Question

Q2. What is the mechanism of action to account for the anti-platelet effect of low-dose aspirin?

Option 1: Inhibition of cyclooxygenase (COX) enzyme.

Option 2: Blockade of adenosine receptors.

Option 3: Activation of platelet aggregation.

Option 4: Suppression of fibrinolysis.

Answer 1

The anti-platelet effect of low-dose aspirin is due to inhibition of the
`COX` enzyme, preventing thromboxane
`A2` synthesis and decreasing platelet aggregation.

Step-by-step explanation:

The mechanism of action to account for the anti-platelet effect of low-dose aspirin is the inhibition of cyclooxygenase enzyme. Aspirin, or acetylsalicylic acid, inactivates the cyclooxygenases
`(COX-1 and COX-2)` by acetylating a serine residue within the enzyme, which prevents the synthesis of prostaglandins and thromboxanes.

This reaction effectively blocks the formation of thromboxane
`A2 (TXA2)`by the platelets, a potent agent that promotes platelet aggregation. By reducing the production of
`TXA2` , aspirin decreases platelet aggregation and thereby exhibits its anticoagulant effect, which is critical in preventing cardiovascular events like heart attacks and strokes.