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Stomach Final PPT 4

The document discusses the physiology and biochemistry of the stomach, detailing its functions, gastric secretion, and motility. It covers the mechanisms of hydrochloric acid secretion, factors affecting it, and the phases of gastric secretion. Additionally, it outlines various gastric function tests used to assess conditions like hyperchlorhydria and achlorhydria.

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0% found this document useful (0 votes)
99 views31 pages

Stomach Final PPT 4

The document discusses the physiology and biochemistry of the stomach, detailing its functions, gastric secretion, and motility. It covers the mechanisms of hydrochloric acid secretion, factors affecting it, and the phases of gastric secretion. Additionally, it outlines various gastric function tests used to assess conditions like hyperchlorhydria and achlorhydria.

Uploaded by

amanmahawar3199
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

Physiology and

Biochemistry of
stomach
By Mohan Gandhi K.E
MBBS Final Year
Department of Surgery
Unit 4
GRMC
Physiology of stomach

• Functions of stomach

• Gastric secretion – composition, regulation, phases.

• GI motility – in empty stomach, related to meals .


Functions of stomach:

• Storage of food.

• Mixing of food with gastric secretion to form


a semisolid mixture called chyme.

• Slow emptying of chyme from stomach into


small intestine at a suitable rate for better
digestion and absorption.
Secretion of gastric juice

• Hydrochloric acid is secreted by Parietal cell(oxyntic cells).


• These cells have a complex network of intracellular
canaliculi into which HCL is secreted.
Mechanism of HCl secretion
• The secretion of HCL can be described in
two steps – secretion of H+ and
secretion of Cl-

• Secretion of H+ :

• H+ ions are produced from metabolic co2


and h2o present within the cell.

• The enzyme carbonic anhydrase accelerates


the formation of H2CO3 which dissociates to
release H+ and HCO3-

• CO2 + H2O  H2CO3  H+ and HCO3-


• The H+ ions are secreted into the lumen of
canaliculi are exchanged with K+ by primary
active transport mediated by H+K+ATPase
pump.

• The HCO3- ions produced in parietal cells are


transported by antiport in the serosal
membrane into the blood in exchange for Cl-
by active transport.
• Secretion of Cl-
• The Na-K pump located on the basolateral membrane
of paritel cell pumps out three Na+ for every two K+
in creating intracellular negativity.

• Because of high intracellular negativity, the Cl- is


forced out into the lumen of the gland through the Cl-
channels located on the apical membrane of the cell.
Factors affecting HCL secretion

• FACTORS STIMULATING HCL SECRETION :

• Vagal stimulation
• Gastrin
• Histamine
Factors affecting HCL secretion

• FACTORS INHIBITING HCL SECRETION :

• Negative feedback due to low pH


• Somatostatin
• Prostaglandins – PGE and PGI
Function of HCL

• It hinders the growth of pathogenic bacteria.

• Provides optimal pH for the action of pepsin.

• It helps in the breakdown of proteins.

• Pepsinogen secreted by chief cells are converted into its active form,
pepsin by the action of HCL.
Regulation of gastric secretion
• It includes neural control and chemical control.
• Neural control:
• Vagal stimulation:
• It increases secretion of HCL by parital cells and pepsin
by chief cells. Vagal stimulation occurs through direct
path and indirect path.

• In the direct path, it stimulates HCL secretion by


releasing acetylcholine which acts on the muscarinic
receptors on parietal cells. Ach also potentiates the
action of histamine on h2 receptors of parietal cells.

• In the indirect path, the vagus nerve causes the release


of gastrin which stimulates H+ secretion.
Regulation of gastric secretion- Chemical
control
• Role of gastrin:
• It stimulates HCL secretion by binding with cholecystokinin receptors on the parietal
cell.
• Gastrin also increases HCL secretion by stimulating secretion of histamine from
ECL(Enterochromaffin like) cells present in the body of stomach.

• Role of histamine:
• Histamine is released from ECL cell on the base of gastric gland.
• Histamine increases HCL secretion by acting on H2 receptors .

• Role of somatostatin:
• Somatostatin is secreted by D cells located adjacent to G cells or parietal cells in the
gastric glands.
• Somatostatin inhibits HCL secretion directly by its action on parietal cells and indirectly
by inhibiting gastrin secretion by G cells.
• Role of low pH:
• Low pH inhibits H+ secretion by parietal cells through negative
feedback mechanism.
• However, if the pH rises above 3.5, the release of gastrin is
stimulated. In this way, the negative feedback maintains pH near 3.

• Intestinal influences:
• Chyme causes the release pf several intestinal hormones like secretin,
CCK and GIP.
Phases of gastric secretion

• Gastric secretion occurs in three phases:

• Cephalic phase
• Gastric phase
• Intestinal phase
Cephalic phase

• Secretion is initiated by the thought,


sight, smell or taste of food.

• Neurogenic signals originate in cerebral


cortex and appetite centres of amygdala
or hypothalamus. The impulses are
transmitted to dorsal vagal nuclei and
then to the stomach.

• Emotions such as anger increase gastric


secretion while fear and depression
decrease gastric secretion.
Gastric phase
• This phase occurs when food enters the
stomach.

• This phase accounts for about 50


percent of total gastric secretion.

• Gastric secretion is produced by:


• Distension of body of stomach acting
through vagovagal and local myenteric
reflex.
• Distension of antrum result in gastrin release
from antral G cells.
Intestinal phase

• It begins when the chyme starts to


empty from stomach into the
duodenum.

• This phase is mainly inhibitory in


nature.

• It occurs through following mechanisms,


• Enterogastric reflex initiated by distension of
small intestine.
• Hormonal through release of secretin, CCK,
GIP, VIP and somatostatin which inhibit
gastric secretion.
Gastric motility

• Gastric motility is the function of gastric musculature


consisting of outer longitudinal layer, middle circular layer
and inner oblique layer.

• Initiation of gastric motility:

• The basal electrical rhythm(BER) or gastric slow waves


are initiated by the pacemaker cells located near the
fundus on the greater curvature of the stomach.
Types of gastric motility

• Motility of empty stomach which includes,


• Migrating motor complexes
• Hunger contractions

• Gastric motility related to meal which includes,


• Receptive relaxation
• Mixing peristaltic waves
• Gastric emptying.
Gastric motility – empty stomach
• Migrating motor complexes:
• It is the peristaltic wave which begins in the
esophagus and travels through the entire GIT.
• This wave remove any food remaining in the
stomach and intestine during the interdigestive
period.

• Hunger contractions:
• These are mild peristaltic contractions occurring
in empty stomach.
• When they become extremely strong, they may
cause tetanic contraction lasting for 2-3 min
which can painful. These are associated with a
sensation of hunger.
Gastric motility – related to meals

• Receptive relaxation and accommodation:

• It is a vasovagal reflex caused by distension of stomach.

• Cholecystokinin participates in receptive relaxation by


increasing distensibility of the stomach.

• By the end of meal, about 1-2L of food can be


accommodated.
• Mixing peristaltic waves:
• The presence of food increases the contractile activity of the
stomach.
• This enhanced contractile activity is called mixing waves , which
mix the food with stomach acid and enzymes and break it into
smaller and smaller pieces to form a pasty consistency called
chyme.

• Gastric emptying:
• Gastric emptying occurs through a progressive wave of
forceful contraction involving antrum, pylorus and
proximal duodenum which together function as a unit.
Gastric mucosal barrier

• It protects the gastric mucosa from damage by the hcl. It is


created by:

• Mucin secretion

• Bicarbonate

• Epithelial barrier

• High mucosal blood flow

• Prostaglandins
Gastric function tests
• These are used to establish the presence of
hyperchlorhydria or achlorhydria.
• Fractional test meal test:
Gastric function tests
• Histamine test:
• After an overnight fast, in the morning the stomach is aspirated and washed with
distilled water, then 0.5mg histamine is injected subcutaneously and the samples
are aspirated and analysed.
• If there is no free acid present, then it is called true achlorhydria or histamine fast
achlorhydria.

• Augmented histamine test:


• The test is performed with increasing dose of histamine till maximum secretory
response is achieved.
Gastric Function Tests

• Pentagastrin test:
• It is similar to histamine test but instead of histamine, 6 mg of
pantagastrin is given as subcutaneous injection.

• Insulin test:
• Hypoglycemia produces vagal stimulation that also causes secretion
of acid from the stomach.
• Seven units of insulin is given intravenously and samples are taken
for presence of free acid.
Gastric Function Tests

• Barium meal study:


• The patient swallows a suspension of radio opaque barium sulphate
and its passage through GIT is observed by radiograph on
fluorescent screen.

• Endoscopic examination and biopsy:


• It is more reliable than conventional barium meal studies. Specimen
can be taken using biopsy forceps for histological and cytological
examination.
Take home messages

• Regulation of gastric secretion:


• Neural control
• Chemical control – Gastrin, Histamine, Somatostatin

• Phases of gastric secretion:


• Cephalic
• Gastric
• Intestinal
Take home messages

• Gastric function tests:


• Fractional meal test
• Histamine test
• Augmented histamine test
• Pentagastrin test
• Insuline test
• Barium meal study
• Endoscopy examination and Biopsy
TEXTBOOKS REFERRED :

1. BAILEY AND LOVE’ SHORT PRACTICE OF SURGERY


TEXTBOOK

2. INDU KHURANA ,TEXTBOOK OF PHYSIOLOGY – 2ND EDITION


Thank you

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