665

Chapter 85: Billary Secretion

Table 85.1: Composition of solids in hunan bile causes steatorrhea. Bile salts perform following important
Bile salts functions:
Bile plgments 1. Absorption of fat: Bile salts are essential for absorption of
Cholesterol fat from intestine.
Inarganic salts This depends on formation of mlcelles by bile salts in
Fatty acids and fat the intestine. For their amphipathic (both hydrophilic
Alkaline phosphatase and hydrophobic domains) property, along with
Cations: Na, K, Cas, and Mg lecithin and cholesterol, bile sats form cylindrical
disks, called as micelles (for details, refer Chapter 94).
Anions: HCO,,C, so and PO) " Liplds are transported in mlcelles from the lumen to
the membrane of intestinal mucosal epithelal cels
Hepatic and Gallbladder Bile where micelle dissociates and liplds are absorbed.
There are differences between 2. Emulsification of fat: Bile salts are surface tension
the liver) and hepatic bile (ble
(bile stored in formed
in
as bile is gallbladder bileand acidified in gallbladder)
reducing agents.

(Table 85,2) concentrated

Along with phospholiplds and monoglycerides, they
1. Water
gallbladder cause emulsification of fat, which is essential for
absorption is the major digestion and absorption of fat.
mechanism
centration of bile that occurs secondary to Na'
for con 3. Source of bile acid: Bile salts are converted to bile acids in
(seccondary actve
2. Na'-K* ATPase in the
oral
absorption the Intestine, which are then absorbed into portal blood.
Thus, bile salts are important sources of bile acids that
transports Na' actively outmembrane
cell lining of
the cell andepithella
of
creates
add to the bile acid pool of the body.
gradient for Na transport into the cell. 4. Bile secretion: Bile salts are important
choleretics.
3. Water is reabsorbed They are constítuent of bile and also they stimulate bile
by Na movement.
passively by osmotic gradient created secretion.
4. H'is exchanged with Na'that causes 5. Absorption of fat-soluble vitamins: Bile salts facilitate
acidification of bile. absorption of fat-soluble vitamins (vitamins A, D, E,
Bile Acids and Salts and K).
"Hence, in obstructive jaundice, features of deficiencies
Bile Acids of fat-soluble vitamins develop.
There are two types of bile acids: Primary and 6. Activation of pancreatic enzymes: Bile salts
secondary. activate
1. The primary bile acids are pancreatic lipase
cholic acid and
deoxycholic acid. The primary bile acids are formedcheno
in the
7. Prevention of gallstone
with lecithin solubillze
formation: Bile salts along
hepatocytes from cholesterol. cholesterol. Thus, they prevent
2. Secondary bile acids (SBAs) are formation of stones in the gallbladder.
deoxycholic acid and 8. Physiological purgatives: Bile salts act as
lithocholic acid. The SBAs are produced in the intestine purgatives. Constipation occurs in conditionsphysiological
where intestinal bacteria convert primary bile acids into of deficiency
of delivery of bile into intestine as occurs in obstructive
SBAS.
jaundice.
9. Stool color: Bile salts add natural brownish color to the
Bile Salts stool.
Bile salts are Na' and K' salts of bile acids. 10. Prevention of bacterial growth: Bile maintains pH of
Bile acids are conjugated with taurine or glycine to form intestinal content and prevents overgrowth of bacteria in
taurocholic acid or glycocholic acid. intestine.
* These acids then combine with sodium and potassium
salts to form Na'-tourocholote, Na'-glycocholate, K-Enterohepatic Circulation
tourocholate, and K'-glycocholate, respectively. Bile acids and salts are absorbed from the intestine and re
Functions of Bile Salts excreted in the bile, and this cycle is repeated so many times,
Bile salts are primarily responsible for absorption of which is called enterohepatic circulation of bile acids and salts
fat and fat-soluble nutrients. Therefore, bile deficiency 1. Bile salts are produced in liver (200-500 mg/day) and
conjugated. Conjugated ble salts (CBS) through bilary
tract enter intestine.
Table 85.2: Ditlerences in hepatic and galibladder bile
Galbladder bile 2. From intestine, they are absortbed into the portal blood to
Hepatic bile reach lvert
Alkaline (8-85) Acidic (about 7)
Wter content 3. Also, in the intestine, CBS is deconjugated and un
96% 85% conjugated bile salt is absorbed into portal circulation
Solids 2g% 10-15 gh 4. The free bile acids in terminal leum and colon by the action
euts and Less More of bacteria are coverted into S8As, Le deoychallc ocid
hgnents and lithochollc acid
 System
644 Sectlon 7 Gastrolntestinal
are the causes of peptic ulcer. Chronically increased secretion
3. Drugs (hyperchlorhydria) produces pepticculcer bry damaging
of acid
4. Chemical and physical agents the mucosal barrier
5. Severe stress hyperchlorhydria are:
Conditlons that cause
Chronic gastritis, if untreated, leads to peptic ulcer Zollinger Elison syndrome
Gastric outlet obstruction syndrome (as occurs in pylore
Peptic Ulcers stenosis) from maes
mastocytosis (histamine secreted
Peptic ulcer means ulcer in the stomach (gastric ulcer) Syrstemic
increases HCI secretion).
or duodenum (duodenal ulcer) Acid of the gastric juice and non-B
Therefore.Zollinger-Ellison
to the syndrome is anon-a gstrin-
or pepsin in the gastric secretion produces damage
tumor of pancreas.
astroduodenal mucosa in abnomal conditions secreting
Helicobacter pylori infection
peptic ulcer is called acid peptic disease. byH.
that infection pyloriissthe major
Recently it is observed
Pathophysiology ulcer,
of pepticGram-negative
mucosal defense, causeThis bacillus that secretes an enzyme
Peptic ulcer is caused either by decreased 1. is a
converts urea into carbon
dioxide
or by hypersecretion of acid or infection. called urease that acid surrounding th
Diminished Effectiveness of Mucosal Barrier ammonia. Ammonia buffers the
mucus coat on the bacteria.
The defense barrier of the stomach is the 2, Helicobacterrpylori colonizes the
antral mucosa, whers
mucosal defense barrier.
gastric epithelium. This is called inflammation and disrupts immune
1. The mucus is secreted by mucus cells.
Mucus is a viscous it causes local somatostatin secretion fr
(mainly responses. It also inhibits
gel that contains mucin, phospholipid, electrolytes that facilitates gastrin release
and consequents
HCO,), and water. D cells
effectively increased HCl secretion.
2. The mucus gel layer is about 0.2 mm thick and gastrin level is moderately
elevate
separates the bicarbonate rich secretion of
epithelial celis 3. Therefore, serum
82.13). duodenal ulcer.
from the acidic content of the stomach (Fig. but later, ulcer
cells to remain alkaline Helicobacter pylori causes gastritis initially,
3. This allows the pH of the epithelial mucosal
despite acidic pH of gastric content. It protects isproduced.
acidic chyme. 5. Therefore, antibiotic therapy to kill H. pylori is frequently
epithelium from injury caused by treatment of peptic ulcer.
of mnucus is impaired, or successful in the
4. However, when secretion mucosal
bicarbonate production is decreased or when the Scientists contributed
cause ulcer
coat is mechanically damaged, acid and pepsin
formation.
use of aspirin and
Such damage is usually produced by drugs) that inhibit
NSAIDs (nonsteroidal anti-inflammatory
bicarbonate. Catecholamines also
the secretion of mucus and
ulcer is produced
inhibit mucus secretion. In chronic stress, Barry J Marshall JRobin Warren
catecholamines
(stress ulcer) by chronically elevated level of The Nobel Prize in Physiology or Medicine 2005 was awar awarded jointly
Barry J Marshall (Born 1951) and J Robin
in blood. to two Australian physicians,
Hypersecretion of Acid Warren (Born 1937) "for their discovery of the bacterium Helicobacter pylori
anxiety. Peptic ulcer and its role in gastritis and peptic ulcer disease
Gastric acid secretion increases in chronic
most of them lead a life
is common in business executives as food is known Features
more spicy
either in hurry or in worry. Intake of
toincrease acid secretion. Chronic stress induces gastric
ulcer. In most of the cases ulcer is located in the duodenum (Fig.
Therefore, it is generally believed that hurry, worry, and curry 82.14), usually above the ampulla of Vater, as in this area
acidic chyme is not neutralized by alkaline pancreatic juice.
The main feature of peptic ulcer is upper abdominal pain
Mucus
(epigastric pain). Typically, pain is experienced in empty
layer HCO, HCO, stomach and is relieved by taking water, food, or antacid.
If disease is untreated, hematemesis (vomiting of blood)
Mucosal surface-pH7 or malena (dark, tarry stool), vomiting (due to pylork
obstruction), and peritonitis due to perforation of ulcer
Mucus into the peritoneal cavity occurs.
droplets
Mucus
cells
Treatment
Interstitial fuid Specific Treatment
Capilary The specific treatment includes use of following drugs.
1. H, receptor antagonists: Ranitidine, cimetidine, famotae
Fig. 82.13: Mucosal defense barrier by bicarbonate. ond nizatidine are different generations of H, recepto
 Anterior
Posterior

Hepatic branch

Celiac branch

Eio, 82.14:
the
duodenum Endoscopic view of
seen through chronic peptic ulcer (note, two
Fligure 2.3. Rao SD endoscope).
Courtes Rioure
ulcers in
thers Medical
Avypee Brothe
Gastroln testinal
Publishers (P) Ltd, 2009. Surgery, 1st ediion Neww Delhl:
blockers. These drugs block the H,
histamine secretion. As histamine is areceptor and inhibit
HCI release from parietal cells, H, potent stimulator of
HCI secretion.
2. receptor blockers itinhibit Fig.82.15:Types of vagotomy. 1.Truncal vagotomy (main
vagus is cut); 2. Selective trunk of the
Proton-pump blocker
inhibits the activity of (H-K*ATPase inhibitor): spared);
This drug are cut),
3. Highly
vagotomy (hepatic and celiac branches
selective vagotomy (branches supplying are

H-K' proton pump, i.e. stomach

is ATPase. Therefore, the final step of the activity of Courtesy Figure 2.2. SD, Gastrointestinal Surgery, 1st edition.
inhibited. This is the most effective acid secretion Jaypee Brothers MedicalRao Publishers (P) Ltd; 2009. New Deihi:
treatment of peptic ulcer. The medicine
usual proton-pump
for the
used is omeprazole. blocker
3.
Sucralfate: This is sucrose octasulfate. Ittprovides a
protective layer on the ulcer. Therefore, it promotes ulcer
healing.
4. Muscarinic Gastrectomy
blockers:
Used to block the M, Atropine and pirenzepine are
and M, receptors. Therefore,
acetylcholine does not act on parietal cells. However, as Stomach
the noncholinergic vagal
cholinergic
innervation dominates over the
innervation for acid secretion, atropine does
not produce encOuraging results. Therefore,
muscarinic
blockers are not used in peptic ulcer treatment.
5. Gastrin blockers: As gastrin is the most potent stimulator
of acid secretion, effort has been made to discover
gastrin
antagonists. However, a successful gastrin blocker has not
yet been discovered. Proglumide, a gastrin blocker, is used
recently for the purpose.
6. Antibiotics: Recently, high dose of antibiotics such as
Stomach Stomach
amoxicillin to killH. pylori has provided promising result.
Nonspecific Measures Duodenum
Antacids
Antacids give immediate and temporary relief from pain. As Billroth Billroth I
e disease is mostly due to stress, measures to reduce the (Gastroduodenostomy) (Gastroduodenostomy)
stress level are very helpful. Fig. 82.16: The procedure of gastrectomy followed by gastro
Yoga Therapy and Other Measures duodenostomy (Bilroth I surgery) or gastrojejunostomy (Bilroth
surgery). Note the portion of stomach (as shown within the two dotted
Toga therapy like practice of relaxation techniques, adequate lines) removed in gastrectomy surgery for peptic ulcer.
eep and rest, regulation of diet, and withdrawal of drugs Courtesy: Figure 4.9, Rao SD. Gastrointestinal Surgery. 1st edition New Deht
Jaypee Brothers Medical Publishers (P) Ltd; 2009
like aspirin and NSAID improve the condition. Use of cold milk
 82.151 Antrum is
To Gastrojejunostomy chyme food, gastric gastricare andthese
(Fig.as the
prejerred jood. Whattests, secretion,
complications.
cells.foodinto
removes iprocedures)
s the glands,gastric
of discovery answer
cell) of killing healthy in of
G o emptying RegulationMechanism function
other,
parietal contains Stasis useful gastricof
HCI
is gastrectomy and relaxation, to
vagotomy propels vagotomy. absorption is
phases for
each expected
gastric of
the with part in drainage controlled level of
secretion, from prize Mechanism
innervate that usually such 82.16).
results
complication, secretion,
Names different
this Mental gastrin Nobel
Classify
cellassociatedstomach (the(Fig.truncal
differ is
as antrectomy
Partial
parietal andB secretion/day,
gastric gastric student
preferentiallystomach, gastrojejunostomy secretion.of
vitamin for they got viva.
gastrectomy food Question.
estimation stimulijuice,
the
areGastrectomy:
with
of how Who in
of for of appetite A
System thetypes of Therefore, performed
SUMMARY
CHAPTER mixing Mechanism ulcer, asked examination.
of pump IF gastric constituent
the and
Usually, portion providing ulcer, Long gastricare pouches
that two with pepticusually
Gastrointestinal the and for ulcer.
acid. peptic aas of What isWhat
2. food, stimulant
grinding peptic
gastric
secretion,
comes Amount
each
gastric and gastric
juice
are theory
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usual as in vagotomy
disease nerve of andand Notes. of gastritis
suchnerves storage, important
digestion gastritis secretion" Function
gastric stomach, the
7:
The
of gastritis
secretion in
Section
in Questions/Short
help the vagotomy vagus theyare gastric
of asked
advocated.selective temporary of
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are for diagnosisgastric of secretion,
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What Causes of
also onlythe s
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are
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functions
over howstudied,
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(cutting of tests,
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is
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types diaphragm), isstomachandcontrol
for causative regulation gastric
for and and are
of surgery
use are:different vagotomy useful emotion,method Short
and
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and pass.
and the have
that Structure
of can Composition
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performed is and as function
sympathetic secretion.
to
food patients, (cutting
thenerve
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secretion to important
surest(Must come secretion ulcer. him
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Treatment are below selective "Mechanism gastric
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and gastricimportantgastric
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primary is tests... and
and difficult
avoidance just stomach.areis
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Composition
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in In Vagotomy: thehighly pylori
parasympathetic of
disease. cured.
the Sometimes abdomen Concepts
Key sleep TO examinations,
gastric examinerof
function be
phases
truncal(cutting the
Though Helicobacter
IMPORTANT thephasesvalues of
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and notsurgical and foodGastric Though of of of different
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646 is in What normal
1. In In the
2. 3. 4. 1. 2. of
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4.
 Penstait
Rraior Antal Retropulsn Antral pump
contractioe

es 91AA te Di Pyono sphiíncter is parialy

D opened causing slow emptying
ginding of food o
Mechaniandsmsthe foodgast naterialemptying
aastris content intooccurs
of
Note, pyloric sphincter is cdosed in step A B, and C
during which thorough miaing and
duodenum h
converted into chyme. In stage D, sphincteris partially opened that causes slow emptying of
d

duodenum,
stomach (Figrather food returns back
. 9148). into the body of the 1. Acid In the duodenum: With
2. After fewsuch decrease in the pH of the
a
3. norrow openingcontractions,
at the pylorus opens partially with
duodenal content, the rate of gastric emptying decreases.
This response is mediated by both
Therefore,wave,
peristaitic
center.in
stomach empties small squirts with each hormonalol mechonisms,
. The acidic chyme in the
neural and
duodenum releases secretin that
Retropulsion
The terminal part of
decreases gastric emptying inhibiting contraction
the antrum and by stimulating the contraction of
pyloric
by of
sphincter.
contractions that antrum exhibits rapid and forceful2. Products of digestion: Products fat digestion like
back toward the force the chyme to be
fat of
of proximal part of the antrum propelled fatty acids and also some fat molecules in the duodenal
the
stomach (Fig. and body content inhibit gastric emptying.
retropulslon, 91.4C). This is movement mediated by CCK and GIP.
This response is
called
.Retropulsion is very
larger fod particles effective in mixing and
grinding the
CCK is secreted from duodenum and jejunum
response to fatty acids and it inhibits gastric emptying
in
into smaller
ones. "GIP, Which is released in response to fatty acids also
Thet
slowly sphincter
fond into partially opens and gastric pump gastric emptying.
duodenum (Fig. 91.4D) 32 Osmolality of
duodenal content: The chyme entering into
Physiological
As the
Significance duodenum has higher osmolality.
" There are osmoreceptors in the mucosa of duodenum
muscle layers in the and jejunum that detect change in osmolality of the
contractions in these parts offundus and body are thin,
the stomach are weak. duodenal content.
Therefore, gastric content in body of stomach settles into " Hypertonic solutions in the duodenum release
different layers based on their density. hormones that inhibit the rate of gastric
1. Fat content of thefood forms an oily 4. Products of protein digestion: Presence of emptying.
layer on the top peptides and
other gastric contents. This is why fat is emptied of the amino acids in the duodenum releases gastrin from the
than thecarbohydrate and protein (Application Boxslower G cells located in the duodenum.
2. Liquid portion of the food flow around the mass and 91.1).
enter
Gastrin increases antral contraction but at the same
the antrum, and from there into the duodenum. Therefore, time also causes constriction of pyloric sphincter.
liquid is emptied faster than the solid. Therefore, the net effect is decreased rate of gastric
emptying.
The products of protein digestion also release CCK and
Application Box 91.1 GIP from duodenum and jejunum that inhibit gastric
Acup of fat is taken in cocktail party:As fat decreases gastric emptying. emptying.
ually a cup of fat is ingested before drinking alcohol in cocktail pary.
Usually 5. Volume of the meal: Whenever a large amount of food
Fat ensures slow gastric emptying and slow absorption ofof alcohol from is taken in a meal, the time taken for gastric emptying
intestine, and thereforethe person drives his car back after the party.
even aftera heavy drink. prolongs. However, if the volume is mainly due to liquld
then emptying is faster.
6. Stretching of duodenum: Entry of chyme into the
Regulation of Gastric Emptying duodenum stretches the wall of duodenum.
Gastric emptying is regulated by both neural and hormonal " This initiates enterogastric reflex that inhibits gastric
mechanisms. The upper part of the small intestine (duodenum emptying.
and jejunum) contains receptors that detect change in pH, " Enterogastric reflex is also activated by acid in the
fat and protein digestion
osmotic pressure, and products of hypertonic
duodenum.
7. Neural factors:
The chyme that enters duodenumishighly acidic and Al these
digestion.
and contains products of protein and fat " Vagal stimulation promotes gastric emptying.
Therefore, vagotomy produces gastric stasis Con
stimul influence gastric emptying
694 Section 7: Gastrointestinal System
3. Hormones like thyroxine
sequently, whenever vagotomy is performed for and intestinal motility. Her
the treatment of peptic ulcer, usually a drainage hyperdefecation are feature
procedure like pyloroplasty or gastrojejunostomy 4. Increased liquid content of
is also performed to ensure proper passage of food ing
from the stomach into the duodenum (Clinical
Box 91.1). Vomiting
" Sympathetic stimulation inhibits gastric emptying. Definition
8. Hormonal factors: Most of the hormones liberated from
duodenum and jejunum like CCK, GIP, secretin, etc. inhibit Vomiting is the expulsion of g
gastric emptying. tract to the external environm
Clinical Box 91.1
Associated Features
Vomiting is usually preced
Drainage procedure is done with vagotomy: As vagotomy decreases
gastric motility and produces gastric stasis, whenever vagotomy is tachycardia, sweating, pall
performed as done for the treatment of peptic ulcer, usually a drainage pupils. It is associated with
procedure like gastrojejunostomy is also performed to ensure proper the stomach into the esopha
passage of food from the stomach into the duodenum.
Stimuli and Vomiting C
APPLIED PHYSIOLOGY Vomiting is a reflex pheno
located in the medulla (Flov
Dysfunctions of Gastric Emptying 1. The receptors present
inputs to the vomiting
Delayed Gastric Emptying center present in the
1. Gastric emptying is delayed in autonomic neuropathy as consists of various scat
occurs in diabetes mellitus. different aspects of va
2. Paralysis of propulsive movements occurs following 2. Vestibular nuclei med
vagotomy, which is called gastroparesis. Therefore, a sickness.
drainage procedure like pyloroplasty is performed to 3. Pharyngeal stimulati
overcome postvagotomy gastric stasis. nucleus tractus solita
3. Hypertrophic pyloric stenosis can cause gastric stasis.
4. Area postrema mec
(opiates, chemother
Rapid Gastric Emptying (as in pregnancy).
Normally, vagus stimulation promotes gastric emptying. 5. Vomiting activated
1, Therefore, states of
emptying
increased vagal activity increase diencephalic inputs
2. Conversely, sympathetic stimulation inhibits The important stimuli t
Therefore, loss of appetite is a feature of acuteemptying. 1, Distention of stoma
state of sympathetic overactivity. stress, a 2. Tickling the back o
3. Painful injury of th
Flowchart 91.2: Mechanism of vomiting reflex.
 the yphate is
muscularis externa (outer longitudinal and inner circular muscles) 6. Therefore, segmentation
movements are also
wel developed mixing movements. They help in digestion
VSubhadra Dev, 1st edition, 2016:
Courte Figure 1325A Basic Histology, by New
of nutrients. and
Javypee Brothers Medical Publishers P) Ltd. Delhi.
Peristalsis
Peristalsissis the progressive contraction of
Electrophysiology of f
Intestinal Smooth Muscles
ofcircular smooth muscles of the small intestine
1. The wave of successive
contraction moves in orthogradee portns
The frequency of slow waves is maximum in small intestine
that occurs regularly. The frequency is highest in duodenum
i.e. toward colon.
" In fact, peristaltic wave spreads in both direction
(about 15/min) and decreases slowly toward ileum where it However, wave oral cavity (oral directions
out after shorttoward
is about 8-10/minute.
1. Slow waves are not always accompanied by bursts of action
a
distance, and wave toward
(aboral spread) continues spreadjcoleedi
potential spikes. When slow wave is associated with spike,
progressively.
This is called law of the intestine.
2. Peristaltic waves involve a smaller length of intestine
the contraction is stronger and, in its absence (no spike), . When chyme
contraction is weaker or absent (refer to Fig. 88.5; Chapter enters the intestine, the bolus of the
88). chyme stretches its wall.
2. A characteristic feature of slow waves of intestine is that . The part of the
they are localized to a short segmnent of the intestine.
intestine behind
and the part of the intestine inthe chyme contracts
front of the chyme
Therefore, contraction is also localized to the segments.
This results in segmentation type of movement in the Segmental contractions
intestine.
3. The basic electrical rhythm is purely intrinsic.
4. The frequency of action potential spike, which determines
the strength of muscle contraction, depends on excitability
of the smooth muscles. The excitability in turn depends
on autonomic innervation, activity of the enteric neurons
and the circulating hormones.
5. Parasympathetic stimulation enhances and sympathetic
stimulation inhibits intestinal contractility. Propulsive segment

TYPES OF INTESTINAL MOVEMENTS

Intestinal movements carry out three primary functions:
1. Mixing the chyme with digestive secretions.
2. Bringing the chyme in contact with the absorptive
of the
surface
microvilli to increase absorption. B
3. Propelling the chyme toward colon. Receiving segment
nese runcions are achieved by various small intestinal Figs. 92.3A and B: Segmentation movement of small intestine
motilities. The motilities are segmentation, peristalsis, migrating the mechanism for mixing of food in segmental contractions ibl
myoelectric complex, contraction of the muscularis mucosa, slightly enlarged view of intestine. The direction of arrows indicate
villus contractions, and movements due to intestinal direction of movement of food particles. Note, in segmental contrac
reflexes. food is grindedand thoroughly mixed between two propulsive seg
 699
Chapter 921 Smal lntestinal Motility
Propulsive segment 1. There are bursts of intense electrical and contractile acthvity,
once in about every 90 minutes. This is called migrating
motor complex or migrating myoelectric complex (MMC
2. MMC starts in the stomach and is propagated throughout
the intestine to the terminal part of theeileum. Once, a
MMC reaches the distal end of the ileum, a next MMC
Peristaltic ring
Receiving segment
begins in the stomach. Likewise, MMC is repeated every
A 75-90 ninutes.
1 MMC results and strong propulsive contraaction;
ins the intestine and empties the
therefore, this
remaining contents into the colon.
4. MMC cleans the entire lumen of the stomach and intestine,
to keep the house ready for the next meal. This is why the
MMC is known as housekeeper of small intestine.
B Peristaltic contraction moving to a 5. MMC also inhibits the migration of colonlcbacterla tron
new forward position colon into the intestine.
Figs. 92.4A and B: Peristalsis in small
intestine. Note the ring of
contraction
forward position moves from the initial position (A) to a new Contraction of Muscularis MucOsa
(B). Thus, peristalsis moves aborally
The muscularis mucosa of small intestine contracts irregularly.
These contractions alterr the patterns
pa of the mucosal folds.
relaxes and the ring of contraction proceeds in forward
direction (Figs. 92.4A and B). 1. Contractions ocCur at a frequency ofabout 3/minute
3. The primary function of peristaltic 2. Such contractions help in mixing the luminal contents and
chyme in forward direction. movements is to propel also in bringing the fresh chyme in contact with mucosal
4. Sometimes, the frequency of surface.
peristalsis increases to an
extent that intestinal contents are emptied very fast (with
a speed of 20 cm/sec) into the Villus Contraction
- This is called rush colon.
peristalsis.
This is typically seen in
The villi of small intestine also contract irregularly. This is
acute diarrhea called villus contraction.
5. There are also
antiperistaltic contractions of intestine 1. This is typically seen in upper part of the small intestine.
Antiperistalsis results in vomiting 2. These contractions are especially meant for emptying the
central lacteals of the villi.
Short Range Peristalsis 3. They also increase intestinal lymph flow.
nort range operistalsis also
occurs in the intestine, but less
frequently. It occurs fora shorter part of intestine. Intestinal Reflexes
1. Short range peristalsis alongwith segmentation
contraction There are two reflexes observed in the
decreases the net rate of propulsion of chyme in forward intestine:
direction. (1)intestinointestinal reflex and (2) gastroileal reflex.
2. This allows the chyme to stay more time in intestine to
Intestinointestinal Reflex
facilitate digestion and absorption. When a part of the intestine is
intestine relaxes. This is called ver-distended,
the rest of the
Clinical Significance mediated by local intestinointestinal
enteric neurons and
reflex. It is
1. Admninistration of codeine decreases the motility of the
vagovagal pathways.
intestine, therefore decreases the frequency of defecation. Gastroileal
When food
Reflex
" The decreased motility also prolongs the transit time the enters
the motility of the stomach (stretching of stomach),
for the intestinal contents so that more water and terminal part of ileum is enhanced and
nutrients are reabsorbed. ileocolic sphincter relaxes.
This increases entry of contents
" Therefore, this also decreases the volume of stool. through ileocecal sphincter.
of
ileum into the colon
2. On the other hand, administration of laxative for example
castor oil produces the reverse effect. This reflex is proposed to be
therefore
nediated by vagus nerve.
" Laxatives increase intestinal motility, and Law of the Intestine
shorten the transít time of the intestinal content.
" This increases the delivery of chyme and water
into When a bolus of chyme enters the
the colon that causes diarrhea. intestine behind the bolus intestine, the part of the
intestine ahead of it relaxes.contracts and the portion of the
. This helps in
Other Motilities propagation of ring of
direction. contraction
in aboral
Migrating Myoelectric Motor Conplex This response is known as law of
This is men the intestine
pattern of motility of small eant to propel the
In the interdigestive phase, the aboral direction as intestinal content in the forward
intestine changes. occurs in
peristalsis.
 1S secreted from Ebners glands secretion of gastr
in the tongue.
2. Gastrie lipase also helps in digestion of fat. However, pH inhibits pancre
salt.
deficiency of lingual and gastric lipase does not result 3. Another cause of s
in malabsorption of fat as pancreatic lipase is actually bile salts in the d
important for lipid digestion. 4. Steatorrhea can a
3. Principal fat digestion starts in the duodenum by the
pancreatic lipase, which hydrolyzes 1 and 3 bonds of Tropical Sprue
triglycerides that result in formation of free fatty acid and In this condition, t
2-monoglycerides (2-monoglycerols). Pancreatic lipase density of microvil
acts on lipids that have been emulsified (emulsification absorption probab
by bile acids). absorption of lipids.
4. Fat digestion is facilitated by pancreatic colipase.
5. There is another lipase secreted from pancreas called Absorption o
as bile salt activated lipase, which also assists in lipid
digestion. Absorption o
6. The dietary cholesterol is hydrolyzed by cholesteryl ester Normally, about 1
is added from GI s
hydrolase.
water is excreted in
Absorption of Lipids 99.5% of water lo
Lipids are absorbed by passive diffusion and carrier-mediated 1. Water is not
transport. As soon as lipids enter the cell they are esterified, stomach.
therefore a gradient is maintained for their entry into the cell. 2. Due to hype
1. For their absorption, fats are emulsified in the intestine by secreted fro
detergent action of bile salts, lecithin, and monoglycerides. nutrients ar
With the help of bile salt, lipids form micelles. jejunum, the
2. Micelles are cylindrical aggregates of lipids like fatty acids, about 600 m
monoglycerides, and cholesterol with their hydrophobic H,0 in the ile
ends at the center. 3. Water is ab
3. Micelle solubilizes the lipids and provides a medium for osmolality
their transport to the intestinal epithelial cells. Thus, water is ma
micelles help in transport of lipids to the enterocytes, (refer to Fig
where they disintegrate into the individual lipids and 4. The absorg
passively diffuse into the cells. electrolyte
Short-chain fatty acids are produced in the colon by the 5. In the colo
colonic bacteria and absorbed there. About 60% of short osmotic pr
chain fatty acid is acetate, 25% propionate and 15% butyrate. standing g
ointestinal System
Short-chain fatty acids are absorbed in exchange for H,
therefore help in acid-base balance. They also promote the
absorption of Na'.
Cholesterol is easily absorbed from the intestine in the
presence of bile, fatty acid and pancreatic juice. The absorbed
cholesterol is incorporated into the chylomicrons that enter
circulation via lymphatics.
The vitamins A, D, E, and Kare fat-soluble vitamins. Their
absorption is facilitated by presence of bile acids and products
of lipid digestion in the intestine. Therefore, in the absence of
bile acids or malabsorption of fat, deficiency of these vitamins
OcCurs.

Disorders of Fat Digestion

Steatorrhea
This is a condition in which there is passage of fatty, bulky,
and clay-colored stool.
1. This occurs due to deficiency of exocrine pancreas.
Pancreatic lipase deficiency results in impairment of fat
digestion.
2. This is also sometimes seen in patients with excess
secretion of gastric acid in which decreased duodenal
pH inhibits pancreatic lipase. Acid also precipitates bile
salt.
3. Another cause of steatorrhea is impaired reabsorption of
bile salts in the distal ileum.
4. Steatorrhea can also occur due to intestinal diseases.
 project into the canaliculi (Fig. 82.b),
is greatly incre0sed
lumen
membrane in contact with gastric microvillaror canalicular
Fusion of tubules and vesicle with activity of the
membrane ensures increased H-KATPase
membrane in the active state.

Nerve Supply of Stomach

Stomach is supplied by both divisions of ANS.
Parasympathetic innervation is by vagus nerve. Vagal
1.
stimulation facilitates gastric secretion and motility.
2. Sympathetic stimulation inhibits gastric secretion and
motility.
Gastric Juice
Volume and pt: The amount of gastric secretion per day
varies from 1 liter to 2.5 liters. The gastric juice is highly acidic,
having pH of 0.7-4.
Composition of Gastric Juice
It has following constituents:
1. Water (99.5%)
2. Solids (0.5%).
tlSolids contain inorganic and organic substances.
 Chapter 82:Gastric Secretion
norganic Constituents: Anions are Cl,
andcations are H,,Na', K', Ca', and Mg PO,,S0,and HCO, ISF Paretal call

Organic Constituents: Pepsinogen, intrinsic factor, mucin,

rennin,gastric lipase, gelatinase, carbonic anhydrase, and co, +HO
jsozyme. Na
CA
Functions of Constituents
Normal concentration of HCI is 40-60 mEq/L. The maximum H,CO
concentration can increase up to 150 mEa/L Na -KATPase
Pepsinogen is secretedifrom the peptic cells. There are two
types of pepsinogens:
Type-i pepsinogen is found in chief cells in fundus and
body.
. Type-ll pepsinogen is found in the chief cells HCO,4 HCO,
throughout the stomach.
CI
2. Pepsinogen is converted into pepsin by HCI.
" Pepsin is a proteolytic enzyme that breaks down
protein molecules into peptones. Pepsin acts best at
pH of 2-4. Fig. 82.7: Mechanism of HCl secretior
(also called chymosin) is a protein igesting dashed lines for K and C depict t
" Rennin gastric lumen. Note the presence of
enzyme. membrane that pumps K* into the cel
The mucin secreted by mucus cells is of two types: the (SF: interstitial fluid; CA: carbonic anhydra
3.
insoluble mucin and the soluble mucin.
Mucin forms a protective layer on the gastric 5. The Cl that enters parieta
"
epithelium. gastric lumen. In the lumen,
bicarbonate and has alkaline pH. Thus, it HCI.
" It retains digestion, as it str
from acid-peptic 6. The HCO, enters blood
protects the stomach
Thus, for each H secrete
buffers HCI. absorption from
vitamin B, HCO, is reabsorbed into t
4. Intrinsic factor helps in Recycling of K': K* that e
terminal ileum. 7.
ATPase is transported bac
is reutilized for further H+
GASTRIC SECRETION other major " K' entering the cell
secretion of HCl and basolateral membrar
Gastric secretionincludes pepsinogen,
secretion of located on basolatera
synthesis and
Constituents Such as
the lumen.
 638 Seten tteintbitem
inoen a covened inte pepn y H Pepn i
trong preteeye enyme
3histamine
Peeingen secretien it atimuiated by gtrin and
Mucus Secretion
Mucus i secretet hy mucus seerettng telte that are plentily
valable n the neckegon of esstrie gland
1 The mucin secreted by cous cell is ef twe types the
obe mucin, which is secreted by imuis secretng celle
of entire gostric mcosa and the solble mucin, secreted
from mainly cardiac and ylorik mucosal cells
Mucin oms a peotective lyer on the gastrik epithelium
tretalins bicarbenate and hacalkaline ph
Thus, it pretects the stomach from acid-peptic
digestion, as it buffers HCI
2. Mucus secretion is stimulated by increased blood flow to
the stomach
Intrinsic Factor Secretion
Intrinsic factor (IF) is secreted from parietal cells along with
HCL. It is a glycoprotein.
1. Itis synthesized like other glycoproteins and its secreton
is stimulated by factors that stimulate HCl secretion like
histamine and gastrin.
2. Intrinsic factor helps in vitamin B,, absorption from
terminal ileum.
Factors that Influence HCI Secretion
Factors that Stimulate Gastric Acid
Secretion
Factors that increase HCl secretion from the parietal cells of
stomach mainly act through locally altering the concentration
of three hormones: acetylcholine, gastrin, and histamine.
In the parietal cells, there are specific receptors for these
hormones and other hormones. Hormones bind with the
receptors and change the intracellular second messenger
concentration that finally stimulates HCl secretion (Fig. 82.8)
Acetylcholine
Acetylcholine is an effective stimulator of gastric acid secretion.
It is released at the nerve endings of vagal cholinergic fibers
that innervate parietal cells.
1. Acetylcholine acts on the M, cholinergic receptors on the
parietal cells and increases intracellular Ca'".
2. It acts directly on the parietal cell to increase HCl secretion Histamine is a powerful stimulator of HCl secretion from
and acts indirectly by secreting histamine and gastrin from stomach.
ECL cells and G cells respectively that in turn stimulate
parietal cells.
Gastrin
Gastrin is the most potent stimulus for HCl secretion.
1. Gastrin acts on gastrin receptors on the parietal cels and
increases HCl secretion by increasing intracellular Ca'"
(Fig. 82.8).
2. Gastrin is secreted fromG cells that are present in the
antral mucosa of the stomach.
3. Vagal fibers innervate G cells and vagal stimulation
increases gastrin release. However, vagal fibers that
6AME
ode kinsses
Paretal ce
ATPaseGastrickmen
Fig. 82.8:t Mechanism of actions of hormones on parietal cell. Note
linally calcium and CAMP act as second messengers for hormones thae
activate H-K ATPase to purmp H into the gastric lumen. Minus sign
indicates inhibition
(GR gastrin recepto, M, muscarinie 3eceptor, H histamine type 2
receptor, ACh acetylcoline, PGE, prostaglandin )
mediate gastrin release are noncholinergic (Fig. 829) as
the neurotransmitter is GRP (gastrin-releasing peptide).
4. Gastrin also stimulates histamine release from ECL cells
that in turn Increases secretion of HCI from parietal
cells.
5. Gastrin secretion from stomach is increased by gastric
distenslon, noncholinergic vagal stimulation, protein
rich food, and catecholamines. Pentagastrin is used for
assessing gastric acid output (Application Box 82.1).
Application Box 82,1
Pentagastrin test and Gastrectomy1 As gastrin is the most potent
stimulator of HCI secretion, exogenously administered synthetic gastrin
(pentagastrin) assesses the degree of acid output
put from parietal cell mas
of the stomach, This forms the physiological basis of pentagastrin test.
As Gcells are present in antral part of stomach and gastrin is the stong
stimulus for parietal cells, antrectomy (partial antral gastrectomy) ls
performed for surgical treatment of protracted peptic ulcer.
Histamine
1. It acts on H, receptors on the parietal cells and increases
Intracellular cyclic AMP as second messenger, Cyclic AMP
stimulates protein kinase, which increases the activity of
H-K* ATPase and HCl secretion.
2. Histamine is secreted from enterochromaffin-ike (ECL)
cells.
3. Histamine release is stimulated by both ocetylcholine and
gostrin.
4. Thus, histamine is considered asa major mediator of HC
secretion. Therefore, patients with peptic ulcer are usually
first treated with histamine type-2 receptor antagonists.
 639
ChepterBi Gestr Secretion
Atechanicaland Chemical Factors
Acrumulatian of tood in the Chyme in the Duodenumduodenum, secretin is secreted
mainly
This ma occurs due stomach
to increases acidWhen acidic chyme enters
ecreton
mechanical distension
t stretches Gcells and stimulates gastrin release. Also. from upper intestinalmmucoss rmolity, and gastrin
inhibits gastrle secretion and
educts sof orotein digestion (peptides and amino acids) Secretin elle
gastrin secretion, and hot and spiey release from G cells digestion in the
foods carbohydrate and lipid content
HaSecretionfrom the stomach (Table 82.1). facilitate Poducts of hyperosmolality of duodenal of an
duodenum, and release
by increasing the peptide).
Factorssthat Inhibit Gastric Inhibit acid secretion GIP (qostric inhibitory
Acid Secretion enterogastrone called gastric
e
increasedacid output, somatostatin, and acidic enterogastrones also that inhibit
duodenumodecrease gastric acid secretton. content of 3. There are other
secretion.
Content
aH of Gastric Luminal
gastric Regulation of Gastric Secretion
Decreased pH of content is an important and natural humoral
secretion, regulated by neural and
inhibitor of HCl Gastric secretion is regulation depends on the
1. When secretion of acid is high enough to decrease pH of mechanisms. The mechanismn of mechanisms
secretion. The neural
stric content to below 2, secretionn of HCI is inhibited phase of gastric acid and long Gl reflexes,
and
Beeative feedback mechanism. Hence, this is called as are autonomic influences, short vagus nerve. The hormonal
autoregulation of acid secretion central influences mediated bysecretion are discus5sed auove
all mechanisms regulating gastric
The highly aciaiC gastric pH does not inhibit nariotal phases (cephalic, gastric,
ectly: rather inhibition of acid secretion is mediated by Gastric secretion occurs in three regulating secretion are
mechanisms
gastrin and somatostatin, and intestinal) and the
different for each phase of secretion.
2 The highly acidic chyme directly inhibits gastrin serretion
rom Gcells, and stimulates somatostatin secretion from Cephalic Phase
stomach. smell,
Dcells of gastric secretion is elicited by
Somatostatin inhibits secretion of gastrin from G cells that The cephalic phase of chewing of food. This is called
decreases acid secretion. sight, thought, taste, and increase acid secretion originate
cephalic phase as impulses to
Somatostatin mainly in the brain.
Camatostatin is secreted trom the D cells of the gastric activate dorsal motor nucleus of
1. The sensory stimuli gastric
cephalic phase of
mucosa. vagus in the medulla. Therefore, vagus nerve and the
Decreased pH of gastric content inhibits
(pH <2) increases the secretion is entirely mediated by
noncholinergic (Fig. 82.9).
secretion of somatostatin, which gastrin release. fibers are both cholinergic and
secretion, directly contact parietal cells are
2 As gastrin is the most potent stimulator of acid 2. The vagal fibers that noncholinergic
decreased gastrin release decreases HCI secretion from cholinergic and fibers that contact Gcells are
the stomach. (neurotransmitter is GRP).
stronger than cholinergic
secretion 3. As noncholinergic effects are prevent vagally
Table 82.1: Stimuli that alter gastric acid effects, atropine cannot effectively
HCl secretion Therefore, atropine is not
A. Factors that increase mediated acid secretion.
ulcer.
Luminal Factors prescribed in the management of peptic
Distension of stomach
Brain
2. Products of protein digestion Vagus nerve
Hormonal Factors (locally acting)
Acetylcholine
Noncholinergic fibers
2. Gastrin Cholinergic fibers
3. Histamine
GRP
Neural Factors
ACh 1 ACh
Vagal stimulation (cholinergic and noncholinergic) G cell
ECL cells Dcell
Blood-borne Factors
Epinephrine Histamine Somatostatin Gastrin
secretion
B. Factors that decrease HCI
Luminal Factors Panetal cell4
Increased acid content (highly acidic chyme) ACh
Hormonal Factors (locally acting)
HCI
Somatostatin
Fig. 82.9: Regulation of gastric secetion by vagus nerve
Blood-borne Factors peptide
(ECL enterochroaffn lke colt GAP gastrin leasing
acetyicholine, Minus sgn-indicates inhibition)
Secretin, GiR, glucagon
Ggtic inhtitory peptidel