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CV Pharm HY
Day 6
| Question | Answer |
|---|---|
| What is the first line drug for essential htn? | Hydrochlorathiazide |
| Name 2 benefits of a common SE of hydrochlorathiazide therapy. | Retains calcium so you have a decreased risk of developing osteoporosis and prevents the development of renal stones! Yippee! |
| Name 4 drug classes that can be used to treat essential HTN. | Diuretics (thiazides), ACE-i, ARBs, and CCBs (nifedipine causes peripheral vasodilation) |
| Which diuretics can precipitate kidney stones? | Loop diuretics like furosemide; Loops Lose calcium in the urine--> stone formation |
| Name 5 classes of drugs used to treat CHF. | Diuretics (loops like furosemide), ACE-i, ARBs, Beta blockers, and K sparing diuretics (spironolactone, triamterene, and amiloride) |
| In which type of CHF are Beta blockers contraindicated? | decompensated CHF (e.g., if patient has fluid in the lungs, do NOT give them beta blockers!) |
| Name 6 classes of drugs that can be used to treat HTN in diabetic patients. | ACE-i, ARBs, CCBs, diuretics, Beta blockers, and alpha blockers |
| Which anti-hypertensives are protective against diabetic nephropathy? | ACE-i (prevents proteinuria in diabetics) |
| Which antihypertensive can be used in severe hypertension and is frequently co-administered with a beta blocker to prevent reflex tachycardia? | Hydralazine |
| Which antihypertensives are considered safe for use in pregnancy (4)? | hydralazine, nifedipine, labetolol, and alpha-methyl dopa |
| Which antihypertensive vasodilates the arterioles more than the veins, leading to a reduction in afterload? | Hydralazine (one of few drugs that can decrease afterload) |
| What is the mechanism of action of hydralazine? | increases cGMP leading to sm m relaxation |
| Which antihypertensive can cause drug induced lupus? | Hydralazine (SHIPP= Sulfonamides, Hydralazine, Isoniazid, Procainamide, and Phenytoin) |
| Why is hydralazine contraindicated in angina/CAD? | B/c it can cause compensatory tachycardia. |
| What is the mechanism of action of calcium channel blockers? | Block voltage-dependent L-type calcium channels of cardiac and smooth m thereby reducing m contractility |
| Which CCB cannot be used to treat arrhythmias? Why not? | Nifedipine; it works on the vascular sm m, NOT on the heart (use verapamil or diltiazem instead) |
| Why is nifedipine therapy useful in patients with bradycardia? | B/c it causes peripheral vasdilation which leads to a reflex tachycardia; it also has a minimal affect on AV conduction (remember it doesn't act directly on the heart) |
| CCBs can be used to treat which 3 "spasmodic" conditions? | Prinzmetal's angina, Raynaud's, and esophageal spasms |
| What CCB toxicities are only attributable to verapamil and diltiazem? | Cardiac depression and AV block |
| What CCB toxicity is mainly caused by nifedipine? | Peripheral edema |
| Which CV drug can be used to treat both severe hypertension and hair loss (topical application)? | Minoxidil |
| What is the mechanism of minoxidil? | Opens K channels and hyperpolarizes sm m, resulting in relaxation of vascular sm m |
| Name 3 drugs that can be used to treat malignant HTN. | Nitroprusside, Fenoldopam, and Diazoxide (labetolol is also commonly used) |
| Which malignant HTN treatment is known to cause hyperglycemia due to reduced insulin release? | Diazoxide (D for Diabetic) |
| Which malignant HTN drug is the only IV agent that improves renal perfusion, so it's beneficial for hypertensive patients with renal insufficiency? | Fenoldopam |
| What is the mechanism of action of fenoldopam? | A dopamine D1 receptor agonist (think fenolDOPAM for DOPAMine) |
| What is the mechanism of action of nitroprusside? | increased cGMP via direct release of NO; short acting |
| What affect does nitroprusside have on preload and afterload? What is the mechanism? | It vasodilates arterioles and vv so it decreases both preload and afterload |
| Which malignant HTN treatment can cause cyanide toxicity | Nitroprusside. NitroprussIDE releases cyanIDE |
| What is the mechanism of action of nitroglycerin and isorbide dinitrate? | Vasodilate by releasing NO in sm m--> increased cGMP--> sm m relaxation |
| What does nitroglycerin preferentially dilate-- aa or vv? What is the resultant effect on preload or afterload? | Dilates vv more than aa, so reduces preload |
| Why can isosorbide be used to treat pulmonary edema? | B/c it pools blood peripherally so there is not as much blood in the lungs |
| What is the goal of anti-anginal therapy? | Reduction of myocardial O2 consumption |
| What are the determinants of myocardial oxygen consumption? | EDV (preload), BP (afterload), HR, contractility, and ejection time |
| EDV: nitrates | decreased |
| EDV: Beta blockers | increased |
| EDV: nitrates + beta blockers | no effect or decreased |
| BP: nitrates | decrease |
| BP: beta blockers | decrease |
| BP: nitrates + beta blockers | greatly decreased |
| Contractility: nitrates | increased (reflex) |
| Contractility: beta blockers | decreased |
| Contractility: nitrates + beta blockers | Little/no effect |
| HR: nitrates | increased (reflex) |
| HR: beta blockers | decreased |
| HR: nitrates + beta blockers | decreased |
| Ejection time: nitrates | decreased |
| Ejection time: beta blockers | increased |
| Ejection time: nitrates + beta blockers | little to no effect |
| myocardial O2 consumption: nitrates | decreased |
| myocardial O2 consumption: beta blockers | decreased |
| myocardial O2 consumption: nitrates + beta blockers | greatly decreased |
| Which partial beta agonists are contraindicated in agina? | Pindolol and acebutolol |
| Which lipid reducing agent shows the greatest reduction of LDL? | HMG-CoA reductase inhibitors (statins) |
| What is the drug of choice for raising HDL? | Niacin (remember niacin is a pharmacologic VITAMIN! B3) |
| What are the side effects of niacin? | Red, flushed face, hyperglycemia (acanthosis nigrans), and hyperuricemia (exacerbates gout) |
| Which lipid lowering agent is known for its bad taste and GI discomfort? | Bile acid resins (cholestyramine, colestipol, and colesevelam) |
| How does cholestyramine affect the absorption of fat soluble vitamins? | Decreases it |
| Which lipid lowering agent prevents cholesterol reabsorption at the small intestine brush border? | Ezetimibe |
| Why is ezetimibe rarely used? | It may increase plaque thickness and may not affect the long term outcome; may also increase LFTs, but this is rare |
| Which lipid lowering agent is the most effective at lowering triglycerides? | Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate) |
| Which lipid lowering agent can be used to lower triglycerides, reduce the severity of Rheumatoid arthritis, and decrease the risk of arrhythmias in patients with heart disease? | Omega 3 fatty acids |
| What is one of the MCC of pancreatits? | High triglyceride levels; can be fatal |
| Which lipid lowering agents can cause cholesterol gallstones? | Bile acid resins (cholestyramine) and fibrates (gemfibrozil) |
| How do bile acid resins like cholestyramine work? | Prevent intestinal reabsorption of bile acids so liver must use up cholesterol to make more. Very clever! |
| How does niacin work? | Inhibits lipolysis in adipose tissue and reduces hepatic VLDL secretion into circulation |
| Which lipid lowering agents require monitoring of liver function tests and muscle function? | HMG-CoA reductase inhibitors (statins) and fibrates (gemfibrozil). It's dangerous to use these drugs in combination. Don't do it! |
| How do cardiac glycosides like digoxin work? | It blocks the Na/K ATPase, so there is less extracellular Na available for use in the Na/Ca exchanger on cardiac myocytes which draws Ca out of the cell. This results in increased Ca inside the cell which increases contractility. |
| Which receptors are the major cellular mediator of calcium-induced calcium release? | Ryanodine receptors (mutated in malignant hyperthermia) |
| An elevation of which electrolyte in serum suggests digoxin toxicity? | K; the higher the K levels in serum, the more digoxin the patient has consumed |
| Name 2 conditions that digoxin is used to treat. | chronic CHF (increases contractility) and a fib (decreases conduction at the AV node and depresses the SA node) |
| What are the side effects of digoxin toxicity? | Cholinergic: nausea, vomiting, diarrhea, blurry yellow vision like Van Gogh (FREQUENTLY TESTED according to UWorld) |
| Which medical conditions worsen digoxin toxicity? | Renal failure (decreased excretion) and hypokalemia (allows for more digoxin binding at the K binding site on Na/K ATPase) |
| Which drug worsens digoxin toxicity? | Quinidine, a class Ia antiarrhythmic (decreases digoxin clearance and displaces digoxin from tissue binding sites) |
| What EKG finding is seen with digoxin toxicity? How is it treated? | Bradycardia; treat with atropine which will increase the HR |
| What are the 4 classes of antiarrhythmics? | Na channel blockers (Class I), Beta blockers (Class II), K channel blockers (Class III), CCB (Class IV); No Bad-Boy Keeps Clean |
| What 3 drugs are in Class IA antiarrhythmics (Na channel blockers)? | Procainamide, Disopyramide, and Quinidine(Police Department Questioned) |
| What 3 drugs are in Class IB antiarrhythmics (Na channel blockers)? | Tocainide, Lidocaine Mexiletine (The Little Man) |
| What 3 drugs are in Class IC antiarrhythmics (Na channel blockers)? | Flecainide, Propafenone, and Encainide (For Pushing Ectasy) |
| How do Class I antiarrhythmics work? | Decrease the slope of phase 0, thereby elongating the ERP (effective refractory period); different classes affect phase 3 differently |
| Which class of antiarrhythmics is best for treating after an MI? | Class IB (Tocainamide, Lidocaine, Mexiletine) |
| Which class of antiarrhythmics is contraindicated after an MI? | Class IC (Flecainide Propafenone Encainide) |
| Which electrolyte abnormality increases toxicity for all Class I drugs? | Hyperkalemia |
| Which class I antiarrhythmic is used to treat Wolf Parkinson White syndrome? | Procainamide (can cause drug induced lupus) |
| Which toxicities are unique to quinidine? | Torsades de pointes (due to increased QT interval), cinchonism (HA, tinnitus), and thrombocytopenia |
| Lidocaine (Class IB) can be used to treat which drug-induced arrhythmias? | Digitalis-induced arrhythmias |
| Which class of antiarrhythmics is used only as a last result against refractory tachyarrhythmias? | Class IC (Flecainide Propafenone Encainide) |
| How do class II antiarrhythmics work? | Class II= beta blockers. Decreases cAMP which decreases Ca currents. This suppresses abnormal pacemakers by decreasing the slope of phase 4. |
| Which class II antiarrhythmic is very short acting? | esmolol (beta blocker) |
| Why are class II antiarrhythmics potentially dangerous for diabetics? | B/c they may mask the signs of hypoglycemia (beta blockers). |
| What are the 2 most commonly used class III antiarrhythmics? | Sotalol and amiodarone (K channel blockers) |
| What is the mechanism of action of bretyllium? | slows release of K, thereby elongating the ERP. Also increases AP duration. (K channel blocker/Class III antiarrhythmic) |
| Which class III antiarrhythmic is known to cause torsades de pointes? | Sotalol (increases the QT interval) |
| What are the toxic SE of amiodarone (Class III antiarrhythmic)? | Pulmonary fibrosis, hepatoxicity, and hypo/hyperthyroidism (check PFTs, LFTs, and TFTs); also corneal deposits, blue/gray skin deposits, and photodermatitis |
| What are the treatment options for Wolf Parkinson White Syndrome? | Amiodarone and procainamide |
| What is the mechanism of action of Class IV antiarrhythmics? | Decrease conduction velocity, increase ERP, and increase PR interval |
| Which category of class III antiarrhythmics work at the heart? at the vessels? | Nondihydropyridine= heart (e.g., verapamil and diltiazem) Dihydropyridine= vessels (e.g., nifedipine, diltiazem) Diltiazem does both |
| Which antiarrhythmic actually stops the heart by increasing K flux out of the cell and decreasing the permeability of the cell to calcium? | Adenosine (can't depolarize if you can't move calcium, so heart just stops) |
| What are the symptoms of adenosine toxicity? | Flushing, hypOtension, and chest pain; blocked by theophylline |
| Which electrolyte antiarrhythmic depresses ectopic pacemakers in hypokalemia (e.g., digoxin toxicity)? | K |
| Which electrolyte antiarrhythmic is useful in treating torsades de pointes and digoxin toxicity? | Mg |
| Adenosine is contraindicated in which type of arrhythmia? | Wolf Parkinson White |
| Which lipid lowering agent has vasodilatory effects that may necessitate reducing the dosage of any anti-hypertensive drugs a patient may be taking? | Niacin (when on niacin, need to reduce dosing of anti-hypertensive drugs and increase dosing of diabetic drugs) |
| What can be used to treat cyanide toxicity from nitroprusside? | Sodium thiosulfate (remember thiosulfate is used to treat general cyanide poisoning) |
| How does digoxin affect parasympathetic tone? | Increases it thru its action on the vagus n which leads to a decreased rate of AV conduction |
| Unmonitored patient on long-term therapy for CHF presents with changes in color vision, nausea, vomiting, anorexia, and diarrhea | Digoxin toxicity (may also be at risk for developing digoxin-induced arrhythmias) |
| Why must patients taking daily, long-acting nitrates have a daily nitrate-free interval (usually b/f going to bed)? | B/c of tolerance development; drug free interval is usually situated at night when cardiac work is the lowest |
| Which agents cause coronary steal phenomenon (selective vasodilation of coronary vessels which may divert blood flow from ischemic areas to non-ischemic areas leading to hypOperfusion and worsening existing ischemia)? | Adenosine and dipyrimadole (vasodilators) |
| To decrease the risk of developing myopathy while taking an agent that inhibits CYP-450 (e.g., erythromycin), which statin is the drug of choice? | Pravastatin (CYP-450 inhibitors greatly increase the serum levels of all statin drugs, EXCEPT for pravastatin, leading to increased risk of rhabdomyolysis and hepatotoxicity) |
| Patient being treated for arrhythmias develops constipation and gingival hyperplasia. What drug was he taking? | Verapamil (Class IV antiarrhythmic) |
| Which cardiac drug is used for chemical stress testing? | Adenosine |
| Patient with mural thrombus receives the std treatment for his condition. He develops skin necrosis. What drug was he given and what protein deficiency does he have? | Warfarin. Pt has protein C deficiency. |
Created by:
sarah3148
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