) GIT) physiology
‫المحاضرة الرابعة‬
‫المرحلة الثانية‬
‫كلية الطب‬
Cell types of gastric mucosa:
The gastric mucosa contains several cells types that secrete gastric juice figure(6)
Intrinsic factor
Hcl
Parietal cells
Pepsinogen
mucous
Chief cells
G cell
Mucous cells
Gastrin to (circulation)
Figure (6)secretary products 0f gastric cells
The lumen of stomach is lined by epithelial cells, deeper are:
1- Mucous cells:-lines the entire surface of the stomach, which responsible for mucus
secretion.
2- oxyntic glands or(gastric glands):-secrete hydrochloric acid, pepsinogen, intrinsic factor,
and mucus. located inside surfaces of the body and fundus of the stomach,its about 80 % of
the stomach mucosa.
3- pyloric glands.
The pyloric glands contain two cell types, the G cells and mucous cells. The G cells secrete
gastrin into circulation. The pyloric glands are located in the antral portion ,its about 20 of
the stomach mucosa.
*oxyntic glands:- is composed of three types of cells:
(1) mucous neck cells, which secrete mainly mucus.
(2) peptic(or chief) cells, which secrete large quantities of pepsinogen.
(3) parietal (or oxyntic) cells, which secrete HCL and intrinsic factor. HCL which acidifies
the gastric contents to pH l-2 to convert inactive pepsinogen ,to pepsin form. Figure (7)
Figure (7)types of cells in the gastric mucosa
Function of HCL:
1-HCL participates in break down of protein.
2- It provides an optimal pH for convert an active pepsinogen to active pepsin.
3- It hinders the growth of pathogenic bacteria.
Mechanism of HCI secretion:
HCL is secreted by the following steps:
1- CL- ions is transported by active transport into the canaliculus. The flow of CL- create a
negative potential inside the canaliculi, causing K+ to flow passively into the canaliculus.
2- H+ ion is then exchanged for K+ ion by H+-K+ ATPase pump. The source of H+ ion is from
the dissociation of carbonic acid (H2C03) into H+ + HCO3- (CO2+ H2O = H2C03). H+ react
with CL_ to form HCL, HC03- diffuse back to plasma. After meal sufficient H+ ions may be
secreted.
3- Water enter canaliculus down the osmotic gradient created by movement of the HCL
into the canaliculus. Figure (8)
HCL secreted
Figure (8) gastric parietal cell
Substances affecting HCL secretion:
A- Stimulation of HCL secretion:
1- Acetylcholine: Stimulation of gastric mucous by distension, tactile stimulation and
chemical stimulation include amino acid. This stimulation can cause two types of reflexes.
a- Long reflex: stomach mucosa
vagus nerve
system of stomach wall and then to
brain stem
enteric nervous
parietal cell.
b- Short reflex: originates locally and transmitted entirely through local enteric nervous
system. The receptor is muscarinic type and mediated is acetylcholine. so parietal cell
stimulated directly by Ach for release HCL.
2- Histamine: the parietal cells operate in close association with another type of cell called
enterochromaffin-like cells (ECL cells) stimulated by gastrin, the primary function of which
is to secrete histamine. The ECL cells lie in the deep of the oxyntic glands and therefore
release histamine in direct contact with the parietal cells of the glands. The rate of
formation and secretion of hydrochloric acid by the parietal cells is directly related to the
amount of histamine secreted by the ECL cells..
The most commonly used anti ulcer drug cimetidine which is histamine antagonists that
block H2 receptor on parietal cell.
3- Gastrin: It is released from G cell through stimulation of vagus nerve in distal stomach.
Gastrin is carried by circulation to stimulate parietal cell for release HCL.
B-Inhibition of HCL :
Somatostatin inhibits HCL secretion by parietal cell and gastrin secretion by G cell.
Somatostatin is released from interneurons within the enteric nervous system.
gastric HCL secretion:is divided into three phases; cephalic, gastric and intestinal. The cephalic and gastric phases
are illustrated in Figure (8).
1- Cephalic phase: 30% of total HCL secreted in response to meal. The stimuli for HCL
secretion in this phase are smelling, tasting, chewing, swallowing and conditioned reflexes.
Two mechanisms promote HCL secretion in this phase.
First is direct stimulation of the parietal cell by vagus nerves, which release Ach. Second is
indirect stimulation of the parietal cells by gastrin. Indirect path vagus nerve release, at G
cells stimulating gastrin secretion, gastrin enters the circulation and stimulate the parietal
cells.
2- Gastric phase: 60% of total HCL secreted in response to meal. The stimuli are
distension of stomach and presence of breakdown products of protein; amino acid and
small peptides. Four physiological mechanism are involved. First two mechanisms which are
initiated by distension of the stomach. Distension causes direct vagus stimulation of the
parietal cells and indirect stimulation of the parietal cells via gastrin release. The third
mechanism is initiated by distension of the stomach antrum and local reflex which
stimulate gastrin release. Fourth mechanism direct effect of amino acid and small peptides
like GRP(gastric releasing polypeptides) to stimulate gastrin release. Alcohol and caffeine
also stimulate gastric HCL secretion .
GRP
))
Figure (8) Cephalic and gastric
3- Intestinal phase: Itphase
is only 10% of HCI secretion. It is mediated by products of protein
digestion.
Peptic ulcer and gastric barrier:
A peptic ulcer is an excoriated area of stomach or intestinal mucosa caused principally by
the digestive action of gastric juice or upper small intestinal secretion.
peptic ulceration is an imbalance between the rate of secretion of gastric juice and the
degree of protection by mucous which secrete along GIT and the alkalinity Secretion of the
small intestinal(bicarbonate secretion)
it caused by:
1- Breakdown of the barrier in which (the Stomach is lined with highly resistant mucous
cells that secrete a viscid and alkaline adherent mucus. And the adjacent epithelial cells has
tight junction between the gastric barrier prevent the stomach from auto digestion and
irritation by gastric secretion or by infection with a bacterium ( Helico bacteria pylori ),
disrupts this barrier, as do aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs),
which inhibit the production of prostaglandins and consequently decrease mucus and HCO3
–secretion. The NSAIDs are widely used to combat pain and treat arthritis.
2- Prolonged excess secretion of acid:two feedback control mechanisms that neutralization of gastric juices:
A- When excess acid enters the duodenum, it reflexly inhibits gastric secretion and
peristalsis in the stomach, both by nervous reflexes and by hormonal feedback from the
duodenum, thereby decreasing the rate of gastric emptying.
B- The presence of acid in the small intestine liberates secretin from the intestinal mucosa,
which then passes by way of the blood to the pancreas to promote rapid secretion of
pancreatic juice. This juice also contains a high concentration of sodium bicarbonate, for
neutralization of the acid .
Gastric and duodenal ulcers can be given a chance to heal by inhibition of acid secretion
with drugs that block the H2 histamine receptors on parietal cells or drugs that inhibit H+–
K+ ATPase. Bacteria can be eradicated with antibiotics, and NSAID-induced ulcers can be
treated by stopping the NSAID.
peptic ulcers most frequently occur, In a few centimeters of the pylorus ,and along the
lesser curvature of the antral end of the stomach or, more rarely, in the lower end of
the esophagus where stomach juices frequently reflux.