Copy of Cardiovascular Rx - Sheet1

Question 1

Nifedipine, verapamil, diltiazem, amlodipine

Answer 1

1) HTN, angina, arrhythmia (not nifedipine) Prinzmetal’s angina, Raynaud’s
2)Ca2+ Channel Blockers/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility
vascular sm. muscle effects: amlodipine=nifedipine > diltiazem > verapamil
Heart: verapamil>diltiazem>amlodipine=nifedipine (verapamil=ventricle!, sim to b blockers; nifedipine=similar to nitrates)
3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
V & d= class Iv antiarrythmics (dec conduction velocity, inc erp & pr interval, used in prevention of nodal arrhythmia a (svt)

Question 2

Hydralazine

Answer 2

1) Severe HTN (first line in pregnancy+ metyldopa), CHF (w/ beta-blocker to prevent reflex tachycardia)
2) Increase cGMP to cause sm. muscle relaxation
- vasodilates arterioles > veins
- Afterload reduction
3) Compensatory tachycardia, fluid retention, nausea, headache, angina, lupus-like syndrome
4) Contraindicated in angina and CAD

Question 2

Nitroprusside

Answer 2

1) Malignant HTN
2) Increases cGMP via direct release of NO; short acting
3) Cyanide toxicity

Question 2

Fenoldopam

Answer 2

1) Malignant HTN
2) Dopamine (D1) receptor agonist
- leads to coronary, peripheral, renal, and splanchnic vasodilation
- decreases BP and increases naturesis

Question 3

Nitroglycerin, isosorbide dinitrate

Answer 3

1) Angina, pulmonary edema
2) Vasodilator – release of NO in sm. muscle –> increases cGMP and sm muscle relaxation
- dilates veins&raquo_space; arteries (decreases preload)
3) reflex tachycardia, hypotension, flushing, headache
4) “Monday Disease” –> devleop tolerance during the week and loss of tolerance during weekend resulting in side effects on reexposure

Question 4

Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

Answer 4

1) Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2) HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3) Hepatotoxicity (increase LFTs), rhabdomyolysis
4) cause hepatocytes to increase LDL receptor density (b/c can’t make LDL anymore)

Question 5

Niacin (B3)

Answer 5

1) Lipid-lowering agent (decreases LDL and TG, sig increases HDL)
2) Inhibits lipolysis in adipose tissue, reduces hepatic VLDL secretion into circulation
3) Red flushed face (dec by aspirin & lt use), hyperglycemia (acanthosis nigrans), hyperuricemia (excerbates gout)

Question 6

Cholestyramine, colestipol, colesevelam

Answer 6

1) Lipid-lowering agents (decrease LDL, slightly increase TG and HDL
2) Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to use cholesterol to make more)
3) Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones
4) unique among hypolidipemic agents in that they inc blood tg levels–> fibrinic acid derivatives=first line tx for hypertg

Question 7

Ezetimibe

Answer 7

1) Lipid-loweing agents (decrease LDL)
2) Cholesterol Absorption Blockers/Prevent cholesterol reabsorption at small intestine brush border
3) Rare increase in LFTs, diarrhea

Question 7

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

Answer 7

1) Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL)
2) Fibrates/Upregulates LPL –> increases TG clearance
3) Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones

Question 7

Digoxin

Answer 7

1)CHF (increase contractility), A.fib (decrease conduction at AV node, depression of SA node)
2)Cardiac Glycoside/Direct inhibition of Na+/K+ ATPase leads to indirect inhibtion of Na+/Ca2+ exchanger/antiport –> increases Ca2+ concentration(positive inotropy)
-stimulates vagus nerve to decrease HR
3)Cholinergic –> N/V/D, blurry yellow vision, EKG changes (increased PR, decrased QT, ST scooping, T-wave inversion, arrhythmia, AV block), hyperkalemia (poor prognostic indicator)
-Factors predisposing to toxicity –> renal failure (dec excretion), hypokalemia (permissive for digoxin binding at k+ binding site on na/k atpase), quinidine (decreases digoxin clearance, displaces digoxin from tissue binding sites)
4)Antidote –> slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab fragments, Mg2+
75% bio available, 20-40% protein bound, t1/2=40 hours, urinary excretion

Question 7

Quinidine, procainamide, disopyramide

Answer 7

1) Atrial and ventricular arrhythmias – re-entrant and ectopic supraventricular, ventricular tachycardia
2) Anti-arrhythmics:Na+ Channel Blocker (Class IA)/ Slow or block conduction – increase AP duration, ERP and QT interval
3) q–>Cinchonism (headache, tinnitus); p–> reversible sle like syndrome; d–> heart failure; thrombocytopenia, Torsades de Pointes (increased QT), hyperkalemia causes increased toxicity

Question 7

Lidocaine, mexiletine, tocainide

Answer 7

1)Acute ventricular arrhythmias (esp post-MI), digitalis-induced arrhythmias
2)Anti-arrhythmics:Na+ Channel Blocker (Class IB)/ Slow or block conduction –decrease AP duration
3)Local anesthetic, CNS stimulation/depression, cardiovascular depression
4)Preferentially affects ischemic or depolarized Purkinje and ventricular tissue, hyperkalemia causes increased toxicity
Phenytoin can also be considered class ib anti arrhythmic

Question 8

Flecainide, propafenone

Answer 8

1) V.tach that progress to V.fib, intractable SVT, last resort in refractory tachyarrhythmias
2) Anti-arrhythmias: Na+ Channel Blocker (Class IC)/ Slow or block conduction – no effect on AP duration
3) Pro-arrhythmic (esp post-MI), prolongs refractory period in AV node
4) Contraindicated post-MI and in pts with structural abnormalities, hyperkalemia causes increased toxicity

Question 9

Metoprolol, propranolol, esmolol, atenolol, timolol

Answer 9

1)V.tach, SVT, slowing ventricular rate during a.fib and a.flutter
2)Anti-arrhythmics: Beta-Blockers (Class II)/ Decrease cAMP and Ca2+ currents to decrease SA and AV nodal activity – suppress abnormal pacemakers by decreasing slope of phase 4
3)Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), mask signs of hypoglycemia, dyslipidemia
4)Treat overdose with glucagon
Av node particularly sensitive–> inc pr interval. Esmolol very short acting. Propanolol–> exacerbate vasospasm in prinzmetal’s angina. Metoprolol–> dyslipidemia

Question 9

Amiodarone, ibutilide, dofetilide, sotalol

Answer 9

1) When other anti-arrhythmics fail
2) Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval
3) sotalol: torsades, excess b block; i: torsades; amioderone: Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (=40% iodine), corneal deposits, skin deposits (blue/grey) – cause photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF) – check PFTs, LFTs, TFTs
4) amioderone Has Class I, II, III and IV effects – alters the lipid membrane

Question 9

Adenosine

Answer 9

1) Diagnosing/abolishing SVT
2) Increase K+ removal from cell –> hyperpolarize the cell and decrease I(Ca), very short-acting (15 secs)
3) Flushing, hypotension, chest pain
4) Effects blocked by theophylline and caffeine

Question 10

Mg2+

Answer 10

1)Torsades de Pointes, Digoxin toxicity

Question 19

Nicardipine, clevidipine, labetolol

Answer 19

Other drugs for malignant HTn