EICOSANOIDS Flashcards
some patients report severe allergic reactions to aspirin consisting of angioedema and difficulty breathing, is this likely to be a true allergic reaction? what mechanism appears to be responsible for most of these reactions? what other drugs should these patients avoid? what questions should you ask the patient?
Aspirin is an inhibitor of prostaglandin production leading to an increase in the production of leukotrienes for compensation that can cause an adverse reaction. The limiting factor in the production of prostaglandins is the availability of arachidonic acid, once the stimulus for the production of AA is released, leukotrienes are also produced as a result of AA metabolism.
All COX inhibitors (NSAIDS) are likely to cause the same reaction –> ask patient if they had any previous reaction to NSAIDs.
Ask if patient had classic triad of aspirin sensitivity (nasal polyps, and asthma).
NSAID reactions are more likely to be fatal in patients with asthma.
how would you treat someone who is allergic to NSAIDS who also has severe arthritis?
most patients tolerate COX2 selective NSAIDS such as celecoxib. Patients can also be desensitized to aspirin by starting them at a small dose and slowly increasing dose, patient must continue to take the aspirin otherwise they will lose desensitization. Salicylate and acetaminophen are usually tolerated, but not first line therapy and usually less effective. Leukotriene inhibitor (montelukast) can prevent symptoms.
provide 3 mechanisms by which analgesics such as aspirin could cause complications during childbirth?
prostaglandins induce uterine contractions, thus aspirin being an inhibitor of prostaglandin production can inhibit labor; prostaglandins also induce platelet aggregation, thus aspirin can inhibit platelet aggregation and increase risk of bleeding and hemorrhage during childbirth; prostaglandins are required to keep the ductus arteriosis open in the fetus, thus aspirin can cause premature closing of the DA.
why is it bad to take NSAIDS for pain at the same time as aspirin for reduction of CV events?
aspirin works by acetylating a serine group on cyclooxygenase enzyme, leading to irreversible inactivation of the enzyme, thus decreasing platelet aggregation.
NSAIDS interact reversibly with COX and block access of aspirin to this serine; thus it blocks the anti platelet effects of aspirin. Other NSAIDS increase risk of CV events because they inhibit the production of prostacyclin and prostaglandins required to decrease risk of CV events.
how does a COX2 specific NSAID increase risk of MI and stroke? What is the data with celecoxib and other NSAIDS?
what other conditions may respond to leukotriene antagonists?
LK inhibitors such as montelukast are tried for asthma, however results came back negative. They have some effect in allergic rhinitis and exercise induced bronchospasm.
