For medical students

1. Physiology of Digestive
system
Physiology of the stomach
Dr. M.Ashraf
M.Ashraf

2. Learning objectives
By the end of this lecture the students should:
– Know functions of the stomach.
– Describe control of gastric secretions and
motility.
– Describe different phases of gastric secretion.
– Describe control of gastric functions.
– Define vomiting and know its causes.
M.Ashraf

3. General Functions of The stomach
The stomach functions as:
1. A short-term food reservoir, The
presence of rugae that line the stomach
allow for expansion
2. A site of digestion. By secreting acid
and enzymes that help food digestion.
3. Churn the food bolus by its three
layers of smooth muscle: longitudinal,
circular, and oblique.
4. Evacuation of gastric contents slowly
into the small intestine through the
pylorus.
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4. Gastric secretion
Gastric secretion is the
function of the gastric
glands
The gastric rugae in both the body
and the fundus contain microscopic
invaginations, called gastric pits,
that each open into 4 or 5 gastric
glands
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5. Cells and secretions of gastric glands
In the body and fundus:
 Parietal (oxyntic) cells: Secrete
HCl and intrinsic factor (IF).
 Chief (peptic) cells: Secrete
pepsinogen.
In the antrum:
 Mucus-secreting cells: Release both
mucus and bicarbonate.
 G cells: Secrete gastrin.
 D cells: secrete somatostatin.
 Enterochromaffin like cells: secrete
serotonin & histamine.
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6. Serotonine: plays a role in regulation of
gastric secretion and motility.
Somatostatin
secreted by
hypothalamus
δ cells of pancreas
GIT
It inhibits
gastric,
pancreatic
, small
intestinal
secretions
and gall
bladder
contraction
inhibits GH &
TSH secretion by
anterior
pituitary
Inhibits insulin and
glucagon release
Histamine: stimulates HCl secretion by
the parietal cells by acting on 𝑯𝟐
receptors.
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7. Gastric juice
 Clear colourless fluid.
 Its pH is 0.9 – 1.5 (the most acidic fluid in the body)
 Volume: about 2-3 Litres / day.
Organic: as pepsin,
rennin, lysozyme, lipase,
intrinsic factor & mucin.
Inorganic: as Na+, Cl- &
K+, PO4
3-, Ca2+ & HCO3
-.
99%
water
Composition
0.5% HCl
0.5%  solids: organic &
inorganic
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8. Functions of gastric HCl
A. It transforms the inactive pepsinogen into active
pepsin.
B. It provides the optimum pH for the action of
pepsin (PH 1.5-2.0).
C. Has an antibacterial function.
D. Help absorption of calcium (by preventing its
precipitation) and iron (by converting ferric iron
into ferrous).
E. Help milk clotting.
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9. Mechanism of secretion of HCl
Inhibited by carbonic
anhydrase inhibitors as
diamox
Inhibited by proton pump
inhibitors as omeperazole
These reactions can be
inhibited using 𝐻2 blockers
as cimitidine
temporary increase in the pH of the blood after meals is called "post prandial alkaline tide".
because for each molecule of HCl formed, one molecule of NaHCO3 is added to the blood.
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10. M.Ashraf
Parietal cells have 3 receptors that increase HCl secretion
when stimulated
 CCK-B receptors for Gastrin.
 M3 receptors for Ach.
 H2 receptors for Histamine.

11. Digestive enzymes and other organic constituents
1- Pepsin
 Proteolytic enzyme (endopeptidase) secreted in an inactive
form (pepsinogen) then activated by HCl to pepsin.
 Its optimum PH is 1.5 - 2.
 It hydrolyzes the proteins into proteoses, peptones &
polypeptides.
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12. Digestive enzymes and other organic constituents
2- Rennin
 Milk clotting enzyme.
 Not present in human but found in gastric juice of young
animals.
 Its function in human is performed by pepsin and HCl.
 Its optimum PH is 6- 6.5.
Importance of milk clotting:
It prevents rapid evacuation of the milk from the stomach.
This allows sufficient time for gastric digestion & the
antibacterial action of HCl to take effect.
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13. Digestive enzymes and other organic constituents
3- Gastric lipase
 Weak lipolytic enzyme.
 Its optimum PH is 5.
 So, it is of less value in the stomach of adults.
 It hydrolyzes the fat (in infants as the gastric juice is less
acidic) into glycerol & fatty acids.
Explain: gastroenteritis is more common in children than
adults.
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14. Digestive enzymes and other organic constituents
4- Intrinsic factor
 glycoprotien secreted from parietal cells.
 Required for absorption of vitamin 𝑩𝟏𝟐
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5- Lysozyme has antibacterial action
 Excellent lubricant.
 Chemical and mechanical barrier: it Protects the wall
of the stomach from HCl or mechanical irritation.
6- Mucin:

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A - The digestive enzymes are secreted
in an inactive form & activated only
in the lumen of the stomach.
B - The presence of thick layers of
mucous.
F - The presence of protective
prostaglandins which: Decrease HCl
secretion & Increase mucous secretion.
C - Secretion of bicarbonate by
mucosal cells.
D - The presence of tight junctions
between mucosal cells prevents the
penetration of HCl.
E - Rapid regeneration of mucosal
cells.
How the stomach is protected against self digestion?

16. Control (regulation) of gastric secretion
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• It passes in 3 phases:
1
• Cephalic phase
• Nervous phase
2
• Gastric phase
• Hormonal mainly
3
• Intestinal phase
• Hormonal mainly

17. A - Cephalic phase
Nervous or Psychic phase
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Occurs before food reaches the stomach
It takes place through
Conditioned
reflexes
Unconditioned
reflexes
Seeing, smelling, hearing
or even thinking about
food reaches the cortex
then stimulates vagus
nerve to increase the
gastric secretion.
presence of food in the mouth
stimulates gastric secretion
either mechanically by
chewing or chemically by
taste.
20%

18. Cephalic phase
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Seeing, smelling, hearing or thinking
vagus nerve
Presence of food in the mouth
Increase gastric secretion

19. B – Gastric phase
Hormonal phase mainly
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Occurs when food reaches the stomach
Mechanically
by gastric
distension
Chemically by
secretagauges
Nervous mechanism
through vagovagal reflex
& local axon reflex
Hormonal through release of
Gastrin hormone
70%
The main mechanism

20. Nervous mechanism of Gastric phase
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Vagovagal reflex
Distension of stomach
Release of acetyl choline 
Increase gastric secretion
Release of GRP or
bombesin  Increase
gastrin hormone secretion
Explain
gastrin secretion isn’t blocked by
atropine

21. M.Ashraf
Vagus nerve stimulates gastric secretion by 2 mechanisms:
1- Directly: through release of Ach on gastric glands.
2- Indirectly: through stimulation of G-cells to secrete gastrin. The post-ganglionic
fibers of the vagus nerve (enteric nerve endings) that innervate the G cells release GRP
also known as Bombesin. Vagus also increases histamine secretion.

22. Gastrin hormone
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Site of release G cells in pylorus
Stimulus of release
a) Mechanically: Distension of the stomach by bulk of food
b) Chemically: by Secretagogues.
They are chemical substances have the power to stimulate
secretion independent of CNS such as:
Extracts of meat
Vegetable extracts
Partially digested proteins
Alcohol & caffeine

23. Gastrin hormone
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Mechanism of release
Local axon reflex and by
vagovagal reflex(by GRP).
Actions
 Stimulate HCl secretion by direct action on parietal cells and by
activation of Histamine secretion .
 Stimulate gastric motility.
 Stimulate pepsinogen secretion.
 Contraction of lower oesophageal sphincter.
 Stimulate growth of mucosa of stomach, small and large intestine
(trophic action).

24. Then, by enterogastric reflex and intestinal hormones as gastric
secretion and evacuation are inhibited.
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C - Intestinal phase
Mechanical Distension of
the duodenum or by chemical stimulation
secretion of intestinal gastrin and entero-oxyntin
stimulate secretion of small amount
of gastric juice
10%

25. Gastric function tests
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I- The residual or fasting juice:
The volume of residual juice is 50 ml:
- Increased volume indicates pyloric obstruction,
- Increased acid indicates ulcer.
- Presence of blood indicates cancer,
- Presence of starch indicates delayed evacuation.
- Presence of bile indicates regurgitation from duodenum.
II-The fractional test meal:
A test meal is given and a sample of gastric juice is collected every 15 minutes
for 2-3hours. The fasting level of acidity is about 20 unite. After 15 min, the
acidity decreases due to dilution with the meal. Then the acidity rises to a
maximum of 30 units in 6O-90 minute and then decline to the fasting level
after 2.5-3.0 hours: -
-If the acidity increased to 60-120 unite, the condition is called hyperacidity.
-If the acidity is below 20 unite, the condition is called hypoacidity.
-Complete absence of HCl is called anacidity.

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27. Gastric function tests
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III-Histamine test:
Histamine test is used to differentiate between anacidity caused
by absence of the function of parietal cell (true anacidity) or
weak stimulant to parietal cells (false anacidity).
IV. Insulin test:
Insulin is injected (subcutaneously) stimulates gastric secretion
by its hypoglycaemic effect.
This hypoglycaemic effect stimulates the hypothalamus, which
discharge impulses through the vagi to stimulate gastric secretion.
Vagotomy with insulin injection produces no secretion.
insulin test is used to assess of vagotomy operation that use to
cure peptic ulcer.

28. Gastric movements
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The stomach’s main motor functions include
Storing Mixing Emptying
1- Receptive relaxation
it is a Vagovagal reflex that occurs in response to esophageal distention
during taking food, the fundus and body of the stomach relax. Efferent
vagal fibers that relax the gastric wall secrete ATP.
Storage time is: Fats – 6 hours, proteins – 4 hours, sacharides – 2
hours.

29. M.Ashraf
Mixing
Mixing waves, a weak constrictor waves started near the
middle of the stomach. It performs the important functions
of grinding the food, mixing it thoroughly with the
digestive juice.
Peristaltic wave
Anti-peristaltic waves

30. M.Ashraf
If no food is taken, the gastric contractions become stronger and
associated with hunger pain.
If no food is taken, they become extremely strong and fuse together to
cause tetanic contraction lasting for 2-3 minutes
They occur through stimulation of glucoreceptors in hypothalamus by
hypoglycaemia then, hypothalamus responds by increasing gastric
motility and secretion through vagus nerve. So, Atropine inhibits hunger
pain but hunger sensation persists.
Hunger contractions
occurs between meals, when the stomach is empty for a long time.
Rate: 2-4 waves /minute.
The person is unconscious of it.
associated with the sensation of hunger
Tonus contraction

31. M.Ashraf
Evacuation of the stomach
When food liquefaction takes place, Emptying of the
stomach is enabled by an intense contraction, which
pushes chyme through the pyloric sphincter.

32. M.Ashraf
Factors affecting the rate of gastric
evacuation
Within limits, the greater the volume of gastric content, the more
rapid will be the evacuation.
Carbohydrate evacuated firstly in few hours, then proteins then
fats.
Type of food
Gastric factors
Gastric distension
Consistency of food
Fluids are evacuated firstly then solids (when liquefied).

33. M.Ashraf
Factors affecting the rate of gastric
evacuation
Delay gastric emptying through release of duodenal hormones.
This is because fat is digested slower than other types of food.
Duodenal factors
Duodenal distension, acidity or hyperosmolarity
Inhibits gastric evacuation by enterogastric reflex and duodenal
hormones
Presence of fat in duodenum

34. Regulation of gastric emptying
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A - Nervous regulation
By Enterogastric reflex
B – Hormonal regulation
released by jejunum. Stimulated by presence of fat
Many hormones are Released from duodenal mucosa in response to the
same stimuli to enterogastric reflex to inhibit gastric motility and
secretion.
The most important are
GIP
Secretin
CCK
(PZN)
VIP
Somatostatin
Peptide
YY

35. Enterogastric reflex
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6- Response: inhibition of gastric
secretion & motility
1- Stimulus: distension of the
duodenum, presence of HCl,
presence of partially digested
proteins, fats & hypertonic
solutions.
2-receptors: mechanical and
chemical duodenal receptors
5- efferent: vagus nerve
4- center:
vagal
nucleus
3- afferent: vagus
nerve

36. M.Ashraf
Gastrin Inhibitory Polypeptide (GIP)
Site of release: K-cells in duodenum and jujenum
Stimulus of release: hyperosmolarity of glucose and by fat in duodenum
Actions:
Stimulate insulin secretion by the pancreas (main action) so
called Glucose-dependent insulinotropic peptide.
Inhibit gastric evacuation and secretion (in large doses higher
than the normal physiological levels).

37. M.Ashraf
Physiological significance of regulation
of gastric evacuation
1
• Protect the duodenum from overdistension
2
•Allow sufficient time for neutralization of HCl
3
•Allow sufficient time for digestion in duodenum.
4
•Prevent rapid flow of hypertonic solutions into small
intestine preventing electrolyte imbalance

38. M.Ashraf
Vomiting
It is reflex expulsion of gastric content outwards through
the mouth and it often starts with sensation of nausea.
Mechanism of vomiting
Controlled by vomiting center in medulla oblongata.
The glottis remains closed, soft palate elevated to prevent vomitus
from entering airways.
Excessive salivary secretion, sweating & rapid heart rate
accompanied by unpleasant sensation of nausea.
1
Deep inspiration then Closure of the glottis with descend of the
diaphragm downwards, this elevates intrabdominal pressure.
2
The abdominal muscles contract while the body of the stomach and
cardiac sphincter relax  marked elevation of intrabdominal
pressure  squeezing the relaxed stomach leading to ejection of its
contents into the eosophagus.
3
4

39. M.Ashraf
Causes of Vomiting
Reflex vomiting
Mechanical irritation of the posterior
part of the tongue or throat
Central vomiting
Chemical irritation of the stomach or
mechanically by overdistention.
Intestinal obstruction
Intense pain as renal or biliary colic or
myocardial infarction
Rotation or acceleration of the head
such as occurs in motion sickness
Psychogenic vomiting
(conditioned reflex)
Acidosis
Head injuries
Increased intracranial tension
as in brain tumors
Anoxia of vomiting center as
in High altitudes
Drugs & chemical agents:
anaethetics, emetics, cancer
chemotherapy, tartar emetate,
apomorphine.

40. M.Ashraf
Effects of vomiting:
1. Dehydration.
2. Alkalosis  tetany.
3. Loss of electrolytes especially K+.

41. Thank you
M.Ashraf