GOVERNMENT

MEDICAL COLLEGE
THIRUVANANTHAPURAM

LUMINAIRE ’18 PATHOLOGY.

MICROBIOLOGY.
PHARMACOLOGY.
FORENSIC MEDICINE.

ANATOMY | PHYSIOLOGY | BIOCHEMISTRY

 luminaire’18 _____________________________________________________

The complete second professional MBBS man-

ual REFERENCES
LUMINAIRE 2018 PATHOLOGY:
9th Edition ROBBINS AND COTRAN PATHOLOGICAL BASIS
JANUARY 2018 OF DISEASE,HARSH MOHAN TEXTBOOK OF PA-
THOLOGY

Published by PHARMACOLOGY:
SFI MEDICAL COLLEGE UNIT ESSENTIALS OF MEDICAL PHARMACOLOGY
Government Medical College K.D.TRIPATHI, TARA V SHENBAGH PHARMACOL-
Thiruvananthapuram OGY FOR MEDICAL GRADUATES

MICROBIOLOGY:
Cover design ANATHANARAYANAN TEXTBOOK OF MICROBIOL-
ABID ALI KHAN OGY, C.P BAVEJA TEXTBOOK OF MICROBIOLOGY ,
PANICKER’S TEXTBOOK OF PARASITOLOGY

FORENSIC MEDICINE:
Type setting THE ESSENTIALS OF FORENSIC AND TOXICOLO-
ABISHEK SWAMI GY, DR K. S. NARAYANAN REDDY

Printing and Binding

SOORYA FINE ARTS
SIVAKASI

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m HARIKRISHNAN M.R.
i 7025149626

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_____________________________________________________ luminaire’18

“Almost everyone knows that years ago I began my career

as a doctor. And when I began as a doctor, I began to
study medicine, most of the concepts I have today, as a
revolutionary were absent from my store of ‘ideas’.
Like everyone, I wanted to succeed. I dreamt of becoming
a famous medical research scientist; I dreamt of tirelessly
working to discover something which could be used to
help humanity, but at that time I thought of it in terms
of personal success. I was, as we all are, a child of my
environment.
After graduation, due to special circumstances and perhaps
also my character, I began to travel throughout Latin
America, and I began acquainted with all of it.
Because of the circumstances in which I traveled, first as
a medical student and later as a doctor, I came in contact
with poverty, hunger and disease.
And at that time, I realized there were things that were as
important to me as becoming a famous scientist for making
a significant contribution to medical science: I wanted to
help those people”.
Dr. Ernesto Che Guevera
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MESSAGE FROM STUDENTS’ FEDERATION OF INDIA

Students Federation of India (SFI) is one of the major student organisations in India.
Founded in 1970. As of 2013, it has a membership strength of nearly 40 lakhs school and
university students. The SFI includes students from all the academic institutions of India -
from schools to colleges, from professional institutions to research academies.

The SFI believes that education is a major tool of social transformation and that this
concept is especially relevant in a country like India, where regressive forces still prevail.
Proper education, we believe, will counteract such forces and will help to build a new society
based on rationality and justice. The SFI is an organization of students which is ever aware
of its role in society. It identifies with a society’s progressive forces and is totally committed
to the idea of independence, democracy, and socialism.

We utilize this occasion to pay our deep respect to great visionaries of past, like Dr.
Ernesto Che Guevara, the doctor -poet-revolutionary who is the thrilling epitome of the
leftist revolutionary movement.

Us together,

Jinan R S Harikrishnan M R
President Secretary

l REVOLUTIONARY GREETINGS
SFI MEDICAL COLLEGE UNIT
u Thiruvananthapuram
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 CONTENTS
PATHOLOGY..................................................006
PHARMACOLOGY........................................065
MICROBIOLOGY...........................................113
FORENSIC MEDICINE.................................141
QUESTION PAPPERS....................................183
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM
PAT H O L O G Y

QUESTION

PATHOLOGY
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PATHOLOGY SYLLABUS

PAT H O L O G Y
QUESTION PAPER PATTERN

PAPER-I General Pathology and Clinical Pathology

PAPER-II Hematology and Systemic Pathology

UNIVERSITY EXAMINATIONS MARKS

Theory Papers I & II 40 + 40 = 80
Internal Assessment 15
Practicals 25
Internal Assessment 15
Viva Voce 15
TOTAL 150

Paper I / II 40 marks
Essay (1 question) 1 x 8 8 marks
Clinical essay (1 questions) 1x6 6 marks
Short notes (4 questions) 4 x 4 16 marks
Short notes (4 questions) 4 x 2 8 marks
Short answers (4 questions) 4 x 1/2 2 marks
PA P E R S

EXAM TIPS

• Learn your CLIP record thoroughly for paper I.

• Learn related hematology portions for paper I.
• Draw histopathological diagrams wherever necessary.
• In case if any tumor is asked, write it under following headings - benign/malignant, etiology,
pathogenesis, gross and microscopic features, clinical features, lab findings, staging and prognosis.

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CLINICAL PATHOLOGY
PAT H O L O G Y

1. FNAC (HM 888) (RB 333) 2. Ova in stools

2. Exfoliative cytology (HM 227) (RB 97) 3. Plasma cell
3. CSF findings in meningitis** 4. Barr body
4. Sperm Analysis.
5. Urine microscopy- casts & crystals**
6. ESR (HM-270)**UQ
7. PCV
8. Coomb‘s test CIPHERS
9. Barr body(HM-252) ANTICOAGULANT OF CHOICE
10. Steps in tissue processing 1. Calcium chelators
11. Frozen section ·· Oxalate-PCV
12. Fixatives(HM-898) ·· EDTA-Cell counts & Peripheral smear
13. Bone marrow aspiration & biopsy(HM preparation.
262-264) ·· S o d i u m c i t r a t e - 1 : 4 ( 3 . 8 % - E S R )
14. Proteinuria- causes 1:9(3.2%-Coagulation studies)
15. Ketonuria – causes**UQ 2. Heparin
16. Leishman‘s stain **UQ ·· Osmotic fragility
17. Anti coagulants ·· Arterial blood gas analysis
18. Pap smear(HM-897)**
19. Lipid special stains 3. Anticoagulants used in blood bank
·· Acid Citrate Dextrose (21days) QUESTION
20. Immunohistochemical stains
·· Citrate Phosphate Dextrose with
21. Flow cytometry
adenine (35days)
DIAGRAMS
1. Urinary casts and crystals (IMP**)

CELL INJURY (IMP)

1. Cell injury – causes, mechanism, reversible and irreversible types(HM-9,RB-

38,44)**ESSAY,UQ
l 2. Reperfusion injury, Free radical injury(HM-14,RB-47,51)
3. Necrosis- Types, Explain each type (HM-26,RB-41,Fig2-8)**ESSAY,UQ
u
4. Apoptosis, difference b/w apoptosis & necrosis(HM-29,RB-52)**ESSAY,UQ
m 5. Gangrene ,difference b/w dry & wet gangrene(HM-32, tab2.5)
i 6. Pathological calcification, types (HM 33-37, RB-65, tab2.6)**UQ
n 7. Metaplasia**UQ
a 8. Fatty change (HM-19,RB-62)**UQ
9. Endogenous pigments.(HM-22,RB-64)
i 10. Dysplasia,Hyperplasia,Hypertrophy,Atrophy(HM 37-41,RB 34-38)**UQ
r 11. Lipofuscin(HM-25,RB-64)**UQ
e 12. Ochronosis(HM-22,RB-64)
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INFLAMMATION AND HEALING (IMP)

PAT H O L O G Y
1. Inflammation- definition, signs, types, vascular & cellular events, mediators,and outcome in
inflammation(hm-116,rb-73)**ESSAY,UQ
2. Wound healing- types, mechanisms, factors and complications. (Hm-158,rb-106)**
3. Chemical mediators of inflammation (hm-122,rb-82,fig5.7)**UQ
4. Morphological patterns & outcome of a/c inflammation(hm-131,rb-90)
5. Granulomatous inflammation(HM-135,RB-97)
6. Granuloma- definition, Evolution & fate of tubercle(HM-136 fig5.18,140 fig5.21)**UQ
7. Fracture healing(HM-161,RB-1193)
8. Cell adhesion molecules(HM-120,RB-76)
9. Granulation tissue- with diagram(HM-157,RB-103)
10. Acute phase reactants(HM-127,RB-702)
11. Difference b/w transudate & exudate(HM-81,RB-73)**UQ
DIAGRAMS
1.Inflammatory cells(hm-129 tab5.4,Rb-70 fig3.1)
2.Giant cells(hm-131)
HAEMODYNAMIC DISORDERS
(IMP) CIPHERS
1. Shock – types, pathogenesis, stages, mani ·· Liquefactive necrosis seen in brain
PA P E R S festations (hm-94,rb-131)**UQ
·· Barretts esophagus –metaplasia from squamous to
2. Embolism- definition, pulmonary embo
columnar.
lism,fat embolism**, air embolism, amni-
·· Wear & tear pigment- lipofuscin
otic fluid embolism (hm-105,rb-127)
**UQ ·· Death ligand – cd 95
3. Thrombosis – defn, pathogenesis (vir- ·· Hydropic change is the earliest manifestation of
chows triad), types, fate (hm-99,rb-122) reversible cell injury
**UQ ·· Ladder patten in agarose gel electrophoresis-apoptosis
·· Smeared pattern –necrosis
5. Chronic venous congestion – lung, liver, ·· Bcl-2+bax+bad –promote apoptosis
spleen.(Hm-90)**UQ ·· Bcl-2+bcl xl–inhibit apoptosis
6. D.I.C(hm-315,rb-127)
7. Infarction-definition, morphology, clinical
outcome(hm-111,rb-129) l
8. Gamma gandy bodies(portal htn, sickle cell u
anaemia,pna,angiosarcoma)(hm-93)**UQ
9. Decompression sickness(hm-108,rb-128) m
Differences between i
i. Hyperemia & congestion(hm-90,rb-115) n
ii. Antemortem & postmortem thrombi(hm-104 tab4.7,Rb-125)
a
iii. Arterial & venous thrombi(hm-103 tab4.6,Rb-125)
iv. Nephrotic edema & nephritic edema(hm-84 tab4.2) i
v. Red infarct & pale infarct(hm-112,rb-129) r
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GENETICS& PEDIATRIC DISORDERS sis(HM-61,RB-211)

1. Karyotyping(HM-252,RB-158)*
PAT H O L O G Y

2. Down‘s syndrome(HM-253,fig 9.3a;RB-

161)*
3. Turner‘s syndrome(HM-253,fig9.3c;RB- INFECTIOUS AND PARASITIC
166)**UQ DISEASE
4. Klinefelters syn-
drome(HM-253,fig9.3b;RB-165)
1. Tuberculosis- primary and secondary tb,
5. Gauchers diseases,Gauchers cell(diagram)
primary sites of tb, pathogenesis, diagnosis,
(HM-257,RB-153)**
mantoux test(hm-137,rb-371)**essay
6. Marfan‘s syn-
2. Leprosy - reactions in leprosy, lepromin
drome(HM-19,387,431;RB-144)
test, difference between lepromatous and
7. Pleiotropism(HM-189,190;RB-140)
tuberculoid leprosy(hm-147,rb-377)**uq
8. Neimann Pick disease(HM-258;RB-152)
3. Infectious mono nucleosis(imn)(hm-
9. Common pediatric malignant
329,rb-360)**uq
tumors(HM-260,tab9.4)**
4. Torch complex(hm-182,rb-460)
5. Syphilis(hm-151,rb-378)
6. Malaria- black water fever(hm-180,rb-390)
7. Mycetoma(hm-173)
IMMUNOLOGY 8. Candidiasis(hm-173,rb-386)
1. SLE - Etiology and pathogenesis, sero- 9. Amoebiasis(hm-178)
logical test, Renal lesions**, cardiac lesions, 10. Aspergillosis(hm-455,rb-388)
morphology of other organs, hematological 11. Rhinosporidiosis(hm-497)** QUESTION
presentation (HM-62,tab3.10,RB-218)**ES-
SAY
2. Amyloidosis –defn, types, classification,
Staining, Morphology in differrent or-
gans(HM-66,RB-256)**ESSAY
DIAGRAMS
3. HIV-Pathogenesis in HIV, neoplasms in
i. Rhinosporidiosis(HM fig16.12)
AIDS, opportunistic reactions in AIDS(HM-
ii. Amoeboma(HM-179,fig6.9)
52,RB-245)
iii. Flask shaped ulcer of amoebia-
4. Hypersensitivity reactions- all types with
sis(HM-556,fig 18.32)v
examples(HM 58-61,RB 201-208)
5. Transplant rejection-mechanisms,-
types(HM-49,50;RB-231)
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6. GVH reaction(HM-50,RB-236)  LE test positive-Rheumatoid arthritis,SLE
u 7. Immune tolerance(HM-61,RB-212)
m 8. Sago spleen, Lardaceous spleen(HM-74)**
9. Dendritic cells(RB-191) DIAGRAMS
i
10. Natural killer cells(HM-46,RB-192)
n 11. Arthus reaction(HM-60,RB-208)* i. LE cell(HM-64,fig3.9)**
12. Serum sickness(RB-207) ii. Tart cell
a
13. Reiters syndrome
i 14. MHC(HM-48,RB-194)
r 15. Autoimmunity-definition,pathogene-
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NEOPLASIA (IMP) 10. Tumour antigens(HM-223,RB-310) 11.

Premalignant lesions- carcinoma in situ(HM-

PAT H O L O G Y
1. Neoplasia- defn, difference between benign 199,RB-271)**
and malignant tumors(hm-186,tab7.2;Rb- 12. Grading & staging of
274,tab 7.2)** cancer(HM-197,RB-332)
2. Carcinogenesis- types, mechanisms, and 13. Hamartoma,Choristoma,Terato-
features (hm-210-214,rb-322-324),ame‘s test** ma(HM-260,RB-266,267)
3. Metastasis- pathways of spread,mechanism 14. RB gene-2 hit hypothesis(HM-206,
of invasion(hm-192,rb-272,306)** fig 7.23,RB-290)*
4. Anaplasia(hm-189,rb-269)**uq 15. Li Fraumeni syndrome
5. Oncogenes- defn, types, mecha- (HM-207,751,851;RB-294)
nisms(hm-202,tab7.4;Rb-283)**uq 16. P53 (HM-206,RB-294)*
6. Tumor suppressor genes- rb gene and 17. Apoptosis inducing genes (RB-301)
p53(hm-205,tab 7.5,Rb-290) 18. Molecular basis of cancer
7. Paraneoplastic syndromes (HM-201,RB-280).
(hm-225,tab 7.11)**
8. Immune surveillance(hm-222,rb-310)
9. Tumour markers (hm-229,tab 7.14;Rb- DIAGRAMS
337)**
10. Tumour antigens(hm-223,rb-310) i. Metastatic cascade(HM-196,fig7.15;RB-
11. Premalignant lesions- carcinoma in 307,fig-7.36)
situ(hm-199,rb-271)** ii. Anaplasia(HM-189,fig7.4)
12. Grading & staging of
PA P E R S cancer(hm-197,rb-332)
13. Hamartoma,choristoma, RBC DISORDERS
teratoma(hm-260,rb-266,267)
14. Rb gene-2 hit hypothesis(hm-206,fig 1. Anaemia-definition and classifica-
7.23,Rb-290)* tion(HM-271,RB-630,tab-14.1)
15. Li fraumeni 2. Megaloblastic anemia- Biochemical basis,
syndrome(hm-207,751,851;rb-294) Classification, Blood and BM findings Perni-
16. P53(hm-206,rb-294)* cious anemia(HM 28283,fig10.18,tab-10.8,RB-
17. Apoptosis inducing genes(rb-301) 645,tab 14.5)**ESSAY,UQ
18. Molecular basis of 3. Iron Deficiency Anemia - etiology, periph-
cancer(HM-201,RB-280) eral smear, bone marrow findings, biochemical
test, RDW(HM 274-276,RB 651-653)**ES-
SAY,UQ l
4. Sickle Cell Anemia - pathogenesis, inves- u
tigation, peripheral smear, Sickling test(HM
DIAGRAMS m
294-296,RB 635638,fig14.7)**ESSAY,UQ
i. Metastatic cascade(HM-196,fig7.15;RB-
5.Thalassemia - pathogenesis, Peripher- i
307,fig-7.36)
al smear investigation(beta thalassemia n
ii. Anaplasia(HM-189,fig7.4)
major**)(HM 296-301,RB 638-642,fig
14.12,tab 14.3)**ESSAY,UQ a
6.Hemolytic anemia - Classification, Investi- i
gations(HM-287,tab10.10) r
7.Immunohemolytic anemia(HM 288-289) e
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8.Hereditary spherocytosis(HM291-292,RB 8. Myelodysplastic syndrome(HM 343-344,RB

632-633,fig 14.3) 614-616)
PAT H O L O G Y

9. Sideroblastic anemia(HM-277) 9. Polycythemia vera(HM 338-339,RB 618-

10.Blood cell indices 619)
11.Aplastic anaemia(HM 301-303,RB 653- 10. Myeloblast, megaloblast, lymphoblast
655) (HM tab12.1)
12.Reticulocyte count(HM-265,RB-631)**UQ 11. Burkitts Lymphoma (HM-357, RB-597)
13.MAHA(HM 289-290) 12. Hairy cell leukemia (HM-358,RB 603-604)
14.PNH(HM-290,RB-642) 13. Follicular lymphoma (HM-356,RB 594-
15.Basophilic stippling(HM-269) 595)
16.Howell Jolly bodies(HM-269,RB-636) 14. Langerhans cell histiocytosis (HM-365,RB
17.Heinz bodies(HM-293,RB-634) 621-622)
18.Cold agglutinin disease(HM-289,RB-644)
19.Coomb’s diesease

PLATELET DISORDERS

1.ITP and TTP(HM-311)**UQ

2.Thrombocytopenia(HM-310)
3.Hemophilias - A & B(HM-313)**
4.Von Willebrand‘s d/s(HM-314)
5.DIC(HM-315)
6.Blood transfusion reactions(HM-318)** QUESTION
7.Hemolytic diseases of new born(HM-319)

WBC DISORDERS

1. AML - FAB & WHO classification of

acute leukemia, peripheral smear find-
ings,special stains(HM 340-343, tab12.5 RB
611614,tab13.10)**ESSAY,UQ
2. ALL - Classifications, Blood picture, Spe-
cial stains(HM 353-354,fig12.19 tab12.6, RB
l 590-592)**ESSAY
3. CML - Molecular abnormality, natural
u history, Blood & Bone marrow picture, DD-
m leukemoid reaction(HM 335-338,fig12.13, RB
i 616-618)**ESSAY,UQ
4. CLL-Peripheral smear(HM-355)**UQ
n 5. Leukemoid reactions (HM 332-333 tab12.3)
a 6. IMN-Pathogenesis,complications, lab find-
i ing, special tests for diagnosis(HM 329-331,RB
360-362)**ESSAY,UQ
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7. Agranulocytosis(RB-582)**
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4. Pericarditis-types(HM 437-439,RB 573-575

tab 12.14)

PAT H O L O G Y
5. Cardiomyopathy-Types(HM 434-436
tab14.10,fig 14.35, RB 564-570 fig12.31)
6. Infective endocarditis(HM 425-429,fig14.30
LYMPHOID SYSTEM ,RB 559-561,tab12.9)**
7. Aschoff bodies (HM-420,fig14.25 RB-
1. Hodgkins lymphoma - classification, reed 558)**UQ
- sternberg cells – types**, ann arbor stag- 8. Mac callam patch(HM-422,RB-558)
ing(hm 348-352 tab12.9,12.10 ,Fig12.16 ,Rb 9. Bread & butter pericarditis (HM-
606-611 tab13.8,13.9)**Uq 422,RB-558)
2. Multiple myeloma - investigations, urinary 10. Libman sacks endocarditis (HM-
findings, bence - jones protein**, plasma cell, 424,RB-562)
russelbodies and dutcher bodies in mm,salm- 11. Myocarditis(HM 432-434 tab14.9,RB 570-
on durie criteria (hm 361-364,fig12.25,12.27, 571 tab12.13)
Rb 599-602)**essay,uq 12. Loefflers endocarditis (HM-436)

THE HEART

1. Mi- gross & light microscopic features**,-

consequences,complications,markers for BLOOD VESSELS AND LYMPHATICS
PA P E R S diagnosis (hm 409-415 tab14.4,Fig14.18, Rb
540-550 tab12.5)*essay 1. Atherosclerosis- Aetiopathogenesis, risk-
2. RHD- aetiopathogenesis,jones criteria,- factors, AHA classification, foam cells, fat-
gross and microscopy with aschoff body (hm ty steak, atheromatous plaques,sequalae
418-424,fig14.24,14.25,14.27 ,Rb 557559)** (HM 373-380 fig13.6,tab14.2,RB 491-501
essay,UQ fig11.10,11.11,11.16)*
3. Vegetations-types(in rhd,sle,nbte,ie)(hm 2. Aneurysms-classsification,dissecting
424-428 tab14.8 ,Rb 559-562 fig12.24)**UQ aneurysm.(HM 386-389 fig13.15,13.18,RB
501-505 fig11.22) 3. Buerger‘s Disease(HM
384-385,RB-512) 4. PAN(HM -383,RB-509)

Salmon Durie Criteria

l
Major- Marrow plasmacytosis >30%, Plasmacytoma on biopsy, M component u
Minor- Marrow plasmacytosis 10-30% , Radiological finding-lytic bone lesion ,M component m
less than in major criteria
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5. Capillary and cavernous hemangioma.(HM 709)

391-392 fig13.19,13.20,RB-516) 6. Wegeners 11. Good pasture syndrome(HM-475 ,RB-
PAT H O L O G Y

granulomatosis(HM 383-384) 7. Vascular 701)

changes in hypertension(RB 490-491) 8. Ar- 12. Mesothelioma(HM-486,RB 723-724)
teriosclerosis(HM 371-372 fig13.2) 9. Classifi- 13. Asbestos body(Ferruginous body)(HM-
cation of arteritis ,Giant cell arteritis(HM-381 472 fig15.31)**
tab13.3,13.4,RB-505)

HEAD AND NECK

THE RESPIRATORY SYSTEM 1. Pleomorphic adenoma(HM-516 fig17.13,

RB-744)**UQ
1. Bronchogenic carcinoma- classifica- 2. Warthins tumor(HM 517-518,RB-745)
tion,etiopathology,histologictypes,gross,mi- 3. Leukoplakia(HM-507,RB-731)
croscopy( hm 477483,tab15.10,15.12,- 4. Hairy leukoplakia(HM-507,RB-730)
Fig15.34,15.35,15.37,15.38,15.39, Rb 712-719 5. Erythroplakia(RB-731)
tab15.9,15.10)** Essay,uq 6. Adenoid cystic Carcinoma(HM-519)
2. Emphysema-aetiopathology,mor- 7. Mucoepidermoid Carci-
phology-gross and microscopy(hm noma(HM-518,RB-745)
459-462,tab15.5,Fig15.18,15.20, Rb 675-678 8. Ameloblastoma(HM-513)
fig15.8)**Uq 9. Classification of salivary gland tu-
3. Bronchiectasis-clinical features,etiopatho-
genesis(rb 683-684,hm 465-466)**uq
4. Pneumoconiosis,anthraco- QUESTION
sis ,silicosis,asbestosis with THE GASTROINTESTINAL SYS-
diagram(hm467-474,fig15.26-15.32,Rb 687- TEM
692)
5. Pneumonia- stages of pneumonia,complica- 1. Gastric Ca- classification(WHO &Lau-
tion(hm 449-452 fig15.6 Tab15.2 , Rb 702-705) ren), risk factors, morphology, spread,-
6. Ards(hm 444-446,fig 15.3,15.4 Rb 672-674 investigations(HM-538,RB-771)**ES-
fig15.3 Tab15.2) SAY,UQ
7. Atelectasis(HM -446, RB 670-671 fig15.2) 8. 2. Colorectal Ca- aetiopathogenisis,clin-
Chronic bronchitis-Reid index(HM 458-459 ical features, morphology, TNM stag-
fig15.17 ,RB 678-679) ing,associated tumor markers, investiga-
9. Bronchial asthma-Curschmann spiral,char- tions(HM-570,RB-810)**ESSAY,UQ
l cot leyden crystals(HM 463-464 fig15.22 3. Peptic ulcer(HM-533,RB-766)**UQ
tab15.6,RB 679-682)**UQ 4. Crohns disease and ulcerative colitis(HM-
u 548,RB-797)*
10. Lung abscess(HM-457 fig 15.15,RB 708-
m 5. Colorectal polyps- definition, types(HM-
i 566,RB-804)*

n JONES CRITERIA
·· MAJOR CRITERIA – Carditis, Polyarthritis, Sydenhams chorea, Erythema marginatum, Sub cutaneous nodules
a ·· MINOR CRITERIA- Fever, Arthralgia, Previous h/o Rheumatic fever, Lab findings of Elevated ESR-Raised
i CRPLeukocytosis, ECG findings-prolonged PR interval.
·· DIAGNOSIS- Any 2 of major criteria or 1 major and 2 minor.
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6. Barrett‘s oesophagus(HM-523,RB-757)**UQ Portal hypertension(HM-615,RB-828)

7. Tuberculous ulcer(HM-553,RB-786) 12. Mallory body(HM-607,RB-842)**

PAT H O L O G Y
8. Typhoid ulcer(HM-554,RB-789) 13. Councilman body(HM-595,RB-842)**
9. Amoebic ulcer(HM-555,RB-794) 14. Haemochromatosis(pigment cirrho-
10. Typhoid nodule(RB-789) sis,bronze diabetes)(HM-611,RB-847)**
11. Carcinoid tumour(HM-559,RB-773) 15. Wilson‘s d/s(HM-612,RB-849)**
12. Carcinoid syndrome(HM-560,RB-773) 16. Piecemeal necrosis(HM-596)
13. Meckel‘s diverticulum(HM-544,RB-751)* 17. Hobnail liver(HM-608)
14. Hiatus hernia(HM-521,RB-750) 18. Liver abcess(HM-600)
15. Achalasia cardia(HM-521,RB-753) 19. Hydatid d/s(HM-601)
16. GERD(HM-523,RB-755) 20. Postnecrosis cirrhosis(HM-609)
17. Ca esophagus(HM-524,RB-758) 21. Chronic cholecystitis(HM-626,RB-878)
18. Hirschprung disease(HM-563,RB-751) 22. Reye‘s syndrome(HM-587).
19. Pseudomembranous enteroco-
litis(HM-556,RB-791)
20. Gastritis(HM-529,RB-763) KIDNEY AND LOWER URINARY
21. GIST(HM-538,RB-775) TRACT
22. Curling ulcer(HM-533,RB-762)*
23. Cushing‘s ulcer(HM-533,RB-762) 1. Post streptococcal glomerulonephritis
24. Gastric lymphoma(HM-543,RB-773) -etiology, urinaryfindings, microscop-
25. Intussusception(HM-546,RB-778)* ic findings in renal biopsy,investiga-
26. Appendicitis(HM-561,RB-816)* tion(HM652,RB-909)**ESSAY,UQ
27. Familial polyposis coli(HM-569,RB- 2. Renal cell carcinoma-histological
PA P E R S 809)**UQ types,morphology,paraneoplastic syn-
28. Difference between benign and malignant dromes(HM-681,RB-953)**ESSAY,UQ
ulcers(HM-543) 3. Nephrotic syndrome-causes,test to
confirm the diagnosis,causes of protein-
uria(HM-648,RB-914)**ESSAY
LIVER AND PANCREAS 4. IgA nephropathy(HM-661,RB-923)
5. C/c glomerulonephritis (HM-
1. Cirrhosis- classification,aetiopathogene- 661,RB-925)
sis,morphology,complication (HM-603)**ES- 6. Diabetic nephropathy (HM-
SAY,UQ 664,RB-926)**
2. Hepatocellular carcinoma (HM-618,RB- 7. Pyelonephritis(HM-667,RB-930)
870)**ESSAY,UQ 8. Hypertensive Changes In Kid-
3. Hepatic failure-hepatorenal syndrome,he- ney(HM-677) l
patic encephalopathy(HM-588,RB-826) 9. Hydronephrosis(HM-674,RB-950)
u
4. Viral hepatitis-hepatitis B,C morpholo- 10. Renal Calculi (HM-
gy(HM-590,RB-831) 672,tab20.15,RB-951) m
5. Alcoholic liver d/s(HM-606,RB-842)** 11. Wilm‘s Tumor(HM-683)**UQ i
6. Primary biliary cirrhosis (HM- 12. Renal Lesion In SLE - Lupus Ne-
n
610,RB-858)** phritis(HM-662)**UQ
7. Jaundice(HM-581,RB-853) 13. PKD(HM-664,RB-945)* a
8. Cholelithiasis(HM-623,RB-876)**UQ 14. RPGN(HM-654,RB-912)* i
9. Gallstones and types(HM-623,RB-877)* 10. 15. Membranous glomerulone- r
Pancreatitis - a/c &c/c(HM-631,RB-884) 11. phritis(HM-656,RB-915)
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

16. MPGN(HM-658,RB-920) esis,morphology,staging,investiga-

17. FSGN(HM-660,RB-918) tion(HM-715,RB-1004)**ESSAY,UQ
PAT H O L O G Y

18. A/c tubular necrosis(HM-666,RB-927) 19. 3. CIN(HM-715,RB-1003)**UQ

Difference between nephritic and nephrotic 4. Endometriosis,Adenomyo-
syndromes(HM-649,RB-898)** 20. Urothelial sis(HM-721,722,RB-1010)**
tumour(HM-687,RB-964) 21. Lipoid necro- 5. CA endometrium(risk factors)(HM-
sis(HM-656,RB-917) 724,RB-1014)**
22. Staghorn calculus(HM-673,RB-952) 6. Leiomyoma uterus(HM-726,RB-1019)**UQ
23. Tumours of bladder(HM-687,RB-964) 7. Surface epithelial tumours-serous and muci-
24. Goodpasture‘s syndrome(HM-655,RB-912) nous tumours(HM-732,733,RB-1023)
8. Germ cell tumour-teratoma,dysgermi-
noma,yolk sac tumour(HM-735,737)**
MALE GENITAL SYSTEM 9. Choriocarcinoma(HM-738,742,RB-1041)**
10. Hydatidiform mole(HM-741,RB-1039)**
1. Testicular tumour – Classifica- 11. Brenners tumor(HM-734,RB-1028)
tion(HM-696,RB-975) 12. Dermoid cyst(HM-736,RB-1029)**UQ
2. Seminoma(HM-697,RB-976)**UQ 13. Krukenberg tumor(HM-740,RB-1034)*
3. BPH(HM-705,RB-982) 14. Struma ovary(HM-737,RB-1030)
4. CA prostate-tumour mark- 15. Chocolate cyst of ovary(HM-722)
er(HM-706,RB-983)** 16. Follicular adenoma thyroid.
5. Bowen‘s disease(HM-702,RB-971) 17.Psammoma Bodies
6. Bowenoid papulosis(HM-703,RB-971)
7. Schiller duval body(HM-699,RB-977)** • Draw and label-early secondary endome-
8. Reinke‘s crystals(HM-691)**UQ trium QUESTION

FEMALE GENITAL TRACT THE BREAST

1. Ovarian tumors-WHO classification ( 1. Ca breast – classification,risk fac-

HM-731,RB-1023)**UQ tors,staging,Paget‘s disease of nip-
2. Cervical Ca–risk factors,pathogen- ple(HM-750,RB-1051)**ESSAY,UQ
2. Fibroadenoma,Phyllodes tu-

Classification of CIN/SIL
l
u Bethesda system CIN Dysplasia
m
i
1.L-SIL(HPV-6,11) CIN-1 Mild
n
a 2.H-SIL(HPV-16,18) CIN-2,3 Moderate,severe, Carcinoma in situ
i
r
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

mour(HM-748,749,RB-1069)**UQ cinoma(HM-754,RB-1066) 7. Inflammatory

3. Prognostic and predictive markers of breast carcinoma(HM-755,RB-1066)

PAT H O L O G Y
carcinoma(RB-1067)**
4. Fibrocystic disease of breast-proliferative 6. Medullary carcinoma (HM-754,RB-1066)
and non-proliferative(HM-746,RB-1048) 7. Inflammatory carcinoma (HM-
5. DCIS and Infiltrating duct carci- 755,RB-1066)
noma(HM-752,RB-1057) 6. Medullary car-
Carcinoma Breast Classification

A.non invasive carcinoma 4.Medullary carcinoma

1.intraductal 5.colloid(mucinous)carcinoma
2.intralobular 6.Other types:papillary carcinoma
Adenoid,cystic carcinoma,secretory
carcinoma,secretory carcinoma,
B.invasive carcinoma secretory carcinoma, inflamatory
1.infiltrating(invasive) Duct ca-NOS. carcinoma, metastatic carcinoma.
2.infiltratring(Invasive) lobular carcinoma.
3.tubular carcinoma (cribriform)
.

SKIN 7. Cushing‘s Syndrome(HM-788,RB-1123)

PA P E R S 8. Addison‘s disease(HM-789,RB-1130)
1. Squamous Cell Carcinoma (HM- 9. Hyper & Hypothyroid-
783,RB-1178)** ism(HM-793,RB-1083)
2. Basal Cell Carcinoma (HM-784,RB- 10. Goitre-Simple &MNG(HM-797,RB-1090)
1180)**UQ (diagram)
3. Malignant Melanoma(HM-787,RB-1171)** 11. Sheehan‘s Syndrome(HM-785,RB-1081)
4. Distinguish b/w benign mole and malig- 12. Psammoma Bodies (HM-803,RB-1096)**
nant melanoma(HM-779,tab 24.3). 13. Riedel‘s thyroiditis(HM-796,RB-1088)
14. Follicular adenoma Thyroid.

ENDOCRINOLOGY
THE MUSCULOSKELETAL SYSTEM
1. Diabetes Mellitus- Including Pathogenesis
l
Of Type 1 &2 DM(HM-809,RB-1109)** 1.Classification of Bone tumour(HM-832,RB-
2. Pheochromocytoma(HM-790) 1197)**UQ u
3. Hashimoto‘s Thyroid- 2. Osteosarcoma-Origin,Etiology,- m
itis(HM-795,RB-1086)**UQ Gross&Microscopy,Radiological Appear-
i
4. Grave‘s disease(HM-796,RB-1089)**UQ 5. ance(HM-832,RB-1198)**ESSAY
5. Ca Thyroid- Papillary**UQ,Follicular,Med- 3. Ewing‘s Sarcoma –Origin,Etiology , n
ullary(with morphology of each)(HM-802,RB- Gross & Microscopy , Radiological Appear- a
1094)**ESSAY ance(HM-839,RB-1203)**ESSAY
i
6. Multiple Endocrine Neopla- 4. Osteochondroma(HM-835,RB-1200)**
sia(HM-819,RB-1136)** 5. Osteoclastoma (Giant Cell Tumor)(HM- r
e
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MEN 1(Wermer‘s syndrome) MEN IIA (Sipple‘s syndrome) MEN IIB

PAT H O L O G Y

1.Parathyroid hyperplasia 1.Parathyroid hyperplasia/ 1. Medullary ca syndrome

2.Pancreatic islet cell hyperplasia Adenoma 2.Pheochromocytoma
3.Pituitary hyperplasia 2.Medullary Ca thyroid 3.Mucosal and gi neuromas
4.Mutant gene is MEN1 3.Pheochromocytoma 4.Marfanoid features
4.Mutant gene is RET

837,RB-1203)** 15. Chondrosarcoma(HM-837,RB-1202)

6. Osteomyelitis –Pyogenic and tubercu- 16. Involucrum(HM-823)**UQ
lous(HM-822,RB-1195)**UQ 17. Sequestrum(HM-823)
7. Paget‘s Disease Of Bone(HM-828,RB-1189)*
8. PNET(HM-839,RB-1209)
9. Rheumatoid Arthritis(HM-843,RB-1209).
10. Osteoporosis(HM-826,RB-1187)
11. Osteogenesis Imperfecta(HM-825) 12. Os-
teoarthritis(HM-842,RB-1208)
13. Pott‘s D/S,Psoas Abcess(HM-824,RB-1196)
14. Gout(HM-845,RB-1214)

PATHO PEARLS
QUESTION
• Most common histologic type of thyroid cancer-Papillary carcinoma(Orphan annie
eye/Ground glass nuclei,Psammoma bodies)
• Feature which differentiates follicular carcinoma from follicular adenoma of thy-
roid-capsular and vascular invasion.
• Medullary carcinoma thyroid-Increased calcitonin,amyloid stroma,associated with
MEN-II
• Primary acute adrenocortical insufficiency-Waterhouse Friderichsen syndrome
• Primary chronic adrenocortical insufficiency-Addison‘s disease
• Neoplasms of thyroid
a.Benign - Follicular adenoma
b.Malignant - Papillary, follicular, anaplastic, medullary
l
SOFT TISSUE TUMOURS THE CENTRAL NERVOUS SYSTEM
u
m 1. Lipoma**,Liposarcoma(HM-857,RB-1220) 1. CSF findings in TB , Pyogenic and Vi-
2. Rhabdomyoma,Rhabdomyosarco- ral Meningitis(Cob web appearance)(HM-
i
ma(HM-859,RB-1222) 867,RB-1272)**UQ
n 2. Meningioma(HM-882,RB-1314)**UQ 3.
3. Myositis Ossificans(HM-854),
a Glioma - Astrocytoma,Glioblastoma multi-
forme(HM-879,RB-1306)
i
4. Brain Abscess(HM-869,RB-1273)
r 5. Medulloblastoma(HM-881,RB-1312)
e
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Classification Of Bone Tumors

PAT H O L O G Y
Benign Malignant

1.Bone forming Osteoma,Osteoid osteoma, classic osteosarcoma,

Osteoblastoma surface osteosarcoma

2.Cartilage forming Enchondroma,Osteochondro- chondrosarcoma

ma, Chondroblastoma

3.Haematopoeitic tumours ----- myeloma,lymphoplasmocytic

Lymphoma

4.Unknown Osteoclastoma Ewing’s sarcoma, adamantino-

ma of long bones

-----
5.Notochordal tumours Chordoma

6. Schwannoma,Neurilemmo- EYES & ENT

ma(HM-885,RB-1247)
7. Oligodendroglioma(HM-880,RB-1309) 1. Retinoblastoma(HM-493)**
8. Von Recklinghausen‘s disease(HM-885) 2. Rhinosporidiosis(HM-497)**
9. Classify intracranial tumours (HM-878 ,
PA P E R S
RB-1306).
DIAGRAMS
1. Schwannoma (HP)
2. Meningioma (HP)

PATHO PEARLS
• Verocay bodies-Schwannoma
• Most common site of Schwannoma-CP angle
• Rosenthal fibres-Pilocytic astrocytoma
• Drop metastasis-Medulloblastoma l
• Fried egg appearance-Oligodendroglioma u
m
i
n
a
i
r
e
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MODEL ESSAYS
PAT H O L O G Y

1. 24 year old female presents with fever, joint pain, puffiness of face since 2 weeks. Irregular
discolouration of facial skin and alopecia was noted.
a) What is the provisional diagnosis?
b) Describe etiology and pathogenesis
c) Mention two serological tests by which you can confirm the diagnosis
d) Describe the renal lesions in this condition and what is the most common pattern of renal
lesion?
e) What are the cardiac lesions that can occur in this patient?
f) Mention the pulmonary manifestations of this condition.
g) What is the usual hematological presentation in this condition?
h) What is the usual cause of death?(renal disease)

2. 25 year old man was involved in a major road traffic accident. He had multiple injuries and
was bleeding profusely. When brought to the casualty, he was in stupor. His BP was 80/40 mm
Hg and pulse 145/min. He was tachypnoeic with cold extremities and died the following day. An
autopsy was done.
a) What type of shock did he develop?
b) What are the other types of shock?
c) Describe the pathogenesis of septic shock
d) What are the stages of shock?
e) What are the morphological changes in the organs at autopsy?
QUESTION
3. 5 year old child was admitted with fever, vomiting, unconsciousness in the hospital. O/E
he showed neck rigidity, petechial spots on the skin. TC-18000 ,DC-P78 L20 E2
a) What is your diagnosis?
b) What is the ideal specimen to be collected for diagnosis?
c) What is the special stain to be used?
d) Mention the etiological agents of this condition.
e) What are the likely CSF findings?
f) What are the complications of lumbar puncture?

3. 5 year old child was admitted with fever, vomiting, unconsciousness in the hospital. O/E
he showed neck rigidity, petechial spots on the skin. TC-18000 ,DC-P78 L20 E2
l a) What is your diagnosis?
u b) What is the ideal specimen to be collected for diagnosis?
m c) What is the special stain to be used?
d) Mention the etiological agents of this condition.
i e) What are the likely CSF findings?
n f) What are the complications of lumbar puncture?
a
4. 60 year old female sustained fracture neck of femur,. On the 2nd day she developed sudden
i severe dyspnoea, tachycardia, tachypnoea and died.
r a) What is the provisional diagnosis?
e
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b) Mention other causes of the diagnosis

c) What is the pathogenesis of this condition?

PAT H O L O G Y
d) Describe the morphology of the lesion in the lung.
e) What are the special stains to be used to reach the diagnosis?

5. 58 year old male came with the h/o c/c bleeding PR since 1 year. O/E he was very pale. Nails
showed koilonychia.
a) What is the diagnosis?
b) Mention the investigations needed to confirm the diagnosis.***
c) What are the etiological factors responsible?
d) What is the blood picture and bone marrow findings in this condition.***

6. 60 year old male presents with gradual darkening and shrivelling of right toe.
a) What is the diagnosis?
b) Name two basic investigations you will do for this patient.

7. 8 year old boy from a tribal village at Wayanad came with the h/o severe pain in fingers and
toes. There is h /o intermittent jaundice. O/E the child had pallor, jaundice and hepatomegaly.
Investigations Hb-6g/dl, Reticulocyte count17%, Urobilinogen +++
a) What is the provisional diagnosis?
b) List other investigations indicated in this patient.
c) How will you confirm your diagnosis?
d) Describe the peripheral smear findings inthe patient.
PA P E R S e) What is the basic abnormality which caused the disease.

8. 24 year old male presented with fatigue, fever, gum hypertrophy and spontaneous mucosal
and cutaneous bleeding. There is also recent h/o recurrent infections of resp tract and oral cavi-
ty. O/E mild lymphadenopathy and hepatosplenomegaly.
a) What is the diagnosis?
b) Mention two investigations.
c) Mention the peripheral smear findings and draw the diagram.
d) What are the special stains used?myeloperoxidase,[immune stain-CD13,33,117]
e) What is the WHO classification of this condition?
f) What is the revised FAB classification of this condition?
l
u
9. 5 year old child presents with fatigue, fever, epistaxis, gum bleeding of 1 week duration. Clin-
m
ical examination reveals generalised lymphadenopathy and hepatosplenomegaly. The child also
complains of episodes of headache and vomiting during this 1 week period. i
a) What is the diagnosis? n
b) Name two investigations
a
c) Describe the blood picture
d) Which special stain will you use? PAS i
e) Which immunostain can be used? Blymphocyte-CD10,19…..Tlymphocyte-CD2,3 r
f) Classify this condition. e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

g) What is the pathogenesis?

PAT H O L O G Y

10. 52 year old male presented with fatigue, weight loss anorexia and left upper quadrant pain.
O/E massive splenomegaly, hepatomegaly and mild lymphadenopathy.
a) What is the diagnosis?
b) What are the investigations?
c) Describe the natural history of the condition.
d) Describe the blood picture with a diagram.
e) What is the bone marrow picture?
f) What is the characteristic molecular abnormality associated with this condition?
g) What are the differential diagnoses?

11. 50 year old male is admitted with weakness and lower back ache. His ESR value is 200
mm/1st hr.
a) What is the probable clinical diagnosis?
b) Mention three lab investigations and their findings which will help in diagnosis
c) Name the organ that is commonly involved as a complication of this condition.
d) How will you confirm the diagnosis?
e) Mention two urinary findings(BJ protein detection,increase uric acid)

12. 15 year old male presented with painful swelling of bony consistency above the knee. Xray
revealed a metaphyseal lesion with characteristic sun-ray spicule appearance.
a) What is the probable diagnosis? QUESTION
b) What are the common sites affected and the common age group involved?
c) Describe the morphology and histology of the lesion.
d) What is the radiological appearance?
e) Common sites of metastasis.(lung,bones,pleura,heart)

13. 45 year old female came with h/o bleeding and foul smelling discharge PV. O/E patient
is emaciated, cervix bleeds to touch.
a) What is the provisional diagnosis?
b) Describe the pathogenesis.
c) How will you stage this lesion?
d) What investigation would have been helpful in detecting this lesion early?
l e) What is the morphology of this lesion?
f) What are the risk factors associated with this condition?
u
m 14. 47 year old lady presents with a hard lump in the breast,fixed to the skin and axillary lymph-
i adenopathy
a) What is your diagnosis?
n
b) Which pre operative investigation will prove the diagnosis?
a c) What is the aetiopathogenesis of this condition?
i d) What are the hisological types of this lesion.Name the histological type with
i) lymphoplasmacytic infiltrate
r
ii) peculiar pattern of metastasis
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

e) What is the likely gross and microscopic picture?

f) What are the prognostic factors of this condition?

PAT H O L O G Y
g) What is the staging of this condition?

15. 5 year old boy presented with painful swelling in the diaphysial region of femur. Xray re-
vealed a “onion peel appearance” at shaft of femur.
a) What is the diagnosis?
b) What is the reason for the typical radiological appearance of the lesion?
c) What is the chromosomal abnormality commonly associated with this condition?
d) Name another condition with similar histology.
e) Describe the gross and microscopy of the lesion.

16. 65 year old male, c/c smoker, complains of cough, hemoptysis. Xray chest shows opacity in
left lower lobe. CT shows solid mass lesion.
a) What is the diagnosis?
b) What are the 2 additional investigations to confirm your diagnosis?
c) What are the four histological types?
d) Describe the pathological features of each type.

17. 12 year old female child presented with puffiness of face and oliguria. Urine examination
showed massive proteinuria.
a) What is the provisional diagnosis?
PA P E R S b) Mention the test for confirming the diagnosis.
c) Mention the principle and procedure of the test for proteinuria.
d) Mention the causes of proteinuria.

18. 52 year old businessman was admitted in the hospital with severe hematemesis. He was a
known alcoholic for the past 20 years. O/E he was anemic, ascites present, liver enlarged.
a) What is the probable diagnosis?
b) Describe the pathology of the condition.
c) What are the complications of this condition?
d) What is the cause of ascites and hepatic enlargement in this case?
e) Mention 4 pathognomonic microscopic changes in this condition.
f) Mention 1 condition occuring in children below 3 years where similar morphological changes
are seen (Wilson‘s disease) l

19. 48 year old male was admitted to the hospital because of hematemesis. O/E he had jaundice, u
ascites, splenomegaly and nodular hepatomegaly. One nodule was large. m
a) What is the most likely diagnosis? i
b) Mention 4 investigations you will do for this patient.
c) Describe the pathogenesis of this condition. n
d) FNAC was unsuccessful. Hence a liver biopsy was done. a
i)Mention why this was done i
ii)What is the histopatholgy likely to be in this patient.
r
e) Mention 1 late sequelae that often occurs in such patients.
e
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20. 6 year old female child presented with fever, puffiness of face and decreased urine output for
PAT H O L O G Y

two days. The child gives a h/o sore throat 3 weeks back.
a) What is the provisional diagnosis?
b) What is the etiology?
c) What investigations will you do?
d) Mention 3 urinary findings.
e) Mention 3 tests to be done in this patient to find out the urinary abnormality.
f) Mention imp light microscopic features in renal biopsy of this case.

21. 52 year old hypertensive male complains of sudden onset of severe retrosternal chest pain
and sweating. O/E rapid and feeble pulse with cold extremities.
a) What is your diagnosis?
b) Describe the gross morphological changes in this condition
c) What are the microscopic changes in this condition.
d) What are the markers for diagnosis?
b) What are the 2 additional investigations to confirm your diagnosis?
c) What are the four histological types?
d) Describe the pathological features of each type.

17. 12 year old female child presented with puffiness of face and oliguria. Urine examination
showed massive proteinuria.
a) What is the provisional diagnosis?
b) Mention the test for confirming the diagnosis. QUESTION
c) Mention the principle and procedure of the test for proteinuria.
d) Mention the causes of proteinuria.

18. 52 year old businessman was admitted in the hospital with severe hematemesis. He was
a known alcoholic for the past 20 years. O/E he was anemic, ascites present, liver enlarged.
a) What is the probable diagnosis?
b) Describe the pathology of the condition.
c) What are the complications of this condition?
d) What is the cause of ascites and hepatic enlargement in this case?
e) Mention 4 pathognomonic microscopic changes in this condition.
f) Mention 1 condition occuring in children below 3 years where similar morphological
l changes are seen (Wilson‘s disease)
u
19. 48 year old male was admitted to the hospital because of hematemesis. O/E he had jaundice,
m ascites, splenomegaly and nodular hepatomegaly. One nodule was large.
i a) What is the most likely diagnosis?
b) Mention 4 investigations you will do for this patient.
n
c) Describe the pathogenesis of this condition.
a d) FNAC was unsuccessful. Hence a liver biopsy was done.
i i)Mention why this was done
r ii)What is the histopatholgy likely to be in this patient.
e) Mention 1 late sequelae that often occurs in such patients.
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

20. 6 year old female child presented with fever, puffiness of face and decreased urine output for

PAT H O L O G Y
two days. The child gives a h/o sore throat 3 weeks back.
a) What is the provisional diagnosis?
b) What is the etiology?
c) What investigations will you do?
d) Mention 3 urinary findings.
e) Mention 3 tests to be done in this patient to find out the urinary abnormality.
f) Mention imp light microscopic features in renal biopsy of this case.

21. 52 year old hypertensive male complains of sudden onset of severe retrosternal chest pain
and sweating. O/E rapid and feeble pulse with cold extremities.
a) What is your diagnosis?
b) Describe the gross morphological changes in this condition
c) What are the microscopic changes in this condition.
d) What are the markers for diagnosis?
a) What is your provisional diagnosis?
b) What relevant investigations will you do?
c) What is the histological type of this lesion?
d) What are the morphological patterns seen
in this condition.
e) Describe the grading of this condition.

PA P E R S 28. A 3 year old boy presented with severe anemia and failure to thrive. His frontal bones were
prominent, Hb- 4gm%, TC10,000/cu.mm
a) What is the clinical diagnosis?
b) Give two investigations to confirm the diagnosis?
c) Describe the blood picture.
d) Pathogenesis

29. A 43 yr old man presents with c/c cough 2 months duration ,evening rise of temp,weight loss
and occasional blood staining of sputum. X-ray revealed a patchy opacity at the apex of the right
lung.
a) What is the clinical diagnosis?
b) How will you classify this condition?
c) What are the primary sites of this lesion? (Lungs, intestine, tonsil, skin, conjunctiva) l
d) Name the best specimen for culture.
u
e) Describe the pathogenesis of this condition.
m
30. 65 year old female came to the medical OPD with complaints of macroglosia of 2 years du- i
ration and slurring of speech. O/E Pallor (+). No organomegaly or lymphadenopathy. ESR – 100
n
mm in 1st hour. Biopsy from tongue- Microscopy showed irregular, homogenous pink material
deposited in the sub epithelial region and vessel wall. Bone marrow trephine biopsy – Plasma a
cells 5% i
a) What is the provisional diagnosis? r
b) How will you confirm the diagnosis?
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

c) Classify the diseases

d) Describe the etiopathogenesis of the commonest type seen in developing countries.
PAT H O L O G Y

• Complications: rupture & fatal hemor-

GROSS SPECIMENS rhage, compression of adjacent structures
(ureter, vertebral bodies), thrombo embo-
1. Gangrene Foot lism, distal ischaemia
• Amputated specimen of foot showing dry • Disorders associated with aneurysm –
shrunken, shrivelled and dark appearance Atherosclerosis > Hypertension
of big toe with marked demarcation be- • Syndromes associated with aneurysm-
tween gangrenous and normal areas. Marfans syndrome, EhlerDanlos syndrome
• Gangrene- massive necrosis with super
added putrefaction.
• Types, causes,diff b/w wet and dry gan- 4. Atheroma Aorta.
grene • Cut opened specimen of a portion of aor-
ta, internal surface showing raised yellow-
2. Calcinosis Cutis ish white plaques and ulcerated areas.
• C/S showing skin with underlying patches • Common sites – Abdominal aorta> tho-
of chalky white deposits. racic aorta> coronary arteries> popliteal
• 2 types of pathological calcification: dys- artery> internal carotid artery> vessels of
trophic and metastatic circle of Willis
• Dystrophic - dead and dying tissues. No • Fatty dots &streaks – Earliest change
hypercalcaemia. E.g.; in atherosclerotic • Atherosclerotic plaque components – Fi-
patches brous cap, Cellular area, Soft core QUESTION
• Special stains- vonkossa, Alizarin red, • Risk Factors of atherosclerosis- Hy-
osmic acid stain pertension, Dyslipidemia, Increasing
• Psammoma bodies - spherules of calcifi- age, male sex, Lipoprotein A levels
cation in some tumors like meningoma, • Complications: Erosion,Ulceration,
papillary serous cystadenocarcionma of Rupture, Hemorrhage into plaque
ovary and papillary serous carcinoma of ,Aneurysmal dilation,Thrombosis
thyroid. • Consequences: MI, cerebral infarc-
• Metastatic; occur in association with tion, Aortic aneurysm, peripheral
hypercalcaemia. Calcium gets deposited vascular disease.
in living and healthy tissue, sites: kidney,
stomach, lungs, BV,cornea.
5. Mural Thrombus - Heart:
l
• Cut open heart showing solid mass of
u 3. Aneurysm Aorta With Thrombus thrombus attached to endocardial surface
m • Specimen heart with dialated aorta. Cut near apex of ventricle.
section showing brownish thrombus filling • Thrombosis is defined as the formation
i
lumen. of clotted mass of blood within the intact
n • Aneurysm is defined as any permanent ab- CVS during life.
a normal localized dilation of a blood vessel • Pathogenesis: Virchow‘s triad, Lines of
or heart Zahn
i
• Sites: large arteries (esp. abdominal aorta • Embolus: An intravascular solid, liquid or
r below renal artery and above bifurcation) gaseous mass
e
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• Types of thrombi: mural, arterial &venous -according to presence or absence

(Diff. b/w arterial & venous thrombi) of infection - bland and septic.

PAT H O L O G Y
Fate: Propagation, Embolisation, Dissolution, • Type of necrosis seen in infarct- coagula-
Organization, Recanalisation. tive (but in brain - liquefactive)
• Causes of infarction: interrupted blood
6. Lymphoma supply(ischemic );venous(stagnant hypox-
• 2 types - Hodgkin‘s disease &non Hod- ia); thrombosis; embolism; non occlusive
gkin‘s lymphoma circulatory insufficiency.
• Hodgkin‘s –localized, extra nodal involve-
ment rare. Ann Arbor staging 9. Amyloid Spleen
• RS cell-types (Popcorn – Lymphocyte pre- • Types of amyloid spleen:
dominant, Lacunar – Nodular Sclerosis, • 1. sago - amyloid deposition limited to
• NHL- involves multiple nodes, extra nodal splenic follicles resembling sago grains.
involvement –common • 2. Lardaceous: deposition in splenic
sinuses and connective tissue in red pulp,
fusion of deposits gives rise to map like
7. Fibrinous Pericarditis (White Heart) areas of amyloid.
• Specimen of heart shows white flaky ap- • Amyloid liver – Specimen of liver showing
pearance. pale waxy grey appearance (deposition
• Fibrinous exudate is formed on the surface starts in the Space of Disse)
of the 2 layers of pericardium and gives a • Special stains (microscopy) – Congo red,
“bread and butter appearance” when the Thioflavin T;
two layers are seperated. • Gross – Lugol‘s Iodine -mahagony brown
PA P E R S C auses - a/c MI, Rheumatic fever, Dressler‘s colour,Sulphuric acid - Blue
syndrome, uraemia, chest radiation, SLE,
10. Cvc Spleen
8. Infarction Spleen • Specimen showing C/S of enlarged, tense
• Specimen showing cut section of spleen and cyanotic spleen.
with wedge shaped pale infarct. • Etiology: RHF, portal hypertension, from
• Causesof splenic infarct- thrombo embo- liver cirrhosis.
lism arising in the heart, obstruction of • Histological features: sinuses are dilated
microcirculation (e.g. in myeloproliferative and congested, foci of recent h‘age
diseases, sickle cell anaemia, arteritis, Hod- • Gamnagandy bodies (Siderofibrotic nod-
gkin‘s disease) ules) - scar tissue laden with Ca,Fe.
• Hereditary disease in which splenic infarc- • Special stains: Prussian and Von kossa.
tion is seen - sickle cell anemia (auto-sple- l
nectomy) 11. Lobar Pneumonia
• Infarction - ischaemic tissue necrosis u
• Specimen of lung showing widespread
caused by occlusion of either arterial fibrinosuppurative consolidation, affected m
supply or venous drainage in a particular part pale with greyish homogenous dry i
tissue. surface
• Types: according to colour— n
• Etiology: staphylococcus, pneumococcus,
-white/anemic- spleen, kidney, klebsiella. a
heart • Stages: 1. stage of congestion i
-red/h‘ gic-intestine, ovarian tor- ·· 2. Stage of red hepatisation r
sion, lung ·· 3. Stage of grey hepatisation e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

·· 4. Stage of resolution Hydatid cyst.

• Complications: lung abscess, partial heal- • How to distinguish between lung abscess
PAT H O L O G Y

ing, organization, empyema, bacteraemic and other cavitary lesions? -Lung abscess is
dissemination to pericardium, brain, kid- a localized area of lung tissue with sup-
neys, heart valves. puration. There will be air fluid level also
• Carnification: Post pneumonic fibrotic within the abscess cavity due to pus collec-
reorganisation. tion.

12. Pulmonary Embolism 14. Caseating Tb Lymphadenitis:

• Occlusion of pulmonary tree by thrombo- • Cut section of enlarged lymph node,
embolism capsule is thickened, c/s showing multi-
• Causes: ple grey white areas with necrosis at the
1. thrombi originating from large veins from centre.
lower legs, • Diff from Hodgkin‘s lymphoma: TB-mat-
2. thrombi in varicosities in superficial veins ted, firm nodules with skin involvement.
of leg and pelvic veins HL -discrete, knotty nodules with no skin
• Consequences: sudden death, corpulmo- involvement
nale, pulmonary infarction, pulmonary • Matting of nodules due to PERIADENITIS
h‘ge, resolution, pulmonary hypertension, • Complications – cold abscess, c/c non
pulmonary atherosclerosis. healing sinus, disseminated TB.
• Paradoxical embolism; may occur by pas- • Investigations - CXR, FNAC lymphnode,
sage of an embolus from right heart to left Mantoux test, TB PCR
heart through atrial or ventricular septal • Common lymph node groups affect- QUESTION
defect. In this way pulmonary emboli may ed- Hilar, Cervical, Mesentric
reach systemic circulation
15. Lung Abscess:
13. Fibrocaseous Tuberculosis: • Specimen of lung showing an abscess
• Pneumonectomy specimen with destruc- cavity with shaggy wall and fibrosis
tion of lung parenchyma producing mul- • It is a local suppurative process with
tiple irregular cavities, lined by caseous necrosis of lung tissue.
material. • Organisms causing- Streptococci,
• 5 primary sites of TB – lung, intestine, staphylococci, other gram -ve organ-
tonsil, conjunctiva, skin. isms.
• Consequences of progressive pulmonary • Complication: Amyloidosis, exten-
l TB – fibrocaseous cavity, miliary TB, tu- sion to pleura, dissemination.
berculous bronchopneumonia.
u 16. Bronchogenic Carcinoma Lung:
• Complications: dissemination, hemor-
m rhage, Amyloidosis. • Pneumonectomy specimen- greyish white,
i • Lung parenchyma destroyed, dystrophic poorly circumscribed firm to hard lesion
calcification maybe seen. Right lung com- ,with focal areas of h‘ge and necrosis.
n • Etiology.- smoking, atmospheric pollution,
monly affected. Cavity formed as a result of
a caseous necrosis. asbestosis, dietary and genetic factors,
i • Cavitary lesions of the lung: pulmonary chronic scarring
TB, lung abscess, bronchiectasis, broncho- • Age group- 40- 70
r
genic carcinoma, congenital cysts of lung, • Metastasis: direct, lymphatic and hema-
e
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togenic spread, prognosis generally poor,

• Histological types: squamous cell carci-

PAT H O L O G Y
noma(25-40% in smokers), adenocarci- 19. Retinoblastoma
noma(25-40% most common in women • C/S showing eye showing grayish white
and non smokers), small cell carcino- mass within the retina, lesion could be
ma(20-25%), large cell carcinoma(10-15%) partly necrotic, partly solid (Tumor may be
• Paraneoplastic syndromes: 1. ectopic endophytic or exophytic)
hormone production.(Cushing‘s syndrome, • Most common intra-ocular malignancy of
hyponatremia, hypercalcaemia, gynae- children.
comastia, carcinoid syndrome) 2. other • 60% sporadic, 40% familial
systemic manifestations (polymyositis, • Knudson‘s two hit hypothesis
myopathy, clubbing, acanthosisnigricans, • Cell of origin: neuroepithelial cells in pos-
trousseau‘s syndrome) terior retina.
• Sites of metastasis- adrenals(>50%), liver, • Types of rosettes: Flexner- Wintersteiner,
brain, bone Homer Wright
• Worst prognosis - Small cell carcinoma • Other rosettes showing tumors: neuroblas-
• Best response to chemo & radiotherapy – toma, medulloblastoma
Small cell ca • Types of RB: autosomal dominant and
autosomal recessive
• Increased risk of developing osteosarcoma
17. Hydatid Cyst: • Trilateral retinoblastoma – Bilateral retino-
• Cystic space seen in lung, inner surface is blastoma + Pinealoblastoma
smooth and contains a whitish translucent • Spread – locally (vitreous, retina, optic
PA P E R S membranous material. - Tender coconut nerve, brain), blood (bone marrow)
appearance.
• Etiology- Echinococcusgranulosus (dog
tape worm)
• Other sites: liver, kidney, eye, brain, bone, 20. Tuberculous Ulcer-INTESTINE
spleen • Section of intestine showing narrowing and
• Complications: anaphylaxis on cyst rup- stricture formation in the intestine with a
ture. dilated proximal segment. Mucosa shaggy
• Diagnosis by Ultrasound, IgM ELISA test, and ulcerated.Lossof normal mucosal folds.
Casoni‘s intradermal test. • Lesion begin in the Peyer‘s patches or
lymphoid follicles with formation of small
18. Lipoma ulcers that spread through the lymphatics
• Well encapsulated, round to oval mass, C/S to form large ulcers which are transverse to l
shows smooth, yellowish, greasy appear- the long axis of the bowel. The ulcers may
be coated with caseous materials. Serosa u
ance
• Most common soft tissue tumor of adult- may be studded with visible tubercles. m
hood • Complication: transverse fibrous strictures i
• Classified based on particular morpho- and intestinal obstruction.
• Causes of ulcer intestine-TB, typhoid, n
logical features like conventional lipoma,
fibrolipoma, angiolipoma, myelolipoma, yersinia, peptic ulcer, malignancy, carci- a
spindle-cell lipoma etc. noid, amoebiasis i
• Special Stains - Sudan III, Sudan IV, Sudan
r
black, oil red O, Osmic acid.
e
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21. Typhoid Ulcer-Intestine out lesion with clear base and mucosal
• Segment of resected small bowel showing folds converging towards the ulcer.
PAT H O L O G Y

thinned out mucosa with surrounding • Aetiology: disruption of the mucosal bar-
mucosal folds. rier, gastritis, bile reflux, alcohol, tobacco.
• Ulcer-longitudinal • Sites :first part of duodenum, pyloric
• Complication: perforation of ulcer, haem- antrum, gastroeosophageal junction in
orrhage. GERD or Barret esophagus, jejunum in
Zollinger Ellison syndrome( in addition to
22. Amoebic Ulcer duodenum & stomach), Meckel‘s divertic-
• Segment of colon showing multiple ulcers ulum.
on the mucosal surface. The ulcers have • Complication: perforation, h‘age, obstruc-
overhanging ragged edges and are covered tion, malignant transformation.
with necrotic tissue. Mucosa between the • Histology from within outwards:
ulcers is not involved. • Zone of necrotic debris
• Early intestinal lesions appear as small area • Zone of non specific inflammation
of elevation on the mucosal surface. In • Granulation tissue zone
advanced cases typical flask shaped ulcers • Zone of fibrosis
having narrow neck and broad base are
seen.
• Most common site- caecum 25. Carcinoma Stomach
• Complication: amoebic liver absecess, • Gastrectomy specimen showing an ulce-
perforation, haemorrhage, and formation of ro-proliferative growth, ill defined border
amoeboma. with irregular papillary projections.Floor
• Diagnosis – demonstration of trophozoite/ is shaggy and necrotic. QUESTION
cyst in stool. • Risk factors: H. pylori infections, c/c
• Special Stain – Gomorri-Trichrome, Fe- gastritis, gastric adenomas, perni-
hematoxylin stain to demonstrate amoeba. cious anemia.
• Early gastric Ca – confined to mu-
cosa & sub-mucosa with or without
lymph node involvement
23. Gangrene Intestine • Advanced gastric Ca.,Linitis plastic
• Coiled loop of intestine with black disc- (leather bottle stomach), Krukenberg
olouration, wall oedematous with loss of Tr., Sister Mary Joseph Nodule
normal mucosal folds, surface is shaggy. • Lauren‘s classification (Intestinal &
• Causes- occlusion of superior mesenteric Diffuse); WHO histological classifi-
l artery, other causes: volvulus, intussus- cation
ception, inferior mesenteric vein throm-
u bus. 26. Intussusception
m • Why does haemorrhagic infarction occur • Specimen showing cut open section of
i in the intestine? = Intestine is a soft tissue portion of intestine with telescoping of
and it has dual circulation a segment of intestine into the segment
n
below. It occurs due to peristalsis of the
a telescoped segment. The telescoped seg-
i 24. Gastric Ulcer ment is called intussusceptum& the lower
• Specimen of cut section of stomach show- receiving part is called the intussuscepiens.
r
ing solitary, small round to oval, punched • Causes: foreign bodies & tumors [adults],
e
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enlargement of lymphoid tissue in ter- half stained with Pearl‘s stain

minal ileum mostly due to viral infection • Hemochromatosis is a condition in which

PAT H O L O G Y
[children] systemic overload of iron in the form of
• Types: ileocolic ,ileoileocolic, colocolic the hemosiderin pigment occurs
• Complications: obstruction, infarction, • Types: Primary [hereditary], Second-
gangrene, perforation, peritonitis ary[acquired]-due to thalassemia, sid-
• Signs & symptoms- Mass in the abdo- eroblastic anemia, multiple transfusion,
men, bleeding PR, other symptoms of a/c alcoholic cirrhosis.
obstruction. • Sites : skin, liver, pancreas, heart, pituitary,
joints (testicular atrophy occurs d/t pitu-
27. Familial Polyposis Coli itary involvement)
• Gross: Cut open segment of colon with
the lumen showing homogenous brownish 30. Fatty Liver
and yellowish areas studded with multiple • Cut section of enlarged liver, bright yellow
polyps colour and soft greasy feel.
• APC gene mutation, chromosome 5q21 • Fatty change (Steatosis) occurs due to
• Risk of early development of Ca. Colon abnormal accumulation of triglycerides
• Prophylactic colectomy advisable within parenchymal cells.
• C/S: Homogenous, brownish, & yellowish. • Special stains: Sudan III, Sudan IV, Oil red
• Types: Non neoplastic :Hamartomatous, O, Osmic acid.
Inflammatory, Lymphoid, Hyperplastic – • Other organs affected- heart, skeletal mus-
Neoplastic: Benign adenomas and malig- cle, kidney
nant polypoid Ca. • Causes: Alcohol, CCl4, OCPs, Obesity,
PA P E R S Bacterial toxins
28. Acute Appendicitis • Types: ileocolic ,ileoileocolic, colocolic
• Specimen of appendix showing oedema- • Complications: obstruction, infarction,
tous walls, ulcerated mucosa and blackish gangrene, perforation, peritonitis
exudates on surface. • Signs & symptoms- Mass in the abdomen,
• Stages: early acute, acute suppurative, bleeding PR, other symptoms of a/c ob-
acute gangrenous struction.
• Causes: obstructive (fecolith, calculi, for- •
eign bodies, tumor, worms), non-obstruc-
tive (vascular occlusion, diet)
31. Cirrhosis Liver
• Specimen of portion of liver having sur-
• Pathogenesis: Obstruction-- Continued
face studded with numerous nodules. Cut
mucus secretion--Increased intraluminal
surface is nodular and greasy with firm l
pressure-- Collapse of draining veins--
consistency( due to fibrosis)
Ischaemic injury-- Bacterial prolifera- u
• Cirrhosis is the end stage of c/c liver dis-
tion--Inflammatory edema and exudation
ease characterised by : m
• Complications: peritonitis, appendicular
■■ a. Bridging fibrous septae i
abscess, adhesions, mucocele.
■■ b. Parenchymal nodules encircled by fibrosis
C/F – fever, vomiting, right sided abdominal n
■■ c. Disruption of liver architecture
pain and tenderness (at Mc Burney‘s point)
• Types:Micronodular, Macronodular, mixed a
• Etiology: Alcoholic liver disease, viral hep- i
29. Hemochromatosis Liver
atitis, biliary disease, wilsons disease.
• Cut section of liver, one half shows ho- r
• Complications: portal hypertension, hepat-
mogenous brownish appearance, other e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

ic failure, hepatocellular Ca • Risk Factors- Female gender, OCPs, preg-

nancy, obesity, biliary infection
PAT H O L O G Y

• Complication: cholecystitis, gall stone ile-

32. Cavernous Angioma Liver us, biliary fistula, mucocoel, gallblader Ca.
• Section of liver with fairly well demarcated
blackish discolouration occupying the one
region. 36. C/C Cholecystitis
• Types of hemangiomas – Cavernous, capil- • One half of cholecystectomy specimen cut
lary, pyogenic granuloma opened, wall thickened, lumen dilated, and
• Other sites – skeletal muscles, bones, lips, shows
tongue, face,brain two calculi.
• Malignant counterpart - Hemangiosarco- • Mucosa shows brownish discolouration,
ma . shaggy serosa.
• Complication: obstructive jaundice,
cholecystitis, biliary cirrhosis, cholangitis,
33. Amoebic Liver Abscess mucocele.
• Section of liver shows large cystic cavi-
ty with irregular thickened shaggy inner
lining, normal compressed tissue at the 37. Granular Contracted Kidney
periphery. • Bisected kidney. Capsule from surface
• Cause: Entamoebahistolytica is peeled off. Exposed cortical surface
• Special stain: PAS, Gomorritrichrome, Fe shows fine granularity. Kidney as such is
hematoxylin. decreased in size. Cut surface shows de-
creased size of renal cortex and slight QUESTION
dilatation of calyces.
34. Carcinoma Liver • Causes: c/c glomerulonephritis, c/c
• Section of liver showing fairly well circum- pyelonephritis, diabetic nephropathy,
scribed grey white mass, periphery shows nephrosclerosis.
compressed liver tissue.
• Etiology: HBV infection, c/c alcoholism,
food contaminants (aflatoxin). 38. Pyelonephritis
• Morphological types: Unifocal, multifocal, • Section of kidney, capsule adherent.
diffusely infiltrating C/S shows yellowish black areas with
• Tumourmarkers : AFP, Des-gammacar- irregular scarring and distended caly-
boxyprothrombin, Alk. PO4ase ces with focal abscess
• Types: Acute and chronic.
l • Variant: fibrolamellar carcinoma which
• Causes: UTI [E.coli, Enterobacter, Klebsi-
occurs in the absence of cirrhosis or HBV
u ella, Proteus], obstructive pyelonephritis
infection, has good prognosis.
m • Complications: papillary necrosis, pyone-
phrosis, perinephric abscess.
i • Variant of c/c pyelonephritis- xanthogran-
35. Gall Stones
n ulomatous pyelonephritis.
• Types: cholesterol, pigment stones
a • Pathogenesis: Cholesterol super-saturation
i in bile and enucleation (cholesterol stones);
39. Hydronephrosis
r Increased bilirubin forming calcium salts • Cut opened kidney which is enlarged and
e (pigment stones)

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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

having dilated pelvis and calyces with 43. Nephroblastoma

thinned out renal cortex. • Specimen of kidney showing a solitary well

PAT H O L O G Y
• Cause- Obstruction to outflow of urine, circumscribed mass.Cut surface is soft,ho-
eg: stricture,calculi, prostatic hypertrophy, mogenous and tan to grey with occasional
tumors foci of haemorrhage,cyst formation and
• Complications: glomerular atrophy, renal necrosis
papillary necrosis, pyelonephrits. • lt is the most common primary renal tu-
mor of childhood.
• Classical triphasic histology – blastemal,
40. Polycystic Kidney stromal & epithelial cell types.
• C/S shows multiple cysts of varying size • Syndromes associated – WAGR syndrome,
• Inheritance type: adult type- autosomal Denys-Drash syndrome, Beckwith Weid-
dominant; infantile- autosomal recessive mann syndrome, Miller syndrome
• The cyst do not communicate with the • C/F-abdominal mass,hematuria,pain in
pelvis of kidney- a feature that helps to abdomen,intestinal obstruction.
distinguish polycystic kidney from hydro-
nephrotic kidney on sectioned surface. 44. Carcinoma Kidney (Renal Cell Carcino-
• Associated lesions: cysts in liver and pan- ma/Grawitz Tumour)
creas; colonic diverticula, berry aneurysm, • C/S of kidney showing spherical masses
MVP (in adult type) of bright yellow/grayish white tissue that
• Complication: nephrosclerosis, fibrosis distorts renal outline with foci of h‘age,
and c/c inflammation. necrosis and areas of softening (variegated
appearance)
41. Calculus Kidney • Causes: cigarette smoking, obesity, hy-
PA P E R S
• Cut opened kidney, showing calculi occu- pertension, long term dialysis and family
pying pelvis, surface has brownish gran- history (von Hippellindau syndrome,
ules, cortex grossly granular.
hereditary papillary ca.)
• Types: Calcium stones[75%], mixed
• Histo types: clear cell (most common),
stones[struvite]-l5%, Uric acid-6%, Cys-
papillary, chromophobe, collecting duct.
tine-2%.
• 3 classical features – costovertebral pain,
• Struvite stones are formed after infection
palpable mass and hematuria
by urea splitting bacteria
• Spread: hematogenous and local.
• Complications: Hydronephrosis and he-
• Paraneoplastic syndromes: polycythemia,
maturia.
hypercalcemia, hypertension, feminization,
• C/F: renal colic, hematuria,
masculinization
42. Staghorn Calculus (With Hydronephro- l
sis) u
• Cut opened kidney with dilated calyces 45. Carcinoma Penis
• Specimen of Penis with scrotum, distal end m
and pelvis, a large brown white calculus
creating of penis shows exophytic growth encircling i
a cast of pelvicalyceal system the shaft.
n
• Composition: magnesium ammonium cal- • Premalignant lesions: Bowens disease,
cium phosphate[triple phosphate stones] bowenoidpapulosis. a
• Etiology, urinary tract infections with urea • Etiological factors: Unidentified carcino- i
splitting organisms like proteus. gens contained in smegma, HPV 16, 18
r
• Commonest type: squamous cell carcino-
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

ma. • Screening – Pap smear

• Types of HPV producing Ca Cervix: low
PAT H O L O G Y

risk-6 & 11; high risk-16; 18,31

46. Seminoma Testis
• Enlarged testis, C/S shows homogenous 49. Teratoma
grey white lobulated tissue; h‘age, necrosis • Teratoma are tumors composed of dif-
not seen. ferent types of tissues derived from three
• Commonest germcelltumour of testis and germ layers - ectoderm, mesoderm, endo-
corresponds to dysgerminoma of ovary. ( derm in different combinations.
peak incidence in 40‘s) • Types: Mature(benign), Immature(malig-
• Tumour markers: AFP, HCG. nant), monodermal or highly specialised
• Tumour cells +ve for PAS due to glycogen. teratomas.
• Sheets of uniform cells divided into lobules • Benign Cystic Teratoma(Dermoid Cyst) -
by delicate fibrous septa unilocular cyst lined by skin
• Types: Typical( 85%), Anaplastic(5-10%), • C/S-Unilocular Cyst filled with sebaceous
Spermatocytic. secretions & desquamated keratin ad-
mixed with masses of hair, tissue elements
47. Endometrial Carcinoma such as tooth, bone, cartilage. Cyst wall is
• Gross: 2 patterns – diffuse(more common) thin and opaque grey white. In one area of
or polypoid, tumor protrudes into endo- the cyst wall, a solid protuberance (Roki-
metrial cavity as irregular friable grey tan tansky‘s protuberance) maybe seen.
mass • Other sites: Ovary, testes, mediastinum,
• Extension into myometrium maybe seen as retro peritoneum, sacrococcygeal region.
soft, friable granular tissue on c/s • Classification of Ovarian Tumors QUESTION
• Peak age: 55 – 65
• Risk factors : DM, HTN, Obesity, Infertil- 50. Adenomyosis
ity • Gross: Enlarged uterus showing
• C/F: irregular vaginal bleed, excessive diffuse thickening of uterine wall
leucorrhea sometimes with areas of reddish
• Diagnosis by curettage and histological brown discolouration within the
examination myometrium
• Presence of endometrial tissue in the
myometrium
• C/F: dysmenorrhoea, abnormal
48. CARCINOMA CERVIX. bleeding, menorrhagia.
l • Section of uterus, both lips of Cervix
shows greyish white necrotic growth. 51. Leiomyoma Uterus
u • Risk factors: early age sexual activity,high • Gross: distorted specimen of uterus, with
m risk male sexual partner such as promis- circumscribed discrete round firm grey
i cous male having history of penile condy- white mass, in a whorled pattern.
loma, multiparity, venerallytransmissable • Leiomyomas/Fibroids-common uterine
n infections. tumor of smooth muscle origin.
a • Most common histological type – squa- • Cause: estrogen, human growth hormone,
i mous cell carcinoma Infertility, estrogen dependent tmr.
• Morphologoical Types: fungating, ulcer- • Types: subserosal, submucosal, intramural
r ative and invasive. • Other sites- esophagus, erector pili mus-
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

cles of skin , nipple, scrotum, labia • Most common benign tumor of breast.,
• 2° Changes- cystic change, myxomatous arises from intra lobular stroma.

PAT H O L O G Y
change, pathological calcification, red de- • Also called ‘mouse-in-breast‘ as its a mo-
generation, hyaline change bile lump.
• Complications: torsion, inversion, capsule • DD‘s - c/c abcess, fat necrosis, Ca breast
rupture, inflammatory changes, associa- • Cytosarcomaphyllodes: bulky breast tumor
tion with endometrial carcinoma. with leaf like gross appearence.
• Phyllode‘stumour histologically distin-
52. Uterus With Vesicular Mole
guished fromfibroadenoma by cellularity,
• Gross: hysterectomy specimen, cut open
mitotic rate & infiltrative borders
uterus, endometrium dilated & filled with
friable,delicate, thin walled translucent
small vesicles forming a cluster(like a
55. Carcinoma Breast With Secondaries In
bunch of grapes)
Lymph Nodes
• significant investigation -urine hcg exam-
ination. • C/S of breast( identify nipple) showing
grey white firm to hard granular growth
• Hydatidiform mole characterised by 2
with irregular borders.
features-hydropic change of chorionic villi
• Types- non-invasive[intra-ductal Ca, Lob-
& trophoblastic proliferation.
ular Ca in situ], invasive[invasive ductal,
• Complications-trophoid disease, chorio-
invasive lobular, medullary Ca, tubular,
carcinoma.
mucinous, papillary]
• Classification-(l) non-invasive mole-com-
• Aetiology: sex, age, genetic (BRCA1,
plete& partial (2)invasive mole
BRCA2), diet, endocrine, geographical,
(chorioadenomadestruens)
PA P E R S mammary dysplasia.
• Spread: lymphatic, local, blood stream.
• Lobular breast Ca- Bilateral, Indian file
53. Choriocarcinoma-Uterus
appearance
• Gross-Cut section of uterus with cervix
• ScirrousCa-infiltrating ductal carcinoma-7
.Endometrial cavity filled with necrotic,
5% of all breast cancer, hard in consistency.
friable, blackish appearing growth, infil-
• Inflammatory Ca-breast cancers with
trating the myometrium.
redness, oedema, tenderness and rapid en-
• Causes-Hydatidiformmole(50%), nor-
largement. Associated with excessive inva-
mal pregnancy (22%), previous abortion
sion of dermal lymphatics; poor prognosis.
(25%), remainder occur in ectopics and
• Paget‘s d/s of nipple -rare type of breast Ca,
genital teratomas.
presents as unilateral erythematous erup-
• Types-(l) gestational {placental origin} (2)
tion with a scaly crust. l
non-gestational (ovarian origin}
• Clinical staging & prognostic factors
• Tumor marker-HCG u
• Sites of metastasis-lungs (50%), vagina m
56. Malignant melanoma skin/eye/rib
(40%), brain, liver, kidney.
• Blackish deposit with intervening necrotic i
areas.
n
• Arise from melanocytes, most rapidly
54. Fibroadenoma
spreading malignant tumor of skin a
• C/S-well circumscribed grey white spheri-
• aetiology: excessive exposure of sunlight i
cal / discoid mass with slit like spaces.
esp. To white skin. r
• Types-pericanalicular, intracanalicular.
• Predisposing factors: naevi, heredity and
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local host immune response.

• Sites: skin {trunk, legs, face, soles, palms 59. Malunion
PAT H O L O G Y

and nail bed), oral and anogenital mucosa, • Two pieces of bone covered by muscle
oesophagus, conjunctiva, uveal epithelium, fibre; Malunion means that the fracture
orbit and leptomeninges. has united in a position of deformity with
• Four types of cutaneous melanomas: angulation, rotation or over riding of the
lentigomalignant melanoma, superficial fragments, results from imperfect reduc-
spreading melanoma, a lentigenous mela- tion and failure to stabilise a previously
noma, nodular melanoma. satisfactory reduction.
• Histology: tumor cells resembling epithe- • Other complications of fractures: fibrous
liod cells with pleomorphic nuclei and union, pseudoarthrosis, non-union, de-
prominent nucleoli are seen solid masses layed union.
in the dermis. Multinucleate giant cells
and mitotic figures are often present. 60. Sequestrum
• Special stain – masson‘s fontana • A tubular piece of bone, cortex shows
marked sclerosis.
57. Basal cell carcinoma • Dead piece of bone formed due to com-
• gross : common pattern is nodulo-ulcer- bination of suppurartion and ishaemic
ative type with a pearly/dark translucent injury in pyogenic osteomyelitis
colour and a network of fiery red blood • Complication: C/c osteomyelitis, amyloi-
vessels on the surface, the surface may dosis
ulcerate with melanin pigmentation. • Formation of the reactive new bone as an
• Sites: upper part of face - cheek, nose and encasing sheath around the necrosed bone
ear. ( Above a line joining tip of ear and - Involucrum. QUESTION
angle of mouth) • Long continued osteogenesis give
• histology: dermis invaded by irregular rise to dense sclerotic pattern of os-
mass of basaloid cells with characteristic teomyelitis called c/c sclerosing non
peripheral palisaded appearence . suppurartive osteomyelitis of garre.
• Highly radio sensitive, does not metasta- • Brodie‘s abscess: occasionaly a/c
sise osteomyelitis may be contained to lo-
• aetiology - chronic sun exposure, immu- calised area and walled off by reactive
nosuppression, defective dna repair bone.
• associated with gorlin‘s syndrome (ptch
gene mutation – nevoid bcc syndrome)
61. Osteogenic sarcoma
l 58. Squamous Cell Carcinoma Foot • Fusiform greyish white tumor involving
• Specimen of foot showing greyish white metaphyseal end and destroying sur-
u rounding cortex, epiphysis free, periosteal
warty growth having cauliflower appear-
m ance elevation.
i • Types : Ulcerating, Fungating, Invasive • Most common primary malignant tumor
• Risk factor: Sun exposure, industrial car- of bone.Characterised by formation of
n osteoid, bone or both, directly by sarcoma
cinogens, chronic ulcers, old burns, scars,
a AIDS cells.
i • Sites: Skin and mucosa of lip, tongue, • Bimodal age distribution – 10 – 20 yrs and
pharynx, oesophagus, vocal cord, anal also in elderly
r
region, vagina, ducts of glands etc • Cells of origin: primitive osteoblast form-
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ing mesenchyme. of ophthalmopathy and dermatopathy.

• Site: lower end of femur, upper end of tibia, • Two forms: simple goitre (diffuse nontox-

PAT H O L O G Y
upper end of humerus and femur. ic/colloid) & nodular goitre (MNG adeno-
• X ray pattern: codman‘s triangle and sun- matous goitre)
burst appearence. • Section from thyroid showing uniform en-
• Two main categories: medullary and cen- largement of the gland.. C/S: greyish white,
tral, parosteal or cortical osteosarcom. with faint lobulation showing salivary
• Associated with hereditary retinoblastoma. gland like appearance.

65. Hashimoto’s Thyroiditis

62. Osteochondroma • Diffuse goitrous enlargement of thyroid,
• Eccentric epiphyseal expansile growth con- lymphocytic infiltration of thyroid, Oc-
tinuous with the cortex of bone. currence of auto antibodies are 3 principle
• Commonest benign tumor of cartilage, features of hashimoto‘s thyroiditis.
may occur as a solitary, sporadic, exostosis • Also called chronic lymphocytic thyroiditis
or multiple hereditary exostosis. (age group – 45 -65)
• Sites: metaphysic of long tubular bones - • HLA association-HLA DR5, HLA DR3.
lower femur, upper tibia, upperhumerus. • Microscopy: loss of architecture, follicles
• Age: late childhood and adolescence atrophied, lymphoid follicles, degeneration
• EXT gene association of follicular lining cells.
• Hurthle cells and fibrosis present. Hurthle
63. Giant Cell Tumour Of Bone cells (askanazy/ oxyphil/ oncocytes) are
• Gross: lower end of femur hemisection, follicular epithelial cells which undergo
PA P E R S grey white friable, expansile growth involv- metaplastic change- abundant oxyphilic
ing epiphysis. Thinned out shell of bony granular cytoplasm due to large number of
cortex.Area of H‘ages seen. mitochondria, large bizarre nucleus.
• It is benign tumour with malignant poten- • Most common antibody- thyroid microso-
tial. (age group – 20 – 40yrs) mal auto antibody. Other autoimmune d/s
• Soap bubble appearance in X-ray. associated with H‘s thyroiditis- pernicious
• Tumor arises from epiphysis of long bone anemia, SLE, rheumatoid arthritis, IDDM,
close to the articular cartilage. Addison‘s disease, myasthenia gravis.
• Association with malignant lymphoma:
increased risk of developing B-cell non
64. Multinodular Goitre Hodgkin‘s lymphoma,(associated with
• Specimen of enlarged and distorted thy- unregulated helper T cell participation in B
roid showing surface nodules. C/S multiple l
cell synthesis of auto antibodies)
nodules of different sizes filled with colloid • Four type of thyroiditis: hashimotos, u
(brownish). Large nodules may show cystic riedel‘s, sub acute(dequervain‘s), chronic
changes, scarring &haemorhages. m
(silent)thyroiditis.
• Aetiology - Impaired thyroid hormone i
synthesis leads to compensatory rise in se- 66. Thyrotoxicosis n
rum TSH level. This results in compensato- • Enlarged, homogenous, reddish brown,
ry hypertrophy & hyperplasia of follicular a
meaty appearance on fresh sections
cells leading to enlargement of the gland. i
• Causes: grave‘s disease, toxic MNG, toxic
• Plummer‘s disease (toxic nodular goitre): adenoma. r
similar to grave‘s disease but lack features • Jodbasedow thyrotoxicosis: (Jod = iodine) e
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when large doses of iodine is given thera- • Also called chronic lymphocytic thyroiditis
peutically for hyperplastic endemic goiter, (age group – 45 -65)
PAT H O L O G Y

temporary hyperthyroidism and occasional • HLA association-HLA DR5, HLA DR3.

persistent hyperthyroidism may occur. • Microscopy: loss of architecture, follicles
• Conditions producing uniform enlarge- atrophied, lymphoid follicles, degeneration
ment of thyroid: physiological goitre, of follicular lining cells.
colloid goitre, primary thyrotoxicosis, • Hurthle cells and fibrosis present. Hurthle
thyroiditis cells (askanazy/ oxyphil/ oncocytes) are
follicular epithelial cells which undergo
67. Adenoma Thyroid metaplastic change- abundant oxyphilic
• Encapsulated, usually solitary, well cir- granular cytoplasm due to large number of
cumscribed nodule with greyish white mitochondria, large bizarre nucleus.
appearance.H‘age& cyst formation may oc- • Most common antibody- thyroid microso-
cur.Normal thyroid tissue seen at one end. mal auto antibody. Other autoimmune d/s
• Clinically- pressure symptoms, sudden associated with H‘s thyroiditis- pernicious
enlargement and pain due to intra lesional anemia, SLE, rheumatoid arthritis, IDDM,
h‘ge. Addison‘s disease, myasthenia gravis.
• Follicular adenoma is the most common • Association with malignant lymphoma:
type of benign thyroid tumor. increased risk of developing B-cell non
• Features to distinguish from a nodule of Hodgkin‘s lymphoma,(associated with
MNG: solitary nodule, complete encapsu- unregulated helper T cell participation in B
lation, clearly distinguishable architecture cell synthesis of auto antibodies)
inside and outside the capsule, compres- • Four type of thyroiditis: hashimotos, rie-
sion of the thyroid parenchyma outside the del‘s, sub acute(dequervain‘s), chron- QUESTION
capsule. ic (silent)thyroiditis.
• Types: micro follicular(foetal adenoma),
normo follicular(simple adenoma), macro 70. Thyrotoxicosis
follicular(colloid adenoma), trabecular • Enlarged, homogenous, reddish
(embryonal adenoma), Hurthle cell, atyp- brown, meaty appearance on fresh
ical . sections
68. Pleomorphic Adenoma • Causes: grave‘s disease, toxic MNG,
• Section of salivary gland showing a well toxic adenoma.
demarcated, faintly lobulated greywhite • Jodbasedow thyrotoxicosis: (Jod =
lesion. Myxoid& blue translucent areas are iodine) when large doses of iodine is
noted at places. given therapeutically for hyperplastic
l • Section from thyroid showing uniform en- endemic goiter, temporary hyperthyroid-
largement of the gland.. C/S: greyish white, ism and occasional persistent hyperthy-
u with faint lobulation showing salivary roidism may occur.
m gland like appearance. • Conditions producing uniform enlarge-
i ment of thyroid: physiological goitre,
69. Hashimoto’s Thyroiditis colloid goitre, primary thyrotoxicosis,
n
• Diffuse goitrous enlargement of thyroid, thyroiditis
a
lymphocytic infiltration of thyroid, Oc-
i currence of auto antibodies are 3 principle 71. Adenoma Thyroid
r features of hashimoto‘s thyroiditis. • Encapsulated, usually solitary, well cir-
cumscribed nodule with greyish white
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appearance.H‘age& cyst formation may

occur.Normal thyroid tissue seen at one

PAT H O L O G Y
end.
• Clinically- pressure symptoms, sudden
enlargement and pain due to intra lesional
h‘ge.
• Follicular adenoma is the most common
type of benign thyroid tumor.
• Features to distinguish from a nodule of
MNG: solitary nodule, complete encapsu-
lation, clearly distinguishable architecture
inside and outside the capsule, compres-
sion of the thyroid parenchyma outside
the capsule.
• Types: micro follicular(foetal adenoma),
normo follicular(simple adenoma), macro
follicular(colloid adenoma), trabecular
(embryonal adenoma), Hurthle cell, atyp-
ical .

72. Pleomorphic Adenoma

• Section of salivary gland showing a well
demarcated, faintly lobulated greywhite
PA P E R S lesion. Myxoid& blue translucent areas are
noted at places.

l
u
m
i
n
a
i
r
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HISTOPATHOLOGY
PAT H O L O G Y

• Heart failure cells or large macrophages

filled with brown pigment in the alveolar
1. Fatty liver wall and in the lumen.
·· Normal liver cells, central vein, portal triad
are seen. 7. Granulation tissue
• The spindle shaped fibroblasts and loose
·· Liver cells with vacuolated cytoplasm showing
oedematousstroma.
fatty change and washed out appearance.
• The newly formed capillary spaces lined
·· by endothelial cells. Inflammatory cells
2. .Atheroma chiefly polymorphs, round cells and mac-
• intima is thickened and show cleft like rophages.
spaces. Innermost endothelial surface is
damaged 8. Cirrhosis liver
• and show adhesion of rbcs media is • Loss of normal architecture of liver lobules
thinned out and fibrosed. • Central vein is eccentric.
• Liver cells arelarge in size and some are
binucleated. Irregular lobules are separat-
3. Melanoma ed by dense fibrous septa. The portal triad
• epidermis of the skin showing pigment show round cell infiltration.
layden cells in the basal layer.
• The groups of cells extend down into deep- 9. .Acute appendicits
er tissue the cells are polygonal spindle or • The destruction of mucosal lining QUESTION
round and arranged in sheets and contain epithelium in places seen.
pigment • Acuteinflalnrnatory exudates in the
lumen.
4. Calcinosis cutis • Cellular infiltration in the mucosa,
• Epidermis of the skin, blood vessels and muscle coat and serosa.
skin appendages are seen. Deep in the
dermis there are irregular bluish calcified 10. Lobar pneumonia
masses lying in spaces or in the tissue • All alveoli are filled with inflamma-
itself. tory exudates and cells are mainly
polymorphs
5. CVC liver • Clear spaces are seen between alveo-
• The central vein is congested. lar wall and exudates
l • The sinusoids in the centrizonal region
u dilated and congested. 11. Tuberculous lymphadenitis
m • The liver cells are compressed and in the • The thickened capsule at the periphery and
periphery of the lobule show fatty change the subcapsular lymphoid follicles
i and brownish pigments scattered in the • The normal architecture of the lymphnode
n parenchyma. is lost in the centre
a • It is replaced by large homogenous eo-
6. CVC lung sinophilic area of caseation surrounded
i • Thickened alveolar wall and congested by multinucleated Langhans giant cells,
r capillaries epitheloid cells and round cells.
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19. Capillary hemangioma

12. Lepromatous leprosy • Benign vascular tumours

PAT H O L O G Y
• The thinned out and atrophied epidermis of • GROSS-Nodular, polypoidal/ pedunculat-
the skin seen. ed , well circumscribed , red/ blue masses ,
• Clear homogenous zone just beneath the measuring <2cm in diameter
epidermis. • MICRO- small thin walled blood vessels
• The dermis shows diffuse collection foamy lined by plump epithelial cells divided into
macrophages and round cells. lobules by fibrous tissue septa

13. Tuberculous Leprosy 20. Fibroadenoma

• Normal epidermis, • Proliferated elongated dilated or distorted
• Dermis shows granulomatous lesions ducts lined by cuboidal epithelium and the
surrounding stroma shows spindle cells.
14. Rhinosporidiosis • The stroma in places show myxomatous
• The submucosa shows rounded capsulated degeneration and round cell infilteration.
sporangia of variable size.
• The interior of the sporangia shows small 21. Teratoma
rounded spores. • Various types of tissues of tridermal orgin.
• Lobules of cartilage cells, mucus secreting
15. Osteochondroma glands, lobules of fat, hair,muscle, brain,
• The lobules of cartilage cells separated by sebaceous glands etc.
fibrous septa.
• The cartilage cells which are arranged in 22. Pleomorphic adenoma
PA P E R S groups or singly are embedded in a bluish • The pleomorphic appearance of the neo-
homogeneous matrix. plasm.
• Areas of calcification may also be seen. • Epithelial cells arranged in sheets, strands
and acinar pattern and acini show colloid
16. Lipoma like or keratinizing material.
• Lobules of fat cells separated by fibrous • Groups of cartilage like cells arranged in
septa. groups or singly in a homogenous matrix.
• The intervening fibrous septa show blood
vessels and nerve bundles. 23. Basal cell carcinoma The cells are of the
basal cell type with scanty basophilic cyto-
17. Leiomyoma plasm and hyperchromatic nuclei. The cells in
• The endometrium of the uterus with tubu- the periphery shows pallisading arrangement
lar glands lined by epithelium. l
The myometrium showing well demarcat- 24. Adenocarcinoma colon
u
ed cellular areas composed of spindle cells • Normal colon mucosa with an ulcerated
running in interlacing bundles. proliferating growth at one end. m
• Groups of carcinomatous cells with ade- i
18. Schwannoma nomatous pattern are seen infiltrating into
n
• Thickened nerve bundles. the deeper tissue.
• Groups of spindle cells arranged in a pal- a
isading manner separated by nuclear free 25. Osteogenic sarcoma i
zones of eosin stained fibres. • Eosinophilic areas of new bone formation r
with strands of osteoid tissue.
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• Spindle cells, round cells and multinucle- brown areas, white areas and haemorrhagic
ated cells with areas of haemorrhage and / red areas.
PAT H O L O G Y

necrosis. • MICRO- clear cell-clear cytoplasm due

to high content of lipid and glycogen,and
26. Giant cell tumour prominent cell border Granular cell-granu-
• The characteristic multinucleated giant lar due to increase content of mitochondria
cells and cellular stroma composed of spin- Cells are arranged in sheets,nests,cords,tu-
dle cells and oval cells. bular or papillary pattern;separated by
• Plenty of vascular spaces, areas of haemor- fibrous septa Little cellular/nuclear pleo-
rhage, cystic spaces and areas of degenera- morphism or mitosis seen 2º changes-ne-
tion. crosis,fibrosis,cholesterol deposit,heamor-
rhage,calcification,cystic change.
27. Hashimoto’s thyroiditis
• The follicles are atrophied and variable in
size. 32. Hodgkin lymphoma
• Some acini are lined by large cells with • Reed –sternbergcell:large cell with bilobed
abundant eosinophilic granular cytoplasm nucleus seen as a mirror image of each
(Askanazy or Hurthle cells) and the colloid other
is scanty or absent. • Each lobe contain prominent eosinophilic
inclusion with clear halo around it.
28. Papillary Ca thyroid • Owls-eye appearance;and cytoplasm abun-
• Papillae composed of fibrovasular stalk and dant and eosinophilic
covered by tumour cells • Classifcn-nodular sclerosis,mixed cellu-
• The tumour cells have overlapping pale larity,lymphocyterich,lymphocyte QUESTION
nuclei (ground glass appearance) depletion,lymphocyte predominance
• Psammoma bodies may be seen. • RS cell positive for CD15,CD30
except in lymphocyte predomi-
29. Adenoma thyroid nance(CD20 +,other markers are
• The capsule at the junction of the adenoma –ve)
and normal thyroid tissue.
• The adenoma is composed of follicles lined
by cuboidal or flattened epithelium.

30. Squamous cell carcinoma

• Section of the tissue showing normal
l epidermis at one end and a proliferating
growth at the other end. Keratin pearls
u
can be seen.
m • Groups of cells are seen infiltrating in the
i deeper tissue. The infiltrating cells are po-
lygonal and show hyperchromatic nuclei
n
a 31. Renal Cell Carcinoma
i • GROSS- usually affects 1 pole of the kid-
r ney , fairly circumscribed.Cut surface(var-
iegated appearance) with yellowish areas ,
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HEMATOLOGY SLIDES

PAT H O L O G Y
1. LE Cell • W.bancrofti – pointed tail tip , gentle flow-
• Mature granulocyte phagocytose homoge- ing smooth curved , nuclear column-nuclei
nous nuclear material discreate, cephalic length same as breadth.
• Phenomenon due to antinuclear Ab • B.malayi – kinked end with two terminal
against nucleprotein nucleus , crinkled secondary curves , nu-
• Tart cell = engulfed by monocyte; in- cleus coloums-smudge, cephalic end longer
clusions not homogenous and will show than broad
chromatin
• Seen in – SLE,Multiplemyeloma,Rheuma-
toidarthritis,Leukemia. 7. PLASMA CELL
• Size 14-20 microns
2. Megakaryocyte • Nucleus – eccentric and small
• Largest cell in bone marrow(30-100 mi- • Increase in – plasma cell leukemia , mea-
cron) sles &german measles , serum sickness,
• 2 types – inactive and active IMN, Chronic infection
• Normal bone marrow contains 1-2 mega- • MYELOMA CELL- atypical and immature
karyocytes/HPF plasma cell.
• Multilobulated nucleus
• No. Increase in-megakaryocytic leuke-
PA P E R S
mia,polycythemia vera,ITP,Hypersplenism
• No. Decrease in – Toxic bone marrow
depression,Heat stroke,Pernicious anae-
mia,acute leukemia,aplastic anaemia.

4. Plasmodium Vivax(Trophozoite Stage)

• Infected red cell large
• Early trophozoite – signet ring shaped
• Late trophozoite – amoeboid trophozoite
with SCHUFFNER‘S DOT  Infective
form – sporozoite
l
u
5. Plasmodium Falciparum (Gametocyte)
• Cause malignant malaria m
• Male gametocyte – banana shaped i
• Female gametocyte – crescent shaped.
n
a
6. Microfilaria i
• Thick smear used to find out microfilaria
r
• 2 common species- W.bancrofti , B. Malayi
e
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CLIP CHARTS
PAT H O L O G Y

CASE 1 week, deepening jaundice - 2 days

Urine Color - deep yel-
low
8 year old boy brought with c/o fever, vomit- Bile pigment - ++
ing and neck rigidity-1 day. LP done. Bile salt - ++
C.S.F Appearance - clear Urobilinogen - absent
Pressure - 250mm of water
Protein - 110mg% Diagnosis -Obstructive Jaundice
Sugar - 20-mg%
Chlorides - 400 mg% CASE 5
Microscopy - 200 cell/c.mm mainly 35 year old female c/o generalized edema -2
lymphocytes Special stain done weeks
Urine - Specific gravity
Diagnosis- Tuberculous meningitis Specific gravity - 1.035
Sugar - nil
CASE 2 Albumin - ++++
10 year old girl brought with c/o fever, vomit- Deposit - granular cast ++,
ing-2 days. O/E febrile.Neckrigidity+.LP done. hyaline cast +,
RBC cast – occasional.
C.S.F Appearance - turbid
Pressure - 250mm of water Diagnosis – Nephrotic syndrome
Protein - 150 mg%
QUESTION
Sugar - 10mg% CASE-6
Chlorides - 400 cells/c.mm
Cells - polymorphs 55 year old female-clinical diagnosis-ure-
mia
Diagnosis- Pyogenic meningitis Urine -
Specific gravity - 1.035
CASE 3 Albumin +
6 year old boy. Puffiness of face - 1 day Sugar - >2g%
Urine - Color - Smoky Acetone - nil
Specific gravity - 1.030
Sugar - nil Diagnosis- Diabetes mellitus.
Albumin - + +
l Blood - + + CASE 7
u Deposit: - RBCs + +, 21 years old female c/o fever, vomiting, loss of
pus cell+, appetitie- 3days
m hyaline casts ++, Color Urine - deep yellow .
i RBC cast ++, Bilepigmen1 - ++
n Granular casts ++ Bile salt - ++
a Urobilinogen - absent
Diagnosis-Glomeruonephritis
i Diagnosis – Obstructive jaundice.
r CASE 4
e Male 50 years, C/o Abdominal discomfort -1
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

CASE 8 CASE 11

PAT H O L O G Y
7 years old girl presented with recurrent jaun- 25 year old male c/o sore throat, fever - 3 days.
dice and pallor- 6months H/o treatment with antibiotic
Urine Blood
Color . - Yellow Hb - 12g%
Bilepigment - absent TC - 4000/c.mm
Bile salt - absent DC - P30 L60 E8 M2
Urobilinogen - +++ Platelet - 2,00,000/c.mm

Diagnosis – Hemolytic anemia, Hemolytic / Diagnosis - Agranuclocytosis.

pre-hepatic jaundice
CASE 12
CASE 9 10 years old girl c/o fever - 1 week, bleeding
from gums - 3 days.O/E Pallor +Cervical
8 years old boy c/o fever with cervical lymph-
lymphadenopathy.
adenopathy- 3 days.
Blood
Blood - 12g%
Hb - 4g%
Hb - 13,500 cells/c.mm TC -50,000/c.mm
TC - - P25 L 65 E5 M5 DC -P3 E0 L3 M2
DC - RBCs normochromic normo- Abnormal cells - 92%
cytic Platelet - 30,000/c.mm
WBCs- Lymphocytes Peripheral Peripheral smearRBC - normochro-
smear mic normocytic,
PA P E R S Numerous atypical lympho- WBC - large number of
cytes, blasts of lymphocytic series,
Platelets- adequate Platelets - reduced in number

Diagnosis – Lymphocytosis with atypical lym- Diagnosis – ALL (Diagnosis confirmed by

phocytes ( suggestive of IMN) PAS staining and IHC)

CASE 10 CASE 13
Male 38 years c/o fatigue O/E pallor ++, 3 year old c/o paroxysmal bouts of coughing
splenomegaly ++ -1 week
Blood Hb - 6 g% Blood
TC - 3,00,000/c.mm Hb - 12 g%
DC - P12,L4,E7,M2,B10 WBC - 30,000/c.mm l
Peripheral smear - Metamyelo- DC - P20 L70 E5 M5
cyte - 40%, Myelocyte - 23%, Blast cells Platelet - 200,000/c.mm u
- 2% Peripheral smear - no imma- m
Plateletcount - 3,20,000/c.mm ture cells
Diagnosis – Absolute lymphocytosis (On clin- i
Diagnosis- Chronic Myeloid Leukemia (to ical correlation, Pertussis) n
be confirmed by karyotyping to demonstrate a
Philadelphia chromosome & LAP to differen- CASE 14
tiate). 30 year old female H/O whole body irradia- i
tion r
Blood e
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Hb - 5g% Platelet - 250000/c.mm

RBC count - 2million/c.mm Peripheral smear RBC -
PAT H O L O G Y

WBC count - 1000/c.mm Show anisocytosis, hypochromia, mi-

Platelet - 20,000/c.mm crocytosis. Numerous polychromatic
ESR - 120mm/lslhour cells, few normoblasts
WBC - Normal
Diagnosis- Pancytopenia ( suggestive of aplas- Platelet - Normal
tic anemia) Diagnosis-Hypochromic microcytic anemia
with evidence of hemolysis, probably Thalas-
CASE 15 semia
20 year old female c/o high fever -10 days,
abdominal discomfort and loose motion - 3 CASE 18
days. O/E spleen palpable. 60 year old male ,weakness,back pain.
Blood findings Investigations:
Hb - 11.5 g% Hb - 6gm%
TC - 3000/c.mm ESR - 110mm 1st hour
P35 L58 E2M5, no X-ray skull and spine - Multiple lytic
abnormal cells lesions
Platelet - 200000/c.mm Peripheral smear - Nor-
mocytic normochromic anemia with
Diagnosis- Leucopenia with lymphocytosis ( increased rouleaux formation.Bone
suggestive of typhoid) . marrow aspiration done.

Diagnosis - Multiple myeloma (to be QUESTION

CASE 16 confirmed by serum electrophoresis).
13 year old male c/o loss of appetite and pallor
-1 month
Blood CASE 19
Hb - 5 g% Male 14 yr old presented with fever ,cer-
TC - 7000/c.mm vical lymph node enlargement and sore
DC - P40 L30 E26 M4 throat
MCV - 80 fl Hb - 12 gm%
Blood picture - RBC anisopoikilo- Tc - 16,000/mm3
cytosis, marked hypochromia,pencil shaped Dc - pol 20%,
cells, Target cells +, WBC - eosinophilia, lymp- 80% Atypical lympho-
l Platelet seen scattered. cyes constitutes about 22% of lym-
Diagnosis-Hypochromic microcytic phocytic series
u
anemia with eosinophilia. Platelet - 1 lakh/mm3 Interpret the
m chart and give your diagnosis.
i
CASE 17 Diagnosis: Absolute lymphocytosis with atyp-
n
3 year old boy c/o pallor and stunted growth ical lymphocytes – IMN (to be confirmed by
a O/E mild icterus, Splenomegaly
i Blood
r Hb - 4.5 g%
TC - 7000/c.mm
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INSTRUMENTS

PAT H O L O G Y
pointed stylet Indications: leukaemia, Meg-
Paul Bunnel test).
aloblastic anaemia , Parasitic infections like
leishmaniasis, malaria etc. Sites: sternum op-
1. HB PIPETTE Vol - 20mm3 Use: Hb esti-
posite to 2nd intercostal space,Upper medial
mation by Sahli‘s haemoglobinometer
end of tibia iliac crest
2. WINTROBE‘S TUBE Length: 11 cm,
12. LUMBAR PUNCTURE NEEDLE Made of
Diameter: 3mm Calibration: 0-10 mm Use:
platinum iridium Site: between L3-L4 or L4-
PCV,ESR
L5
Indications: Meningitis, Encephalitis , Sub-
3. WESTERGREN‘S TUBE Length: 30 cm,
arachnoid h‘age Contraindication: Presence
diameter: 2.5 mm Calibration: 0-200[top to
of papilloedema, Bleeding tendency , Infec-
bottom] Use:ESR
tion of site.
4. WBC PIPETTE Whitehead; Markings:
13. LIVER BIOPSY NEEDLE Has 3 parts:
0.5,1,11 Use: WBC count, RBC count in
Cannula or outer needle, Trocar , 3rd part as
erythropenia, semen, CSF
a bifid or split needle Indication: Cirrhosis,
Hepatoma, Granuloma: Tb, schistosomia-
5. RBC Pipette Uses: WBC count, RBC count,
sis Contraindication: coagulative disorders,
Platelet count, Sperm count
hydatid cyst of liver ,hemangioma liver Site:
Midaxillary line in the 10th intercostal space
6. LANCET used to collect blood by finger
PA P E R S
puncture made of steel up to 3 mm tip
14. AYRES SPATULA Made of soft wood and
has two ends: one plain and one bifid Bifid
7. NEUBEAUR‘S Counting chamber depth
end: used to collect cervical smear Plain end:
: 0.1 mm uses: WBC count, RBC count,
buccal smear
Platelet count, Sperm count 8. Urinometer
to determine the specific gravity of the urine
15. NEUBAUER‘S COUNTING CHAMBER
minimum 25 ml of urine
Depth is 0.1 mm Uses: WBC count, RBC
count, platelet count, Sperm count.
9. Esbach‘s Albuminometer Quantitative
estimation of albumin in urine .U‘ marking
16. L BLOCK Leuckhart‘s L block Used as a
for urine, .R‘ marking for reagent . Reagent
mould while producing wax blocks
+ Urine mixed and kept vertically for 24 hrs
Height of coagulation measured and l
17. TISSUE PROCESSING CAPSULE Use: to
expressed in g/dl Esbach‘s reagent: Picric acid, u
bath the tissue in the processing fluid.
Citric acid, Distilled water m
10. MULTISTIX REAGENT STRIPS to detect 18. PARAFFIN BLOCK Used for embedding i
urinary constituents like Glucose, Albumin the tissue in wax.
etc Indicators: tetrabromophenol blue, or- n
thotoluidene a
i
11. BONE MARROW BIOPSY NEEDLE Iden-
r
tification: short and stout needle sharp
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BLOOD GROUPING (IMP)

PAT H O L O G Y

• Transfusion reactions, transfusion trans-

mitted diseases (HIV, Hepatitis B, Malaria)
Oxalated blood used • Blood component preparation(FFP,
Methods: Direct (tube & tile/slide methods), cryopptetc), blood substitutes
Indirect (serum grouping) • Plasma substitutes – Albumin, Hydroxy
Bombay Group ethyl starch, Dextran
• Anticoagulants used in blood bank (CPD,
H gene CPD-A, APD)
A, B, or O gene • Rh: chromosome 1;
Precursor substance →a H antigen →a A/B ABO: Chr 9;
antigen H: Chr 19 \
• Why saline preparation of RBCs for ABO
If H gene is recessive , H antigen is not grouping??? (prozone phenomenon)
formed hence A/B antigens are also not • Why whole blood for Rh grouping? (weak
formed. So person‘s blood group is O. Since A, antigenicity of Rh )
B or H antigens are absent on RBC membrane • Use of control (to detect auto agglutination
of Bombay blood group, their plasma contains if present)
anti-A, anti-B and antiH antibodies. Due to • Difference between rouleaux formation
presence of anti-H antibody, their blood can and agglutination (rouleaux formation is
not be transfused with any other blood other reversible while other is not, on adding a
than Bombay group. drop of water – rouleaux disperses, QUESTION
while agglutination persists)
Dangerous O group – persons with O group
having very high titres of anti-A and anti-B Hb estimation
antibodies. PCV
ESR ( note the time immediately
Landsteiner‘s laws after dipping the esrite tube into
Other blood group systems – MN system, the vial)
Lewis, Kell, Duffy Lutheran Anticoagulant of choice – 3.8%
Colouring agent - methylene sodium citrate 1:4
blue(anti-A) WBC count
- acriflavin yel Peripheral smear preparation
low(anti-B) and staining
l Du antigen – it is a variant of D antigen and is
u weak. So, during group determination, patient Stains used :
m may be labeled –ve, and when he becomes a 1.Romanowsky group of dyes – Leishman,
donor , he may be giving Du positive blood Wright, Giemsa, May – Grunwald and Jenner
i to a Rh-ve person and can cause transfusion stain.
n reaction. 2.Leishman‘s stain – composition
a 1.Methylene blue acts as nuclear stain
• Rh incompatability 2.Eosin acts as cytoplasmic stain
i • Coomb‘s test (direct & indirect) 3.Acetone free methyl alcohol - acts
r • Erythroblastosisfoetalis
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as solvent and fixative.

PAT H O L O G Y
STAINING TECHNIQUE PERIPHERAL SMEAR EXAMINATION
FORMAT
1. Keep the slide in a horizontal position
2. Leishmann‘s stain is added to cover the 1. Under Low Power
entire smear Preparation and staining ( smear shows ade-
3. Add distilled water( double the amount quate staining with no stain deposits and cells
of stain) are evenly distributed)
4. Mix the stain and water properly by WBC count increased or not
blowing air Parasites seen or not
5. Keep it for 7- 10 minutes. 2. Under oil immersion
6. Pour water and wash thoroughly with RBC
Shape and color of RBC
running water.
Nucleated RBCs – present or not P
7. Wipe the other side of slide with cotton
olychromasia – present or not
8. Dry the smear by placing the slide in a Inclusion bodies – present or not
slanting position with tail end upwards. Parasites –seen or not
Excessive rouleoux formation – seen
Criteria for Good staining or not
1. Should be pinkish in colour. WBC
2. There should not be any stain deposits Apparent count, distribution, nuclear
3. Should be tongue shaped and cytoplasmic characteristics, im-
PA P E R S 4. No serrations and vacuoles mature cells, blast cells, any other cells
5. RBCs coppery red in color, no shrinkage Platelets
or swelling, eosinophils orange red. Apparent count, distribution, mor-
phology
IMP – if there is excess staing, add stain
again. if it is understained, repeat the staining
Preparation Diagnosis / Impression

Preparation Of Thick Smear – ( For apparent WBC count: No. of WBC / HPF
Prepared by placing 4 drops of blood on a X 1000
slide and join the 4 drops of blood togeth- For apparent platelet count: No. of platelets /
er into an area of 1sq:cm or a similar sized oil immersion field X 15000)
circle. l
Use – for demonstration of parasites such as u
malaria and microfilaria.
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ALGORITHM FOR PERIPHERAL SMEAR

EXAMINATION
PAT H O L O G Y

STEP1 STEP3
Low Power – focus on areas of uniform cel- Under oil immersion –
lularity and staining If all immature blast cells – AML
If all series of maturation and baso-
STEP2 philia – CML
High power – assess WBC count, if Look at granules in case of mature
high(more bluish) think in terms of AML WBC I
and CML, if normal, think in terms of neu- f pink granules – neutrophilia
trophilia and eosinophilia.
If orange granules – eosinophilia.
If WBC count appears normal, RBCs hypo-
chromic and different shapes of RBCs seen,
think in terms of HMA

NORMAL VALUES
Specific gravity 1.003 – 1.030
Urea 25 – 30G/ 24 HR urine excreted
Creatinine 1 – 1.8G/ 24 HR urine excreted
Protein 30 -150MG/ 24 HR urine excreted
Glucose 2 – 20MG/DL in fasting urine QUESTION

PRESERVATIVES
Toluene all round preservative
Formal excellent for formed elements
Sodium bicarbonate preserve UBG and porphyrin
Hibitane (Chlorhexidine) preserve glc in 24hr urine sample

l
u
m
i SPECIAL PRESERVATIVES
n Addis Count 40% formaldehyde
a
Estimation of VMA conc.HCl
Estimation of catecholamines conc. H2SO4
i
r Estimation of aldosterone CHCL3
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TESTS OF PROTEIN

PAT H O L O G Y
1. Heat and acetic acid test
Drop of acetic acid – turbidty due to phosphate
& carbonate disappear
Drop of nitric acid – turbidty due to mucin
disappear
2. Sulphosalicylic acid test(done in CLIP lab, MCH)
3. Heller‘s test
4. Esbach‘s reagent test
5. Dipstick method

INTERPRETATION
traces barely visible cloudiness
1+ cloudiness without granular ppt
2+ cloudiness with granular ppt but no flocculation
3+ loudiness with granular ppt and flocculation
4+ thick curdy ppt and coagulation
PA P E R S BJP tests DDs for BJP
1. Heat and coagulation test – BJP ppt at45ºC,
max ppt at 60ºC;At 80ºC ppt start to disap- 1. Multiple myeloma
pear,at 100ºC completely disappear& reap- 2. Amylodosis
pear on cooling 3. Walderstrom‘smacroglobulinemia
2. Toluene sulphonic acid test 4. CML
3. HCl test (bradshaw”s test:2ml urine+con-
cHCl—>white ring) Quantitative estimation of protein
• Albumin - Esbach‘s method
• Globulin – urine + amm.sulphate

l
u
REAGENT COMPONENTS
m
Benedict‘s reagent Copper sulphate,anhydroussod. bicarbon-
ate,sod. citrate, D/W i
Esbach‘s reagent picric acid,citricacid,distilled water n
Fouchet‘s reagent trichloroaceticacid,ferricchloride,distilled a
water i
Ehrlich‘s reagent p-dimethylaminobenzaldehyde,HCl r
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TESTS FOR GLUCOSE

PAT H O L O G Y

1. Benedict’s test –semiquantitative test

Sod.bicarbonate – provide alkaline medium
Sod.citrate – prevent pptn of cupric oxide by forming deep blue complexes which dissociates to
supply cupric ions for oxidation

INTEPRETATION
Trace slight yellow ppt with greenish blue/bluish green mixed sol <0.5 g/dL
1+ greenish yellow ppt with apple green mixed soln =0.5 g/dL
2+ large amount of yellowish green ppt =0.75 g/dL
3+ orange ppt =1 g/dL
4+ large amount of yellow to red ppt. no blue in supernatant >2 g/dL

2. Glucose oxidase test(specific for glucose)

TESTS FOR KETONE BODIES

Ketone bodies are acetone, aceto acetic acid and beta hydroxy butyric acid. Ketonuria is QUESTION
seen
in anorexia, fasting, starvation, DKA, prolonged vomiting.

Rothera‘s test acetone & aceto acetic acid

Beta hart test Beta hydroxy butyric acid
Gerhardt‘s test acetoacetic acid
In Rothera‘s test, urine saturated with NH2 SO4 to keep liquor ammonia above the urine
solution.

l TEST FOR BILE PIGMENTS

u MODIFIED FOUCHET’S TEST
m BPs adsorbed on barium sulphate Fouchet‘s reagent: 10% Ferric chloride, trichloro acetic acid,
i distilled water Biliverdin(green), Bilicyanin (blue)
n
a TEST FOR BILE SALTS
i
HAY’S TEST
r
Based on the physical property of surface tensioN.
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TESTS FOR UROBILINOGEN

PAT H O L O G Y
EHRLICH’S TEST
Pale pink color – UBG normal
Cherry red color - UBG increased
Watch the color through the mouth to increase the depth of liquid column for better appreciation
of the color.
CLINICAL BILE PIGMENT BILE SALT UBG
CONDITION
Prehepatic - - +++ to ++++
Hepatic + to ++++ + ++
Posthepatic ++ to ++++ + +/-

TEST FOR BLOOD SAMPLE C

Male 50 yrs complains of abdominal discom-
fort 1 week and deepening of jaundice 3 days.
BENZIDINE TEST
Diagnosis: obstructive jaundice
Boiled and cooled urine is used to destroy
Test to be done: 1. Fouchet‘s test-for bile
peroxidase enzyme present in pus cells, bacteria
pigments
etc. positive test in hematuria,hemoglobinuria
2. Hay‘s test-for bile salts
& myoglobinuria.
PA P E R S Trace Faint green 3. Ehrlichs test-for
1+ green urobilinogen.
2+ greenish blue
3+ blue
4+ deep blue

SAMPLE A
Male, 60yrs, presented with loss of appetite,
nausea & vomiting in casualty.
Diagnosis: Diabetic ketoacidosis
Tests to be done: 1. Benedicts test-for sugar
2. Rothera‘s test-for ketone bodies l
u
SAMPLE B m
6 yr old male child, complains of puffy face of 1
day duration. i
Diagnosis: acute glomerulonephritis. n
Test to be done: 1. heat and acetic acid test-for a
protein , 2. benzidine test-for blood
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PAT H O L O G Y

CRYSTALS IN ACIDIC URINE

Type Appearance Disease associated

Uric acid yellow brown rhombic c/c nephritis, gout

plates rossets
Ca oxlate colourless envelope/dumb liver ds, DM ,
bell shaped hyperparathyroidism
Sod.urate colourless/yellowish slen- no clinical
der prism in fan/sheaf like significance
pattern
Cystine large flat transparent with nephritis, chyluria,
1 or more Corners cut off nephritic syndrome
Leucine highly refractile yellow/ severe hepatitis, MSUD
brown spheres With radi-
al/concentric striations

CRYSTALS IN ALKALINE URINE

Type Appearance Disease
QUESTION
Struvite/triple phosphate coffin lid appearence Seen in normal urine or UTI
due to urease+ve Organisms
Calcium carbonate large yellow brown/colorless
spheroids or small round/
ovoid/dumb bell forms
Amm.biurate Apple thorn crystals
Calcium phosphate Large thin irregular granular
colorless plates

l
u CASTS
m Type Disease associated
i Hyaline Few in normal & increased in proteinuria or renal/extrarenal origin
n Granular c/c nephritis
RBC Glomerulo nephritis
a
WBC a/c pyelonephritis &glomerulo nephritis
i
Epithelial c/c renal d/s
r
Fatty Nephrotic syndrome & c/c glomerulo nephritis
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PAT H O L O G Y
HISTOPATHOLOGICAL TECHNIQUES

Registration→fixation→grossing labeling→decalcification→dehydration→Clearing→impregna-
tion→emb edding→cutting→staining→mounting→reporting

Ideal fixative Disadvantages of formalin

1. Should penetrate tissue easily • loss of fat & glycogen
2. Rapid in action • shrinkage of tissue acid form of hematin
3. Be isotonic in bloody tissue
4. Cause min.physical and chemical alteration • Formol saline is the fixative in renal, skin
5. Cheap, stable and safe to handle and eyeball biopsy
Volume 10-20 times the volume of the
specimen except OsO4
Routine fixative 10% neutral buffered
formalin.

Special fixatives
• Glycogen storage diseases - Carnoy fixative.
• Testicular biopsy - Bowins fluid(Picric acid)
• Enzyme histochemistry - Cold acetone
• Electron microscopy - 4% glutaraldehyde,
PA P E R S
Osmium tetroxide

Decalcifying agents 1.dilute mineral acids

2.chelating agents
3.organic acids(acetic acid & formic acid)
Tissue processing(dehydration) Agent Ethyl alcohol (ascending grades)
Clearing(dealcoholism) agents 1.chloroform
2.xylene
3.toluene
4.benzene
l
Embedding Impregnation of tissue with medium-3 meth- u
ods m
1.paraffin wax
2.celloidin i
3.gelatin n
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MICROTOME
PAT H O L O G Y

• used for cut the section

• Normaly-6-8micrometer thickness t
• For immunohistochemistry and AgNOR study-4-5 micrometer
• Types-rotary microtome(routinely)
• Sledge microtome,saw microtome,vibrating microtome,rocking microtome

SPECIAL STAINS ( WRITE APPR.STAINS IN SHORT NOTES TO GET EXTRA MARKS)

Van gieson yellow collagen and other connective tissues
Verhoeff ‘s method elastic fibres
Von kossa stain Calcium
Perl‘s stain Iron
Congo red Amyloid
Rhodanineorcein Copper
Mayer‘s mucicarmine Mucin
QUESTION
PAS Glycine

CYTOPATHOLOGY
Ideal fixative -95% ethyl alcohol and ether in the ratio 1:1

PAPANICOLAOU STAINING PROCEDURE

Fixation →hydration(descending grades of alcohol)→haematoxylin (nuclear stain)→Wa-
ter rinses→blueing soln.(raise pH,turns red to blue)→water rinses→dehydration (prepare for
l
alcohol counterstains)→OG(cytoplasmic stain) and rinses→EA(cytoplasmic stain) rinses→al-
u
coholic rinse(prepare for xylene)→learing with xylene
m
i
FNAC (FINE NEEDLE ASPIRATION CYTOLOGY)
n 10-20 cc syringe and 22-23 guage needle is used Advantages -Done as OPD procedure , No
a anaesthesia required , Low cost procedure ,Results on the same day ,No much trauma
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PAT H O L O G Y
PA P E R S

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PAT H O L O G Y

QUESTION

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PAT H O L O G Y
PA P E R S

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PAT H O L O G Y

QUESTION

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PAT H O L O G Y
PA P E R S

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PAT H O L O G Y

QUESTION

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Pathogenesis PS BM

PAT H O L O G Y
Fe def anemia Decreased Fe for Hb Microcytic hypo- Hypercellular BM
synthesis chromic red cells, reversal of M:E ratio
- ^ed blood loss Poikilocytosis – small Ed BM Fe store
- ^Ed requirement and elongated cells (
- ^Ed intake pencil cells), Ovalocy-
- ^Ed absorbsion tes, target cells, Mild
reticulocytosis
Megaloblastic Anemia Impaired DNA Pancytopenia with Hypercellular BM,
synthesis due to macrocyts lacking Megaloblast + Giant
malfunction of thymi- central pallor, How- metamyelocyte and
dylate synthetase, 20 ell Jolly body ( RBC band forms Large
folate def nuclr remnants) megakaryocytes with
Basophilic stippling bizarre nuclei
Hypersegmented
neutrophils ( earliest
finding)
c/c myeloid leukemia T(9;22) producing Marked leukocytosis BM is 100% cellular
BCR-ABL fusion with cells of myeloid Erythroid precursors
gene on Philadelphia series in all stages of are decreased, Ab-
chrom causing unop- dvlpmnt, Thrombo- normal megakaryo-
posed tyrosine kinase cytosis, Eosinophilia cytes, Pseudo gaucher
PA P E R S activity and basophilia cells, ^ In reticulin
fibre
Thalassemia (ß major) Mutations on ß glo- Microcytic hypochro- Hypercellular with
bin chain gene leading mic RCs, Poikilocy- erythroid hyperplasia
to its absent produc- tosis – target cells, (M:E ratio rever-
tion nucleated red cells sed), Pink inclusions
Basophilic stippling, in normoblast d/t
Howell Jolly bodies, alphachain accumuln
reticulocytosis, left
shift in leukocytes
Sickle cell anemia Point mutation in the RBCs aresickle shaped Vaso occlusive epi-
chain for b globin Target cells Howell sodes ( a/c chest s/d
chain causing replace- Jolly bodies + ) Autosplenectomy, l
ment of GLU by Val @ +ve sickling test with u
6th position sodium dithionit
m
Hereditary spherocy- Defect in RBC mem- Microspherocytes, increased osmotic fra-
tosis brane cytoskeletal MCHC ^ ed, Mild gility, Triad of anemia i
protins – ankyrin, reticulocytosis gallstones splenome- n
spectrin, band 4 galy, -ve coomb’s test ( a
diff from AIHA )
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PAT H O L O G Y

QUESTION

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PHARMACOLOGY
PHARMACOLOGY
PA P E R S

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SYLLABUS

Paper I-General pharmacology, ANS, CVS, Blood, Diuretics, CNS, Autacoids, Respiratory sys-
tem

Paper II-GIT, Hormones, Antibiotics, Chemotherapy, Miscellaneous

PHARMACOLOGY

QUESTION PATTERN
ESSAYS 2X6=12

SHORT NOTES 5X3=15

ANSWER BRIEFLY 5X1=5

NAME TWO DRUGS FOR 8X1=8

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INTRODUCTION; ROUTES OF AD- Rifampicin, Carbamezapine, Phenobarbi-

tone
MINISTRATION • INHIBITORS - Valproate, Ketoconazole,
Cimetidine, Ciprofloxacin, Erythromycin,
1. Drug ,Orphan drugs - Defini-
INH
tion(TP-2,5;TV-1,2)
• Drugs with ZERO ORDER kinetic - War-
2. Source of drugs (refer record)(TV-3)
farin, Alcohol & Aspirin, Theophilline,
3. Transdermal Therapeutic Sys-
Tolbutamide, Phenytoin
tems(TP-6,TV-8)
4. Sublingual ,rectal , transdermal, subcuta-
neous ,inhalational routes -Example (TP-

PHARMACOLOGY
6,TV-5)**
5. Limitations of oral route of administration/ PHARMACODYNAMICS
Advantages of i.v(TP-6,TV-5)
6. Inhalational and sublingual routes of ad-
ministration-advantages (TP-6,8;TV-5,6)** 1. Pharmacodynamics-Defini-
7. Special drug delivery system(TV-9)** tion(TP-37,TV-26)
2. Affinity, Efficacy, Potency(TP-41,TV-28)
• Drugs given rectally-PEDI- Paralde- 3. Partial agonists, inverse ago-
hyde, Ergotamine, Diazepam, Indo- nists(TP-42,TV-28)**
methacin 4. Receptors- Types, functions(TP-40,TV-28)
• 2 orphan drugs- Fomepizole, Sodium 5. Therapeutic window Phenomenon, Thera-
nitrate peutic index(TP-55,56;TV-32,33)**
• 2 drugs from animal source- porcine 6. Synergism / Antagonism(TP-57,TV-34)**
insulin (pig), Heparin (ox lung) 7. Dose Response Curves(TP-53,TV-32)**
• 2 drugs given sub lingually-GTN,
Buprenorphine
• 2 drugs given as transdermal patches- PHARMACOTHERAPY
Nicotine, Fentanyl
1. Pharmacogenetics, Pharmacogenom-
PHARMACOKINETICS ics(TP-65)
2. Tolerance(TP-70,TV-38)
1. Pharmacokinetics- Definition(TP-10,TV-9)
3. Tachyphylaxis(TP-70,TV-39)**
2. Bioavailability(TP-16,TV-12)**
3. Redistribution(TP-18,TV-14)
4. Plasma Protein Binding(TP-19,TV-15)
5. Volume of Distribution(TP-17,TV-13) l
ADVERSE DRUG EFFECTS
6. Prodrug(TP-22,TV-16)**
u
7. Hoffman elimination(TP-25,TV-18)
1. Adverse drug reactions- Definition,- m
8. First Pass Metabolism(TP-27,TV-12)**
types(TP- 82,TV-42)
9. Microsomal Enzyme Induction and Inhibi- i
2. Idiosyncracy, Drug allergy(mechanism,
tion(TP-26,TV-19)
types, treatment)(TP-85,TV-44) n
10. HalfLife(TP-31,TV-21)**
3. Teratogenicity(TP-89,TV-45)** a
11. Therapeutic drug monitor-
2 drugs showing tachyphylaxis- Ephedrine
ing(TP-34,TV-24)** i
, Nicotine
12. Kinetics of Elimination(TP-30,TV-21) r
• INDUCERS - Griseofulvin, Phenytoin,
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cation (Reduces tracheobronchial & salivary

CHOLINERGIC SYSTEM IN BODY secretions→prevent laryngeal spasm)
8. Mydriatics of choice in elderly (phenyleph-
1.Types of cholinergic receptors, sites, agonists rine) & children <5 (atropine)
and antagonists(TP-101 fig7.1,TV-56) 9. Atropine – specific antidote of anti ChE
2. Pilocarpine and occusert, Bethanechol us- 10. Ipratropium and its rationale in COPD
es(TP-104,TV-60)** (Reverse bronchoconstriction due to stim of
3. Anti-ChEs – Classification, MOA, egs, us- M3 receptors,Inhaled- decreases bronchial
es(TP-105,TV-57,62)** secretions)
4. Physostigmine v/s Neostigmine(TP-108
tab7.6,TV-64 tab2.4) TIPS
PHARMACOLOGY

5. Belladona poisoning –clinical features, man- 1. Two drugs in Alzeimer‘s disease-Donapez-

agement with dose(TP-110,TV-68,75) il, Rivastigmine
6. OP poisoning –MOA, clinical features , 2. DOC in Belladonna poisoning -Physostig-
Management(TP-111,TV-68,69)** mine 0.5 to 2 mg i.v
7. Myasthenia gravis- Rx,myasthenic&cholin- 3. DOC in Organophosphate poisoning -
ergic crisis (TP-109,TV-67,68) Atropine 2mg i. v every 1Omts
8. Anti cholinergics- Classification, Uses, ex- 4. DOC in Motion sickness-Hyoscine
amples (TP-113,TV-70)** 5. Shortest acting carbamate- Edrophonium ,
9. Glycopyrrolate, dicyclomine, cyclopentolate, use in myasthenia
tropicamide(TP-117,TV-73) 6. Cerebroselective carbamates-Rivastigmine
10. Vesicoselective anticholinergics (TP- &Donepezil
117,TV-75)** 7. Only water soluble OP & used in aphakic
glaucoma-Echothiophate
8. 2 drugs used in Myasthenia gravis-Neostig-
P.B. mine, Pyridostigmine
1. Pralidoxime for tacrine poisoning (Ta- 9. Drugs c/I in myasthenia - Aminoglycoside
crine-reversible Anti-ChE , Oxime- Enzyme antibiotics, Quinine, Pancuronium , Tubocu-
reactivator) rarine.
2. Betaxolol/Physostigmine -1st choice in glau- Anticholinergic drugs used in
coma (Betaxolol bcoz decreases IOP, protective a) Peptic ulcer-Propanthelene, Pirenzepine
effect on retinal neurons by reducing Na-Ca b) COPD-Ipratropium, Tiotropium
influx, less bronchpulmonary and cardiac side c) Abdominal colic-Dicyclomine
effects, no consistent effect on pupil size or d) Refractory error testing in children- Atro-
accommodation) pine 1% ointment.
l 3. Neostigmine/Physostigmine in my.gravis
(Neostigmine bcoz anti-ChE with prominent
u action on skeletal muscles and less CNS ef-
m fects) ADRENERGIC SYSTEM IN BODY
i 4. Neostigmine+Atropine in cobra bite (At-
ropine prevents cholinergic adv effects of 1. Distribution and actions of α&β receptors,
n neostigmine) agonists and antagonists(TP-127,TV-86)
a 5. PB of oximes in OP poisoning 2. Adrenergic drugs- Therapeutic classifica-
i 6. Hyoscine in motion sickness (more com- tion(TP-133,TV-90)**
pletely metabolized, better BBB penetration) 3. Dales vasomotor reversal(TP-131,TV-91)**
r
7. Glycopyrrolate in Pre Anaesthetic Medi- 4. Nasal decongestants-systemic and topical,
e
’18 68
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

Anorectic agents(TP-136,TV-96) congest eye by osmotic action))

5. α blockers- Classification (selectivity), 8. Atropine C/I in glaucoma(IOP increase in
uses and adverse effects(TP-140,TV-99,102) narrow angle G))
6. Phentolamine, Prazosin, Tamsu- 9. α+β blockers in pheochromocytoma(de-
losin(TP-141,TV-101,1020 crease BP by both ἀ1and β1 blockade and β2
7. β blockers- Classification, MOA, Uses and agonism, by ἀ blocking, they maintain bld vol,
Adverse effects(TP-144,TV-103)** decrease BP and antagonize fall in BP aftr sur-
8. Cardioselective β blockers, β blockers with gry by maintaining bld vol, by β blocking they
ISA (Acebutolol, Pindolol)(TP-147,TV-103) 9. decrease tachycardia and arrhythmia)
Propranolol {Class of drug, MOA, Kinetics, 10. Verapamil C/I with propranolol (cardiac
Interactions, Adverse effects,C/I, Uses}(TP- arrest, safe with nifedipine)

PHARMACOLOGY
145,TV-103)
10. α +β blockers- Labetalol, Carve-
dilol(TP-151,TV-107)** TIPS
11. Glaucoma- ESSAY(TP-151,TV-64)
a) Rx of open angle, angle closure (Drugs • Clonidine congeners- Apraclonidine, Bri-
with priority) monidine
b) CA inhibitors used in glaucoma • 2 drugs used for hypotension- Ephedrine,
c) Mydriatics c/I in a/c congestive glaucoma Mephentermine
• Topically useful C.A-Dorzolamide
• β1 selective blocker used in the Rx of glau-
P.B coma-Betaxolol
• Topical carbonic anhydrase inhibitor used
1. Dopamine/adrenaline in shock(Hint:dopa- in glaucoma-Dorzolamide
mine-cardiogenic shock,septic shock,adrena- • Selective β1 agonist-Dobutamine
line-anaphylactic shock) • Ultra short acting β blocker-Esmolol
2. Adrenaline in anaphylactic shock & its • Longest acting β blocker-Nadolol
route (^BP,counteracts bronchospasm/laryn- • 2 lipid soluble β blockers- Atenolol, Sotalol
geal edema) • 2 β blockers with NO mediated vasodila-
3. Lignocaine +adrenaline in local anesthesia tation-Nebivolol, Celiprolol
(duration of anaesthesia ‘^’,systemic toxicity of • β1 blocker with β2 agonism-Celiprolol
LA and bleeding ‘√’)
4. Tamsulosin +finasteride in BPH (Tamsu-
losin- decrease prostatic/bladder neck mus AUTACOIDS
tone, finasteride decrease prostate size
5. Propranolol in thyrotoxicosis (rapidly con- 1. 2nd generation v/s 1st generation anti l
trols sympathetic symptoms, inhibits peripher- histaminics(TP-163,TV-250)
u
al convn of T4→T3 2. Fexofenadine, Loratadine, Cetrizine, Azelas-
6. Propranolol C/I in diabetes, variant angina tine(TP-166,TV-252) m
& hyperlipedimia(delays recovery from hy- 3. Uses of anti histaminics(TP-167,TV-251) i
poglycaemia due to insulin and OHGA and 4. Drug therapy of Vertigo(TP-168,TV-253) 5.
n
warning signs of the same are suppressed, Ketanserin(TP-174,TV-253)
exacerbates variant angina by unopposed ἀ 6. Drug therapy & Prophylaxis of migraine, a
mediated coronary constrctn, alters lipid pro- MOA of Sumatriptan(TP-176,TV-255)** i
file TG,LDLincreaes,HDLdecrease) 7. Clinical uses of Prostaglan-
r
7. Mannitol in acute congestive glaucoma(de- dins(TP-!89,TV-257)
e
69 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

8. NSAIDs (TP-192,TV-260)**ESSAY • 2 5HT3 Antagonists – Ondansetron ,

9. Selective COX-2 inhibitors (TP- Granisetron
205,TV-267)** • Drugs used for the induction of la-
10. Aspirin(TP-195,TV-261) bour-PGE-2
11. Diclofenac Na(TP-204,TV-266) • Drugs used for midterm abortion-PGF-2ἀ
12. Acute salicylate poisoning (TP- • DMARDs-GOLD CLIPS(Gold, Chloro-
197,TV-264) 13. Ketorolac(TP-204,TV-266) quine, Leflunomide, Immunosuppressants,
14. Acute paracetamol poisoning (NABQI d-Penicillamine, Sulfasalazine)
metabolite, antidote N-acetyl cysteine) (TP-
206,TV-268)
15. Topical NSAIDS(TP-208,TV-269)
PHARMACOLOGY

16. DMARDS-Methotrexate, Leflunomide, RESPIRATORY SYSTEM

Gold CLIPS-(refer mnemonic section) (TP-
210,TV-273)** 1. Drugs used for Dry Cough(TP-218,TV-276)
17. Biological Response Modifiers- Infliximab, 2. Mucolytics – Bromhexine , Ambroxol-
Adalimumab, Anakinra(TP-212,TV-275) (TP-219,TV-277)
18. Drugs used in gout- Colchicine, Probene- 3. Drugs in Bronchial Asthma- classifica-
cid , Allopurinol(TP-213,TV-269) tion(TP-222,TV-278) **ESSAY
4. Salbutamol (Class of drug, MOA, Kinetics,
Interactions, Adverse effects, C/I, Uses)(TP-
P.B. 223,TV-278)
5. Theophylline(TP-224,TV-278)
1. P.B. Terfenadine cardiotoxicity. (Erythromy- 6. LT antagonists- Montelukast , Zafirlu-
cin+ terfenadine) kast(TP-228,TV-281)
2.P.B. Promethazine in motion sickness (antag 7. Mast cell stabilizers-Ketotifen, Sodium cro-
of histamine in brain/antimuscarinic ppty) moglycate(TP-229,TV-282)**
3.P.B NSAIDS in PDA (DA kept patent by 8. Inhalational steroids- Budesonide, Flutica-
PGE2 and PGI2) sone(TP-230,TV-283)
4.PB. Aspirin in post M.I. patients (inhibit 9. Rx of Status Asthmaticus (TP-
platelet aggregation) 233,TV-284)** ]
5. PB. Sulphonyl ureas and Salicylates (Aspirin 10. Inhalation therapy in asthma (TP-231
displaces sulfonyl ureas from plasma protein ,TV-283)
binding site→toxicity)
P.B

l 1. Ciprofloxacin + Theophylline (Cipro inhib-

TIPS its theophylline metabolism and increase in
u
plasma level)
m • DOC in Patent ductus arteriosus - indo-
i methacin 0.1-0.2 mg/kg , 12th hrly
• A/C paracetamol poisoning - N acetyl
n
cysteine 150 mg/kg i.v over 15 mts
a • 2 antihistamines used in vertigo-cin-
i narizine, promethazine
r • 2 5HT antagonists- Ketanserin, Cypro-
heptadine
e
’18 70
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

6. Classification of Oral hypoglycemics (TP-

ENDOCRINE PHARMACOLOGY 270,TV-383)**ESSAY
7. Sulphonylureas {Class of drug, MOA, Ki-
PITUITARY netics, Interactions, Adverse effects, C/I, Uses}
(TP-270,TV-383)**
1. Somatostatin, Octreotide ( GH inhibitors) 8. Biguanides(TP-275,TV-386)
(TP-237,TV-335) 9. MOA Thiazolidinediones(TP-276,TV-388)
2. Bromocriptine ( Actions , uses, adverse ef- 10. α Glucosidase Inhibitor(TP-277,TV-389)
fects- Livedo reticularis)(TP-239,TV-338)
3. Uses of Gonadotropin(TP-241,TV-336)
4. Examples of GnRH agonists (Nafarelin, P.B

PHARMACOLOGY
Leuprolide), GnRH antagonists (Ganirelix,
cetrorelix)(TP-242,TV-337) 1. P.B Biguanide/sulphonyl urea in obese pts
(Anorectic action )
THYROID 2. P.B. Metformin safer than Phenformin
(Lesser chance for lactic acidosis)
1. Synthesis, storage and secretion of thyroid 3. P.B. Tolbutamide preferred over Chlorpro-
hormone(TP-245,TV-340) pamide in elderly(hypoglycaemia in elderly
2. Uses of T3, T4(TP-251,TV-342) more common with use of chlorpropamide
3. Thyroid inhibitors drugs – classification due to its longer action)
(TP-252,TV-343)**ESSAY 4. P.B Regular insulin in DK (after i.v. injection
4. Propylthiouracil(TP-252,TV-345)** hexameric reg.insulin dissociates rapidly to
5. Rx of thyrotoxicosis, Thryoid storm(TP- produce prompt action, rapidly corrects meta-
256,TV-347) bolic abnormalities)

P.B CORTICOSTEROIDS
1. PB. Propylthiouracil/ Carbimazole in preg- 1. Corticosteroids- MOA, Uses, Adverse ef-
nancy (propylyhiouracil-greater protein bind- fects, C/I(TP-282,TV-364)**
ing, less transfer to foetus) 2. DOC of cerebral edema (Dexamethasone /
2. PB.Iodine + Carbimazole in Preop prepa- Betamethasone)(TP-292,TV-374)**
ration for thyrotoxicosis (to attain euthyroid 3. Methyl prednisolone(TP-288,TV-366
state) tab9.6)
3. Propranalol in thyrotoxicosis. 4. Classification of steroids based on duration
of action(TP-289 tab20.1,TV-386 tab9.6) l
5. 2 uses of steroids where high dose ad-
u
INSULIN,ORAL HYPOGLYCAEMIC ministration & long term therapy is needed
DRUGS AND GLUCAGON (organ transplantation,collagen vascular d/s) m
6. How to stop treatment with corticoste- i
1. Human insulin –indications(TV-381) roids?(TP-294,TV-372)
2. Insulin Analogues (TP-264,TV-378)** n
3. RX of diabetic ketoacidosis(TP-267,TV-382) a
4. Insulin resistance(TP-269) P.B i
5. Insulin secretagogues (Sulphonyl ureas,
r
meglitinide analogues)(TP-270,TV-383) 1. P.B Hydrocortisone in Addisons d/s (acts e
71 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

rapidly, short duration of action, has both relaxation b/w contractions preventing fetal
primary glucocorticoid and mineralocorticoid asphyxia, fetal descent not compromised)
activity) 4. PB Methyl ergometrine in PP (sustained
tonic uterine contractions→compress uterine
bld vessels→stops bleeding)
5. Rationale for the combination of oestrogen
GONADAL HORMONES and progesterone in OCPs (both synergise to
inhibit ovulation, progestin ensures prompt
1. Androgens- Side effects and us- bleeding at the end of a cycle and blocks risk
es(TP-299,TV-348) of developing endo.Ca due to estrogen)
2. Anabolic steroids(TP-300,TV-349)
PHARMACOLOGY

3. Anti Androgens – Danazol ,Flutamide

(TP-301,TV-349) CALCIUM BALANCE
4. 5 α reductase inhibitors – Finasteride ,
Dutasteride(TP-302,TV-349)** 1. Parathormone – MOA(TP-338,TV-391)
5. Sildenafil(TP-303,TV-129,137)** 2. Vitamin D –Uses (TP-342,TV-395)
6. Oestrogens – Uses(TP-309,TV-352) 3. Bisphosphonates – MOA, Uses ( Alendro-
7. Hormone replacement therapy- nate, Zolendronate)(TP-343,TV-395)**
(TP-309,TV-352)
8. SERMs – Tamoxifen, Raloxifene, Ormelox-
ifene(TP-313,TV-355)** TIPS
9. Clomiphene citrate(TP-312,TV-354)
10. SERD – Fulvestrant(TP-313,TV-355) • GnRH agonist used as nasal spray-Na-
11. Progesterone – uses(TP-318,TV-356) farelin
12. Mifepristone(TP-319,TV-357)** • Anti-thyroid drug used in pregnancy-Pro-
13. Oral Contraceptive Pills – Classifi- pyl thiouracil
cation , Uses , Adverse Effects(TP-321 • Commonly used iodine isotope-I-131
tab22.2,TV-359) • Rx of hypoglycaemia- Glucose, glucagon
14. Post coital contraception(TP-322,TV-361) • Hypoglycemic drug used in the Rx of
15. Injectable contraceptive prepara- PCOD-Metformin
tions(TP-323,TV-362) • Corticosteroids used in cerebral oede-
16. Uses of Oxytocin (TP-330,TV-397) ma-Dexamethasone, Betamethasone**
17. Uterine Stimulants and Relaxants – clas- • 2 synthetic androgens- Methyl testoster-
sification and egs(TP-329,332;TV-397,401) one, Fluoxymesterone
• PDE-5 inhibitor-Sildenafil
l • Pure estrogen antagonist, selective estro-
PB gen receptor down regulator-Fulvestrant
u
• Oxytocin antagonist-Atosiban**
m 1. PB. Clomiphene citrate in multiple preg- • 2 drugs for osteoporosis- Raloxifene, Alen-
i nancy (blocks estrogen receptors→stim LH, dronate
FSH secretion→induce ovulation and may→- • Non steroidal estrogen antagonist used as
n
multiple pregnancy) contraceptive-Centchroman**
a 2. PB. OCP + Rifampicin (contraceptive fail- • 2 uterine relaxants/Tocolytics- Ritodrine,
i ure ) Nifedipine
r 3. Oxytocin / Methyl ergometrine- for induc-
tion of labour (oxytocin-short t1/2 , complete
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

SKELETAL MUSCLE RELAXANTS ionizing to a very small extent even at low pH.
So effective in anaesthetising gastric mucosa
1. Classify Skeletal Muscle relax- despite acidity of the medium).
ants(TP-347,TV-78)**ESSAY
2. Difference between competitive and depo-
larization blockade(TP-350,TV-80) TIPS
3. Pancuronium, Succinylcholine (uses)(TP-
353,TV-78)** • LA with antiarrythmic ppty-Lignocaine
4. Dantrolene sodium – MOA ,Us- • LA with sympathomimetic ppty-Cocaine
es(TP-356,TV-83)** • LA causing methaemoglobinemia-Prilo-
5. Centrally acting muscle relax- caine

PHARMACOLOGY
ants(TP-357,TV-78)** • Pre anaesthetic medication-OHSA-
NA-Opioids, H2 blockers, Sedatives, Anti-
TIPS cholinergics, Neuroleptics, Antiemetics
• Most cardiotoxic LA-Bupivacaine.
• DOC in Malignant hyperthermia - Dan-
trolene sodium 1 mg /kg i.v
• Hoffmans elimination-Atracurium GENERAL ANAESTHESIA
• Shortest acting NM blocker-Succinyl cho-
line(2-5 min) 1. Define general anaesthesia, Stages,
• Shortest acting competitive NM block- Second gas effect and diffusion hypox-
er-Mivacurium(10-20 min) ia(TP-372,TV-185)
• 2 Intermediate acting competitive Nm 2. General anaesthesia-Classification( TP-
blockers- Atracurium, Vecuronium 377,TV-186)**ESSAY
• 2 long acting competitive Nm blockers- 3. Halothane(TP-379,TV-188)**
Pancuronium, Doxacurium 4. Inducing agents (Thiopentone, Propofol)
• 2 Nn blockers-Trimethaphan, Hexame- (TP-381,TV-190)**
thonium 5. Ketamine, Fentanyl(TP-383,TV-192)
6. Neuroleptics(TP-387)
7. Pre anaesthetic medication (TP-
LOCAL ANAESTHETICS 385,TV-193)**
8. Desflurane(TP-380,TV-188)
1. Classification of local anesthetics and
MOA(TP-360,TV-194)
2. Lignocaine**, Bupiva- TIPS
caine(TP-366,367;TV-200) l
3. Conduction block(TP-368,TV-202) • GA C/I epilepsy- Enflurane
u
4. Spinal anaesthesia- Complications and con- • Most common ADRs of Halothane-CV
traindications(TP-369,TV-202) and Respiratory depression m
5. Eutectic mixture(TP-366,TV-200) • GA producing malignant hyperther- i
mia-Halothane
n
• Dissociative anaesthesia-Ketamine
P.B • PROPOFOL-Popular, Rapid acting, pre- a
ferred for OP surgical prOcedures, causes i
1.PB Adrenaline + local anesthetics FOL(fall) in BP r
2.PB Oxethazaine in gastritis (unique in e
73 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

ALCOHOL 6. Flumazenil- Uses(TP-408,TV-182)**

1. Uses of ethanol(TP-394,TV-204)
2. Disulfiram, MOA, Drugs with disulfiram P.B
like action(TP-394,TV-205) **
3. RX of methyl alcohol poison- 1.PB Barbiturates contraindicated in acute in-
ing(TP-395,TV-205)** termittant porphyria (hint: enzyme induction)
4. Fomepizole(TP-395,TV-206)** 2.PB phenobarbitone in neonatal jaundice
(hint: enzyme induction )

P.B.
PHARMACOLOGY

1. PB Ethanol in Methyl alcohol poisoning ANTI-EPILEPTICS

(competes with methanol for metabolic en-
zymes and saturates them preventing forma- 1. Phenytoin – MOA , Adverse effects , us-
tion of toxic metabolites) es(TP-413,TV-208)**
2. Carbamazepine - Class of drug, MOA,
Kinetics, Interactions, Adverse effects, C/I,
TIPS Uses}[note: DOC in trigeminal neuralgia,
used in bipolar disease, has ADH like action,
• Methanol poisoning - Ethanol loading nd prefrd in pregnancy](TP-415,TV-210)
dose 0.7ml/kg followed by 0.15 ml/kg /hr 3. Sodium valproate – MOA , Adverse Effects
drip ,Uses(TP-417,TV-211)**
• Drugs causing disulfiram like reaction-Sul- 4. Broad spectrum anti convulsant(Lamotrigi-
phonyl urea, Cephalosporins(cefopera- ne, Topiramate)(TP-419,420;TV-213 tab5.10)
zone, moxalactam, cefamandole), Metroni- 5. Newer generation anti convul-
dazole, Griseofulvin sants(TP-419,TV-213)**
• Drugs used to treat withdrawal syn- 6. Gabapentin, Vigabatrine, Tiaga-
drome-Benzodiazepines(chlordiazepoxide, bine(TP-419,421;TV-214)
diazepam), Naltrexone, Acamprosate 7. RX of status epileptics, Febrile convul-
• Specific toxicity of formic acid in methanol sions(TP-424,TV-215)**
poisoning-Retinal damage 8. DOC for absence seizures-Ethosuximide

TIPS
SEDATIVES AND HYPNOTICS • 2 drugs for grandmal epilepsy- Phenytoin,
l Carbamazepine
1. Benzodiazepines v/s barbiturates- MOA, • Drugs for absent seizure - ethosuximide,
u Sodium Valproate
advantages, Uses(TP-398,TV-178)**
m 2. Drugs affecting GABA receptor gated chlo- • DOC in Absence seizures - sodium val-
i ride channel (Fig 29.3)(TP-403)** proate
3. Acute barbiturate poisoning, Drug automa- • DOC in Myclonic seizures -sodium val-
n proate
tism(TP-400,TV-183)
a 4. Classification of BZDs based on pharmaco-
i kinetic profile(TP-404)
r 5. Non benzodiazepine hypnotics (Zopiclone, PARKINSONISM
e Zolpidem)(TP-406,TV-184)
’18 74
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

1. Drugs for PARKINSONISM – Classifica- 9. RIMA (Moclobemide)(TP-455,TV-243)

tion (TP-425,TV-228)**ESSAY 10. Tricyclic Antidepressants(TP-455,TV-241)
2. Levodopa {Class of drug, MOA, Kinetics, 11. Cheese reaction(TP-455,TV-244)
Interactions, Adverse effects, C/I, Uses}(TP- 12. Selective Serotonin Reuptake Inhibi-
426,TV-229)** tors(TP-460,TV-242)**
3. MAO- B inhibitor, Amanta- 13. Atypical anti depressants(TP-462,TV-243)
dine(TP-431,TV-232) 14. Anti anxiety drugs(TP-465,TV-240)
4. Central anti- cholinergics in Parkinson-
ism(TP-433,TV-232) P.B
1.PB Lithium plus diuretics esp Thiazides(as a
P.B compensatory response to excessive loss of Na

PHARMACOLOGY
1. P.B. Levodopa+ Carbidopa** by the use of diuretics, renal excretion of Li is
2. P.B Levodopa and Vit B (Vit.B6 enhances decreased→toxicity).
peripheral decarboxylation)
3. Metoclopramide/ Domperidone in L-dopa
induced vomiting (Domperidone does not TIPS
cross BBB)** • Plasma concentration of Li-0.5-0.8mEq/L
for bipolar disease, 0.8-1.2mEq/L for acute
TIPS mania**
• Drugs causing secondary parkinson- • Rx of Bipolar disease- Carbamazepine and
ism-Resepine, Methyl dopa, Chlorproma- Valproate
zine, Metoclopromide • 2 uses and 2 ADRs of Clozapine-An-
• 2 uses and 2 adverse effects of Amanta- ti-psychotic, Resistant Schizophrenia,
dine-anti parkinsonian, anti influenza, ADRs-Paradoxical hypersalivation, agran-
ADR-Livedo reticularis, Ankle edema ulocytosis, myocarditis**
• DOC in Drug induced parkinsonism - • HIT and RUN drugs-non-selective irre-
Benzhexol, Procyclidine. versible MAO inhibitors
• Rx of cheese reactn-i/v Phentoalmine
• DOC in A/C schizophrenia - Haloperidol
DRUGS USED IN MENTAL ILLNESS 2 -20 mg/day
• 2 anti-depressants effective in chronic
1. Classification of anti-psychot- pain-Imipramine, Amitriptyline.
ics(TP-436,TV-236)**ESSAY
2. Chlorpromazine - MOA, Uses , Advere
Effects(TP-437,TV-236) OPIOIDS
3. Non psychiatric uses of antipsychot- l
ics(TP-447,TV-239) 1. Morphine {Class of drug, MOA, Kinetics,
u
4. Haloperidol(TP-441,TV-237)** Interactions, Adverse effects, C/I, Uses}(TP-
5. Atypical Antipsychotics ( Risperidone , 469,TV-217) m
Clozapine , Olanzapine , Quetiapine)(TP- 2. Morphine poisoning – Treat- i
441,TV-238 tab5.17) ment(TP-472,TV-220)
n
6. Extra pyramidal side effects of anti psy- 3. Pethidine(TP-475,TV-222)
chotics(TP-444,TV-237) 4. Methadone – Maintenance Therapy- a
7. Lithium(TP-447,TV-246)** (TP-476,TV-224) i
8. Antidepressants- Classification, Us- 5. Tramadol(TP-477,TV-224) r
es(TP-454,TV-240) 6. Opioid receptors- MOA (TP-478 fig34.1)
e
75 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

7. Pentazocine, Buprenor- 5. Rationale behind combining ACEI & ARB

phine(TP-480,TV-225)
8. Naloxone, Naltrexone(TP-483,TV-227)
TIPS
• Longest acting- Ramipril
P.B • All prodrugs EXCEPT captopril, lisinopril
1. PB Morphine in asthmatics (histamine • ADR ACEI Inhibitor- CAPTOPRIL:
releasing action) Cough, Anaphylaxis, Palpitation, Taste,
2. PB Morphine contraindicated in head Orthostatic hypotension, Potassium in-
injury** creased, Renal impairment, Impotence,
3. PB Morphine in acute LVF Leucopenia)
PHARMACOLOGY

4. PB Pethidine preferred as obstetric analgesic • Only ACEI available in i/v - Enalapril

(less neonatal respiratory depression)

TIPS DRUGS FOR HEART FAILURE

• 2 uses , 2 ADRs of Naloxone-A/C Opioid 1. Drugs used in CCF – Classifica-
poisoning, Neonatal resuscitation follow- tion(TP-519,TV-138)**ESSAY
ing morphine use in mothers,ADRs 2. Digoxin-{Class of drug, MOA, Kinetics,
• in BP, pulmonary edema Interactions, Adverse effects, C/I, Uses}(TP-
• Opioid used in non specific diarrhoea- 512,TV-141)**
Loperamide 3. Digoxin Poisoning**, drug holiday, slow
• Buprenorphine- partial agonist at mu digitalization(TP-516,TV-143) 3. Inodialators
receptor (Amrinone, Milrinone)(TP-525,TV-146)
• Pentazocine- agonist(k) antagonist(mu)
• DOC in A/c morphine poisoning- Nalox- P.B
one 0.4- 0.8 mg i.v every 2-3min till resp
picks up 1.PB digoxin in AF
2. PB digoxin + Quinidine (hint: decreases
renal clearance of digoxin, displaces it from
RAAS tissue binding sites→ toxicity)
1. RAAS, Inhibition of RAAS(TP-495) 3. PB digoxin +Furosemide (hint: frusemide→
2. ACE inhibitors (Captopril,Enalapril) hypokalemia→digoxin toxicity)
{Class of drug, MOA, Kinetics, Interactions, 4. PB digoxin + Propranolol (hint : addictive
Adverse effects, C/I , Uses)(TP-500,TV112)** depressivent action on SA and AV node, ppt
3. ARBs (Losartan) advantages over ACE AV block)
l inhibitors(TP-505,TV-115) 5. PB digoxin + Ca (hint : synergises with
digitalis→ toxicity)
u
6. PB digoxin + CCB (hint-same as 4)
m P.B 7. PB: β-blockers in CHF (hint : sympathet-
i 1. PB -Lithium + ACEI (hint: reduce Li clear- ic activity →ventricular wall stress, apoptosis
ance→ toxicity) promotion, pathological remodelling, sinister
n
2. NSAIDs + ACEI ( attenuate the hypoten- arrhythmias; all these actions antagonised by
a sive action) beta blocker)
i 3. ACEI +K sparing diuretics (hyperkalemia
r produced)
e 4. ACEI in HTN and CHF TIPS

’18 76
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

• Specific antidote for Digoxin : Digibind caine

• ECG changes in digoxin therapy-T invn,
increasePR interval,decrease QT interval
• DOC for digoxin induced ventricular ANTI-ANGINAL DRUGS
arrhythmias-Lignocaine
• Most characteristic arrhythmia d/t di- 1. Drugs in angina – Classification (TP-
goxin-non-paroxysmal supraventricular 540,TV-126)**ESSAY
tachycardia 2. Nitrates -{Class of drug, MOA, Kinetics,In-
• Hypokalemia, hypomagnesemia, hypercal- teractions,Adverse effects, C/I, Uses}(TP-
cemia increase risk of digoxin toxicity 540,TV-126)**
3. Calcium Channel Blockers- Classification,

PHARMACOLOGY
Uses , Adverse Effects(TP-546,TV-131)** 4.
ANTI-ARRYTHMICS Nifedipine, Nimodipine ,Verapamil (TP-
548,549;TV-131,132)
1. Classification of Anti- Arrythmic drugs, 5. Rational drug Combinations (Nitrates+
MOA(TP-529,TV-148)** CCB, Nitrates +Propranolol)(TP-551,TV-135)
2. Procainamide(TP-529,TV-150) 6. Nicorandil (TP-552,TV-134)
3. Lignocaine in Ventricular arrhyth- 7. Dipyridamole (Steal phenomenon),
mia(TP-530,TV-150)** Trimetazidine(TP-553)
4. Propranolol in Arrythmia(TP-532,TV-152) 8. Drug therapy in MI (TP-556,TV-137)
5. Adenosine(TP-536,TV-154) **ESSAY
6. Beta blockers in Arrhyth-
mia(TP-532,TV-152)
7. Amiodarone(TP-533,TV-152)**

PB
P.B 1. P.B- Sodium Nitrite in cyanide poisoning
1.PB Propranolol + Lignocaine (propranolol (generate methaemoglobin which has high
prolongs t1/2 of lidocaine by reducing hepatic affinity for cyanide forming cyanmethaemo-
blood flow) globin. Cytochrome & other oxidative enzymes
2.PB Amiodarone + Warfarin (increase war- are thus protected from cyanide)
farin level by reducing renal clearance{same
with digoxin})
TIPS
• Shortest acting nitrate- Amyl nitrite(inha-
TIPS lational) l
• DOC in Supraventricular tachycardia- Ve- • Other uses of nitrates-Cyanide poisoning,
u
rapamil biliary colic, esophageal spasm
• PSVT - Adenosine , Propranolol • Cerebroselective CCB-Nimodipine m
• ADRs of Amiodarone-The Periphery of • CCB which release NO-Nitrendipine i
My Lung, Liver and Cornea is Photosensi- • Longest acting CCB-Amlodipine
n
tive (Thyroid{both hyper and hypothyroid- • K+ channel openers-Nicorandil, Minoxi-
ism}, Peripheral neuropathy, Myocardial dil a
depression, Lung fibrosis, Liver toxicity, • DOC in vasospastic angina-CCB i
Corneal microdeposits, Photosensitivity) • Coronary steal phenomenon-Dipyrida-
r
• DOC of ventricular tachycardia-Ligno- mole, Hydralazine
e
77 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

ANTI HYPERTENSIVES RENAL PHYSIOLOGY

1. Classification of Anti Hyperten- 1. Diagram of nephron with sites of action of
sives(TP-558,TV-111)**ESSAY diuretics(TP-575 figIX.1,TV-163 fig4.1)
2. Clonidine, Methyl dopa(TP-565,TV-118) 2. Classification of Diuretics (TP-579,TV-
3. Hydralazine, Nitroprusside(TP-566,TV-121) 163)**ESSAY
4. Drugs for HT in Pregnancies(TP-572)** 3. High Ceiling diuretics - {Class of drug,
5. Hypertensive emergen- MOA, Kinetics, Interactions, Adverse effects,
cies(TP-572,TV-124)** C/I, Uses}(TP-579,TV-166)**
PHARMACOLOGY

4. Non diuretic uses of diuret-

ics(TP-581,TV-167)
P.B 5. Complications of diuretic therapy-
1. PB diuretics in HT, Thiazides/ Loop diuret- (TP-584,TV-167)
ics in HT (refer MOA thiazides. Thiazides have 6. Which is preferred in Ca stones of renal
long duration of action, well tolerated and pelvis- Thiazides/ Furosemide
cheap. Loop D-short duration, used only when 7. Acetazolamide, Spironolac-
complications present) tone(TP-586,TV-164)**
2.PB. CCB not in pregnancy (weaken labour) 8. Inhibitors of renal epithelial Na channel-
3.PB. Verapamil + β blocker(marked bradycar- Triamterene, Amiloride(TP-589,TV-171)
dia, AV block) 9. Mannitol- MOA, Uses(TP-590,TV-165)**
10. ADH,Desmopressin(TP-593,TV-172)

P.B
1.PB Loop diuretics+ Aminoglycosides (both
ototoxic and nephrotoxic→additive toxicity)
TIPS 2. PB Furosemide in acute LVF (vasodilator
• A/E of Methyl dopa-METHYL DO- action that precedes saluretic action→↓in
PA-Mental retardation, Electrolyte imbal- blood volume and venous return)
ance, Tolerance, Headache, Impotence, 3. PB. Thiazides/ Furosemide in hypercalce-
Lactation, Dry mouth, Oedema, Parkin- mia (Frusemide ↑Ca excretion→↓S.Ca level)
sonism, Anaemia 4. PB Thiazide in diabetes insipidus
• Anti-hypertensives safe in pregnancy-Bet- (hint:paradoxical antidiuretic effect)
ter Mother Care During Hypertensive 5. PB Mannitol used in cerebral edema, C/I
l Pregnancy-Beta blockers, Methyl dopa, in pulmonary and cardiac edema (by osmotic
Clonidine, Dihydropyridine, Hydralazine, action it ↑movt of water from brain paren-
u Prazosin chyma, CSF and aq.humour;hence used in
m • DOC for hypertensive emergencies in cerebral edema, if ARF already set in kidney
i pregnancy-Hydralazine is incapable of forming urine→↑plasma vol-
• First dose effect-Prazosin ume→pulmonary edema and heart failure)
n • Antihypertensive drug in Rx of alope-
a cia-Minoxidil TIPS
i • Least potent and most ototoxic loop di-
r uretic-Ethacrynic acid
• DOC of Li induced Diabetes Insipi-
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

dus-Amiloride 25. Wide spectrum hypolipidimic drug - Nic-

• K+ sparing diuretic used for Rx cystic otinic acid(TP-640,TV-159)
fibrosis-Amiloride 26. Plasma expanders(TP-644,TV-160)
• 2 drugs used in cerebral edema- Mannitol,
Furosemide
P.B
• Folic acid /folinic acid in methotrexate
BLOOD AND BLOOD FORMING therapy [folinic acid-active coenzyme, no
DRUGS need to be reduced by DHFRase so meth-
otrexate(DHFRase inhibitor)toxicity is
1. Mucosal block theory(TP-601,TV-325) antagonised by it]

PHARMACOLOGY
2. Oral formulations of Fe and its adverse • Menadione contra indicated in newborn
effects(TP-601,TV-325) [ppt kernicterus by inducing hemoly-
3. Parenteral Fe therapy, A/C iron poison- sis→↑bilirubin load, competitively inhibit-
ing(TP-604,TV-326) ing bilirubin glucuronidation]
4. Erythropoeitin(TP-611,TV-331) • Heparin/ Warfarin in pregnancy [foetal
5. Vitamin K(TP-613,TV-530) warfarin syndrome]**
6. Ethamsylate(TP-616)
7. Anticoagulants- In vivo, In vit- TIPS
ro(TP-617,TV-313) • Clot specific fibrinolytic agent-Alteplase
8. Heparin -{Class of drug, MOA, Kinetics, • Specific antidote for fibrinolytics-Epsilon
Interactions,Adverse effects, C/I, Uses}(TP- Amino Caproic Acid(EACA)
617,TV-313)** • Atorvastatin-Antioxidant property
9. LMW heparin(TP-619,TV-313) • ADR of Heparin-Bleeding,thrombocyto-
10. Protamine sulphate(TP-620,TV-314)** 11. penia,osteoporosis,alopecia
Warfarin – MOA ,uses ,interactions ,Warfarin • Antidote of heparin-Protamine sulphate
toxicity(TP-617,TV-316)** • Monoclonal antibody used as anti-platelet
12. Uses of anticoagulants(TP-624,TV-314) drug-Abciximab (Gp IIb-IIIa Inhibitor)
13. Oral anticoagulants-MOA,adverse effects, • Drug causing maximum HDL rise-Nico-
interactions(TP-620,TV-313) tinic acid
14. Fibrinolytics-MOA,uses(TP-625,TV-514) • 2 low molecular weight heparins-Enoxa-
15. Clot specific fibrinolytics(Hint:Alteplase) parin, Reviparin
(TP-625) • 2 antiplatelet drugs-Aspirin, Dipyridamole
16. Antifibrinolytics-MOA,uses,-
source(TP-628,TV-321)
17. Anti platelet drugs, uses(TP-629,TV-322) PEPTIC ULCER l
18. Aspirin, Uses(TP-629,TV-322)
19. Ticlopidine, Clopidogrel(TP-630,TV-324) u
1. Drugs in peptic ulcer – Classification with
20. Abciximab(TP-631,TV-323)** examples(TP-649,TV-301)**ESSAY m
21. Hypolipidemic drugs – Classification with 2. Proton pump inhibitors(TP-651,TV-301)** i
MOA(TP-635,TV-156)**ESSAY 3. H2 antagonists(TP-649,TV-302)
22. HMGCoA Reductase Inhibitor- ( Class of n
4. CBS(TP-656,TV-306)
drug, MOA, Kinetics, Interaction, Adverse 5. Anti- H Pylori drugs(atleast one triple a
reaction, C/I, Uses)(TP-636,TV-156)** 23. drug regimen with dose)(TP-657,TV-308) i
Gemfibrozil(TP-639,TV-158)
r
24. Ezetimibe-MOA(TP-641,TV-156) P.B
e
79 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

1. Cimetidine/ Ranitidine in 30 yr old male tives(TP-672,TV-297)

suffering from severe ulcer [Ranitidine pre- 2. Lactulose- Why it is used in Hepatic en-
ferred since cimetidine has antiandrogenic cephalopathy?(TP-676,TV-300)
action] 3. WHO recommended ORS formu-
2. Sucralfate ineffective in patients with antacid la(TP-680,TV-293)
therapy [antacids reduce efficacy of sucralfate 4. Super ORS(TP-680,TV-294)
by raising the pH. Sucralfate needs pH <4 for 5. Drug therapy of diarrohea(TP-681,TV-224)
its action]** 6. Loperamide(TP-686,TV-226)
3. Ranitidine + Sucralfate : basis of combina- 7. Laxative used in hepatic encephalopathy
tion (same as prev. qn)
4. Tetracycline + Antacid combination not
PHARMACOLOGY

used why? [antacids reduce absorption of TIPS

tetracycline] • Prokinetic drug with little anti emetic
5. P.B Mg(OH)2 + Al(OH)3 ; P.B NaHCO3/ ppty-Cisapride(no D2 action)
Mg trisilicates-good antacid. • Somatostatin analogue used in secretory
6. PB Rabeprazole in peptic ulcer [fastest acid diarrhea-Octreotide
suppression, aid gastric mucin synthesis]. • PPIs given i/v-Pantoprazole, Lansoprazole
• Laxative in cardiac patients-Liquid paraf-
fin(prevents straining)
ANTI-EMETICS • DOC of chemo and radiotherapy induced
vomiting-Ondansetron(5HT3 antagonist)
1. Classification with exam-
ples(TP-662,TV-286)**ESSAY
2. Metoclopramide- { Class of drug , MOA,
Kinetics, Interactions, Adverse effects, C/I, ANTIBIOTICS- GENERAL
uses}(TP-664,TV-284)** CONSIDERATION
3. Anti-dopaminergic S/E of Metoclopra- 1. Drug resistance- Mechanism , Cross resis-
mide(TP-665,TV-284) tance(TP-691,TV-405)
4. Domperidone-DOC in drug induced 2. Super infection(TP-693,TV-406)**
vomiting, DOC Chemo/radiotherapy, DOC 3. MOA of antimicrobials – 2 examples of each
levodopa induced vomiting(TP-666,TV-251) with diagram
5.Cisapride, Ondansetron(TR-667,TV-292) 4. Post antibiotic Effect( Long PAE – fluoro-
6.Diagram showing MOA of prokinetic quinolones, Aminoglycosides, B- lactam)
drugs(TP-665)
7.Methyl Polysiloxane(TP-670) P.B
l 1. Combination of antibiotics – Rationale
P.B - Broadens the spectrum of activity (Eg:
u
1. PB: Promethazine + Metoclopramide [Pro- Metronidazole+Ceftriaxone)
m methazine supplement antiemetic action and - Supradditive synergism (Eg: Penicillin+-
i reduce the attending dystonic reactions] Gentamicin)
- Prevents emergence of resistance (Multi-
n
drug therapy in TB & Leprosy)
a CONSTIPATION AND DIARRHOEA - Reduces duration of therapy ((Multi-
i drug therapy in TB & Leprosy)
r 1. Classification – Bulk forming, stool - Reduces adverse effects (Amphotericin-
softners, stimulants, osmotic purga- B+Flucytosine)
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

- Combination acts faster (Sulfadox- pus-Mafenide

ine+Pyrimethamine) • ADRs of Sulfonamides-RASH AB-
- Sequential blockade (Eg: Sulfamethox- C(RAsh, SLE, Hemolysis in G6PD,
azole+Trimethoprim, Sulfadoxine+Pyri- Aplastic anaemia, Bilirubin displace-
methamine) ment{Kernicterus}, Crystalluria)
- Combination may produce cidal effect
(Eg: Sulfamethoxazole+Trimethoprim)
QUINOLONES
SULFONAMIDES 1. Nalidixic acid-Uses(TP-709,TV-416) 2.
Fluroquinolones - Ciprofloxacin {Class

PHARMACOLOGY
1. Sulfonamides - MOA, Development of of drug, MOA, Kinetics, Interactions,
resistance, Adverse effects(TP-704,TV-450) Spectrum, Adverse effects, C/I, Uses }
2. Topically used Sulfon- (TP709,TV-416)**ESSAY
amides(TP-705,TV-450) 3. Sparfloxacin, Levofloxacin, Gatifloxacin,
3. Sulfadiazine,Mafenide(TP-705,TV-450) Ofloxacin(TP-713,TV-418)
4. Cotrimoxazole { Class of drug, MOA, 4. Rx typhoid (also in pregnancy)(TP-
Kinetics, Interactions, Spectrum,Adverse 712,TV-416)
effects, C/I, Uses}(TP-706,TV-414)**
5. Site of action of Sulfonamides and Tri- P.B
methoprim(TP fig50.1)** 1. PB: Pefloxacin/Ciprofloxacin in meningi-
tis - Pefloxacin - Passage into CSF is higher
P.B than other FQs

1. PB: Sulfadoxine + Pyrimethamine in ma- TIPS

laria (supra-additive synergistic combina- • DOC in Typhoid - Ciprofloxacin 500mg
tion due to sequential blockade in bac.folate BD x 10 day
meta. However use is limited to chloroquine • Urinary antiseptics-Nalidixic acid, Ni-
resistant falciparum malaria since the com- trofurantoin, Methenamine
bination cause serious adverse effects) • F.Q effective against M.leprae-Ofloxacin
2. PB: Sulfamethoxazole + Trimethoprim • F.Q effective against Atypical MB and
(Cotrimoxazole-supra-additive synergism anaerobes-Sparfloxacin
due to sequential blockade in bacterial folate • F.Q causing QT prolongation-Lome-
metabolism) floxacin, Sparfloxacin, Gatifloxacin

TIPS l
• DOC in Chancroid – Cotrimoxazole BETALACTAM ANTIBIOTICS u
(800+160)BD x 7 days / Erythromycin 2
gm /day x 7 days 1. MOA, Classification(TP-716,TV-420) m
• DOC in Pneumocystis carinii - Cotri- 2. Benzyl Pencillin ( Class of drug, MOA, i
moxazole(800+ 160) BD 4-6 times Kinetics, Interactions, Spectrum, Adverse n
• DOC inToxoplasmosis - Pyrimethamine effects, C/I, Uses)(TP-717,TV-421)**
+ Sulfadiazine 3. Semi synthetic pencillins – Classifica- a
• Sulphonamide used in ophthalmia neo- tion(TP-720,TV-425) i
natorum-Sulfacetamide 4. Repository Pencillin G injec- r
• Sulphonamide used in the presence of tion(TP-720,TV-423) e
81 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

5. Ampicillin, Amoxicil- • DOC in Rheumatic fever (prophylaxis)

lin(TP-722,723;TV-426) - Benzathine penicilline 1 - 2 mg every 4
6. Rx of MRSA(TP-721)** weeks
7. β Lactamase inhibitors(TP-724,TV-343)** • DOC in Meningitis (pseudomonas) - Cef-
8. Anti pseudomonal penicillins(Carbene- tazidime + Gentamycin
cillin, Ticarcillin, Piperacillin)(TP-723) • DOC in Meningitis(H.infl, enterobact) -
9. Cephalosporins- Classification, Adverse Ceftriazone, Cefuroxime
effects, Uses(TP-725,TV-428)**ESSAY • DOC in Gonorrhea- non penicillinase
{Third gen Cephalosporins**} producing organisms –Amoxicllin 3.5g
10. Ceftriaxone , Cefuroxime , Cefotaxi- oral / Procaine PenicillinG 4.8 mu i .m
me,Cefpirome(TP-727,729;TV-408) ; Penicillinase producing - Ceftriaxone
PHARMACOLOGY

11. Rx of Ophthalmia neonatorum,Syphilis 250mg i.m

• Cefazolin-Surgical Prophylaxis
P.B
• PB: Amoxicillin + Clavulanic acid, Aug- TETRACYCLINE AND
mentin** CHLORAMPHENICOL
• PB: Ampicillin + Sulbactum,Sulbacin**
{Ampicillin and Amoxicillin are β lactam 1. MOA of Tetracycline and Chlorampheni-
antibiotics, Clavulanic acid and Sulbac- col(fig 52.1)
tam are β lactamase inhibitors.There- 2. Tetracycline- Spectrum, Uses and Adverse
fore,combination increases activity by Effects(TP-734,TV-437)**ESSAY
preventing β lactamase mediated enzyme 3. Chloramphenicol- Uses and Adverse Ef-
destruction} fects(TP-739,TV-440)
• PB: Procaine Pencillin should not be
used as IV(I.V. Inj. Of Procaine Penicillin TIPS
produces CNS stimulation, hallucination • DOC in Atypical pneumonia - tetracycline
& convulsions due to Procaine Causes / erythromycin
microembolism) • DOC in Cholera, plague, relapsing fever,
• PB: Procaine Pencillin + Probenecid – rickettsial infection - tetracycline
Beneficial (Probenecid competes for tu- • DOC in Brucellosis - doxycycline 200mg/
bular secretion & thus retards excretion day x 6 weeks
of Penicillin/Cephalosporin- Increases • Minocycline-Vestibular toxicity
the blood levels and volume of distribu- • Tetracycline with enterohepatic circula-
tion) tion-Doxycycline
• PB: Imipenem + Cilastatin in hospital • Advantages of Doxycycline over Tetracy-
l acquired infection –Beneficial -Cilastatin cline
inhibits Dihydropeptidase I on the brush
u
border of renal tubular cells, which rap-
m idly metabolises Imipenem AMINOGLYCOSIDE
i
1. Classification, MOA of Aminoglyco-
n
TIPS side(TP-743),Adverse Effects**
a • DOC in A/C rheumatic fever – Penicillin 2. Toxicity of Aminoglycosides, Mechanism of
i • DOC in Syphilis-Penicillin resistance(TP-744,TV-432)
• DOC in Anthrax, actinomycosis, trench 3. Neomycin, Gentamycin , Streptomycin ,
r
fever - PnG Amikacin(TP 747-750,TV-434,435)
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

4. Draw and label MOA of Aminoglyco- ■■ Pseudomembanous enterocolitis –

sides(fig 52.1) Vancomyin, Metronidazole
• Uses of Macrolides-CLAW(Chancroid,
P.B Legionella, Atypical pneumonia, Whoop-
1. PB: Aminoglycoside + Amphotericin B not ing cough)
used – Adverse- Additive nephrotoxicity • Prokinetic macrolide antibiotic-Erythro-
2. PB: Aminoglycoside + Frusemide not used – mycin
Adverse - Additive ototoxity • Erythromycin esteolate salt causes choles-
3. PB: Gentamycin + Penicillin in SABE - Ben- tatic jaundice
eficial - Penicillin inhibits cell wall synthesis &
facilitate entry of Gentamicin - Other relevant

PHARMACOLOGY
points from “Combination Of Antibiotics” ANTI TB DRUGS
1. Treatment of TB – DOTS(TP-774,TV-
TIPS 457)**ESSAY
• DOC in Tularemia-Streptomycin 2. Rifampicin {Class of drug, MOA, Kinetics,
• DOC in SABE-Penicillin/Gentamicin Interactions, Spectrum, Adverse effects, C/I,
• Aminoglycoside with widest spectrum of Uses}(TP-767,TV-454)
action-Amikacin(resistant to inactivating 3. INH(Chemoprophylaxis**), Pyrazinamide ,
enzymes) Ethambutol
• AG with highest nephrotoxicity-Neomycin 4. Adverse effects of anti TB drugs
• AG with lowest nephrotoxicity-Streptomy- 5. PB of employing multiple drug therapy-
cin (TP-772)
• AG used topically-Neomycin, Framycetin 6. TB in pregnancy(TP-777,TV-459)**
7. TB in AIDS(TP-778,TV-456)**
8. 2nd line drugs- Cycloserine, Clarithromy-
MACROLIDES AND OTHER ANTIBAC- cin(TP-770,TV-459),MDR-TB**
TERIALS 9. Role of steroids in TB(TP-776,TV-459)
1.MOA of Macrolides(fig 52.1)
2. Erythromycin {Class of drug, MOA, Kinet-
ics, Interactions, Spectrum, Adverse effects, TIPS
C/I, Uses}(TP-752,TV-442)** • A/E of INH-Hepatotoxicity,peripheral
3. Azithromycin(TP-754,TV-444) neuritis
4. Clarithromycin(TP-754,TV-443) • A/E of Pyrazinamide-Hyperuricemia
5. Clindamycin (causes Cl. difficile superinfec- • A/E of Ethambutol-Retrobulbar neuritis,
tion)(TP-756,TV-492) hyperuricemia
6. Vancomycin - Redman‘s syn- • Rifampicin-Uses-TB, leprosy, prophylax- l
drome(TP-757,TV-468) is of streptococcal and meningococcal
u
7. Linezolid(TP-758,TV-468),MOA** carriers, A/E-Orange-red discoloration of
8. Rx of UTl(TP-761,TV-415) urine m
9. Streptogramin • Streptomycin-Only parenteral anti-TB i
drug(i.m), primary anti TB drug C/I in
n
TIPS pregnancy**
• DOC in Whooping cough - Erythromycin • Standard drug for chemoprophylaxis of a
■■ MRSA- Vancomycin , Linezolid** TB-INH 300mg daily ,6 to 12 months** i
■■ Chlamydia trachomatis - Azithromycin 1 • Rifampicin is the safest drug in renal r
g oral OD failure e
83 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

• Rifampicin- active against persisters. 2. PB. Amphotericin B+ Flucytosine in myco-

sis
- Beneficial
ANTI LEPROTICS (ESSAY) - Amphotericin B increses the perme-
ability of fungal cell membrane by forming
1. Dapsone - MOA, Uses , Adverse Ef- pores 7 channels and facilitate the entry of
fects(TP-780,TV-461) Flucytosine
2. Clofazimine (in lepra reaction)(TP- - Other relevant points from
781,TV-462) “Combination Of Antibiotics”
3. MDT of Leprosy(TP-783,TV-409)** 3. PB Fluconazole in fungal meningitis (good
4. Reactions in leprosy, Manage- CSF penetration) - Good CSF penetration &
PHARMACOLOGY

ment(TP-786,TV-463)** less toxic

5. ROM Regimen in leprosy(TP-785)
TIPS
TIPS • Antifungal drug with disulfiram like reac-
• Leprostatic drug with anti-inflammatory tion-Griseofulvin
property- Clofazamine • AF with anti-androgenic action-Keto-
• Dapsone- DOC of dermatitis herpetiformis conazole
-produces sulfone syndrome • Luminal antibiotic with antifungal and
• DOC for type 1 and type 2 lepra reaction- antibacterial- Quiniodochlor
steroid • Dose limiting activity of Amphotericin B-
• THALIDOMIDE- gold std for treatment of Nephrotoxicity
type 2 reaction • Doc for candidiasis, coccidioidal and cryp-
tococcal meningitis- Fluconazole
• 2 drugs for superficial mycosis- AMB,
ANTI FUNGALS(ESSAY) Nystatin
• 2 drugs used in dermatophytosis- Griseo-
1. Amphotericin B(TP-787,TV-464)** fulvin, Ketoconazole
2. Nystatin(TP-789,TV-464) • DOC for Blastomycosis, histoplasmosis,
3. Griseofulvin {Class of drug, MOA, Kinetics, coccidiomycosis, paracoccidiomycosis,
Interactions, Spectrum, Adverse effects, C/I, sporotrichosis-Itraconazole
Uses}(TP-790,TV464)[disulfiram likr action]** • DOC for Invasive aspergillo-
4. Clotrimazole(TP-792,TV-465)** sis-Voriconazole
5. Ketoconazole {Class of drug, MOA, Kinet-
ics, Interactions, Spectrum, Adverse effects,
l C/I , Uses }(TP-792,TV-469)** ANTI VIRAL DRUGS
6. Fluconazole(TP-793,TV-470)
u 7. Terbinafine(TP-795,TV-469) 1. Acyclovir(TP-799,TV-473)**
m 8. Mention 2 uses and 2 adverse effects of Flu- 2. AntiRetroviral Therapy-
i conazole (TP-805,TV-476)**ESSAY
3. Zidovudine(TP-806,TV-476)**
n P.B 4. Anti-influenza drugs (Amantadine, Osel-
a 1. PB Terfinadine/ Astemizole/ Cisapride +Ke- tamivir)(TP-801,TV-475)
i toconazole (ketoconazole causes excessive rise 5. NNRTIs(TP-808,TV-477)** 6. Amanti-
in plasma levels of these drugs→polymorphic dine- uses(TP-801,TV-475) 7. Interferon
r
ventricular tachycardia) alpha(TP-801,TV-481) 8. Protease inhibi-
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

tors(TP-809,TV-478)** • DOC for radical cure of vivax and ovale

malaria-Primaquine
TIPS • DOC for malaria in pregnancy-Chloro-
• DOC in Herpes infection -Acyclovir quine
CMV infection - Gancyclovir • Chloroquine uses-MALARID(MAlar-
• Acyclovir-Least toxic antiviral drug, pro- ia,Lepra reactions,Amoebiasis,Rheumatoid
phylaxis for recurrent genital herpes arthritis,Infectious mononucleosis,Discoid
• Gancyclovir-used only i/v.A/E- Myelosup- lupus erytthematoses)
pression, CNS S/E(Headache to convul- • Chloroquine causes Bull‘s eye maculopa-
sions) thy
• Stavudine- NRTI causing peripheral neu-

PHARMACOLOGY
ropathy, lactic acidosis ANTI AMOEBIASIS(ESSAY)
• NRTI causing bone marrow suppres- 1. Classification of Anti Amoebic Drugs(TP-
sion-Zidovudine Pancreatitis-Didanosine 837,TV-493)**
Increased risk of MI-Abacavir 2. Metronidazole-Class of drug, MOA, Kinet-
ics, Interactions, Spectrum, Adverse effects,
ANTI MALARIAL DRUGS C/I, Uses}(TP-837,TV-493)**
(ESSAY) 3. Diloxanide furoate(TP-840)**
4. Pentamidine(TV-497)
1. Classify AntiMalarial Drugs(TP-
816,TV-481)** P.B
2. Chloroquine(TP-821,TV-484)** 1. PB.Metronidazole +Diloxanide furoate in
3. RX of cerebral malaria(TP-821,TV-486) intestinal amoebiasis
4. Primaquine(TP-828,TV-490)** - Beneficial
5. Artemisinine derivatives(TP-829,TV-491) - Metronidazole is a tissue amoebicide
6. ACT(TP-831,TV-492)** whereas Diloxanide furoate is a luminal
7. Diagram showing site of action of drugs amoebicide, provoding complete cure

P.B
1.Quinine,why is it given in 5%dextrose TIPS
-Beneficial • DOC in Trichomonas vaginitis and
- Quinine produces hypoglycemia due to Dracunculus mediensis- Metronidazole
hyperinsulinemia 400mg TDS x 7 days
2.Chloroquine+Primaquine • DOC in Anaerobic infection-Metronida-
- Beneficial zole
- Chloroquine is mainly blood schizontici- • DOC for asymptomatic amoebiasis and l
dal(Erythrocytic stage) whereas Primaquine effective against C/c cyst carrier-Diloxa-
u
is tissue schizonticidal (Preerythrocytic nide furoate
stage & Hypnozoites) & gametocidal, pro- m
viding complete cure • DOC for kala-azar-Sodium stibogluconate i
• Drug used for extraintestinal amoebia-
n
sis-Chloroquine
TIPS a
• DOC in F. malaria- Chloroquine 600mg i
stat followed by 300mg daily - next 2 days. ANTI HELMINTHICS (ESSAY) r
Cerebral malaria - Quinine i. v
e
85 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

1. Albendazole(TP-850,TV-500)** tein kinases in CML cells)

2. Pyrantel palmoate(TP-852,TV-501)** 2. PB. Mercaptopurine+Allopurinol (6-MP
3. Piperazine-flaccid paralysis(TP-852,TV-501) meta by xanthine oxidase, which is inhibited
4. DEC with dose(TP-853,TV-501)** by allopurinol; dose must be reduced if allo-
5. Ivermectin(TP-853,TV-503)** purinol given concurrently)
6. Niclosamide, Praziquan-
tel(TP-854,TV-504)** TIPS
• DOC in Hemorrhagic cystitis - MESNA
TIPS • DOC in Multiple myeloma- Melphalan
• Filariasis- DEC 2mg/kgTDS x 7days • DOC in C/c lymphoid leukaemia— Chlo-
• Tropical eosinophilia - 2-4 mg/kg DEC rambucil
PHARMACOLOGY

TDS x 2-3 wks • DOC in C/c myeloid leukaemia— Busul-

• Albendazole is the DOC for most nem- phan
atode infections except filariasis(DEC), • DOC in Ca breast— Tamoxifen,Metho-
onchocerca and strongyloides(Ivermectin) trexate
• Praziquantel is the DOC for all trematode • DOC in Ca cervix—Mitomycin C,metho-
and cestode infections except fasciola(Bi- trexate
thionol) and hydatid(Albendazole) • Cardiotoxic anticancer antibiotics- Doxo-
• Tinea infection-Niclosamide rubicin, Daunorubicin
• Anti-helminthic acting as immunomodula- • Most common side effect of Cyclophos-
tor-Levamisole phamide- Hemorrhagic cystitis
• Only orally effective drug for pediculosis • Glove and stocking neuropathy is the s/e
and scabies-Ivermectin of- Paclitaxel

ANTI-CANCER DRUGS IMMUNOSUPPRESSANTS

1.Cyclosporine(TP-878,TV-520)**
1. Toxicity of cytotoxic drugs(TP-876,TV-506) 2.Tacrolimus(TP-881,TV-520)
2. Cell cycle specific anti neoplastic agents(TP- 3.Immunosuppressant antibod-
862,TV-510) ies(TP-884,TV-522)
3. Alkylating agents(TP-860,TV-507)** 4.Drugs used for graft rejection- Methyl pred-
4. Cyclophosphamide(TP-860,TV-508)** nisolone, Muromonab
5. Busulfan, Chlorambucil(TP-860,TV-509)
6. Methotrexate(TP-862,TV-510)** CHELATING AGENTS
7. Leucovorin rescue(TP-862,TV-511) 1. BAL(TP-905,TV-517)
l 8. Mercaptopurine, Azathioprine (TP- 2. D- Penicillamine(TP-907,TV-518)
863,TV-511) 3. Desferrioxamine(TP-907,TV-519)
u
9. Anti cancer antibiotics(TP-867,TV-513) 4. Desferrioxamine/ Dimercaprol in Fe poi-
m 10. Vinca alkaloids(TP-865,TV-512)** soning
i 11. Paclitaxel(TP-865,TV-513)**
12. Camptothecin analogues(TP-866,TV-513) Name two drugs:
n
13. L- asparaginase(TP-868,TV-514) 1. Given Sublingually – GTN , Buprenoph-
a rine
i 2. Given Rectally – Diazepam , Indomethacin
P.B 3. Given as Transdermal patches - Nicotine ,
r
1. P.B-Imatinib in CM (inhibits tyrosine pro- Fentanyl
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

4. Microsomal Enzyme Inhibitors – Erythro- 27. Anticholinergics used in motion sickness –

mycin , Ketoconazole Hyoscine , Dicyclomine
5. Microsomal Enzyme Inducers - Phenobar- 28. Anticholinergics used in Pre Anaesthetic
bitone , Rifampicin Medication – Glycopyrrolate , Atropine
6. Low First Pass Metabolism – Phenobarbi- 29. Selective β2 Agonists – Salbutamol , Ter-
tone , Theophylline butaline
7. High First Pass Metabolism- Lignocaine , 30. Selective β1 Antagonists – Atenolol , Me-
Isoprenaline, Propranolol toprolol

PHARMACOLOGY
8. Zero Order Kinetics – Phenytoin , Warfarin 31. Selective α1 Agonists- Phenylephrine ,
9. Low Safety Margin – Digoxin , Anticonvul- Methoxamine
sants , Lithium 32. Nasal Decongestants – Phenylephrine ,
10. Competitive Inhibiton – Neostigmine , Xylometazoline , Oxymetazoline
Sulfonamides , Captopril 33. Indirectly Acting Sympathomimetics –
11. Non Competitive Inhibition – Acetazol- Amphetamine , Tyramine , Methamphetamine
amide , Aspirin 34. Anoretics – Fenfluramine , Dexfenflur-
12. Therapeutic Window Phenemenon- Tricy- amine
clic Antidepressants , Clonidine 35. Uterine Relaxants – Isoxsuprine , Ritodrine
13. Tachyphylaxis – Tramine , Ephedrine , 36. Selective α1 Blockers – Prazosin , Tera-
Nicotine zosin
14. Idiosyncrasy – Barbiturates , Quinine , 37. Treatment of BPH – Prazosin , Terazosin
Chloramphenicol 38. Selective α2 Blockers – Yohimbine , Rau-
15. Phototoxicity – Tetracycline , Amiodarone wolscine
16. Teratogenicity – Thalidomide , Sodium 39. Non selective β blockers – Propranolol ,
Valproate , phenytoin Timolol
17. Centrally Actind anti-AChE – Rivastig- 40. Cardio selective β blockers (β1Selective
mine , Donapezil blocker ) – Metoprolol , Atenolol
18. Treatment of Alzhimers – Rivastigmine , 41. β + αAction – Labetalol , Carvedilol
Donapezil 42. Used for Open Angle Glaucoma – Timolol
19. Cobra bite , Post Operative Decurarisa- , Betoxolol , Latanoprost
tion – Neostigmine + Atropine 43. Used for Angle Closure Glaucome – Hy-
20. AntiCholinesterase Poisoning – Atropine pertonic Mannitol , Acetazolamide
and Pralidoxime 44. Carbonic Anhydrase Inhibitor – Acetazol-
21. Miotics – Pilocarpine , Physostigmine amide , dorzolamide l
22. Mydriatics – Atropine , Cyclopentolate , 45. H1 receptor Antagonists – Promethazine ,
Diphenhydramine , Dimenhydrinate u
Tropicamide
23. Vasicoselective AntiCholinergics – Oxy- 46. Second Generation Antihistaminics – Cer- m
butynin , Flavoxate trizine , Loratidine , Azelastine i
24. Centrally Acting Anticholinergics – Ben- 47. Vertigo – Cinnarizine , Betahistine
48. H2 Antagonists – Cimetidine , Ranitidine n
zhexol , Procyclidine (AntiParkinsonian)
25. Anticholinegics used in Bronchial Asthma 49. 5HT3 Antagonists – Ondansetron , Gran- a
– Ipratropium Bromide , Tiotropium Bromide isetron
i
26. Anticholinergics used in Peptic Ulcer – 50. Ergot Alkalois – Ergotamine , Ergometrine
51. Migraine – Sumatriptan , Ibuprofen r
Pirenzepine , Propantheline
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

52. Prophylaxis of Migraine – Beta blocker + 78. AntiThyroid Drugs – PropylThiouracil ,

CCB + Amitriptyline Methimazole
53. 5HT2 Antagonists – Ketanserin , Cypro- 79. Inhibit Iodide Trapping – Thiocyanates ,
heptadine , Methysergide Perchlorates
54. Postpartum Haemorrhage – Carboprost , 80. Radioactive Iodine – I 131 , I 125
Dinoprost 81. Inhibit peripheral conversion f T4 to T3 –
55. Abortion – Mifepristone , Misoprostol Propylthiouracil , Propranolol , Amiodarone
56. Induction of Labour – Misoprostol , Dino- 82. Treatment of Thyrotoxicosis – PropylTh-
prostone iouracil , Propranolol
57. Preferential COX 2 Inhibitors – Nime- 83. Rapid Acting Insulin – Insulin Lispro ,
sulide , Meloxicam Insulin Aspart
PHARMACOLOGY

58. Selective COX 2 Inhibitors – Etoricoxib , 84. Long Acting Insulin – Insulin Glargine ,
Parecoxib (Gastro Protective) Insulin Detimer
59. Topical NSAIDS – Diclofenac , Ibuprofen 85. Intermediate Acting Insulin – Insulin
60. Acute Musculoskeletal and osteoarthritic Lente , Isophane Insulin
pain – Paracetamol , Diclofenac 86. First Generation SulfonylUrea – Tolbut-
61. DMARDS – Methotrexate , Sulphasalazine amide , Chlorpropamide
62. Biologic Response Modifiers – Etanercept , 87. Second Generation SulfonylUrea- Gliben-
Infliximab , Anakinra clamide , Glipizide
63. Acute Gout – NSAIDs , Cochicine 88. BIguanide-Metformin , Phenformin
64. Uricosuric Drugs – Probenecid , Sulfinpyr- 89. Thiazolidinediones – Rosiglitazone , Piogl-
azone itazone
65. Uric acis synthesis Inhibitor – Allopurinol 90. α glucosidase inhibitor – Acarbose , Migli-
, Febuxostat tol
66. Pharyngeal Demulcents – Lozenges , Linc- 91. Meglitinide – Rosiglitazone , Pioglitazone
tuses 92. Treatment of Ulcerative Colitis- Hydro-
67. Mucolytics – Bromhexine , Ambroxol cortisone , MethylPrednisolone
,Acetylcystiene 93. Treatment of Cerebral Edema – Dexa-
68. Antitussives – Codiene , Dextrometho- methasone , Betamethasone
rphan 94. Treatment of Adrenal Insufficiency – Hy-
69. Broncho Dilalators – Salbutamol , Salmet- drocortisone , Dexamethasone
erol 95. Anabolic Steroids – Nandrolone , Stanozo-
70. Anticholinergics used in Bronchial Asthma lol , Oxymetholone
– Ipratropium Bromide , TioTropium Bromide 96. AntiAndrogens- Flutamide , Danazol
71. Leukotriene Antagonists – Montelukast , 97. 5α reductase Inhibitor – Finasteride ,
l Zafirukast Dutasteride
72. Mast Cell Stabilizers – Na Cromoglycate , 98. Treatment of Erectile Dysfunction –
u
Ketotifen (PDE-5 inhibitors) – Sildenafil , Tadalafil
m 73. Inhalational Corticosteroids in Bronchial 99. Synthetic Estrogens – Ethinyl Estradiol ,
i Asthma – Fluticasone , Budesonide Diethylstilbestrol
74. GH Inhibitors – Somatostatin , Octreotide 100. AntiEsrtogens – Clomiphine Citrate ,
n
75. Prolactin Inhibitors – Bromocriptine , Fulvestrant
a Cabergoline 101. SERMs – Tamoxifen , Raloxifene
i 76. GnRH Agonists – Gonadorelin , Triptore- 102. Aromatase Inhibitors – Letrozole , Anas-
r lin , Nafarelin trozole
77. GnRH Antagonists- Ganirelix , Cetorelix 103. Antiprogestins – Mifepristone , Onapri-
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

stone nytoin
104. Tocolytics – Isoxsuprine , Ritodine , 128. Peripheral Decarboxylase Inhibitor –
Nifedipine , Atosiban Carbidopa , Benserazide
105. Bisphosphonates – Alendronate , Zole- 129. Dopaminergic Agonists – Bromocriptine
dronate , Ropinirole , Pramiprexole
106. Treatment of Osteoporosis – Alendronate 130. MAO-B Inhibitors – Selegiline ,
, Raloxifene Rasagiline
107. Non depolarizing Neuromuscular block- 131. MAO- A Inhibitors (RIMA) – Moclobe-
ers- Tubocurarine , Pancuronium mide , Clorgyline
108. Depolarizing Neuromuscular blockers – 132. COMT inhibitors – Entacapone , Tolca-
Succinylcholine , Decamethonium pone

PHARMACOLOGY
109. Directly Acting Skeletal Muscle Relaxants 133. Centrally Acting Anticholinergics in Par-
– Dantrolene sodium , Quinine kinsonism – Benhexol , Procyclidine
110. Injectable Local Anaesthetic – Procaine , 134. Antipsychotics (Neuroleptics) – Chlor-
Lignocaine , Tetracaine , Bupivacaine promazine , Fluphenazine , Haloperidol 135.
111. Surface Anaesthetics – Lidocaine , Tetra- Atypical Antipsychotics- Clozapine , Risperi-
caine , Benzocaine done , Olanzapine , Quetiapine
112. Inhalational GAs – Nitrous Oxide . Halo- 136. Schizophrenia - Haloperidol , Risperi-
thane , Isoflurane done , Quetiapine
113. Intravenous GAs Inducing Agents – Thio- 137. Mania- Haloperidol , Lithium , Olanzap-
pentone Sodium , Propofol ine
114. Disulfuram Like Reaction – Metronida- 138. Bipolar Disorders – Lithium , Carba-
zole , Gresiofulvin mezepine
115. Withdrawal Syndrome – Naltrexone , 139. Hallucinogens – LSD , Cannabinoids
Acamprostate 140. TCAs – Amitriptyline , Imipramine
116. Nonbenzodiazepine Hypnotics ( Z hyp- 141. SSRI- Fluoxetine , Fluoxamine , Citalo-
notics ) – Zopiclone , Zolpidem pram
117. Long Acting Benzodiazepene – Diazepam 142. SNRI – Venalafaxine , Duloxetine
, Flurazepam 143. Atypical Antidepressants SNRI , Trazo-
118. Short Acting Benzodiazepenes – Alpro- done
zolam , Triozolam 144. AntiAnxiety – Diazepam , Buspirone ,
119. Generalised Tonic Clonic Seizures Hyroxyzine
(Grand Mall Epilepsy) – Sodium Valproate , 145. Natural Opium Alkalois – Morphine ,
Carbamezepine Coedine
120. Absence Seizure – Ethosuximide , Sodi- 146. Semisynthetic Opiates – Pholcodiene ,
um Valproate DiacetylMorphine l
121. Simple Partial Seizures- Sodium Val- 147. Synthetic Opiods – Pethidine , Fentanyl ,
proate , Carbamezepine u
Tramadol
122. Complex Partial Seizures – Sodium Val- 148. Opioid Antagonist – Naloxone , Naltrex- m
proate , Carbamezepine one i
123. Newer Antiepileptics – Vigabatrine , 149. CNS stimulants – Amphetamine , Modaf-
Topiramate n
inil
124. Myoclonic Seizures- Sodium Valproate , 150. ACE Inhibitors – Captopril , Lisinopril a
Lamotrigine 151. ARBs – Losartan , Candesaratan i
125. Atonic Seizures – Valproate , Clonazepam 152. Direct Renin Inhibitors – Aliskiren ,
r
126. Trigeminal Neuralgia – Carbamezepine Remikiren
e
(DOC) 153. Cardiac Glycosides – Digoxin , Digitoxin
127. Status Epilepticus – Lorazepam , Phe- 89 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

154. Inodilators ( PDE-3 inhibitors) – Milri- tomenaphthone

none ,AMrinone 181. Parentral Anticoagulants – Heparan Sul-
155. Used In CHF – Digoxin , Carvedilol fate , Heparin , LMW Heparin
156. PSVT – Adenosine , Propranolol 182. Oral Anticoagulants – Dicumarol , Warfa-
157. Widens Action Potential – Amiodarone , rin Sod
Bretylium 183. LMW heparin – Enoxaparin , Reviparin
158. AV block – Isoprenaline , Atropine 184. Fibrinolytics (Thrombolytics)- Streptoki-
159. Prolong QT interval – Quinidine , Spar- nase , Alteplase
floxacin ,Terfenadine 185. Antifibrinolytics – Epsilon amino Caproic
160. Venticular Fibrillation – Lignocaine , Acid , Tranexaemic Acid
Amiodarone 186. Antiplatelet Drugs (AntiThrombotic) –
PHARMACOLOGY

161. Atrial Fibrillation – Esmolol , Verapamil Apirin , Dipyridamole , Clopidogrel

162. Nitrates – GTN , Isosorbide mononitrate 187. GP IIb/IIIa receptor antagonists – Abcix-
163. CCBs – Verapamil , Diltiazem , Nifedipine imab , Eptifibatide
164. Potassium Channel Openers – Nicorandil 188. HMG-CoA reductase inhibitors – Ator-
, Minoxidil vastatin , Rosuvastatin
165. Central Sympatholytics – Clonidine , 189. Bile acid sequestrants – Cholestyramine ,
MethylDopa Colestipol
166. Antihypertensives Safe in Pregnancy – 190. Activate lipoprotein Lipase (Fibric Acid
Hydralazine , MethylDopa Derivatives )- Gemfibrozil , Fenofibrate
167. Antihypertensive Unsafe In Pregnancy – 191. Plasma Expanders – Human Albumin ,
Diuretics , ACE inhibitors , Propranolo 168. Dextran
Hypertensive Emergencies – Sodium Nitro- 192. H2 AntiHistaminics – Cimetidine , Ranit-
prusside , GTN , Hydralazine idine
169. High Ceiling Diuretics – Furosemide , 193. Proton Pump Inhibitors – Omeprazole ,
Bumetanide Pantoprazole
170. Thiazide Diuretics- Hydrochlorthiazide , 194. Systemic Antacids – Sodium bicarbonate ,
Benzthiazide Sodium Citrate
171. Thiazide Like Diuretics – Chlorthalidone 195. Nonsystemic Antacids – Magnesium Hy-
, Xipamide droxide , Aluminium Hydroxide
172. Potassium Sparing Diuretics – Spirinolac- 196. Ulcer Protectives – Sucralfate , Colloidal
tone , Triamterene Bismuth subcitrate
173. Epithelial Sodium Channel Inhibitors – 197. Anti-H pylori Drugs – Amoxicillin , Clar-
Triamterene , Amiloride ithromycin , Tinidazole
174. Osmotic Diuretics – Mannitol , Glycerol 198. Prokinetic Drugs – Metoclopramide ,
l 175. Aldosterone Antagonists – Spirinolactone Domperidone , Cisapride
, Elperenone 199. Motion Sickness – Hyoscine , DIcyclo-
u 176. Vasopressin Analogues – desmopressin , mine, Promethazine
m Terlipressin 200. GERD – Omeprazole , Ranitidine 201.
i 177. Oral Iron Preparations – Ferrous Sulfate , 5HT4 Agonists – Cisapride , Tegaserod
Ferrous Gluconate 202.Carminatives – Sodium Bicarbonate , Oil
n 178. Parentral Iron – Iron Dextran , Iron Sorbi- Peppermint
a tol Citric Acid 203. Gall stone dissolving Drugs – Chenodiol ,
i 179. Vit B12 Preparations – Cyanocobalamin , Ursodiol
Hydroxycobalamin 204. Bulk forming Laxatives – Dietary Fibre :
r
180. Synthetic Vitamin K – Menadione , Ace- Bran , Methylcellulose
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

205. Stool Softners – Docusates , Liquid Par- cillin , Piperacillin

affin 229. First Generation Cephalosporins – Ce-
206. Stimulant Purgatives – Bisacodyl , Phe- fazolin , Cephalexin
nolpthalein , tegaserod 230. Second Generation Cephalosporins- Ce-
207. Osmotic Purgative s- Lactulose , Sod. Pot. furoxime , Cefuroxime axetil
Tartrate 231. Third Generation Parenteral Cephalospo-
208. Travellers Diarrhoea – Cotrimoxazole , rins – Cefotaxime , Ceftriaxone , Cefoperazone
Norfloxacin , Doxycycline 232. Third Generation Oral Cephalosporins –
209. Shigella Enteritis – Ciprofloxacin , Nali- Cefixime , Cefpodoxime
dixic Acid , Cotrimoxazole 233. Fourth Generation Cephalosporin –
210. Antisecretory Drugs used in Diarrhoea – Cefepime , Cefpirome

PHARMACOLOGY
Sulfasalazine, Mesalazine 234. Carbapenems – Imipenem , Meropenem
211. Anti Motility Drugs Used in Diarrhoea- 235. Topical Aminoglycoside s- Neomycin ,
Diphenoxylate , Loperamide Framycetin
212. Cause Superinfection ( Pseudomem- 236. Lincosamide Antibiotics – Clindamycin ,
braneous Enterocolitis) – Aminoglycosides , Lincomycin
Clindamycin 237. Glycopeptide Antibiotics – Vancomycin ,
213. Treatment of Pseudomembraneous En- Teicoplanin
terocolitis – Metronidazole , Vancomycin 238. Urinary Antiseptics – Nitrofurantoin ,
214. UTI and Enteritis caused by Proteus – Nalidixic Acid
Cefixime , Gentamicin 239. MAC – Clarithromycin , Ethambutol ,
215. Psedomonas Infection – Carbenicillin , Rifabutin , Ofloxacin
Piperacillin 240. Lepra Reaction – Clofazimine , Predniso-
216. Drugs that show Post Antibiotic Effect – lone, Thalidomide
FQs , Aminoglycosides 241. Multibacillary Leprosy – Rifamoin , Dap-
217. Surgical Site Infection – Cefazolin , Van- sone , Clofazimine
comycin 242. Paucibacillary Leprosy – Rifampi , Dap-
218. Infection on burn surfaces – Silver sulfa- sone
dizine , Mafenide 243. Topical Antifungals – Clotrimazole ,
219. First Generation Fluroquinolone – Nor- Econazole , Miconazole
floxacin , Ciprofloxacin , Ofloxacin 244. Systemic Antifungals – Fluconazole ,
220.Second Genaration Fluroquinolone – Voriconazole , Ketoconazole
Levofloxacin , Sparfloxacin , Gatifloxacin 245. Antiviral Drugs – Acyclovir , Valacyclovir
221. Chancroid – Ceftriaxone , Erythromycin , 246. Cytomegalovirus – Ganciclovir , Foscar-
Ciprofloxacin net
222. Typhoid – Ciprofloxacin , Ceftriaxone 247. NRTI – Zidovudine , Stavudine , Lamivu- l
223. Fluroquinolones that prolong QT interval dine
248. NNRTI – Nevirapine , Efavirenz u
– Gatifloxacin , Sparfloxacin , Moxifloxacin
224. MRSA – Vancomycin , Linezolid m
225. Penicillinase resistant Penicillins – Meth- 249. Protease Inhibitor – Ritonavir , Indinavir , i
icillin , Cloxacillin Saquinavir
250. Anti- Influenza Drugs – Amantidine , n
226. Extended Spectrum Penicillins – Ampi-
cillin , Amoxycillin , Oseltamivir a
227. β Lactamase Inhibitors – Clavulanic Acid 251. Antimalarial Drugs – Chloroquine , Pri- i
, Sulbactam maquine
r
228. Anti Pseudomonal Penicillins – Carbeni- 252. Vivax Malaria – Cholroquine , Pri-
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

maquine 276. Breast CA – Tamoxifen , Methotrexate

253. Cholroquine resistant vivax malaria – 277. Ewings Sarcoma – Vincristine , Doxoru-
Quinine , Doxycycline , Primaquine bicin
254. Falciparum Malaria – Artesunate , Sulfa- 278. CML – Imatinib , Busulfan
doxine , Pyrimethamine 279. Acute Leukemias – Daunorubicin , Cyclo-
255. Severe and Complicate Falciparum Ma- phosphamide
laria – Artesunate , Artemether 280. Calcineurin Inhibitors (Specific T cell
256. Tissue Amoebicides – Metronidazole , Inhibitors) – Cyclosporine , Tacrolimus
Tinidazole 281. Immunosuppresants – Cyclosporine ,
257. Luminal Amoebicides – Diloxanide Furo- Tacrolimus , Azathioprine
ate , Nitazoxanide 282. Chelating Agents – BAL , Penicillamine ,
PHARMACOLOGY

258. Giardiasis – Metronidazole , Tinidazole , Disodium Edetetate

Nitazoxanide
259. Trichomonas Vaginitis – Metronidazole ,
Tinidazole , Nimorazole
260. Leishmaniasis – Sodium Stibogluconate ,
Pentamidine
261. Ascariasis – Mebendazole , Albendazole
262. Filariais – DEC , Ivermectin , Albenda-
zole
263. Tapeworm – Praziquantel , Niclosamide ,
Albendazole
264. Hydatid Disease , WhipWorm , Hook-
worm – Albemdazole , Mebendazole
265. Alkylating Agents – Cyclophosphamide ,
Chlorambucil ,Busulfan
266. Antimetabolites – Methotrexate , Azathi-
oprine
267. Vinca Alkaloids – Vincristine , Vinblas-
tine
268. Taxanes – Paclitaxel , Docetaxel
269. Anticancer Antibiotics – Actinimycin D ,
Doxorubicin , Mitomycin C
270. Cell Cycle Nonspecific Anticancer Drugs
– Cyclophosphamide , Chlorambucil , Cispla-
l tin
271. Cell Cycle Specific – Vinblastine , Vin-
u
cristine , Methotrexate , Paclitaxel
m 272. S phase selective Cytotoxic Drugs –
i Methotrexate , 5 Fluro Uracil , Doxorubicin
273. G2 phase selective cytotoxic Drugs –
n
Bleomyci , Etoposide , Topotecan
a 274. M phase Selective Cytotoxic Drugs – Vin-
i cristine , Vinblastine , Paclitaxel
r 275. Hodgkins Lymphoma – Vinblastine ,
Doxorubicin , Dacarbazine
e
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ESSAYS ing? Explain b) How do you confirm the

diagnosis c) Outline the management of this
PAPER 1 poisoning

1) Devi had prosthetic valve replacement 5) 50 yr old female patient suffering from
2 yrs back. She was prescribed some drugs chronic Rheumatoid arthritis, on treatment.
which she was taking regularly, she developed He was brought to hospital with following
bleeding from the gums and on investigation features tinnitus, nausea, vomiting, sweating,

PHARMACOLOGY
prothrombin time was prolonged 5 times the hypoventilation
control. a) What is the drug she is taking b) a) Diagnosis ?
How will you manage the case c) Name 2 oth- b) What drug has produced these effects ?
er drugs which has same action d) Mention c) Therapeutic effects of this drug in RA
an important drug interaction of this drug d) Biochemical abnormalities to be present in
the patient
2) Latha 40 yrs was brought to doctor with e) Outline treatment approach giving pharma-
complaints of stiffness of body and tremor for cological basis
3 days, she has been taking chlorpromazine for
the last 1 month for some mental illness. The 6) Working woman with h/o mild asthmat-
Dr. diagnosed it as drug induced parkinsonism ic attacks in the past. Had an acute attack of
a) Explain the mechanism of this side effect bronchoconstriction, repeated self adminis-
of CPZ b) How will you manage c) Name 3 tration from inhaler did not provide relief and
other drugs used in parkinsonism with MOA symptoms progressed until she became cya-
d) Role of carbidopa in parkinsonism e) Anti notic.She was admitted to hospital in severe
emetic which can induce parkinsonism respiratory distress. She was given a medica-
tion IV which lead to marked improvement of
3) 65 yr old male admitted in hospital. O/E symptoms in 15 mins
his BP was 150/90, LDL 250mg/dl, he is a a)What are the probable mediators or bron-
known asthmatic on salbutamol inhalation chial asthma
a) Which anti hypertensive will you use on b)What are the medications commonly used
this patient? Why b) Name anti hyperten- for the treatment of asthma
sives to be avoided in this patient with reasons c)What drug was administered in the hospital
c) which drug will you use to lower his LDL room
levels what is its MOA? d) Name two other d)What agents are used as nebulisers l
drugs that lower LDL levels e) What life style e) What instructions will you give the patient
modification will you advice for this patient regarding the use of metered dose inhaler u
f) Name four drugs used to treat hypertensive m
emergencies 7) After consuming country made alcohol, i
people developed vomiting, blurring of vision
4) A farmer while spraying and insecticide and within a few hours they went to coma. n
develops profuse sweating and muscle weak- a) How will you account for the symptoms a
ness with bronchospasm O/E his pulse rate is b) Outline treatment of this condition with
i
68/min and pupils constricted. a) What type rationale
of insecticide could have caused this poison- r
e
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8) 20 yr old man brought to casualty with h/o b) What is the total dose of iron required and
seizures. His father said he is an epileptic pa- in how many injections/day can the treatment
tient on phenobarbitone which he was taking be completed
irregularly. He again developed seizures while c) Name 4 indications of parenteral iron ther-
in the casualty a) Mention dosage schedule apy
and MOA of phenobarbitone b) What other
drugs can you use for long term control of 13) 40 yr old patient with a/c attack of gout
seizures c) Mention A/E of long term use of treated with 10 day course of naproxen
phenobarbitone d) Mention 4 recently devel- a) Why naproxen was given for a/c gout
oped anti epileptics e) Which drug will you b) What other drugs can be given for a/c gout
use to treat the seizure immediately c) Is naproxen sufficient for long term treat-
PHARMACOLOGY

ment
9) 53 yr old house wife, admitted with com- d) Which drug do you like to give with naprox-
plaints of dyspnoea, palpitation and b/l pedal en
edema, diagnosed as CCF a) Enumerate e) Write its MOA
drugs used in CCF b) Explain PB of each
drug usage c) 3 important A/E of 3 drugs 14) A diabetic patient was found to have a BP
used in this patient of 140/100 mm of Hg and was prescribed an
antihypertensive. After one week the patient
10) 70 yr old patient brought with dyspnoea, complained of dry cough.
froathy sputum, BP 200/120, later patient was a) Which is the most probable antihyperten-
given aminophylline a) Which drugs will you sive that can produce cough? Why is this drug
use. Justify b) What is the dose, route and preferred in diabetes?
rationale of using aminophylline b) Mention two other indications of the above
drug.
11) 30 yr old male presentswith severe ret- c) Mention four other adverse effects of this
rosternal pain precipitated by exertion, he drug.
was sweating profusely and was confirmed as d) Name two groups of antihypertensives not
having angina pectoris. He was given a tablet indicated in this patient.
under the tongue a) What can be the drug
given by the doctor b) What are the advan- 15) A 60 year old man with hypertension and
tages of this route of administration c) Write type2 diabetes comes for a follow up visit. He is
MOA of the above drug d) Mention other found to have elevated total cholesterol and el-
routes by which this drug can be administered evated LDL levels. The doctor prescribes some
e) Name a poisoning for which this drug can hypolipidemic drugs.
l be administered a) Enumerate the different types of hypolipid-
emic drugs with one example each.
u
12) Lady aged 45 weighing 50 kg attented b) Mention two groups of hypolipidemics
m clinic with signs and symptoms of severe which can selectively lower elevated LDL lev-
i anemia, on investigation she was found to els.
have microcytic hypochromic anemia, she c) Write their mechanism of action
n
was started on oral iron but could not contin- d) Name one newer hypolipidemic drug which
a ue as sshe developed severe nausea and vomit- can be combined with statins.Write the mecha-
i ing. Her Hb was 69% nism of action of the new drug.
r a) Name 2 parenteral iron preparation that can
be used here
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v16) Mrs. Lobo , A 30year old female, moth- a) What is the probable cause for this?
er of a 4year old boy, was admitted to the b) Can you treat this with edrophonium?
emergency ward with following complaints c) Mention the line of treatment with reasons.
of giddiness, headache, slight breathlessness, d) What other drugs can be given instead of
amenorrhoea for 5months, fainting attacks. succinyl choline ?
On examination, pulse – 110/min, e) Name 2 centrally acting muscle relaxants.
BP – 150/104 mmHg. Urine analysis – pro-
teinuria ++ Hb – 9g/dl, CVS – NAD, RS – oc- 19) A man aged 40 years was on a mainte-
casional crepitations, rhonchi, pregnancy test nance dose of warfarin 5mg/day for his angina
+. Past history – not a known hypertensive, attacks. Subsequently he developed rheumatic
had seasonal asthma. joint pain for which he was advised to take

PHARMACOLOGY
a) Mention safer antihupertensive drugs for aspirin(300mg tablets) 4-4-4 after food. One
her. week later, he was brought to casuality in a
b) What advice would you give for her asthma state of shock due to severe hematemesis.
attacks? a) Explain the reason for this.
c) What drugs with route of administration b) How it could have been prevented?
and duration would you advice to improve her c) How will you treat this emergency?
Hb levels? d) Name 2 oral anti-coagulants
d) Enumerate the drugs used in hypertensive
emergencies , mentioning the routes of ad- 20) A patient who was on large doses of Halo-
ministrations and precautions. peridol for two weeks , has developed rigidity,
e) What antihypertensive drugs are avoided tremor and mask like facies.
in this patient with reasons? a) What can be the clinical condition for which
the patient was taking haloperidol?
17) Sudha 34years was brought to casuality b) Name 2 other drugs useful in the manage-
with history of continuous wheezing for the ment of same conditions?
past 3 hours which was not responding to c) What is the probable cause of side effects?
Salbutamol orally or Adrenaline s/c. d) How will you treat the adverse effects?
a) What is her condition and which drug will e) Name another group of drug with same side
you give for immediate relief ?mention the effect?
dose and route of administration.
b) Mention the various drugs in a classified 21) Dr. Mohan a lecturer in anaesthesia inject-
manner used foe wheezing. ed 2mg of 2.5% solution of thiopentone sodi-
c) On chest examination she had chest infec- um iv for open reduction for fracture humerus.
tion. What drug will you prescribe? 15minutes after the injection, patient recov-
d) If she complains of allegry to jute, what non ered from anaesthesia and hence thiopentone l
hormonal preparation will you advice and sodium was repeated many times making a
u
what is the method? total of 5 injections.
e) What is the hormonal inhalation useful for a) What is the reason for quick recovery from m
Sudha , and how will you advise her the use? anaesthesia and does the repeated injections i
f) What is the advantage of this preparation modify recovery?
b) What are the drawbacks of thiopentone n
?what adverse reaction can you expect in her?
sodium? a
18) An injection of succinylcholine IV to pro- c) Name other iv administered general anaes- i
vide muscle relaxation during an operation thetics.
r
patient developed prolonged apnoea. d) Write 2 other uses of thiopentone sodium.
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

e) What are the components of neuroleptic b)Mention its MOA

anaesthesia and write its advantages. c)Name 1 drug used in ventricular tachycardia
d)Mention its MOA
22. Ramesh, 28 yrs was administered an in- e)Name 2 drugs used in Heart block.
jection of adrenaline with lignocaine at base
of his thumb for nail extraction. Later he
developed severe gangrene of thumb:
a)Why has gangrene developed and how could PAPER 2
this have been avoided.
b)Mention the mechanism & pharmacological 1)Ravi 38 yr old recently diagnosed as pulmo-
actions of adrenaline and lignocaine nary TB
PHARMACOLOGY

c)List 2 other surface anaesthetics and men- a) What are the 1st line drugs given in TB
tion their a/e. b) Give MOA of each
d) Mention the cardiac uses of lignocaine c) Name drug effective against persisters
with dose and rationale. d) Mention its 2 other uses and also 2 drug
interactions
23. A 24 yr old man is bought to the hospital e) His 4 yr old daughter was also diagnosed
with complaints of unconsciousness, sus- as pulmonary TB but was given Pyrazinamide
tained contractions (tonic) of all body muscles instead of Ethambutol. Why?
followed by periods of muscle contraction f) List 2 important adverse effects of Pyrazin-
alternating with periods of relaxation (clonic) amide
lasting 1-2 min. g) Mention 2 situations where Prednisolone is
a) What are the drugs that can be prescribed used with anti TB drugs
for this patient? h) Write a short note on DOTS
b) Describe the pharmacokinetics and adverse
effects of any one such drug 2) 25 yr old business man from Bangalore
c) What is the treatment of status epilepticus admitted at hospital with high grade fever,
(2+3+1=6) malaise and chills in 3 day cycle, his peripherl
smear was positive for P. vivax.
24. A 50 year old man develops pedal edema a) Prescribe suitably for him
and also has difficulty in breathing.Echocar- b) With the help of schematic diagram of life
diography confirms mild congestive cardiac cycle of parasite, Classify antimalarial agents
failure. Answer the following: c) What are the important side effects of the
a) What are the first line drugs in congestive prescribed drugs
cardiac failure. d) Outline management of cerebral malaria
l b) What is the rationale for use of each of e) Mention 2 drugs for chemoprophylaxis of
them in congestive cardiac failure malaria with dosage schedule
u
c) Mention the life style modification that you
m would advise to this patient 3) 30 yr old lady was admitted with tremor,
i d) Add a note on treatment of digoxin over loose stools, sweating, loss of weight inspite of
dosage (1+2+1+2=6) increased appetite. O/E HR was 120/min, she
n
had a uniform thyroid swelling.
a 25. Dhruva, 49 yrs, was admitted to the hosp a) Provisional diagnosis
i with complaints of palpitation, tachycardia, b) Drug for immediate control of symptoms
r chest pain. The diagnosis was PSVT. c) Drug used if she was pregnant
a)Name the drug used for this patient. d) What is the MOA of this drug
e
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e) Mention pre-operative drug therapy in this level

condition d) What are the common adverse effects of
\ statins

4) Male truck driver detected to be HIV posi- 8) 30 yr old female patient suffering from
tive, develops cough, fever, loss of weight. He chronic asthma well controlled with amino-
was admitted for investigation a) Most likely phylline developed respiratory infection was
cause of his present complaints b) Name four brought to the medical op for treatment, she
drugs to be prescribed to him for treatment of was prescribed erythromycin 500mg QID
HIV c) If there is associated infection with a) Is erythromycin appropriate for the patient
pneumocystis carni, what is the drug of choice b) Mention 2 antibiotics suitable and 2 antibi-

PHARMACOLOGY
d) What drugs will you use if his sputum shows otics that should not be used in this patient
growth of TB bacilli e) Discuss limitations of c) Write two clinical conditions where eryth-
anti HIV therapy romycin is used as DOC
d) Write down MOA of erythromycin
5) Ravi 48, habitual smoker and alcoholic
complaints of recurrent paint in epigastrium,
nausea and belching. Complaints started 2 9) The leprologist Dr. Madhavan, on clinical
yrs back and he used to take antacids for pain examination found a patient suffering from
relief. Endoscopy confirmed gastric ulcer. pauci bacillary leprose
On serological examination, he had H. pylori a) Classify anti-leprosy drugs
infection. b) Write the MOA and important S/E of drugs
a) What drugs will you prescribe. Justify and used
write dosage schedule c) Mention 2 reaction states that follow the
b) MOA of Omeprazole, Pirenzepine, Raniti- chemotherapy. Explain
dine d) Write two drugs effective in this reaction
c) Mention 4 drugs C/I in this patient e) Write the dosage schedule in pauci bacillary
d) List advantages and disadvantages of leprosy
1) aluminium hydroxide gel
2) Mg trisilicate 10) A 40 yr old man attended the op with
3)NaHCO3 a h/o dysentery. The attending doctor pre-
e) Classify drugs used in peptic ulcer scribed metronidazole 400mg for 5 days. The
dysentery subsided temporarily and recurred
6) 20 yr old male hospitalized with dehydra- after 2 weeks
tion, kussmauls breathing and unconscious- a) Was it appropriate to start metronidazole
ness, urine shows severe glycosuria and keton- initially l
uria b) How will you confirm your diagnosis
u
a) Diagnosis c) What is the reason for relapse
b) Management m
c) Rationale of all the drugs used 11) A 45 yr old male with type II diabetes i
mellitus had been on treatment with a com-
n
7) 75 yr old woman, cholesterol level of 325 bination of two oral hypoglycaemic drugs.
mg/dl and is put on anti cholesterol therapy a) As his blood sugar was not lowered with the a
Mention drugs used as hypolipidemics above drugs, 40 units of insulin was added to i
b) Mention MOA the therapy. Later the dose of insulin had to be
r
c) What are the different statins and their dose increased to control hyperglycaemia.
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

a) What is insulin resistance and how will you loss of weight . heart rate 126/min. she has
manage it? exophthalmos.
b) Name the different insulin preparations and a) Name the drugs that you will give to get rid
mention the methods of its delivery. of the symptoms at the earliest. Mention the
c) Give two important adverse effects of insulin dose , route and rationale for use.
and how will you manage it. b) Which are the specific drugs you can give
for long term management for this condition?
12) A middle aged man was admitted to the What is the mechanism of action and ADR of
hospital with severe epigastric pain which ag- one of this?
grevated with food intake. Diagnosis is peptic c) Which drug is contraindicated in this age
ulcer. group? Why ?
PHARMACOLOGY

a) Enumerate the different groups of drugs that d) Will you give cyanates? Justify
can be used in such patients. Name one drug
from each group. 15) A diabetic patient receiving Tolbutamide
b) Name 2 drugs which can be used in NSAID is also suffering from right knee joint pain for
induced peptic ulcer. which he administered salicylates. He sudden-
c) What is the cause for recurrence of peptic ly developed flushing, headache and sweating.
ulcer ?outline the drug treatment for the same. a) Explain the reason for this .
d) What advice on lifestyle modification b) Mention 2 other drugs with similar action.
should be given to him? c) Alternatively , how will you treat the patient
e) Name two drugs from different groups that for joint pain?
can cause peptic ulcer. d) Name 2 selective COX-2 inhibitors.
e) What are the adverse effects of Tolbut-
13) A 50 year old male patient was admitted amide?
to emergency ward with the following features
: unconscious , rapid shallow breathing with 16) A female patient receives Rifampicin ther-
smell of acetone, tachycardia, thready pulse apy for tuberculosis and is also administered
, dry tongue, wasting of muscles. HIS TEM- oral contraceptive pills to prevent pregnancy.
PERATURE WAS 100 F .skin dry , non elastic, However she conceives.
blood sugar – 600 mg%, urine sugar +++. BP a) Explain the reason for contraceptive failure.
80/60 mmHg . b) Name 2 other drugs with similar effects. c)
a) What is your diagnosis? Which drug would How will you prevent this?
you administer initially ? Name the prepara- d) Mention 2 adverse effects of oral contracep-
tion , dose, route. tives.
b) What are the follow up measures in treat- e) Mention 2 other indications of rifampicin.
l ment you would undertake for this patient?
c) What is insulin resistance? How will you 17) Raju 35 years , presents with fever for
u
manage? more than a week duration and his WBC
m d) Mention different groups of oral antidiabet- count was 4000/mm3 . Widal test was found
i ic grugs with examples. to be positive.
e) Enumerate the various preparations of a) What is the probable diagnosis?
n
human insulins available with a note on their b) How will you treat?
a advantages. c) Name 4 other drugs effective in managing
i this condition and mention the side effect of
14) Ragini, 26years complains of a thyroid any of two?
r
swelling , sweating , shivering of hands , and d) What is the DOC for the same condition in
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

a child of 6 years? Give reason.

e) What is the drug treatment for carrier state?

18) A 30 year old lady came to gynaec OP with complaints of itching vulva and profuse discharge
from vagina. After proper investigations she was diagnosed to have trichomonal vaginitis.
a) How do you treat this patient?
b) What advice would you give to this patient? c) Mention two drugs not advisable in this pa-
tient during treatment and why.
d) Write 4 other indications of the drug to be used in this patient.
e) Write 2 differences between tinidazole and metronidazole.

PHARMACOLOGY
19)A young businessman with Amoebic dysentery was given Metronidazole and Diloxanide fu-
roate. While on Rx he went for a party and consumed liquor. Immediately he developed flushing
of the face, throbbing headache and tightness in the chest.
a)Why did he develop these symptoms while on Rx?
b)Why is Metronidazole combined with diloxanide furoate?
c)Write the MOA and two other uses of Metronidazole
d)List 4 groups of drugs used in amoebiasis

20)A 20 years old pregnant woman developed a mild upper respiratory tract infection .She was
given cap. Tetracycline 250mg thrice daily for three days.
a)Comment on the treatment for a mild bacterial infection.
b)Comment on the use of tetracycline in pregnancy.
c)If it was a severe infection, what will be your choice of antibiotic in a pregnant woman.
(2+2+2=6)

l
u
m
i
n
a
i
r
e
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SPOTTERS mia,phentolamine controls hypertension)

DRUGS
6. Low dose Aspirin
1. Streptokinase • Dose – 75 mg OD orally
• Use – dissolve clots; used in MI • Monoclonal antibody used in unstable
• Loading dose is required since antibodies angina – Abciximab
PHARMACOLOGY

from past streptococcal infections can • Other antiplatelet drug – Clopidogrel

neutralize the drug
• Longest acting fibrinolytic – Tenectiplase 7. Amlodipine
• Drug with highest fibrin selectivity – • Higher vascular selectivity – Felodipine,
Tenectiplase Lacidipine
• Drug used in Streptokinase overload – Ep- • Congener which prevents atherosclerosis –
silon amino caproic acid Nitrendipine
• Cerebro selective CCB - Nimodipine
2. Enalapril
• Active metabolite – Enalaprilat (adminis- 8. Indapamide
tered IV in hypertensive emergency) • Thiazide diuretic
• Not used along with spironolactone – the • Endocrine side effects – Diabetes mellitus,
combination causes fatal hyperkalemia Impotence

3. Furosemide 9. Propofol
• Causes hypocalcemia • IV induction agent
• Frusemide = Lasix (last six hours) • Used for day care surgery (short duration
• Longest acting loop diuretic – Torsemide of anesthesia, rapid induction & recovery,
• Most potent loop diuretic – Bumetanide lacks airway resistance, residual impair-
ment less)
4. Dorzolamide • Disadv: Pain during induction, No analge-
• Carbonic anhydrase inhibitor used topical- sia & skeletal muscle relaxation
ly in glaucoma (8th hourly)
• Other topical drugs in glaucoma – Lata- 10. Lignocaine
noprost (Prostaglandin), Betaxolol (beta • Dosage forms – Topical solution, gel, oint-
l
blocker) ment, spray
u • ADR: arrhythmia, hypotension, respirato-
m 5. Propranolol ry depression
• Causes bronchoconstriction; hence not • Not used in liver disease since it is metab-
i
used in asthmatics olised in liver
n • Sudden withdrawl causes rebound hy-
a pertension d/t receptor upregulation and 11. Olanzapine
hypersensitivity • Atypical antipsychotic
i
• Used in pheochromocytoma with phen- • Used with caution in Diabetes, Obesity,
r Hypertension
tolamine (propranolol prevents arrhyth-
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

• Adv. Over Clozapine – no agranulocytosis, 17. Cefixime

no hypersalivation • 3rd gen cephalosporin given orally
• Dose in severe UTI-
12. Fluoxetine • Not sensitive against Staphylococcus,
• Longest acting SSRI Pseudomonas
• Dose; 20-40 mg OD daily • ADR- Diarrhea, Stool changes
• Other uses: Social phobias, Obsessive
Compulsive Disorder 18. Levocetrizine
• Not used in acute depression d/t slower • Uses: Allergic rhinitis, Urticaria
onset of action • Adv: No sedation, no anticholinergic side
effects

PHARMACOLOGY
13. Zolpidem • Dose: 10 mg OD orally
• Used in short term insomnia (5-10mg oral-
ly at bedtime) 19. Atorvastatin
• Adv over BZD: minimal residual daytime • Inhibits HMG CoA reductase; reduces
sedation, no rebound insomnia, less de- LDL fraction
pendence & tolerance • Has antioxidant property & long t1/2
• Antidote: Flumazenil • Most potent statin: Rosuvastatin

20. Metoclopramide
14. Tizanidine • Antiemetic with prokinetic action (10mg
• Centrally acting alpha 2 agonist with mus- TID orally)
cle relaxant property • Can be given orally, IM, IV
• Uses: Spastic neurologic diseases, muscle
spasms, spinal diseases 21. Ciprofloxacin
• Other centrally acting SMR: Baclofen • MOA- inhibits DNA gyrase
(GABAB agonist), Diazepam • Dose in Enteric fever: 500mg BD X 7 days
• Not sensitive against Bacteroids, Clostridia
15. Paracetamol • Pefloxacin is safe in renal insufficiency
• Sparfloxacin has highest incidence of pho-
• Preferred over aspirin in tophobia
··1) children • QT interval prolongation: Sparfloxacin,
··2) patients with peptic ulcer Gatifloxacin
• Toxicity affects liver and kiney (analgesic
nephropathy) 22. Anti TB Combination
• Antidote: N-acetyl cysteine • First line anti TB drug given parenterally – l
Streptomycin
u
16. Diclofenac • 4 drugs / pellet - thrice weekly X 2 months;
• Route: IM, topical 2 drugs / pellet – thrice weekly X 4 months m
• Uses: Toothache, Rheumatoid arthritis (50 • Rifampicin – acts on persistor bacilli pre- i
mg TID, orally) venting relapse
n
• Aceclofenac is its congener with chon-
droproctive action and selective COX-2 23. Acyclovir a
inhibition • Dose in Chicken pox: 400 mg QID X 5 i
days r
• Other uses: Herpes simplex encephalitis,
e
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Mucocutaneous herpes Causes Nephro- • Contraindications: pregnancy, Intestinal

toxicity Congener active against CMV- obstruction
Ganciclovir • Drug with similar action: Sodium picosul-
phate
24. Fluconazole
• Adv. over ketoconazole: less potent enzyme 31. Azhithromycin
inhibitor, less anti androgenic side effects • Adv. Over erythromycin: longer duration,
• Preferred in fungal meningitis (good CNS less enzyme inhibition, intracranial pene-
penetration) tration
• Voriconazole – used in aspergillosis • Not active against MRSA
• DOC: Mycoplasma pneumonia, Chla-
PHARMACOLOGY

25. Efavirenz mydiasis

• Used in HIV infection • Dose in Respiratory infection: 500 mg OD
• Other anti HIV drugs – Zidovudine, lami- X 3 days; 1 hour before or after food
vudine
• Nevirapine: prevents vertical transmission 32. Artemesia annua
of HIV from mothers to kids • Part used-Alkaloids from leaves and stem
• Active principle - Artemesine
26. Esomeprazole • MOA
• Longer half life • Derevatives- Artether, Artemether, Arte-
• Lansoprazole: partly reversible blocker H+ sunate
K+ ATPase • Uses- Multi drug resistant malaria
• Fastest acting • ADR- Nausea, Vomiting, abdominal pain,
• PPI- Rabeprazole PPI given IV- Pantopra- QT prolongation
zole, Lansoprazole
33. Adathoda vasica
27. Albendazole • Parts used-Alkaloids from leaves, roots ,
• Uses: Ascariais, Giardiasis flowers,fruits, bark
• Preferred in neurocysticercosis (short • Active principle-Vasicine, Vasicinone
course, cheaper) • MOA
• Semisynthetic derivatives- Bromhexine,
28. Tinidazole Ambroxol
• Uses: Amebiasis, Trichomoniasis • Uses- Bronchitis, Asthma
• Dosage: 2gm orally X 3 days
34. Atropa belladona
l 29. Dicyclomine • Parts used - Alkaloids from roots and
• Uses: Abdominal colic, Morning sickness, berries
u
Motion sickness • Active principles- Atropine , Hyoscina-
m • Dose for abd. Colic: 20 mg SOS mine, Belladona
i • Not used in children below 6 months (ex- • Semisynthetic derivative - Tropicamide
hibit fever symptoms)
n
• Other drugs for morning sickness: Doxyl- 35. Digitalis - Digitalis purpura, Digitalis
a amine, Cyclizine lanta
i • Parts used - alkaloids from leaves
30. Bisacodyl • Active principles - Digoxin, Digitoxin
r
• Route: Oral, suppository MOA,Uses, Toxicity, Treatment
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36. Papaver somniferum INSTRUMENTS

• Part used - exudate from unripe capsule of
poppy seed 1.Tuberculin syringe
• Active principle - Opium 2.Frontal writing lever
• MOA, Uses ,Poisoning, Treatment 3.Metered dose inhaler
4.Spacer
37. Cinchona pubescens 5.Insulin syringe
• Part used - Alkaloids from bark 6.Nebuliser
• Active principle - Cinconin, Cinconidine, 7.Rotahaler
Quinine, Quinidine MOA,Uses,Poisoning 8.Needles

PHARMACOLOGY
38. Chondrodendron tomentosum
• Parts used-Alkaloids from leaves and roots
• Active principle - d-tubocuramine
• MOA - Competitive blocker of Nm recep-
tors Uses, Poisoning, Treatment 39.

39.Physostigma venenosum
• Parts used - Alkaloids from bean
• Active principle - Physostigmine
• MOA-reversible anticholinesterase
• Uses, Poisoning, Management

40. Vinca rosea

• Alkaloids from dried leaves
• Active principle- Vincristine, Vinblastine,
Vindesine
• MOA,Uses,ADR

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ADVERSE EFFECT DRUG CAUSING

Teeth discoloration Tetracycline Ciprofloxacin Fe preparations

Alopecia Anticancer drugs (Cisplatin, Paclitaxel) Anti-

coagulants (Heparin, Warfarin) Gentamicin,
Valproate
Cushing syndrome Corticosteroids OCPs
Steven –Johnson syndrome Sulfonamides, Penicillin Phenytoin Allopuri-
PHARMACOLOGY

nol
Hirsuitism Phenytoin Cyclosporine Metoclopramide

Spina bifida Sodium valproate Carbamazepine

Gingival hypertrophy Phenytoin Amlodipine Cyclosporine

Oral thrush Inhalational corticosteroids, Antibiotics
Cleft palate Phenytoin, Valproate, Methotrexate, Ami-
nopterin
Gynecomastia Digoxin Spirinolactone Ketoconazole Risper-
idone

Drugs Type of interaction Clinical significance

Captopril + Spironolac- Pharmacodyna mic; Dangerous hyperkalemia
tone Synergism
Aspirin + Thiazide Pharmacodyna mic; Diuretic action of thiazide is PG mediated;
Antagonism Aspirin inhibit PG synthesis à Failure of
diuretic therapy
OCP + Rifampicin Pharmacokineti c; Rifampin is a microsomal enzyme inducer
Metabolism à increase OCP metabolism à contraceptive
l failure
u Sucralfate + Anatacids Pharmacodyna mic; Sucralfate polymerizes at pH <4; Antacids
Antagonism increase pH à prevents action of sucralfate
m
Sucralfate + tetracycline/ Pharmacokineti c; Sucralfate prevents absorption of tetracy-
i phenytoin Absorption cline / phenytoin à therapeutic failure
n
a Insulin + Propranolol Pharmacodyna mic;
Antagonism
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Diclofenac + Salbutamol Pharmacodyna mic; NSAID inhibits PG synthesis à Arachdonic

(Asthma) Antagonism acid channelled to Leukotriene synthesis à
bronchoconstrictionà worsens asthma
Astemizole + Erythromy- Pharmacokineti c; Erythromycin is a enzyme inhibitor à de-
cin Metabolism creases Astemizole metabolismà arrhythmia
Diuretic + Lithium Pharmacokineti c; Diuretic cause Na+ loss à Body tries to
Excretion increase Na conc. à Li gets reabsorbed along
with Naà Lithium toxicity
Neostigmine + Atropine Pharmacodyna mic; Neostigmine given to reverse muscle paraly-
Antagonism sis after ansesthesiaà causes muscarinic side

PHARMACOLOGY
effectsà reversed by atropine (anti muscarin-
ic)
Ciprofloxacin + Theoph- Pharmacokineti c; Ciprofloxacin is a enzyme inhibitor à de-
ylline Metabolism crease theophylline metabolism à CVS &
CNS toxicity
Tetracycline + Iron/Ant- Pharmacokineti c; Tetracycline absorption decreased à thera-
acid Absorption peutic failure
Digoxin + Quinidine Pharmacokineti c; Quinidine displaces Digoxin from PPB sites
Distribution à Digoxin levels increased (Quinidine also
decreases the renal clearance of digoxin)
Digoxin + Propranolol Pharmacodyna mic; both decreases AV conduction and precipi-
Synergism tates AV block

Aspirin + Methotrexate Pharmacokineti c; Aspirin displaces MTx from PPB site à pre-
Distribution cipitates MTx toxicity
Penicillin + Probenecid Pharmacokineti c; Blocks tubular secretion of penicillin à
Excretion decrease penicillin excretionà prolong its
duration of action à therapeutic efficacy
increased

Warfarin + Ceftriaxone Pharmacodyna mic; Hypoprothrombinemia- ADR of Ceftriax-

Synergism one à potentiates the anticoagulant effect of
warfarin à increased risk of bleeding l
Clopidogrel + Warfarin Pharmacodyna mic; Clopidogrel- antiplatelet action; Warfa- u
Synergism rin-anti coagulant à increased risk of bleed- m
ing
i
Frusemide + Aminogly- Pharmacodyna mic; Both are ototoxic drugs à additive toxicity
coside Synergism n
a
Penicillin + tetracycline Pharmacodyna mic; Penicillin- bactericidal; Tetracycline – bace- i
Antagonsim riostatic à efficacy of combination reduced r
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Levodopa + Metoclopra- Pharmacodyna mic; L-dopa relieves parkinsonian symptoms by

mide Antagonism D2 agonism; Metoclopramide blocks central
D2 receptors reduces efficacy of L-dopa
Statins + Gemfibrozil Pharmacodyna mic; Both causes myopathy a-additive toxicity
Synergism
Amitryptiline + Atropine Pharmacodyna mic; Both have anti-cholinergic acton.
Synergism
Sulfamethoxazole + Tri- Pharmacodyna mic; Sequential blockade of folate metabolism
methoprim Synergism pathway in microbes
Amoxicillin + Clavulanic Pharmacodyna mic; Amoxicillin is destroyed by beta lactamase ;
PHARMACOLOGY

acid Synergism Clavulanic acid is a betalactamase inhibitor

increases amoxicillin concentration same t
1/2 = 10 hours
Nitrates + Beta blockers Pharmacodyna mic; Tachycardia caused by nitrates is nullified by
(angina) Antagonism beta blocker action
Nitates + CCB (angina) Pharmacodyna mic; Nitrates reduces preload(venodilators) CCB
Synergism reduces afterload (arteriodilators) à reduces
the workload of ischemic heart
TCA + Clonidine Pharmacodyna mic; TCA abolishes antihypertensive action of
antagonism clonidine by inhibiting its transport into
adrenergic neurons
Cholestyramine + Digox- Pharmacokineti c; Effectve blood concentration of digoxin is
in absorption decreased
Tolbutamide + Salicylate Pharmacokineti c; Salicylates displaces sulfonylureas from PPB
Distribution sites à cause dangerous hypoglycemia
Lignocaine + Adrenaline Pharmacokineti Adrenaline causes vasoconstriction à de-
c-Absorption creases absorption of lignocaine decreasing
the systemic toxicity and increasing the
duration of action
L-Dopa + Pyridoxine Pharmacokineti c Pyridoxine as co-factor for carboxylase en-
Metabolism zyme à increased peripheral decarboxylation
of L-Dopa à decreased efficacyt

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CHARTS effects Ans: ephedrine, nicotine c. Write

their MOA Hint: NA release
1. Effects on the cat’s tibialis anterior muscle
nerve preparation 6. Graph of failing heart
a. Explain the graph a. Explain the graph
b. Classify neuromuscular blockers. b. What are the effects of digoxin on a failing
c. Write the uses of neostigmine heart Hint: positive inotropic effect
ans: 1. post operative paralytic ileus c. Write its cardiac adverse effects Ans: ar-
2. post operative urinary retention rythmia, AV block, bradycardia
3. myasthenia gravis
4. cobra bite 7. Nicotinic action of ACh on dogs BP

PHARMACOLOGY
d. Shortest acting Nm blocker: succinyl a. Explain the graph
choline b. Explain mechanism behind nictinic action
e. Longest acing Nm blocker: doxacurium of Ach
c. Write the distribution of nicotinic receptors.

2. Experiment on frog rectus abdominis 8. Effect of drugs on anaesthetised dogs BP

muscle a. Explain the graph
a. Name the different drugs which blocks the b. Identify drug A and write its 2 non cardiac
action of ACh at diff. sites. uses Ans: non selective β blocker [propran-
b. What is the nature of Drug D? Ans: olol] Uses: prophylaxis of migraine, thyro-
sk.muscle relaxant toxicosis
c. Mention 2 drugs with similar MOA c. Write 3 most important clinical uses of
d. How can you reverse the action of drug D. adrenaline Ans: anaphylaxis, to control
Ans: increase the dose of ACh bleeding from skin and mucous membrane,
given along with local anaestheic.
3. Experiment on rat phrenic nerve
a. What type of Nm blocker is drug A? give 9.Effect of drug on respiratory smooth mus-
reason Hint: depolarising blocker. cle
b. Name 2 other drugs with MOA similar to a. What is drug D? Ans: Bronchodilator-it
drug A. Ans: dexamethonium, succinyl relaxes respiratory smooth muscle.
choline. b. Classify drugs with actions similar to drug
c. Write 3 uses of Nm blocker. D
Ans: 1. adjuvant to general anaesthesia c. Mention their routes of administration
2. endotracheal intubation Hint: 1. Injection: salbutamol
3. electroconvulsive therapy 2. Inhalation: salbutamol, ipratropium l
bromide
u
4 .Effect of drugs on anaesthetised dogs BP 3. Subcutaneous: adrenaline
a. Explain the graph . 4. Oral: salbutamol, theophylline m
b. What is drug A Ans: alpha 1 blocker i
c. Mention the alpha adrenergic receptors 10. Effects of drugs on respiration on anaes-
n
with its distribution and action. thetised cat
a. Expain the graph a
5. Effect of drugs on anaesthetised dogs BP b. Why is morphine used cautiously in asth- i
a.Explain the graph. Hint: Tachyphylaxis matic patients r
b.Mention 2 other drugs producing the above 1. Histamine release
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2. Respiratory depressant c. Mention 2 other drugs with similar MOA.

3. Cough depressant Hint: Directly acting: KCl and nitrates
4. Smooth muscle contraction. d. Why barium sulphate is used instead of
c. Which effect of morphine is not antagono- barium chloride in barium enema? Hint:
sed by nalorphine Ans: sedation Barium enema material should be radio-
opaque
11.Effects of drugs on intestinal smooth mus-
cle 13 Graph on human uterus
a. Explain the graph a. What is the action of oxytocin and isoxsu-
b. What type of drug is bethanechol, mention prine on uterus?
its clinical use Ans:- cholinergic drug Uses b. Write 2 clinical uses of oxytocin Ans: milk
PHARMACOLOGY

:- postoperative urinary retention, congenital ejection and induction of labour

megacolon, GERD c. What is a tocolytic agent? Give 2 reasons .
c. Which is the unknown drug ? What are its
clinical use? Ans:- Antimuscarinic agent 14. Action of mepyramine maleate on hista-
Use:- AV block, OP poisonong, refraction test- mine receptor of Guin
ing in children, abdominal colic a. What is the effect of histamine on intestine.
b. What is pretreatment with antihistamine.
12. Effects of drugs on intestinal smooth c. Name 2 second generation antihistamines
muscle with dose
a. Explain the graph
b. What is drug A? What is its MOA? Hint:
Smooth muscle relaxant- directly acting.

BaCl2 BaSO4
Slimulate smooth muscle radio opaque
Not radio opaque does not produce systemic effects
No smooth muscle contraction
15.. Dose Response Relationship

a.Define Bioassay
b. Mention 2 types of Bioassay where rectus muscle is used
c.Define supramaximal dose
d.What is dose-response relation
l e.Advantages of frog rectus muscle
u f.Receptor responsible for above action 16.Effect of drugs on rabbits eye
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PHARMACOLOGY
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PHARMACOLOGY

a)Interpret the findings

b)Identify the drugs (Hint:- A –Phenyl ephrine B- Atropine C-Miotic D-Local Anaesthetic)
c)Other drugs with same effect
vd)Opthalmologic Uses

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DRUG OF CHOICE

• Belladonna poisoning – physostigmine 0.5 to 2 mg IV

• Organophosphate poisoning – atropine 2mg IV every 10 mts
• Motion sickness – hyoscine
• Patent ductus arteriosus – indomethacin 0.1 – 0.2 mg / kg, 12th hrly
• a/c paracetamol poisoning- n- acetyl cysteine 150mg/kg IV over 15mts
• malignant hyperthermia – dantrolene sodium 1mg/kg IV
• methanol poisoning- ethanol loading ,dose 0.7ml/kg followed by 0.15ml/kg /hr drip
• BZD overdose – flumanezil 0.2 mg IV
• Absence seizure – sodium valproate

PHARMACOLOGY
• myclonic seizures – sodium valproate
• drug induced parkinsonism – benz hexol 2-20 mg/day
• a/c schizophrenia – haloperidol 2-20mg/day
• a/c morphine poisoning – naloxone 0.4-0.8mg IV evry 2-3 mts till resp picks up
• supraventricular arrhythmias – propranolol, verapamil
• PSVT – adenosine 6-12mg IM
• Typhoid – ciprofloxacin 500mg BD x 10 days
• Chancroid – cotrimoxazole ( 800 + 160 ) BD x 7 days or erythromycin 2g/day x 7 days
• Pneumocystitis carinii – cotrimoxazole ( 800 + 160 ) BD x4-6 times
• Syphilis – penicillin
• Anthrax , actinomycosis, trench fever- PnG
• Rheumatic fever ( prophylaxis ) – benzathine penicillin 1-2mg every 4 wks
• Meningitis ( pseudomonas) – ceftazidime + gentamycin
• Meningitis ( H.infl.enterobact.) ceftriazone, cefuroxime
• Atypical pneumonia – tetracycline / erythromycin
• Cholera, plague, relapsing fever, ricketisial infection – tetracycline
• Brucellosis – doxicycline 200mg/day x 6 wks
• Tularemia – streptomycin
• Whooping cough – erythromycin
• MRSA – vancomycin
• Gonorrhea – non penicillinase producing orgnsms – amoxicillin 3.5g oral or procaine peni-
cillin G 4.8 milliunit IM ; penicillinase producing – ceftriaxone 250mg IM
• Clamidiatrachomitias – azithromycin 1g oral OD
• Herpes infection – acyclovir
• CMV infection - ganciclovir or foscarnet l
• F. malaria – chloroquine 600mg stat followed by 300mg daily-next two days u
• Cerebral malaria – quinine IV
• Toxoplasmosis – pyrimethamine + sulfadiazine m
• Trichomonas vaginitis – metronidazole 400mg TDS x 7 days i
• Amebic dysentery ,giardiasis – metronidazole n
• Pseudomembanous enterocolitis – vancomycin/metronidazole
• Filariasis – DEC 2mg /kg TDS x 3 wks a
• Tropical eosinophilia – 2-4 mg/kg DEC TDS x 2 wks i
• Loa loa / Onc.s volvulus – DEC r
• Tinea infection – niclosimide e
• Hemorrhagic cystitis - MESNA
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NOTES
PHARMACOLOGY

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MICROBIOLOGY
MICROBIOLOGY
QUESTION PAPER PATTERN - THEORY
• Clinical essay (structured)- 10 marks
• Short essays – 2 X 5 = 10 marks
• Short notes- 10 X 2 = 20 marks
l
QUESTION PAPER PATTERN - PRACTICAL
• Gram staining- 5 marks u
• AFB staining- 5 marks m
• Clinical question- 5 marks i
• Spotters – 10 mark
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GENERAL MICROBIOLOGY 9. Filters with examples(A-32,33;B-33)(impor-

tance in practicals)
Historical introduction 10. Cold sterilization (A-33)
1. Louis Pasteur(A-3,B-4)**UQ 11. Aldehydes (A-34,B-35)
2. Contributions of Robert Koch(A-4,B- 12. Gaseous disinfectants(formaldehyde, eth-
4)**UQ ylene oxide, BPL)(A-35,36;B-37)
3. Koch‘s postulates(A-4,B-5)
Diagrams
Morphology & Physiology of Bacteri 1.Methods of sterilization by dry heat(A-29 fig
1. Dark ground microscopy (A-11 fig2.2,B- 3.1)
10)**UQ 2.Methods of sterilization by moist heat(A-31
2. Negative staining(A-12,B-11) fig3.3)
3. Cell wall(A-15 fig2.8,B-14)
4. L- form(A-21,B-16)**UQ
5. Mesosomes(A-16,B-16)* Culture media
6. Intracytoplasmic inclusions(especially volu- 1. Culture media – definition and types (short
tin granules)(A-18) essay)(A-39,B-42)(Code for special me-
7. Capsule(A-17,B-17)**UQ dia-SEED IT)
8. Flagella(A-19 fig2.10,2.11,B-17)**UQ 9. 2. Agar(A-39,B-42)**
Fimbriae(A-20,B-18) 3. Enriched media with examples (A-40,B-
10. Spore (A-20 fig 2.12,2.13,B-19) 43)**UQ
4. Enrichment media with examples (A-42,B-
MICROBIOLOGY

11. Bacterial growth curve(A-22 fig2.14,B-24)

12. Difference between vital and supravital 44)**UQ
staining 5. Differential media with exam-
ples(A-42,B-44)**UQ
6. Indicator media with examples(A-42,B-44)
Figures 7. Transport media with exam-
i. Bacterial cell(A-15 fig2.6) ples(A-43,B-44)**UQ
ii. Cell wall(Gram+ve and Gram-ve)(A-17 8. MacConkey agar and its constitu-
fig2.8) ents(A-42,B-46)(Code-PLANT)
iii. Flagella(A-19 fig2.10)* 9. Difference between enrichment media and
iv. Bacterial spore(A-21 fig2.12,2.13)*UQ selective media
v. Bacterial growth curve(A-22 fig2.14) 10. Give examples for the following
a) Simple media
Sterilisation And Disinfection b) Enriched media
l 1. Sterilization- definition, agents, methods c) Enrichment media
(A 28-32,B 29-31)**ESSAY,UQ d) Selective media
u
2. Disinfectants & Antiseptics (A-28,B-24) e) Indicator media
m 3. Incineration(A-29,30;B-30)* f) Differential media
i 4. Hot air oven-temp,duration,holding period,- g) Transport media
control(A-30 fig3.1 tab3.1,B-30)* h) Anaerobic media
n
5. Pasteurization (A-30,B-31)**UQ
a 6. Inspissation(A-30,B-31) Culture methods
i 7. Tyndallisation(A-31,B-31) 1.Anaerobic cultural methods (short essay)
r 8. Autoclave (short essay)(A-31,32 (A-46,47 fig5.2,B-49)**UQ
fig3.3;B-32)** 2. McIntosh - Fildes jar-action of palladinised
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asbestos(A-46 fig5.2;B-50) \
3. Robertson‘s cooked meat medium(B-51) Microbial pathogenicity
1. Nosocomial infection (A-71,B-80)**UQ
Bacterial genetics 2. Iatrogenic infection (A-71,73;B-81,83)**UQ
1. Plasmids(A-55,B-65)**UQ 3. Latent infection (A-72,B-81)
2. Episomes(A-55,B-65)**UQ 4. Pathogenicity & virulence(A-73,B-83)
3. Mutation- types (short essay)(A-57,58;B- 5. Exaltation & attenuation (A-74,B-83)
67),One step mutation 6. Differences between exotoxins & endotoxins
4. Modes of transmission of genetic material in (A-75,B-84)**UQ
bacteria(A-59,60;B-69)** 7. Carriers- types ; Paradoxical carrier
5. Lysogenic conversion (A-60,B-70)** (A-72,B-81)**
6. Prophage (A-62,B-72) 8. Septicemia –define(A-76,B-86).
7. R factor (A-62,B-72) 9. Endemic, epidemic and pandemic diseas-
8. Genetic mechanisms of drug resistance(A-63 es,biological vector (A-72,76;B-82,86)
fig7.8,B-72)
9. Diff. between mutational and transferable
drug resistance(A-62,B-73)
10. Transposons (A-63 fig7.9,B-73)**
11. Genetic engineering(A-64,B-74)
12. Southern blotting (A-65,B-75)
13. Polymerase chain reaction (A-65,66
fig7.1,B-75)

MICROBIOLOGY
14. Phage typing
15. Gene therapy(B-77)

Method Temperature(°C) Holding time Articles

1.Autoclave 121 15 min Dressings,surgical
instruments,culture
media,labware,gloves
2.Inspissation 80-85 Half an hour for 3 LJ medium,Loeffler‘s
successive days serum slope
3.Hot air oven 150 1 hr Scissors,glass forceps-
,oil,glycerol scalpels
4.Tyndallisation 100 20 min for 3 succes- Media containing
sive days sugars or gelatin l
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IMMUNOLOGY
6. Agglutination reactions- types, mechanisms,
applications (short essay)(A-108,B-110)**UQ
Immunity 7. Coomb‘s test- types, mechanisms (short
essay)(A-109,B-110)
1. Types of immunity, examples(A-78,B-87) 2. 8. Co-agglutination reactions, co-agglu-
Acute phase proteins (A-81,B-89) tinin(A-110,B-111)
3. Differences b/w active & passive immunity 9. Complement fixation test(A-110,B-112)
(A-83,B-90) 10. Opsonisation(A-112,B-114)
4. Artificial immunity- Types- Active and 11. Immunofluorescence (A-116,B-114)
passive(A-81,B-89) 12. Enzyme immunoassays(A-114,B-116)
5. Local immunity (A-85,B-90)
6. Adoptive immunity, Transfer fac-
tor(A-84,B-91) Complement system
7. Herd immunity (A-85,B-91)**UQ
8. Immune elimination(A-82,147) 1. Complement - definition, classical & alter-
9. Premunition(A-83) native pathways (short essay)(A-121,B-121)
2. Biological effects of comple-
ment(A-125,B-123)
Antigen 3. Regulation of complement activa-
MICROBIOLOGY

tion(A-124,B-124)
1. Antigen(A-87,B-93)**UQ 4. Hereditary angioneurotic edema
2. Hapten (A-87,B-93)**UQ
3. Paratope and Epitope(A-88)
4. Heterophile antigen- egs (A-89,B-95)**UQ Immune system & Immune
5. Super antigen(A-90,B-95)**UQ response

Antibodies 1. Helper T cells, Cytotoxic T cells

(A-135,B-130)
1.Immunoglobulins- types , structure and 2. Null cells(A-137,B-131)**UQ
functions(short essay)(A-93,B-97)** 3. MHC (HLA antigen)- Applica-
2. Bence Jones Protein(A-99,B-102)* tion(A-139,B-133)
3. Reagin antibody 4. MHC restriction(A-142,B-134)
5. Antigen presenting cells(A-138)
l 6. Clonal selection theory (A-159,B-138)
u Antigen-Antibody reactions 7. Monoclonal antibodies
8. Hybridoma (short essay)(A-148,B-
m
1. Precipitation- mechanism, applications 138)**UQ
i (short essay)(A-105,B-106) 9. Adjuvants(A-150,B-140)**UQ
n 2. Flocculation- types , mechanisms, applica- 10. Cell mediated immunity(A-156,B-136)
tions(short essay)(A-105,B-106) 11. Cytokines(A-152,155;B-141)**UQ
a
3. Prozone phenomenon(A-105,B-106)**UQ 12. Transfer factor(A-156,B-143)**UQ
i 4. Immunoelectrophoresis(A-106,B-108) 13. Immunological tolerance(A-157,B-144)
r 5. Immunodiffusion(A-107,B-107)
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Immunodeficiency diseases 2. Sequestered antigen(A-178,B-160).

1. Give examples of humoral and cellular im-

munodeficiencies(A-171,B-136) Transplantation and Tumour
immunity

Hypersensitivity 1. Autograft(A-184,B-163)
2. Isograft (A-184,B-163)
1. Hypersensitivity- definition, types, mech- 3. Allograft (A-185,B-163)
anisms and examples in detail(short essay) 4. Xenograft (A-185,B-163)
(A-161,B-152)** 5. Graft versus host reaction(short essay)
2. Type I hypersensitivity reaction (A-163,B- (A-186,B-164)**UQ
153)**UQ 6. Immunological surveil-
3. Atopy(A-165,B-155)**UQ lance(A-188,B-165)**UQ
4. Type II hypersensitivity reaction
(A-165,B-155)**
5. Type III hypersensitivity reac- Immunohaematology
tion(A-167,B-156)**UQ
6. Type IV hypersensitivity reac- 1. ABO blood group (A-191,B-168)
tion(A-166,B-156)**UQ 2. Bombay group(A-192,B-168)
7. Type V hypersensitivity reaction 3. Rh incompatibility, prevention, HD-
8. Shwartzman reaction(A-168,B-157) N(A-193,B-169)

MICROBIOLOGY
4. Diseases spread through blood transfu-
Autoimmunity sion(B-170)

1. Autoimmunity- definition, pathogen-

esis, mechanism, examples(short essay)
(A-178,B-160)

SYSTEMIC BACTERIOLOGY
Staphylococcus (Essay) SA(A-201,204;B-178)
10. Pathogenesis,lab diagnosis and treat-
1. Morphology, Characteristics of colo- ment(A-204,205;B-179,180)
nies(A-199,200;B-174) 11. Micrococci(A-206,B-181)
2. Coagglutination(A-201,B-176) 12. Coagulase negative staphylococ- l
3. Heat cold phenomenon(A-202,B-176) cus(A-203,B-181)
u
4. Toxins of Staphylococcus(A-202,B-176)
5. TSS Toxin(A-202,B-176)**UQ m
6. Staphylococcal food poison- i
ing(A-202,B-176)
n
7. Coagulase test- slide and tube(A-204,205:B-
177)**UQ a
8. Staphylococcal Scalded Skin Syndrome i
(SSSS)(A-203,B-176) r
9. Penicillin resistance- MR- e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

MNEMONIC nies(A-220,B-196)
Staph aureus : Diseases caused - SOFT PAIN 3. Optochin sensitivity(A-222,B-197)
1.Skin infections 4. Soluble specific substance(A-222,B-197)
2.Osteomyelitis 5. Quellung reaction (A-222,B-197)**UQ
3.Food poisoning 6. CRP- Importance(A-223,B-197)
4.Toxic shock syndrome 7. SR variation(A-223,B-198)
5.Pneumonia 8. Streptococcus viridans(A-218,B-199)**UQ
6.Acute endocarditis
7.Infective arthritis
8.Necrotising fascitis MNEMONICS

Streptocoocus and Enterococcus I.Pneumococcal diseases : COMPS

(Essay) -Conjunctivitis, Otitis media, Meningitis,
Pneumonia, Sinusitis.
1. Streptokinase and Streptodornase II.Capsulated microbes : Some Nasty Killers
(A-213,B-188)** Have Some Capsule Protection
2. Group A Streptococci - Lab diagno- -Streptococcus pneumoniae,
sis, pathogenesis, treatment(A-213,B-188) N.meningitidis, K.pneumoniae, H.influ-
3. Morphology and classifica- enza, S.typhi ,C.neoformans, P.aeruginosa
tion(A-209,211;B-184,185) Neisseria (Essay)
4. Streptolysin(A-212,B-187)
5. ASO titre- Importance(B-187)**
MICROBIOLOGY

6. Dick test(A-213,B-187) 7. Suppurative and Meningococcus

non suppurative infections caused, puerperal
sepsis(A-214,B-188) 1. Pathogenesis, lab diagnosis, treatment(A-
8. Group B streptococci(A-216,B-191)**UQ 229,B-202)**UQ
9. CAMP reaction(A-216,B-191)**UQ 2. Gonococcus- Pathogenesis, lab diagnosis,
10. Group D streptococci(A-218,B-192) treatment(A-232,B-205)**UQ
3. Kovac‘s method(A-228)
MNEMONIC 4. Meningococcal septicemia(A-229)
Streptococcus pyogenes: 5. Waterhouse Friderichsen syndrome(A-
Disease caused-NIPPLES 229,B-202)**UQ
1. Necrotising fasciitis and myositis 6. Non gonococcal urethritis(A-234,B-
2. Impetigo 207)**UQ
3. Pharyngitis 7. Fitz Hugh Curtis Syndrome(A-232)
l 4. Pneumonia 8. Watercan perineum(A-232)
5. Lymphangitis 9. Reiter‘s syndrome (A-234)
u 6. Erysipelas and cellulitis
m 7. Scarlet fever MNEMONICS -
i Meningitis most common organisms-NHS
*N.meningitidis, H.influenza, S.pneumoniae(-
n Pneumococcus (Essay) most severe)
a 1. Pneumococcal meningitis & Pneumococ-
i cal pneumonia- Pathogenesis, lab diagnosis, Corynebacterium (essay) \
treatment(A223,B-198)
r
2. Morphology and characteristics of colo- 1. Diphtheria- Pathogenesis, complications,
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

lab diagnosis, treatment & prophylaxis 1. Classification, examples(A-268,B-238)

(A-239,B-212)**UQ 2. Peptostreptococcus (A-269,B-238)
2. Volutin granules(A-237,B-210) 3. Doderlein‘s bacillus/ Lactobacil-
3. Special stains for Corynebacterium(B-210) lus(A-269,B-238)
4. Diphtheria toxin, MOA(A-237,B-212) 4. Bacteroides(A-269,B-239)**UQ
5. Lysogenic conversion(A-238,B-212)**UQ 5. Treatment of anaerobic infection and predis-
6. Eleks test(A-240,B-214)**UQ posing factors(A-270,272;B-240,241)
7. Virulence tests(A-240,B-214)**
8. Diphtheroids(A-242,B-216)
9. Danysz phenomenon 10. Ehrlich phenome- Enterobacteriaceae
non
1. Classification of enterobacteriace-
ae(A-273,B-244)
Bacillus 2. IMViC test(A-274,B-245)
3. Shiga like toxin(A-277,B-248)
1. Cultural characteristics(A-245,B-220) 4. E. coli- Pathogenesis, lab diagnosis, treat-
2. String of pearl reaction(A-246,B-220) ment(A-276,B-247)**UQ
3. PLET medium(A-246,B-220) 5. Traveler‘s diarrhoea(A-279,B-247)**UQ
4. Human anthrax- Types, Pathogenesis, lab 6. EPEC, ETEC, EIEC, EAEC & EHEC
diagnosis, treatment,prophylaxis(A-246,221) [VTEC](A-279,B-247)**UQ
5. Malignant pustule(A-247,B-221)**UQ 7. Bacteriological diagnosis of UTI (essay) ;
6. McFadyean‘s reaction(A-248,B-222)**UQ Screening techniques(A-278,670;B-249,578)

MICROBIOLOGY
7. Ascoli‘s test(A-248,B-222)**UQ 8. Significant bacteruria(A-278,B-249)**UQ
8. Bacillus cereus(B-223) 9. Klebsiella pneumonia (Friedlanders bacil-
9. Wool Sorters disease(A-247,B-221)**UQ lus)(A-280,B-251)

Clostridium- (Essay) Shigella (Essay)

1. Gas gangrene- pathogenesis, lab diagnosis, 1. Shigellosis- pathogenesis, lab diagnosis &
prophylaxis & treatment(A-255,B-229)**UQ treatment(A-286,B-259)
2. Tetanus - Pathogenesis, lab diagnosis, pro-
phylaxis & treatment(A-260,B-231)
3. Clostridium spores(A-252,B-227) Salmonella (Very imp Essay)
4. Stormy fermentation(A-254,B-228)
5. Lecithinase and Lecithinase ef- 1. Enteric fever- Pathogenesis, lab diagnosis, l
fect(A-254,B-228) Prophylaxis & treatment(A-295,B-266)**UQ
6. Nagler reaction(A-254,B-228)**UQ u
2. Craigie‘s tube(A-293,B-264)
7. Tetanospasmin & tetanolysin(A-260,B-231) 3. HO variation(A-293,B-264) m
8. Botulism- types, lab diagnosis(A-264,B-233) 4. V-W variation(A-294,B-265) i
9. Cl. difficile- Antibiotic associated colitis, 5. Clot culture(A-297,B-268)
pseudomembranous(A-265,B-234)**UQ n
6. Widal test (A-298,B-269)**UQ
7. Coagglutination(A-299,B-270)**UQ a
8. Typhoid carriers(A-296,B-271) i
Nonsporing anaerobes 9. Typhoid vaccines(A-299,B-272) r
10. Salmonella gastroenteritis(A-300,B-272)
e
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Vibrio (Essay) Legionella

1. Cholera – Pathogenesis, lab diagnosis, 1. Pontiac fever(B-309)

complications, prophylaxis & treatment(A- 2. Legionnaire‘s disease(B-309)**
307,B-281)**UQ
2. Special culture media(A-304,B-277) Haemophilus and Gardnerella
3. Cholera red reaction , String test(A-
304,B-278) 1. Satellitism(A-328,B-312)**UQ
4. Classification, El tor strain, sero- 2. H. influenza- Pathogenesis, lab diagnosis,
types(A-306,tab 32.3;B-279,fig34.2) prophylaxis, treatment(A-329,B-313)
5. Halophilic vibrios(A-311,B-283)**UQ 3. H. ducreyi(A-331,B-315)
6. Kanagawa phenomenon- Wagatsuma 4. Chancroid(A-331,B-315)
agar(A-312,B-283) 5. HACEK bacteria(A-331,B-316)**
7. Copro antibodies (local antibodies)(A-310) 6. Clue cells(B-316)
7. Gardnerella vaginalis , bacterial vagino-
MNEMONICS sis(B-316)
*Reactions of v.cholerae-COINS

-Catalase+ve, Oxidase+ve, Indole+ve, Nitrates Bordetella

reduced to nitrites, Sucrose fermentation
1. Antigens & virulence factors(A-334,B-320)
MICROBIOLOGY

2. Pathogenesis, lab diagnosis, prophylaxis

Campylobacter and Helicobacter and treatment(A-334,B-321)
1. Campylobacter (B-287)
2. H. pylori- Pathogenesis, lab diagnosis, treat-
ment(B-289)**UQ Brucella

1. Casteneda‘s method(A-342,B-327)**UQ
Pseudomonas and Burkholderia 2. Brucellosis- Lab diagnosis,Prophylaxis,
Treatment(A-342,B-326)
1. Pigment production(A-315,B-293) 3. Milk ring test(A-343,B-328)**UQ
2. Pathogenesis(A-316,B-295)
3. Nosocomial infections- Control & treat-
ment(A-315,B-295)**UQ Mycobacterium tuberculosis (Essay)
l 4. Melioidosis(A-317,B-297)**UQ
1. Tuberculosis- Pathogenesis, lab diagnosis
u
Yersinia and Francisella & treatment(A-351,B-335)**
m 2. BCG vaccine & complications
i 1. Stalactite growth(A-320,B-301)**UQ (A-355,B-341)
2. Plague- Pathogenesis, lab diagnosis, pro- 3. Koch‘s phenomenon(A-350,B-335)
n 4. Culture media – Lowenstein Jenson me-
phylaxis, treatment(A-322,B-302)
a 3. Clinical features of plague(A-322,B-302) dia(A-353,B-332)
i 4. Tularemia (Francisella)(A-325,B-305)**UQ 5. Petroff ‘s method(A-352,B-337)
6. Mantoux test(A-354,B-336)
r
7. MDR-TB,XDR-TB(A-357,B-340)
e
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8. Antibiotic sensitivity testing of Mycobacte- 1. Human actinomycosis- Lab diagnosis, treat-

rium tuberculosis(B- 339) ment (A-391,B-382)
2. Nocardiosis(A-393,B-383)
Non-tuberculous mycobacteria 3. Differentiate actinomycotic & fungal myce-
toma(A-360,B-384)*
1. Classification with examples, lab diag-
nosis & treatment (short essay)(A-359,Bt-
ab39.1;B347,tab43.1)**UQ Miscellaneous bacteria
2. MAC (Battey bacillus)(A-360,B-347)**UQ
3. Swimming pool granulo- 1. Listerial infections & their lab diagno-
ma(A-360,B-349)**UQ sis(A-395,B-387)
2. Rat bite fever (Streptobacillus moniliformis
& Spirillum minus)(A-398,B-389)
Mycobacterium leprae (Essay) 3. Donovaniosis (Klebsiella granulomatis)
(A-397,B-390)
1. Leprosy- pathogenesis, lab diagnosis & 4. Cold enrichment(A-396)
treatment(A-368,B-354) 5. Acinetobacter bowmani(B-391)
2. Lepra reactions(A-367,B-355)**UQ
3. Lepromin test(A-367,B-355)**UQ
Rickettsiaceae
Spirochaetes
1. Neil Mooser reaction(A-407,B-395)**UQ

MICROBIOLOGY
1. Syphilis- Stages, lab diagnosis, prophylax- 2. Epidemic typhus, endemic typhus, tick ty-
is, treatment (Essay)(A-372,B-362) phus- Agent & Vector(A-406,B-395)
2. Leptospirosis- Pathogenesis, lab diagno- 3. Weil Felix reaction(A-410,B-396)**UQ
sis, prophylaxis, treatment (Essay)(A-381,B- 4. Scrub typhus (A-408,B-397)*
370)**UQ 5. Q-fever (A-411,B-397)**
3. Chancre & chancroid(A-372,B-362) 6. Cat scratch disease(A-413,B-399)
4. Serological tests for syphi-
lis(A-374,B-363)**UQ
5. VDRL test(A-374,B-363) Chlamydia
6. Biological false positive reaction; examples
(acute, chronic)(A-374,B-364)**UQ 1. Chlamydia life cycle (A-416,B-403)
7. Relapsing fever(A-378,B-368)**UQ 2. TRIC agents(A-417,B-404)**UQ
8. Vincent‘s angina(A-379,B-369) 3. Trachoma, HP body(A-419,B-405)
9. Lyme disease(A-380,B-369)**UQ 4. Inclusion conjunctivitis (swimming pool) l
(A-420,B-404)**
u
5. TWAR agents- C. pneumoni-
Mycoplasma ae(A-421,B-405) m
6. Lab diagnosis of chlamydial infec- i
1. Atypical pneumonia(A-388,B-377) tion(A-417,B-405)
n
2. Cold agglutination test(A-389,B-378)**UQ 7. LGV , Freis test(A-420,B-407)**UQ
8. Psittacosis (A-421,B-405) . a
i
Actinomycetes r
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

CLINICAL MICROBIOLOGY (paper I)

1. Name some organisms causing Antimicrobial sensitivity testing

a. Pneumonia(A-666 tab74.3,B-579) b. a. Diffusion tests (Stokes method,
UTI(A-671 tab76.3,B-584) Kirby-Bauer method, E test)(A-635
c. Diarrhoea(A-677 tab78.2,B-588) fig67.1,67.2;B-628)
d. Dysentery(A-676 tab78.1,B-593) b. Dilution tests(A-637,B-632)
e. Food poisoning(A-676 tab78.1,B-594) 3. Bacteriological analysis of drinking wa-
f. Meningitis(A-667 tab75.1,B-596) ter(A-625,B-640)
g. Sexually transmitted diseases(P-673 4. Presumptive and differential coliform
tab77.1,B-607) count(A-626,627;B-640)
h. Pyrexia of unknown origin(A-681 5. Water borne diseases(A-626 tab66.1,B-640)
tab80.1,B-604) 6. Milk borne diseases(A-631 tab66.4,B-642)

VIROLOGY
General Properties of Viruses Bacteriophage (Short essay)
MICROBIOLOGY

1. Haemagglutination test (A-430,B-414) 1. Morphology of bacteriophage(A-456

2. Steps in viral multiplica- fig49.1,B-434 fig53.1)
tion(A-431,B-415)**UQ 2. Phage conversions, transduc-
3. Von magnus phenomenon, Abortive virus, tion((A-458,459;B-436,437)
Defective virus(A-433,434;B-416) 3. Prophage(A-458,B-436)
4. Pseudovirion, Viroids(A-442,B- 4. Bacteriophage typing(A-459,B-436)
416,421)**UQ 5. Bacteriocin(A-26)
5. Tissue culture, Cell culture(A-435,436;B
417-419)**UQ
6. Cytopathic effect(A-436,B-418,419)**UQ Pox viruses
7. Prions(A-442,B-421)**UQ
8. Examples of DNA & RNA virus(A-440 1. Small pox vaccination(A-463,B-441)
tab47.4,B-423,tab 51.5) 2. Molluscum contagiosum(A-465,B-441)

l
u Virus-Host Interactions Herpes viruses
m 1. Herpes simplex- Pathogenesis, clinical
1. Inclusion bodies(A-444,B-426)**UQ
i 2. Interferons, cytokines (A-448,152;B- features, lab diagnosis, treatment (Essay)(A
n 428,141)**UQ 468-470,B 443445)
3. Immunoprophylaxis- live & killed vaccines 2. Tzanck smear(A-470,B-445)
a 3. Varicella zoster, Fetal varicella syndrome(A
with examples(imp)(A-451,B-430)
i 471-472,B-445)**UQ
r 4. Herpes zoster(A 472-473,B-445)**UQ
e 5. CMV(A 473-474,B-446)**UQ
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

6. EBV(A 474-477,B-447)**UQ prophylaxis, complication(A 507-509,B-

7. IMN- Paul-Bunnel test (short essay)(A 474)**
475-477,B-447)**UQ 3. Measles- Clinical features, pathogenesis,
lab diagnosis, complications(A-512,513;B-47
Adeno viruses 4,475)**UQ
4. Prophylaxis of measles(A-513,B-475)
1. Adenovirus- Pathogenesis(A 481-482,B- 5. RSV(A-510,511;B-476)
453)
2. Epidemic keratoconjunctivitis(A-482,B-453)
Arbo viruses

Picorna viruses 1. Mosquito borne group(A-520,B-480

tab60.1)
1. Polio virus- Pathogenesis, clinical features, 2. Tick borne group(A-523,B-480 tab60.1)
lab diagnosis(Essay)(A 486-487,B-457)**UQ 3. Chikungunya-Agent and vector(A-519,B-
2. Polio prophylaxis, complications of polio 482)**UQ
vaccination(A-487,B-457)**UQ 4. Japanese encephalitis(A-520,B-483)**UQ
3. OPV v/s IPV(imp)(A-489 tab53.2,B-458 5. Yellow fever(A-522,B-483)
tab57.3) 6. Dengue fever(A-523,B-484)**UQ
4. Manifestations of Coxsackie virus infec- 7. KFD(A-524,B-485)**UQ
tion(A 491-492,B 459-460)**UQ 8. Arboviruses seen in India
5. Echovirus, Rhinovirus(A 492,493;B

MICROBIOLOGY
460,461)
Rhabdoviruses (Essay)
Orthomyxoviruses
1. Diagram-Rabies virus(A-531 fig57.1,B-489
1. Diagram of influenza virus (A-497 fig61.1)**UQ
fig54.1,B-465 fig58.1)**UQ 2. Pathogenesis,lab diagnosis of Ra-
2. Morphology of influenza vi- bies(A-532,533;B-490,491)
rus(A-497,B-465) 3. Negri bodies(A-534,B-491)**UQ
3. Haemagglutination & Elution 4. Prophylaxis of Rabies(A 534-537,B 492-
(A-498,B-466) 494)**UQ
4. Antigenic drift and shift (A-499,B- 5. Non-neural vaccines,Intradermal Rabies
466)**UQ vaccination(A-535,B-493)**UQ
5. Pathogenesis of influenza, lab diagno-
sis(A-500,501;B-467) l
6. Prophylaxis & treatment of influen- Hepatitis Viruses (Essay) u
za(A-503,504,B-469)
7. Hemoagglutination inhibitors(A-501) 1. Hepatitis A(A-541,B-498)**UQ m
2. Parenterally transmitted hepatitis virus- i
es-HBV,HCV,HDV,HGV
n
Paramyxoviruses 3. Diagram of HBV(A-543 fig58.3,B-500
fig62.3) a
1. Diagram- Rubeolavirus (A-507 4. Hepatitis B carriers(A-545,B-502)**UQ i
fig55.1;B-473 fig59.1) 5. Hepatitis B- pathogenesis, lab diagnosis, r
2. Mumps- Clinical features, lab diagnosis, treatment and prophylaxis of hepatitis B(A-
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

546,B-502)**UQ 9. Viral hemorrhagic fever(A-558,B-527)**UQ

6. Serological markers of HBV(A-546,B-502) 10. Slow viruses, Prion disease(A-556,B-
7. Methods of detection HbsAg & anti- 531)**UQ
Hbs(A-546,B-502) 11. SSPE(A-557,B-533)**UQ
8. Hepatitis B vaccine(A-548,B-504) 12. Viral URT infections
9. Hepatitis C(A-548,B-504)**UQ 13. Aseptic meningitis(A-491,667;B-591)**UQ
10. Hepatitis D&E(A-549,B-505)
11. Hepatitis virus superinfec-
tion(A-549,B-505) Oncogenic Viruses
12. Enterically transmitted hepatitis virus-
es(A-550,B-505) 1. Mechanism of viral oncogene-
sis(A-569,B-536)
2. Oncogenic Viruses(RNA/DNA)(A-565
Retroviruses- HIV (Essay) tab60.2;B-537 tab65.1,65.3)

1. Diagram(A-571 fig61.1,B-510 fig63.1)**UQ

2. Morphology of HIV(A-571,B-510)
3. HIV structural antigens & their role in diag- MYCOLOGY (very imp)
nosis of HIV infections(A-571,B-510) **UQ
4. Antigenic variation of HIV(A-572,B-511)
5. Pathogenesis, clinical features, lab diagno- 1. Mycological culture media(A-592,B-546) \
sis(A 574-581,B 512-518) 2. Commonly used fungal stains(A-592,B-546)
MICROBIOLOGY

6. Oppurtunistic infections in AIDS(A-576 3. Zygomycetes(A-595,B-547)

tab61.5,B-513 tab63.4)**UQ 4. Pityriasis versicolor, Piedra(A-595,B-547)
7. Window period- lab diagnosis in window 5. Dermatophytoses (short essay)(A 596-
period(A-581 tab61.6,B-515 tab63.6) 600,B 548-550)**UQ
8. Serological detection- applica- 6. Candidiasis- local & systemic (A-611,B-
tions(A-581,B-517) 557)**UQ
9. Epidemiology/prevention(A-581,B-518) 10. 7. Systemic candidiasis(A-611,B-557)
Treatment of HIV(A-583,B-518) 8. Reynolds-Braude phenome-
11. Post exposure prophylaxis(A-583,B-518) non(A-612,B-558)
9. Deep mycoses(A-600,B-550)
10. Mycetoma(A-600,B-550)**UQ
Miscellaneous Viruses 11. Chromoblastomycoses-sclerotic bod-
ies(A-601 fig63.16,B-551 fig66.13)**UQ
l 1. Papova virus (A-551,B-523)**UQ 12. Sporotrichosis(A-602 fig63.17,B-551
2. Ebola/Marburg disease(A-558,559) fig66.14)**UQ
u
3. German measles /Rubella virus 13. Rhinosporidiosis(A-603,B-552)**UQ
m (A-554,B-528) 14. Histoplasmosis- tuberculate spores(A-
i 4. Congenital rubella syndrome(A-555,B-528) 607,B-552)**UQ
5. Prophylaxis of Rubella(A-556,B-529) 15. Cryptococcus neoformans/pathogenic
n
6. Rotavirus- Clinical features, pathogenesis, yeast(A-606,B-555)**UQ
a lab diagnosis, treatment(A-560,B-529) 16. Oppurtunistic myco-
i 7. Diarrheagenic viruses (Essay)(A 560-562,B ses(A-608,B-556)**UQ
r 529-531) 17. Aspergillosis(A-608,B-559)**UQ
8. Viral gastroenteritis(A 560-562,B-530) 18. Mucormycosis(A-610,B-560)**UQ
e
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19. Otomycosis (A-614,B-561)**UQ 22.Aspergillus flavus(A-608,B-559)

20.Oculomycosis- Mycotic kerati- 23. Dematiaceous fungi(A-601,B-551)
tis(A-614,B-562)**UQ 24. Dimorphic fungi(A-590,B-544)**UQ
21.Mycetism/mycotic poison- 25. Penicillosis(A-610,B-560)
ing(A-614,B-562)**UQ

PARASITOLOGY
General Introduction (J-39)
7. Blood Incubation Infectivity Test (BIIT)
1. Host-Definitive(UQ),Intermedi- (J-44)
ate,Paratenic,Reservoir and Amplifier host(J-2) 8. Life cycle & lab diagnosis of T. cruzi(J-46) 9.
2. Zoonoses(J-2) Romana‘s sign, Chagoma(J-47)
3. Incubation period(J-4) 10. Life cycle of L. donovani, Leishman Don-
4. Types of parasites(diag 1.1,J- ovan bodies(J-52)
11. Kala azar- pathogenesis, lab diagnosis,
Amoebae treatment and prophylaxis(J-54)
12. Post Kala azar Dermal Leishmaniasis
1. Life cycle of Entamoeba histolytica(J-17) (PKDL)(J-55)
2. Amoebic ulcer; Amoebic hepatitis; Amoebic 13. Formol gel test, Montenegro skin test(J-58)

MICROBIOLOGY
abscess; Amoeboma(J-18) 14. Cutaneous Leishmaniasis(J-60)
3. Intestinal amoebiasis- pathogenesis, lab . Oriental sore(J-60)
diagnosis, treatment(J-16)**Essay 16. Espundia- mucocutaneous(J-61)
4. Extraintestinal amoebiasis- pathogenesis,
lab diagnosis and treatment (J-16)**Short
Essay Malaria parasites
5. Diff b/w bacillary and amoebic dysen-
tery(J-20) 1. Malaria- pathogenesis, lab diagnosis, treat-
6. Primary amoebic meningoencephalitis ment and prophylaxis(J-65)**ESSAY
(PAM)((J-25) 2. Life cycle of Plasmodium vivax(J-65)**
7. Acanthamoeba(J-27)**UQ 3. Exo-erythrocytic stage(J-66)
8. Naegleria(J-25)**UQ 4. Erythrocytic stage(J-66)
5. Hypnozoites (J-66)**
6. Difference between relapse and recrudes-
Flagellates cence(J-79) l
7. Schuffner‘s dots(J-69)**UQ u
1. Giardia lambia(J-30)**UQ 8. Malignant tertian malaria/pernicious ma- m
2. Trichomonas Vaginalis(J-34)**UQ laria(J-77)
3. Entero test(J-33) 9. Blackwater fever(J-77)**UQ i
4. Morphological stages of haemoflagel- 10. Tropical splenomegaly syndrome(J-77) n
lates(J-39,tab5.1) 11. Cerebral malaria(J-76)** a
5. Inoculative transmission. Give exam- 12. Merozoite induced malaria(J-77)**UQ
ple(J-39) 13. QBC test(J-80) i
6. Stercorarian transmission. Give example r
e
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(pork taperworm)(J-124,125)
Miscellaneous Sporozoa and 7. Cysticercus cellulosae (J-122)**UQ
Microspora 8. Life cycle,lab diagnosis of Echinococcus
granulosus(J-129,131)**UQ,Short Essay
1. Endodyogeny(J-88) 9. Hydatid cyst(J-129)**UQ
2. Tachyzoites & bradyzoites(J-88) 10. Osseous hydatid(J-131)
3. Life cycle of Toxoplasma gondii(J-89)** 11. Casoni‘s intradermal test(J-131)
4. Toxoplasmosis (J-90)**UQ 12. Cysticercosis(J-124)
5. Babesia(J-83)
6. Life cycle of Pneumocystis carini & lab
diagnosis(J-104)** Nematodes: General features, Whip
7. Isospora belli(J-93) worm & Strongyloides
8. Cryptosporidium parvum(J-94)**UQ
1. Name some viviparous nematodes(J-161)
2. Name some oviparous nematodes (J-161) 3.
Ciliate protozoa Name an ovoviviparous nematode(J-161)
1. Balantidium coli-largest protozoan para- 4. Life cycle,lab diagnosis and treatment of
site(J-108) Trichuris trichura(J-173)
5. Life cycle of Strongyloides(J-178)
Trematodes: Flukes 6. Larva currens(J-180)**

1. Diecious blood flukes(J-139) 2. Hermaphro-

MICROBIOLOGY

ditic flukes(J-139) Hookworm

3. Life cycle of Schistosoma hematobium (J- 1. Ancylostoma duodenale- Life cycle,
142) clinical features, diagnosis, treatment
4. Clinical features of schistosomiasis (J- (J-184)**UQ,Essay
142)** 2. Diff b/w Ancylostoma & Necator(J-185)
5. Katayama fever(J-143,147)**UQ 3. Ground itch(J-187)**
6. Lab diagnosis of Schistosoma hematobium,
Fairley‘s test(J-144,145)
7. Cercarian hullen reaction Pinworm
8. Life cycle of Clonorchis sinensis(J-148) 9. 1. Enterobius- life cycle, clinical fea-
Life cycle of Fasciola hepatica (J-151) tures(J-191)**UQ,Essay
10. Halzoun(J-153) 2. Lab diagnosis, NIH swab(J-193)**
11. Life cycle of Paragonimus westermani(J-1 3. Oxyuriasis
l 58)**UQ
u
Cestodes: Tapeworms Roundworm
m 1. Life cycle of Diphyllobothrium la- 1. Life cycle, lab diagnosis, treatment of As-
i tum(J-117)** caris(J-197)**UQ,Essay
2. Sparganosis(J-120)** 2. Ascaris eggs(J-196)**
n
3. Life cycle of Taenia saginata(beef tape- 3. Loeffler‘s syndrome(J-198)**UQ
a worm)(J-123)
i 4. Hexacanth embryo(J-116)
r
5. Cysticercus bovis(J-122)**UQ Filarial worms
6. Life cycle,lab diagnosis of Taenia solium 1. Filariasis- pathogenesis, lab diagnosis and
e
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treatment (J-209)**UQ,Essay Guinea worm

2. Worms causing lympatic,subcutaneous,se-
rous cavity filariasis(J-203) 1. Life cycle of Dracunculus medinensis,
3. Life cycle of W. bancrofti(J-207) Infective stage(J-222)**UQ,Essay
4. Microfilaria(J-206)** 2. Dracunuculosis- clinical features, diagno-
5. Occult filariasis- Tropical Pulmonary Eo- sis(J-223)
sinophilia(J-210)**UQ
6. DEC provocation test(J-212)**UQ
7. Distinguishing features of Mf. bancrofti & Miscellaneous Nematodes
Mf. Malayi(J-214)
8. Loa Loa(J-216)**UQ 1. Larva migrans- Cutaneous and Viscer-
9. Onchocerca volvulus, vector(J-217) al(J-162)**UQ

Paper I
1. A 4 yr old boy was brought to the hospital (or) What advice will you give to the family
with fever and sore throat and toxemic appear- members and the people in the neighbour-
ance. O/E there was pseudomembrane over hood?
the tonsillar area and a bull neck appearance. e. What is the pathogenesis?
Cervical lymphadenopathy, pallor, tachycardia f. How will you confirm the diagnosis?

MICROBIOLOGY
and dyspnoea present. g. What are the lab findings?
a. What is your diagnosis? h. Explain the MOA of this toxin in this
b. Describe the morphology and staining illness.
characteristics of the etiological agent.
c. What staining procedures are useful in the 3. A 10 yr old boy presented with fever and
diagnosis? pain with swelling of joints. He gave a h/o sore
d. Pathogenesis throat 5 weeks earlier.
e. What are the toxigenicity tests used? a. What is your diagnosis?
f. How do you culture the organism? b. Name and draw the causative organism.
g. Immunoprophylaxis c. Name and describe the important serolog-
h. Lab diagnosis ical tests for the diagnosis.
i. List the other organisms causing URTI d. Name the important toxins.
e. Describe the immunological phenomenon
in pathogenesis of this d/s.
2. A 35 yr old female was admitted with vom- l
iting and watery diarrohea. O/E severe dehy- u
dration was noticed and motion was like rice 4. 3 young men in a canal work developed flu m
water. No mucous or blood in the stools. like symptoms. About a week later one of them
a. What is your diagnosis? Name the etiologi- started to feel worse and was hospitalized. O/E i
cal agents and describe its morphology. he was febrile and jaundiced. n
b. Media used to identify the organism. a. What bacterial infection he might be a
c. Treatment having?
d. Mention the prophylactic measures to be b. What is the significance of his condition? i
followed to prevent the spread of infection. c. How do you confirm your diagnosis? r
e
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d. What other serious complications may canned food.

occur? a. What is the diagnosis and what is the
e. Prophylaxis organism responsible?
b. What is the virulence factor?
5. A 40 yr old man was brought to the hospital c. Lab diagnosis and treatment d. Enumerate
with c/o fever and vomiting. O/E there was the other important bacteria causing food
neck rigidity and signs of meningeal irritation. poisoning
There is petechial rash all over the body.
a. What is the probable diagnosis? 9. An adult male patient complains of sudden
b. What is the pathogenesis? onset of fever with rigor, dysuria and pain in
c. Mention the lab diagnosis. the loins and flanks. Midstream clean catch
d. What is the treatment? urine yielded significant growth of E. coli
more than 1 lakh colonies per ml of urine.
a. What is your diagnosis?
6. A 10 yr old boy was brought to the hospital b. What are the bacterial causes of this clini-
with acute respiratory distress and convul- cal infection?
sions, there was a h/o penetrating injury of the c. How do you identify the urinary isolates?
leg 3 weeks back. The unhealed contaminated
wound was persisting. 10. A male patient aged 25 yrs was brought
a. What is the clinical diagnosis? Name the to the hospital with the following complaints.
etiological agent Fever, ulcer on the shaft of the penis and h/o
b. Describe briefly the pathogenetic mecha- exposure:
MICROBIOLOGY

nism of this organism and typical features of a. What is the diagnosis?

the convulsion. b. What are the serological tests to be done?
c. How will you manage this case? c. What is the procedure of routine serologi-
d. Prevention of this d/s in a cal test done for this condition?
i) new born d. What is biological false positive?
ii) a pregnant lady in early pregnancy e. What is the non-venereal mode of trans-
iii) a 25 yr old healthy man mission of this d/s?
e. How is the pathogenicity of the organism
confirmed? (lab diagnosis) 11. A 39 yr old male consulted a doctor com-
plaining of fever and abdominal discomfort
7. A 33 yr old man complaining of evening rise for one week duration. O/E coated tongue,
of temp, weight loss and cough. O/E axillary temp 103F, pulse 65 per min, spleen tip palpa-
and cervical lymph nodes palpable. ble.
l a. What is your diagnosis? a. What is your diagnosis?
b. Lab diagnosis b. Lab investigations
u c. Pathogenesis of gastrointestinal lesions.
c. Concentration methods
m d. Culture media used. d. Complications
i e. Organism causing the d/s in AIDS pa- e. Enumerate the specific serological tests
tients. f. Pathogenesis. f. Treatment and prophylaxis.
n
a 12. A 20 yr old male presented with dysuria
i 8. A 25 yr old male present with sudden onset and urgency of micturition. O/E he was afe-
of diplopia, dry mouth, weakness, dysarthria brile.
r
and dysphagia. Last night he ate some home a. What is your diagnosis?
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b. What are the bacteriological agents? a. What is your diagnosis?

c. How do you collect the specimen and b. Lab diagnosis
transport? c. Pathogenesis
d. How do you diagnose the condition by lab d. Culture media and appearance of colony
methods? e. Stages of d/s? Which is the most infective
e. What are the predisposing conditions? stage?
f. Complications and prophylaxis

13. A 25 yr old female complaints of fever, 17. A 25 yr old female patient was brought to
gripping abdominal pain, passage of blood and the op with complaints of fever, malaise and
mucous in the stool. Stool culture shows non loss of appetite of 8 days duration. O/E patient
motile gram negative bacilli. was febrile, pale, tongue was coated and mild
a. What is your diagnosis? dehydration present. There was marked hepa-
b. What are the causes of dysentery? tosplenomegaly.
c. How do you identify the organism? a. What is your diagnosis?
b. What are the lab findings?
c. What is the causative agent and name other
14. A 50 yr old male with varicose ulcer on agents included in third group.
medial maleolus was hospitalized and had d. What is the pathogenesis of this condition
secondary infection. The ulcer O/E had earthy and where is the organism stored in carriers?
smell and bluish pus and a swab was taken and e. What is the treatment given? Also write the
sent for investigation. prophylactic measures.

MICROBIOLOGY
a. What is the infection due to?
b. Nosocomial infections and problems? 18. A 25 year old male patient with burning
c. Common infection caused by the organism urination, profuse urethral discharge. 4 days
d. Treatment and management ago he had unprotected sexual contact with a
e. Prophylaxis prostitute. Smear of urethral discharge reveals
intracellular gram negative diplococci.
15. A 43 yr old man presents with c/c cough 2 a. What is the diagnosis and what is the organ-
months duration, evening rise of temp, weight ism responsible?
loss and occasional blood staining of sputum. b. How do you diagnose the condition by lab
X-ray revealed a patchy opacity at the apex of methods?
the right lung. c. Treatment of this condition.
a. What is the clinical diagnosis? d. Enumerate other bacteria causing sexually
b. Name the best specimen for culture. How transmitted d/s.
is it collected and processed? l
c. How will you culture and confirm the 19. A 25 yr old male patient came to the STD
diagnosis? u
clinic with fever, myalgia and mucocutaneous
d. What is the immunoprophylaxis available? rash. He gave past h/o sexual exposure and m
painless ulcer over the genitals. O/E general- i
16. An 8 month old child presenting with ized lympadenopathy was present.
paroxysmal cough for 2 weeks. The cough is n
a. What is your diagnosis?
increasing in intensity and comes in distinc- b. What is the pathogenesis? a
tive bouts which end in a whoop. O/E there is c. What is the lab test for diagnosis? i
marked leucocytosis and relative lymphocyto- d. What is the treatment? Serological test r
sis. done? Various stages of this infection?
e
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e. Enumerate other STDs & causative organ- Answers

isms 1- Diphtheria,
2- Cholera,
20. A 50 yr old man came to the hospital with 3- Strep. pyogenes,
complaints of loss of appetite, loss of weight, 4- Leptospirosis,
cough with blood stained sputum, evening rise 5- Meningococcal meningitis,
of temp. 6- Tetanus,
a. What is your diagnosis? 7- TB,
b. Name the etiological agents; describe its 8- Botulism,
morphology and staining characteristics. 9- UTI,
c. How will you grow this organism in the lab? 10- Syphilis,
d. Name the drugs used in the treatment. 11- Typhoid,
e. Immunoprophylaxis against this d/s 12- UTI,
13- Dysentery (Shigella),
21. A 35 yr old agricultural worker was 14- Pseudomonas,
brought to the medical op with irregular fever, 15- TB,
severe muscle pain, malaise and yellow disc- 16- Whooping cough,
olouration of eye of 10 days duration. O/E he 17- Typhoid,
was febrile, mild hepatomegaly, subconjuctival 18- Gonococci,
hemorrhage present 19- Syphilis,
a. What is the diagnosis? 20- TB,
b. What is the pathogenesis of this condition? 21- Leptospirosis,
MICROBIOLOGY

c. Name the etiological agent and describe its 22- Tetanus

morphology.
d. Explain the epidemiology and method of
lab diagnosis.
e. Treatment and prophylaxis.
f. What is the source of infection?
g. Which are the other human pathogens mor-
phologically resembling
h. What is the mode of transmission?

22.A 5 yr old boy complaining of a/c pain and

discharge from right ear. Doctor diagnosed as
acute otitis media. Later he developed muscle
l rigidity, spasm and convulsions.
a. What is your diagnosis?
u
b. Pathogenesis
m c. Management of this condition.
i d. Write the prophylaxis in this condition.
n
a
i
r
e
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Paper II
1. A 10yr old boy was brought to casualty with c. Lab diagnosis
anxiety, irritability and difficulty in drinking d. Serological markers of the virus e. Pro-
and intense thirst. Attempts to drink brings phylaxis
painful spasm of pharynx
a. What is the diagnosis 5. A 40 yr old man came to hospital with com-
b. What is mode of transmission plaints of epigastric tenderness. O/E there was
c. Describe pathogenesis, lab diagnosis & extreme pallor of mucous membrane of eyes,
prophylaxis lips, tongue, with puffiness of face, edema of
d. Stages of this disease, different vaccines lower eyelid and feet. Patient had protuberant
along with schedule of administration and lusterless hair
a. Diagnosis
2. A 4 yr old child admitted with h/o fever, sore b. Direct and indirect methods to confirm
throat and weakness of right lower limb, on diagnosis
examination child has neck rigidity and signs c. Infective form of nematode with mode of
of flaccid paralysis. No h/o immunization transmission
a. Diagnosis d. Pathogenic effects
b. Pathogenesis e. Treatment
c. Lab diagnosis

MICROBIOLOGY
d. How can u prevent this disease? Give 6. A 60 yr old male presented with periodic
schedule of immunization with age. attacks of fever, associated with painful swell-
ing of scrotal contents, arms and legs due to
3. A 40 yr old male presented with profound lymphadenitis and lymphangitis.
weight loss and persistent diarrhoea. O/E a. Diagnosis
generalized lymphadenopathy. H/o exposure to b. Enumerate tissue nematodes
multiple sexual partners c. Lab diagnosis
a. Diagnosis d. What is DEC provocation test?
b. Draw and label the causative organism e. Draw and label larval stages of different
c. Various structural antigens of the virus species
d. Name organisms causing diarrhoea in this f. Outline life cycle
disease
e. Lab diagnosis 7. A 22 yr old male presented with fever with
f. Window period chills and rigor, sweating episodes. Fever is l
periodic and showed rise in temperature every
4. A 20 yr old student presented with jaun- 3rd day. He gave h/o travel outside Kerala. u
dice and dark yellow urine. O/E there was a. Diagnosis m
hepatomegaly and no evidence of ascitis and b. Pathogenesis and life cycle
i
splenomegaly. He also complained of nausea, c. Lab diagnosis
low grade fever and loss of appetite. There was d. Treatment n
a h/o accidental needle stick injury 2 months a
back. 8. A 25 year old male presented with a visible
i
a. Diagnosis swelling of the abdomen. O/E, it was cystic
b. Causative agent in nature and there were associated pres- r
e
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sure symptoms. The patient gave a history of b. Draw and label the causative organism. c.
association with dogs for the past few years a. Classify the groups of microbes to which the
What is the probable diagnosis? b. What is the organism belongs.
mode of transmission? c. Describe the patho- d. Briefly describe the pathogenesis.
genesis. d. Discuss the laboratory diagnosis. e. e. Mention 2 complications. f
What is the prophylaxis? . Name the drug used for the treatment.

9. A 5 year old boy presented with history 12. 6 year old boy with fever, running nose and
of eating sand and mud and failure to gain cough brought to pediatric OP. Conjunctival
weight. On examination severe pallor++, no injection present. Bluish white ulcerations are
hepatosplenomegaly, slight pedal edema; other seen on the buccal mucosa opposite the lower
systems within normal limits. Lab findings: molars.
Hb-8 mg%, TC- nl, DC showed eosinophil- a. What is the provisional diagnosis?
ia-30% and ESR- 5 mm b. Name the causative organism.
a. Diagnosis c. Briefly describe the pathogenesis.
b. Describe the lifecycle of the pathogen with d. How will you confirm the diagnosis?
fig. e. What are the complications?
c. How will you confirm the diagnosis? f. What prophylaxis is advised?
d. What are the concentration techniques for
helminthic ova? 13. A 40year old male presented with intermit-
e. Describe the management and prophylac- tent bouts of high fever with rigor and pain-
tic measures to be taken to prevent nema- ful swellings of inguinal region. He gave past
MICROBIOLOGY

tode infection. history of a few similar episodes within last 3

years. He belongs to Sherlallai of Allepey dis-
10. A 3 month old baby was brought to the trict in Kerala. O/E inguinal lymph nodes were
paediatrics out-patient department with com- enlarged and tender with associated lymphan-
plaints of passing loose stool 8 times/day, fever gitis.
and vomiting. On examination, the stool was a. What is the provisional diagnosis? Name 2
greenish in colour. etiological agents.
a. Which is the most common virus causing b. Enumerate 3 other common clinical mani-
diarrhoea in infants? festations which can be present in this patient.
b. Describe the morphology of the virus.
c. What are the other viruses causing diar-
rhoea?
d. Describe the pathogenesis of viral diar- Answers
l rhoea. 1- Rabies, 12- measles,
e. How will you prove the diagnosis and treat 2- Polio, 13- Filariasis
u the case? 3- AIDS,
m 4- Hepatitis B,
i 11. 30 year old business man was brought to 5- Hookworm,
casualty with complaints of fever, pain radiat- 6- Filariasis,
n ing from the back of epigastrium of 2 days du- 7- Malaria,
a ration. He noticed multiple vesicular eruptions 8- Hydatid cyst,
i confined only to left side. He gives h/o chicken 9- Hookworm,
pox when he was 8 years old. 10- Rota virus,
r
a. What is the provisional diagnosis? 11- Herpes zoster,
e
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SPOTTING
1. Lowenstein-Jensen Medium with Infective endocarditis, Brucellosis, IMN,
growth Leptospirosis, Pyrexia of unknown origin
• PUO- Incubated for 24 hrs.
• Use- isolation of Mycobacterium tubercu-
losis Haemagglutination plate
• Ingredients- coagulated hens‘ egg, mineral
salt solution (potassium dihydrogen phos- • Identification- Numerous pits & large de-
phate, magnesium sulphate), asparagine, pressions.
malachite green, distilled water, glycerol • Use- To perform the following serological
• Functions of ingredients- Malachite green- investigations
selective media; inhibits other bacteria, • a. Haemagglutination test for
gives colour to the media ·· Influenza
• Sterilisation - By inspissation ·· Parainfluenza
• Nature of colonies- dry, rough, raised, ·· Rubella
irregular with wrinkled surface, creamy ·· Mumps
white, buff coloured colonies. (rough, • b. Haemagglutinaton inhibition tests
tough, buff) • c. Titration of viruses- influenza
• Rapid growth (within 7days)- Atypical

MICROBIOLOGY
mycobacteria
• Other media for M. tuberculosis VDRL slide
• Solid media- With egg- LJ, Petragnini, • Identification- slide is 75*56 mm & 3 mm
Dorset; With blood- Tarshis; With serum- thick, 12 polished concavities, each 16mm
Loeffler; With potato- Pavlovsky diameter & 1.7 mm deep
• Liquid media- Dubos‘, Middlebrook‘s, Su- • Use- diagnosis of syphilis
la‘s and Sauton‘ media • Advantage - simple, rapid, sensitive, small
• Reason for incubating the inoculated amount of serum is required, can be used
medium at 25oC & 37oC- M. tuberculosis to assess treatment, quantitative, CSF can
grows only at 37oc, while atypical myco also be used.
grows at both temperatures • Method- Slide flocculation-0.05ml heat in-
• Guinea pig is commonly used for animal activated (56oC for 30mins) serum is taken
inoculation studies . in depressions and a drop of freshly pre-
pared Cardiolipin antigen is added, mixed l
with syringe, slide is rotated at 180 rpm in
u
2. Blood culture bottle a VDRL rotator for 4min. Examine under
microscope under low power- formation of m
• Contains brain heart infusion broth floccules or clumps indicate reactive serum. i
• Method- 5 ml blood is collected by ve- • Modified test with carbon particles coat-
n
nepuncture & inoculated into the bottle ed with cardiolipin is RPR (Rapid Plasma
with 50 ml brain heart infusion broth. Reagin) test. a
Ideally 3 sets of samples are to be collected • Biological false positive- Tropical eosino- i
from different sites at 1/2 hr interval. philia, Malaria, Leprosy, Relapsing fever,
r
• Indications-1st week of typhoid fever, RA, IMN, Hepatitis, SLE, (Code- Tropical
e
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MALARIAHS); Chronic(>6 months)- SLE MacConkey’s agar

and other collagen diseases; Acute- Acute • Use- Differential media for cultivation of
infections and inflammations enteric
• False negative- Sera with high titres of an- • Ingredients- Peptone, Lactose, Agar, Neu-
tibody- prozone phenomenon, dilute sera tral red, Sod. taurocholate (Code- PLANT)
and repeat test • Functions of ingredients:
·· Bile salt inhibits the growth of non enteric
bacteria
• Robertson’s cooked meat ·· Neutral red is the indicator
medium • Lactose fermenters form pink colonies eg.
E. coli, Klebsiella
• Identification- Test tube containing fat • Non lactose fermenters form colourless
free minced cooked meat of ox heart in colonies eg. Salmonella, Proteus
infusion broth with peptone and a layer of • Late lactose fermenters eg. Vibrio cholera,
sterile liquid paraffin over it. Sh. sonnei
• Uses - Suitable for growing anaerobes,
preservation of stock cultures (Bacterioi-
des, Clostridium) Agar Agar
• Production of gas- bubbles, change in • Use- For solidification of media
colour of meat, turbidity of broth indicate • Agar melts at 98oC and solidifies at 42oC,
growth of organism obtained from sea weeds, contains long
• Saccharolytic- meat turns pink (Clostridi-
MICROBIOLOGY

chain fatty acids

um perfringens) • Adv- Bacteriologically inert, free from
• Proteolytic- meat turns black (Clostridium growth promoting and inhibiting substanc-
tetani) es, do not add to nutritive property of the
media
Widal test • Concentration- 2% for solid media, 0.2-
0.5% for semisolid, 6% for prevention of
• Tube agglutination test for the lab diagno- swarming of Proteus and in Nagler reaction
sis of enteric fever (Cl. perfringens)
• Identification- many test tubes- To esti-
mate serum agglutination titres of O & H Membrane Filter
antigens of Salmonella typhi and H anti-
gen of Sal. paratyphi A & B. Agglutination • Identification- Consists of two chambers
appears by the end of 1st week. with a cellulose acetate membrane in b/w.
l • Narrow tube with conical bottom {Drey- • Use- Water purification & analysis, Ster-
er‘s} for H agglutination, round bottom ilisation, Sterility testing, Preparation of
u
{Felix} for O agglutination. solutions for parenteral use, to filter serum,
m • H agglutination- loose, cotton woolly antibiotic solution, liquid media & exu-
i clumps, O agglutination- disc like pattern dates.
• False positive- TAB vaccine • Membrane is made up of cellulose nitrate
n
• False negative- Treatment with chloram- & cellulose acetate.
a phenicol • Total capacity-115 ml with markings at 20,
i 40, 60, 80, 100. Average pore diameter of
r 0.22 micrometre is widely used.
e •
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Seitz filter Stokes antibiotic sensitivity test

• Consists of a disc of asbestos composition • Disc diffusion technique for antibiotic sen-
through which the fluid is passed. sitivity testing.
• Composed of Magnesium silicate • Both test and control organisms are inocu-
• Use- a. Sterilization of serum b. To obtain lated on same plate with inoculums which
bacteria free filtrates of toxins and bac- give semiconfluent growth. Inhibition zone
teriophages c. Sterilization of antibiotic size of test can be compared with that of
solution, urease medium, hydatid fluid control, so easier to do.
(Casoni‘s test) • Method- Standard sensitive strains of the
• Disadvantage- Passing of viruses & myco- bacteria to be tested is inoculated into the
plasma, carcinogenic potential of asbestos middle 1/3rd of the plate eg. Bacillus cul-
ture plate. Control bacterium is inoculated
into the upper and lower 1/3rd. Antibiotic
Mandlers candle filter discs (small 6mm discs) are applied in
between the standard and test inocula such
• Hollow open candles made of Kieselghur, that the zones of inhibition are around
asbestos, plaster of paris each disc
• Use- For purification of water for industri- • Interpretation-
al & drinking purposes ·· If zones are equal, test bacteria are sensitive
to antibiotic
·· if zone around test is smaller than control,

MICROBIOLOGY
Sterile cotton swab moderately sensitive
·· if there is no zone of inhibition then test
• Identification- A stick with cotton at its bacteria are resistant
end in a closed test tube. • MIC & MBC- from dilution tests, tube
• Use- To take specimen from throat, anteri- dilution and agar dilution tests
or nares, conjunctiva, uterus and cervix. • Medium used- Mueller Hinton agar/ Nu-
• Method of sterilization- Hot air oven, trient agar
alpha radiation, autoclave
Kirby bauer antibiotic sensitivity
method
Mclntosh Fildes jar
• Disc diffusion technique used for antibiotic
• Identification- Metallic container with a sensitivity testing.
lid having outlet & inlet tubes. Blood agar • Done in a lawn culture of the organism l
plate is kept inside. Outer tubes connected being tested u
to vacuum pump while the inner to hydro- • Other methods
gen source. Two terminals are present for ·· Diffusion tests- Stoke‘s method, E test m
electric supply & catalyst- modified alumi- ·· Dilution tests- Tube dilution, Agar dilution i
na pellets coated with palladium n
• Use- for anaerobic culture
• Disadv- Risk of explosion Western blot paper test a
i
• Use: Confirmatory test for HIV antibody r
e
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• Method- Nitrocellulose strips with HIV Sabouraud’s dextrose agar with

proteins are reacted with test & control- colonies
strong positive, weak positive, negative sera.
• In positive sera, bands will be seen with • Greenish- Penicillium
multiple proteins, atleast 1 core and 2
• Blackish- Aspergillus
envelope proteins. (p18, p24, p55, gp120,
gp160, gp41) • Creamy white, smooth- Candida
• pH of medium- 5.4 17. Beta-Hemolytic

Candida microscopy & Candida germ

tube Steptococci on blood agar

• Identification- Violet coloured oval budding • Identification- Clear, complete zone of

cells hemolysis around the colonies.
• They are normal inhabitants of skin and • Infections produced- Suppurative, non
mucosa suppurative (Rheumatic fever, Acute
• Diseases caused- Candidiasis- opportunistic glomerulonephritis)
fungal infection (predisposing factors
- DM, prolonged antibiotic therapy,
i m mu n o s u p p r e s s i o n ) , o t o my c o s i s , Staphylococcus aureus on blood agar
keratomycosis
MICROBIOLOGY

• Reynolds-Braude phenomenon- Ability to • Identification- Hemolytic golden yellow

form germ tubes within 2 hrs in human colonies, zone of complete hemolysis
serum at 37oC surrounds the colonies.
• Diseases caused- Abscesses, skin infections,
Penicillium tonsillitis, pneumonia,osteomyelitis
(Streptococci, E. coli, Psuedomonas,
• Identification- Brush like arrangement Klebsiella)
of conidiophores & chains of spores
extending from the ends of short branches
of conidiophores. Corynebacterium diphteriae on
• Causes Penicilliosis in HIV, Otomycosis tellurite blood agar or microscopy

• Selective medium for the isolation of C.

l Aspergillus diphtheriae, reduces potassium tellurite to
metallic tellurium producing black colonies.
u
• Mycelium consists of septate hyphae • Colonies are at first small, circular, white
m opaque discs but enlarge on continued
• Conidiophores arise from a foot cell &
i terminate in a vesicle from which flask incubation & acquire a yellow tint.
n shaped sterigmata arises • Cuneiform arrangement of bacteria (Chinese
• Microconidia arranged in chains on letter pattern)
a • Special stains- Albert‘s stain, Neisser‘s,
sterigmata
i Ponder‘s
• Aspergillosis, Otomycosis, Oculomycosis
r • Other selective media for the same bacteria-
e Loeffler‘s serum slope
’18 136
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

• Morphological classification of the bacteria 23. Microfilaria

grown in this medium- gravis, intermedius
and mitis. • Identification- Larvae of filarial worm in
• Volutin granules peripheral smear.
• Differences between microfilaria of W.
bancrofti and B. malayi
Pseudomonas on nutrient agar • Blood is collected between 10 pm and 4 am
because of its nocturnal periodicity
• Identification- Green diffusible pigment
production of Pseudomonas aeruginosa on
nutrient agar. Aerobic spore bearer
• Pigments produced- Pyocyanin, Pyoverdin,
Pyomelanin, Pyorubin • Identification- Gram positive bacilli ar-
• Diseases caused ranged in long chains with a central spore.
• Eg. Bacillus anthracis, Nocardia
• Destruction of spores by Duckering pro-
• Proteus- swarming growth on cess, using 2% formaldehyde.
blood agar
Clostridium tetani
• Identification- Gram positive bacillus with
• Culture media- Blood agar, MacConkey agar
rounded, bulging terminal spores.
(no swarming)

MICROBIOLOGY
• Culture medium- Robertson‘s cooked meat
• Characteristic odour- fishy odour medium.
• Methods to inhibit swarming- (i) increase • Toxigenicity test in tail of mouse
concentration of agar (6%) (ii) Incorporate • Toxins produced- Tetanospasmin, Tetano-
chloral hydrate (1:500), sodium azide (1:500) lysin (toxin responsible for tetanus - teta-
[No swarming in MacConkey agar.] nospasmin)
• Gram negative bacilli
• Identification with examples (E. coli, Kleb-
Demonstration of capsule- siella, Salmonella)  Enumerate diseases
Pneumococci caused- UTI, diarrhoea, septicemia  Me-
dium used for culture- MacConkey‘s agar
• Identification- Diploocci with clear halo
around it Satellitism (pic)
• Diseases caused- Pneumonia, otitis media, l
sinusitis, meningitis • For identification of H. influenza
• Organism used for isolation- Mice • Blood agar deficient in factor V u
• O t h e r u s e s o f n e g a t i v e s t a i n i n g - • Staph. aureus streaked across a plate of m
Demonstration of capsule of Cryptococci, blood agar inoculated with H. influenza
i
Spirochaete demonstration (Negative • H. influenza colonies near the Staph. au-
reus colonies are bigger in size n
staining for spirochetes different from that
used for capsule demonstration) a
Castaneda’s method of blood
i
culture (pic)
r
e
137 ’18
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

• Biphasic medium with both solid and liq- • No intermediate host

uid media
• Use- Brucella isolation and Salmonella
culture Cyclops
• Adv- Minimum material, manipulation,
contamination, lab worker infection, for • Vector for
slow growing organisms a. fish tape worm (1st stage larva- coracidi-
um)
b. guinea worm (3rd stage larva)
Elek’s gel precipitation test (pic)

• Virulence test for C. diphtheriae Tapeworm

• On 20% horse serum agar
• Animal used for inoculation studies- guin- • Infective form form for humans- Cysticer-
ea pig, rabbit cus cellulosae or bovis
• Intermediate host- Pig or Cow
• Peculiarity of embryo- 3 pairs of hooklets
HIV (pic)

• Genes in HIV- env, gag, pol (structural • Pinworm

genes) • Infective form- Egg containing larvae
• HIV proteins- p24, gp120, gp41 • Egg- Planoconvex, double layered, colour-
MICROBIOLOGY

• Screening test & Confirmatory test 31. less

Ascaris egg- fertilized
• Infective form of the parasite- egg contain-
ing rhabditiform larva
• Methods of diagnosis- demonstration of
eggs in feces, larvae and Charcot Leyden
crystals in sputum.

• Chemotherapy- Pyrantel
• pamoate, Albendazole

• Methods to prevent infection- treatment

l of vegetables with iodine 200 ppm for 15
minutes kills egg and larvae.
u
m
i Trichuris trichura (whip worm) egg
n
• Identifying features- barrel shaped, mucus
a plug on both sides, bile stained
i • Infective form- embryonated egg
• Part of the intestine where adult form of
r
the parasite reside- caecum
e
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

STAINING PROCEDURES
GRAM STAINING (The given smear contains....)
b. Draw diagram ( don‘t draw pus cells if
1. Place the slide on the staining rack not seen in field of observation)
2. Cover the slide with Gentian violet/Methyl
violet/Crystal violet & keep it for 1 min. • Acid fast staining - Mycobacterium tuber-
3. Wash with water, cover the slide with culosis (with 20% sulphuric acid)
Gram‘s iodine & keep it for 1 min.
4. Wash the slide with water • Modified acid fast staining
5. Decolorise with acetone, keep the slide in a.M. lep r a e (with 5% sulphuric acid)
a slanting position and add acetone drop by b.Nocardia (with 1% sulphuric acid)
drop for 2-3 sec (until the draining fluid is c.Spores (with 0.25 - 0.5% sulphuric acid)
colourless) d.Cryptosporidi um parvum, Isospora belli
6. Immediately wash with water. (cold acid fast staining)
7. Cover the slide dil. carbol fuschin & allow
to stand for 30 sec.
8. Wash thoroughly with water, blot & dry in
air.
9. Examine under oil immersion.

MICROBIOLOGY
10. Write down observations

ZIEHL-NEELSEN STAINING [ACID

FAST STAINING]

1. Place the slide on the staining rack

2. Cover the smear with con. carbol fuschin.
Heat until steam rise. Do not boil. Allow the
preparation to stain for 7 min, heat being
applied at intervals to keep the stain hot. The
stain must not be allowed to evaporate or dry.
If necessary pour more con. carbol fuschin to
cover it.
3. Wash with water l
4. Cover the slide with 20% Sulphuric acid. u
Keep it for 1 min. Decolorisation is finished m
when the film is colorless or faintly pink.
5. Wash with water i
6. Counterstain with Loeffler‘s methylene blue n
for 3 min. a
7. Wash with water, blot, dry.
8. Examine under oil immersion. i
9. Write down observations as follows r
a. Colour, Shape, Arrangement, Inference e
139 ’18
 OSPE
MICROBIOLOGY

QUESTION

• ZN SMEAR EVALUATION AND AFB REPORT

No. of AFB Seen in oil immersion field (F) Report
0 300 F AFB not seen
1-9 100 F 1+
1-9 10 F 2+
1-9 1F 3+
10 or >10 1F 4+

140
 FORENSIC MEDICINE
FORENSIC
PA P E R S

MEDICINE
QUESTION PAPER PATTERN

ESSAY – 7 marks
SHORT NOTES – 5 x 3 = 15 marks
ANSWER BRIEFLY – 5 x 2 = 10 marks
DIFFERENTIATE BETWEEN – 2 x 2 = 4 marks
DIAGRAM – 2 x 2 = 4 marks

141
 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM
FORENSIC MEDICINE

DIAGRAMS 6. Courts of Law and their powers(R-7)

7. Punishments(R-7)
1. Ossification centres of shoulder joint(R-73) 8. Cognisable offence(R-8)
2. Ossification centres of wrist joint(R-75) 9. Subpoena/Summons/Litigation(R-8)
3. Ossification centres of hip joint(R-73) 10. Conduct Money(R-9)
4. External appearance of wounds caused 11. Dying Declaration,Compos mentis(R-10)
by a single edged weapon & rubber tapper‘s 12. Dying Deposition(R-11)
knife(R-202) 13. Oral evidence and exceptions(R-11)
5. Cross section of rifled barrel(R-209) 14. Witness & types(R-12)
6. Shotgun catridge(R-213) 15. Hostile witness(R-13) 16. Perjury(R-13)
7. Parts of catridge of a rifled weapon(R-213) 17. Steps in record of evidence(R-13)
8. Types of hymen(R-391) 18. Leading question(R-14)
9. Sex chromatin(R-59) 19. Summons case(R-20) 20. Warrant
10. Shotgun wounds at varying distanc- case(R-20)
es(R-219)
11. Abrasion collar of an entrance bullet MEDICAL LAW AND ETHICS
wound(R-224)
12. Estimation of extent of body surface 1. Function of Indian and state medical coun-
burns(R-321) cils(R-24)
13. Belly scales and head scales of snake 2. Warning notice, Penal erasure(R-27)
14. Fractures of hyoid bone(R-357) 3. Infamous conduct(R-27)
15. Diatoms(R-371) 4. Dichotomy, Covering(R-645,646)
16. Complications of criminal abortion(R-410) 5. Duties of medical practioner(R-29)
17. Human spermatozoa(R-436) 6. Professional secrecy and Privileged QUESTION
18. Signs of strangulation(R-349) communication(R-32)
19. Human hair and animal hair(R-95) 7. Professional negligence- types, differ-
20. Gastric lavage tube(R-515) ence(R-35,tab3-1)
21. Fundal heights during pregnancy(R-393) 8. When does liability for negligence
22. Coup and contrecoup injuries(R-252,253) arise? (4 D‘s)(R-35)
23. Chart showing the major changrs to esti- 9. Res Ipsa loquitur(R-38)
mate time since death(R-158) 10. Calculated risk(R-38)
24. Fingerprint patterns(R-86) 11. Novus actus intervenience(R-39)
25. Fusion of epiphysis in sternum 12. Difference between professional negli-
26. Vertical section of incisor tooth and gence & infamous conduct(tab 3-2)
age-process in teeth(R-71) 13. Medical maloccurance(R-39)
l 14. Corporate negligence(R-41)
15. Contributory negligence(R-41)
u
INTRODUCTION & LEGAL 16. Defence against neglence(R-46)
m PROCEDURES 17. Therapeutic misadventure(R-46)
i 18. Vicarious liability(R-47)
1. Forensic medicine, legal medicine(R-1) 19. Products Liability(R-48)
n
2. Medical Jurisprudence(R-1) 20. Euthanasia(R-54)
a 3. Medical etiquette(R-1) 21. Consent in medical practice- Types,
i 4. Inquest & procedure(R-6) MLI(R-50)
r 5. Situations where magistrate inquest is re- 22. Therapeutic privilege(R-51)
quired(R-7) 23. Loco parentis(R-53)
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FORENSIC MEDICINE
24. Malingering(R-56) 6. Undertaker‘s fractures(R-110)
25. Consumer protection act (COPRA 1986) 7. Preservation of viscera(R-123)
(R-649) 8. Preservatives(R-124)
9. Conditions where preservation is not neces-
sary(R-125)
IDENTIFICATION 10. Ostometric board(R-129)
11. Karl pearson formula(R-129)
1. Corpus delicti(R-57) 12. Exhumation & its authorization(R-132)
2. Cephalic Index, types of skulls(R-58)
3. Sex chromatin(R-59)
4. Sex difference in bones(Tab 4-3) DEATH AND ITS CAUSES
5. Medullary Index(R-65)
6. Intersex, Concealed sex(R-60,65) 1. Somatic death, Bishop‘s tripod of life(R-134)
7. Gustafson‘s method(R-70) 2. Brain death, Moment of death(R-134)
8. Difference between temporary & permanent 3. Harvard criteria of brain death.(R-135)
teeth(Tab 4-6) 4. Molecular death(R-136)
9. Eruption of teeth (Age)(R-71,tab 4-7) 5. Asphyxia and asphyxial stigmata(R-137,140)
10. Diff b/w mandible in infants, adult and old 6. Tardieu spots(R-141)
age(R-79,tab4-10) 7. Classification of cause of death(R-142)
11. MLI of Age (esp 10, 12, 14, 15, 16, 18, 21) 8. Causes of sudden death(R-150)
(R-82) 9. Negative autopsy(R-143)
12. Age of fetus(R-83) 10. Obscure autopsy(R-144)
13. Rule of Haase(R-84) 11. Concealed trauma(R-146)
PA P E R S 14. Anthropometry(R-85) 12. Signs of death(R-152)
15. Dactylography(R-85) 13. Suspended animation -Causes, MLI(R-152)
16. Types of fingerprints(R-86) 14. Changes in eye- Tache noir, Kevorkian
17. Poroscopy, podogram(R-86) sign(R-153,154)
18. Cheiloscopy(R-88) 15. Postmortem fluidity of the blood(R-153)
19. Super imposition(R-89) 16. Postmortem cooling of body(R-154)
20. Scars,MLI(R-91) 17. Postmortem caloricity(R-155)
21. Tattoo marks- MLI, Removal, Dyes(R-92) 18. Postmortem hypostasis - synonyms,cause,-
22. Difference between human & animal fixation & nonfixation,MLI(R-155)
hair-Diagram,MLI(R-96,tab4-11,4-45) 19. Diff b/w postmortem hypostasis and con-
23. Forensic odontology,MLI(R-97) gestion(R-158)
24. Bite marks(R-98) 20. Primary flaccidity & secondary flaccidi-
25. FDI two digit system, modified FDI sys- ty(R-160) l
tem(R-99) 21. Rigor mortis - mechanism of production,-
time,order of appearence,MLI(R-160) u
22. Conditions simulating rigor mortis(R-163) m
MEDICO LEGAL AUTOPSY 23. Cadaveric spasm- MLI, difference from rig- i
or mortis(R-162,163)
1. Skin incisions(R-107) 24. Putrefaction – cause,bacteria associated n
2. Objectives of medicolegal autopsy(R-102) with,enzymes,features of putrefaction, site,fac- a
3. Method of removal of organs(R-109) tors affecting(R164) i
4. Post mortem clots(R-113) 25. Marbling(R-166)
r
5. Unclotted blood- conditions(R-113) 26. Glove-stocking appearance(R-167)
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM
FORENSIC MEDICINE

27. Casper‘s dictium(R-170) 27. Fishtailing(R-200)

28. Adipocere -morphology, cause, predispos- 28. Penetrating and Perforating
ing factor,MLI(R-171) wounds(R-197)
29. Mummification — morphology, cause, 29. Concealed puncture wound(R-202)
predisposing factor, MLI(R-172) 30. MLI of stab wound, Important dimen-
30. Maceration (asepctic autolysis, signs of sions(R-204)
dead born, refer chapter—infant death) 31. Difference between incised & lacerated
31. Embalming, embalming fluid(R-173) wound(R-205)

MECHANICAL INJURIES FORENSIC BALLISTICS

1. Define injury(R-179) 1. Rifling & its advantages.

2. Classification of injuries(R-179) 2. Choking of a shotgun, Paradox guns
3. Abrasion & types(R-181) 3. Calibre and gauge
4. Patterned abrasion(R-182) 4. Composition of priming mixture
5. Brush burn (mech of production)(R-181) 6. 5. Powder (1) black powder constituents
Pressure abrasion(R-182) (2) smokeless powder constituents
7. Age of abrasion(R-182) 6. Dum dum bullet
8. Difference between AM & PM abra- 7. Shot gun wounds at varying distance,
sion(R-183) Diagram
9. MLI of abrasion(R-183) 8. Features of contact wound for shot gun
10. Contusion, MLI(R-184) 9. Wounds from rifled weapons- assessment of
11. Ectopic bruising, come-out bruise(R-185) range QUESTION
12. Patterned bruising(R-185) 10. Backspatter, corona, abrasion collar,
13. Age of bruise(R-185) dirt collar
14. Difference between hypostasis & bruis- 11. Contusion collar, point blank
ing(R-188) 12. Puppe‘s rule
15. Define laceration, types(R-189) 13. Dermal nitrate test, MLI
16. Differences between incised looking lac- 14. Difference between entrance & exit
erated wound & incised wound(R-191,192) wound 15. Supported exit wound
17. Incised wound & MLI, tailing of 16. Ricochet bullet, exhibit bullet, test
wound(R-192) bullet 17. Primary & secondary markings
18. Beveling cut, MLI(R-193) of a bullet 18. Neutron activation analysis
19. Difference between suicidal & homicidal 19. Blast lung
l cut throat(R-195) 20. Tandem bullet, yawning bullet, tumbling
20. Self inflicted and fabricated wounds(R-194) bullet
u
21. Hesitation marks(R-194)
m 22. Complications in a cut throat inju-
i ry(R-195) REGIONAL INJURIES
23. Chop wound(R-196)
n
24. Defence wounds(R-207) 1. Causes of black eye(R-243)
a 25. Stab wound, Punctured wound, Complica- 2. Types of fracture of skull(R-243)
i tions(R-197) 3. Depressed fracture of skull, MLI(R-245) 4.
26. Shapes of wounds, Kinds of weapons Signature fracture, Pond fracture, Gutter frac-
r
used(R-199) ture(R-245,246)
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FORENSIC MEDICINE
5. Contrecoup injury(R-251) 17. Shock lung(R-306)
6. Commotio cerebri, Commotio cordis(R-251) 18. Remote causes of death from
7. Lucid interval(R-251) wounds(R-306)
8. Causes & features & MLI- Extadural, Sub- 19. Crush syndrome(R-307)
dural,Sub arachnoid, intra cerebral haemor- 20. Difference between AM & PM
rhage(R 258-263) Wounds(R-312)
9. Apoplexy(R-259)
10. Punch drunk syndrome(R-284)
11. Whiplash injury(R-266) THERMAL DEATHS
12. Railway spine(R-267)
13. Concussion of brain (R-253) 1. Trench foot, Immersion foot(R-317)
14. Injuries of pedestrains (Primary impact 2. Frost bite (R-317)
injuries)(R-277) 3. Heat stroke(R-319)
15. Bumper injury(R-277) 4. New classification of burns(R-320)
16. Under running / tail-gating(R-284) 5. Rule of nine (R-321)
17. Motor cyclist‘s fracture(R-283) 6. Pugilistic attitude(R-322)
18. Fracture of pontine haemorrhage 7. Heat haematoma(R-324)
19. Buckling up of sterum 8. Scalds(R-329)
20. Steering wheel impact type of inju- 9. Thermal fractures of skull(R-325)
ry(R-281) 10. Difference between external haematoma
21. Seat belt syndrome(R-282) due to burns & due to blunt force(R-324)
22. Triage(R-283) 11. Difference between antemortem & post-
23. Cardiac tamponade mortem burns(R-326)
PA P E R S 24. Boxer fracture(R-287) 12. Joule burns(R-330)
13. Crocodile flash burn(R-331)
14. Current pearls(R-332)
MEDICO LEGAL ASPECTS OF 15. Bone pearls / wax drippings(R-332)
WOUNDS 16. Filigree burns(R-334)
17. Cause of death in burns, Electrocu-
1. Define injury (Sec 44 IPC)(R-291) tion(R-321)
2. Murder (Sec 300 IPC)(R-291) 18. Artifacts due to burns(R-470)
3. Dowry death (Sec 304-B IPC)(R-295) 19. Healing of burns(R-325)
4. Homicide(R-290)
5. Culpable homicide(R-290)
6. Hurt ( Sec 319 IPC) (R-292) MECHANICAL ASPHYXIA
7. Grevious hurt (Sec 320 IPC)(R-292) l
8. Dangerous weapon(R-294) 1. Definition of hanging (R-338)
9. Assault(R-295) 2. Partial hanging ,Typical hanging,Atypical u
10. Medicolegal classification of injury(R-290) hanging(R-338) m
11. Classification of Fatal/ Dangerous Inju- 3. Features of AM hanging(R-342) i
ries(R-293) 4. Causes of death in hanging & commonest
12. Fat embolism(R-308) cause(R-339) n
13. Air embolism(R-309) 5. Features of Asphyxial death- cyanosis, a
14. Cause of death from wounds(R-302) 15. congestion, petechial h‘ge, edema, fluidity of i
Primary shock(R-303) blood(R-344)
r
16. Secondary shock(R-303) 6. Le-facie sympathique & its mecha-
e
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FORENSIC MEDICINE

nism(R-344) MLI of impotence and sterility

7. Lynching (R-346) 9. Quoad hoc(R-384)
8. Strangulation –Types, cause of death, mech- 10. Artificial Insemination- Indications, types,
anisms(R-347) precautions, legal problems(R-386)
9. Diagram—signs of strangulation(R-349) 11. Sterilization- Indications, types(R-386) 12.
10. Differentiating features between strangula- Fecundation ab extra(R-385) 1
tion & hanging(R-351) 3. Indications, legal problems of surrogate
11. Pseudo strangulation, Subpleural emphy- motherhood(R-388)
sematous bullae(R-348,349) 14. Lerische ssyndrome
12. Bansdola / garroting / mugging / throttling
/smothering / overlying / burking/ Gagging(R
353360) VIRGINITY, PREGNANCY AND DELIVERY
13. Define suffocation(R-360)
14. Commando punch(R-356) 1. Define virgin, virginity, defloration, divorce,
15. Hyoid bone fractures — type & its nullity of marriage(R-389)
MLI(R-357) 2. Hymen, types of hymen with figure(R 390-
16. Café coronary & mechanism of 391)
death(R-363) 3. How to differentiate between tear of hymen
17. Traumatic asphyxia(R-363) 18. Drowning produced by sexual offences & notched hy-
& types(R-365) men?(R-390)
19. Immersion syndrome(R-366) 4. Cause of rupture of hymen(R-390)
20. Difference between drowning in fresh & 5. MLI of hymen, virginity(R-392)
sea water(R-370) 6. Features in genitalia of a virgin(R-389) 7.
21. Cutis anserine, Cadaveric spasm(R-368) MLI of pregnancy(R-392) QUESTION
22. Patho- physiology & mechanism of death 8. Affiliation(R-397)
in fresh & sea water drowning(R-366) 9. Presumptive signs , probable signs &
23. Emphysema aquosum and odema aquo- positive signs of pregnancy(R 392-396)
sum(R-369) 10. Lochia and its types(R-398)
24. Paltauf ‘s haemorrhage(R-369) 11. What is (a) Chadwick‘s sign
25. Dry drowning(R-370) (b) Hegar‘s sign
26. Gettler‘s test(R-371) (c) Goodell‘s sign
27. Diatom test(R-371) (d) Osiander‘s sign & when
28. Sexual asphyxia(R-375) do they appear?(R 393-394)
29. Wrinkling, bleaching, soddening- Times of
occurrence(R-368) 12. Radiological signs of fetal death in
l utero(R-396)
13. Pseudocyesis / phantom pregnancy (R-396)
u IMPOTENCE AND STERILITY 14. Pseudo virgin
m 1. Impotence(R-382) 15. Posthumous child(R-396)
i 2. Sterility(R-382) 16. Superfecundation, superfoetation, sup-
3. Frigidity(R-382) posititious child(R-396,397)
n 4. Sterilization(R-386) 17. Prenatal diagnostic act :-a) objectives (b)
a 5. Surrogacy(R-388) punishment(R-652)
i 6. Artificial Insemination(R-386) 18. Legitimacy, MLI(R-397)
7. Causes (permanent & temporary) of im- 19. Estimation of paternity of a child , Disput-
r
potence in male & female, MLI(R 383-385) 8. ed paternity(R-397)
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FORENSIC MEDICINE
20. Difference between parous and nulliparous 33. Proof of semen(R-436)
uterus(R-399)
21. Signs of virginity(R-392)
ABORTION
SEXUAL OFFENCE 1. Abortion – classify(R-400)
2. Justifiable &criminal abortion(R-400)
1. Classify sexual offence(R-411) 3. Difference between natural and criminal
2. Define rape, punishment (Sec 375, 376 IPC) abortion(R-409)
(R-411,412) 4. Any 4 sections of IPC dealing with criminal
3. Statutory rape(R-414) abortion(R-400,401)
4. Features of a voluntary consent 5. MTP act – indications, Who can do abor-
5. Objectives of doing medical examina- tion & where(R-401)
tion(R-416) 6. Duties of a doctor in case of therapeutic &
6. Examination of a victim- features looked criminal abortion(R-408)
for, calculation of time of assault, specimens 7. Enumerate the methods of therapeutic &
collected(R 416422) criminal abortion(R 402-405)
7. Examination of the accused(R-425) 8. Hy- 8. Abortifacient drugs(R-402)
menal tear & its healing(R-419) 9. Abortion stick(R-404)
9. Corroborative signs of rape(R-422) 10. MLI of placenta(R-408)
10. Incest(R-427) 11. Complications of criminal abor-
11. Unnatural sexual offences(R-427) 12. Sod- tion(R-410,fig 17-4)
omy ( & its other names), procedure of exam- 12. Causes of death in abortion(R-410)
PA P E R S ination ,MLI(R-427) 13. Punishment for criminal abortion (Sec 312
13. Buccal coitus(R-429) – 316 IPC)(R-400,401)
14. Sexual perversions(R-430)
15. Tribadism(R-430)
16. Bestiality(R-430) INFANT DEATHS
17. Uranism(R-431)
18. Sadism(R-431) 1. Define infanticide, Stillbirth, live birth
19. Lust murder(R-431) 2. Viability
20. Necrophagia(R-431) 3. Dead birth & its features
21. Masochism(R-431) 4. Spalding sign
22. Fetichism(R-432) 5. Difference in lungs before & after respira-
23. Transvestism(R-433) tion
24. Exhibitionism(R-433) 6. Ploucquet‘s test l
25. Voyerism(R-433) 7. Hydrostatic lung test (Raygat‘s test) – con-
u
26. Troilism(R-433) ditions where it is unnecessary, fallacies
27. Frotteuerism(R-433) m
28. Undinism(R-433) i
29. Indecent assault(R-411)
n
30. Catamite(R-427)
31. Chemical tests for semen(R-434) a
32. Microscopic examination, Motility of sper- i
m(R-436) r
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8 Breslaus second life test, Wredin‘s test 3. Hallucination & its types(R-481)
9. Caput succedaneum 4. Illusion(R-482)
10. Cephal hematoma 5. Impulse & types(R-482)
11. Precipitate labour, MLI 6. Phobia- types(R-482)
12. Difference between head injury due to 7. Lucid interval(R-482)
labour and blunt force 8. Diff b/w lucid interval in insanity & head
13. Battered baby syndrome ( Cafey‘s syn- injury(R-483,tab 23-1)
drome) 9. Diff b/w psychosis & neuro-
14. Concealment of birth sis(R-483,tab23-2)
15. Abandoning of infants 10. Diff b/w real and feigned insani-
16. Infantile whiplash syndrome ty(R-488,tab23-3)
17. Munchhausen‘s syndrome by Proxy 11. Restraint of the insane(R-489)
18. Sudden infant death syndrome (imp) 12. Delirium tremens(R-580)
19. Ossification centres in sternum, sacrum 13. Civil & criminal responsibilities of an
20. Umblicical cord changes after birth insane person(R-491,493)
21. Non accidental trauma – Battered baby, 14. Testamentory capacity(R-492)
Munchausen‘s, SIDS 15. Mc naughten‘s rule - Section 84 IP-
C(R-493)
16. Automatism(R-496)
BLOOD STAINS 17. Post - epileptic insanity(R-485)
18. Drunkenness & law [Sec 85,86 IPC](R-
1. Screening tests for blood – benzidene, 497)
phenolphthalein, o-toluidine, mucomalachite
green tests(R-450) FORENSIC SCIENCE LABORATO- QUESTION
2. How will you differentiate human blood RY
stain from other species by microscopic exam- 1. Locard‘s exchange principle(R-475)
ination of blood?(R451) 2. Difference between colostrum & milk
3. Examination of blood stains- Age of blood 3. Microscopic appearance of
stains,sex and age of person,living or dead blood(R-451) 4. Confirmatory test for
body(R-450) semen(R-476)
4. Benzidine test(R-450) 5. Polygraph(R-477)
5. Confirmatory test for blood(R-451) 6. Narco analysis- Truthserum
6. Teichmann‘s test(R-451) drugs(R-478)
7. Takayama test(R-451)
8. Precipitin test(R-452)
l 9. MLI of blood group(R-458) ARTEFACTS
10. DNA finger printing(R-459) 1. Resuscitation of artefacts(R-468)
u 11. Difference between AM & PM blood stains 2. Artefacts related to rigor mortis and
m 12. Microscopic appearance of RBC‘s – dia- burns(R-469)
i gram(R-451)
13. PCR v/s RFLP(R-463)
n
TOXICOLOGY
a
i FORENSIC PSYCHIATRY 1. Toxicology and poison, classification of
1. Delirium(R-480) poisons(R-498,504)
r
2. Delusion & its types(R-481) 2. Duties of a doctor in suspected case of poi-
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soning (R-513) 2. Viscera preserved in arsenic poisoning
3. Gastric lavage – method, C/I (R-514) 3. Difference between arsenic poisoning &
4. Preservation for organs in poisoning cholera(R-539)
5. Antidotes – Types(R-516) 4. Hg poisoning –treatment(R-542)
6. Universal & physiological antidotes(R-517) 5. Signs & Symptoms of plumbism(R-544,545)
7. Chelating agents(R-518) 6. Cu poisoning(R-547)
8. Name some poisoning substances used as 7. Aldrich -mess lines(R-540)
abortifacients 8. Rain drop pigmentation(R-540)
9. Contraindications in corrosive poisoning 10. 9. Mercurial erithism(R-543)
Give examples for - Stupefying agents, Cattle 10. Hatter‘s hakes(R-543)
poisons, Household emetics 11. Mercuria lentis(R-543)
11. Corrossive poisons 12. Acrodynia(R-543)
12. Deliriants 13. Punctuate basophilia(R-544)
13. Diaphoretics(R-519) 14. Activated char- 14. Bartonian lines(R-544)
coal(R-516)
INORGANIC IRRITANT POISONS
1. Phossy jaw(R-551)
AGRICULTURAL POISONS 2. Antidote in P poisoning(R-551)
‘ 3. Difference in P poisoning and acute yellow
‘1. Organo phosphorus poisoning – MOA, atrophy(R-551)
manifestation, causes of death, diagnosis, man- 4. Difference between red and white phospho-
agement, PM findings(R 521-524) rus(R-550)
2. Cholinesterase reactivators(R-523)
PA P E R S 3. Plant penicillin(R-525)
4. Zinc phosphide, Al phosphide(R-527,529) ORGANIC IRRITANT POISONS

1. Toxalbumin / phytotoxin – examples (R-

CORROSIVE POISONS 554)
2. Active principles in (1)Ricinus communis
1. Sulphuric acid poisoning – signs and (2)Abrus precatorius (3)semecarpus anacardi-
symptoms, Causes of death , Rx, PM fea- um (4) Calotropis(R-554,555)
tures(R-530,531) 3. Suis(R-556)
2. Vitriolage and treatment(R-532) 4. Ergotism(R-556)
3. Nitric acid poisoning, Xanthoproteic reac- 5. Difference between poisonous & non-poi-
tion(R-532) sonous snakes, their bite marks(R 559-563)
4. HCl(R-532,533) 6. Belly scales(Diagram) l
5. Oxalic acid(R-533) 7. Difference between Cobra & Viper(R-559)
6. Formic acid poisonings(R-535,536) 8. Clinical features of Cobra bite & viper bit- u
7. Carboluria(R-535) eR-563) m
8. Ochronosis(R-537) 9. Snake venom(R-561) i
10. Snake bite management(R-564)
11. Anti- snake venom, dosage(R-564) n
METALLIC POISONS a
i
1. Arsenic poisoning - MOA, Rx, specific anti- CNS DEPRESSANTS
r
dote(R 538-541)
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1. Factors affecting alcohol absorption(R-569)

2. Metabolism of alcohol(R-570) 1. Drug & drug dependence(R-604)
3. Mc ewan‘s sign , alchohol gaze nystag- 2. Substance abuse(R-604)
mus(R-571,572) 3. Substance dependence(R-604)
4. Critical level of alchohol in blood 4. Difference between drug addiction & drug
5. Define drunkenness(R-573) habituation(R-605)
6. Collection of blood in alcoholics – precau- 5. Withdrawal symptoms(R-605,606)
tions(R-576) 6. Body packer & Body stuffer(R-607)
7. Widmark‘s formula, Henry‘s law(R-577)
8. Methods to determine blood alcohol(R-577)
9. Alcoholic blackout(R-579) SPINAL POISONS
10. Delirium tremens(R-580)
11. Korakoff ‘s psychosis(R-580) 1. Active principles in Strychnine, mechanism
12. Rx of acute & chronic alchohol- of action(R-612)
ism(R-572,573) 2. Signs & symptoms in Strychnine poisoning,
13. Rx of methanol poisoning(R-582) Rx, Antidote(R-613)
14. DD of alcoholism 3. Difference between Strychnine poisoning &
15. Level of alchohol in blood above which tetanus (R-614)
driving is not allowed
16. DD of contracted pupil due to poisoning
17. DD of dilated pupil 18. Micke finn(R-590) CARDIAC POISONS
19. Disulfiram reaction(R-573)
20. Wernickers encephalopathy(R-580) 1. Active principles in nerium odorum,
21. Barbiturate blisters(R-588) cerbera thevetia, cerbera odalla- QUESTION
22. Knock out drops(R-590) m(R-616,R-617) 2. Cerbera odallam –
signs & symptoms, ECG changes, man-
agement(R-617)
PSYCHOTROPIC DRUGS 3. BHIST regimen
4. Aconite poisoning (Hippus)(R-619)
1. Flashback phenomenon-LSD(R-596)
2. Benzodiazepines(R-595)
ASPHYXIANTS
DELIRIANT POISONS 1. Critical level of CO in blood(R-620)
2. Postmortem appearance & staining in
l 1. Toxins in Datrura, mechanism of action, CO poisoning, Reason(R-623)
symptoms ( 8D‘s)(R-598) 3. Tear gases(R-625,626)
u
2. Management of Datrura poisoning(R-599) 4. HCN poisoning – signs & symptoms,
m 3. Active principles in Cannabis(R-600) Mechanism of action, Fatal dose(R 626-628) 5.
i 4. Run amok(R-601) Management of HCN poisoning – Antidote &
5. Street poison(R-599) its mechanism of action(R-628)
n
6. Cocaine bugs ( Magnan‘s phenomenon)(R- 6. Food poisoning
a 603) 7. Active neurotoxic principles in Lathyrus
i sativus(R-638)
r
DRUG DEPENDENCE AND DRUG 8. Botulism(R-637)
ABUSE 9. Ptomaines(R-638)
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CLINICAL QUESTIONS
1. An adult male was brought to the casuality dead to the hospital with history of excessive
dead with history of sudden loss of conscious- intake of some tablets .postmortem examina-
ness .Postmortem examination revealed corro- tion revealed multiple white tablets and pow-
sion of stomach and lower part of oesophagus dery particles in the stomach .Anoxic bullae
with smell of bitter almond.Blood was bright were present on front of both knees and back
red in colour . of elbows .Internal capsules of brain showed
a)what is your diagnosis ? softening.
b) mechanism of death ? a)wht is your diagnosis?
c)what are the important clinical features in b)what is the line of management?
this case? c)what is the fatal dose of the poison in this
d)briefly outline the treatment in this case case?
e)what is the antidote? d)what are the materials send for chemical
analysis in this case?
2. A 50 year old female was found dead inside e)what are the duties of the doctor attending
a well at about 6am on 31-3-07 at lokarnakavu this case at the casualty of hospital?
temple premises .Recovery of the body from
the well reaveled the same in two pieces .Head 5. A 30 year old female was brought to the hos-
and portion of neck amputed at the level of 3rd pital with history of alleged consumption of the
cervical vertebra and rest of the body .A plastic kernel of a mango like fruit .she complained
rope with soft tissues and scalp hairs entangled of nausea ,vomiting and abdominal pain .on
in it .postmortem examination revealed a examination there were signs like bradycar-
PA P E R S lacerated wound 27.5cm all around the neck dia,irregular pulse,and respiration.
at the level of 3rd intervertebral .the amputed a)what is your diagnosis?
pieces could be well approximated. b)mention the names of the toxic principles
a)what is the mode of production of injury? contained in this fruit
b)what is the cause of death? c)what is the line of management?
c)what is the circumstance of death? d)what could be the likely findings at the au-
topsy?
3. A 50 year old female was brought dead to e)how will you preserve the viscera and tissues
hospital with history of poisoning .during for chemical analysis?
postmortem examination there were blackish
discolouration and thickening of mucosa of 6. A 45 year old man was brought to the hos-
mouth,oesophagus ,stomach and small intes- pital with watery diarrhoea ,tenesmus,pain
tine. Stomach contained brownish black fluid l
and irritation around the anus .The stools were
with pungent smell. initially dark coloured ,bloody and foul smell- u
a)what is your diagnosis? ing,but later on became involuntary,colourless m
b)what are the poisons producing the above and watery.The provisional diagnosis was food
change? poisoning(bacterial)but the patient suspected i
c)what is the antidote? homicidal poisoning and gave a statement to n
d)enumerate the line of management that effect before lapsing in to coma. a
e)what is VITRIOLAGE? a)what is your diagnosis?
b)what are the skin manifestations in chronic i
4. A 45 year old female nurse was brought poisoning? r
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c)what is the specific antidote ? congested. Brain showed an “cooked”

d)what is the line of management? appearance, stomach empty, uterus contained
e)what are the specific tissues to be sent for a foetus of 16cm length.
analysis in this poisoning a. Who should conduct the inquest and why?
b. What is the term used for the flexed attitude
7. A 20 year old young man was brought to of the body and its MLI
the hospital with a history of a bite by a reptile c. Calculate the percentage of burns in this
on the leg,ten minutes ago.on examination case.
there were two small puncture marks on the rt d. What is the gestational age of the fetus?
leg with pain and swelling around.He com- e. What is the cause and manner of death?
plained of progressively increasing weakness
of the muscles of limbs and face. 10. The body of a male recoverd from a paddy
a)what is your diagnosis? field showing post mortem lividity of the left
b)what is the line of management? side of the face, trunk, left upper and lower
c)how will you test for the sensitivity of the limbs( outer aspects ) and fixed. Rigor present
antidote? all over the body. Blood was oozing out of the
d)draw a diagram showing the peculiarity of left ear. Contusion 5x2cm obliquely placed was
the head scales of the involved reptile. present on the outer aspect of right forearm at
e)if this patient dies,what special tis- about its middle.
sues will you collect for chemical analysis a. What type of inquest should be conducted
and what presevatives will you use? b. What steps have to be taken to identify the
f) Diff b/w poisonous & nonpisonous snakes& deadbody?
their bite marks. c. What was the position of the body when it
was recovered? QUESTION
8. A person was brought to the casulty in an d. What was the time since death?
unconscious state with history of consump- e. What is the reason for bleeding from
tion of poison.it is alleged that the poison was left ear?
forcibly administered.on examination it was
found that pupils were consticted and there 11. The body of a 20 year old female is re-
was muscle twitching with smell of kerosene covered from a river showing the clothes
in the breath. wet, rigor was present in the lower half of
a)mention the legal responsibility of doctor the body. Right hand was clenched tight-
attending thus case ly. Postmortem lividity seen on the face,
b)what is your diagnosis? front of the neck and the dependent parts
c)mechanism of action of this poison of upper and lower limbs. Froth is seen
l d)what are the important clinical features? oozing out of the mouth and nose. Uterus con-
e)what are the antidotes that can be given? tained a fetus 9 cm long and 30gms in weight.
u a. What is the time since death?
m 9. A twenty year old woman died of burns b. What is the probable cause of death?
i after 2 years of her marriage at her home. c. What was the position in which the body
The body was in flexed attitude, all fingers was floating?
n d. Comment on the clenched right hand?
were hooked like claws. The clothing and skin
a showed evidence of charring, in several plac- e. What is the age of the fetus? Describe the
i es. The following parts showed burns. Head method of calculation?
and neck, both upper limbs, front of the trunk
r
and both lower limbs. The internal organs are
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12. A 3 year old child was brought to casualty e, PMA: congestion, h‘age in the GIT, tubular
with the history of swallowing some seeds. degeneration in the kidney.
The parents described them as soft spiny small
seeds, blue-green or rose-red in color. The
child on examination showed increased sali- 3.Endrin (plant penicillin)-dieldrin
vation, weak and rapid pulse and was drowsy.
The symptoms included nausea vomiting and a. Chemical nature : organochloro compound
bloody diarrhea with abdominal pain and –broad spectrum action
cramps. b. FD: 3-6gm, FP- l/2-6hrs.
a. What is your diagnosis? c. MOA: considered as a neuro toxin
b. What is a toxalbumin? d. CF: dyspnoea, dilated pupil, tremor, ataxia,
c. What is the mechanism of action? convulsions, failure of respiratory centres.
d. What is the line of management? e. Treatment: i.v Ca gluconate or oral Ca lac-
e. What are the post mortem appearances? tate. Cholestyramine-incr excretn
f. PMA: kerosine like odour of stomach con-
tents.

SPOTTERS 4.Tik-20- organophosphate

1. Zinc phosphide (Rat Poison) a. Chemical nature: diazinone

b. Organophoshorus compound.
a. FD: 5gm; F.P:24hours c. FD: l gm oral, FP : within 24 hrs
PA P E R S b. M.0.A: on hydrolysis with dilute HC1 of d. MOA: inhibits the enzyme choline esterase,
stomach, phosphine is liberated which acts as results in the accumulation of Ach.
a powerful respiratory poison. e. CF:
c. C/F: vomiting with retching, tremor, drows- i) Muscarine like effect: Salivation, Lacri-
iness, respiratory distress, mation, Urination, Defecation, G.I distur-
d. Cause of death: respiratory failure bance, emesis.[ code- SLUDGE]
e. Treatment: Stomach wash, demulscent, ii) Nicotinic manifestation: muscle twitch-
calcium disodium versanate ing, fasciculations, weakness, paralysis.
f. post mortem appearence: Stomach mucosa iii) CNS effects: headache, giddiness, drows-
shows tiny granular appearence. Sticking iness. COD: respiratory failure
on the crypts with garlicky order. All other f. Treatment: atropinisation, oximes(learn
organs congested. Blood cherry red doses).
g. PMA: kerosine like smell in stomach, froth l
in air passages, cyanosis
u
2.Methylated spirit
a. F.D: 60-200 ml, F.P: 24-36 hrs m
b. C/F: headache, dizziness, visual distur- 5.Oxalicacid (salt of sorrel) i
bances, metabolic acidosis- CNS depressant c. n
C.O.D: acidosis and respiratory failure a. FD 15-20 mg FP: 1-2 hrs
d, Treatment: stomach wash with sodium b. CF: nausea, vomiting, tenesmus, shock, a
bicarbonate, correction of metabolic acido- hypocalcemia, hematuria due to renal tubular i
sis,ethanol 50% 1 ml/kg body wt/2 hrs for 5 necrosis,vomit-coffee coloured
r
days. c. Treatment: Specific Ca preparation-
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1. Calcium disodium versanate 10. Oxime

2. Ca gluconate I.V.,
3. Saccharated soln of lime a. Pralidoxime dephosphrylates the inactivat-
4. I.V fluids, ed choline esterases
5. Dialysis b, Dose: 1 gm PAM is given i.v as 5% soln in
d. PMA: corrosion of upper GIT, white shriv- water over 5 min. Repeat 4 times every 8 hrs.
elled mucosa of GIT, dark brown streaks of
blood on stomach
e. MLA: accidental, suicidal poisoning 11. Carbolic acid / phenol (black liquid
with phenolic smell)

6.Gardenal sodium a. FD – l0 - 15gm, Fp: 3-4hrs

b. Locally acts a corrosive later anaesthetic
a. FD 3-4 gm orally, FP: 1 -2 days.‘ effect, systemically act as a narcotic.
b. CF: slow respiration, anoxic blebs, coma, c. CF: a/c poisoning is known as carbolism.
shock, drowsiness. Burning, numbness, anaesthesia at the area
c. MOA: CNS depressant of contact, smell of phenol in breath, pupils
d. COD: respiratory failure, irreversible cere- constricted, shallow and rapid respiration –
beral anoxia, bronchopneumonia. oochronosis(blackening) Urine: hematuria,
e. Treatment: stomach wash, forced alkaline albuminuria, carboluria [urine turns to olive
diuresis, dialysis, symptomatic treatment. green due to oxidation of metabolic prod-
f. PMA: particles of tablet in stomach, general ucts-Pyrrocatecholes and hydroquinones.
visceral congestion, softening of basal ganglia. d. COD: respiratory failure, cardiac failure.
g. MLI: suicidal, accidental, automatism, hom- e. Treatment: stomach wash with MgS04, QUESTION
icidal. demulscents, liquid paraffin, i.v fluids.
f. PMA: stomach- ash grey in colour,
hard, leathery, velvety contents having
7.Charcoal powder smell of phenol.
g. MLI: suicidal, accidental poisoning,
a. MO A: adsorbs within its pores poisons de- abortifacient.
laying systemic absorption.
b. Universal antidote- animal charcoal : mgo :
tannic acid -2:1:1. Two table spoons of this is 12. Formic acid
taken in a glass of water and glucose.
c. Animal charcoal adsorbs alkaloids, mgo-ac- a. Black corroded thickened rugae and mucosa
l ids, tannic acid ppts metals, alkaloids. b. FD 50-200 ml
u c. CF- burning pain, vomiting, altered blood,
oliguria, hematuria
m 8.Stomach tube(Ewald/ Boa’s tube) d. Treatment: intragastric milk drip, careful
i aspiration of stomach contents, symptomatic
a. For gastric lavage. 1and half meters long. treatment- Folinic Acid(1mg/kg)
n b. Contraindications: Corrosive poisoning (ex- e. Cause of death: acidosis, respiratory failure
a cept phenol),convulsant poisoning, oesopha- f. PMA: corrosion of GIT, blatubular necrosis
i geal varices, hypothermia, volatile poisons. of kidney
r g. MLI: suicidal, accidental.
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13. Sulphuric acid f. PMA: corrosion of mucosa with grey colour
and blackish streaks of blood vessels, oedema
a. FD: 10 - 15ml, FP: 12-24hrs of glottis present.
b. CF: burning, vomiting, difficulty in breath- g. MLI: vitriolage, accidental and suicidal
ing and swallowing poisoning.
c. Treatment: morphine for pain, antidote is
cao, mgo, i.v fluids, milk of magnesia, Alu- 16. Hammer
minium hydroxide gel
d. Contraindications: gastric lavage, bicarbon- a. Dangerous weapon-any instrument for
ates by mouth shooting, stabbing, cutting or any instrument
e. COD: circulatory collapse, spasm and oede- which is used as a weapon of offence and is
ma of glottis, perforation of stomach, toxemia likely to cause death
f. PMA: Blackish corrosion of upper GIT, b. Produces blunt injury- heavy weapon
chalky white teeth, perforation of stomach, c. MLI- weapon can be identified- imprint
corrosion of abdominal viscera. injury
g. MLI: vitriolage, grevious hurt, accidental or d. Types of injuries produced: contusion, lac-
suicidal poisoning. eration, abraded contusion, depressed fracture
[fractured bone is driven into the skull cavity.
14. Nitric acid Also called as signature fracture because shape
of fracture resembles shape of weapon.
a. Nature: corrosive mineral acid
b. FD: 10-15 ml, Fp: 12-24hrs
c. CF: burning pain, suffocation, vomiting 17. Lathi
PA P E R S [yellowish]
d. Treatment: antidote-Ca/mgo. a. Dangerous weapon
e. Contraindication: gastric lavage, bicarbonate b. Tramline contusion
by mouth. c. Types of injuries produced: contusion [a pat-
f. COD: spasm and oedema of glottis, circula- terned contusion /bruise is produced {2 lines
tory collapse, remote: starvation due to stric- of contusion seperatedby normal skin}], lacera-
ture. tion, abraded contusion, comminuted fracture
g. PMA: yellowish corrosion of GIT due to or depressed localized fracture.
xanthoproteic reaction, inflammation of
respiratry tract, peeling of mucosa of GIT.
h. MLI: vitriolage, grevious hurt, accidental or 18.Stone
suicidal poisoning.
a. Dangerous weapon, Produces blunt injury l
b. Can produce depressed fracture in skull.
u
15. HCL c. Types of injuries produced: contusion, lacer-
ation, abraded contusion, depressed fracture in m
a. Nature of poison: corrosive mineral acid skull [may be irregular or triangular] i
b. FD: 15-20 ml, FP: 12-24 hrs. n
c. CF: burning, pain, suffocation, vomiting
d. COD: suffocation, shock. Remote cause: 19.Cutting sharp weapon a
bronchopneumonia, stricture formation i
e. Treatment: antidote: Ca/mgo, morphine, i.v a. Dangerous weapon
r
fluids, demulscents b. Injuries produced: abrasion, punctured
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wound, penetrating wound, chop wound- b. Blow on vertex- extradural heamorrhage

depth of injury more, deeper sructures are from sagittal sinus.
involved. c. Symptoms: immediate but temporary loss
of memory/ consciousness, return of con-
20.Rubber tappers knife- wound shape- sciousness after a period of hours to weeks-
boat shaped lucid interval. Death occurs due to respiratory
failure due to brain stem compression.
a. Dangerous weapon d. MLI- lucid interval.
b. Square bracket shaped ( [ ) wound is
produced.
25. Subdural clot
a. Causes rupture of bridging parasagittal
21.Rope veins, dural venous sinuses, aneurysm, injury
a. Dangerous weapon to cortical veins.
b. Used for: hanging and strangulation b. Drugs: dicoumarol, heparin, warfarin.
c. Types: acute, sub acute, chronic
d. Death due to secondary pressure on brain
22.Single edged light cutting sharp stem.
weapon e, MLI: mistaken for schizophrenism in young
and senile dementia in the elderly.
a. Dangerous weapon
b. Injuries produced: abrasion, incised wound, 26. Subarachnoid h’age(diffuse hmg- ID)
stab wound-perforating and penetrating.
Perforating:- through and through injury a. Usually starts at the base of the brain. QUESTION
Penetrating:- enters into the body cavity Never localized as easily mixes up with
c. Produces a triangular or wedge shaped sur- the CDF, diffuses and spreads over the
face wound. Blunt end may show fish tailing of entire surface of the brain.
wounds (small splits in skin) b. Causes: rupture of aneurysm is Circle
of Willis; Traumatic usually follows rup-
ture of vertebral atery following a blow
23. Double edged light weapon on the side, neck, below the ear-Com-
mando chop. BALA B- Berry aneurysm
a. Injuries produced: abrasion, incised wouind, rupture A- Angioma, AV malformation
stab wound [depth greater than length and L- Leaukemia, blood dyscrasia A-As-
breadth] phyxia
l b. Shape of the wound elliptical or slit like and c. Symptoms – headache, stiff neck, photo-
both angles are sharp or pointed. phobia, deterioration of consciousness.
u
m
i 24. Extradural blood clot- least 27. Intracerebral / brainstem h’age
common(3%)
n
a. Causes:
a a. Cause: blow over the lateral convexity of 1. Bleeding from lenticulostriate artery near
i head injury the middle meningeal artery, vein basal ganglia.
and less commonly posterior meningeal artery 2. Hypertension and vascular disease
r
and anterior ethmoid artery. 3. Angioma
e
4. Malignant tum ors of brain.
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c. MLI: accidental- done by convulsive thera-

FORENSIC MEDICINE
b. Symptoms- Unconsciousness from the py, rarely homicidal, judicial execution in the
moment of injury. U.S.

32. Crocodile skin

28. Specimen of heart and lung a. Piece of skin showing multiple burnt/
punched out lesions- flash burns,arc eye
a. Rt ventricle and pulmonary artery seen b. Multiple burned out or punched out le-
opened with thrombus in situ. sions, due to the electric arc dancing over the
b. Causes: body surface.
1. Emboli from lower legs in bed ndden c. COD: paralysis of medullary centre, ven-
patients. tricular fibrillation
2. Varicosities of superficial veins of leg
3. Hypertension, diabetes mellitus, ath-
erosclerosis 33. Depression fracture skull
c. MLI: sudden natural death.
a. Portion of skull and brain showing a de-
29. Cross section of kidney with Bilat- pression of skull with corresponding de-
eral adrenal h’age pression of brain.
b. MLI: signature fracture [resembles shape of
a. Causes : meningococcal septicemia, weapon].
bleeding diathesis, hypertension, shock.
b. MLI: sudden natural death, Water- 34. Stab injury head involving skull, dura
house-frederichsen syndrome and brain
PA P E R S
a. Penetrating injury.
30. Sternum showing incised pene-
trating wound (cut fracture sternum)
35. Abortion stick
a. One end of the wound is cleanly cut
and the other end is split. The weapon a. Abortion stick in-situ with perforated fun-
used is single edged. dus of the uterus and wall of large intestine.
b. COD: injury to the vital organs. b. Inference: criminal abortion using abortion
stick.
31. Piece of skin showing an injury
with a pale base
36. Uterus with appendage- l
a. Electric burn mark [joule burn]- diag- u
nostic of contact with electricity. - a. wet specimen showing ruptured tubal
m
Found at the point of entry of current an pregnancy
oval shallow crater 1 -3 cms in diameter Right ovary is covered with ampulla; portion i
with a ridge of skin around the circumfer- of fallopian tube where an embryo developed. n
ence, there is conversion of electricity into b. Causes: IUCD, tube pathology
a
heat energy. c. MLI-sudden natural death.
b. COD: paralysis of medullary respiratory i
centre, ventricular failure, cardiac arrest. r
e
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36.Wet specimen of cervix showing sion, diffuse extravasation of blood, thyroid

cervical os and cricoid fracture, asphyxial signs.

a. Multipara(transverse)
b. Nullipara(round) 42. Piece of skin showing patterned abra-
c. Diff b/n multipara, nullipara sion of a coir rope.

a. Features of pressure abrasion seen; typical

37.Wet specimen of uterus with coppert hanging, ligature strangulation
insitu b. COD: asphyxia, venous congestion, com-
bined asphyxia and venous congestion.
a. MTP act, abortion and delivery

43. Piece of skin showing abraded contu-

38. Laceration of liver sion

a. Cause: blunt force like kicking, fall from a. MLI:

height 1. Evidence of aplication of blunt force.
b. COD: bleeding, shock 2. Degree of violence may be determined
3. Age of injury from colour changes

39. Specimen of oesphagus showing ruptured

oesophageal varices 44. Tatoo marks
QUESTION
a. Causes: a. wet specimen of forearm showing
1. Increased portal venous presssure tattoo marks on ant aspect
2. Portal vein thrombosis b. Dyes used: indigo, cobalt, cinnabar,
3. Hepatic vein thrombosis carbon, vermilion
4. Pyelophlebitis c. Erasure
b. CF: hematemesis, anemia. . l. Surgical methods
c. MLI: sudden natural death. 2. Electrolysis
3. Caustic substances
4. Laser beam
40. Degloved skin- preserved in 10% d. MLI: identity, religion, God of wor-
formalin ship, social status, drug addicts, any sexual
l perversions.
a. Skin of hand is kept
u
b. Causes: burns, drowning, putrefaction.
m c. MLI: fingerprints 46. Malunion fracture
i
n a. MLI : Identification, to sue for damage –
41. Hyoid bone adduction fracture (inward medical negligence, grevious hurt.
a displacement of broken bone)
i
r a. Cause: manual stangulation [throttlirig] 47. Foetal Sternum
b. PMA: fingernail marks, bruise and contu-
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a. Five osscification centres appear in the fol-
lowing order:
1 st- 6 months
2nd-6 months
3rd-7 months (viable)
4th-7 months
5th- 9 months.
Here 5th ossification centre appeared - So age 49. Scrotum of fetus with testis
of the foetus is 9 months
a. Scrotum showing descended testis.
b. Descends to scrotum at 9th month of IUL
48. Infant sacrum c. MLI: full term

a. 5 centres appear in the following order:

1st-4 to 5 months
2nd - 4 to 5 months
3rd - 6 to 7 months
4th - 6 to 7 months
5th - 8 months.
If age is 8 months then MLI: viable foetus.

PA P E R S
Entrance wound Exit wound
Size Smaller than diameter of the Diameter bigger than bullet
bullet
Edges Inverted Everted
Grease collar Present Absent
Burning / Tattooing May be seen around the Absent
wound
Bleeding Less More
Tissues Cherry red Absent

l
u
m
i
n
a
i
r
e
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Plants f. MLI- suicidal poison, abortifacient, cattle

poison
50. Cannabis sativa
53. Cerbera odallam
a. Toxic principle- tetrahydrocannabinol, can-
nabinol, cannabidiol, cannabinic acid a. Poisonous part- kernel of fruit
b. FD- l-2 mgof THC b. Active principles- cerberin, cerberoside,
c. Preparation- bhang,majoon, ganja, charas. odollin, odollotoxin, thevetin, cerapain
d. C/F- Stage of inebriation- euphoria, in- FD- kernel of one fruit
creased appetite, loss of perception of time & c. FP - 1-2 days
space. d. C/F-bradycardia, cardiac arrthymia, con-
e. Treatment- Stomach wash, symptomatic duction defects, hyperkalemia
f. MLI- Run amok, drug dependence, acciden- e. Treatment- stomach wash, atropine 0.5 mg
tal poison, stupefying agent iv, correct hyperkalemia
f. PMA- petechial h‘ age in the heart, conges-
tion of internal organs
51. Abrus precatorius g. MLI-suicidal, accidental in children.

a. Identification: small, round smooth bright

scarlet colour seeds with a large black spot at 54. Cerbera thevetia
one end.
b. Nature of poison: vegetable irritant, locally- a. Active principles: thevetin, thevatoxin, cer-
inflammation, vessication, ulceration, orally- berin, peruvoside, nerifolin.
GI irritation b. FD: 15-20gm root - QUESTION
c. Active principles: abrin [toxalbumin], c. FP: 2-3hrs.
abrine, abralin [glycoside] d. CF: rapid weak and irregular pulse,
d. MOD: Abrin inhibits protein synthesis & tingling and numbness of tongue, loss of
cause cell death. . muscular power and death from periph-
e. FD-90-120 mg by inj, 10mg orally eral circulatory failure.
f. FP- 3-5 days e. Treatment: BHIST regime: sodium mo-
g. MLI- lar lactate transfusion with glucose and 1
1 .cattle poison in the form of suis mg atropine, 2 ml adrena-line and 2 mg
2. Accidental poison noradrenaline.
3. Abortifacient f. MLI: suicidal, abortifacient, cattle poi-
h. Specific antidote-antiabrin son.
l
u
52. Nerium odorum 55. Calotropis
m
i a. MOA: cardiac poison a. Nature of poison: vegetable irritant.
b. Toxic principle: nerin, oleandrin b. Locally produces inflammation, vesication,
n
c. FD-15-20 gm of the root,5-l 5 leaves ulceration, orally produces GI irritation and
a d. FP- 20-36hrs CNS irritation.
i e. C/F - slow & weak pulse, muscular twitch- c. Active principles: gigantin, urcharin, calo-
r ings, coma, difficulty in swallowing, dilated toxin, calactin, calotropin.
pupils, signs of cardiac failure. d. MLI:abortifacient, cattlepoison, infanticide,
e
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fabricating injuries, vitriolage.
59. Strychnine- Nux vomica
56. Ricinus communis
a. Active principles- strychnine, brucine, log-
a. Nature of poison: vegetable irritant. anin
b. Locally produces inflammation, vescication, b. Action- prevents the eff of glycine(inhib
ulceration, orally produces GI irritation. transmitter)- release excitation
c. MOA- ricin blocks protein synth by inhibit- Read Diff b/n strychn poisng and tetanus
ing RNA polymerase c. C/F- convulsion, risus sardonicus, ophistho-
d. Active principle is a toxalbumen known as tonus.
Ricin. Cake obtained after oil extraction con-
tains more of ricin
e. FD: 10 castor seeds Snakes
f. FP: 7 days
g. MLI: accidental poisoning in children. Large 60. Sea snake
doses of castor oil may prove fatal in children.
a. Identifying features: small eyes, prominent
57. Semecarpus Anacardium [marking nut] nostrils on the top of head, black in colour,
compressed paddled tail, small tuberculated
a. Nature of poison: vegetable irritant. dorsal scales, broad ventrals.
b. Locally produces inflammation, vescication, b. Nature of venom: myotoxin.
ulceration, orally produces GI irritation. c. Signs and symptoms: muscle pain, stiffness,
c. Active principles: Semecarpol, Bhilawanol. muscle weakness, ptosis, visual disturbances,
PA P E R S d. FD: 5-10gm urine may contain albumin, erythrocytes and
e. FP: 24-48 hrs myoglobin.
f. MLI: d. COD: acute renal failure due to myoglobin-
1. To fabricate an injury uria, respiratory failure.
2. Throwing juice to produce disfiguration of
face[grevious hurt] 61. Russel’s viper
3. Abortifacient a. Identifying features: flat heavy traingular
head-with V shaped mark, angle of the V
58. Datura pointing forwards.It has three rows of dia-
mond shaped black or brown spots along the
a. Active principles- Hyoscine, hyoscyamine, back. Viviparous
Atropine b. Nature of venom: hemotoxic
b. Action- first stim higher centres of brain, c. Signs and symptoms: l
motor cntr, finally-depression, paralysis *Local symptoms: severe pain, ecchymosis,
u
c. C/F- corn picker‘s pupil(unilat mydriasis), swelling, blood stained discharge.
(8Ds-dryness of mouth, dysphagia, dil pupil, *Systemic symptoms: blurring of vision, signs m
dry hot skin,drunken gait, delirium, drowsi- of collapse, h‘age, renal failure i
ness, death due to resp failure) -Mydriatic test f. COD: shock and h‘age.
n
d. Circumstances – Road poison, abortifacient, g. FD: 15 mg, FP: 1-2 days.
aphrodisiac, accidnt cause h. Treatment: RIGHT(Reassure, Immobilise, a
e. MLI: person suffering from delirium due to Get to Hospital, Treatment) i
poisoning- not criminal responsible 1. First aid r
2. Specific: polyvalent antisnake venom serum e
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20 ml i.v algae.
b. Appearence: spindle shaped, colourless,
62. Cobra glassy/silicacious capsule
c. MLI: drowning
a. Identification: dorsal side of head bears
spectacle like mark, tail shields are divided.
Third labial touches the eye. Head scales large. 66. Unrespired lung( ID-glandular lobulated
-oviparous app)
b. Nature of venom: neurotoxic
c. Affects respiratory and cardiac centres. a. Alveolar sacs are closed and lined with
d. Treatment: Refer Russel‘s viper treatment. columnar cells
b. MLI: not live birth, indicates still birth or
dead birth.

Microscopy
67.Respired lung (ID- alveoli with a lot of air
spaces, cartilage can be seen)
63. Human hair and animal hair.
a. Alveolar cells are dilated and lined with flat
human hair animal hair cells, vascularity prominent
b. MLI: live birth
General fine and thin Coarse and
thick
Cortex Thick Thin 68. Chorionic villi QUESTION
Medulla usually nar- Wider
row a. MLI: sure sign of pregnancy.

MLI: 69. Alcohol content of beverages

1. Differentiate b/w hair and fibre
2.Crime, investigations Beer – 4-8% Toddy – 2-5%
A. RTA [hair root-blood group] Wine – 10-15% Sherry – 20%
B. Rape, bestiality, sodomy C. Stains-nature Arrack/Brandy – 40-50%
of assaults Rum/Whisky/Gin – 50-60%
3.Identification- age, sex
l 4.Texture of hair indicates from which part of 70. Ossification of bones (dates followed in
body it is from our state medicolegal institute)
u 5. Chronic metal poisoning-arsenic
m a. Eruption of permenant tooth
i b. Ist molar 6-7yrs
64.Intracerebral h’age, subarachanoid c. Medial incisor 7-8yrs
n h’age[for questions refer wet specimens] d. Lateral incisor 8-9yrs
a e. Canine 11-12yrs
i f. I premolar 9-11 yrs
65. Diatoms g. II premolar 10-12 yrs
r
a. Microscopic unicellular or colonial aquatic h. II molar 12-14 yrs
e
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i. III molar 17 or above or never
Bone Appearance Fusion
Acromion 14 18
Coracoid process 14 18
Head of humerus 1
Lesser tuberosity 5 coposite mass-6 16-18
Greater tuberosity 3
Medial epicondyle 8 14-17
Capitulum 2
Trochlea 11-composite mass-14 14-17
Lateral epicondyle 13
Olecranon 10 14-17
Head of radius 6 14-17
Lower end of radius 2 14-18
Lower end of ulna 6 14-18
Base of 1st metacarpal 2-4 14-17
Head of other MC’s 2-4 14-17
Head of femur 1 15
Lesser trochanter 11 14-17
PA P E R S Greater trochanter 4 14-17
Iliac crest 14-16 18
Ischial tuberosity 16 19 (f) 21(m)
Ischiopubic ramus - 7-8
Triradiate cartilage - 11-14
72. Fetal foot Pisiform – 11 to 12 yrs

Find the time of appearance of ossification 75.Specimen of stomach in various

centres, diagram of bones forming fetal foot, poisoning
calcaneum 5th month, talus-7, cuboid-9
CuSO4, Phenol, Formic acid, Nitric acid, HCl
Analysis of postmortem certificate will be one
73. Wet specimen of transection aorta- ul- of the compulsory exercise for practical exam- l
cerated and calcified ination. One should know the objective of do- u
ing a medico- legal autopsy for proper analysis m
a. Atheromatous plaque- rupture, thrombosis. of postmortem certificate
1.To find out the cause of death. i
2.To find out the time since death n
74. Appearance of carpal bones 3.To get some clues regarding the manner of a
death
Capitate – 1yr Hamate – 2yrs 4.To establish the identity of unknown per- i
Triquetral – 3 yrs Lunate – 4 yrs sons 5.In foetal autopsies to find out wheth- r
Trapezoid, scaphoid – 5 yrs Trapezium – 6 yrs er it was live born, still born or dead born e
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and to find out its intrauterine age. Here we need mention only whether the death
An actual postmortem certificate will was due to hanging or not.
contain 4 paragraphs and an opinion as to the
cause of death. The first paragraph will be pre-
amble. In the certificate given for examination Opinion in injury cases
there will not be any preamble, instead you will
be given a history of the case. The history may After sustaining an injury, if the victim is left to
contain relevant and irrelevant details. Ques- the ordinary course of nature (without treat-
tions can be asked from history part also. ment), if death is most probable, it is called an
The second paragraph will be about the injury which is sufficient in the ordinary course
external appearances of the body like height, of nature to cause death. All penetrating inju-
weight, scale of body orifices, colour of nails, ries are considered as sufficient inthe ordinary
blood stains, salivary stains etc. course of nature to cause death. Ligature marks
The third paragraph will be about post- the neck in hanging and strangulation are
mortem changes like rigor mortis, postmortem other samples. Fracture skull, with or with-
staining, signs of decomposition if any, wheth- out brain damage is sufficient in the ordinary
er the body was refrigerated etc. course of nature to cause death. Brain damage
Then there will be a list of injuries if any in alone also is sufficient. Multiple rib fracture
the body. is another example, Fracture of femur, pelvis,
The last paragraph will be about other spine etc. are sufficient in the ordinary cours of
positive findings and relevant negative find- nature to cause death. In any injury if a major
ings. The state of internal organs are described blood vessel is involved it is sufficient in the or-
in this paragraph. There will not be any opin- dinary course of nature to cause death. Rapid
ion as to the cause of death in the certificates loss of 1/3 of total blood volum Read all QUESTION
given to you. Forming and wording the opin- the antemortem injuries carefully and find
ion will be one of the questions. out the fatal nature of the injuries. The
fatal injuries are classified into 3
(a) Necessarily fatal
(b)One which is sufficient in the ordi-
Forming and wording the cause of nary course of nature to cause death
death (c) One which is likely to cause death.
A necessarily fatal injury is one
While wording the opinion as to the cause which is incompatible with life. Examples
of death you should remember that the post- are decapitation, transection of the trunk,
mortem certificates are sent to the concerned avulsion of the heart, mangling of the
l magistrates and police officers, who are laymen body etc. There is not even 1 % of chance of
as far as we medical people are concerned. So survival after sustaining such injuries.
u
wording should be in such a way that they can after sustaing an injury ,if the victim is left to
m understand it. In all cases laymen‘s language the ordinary course of nature (without treat-
i alone may not be sufficient to express the ment), if death is most probable, it is called
opinion. Here you can add an explanatory sen- an injury which is sufficient in the ordinary
n
tence or word. We need not mention the exact course of nature to cause death. Burns affect-
a mode of death (and it is not always possible ing more than 1/3rd \ of the body surface is
i also) since the law enforcing authorities are another example
not bothered about it. For example in a case of If death is the probable result of an
r
hanging the mode of death may be asphyxia. injury (left untreated) it is an injury which is
e
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likely to cause death. Examples are fracture of “Death was due to dermoepidermal burns
long bones other than femur, burns affecting affecting it, scale of about 70% of body sur-
less than 1/3rd of the body surface etc. face”or “Death was due to infection following
While forming the opinion as to the second degree burns affecting about 30%
cause of death if there is only fatal injury, you of body surface’” or “Death was due to the
can state that as the cause of death. If there is complications of dermo-epidermal burns af-
a penetrating injury to the chest, others being fecting about 20% of body surface” depending
nonfatal you can word the opinion that “Death upon the findings furnished in the P.M.C.
was due to the penetrating injury sustained to
the chest”. If there is a fatal head injury also the
wording shall be “Death was due to the injuries Hanging cases
sustained to the the head and chest.. If there
is a fatal injury on the abdomen also then you Vertical salivary dribble mark and ‘Le facie
may word your opinion as “Death was due to sympathique; are the conclusive evidence of
the injuries sustained to the head, chest and antemortem hanging.If any one or both signs
abdomen.” The terms bleeding, shock etc. shall are present you should word the opinion as
not be incorporated in the opinion. Where “Death was due to hanging”. Never add as-
there are more than 3 fatal injuries you can phyxia due to hanging etc. If there is a noncon-
word the opinion as “Death was due to multi- tinuous oblique pressure abrasion on the neck
ple injuries sustained”. In deciding whether a and underlying pale and dry subcutaneous
culpable homicide is murder or not the fatal tissue along with other signs of suspension, in
nature of the injury inflicted is very important. the absence of other causes of death, you can
word the opinion as “Postmortem findings are
PA P E R S consistent with death due to hanging” even if
conclusive signs are absent.
Forming Opinions in poisoning
cases
Drowning cases
In suspected poisoning, if the stomach con-
tents has an unusual smell or colour the Presence of sand, mud, leaves etc. in the air
opinion shall be “Postmortem findings are passages is a conclusive evidence of drown-
consistent with death due to poisoning, Final ing. If identical diatoms are detected in bone
opinion is reserved pending the report of marrow of the deceased and in the drowning
chemical analysis”If there is no obvious cause medium it is another evidence
of death the opinion will be “Reserved pend- of drowning. Some experts consider fine white
ing the report of chemical analysis” lathery tenacious consistent mushroom shaped l
froth at nostrils together with emphysema
u
aquosum as a conclusive evidence of drown-
Cases of Burns ing. So if any of the above findings are present m
in the body the wording of the opinion shall i
Presence of soot in the air passages, red line of be “Death was due to drowning”. If the signs of
demarcation between the affected and nonaf- n
submersion of the body in water like washer
fected area, blisters containing serum rich in woman‘s hand, cutis anserina etc. are present a
protein and choride etc. are the antemortem and the conclusive proofs of drowning are i
features of burns. If the bums are antemortem absent, in the absence of other causes of death r
the opinion as to the cause of death shall be you can furnish the opinion as “Postmortem e
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findings are consistent with death due to ·· The foetus was dead -born (only when signs
drowning”. In a case of drowning if there is a of maceration or putrefaction is present)
fatal head injury also opinion shall be “Death ·· The foetus was not live born (It is difficult to
was due to the combined affects of drowning give an opinion that a foetus was still born
and head injury”. If a body is recovered from ·· By naked eye examination it is not possible
water in a decomposed state and if diatom test to determine the sex of a foetus if it is less
is negative the opinion as to the cause of death than 4 months.
shall be reserved pending the report of chemi-
cal analysis though presence of sand etc. in the
air passages is indicative of drowning.
Sudden deaths

Electrocution Death occurring suddenly and unexpectedly

in an apparently healthy individual under
If there is a joule burn on the body in the ab- suspicious circumstances due to natural causes
sence of other causes of death you can give an are called sudden deaths. The most common
opinion “Death was due to electrocution”. cause of sudden death is myocardial infarction.
Some sample opinions in sudden death is given
below.
Foetal autopsy • Death was due to coronary thrombosis - a
disease of the heart (Natural cause).
In foetal autopsy one has to find out whether it • Death was due to pneumonia - a disease of the
was live born, dead born or still born. If it was lung (Natural cause).
live cause of death is to be determined. Apart • Death was due to subarachnoid bleeding QUESTION
from these the intrauterine age of the foetus - a disease of the brain (Natural death).
also has to be found • Death was due to advanced tuberculosis
Even without an autopsy we can of the lungs.
certify live birth if there is physiological jaun-
dice, erythema around umbilicus etc. Pres- Estimation of time since death
ence of milk in the stomach, air in the G.I.T. • Time since death is determined from
and the middle ear etc. are other conclusive postmortem changes like rigor mortis,
evidence of live birth. In the absence of the postmortem staining, of decomposition etc.
above Breslau‘s 2nd Life test has to be done • Rigor mortis will appear in head and neck
to ascertain livebirth. Microscopy of lung is by 1 -2 hours, in the upper limbs by 2-4
almost confirmatory. hours and in the lower limbs by 6 hours.
l In a live born foetus presence of The whole body will become stiff due to rigor
Circumoral pallor is an evidence of smoth- mortis by 6 hours. Rigor mortis will start passing
u
ering. By applying Haase‘s rule the age of a off by 18 hours. Complete disappearance is by
m foetus can be determined from it length. This 48 to 72 hours. • Postmortem staining will get
i is only an estimate. Conclusive proof is ap- fixed by 6 to 12 hours. If postmortem staining
pearance of ossification centres in sternum, is fixed time since death is more than 6 hours.
n
ankle and sacrum. Some opinions given after If not fixed then less than 12 hours (exception
a foetal autopsy are: being asphyxia).
i ·· The foetus was viable and live born • Greenish discolouration will appear in right
·· Death was due to smothering. iliac fossa by 18 - 24 hours. Marbling will be seen
r
·· The foetus was not viable. by 36 .hours.
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• If rigor mortis is fully present all over the injury from a distant range cannot be suicidal.
body the minimum time since death is 6 hours. In a case of hanging if poison also is found in
If it has started passing off 18 hours elapsed the stomach it is in favour of a suicide. A body
after death. Temperature, muscle mass exertion recovered from a well with “brush burns” on the
prior to death etc. are the conditions which can palms is in favour of accidental fall. Applicatiin of
modify the onset and duration of rigor mortis. Locard‘s principle of exchange may help in fixing
• If rigor mortis is present all over the body and the manner of death in hanging. Examination
postmortem staining is not fixed, the time since of finger prints in weapons also will help to get
death is more than 6 hours and less than 12 hours. some clues regarding the manner of death.
• If rigor mortis is retained all over and
postmortem staining is fixed time since death is Identity
more than 6 hours and less than 18 hours. • In unknown bodies, its identity has to be
• If rigor mortis started passing off and greenish established.
discolouration is present in right iliac fossa time • Sex determination will not be a problem
since death is more than at least 18 hours and unless the body is highly decomposed.Prostate
less than 36 hours, (since marbling the next and nongravid uterus resist putrefaction for a
postmortem change has not appeared). long time.
• Age can be determined from obliteration of
skull sutures, fusion of manubrium and xiphoid
process with the body of sternum etc. Age can
Time of death from stomach contents be determined from a single tooth by Gustafsson
technique.
• The gastric emptying time is 4-6 hours. If the • Pierced ear lobule in a male indicates that
PA P E R S stomach is empty the time of death is at least 4 the victim is a Hindu. Circumscised penis is in
hours after the last solid meal. If the stomach favour of the deceased being a Muslim.
contains food time of death is less than 6 hours • See whether there are callosities or other
after the last solid meal. Hence if the time of occupational mark.
last meal is known, the time of death can be • Dental formula of unknown bodies are
determined. expressed in modified F.D.I. (Federation
• Stomach emptying time maybe delayed in Dentaire International)Code
head injury, shock etc. The rate of formation
of urine in the bladder is 1 ml/mt. This will help Conclusion
to fix the time of death to a certain extent only. What is given above is not an exclusive note. To
answer the questions given along with the P.M.C.
a thorough knowledge of the subject is necessary.
l
Manner of death u
Manner of death means whether a death is m
accidental, suicidal or homicidal. It is not always i
possible to state the manner of death. In certain
n
cases from the history and postmortem findings
some clues regarding the a
anner of death can be obtained. A chop wound on i
the top of head and a stab injury in an inaccessible r
area is strongly in favour of homicide. A firearm e
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Rigor mortistis
Appearance on the face 1 to 2 hours
Upper limb 2 to 4 hours
Whole body stiffness 4 to 6 hours
Starts disapperaing by 18 hours
18 hours 48-72 hours
t Postmortem staining (PM Lividity)
Starts appearing 2 to 4 hours
Fixation 6 to 12 hours (if fixed > 6 hours)
Decomposition changes
Greenish discolouration- Rt iliac fossa 24 hours (18-24 hours)
Marbling 36 hours
Gaseous distention, PM blebs & peeling of 48 to 72 hours
cuticle
Loosening of teeth 72 hours
Liqefaction of brain 3 days
Skeletonisation
Exposed body 1 to 2 days
Buried body 2 to 6 days
ADIPOCERE 3 days to 15 days QUESTION
Mummification 3 weeks to 3 months
Gastric emptying time 4 to 6 hours

Examples of postmortem
certificates • Blood stained frothy discharge at
mouth and nostrils. Multiple small pete-
The history and Post mortem findings of the chial haemorrhages were present under
case are given below. Read it carefully and an- the conjuctiva, on the eye lids and on the
swer the questions given which follow. forehead. Nails bluish. Rigor months es-
tablished all over. Post - mortem staining
l on the back, fixed. Vulva and vagina were nor-
CASE NO 1 mal, carunculae hymenalis present Injuries
u (Antemortem)
History:
m • Body of a female aged about.30 years was 1. Contusion 2 x 1.5 cm on the right side of the
i found in a rubber estate in a semi -naked state. front of neck over the thyroid, infiltration of
The body was identified as that of an agricul- blood in the subcutaneous tissue underneath.
n 2. Four contusions each 1.5 x 1 cm one below
tural labourer. Her golden ear rings were found
a missing from the body. the other, obliquely placed on the left side of
i the front of neck with infiltration of blood in
Post-mortem findings: the subcutaneous tissue underneath.
r
General 3. Fracture of the right ala of the thyroid carti-
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lage with infiltration of blood around. • The history and post mortem findings of
4. Multiple finger nail abrasions on the inner the case are given below. Read it carefully and
aspects of both thighs. answer and answer the questions given which
follow.
Other findings
• Lungs were congested and oedematous with History:
multiple subpleural petechial haemorrhages. • Body of a female, aged about 28 years, was
Heart showed rnultiple sub-epicardial petechi- found hanging in a room of her husband‘s
al haemorrhages. Brain was normal. Stomach house. The doors off the room were found to
contained partly digested food particles with- be locked from inside. She was staying with her
out any unusual smell, it‘s mucosa was normal. husband and his relatives after her marriage
Liver, Spleen and Kidneys were congested. which took place 3 years ago. There is history
• Vaginal smear showed the presence of Sper- of harrasment by the husband and his mother.
matazoa.
POST MORTEM FINDINGS
Questions:
• What is the cause of death ? Hint: Death was General
due to throttling. • Rigor mortis established and retained all over
• What are the various mechanisms of death in the body. Post mortem staining in the lower
such a case ? Hint: (i) Asphyxia (ii) fracture limbs and fixed
of hyoid bone (Hi) fracture of thyroid bone. • • Conjuctiva and nails were bluish extemal
What is the manner of death ? Hint: Homi- body orfices were nomal vulva and vagina
cide were normal salivary dribble marks were found
PA P E R S • What is the approximate time since death ? on the right side of the mouth. A ligature mark
Hint:>6hrs&<18hrs made of a saree was found tied around the
• She died within how many hours of her last neck with a slip knot on the left side of neck
meal ? Hint:<6hrs head was found slightly titled to the right side
• In what position was the body lying after
death ? Hint: Supine Position Injury ante-mortem
• What is the significance of injury no. 4 ? • Ligature marks were found on the fornt and
Hint: Rape attempt sides of the neck above the level of thyroid
• Comment on the sexual habit of the de- cartilage with a discontinuity on the left side of
ceased. Hint: Has undergone sexual inter- the back of neck. The subcutaneous tissue un-
course - Carunculae hymenalis. derneath was dry and pale. Muscles bones and
• Can you explain the absence of genital inju- cartilages of the neck were normal and in tact.
ries in this case? No other injury was found on the body Other l
• What were the probable motives of the ac- findings
u
cused in this case ? • Lungs were congested and oedematous stom-
Hint: Rape & Theft ach was empty liver spleen and kidneys were m
• What are the sections of the Indian Penal congested the uterus was normal it scavity was i
Code under which the accused maybe charged empty vaginal smears showed the presence of
n
? Hint: IPC 302 & 376 motile spematazoa
• What is Florence Reagent.? Hint: I +KI + a
H2O Questions i
1 What is the cause of death ? Hint : death r
CASE NO .2 was due to hanging
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2 What are the various mechanisms of death

in such a case? POST-MORTEM FINDINGS:
Hint : Asphyxia, vagal inhibition, venous con-
gestion ,cervical vertebrae ,cerebral anaemia POSTMORTEM FINDINGS
3. What is the manner of death ? Hint: sui- External:
cide • Fine white lathery froth at mouth and nos-
4. What is the approximate time since death? trils. Conjunctiva normal. Nails were bluish.
Hint . >6hr & < 18hrs Palms and soles showed soddening. Rig-
5. She died within how many hours of her last or mortis established and retained all over.
meal Hint > 4 hr Post-mortem staining on the front of chest,
6. She died within how many how many hours fixed.
[maximum after her last intercourse ] Hint : • Hymen showed a recent tear. No other injury
24 <hours was found on the body.
7. There is an allegation that it is a case of post
mortem suspension write three points against Internal:
this allegation hint • Lungs were ballooned, pale and cut section
1) Room locked from inside exuded frothy fluid on compression. Right
2) No external injuries lung weighed 35 gms and Left lung weighed
3) Salivary dribble marks 300 gms. Sand particles were present in the
8. What is the time required for death to take bronchioles. Stomach was empty. Liver, Spleen
place in a case of hanging? Hint : 3-5 minutes and Kidneys were congeted. Uterus was nor-
9. Hanging is considered as the most painless mal in size and it‘s cavity was empty. Vaginal
from of death, Why it is painless? Hint Loss smear showed the presence of spermatazoa.
of consciousness QUESTION
10. under what section of IPC, the husband Questions:
and his parents can be chargted Hint S 304 B 1. What is your opinion as to the cause of
(Dowry Death) death? Hint: Death was due to drown-
ing.
Other Questions 2 Write 4 points in support of your opin-
1. Judicial hanging COD : ion as to the cause of death. Hint: i)
i) #- dislocation at level of 2nd /3rd or 3rd/ Fine white leathery froth. ii) Sodden-
4th cervical vertebrae ing. iii) Sand in bronchioles. iv)
ii) rupture of brain strem (less commonly) Ballooning of lungs
2. Lynching Homicidal hanging of a suspect, 3. What is the manner of death? Hint:
enemy by a rope from a tree by the mob Suicide
l 4. What is the approximate time since death?
Hint: >6hrs& 18hrs.
u
CASE NO .3 5. How long was the body lying submerged
m in water? (State the minimum time). Hint:
i History : 24hrs.
• Body of a 15 year old girl was recovered from 6. What is the normal chloride content of
n
a well near her house. Two days agop she had blood? Hint:600 mg/100ml.
a eloped with a man and stayed with him for 7. Which is more dangerous and why? Hae-
i a day. When she returened home, she was modilution / Hemoconcentration. Hint: He-
r severely scolded by her parents for her grave modilution
misdeed. 8. Water may not enter the lungs yet a person
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may die. How? Hint: COD: Laryngeal spasm Rigor mortis passed off from head and neck,
(Dry drowning) but retained in the upper and lower limbs.
9. Which finding show that the deceased was Vulva and Vagina were normal. Caranculae
alive at the time of submersion? Hint: Sand hymenalis present.
in bronchioles. • Injection marks present on the front of right
10. What are the offences committed by the elbow and on the back of right wrist. No other
man with whom the deceased eloped? Hint: injury present on the body.
Rape, Abduction Internal:
11. Under what sections of the Indian Penal • Air passages contained blood stained mu-
Code the man may be charged? Hint: S.376. cous froth. Lungs were congested and oedem-
IPC, S.362 IPC atous. Stomach contained 260ml of greenish
12. What is the maximum punishment which fluid with a kerosene like smell,it‘s mucosa
can be given to the man if charges against him was congested. Liver, Spleen and Kidneys were
are proved? Hint: Ten years congested. Uterus was enlarged in size and it‘s
13. In order to teach the man a lesson, the par- cavity contained a male foetus. The crown -
ents of the deceased falsely allege that the man heal length of the foetus was 16cms.
had killed his daughter and put her body in the
well. Write 2 points against the allegation of Questions:
the parents of the deceased. 1.What is your opinion as to the cause of
Hint: i) No external injuries, death? Hint: Death was due to poisoning.Final
ii) post mortem findings of drowning opinion reserved pending chemical analysis
are present report
14. Fatal period is less in which of the follow- 2.What is the manner of death ? Hint: Suicide
PA P E R S ing -a) Fresh water drowning or 3.What is the time since death? Hint: 18-24hrs.
b) Sea water drowning. 4.What findings show that she has had fre-
quent intercouse?
Other Questions: Hint: Caranculae hymenalis.
1.Emphysema Aquosum 5.She has been pregnant for how many
2.Gettler‘sTest months? Hint: 4 months.
3.Cadaveric Spasm 6.State whether her pregnancy could have
4.Paltaufs haemorrhages. 5.Washerwoman‘s been medically terminated if it was due to
hand. contraceptive failure? Hint: Yes. (Refer MTF
Act)
7.What was the poison consumed by the de-
CASE NO. 4 ceased? Hint: organophosphates
8.If you are treating such a case, what speci- l
History: mens you will collect from the patient, while
• A 20 years old unmarried female died in a u
under treatment, for chemical analysis? Hint:
hospital while under treatment for poisoning. i) Blood ii) Urine iii) Aspirated gastric m
She was admitted in the hospital 2 days ago, contents. i
with a history of taking some poison. 9.What are the antidotes used for treating such
n
a case? Mention the dose of each ante-dote.
POST-MORTEM FINDINGS: Hint: i) Atropine Sulphate 2-4 mg i.v. a
External: ii) Oximes - l-2g i.v. as 5% solution i
• Blood stained frothy discharge from mouth 10. While conducting post-mortem examina-
r
and nostrils. Conjunctiva normal. Nails bluish. tion in a case of poisoning, the stomach and
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intestine is collected in one bottle and the liver wound was directed backward downwards
and kidney is collected in another bottle for and to the right and the total minimum depth
chemical analysis. Why in 2 separate bottles was 11.5cm. Incised wound 5x5x 1.5cm hor-
? Hint: To prevent contamination of solid izontally on the front of right fore arm 6cm
viscera with GIT contents. below the elbow.
11. Formalin should not be used in preserv-
ing the viscera. Why ? Hint: Extraction of POST-MORTEM INJURIES:
poison become difficult. 1. Crushed decapitating wound on the neck
12. What preservative will you use for blood at the level of 4th vertebrae.
and urine? Hint: NaF / KF 2. Grazed abrasion 30 x 20cm on the back of
13. Who will conduct the inquest in such a middle of trunk, 6cm below root of neck.
case? • Air passages contained blood. Lungs were
pale. Stomach was empty.- heart showed
subendocardial bleeding. Spleen was found to
CASE NO. 5 be shrunken. All internal organs were pale.
History:
Questions:
• A 30 year old male was found dead on a rail- 1.Who should hold the inquest in this case?
way track (Meter gauge) with injuries on the Hint: Police
body. After the inquest the body was sent for 2.Estimate the time since death from the
post-mortem. post-mortem changes. Hint: 36 - 48 hrs.
3.How can you account for the post-mortem
POST-MORTEM APPEARANCES: skin slippages? Hint: Hot surface contact of
railway line. QUESTION
• Body was that of an adult male of height 173 4.What is the fatal nature of the An-
cm and weight 60 kg and having fair com- te-mortem injury no. 1. Hint: Sufficient
plexion. Conjunct were pale. Dry blood stains in the ordinary course of nature to cause
were seen in and around the mouth and nos- death.
trils. Other body orifices were normal Nails 5.What will you call me injury which
were blue. Post-mortem skinslippages were was seen on the right fore arm? Hint:
seen at several sites. Defence wound. 6.How much time might
• Rigor mortis was retained over the lower have elapsed after his last solid meal ?
limbs only. Post-mortem staining was not Hint: >6hrs.
clear. Greenish discoloration was noticed in 7.What is your conclusion from the
the lower abdomen. Marbling was seen on the sub-endocardial bleeding? Hint: Head
l arms. (Body was not refigerated). Ante-mor- injury.
tem injuries: 8. What is the reason why the spleen was
u
• Incised penetrating wound 5x1.5cm oblique- found to be shrunken? Hint: H‘age
m ly placed on the left side of the front of chest 9.Is this a case of murder? State Yes / No / Can-
i with it‘s lows border sharply cut and 5 cm not be stated? Hint: Yes, incised penetrating
outer to the midline and 8cm below the collar wound.
n
bone. It‘s outer end was blunt. Left chest cavity 10.What is your impression regarding the
a was seen penetrated through the 6th inter- manner of death ? Give reasons. Hint: Hom-
i coastal space. Lower lobe of left lung was seen icidal
underfixed. The chamber of the left ventri- 11.What laboratory investigations will you do
r
cle was found to be pierced. The track of the in such a case?
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12.How will you word your opinion as to the broad) with the discontinuity of 2cm below
cause of death? left ear. On flap dissection of neck done under
bloodless field the subcutaneous tissue under-
neath the injury appeared pale and dry. Hyoid
bone, cartilages and other neck structures were
found to be intact.
CASE NO.6 2. Abrasion 3x3cm overlying the left malar
eminence.
HISTORY 3. Two skin deep incised wounds 3x0.2cm and
4x0.3cm on the front of left wrist.
A 26 year old christian married woman was • The air passages were congested. Lungs were
found hangibg in a ceiling fan in her own congested and oedematous. The stomach con-
house . Her husband left her two years ago tained 200ml of bile stained fluid without any
for employement in Abu Dhabi. thw circle unusual smell its mucosa was normal. Uterus
inspecter conducted the inquest and sent the measured 16x 10x5cm and its cavity contained
body for post mortem. a male foetus having a crown heel length of
40cm within intact membranes. All other
POST MORTEM APPEARENCES organs were congested, otherwise normal,
Urinary bladder was empty.
Body was thats of a well nourished and mod-
erately built adult female of height 157 cm Questions
and weight 50 kg. a ligature made of synthetic 1.How will you word your opinion as to the
sari was seen tied around the neck with a slip cause of death ?
PA P E R S knot on the right side. the nosose measured 2.What is the fatal nature of injury No. 1?
30cm , long free portion 147cm and short free 3.How Locards‘ principle of exchange can be
portion 10cm.right eye was open and its pupil applied in this case to ascertain the manner of
was dilated while the left ey was closed and death ?
the pupil was constricted. tip of the tounge 4.What is the age of the foetus ? Give reasons.
was protruded- not bitten. vuvlva an vagina 5.What could be the time since death ? Give
and other body orifices were normal, hymen reasons for your opinion ?
shows multipleold healed tears and vagina ad- 6.What could be the manner of death ? Sub-
mitted three fingers. Other body orifices were stantiate your answer.
normal. Nails were bluish. Salivary dribble
mark was not seen.
• Body was cold. Rigor mortis retained only
in lower limbs. Postmortem staining was seen l
at the lower part of limbs and was fixed. Both
u
iliac fossae showed greenish discolouration.
(Body was not refrigerated). m
i
Injuries (antemortem)
n
1.Pressure abrasion 29cm long noncontinu-
ous, obliquely placed on the neck, above the a
level of thyroid cartilage being 6cm below the i
chin (3cm broad), 8cm below occiput (2.5cm r
broad) and 7cm below left ear lobule (3cm
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WOUND CERTIFICATE
SI no: Date of : Date and time of examination:
Medical College :
l. Name
2. Age
3. Sex
4. Address
5. Occupation
6. Brought by whom (as per requisition of CI of police, a person named………….., aged
………….. was brought for examination of injury involving Cr No………. He was accompa-
nied by PC No…...)
7. Consent of subject a) expressed b) implied
8. Two Marks of identification
9. History and alleged cause of injury
10. Details of injury
• Age of injury, Name, Size, part, kind of weapon
• Simple/grevious
11. No: of additional sheets
12. Whether dying declaration was required
• if yes whether police or magistrate was informed 13. Investigation results, if any
14. .DOA IP no: DOD:
15. Condition on discharge
16. Opinion, with details including Cause of injury, Nature of injury, age of injury, simple/
grevious, Whether injury could be caused as alleged by subject QUESTION

Place: Name:
Date : Designation:
Issued to ————————— as per requisition no ———dated--------------------------

Signature of issuing authority

Case 1 : RTA
A patient in coma stage brought to the casualty with a head injury.(More details will be
given in the question paper)

l Questions:
1. What is bumper injury?
u 2. Classify injuries in RTA in case of a pedestrian
m 3. What is brushburn abrasion?
i 4. What will be the cause of death if femur fracture occurs?
ans: 1. fat embolism
n 2. rapid loss of blood
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Case 2 : RTA
An RTA brought to casualty with fracture on left tibia and fibula,CT scan showed extradural
hemorrhage.

Questions:
1. If bumper height is >20cm, how will u explain the injury.
Hint: 20cm from above heel,so its a primary impact injury-(bumper&acture).
2. Can the neurosurgeon do surgery for hematoma? substantiate
Hint: Yes, as per the law of emergency doctrine section 92 of IPC, he can do for the benefit of
the person even without the consent& is not an offence.
3. If power failure during surgery and failure of surgery occured,then what is the best defence
plea?
Hint: Inevitable acident
4. What is underrunning / tailgating?
5. Seatbelt syndrome , whiplash injury?

Case 3 : RTA
An RTA, patient was first taken to thaluk hospital then reffered to medical college. X ray revealed
fracture of right tibia.

Questions
1. Who should issue the wound certificate?
PA P E R S 2. Is it a Grevious hurt?

Case 4 : RTA

An 9 yr old student was hit by an auto while he was crossing the road. The auto driver took him
to the hospital. On examination the child had fracture in his Lt upper arm. The auto driver gave
the consent for treatment
Questions
1. Is the consent valid?
Questions of drunkenness
A man driving carelessly hit an old lady and she died, police arrested the man and he was drunk.
Questions: l
1. What was the crime committed and under which session?
Hint: Rash and negligent act-section 304-A of IPC. u
2. What is sec 53 Cr PC? m
Hint: a person under arrest can be examined without consent i
3. Rate of metabolism of alcohol?
Hint: Follows zero order kinetics n
a
Other questions which can be asked: i
1. DD of alcoholism.
r
2. Tests for muscle coordination.
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3. Preservatives used
4. MLI of drunkenness
5. Delirium tremens.
6. Wernicke‘s encephalopathy
7. Precautions taken for collection of blood.
8. The statutory limit of blood alcohol level in india is- 30mg%
9. Alcoholics anonymous

CERTIFICATE OF DRUNKENESS
Requisition for examination was received from ………………………….with his letter no:
…………….dated…………….through PC no……………

1. Name
2. Age,sex
3. Address
4. Escorted by
5. Informed written consent
6. Date,time and place of examination
7. Consent

QUESTION

8.Marks of identification
9.History:
a) Did he suffer from fits or any other illness or disability previously
b) What food and drink he took and when
c) Whether he took alcohol
10.General appearance(clothing,speech etc)
11.Higher functions(orientation,memory,intelligence,power of interpretation etc)
l 12.Examination of mouth
13.Examination of eyes
u 14.Test for reaction time,reflexes,muscle coordination(walk along straight line,finger nose
m test,Romberg’s sign etc)
i 15.General examination
16.Systemic examination
n 17.Examination of injuries
a 18.Collection of blood,urine for chemical examination
i 19.Opinion
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I am of the opinion that the above person has:
i. Consumed alcohol and is under its influence
ii. Consumed alcohol but is not under its influence
iii. Has not consumed alcohol

Signature
Name:
Station: Designation
Date: Address

PA P E R S

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Examination and report of a person regarding potency

MEDICAL COLLEGE,TRIVANDRUM
Ref no;ML…………../……………/P
Dated………………

EXAMINATION OF POTENCY

Requisition received from the……………….vide his letter no…………………..

dated…………….through PC/HC No……… For examination of potency of……………….
aged………………yrs involved in Cr No:………………..of………………….Police Station

1. Name and Address of the Subject:

2. Age:
3. Occupation:
4. Accompanied by:
5. Date,time and place of examination:
6. Consent

QUESTION

7.Marks of identification
8.Clinical history: DM/Drug Addiction/Trauma/Exposure to Venereal Disease/Others,if
any
9.History of sexual development: Masturbation/Night emissions/Homosexual practice/Sex-
ual intercourse
10.Physical Examination
a.General
i. Height……………cm
ii. Weight…………….kg
l iii. Build:(good,moderate,poor)
iv. Adam’s Apple
u
v. Hair(Pubic or axillary:facial,chest)
m b.Local
i i. Penis
• Present/Absent
n
• Length………………..cm(flaccid state)
a • Circumference……………….cm(flaccid state)
i • Disease(if any)
r • Deformity(if any)
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• Injury(if any)
• Sensation over glans penis
• Foreskin retractable/not
• ii.Scrotum
• Pendulous /not
• Right testis present/absent
• Left testis present/absent
• Development of testis(small,medium or adult size)
• Sensations
• Diseases,deformity,injury if any
• Epididymis and cord
•
c.Systemic Examination
CVS,GIS,CNS,RS
11.Special examinations(if relevant)
12.Opinion
a)There is nothing to suggest thst the above person is incapable of performing the sexual act
b)The above subject is incapable of performing the sexual act because of the following impedi-
ments;

Signature:
Name:
PA P E R S Designation:

*delete whichever is not applicable.vv

Probable questions 6. Quoad hoc

1. What is impotence,sterility? 7. Vaginismus
2. The term for impotency in female
3. Test for evidence of recent sexual inter-
course hint: penile wash
4. Name two civil and criminal cases each in
which examination of potency is asked for. l
5. How can a person can have a child of his u
own if he is impotent
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CERTIFICATE OF EXAMIANTION OF VICTIM OF RAPE

MEDICAL COLLEGE,TRIVANDRUM
ML.No………….. Date……………
REPORT OF MEDICAL EXAMINATION OF FEMALE IN SEXUAL OFFENCES

1. Name and Address

2. Age(as stated by the individual)
3. Referred by
4. Brought by
5. Crime no: Police Station
6. Date and time of examination
7. Informed consent given by (signature and name)

8.Female witness present during examination (signature,name,address)

9.Marks of identification QUESTION
10.History
General-Past illness,accidents,operations,medications,drug addictions
Sexual-Previous sexual experience,frequency,date of last sexual act
Menstrual-Dates of first and last menstrual period,regular/not,no:of flow days,frequen-
cy,h/o dysmenorrhea
Obstetric-No of pregnancies,type of delivery,surgical repair etc.
Specific
• Date,time and place of alleged act
• Reason for delay in complaint,if any
• Details of position,no of persons involved
• Degree of penetration and violence used by both parties
l • Resistance offered(if no resistance was offered,the reason for that)
u • If experienced any pain
m • Details of washing the local areas since the incident
• State of consciousness
i
• Whether clothes have been changed or washed since act
n •
a General examination findings
i • Mental state
• Height…………cms
r • Weight……………….kg
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FORENSIC MEDICINE
• Secondary sexual characters
• Appearance of breast
• Condition of clothes(indication of struggle,presence of stains,any other findings)
• Gait-pain during walking-yes/no

Injuries
1.General
2.Genital

Local examination
• Condition of pubic hair-matted/non matted
• Appearance of labia/clitoris
• Condition of hymen-intact/elastic/torn-fresh/old
,carunculae hymenalis
• Fourchette-intact/torn
• Condition of vagina-admits one/two/more than two fingers,
rugae-distinct/not,
dischargepresent/not
• Appearance of perineum and thighs
• Signs of venereal disease
Nature of specimens sent for chemical analysis/preserved for DNA profile (no and
date of letter sending the specimen)

PA P E R S Results of chemical examination

Any additional findings

OPINION
Based on the above facts I certify that,
1. There is evidence or no evidence of general injuries on the body
2. There is evidence or no evidence of genital injuries,it could be due to penetration,recent or old
3. Final opinion is reserved pending the chemical analysis report

Signature
Name and designation
Probable questions Hint: presence of atleast 1 unbroken sper- l
1. A girl 15 year old raped with consent by matozoan or electrophoretic LHD isoenzyme
fisherman Ratheesh and she was brought for detection of sperms u
examination. (Details will be given in the 4. How will you determine sexual intercourse m
question paper). from vaginal swab? i
How will you differentiate between torn and Hint: from motility of sperm
fimbriated hymen? full => 3 hrs n
2. What is the time taken for complete healing 50% => 8 hrs‘ a
of torn hymen? Hint: 1 week 10% => 24 hrs i
3. What is the absolute proof of presence of 5. Write 4 causes of rupture of hymen other
r
semen? than sexual intercourse
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FORENSIC MEDICINE

Hint: accidental 5. Rape trauma syndrome

surgical operation
ulceration
masturbation
Other questions
1. Define adultery
2. Statutory rape,
3. Test for evidence of recent sexual inter-
course in male
hint: penile washing-method: retract the fore-
skin of the penis and wash glans penis- cen-
Q U E S T I O N PA P E R S

trifuge the washing-take sediment and add KI.

If vaginal epithelial cells are present, glycogen
in the cells wll take up Iodine and stain brown.
4. Two tests for spermatozoa:
Hint: Florence test and Barberio test

QUESTION

l
u
m
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Q.P. Code: 201001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
October 2016
Pharmacology- Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)

Q U E S T I O N PA P E R S
1. Classify NSAIDs. Mention the therapeutic uses and adverse effects of salicylates. (2+2+2=6)
2. Read the case history and answer the following questions. A 25 years old man had a gradual
onset of delusions and auditory hallucinations. He was taken to a psychiatrist who started
him on tab. haloperidol 2mg twice daily. A few weeks later although he improved clinically he
developed stiffness and rigidity of upper and lower limbs.
• Comment on the response of the patient to haloperidol.
• Outline the further line of management.
• Name two atypical antipsychotics. (2+2+2=6)

Short notes: (5x3=15)

3. Carvedilol
4. COMT inhibitors.
PA P E R S 5. Therapeutic uses and adverse effects of atropine.
6. Furosemide.
7. First pass metabolism.
Answer briefly: (5x1=5)

8. Rationale for the use of glycopyrrolate in pre-anesthetic medication.

9. Mechanism of action of pancuronium.
10. New drug delivery systems.
11. Two uses and two adverse effects of morphine.
12. Young’s formula.

Name two drugs: (8x1=8)

l
13. Status epilepticus.
14. Febrile convulsions in a child aged six years.
u
15. Drugs used in myasthenia gravis. m
16. Acute myocardial infarction.
i
17. Congestive cardiac failure.
18. Iron deficiency anemia. n
19. Motion sickness. a
20. Acute severe asthma.
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Q.P. Code: 206001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
October 2016
Microbiology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Q U E S T I O N PA P E R S

Essay: (10)
1. Read the following clinical history and answer the following
Mother of a small child was complaining about passing half an inch pale white motile
worms in stool.
• What is the probable diagnosis.
• What sample will you collect from the patient.
• What do you expect to see in light microscopy.
• What would be the child’s symptoms.
• What are the complications expected (1+1+4+2+2 =10)

Short essay: (2x5=10)

2. Dimorphic fungi
3. Japanese encephalitis

Short notes: (10x2=20)

4. Virus cultivation by cell culture method.
5. Prophylaxis of rabies
6. Herpes simplex virus 1 ( HSV1 )
7. Viral diarrhea
l 8. Non-bile stained eggs
u 9. Cryptosporidium
m 10. Dermatophytes
i 11. Hydatid disease
n 12. Cyclops
a 13. Cryptococcosis
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Q.P. Code: 205001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
October 2016
Microbiology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Q U E S T I O N PA P E R S
Essay: (10)
1. A male patient aged 20 years came with a history of fever for 15 days duration with
coated tongue and soft palpable spleen. Answer the following:
• Mention the probable diagnosis and source of infection
• List the specimens to be sent for lab. diagnosis in this case
• How will you proceed with lab. diagnosis in this case .
• What is anamnestic reaction
• How the disease can be prevented (1+1+4+2+2=10)

Short essay: (2x5=10)

2. Lab diagnosis of helicobacter infection
3. Graft – versus – host ( GVH ) reaction

Short notes: (10x2=20)

4. Adjuvants
5. Rapid plasma reagin test
6. Acinetobacter
7. Prophylaxis of whooping cough
8. Bacterial capsule
l
9. Innate immunity
u
10. Super antigens
m
11. CAMP reaction
i
12. Non – gonococcal urethritis
n
13. Q- fever
a

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Q.P. Code: 204001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
October 2016
Hematology and Systemic Pathology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Q U E S T I O N PA P E R S

Essay: (8)
1. Classify tumors of the kidney. Discuss the gross and microscopy of the most common
renal tumor in adults (2+3+3= 8)

Short essay: (6)

2. An 18 years old lady presented with fatigue. Investigations: Hb5 g/dl TC 10,000 /cmm
platelet count 1.8 lakh/cmm. MCV 60 fl MCH 20 pg. Answer the following:
• What is your morphological diagnosis.
• Describe the peripheral blood picture
• Name the conditions in which this blood picture is seen
• How will you differentiate the above two conditions with laboratory tests
(1+2+1+2=6)

Short notes: (4x4=16)

3. Etiopathogenesis of bronchiectasis
4. Lab diagnosis of immune thrombocytopenic purpura
5. Peripheral smear findings in chronic lymphocytic leukemia
6. Teratoma

Answer briefly: (4x2=8)

7. List two causes of extra medullary hemopoiesis
8. Classification of tumors of the breast
9. Seminoma
10. Malignant melanoma

l Answer in single sentence: (4x½=2)

u 11. Mott cell
12. Endometriosis
m 13. Hydatidiform mole
i 14. Reinke crystals
n
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Q.P. Code: 203001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
October 2016
Clinical Pathology and General Pathology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Q U E S T I O N PA P E R S
Essay: (8)
1. Define shock. Mention four types of shock. Describe the morphological changes in
various organs in shock. Add a note on pathogenesis of septic shock (1+2+3+2=8)

Short essay: (6)

2. A 5 years old boy was admitted with history of oliguria, facial edema and dark colored
urine. His BP was 140/100 mm of Hg. Answer the following:
• What is your provisional diagnosis.
• What are the laboratory findings in urine examination in this patient
• How do you examine urinary sediments and describe the sediments seen in
urine (1+2+3=6)

Short notes: (4x4=16)

3. Metaplasia
4. Blood transfusion reaction
5. Primary wound healing
6. Miliary tuberculosis

Answer briefly: (4x2=8)

7. Anti nuclear antibodies
8. Name four carcinogenic viruses
9. CSF findings in pyogenic meningitis.
10. Erythrocyte sedimentation rate

Answer in single sentence: (4x½=2) l

11. Define necrosis u
12. Cardinal signs of inflammation
m
13. Fate of thrombus
14. Skeletal changes in rickets i
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Q.P. Code: 202001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
October 2016
Pharmacology- Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essays: (2x6=12)
Q U E S T I O N PA P E R S

1. A 50 years old lady complains of pain in the throat and has been diagnosed to
have streptococcal tonsillitis. Answer the following:
• Name two appropriate drugs for it.
• Name two bactericidal and two bacteriostatic drugs
• Explain briefly the mechanism of action of penicillins
• What are the adverse effects of amino glycosides. (1+1+2+2=6)
2. Classify oral anti diabetic drugs and explain the mechanism of action of any two
groups. Mention one insulin analog and list one advantage of it over conventional
insulin (2+3+1=6)

Short notes: (5x3=15)

3. Methotrexate
4. Non systemic antacids
5. Rifampicin
6. Artemisinin based combination therapy (ACT ) in malaria
7. Post coital contraceptives
Answer briefly: (5x1=5)
8. Two differences between ketoconazole and fluconazole
9. Mention four uses of metronidazole
10. Mechanism of action of hydrocortisone
11. What is post antibiotic effect and mention one example
12. What are streptogramins and mention one use of it

Name two drugs: (8x1=8)

l 13. Peptic ulcer
u 14. Chemoprophylaxis in tuberculosis
15. Anti emetics
m 16. Antibiotics given only parenterally
i 17. Anti thyroid drugs
18. Typhoid fever
n 19. Antiretroviral drugs
a 20. Round worm infestation

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Q.P. Code: 201001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
October 2016
Pharmacology- Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)

Q U E S T I O N PA P E R S
1. Classify NSAIDs. Mention the therapeutic uses and adverse effects of salicylates. (2+2+2=6)
2. Read the case history and answer the following questions. A 25 years old man had a gradual
onset of delusions and auditory hallucinations. He was taken to a psychiatrist who started
him on tab. haloperidol 2mg twice daily. A few weeks later although he improved clinically he
developed stiffness and rigidity of upper and lower limbs.
• Comment on the response of the patient to haloperidol.
• Outline the further line of management.
• Name two atypical antipsychotics. (2+2+2=6)

Short notes: (5x3=15)

3. Carvedilol
4. COMT inhibitors.
5. Therapeutic uses and adverse effects of atropine.
6. Furosemide.
7. First pass metabolism.
Answer briefly: (5x1=5)

8. Rationale for the use of glycopyrrolate in pre-anesthetic medication.

9. Mechanism of action of pancuronium.
10. New drug delivery systems.
11. Two uses and two adverse effects of morphine.
12. Young’s formula.

Name two drugs: (8x1=8)

13. Status epilepticus. l

14. Febrile convulsions in a child aged six years. u
15. Drugs used in myasthenia gravis.
16. Acute myocardial infarction.
m
17. Congestive cardiac failure. i
18. Iron deficiency anemia.
n
19. Motion sickness.
20. Acute severe asthma. a
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Q.P. Code: 207001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2016
Forensic Medicine & Toxicology
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essay: (7)
1. A 20 years old male was bitten on the foot by a snake while he was working in fields.
He killed the snake and brought it to casualty along with him. It had a triangular head
Q U E S T I O N PA P E R S

and black diamond shaped patches on the back. There was swelling and blood oozing
from the site of bite. Answer the following:
• Identify the snake
• What is the nature of its venom
• Mention the first aid management that can be given in such a bite
• What is the specific management to be given in this case (1+1+3+2=7)
Short notes: (5x3=15)
2. Pathophysiology of fresh water drowning
3. Police inquest
4. Functions of state medical council
5. Ingredients of medical negligence
6. Dactylography

Answer briefly: (5x2=10)

7. Maceration
8. Objectives of medico legal autopsy
9. Signs of virginity
10. Positive signs of pregnancy
11. Delusion
l
Differentiate between: (2x2=4)
u
12. Post mortem lividity and contusion
m
13. Somatic and molecular death
i
Draw and label: (2x2=4)
n
14. Longitudinal section of shot gun cartridge
a
15. Stomach wash tube
i
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Q.P. Code: 205001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2016
Microbiology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)

Q U E S T I O N PA P E R S
1. Read the clinical history and answer the following questions:
A 24 years old man was admitted in medical ward with a history of diarrhea for the
past two days. On clinical examination he was severely dehydrated. The macroscopic
appearance of the stool resembled ‘rice water’. Answer the following:
• What is the probable diagnosis and name the causative agent
• Mention the method of sample collection and transportation of the sample to the
laboratory.
• What is the pathogenesis of the above disease.
• Describe the laboratory diagnosis.
• What is the prophylaxis. (1+2+2+4+1=10)

Short essay: (2x5=10)

2. Type IV hypersensitivity reaction.
3. Pathogenesis and laboratory diagnosis of enteric fever.

Short notes: (10x2=20)

4. Tyndallisation.
5. T-helper cells.
6. Transduction
7. Bacterial flagella
l

8. Enrichment medium.
u

9. Lymphogranuloma venereum.
m

10. Helicobacter pylori. i

11. Coagulase test. n
12. Nagler reaction. a
13. Types of diarrhoeogenic esherichia coli. i
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Q.P. Code: 206001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2016
Microbiology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)
Q U E S T I O N PA P E R S

1. Read the clinical history and answer the following questions:

A 27 years old male was admitted in intensive medical care unit with drooling of saliva
and fear for intake of liquids since morning. There was a past history of dog bite on
his right leg ten days back.
• What is the provisional diagnosis
• Discuss briefly about the pathogenesis of the above clinical condition.
• Describe the laboratory investigations to confirm the diagnosis
• Explain the prophylaxis of this condition (1+3+2+4=10)

Short essay: (2x5=10)

2. Ascaris lumbricoides.
3. Pathogenesis and laboratory diagnosis of lymphatic filariasis.

Short notes: (10x2=20)

4. Serological markers of hepatitis B infection.
5. Prophylaxis of poliomyelitis.
6. Tissue culture
7. Cryptococcosis
l 8. Life cycle of plasmodium falciparum.
u 9. Piedra
m 10. Laboratory diagnosis of dermatophytosis.
i 11. Histoplasma capsulatum.
n 12. Viral haemorrhagic fever.
a 13. Cysticercus cellulosae.
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Q.P. Code: 204001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2016

Hematology and Systemic Pathology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)

Q U E S T I O N PA P E R S
1. Classify breast tumors. Mention the risk factors and pathogenesis of breast cancer.
Describe the gross and microscopic features of infiltrating duct carcinoma. (3+3+2=8)
Short essay: (6)
2. A young boy aged 3 years was admitted for compliants of yellowish
discoloration of eyes.He has past history of repeated blood transfusions.On
examination severe pallor and splenomegaly present.X ray showed crew cut
appearance.Peripheral smear showed microcytic hypochromic RBCs. Answer the
following :
• What is the most probable diagnosis.
• Describe the various lab investigations to establish the diagnosis.
• What is the pathogenesis of the disease (1+3+2=6)

Short notes: (4x4=16)

3. Lab investigations for diagnosis of acute leukemia
4. Pathology of grave’s disease.
5. Vegetations in bacterial endocarditis
6. Etiopathogenesis of cirrhosis

Answer briefly: (4x2=8)

7. Clinico-pathological features of leiomyoma
8. Name four conditions associated with development of osteosarcoma
9. Gall stones – types and complications
10. Malignant melanoma

Answer in single sentence: (4x½=2) l

11. Myelodysplastic syndrome u
12. Leukoplakia m
13. Osteoporosis
14. Aschoff nodule i
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Q.P. Code: 203001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2016

Clinical Pathology and General Pathology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)
Q U E S T I O N PA P E R S

1. Define necrosis. Describe the various types of necrosis with suitable examples. How
does it differ from apoptosis. (1+4+3=8)

Short essay: (6)

2. A 14 years old boy presented with fever, cervical lymphadenopathy, rashes, mild
hepatomegaly. No bleeding manifestation. TC: 20,000 cell/mm3; predominantly
lymphocytes in peripheral blood. Answer the following:
• What is your provisional diagnosis
• What are the confirmatory tests
• What is the complication
• What is the etiologic agent (1+2+2+1=6)
Short notes: (4x4=16)
3. Spleen in amyloidosis
4. Radiation and cancer
5. Metaplasia
6. Dystrophic calcification

Answer briefly: (4x2=8)

7. Thromboembolism
8. Erythrocyte sedimentation rate.
9. Healing by secondary intention
10. Chemotaxis

l Answer in single sentence: (4x½=2)

u 11. Define gangrene

12. Principle of Benedict’s test
m 13. Draw Langhan’s giant cell.
i 14. Normal reticulocyte count.
n
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Q.P. Code: 201001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2016

Pharmacology- Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. Enumerate four groups of antiepileptic drugs with examples of each. Mention four newer anti

Q U E S T I O N PA P E R S
epileptics. Describe the pharmacological actions, adverse effects and therapeutic uses of any
one of them. (2 + 2+ 2 = 6)
2. Read the clinical problem and answer the following question: Master. Vijay, 12 years had
severe fever for the past 3 days and he was under treatment with antibiotics and analgesics.
He developed severe pain in the stomach after taking the analgesics and he was admitted to
the Hospital for severe gastritis
• List four groups of analgesics and antipyretics that produces gastritis ,
• Mention the mechanism of action and advantages of propionic acid derivatives
• Name two selective COX-2 inhibitors and its advantages (2+ 2+ 2 = 6)

Short notes: (5x3=15)

3. Therapeutic uses of adrenergic drugs.

4. Dopamine in cardiogenic shock.
5. Bioavailability.
6. Mechanism of action of loop diuretics.
7. Rationale of ethanol in methanol poisoning.

Answer briefly: (5x1=5)

8. Explain why morphine is contraindicated in patients with head injury.

9. Two uses and two adverse effect of nifedipine.
10. Mechanism of action of diazepam.
11. Plasma half life and its clinical relevance.
12. Nitrates in acute attack of angina.

Name two drugs: (8x1=8)

l
13. Fibrinolytics.
14. Treatment of rheumatoid arthritis. u
15. Hyperlipidemia. m
16. Hypertensive emergencies.
17. Parkinson’s disease i
18. Causing teratogenicity n
19. Management of organophosphorus poisoning.
20. Migraine. a
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Q.P. Code: 202001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2016

Pharmacology- Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. Classify cephalosporins. Describe the mechanism of action and clinical uses of ceftriaxone.
Q U E S T I O N PA P E R S

Which drug can be combined with amoxicillin to treat infection due to beta lactamase
producing staph. aureus. ( 2+1+2+1 = 6)
2. A 25years old insulin dependent diabetes mellitus patient develops sweating, anxiety,
palpitations and tremors after performing vigorous exercise. Answer the following:
• What is the cause of these symptoms.
• Would you prescribe beta blockers to this patient if he develops hypertension and why.
• How will you treat diabetic keto acidosis. (1+2+3=6)

Short notes: (5x3=15)

3. Adverse effects of aminoglycoside antibiotics

4. Uses of chloroquine
5. Methotrexate
6. Cyclosporine
7. Uses of glucocorticoids
Answer briefly: (5x1=5)

8. Mechanism of action of cotrimoxazole

9. Uses of azole antifungal agents
10. Centchroman
11. Aprepitant
12. Uses of clofazimine
Name two drugs: (8x1=8)

13. Treatment of onchocercosis

14. Anti tumor antibiotics
15. Non nucleoside reverse transcriptase inhibitors
l
16. Treatment of multi drug resistant tuberculosis
u 17. Monoclonal antibodies
m 18. Chelating agents
19. Uterine stimulants
i 20. Treatment of Paget’s disease
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Q.P. Code: 201001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2015
Pharmacology- Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)

Q U E S T I O N PA P E R S
1. Enumerate four groups of drugs used in the treatment of Parkinson’s disease. Describe the
pharmacological actions and adverse effects of levodopa. What is the advantage of combining
levodopa with the peripheral decarboxylase inhibitor. (2+3+1= 6)
2. Read the clinical problem and answer the following questions: 30 years old man was admitted
in emergency ward with acute abdominal pain. After diagnosed with acute appendicitis, he was
taken for surgery. On the operation table, after administration of a skeletal muscle relaxant,
patient developed difficulty in breathing and went in for apnoea.
• Which skeletal muscle relaxant is responsible for this reaction.
• What is the reason for the apnoea.
• How will you manage the patient. (1+3+2=6)

Short notes: (5x3=15)

3. Trans dermal therapeutic system

4. Amphetamine
5. Second generation antihistamines
6. Tramadol
7. Ramipril
Answer briefly: (5x1=5)

8. Rationale for use of calcium channel blockers in angina

9. Rationale for use of ethanol in methanol poisoning
10. Rationale for use of prostaglandin in acid peptic disease
11. Rationale for use of physostigmine in atropine poisoning
12. Pharmacovigilance

Name two drugs: (8x1=8) l

u
13. Cholinesterase reactivators
14. Intravenous general anesthetics m
15. Inhalational steroids i
16. Centrally acting muscle relaxants
17. Nasal decongestants n
18. Pure opioid antagonists a
19. Low molecular weight heparins
20. Cardio selective beta blockers
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Q.P. Code: 202001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2015
Pharmacology- Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
Q U E S T I O N PA P E R S

1. List aminoglycoside antibiotics. Mention its four common properties and two adverse effects.
2. Read the clinical problem and answer the following questions: A 28 years old woman
having two children wanted to follow a contraceptive method. Patient was advised to take
oral contraceptive pills. She is a known case of pulmonary tuberculosis for which she is on
Rifampicin 450mg. INH300mg and ethambutol 300mg per day.
• What are the expected complications.
• Why.
• What will you suggest (2+2+2=6)

Short notes: (5x3=15)

3. Interferon alfa
4. Therapeutic uses of glucocorticoids.
5. Clomiphene citrate.
6. Rabeprazole.
7. Gatifloxacin.
Answer briefly: (5x1=5)

8. Rationale for the combined use of aluminium and magnesium salts in antacid preparations.
9. Mechanism of action of co-trimoxazole.
10. Rationale for the use of folinic acid in methotrexate toxicity.
11. Comment on the interaction between itraconazole and omeprazole.
12. Pharmacological basis for the combined use of drugs in cancer chemotherapy.

Name two drugs: (8x1=8)

l
13. Dermatophytosis.
u
14. GERD.
m 15. Brucellosis.
i 16. Thyrotoxic crisis.
17. Intestinal amoebiasis.
n
18. Hookworm infestation
a 19. Burns infected with pseudomonas aeruginosa
i 20. H1N1 viral infection.
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Q.P. Code: 203001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2015
Clinical Pathology and General Pathology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)

Q U E S T I O N PA P E R S
1. Define granuloma. Describe the morphology of a classical granuloma. Discuss the
evolution granulomatous inflammation. Mention three examples of granulomatous
diseases (1+2+3+2=8)

Short essay: (6)

2. A 55 years old man presented with generalised edema and shortness of
breath.On examination he has distended jugular veins. He gives previous history of
rheumatic heart disease.
• What is your diagnosis.
• Describe the gross and microscopic features of liver, spleen and lung.
• What is the pathogenesis of edema in this case (1+ 3+2=6)

Short notes: (4x4=16)

3. Define necrosis. Describe the types of necrosis with examples
4. Microscopic examination of urine
5. Causes of impaired wound healing
6. Chemical carcinogenesis

Answer briefly: (4x2=8)

7. Transfusion transmitted diseases
8. Rickets
9. HIV associated changes in immune function
10. Balanced translocation
l
Answer in single sentence: (4x½=2)
u
11. Define atrophy
12. Principle of reagent strip test for glycosuria m
13. Anaphylaxis i
14. Sago spleen
n
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Q.P. Code: 204001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2015
Hematology and Systemic Pathology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Q U E S T I O N PA P E R S

Essay: (8)
1. Define rheumatic fever. Describe the etiopathogenesis and pathology of rheumatic
heart disease. (1+3+4 =8)

Short essay: (6)

2. A 72 years old male presented with changes in the bowel habit, bleeding per rectum,
loss of weight, fatigue and weakness of six months duration. After endoscopic biopsy
of colon, a left sided hemicolectomy was done. Answer the following:
• What is the probable diagnosis.
• Describe the etiopathogenesis.
• Describe the gross and microscopic features of the resected colon
• Mention the serological marker which is increased. (1+2+2+1=6)

Short notes: (4x4=16)

3. Laboratory diagnosis of megaloblastic anemia.
4. Idiopathic thrombocytopenic purpura.
5. Bronchiectasis
6. Cholelithiasis

Answer briefly: (4x2=8)

7. Gross features of adult polycystic kidney.
8. Microscopic appearance of seminoma.
9. Kruckenberg’s tumor
l 10. Paget’s disease of the breast.
u Answer in single sentence: (4x½=2)
m
11. Sequestrum
i 12. Target cells
n 13. Migratory thrombophlebitis
14. Mention two advantages of FNAC over biopsy.
a
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Q.P. Code: 205001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2015
Microbiology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)

Q U E S T I O N PA P E R S
1. A twenty five years old lady presented with frequency in passing urine and pain during
micturition along with fever for the last five days. Microscopy of urine showed plenty of
pus cells and bacilli . Answer the following:
• What is your diagnosis .
• Name of the common bacteria causing this condition .
• What is significant bacteriuria .
• How will you confirm the diagnosis in the laboratory.
• What are the screening techniques for the presumptive diagnosis of significant
bacteriuria (1+2+1+4+2=10)

Short essay: (2x5=10)

2. Pathogenesis of autoimmune diseases
3. Compare exotoxin and endotoxin

Short notes: (10x2=20)

4. Halophilic vibrios
5. Pasteurization
6. Transport media
7. Gene therapy
8. ELISA l
9. B-lymphocytes u
10. Toxic shock syndrome m
11. Coagulase negative staphylococci i
12. Tric agents n
13. L-forms a
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Q.P. Code: 206001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2015
Microbiology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)
Q U E S T I O N PA P E R S

1. A male patient aged 35 years came to STD outpatient department with a history of
exposure and is complaining of intractable diarrhea of one month duration with loss of
weight and prolonged fever. Answer the following:
• Mention the probable diagnosis
• Describe the morphology of the virus causing the disease
• How will you proceed with laboratory diagnosis in this case
• Discuss the other modes of transmission
• How the disease can be prevented (1+2+3+2+2=10)

Short essay: (2x5=10)

2. Prophylaxis of poliomyelitis

3. Larva migrans

Short notes: (10x2=20)

4. Pencilliosis

5. Hydatid cyst

6. Cell cultures for growing viruses

7. Eggs of nematodes

8. Germ tube test

l 9. Intestinal flagellates
u
10. Mycotic poisoning
m
11. Name four viruses causing diarrhea
i
n 12. Live attenuated vaccines
a 13. Name four parasites causing water borne diseases.
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Q.P. Code: 201001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2015
Pharmacology- Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. Enumerate four groups of non-steroidal anti-inflammatory drugs with the example each.

Q U E S T I O N PA P E R S
Describe the pharmacological actions, adverse effects and therapeutic uses of any one of
them. (2+2+1+1=6)
2. Read the clinical problem and answer the following question: Mr.Shankar, 54 years suddenly
developed severe chest pain. He was a diabetic and admitted in the ICCU with the diagnosis of
acute myocardial infarction,
• List the drug to be started immediately after acute myocardial infarction.
• Write the mechanism of action and two adverse effects of fibrinolytics
• Name the analgesics used to relieve pain and its rationale for the same (2+ 2+ 2 = 6)

Short notes: (5x3=15)

3. Atropine
4. Drug antagonism.
5. Halothane
6. Diazepam
7. Heparin.
Answer briefly: (5x1=5)

8. Two uses and two adverse effects of propranolol.

9. Explain briefly why physostigmine is preferred over neostigmine for the treatment of glaucoma.
10. Rationale of using terazosin in benign prostatic hypertrophy
11. Mechanism of action of lignocaine.
12. Teratogenecity with one example.

Name two drugs: (8x1=8)

l
13. Angiotensin converting enzyme inhibitor
u
14. The treatment of migraine.
15. Nasal decongestants. m
16. The treatment of cardiac failure. i
17. Ototoxic diuretics.
18. Short acting agents for insomnia. n
19. Treatment of methanol poisoning. a
20. Opioid antagonist.
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Q.P. Code: 202001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2015
Pharmacology- Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. Classify drugs used in treatment of malaria. Explain the mechanism of action, adverse effects
and dose of any one such drug. Which drug is used for radical cure of acute vivax malaria.
Q U E S T I O N PA P E R S

2. A 35 years old woman came with complaints of heat intolerance, retraction of upper eyelid
and menstrual irregularities. Her T3 , T4 , FT4 & FT3 are elevated while TSH is suppressed.
Answer the following:
• Which drugs can be administered to reduce the thyroid activity in this patient.
• What is its mechanism of action.
• Which drug is preferred, if the patient is pregnant.
• What is the route of administration of I131. (2+2+1+1=6)

Short notes: (5x3=15)

3. Proton pump inhibitors
4. Fluconazole
5. Lepra reaction
6. Adverse effects of oral contraceptives
7. Bisphosphonates
Answer briefly: (5x1=5)
8. Prevention of vertical transmission HIV infection
9. Mechanism of action of ciprofloxacin
10. Anti malignancy drugs producing gouty arthritis
11. Immunotherapy for Rh negative woman with Rh positive baby
12. Longest acting insulin given as once daily dose
Name two drugs: (8x1=8)
13. Treatment of pneumocystis carnii
14. Peroxysome proliferator activated receptor gamma agonists
15. Drugs causing haemolytic anemia in glucose 6 phosphate dehydrogenase deficiency patients
16. Cell cycle specific anti metabolites
17. Treatment of extra intestinal amoebiasis
l
18. Selective estrogen receptor modulators
u 19. Treatment of ascariasis
20. Antiemetic agents
m
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Q.P. Code: 203001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2015
Clinical Pathology and General Pathology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)
1. Define reversible and irreversible cell injury. What is the pathogenesis of irreversible

Q U E S T I O N PA P E R S
cell injury. Define and describe the type of necrosis and gangrene (1+3+4=8)

Short essay: (6)

2. A 45 years old male was admitted with complaints of yellowish discoloration of eyes
and distension of abdomen since 15 days. USG abdomen shows contracted liver with
loss of architecture and splenomegaly. Patient is a chronic alcoholic since 15 years.
Answer the following:
• What is your most probable diagnosis.
• Describe the gross and microscopic features of the organs involved.
• Name the laboratory investigation to be done in this case and the expected
variation in this values
• List three complications of the above condition.

Short notes: (4x4=16)

3. Erythrocyte sedimentation rate
4. Pathogenesis of amyloidosis
5. Staining of peripheral blood film
6. Transudate and exudate

Answer briefly: (4x2=8)

7. Actinomycosis
8. Pathogenises of CNS lesions seen in HIV infection
9. Exfoliative cytology
10. Manifestations of vitamin A deficiency

Answer in single sentence: (4x½=2)

l
11. Define delayed hypersensitivity reaction.
12. Define fixed specific gravity. u
13. Define dysplasia. m
14. Mention two anticoagulants.
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Q.P. Code: 204001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2015
Hematology and Systemic Pathology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)
Q U E S T I O N PA P E R S

1. Classify the tumors of the uterus. Discuss the pathology of leiomyoma. Add a note
on secondary changes in leiomyoma. (2+3+3=8)

Short essay: (6)

2. A 50 years old male presented with weakness, pallor and massive splenomegaly.
Blood examination revealed marked increase in the total count. Answer the following:
• What is the probable diagnosis.
• What are the peripheral smear findings.
• What is the genetic abnormality.
• What are the different stages of disease progression. (1+2+1+2=6)

Short notes: (4x4=16)

3. Medullary carcinoma of the thyroid.
4. Osteosarcoma
5. Emphysema
6. Meningioma

Answer briefly: (4x2=8)

7. Gross and microscopy of ulcerative colitis.
8. Nephroblastoma
9. Dermoid cyst of ovary
10. Aschoff’s body

Answer in single sentence: (4x½=2)

l
11. Principle of sickling test
u 12. Leukoplakia
13. Mott cell
m
14. Barett’s eosophagus.
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Q.P. Code: 205001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2015
Microbiology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)

Q U E S T I O N PA P E R S
1. Read the following clinical history and answer the following questions:
A young adult male met with an accident on the high way and sustained severe injury
to the right thigh. On examination there was foul smelling discharge and crepitus at
some of the areas.
• What is the probable diagnosis
• Name the etiological agents
• What are the specimens to be sent for the laboratory
• Describe the laboratory diagnosis briefly
• What is the prophylaxis. (1+2+2+4+1= 10)

Short essay: (2x5=10)

2. Leptospirosis
3. Agglutination reactions

Short notes: (10x2=20)

4. Super antigen with an example
5. Immunological effects of TNF
6. Immunological tolerance
7. Hereditary angioneurotic edema
l
8. Primary mediators of type I hypersensitivity
u
9. Diarrhaegenic escherichia coli.
m
10. Non-gonococcal urethritis
i
11. Mycobacterium avium – intracellular complex
n
12. Satellitism. a
13. Scrub typhus. i
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Q.P. Code: 206001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2015
Microbiology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)
Q U E S T I O N PA P E R S

1. 19 years old female patient complaints of fever biphasic in nature with severe bone
pains in the back and limbs. She had maculopapular rash and developed

haemorrhagic manifestations. Answer the following:

• What is the probable diagnosis.
• What is the transmitting vector for this disease.
• Discuss the laboratory diagnosis of this disease
• List two complications of this disease
• Mention the preventive measures to prevent this disease (1+1+4+2+2=10)

Short essay: (2x5=10)

2. Pathogenesis and complications of ascariasis
3. Discuss the lab diagnosis of candidiasis

Short notes: (10x2=20)

4. Non-neural vaccines for rabies
5. Presumptive coliform count
6. Mycetism
7. Rhinosporidiosis
l
8. Otomycosis
u
9. Microfilaria
m
10. Molluscum contagiosum
i
11. Trichomonas vaginalis
n
12. Continuous cell lines
a
i 13. Hospital acquired infection
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Q.P. Code: 202001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2015
Pharmacology- Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. Classify drugs used in treatment of malaria. Explain the mechanism of action, adverse effects

Q U E S T I O N PA P E R S
and dose of any one such drug. Which drug is used for radical cure of acute vivax malaria.
2. A 35 years old woman came with complaints of heat intolerance, retraction of upper eyelid
and menstrual irregularities. Her T3 , T4 , FT4 & FT3 are elevated while TSH is suppressed.
Answer the following:
• Which drugs can be administered to reduce the thyroid activity in this patient.
• What is its mechanism of action.
• Which drug is preferred, if the patient is pregnant.
• What is the route of administration of I131. (2+2+1+1=6)

Short notes: (5x3=15)

3. Proton pump inhibitors
4. Fluconazole
5. Lepra reaction
6. Adverse effects of oral contraceptives
7. Bisphosphonates
Answer briefly: (5x1=5)
8. Prevention of vertical transmission HIV infection
9. Mechanism of action of ciprofloxacin
10. Anti malignancy drugs producing gouty arthritis
11. Immunotherapy for Rh negative woman with Rh positive baby
12. Longest acting insulin given as once daily dose
Name two drugs: (8x1=8)
13. Treatment of pneumocystis carnii
14. Peroxysome proliferator activated receptor gamma agonists
15. Drugs causing haemolytic anemia in glucose 6 phosphate dehydrogenase deficiency patients
16. Cell cycle specific anti metabolites l
17. Treatment of extra intestinal amoebiasis u
18. Selective estrogen receptor modulators
19. Treatment of ascariasis m
20. Antiemetic agents i
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Q.P. Code: 207001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, February 2015
Forensic Medicine & Toxicology
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essay: (7)
1. A 30 years old male comes to trauma center with history of head injury. He does not
Q U E S T I O N PA P E R S

remember the incident. After a couple of hours he loses consciousness and his
condition progressively deteriorates and he dies. Answer the following:
• What is the likely diagnosis
• Mention the source of bleeding
• What is the medico legal importance of this condition
• What is the emergency procedure that needs to be done (2+3+1+1=7)

Short notes: (5x3=15)

2. Traumatic asphyxia
3. Magistrate inquest
4. Infamous conduct
5. Vicarious liability
6. Presumptive signs of pregnancy

Answer briefly: (5x2=10)

7. Cadaveric spasm
8. Tattoos
9. Sudden infant death syndrome
10. Testamentary capacity
11. Chelating agents
l
u Differentiate between: (2x2=4)

m 12. Medico legal and pathological autopsy

i 13. Strychnine poisoning and tetanus

n Draw and label: (2x2=4)

a
14. Types of finger print pattern
i
15. Entry wound of rifled firearm from a close range
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Q.P. Code: 201001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2014
Pharmacology- Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)

Q U E S T I O N PA P E R S
1. Classify beta blockers with one example for each. Mention the therapeutic uses and adverse
effects of propranolol (2+2+2=6)
2. Read the case history and answer the following questions. Mr.George aged 45 years was
on maintenance dose of warfarin 5 mg /day for his ischaemic heart disease. Subsequently
he developed joint pains for which he was administered tab. aspirin 300mg thrice daily after
food. One week later he was brought to casualty in a state of shock due to severe
haemetemesis.
• How will you explain haemetemesis in this patient.
• How it could have been prevented.
• How will you treat the present emergency (2+2+2=6)

Short notes: (5x3=15)

3. Propofol
4. Dopamine
5. Ramipril
6. Treatment of organophosphorous poisoning
7. Mention SSRI and its advantages.
Answer briefly: (5x1=5)

8. Rationale for the use of adrenaline along with local anesthetics.

9. Two uses and two adverse effects of calcium channel blockers.
10. Mechanism of action of dantrolene sodium.
11. Rationale for the use of nitrates in angina pectoris.
12. Chemical antagonism with one example.
Name two drugs: (8x1=8)

13. Drugs administered by inhalation route. l

14. Anaphylactic shock. u
15. Hypertensive emergencies.
16. Pre-anesthetic medication
m
17. Treatment of migraine. i
18. Supra ventricular tachycardia.
19. Benign prostatic hypertrophy.
n
20. Cerebral edema. a
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Q.P. Code: 202001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2014
Pharmacology- Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. Classification of fluoroquinolones .Describe the mechanism of action, therapeutic uses and
Q U E S T I O N PA P E R S

adverse effects of sparfloxacin. (2 + 2+ 2 =6)

2. Read the case history and answer the following questions. Mr. Raman 32 years has
developed severe epigastric pain after taking tab. Ibuprofen 400mg tds for his joint pain
• Mention two drugs used in NSAID induced gastric ulceration
• Mechanism of action of proton pump inhibitors
• Drugs for eradication of H.pylori infection

Short notes: (5x3=15)

3. Bisphosphonates
4. Adverse effects of aminoglycosides
5. Anti thyroid drugs
6. Rifampicin.
7. Taxanes in cancer chemotherapy.

Answer briefly: (5x1=5)

8. Two uses and two adverse effects of oral contraceptive pills

9. Mechanism of action of metoclopramide
10. Two advantages of human insulin
11. Specify the important spectrum of vancomycin
12. Rationale of estrogen in hormone replacement therapy

Name two drugs: (8x1=8)

13. Chloroquine resistant malaria.

14. Urinary tract infections
15. Immunosuppressive in organ transplantation
l 16. Irritable bowel syndrome.
17. Gram negative septicemia
u
18. Tocolytics
m 19. Aromatase inhibitors
20. Retro viral infections
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Q.P. Code: 203001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2014
Clinical Pathology and General Pathology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Q U E S T I O N PA P E R S
Essay: (8)
1. Define inflammation. Explain the sequential vascular changes in acute inflammation.
What are the outcomes of acute inflammation. (1+4+3 =8)

Short essay: (6)

2. 35 years male had low grade evening rise of temperature, loss of weight, cough and
weakness Answer the following:
• What is your probable clinical diagnosis.
• What are the investigations required for the diagnosis.
• What is the microscopic finding.
• What is the etiology of the disease (1+2+2+1=6)

Short notes: (4x4=16)

3. Role of free radicals in cell injury.
4. Pathogenesis of renal oedema
5. Semen analysis
6. Coomb’s test

Answer briefly: (4x2=8)

7. Ketonuria
8. CSF findings in pyogenic meningitis.
9. Virchow’s triad
10. Epstein bar virus induced tumors in humans.

Answer in single sentence: (4x½=2) l

u
11. Define metaplasia
12. Barr body m
13. List two urinary casts i
14. Two uses of PCV tube
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Q.P. Code: 204001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2014
Hematology and Systemic Pathology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Q U E S T I O N PA P E R S

Essay: (8)
1. Define infarction. Discuss the etiopathogenesis, morphology and complications of
myocardial infarction. (1+3+3+1=8)

Short essay: (6)

2. Five years old boy presented with recurrent fever, generalized lymphadenopathy,
hepatosplenomegaly and severe anemia. His total WBC count was more than a lakh
with numerous blasts. Answer the following:
• What is your diagnosis.
• Describe the types of blast with diagram.
• What is the bone marrow picture in this condition. (2+2+2=6)

Short notes: (4x4=16)

3. Basal cell carcinoma
4. Chronic venous congestive liver
5. Papillary carcinoma thyroid
6. Post-streptococcal glomerulonephritis.

Answer briefly: (4x2=8)

7. Cystic teratoma
8. Sickle cell anemia
9. Fibro adenoma breast.
10. Chronic osteomyelitis
l
Answer in single sentence: (4x½=2)
u
11. Russell body
m 12. What is leukoplakia.
i 13. Pigment stones
14. Curshmann spirals.
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Q.P. Code: 205001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2014
Microbiology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Q U E S T I O N PA P E R S
Essay: (10)
1. A 10 years old boy was admitted in pediatric ward with history of fever, toxaemia and
on examination. A white patch seen of fauces which bleeds on removal. He was not
immunized properly. Answer the following:
• Explain the probable diagnosis and name the causative agent
• Describe the laboratory diagnosis mentioning the methods of sample collection
• What are the complications of the disease
• How is the disease treated
• Describe the method of prophylaxis briefly (2+4+1+1+2 = 10)

Short essay: (2x5=10)

2. Pathogenesis and laboratory diagnosis of enteric fever
3. Monoclonal antibodies and its application in clinical microbiology

Short notes: (10x2=20)

4. Bacterial capsule
5. Sterilization using dry heat
6. Enrichment media with an example
7. Toxic shock syndrome
8. Differences between exotoxin and endotoxin l
9. Herd immunity u
10. Lyme disease m
11. Opsonization i
12. Differences between ‘T’ & ‘B’ lymphocytes n
13. Secretory IgA a
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Q.P. Code: 206001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2014
Microbiology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)
Q U E S T I O N PA P E R S

1. A 45 years old male complaints of intermittent high grade fever which was cyclical and
associated with rigor and chills. On examination he has hepatosplenomegaly. Answer
the following:
• What is the probable diagnosis.
• List the species of organism which can cause this type of disease
• Discuss briefly the pathogenesis of the condition
• Discuss in detail the laboratory diagnosis of this disease (1+2+3+4=10)

Short essay: (2x5=10)

2. Discuss the laboratory diagnosis of mycetoma
3. Discuss the laboratory diagnosis of hepatitis B virus Infection

Short notes: (10x2=20)

4. Rhinosporidiosis
5. Naegleria fowleri
6. Normal flora of skin
7. Hydatid cyst
8. Cryptosporidium
9. Mycotoxins
l
10. Dermatophytes
u
11. Cutaneous larva migrans
m
12. Papilloma virus
i
13. Morphology of influenza virus
n
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Q.P. Code: 207001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2014
Forensic Medicine & Toxicology
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (7)

Q U E S T I O N PA P E R S
1. A dead fetus was recovered from the dust bin. Crown heel length was 35 cms. Finger
nail marks with contusions were noted in the neck. Answer the following:
• Estimate the gestational age with reason
• Mention the ossification centers which are likely to be found in this case
• Is this fetus viable or not
• What is the cause of death (2+3+1+1=7)

Short notes: (5x3=15)

2. Signs of ante mortem hanging
3. Cross examination
4. Informed consent
5. Plumbism
6. Section 375 of Indian penal code

Answer briefly: (5x2=10)

7. Lochia
8. Bloodless dissection of neck
9. Hallucination
10. Filigree burns
11. Ectopic contusion
l
Differentiate between: (2x2=4) u
12. Complete and partial hanging m
13. Adipocere and mummification i
n
Draw and label: (2x2=4)
a
14. Skin incisions at autopsy
i
15. Longitudinal section of rifled cartridge
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Q.P. Code: 203001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, March 2014
Clinical Pathology and General Pathology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)
Q U E S T I O N PA P E R S

1. Define thrombosis. Describe the pathogenesis and pathology of arterial and venous
thrombosis (2+ 3+ 3=8)

Short essay: (6)

2. A 30 years old man presented with tiredness and numbness of feet. Investigations
showed Hb 6 g/dl TC 3500/c.mm. MCV 104fl . Answer the following:
• What is your diagnosis
• Describe the peripheral blood picture
• What are the causes of this condition (1 + 3 + 2=6)

Short notes: (4x4=16)

3. Apoptosis
4. Urinary casts
5. Oncogenes
6. Ghon complex

Answer briefly: (4x2=8)

7. Endogenous pigments
8. Characteristics of normal seminal fluid
9. Vascular changes in inflammation
10. Opportunistic infections

Answer in single sentence: (4x½=2)

11. Define hyperplasia
l 12. List two salient CSF findings in TB meningitis
13. Name two causes of proteinuria
u 14. Define dystrophic calcification with an example
m
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 GOVT. MEDICAL COLLEGE, THIRUVANANTHAPURAM

Q.P. Code: 207001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, March 2014
Forensic Medicine & Toxicology
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (7)

Q U E S T I O N PA P E R S
1. A forty years old man’s body is brought for post mortem. An oblique ligature main is
present over the neck. Dried salivary stain over right angle of mouth. Hyoid bone is intact.
Answer the following:
• What is your probable opinion regarding cause of death.
• Difference between hanging and strangulation.
• How will you differentiate ante mortem hanging from post mortem hanging.
(1+3+3=7)

Short notes: (5x3=15)

2. Color changes in contusion
3. Procedure in admission of an insane person in a mental asylum
4. Changes of body in putrefaction
5. Mercuria lentis
6. Intra cranial hemorrhage

Answer briefly: (5x2=10)

7. Carboluria
8. Burtonian line
9. Calibre of a fire arm
10. Cadaveric spasm
11. Disputed paternity l
Differentiate between: (2x2=4) u
12. Ante mortem and post mortem bruise m
13. Arsenic poisoning and cholera i
Draw and label: (2x2=4) n
14. Different types of finger prints a
15. Ligature mark pattern in strangulation. i
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Q.P. Code: 204001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, March 2014

Hematology and Systemic Pathology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)
Q U E S T I O N PA P E R S

1. Classify bone tumors. Describe the etiopathogenesis and clinico-pathological features of

osteosarcoma (2+3+3=8)
Short essay: (6)
2. 45 years old male presented with splenomegaly and anemia. His total WBC count was
1.5 lakhs per cu mm with myeloid precursors of all series in peripheral blood. Answer the
following:
• What is your diagnosis.
• Describe the peripheral blood and bone marrow findings.
• What is the cytogenetic abnormality (1+4+1=6)

Short notes: (4x4=16)

3. Acute glomerulonephritis
4. Malignant melanoma
5. Cervical intraepithelial neoplasia
6. Seminoma

Answer briefly: (4x2=8)

7. Megaloblast
8. Carcinoid
9. Clotting time
10. Lung absess

Answer in single sentence: (4x½=2)

l 11. What is paraneoplastic syndrome

12. Mention two causes of cirrhosis
u 13. Reed Sternberg cell
m 14. Name two haemoparasites.
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Q.P. Code: 205001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, March 2014
Microbiology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)

Q U E S T I O N PA P E R S
1. A 25 years old male comes to a medical outpatient department with complaints of high
fever with relative bradycardia for the past one week, he has headache, coated tongue
and hepatosplenomegaly. Answer the following:
• What is the probable diagnosis.
• What is the causative organism.
• Describe the pathogenesis of this disease.
• Discuss the laboratory diagnosis of this disease.
• Discuss the vaccines used for prevention of this disease. (1+1+3+3+2=10)

Short essay: (2x5=10)

2. Discuss about autoclave and its uses.
3. Discuss type I hypersensitivity reaction

Short notes: (10x2=20)

4. Louis Pasteur
5. Lowenstein jensen medium
6. Coagulase test
7. Bacteroides fragilis
8. Satellitism
l
9. Weil-felix reaction
u
10. Natural killer cells
m
11. Transduction
i
12. Incineration
n
13. Acinetobacter baumannii
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Q.P. Code: 206001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, March 2014
Microbiology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (10)
Q U E S T I O N PA P E R S

1. Read the following clinical history and answer the following questions
A one year old child presented with h/o inability to move the limbs associated with neck
stiffness following a bout of fever. Immunization history was not available. O/E the child
had flaccid paralysis.
• What is the probable clinical diagnosis and name the etiologic agent
• Describe the pathogenesis of the disease .
• How it is diagnosed in the lab and mention the prophylaxis available (2+3+5=10)
Short essay: (2x5=10)
2. Life cycle of dracunculsis medinensis.
3. Dengue hemorrhage fever

Short notes: (10x2=20)

4. Otomycosis.
5. Cyst of giardia.
6. Acanthamoeba.
7. Intermediate and definitive host for toxoplasma gondii.
8. Hydatid cyst
9. Egg of schistoma hematobium.
l 10. Eclipse phase in viral replication.
u 11. Significance of p24 antigen.
m 12. Enumerate enterically transmitted hepatitis viruses.
i 13. Cryptosporidium parvum
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Q.P. Code: 201001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, March 2014
Pharmacology- Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. A 28 years old man, while working on his computer in an IT company, suddenly went

Q U E S T I O N PA P E R S
blank, fell down and appeared to be unconscious. He regains consciousness in the
next 5 minutes but was confused and could not remember what happened. When he
consulted a neurologist, he was diagnosed to have absence seizures. Answer the
following:
• Name two drugs useful in absence seizures
• Explain the mechanism of action of phenytoin
• List four uses of carbamazepine
• Mention two drugs used in status epilepticus (1+2+2+1=6)

2. Enumerate  blockers. Explain any six uses and two contraindications of  blockers
(2+3+1=6)

Short notes: (5x3=15)

3. Sodium nitroprusside
4. Sevoflurane
5. Bronchodilators
6. Plasma half-life
7. Selective serotonin reuptake inhibitors

Answer briefly: (5x1=5)

8. Two uses and two adverse effects of atropine
9. Rationale for use of frusemide in acute pulmonary edema
10. Mechanism of action of diazepam
11. Two differences between heparin and warfarin
12. Mention the antidote in over dosage of morphine

Name two drugs: (8x1=8)

l
13. Supraventricular arrhythmias
14. Non sedative antihistamines
u
15. Idiopathic parkinsonism m
16. Enzyme inducers
17. Mucolytics i
18. Drugs for the prophylaxis of angina pectoris n
19. Relief of somatic pain
20. Hyperlipidemia a
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Q.P. Code: 202001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, March 2014
Pharmacology- Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. Enumerate the antibiotics which act by inhibiting cell wall synthesis. Mention the detailed
Q U E S T I O N PA P E R S

mechanism of action of any one of them on bacterial cell wall synthesis. Add a note on beta
lactamase inhibitors (2 + 2 +2 = 6)
2. Read the clinical problem and answer the following questions: 40 years old man who was on
metronidazole for amoebic dysentery went to a cocktail party where he consumed alcohol. After
some time, he started developing symptoms like flushing, burning sensation, throbbing headache,
dizziness, tightness in chest, vomiting.
• What is the reason for his symptoms.
• What are the other uses of metronidazole.
• What are the adverse effects produced by metronidazole (2 + 2 + 2 = 6)

Short notes: (5x3=15)

3. Alpha glucosidase inhibitors
4. Serious adverse effects produced by oral contraceptive pills
5. Azithromycin
6. Vinca alkaloids
7. Proton pump inhibitors
Answer briefly: (5x1=5)
8. Radical cure in plasmodium vivax infection
9. Drug used in thyrotoxic crisis
10. Super ORS
11. Adverse effects of metoclopramide
12. Antiseptics

Name two drugs: (8x1=8)

l 13. Topical anti fungals
u 14. Anti pseudomonal drugs
15. H2 blockers
m 16. Calcineurin inhibitors
i 17. Fluoroquinolones
18. Selective estrogen receptor modulators
n
19. First line anti tubercular drugs
a 20. Bisphosphonates
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Code: 203001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, April 2013
Clinical Pathology and General Pathology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)

1. Define an embolus. What are the types of emboli. Discuss the etiopathogenesis,

Q U E S T I O N PA P E R S
morphology and complications of embolism. (1+3+3+1=8)

Short essay: (6)

2. 40 yrs old female complained of easy fatigue and dyspnea. PCV 25% and Hb 5gm/dl.
MCV 40 fl, MCH 10 pg, MCHC 18 g/dL. Reticulocyte count 0.5%. Answer the following:
• What is your diagnosis
• What is the etio-pathogenesis of this condition
• What are the laboratory findings (1+3+2=6)
Short notes: (4x4=16)

3. Septic shock
4. Fatty liver
5. Granuloma
6. CSF in tuberculous meningitis.

Answer briefly: (4x2=8)

7. Anaplasia
8. Classify leprosy
9. Causes of thrombocytopenia
10. Leishmans stain

Answer in single sentence: (4x½=2)

11. What is an abscess.

12.Lipoma
13. What is lipofuscin.
14. Aim of Rothera’s test. l
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Q.P. Code: 203001 Reg. no.: …………………

Second Professional MBBS Degree Supplementary Examinations,
September 2013
Clinical Pathology and General Pathology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)
Q U E S T I O N PA P E R S

1. Define amyloidosis. Explain gross and microscopic features of organs involved in

secondary amyloidosis. Mention the special stains for amyloid. (1+4+3 =8)

Short essay: (6)

2. 50 years old female underwent abdominal surgery and was bedridden for 10 days. She
suddenly developed dyspnoea and collapsed. She died a few minutes later. Answer the
following:
• What is the diagnosis.
• What are the postmortem findings relevant to the diagnosis.
• What is the etiopathogenesis
• What are the preventive measures. (1+2+2+1=6)

Short notes: (4x4=16)

3. Modes of spread of malignant tumors with suitable examples
4. Dystrophic calcification
5. CSF findings in meningitis
6. How do you screen a blood donor. Mention the screening tests performed.

Answer briefly: (4x2=8)

7. Hypertrophy
8. Microscopic appearance of granuloma
9. Uses of buffy coat
10. Renal causes of haematuria

l Answer in single sentence: (4x½=2)

u 11. FNAC
12. Define oligospermia
m 13. List two tumor markers
i 14. Define chemotaxis
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Code: 207001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, April 2013
Forensic Medicine & Toxicology
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (7)

Q U E S T I O N PA P E R S
1. Define ‘Drunkenness’. Explain, how the state of drunkenness renders the driving of a
vehicle dangerous. What is Widmark’s formula. (2+4+1=7)

Short notes: (5x3=15)

2. Post mortem lividity
3. Estimation of time since injury in contusion
4. Functions of the state medical council
5. Examination findings in a 14 year old victim of rape
6. Neck findings in a case of death due to hanging

Answer briefly: (5x2=10)

7. Hesitation cuts
8. Contributory negligence
9. Primary impact injuries
10.Delusion
11. Testamentary capacity

Differentiate between: (2x2=4)

12. Male pelvis and female pelvis

13. Entrance wound and exit wound caused by a bullet
l
Draw and label: (2x2=4) u
14. Different types of finger prints m
15. Cross section of a rifled barrel i
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Code: 204001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, April 2013
Haematology and Systemic Pathology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary

Essay: (8)
Q U E S T I O N PA P E R S

1. Classify bone tumors. Describe the gross (including x-ray appearances) and microscopic
features of the most common malignant bone tumor (3+3+2= 8)

Short essay: (6)

2. A 53 year old male presented with pain abdomen. Investigations: Hb 8g/dl TC
70,000/cmm DC N 55 L 10 myelocyte 15 metamyelo 10 band 1 eosino 6 baso 3 platelet
count 5.8 lakh/cmm. Answer the following:
• What is your diagnosis.
• Describe the peripheral blood picture and bone marrow findings in this condition
• Name the cytogenetic abnormality associated (1+4+1=6)

Short notes: (4x4=16)

3. Hemophilia
4. Hydatidiform mole
5. Papillary carcinoma of thyroid
6. Renal cell carcinoma

Answer briefly: (4x2=8)

7. List two hematological evidences of DIC
8. Basal cell carcinoma
9. Lab diagnosis of Thalassemia
10. Cholelithiasis

Answer in single sentence: (4x½=2)

11.Auer rod
l 12.Involucrum
13.Cirrhosis
u 14.Carcinoid
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Code: 205001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, April 2013
Microbiology - Paper I
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essay: (10)
1. Read the clinical history and answer the following questions:

Q U E S T I O N PA P E R S
A 20 year old young male was admitted with history of fever with evening rise of
temperature and cough since two months. Recently he developed haemoptysis. X-ray
showed features of right lobe consolidation
• Mention the probable diagnosis and name the causative agent.
• Describe briefly the methods of laboratory diagnosis.
• What are the complications of the disease
• How the disease is treated
• What is the prophylaxis. (2+4+1+1+2 =10)
Short essay: (2x5=10)
2. Pathogenesis and lab diagnosis of syphilis.
3. Agglutination type of reaction in antigen-antibody combination.

Short notes: (10x2=20)

4. R plasmid
5. Method of moist heat sterilization.
6. Enrichment media.
7. lgM.
8. Elek’s test
9. Prophylaxis of tetanus.
10. Wool sorter’s disease. l
11. Clostridium difficile u
12. Enterotoxigenic escherichia coli m
13. Chlamydial conjunctivitis. i
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Code: 206001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, April 2013
Microbiology - Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essay: (10)

1. Read the clinical history and answer the following questions:

Q U E S T I O N PA P E R S

A 35 year old man presented to the medical OPD with a history of intractable diarrhea for
the past one week. He gave past history of multiple exposures six months back. On
clinical examination he was emaciated and oral thrush was present.
• What is the provisional diagnosis.
• Mention the different routes of transmission in this condition.
• Explain the pathogenesis of the above clinical condition.
• Describe briefly the laboratory investigations.
• What is the confirmatory test.
• Mention any four important opportunistic infections associated with this disease.
(1+1+2+3+1+2=10)
Short essay: (2x5=10)
2. Hydatid disease.
3. Pathogenesis and laboratory diagnosis of faciparum malariae.

Short notes: (10x2=20)

4. Giardiasis.
5. Cryptosporidium parvum.
6. Tinea versicolor
7. Candida albicans.
l 8. Mycotoxins.
u 9. Mucormycosis
m 10. Infectious mononucleosis.
i 11. Prophylaxis of rabies.
n 12. Inclusion bodies.
a 13. MMR vaccine.

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Code: 201001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, April 2013
Pharmacology- Paper I
Time: 3 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)
1. A 24year old man is brought to the hospital with complaints of unconsciousness , sustained
contractions (tonic) of all the body muscles followed by periods of muscle contraction alternating

Q U E S T I O N PA P E R S
with periods of relaxations(clonic) lasting 1 to 2 minutes . Answer the following:
• What are the drugs that can be prescribed to this patient.
• Describe the pharmacokinetics and adverse effects of any one such drug.
• What is the treatment of status epilepticus. (2+3+1=6)

2. Classify diuretic agents. Describe the mechanism of action, uses and adverse effects of
furosemide. (2+2+1+1=6)

Short notes: (5x3=15)

3. Calcium channel blockers

4. Drug treatment of anti cholinesterase poisoning
5. Kinetics of elimination
6. Halothane
7. Nicorandil
Answer briefly: (5x1=5)

8. Rationale of combining beta blockers with long acting nitrates

9. Clinical uses of prostaglandins
10. Mechanism of action of disulfiram
11. Flumazenil
12. Hofmann elimination
Name two drugs for: (8x1=8)

13. Drugs used in Myasthenia gravis

14. Uterine relaxants
15. Mast cell stabilizers
16. Mucolytics
l
17. Low molecular weight heparins u
18. Anti platelet drugs
m
19. Drug induced parkinsonism
20. 5HT antagonists i
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Code: 202001 Reg. no.: …………………

Second Professional MBBS Degree Examinations, April 2013
Pharmacology- Paper II
Time: 2 Hours Total Marks: 40
• Answer all questions
• Draw diagrams wherever necessary
Essays: (2x6=12)

1. A 60 year old lady is suffering from rheumatoid arthritis and has been prescribed
Q U E S T I O N PA P E R S

prednisolone. Answer the following:

• What is the mechanism of action of glucocorticoids.
• Name two glucocorticoids which have no mineralocorticoid activity
• Enumerate the adverse effects that you expect in this patient (2+1+3=6)

2. Enumerate macrolide antibiotics. Describe briefly its mechanism of action and mention
four uses. Add a note on linezolid. (1+2+1+2=6)

Short notes: (5x3=15)

3. Metronidazole
4. Cyclophosphamide
5. Mifepristone
6. Insulin analogs
7. Ciprofloxacin

Answer briefly: (5x1=5)

8. Omeprazole is used in peptic ulcer – State reason
9. Mention four adverse effects of rifampicin
10. Mention two differences between tetracycline and doxycycline
11. Treatment of multi drug resistant falciparum malaria
12. Mechanism of action of acyclovir

Name two drugs for: (8x1=8)

13. Prevention of constipation
14. Systemic antifungal drugs
15. Prevention of AIDS in the new born
16. Treatment of amoebiasis (from different groups)
l 17. Antithyroid drugs
u 18. Chemoprophylaxis of surgical site infection
19. Uterine stimulants
m 20. Lepra reactions
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