Kadasne's Textbook of Embryology PDF

Contents i
Kadasne’s
TEXTBOOK OF EMBRYOLOGY
Kadasne’s
TEXTBOOK OF EMBRYOLOGY
DK Kadasne MS FRCS FICS

Emeritus Professor of Anatomy
Pandit Jawaharlal Nehru Medical College
Datta Meghe Institute of Medical Sciences
(A Deemed University)
Sawangi, Wardha, Maharashtra, India
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Kadasne’s Textbook of Embryology

© 2011, Jaypee Brothers Medical Publishers
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First Edition: 2011
ISBN 978-93-5025-152-2
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Printed at
Dedicated to
The Sacred Memory
of
My late beloved
Parents
FOREWORD
DK Kadasne is known to me for the last 50 years. He was my junior colleague in the Department
of Anatomy at the Government Medical College, Nagpur, Maharashtra, India for a period of 12
years. He was extremely popular with the students as his teaching was making anatomy clearly
understandable to them. He is a born teacher, very comfortable with teaching students. Later he
went to the UK, and because of his lucid understanding and knowledge of anatomy, he did his
FRCS in general surgery from Royal College of Surgeons of Edinburgh (UK) in a short period of
one year. After returning from the UK, he was offered the post of professor and the head of
department of anatomy at BJ Medical College, Pune. However, this surgeon anatomist preferred
to join as Civil Surgeon, Jalgaon. During 20 years of his tenure of civil surgeon, he did incredible
job in rendering service to the poor and needy. At the same time, his contribution to the general
up-keep, cleanliness of the hospitals, patient care, public relations and administrative skill is
remembered by the authorities and the masses even today.
He is already an author for his three-volume book on anatomy entitled as Kadasne’s Textbook of
Anatomy (Clinically Oriented) published by M/s Jaypee Brothers Medical Publishers (P) Ltd. It
must be mentioned here that all the figures in the textbook are drawn by Dr Kadasne himself. I
consider this as a unique accomplishment for the author, for the book in general and the anatomy
in particular. At present, he is Professor Emeritus at Pandit Jawaharlal Nehru Medical College,
Sawangi, Datta Meghe Institute of Medical Sciences, A Deemed University, Sawangi, Wardha,
Maharashtra, India. I am glad that he has written the textbook on human embryology and I am
sure with his genius and sincere efforts that the book will be accepted well by students as well as
teachers. The striking thing which I have found in Kadasne’s book is excellent, linear and
reproducible diagrams. The highlight of the book is the presentation of beautiful clinical
photographs related to the subject.
At last, I would like to mention that this book of embryology is a perfect example of the definition
of a very good book.
I wish the book to be a great success.
BR Kate MBBS, MS, FAMS

Retired Director of Medical
Education and Research
Maharashtra, India
PREFACE
Kadasne’s Textbook of Embryology is written with the sole object of making the subject clearly
understandable and interesting. Study of embryology should not be done in isolation, on the
other hand, it should be the integral part of the subject of anatomy as a whole. The contents of the
book is the representation of my lectures on human embryology.
Every structure in the body has the hidden surgical and clinical thrill of practical importance.
It is only on the foundation of embryology and anatomy that the clinical sciences have progressed
to the stage of organ transplant. The non-invasive techniques of investigation have acted as a
boon for embryology and anatomy in its further research.
“No book is complete and no book can be comprehensive!”
DK Kadasne
ACKNOWLEDGMENTS
I am thankful to Mr Datta Meghe, MP and Chancellor of the Datta Meghe Institute of Medical
Sciences (DMINS) who gave me an opportunity to enter the academic field of teaching anatomy, in
addition to my surgical practice is the major factor which inspired me to write a book of this type.
I am also thankful to Mr Sagar Meghe, MLA who played a pivotal role in keeping me engaged
in the teaching of anatomy. Dr Dilip Gode, presently the Professor of Surgery in Pt JNM College,
Sawangi, Wardha has always acted as my well-wisher and supporter, which I can never forget.
I am indebted to Late Dr Joharapurkar, Director, Datta Meghe Institute, Department of Post-
Graduate Research and Medical Education and the member of the management council for
encouragement and support. My thanks are due to Dr Deshpande, the Dean of the Pandit Jawaharlal
Nehru Medical College, Sawangi for appreciation. Dr (Mrs) Jayashree Deshpande, Prof and Head
of Department of Anatomy, Dr (Mrs) Fulzele Prof of Anatomy of the Pandit Jawaharlal Nehru
Medical College, Sawangi deserve grateful thanks for meaningful discussions. Dr Yogesh Sontakke
MD Anatomy of Cytogenetics and Assistant Professor, Department of Anatomy, JN Medical College,
Sawangi, Wardha was instrumental in writing the chapter on genetics, I am thankful to him for his
generous help and assistance.
I could not have presented the book in the present form without the generous donation of the
clinical material by my friends who are renowned experts in their respective fields. Dr Shirish
Dhande, a renowned radiologist of the city made the X-rays and the MRI available.
My grateful thanks to Dr Vedprakash Mishra, Vice Chancellor of the DMIMS University,
Sawangi, Wardha, and the Chairman of Postgraduate Medical Education Committee, Medical
Council of India, New Delhi, a doyen in the science of physiology for appreciation and time-to-
time encouragement.
I feel honored as Dr BR Kate Retired Director of Medical Education and Research, Maharashtra
has willingly consented to write the foreword for the book.
Dr Prakash Heda of Nairobi, student and friend of mine has constantly been remained by my
side whether it is in India or abroad. I thank him sincerely.
I am grateful to Dr (Mrs) Sushma Deshmukh, Gynecologist, Dr Ravi Deshmukh, urosurgeon,
Dr Tule, pediatric surgeon and Dr Parimal Fukey, Dr Dinesh Singh, Dr Sudhanshu Kothe, Dr BK
Sharma, Dr Madan Kapre, ENT surgeon, Nagpur for clinical photographs, Dr Anupam Dasgupta,
Dean of Lata Mangeshkar College of Medical Sciences, Nagpur. My thanks are due to Dr Sunil
Deshpande, physician for appreciation of my work from time to time.
Dr SD Suryawanshi Retd Prof and Head of Department of Medicine, Indira Gandhi Medical
College, Nagpur, acted as constant critic of mine during the preparation of this book. I thank him
profusely. Dr (Mrs) Rajani Suryawanshi, Gynecologist provided the material on hydatid mole.
My sincere thanks to Mr Dr Vikrant Sawaji, Dermatologist, Nagpur who was very helpful and
enthusiastic to provide clinical photographs for the chapter on the development of skin and its
anomalies.
xii Kadasne’s Textbook of Embryology
I have all the appreciation for the work done by Manoj Dharmadhikari for computerized typing
of the manuscript of this book. Mr Avinash Kokate did an excellent work in reproducing the
diagrams drawn by me in the form of beautifully colored pictures.
My better-half Mrs Arti Kadasne took pains to go through the manuscript and helped me
untiringly till the completion of the book.
My sincere thanks are due to Dr Shivraj Mulik, ophthalmic surgeon who provided superb
photographs of coloboma iris. Dr BJ Chikodi, ex-civil surgeon and Dr JS Mulik, ophthalmic surgeon
encouraged me in the production of this book. I expressed my gratitude to them.
My thanks are due to Dr Padole, surgeon and Dr Neral, and Dr Jape, radiologists for their
encouraging comments and helpful hands.
Dr (Mrs) Pushpa Jagtap, Ex-Dean of Indira Gandhi, Medical College, Nagpur and her brilliant
sons Dr Prashant, cardiovascular surgeon of Wockhardt Hospital, Nagpur, and Dr Satyajeet Jagtap
renowned orthopedic surgeon have extended helping hands wholeheartedly, I cannot forget them.
Dr Mangrulkar took pains to provide necessary photographs and their reproduction, I am
grateful to him.
Dr KN Ingle, Professor of Pandit Jawaharlal Nehru College, Sawangi, Wardha has always
acted as a source of inspiration. Dr Dhananjay Patrikar, radiologist assisted me in providing
necessary radiological pictures, I thank him sincerely.
I am grateful to Shri Jitendar P Vij, CMD of M/s Jaypee Brothers Medical Publishers (P) Ltd,
New Delhi for publishing this book. I acknowledge the contribution of Mr Tarun Duneja (Director-
Publishing) and his team members, who deserve my sincere thanks. Mr AV Gujar, Author Co-
ordinator of the Publishers acted as a driving force during the entire period of production of this
book, I am extremely grateful to him. Mr Prasun Bhattacharjee, Branch Manager acted as an
inspiring force during the production of this book, I thank him profusely.
I am extremely grateful to my beloved students who always appreciated and inspired me for
teaching the subject.
I am extremely grateful to Almighty who allowed me to complete my desired object.
I am under the heavy obligations of Almighty for allowing me to complete this work.
CONTENTS
1. Embryology ........................................................................................................................................... 1
Let Us See Some of the Terms Used in the Embryology 1; Let Us Get Familiar with the
Terms often Used in Embryological Text 1; Growth 2; Turnover 2; Auxetic Growth 2;
Totipotent 2; Chemodifferentiation 3
2. ABC of Genetics .................................................................................................................................. 4
Study of the Common Terms Used in Genetics 4; Allele 4; Genes 5; Autosomal Domi-
nant Disorders 5; Autosomal Recessive Disorders 6
3. Introduction to Chromosomes and Cell Division ......................................................................... 7
Chromosomes 7; Structure of Chromosomes 7; Classification of Chromosomes 7; Karyo-
typing 8; Functions of Chromosomes 8; Chromosomal Abnormalities 8; Deletion 11;
Cell division 11; Mitosis 11; Meiosis 12; Stem Cells 13; Parkinson’s Disease 14;
Alzheimer’s Disease 14; Blood Diseases 14; Spinal Cord Injury 14
4. Development of the Tissues of the Body ...................................................................................... 15
Epithelia 15; Development of Glands 15; Glands Arising from Ectoderm 15; Glands
Arising from Mesoderm 15; Glands of Mixed Origin 15; Mesenchyme 16; Connective
Tissue 16; Blood Formation 16; Histogenesis of Cartilage 16; Histogenesis of Bone 17;
Enchondral Ossification 18; Development of Long Bone 18; Epiphyseal Zones 18; Meta-
physis 19; Anomalies of Bones 19; Development of Striated Muscle 20; Sclerotome 21;
Dermatome 21; Myotome 21; Development of Smooth Muscle 21; Cardiac Muscle 22;
Development of the Neurones 22; Spongioblast 23; Formation of Myelin Sheath 23
5. Structure of Sperm ............................................................................................................................ 25
Head 26; Body 26; Tail 27; Spermatogenesis 27; Spermatogonia A 28; Ovum 29; Oogen-
esis 29; Formation of Ovarian Follicle 31; Role of Follicular Cells and the Oocyte 34
6. Ovulation ............................................................................................................................................ 35
What Promotes Ovulation? 35; Structure of the Ovum 35; Future of the Ovum 37; Cor-
pus Luteum 37; Corpus Luteum of Menstruation 37; Corpus Luteum of Pregnancy 38
7. Ovarian Cycle ..................................................................................................................................... 41
Ovulation 41
8. Menstrual Cycle ................................................................................................................................. 43
Follicular Phase 45; Secretory Phase (Progestational Phase) 45; Formation of Decidua
46; Menstrual Phase 48
9. Fertilization ........................................................................................................................................ 49
Capacitation 51; Acrosomal Reaction 51; Secondary Oocyte 51; Disintegration of the
Barriers 51; Vitelline Block 52; Effects of Fertilization 52; Parthenogenesis 52; Infertility,
Causes and Remedy 52; In Vitro Fertilization of Female Gamete 53; Surrogate Mother
53; Period of Gestation 53; Determination of Sex 53; Cleavage 54; Role of Zona Pellu-
cida 55; Implantation of Blastocyst 56; Abnormal Implantation of the Blastocyst 56;
Extrauterine Implantation of Blastocyst 57; Definition of Shock 57; Hydatidiform Mole
xiv Kadasne’s Textbook of Embryology
57; Stages of Labor 58; Formation of Germ Layers 58; Formation of Primary Yolk Sac 59;
Formation of Extraembryonic Mesoderm 59; Chorion 61; Amnion 61; Formation of the
Primitive Streak 61; Gastrulation 62; Intraembryonic Mesoderm 62; Paraxial Mesoderm
63; Intermediate Mesoderm 64; Lateral Plate Mesoderm 64; Splanchnopleuric Layer 65;
Neural Tube 65; Formation of Notochord 66; Formation of Secondary Yolk Sac 66; Fold-
ing of the Embryonic Disk 67; Connecting Stalk 68; Allantoenteric Diverticulum 69;
Meckel’s Diverticulum 71; Arrangement of Structures of Embryo before and after the
Formation of the Head and the Tail Folds 72
10. The Placenta ....................................................................................................................................... 75
Types of Implantation 81; Decidua 81; Process of Formation of Villi 82; Development of
Placenta 82; Placental Barrier 83; Aid to Memory 83; Functions of Placenta 83; Normal
Human Placenta is Hemochorial 84; Placental Circulation 84; Abnormal Implantation
of the Ovum 84; Extrauterine Implantation 85; Intrauterine Abnormal Implantation 85;
Anomalies of the Placenta 85; Variations of Umbilical Cord Attachments 85; Placental
Classification as per the Tissues Involved 87; Hormones 88; Placental Estrogen 88;
Action of Placental Estrogen 88; Placental Progesterone 88; Placental Lactogen 88; Pros-
taglandins 88; Placental – Homograft 88; Hydatidiform Mole 89; The Umbilical Cord
90; Wharton’s Jelly 91; Meckel’s Diverticulum 91; Allanto-enteric Diverticulum 92;
Physiological Umbilical Hernia 92; Amniotic Cavity 92; Amniotic Fluid 94; Functions
of Liquor Amnii 94; Amniocentesis 95; Hormones 95; Production of Hormones by
Placenta 95
11. Prenatal Diagnosis of Birth Defects .............................................................................................. 96
Types of Abnormalities 96; Syndrome 96; Association 96; Teratogens 96
12. Methods of Prenatal Disease Detection ........................................................................................ 97
Treatment 97; Stem Cell Transplantation 97
13. Formation of Branchial (Pharyngeal) Arches ............................................................................... 98
First Arch Syndrome (Treacher Collins Syndrome) 99; Derivatives of the First Pharyn-
geal Arch 101; Derivatives of the Second Arch 101; Derivatives of the Third Arch 101;
Skeletal Components Derived by the Pharyngeal Arches 102; Meckel’s Cartilage 102;
Second Arch 102; Third Arch 103; Morphology of the Nerves of the First Arch 103;
Comment on Nerve Supply of Pharyngeal Muscles 103; An Account of the Ectodermal
Clefts 103; Branchial Fistula 104; Branchial Sinus 105; Modern Theory of Branchial Cyst
Formation 106; Branchiogenic Carcinoma 106; Future of the Endodermal Pouches 106;
First Pouch 106; Second Pouch 107; Third Pouch 107; Development of the Thymus 107;
Fourth Pouch 107; Fifth Pouch 108
14. The Skin and its Appendages ....................................................................................................... 109
Epidermis 109; Dermis 110; Nails 110; Hair 111; Sebaceous Gland 111; Sweat Glands
112;Anomalies of the Skin and its Associates 112; Aplasia 112; Dysplasia 112; Alopecia
112; Congenital Alopecia 113
15. Development of Mammary Gland ............................................................................................... 114
Anomalies of the Breast 115
Contents xv
16. The Skeleton ..................................................................................................................................... 116

Cartilage Bones 116; Cleidocranial Dysostosis 117; Development of Vertebral Column
117; Congenital Anomalies of the Vertebral Column 118; Spina Bifida 119; Hemivertebra
119; Anterior Spina Bifida 119; Congenital Fusion of Vertebral Bodies 120; Develop-
ment of Ribs 121; Development of Sternum 121; Accessory Ribs 121; Anomalies of Ribs
and Chest Wall 122
17. The Skull and Limbs ...................................................................................................................... 123
Anomalies of the Skull 124; Radial Club Hand 124; Ulnar Club Hand 125; Radioulnar
Synostosis 125; Pseudoarthorsis of the Clavicle 125; Club Foot (Talipes Equinovarus)
125; Treatment of Club Foot in Early Cases 125
18. Mouth and Teeth ............................................................................................................................. 127
19. Development of Teeth .................................................................................................................... 128
Formation of Temporary or Milk Teeth 131; Formation of Permanent Teeth 132
Anomalies of Teeth132; Inherited Abnormalities 132
20. Development of the Tongue ......................................................................................................... 133
Development of Alveolingual Groove 135; Anomalies of the Tongue 135; Salivary Glands
135; Development of Parotid Gland 135; Submandibular Salivary Glands 135; Sublin-
gual Salivary Glands 136; Tonsil 136; Pharynx 137
21. Development of the Thyroid Gland ............................................................................................ 138
Histogenesis of Thyroid Gland 138; Median Ectopic Thyroid 139; Pyramidal Lobe140;
Lateral Aberrant Thyroid 140; Anomalies of the Thyroid Gland 140; Isthmus 140; Lobes
140; Abnormal Sites of Thyroid 140; Sites of Ectopic Thyroid Tissue 141; Anomalies of
the Thyroglossal Duct 141; Thyroglossal Cyst 141; Thyroglossal Fistula or Sinus 142;
Treatment of Thyroglossal Fistula 142
22. Development of Parathyroids ....................................................................................................... 143
23. Development of Face ...................................................................................................................... 144
Nose 145; Intermaxillary Segment 147; Cleft Lip 148; Oblique Facial Cleft 149; Median
Cleft Lip 150; Nasal Cavities 150; Vomeronasal Organs of Jacobson 151
24. Development of Palate ................................................................................................................... 152
Secondary Palate 152; Anomalies of the Palate 152; Anomalies of Lip, Palatal and the
Drugs 155; Other Anomalies of the Face 155
25. Body Cavities ................................................................................................................................... 156
Mesothelium 157; Separation of Cavities 157
26. Development of Respiratory System ........................................................................................... 158
Development of Larynx 159; Lungs 160; Bronchopulmonary Segments 162; Anoma-
lies of the Larynx 162; Anomalies of the Trachea 162; Anomalies of the Lung 163
27. Development of Diaphragm ......................................................................................................... 166
Separation of Pericardial, Pleural and the Peritoneal Cavities 167; Anomalies of the
Diaphragm 168; Congenital Diaphragmatic Hernia 168; Parasternal Hernia 168; Fora-
men of Bochdalek 169; Eventration of Diaphragm 169; Accessory Diaphgram 169
28. Alimentary System .......................................................................................................................... 170
Esophagus 172; Esophageal Stenosis 172; Congenital hiatal Hernia 172; Esophageal
Atresia 173; Highlight of Ten’s 174; Achalasia Cardia 174; Dysphagia lusoria 174; Stom-
ach 175; Formation of Curvatures 177; Histogenesis of the Stomach 177; Congenital
xvi Kadasne’s Textbook of Embryology
Anomalies of the Stomach 177; Congenital Hypertrophic Pyloric Stenosis 177; Forma-
tion of Lesser Sac or Omental Bursa 177; Development of Spleen 179; Histogenesis of
the Spleen 179; Anomalies of the Spleen 179; Duodenum 180; Anomalies of the Duode-
num 180; Duodenal Atresia 180; Duodenal Stenosis 180; Duodenal Diverticuli 181;
Development of Liver 181; Congenital Anomalies of Liver 183; Development of the
Gallbladder 183; Anomalies of the Biliary Apparatus 183; Biliary Ducts (Extrahepatic)
184; Atresia 184; Development of Pancreas 186; Histogenesis of Pancreas 188; Annular
Pancreas 188; Ectopic Pancreatic Tissue 188; Inversion of the Pancreatic Ducts 188; De-
rivatives of the Midgut 189; Development of Jejunum and Ileum 189; Development of
Cecum and Appendix 189; Development of Ascending Colon 190; Development of
Transverse Colon 190; Development of Descending Colon 191; Development of Rec-
tum 191; Endodermal Cloaca 191; Development of Anal Canal 191; Anomalies of the
Hindgut 193; Congenital Megacolon (Hirschsprung's Disease)193; Common Cloaca 193;
Rectovesical Fistula 193; Rectovaginal Fistula 194; Rectourethral Fistula 194; Imperfo-
rate Anus 195; Ectopic Anus 195; Physiological Herniation 195; Rotation of the Midgut
195; Formation of Mesentery 197; Congenital Umbilical Hernia 199; Comparison
between Omphalocele and Gastroschisis 199; Anomalies of Vitellointestinal Duct 199;
Duplication and Diverticuli of the Gut 200; Jejunal Diverticuli 201; Meconium 201;
Errors of Rotation 201; Errors of Fixation 202; Situs Inversus 202; Recall of the Develop-
mental Anomalies of the Gut 202
29. Cardiovascular System ................................................................................................................... 203
Atria 204; Division of Atrioventricular Canal 205; Separation of Primitive Atrium 205;
Formation of Septum Primum 207; Development of Atria 208; Absorption of Sinus
Venosus into the Right Atrium 208; Absorption of Pulmonary Veins 209; Development
of Aorticopulmonary Septum 210; Primitive Ventricle and Part of the Right Atrium
210; Ventricular Cavity 212; Formation of the Valves of the Heart 213; Development of
Aortic and the Pulmonary Valves 213; Conducting System of the Heart 214; Pericar-
dial Cavity 214; Formation of Sinuses of the Pericardial Cavity 216; External Form of
Heart 216; Congenital Anomalies of the Heart 216; Arch Arteries 220; Patent Ductus
Arteriosus 223; Aortic Arches and their Derivatives 224; Highlights of 4 225; Coronary
Artery Dominance 225; Brachiocephalic Artery 225; Right Subclavian Artery 226; De-
velopment of Left Subclavian Artery 226; Development of Common Carotid Artery
226; Internal Carotid Artery 226; Descending Aorta 228; Pulmonary Arteries 228; De-
velopmental Anamolies of the Arch Arteries 228; Septal Anomalies 229; Abnormal Right
Subclavian Artery 229; Aortic Stenosis 229; Coarctation of Aorta 230; Branches of
Dorsal Aorta 230; Pre-costal Anastomosis 231; Seventh Cervical Intersegmental Artery
231; Derivatives of Anastomoses 232; Formation of the Vertebral Artery 232; Internal
Mammary Thoracic Artery 233; Limb Arteries-Upper Limb 233; Anomalies of the Ra-
dial Artery 233; Right Subclavian Artery 234; Lower Limb 234; Axis Artery of the Lower
Limb 234; Umbilical artery 234; Veins of the Embryo 235; Portal Vein 237; The Umbili-
cal Veins 239; Cardinal Veins 239; Development of Intracranial Venous Sinuses 240;
Cavernous Sinus 240; Sigmoid Sinus 240; Transverse Sinus 240; Superior Petrosal Sinus
241; Inferior Petrosal Sinus 241; Sagittal Sinus 241; Left Brachiocephalic Vein 241; Inter-
nal Jugular Vein 241; Superior Vena Cava 241; Double Superior Vena Cava 244; Left
Superior Vena Cava 244; Posterior Cardinal Veins 244; Subcardinal Veins 244;
Contents xvii
Supracardinal Veins 245; Azygos Venous Lines 245; Subcentral Veins 247; Renal Collar
247; Formation of the Inferior Vena Cava 247; Anomalies of the Inferior Vena Cava
248; Double Inferior Vena Cava 248; Retrocaval Ureter 248; Development of Left Renal
Vein 248; Fetal circulation 249
30. Development of Lymphatic System ............................................................................................ 252
Development of Thoracic Duct 252
31. Urogenital System ........................................................................................................................... 255
Development of Kidney 256; Pronephros 257; Mesonephros 258; Metanephros 258;
Ascent of the Kidney 260; Rotation of Kidneys 261; Juxtaglomerular Apparatus 261;
Probable Causes of Rotation of the Kidney 261; Anomalies of the Kidneys 261; Hydro-
nephrosis 262; Anomalies in the Ascent of Kidneys 262; Defects of Rotation 264; Con-
genital Polycystic Kidney 264; Congenital Polycystic Kidney is of Two Types 264; Treat-
ment 264; Aberrant Renal Artery 265; Dietl’s Crisis 265; Absorption of Caudal Part of
the Mesonephric Ducts into the Cloaca 265; Development of the Ureter 266; Anomalies
of the Ureter 266; Development of the Urinary Bladder 268; Congenital Anomalies of
the Urinary Bladder 268; Development of the Female Urethra 270; Development of the
Male Urethra 270; Anomalies of the Urethra 271; Development of Prostate 272; Female
Homologues of Prostate 274; Paramesonephric Duct 274; Development of the Uterus
274; Anomalies of the Uterus 276; Anomalies of the Uterine Tubes 276
32. Development of Vagina .................................................................................................................. 277
Summary of Development of Vagina 277; Anomalies of the Vagina 278; Paramesonephric
Ducts in Males (Mullerian Ducts) 278; Development of External Genitalia 279; Devel-
opment of Female External Genitalia 279; Development of Male External Genitalia 279;
Development of Male Urethra 279; Prenatal Diagnosis of Sex 281; Anomalies of Male
External Genitalia 282; Anomalies of Female External Genitalia 282; Development of
Testes 283; Duct System of Testis 284; Descent of Testis 285; Processus Vaginalis 286;
Anomalies of the Testis 288; Ectopic Testis 289; Tails of Lockwood 290; Anomalies of
the Duct System of Testis 291; Anomalies of the Processus Vaginalis 291; Develop-
ment of the Ovary 291; Descent of the Ovary 293; Succus Vaginalis in Females 293;
Anomalies of the Ovary 293; Derivatives of the Mesonephric Duct 293; Remnants of
Mesonephric Tubules 294; Factors Responsible for Determination of the Sex 295; True
Hermaphrodite 296; Pseudohermaphroditism 296; Greater Vestibular Glands 296; Com-
parison between Bulbourethral and Greater Vestibular Glands 296
33. Nervous System ............................................................................................................................... 297
Nervous System 297; Neural Tube 297; Cavities of the Brain 298; The Neural Crest 298;
Spinal Cord 300; Neurons of the Posterior Gray Column 301; Histogenesis of the Neu-
ral Tube 302; Medulla Oblongata 304; Pons 304; The Midbrain 305;
34. Cerebellum ........................................................................................................................................ 307
Formation of Peduncles 308; Formation of Cerebral Hemisphere 309; Development of
Thalamus and the Hypothalamus 311; Development of Corpus Striatum 311; Cerebral
Cortex 313; Commissural Fibers 314; Association Fibers 314; Interconnecting Axons
314; Asending Fibers 314; Cerebral Commissures 315; Anomalies of the Brain and the
Spinal Cord 315; Variation of Spina Bifida 315; Arnold-Chiari Deformity 316; Dandy
xviii Kadasne’s Textbook of Embryology
Walker Syndrome 317; Hydranencephaly 317; Autonomic Nervous System 317; Para-
sympathetic Neurons 318; Sacral Parasympathetic Outflow 319
35. Ear ...................................................................................................................................................... 320
Development of the Internal Ear 320; Middle Ear 321; External Ear 323; Auricle 324;
Congenital Anomalies of the Ear 325
36. Eye ...................................................................................................................................................... 327
Development of Retina 330; Development of Ciliary Body 331; Development of Iris
331; Development of the Lens 332; Development of the Anterior and Posterior Cham-
ber of the Eye 333; Development of the Cornea 333; Development of the Choroids and
the Sclera 334; Eyelids 334; Ptosis 335; Lacrimal Gland 335; Nasolacrimal Duct 335;
37. Hypophysis Cerebri ........................................................................................................................ 338
38. Pineal Gland ..................................................................................................................................... 340
39. Adrenal Gland ................................................................................................................................. 341
Adrenal Gland 341; Anomalies of the Adrenal Gland 342; Chromaffin Tissue 342
40. Formation of Limbs ......................................................................................................................... 343
The Skull of Newborn 343; Functions of the Fontanelle 343; Joints 344; Other Anoma-
lies of the Limbs 345; Story of Thalidomide 346
41. Age of an Embryo ............................................................................................................................ 347
42. Twining ............................................................................................................................................. 348
Dizygotic Twins 348; Monozygotic Twins 349; Parasitic Twins 351
43. Role of Ultrasound in Pregnancy ................................................................................................. 352
44. Stages in Embryology ..................................................................................................................... 354
Highlights of the 2nd Week 354
Prologue to Human Molecular Biology ........................................................................................ 355

Index .................................................................................................................................................... 357
Embryology 1
Embryology
1
Embryology is the study of intrauterine development of an individual. Total period of development
is of 38 weeks. The development is divided into two stages, i.e. embryonic and fetal. Embryonic
stage covers first two months while the fetal period of development runs from 3rd month to the
birth. Embryonic period is important as the embryo obtains human look during the period. This is
due to the development of organs and different systems of the body.
Organisms are added to the world as a continuous stream due to reproduction. One must
remember that elimination (extinction) of species is prevented by adding new generations by
reproduction. For reproduction in vertebrates, male and female are required. Sex cells are produced
by sex glands known as gonads. Testes are the male gonads and the ovaries are the female.
Intrauterine development total period 38 weeks
Embryo Fetus
0-2 months 3 months to birth
Let Us See Some of the Terms Used in the Embryology

1. Ontogeny: It is an account of complete life cycle of an organism.
2. Phylogeny: It includes evolutionary or ancestral history of a group of organisms. In the ascending
order are the pisces, amphibians, reptiles, avians and the mammals at the top.
Let Us Get Familiar with the Terms often Used in Embryological Text
1. Oocyte: Female germ cell produced by ovary.
2. Sperm: Male germ cell produced by testes.
3. Fertilization: Union of male and female gametes.
4. Zygote: It is a cell formed after union of male and female gametes (see fertilization).
5. Cleavage: Cell division by mitosis.
6. Blastomere: Early embryonic cell, formed as a result of division of zygote, size of the zygote
remains unchanged as the size of the cells formed after division, continues to become smaller.
2 Kadasne’s Textbook of Embryology
7. Morula: Means one which looks like a mulberry fruit. Morula is a compact mass of cells formed
by 16 cell (The cells may vary from 12-32).
8. Blastocyst: Fluid enters the morula forming a fluid lake inside the morula. Morula which is
transformed into the fluid-filled cavity is called the blastocyst. Cells divide to form inner and
outer cellular mass. The inner cell mass forms the embryo which is called the embryoblast.
9. Primordium: It is the early form.
10. Implantation: Attachment of blastocyst to the endometrium and its embedding in the
endometrium.
11. Gastrula: Formation of three germ layers, e.g. endoderm, mesoderm and the ectoderm.
12. Neurula: Formation of neural tube from the neural plate.
13. Conceptous: Structures derived from the zygote and the embryonic part.
14. Abortion: Expulsion of embryo or the fetus before maturation.
15. Habitual abortion: Spontaneous expulsion of the nonviable embryo or the fetus from the uterine
cavity successively for more than three times.
16. Missed abortion: Retention of the embryo or the fetus in the uterine cavity after death.
17. Trimester: Duration of first three calendar months.
18. Teratology: Deals with abnormal development.
Growth
It includes increase in cell number, cell size and the intercellular substance.
Turnover
Cells of the epidermis and circulating erythrocytes are lost due to wear and tear. They are replaced
by stem cells through mitosis. Thus, the cell population is maintained at the optimum level.
Maintenance of steady state of cell population is called ‘Turn over’.
Auxetic Growth
It is observed in oocytes and some neurones. Large cell lies in the center surrounded by the small
cells. Example: oocytes are surrounded by follicular cells while the neurons are surrounded by
neuroglial cells. Accretionary growth is by increase in quantity of the intercellular substance, which
is seen in bones and cartilages.
Totipotent
Following division of zygote (first cleavage) two cells are formed (two-cell stage). Now each cell
can form separate embryo having three germ layers, e.g. ectoderm, endoderm and mesoderm.
This explains formation of uniovular twins. Totipotent character of the cells exists only up to the
8-cell stage. After 8-cell stage, morula is formed (16-cell stage). Cells of the morula become
pluripotent which are capable of producing specific types of tissues. This phase is also called the
plastic phase.
Embryology 3
Chemodifferentiation
It is the physiochemical event seen in the cells of the dorsal lip of the blastopore and the primitive
streak of the higher vertebrates. This cellular zone of embryo is capable of inducing the process of
tissue differentiation through chemical substances. Hence, these cellular zones are called organizers.
Primitive streak becomes the primary organizer for inducing formation of notochord and the
mesoderm. Notochord becomes the secondary organizer forming the brain and the spinal cord
from the neuroectodermal plate.
Now the neural tube becomes the tertiary organizer and forms the somites (paraxial mesoderm).
Chemodifferentiation is followed by histodifferentiation and later by the organogenesis. Hemodynamics
of the circulation makes the walls of the arteries thicker. Thus, the structural change related to the
function is called functional differentiation.
Importance of embryology in medicine:
1. With the study of development, anatomical relations can be explained and better understood.
2. One gets an insight regarding the abnormal development, their prenatal detection, prevention
and treatment.
3. Use of alcohol, smoking, drugs, viral infections and teratogens including the external
envirnoment are blamed for the abnormal development. The incidence of the abnormal
development can be reduced to the minimum by rendering advice and adopting preventive
measures.
4. Ex-utero surgery for congenital diaphragmatic hernias, removal of the cyst and repairing of
the spinabifida is possible, only due to in-depth study of the embryology by the medical faculty.
ABC of Genetics
of
2
Study of the Common Terms Used in Genetics
Depletion: It means loss of a segment of the chromosome.
Invertion: After detachment the detached segment joins the same chromosome in inverted position.
There is no loss of genes, however, their sequence gets changed due to changed loci.
Isochromosomes: The centrosomes of the chromosomes split transversely in place of normal
longitudinal. This forms chromosomes of different lengths. The chromosomes formed as a result
of transverse splitting of the chromosomes are called isochromosomes.
Ring chromosomes: When the part of the chromosome is detached at both the ends, the detached
sticky ends join and form a ring.
Duplication: In this, the portion from the other homologous chromosomes with duplication of genes
occurs.
Translocation: When there is exchange of segments between nonhomologous chromosomes, it is
called translocation.
Polyploidy: In this, the number increases by multiple of haploid (23) chromosomes. This can occur
due to fertilization of an ovum by two sperms seen in formation of hydatidiform mole. Now the
zygote has two male pronuclei and one X-chromosome. In pregnancy, trophoblastic membranes
are formed however, there is no formation of an embryo. Maternal chromosomes regulate
embryoblast while the paternal chromosomes regulate the development of the trophoblast. It is
obvious from the above phenomenon that it is the maternal chromosomes which regulate
development of an embryo and the paternal chromosomes regulate development of the trophoblast.
(Mother forms the fetus and father provides nutrition).
Allele
One of the two or more genes occupy corresponding positions (loci) on paired chromosomes. The
person with the pair of identical alleles either dominant or recessive is said to be homozygous for
this gene. Union of a dominant and its recessive alleles produces heterozygous individual.
Heterozygous: It means having different alleles at a given position (locus).
Homozygous: It means produced by similar alleles.
ABC of Genetics 5
Genes
• Genes are the units of heredity.
• They are carried by deoxyribonucleic acid (DNA).
• About 30,000-40,000 genes are present in total human genome with 3 billion base pairs.
• Locus is the position of the gene on chromosome.
• Genes cannot be observed under microscope like chromosomes.
• Genome is the full set of genes of an individual.
• Genotype is the genetic constitution of an individual.
• Phenotype is the physical or biochemical expression of the genotype.
• Allelomorphs or alleles are the genes having identical loci on homologous chromosomes.
• If both allelomorph genes regulate similar characters, they are homozygous and if nonsimilar
characters then they are heterozygous.
• Recombination: During crossing over in meiosis there is exchange of genetic material between
homologous chromosomes. This produces recombination of gene.
• Mutation:
– Definition: Mutation is the change in a base pair of DNA molecule. It is also known as
point mutation.
– Due to the mutation, altered protein may be produced with alteration in biological function
of that protein.
– Mutations may be spontaneous or induced by various chemicals and physical agents.
– Mutagenic substances are the agents which induce mutation, e.g. X-rays, gamma rays,
atomic radiations, mustard gas, etc.
• Classification of inheritance/genes:
Inheritance depends upon the gene which may be dominant of recessive in nature.
– Dominant gene: Dominant gene always expresses character when the allelic genes are either
homozygous or heterozygous, e.g. gene for tallness.
– Recessive gene: Recessive gene expresses character only when allelic genes are homozygous,
e.g. gene for shortness.
Carrier: Carrier is the person with heterozygous recessive gene which may express in subsequent
generations.
Autosomal Dominant Disorders

Marfan’s syndrome: Elongated extremities, dislocation of lens of eyes, cardiovascular abnormalities.
Nail-patella syndrome: Dystrophy of nails, absence of patella.
Achondroplasia: An inherited skeletal disorder beginning before birth. Cartilage converted to bone
resulting in dwarfism.
Huntington’s chorea: A CNS disorder which affects muscle coordination and some cognitive function.
Multiple neurofibromatosis: A genetic disease in which multiple soft tumors develop under the skin
and throughout the nervous system.
Osteogenesis imperfecta: An autosomal dominent disorder of connective tissue characterized by brittle

bones that fracture easily.
Autosomal Recessive Disorders

Hemoglobinopathies such as sickle cell anemia, thalassemia.
Alkaptonuria: There is excretion of a large amount of homogentisic acid in the urine as a result of
incomplete metabolism of tyrosine and phenylalanine.
Galactosemia: Inability to metabolize galactose into glucose due to congenital absence of enzyme.
Phenylketonuria: Inability to metabolize a protein called phenylalanine.
Tay-Sach’s disease: It is a most severe type of lipoid storage disease, marked by neurological
deterioration in the first year of life.
Introduction to Chromosomes and Cell Division 7
Introduction to
Chromosomes and
3 Ce ll Division
Cel
Chromosomes
Chroma means color and soma stands for the body, i.e. colored body. Chromosomes stain deeply
with basic dyes and are prominent during mitosis. In every species including man, the total number
of chromosomes is fixed as the 46. Out of these 44 chromosomes are known as autosomes and the
remaining two as the sex chromosomes. In male, they are X and Y while in female they are X and
X. The Y chromosomes is the sex deciding factor. Chromosomes are arranged in pairs. Genes located
on the chromosome are made of nucleic acid known as deoxyribonucleic acid (DNA). The site of
gene location is called the locus.
Structure of Chromosomes (Fig. 3.1)

Chromosomes are visible only during the cell
division due to the fact that the chromatin of
the nucleus gets condensed. Each chromosome
is made of two rod-shaped structures which are
known as chromatids. Chromatids lie parallel
to each other. Union of the chromatids occurs
at a site which is known as the centromere or
kinetochrome. Each chromatid presents two
arms, long and the short. Based on the total
length, length of the short and long arms
chromosomes are classified. This method of
classification of the chromosomes is known as
karyotyping.
Fig. 3.1: Typical chromosome
Classification of Chromosomes— According to Location of the Centrosome (Fig. 3.2)

Human chromosomes are classified in seven groups from A to G.
Fig. 3.2: Classification according to the position of centromere
Karyotyping
Chromosomes are arranged in order. Longest chromosomes is put first and the shortest at the last.
In case, there are more than one pair of the chromosomes having same length, the metachromatic
chromosomes is put first. Each chromosome is identified according to the length, position of
centromeres and the satellite bodies on their arms. Karyotyping helps in finding chromosomal
abnormalities.
Functions of Chromosomes
All the information regarding the formation of the various tissues and the organs of the body are
inherited through the chromosomes. Chromosomes can be considered as treasure of information.
Chromosomal Abnormalities
Philadelphia Chromosomes
It is an abnormal chromosome 22 in which there is translocation of the distal portion of the long
arm to the chromosome 9. It is found in many patients with chronic myelocytic luekemia. In this
condition autosomes are affected.
Nondysjunction
At first meiotic division, two chromosomes of a pair do not separate at anaphase and prefer to go
to the same pole. It is known as non-dysjunction. As a result, the gamete formed has 24 chromosomes
in place of 23. When the gamete is fertilized, the zygote has 47 chromosomes. There are three
identical chromosomes instead of one of the normal pair. Hence called trisomy.
Trisomy of chromosomes 21 is seen into Mongolism (Down’s syndrome) which is due to
affection of autosomes.
Particulars of the Down’s syndrome are

1. Broad face
2. oblique palpebral fissures
3. Furrowed lip
4. Broad hands with single transverse palmar line
5. Mental retardation
6. Congenital heart defects
Presence of extra X or Y chromosome causes different syndromes which exhibit abnormal
growth, abnormal genital development and mental retardation, e.g. XXX (Abnormal female) and
XXY abnormal male.
XXY (Klinefilter syndrome) As it has Y chromosome the individual is male and has poor testicular
development, sterility and gynecomastia. Subjects with XXX chromosomes present two masses of
sex chromatin in their cells. Although they are called super female, the adjective ‘super’ is improper.
They have poor sexual development with scanty menstruation and mental retardation. In this
condition sex chromosomes are affected.
When both the chromosomes of a pair prefer to go to one gamete resulting gamete has only
22 chromosomes in place of 23. Therefore zygote has 45 chromosomes. One pair being represented
by a single chromosome, it is known as monosomy, e.g. Turner’s syndrome. In this condition, sex
chromosomes are affected.
Turner’s syndrome
Subject is female with only X chromosome.
• It is monosomy
• Due to the absence of Y chromosome, the subject is always female
• They have agenesis of ovaries
• Webbed neck
• Skeletal defects
• Mental retardation.
At times the gamete has diploid number of chromosomes, naturally the zygote has 46 + 23 =
69 chromosomes (Triploidy). Fetus born in this category is invariably born dead. When the part of
the chromosome gets attached to the chromosome of different pair, it is known as translocation.
Fragile sites (Martin-Bell Syndrome)

In this condition, sex chromosome are affected. Abnormal gaps are seen in the staining pattern of
some chromosomes. They are known as fragile sites. When X chromosome is affected with fragile
site. It presents with:
1. Mental retardation.
2. Skeleton deformities
3. Other anomalies
It is known as fragile X syndrome or Martin-Bell syndrome.
Barr Body (Fig. 3.3A)

One of the X chromosomes remains
synthetically inert. It is heterochromic
planoconvex structure, present on the inner
side of the nuclear membrane of the somatic
cells in female, is called Bar body. It represents
inactivated X chromosome. Commonly
the cells from the oral mucosa are taken for
the purpose. Within the nuclei of the
polymorphonuclear leukocyte drumstick
bodies are present (Fig. 3.3B). The number of Fig. 3.3A: Barr body
Barr bodies in the cell is equal to the number
of X-chromosomes less one.
• XX chromosome—has one Barr body
• XXX (Triple X)— has two Barr bodies.
• The female of Turner’s syndrome has only
one X chromosome and therefore no Barr
body.
• Male of Klinefilter’s syndrome has XXY
chromosome has one Barr body.
Barr bodies help in nuclear sexing of the
tissues.
Fig. 3.3B: Polymorphonuclear leukocyte
Note: Murray Barr Canadian anatomist
described barr in 1908.
Cri-du-chat syndrome
The child has hypertellorism, round face, micrognathia, mental retardation and child cries and the
cry is similar to that of a cat. In this condition, autosomes are affected.
Patau’s syndrome
Subject has gross brain malformation, macrophthalmia, hare lip or cleft palate, polydactyly and
other congential malformations. The survival of the subject is short, i.e. hardly for few weeks. In
this condition autosomes are affected.
Edward’s syndrome
It is due to trisomy 18. The subject has long head, broad and flat nose, low-set ears, micrognathia,
contraction of fingers, rocker bottom foot due to vertical talus and congenital heart malformation.
The life of the subject is short, i.e. dies within a few weeks. In this condition, autosomes are affected.
XYY syndrome
The subject is male and is abnormally tall, i.e. above 6 ft with unsound mind, agressive nature and
antisocial in behavior.
Deletion
When the part of the chromosome gets lost it is called deletion. Two chromosomes from the pair
may get broken into unequal segments. After joining the opposite chromosome they may present
with different lengths. One which gets longer than normal have some of the genes duplicated and
the chromosome which gets shorter, has missing genes. When a piece of the chromosome gets
inverted before joining it is called inversion. This does not change the number of genes however
their sequence undergoes gross alteration.
When chromosomes split transversely, they produce two different chromosomes. One
chromosome is formed by the short arms of the both the chromosomes and the other is formed by
the long arms of both the chromosomes (Isochromosomes). When the chromosomal error occurs
during segmentation of the ovum, fetus is having combination of cells with normal and abnormal
chromosomes (Mosaicim).
Cell Division
Cell multiplication occurs due to division of
the cell. Cell division is an important part of
the development. Its death and replacement
are the vital phases of embryonic growth.
During cell division the genetic information is
passed to the daughter cells. As a result, the
daughter cells have the same number of
chromosomes having genetic material similar
to that of the mother. This process of division
is known as mitosis. Second type of division is
known as meiosis which occurs in formation of
gametes. The cell formed as a result of meiotic
division contains half the number of
chromosomes.
Mitosis (Fig. 3.4)

It is the phase in which cell undergoes active
division. Interphase is the period between two
serial divisions. This type of cell division occurs
in somatic cells. Each daughter cell contains
the same number of chromosomes as those of
the parent cell. Body grows by following the
process of mitosis. Mitosis is divided into four
phases as:
1. Prophase
2. Metaphase
3. Anaphase
4. Telophase Fig. 3.4: Stages of mitosis
Prophase
Chromatin material gets organized into chromosomes. They appear as long filaments each having
two identical chromatids due to DNA replication. Each pair is joined at the centromere. Nuclear
membrane disappears along with the nucleoli, centriole divides and migrates to each pole. They
are connected by achromatic spindle.
Metaphase
Paired chromosomes get arranged at the equatorial plane half away between two centrioles.
Anaphase
Chromosomes move towards respective centriole.
Telophase
Chromosomes become long and get loosely spiralled. Nuclear membrane and nucleus reappear.
Chromosomes become less distinct and appear as granules in the nucleus. Cytoplasm divides
with appearance of constriction at the equatorial region. Each chromosome has single chromatid.
During later period of interphase another
chromatid is formed due to DNA replication.
Now chromosome is made of two chromatids.
This is followed by the mitosis. During
prophase thread-like chromosome becomes
rod-like. At the end of the prophase chromatids
become distinct. Centrioles go apart and form
the spindle. The nuclear membrane breaks and
the nucleus becomes invisible. Chromosomes
occupy the equator of the spindle. They are
seen attached to the microtubules of the
spindle through the medium of the
centromeres. Metaphase is followed by
anaphase during which the centromere splits
longitudinally converting the chromatids into
the chromosomes. Now one chromosome of
the pair follows the spindle and reaches each
pole of the cell. In telophase, daughter nuclei
are formed with reappearance of nuclear
membrane. Chromosomes become clearly
visible with nucleoli. The centriole gets
duplicated which is followed by division of the
nucleus with division of the cytoplasm. Each
daughter cell receives quota of organelles as
per the norms.
Fig. 3.5: Prophase of first meiotic division
Meiosis (Figs 3.5 and 3.6)
Meiosis occurs in two phases, i.e. I and the II meiotic divisions.
First Meiotic Division

It appears in prophase and is divisible under
four heads as:
1. Leptotene
2. Zygotene
3. Pachytene
4. Diplotene.
Leptotene: Chromosomes become visible and
two chromatids are visualised separately.
Zygotene: Chromosomes are paired and come
close (Synapsis or conjugation).
Pachytene: Two chromatids of each chromo-
somes become clearly visible. As a result of
bivalent has four chromatids and is called as a
tetrad. There are two peripheral and two
central chromatids in each chromosome. Two
central chromatids cross at many points. It is
called crossing over. The point of crossing is
known as chiasmata.
Diplotene: Two bivalent chromosomes move
apart. In the process the chromatid Fig. 3.6: Metaphase, anaphase and
participation in crossing over breaks at the telophase of the first meiotic division
points of crossing and the loose pieces get
attached to the opposite chromatid leading to the exchange of genetic material. This is followed by
the metaphase as seen in mitosis. 46 chromosomes get attached to the spindle at the equator. Since
the chromosomes are in pairs, they are close to each other. Anaphase is totally different from the
mitosis as there is no splitting of centromeres. Entire chromosomes of each pair go to each pole of
the spindle. This results in daughter cells having 23 chromosomes, each consisting of two
chromatids. Anaphase is followed by telophase in which two nuclei are formed which is followed
by the division of cytoplasm.
Second Meiotic Division

After the first meiotic division, there is a short interval known as short interphase. There is no
duplication of DNA being redundant as the chromosomes of the cells resulting from first division
already have two chromatids. It must be remembered that the second meiotic division is similar to
mitosis. Due to phenomenon of crossing over during the first division the daughter cells do not
have identical genetic material.
Stem Cells
The inner cell mass is capable of forming all three layers, e.g. ectoderm, endoderm and the
mesoderm. Hence, the inner cell mass is called the embryonic stem cells. They can be kept in the
undifferential state in a laboratory in culture. By using growth factors, they can be made to form
different tissues like muscle cells, cartilage cells, neurones and blood cells. It is the immune reaction
which stands in the way of success. Therapeutic stem cells cloning (TSCC) is being tried. TSCC in
which nucleus of the patient cell is put into the embryonic stem cell.
Diseases which are likely to be Benefited are by the Stem Cells
Parkinson’s disease
It is a chronic degenerative disease of the central nervous system. The disease is commonly seen
after the age of 65 years. It is characterized by tremors in limbs, stooping posture and mask-like
face, (e.g. expression less). Presence of the tremors at rest particularly involving one limb is the key
for the diagnosis of the disease.
Alzheimer’s disease
It is a chronic progressive degenerative disease of elderly people. It presents as loss of memory.
Later there are behavioral changes and the patient is unable to look after himself or herself and has
to be assisted in daily activities.
Blood Diseases
Spinal cord injury
It is known that due to the absence of centrosomes nerve cells do not divide and do not undergo
regeneration. One is born with fixed number of neurons and die with same number, only in the
absence of an accident in which the neurons are lost.
Development of the Tissues of the Body 15
Deve lopment o
Development f the
of
4 Tissues of the Body
of
Epithelia
Source of formation of epithelium can be from the three basic embryonic layers like ectoderm,
endoderm and the mesoderm, i.e. the epithelium arising from the ectoderm are epithelium of the
skin, epithelium of the cornea and the conjunctiva. Epithelium of the gastrointestinal tract except
some part of the mouth and the anal canal come from the endoderm.
The epithelium of the renal tubules, urinary bladder, uterine tubes and the testes develop from
the mesoderm.
Development of Glands
Glands develop from the diverticulum or diverticuli of the epithelium. Initially the diverticulum is
solid which gets canalized later. The site of origin of the gland is maintained as the opening of the
duct of the gland. (Duct of the submandibular salivary gland). Contrary to this the duct of the
parotid gland opens in the vestibule of the mouth though the origin of the duct is at the primitive
angle of wide mouth.
Glands Arising from Ectoderm

• Sweat
• Sebaceous
• Mammary
• Parotid gland.
Glands Arising from Mesoderm

Suprarenal.
Glands of Mixed Origin

Prostate.
Mesenchyme
It has already been seen that the mesoderm develops from mesenchyme which is capable of forming
chondroblast, osteoblast and erythroblast while rest of the mesenchyme forms the connective tissue.
Connective Tissue
It does the job of binding the tissues of the body. Mesenchyme gives rise to fibroblast and the
fibroblast produce ground substance and the collagen fibers. In addition to it, the mesenchyme
contribute to the formation of histiocyte, plasma cells, mast cells including the fat cells.
Blood Formation (Fig. 4.1)

Blood formation begins before the somites
appear and continues till the end. The wall of
the yolk sac, allantoenteric diverticulum and
the connecting stalk are the sites of blood
formation. In the third week of intrauterine life
mesodermal cells form blood islands forming
blood vessels and the blood cells. The cells at
the periphery form the angioblasts form the
blood vessels while the cells in the center form
the hemopoietic stem cells. Yolk sac blood cells
Fig. 4.1: Formation of blood cells and the vessel wall
are replaced by permanent cells arising from
the mesoderm around the aorta. They form colonies in the liver. These colonies are engaged in the
process of blood formation till the 6th month of intrauterine life. Liver remains the vital source of
blood formation. From the liver hemopoietic cells migrate to the bone marrow. These stem cells
form colony forming units which produce certain type of cells like erythrocyte, megakaryocyte,
granulocyte, monocyte, macrophages and lymphocyte. Due to rapid division of the erythropoietic
stem cells it appears as if the cell is on the verge of bursting (BFU).
Histogenesis of Cartilage (Figs 4.2 to 4.4)

Chondroblasts are formed from mesen-
chymal cells. Chondroblasts lay down
intercellular substance. As the chondroblast
gets trapped and isolated they become the
chondrocyte. Collagen fibers are not visible
in the hyaline cartilage, however plenty of
collagen fibers make their appearance in the
fibrocartilage, and elastic fibers are
predominantly present in the elastic
cartilage. Mesodermal covering of the
cartilage is known as perichondrium.
Fig.4.2: Hyaline cartilage
Fig.4.3: Fibrocartilage Fig. 4.4: Elastic cartilage
Histogenesis of Bone (Figs 4.5 and 4.6)

Osteocytes, osteoblasts and osteoclasts are the
bone cells. Bones develop from the mesoderm.
Mesenchymal cells form the cartilage which is
replaced by the bone. This formation of bone
is called enchondral ossification and the bone
is known as cartilage bone. Defective
formation of the cartilage bones, results in
formation of a dwarf. When bone is formed
directly from the mesenchyme is called the
membrane bone. Due to defective formation
of the membrane bones results in cleidocranial
dysostosis. In this condition, the shape of the
skull is deformed and the clavicles are absent. Fig. 4.5: Mesenchyme
Fig. 4.6: Roll of osteoblasts and osteoclasts in addition and the

depletion of the bone
Enchondral Ossification
Mesenchymal condensation forms chondroblast which forms hyaline cartilage.
Chondroblasts enlarge and the intercellular matrix gets calcified. Calcification of the matrix obstructs
the flow of nutrition of the chondroblast. Eventually, they die leaving the empty spaces behind
which are called primary areolae. Periosteal bud consisting of osteoblasts, the osteoclasts and blood
vessels grow from the periosteum. It grows inside and engulf the calcified matrix surrounding the
primary areolae. It is due to the erosion of the walls of the primary areolae by the osteoclast, the
smaller primary areolae get converted into larger secondary areolae. The plates of the calcified
cartilage bounding the secondary areolae get lined by the osteoblast. Osteoblast lay down osteoid
tissue which is made of ossein fibres + gelatin matrix. After calcification of the osteoid tissue, the
bony lamellus is formed. Number of lamellae are piled on the top of each other. Osteoblast caught
in between the lamillae becomes the osteocyte. This leads to the formation of bony trabeculae
Development of Long Bone (Fig. 4.7)

At first let us see the definition of ossification.
Ossification is the process of deposition of
calcium in the osteoid tissue. It begins in the
middle of the long bone forming primary
center of ossification which forms the
diaphysis. When the center of ossification
appears at the ends of the bone, the part of the
long bone formed by the secondary center of
ossification is known as the epiphysis. At the
same time, layer on the surface of the cartilage
model forms the perichondrium. With the bone
formation the perichondrium is called as
periosteum. The process of formation of the
Fig. 4.7: Parts of the developing long bone
bone by the osteogenic cells of the periosteum
is known as intramembraneous ossification. This forms the periosteal collar around the cartilaginous
model of the long bone. Periosteal collar provides strength to the cartilage bone particularly at the
zones weakened by formation of secondary areolae. Periosteal collar extends towards both ends of
the bone. The process of addition of new bone by the osteoblast on the periphery and the depletion
of the bone by the osteoclasts from inside, keeps formation of the bone under control. As a result
the cartilage bone is completely replaced by the membrane bone added from the periphery by the
osteoblasts. It can be inferred that the major portion of the long bone is formed by the membrane
bone. Plate of cartilage separating the epiphysis and the diaphysis is called the epiphyseal plate,
which plays an important role in growth of the bone. Trabeculae in the center of the bone are
removed by the osteoclasts forming the marrow cavity. The epiphyseal plate is not encroached by
the marrow cavity.
The Epiphyseal Plate has Three Zones

1. Zone of resting cartilage
2. Zone of proliferating cartilage
3. Zone of calcifying cartilage
The zone of calcifying cartilage is followed by the zone of bone formation. The conversion of
epiphyseal cartilage into bone helps in increasing the length of the bone.
Metaphysis (Figs 4.7 to 4.9)

Metaphysis is the part of the diaphysis in close proximity of the epiphyseal plate. Important factors
regarding the metaphysis are as under:
1. Metaphysis is more vascular where the blood vessels form the hairpin bends. Due to the
formation of hairpin bends, blood flow slows enabling the organisms (staphyloccoci) to settle
in the metaphysis leading to the condition of acute osteomyelitis.
2. The zone is susceptible to infections.
3. It has high calcium turnover after completion of the bone growth.
When growth occurs through cell multiplication and adding of the intercellular substance it is
called interstitial growth. As the growth occurs in all the directions the original shape of the bone
remains unchanged. When the growth of the bone is by deposition of bone on the surface it is
known as oppositional growth.
Process of removing the redundant bone is called modeling which maintains the shape of the
bone. Trabeculae are formed and get organized as per the needs of weight transmission and weight
bearing. It is called the internal modeling.
Anomalies of Bones
Molecular biology and genetics have succefully found the role of fibroblast growth factor (FGF)
and fibroblast growth factor recepter (FGFR) in producing skeletal dysplasias. Nine members of
the FGF and four (4) receptors regulate the cellular proliferation, differentiation and migration.
Fig. 4.8: Formation and growth of periosteal collar Fig. 4.9: Development of long bone
progressing towards the ends of the long bone Note that 1st, 2nd and the 3rd layers have disappeared.
The 4th and 5th layers are newly added remain. Addition
from out and depletion from in keeps the bony mass
relatively static in spite of addition of the layers. Thus
preventing ugly and extrabone formation
Achondroplasia: Due to the defective bone formation of the epiphyseal plate the growth of the long
bone is affected and the individual becomes a dwarf.
Cleidocranial dysostosis: In this condition, there is defective formation of the membrane bones leading
to deformed vault of the skull and the absence of the clavicles.
Osteogensis imperfecta: Due to abnormality of collagen I, there is deficient bony matrix leading to
fragility and short strature. The condition is marked with multiple repeated fractures.
Marble bone disease: Fragility and density (Osteopetrosis) of the bone is increased with sclerosis
which is classically described as bone within the bone. The condition is associated with cardiovascular,
ophthalmic, skeletal and the soft tissue defects.
Multiple epiphyseal dysplasia: Patients suffer from joint pains, and waddling gait.
Diatropic dysplasia: The condition is marked by short stature and typical thumb deformity
(Hitchhiker’s thumb).
Development of Striated Muscle (Figs 4.10 and 4.11)

The voluntary muscles of the body wall develop from the paraxial mesoderm which is the medial
most column of the intraembryonic mesoderm. Each somite has three parts.
• Sclerotome
• Dermatome
• Myotome
Fig. 4.10: Skeletal muscles of the body wall and the limb
Fig. 4.11: Parts of the paraxial mesoderm
Sclerotome
It migrates medially towards the notochord and the nural tube and contributes to the formation of
the vertebral column.
Dermatome
It forms the skin of the back and the subcutaneous tissue.
Myotome
It gets segmented and form the myotomes having cavity in the middle known as mycele.
Occipital myotomes give rise to the muscles of the tongue which are supplied by the 12th
cranial nerve. Preoccipital myotomes form the muscles of the eyeball which are supplied by the
3rd, 4th and the 6th cranial nerves. Each myotome of the cervical and thoracic region divides into
two forming the epimere and the hypomere. The muscles of the epimere are supplied by dorsal
primary ramus of the spinal nerve. Muscles of the hypomere are supplied by the ventral ramus of
the spinal nerves. Epimeres forms the extensor muscles of the back, while the hypomeres give rise
to the muscles of the body wall and the limbs. Epimere forms two muscular columns, the lateral
and the medial. The lateral column forms the longissimus and the iliocostalis muscles and the
medial column forms spinalis, semispinalis capitis and multifidus muscles. The hypomere forms
the transversus abdominis, internal oblique and the external oblique muscles of the body wall.
The ventral extensions of the muscles fuse infront of the anterior abdominal wall forming the
rectus abdominis muscle. Similarly, sternalis muscle is seen at times infront of the thorax. In addition
to it, the hypomeres also form the extensors and the flexors of the limb.
Development of Smooth Muscle

Smooth muscles of the viscera come from the splanchnopleuric mesoderm such as that of stomach
and intestine. It must be remembered that the muscles of the iris, i.e. sphincter and dialator pupillae
and the myoepithelial cells of the sweat glands are ectodermal in origin.
Cardiac Muscle
It develops from the myoepithelial mantle of the splanchnopleuric mesoderm of the pericardium.
Each muscle cell gives number of branches which join each other. Each muscle cell elongates and
comes into contact with the adjacent muscle cell. However, their cell membranes remain intact.
The junctional zone of the cell membranes forms the intercalated disk. Myofibrills appear within
the cells which give striated appearance to the cardiac muscle.
In brief the microscopic appearance of the cardiac muscle can be described as under:
Short, branched, striated with central nucleus and the intercalated disk.
Intercalated disk contains inter cellular junctions for electrical and mechanical linkage of
cotinguous cells.
Development of the Neurones (Fig. 4.12)

It has already been seen that the neural tube has three layers namely the ependymal, mantle and
the marginal from inside out. Essentially, the ependymal layer forms the ependymal lining of the
ventricles and the central canal of the spinal cord.
The fate of the ependymal cells is as under:
Ependymal cells go to the mantle layer and form apolar neuroblast.
The cell develops processes on both sides and becomes bipolar neuroblast.
One process disappears and the neuroblast becomes unipolar.
Only one process elongates to form axon while other processes form the dendrites, forming the
multipolar neuroblast.
Fig. 4.12: Histogenesis of spinal cord

Spongioblast (Fig. 4.12)

Spongioblasts form astrocytes and the oligodendrocytes. Some of the ependymal cells migrate to
the mantle and the marginal layers to form the astroblasts which get converted into astrocyte.
Some of the ependymal cells migrate to the mantle and the marginal layers and form
oligodendroblasts which get converted into the oligodendrocytes. Oligodendrocytes get lined on
either side of the nerve fiber and the tracts in the marginal layer. They form the myelin sheath for
the nerve fibers of the central nervous system. Due to the myelination of the tracts, the area of the
tracts look white. Axons of the multipolar neurones enter the marginal layer to form the tracts.
Appearance of the Nissl’s granules or bodies makes the neuron incapable of further divisions. The
microglia arise from the mesoderm and not from the neuroectoderm.
The neuroblasts as well as the neuroglia come from the ependymal cells arising from neuro-
ectoderm.
Formation of Myelin Sheath (Figs 4.13 and 4.14)

Nerve fibers within the brain, spinal cord and the peripheral nervous system are provided with a
sheath from the neuroglial cells. The nerve fibres outside the central nerovous system are provided
with a sheath called the neurolemma. Neural crest gives rise to the Schwann cells. The covering
which develops on the inner side of the neurolemma is called myelin sheath. Schwann cells give
rise to the myelin sheath of the peripheral nerves while the myeline sheath for the nerves in the
central nervous system comes from oligodendrocytes of due to the absence of the Schwann cells in
Fig. 4.13: Formation of myelin sheath
Fig. 4.14: Myelination of nerve fiber in the central nervous system by an

oligodendrocyte
the central nervous system. Axon invaginates the Schwann cell forming the double layered
mesoaxon. It is due to elongation and the rotation of the mesoaxon, typical myelin sheath is formed.
The myelination of the nerve fibers of the central nervous system begins in the 4th month of the
intrauterine period and is not complete upto 2 to 3 years of the life. It is well known clinically that
the extensor response of the great toe becomes flexor only after the completion of myelination of
the nerves in the central nervous system. In cases of the head injury normal flexor response of the
great toe becomes extensor (Babinki’s sign or reflex) in case of damage to the upper motor neurons
(Damage to the pyramidal tract).
Blood vessels of the brain are mesodermal in origin. It is believed that the pia and the arachnoid
mater of the brain and the spinal cord arise from the neural crest. However, the dura mater comes
from the mesoderm.
Clinical
There is dorsiflexion of the great toe instead of plantar when the lateral aspect of the sole of the
foot is stroked. It is known as Babinski’s sign or reflex.
Structure of Sperm 25
Structure of Sperm
of
5
Sperm is highly specialized and is smaller than the oocyte. It has head containing the nucleus.
Anterior 2/3rd of the nucleus is covered with the acrosomal cap which comes from Golgi apparatus.
Behind the head is the neck, body and the tail. Sheath of the body of the sperm is formed by the
mitochondria. It is known as mitochondrial sheath (Figs 5.1 and 5.2).
Body of the sperm is also called the middle piece and the tail is known as the principle piece.
Length of the sperm is about 50 microns, out of which 4/5th is formed by the tail.
Fig. 5.1: Parts of spermatozoon

Fig. 5.2: Parts of spermatozoon and their origin
Head
Length of the head of the sperm is about 4 microns and it contains 23 chromosomes (Haploid).
Anterior 2/3rd of the nucleus is covered by the acrosomal cap or the head cap. Acrosomal cap of
the human spermatozoon contains enzymes, e.g. acid phosphatase, hyaluronidase and protease
or acrosomase which are involved in the penetration of the oocyte. Head of the sperm has complete
covering of the cell membrane having no cytoplasm inside. Neck of the sperm contains one centriole
having two cylinders one transverse and other longitudinal. The covering of the longitudinal
cylinder is made of nine thick filaments which are continuous with axial filament of the body and
the tail.
Body
Body of the sperm measures 4 microns in length and is cylindrical. It is made of the following
structures from inside out, e.g. axial filaments, mitochondrial sheath, cytoplasm and the cell
membrane. Axial filament contains pair of central fibrils which are surrounded by two rows of
peripheral fibrils. At the junction of the body and the tail is the terminal centriole which is also
known as ring centriole.
Tail
Tail is the mobile part of the spermatozoon. It is 40 micron in length (Ten times the length of the
head of the sperm) and is made of axial filament, fibrous sheath, cytoplasm and the cell membrane.
Axial filament represents the continuation of the body. Fibrous sheath contains two thick
longitudinal bands placed on each side of the axial filament. The bands are inter-connected by
transverse fibrils. The thick bands decide the plane of movement of spermatozoa. Last part of the
tail is known as end piece and it has no fibrous sheath.
Single ejaculation of semen amounts to 2.5 ml. In normal semen contains 200 to 300 million
sperms. One can remember these figures as under:
• 2.5 ml. and 250 millions.
• If the total number of sperms in the semen comes to 20 million or less per ml. the person is
considered sterile.
Note : Acrosomal cap of the sperm contains:
1. Hyaluronidase
2. Acid phosphatase
3. Protease.
Spermatogenesis (Figs. 5.3 and 5.4)

The formation of spermatozoon is known as spermatogenesis. Spermatogonium having 44
autosomes and X and Y sex chromosomes forms primary spermatocyte. Primary spermatocyte
undergoes first meiotic division forming two daughter cells of equal size. In the daughter cells the
chromosomal number is haploid. The resultant daughter cells are known as secondary
spermatocytes. Secondary spermatocyte undergoes second meiotic division and forms four
spermatids.
Fig. 5.3: Section through human testis

Fig. 5.4: Spermatogenesis
Spermatogonia A
The germ cells have 44 chromosomes + XY sex chromosomes which undergo mitotic division and
give rise to more spermatogonia of type A and also spermatogonia of type B. Spermatogonia of
type B having 44 chromosomes + XY sex chromosomes undergo mitotic division and form primary
spermatocyte. Primary spermatocyte undergoes first meiotic division reducing the number of
chromosomes to the half. Thus secondary spermatocyte contains 22 + X and 22 +Y chromosomes.
Secondary spermatocyte now undergoes second meiotic division giving rise to four spermatids.
22 + X
22 + X
22 + Y
22 + Y
The spermatids get transformed into spermatozoa. The shape of the spermatid is circular having
a nucleus, Golgi apparatus, centriole and mitochondria. The nucleus forms the head and the Golgi
apparatus forms the acromic cap. Centriole divides into two and go apart. One lies at the neck
while the other goes away to form the annulus. The axial filament placed in between the neck and
the annulus gets surrounded by the mitochondria and froms the middle piece. Rest of the axial
filament becomes the tail. It is important to note that the most of the cytoplasm of the spermatid
gets parted, however the cell membrane is maintained as the covering of the spermatozoon, being
vital. The total period required for the process of spermatogenesis including spermiogenesis is of
60 days.
Ovum
Cytoplasm is surrounded by the vitelline membrane. The nucleus is not visible due to dissolution
of the nuclear membrane. However the spindle for second meiotic division is clearly visible. The
perivitelline space lies between the vitelline membrane inside and the zona pellucida outside.
Surrounding the zona pellucida are the radially arranged cells called the corona radiata.
Oogenesis (Figs 5.5 to 5.7)

Process of formation of the ovum is known as oogenesis. Cortex of the ovary has large number of
oogonia which are present long before birth and they do not multiply. As the oogonium enlarges
it becomes the primary oocyte. Primary oocyte undergoes first meiotic division and forms two
daughter cells of unequal size. The larger cell is known as secondary oocyte and the smaller one is
called the first polar body. The daughter cells have haploid number of chromosomes. All the
cytoplasm goes to the larger daughter cell and practically none to the smaller. The secondary
oocyte undergoes second meiotic division and forms the ovum and the second polar body.
The oogonia are in prophase of the first meiotic division and do not complete at this stage. The
first meiotic division gets completed only when the oogonia start maturing and are getting prepaired
for ovulation. At the time of ovulation the secondary oocyte is in metaphase which continues till
fertilisation. During reproductive life of the female which ranges from 12 to 50 years, 40000 primary
oocytes are in stock out of which hardly 10% of them are discharged.
Comments
1. It is interesting to note that the one spermatocyte is able to produce four spermatozoa as against
the one primary oocyte which produces only one ovum.
2. When the primary oocyte divides almost all cytoplasm is donated to the daughter cell forming
the secondary oocyte. The other daughter cell (1st polar body) receives its half quota of
chromosomes but none of the cytoplasm.
Fig. 5.5: Oogenesis
Fig. 5.6: Section of ovary

Fig. 5.7: Primary oocyte
Primary oogonia become larger and form the primary oocyte. The primary oocyte continues
in prophase without completing meiotic division till it gets matured. In each menstrual cycle
about five to thirty primary oocytes get matured and complete their 1st meiotic division prior to
ovulation.
Formation of Ovarian Follicle (Figs 5.8 to 5.14)

Oogonia developing in the cortex of the ovary are surrounded by the stromal cells. The oogonia
surrounded by the stromal cells are called ovarian or the Graafian follicles. Zona pellucida appears
between the follicular cells and the oocyte. Due to rapid proliferation of the follicular cells, multiple
layers are laid down forming the membrana granulosa. The cells are called granulosa cells. Cavities
appear in the granulosa cells which join and form larger cavity. This makes the wall of the follicle
thin and shifts the oocyte to one side of the cavity. The eccentric oocyte is surrounded by granulosa
cells known as cumulus oophorus. The cells which attach the oocyte to the follicular wall is called
the discus proligerus.
Fig. 5.8: Formation of ovarian follicle Fig. 5.9: Formation of ovarian follicle
Note zona pellucida and columnar follicular cells
Fig. 5.10: Formation of ovarian follicle and appearance of membrana granulosa
Fig. 5.11: Appearance of lacunae in granulosa cells.

Fig. 5.12: Appearance of follicular cavity
Fig. 5.13: Fully formed ovarian follicle reaching the surface of the ovary in an attempt to get
released after rupture of the follicle
Fig. 5.14: Fully formed Graafian follicle

Note theca externa and interna. Basement membrane lies between membrana granulosa and theca interna
Due to pressure exerted by the expanding follicle the stromal cells around the follicle get
compressed to form the theca interna. As the theca interna starts secreting estrogen it is called the
thecal gland. Outside the theca interna the second covering is formed due to compression of the
stromal tissue. It is known as the theca externa.
The cells surrounding oogonium are flat as they become columnar, the primordial follicle is
formed.
Role of Follicular Cells and the Oocyte

Follicular cells and the oocyte are complementary to each other regarding their growth and
development. The primary oocyte is not allowed to mature beyond the prophase of the first meiotic
division due to the meiotic inhibition factor. (MIF) produced by the follicular cells. MIF reaches the
oocyte through the gaps between the microvilli of the oocyte and follicular cells. These interlocking
microvilli are placed in the zona pellucida giving striated appearance to the zona pellucida. Follicular
cells help in the metabolism, growth and the maturation of the oocyte, while the oocyte helps in
the proliferation and differentiation of the follicular cells.
Ovulation 35
Ovulation
6
The act of the shedding ovum from the
surface of the ovary is called ovulation. As
the ovarian follicle increases in size, it reaches
the surface of the ovary and projects in the
peritoneal cavity in the form of a bulge. Due
to the pressure of the convexity of the bulge,
the area goes ischemic causing avascular
necrosis. This causes rupture of the follicle
and release of the ovum. Unruptured follicles
disappear and the theca interna forms the
interstitial gland. Finally it ends by forming
the corpus albicans which is similar to the
corpus albicans formed after degeneration of
Fig. 6.1: Ovulation
the corpus luteum (Figs 6.1 and 6.2).
What Promotes Ovulation?

The most important factor is the digestion of the wall of the follicle by enzymes. However other
contributing factors are as under:
1. Raised level of luteinizing hormone which activates collagenase.
2. Prostaglandins cause contraction of smooth muscles of the ovarian wall.
3. Increased hydrostatic pressure inside the follicular cavity acts as the physical factor.
Structure of the Ovum (Fig. 6.3)

Ovum has a protective covering of the zona pellucida. Zona pellucida is surrounded by cells of
corona radiata. The vitellus is surrounded by the vitelline membrane and the spindle of the second
meiotic division is visible. Perivitelline space is the space between the vitelline membrane inside
and the zona pellucida outside. Note the presence of the first polar body in the perivitelline space.
The ovum is larger in size, i.e. almost 10 times the size of the normal body cell.
Fig. 6.2: Rupture of graafian follicle, formation of corpus luteum and corpus albicans
Fig. 6.3: Ovum

Ovulation 37
Future of the Ovum (Figs 6.4 and 6.5)

After its release from the ovary at the ovulation, the ovum enters the fimbriated end of the uterine
tube and enters the ampulla. Its journey is helped by the ciliary movements of cells of the tube,
flow of fluid and the contractions of the tubal muscles. Following intercourse the spermatozoa
reach the ampullary part of the tube mostly due to self motility and surround the ovum. Only one
spermatozoon penetrates the ovum. Now the fertilised ovum reaches the uterus for implantation.
In the absence of fertilisation the secondary oocyte dies.
Corpus Luteum (Refer Figs 6.1 and 6.2)

Following rupture of the ovarian follicle and release of the ovum, the remains of the follicle form
the corpus luteum. With rupture of the follicle, its wall collapses, crumbles and gets folded.
Follicular cells enlarge and become polyhydral. They obtain lutein pigments which are yellow in
color and are called the luteal cells. Few cells of the theca interna grow in size and may help in the
formation of corpus luteum. With the formation of corpus luteum the blood vessels from the theca
interna invade the corpus luteum and help in transport of progesterone secreted by the corpus
luteum (Ovarian follicle itself being avascular).
Corpus Luteum of Menstruation

In the absence of fertilization, the corpus luteum has life of 14 days and it undergoes degeneration
and gets converted into the mass of fibrous tissue. It is known as the corpus albicans.
Fig. 6.4: Path of sperm and ovum for reaching the ampullary part of the uterine tube for fertilization
Fig. 6.5: Maturation of the ovum
Corpus Luteum of Pregnancy (Figs 6.6 and 6.7A and B)

In the event of fertilization of the ovum, the corpus luteum has life span of four months. During this
period progesterone secreted by the corpus luteum helps in maintenance of pregnancy. However,
after four months the trophoblast of the placenta secretes progesterone. Degeneration of corpus luteum
in early period of pregnancy is prevented by human chorionic gonadotropin (hCG) formed by the
trophoblast of the embryo. Corpus luteum of pregnancy is larger than the corpus luteum of
menstruation.
Ovulation 39
Fig. 6.6: Changes in uterine mucosa in relation with the ovarian changes.
Observe implanted blastocyst and corpus luteum of pregnancy. In the absence of implantation of blastocyst there is
no gravid phase, no corpus luteum. Instead, there is menstrual phase with degenerating corpus luteum
Fig. 6.7A: Menstrual phase

Fig. 6.7B: Hormonal control of menstrual cycle

Ovarian Cycle 41
Ovarian Cycle
7
Ovulation (Figs 7.1 and 7.2)
At ovulation, the graafian follicle ruptures and the ovum is released from the cortex of ovary.
Ovulation takes place in the middle of the menstrual cycle, i.e. on 14th day. It occurs due to increased
secretion of LH from the anterior lobe of the pituitary. After ovulation the empty follicular cavity
crumbles and collapses. There is no initial bleeding as the layer of stratum granulosum is avascular.
The cells of the stratum granulosum proliferate by undergoing mitosis. They increase in the size
and contain yellowish carcinoid pigments in the cytoplasm. Capillaries encroach the center of the
follicle from the peripheral stroma. The enlarged granulosa cells are known as granulosa lutein
cells. At the periphery the cells of the theca interna increase in size and are called paraluteal cells.
Granulosa lutein cells produce progesterone and small quantity of estrogen, while the theca lutein
cells secrete estrogen only. Luteinizing hormone of the anterior lobe of the pituitary stimulates
formation of the corpus luteum.
The role of the progesterone of the corpus luteum in the female.
1. Promotes secretary phase of endometrium and makes the uterus ready for reception and
nourishment of fertilized ovum.
2. It prevents expulsion of the developing embryo due to increased tone of the smooth muscles of
the uterus.
3. It depresses the secretion of follicle
stimulating hormone (FSH) from the
anterior lobe of the pituitary.
4. FSH—stimulates release of luteinizing
harmone (LH) through the estrogen
secreted by the follicle. On the other hand
LH depresses secretion of follicle
stimulating hormone (FSH) through
progesterone released by the corpus
luteum. When pregnancy fails, life span
of the corpus luteum is of 12 to 14 days
after ovulation. The corpus luteum
formed in this process is known as Fig. 7.1: Ovulation
Fig. 7.2: Rupture of Graafian follicle, formation of corpus luteum and corpus albicans.
corpus luteum of menstruation. Following this there is degeneration of the luteal cells. Sudden
withdrawal of progesterone from the blood results in menstrual bleeding. Corpus luteum is converted
into a fibrous nodule later and is called the corpus albicans. In case the fertilized ovum gets
embedded in the uterine wall, the trophoblast formed during the process, secretes chorionic
gonadotrophic hormone. The chorionic gonadotrophic hormone, helps the corpus luteum to
survive and grow. Corpus luteum formed in the process is known as the corpus luteum of
pregnancy which continues to secrete progesterone only up to the 4th month and undergoes slow
regression later.
Menstrual Cycle 43
Menstrual Cycle
8
Uterine endometrium undergoes cyclical changes during reproductive life of a woman which is
known as menstrual cycle. At the age of forty-five menstruation ceases and the stage is called the
menopause. Similarly, cyclical changes occur in the ovaries which constitute the ovarian cycle (Figs
8.1A to C and 8.2).
Endometrial changes during the menstrual cycle include growth, degeneration and the repair. It
is associated with exfoliation of the endometrial tissue in the uterine cavity and the uterine bleeding.
This is known as menstruation (GRREB).
Fig. 8.1A: Changes in uterine mucosa in relation with the ovarian changes: Observe implanted blastocyst and corpus
luteum of pregnancy. In the absence of implantation of blastocyst there is no gravid phase, no corpus luteum. Instead,
there is manstrual phase with degenerating corpus luteum.
The period of menstruation lasts for 3 to 4 days.

Menstrual cycle is counted from 1st day of bleeding
of one menstrual cycle to the 1st day of bleeding of the
next menstrual cycle. Repetition of the cycle occurs at
an interval of 28 days.
Menstrual cycle is divided into 4 phases:
1. Postmenstrual is due to estrogen of the follicles
of the ovary.
2. Proliferative is due to estrogen of the follicles
of the ovary.
3. Secretory
Fig. 8.1B: Menstrual phase
4. Menstrual.
The changes seen in the postmenstrual phase and during the proliferative phase are due to the
action of estrogen produced by the follicles in the ovary (hence, rightly labeled as follicular phase).
Initial half of the menstrual cycle covers the follicular phase. Rest half of the menstrual cycle is due
to changes in the endometrium under the influence of corpus luteum through the release of
progesterone and the estrogen. It is known as luteal phase. Before beginning of the next menstrual
period, progesterone and estrogen level goes down causing the menstrual bleeding.
Menstrual cycle is regulated by the hormones liberated by the ovarian follicle and the corpus
luteum.
Fig. 8.1C: Hormonal control of menstrual cycle

Menstrual Cycle 45
Before we go to the details of the menstrual

phase one would like to know the structure of
the endometrium. The endometrial stroma is
arranged in three layers: (1) Stratum basale, (2)
Stratum spongiosum, (3) Stratum compactum,
from outside in, which can be memorized
as BSC, B – Basal, S – Spongiosum, C-
Compactum.
Menstrual changes occur in following
phases:
1. Follicular (Proliferative)
2. Secretory (Progestinal phase)
Follicular Phase Fig. 8.2: Diagrammatic representation of menstrual cycle
Follicular phase covers the initial half of the menstrual cycle. After menstruation which ends on
4th day, the endometrium undergoes the process of repair and growth. Period of repair lasts for
further 4 days. After the period of repair, growth of the endometrium takes place. This period is
known as interval phase. Cells become columnar from cuboidal, glands elongate and become straight.
It is the mature follicle’s estrogen which is responsible for the endometrial changes during the
follicular (Proliferative) phase. It must be remembered that the ovulation occurs at the end of the
follicular phase. Endometrium becomes clearly divisible in three layers as basalis, spongiosum
and the compactum. The estrogen produced by the mature ovarian follicle is responsible for the
changes in the endometrium.
Secretory Phase (Progestational Phase)

It covers the later ½ of the menstrual cycle. It is the corpus luteum which releases estrogen and
progesterone causing this phase. Predominant changes occur in the thickness of the endometrium
which increases from 3 mm to 5 to 7 mm. The thickness of endometrium is attributed to the following
factors:
1. Stromal edema.
2. Dilatation of the glands due to increased secretions.
3. Elongation, enlargement and convolutions of the glands with saw tooth appearance.
4. Stromal cells increase in size due to storage of glycogen and lipids. It is called decidual reaction
which is the landmark event of the pregnancy.
5. Arteries become tortuous. Spiral arteries supply inner two layers of the endometrium, i.e.
stratum compactum and stratum spongiosum. Stratum basale does not take part in the process of
menstrual cycle (One may say that the basale is banned).
The regressional changes start before the actual menstrual period which is known as pre-
menstrual phase.
Formation of Decidua (Figs 8.3 to 8.6)

After implantation of the fertilized ovum, uterine endometrium undergoes certain changes leading to
the formation of the decidua. In other words changed character of the endometrium after implantation of
the fertilized ovum is called the decidua.
Fig. 8.3: Implantation of blastocyst with formation of decidua
Fig. 8.4: Implantation of blastocyst

Menstrual Cycle 47
Fig. 8.5: Implantation of blastocyst
Fig. 8.6: Showing decidua in three regions: 1. At the base. 2. Which separate the embryo from the uterine cavity.
3. Lining the uterine cavity respectively known as decidua basalis, decidua capsularis and decidua parietalis
The decidual changes include increase in thickness of the endometrium, collection of fluid
(oedema), increase in vascularity, increase in cell population and glandular proliferation. In brief
the endometrium becomes thick, edematus, cellular, vascular and glandular. The cells are larger oval in
shape having glycogen and lipids, are called the decidua cells.
Menstrual Phase
Due to further coiling of the spiral arteries, circulation in the endometrium becomes slow causing
reduction of the circulatory flow in the endometrium. Spiral arteries undergo vasoconstriction
leading to transient ischemia of the endometrium. Ischemia of the endometrium is reversed as the
spiral arteries start dilating. Damaged capillary walls allow escape of blood into the intercellular
spaces. This is associated with piece-meal detachment of endometrium accompanied with bleeding.
This phase continuous for 3-5 days. It is only the stratum compactum and spongiosum which are shed
off. Amount of blood loss is about 50 – 60 ml. Menstrual blood of menstruation does not clot due to
proteolytic enzymes in the blood.
Menstrual bleeding occurs due to sudden withdrawal of progesterone. In anovular menstruation,
ovulation and formation corpus luteum are absent and yet the bleeding occurs. Possibly it is due to
the withdrawal of estrogen from the blood. After fertilization of the ovum, the secretary phase of the
endometrium is continued further by the progesterone from the corpus luteum of pregnancy. Endometrium
is prepared with a red carpet to welcome and receive the fertilized ovum for getting implanted. As
a result menstruation stops till the period of gestation.
Fertilization 49
Fertilization
9
Fusion of the two mature germ cells, an ovum and the spermatozoon resulting in formation of the
zygote, is called fertilization. Fertilization takes place in the ampullary part of the uterine tube. It
can be described in brief as an approximation of gametes, fusion of cell membranes and the effects
(Figs 9.1 to 9.3).
Journey of spermatozoa from vagina to the ampullary part of the uterine tube is promoted by
the prostaglandins present in the semen. Prostaglandins cause powerful contractions of the uterine
muscles. Oxytocin released from the neurohypophysis adds to the contractions of uterine muscles.
Uterine contractions create negative pressure in the uterine cavity. Sperms are aspirated (sucked
in) from the vagina into the uterine cavity. Spermatozoa get reduced in number during upward
journey mainly due to the sphincteric action of the cervix and the ostium of the uterine tube. They
act as filters and permit entry only to the competent spermatozoa. Majority of the spermatozoa die
within 24 hours. Oocyte reaches the ampullary part of the tube due to movements of cilia of the
Fig. 9.1: Spermatozoa passing through corona radiata

Fig. 9.2: Spermatozoa penetrating zona pellucida
Fig. 9.3: Fusion of oocyte with sperm cell membrane
uterine tube, fluid in the tube and the contractions of the tubal muscles. Trans coelomic migration
can carry the oocyte to the opposite uterine tube.
Out of 300 million sperms, only 300 reach the ovum (only hundreds out of millions). Remaining
army of sperms start destroying the corona radiata with the help of hyaluronidase from the
acrosomal caps of the heads of the sperm. Corona radiata forms the first barrier, zona pellucida
the second and the vitelline membrane of the secondary oocytes becomes the third barrier trying
to obstruct the advance of the sperm.
Before penetration, the sperm has to undergo capacitation and the acrosomal reaction.
Fertilization 51
Capacitation
The mechanism of the capacitation is not fully known, however, it requires 7 hours for its completion.
Antigenic coating of the sperm initiates an immunological reaction between the oocyte’s fertilizin
and the spermatozoon’s anti-fertilizin.
Acrosomal Reaction
Acrosomal reaction is the process of multiple contacts of the sperm with various barriers protecting
the oocyte. Acrosomal cap contains hyluronidase, acid phosphatase and protease which are released
at various levels of the barriers. This helps the spermatozoon to enter the oocyte.
Secondary Oocyte
It has following components:
• Cell membrane (vitelline membrane)
• Cytoplasm
• Nucleus – it is eccentric – germinal vesicle, nucleolus as germinal spot.
• Zona pellucida
• Cells of corona radiata
• Polar bodies
Nucleus of the secondary oocyte contains 23 chromosomes.
Disintegration of the Barriers

First Barrier
It is formed by the cells of corona radiata and the cumulus oopharicus. Its disintegration occurs due
to hyluronidase of the acrosomal cap of the sperm.
Second Barrier
Zona pellucida is the second barrier which looks striated and thick. It is formed by glycoproteins
ZP1, ZP2, and ZP3.
Binding of the sperm head to the specific glycoprotein site starts acrosomal reaction, releasing
acrosin. Acrosin digests zona pellucida in proximity of the sperm head. With disappearance of
zona pellucida, the sperm head enters the perivitelline space.
Third Barrier
Third barrier is the vitelline membrane of the secondary oocyte. After fusion of the sperm head with
the vitelline membrane, it gets armed with two disintegrin peptides on the head of the sperm,
which open the gate (door) through which the head of the sperm enters the cytoplasm of the
oocyte. With the entry of the sperm head, the gate gets closed by integrin peptides of the vitelline
membrane.
Calcium Wave
Calcium wave appears in the cytoplasm of the oocyte. Calcium waves help in the formation of the
mature ovum from the secondary oocyte. It also initiates release of the second polar body in the
perivitelline space. The calcium waves initiate release of enzymes from the peripheral cortical
granules, ZP3 receptors are hydrolysed by the enzymes.
This does two remarkable things:
1. It prevents the entry of the other sperms thus preventing polyspermy.
2. Secondly, it prevents acrosomal reaction. With the help of the above two mechanisms,
polyspermy is prevented.
Vitelline Block
Vitelline membrane undergoes change due to secretion of the cortical granules. Changed vitelline
membrane works as vitelline block and prevents entry of sperms and thereby polyspermy.
Now the mature ovum contains two pronuclei, male and female. Head of the sperm forms
male pronucleus and the nucleus of the mature ovum forms female pronucleus. Pronuclei swell
and come closer. They loose their envelopes. After DNA replication 1-N to 2-N DNA complex is
formed. Centrioles of the spermatozoon migrate to the opposite poles. Nuclear membrane disappers
and chromosomes of the zygote get arranged at the equatorial plane of the achromatic spindle of
the first division, as a result two cells appear within the zona pellucida.
Effects of Fertilization
• Restoration of number of chromosomes from haploid to diploid.
• End of second meiotic division, maturation of ovum with release of the second polar body.
• Determination of sex
• Stimulus to divide
• Establishment of polarity: It is decided by the line of entry of the spermatozoon.
• Restoration of cell size: Equal to that of body cell.
Parthenogenesis
Embryo is formed following cleavage without the male gamete.
Infertility, Causes and Remedy

Infertility in male is due to poor sperm count, distorted morphology and sluggish motility of the
sperms. Volume of semen per ejaculation is about 2.5 to 3 ml with sperm count of 100 millions per
ml. Men having 20 millions sperm count and below are likely to be sterile.
Causes of infertility in female:
• Congenital anomaly of uterus such as agenesis.
• Tubal obstruction due to pelvic infections.
• Absence of ovulation.
• Unfriendly cervical mucosa.
Fertilization 53
Remedies
They are as under:
1. ART: Assisted reproductive technology.
2. IVF: In vitro fertilization.
3. GIFT – Gametes Intra-fallopian tube transfer.
4. Zygote intrafallopian transfer.
Oligospermia means very low count of live sperms. Azospermia means absence of live sperm.
Azospermia can be treated with the help of intracytoplasmic sperm injection (ICSI). Sperm is
obtained from the male and injected into the cytoplasm of the oocyte for fertilization to occur.
In Vitro Fertilization of Female Gamete

Females with bilateral tubal blockage (atresia) although have normal ovaries cannot reproduce.
They are given clomiphene to stimulate maturation of ovarian follicles. Through laparoscopy
oocytes are obtained from the ovarian follicle and added to the cultural medium having standard
pH and temperature. Sperms from husband are collected and placed in the same cultural medium.
Appearance of two polar bodies in the perivitelline space confirms fertilization which is viewed
through the stereoscopic microscope. When fertilized ovum undergoes cleavage up to 8-cell stage,
it is introduced into the uterine cavity. Prior to this, female partner is put on progesterone for
decidual reaction with secretory phase.
Surrogate Mother
Female having normal ovaries but blocked tubes with agenesis of uterus cannot produce. In such
cases in vitro fertilization of the oocyte belonging to the female is done with the husband’s semen.
The embryo obtained by this method is transferred to the uterine cavity of a different female after
pretreatment with progesterone compound.
Period of Gestation
Period of pregnancy in human is 40 weeks (280 days). It is to be remembered that the ovulation
occurs 14 days before the onset of next menstruation. Date of pregnancy is calculated from the
first day of last menstrual period (menstrual age of the baby). Naturally, fertilization age of the
baby is two week less than the menstrual age.
Determination of Sex
Ovum has 22 + X
Spermatozoa are of two types:
50% = 22 + X
50% = 22 + Y
X bearing spermatozoon gives rise to zygote having 44 + XX, i.e. offspring is female.
Y bearing spermatozoon produces zygote having 44 + XY, i.e. offspring is male.
Cleavage (Figs 9.4 to 9.7)

Cleavage is the process of subdivision of the ovum into the smaller units. During the process of
division ovum reaches two-cell stage, three-cell stage (as the larger cell divides first) and four cell
stage. As it reaches 16-cell stage, it is called the morula. Dividing cells are surrounded by the zona
pellucida. Cells inside the zona pellucida are arranged into two groups—the inner and the outer
called the inner cell mass and the trophoblast respectively. The inner cell mass forms the embryo
and is called the embryoblast. Outer layer forming the trophoblast supplies nutrition to the embryo.
(Trophe – means nutrition).
As the fluid from the uterine cavity enters the morula, the inner cell mass gets physically
separated from the trophoblast. With the increase in quantity of fluid, the morula becomes a fluid
filled lake with an island of cells at the periphery. The cystic cavity thus formed is known as
blastocele and the transformed morula is called the blastocyst (Refer Fig. 9.7).
Fig. 9.4: Segmentation of the fertilized ovum

Fertilization 55
Fig. 9.5: Formation of embryoblast and trophoblast Fig. 9.6: Formation of blastocyst (early stage)
The inner cell mass lies on one side of

the blastocystic cavity. Due to increase in
hydrostatic pressure inside the blastocyst, the
trophoblast gets flattened. The side where
the inner cell mass is attached to the wall of
the blastocyst is called the embryonic pole
and the diagonally opposite side is called the
ab-embryonic pole (Refer Figs 9.5 and 9.6).
Role of Zona Pellucida (Refer Figs 9.5 and

9.8)
As the trophoblast has strong tendency to
Fig. 9.7: Formation of blastocyst (further stage)
develop intimate contact with the uterine
endometrium with which it establishes
nutrient relationship and eats up the uterine
epithelium. It invades and burrows into the
endometrium.
It is important to remember that the zona
pellucida prevents sticking of the trophoblast
to the uterine epithelium during journey of
the fertilized ovum from the ampullary part
of the uterine tube to the uterine cavity.
During the journey, the embryo receives
nutrition from the stored yolk inside the
ovum and also from the uterine secretions. Fig. 9.8: Schematic representation of microscopic structure
of zona pellucida
With the formation of the blastocyst, the
embryo is in urgent need of additional nutrition. This is possible only by sticking of the blastocyst
to the uterine endometrium and finally getting implanted into it. This is made possible by the
disappearance of the zona pellucida. The most important function of the zona pellucida is to
prevent implantation of the blastocyst at sites other than normal (preventing ectopic pregnancy).
(Refer Fig. 8.3).
Coming together of the maternal and embryonic tissues can trigger immunological response
due to the fact that the maternal and the embryonic tissues are genetically different. Zona pellucida
acts as a barrier separating the maternal and the fetal tissues. Zona pellucida by itself is inert and
does not give rise to immune reaction. After the disappearance of the zona pellucida immuno-
suppressive cytokines and some proteins formed by the embryo come in the way of recognition of
the embryonic tissue as foreign to the mother.
Implantation of Blastocyst (Refer Figs 8.3 and 8.4)

After disappearance of the zona pellucida, the blastocyst is free in the uterine cavity. Meanwhile
the uterine endometrium forms the decidua having three layers from outside within as under:
1. Stratum basale
2. Stratum spongiosum
3. Stratum compactum (BSC)
With the disappearance of the zona pellucida, the trophoblast at the embryonic pole gets
implanted on the decidual wall of the uterus by eroding the stratum compactum and the stratum
spongiosum. This is achieved through the proteolytic enzymes of the trophoblast. Trophoblastic
cells make an entry through the gap between the epithelial cells of the uterine mucosa. Later they
erode the cells with the help of proteolytic enzymes and get implanted. It is important to note that
the epithelial cells of the endometrium do not remain merely passive as it allows the trophoblastic
invasion with its own consent and full cooperation, keeping in mind the sole and strong desire of
child bearing (being the main function of the womb.)
Abnormal Implantation of the Blastocyst (Figs 9.9 and 9.10)

It can be intrauterine as well extrauterine. Intrauterine abnormal implantation can occur in the
lower segment of the uterus close to the internal os. It may completely cover the os. This is known
Fig. 9.9: Sites of abnormal implantation of the fertilized ovum, A- Normal, B- Placenta previa, C - Interstitial type,
D- Tubal, E- Ovarian, F- Peritoneal
Fertilization 57
Fig. 9.10: Abdominal pregnancy in the rectouterine pouch
as placenta previa, which can cause life-threatening bleeding during labor. Placenta previa is
classified into four grades.
Extrauterine Implantation of Blastocyst (Refer Fig. 9.9)

When the implantation occurs outside the uterus, it is called as ectopic pregnancy.
1. Tubal-95%
2. Ovarian-When the blastocyst grows in the ovary itself, it is called primary ovarian pregnancy.
3. In the pouch of Douglas
4. Peritoneal coverings
5. Greater omentum.
Normally, the embryo does not survive beyond two months of gestation in tubal pregnancy.
Rupture of the ectopic tubal pregnancy causes severe abdominal pain and bleeding leading to the
state of shock.
Definition of Shock
When there is gross disproportion between the circulating volume and the capacity, leading to
interference in vital tissue perfusion leading to serious pathophysiological changes, it is called
shock.
Hydatidiform Mole
At times the trophoblast is formed leading to the formation of the placental membranes without
formation of embryonic tissue.
This is called hydatidiform mole which secretes high level of hCG leading to formation of
benign or malignant tumors (choriocarcinoma).
Stages of Labor
There are 3 stages of labour.
1. Effacement of the cervix
2. Delivery of the fetus
3. Delivery of the placenta and the membranes.
Formation of Germ Layers (Figs 9.11 to 9.13)

Embryonic disk is made of three germ layers, i.e. ectoderm, endoderm and mesoderm. The
fundamentals of the embryology revolve around the axis of the three basic germ layers. Their
formation and the fate should be studied with concentration. Cells on the inferior surface of the
inner cells mass become cuboidal to form the endoderm. The endoderm is the first germ layer to form in
Fig. 9.11: Formation of ectoderm and endoderm Fig. 9.12: Formation of ectoderm and endoderm with
development of amniotic cavity and primary yolk sac
Fig. 9.13: Intra-embryonic mesoderm arising from the primitive streak spreading between
the ectoderm above and the endoderm below
Fertilization 59
the embryonic disk. The cells above the newly formed endodermal cells become columnar and form
the ectodermal layer.
Thus the bilaminar embryonic disk is formed. A cavity appears between the trophoblast above
and the ectoderm below. It is known as the amniotic cavity. Its roof is formed by the amniogenic
cells which are derived from the trophoblast and the floor is formed by the tall ectodermal cell of
the superior surface of the bilaminar embryonic disc. The cavity is filled with amniotic fluid.
Formation of Primary Yolk Sac (Refer Fig. 9.12)

Flattened cells on the inferior surface of the bilaminar embryonic disk start growing inside the
wall of the blastocyst. This is known as Heuser’s membrane. Thus the cavity lined by the endoderm
is formed inside the blastocyst. It is called the primary yolk sac (cavity within the cavity).
Formation of Extraembryonic Mesoderm (Figs 9.14 and 9.15)

Trophoblast gives rise to the extraembryonic mesoderm which fills the gap between the trophoblast
outside and the Heuser’s membrane inside.
Fig. 9.14: Formation of extraembryonic mesoderm and development of extra embryonic coelom
and formation of secondary yolk sac
Fig. 9.15: Appearance of amniotic cavity and primitive yolk sac. Note brown-colored extraembryonic
mesoderm with white spaces forming extraembryonic coelom after joining
Fig. 9.16: Blastocyst with amniotic cavity, secondary yolk sac and formation of
extraembryonic coelom in the extraembryonic mesoderm
Extraembryonic mesoderm is also known as the primary mesoderm. Small cavities appear in
the extraembryonic mesoderm. They enlarge and join to form the large single cavity. It is known
as the extraembryonic coelom (Fig. 9.16). Due to appearance of extraembryonic coelom, the
extraembrynic mesoderm gets split into two i.e. outer and the inner layers. The outer layer of the
extraembryonic mesoderm is called the somatopleuric layer and the inner layer is called the
splanchnopleuric layer. Both layers are in continuity in the region of the connecting stalk.
The somatopleuric layer of the extraembryonic mesoderm covers the trophoblast from inside
forming the chorion. Covering of the yolk sac from outside is known as the splanchnopleuric layer
of mesoderm. The part of the extraembryonic mesoderm extending from the caudal end of the
embryonic disk to the trophoblast is not invaded by the extraembryonic coelom. The unsplit part
of the extraembryonic mesoderm forms the connecting stalk which becomes the umbilical cord later.
Fertilization 61
Chorion (Refer Fig. 9.14)

Chorion is formed by the combination of the trophoblast from outside and the somatopleuric layer of
the extraembryonic mesoderm on inside. The finger-like outward projections of the chorion are called
the chorionic villi. Blastocystic cavity becomes the chorionic cavity in the later part of the 2nd week.
Blastocytes has two cavities inside i.e. amniotic and the yolk sac. The portion between the amniotic
cavity above and the yolk sac below forms the bilaminar embryonic disc.
Amnion (Refer Fig. 9.14)

It is formed by the combination of the amniogen cell wall of the amniotic cavity inside and the
somatopleuric layer of the extraembryonic mesoderm outside.
We have already seen that amniogen cell layer develops from the trophoblast forming the roof
of the amniotic cavity. It lines the roof and the lateral walls of the amniotic cavity and does not
cover the floor. Amnion has two types of cells, i.e. Golgi and the fibrillar. The cuboidal cells of the
inferior surface of the embryonic disk near the cranial end become columnar, forming the circular
area known as the prochordal plate.
With the appearance of the prochordal plate, the cranial and the caudal ends of the embryonic
disk are defined denoting the central axis.
Note : Chorion is the combination of trophoblast and the mesoderm, while amnion is a combination
of amniogenic cells and the mesoderm.
Formation of the Primitive Streak (Fig. 9.17)

Superior surface of the embryonic disk shows the linear raised area towards the caudal end of the
embryo. This is due to linear proliferation of ectodermal cells on the superior surface of the
embryonic disk along the central axis of the embryo near the tail. This is known as primitive streak.
As a result of the elongation of the embryonic disk, the primitive streak gets enlarged.
Fig. 9.17: Formation of primitive streak, Hensen’s node, blastopore and the notochordal process
The primitive streak gives rise to the third

layer of the embryonic disk the intraembryonic
mesoderm.
Gastrulation (Fig. 9.18)

Gastrulation includes the formation of the
primitive streak and formation of the intra-
embryonic mesoderm.
Intraembryonic mesoderm spreads in the
cranial, caudal and the lateral directions. It
absent in three regions:
1. Region of the prochordal plate
2. Region of notochord
3. Region of cloacal membrane.
Due to the absence of the intervening
mesoderm, the prochordal plate and the Fig. 9.18: Gastrulation includes formation of primitive
cloacal membrane become thin, forming the streak and intra-embryonic mesoderm
buccopharyngeal and the cloacal membranes Note that the prochordal plate and cloacal membrane are
respectively. without intervening mesoderm. Green arrows indicate spread
of intraembryonic mesoderm from primitive streak
Growth of the primitive streak makes the
embryonic disk change its shape from circular to pear-shaped.
The caudal end of the embryonic disk along with the amniotic, cavity and the yolk sac is
attached to the trophoblastic wall through the connecting stalk. With growth of the embryo the
connecting stalk gets thinner and longer. As a result, the embryonic disk is seen hanging from the
trophoblastic wall with the help of elongated connecting stalk which becomes the umbilical cord
later.
Intraembryonic Mesoderm (Figs 9.19 and

9.20)
The primitive streak is the mother of the
intraembryonic mesoderm. The intraembr-
yonic mesoderm lies in between the ectoderm
and the endoderm of the embryonic disc
except at three sites mentioned earlier.
Intraembryonic mesoderm meets its
counterpart of the other side in front of the
prochordal plate forming the cardiogenic plate.
Intraembryonic mesoderm is subdivided
into 3 columns as the paraxial mesoderm,
intermediate mesoderm and the lateral plate
mesoderm from medial to lateral side.
Fig. 9.19: Three columns of intraembryonic mesoderm
Fertilization 63
Fig. 9.20: Cross section of embryonic disk showing three parts of intraembryonic mesoderm.
Note formation of intraembryonic coelom between the somatopleuric and the splanchnopleuric layers
of lateral plate mesoderm
Paraxial Mesoderm (Refer Figs. 9.19 and 9.20)

It comes from the primitive node and the anterior part of the primitive streak. As it lies parallel to
central axis of the embryonic disk it is called the paraxial mesoderm. Cranial part of it is
unsegmented, while rest of the paraxial mesoderm gets divided in 44 pairs of segments. They are
known as somites. Cranial 4-5 somites lie lateral to the hind brain and contribute to the formation
of the skull. A cavity develops inside the somite is called the myocele. The cavity is transitory and
gets obliterated due to proliferation of cells of the cavity.
Each somite gets divided into two parts, ventri-medial and the dorsilateral parts. They are
called the sclerotome and the dermomyotome respectively. Sclerotome migrates towards notochord
and neural tube medially to form the primitive vertebrae. Dermomyotome has two parts namely
the lateral dermal plate and the medial muscle plate. Dermal plate forms the dermis of the skin and
the subcutaneous tissue under the surface ectoderm. Muscle plate forms skeletal muscles. The
mesodermal somite gets its nerve supply from the corresponding spinal nerve. The muscle carries
its nerve supply with it, during migration. Thus, the muscle sticks to its nerve and does not depart.
Distribution of the 44 somites is as under:
1. Occipital – 4
2. Cervical – 8
3. Thoracic – 12
4. Lumbar – 5
5. Sacral – 5
6. Coccygeal – 8-10
Note: Unsegmented cranial part of the paraxial mesoderm and the occipital myotomes helps in
the development of skull cap and the base of the skull.
Please remember that all the skeletal muscles of the trunk are mesodermal in origin including
the muscles of the tongue, diaphragm and the limbs. The muscles of the tongue are derived from
the occipital myotomes. Muscles carry the hypoglossal nerve forwards towards the tongue crossing
the internal and external carotid arteries, superficially.
Intermediate Mesoderm (Fig. 9.21)

It lies between the paraxial mesoderm medially and the lateral plate mesoderm laterally. The
column of intermediate mesoderm in the cervical and upper half of the thoracic region is segmented.
The caudal part of it remains unsegmented and forms the nephrogenic chord. With the appearance
of the intraembryonic coelom, intermediate mesoderm projects as a bulging from dorsal wall of
the intraembryonic coelom on both sides of the primitive dorsal mesentery.
Lateral Plate Mesoderm (Refer Fig. 9.20)

Lateral plate mesoderm arises from the middle of the primitive streak and remains unsegmented. It
spreads laterally up to the lateral limit of the embryonic disk. Its cranial migration extends cephalic
to the prochordal plate and joins with counterpart of the other side forming the pericardial bar. A
cavity appears in the pericardial bar which is known as the pericardial sac. Probably this is the
beginning of the formation of intraembryonic coelom. Similar clefts or cavities appear in the lateral
plate mesoderm and join, forming intraembryonic coelom inside the embryonic disk. Due to
appearance of the intraembryonic coelom the lateral plate mesoderm gets split into two layers
somatopleuric and splanchnopleuric. Intraembryonic coelom is like an inverted U or horse-shoe
shaped. The cavity extends in front of the prochordal plate and its diverging limbs occupy the
lateral part of the embryonic disk. Intraembryonic coelom does not reach the mesoderm between
cranial edge of the disk and the cardiogenic area. This part of the mesoderm forms the septum
transversum which gives rise to the major part of respiratory diaphragm.
Somatopleuric layer of the lateral plate mesoderm forms parietal layer of pleural, peritoneal
and pericardial sacs, subcutaneous tissue of the body wall. The muscles of the trunk both of back
and the front include the extensors and flexors muscles of the limbs are derived from paraxial
mesoderm.
Fig. 9.21: Nephrogenic cord projecting from the dorsal wall

in the intraembryonic coelom by the side of dorsal mesentery
Fertilization 65
Splanchnopleuric Layer
It contributes to visceral layer of the sacs, i.e. pericardial, pleural and the peritoneal, smooth muscles
and connective tissue of the gut, respiratory tree and the heart.
In early stages, the intraembryonic coelom is a closed cavity. However, it communicates with
the extraembryonic coelom later. The heart tube develops from the splanchnopleuric mesoderm
of the floor of the pericardial cavity.
Neural Tube (Fig. 9.22)

“The process of formation of the neural plate, neural folds and their fusion to form the neural tube
is called “Nurulation”. The ectoderm above the notochord gets thickened to form the neural plate.
The neural groove appears on the neural plate with the formation of neural folds. Neural folds
Fig. 9.22: Development of neural tube anterior and posterior neuropores.

Note the circulation of the amniotic fluid into the cavity of the neural tube when the neuropores get closed.
The amniotic fluid gets trapped within embryonic body
start fusing in the middle and the process of fusion proceeds cranially and caudally. Before
completion of the process of fusion, the neural tube presents two openings. The cranial opening is
called the anterior neuropore and the caudal is called the posterior neuropore. Amniotic fluid
circulates in the tube through the neuropores. With the closure of the openings, amniotic fluid gets
trapped in the neural tube. [It is said that we have imbibed (take in) the sea water in our body].
Neural tube has two—parts the larger cranial and the smaller and narrower caudal. Cranial part
forms brain and the caudal part forms the spinal cord.
Formation of Notochord (Fig. 9.23) (Refer Figs 9.17 to 9.19)

The primitive streak is formed due to the linear proliferation of the cells of the ectoderm on the
superior surface of the embryonic disk, producing the linear strip in the floor of the amniotic
cavity. At the cranial end of the primitive streak, there is localized proliferation cells forming the
primitive knot or Hensen’s node. A depression appears in the center of the Hensen’s node. It is known
as the blastopore. Solid cord of cell grows cranially from the Hensen’s node between the ectoderm
and the endoderm which reaches the caudal margin of the prochordal plate. This is known as head
process. The cavity of the blastopore grows into the head process and forms the notochordal canal.
The cells of the floor of the canal get mixed up with the cells of the roof of the yolk sac. Finally, the
floor of the notochordal canal disappears and the channel communicating the amniotic cavity and
the yolk sac is established. It is called the notochordal canal.
1. Floor of the notochordal canal breaks.
2. Wall of the canal becomes flattened which is called the notochordal plate.
3. The notochordal plate gets curved and forms the tube. Cells of the tube undergo rapid
proliferation converting the hollow notochordal tube into the solid notochord.
Clinical
Caput succedaneum: It develops as a large swelling on the presenting part of the fetal head over the
scalp. It is often seen during labor in case of contracted pelvis. Caput comes down ahead of the
head. Hence it can be mistaken for the head itself. It may result in taking unwise and unwarranted
decision of applying forceps to caput instead of the head during conducting delivery. Normally
caput succendeneam resolves, without treatment.
Chordoma: It may arise from the remnants of the notochord. They are seen at the base of the cranium
and have tendency to spread to the nasopharynx. Thirty percent of these tumors are malignant.
Sacrococcygeal teratoma: It is a large precoccygeal tumour arising from the totipotent cells of the
Hensen’s node. Its large size can cause infant death or obstructed labor.
Formation of Secondary Yolk Sac (Refer Fig. 9.14)

Due to formation of the extra-embryonic coelom and its enlargement, the primary yolk sac becomes
smaller in size and the flattened cells lining the cavity become cuboidal. The differences between
the primary yolk sac and the secondary yolk sac are as under.
Secondary yolk sac is smaller in size and it is lined by the cuboidal cells.
Fertilization 67
Fig. 9.23: Stages of formation of the notochord
Role of Yolk Sac

1. Does not store yolk
2. Helps in transfer of nutrient to the embryo.
3. Wall of it is the first site of blood formation.
4. Forms endodermal lining of the GI tract and the respiratory system.
5. Source of primordial germ cells.
Folding of the Embryonic Disk (Figs 9.24 and 9.25)

The enlargement of the embryonic disk results in increasing the length of the disk. Due to increased
length, the embryonic disk bends producing a convexity dorsally. It is seen as a bulging in the
floor of the amniotic cavity.
Due to the formation folds on all sides, the curved embryo becomes cylindrical leaving an
opening on the ventral aspect called the umbilical opening. Due to formation of the head and the
tail folds, part of the yolk sac is taken inside the embryonic disk. It forms the primitive gut which
is lined by endoderm. Part of the yolk sac taken in as a result of formation of the head fold is
Fig. 9.24: With formation of head and tail folds, forgeut, midgut and the hindgut are formed.
Note that the amniotic cavity covers the embryonic disk on all sides except at the umbilical opening
Fig. 9.25: Foregut, midgut, hindgut and vitelllointestinal duct with stomodeum and proctodeum
known as the foregut and the part of the yolk sac taken in, due to the formation of the tail fold, is
called the hindgut. Middle part of the primitive gut communicates with the vitellointestinal duct
which is called the midgut. The yolk sac which becomes smaller in size is called the umbilical
vesicle. Following the extensive folding, the amniotic cavity expands all around the embryonic
disk forming the ectodermal cover for the embryo except at the site of entry of the vitellointestinal
duct. The opening thus formed is called the umbilical opening. The enlargement of the amniotic
cavity filled with the amniotic fluid to the brim provides a swimming pool for the embryo. Due to
the large sized amniotic cavity and plenty of amniotic fluid, the small-sized embryo is seen hanging
from the placenta by the umbilical cord. The embryo is free to move and rotate resulting in torsion
of the umbilical cord leaving rotational marks on the umbilical cord.
Connecting Stalk (Fig. 9.26)

The extraembryonic mesoderm running from amniotic cavity and yolk sac to the trophoblastic
wall is called the connecting stalk. Formation of the connecting stalk is due to the noninvasion of
the mesoderm by the extraembryonic coelom.
Uterine endometrium and the trophoblast form the placenta, which is the main source of the nutrition
and oxygen to the growing embryo. It removes the waste products of the metabolic processes of the
embryo. To highlight the importance of the connecting stalk, one can say that the connecting stalk is
the life line of the embryo. With the development of the embryo, the connecting stalk gets narrower
and longer to form the umbilical cord. It is attached to the embryonic disk at the caudal end. After
the formation of the tail fold, the attachment of the connecting stalk shifts to the ventral aspect of
the embryo at the site of umbilical opening. As the blood vessels develop in the embryo and the
placenta they establish communications.
There are two umbilical arteries and two umbilical veins in the connecting stalk. However, the
right umbilical vein disappears and the left vein becomes the ligamentum teres hepatis.
Ligamentum teres hepatis lies in the free border of the falciform ligament. It is accompanied by the
paraumbilical veins which open into the left branch of the portal vein.
Fertilization 69
Fig. 9.26: Formation of connecting stalk and the umbilical cord
Following are the constituents of the umbilical cord: (Fig. 9.27)

1. Cover of the amnion all around
2. Wharton’s jelly
3. To and fro blood vessels, i.e. from placenta to the embryo and from the embryo to the placenta.
4. Part of the extraembryonic coelom.
At birth umbilical cord has length of fifty centimeters and a diameter of two centimetres. Freely
hanging embryo in the amniotic cavity rotates and the rotational marks are left on the umbilical
cord. Too short umbilical cord creates problems at the time of delivery. Long umbilical cord may
form loop or loops around the neck of the baby causing strangulation and death.
Allantoenteric Diverticulum (Fig. 9.28)

At the caudal end of the embryonic disc the yolk sac gives a small diverticulum known as the
allantoenteric diverticulum. It grows in the connecting stalk. Absorption of the diverticulum into
the hindgut takes place after formation of the tail fold.
Fig. 9.27: Cross section of umbilical cord
Fig. 9.28: Allantoic enteric diverticulum arising from yolk sac (A)
Allantoenteric diverticulum projecting from hindgut into the connecting stalk (B)
Fertilization 71
Now the diverticulum apparently arises from the ventral aspect of the hindgut and is seen
entering the connecting stalk.
Meckel’s Diverticulum (Fig. 9.29)

It is the remnant of the vitello-intestinal duct seen at the antimesenteric border of the ileum having
2" in length, 2" feet away from the ileocecal junction with two types of ectopic tissues, i.e. gastric or
Fig. 9.29: Development of Meckel’s diverticulum and other anomalies

pancreatic. Normally it does not give rise to symptoms. However, presence of gastric tissue can cause
peptic ulcer at the mesenteric border leading to bleeding and perforation. Treatment is resection of the
segment bearing Meckel’s diverticulum and anastomosis. Mere diverticulectomy is irrational as
the ulcer along the mesenteric border is left unattended. As the Meckles’ diverticulum has 3 coats,
own blood supply, mouth and the lumen, is the true diverticulum.
Arrangement of Structures of Embryo before and after the Formation of the Head and the
Tail Folds (Figs 9.30 to 9.33)
Before formation of head fold After formation of head fold

The sequence is cranio-caudal.
1. Septum transversum 1. Septum transversum which was the cranial most structure
becomes caudal most.
2. Pericardium and heart tube lie in the 2. Pericardium and the heart lie ventral to the foregut.
floor of the pericardial cavity.
3. Prochordal plate 3. Heart tube jumps from the floor of the pericardial cavity to the
roof (reversal).
4. Neural plate
5. Primitive streak
6. Cloacal membrane
Fig. 9.30: Position of septum transversum, pericardial cavity and prochordal plate from before backwards
Note intraembryonic coelom in the lateral plate mesoderm
Fertilization 73
Fig. 9.31: Embryonic disk with important components, e.g. septum transversum, pericardial
cavity, heart tube, prochordal plate, neural plate, notochord, primitive streak, cloacal
membrane and allantoenteric diverticulum arranged from craniocaudally
Fig. 9.32: Embryonic disk after formation of head fold. The heart tube has jumped from floor of the
pericardial cavity to the roof and the septum transversum goes caudal to the pericardial cavity and the heart tube
Fig. 9.33: Further stage of formation of head and tail folds. Study the changed relation of septum transversum,
pericardial cavity, buccopharyngeal membrane, cloacal membrane and the allantoenteric diverticulum
The Placenta 75
The Placenta
10
The placenta includes chorionic plate of the fetal side and the basal plate of the maternal side.
After fertilization in the ampullary part of the uterine tube fertilized ovum reaches the uterine
cavity. Due to the process of cell division morula is formed which soon gets converted into the
blastocyst. Due to presence of zona pellucida, the trophoblast of the blastocyst fail to stick to the
uterine wall. After disappearance of zona pellucida, trophoblast of the blastocyst get attached to
the uterine wall (implantation). Due to proteolytic activity, trophoblast invade and go deeper in
the decidua basalis. This is known as interstitial type of implantation (Figs 10.1 to 10.12).
Fig. 10.1A: Changes in uterine mucosa in relation with the ovarian changes.
Observe implanted blastocyst and corpus luteum of pregnancy. In the absence of implantation of blastocyst there is
no gravid phase, no corpus luteum. Instead, there is menstrual phase with degenerating corpus luteum
After implantation of the fertilized ovum, the

changed character of the endometrium is known as the
decidua. The uterine lining becomes thick,
edematous, vascular, glandular and cellular in the
decidua.
Fig. 10.1B: Menstrual phase
Fig. 10.2A: Relation of circulating fetal blood in the villi floating in the intervillus spaces filled with maternal blood
Fig. 10.2B: Structures of primary, secondary and tertiary villi in cross-section

The Placenta 77
Fig. 10.2C: Placental barrier Fig. 10.2D: Types of implantation
Fig. 10.3: Formation of chorion frondosum and chorion laeve.

Note: Three parts of decidua 1. Decidua basalis 2. Decidua capsularis, and 3. Decidua parietalis
Fig. 10.4: Placenta with gaint cells and Nitabuch’s layer having fibrinoid deposits
Fig. 10.5: Trabeculae and lacunae surrounding the blastocyst
Fig. 10.6: Layers of endometrium. Note the spiral arteries supply the stratum spongiosum
and straight arteries supply the stratum basale
The Placenta 79
Fig. 10.7: Formation of outer shell of trophoblast dividing syncytiotrophoblast into inner and outer layers of
syncytiotrophoblast undergoes fibrinoid degeneration. Inner layer of syncytiotrophoblast undergoes
fibrinoid degeneration known as Rohr’s stria
Fig. 10.8: Anchoring villi with intervillus spaces in the placenta.

Note truncus ramus and ramuli chorii
Fig. 10.9: Cotyledons of placenta
Fig. 10.10: Circulation of maternal blood in the placenta
Fig. 10.11: Fetal surface of placenta. Fig. 10.12A: Maternal surface of placenta.
Courtesy: Dr Mrs Sushma Deshmukh Courtesy: Dr Mrs Sushma Deshmukh
The Placenta 81
Types of Implantation (Fig. 10.12B)

1. Interstitial: Lies in the uterine wall.
2. Central implantation: Lies in the uterine cavity.
3. Eccentric implantation: It lies in the uterine crypt.
Decidua
After implantation of the ovum uterine endometrium undergoes radical changes which include
enlargement of the stromal cells filled to the brim with glycogen and lipids. The changes in the
stromal cells are known as decidual reaction. The zone of attachment of the blastocyst to the uterine
endometrium is known as decidua basalis. The decidua which covers the embryo is called decidua
capsularis and one which lines the uterine cavity is known as decidua parietalis.
Area of the decidua basalis is also known as the decidual plate. The end of pregnancy is
marked by the process of shedding the decidua along with the placenta and its membranes.
(Meaning of the word decidua is shedding off).
The finger like processes arising from all sides of the blastocyst are called the villi (chorionic
villi). At the basal plate villi grow faster and those arising from the decidua capsularis have slow growth.
Here the villi degenerate and form smooth area known as chorion laeve. Full grown villi at the
decidua basalis are called chorion frondosum. Trophoblast with the extraembryonic mesoderm is known
as the chorion. The combination of the chorion and the tissue from the decidua basalis together form the
placental mass.
Note:
1. Decidua basalis has isolated multinucleated giant cells which secret placental hormones.
2. In certain areas of the terminal villi, syncytium joins the capillary walls. They known as vasculo-
endothelial membranes. The villus has membranous and the non-membranous areas.
Fig. 10.12B Relation of circulating fetal blood in the villi floating in the intervillus spaces filled with maternal blood
Membranous area is called as “alpha zone”. It is the site for maternal and fetal exchange.
Non-membranous area is known as “beta zone”. It probably produces hormones.
Process of Formation of Villi (Refer Fig. 10.2)

1. Primary villus: Single layer of cytotrophoblast forms the core of the villus which is covered by
the syncytiotrophoblast (only cells).
2. Secondary villus: Extraembryonic mesoderm is added to the core of the primary villus. It is
known as secondary villus. (Cells + mesoderm)
3. Tertiary villus: When the blood vessels develop in the core of the extraembryonic mesoderm, it
is called the tertiary villus. (Cells + mesoderm + blood vessels)
Syncytiotrophoblast grows rapidly and forms a syncytium with no clearly visible cell walls
but having prominent nuclei. Deep to the syncytiotrophoblast is the layer having clear cell wall and
nuclei. It is called the cytotrophoblast. (Langhan’s layer).
Syncytiotrophoblast grows rapidly and proliferates forming the small cavities within. The
cavities are called the lacunae.
The lacunae get radially arranged (Fig. 10.5). Cells of the syncytiotrophoblast from trabeculi
which act as partitions between the lacunae. Lacunae join to form larger lacunae. Syncytio-
trophoblast on embryonal side, grows excessively and erodes the endometrium of the uterus leading
to the rupture of the maternal blood vessels. It fills the lacunar spaces with maternal blood.
Trabecular columns of syncytiotrophoblast are invaded by the cytotrophoblast. Each trabeculum
consists of central core of cytotrophoblast surrounded by the collar of syncytiotrophoblast. The
primary villus thus formed is seen floating in the pool of maternal blood. Trabeculae become the
primary villi and the lacunae get converted into the intervillus spaces.
Please note, that the intravillus circulation is fetal while the intervillus circulation is maternal.
Cytotrophoblast entering the trabeculum fails to penetrate the layer of syncytiotrophoblast and
hence does not reach the decidua. However, cytotrophoblast succeeds in coming out of the
syncytium at the apex of the villus. The cells of the cytotrophoblast join the cytotrophoblastic arm
of adjoining villus and form the trophoblastic shell. Due to the intervention of cytotrophoblastic
shell, syncytiotrophoblast gets isolated from the decidua and also divide into the outer and the
inner layers.
Villi are attached to the maternal and the fetal side. As the villi are fixed at both the ends they
are called the anchoring villi. Branching pattern of the villus is in the form of truncus chorii, rami chorii
and the ramuli chorii. Ramuli chorii are attached to the cytotrophoblastic shell. Intervillus space is
filled with branches of anchoring villi. Anchoring villi give number of offshoots which move as
the free villi. In addition to this, new villi are added from the chorionic side converting the intervillus
space into a bag of vascular sponge. This increases the surface area for exchange of fetal and maternal
circulatory bed. Every new villus formed has to pass through three stages i.e. primary, secondary
and the tertiary.
Development of Placenta (Refer Fig. 10.9)

Intervillus septa from the maternal side divide placenta into lobes known as the cotyledons. In
fully developed placenta there are 15 to 30 cotyledons. Each lobe is made of large number of
The Placenta 83
anchoring villi, with branches. Fully developed placenta has 60-100 fetal cotyledons. Hence each
cotyledon has at least two villi. Weight of the placenta is around 500 gm and its diameter is 20 cm.
After birth of the baby the placenta is shed off along with the decidua. Maternal surface of the
placenta has grooves and elevations having cobble stone appearance. (cobble means rounded stones
used for paving the roads particularly in the public gardens) (Reference Figure 71-72 – Photographs)
Fetal surface of the placenta is smooth shining and is covered with the amnion.
Placental Barrier (Refer Fig. 10.2C)

Fetal blood and the maternal blood do not mix. The medium of separation between the two from
inside out are as under
1. Endoderm
2. Basement membrane
3. Mesoderm
4. Cytotrophoblast
5. Syncytiotrophoblast
Aid to Memory
EBMCS - Eastern Bureau of Mines supplies Coal to South.
Placental membrane barrier measures up to 14 mtr, i.e. equal to the absorptive area of the gastro-
intestinal tract. There are microvilli on the surface of the cytotrophoblast which further increase the
absorptive capacity.
Functions of Placenta
1. Transport of oxygen, water, electrolyte, nutrition, carbohydrates, lipids, polypeptides amino-
acids and vitamins from the mother to the fetus.
2. Fetal blood takes about 25 ml of oxygen per minute from the maternal blood. Therefore, even
the brief disturbance of oxygen supply to the fetus can be hazardous.
3. Excretion of CO2 and urea.
4. Maternal antibodies (IgG) gamma globulins, immunoglobulins cross the placental barrier which
give immunity to the fetus against diseases like diphtheria, measles and poliomyelitis but not
against chickenpox and whooping cough.
5. Helps in exchange of gases and excretion products of metabolism from fetal and maternal
circulation.
It is achieved through simple process of diffusion or through an active process. PO2 tension in
maternal blood is 50 mm Hg while in the fetus is only 20 mm Hg.
Glucose level of the fetal blood is lower than that of the maternal blood due to rapid metabolic
action. Active diffusion of amino acid, calcium and inorganic phosphate is carried by carrier
molecules or phagocytosis. As the fetal and maternal RBCs, can cross the placental barrier they
may create Rh incompatibility.
Placenta acts as the storage house for the glycogen, calcium and iron in the early months of
pregnancy, however this function is taken over by liver soon.
Normal Human Placenta is Hemochorial
Placental Circulation (Refer Figs 10.7 and 10.8)

Maternal blood develops direct contact with the placental villi
due to disappearance of the endothelial of the maternal blood
vessels. As a result the intervillus space is filled by maternal
blood coming from the uterine vessels after endothelial loss.
Umbilical artery gives terminal branch in the form of spiral
arteries which enters the intervillus space. The terminal
opening of the spiral artery has hypertrophied cells which slow
down the placental circulation leading to lowering of the
arterial blood pressure.
Small fragments syncytiotrophoblast are released in the
intervillus space which are carried to the lungs through the
uterine vein. This is the probable reason why mother starts
recognizing the fetal tissue as her own and not foreign.
Short circuit between the umbilical vein and the artery is
prevented by high perfusion pressure of the endometrial
arteries. As a result blood is forced to go towards chorionic
plate. Uterine muscle contractions and the fetal pulse in the
villi help intervillus circulation. It must be noted that the blood
pressure in the intervillus space is around 15 mm of mercury.
There is one spiral artery for each intervillus space. Ramuli go
to basal plate and turn back to the intervillus space. Maternal
and fetal blood flow in opposite direction (Counter current)
increasing the surface area for the gaseous exchange. The
vascular branching of the villi arising from the tertiary stem villus
ramify in the form of hollow drums system (Tambour). Tambour is
a drum like shallow appliance for recording pulse, pressure
(BP) and respiration. The branches of the third order pass
through the intervillus space and go to the basal plate. Finally,
it returns to the intervillus space, forming the terminal villus
network. This terminal network is at the periphery of
imaginary cylindrical core which is villus free. There is one
spiral artery from the mother to each Tambour system. As a
result the maternal blood enters into the villus free central area
of the Tambour system. About 300 ml of fetal blood circulates
through the chorionic villi every minute. It must be
remembered that the pressure of the fetal blood capillaries is
around 30 mm of mercury.
Abnormal Implantation of the Ovum (Fig. 10.13A)

This can be intrauterine or extrauterine.
Fig. 10.13A: Placenta previa
The Placenta 85
A) Extrauterine Implantation (Fig. 10.13B)

1. Tubal pregnancy (ectopic tubal
pregnancy: It cannot continue beyond
three month due to the non-development
of the decidua.
2. Abdominal pregnancy
3. Interstitial tubal implantation occurs in
tubal ostium
4. Ovarian implantation: Recently a live
birth in event the ovarian implantation has
been reported in Australia.
Fig. 10.13B: Ovarian ectopic pregnancy
B) Intrauterine Abnormal Implantation Courtesy: Dr Parimal Fukey, Nagpur, Maharashtra, India
(Fig. 10.13C)
Implantation of the placenta in the lower
uterine segment is called placenta praevia.
Placenta previa is divided into 4 degrees.
1st degree – Occupies the lower uterine
segment but fails to reach the internal os.
IInd degree – Reaches the margin of the
internal os.
IIIrd degree –Partially covers the internal os.
IVth degree –Totally covers the internal os. It
causes severe bleeding during early stages
of labor (Parturition).
Anomalies of the Placenta (Figs 10.14. and

10.15) Fig. 10.13C: IV degree placenta previa totally covering the
internal os Courtesy: Dr Parimal Fukey, Radiologist,
1. Bilobed placenta Nagpur, Maharashtra, India
2. Lobed placenta
3. Diffuse placenta: In diffuse placenta the chorionic villi at the site of chorion laeve continue to
grow along with the villi of chorion frondosum.
4. Placenta succenturia: Small part of the placenta is detached from the main placental mass but
remains connected through the placental membranes.
5. Fenestrated placenta: a hole exist in this type of placenta.
6. Circumvallet placenta: Decidual fold covers outer margin of the placenta.
Variations of Umbilical Cord Attachments

• Marginal
• Velamentous
• Furcate
Fig. 10.14A: Bilobed placenta Fig.10.14B: Lobed placenta
Fig. 10.14C: Diffuse placenta Fig. 10.14D: Placenta succenturia
Fig. 10.14E: Circumvallate type of placenta Fig. 10.14F: Fenestrated placenta

The Placenta 87
Fig. 10.15A: Variations of attachments of umbilical cord to the placenta
Fig. 10.15B: Bunch of grapes reminds look of hydatidiform mole
Placental Classification as Per the Tissues Involved

After going through the phylogenetic events it is observed that the placenta can be classified into
five types:
1. Epitheliochorial: It is also called non-deciduas as the decidua is not shed.
2. Syndesmochorial
3. Endotheliochorial
4. Hemochorial (Human)
Due to erosion of the endothelium of the maternal blood vessels, maternal blood comes in
contact of the chorionic villi. The intervillus spaces get filled with maternal blood rushing
from the eroded uterine vessels from the openings in the desidual plate.
5. Hemoendothelial type (Rabbit): In this type of placenta the endothelium of the fetal blood vessels
forms the barrier between the maternal and the fetal blood.
Hormones
hCG (Human chorionic gonadotropin) estrogen, progesterone and hPL (human placental lactogen)
along with prostaglandins are the hormones produced by the placenta. Human chorionic
gonadotropin is formed by cytotrophoblast and syncytiotrophoblast. It can be detected in urine of the
mother after 8 days of pregnancy (2 weeks). hCG level goes down after 16th week. In case of its
persistance even after two months, molar pregnancy should be suspected.
hCG is responsible for growth of corpus luteum up to 3rd month. It produces testosterone
from the interstitial cells causing testicular descent.
Placental Estrogen
It is synthesized by syncytiotrophoblast from dehydroepiandrosterone (DHEA) which is
manufactured by the suprarenal cortex. Abrupt fall of estrogen level in the maternal blood could be
indicative of fetal death.
Action of Placental Estrogen

It causes enlargement of uterus, breast and female external genitalia and relaxation pelvic muscles.
Placental Progesterone
Action: Development of decidual cells, provides nutrition to embryo, decreases uterine contraction
and gets breast ready for the lactation.
Placental Lactogen
It is a protein hormone made of 190 amino acids. It is synthesized by syncytiotrophoblast.
Prostaglandins
Are the fatty acid compounds secreted by placenta. They help in the maintenance of the pregnancy
and the onset of labor. Decrease ratio of progesterone estrogen is marked by increased secretion of
prostaglandins by the placenta.
Placental – Homograft
Nonreaction of mother to the antigens of the embryo continues until pregnancy which is probably
due to lac of excessive lymphatic drainage. Trophoblast do not carry antigens.
The Placenta 89
Clinical
Hydatidiform Mole (Fig. 10.15C)
The formation of the hydatidiform mole basically involves an abnormal growth of the trophoblast.
As the embryo dies, the chorionic villi do not develop further failing to form the tertiary villi as
they remain avascular. Cystic swellings develop from the degerating villi. Around 3 to 5% of the
hydatidiform mole undergoes malignant change forming the choriocarcinoma. There are two
clinical type of the hydatidiform mole:
1. Complete – No embryo
2. Partial – Part of embryo is seen
Majority of hydatidiform are monospermatic. An empty oocyte having no female pronucleus
is fertilized by a single sperm, it is called monospermic hydatidi form mole.
Note: One who has seen the hydatidiform mole, would love to compare it with the bunch of grapes
(Figure 10.15A).
Diagnosis
1. Ultrasound – ‘Snow storm’ appears of the whole of uterine cavity.
2. Finding of vesicles in urine.
3. Uterine enlargement
4. No fetal movements
5. No fetal heart sounds
6. High level of hCG and hPL
Fig. 10.15C: Ultrasonograph of Hydatidiform mole (Snow storm appearance of uterine

cavity) Courtesy: Dr Dinesh Singh, Radiologist, Nagpur, Maharashtra, India
The Umbilical Cord (Fig. 10.16)

Umbilical cord is a rope like structure connecting umbilicus of the fetus to the center of the fetal
surface of the placenta. It has covering of the smooth glistening amniotic membrane on the fetal
side. The mesodermal bar connecting the tail end of the germinal disk to the wall of the blastocyst
forms the umbilical cord (connecting stalk). Umbilical cord consists of primary mesoderm, umbilical
vessels, the allanto-enteric diverticulum and the remnants of vitellointestinal duct. Length of the
umbilical cord at the full-term is approximately 50 cm and breadth being 2 cm. Long umbilical
cord can strangulate the baby while the short umbilical cord can create problems during delivery.
Long umbilical cord can prolapse in the cervical canal (Prolapse of the umbilical cord).
Umbilical cord has twisted appearance which is attributed to the freely hanging fetus which is
able to move and rotate in the amniotic cavity (the so called amniotic swimming pool). Differential
growth of the vessel wall muscles may add to twists.
Contents
1. Two umbilical arteries
2. Initially two umbilical veins of which the right umbilical vein disappears and the left umbilical
vein forms ligamentum teres hepatis.
3. Remnants of allantoenteric diverticulum.
4. Remnants of vitellointestinal duct
5. Wharton’s jelly.
Two umbilical arteries arising from the ventral divisions of the internal iliac arteries bring
deoxygenated blood to the placenta. After oxygenation the blood is returned by the left umbilical
vein to the left branch of the portal vein. The special intrahepatic channel runs from left branch of
the portal vein to the hepatic segment of inferior vena cava. It is known as the ductus venosus,
which gets atrophied and forms the ligamentum venosum.
Fig. 10.16: Cross-section of umbilical chord

The Placenta 91
After birth distal part of the umbilical arteries gets fibrosed forming the medial umbilical
ligaments, while the proximal part forms the superior vesicle artery.
Wharton’s Jelly
Wharton’s jelly is formed for the protection of the umbilical vessels. It is derived from the primary
mesoderm of the connecting stalk. The jelly is formed due to mucoid degeneration of the primary
mesoderm.
Distal part of the allanto-enteric diverticulum gets fibrosed and forms urachus, connecting the
apex of the urinary bladder to the umbilicus. It forms the median umbilical ligament in the adult.
Meckel’s Diverticulum (Fig. 10.17)

Midgut is connected with the vitellineintestinal duct which normally disappears. It may persist in
its proximal part and forms the Meckel’s diverticulum arises from the antimesenteric border of the
gut.
Fig. 10.17: Allantoic enteric diverticulum arising from yolk sac (A), Allanto enteric diverticulum
projecting from hindgut into the connecting stalk (B)
Allanto-enteric Diverticulum
Distal part of the allanto-enteric diverticulum gets fibrosed to form the urachus which becomes
the median umbilical ligament.
Physiological Umbilical Hernia (Fig. 10.18)

Communication between extra and intraembryonic celoms remains patent around the vitello-
intestinal duct. U-shaped loop of the midgut herniates into the extraembryonic celom. It is called
the physiological umbilical hernia. Celomic space gets closed after the return of the midgut loop to
the abdominal cavity.
Amniotic Cavity (Figs 10.17 to 10.21)

It appears as a space between amniogenic cell layer formed by the trophoblast above and the
ectodermal layer of the floor of amniotic cavity below. Meeting of the roof and the floor is at the
periphery of the disk and is called amnio-ectodermal junction.
As the extraembryonic celom extends the amniotic cavity and the yolk sac get covered with
primary mesoderm which is continuous with the connecting stalk. Due to the formation of
embryonic folds amnio-ectodermal junction starts meeting on the ventral aspect of the cylindrical
embryonic disk to form the umbilical opening.
Amniotic cavity grows at the expenses of the extraembryonic celom which gets obliterated
after fusion of the amnion and the chorion.
Fig. 10.18: Midgut loop attached to the dorsal wall by the mesentery.
Note the superior mesenteric artery arising from dorsal aorta going to the apex of the midgut loop
The Placenta 93
10.19: Amniotic cavity, extraembryonic celom and the uterine cavity
Fig. 10.20: Amniotic and uterine cavities

Please note enlargement of amniotic cavity at the expence of extraembryonic celom which has disappeared
Fig. 10.21: Amniotic cavity has grown at the expense of extraembryonic celom.
Note: With fusion of amnion and chorion the extraembryonic celom disappear. When the decidua capsularis and
parietalis fuse the uterine cavity disappears. As a result large amniotic cavity is the only occupant of the uterine cavity
along with the fetus
Amniotic Fluid
It is clear, watery and has salt, sugar, urea and proteins. The fluid is produced by the cuboidal
amniotic cells which are of two types:
1. Golgi type
2. Fibrillar type.
Increase in the quantity of the amniotic fluid continues up to the 6th month of gestation and the
recession begins towards the end of gestation.
Functions of Fliquor Amnii

1. Acts as the protective fluid cushion for the embryo in which the swimming and rotating embryo
grows.
2. Fluid maintains pressure suitable for differentiation and growth of delicate organs.
3. Allows free movements of the embryo.
4. Maintains environmental temperature.
5. By forming the hydrostatic bag it helps in dilation of the cervical canal at the time of parturition
(during labor).
The Placenta 95
Addition of fetal urine and swallowing of liquor amnii by the fetus maintain the quantity of
the amniotic fluid to the optimum.
Abnormal of liquor amnii
Hydramnios Oligoamnios
Fluid content in excess, i.e. more than 2 liters. Fluid is scanty
Excess collection of amniotic fluid occurs when the Due to congenital absence of metanephros on both sides,
fetus is unable to swallow it due to esophageal urine is not added to the amniotic fluid. (Bilateral renal
atresia. agenesis.)
Amniocentesis
Amniocentesis is done through the cervix or the anterior abdominal wall for the purpose of nuclear
sexing and diagnosis of the deformities.
Hormones
As a rule maternal hormones do not reach the fetus due to the placental barrier. However, synthetic
hormones like progestin and synthetic oestrogen can pass through the placental barrier causing lethal
changes. As the maternal and fetal bloodstreams are circulating in isolation, antigenic reactions are rare.
Production of Hormones by Placenta

Syncytiotrophoblast produces number of hormones of which progesterone is essential for
continuation of pregnancy after the fourth month, i.e. at the time when the corpus luteum becomes
non-functional. Estrogen from the placenta promotes growth of uterus and development of the
mammary glands.
Clinical
1. Human chorionic gonadotropin (hCG) is produced by the syncytiotrophoblast which can be
detected in urine in the second week pregnancy.
2. Sommatomammotrophin has an anti-insulin effect leading to increase in glucose and amino
acid level of the maternal blood. Recollect the word, diabetes of pregnancy.
3. Pre-eclampsia: It is one of the complications of the pregnancy marked by hypertension and the
presence of albumin in the urine. It is attributed to the developmental defect of the
cytotrophoblast. It is the leading cause of fetal and maternal deaths.
4. Red cell antigen can form maternal antibodies against the foetal cells leading to their breakdown.
(Erythroblastosis fetalis). It causes severe anemia, hydrops which is characterized by edema
and effusion in the body cavities. Red cells hemolysis can be detected by finding bilirubin in
the amniotic fluid. Antigens from ABO blood group evoke antigenic response however the
effect is mild.
Prenatal Diagnosis of
of
11 Birth Defe
Def cts
ec
Study of congenital defects is called teratology. (Teratos-Monster). About 20-21% of infant deaths
are attributed the birth defects. Presence of minor anomalies like small ears may be an indication
of the major underlying defects.
Types of Abnormalities
1. Malformation: They are seen during formation of the organs (i.e. 3-8 weeks).
2. Disruption: Damage and destruction can be detected by finding of vascular defects leading to
atresia of the bowel. Formation of amniotic bands causes limb anomalies in fetal alcohol syndrome.
Syndrome
Presence of number of anomalies together due to particular common factor is called the syndrome.
Association
It is an orderly appearance of two or more anomalies with a tendency to occur in a group instead
of making the single appearance. Classical example of the association is VACTERL which means
vertebral, anal, cardiac and tracheoesophageal fistula, renal and limb defects.
V - Vertebral
A - Anal
C - Cardiac
T - Tracheoesophageal fistula
R - Renal
L - Limbs
Teratogens
1. Teratogens include infective agents such as viruses.
2. Ionizing radiation.
3. Chemicals – thalidomide can cause ameli (absence of limbs).
Phenytoin, diazepam, warfarin, aspirin, LSD (lysergic acid diethylamine), alcohol, smoking, oral
contraceptives, diabetes, iodine deficiencies, obesity, mercury and lead can cause anomalies.
Methods of Prental Disease Detection 97
Methods o f Prenatal
of
12 Disease Dete ction
Detection
1. Ultrasound: Ultrasound tells about the age, CR length, BPD and ossification of femur.
2. Growth and anomalies
3. Maternal serum screening(MSC): Serum alphaprotein.
4. Aminocentesis: It is done by transabdominal insertion of a needle into the amniotic cavity and is
undertaken only after 14 weeks. Similarly the cells can be subjected to study on the basis of
karyotyping.
5. Chorionic villus biopsy: It is done by passing a needle through the anterior abdominal wall into
the placenta to take a sample of the villi. It is risky and is not done in high-risk cases. Alpha-
fetoprotein is produced by the liver which enters maternal circulation through the placenta.
Defects as neural tube defects, anencephaly, spina bifida, omphalocele, hare lip and cleft palate
can be detected. Advanced age of the mother and diabetes are prone to cause congenital
anomalies.
Treatment
Fetal transfusion: Blood transfusion and medication can be given during prenatal period.
Fetal surgery: Fetus is operated after opening the uterus for congenital diaphragmatic hernia, removal
of a cyst, adenomatous lesion of the lung and repairing the spina bifida. Repair of the neural tube
defect does not guarantee the improvement of neurological functions. However, it does help in partial relief
of the hydrocephalus. It does prevent the herniation of the cerebellum and its tonsils into the foramen
magnum. Putting a shunt to remove fluid from the cavity obstructing the urinary system, e.g.
pigtail shunt is put into the fetal bladder to prevent renal damage.
Exposure to chemicals and radiation can cause mutation in male germ cells. Various chemicals
are blamed, e.g. mercury, lead, alcohol and smoking can cause abortions and birth detectors. Neural
tube and limb defects are attributed to the advanced age of the father. A young father of less than
20 years of age may produce birth defects in the offspring.
Stem Cell Transplantation

Fetus is not immunologically competent up to the age of 18 weeks of gestation. There is no rejection
phenomenon before 18 weeks. Hematopoietic stem cells can be used for treating hemorrhagic
disorders. Inherited metabolic diseases like cystic fibrosis can be subjected to gene therapy.
Formation of Branc
of hial
Branch
13 (Pharyngeal) Arc
(Pharynge hes
ches
Forehead prominence is formed by the brain bulge which lies above the depression called the
stomodeum. Pericardial prominence is formed by the developing heart which lies below the
stomodeum depression. The small area between the brain and the pericardial bulges shows
appearance of the pharyngeal arches. They are six in number, and are named numerically as 1, 2,
3, 4, 5 and 6. It must be noted that the 5th arch is transitory which finally disappears. The mesodermal
bars surround the ventrolateral aspect of the cranial part of the foregut and unite ventrally in the
floor of the pharynx. This makes floor of the pharynx full of elevations and the depressions. With
rupture of buccopharyngeal membrane the foregut opens to the exterior. The unsegmented
mesoderm forming the wall of the pharynx lies between the ectoderm outside and the endoderm
inside. It gets organized to form mesodermal bars, known as the pharyngeal arches. They are
covered with the endoderm from inside and the ectoderm from outside. Internally, the endodermal
depressions between the two arches are called the pouches while the ectodermal depressions outside
are called the clefts. Small area originally marked by the pharyngeal arches grows caudally pushing
the developing heart down. As a result the region, elongates and forms the neck of the embryo
(Figs 13.1 and 13.2).
Fig. 13.1: Appearance of pharyngeal arches

Formation of Branchial (Pharyngeal) Arches 99
Fig. 13.2: Cranial part of the foregut in a section after formation of pharyngeal arches
First arch is known as the mandibular arch and the second as the hyoid. Each pharyngeal arch
consists of following components (Fig. 13.3).
1. Cartilage
2. Bone
3. Striated muscle: When the muscle migrates to the distant region, it carries its nerve with it.
4. Each pharyngeal arch has the arterial arch connecting the dorsal and the ventral aortae.
5. Nerve: Each arch is provided with a nerve which supplies striated muscles arising from the
arch. Its sensory component of the nerve supplies the overlying ectoderm and the underlying
endoderm (Fig. 13.4).
Each arch is provided with two nerves, i.e. the post-trematic and the pretrematic. Nerve which
runs along the cranial border of the arch is known as the post-trematic nerve and the nerve running
along the caudal border is called the pretrematic nerve. Mandibular nerve is the postrematic nerve and
the chorda tympani is pretrematic nerve of the first arch.
First Arch Syndrome (Treacher Collins Syndrome)

It is an autosomal dominant genetic malformation. It involves the defective development of the
derivatives of the first arch, which includes:
• Maxilla
• Mandible
Fig. 13.3: Components of pharyngeal arch
Fig. 13.4: Nerves of pharyngeal arches, Pretrematic and post-trematic
• Cheek
• Displacement of external ear
• Cleft palate
• Defective dentition.
Derivatives of the First Pharyngeal Arch (Fig. 13.5)

1. Malleus
2. Incus
3. Anterior ligament of malleus
4. Sphenomandibular ligament.
Note: Maxilla, mandible, zygoma, palatine and part of temporal bones come from the 1st arch.
Fig. 13.5: Derivatives of 1st arch
Derivatives of the Second Arch (Fig. 13.6)

1. Stapes
2. Styloid process
3. Stylohyoid ligament
4. Lesser cornu of hyoid bone
5. Upper half of the body of hyoid.
Derivatives of the Third Arch

1. Lower half of the body of the hyoid
2. Greater cornu of the hyoid.
3. Posterior 1/3rd of the tongue including the circumvallate papillae.
Cartilages of the larynx come from the 4th and the 6th arches (contribution of the 5th arch is
doubted).
Fig. 13.6: Derivatives of second and third arches. 2nd arch derivative shown
in yellow color. Derivatives of third arch shown in blue color
Skeletal Components Derived by the Pharyngeal Arches
Meckel’s Cartilage (Refer Fig. 13.5)

The cartilage arising from the first arch is known as the Meckel’s cartilage. Two ossicles of the
middle ear namely the malleus and the incus are derived from the dorsal end of the Meckel’s
cartilage. However, the ventral part of the Meckel’s cartilage, surrounded by the developing
mandibular element, disappears.
The 1st arch is called the mandibular. The nerve of the 1st arch is also called the mandibular
nerve. It supplies muscles of mastication. They are eight muscles supplied by the mandibular
nerve. The easy way to remember the names of the muscles is by remembering the following
sentence: Therapeutic Trial of Four Medicines by MD (Doctor having qualification of MD), e.g.
Doctor of Medicine.
T - Tensor tympani
T - Tensor palati
4M - Four muscles of mastication (masseter, temporalis, medial pterygoid, lateral pterygoid)
M - Mylohyoid
D - Anterior belly of digastric.
(TT 4M by MD)
Second Arch (Refer Fig. 13.6)

Cartilaginous bar of the second arch is called the Reichert’s cartilage which extends dorsally up to
the cartilaginous ear capsule. Dorsal end of the cartilage forms stapes. The other derivatives being
styloid process, stylohyoid ligament, lesser cornu of the hyoid and the upper part of the body of
hyoid bone.
Third Arch (Refer Fig. 13.6)

It gives rise to the lower part of the body of the hyoid and its greater cornu. The nerve of the third
arch is glossopharyngeal, i.e. the 9th cranial nerve. Its motor element supplies only one muscle, i.e.
stylopharyngeus while the sensory element is distributed to many structures. In order to remember
the structures supplied by the glossopharyngeal nerve, I would like you to remember the following
sentence: “Glosso/Pharyngeal nerve supplies Parotica, Carotica, Tympani, Tonsili”.
Glosso - Supplies general and special sensations to the posterior 1/3rd of the tongue
including the circumvallate papillae.
Pharyngeal - Supplies stylopharyngeus muscle.
Parotica - Supplies parotid gland with secretomotor fibers
Carotica - Supplies carotid body and carotid sinus.
Tympani - Supplies tympanic cavity.
Tonsili - Supplies tonsil.
Morphology of the Nerves of the First Arch

As the anterior 2/3rd of the tongue develops from the first arch the nerve of the general sensation
is the lingual branch of the mandibular and the chorda tympani the branch of the facial forms the
nerve of special sensation.
Comment on Nerve Supply of Pharyngeal Muscles

It has been stated by some authorities that the paraxial mesoderm anterior to the occipital somites
may contribute to the formation of pharyngeal muscles under the influence of the neural crest.
An Account of the Ectodermal Clefts (Figs 13.7 to 13.9)

Ectodermal clefts appear during the 5th week of intrauterine life. Each ectodermal cleft has two
parts, dorsal and the ventral. Dorsal part of the first cleft forms the external acoustic meatus. Ventral
part of it forms ear plug which disappear. Persistence of the ear plug causes congenital deafness.
Pinna of the ear is formed by the small mesodermal hillocks arising from the first and the second
pharyngeal arches around the external acoustic meatus. The clefts lying caudal to the first cleft are
the second, third and the fourth. They get covered by caudally growing operculum or the lid of the
second arch. Operculum of the second arch fuses with the caudal pharyngeal complex enclosing
the 2, 3 and the 4th clefts. The enclosed cavity is lined by the ectoderm and is called the cervical
sinus. The cavity of the cervical sinus disappears. The persistence of the cervical sinus leads to
formation of the branchial cyst. Branchial cyst appears along the anterior border of the sterno-
cleidomastoid muscle at the junction of upper 1/3rd and lower 2/3rd. It is placed below and
behind the angle of the mandible. Deep extension of the cyst tends to pass between the carotid fork
(Division of the common carotid artery into the external and the internal carotid arteries). Branchial
cyst passes superficial to the 9th and the 12th cranial nerves and lies deep to the posterior belly of
the digastric. Presence of cholesterol crystals in an aspirate of the branchial cyst confirms the
diagnosis of the branchial cyst. Wall of the cyst is lined by the lymphoid tissue making it prone to
infection. In case of the rupture of the branchial cyst, branchial fistula is formed. Tract of the branchial
fistula passes between the internal and external carotid arteries. It opens into the tonsillar sinus.
The fistulus tract is lined with the ciliated columnar epithelium which gives mucus discharge.
Fig. 13.7: Formation of cervical sinus in section of pharynx corneal
Fig. 13.8: Site of branchial cyst and opening of branchial fistula
Branchial Fistula (Fig. 13.10)

It results due to the persistence of the second cleft and the second pouch. It runs subcutaneously in
the platysma. As already mentioned the tract of the branchial fistula passes between the external
and the internal carotid arteries. The tract opens on the surface at the junction of upper 2/3rd and
the lower 1/3rd of the anterior border of the sternomastoid muscles.
Fig. 13.9: Derivatives of pharyngeal clefts and pharyngeal pouches (Kadasne’s Anatomy Vol. 3)
Branchial Sinus
Middle portion of the branchial fistular tract gets obliterated leaving blind ends of the tracts at
both the ends.
Fig. 13.10: Course of branchial fistula passing through the carotid fork
Clinical
1. Cyst: Cyst is a closed cavity lined by epithelium containing fluid.
2. Fistula: It is an abnormal communication between two epithelial surfaces, i.e. from surface
epithelium to bowel, from artery to the vein and from one tube to the other, (Tracheobronchial
fistula).
3. Sinus: It is a blind ending tract extending from the surface epithelium to the nearby tissue, e.g.
preauricular sinus.
Modern Theory of Branchial Cyst Formation

According to this, branchial cyst arises from branchial epithelium caught in the lymphoid tissue.
Branchiogenic Carcinoma
Occurrence of primary carcinoma from the branchial cyst is doubted. It may be the result of cystic
degeneration in the core of the lymph nodes having deposits of squamous carcinoma. Possible
primary focus is in the nasopharynx, tonsil, tongue or the pyriform fossa.
Future of the Endodermal Pouches (Fig. 13.11)
First Pouch
It forms diverticulum called the tubotympanic recess. It comes into contact with the epithelium of
the first cleft. First pharyngeal cleft forms the external acoustic meatus. Proximally, the tubotympanic
recess forms the pharyngotympanic tube and distally its dilated part forms middle ear, tympanic
antrum, mastoid air cells and the inner lining of the tympanic membrane.
Fig. 13.11: Diagrammatic presentation of the derivatives of pharyngeal pouches

Second Pouch
The epithelial lining of the second pharyngeal pouch proliferates and grows in the mesenchyme
around. These buds are enchroached by the mesoderm which form the primordium of the palatine
tonsil. The tonsillar primordeum gets infilterated by the lymphatic tissue in the fourth month.
Tonsillar fossa seen in the adult represents the part of the second pharyngeal pouch.
Third Pouch
It contributes to the formation of two structures, i.e. inferior parathyroids and the thymus. (Thymus
three, inferior stands for IIIrd grade).
Development of the Thymus (Fig. 13.12)

Thymus develops from the endoderm of the ventral part of the third pharyngeal pouch. Two diverticuli
grow caudally with the primordium of the inferior parathyroid in front of the aortic sac. Later the
diverticuli become cellular and get invaded by the surrounding mesenchyme. The cellular masses
of the thymus get invaded by the mesenchyme having lymphoid stem cells, converting thymic
mass into the partially lobulated structure. Hassall’s corpuscles are derived from the endoderm. Thymus
is larger at birth and and atrophies in old age. Narrow cervical part of the thymus forms the accessory
thymic tissue. Dorsal part of the 3rd pharyngeal pouch forms the inferior parathyroid gland.
Fig. 13.12: Development of thymus and parathyroids
Fourth Pouch
It gives rise to superior pair of parathyroids. The contribution of the fourth pouch in the formation
of thyroid gland is disputed (Refer Fig. 13.12).
Fifth Pouch
It is also known as the ultimobranchial pouch. Fifth pouch is transitory like the fifth arch. However,
it forms the ultimobranchial body in some lower forms. It may join the 4th pouch to form caudal
pharyngeal complex. Parafollicular cells “C” cells of the thyroid may arise from the caudal
pharyngeal complex. According to some authorities the origin of the “C” cells is form the neural
crest. The C cells secrete thyrocalcitonin the action of which is the deposition of the calcium in the
bones, as against the action of the parathormone which takes away calcium from the bone.
It is easy to remember the nerve supply of muscles derived from somitomeres following the game
of numericals.
Muscles derived from 1 and 2 = Supplied Oculomotor nerve
somitomeres by the 3rd All muscles supplied by
Oculomotor nerve
Muscles derived from 3 = Supplied Trochlear nerve supplies
somitomeres by the 4th superior oblique muscle
Muscles derived from 4 = Supplied Trigeminal 5th cranial nerve.
somitomeres by the 5th
Muscles derived from 5 = Supplied Abducent nerve supplies the
somitomeres by the 6th lateral rectus muscle.
Muscles derived from 6 = Supplied Facial muscles are derived from
somitomeres by the 7th second pharyngeal arch are
supplied by the 7th nerve
(facial) the nerve of the second
arch.
Others
1. Stylopharyngeus muscle arises from 7th somitomere of the third arch and is supplied by the
nerve of the 3rd arch, the glossopharyngeal.
2. Laryngeal muscles are derived from occipital somites 1 and 2. They arise from 4 to 6 arches
and are supplied by the branches of vagus.
3. Occipital somites 3 to 5 form muscles of the tongue and are supplied by the 12th cranial nerve
(hypoglossal).
Note: All the muscles of the tongue are supplied by the hypoglossal nerve except the palatoglossus
which being a muscle of palate is supplied by a cranial root of the accessory, the 11th cranial nerve.
The Skin and its Appendages 109
The Skin and its

14 Appendag
Appendage es
Skin develops from three sources:

1. Epidermis is ectodermal.
2. Dermis is mesodermal.
3. Melanoblasts arise from the neural crest.
Epidermis (Fig.14.1)
Initially, epidermis is made of single layer. However, it divides forming the flattend cell layer
called the epitrichium which forms the superficial covering. It is due to proliferation of the basal
layer or germinal layer, the intermediate layer is laid down. At the end of the 4th month of
intrauterine life epidermis is fully formed. At this stage, epidermis shows 5 layers (4th month –5th
layers). They are as under from superficial to deep:
1. Stratum corneum
2. Stratum lucidum—very few nuclei
3. Stratum granulosum—keratin granules in the cell protoplasm.
4. Stratum spinosum—prickle cells
5. Stratum basale—columnar cells and melanoblasts derived from the neural crest.
New cells are added to the epidermis by the germinal layer. The layer gets wavy forming
ridges and the depressions which are carved at the tip of the fingers. They form archer, loops and
whorls (fingerprints).
Horny layer is tough, scaly and is formed by the dead cells containing keratin within the
epidermis. The layer is invaded by the neural crest cells which form melanin pigment in the
melanoblasts.
Due to rapid proliferation of cells the epidermis gets stratified. Shedding of the superficial
cells get mixed with secretions of the sebaceous glands. This forms sticky, white looking substance
known as vernix caseosa. It covers the skin of the newborn and acts as a protector of the tender
skin.
Fig. 14.1: Development of epidermal layer of skin
Dermis
It develops from mesenchyme derived from the somatic dermatome. The junctional zone between
the epidermis and the dermis is straight earlier. Due to thickening of the epidermis, projections are
seen enchroaching the dermis. Part of the dermis between the two epidermal projections is known
as dermal papilla.
Nails (Fig. 14.2)
Development of the nails is from the surface
ectoderm. Primary nail field is formed at the
tip of digits, which is due to thickened
ectoderm.
At the proximal part of the nail field the
proliferation of cells forms the root of the nail.
Germinal matrix is formed from the germinal
layer. Proliferation of the cells of the matrix
gives rise to nail substance. Morphologically,
it corresponds to the stratum lucidum. Primary
nail field migrates dorsally from the tips of the Fig. 14.2: Development of nail
fingers. This explains nerve supply of the dorsal aspect of the digit from the nerves of the ventral
aspect.
Hair (Fig. 14.3)
Hair develops from the surface ectoderm. It is formed by the cells of the germinal layer on the top
of the papilla. At the site of the future hair follicle epidermis proliferates locally and forms the
cylinder of the cells which grow into the dermis. The lower end of the cylindrical mass enlarges and
gets invaginated by the mesoderm of the dermis. This forms the papilla. With growth of the hair
towards the surface the cells around the down growth form the epithelial root sheath. Surrounded
mesenchymal tissue around forms the dermal root sheath. Mesoderm gets transformed into a
delicate band of smooth muscle. It is known as the arrector pili. The muscle is attached to the dermal
root sheath.
Sebaceous Gland (Fig. 14.3)

Ecodermal cells of the wall of the hair follicles give rise to the sebaceous glands.
Fig. 14.3: Development of sebaceous gland and hair

Sweat Glands (Fig. 14.4)

They are ectodermal in origin and develop from the solid epidermal growths which go down in
the dermis. The solid down growth get canalized. Its lower part becomes coiled which forms the
secreting part of the gland.
Fig. 14.4: Development of sweat gland
Anomalies of the Skin and its Associates

1. Albinism (Fig. 14.5): Albinism is autosomal recessive trait in which lack of pigment is seen in skin,
hair and the retina. It is due to deficiency of enzyme called tyrosinase, the melanocytes are
unable to produce melanin pigments.
2. Vitiligo (Fig. 14.6): In this condition white patches are seen on the skin and are unevenly
distributed as a result of degeneration of the prior existing melanocytes. It is an autoimmune disorder.
Note: Albinos are labeled medically unfit in the army, although albinisim is not a disease.
Aplasia
There is regional failure of formation of
skin.
Dysplasia
The skin is abnormal in structure.
Maldevelopment of other associates of
the skin, i.e. teeth, hair, sebaceous and
sweat glands may form the part of the
dysplasia of the skin.
Alopecia
Alopecia means absence of scalp hair. Fig. 14.5: Albinism
(Courtesy: Dr Vikrant Saoji, Dermatologist, Nagpur, Maharashtra, India)
Fig. 14.6: Vitiligo (Courtesy: Dr Vikrant Saoji, Dermatologist, Nagpur, Maharashtra, India)
Fig. 14.7: Ichthyosis (Courtesy: Dr Vikrant Saoji, Dermatologist, Nagpur, Maharashtra, India)
Congenital Alopecia
Absence of the hair over the scalp is known as alopecia. This can be associated with absence of the
eyebrows and eye lashes.
Atrichia is absence of the hair in any part of the body.
Hypertrichia is overgrowth of hair.
Anonychia is absence of nails.
Ichthyosis (Fig. 14.7): It is the disorders of the skin, which presents as excessive keratinization.
Skin is dry with fish skin-like scales.
Development o
Development f
of
15 Mammary Gland
An ectodermal ridge extends from the base of the upper limb to the base of the lower limb, i.e. from
axilla to the groin. It is called the milk ridge or the mammary ridge. Over the pectoral region
milk ridge stays and forms the mammary gland. The remaining part of it disappears
(Figs 15.1 and 15.2).
At the site of development of the mammary gland ectoderm gets thickened and projects into
the dermis. Sixteen to twenty solid buds grow down into the dermis. The buds get canalized. The
terminal part of the canalized bud froms the secretary element of the gland. Proximal part of this
buds form the lactiferous ducts. Lactiferous ducts open into the pit formed as the depression on
Fig. 15.1: Development of mammary gland

Development of Mammary Gland 115
Fig. 15.2: Milk ridge extending from axilla to groin
the top of the ectodermal thickening. The mesoderm at this site grows and converts the pit into an
elevation in the form of nipple projecting on the surface of the gland (everted normal nipple).
In female, there is fast growth of ducts and the secretary part at puberty. Adipose tissue adds
to the size and smooth globular contour of the breast. Myoepithelial cells around the ducts help in
bringing the milk out through their contractions. In male, the mammary gland remains rudimentary.
Anomalies of the Breast

• Amastic: Absence of the mammary gland on one or both sides.
• Polymastia: The mammary glands more in number. They develop along the milk ridge and
may be seen anywhere along the path of the milk ridge from the axilla to the groin.
• Athelia: Absence of nipple.
• Polythelia: More number of nipples (accessory breast).
• Inverted nipple: The inverted nipple is seen in advanced cases of breast cancer, however inversion
of the nipple can also be due to developmental anomaly which creates difficulty in sucking.
This can be made to evert, surgically.
• Micromastia: Abnormal small breast.
• Macromastia: Abnormal large breast.
The Skeleton
16 Skeleton
Bones are developed from the mesoderm: Mesenchyme gets converted into the cartilage which
subsequently gets replaced by the bone. The bone formed in this manner is known the cartilage bone.
When the mesenchyme bypasses the cartilaginous stage and directly forms the bone, is called the
membrane bone.
Cartilage Bones (Fig. 16.1)

Cartilage bones form the base of the skull and the long bones of the limbs. The mesenchymal
conversion into cartilage and the bone occurs as under.
Mesenchyme → cartilage → Bone (Cartilage bone).
Mesenchyme ⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯⎯→ Bone (Membrane bone)
Clinical
Defective development of the long bones leads to a clinical condition known as achondroplasia
(dwarf). Defective development of the membrane bones leads to clinical condition called cleido-
cranial dysostosis.
Fig. 16.1: Development of bone

The Skeleton 117
Achondroplasia: Dwarf – (Abnormally short person) seen circus as a joker.

It is an inherited autosomal dominant trait (IADT). Mutation in the FGHR 3 gene leads to
adverse effect on growth of cartilages reducing the height of the individual. Due to short vertebral
pedicles the condition is associated with spinal canal stenosis (narrowing of the spinal canal).
Cleidocranial Dysostosis
There is defective ossification of the bones of the vault of the skull and partial or complete absence
of the clavicles. In the event of the bilateral absence of clavicles both shoulders of the subject can be
made to touch each other in front of the chest.
Development of Vertebral Column (Figs 16.2 to 16.7)

It has been seen that the sclerotome of the somites grows medially around the notochord and the
neural tube to form the vertebral body. Lateral extension of the mesenchyme forms the transverse
process of the vertebra while its ventral extension forms the rib. There is condensation of cells in
the middle of the segment. This condensed part is called perichordal disk. The perichordal disk
intervenes between the two vertebral bodies and forms the intervertebral disk. The notochord gives
rise nucleus pulposus while the rest of the notochord disappears. Neural arches, transverse processes
and the costal elements develop as an extensions of the mesenchyme of the vertebral body. The
intervening tissue between the spines and the transverse processes forms the interspinous and
intertransverse ligaments.
Remember that the vertebra is an example of intersegmental structure which is formed by the
parts of the two somites. Intervertebral disk or the perichordal disk marks the site of the center of
the somite. Similarly, transverse processes, ribs and the blood vessels are intersegmental in origin.
It should be noted that the spinal nerves are segmental therefore lie between the two vertebrae
and the ribs.
The mesenchymal premordium of the vertebral body gets chondrified. The condrified vertebra
gets ossified from three centers, i.e. one for the body and one for each half of the neural arch. At
birth two neural arches are connected by the cartilage in the midline. Centrum (body) of the vertebra
is connected to the neural arches by means of cartilages. Posterolateral part of the vertebral body
receives contribution from neural arch. The original joint thus formed is known as neurocentral
joint and is called the neurocentral line later.
Fig. 16.2: Mesenchymal components of vertebra

Fig. 16.3: Formation of vertebral bodies

(Note that the each vertebral body is formed by two less condense parts)
Fig. 16.4: Vertebra at birth having three Fig. 16.5: Neurocentral line at the fusion of body
separate pieces of the vertebra and neural arch
Congenital Anomalies of the Vertebral Column

1. Absence of vertebra: Coccyx or sacrum.
2. Spina bifida: Neural arches fail to fuse dorsally. Large gap allows protrusion of the meninges
alone or accompanied by the neural element. The anomalies are respectively known as
meningocele, and meningomylocele.
The Skeleton 119
Fig. 16.6: Nonunion of neural arches producing spina bifida and formation of meningocele
3. Klippel-Feil syndrome: In this condition, the number of cervical vertebrae are not normal. Individual
has short neck with restricted movements of the neck.
Spina Bifida is Clinically Divided into Three (Fig. 16.7)

1. Spina bifida aperta: In this condition, neural tube is open and there is no skin coverage.
2. Spina bifida cystica: Bony defect is covered with the skin and there is CSF in the meningeal sac.
3. Spina bifida occulta: The defect in the neural arch is covered with the skin. There is pigmentation
of the skin, hairy patches, fatty lump or a dermal sinus at the site.
Note: The condition of the spina bifida is associated with Arnold-Chiari malformation and
hydrocephalus. Due to the presence of spina bifida, medulla oblongata and the tonsils of the
cerebellum sag down in the foramen magnum. This obstructs the flow of CSF causing
hydrocephalus.
Diagnosis
Prenatal diagnosis of spina bifida can be made with the help of ultrasonography and finding of
alpha fetoproteins (AEP) in the amniotic fluid.
Hemivertebra
At times the body of the vertebra ossifies from two primary centers. In the event of failure of
appearance of one center, it leads to failure of formation of the half of the vertebral body. It is
known as hemivertebra, which is one of the causes of the congenital scoliosis. (Lateral bending of
spine).
Anterior Spina Bifida

Two halves of the vertebral body are placed apart creating a gap between the two. The meninges
and the neural tissue may herniate through the gap leading to anterior spina bifida.
Fig. 16.7: Formation of sacrum by contribution from neural arch, centrum and costal element
Congenital Fusion of Vertebral Bodies

1. When two or more cervical vertebral bodies fuse, it leads to the formation of a clinical condition
known as Klippel-Feil syndrome
2. Occipitalization of atlas
3. Sacralization of 5th lumbar vertebra
The Skeleton 121
4. Lumbarization of 1st sacral vertebra.

5. Spondylolisthesis: Due to non-development of the inferior articular processes of the 5th lumbar
vertebra, the body of it has tendency to go forward over the sacrum. Due to similar
developmental anomaly of 4th lumbar vertebra, it slips anteriorly over the 5th lumbar.
6. Diastematomyelia: It is a condition in which spinal cord gets split into two due to sharp projecting
ridge in the vertebral canal.
7. Chondro-osteodystrophy: Defective ossification of the vertebral bodies leads to reduction in height
of an individual.
8. Sacrococcygeal teratoma: It arises from Hensen’s node.
Clinical
There are three known common causes of backache, i.e. trauma, tumor and tuberculosis. (3 T’s).
The fourth cause is due to the congenital malformation of the spine, i.e. congenital scoliosis.
Development of Ribs (Fig. 16.8)

Ribs arise from the ventrolateral extension of the vertebra in front of the transverse process.
Formation of the ribs is not peculiar to the thoracic region as it is seen in cervical, lumbar and the
sacral regions too. Cervical rib is the condition causing compression of the neurovascular bundle
of the upper limb leading to the vascular changes and neuralgia. It is an extra rib which develops
from the costal element of the 7th cervical vertebra.
Development of Sternum (Refer Fig. 16.8)

Mesodermal sternal bars appear on either side of the midline of the chest and get converted into
the cartilage. These cartilaginous sternal plates are in continuity with the ribs laterally. Fusion of
the sternal plates begins in the midline and extends craniocaudally direction. Ossification of the
body and manubrium takes place independently. Ossification of the xiphoid process is late.
Accessory Ribs
Lumbar accessory rib is the commonest, however it does not attract attention as it is symptomless.
The incidence of accessory cervical rib is 0.5 to 1%. It arises from the costal element of the 7th cervical
Fig. 16.8: Development of sternum and ribs

Fig. 16.9: Radiograph of the root of the neck showing bilateral cervical rib, bilateral cervical rib
vertebra. It can be unilateral or bilateral. It presses the brachial plexus and the subclavian artery
leading to neurovascular symptoms..
Anomalies of Ribs and Chest Wall

Absence of rib on one side is commonly seen in condition of hemivertebra.
• Cervical rib (Refer Fig. 16.9)
• Lumbar rib
• Split sternum
• Funnel chest: In this the lower half of the sternum and the attached costal cartilages are pulled
inwards due to short central tendon of the diaphragm.
• Pigeon chest: The upper half of the sternum and attached costal cartilages project forwards.
The Skull and Limbs 123
The Skull and Limbs

17
The skull is divided into two parts, i.e. neurocranium which protects the brain and the
viscerocranium which forms the bones of the face (Fig. 17.1).
1. Formation of the base of the skull is from the cartilage while the vault of the skull develops
from the membrane. Four precervical occipital somites contribute sclerotome for the formation
of the occipital part of the base of the skull.
2. Mesenchyme of the otic and nasal capsules help in the formation of the skull.
3. Mandibular and maxillary processes of the first arch contribute to the formation of the face
and the skull.
Bones forming the skull are of three types:
Membrane bones Cartilage bones Membrane and Cartilage bones
Frontal Ethmoid bone Ooccipital: Part above the superior nuchal line
develops from membrane and rest of the occipital
bone develops from cartilage.
Maxilla Inferior nasal concha Sphenoid: Lateral part of greater wings of
sphenoid and pterygoid processes develop in
membrane and the rest in cartilage.
Zygomatic Hyoid : Lesser cornu and the upper Temporal bone: Squamous and tympanic parts
part of the body of the hyoid develop of the temporal bone develop from the membrane.
in cartilage from the IInd pharyngeal The petro-mastoid and styloid processes develop
arch. Lower part of the body of the from the cartilage.
hyoid and the greater cornu arise
from the cartilages of the third
pharyngeal arch.
Mandible Mandible: Every part of the mandible develops
from the membrane while the condylar and the
coronoid processes develop from the cartilage.
Nasal Ossifies in membrane —
Vomer Ossifies in membrane —
Lacrimal Ossifies in membrane —
Fig. 17.1: Skull at birth
Anomalies of the Skull

1. Anencephaly: Major part of the vault of the skull is missing due to failure of the neural tube to
close in the area of the brain.
2. Cleidocranial dysostosis: It has deformed skull with missing clavicles.
3. Scaphocephaly: Boat shaped skull due to early fusion of sagittal suture.
4. Acrocephaly or pointed skull. It is due to the early fusion of coronal suture.
5. Plagiocephaly: It occurs when the union of the sutures is asymmetrical.
6. Microcephaly: It is due to failure of the development of the brain.
7. Schuller-Christan Syndrome: There are large defects in the skull bones.
8. Fusion of the atlas with the occipital bone.
9. Mandibulofacial dysostosis (Treacher Collin Syndrome or First Arch Syndrome). It has
following defects.
a. Coloboma of eye
b. Nondevelopment of maxilla, mandible and zygomatic bones.
c. Displacement of external ear.
d. Cleft palate
e. Defective dentition
f. Absence of cheek
g. Retroganthia—receding mandible
h. Proganthia—protruding mandible
Radial Club Hand

In this condition there is partial or total absence of the radius with radial deviation of the hand
(Med-lung’s deformity).
The Skull and Limbs 125
Ulnar Club Hand

In this condition, there is partial or total absence of the ulna.
Radioulnar Synostosis
Synostosis between radius and the ulnar is more common in proximal part. The congenital anomaly
interferes with the movements of pronation and supination.
Pseudoarthorsis of the Clavicle

There is a gap in the middle of the shaft of the clavicle. The gap is filled by the fibrocartilaginous
tissue.
Club Foot (Talipes Equinovarus) (Fig. 17.2)

Deformities in clubfoot are
a. Plantar flexion of the foot
b. Adduction of the forefoot
c. Medial roration of the forefoot.
d. Raising of the medial longitudinal arch of the foot.
Treatment of Club Foot in Early Cases

In early stages, the deformity can be corrected without anasthesis as a part of the regular manual
exercise.
• Plantar flexion is counteracted by dorsiflexion.
• Adduction of the fore foot is counteracted by abduction.
• Medial rotation is counter-acted by the lateral rotation.
Fig. 17.2: Club foot (Talipes equinovarus) (Courtesy: Dr Sudhanshu Kothe, Nagpur, Maharashtra, India)
Fig. 17.3: Lobester foot (Cleft foot) (Courtesy: Dr Sudhanshu Kothe, Nagpur, Maharashtra, India)
Lobster foot or split foot: In lobster foot, foot is split into two through a large longitudinal cleft. This
condition is similar to the anomaly of the split hand (Fig. 17.3).
Rocker bottom foot: It is an equinus deformity with vertical talus.
Nail Patella Syndrome: Patella may be absent or poorly developed with spitting of the nails.
Discoid lateral semilunar cartilage: Due to presence of the discoid cartilage separating the femoral
and tibial articular surfaces, there is loss of proprioception. Mother who brings the child to the
doctor says, “Doctor on standing my child’s leg gives way”.
Congenital dislocation of hip: When there is total disruption of the articular surfaces of the bones
forming the joint, it is calld as dislocation.
The basic congenital defect is the shallow acetabulum due to dysplasia and the anti-version of
the femoral neck. Congenital dislocation of hip can be diagnosed in utero with the help of ultrasound.
Mechanical forces in the uterus are being blamed for the deformity. If so they can be corrected
in utero itself. The final answer on this is yet to come.
Mouth and Teeth 127
Mouth and Teeth

18 Te
The mouth develops from two sources (Fig. 18.1):

1. Stomodeum (ectodermal)
2. Foregut (endodermal)
Fig. 18.1: Development of floor of mouth. Cheeks, lips and gums are ectodermal in origin shown
in green color and the tongue is endodermal in origin shown in pink color
As the buccopharyngeal membrane disappears, the foregut communicates with the exterior.
The epithelium lining the inner side of the lips, cheeks and the palate is ectodermal. The gums and
the teeth are ectodermal in origin while the epithelium covering of the tongue is endodermal. In
the floor of the mouth, three structures can be identified from before backwards, i.e. lower lip,
lower jaw and the tongue. Tongue gets separated from the mandibular process by the linguo-
gingival sulcus. Second sulcus appears distal to the linguogingival sulcus. It is known as the
labiogingival sulcus. As the sulci get deepened, the area between the sulci forms the raised platform
called the alveolar process.
Deve lopment
Development
19 ofT eeth
Te
The development of teeth is closely associated with the development of alveolar processes of the
jaws. The epithelial lining covering the alveolar process gets thickened to form the dental lamina.
Soon the dental lamina sends projections into the underlying mesenchyme. Series of thickened
patches are seen in the dental lamina. They are known as the enamel organs. Each enamel organ
gives rise to milk tooth (Fig. 19.1).
Development of Tooth
We have already seen that the dental lamina forms thickened patches due to cell proliferation.
They are known as the enamel organs. Enamel organ grows deep into the mesenchyme of the alveolar
process. The lower end of each enamel organ becomes cup shaped (Inverted cup). The cup gets
filled with mesenchymal tissue which is called the dental papilla. Enamel organ with the dental
papilla forms the tooth germ. The developing tooth looks like cap, hence the stage itself is called
capstage of development of tooth.
Fig. 19.1: Development of floor of mouth, alveolar process, dental lamina,

linguogingival and labiogingival grooves
Development of Teeth 129
Cells of the enamel organ covering the papilla become columnar. These cells are called the
ameloblasts. Mesodermal cells at the periphery of the papilla form epithelial cell layer known as the
odontoblasts which lies on the inner aspect of the ameloblasts. The layer of odontoblasts covers the
mass of the pulp. Between the outer ameloblasts and the inner odontoblasts lies the basement
membrane. The pulp is formed by the cells of the papilla.
Ameloblasts produce enamel on the outer side of the basement membrane and the dentin is
produced by the odontoblasts on the inner side of the basement membrane. Dentin is the structure
similar to the bone formed by the osteoblasts. The dentin separates the ameloblasts and the
odontoblasts. After formation of the enamel, the ameloblasts disappear, and get converted into a
thin membrane known as enamel cuticle. Enamel cuticle forms the cover for the enamel organ.
Odontoblasts do not disappear and stay for the life, between the dentin and the pulp. With
ossification of jaws, roots of the teeth get firmly anchored to the developing jaws. Due to the
deposition of the dentin, the pulp space gets reduced, becomes narrow and gets converted into the
canal. The canal acts as the gate for the entry of the vessels and the nerves of the pulp space. At the
root, the ameloblastic layer is absent and the dentin gets covered with the mesenchymal layer
known as the cementoblast which forms dense bone called the cementum. Outside the cementum,
the periodontal ligament is formed. It acts as the main connecting medium between the root of the
tooth and the socket of the jaw (Gomphosis).
Formation of Permanent Teeth (Figs 19.2 to 19.6)

Number of buds develop on the inner aspect of the developing milk teeth. The buds form enamel
organs in the same manner as before. Permanent incisors, canines and premolars are developed from
these buds. On the other hand, the permanent molars develop from the buds arising from the
dental lamina posterior to the last milk tooth. At birth, germs of all temporary teeth and the
permanent incisors, canines and the first molars are in the state of advanced development. The
germs of the permanent premolars and second molars are rudimentary. The germs of the third
molar is formed only after birth. All the temporary teeth including the permanent lower first molars
start calcifying before birth and the other permanent teeth calcify at varied ages after birth.
Fig. 19.2: Development of enamel organ from dental lamina

Fig. 19.3: Development of tooth. Please note that ameloblasts lay down enamel and dentin is formed by odontoblasts
Fig. 19.4: Erupting temporary tooth

Development of Teeth 131
Fig. 19.5: Stages in formation of tooth
Fig. 19.6: Structure of tooth
Formation of Temporary or Milk Teeth

It is interesting to know and remember the eruption of Ist, IInd and the IIIrd Molar as under:
Key of multiples of six.
I Molar - 6 Years
II Molar - 12 Years
III Molar - 18 Years
Lower central incisors 6 to 9 months
Upper incisors 8 to 10 months
Lower lateral incisors 12 to 20 months

First molars 12 to 20 months
Canines 16 to 20 months
Second molars 20 to 39 months
Formation of Permanent Teeth

First molars 6 to 7 years
Central incisors 6 to 8 years
Lateral incisors 7 to 9 years
Premolars 10 to 12 years
Canines 10 to 12 years
Second molars 11 to 13 years
Third molars 17 to 21 years
In brief, the question on the development of the tooth can be answered as under:
Tooth develops from two sources enamel from the ectoderm and the dentin from the
mesoderm.
Anomalies of Teeth
1. Anodentia: means complete absence of teeth.
2. Gemination: Fusion of teeth.
3. Malocclusion: Loss of alignment of upper and lower teeth or incorrect alignment.
4. Precocious teeth: Commonly the lower incisors may erupt at the time of birth (The word
‘precocious’ means having developed earlier.)
5. Natal teeth: Teeth which erupt at birth are also known as natal teeth. They are two mandibular
incisors appearing at birth. Natal teeth produce maternal discomfort during breastfeeding or
may cause injury to the infants tongue. Worst can happen when the detached tooth gets aspirated
in the upper respiratory tract. Extraction of the natal teeth avoids the complication.
6. Delayed eruption of teeth.
7. Ectopic tooth: Tooth may be seen at an abnormal sites such as the ovary or the pituitary.
8. Tooth and Nail syndrome: It is also called as Withop syndrome (ADI). Teeth are malformed
or absent with defects in nail plate development. It is an autosomal dominant inherited
syndrome.
9. Dentigerous cyst: Cyst contains unerupted tooth. It occurs due to cystic degeneration of enamel
reticular of the enamel organ. The dentigerous cysts are seen in mandible and the maxilla.
Inherited Abnormalities
1. Amelogenesis imperfecta: There is anomaly of the enamel in which enamel becomes soft and
friable due to hypocalcification.
2. Dendinogenesis imperfecta: There is anomaly of dentin.
Note: Abnormalities of the dentin are seen in osteogenesis imperfecta.
Congenital syphilitic: Incisors are screw shaped with central notching at the edges.
Development of the Tongue 133
Deve lopment o
Development f
of
20 the Tong
Tongue
ongue
In the floor of the mouth six pharyngeal arches are seen running from the lateral wall of the foregut
which fuse with each other in the midline. In the midline over the first arch three swellings appear,
two laterals known as the lingual swellings and one which appears in the middle is called the
tuberculum impar. Anterior 2/3rd of the tongue develops from the first pharyngeal arch. Posterior
to the tuberculum impar, there is a small pit which marks the site of descent of the median thyroid
diverticulum. Median thyroid diverticulum forms the thyroid. It is known as the foramen cecum.
Behind the foramen cecum the swelling appears at the medial ends of the second, third and fourth
pharyngeal arches. It is called the hypobranchial eminence (Copula of His). Cranial part of the
hypobranchial eminence joins the tongue to form the posterior 1/3rd, the tongue including the
circumvallate papillae. The caudal part of the hypobranchial eminence forms the epiglottis
(Figs 20.1 to 20.3).
Fig. 20.1: Development of tongue

Fig. 20.2: Development of tongue (diagrammatic)
Fig. 20.3: Development of tongue (diagrammatic)
Muscles of the tongue are developed from 3-5 occipital myotomes and are supplied by the
hypoglossal nerve. The migration of the occipital myotomes to the tongue explains the course of
the hypoglossal nerve and its superficial crossing of the external and internal carotid arteries.
Anterior 2/3rd of the tongue is supplied by the lingual nerve. Lingual is the nerve of general
sensation, while the chordi tympani is the nerve of special sensation of the anterior 2/3rd of the
tongue. Posterior 1/3rd of the tongue is supplied by the glossopharyngeal nerve which is the
nerve of general and special sensation for the posterior 1/3rd of the tongue including the
circumvillate papillae. Posteriormost part of the tongue develops from the fourth arch and is
supplied by the internal laryngeal nerve, the branch of the superior laryngeal nerve which is branch
of the vagus.
Note: Beer is tasted at the posterior most part of the tongue supplied by the internal laryngeal
nerve. Hence the internal laryngeal nerve is called the Beer drinker’s nerve.
Development of Alveolingual Groove

The alveolingual groove separates the peripheral part of the tongue from the floor of the mouth.
Anomalies of the Tongue

1. Macroglossia
2. Microglossia
3. Bifid tongue
4. Tongue tie (Fig. 20.4)
5. Ankyloglossia: Lingual frenulum runs from the under surface of the tongue to the floor of mouth,
extension of it to the tip of the tongue interferes with the free movement of the tongue as a
result the patient is unable to protrude tongue and the babies face difficulty during breast-
feeding. One baby out of three hundred do suffer from tongue tie in which surgery is hardly
required as most cases are symptomless. Remember the function of the tip of tongue in adults.
The tip of the tongue being freely mobile cleans the debris from the back of the incisors in
adults.
6. Fissured tongue
7. Intralingual thyroid
8. Lingual cysts: They arise from the remnants of the thyroglossal duct and the enlarged lingual
cyst causes discomfort in the pharynx and dysphagia.
Salivary Glands
Buccal epithelium grows as solid outgrowths which get canalized, branched and finally form the
alveoli of the secretary acini.
Development of Parotid Gland (Fig. 20.5)

Parotid gland is ectodermal in origin. It develops at the primitive angle of the mouth (stomodeum)
in the form of a groove which becomes the duct acquires the length and divides and subdivides in
the substance of the cheek, forming the gland. As the maxillary and the mandibular arches come
closer, the opening of the parotid duct goes posteriorly to the level of upper second molar, in the
vestibule of mouth.
Submandibular Salivary Glands

Submandibular salivary gland develops from endodermal buds arising from the floor of the mouth.
The cellular processes are solid earlier. They grow in the posterior direction lateral to the tongue.
The processes branch and develop to form the acni. Mucous acni develop after birth. Duct of the
submandibular salivary gland develops from the groove in the floor of the mouth lying lateral to
the developing tongue.
Fig. 20.4: Tongue tie (Courtesy: Dr Kadasne, surgeon, Nagpur, Maharashtra, India)
Fig. 20.5: Development of parotid gland
Sublingual Salivary Glands

Sublingual salivary glands develop in the form of multiple buds, e.g. 10 to 12 from the floor of the
mouth. They get canalized and form 10-12 ducts, which open independently in the floor of mouth.
Tonsil (Fig. 20.6)

Palatine tonsils are endodermal in origin. They develop from the second pharyngeal pouch (Tonsil –
two). Tonsillar stroma is derived from the mesoderm of the second pharyngeal arch. Pockets
surrounding the mesoderm form intratonsillar clefts. They represent the remains of the second
pharyngeal pouch. Lymphoid tissue of the tonsil either develops in situ or is derived from blood in
the form of lymphoblasts. Localized collection of lymphatic tissue leads to formation of tubal and
the pharyngeal tonsils. Palatine tonsils belong to the inner ring of Waldyer, i.e. palatine, lingual,
tubal tonsils and the adenoids.
Fig. 20.6: Diagrammatic presentation of the derivatives of pharyngeal pouches
Pharynx
Cranial part of the foregut forms the pharynx. Endodermal pharyngeal pouches project out from
the lateral walls of the foregut. First tubal recess forms the auditory tube, middle ear cavity, mastoid
antrum and the inner lining of the tymepanic membrane. Floor of the foregut gives rise to an
endodermal diverticulum known as tracheobronchial diverticulum. The development of the larynx,
trachea is closely related to the development of the foregut. As the palate develops, the naso-
pharynx and the oropharynx get defined and are separated. The lower part of the pharynx is called
the laryngeal part of the pharynx. The muscles of the pharynx are derived from third and the other
pharyngeal arches.
Development o
Development f the
of
21 Thyroid Gland
Thyroid gland is endodermal in origin. It develops in the form of median thyroid diverticulum
which descends into the neck from the site of the future foramen cecum and divides into two lobes.
The lobes of the thyroid are connected through the isthmus. Isthmus of the thyroid lies on the 2nd,
3rd and the 4th tracheal rings. Thyroglossal duct passes through the substance of the tongue and
infront, below, behind the body of the hyoid (Figs 21.1 to 21.3).
Parafollicular cells (C-cells) arise from the neural crest and enter the thyroid gland through the
ultimobranchial body.
Ectopic thyroid tissue can be seen along the path of the thyroglossal duct.
Histogenesis of Thyroid Gland

Solid mass of endodermal cell breaks into small clumps of cells and form cavities within. The
cavities get lined by single layer of cells. As the cellular masses gets vascularized, the colloidal
material appears in the cavities converting them into the thyroid follicles. Iodine concentration
and formation of thyroid hormones begins later.
Fig. 21.1: Diagrammatic representation of formation of thyroid

Development of the Thyroid Gland 139
Fig. 21.2: Path of thyroglossal duct and abnormal sites of the thyroid tissue
Fig. 21.3: Common sites of thyroglossal cyst in order of preference
Median Ectopic Thyroid

It appears as a swelling in the mid-line of the upper part of the neck. At times, it could be the only
functioning thyroid tissue. If diagnosed as the thyroglossal cyst and removed by mistake, patient
suffers thyroid deficiency for the life.
Pyramidal Lobe
It is the normal constituent of the thyroid gland arising from the left side of the isthmus. The apex
of the pyramidal lobe is attached to the hyoid bone through fibromuscular band called the lavatory
glandulae thyroidia.
Lateral Aberrant Thyroid

In fact the lateral aberrant thyroid does not exist. The normal thyroid tissue found away from the
gland is considered as the metastasis in the cervical nodes from occult carcinoma of thyroid. When
the carcinoma of thyroid is less than 1.5 cm in diameter is called occult carcinoma of thyroid.
Anomalies of the Thyroid Gland

Anomalies of the thyroid gland can be classified into four groups:
• Pyramidal lobe
• Isthmus
• Lateral lobes
• Sites
Pyramidal Lobe Anomalies

• It may be detached from gland
• It can be too small
• It can be too large—reaching the hyoid bone
• It can be on the right side of the isthmus
Isthmus
Isthmus of thyroid may be missing.
Lobes
One or both the lobes of the thyroid may be missing. Thyroid hemiagenesis is commonly on the
left.
Abnormal Sites of Thyroid (Refer Fig. 21.2)

1. Lingual
2. Sublingual thyroid: It is seen in the neck below the hyoid bone. Sublingual thyroid needs to be
highlighted as it always and invariably forms the only functioning thyroid tissue. After its
removal by mistake the patient is left at the mercy of thyroid drug regime for the life.
3. Suprahyoid
4. Infrahyoid
5. Thyroid
6. Cricoid
Development of the Thyroid Gland 141
7. Intrathoracic: Intrathoracic thyroid is not a congenital malformation. It occurs due to sucking in

of the thyroid growth in the thorax behind the sternum due to negative intrathoracic pressure.
Sites of Ectopic Thyroid Tissue

• Larynx
• Trachea
• Esophagus
• Pericardium
• Pleura
• Ovaries
Anomalies of the Thyroglossal Duct

• Thyroglossal cyst
• Thyroglossal fistula
Thyroglossal Cyst (Figs 21.3 and 21.4)

It appears anywhere along the thyroglossal tract. However,
the common sites are as under in order of frequency.
• Infrahyoid
Fig. 21.4: Thyroglossal cyst
• Near the thyroid cartilage (Courtesy: Dr Sudhanshu Kothe, Plastic
• Suprahyoid Surgeon, Nagpur, Maharashtra, India)
Fig. 21.5: Branchial cyst and opening of branchial fistula

Thyroglossal cyst lies in the midline of the neck. It moves upwards on protrusion of the tongue
and also during swallowing due to the attachment of the thyroglossal tract at the foramen cecum
above. Thyroglossal cyst is lined with lymphoid tissue making it prone for infections. Inflamed
thyroglossal cyst is likely to be opened in case, mistaken for an abscess. Rupture of the thyroglossal
cyst ends in formation of the thyroglossal sinus rather than the fistula.
Thyroglossal Fistula or Sinus (Fig. 21.5)

Opening of the fistula or sinus is in the midline of the neck anterior to the laryngeal cartilages.
Thyroglossal fistula can never be congenital. Thyroglossal fistula occurs due to the failure of the complete
removal of the thyroglossal cyst or the removal of the entire thyroglossal track.
Treatment of Thyroglossal Fistula

Due to close proxomity of the thyroglossal tract to the body of the hyoid, excision of the central
part of the body of hyoid is mandatory for the removal of the cyst or the fistula. The sleeve of
lingual muscles around the tract is also removed (Sistrunk’s operation).
Development of Parathyroids 143
Deve lopment o
Development f
of
22 Parathyroids
There are two pairs of parathyroid glands, the superior and the inferior placed along the posterior
borders of the thyroid gland. Parathyroids are endodermal in origin and develop from the dorsal
parts of the 3rd and 4th pharyngeal pouches. Inferior parathyroids develop from the 3rd pharyngeal
pouch with the thymus (Fig. 22.1).
Third pharyngeal pouch gives rise to the thymus and the inferior parathyroids. Descent of,
thymus into the thorax carries the parathyroid III caudally. The parathyroids IV remains static due
to their attachment to the lateral lobes of thyroid. It can be said that the parathyroids IV are static
and the parathyroids III are mobile. Parathyroids III may go to the superior mediastinum with the
thymus.
Fig. 22.1: Development of thymus and parathyroids

23 Development o
Development f Face
of
Facial components are derived from the mesenchyme of the neural crest. The first pair of pharyngeal
arches contributes to the formation of the face through the frontonasal, maxillary and mandibular
prominences. Frontonasal prominence is formed by the mesenchyme ventral to the brain vesicle
forming the upper limit of the stomodeum. Maxillary prominances are lateral and mandibular
prominances are caudal to the stomodeum (Figs 23.1 and 23.2).
On either side of the frontonasal prominence the ectoderm gets thickned to form the nasal
placodes due to induction of the ectoderm by the forebrain. Invagination of the nasal placodes leads
to the formation of nasal pits. As the nasal pits deepen, medial and the lateral nasal prominences
are formed.
The maxillary prominences grow medially, meeting the medial nasal processes in the midline.
As a result, the upper lip is formed by the two medial nasal prominences and the two maxillary prominences.
Maxillary prominences first fuses with the lateral nasal prominence and next with the medial nasal
Fig. 23.1: Formation of frontonasal process. Note foregut and buccopharyngeal membrane
Development of Face 145
Fig. 23.2: Development of mandibular and maxillary processes.

Note stomodeum, frontonasal process and the bulge of pericardial
prominence. It must be noted that the

contribution from frontonasal process is overlapped
by the maxillary processes as they fuse in the
midline. This explains nerve supply of the upper
lip from the maxillary nerves. Mesoderm from the
frontonasal process forms the filtrum of the
upper lip while the skin comes from the
maxillary processes. The lateral nasal Fig. 23.3: Overlapping of the frontonasal process
prominences do not participate in the formation of by extensions from maxillary processes
the upper lip. Lower lip and the lower jaw are formed
by the mandibular prominence (Fig. 23.3)
The deep groove between the lateral nasal prominence and the maxillary prominence is called
the nasolacrimal groove. Ectoderm in the floor of the groove proliferates and forms a solid cord
which gets detached from the surface. The solid cord gets canalized and forms the naso-lacrimal
duct. The nasolacrimal duct at the upper end becomes wide to form the lacrimal sac. However the
lower tubular portion of it forms the nasolacrimal duct. After detachment, the solid cord the
maxillary and the lateral nasal prominences get fused. The nasolacrimal duct runs between the
medial angle of the eye and the inferior meatus of the nose. Cheek is formed by fusion of the
maxillary and the mandibular processes or prominences.
Nose (Figs 23.4 to 23.7)

Five different facial components contribute to the formation of the nose:
Frontal prominence forms the bridge of the nose.
Medial nasal prominences form, crest and the tip of the nose.
Lateral nasal prominences form, the alae of the nose.
Fig. 23.4: Development of face. A) Nasal placodes appear in the zone of frontonasal process.
Appearance of lens placode is seen above the nasal placode. B) Nasal placodes develop nasal
pits, marking the medial and lateral nasal processes
Fig. 23.5: Development of face. The nasal pits get closer. Lateral nasal process
is separated from the maxillary process through the naso-optic furrow
Fig. 23.6: Development of face. The nasal pits get closer. Lateral nasal process is
separated from maxillary process through the naso-optic furrow. The figure is
diagrammatic
Fig. 23.7: Formation of face from various sources
Intermaxillary Segment (Fig. 23.8)

Two medial nasal prominences fuse at the surface and also in the depth. They form the band of
tissue between the maxillary prominences which is called the intermaxillary segment. Intermaxillary
segment consists of three components as under.
Fig. 23.8: Components derived from the intermaxillary segment
Labial: It forms the philtrum of the upper lip.

Upper Jaw: It forms the part of the upper jaw having four incisors.
Palatal: It forms the triangular primitive palate.
Cleft Lip (Figs 23.9 and 23.10)

It is the upper lip which is commonly involved in the anomaly. Incidence of the cleft lip is 1 in
1000. It is interesting to note that more than 60 to 80% of infants having deformity of cleft lip are
males. Cleft lip deformity varies from the simple notch to a large gap extending into the nostril
and the alveolus. It can be unilateral or bilateral. Cleft lip results due to the failure of the maxillary
prominence to fuse with the medial nasal prominence. The main fault is with the intervening
mesenchyme between the two prominences. The mesenchyme fails to proliferate and as a result a
Fig. 23.9: Cleft palate.

(Courtesy: Dr Sudhanshu Kothe, Nagpur, Maharashtra, India)
Fig. 23.10: Unilateral cleft lip (Harelip)

groove is formed in the upper lip. The epithelium of the floor of the groove gets stretched leading
to the rupture and separation of the medial and the lateral parts of the upper lip. At times the
divided parts of the upper lip are connected by means of a tissue bridge called as a Simonart band.
Oblique Facial Cleft (Fig. 23.11)

They are also known as the orbitofacial fissures. Usually, they are bilateral and extend from the
upper lip to the medial angle of the orbit. This converts the nasolacrimal ducts into grooves. Oblique
Fig. 23.11: Oblique facial cleft

facial clefts with cleft lip occur due to failure of union of the maxillary prominences with the
medial and the lateral nasal prominences.
Median Cleft Lip (Fig. 23.12)

The subjects affected are generally mentally retarded. This condition is very rare.
Nasal Cavities (Fig. 23.13)

As a result of faster growth of the nasal prominences, the nasal pits deepen. Initially, the oronasal
membrane separates the primitive nasal pits from the primitive oral cavity. The conchae are placed
on either side of the midline caudal to the primary palate (premaxillary). With the development of
secondary palate and the nasal chambers, primitive conchae are placed at the junction of the nasal
cavity and the pharynx. Later, they form three nasal conchae the superior, middle and the inferior.
Paranasal sinuses develop from mucus membrane of the lateral nasal wall in the form of
diverticuli. The diverticuli encroach and grow into the sphenoid, ethmoid, frontal and the maxillae.
First sinus to develop is the maxillary air sinus which appear at the 4th month of intrauterine life.
As a result, maxillary air sinus is the only air sinus present at birth having diameter of 4 mm
(4 months in intrauterine life and 4 mm at birth).
Fig. 23.12: Types of harelip

Fig. 23.13: Development of nasal cavity
Vomeronasal Organs of Jacobson

They are the chemosensory structures on either side of the nasal septum. Vomeronasal organs in
humans are tubular having minute anterior openings. They represent vomeronasal organs in other
animals. During development they appear in the 5th week and continue to stay for the life. In
animals they play an important part in reproduction and feeding habits.
Development o
Development fP
of alate
Pa
24
Intermaxillary segment is formed by the maxillary prominences and two medial nasal prominences.
The intermaxillary segment forms (Fig. 24.1)
• Lip
• Upper jaw
• The palatal component, i.e. the primary
palate.
The intermaxillary segment has
continuity with the nasal septum. It is to be
remembered that the nasal septum develops
from the frontonasal process.
Fig. 24.1: Components derived from the inter-
maxillary segment
Secondary Palate (Figs 24.2 to 24.7)
Secondary palate is formed by two palatine processes of the maxillae which unite in the midline.
The plates are also called as palatine shelves. Initially, the palatine plates or shelves are directed
downwards and medially. It is due to the presence of the developing tongue in the floor of mouth.
Later the oblique palatine processes become horizontal and unite above the developing tongue,
which becomes smaller and moves down due to the development of jaws. The site of fusion of the
primary palate and the secondary palate is marked by the foramen called the incisive foramen.
Finally the developing nasal septum from the frontal nasal process joins the secondary palate. The
incisive foramen forms the landmark between the anterior and posterior anomalies of the palate.
Anomalies posterior to the incisive foramen include the anomalies of the cleft palate and the cleft
uvula. Anterior anomalies include those of the lip, jaw and the primitive palate.
Anomalies of the Palate (Fig. 24.8)

• Y-shaped cleft palate with bilateral cleft lip
• Unilateral cleft palate
• Midline cleft palate
• Bifid uvula.
Development of Palate 153
Fig. 24.2: Formation of nasal septum. With rupture of the

bucconasal membrane, nasal sac opens into stomatodeum
Fig. 24.3: Palatal processes of maxillae are directed downward due to the intervening tongue
Fig. 24.4: Tongue has sagged down. The palatal Fig. 24.5: Development of palate
processes become horizontal and unite above the
tongue
Fig. 24.6: Intermaxillary segment
Fig. 24.7: Development of palate

Development of Palate 155
Fig. 24.8: Types of cleft palate
Anomalies of Lip, Palatal and the Drugs

Anticonvulsant drugs like dylantoin if administered during pregnancy for the treatment of epilepsy,
cause cleft palate, the incidence of which goes very high.
Other Anomalies of the Face

A. Macrostoma: Transverse facial clefts extends from the angle of the mouth to the external ear
resulting in macrostoma.
B. Microstoma: It occurs due to excessive fusion of the maxillary and the mandibular prominences.
C. Anomalies of the nose:
i. Absence of nose
ii. Bifid nose
iii. Humped nose
iv. Crooked nose.
25 Body Cavities
All the three body cavities, i.e. pericardial, pleural and peritoneal arise from the intraembryonic
coelom. Intraembryonic coelom appears in the lateral plate mesoderm dividing it into, the
somatopleuric and the splanchnopleuric layers (Fig. 25.1). The parietal and visceral layers of the
pericardium, pleura and the peritoneal cavities are formed by the mesoderm. Intraembryonic coelom
is horse-shoe shaped. Two lateral limbs of the intraembryonic coelom meet in front of the prochordal
plate and forms the pericardial cavity. Pericardial cavity communicates with the peritoneal cavity
through the pericardio-peritoneal canals. The pericardio-peritoneal canals expand dorsally, cranially
and caudally due to the invagination of the lungs forming the pleural cavities. Mesoderm of the
lateral thoracic wall splits into two parts, the medial and the lateral. Lateral part forms thoracic
wall and the medial forms the pleuro-pericardial membrane. The phrenic nerve runs through the
membrane which forms the fibrous pericardium. In adult, the phrenic nerve has intimate
relationship with the fibrous pericardium. The lateral limbs of the intraembryonic coelom unite
caudally to form the large cavity called the peritoneal (Fig. 25.1).
Fig. 25.1: Formation of pericardial and peritoneal cavities

Body Cavities 157
Mesothelium
Linings of the pericardial, pleural and the peritoneal cavities are formed by the epithelial cells
called the mesothelium. Initially all the three cavities are in communication through the pericardio-
pleural and the pleuroperitoneal openings. Later the openings are closed by the pericardiopleural
and the pleuroperitoneal membranes isolating the cavities.
Separation of Cavities (Figs 25.2A and B)
Fig. 25.2A: Pericardial, pleural and peritoneal cavities before separation (Diagrammatic)
Fig. 25.2B: Pericardial, pleural and peritoneal cavities after separation (Diagrammatic)
Deve lopment o
Development f
of
26 Respiratory System
Respiratory system develops from the endodermal diverticulum of the foregut (Fig. 26.1). Epithelial
lining of the entire respiratory system is derived from the endoderm. Rest of the constituents of the
respiratory system, e.g. cartilage, muscle and connective tissue come from the splanchnopleuric
mesoderm. Visceral layer of the pleura develops from splanchnopleuric mesoderm the parietal
layer develops from the somatopleuric mesoderm. The median diverticulum which develops from
the floor of the pharynx is called the tracheobronchial diverticulum. First indication of formation of
the respiratory system is the appearance of the tracheobronchial groove behind the hypobranchial
eminence (Fig. 26.1). Tracheobronchial diverticulum gets separated from the foregut due to the
formation of the tracheoesophageal septum. Larynx is placed at the cranial end of the trachea. It
opens in the lower part of the pharynx called the laryngeal part of the pharynx.
Tracheobronchial diverticulum has blind caudal end which divides and forms two lung buds.
They form right and the left bronchi. Right bronchus is wider and more in line with the trachea.
This tempts foreign bodies to go to the right bronchus. Left bronchus is narrower and makes an
angle of 45 degrees with the trachea. Lung bud divides into 3 lobar bronchi on the right and 2 on
Fig. 26.1: Development of esophagus and respiratory diverticulum

Note the positions of septum transversum and the pericardium
Development of Respiratory System 159
Fig. 26.2: Site of origin of the tracheobronchial groove in the floor of pharynx behind hypobranchial eminence
Fig. 26.3: Development of tracheobronchial diverticulum from the foregut
the left. Cranial end of the tracheobronchial diverticulum forms the larynx and the rest extending
from the larynx to the tracheal bifurcation forms the trachea.
Development of Larynx (Figs 26.2 and 26.3)

Larynx is the box like structure situated at the cranial end of the trachea. It has dual functions, e.g.
respiration and phonation.
Laryngeal epithelium develops from the endoderm of the cranial part of the laryngotracheal
bud. The laryngeal cartilages develop from the mesenchyme derived from the neural crest.
Fig. 26.4: Subdivisions of lung buds
Original opening of the tracheobronchial diverticulum is like a vertical slit. It becomes T-shaped
due to growth of the arytenoid swellings.
Due to rapid proliferation of the laryngeal epithelium, the lumen of the larynx gets temporarily
occluded. It gets canalized forming the laryngeal ventricles separated by the mucous folds which
form the vocal and the vestibular folds. Cranial part of the hypobranchial eminence forms the
posterior 1/3rd of the tongue and the caudal part forms the epiglottis. Fourth and the 6th arch
mesenchyme form the muscles of the larynx which are supplied by the laryngeal branches of the
vagus.
Note
All the intrinsic muscles of the larynx are supplied by the recurrent laryngeal nerve except the cricothyroid
muscle which is the only intrinsic muscle of the larynx situated outside, supplied by the external laryngeal
nerve and is the only tensor of the vocal cords. Being the tensor of the vocal cords, it is of great value to the
singers (melodius singer’s muscle). The other muscle of the larynx, the posterior cricoarytenoid is the only
abductor of the vocal cords. Being the only abductor, I would call it the most important muscle of the body
next to the heart. This muscle saves person from harm and even from death (The saviour muscle).
Lungs (Figs 26.4 to 26.6)

Lung buds called the primary bronchial buds grow in the lateral direction encroaching the
pericardio-pleural canals which form the pleural cavities. Further subdivisions of the lobar bronchi
contributes to the formation of the lung. Each bronchus has 17 divisions before birth and the 7 are
added after birth. The terminal part of the bronchial tree develops into the alveoli. Parenchyma of
the lobar bronchus is separated from the adjoining bronchus by the mesoderm. The lobes are
separated by the fissures which are lined by the pleura. In the canalicular phase, the lining cells of
the air passages are cubical, and with the onset of the respiration cells get flattened forming the
Fig. 26.5: Pericardioperitoneal canal are invaginated by the lungs
Fig. 26.6: Expanded lungs encroach the pleural cavities forming visceral,
parietal layers of pleura and the pleural cavity
alveoli. The alveoli dilate later. Right bronchus divides into 3 bronchi and the left bronchus into 2.
This is followed by the formation of the lobar, segmental and the intrasegmental bronchi. Lung
develops in 4 phases:
Pseudoglandular phase
Canalicular phase
Saccular phase
Alveolar phase
In the saccular phase there is intimate contact between the epithelium and the endothelium
which is called as the blood air barrier.
Bronchopulmonary Segments
Bronchopulmonary segment is the part of the lung tissue supplied by the tertiary division of the
bronchus. Each bronchopulmonary segment is triangular with the base directed at the periphery
and the apex towards the hilum. Each segment has its independent blood supply and air supply.
However, the venous drainage is common through the vein called the intersegmental vein. Thoracic
surgeons perform segmental resections by taking help of this plane called the the intersegmental plane.
There are 10 bronchopulmonary segments on the right lung and 9 on the left.
Before birth, the respiratory passage contains fluid and surfactant. With onset of the respiration,
fluid is absorbed and expelled. The surfactant covers the alveolar lining and prevents collapse of
them during expiration.
Premature babies do not have surfactant causing difficulty in the lung expansion and finally
die due to respiratory failure.
By the 7th month, the development of pulmonary respiration is optimum for supplying the
much needed oxygen to the infants even in the presence of shunts like the foramen ovale and the
ductus arteriosus. Infants born after the 7th month are considered as viable.
Anomalies of the Larynx

1. Laryngocoele is an excessive enlargement of saccule of the larynx. In south, musical instrument
similar to shahanai is played putting the proximal end of the instrument on the neck surface
(Sundri).
2. Congenital stenosis/atresia: Stenosis occurs due to partial failure of recanalization of the larynx
while the atresia occurs due to complete failure of the recanalization.
3. Duplication of larynx including that of the vocal cords.
4. Laryngoptasis – Larynx is situated lower down in the neck, which may be retrosternal.
5. Laryngeal web – It is called congenital high airway obstructive syndrome. Vocal cords are connected
anteriorly by the mucus fold due to incomplete canalization of the larynx. As a result, the child
is unable to cry after birth, disappointing the anxious relatives waiting outside the labour
room. (Figure from Author’s Anatomy Vol-III).
Anomalies of the Trachea (Figs 26.7 to 26.11)

1. Tracheoesophageal fistula is the commonest anomaly of the respiratory tract. Due to aspiration
of feeds in the pulmonary tree, the child develops pneumonia. Due to esophageal atresia there
is polyhydramnios. Recall the fact that the 85% cases of esophageal atresia have
tracheoesophageal fistula.
2. Tracheal diverticuli.
3. Accessory bronchi rise from the trachea. They are of different varieties:
• Blind
• Accessory lobe
• Replacing the normal bronchus
• Absence of trachea: Bronchus may arise from the blind tracheal end.
4. Congenital stenosis/atresia.
5. Displaced bronchi: They may arise from trachea near its bifurcation or from the esophagus.
Fig. 26.7: Anomalies of tracheal bronchi. All the three anomalies are shown
Fig. 26.8: Esophageal atresia and various types of tracheoesophageal fistulae
Anomalies of the Lung

1. Agenesis: Nondevelopment of the complete lung or its lobes.
2. Hypoplasia: Poor amount of amniotic fluid in the lung retards its growth.
3. Absence of fissures: Right lung has oblique and transverse fissures. In case of absence of the
transverse fissure of the right lung, the right lung presents only two lobes.
Fig. 26.9: Azygos lobe of the lung
Fig. 26.10: Bronchus arising from esophagus supplying Fig. 26.11: Congenital laryngeal web
accessory lobe of lung
4. Azygos lobe: Portion of the upper lobe of the right lung lies medial to the arch of azygos vein is
called the azygos lobe. The vein lies at the floor of the fissure. Azygos lobe is present on the right
as the arch of the azygos vein itself is on the right (Fig. 26.9).
5. Accessory lobe: May arise from trachea or the esophagus.
6. Sequestration: Lung tissue is completely separated from the tracheobronchial tree. It may replace
the complete lobe (Lobar sequestration). When the lung tissue gets trapped in the core of the
lobe, it is known as the intralobular sequestration.
7. Herniation of the lung: The lung herniates through the thoracic inlet or through the defect in the
thoracic wall. The herniation can occur in the mediastinum or the pleural cavity of the same or
the opposite side.
8. Accessory lung: It is present at the base of the lung and has no communication with the tracheo-
bronchial tree. It draws its blood supply from the systemic circulation rather than pulmonary.
9. Honey comb lungs: Multiple cysts are formed in the lungs due to abnormal dilatation of the
terminal bronchioles. It has honey comb appearance which can be seen in the radiograph.
10. New born lung: The lung of infant born-alive, floats in water due to the presence of air within.
The lung of the infant born-dead (still-born) is firm and does not crepitate due to the absence
of air within and sinks in water. This is of a medicolegal importance as it tells wheather the
infant was born alive or born dead (still-born).
11. Respiratory distress syndrome (RDS): Infant develops labored respiration just after birth and
gets cyanosed, the condition is called the hyaline membrane disease (HMD). It occurs due to
the deficiency of the surfactant. When the surfactant is deficient the primordial lung alveoli do
not open and remain collapsed. Thirty present of the premature infants die due to HMD.
Thyroxine and glucocorticoids help formation of surfactant and can be used therapeutically.
12. Potter's syndrome: Development of (Fetal) lungs depen on the volume the amniotic fluid. In
bilateral renal agenesis, no urine in added to the amniotic fluid resulting in pulmonary
hypoplasia. In Potter syndrome there is pulmonary hypoplasia with congenital urinary
obstruction pathology.
Development o
Development f
of
27 Diaphragm
Pleural cavities are in communication with the peritoneal cavity prior to the development of
diaphragm. Soon pleuroperitoneal folds appear in the caudal parts of the pericardio-peritoneal
canals. They grow medially and fuse with the mesentry of the esophagus and the septum
transversum. The communication between the pleural and the peritoneal cavities is closed by the
pleuroperitoneal membranes. With the enlargement of the pleural cavities the mesenchyme from
the body wall contribute to the the peripheral portion of pleuroperitoneal membranes. Later the
myoblasts from the bodywall enter the pleuroperitoneal membranes forming the muscular part of
the diaphragm. Diaphragm originally develops in the neck at the level of 4th cervical segment. It
draws its nerve supply from 3, 4 and 5 cervical segments. As a result of elongation of the neck and
caudal migration of the heart, and lungs, diaphragm descends and forms partition between the
thorax and the abdomen. However, its nerve supply is retained from the phrenic nerve, the root
value being 3,4,5. The development of the diaphragm can be summarized as below (Figs 27.1 and
27.2A):
1. Septum transversum: It forms the central tendon of the diaphragm.
2. Right and left pleuroperitoneal membranes.
Fig. 27.1: Components forming respiratory diaphragm

Development of Diaphragm 167
Fig. 27.2A: Sites of diaphragmatic hernias
Fig. 27.2B: Diagrammatic representation of developing liver pancreatic buds and cystic bud
3. Contribution from the body wall.

4. Mesentery of the esophagus.
Phrenic nerve is motor and the sensory to the diaphragm, however, the lower intercostals
nerves are the sensory nerves of the diaphragm at the periphery.
Separation of Pericardial, Pleural and the Peritoneal Cavities

Pericardial and pleural cavities are separated by the pericardiopleural membrane. Pleural and
peritoneal cavities are separated by the pleuroperitoneal membrane.
Fig. 27.3: Participation of thoracic wall in the formation of diaphragm
Fig. 27.4: Congenital diaphragmatic due to short esophagus
Anomalies of the Diaphragm (Fig. 27.2A)
Congenital Diaphragmatic Hernia (Fig. 27.4)

It is also called congenital hiatal hernia in which the fetal stomach is pulled into the thorax. It is
associated with congenital short esophagus and the large esophageal opening. Hiatal hernias are
mostly seen in adults which are of acquired variety. The congenital diaphragmatic hernia can be
detected before birth with the help of ultrasound and MRI (Magnetic Resonance Imaging).
Parasternal Hernia
The defect is in the anterior part of the diaphragm on the right. Part of the intestinal loop mostly
colon enters the thorax between the sternal and the costal origins of the diaphragm (The opening
is called foramen of Morgagni) (Fig. 27.2B).
It is also called parasternal hernia. The hernia mostly contains fat hence is of little clinical
importance.
Development of Diaphragm 169
Foramen of Bochdalek (Fig. 27.2A)

It is formed due to the nonfusion of the pleuroperitoneal membrane with other diaphragmatic
components on the left. It is a triangular gap in the diaphragm on the left side bounded by the 12th
rib below, vertebral origin of the diaphragm medially and the costal laterally. As the abdominal
contents enter the thorax, the heart is shifted to the right causing cardiac and the respiratory distress.
Surgery within hours can reduce mortality as adhesions develop within hours. It presents as the
triad (RDS) which do not stand for Respiratory Disease Syndrome).
a. Respiratory distress
b. Dextrocardia and
c. Scaphoid abdomen.
Dome: The defect is placed in the dome of the diaphragm.
Eventration of Diaphragm
Due to thin muscles and the weak aponeurosis, the half of diaphragm gets ballooned into the
thorax. The abdominal structures entering the thorax are covered with thin capsule formed by the
thin diaphragm itself. Latissimus dorsi can be used to strengthen the weak part of the diaphragm
or the synthetic material can also be considered for the surgical repair. Clinically the patient has
paradoxical respiration which can be prevented by surgery which is done by fixing the diaphragm
in inspiration. For the relief, the redundant part of the diaphragm can also be plicated.
Accessory Diaphgram
It is commonly associated with hypoplasia of the lung and can be diagnosed by CT and MRI.
Treatment of the accessory diaphragm is surgical which includes excision.
28 Alimentary System
Endoderm forms the lining of the gastrointestinal tract. Two depressions, i.e. cephalic and the
caudal lined by ectoderm are called the stomodeum and the proctodeum respectively. The
membrane lining stomodeum is known as the buccopharyngeal membrane and the membrane
lining proctodeum is called the cloacal membrane. Both the membranes are devoid of the middle
mesodermal layer. As the flat embryonic disk undergoes folding, larger part of the yolk sac is
taken inside the embryonic disk forming the primitive gut. The gut is divided in three, i.e. the
foregut, midgut and the hindgut (Fig. 28.1).
The yolk sac freely communicates with the midgut through the vitellointestinal duct. Due to
formation of the head fold cephalic part of the primitive gut becomes the foregut and as a result of
formation of tail fold the caudal part of the primitive gut becomes the hindgut. Foregut is closed
anteriarly by the buccopharyngeal membrane. Similarly cloacal membrane separates the hindgut
from the proctodeum. With rupture of the membranes, i.e. buccopharyngeal and cloacal, the foregut
and the hindgut get opened to the exterior (Fig. 28.2).
The main midline dorsal artery develops on the dorsal abdominal wall. Number of ventral
branches arise from the dorsal artery. Out of these many disappear leaving only three to survive,.
i.e. one each, for the foregut, midgut and the hindgut. Artery for the foregut is known as the coeliac
trunk, for the midgut is called the superior mesenteric artery and the artery of the hindgut is known
as the inferior mesenteric artery.
Midgut loop is seen attached to the dorsal abdominal wall through the mesentry with the
superior mesenteric artery forming an axis. Due to rapid growth the midgut becomes U shaped.
When seen from the front, the loop lies vertical with pre-arterial segment above, and the post-
arterial segment below in relation to the superior mesenteric artery. Small dilatation appears on
the postarterial segment close to the apex of the loop. It is the primordium of the caecum.
Due to rapid growth of the pre-arterial segment, the loops herniate through the umbilical
opening into the extra-embryonic coelom. It is known as the physiological umbilical hernia which
gets reduced soon. An endodermal evagination is seen arising from the hindgut going to the
connecting stalk (Umbilicus). It is known as the allanto-enteric diverticulum. Allanto-enteric
diverticulum divides the hindgut into the larger anterior and the smaller posterior parts. Larger
anterior part is known as the urogenital sinus while the smaller posterior part is called the primitive
rectum. They are separated by the urorectal septum. The cloacal membrane gets divided into the
Alimentary System 171
Fig. 28.1: With formation of head and tail folds, foregut, midgut and the hindgut are formed.
Note that the amniotic cavity covers the embryonic disk on all sides except at the unbilical opening.
Fig. 28.2: Foregut, midgut, hindgut, vitelllointestinal duct with stomodeum and proctodeum
anterior urogenital membrane and the posterior anal membrane after joining of the uro-rectal
septum. Mesodermal tubercles develop around the anal pit, which is floored by the anal membrane.
(proctodeum) (Figs 28.3 to 28.5).
Table 28.1: Derivatives of the gut
Foregut Midgut Hindgut
Tongue and the floor of mouth, Distal half of the duodenum Left 1/3rd of the transverse colon,
pharyngeal pouches, thyroid, caudal to the duodenal papilla, descending colon, pelvic colon, rectum
esophagus, stomach, proximal half jejunam, ileum, cecum, upper ½ of anal canal. urogenital system
of the duodenum, liver, extrabiliary appendix, ascending colon and
apparatus, pancreas, respiratory the right 2/3rd of the transverse
system. colon.
Note: Smooth muscles, peritoneum and the connective tissue, are derived from the splanchnopleuric
mesoderm.
The ventral wall of the midgut gets closed after

regression of the vitellointestinal duct.
Foregut is attached to the dorsal and the
ventral abdominal walls through the dorsal
and the ventral mesentries. Midgut and the
hindgut are devoid of ventral mesentries.
Esophagus (Figs 28.6 to 28.8)

The esophagus is endodermal in origin and
develops from the foregut between developing Fig. 28.3: Divisions of cloaca in cross-section
pharynx and the fusiform dilatation of the
stomach. Initially esophagus is short and has
a lumen. It elongates with the descent of the
diaphragm resulting in obliteration of its
lumen. The esophagus gets recanalized later.
Failure of recanalization of the esophagus leads
to esophageal atresia.
Upper 1/3rd of the esophagus has striated
musculature while the middle 1/3rd has mixed
and the lower 1/3rd has only smooth. The
respiratory system develops from the foregut
Fig. 28.4: Process of divisions of cloaca
as the bifid ventral diverticulum. It is known Note nloacal duct before division of the cloaca
as tracheo-bronchial diverticulum. Caudal part
of the groove gets separated from the lumen
of the foregut while the cranial part remains
in communication. Failure of separation of the
tracheo-bronchial diverticulum and the
foregut results in the formation of tracheo-
esophageal fistula.
In 85% of the cases of the tracheo-
esophagial fistula, the lower segment of the
esophagus is connected to the trachea.
Clinically, infant vomits every feed. The
presence of the air in the fundus of the stomach Fig. 28.5: Divisions of cloaca
is the diagnostic sign of tracheo-esophagial
fistula (see Fig. 28.7).
Esophageal Stenosis
In this condition, esophageal lumen is narrowed due to incomplete canalization.
Congenital Hiatal Hernia

It is associated with congenital short esophagus. As seen earlier, the infantile stomach is pulled up
through the large esophageal opening.
Fig. 28.6: Development of esophagus and trachea from the foregut
Fig. 28.7: Tracheo-esophageal fistula with atresia of Fig. 28.8: Development of esophagus
esophagus observe air in the fundus of stomach. It is the
commonest type of TO fistula (85%)
Esophageal Atresia
It occurs due to failure of recanalization of esophagus. It is due to the deviation of the tracheo-
esophageal septum in the posterior direction. Infant accepts first feed normally, but the subsequent
feeds are returned through the nose and the mouth causing respiratory distress and cynosis.
Continuous pouring of saliva from mouth is the most important confirmatory sign of the esophageal
atresia which is not seen in any other condition. Site of atresia can be assessed by passing a catheter
under fluoroscopic control. It is gratifying to know that the surgical treatment gives 85% survival
rate. As amniotic fluid is not swallowed by the fetus due to atresia, which results in polyhydramnios.
Highlight of Ten’s
There are ten alphabets in the word oesophagus. The length of the oesophagus is ten inches and it
pierces the diaphragm at the level of 10th thoracic vertebra. If number ten catheter is passed in a
newborn and in case, it gets obstructed at mark ten at the level at the lips, diagnosis of the tracheo-
esophageal fistula is confirmed.
Achalasia Cardia
There is failure of relaxation of the lower part of the esophageal musculature leading to pencil
shaped narrowing of lower end the esophagus or the bird-beak deformity seen in barium swallow.
Above the narrow lower segment there is dilatation of the esophagus. There is loss of ganglion
cells in Aurbach plexus.
Dysphagia Lusoria
Abnormal right subclavian artery passes behind the esophagus causing its compression leading to
dysphagia (Fig. 28.9).
Fig. 28.9: Formation of abnormal right subclavian artery causing dysphagia lusoria
Table: 28.2: The differences between the achalasia cardia and the congenital megacolon
Achalasia cardia Congenital megacolon

There is loss of ganglion cells in the Auerbach plexus. The constricted lower segment is aganglionic
and non-peristaltic.
Dilated segment of esophagus contains few ganglion cells. Dilated segment contains normal ganglion cells.
Stomach (Figs 28.10 to 28.13)

Stomach is endodermal in origin. It develops from the foregut as the fusiform dilatation between
the developing esophagus and the duodenum. A line connecting the cardiac and the pyloric ends
of the stomach marks its long axis.
Fig. 28.10: Parts of stomach with greater omentum and the lesser omentum
Fig. 28.11: Development of spleen and its earlier position before rotation of stomach (seen from above)
Fig. 28.12: Gastrosplenic and lienorenal ligaments after rotation of stomach.

Note that the spleen is pushed to the left (seen from above)
Fig. 28.13: Development of lesser sac and rotation of stomach to the left
Stomach is attached to the dorsal and the ventral abdominal walls by the dorsal mesogastrium
and the ventral mesogastrium. Ventral mesogastrium extends from the ventral border of the stomach
to the septum transversum. With the development of the liver, ventral mesogastrium gets divided
into two:
1. Part extending from stomach to the liver
2. Part extending from liver to the anterior abdominal wall.
Part of the ventral mesogastrium between the stomach and the liver forms the lesser omentum.
Part of the ventral mesogastrium between the liver and anterior abdominal wall and diaphragm
forms the falciform and the coronary ligaments.
Spleen develops in the left layer of the dorsal mesogastrium. Part of the dorsal mesogastrium
between stomach and the hilum of spleen is called the gastrosplenic ligament. The part extending
from the hilum of spleen to the front of the left kidney is called the lienorenal ligament. Stomach
undergoes 90° clockwise rotation along its long axis. As a result right surface of the stomach becomes
posterior and the left anterior. This explains the fact that the right vagus presents as the posterior
gastric nerve and the left vagus as the anterior gastric nerve. Stomach also undergoes rotation
along its anteroposterior axis.
Formation of Curvatures
Rapid growth of the dorsal border of the stomach forms the fundus and the greater curvature
while the ventral border of the stomach forms the lesser curvature.
Histogenesis of the Stomach

It occurs stagewise:
• Gastric glands appear in the 3rd month of intrauterine life.
• Oxyntic and zymogenic cells appear in the 4th month of intrauterine life.
• Renin starts functioning at the 5th month of intrauterine life.
Formation ends: It is the antero-posterior rotation of the stomach which brings cardiac end to the
left and the pyloric end to the right.
Congenital Anomalies of the Stomach

Congenital Hypertrophic Pyloric Stenosis
There is failure of the pylorus to relax due to hypertrophy of pyloric sphincter. As the circular
musculature of the pylorus and gastric antrum undergo hypertrophy, the mucosal lining of the
pyloric canal gets compressed, converting it into a probe admitting channel (Probe patency).
Stomach distends leading to forceful, progressive projectile vomiting. The vomitus does not contain
bile. Clinically there is enlargement of the abdomen with palpable mass under the right
hypochondric region with visible peristalsis.
Formation of Lesser Sac or Omental Bursa (Figs 28.14 and 28.15)

Stomach is attached to the dorsal abdominal wall by the dorsal mesogastrium and to the ventral
abdominal by the ventral mesogastrium. On either side of the dorsal mesogastrium small recesses
appear. They are called the right and the left pneumoenteric recesses. The left pneumoenteric
recess disappears while the right persists and continues to grow. The stomach rotates to the left
which carries the right pneumoenteric recess posterior to the stomach. It forms the main part of
the lesser sac. Due to the rotation the stomach to the left the ventral mesogastrium shifts to the
right with a part of the peritoneal cavity behind it. It forms the vestibule of the lesser sac. As a
result of the rotation of the stomach to the left the dorsal mesogastrium shifts to the left. Spleen
develops in the left layer of the dorsal mesogastrium which divides it in two parts: (1) The gastro-
splenic ligament and (2) Lienorenal ligaments. Gastrosplenic ligament runs between the greater
curvature of the stomach and the hilum of the spleen. The lienorenal ligament extends between
the hilum of the spleen and the front of the left kidney. Now the hilum of spleen and both the
ligaments, e.g. gastrosplenic and the lienorenal form the left limit of the lesser sac.
Fig. 28.14: Formation of lesser sac and

participation of the transverse mesocolon in its
formation
Fig. 28.15: Sagittal section of

developing peritoneal cavity showing
development of lesser sac
Note the red arrow indicating fusion
of anterior layer of transverse
mesocolon with posterior layer of
greater omentum
Lesser sac or the omental bursa is formed from the following:

1. Right pneumoenteric recess
2. Contribution from the part of the peritoneal cavity lying behind the lesser omentum. It forms
the vestibule of the lesser sac.
3. Growth of dorsal mesogastrium from the greater curvature of the stomach, extends below,
gets folded upon itself and passes in front of the transverse colon and mesocolon. It is important
to remember that the anterior layer of the transverse mesocolon fuses with the posterior layer
of the greater omentum. The cavity which appears between the layers of the greater omentum
forms the lowest part of the lesser sac.
4. The right pneumoenteric recess extends cranially on the right side of the esophagus and behind
the liver. The cranial extension of the right pneumoenteric recess goes above the diaphragm.
The part of it above the diaphragm forms the infracardiac bursa and the part below the
diaphragm forms the superior recess of the lesser sac.
On the right, the lesser sac opens into the greater sac through an opening which lies behind the
lesser omentum. The opening is called the foramen of Winslow or the aditus to the lesser sac. The
opening lies behind the free margin of the lesser omentum.
Development of Spleen (See Figs 28.11 and 28.12)

Spleen is mesodermal in origin. It develops from the mesoderm lying between the two layers of
dorsal mesogastrium. Small lobules of the splenic tissue are formed. They join forming the
identifiable splenic mass. The notches at the superior border of the adult spleen is a reflextion of
the lobular origin of the spleen. Growth of the spleen is rapid on the left which forms the prominent
projection on the left layer of the dorsal mesogastrium. Rotation of the stomach carries the spleen
to the left. Due to appearance of the spleen, dorsal mesogastrium gets divided into two: (1) The
part extending from the greater curvature of the stomach to the hilum of spleen, is called the
gastrosplenic ligament, and (2) the part extending from the hilum of spleen to the front of the left
kidney is called lienorenal ligament.
Histogenesis of the Spleen

The primordium of the splenic tissue forms branching cords and the isolated free cells. The free
cells form erythroblasts, myoblast and the lymphoblasts. The process of the blood formation by
the spleen begins in early embryonic age, however, the process stops at birth with the exception of
the lymphoblasts which continues its formation even after birth. This is followed by appearance
splenic vessels and the sinusoids.
Anomalies of the Spleen

1. Accessory splenic tissue is found around the spleen, in the gastrosplenic ligament, greater
omentum and the left spermatic cord. After removal of the spleen the accessory splenic tissues
enlarge and take over the function of the lost spleen.
2. Hamartomas: It is a tumor arising from the part of the body having tissues not foreign body to
the part. They do not become malignant.
3. Splenic cyst: They are of two types (i) True and (ii) False. True cysts of the spleen arise from the
embryonal remnants and the false cysts of the spleen occur due to trauma.
Fig. 28.16: After rotation of duodenal

loop it falls on the right. Posterior layer
of the mesoduodenum fuses with the
peritoneum of the dorsal abdominal
wall as a result duodenum becomes
retroperitoneal
Duodenum (Fig. 28.16)

The duodenum has dual origin. Proximal half of the duodenum is derived from the foregut and
the distal half from the midgut.
Proximal half of the duodenum which develops from the foregut and is supplied by the artery
of the foregut, i.e. celiac trunk through the superior pancreatico-duodenal. Distal half of the
duodenum develops from the midgut and is supplied by the artery of the midgut, i.e. superior
mesenteric artery through the inferior pancreatico-duodenal artery.
Duodenal loop with head of the pancreas falls on the right due enlargement of the right lobe of
liver and the return of the large gut to the abdominal cavity. Rotation of the stomach to the left
makes duodenum to fall on the right. Its peritoneum fuses with the peritoneum of the posterior
abdominal wall and disappears (Zygosis). It makes the duodenum retroperitoneal.
Anomalies of the Duodenum
Duodenal Atresia (Fig. 28.17)

Failure of canalization of the duodenum leads to atresia of the second part of the duodenum distal
to the opening of the common bile duct. Diagnosis of the duodenal atresia is suspected due to
double bubble sign seen in radiograph or the ultrasound picture of the abdomen. Duodenal atresia
is associated with polyhydramnios.
Duodenal Stenosis
It results due to defective vacuolization of the tissue occupying duodenal lumen. The duodenal
stenosis affects the 3rd and the 4th parts of the duodenum.
Septum : The septum develops in the duodenum separating the duodenal lumen into the proximal
and the distal parts.
Fig. 28.17: Duodenal atresia Fig. 28.18: Duodenal diverticuli
Duodenal Diverticuli (Fig. 28.18)

They are seen along the inner border of the second and the third parts of the duodenum.
Clinical
In duodenal atresia, infant vomits bile right from the time of birth and looses weight. Surgery is
done by joining the dilated proximal part of duodenum to the jejunum (Duodeno-jejunostomy).
The basic difference, in the clinical presentations of the duodenal atresia and the congenital
pyloric stenosis, is the absence of bile in the vomitus of congenital pyloric stenosis.
Development of Liver (Figs 28.19 to 28.21)

Liver is endodermal in origin and develops from
the caudal part of the foregut in the form of
hepatic bud. It grows into the ventral
mesogastrium and the septum transversum. The
bud divides into the large cranial and the caudal
small parts. The larger cranial part is known as
the pars hepatica and the smaller caudal part is
called the pars cystica. Pars cystica forms the gall-
bladder and the cystic duct. Hepatic bud divides
into two—the larger right and the smaller left
lobes forming the right and the left lobes of the
liver. Earlier both the lobes of the liver are of the
equal size.
With the formation of the liver, the umbilical
and the vitelline veins get distorted and broken
forming the hepatic sinusoids.
Due to rapid enlargement, liver occupies
Fig. 28.19: Showing development of liver and
major portion of the abdominal cavity forcing gallbladder from the caudal part of the foregut
coils of the gut to herniate at the umbilicus. This
Fig. 28.20: Development of pancreas, liver, gallbladder and spleen.

Note: Allantoenteric diverticulum, primitive urogenital sinus and common cloaca
Fig. 28.21: Development of liver and gallbladder
is known as the physiological herniation. Oxygen rich blood and the proliferation of the hemopoietic
tissue are responsible for the large size of the liver during development.
Septum transversum takes part in forming the constituents of the liver in the form of
hepatocytes, hemopoietic cells, Kuffer cells and the stroma of the liver.
Mesoderm around the liver forms the fibrous capsule of the liver (Glisson’s capsule). Upper
part of the liver lies in direct contact with the diaphragm and is devoid of the peritoneal covering
(Bare area of liver).
Hemopoietic function of the liver starts in the 10th week. The tissue gives white and red cells
which occupy the gaps between the liver cells and the walls of the blood vessels. Production of
WBC and RBC continues till birth.
After production of the bile by the liver cells, the bile enters the gallbladder. Later the cystic
duct joins the common hepatic duct to form the common bile duct. The common bile duct goes
behind the first part duodenum and opens into the postero-medial part of the second part of the
duodenum.
Congenital Anomalies of Liver

Congenital anomalies of the liver are not common, however, the anomalies of the extrahepatic
biliary system are common. They are of great clinical importance. The presence of accessory hepatic
duct of Luschka which comes from right lobe of liver opens into the gallbladder or the cystic duct
has important surgical bearing. At times the duct may open into the common bile duct. Intrahepatic
biliary atresia cannot be subjected to surgical corrections as a result the child has only two options, i.e.
liver transplant or death.
1. Rudimentary liver
2. Riedel’s lobe – is a tongue-like extension of the right lobe of the liver.
3. Absence of quadrate lobe
4. Accessory liver tissue in falciform ligament
5. Caroli’s disease: There is congenital dilatation of intrahepatic biliary tree leading to formation of
sepsis, stone and even the carcinoma (SSC).
6. Polycystic disease of the liver. It is a congenital anomaly seen in the liver associated with cystic
diseases of kidney and the pancreas.
Development of the Gallbladder (See Fig. 28.21)

Gallbladder is endodermal in origin. It develops from the caudal part of the foregut. It arises from
the par cystica of the hepatic bud. The proximal part of the pars cystica forms the cystic duct. The
part of the hepatic bud below the pars cystica becomes the common bile duct. The opening of the
common bile duct gets shifted to the dorsomedial aspect of the second part of duodenum. It occurs
due to the differential growth of the right wall of the duodenum.
Anomalies of the Biliary Apparatus (Figs 28.22 to 28.25)

Basic congenital defect in the biliary duct system is the failure of the canalization, which can be
extrahepatic or intrahepatic. Extrahepatic patent proximal ducts are surgically correctable and
those with intrahepatic atretic ducts have poor prognosis.
1. Agenesis or atretic gallbladder
2. Septate gallbladder
3. Double gallbladder
4. Intrahepatic gallbladder
5. Floating gallbladder
6. Hepatocystic duct—Duct from the liver directly opens into gallbladder.
Fig. 28.22: Anomalies of gallbladder Fig. 28.23: Anomalies of gallbladder
Fig. 28.24: Anomalies of gallbladder Fig. 28.25: Visceral surface of liver with left sided
gallbladder
7. Hartmann’s pouch—Pouch arises from the neck of the gallbladder, either due to stone or the
congenital malformation (This is controversial).
8. Phrygian cap—It is due folded fundus of gallbladder which may be due to failure of canalization
of the fundus of the gallbladder. Folded fundus looks like a cap worn by the people of Phrygia,
an ancient country of Asia Minor.
9. Left sided gallbladder
10. Moynihan’s hump—In this condition the hepatic artery lies in front of the common bile duct
forming a loop (Fig. 28.26).
Biliary Ducts (Extrahepatic) (Fig. 28.27)

Atresia
Bile duct atresia is due to failure of canalization of the biliary passage. It manifests as persistent
progressive jaundice of the newborn and may be associated with absence of the ampulla of Vater.
Fig. 28.26: Relation of tortuous hepatic artery to the common bile duct called the caterpillar turn
(Moynihan’s hump)
Fig. 28.27:Thick green lines indicates normal duct pattern broken lines indicate atresia.
No. 8th shows accessory duct joining neck of gallbladder (Duct of Luschka)
i. Long cystic duct

ii. Long hepatic duct
iii. Cystic duct infront of common hepatic duct
iv. Cystic duct behind common hepatic duct
v. Agenesis of cystic duct
vi. Agenesis of the common bile duct.
Development of Pancreas (Figs 28.28 to 28.31)

Pancreas is endodermal in origin. It develops from the caudal part of the foregut in the form of
dorsal and the ventral pancreatic buds. Dorsal pancreatic bud occupies the dorsal mesoduodenum.
Ventral bud appears near the root of the bile duct.
Due to the rapid growth of the right duodenal wall the ventral bud goes to the left and takes
the position below the dorsal bud and finally fuses with it.
Main pancreatic duct is formed by the left ¾ of the dorsal pancreatic duct and the remaining
right ¼ is formed by the duct of the ventral pancreatic bud. The pancreatic duct opens in the
second part of the duodenum at the major duodenal papilla.
Fig. 28.28: Development of pancreas

Fig. 28.29: Pancreatic duct
Fig. 28.30: Hepatopancreatic buds
Fig. 28.31: After axial rotation of duodenum

Histogenesis of Pancreas
Endoderm of the pancreatic buds forms mesh of tubules. Group of cells get detached from the
tubule and form pancreatic islands. Insulin secretion starts in the 10th week and the glucogon and
somatostatin processing cells develop prior to the insulin secreting cells.
Connective tissue and the thin capsule with the septae are formed from the splanchnopleuric
mesoderm. In maternal diabetes beta cells secrete insulin and are exposed to high glucose leading
to hypertrophy.
Annular Pancreas (Fig. 28.32)

Ventral pancreatic bud has two divisions the right and the left. Normally they go to the left to join
the dorsal pancreatic bud. In case of their migration in the opposite directions they encircle the
second part of duodenum and form the collar of pancreatic tissue. This may throttle the duodenum
and cause duodenal obstruction. It could be associated with the duodenal stenosis (Double bubble
appearance). Treatment is duodenojejunostomy and not cutting of the pancreatic collar.
Double bubble appearance is due to gas in the stomach and in the dilated part of the duodenum proximal
to the site of atresia.
Clinical: Pancreatitis or the malignancy of the annular pancreas can cause duodenal obstructions.
Ectopic Pancreatic Tissue

1. Wall of the duodenum
2. Lower end of esophagus
3. Wall of the stomach
4. Wall of the small intestine
5. Meckel’s diverticulum.
Inversion of the Pancreatic Ducts

Main pancreatic duct is mostly formed by the duct of the dorsal pancreatic bud. It opens at the
minor duodenal papilla. The development of the duct of the ventral bud remains poor and it
opens at the major duodenal papilla.
Fig. 28.32: Annular pancreas

Divided pancreas: In this condition dorsal and ventral pancreatic buds do not fuse.
Midgut: The midgut is attached to the dorsal abdominal wall through the mesentery. Lumen of the
midgut communicates with lumen of the vitellointestinal duct.
Derivatives of the Midgut

1. Distal half of the duodenum
2. Jejunum
3. Ileum
4. Caecum
5. Appendix
6. Ascending colon
7. Right 2/3rd of the transverse colon.
Development of Jejunum and Ileum

Whole of the jejunum and the proximal part of the ileum are developed from the pre-arterial
segment of the midgut loop and the distal part of the ileum is derived from post-arterial segment.
Development of Cecum and Appendix (Figs 28.33 to 28.35)

On the post-arterial segment the diverticulum appears near the apex of the midgut loop. It is
known as the caecal diverticulum. The proximal dilated part of the caecal bud forms the caecum
and the distal narrow part forms the appendix. Due to faster growth of the right wall of the caecum
appendix gets shifted to the left.
Cranial limb Caudal limb
1. Caudal ½ of the duodenum Distal ½ of the ileum

2. Jejunum Caecum
3. Proximal part of the ileum Appendix
Ascending colon
Right 2/3 of the transverse colon.
Note: The ileum developes from both the cranial and the caudal limbs of the midgut loop.
Fig. 28.33: Development of appendix

Fig. 28.34: Positions of appendix
Fig. 28.35: Descent of caecum
Development of Ascending Colon

The ascending colon has its origin from the post-arterial segment of midgut caudal to the caecal
bud.
Development of Transverse Colon

The transverse colon has dual origin, i.e. right 2/3rd of the transverse colon develops from the
midgut and the left 1/3rd of it from the hindgut. Superior mesenteric artery is the artery of midgut.
It supplies right 2/3rd of the transverse colon, while the left 1/3rd of the transverse colon is supplied
by the inferior mesenteric artery, the artery of the hindgut.
Development of Descending Colon

It develops from the hindgut.
Development of Rectum (Figs 28.36 to

28.38)
Rectum develops from the dorsal part of the
cloaca called the primitive rectum.
Endodermal Cloaca
The rectum, upper half of the anal canal Fig. 28.36: Divisions of cloaca in cross-section
including the mucous membrane of the urinary
bladder and the urethra develop from the post-
allantoic part of the cloaca (Endodermal
cloaca).
The endodermal cloaca is divided into the
ventral and the dorsal parts by the urorectal
septum. The ventral part is called the primitive
urogenital sinus and the dorsal part is called
the primitive rectum. The urogenital septum
develops from an angle between the hindgut
and the allantois. It descends to join the cloacal
membrane. As this attempt fails initially,
leaving the gap between the lower edge of the Fig. 28.37: Process of divisions of cloaca.
Note: Cloacal duct before division of the cloaca
urorectal septum and the cloacal membrane.
The gap connects the primitive urogenital
sinus with the primitive rectum. It is called the
cloacal duct which gets closed with the
development of the perineal body. After
joining of the urorectal septum the cloacal
membrane gets divided into the anterior part
known as the urogenital membrane and the
posterior as the anal membrane. The tissue at
the site of fusion of the urorectal septum and
the cloacal membrane forms the perineal body.
Development of Anal Canal Fig. 28.38: Divisions of cloaca

(Figs 28.39 and 28.40)
The anal canal develops from two sources, i.e. upper half is endodermal in origin which develops
from the hindgut. Lower half of the anal canal is ectodermal in origin and develops from the anal
pit. It has already been mentioned that the anal pit is surrounded by anal tubercles. They give
Fig. 28.39: Development of anal canal
Fig. 28.40: Anomalies of anal canal
depth to the ectodermal depression, the anal pit. As the anal membrane ruptures the rectum
establishes communication with the anal canal. The site of anal membrane is represented by the
pectinate line in the adults.
In brief the anal canal has a dual origin, i.e. the part of the anal canal above the pectinate line
develops from the endodermal cloaca, the part of the hindgut. The lower part of the anal canal
below the pectinate line develops from the ectodermal anal pit or the proctodeum. Upper half of
the anal canal is supplied by the superior rectal artery while the lower half is supplied by the
inferior rectal artery. The nerve supply of the upper half of the anal canal is autonomic, while
nerve supply of the lower half of the anal canal is somatic.
Main differences between the upper and lower halves of the anal canal regarding development,
blood supply, venous drainage and the nerve supply are as under:
Item Upper half Lower half
Development Endodermal Ectodermal

Blood supply Superior rectal artery Inferior rectal artery
Venous drainage Superior rectal vein goes to portal vein Inferior rectal vein goes to systemic veins
Nerve supply Autonomic Somatic
Anomalies of the Hindgut

Congenital Megacolon (Hirschsprung's Disease) (Fig. 28.41)
In this condition the part of the hindgut proximal to the anal canal is narrow right from the time of
birth. It is due to the congenital absence of the nerve cell in the myenteric and the submucous
plexuses. The narrow part of the gut has no parasynthetic innervation and as a result is the
nonperistaltic. The sympathetic nerve causes persistent spasm of the affected narrow segment.
Part of the gut proximal to the narrow segment gets dilated, which is called congenital megacolon.
Surgical correction includes resection of the narrow segment of the gut and anastomosis of the
dilated part of the gut to the remaining anal canal.
Fig. 28.41: Congenital megacolon during surgery

Courtesy: Dr Manohar Tule, Pediatric Surgeon, Nagpur, Maharashtra, India
Common Cloaca (Fig.28.42)

The urorectal septum fails to develop completely as a result undivided common cloaca opens after
rupture of the cloacal membrane through a common perineal opening. As a result the urinary, the
genital and the intestinal passages have the common perineal openings in female.
Rectovesical Fistula (Fig. 28.43)

It occurs as a result of defective development of the urorectal septum leaving the cloacal duct
patent. In this condition rectum communicates with the urinary bladder.
Fig. 28.42: Common cloaca (Perineal cloaca) in female
Fig. 28.43:Types of fistulae in male and female
Rectovaginal Fistula (Fig. 28.43)

In this condition rectum communicates with the vagina in female.
Rectourethral Fistula (Fig. 28.43)

It is commonly seen in the males in which the rectum communicates with the prostatic part of the
urethra. In this type of anomalies the anal pit is poorly developed or is absent.
Imperforate Anus (Refer Fig. 28.40)

It is a primary defect. However, when present in association with the rectal fistulae, it is called
secondary defect. The causes of imperforate anus are as under:
• Persistence of the anal membrane
• Failure of development of proctodeum
• Lower rectal atresia.
Ectopic Anus
It is due to failure of migration of the perineal body posteriorly, hence the anal and the urinogenital
openings are placed closer. Opening of the anal canal and the opening of the vagina are placed
within the vestibule in the female. Other sites of ectopic anus could be perineal, scrotal and penile.
Physiological Herniation
Cranial limb of the primary intestinal loop undergoes rapid elongation. Due to the large size of the
liver, the loops find it difficult to get accommodated in the abdominal cavity. This compels the
intestinal loops to herniate to the extraembryonic coelom near the umbilicus. This is known as
physiological umbilical hernia.
Look at the herniated loop placed vertically, from the front. It presents central axis formed by
the superior mesenteric artery, cranial limb of the midgut above and caudal below.
Caudal limb shows a small dilatation marking the site of the development of the caecum
(caecum means blind).
Non-return of the intestinal loops to the abdomen causes omphalocele.
Rotation of the Midgut (Figs 28.44 to 28.51)

Midgut loop is seen in the extra-embryonic coelom near the umbilicus. It hangs from the dorsal
wall of the embryo by the primitive mesentery. When seen from the front superior mesenteric
artery is seen in the middle at the apex of the loop. The pre-arterial segment is above and the post-
arterial below the artery. All the three structures are in the vertical plane. Due to 90 degrees
anticlockwise rotation the pre-arterial segment comes to the right and the post arterial segment
goes to the left. All the three structures are in horizontal plane.
Due to elongation and the growth of the pre-arterial segment the mass of jejunal and ileal coils
lie on the right side of the superior mesenteric artery outside the abdominal cavity. Coils of jejunum
and ileum return to the abdominal cavity first. During return the loop undergoes next anti-clockwise
rotation. During the process the coils of jejunum and ileum pass behind the superior mesenteric
artery. As a result the duodenum goes behind the superior mesenteric artery. A small diverticulum
appears on the post-arterial segment near the apex of the loop. It is known as the caecal bud. It is
believed that the caecal bud comes in the way of early return of the intestinal coils to the abdominal
cavity and probably it guides and commands the process of return. Lastly the post-arterial segment
enters the abdominal cavity and due to anticlockwise rotation, the transverse colon goes in front of
the superior mesenteric artery. Now the caecum lies below the visceral surface of the liver, and
descends from the liver to the right iliac fossa. The ascending colon, the transverse colon and
descending colon get defined.
Fig. 28.44: Rotation of midgut (first phase)
Fig. 28.45: Preaxial limb’s elongation on the right

of the superior mesenteric artery forming jejunum
and ileum
Fig. 28.46: Third part of duodenum going Fig. 28.47: Caecum enters abdominal cavity last
behind the superior mesenteric artery and is seen on left side of superior mesenteric artery
Fig. 28.48: Caecum alongwith transverse colon rotate Fig. 28.49: Position of the caecum after its descent
to the right anterior to the superior mesenteric artery from sub-hepatic position to the right iliac fossa
Fig. 28.51: Reverse rotation of midgut which

Fig. 28.50: Non-rotation of midgut. Small brings duodenum anterior to superior mesenteric
intestine goes to right and the colon to the left artery and makes the colon lie behind the artery
Formation of Mesentery
Mesentery of the primary intestinal loop forms the mesentery of the small intestine. Initially
ascending colon, caecum and the appendix are attached to the dorsal abdominal wall through the
mesocolon. Similarly transverse colon, the whole of the descending colon and the sigmoid colon
are attached to the dorsal abdominal wall by the mesocolon. As the ascending colon reaches its
normal anatomical position its mesocolon gets fused with peritoneum of the posterior abdominal
wall and disappears. As a result the ascending colon becomes retroperitoneal. The appendix and
the caecum retain their mesenteries. Descending colon also becomes retroperitoneal after loosing
its mesocolon. However, the transverse colon and the sigmoid colon retain their dorsal attachments
through the transverse and the pelvic mesocolons.
Root of the mesentery of the small intestine is attached to the posterior abdominal wall extending
from duodenojejunal junction to the right iliac fossa. Duodenum looses mesoduodenum due to
fall of the duodenal loop on the right. As a result the duodenal loop along with the head of the
pancreas become retroperitoneal following the fusion of the mesoduodenum with the peritoneum
of the posterior abdominal wall.
Hepatic and splenic flexors loose their mesocolons and come to lie in direct contact with the
liver on the right and the spleen on the left.
Please recall that the right part of the transverse colon lies directly on the second part of the
duodenum, front of the right kidney and the head of the pancreas.
However, the transverse colon retains its mesocolon, the root of which is attached to antero-
inferior border of the body of the pancreas.
Anterior layer of the transverse mesocolon gets fused with the posterior layer of the greater
omentum, thus helps in the formation of the omental bursa or lesser sac.
Anomalies
1. Persistence of the mesentery of the caecum and mesocolon (Mobile - caecum).
2. Persistence of long mesocolon for the ascending colon. This can cause volvulus of the colon
and the caecum (Volvulus mean rotation).
3. Persistence of retrocolic space. The loops of small intestine may go for internal herniation
leading to the intestinal obstruction and strangulation.
4. Omphalocele (exomphalos) (Figs 28.52 and 28.53).
Herniated loops of small intestine pass through the wider umbilical orifice and refuse to return
to the abdominal cavity. It could be associated with the cardiac and neural tube defects due to
possible involvement of the neural crest. Its contents are covered with the amnion:
Fig. 28.52: Exomphalos
Fig. 28.53: Exomphalos (Author’s Anatomy Vol. 2, Courtesy: Dr Manohar Tule, Pediatric Surgeon,
Nagpur, Maharashtra, India)
Fig. 28.54: Congenital umbilical hernia

(Courtesy: Dr. Manohar Tule, Pediatric Surgeon, Nagpur, Maharashtra, India)
Congenital Umbilical Hernia (Figs 28.54)

In this anomaly there is herniation of the abdominal viscera through the poorly closed umbilicus.
The contents are covered with peritoneum, subcutaneous tissue and the skin. The defect is placed
in the linea alba. The hernial bulge gets prominent during crying, coughing and straining. The
child is subjected to surgery only when the hernia stays upto the age of 2-3 year and never before
that. It is important to remember that the congenital umbilical hernia gets regressed within first 2
years of life and disappears for the good.
Comparison between Omphalocele and Gastroschisis
Omphalocele Congenital Umbilical Hernia (Gastroschisis)
1. Herniation through the umbilical opening. 1. Herniation through the weak umbilical opening
2. Covered with amnion 2. Covered with the peritoneum
3. Has genetic basis 3. Has no genetical basis
4. Has bad prognosis 4. Has good prognosis
Anomalies of Vitellointestinal Duct

Vitellointestinal duct normally disappears. In case of its persistence, the Meckel's diverticulum is
formed. Anomalies of vitellointestinal duct can summarized as (Fig. 28.55).
i. Meckel's diverticulum
ii. Meckel's diverticulum with fibrous band attached to the umbilicus. The intestine can rotate
along the fibrous band and can cause intestinal obstruction.
iii. Vitelline cyst.
iv. Vitelline fistula connecting the lumen of the ileum with the umbilicus (Umbilical fecal fistula).
Fig. 28.55: Development of Meckel’s diverticulum and other anomalies
Duplication and Diverticuli of the Gut (Figs 28.56)

It can involve long or the short segment of the intestine. Atresia can occur due to the failure of
canalization while partial failure of canalization leads to stenosis.
Atresia and stenosis can also occur due to vascular defects (Vascular insults). Congenital
diverticulum is of true variety as it has all the three layers.
Diverticulii in case of the duodenum are seen at the inner border of the 2nd and 3rd part of the
duodenum. The diverticuli in the IInd part of the duodenum usually obstruct the view of duodenum
papilla during endoscopy.
Fig. 28.56: Duodenal diverticuli from second and third part of duodenum
Jejunal Diverticuli
They can involve the long or the short segment of the gut.
They are multiple and normally do not give rise the symptoms. As they act as the way side
houses of ill fame, can cause malabsorption, anemia and avitaminosis. Resection of the affected
segment is done as a surgical measure.
Meconium
It is the discharge of the large intestine after birth. It is the mixture of bile, intestinal secretions and
the amniotic fluid.
Errors of Rotation
1. Non-rotation of the midgut loop: In this condition the small intestine is on the right side of the
abdominal cavity while the large intestine is on the left.
2. Reversed rotation: In this condition transverse colon goes behind the superior mesenteric artery
and the duodenum lies infront.
3. Non-return of umbilical hernia: In this condition child is born with loops of intestine coming out
of the umbilical opening. It is called the exomphalos or omphalocele. In exomphalos contents
are covered with amnion.
Errors of Fixation
A. Parts of the intestine normally supposed to be retroperitoneal are provided with the mesentery.
Long mesentery causes twisting of the coils of intestine which is called volvulus. Twisting of
the coils of the intestine causes intestinal obstruction and interruption of its blood supply results
in formation of gangrene.
B. Sub-hepatic caecum
C. The descent of the caecum stops at the lumbar region instead going to the right iliac fossa.
However, normally caecum descends and reaches the right iliac fossa.
Situs Inversus
The condition carries abdominal and thoracic viscera to the opposite side. This leads to the condition
in which the parts normally supposed to be on the right side are shifted to the left (Transposed).
Good examples of this condition are the left sided appendix and the left sided duodenum.
Recall of the Developmental Anomalies of the Gut

Summary of developmental anomalies
1. Atresia
There is total failure of canalization leading to atresia. At times the segment is missing or it
is replaced by the fibrous tissue. The development of the septum in the lumen of the gut
causes intestinal obstruction.
2. Stenosis
Abnormally narrow lumen.
3. Non-development of nerve plexuses in the certain parts of the intestine does not allow passage
of food as the segment is non-peristaltic hence remains contracted. The part proximal to the
non-peristaltic segment gets dilated (Congenital Megacolon, Hirschsprung disease).
4. Abnormal hypertrophy of the pyloric sphincter throttles the lumen of the pyloric canal leading
to congential pyloric stenosis.
5. Apple peel atresia: Atresia is present in the proximal jejunum. Portion of the jejunum distal
to the lesion is coiled around the mesenteric remnants.
6. Compression from outside due to abnormal peritoneal bands (Cystocolic band compresses
the duodenum). Peritoneal band infront of the ascending colon leads to large bowel
obstruction.
7. Annular pancreas causes duodenal obstruction.
8. Imperforate anus : It is due to the failure of rupture of anal membrane. It can be associated
with other malformations of the region, e.g. anal stenosis, non-development of proctodeal
pit (anal pit) or a big gap between the anal pit and the hindgut.
9. Fistulae (Tracheoesophageal fistula) In 85% of cases the lower segment of the esophagus
communicates with the trachea. Infant vomits after every feed and there is presence of air in
the fundus of the stomach (see Fig. 28.43).
10. Rectovesical, rectovaginal, rectourethral fistulae are known to occur.
Cardiovascular System 203
Cardiovascular System
29
The heart is mesodermal in origin. It develops from splanchnopleuric mesoderm in front of the
prochordal plate, in the area called the cardiogenic area. The heart develops from the angioblastic
tissue appearing in the floor of the pericardial cavity. Before formation of the head fold the
endothelial heart tubes are at the floor of the pericardial cavity. Soon the tubes fuse and form the
single tube becomes ‘U’ shaped and ‘S’ shaped later. The heart tube has posterior arterial and the
anterior venous ends. After formation of the head fold, the pericardial cavity and the heart tube
come to lie ventral to the foregut and the heart tube goes from the floor of the pericardial cavity to
its roof (Figs 29.1A and 29.2).
Splanchnopleuric mesoderm on the dorsal aspect of the pericardial cavity, proliferates and becomes thick,
forming the myoepicardial mantle. As the heart tube starts invaginating from the dorsal aspect of the
pericardial cavity, the myoepicardial mantle covers the heart tube from all sides. The myoepicardial
Fig. 29.1A: Heart tube is seen at the floor of the pericardial cavity.
Note the position of the septum transversum which is anterior to the heart tube and the pericardial cavity
mantle gives rise to the

myocardium and the visceral layer
of the serous pericardium and
somatopleuric mesoderm gives
rise to the parietal layer of the
serous pericardium. The heart tube
gets subdivided into four
dilatations named as bulbus
cordis, ventricle, atrium and the
sinus venosus craniocaudally (Figs
29.1B and C).
The sinus venosus has two Fig. 29.1B: Two heart tubes fuse to form single tube which gets divided
horns: the right and the left. The into four parts, e.g. bulbus cordis, ventricle, atrium and the sinus venosus
opening between the ventricle and
the atrium is called the atrio-
ventricular canal. It is important to
remember that the formation of the
head fold makes the anterior end of
heart tube arterial and the posterior
venous.
Two arteries arising from the
anterior end of the heart tube
continue as ventral and dorsal
aortae (Figs 29.3 and 29.4).
Each horn of the sinus venosus
receives three veins.
1. One from the body wall,
i.e. common cardinal vein.
2. One from yolk sac, i.e.
vitelline vein
3. One from the placenta, i.e.
umbilical vein
Atria
Sinus venosus is connected with
the primitive atria through a
horizontal large opening. The
opening gets smaller and shifts to
the right. It becomes vertical and
is guarded by the right and the left
venous valves. The valves fuse
cranially to form the septum
Fig. 29.1C:Invagination of the heart tube from the dorsal aspect of the
spurium and caudally to form the pericardial cavity
sinus septum.
Fig. 29.2: Heart tube has jumped to the roof of the pericardial cavity and septum transversum
has gone posterior to the heart tube and the pericardial cavity
Fig. 29.3: Arterial and venous ends of the heart tube
Division of Atrioventricular Canal (Fig. 29.5)

Atrioventricular canal is divided with the appearance of the ventral and the dorsal endocardial
cushions. The fused endocardial cushion is called the septum intermedium.
Separation of Primitive Atrium (Fig. 29.6)

The primitive atrial chamber gets divided into two by the septum primum and the septum
secundum.
Fig. 29.4: Subdivisions of heart tube. 1. Ascending aorta and pulmonary trunk. 2. Outflow tracts of ventricles. 3. Trabeculated
part of primitive right ventricle. 4. Trabeculated part of primitive left ventricle. 5. Right and left atria. 6. Sinus venosus gets
absorbed into right atrium
Figs 29.5: (A) Atrioventricular cushion and the line of cross section (B) Actual cross section showing fusion of
endocardial cushions and formation of atrioventricular openings
Formation of Septum Primum (Fig 29.6)

Septum primum appears at the roof of atrium on the left of the septum spurium. It grows down to
meet the septum intermedium. Before their fusion an opening between the lower edge of the septum
primum and the septum intermedium exists. It is called the ostium primum. The fusion of the
septum primum with the septum intermedium is followed by the appearance of another opening
in the dorsal part of the septum primum. The opening is known as the ostium secundum. Meanwhile
septum secundum appears and grows down from the roof of the atrium on the right side of the
septum primum. As it grows down and its lower cresentic edge overlaps the upper edge of the
septum primum. The gap between the two, forms the valvular slit allowing blood from right to the
left. This opening is known as the foramen ovale. With the onset of respiration at birth, left atrium
starts receiving oxygenated blood from the lungs. With the rise in pressure in the left atrium, the
septum primum gets stuck to the septum secundum form the left atrial side closing the foramen
ovale.
Fig 29.6: Formation of right and left atria

Note: Septum secundum is tough and can resist pressure. However, septum primum is thin and
pliable. As blood goes from right to the left, the septum primum gives way easily allowing entry of
blood from right to the left. With the rise of pressure in the left atrium at the onset of respiration at
birth, the septum primum gets stuck against the structurally tough septum secundum.
In the adult, anulus ovalis or limbus fossae ovalis represents the lower edge of the septum
secundum while the fossa ovalis represents the septum primum.
Development of Atria
Sr. No. Right atrium Left atrium
1. Right ½ of primitive atrium Left ½ of primitive atrium
2. Sinus venosus Pulmonary veins
3. Right ½ of atrioventricular canal Left ½ of atrioventricular canal
Absorption of Sinus Venosus into the Right

Atrium (Figs 29.7 to 29.9)
Atria and sinus venosus are in communication
through a wide opening. Soon they get
separated from each other partially on the right
and completely on the left. As a result, left of
the sinus venosus is totally isolated from the
atrium.
We have already seen that the centrally
placed, horizontal sinoatrial orifice shifts to the
right, and becomes vertical.
The sinoatrial orifice is guarded by the right
and the left sinoatrial valves. The left sinuatrial
valve fuses with the interatrial septum.
However, the right sinoatrial valves form three
structures as underneath (Figs 29.10A and B).
Crista terminalis
Valve of the inferior vena cava
Valve of the coronary sinus.
Left horn of the sinus venosus becomes
smaller and forms the coronary sinus which
opens into the right atrium. Proximal part of
the superior vena cava is formed by the right
common cardinal vein and the right anterior
cardinal vein caudal to anastomotic channel.
The terminal part of the inferior vena cava is formed
Fig. 29.7: Changes in size and position of the sinoatrial orifice
by the right vitelline vein. With completion of the with right and left venous valves. Note septum spurium above
process of absorption of the sinus venosus into and the sinus septum below
Figs 29.8A and B: Process of absorption of sinus venosus in to the right atrium
Note: Fig. 29.8B which is diagrammatic for the purpose of understanding. This figure shows that
the absorbed part of sinus venosus into the right atrium represents the smooth part of the
atrium into which superior vena cava, inferior vena cava and coronary sinus open
the right atrium all the three venous channels, i.e. superior vena cava, inferior vena cava and the
coronary sinus open into the right atrium.
Absorption of Pulmonary Veins (Fig. 29.11)

Earlier, only one pulmonary vein opens into the left atrium. The single pulmonary vein divides
into two which undergo further division forming four pulmonary veins. During the process of
absorption of the pulmonary veins, the part up to the four pulmonary veins gets absorbed into the
left half of the primitive atrium. Now the posterior wall of left atrium shows four openings of the
pulmonary veins.
In total anomalies of the pulmonary vein, none of the pulmonary vein gets connected with the
left atrium. However, they open into the right atrium.
Fig. 29.9: Absorption of left horn of the sinus venosus in to the right atrium
Note: The sinoatrial opening is shifted to the right and is guarded by right and left venous valves
Development of Aorticopulmonary Septum (Figs 29.12A and B)

Bulbus cordis has three subdivisions, i.e. truncus arteriosus, conus and proximal dilated part
arranged craniocaudally. Truncus arteriosus gets divided into the ascending aorta and the
pulmonary trunk by the spiral septum. The spiral septum is formed by the fusion of right superior
and left inferior truncal cushions. Proximally the horizontal spiral septum forms partition between
the pulmonary trunk in front and the ascending aorta behind. However, in the middle the partition
becomes vertical and forms partition between the pulmonary trunk on the left and the ascending
aorta on the right. Distally the septum again becomes horizontal forming the partition between
the ascending aorta in front and the pulmonary trunk behind. In brief, the partition between the
ascending aorta and the pulmonary trunk is horizontal proximally, vertical in the middle and
horizontal distally.
Primitive Ventricle and Part of the Right Atrium

Conus gives rise to the smooth parts of the right and left ventricles and the proximal 1/3rd dialated
part of the bulbus cordis foms the primitive ventricle. Proximal 1/3rd of the bulbus cordis forms
the trabeculated part of the right atrium.
Figs 29.10A and B: Right venous valve forms. 1. crista terminalis. 2. Valve of inferior vena cava.
3. Valve of coronary sinus
Fig. 29.11: Absorption of pulmonary veins into posterior wall of left atrium
Fig. 29.12A: Spiral aorticopulmonary septum in

transverse section at proximal A, middle B
and the distal C. Note the septum is horizontal
proximally vertical in the middle and again horizontal
distally Fig. 29.12B: Components forming
interventricular septum
Ventricular Cavity (Figs 29.13 and 29.14)

Formation of ventricular cavity is from three sources:
1. Conus
2. Dilated proximal 1/3rd of bulbus cordis.
3. Primitive ventricle
Fig. 29.13: Separation of ventricles. Pulmonary trunk and aorta are separated by spiral septum and bulbar septum.
The ventricles are separated by interventricular septum and contribution from AV cushions (diagrammatic)
Fig. 29.14: Formation of interventricular septum. Note that the septum primum joins the endocardial cushion
in the middle while the interventricular septum joins the endocardial cushion at its extreme right end
Interventricular septum grows from the bottom of the bulboventricular cavity. It grows towards
the atrioventricular canal and fuses with the septum intermedium at its extreme right. Externally
the site of formation of the interventricular septum is marked by the bulboventricular sulcus. Bulbar
septum is formed by right and the left bulbar ridges, which grow from the walls of the
bulboventricular canal. Its growth stops near the interventricular septum leaving a gap between
the two. The opening between the lower edge of the bulbar septum and the superior edge of the
interventricular septum is filled by the proliferation and growth of the endocardial cushions. The
endocardial cushions form the membranous part of the interventricular septum. The anterior
membranous part of the septum separates ventricles from each other while its posterior part
separates the left ventricle from the right atrium.
Formation of the Valves of the Heart

Left atrioventricular opening has two valves and the opening is called bicuspid. While the right
atrioventricular opening has three valves and is called the tricuspid opening. The valves develop
from the endocardial cushions under the endocardium. They develop at the junction of the truncus
arteriosus and the conus.
Development of Aortic and the Pulmonary Valves (Fig. 29.15)

Two endocardial cushions develop from the right and the left walls of the conus. Due to there
fusion, the aortic and the pulmonary openings are formed. Soon the right and the left cushions get
divided into the anterior and the posterior parts. Anterior part forms aortic cusps and the posterior
forms the pulmonary.
Meanwhile dorsal and ventral cushions appear. Now each opening has three cusps. Cusps
acquire anatomic positions only after the rotation. After rotation, the pulmonary opening lies
anterior and to the left of the aortic opening. Aorta has one anterior and the pulmonary trunk has one
posterior valve.
Fig. 29.15: Formation of aortic and pulmonary valves. A B - indicates the line of division of aorta and the pulmonary
trunk. Aorta has one cusp anteriorly while the pulmonary trunk has two anterior cusps
Aid to Memory
Keep Figure – 1 as the common figure for the
aortic and the pulmonary openings.
A—Aorta, Anterior 1, P—Pulmonary,
Posterior 1.
Conducting System of the Heart

(Fig. 29.16— Author’s Anatomy Vol-II)
Before fusion of the heart tubes, sinoatrial
node is in the posterior part of the left heart
tube. Fusion of the heart tubes shifts the SA
node to the sinus venosus. As we know that
the sinus venosus gets absorbed and becomes
the part of the right atrium, the SA node is in
the proximity of the opening of the superior
vena cava, near the interatrial septum. AV
node and the bundle of His are formed in the
left wall of the sinus venosus in proximity
with the atrioventricular canal and to stay near
the interventricular septum.
Pericardial Cavity (Figs 29.17 and 29.2)

1. Intraembryonic coelom in the midline in
front of the prochordal plate forms the
pericardial cavity. Fig. 29.16: Conducting system of the heart
Fig. 29.17: Developing heart tube in the floor of pericardial cavity before formation of head fold
2. Following formation of the head fold pericardial cavity comes to lie ventral to the foregut.
3. The heart tube jumps from the floor to the roof of the pericardial cavity. It starts invaginating
the pericardial cavity from the dorsal aspect.
4. Somatopleuric mesoderm gives rise to parietal layer of serous pericardium and the fibrous
pericardium.
5. Splanchnopleuric mesoderm on the dorsal aspect of the pericardial cavity forms the
myoepicardial mantle.
The heart tube invaginates the pericardial cavity from the dorsal aspect hence, gets completely
covered with the myoepicardial mantle. Finally, it is seen hanging from the dorsal aspect of the
pericardial cavity through the dorsal mesocardium. As the dorsal mesocardium disappears, the
transverse sinus venosus appears (Refer Fig. 29.2).
Due to disappearance of the dorsal mesocardium the parietal and the visceral layers of the
serous pericardium get in continuity at the arterial and the venous ends of the heart tube.
With the formation of head fold the arterial and the venous ends of the heart tubes come
closure. Serous layer of pericardium gets arranged in to two tubes, i.e. one for the aorta and the
pulmonary trunk and other for superior vena cava, inferior vena cava and the four pulmonary
veins.
Formation of Sinuses of the Pericardial Cavity (Figs 29.18 and 29.19)

The tube I encloses the aorta and the pulmonary trunk forming the anterior limit of the transverse
sinus of the pericardium. The posterior limit of the transverse sinus of the pericardium is formed
by the superior border of the left atrium. Now the tube II is meant for the superior vena cava,
inferior vena cava and the four pulmonary veins. Thus oblique sinus is formed by the peculiar
situations of these veins.
Fig. 29.18: Formation of bulboventriclular loop and appearance of transverse

sinus of pericardium in the dorsal mesocardium
External Form of Heart (Figs 29.20 and 29.21)

We have seen that the heart tube is suspended in the pericardial cavity by the dorsal mesocardium.
As the dorsal mesocardium disappears, the transverse sinus appears in the dorsal mesocardium.
Now the tube is lying free in the pericardial cavity between two fixed ends. Due to growth of the
heart tube, it becomes ‘U’shaped. The bulboventricular loop is within the pericardial cavity while
the atrium and sinus venosus are outside the pericardial cavity buried in the septum transversum.
As the atrium and the sinus venosus get freed from the septum transversum, they enter in the
pericardial cavity and occupy superoposterior aspect of the ventricle. The conus, proximal dilated
1/3rd part of the bulbus cordis and the ventricle loose their individual identity and form one
common chamber. Atrium which has gone posterior to the truncus arteriosus and the ventricles
grows and projects anteriorly on the either side of the truncus arteriosus, similar to ears of the dog
flanking the snout of the forehead.
Congenital Anomalies of the Heart

They are classified as the cyanotic and acyanotic.
In cyanotic type of congenital anomalies of the heart there is central cyanosis and bluish tinge
of the mucous membrane. Cyanotic type of anomalies constitute 1/3rd of the cardiac anomalies.
Fig. 29.19: Formation of transverse and the oblique sinuses of the pericardium as viewed from behind
Cyanotic Acyanotic
Tetralogy of Fallot PDA patent ductus arteriosus
Transposition of great arteries (TGA) ASD atrial septal defect
Total anomaly of the pulmonary venous drainage. VSD ventricular septal defect
Aortic stenosis
Coarctation of aorta
All the anomalies increase pressure load of the heart.
Note: Three cyanotic heart anomalies can be remembered as 3T’s.

1. Tetralogy of fallot
2. Transposition of great arteries
3. Total anomalus pulmonary venous drainage.
1. Situs inversus: In this condition, all the structures on one side go to the opposite side, i.e. right
atrium is on the left and the superior and inferior vena cavae lie on the left instead of the right.
2. Dextrocardia: It is the total reversal of the chambers of the heart with blood vessels. Left ventricle
and arch of aorta are on the right side.
3. Ectopia cordis (Figure 29.22 – Photograph Courtesy of Dr PK Deshpande, Cardiac Surgeon,
Nagpur.)
Nonunion of the sternal plate exposes the heart to the exterior.
Fig. 29.20: Formation of external form of the heart
Fig. 29.21: External form of heart as right and left atria go dorso superior to the truncus arteriosus
4. Septate left atrium

5. Myocardial hypoplasia – Hypoplastic left ventricular syndrome.
6. Patent osteum primum
7. Patent osteum secondum
8. Patent foramen ovale
9. Probe patency of the foramen ovale
10. Interventricular septal defects: The interventricular septal defect is the commonest congenital
anomaly of the heart (20%). The defect commonly involves the membranous part of the inter-
ventricular septum.
It results due to failure of the membranous part of the interventricular septum to develop.
It is due to the failure of fusion of the endocardial cushions with the aorticopulmonary septum
and the muscular part of interventricular septum. It leads to pulmonary hypertension causing
difficulty in breathing. Interventricular septal defect in the muscular part is not common. When
the muscular part of the interventricular septum is studded with multiple small openings, it is
called Swiss Cheese Ventricular Defect- SCVD. Interventricular septal defect increases the
pulmonary pressure causing difficulty in breathing.
11. Transposition of great arteries: This cyanotic disease of the heart mostly occurs due to transposition
of great vessels. It is due to failure of the aorticopulmonary septum to follow its normal spiral
course.
12. Patent truncus arteriosus: Due to failure of formation of the spiral septum, ascending aorta and
the pulmonary trunk, form the common chamber while the partial separation leads to
aorticopulmonary shunt (fistula).
Four chambers of the heart freely communicate with each other, due to anomalus formation
of AV cushions.
Fig. 29.22: Ectopia cordis (Courtesy: Dr PK Deshpande, Cardiac Surgeon, Nagpur)

13. Tetralogy of fallots (Fig. 29.23): It is the cyanotic congenital heart malformation.
In this condition, there are four defects, hence the name (four).
1. Pulmonary stenosis
2. Overriding of the aorta
3. Ventricular septal defect
4. Hypertrophy of the right ventricle.
14. Taussing-bing-syndrome: The aorta arises from the right ventricle and the pulmonary trunk
overrides both the ventricles in the presence of the interventricular septal defect. Superior and
inferior vena cavae with pulmonary veins may open into right atrium.
Arch Arteries (Figs 29.24 to 29.27)

Fused cranial ends of the endocardial tubes form aortic sac and its right and left horns. Arterial
arches from 1 to 6 appear stage-wise. The arches are connected ventrally with the horn of aortic sac
and dorsally with the dorsal aorta.
Major parts of the first and second arterial arches disappear. However, the maxillary artery
represents the artery of the first arch while hyoid and the stapedial arteries represent the arteries
of the second arch. With the disappearance of the fifth arch artery third and the fourth and 6th arteries
get communicated with the aortic sac. Aortic sac has two parts the ventral and the dorsal. Third
and the fourth arch arteries have communication with the ventral part of the aortic sac while the
6th arch artery communicates with the dorsal part of the aortic sac.
It is due to peculiar course of the spiral septum developing in the truncus arteriosus and its
fusion with the posterior wall of the aortic sac, blood from the pulmonary trunk goes to the 6th
arch and blood from the asceding aorta goes to the 3rd and the 4th arch arteries.
Dorsal aortae grow cranially, distal to the first arch artery.
Fig. 29.23: Tetralogy of Fallot

Fig. 29.24: Formation of aortic arches
Fig. 29.25: Formation of aortic arches. 1st, 2nd and the 5th arches are transitory
Fig. 29.26: Disappearance of ductus caroticus on both sides. Please note the right dorsal aorta disappears. Part of six
arch between the left lung bud and the left dorsal aorta does not disappear and forms ligamentum arteriosum. Hence left
recurrent laryngeal nerve hooks around the ligamentum arteriosum while the right recurrent laryngeal nerve escapes and
goes to neck
Fig. 29.27: Development of arch of aorta and descending aorta

Part of the dorsal aorta connecting the 3rd and the 4th arch arteries is known as ductus caroticus.
Right dorsal aorta between the 4th arch and the point of fusion of dorsal aortae disappears.
Part of the 6th arch artery between the lung bud and the dorsal aorta is known as ductus
arteriosus. The recurrent laryngeal nerves lies caudal to the ductus arteriosus on both the sides.
Ductus arteriosus disappears on the right side. On the left, ductus arteriosus persists as the
ligamentum arteriosum. Due to disappearance ductus arteriosus on the right side, the right recurrent
laryngeal nerve goes to the neck and hooks the right subclavian artery. However on the left, ductus
arteriosus persist as the ligamentum arteriosum. Ligamentum arteriosum prevents the left recurrent
laryngeal nerve from going up. The left recurrent laryngeal nerve hooks the arch of aorta and the
ligamentum arteriosum before its head-ward journey to the neck (Fig. 29.28).
The recurrent laryngeal nerves are obliged to take recurrent course, due to the descent of the
heart. The right recurrent laryngeal nerve becomes nonrecurrent in the presence of the abnormal
right subclavian artery.
Patent Ductus Arteriosus

Patent ductus arteriosus is the common anomaly often seen in female. Functional closure of the
ductus arteriosus occurs at birth. In case of its patency, blood from the aorta goes to the pulmonary
trunk. Maternal rubella infection in the early part of the pregnancy is the commonest cause of the
anomaly.
Fig. 29.28: Right recurrent laryngeal nerve hooks the right subclavian artery and the left recurrent
laryngeal nerve hooks the arch of aorta
The factors which contribute to the closure of the ductus arteriosus are:
1. Rotation of the heart: Occurs at the onset of respiration causing twisting of the ductus
arteriosus.
2. Anoxia: (HMD) Hyaline Membrane Disease.
3. Prematurity
4. Prostaglandins
5. The failure of normal process of obliteration which involves cellular hyperplasia of the
lining of the duct.
6. The most relevant cause appears to be the contraction of the muscles of the ductus arteriosus.
In coarctation of aorta blood pressure in the aorta is high which forces the blood to flow into
the pulmonary trunk through the ductus arteriosus (Road in use is never gets closed). Surgical
treatment of the patent ductus arteriosus is limited to its ligation and division.
Aortic Arches and their Derivatives

Arch arterial derivative truncus arteriosus aorta and pulmonary aorta
1st arch – Maxillary artery
2nd arch – Hyoid and stapedial arteries
3rd arch – Common carotid proximal to the external carotid and first part
of the internal carotid.
4th arch left – Arch of aorta.
4th arch right – Right subclavian artery.
6th left arch – Left pulmonary artery
6th right arch – Right pulmonary artery.
Development of arch of aorta is from 4 sources. (Fig. 29.29) (A Kadasne’s Anatomy Volume – II Page 456)
1. Aortic sac
2. Left horn
3. Left 4th arch
4. Left descending aorta.
Fig. 29.29: Development of arch of aorta and brachiocephalic artery (Kadasne’s Anatomy Vol 2)
Highlights of 4
The word arch has 4 alphabets. It lies at the level of 4th thoracic vertebra, it has 4 branches and it
develops from 4 sources.
Four branches of the arch of aorta are:
1. Brachiocephalic
2. Thyroidea ima
3. Left common carotid artery
4. The left subclavian artery.
Coronary Artery Dominance

It is the posterior interventricular artery which decides the coronary dominance. Normally the
posterior interventricular branch arises from the right coronary artery which is called the right
coronary dominance. As against this when the posterior interventricular artery arises from the left
coronary artery (Circumflex) is called the left coronary dominance.
Anomalies of the arch of aorta: are as under:

1. Double aortic arch: It is due to non-regression of the right fourth aortic arch distal to the 7th
intersegmental artery. Right sided aortic arch is common in birds.
Brachiocephalic Artery (Figs 29.30 and 29.31)

Brachiocephalic artery develops from right horn of the aortic sac.
Figs 29.30 and 29.31: Development of brachiocephalic artery and right subclavian artery
Right Subclavian Artery (Figs 29.32 and 29.33)

Right subclavian artery develops from two sources. Proximal part arises from right 4th arch artery
and the distal develops from the right 7th cervical intersegmental artery.
Development of Left Subclavian Artery (Fig. 29.34)

It develops from the 7th left intersegmental artery.
Fig. 29.32: Formation of abnormal right subclavian artery, right recurrent laryngeal nerve does not hook the
right subclavian artery and goes up in the neck. Hence becomes non-recurrent
Development of Common Carotid Artery (Fig. 29.34)

Common carotid artery arises from 3rd arch artery proximal to the external carotid bud.
Internal Carotid Artery

Internal carotid artery develops from 3rd arch artery distal to the external carotid bud and the
cranial part of the dorsal aortae beyond the attachment of the 3rd arch artery.
Fig. 29.33: Formation of abnormal right subclavian artery
Fig. 29.34: Development of common carotid artery and internal carotid artery
Fig. 29.35: Development of external carotid artery, pulmonary artery and the ductus arteriosus
Descending Aorta (Refer Fig. 29.27)

Descending aorta develops from left dorsal aorta distal to the attachment of 4th arch artery. Its
distal part develops from the fused dorsal aortae forming the single median artery.
Note: It must be remembered that the 3rd and the 4th arch arteries have their origin from the right
horn of the aortic sac which forms the brachiocephalic artery. As a result the common carotid and
subclavian arteries of the right side appear as branches of the brachiocephalic artery.
Pulmonary Arteries (Fig. 29.35)

Pulmonary arteries are derived from the part of the 6th arch arteries placed between the pulmonary
trunk and the lung bud.
Developmental Anamolies of the Arch Arteries

Cranial ends of the endothelial heart tubes fuse and form aortic sac with the left and the right
horns. Following this there is appearance of arterial arches numbering six. The aorta which is
placed ventral to the foregut is known as ventral aorta and the dorsally placed part of it is called as
dorsal aorta. The ventral aorta communicates with the dorsal aorta through the arch arteries. Each
arch communicates with right or left horn of the aortic sac.
The fifth arch artery disappears. Third, fourth and the sixth arch arteries communicate with
the aortic sac. Ventral part of the aortic sac receives third and fourth arch arteries while the dorsal
part of the aortic sac receives 6th arch artery.
Septal Anomalies
Ostium primum defect: It is due to failure of the
septum primum to reach the endocardial
cushion.
Ostium secundum: It occurs due to failure of

formation of the septum secundum.
Patent foramen ovale: It is due to non-fusion of
the septum primum and the septum secundum.
(Fig. 29.36).
Fig. 29.36: Patent foramen ovale
Early closure of foramen ovale: In this condition
right sided chambers of the heart get dilated.
Tricuspid atresia: Endocardial fusion extends
more to the right leading to the formation of
tricuspid atresia. Tricuspid atresia increases
pressure in the right atrium as a result there is
non-closure of the foramen ovale (Fig. 29.37).
Other Anomalies
Hypoplasia : left ventricular syndrome. The left
ventricle is poorly developed and is non-
functional.
Cor biloculare – two chambered heart Fig. 29.37: Separation of common ventricular chamber in to
the right and the left by the inter-ventricular septum proper
Cor triloculare – three chambered heart
and the endocardial cushion
Single ventricle and two atria
Double ventricles and one atrium
Absence of pericardium (Complete or partial).
Abnormal Right Subclavian Artery

Abnormal right subclavian artery arises from
the left dorsal aorta and passes behind the
esophagus to the right. Due to the esophageal
compression it causes dysphagia (difficulty in
swallowing). It is called dysphagia lusoria.
Aortic Stenosis (Fig. 29.38)

It leads to hypertrophy of the left ventricle.
Supravalvular aortic stenosis is surgically
repaired by using a graft. Infravalvular aortic
stenosis is surgically treated by excising the Figs 29.38A and B: Aortic stenosis, (A) Supravalvular and
obstructing membrane. (B) Infravalvular
Coarctation of Aorta (Fig. 29.39)

Coarctation means narrowing of the lumen of
the aorta. It occurs due to extension of process
of obliteration of ductus arteriosus to the aorta.
It can be preductal or postductal. Blood
pressure in the upper limb arteries is more than
blood pressure in the lower limb arteries. In
an attempt to overcome the obstruction large
collateral channels develop between the
branches of the descending aorta, internal
mammary thoracic and the axillary arteries.
Enlarged collateral arteries produce notching
of the lower border of the ribs. Radiographs of
the chest shows prominent ascending aorta
and the double aortic knuckle.
There are three sets of arteries arising from Fig. 29.39: Coarctation of aorta
the dorsal aorta.
Branches of Dorsal Aorta (Fig. 29.40)

1. Ventral splanchnic form superior and inferior mesenteric artery. The arteries for bronchi and
the esophagus also arise from the ventral splanchnic branches.
2. Lateral splanchnic branches forms renal, suprarenal, phrenic, spermatic and ovarian vessels.
3. Somatic intersegmental branches somatic intersegmental are the intercostal and the lumbar
arteries.
Fig. 29.40: Branches of embryonic dorsal aorta, e.g. ventral, lateral and the somatic intersegmental
Intersegmental arteries of the cervical region join each other and form as longitudinal
anastomotic channel, i.e. pre-costal, post-costal, post-transverse.
Precostal – In front of the neck of the rib.
Post-costal – Behind the neck of the rib.
Post-transverse – Behind the transverse process
Pre-costal Anastomosis (Fig. 29.41)

Thyrocervical trunk, ascending cervical and the superior intercostal arteries are formed from
precostal part of the anastomosis (T-A-S). The part of vertebral artery is formed from the post
costal anastomosis. Deep cervical artery is formed by the post-transverse anastomosis. Ventral
divisions of the somatic intersegment arteries anastomose and form internal mammary thoracic
artery, superior and inferior epigastric arteries. The anastomatic chain lies on the ventral aspect of
the body near the mid-line.
Seventh cervical intersegmental artery forms the stem of the subclavian artery. Dorsal division
forms the stem of the vertebral artery, lateral division goes the superior limb and form axillary and
branchial arteries. Ventral division becomes the stem of internal mammary thoracic artery.
Seventh Cervical Intersegmental Artery

It’s stem forms the subclavian artery and its dorsal division forms the stem of the vertebral artery.
It’s superolateral division forms the artery of the limb bud in the form of axillary and brachial arteries.
The ventral division forms the stem of the internal mammary thoracic artery.
Fig. 29.41: Vertical anastomoses between branches of dorsal aorta

Derivatives of Anastomoses
Precostal Postcostal Post Transverse
Thyrocervical Vertebral Deep cervical
Ascending cervical
Superior intercostals
TAS V D
Formation of the Vertebral Artery (Fig. 29.42)

First part of the vertebral artery, i.e. from origin to the entry into the foramena transversarium of
the sixth cervical vertebra develops from the dorsal division of 7th cervical intersegmental artery.
The part of the vertebral artery from the foramen transversarium of the sixth cervical vertebra
to that of the first cervical comes from postcostal anastomosis.
The part of the vertebral artery which lies on the arch of atlas develops from the spinal branch
of first cervical intersegmental artery.
Fig. 29.42: Development of vertebral artery

Internal Mammary Thoracic Artery (Fig. 29.43)

Its stem comes from the ventral division of 7th cervical intersegmental artery.
Vertical part of the artery develops from the ventral anastomoses between ventral divisions of
thoracic intersegmental arteries (intercostals artery).
Limb Arteries - Upper Limb (Fig. 29.44)

Each limb has an axis artery. Axis artery of the upper limb is formed from the 7th cervical
intersegmental artery. It forms the axillary, brachial, anterior interosseous artery, deep palmar
arch. The appearance of the radial and the ulnar arteries is later.
Anomalies of the Radial Artery

Anatomical pattern of the radial artery has gained importance since it has replaced the femoral
artery for the purpose of introduction of the cardiac catheter. Anomalies of the radial artery are
responsible for forming a loop of a cardiac catheter and return. (Radioulnar loop). Anomalies of
the radial artery are described as
A, AB, aB
A – Arises from the axillary artery.
AB – Arises from both the axillary and the brachial.
aB – a – negligible from the axillary and B - mostly from the brachial.
Fig. 29.43: Development of internal mammary thoracic artery

Fig. 29.44: Development of arteries of the upper limb
Right Subclavian Artery

Proximal part of the right subclavian artery is formed by the right 4th arch artery and the distal
part is formed by the 7th cervical intersegmental artery.
Lower Limb (Fig. 29.45)

5th lumbar intersegmental artery gives rise to the axis artery of the lower limb and appears as the
branch of internal iliac artery.
The femoral artery appears as entirely new arterial channel on the ventral aspect of the thigh.
It develops connection with external iliac artery above and the popliteal below. Please note that
the external iliac artery is an offshoot of the axial artery.
Following Components Belong to the Axis Artery of the Lower Limb

Inferior gluteal artery
The artery is the branch of the inferior gluteal artery which supply the sciatic nerve. It is known
as arteria nervi ischiadici.
Popliteal artery above the popliteus.
Lower part of the peroneal artery.
Some part of the plantar arch.
Umbilical Artery (Fig. 29.45)

Umbilical arteries are continuous with dorsal aortae before their fusion. With the fusion of dorsal
aortae they become the lateral branches of the fused dorsal aorta. Umbilical artery develops
Fig. 29.45: Development of umbilical artery and the fate of the 5th lumbar intersegmental artery
communication with the newly formed 5th lumbar intersegmental artery. Fifth lumbar
intersegmental artery becomes the internal iliac artery. Part of the umbilical artery between the
dorsal aorta and the site of anastomoses of umbilical artery with 5th lumbar intersegmental artery
disappears as a result, it appears as the branch of the internal iliac artery.
Veins of the Embryo are Divided into three Groups (Figs 29.46 and 29.47)
• Vitelline veins from yolk sac
• Umbilicus vein – carry oxygenated blood from the placenta.
• Cardinal venous system.
There are two vitelline veins from the yolk sac, and the two umbilical veins from the placenta.
Each horn of the sinus venosus receives one umbilical vein and one vitelline vein. As the sinus
venosus itself is embedded in the septum transversum, all the four veins travel through the septum
transversum.
As the liver develops in the septum transversum all the 4 veins get distorted and broken to
form sinusoids of the liver. Sinusoids drain into the sinus venosus through the remaining parts of
the vitelline veins which are called as the right and the left hepato-cardiac channels. The umbilical
veins get disconnected from the sinus venosus.
Fig. 29.46: Development of umbilical and vitelline veins. Note the liver bud appearing
Fig. 29.47: Development of umbilical veins, vitelline veins and the right hepatocardiac channel
The shift of blood from left to the right results in obliteration of the right umbilical vein and the
left vitelline vein. As a result the left horn of the sinus venous looses its prominence. The left common
cardiac vein gets obliterated forming the oblique vein of Marshal, (the oblique vein of the left atrium) and the
coronary sinus. Due to shunting of blood from left to the right the right hepatocardiac channel
enlarges and the left hepatocardiac channel undergoes regression. Now the right hepatocardial
channel is the only channel which has communication with the sinus venosus. As the blood from
the umbilical and vitelline veins goes to the sinus venosus through the hepatocardiac channel it is
called the common hepatic vein. This part of the vein forms the cranial part of the inferior vena cava.
Due to obliteration and final disappearance of the right umbilical vein blood from the placenta
goes to liver only through the left umbilical vein. (Left lives) To facilitate transport of blood the
special channel develops in the substance of the liver, i.e. intrahepatic channel which connects the
left branch of the portal vein to the right hepatocardiac channel. It bypasses the circulation through
the liver substance and is called the ductus venosus.
Portal Vein (Figs 29.48 and 29.49)

Two vitelline veins lying on either sides of the developing duodenum get connected through three
connecting channels, e.g. two ventral and one dorsal.
• Cranial ventral
• Middle dorsal
• Caudal-ventral
Portal Vein is formed by Three Components

a. Caudal part of the left vitelline vein up to joining of the splenic and the superior mesenteric
veins
b. Dorsal anastomosis
c. Cranial part of the right vitelline vein between the dorsal and cranial ventral anastomosis.
Cranial ventral anastomosis and the left vitelline vein cranial to the anastomosis form the left
branch of the portal vein. Right vitelline vein cranial to the anastomoses forms the right branch of
the portal vein.
Finally the portal, caval and the azygos systems are formed to stay permanently in the adults.
The vitelline veins are two the right and the left. They arise from the capillary plexus of the yolk
sac. The vitelline veins run on the either side of the developing duodenum and the septum
transversus and enter the sinus venosus.
Fig. 29.48: Formation of ductus venosus, portal vein and hepatic portion of inferior vena cava
Due to the emergence of the hepatic bud in the substance of the septum transversum the
vitelline veins get divided into three parts they are as under:
1. Supra-hepatic part
2. Intra-hepatic part
3. and the infra-hepatic part.
The story of the infrahepatic part has already been covered.
Intra-hepatic Part (Fig. 29.49)

Due to the growth of the liver cells the vitelline veins break to form the capillary plexus. The
capillary plexus thus formed opens into the hepatic sinusoid, which are formed between the liver
cells.
The vitelline capillary network is arranged into two
1. Venae advehentes (afferent)
2. Venae revehentes (efferent)
Fig. 29.49: Development of portal vein

Venae advehentes belong to the afferent system as they form the branches of the portal vein.
Venae revehentes form the part of the efferent system as they drain into the hepatic veins (Inferior
vena cava).
Suprahepatic Part
Due to disappearance of the suprahepatic part of the left vitelline vein, the suprahepatic part of the
right vitelline vein undergoes enlargement and forms hepatocardiac vein. The hepatocardiac vein
forms the terminal part of the inferior vena cava.
The Umbilical Veins

There are two umbilical veins, the right and the left. They carry oxygenated blood from the placenta
to the fetus and open into the respective horn of the sinus venosus. With the development of the
hepatic bud in the septum transversum the right umbilical vein disappears. The left umbilical vein
communicates with the hepatic sinusoid and joins the left branch of the portal vein. New intrahepatic
communicating channel develops, connecting the left branch of the portal vein with the inferior
vena cava bypassing the hepatic
circulation. It is known as the ductus
venosus. At birth the ductus venosus
get fibrosed and forms the ligamentum
venosum. The left umbilical vein
undergoes fibrosis and forms the
ligamentum teres-hepatis.
Cardinal Veins (Figs 29.50 and

29.51)
Anterior cardinal vein carry blood from
the head, brain, neck and the superior
limb. Caudally the anterior cardinal
vein joins the posterior cardinal vein
and forms the right common cardinal
vein. The common cardinal vein of the
respective side open into the respective
sinus horns.
The cranial part of the anterior
cardinal vein is known as the primary
head vein. It receives blood from the
brain. There are three primary dural
stems, which join the primary head
vein. The venous plexus of the
cranium is divided into the superficial
and the deep parts. Superficial part of
the venous plexus forms the dural
venous sinuses while the deep part of Fig. 29.50
Fig. 29.50 and 29.51: Development of major veins of the upper part of the body
the plexus forms the cerebral veins. The anterior dural stem carries blood from the midbrain and
the middle dural vein drains blood from the metencephalon, while the posterior dural stem drains
blood from the mylencephalon.
Development of Intracranial Venous

Sinuses (Fig. 29.52)
Cavernous Sinus
Cavernous sinus develops from the primary
head vein medial to the trigeminal ganglion.
Sigmoid Sinus
Sigmoid sinus develops from the connecting
channel between the middle and the posterior
dural stems and the posterior dural stem itself.
Transverse Sinus
Transverse sinus develops from the
communicating channel between the anterior
and the middle dural stems.
Fig. 29.52: Formation of intracranial venous sinuses
(highly diagrammatic)
Fig. 29.53: Sinuses developing from sagittal plexus including great cerebral vein of Galen
Superior Petrosal Sinus

It develops from the middle dural stem.
Inferior Petrosal Sinus

It develops from the channel connecting the cavernous sinus and the primary head vein.
Sagittal Sinus
Sagittal sinus develops from the sagittal plexus. It forms the superior sagittal sinus, straight sinus
and the great cerebral vein of Galen (Fig. 29.53).
Left Brachiocephalic Vein (Fig. 29.54)

Develops from the caudal part of the left anterior cardinal and the oblique channel connecting the
left and the right anterior cardinal veins.
Internal Jugular Vein (Refer Fig. 29.54)

It develops from the anterior cardinal vein, cephalic to the joining of the subclavian vein.
Superior Vena Cava (Figs 29.51, 29.55 to 29.58)

It develops from two sources.
1. Right anterior cardinal vein - caudal to the opening of the oblique communication between two
anterior cardinal veins. This part of the superior vena cava is extrapericardial (Refer Figs 29.53
and 29.54). In brief the superior vena cava develops from the right common cardinal and the
proximal part of the right anterior cardinal veins.
2. Right common cardinal vein – forms the proximal part of the superior vena cava.
Subclavian, internal jugular and left brachiocephalic veins
Fig. 29.54: Development of major veins of the upper part Fig. 29.55: Development of left superior intercostal
of the body vein from the left anterior cardinal vein. The 2nd
and 3rd intercostal veins develop from left posterior
cardinal vein
Fig. 29.56: Development of superior vena cava and coronary sinus, oblique vein of left atrium, left superior intercostal
vein and superior vena cava
Fig. 29.57: Development of coronary sinus and Fig. 29.58: Formation of superior vena cava,
absorption of sinus venosus into the right atrium. coronary sinus and oblique ligament
As if viewed from behind
The vein draining the upper limb joins the anterior cardinal vein, cephalic to the oblique
communicating channel. This is known as the subclavian vein. Parts of the anterior cardinal vein
cephalic to the joining of the subclavian vein forms the internal jugular vein. The portion of the right
anterior cardinal vein caudal to the opening of the subclavian vein forms the right brachiocephalic
vein. While the oblique communicating channel between the anterior cardinal veins and the small
part of the left anterior cardinal veins form the left brachiocephalic vein (Fig. 29.59).
On the left side the caudal part of the left anterior cardinal vein regresses and forms the left
superior intercostal vein and the ligament of the left vena cava. The left common cardinal vein forms
the oblique vein of the left atrium (Oblique vein of Marshall) and the coronary sinus.
Fig. 29.59: Veins from the body wall draining in to the anterior and posterior cardinal veins
Double Superior Vena Cava (Fig. 29.60)

In the absence of development of the left brachiocephalic vein, the caudal part of the left anterior
cardinal vein and left common cardinal vein forms the superior vena cava of the left. Both the
superior vena cavae join the left atrium. The right superior vena cava directly goes to the right
atrium while the left superior vena cava joins the coronary sinus.
Fig. 29.60: Left superior vena cava draining into the right atrium
through the coronary sinus (A) Double superior vena cava (B)
Left Superior Vena Cava (Refer Fig. 29.60)

In this condition the caudal part of the right anterior cardinal vein and the right common cardinal
vein disappear as soon as the left brachiocephalic vein develops. In such cases the same veins of
the left side do not disappear.
Posterior Cardinal Veins (Fig. 29.61)

They are paired longitudinal channels which appear on the dorsolateral aspect of the mesonephric
ridge. At the cranial end it joins the anterior cardinal vein and forms the common cardinal vein of
the respective site. At their caudal ends they receive external iliac and the internal iliac veins from
lower limb bud (Fig. 29.62) and the pelvis.
Subcardinal Veins (Refer Fig. 29.55)

Each subcardinal vein develops on the ventromedian aspect of the mesonephric ridge. Two
subcardinal veins are connected in front of the aorta. It is known as pre-aortic anastomosis. Pre-
aortic anastomosis forms the part of the left renal vein. The subcardinal veins are connected to the
posterior cardinal veins. At the cephalic end of the right subcardinal vein a new channel grows
towards head after receiving the supracardinal vein. It joins the right hepatocardiac segment. The
new channel forms the hepatic segment of the inferior vena cava and the common hepatic channel
Fig. 29.61: Development of inferior vena cava
forms the terminal part of the inferior vena cava. It must

be remembered that major part of the right subcardinal vein
forms the renal segment of the inferior vena cava on the right
and the left subcardinal vein forms the part of the left renal
vein on the left.
Supracardinal Veins (Refer Fig. 29.61)

They appear as two longitudinal channels. They are
connected cranially and caudally with the subcardinal
vein of the same side. The right supracardinal vein
develop communication with the right subcardinal vein.
The supracardinal and subcardinal anastomosis of the
Fig. 29.62: Enlarged vein opposite the
right receives testicular or the ovarian vein of the right limb bud
side. As the right supra-cardinal subcardinal anastomosis
forms part of the post-renal segment of the inferior vena cava. The right testicular or right ovarian vein opens
into the inferior vena cava on the right. Anastomosis between the two subcardinal veins forms the left
renal vein. Hence, the left testicular or ovarian vein opens into the left renal vein.
Azygos Venous Lines (Figs 29.63 and 29.64)

The paired veins appear longitudinally. They have communication with the posterior cardinal
veins. Azygos venous lines are joined by transverse connections with the supracardinal veins.
Right azygos venous line forms the vertical part of the azygos vein while the cephalic part of the right
Fig. 29.63: Cross section of the embryo showing venous drainage of body wall
Fig. 29.64: Veins of the body wall joining the anterior and the posterior cardinal veins
posterior cardinal vein forms the arch of the azygos vein. The left azygos venous line forms the superior
and the inferior hemi-azygos veins.
Subcentral Veins
Their appearance is transitory. They are posterior to the primitive dorsal aorta. Two subcentral
veins are connected with each other.
Renal Collar (Fig. 29.65)

The primitive dorsal aorta is surrounded by the ring of veins and their inter-connections. Following
veins take part in the formation of the renal collar.
• Pre-aortic anastomosis joining two subcardinal veins in front of the primitive dorsal aorta.
• Anastomosis between the subcardinal and the supracardinal veins.
• Anastomosis between the supracardinal veins and the azygos venous lines.
• Anastomosis between azygos venous lines and the subcentral veins.
• Post aortic anastomosis connecting the two subcentral veins.
It must be remembered that the pre-aortic anastomosis between the subcardinal veins forms the
left renal vein. Caudally the subcardinal veins receives venous channel which forms the left common
iliac vein. Major portion of the left posterior cardinal vein regress caudally, while it forms the left superior
intercostal vein cranially.
Fig. 29.65: Veins of the renal collar in cross section of mesonephric ridges
Formation of the Inferior Vena Cava (Figs 29.61 and 29.66)

It is formed by the following veins:
• Right posterior cardinal – caudal part
• Right supra-cardinal – caudal part
The anastomosis between the right supracardinal and the right subcardinal veins which receives right
testicular or ovarian vein.
Upper part of the right subcardinal vein: This portion of the inferior vena cava receives both the
renal veins and the right supra-renal vein.
Fig. 29.66: Development of inferior vena cava. Development of inferior vena cava can be remembered by the following
short sentence RIGHT POSTERIOR CARDINAL — SUPRA — SUB — HEPATIC and anastomoss between them
Channel communicating the right subcardinal and the common hepatic vein.
Common hepatic vein: It develops from the suprahepatic segment of the right vitelline vein.
Note: In brief the development of the inferior vena cava can be described as “Supra-sub-hepatic”
with their intercommunicating channels.
Anomalies of the Inferior Vena Cava
Double Inferior Vena Cava

When the infrarenal segment of the left subcardinal vein and the left common iliac veins fail to
disappear.
Retrocaval Ureter
In this case the right ureter passes behind the inferior vena cava which generally is found fibrosed.
This occurs when the postrenal segment of the vena cava which comes from the right posterior
cardinal vein and the right supracardinal vein completely disappear.
Development of Left Renal Vein (Figs 29.65 and 29.67)

Left renal vein develops from the following.
1. The mesonephric vein draining in to the left subcardinal vein.
2. Part of the left subcardinal vein.
3. Communicating channel between the subcardinal veins. The communicating channel lies in
front of the aorta and is called the preaortic channel. It explains why the left renal vein lies
infront of the aorta.
Fig. 29.67: Development of left renal vein from three sources 1. Mesonephric vein
2. Left sub-cardinal vein 3. Anastomosis between two subcardinal veins
Fetal Circulation (Figs 29.68 and 29.69)

Gases exchange between the mother and the fetus occurs by a process of diffusion through the
placental barrier. The left umbilical vein enters the free margin of the falciform ligament of the
liver, and joins the left branch of the portal vein. Due to development of the ductus venosus, major
portion of the blood is carried into the inferior vena cava directly, however part of the blood goes
through the hepatic circulation and reaches the inferior vena cava. This explains the larger size of
the liver in a newborn. The terminal portion of the inferior vena cava receives mixed blood
(1) oxygenated from the left umbilical vein and (2) deoxygenated blood from the embryo. The
sphincter is placed at the caudal end of the ductus venosus which can regulate the entry of the
blood from the left umbilical vein. When the sphincter is relaxed, the oxygen content of the blood
is increased. Dut to the sphincteric control the load on the fetal heart can be lessened. After entry
in the right atrium the blood from the inferior vena cava is guided by the valve of the inferior vena
cava to the left atrium through the foramen ovale. The foramen ovale is bounded above by the
lower edge of the septum secondum called the crista dividens. Due to the crista dividens the blood
from the inferior vena cava is divided into two flows right and the left. Major portion of the blood
reaches the left atrium and small quantity of blood goes to the lung. On the other hand the right
atrium receives large amount of deoxygenated blood as small amount of oxygenated blood brought
by the inferior vena cava stays in the right atrium. The blood from the left ventricle goes to the
ascending aorta and is carried to the head, neck, brain and the upper limb. As a result essential
organs are provided with the oxygenated blood. The blood in the right ventricle with poor oxygen
content is pushed into the pulmonary circulation. However the major portion of the blood goes to
the distal part of the aorta through the ductus arteriosus. The blood in the descending aorta goes to
Fig. 29.68: Fetal circulation (Highly diagrammatic)
the thoracic viscera, abdominal viscera and limbs. De-oxygenated blood reaches the placenta
through the right and the left umbilical arteries. Blood is oxygenated in the placenta and gets
prepared for further circulation. Due to the aortic pressure and the solid lung structure the right
ventricle is compelled to push blood against resistance. Due to more work undertaken by the right
ventricle, its musculature gets thicker in the fetal life. However, after birth as the job of forceful
pushing of the blood is assigned (given) to the left ventricle, as a result the wall of the left ventricle
becomes thicker than that of the right.
Fig. 29.69: Circulation in adult (Highly diagrammatic)
Factors of Importance for Normal Foetal Circulation

1. Left umbilical vein
2. Ductus venosus
3. Valve of the inferior vena cava
4. Foramen ovale
5. Ductus arteriosus
6. The umbilical arteries.
Development o
Development f
of
30 Lymphatic System
There are two theories regarding the origin of the lymphatic system (Figs 30.1 and 30.2).
1. Develops from the mesenchyme.
2. Develops as outgrowths from the existing venous system.
Five lymph sacs develop in the embryo, i.e. two jugular, two iliac, one retroperitoneal and the
cisterna chyli. The sacs are connected by the numerous channels for the drainage of the different
parts of the body.
Development of Thoracic Duct (Fig. 30.2)

Two lymphatic ducts develop on either side of the vertebral column. They are connected by the
cross channel at the level of 5th thoracic vertebrae. Thoracic duct is formed by the caudal part of
Fig. 30.1: Development of lymphatic system

Development of Lymphatic System 253
Fig. 30.2: Development of thoracic duct multilocular and unilocular cystic hygromas
Fig. 30.3A: Cystic hygroma (Courtesy: Dr Manohar Tule, Pediatric surgeon, Nagpur, Maharashtra, India)
the right lymphatic duct, communicating channel between the two lymphatic ducts at the 5th
thoracic vertebra and the cranial part of the left lymphatic duct. The right lymphatic duct develops
from the cranial part of the right thoracic channel.
Fig. 30.3B: Ultrasound of cystic hygroma of neck. It is multilocular
Clinical
1. Cystic hygroma: Primitive lymph sacs in the neck between the internal jugular and the subclavian
veins are commonly involved. It is the sequestration or pinching of the jugular lymph sacs
which leads to the formation of soft, partly compressable and brilliantly translucent swellings in the
neck. It appears before birth or during early infancy. Large cystic hygroma can be the cause of
obstructed labor. Cystic hygroma can be unilocular or multilocular (Figs 30.3A and B).
The cysts are lined with single layer of epithelium and are filled with clear lymph. It may
resolve or increase in size causing respiratory distress. Treatment of the cystic hygroma includes
aspiration, injection of sclerosing agents (Picibanil) or the surgery.
2. Congenital lymphoedema of the skin: Appears in the form of diffuse swellings on the surface of
the body as a result of primary dilatations of the primordial lymphatic channels.
Urogenital System 255
Urogenital System
Urogenital
31
Intraembryonic mesoderm is arranged in 3 columns, the paraxial, intermediate and the lateral
plate mesoderm. The intermediate mesoderm froms the urogenital system. It is called nephrogenic
cord which extends from the cervical to the sacral regions (Figs 31.1 and 31.2).
Nephrogenic cord has two parts medial gonadal and the lateral urinary. They are seen bulging
in the coelomic cavity on the dorsal abdominal wall by the side of the root of the dorsal mesentery.
The bulgings are covered with the coelomic epithelium.
Following structures appear in the nephrogenic cord at different stages:
1. Excretory tubules of kidney.
2. Nephric duct.
3. Paramesonephric duct.
4. Gonads (testis or ovary): Gonads develop from the coelomic epithelium covering the
gonadal part of the urogenital ridge.
Fig. 31.1: Nephrogenic cord projecting from the dorsal wall in the intraembryonic coelom
by the side of dorsal mesentery
Fig. 31.2: Urogenital ridge with its gonadal and the urinary parts
Development of Kidney (Figs 31.3 and 31.4)

Kidneys are mesodermal in origin and develop from two sources:
1. Excretory part of the kidney develops from the metanephric cap.
2. The collecting portion of the kidney develops from the ureteric bud which arises from the
mesonephric duct.
Fig. 31.3: Development of kidney. Note ureteric bud arising from mesonephric duct. Observe capping of ureteric bud
by the metanephros. Note ejaculatory duct
Fig. 31.4: Stages of development of metanephric kidney
Developmental events of the formation of kidneys prove the saying “Ontogeny repeats the
phylogeny”.
The evolutionary stages of kidneys:
1. Pronephros in fishes.
2. Mesonephros in amniotes
3. Metanephros duct in amniotes (Human)
Pronephros appears in the cervical, mesonephros in the thoracolumbar and the metanephros
in the sacral regions.
Pronephros
Pronephros is non-functioning however its nephric duct opens into the cloaca. Mesonephros is
made of large number excretory tubules appearing in the thoracolumbar region. Mesonephric
tubules join the nephric duct which acquires the name as the mesonephric duct.
Pronephros consists of 7-8 pronephric tubules and the pronephric tubes join the successive
pronephric tubul caudally and from the pronephric duct. The pronephric duct caudally opens into
ventral part of cloaca which forms the urinary bladder. The proximal part of each pronephric tube
(Nephrocele) opens in the coelomic cavity forming peritoneal funnel. Near the peritoneal funnel
external glomerulus is formed by the lateral branch of the aorta. The external glomerulus is seen
projecting into the coelomic cavity from the dorsal wall. Artery from the aorta enter the cavity of
the pronephric tubule forming the internal glomerulus. Later the pronephric tubules degenerate
and disappear deserting the pronephric duct.
Mesonephros
Following disappearance of the pronephric tubules 70-80 mesonephric tubules appear. The
mesonephric tubules join the pronephric duct. Now the pronephric duct is called the mesonephric
duct or Wolffian duct. Medial end of the mesonephric tubule gets dilated to receive capillary tuft
from the lateral branch of the aorta. This forms the internal glomerulus. Mesonephric tubule becomes
S shaped. Its medial part is lined by the columnar epithelial and the lateral with cubical epithelial.
Medial part lined by the columnar epithelium is representative of the secretory part while the lateral
part lined by the cubical epithelium represents the collecing part of the tubule.
Number of mesonephric tubules in the lumbar region form a mass projecting into coelomic
cavity lateral to the root of mesentery forming the mesonephric ridge. Proliferation of cell covering
the medial part of the nephrogenic cord forms the gonadal ridge from which gonads develop. The
mesonephric kidney’s function involves filteration for removing the waste products from the blood.
It is not able to function as the selective absorber of the glomerular filtrate due to the absence of the
loop of Henle and the capillary plexus surrounding the nephric tubules.
Mesonephric tubules in male forms vasa efferentia. The mesonephric duct gives rise to epididymis,
vas deferens, seminal vesicles and the ejaculatory ducts. However proximal mesonephric tubules form
ductus aberrant superior and the distal one forms the ductus aberrant inferior. In female mesonephric
tubules form epoophoron and the paroophoron. In female the mesonephric duct itself forms the duct
of epoophoron called the Gartner’s duct.
Metanephros (Figs 31.5 to 31.8)

It develops in the 5th week and starts functioning 5 weeks later.
Permanent kidney develops from two sources, (1) ureteric bud and (2) the metanephric gap.
The ureteric bud arises from the caudal part of the mesonephric duct long before the duct joins the
cloaca. It approaches the mesonephric ridge which forms the metanephric cap. Part of the
mesonephric duct caudal to the origin of the ureteric bud forms the ejaculatory duct.
Metanephric kidney appears at the lumbosacral
region. Ureteric bud forms the collecting part and
metanephric part forms the excretory part. Ureteric bud
bifurcates to form the major calyces. Each major calyx
divides repeatedly and its two, three four divisions form
the minor calyces. Beyond the fifth division the collecting
tubules are formed. The cranial end of the ureteric bud dilates
forming the pelvis of the ureter and the narrow caudal part
becomes the ureter. Two dilatations appear in the ureteric
bud, e.g. pelvic and the lumbar regions. These two
dilatations form three constrictions of the ureter, i.e. at
the pelviureteric junction, at the brim of pelvis and the Fig. 31.5: Development of metanephric vesicle
third at the ureterovesical junction. and the ampulla of the collecting duct
Fig. 31.6: Stages of development of the nephron
The mesonephric ducts form the trigone of the urinary

bladder as they get absorption in the dorsal wall of the
cloaca. This makes the ureteric bud to open proximally
in the urinary bladder while mesonephric ducts
proceed caudally to open into the pelvic part of the
urogenital sinus as the ejaculatory ducts.
Each branch of the ureteric bud of the first order
gets capped by the metanephric blastema. Initially it
is solid consisting of bilaminar cells. Group of cells
get separated from main mesenchymal mass. They lie
on either side of the tubule and the remaining
mesenchymal mass goes at the tips of the branches.
Solid cluster of cells develop a cavity. It is called the renal
Fig. 31.7: Dividing ureteric bud in the
vesicle which gives rise to the nephron. One end of the metanephros
renal vesicle touches the collecting tubule and the other end
gets dilated and invaginated by the internal glomerular
plexus. The internal glomerular plexus is formed from
the angiogenic tissue of the nephrogenic cord.
Angiogenic tissue of the mesenchyme also forms the
endothelial and mesengeal cells of glomerulas. The
renal vesicle becomes S shaped. The middle part of
the renal vesicle forms the loop of Henle. Loop of
Henle occupies the medullary part of the kidney.
Finally the loop of Henle forms proximal and the distal
convoluted tubules. As the walls of the excretory and
the collecting tubules fuse and break, communication
opens between the two, heralding the beginning of Fig. 31.8: Ureter, pelvis and calyces
the tubular function. However the reabsorption of the glomerular filtrate by the loop of Henle
occurs later. The nephrons which develop earlier form the Juxta Medullary Apparatus, which lies at
the junction of medulla and the cortex of the kidney.
Ascent of the Kidney (Fig. 31.9)

Metanephros is the adult kidney which develops in the sacral region. It is probably due to differential
growth of the posterior abdominal wall the kidneys ascend. Location of the kidney changes its
blood supply. Initially kidney is supplied by the branch from the median sacral artery. As it reaches
the iliac fossa, it is supplied by the branch of comman iliac artery. As the kidneys reach under the
diaphragm, its upward journey is stopped by the developing large suprarenals. The lower
suprarenal artery supplies the kidney. As a result the lower suprarenal artery forms the permanent
renal artery. In brief the ascent of the kidney is attributed to the following factors:
• Growing length of the ureteric bud
• Reduction of the fetal curvature
• Due to smaller pelvic cavity it faces space crunch
• It ascend in search of better blood supply.
The kidneys at birth are lobulated and remain in the lobulated form upto 1st year of life.
Fig. 31.9: Ascent of kidney and changing blood supply

Rotation of Kidneys
Kidney rotate medially around the vertical axis during the ascent. As a result the hilum of the
kidney faces medially.
Juxtaglomerular Apparatus
Blood supply of the medulla of the kidney is controlled by juxtaglomerular apparatus. The juxta-
glomerular apparatus contains macula densa, juxtaglomerular cells and mesangeal cells.
Probable Causes of Rotation of the Kidney

It is of interest to ponder about the hilum of the kidney which is directed ventrally, while in the
pelvis. This appears to be the due to space crunch as a result of small pelvic cavity. As the kidney
reaches the posterior abdominal wall it is offered broad and comfortable bed on the posterior
abdominal wall. This makes the kidney to undergo the medial rotation where the hilum of the
kidney points towards the vertebral column. In other words kidney undertakes upward journey
in the search of better accommodation and the blood supply.
Anomalies of the Kidneys

1. Agenesis: It may be of one or both the kidneys. Agenesis of one kidney does not give rise to
symptoms as the job of the missing kidney is taken over by the one which is present. Due to
overwork it undergoes compensatory hypertrophy (It increases in size) Finding of the single
umbilical artery in an infant is enough to raise suspision of unilateral agenesis of the kidney. Bilateral
agenesis of kidney is always associated with oligohydramnios as no urine is added to the amniotic
cavity. This condition is incompitable with life.
2. Hypoplasia and hyperplasia.
3. Hydronephrosis: Due to congenital obstruction.
Shape
A. Horseshoe kidney (Fig. 31.10): The lower poles of the kidneys get fused. Both the ureters pass in
front of the connecting bridge causing compression of the ureter leading to hydronephrosis. It
should be noted that the inferior mesenteric artery also runs in front of the connecting bridge.
Clinical
Horseshoe kidney is prone to develop following complications:
a. Infection.
b. Stone formation: Removal of a stone from pelvis of ureter in case of horseshoe kidney is relatively
easy due to position of pelvis of ureter.
c. Tuberculosis: Treatment of horseshoe kidney is not to cut the bridge but to re-route the ureters.
Ureters are sectioned and brought in front of the kidney bridge and joined (Anastomosed).
(Cutting of the kidney bridge is undertaken only during the surgery for the aortic aneurysm.)
Fig. 31.10: Horseshoe kidney

Hydronephrosis
It is an aseptic dilation of the kidney due to partial obstruction to the outflow of urine accompanied
by stretching the renal pelvis.
B. Pancake kidney (Fig. 31.11): Two kidneys join to form a single cake like mass
C. Crossed ectopia (Fig. 31.12): Kidney crosses to the opposite side.
Anomalies in the Ascent of Kidneys

1. Pelvic kidney (Fig. 31.13).
2. Lower lumbar kidney: The kidney at the brim of
the pelvis is commonly seen on left. Acute
renal disease of the kidney at the brim of
pelvis may create diagnostic problem. The
bizarre (odd) pelvic mass may tempt, an
inexperienced surgeon to go for its removal.
3. Thoracic kidney.
4. Both kidney on one side one above the other
(‘S’ shaped kidney).
5. Both kidneys cross each other through their
ureters in the midline.
6. Lobulated kidney (Fig. 31.14): It is normal
developmental form which persists upto one
year of life. However lobulated kidney may
Fig. 31.11: Pancake kidney
continue in the same form upto adulthood.
Fig. 31.12: Cross ectopia Fig. 31.13: Pelvic kidney
It is thought pertinent to study the derivatives of the pronephros and the mesonephros at this
stage in the form of a chart.
Pronephros Mesonephros
Situation Cervicothoracic Thoracolumbar
No. of tubules 7–8 700–800
Communication Communicates with celomic cavity through Totally disconnected from the coelomic
a funnel. cavity.
Glomeruli Has external glomeruli Has only internal glomeruli
At times internal glomeruli too
Elimination of Indirectly through coelomic cavity Waste products from blood go to
waste products mesonephric tubules by way of
filteration. Due to the absence of loop
of Henle no selective reabsorption.
Duct Has its own duct i.e. pronephric duct. Does not have its own duct hence
borrows pronephric duct and give its own
name to it (mesonephric duct.)
Remnants No remnants in male Mesonephric duct persists in the form
of structures both in the male and the
female.
MALE : Vasa efferentia, canal of
epididymis, vas deferens, seminal
vesicles, ejaculatory ducts.
FEMALE: Epoophoron and paroophoron and
Gartner’s duct.
Defects of Rotation (Fig. 31.15)

No rotation: Hilum looks forward.
Normal medial rotation: Hilum look medially.
Incomplete rotation: Hilum looks anteromedially.
Reverse rotation: Hilum looks anterolaterally.
Congenital Polycystic Kidney (Fig. 31.16)

Kidney is studded with cysts pressing and destroying
the renal parenchyma causing the renal failure.
Note: According to some of the authorities, formation
of the cyst is not due to the non-union of the collecting
Fig. 31.14: Lobulated kidney
and the excreting portions of the kidney but is due
to the abnormal dilatation of urinary tubules. Uriniferous tubules arise from two different
embryological components. Nephrons develop from the metanephros belonging to the intermediate
mesoderm while the collecting tubules develop from the ureteric bud, the diverticular of the
mesonephric duct.
Fig. 31.15: Defects of rotation of kidney
Congenital Polycystic Kidney is of Two Types
Adult type Childhood type

Autosomal dominant Autosomal recessive
Causes hypertension,
pain, renal failure.
Appears after 20 years and Appears before 20 and
patient survives upto 60 years. patient dies earlier.
Treatment
1. Low protein diet may help in delaying renal
transplant.
Fig. 31.16: Congenital polycystic kidney
2. De-roofing of the cyst (Rousing’s operation) with the hope of reducing the renal pressure. It can
be done laproscopically for the relief of pain.
3. Finally the patient of polycystic kidney requires renal transplant.
Aberrant Renal Artery (Fig. 31.17)

Renal arteries are the functional end arteries. Ligation of an abnormal renal artery can lead to renal
ischemia of the part supplied. Two or more renal arteries are commonly seen on the left. Renal
arteries supplying the poles of the kidneys are called polar arteries. Aberrant renal artery of the left
passes anterior to the left ureter and causes enlargement of the left renal pelvis (Hydronephrosis). Aberrant
renal artery of the right passes anterior to the inferior vena cava and the right ureter.
Abnormal sites of opening of the ureter (Ectopic
openings of ureter).
The ureter which opens anywhere except the in
urinary bladder is called the ectopic ureter.
Female Male
1. Urethra 1. Seminal vesicles
2. Vagina 2. Ejaculatory ducts
3. Rectum 3. Rectum, prostatic part of urethra
4. Vestibule
Note: In female opening of ectopic ureter is placed

below the sphincter which causes troublesome
incontinence. However, in male the ectopic ureteric
opening is above the sphincter hence causing no
incontinence. (Incontinence – means loss of self control Fig. 31.17: Aberrant renal artery
in passing of urine). (more common on left)
Dietl’s Crisis
It is seen in cases of pelviureteric obstruction. It is more common on the right. Attacks of pain is
followed by the appearance of swelling in the loin. Hours after, patient passes large quantity of
urine leading to disappearance of pain and the swelling. The condition is also labeled as the
intermittent hydronephrosis.
Note: Some authors have mentioned occurance of Dietl’s crisis in floating kidney, which is not
correct. The pressure on the kidney pedicle suppresses urine formation, causing renal failure rather
than Dietl’s crisis. In floating the kidney its pole gets tilted down causing the compression of the
kidney pedicle.
Absorption of Caudal Part of the Mesonephric Ducts into the Cloaca (Fig. 31.18)
Caudal ends of the mesonephric ducts open into the part of the cloaca which forms the vesicourethral
canal. Mesonephric duct give ureteric bud cranial to the wall of the cloaca. The part of the
mesonephric duct caudal to the origin of the ureteric bud gets absorbed in the dorsal wall of the
cloaca. This creates separate openings for the mesonephric ducts and the ureteric buds. Absorption
of the ureteric buds shifts their openings in cephalolateral direction. The triangular area on the
Fig. 31.18: Absorption of mesonephric ducts in the dorsal wall of the urogenital sinus
dorsal wall of the vesicourethral canal marked by the openings of ureteric buds and the mesonephric
ducts, forms the trigone of the urinary bladder. It is mesodermal in origin and is very vascular and
extra sensitive.
Development of the Ureter

Ureters develop from the part of the ureteric buds between the pelvis of the ureter above and the
uretrovesical junction below. The ureters are mesodermal in origin. They develop two dilatations
forming three constrictions, e.g. pelvic, ureteric, at the brim of pelvis and at the ureterovesical
junction.
Anomalies of the Ureter (Fig. 31.19)

1. Unilateral agenesis.
2. Duplication of ureter partial or complete.
3. Ectopic opening of the ureter, e.g. prostatic part of urethra, seminal vesicle, ductus deferens or
the rectum in the male. Vagina, vestibule and rectum in the female.
4. Blind upper end of the ureter.
5. Hydroureter: It is also known as congential megaureter. It is due to the functional obstruction
at the lower end of the ureter (Fig. 31.20).
6. Ureter having valves or diverticuli.
7. Retrocaval ureter: Right ureter lies behind the inferior vena cava. It is usually fibrotic.
8. Ureterocele (Fig. 31.21): Congenital atresia of the lower end of the ureter causes dilatation of
intramural part of the ureter. (Intramural means portion of the ureter in the wall of the urinary
bladder.) The part of the ureter in the wall of the urinary bladder gets dilated due to
ureterovesicle obstruction.
9. Double ureter: Mesonephric duct gives rise to two ureteric buds, i.e. upper and the lower forming
two kidneys on the same side. Lower ureter opens proximally in the urinary bladder while the
upper one goes distally along with the distal migration of the mesonephric duct and opens in
the prostatic part of the urethra. It is interesting to note that these two ureters cross each other
near the urinary bladder. At times

both the ureters open into the
urinary bladder by a common
opening.
Before we go for the study of the
development of the urinary bladder
and urethra, it is advisable to go
through the development of vesico-
urethral canal and the urogenital
sinus. Vesicourethral canal gets
divided into cranial and the caudal
parts. The cranial parts forms the
urinary bladder and the caudal part
Fig. 31.19: Anomalies of urinary system Fig. 31.20: Hydroureter (IVP) (Courtesy: Dr Ravi
Deshmukh, Urosurgeon, Nagpur, Maharashtra,
India)
forms the primitive urethra. The

urogenital sinus also divides into two
parts the cranial and the caudal.
Cranial part is known as the pelvic
part of the urogenital sinus while the
caudal part is called the phallic part
of the urogenital sinus.
Fig. 31.21: Ureterocele

Development of the Urinary Bladder

(Figs 31.22 and 31.23)
Urinary bladder is endodermal in
origin. It develops from the cranial part
of the vesicourethral canal. Trigone of
the urinary bladder is mesodermal in
origin. It develops from the absorbed
mesonephric ducts. Epithelium of the
trigone is gradually replaced by the
surrounding endoderm.
Allanto-enteric diverticulum gets
fibrosed and forms the urachus which
runs from the apex of the urinary
bladder to the umblilicus. In adult, it
forms the median umbilical ligament. Fig. 31.22: Development of urinary bladder
Allanto-enteric diverticulum does not
contribute to the formation of the
urinary bladder.
Congenital Anomalies of the

Urinary Bladder
1. Absence of urinary bladder.
2. Duplication of urinary bladder.
3. Absence of sphincter vesica.
4. Compartmental urinary bladder.
5. Hourglass urinary bladder.
6. Ectopia vesicae (Figs 31.24 and
31.25 Courtesy: Dr Ravi Deshmukh,
Urologist, Nagpur). In this condition
the lower part of the anterior
abdominal wall is missing along
with ventral wall of the urinary
bladder. As a result interior of the
urinary bladder, i.e. trigone and
ureteric openings can be viewed
from outside. It is associated with
epispadias with missing of the umbilicus
and absence of pubic bones are
the hallmarks of ectopia vesicae.
7. Urachal cyst: Middle part of the
allantoic diverticulum forms a cyst
while its proximal and the distal
part get fibrosed. Fig. 31.23: Divisions of primitive urogenital sinus
Fig. 31.24: Ectopia vesicae. Note the absence of the umbilicus
Fig. 31.25: Ectopia vesicae (Courtesy: Dr Ravi Deshmukh, Urologist, Nagpur, Maharashtra, India)
8. Urachal fistula: Total patency of the allantois leads to formation of the urachal fistula. (Urinary
umbilical fistula).
9. Rectovesical fistula.
10. Vesicovaginal fistula: Mullerian tubercles bulge into the vesicourethral canal instead of the
opening into the urogenital sinus. After disappearance of the tubercle vasicovaginal fistula is
formed.
11. Congenital diverticula: They are seen at the

junctional zone between the trigone and the
rest of the bladder wall.
12. Megalocystis: Large urinary bladder can
result due to distal obstruction in the
posterior urethra due to the urethral valves.
This causes renal failure which can be
prevented by performing ex-utero surgery.
Development of the Female Urethra

(Fig. 31.26) Fig. 31.26: Development of female urethra
Female urethra develops from the caudal part of the vesico-urethral canal. It is endodermal in
origin. However the dorsal wall of the urethra develops from the mesonephric ducts, hence
mesodermal. It corresponds to the prostatic part of the male urethra above the colliculas seminalis.
Development of the Male Urethra (Figs 31.27 to 31.29)

1. Male urethra between the urinary bladder and the colliculus seminalis (openings of the
ejaculatory ducts) develops from the caudal part of the vesicourethral canal. However its dorsal
wall is mesodermal in origin as it develops from the mesonephric ducts.
2. Prostatic part of the urethra below the colliculus seminalis and the membranous part of the
urethra are formed by the pelvic part of the definitive urogenital sinus.
Fig. 31.27: Development of male urethra

Fig. 31.29: Transverse section of glans showing development of urethra of glans from
the ectodermal terminal urethral plate
3. Penile part of the urethra is formed from the phallic part of the definitive urogenital sinus.
4. Terminal part of the urethra which occupies the glans penis develops from the ectoderm.
Anomalies of the Urethra

1. Bladder neck obstruction.
2. Diverticula.
3. Duplication of urethra partial or complete.
4. Valves (urethral valves): They allows the entry of the catheter but stops exit of urine (Fig. 31.30).
5. Hypospadias (Figs 31.31 and 31.32).
6. Epispadias – mostly associated with ectopia vesicae.
7. Fistula between the urethra and the rectum, vagina or the ureter.
Development of Prostate (Figs 31.33 to 31.36)

Five epithelial buds grow from the caudal part of the vesico-urethral canal and the pelvic part of
the definitive urogenital sinus. They are, one anterior, two lateral and two posterior.
Buds arising from the mesodermal posterior wall of the urethra form the inner glandular zone
of the prostate. Remaining buds arising from the endoderm form the outer zone of the prostate.
Inner glandular zone is prone to undergo benign prostatic hypertrophy. Outer zone of the prostate
is the zone is prone to develop cancer (Fig. 31.37). Capsule, muscles and the connective tissue of
the prostate develop from the surrounding mesenchyme. Secretary zone of the prostate at puberty
undergoes radical changes. In old age it may undergo atrophy or hypertrophy.
Fig. 31.30: Urethral valves Fig. 31.31: Sites of hypospadius
Fig. 31.32: Hypospadius (Courtesy: Dr Ravi Deshmukh, Kadasne’s Textbook Vol ll,
Urologist, Nagpur, Maharashtra, India)
Fig. 31.33: Vesicourethral canal viewed from side Fig. 31.34: Vesicourethral canal seen from
presenting one anterior and two posterior prostatic behind presenting two lateral prostatic buds
buds
Fig. 31.35: Prostatic part of urethra
Fig. 31.36: Sagittal section through prostatic part of urethra showing median lobe of prostate
Fig. 31.37: Outer and inner zones of prostate with their source of origin
Female Homologues of Prostate

Buds arising from the caudal part of the vesicourethral canal develop into the urethral gland,
while the buds arising from the urogenital sinus form paraurethral glands of Skene. The paraurethral
glands of Skene correspond to the true prostatic glands of the male.
Paramesonephric Duct
They are formed as the surface coelomic epithelium undergoes invagination. The paramesonephric
ducts develop in the intermediate mesoderm in the cranial part of the nephrogenic cord and are
lateral to the mesonephric duct.
Paramesonephric duct has three parts, (1) cranial vertical, (2) middle horizontal (3) and the
caudal vertical. The middle horizontal part of the paramesonephric ducts crosses in front of the
mesonephric ducts and approach each other, to fuse and form the uterovaginal canal. Caudal ends
of the paramesonephric ducts produce tubercles in the dorsal wall of the definitive urogenital
sinus. They are called the Mullerian tubercles. This part of definitive urinogenital sinus forms the
vestibule of vagina in the female. Uterine tubes, uterus and the upper part of the vagina develop
from the paramesonephric ducts in the female.
Derivatives of the paramesonephric ducts in the male are as under:
1. Appendix of the testes
2. Prostatic utricle
Development of the Uterus (Figs 31.38 and 31.39)

Uterus is mesodermal in origin and develops from the uterovaginal canal. Uterovaginal canal is
formed by fusion of the paramesonephric ducts. Caudal vertical part of the paramesonephric ducts
unite caudocranially to form the uterovaginal canal. Blind caudal ends of the paramesonephric
duct form tubercles in the dorsal wall of the urogenital sinus. The tubercles are called the Mullerian
tubercles. The surrounding mesenchyme forms the myometrium of the uterus. Horizontal non-
Fig. 31.38: Formation of uterovaginal canal after fusion of two paramesonephric ducts
united parts of the paramesonephric ducts get buried in the heap of mesoderm and form the fundus
of the uterus. Uterine tubes develop from the rest of the horizontal portion of the paramesonephric
ducts. The sites of invagination of the paramesonephric ducts are maintained as the peritoneal
ostia. (Ostium – opening of the uterine tubes in celomic cavity). Through the tubal opening, the
peritoneal cavity of the female communicates with the exterior. Hence is not the closed cavity as
against the peritoneal cavity of the male which is closed. This explains the higher incidence of
pelvic infections in the female.
Fig. 31.39: Formation of uterus from uterovaginal canal

Fig. 31.40: Anomalies of the uterus
Anomalies of the Uterus (Fig. 31.40)

1. Duplication of uterus: Complete duplication of the uterus is known as uterus didelphys.
2. Septate uterus.
3. Agenesis of uterus.
4. Half of the uterus is missing (Unicornuate uterus).
5. Rudimentary uterus.
6. Atresia of the body of the uterus or the cervix.
7. Infantile uterus: Fetal cervix is two times longer than the body of the fetal uterus.
Anomalies of the Uterine Tubes

1. Absence of one or both uterine tubes.
2. Duplication of uterine tubes.
3. Tubal atresia.
Development of Vagina 277
Development o
Development fV
of agina
Vagina
32
Caudal end of the uterovaginal canal reaches the dorsal wall of the urogenital sinus. The endodermal
cells of the wall of the urogenital sinus form two solid masses. They are called as the sinovaginal
bulbs (Fig. 32.1A). The sinovaginal bulbs intervene between uterovaginal canal and the dorsal wall
of the urogenital sinus. Union of the sinovaginal bulbs forms the vaginal plate. Although the larger
part of the vaginal plate arises from the sinovaginal bulbs, the part of it near the cervix is mesodermal
in origin. Uterovaginal canal and the urogenital sinus are separated by the vaginal plate (Fig. 32.1A).
Hymen lies at the lower end of the viginal plate which is the junction of vaginal plate and the
urogenital sinus. It is important to remember that both the surfaces of the hymen are covered by
the endoderm.
Summary of Development of Vagina (Fig. 32.1A)

1. Upper 4/5th part of vagina above the hymen is develops from endoderm by canalization of
the sinovaginal bulbs (vaginal plate).
Fig. 32.1A: Formation of vagina

2. Lower 1/5th of vagina below the hymen develops from endoderm of the urogenital sinus.
3. External orifice of the vagina is ectodermal and develops from the genital folds after disappearance
of the urogenital membrane.
4. Part of the vagina near the cervix is derived from the mesoderm of the uterovaginal canal. The
cavitation of the mesoderm around the cervix forms the vaginal fornices.
Anomalies of the Vagina

1. Duplication of vagina
2. With duplication of the uterus
3. Compartmental vagina in which vagina is divided longitudinally or transversely.
4. Absence of uterus.
5. Imperforate hymen is due to nondisintegration of the central part of the Mullerian eminence.
At the onset of menstruation at puberty, leads to collection of menstrual blood in the uterine
cavity. It is called hematocolpos.
6. Rectovaginal fistula (RVF) (Fig. 32.1B)
7. Vasicovaginal fistula (VVF): Mullerian tubules bulge in the vesicourethral canal and not in
the urogenital sinus. After disappearance of the tubercles vasicovaginal fistula is formed
(Fig. 32.1B).
Paramesonephric Ducts in Males (Mullerian Ducts)

Paranephric duct forms the appendix of the testis and the prostatic utricle in the males.
Fig. 32.1B: Types of fistulae in male and female

Major portion of the paramesonephric duct disappears in the male, however, cephalic end of
each duct forms an appendix of the testis. Appendix of the testis may give rise to cysts. It is believed
that prostatic utricle represents the uterovaginal canal and considered as the homologue of the
uterus.
Development of External Genitalia (Fig. 32.2)

As the urorectal septum meets the cloacal membrane, it divides the cloacal membrane into ventral
and dorsal parts. Ventral part is called the urogenital membrane and the dorsal as the anal
membrane. Urogenital membrane elongates in cephalocaudal direction. Mesoderm on either side
of the cloacal membrane grows from the primitive streak and forms two longitudinal elevations.
They are known as the primitive urethral folds. Apart from these folds there are three mesodermal
elevations in this area which are as under:
1. Genital tubercle: Genital tubercle is placed in the midline occupying the gap between the
urogenital membrane and the lower part of the anterior abdominal wall.
2. The right and the left genital swellings.
Development of Female External Genitalia (Figs 32.2 and 32.3)

Genital tubercle changes its shape and becomes cylindrical. It forms the clitoris. The genital swellings
grow in size and form the labia majora. The swellings are connected in the midline caudally forming
the posterior commissure. Continuity is established with breakdown of the urogenital sinus with
the exterior. Primitive urethral folds form the labia minora. It is important to remember that the
labia minora has outer ectodermal and inner endodermal linings.
Development of Male External Genitalia (Fig. 32.2)

Genital tubercle assumes cylindrical shape and becomes the phallus. Enlargement of the phallus
converts it into the penis. At a later stage along with the growth of the phallus, glans and the
coronary sulcus are defined. Prepuce of the penis is formed due to duplication of the ectoderm
covering the terminal part of the phallus. Genital swellings fuse in the midline forming the scrotal
sacs for the testes.
Development of Male Urethra (Fig. 32.4)

Longitudinal groove appears on the caudal surface of the phallus. It is lined by the ectoderm and
called the primary urethral groove. The primary urethral groove is guarded by the genital folds.
The primary urethral groove reaches the base of the developing glans penis. Now the phallic part
of the urogenital sinus forms the urethral plate which extends up to the base of the developing
glans penis all along the roof of the primary urethral groove.
Solid urethral plate gets canalized forming the hollow tube. Bilaminar urogenital membrane
separates the newly formed endodermal tube from the primary urethral groove. The urogenital
membrane breaks forming the definitive urethral groove flanked by definitive urethral folds.
The urethral folds start fusing in the caudocranial direction, forming the spongy urethra up to
the base of glans where it opens forming the primary urethral meatus. Solid plate of ectoderm
develops on the under surface of the glans. It forms a groove and the groove gets converted into
Fig. 32.2: Development of external genitalia of male and female

the ectoderm lined canal. It opens at the tip

of the glans penis forming the permanent
external urethral meatus. Proximally the
newly formed ectodermal tube develops
communication with the spongy urethra.
External urethral meatus is the narrowest part
of the male urethra is lined with the stratified
squamous epithelium being ectodermal in
origin.
Prenatal Diagnosis of Sex

Ultrasound can help in the identification of
the sex before birth. At the 3 to 4 months of
the intrauterine life genital tubercles have
same rate of growth both in male and female.
Conclusion of the male or the female at this
stage can be erroneous as the clitoris can be
mistaken for the penis.
Fig. 32.3: Development of female external genitalia

Anomalies of Male External Genitalia

1. Micropenis: It is attributed to poor androgenic stimulation.
2. Absence of penis.
3. Phimosis: Opening of the prepuce is narrow and cannot be retracted.
4. Double penis.
5. Bifid penis.
6. Hypospadias (Figs 32. 5 and 32.6): The defect is on the under surface of the penis. The hypospadias
is classified as (1) Balanic—in this condition urethra opens on the undersurface of the glans
penis. It is due to nonclosure of the ectodermal groove. (2) Penile—nonunion of the anterior
part of the genital folds leads to penile type of hypospadias. The defect is on the undersurface
of the body of the penis. (3) Coronal type—the urethra opens at the undersurface of the glans
penis. (4) Complete perineal type—when the genital folds fail to unite even after the rupture
of the urogenital membrane, it leads to penile hypospadias, divided scrotum and undescended
testes. The external appearance resembles female external genitalia. It is known as male pseudo-
hermaphroditism.
7. Epispadias: When urethra opens on the dorsal surface of the penis it is known as epispadias. It
may be associated with ecopia vesicae (Figs 32.7 and 32.8).
8. Congenital stenosis of urethra.
9. Formation of urethral valves (Fig. 32.9).
Anomalies of Female External Genitalia

1. Clitoris can be absent, double or bifid.
2. In case of enlargement of clitoris it is known as hermaphroditism.
3. Labia minora are fused.
4. Urethral opening may be seen on the anterior vaginal wall which morphologically corresponds
to the male hypospadias.
Fig. 32.5: Sites of hypospadius Fig. 32.6: Hypospadius (Courtesy: Dr Ravi Deshmukh,
Kadasne’s Textbook Vol ll, Urologist, Nagpur, Maharashtra,
India)
Fig. 32.7: Ectopia vesicae. Note the absence of the umbilicus
Fig. 32.8: Ectopia vesicae (Courtesy: Dr Ravi Deshmukh, Fig. 32.9: Urethral valves
Urologist, Nagpur, Maharashtra, India)
Development of Testes (Fig. 32.10)

Testes are mesodermal in origin and develop from genital part of the urogenital ridges. It is believed
that the primordial egg cells develop in the wall of the yolk sac and migrate to developing gonads along
the dorsal mesentery. They probably have an inductive effect on the gonads.
Fig. 32.10: Development of testes
The epithelium covering the genital part of the urogenital ridge gets thickened to form the
genital ridge. The cells of the germinal epithelium proliferate forming the number of sex cords. As
they reach the deeper surface of the gonad they are called medullary cords. These medullary cords
get canalized and form the seminiferous tubules. The primordial germ cells are already present
amongst the crowded medullary cords. Interstitial cells of Leydig develop from the sex cords which
do not undergo canalization. The mesenchyme surrounding the testis forms a thick fibrous layer
which is called the tunica albugenia. The tunica albugenia separates the sex cords from the germinal
epithelium thus blocking its contribution to the formation of sex cords permanently.
It is to be noted that the interstitial cells of Leydig start producing androgenic hormones leading
to masculine changes in the mesonephric ducts and the external genitalia. Fetal testis produces anti-
Mullerian hormone (AMH) till the stage of puberty, the level of which falls later. Seminiferous tubules
do not develop lumen and are in the form of solid-plates. The spermatogonia develop only after puberty.
This anatomical fact has clinical importance. Testicular tumor called the seminoma is unknown before
puberty as the seminoma itself arises from the seminiferous tubules which do not develop before puberty.
Duct System of Testis (Fig. 32.11)

The testis develops in close association with the mesonephros. Although majority of the mesonephric
tubules degenerate, some of these near the testis persist and form duct system of the testis. Seminiferous
tubules have two parts, i.e. coiled and the straight. It is the straight part of the seminiferous tubules
that forms rete-testes. Rete-testes communicate with remaining mesonephric ductules forming
vasa-efferentia. Cephalic portion of the mesonephric duct gets coiled and forms epididymis and uncoiled
part forms the ductus deference. Seminal vesicles develop as the diverticuli from the lower ends of
the mesonephric ducts. Mesonephric duct between its opening into the prostatic part of the
urethra and the diverticulum of the seminal

vesicle forms the ejaculatory duct.
Descent of Testis (Figs 32.12 and 32.13)

Testis develops on the posterior abdominal wall
in the lumbar region, from the genital part of
the urogenital ridge. It is mesodermal in origin.
Lower pole of the testis is attached to the scrotal
skin through the band of mesenchyme known
as the gubernaculum. Testis reaches the iliac
fossa in the third month, at the deep ring in the 7th
month in the inguinal canal at the 8th month and
finally reaches scrotum by the end of 9th month.
Causes of Descent of Testis

1. Differential growth of the posterior abdominal
wall.
2. Formation of inguinal bursa: Note that the
inguinal bursa is formed before the entry
of the testis. The cavity of the inguinal bursa Fig. 32.11: Genital ducts in the male
forms the inguinal canal.
3. Gubernaculum: It is the mesenchymal band extending from the lower pole of the testis to the
bottom of scrotal skin. The gubernaculum being devoid of contractile tissue its role in pulling
the testis out from the abdominal cavity is disputed. Due to differential growth of the posterior
abdominal wall the gubernaculum gets shortened. The gubernaculum helps in dilating the
inguinal bursa and also lays down the path for the descend of the testis.
Fig. 32.12: Five sites of ectopic testis starting from letter ‘S’
Fig. 32.13: Coverings of the testis from outer side to inside are: 1. Skin and dartos
2. External spermatic fascia 3. Cremastric fascia 4. Internal spermatic fascia
4. Intra-abdominal pressure: It is responsible for pushing the testis out.

5. Squeezing action of the internal oblique muscle: As the rounded surface of the testis comes into
the contact of the arched fiber of the internal oblique muscle of the abdomen, it squeezes the
testis out.
6. Hormones secreted by the anterior lobe of hypophysis cerebri in the testis play part in the descent
of the testis.
Note: Testis descends into the scrotum, from its original position on the posterior abdominal wall
above. It carries the vas and the blood vessels along with it. Crossing of the vas deferens anterior to
the ureter near the urinary bladder can be explained from this developmental fact. During desend
the testis and vas deferens obtained their coverings from the anterior abdominal wall. The members
of the cover are arranged from inside-out.
1. Internal spermatic fascia comes from the fascia transversalis.
2. Cremastric fascia comes from the internal oblique muscle of abdomen.
3. External spermatic fascia is derived from the aponeurosis of the external oblique muscle of
abdomen.
Processus Vaginalis (Figs 32.14A to C)

Processus vaginalis is the diverticulum of the peritoneal cavity growing into the mesenchyme of
the gubernaculum, inguinal canal and the scrotum. Testis descents and invaginates the processus
vaginalis from behind. Once the descent of the testis is complete, the processus vaginalis gets
Fig. 32.14A: Types of hydrocele
Fig. 32.14B: Anomalies of the processus vaginalis
atrophied between the testis and the deep inguinal ring. The part of the processus vaginalis which
covers the testis is known as tunica vaginalis testis. As the testis enters the tunica vaginalis from
behind all the surfaces of the testis except its posterior border get covered by the peritoneal sac.
Fig. 32.14C: Three types of oblique inguinal hernia
Anomalies of the Testis (Fig. 32.14D)

1. Absence of testis
2. Duplicated testis
3. Fusion of testis
Fig. 32.14D: Types of testis

4. Undescended (Cryptorchitism means hidden testis): It cannot be brought to the scrotum manually
whereas the retractile testis can be brought to the scrotal floor.
5. Anteverted testis: In this condition epididymis lies infront.
6. Inverted testis: The testis lies upside down. Its upper pole points downwards and lower upwards.
7. Higher extension of the tunica vaginalis: It promotes tortion of the testis.
Anomalies of the Descent (Figs 32.15 and 32.16)

It is known as cryptorchitism. It involves nondescent or incomplete descent. Testis is found in the
iliac fossa, inguinal canal or at the superficial inguinal ring.
Clinical
Undescended testis carries following risks:
1. Undescended testis does not produce sperms due to its poor development and higher abdominal
temperature. In bilateral undescended testis the individual is sterile.
2. Susceptible to injury.
3. Likely to develop malignancy.
4. Atrophy.
Ectopic Testis
The sites of ectopic testis are as under (see Fig. 32.12)
1. In the lower part of the anterior abdominal wall it is called interstitial type. The testis lies external
to the aponeurosis of the external oblique muscle. It is common while other types of ectopic
testis are rare.
Fig. 32.15: Factors responsible for descent of testis

Fig. 32.16: Descent of the testis in various locations and the periods
2. Anteromedial aspect of the thigh.

3. Near the anterior superior iliac spine.
4. Root of penis.
5. In the perineum posterior to the scrotum.
6. Monorchism: One testis is intra-abdominal and the other follows the normal descent.
7. Crossed ectopia of testis: Testis goes to the opposite side.
If testis is found arrested at the deep ring, inguinal canal or at the superficial inguinal ring,
testicular hormone may be tried for promoting the descent. Testis can be surgically mobilized and
fixed to the scrotal floor (orchidopexy) in the event of failure of the hormonal therapy.
Tails of Lockwood
The lower pole of the testis has five fibrous bands. They are called the tails of Lockwood. Bands
have five sites of attachment distally and three proximally. The proximal attachments are:
1. Lower pole of the testis
2. Peritoneum
3. Mesonephric duct.
All the five distal attachments of the testis start from the letter ‘S’ as under:
1. S—Scrotum
2. S—Superficial perineal pouch
3. S—Symphysis pubis
4. S—Saphenous opening
5. S—Spine—anterior superior iliac spine.
The phenomenon of the ectopic testis can be explained with the help of hypothetical bands of
Lockwood. They carry the testis else where away from the expected path where the size and strength
of the tail matters.
Anomalies of the Duct System of Testis

1. No connection between seminiferous tubules and the vasa efferentia.
2. No connection between vas deferens and the epididymis.
3. Absence of vas deferens in part or complete.
Anomalies of the Processus Vaginalis

Patent processus—vaginalis can form congenital indirect inguinal hernia or the hydrocele
(see Fig. 32.14A).
Vestigial remnants in the testicular region.
1. Appendix of testis (hydatid of Morgagni).
2. Appendix of epididymis.
3. Superior and inferior aberrant ductules.
4. Paradidymis.
Clinical
Any of these can form the cyst.
Development of the Ovary (Figs 32.17 and 32.18)

Ovaries are mesodermal in origin and develop from the genital part of the urogenital ridge on the
posterior abdominal wall. However, primordial germ cells on the wall of the yolk sac migrate
along the dorsal mesentery and reach the gonads (ovaries).
Following is the sequence of the formation of the ovary:
1. Formation of genital ridges due to thickening of the coelomic epithelium.
2. Sex cord or the medullar cord grow from the germinal epithelium and enter the under-
lying mesoderm.
3. Primordial germ cells formed on the wall of the yolk sac migrate along the dorsal mesentery
and reach the ovary to form the oocyte.
4. Sex cord cells form clusters of cells around the primordial germ cells and form the primordial
follicle.
5. Medullary sex cords regress and are replaced by cortical cords which arise from the coelomic
epithelium. Cortical cords give rise to follicular cells.
6. Mesenchyme of the gonad forms interstitial cells.
7. Contribution of the germinal epithelium to the ovary continues due to nondevelopment of
the tunica albuginea.
Fig. 32.17: Migration of primordial germ cells to the genital ridge
Fig. 32.18: Development of ovary

Descent of the Ovary

Ovaries develop in the lumbar region and descend into the pelvis. Lower pole of the ovary is
attached to the labium majus through the gubernaculum. During descent middle part of the
gubernaculum gets attached to the body of the uterus. The part of the gubernaculum between the
ovary and the uterus is called the suspensory ligament of the ovary and the part of the gubernaculum
between the uterus and labium majus forms the round ligament of the uterus.
Succus Vaginalis in Females

Its extension in the inguinal canal is called the canal of Nuck. Normally the canal of Nuck gets
obliterated, however, in case of its patency it forms oblique potential sac of the inguinal hernia.
Anomalies of the Ovary

1. Absence of ovary on one or both the sides.
2. Duplication of ovary.
3. Ovary is found in the inguinal canal or labium majus.
4. Presence of thyroid and adrenal tissue in the ovaries.
5. Cell-rest capable of forming tissues like cartilage and bones can form teratoma of the ovary.
Derivatives of the Mesonephric Duct (Figs 32.19 and 32.20)

1. Ureteric bud develops into ureter, pelvis, calyces, the collecting tubules and the ducts.
2. Trigone of the urinary bladder.
Fig. 32.19: Derivatives of mesonephric duct

Fig. 32.20: Absorption of mesonephric ducts in the dorsal wall of the urogenital sinus and formation
of the trigone of the urinary bladder
3. Posterior wall of the prostatic part of the urethra above the openings of the ejaculatory ducts.
4. Vas deferens, epididymis, seminal vesicle and ejaculatory ducts.
5. Appendix of the epididymis arises from the mesonephric duct (appendix of the testis is derived from
the paramesonephric duct.)
Remnants of Mesonephric Tubules (Fig. 32.21)

1. Vasa efferentia.
2. Superior aberrant ductules: They are cranial to the vasa efferentia and are connected to the testis.
Fig. 32.21: Derivatives mesonephric tubules and the mesonephric duct

Fig. 32.22: The only remnants of the mesonephric duct in female are epoophoron, paroophoron and Gartner’s duct
3. Inferior aberrant ductules: They are caudal to the vasa-efferentia and connected to the epididymis.
4. Paradidymis lies between the testis and the epididymis having no connection with the testis or
the epididymis.
5. Epoophoron (Fig. 32.22): It forms the duct which runs along the side of the uterus, the caudal
portion of which gets embedded in the cervix. The duct is joined by the transverse tubule and
morphologically it corresponds to the vas deferens of the male. In female the duct of the
epoophoron may persist as the Gartner’s duct.
6. Paroophoron (Fig. 32.22): It consists of blind tubules which lie between the ovary and the uterus.
It is the remnant of paradidymis of the male.
Factors Responsible for Determination of the Sex

A gene SRY is present on the short arm of the Y chromosome. It produces testis determining factor.
Testis determining factor has an important role of converting the gonad into the testis. Testis
determining factor controls other genes too. They control formation of Sertoli cells from the sex
cords and Leydig cells from the mesenchymal cell of the gonadal ridge.
After formation of the testis, Leydig cells produce testosterone which helps in differentiation
of genital ducts and the external genitalia. At the age of eighteen weeks, fetal Leydig cells disappears
only to reappear at puberty.
Sertoli cells form Mullerian Inhibiting Substance (MIS) which causes regression of the
paramesonephric ducts. Androgen of the cells of Sertoli assist in conversion of the spermatogonia
to the spermatozoa.
Female has no Y chromosomes. Ovary is formed under the influence of WNT 4 gene. It is the
estrogen of the mother and the placenta which help the formation of external and internal genital
organs of the female.
True Hermaphrodite
The person has both testis and the ovary.
Pseudohermaphroditism
In this condition the person having external genitalia of one sex and the gonads of the opposite
sex. The person having testis is called male hermaphrodite and one having ovary is known as
female hermaphrodite.
Excessive amount of androgens formed by the fetal suprarenal gland causes pseudoherma-
phroditism (adrenogenital syndrome).
Greater Vestibular Glands

Greater vestibular glands also called the Bartholin’s glands lie in the superficial perineal pouch
caudal to the bulb of the vestibule. The ducts of the greater vestibular gland open in the vagina
below the hymen. Greater vestibular glands develop from the urogenital sinus and are
morphologically similar to the bulbourethral glands of the male.
Comparison between Bulbourethral and Greater Vestibular Glands
Bulbourethral Greater vestibular glands (Bartholin’s gland)

Sex Male Female
Situation Deep perineal pouch Superficial perineal pouch
Relation Are on either side of the membranous Are caudal to the bulb of the vestibule
part of urethra
Duct Opens into the bulb of the urethra Opens into the vigina below the hymen
Development From urogenital sinus From urogenital sinus
Note 1: Greater vestibular glands of the female are morphologically similary to the bulbourethral glands of the male.
Note 2: It is important to remember that the testes are responsible for induction and promotion of masculinity. At the same
time testes play an important role in suppression of the feminity. This clearly shows that the ovaries have no role in the
development of the primary sexual development.
Nervous System 297
Nervous System
33
Nervous System
Nervous system is ectodermal in origin.
Neural Tube
Ectoderm above the notochordal process gets thickened to form the neural plate. It is as a result of
induction by the notochord, the neural plate is formed. The groove appears on the surface of the
neural plate which deepens forming the deep groove with the neural folds. The neural folds grow
and begin to fuse in middle of the tube and proceeds cranially and caudally. The fusion converts
the neural groove into the neural tube. Formation of the neural tube is called neurulation. Non-
closure of the tube in the cranial and the caudal ends leaves the transient openings. The openings
are known as the anterior and the posterior neuropores. Anterior neuropore corresponds the lamina
terminalis of the adult. Neural tube gets detached from the surface and the gap between the neural
tube and the covering ectoderm is filled by the neural crest cells. Amniotic fluid enters the
neuropores and circulates within the neural tube. With the closure of the neuropores amniotic
fluid gets trapped inside the tube. Closure of the neuropores is marked by the beginning of the
circulation. It has been said that we have imbibed sea-water in our body. Just before the closure the
tube, it gets subdivided into two parts the cranial and the caudal. Cranial part enlarges to the brain
and the caudal tubular part forms the spinal cord. The neural canal becomes the ventricles of the
brain and the central canal of the spinal cord. Brain cavity gives rise three cavities. Cranio-caudally
and are labelled as:
1. Prosencephalon
2. Mesencephalon
3. Rhombencephalon
Prosencephalon further gets subdivided into the telencephalon and the diencephalon.
Telencephalon forms the cerebral vesicles. Diencephalon forms the cavity of the thalamic region.
Rhombencephalon gets subdivided into the cranial and the caudal parts. The cranial part is called
as the metencephalon and the caudal the myelencephaln.
Initially, the prosencephalon, mesenc-

ephalon and rhombencephalon are in one
horizontal plane.The linear arrangement
undergoes radical changes due to the formation
of four flexures. The flexures are as under (Fig.
33.1).
1. Cervical flexure
2. Mesencephalic flexure
3. Pontine flexure
4. Telencephalic flexure
Cervical flexure: Develops at the meeting point
of the rhombencephalon and the spinal cord.
Mesencephalic flexure: Appears at the midbrain.
Pontine flexure: Develops in the middle of the
rhombencephalon subdividing it into the cranial
metancephalon and the caudal mylencephalon.
Telencephalic flexure: Appears between the
telencephalon and the diencephalons.
Cavities of the Brain

1. Lateral ventricles: Telencephalon forms the
lateral ventricles.
Fig. 33.2A: Early development of brain
2. IIIrd ventricle: Cavity of the diencephalon

and the central part of the telencephalon
form cavity of the third ventricle (Figs 33.2A
and B).
3. Aqueduct is formed from the cavity of the
mesencephalon.
4. Fourth ventricle is formed from the cavity
of the rhombencephalon.
The Neural Crest

Neural crest cells appear at the junction of the
neural plate and the adjoining ectoderm. When
Fig. 33.1: Formation of flexures of brain the neural tube gets closed, islands of neural
Nervous System 299
Fig. 33.2B: Development of choroidal fissure and formation of the lateral ventricle, its body, anterior horn, posterior
horn and the inferior horn. Note the shape of the choroidal fissure
crest cells lie dorsolateral to the neural

tube. Unlike the property of the
neural tissue of the neural tube, i.e.
like joins the like, the neural crest cells
loose this character and get freed to
migrate to the distant parts of the
body, e.g. skull, face, thyroid, dorsal
root ganglion, skin and the suprarenal
etc. Let us list the structures derived
from the neural crest (Fig. 33.3).
1. Neurons of the dorsal root
ganglion.
2. Neurons of the sensory ganglion
5, 7, 8, 9, 10 cranial nerves.
3. Neurons and satellite of cell
sympathetic ganglion.
Fig. 33.3: Some derivatives of the neural crest.
4. The Schwann cell
5. Medulla of the suprarenal
6. Melanoblast of the skin
7. Neurons with satellite cells of the parasympathetic ganglia like:
a. Ciliary
b. Submandibular
c. Sphenopalatine and the
d. Otic ganglions
8. Parasympathetic ganglia of GI tract and ganglia of pelvic visceral

9. Parafollicular ‘C’ cells of the thyroid gland.
10. Piamater and arachnoid mater.
11. Dental papilla, odontoblasts and dentine.
12. Bones of the face and vault of the skull.
13. Connective tissue of the thyroid, parathyroid, thymus and the salivary glands.
Note: The parafollicular cells ‘C’ of the thyroid are in the list of probables.
Many clinical conditions are enlisted as a result of neural crest disturbance.
1. Septal defects of the heart
2. Cleft lip
3. Cleft palate
4. Neurofibroma
Spinal Cord (Figs 33.4 and 33.5)

Caudal cylindrical portion of the neural tube forms the spinal cord. Cavity of the neural tube is
almost like a vertical slit as seen in the cross section. Due to the formation vertical slit, lateral walls
get thickened and the floor and roof become thin. Wall of the tube gets subdivided into three
layers, e.g. ependymal, mantle and the marginal layers, from inside out.
Rapid growth of the mantle layer in the ventral part, makes ventral part thicker which reduces
the lumen of the tube ventrally. The line of demarcation appears in the lateral wall of the tube. It is
known as the sulcus limitans.
Part of the lateral wall of the
neural tube ventral to the
sulcus limitans is called the
basal lamina and the part
dorsal to the sulcus is
labelled as the alar. The alar
lamina grows in size,
obliterating the dorsal part
of the cavity of the neural
tube, forming the median
septum. The ventral part of
the cavity forms the central
canal of the spinal cord.
Basal lamina enlarges
anteriorly forming ventral
projections. It creates the
space between two anterior
projections of the basal
laminae, called the anterior
median fissure. The nerve Fig. 33.4: Development of spinal cord
Nervous System 301
cells in the mantle layer of the basal lamina

form the neurons of the anterior gray
column. The axons of these nerve cells leave
the spinal cord ventrolaterally and form the
anterior or the motor nerve roots of the
spinal nerves (Figs 33.4 and 33.5).
Neurons of the Posterior Gray Column

They are formed from the nerve cells which
develop in the mantle layer of the alar Fig. 33.5: Formation of neuroblast
lamina. The neurons of the posterior gray
column are sensory. They form the sensory neurons of the second order. The axons of the neurons
of the posterior gray column go upward in the marginal layer forming the ascending tracts of the
spinal cord. Interneurons are formed from the neurons of the posterior gray column.
Neural crest cells collect near the dorsilateral aspect of the neural tube. The neural crest cells
gives rise to the dorsal root ganglion or the spinal ganglion. The nerve cells of the ganglion being
unipolar, their axons divide into peripheral and the central processes. Central processes go towards
the dorsilateral parts of the spinal cord synap with the neurons of the posterior gray column (Fig. 33.6).
Fig. 33.6: Development of spinal cord in relation to the growth of the vertebral column
Peripheral processes of the unipolar cells of the dorsal root ganglion form the sensory part of the
spinal nerves.
The axons of the neurons of the posterior grey column make an entry into the marginal layer,
go upward toward the brain forming the ascending tracts. Similarly axons of the neuron of the
developing brain grow down, enter the marginal layer of the spinal cord thus forming the
descending tracts of the spinal cord. The gray mater of the spinal cord becomes ‘H’ shaped. It
divide the white mater of the spinal cord into anterior, posterior and the lateral columns
(Fig. 33.6).
During early stage of development the lengths of the spinal cord and the vertebral column are
equal. Due to the rapid growth of the vertebral column, the length of the spinal cord falls short. As
a result the lower end of the spinal cord is at the 3rd lumbar vertebra at birth.
Further recession of the spinal cord leads to the upward shift of the spinal cord. As a result in
adult spinal cord ends at the lower border the 1st lumbar vertebra.
Due to differential growth of the cord and the vertebral column intervertebral formina do not
remain at the level of the spinal nerves. The spinal nerves are forced to go down oblique.
Naturally, the obliquity is minimum in the cervical region and maximum in the sacral and
coccygeal regions. This explains the formation of cauda equina at the tail of the spinal cord around
the filum terminale.
In spina bifida occulta due to the upward pull of the spinal cord, the nerves are stretched
causing paresis or paralysis of the lower limbs. The nerves are invariably adherent to the dural
sheath of the meningocele. During surgery the nervous tissue is carefully separated from the dura.
Now we go to the details of the histogenesis of the neural tube.
Histogenesis of the Neural

Tube
The cavity of the neural tube
is lined by the tall columnar
cells. Due to changed
position of the nuclei of the
cells, the columnar layer
becomes psedostratified.
Proliferation of the cells
makes the wall of the neural
tube thicker and the cell layer
multilayered. As a result 3
zones are formed in the wall
of the neural tube from inside
out (Fig. 33.7).
Fig. 33.7: Histogenesis of neural tube

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1. Ependymal layer: It is also called germinal layer.

2. Mantle layer: Has neurons and spongioblasts.
3. Marginal layer: Forms white mater of the spinal cord and contains axonal processes of the
neuroblasts and the neuroglia. It looks white as a result of myelination. Ependymal cell migrates
to the mantle layer forming:
a. Apolar neuroblast
b. Bipolar neuroblast
c. Multipolar neuroblast
Apolar neuroblast comes from the ependymal zone. They withdraw the processes and becomes
apolar neuroblasts. They enter the mantle zone and form bipolar neuroblasts. After withdrawal of
one process it becomes unipolar neuroblast. Single process forming the axon and multiple small
protoplasmic processes arising from the cell body of the neuroblast form the multipolar neuroblast.
Spongioblasts form astrocytoblast and oligodentroblasts. Astrocytoblast forms the astrocyte
and the oligodendroblasts forms the oligodendrocyte. Processes of the astrocytes develop attachment
with the endothelium of the nearby capillaries forming the perivascular feet, which take nutrition
to the neurones across the blood brain barrier. Ependymal cells which withdra from the membranes
migrate to the mantle and the marginal layers as oligodendroblast which form oligodendrocyte.
They lay down myelin sheath for the nerves and the tracts in the central nervous system. Oligodendrocyte
form the linear rows by the side of the nerves and the tract in the marginal zone and form myelin
sheath. The primitive spinal ganglion form dorsal and ventral masses. Dorsal mass gives rise to
dorsal root ganglia of the spinal nerves, in addition to the sensory ganglia of the 5th, 7th, 9th and
the 10th cranial nerves. Dorsal mass form three types of cells, e.g. neuroblast, spongioblast and the
pleuripotent cells.
Initially, the neuroblast is oval which becomes bipolar. It has two processes the central and the
peripheral. Central process enters the neural tube forming the sensory root. Soon the processes of
the bipolar cells come closure and fuse to form a single process and divides like a letter T. These T
shaped pseudounipolar cells are present in the dorsal root ganglia of all the spinal nerves. However,
the retina and the vestibule-cochlear nerves retain the bipolar neurones. Neural crest cells also give rise
to skeletal elements of the branchial arches, odontoblasts and the parafollicular or ‘C’ cells of thyroid.
Spongioblasts form capsular cells which cover for the cell bodies of the dorsal root ganglion cells.
Schwann cells form myelin sheath and the neurilema, Schwann cell get arranged along axon forming the
cover. Axon gets suspended by mesoaxon formed by the outer cell membrane of the Schwann cell.
As a result of rotation of the Schwann cells around the axon the myelin sheath is formed. Myelin
sheath consists of alternate layers of protein and lipids. Cytoplasm and the nucleus of the Schwann
are pushed to the periphery.
Due to lack of rotation although the Schwann cells cover the unmyelinated peripheral fibers, myelin is
not led down. Hence, unmyelinated peripheral fibers are covered only with the neurolemma.
Pleuripotent cells of the dorsal mass form melanoblasts, odontoblasts, cartilage cells and the pia and
the arachnoid (leptomeninges). The dura mater comes from the mesenchyme around.
The ventral mass forms the sympathochromaffin organs, which form two types of cells, the small and the
large. The small cells are called sympathoblast which form sympathetic chain, the paired chain lying by the
side of the vertebral column. Other ganglion cells migrate to form parasympathetic ganglion cells of the
ciliary, pterygopalatine, submandibular and the otic ganglia. The large cells form chromaffin cells secreting
noradrenaline. Majority of the cells from the medulla of the suprarenal secret mostly adrenaline.
Due to the fact that adrenal cortex near the medulla converts noradrenalin into adrenaline by
methylation of the primary amines. Chromaffin cells placed within the sympathetic ganglian are
called paraganglia.
The cells which migrate along the preaortic plexus form para-aortic bodies. Some cells migrate
and reside on the surface of the epithelium of the mucous membrane of the gastrointestinal and
respiratory tracts are called enterochromaffin cells. They produce regional peptide hormones and
are called as APUD cells (Amine Precursor Uptake Decarboxylation cells).
Remaining ependymal cells form the lining of the ventricles of the brain and the lining of the
central canal of the spinal cord.
Medulla Oblongata
It is derived from the myencephalon, the caudal part of the rhombencephalon. Sulcus limitans
appears on the lateral wall of the medulla separating the alar and the basal laminae. Original thin
roof of the medulla gets stretched due to formation of the pontine flexure.
Note: Take 4 inch piece of a rubber tube. Make a vertical slit and bend the tube.
This converts the linear slit into the rhomboid shaped aperture.
I have seen Prof GJ Romanes of Medical School Edinburgh, UK bringing the rubber tube for
demonstration in the pocket of his long white coat.
The cells form the caudal part of the bulbo-pontine extension form the olivary nuclei. Rest of
the alar lamina forms the sensory nuclei of the cranial nerves of the medulla. Basal lamina of the
medulla gives rise to the motor nuclei of the nerves of the medulla.
The arrangement of the nerve cells of the alar and the basal laminae is based on their functional
role. However, the nuclei migrate from the floor of the 4th ventricle. Somatic efferent column
migrates to form the 3rd and the 4th nuclei in the midbrain and the nucleus of the 6th nerve in the
pons, while the hypoglossal nucleus is formed in the middle.
Nucleus gracilis and the nucleus cuneatus are derived from the general somatic afferent column.
White mater of the medulla is mostly extraneous (External in origin) as it is formed by the ascending
and descending tracts.
Pons
Pons has its origin from the ventral part of the metencephalon. However, the alar lamina of
myelencephalon do contribute its formation which comes as the cranial part of the bulbopontine
extension. The pontine nuclei are derived from the bulbopontine extension. Cells in the pontine
nuclei send their axons, which go transversely forming the middle cerebellar peduncles. Cells of the
lateral part of the alar lamina migrate anteriorly to the marginal layer ventrolateral to the basal
plate lamina. The cells are from the caudal part of the bulbopontine extension (Fig. 33.8).
Lateral part of the alar lamina forms the rhombic lip. Cerebellum develops from the rhombic lip.
Sensory cranial nuclei of pons develop from the rest of the alar lamina. Motor cranial nucleus of
the pons develop from the basal lamina.
Nervous System 305
Bulbopontine extension
forms the pontine nuclei in the
pons while caudally it forms
olivary nuclei in the medulla.
Ventral part of the pons
itself is formed by:
1. Pontine nuclei, the axons,
which grow transversly
to become the middle
cerebellar peduncle.
2. Carticobulbar and cortico-
spinal fibres descend from
the cerebral cortex pass
through the area, on their
way to the medulla and
spinal cord. Fig. 33.8: Section through lower part of pons
The Midbrain
Mesencephalon forms the midbrain. Cavity of the mesencephalon becomes the aqueduct of Sylvius.
Fig. 33.9: Transverse section of midbrain at the level of superior colliculus

Fig. 33.10: Transverse section of midbrain at the level of inferior colliculus
• Sulcus limitations demarcates the mantle layer into the alar and the basal laminae.
• Three nuclei are derived from the basal lamina, i.e.
– Oculomotor nucleus
– Trochlear nerve nucleus
– Edinger West-phal nucleus
• Alar lamina forms
• Red nucleus
• Sustantia nigra
• Cells of the corpora quadrigemina (Figs 33.9 and 33.10)
Marginal layer of the midbrain is occupied by fibers going down from the cerebral cortex, they
are corticospinal.
• Corticobulbar
• Corticopontine.
The ventrally projecting parts of the midbrain form the cerebral peduncles or the basis pedunculus
or the crus cerebri of the midbrain.
Cerebellum 307
Cerebe
Cerebe llum
bellum
34
Dorsolateral part of the alar lamina of the metencephalon forms the rhombic lips which forms the
cerebellum. Two primordia of the cerebellum grows medially in the roof plate of the metencephalon
and fuses in the midline. They form two lateral lobes and the vermis in the middle. This forms
dumbbell shaped structure on the roof plate of the fourth ventricle. Due to rapid growth of
cerebellum, fissures appear on the surface of the developing cerebellum (Figs 34.1 and 34.2).
During development, the cerebellum presents two parts, i.e. intraventricular and the extra-
ventricular. Intraventricular part is larger than the extraventricular part. Intraventricular part
projects into the cavity of the fourth ventricle. As the development of the cerebellum proceeds, the
extraventricular part grows faster on the roof plate presenting the whole of the cerebellum. Cells
of the mantle layer enter the marginal layer and form the cerebellar cortex. The neuroblasts of the
mantle layer form four nuclei of the cerebellum. The nuclei are:
Fig. 34.1: Development of cerebellum in the roof of the fourth ventricle

Fig. 34.2: Formation of pontine flexure, rhombic lip, hypophysis cerebri and superior and inferior colliculi
1. Dentate
2. Emboliformis
3. Globosus
4. Fastigium
Formation of Peduncles
1. Superior cerebellar peduncle is formed by the axons of the dentate nucleus.
2. Middle cerebellar peduncle is formed by the transversely placed axons of the cells of the
pontine nuclei.
3. Inferior cerebellar peduncle is formed by the fiber entering the cerebellum from spinal cord
and the medulla.
The flocculonodular lobe is called the archicerebellum. It has connections with the vestibular
nuclei which control posture and the equilibrium. Archicerebellum is the oldest part of the cerebellum
which is present in the aquatic vertebrates.
V-shaped fissure-prima appears on the dorsal aspect of the cerebellum. It separates the anterior
lobe from the rest of the cerebellum. The anterior lobe, uvula with the pyramid forms the paleo-
cerebellum. It is connected to the spinal cord and thereby controls the tone and posture of the
muscles of the limb. When the cerebellum develops connections with the cerebral cortex, it is able
to coordinate voluntary and skilled movements. This forms the neocerebellum.
Note: The process of differentiation of the basket and stellate cells continues till 1 to 2 year of post-
natal life.
In the event of administration of DNA blocking, drugs for the treatment of viral infections in
infants of 1 to 2 years of age can damage the cerebellar neurons.
Nucleus of the 4th nerve and the mesencephalic nucleus of the 5th nerve develop from the
isthmus rhombencephali which migrate cranially to the midbrain.
Cerebellum 309
Formation of Cerebral Hemisphere (Figs 34.3 to 34.5)

The telencephalic vesicles give rise to the cerebral cortex and the corpus striatum. The diencephalon
gives origin to the thalamus, hypothalamus and the associated structures.
Smaller telencephalic vesicles of both the sides start growing faster in three directions, e.g.
forward, backward and upward. The telencephalon’s fast growth hides the diencephalon from the
lateral aspect and gets fused with it. As a result, the cerebral cortex and the corpus striatum is
placed lateral to the thalamus. Due to growth of the telencephalic vesicles of both the sides, they
come closure. The meeting line of the telencephalic vesicles is in the front, behind and above the
diencephalon.
Fig. 34.3: Transverse section of midbrain at the level of inferior colliculus
Lateral ventricles are derived from the telencephalic vesicles and the 3rd ventricle develops
from the cavity of the diencephalon.
Initial spherical telencephalic vesicles grow forward and backward, and acquire shape of an
egg. As the posterior end of the vesicle grows downwards and forwards ending in the formation
of the temporal lobe and the inferior horn of the lateral ventricle within. Backward growth gives
rise to the occipital lobe and the posterior horn of the lateral ventricle.
Medial walls of telencephalic vesicle come nearer. This leads to the formation of a grooved
channel, in the midline. The mesenchyme in the grooved channel forms the falx cerebri. The lateral
Fig. 34.4: Development of cerebral hemisphere. Note how the overgrowth of the cerebral
hemisphere hides the diencephalon
Fig. 34.5: Three developing brain ventricles (Anterior view)

Cerebellum 311
walls of the grooved channel are formed the medial surfaces of the telencephalic vesicles. Floor of
the groove becomes the roof of the 3rd ventricle.
The gap between the floor of the groove and the medial wall of the telencephalic vesicles
forms the choroid fissure. Pia mater invaginates in the fissure which is called the telachoroidea.
With the invasion of capillaries, the telachoroidea becomes the choroid plexus. Through the choroid
fissure of the the telachoroidea enters the lateral and the 3rd ventricles. With the formation of the
temporal pole, inferior horn of the lateral ventricles grows within it. With these changes the choroids
fissure becomes ‘C’ shaped (Fig. 34.6).
Fig. 34.6: Formation of corpus callosum and the choroid plexus
Development of Thalamus and the Hypothalamus

The thalamus and the hypothalamus are derived from the diencephalon. Lateral wall of the
diencephalon becomes thick. It shows appearance of two grooves namely the epithalamic sulcus
above and hypothalamic sulcus below. The part between the epithalamic and the hypothalamic
sulci is called the thalamus. Part above the thalamus is called the epithalamus and the part below
it is called the hypothalamus. Epithalamus forms the pineal body and habenular nuclei.
Nuclei of the thalamus and the hypothalamus are formed due to multiplication of the cells of
the mantle layer of the lateral wall of the diencephalon (Fig. 34.7).
Development of Corpus Striatum (Figs 34.8 and 34.9)

The corpus striatum develops from the thick basal part of the telencephalic vesicle. Initially, the
telencephalic vesicle is subdivided into upper thin and the lower thick parts. Cells of the mantle
layer of the thick part migrate to the adjoining marginal layer and form the cerebral cortex.
Fig. 34.7: Formation of thalamus and hypothalamus. Please note that the epithalamic and
hypothalamic sulci mark three parts of diencephalon, e.g. thalamus, epithalamus and hypothalamus
Rest of the cells of the mantle layer give rise to the corpus striatum. The medial and the lateral
parts of the corpus striatum get divided by the axons of the cells of the cerebral cortex. The axons
bisect the corpus striatum into the superficial and the deep parts. The deep part becomes the caudate
nucleus while the superficial part forms the lentiform nucleus. The lentiform nucleus gets
subdivided to the putamen and globus pallidus. Out of these, globus pallidus is medial and the
putamen is lateral.
Fig. 34.8: Formation of caudate nucleus from the deep part of the corpus striatum and formation of
lentiform nucleus from the superficial part of the corpus striatum
Cerebellum 313
Fig. 34.9: Formation of caudate nucleus from deep part of corpus striatum and formation of lentiform nucleus from
superficial part of corpus striatum
Cerebral Cortex
Cells from the mantle layer migrate into adjoining marginal layer and form the cereberal cortex.
As a result of repeated divisions, several layers are formed. Growth of the covering cortex being
faster than the overall growth of cerebral hemisphere, the cortical layer undergoes folding forming
the sulci and the gyri. It is obviously due to the space crunch. The formation of the sulci and the
gyri helps in accommodating the larger cortical area in the relatively smaller zone. Due to the slow
growth at the insular area, the insula gets buried under the overgrowing operculi of the cortex on
the superolateral surface of the cerebrum. The cortex constitutes (1) Hippocampal cortex (2) Neocortex
3) Piriform cortex. Most of the cerebral cortex of the superolateral, medial and the interior surfaces
of cerebrum is derived from the neocortex (Fig. 34.10).
Fig. 34.10: Development of cerebral cortex. Part of the limbic system develops frofm piriform cortex (Highly diagrammatic)
As the hippocampal cortex has close relation with the choroidal fissure, the hippocampal cortex
follows the ‘C’ shaped choroidal tissue and acquires ring shape. It occurs due to the formation of
the inferior horn of the lateral ventricle. As a result of formation of the corpus callosum, small part
of the hippocampal formation gets isolated from the choroidal fissure. It forms the indusium
griseum. Hippocampus and the dentate gyrus are developed from the lower part of the hippocampal
cortex. With expansion of the neocortex, the hippocampus and the dentate gyrus are pushed deep
into the inferior horn of the lateral ventricle. White matter of cerebrum: White matter has the major
contribution in forming the bulk of the cerebrum. The contribution comes from the following:
Commissural Fibers (Fig. 34.11)

• Corpus callosum
• Anterior commissure
• Posterior commissure
• Habelunar commissure
Association Fibers
• Long association fiber
• Short association fiber
• Projection fibers
• Cortical cells (Pyramidal cell of motor cortex), send their axons to the lower centers through
the cerebrum.
Interconnecting Axons
Thalamus, hypothalamus and the basal ganglia are interconnected with each other and also with
the cerebral cortex.
Asending Fibers
Brainstem and the spinal cord axons go to the cerebral hemisphere.
Fig. 34.11: Development of interventricular foramen, rudimentary corpus callosum, septum pellucidum and optic chiasma
Cerebellum 315
Cerebral Commissures
Lamina terminalis closes the cranial end of the prosencephalon. With the development of the
telencephalic vesicles, lamina terminalis forms the anterior wall of the third ventricle. Lamina
terminalis acts as the bridge between the two hemispheres. It becomes thick and is known as the
commissural plate. Nerve fibers from one cerebral hemisphere go to other through the commissural
plate.
Following Commissures Develop Later

• Anterior commissure
• Corpus callosum (Fig. 34.11)
• Hippocampal commissure
• Optic chiasma
• Habelunar chiasma
Corpus callosum due to extensive growth of the cerebral hemisphere, grows in size.
Anomalies of the Brain and the Spinal Cord

1. Posterior rachischisis – Whole neural tube remains open.
2. Anencephaly – Nonclosure of the neural tube in region of the brain.
3. Spina bifida – Nonclosure of the vertebral canal.
4. Cranium bifidum – Nonclosure of the cranium (Fig. 34.12).
Note: When neural tissue lies out side vertebral canal or the cranial cavity, it is called myelocele
and encephalocele respectively.
Variation of Spina Bifida

Meningomyelocele: Outward bulging contains neural tissue and is covered with meninges and the
skin.
Fig. 34.12: Anomalies of neural tube

Meningocele (Fig. 34.13): Bulging

is formed by the membranes
containing CSF with no neural
tissue.
Arnold-Chiari Deformity
In the presence of a
meningomyelocele, the medulla
oblongata and the inferior vermis
of the cerebellum sags downward
and enters the foramen magnum,
obstructing the flow of
cerebrospinal fluid causing
hydrocephalus.
Note: Please remember, that the
medulla oblongata passes
through the foramen magnum. It Fig. 34.13: Occipital meningocele
(Courtesy: Dr Pavitra Patnaik, Neurosurgeon, Nagpur, Maharashtra, India)
is the low intraspinal pressure
due to the meningomyelocele which makes the medulla and the vermis sag down into the foramen
magnum.
Hydrocephalus (Figs 34.14 and 34.15): It is an abnormal collection of cerebrospinal fluid in the
ventricular system. It occurs due to overproduction of the cerebrospinal fluid or the obstruction to
its flow. Ventricles dilate, head becomes large and due to pressure, nerve tissue undergoes
degenarative changes. Large head creates difficulty in labor.
Fig. 34.14: Hydrocephalus Fig. 34.15: Hydrocephalus. Dilated lateral ventricle

(Courtesy: Lt Dr Joharapurkar, Ex Director, (Courtesy: Lt Dr Joharapurkar, Ex Director,
Postgraduate studies, JNMC, Sawangi) Postgraduate studies, JNMC, Sawangi)
Cerebellum 317
Hydrocephalus is clinically divisible into obstructive or noncommunicating type. In obstructive

type, the whole of the ventricular system is enlarged. When the hydrocephalus results, due to
obliteration of the subarachnoid cistern or malformation of the arachnoid villi is called non-
obstructive or communicating type of hydrocephalus.
Hydromyelia: It is the condition of spinal cord similar to hydrocephalus.
Syringocele: Dilation of the central canal of the spinal cord.
Syringomyelia: Abnormal cavities develop around the central canal of the spinal cord destroying
the nerve tissue around. As the spinothalamic tracts cross infront of the central canal, it leads to
loss of bilateral pain sensation below the site of the lesion.
Dandy Walker Syndrome

Due to the blockage of median aperture in the roof (Foramen of Magendie) and the lateral apertures
(Foramina of Luschka), the cavity of the fourth ventricle enlarges. The enlargement of the brain is
limited to the posterior cranial fossa. Stenosis of aqueduct of sylvius causes hydrocephalus as a
result of enlargement of the third ventricle.
Indulgence of the mother in alcoholic abuse has proved to be common cause of mental
retardation.
Hydranencephaly
In this condition, cerebral hemispheres are absent and they present in the form of membranous
bag. Due to accumulation of the CSF, the head grows larger. Further enlargement of the head can
be prevented by making the ventriculoperitoneal shunt.
1. Microcephaly
2. Macrocephaly
3. Poor development of the cerebral cortex may lead to low intelligence
4. Some parts of the nervous system fail to develop, they are three ‘C’s
5. Corpus callosum: Failure of development of corpus callosum may remain asymptomatic.
However, epileptic attacks and mental retardation are associated with the absence or
malformations as below:
• Corpus callosum
• Cord (spinal cord)
• Cerebellum
Autonomic Nervous System

Nervous system is divided into somatic and the autonomic. Autonomic nervous system is further
divided into the sympathetic and the parasympathetic. Sympathatic system is thoracolumbar and
the parasympathetic system is craniosacral (Figs 34.16 to 34.18).
Sympathetic pathway has two neurons, e.g.
1. Preganglionic
2. Postganglionic
Fig. 34.16: Development of preganglionic and postganglionic sympathetic neurons
Sympathetic preganlionic neurons develop in the thoracolumbar region extending from T1 to L1.
They arise from the cells of the lateral horn of the spinal cord. Axons of the neurons are myelinated
and leave the cord to enter the ventral nerve root of the spinal nerve. They leave the spinal nerve
and grow in the direction of the postganglionic sympathetic neurons. Postganglionic neurons reach
the viscera and form the visceral sympathetic ganglia. Preganglionic fibers for the viscera do not
relay in the sympathetic ganglia and directly go to the visceral ganglia. They innervate the blood
vessels, sweat glands and the hair follicles. It has already been mentioned, i.e. postganglionic
neurons arise from the neural crest.
Parasympathetic Neurons
Edinger-Westphal salivary, lacrimatory nuclei and the dorsal nucleus of the vagus arise from general
visceral efferent column. Preganglionic parasympathetic fibers arising from the Edinger-Westphal
nucleus join the oculomotor nerve and enter the ciliary ganglion. Preganglionic fibers arising from
the superior salivatory and lacrimal nuclei join the facial nerve and go to the pterygopalatine and
submandibular ganglia.
Fibers arising from the inferior salivary nucleus join the glossopharyngeal nerve and take part
in the formation of tymphanic plexus. They leaves tymphanic plexus as the lesser superficial petrosal
nerve and enters the otic ganglion and go to the parotid gland through the auriculo-temporal
nerve. The secretomotor fibers for the subminadibular salivary gland come from the superior
Cerebellum 319
Fig. 34.17: Cranial outflow of preganglionic and postganglionic parasympathetic neurons
Fig. 34.18: Sacral outflow of preganglionic and postganglionic parasympathetic neurons
salivary nucleus. The fibers travel in the 7th nerve and through the chordae tympani, they leave
the facial nerve to join the lingual nerve at an acute angle. The fibers are relayed in the
submandibular salivary ganglion and the post ganglionic fibers go to the sumbandibular and the
sublingual salivary glands. Preganglion parasympathetic fibers which terminate in the ganglia
situated in the walls of the viscera are from the dorsal nucleus of the vagus.
Sacral Parasympathetic Outflow

The mantle layer of the sacral part of the neural tube is the source of formation of the preganglionic
neurons. Their axons form the preganglionic parasympathetic fibers which terminate after
synapsing with the postganglionic neurons in walls of the pelvic viscera and the hindgut.
Ear
35
Human ear has three parts (1) External (2) Middle (3) Internal. They are arranged from lateral to
the medial side. External ear is closed medially by the tympanic membrane (Fig. 35.1).
The external ear has two parts, e.g. auricle and the external acoustic meatus. The middle ear
cavity is like a room having four walls roof and the floor. It contains air and 3 ossicles, e.g. malleus,
incus and the stapes. Foot of the stapes transfers vibrations to the fenestra vestibuli. The internal
ear is made of bony and the membrane labyrinths. The bony labyrinth contains perilabyrinth which
surrounds the membrane labyrinth. The membranous labyrinth contains endolymph. The
perilymph is in communication with sub-arachnoid space through the cochlear duct.
The membranous labyrinth consists of following structures placed anteroposterior as below:
• Cochlear duct
• Saccule
• Utricle
• Semicircular canals.
At birth, the position of the tympanic membrane is horizontal. (It looks down). The internal
ear, tympanic cavity, the middle ear and the ossicles attend their adult size at the time of birth.
Development of the Internal Ear

Ectodermal thickenings appear on either side of the rhombencephalon. They are known as the otic
placodes. On each placode, the pit appears which is called the otic pit. Otic pit separates from the
Fig. 35.1: Formation of otic vesicle

Ear 321
surface ectoderm and forms the otic vesicles. The wall of the otocyst gives neuroepithelial cells
which get mixedup with the neural crest cells. They form the bipolar cells of the vestibulochoclear
ganglia. Peripheral process of the biopolar cells carry sensation of equilibrium from the seccule,
utricle and semicircular canals through the vestibular nerve. The hearing is carried through the
auditory nerve. Otocyst forms the saccule and the ducts endolymphaticus. Otocyst shows two
parts marked along the line running from the opening of the ductus endolymphaticus. They are
the utricle and the saccule. Semicircular ducts develop from the utricle. One end of the duct is
dilated which is known as the ampullary end. It has sensitive hair cells of crestae ampullae. The
macula/the gravity receptor develop from the utricle and the saccule. Chochlear duct arises from
the saccule in the form of a spiral duct. Bony labyrinth forms the socket for the saccule and the
utricle. Mesenchyme of the bony labyrinth forms two perilymphatic spaces near the cochlear duct,
e.g. scala vestibuli above and the scala tympani below. Out of these, the scala vestibuli is separated
from the chochlear duct by the vestibular membrane (Reisser’s membrane) and the scala tympani
is separated from the chochlear duct by the basilar membrane. The outer wall of the chochlear
duct is connected to the bony chochlear canal by the spiral ligaments. The chochlear duct has
communication with the scala vestibuli and the scala tympani at its apex through an opening. The
opening is called the helicotrema (Figs 35.2 to 35.6).
Two ridges develop on the basilar membrane. They are known as the inner and the outer
ridges. Cells of the outer ridge form Two rows of inner cells 3 to 4 rows of outer hair cells.
Cells of the inner ridge form the spiral limbus which gives attachment to the membrana tectoria.
When the membrana tectoria touches the inner and outer cells, it creates sound waves in the form
of vibrations which are carried to the brain through the auditory nerve. The inner and the outer
ridges constitute the organ of Corti.
Middle Ear
It develops from the tubotympanic recess of the first pharyngeal pouch alongwith the mastoid
antrum, mastoid air cells and the inner lining of the tympanic membrane. The tubotympanic recess
is formed by the 1st pharyngeal pouch with small contribution from the second. External acoustic
meatus and the external auditory canal are formed by the 1st pharyngeal cleft. Medial part of the
tubotympanic recess gets narrowed and forms the auditory tube. The malleus and the incus develop
from the dorsal end of the cartilaginous bar of the 1st arch (Meckel’s cartilage) while the stapes
develops from the second arch cartilage known as (Reicher’s cartilage). The muscle tensor tympani
Fig. 35.2: Development of membranous labyrinth

Fig. 35.3: Fully formed internal ear
Fig. 35.4: Development of internal ear
Fig. 35.5: Development of internal ear

Ear 323
Fig. 35.6: Perilymph communicates with subarachnoid space through the cochlear duct
develops from the 1st arch and is supplied by the mandibular nerve. The stapedius muscle develops
from the second arch and is supplied by the facial nerve. Posterior extension of the middle ear
cavity forms the mastoid antrum (Figs 35.7 and 35.8).
External Ear
The primary meatus develops from the 1st ectodermal cleft. Ectodermal plate develops in the floor
of the primary meatus. The solid meatal plate gets canalised and forms the secondary meatus.
Outer lining of the tympanic membrane develops from the ectoderm of the 1st pharyngeal cleft
Fig. 35.7: External, middle and the internal ears during development. (Diagrammatic)
1. Malleus 2. Incus 3. Stapes
Fig. 35.8: Microscopic features of the internal ear
and the inner lining of it comes from the endoderm of the tubotympanic recess. The mesoderm
sandwitched between the inner endoderm layer and the outer ectodermal layer forms the fibrous
layer of the tympanic membrane (Fig. 35.9).
Auricle
Six mesodermal hillocks develop around the first pharyngeal cleft. Each arch i.e. the first and the
second contributes three tubercles. Mandibular arch tubercles form the tragus, crus of the helix.
Three tubercles of the second arch form the antihelix, tragus and lobule of the ear. It occurs due to
poor development of auricular hillocks leading to microtia. [Fig. 35.10A–Clinical Photograph
Fig. 35.9: Development of the auricle

Ear 325
Fig. 35.10A: Microtia (Courtesy: Dr BK Sharma, ENT Surgeon, Nagpur, Maharashtra, India)
(Courtesy: Dr BK Sharma, MS, ENT Surgeon, Nagpur, Maharashtra, India) It may result due to drugs
consumed during pregnancy such as trimethodione. It may be an indicative of the malformations
of the middle ear.
Congenital Anomalies of the Ear

1. Congential deafness: It is mostly due to failure of canalization of the meatus plate. Poorly
developed auricle may present as small tubercles. The auricle can be small or of the large size.
As regards the meatus, the curvature may be acute making it difficult to have a look at the
tympanic membrane and creating difficulty in removing the foreign body.
a. External auditary meatus and the ossicles of the middle ear are poorly developed or fused
leading to deafness.
b. Membranous labyrinth may fail to develop properly, leading to congenital deafness.
c. Defeciant facial canal poses risk of involvement of the facial 7th nerve in the presence of
otitis media causing 7th nerve palsy.
Note:
1. Congenital deafness is cuased by the genetic factors. In deaf mutism there is defect of perception.
This defect could be the part of the 1st arch syndrome in which the anomalies of the malleus
and the incus are present.
Rubella infection in 8th week can cause mal development of spiral organ of Corti of the 8th
nerve (One may remember 8th nerve affection and the time of affection is also 8th week of
intrauterine life.) Congenital fixation of stapes may occur due to failure of formation of the
anular ligament.
Fig. 35.10B: Preauricular sinus (Courtesy: Dr Madan Kapre)
2. Preauricular fistula/Sinus: (Fig. 35.10B – Courtesy: Dr Madan Kapre, FRCS, ENT Surgeon, Nagpur,
Maharashtra, India). They are small pit like depressions in the preauricular region. Their mere
presence is enough to raise suspicion of the underline anomalies of the deafness and renal
malformation.
3. Accessory tubercles.
4. Otocephaly – due to the failure of the development of the mandible, ears fuse in the midline of
the neck.
5. Anotia – absence of auricle.
6. Congenital cholesteotoma – white crystalline structure may lie medial to the tympanic
membrane and may represent the cell rest of the meatal plug.
Eye 327
Eye
36
Eye develops from four different components which include neuroectoderm of the forebrain vesicle,
ectoderm of the head, neural crest and the mesoderm around. Retina, optic nerve and the posterior
layer of the iris come from the neuroectoderm of the forebrain vesicle. Ectoderm of the head gives
rise to the lense and the epithelium covering the anterior aspect of the cornea. The mesoderm
sandwitch in between the neuroectoderm and the surface ectoderm give rise to fibrovascular
element of the eye. It must be remembered that the sclera, choroid and the epithelium of the cornea
develop from two sources, i.e.
1. mesenchyme
2. neural crest (Figs 36.1 to 36.5).
Fig. 36.1: Layers of eyeball, ciliary body, iris, lens, anterior and posterior chambers of the eye
Fig. 36.2: Structure of cornea
Fig. 36.3: Sclerocorneal junction
Optic grooves appear at the cranial end of the forebrain. They grow and evaginate to form the
hollow optic vesicle. The distal part of the optic vesicle enlarges while its proximal part near the
forebrain undergoes narrowing. As the optic vesicle comes in contact with the surface ectoderm.
The part of the surface ectoderm gets thickened and forms the lens placode. Formation of the lens
placode is due to induction by the optic vesicles. Now the lens placode undergoes invagination
and form the lens pits. Approximation of the folds of the lens pit and their fusion converts the lens
pit into the lens vesicle. It gets detached from the surface ectoderm later.
Optic vesicle soon invaginates and forms the double wall optic cups. After detachment from
the surface ectoderm the lens vesicle enters the entrance or the gate of the cavity of the optic cup.
Eye 329
Under surface of the optic cup and the optic stalk develop the groove called the choroidal groove
or the choroidal fissure. The groove or the fissure is encroached by the mesenchymal cells and the
hyloid vessels. The hyloid artery arises from the opthlamic and supplies the inner layer of the
optic cup, lens vesicle and the mesenchymal tissue. Proximal part of the hyloid artery forms the
central artery of retina. With the closure of the retinal fissure the axons of the ganglion cells from
the retina get locked up in the optic stalk forming the optic nerve.
Fig. 36.4: Development of optic vesicle
Fig. 36.5: Formation of optic vesicle and optic stalk

Fig. 36.6: Early development of retinal and the lens layers. Few lens primarily retain nuclei for long time
Development of Retina
Before we go to the development of the retina it is advisable to remember the layers of the retina,
which can be memorised by remembering the following sentence (Fig. 36.6).
Pigment Royal Chemicals (manufactures) Non Protein Nitrogenous Products (under) Greater Supervision.
P – Pigment layer
R – Rods
C – Cones
N – Nuclear layer – outer
P – Plexiform layer – outer
N – Nuclear – inner
P – Plexiform layer – inner
G – Ganglion cell layer
S – Stratum opticum.
Walls of the optic cup give rise to the retina. Outer layer of the optic cup is thin, which forms
the retinal pigment epithelial layer. The inner layer of the optic cup is thick and it forms the neural
layer of the retina. During the early period of development these two layers are separated through
the intraretinal space. As the intraretinal space disappears the two layers lie very close. However,
they don’t get firmly fixed to each other. Their relationship remains as the close contact association
and not the real fusion. It must be noted here that the association of the pigment layer and the
choroid is the real fusion of two layers and not mere association. During detachment of the retina,
the neural layer gets separated from the pigment layer of the retina. It is observed that during
boxing where a mere blow on the eye can lead the detachment of retina.
Eye 331
Neuroepithelial layer of the retina develops into a light sensitive zone of the optic part of the
retina. It is called the neural retina. This layer is studed with the cells of rods and cones, bipolar
neurons and the ganglion cells. Axons from the ganglion cells go towards the optic stalk and from
there they go to the brain. Due to obliteration of the optic stalk cavity the axons of the ganglion
cells get buried in the substance of the optic stalk thus forming the optic nerve. Optic nerve fibers
are unmyelinated at the time of birth; however it takes ten weeks for the mylination of the fibres
after exposure of the eye to the light for the duration of 10 weeks. Myelination stops at the site of
the entry of the optic nerve.
New born infants react to sudden changes of illumination, however the vision remains poor.
They are able to see large objects like balloons.
Development of Ciliary Body

Ciliary body develops from anteriormost part of the choroids. Its ciliary processes point towards
the lens. Pigment layer of the ciliary epithelium comes from the outer layer of the optic cup. The
non-pigmented layer of the ciliary epithelium is an anterior extension of the neural retina which
lacks neural tissue. Ciliary muscle is smooth muscle responsible for focusing of lens with the
assistance of mesenchymal tissue of the ciliary body.
Development of Iris
Rim of the optic cup covering the lens partially forms the iris. The epithelium of the iris comes
from both the layers of the optic cup. The connective tissue of the iris originates from the neural
crest. It is of the importance to remember that the dilator and the sphincter muscles of the iris are
neuroectodermal in origin (Figs 36.7 and 36.8).
Fig. 36.7: Anterior chamber of the eye, iridopupillary membrane, inner and outer vascular layers, choroid and the
sclera. With disappearance of the hyaloid artery is followed by formation of hyaloid canal
Fig. 36.8: Degeneration of distal part of hyaloid artery and formation of hyaloid canal
Development of the Lens

Surface ectoderm forms the lens vesicle. Anterior wall of the lens vesicle is lined by the cuboidal
cells and the posterior wall by the tall columnar cells. Nuclei of the columnar cells of the posterior
wall of the lens vesicle are not clearly visible due to the process of their dissolution (Figs 36.9 and
36.10).
The tall columnar cells grow and elongate towards the anterior wall of the lens vesicle. The
cells are transparent and are called the Primary lens fibers. Due to the formation of the primary lens
fibers the cavity of the lens vesicle gets obliterated. Now cuboidal cells at the equator of the lens
elongate and loose their nuclei. They form the secondary lens fibers. Due to the addition of the
Fig. 36.9: Development of optic cup and formation of lens vesicle

Eye 333
Fig. 36.10: Development of lens of the eye
secondary lens fibers the diameter of the lens increases. It is pertinent to remember here that the
primary lens fibers stay permanently for the life.
During development, the lens receives its blood supply from the hyloid artery the branch of
the ophthalmic. Due to degeneration of the distal part of the hyloid artery, the blood supply of the
lens is stopped making it avascular. However the lens is able to draw its nutrition from the aqueous
humor in the front and the vitreous humor at the back. As the lens lies between the two fluid filled
lakes, need not worry about the nutrition.
The lens has a covering of a vascular capsule which is called as the tunica vasculosa lentis. The
papillary membrane forms the anterior part of the vascular part of the lens. As a result of regression
and degeration of the distal part of the hyliod artery the vascular capsule of the lens degerates and
disappears. Now the thick basement membrane forms the lens capsule. Disappearance of the distal
part of the hyloid artery leaves an empty canal in the vitreous body which is called the hyloid
canal.
Vitreous body is a jel like material, avascular and transparent. Vitreous humor develops in
two stages the primary and the secondary. Primary vitreous humor comes from the neural crest
cells. The secondary vitreous humor probably arises from the inner cell of the optic cup.
Development of the Anterior and Posterior Chamber of the Eye

The anterior chamber of the eye develops as a cleft in the mesenchyme between the lens and the
cornea while the posterior chamber of the eye develops from the cleft in the mesenchyme between
the iris and the lens. With the disappearance of the papillary membrane the anterior and the
posterior chambers freely communicate with each other.
Development of the Cornea

Substantia proprea and the inner layer of the cornea develop from the neural crest. The epithelial
over of the cornea comes from the surface ectoderm. Differentiation of the cornea occurs due to
induction by the lens. Due to induction by the the lens vesicle the surface ectoderm gets transformed
into the transparent, avascular and multilayered cornea.
Development of the Choroids and the Sclera

Mesenchymal tissue around the optic cup divides into the inner vascular layer known as choroid
and the outer fibrous layer called the sclera. The sclera continues with the cornea. Anterior part of
the choroids forms the ciliary body and the ciliary processes.
Eyelids
The upper and the lower cutaneous folds containing mesoderm approach each other infront of the
cornea. On the inner side, the cutaneous folds are covered with the ectodermal conjuctival sac. The
lids are fused and with their separation, the palpebral fissure is formed. The mesodermal core of
the cutaneous folds forms the tarsal plates (Figs 36.11 and 36.12). Anomalies of eylids include:
Fig. 36.11: Development of eyelids and lacrimal gland
Fig. 36.12: Formation of the eyelids

Eye 335
Ptosis
It is dropping of the eyelids. Margins are diverted outward is called ectropion and when the lead
margins pointing inwards, it is called entropion.
Lacrimal Gland
Superolateral part of the ectodermal conjunctival sac gives rise to two buds, i.e. the orbital and the
palpabral. Multiple solid buds get canalized to form the acini and the ductules of the lacrimal
gland.
Anomalies of the Lacrimal Gland

Agenesis, ectopic or nonfunctioning lacrimal glands.
Nasolacrimal Duct
Thickened ectoderm along the line of the fusion of the lateral nasal process and the maxillary process gets
buried in the form of the solid cord after getting separated from the surface ectoderm. The cord gets canalized.
It forms the lacrimal sac at the cranial end and the nasolacrimal duct at the caudal. The caudal end
opens into the inferior meatus of the nose. Superior and
the inferior canaliculi connect the conjunctival sac with
the lacrimal sac. The inferior canaliculus separates
the part of the lower lid to form the lacrimal caruncle
(Figs 36.13 to 36.15).
Anomalies of the nasolacrimal duct and canaliculi: It is
commonly associated with the oblique facial cleft defect.
In this condition the nasolacrimal duct is converted into
an open gutter. Atresia of the nasolacrimal duct.
Supernumerary canaliculi or puncti.
Anomalies
1. Coloboma of the retina: The defect is in the retina
placed inferior to the optic disc. It occurs due to
defective closure of the retinal fissure (Choroidal
fissure).
2. Coloboma of the iris: (Fig. 36.16): It is the defect in
the inferior part of the iris and gives an appearance
of a key-hole. The defect may extend to the ciliary
body and the retina. It results due to failure of
closure of the retinal fissure. Coloboma of the iris is
usually hereditary.
3. Coloboma of the eyelid: It is also known as
palpebral coloboma which is rare. Epicanthic fold
is seen at the medial angle of the eye in certain races
like Chinese (Mangolian). Fig. 36.13: Development of nasolacrimal duct
Fig. 36.14: Development of face. Please note that the nasal pits have come closer. Lateral nasal process is separated
from the maxillary process through the intervention of the naso-optic furrow
Fig. 36.15: Development of nasolacrimal duct
4. Persistent pupillary membrane: Persistence of the anterior part of the vascular membrane of
the lens may completely cover the pupil. It is commonly seen the premature infants. Normally
the membrane undergoes atrophy and rarely interferes with the vision. However when the
entire papillary membrane persists it is called the atresia of the pupil and needs surgical
treatments.
5. Congenital aphakia: There is absence of lens due to non development of the lens placode.
6. Persistence of the hyaloid artery: It has already been seen that the proximal part of the hyloid
artery forms the central artery of the retina. In case the distal part of the hyaloid artery persists
it stays in the form of a nonfunctional vessel, almost looking like a moving worm arising from
the optic disk.
Eye 337
Fig. 36.16: Coloboma iris (Courtesy: Dr Shivraj Mulik, Ophthalmologist, Jalgaon)
7. Congenital cataract: In this condition, the lens remains opaque causing blindness. It occurs
due to rubella virus, radiation or congenital galactosemia in which large amount of glucose is
present in the blood of the infant resulting in injury to the lens causing cataract. Congenital
cataract is seen in avitominosis and the parathyroid deficiency.
8. Congenital glaucoma: Occurs due to defective development of the drainage apparatus of the
aqueous humour leading to increased intraoccular pressure.
9. Congenital ptosis of the eyelid: It is due to the failure of developement of the muscle levator
palpabrae superioris. However, it can occur due to injury to the occulomotor nerve.
10. Cryptophthalmos: In this condition eyelids do not develop as a result the eye is covered with
skin.
11. Cyst: Occurs due to failure of the optic cup to invaginate.
12. Anophthalmos: Complete failure of development of eye.
13. Cylopia: There is fusion of two eyes in the midline. When the nose placed above the fused
single eye it is known as proboscis.
14. Blue sclera: It is due to extreme thinness the pigments of the choroid are visible through the
sclera.
15. Absence of sphincter or dilator pupillae.
16. Albinism: Absence of pigment in part or total.
17. Visual defect and color blindness.
18. Single median eye: Cyclop.
19. Synophthalmos: When the eyes are partially fused it is called synophthalmos.
20. Anophthalmos: It is a rare anomaly occurs due to total failure of the eyes to develop.
21. Micro-ophthalmos: When the development of the eye is tiny it is called micro-ophthalmos.
Hypophysis Cerebri
Cereb
37
The hypophysis cerebri develops from two sources:
1. Its anterior lobe develops from the roof of stomatodeum in the form of an ectodermal
diverticulum (Rathke’s pouch).
2. Posterior lobe, i.e. pars neurvosa and stalk of the hypophysis develop as the neuroectodermal
diverticulum from the floor of the 3rd ventricle. It meets the Rathke’s pouch and fuses with it.
Rathke’s pouch presents a cavity which divides the diverticulum into anterior and posterior
walls. Anterior wall of Rathke’s pouch proliferates to form pars anterior of the hypophysis
and posterior wall from pars intermedia. Pars tuberalis is formed by the upward growth of the
pars anterior infront of the infundibulum. Original site of attachment of the Rathke’s pouch
gets closed. With formation of the mouth and it lies in the roof of the nasopharynx. The tract of
the Rathke’s pouch forms the craniopharyngeal canal. Remnant of the canal may form the
craniopharyngiomas. It must be remembered that the craniopharyngeal canal runs between
Fig. 37.1: Development of hypophysis cerebri

Hypophysis Cerebri 339
the roof of nasopharynx to the floor of the hypophyseal fossa. In the event of nondevelopment
of the hypophysis, the accessory hypohyseal tissue may develop in the posterior wall of the
pharynx (Figs 37.1 and 37.2).
Fig. 37.2: Development of hypophysis cerebri

Pineal Gland
38
Pineal Gland
It develops from the roof of the diencephalon in the form of a small hollow diverticulum, which
gets obliterated forming the bud. Modified neuroglial cells form the cells of the pineal gland. The
peneal gland was considered as a vestigial structure and hence no importance was attributed to it.
Recently the gland has come to lime-light due to the fact that it is said to be concerned with the
secretion of the hormones and control over the other endocrine glands (Fig. 38.1).
Fig. 38.1: Development of pineal gland from roof of diencephalon

Adrenal Gland 341
Adrenal Gland
39
Adrenal Gland
Adrenal gland develops from two sources (Figs 39.1 and 39.2).
1. Cortex of the adrenal gland develops from the coelomic epithelium and is mesodermal in
origin.
2. Medulla of the adrenal gland develops from the neural crest which comes the neuroectoderm.
Proliferation of the mesothelium of the dorsal coelomic wall forms a ridge called as the
suprarenal ridge. The suprarenal ridge lies between the root of the dorsal mesentry medially
and the developing gonad laterally. Mesenchymal cells of the coelomic epithelium reach the
zone of development of the adrenal
gland in two batches. The first batch
consists of large and acidophilic cells.
They surround the cells arrived from
the neural crest destined to form the
medulla of the adrenal gland. Three
large acidophilic cells of the first
batch form the fetal cortex.
The cells of the second batch
are of small size and they cover the
foetal cortex from outside. They form
the definitive cortex of the adrenal
gland. Due to differentiation of the
cells of the definitive cortex, zona
glomerulosa and zona faciculata
are formed at the birth. However, the
zona reticularis is identifiable only
during the third year of life.
The cells forming the medulla
of the adrenal gland are derived
from the neural crest. They belong to
the category of postsympathetic Fig. 39.1: Development of adrenal gland
ganglionic neurons in which

the preganglionic sympathetic
neurons terminate. The cells of
the neural crest also give rise
to sympathetic ganglion. Cells
forming the medulla of the adrenal
gland migrate from the neural
crest and enter the foetal cortex
from the medial side.
Fetal adrenal gland is 10 to 20
times larger than the adult adrenal
gland. Large size of the adrenal
gland is attributed to the large size
of the fetal cortex. Regression of
the fetal cortex occurs at birth
during the first year life.
1/3rd weight of the adrenal
gland is lost during three months
after the birth.
Anomalies of the Adrenal Gland

1. Ectopic adrenal tissue. The adrenal
tissue or the complete gland may
be found fused to the kidney or the
liver of the right.
2. Adrenogenital syndrome: It is due to
hyperplasia of cells of the adrenal Fig. 39.2: Microscopic anatomy of suprarenal gland
cortex, which secrets androgens.
The condition is marked by the premature development of the secondary sexual characters. In
case of female, the clitoris shows an enormous enlargement like the penis. The child can be
mistaken and labelled as the male. This condition is called as pseudohermaphroditism.
Chromaffin Tissue
Chromaffin tissue comes from the neural crest. Normally chromaffin tissue is seen in the para-
aortic bodies. It is also seen along the sympathetic chain near the sympathetic ganglion and along
the sympathetic plexuses and near the splanchnic nerves.
Formation of Limbs 343
Formation of
of
40 Limbs
Formation of Limbs
Limb buds are the bars of mesenchyme covered with the ectoderm. The limb buds arise from the
side of the body of an embryo at angle of 90°. Each bud has preaxial and the postaxial borders. The
base of the limb bud is at the body and the apex is at the tip. An ectodermal ridge appears at the
apex of the limb. The mesenchyme adjacent to the ectodermal ridge do not differentiate, however,
the mesenchyme away from ectodermal ridge undergoes differentiation forming muscles and
cartilages. Forelimb gets marked in three zones, i.e. arm, forearm and the hand due to appearance
of two constrictions. Appearance of the digits in the hand is due to death and disolution of the
intervening tissue. Mesenchyme of the bud is converted into cartilages, which are replaced by the
bones of the limb.
Preaxial bone of the forearm is the radius while the preaxial bone of the leg is tibia. Upper limb
gets adducted and lies by the side of the embryo with thumb pointing outwards. The ventral
surface of the upper limb becomes the flexor surface of the arm, forearm and the hand.
Inferior limb undergoes adduction and medial rotation which brings the tibia and great toe on
the medial side. Due to medial rotation, the knees face anteriorly. Due to adduction of the forelimb
elbows point posteriorly. The development of the forelimb is from C5,C6,C7,C8 and T1. and that
of the lower limb is from L2, L3, L4, L5, S1 and S2 segments.
The Skull of New Born

Flat bones of the vault of the skull are joined by the fibrous sutures derived from the neural crest.
Neural crest forms the sagittal suture and the paraxial mesoderm forms the coronal. Mastoid process
is not developed. The gaps between the bones are filled by the membranous tissue. They are called
as fontanelle. Anterior fontanelle is placed at the junction of two parietal bones and the two halves
of the frontal. It closes at the half year of life.
Functions of the Fontanelle

1. They facilitate delivery, due to overlapping of the bones during passage of fetal head through
birth canal.
2. Allows growth of the brain.
3. Helps in accessing the state of ossification of bones of the vault of skull.

4. Helps in dignosing dehydration and hyperhydration.
5. Blood can be obtained from the superior sagittal sinus for examination and the drugs can be
infused and transfusions can be given.
Joints
Mesenchyme between the ends of the developing bones—forms the tissues of the joint. The
mesenchyme gets converted into fibrous, and cartilaginous tissues. They form the fibrous and the
cartilaginous joints. Fibrous joints form sutural joints, gamphosis and the syndesmosis. (Inferior –
tibiofibular joint is a classical example of syndesmosis (Fig. 40.1).
Fig. 40.1: Formation of a synovial joint
Primary cartilaginous joints are at the ends of the long bones between the epiphysis and the
metaphysic before union. They are temporary as they get ossified and do not allow movements. In
synovial joints cavity appears in the mesenchyme, between the bones. Mesothelium linining of the
cavity forms the synovial membrane. Mesenchyme around the joint forms the capsule and the
ligaments.
Formation of Limbs 345
Other Anomalies of the Limbs

1. Phocomelia: In this condition, proximal part of the limb is absent or poorly developed. The
hand or the foot is directly attached to the trunk.
2. Amelia: Total absence of the limb.
3. Talipes equinovarus (Club foot) (Fig. 40.2).
Fig. 40.2: Club foot (Talipes equinovarus) (Courtesy: Dr Sudhanshu Kothe, Nagpur, Maharashtra, India)
4. Congenital amputations: The congenital amputations are due to constricting bands, as seen in
the fetal alcohol syndrome (Fig. 40.3).
Fig. 40.3: Congenital amputation of fingers due to constriction bands

5. Fused digits (Fig. 40.4): Syndactyly (syndactyly

can be cutaneous or osseous), macrodactyly,
synphalangia, brachydactyly, arachnodactyly
(Spider fingers) polydactyly. Normally thumb
has two phalanges and at times it may have one
additional phalange.
Fig. 40.4: Syndactyly (Courtesy: Dr Sudhanshu Fig. 40.5: Lobster foot (Cleft foot) (Courtesy:
Kothe, Nagpur, Maharashtra, India) Dr Sudhanshu Kothe, Nagpur, Maharashtra, India)
6. Cleft, palm or sole of the foot. (Lobsters claw) (Fig. 40.5).

7. Unusual anomaly of the limbs. Teratogens have their maximum influence on developing limbs
during the period of 4 to 7 weeks of the intrauterine life.
Story of Thalidomide
The drug was widely used as a sleeping pill and anti-nauseating agent. It was withdrawn from the
market when discovered that the drug causes severe malformations of the limbs. However, the
drug has resurfaced on the counters of the medical stores as a remedy for diseases like cancer,
Aids and certain immunological diseases. The drug is contraindicated for women during the child
bearing age.
Age of an Embryo 347
Ageo
Age f
of
41 an Embryo
1. The age of an embryo is calculated considering the date of conception.

2. By the presence of number of somites
a. Presomite
b. Somite stages
3. Measurement of the length called as crown-rump (CR length), i.e. the length of 2-month-old
embryo is 30 mm while at the time of birth the CR length is 10 times more, i.e. 300 mm.
Twining
42
Twining
Birth of two infants at the same time is known as twins. Similarly there can be birth of three or
four infants at the same time. The former is known as triplets and the later is called quadruplates
(Figs 42.1A and B).
Dizygotic Twins (Fig. 42.2)

Two separate ova are fertilized independently resulting in dizygotic twins. In production of
dizygotic twins ovum and the spermatozoon are separate. The twins do not look alike and can be
of different sex. In addition to these the chorionic and the amniotic sacs are separate and
independent.
Fig. 42.1A: Ultrasound showing twin pregnancy (Courtesy: Dr Dinesh Singh, Radiologist, Nagpur, Maharashtra, India)
Twining 349
Fig. 42.1B: Monozygotic twins with separate amniotic, chorionic sacs and separate placentas
Monozygotic Twins
When the single fertilized ovum forms twins, it is called monozygotic twins. In a monozygotic
twins, genetic constitution, sex and the looks are the same. Totipotent cell give rise to the complete
Fig. 42.2: Dizygotic twins having its own amnion, chorion and placenta, however placentas get fused
embryo when single cell gets divided and separate to

develop independently. Naturally they have separate
chorionic and the amniotic sacs. When the
development of the embryo reaches the blastocystic
stage, inner cell mass gets divided into independent
complexes and form complete fetus. In this there is
common chorionic sac and separate amniotic cavities.
When the inner cell mass gets divided into two, two
embryonic axises are formed resulting in formation
of two separate embryonic disks, each having the
separate prochordal plate and the primitive streak.
They have common chorionic and amniotic cavities.
In such cases, the placenta is one with two umbilical
cords. At times two independent placentae are formed
which may fuse with each other having no
anastomosis of the blood vessels. When there is a
fusion of the placentae mixing of the blood of two
fetuses occur. Naturally the infants have two different
types of erythrocytes (Erythrocyte mosaicism).
When there is partial separation of monozygotic
twins, two infants are born with fusion of the part of
the body. They are known as conjoint twins or Siamese
twins. The incidence of twining is seen in 1% to 2% of
pregnancies which are mostly dizygotic. Classification
of conjoint twins is based on the site and extent of the
fusion (Figs 42.3A and B). Fig. 42.3A: Conjoint twins
Twining 351
Fig. 42.3B: Conjoint twins having four upper limbs and three lower limbs (From the news)
• Craniophagus—Fusion of heads
• Thoracophagus—Fusion of thorax
• Pygopagus—Fusion at sacral region.
• Cephalothoracic—Fusion of head and thorax.
Parasitic Twins
The development of one of the twins remains rudimentary due to poor blood supply. It lives like
a parasite on the body of developed co-twin. When twins develop within the body of the developed
twin (Intrafetal) is called as fetus in fetus.
Role o
off Ultrasound
43 in Pregnancy
egnancy
Ultrasonography has become the inseparable and integral part of diagnosis, care and management
of the cases of pregnancies (Fig. 43.1).
Ultrasonography helps in the following ways:
1. Age—Age of the embryo/fetus can be estimated.
2. Growth—Progress or retardation can be assessed.
3. Provides guide during chorionic villus biopsy.
4. Detection of abnormal pelvic mass
5. Diagnosis of ectopic pregnancy.
Fig. 43.1: Sonography

Role of Ultrasound in Pregnancy 353
6. Detection of congenital anomalies, particularly of the heart at 16 weeks. Finding of the low
pulse rate is an enough indication of the underlying cardiac anomaly.
7. Abnormality and pathology of the uterus, tubes and the ovaries.
8. Detection of placenta praevia.
9. Nuchal translucency (NT) by ultrasound is a commonly used soft tissue marker between 11th
to 13th weeks gestation along with other marker’s and biochemical tests in screening for
chromosomal and genetic disorders.
Other soft tissue markers are nasal bone, facial angle, echogenic bowel, tricuspid
regurgitation and ductus venosus Doppler. Biochemical tests are free β-hCG estriol,
inhibin-A, AFP.
Stages in
Stage
44 Embryology
There are three stages in the development of an individual from fertilization onwards:
Germinal period (1 to 3 weeks): It covers fertilization to the formation of trilaminar disk.
Embryonic period (4 to 8 weeks): There is differentiation of three germ layers to form tissues and
organs.
Fetal period (3 months to birth): It includes growth of the fetus and formation of placenta.
Highlights of the 2nd Week

It is known as the week of two’s (2)
1. Trophoblast divides into two, i.e. the cyto and the syncytiotrophoblast.
2. Embryo has two layers, i.e. epiblast and hypoblast. Epiblast is ectodermal and the hypoblast is
endodermal.
3. Extraembryonic mesoderm divides into two layers, i.e. somatopleuric and the splanchnopleuric
layers.
4. Two cavities are formed, i.e. amniotic cavity and the yolk sac.
5. Pregnancy can be diagnosed in the second week by doing RIA test. Syncytiotrophoblast secretes
gonadotrophic hormone which is detected in urine in pregnancy test.
6. There are two common tumors:
• Hydatid form mole.
• Choriocarcinoma.
Prologue to Human
Prologue
Molecular Biology
Molecular
Due to achievements in the field of molecular biology, advanced laboratory techniques are used
for the study of gene regulation and expression. Now we have an assess to the time-table of genes
regarding their activation and expression in the embryo during normal and abnormal development.
Recognition of the gene controlling the embryonic development unfolds the secret of genesis of
congenital anomalies. Pleuripotent embryonic stem cells have capability to differentiate into various
types of tissues.
Human embryonic stem cells (HESC) can be obtained and cultured in a laboratory. This has
opened the door for the molecular therapy for the various diseases.
It cannot be denied that the present progress of embryology is due to anatomy, biochemistry
and molecular level study of the development.
One gene one enzyme hypothesis has gone underground and the new hypothesis “Single
gene and many proteins” has emerged.
Let us see the molecular regulation of gastrointestinal tract. Different transcription factors are
expressed region-wise. SOX2 specifies esophagus and the stomach, POX1 the duodenum, CDXC
small intestine, CDXA the large intestine and the rectum.
Index
A lobe 162, 164 Annular pancreas 188

ABC of genetics 4 lung 164 Anodentia 132
Abdominal pregnancy 57, 85 ribs 121 Anomalies 198, 335
Aberrant renal artery 265 Account of ectodermal clefts 103 in ascent of kidneys 262
of right 265 Achalasia cardia 174 Anomalies of
Abnormal Achondroplasia 5, 20, 117 anal canal 192
implantation of Acid phosphatase 27 biliary apparatus 183
blastocyst 56 Acrosomal reaction 51 bones 19
ovum 84 Action of placental estrogen 88 brain and spinal cord 315
right subclavian artery 229 Adrenal gland 341 breast 115
sites of Adrenogenital syndrome 342 descent 289
opening of ureter 265 After axial rotation of diaphragm 168
thyroid 140 duodenum 187 duct system of testis 291
Abortion 2 Age of embryo 347 duodenum 180
Absence of Agenesis of face 155
fissures 163 common bile duct 186 female external genitalia 282
nose 155 cystic duct 186 gallbladder 184
ovulation 52 uterus 276 hindgut 193
penis 282 Albinism 112, 337 inferior vena cava 248
pericardium 229 Alimentary system 170 kidneys 261
quadrate lobe 183 Alkaptonuria 6 lacrimal gland 335
sphincter 337 Allantoenteric diverticulum 69, 92 larynx 162
testis 288 Allele 4, 5 limbs 345
uterine tubes 276 Allelomorphs 5 lip, palatal and drugs 155
uterus 278 Alopecia 112 lung 163
vertebra 118 Alveolar process 127 male external genitalia 282
Absorption of Alzheimer’s disease 14 neural tube 315
caudal part of mesonephric Ameloblasts 129 nose 155
ducts 265 Aminocentesis 95, 97 ovary 293
mesonephric ducts in dorsal Amnio-ectodermal junction 92 palate 152
wall 266, 294 Amniogen cell 61 placenta 85
pulmonary veins 209 Amnion 61 processus vaginalis 287, 291
into posterior wall 211 Amniotic radial artery 233
sinus venosus into right cavity 60, 92-94 ribs and chest wall 122
atrium 208 fluid 94 skin 112
Accessory Anamolies of adrenal gland 342 skull 124
diaphgram 169 Anencephaly 124 spleen 179
hepatic duct of Luschka 183 Ankyloglossia 135 teeth 132
testis 288 B rib 122

thyroglossal duct 141 Babinski’s sign or reflex 24 Chondro-osteodystrophy 121
thyroid gland 140 Barr body 10 Chordoma 66
tongue 135 Basement membrane 83 Choriocarcinoma 354
trachea 162 Bifid Chorion 60, 61
tracheal bronchi 163 nose 155 Chorionic
ureter 266 penis 282 gonadotrophic hormone 42
urethra 271 tongue 135 villus biopsy 97
urinary system 267 Biliary ducts 184 Chromaffin tissue 342
uterine tubes 276 Bilobed placenta 85, 86 Chromosomal abnormalities 8
uterus 276 Blastocyst 2, 60 Chromosomes 7
vagina 278 Blastomere 1 Ciliary body 327
vitellointestinal duct 199 Blastopore 66 Circulation of maternal blood in
Anonychia 113 Blood placenta 80
Anophthalmos 337 diseases 14 Circumvallate type of placenta 86
Anterior formation 16 Classification of
belly of digastric 102 Blue sclera 337 chromosomes 7
cardinal vein 239 Body cavities 156 inheritance/genes 5
chamber of eye 331 Bone 99 Cleft
commissure 314, 315 Brachiocephalic artery 225 foot 26, 346
ligament of malleus 101 Brain ventricles 310 lip 148
spina bifida 119 Branches of palate 100, 148
Anteverted testis 289 dorsal aorta 230 Cleidocranial dysostosis 20, 117, 124
Anti-mullerian hormone 284 embryonic dorsal aorta 230 Clitoris 282
Aortic Branchial Club foot 125, 345
arches 224 cyst 141 Coarctation of aorta 230
stenosis 229 fistula 104 Cochlear duct 320
Aplasia 112 sinus 105 Coeliac trunk 170
Appearance of Branchiogenic carcinoma 106 Coloboma iris 337
amniotic cavity 60 Bronchopulmonary segments 162 Coloboma of
follicular cavity 33 eyelid 335
lacunae in granulosa cells 32 iris 335
pharyngeal arches 98 C retina 335
Appendix 189 Caecum 189 Columnar cells 109
Arch arteries 220 Calcium wave 52 Commissural fibers 314
Arnold-Chiari deformity 316 Caput succedaneum 66 Common
Arrangement of structures of Cardiac muscle 22 cloaca 193
embryo 72 Cardinal veins 239 in female 194
Ascending colon 189 Cardiovascular system 203 hepatic
Ascent of kidney 260 Caroli’s disease 183 duct 186
Asending fibers 314 Cartilage bones 116, 123 vein 248
Association fibers 314 Caudal limb 189 sites of thyroglossal cyst 139
Athelia 115 Causes of descent of testis 285 Conducting system of heart 214
Atresia 184, 202 Cavernous sinus 240 Congenital
Atretic gallbladder 183 Cavities of brain 298 alopecia 113
Atria 204 Cell amputation of fingers 345
Atrichia 113 division 11 anomalies of
Atrioventricular cushion 206 membrane 51 ear 325
Auricle 324 Cells of corona radiata 51 heart 216
Autonomic nervous system 317 Cementoblast 129 liver 183
Autosomal Cementum 129 stomach 177
dominant disorders 5 Cerebellum 307 urinary bladder 268
recessive disorders 6 Cerebral vertebral column 118
Auxetic growth 2 commissures 315 anomaly of uterus 52
Azygos cortex 313 aphakia 336
lobe of lung 164 Cervical cataract 337
venous lines 245 flexure 298 diaphragmatic hernia 168
Index 359
dislocation of hip 126 Defects of ciliary body 331

diverticula 270 rotation 264 common carotid artery 226, 227
fusion of vertebral bodies 120 rotation of kidney 264 cornea 333
glaucoma 337 Definition of shock 57 corpus striatum 311
heart defects 9 Degeneration of distal part of descending colon 191
hiatal hernia 172 hyaloid artery 332 diaphragm 166
hypertrophic pyloric stenosis 177 Delivery of enamel organ from dental
laryngeal web 164 fetus 58 lamina 129
lymphoedema of skin 254 placenta and membranes. 58 epidermal layer of skin 110
megacolon 174, 193 Dental esophagus 158, 173
polycystic kidney 264 lamina 128 external
ptosis of eyelid 337 papilla 128 carotid artery 228
stenosis of urethra 282 Dentigerous cyst 132 genitalia 279, 280
syphilitic 132 Derivatives mesonephric tubules 294 eyelids and lacrimal gland 334
umbilical hernia 199 Derivatives of face 144, 146, 147, 336
Conjoint twins 351 anastomoses 232 female
Connecting stalk 60, 68 first pharyngeal arch 101 external genitalia 279, 281
Connective tissue 16 gut 171 urethra 270, 271
Copula of his 133 mesonephric duct 293 floor of mouth 127, 128
Corona radiata 51 midgut 189 gallbladder 183
Coronary pharyngeal glands 15
artery dominance 225 clefts 105 hypophysis cerebri 338, 339
sinus 208 pouches 106, 137 inferior vena cava 245, 248
Corpus second internal
callosum 314, 315, 317 and third arches 102 ear 320, 322
luteum 37, 41, 44 arch 101 mammary thoracic artery 233
luteum of third arch 101 interventricular foramen 314
menstruation 37 Dermatome 20, 21 intracranial venous sinuses 240
pregnancy 38 Dermis 110 iris 331
Cotyledons of placenta 80 Descending aorta 228 jejunum and ileum 189
Course of branchial fistula 105 Descent of kidney 256
Cranial limb 189 caecum 190 larynx 159
Cranium bifidum 315 ovary 293 left
Cri-du-chat syndrome 10 testis 285 renal vein 248, 249
Crista terminalis 208, 211 in various locations 290 subclavian artery 226
Crooked nose 155 Determination of sex 53 superior intercostal vein 242
Cross Development of lens 332
ectopia 263 adrenal gland 341 of eye 333
section of umbilical cord 70 alveolingual groove 135 lesser sac 176
Crossed ectopia of testis 290 anal canal 191, 192 liver 181
Cryptophthalmos 337 anterior and posterior chamber 333 and gallbladder 182
Cumulus oophorus 31 aortic and pulmonary valves 213 long bone 18
Cylopia 337 aorticopulmonary septum 210 lymphatic system 252
Cyst 106, 337 appendix 189 male
Cystic hygroma 254 arch of aorta 222, 224 external genitalia 279
Cytoplasm 51 arteries of upper limb 234 urethra 270, 271, 279, 281
Cytotrophoblast 83, 88 ascending colon 190 mammary gland 114
atria 208 mandibular and maxillary
D auricle 324 processes 145
bone 116 Meckel’s diverticulum 71, 200
Dandy Walker syndrome 317 brachiocephalic artery 225 metanephric vesicle and
Decidua 46, 81 cecum and appendix 189 ampulla 259
basalis 81 cerebral nail 110
cells 48 cortex 313 nasal cavity 151
parietalis 81 hemisphere 310 nasolacrimal duct 334, 336
Decidual reaction 45, 81 choroidal fissure 299 neural tube 65
Defective dentition 100 choroids and sclera 334 neurones 22
optic Dividing ureteric bud in Enamel

cup 332 metanephros 259 cuticle 129
vesicle 329 Divisions of organs 128
ovary 291, 292 atrioventricular canal 205 Enchondral ossification 18
palate 152, 154 cloaca 172, 191 Endoderm 83
pancreas 182, 186 Dizygotic twins 348 Endodermal cloaca 191
parathyroids 143 Dominant gene 5 Endotheliochorial 87
parotid gland 135, 136 Dorsal aorta 247 Epidermis 109
pineal gland 340 Double Epiphyseal plate has three zones 18
placenta 82 aortic arch 225 Epispadias 282
portal vein 238 bubble appearance 188 Epithelia 15
prostate 272 gallbladder 183 Epoophoron 295
rectum 191 inferior vena cava 248 Errors of
respiratory system 158 penis 282 fixation 202
retina 330 superior vena cava 244 rotation 201
ribs 121 ureter 266 Erupting temporary tooth 130
sebaceous gland and hair 111 Duct system of testis 284 Esophageal
smooth muscle 21 Ductus atresia 163, 172, 173
spinal cord 300 arteriosus 251 stenosis 172
spleen 175, 179 venosus 251 Esophagus 172
sternum 121 Duodenal Eventration of diaphragm 169
striated muscle 20 atresia 180, 181 Exomphalos 198
superior vena cava 242 diverticuli 181, 201 External
sweat gland 112 stenosis 180 ear 323
teeth 128 Duodenum 180 form of heart 216, 218
testes 283, 284 Duplicated testis 288 Extraembryonic celom 93
thalamus and hypothalamus 311 Duplication and diverticuli of gut 200 Extraembryonic mesoderm 60, 61
thoracic duct 252 Duplication of Extrauterine implantation 85
thymus 107 uterine tubes 276 of blastocyst 57
thyroid gland 138 vagina 278 Eyelids 334
tissues of body 15 Dysphagia lusoria 174
tongue 133, 134 Dysplasia 112
F
tooth 128, 130
tracheobronchial diverticulum 159 E Factors responsible for
transverse colon 190 descent of testis 288
Early determination of sex 295
umbilical closure of foramen ovale 229
and vitelline veins 236 Female homologues of prostate 274
development of brain 298 Fenestrated placenta 86
veins 236 development of retinal and
ureter 266 Fertilization 1, 49
lens layers 330 Fertilized ovum 46
urinary bladder 268 Ectodermal layer 59
uterus 274 Fetal
Ectopia
vagina 277 circulation 249, 250
cordis 217, 219
vertebral period 354
vesicae 268, 269, 283
artery 232 surface of placenta 80
Ectopic
column 117 surgery 97
adrenal tissue 342
Developmental anamolies of arch transfusion 97
anus 195
arteries 228 First arch syndrome 99
pancreatic tissue 188
Dextrocardia 217 Fissured tongue 135
testis 289
Diastematomyelia 121 Fistula 106
tooth 132
Diatropic dysplasia 20 Floating gallbladder 183
Edward’s syndrome 10
Dietl’s crisis 265 Folding of embryonic disk 67
Effacement of cervix 58
Diffuse placenta 85, 86 Follicle stimulating hormone 41
Effects of fertilization 52
Diplotene 13 Follicular phase 45
Elastic cartilage 17
Discoid lateral semilunar cartilage 126 Foramen
Embryology 1
Discus proligerus 31 cecum 133
Embryonic
Displacement of external ear 100 of Bochdalek 169
disk 59
Distal half of duodenum 189 ovale 207, 251
period 354
Index 361
Formation of temporary 131 H

abnormal right subclavian thalamus and hypothalamus 312 Habelunar
artery 174, 226, 227 thyroid 138 chiasma 315
aortic transverse 217 commissure 314
and pulmonary valves 214 urethral valves 282 Habitual abortion 2
arches 221 uterovaginal canal 275 Hair 111
blastocyst 55 uterus from uterovaginal Hamartomas 179
blood cells and vessel wall 16 canal 275 Hartmann’s pouch 184
branchial arches 98 vagina 277 Heart tube 203, 205
bulboventriclular loop 216 valves of heart 213 Hemivertebra 119
caudate nucleus 312, 313 vertebral Hemoendothelial type 88
cerebral hemisphere 309 artery 232 Hemoglobinopathies 6
cervical sinus in section bodies 118 Hepatocystic duct 183
of pharynx 104 Fragile sites 9 Hepatopancreatic buds 187
chorion frondosum 77 Frontal prominence 145 Herniation of lung 164
connecting stalk 69 Functions of Heuser’s membrane 59
corpus 36 chromosomes 8 Higher extension of tunica
callosum 311 fontanelle 343 vaginalis 289
curvatures 177 placenta 83 Hippocampal commissure 315
decidua 46 Funnel chest 122 Hirschsprung’s disease 193
ductus venosus 237 Fusion of Histogenesis of
ectoderm and endoderm 58 oocyte with sperm cell bone 17
embryoblast and trophoblast 55 membrane 50 cartilage 16
external form of heart 218 testis 288 neural tube 302
extraembryonic mesoderm 59 Future of pancreas 188
eyelids 334 endodermal pouches 106 spleen 179
face from various sources 147 ovum 37 stomach 177
flexures of brain 298 thyroid gland 138
frontonasal process 144 G Homozygous 4
germ layers 58 Honey comb lungs 164
inferior vena cava 247 Galactosemia 6
Gastroschisis 199 Hormonal control of menstrual
interventricular septum 213 cycle 40, 44
intracranial venous sinuses 240 Gastrula 2
Gastrulation 62 Hormones 88, 95
lesser sac 177 Horseshoe kidney 261, 262
limbs 343 Gemination 132
Genes 5 Human
mesentery 197 chorionic gonadotropin 38, 88, 95
myelin sheath 23 Genital
ducts in male 284 ear 320
nasal septum 153 Humped nose 155
neuroblast 301 tubercle 279
Genome 5 Huntington’s chorea 5
notochord 66 Hyaline cartilage 16
optic vesicle and optic stalk 329 Genotype 5
Germinal period 354 Hyaluronidase 27
ovarian follicle 31, 32 Hydatidiform mole 57, 89, 354
peduncles 308 Glands arising from
ectoderm 15 Hydranencephaly 317
pericardial and peritoneal Hydrocephalus 316
cavities 156 mesoderm 15
Glands of mixed origin 15 Hydromyelia 317
permanent teeth 129, 132 Hydronephrosis 261, 262, 265
pontine flexure 308 Graafian follicles 31
Granulosa Hydrostatic bag 94
primary yolk sac 59 Hydroureter 266, 267
primitive streak 61 cells 31
lutein 41 Hyperplasia 261
right and left atria 207 Hypertrichia 113
secondary yolk sac 66 lutein cells 41
Greater Hypobranchial eminence 133
septum primum 207 Hypophysis cerebri 338
sinuses of pericardial cavity 216 cornu of hyoid 101
omentum 57 Hypoplasia 163, 229
superior vena cava 243 Hypospadias 282
synovial joint 344 vestibular glands 296
I L Medial nasal prominences 145

Median
Ichthyosis 113 Labia minora 282
cleft lip 150
Ileum 189 Lacrimal gland 335
Laryngeal web 162 ectopic thyroid 139
Imperforate anus 195
Laryngoptasis 162 thyroid diverticulum 133
Implantation of blastocyst 46, 47, 56 Medulla oblongata 304
Importance of embryology in Lateral
Medullary cords 284
medicine 3 aberrant thyroid 140
Meiosis 12
In vitro fertilization of female lobes 140
Meiotic inhibition factor 34
gamete 53 nasal prominences 145
plate mesoderm 64 Membrane
Inferior and cartilage bones 123
splanchnic branches 230
aberrant ductules 295 bones 123
ventricles 298
petrosal sinus 241 Meningocele 316
Layers of
Inherited autosomal dominant Meningomyelocele 315
endometrium 78
trait 117 Menopause 43
eyeball 327
Interconnecting axons 314 Left Menstrual
Intermaxillary segment 147, 148, 154 brachiocephalic vein 241, 243 bleeding 44, 48
Intermediate mesoderm 64 cycle 43-45
horn 208
Internal period 44
sided gallbladder 184
carotid artery 226 phase 39, 44, 48, 76
superior vena cava 244
jugular vein 241, 243 Mental retardation 9
umbilical vein 251
mammary thoracic artery 233 Lesser cornu of hyoid bone 101 Mesencephalic flexure 298
Interstitial cells of Leydig 284 Limb arteries 233 Mesenchymal components of
Interventricular septal defects 219 vertebra 117
Lingual cysts 135
Mesenchyme 16, 17
Intervertebral disk 117 Lobed placenta 85, 86
Mesenteric artery 170
Intracytoplasmic sperm injection 53 Lobes 140
Mesoderm 83
Intra-embryonic mesoderm 58 Lobester foot 126, 346
Lobulated kidney 265 Mesonephric
Intraembryonic mesoderm 62
Long duct 290
Intrahepatic tubules 258
biliary atresia 183 cystic duct 186
Mesonephros 258
gallbladder 183 hepatic duct 186
Mesothelium 157
part 238 Lower
Metanephros 258
Intralingual thyroid 135 end of esophagus 188
half of body of hyoid 101 Metaphysis 19
Intrauterine abnormal Methods of prenatal disease
limb 234
implantation 85 detection 97
lumbar kidney 262
Introduction to chromosomes Microcephaly 124, 317
pole of testis 290
and cell division 7 Microglossia 135
Lumbar
Inversion of pancreatic ducts 188 Micromastia 115
accessory 121
Inverted rib 122 Micro-ophthalmos 337
nipple 115 Lungs 160 Micropenis 282
testis 289 Microscopic
Luteinizing harmone 41
Ionizing radiation 96 anatomy of suprarenal gland 342
Isochromosomes 4 features of internal ear 324
M Microstoma 155
Isthmus 140
Macrocephaly 317 Microtia 325
Macroglossia 135 Midbrain 305
J
Macromastia 115 Middle ear 321
Jejunal diverticuli 201 Macrostoma 155 Midgut loop attached to dorsal
Jejunum 189 Marble bone disease 20 wall 92
Joints 344 Marfan’s syndrome 5 Milk ridge extending 115
Juxtaglomerular apparatus 261 Martin-Bell syndrome 9 Missed abortion 2
Maternal surface of placenta 80 Mitosis 11
Maturation of ovum 38 Modern theory of branchial cyst
K
Maxilla 99 formation 106
Karyotyping 8 Meckel’s Monozygotic twins 349
Klinefilter syndrome 9 cartilage 102 Morphology of nerves of first
Klippel-Feil syndrome 119 diverticulum 71, 91, 188, 191 arch 103
Index 363
Morula 2 Ontogeny 1 Phimosis 282

Moynihan’s hump 184 Oocyte 1 Phrygian cap 184
Muconeum 201 Oogenesis 29, 30 Phylogeny 1
Mullerian Opening of branchial fistula 141 Pigeon chest 122
ducts 278 Optic chiasma 315 Pineal gland 340
inhibiting substance 295 Osteogenesis imperfecta 6, 20 Placenta 38, 75
Multiple Ostium previa 84
epiphyseal dysplasia 20 primum defect 229 succenturia 85, 86
neurofibromatosis 5 secundum 207, 229 Placental
Mylohyoid 102 Outer and inner zones of prostate 274 barrier 77, 83
Myocardial hypoplasia 219 Ovarian circulation 84
Myotome 20, 21 cycle 41 estrogen 88
ectopic pregnancy 85 lactogen 88
N follicle 44 membrane 83
Overlapping of frontonasal progesterone 88
Nail-patella syndrome 5, 126 process 145 Plagiocephaly 124
Nails 110 Ovulation 35, 41 Polar bodies 51
Nasal Ovum 29, 36 Polycystic disease of liver 183
cavities 150 Polymastia 115
placodes 144 Polymorphonuclear leukocyte 10
Nasolacrimal P
Polyploidy 4
duct 335 Pachytene 13 Polythelia 115
groove 145 Pancake kidney 262 Pontine flexure 298
Natal teeth 132 Pancreatic duct 187 Portal vein 237
Nephrogenic cord projecting from Parafollicular cells 108 Position of
dorsal wall 64, 255 Paraluteal cells 41 appendix 190
Nerve supply of pharyngeal Paramesonephric duct 274 caecum 196
muscles 103 in males 278 septum transversum 72
Nerves of pharyngeal arche 100 Parasitic twins 351 Posterior
Nervous system 297 Parasternal hernia 168 cardinal veins 244
Neural Parasympathetic neurons 318 commissure 314
crest 298, 299 Paraxial mesoderm 63 Potter’s syndrome 165
tube 65, 297 Parkinson’s disease 14 Preauricular sinus 326
defect 97 Paroophoron 295 Preaxial limb’s 196
Neurons of posterior gray column 301 Participation of thoracic wall 168 Precocious teeth 132
Nitabuch’s layer 77 Particulars of Down’s syndrome 9 Pre-costal anastomosis 231
Non-return of umbilical hernia 201 Parts of spermatozoon 25, 26 Prenatal diagnosis of
Non-rotation of midgut 197, 201 Patau’s syndrome 10 birth defects 96
Nonunion of neural arches Patent sex 281
producing spina bifida 119 ductus arteriosus 223 Preventing ectopic pregnancy 55
Normal medial rotation 264 foramen ovale 229 Prickle cells 109
Notochordal canal 66 truncus arteriosus 219 Primary
Nuchal translucency 353 Path of thyroglossal duct 139 oocyte 31
Pelvic kidney 262, 263 villus 82
O Pericardial cavity 214 Primitive rectum 170
Pericardioperitoneal canal 161 Primordium 2
Oblique Perichordal disk 117
facial cleft 149 Process of
Period of gestation 53 divisions of cloaca 172, 191
inguinal hernia 288 Periodontal ligament 129
vein of left atrium 243 formation of villi 82
Peritoneal coverings 57 Processus vaginalis 286
Observe implanted blastocyst 75 Persistance of hyaloid artery 336
Occipital Prochordal plate 61
Persistent pupillary membrane 336 Production of hormones 95
meningocele 316 Pharyngeal pouches 143
myotomes 64 Progestational phase 45
Pharynx 137 Progesterone 38
Odontoblasts 129 Phenotype 5
Oligospermia 53 Prolapse of umbilical cord 90
Phenylketonuria 6 Prophase of first meiotic division 12
Omphalocele 198, 199 Philadelphia chromosomes 8 Prostaglandins 88
Prostatic S at birth 124

part of urethra 273 Saccule 320 of new born 343
utricle 279 Sacral parasympathetic outflow 319 Somatic intersegmental branches 230
Protease 27 Sacrococcygeal teratoma 66, 121 Somatopleuric layer 60
Pseudoarthorsis of clavicle 125 Sagittal Sonography 352
Pseudohermaphroditism 296 plexus 241 Sperm 1
Ptosis 335 sinus 241 Spermatogenesis 27, 28
Pulmonary arteries 228 Salivary glands 135 Spermatogonia 28
Pyramidal lobe 140 Scaphocephaly 124 Spermatozoa
anomalies 140 Schuller-Christan syndrome 124 passing through corona radiata 49
Schwann cell 299 penetrating zona pellucida 50
R Sclerocorneal junction 328 Sphenomandibular ligament 101
Sclerotome 20, 21 Spina bifida 118
Radial club hand 124
Sebaceous gland 111 aperta 119
Radioulnar synastosis 125
Second meiotic division 13 cystica 119
Rapture of graafian follicle 42
Secondary occulta 119
Rathke’s pouch 338
oocyte 51 Spinal cord 300
Recessive gene 5
palate 152 injury 14
Rectourethral fistula 194
villus 82 Splanchnopleuric
Rectouterine pouch 57
Secretory phase 45 layer 60, 65
Rectovaginal fistula 194, 278
Section of ovary 30 mesoderm 203
Rectovesical fistula 193, 269
Section through Splenic cyst 179
Relation of circulating fetal
human testis 27 Split sternum 122
blood 76, 81
lower part of pons 305 Spondylolisthesis 121
Remnants of mesonephric tubules 294
Renal Semicircular canals. 320 Spongioblast 23
and limb defects 96 Separation of Stages in
collar 247 cavities 157 embryology 354
Repair of neural tube defect 97 common ventricular chamber 229 formation of tooth 131
Replacing normal bronchus 162 pericardial 167 Stages of
Respiratory distress syndrome 165 primitive atrium 205 development of
Restoration of cell size 52 ventricles 212 metanephric kidney 257
Retrocaval ureter 248, 266 Septal anomalies 229 nephron 259
Reverse rotation 197, 264 Septate formation of notochord 67
Riedel’s lobe 183 gallbladder 183 labor 58
Right left atrium 219 mitosis 11
anterior cardinal vein 241, 243 uterus 276 Stem cell transplantation 97
common cardinal vein 241 Septum 180 Stomach 175
subclavian artery 226, 234 intermedium 207 Stomodeum 127
venous valve forms 211 primum 207 Stone formation 261
Ring secundum 207, 208 Story of thalidomide 346
chromosomes 4 Seventh cervical intersegmental Stratum
of veins 247 artery 231 basale 45, 56, 109
Rocker bottom foot 126 Sex cords 284 compactum 45, 56
Role of Sigmoid sinus 240 corneum 109
follicular cells and oocyte 34 Single median eye 337 granulosum 109
ultrasound in pregnancy 352 Sinovaginal bulbs 277 lucidum 109
yolk sac 67 Sistrunk’s operation 142 spinosum 109
zona pellucida 55 Sites of spongiosum 45, 56
osteoblasts 17 branchial cyst 104 Stromal edema 45
Rotation of diaphragmatic hernias 167 Structure of
kidneys 261 ectopic thyroid tissue 141 chromosomes 7
midgut 195, 196 hypospadius 272, 282 cornea 328
stomach 176 Situs inversus 202, 217 ovum 35
Rudimentary Skeleton 116 sperm 25
liver 183 Skeleton deformities 9 tooth 131
uterus 276 Skull Stylohyoid ligament 101
Rupture of graafian follicle 36 and limbs 123 Styloid process 101
Index 365
Subcardinal veins 244 fistula 106 fistula 269

Subcentral veins 247 groove 158 Ureterocele 266, 267
Subdivisions of Tracheoesophageal fistula 96, 173 Urethral valves 272, 283
heart tube 206 Transposition of great arteries 217, 219 Urogenital
lung buds 160 Transverse section of ridge 256
Sublingual glans 271 sinus 170
salivary glands 136 midbrain 306, 309 system 255
thyroid 140 Transverse sinus 240 Uterine endometrium 68
Submandibular salivary glands 135 Treacher Collins syndrome 99 Utricle 320
Succus vaginalis in females 293 Treatment of
Summary of development of vagina club foot 125
V
277 thyroglossal fistula 142
Superior Tricuspid atresia 229 Vaginal plate 277
aberrant ductules 294 Trophoblast 38, 61 Valve of
petrosal sinus 241 True hermaphrodite 296 coronary sinus 208
vena cava 241 Truncus chorii 82 inferior vena cava 208, 251
Supracardinal veins 245 Tubal Variations of
Suprahepatic part 239 atresia 276 spina bifida 315
Surrogate mother 53 obstruction 52 umbilical cord attachments 85
Sweat glands 112 Tuberculosis 261 Vasicovaginal fistula 278
Syncytiotrophoblast 83, 88 Turner’s syndrome 9 Veins of
Synophthalmos 337 Twin pregnancy 348 embryo 235
Syringocele 317 Twining 348 renal collar 247
Syringomyelia 317 Types of Venous ends of heart tube 205
abnormalities 96 Ventral splanchnic 230
T cleft palate 155 Ventricular cavity 212
fistulae in male and female 194, 278
Tails of lockwood 290 Vesicourethral canal 273
harelip 150
Talipes equinovarus 125, 345 Vesicovaginal fistula 269
hydrocele 287
Taussing-Bing-syndrome 220 Visual defect and color blindness 337
implantation 77, 81
Tay-Sach’s disease 6 Vitelline
testis 288
Telencephalic flexure 298 block 52
Typical chromosome 7
Tensor cyst 199
palati 102 membrane 51
tympani 102 U Vitellointestinal duct 170
Teratogens 96 Ulnar club hand 125 Vitiligo 112, 113
Tertiary villus 82 Ultimobranchial pouch 108 Vomeronasal organs of Jacobson 151
Testicular tumor 284 Ultrasonograph of hydatidiform
Tetralogy of Fallot 217, 220 mole 89 W
Theca Ultrasound 97, 348
externa 34 Umbilical Wall of
interna 34 arteries 251 duodenum 188
Thecal gland 34 cord 60, 90 small intestine 188
Third arch 103 hernia 92, 170 stomach 188
Thoracic kidney 262 veins 239 Wharton’s jelly 69, 90, 91
Thymus 107 Unfriendly cervical mucosa 52
Thyroglossal Unilateral X
cyst 141 agenesis 266
fistula 141, 142 cleft lip 149 XYY syndrome 10
Tongue tie 135, 136 Upper
Tonsil 136 half of body of hyoid 101 Z
Tooth and nail syndrome 132 jaw 148, 152 Zona pellucida 31, 51, 56
Total anomalus pulmonary venous limb 233 Zygote 1
drainage. 217 part of right subcardinal vein 247
intrafallopian transfer 53
Tracheobronchial Urachal
Zygotene 13
diverticulum 158 cyst 268

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Contents i

DK Kadasne MS FRCS FICS

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

Kadasne’s Textbook of Embryology

First Edition: 2011

Typeset at JPBMP typesetting unit

BR Kate MBBS, MS, FAMS

16. The Skeleton ..................................................................................................................................... 116

Prologue to Human Molecular Biology ........................................................................................ 355

Intrauterine development total period 38 weeks

Let Us See Some of the Terms Used in the Embryology

Autosomal Dominant Disorders

Osteogenesis imperfecta: An autosomal dominent disorder of connective tissue characterized by brittle

Autosomal Recessive Disorders

Structure of Chromosomes (Fig. 3.1)

Classification of Chromosomes— According to Location of the Centrosome (Fig. 3.2)

Fig. 3.2: Classification according to the position of centromere

Particulars of the Down’s syndrome are

Fragile sites (Martin-Bell Syndrome)

Barr Body (Fig. 3.3A)

Mitosis (Fig. 3.4)

First Meiotic Division

Second Meiotic Division

Diseases which are likely to be Benefited are by the Stem Cells

Glands Arising from Ectoderm

Glands Arising from Mesoderm

Glands of Mixed Origin

Blood Formation (Fig. 4.1)

Histogenesis of Cartilage (Figs 4.2 to 4.4)

Fig.4.3: Fibrocartilage Fig. 4.4: Elastic cartilage

Histogenesis of Bone (Figs 4.5 and 4.6)

Fig. 4.6: Roll of osteoblasts and osteoclasts in addition and the

Development of Long Bone (Fig. 4.7)

The Epiphyseal Plate has Three Zones

Metaphysis (Figs 4.7 to 4.9)

Development of Striated Muscle (Figs 4.10 and 4.11)

Fig. 4.11: Parts of the paraxial mesoderm

Development of Smooth Muscle

Development of the Neurones (Fig. 4.12)

Fig. 4.12: Histogenesis of spinal cord

Spongioblast (Fig. 4.12)

Formation of Myelin Sheath (Figs 4.13 and 4.14)

Fig. 4.13: Formation of myelin sheath

Fig. 4.14: Myelination of nerve fiber in the central nervous system by an

Fig. 5.1: Parts of spermatozoon

Fig. 5.2: Parts of spermatozoon and their origin

Spermatogenesis (Figs. 5.3 and 5.4)

Fig. 5.3: Section through human testis

Fig. 5.4: Spermatogenesis

Oogenesis (Figs 5.5 to 5.7)

Fig. 5.5: Oogenesis

Fig. 5.6: Section of ovary

Fig. 5.7: Primary oocyte

Formation of Ovarian Follicle (Figs 5.8 to 5.14)

Fig. 5.10: Formation of ovarian follicle and appearance of membrana granulosa

Fig. 5.11: Appearance of lacunae in granulosa cells.

Fig. 5.12: Appearance of follicular cavity