Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
62 Cards in this Set
- Front
- Back
|
Cardiology
|
[MOA/Clinical use/TOX]
|
|
|
Calcium Channel Blockers
|
Nefedipine, Verapamil, Diltiazem, Amlodipine
|
|
|
Ca Channel Blockers MOA
|
Block volume-dependent L-type Ca channels of cardiac and smooth muscle --> REDUCE contractility
-Vascular smooth muscle: Amlodipine -Heart: Verapamil |
|
|
Ca Channel Blockers clinical use
|
Hypertension, angina, arrhythmias (not nifedipine), prinzmetal angina, Raynaud's
|
|
|
Ca Channel blockers Tox
|
-Cardiac depression & AV block
-Peripheral edema -Flushing -Dizziness -Constipation |
|
|
Hydralazine MOA
|
INCREASE cGMP-->smooth muscle relaxation
Vasodilate arterioles>>veins = AFTERLOAD REDUCTION |
|
|
Hydralazine clinical use
|
First line therapy for hypertension in pregnancy (w/ methyldopa)
Frequently combined with B-blocker to prevent reflex tachycardia |
|
|
Hydralazine Tox
|
-Lupus-like syndrome
-Compensatory tachycardia (contra in angina/CAD) -Angina -Fluid retention, nausea, headache |
|
|
TX for malignant hypertension
|
Nitroprusside, Fenoldopam
|
|
|
Nitroprusside MOA
|
Short acting; INCREASE cGMP via direct release of NO
(can cause cyanide tox) |
|
|
Fenoldopam MOA
|
DA D1 receptor agonist--> coronary, peripheral, renal and splanchnic vasodilation
= DECREASE BP and INCREASE natriuresis |
|
|
Nitroglycerin, isosorbide dinatrate MOA
|
Vasodilate by releasing nitric oxide in sm mm, causing INCREASE in cGMP and sm mm relaxation.
Dilate veins >> arteries = DECREASE PRELOAD |
|
|
Nitroglycerin, isosorbide nitrate clinical use
|
Angina, pulmonary edema
|
|
|
Nitorglycerin, isosorbide nitrate TOX
|
-Reflex tachycardia & Hypotension
-Flushing & Headache -MONDAY DISEASE (tolerance during work week, loss of tolerance over wknd-->tachy, dizziness and headache upon reexposure) |
|
|
Goal of antianginal Therapy?
|
Goal: reduce myocardial O2 consumption (MVO2) by decreasing EDV, BP, HR, contractility, or ejection time
|
|
|
Effects of combination antianginal therapy (nitrates + B-blockers)
|
Greatly reduces: myocardial O2 consumption (MVO2)
Reduces: blood pressure, heart rate Has little-to-no effect on: EDV, contractility, and ejection time |
|
|
HMG-CoA reductase inhibitors
|
-statins
|
|
|
HMG-Coa reductase inhibitors MOA
|
Inhibit conversaion of HMG-CoA to mevalonate (a cholesterol precursor)
=decrease circulating cholesterol (LDL) |
|
|
HMG-CoA reuctase inhibitors TOX
|
Hepatotoxicity (if LFT > 3x, stop therapy)
Rhabdomyolysis |
|
|
Niacin (vit. B3) MOA
|
Inhibits lipolysis in adipose tissue; reduce hepatic VLDL secretion into circulation
Decreases LDL, Increases HDL |
|
|
Niacin Tox
|
-Red, flushed face (dec by aspirin)
-Hyperglycemia (acanthosis nigricans) -Hyperuricemia (exacerbates gout) |
|
|
Bile acid resins
|
Cholestyramine, colestipol, colesvelam
|
|
|
Bile acid resins MOA
|
Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
Decreases LDL, slightly increases HDL |
|
|
Bile acid resins TOX
|
-Tastes bad, causes GI discomfort
-Decreased absorption of fat-soluble vitamins (ADEK) -Cholesterol gallstones |
|
|
Cholesterol absorption blockers MOA
(Ezetimibe) |
Prevent cholesterol reabsortion at small intestine brush border
|
|
|
Ezetimibe TOX
|
Increases LFTs (rarely), diarrhea
|
|
|
Fibrates
|
Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate
|
|
|
Fibrates MOA
|
DECREASE Triglycerides
Upregulate LPL= INCREASE TG clearance |
|
|
Fibrates TOX
|
-Myositis
-hepatotoxicity (increases LFTs) -Cholesterol gallstones |
|
|
Cardiac glycosides
(Digoxin) |
-75% bioavaliabilty
-20-40% protein bound -t(1/2) = 40 hours URINARY EXCRETION |
|
|
Digoxin MOA
|
Direct inhibition of Na/K ATPase = indirect inhibition of Na/Ca exchanger/antiport
-Increases [Ca]--> positive inotropy (contractiliy) -stimulates vagus n. --> Decreases HR |
|
|
Digoxin clinical use
|
CHF (inc contractility)
A fib (DEC conduction at AV node and depresion of SA node) |
|
|
Digoxin TOX
|
-Cholinergic: N/V/D, BLURRY YELLOW VISION
-ECG: INC PR, DEC QT, ST scooping, T-wave INVERSION, arrythmia, AV block -hyperkalemia= POOR PROGNOSTIC INDICATOR |
|
|
Digoxin antidote
|
-Slowly normalize K
-Lidocaine -Cardiac pacer -Anti-digoxin Fab fragments -Mg2+ |
|
|
What factors predispose a patient to cardiac glycoside toxicity?
|
Renal failure, hypokalemia, quinidine (dec clearance; displaces digoxin from tissue binding sites)
|
|
|
Anti-Arryhthmics
|
Mnemonic: No Bad body keeps clean
Na+, B-blockers, K+, Ca2+ |
|
|
Class 1: Na channel blockers
|
-Slow or block conduction
-DEC slope of phase 0 -INC threshold for firing in abnormal pacemaker cells -Hyperkalemia causes INC tox for all class 1 drugs |
|
|
Class 1A drugs and MOA
|
Disopyramide, Quinidine, Procainamide
(Mneumonic: Double quarter pounder) INC AP duration and effective refractory period INC QT interval |
|
|
Class 1A clinical use
|
Re-entrant and ectopic supraventricular and ventricular tachycardia
Procainamide --> WPW |
|
|
Class 1A Tox
|
Disopyramide: heart failure
Quinide: cinchonism (headache, tinnitus) Procainamide (reversible SLE-like syndrome) All: Torsades de pointes due to INC QT interval |
|
|
Class 1B drugs and MOA
|
Lidocaine, Tocainide, Mexiletine
(Mneumonic: Lettuce, tomato, mayo) DEC AP duration |
|
|
Class 1B clinical use
|
Acute ventricular arrhythmias (especially POST- MI)
Digitalis-induced arrythmias |
|
|
Class 1B TOX
|
-Local anesthetic
-CNS stimulation/depression -Cardiovascular depression |
|
|
Class 1C
|
Flecainide, Propafenone
(Fries please) No effect on AP duration |
|
|
Class 1C clinical use
|
Last resort in refractory tachyarrythmias
useful in V-Tach that progress to VF |
|
|
Class 1C tox
|
contraindicated in structural heart disease and post-MI
|
|
|
Class II: B-Blockers
|
Metoprolol, Propranolol, Esmolol, Atenolol, Timolol
Esmolol is very short acting |
|
|
B-Blockers MOA
|
-Decreases SA and AV nodal activity by decreasing cAMP and Ca currents
-Suppress abnormal pacemakers by decreasing slope of phase 4 (takes longer time to reach threshold) -AV node particularly sensitive--INC PR interval |
|
|
B-Blockers clinical use
|
-V-Tach
-SVT -slowing ventricular rate during A FIB and A flutter |
|
|
B-Blockers TOX
|
-Impotence
-Cardio (Bradycardia, AV block, CHF); worsen ASTHMA -CNS (sedation, sleep alterations) -Mask hypoglycemia in diabetes; can cause dyslipidemia -Treat OD with GLUCAGON |
|
|
Class III K channel blockers
|
Amiodarone, Ibutilide, Dofetilide, Sotalol
(mnemonic AIDS) |
|
|
Class III MOA
|
Increases AP duration, ERP (effective refractory period) and QT interval
*Used when other anti-arrythmics fail |
|
|
Amiadorone toxicity?
|
-Pulmonary fibrosis & hepatotoxicity (check LFT)
-Thyroid problems (amiodarone 40% iodine) -corneal and skin deposits (blue/gray) = photodermatitis -Neurologic effects -Cardio (brady, heart block, CHF). |
|
|
What classes of antiarrhythmics can amiadarone be categorized as?
|
Amiodarone has class I, II, III, IV effects bc it alters the lipid membrane.
|
|
|
Sotalol toxicity?
|
Torsades de pointes, excessive beta-blockade
|
|
|
Ibutalide toxicity?
|
Torsades de pointes
|
|
|
Class IV
|
Ca channel blockers (Verapamil, Diltiazem)
|
|
|
Class IV MOA
|
Decreases conduction velocity
Increases ERP (effective refractory period) and PR interval |
|
|
Class IV clinical use
|
Preventing nodal arrythmias
|
|
|
Class IV TOX
|
Constipation
Flushing Edema CV (CHF, AV block, sinus node depression) |
|
|
Other antiarrhythmics: Adenosine
|
-Increases K out of cells-->hyperpolarize cell--> decreases calcium influx
-DOC in diagnosing/abolishing SVT -TOX: Flushing, hypotension, chest pain -Effects blocked by THEOPHYLLINE and caffeine |
|
|
Other antiarrhythmics: Mg
|
Effective in Torsades and digoxin toxcity
|
