NSAIDs MCQs

Drugs acting as inhibitors COX NSAID Aspirin: Inhibits COX-1 and COX-2. Indomethacin and ibuprofen-inhibit cyclooxyge- nases by competing with arachidonate. Coxibs: Selectively inhibit COX-2 Some coxibs have been withdrawn or suspended from the market due to undesirable side effects and safety issues. Reference: Harper's 32 nd edition, page 241

Aspirin, even in small doses, irreversibly inhibits TXA2 synthesis by platelets. Thus, it interferes with platelet aggregation and bleeding time is prolonged to nearly twice the normal value. Long-term intake of large doses decreases synthesis of clotting factors in the liver and predisposes to bleeding. This can be prevented by prophylactic vit K therapy. Aspirin particles coming in contact with gastric mucosa promotes local back diffusion of acid. This causes focal necrosis of mucosal cells and capillaries→acute ulcers, erosive gastritis, congestion and microscopic haemorrhages. The occult blood loss in stools is increased by even a single tablet of aspirin.

Ductus arteriosus closure During foetal circulation ductus arteriosus is kept patent by local elaboration of PGE2 by COX-2. Unknown mechanisms switch off this synthesis at birth and the ductus closes. When this fails to occur, small doses of indomethacin or aspirin bring about closure in the majority of cases within a few hours by inhibiting PG production. Administration of NSAIDs in late pregnancy has been found to promote premature closure of ductus in some cases. Risk of postpartum haemorrhage is increased. Prescribing of NSAIDs near term should be avoided

Celecoxib is a COX-2-selective inhibitor. Although the COX-2 inhibitors have the advantage over nonselective NSAIDs of reduced gastrointestinal toxicity, clinical data suggest that they are more likely to cause arterial thrombotic events. A history of myocardial infarction would be a compelling reason to avoid a COX-2 inhibitor. Reference: Basic & Clinical Pharmacology, Fourteenth Edition By Bertram G. Katzung Pg no. 650

Salicylate intoxication is associated with metabolic acidosis, dehydration, and hyperthermia. If these problems are not corrected, coma and death ensue. Reference: Basic & Clinical Pharmacology, Fourteenth Edition By Bertram G. Katzung Pg no. 647

Morphine helps in pulmonary oedema by reducing the preload by redistributing the blood and therefore reducing the pulmonary capillary pressure. Indomethacin like many other NSAIDS inhibit the synthesis of prostaglandins and relieve symptom of headache. Aspirin is a non competitive inhibitor of COX and causes gastric ulcers, does not relieve dyspepsia. Opioids produce a general increase in resting tone of the gut wall and sphincters. These effects arise from stimulation of both µ- and κ-receptors on neuronal plexuses in the gut wall. An increase in biliary pressure caused by opioid-induced spasm at the sphincter of Oddi can exacerbate biliary colic. Hence, Pethidine can be used in the treatment of biliary colic.

Ketorolac exerts typical NSAID effects. It prolongs the bleeding time and can impair renal function, especially in a patient with preexisting renal disease. Its primary use is as a parenteral agent for pain management, especially for treatment of postoperative patients. Reference: Basic & Clinical Pharmacology, Fourteenth Edition By Bertram G. Katzung Pg no. 648

Paracetamol (acetaminophen) Actions: The central analgesic action of paracetamol is like aspirin, i.e. it raises pain threshold, but has weak peripheral anti-inflammatory components. Analgesic action of aspirin and paracetamol is additive. Paracetamol is a good and promptly acting antipyretic. Paracetamol has negligible anti-inflammatory action. In contrast to aspirin and other NSAIDs, paracetamol does not stimulate respiration or affect acid-base balance; it does not increase cellular metabolism. It has no effect on CVS. Gastric irritation is insignificant-mucosal erosion and bleeding occur rarely only in overdose. It does not affect platelet function or clotting factors and is not uricosuric.