March 24, 2023

💡💡 Learn Pharmacology?

In the previous lecture we discussed an introduction about hemostasis and how the body responds to an injury so in this lecture we’ll start talking about the drugs that are used to either prevent or dissolve unwanted clots that may arise in the blood vessels under some pathological conditions we already know from the previous lecture that we have three main

Mechanisms involved in the clot formation and dissolution platelet aggregation blood coagulation and fibrinolysis so we can conclude that the drugs used to stop any of these mechanisms can be classified to antiplatelet drugs anticoagulants and thrombolytic agents also known as fiber analytics today we’ll discuss the antiplatelet drugs we already know from the

Previous lecture that platelet activation process depends on several chemical mediators such as thromboxane a2 adenosine diposphate thrombin serotonin and collagen these platelet activators promote the conformational change needed for the glycoprotein 2b3a receptor to bind ligands particularly fibrinogen fibrinogen simultaneously binds to glycoprotein 2b3a receptors

On two separate platelets resulting in cross-linking and aggregation so we can conclude that antiplatelet drugs can be classified to thromboxane a2 inhibitors adp receptor inhibitors and glycoprotein 2b3a inhibitors let’s start by thromboxane a2 inhibitors the famous drug aspirin in small dose of 75 to 150 milligrams works as thromboxane a2 inhibitor so what is

The exact mechanism stimulation of platelets by thrombin adp and collagen results in activation of platelet membrane phospholipase that liberate arachidonic acid from membrane phospholipids arachidonic acid is first converted to prostaglandin h2 by cox 1. prostaglandin h2 is further metabolized to thromboxane a2 which is released into plasma and we know the rest

Of the story thromboxane a2 promotes the aggregation process so what aspirin does is that it irreversibly inactivates the enzyme cox 1 leading to inhibition of thromboxane a2 synthesis thereby preventing platelet aggregation aspirin is used in the prophylactic treatment of transient cerebral ischemia and to reduce the incidence of recurrent myocardial infarction

The second category adenosine diphosphate inhibitors clopidogrel tyclopidine prasugrul and tychogralore these drugs inhibit the binding of adp to its receptors on platelets and thereby inhibit the activation of the glycoprotein 2b3a receptors required for platelets to bind to fibrinogen and to each other clopidogrel is approved for prevention of atherosclerotic

Events in patients with a recent myocardial infarction or stroke and in those with established peripheral arterial disease it is also approved for prophylaxis of thrombotic events in acute coronary syndromes ticlopidine is indicated for the prevention of transient islamic attacks and strokes in patients with a prior cerebral thrombotic event prasugrel is approved

To decrease thrombotic cardiovascular events in patients with acute coronary syndromes tychogrilor is approved for the prevention of arterial thromboembolism in patients with unstable angina and acute myocardial infarction the third category is the glycoprotein 2b3a inhibitors it includes absence and mab eptibitide and tyrofiban they simply inhibit the glycoprotein

2b3a receptor complex by blocking the binding of fibrinogen and vanulla brand factor leading to inhibition of aggregation these agents are given intravenously along with heparin and aspirin as an adjunct to percutaneous coronary intervention for the prevention of cardiac islamic complications and the last two agents are diapered amole and cylostozole dipyridamole

A coronary vasodilator increases intracellular levels of camp resulting in decreased thromboxane a2 synthesis it is used for stroke prevention and is usually given in combination with aspirin celostazole is an oral antiplatelet agent that also has vasodilating activity still osteozole and its active metabolites inhibit phosphate esterase type 3 which prevents

The degradation of camp thereby increasing levels of camp and platelets and vascular tissues this increase in camp levels in platelets and the vasculature prevents platelet aggregation and promotes vasodilation of blood vessels this drug is approved to reduce the symptoms of intermittent claudication that’s all for this video in the next lecture we’ll discuss the

Anticoagulants so subscribe and wait for the next video

Transcribed from video
Pharmacology [CVS] 20- Antiplatelet Drugs Mechanism Of Action [ Aspirin – Clopidogrel – Cilostazol ] By Medical Videos [ ANIMATED ]