Section

4
Digestive System

36. Introduction to Digestive System ............................................................. 219

37. Mouth and Salivary Glands ..................................................................... 223
38. Stomach .................................................................................................. 230
39. Pancreas ................................................................................................. 241
40. Liver and Gallbladder .............................................................................. 249
41. Small Intestine ......................................................................................... 261
42. Large Intestine ........................................................................................ 266
43. Movements of Gastrointestinal Tract ....................................................... 270
44. Gastrointestinal Hormones ...................................................................... 281
45. Digestion, Absorption and Metabolism of Carbohydrates ....................... 287
46. Digestion, Absorption and Metabolism of Proteins .................................. 290
47. Digestion, Absorption and Metabolism of Lipids ..................................... 292
 Chapter
Introduction to
Digestive System 36
„ INTRODUCTION
„ FUNCTIONAL ANATOMY
„ WALL OF GASTROINTESTINAL TRACT
„ MUCUS LAYER
„ SUBMUCUS LAYER
„ MUSCULAR LAYER
„ SEROUS OR FIBROUS LAYER
„ NERVE SUPPLY TO GASTROINTESTINAL TRACT
„ INTRINSIC NERVE SUPPLY
„ EXTRINSIC NERVE SUPPLY

„ INTRODUCTION 5. Digestion of the food particles

6. Absorption of the digestive products (nutrients)
Digestion is defined as the process by which food is 7. Removal of unwanted substances from the body.
broken down into simple chemical substances that can
be absorbed and used as nutrients by the body. Most „ FUNCTIONAL ANATOMY OF
of the substances in the diet cannot be utilized as such.
DIGESTIVE SYSTEM
These substances must be broken into smaller particles,
so that they can be absorbed into blood and distributed Digestive system is made up of gastrointestinal tract
to various parts of the body for utilization. Digestive (GI tract) or alimentary canal and accessory organs,
system is responsible for these functions. which help in the process of digestion and absorption
Digestive process is accomplished by mechanical (Fig. 36.1). GI tract is a tubular structure extending from
and enzymatic breakdown of food into simpler chemi- the mouth up to anus, with a length of about 30 feet. It
cal compounds. A normal young healthy adult consumes opens to the external environment on both ends.
about 1 kg of solid diet and about 1 to 2 liter of liquid GI tract is formed by two types of organs:
diet every day. All these food materials are subjected to 1. Primary digestive organs.
digestive process, before being absorbed into blood and 2. Accessory digestive organs.
distributed to the tissues of the body. Digestive system
plays the major role in the digestion and absorption of 1. Primary Digestive Organs
food substances.
Thus, the functions of digestive system include: Primary digestive organs are the organs where actual
1. Ingestion or consumption of food substances digestion takes place.
2. Breaking them into small particles Primary digestive organs are:
3. Transport of small particles to different areas of the i. Mouth
digestive tract ii. Pharynx
4. Secretion of necessary enzymes and other subs- iii. Esophagus
tances for digestion iv. Stomach
 220 Section 4 t Digestive System

v. Small intestine Mucosa has three layer of structures:

vi. Large intestine. i. Epithelial lining
ii. Lamina propria
2. Accessory Digestive Organs iii. Muscularis mucosa.
Accessory digestive organs are those which help prim-
ary digestive organs in the process of digestion. Epithelial Lining
Accessory digestive organs are: Epithelial lining is in contact with the contents of GI tract.
i. Teeth The type of cells in this layer varies in different parts of
ii. Tongue GI tract. The inner surface of mouth, surface of tongue,
iii. Salivary glands inner surface of pharynx and esophagus have stratified
iv. Exocrine part of pancreas squamous epithelial cells. However, mucus membrane
v. Liver lining the other parts such as stomach, small intestine
vi. Gallbladder. and large intestine has columnar epithelial cells.

„ WALL OF GASTROINTESTINAL TRACT Lamina Propria

In general, wall of the GI tract is formed by four layers Lamina propria is formed by connective tissues, which
which are from inside out: contain fibroblasts, macrophages, lymphocytes and
1. Mucus layer eosinophils.
2. Submucus layer
3. Muscular layer Muscularis Mucosa
4. Serous or fibrous layer.
Muscularis mucosa layer consists of a thin layer of
„ 1. MUCUS LAYER smooth muscle fibers. It is absent in mouth and pharynx.
It is present from esophagus onwards.
Mucus layer is the innermost layer of the wall of GI
tract. It is also called gastrointestinal mucosa or mucus „ 2. SUBMUCUS LAYER
membrane. It faces the cavity of GI tract.
Submucus layer is also present in all parts of GI tract,
except the mouth and pharynx. It contains loose collagen
fibers, elastic fibers, reticular fibers and few cells of
connective tissue. Blood vessels, lymphatic vessels and
nerve plexus are present in this layer.

„ 3. MUSCULAR LAYER
Muscular layer in lips, cheeks and wall of pharynx
contains skeletal muscle fibers. The esophagus has both
skeletal and smooth muscle fibers. Wall of the stomach
and intestine is formed by smooth muscle fibers.
Smooth muscle fibers in stomach are arranged in
three layers:
i. Inner oblique layer
ii. Middle circular layer
iii. Outer longitudinal layer.
Smooth muscle fibers in the intestine are arranged
in two layers:
i. Inner circular layer
ii. Outer longitudinal layer.
Auerbach nerve plexus is present in between the
circular and longitudinal muscle fibers. The smooth
muscle fibers present in inner circular layer of anal
canal constitute internal anal sphincter. The external
FIGURE 36.1: Gastrointestinal tract anal sphincter is formed by skeletal muscle fibers.
 Chapter 36 t Introduction to Digestive System 221

„ 4. SEROUS OR FIBROUS LAYER

Outermost layer of the wall of GI tract is either serous or
fibrous in nature. The serous layer is also called serosa
or serous membrane and it is formed by connective
tissue and mesoepithelial cells. It covers stomach, small
intestine and large intestine.
The fibrous layer is otherwise called fibrosa and it
is formed by connective tissue. It covers pharynx and
esophagus.

„ NERVE SUPPLY TO
GASTROINTESTINAL TRACT
GI tract has two types of nerve supply: FIGURE 36.2: Structure of intestinal wall with
I. Intrinsic nerve supply intrinsic nerve plexus
II. Extrinsic nerve supply.
Functions of Meissner plexus
„ INTRINSIC NERVE SUPPLY –
ENTERIC NERVOUS SYSTEM Function of Meissner plexus is the regulation of
Intrinsic nerves to GI tract form the enteric nervous secretory functions of GI tract. These nerve fibers cause
system that controls all the secretions and movements constriction of blood vessels of GI tract.
of GI tract. Enteric nervous system is present within the
wall of GI tract from esophagus to anus. Nerve fibers „ EXTRINSIC NERVE SUPPLY
of this system are interconnected and form two major
Extrinsic nerves that control the enteric nervous system
networks called
are from autonomic nervous system. Both sympathetic
1. Auerbach plexus
2. Meissner plexus. and parasympathetic divisions of autonomic nervous
These nerve plexus contain nerve cell bodies, system innervate the GI tract (Fig. 36.3).
processes of nerve cells and the receptors. The recep-
tors in the GI tract are stretch receptors and chemo- Sympathetic Nerve Fibers
receptors. Enteric nervous system is controlled by Preganglionic sympathetic nerve fibers to GI tract arise
extrinsic nerves. from lateral horns of spinal cord between fifth thoracic
and second lumbar segments (T5 to L2). From here, the
1. Auerbach Plexus
fibers leave the spinal cord, pass through the ganglia of
Auerbach plexus is also known as myenteric nerve sympathetic chain without having any synapse and then
plexus. It is present in between the inner circular muscle terminate in the celiac and mesenteric ganglia. The
layer and the outer longitudinal muscle layer (Fig. 36.2). postganglionic fibers from these ganglia are distributed
Functions of Auerbach plexus throughout the GI tract.

Major function of this plexus is to regulate the move- Functions of sympathetic nerve fibers
ments of GI tract. Some nerve fibers of this plexus
Sympathetic nerve fibers inhibit the movements
accelerate the movements by secreting the excitatory
and decrease the secretions of GI tract by secreting
neurotransmitter substances like acetylcholine, sero-
the neurotransmitter noradrenaline. It also causes
tonin and substance P. Other fibers of this plexus
inhibit the GI motility by secreting the inhibitory neuro- constriction of sphincters.
transmitters such as vasoactive intestinal polypeptide
(VIP), neurotensin and enkephalin. Parasympathetic Nerve Fibers

Parasympathetic nerve fibers to GI tract pass through

2. Meissner Nerve Plexus some of the cranial nerves and sacral nerves. The pre-
Meissner plexus is otherwise called submucus nerve ganglionic and postganglionic parasympathetic nerve
plexus. It is situated in between the muscular layer and fibers to mouth and salivary glands pass through facial
submucosal layer of GI tract. and glossopharyngeal nerves.
 222 Section 4 t Digestive System

FIGURE 36.3: Extrinsic nerve supply to GI tract.

T5 = 5th thoracic segment of spinal cord
L1 = 1st lumbar segment of spinal cord
S2 = 2nd sacral segment of spinal cord

Preganglionic parasympathetic nerve fibers to eso- with the postganglionic nerve cells in the myenteric and
phagus, stomach, small intestine and upper part of large submucus plexus.
intestine pass through vagus nerve. Preganglionic nerve Functions of parasympathetic nerve fibers
fibers to lower part of large intestine arise from second,
Parasympathetic nerve fibers accelerate the move-
third and fourth sacral segments (S2, S3 and S4) of ments and increase the secretions of GI tract. The
spinal cord and pass through pelvic nerve. All these neurotransmitter secreted by the parasympathetic nerve
preganglionic parasympathetic nerve fibers synapse fibers is acetylcholine (Ach).
 Chapter
Mouth and Salivary Glands
37
„ FUNCTIONAL ANATOMY OF MOUTH
„ FUNCTIONS OF MOUTH
„ SALIVARY GLANDS
„ PROPERTIES AND COMPOSITION OF SALIVA
„ FUNCTIONS OF SALIVA
„ REGULATION OF SALIVARY SECRETION
„ EFFECT OF DRUGS AND CHEMICALS ON SALIVARY SECRETION
„ APPLIED PHYSIOLOGY

„ FUNCTIONAL ANATOMY OF MOUTH „ MAJOR SALIVARY GLANDS

Mouth is otherwise known as oral cavity or buccal Major glands are:
cavity. It is formed by cheeks, lips and palate. It encloses 1. Parotid glands
the teeth, tongue and salivary glands. Mouth opens
2. Submaxillary or submandibular glands
anteriorly to the exterior through lips and posteriorly
through fauces into the pharynx. 3. Sublingual glands.
Digestive juice present in the mouth is saliva, which
is secreted by the salivary glands. 1. Parotid Glands

„ FUNCTIONS OF MOUTH Parotid glands are the largest of all salivary glands,
situated at the side of the face just below and in front of
Primary function of mouth is eating and it has few other
the ear. Each gland weighs about 20 to 30 g in adults.
important functions also.
Secretions from these glands are emptied into the oral
Functions of mouth include:
1. Ingestion of food materials cavity by Stensen duct. This duct is about 35 mm to 40
2. Chewing the food and mixing it with saliva mm long and opens inside the cheek against the upper
3. Appreciation of taste of the food second molar tooth (Fig. 37.1).
4. Transfer of food (bolus) to the esophagus by
swallowing 2. Submaxillary Glands
5. Role in speech
6. Social functions such as smiling and other Submaxillary glands or submandibular glands are
expressions. located in submaxillary triangle, medial to mandible.
Each gland weighs about 8 to 10 g. Saliva from these
„ SALIVARY GLANDS glands is emptied into the oral cavity by Wharton duct,
In humans, the saliva is secreted by three pairs of major which is about 40 mm long. The duct opens at the side
(larger) salivary glands and some minor (small) salivary of frenulum of tongue, by means of a small opening on
glands. the summit of papilla called caruncula sublingualis.
 224 Section 4 t Digestive System

TABLE 37.1: Ducts of major salivary glands

Gland Duct
Parotid gland Stensen duct
Submaxillary gland Wharton duct
Sublingual gland Ducts of Rivinus/Bartholin duct

5. Palatal Glands
Palatal glands are found beneath the mucus membrane
of the soft palate.

„ CLASSIFICATION OF SALIVARY GLANDS

Salivary glands are classified into three types, based on
the type of secretion:

1. Serous Glands
FIGURE 37.1: Major salivary glands Serous glands are mainly made up of serous cells. These
glands secrete thin and watery saliva. Parotid glands
3. Sublingual Glands and lingual serous glands are the serous glands.

Sublingual glands are the smallest salivary glands 2. Mucus Glands

situated in the mucosa at the floor of the mouth. Each
gland weighs about 2 to 3 g. Saliva from these glands is Mucus glands are mainly made up of mucus cells.
poured into 5 to 15 small ducts called ducts of Rivinus. These glands secrete thick, viscous saliva with high
These ducts open on small papillae beneath the tongue. mucin content. Lingual mucus glands, buccal glands
One of the ducts is larger and it is called Bartholin duct and palatal glands belong to this type.
(Table 37.1). It drains the anterior part of the gland and
opens on caruncula sublingualis near the opening of 3. Mixed Glands
submaxillary duct. Mixed glands are made up of both serous and mucus
cells. Submandibular, sublingual and labial glands are
„ MINOR SALIVARY GLANDS the mixed glands.
1. Lingual Mucus Glands „ STRUCTURE AND DUCT SYSTEM
Lingual mucus glands are situated in posterior one third OF SALIVARY GLANDS
of the tongue, behind circumvallate papillae and at the Salivary glands are formed by acini or alveoli. Each
tip and margins of tongue. acinus is formed by a small group of cells which surround
a central globular cavity. Central cavity of each acinus
2. Lingual Serous Glands is continuous with the lumen of the duct. The fine duct
Lingual serous glands are located near circumvallate draining each acinus is called intercalated duct. Many
papillae and filiform papillae. intercalated ducts join together to form intralobular duct.
Few intralobular ducts join to form interlobular ducts,
3. Buccal Glands which unite to form the main duct of the gland (Fig. 37.2).
A gland with this type of structure and duct system is
Buccal glands or molar glands are present between called racemose type (racemose = bunch of grapes).
the mucus membrane and buccinator muscle. Four to
five of these are larger and situated outside buccinator, „ PROPERTIES AND COMPOSITION
around the terminal part of parotid duct. OF SALIVA
4. Labial Glands „ PROPERTIES OF SALIVA
Labial glands are situated beneath the mucus membrane 1. Volume: 1000 mL to 1500 mL of saliva is secreted
around the orifice of mouth. per day and it is approximately about 1 mL/minute.
 Chapter 37 t Mouth and Salivary Glands 225

2. Reaction: Mixed saliva from all the glands is slightly

acidic with pH of 6.35 to 6.85
3. Specific gravity: It ranges between 1.002 and 1.012
4. Tonicity: Saliva is hypotonic to plasma.

„ COMPOSITION OF SALIVA

Mixed saliva contains 99.5% water and 0.5% solids.

Composition of saliva is given in Figure 37.3.

„ FUNCTIONS OF SALIVA
Saliva is a very essential digestive juice. Since it has many
functions, its absence leads to many inconveniences.

„ 1. PREPARATION OF FOOD FOR SWALLOWING

When food is taken into the mouth, it is moistened and
dissolved by saliva. The mucus membrane of mouth is
also moistened by saliva. It facilitates chewing. By the
movement of tongue, the moistened and masticated
FIGURE 37.2: Diagram showing acini and duct system food is rolled into a bolus. Mucin of saliva lubricates the
in salivary glands
bolus and facilitates swallowing.
Contribution by each major salivary gland is:
„ 2. APPRECIATION OF TASTE
i. Parotid glands : 25%
ii. Submaxillary glands : 70% Taste is a chemical sensation. By its solvent action,
iii. Sublingual glands : 5%. saliva dissolves the solid food substances, so that the

FIGURE 37.3: Composition of saliva

 226 Section 4 t Digestive System

dissolved substances can stimulate the taste buds. The iv. Lactoferrin of saliva also has antimicrobial
stimulated taste buds recognize the taste. property.
v. Proline-rich proteins and lactoferrin protect the
„ 3. DIGESTIVE FUNCTION teeth by stimulating enamel formation.
Saliva has three digestive enzymes, namely salivary vi. Immunoglobulin IgA in saliva also has
amylase, maltase and lingual lipase (Table 37.1). antibacterial and antiviral actions.
vii. Mucin present in the saliva protects the mouth
Salivary Amylase by lubricating the mucus membrane of mouth.

Salivary amylase is a carbohydrate-digesting (amylolytic) „ ROLE IN SPEECH

enzyme. It acts on cooked or boiled starch and converts
it into dextrin and maltose. Though starch digestion By moistening and lubricating soft parts of mouth and
starts in the mouth, major part of it occurs in stomach lips, saliva helps in speech. If the mouth becomes dry,
because, food stays only for a short time in the mouth. articulation and pronunciation becomes difficult.
Optimum pH necessary for the activation of salivary
amylase is 6. Salivary amylase cannot act on cellulose. „ EXCRETORY FUNCTION
Many substances, both organic and inorganic, are
Maltase
excreted in saliva. It excretes substances like mercury,
Maltase is present only in traces in human saliva and it potassium iodide, lead, and thiocyanate. Saliva also
converts maltose into glucose. excretes some viruses such as those causing rabies
and mumps.
Lingual Lipase In some pathological conditions, saliva excretes
certain substances, which are not found in saliva under
Lingual lipase is a lipid-digesting (lipolytic) enzyme. It
normal conditions. Example is glucose in diabetes
is secreted from serous glands situated on the posterior
mellitus. In certain conditions, some of the normal
aspect of tongue. It digests milk fats (pre-emulsified
constituents of saliva are excreted in large quantities.
fats). It hydrolyzes triglycerides into fatty acids and
For example, excess urea is excreted in saliva during
diacylglycerol (Table 37.2).
nephritis and excess calcium is excreted during
hyperparathyroidism.
„ 4. CLEANSING AND PROTECTIVE FUNCTIONS
i. Due to the constant secretion of saliva, the „ REGULATION OF BODY TEMPERATURE
mouth and teeth are rinsed and kept free off
In dogs and cattle, excessive dripping of saliva during
food debris, shed epithelial cells and foreign
panting helps in the loss of heat and regulation of body
particles. In this way, saliva prevents bacterial
temperature. However, in human beings, sweat glands
growth by removing materials, which may serve
play a major role in temperature regulation and saliva
as culture media for the bacterial growth.
does not play any role in this function.
ii. Enzyme lysozyme of saliva kills some bacteria
such as staphylococcus, streptococcus and
„ REGULATION OF WATER BALANCE
brucella.
iii. Proline-rich proteins present in saliva posses When the body water content decreases, salivary secre-
antimicrobial property and neutralize the toxic tion also decreases. This causes dryness of the mouth
substances such as tannins. Tannins are present and induces thirst. When water is taken, it quenches the
in many food substances including fruits. thirst and restores the body water content.

TABLE 37.2: Digestive enzymes of saliva

Enzyme Source of secretion Activator Action

Salivary amylase All salivary glands Acid medium Converts starch into maltose
Maltase Major salivary glands Acid medium Converts maltose into glucose
Lingual lipase Lingual glands Acid medium Converts triglycerides of milk fat into fatty
acids and diacylglycerol
 Chapter 37 t Mouth and Salivary Glands 227

„ REGULATION OF SALIVARY SECRETION pass through the tympanic branch of glossopharyngeal

nerve, tympanic plexus and lesser petrosal nerve and
Salivary secretion is regulated only by nervous mech- end in otic ganglion (Fig. 37.5).
anism. Autonomic nervous system is involved in the Postganglionic fibers arise from this ganglion and
regulation of salivary secretion. supply the parotid gland by passing through auriculo-
temporal branch in mandibular division of trigeminal
„ NERVE SUPPLY TO SALIVARY GLANDS nerve.
Salivary glands are supplied by both parasympathetic
and sympathetic divisions of autonomic nervous system. Function of Parasympathetic Fibers
Stimulation of parasympathetic fibers of salivary glands
„ PARASYMPATHETIC FIBERS causes secretion of saliva with large quantity of water.
It is because the parasympathetic fibers activate the
Parasympathetic Fibers to Submandibular acinar cells and dilate the blood vessels of salivary
and Sublingual Glands glands. However, the amount of organic constituents in
Parasympathetic preganglionic fibers to submandibular saliva is less. The neurotransmitter is acetylcholine.
and sublingual glands arise from the superior salivatory
nucleus, situated in pons. After taking origin from this „ SYMPATHETIC FIBERS
nucleus, the preganglionic fibers run through nervus Sympathetic preganglionic fibers to salivary glands
intermedius of Wrisberg, geniculate ganglion, the motor arise from the lateral horns of first and second thoracic
fibers of facial nerve, chorda tympani branch of facial segments of spinal cord. The fibers leave the cord
nerve and lingual branch of trigeminal nerve and finally through the anterior nerve roots and end in superior
reach the submaxillary ganglion (Fig. 37.4). cervical ganglion of the sympathetic chain.
Postganglionic fibers arising from this ganglion Postganglionic fibers arise from this ganglion and
supply the submaxillary and sublingual glands. are distributed to the salivary glands along the nerve
plexus, around the arteries supplying the glands.
Parasympathetic Fibers to Parotid Gland
Function of Sympathetic Fibers
Parasympathetic preganglionic fibers to parotid gland
arise from inferior salivatory nucleus situated in the Stimulation of sympathetic fibers causes secretion of
upper part of medulla oblongata. From here, the fibers saliva, which is thick and rich in organic constituents such

FIGURE 37.4: Parasympathetic nerve supply to submaxillary and sublingual glands

 228 Section 4 t Digestive System

„ EFFECT OF DRUGS AND CHEMICALS

ON SALIVARY SECRETION
Substances which increase salivary secretion
1. Sympathomimetic drugs like adrenaline and
ephedrine.
2. Parasympathomimetic drugs like acetylcholine,
pilocarpine, muscarine and physostigmine.
3. Histamine.
Substances which decrease salivary secretion
1. Sympathetic depressants like ergotamine and
dibenamine.
2. Parasympathetic depressants like atropine and
scopolamine.
3. Anesthetics such as chloroform and ether stimulate
the secretion of saliva. However, deep anesthesia
decreases the secretion due to central inhibition.

„ APPLIED PHYSIOLOGY
„ HYPOSALIVATION
FIGURE 37.5: Parasympathetic nerve supply to parotid gland
Reduction in the secretion of saliva is called
hyposalivation. It is of two types, namely temporary
as mucus. It is because, these fibers activate the acinar
hyposalivation and permanent hyposalivation.
cells and cause vasoconstriction. The neurotransmitter
1. Temporary hyposalivation occurs in:
is noradrenaline.
i. Emotional conditions like fear.
ii. Fever.
„ REFLEX REGULATION OF
SALIVARY SECRETION iii. Dehydration.
2. Permanent hyposalivation occurs in:
Salivary secretion is regulated by nervous mechanism i. Sialolithiasis (obstruction of salivary duct).
through reflex action. ii. Congenital absence or hypoplasia of salivary
Salivary reflexes are of two types: glands.
1. Unconditioned reflex. iii. Bell palsy (paralysis of facial nerve).
2. Conditioned reflex.
„ HYPERSALIVATION
1. Unconditioned Reflex
Excess secretion of saliva is known as hypersalivation.
Unconditioned reflex is the inborn reflex that is present
Physiological condition when hypersalivation occurs is
since birth. It does not need any previous experience
pregnancy. Hypersalivation in pathological conditions is
(Chapter 162). This reflex induces salivary secretion
called ptyalism, sialorrhea, sialism or sialosis.
when any substance is placed in the mouth. It is due to
Hypersalivation occurs in the following pathological
the stimulation of nerve endings in the mucus membrane
conditions:
of the oral cavity.
1. Decay of tooth or neoplasm (abnormal new growth
or tumor) in mouth or tongue due to continuous
2. Conditioned Reflex
irritation of nerve endings in the mouth.
Conditioned reflex is the one that is acquired by 2. Disease of esophagus, stomach and intestine.
experience and it needs previous experience (Chapter 3. Neurological disorders such as cerebral palsy, mental
162). Presence of food in the mouth is not necessary to retardation, cerebral stroke and parkinsonism.
elicit this reflex. The stimuli for this reflex are the sight, 4. Some psychological and psychiatric conditions.
smell, hearing or thought of food. 5. Nausea and vomiting.
 Chapter 37 t Mouth and Salivary Glands 229

„ OTHER DISORDERS procedure, some of the parasympathetic nerve fibers to

salivary glands may be severed. During the regeneration,
In addition to hyposalivation and hypersalivation,
some of these nerve fibers, which run along with chorda
salivary secretion is affected by other disorders also,
tympani branch of facial nerve may deviate and join with
which include: the nerve fibers supplying sweat glands. When the food
1. Xerostomia is placed in the mouth, salivary secretion is associated
2. Drooling with sweat secretion.
3. Chorda tympani syndrome
4. Paralytic secretion of saliva 4. Paralytic Secretion of Saliva
5. Augmented secretion of saliva
6. Mumps When the parasympathetic nerve to salivary gland
7. Sjögren syndrome. is cut in experimental animals, salivary secretion
increases for first three weeks and later diminishes;
1. Xerostomia finally it stops at about sixth week. The increased
secretion of saliva after cutting the parasympathetic
Xerostomia means dry mouth. It is also called pasties or nerve fibers is called paralytic secretion. It is because
cottonmouth. It is due to hyposalivation or absence of of hyperactivity of sympathetic nerve fibers to salivary
salivary secretion (aptyalism). glands after cutting the parasympathetic fibers. These
Causes hyperactive sympathetic fibers release large amount
of catecholamines, which induce paralytic secretion.
i. Dehydration or renal failure. Moreover, the acinar cells of the salivary glands become
ii. Sjögren syndrome (see below). hypersensitive to catecholamines after denervation. The
iii. Radiotherapy. paralytic secretion does not occur after the sympathetic
iv. Trauma to salivary gland or their ducts. nerve fibers to salivary glands are cut.
v. Side effect of some drugs like antihistamines,
antidepressants, monoamine oxidase inhibitors, 5. Augmented Secretion of Saliva
antiparkinsonian drugs and antimuscarinic drugs. If the nerves supplying salivary glands are stimulated
vi. Shock. twice, the amount of saliva secreted by the second
vii. After smoking marijuana (psychoactive com- stimulus is more than the amount secreted by the first
pound from the plant Cannabis). stimulus. It is because, the first stimulus increases
Xerostomia causes difficulties in mastication, swa­ excitability of acinar cells, so that when the second stimulus
llowing and speech. It also causes halitosis (bad breath; is applied, the salivary secretion is augmented.
exhalation of unpleasant odors).
6. Mumps
2. Drooling Mumps is the acute viral infection affecting the parotid
Uncontrolled flow of saliva outside the mouth is called glands. The virus causing this disease is paramyxovirus.
drooling. It is often called ptyalism. It is common in children who are not immunized. It
occurs in adults also. Features of mumps are puffiness
Causes of cheeks (due to swelling of parotid glands), fever, sore
Drooling occurs because of excess production of saliva, in throat and weakness. Mumps affects meninges, gonads
association with inability to retain saliva within the mouth. and pancreas also.
Drooling occurs in the following conditions:
7. Sjögren Syndrome
i. During teeth eruption in children.
ii. Upper respiratory tract infection or nasal allergies Sjögren syndrome is an autoimmune disorder in which
in children. the immune cells destroy exocrine glands such as
iii. Difficulty in swallowing. lacrimal glands and salivary glands. It is named after
iv. Tonsillitis. Henrik Sjögren who discovered it. Common symptoms
v. Peritonsillar abscess. of this syndrome are dryness of the mouth due to lack
of saliva (xerostomia), persistent cough and dryness of
3. Chorda Tympani Syndrome eyes. In some cases, it causes dryness of skin, nose and
vagina. In severe conditions, the organs like kidneys,
Chorda tympani syndrome is the condition characterized lungs, liver, pancreas, thyroid, blood vessels and brain
by sweating while eating. During trauma or surgical are affected.
 Chapter
Stomach
38
„ FUNCTIONAL ANATOMY OF STOMACH
„ GLANDS OF STOMACH – GASTRIC GLANDS
„ FUNCTIONS OF STOMACH
„ PROPERTIES AND COMPOSITION OF GASTRIC JUICE
„ FUNCTIONS OF GASTRIC JUICE
„ SECRETION OF GASTRIC JUICE
„ REGULATION OF GASTRIC SECRETION
„ COLLECTION OF GASTRIC JUICE
„ GASTRIC ANALYSIS
„ APPLIED PHYSIOLOGY

„ FUNCTIONAL ANATOMY OF STOMACH 3. Body or Corpus

Stomach is a hollow organ situated just below the Body is the largest part of stomach forming about 75%
diaphragm on the left side in the abdominal cavity. to 80% of the whole stomach. It extends from just below
Volume of empty stomach is 50 mL. Under normal the fundus up to the pyloric region (Fig. 38.1).
conditions, it can expand to accommodate 1 L to 1.5 L of
solids and liquids. However, it is capable of expanding 4. Pyloric Region
still further up to 4 L.
Pyloric region has two parts, antrum and pyloric canal.
„ PARTS OF STOMACH The body of stomach ends in antrum. Junction between
body and antrum is marked by an angular notch called
In humans, stomach has four parts: incisura angularis. Antrum is continued as the narrow
1. Cardiac region canal, which is called pyloric canal or pyloric end. Pyloric
2. Fundus canal opens into first part of small intestine called duo­
3. Body or corpus denum. The opening of pyloric canal is guarded by a sphin­
4. Pyloric region. cter called pyloric sphincter. It opens towards duodenum.
Stomach has two curvatures. One on the right side
1. Cardiac Region is lesser curvature and the other on left side is greater
Cardiac region is the upper part of the stomach where curvature.
esophagus opens. The opening is guarded by a sphinc­
ter called cardiac sphincter, which opens only towards „ STRUCTURE OF STOMACH WALL
stomach. This portion is also known as cardiac end.
Stomach wall is formed by four layers of structures:
1. Outer serous layer: Formed by peritoneum
2. Fundus
2. Muscular layer: Made up of three layers of smooth
Fundus is a small dome­shaped structure. It is elevated muscle fibers, namely inner oblique, middle circular
above the level of esophageal opening. and outer longitudinal layers
 Chapter 38 t Stomach 231

„ STRUCTURE OF GASTRIC GLANDS

1. Fundic Glands
Fundic glands are considered as the typical gastric
glands (Fig. 38.2). These glands are long and tubular.
Each gland has three parts, viz. body, neck and
isthmus.
Cells of fundic glands
1. Chief cells or pepsinogen cells
2. Parietal cells or oxyntic cells
3. Mucus neck cells
4. Enterochromaffin (EC) cells or Kulchitsky cells
5. Enterochromaffin­like (ECL) cells.
Parietal cells are different from other cells of the
gland because of the presence of canaliculi (singular
FIGURE 38.1: Parts of stomach = canaliculus). Parietal cells empty their secretions into
the lumen of the gland through the canaliculi. But, other
cells empty their secretions directly into lumen of the
3. Submucus layer: Formed by areolar tissue, blood gland.
vessels, lymph vessels and Meissner nerve plexus.
4. Inner mucus layer: Lined by mucus­secreting 2. Pyloric Glands
columnar epithelial cells. The gastric glands are
Pyloric glands are short and tortuous in nature. These
situated in this layer. Under resting conditions,
glands are formed by G cells, mucus cells, EC cells and
the mucosa of the stomach is thrown into many
ECL cells.
folds. These folds are called rugae. The rugae
disappear when the stomach is distended after 3. Cardiac Glands
meals. Throughout the inner mucus layer, small
depressions called gastric pits are present. Glands Cardiac glands are also short and tortuous in structure,
of the stomach open into these pits. Inner surface of with many mucus cells. EC cells, ECL cells and chief
mucus layer is covered by 2 mm thick mucus. cells are also present in the cardiac glands

„ GLANDS OF STOMACH –
GASTRIC GLANDS
Glands of the stomach or gastric glands are tubular
structures made up of different types of cells. These
glands open into the stomach cavity via gastric pits.

„ CLASSIFICATION OF GLANDS
OF THE STOMACH
Gastric glands are classified into three types, on the
basis of their location in the stomach:
1. Fundic glands or main gastric glands or oxyntic
glands: Situated in body and fundus of stomach
2. Pyloric glands: Present in the pyloric part of the
stomach
3. Cardiac glands: Located in the cardiac region of the
stomach. FIGURE 38.2: Gastric glands
 232 Section 4 t Digestive System

Enteroendocrine Cells „ 4. HEMOPOIETIC FUNCTION

Enteroendocrine cells are the hormone­secreting cells Refer functions of gastric juice.
present in the glands or mucosa of gastrointestinal tract,
particularly stomach and intestine. The enteroendocrine „ 5. EXCRETORY FUNCTION
cells present in gastric glands are G cells, EC cells and Many substances like toxins, alkaloids and metals are
ECL cells (Table 38.1). excreted through gastric juice.

„ FUNCTIONS OF GASTRIC GLANDS „ PROPERTIES AND COMPOSITION

Function of the gastric gland is to secrete gastric juice. OF GASTRIC JUICE
Secretory activities of different cells of gastric glands
Gastric juice is a mixture of secretions from different
and enteroendocrine cells are listed in Table 38.1.
gastric glands.
„ FUNCTIONS OF STOMACH „ PROPERTIES OF GASTRIC JUICE
„ 1. MECHANICAL FUNCTION Volume : 1200 mL/day to 1500 mL/day.
Reaction : Gastric juice is highly acidic with a pH
i. Storage Function of 0.9 to 1.2. Acidity of gastric juice is
Food is stored in the stomach for a long period, i.e. due to the presence of hydrochloric
for 3 to 4 hours and emptied into the intestine slowly. acid.
The maximum capacity of stomach is up to 1.5 L. Slow Specific gravity : 1.002 to 1.004
emptying of stomach provides enough time for proper
digestion and absorption of food substances in the small „ COMPOSITION OF GASTRIC JUICE
intestine. Gastric juice contains 99.5% of water and 0.5% solids.
Solids are organic and inorganic substances. Refer Fig.
ii. Formation of Chyme 38.3 for composition of gastric juice.
Peristaltic movements of stomach mix the bolus with
gastric juice and convert it into the semisolid material „ FUNCTIONS OF GASTRIC JUICE
known as chyme.
„ 1. DIGESTIVE FUNCTION
„ 2. DIGESTIVE FUNCTION Gastric juice acts mainly on proteins. Proteolytic enzymes
Refer functions of gastric juice. of the gastric juice are pepsin and rennin (Table 38.2).
Gastric juice also contains some other enzymes like
„ 3. PROTECTIVE FUNCTION gastric lipase, gelatinase, urase and gastric amylase.
Refer functions of gastric juice. Pepsin
TABLE 38.1: Secretory function of cells in gastric glands Pepsin is secreted as inactive pepsinogen. Pepsinogen
Cell Secretory products is converted into pepsin by hydrochloric acid. Optimum
Pepsinogen pH for activation of pepsinogen is below 6.
Rennin
Chief cells Lipase Action of pepsin
Gelatinase
Urase
Pepsin converts proteins into proteoses, peptones and
polypeptides. Pepsin also causes curdling and digestion
Hydrochloric acid
Parietal cells of milk (casein).
Intrinsic factor of Castle
Mucus neck cells Mucin Gastric Lipase
G cells Gastrin
Gastric lipase is a weak lipolytic enzyme when compared
Enterochromaffin (EC) cells Serotonin
to pancreatic lipase. It is active only when the pH is
Enterochromaffin­like (ECL) cells Histamine between 4 and 5 and becomes inactive at a pH below
 Chapter 38 t Stomach 233

2.5. Gastric lipase is a tributyrase and it hydrolyzes Vitamin B12 is an important maturation factor during
tributyrin (butter fat) into fatty acids and glycerols. erythropoiesis. Absence of intrinsic factor in gastric
juice causes deficiency of vitamin B12, leading to
Actions of Other Enzymes of Gastric Juice pernicious anemia (Chapter 14).
i. Gelatinase: Degrades type I and type V gelatin
and type IV and V collagen (which are proteo­ „ PROTECTIVE FUNCTION –
glycans in meat) into peptides FUNCTION OF MUCUS
ii. Urase: Acts on urea and produces ammonia Mucus is a mucoprotein, secreted by mucus neck cells
iii. Gastric amylase: Degrades starch (but its action of the gastric glands and surface mucus cells in fundus,
is insignificant) body and other parts of stomach. It protects the gastric
iv. Rennin: Curdles milk (present in animals only). wall by the following ways:

„ 2. HEMOPOIETIC FUNCTION Mucus:

Intrinsic factor of Castle, secreted by parietal cells of i. Protects the stomach wall from irritation or
gastric glands plays an important role in erythropoiesis. mechanical injury, by virtue of its high viscosity.
It is necessary for the absorption of vitamin B12 (which ii. Prevents the digestive action of pepsin on the
is called extrinsic factor) from GI tract into the blood. wall of the stomach, particularly gastric mucosa.

FIGURE 38.3: Composition of gastric juice

TABLE 38.2: Digestive enzymes of gastric juice

Enzyme Activator Substrate End products

Pepsin Hydrochloric acid Proteins Proteoses, peptones and polypeptides
Gastric lipase Acid medium Triglycerides of butter Fatty acids and glycerols
Gastric amylase Acid medium Starch Dextrin and maltose (negligible action)
Gelatinase Acid medium Gelatin and collagen of meat Peptides
Urase Acid medium Urea Ammonia
 234 Section 4 t Digestive System

iii. Protects the gastric mucosa from hydrochloric Factors Stimulating the Secretion
acid of gastric juice because of its alkaline of Hydrochloric Acid
nature and its acid­combining power.
1. Gastrin
2. Histamine
„ 4. FUNCTIONS OF HYDROCHLORIC ACID
3. Vagal stimulation.
Hydrochloric acid is present in the gastric juice:
i. Activates pepsinogen into pepsin Factors Inhibiting the Secretion
ii. Kills some of the bacteria entering the stomach of Hydrochloric Acid
along with food substances. This action is called 1. Secretin
bacteriolytic action 2. Gastric inhibitory polypeptide
iii. Provides acid medium, which is necessary for 3. Peptide YY.
the action of hormones.
„ REGULATION OF GASTRIC SECRETION
„ SECRETION OF GASTRIC JUICE
Regulation of gastric secretion and intestinal secretion
„ SECRETION OF PEPSINOGEN is studied by some experimental procedures.

Pepsinogen is synthesized from amino acids in the „ METHODS OF STUDY

ribosomes attached to endoplasmic reticulum in chief
cells. Pepsinogen molecules are packed into zymogen 1. Pavlov Pouch
granules by Golgi apparatus. Pavlov pouch is a small part of the stomach that is
When zymogen granule is secreted into stomach incompletely separated from the main portion and made
from chief cells, the granule is dissolved and pepsinogen into a small bag­like pouch (Fig. 38.5). Pavlov pouch
is released into gastric juice. Pepsinogen is activated was designed by the Russian scientist Pavlov, in a dog
into pepsin by hydrochloric acid. during his studies on conditioned reflexes.
„ SECRETION OF HYDROCHLORIC ACID Procedure

According to Davenport theory, hydrochloric acid To prepare a Pavlov pouch, stomach of an anesthetized
secretion is an active process that takes place in the dog is divided into a larger part and a smaller part by
canaliculi of parietal cells in gastric glands. The energy making an incomplete incision. The mucus membrane
for this process is derived from oxidation of glucose.
Carbon dioxide is derived from metabolic activities
of parietal cell. Some amount of carbon dioxide is
obtained from blood also. It combines with water to form
carbonic acid in the presence of carbonic anhydrase.
This enzyme is present in high concentration in parietal
cells. Carbonic acid is the most unstable compound and
immediately splits into hydrogen ion and bicarbonate
ion. The hydrogen ion is actively pumped into the
canaliculus of parietal cell.
Simultaneously, the chloride ion is also pumped
into canaliculus actively. The chloride is derived from
sodium chloride in the blood. Now, the hydrogen ion
combines with chloride ion to form hydrochloric acid. To
compensate the loss of chloride ion, the bicarbonate ion
from parietal cell enters the blood and combines with
sodium to form sodium bicarbonate. Thus, the entire
process is summarized as (Fig. 38.4):
FIGURE 38.4: Secretion of hydrochloric acid in the
CO2 + H2O + NaCl → HCl + NaHCO3 parietal cell of gastric gland
 Chapter 38 t Stomach 235

is completely divided. A small part of muscular coat 3. Bickel Pouch

called isthmus is retained. Isthmus connects the two
In this, even the sympathetic nerve fibers are cut by
parts.
removing the blood vessels. So, Bickel pouch is a totally
The cut edges of major portions are stitched. Smaller denervated pouch.
part is also stitched, leaving a small outlet. This outlet
is brought out through the abdominal wall and used to Uses of Bickel pouch
drain the pouch. Bickel pouch is used to demonstrate the role of hormones
Nerve supply of Pavlov pouch in gastric secretion.

Pavlov pouch receives parasympathetic (vagus) nerve 4. Farrel and Ivy Pouch
fibers through isthmus and sympathetic fibers through
blood vessels. Farrel and Ivy pouch is prepared by completely removing
the Bickel pouch from the stomach and transplanting it
Use of Pavlov pouch in the subcutaneous tissue of abdominal wall or thoracic
Pavlov pouch is used to demonstrate the different wall in the same animal. New blood vessels develop
phases of gastric secretion, particularly the cephalic after some days. It is used for experimental purpose,
phase and used to demonstrate the role of vagus in when the new blood vessels are developed.
cephalic phase. Uses of Farrel and Ivy pouch
This pouch is useful to study the role of hormones during
2. Heidenhain Pouch
gastric and intestinal phases of gastric secretion.
Heidenhain pouch is the modified Pavlov pouch. It is
completely separated from main portion of stomach by 5. Sham Feeding
cutting the isthmus without damaging blood vessels. So,
Sham feeding means the false feeding. It is another
the blood vessels are intact. Thus, Heidenhain pouch
experimental procedure devised by Pavlov to demons­
does not have parasympathetic supply, but the sym­
trate the regulation of gastric secretion.
pathetic fibers remain intact through the blood vessels.
Procedure
Uses of Heidenhain pouch
i. A hole is made in the neck of an anesthetized
Heidenhain pouch is useful to demonstrate the role of dog
sympathetic nerve and the hormonal regulation of gastric ii. Esophagus is transversely cut and the cut ends
secretion after vagotomy (cutting the vagus nerve). are drawn out through the hole in the neck
iii. When the dog eats food, it comes out through
the cut end of the esophagus
iv. But the dog has the satisfaction of eating the
food. Hence it is called sham feeding.
This experimental procedure is supported by the
preparation of Pavlov pouch with a fistula from the
stomach. The fistula opens to exterior and it is used to
observe the gastric secretion. The animal is used for
experimental purpose after a week, when healing is
completed.
Advantage of sham feeding
Sham feeding is useful to demonstrate the secretion of
gastric juice during cephalic phase. In the same animal
after vagotomy, sham feeding does not induce gastric
secretion. It proves the role of vagus nerve during
cephalic phase.

„ PHASES OF GASTRIC SECRETION

Secretion of gastric juice is a continuous process. But
FIGURE 38.5: Pavlov pouch the quantity varies, depending upon time and stimulus.
 236 Section 4 t Digestive System

Accordingly, gastric secretion occurs in three different Nervous mechanism regulates cephalic phase
phases: through reflex action. Two types of reflexes occur:
I. Cephalic phase 1. Unconditioned reflex
II. Gastric phase 2. Conditioned reflex.
III. Intestinal phase.
In human beings, a fourth phase called interdigestive 1. Unconditioned Reflex
phase exists. Each phase is regulated by neural mechan­
ism or hormonal mechanism or both. Unconditioned reflex is the inborn reflex. When food
is placed in the mouth, salivary secretion is induced
„ CEPHALIC PHASE (Chapter 37). Simultaneously, gastric secretion also
occurs.
Secretion of gastric juice by the stimuli arising from
head region (cephalus) is called cephalic phase (Fig. Stages of reflex action:
38.6). This phase of gastric secretion is regulated by
i. Presence of food in the mouth stimulates the
nervous mechanism. The gastric juice secreted during
taste buds and other receptors in the mouth
this phase is called appetite juice.
During this phase, gastric secretion occurs even ii. Sensory (afferent) impulses from mouth pass via
without the presence of food in stomach. The quantity of afferent nerve fibers of glossopharyngeal and
the juice is less but it is rich in enzymes and hydrochloric facial nerves to amygdala and appetite center
acid. present in hypothalamus

FIGURE 38.6: Schematic diagram showing the regulation of gastric secretion

CCK­PZ = Cholecystokinin­pancreozymin, GIP = Gastric inhibitory peptide, VIP = Vasoactive intestinal peptide.
 Chapter 38 t Stomach 237

iii. From here, the efferent impulses pass through 1. Nervous Mechanism
dorsal nucleus of vagus and vagal efferent nerve
Local myenteric reflex
fibers to the wall of the stomach
iv. Vagal efferent nerve endings secrete acetylcho­ Local myenteric reflex is the reflex elicited by stimulation
line, which stimulates gastric secretion. of myenteric nerve plexus in stomach wall. After
entering stomach, the food particles stimulate the local
2. Conditioned Reflex nerve plexus (Chapter 36) present in the wall of the
stomach. These nerve fibers release acetylcholine,
Conditioned reflex is the reflex response acquired by which stimulates the gastric glands to secrete a large
previous experience (Chapter 162). Presence of food in quantity of gastric juice. Simultaneously, acetylcholine
the mouth is not necessary to elicit this reflex. The sight, stimulates G cells to secrete gastrin (see below).
smell, hearing or thought of food, which induce salivary
secretion induce gastric secretion also. Vagovagal reflex

Stages of reflex action: Vagovagal reflex is the reflex which involves both afferent
and efferent vagal fibers. Entrance of bolus into the
i. Impulses from the special sensory organs (eye, stomach stimulates the sensory (afferent) nerve endings
ear and nose) pass through afferent fibers of of vagus and generates sensory impulses. These
neural circuits to the cerebral cortex. Thinking of sensory impulses are transmitted by sensory fibers of
food stimulates the cerebral cortex directly vagus to dorsal nucleus of vagus, located in medulla of
ii. From cerebral cortex, the impulses pass through brainstem. This nucleus in turn, sends efferent impulses
dorsal nucleus of vagus and vagal efferents and through the motor (efferent) fibers of vagus, back to
reach the stomach wall stomach and cause secretion of gastric juice. Since,
iii. Vagal nerve endings secrete acetylcholine, both afferent and efferent impulses pass through vagus,
which stimulates the gastric secretion. this reflex is called vagovagal reflex (Fig. 38.7).

Experimental evidences to prove cephalic phase 2. Hormonal Mechanism – Gastrin

i. Unconditioned reflex of gastric secretion is prov­ Gastrin is a gastrointestinal hormone secreted by the G
ed by sham feeding along with Pavlov pouch cells which are present in the pyloric glands of stomach.
(see above). After vagotomy, sham feeding Small amount of gastrin is also secreted in mucosa of
does not cause gastric secretion. It proves the upper small intestine. In fetus, it is also secreted by islets
importance of vagus nerve in this phase. of Langerhans in pancreas. Gastrin is a polypeptide
ii. Conditioned reflex of gastric secretion is proved containing G14, G17 or G34 amino acids.
by Pavlov pouch and belldog experiment Gastrin is released when food enters stomach.
(Chapter 162). Mechanism involved in the release of gastrin may be the
local nervous reflex or vagovagal reflex. Nerve endings
„ GASTRIC PHASE release the neurotransmitter called gastrin­releasing
peptide, which stimulates the G cells to secrete gastrin.
Secretion of gastric juice when food enters the stomach
is called gastric phase. This phase is regulated by both Actions of gastrin on gastric secretion
nervous and hormonal control. Gastric juice secreted Gastrin stimulates the secretion of pepsinogen and
during this phase is rich in pepsinogen and hydrochloric hydrochloric acid by the gastric glands. Refer Chapter
acid. 44 for other actions of gastrin.
Mechanisms involved in gastric phase are:
1. Nervous mechanism through local myenteric reflex Experimental evidences of gastric phase
and vagovagal reflex Nervous mechanism of gastric secretion during gastric
2. Hormonal mechanism through gastrin phase is proved by Pavlov pouch. Hormonal mechanism
Stimuli, which initiate these two mechanisms are: of gastric secretion is proved by Heidenhain pouch,
1. Distention of stomach Bickel pouch and Farrel and Ivy pouch.
2. Mechanical stimulation of gastric mucosa by bulk of
food „ INTESTINAL PHASE
3. Chemical stimulation of gastric mucosa by the food Intestinal phase is the secretion of gastric juice when
contents. chyme enters the intestine. When chyme enters the
 238 Section 4 t Digestive System

FIGURE 38.7: Vagovagal reflex

intestine, initially, the gastric secretion increases but 2. Gastrointestinal hormones

later it stops. Intestinal phase of gastric secretion is
regulated by nervous and hormonal control. Presence of chyme in the intestine stimulates the secre­
tion of many GI hormones from intestinal mucosa and
Initial Stage of Intestinal Phase other structures. All these hormones inhibit the gastric
secretion. Some of these hormones inhibit the gastric
Chyme that enters the intestine stimulates the duodenal motility also.
mucosa to release gastrin, which is transported to
stomach by blood. There it increases gastric secretion. GI hormones which inhibit gastric secretion:
i. Secretin: Secreted by the presence of acid
Later Stage of Intestinal Phase chyme in the intestine
After the initial increase, there is a decrease or complete ii. Cholecystokinin: Secreted by the presence
stoppage of gastric secretion. Gastric secretion is of chyme containing fats and amino acids in
inhibited by two factors: intestine
1. Enterogastric reflex iii. Gastric inhibitory peptide (GIP): Secreted by the
2. Gastrointestinal (GI) hormones. presence of chyme containing glucose and fats
in the intestine
1. Enterogastric reflex iv. Vasoactive intestinal polypeptide (VIP): Secreted
Enterogastric reflex inhibits the gastric secretion and by the presence of acidic chyme in intestine
motility. It is due to the distention of intestinal mucosa v. Peptide YY: Secreted by the presence of fatty
by chyme or chemical or osmotic irritation of intestinal chyme in intestine.
mucosa by chemical substances in the chyme. It is media­ In addition to these hormones, pancreas also
ted by myenteric nerve (Auerbach) plexus and vagus. secretes a hormone called somatostatin during
 Chapter 38 t Stomach 239

intestinal phase. It also inhibits gastric secretion. Refer i. A piece of bread and a cup of tea
Chapter 44 for details of GI hormones. ii. Wheat biscuit and 400 mL of water
Thus, enterogastric reflex and intestinal hormones iii. 300 mL of oatmeal gruel.
collectively apply a strong brake on the secretion and
motility of stomach during intestinal phase. Fractional gastric analysis

Experimental evidences for intestinal phase After the ingestion of a test meal, gastric juice is collected
at every 15th minute for a period of two and a half hours.
Intestinal phase of gastric secretion is demonstrated by All these samples are analyzed for peptic activity and
Bickel pouch and Farrel and Ivy pouch. acidity.

„ INTERDIGESTIVE PHASE 2. Nocturnal Gastric Analysis

Secretion of small amount of gastric juice in between Patient is given a clear liquid diet at noon and at 5 pm.
meals (or during period of fasting) is called interdigestive At 7.30 pm, the tube is introduced into the patients’s
phase. Gastric secretion during this phase is mainly stomach. Then from 8 pm to 8 am, hourly samples of
due to the hormones like gastrin. This phase of gastric gastric juice are collected and analyzed.
secretion is demonstrated by Farrel and Ivy pouch.
3. Histamine Test
„ FACTORS INFLUENCING GASTRIC SECRETION After overnight fasting, the stomach is emptied in the
Gastric secretion is also influenced by some factors morning by aspiration. Then histamine is injected
which increase the gastric secretion by stimulating subcutaneously (0.01 mg/kg). Histamine stimulates
gastric mucosa such as: secretion of hydrochloric acid in the stomach. After 30
1. Alcohol minutes, 4 samples of gastric juice are collected over a
2. Caffeine. period of 1 hour at 15 minutes interval and analyzed.

„ COLLECTION OF GASTRIC JUICE „ APPLIED PHYSIOLOGY

In human beings, the gastric juice is collected by using Gastric secretion is affected by the following disorders:
Ryle tube. The tube is made out of rubber or plastic. It is
passed through nostril or mouth and through esophagus „ 1. GASTRITIS
into the stomach. A line is marked in the tube. The Inflammation of gastric mucosa is called gastritis. It may
entrance of the tip of the tube into stomach is indicated be acute or chronic. Acute gastritis is characterized by
when this line comes near the mouth. Then, the contents inflammation of superficial layers of mucus membrane
of stomach are collected by means of aspiration. and infiltration with leukocytes, mostly neutrophils.
Chronic gastritis involves inflammation of even the
„ GASTRIC ANALYSIS deeper layers and infiltration with more lymphocytes. It
For analysis, the gastric juice is collected from patient only results in the atrophy of the gastric mucosa, with loss
in the morning. Analysis of the gastric juice is done for the of chief cells and parietal cells of glands. Therefore, the
diagnosis of ulcer and other disorders of stomach. secretion of gastric juice decreases.
Gastric juice is analyzed for the following:
1. Measurement of peptic activity Causes of Acute Gastritis
2. Measurement of gastric acidity: Total acid, free acid i. Infection with bacterium Helicobacter pylori
(hydrochloric acid) and combined acid. ii. Excess consumption of alcohol
iii. Excess administration of Aspirin and other non­
„ METHODS OF GASTRIC ANALYSIS
steroidal antiinflammatory drugs (NSAIDs)
iv. Trauma by nasogastric tubes
1. Fractional Test Meal (FTM) v. Repeated exposure to radiation (rare).
After overnight fasting, the gastric juice is collected.
Then, the patient takes a small test meal called fractional Causes of Chronic Gastritis
test meal (FTM). i. Chronic infection with Helicobacter pylori
Typical test meals are:
 240 Section 4 t Digestive System

ii. Long­term intake of excess alcohol Causes

iii. Long­term use of NSAIDs i. Increased peptic activity due to excessive
iv. Autoimmune disease. secretion of pepsin in gastric juice
ii. Hyperacidity of gastric juice
Features iii. Reduced alkalinity of duodenal content
iv. Decreased mucin content in gastric juice or
Features of gastritis are nonspecific. Common feature
decreased protective activity in stomach or
is abdominal upset or pain felt as a diffused burning
duodenum
sensation. It is often referred to epigastric pain. Other
v. Constant physical or emotional stress
features are: vi. Food with excess spices or smoking (classical
i. Nausea causes of ulcers)
ii. Vomiting vii. Long­term use of NSAIDs (see above) such as
iii. Anorexia (loss of appetite) Aspirin, Ibuprofen and Naproxen
iv. Indigestion viii. Chronic inflammation due to Helicobacter pylori.
v. Discomfort or feeling of fullness in the
epigastric region Features
vi. Belching (process to relieve swallowed air Most common feature of peptic ulcer is severe burning
that is accumulated in stomach). pain in epigastric region. In gastric ulcer, pain occurs
while eating or drinking. In duodenal ulcer, pain is felt 1
„ 2. GASTRIC ATROPHY or 2 hours after food intake and during night.
Gastric atrophy is the condition in which the muscles of Other symptoms accompanying pain are:
the stomach shrink and become weak. Gastric glands i. Nausea
also shrink, resulting in the deficiency of gastric juice. ii. Vomiting
iii. Hematemesis (vomiting blood)
iv. Heartburn (burning pain in chest due to regurgi­
Cause
tation of acid from stomach into esophagus)
Gastric atrophy is caused by chronic gastritis called v. Anorexia (loss of appetite)
chronic atrophic gastritis. There is atrophy of gastric vi. Loss of weight.
mucosa including loss of gastric glands. Autoimmune
atrophic gastritis also causes gastric atrophy. „ 4. ZOLLINGER-ELLISON SYNDROME
Zollinger­Ellison syndrome is characterized by secretion
Features of excess hydrochloric acid in the stomach.
Generally, gastric atrophy does not cause any noticeable
symptom. However, it may lead to achlorhydria (absence Cause
of hydrochloric acid in gastric juice) and pernicious This disorder is caused by tumor of pancreas. Pancreatic
anemia. Some patients develop gastric cancer. tumor produces a large quantity of gastrin. Gastrin
increases the hydrochloric acid secretion in stomach by
„ 3. PEPTIC ULCER stimulating the parietal cells of gastric glands.
Ulcer means the erosion of the surface of any organ due
to shedding or sloughing of inflamed necrotic tissue that Features
lines the organ. Peptic ulcer means an ulcer in the wall i. Abdominal pain
of stomach or duodenum, caused by digestive action ii. Diarrhea (frequent and watery, loose bowel
of gastric juice. If peptic ulcer is found in stomach, it movements)
is called gastric ulcer and if found in duodenum, it is iii. Difficulty in eating
called duodenal ulcer. iv. Occasional hematemesis (see above).
 Chapter
Pancreas
39
„ FUNCTIONAL ANATOMY AND NERVE SUPPLY OF PANCREAS
„ PROPERTIES AND COMPOSITION OF PANCREATIC JUICE
„ FUNCTIONS OF PANCREATIC JUICE
„ DIGESTIVE FUNCTIONS
„ DIGESTION OF PROTEINS
„ DIGESTION OF LIPIDS
„ DIGESTION OF CARBOHYDRATES
„ NEUTRALIZING ACTION
„ MECHANISM OF PANCREATIC SECRETION
„ SECRETION OF PANCREATIC ENZYMES
„ SECRETION OF BICARBONATE IONS
„ REGULATION OF PANCREATIC SECRETION
„ STAGES OF PANCREATIC SECRETION
„ CEPHALIC PHASE
„ GASTRIC PHASE
„ INTESTINAL PHASE
„ COLLECTION OF PANCREATIC JUICE
„ IN ANIMALS
„ IN HUMAN
„ APPLIED PHYSIOLOGY
„ PANCREATITIS
„ STEATORRHEA

„ FUNCTIONAL ANATOMY AND has a single layer of acinar cells with a lumen in the
NERVE SUPPLY OF PANCREAS center. Acinar cells contain zymogen granules, which
possess digestive enzymes.
Pancreas is a dual organ having two functions, namely
endocrine function and exocrine function. Endocrine A small duct arises from lumen of each alveolus.
function is concerned with the production of hormones Some of these ducts from neighboring alveoli unite to
(Chapter 69). The exocrine function is concerned with form intralobular duct. All the intralobular ducts unite
the secretion of digestive juice called pancreatic juice. to form the main duct of pancreas called Wirsung duct.
Wirsung duct joins common bile duct to form ampulla of
„ FUNCTIONAL ANATOMY OF EXOCRINE Vater, which opens into duodenum (see Fig. 40.3).
PART OF PANCREAS In some persons, an accessory duct called duct of
Exocrine part of pancreas resembles salivary gland in Santorini exists. It also opens into duodenum, proximal
structure. It is made up of acini or alveoli. Each acinus to the opening of ampulla of Vater.
 242 Section 4 t Digestive System

„ NERVE SUPPLY TO PANCREAS i. High bicarbonate content makes the pancreatic

juice highly alkaline, so that it protects the intes­
Pancreas is supplied by both sympathetic and para­
tinal mucosa from acid chyme by neutralizing it
sympathetic fibers. Sympathetic fibers are supplied
ii. Bicarbonate ions provide the required pH (7 to
through splanchnic nerve and parasympathetic fibers
9) for the activation of pancreatic enzymes.
are supplied through vagus nerve.

„ PROPERTIES AND COMPOSITION „ FUNCTIONS OF PANCREATIC JUICE

OF PANCREATIC JUICE Pancreatic juice has digestive functions and neutralizing
action.
„ PROPERTIES OF PANCREATIC JUICE
„ DIGESTIVE FUNCTIONS OF PANCREATIC JUICE
Volume : 500 to 800 mL/day
Reaction : Highly alkaline with a pH of 8 to 8.3 Pancreatic juice plays an important role in the digestion
Specific gravity : 1.010 to 1.018 of proteins and lipids. It also has mild digestive action
on carbohydrates.
„ COMPOSITION OF PANCREATIC JUICE
„ DIGESTION OF PROTEINS
Pancreatic juice contains 99.5% of water and 0.5%
of solids. The solids are the organic and inorganic Major proteolytic enzymes of pancreatic juice are trypsin
substances. Composition of pancreatic juice is given in and chymotrypsin. Other proteolytic enzymes are carbo­
Fig. 39.1. xypeptidases, nuclease, elastase and collagenase.
Bicarbonate content is very high in pancreatic juice.
1. Trypsin
It is about 110 to 150 mEq/ L, against the plasma level of
24 mEq/L. High bicarbonate content of pancreatic juice Trypsin is a single polypeptide with a molecular weight
is important because of two reasons: of 25,000. It contains 229 amino acids.

FIGURE 39.1: Composition of pancreatic juice

 Chapter 39 t Pancreas 243

It is secreted as inactive trypsinogen, which ii. Digestion of milk: Chymotrypsin digests caseino­
is converted into active trypsin by enterokinase. gen faster than trypsin. Combination of both
Enterokinase is also called enteropeptidase and it enzymes causes rapid digestion of milk
is secreted by the brush­bordered cells of duodenal iii. On blood clotting: No action.
mucus membrane. Once formed, trypsin itself activates
trypsinogen by means of autocatalytic or autoactive 3. Carboxypeptidases
action.
Carboxypeptidases are carboxypeptidase A and carboxy­
Trypsin inhibitor peptidase B. Carboxypeptidase A is derived from the
precursor procarboxypeptidase A. Carboxypeptidase B
Trypsinogen is activated only when it reaches the small
is derived from procarboxypeptidase B. Procarboxypep­
intestine. If trypsin is activated when it is in pancreas, it
tidases are activated into carboxypeptidases by trypsin.
may hydrolyze the pancreatic tissue proteins, resulting
in pancreatic damage. But its activation in the secretory Actions of carboxypeptidases
cells, acini and ducts of pancreas is prevented by an Carboxypeptidases are exopeptidases and break the
inhibitor protein called trypsin inhibitor. Any abnormality or terminal bond of protein molecules. Exopeptidases split
deficiency of the trypsin inhibitor will result in unopposed the polypeptides and other proteins into amino acids.
trypsin activity, which damages the pancreas. Carboxypeptidase A splits the proteins into
Actions of trypsin amino acids having aromatic or aliphatic side chains.
Carboxypeptidase B converts the proteins into amino
i. Digestion of proteins: Trypsin is the most powerful acids having basic side chains.
proteolytic enzyme. It is an endopeptidase
and breaks the interior bonds of the protein 4. Nucleases
molecules and converts proteins into proteoses
and polypeptides Nucleases of pancreatic juice are ribonuclease and
deoxyribonuclease, which are responsible for the
ii. Curdling of milk: It converts caseinogen in the
digestion of nucleic acids. These enzymes convert the
milk into casein
ribonucleic acid (RNA) and deoxyribonucleic acid (DNA)
iii. Blood clotting: It accelerates blood clotting
into mononucleotides.
iv. It activates the other enzymes of pancreatic
juice, viz. 5. Elastase
a. Chymotrypsinogen into chymotrypsin
b. Procarboxypeptidases into carboxypeptidases Elastase is secreted as inactive proelastase, which is
activated into elastase by trypsin. Elastase digests the
c. Proelastase into elastase
elastic fibers.
d. Procolipase into colipase
v. Trypsin also activates collagenase, phospholi­ 6. Collagenase
pase A and phospholipase B
vi. Autocatalytic action: Once formed, trypsin itself Collagenase is secreted as inactive procollagenase,
converts trypsinogen into trypsin. which is activated into collagenase by trypsin. It digests
collagen.
2. Chymotrypsin
„ DIGESTION OF LIPIDS
Chymotrypsin is a polypeptide with a molecular weight
Lipolytic enzymes present in pancreatic juice are pan­
of 25,700 and 246 amino acids. It is secreted as inactive
creatic lipase, cholesterol ester hydrolase, phospholipase
chymotrypsinogen, which is activated into chymotrypsin
A, phospholipase B, colipase and bile­salt­activated
by trypsin.
lipase.
Actions of chymotrypsin
1. Pancreatic lipase
i. Digestion of proteins: Chymotrypsin is also an
endopeptidase and it converts proteins into Pancreatic lipase is a powerful lipolytic enzyme. It
polypeptides digests triglycerides into monoglycerides and fatty
 244 Section 4 t Digestive System

acids. Activity of pancreatic lipase is accelerated in the „ NEUTRALIZING ACTION OF

presence of bile. Optimum pH required for activity of this PANCREATIC JUICE
enzyme is 7 to 9.
Digestion of fat by pancreatic lipase requires two When acid chyme enters intestine from stomach,
more factors: pancreatic juice with large quantity of bicarbonate is
i. Bile salts, which are responsible for the emulsi­ released into intestine. Presence of large quantity of
fication of fat, prior to their digestion bicarbonate ions makes the pancreatic juice highly
ii. Colipase, which is a coenzyme necessary for alkaline. This alkaline pancreatic juice neutralizes acidity
the pancreatic lipase to digest the dietary lipids. of chyme in the intestine.
About 80% of the fat is digested by pancreatic lipase. Neutralizing action is an important function of
Deficiency or absence of this enzyme leads to excretion pancreatic juice because it protects the intestine from
of undigested fat in feces (steatorrhea; see below). the destructive action of acid in the chyme.

2. Cholesterol ester hydrolase „ MECHANISM OF

PANCREATIC SECRETION
Cholesterol ester hydrolase or cholesterol esterase
converts cholesterol ester into free cholesterol and fatty „ SECRETION OF PANCREATIC ENZYMES
acid by hydrolysis.
Pancreatic enzymes are synthesized in ribosomes,
3. Phospholipase A which are attached to the endoplasmic reticulum of
acinar cells in pancreas. The raw materials for the
Phospholipase A is activated by trypsin. Phospholipase synthesis of pancreatic enzymes are the amino acids,
A digests phospholipids, namely lecithin and cephalin which are derived from the blood. After synthesis, the
and converts them into lysophospholipids. It converts enzymes are packed into different zymogen granules
lecithin into lysolecithin and cephalin into lysocephalin. by Golgi apparatus and stored in cytoplasm. When
stimulated, the acinar cells release zymogen granules
4. Phospholipase B into the pancreatic duct. From the granules, the enzymes
Phospholipase B is also activated by trypsin. It converts are liberated into intestine.
lysophospholipids (lysolecithin and lysocephalin) to
phosphoryl choline and free fatty acids. „ SECRETION OF BICARBONATE IONS
Bicarbonate ions of pancreatic juice are secreted from
5. Colipase the cells of pancreatic ductules and released into the
Colipase is a small coenzyme, secreted as inactive pancreatic duct.
procolipase. Procolipase is activated into colipase by Mechanism of bicarbonate secretion
trypsin. Colipase facilitates digestive action of pancreatic
lipase on fats. 1. Carbon dioxide derived from blood or metabolic
process combines with water inside the cell to
6. Bile-salt-activated lipase form carbonic acid in the presence of carbonic
anhydrase
Bile­salt­activated lipase is the lipolytic enzyme activated
2. Carbonic acid dissociates into hydrogen and bicar­
by bile salt. It is also called carboxyl ester lipase or
bonate ions
cholesterol esterase. This enzyme has a weak lipolytic
3. Bicarbonate ions are actively transported out of the
action than pancreatic lipase. But it hydrolyses a variety
cell into the lumen
of lipids such as phospholipids, cholesterol esters and
triglycerides. Human milk contains an enzyme similar to 4. Hydrogen ion is actively transported into blood in
bile-salt-activated lipase (Table 39.1). exchange for sodium ion
5. Sodium ion from the cell is transported into the
„ DIGESTION OF CARBOHYDRATES lumen, where it combines with bicarbonate to form
sodium bicarbonate
Pancreatic amylase is the amylolytic enzyme present in 6. Because of the loss of sodium and bicarbonate
pancreatic juice. Like salivary amylase, the pancreatic ions from the blood, there is some disturbance in
amylase also converts starch into dextrin and maltose. the osmotic equilibrium of the blood. To maintain
 Chapter 39 t Pancreas 245

TABLE 39.1: Digestive enzymes of pancreatic juice

Enzyme Activator Acts on (substrate) End products

Enterokinase
Trypsin Proteins Proteoses and polypeptides
Trypsin
Chymotrypsin Trypsin Proteins Polypeptides
Carboxypeptidases Trypsin Polypeptides Amino acids
Nucleases Trypsin RNA and DNA Mononucleotides
Elastase Trypsin Elastin Amino acids
Collagenase Trypsin Collagen Amino acids
Pancreatic lipase Alkaline medium Triglycerides Monoglycerides and fatty acids
Cholesterol ester hydrolase Alkaline medium Cholesterol ester Cholesterol and fatty acids
Phospholipase A Trypsin Phospholipids Lysophospholipids
Phospholipase B Trypsin Lysophospholipids Phosphoryl choline and free fatty acids
Facilitates action of
Colipase Trypsin –
pancreatic lipase
Phospholipids Lysophospholipids
Bile­salt­activated lipase Trypsin Cholesterol esters Cholesterol and fatty acids
Triglycerides Monoglycerides and fatty acids
Pancreatic amylase – Starch Dextrin and maltose

the osmotic equilibrium, water leaves the blood and Unconditioned Reflex
enters the lumen of pancreatic duct by osmosis
Unconditioned reflex is the inborn reflex. When food
7. In the lumen, bicarbonate combines with water
is placed in the mouth, salivary secretion (Chapter
forming the solution of bicarbonate. 37) and gastric secretion (Chapter 38) are induced.
Simultaneously, pancreatic secretion also occurs.
„ REGULATION OF PANCREATIC
SECRETION Stages of reflex action:

Secretion of pancreatic juice is regulated by both i. Presence of food in the mouth stimulates the
nervous and hormonal factors. taste buds and other receptors in the mouth
ii. Sensory (afferent) impulses from mouth reach
„ STAGES OF PANCREATIC SECRETION dorsal nucleus of vagus and efferent impulses
reach pancreatic acini via vagal efferent nerve
Pancreatic juice is secreted in three stages (Fig. 39.2) fibers
like the gastric juice: iii. Vagal efferent nerve endings secrete acetyl­
1. Cephalic phase choline, which stimulates pancreatic secretion.
2. Gastric phase
3. Intestinal phase. Conditioned Reflex
These three phases of pancreatic secretion Conditioned reflex is the reflex response acquired by
correspond with the three phases of gastric secretion. previous experience (Chapter 162). Presence of food in
the mouth is not necessary to elicit this reflex. The sight,
„ 1. CEPHALIC PHASE smell, hearing or thought of food, which induce salivary
secretion and gastric secretion induce pancreatic
As in case of gastric secretion, cephalic phase is regulat­
secretion also.
ed by nervous mechanism through reflex action.
Two types of reflexes occur: Stages of reflex action:
1. Unconditioned reflex i. Impulses from the special sensory organs (eye,
2. Conditioned reflex. ear and nose) pass through afferent fibers of
 246 Section 4 t Digestive System

neural circuits to the cerebral cortex. Thinking of Hormones Stimulating Pancreatic Secretion
food stimulates the cerebral cortex directly
ii. From cerebral cortex, the impulses pass through i. Secretin
dorsal nucleus of vagus and vagal efferents and ii. Cholecystokinin.
reach pancreatic acini
iii. Vagal nerve endings secrete acetylcholine, Secretin
which stimulates pancreatic secretion.
Secretin is produced by S cells of mucous membrane
„ 2. GASTRIC PHASE in duodenum and jejunum. It is secreted as inactive
prosecretin, which is activated into secretin by acid
Secretion of pancreatic juice when food enters the chyme.
stomach is known as gastric phase. This phase of The stimulant for the release and activation of
pancreatic secretion is under hormonal control. The prosecretin is the acid chyme entering intestine.
hormone involved is gastrin.
Products of protein digestion also stimulate the hormo­
When food enters the stomach, gastrin is secreted
nal secretion.
from stomach (Chapter 39). When gastrin is transported
to pancreas through blood, it stimulates the pancreatic Action of secretin
secretion. The pancreatic juice secreted during gastric
phase is rich in enzymes. Secretin stimulates the secretion of watery juice which is
rich in of bicarbonate ion and high in volume. It increases
„ 3. INTESTINAL PHASE the pancreactic secretion by acting on pancreatic
ductules via cyclic AMP (messenger). Other actions of
Intestinal phase is the secretion of pancreatic juice when secretin are explained in Chapter 44.
the chyme enters the intestine. This phase is also under
hormonal control.
Cholecystokinin
When chyme enters the intestine, many hormones
are released. Some hormones stimulate the pancreatic Cholecystokinin (CCK) is also called cholecystokinin­
secretion and some hormones inhibit the pancreatic pancreozymin (CCK­PZ). It is secreted by I cells in
secretion. duodenal and jejunal mucosa. The stimulant for the

FIGURE 39.2: Schematic diagram showing the regulation of pancreatic secretion

 Chapter 39 t Pancreas 247

release of this hormone is the chyme containing 1. Acute Pancreatitis

digestive products such as fatty acids, peptides and
amino acids. Acute pancreatitis is more severe and it occurs because
of heavy alcohol intake or gallstones.
Action of cholecystokinin
Features of acute pancreatitis:
Cholecystokinin stimulates the secretion of pancreatic
juice which is rich in enzyme and low in volume, i. Severe upper abdominal pain
by acting on pancreatic acinar cells via inosine ii. Nausea and vomiting
triphosphate (second messenger). The other actions of iii. Loss of appetite and weight
cholecystokinin are described in Chapter 44.
iv. Fever
Hormones Inhibiting Pancreatic Secretion v. Shock.

i. Pancreatic polypeptide (PP) secreted by PP 2. Chronic Pancreatitis

cells in islets of Langerhans of pancreas
ii. Somatostatin secreted by D cells in islets of Chronic pancreatitis develops due to repeated acute
Langerhans of pancreas inflammation or chronic damage to pancreas.
iii. Peptide YY secreted by intestinal mucosa
Causes of chronic pancreatitis
iv. Peptides like ghrelin and leptin
Refer Chapter 44 for details of these hormones. i. Long­time consumption of alcohol
ii. Chronic obstruction of ampulla of Vater by
„ COLLECTION OF PANCREATIC JUICE gallstone
„ IN ANIMALS iii. Hereditary cause (passed on genetically from
one generation to another)
In animals, the pancreatic juice is collected by connecting
a fistula between the pancreatic duct and the opening in iv. Congenital abnormalities of pancreatic duct
the abdominal wall. v. Cystic fibrosis, a generalized disorder affecting
the functions of many organs such as lungs
„ IN HUMAN (due to excessive mucus), exocrine glands like
In human beings, a multilumen tube is inserted through pancreas, biliary system and immune system
nose or mouth, till the tip of this tube reaches the intestine vi. Malnutrition (poor nutrition; mal = bad)
near the ampulla of Vater. The tube has a marking. The vii. Idiopathic pancreatitis (due to unknown cause).
entrance of the tip of the tube into the intestine near
the ampulla is indicated when this line comes near the Features of chronic pancreatitis
mouth. The tube has three lumens. Small balloons are i. Complete destruction of pancreas: During the
attached to the two outer lumens. When balloons are
obstruction of biliary ducts, more amount of
inflated by air, the intestine near the ampulla is enlarged.
trypsinogen and other enzymes are accumulated.
Now, the pancreatic juice is collected through the middle
lumen by means of aspiration. In spite of the presence of trypsin inhibitor in
acini, some trypsinogen is activated. Trypsin
„ APPLIED PHYSIOLOGY in turn activates other proteolytic enzymes. All
these enzymes destroy the pancreatic tissues
„ PANCREATITIS completely
Pancreatitis is the inflammation of pancreatic acini. It is ii. Absence of pancreatic enzymes: Pancreatitis
a rare but dangerous disease. is more dangerous because the destruction of
Pancreatitis is of two types: acinar cells in pancreas leads to deficiency or
1. Acute pancreatitis total absence of pancreatic enzymes. So the
2. Chronic pancreatitis. digestive processes are affected; worst affected
 248 Section 4 t Digestive System

is fat digestion that results in steatorrhea (see Causes of Steatorrhea

below)
Any condition that causes indigestion or malabsorption
iii. Severe pain in upper abdominal region, which of fat leads to steatorrhea. Various causes of steatorrhea
radiates to the back are:
iv. Fever, nausea and vomiting 1. Lack of pancreatic lipase: Since most of the fat is
v. Tender and swollen abdomen digested only by pancreatic lipase, its deficiency
vi. Weight loss. leads to steatorrhea
2. Liver disease affecting secretion of bile: Bile salts
„ STEATORRHEA are essential for the digestion of fat by lipase and
absorption of fat from intestine. Absence of bile
Steatorrhea is the formation of bulky, foul­smelling, salts results in excretion of fatty stool
frothy and clay­colored stools with large quantity of 3. Celiac disease: Atrophy of intestinal villi leads to
undigested fat because of impaired digestion and malabsorption, resulting in steatorrhea
absorption of fat. 4. Cystic fibrosis (see above).
 Chapter
Liver and Gallbladder
40
„ FUNCTIONAL ANATOMY OF LIVER AND BILIARY SYSTEM
„ BLOOD SUPPLY TO LIVER
„ PROPERTIES AND COMPOSITION OF BILE
„ SECRETION OF BILE
„ STORAGE OF BILE
„ BILE SALTS
„ BILE PIGMENTS
„ FUNCTIONS OF BILE
„ FUNCTIONS OF LIVER
„ GALLBLADDER
„ REGULATION OF BILE SECRETION
„ APPLIED PHYSIOLOGY

„ FUNCTIONAL ANATOMY OF LIVER Hepatocytes and Hepatic Plates

AND BILIARY SYSTEM Hepatocytes are arranged in columns, which form the
Liver is a dual organ having both secretory and excretory hepatic plates. Each plate is made up of two columns of
functions. It is the largest gland in the body, weighing cells. In between the two columns of each plate lies a
about 1.5 kg in man. It is located in the upper and right bile canaliculus (Fig. 40.2).
side of the abdominal cavity, immediately beneath In between the neighboring plates, a blood space
called sinusoid is present. Sinusoid is lined by the
diaphragm.
endothelial cells. In between the endothelial cells some
special macrophages called Kupffer cells are present.
„ LIVER

Hepatic Lobes Portal Triads

Liver is made up of many lobes called hepatic lobes Each lobule is surrounded by many portal triads. Each
(Fig. 40.1). Each lobe consists of many lobules called portal triad consists of three vessels:
hepatic lobules. 1. A branch of hepatic artery
2. A branch of portal vein
Hepatic Lobules 3. A tributary of bile duct.
Branches of hepatic artery and portal vein open
Hepatic lobule is the structural and functional unit of into the sinusoid. Sinusoid opens into the central vein.
liver. There are about 50,000 to 100,000 lobules in the Central vein empties into hepatic vein.
liver. The lobule is a honeycomb-like structure and it is Bile is secreted by hepatic cells and emptied into
made up of liver cells called hepatocytes. bile canaliculus. From canaliculus, the bile enters the
 250 Section 4 t Digestive System

hepatic artery divides into many branches. Each branch

enters a portal triad.

FIGURE 40.1: Posterior surface of liver

tributary of bile duct. Tributaries of bile duct from

canaliculi of neighboring lobules unite to form small bile
ducts. These small bile ducts join together and finally
form left and right hepatic ducts, which emerge out of
liver.

„ BILIARY SYSTEM
Biliary system or extrahepatic biliary apparatus is
formed by gallbladder and extrahepatic bile ducts (bile
ducts outside the liver). Right and left hepatic bile ducts
which come out of liver join to form common hepatic
duct. It unites with the cystic duct from gallbladder to
form common bile duct (Fig. 40.3). All these ducts have
similar structures.
Common bile duct unites with pancreatic duct to
form the common hepatopancreatic duct or ampulla of
Vater, which opens into the duodenum.
There is a sphincter called sphincter of Oddi at FIGURE 40.2: Hepatic lobule
the lower part of common bile duct, before it joins the
pancreatic duct. It is formed by smooth muscle fibers of
common bile duct. It is normally kept closed; so the bile
secreted from liver enters gallbladder where it is stored.
Upon appropriate stimulation, the sphincter opens and
allows flow of bile from gallbladder into the intestine.

„ BLOOD SUPPLY TO LIVER

Liver receives maximum blood supply of about 1,500
mL/minute. It receives blood from two sources, namely
the hepatic artery and portal vein (Fig. 40.4).

„ HEPATIC ARTERY
Hepatic artery arises directly from aorta and supplies
oxygenated blood to liver. After entering the liver, the FIGURE 40.3: Biliary system
 Chapter 40 t Liver and Gallbladder 251

FIGURE 40.5: Enterohepatic circulation

FIGURE 40.4: Schematic diagram of blood flow through liver

pH : 8 to 8.6
Specific gravity : 1.010 to 1.011
„ PORTAL VEIN Color : Golden yellow or green.
Portal vein is formed by superior mesenteric vein and
splenic vein. It brings deoxygenated blood from stomach, „ COMPOSITION OF BILE
intestine, spleen and pancreas. Portal blood is rich in
Bile contains 97.6% of water and 2.4% of solids. Solids
monosaccharides and amino acids. It also contains bile
include organic and inorganic substances. Refer Fig.
salts, bilirubin, urobilinogen and GI hormones. However,
40.6 for details.
the oxygen content is less in portal blood.
Flow of blood from intestine to liver through portal
vein is known as enterohepatic circulation (Fig. 40.5). „ SECRETION OF BILE
The blood from hepatic artery mixes with blood from Bile is secreted by hepatocytes. The initial bile secreted
portal vein in hepatic sinusoids. Hepatic cells obtain by hepatocytes contains large quantity of bile acids,
oxygen and nutrients from the sinusoid. bile pigments, cholesterol, lecithin and fatty acids.
From hepatocytes, bile is released into canaliculi. From
„ HEPATIC VEIN here, it passes through small ducts and hepatic ducts
Substances synthesized by hepatic cells, waste products and reaches the common hepatic duct. From common
and carbon dioxide are discharged into sinusoids. hepatic duct, bile is diverted either directly into the
Sinusoids drain them into central vein of the lobule. intestine or into the gallbladder.
Central veins from many lobules unite to form bigger Sodium, bicarbonate and water are added to bile
veins, which ultimately form hepatic veins (right and left) when it passes through the ducts. These substances
which open into inferior vena cava. are secreted by the epithelial cells of the ducts. Addition
of sodium, bicarbonate and water increases the total
„ PROPERTIES AND COMPOSITION quantity of bile.
OF BILE
„ STORAGE OF BILE
„ PROPERTIES OF BILE
Most of the bile from liver enters the gallbladder, where it
Volume : 800 to 1,200 mL/day is stored. It is released from gallbladder into the intestine
Reaction : Alkaline whenever it is required. When bile is stored in gallbladder,
 252 Section 4 t Digestive System

TABLE 40.1: Differences between liver bile

and gallbladder bile

Types of entities Liver bile Gallbladder bile

pH 8 to 8.6 7 to 7.6
Specific gravity 1010 to 1011 1026 to 1032
Water content 97.6% 89%
Solids 2.4% 11%
Organic substances
Bile Salts 0.5 g/dL 6.0 g/dL
Bile Pigments 0.05 g/dL 0.3 g/dL
Cholesterol 0.1 g/dL 0.5 g/dL

FIGURE 40.6: Composition of bile Fatty Acids 0.2 g/dL 1.2 g/dL
Lecithin 0.05 g/dL 0.4 g/dL
it undergoes many changes both in quality and quantity Mucin Absent Present
such as: Inorganic substances
1. Volume is decreased because of absorption of Sodium 150 mEq/L 135 mEq/L
a large amount of water and electrolytes (except
calcium and potassium) Calcium 4 mEq/L 22 mEq/L
2. Concentration of bile salts, bile pigments, cholesterol, Potassium 5 mEq/L 12 mEq/L
fatty acids and lecithin is increased because of Chloride 100 mEq/L 10 mEq/L
absorption of water and electrolytes
Bicarbonate 30 mEq/L 10 mEq/L
3. The pH is decreased slightly
4. Specific gravity is increased
5. Mucin is added to bile (Table 40.1). „ ENTEROHEPATIC CIRCULATION
OF BILE SALTS
„ BILE SALTS Enterohepatic circulation is the transport of substances
Bile salts are the sodium and potassium salts of bile from small intestine to liver through portal vein. About
acids, which are conjugated with glycine or taurine. 90% to 95% of bile salts from intestine are transported to
liver through enterohepatic circulation. Remaining 5% to
„ FORMATION OF BILE SALTS 10% of the bile salts enter large intestine. Here, the bile
salts are converted into deoxycholate and lithocholate,
Bile salts are formed from bile acids. There are two which are excreted in feces.
primary bile acids in human, namely cholic acid and
chenodeoxycholic acid, which are formed in liver and „ FUNCTIONS OF BILE SALTS
enter the intestine through bile. Due to the bacterial action
in the intestine, the primary bile acids are converted into Bile salts are required for digestion and absorption of
secondary bile acids: fats in the intestine. The functions of bile salts are:
Cholic acid → deoxycholic acid
Chenodeoxycholic acid → lithocholic acid 1. Emulsification of Fats
Secondary bile acids from intestine are transported Emulsification is the process by which the fat globules
back to liver through enterohepatic circulation. In liver, are broken down into minute droplets and made in the
the secondary bile acids are conjugated with glycine form of a milky fluid called emulsion in small intestine,
(amino acid) or taurin (derivative of an amino acid) and by the action of bile salts.
form conjugated bile acids, namely glycocholic acid Lipolytic enzymes of GI tract cannot digest the fats
and taurocholic acids. These bile acids combine with directly because the fats are insoluble in water due to the
sodium or potassium ions to form the salts, sodium surface tension. Bile salts emulsify the fats by reducing
or potassium glycocholate and sodium or potassium the surface tension due to their detergent action. Now
taurocholate (Fig. 40.7). the fats can be easily digested by lipolytic enzymes.
 Chapter 40 t Liver and Gallbladder 253

FIGURE 40.7: Formation of bile salts

Unemulsified fat usually passes through the intes­ salts act as cholagogues indirectly by stimulating the
tine and then it is eliminated in feces. secretion of hormone cholecystokinin. This hormone cau­
Emulsification of fats by bile salts needs the pres­ ses contraction of gallbladder, resulting in release of bile.
ence of lecithin from bile.
5. Laxative Action
2. Absorption of Fats Laxative is an agent which induces defecation. Bile salts
act as laxatives by stimulating peristaltic movements of
Bile salts help in the absorption of digested fats from
the intestine.
intestine into blood. Bile salts combine with fats and
make complexes of fats called micelles. The fats in the 6. Prevention of Gallstone Formation
form of micelles can be absorbed easily.
Bile salts prevent the formation of gallstone by keeping
3. Choleretic Action the cholesterol and lecithin in solution. In the absence
of bile salts, cholesterol precipitates along with lecithin
Bile salts stimulate the secretion of bile from liver. This and forms gallstone.
action is called choleretic action.
„ BILE PIGMENTS
4. Cholagogue Action
Bile pigments are the excretory products in bile. Bilirubin
Cholagogue is an agent which causes contraction of and biliverdin are the two bile pigments and bilirubin is
gallbladder and release of bile into the intestine. Bile the major bile pigment in human beings.
 254 Section 4 t Digestive System

Bile pigments are formed during the breakdown of „ FATE OF CONJUGATED BILIRUBIN
hemoglobin, which is released from the destroyed RBCs
Stages of excretion of conjugated bilirubin:
in the reticuloendothelial system (Fig. 40.8).
1. In intestine, 50% of the conjugated bilirubin is
converted into urobilinogen by intestinal bacteria.
„ FORMATION AND EXCRETION
First the conjugated bilirubin is deconjugated into free
OF BILE PIGMENTS
bilirubin, which is later reduced into urobilinogen.
Stages of formation and circulation of bile pigments: 2. Remaining 50% of conjugated bilirubin from intestine
1. Senile erythrocytes are destroyed in reticuloen­ is absorbed into blood and enters the liver through
dothelial system and hemoglobin is released from portal vein (enterohepatic circulation). From liver, it
them is re­excreted in bile
2. Hemoglobin is broken into globin and heme 3. Most of the urobilinogen from intestine enters liver
3. Heme is split into iron and the pigment biliverdin via enterohepatic circulation. Later, it is re­excreted
4. Iron goes to iron pool and is reused through bile
5. First formed pigment biliverdin is reduced to bilirubin. 4. About 5% of urobilinogen is excreted by kidney
6. Bilirubin is released into blood from the reticulo­ through urine. In urine, due to exposure to air, the
endothelial cells urobilinogen is converted into urobilin by oxidation
7. In blood, the bilirubin is transported by the plasma 5. Some of the urobilinogen is excreted in feces as
protein, albumin. Bilirubin circulating in the blood is stercobilinogen. In feces, stercobilinogen is oxidized
called free bilirubin or unconjugated bilirubin to stercobilin.
8. Within few hours after entering the circulation, the
free bilirubin is taken up by the liver cells „ NORMAL PLASMA LEVELS OF BILIRUBIN
9. In the liver, it is conjugated with glucuronic acid to Normal bilirubin (Total bilirubin) content in plasma is 0.5
form conjugated bilirubin to 1.5 mg/dL. When it exceeds 1mg/dL, the condition is
10. Conjugated bilirubin is then excreted into intestine called hyperbilirubinemia. When it exceeds 2 mg/dL,
through bile. jaundice occurs.

FIGURE 40.8: Formation and circulation of bile pigments

 Chapter 40 t Liver and Gallbladder 255

„ FUNCTIONS OF BILE „ FUNCTIONS OF LIVER

Most of the functions of bile are due to the bile salts. Liver is the largest gland and one of the vital organs of the
body. It performs many vital metabolic and homeostatic
„ 1. DIGESTIVE FUNCTION functions, which are summarized below.
Refer functions of bile salts.
„ 1. METABOLIC FUNCTION
„ 2. ABSORPTIVE FUNCTIONS
Liver is the organ where maximum metabolic reactions
Refer functions of bile salts. such as metabolism of carbohydrates, proteins, fats,
vitamins and many hormones are carried out.
„ 3. EXCRETORY FUNCTIONS
Bile pigments are the major excretory products of the „ 2. STORAGE FUNCTION
bile. Other substances excreted in bile are: Many substances like glycogen, amino acids, iron, folic
i. Heavy metals like copper and iron acid and vitamins A, B12 and D are stored in liver.
ii. Some bacteria like typhoid bacteria
iii. Some toxins „ 3. SYNTHETIC FUNCTION
iv. Cholesterol
v. Lecithin Liver produces glucose by gluconeogenesis. It synthe­
vi. Alkaline phosphatase. sizes all the plasma proteins and other proteins (except
immunoglobulins) such as clotting factors, complement
„ 4. LAXATIVE ACTION factors and hormone­binding proteins. It also synthesizes
steroids, somatomedin and heparin.
Bile salts act as laxatives (see above).
„ 4. SECRETION OF BILE
„ 5. ANTISEPTIC ACTION
Bile inhibits the growth of certain bacteria in the lumen Liver secretes bile which contains bile salts, bile
of intestine by its natural detergent action. pigments, cholesterol, fatty acids and lecithin.
The functions of bile are mainly due to bile salts. Bile
„ 6. CHOLERETIC ACTION salts are required for digestion and absorption of fats in
the intestine. Bile helps to carry away waste products
Bile salts have the choleretic action (see above).
and breakdown fats, which are excreted through feces
or urine.
7. MAINTENANCE OF pH IN
GASTROINTESTINAL TRACT
„ 5. EXCRETORY FUNCTION
As bile is highly alkaline, it neutralizes the acid chyme
which enters the intestine from stomach. Thus, an Liver excretes cholesterol, bile pigments, heavy metals
optimum pH is maintained for the action of digestive (like lead, arsenic and bismuth), toxins, bacteria and
enzymes. virus (like that of yellow fever) through bile.

„ 8. PREVENTION OF GALLSTONE FORMATION „ 6. HEAT PRODUCTION

Refer function of bile salts. Enormous amount of heat is produced in the liver
because of metabolic reactions. Liver is the organ where
„ 9. LUBRICATION FUNCTION maximum heat is produced.
The mucin in bile acts as a lubricant for the chyme in
intestine. „ 7. HEMOPOIETIC FUNCTION

In fetus (hepatic stage), liver produces the blood

„ 10. CHOLAGOGUE ACTION
cells (Chapter 10). It stores vitamin B12 necessary
Bile salts act as cholagogues (see above). for erythropoiesis and iron necessary for synthesis
 256 Section 4 t Digestive System

of hemoglobin. Liver produces thrombopoietin that „ FUNCTIONS OF GALLBLADDER

promotes production of thrombocytes.
Major functions of gallbladder are the storage and
„ 8. HEMOLYTIC FUNCTION concentration of bile.

The senile RBCs after a lifespan of 120 days are 1. Storage of Bile
destroyed by reticuloendothelial cells (Kupffer cells) of
liver. Bile is continuously secreted from liver. But it is released
into intestine only intermittently and most of the bile is
„ 9. INACTIVATION OF HORMONES stored in gallbladder till it is required.
AND DRUGS
2. Concentration of Bile
Liver catabolizes the hormones such as growth hormone,
parathormone, cortisol, insulin, glucagon and estrogen. Bile is concentrated while it is stored in gallbladder.
It also inactivates the drugs, particularly the fat­soluble The mucosa of gallbladder rapidly reabsorbs water and
drugs. The fat­soluble drugs are converted into water­ electrolytes, except calcium and potassium. But the
soluble substances, which are excreted through bile or bile salts, bile pigments, cholesterol and lecithin are not
urine. reabsorbed. So, the concentration of these substances
in bile increases 5 to 10 times (Fig. 40.9).
„ 10. DEFENSIVE AND DETOXIFICATION
FUNCTIONS 3. Alteration of pH of Bile
Reticuloendothelial cells (Kupffer cells) of the liver play The pH of bile decreases from 8 – 8.6 to 7 – 7.6 and it
an important role in the defense of the body. Liver is also
becomes less alkaline when it is stored in gallbladder.
involved in the detoxification of the foreign bodies.
i. Foreign bodies such as bacteria or antigens are
4. Secretion of Mucin
swallowed and digested by reticuloendothelial
cells of liver by means of phagocytosis. Gallbladder secretes mucin and adds it to bile. When bile
ii. Reticuloendothelial cells of liver also produce is released into the intestine, mucin acts as a lubricant
substances like interleukins and tumor necrosis for movement of chyme in the intestine.
factors, which activate the immune system of
the body (Chapter 17). 5. Maintenance of Pressure in Biliary System
iii. Liver cells are involved in the removal of toxic
property of various harmful substances. Removal Due to the concentrating capacity, gallbladder maintains
of toxic property of the harmful agent is known a pressure of about 7 cm H2O in biliary system. This
as detoxification. pressure in the biliary system is essential for the release
Detoxification in liver occurs in two ways: of bile into the intestine.
a. Total destruction of the substances by means
of metabolic degradation. „ FILLING AND EMPTYING OF GALLBLADDER
b. Conversion of toxic substances into non­
toxic materials by means of conjugation with Usually, the sphincter of Oddi is closed during fasting
glucuronic acid or sulfates. and the pressure in the biliary system is only 7 cm H2O.
Because of this pressure, the bile from liver enters the
„ GALLBLADDER gallbladder.
While taking food or when chyme enters the
Bile secreted from liver is stored in gallbladder. The
intestine, gallbladder contracts along with relaxation of
capacity of gallbladder is approximately 50 mL.
sphincter of Oddi. Now, the pressure increases to about
Gallbladder is not essential for life and it is removed
(cholecystectomy) in patients suffering from gallbladder 20 cm H2O. Because of the increase in pressure, the
dysfunction. After cholecystectomy, patients do not bile from gallbladder enters the intestine. Contraction
suffer from any major disadvantage. In some species, of gallbladder is influenced by neural and hormonal
gallbladder is absent. factors.
 Chapter 40 t Liver and Gallbladder 257

FIGURE 40.9: Diagram showing the formation of bile from liver and changes taking place in the composition of gallbladder bile

1. Neural Factor 1. Choleretics

2. Cholagogue
Stimulation of parasympathetic nerve (vagus) causes
3. Hydrocholeretic agents.
contraction of gallbladder by releasing acetylcholine.
The vagal stimulation occurs during the cephalic phase
and gastric phase of gastric secretion. 1. Choleretics

Substances which increase the secretion of bile from

2. Hormonal Factor liver are known as choleretics.
When a fatty chyme enters the intestine from stomach, Effective choleretic agents are:
the intestine secretes the cholecystokinin, which causes i. Acetylcholine
contraction of the gallbladder. ii. Secretin
iii. Cholecystokinin
„ REGULATION OF BILE SECRETION iv. Acid chyme in intestine
Bile secretion is a continuous process though the amount v. Bile salts.
is less during fasting. It starts increasing after meals and
continues for three hours. Secretion of bile from liver 2. Cholagogues
and release of bile from the gallbladder are influenced
by some chemical factors, which are categorized into Cholagogue is an agent which increases the release of
three groups: bile into the intestine by contracting gallbladder.
 258 Section 4 t Digestive System

Common cholagogues are: Common causes of hemolytic jaundice are:

i. Bile salts i. Renal disorder
ii. Calcium ii. Hypersplenism
iii. Fatty acids iii. Burns
iv. Amino acids iv. Infections such as malaria
v. Inorganic acids v. Hemoglobin abnormalities such as sickle cell
All these substances stimulate the secretion of anemia or thalassemia
cholecystokinin, which in turn causes contraction of vi. Drugs or chemical substances causing red cell
gallbladder and flow of bile into intestine. damage
vii. Autoimmune diseases.
3. Hydrocholeretic Agents
Hydrocholeretic agent is a substance which causes 2. Hepatic or Hepatocellular or
the secretion of bile from liver, with large amount of Cholestatic Jaundice
water and less amount of solids. Hydrochloric acid is a Hepatic jaundice is the type of jaundice that occurs due
hydrocholeretic agent. to the damage of hepatic cells. Because of the damage,
the conjugated bilirubin from liver cannot be excreted
„ APPLIED PHYSIOLOGY and it returns to blood.
„ JAUNDICE OR ICTERUS Causes
Jaundice or icterus is the condition characterized by i. Infection (infective jaundice) by virus, resulting
yellow coloration of the skin, mucous membrane and in hepatitis (viral hepatitis)
deeper tissues due to increased bilirubin level in blood. ii. Alcoholic hepatitis
The word jaundice is derived from the French word iii. Cirrhosis of liver
‘jaune’ meaning yellow. iv. Exposure to toxic materials.
The normal serum bilirubin level is 0.5 to 1.5 mg/dL.
Jaundice occurs when bilirubin level exceeds 2 mg/dL. 3. Posthepatic or Obstructive or
Extrahepatic Jaundice
Types of Jaundice
Posthepatic type of jaundice occurs because of the
Jaundice is classified into three types: obstruction of bile flow at any level of the biliary system.
1. Prehepatic or hemolytic jaundice The bile cannot be excreted into small intestine. So, bile
2. Hepatic or hepatocellular jaundice salts and bile pigments enter the circulation. The blood
3. Posthepatic or obstructive jaundice. contains more amount of conjugated bilirubin (Table
40.2).
1. Prehepatic or Hemolytic Jaundice
Causes
Hemolytic jaundice is the type of jaundice that occurs
i. Gallstones
because of excessive destruction of RBCs resulting in
ii. Cancer of biliary system or pancreas.
increased blood level of free (unconjugated) bilirubin. In
this condition, the excretory function of liver is normal.
„ HEPATITIS
But the quantity of bilirubin increases enormously. The
liver cells cannot excrete that much excess bilirubin Hepatitis is the liver damage caused by many agents. It
rapidly. Unconjugated bilirubin is insoluble in water and is characterized by swelling and inadequate functioning
is not excreted in urine. So, it accumulates in the blood of liver. Hepatitis may be acute or chronic. In severe
resulting in jaundice. conditions, it may lead to liver failure and death.
Formation of urobilinogen also increases resulting in
the excretion of more amount of urobilinogen in urine. Causes and Types
Causes 1. Viral infection (viral hepatitis: see below)
Any condition that causes hemolytic anemia can lead to 2. Bacterial infection like leptospirosis and Q fever
hemolytic jaundice. 3. Excess consumption of alcohol
 Chapter 40 t Liver and Gallbladder 259

TABLE 40.2: Features of different types of jaundice

Prehepatic jaundice Hepatic jaundice Posthepatic jaundice

Features
(Hemolytic) (hepatocellular) (Obstructive)
Cause Excess breakdown of RBCs Liver damage Obstruction of bile ducts
Type of bilirubin in blood Unconjucated Conjugated and unconjugated Conjugated
Urinary excretion of Decreases
Increases Decreases
urobilinogen Absent in severe obstruction
Fecal excretion of
Increases Decreases (pale feces) Absent (clay­colored feces)
stercobilinogen
van den Bergh reaction Indirect – positive Biphasic Direct – positive
Liver functions Normal Abnormal Exaggerated
Anemia
Blood picture Reticulocytosis Normal Normal
Abnormal RBC
Albumin – increases
Plasma albumin and
Normal Globulin – increases Normal
globulin
A : G ratio – decreases
Hemorrhagic tendency Absent Present due to lack of vitamin K Present due to lack of vitamin K

4. Excess administration of drugs like paracetamol i. Stomach pain

5. Poisons like carbon tetrachloride and aflatoxin ii. Paleness of skin
6. Wilson disease (Chapter 151) iii. Dark­colored urine and pale stool
7. Circulatory insufficiency iv. Jaundice
v. Personality changes.
8. Inheritance from mother during parturition.

Viral Hepatitis „ CIRRHOSIS OF LIVER

Cirrhosis of liver refers to inflammation and damage of
Viral hepatitis is the type of hepatitis caused by viruses. parenchyma of liver. It results in degeneration of hepatic
It is caused by two types of viruses, hepatitis A and cells and dysfunction of liver.
hepatitis B.
Causes of viral hepatitis Causes

i. Mainly by intake of water and food contaminated 1. Infection

with hepatitis virus 2. Retention of bile in liver due to obstruction of ducts
ii. Sharing needles with infected persons of biliary system
iii. Accidental prick by infected needle 3. Enlargement of liver due to intoxication
iv. Having unprotected sex with infected persons 4. Inflammation around liver (perihepatitis)
v. Inheritance from mother during parturition
5. Infiltration of fat in hepatic cells.
vi. Blood transfusion from infected donors.
Hepatitis caused by hepatitis B virus is more Features
common and considered more serious because it may
lead to cirrhosis and cancer of liver. 1. Fever, nausea and vomiting
2. Jaundice
Features of Hepatitis 3. Increased heart rate and cardiac output
1. Fever 4. Portal hypertension
2. Nausea 5. Muscular weakness and wasting of muscles
3. Vomiting, diarrhea and loss of appetite 6. Drowsiness
4. Headache and weakness 7. Lack of concentration and confused state of mind
5. In addition, chronic hepatitis is characterized by 8. Coma in advanced stages.
 260 Section 4 t Digestive System

„ GALLSTONES 5. Damage or infection of gallbladder epithelium. It

alters the absorptive function of the mucous mem­
Definitions brane of the gallbladder. Sometimes, there is
Gallstone is a solid crystal deposit that is formed by excessive absorption of water or even bile salts,
cholesterol, calcium ions and bile pigments in the gall­ leading to increased concentration of cholesterol,
bladder or bile duct. Cholelithiasis is the presence of bile pigments and calcium ions
gallstones in gallbladder. Choledocholithiasis is the 6. Obstruction of bile flow from the gallbladder.
presence of gallstones in the bile ducts.
Diagnosis of Gallstone
Formation of Gallstones Presence of gallstone is diagnosed by ultrasound
scanning and cholangiography. Cholangiography is the
Normally, cholesterol present in the bile combines
radiological study of biliary ducts after the administration
with bile salts and lecithin, which make the cholesterol
of a contrast medium.
soluble in water. Under some abnormal conditions, this
water­soluble cholesterol precipitates resulting in the
Features
formation of gallstone.
Initially, small quantity of cholesterol begins to Common feature of gallstone is the pain in stomach area
precipitate forming many small crystals of cholesterol or in upper right part of the belly under the ribs. Other
in the mucosa of gallbladder. This stimulates further features include nausea, vomiting, abdominal bloating
formation of crystals and the crystals grow larger and and indigestion.
larger. Later, bile pigments and calcium are attached to
these crystals, resulting in formation of gallstones. Treatment for Gallstone
Simple cholesterol gallstones can be dissolved over
Causes for Gallstone Formation a period of one or two years by giving 1 to 1.5 gm
1. Reduction in bile salts and/or lecithin of chemodeoxycholic acid daily. This increases the
concentration of bile acids. So, excessive concentration
2. Excess of cholesterol
of bile does not occur.
3. Disturbed cholesterol metabolism In severe conditions, the gallbladder has to be
4. Excess of calcium ions due to increased concen­ removed (cholecystectomy). Laparoscopic surgery is
tration of bile the common method.
 Chapter
Small Intestine
41
„ FUNCTIONAL ANATOMY
„ INTESTINAL VILLI AND GLANDS
„ PROPERTIES AND COMPOSITION OF SUCCUS ENTERICUS
„ FUNCTIONS OF SUCCUS ENTERICUS
„ FUNCTIONS OF SMALL INTESTINE
„ REGULATION OF SECRETION OF SUCCUS ENTERICUS
„ METHODS OF COLLECTION OF SUCCUS ENTERICUS
„ APPLIED PHYSIOLOGY

„ FUNCTIONAL ANATOMY the surface area of mucous membrane by many folds.

Within each villus, there is a central channel called
Small intestine is the part of gastrointestinal (GI) tract,
lacteal, which opens into lymphatic vessels. It contains
extending between the pyloric sphincter of stomach
blood vessels also.
and ileocecal valve, which opens into large intestine. It
is called small intestine because of its small diameter,
„ CRYPTS OF LIEBERKÜHN OR
compared to that of the large intestine. But it is longer
INTESTINAL GLANDS
than large intestine. Its length is about 6 meter.
Important function of small intestine is absorption. Crypts of Lieberkühn or intestinal glands are simple
Maximum absorption of digested food products takes tubular glands of intestine. Intestinal glands do not
place in small intestine. penetrate the muscularis mucosa of the intestinal wall,
Small intestine consists of three portions: but open into the lumen of intestine between the villi.
1. Proximal part known as duodenum Intestinal glands are lined by columnar cells. Lining of
2. Middle part known as jejunum each gland is continuous with epithelial lining of the villi
3. Distal part known as ileum. (Fig. 41.1).
Wall of the small intestine has all the four layers as Epithelial cells lining the intestinal glands undergo
in stomach (Chapter 36). division by mitosis at a faster rate. Newly formed cells
push the older cells upward over the lining of villi.
„ INTESTINAL VILLI AND GLANDS These cells which move to villi are called enterocytes.
OF SMALL INTESTINE Enterocytes secrete the enzymes. Old enterocytes are
continuously shed into lumen along with enzymes.
„ INTESTINAL VILLI Types of cells interposed between columnar cells of
Mucous membrane of small intestine is covered by intestinal glands:
minute projections called villi. The height of villi is about 1. Argentaffin cells or enterochromaffin cells, which
1 mm and the diameter is less than 1 mm. secrete intrinsic factor of Castle
Villi are lined by columnar cells, which are called 2. Goblet cells, which secrete mucus
enterocytes. Each enterocyte gives rise to hair-like 3. Paneth cells, which secrete the cytokines called
projections called microvilli. Villi and microvilli increase defensins.
 262 Section 4 t Digestive System

„ FUNCTIONS OF SUCCUS ENTERICUS

„ 1. DIGESTIVE FUNCTION
Enzymes of succus entericus act on the partially
digested food and convert them into final digestive
products. Enzymes are produced and released into
succus entericus by enterocytes of the villi.

Proteolytic Enzymes
Proteolytic enzymes present in succus entericus are
the peptidases, which are given in Fig. 41.2. These
peptidases convert peptides into amino acids.

Amylolytic Enzymes
Amylolytic enzymes of succus entericus are listed in
Fig. 41.2.
Lactase, sucrase and maltase convert the
disaccharides (lactose, sucrose and maltose) into two
molecules of monosaccharides (Table 41.1).
Dextrinase converts dextrin, maltose and maltriose
into glucose. Trehalase or trehalose glucohydrolase
FIGURE 41.1: Intestinal gland and villus
causes hydrolysis of trehalose (carbohydrate present in
mushrooms and yeast) and converts it into glucose.

Lipolytic Enzyme
„ BRUNNER GLANDS
Intestinal lipase acts on triglycerides and converts them
In addition to intestinal glands, the first part of duodenum
into fatty acids.
contains some mucus glands, which are called Brunner
glands. These glands penetrate muscularis mucosa and
„ 2. PROTECTIVE FUNCTION
extend up to the submucus coat of the intestinal wall.
Brunner glands open into the lumen of intestine directly. i. Mucus present in the succus entericus protects
Brunner gland secretes mucus and traces of enzymes. the intestinal wall from the acid chyme, which
enters the intestine from stomach; thereby it
„ PROPERTIES AND COMPOSITION prevents the intestinal ulcer.
OF SUCCUS ENTERICUS ii. Defensins secreted by paneth cells of intestinal
glands are the antimicrobial peptides.
Secretion from small intestine is called succus These peptides are called natural peptide antibiotics
entericus. because of their role in killing the phagocytosed
bacteria.
„ PROPERTIES OF SUCCUS ENTERICUS
Volume : 1800 mL/day „ 3. ACTIVATOR FUNCTION
Reaction : Alkaline Enterokinase present in intestinal juice activates
pH : 8.3 trypsinogen into trypsin. Trypsin, in turn activates other
enzymes (Chapter 39).
„ COMPOSITION OF SUCCUS ENTERICUS
„ 4. HEMOPOIETIC FUNCTION
Succus entericus contains water (99.5%) and solids
(0.5%). Solids include organic and inorganic substances Intrinsic factor of Castle present in the intestine plays
(Fig. 41.2). Bicarbonate concentration is slightly high in an important role in erythropoiesis (Chapter 10). It is
succus entericus. necessary for the absorption of vitamin B12.
 Chapter 41 t Small Intestine 263

FIGURE 41.2: Composition of succus entericus

„ 5. HYDROLYTIC PROCESS „ 5. ACTIVATOR FUNCTION

Intestinal juice helps in all the enzymatic reactions of Refer functions of succus entericus.
digestion.
„ 6. HEMOPOIETIC FUNCTION
„ FUNCTIONS OF SMALL INTESTINE Refer functions of succus entericus.
„ 1. MECHANICAL FUNCTION
„ 7. HYDROLYTIC FUNCTION
Mixing movements of small intestine help in the thorough
mixing of chyme with the digestive juices like succus Refer functions of succus entericus.
entericus, pancreatic juice and bile.
TABLE 41.1: Digestive enzymes of succus entericus
„ 2. SECRETORY FUNCTION Enzyme Substrate End products
Small intestine secretes succus entericus, enterokinase Peptidases Peptides Amino acids
and the GI hormones.
Sucrase Sucrose Fructose and glucose

„ 3. HORMONAL FUNCTION Maltose and

Maltase Glucose
maltriose
Small intestine secretes many GI hormones such as
Galactose and
secretin, cholecystokinin, etc. These hormones regulate Lactase Lactose
glucose
the movement of GI tract and secretory activities of small
intestine and pancreas (Chapter 44). Dextrin, maltose
Dextrinase Glucose
and maltriose
„ 4. DIGESTIVE FUNCTION Trehalase Trehalose Glucose
Intestinal lipase Triglycerides Fatty acids
Refer functions of succus entericus.
 264 Section 4 t Digestive System

„ 8. ABSORPTIVE FUNCTIONS entericus. Stimulation of sympathetic nerves causes

vasoconstriction and decreases the secretion of succus
Presence of villi and microvilli in small intestinal mucosa
entericus. But, the role of these nerves in the regulation
increases the surface area of mucosa. This facilitates
of intestinal secretion in physiological conditions is
the absorptive function of intestine.
Digested products of foodstuffs, proteins, carbo- uncertain.
hydrates, fats and other nutritive substances such as However, the local nervous reflexes play an
vitamins, minerals and water are absorbed mostly in small important role in increasing the secretion of intestinal
intestine. From the lumen of intestine, these substances juice. When chyme enters the small intestine, the mucosa
pass through lacteal of villi, cross the mucosa and enter is stimulated by tactile stimuli or irritation. It causes the
the blood directly or through lymphatics. development of local nervous reflexes, which stimulate
the glands of intestine.
Absorption of Carbohydrates
„ HORMONAL REGULATION
Refer Chapter 45.
When chyme enters the small intestine, intestinal mucosa
Absorption of Proteins secretes enterocrinin, secretin and cholecystokinin,
which promote the secretion of succus entericus by
Refer Chapter 46.
stimulating the intestinal glands.
Absorption of Fats
„ METHODS OF COLLECTION
Refer Chapter 47. OF SUCCUS ENTERICUS
Absorption of Water and Minerals „ IN HUMAN
i. In small intestine, sodium is absorbed actively. It In human beings, the intestinal juice is collected by
is responsible for absorption of glucose, amino using multilumen tube. The multilumen tube is inserted
acids and other substances by means of sodium through nose or mouth, until the tip of this tube reaches
cotransport. the intestine. A line is marked on the tube. Entrance of
ii. Water moves in or out of the intestinal lumen tip of the tube into small intestine is indicated when this
until the osmotic pressure of intestinal contents line comes near the mouth. This tube has three lumens.
becomes equal to that of plasma. To the outer two lumens, small balloons are attached.
iii. In ileum, chloride ion is actively absorbed in When these balloons are inflated, the intestine is
exchange for bicarbonate. The significance of enlarged. Now, the intestinal juice is collected through
this exchange is not known. the middle lumen, by means of aspiration.
iv. Calcium is actively absorbed mostly in upper
part of small intestine. „ IN ANIMALS

Absorption of Vitamins Thiry Loop

Most of the vitamins are absorbed in upper part of A portion of intestine is separated from the gut by
small intestine and vitamin B12 is absorbed in ileum. incising at both ends. The cut ends of the main gut are
Absorption of water-soluble vitamins is faster than fat- connected and the continuity is re-established. One
soluble vitamins. end of isolated segment is closed and the other end is
brought out through abdominal wall. It is called Thiry
„ REGULATION OF SECRETION loop or Thiry fistula.
OF SUCCUS ENTERICUS
Secretion of succus entericus is regulated by both Thiry-Vella Loop
nervous and hormonal mechanisms. Thiry-Vella loop is the modified Thiry loop. In this, a
long segment of intestine is cut and separated from the
„ NERVOUS REGULATION main gut. Both the ends of this segment are brought out
Stimulation of parasympathetic nerves causes vaso- through the abdominal wall. The cut ends of the main
dilatation and increases the secretion of succus gut are joined.
 Chapter 41 t Small Intestine 265

„ APPLIED PHYSIOLOGY Cause

„ 1. MALABSORPTION The cause of this disease is not known and it may be

related to infectious organisms.
Malabsorption is the failure to absorb nutrients such as
proteins, carbohydrates, fats and vitamins.
Features
Malabsorption affects growth and development of
the body. It also causes specific diseases (see below). i. Indigestion
ii. Diarrhea
„ 2. MALABSORPTION SYNDROME
iii. Anorexia and weight loss
Malabsorption syndrome is the condition characterized iv. Abdominal and muscle cramps.
by the failure of digestion and absorption in small
intestine. Malabsorption syndrome is generally caused „ 5. STEATORRHEA
by Crohn’s disease, tropical sprue, steatorrhea and
celiac disease. Steatorrhea is the condition caused by deficiency of
pancreatic lipase, resulting in malabsorption of fat. Refer
„ 3. CROHN’S DISEASE OR ENTERITIS Chapter 39 for details.
Enteritis is an inflammatory bowel disease (IBD), charac-
„ 6. CELIAC DISEASE
terized by inflammation of small intestine. Usually, it
affects the lower part of small intestine, the ileum. The Celiac disease is an autoimmune disorder characterized
inflammation causes malabsorption and diarrhea. by the damage of mucosa and atrophy of villi in small
intestine, resulting in impaired digestion and absorption.
Causes It is also known as gluten-sensitive enteropathy, celiac
Crohn’s disease develops because of abnormalities of sprue and non-tropical sprue.
the immune system. The immune system reacts to a virus
or a bacterium, resulting in inflammation of the intestine. Cause

Celiac disease is caused by gluten. It is a protein present

Features
in wheat, oats, rye, barley and other grains. Gluten is
i. Malabsorption of vitamin like a poison to individuals with celiac disease, because
ii. Weight loss it damages the intestine severely.
iii. Abdominal pain
iv. Diarrhea Features
v. Rectal bleeding, anemia and fever
vi. Delayed or stunted growth in children. i. Diarrhea
ii. Steatorrhea
„ 4. TROPICAL SPRUE iii. Abdominal pain
Tropical sprue is a malabsorption syndrome, affecting iv. Weight loss
the residents of or the visitors to tropical areas where v. Irritability
the disease is epidemic. vi. Depression.
 Chapter
Large Intestine
42
„ FUNCTIONAL ANATOMY
„ PARTS OF LARGE INTESTINE
„ STRUCTURE OF WALL OF LARGE INTESTINE
„ SECRETIONS OF LARGE INTESTINE
„ COMPOSITION OF LARGE INTESTINAL JUICE
„ FUNCTIONS OF LARGE INTESTINAL JUICE
„ FUNCTIONS OF LARGE INTESTINE
„ ABSORPTIVE FUNCTION
„ FORMATION OF FECES
„ EXCRETORY FUNCTION
„ SECRETORY FUNCTION
„ SYNTHETIC FUNCTION
„ DIETARY FIBER
„ APPLIED PHYSIOLOGY
„ DIARRHEA
„ CONSTIPATION
„ APPENDICITIS
„ ULCERATIVE COLITIS

„ FUNCTIONAL ANATOMY OF „ STRUCTURE OF WALL OF

LARGE INTESTINE LARGE INTESTINE
Large intestine or colon extends from ileocecal valve up Wall of large intestine is formed by four layers of
to anus (Fig. 36.1). structures like any other part of the gut.
1. Serous layer: It is formed by peritoneum
„ PARTS OF LARGE INTESTINE 2. Muscular layer: Smooth muscles of large intestine
Large intestine is made up of the following parts: are distributed in two layers, namely the outer
1. Cecum with appendix longitudinal layer and inner circular layer. The
2. Ascending colon longitudinal muscle fibers of large intestine are
3. Transverse colon arranged in the form of three long bands called
4. Descending colon tenia coli. The length of the tenia coli is less when
5. Sigmoid colon or pelvic colon compared to the length of large intestine. Because
6. Rectum of this, the large intestine is made into series of
7. Anal canal. pouches called haustra
 Chapter 42 t Large Intestine 267

3. Submucus layer: It is not well developed in large „ FUNCTIONS OF LARGE INTESTINE

intestine
4. Mucus layer: The crypts of Leiberkühn are present „ 1. ABSORPTIVE FUNCTION
in mucosa of large intestine. But the villi, which are
Large intestine plays an important role in the absorption
present in mucus membrane of small intestine, are
of various substances such as:
absent in the large intestine. Only mucus-secreting
i. Water
glands are present in the mucosa of large intestine.
ii. Electrolytes
„ SECRETIONS OF LARGE INTESTINE iii. Organic substances like glucose
iv. Alcohol
Large intestinal juice is a watery fluid with pH of 8.0. v. Drugs like anesthetic agents, sedatives and
steroids.
„ COMPOSITION OF LARGE INTESTINAL JUICE
Large intestinal juice contains 99.5% of water and 0.5% „ 2. FORMATION OF FECES
of solids (Fig. 42.1). Digestive enzymes are absent and
concentration of bicarbonate is high in large intestinal After the absorption of nutrients, water and other
juice. substances, the unwanted substances in the large
intestine form feces. This is excreted out.
„ FUNCTIONS OF LARGE INTESTINAL JUICE
„ 3. EXCRETORY FUNCTION
Neutralization of Acids
Strong acids formed by bacterial action in large intestine Large intestine excretes heavy metals like mercury,
are neutralized by the alkaline nature of large intestinal lead, bismuth and arsenic through feces.
juice. The alkalinity of this juice is mainly due to the
presence of large quantity of bicarbonate. „ 4. SECRETORY FUNCTION

Large intestine secretes mucin and inorganic substances

Lubrication Activity
like chlorides and bicarbonates.
Mucin present in the secretion of large intestine lub-
ricates the mucosa of large intestine and the bowel „ 5. SYNTHETIC FUNCTION
contents, so that, the movement of bowel is facilitated.
Mucin also protects the mucus membrane of Bacterial flora of large intestine synthesizes folic acid,
large intestine by preventing the damage caused by vitamin B12 and vitamin K. By this function, large
mechanical injury or chemical substances. intestine contributes in erythropoietic activity and blood
clotting mechanism.

„ DIETARY FIBER
Dietary fiber or roughage is a group of food particles
which pass through stomach and small intestine without
being digested and reach the large intestine unchanged.
Other nutritive substances of food are digested and
absorbed before reaching large intestine.
Characteristic feature of dietary fiber is that it is
not hydrolyzed by digestive enzymes. So, it escapes
digestion in small intestine and passes to large intestine.
It provides substrate for microflora of large intestine and
increases the bacterial mass. The anaerobic bacteria,
in turn, degrade the fermentable components of the
fiber. Thus, in large intestine, some of the components
of fiber are broken down and absorbed and remaining
FIGURE 42.1: Composition of large intestinal juice components are excreted through feces.
 268 Section 4 t Digestive System

Components of Dietary Fiber 1. Dietary abuse: Diarrhea is caused by intake of

contaminated water or food, artificial sweeteners
Major components of dietary fiber are cellulose,
found in food, spicy food, etc.
hemicelluloses, D-glucans, pectin, lignin and gums. 2. Food intolerance: Acute diarrhea is caused mainly
Cellulose, hemicelluloses and pectin are partially by indigestion of food substances, particularly
degradable, while other components are indigestible. lactose, a sugar present in milk and milk products
Dietary fiber also contains minerals, antioxidants and may not be digested easily
other chemicals that are useful for health. 3. Infections by:
i. Bacteria such as Escherichia coli, Salmonella,
Sources of Dietary Fiber Shigella, etc.
Sources of dietary fiber are fruits, vegetables, cereals, ii. Viruses like rotavirus, hepatitis virus, etc.
bread and wheat grain (particularly its outer layer). iii. Parasites like Entamoeba histolytica, Giardia
lamblia, etc.
Significance of Dietary Fiber 4. Reaction to medicines such as:
Diet with high dietary fiber has health benefits since i. Antibiotics
dietary fiber: ii. Antihypertensive drugs
1. Delays emptying of stomach iii. Antacids containing magnesium
2. Increases formation of bulk and soft feces and iv. Laxatives
eases defecation 5. Intestinal diseases: Chronic diarrhea occurs during
3. Contains substances such as antioxidants and other inflammation of intestine, irritable bowel syndrome
useful substances.
and abnormal motility of the intestine.
When high dietary fiber food is taken, other foods,
which may cause some diseases may be decreased in
Features
quantity or completely excluded from diet. Diet with high
fiber content tends to be low in energy and it may be Severe diarrhea results in loss of excess water and
useful in reducing the body weight. Some components electrolytes. This leads to dehydration and electrolyte
of dietary fiber also reduce blood cholesterol level and imbalance. Chronic diarrhea results in hypokalemia
thereby decrease the risk for coronary heart disease and metabolic acidosis. Other features of diarrhea are
and gallstones. abdominal pain, nausea and bloating (a condition in
Dietary fiber is suggested for treating or to prevent which the subject feels the abdomen full and tight due
constipation and bowel syndrome. It is also useful in to excess intestinal gas).
treatment of some disorders such as diabetics, cancer,
ulcer, etc.
„ CONSTIPATION

„ APPLIED PHYSIOLOGY Failure of voiding of feces, which produces discomfort is

known as constipation. It is due to the lack of movements
„ DIARRHEA necessary for defecation (Chapter 43). Due to the
Diarrhea is the frequent and profuse discharge of absence of mass movement in colon, feces remain in
intestinal contents in loose and fluid form. It occurs due the large intestine for a long time, resulting in absorption
to the increased movement of intestine. It may be acute of fluid. So the feces become hard and dry.
or chronic.
Causes
Causes
1. Dietary causes
Normally, when digested food passes through colon,
large portion of fluid is absorbed and only a semisolid Lack of fiber or lack of liquids in diet causes
stool remains. In diarrhea, the fluid is not absorbed constipation.
sufficiently, resulting in watery bowel discharge. Acute 2. Irregular bowel habit
diarrhea may be caused by temporary problems like
infection and chronic diarrhea may be due to disorders Irregular bowel habit is most common cause for
of intestinal mucosa. Thus, the general causes of constipation. It causes constipation by inhibiting the
diarrhea are: normal defecation reflexes.
 Chapter 42 t Large Intestine 269

3. Spasm of sigmoid colon lower right side of the abdomen. It becomes severe
within 6 to 12 hours
Spasm in the sigmoid colon (spastic colon) prevents its
2. Nausea
motility, resulting in constipation.
3. Vomiting
4. Diseases 4. Constipation or diarrhea
Constipation is common in many types of diseases. 5. Difficulty in passing gas
6. Low fever
5. Dysfunction of myenteric plexus 7. Abdominal swelling
in large intestine – megacolon 8. Loss of appetite.
Megacolon is the condition characterized by distension If not treated immediately, the appendix may rupture
and hypertrophy of colon, associated with constipation. and the inflammation will spread to the whole body,
It is caused by the absence or damage of ganglionic leading to severe complications, sometimes even death.
cells in myenteric plexus, which causes dysfunction Therefore, the treatment of appendicitis is considered
of myenteric plexus. It leads to accumulation of large as an emergency.
quantity of feces in colon. The colon is distended to a Usual standard treatment for appendicitis is
diameter of 4 to 5 inch. It also results in hypertrophy of appendectomy (surgical removal of appendix).
colon. Congenital development of megacolon is called
Hirschsprung disease. „ ULCERATIVE COLITIS

6. Drugs Ulcerative colitis is an inflammatory bowel disease

(IBD), characterized by the inflammation and ulcerative
The drugs like diuretics, pain relievers (narcotics), aberrations in the wall of the large intestine. It is also
antihypertensive drugs (calcium channel blockers), known as colitis or proctitis. Rectum and lower part of
antiparkinson drugs, antidepressants and the anticon- the colon are commonly affected. Sometimes, the entire
vulsants cause constipation. colon is affected.
Ulcerative colitis can occur at any age. More
„ APPENDICITIS commonly, it affects people in the age group of 15 to 30
Inflammation of appendix is known as appendicitis. years. Rarely it affects 50 to 70 years old people.
Appendix is a small, worm-like appendage, projecting
from cecum of ascending colon. It is situated on the Cause
lower right side of the abdomen. Exact cause for ulcerative colitis is not known. However,
Appendix does not have any function in human it is believed that the interaction between the immune
beings. But, it can create major problems when diseased.
system and viral or bacterial infection causes this
Appendicitis can develop at any age. However, it is very
disease.
common between 10 and 30 years of age.
Features
Causes
1. Abdominal pain
The cause for appendicitis is not known. It may occur by
2. Diarrhea with blood in the stools
bacterial or viral infection. It also occurs during blockage
3. Early fatigue
of connection between appendix and large intestine by
4. Loss of appetite and weight
feces, foreign body or tumor.
5. Arthritis and osteoporosis
6. Eye inflammation
Features
7. Liver diseases like hepatitis, cirrhosis, etc.
1. Main symptom of appendicitis is the pain, which 8. Skin rashes
starts around the umbilicus and then spreads to the 9. Anemia.
 Movements of Chapter
Gastrointestinal Tract 43
„ MASTICATION
„ DEGLUTITION
„ MOVEMENTS OF STOMACH
„ FILLING AND EMPTYING OF STOMACH
„ VOMITING
„ MOVEMENTS OF SMALL INTESTINE
„ MOVEMENTS OF LARGE INTESTINE
„ DEFECATION
„ EVACUATION OF GASES FROM GASTROINTESTINAL TRACT

„ MASTICATION „ CONTROL OF MASTICATION

Mastication or chewing is the first mechanical process Action of mastication is mostly a reflex process. It is
in the gastrointestinal (GI) tract, by which the food carried out voluntarily also. The center for mastication
substances are torn or cut into small particles and is situated in medulla and cerebral cortex. Muscles of
crushed or ground into a soft bolus. mastication are supplied by mandibular division of 5th
cranial (trigeminal) nerve.
Significances of mastication
„ DEGLUTITION
1. Breakdown of foodstuffs into smaller particles
2. Mixing of saliva with food substances thoroughly Definition
3. Lubrication and moistening of dry food by saliva, so
that the bolus can be easily swallowed Deglutition or swallowing is the process by which food
4. Appreciation of taste of the food. moves from mouth into stomach.

„ MUSCLES AND THE MOVEMENTS Stages of Deglutition

OF MASTICATION Deglutition occurs in three stages:
I. Oral stage, when food moves from mouth to
Muscles of Mastication
pharynx
1. Masseter muscle II. Pharyngeal stage, when food moves from
2. Temporal muscle pharynx to esophagus
3. Pterygoid muscles III. Esophageal stage, when food moves from
4. Buccinator muscle. esophagus to stomach.

Movements of Mastication „ ORAL STAGE OR FIRST STAGE

1. Opening and closure of mouth Oral stage of deglutition is a voluntary stage. In this
2. Rotational movements of jaw stage, the bolus from mouth passes into pharynx by
3. Protraction and retraction of jaw. means of series of actions.
 Chapter 43 t Movements of Gastrointestinal Tract 271

Sequence of Events during Oral Stage iv. All these movements arrest respiration for a few
seconds. It is called deglutition apnea.
1. Bolus is placed over postero-dorsal surface of the
tongue. It is called the preparatory position Deglutition apnea
2. Anterior part of tongue is retracted and depressed.
Apnea refers to temporary arrest of breathing. Deglutition
3. Posterior part of tongue is elevated and retracted
apnea or swallowing apnea is the arrest of breathing
against the hard palate. This pushes the bolus
during pharyngeal stage of deglutition.
backwards into the pharynx
4. Forceful contraction of tongue against the palate
4. Entrance of Bolus into Esophagus
produces a positive pressure in the posterior part of
oral cavity. This also pushes the food into pharynx As the other three paths are closed, the bolus has to
(Fig. 43.1). pass only through the esophagus. This occurs by the
combined effects of various factors:
„ PHARYNGEAL STAGE OR SECOND STAGE i. Upward movement of larynx stretches the
opening of esophagus
Pharyngeal stage is an involuntary stage. In this stage,
the bolus is pushed from pharynx into the esophagus. ii. Simultaneously, upper 3 to 4 cm of esophagus
Pharynx is a common passage for food and air. It relaxes. This part of esophagus is formed by the
divides into larynx and esophagus. Larynx lies anteriorly cricopharyngeal muscle and it is called upper
and continues as respiratory passage. Esophagus lies esophageal sphincter or pharyngoesophageal
behind the larynx and continues as GI tract. Since sphincter
pharynx communicates with mouth, nose, larynx and iii. At the same time, peristaltic contractions start in
esophagus, during this stage of deglutition, bolus from the pharynx due to the contraction of pharyngeal
the pharynx can enter into four paths: muscles
1. Back into mouth iv. Elevation of larynx also lifts the glottis away from
2. Upward into nasopharynx the food passage.
3. Forward into larynx All the factors mentioned above act together so
4. Downward into esophagus. that, bolus moves easily into the esophagus. The whole
However, due to various coordinated movements, process takes place within 1 to 2 seconds and this
bolus is made to enter only the esophagus. Entrance of process is purely involuntary.
bolus through other paths is prevented as follows:
„ ESOPHAGEAL STAGE OR THIRD STAGE
1. Back into Mouth
Esophageal stage is also an involuntary stage. In
Return of bolus back into the mouth is prevented by: this stage, food from esophagus enters the stomach.
i. Position of tongue against the soft palate (roof Esophagus forms the passage for movement of bolus
of the mouth) from pharynx to the stomach. Movements of esophagus
ii. High intraoral pressure, developed by the are specifically organized for this function and the
movement of tongue. movements are called peristaltic waves. Peristalsis
means a wave of contraction, followed by the wave
2. Upward into Nasopharynx of relaxation of muscle fibers of GI tract, which travel
in aboral direction (away from mouth). By this type of
Movement of bolus into the nasopharynx from pharynx movement, the contents are propelled down along the
is prevented by elevation of soft palate along with its GI tract.
extension called uvula. When bolus reaches the esophagus, the peristaltic
waves are initiated. Usually, two types of peristaltic
3. Forward into Larynx contractions are produced in esophagus.
Movement of bolus into the larynx is prevented by the 1. Primary peristaltic contractions
2. Secondary peristaltic contractions.
following actions:
i. Approximation of the vocal cords
1. Primary Peristaltic Contractions
ii. Forward and upward movement of larynx
iii. Backward movement of epiglottis to seal the When bolus reaches the upper part of esophagus, the
opening of the larynx (glottis) peristalsis starts. This is known as primary peristalsis.
 272 Section 4 t Digestive System

FIGURE 43.1: Stages of deglutition. A. Preparatory stage; B. Oral stage; C. Pharyngeal stage; D. Esophageal stage.

After origin, the peristaltic contractions pass down „ DEGLUTITION REFLEX

through the rest of the esophagus, propelling the bolus
Though the beginning of swallowing is a voluntary
towards stomach. act, later it becomes involuntary and is carried out by
Pressure developed during the primary peristaltic a reflex action called deglutition reflex. It occurs during
contractions is important to propel the bolus. Initially, the pharyngeal and esophageal stages.
the pressure becomes negative in the upper part of
esophagus. This is due to the stretching of the closed Stimulus
esophagus by the elevation of larynx. But immediately,
When the bolus enters the oropharyngeal region, the
the pressure becomes positive and increases up to 10
receptors present in this region are stimulated.
to 15 cm of H2O.
Afferent Fibers
2. Secondary Peristaltic Contractions
Afferent impulses from the oropharyngeal receptors
If the primary peristaltic contractions are unable to propel pass via the glossopharyngeal nerve fibers to the
the bolus into the stomach, the secondary peristaltic deglutition center.
contractions appear and push the bolus into stomach.
Secondary peristaltic contractions are induced by Center
the distention of upper esophagus by the bolus. After Deglutition center is at the floor of the fourth ventricle in
origin, these contractions pass down like the primary medulla oblongata of brain.
contractions, producing a positive pressure.
Efferent Fibers
Role of Lower Esophageal Sphincter
Impulses from deglutition center travel through
Distal 2 to 5 cm of esophagus acts like a sphincter glossopharyngeal and vagus nerves (parasympathetic
and it is called lower esophageal sphincter. It is motor fibers) and reach soft palate, pharynx and
constricted always. When bolus enters this part of the esophagus. The glossopharyngeal nerve is concerned
esophagus, this sphincter relaxes so that the contents with pharyngeal stage of swallowing. The vagus nerve
enter the stomach. After the entry of bolus into the is concerned with esophageal stage.
stomach, the sphincter constricts and closes the lower
end of esophagus. The relaxation and constriction of Response
sphincter occur in sequence with the arrival of peristaltic The reflex causes upward movement of soft palate, to
contractions of esophagus. close nasopharynx and upward movement of larynx,
 Chapter 43 t Movements of Gastrointestinal Tract 273

to close respiratory passage so that bolus enters the Types of movements in stomach
esophagus. Now the peristalsis occurs in esophagus,
1. Hunger contractions
pushing the bolus into stomach.
2. Receptive relaxation
„ APPLIED PHYSIOLOGY 3. Peristalsis.

1. Dysphagia „ 1. HUNGER CONTRACTIONS

Dysphagia means difficulty in swallowing. Hunger contractions are the movements of empty
Causes of dysphagia stomach. These contractions are related to the sensa-
tions of hunger.
i. Mechanical obstruction of esophagus due to Hunger contractions are the peristaltic waves
tumor, strictures, diverticular hernia (out pouch- superimposed over the contractions of gastric smooth
ing of the wall), etc.
muscle as a whole. This type of peristaltic waves is
ii. Decreased movement of esophagus due to different from the digestive peristaltic contractions.
neurological disorders such as parkinsonism The digestive peristaltic contractions usually occur in
iii. Muscular disorders leading to difficulty in swall- body and pyloric parts of the stomach. But, peristaltic
owing during oral stage or esophageal stage. contractions of empty stomach involve the entire
stomach. Hunger contractions are of three types:
2. Esophageal Achalasia or Achalasia Cardia
Esophageal achalasia or achalasia cardia is a neuro- Type I Hunger Contractions
muscular disease, characterized by accumulation of Type I hunger contractions are the first contractions
food substances in the esophagus preventing normal
to appear in the empty stomach, when the tone of the
swallowing. It is due to the failure of lower esophageal
gastric muscles is low. Each contraction lasts for about
(cardiac) sphincter to relax during swallowing. The accu-
20 seconds. The interval between contractions is about
mulated food substances cause dilatation of esophagus.
3 to 4 seconds. Tone of the muscles does not increase
Features of esophageal achalasia between contractions. Pressure produced by these
i. Dysphagia contractions is about 5 cm of H2O.
ii. Chest pain
iii. Weight loss Type II Hunger Contractions
iv. Cough. Type II hunger contractions appear when the tone of
stomach is stronger. Tone increases in stomach if food
3. Gastroesophageal Reflux Disease (GERD) intake is postponed, even after the appearance of the
GERD is a disorder characterized by regurgitation type I contractions. Each of the type II contractions
of acidic gastric content through esophagus. The lasts for 20 seconds like type I contractions. But the
regurgitated gastric content flows into pharynx or mouth. pause between the contractions is decreased. Pressure
Regurgitation is due to the weakness or incompetence produced by these contractions is 10 to 15 cm of H2O.
(failure to constrict) of lower esophageal sphincter.
Type III Hunger Contractions
Features of GERD
Type III hunger contractions are like incomplete tetanus.
i. Heart burn or pyrosis (painful burning sensation
These contractions appear when the hunger becomes
in chest due to regurgitation of acidic gastric
severe and the tone increases to a great extent. Type III
content into esophagus)
ii. Esophagitis (inflammation of esophagus) hunger contractions are rare in man as the food is taken
iii. Dysphagia usually before the appearance of these contractions.
iv. Cough and change of voice These contractions last for 1 to 5 minutes. The pressure
v. Esophageal ulcers or cancer (in chronic cases). produced by these contractions increases to 10 to 20
cm of H2O.
When the stomach is empty, the type I contractions
„ MOVEMENTS OF STOMACH
occur first, followed by type II contractions. If food intake
Activities of smooth muscles of stomach increase during is still postponed, then type III contractions appear and
gastric digestion (when stomach is filled with food) and as soon as food is consumed, hunger contractions
when the stomach is empty. disappear.
 274 Section 4 t Digestive System

„ 2. RECEPTIVE RELAXATION Chyme

Receptive relaxation is the relaxation of the upper por- Chyme is the semisolid mass of partially digested food
tion of the stomach when bolus enters the stomach from that is formed in the stomach. It is acidic in nature.
esophagus. It involves the fundus and upper part of the Acid chyme is emptied from stomach into the intestine
body of stomach. Its significance is to accommodate the slowly, with the help of peristaltic contractions. It takes
food easily, without much increase in pressure inside about 3 to 4 hours for emptying of the chyme. This slow
the stomach. This process is called accommodation of emptying is necessary to facilitate the final digestion and
stomach. maximum (about 80%) absorption of the digested food
materials from small intestine. Gastric emptying occurs
„ 3. PERISTALSIS
due to the peristaltic waves in the body and pyloric part
When food enters the stomach, the peristaltic contrac- of the stomach and simultaneous relaxation of pyloric
tion or peristaltic wave appears with a frequency of 3 sphincter.
per minute. It starts from the lower part of the body of Gastric emptying is influenced by various factors of
stomach, passes through the pylorus till the pyloric the gastric content and food.
sphincter.
Initially, the contraction appears as a slight indenta- Factors Affecting Gastric Emptying
tion on the greater and lesser curvatures and travels
towards pylorus. The contraction becomes deeper while 1. Volume of gastric content
traveling. Finally, it ends with the constriction of pyloric
For any type of meal, gastric emptying is directly
sphincter. Some of the waves disappear before reaching
proportional to the volume. If the content of stomach
the sphincter. Each peristaltic wave takes about one
is more, a large amount is emptied into the intestine
minute to travel from the point of origin to the point of
ending. rapidly.
This type of peristaltic contraction is called digestive 2. Consistency of gastric content
peristalsis because it is responsible for the grinding of
food particles and mixing them with gastric juice for Emptying of the stomach depends upon consistency
digestive activities. (degree of density) of the contents. Liquids, particularly
the inert liquids like water leave the stomach rapidly.
„ FILLING AND EMPTYING OF STOMACH Solids leave the stomach only after being converted
into fluid or semifluid. Undigested solid particles are not
„ FILLING OF STOMACH easily emptied.
While taking food, it arranges itself in the stomach in 3. Chemical composition
different layers. The first eaten food is placed against
the greater curvature in the fundus and body of the Chemical composition of the food also plays an important
stomach. The successive layers of food particles lie role in the emptying of the stomach. Carbohydrates are
nearer, the lesser curvature, until the last portion of emptied faster than the proteins. Proteins are emptied
food eaten lies near the upper end of lesser curvature, faster than the fats. Thus, the fats are emptied very
adjacent to cardiac sphincter. slowly.
The liquid remains near the lesser curvature and
flows towards the pyloric end of the stomach along a 4. pH of the gastric content
V-shaped groove. This groove is formed by the smooth
Gastric emptying is directly proportional to pH of the
muscle and it is called magenstrasse. But, if a large
quantity of fluid is taken, it flows around the entire food chyme.
mass and is distributed over the interior part of stomach, 5. Osmolar concentration of gastric content
between wall of the stomach and food mass.
Gastric content which is isotonic to blood, leaves the
„ EMPTYING OF STOMACH stomach rapidly than the hypotonic or hypertonic
content.
Gastric emptying is the process by which the chyme
from stomach is emptied into intestine. Food that is „ REGULATION OF GASTRIC EMPTYING
swallowed enters the stomach and remains there for
about 3 hours. During this period, digestion takes place. Gastric emptying is regulated by nervous and hormonal
Partly digested food in stomach becomes the chyme. factors.
 Chapter 43 t Movements of Gastrointestinal Tract 275

Nervous Factor symptoms. It is due to the rapid or quick dumping

of undigested food from stomach into the jejunum.
Nervous factor which regulates the emptying of stomach
is the enterogastric reflex. It occurs in patients following partial gastrectomy
(removal of stomach) or gastroenterostomy (gastric
Enterogastric Reflex bypass surgery). The rapid gastric emptying may begin
immediately after taking meals (early dumping) or about
Enterogastric reflex is the reflex that inhibits gastric few hours after taking meals (late dumping).
emptying. It is elicited by the presence of chyme in
the duodenum, which prevents further emptying of Causes
stomach.
i. Gastric surgery.
Mechanism of enterogastric reflex ii. Zollinger-Ellison syndrome (rare disorder due to
1. Presence of chyme in duodenum causes generation severe peptic ulcer and gastrin-secreting tumor
of nerve impulses which are transmitted to stomach in pancreas).
by the intrinsic nerve fibers of GI tract. After reaching Symptoms of early dumping
the stomach, these impulses inhibit emptying.
2. Impulses from duodenum pass via extrinsic i. Nausea and vomiting
sympathetic fibers to stomach and inhibit emptying. ii. Bloating (increase in abdominal volume with
3. Some impulses from duodenum travel through feeling of abdominal fullness and tightness)
afferent vagal fibers to the brainstem. Normally, iii. Diarrhea
brainstem neurons send excitatory impulses to
iv. Sweating and weakness
stomach through efferent vagal fibers and stimulate
gastric emptying. However, the impulses from v. Fatigue and dizziness
duodenum inhibit these brainstem neurons and vi. Fainting and palpitations (sensation of heart
thereby inhibit gastric emptying. beat).
Factors which initiate enterogastric reflex Symptoms of late dumping
1. Duodenal distension i. Hypoglycemia
2. Irritation of the duodenal mucosa ii. Sweating and weakness
3. Acidity of the chyme
iii. Dizziness.
4. Osmolality of the chyme
5. Breakdown products of proteins and fats.
2. Gastroparesis
Hormonal Factors Gastroparesis is a chronic disorder characterized
When an acid chyme enters the duodenum, the by delayed gastric emptying. It usually occurs as a
duodenal mucosa releases some hormones which secondary disorder, precipitated by a primary cause.
enter the stomach through blood and inhibit the motility Causes
of stomach.
i. Diabetes mellitus
Hormones inhibiting gastric motility and emptying
ii. Postsurgical complications
1. Vasoactive intestinal peptide (VIP) iii. Motility disorder
2. Gastric inhibitory peptide (GIP) iv. Gastric infection
3. Secretin
v. Metabolic and endocrine disorder
4. Cholecystokinin
5. Somatostatin vi. Decrease in myenteric ganglia (rare).
6. Peptide YY. Symptoms

„ APPLIED PHYSIOLOGY – ABNORMAL i. Early satiety (feeling full with small quantity of
GASTRIC EMPTYING food)
ii. Nausea
1. Gastric Dumping Syndrome iii. Vomiting
Gastric dumping syndrome or rapid gastric emptying is iv. Bloating
the condition characterized by series of upper abdominal v. Upper abdominal discomfort.
 276 Section 4 t Digestive System

„ VOMITING 3. Closure of glottis

4. Upward and forward movement of larynx and hyoid
Vomiting or emesis is the abnormal emptying of stomach
bone
and upper part of intestine through esophagus and
mouth. 5. Elevation of soft palate
6. Contraction of diaphragm and abdominal muscles
„ CAUSES OF VOMITING with a characteristic jerk, resulting in elevation of
intra-abdominal pressure
1. Presence of irritating contents in GI tract 7. Compression of the stomach between diaphragm
2. Mechanical stimulation of pharynx
and abdominal wall leading to rise in intragastric
3. Pregnancy
pressure
4. Excess intake of alcohol
8. Simultaneous relaxation of lower esophageal sphinc-
5. Nauseating sight, odor or taste
6. Unusual stimulation of labyrinthine apparatus, as in ter, esophagus and upper esophageal sphincter
the case of sea sickness, air sickness, car sickness 9. Forceful expulsion of gastric contents (vomitus)
or swinging through esophagus, pharynx and mouth.
7. Abnormal stimulation of sensory receptors in other Movements during act of vomiting throw the vomitus
organs like kidney, heart, semicircular canals or (materials ejected during vomiting) to the exterior
uterus through mouth. Some of the movements play important
8. Drugs like antibiotics, opiates, etc. roles by preventing the entry of vomitus through other
9. Any GI disorder routes and thereby prevent the adverse effect of the
10. Acute infection like urinary tract infection, influenza, vomitus on many structures.
etc. Such movements are:
11. Metabolic disturbances like carbohydrate starvation 1. Closure of glottis and cessation of breathing
and ketosis (pregnancy), uremia, ketoacidosis prevents entry of vomitus into the lungs
(diabetes) and hypercalcemia.
2. Elevation of soft palate prevents entry of vomitus
into the nasopharynx
„ MECHANISM OF VOMITING
3. Larynx and hyoid bone move upward and forward
Nausea and are placed in this position rigidly. This causes
the dilatation of throat, which allows free exit of
Vomiting is always preceded by nausea. Nausea is
vomitus.
unpleasant sensation which induces the desire for
vomiting. It is characterized by secretion of large amount
of saliva containing more amount of mucus. „ VOMITING REFLEX

Vomiting is a reflex act. Sensory impulses for vomiting

Retching arise from the irritated or distended part of GI tract or
Strong involuntary movements in the GI tract which other organs and are transmitted to the vomiting center
start even before actual vomiting. These movements through vagus and sympathetic afferent fibers.
intensify the feeling of vomiting. This condition is called Vomiting center is situated bilaterally in medulla
retching (try to vomit) and vomiting occurs few minutes oblongata near the nucleus tractus solitarius.
after this. Motor impulses from the vomiting center are
transmitted through V, VII, IX, X and XII cranial nerves
Act of Vomiting to the upper part of GI tract; and through spinal nerves
Act of vomiting involves series of movements that takes to diaphragm and abdominal muscles.
place in GI tract.
Center for Vomiting during Motion Sickness
Sequence of events:
and Vomiting Induced by Drugs
1. Beginning of antiperistalsis, which runs from ileum
towards the mouth through the intestine, pushing Center for vomiting during motion sickness and vomiting
the intestinal contents into the stomach within few induced by drugs such as morphine, apomorphine, etc.
minutes. Velocity of the antiperistalsis is about 2 to is on the floor of fourth ventricle. This area is called
3 cm/second chemoreceptor trigger zone. During motion sickness,
2. Deep inspiration followed by temporary cessation of the afferent impulses from vestibular apparatus reach
breathing vomiting center through this zone.
 Chapter 43 t Movements of Gastrointestinal Tract 277

Center for Psychic-stimuli-induced Vomiting clock. Small portions of intestine (loops) sweep forward
and backward or upward and downward. It is a type of
Center for vomiting due to psychic stimuli such as
mixing movement, noticed only by close observation.
nauseating odor, sight or noise is in cerebral cortex.
It helps in mixing of chyme with digestive juices.
„ MOVEMENTS OF SMALL INTESTINE „ 2. PROPULSIVE MOVEMENTS
Movements of small intestine are essential for mixing Propulsive movements are the movements of small
the chyme with digestive juices, propulsion of food and intestine which push the chyme in the aboral direction
absorption. through intestine. The propulsive movements are
peristaltic movements and peristaltic rush.
Types of Movements of Small Intestine
Movements of small intestine are of four types: i. Peristaltic Movements
1. Mixing movements:
Peristalsis is defined as the wave of contraction
i. Segmentation movements
followed by wave of relaxation of muscle fibers. In GI
ii. Pendular movements. tract, it always travels in aboral direction. Stimulation of
2. Propulsive movements: smooth muscles of intestine initiates the peristalsis. It
i. Peristaltic movements travels from point of stimulation in both directions. But
ii. Peristaltic rush. under normal conditions, the progress of contraction in
3. Peristalsis in fasting – migrating motor complex an oral direction is inhibited quickly and the contractions
4. Movements of villi. disappear. Only the contraction that travels in an aboral
direction persists.
„ 1. MIXING MOVEMENTS
Starling’s law of intestine
Mixing movements of small intestine are responsible
for proper mixing of chyme with digestive juices such Depending upon the direction of the peristalsis, ‘Law of
as pancreatic juice, bile and intestinal juice. The intestine’ was put forth by Starling.
mixing movements of small intestine are segmentation According to the law of intestine, the response of
contractions and pendular movements. the intestine for a local stimulus consists of a contraction

i. Segmentation Contractions
Segmentation contractions are the common type of
movements of small intestine, which occur regularly or
irregularly, but in a rhythmic fashion. So, these movements
are also called rhythmic segmentation contractions.
The contractions occur at regularly spaced intervals
along a section of intestine. The segment of the intestine
involved in each contraction is about 1 to 5 cm long.
The segments of intestine in between the contracted
segments are relaxed. The length of the relaxed
segments is same as that of the contracted segments.
These alternate segments of contraction and relaxation
give appearance of rings, resembling the chain of
sausages.
After sometime, the contracted segments are
relaxed and the relaxed segments are contracted (Fig.
43.2). Therefore, the segmentation contractions chop
the chyme many times. This helps in mixing of chyme
with digestive juices.

ii. Pendular Movement

Pendular movement is the sweeping movement of small
intestine, resembling the movements of pendulum of FIGURE 43.2: Movements of small intestine
 278 Section 4 t Digestive System

of smooth muscle above and relaxation below the „ 4. MOVEMENTS OF VILLI

stimulated area.
Intestinal villi also show movements simultaneously
Peristaltic contractions start at any part of the
along with intestinal movements. It is because of the
intestine and travel towards anal end, at a velocity of
1 to 2 cm/sec. The contractions are always weak and extension of smooth muscle fibers of the intestinal wall
usually disappear after traveling for few centimeter. into the villi.
Because of this, the average movement of chyme Movements of villi are shortening and elongation,
through small intestine is very slow and the average which occur alternatively and help in emptying lymph
velocity of movement of the chyme is less than 1 cm/ from the central lacteal into the lymphatic system. The
sec. So, the chyme requires several hours to travel from surface area of villi is increased during elongation. This
duodenum to the end of small intestine. helps absorption of digested food particles from the
Peristaltic waves in small intestine increase to a lumen of intestine.
great extent immediately after a meal. This is because of Movements of villi are caused by local nervous
gastroenteric reflex, which is initiated by the distention reflexes, which are initiated by the presence of chyme
of stomach. Impulses for this reflex are transmitted from in small intestine. Hormone secreted from the small
stomach along the wall of the intestine via myenteric intestinal mucosa called villikinin is also believed to play
plexus. an important role in increasing the movements of villi.

ii. Peristaltic Rush „ MOVEMENTS OF LARGE INTESTINE

Sometimes, the small intestine shows a powerful peris- Usually, the large intestine shows sluggish movements.
taltic contraction. It is caused by excessive irritation of Still, these movements are important for mixing,
intestinal mucosa or extreme distention of the intestine. propulsive and absorptive functions.
This type of powerful contraction begins in duodenum
and passes through entire length of small intestine and Types of Movements of Large Intestine
reaches the ileocecal valve within few minutes. This is
called peristaltic rush or rush waves. Movements of large intestine are of two types:
Peristaltic rush sweeps the contents of intestine into 1. Mixing movements: Segmentation contractions
the colon. Thus, it relieves the small intestine off either 2. Propulsive movements: Mass peristalsis.
irritants or excessive distention.
„ 1. MIXING MOVEMENTS –
„ 3. PERISTALSIS IN FASTING – SEGMENTATION CONTRACTIONS
MIGRATING MOTOR COMPLEX Large circular constrictions, which appear in the colon,
Migrating motor complex is a type of peristaltic are called mixing segmentation contractions. These
contraction, which occurs in stomach and small intestine contractions occur at regular distance in colon. Length
during the periods of fasting for several hours. It is also of the portion of colon involved in each contraction is
called migrating myoelectric complex. It is different nearly about 2.5 cm.
from the regular peristalsis because, a large portion of
stomach or intestine is involved in the contraction. The „ 2. PROPULSIVE MOVEMENTS –
contraction extends to about 20 to 30 cm of stomach or MASS PERISTALSIS
intestine. This type of movement occurs once in every
1½ to 2 hours. Mass peristalsis or mass movement propels the feces
It starts as a moderately active peristalsis in the from colon towards anus. Usually, this movement occurs
body of stomach and runs through the entire length of only a few times every day. Duration of mass movement
small intestine. It travels at a velocity of 6 to 12 cm/min. is about 10 minutes in the morning before or after
Thus, it takes about 10 minutes to reach the colon after breakfast. This is because of the neurogenic factors
taking origin from the stomach. like gastrocolic reflex (see below) and parasympathetic
stimulation.
Significance of Peristalsis in Fasting
„ DEFECATION
Migrating motor complex sweeps the excess digestive
secretions into the colon and prevents the accumulation Voiding of feces is known as defecation. Feces is formed
of the secretions in stomach and intestine. It also sweeps in the large intestine and stored in sigmoid colon. By the
the residual indigested materials into colon. influence of an appropriate stimulus, it is expelled out
 Chapter 43 t Movements of Gastrointestinal Tract 279

through the anus. This is prevented by tonic constriction nerve fibers of pelvic nerve. Motor impulses cause
of anal sphincters, in the absence of the stimulus. strong contraction of descending colon, sigmoid colon
and rectum and relaxation of internal sphincter.
„ DEFECATION REFLEX Simultaneously, voluntary relaxation of external
sphincter occurs. It is due to the inhibition of pudendal
Mass movement drives the feces into sigmoid or pelvic
nerve, by impulses arising from cerebral cortex (Fig.
colon. In the sigmoid colon, the feces is stored. The
43.3).
desire for defecation occurs when some feces enters
rectum due to the mass movement. Usually, the desire
„ CONSTIPATION
for defecation is elicited by an increase in the intrarectal
pressure to about 20 to 25 cm H2O. Constipation is the failure of voiding of feces. Refer
Usual stimulus for defecation is intake of liquid Chapter 42 for details.
like coffee or tea or water. But it differs from person to
person. „ EVACUATION OF GASES FROM
GASTROINTESTINAL TRACT
Act of Defecation
Normally, gas accumulates in the GI tract either because
Act of defecation is preceded by voluntary efforts like of entrance of outside air or production of gases in the
assuming an appropriate posture, voluntary relaxation body. Accordingly, the gases accumulated in GI tract are
of external sphincter and the compression of abdominal classified into two groups:
contents by voluntary contraction of abdominal 1. Exogenous gases
muscles. 2. Endogenous gases.
Usually, the rectum is empty. During the development
of mass movement, the feces is pushed into rectum
and the defecation reflex is initiated. The process of
defecation involves the contraction of rectum and
relaxation of internal and external anal sphincters.
Internal anal sphincter is made up of smooth muscle
and it is innervated by parasympathetic nerve fibers via
pelvic nerve. External anal sphincter is composed of
skeletal muscle and it is controlled by somatic nerve
fibers, which pass through pudendal nerve. Pudendal
nerve always keeps the external sphincter constricted
and the sphincter can relax only when the pudendal
nerve is inhibited.

Gastrocolic Reflex
Gastrocolic reflex is the contraction of rectum, followed
by the desire for defecation caused by distention of
stomach by food. It is mediated by intrinsic nerve fibers
of GI tract.
This reflex causes only a weak contraction of
rectum. But, it initiates defecation reflex.

„ PATHWAY FOR DEFECATION REFLEX

When rectum is distended due to the entry of feces by
mass movement, sensory nerve endings are stimulated.
Impulses from the nerve endings are transmitted via
afferent fibers of pelvic nerve to the defecation center, FIGURE 43.3: Defecation reflex. Afferent and efferent fibers
situated in sacral segments (center) of spinal cord. of the reflex pass through pelvic (parasympathetic) nerve.
The center in turn, sends motor impulses to the Voluntary control of defecation is by pudendal (somatic) nerve.
descending colon, sigmoid colon and rectum via efferent Defecation center is in the sacral segments of spinal cord
 280 Section 4 t Digestive System

1. Exogenous Gases 3. Opening of lower esophageal sphincter.

4. Descent of diaphragm, which increases abdominal
Exogenous gases form about 90% of accumulated gases.
pressure and decreases intrathoracic pressure.
These gases enter the GI tract either by swallowing
All these activities are responsible for the expulsion
through mouth or drinking carbonated beverages.
of air from stomach to the exterior via esophagus.
2. Endogenous Gases
„ FLATULENCE
Endogenous gases form about 10% of accumulated
gases. These gases are produced by digestion of food Flatulence is the production of a mixture of intestinal
stuffs and interaction between bacteria and food stuffs gases. The mixture of gases is known as flatus (in
in the intestine. Latin, flatus = wind). Expulsion of flatus through anus
under pressure is called farting or passing gas. Farting
„ EVACUATION OF ACCUMULATED GASES is associated with disagreeable odor (due to odorous
gases) and sound (due to vibration of anal sphincter).
Evacuation of accumulated gases usually occurs by two
processes: Quantity of Flatus
1. Belching
2. Flatulence. Average flatus released by human is about 500 to 1500
mL per day, with 10 to 25 episodes throughout the day.
„ BELCHING
Source of Gases in Intestine
Belching is the process by which the gas accumulated
in stomach is expelled through mouth. It is also called Flatulence is the mixture of gases present in the intestine.
burping. It occurs because of inflation (distention) of Flatulence by swallowed air is rare.
stomach by swallowed air. The distention of the stomach Common sources of gases in flatulence are:
causes abdominal discomfort and the belching expels 1. Bacterial action on undigested sugars and polysac-
the air and relieves the discomfort. charides (e.g. starch, cellulose)
Most of the gas accumulated in stomach is expelled 2. Digestion of some flatulence producing food stuffs
through mouth. Only a small amount enters the intestine. such as cheese, yeast in bread, oats, onion, beans,
cabbage, milk, etc.
Causes for Accumulation of Gases in Stomach
Constituents of Flatus
1. Aerophagia: Swallowing large amounts of air due to
gulping the food or drink too rapidly Major constituents of flatus:
2. Drinking carbonated beverages 1. Swallowed non-odorous gases
3. During some emotional conditions like anxiety lot of i. Nitrogen (major constituent)
air enters the stomach through mouth. ii. Oxygen
2. Non-odorous gases produced by microbes
Act of Belching i. Methane
Belching is not a simple act and it requires the ii. Carbon dioxide
coordination of several activities such as: iii. Hydrogen
1. Closure of larynx, which prevents entry of liquid or 3. Odorous materials such as
food with the air from stomach into the lungs. i. Low molecular weight fatty acids like butyric
2. Elevation of larynx and relaxation of upper acid
esophageal sphincter. It allows exit of air through ii. Reduced sulfur compounds (hydrogen sulfide
esophagus more easily. and carbonyl sulfide).
 Chapter
Gastrointestinal Hormones
44
„ INTRODUCTION
„ CELLS SECRETING THE HORMONES
„ DESCRIPTION OF GASTROINTESTINAL HORMONES
„ GASTRIN
„ SECRETIN
„ CHOLECYSTOKININ
„ GLUCOSE-DEPENDENT INSULINOTROPIC HORMONE
„ VASOACTIVE INTESTINAL POLYPEPTIDE
„ GLUCAGON
„ GLICENTIN
„ GLUCAGON-LIKE POLYPEPTIDE-1
„ GLUCAGON-LIKE POLYPEPTIDE-2
„ SOMATOSTATIN
„ PANCREATIC POLYPEPTIDE
„ PEPTIDE YY
„ NEUROPEPTIDE Y
„ MOTILIN
„ SUBSTANCE P
„ GHRELIN
„ OTHER GASTROINTESTINAL HORMONES

„ INTRODUCTION Neuroendocrine Cells or APUD Cells

Gastrointestinal (GI) hormones are the hormones secreted Enteroendocrine cells which secrete hormones from
in GI tract. These hormones are polypeptides in nature amines are known as amine precursor uptake and
and belong to the family of local hormones (Chapter decarboxylation cells (APUD cells) or neuroendocrine
73). Major function of these hormones is to regulate the cells. For the synthesis of a GI hormone, first a precursor
secretory activities and motility of the GI tract.
substance of an amine is taken up by these cells. Later,
this precursor substance is decarboxylated to form the
„ CELLS SECRETING THE HORMONES
amine. From this amine, the hormone is synthesized.
Enteroendocrine Cells Because of the uptake of the amine precursor and
Enteroendocrine cells are the hormone-secreting cells decarboxylation of this precursor substance, these cells
in GI tract. These are the nerve cells and glandular are called APUD cells. This type of cells is also present
cells which are present in the gastric mucosa, intestinal in other parts of the body, particularly the brain, lungs
mucosa and the pancreatic cells. and the endocrine glands.
 282 Section 4 t Digestive System

Enterochromaffin Cells Gastrin is secreted from stomach during the gastric

(second) phase of gastric secretion and from small intestine
Enteroendocrine cells which secrete serotonin are called
during the intestinal (third) phase of gastric secretion.
enterochromaffin cells.
Stimulant for Secretion
„ DESCRIPTION OF
GASTROINTESTINAL HORMONES Stimulants for secretion of gastrin are:
i. Presence of food in the stomach.
„ 1. GASTRIN ii. Stimulation of local nervous plexus in stomach
and small intestine.
Gastrin is a peptide with 34 amino acid residues. It iii. Vagovagal reflex during the gastric phase of
is secreted mainly by the G cells of pyloric glands of gastric secretion: Gastrin-releasing polypeptide
stomach. It is also secreted by TG cells in stomach, is released at the vagal nerve ending. It causes
duodenum and jejunum. In fetus, the islets of the secretion of gastrin by stimulating the G cells
Langerhans also secrete this hormone (Table 44.1). or TG cells.

TABLE 44.1: Gastrointestinal hormones

Hormone Source of secretion Actions

G cells in stomach Stimulates gastric secretion and motility
TG cells in GI tract Promotes growth of gastric mucosa
Gastrin Islets in fetal pancreas Stimulates release of pancreatic hormones
Anterior pituitary Stimulates secretion of pancreatic juice
Brain Stimulates secretion of pancreatic hormones
Stimulates secretion of watery and alkaline pancreatic
secretion
Secretin S cells of small intestine Inhibits gastric secretion and motility
Constricts pyloric sphincter
Increases potency of cholecystokinin action
Contracts gallbladder
Stimulates pancreatic secretion with enzymes
Accelerates secretin activity
Increases enterokinase secretion
Cholecystokinin I cells of small intestine Inhibits gastric motility
Increases intestinal motility
Augments contraction of pyloric sphincter
Suppresses hunger
Induces drug tolerance to opioids
Gastric inhibitory peptide K cells in duodenum and jejunum Stimulates insulin secretion
(GIP) Antrum of stomach Inhibits gastric secretion and motility
Dilates splanchnic (peripheral) blood vessels
Inhibits Hcl secretion in gastric juice
Vasoactive intestinal Stomach Stimulates secretion of succus entericus
polypeptide (VIP) Small and large intestines Relaxes smooth muscles of intestine
Augments acetylcholine action on salivary glands
Stimulates insulin secretion
α-cells in pancreas
Glucagon A cells in stomach Increases blood sugar level
L cells in intestine
Glicentin L cells in duodenum and jejunum Increases blood sugar level
Glucagon-like polypeptide-1 α-cells in pancreas Stimulates insulin secretion
(GLP-1) Brain Inhibits gastric motility
GLP-2 L cells in ileum and colon Suppresses appetite
Contd...
 Chapter 44 t Gastrointestinal Hormones 283

Contd...
Hormone Source of secretion Actions
Hypothalamus Inhibits secretion of growth hormone
D cells in pancreas Inhibits gastric secretion and motility
Somatostatin
D cells in stomach and small Inhibits secretion of pancreatic juice
intestine Inhibits secretion of GI hormones
PP cells in pancreas Increases secretion of glucagons
Pancreatic polypeptide
Small intestine Decreases pancreatic secretion
Inhibits gastric secretion and motility
Reduces secretion of pancreatic juice
Peptide YY L cells of ileum and colon
Inhibits intestinal motility and bowel passage
Suppresses appetite and food intake
Ileum and colon
Neuropeptide Y Brain and autonomic nervous system Increases blood flow in enteric blood vessels
(ANS)
Mo cells in stomach and intestine Accelerates gastric emptying
Motilin Enterochromoffin cells in intestine Increases movements of small intestine
Increases peristalsis in colon
Brain
Substance P Increases movements of small intestine
Small intestine
Stomach
Hypothalamus Promotes growth hormone (GH) release
Ghrelin Pituitary Induces appetite and food intake
Kidney Stimulates gastric emptying
Placenta

Actions Products of protein digestion also stimulate secretin

secretion.
Gastrin:
i. Stimulates gastric glands to secrete gastric juice
Actions
with more pepsin and hydrochloric acid.
ii. Accelerates gastric motility. Major actions
iii. Promotes growth of gastric mucosa. Secretin stimulates exocrine pancreatic secretion. It acts
iv. Stimulates secretion of pancreatic juice, which on the cells of pancreatic ductule via cyclic AMP and
is rich in enzymes. causes secretion of large amount of watery juice with
v. Stimulates islets of Langerhans in pancreas to high content of bicarbonate ion. Bicarbonate content of
release pancreatic hormones. pancreatic juice (released by secretin) has functional
significance (Chapter 39).
„ 2. SECRETIN
Other actions
Secretin is a peptide hormone with 27 amino acid
residues. Historical importance of secretin is that, it was Secretin:
i. Inhibits secretion of gastric juice
the first ever hormone discovered. It was discovered
in 1902 by Bayliss and Starling. It is secreted by the S ii. Inhibits motility of stomach
cells of duodenum, jejunum and ileum. iii. Causes constriction of pyloric sphincter
Secretin is first produced in an inactive form called iv. Increases the potency of action of cholecystokinin
prosecretin. It is converted into secretin by the acidity on pancreatic secretion.
of chyme.
„ 3. CHOLECYSTOKININ
Stimulant for Secretion Cholecystokinin is made up of 39 amino acid residues.
Stimulant for the release and activation of prosecretin is Previously it was thought that there were two separate
the acid chyme entering the duodenum from stomach. hormones, namely pancreozymin and cholecystokinin. It
 284 Section 4 t Digestive System

was thought that pancreozymin stimulated the secretion Actions

of pancreatic juice with large amount of enzymes and the
Gastric inhibitory peptide (GIP):
cholecystokinin stimulated the contraction of gallbladder.
i. Stimulates the beta cells in the islets of
But now it is established that the same hormone has
Langerhans in pancreas to release insulin.
actions on both pancreas and gallbladder. So, it is
It causes insulin secretion, whenever chyme
named as cholecystokinin-pancreozymin (CCK-PZ) or
with glucose enters the small intestine. Hence
cholecystokinin (CCK).
it is called glucose-dependent insulinotropic
Cholecystokinin is secreted by I cells in mucosa of
hormone.
duodenum and jejunum. A small quantity of the hormone
ii. Inhibits the secretion of gastric juice.
is secreted in the ileum also.
iii. Inhibits gastric motility.
Recent studies reveal that GIP does not show
Stimulant for Secretion
significant action on gastric secretion.
Stimulant for the release of this hormone is the presence
of chyme-containing digestive products of fats and „ 5. VASOACTIVE INTESTINAL POLYPEPTIDE
proteins, viz. fatty acids, peptides and amino acids in
Vasoactive intestinal polypeptide (VIP) contains 28
the upper part of small intestine.
amino acid residues. This polypeptide is secreted in the
stomach and small intestine. A small amount of this
Actions
hormone is also secreted in large intestine.
Major actions
Stimulant for Secretion
Cholecystokinin:
i. Contracts gallbladder. Presence of acid chyme in the stomach and intestine
ii. Stimulates exocrine pancreatic secretion: It causes secretion of VIP.
activates the pancreatic acinar cells via the
Actions
second messenger inositol triphosphate.
Cholecystokinin causes secretion of pancreatic Vasoactive intestinal polypeptide (VIP):
juice with large amount of enzymes. i. Dilates splanchnic (peripheral) blood vessels.
ii. Inhibits hydrochloric acid secretion in gastric
Other actions juice.
Cholecystokinin: iii. Stimulates secretion of succus entericus with
i. Accelerates the activity of secretin to produce large amounts of electrolytes and water.
alkaline pancreatic juice, with large amount of iv. Relaxes smooth muscles of intestine.
bicarbonate ions. v. Augments action of acetylcholine on salivary
ii. Increases the secretion of enterokinase. glands.
iii. Inhibits the gastric motility. vi. Stimulates insulin secretion.
iv. Increases the motility of intestine.
„ 6. GLUCAGON
v. Augments contraction of pyloric sphincter.
vi. Plays an important role in satiety by suppressing Glucagon has 29 amino acid residues. It is secreted
hunger. mainly by alpha cells of islets of Langerhans in
vii. Induces drug tolerance to opioids. pancreas. It is also secreted by A cells in the stomach
and L cells in the intestine. In intestine, it is secreted as
„ 4. GLUCOSE-DEPENDENT preproglucagon.
INSULINOTROPIC HORMONE
Stimulant for Secretion
Earlier it was called gastric inhibitory peptide (GIP). It is
a peptide hormone, formed by 42 amino acid residues. Presence of food with more fat and protein in the
It is secreted by K cells in duodenum and in jejunum. It stomach is the stimulant for glucagon secretion in
is also secreted in antrum of stomach. stomach and duodenum. Hypoglycemia is the stimulant
for secretion of pancreatic glucagon.
Stimulant for Secretion
Action
GIP is secreted when chyme containing glucose and fat
enters the duodenum. Glucagon increases blood sugar level (Chapter 69).
 Chapter 44 t Gastrointestinal Hormones 285

„ 7. GLICENTIN and D cells of pancreatic islets also. Somatostatin is

secreted in two forms, one with 14 amino acids and the
Glicentin polypeptide is secreted by L cells in duodenum
other one with 28 amino acids.
and jejunum and α-cells of pancreatic islets. It is also
secreted in brain.
Stimulant for Secretion
Precursor of this hormone is the preproglucagon. In
intestine, the preproglucagon is converted into glicentin Presence of chyme with glucose and proteins in stomach
and glucagon-like polypeptide-2 (GLP-2). In pancreas, it and small intestine causes release of somatostatin.
is converted into glucagon, glucagon-like polypeptide-1
(GLP-1) and major proglucagon fragment. Actions

Stimulant for Secretion Somatostatin:

i. Inhibits the secretion of growth hormone (GH)
Glicentin is secreted when chyme with fat and protein and thyroid-stimulating hormone (TSH) from
enters the intestine. anterior pituitary
ii. Inhibits gastric secretion and motility
Action
iii. Inhibits secretion of pancreatic juice
Like glucagon, glicentin also increases the blood sugar iv. Inhibits secretion of GI hormones such as:
level. a. Gastrin
b. Cholecystokinin (CCK)
„ 8. GLUCAGON-LIKE POLYPEPTIDE-1 c. Vasoactive intestinal polypeptide (VIP)
Glucagon-like polypeptide-1 (GLP-1) is secreted in d. Gastric inhibitory peptide (GIP).
α-cells of pancreatic islets (see above). Structurally, it is
similar to GLP-2 and glucagon. It is found in brain also. „ 11. PANCREATIC POLYPEPTIDE

Stimulant for Secretion Source of Secretion

Presence of food with glucose in the small intestine Pancreatic polypeptide is a polypeptide with 36 amino
stimulates the release of GLP-1. acid residues. It is secreted mainly by the PP cells of
the islets of Langerhans in pancreas. It is also found in
Actions small intestine (Table 44.1).
Glucagon-like polypeptide-1 (GLP-1):
Stimulant for Secretion
i. Stimulates the insulin secretion from β-cells of
islets in pancreas Pancreatic polypeptide is secreted by the presence of
ii. Inhibits gastric motility. chyme with proteins in the small intestine. It is also
secreted in conditions like hypoglycemia, fasting and
„ 9. GLUCAGON-LIKE POLYPEPTIDE-2 exercise.

Glucagon-like polypeptide-2 (GLP-2) is secreted by L Actions

cells in ileum and colon (see above). Structurally, it is
similar to GLP-1 and glucagons. Like GLP-1, it is also Pancreatic polypeptide:
found in brain. i. Increases the secretion of glucagon from α-cells
of islets of Langerhans in pancreas.
Stimulant for Secretion ii. Decreases the secretion of pancreatic juice from
Presence of food with glucose in the small intestine exocrine part of pancreas.
stimulates the release of GLP-2 also.
„ 12. PEPTIDE YY
Action Polypeptide YY with 36 amino acid residues, is struct-
GLP-2 is believed to suppress appetite. urally related to pancreatic polypeptide and neuro-
peptide Y. It is secreted in L cells of ileum and colon.
„ 10. SOMATOSTATIN
Stimulant for Secretion
Somatostatin was first found in hypothalamus and named
as growth hormone-inhibiting hormone. Now it is found Presence of fat-containing chyme stimulates the release
in D cells of stomach and upper part of small intestine of peptide YY.
 286 Section 4 t Digestive System

Actions Stimulant for Secretion

Peptide YY: Secretion of substance P in intestine is caused by the
presence of chyme.
i. Inhibits gastric secretion and motility
ii. Reduces secretion of pancreatic juice
Actions
iii. Inhibits the intestinal motility and stops passage
of bowel beyond ileum (ileal brake) In GI tract, substance P increases the mixing and
iv. Suppresses appetite and food intake. propulsive movements of small intestine (refer Chapter
141 for its actions in brain).
„ 13. NEUROPEPTIDE Y
„ 16. GHRELIN
Neuropeptide Y contains 36 amino acid residues. It is
structurally related to pancreatic polypeptide and peptide Ghrelin is a recently discovered hormone. This 28
YY. It is secreted by enteric nerve endings particularly in amino acid polypeptide is synthesized by epithelial
ileum and colon. It is also secreted in medulla, hypo- cells in the fundus of stomach. It is also produced in
thalamus and neurons of autonomic nervous system smaller amounts in hypothalamus, pituitary, kidney and
(ANS). placenta.

Stimulant for Secretion Stimulant for Secretion

Secretion of neuropeptide Y is stimulated by fat- Secretion of ghrelin increases during fasting and
containing chyme. decreases when stomach is full.

Action Actions
Neuropeptide Y increases the blood flow in enteric blood Ghrelin:
vessels and stimulates food intake (Chapter 141).
i. Promotes the secretion of growth hormone (GH)
by stimulating somatotropes (growth hormone
„ 14. MOTILIN
synthesizing cells) in anterior pituitary. Receptors
Motilin is built by 22 amino acid residues. It is secreted for this hormone called growth hormone
by Mo cells, which are present in stomach and intestine. secretogogues receptor (GHS-R) were identified
It is also believed to be secreted by enterochromoffin in the somatotropes before the discovery of the
cells of intestine. hormone itself. These receptors are also found
in adipose tissue, heart and hypothalamus.
Stimulant for Secretion ii. Induces appetite and food intake by acting via
Motilin is secreted when the chyme from stomach enters feeding center in hypothalamus (Chapter 149).
the duodenum. iii. Stimulates gastric emptying.

Actions „ OTHER GASTROINTESTINAL HORMONES

Motilin: Mucosa of GI tract secretes many other hormones such
as:
i. Accelerates gastric emptying 1. Enkephalins
ii. Increases the mixing and propulsive movements 2. Dynorphin
of small intestine 3. Neurotensin
iii. Increases the peristalsis in colon. 4. Serotonin
5. Urogastrone
„ 15. SUBSTANCE P 6. Enterocrinin
7. Villikinin
Source of Secretion
8. Guanylin
Substance P is a neurotransmitter with 11 amino acid 9. Bombesin.
residues. It is secreted at the pain nerve endings in However, the significant biological actions of these
brain and enteric nerve endings in small intestine. hormones on GI tract are not clear.
 Digestion, Absorption Chapter
and Metabolism
of Carbohydrates 45
„ CARBOHYDRATES IN DIET
„ DIGESTION
„ ABSORPTION
„ METABOLISM
„ DIETARY FIBER

„ CARBOHYDRATES IN DIET „ DIGESTION OF CARBOHYDRATES

Human diet contains three types of carbohydrates: „ IN THE MOUTH

„ 1. POLYSACCHARIDES Enzymes involved in the digestion of carbohydrates

are known as amylolytic enzymes. The only amylolytic
Large polysaccharides are glycogen, amylose and enzyme present in saliva is the salivary amylase or
amylopectin, which are in the form of starch (glucose ptyalin (Chapter 37).
polymers). Glycogen is available in non-vegetarian diet.
Amylose and amylopectin are available in vegetarian „ IN THE STOMACH
diet because of their plant origin.
Gastric juice contains a weak amylase, which plays a
minor role in digestion of carbohydrates.
„ 2. DISACCHARIDES
Two types of disaccharides are available in the diet. „ IN THE INTESTINE
i. Sucrose (Glucose + Fructose), which is called
Amylolytic enzymes present in the small intestine are
table sugar or cane sugar
derived from pancreatic juice and succus entericus
ii. Lactose (Glucose + Galactose), which is the
(Table 45.1).
sugar available in milk.
Amylolytic Enzyme in Pancreatic Juice
„ 3. MONOSACCHARIDES
Pancreatic juice contains pancreatic amylase (Chapter
Monosaccharides consumed in human diet are mostly 39).
glucose and fructose.
Other carbohydrates in the diet include Amylolytic Enzymes in Succus Entericus
i. Alcohol
Amylolytic enzymes present in succus entericus are
ii. Lactic acid
maltase, sucrase, lactase, dextrinase and trehalase
iii. Pyruvic acid
(Chapter 41).
iv. Pectins
v. Dextrins
„ FINAL PRODUCTS OF
vi. Carbohydrates in meat.
CARBOHYDRATE DIGESTION
Diet also contains large amount of cellulose, which
cannot be digested in the human GI tract so it is not Final products of carbohydrate digestion are monosac­
considered as a food for human beings. charides, which are glucose, fructose and galactose.
 288 Section 4 t Digestive System

TABLE 45.1: Digestion of carbohydrates

Area Juice Enzyme Substrate End product

Polysaccharides – cooked Disaccharides – dextrin and
Mouth Saliva Salivary amylase
starch maltose
Stomach Gastric juice Gastric amylase Weak amylase The action is negligible
Disaccharides
Pancreatic juice Pancreatic amylase Polysaccharides
– Dextrin, maltose and maltriose
Sucrase Sucrose Glucose and fructose
Small Maltase Maltose and maltriose Glucose
intestine
Succus entericus Lactase Lactose Glucose and galactose
Dextrinase Dextrin, maltose and maltriose Glucose
Trehalase Trehalose Glucose

Glucose represents 80% of the final product of carbo­ digestion and absorption, food substances must be
hydrate digestion. Galactose and fructose represent the utilized by the body. The utilization occurs mainly by
remaining 20%. oxidative process in which the carbohydrates, proteins
and lipids are burnt slowly to release energy. This
„ ABSORPTION OF CARBOHYDRATES process is known as catabolism.
Part of the released energy is utilized by tissues for
Carbohydrates are absorbed from the small intestine physiological actions and rest of the energy is stored as
mainly as monosaccharides, viz. glucose, galactose rich energy phosphate bonds and in the form of proteins,
and fructose. carbohydrates and lipids in the tissues. This process is
called anabolism.
„ ABSORPTION OF GLUCOSE Metabolism of carbohydrates is given in the form of
schematic diagram (Fig. 45.1).
Glucose is transported from the lumen of small intestine
into the epithelial cells in the mucus membrane of small
„ DIETARY FIBER
intestine, by means of sodium cotransport. Energy for
this is obtained by the binding process of sodium ion Dietary fiber or roughage is a group of food particles
and glucose molecule to carrier protein. which pass through stomach and small intestine, without
From the epithelial cell, glucose is absorbed into the being digested and reach the large intestine unchanged.
portal vein by facilitated diffusion. However, sodium ion Other nutritive substances of food are digested and
moves laterally into the intercellular space. From here, it absorbed before reaching large intestine.
is transported into blood by active transport, utilizing the Characteristic feature of dietary fiber is that it is
energy liberated by breakdown of ATP. not digestible by digestive enzymes. So it escapes
digestion in small intestine and passes to large intestine.
„ ABSORPTION OF GALACTOSE It provides substrate for microflora of large intestine and
increases the bacterial mass. The anaerobic bacteria
Galactose is also absorbed from the small intestine in in turn, degrade the fermentable components of the
the same mechanism as that of glucose. fiber. Thus, in large intestine, some of the components
of fiber are broken down and absorbed and remaining
„ ABSORPTION OF FRUCTOSE components are excreted through feces.
Fructose is absorbed into blood by means of facilitated Components of Dietary Fiber
diffusion. Some molecules of fructose are converted
into glucose. Glucose is absorbed as described above. Major components of dietary fiber are cellulose,
hemicelluloses, D­glucans, pectin, lignin and gums.
„ METABOLISM OF CARBOHYDRATES Cellulose, hemicelluloses and pectin are partially
degradable, while other components are indigestible.
Metabolism is the process in which food substances Dietary fiber also contains minerals, antioxidants and
undergo chemical and energy transformation. After other chemicals that are useful for health.
 Chapter 45 t Digestion, Absorption and Metabolism of Carbohydrates 289

FIGURE 45.1: Schematic diagram of carbohydrate metabolism

Source of Dietary Fiber 3. Diet with high fiber content tends to be low in energy
and it is also useful in reducing the body weight
Source of dietary fiber are fruits, vegetables, cereals,
4. Dietary fiber increases the formation of bulk and
bread and wheat grain (particularly its outer layer).
soft feces and eases defecation
5. It contains some useful substances such as
Health Benefits of Dietary Fiber
antioxidants
1. By intake of high dietary fiber food, some disease­ 6. Some components of dietary fiber also reduce blood
producing food substances may be decreased in cholesterol level and thereby, decrease the risk of
quantity or completely excluded in diet some diseases such as coronary heart disease and
2. Dietary fiber helps in weight maintenance because it gallstones
requires more chewing and promotes hunger satis- 7. Dietary fiber is also suggested to prevent or to
faction by delaying the emptying of stomach and by treat some disorders such as constipation, bowel
giving the person a sense of fullness of stomach syndrome, diabetics, ulcer and cancer.
 Digestion, Absorption Chapter
and Metabolism
of Proteins 46
„ PROTEINS IN DIET
„ DIGESTION
„ ABSORPTION
„ METABOLISM

„ PROTEINS IN DIET Dietary proteins are formed by long chains of amino

acids, bound together by peptide linkages.
Foodstuffs containing high protein content are meat,
fish, egg and milk. Proteins are also available in wheat, „ DIGESTION OF PROTEINS
soybeans, oats and various types of pulses.
Enzymes responsible for the digestion of proteins are
Proteins present in common foodstuffs are:
called proteolytic enzymes.
1. Wheat: Glutenin and gliadin, which constitute
gluten „ IN THE MOUTH
2. Milk: Casein, lactalbumin, albumin and myosin Digestion of proteins does not occur in mouth, since
3. Egg: Albumin and vitellin saliva does not contain any proteolytic enzymes. So, the
4. Meat: Collagen, albumin and myosin. digestion of proteins starts only in stomach (Table 46.1).

TABLE 46.1: Digestion of proteins

Area Juice Enzyme Substrate End product

Polysaccharides – Disaccharides – dextrin and
Mouth Saliva No proteolytic enzyme
cooked starch maltose
Proteoses, peptones, large
Stomach Gastric juice Pepsin Proteins
polypeptides
Trypsin Dipeptides
Proteoses
Tripeptides
Peptones
Chymotrypsin Polypeptides
Pancreatic juice
Dipeptides
Small Carboxypeptidases A and B Tripeptides Amino acids
intestine Polypeptides
Dipeptidases Dipeptides
Succus entericus Tripeptidases Tripeptides Amino acids
Amino peptidases Large polypeptides
 Chapter 46 t Digestion, Absorption and Metabolism of Proteins 291

FIGURE 46.1: Schematic diagram of protein metabolism

„ IN THE STOMACH dipeptidases, tripeptidases and aminopeptidases

(Chapter 41).
Pepsin is the only proteolytic enzyme in gastric juice
(Chapter 38). Rennin is also present in gastric juice. But
„ FINAL PRODUCTS OF PROTEIN DIGESTION
it is absent in human.
Final products of protein digestion are the amino acids,
„ IN THE SMALL INTESTINE which are absorbed into blood from intestine.
Most of the proteins are digested in the duodenum and
jejunum by the proteolytic enzymes of the pancreatic „ ABSORPTION OF PROTEINS
juice and succus entericus. Proteins are absorbed in the form of amino acids from
small intestine. The levo amino acids are actively
Proteolytic Enzymes in Pancreatic Juice absorbed by means of sodium cotransport, whereas,
Pancreatic juice contains trypsin, chymotrypsin and the dextro amino acids are absorbed by means of
carboxypeptidases. Trypsin and chymotrypsin are facilitated diffusion.
called endopeptidases, as these two enzymes break the Absorption of amino acids is faster in duodenum
interior bonds of the protein molecules (Chapter 39). and jejunum and slower in ileum.

Proteolytic Enzymes in Succus Entericus „ METABOLISM OF PROTEINS

Final digestion of proteins is by the proteolytic Metabolism of proteins is given in the form of a schematic
enzymes present in the succus entericus. It contains diagram (Fig. 46.1).
 Digestion, Absorption Chapter
and Metabolism
of Lipids 47
„ LIPIDS IN DIET
„ DIGESTION
„ ABSORPTION
„ STORAGE
„ TRANSPORT IN BLOOD – LIPOPROTEINS
„ ADIPOSE TISSUE
„ METABOLISM
„ LIPID PROFILE

„ LIPIDS IN DIET 1. Monounsaturated Fats

Lipids are mostly consumed in the form of neutral fats, Unsaturated fats which contain one double bond bet­
which are also known as triglycerides. Triglycerides ween the carbon atoms are called monounsaturated
are made up of glycerol nucleus and free fatty acids. fats.
Triglycerides form the major constituent in foods of
animal origin and much less in foods of plant origin. 2. Polyunsaturated Fats
Apart from triglycerides, usual diet also contains small
Unsaturated fats with more than one double bond
quantities of cholesterol and cholesterol esters.
between the carbon atoms are called polyunsaturated
Dietary fats are classified into two types:
fats. Polyunsaturated fats belong to the family of
1. Saturated fats
essential fatty acids (fatty acids required in diet).
2. Unsaturated fats.
Polyunsaturated fats are of two types:
1. Omega-3 fats or omega­3 fatty acids having double
„ SATURATED FATS
bond in the third space from the end of the carbon
Saturated fats are the fats which contain triglycerides chain
formed from only saturated fatty acids. The fatty acids 2. Omega-6 fats or omega­6 fatty acids having double
having maximum amount of hydrogen ions without bond in the sixth space from the end of the carbon
any double bonds between carbon atoms are called chain.
saturated fatty acids. Both omega-3 and omega-6 fatty acids are beneficial
to the body. However, consuming too much of omega­6
„ UNSATURATED FATS fatty acids results in hazards than benefits. So, the diet
containing 3 : 1 ratio of omega-6 to omega-3 fatty acids
Fats containing unsaturated fatty acids are known as
is often recommended by experts.
unsaturated fats. Unsaturated fatty acids are fatty acids
formed by dehydrogenation of saturated fatty acids.
3. Trans Fats
Unsaturated fats are classified into three types:
1. Monounsaturated fats Trans fats or trans fatty acids are unsaturated fatty acids,
2. Polyunsaturated fats with molecules containing trans (across or opposite
3. Trans fats. side) double bonds between carbon atoms.
 Chapter 47 t Digestion, Absorption and Metabolism of Lipids 293

Sources and the functions of the different types of Lipolytic Enzymes in Pancreatic Juice
dietary fats are listed in Table 47.1.
Pancreatic lipase is the most important enzyme for the
digestion of fats. Other lipolytic enzymes of pancreatic
„ DIGESTION OF LIPIDS juice are cholesterol ester hydrolase, phospholipase A
Lipids are digested by lipolytic enzymes. and phospholipase B (Chapter 39).

„ IN THE MOUTH Lipolytic Enzyme in Succus Entericus

Saliva contains lingual lipase. This enzyme is secreted Intestinal lipase is the only lipolytic enzyme present in
by lingual glands of mouth and swallowed along with succus entericus (Chapter 41).
saliva. So, the lipid digestion does not commence in the
mouth (Table 47.2) (Chapter 37). „ FINAL PRODUCTS OF FAT DIGESTION
Fatty acids, cholesterol and monoglycerides are the
„ IN THE STOMACH
final products of lipid digestion.
Gastric lipase or tributyrase is the lipolytic enzyme
present in gastric juice (Chapter 38). „ ABSORPTION OF LIPIDS

„ IN THE INTESTINE Monoglycerides, cholesterol and fatty acids from the

micelles enter the cells of intestinal mucosa by simple
Almost all the lipids are digested in the small intestine diffusion.
because of the availability of bile salts, pancreatic From here, further transport occurs as follows:
lipolytic enzymes and intestinal lipase. 1. In the mucosal cells, most of the monoglycerides
are converted into triglycerides. Triglycerides are
Role of Bile Salts also formed by re-esterification of fatty acids with
Bile salts play an important role in the digestion of lipids more than 10 to 12 carbon atoms. Some of the
(Chapter 40). cholesterol is also esterified.

TABLE 47.1: Sources and functions of dietary fats

Type of fat Sources Functions

Full fat milk, cheese, cream, butter. Commercially
baked biscuits and pastries Increase blood cholesterol and thereby increase
Saturated fats Deep­fried fast food the risk of atherosclerosis and coronary heart
Coconut oil and palm oil diseases
Fatty meat
Oils (canola, olive and peanut oils)
Monounsaturated fats Decrease blood cholesterol and thereby
Nuts (cashews, almonds, hazelnuts and peanuts)
decrease the risk of coronary heart diseases
Margarine
Decrease
Fruits and vegetables Blood cholesterol and triglycerides and thereby
Vegetable oils (sunflower, safflower, corn or soy reduces blood pressure
oils) Risk of coronary heart diseases
Nuts (walnuts) Risk of obesity
Polyunsaturated fats Flax seeds Platelet aggregation and prevents excess blood
Polyunsaturated margarines clotting
Lean meat Inflammation throughout body
Fish and sea foods
Egg Increase
Disease­countering actions in the body
Milk Increase low density lipoproteins and thereby
Trans fats Cheese and table margarines increase the risk of atherosclerosis and
Lamb and beef coronary heart diseases
 294 Section 4 t Digestive System

TABLE 47.2: Digestion of lipids

Area Juice Enzyme Substrate End product

Fatty acid
Mouth Saliva Lingual lipase Triglycerides
1, 2­diacylglycerol
Fatty acids
Stomach Gastric juice Gastric lipase (weak lipase) Triglycerides
Glycerol
Monoglycerides
Pancreatic lipase Triglycerides
Fatty acid
Free cholesterol
Cholesterol ester hydrolase Cholesterol ester
Fatty acid
Phospholipase A Phospholipids Lysophospholipids
Phosphoryl choline
Pancreatic juice
Small Phospholipase B Lysophospholipids Free fatty acids
intestine
Facilitates action of
Colipase –
pancreatic lipase
Phospholipids Lysophospholipids
Bile­salt­activated lipase
Cholesterol esters Cholesterol and fatty acids
Fatty acids
Succus entericus Intestinal lipase Triglycerides
Glycerol (weak action)

Triglycerides and cholesterol esters are coated with When other tissues of the body need energy,
a layer of protein, cholesterol and phospholipids to form triglycerides stored in adipose tissue is hydrolyzed into
the particles called chylomicrons. FFA and glycerol. FFA is transported to the body tissues
Chylomicrons cannot pass through the membrane through blood.
of the blood capillaries because of the larger size. So,
these lipid particles enter the lymph vessels and then „ TRANSPORT OF LIPIDS IN
are transferred into blood from lymph. BLOOD – LIPOPROTEINS
2. Fatty acids containing less than 10 to 12 carbon
atoms enter the portal blood from mucosal cells and Free fatty acids are transported in the blood in
are transported as free fatty acids or unesterified combination with albumin. Other lipids are transported
fatty acids. Most of the fats are absorbed in the in the blood, in the form of lipoproteins.
upper part of small intestine. Presence of bile is
essential for fat absorption. „ LIPOPROTEINS
Lipoproteins are the small particles in the blood which
„ STORAGE OF LIPIDS
contain cholesterol, phospholipids, triglycerides and
Lipids are stored in adipose tissue and liver. Fat stored proteins. Proteins are beta­globulins called apoproteins.
in adipose tissue is called neutral fat or tissue fat.
When chylomicrons are traveling through capillaries of Classification of Lipoproteins
adipose tissue or liver, the enzyme called lipoprotein
lipase present in the capillary endothelium hydrolyzes
Lipoproteins are classified into four types on the basis
triglycerides of chylomicrons into free fatty acids (FFA) of their density:
and glycerol. FFA and glycerol enter the fat cells 1. Very-low-density lipoproteins (VLDL): Contain high
(adipocytes or lipocytes) of the adipose tissue or liver concentration of triglycerides (formed from FFA and
cells. Then, the FFA and glycerol are again converted glycerol) and moderate concentration of cholesterol
into triglycerides and stored in these cells. Other contents and phospholipids
of chylomicrons such as cholesterol and phospholipids, 2. Intermediate-density lipoproteins (IDL): Formed
which are released into the blood combine with proteins by the removal of large portion of triglycerides
to form lipoproteins. from VLDL by lipoprotein lipase. Concentration of
 Chapter 47 t Digestion, Absorption and Metabolism of Lipids 295

cholesterol and phospholipids increases because of Very-low-density lipoprotein

removal of triglycerides
Very­low­density lipoprotein (VLDL) carries cholesterol
3. Low-density lipoproteins (LDL): Formed from IDL by
from liver to organs and tissues in the body. It is also
the complete removal of triglycerides. These lipo­
associated with atherosclerosis and heart disease.
proteins contain only cholesterol and phospholipids
4. High-density lipoproteins (HDL): Contain high
concentrations of proteins with low concentration of „ ADIPOSE TISSUE
cholesterol and phospholipids. Adipose tissue or fat is a loose connective tissue that
All the lipoproteins are synthesized in liver. HDL is forms the storage site of fat in the form of triglycerides.
synthesized in intestine also. It is composed of adipocytes, which are also called
fat cells or lipocytes. Obesity does not depend on the
Functions of Lipoproteins
body weight, but on the amount of body fat, specifically
Primary function of lipoproteins is to transport the lipids adipose tissue.
via blood to and from the tissues. Functions of each type Adipose tissue is of two types, white adipose tissue
of lipoproteins are given in Table 47.3. and brown adipose tissue.

Importance of Lipoproteins „ WHITE ADIPOSE TISSUE OR WHITE FAT

High-density lipoprotein White adipose tissue is distributed through the body
High­denisty lipoprotein (HDL) is referred as the beneath the skin, forming subcutaneous fat. It also
‘good cholesterol’ because it carries cholesterol and surrounds the internal organs. This adipose tissue is
phospholipids from tissues and organs back to the formed by fat cells which are unilocular, i.e. these cells
liver for degradation and elimination. It prevents the contain one large vacuole filled with fat.
deposition of cholesterol on the walls of arteries, by
carrying cholesterol away from arteries to the liver. Functions of White Adipose Tissue
High level of HDL is a good indicator of a healthy
White adipose tissue has three functions:
heart, because it reduces the blood cholesterol level.
HDL also helps in the normal functioning of some 1. Storage of energy: Main function of white adipose
hormones and certain tissues of the body. It is also used tissue is the storage of lipids. Utilization or storage
for the formation of bile in liver. of fat is regulated by hormones, particularly insulin,
depending upon the blood glucose level. If the
Low-density lipoprotein blood glucose level increases, insulin stimulates
Low­density lipoprotein (LDL) is considered as the synthesis and storage of fat in white adipose tissue
‘bad cholesterol’ because it carries cholesterol and (Chapter 69). On the other hand, if blood glucose
phospholipids from the liver to different areas of the level decreases insulin causes release of fat from
body, viz. muscles, other tissues and organs such as adipose tissue. Released fat is utilized for energy
heart. It is responsible for deposition of cholesterol on 2. Heat insulation: Insulation function is due to
walls of arteries causing atherosclerosis (blockage and the presence of adipose tissue beneath the skin
hardening of the arteries). High level of LDL increases (subcutaneous adipose tissue)
the risk of heart disease. 3. Protection of internal organs: White adipose tissue
TABLE 47.3: Functions of lipoproteins protects the body and internal organs by surrounding
them and by acting like a mechanical cushion.
Lipoproteins Functions

VLDL
Transports triglycerides from liver to „ BROWN ADIPOSE TISSUE OR BROWN FAT
adipose tissue
Brown adipose tissue is a specialized form of adipose
Transports triglycerides, cholesterol and
IDL phospholipids from liver to peripheral tissue, having the function opposite to that of white
tissues adipose tissue. It is present only in certain areas of the
body such as back of neck and intrascapular region.
Transports cholesterol and phospholipids
LDL from liver to tissues and organs like It is abundant in infants forming about 5% of total
heart adipose tissue. After infancy, brown adipose tissue
Transports cholesterol and phospholipids
disappears gradually and forms only about 1% of total
HDL from tissues and organs like heart back adipose tissue in adults. It is formed by fat cells which
to liver are multilocular, i.e. these cells contain many small
 296 Section 4 t Digestive System

FIGURE 47.1: Schematic diagram of lipid metabolism

vacuoles filled with fat. The coloration of this adipose non-shivering thermogenesis. Heat production in
tissue is due to high vascularization and large number brown fat is very essential for survival of infants and
of iron-rich mitochondria. small animals in cold environment. It is because,
the lipid in this tissue releases energy directly as heat.
Functions of Brown Adipose Tissue The mitochondria found in brown adipose tissue
contain a unique uncoupling protein called mitochondrial
Brown adipose tissue does not store lipids but uncoupling protein 1 (UCP1). Also called thermogenin,
generates heat by burning lipids. In infants and this protein allows the controlled entry of protons without
hibernating animals, brown adipose tissue plays an adenosine triphosphate (ATP) synthesis, in order to
important role in regulating body temperature via generate heat.
 Chapter 47 t Digestion, Absorption and Metabolism of Lipids 297

TABLE 47.4: Values of lipid profile

Lipids Desirable optimal level Borderline range High-risk level

Total cholesterol < 200 mg/dL 200 to 240 mg/dL > 240 mg/dL
Triglycerides < 150 mg/dL 150 to 200 mg/dL > 200 mg/dL
HDL > 60 mg/dL 40 to 60 mg/dL < 40 mg/dL
LDL < 60 mg/dL 60 to 100 mg/dL > 100 mg/dL
Total cholesterol – HDL ratio < 2 2 to 6 > 6

„ METABOLISM OF LIPIDS lipid profile are correlated with age, sex and other risk
factors of heart disease.
Metabolism of lipids is given in the form of schematic
Tests included in lipid profile are total cholesterol,
diagram (Fig. 47.1).
triglyceride, HDL, LDL, VLDL and total cholesterol –
„ LIPID PROFILE HDL ratio.
Total cholesterol to HDL ratio is helpful in predicting
Lipid profile is a group of blood tests which are carried atherosclerosis and CAD. It is obtained by dividing total
out to determine the risk of coronary artery diseases cholesterol by HDL. High total cholesterol and low HDL
(CAD). Results of lipid profile are considered as good increases the ratio. The increase in the ratio is undesirable.
indicators of whether someone is prone to develop Conversely, high HDL and low total cholesterol lowers
stroke or heart attack, caused by atherosclerosis. In the ratio and the decrease in the ratio is desirable. The
order to plan the course of treatment, the results of the values of lipid profile are given in Table 47.4.
 298 Questions in Digestive System

QUESTIONS IN DIGESTIVE SYSTEM

„ LONG QUESTIONS 17. Properties and composition of pancreatic juice.

18. Functions of pancreatic juice.
1. What are the different types of salivary glands?
19. Regulation of exocrine function of pancreas.
Describe the composition, functions and regulation
20. Steatorrhea.
of secretion of saliva.
21. Secretin.
2. Explain the composition and functions of gastric 22. Cholecystokinin.
juice and give an account of hormonal regulation 23. Composition of bile.
of gastric secretion. 24. Functions of bile.
3. Describe the different phases of gastric secretion 25. Bile salts.
with experimental evidences. 26. Bile pigments.
4. Explain the composition, functions and regulation 27. Enterohepatic circulation.
of secretion of pancreatic juice. 28. Functions of liver.
5. Describe the composition, functions and regulation 29. Differences between liver bile and gallbladder bile.
of secretion of bile. Enumerate the differences 30. Functions of gallbladder.
between the liver bile and gallbladder bile. Add a 31. Jaundice.
note on enterohepatic circulation. 32. Hepatitis.
6. Give an account of succus entericus. 33. Gallstones.
7. Write an essay on gastric motility. What are the 34. Succus entericus.
factors influencing gastric emptying? 35. Functions of small intestine.
8. Describe in detail, the gastrointestinal movements. 36. Functions of large intestine.
37. Mastication.
„ SHORT QUESTIONS 38. Swallowing.
39. Dysphagia.
1. Properties and composition of saliva. 40. Movements of stomach.
2. Functions of saliva. 41. Filling and emptying of stomach.
3. Nerve supply to salivary glands. 42. Hunger contractions.
4. Glands of stomach. 43. Vomiting.
5. Functions of stomach. 44. Movements of small intestine.
6. Properties and composition of gastric juice. 45. Peristalsis.
7. Functions of gastric juice 46. Movements of large intestine.
8. Mechanism of secretion of hydrochloric acid in 47. Defecation.
stomach. 48. Constipation.
9. Pavlov’s pouch. 49. Diarrhea.
10. Sham feeding. 50. Gastrointestinal hormones.
11. Cephalic phase of gastric secretion. 51. Digestion and absorption of carbohydrates.
12. Gastrin. 52. Dietary fiber.
13. Hormones acting on stomach. 53. Digestion and absorption of proteins.
14. FTM. 54. Digestion and absorption of lipids.
15. Peptic ulcer. 55. Lipoproteins.
16. Exocrine function of pancreas. 56. Brown fat.