2. GASTRIC(physiology)
The stomach functions as three distinct units.
The fundus and proximal part act as a reservior with absence of motor activity and a volume capacity of 1-1.5 liters.
The antrum with major motor activity acts as the grinder and separator with wave pattern of 3 per minute.
The pylorus controls the emptying through its sphincter action. Acid bathing, fats with CCK release hypertonic content decrease gastric emptying 4-6 hours after meal the wave pallers changes to frequent 1-5 per minute lasting 10-20 minutes this last phase effectively empties the stomach.
The fundus is the portion of the stomach that secretes acid and intrinsic factor produced by the parietal cells.
The distal portion of the stomach, the antrum, contains G cells that secrete gastrin the endocrine hormone for parietal cell stimulation.
Both the fundus and the antrum contain epithelial cells that line the surface mucosa. The primary products of these cells are mucus and bicarbonate, which provides protection against the secreted acid in the gastric lumen.
CELL FUNCTIONS AND CONTROL
The cardia, antrum and pylorus produce an alkaline viscid mucus,
this secretion is not controlled by the stimulus of food.
CHIEF CELLS
The peptic cells are serous cells and show zymogen granules
containing pepsinogen the precursor of pepsin.
Chief Cell Secretion
The chief cell of the gastric fundus synthesizes pepsinogen. The chief cell can be stimulated by vasoactive intestinal polypeptide (VIP)/ secretin, epinephrine, acetylcholine, and gastrin.
In addition to activation of any of these receptor, acid bathing the lumen also stimulates the release of pepsinogen. Pepinogen, on entering the acidic environment of lumen of the stomach, is converted to the active form of the proteolytic enzyme, pepsin.
THE PARIETAL CELLS
The secretion of these cells closely resembles plasma except that
Na is replaced by H+.
The H+ and chloride ions are actually transported across the
brush border of the parietal cells.
The control of gastric secretions is in three phases
Parietal cell secretion & control;
The secretory surface of the parietal cells is lined with a number of H+, K+-ATPase units.
It is thought that the parietal cell is the only cell in the body that contains this H+, K+-ATPase.
The parietal cell has three main receptors that, when activated, result in stimulation of H+, K+-ATPase units. These receptors are:
1. The Gastrin receptor also referred to as the cholecystokinin B receptor (CCKB).
2. The cholinergic (M3) receptor
3. The histamine2 (H2) receptor
It has been found recently, that a primary effector cell for stimulation of acid secretion is the (entero chromofin / ike) ECL cell, which is placed in close proximity to the parietal cells. It also contains the gastrin/CCKB receptor, as well as the cholinergic muscarin M1 receptor, both of which, when activated, cause the ECL cell to release histamine. Histamine acts as a paracrine agent to activate the H2 receptor on the parietal cell.
The parietal cell can be inhibited by two classes of compounds. The H2 receptor antagonists block the H2 receptor on the parietal cell. These are compounds that are similar in structure to histamine, allowing them to bind to the H2 receptor without activating the cell.
A second group of compounds, the substituted benzimidazoles, are direct inhibitors of H+, K+-ATPase. They are weak bases that enter the lumen, where they are acidified. The acidified form of the substituted benzimidazole then binds irreversibly to a portion of H+, K+-ATPase, thus inhibiting all forms of stimulation of acid secretion.
The parietal cell also synthesizes and releases intrinisic factor which combines with B12 a complex, forming which moves down the gastrointestinal tract where, in the terminal ilium, the components are dissociated and there is active transport of vitamin B12 across the enterovte, into the portal circulation.
Patients who have had a near-total gastrectomy or have has resection of their terminal ilium are likely to require parenteral vitamin B12 administration on a routine basis to replace this function, and to prevent the development of a macrocytic anemia.
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