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Lecture

PHGY210- Lecture 30- Dr. Wechsler.docx

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Department
Physiology
Course
PHGY 210
Professor
Ann Wechsler
Semester
Winter

Description
Lecture 29- Friday, March 19 , 2010h Ulcers 1. Normal HCl output  Weak barrier (agents responsible: Aspirin and NSAIDs, Heliobacter pylori) 2. Normal Barrier  Excessive HCl output (eg: Gastrin producing factors) Phases of Gastric Secretion:  Cephalic psychic, gustatory  Gastric  Intestinal Cephalic Phase (Vagally-mediated) -All regulatory cells are secreting. Accompanied by vasodilation. Distension leads to short intramural reflexes. Also results in afferent fibres going up and efferent fibres as well. Called vagal-vagal reflex. GASTRIN is released in response to: a) SECRETAGOGUES (products of protein digestion) (Antrum Lumen) b) Local enteric reflexes c) Vagally-mediated reflexes Physiological Role of Gastrin a) HCl secretion b) Trophic effect Histamine Lots of Histamine in gastric mucosa. Histamine administration elicits large volume of gastric juice with lots of HCl. PERMISSIVE HYPOTHESIS (Paracrine Fashion)– Histamine is constantly released and presented to the Parietal Cells as a tonic background, sensitizing them to other stimuli. Blocking this tonic background by H2-antagonists, inhibits acid secretion in response to ACh and Gastrin. (H+/K+ ATPase, eg: Nexium) H2 blockers are widely used to decrease HCl secretion (eg: Pepsid). Intestinal Phase Intestinal Phase – Inhibitory Optimal secretory activity is the result of an interplay between neural and hormonal mechanisms. Gastri
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