Salicylates

Aspirin

Mechanism of action
Aspirins main effect is blockade of thromboxane A2 production
from arachidonic acid (Fig. 7-5; see also Fig. 7-4)
in platelets, by irreversibly acetylating the enzyme cyclooxygenase,
the rate-limiting step in thromboxane synthesis.
Remember that aspirin is acetylsalicylic acid and that acetylation
of cyclooxygenase leads to inactivation of this enzyme.
Platelets lack nuclei, so once aspirin inactivates cyclooxygenase,
additional enzyme cannot be resynthesized, which
limits most of the actions of aspirin to platelets. Aspirin also
inhibits production of prostacyclin from endothelial cells, a
prostaglandin that inhibits platelet aggregation (see Fig. 7-4).
However, this endothelium-specific effect is short lived
because endothelial cells, unlike platelets, can resynthesize
cyclooxygenase.
Clinical use
The most common uses of aspirin are preventing and
treating myocardial infarctions and cerebrovascular accidents.
Aspirin may also be used in atrial fibrillation and
transient ischemic attacks. Of course, aspirin is also used
for its analgesic, antipyretic, and antiinflammatory effects
as well.
Adverse effects
Children younger than 12 years may develop Reye syndrome
if given aspirin products. Aspirin is known to induce bronchospasm
and gastrointestinal hemorrhage, thereby limiting its
utility in patients with asthma or peptic ulcer disease