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57 Cards in this Set
- Front
- Back
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Cardiology
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[MOA/Clinical use/TOX]
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Calcium Channel Blockers
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Nefedipine, Verapamil, Diltiazem, Amlodipine
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Ca Channel Blockers MOA
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Block vol-dep L-type Ca channels of cardiac and smooth mm and thereby REDUCE mm contractility
Vascular sm mm--Amlodipine Heart--Verapamil |
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Ca Channel Blockers clinical use
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Hypertension, angina, arrhythmias (not nifedipine), prinzmetal angina, Raynaud's
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Ca Channel blockers Tox
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Cardiac depression
AV block Peripheral edema Flushing Dizziness Constipation |
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Hydralazine MOA
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INCREASE cGMP-->sm mm relaxation
Vasodilate arterioles>>veins = AFTERLOAD REDUCTION |
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Hydralazine clinical use
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First line therapy for hypertension in pregnancy (w/ methyldopa)
Frequently combined with B-blocker to prevent reflex tachycardia |
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Hydralazine Tox
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Compensatory tachycardia (contra in angina/CAD)
Fluid retention Nausea Headache Angina LUPUS-LIKE SYNDROME |
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TX for malignant hypertension
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Nitroprusside, Fenoldopam
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Nitroprusside MOA
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Short acting; INCREASE cGMP via direct release of NO
(can cause cyanide tox) |
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Fenoldopam MOA
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DA D1 receptor agonist--> coronary, peripheral, renal and splanchnic vasodilation = DECREASE BP and INCREASE natriuresis
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Nitroglycerin, isosorbide dinatrate MOA
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Vasodilate by releasing nitric oxide in sm mm, causing INCREASE in cGMP and sm mm relaxation.
Dilate veins >> arteries = DECREASE PRELOAD |
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Nitroglycerin, isosorbide nitrate clinical use
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Angina, pulmonary edema
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Nitorglycerin, isosorbide nitrate TOX
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Reflex tachycardia
Hypotension Flushing Headache MONDAY DISEASE (tolerance during work week, loss of tolerance over wknd-->tachy, dizziness and headache upon reexposure) |
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Antianginal Therapy
Goal & effect of Nitrates + B-Blocker combo therapy |
Goal: reduce myocardial O2 consumption (MVO2) by decreasing 1 or more:
EDV BP, HR, contractility, ejection time Nitrates + B-Blockers = No effect/DEC in EDVV DEC BP No effect/DEC contractility DEC HR Little/no effect ejection time DECREASE MVO2 Ca channel blockers- Nifedipine=nitrates; verapamil=B-blockers |
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HMG-CoA reductase inhibitors
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-statins
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HMG-Coa reductase inhibitors MOA
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Inhibit conversaion of HMG-CoA to mevalonate (a cholesterol precursor)
=decrease circulating cholesterol (LDL) |
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HMG-CoA reuctase inhibitors TOX
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Hepatotoxicity (if LFT > 3x, stop therapy)
Rhabdomyolysis |
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Niacin (vit. B3) MOA
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DEC LDL, INC HDL
Inhibits lipolysis in adipose tissue; reduce hepatic VLDL secretion into circulation |
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Niacin Tox
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Red, flushed face (dec by aspirin)
Hyperglycemia (acanthosis nigricans) Hyperuricemia (exacerbates gout) |
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Bile acid resins
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Cholestyramine, colestipol, colesvelam
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Bile acid resins MOA
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Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
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Bile acid resins TOX
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Patients hate it!
tastes bad GI discomfort DEC absorption of fat-soluble vitamins (ADEK) Cholesterol gallstones |
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Cholesterol absorption blockers MOA
Ezetimibe |
Prevent cholesterol reabsortion at small intestine brush border
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Ezetimibe TOX
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Rare INC LFTs, diarrhea
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Fibrates
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Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate
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Fibrates MOA
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DECREASE Triglycerides
Upregulate LPL= INCREASE TG clearance |
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Fibrates TOX
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Myositis
hepatotoxicity (INC LFTs) Cholesterol gallstones |
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Cardiac glycosides
Digoxin |
75% bioavaliabilty
20-40% protein bound t(1/2) = 40 hours URINARY EXCRETION |
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Digoxin MOA
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Direct inhibition of Na/K ATPase = indirect inhibition of Na/Ca exchanger/antiport
INC [Ca]--> positive inotropy (contractiliy) stimulates vagus n. --> DEC HR |
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Digoxin clinical use
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CHF (inc contractility)
A fib (DEC conduction at AV node and depresion of SA node) |
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Digoxin TOX
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Cholinergic: N/V/D, BLURRY YELLOW VISION
ECG: INC PR, DEC QT, ST scooping, T-wave INVERSION, arrythmia, AV block Can lead to hyperkalemia= POOR PROGNOSTIC INDICATOR Predisposing to tox: Renal failure, hypokalemia, quinidine (dec clearnace; displaces digoxin from tissue binding sites) |
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Digoxin antidote
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Slowly normalize K
Lidocaine Cardiac pacer Anti-digoxin Fab fragments Mg |
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Anti-Arrythmics
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No Bad body keeps clean
Na, B-blockers, K, Ca |
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Class 1: Na channel blockers
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1A: Disopyramide, Procainamide, Quinidine
1B: Lidocaine, Tocainide, Mexiletine 1C: Flecainide, Propafenone Slow or block conduction DEC slope of phase 0 INC threshold for firing in abnormal pacemaker cells State dependent Hyperkalemia causes INC tox for all class 1 drugs |
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Class 1A
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Disopyramide, Quinidine, Procainamide
(Double quarter pounder) INC AP duration INC effective refractory period INC QT interval |
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Class 1A clinical use
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Re-entrant and ectopic supraventricular and ventricular tachycardia
Procainamide --> WPW |
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Class 1A Tox
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Disopyramide: heart failure
Quinide: cinchonism (headache, tinnitus) Procainamide (reversible SLE-like syndrome) All: Torsades de pointes due to INC QT interval |
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Class 1B
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Lidocaine, Tocainide, Mexiletine
(Lettuce, tomato, mayo) DEC AP durection Preferentially affect ischemic or depolarized Purkinje and ventricular tissue |
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Class 1B clinical use
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Acute ventricular arrhythmias (especially POST- MI)
Digitalis-induced arrythmias |
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Class 1B TOX
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Local anesthetic
CNS stimulation/depression Cardiovascular depression |
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Class 1C
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Flecainide, Propafenone
(Fries please) No effect on AP duration |
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Class 1C clinical use
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Last resort in refractory tachyarrythmias
useful in V-Tach that progress to VF |
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Class 1C tox
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contraindicated in structural heart disease and post-MI
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Class II: B-Blockers
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Metoprolol, Propranolol, Esmolol, Atenolol, Timolol
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B-Blockers MOA
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DEC SA and AV nodal activity by DEC cAMP, DEC Ca currents
Supress abnormal pacemakers by DEC slope of phase 4 (takes longer time to reach threshold) AV node particularly sensitive--INC PR interval ESMOLOL very short acting |
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B-Blockers clinical use
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V-Tach, SVT, slowing ventricular rate during A FIB and A flutter
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B-Blockers TOX
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Impotence
Exacerbation of asthma Cardio (Bradycardia, AV block, CHF) CNS (sedation, sleep alterations) Mask signs of hypoglycemia in diabetes Metoprolol can cause dyslipidemia Propranolol can exacerbate vasospasm in Prinzmetal's angina Treat OD with GLUCAGON |
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Class III K channel blockers
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Amiodarone, Ibutilide, Dofetilide, Sotalol
(AIDS) |
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Class III MOA
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INC AP durection
INC ERP (effective refractory period) INC QT interval *Used when other anti-arrythmics fail |
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Class III TOX
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Amiodarone: Pulmonary fibrosis, hepatotox, hypo/hyperthyroidism (amiodarone 40% iodine), corneal deposits, skin deposits (blue/gray) = photodermatitis, neurologic effects, constipation, cardio (brady, heart block, CHF)
Amiodarone has class I, II, III, IV effects bc it alters the lipid membrane CHECK PFTs, LFTs, and TFTs when using amiodarone Sotalol: Torsades, excessive B block Ibutilide: Torsades |
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Class IV
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Ca channel blockers (Verapamil, Diltiazem)
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Class IV MOA
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DEC conduction velocity
INC ERP (effective refractory period) INC PR interval |
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Class IV clinical use
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Preventing nodal arrythmias
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Class IV TOX
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Constipation
Flushing Edema CV (CHF, AV block, sinus node depression) |
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Other antiarrhythmics: Adenosine
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INC K out of cells-->hyperpolarize cell--> DEC I(ca)
DOC in diagnosing/abolishing SVT TOX: Flushing, hypotension, chest pain Effects blocked by THEOPHYLLINE and caffeine (Theophylline used in asthma: methylxanthine that causes bronchodilation by inhibiting phosphdiesterase--> DEC cAMP hydrolysis) |
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Other antiarrhythmics: Mg
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Torsades and digoxin toxcity
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