MOA of Na+ Channel Blockers 




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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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Compare the pharmacology of Aspirin, Diclofenac, and Paracetamol. Aspirin (Acetylsalicylic acid) : Mechanism of Action: Aspirin inhibits both COX-1 and COX-2 enzymes, which are responsible for the production of prostaglandins ( PGF2alpha ), substances that mediate pain and inflammation . It also inhibits the conversion of arachidonic acid to thromboxane A2 , a potent inducer of platelet aggregation. Low-dose aspirin use irreversibly blocks the formation of  thromboxane A 2  in mature platelets by inhibiting the COX-1 enzyme, producing an inhibitory effect on platelet aggregation during the lifetime of the affected platelet (8–9 days) and acts as a blood thinner. Indications: Aspirin is used to treat pain, fever, and inflammation associated with various conditions. It is also used as antiplatelet agent sometimes in low doses. Pharmacokinetics: Aspirin is rapidly and completely absorbed after oral administration. It is widely distributed in the body in protein-bound form. Preventi
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