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"Gastropathy refers to the damage of the epithelial cells of the gastric mucosa and disturbance of epithelial cell regeneration unaccompanied by inflammation. Gastropathy occurs due to irritation by chemical agents (such as non-steroidal anti inflammatory drugs - NSAIDs and alcohol), bile reflux, hypovolemic conditions, and chronic obstruction.NSAIDs in general are chemical agents that cause irritation of the upper gastrointestinal tract through direct and indirect topical effects and by inhibiting prostaglandin synthesis through inhibition of COX-1 and COX-2. There are many data that demonstrates that the anti-inflammatory function of NSAIDs is mainly through inhibition of COX-2, while many of their side effects are due to inhibition of COX-1.In general, there is a correlation between the influence of NSAID and the administered dose. The higher the dose, the higher the risk for upper gastrointestinal tract disorder. NSAID users who frequently switch drugs have a risk twice higher than those only receiving one kind of NSAID. Those who use NSAID with corticosteroids have 15 times the risk. Use ofNSAID simultaneously with anticoagulants increases the risk of bleeding from ulcer 13 times compared to control subjects. NSAID use in a patient with history of bleeding from the gastrointestinal tract is 17.2 times non-users. Smoking also increases the percentage of gastroduodenal ulcer due to NSAID.Clinical symptoms ofNSAID gastropathy are often only dyspepsia syndrome. There is no correlation between symptoms and endoscopic findings.The first step in the therapy ofNSAID gastropathy is termination ofNSAID administration. To treat and prevent risks of gastropathy due to NSAID, mucosal protection agents may be used. Out of the various kinds of medicine available, proton-pump inhibitors turn out to be more effective compared to H2 receptor antagonists or cytoprotectiveagents."

"Non-steroidal anti-inflammatory drugs (NSAIDs) is a group of drugs used to treat pain, inflammation, and fever. High consumption of NSAIDs associated with high gastrointestinal side effects. Common complaint from patients, which ranging from mild heartburn to the onset of gastrointestinal bleeding, often complicates the adequate administration of NSAIDs. Various methods have been developed to reduce the likelihood of gastroenteropathy complication. Early diagnosis, appropriate prompt treatment, as well as adequate monitoring will reduce morbidity and mortality from complications due to NSAIDs. This paper will discuss the diagnosis and management of gastro-enteropathy NSAID through approaching the underlying pathophysiology."

"Non-steroid anti-inflammatory drugs (NSAID) can cause gastropathy and gastric mucosa, especially the mucous may play an important prevention role. This cross-sectional, single group study was conducted to evaluated the difference of mucous thickness in antrum or corpus mucosa and the correlation of gastric mucous thickness to gastropathy. Patients who received NSAID from the rheumatology clinic were studied. Healthy subjects of 14 - 65 years old who never received NSAID were included as normal controls. Piroxicam 20 mg daily was given to the patients for 7 days, then gastroscopy and gastric mucosa biopsy with frozen section were performed. Specimens were stained with haematoxyline eosin and thickness of the mucous layer was measured using ocular micrometer. Thirty-two out of 70 patients participated in the study. All cases had hyperemia on gastroscopy with erosions and ulcer in 32 and 9 cases, respectively. The mean thickness of mucosa in distal antrum, proximal antrum and corpus was 28.5 ± 9, 37.4 ± 13.1 and 43.3 ± 13.1 microns, respectively. There was significant relationship between gastric mucosa mucous thickness with gastroscopic findings. In conclusion, this study confirmed that thickness of gastric mucosa mucous has an important role in preventing NSAID gastropathy and dyspeptic complaints in this kind of patients does not suggest abnormalities of gastric mucosa."

"Intracoronary thrombosis plays an important role in the pathogenesis of acute coronary syndrome. It occurs due to a rupture of an atherosclerotic plaque, which may be spontaneous, as in the case of acute coronary syndrome, or due to procedures such as percutaneous intervention (PCI). Atherosclerotic plaque rupture causes exposure of thrombogenic subendothelial components and initiates platelet aggregation, which then initiates the coagulation cascade. In stable angina, the formation of platelet thrombus is the most important tiling to occur on plaque progressiveness as a result of rupture and episodic formation of thrombi.' Arterial thrombi contain many platelets. Anti-platelet agents are greatly beneficial in acute and chronic coronary heart disease. This paper discusses the use of anti-platelet agents in coronary heart disease."