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Cardiac Pharmacology
Cardiovascular module
Question | Answer |
---|---|
What are three main classes of cardiac drugs | 1. Drugs that directly affect myocardial cels 2. Drugs that have an indirect effect on cardiac function (e.g. Organic Nitrates) 3. Calcium Antagonist |
What are the four main types of drugs that act directly on myocardial cells | 1. Autonomic neurotransmitter & related drugs 2. Antidysarrthymics 3. Cardiac Glycosides and other Inotropic Drugs 4. Miscellaneous drugs and endogenous substances |
What are the four classes of anti-dysrhythmic drugs | Class I - Sodium channel blockers Class II - beta-blockers Class III - Potassium Channel BLockers Class IV- Calcium Channel BlockersWhat are the types of Class I anti-dysarhythmics |
What are the types of Class I anti-dysarhythmics | Class IA - intermediate onset Class IB - fast onset Class IC- slow onset |
What are some class II drugs | Beta blockers: Propanalol, metoprolol, esmolol |
What are some Class III drugs | K+ channel blockers: Amiodarone, Sartalol |
What are some Class IV drugs | Verapamil, diltiazem |
What are Cardiac Glycosides | Drugs that increases inotropy and cardiac output. E.g. Digoxin Used for congestive heart failure and arrhythmias |
How do Calcium Antagonists work? | They prevent Ca+ entry into cells by blocking L-type Ca2+ channels --> slows conduction and causes casodilation Indications: HTN, Angina, arrhythmias |
How do Organic Nitrates work? | 1. They cause vasodilation which decreases arterial and venous pressure --> leads to decreased TPR and venous return as well as afterload --> decreases work of the heart and O2 consumption 2. Decrease platelet aggregation 3. Dilates Collateral vessels |
How do Beta-blockers work? | They block beta-adrenoceptors which are part of the sympathetic NS --> in heart (B1), causes decreased HR and Inotropy + Increases diastolic time which increases time for coronary flow Also causes vasodilation as B2 receptors are found in smooth musc |
What are the two main classes of lipid lowering drugs | 1. Statins 2. Anion-exchanging resins |
What are anion-exchanging resins? | Binds to bile salts to prevent their circulation in the GI tract --> increases hepatic LDL receptors which uptakes plasma LDL |
What are statins? | They inhibit HmG-CoA reductase which is the rate limiting step in intracellular cholesterol synthesis --> upregulate LDL receptors --> inc uptake of plasma LDL Also inc epithelial function, dec inflammation & platelet aggregation and incr fibronolysis |
What are the three types of thrombolytics? | 1. Anti-coagulant 2. Anti-platelet 3. Fibrinolytics |
What are the types of anti-coagulant | Heparin - inhibits coagulation by inactivating thrombin and factor Xa and ATIII Direct Thrombin Inhibitors - binds to thrombin to prevent fibrin formation Vitamin K antagonist (warfarin) - binds to Vitamin K reductase to prevent synthesis of vitamin |
What are the different types of anti-platelets | Aspirin - Inhibits COX Glycoprotein IIb/IIIa inhibitors - inhbits integrins GPIIb and GPIIIa which are what fibrinogen binds to to convert into fibrin P2& antagonist- Targets P2Y receptors that prevents platelet aggregation |
How do fibrinolytics work | They convert plasminogen into plasmin which degrades fibrin products, fibronogen, ECM proteins and clotting factors E.g. Streptokinase, tPa |