Sun28November0628PM 30

The non-steroidal anti-inflammatory analgesics (NSAIDs) are relatively contraindicated in asthmatic patients.

Which of the following products of membrane phospholipid metabolism is most likely to lead to NSAID-induced bronchospasm in predisposed asthmatic patients?

(Please select 1 option)

PGE2

Arachidonic acid

Leukotrienes Correct

Thromboxanes (TXA2)

Prostacycline (PGI2)

Explanation

In some asthma patients, non-steroidal anti-inflammatory drugs (NSAIDs) induce bronchospasm, rhinorrhoea, and nasal obstruction.

NSAID-induced reactions appear to be caused by the inhibition of cyclooxygenase-1 (Cox-1); this in turn activates the lipoxygenase pathway, which eventually increases the release of cysteinyl leukotrienes (Cys-LTs) that induces bronchospasm and nasal obstruction.

With regard to the metabolism of arachidonic acid (AA) in NSAID-intolerant asthmatic patients, the following changes have been observed:

A low production of prostaglandin E2, seemingly due to deficient Cox-2 regulation

An increased expression of leukotriene-C4 synthase and

A reduced production of metabolites (lipoxins) released through the transcellular metabolism of AA.

Arachidonic acid is derived from membrane phospholipids formed by the action of phospholipase A.

TXA2 induces platelet aggregation and adhesion and also causes vasoconstriction.

PGI2 causes vasodilatation and decreases platelet adhesiveness.

PGE2 participates in the initiation and maintenance of parturition and has a role in thermoregulation.

Answer Statistics

1

18%

2

9%

3

57%

4

4%

5

13%

Times answered: 248