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Pharm - Ch. 48-9, 51
Antidysrhythmic, Anticoagulant/Antiplatelet/Thrombolytics, and LDL Lowering Drug
| Question | Answer |
|---|---|
| Define dysrhythmia | Abnormality in rhythm of the heartbeat |
| True or false: there are two types of dysrhythmias | True. Bradydysrhythmias and tachydysrhythmias |
| In nerve cells, Na+ rushes inside the cell and __ rushes out | K+ (potassium) |
| True or false: muscle cells repolarize more steadily than nerve cells | True. K+ takes a longer time to bring the charge of the cell back down to resting state because Ca2+ is rushing inside the cell |
| True or false: there are only four GROUPS of antidysrhythmic drugs | False. There are four major classes, but there is also an "other" category for digoxin and adenosine. These two drugs can be used to treat dysrhythmias. |
| Class I antidysrhythmic drugs inhibit ___ | Na |
| Class II antidysrhythmic drugs inhibit ___ | Ca |
| Class III antidysrhythmic drugs inhibit ___ | K |
| Class IV antidysrhythmic drugs inhibit ___ | Ca |
| List the different types of drugs used for each of the four classes. | Class I: sodium channel blockers. Class II: beta blockers. Class III: potassium channel blockers. Class IV: calcium channel blockers |
| How is digoxin used to treat dysrhythmias? | Digoxin can inhibit the movement of Ca by working on Na-K ATPase. |
| True or false: nifedipine is a Class IV drug | False. Only verapmil as nifedipine does not block the calcium channels of the heart. |
| List a Class I drug | Lidocaine |
| What is the mechanism of action for Lidocaine? | Blocks sodium channels and accelerates repolarization with little or no effect on ECG |
| What are the major adverse effects of Lidocaine? | Dysrhythmias, CNS effects, confusion, paresthesias |
| True or false: metoprolol is NOT used as a Class II drug | False. Metoprolol has same actions as propranolol in blocking calcium. |
| Propranolol is a ____ beta adrenergic antagonist | nonselective |
| What are the adverse effects of propranolol? | When blocking cardiac beta1 receptors, can cause heart failure, AV block, sinus arrest, hypotension. When blocking beta2 receptors, can cause bronchospasm in patients with asthma. |
| True or false: when treating dysrhythmias in asthmatic patients, it is preferable to give metoprolol | True because metoprolol is beta1 selective |
| List a Class III drug | Bretylium |
| What is the mechanism of action for Bretylium? | Delays the repolarization of past potentials. By prolonging action potential duration, one can treat tachycardia or v-fib. |
| True or false: Bretylium's primary adverse effect is profound hypertension | False. HYPOtension is the adverse effect. |
| A patient given a class III drug has extremely low BP. You would treat with the following ______ or _______ | Dopamine or norepinephrine |
| A patient is given an antidysrhythmic drug that results in hypotension, edema, and constipation. Which drug was administered? | Verapamil. These are some of its adverse effects. |
| List the adverse CARDIAC effects of verapamil | Bradycardia, AV block, heart failure with effects on vascular smooth muscle, hypotension, and edema |
| Describes the stages of hemostasis | Stage 1 - formation of platelet plug. Stage 2 - coagulation by intrinsic and extrinsic systems |
| What is the difference between an anticoagulant drug and a thrombolytic drug? | Anticoagulants disrupt the coagulation cascade. Thrombolytic drugs dissolve clots by causing fibrin lysis. |
| _____ is used to treat arterial thrombosis | Antiplatelet drugs |
| _____ is used to treat venous thrombosis | Anticoagulant drugs |
| List the drugs used as anticoagulants, antiplatelets, and thrombolytics respectively | Anticoagulants: heparin and warfarin. Antiplatelets: Aspirin and clopidogrel. Thrombolytic drugs: streptokinase and tPA |
| True or false: antiplatelet drugs are commonly administered after a patient experiences heart failure | True. Aspirin and clopidogrel commonly administered. (Heparin is not an antiplatelet drug, but it is also commonly given as well.) |
| A nurse receives an order for low MW heparin given PO at 1400. What should she do? | Recheck the order because heparin is given via injection or IV. It cannot be given PO. |
| In an emergency, which drug would you use? Heparin or warfarin? | Heparin because it is rapid-acting and can be used in emergency situations. Warfarin is commonly indicated for long-term prevention of venous thrombosis. |
| True or false: warfarin is an only oral anticoagulant | True. At the moment, only oral anticoagulant available in US. |
| Explain the mechanism of action for heparin | Heparin enhances the activity of antithrombin, which inactivates clotting factors. |
| List three indications for heparin | Pulmonary embolism, evolving stroke, prevention of venous thrombosis |
| What are the SE of heparin? | Hemorrhage, heparin-induced thrombocytopenia, hypersensitivity reactions |
| What is the advantage of using low molecular weight heparin versus regular heparin? | Unfractionated heparin was discovered to cause more SE. Low molecular weight heparin has a smaller chunk of active heparin molecule so there are fewer side effects associated. |
| True or false: warfarin is an agonist of vitamin K | False. Antagonist. |
| What is the mechanism of action for warfarin? | Decrease synthesis of clotting factors by antagonizing vitamin K |
| What is a use for warfarin? | Long-term prevention of venous thrombosis |
| List the SE of warfarin | Hemorrhage, multiple DDIs (which can increase/decrease anticoagulant effect and/or promote bleeding) |
| True or false: any drug with an affinity for albumin will alter warfarin binding | True. Warfarin is 99% bound to albumin so DDI can occur as result of changes in albumin binding |
| What is the mechanism of action for aspirin and clopidogrel? | They decrease platelet aggregation |
| Aspirin is indicated for what uses? | Prevention of arterial thrombosis and prevention of MI |
| What is an adverse effect of aspirin and clopidogrel? | Major GI bleeding |
| Explain how a GI bleed may be caused by aspirin | Aspirin antagonizes an enzyme known as COX, which activates platelets and also produces a protective layer for stomach mucosa. Both functions can be affected if aspirin given too much |
| True or false: baby aspirin can be given to children | False. Due to concern of Reye's syndrome, aspirin not administered to pediatric patients |
| Explain the mechanism of action of streptokinase and tPA | They bind to plasminogen and promote lysis of fibrin to dissolve clots |
| What are the uses of thrombolytic drugs? | MI, DVT, massive pulmonary emboli |
| List the SE of streptokinase and tPA | Bleeding, antibody production, hypotension, fever |
| True or false: thrombolytic drugs can be used prophylactically | False. These drugs can only remove thrombi that have already formed. Anticoagulants are used as prophylaxis of thrombus formation. |
| Drugs used to lower LDL cholesterol levels work through ___ mechanisms | Indirect |
| What is an HMG-CoA Reductase Inhibitor? | A class of drugs that inhibit HMG-CoA reductase, a liver enzyme that produces cholesterol. |
| What is the prototype of HMG-CoA reductase inhibitors? | Lovastatin. |
| Lovastatin increases the number of LDL receptors. Explain how this works to lower LDL levels | Inhibits the enzyme producing cholesterol, causing a decrease in cholesterol production within the liver. Liver looks for other sources of cholesterol. Liver cells increase # of LDL receptors and grab onto free floating LDL molecules, lowering LDL levels |
| What are the benefits of using a HMG-CoA Reductase inhibitor? | Lower LDL, increase HDL, increase plaque stability |
| What are the adverse effects of Lovastatin? | Headache, rash, muscle soreness, heptaotoxicity. Also classed as a category X drug |
| Nicotinic acid decreases the production of _____ and ______ | VLDLs and LDLs |
| Nictonic acid ____ the ______ inside adipose tissue | Inhibit, lipolysis |
| What are the SE of niacin? | Skin flushing, hepatotoxicity, GI-related, hyperglycemia |
| List the types of drugs used to lower LDL cholesterol levels | HMG-CoA reductase inhibitors, bile acid-binding resins, nicotinic acids, fibric acid derivatives |
| What is a drug classified as a bile acid-binding resin? | Cholestyramine |
| Explain the mechanism of action for cholestyramine | Increases LDL receptors in liver, prevents reabsorption of bile in intestine. As a result, bile excretion accelerated. Body compensates by synthesizing bile from LDLs. |
| List adverse effects of cholestyramine | Constipation, decrease absorption of fat-soluble vitamins (ADEK) |
| True or false: cholestyramine is not absorbed through GI | True |
| List the therapeutic uses of aspirin (that aren't related to platelet aggregation) | 1) relief of mild-to-moderate pain, 2) analgesic, antipyretic, anti-inflammatory, 3) dysmenorrhea |
| What are the mechanisms of action for aspirin as related to COX enzymes? | Aspirin can irreversibly inhibit COX enzymes. COX-2 inhibition suppresses inflammation, pain and fever. COX-1 inhibition protects against MI by suppressing platelet aggregation |
| True or false: aspirin is contraindicated in pregnancy | True. Category D drug! |
| What is the prototype for fibric acid/fibrates? | Gemfibrozil |
| True or false: gemfibrozil increases the clearance of LDLs | False. Increases clearance of VLDLs |
| What is the mechanism of action of gemfibrozil? | Activates PPAR-gamma, which increases clearance of VLDLs and reduces high triglyceride levels |
| List the adverse effects of gemfibrozil | Rashes, GI, gallstones, hepatotoxicity |
| True or false: gemibrozil's SE are relatively mild | True |
Created by:
choel
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