University:
Western Sydney University
Course:
MEDI 2003 | Clinical Sciences 2
Academic year:

2024
Views:

345

Pages:

2
Author:

Mariam A. A.

NSAIDs The components of gastric & duodenal mucosal barrier against being digested by acid's pepsin. HCO3- neutralization Mucosal PG stimulates = mucid by HCO3 secretion, mucosal BF & hydrophobic phospholipid synthesis Tight junctions between cells Biochemistry of prostaglandins & their physiological & pathological roles in gastric protection maintaining inflammation Prostaglandins are made from middle part of arachidonic acid Prostaglandins = basic prostanoic molecule Arachidonic acid = refer to tablet mechanism PGE2, PGI2 Inflammation → neutrophils → cytokines → PGEs ↑ temp & cAMP Pyrogens → cytokines → ↑ sensitivity of receptors to pain stimuli PGI2 & PGE2 = hyperalgesic Pharmacological actions of prostaglandins - GI Tract Vascular → PGI2, PGE2 → relaxation Bronchial → PGI2, PGE2 → contraction Uterine → PGE2, PGF2α → contraction GIT → PGE2, PGF2α → contraction Pharmacological actions of prostaglandins - Kidney PGI2, PGE2 → ↑ Renal BF TXA2 → ↓ Renal BF, ↑ K+, ↑ aldosterone Thrombosis PGI2 = anti-thrombotic TXA2 = pro-thrombotic COX-1 is anti-thrombotic COX-2 is pro-thrombotic Mode of action of NSAIDs & ulcerogenic effects The different functions of COX-1 & COX-2 & how these are pharmacologically modified Refer to tablet mechanisms COX-1 Bin most cells Constitutive COX-2 Inducible