Header Ads Widget

Pharmacology MCQs|| Which medication inhibit cyclooxygenase?

 

Pharmacology MCQs|| Which medication inhibit cyclooxygenase?

Which medication inhibit cyclooxygenase

a)    Indomethacin
b)   Aspirin
c)    Diclofenac

    d)   All 

Answer:

All 

Cyclooxygenase

Cyclooxygenase (COX) is a group of enzymes that catalyzes the conversion of arachidonic acid to prostaglandin H2 (PGH2). This process results in the formation of prostaglandins and thromboxane, which are important mediators in the body's inflammatory response.

There are two main families of cyclooxygenase (COX): COX-1 (prostaglandin synthase) and COX-2 (prostaglandin H synthase). COX-2 is thought to be involved in immune responses and may also play a role in angiogenesis or blood vessel growth.

Prostaglandins are produced from arachidonic acid by various enzymes called cyclooxygenases (COX). These enzymes include three different isoforms—

cyclooxygenase 1 (COX-1),

2 (COX-2), and

3 (COX-3) —

and several variants. The function of these proteins is to convert arachidonic acid into prostanoids known as prostaglandins. Prostanoids can act as hormones or neurotransmitters, but they also have many other functions including regulating cell growth, differentiation, and apoptosis.

Cyclooxygenase, or COX, is an enzyme that plays a critical role in the body's inflammatory response. COX is responsible for the synthesis of prostaglandins, which are lipid compounds that act as mediators of inflammation and pain. In this article, we will discuss the structure, function, and inhibition of cyclooxygenase.

I. Structure of Cyclooxygenase

Cyclooxygenase is a homodimeric protein composed of two identical subunits. Each subunit has three distinct domains: an N-terminal domain, a C-terminal domain, and a catalytic domain. The catalytic domain contains the active site of the enzyme, which is responsible for the conversion of arachidonic acid into prostaglandins.

II. Function of Cyclooxygenase

Cyclooxygenase plays a critical role in the body's inflammatory response. When tissues are damaged, arachidonic acid is released from the cell membrane and converted by COX into prostaglandins. Prostaglandins are important mediators of inflammation, causing vasodilation, increased permeability of blood vessels, and recruitment of immune cells to the site of injury. Prostaglandins also cause pain by sensitizing nerve endings.

There are two isoforms of cyclooxygenase: COX-1 and COX-2. COX-1 is constitutively expressed in most tissues and is responsible for the production of prostaglandins that maintain normal physiological functions, such as protection of the gastric mucosa and regulation of blood flow to the kidneys. COX-2 is induced in response to inflammation and is responsible for the production of prostaglandins that promote inflammation, pain, and fever.

III. Inhibition of Cyclooxygenase

The inhibition of cyclooxygenase is the basis for the anti-inflammatory and analgesic effects of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen. NSAIDs inhibit both COX-1 and COX-2, leading to decreased production of prostaglandins and reduced inflammation and pain.

Selective COX-2 inhibitors, such as celecoxib, were developed to reduce the risk of gastrointestinal side effects associated with NSAIDs. However, these drugs have been associated with an increased risk of cardiovascular events and have been the subject of controversy.

IV. Conclusion

Cyclooxygenase is an enzyme that plays a critical role in the body's inflammatory response. It is responsible for the synthesis of prostaglandins, which are important mediators of inflammation, pain, and fever. The inhibition of cyclooxygenase is the basis for the anti-inflammatory and analgesic effects of NSAIDs, but can also lead to unwanted side effects. The development of selective COX-2 inhibitors was an attempt to reduce the risk of gastrointestinal side effects, but these drugs have been associated with an increased risk of cardiovascular events.

For More MCQs:

What is an ocular anti-inflammatory drug

Post a Comment

0 Comments