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GI Disorders

Cell Types

Cell TypeNormal functionStimulate byInhibited byEffect – H. pylori PUD (ureaseEffect – NSAID PUD
Parietal cell Secretes H+ (gastric acid) ACh (M3R), Histamine (H2R), Gastrin (CCKR) Prostaglandins, Somatostatin ↑ acid via ↑ gastrin → ↑ ECL histamine ↑ acid (loss of PGE-mediated inhibition)
G cell Secretes gastrin ACh, GRP, peptides/aa Somatostatin ↑ gastrin Generally unchanged
D cell Secretes somatostatin (SST) High [H+] (low pH) Low [H+] (high pH); Ach ↓ SST (disinhibits gastrin and histamine) No primary direct change
Enterochromaffin-like (ECL) cell Secretes histamine ACh (M3) and Gastrin (CCK) Somatostatin ↑ histamine (2/2 hypergastrinemia) No primary direct change
Mucous cell Secretes mucus and HCO3- (barrier protection) ACh, Prostaglandins, Somatostatin Low PGE, SST Barrier compromised by inflammation (functional reduction) ↓ mucus/HCO3- due to ↓ prostaglandins
H+/K+/-ATPase (Proton pump) Final pathway for acid secretion; exchanges H+ for K+ in parietal cells Activated downstream of ACh (M3), Histamine (H2), Gastrin (CCK-B) Prostaglandins, Somatostatin; PPIs directly inhibit pump ↑ activity due to ↑ gastrin → ↑ ECL histamine ↑ activity due to loss of PGE inhibition
H2 receptor (Parietal cell) ↑ cAMP → ↑ H+ secretion Histamine from ECL cells Somatostatin; H2 blockers ↑ activation due to ↑ ECL histamine No primary change
M3 receptor (Parietal cell receptor) Increase intracellular Ca2+ to drive acid secretion Acetylcholine (vagal input) Somatostatin; antimuscarinics Indirect ↑ effect via ↓ SST No primary change
CCK-B receptor (Parietal & ECL receptor) Gastrin → CCK-B → ↑ H+ secretion & ↑ histamine release Gastrin from G cells Somatostatin ↑ activation due to ↑ gastrin No primary change
Acetylcholine Stimulate muscarinic M3 signaling to increase intracellular Ca2+ Cephalic-phase: sight/smell/taste/ingestion Somatostatin (reduces ACh effects on D-cells); antimuscarinics (not primary in this deck) Relative ↑ effect via ↓ SST (D-cell) disinhibition No primary change
CCK-B (gastrin receptor) Stimulate parietal H+ secretion and ECL histamine release Gastrin from G-cells (triggered by peptides/aa; GRP) Somatostatin ↑ activation due to hypergastrinemia No primary change
Peptides/amino acids; GRP (trigger for gastrin) Stimulate G-cells to release gastrin Protein in lumen; vagal GRP Somatostatin Amplifies ↑ gastrin state (disinhibited G-cells) No primary change
cAMP (parietal cell) Second messenger downstream of H2 to activate H+/K+-ATPase Histamine → H2 (Gs) Prostaglandins; H2 antagonists (pharmacologic) ↑ drive via ↑ histamine from ECL Relative ↑ due to loss of PGE brake
Prostaglandins (PGE) Inhibit parietal acid and stimulate mucus/HCO3- production Arachidonic acid via COX NSAIDs (COX inhibition) No primary change (physiology intact) ↓ PGE → ↓ mucus/HCO3, blood flow → gastric acid secretion
Created by: CaristW
 

 



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