Final answer:
Cilostazol and dipyridamole inhibit platelet aggregation through differing mechanisms involving cyclic adenosine monophosphate and extracellular adenosine levels, respectively. They are used for conditions like intermittent claudication and preventing thromboembolic events, but can also have side effects including headaches, gastrointestinal issues, and in some cases, cardiac arrhythmias or thrombocytopenia.
Step-by-step explanation:
Understanding Cilostazol and Dipyridamole:
The mechanisms of action for cilostazol and dipyridamole are both centered on their capacity to inhibit platelet aggregation, though they do so through differing pathways. Cilostazol works by inhibiting phosphodiesterase type 3, leading to an increase in cyclic adenosine monophosphate (cAMP) levels, which results in the inhibition of platelet aggregation and vasodilation. On the other hand, dipyridamole inhibits the uptake of adenosine into platelets, endothelial cells and erythrocytes, leading to increased extracellular adenosine levels and stimulation of adenosine A2 receptors that also induce platelet aggregation inhibition and vasodilation.
Clinical uses of cilostazol include its use in the treatment of intermittent claudication in peripheral arterial disease. Dipyridamole is often prescribed in the prevention of thromboembolic complications associated with cardiac valve replacement and is sometimes used in combination with other antiplatelet drugs. Potential toxicities of cilostazol include headache palpitations and diarrhea. It may also cause cardiac arrhythmias, hypotension or tachycardia. Dipyridamole might lead to side effects such as headache dizziness and gastrointestinal distress, and in rare cases, it can cause thrombocytopenia or hepatic dysfunction.