A 25-year-old woman develops a sore, red, hot, swollen left knee. She has no history of trauma and no familial history of joint disease. Fluid aspirated from the joint space shows an abundance of segmented neutrophils. Aspirin is effective in relieving symptoms of acute inflammation in the patient because it inhibits which of the following enzymes?
**Core Concept**
Aspirin's mechanism of action in relieving symptoms of acute inflammation involves the inhibition of an enzyme that plays a crucial role in the production of pro-inflammatory mediators. This enzyme is involved in the metabolism of arachidonic acid, a key player in the inflammatory response.
**Why the Correct Answer is Right**
Aspirin exerts its anti-inflammatory effects by irreversibly inhibiting the enzyme cyclooxygenase (COX), specifically COX-1 and COX-2 isoforms. This inhibition leads to a decrease in the production of prostaglandins, which are pro-inflammatory mediators that contribute to the symptoms of acute inflammation. The reduction in prostaglandin production results in decreased pain, swelling, and fever. COX enzymes catalyze the conversion of arachidonic acid to prostaglandin H2, which is then further metabolized to other prostaglandins that mediate inflammation.
**Why Each Wrong Option is Incorrect**
**Option A:** This option is incorrect because aspirin does not inhibit the enzyme phospholipase A2, which is involved in the release of arachidonic acid from membrane phospholipids. While aspirin does affect arachidonic acid metabolism, it does so by inhibiting COX enzymes, not phospholipase A2.
**Option B:** This option is incorrect because aspirin does not inhibit the enzyme lipoxygenase, which is involved in the production of leukotrienes from arachidonic acid. Leukotrienes are also pro-inflammatory mediators, but aspirin's mechanism of action does not involve the inhibition of lipoxygenase.
**Option C:** This option is incorrect because aspirin does not inhibit the enzyme thromboxane synthase, which is involved in the production of thromboxane A2 from prostaglandin H2. While thromboxane A2 is a pro-thrombotic and vasoconstrictive mediator, aspirin's anti-inflammatory effects are primarily due to the inhibition of COX enzymes.
**Option D:** This option is incorrect because aspirin does not inhibit the enzyme prostaglandin E synthase, which is involved in the production of prostaglandin E2 from prostaglandin H2. Prostaglandin E2 is a pro-inflammatory mediator, but aspirin's mechanism of action does not involve the inhibition of prostaglandin E synthase.
**Clinical Pearl / High-Yield Fact**
Aspirin's mechanism of action is unique in that it irreversibly inhibits COX enzymes, leading to a long-lasting decrease in prostaglandin production. This property makes aspirin a useful medication for the treatment of acute inflammation, but it also increases the risk of gastrointestinal side effects due to the inhibition of COX-1 in the stomach lining.
**Correct Answer:** C. cyclooxygenase (COX)