Term
|
Definition
MOA - osmotic diuretic.
Use - shock, drug overdose, decrease intracranial/intraocular pressure |
|
|
Term
|
Definition
| Tox - pulmonary edema, dehydration, contraindicated in anuria, CHF |
|
|
Term
|
Definition
MOA - carbonic anhydrase inhibitor, causes HCO3 diuresis and reduction in total body HCO3. acts at proximal convoluted tubule.
Use - glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness |
|
|
Term
|
Definition
Hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
(ACIDazolamide causes ACIDosis) |
|
|
Term
|
Definition
MOA - sulfonamide loop diuretic. inhibits cotransport system (Na, K, Cl) of thick ascending loop of Henle. increase Ca excretion (Loops Lose calcium).
Use - edematous states, HTN, hypercalcemia |
|
|
Term
|
Definition
| OH DANG - Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout |
|
|
Term
|
Definition
MOA - phenoxyacetic acid derivative. same MOA as furosemide - inhibits cotransport system of thick ascending loop of Henle.
Use - diuresis in patients allergic to sulfa drugs |
|
|
Term
|
Definition
| similar to furosemide, but can be used in hyperuricemia |
|
|
Term
|
Definition
MOA - thiazide diuretic. inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron. decreased calcium excretion.
Use - HTN, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus |
|
|
Term
| Hydrochlorothiazide toxicity |
|
Definition
| hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia. sulfa allergy |
|
|
Term
|
Definition
| spironolactone, triamterene, amiloride, eplereone |
|
|
Term
| K+ sparing diuretic use and toxicity |
|
Definition
Use - Hyperaldosteronism, K+ depletion, CHF.
Toxicity - hyperkalemia, endocrine effects (gynecomastia, antiandrogen...) |
|
|
Term
|
Definition
| MOA - K+ sparing diuretic, competitive aldosterone receptor antagonist in the cortical collecting tubule |
|
|
Term
| Triamterene and Amiloride MOA |
|
Definition
| block Na+ channels in the CCT |
|
|
Term
|
Definition
MOA - increase cGMP leading to smooth muscle relaxation. vasodilates arteries more than veins. afterload reduction.
Use - severe HTN, CHF |
|
|
Term
|
Definition
| compensatory tachycardia, fluid retention, lupus-like syndrome |
|
|
Term
| Calcium channel blockers (3) |
|
Definition
| nifedipine, verapamil, diltiazem |
|
|
Term
| Calcium channel blocker MOA and Use |
|
Definition
MOA - block voltage dependent L type calcium channels of cardiac and smooth muscle thereby reducing contractility.
Use - HTN, angina, arrhythmias (not nifedipine. |
|
|
Term
| Calcium channel blocker order of activity on vascular smooth muscle |
|
Definition
| nifedipine > diltiazem > verapamil |
|
|
Term
| Calcium channel blocker order of activity on cardiac muscle |
|
Definition
| verapamil > diltiazem > nifedipine |
|
|
Term
|
Definition
| "prils" - captopril, enalapril, lisinopril |
|
|
Term
| ACE inhibitor MOA and use |
|
Definition
MOA - inhibit ACE, reducing levels of angiotensin II and preventing inactivation of bradykinin, a potent vasodilator. Renin release is increased due to loss of feedback inhibition.
Use - HTN, CHF, diabetic renal disease |
|
|
Term
|
Definition
| CAPTOPRIL - Cough, Angioedema, Proteinuria, Taste changes, hypOtention, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II. also hyperkalemia |
|
|
Term
|
Definition
| angiotensin II receptor antagonist. it is not an ACE inhibitor and does not cause cough. |
|
|
Term
| Nitroglycerin and Isosorbide dinitrate |
|
Definition
MOA - vasodilate by releasing NO in smooth muscle, causing increased cGMP and smooth muscle relaxation. it dilates veins >> arteries.
Use - angina, pulmonary edema. also used as an aphrodisiac and erection enhancer. |
|
|
Term
| Nitroglycerin and Isosorbide dinitrate toxicity |
|
Definition
| tachycardia, hypotension, headache, "Monday disease" in industrial exposure (development of tolerance in work week and loss of tolerance over weekend resulting in tachycardia, dizziness, and headache) |
|
|
Term
| Cardiac glycoside bioavailability, t 1/2, excretion |
|
Definition
| 75% bioavailability, 20-40% protein bound, t1/2 = 40 hours, urinary excretion. |
|
|
Term
| Digoxin MOA and effects on ECG |
|
Definition
| inhibits the Na/K ATPase causing increased intracellular Na, thus impeding the Na-Ca antiport causing increased intracellular Ca. leads to positive inotropy. On ECG - increased PR, decreased QT, scooping of ST segment, T-wave inversion. |
|
|
Term
|
Definition
Use - CHF to increase contractility, atrial fibrillation to decrease conduction at the AV node.
Toxicity - nausea, vomiting, diarrhea, blurry yellow vision, arrhythmia. Toxicities increase with renal failure, hypokalemia (potentiates drug's effects), and quinidine (decreases digoxin clearance; displaces digoxin from tissue binding sites). |
|
|
Term
|
Definition
| slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments |
|
|
Term
| Class IA antiarrhythmics (4) and MOA |
|
Definition
Quinidine, Amiodarone, Procainamide, Disopyramide.
MOA - inhibit fast Na channel by blocking activated Na channels. |
|
|
Term
| Class IA effects and toxicity |
|
Definition
effects - increased action potential duration, increased ERP, increased QT interval. affect both atrial and ventricular arrhythmias.
toxicity - Quinidine causes cinchonism (headache, tinnitus) thrombocytopenia, torsades de pointes due to prolonged QT. Procainamide causes reversible SLE-like syndrome |
|
|
Term
| Class IB antiarrhythmics (3) and MOA |
|
Definition
Lidocaine, Mexiletine, Tocainide.
MOA - inhibit both inactive and active Na channels. act preferentially on depolarized arrhythmogenic tissue |
|
|
Term
| Class IB effects and toxicity |
|
Definition
effects - affect ischemic or depolarized Purkinje and ventricular tissue. useful inacute ventricular arrhythmias (esp. post-MI) and in digitalis-induced arrhythmias.
Toxicity - local anesthetic. CNS stimulation/depression, cardiovascular depression. |
|
|
Term
| Class IC antiarrhythmics (3) and MOA |
|
Definition
Flecainide, Encainide, Propafenone.
MOA - inhibit fast Na channels. |
|
|
Term
|
Definition
effects - has no effect on AP duration. useful in V-tachs that progess to VF and also in intractable SVT. usually used only as a last resort in refractory tachyarrhythmias.
Toxicity - proarrhythmic, especially post-MI. *Contraindicated post-MI |
|
|
Term
| Class II antiarrhythmics and MOA |
|
Definition
| beta blockers. they decrease cAMP and decrease Ca++ currents. suppress abnormal pacemakers by decreased slope of phase 4. the AV node is particularly sensitive - increased PR interval. Esmolol is very short acting. |
|
|
Term
|
Definition
| impotence, exacerbation of asthma, cardiovascular effects (bradycardica, AV block, CHF), CNS effects (sedation, sleep alerations). May mask the signs of hypoglycemia. |
|
|
Term
| Class II antiarrhythmics and MOA |
|
Definition
Soltalol, Ibutilide, Bretylium, Amiodarone, Dofetilide.
MOA - block K+ channels |
|
|
Term
|
Definition
| increased AP duration, increased ERP. Used when other antiarrhythmics fail. increased QT. |
|
|
Term
|
Definition
| torsades de pointes, excessive beta block |
|
|
Term
|
Definition
| new arrhythmias, hypotension |
|
|
Term
|
Definition
pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF), hypothyroidism/hyperthyroidism.
*remember to check PFTs, LFTs, and TFTs when using amiodarone. |
|
|
Term
| Class IV antiarrhythmics and MOA |
|
Definition
| Verapamil, Diltiazem. MOA - Ca channel blockers. |
|
|
Term
|
Definition
| primarily affect AV nodal cells. decreased conduction velocity, increased ERP, increased PR interval. Used in prevention of nodal arrhythmias (eg. SVT) |
|
|
Term
|
Definition
| constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression) |
|
|
Term
|
Definition
| drug of choice in diagnosing/abolishing AV nodal arrhythmias |
|
|
Term
|
Definition
| depresses ectopic pacemakers, especially in digoxin toxicity |
|
|
Term
|
Definition
| effective in torsades de pointes and digoxin toxicity |
|
|
Term
| HMG-CoA reductase inhibitor effects and problems |
|
Definition
| large decrease in LDL, small increase in HDL, small decrease on triglycerides. Problems - expensive, reversible increased LFTs, myositis |
|
|
Term
| Niacin effects and problems |
|
Definition
| Inhibits release of VLDL into circulation. decreased LDL, increased HDL, decreased triglycerides. Problems - red,flushed fase, whichis decreased by aspirin or long term use. |
|
|
Term
| Bile acid resins, effects, and problems |
|
Definition
| Cholestyramine, Colestipol. inhibit absorption of bile acids from gut. decreases LDL, no effect on HDL, slightly increased triglycerides. Problems - patients hate it because it tastes bad and causes GI discomfort. |
|
|
Term
| Cholesterol absorption blocker, effects and problems |
|
Definition
| decreased LDL. no effect on HDL or triglycerides. Problem - rare increased LFTs. |
|
|
Term
| "Fibrates", effects, and problems |
|
Definition
| Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate. inhibit lipoprotein lipase. decreased LDL, increased HDL, greatly decreased triglycerides. Problems - myositis, increased LFTs |
|
|
