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Function of Stomach
Dr. Farhad Shaker
ο‚— . The stomach has five recognizable
parts and two curvatures; parts – the
cardia (around the oesophageal
opening), the fundus (above the level of
the oesophageal opening), the body
(central portion), the antrum - also
referred to as the pyloric antrum – (lower
part) and the pylorus (the most distal
part)
ο‚— curvatures – the lesser curvature
(forming the upper concave border) and
the greater curvature (forming the lower
and longer convex border).
ο‚— Sphincters exist at the entry and exit
parts of the stomach. Although there is
no distinct specialization of stomach
muscle fibres at the cardia, several
mechanisms have been implicated in
preventing reflux of stomach contents
into the oesophagus; these mechanisms
will be outlined. At the pyloric end, the
circular muscle coat is thickened to
produce the pyloric sphincter which
controls the flow of stomach contents
into the duodenum.
Functional and applied anatomy
of the stomach
ο‚— The adult stomach can hold 2 to 3
litres of food.
ο‚— The size and position of the stomach
varies, depending upon body shape,
degree of distension and posture.
Physiology of the Stomach
ο‚— Food is ingested faster than it can be
digested. The stomach stores food whilst
subjecting it to preliminary physical and
chemical disruption to form chyme, which
is then delivered at a controlled rate to the
intestines.
ο‚— This is achieved by a complex of
secretion and specialised motility. The
stomach secretes acid and enzymes,
mostly proteolytic. This generates a
luminal environment very hostile to
biological material, so the stomach
mucosa must be protected by further
secretion of mucus and alkali.
Stomach acid
ο‚— The luminal pH is normally below 2.0,
with a concentration of up to
100mmol.l-1 of hydrochloric acid. This
is secreted by the parietal (oxyntic)
cells located in the gastric pits.
ο‚— Most body fluids are slightly alkaline,
so if H+ ions are to be secreted they
must first be created in quantity. This
happens at numerous mitochondria in
parietal cells by, in effect, splitting
water. This inevitably generates OH-,
which then combines with CO2 from
metabolism to form HCO3-, which is
exported to the blood.
ο‚— Very importantly therefore, every mol
of H+ secreted into the stomach
results in 1 mol of HCO3-, entering the
blood, the so-called β€˜alkaline tide’.
This is subsequently re-secreted into
the GI tract by the pancreas and liver
to neutralise the acid as it leaves the
stomach.
ο‚— The H+ ions produced by the
mitochondria are concentrated by
proton pumps in the walls of canaliculi
which invaginate the luminal surface
of parietal cells and carry the
concentrated acid into the stomach
contents through the gastric pits.
ο‚— At the same time the chief cells, also
in the gastric pits secrete enzymes,
principally pepsin, in the form of an
inactive precursor pepsinogen, which
is cleaved by acid in the stomach into
its active form
ο‚— Acid and enzyme secretion is
controlled by a complex of neural and
endocrine systems. Parietal cells are
stimulated by Acetylcholine, Gastrin
and Histamine, which act through
separate receptors to promote acid
secretion.
ο‚— Acetylcholine is released from post
ganglionic, parasympathetic nerves,
stimulated by gastric distension as
food arrives and acts upon muscarinic
receptors.
ο‚— Gastrin is released from endocrine
cells in the stomach. It is a
polypeptide from the Gastrin/CCK
family, produced by G cells. These
are stimulated by amino acids and
peptides in the stomach content, but
inhibited by low pH.
ο‚— Histamine is released from mast cells,
and diffuses locally to parietal cells
where it acts via H2 receptors which
are almost exclusive to the stomach.
Histamine release is stimulated by
both Gastrin and Acetylcholine, so it
amplifies their action.
Phases of gastric secretion
ο‚— There are three phases of gastric
secretion.
ο‚— 1. Cephalic phase
ο‚— 2. Gastric phase
ο‚— 3. Intestinal phase
ο‚— The sight and smell of food, and the
act of swallowing, activates the
parasympathetic system, which
stimulates the release of
Acetylcholine. This is known as the
Cephalic Phase
ο‚— Once food reaches the stomach its initial
effect is to distend the stomach, further
stimulating Acetylcholine release, and to
raise the pH of the stomach contents by
buffering the relatively small amount of
acid present between meals. The rise in
pH disinhibits gastrin secretion. Acid and
enzymes then act on proteins to produce
peptides which further stimulate gastrin
release as the pH falls and that
disinhibition is removed. This is the
gastric phase.
ο‚— Once chyme leaves the stomach in
significant quantities it stimulates the
release of chemicals from the
intestines (Cholecystokinin and
Gastric Inhibitory Polypeptide) which
reduce acid secretion. This is the
Intestinal Phase.
Stomach Defences
ο‚— The surface cells of the stomach
mucosa secrete a thick layer of
alkaline mucus, which offers some
mechanical protection, and traps H+
ions diffusing into it from the stomach
lumen, by reacting with HCO3- ions
also produced from the surface cells.
This prevents the pH of the surface of
the mucosa cells from falling too low.
The production of defences is
stimulated by prostaglandins.
Peptic Ulceration
ο‚— If the defences of the stomach are
damaged or overwhelmed the acids
attacks cells and produces gastritis
then ulceration. Defences are
damaged by infection with H Pylori by
excess alcohol ingestion, and by non-
steroidal anti inflammatory drugs
which inhibit prostaglandin production.
Reducing Acid Secretion
ο‚— Acid secretion may be reduced by
drugs antagonising the action of
histamine at H2 receptors (eg
cimetidine), or by drugs which inhibit
proton pumps.
Gastric Motility
ο‚— When food is swallowed a vagal reflex
produces receptive relaxation, which
causes the resting tension in the walls
of the stomach to reduce. Food is
therefore accommodated without a
rise in intragastric pressure, reducing
the risk of reflux of acid into the
oesophagus.
ο‚— The full stomach begins regular
peristaltic contractions, triggered by a
pacemaker, in the cardiac region about
three times a minute. These sweep over
the stomach from cardia to pylorus,
accelerating as they move. This
combined with the funnel shape of the
stomach both mixes the contents and
decants liquid chyme into the pyloric
region. A small squirt of chyme leaves
the pylorus with each peristaltic wave
before the pylorus shuts.
ο‚— Gastric emptying rate is controlled by
feedback from the duodenum via
chemical signals, so that the rate of
emptying of the stomach is
appropriate for further digestion and
absorption. Fats greatly slow gastric
emptying as they take more time to
digest and absorb.
ο‚— When empty, the gastric muscosa is
thrown into longitudinal folds (called
rugae); a gastric canal forms
temporarily between the gastric folds
along the lesser curvature to allow
saliva and other fluids and small
amounts of masticated food to pass
along to the pyloric part.
ο‚— The gastric mucosa has three
histologically different zones. The cardia
contains mostly mucus- secreting
glands. The fundus and the body
contain gastric glands that consist of
mucus-secreting neck cells, acid-
secreting (parietal or oxyntic) cells, chief
peptic cells (that secrete pepsinogen, a
precursor of the enzyme pepsin) and
other local hormone-producing (APUD)
cells. The pyloric region contains glands
whose cells secrete mucus and hormone
gastrin (produced by G-cells).
ο‚— Gastric ulcers occur commonly in the
antrum and along the lesser curvature
of the stomach. Perforation of ulcers
leads to the spillage of gastric
contents into the peritoneal cavity; the
spillage may affect abdominal
structures such as the pancreas and
associated blood vessels lying in close
proximity to the stomach.
ο‚— Knowledge of the anatomy of the
stomach and its immediate relations is
important in predicting structures at
risk to damage due to spillage of
gastric contents onto them.
ο‚— Reflux of gastric contents into the
oesophagus is a common condition. If
it is frequent and/or clearance of reflux
material is deficient, β€œheartburn”
and/or inflammation with ulceration
may result.
ο‚— Chronic reflux may result in
metaplastic changes in the mucosa
(Barrett’s oesophagus) with an
increased risk of developing
oesophageal carcinoma. Alcohol and
smoking are other factors that may be
involved in oesophageal cancer which
occurs commonly in the lower part of
the tube. The cancer may obstruct the
lumen, leading to dysphagia (painful
and difficulty in swallowing).
ο‚— Inflammation (gastritis) of the stomach
may be acute (caused by aspirin and
non-steroidal anti-inflammatory drugs or
by alcohol) causing exfoliation of the
surface epithelial cells and decreasing
the secretion of protective mucus.
Gastritis may also be chronic (caused by
infection with the bacterium Helicobacter
pylori; inflammatory changes in the
mucosa result in atrophy and epithelial
metaplasia (which may develop into
carcinoma).
THANK YOU

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Functions of the Stomach Explained

  • 1. Function of Stomach Dr. Farhad Shaker
  • 2.
  • 3. ο‚— . The stomach has five recognizable parts and two curvatures; parts – the cardia (around the oesophageal opening), the fundus (above the level of the oesophageal opening), the body (central portion), the antrum - also referred to as the pyloric antrum – (lower part) and the pylorus (the most distal part) ο‚— curvatures – the lesser curvature (forming the upper concave border) and the greater curvature (forming the lower and longer convex border).
  • 4.
  • 5. ο‚— Sphincters exist at the entry and exit parts of the stomach. Although there is no distinct specialization of stomach muscle fibres at the cardia, several mechanisms have been implicated in preventing reflux of stomach contents into the oesophagus; these mechanisms will be outlined. At the pyloric end, the circular muscle coat is thickened to produce the pyloric sphincter which controls the flow of stomach contents into the duodenum.
  • 6.
  • 7. Functional and applied anatomy of the stomach ο‚— The adult stomach can hold 2 to 3 litres of food. ο‚— The size and position of the stomach varies, depending upon body shape, degree of distension and posture.
  • 8. Physiology of the Stomach ο‚— Food is ingested faster than it can be digested. The stomach stores food whilst subjecting it to preliminary physical and chemical disruption to form chyme, which is then delivered at a controlled rate to the intestines.
  • 9.
  • 10. ο‚— This is achieved by a complex of secretion and specialised motility. The stomach secretes acid and enzymes, mostly proteolytic. This generates a luminal environment very hostile to biological material, so the stomach mucosa must be protected by further secretion of mucus and alkali.
  • 11. Stomach acid ο‚— The luminal pH is normally below 2.0, with a concentration of up to 100mmol.l-1 of hydrochloric acid. This is secreted by the parietal (oxyntic) cells located in the gastric pits.
  • 12. ο‚— Most body fluids are slightly alkaline, so if H+ ions are to be secreted they must first be created in quantity. This happens at numerous mitochondria in parietal cells by, in effect, splitting water. This inevitably generates OH-, which then combines with CO2 from metabolism to form HCO3-, which is exported to the blood.
  • 13. ο‚— Very importantly therefore, every mol of H+ secreted into the stomach results in 1 mol of HCO3-, entering the blood, the so-called β€˜alkaline tide’. This is subsequently re-secreted into the GI tract by the pancreas and liver to neutralise the acid as it leaves the stomach.
  • 14.
  • 15. ο‚— The H+ ions produced by the mitochondria are concentrated by proton pumps in the walls of canaliculi which invaginate the luminal surface of parietal cells and carry the concentrated acid into the stomach contents through the gastric pits.
  • 16. ο‚— At the same time the chief cells, also in the gastric pits secrete enzymes, principally pepsin, in the form of an inactive precursor pepsinogen, which is cleaved by acid in the stomach into its active form
  • 17. ο‚— Acid and enzyme secretion is controlled by a complex of neural and endocrine systems. Parietal cells are stimulated by Acetylcholine, Gastrin and Histamine, which act through separate receptors to promote acid secretion.
  • 18. ο‚— Acetylcholine is released from post ganglionic, parasympathetic nerves, stimulated by gastric distension as food arrives and acts upon muscarinic receptors.
  • 19. ο‚— Gastrin is released from endocrine cells in the stomach. It is a polypeptide from the Gastrin/CCK family, produced by G cells. These are stimulated by amino acids and peptides in the stomach content, but inhibited by low pH.
  • 20. ο‚— Histamine is released from mast cells, and diffuses locally to parietal cells where it acts via H2 receptors which are almost exclusive to the stomach. Histamine release is stimulated by both Gastrin and Acetylcholine, so it amplifies their action.
  • 21. Phases of gastric secretion ο‚— There are three phases of gastric secretion. ο‚— 1. Cephalic phase ο‚— 2. Gastric phase ο‚— 3. Intestinal phase
  • 22.
  • 23. ο‚— The sight and smell of food, and the act of swallowing, activates the parasympathetic system, which stimulates the release of Acetylcholine. This is known as the Cephalic Phase
  • 24. ο‚— Once food reaches the stomach its initial effect is to distend the stomach, further stimulating Acetylcholine release, and to raise the pH of the stomach contents by buffering the relatively small amount of acid present between meals. The rise in pH disinhibits gastrin secretion. Acid and enzymes then act on proteins to produce peptides which further stimulate gastrin release as the pH falls and that disinhibition is removed. This is the gastric phase.
  • 25. ο‚— Once chyme leaves the stomach in significant quantities it stimulates the release of chemicals from the intestines (Cholecystokinin and Gastric Inhibitory Polypeptide) which reduce acid secretion. This is the Intestinal Phase.
  • 26. Stomach Defences ο‚— The surface cells of the stomach mucosa secrete a thick layer of alkaline mucus, which offers some mechanical protection, and traps H+ ions diffusing into it from the stomach lumen, by reacting with HCO3- ions also produced from the surface cells. This prevents the pH of the surface of the mucosa cells from falling too low. The production of defences is stimulated by prostaglandins.
  • 27.
  • 28. Peptic Ulceration ο‚— If the defences of the stomach are damaged or overwhelmed the acids attacks cells and produces gastritis then ulceration. Defences are damaged by infection with H Pylori by excess alcohol ingestion, and by non- steroidal anti inflammatory drugs which inhibit prostaglandin production.
  • 29. Reducing Acid Secretion ο‚— Acid secretion may be reduced by drugs antagonising the action of histamine at H2 receptors (eg cimetidine), or by drugs which inhibit proton pumps.
  • 30. Gastric Motility ο‚— When food is swallowed a vagal reflex produces receptive relaxation, which causes the resting tension in the walls of the stomach to reduce. Food is therefore accommodated without a rise in intragastric pressure, reducing the risk of reflux of acid into the oesophagus.
  • 31. ο‚— The full stomach begins regular peristaltic contractions, triggered by a pacemaker, in the cardiac region about three times a minute. These sweep over the stomach from cardia to pylorus, accelerating as they move. This combined with the funnel shape of the stomach both mixes the contents and decants liquid chyme into the pyloric region. A small squirt of chyme leaves the pylorus with each peristaltic wave before the pylorus shuts.
  • 32. ο‚— Gastric emptying rate is controlled by feedback from the duodenum via chemical signals, so that the rate of emptying of the stomach is appropriate for further digestion and absorption. Fats greatly slow gastric emptying as they take more time to digest and absorb.
  • 33. ο‚— When empty, the gastric muscosa is thrown into longitudinal folds (called rugae); a gastric canal forms temporarily between the gastric folds along the lesser curvature to allow saliva and other fluids and small amounts of masticated food to pass along to the pyloric part.
  • 34. ο‚— The gastric mucosa has three histologically different zones. The cardia contains mostly mucus- secreting glands. The fundus and the body contain gastric glands that consist of mucus-secreting neck cells, acid- secreting (parietal or oxyntic) cells, chief peptic cells (that secrete pepsinogen, a precursor of the enzyme pepsin) and other local hormone-producing (APUD) cells. The pyloric region contains glands whose cells secrete mucus and hormone gastrin (produced by G-cells).
  • 35. ο‚— Gastric ulcers occur commonly in the antrum and along the lesser curvature of the stomach. Perforation of ulcers leads to the spillage of gastric contents into the peritoneal cavity; the spillage may affect abdominal structures such as the pancreas and associated blood vessels lying in close proximity to the stomach.
  • 36. ο‚— Knowledge of the anatomy of the stomach and its immediate relations is important in predicting structures at risk to damage due to spillage of gastric contents onto them.
  • 37. ο‚— Reflux of gastric contents into the oesophagus is a common condition. If it is frequent and/or clearance of reflux material is deficient, β€œheartburn” and/or inflammation with ulceration may result.
  • 38. ο‚— Chronic reflux may result in metaplastic changes in the mucosa (Barrett’s oesophagus) with an increased risk of developing oesophageal carcinoma. Alcohol and smoking are other factors that may be involved in oesophageal cancer which occurs commonly in the lower part of the tube. The cancer may obstruct the lumen, leading to dysphagia (painful and difficulty in swallowing).
  • 39. ο‚— Inflammation (gastritis) of the stomach may be acute (caused by aspirin and non-steroidal anti-inflammatory drugs or by alcohol) causing exfoliation of the surface epithelial cells and decreasing the secretion of protective mucus. Gastritis may also be chronic (caused by infection with the bacterium Helicobacter pylori; inflammatory changes in the mucosa result in atrophy and epithelial metaplasia (which may develop into carcinoma).