Explain why aspirin is effective at preventing heart attacks...

Explain WHY aspirin is effective at preventing heart attacks: Group of answer choices Endothelial cells are able to produce more COX-2, which leads to more PGI2 production COX-1 and COX-2 work with synthetases to break down different molecules in the presence of aspirin Aspirin can only cross the membrane of platelet cells, but not capillary endothelial cells Platelet cells are not affected by aspirin as much because they contain TAX2 enzymes

Transcript

0:00 Hello everyone.

00:01 In this lesson, we'll explore how aspirin, a commonly used non -steroidal anti -inflammatory drug, nsaid, affects the synthesis of prostaglandins, thromboxanes, and leukotrionis.

00:15 So let's get started.

00:21 Aspirin inhibits cyclo -oxygenous enzymes.

00:42 So that's cox1 and cox2.

00:51 Primarily by irreversibly inhibiting the enzyme cooxygenous, there are two main isoforms of this enzyme, cox1, which is expressed constituently in most tissues, and clx2, which is induced during inflammation.

01:10 So by acetylating serine residue in the active site of these enzymes, aspirin prevents them from converting rachidonic acid to prostaglandin h2, which is pgh2, an immediate precursor to various prostaglandins and thromboxanes.

01:37 Reduction in prostaglandin and thromboxane production.

02:01 The inhibition of cox enzymes leads to a decrease in the production of prostate glandins and thromboxins.

02:08 Prostal glandins such as pge2 and pgd2 are involved in mediating inflammation and pain responses, as well as regulating body temperature and gastric mucosa protection.

02:21 Thromboxins, particularly thrombocin a2, play a critical role in platelet aggregation and vasco -constriction.

02:30 As a result, aspirin's action produces inflammation, pain, fever, and the likelihood of blood clots forming.

02:43 Aspirin's effect on leucotrian pathway...

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