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Pharmacology > Renal/Cardio Drugs > Flashcards

Renal/Cardio Drugs Flashcards

1
Q

Treatment of acute decompensated CHF

A 
"LMNOP"
Lasix (furosemide)
Morphine
Nitrates
O2
Position (better to sit up)
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2
Q

Acute treatment of MI

A

“MONA”
Morphine, O2, Nitroglycerin, Aspirin
If w/in 6 hrs of ST elevation onset: fibrinolytic drugs (“-teplase”)
Heparin is also used for acute MI

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3
Q

Nesiritide (mechanism)

A

Recombinant form of B-type Natriuretic Peptide (BNP)

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4
Q

Nesiritide (use)

A

HF

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5
Q

Dihydropiridine and other “-dipine” (mechanism)

A 
Vasoselective CCB (blocks SLOW TYPE Ca2+ channels of vascular smooth muscles) -> the other CCBs work on L-type
Think of effects being similar to nitrates (as opposed to b-blockers)
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6
Q

Dihydropiridine and other “-dipine” (4 uses)

A

For vasospasm stuff (because work on SLOW TYPE Ca2+ channels, unlike fast L-type like the other CCBs) -> HTN, angina (CCB is DOC for Prinzmetal), Raynaud phenomenon, SAH (nimodipine only; prevents cerebral vasospasm)

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7
Q

Dihydropiridine and other “-dipine” (side effects)

A 
Reflex tachycardia (nifedipine), flushing
Hyperprolactinemia, edema
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8
Q

Diltiazem (mechanism)

A 
Nonselective CCB (blocks FAST voltage-dependent L-type Ca2+ channels of cardiac AND vascular smooth muscles)
Class IV antiarrhythmic: reduces conduction velocity, increases ERP and PR interval
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9
Q

Diltiazem (3 uses)

A

HTN, angina, A-fib/flutter

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10
Q

Diltiazem (side effects)

A

Flushing, gingival hyperplasia
Constipation, bradycardia, AV block
CI in CHF (potent negative inotropic effect)

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11
Q

Verapamil (mechanism)

A 
Nonselective CCB (blocks FAST voltage-dependent L-type Ca2+ channels of cardiac AND vascular smooth muscles)
Think of effects being similar to b-blockers for angina (as opposed to nitrates)
Class IV antiarrhythmic: reduces conduction velocity, increases ERP and PR interval
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12
Q

Verapamil (3 uses)

A

HTN, angina, A-fib/flutter

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13
Q

Verapamil (side effects)

A

Flushing, gingival hyperplasia
Constipation, bradycardia, AV block
CI in CHF (potent negative inotropic effect)
Fetal limb defects and fetal loss from decreased placental perfusion

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14
Q

Hydralazine (mechanism)

A

Increases cGMP -> SMC relaxation (arterioles > veins; so effect is mainly afterload reduction)

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15
Q

Hydralazine (2 uses)

A 
Severe HTN (first line for HTN in pregnancy with methyldopa)
CHF
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16
Q

Hydralazine (side effects)

A

Compensatory tachycardia (prevent by using b-blocker) -> contraindicated in angina/CAD
Lupus-like syndrome
Fluid retention, nausea, headache

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17
Q

Nitroprusside (mechanism)

A

Releases NO -> rapid reduction of SVR and BP

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18
Q

Nitroprusside (use)

A

HTN emergency

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19
Q

Nitroprusside (side effects)

A 
Cyanide toxicity (from metabolites) -> risk increases w/ renal insufficiency -> fix cyanide toxicity w/ sodium thiosulfate (sulfur is the functional part here b/c it helps liver rhodanase metab and detox cyanide to thiocyanate)
Hypotension, reflex tachycardia, acidosis
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20
Q

Fenoldopam (mechanism)

A

D1 agonist -> decreases BP and increases natriuresis

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21
Q

Fenoldopam (2 uses)

A

HTN emergency

Cardiogenic shock

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22
Q

Fenoldopam (side effects)

A

Increases IOP -> avoid in glaucoma

Reflex tachycardia, headache, flushing

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23
Q

Minoxidil (mechanism)

A

Opens K+ channels -> arteriolar dilation

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24
Q

Minoxidil (2 uses)

A

Mild-moderate HTN

Baldness

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25
Q

Minoxidil (side effects)

A

Hirsutism (hypertrichosis)

Refkex tachycardia, Na+ retention (so given with b-blocker and diuretic)

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26
Q

Nitroglycerine (mechanism)

A

Increases NO, relaxes veins (incl large veins) more than arteries so main effect is preload reduction (blood collects in venous system)

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27
Q

Nitroglycerine (3 uses)

A

Angina
Acute coronary syndrome
Pulm edema

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28
Q

Nitroglycerine (side effects)

A 
Monday disease
Reflex tachycardia (so use with b-blocker), hypotension, flushing, headache
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29
Q

Isosorbide dinitrate (mechanism)

A

Increases NO, relaxes veins more than arteries so main effect is preload reduction

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30
Q

Isosorbide dinitrate (3 uses)

A

Headache and cutaneous flushing!
Angina
Acute coronary syndrome
Pulm edema

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31
Q

Isosorbide dinitrate (side effects)

A 
Monday disease
Reflex tachycardia (so use with b-blocker), hypotension, flushing, headache
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32
Q

Diazoxide (mechanism)

A

Activates K+ channels -> fall in PVR and BP

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33
Q

Diazoxide (side effects)

A

Ischemia -> DONT use in ischemic heart disease

Hypouricemia, hyperglycemia, angina

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34
Q

“-statin” (side effects)

A

Hypatotoxicity (elevated LFTs), rhabdomyolysis (esp w/ fibrates and niacin)
Metabolized by P450 3A4 so don’t use w/ inhibitors or might get renal failure (from rhabdomyolysis)
If pt on P450 inhibitors, prescribe pravastatin! (only one not metab by P450)

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35
Q

Niacin (mechanism)

A

Reduces VLDL synthesis in liver

Inhibits lipolysis in adipose tissue

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36
Q

Niacin (use)

A

Lipid-lowering drug (low HDL as main indication)

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37
Q

Niacin (side effects)

A

Flushing (fixed with aspirin), hyperglycemia (thus acanthosis nigricans -> increase DM med), hyperuricemia (don’t use in gout), hepatitis
Vasodilatory effects potentiate effects of some ATN meds so decrease dose of HTN med to prevent postural hypotension

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38
Q

Cholestyramine, cholestipol, colesevelam (mechanism)

A

Bile acid resins (prevents intestinal reabsorption of bile acids so liver has to use cholesterol to make more)

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39
Q

Cholestyramine, cholestipol, colesevelam (use)

A

Lipid-lowering drug (high LDL as main indication)

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40
Q

Cholestyramine, cholestipol, colesevelam (side effects)

A

Tastes bad & GI discomfort so poor compliance
Cholesterol gallstones
Increases TG as a monotherapy (the only one that does this)
Lowers fat-soluble vitamin absorption -> esp vit K
If used in combination w/ statins, administer at least 4 hrs apart (otherwise will reduce statin absorption)
Binds warfarin and many other drugs in intestine -> decrease their therapeutic effects

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41
Q

Ezetimibe (mechanism)

A

Prevents cholesterol absorption from intestine

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42
Q

Ezetimibe (use)

A

Lipid-lowering drug (primarily used in conjunction w/ statin)
High LDL as main indication

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43
Q

Ezetimibe (side effects)

A

Rare elevation in LFTs, diarrhea, myopathy

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44
Q

Fibrates (gemfibrozil and other “-fibrate”) (mechanism)

A

Upregulates LPL –> lowers TG (main)

Activates PPAR-a (so considered a “transcription factor ligand”) –> HDL synthesis

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45
Q

Fibrates (gemfibrozil and other “-fibrate”) (use)

A

Lipid-lowering drug (high TG as main indication) -> primarily used to prevent pancreatitis in pts w/ very high TG

46
Q

Fibrates (gemfibrozil and other “-fibrate”) (side effects)

A

Myositis, hepatotoxicity, cholesterol gallstone (by suppressing cholesterol 7a-hydroxylase activity)

47
Q

Digoxin (mechanism)

A

Cardiac glycoside
Inhibits Na+/K+ ATPase –> indirectly inhibits Na+/Ca2+ antiport –> get more Ca2+ in cells from DECREASED Ca2+ EFFLUX and thus increases inotropy

48
Q

Digoxin (2 uses)

A

CHF

A-fib

49
Q

Digoxin (side effects)

A

Most concerning effect is fatal arrhythmia! (increasing intracellular Ca2+ causes DELAYED AFTERDEPOLARIZATION)
AV nodal blockade from increased para tone (thru its action on VAGUS nerve)
Cholinergic (+ blurry yellow VISION)
Hyperkalemia b/c digoxin and K+ competes w/ each other fro Na+/K+ ATPase (but don’t give calcium gluconate in digoxin toxicity!)
Don’t use w/ RENAL FAILURE or older ppl w/ decreased renal fx (excreted unchanged in kidney!), hypokalemia worsens toxicity
Verapamil, amiodarone, and quinidine (all antiarrhythmics) predispose to toxicity

50
Q

Digoxin (2 antidotes)

A

Mg2+, anti-digoxin Fab fragments

51
Q

Class IA antiarrhythmics (mechanism)

A 
"Double Quarter Pounder" -> Disopyramide, Quinidine, Procainamide
Class I antiarrhythmic: Na+ channel blocker (decreases slope of phase 0 depolarization), state-dependent (selective depression of tissue that's frequently depolarized)
Unlike other class I's, class IA also prolongs AP duration (longer QRS complex; the distance at base of AP graph is wider) -> why you get longer ERP (effective refractory period) and QT interval
52
Q

Class IA antiarrhythmics (use)

A

“Double Quarter Pounder” -> Disopyramide, Quinidine, Procainamide
First line for rhythm control of SVTs (A-fib/flutter)
Can use for BOTH SVTs and VT (esp re-entrant and ectopic SVT and VT)

53
Q

Class IA antiarrhythmics (side effects)

A

“Double Quarter Pounder” -> Disopyramide, Quinidine, Procainamide
Quinidine: cinchonism (headache, tinnitus)
Procainamide: SLE-like syndrome (reversible)
Disopyramide: HF
All: Thrombocytopenia, TdP

54
Q

Class IB antiarrhythmics (mechanism)

A 
"Lettuce, Tomato, Mexican" -> Lidocaine, Tocanide, Mexiletine
Class I antiarrhythmic: Na+ channel blocker (decreases slope of phase 0 depolarization), state-dependent (selective depression of tissue that's frequently depolarized)
Unlike other class I's, class IB shortens AP duration (narrower QRS; the distance at base of AP graph is narrower) and prefers Purkinje and ventricular tissue
55
Q

Class IB antiarrhythmics (use)

A

“Lettuce, Tomato, Mexican” -> Lidocaine, Tocanide, Mexiletine
First line for rhythm control of VT (esp post-MI -> b/c lidocaine is very good at selectively depressing conduction in rapidly depol and these depol cells are found in ischemic myocardium)

56
Q

Class IB antiarrhythmics (side effects)

A

“Lettuce, Tomato, Mexican” -> Lidocaine, Tocanide, Mexiletine
CNS (stimulates and depresses), cardiovascular depression

57
Q

Class IC antiarrhythmics (mechanism)

A 
"More Fries, Please" -> Moricizine, Flecainide, Propafenone
Class I antiarrhythmic: Na+ channel blocker (decreases slope of phase 0 depolarization), state-dependent (selective depression of tissue that's frequently depolarized)
Unlike other class I's, class IC doesn't do anything to AP duration (so the distance at base of AP graph is the same as normal), but significantly prolongs ERP in AV node
58
Q

Class IC antiarrhythmics (use)

A 
"More Fries, Please" -> Moricizine, Flecainide, Propafenone
Refractory VT (second line after class IB failed)
59
Q

Class IC antiarrhythmics (side effects)

A

“More Fries, Please” -> Moricizine, Flecainide, Propafenone

Contraindicated post-MI, structural, and ischemic heart disease (proarrhythmic)

60
Q

Class II antiarrhythmics (mechanism and use)

A

B blockers: metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol
Decreases phase 4 slope in abnormal pacemaker, prolongs repolarization at AV node (so get LONGER PR INTERVAL) -> decrease cardiac work by slowing ventricular rate and decreasing afterload so good for stable HF too
Use: 2nd line for HR control for SVTs (A fib/flutter) and Vtach

61
Q

Class III antiarrhythmics (mechanism)

A 
SAID: Sotalol, Amiodarone, Ibutilide, Dofetilide
K+ channel blocker --> increases AP duration (base of AP graph is wider than normal), ERP, QT interval (so just like class IA but no depression of phase 0 slope)
Amiodarine also has class I, II, IV activity --> "antiarrhythmic shotgut"
62
Q

Class III antiarrhythmics (2 uses)

A

SAID: Sotalol, Amiodarone, Ibutilide, Dofetilide

First line for rhythm control of SVTs (A-fib/flutter) and Vtach (amiodarone and sotalol only)

63
Q

Amiodarone (side effects)

A

Class III antiarrhythmic
LESS RISK OF TdP THAN OTHER DRUGS THAT PROLONG QT
Pulm fibrosis (check PFTs) -> cause of death
Hepatotoxicity (check LFTs)
Hyper/hypothyroid (has iodine component; check TFTs)
Corneal deposits, photodermatitis (blue/grey skin deposits), neurologic, constipation, cardiovascular effects

64
Q

“-tilide” (side effect)

A

Class III antiarrhythmics: Ibutilide, Dofetilide

TdP

65
Q

Sotalol (side effects)

A

Class III antiarrhythmic
TdP
Excessive b blockade

66
Q

Adenosine (mechanism)

A

Increases K+ efflux –> hyperpolarization –> decreases Ca2+ current

67
Q

Adenosine (use)

A

DOC for dx/tx of SVT (very short acting)

68
Q

Adenosine (3 side effects)

A

Flushing
Hypotension, chest pain (from bronchospasm)
AV block
Effects interfered by theophylline and caffeine

69
Q

Mg2+ (2 uses)

A

Digoxin toxicity

TdP

70
Q

Mannitol (mechanism)

A

Osmotic diuresis (mainly at proximal tubule - site of major water permeability)

71
Q

Mannitol (3 uses)

A

Increased ICP
Increased IOP
Drug overdose

72
Q

Mannitol (side effects)

A

Major problem if anuria –> PULM EDEMA most worrisome (rapid rise in vol increases overall hydrostatic pressure in vasculature)
(so CI in anuria, CHF, preexisting pulm edema)

73
Q

Acetazolamide (mechanism)

A

CA inhibitor at proximal convoluted tubule (prevents HCO3- from being converted into CO2 so HCO3- gets excreted out with water)

74
Q

Acetazolamide (5 uses)

A

Metabolic alkalosis
Altitude sickness
Glaucoma (decreases aq humor synthesis from inhibiting CA -> need HCO3- to make aq humor)
Intracranial HTN (pseudotumor cerebri)
Altitude sickness (stimulates ventilation via metabolic acidosis)

75
Q

Acetazolamide (4 side effects)

A

Hyperchloremic metabolic acidosis (bicarb wasting -> but this actually worsens hypercalciuria by causing compensatory release of calcium phosphate from bone -> calcium stone formation)
Sulfa allergy
NH3 toxicity
Paresthesias & somnolence
No pupilary/vision changes like cholinomimetic glaucoma meds

76
Q

Furosemide (mechanism)

A 
Loop diuretics (most efficacious diuretics): inhibits NKCC2 receptors at thick asc limp of loop of Henle (normally takes Na+, K+, and 2Cl- into cells from lumen) --> so gets increased excretion of all those ions, also gets more Ca2+ excretion b/c of reduced lumen positive potential
Stimulates PGE release (vasodilatory on afferent arteriole) -> why inhibited by NSAIDs
77
Q

Furosemide (3 uses)

A

Edema
Moderate-severe HTN
Hypercalcemia
Works well for pts w/ renal insufficiency

78
Q

Furosemide (side effects)

A

“OH DANG”
Ototoxicity, Hypokalemia&Hypocalcemia (and thus hypercalciuria), Dehydration, Allergy to sulfa, Nephritis, Gout
Can increase creatinine (prerenal cause of renal insufficiency -> bc it reduces renal blood flow)
Loops Lose calcium

79
Q

Ethacrynic acid (mechanism)

A 
Loop diuretics (most efficacious diuretics): inhibits NKCC2 receptors at thick asc limp of loop of Henle (normally takes Na+, K+, and 2Cl- into cells from lumen) --> so gets increased excretion of all those ions, also gets more Ca2+ excretion b/c of reduced lumen positive potential
Stimulates PGE release (vasodilatory on afferent arteriole) -> why inhibited by NSAIDs
80
Q

Ethacrynic acid (3 uses)

A

Edema
Moderate-severe HTN
Hypercalcemia
Works well for pts w/ renal insufficiency & sulfa allergy

81
Q

Ethacrynic acid (side effects)

A

“OH DANG”
Ototoxicity (WORST out of all loop diuretics), Hypokalemia&Hypocalcemia (and thus hypercalciuria), Dehydration, Allergy to sulfa (DOESNT APPLY TO ETHACRYNIC ACID), Nephritis, Gout
Can increase creatinine (prerenal cause of renal insufficiency -> bc it reduces renal blood flow)
Loops Lose calcium

82
Q

Bumetanide (mechanism)

A 
Loop diuretics (most efficacious diuretics): inhibits NKCC2 receptors at thick asc limp of loop of Henle (normally takes Na+, K+, and 2Cl- into cells from lumen) --> so gets increased excretion of all those ions, also gets more Ca2+ excretion b/c of reduced lumen positive potential
Stimulates PGE release (vasodilatory on afferent arteriole) -> why inhibited by NSAIDs
83
Q

Bumetanide (3 uses)

A

Edema
Moderate-severe HTN
Hypercalcemia
Works well for pts w/ renal insufficiency

84
Q

Bumetanide (side effects)

A

“OH DANG”
Ototoxicity, Hypokalemia&Hypocalcemia (and thus hypercalciuria), Dehydration, Allergy to sulfa, Nephritis, Gout
Can increase creatinine (prerenal cause of renal insufficiency -> bc it reduces renal blood flow)
Loops Lose calcium

85
Q

HCTZ (mechanism)

A

Thiazide diuretics: inhibits NCC symporter in distal convoluted tubule (normally takes Na+ and Cl- into cells from lumen) –> so gets increased excretion of those ions, but gets more Ca2+ REABSORPTION (difference from loop diuretics)
Long-term effects on HTN is actually from decreased peripheral resistance tho

86
Q

HCTZ (5 uses)

A 
Mild-moderate HTN (first step anti-HTN)
Mild CHF
Nephrogenic DI (paradoxic antidiuretic effect)
Idiopathic hypercalciURIA
Osteoporosis
87
Q

HCTZ (side effects)

A

“hyperGLUC” –> hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia
Sulfa allergy, hypokalemic metabolic alkalosis, hyponatremia

88
Q

Metolazone (mechanism)

A

Thiazide diuretics: inhibits NCC symporter in distal convoluted tubule (normally takes Na+ and Cl- into cells from lumen) –> so gets increased excretion of those ions, but gets more Ca2+ REABSORPTION (difference from loop diuretics)
Long-term effects on HTN is actually from decreased peripheral resistance tho

89
Q

Metolazone (4 uses)

A

Mild-moderate HTN (first step anti-HTN)
Mild CHF
Nephrogenic DI
Idiopathic hypercalciURIA

90
Q

Metolazone (side effects)

A

“hyperGLUC” –> hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia
Sulfa allergy, hypokalemic metabolic alkalosis, hyponatremia

91
Q

Spironolactone and eplerenone (mechanism)

A

K+ sparing diuretics

Competitive agonist at aldosterone receptor (on blood side) in collecting tubule

92
Q

Spironolactone and eplerenone (4 uses)

A

w/ other more efficacious diuretics to prevent K+ wasting
CHF (increases survival by inhibiting aldos -> inhibits heart remodeling)
PCOS (anti androgen)
Hirsutism (anti androgen)

93
Q

Spironolactone and eplerenone (side effects)

A

Gynecomastia (spironolactone is antiandrogen)

Hyperkalemia (so avoid in renal failure)

94
Q

Triamterene and amiloride (mechanism)

A

K+ sparing diuretics

Directly blocks ENaC (normally brings Na+ from lumen into cells) in collecting tubule

95
Q

Triamterene and amiloride (2 uses)

A

w/ other more efficacious diuretics to prevent K+ wasting

Liddle syndrome

96
Q

Triamterene and amiloride (side effects)

A 
Hyperkalemia (so avoid in renal failure)
Megaloblastic anemia (triamterene)
Glucose intolerance in DM (amiloride)
Increased BUN (amiloride)
Leg cramps (triamerene)
97
Q

“-pril” (mechanism)

A

Blocks ACEi at the active site

Inhibits bradykinin degradation

98
Q

“-pril” (3 uses)

A

Mild-moderate HTN (1st line for diabetics and CHF w/ HTN -> improve mortality in CHF from inhibiting aldos -> inhibits remodeling)
HF
Diabetic renal disease

99
Q

“-pril” (side effects)

A 
"CAPTOPRIL": Cough, Angioedema (so CI in C1 esterase inhibitor deficiency), Proteinuria, Taste changes, hypOtension (on first dose), Pregnancy problems (fetal renal malformations -> Potter sequence), Rash, Increased renin, Lower Ang II
Also hyperkalemia (b/c it reduces aldosterone) esp when combined w/ K+ sparing diuretics and nonselective beta blockers
Avoid in bilateral renal artery stenosis b/c will further decrease GFR and precipitate renal failure
STOP drug if signs of angioedema
100
Q

Aliskiren (mechanism)

A

Renin inhibitor

101
Q

Aliskiren (side effects)

A

Don’t use if pregnant, hyperkalemia

Headache/diarrhea

102
Q

“-sartan” (side effect)

A

Fetal renal damage

Less cough than ACEi b/c doesn’t inhibit bradykinin degradation (so use in pts who can’t tolerate ACEi)

103
Q

“-rinone” (mechanism)

A

Inamrinone, Milrinone
Phosphodiesterase inhibitors –> increases cAMP –> increases Ca2+ flow into cardiac myocytes –> increases contractility and CO

104
Q

“-rinone” (use)

A

Acute exacerbation of HF (IV only)

105
Q

“-rinone” (side effect)

A

Arrhythmias

Vasodilation! (from increased cAMP) -> limited use in hypotensive pts

106
Q

Indapamide (mechanism)

A

Thiazide diuretics

107
Q

Iloprost (mechanism and 2 uses)

A 
PGI2 analog (longer HL)
For Raynaud's phenomenon (peripheral vascular diseases), MI
108
Q

Alprostadil (mechanism and 2 uses)

A

PGE1 analog

Used as vasolidator for neonates, erectile dysfx

109
Q

“-statin” (use)

A

Lipid-lowering drug (high LDL as main indication)

110
Q

Drugs for SVTs (A fib/flutter) and Vtach control

A

(Ignore V-fib because have to defib only, no medical management)
Control HR first! (meaning PR interval; think of affecting
pacemaker graph): so 1st line CCB (the fast type -> verapamil, diltiazam), 2nd line B-blocker, 3rd line digoxin
Then, control rhythm (meaning QRS complex; think of affecting ventricular AP graph): so 1st line for SVTs are IA and III; 1st line for Vtach are IB and III, 2nd line for Vtach is IC

111
Q

Omega-3 fatty acids (mechanism, use, and side effect)

A

Lower TG synthesis (but not as well as fibrates)
Antihyperlipidemic (high TG as main indication)
Side effect: nausea

112
Q

Magnesium sulfate (use)

A

Tx of TdP

Pharmacology (12 decks)

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