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What are antiplatelet drugs?
Antiplatelet drugs aWhat are antiplatelet drugs?re medications that prevent blood clots from forming. They work by stopping your platelets from sticking together. Antiplatelet drugs are used to avoid blood clots, which can cause heart attacks and strokes
Who should use antiplatelet drugs?
Blood clots are an important and natural way your body protects itself. But blood clots in your bloodstream can cause heart attack and stroke. This is more common in people with certain medical conditions, such as:
Angina.
Atrial fibrillation.
Coronary artery disease.
History of heart attack or warning signs of a possible heart attack in the future.
History of stroke or warning signs of a possible stroke in the future.
Peripheral vascular disease .
Types:
The most commonly used antiplatelet is aspirin, but other kinds include:
*Adenosine diphosphate (ADP) receptor inhibitors (clopidogrel, ticagrelor, ticlopidine, prasugrel) make platelets less sticky.
*Adenosine reuptake inhibitors (dipyridamole) block enzymes involved in clotting.
*Glycoprotein platelet inhibitors (abciximab, eptifibatide, tirofiban) block substances that help clots stick together.
*Phosphodiesterase inhibitors (cilostazol) widen blood vessels and stop platelets from sticking together.
Administration:
Antiplatelet agent administration can be via oral, rectal, or intravenous routes. Oral medications include aspirin, clopidogrel, ticagrelor, cilostazol, and dipyridamole. Intravenous drugs include GpII-IIIA inhibitors and can be used for a short period, most commonly during acute coronary syndromes before or during PCI. Aspirin is available as a rectal suppository if the patient cannot take the drug orally.
Mechanism of Action :
Antiplatelets can be classified based on the mechanism of action as follows:
Platelet aggregation inhibitors such as
Aspirin and related cyclooxygenase inhibitors
Oral thienopyridines such as clopidogrel, ticagrelor, ticlopidine, and prasugrel
Glycoprotein platelet inhibitors (e.g., abciximab, eptifibatide, tirofiban)
Protease-activated receptor-1 antagonists (e.g., vorapaxar)
Miscellaneous (e.g., dipyridamole - a nucleoside transport inhibitor and phosphodiesterase type 3 (PDE3) inhibitor, cilostazol - also a PDE3 inhibitor)
Aspirin is the most commonly used oral antiplatelet drug. It works by irreversibly inhibiting the cyclooxygenase enzyme (COX) activity in the prostaglandin synthesis pathway (PGH2). This prostaglandin is a precursor of thromboxane A2 (TXA2) and PGI2. Thromboxane A2 works by inducing platelet aggregation and vasoconstriction, and COX-1 mediates its production, while PGI2 works by inhibiting platelet aggregation and induces vasodilation, and is mediated by COX-2. Low-dose aspirin (75 mg to 150 mg) can induce complete or near-complete inhibition of COX-1, thus inhibiting the production of TXA2, while larger doses are required to inhibit COX-2.
Contraindications:
The most common contraindications for using antiplatelet agents are as follows:
.Large esophageal varices
.Recent stroke within two years
.History of intracranial
hemorrhage
.Significant thrombocytopenia
.Major surgery with 72 hours
.Hypersensitivity to the medication
.Acute clinically significant bleed
End-stage renal disease on hemodialysis
.Decompensated liver cirrhosis
.Severe hypertension with a BP over 200/110 mmHg
.Congestive heart failure is a contraindication for the use of cilostazol
common side effects of antiplatelet therapy include:
Aspirin-induced asthma.
Shortness of breath.
Bleeding longer or heavier with cuts or menstrual periods.
Bruises.
Hemorrhage.
Nose bleeds (epistaxis).
Upset stomach.
Some side effects can be signs of serious problems. If you have any of the following symptoms, contact your healthcare provider:
Blood in your urine (pee), which may look red, pink or brown.
Blood in your stool (poop), which may look red or black.
Chest pain.
Coughing up or vomiting blood, which may look like blood or coffee grounds.
Hematoma (a large, raised bruise).
Ringing in your ears (tinnitus).
Stomach pain.
Toxicity:
Aspirin is the most commonly used of all antiplatelet drugs, so accidental intake is common. The effect can be life-threatening if taken over 150 mg/kg of body weight. Supportive measure to decrease the absorption of the drug is achievable by using activated charcoal but only if administered within 4 hours of ingestion. The patient will need monitoring for signs and symptoms of bleeding and the development of metabolic derangements, such as acidosis. If acidosis develops, immediate dialysis is indicated.
There is no antidote available for most of these drugs; however, a monoclonal antibody against ticagrelor is in development, but it is not commercially available as yet.
Drug interactions:
Both laboratory studies in healthy volunteers and clinical studies have suggested adverse interactions between antiplatelet drugs and other commonly used medications. Interactions described include those between aspirin and ibuprofen, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and the thienopyridine, clopidogrel, and drugs inhibiting CYP2C19, notably the proton pump inhibitors (PPI) omeprazole and esomeprazole. Other interactions between thienopyridines and CYP3A4/5 have also been reported for statins and calcium channel blockers. The ibuprofen/aspirin interaction is thought to be caused by ibuprofen blocking the access of aspirin to platelet cyclo-oxygenase. The thienopyridine interactions are caused by inhibition of microsomal enzymes that metabolize these pro-drugs to their active metabolites. We review the evidence for these interactions, assess their clinical importance and suggest strategies of how to deal with them in clinical practice. We conclude that ibuprofen is likely to interact with aspirin and reduce its anti-platelet action particularly in those patients who take ibuprofen chronically. This interaction is of greater relevance to those patients at high cardiovascular risk. A sensible strategy is to advise users of aspirin to avoid chronic ibuprofen or to ingest aspirin at least 2 h prior to ibuprofen. Clearly the use of NSAIDs that do not interact in this way is preferred. For the clopidogrel CYP2C19 and CYP3A4/5 interactions, there is good evidence that these interactions occur. However, there is less good evidence to support the clinical importance of these interactions. Again, a reasonable strategy is to avoid the chronic use of drugs that inhibit CYP2C19, notably PPIs, in subjects taking clopidogrel and use high dose H2 antagonists instead. Finally, anti-platelet agents probably interact with other drugs that affect platelet function such as selective serotonin reuptake inhibitors, and clinicians should probably judge patients taking such combination therapies as at high risk for bleeding.
What's the difference between anticoagulants and antiplatelet?
Both anticoagulants and antiplatelets reduce or prevent clotting. But they work in different ways.
Antiplatelets interfere with the process of platelets binding together. Anticoagulants, also called blood thinners, interfere with proteins in your blood that are involved with clotting.
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