How do NSAIDs affect respiratory system?
Within 20 minutes to 3 hours of ingestion of a NSAID, aspirin-sensitive asthmatics can develop: respiratory symptoms such as acute bronchospasm, rhinorrhoea, conjunctival irritation and/or cutaneous flushing of the head and neck, and even circulatory collapse and respiratory arrest. urticaria/angiodema or.
How do NSAIDs cause ulcers mechanism?
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 do NSAIDs affect gastric acid secretion?
Several studies have shown that NSAIDs can potentiate secretagogue-stimulated acid secretion in vivo and in vitro (17,18, 26). This effect is attributable to inhibition of PG synthesis, since PGs inhibit acid secretion by reducing adenylate cyclase activity in the parietal cell (28).
How do NSAIDs treat stomach ulcers?
Treatment of NSAID-induced ulcers involves discontinuing the NSAID, reducing stomach acid with H2-blockers, for example, cimetidine (Tagamet), famotidine (Pepcid), and nizatidine (Axid), or, more effectively, with proton pump inhibitors, such as omeprazole (Prilosec) or synthetic prostaglandins, specifically …
How do NSAIDs cause bronchoconstriction?
NSAID-induced reactions appear to be caused by the inhibition of cyclooxygenase-1 (Cox-1); this in turn activates the lipoxygenase pathway, which eventually increases the release of cysteinyl leukotrienes (Cys-LTs) that induces bronchospasm and nasal obstruction.
Why NSAIDs are contraindicated in asthma?
Paradoxically, NSAIDs, including aspirin, possibly cause asthma exacerbations, particularly in patients allergic to these drugs. Aspirin/NSAIDs inhibit cyclooxygenase (COX) and reduce prostaglandin synthesis, thereby reducing fever and relieving pain and inflammation.
How do NSAIDs inhibit COX enzymes?
The classic non-aspirin NSAIDs block both COX-1 and COX-2 isozymes to varying degrees, by binding an arginine molecule at position 120 halfway up their channel, thereby inhibiting access of arachidonic acid to the catalytic site and thus ultimately inhibiting the synthesis of prostaglandins, PGI2, and thromboxanes [22.
What is the mechanism of action of nonsteroidal antiinflammatory drugs NSAIDs quizlet?
Nonsteroidal anti-inflammatory drugs (NSAIDs) produce their therapeutic activities through inhibition of cyclooxygenase (COX), the enzyme that makes prostaglandins (PGs). They share, to a greater or lesser degree, the same side effects, including gastric and renal toxicity.
Can NSAIDs cause shortness of breath?
Patients taking NSAIDs should seek medical attention immediately if they experience symptoms such as chest pain, shortness of breath or trouble breathing, weakness in one part or side of their body, or slurred speech.
Do NSAIDs inhibit prostaglandins?
Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for their anti-inflammatory, analgesic, and antipyretic effects. NSAIDs generally work by blocking the production of prostaglandins (PGs) through the inhibition of two cyclooxygenase enzymes.
What is the pathophysiology of NSAID-induced ulcers?
Cellular and molecular pathogenesis of NSAID-induced ulcers: NSAIDs cause ulcers by both topical and systemic effects, and the latter may be prostaglandin-dependent (through COX-1 and COX-2 inhibition), or prostaglandin-independent (e.g. through inhibition of NO, H 2 S and polyamines).
What is the role of aspirin in the pathogenesis of NSAID-induced gastric damage?
Since PGs play a critical role in maintaining gastric mucosal defense system, the inhibition of COX leading to decreased mucosal PGs is considered as the most important in the pathogenesis of NSAID-induced gastric damage. Aspirin inhibits COX irreversibly, while other NSAIDs inhibit COX in a reversible, concentration-dependent manner.
How do NSAIDs cause damage to the gastroduodenal mucosa?
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 repair of superficial injury.
What is the mechanism of action of NSAIDs?
NSAIDs induce, probably through up-regulation of proapoptotic proteins and/or down regulation of antiapoptotic proteins of the Bcl-2 family, the translocation of proapoptotic Bax protein toward mitochondria, which further induces and opens MPTP.