Gastric Function PDF

GASTRIC SECRETION  Gastric Mucosa * Arranged in folds or rugae covered by simple columnar epithelium. * Opening onto the surface  gastric pits- 100 /cm2 lined by surface mucus cells. * 3 – 7 tubular glands empty into each gastric pit.  Functions of Stomach 1. St...

GASTRIC SECRETION  Gastric Mucosa * Arranged in folds or rugae covered by simple columnar epithelium. * Opening onto the surface  gastric pits- 100 /cm2 lined by surface mucus cells. * 3 – 7 tubular glands empty into each gastric pit.  Functions of Stomach 1. Storage of ingested meal. 2. Regulate rate of emptying into small intestine. 3. Mix contents of stomach. 4. Dissolve meal  chemical action of HCL. 5. Inhibit bacterial growth  by acid. 6. Provide intrinsic factor for vitamin B12 absorption.  Four cell types make up the gastric mucosa: 1. Parietal (Oxyntic) Cells: - HCL secretion. - Intrinsic Factor. 2. Chief (Zymogen) Cells: - Pepsinogen secretion. 3. Mucus Neck Cells: - Mucus secretion. 4. Argentaffin Cells: ? Uncertain function.  Stomach is divided into Three Areas: Cardia Fundic Pyloric Mucus secreting All 4 cell types -Mucus mainly Cells -Gastrin(G-cells) - ↑↑HCL - ↑↑Pepsinogen - ↑↑Intrinsic Factor  Gastric Juice: * Normal secretion  1.5 – 2 L /day. - Exact amount determined by quantity & quality of ingested food. * Isotonic. * Rates: - With a decreased rate  main cation is Na+. - With an increased rate  Na+ replaced by H+. * Ph may drop < Ph 1. * Chief cells →→secrete    Pepsins (I,II,III) secreted as Cholinergic Gastrin Histamine Pepsinogens Impulse (Inactive form) HCL Pepsins * Lipase enzyme  Small amount for fat digestion. (cellular origin is unknown!) * Parietal cells secrete  Intrinsic Factor (macromolec.polyp.) - I.F + Vit. B12 Cobalamine complex→absorbed in ileum Deficiency of I.F Pernicious Anaemia.  CONTROL OF GASTRIC SECRETION Stimulation of Gastric secretion Gastric secretion is controlled through: 1. Neural Stimulation :    Extrinsic Nerves    Intrinsic Nerves 2. Hormonal Stimulation :   G.I.T Hormones * Both mechanisms(1&2) involved in the gastric secretory response to a meal.  NEURAL STIMULATION CEPHALIC PHASE: * Vagal impulses release acetylcholine from nerve endings in the neighbourhood of the acid & pepsin producing cells    Secrete. * Tonic impulses in the vagus nerve →→ Basal or continuous secretion of gastric juice. * Eating   Immediate & profound stimulation. * Impulses in the vagus N Aroused reflexly by the Sight, Odour & Taste of Palatable Food. * ↑↑ increase in acid secretion  Exposure to : appetizing meal or (anticipation) + strong response to a meal of choice. (see fig.) * No response to a meal dutifully eaten. * Psychic Stimulation  Maximal Acid Secretion.  GASTRIC PHASE: 1) Nervous Stimulation after Distension of Fundus: * Distention of oxyntic gland area (by food) :  Copious Acid & Pepsinogen secretion. This response is partially suppressed If oxyntic area is extrinsically denervate (Both Afferent & Efferent are in the vagus nerve.) ↠Another reflex is local through intrinsic plexuses 2) The Pyloro-Oxyntic Reflex: * Acid secretion in response to antral distension. * This is a gastrin independent mechanism. * The stimulus is mediated by a long reflex Vago- Vagal & a short reflex  Local. * This mechanism operates only in patients with Duodenal Ulcer i.e not in normal humans. * Marked Acid response in patients with active D.U Regulation of Gastric Activity  HORMONAL STIMULATION ▪ In 1905, Edkins → Food stuffs released from the pyloric area   a chemical substance which stimulates oxyntic cells. * I.V. injections of extracts of pyloric mucosa result in increased gastric secretion. * Extracts of oxyntic gland area  No response. *  The chemical substance is named GASTRIN  Stimulation of Gastrin Release: * Gastrin  released by the antrum (pyloric) by 3 mechanisms: A- Mechanical B- Chemical Stimulation C- Vagal A- Mechanical: * Mechanical distension of the antrum ↑Gastrin. * Exists in the absence of nervous pathways betw- een the pyloric & the fundic gland. B- Chemical: * Various secretagogues(e.g. meat extracts) ↑Gastrin + some chemical compounds: 1) Small peptides & āā  Most important natural stimulants. 2) Acetylcholine. 3) Adrenaline: thro. β-adrenergic receptors:  Important in causing Stress Ulcer. 4) Elevation of serum ca++. 5) Bile Acids Importance in causing Gastric ulcer in pts. with significant duodeno-gastric reflux. 6) Coffee. 7) Alcohol. C- Vagal: * Gastrin  The only G.I. hormone released by direct neural stimulation.  Inhibition of Gastrin Release: * Gastrin secretion in response to all stimuli is :  inhibited at a pH < 3 in the antrum. - This mechanism  main form of feedback auto- regulation of gastric secretion. HOW? - During interdigestive period → pH of antrum is low & gastrin is inhibited: - On eating  Vagus stimulates Acid secretion:.. Food buffers, neutralizes & dilutes gastric acid: This removes inhibition of Gastrin release i.e. Gastrin is released + Mechanical & chemical stimuli effects: ∴Released Gastrin ↑Acid ↑Gastric Acidity i.e pH < 3   Inhibiting Gastrin Release.  Interaction of Vagal & Gastrin Stimulation: * The Pavlov pouch is more sensitive to gastrin stimulation & responds with a great output of gastric juice than Heidenhain pouch. i.e. Gastric glands become more sensitive when under the influence of the Vagus nerve. i.e. Synergism exists between gastrin & the physio- logical vagal excitation of the acid-secreting glands.  Histamine & Gastric Secretion: * Histamine is widely distributed in the body. * Its actions divided into 2 groups according to type of receptors: a) H1 Receptor : contraction of gut & bronchial smooth muscle  blocked by antihistamines. b) H2 Receptor: e.g. gastric acid secretion blocked by  e.g. Cimitidine (Tagamet). * Histamine blockers on H2 receptor also inhibit the response due to gastrin & vagal stimulation.  Conclusion: * For full response   Interaction of Histamine with Acetylcholine & Gastrin would be needed. * This explains why Vagotomy also decreases the gastric acid response to Histamine.  Vagus Gastrin Producing producing Vagus cell cells Histamine Histamineproducing producing Inhibited cell Cell by Vagotomy inhibited by inhibited by cimitidine secretin Acetylcholine Histamine Gastrin Inhibited by Atropine Synergistic Effect Oxyntic cell HCL Full Response  CONTROL OF GASTRIC SECRETION Inhibition of Gastric secretion * Chyme entering the duodenum  Stimulates the release of 2 G.I. hormones: 1. Secretin 2. Cholecystokinin(CCK) Inhibition by Secretin: * Secretin released into blood when Acid is introd- uced into the duodenum(S-cells)  stimulates pancreatic secretion. * I.V. injection of secretin  blocks completely the stimulation of gastric secretion in the Heidenhain pouch in response to a meal. * The major inhibitory effect of secretin on gastric secretion is exerted on  gastrin-producing cells. i.e Secretin is the nature’s Antiacid  Inhibition by CCK: * CCK is released by āā & fatty acids when they reach duodenum(I-cells). * CCK is chemically similar to Gastrin : Competitive Inhibition of gastric secretion  Inhibition by other Intestinal Polypeptides: 1. Somatostatin. 2. Bulbogastrone. 3. Gastric Inhibitory Polypeptide (GIP). 4. Vasoactive Intestinal Polypeptide (VIP). 5. Glucagon.  Factors Increasing HCL Secretion in D.U. Pts: 1) More parietal cells i.e. ↑capacity to secrete Acid. 2) More secretion of Acid at rest & in response to stimulants like histamine, a meal etc… 3) 2 or 3 times more gastrin activity per gram of antral mucosa than normals. 4) Ulcer pts. release more gastrin than normals. 5) Gastrin release is not suppressed normally by antral acidification.