Mechanism of Insulin Resistance 



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MOA of Nitroglycerine  Nitroglycerine converted to NO (Active Metabolite)  NO bonds with Guanylyl cyclase and catalyzes the conversion of GTP to cyclic GMP. cGMP induces the enzyme Myosin LC phosphatase  Myosin-LC phosphatase dephosphorylates the phosphorylated myosin-LC (Contraction) to Myosin-LC (Relaxation)  Reducing Preload : Vasodilation promotes peripheral pooling of blood and decreases venous return to the heart , reducing preload. This results in decreased myocardial oxygen demand. Reducing Afterload : Arteriolar relaxation reduces systemic vascular resistance and arterial pressure, also known as afterload. This decreases the resistance the heart must overcome to eject blood, which reduces the workload of the heart. 
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Illustrate the overview of the different classes of anti-anginal drugs and discuss their specific mechanisms of action and indications for use? Classification of Antianginal Drugs MODE of ACTION  Organic Nitrates: (Increasing O2 Supply)           MOA (Vein)            Calcium Channel Blockers: (Increasing O2 supply & Decreasing O2 Demand)          MOA - CLICK HERE         In case of the smooth muscles of coronary artery , the CCBs prevents the contraction of arterial smooth muscle leading to Arterial Dilation . → Increased  O2 Supply   In Case of Cardiac smooth muscle , CCBs prevents the contraction (inhibiting the formation of MLCK+ ) results in Negative inotropic effect ( Decreased Force of Contraction ) in Heart. Potassium Channel Opener: (Increased O2 Supply)           MOA -            Beta Blockers: (Decreasing O2 Demand)           MOA -  Block the  adrenergic  beta (BETA 2) receptor of the heart leading to Decreased sympathetic outflow leading to Decreased HR (Negativ
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Explain in detail the role of prostacyclin and thromboxane on platelet aggregation Prostacyclin and thromboxane are two opposing eicosanoids (locally-acting hormones) that play a critical role in platelet aggregation. These 2 Local hormones are produced in the Arachidonic Acid Metabolism Pathway. Role of TXA2 on platelet Aggregation: Thromboxane A2 is produced from Prostaglandin H2 by the Enzyme Thromboxane A synthase. Mature platelets express only COX-1 and releases TxA2. This TxA2 then binds with TP receptor and induces platelet Aggregation by Protein Kinase C Dependent pathways . ( increased Stickiness) PGI2 also binds with TP receptor of Vascular smooth muscle inhibiting PKC pathway causing increased cAMP level causing Vasoconstriction.   The role of TXA2 in platelet aggregation is so important that aspirin, which inhibits TXA2 production by blocking the cyclooxygenase-1 (COX-1) enzyme, is one of the most widely used antiplatelet drugs in the world. Aspirin is used to prevent
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