Gastric Secretion

Gastric Secretion
 Describe the three types of gastric exocrine secretory
cells and their secretions.
 Summarize the mechanism of HCl secretion.
 Explain the role of HCl and pepsinogen in digestion.
 Emphasize the protective role of mucus and its
applied importance.
 Describe the multiple regulatory pathways that
control stomach secretion.
 Appreciate
the role of stomach in digestion and
 Gastric Secretion is about 2 liters per day.
There are Gastric Glands present in
stomach. They lie at the base of ‘Gastric Pits’.
 Gastric Glands have exocrine & endocrine
 Two distinct areas of gastric mucosa that
secrete gastric juice:
1- Oxyntic mucosa:
Lines body & fundus.
2- Pyloric gland area (PGA):
Lines antrum.
Exocrine Cells in Gastric Gland
1. Mucus Cells: Secrete thin watery mucus.
2. Chief Cells: Secrete enzyme precursor
pepsinogen. Chief cells are present in oxyntic
mucosa (fundus and body).
3. Parietal [=Oxyntic cells]: Secrete HCL and
intrinsic factor. They are present in fundus and
body. Therefore, pH in stomach lumen is below
Mechanism of HCL Secretion
 Hydrogen [H+] is actively transported in parietal cell
membrane, from cell to the lumen.
 Chloride [Cl-] is secreted by secondary active transport
1- Functions of HCL:
1) Digestion of protein by activation of Pepsinogen
into pepsin & give optimum pH of its effect &
hydrolysis of protein.
2) Sterilization by acidity. It kills microorganisms
ingested with food.
3)  Absorption of iron (by converting ferric into
ferrous) & calcium (by prevention of calcium salts
4) When HCl enters duodenum   secretin
hormone   bile & pancreatic secretion.
2- Secretion of Enzymes:
1- Pepsinogens:
• Secreted by chief cells & Optimum pH = 1 – 3.
• Inactive pepsinogen  active pepsin (by HCl &
auto activation).
• Pepsin initiates protein digestion.
2- Gelatinase: which liquefies gelatin.
3- Gastric lipase: acts on short chain fat. Its
optimum pH = 3.
4- Rennin: milk clotting enzyme (not present in
3- Function of Intrinsic Factor:
 It is secreted by parietal cells.
 It is essential for absorption of vitamin B12 [vitamin B12
is only absorbed when in combination with intrinsic factor].
 Intrinsic factor – vitamin B12 complex have special
receptors in terminal ileum, where vitamin B12 is absorbed.
 Vitamin B12 is essential for Maturation of RBCs &
Myelination of nerves.
 If no intrinsic factor (either in deficiency of intrinsic factor or
gastrectomy), vitamin B12 is not absorbed, it causes
pernicious anemia.
4- Functions of Mucus:
 Surface of gastric mucosa is covered by mucus.
 It is derived from surface epithelial cells and
mucous cells.
 Mucus works as a protective barrier. It protects
stomach wall from self-digestion by pepsin.
 As mucus is alkaline (pH=7), it protects stomach
from HCL [pH=2].
 Lubricating: protection from mechanical injury.
Stomach Is Protected From Acidity
& Pepsin, How?
 Gastric mucosal barrier is protected by:
1) Insoluble thick alkaline mucus (HCO3-).
2) Tight junctions between mucosal cells to prevent
passing HCl in between.
3) Mucosal cells are impermeable to H+ pumped to
the lumen.
4) Entire stomach lining is replaced every 3 days.
5- Gastrin secretion:
 Gastrin is a major GIT hormone.
 It is released from G-cells in pyloric antrum.
 It is secreted in response to protein products in lumen of
stomach and in response to ACh.
 It is the main factor increasing HCL during meal digestion.
 Gastrin is carried by blood to the fundus and body of the
stomach and then stimulates parietal & chief cells,
therefore, causes secretion of HCL and pepsinogen.
 Gastrin stimulates Entero Chromaffin Like Cells
(ECLC) to release histamine and increase HCL secretion.
 It causes growth of mucosa of stomach & small
Endocrine & Paracrine Cells in Gastric Glands
1) G-cells: secrete Gastrin (antrum).
2) ECLC (Entero Chromaffin Like Cells): secrete Histamine
(Fundus and body )
3) D-cells:
 Gastrin, Histamine & Acetylcholine [ACh] stimulate
parietal cells to secrete HCL.
 Somatostatin inhabits HCL secretion.
 ACh & Gastrin increase pepsinogen by acting on chief
N.B. Alcohol & caffein stimulate HCl secretion
Gastric juice is increased
before food reaches
Stimuli: thinking, smelling, tasting, chewing
and swallowing  vagal nerve activity.
 Vagus stimulates intrinsic plexus  increases
 Vagus stimulates G-cells  release of gastrin
which increases HCL and pepsinogen.
2- GASTRIC PHASE (75 %):
• Presence of food in stomach as protein, caffeine,
alcohol & by distension   gastric secretion by:
1- Local nerve plexus.
2- Vagus.
3- Gastrin secretion from G-cells.
N.B. Protein is most potent stimulus. It acts via local
plexus, vagus and stimulates gastrin release.
N.B. People with hyper-acidity or peptic ulcer
should avoid caffeine and alcohol.
3- INTESTINAL PHASE (inhibitory):
•The presence of food in duodenum   gastric secretion.
•This inhibition occurs by nervous & hormonal mechanisms.
•Stimulus: presence of acid, fats or hyperosmotic solution
in duodenum or distention of duodenum.
•Response: inhibition of gastric secretion and motility.
•Center: local or vago – vagal reflex.
•Importance of enterogastric reflex:
•Protection of duodenum from over distention by delay
•Protection of duodenum from hyperacidity (till neutralized
by alkaline duodenal secretion).
•Insure Protein digestion.
•Stimulus: presence of fats and fatty acids in
•Response: release of Cholycystokinin (CCK),
Secretin, Gastric Inhibitory Peptide (GIP) & Vaso
Active Inhibitory Peptide (VIP) from duodenum 
inhibition of gastric secretion and motility for
complete digestion of fat.
How Gastric Secretion Decreases After It
Is Produced?
 It decreases by three ways:
i). As a meal gradually leaves the stomach, major
stimulus that is protein in stomach is withdrawn.
ii). Somatostatin is released when food goes to
duodenum. It has an inhibitory effect.
iii). Stimuli which inhibit gastric motility are fat,
acid, hypertonicity or distension in the duodenum.
 Protein digestion begins in the antrum of stomach,
where food is mixed with HCL and pepsin.
 Carbohydrate digestion which started in mouth due to
action of salivary amylase, continues in the stomach, till
amylase is destroyed by the HCL.
 Stomach absorbs alcohol and aspirin. Alcohol is lipid
soluble, therefore, can diffuse through lipid membrane of
epithelial cells lining stomach. Alcohol is absorbed more
rapidly in small intestine.
Peptic Ulcer
Sites: Ulcer or erosion in the stomach, duodenum or
esophagus can occur due to increased acidity and pepsin.
1- ‘Helicobacter pylori’ bacterium that causes peptic ulcer
by toxins which cause gastritis & weakening gastric mucosal
2- Ethyl alcohol.
3- NSAIDS [Non Steroidal Anti-Inflammatory Drugs] e.g.
Aspirin, Ibuprofen [used for arthritis, pain].
4- Stress: probably by increased gastric secretion.
1) Anta-acids.
2) H2 Histamine receptor Blockers e.g.
Cimetidine & Ranitidine.
3) Proton pump Blockers (it blocks H+ - K+
ATP pump) e.g. Omeprazole.
4) Antibiotics for H.Pylori.
‫تاج األدعية‬
‫(ربنا آتنا في الدنيا حسنة‬
‫وفي اآلخرة حسنة وقنا‬
‫عذاب النار)‪.‬‬

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