7. Stomach (Histology)
Gastric gland cells
• Mucous neck cells – produce mucus.
• Parietal cells – produce hydrochloric acid and intrinsic
factor.
• Chief cells – produce pepsinogen.
• Endocrine cells –produce regulatory hormones.
8. Gastric Secretions
Chyme – food and stomach secretions mixed
SECRETION SOURCE FUNCTION
Mucus Mucus cells Lubricates, protects
Intrinsic
factor
Parietal cells Binds with and makes more readily
absorbed in the ilium VITAMIN
B12
Hydrochloric
acid
Parietal cells Low pH bactericidal, denature
proteins, provides proper pH for
pepsin.
Pepsinogen Chief cells Converts to pepsin, catalyzes the
cleavage of peptide bonds in
proteins.
9.
Parietal (Oxyntic) cells: present in the body
of stomach. Secrete HCl & Intrinsic factor
[combines with Vit-B12 & reabsorbed in
distal ileum]
Chief (Zymogen/peptic) cells: present in the
body& fundus of stomach. Secretes
Pepsinogen, converted to pepsin by acid.
Pepsin begins the digestion of protein.
Mucus cells: secretes mucus, HCO3.
Stimulated by prostaglandins. Protects the
stomach.
GASTRIC SECRETIONS..
10. Contents of Normal Gastric Juice
(Fasting State).
Cations: Na+, K+, Mg2+, H+ (pH
approximately 1.0)
Anions: Cl–, HPO4
2–, SO4
2–
Pepsins
Lipase
Mucus
Intrinsic factor
20. Gastric juice secretion is,
*Accurately synchronized with the need for it.
*Secretion persists since, food is about to
enter the stomach and continues till food is
present in the stomach.
Digestive phase x Inter-Digestive phase.
Secretion is regulated by,
Neurocrine /endocrine/ paracrine methods.
21. Agents that stimulate parietal cells.
1.Acetylcholine.
Post ganglionic parasympathetic fibres (vagus)
Acetylcholine
Parietal cells G cells(gastrin) ECL cells
(HCL) (histamine)
Atropine-blocker.
22.
23. 2.Gastrin : G cells in Antral mucosa
Expt : gastric antral removal -- gastrin secretion.
Vagal stimulation – Ach - gastrin
Inhibited by – somatostatin
Gastrin + Ach – more powerful ( potentiation)
(A+B+C) > (A)+(B)+(C)
26. Agents that inhibit parietal cells
1.Acid
Secreted acid--inhibits release of gastrin from G cells
Negative feedback mechanism
(prevents damage of gastric mucosa)
Acidic chyme –enters duodenum-gastric secretion is further inhibited.
(intramural neural reflex operating via pH sensitive duodenal
receptors).
27. 2.Somatostatin
D cells – inhibits {G cells + ECL cells}
Stimulus-gastric acidity
Negative feedback mechanism
Others involved- gastrin, CCK-PZ, secretin and
vasoactive intestinal peptide{VIP},prostaglandins
Stimulus-entry of acid & food into the duodenum.
3.Food
*Carbohydrates, lipids & high osmolar contents of the chyme entering
the duodenum.
GIP & CCK-PZ Inhibits gastric juice secretion
30. Digestive phase regulation can be explained in terms of 3 arbitrary
phases,
1.Cephalic phase;
Sight/Smell or even thought of food—stomach starts secreting the
gastric juice.
Stimulus 1.Unconditioned reflex : food in mouth
2.Conditoned reflex : smell/ sight/ thought or awareness
of food in the mouth.
(psychic or appetite juice)
30% of total gastric juice secretion secreted.
31. Experimental evidence:
1.Sham feeding : Animal feels that it is eating whereas nothing
really reaches its stomach.
Oesophageal fistula
Mediated by : Vagus nerve
Proof: Vagotomised animal does not show any secretion.
Vagus – Ach + GRP released on G cell – gastrin secretion- gastric
juice secretion.
35. 2.Gastric phase:
Food is in the stomach
*Secretion rate is increased.
*60% of the gastric juice secretion during the
digestive phase of stomach happens in this phase.
Stimuli:
1.distension of the stomach
2.chemicals released due to distension
3.chemicals present in the food.
36. Expt: Infusing saline directly into the stomach.
Proof: 20-50% of the peak acid output(PAO).
Via Vagus nerve
afferent convey the information to CNS
Vagus
efferent Motor nucleus of vagus
gastric secretion
Expt :Role of vagus nerve
Sectioning of one of the two vagi leaving the other intact +
stimulation of the central end of vagus - gastric secretion
37. Stretching of the gastric mucosa by the presence of food in
stomach leads to secretion of acid and enzyme.
1.Long vagovagal reflex action –Ach secretion by vagus.
2.Local reflexes in the intrinsic neural plexus.
stretch of mucosa causes activation of Meissner’s plexus which
stimulates secretions.
local reflex
Stretch
vagovagal reflex.
38. 2.Chemical stimuli
Expt : 1) Watery meal infusion
60-70% of peak acid output
2) equivalent amount of saline
Most important stimuli,
a) Proteins b) partially digested proteins and aminoacids.
Humoural mechanism
Gastrin + Acetylcholine + Histamine
39. a) Gastrin
G cells in the antrum
stimuli – a) distension of the gastric mucosa by
food in the stomach.
b) chemicals released on digestion,
1) peptones + aminoacids
Released gastrin increases gastric juice secretion
By some hypothetical pathways.
1) incr.HCL + pepsin secretion
2) Incr. Histamine secretion from ECL cells.
40. b) Acetylcholine
stimuli: distension of gastric mucosa
Ach release from vagus—acts via M1 receptors –can be blocked by
atropine.
Ach – release of Histamine from ECL cells.
c) Histamine
ECL (mast cells) in gastric mucosa.
distension of gastric mucosa.
Ach & gastrin stimulates its secretion
acts via H2 receptors – Cimetidine and Ranitidine.
41. Intestinal Phase
Presence of food in intestine-mechanical & chemical stimuli.
Mechanism is unclear-how it regulates gastric secretion.
presence of chyme in duodenum- Enterooxyntin
contribution is very minimal
Actually this phase has a major role in inhibition of gastric juice
secretion.
a) Acid / fat and hyper osmolar substances enters duodenum.
42. Duodenum and jejunum secretes,
a) secretin, b) bulbogastrone, c)CCK PZ, d)GIP
Inhibits gastrin release –gastric juice secretion.
b) Enterogastric reflex.
food distends duodenum- local plexus is activated-inhibits through
sympathetic fibres-secretion & motility of the stomach is inhibited.
Stimuli : Fat
Cerebral cortex, hypothalamus and limbic system influences gastric
secretion.
43. INTER DIGESTIVE Phase.(Resting Phase)
No food in stomach – minimal secretion of Gastric juice
Represents basal gastric secretion.