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Anti-ulcer / Anti-acids - Coggle Diagram
Anti-ulcer / Anti-acids
Gastric Acid Physiology
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Pathway
- Histamine release from ECF binds to H2, increased cAMP
- ACh released from nerves in intestines binds to M3, activates PLC and DAG-IP3 system, increasing Ca2+
- Increased Ca2+ and cAMP activate protein kinases, phosphorylating poton pump
- Proton pump translocated to apical surface
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NSAIDs
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Systemic Effects
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- Increases expression of Intracellular adhesion molecules in gastric vascular endothelium
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H. Pylori
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Pathogenesis
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- Decreases bicarb production
- Secreted immunopathogenic proteins
- Immune cell invasion and inflammation occurs
- Responsible for most gastric/ duodenal ulcers of non-NSAIDs origin
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Treatment
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Quadruple therapy
PPI, tetracycline, metronidazole, bismuth
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Antiulcer Drugs
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Bismuth
Selectively binds to ulcer crater to protect it from acid & pepsin.
Inhibit pepsin & stimulate mucus production
Toxic to H. Pylori
Misoprostol
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Activates E1 Prostaglandin receptor (Gi) to prevent cAMP accumulation, inhibiting parietal cell activation and activating epithelial mucosal production
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