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GI Disorders

Activators & Inhibitors

TypeChemicalReleased by / TriggerPrimary gastric effectsPrimary target(s)
Activator Acetylcholine (ACh) sight, smell, taste, ingestion of food ↑ Histamine ECL cells
Activator Acetylcholine (ACh) sight, smell, taste, ingestion of food ↑ H+ release Parietal cells
Activator Acetylcholine (ACh) sight, smell, taste, ingestion of food ↓ Somatostatin D-cells
Activator Gastrin Dietary peptides; GRP receptor stimulation ↑ Histamine ECL cells
Activator Gastrin Dietary peptides; GRP receptor stimulation ↑ H+ release Parietal cells
Activator Histamine ACh or Gastrin ↑ H+ release Parietal cells
Inhibitor Prostaglandins (PGEs) fatty acids (e.g., arachidonic acid) ↓ H+ release Parietal cells
Inhibitor Prostaglandins (PGEs) fatty acids (e.g., arachidonic acid) ↑ mucus production Mucous cells
Inhibitor Somatostatin Luminal acid ↓ H+ release Parietal cells
Inhibitor Somatostatin Luminal acid ↓ gastrin G-cells
Inhibitor Somatostatin Luminal acid ↓ Histamine ECL cells
Inhibitor Somatostatin Luminal acid ↓ pepsin Chief cells
Inhibitor Somatostatin Luminal acid ↑ mucus secretion Mucous neck
Pathophysiology H. pylori urease Infection of gastric mucosa ↓ D-cell SST; ↑ Gastrin (hypergastrinemia) D cells (inhibition), G cells (disinhibition)
Pathophysiology Gastrin cascade D-cell suppression ↑ ECL histamine → ↑ Parietal H+ ECL → Parietal
Pathophysiology NSAIDs → COX inhibition NSAID therapy ↓ Prostaglandins → ↓ mucus/HCO3-; loss of parietal inhibition Mucous cells; Parietal cells
Drug H2 antagonists Drug administration Block H2 → ↓ cAMP → ↓ H+ (works early in pathway) Parietal H2
Drug PPIs Prodrug activation in parietal cell Irreversibly inhibit H+/K+-ATPase → ↓↓ H+ (works later in pathway) Parietal proton pump
Drug PCAB Drug administration Reversibly competes with K+ at H+/K+-ATPase → ↓ H+ Parietal proton pump (K+ site)
Drug Antacids Drug administration Neutralize luminal H+ → ↑ pH Luminal H+ (non-cellular)
Drug Bismuth Drug administration Coat mucosa; protect ulcers; H. pylori inhibition Mucosal surface / bacterial factors
Drug Sucralfate Drug administration Coat mucosa; protect ulcers Mucosal surface / bacterial factors
Neural node Chemoreceptor Trigger Zone (CTZ) – D2, 5HT3, CB1 Circulating emetogens/toxins Initiates emetic signaling (central) Vomiting center
Neural node Vomiting Center – H1, M1, NK1, 5HT3 Inputs from CTZ, vestibular, GI Coordinates motor pattern of emesis Brainstem nuclei / GI efferents
Neural node Vestibular system – H1, M1 Motion/inner ear stimuli Activates emesis (motion sickness) Vomiting center
Neural node GI tract afferents – 5HT3, D2, M1, H1, CB1/2 GI irritation, chemotherapy Serotonin from enterochromaffin cells stimulates vagal afferents CTZ / Vomiting center
Created by: CaristW
 

 



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