Most specific drug used for NSAID induced peptic ulcer

Gastric mucosal damage:- Gastric pain, mucosal erosion/ulceration and blood loss are produced by all NSAIDs to varying extents. Mech of peptic ulcer formation:- Inhibition of COX-1 mediated synthesis of gastroprotective PGs (PGE2, PGI2) is clearly involved. Deficiency of PGs reduces mucus and HCO3- secrection, tends to enhance acid secretion and may promote mucosal ischaemia. Thus, NSAIDs enhance aggressive factors and contain defensive factors in gastric mucosa--are ulcerogenic. Paracetamol, a very weak inhibitor of COX is practically free of gastric toxicity and selective COX-2 inhibitors are relatively safer. Treatment:- PGE2 analogue (misoprostol) administered concurrently with NSAIDs counteract their gastric toxicity. DOC for NSAID induced peptic ulcer is PPI. Ref:- kd tripathi;pg num:-194