‫المرحلة الثانية‬
‫كلية الطب‬
) GIT) physiology
‫المحاضرة الرابعة‬
Stimulation of HCL secretion:
1- Acetylcholine: Stimulation of gastric mucosa by distension. tactile stimulation or
chemical stimulation include amino acid can cause two types of reflexes.
˲a- Long reflex: stomach mucosa…… through vagus nerve ….to brain stem…back to enteric
nervous system of stomach wall and then to 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), the primary function of which is to secrete histamine.
ECL cells lie in the deep of the oxyntic glands and therefore release histamine in direct
contact with the parietal cells of the glands.stimulated by gastrin.
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- Gastrine: It is released from G cell through stimulation of vagus nerve in the antrum of
stomach. Gastrine is carried by circulation to stimulate parietal cell for release HCL.
Inhibition of HCL :Somatostatin: secret by Delta cells (or D cells), inhibits HCL secretion by parietal cell directly
and indirectly by inhibits gastrine secretion by G cell.
Phases of gastric HCL secretion:divided into three; phases cephalic, gastric and intestinal.
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.
stimulation of the parietal cell by vagus nerves, which release Ach (direct). And stimulation
of the parietal cells by gastrin (indirect), 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 the stomach causes direct stimulation of the parietal cells by vagus nerve and indirect
stimulation of the parietal cells via gastrin release .presence of breakdown products of
protein, amino acid and small peptides gastrin releasing peptide(GRP)to stimulate gastrin
release. Alcohol and caffeine also stimulate gastric HCL secretion
GRP
))
3- Intestinal phase: It 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 mucous. 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 mucous 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.
Gastric digestion and absorption:
*Carbohydrate digestion in the stomach depend on the action of salivary amylase, which
remains active until by low pH in the stomach.
*Protein digestion occur in the stomach by about 10% and mediated by HCL and gastric
pepsin.
*Fat digestion is minimal in the stomach due to restriction of gastric lipase activity.
Very little absorption of nutrients take place in stomach. The stomach is a poor absorptive
area of the gastrointestinal tract because:1)( it lacks the typical villus type of absorptive membrane)
2) the tight junctions between the epithelial cells.
Only a few highly lipid-soluble substances, such as alcohol and some drugs like aspirin, As
well as( non-ionized triglycerides of acetic ,propionic and butyric acid can be absorbed in
small quantities).
Aspirin at gastric pH is non-ionized and fat soluble, after absorption, it ionizes intracellular
which damaging mucosal cells. Ethanol is rapidly absorbed by a process of simple passive
diffusion along concentration gradients. water moves in both direction across mucous,
Water-soluble substances including Na+ , K-,glucose and amino acid are very poorly
absorbed.
Vomiting (emesis):
The sensory signals that initiate vomiting originate mainly from the pharynx, esophagus,
stomach, and upper portions of the small intestines.
It is reflex coordinated by multiple distributed nuclei in the brain stem called the “vomiting
center". Or by“Chemoreceptor Trigger Zone” in the Medulla for Initiation
of Vomiting by Drugs or by Motion Sickness.
Causes of vomiting
increased pressure within skull, rotating movement of head, intense pain, tactile stimuli
applied to back of the throat and excessive distention or irritation of the duodenum.
provides strong stimulus for vomiting when the vomiting center is directly activated.
Define
It is a forceful expulsion of contents of stomach and upper intestinal tract through mouth.
In the early stages antiperistalsis begins to occur often many minutes before vomiting
appears. (Antiperistalsis means peristalsis up the digestive tract rather than down ward),
antiperistaltic wave travels backward up the intestine at a rate of 2 to 3 cm/sec; this
process can actually push a large share of the lower small intestine contents all the way
back to the duodenum and stomach within 3 to 5 minutes.
Vomiting is preceded by increase salivation, sweating, increased HR, pallor and feeling of
nausea. Vomiting begin deep inspiration, closure of glottis, elevation of soft palate,
abdominal and thoracic muscles contract. Upper small intestine contract lower esophageal
sphincter relax. Event occur repeatedly without vomiting is known retching
Importance of vomiting with nausea:when the vomiting center is directly activated, it causes projectile vomiting not
accompanied by nausea while stimulation of chemoreceptor trigger-zone is accompanied
by nausea, to remove the ingested toxic substances before they can be absorbed. Nausea
importance to avoid ingestion of food containing the same toxic substances.