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This effect is mediated by the irreversible blockage of COX-1 in platelets, since mature platelets don't express COX-2. [ 14 ] This antiplatelet property makes aspirin useful for reducing the incidence of heart attacks; [ 13 ] heart attacks are primarily caused by blood clots, and their reduction with the introduction of small amounts of ...
An antiplatelet drug (antiaggregant), also known as a platelet agglutination inhibitor or platelet aggregation inhibitor, is a member of a class of pharmaceuticals that decrease platelet aggregation [1] and inhibit thrombus formation. They are effective in the arterial circulation where classical Vitamin K antagonist anticoagulants have minimal ...
NSAIDs cause decreased ability to form blood clots, which can increase the risk of bleeding when combined with other drugs that also decrease blood clotting, such as warfarin. [113] NSAIDs may aggravate hypertension (high blood pressure) and thereby antagonize the effect of antihypertensives, [113] such as ACE inhibitors. [114]
Aspirin and other NSAIDs can cause abnormally high blood levels of potassium by inducing a hyporeninemic hypoaldosteronism state via inhibition of prostaglandin synthesis; however, these agents do not typically cause hyperkalemia by themselves in the setting of normal renal function and euvolemic state. [220]
Prostaglandin inhibitors are drugs that inhibit the synthesis of prostaglandin in human body. [1] There are various types of prostaglandins responsible for different physiological reactions such as maintaining the blood flow in stomach and kidney, regulating the contraction of involuntary muscles and blood vessels, and act as a mediator of inflammation and pain.
In whole, the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the inflammation and resulting pain. [citation needed] Some common examples of NSAIDs are aspirin, ibuprofen, and naproxen. The newer specific COX-inhibitors are not classified together with the traditional NSAIDs, even though they presumably ...
Different antithrombotics affect different blood clotting processes: Antiplatelet drugs limit the migration or aggregation of platelets. Anticoagulants limit the ability of the blood to clot. Thrombolytic drugs act to dissolve clots after they have formed.
Platelets are small blood components that form a plug in the blood vessel wall that stops bleeding. Platelets also produce a variety of substances that stimulate the production of a blood clot. One of the most common causes of increased bleeding risk is exposure to nonsteroidal anti-inflammatory drugs (NSAIDs). The prototype for these drugs is ...