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CV Pharm HY

Day 6

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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