What is the mechanism for Nsaid induced peptic ulcer disease?
NSAIDs can cause damage to the gastroduodenal mucosa via several mechanisms, including the topical irritant effect of these drugs on the epithelium, impairment of the barrier properties of the mucosa, suppression of gastric prostaglandin synthesis, reduction of gastric mucosal blood flow and interference with the …
How does H pylori infection contribute to the development of peptic ulcers?
The H. pylori bacteria weakens the protective mucous coating of the stomach and duodenum, thus allowing acid to get through to the sensitive lining beneath. Both the acid and the bacteria irritate the lining and cause a sore, or ulcer.
What is NSAIDs induced ulcer?
By blocking the Cox-1 enzyme and disrupting the production of prostaglandins in the stomach, NSAIDs can cause ulcers and bleeding. Some NSAIDs have less effect on prostaglandins in the stomach than others, and, therefore, may have a lower risk of causing ulcers, but the increased risk of ulcers still exists.
What is the pathophysiology of peptic ulcers?
Peptic ulcer disease is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum.
How do NSAIDs affect the GI tract?
NSAIDs injure the GI tract by causing topical injury to the mucosa and by systemic effects associated with mucosal prostanoid depletion derived from COX inhibition. The main clinically relevant GI side effects include GI bleeding, perforation and obstruction.
Why NSAIDs are contraindicated in peptic ulcer?
Peptic ulcer disease is a well-recognised complication of NSAID use. Inhibition of COX-1 in the gastrointestinal tract leads to a reduction of prostaglandin secretion and its cytoprotective effects in gastric mucosa. This therefore increases the susceptibility to mucosal injury.
What is the main cause of H. pylori?
H. pylori bacteria may be passed from person to person through direct contact with saliva, vomit or fecal matter. H. pylori may also be spread through contaminated food or water.
Why does NSAIDs cause bleeding?
NSAIDs increase bleeding by decreasing the activity of blood platelets and therefore formation of blood clots. When used with other drugs that also increase bleeding, for example, warfarin (Coumadin), the likelihood of bleeding complications is increased.
What are the clinical manifestation of peptic ulcer?
The most common peptic ulcer symptom is burning stomach pain. Stomach acid makes the pain worse, as does having an empty stomach. The pain can often be relieved by eating certain foods that buffer stomach acid or by taking an acid-reducing medication, but then it may come back.
What is pathophysiology of gastritis?
Pathogenesis. The continuous mucosal injury due to long-standing H. pylori infection, leads to atrophy of stomach. This continuous pathological process results in erosion or ulceration of the mucosa leading to the destruction of the glandular layer and followed by fibrous replacement.
How are NSAIDs metabolized?
Most NSAIDs are absorbed completely, have negligible first-pass hepatic metabolism, are tightly bound to serum proteins, and have small volumes of distribution. NSAIDs undergo hepatic transformations variously by CYP2C8, 2C9, 2C19 and/or glucuronidation.
Can NSAIDs cause gastroduodenal mucosal ulcers?
Pathogenesis of NSAID-induced gastroduodenal mucosal injury The use of non-steroidal anti-inflammatory drugs (NSAIDs), even in the era of selective COX-2 inhibitors, remains limited by the ability of these agents to cause gastroduodenal ulceration and bleeding.
What is the pathogenesis of NSAID-induced ulcers and bleeding?
The presence of acid in the lumen of the stomach also contributes to the pathogenesis of NSAID-induced ulcers and bleeding, by impairing the restitution process, interfering with haemostasis and inactivating several growth factors that are important in mucosal defence and repair.
What are the limitations of non-steroidal anti-inflammatory drugs (NSAIDs)?
Gastroduodenal ulceration and bleeding are the major limitations to the use of non-steroidal anti-inflammatory drugs (NSAIDs). The development of safer NSAIDs or of effective therapies for the prevention of the adverse effects of existing NSAIDs requires a better understanding of the pathogenesis of NSAID-induced ulcer disease.
What is the role of NSAIDs in small intestinal injury?
Many NSAIDs also have topical irritant effects on the epithelium which may be particularly important in the production of small intestinal injury.