Test: Autacoids - 4 - NEET PG MCQ

PGE₂ analogues are employed to preserve the patency of the ductus arteriosus, while aspirin or indomethacin are utilised for managing PDA. PGE₂ acts as a bronchodilator and can be administered to treat bronchial asthma through inhalation. Other indications for this agent include cervical priming and NSAID-induced PUD.

• Platelets do not possess a nucleus, which means they cannot regenerate COX.
• In contrast, the endothelium is capable of producing new enzyme.

Prothrombin time is prolonged by medications that disrupt the coagulation pathway (for instance, warfarin). Since COX does not play a part in coagulation, inhibitors of prostaglandin synthesis do not extend PT. However, bleeding time (BT) is lengthened by drugs that affect platelet function.

• Aspirin raises BT by functioning as an antiplatelet agent.

Aspirin and various salicylates exhibit saturation kinetics (zero order), leading to a non-constant half-life.

• At elevated doses (anti-inflammatory), the clearance is lower compared to reduced doses (analgesic).
• Consequently, the half-life (t_1/2) is longer for the anti-inflammatory dosage than for the analgesic dosage.

• Taking aspirin beforehand can reduce this side effect.
• Aspirin has the potential to lead to hyperthermia in cases of overdose.
• It also lowers the risk of developing colon cancer.

Sedation resulting from indomethacin may affect driving abilities.

Selective COX-2 inhibitors tend to be less prone to causing gastrointestinal issues such as peptic ulcer disease (PUD). However, since COX-2 is also naturally occurring in the kidneys, the risk of renal complications remains comparable. The effectiveness of these medications is generally similar to or less than that of non-selective COX inhibitors.

Aspirin functions by inhibiting the synthesis of thromboxane through the blockade of cyclooxygenase (COX). This mechanism provides a clearer understanding of its role in antiplatelet activity.

Aspirin inhibits the COX enzyme, leading to the rerouting of the AA pathway towards the synthesis of LTs. As LTs are potent broncho-constrictors, they may cause shortness of breath in prone patients.

Aspirin-acetylated COX then begins to produce lipoxins (referred to as aspirin-triggered lipoxins), which also possess broncho-constrictor characteristics.

Aspirin may elevate the likelihood of Reye’s syndrome when administered to children suffering from viral illnesses.

This patient presents with salicylate poisoning. Gastric lavage is performed to eliminate any unabsorbed poison.

• Metabolic acidosis needs to be addressed using sodium bicarbonate.
• Alkalinising the urine will enhance the excretion of this weakly acidic medication.
• Treatment with acetylcysteine is not applicable in cases of salicylate poisoning; it is the preferred antidote for paracetamol poisoning.

Prostaglandins (such as alprostadil) are employed to maintain the patency of the ductus arteriosus, while aspirin or indomethacin are utilised for the treatment (closure) of a patent ductus arteriosus (PDA).