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Drugs > CV Drugs/Renal > Flashcards

CV Drugs/Renal Flashcards

1
Q

Nifedipine

A

1) HTN, angina, 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 -more vascular sm. muscle effects 3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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2
Q

Verapamil

A

1) HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s, nodal arrhythmias (SVT) 2)Anti-arrhythmics: Ca2+ Channel Blockers(Class IV)/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility -more heart effects – decrease conduction velocity, increase ERP and PR interval 3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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3
Q

Diltiazem

A

1) HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s, nodal arrhythmias (SVT) 2)Anti-arrhythmics: Ca2+ Channel Blockers (Class IV)/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility -more heart effects – decrease conduction velocity, increase ERP and PR interval 3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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4
Q

Amlodipine

A

1) HTN, angina, arrhythmias, 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 -more vascular smooth muscle effects 3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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5
Q

Hydralazine

A

1)Severe HTN (pregnancy), CHF, reflex tachycardia (w/ beta-blocker) 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

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5
Q

Hydrochlorothiazide

A

1) Use: HTN, CHF, idiopathic hypercalciuria, nephrogenic DI 2) Class/MOA: Inhibits NaCl reabsorption in early DCT, limiting diluting capacity. Decrease calcium excretion. 3) Side effects/ADEs: HyperGLUC (hyperglycemia, hyperlipidemia, hyperuricemia, hpercalcemia). Hypokalemic matabolic alkalosis, hyponatremia, sulfa allergy. 4) Fun Facts:

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6
Q

Nitroprusside

A

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

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7
Q

Fenoldopam

A

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

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8
Q

Nitroglycerin, isosorbide dinitrate

A

1)Angina, pulmonary edema 2)Vasodilator – release of NO in sm. muscle –> increases cGMP and sm muscle relaxation -dilates veins >> 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

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8
Q

Amiloride

A

1) Use: Hyperaldosteronism, K+ depletion, CHF 2) Class/MOA: K+ sparing diuretic. Triamterene and amiloride block Na channel in CCT. 3) Side effects/ADEs: Hyperkalemia (arrhythmias), endocrine effects (gynecomastia and other androgen effects) 4) Fun Facts: The K+ STAys (Spironolactone, triamterene, amiloride)

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9
Q

Lovastatin

A

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

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10
Q

Pravastatin

A

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

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10
Q

Enalapril

A

1) Use: HTN, CHF, diabetic renal disease, prevent heart remodeling from HTN 2) Class/MOA: Inhibit ACE to reduce angiotensin II/bradykinin and vasodilation. Renin release increases 3) Side effects/ADEs: CAPTOPRIL (Cough, Angioedema, Proteinuira, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower ATII) Hyperkalemia. Avoid with bilateral renal artery stenosis becauase ACE inhibitors reduce GFR. 4) Fun Facts: ATII receptor blockers (sartans) are similar to these without the cough.

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11
Q

Simvastatin

A

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

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12
Q

Atorvastatin

A

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

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13
Q

Rosuvastatin

A

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

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13
Q

What do all diuretics do to serum/urine K?

A

Increase urine K. Decrease serum K

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14
Q

Niacin (B3)

A

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, hyperglycemia (acanthosis nigrans), hyperuricemia (excerbates gout)

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15
Q

Cholestyramine

A

1)Lipid-lowering agents (decrease LDL, slightly increase TG and HDL 2)Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more) 3)Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones

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16
Q

Colestipol

A

1)Lipid-lowering agents (decrease LDL, slightly increase TG and HDL 2)Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more) 3)Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones

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17
Q

Colesevelam

A

1)Lipid-lowering agents (decrease LDL, slightly increase TG and HDL 2)Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more) 3)Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones

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18
Q

Ezetimibe

A

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

19
Q

Gemfibrozil

A

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

20
Q

Clofibrate

A

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

21
Q

Bezafibrate

A

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

22
Q

Fenofibrate

A

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

23
Q

Digoxin

A

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 -Factors predisposing to toxicity –> renal failure, hypokalemia, quinidine (decreases clearance) 4)Antidote –> slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab fragments, Mg2+

24
Q

Quinidine

A

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)Cinchonism – headache, tinnitus; thrombocytopenia, Torsades de Pointes (increased QT), hyperkalemia causes increased toxicity

25
Q

Procainamide

A

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)Reversible SLE-like syndrome, thrombocytopenia, Torsades de Pointes (increased QT),hyperkalemia causes increased toxicity

26
Q

Disopyramide

A

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)Heart failure, thrombocytopenia, Torsades de Pointes (increased QT), hyperkalemia causes increased toxicity

27
Q

Lidocaine

A

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

28
Q

Mexiletine

A

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

29
Q

Tocainide

A

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

30
Q

Flecainide

A

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

31
Q

Propafenone

A

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

32
Q

Metoprolol

A

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

33
Q

Propranolol

A

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 4)Exacerbate vasospasm in Prinzmetal’s angina

34
Q

Esmolol

A

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 4)Very short-acting

35
Q

Amiodarone

A

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)Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, corneal deposits, skin deposits (blue/grey) – cause photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF) – **check PFTs, LFTs, TFTs** 4) Has Class I, II, III and IV effects – alters the lipid membrane

36
Q

Ibutilide

A

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)Torsades de Pointes

37
Q

Dofetilide

A

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

38
Q

Sotalol

A

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)Torsades de Pointes, excessive beta-block

39
Q

Adenosine

A

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

40
Q

Mg2+

A

1)Torsades de Pointes, Digoxin toxicity

41
Q

Mannitol

A

1) Use: Shock, drug overdose 2) Class/MOA: Osmotic diuretic 3) Side effects/ADEs: Pulmonary edema, dehydration, CHF, contraindicated in anuria 4) Fun Facts:

42
Q

Acetazolamide

A

1) Use: Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness 2) Class/MOA: Carbonic anhydrase inhibitor, prevents bicarb reabsorption in PCT 3) Side effects/ADEs: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy 4) Fun Facts: ACIDazolamide causes ACIDosis

43
Q

Furosemide

A

1) Use: Edema (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia 2) Class/MOA: Loop diuretic. Inhibits cotransport system (Na, K, 2Cl) of thick ascnding limb, preventing solutes from entering medulla. Prevents concentration of urine. Stimulates PGE release for vasodilation. Increases calcium release. 3) Side effects/ADEs: OH DANG! (Ototoxicity, hypokalameia, dehydration, allergy-sulfa, nephritis, gout) 4) Fun Facts: Inhibited by NSAIDS

44
Q

Ethacrynic acid

A

1) Use: Diuresis for people with sulfa allergies 2) Class/MOA: Phenoxyacetic acid derivative. Inhibits Na, K, Cl cotransporter in ascending limb 3) Side effects/ADEs: OH DANG! (Same as furosemide) 4) Fun Facts: Same MOA as furosemide. Can be used in hyperuricemia

46
Q

Spironolactone

A

1) Use: Hyperaldosteronism, K+ depletion, CHF 2) Class/MOA: K+ sparing diuretic. Spironolactone is a competitive aldosterone receptor antagonist in cortical collecting duct. 3) Side effects/ADEs: Hyperkalemia (arrhythmias), endocrine effects (gynecomastia and other androgen effects) 4) Fun Facts: The K+ STAys (Spironolactone, triamterene, amiloride)

47
Q

Triamterene

A

1) Use: Hyperaldosteronism, K+ depletion, CHF 2) Class/MOA: K+ sparing diuretic. Triamterene and amiloride block Na channel in CCT. 3) Side effects/ADEs: Hyperkalemia (arrhythmias), endocrine effects (gynecomastia and other androgen effects) 4) Fun Facts: The K+ STAys (Spironolactone, triamterene, amiloride)

49
Q

Captopril

A

1) Use: HTN, CHF, diabetic renal disease, prevent heart remodeling from HTN 2) Class/MOA: Inhibit ACE to reduce angiotensin II/bradykinin and vasodilation. Renin release increases 3) Side effects/ADEs: CAPTOPRIL (Cough, Angioedema, Proteinuira, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower ATII) Hyperkalemia. Avoid with bilateral renal artery stenosis becauase ACE inhibitors reduce GFR. 4) Fun Facts: ATII receptor blockers (sartans) are similar to these without the cough.

51
Q

Lisinopril

A

1) Use: HTN, CHF, diabetic renal disease, prevent heart remodeling from HTN 2) Class/MOA: Inhibit ACE to reduce angiotensin II/bradykinin and vasodilation. Renin release increases 3) Side effects/ADEs: CAPTOPRIL (Cough, Angioedema, Proteinuira, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower ATII) Hyperkalemia. Avoid with bilateral renal artery stenosis becauase ACE inhibitors reduce GFR. 4) Fun Facts: ATII receptor blockers (sartans) are similar to these without the cough.

52
Q

What do all diuretics do to serum/urine NaCl?

A

Increase NaCl in urine. Decrease NaCl in serum

54
Q

What do all loop diuretics vs thiazides do to urine calcium?

A

Loop diuretics increase it. thiazides decrease it from enhanced paracellular calcium reabsorption in PCT and loop of henle.

Drugs (11 decks)

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