Renal/Cardio Drugs Flashcards
1
Q
Treatment of acute decompensated CHF
A
"LMNOP" Lasix (furosemide) Morphine Nitrates O2 Position (better to sit up)
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
3
Q
Nesiritide (mechanism)
A
Recombinant form of B-type Natriuretic Peptide (BNP)
4
Q
Nesiritide (use)
A
HF
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)
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)
7
Q
Dihydropiridine and other “-dipine” (side effects)
A
Reflex tachycardia (nifedipine), flushing Hyperprolactinemia, edema
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
9
Q
Diltiazem (3 uses)
A
HTN, angina, A-fib/flutter
10
Q
Diltiazem (side effects)
A
Flushing, gingival hyperplasia
Constipation, bradycardia, AV block
CI in CHF (potent negative inotropic effect)
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
12
Q
Verapamil (3 uses)
A
HTN, angina, A-fib/flutter
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
14
Q
Hydralazine (mechanism)
A
Increases cGMP -> SMC relaxation (arterioles > veins; so effect is mainly afterload reduction)
15
Q
Hydralazine (2 uses)
A
Severe HTN (first line for HTN in pregnancy with methyldopa) CHF
16
Q
Hydralazine (side effects)
A
Compensatory tachycardia (prevent by using b-blocker) -> contraindicated in angina/CAD
Lupus-like syndrome
Fluid retention, nausea, headache
17
Q
Nitroprusside (mechanism)
A
Releases NO -> rapid reduction of SVR and BP
18
Q
Nitroprusside (use)
A
HTN emergency
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
20
Q
Fenoldopam (mechanism)
A
D1 agonist -> decreases BP and increases natriuresis
21
Q
Fenoldopam (2 uses)
A
HTN emergency
Cardiogenic shock
22
Q
Fenoldopam (side effects)
A
Increases IOP -> avoid in glaucoma
Reflex tachycardia, headache, flushing
23
Q
Minoxidil (mechanism)
A
Opens K+ channels -> arteriolar dilation
24
Q
Minoxidil (2 uses)
A
Mild-moderate HTN
Baldness
25
Minoxidil (side effects)
Hirsutism (hypertrichosis)
| Refkex tachycardia, Na+ retention (so given with b-blocker and diuretic)
26
Nitroglycerine (mechanism)
Increases NO, relaxes veins (incl large veins) more than arteries so main effect is preload reduction (blood collects in venous system)
27
Nitroglycerine (3 uses)
Angina
Acute coronary syndrome
Pulm edema
28
Nitroglycerine (side effects)
```
Monday disease
Reflex tachycardia (so use with b-blocker), hypotension, flushing, headache
```
29
Isosorbide dinitrate (mechanism)
Increases NO, relaxes veins more than arteries so main effect is preload reduction
30
Isosorbide dinitrate (3 uses)
Headache and cutaneous flushing!
Angina
Acute coronary syndrome
Pulm edema
31
Isosorbide dinitrate (side effects)
```
Monday disease
Reflex tachycardia (so use with b-blocker), hypotension, flushing, headache
```
32
Diazoxide (mechanism)
Activates K+ channels -> fall in PVR and BP
33
Diazoxide (side effects)
Ischemia -> DONT use in ischemic heart disease
| Hypouricemia, hyperglycemia, angina
34
"-statin" (side effects)
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)
35
Niacin (mechanism)
Reduces VLDL synthesis in liver
| Inhibits lipolysis in adipose tissue
36
Niacin (use)
Lipid-lowering drug (low HDL as main indication)
37
Niacin (side effects)
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
38
Cholestyramine, cholestipol, colesevelam (mechanism)
Bile acid resins (prevents intestinal reabsorption of bile acids so liver has to use cholesterol to make more)
39
Cholestyramine, cholestipol, colesevelam (use)
Lipid-lowering drug (high LDL as main indication)
40
Cholestyramine, cholestipol, colesevelam (side effects)
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
41
Ezetimibe (mechanism)
Prevents cholesterol absorption from intestine
42
Ezetimibe (use)
Lipid-lowering drug (primarily used in conjunction w/ statin)
High LDL as main indication
43
Ezetimibe (side effects)
Rare elevation in LFTs, diarrhea, myopathy
44
Fibrates (gemfibrozil and other "-fibrate") (mechanism)
Upregulates LPL --> lowers TG (main)
| Activates PPAR-a (so considered a "transcription factor ligand") --> HDL synthesis
45
Fibrates (gemfibrozil and other "-fibrate") (use)
Lipid-lowering drug (high TG as main indication) -> primarily used to prevent pancreatitis in pts w/ very high TG
46
Fibrates (gemfibrozil and other "-fibrate") (side effects)
Myositis, hepatotoxicity, cholesterol gallstone (by suppressing cholesterol 7a-hydroxylase activity)
47
Digoxin (mechanism)
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
Digoxin (2 uses)
CHF
| A-fib
49
Digoxin (side effects)
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
Digoxin (2 antidotes)
Mg2+, anti-digoxin Fab fragments
51
Class IA antiarrhythmics (mechanism)
```
"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
Class IA antiarrhythmics (use)
"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
Class IA antiarrhythmics (side effects)
"Double Quarter Pounder" -> Disopyramide, Quinidine, Procainamide
Quinidine: cinchonism (headache, tinnitus)
Procainamide: SLE-like syndrome (reversible)
Disopyramide: HF
All: Thrombocytopenia, TdP
54
Class IB antiarrhythmics (mechanism)
```
"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
Class IB antiarrhythmics (use)
"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
Class IB antiarrhythmics (side effects)
"Lettuce, Tomato, Mexican" -> Lidocaine, Tocanide, Mexiletine
CNS (stimulates and depresses), cardiovascular depression
57
Class IC antiarrhythmics (mechanism)
```
"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
Class IC antiarrhythmics (use)
```
"More Fries, Please" -> Moricizine, Flecainide, Propafenone
Refractory VT (second line after class IB failed)
```
59
Class IC antiarrhythmics (side effects)
"More Fries, Please" -> Moricizine, Flecainide, Propafenone
| Contraindicated post-MI, structural, and ischemic heart disease (proarrhythmic)
60
Class II antiarrhythmics (mechanism and use)
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
Class III antiarrhythmics (mechanism)
```
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
Class III antiarrhythmics (2 uses)
SAID: Sotalol, Amiodarone, Ibutilide, Dofetilide
| First line for rhythm control of SVTs (A-fib/flutter) and Vtach (amiodarone and sotalol only)
63
Amiodarone (side effects)
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
"-tilide" (side effect)
Class III antiarrhythmics: Ibutilide, Dofetilide
| TdP
65
Sotalol (side effects)
Class III antiarrhythmic
TdP
Excessive b blockade
66
Adenosine (mechanism)
Increases K+ efflux --> hyperpolarization --> decreases Ca2+ current
67
Adenosine (use)
DOC for dx/tx of SVT (very short acting)
68
Adenosine (3 side effects)
Flushing
Hypotension, chest pain (from bronchospasm)
AV block
Effects interfered by theophylline and caffeine
69
Mg2+ (2 uses)
Digoxin toxicity
| TdP
70
Mannitol (mechanism)
Osmotic diuresis (mainly at proximal tubule - site of major water permeability)
71
Mannitol (3 uses)
Increased ICP
Increased IOP
Drug overdose
72
Mannitol (side effects)
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
Acetazolamide (mechanism)
CA inhibitor at proximal convoluted tubule (prevents HCO3- from being converted into CO2 so HCO3- gets excreted out with water)
74
Acetazolamide (5 uses)
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
Acetazolamide (4 side effects)
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
Furosemide (mechanism)
```
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
Furosemide (3 uses)
Edema
Moderate-severe HTN
Hypercalcemia
Works well for pts w/ renal insufficiency
78
Furosemide (side effects)
"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
Ethacrynic acid (mechanism)
```
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
Ethacrynic acid (3 uses)
Edema
Moderate-severe HTN
Hypercalcemia
Works well for pts w/ renal insufficiency & sulfa allergy
81
Ethacrynic acid (side effects)
"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
Bumetanide (mechanism)
```
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
Bumetanide (3 uses)
Edema
Moderate-severe HTN
Hypercalcemia
Works well for pts w/ renal insufficiency
84
Bumetanide (side effects)
"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
HCTZ (mechanism)
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
HCTZ (5 uses)
```
Mild-moderate HTN (first step anti-HTN)
Mild CHF
Nephrogenic DI (paradoxic antidiuretic effect)
Idiopathic hypercalciURIA
Osteoporosis
```
87
HCTZ (side effects)
"hyperGLUC" --> hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia
Sulfa allergy, hypokalemic metabolic alkalosis, hyponatremia
88
Metolazone (mechanism)
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
Metolazone (4 uses)
Mild-moderate HTN (first step anti-HTN)
Mild CHF
Nephrogenic DI
Idiopathic hypercalciURIA
90
Metolazone (side effects)
"hyperGLUC" --> hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia
Sulfa allergy, hypokalemic metabolic alkalosis, hyponatremia
91
Spironolactone and eplerenone (mechanism)
K+ sparing diuretics
| Competitive agonist at aldosterone receptor (on blood side) in collecting tubule
92
Spironolactone and eplerenone (4 uses)
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
Spironolactone and eplerenone (side effects)
Gynecomastia (spironolactone is antiandrogen)
| Hyperkalemia (so avoid in renal failure)
94
Triamterene and amiloride (mechanism)
K+ sparing diuretics
| Directly blocks ENaC (normally brings Na+ from lumen into cells) in collecting tubule
95
Triamterene and amiloride (2 uses)
w/ other more efficacious diuretics to prevent K+ wasting
| Liddle syndrome
96
Triamterene and amiloride (side effects)
```
Hyperkalemia (so avoid in renal failure)
Megaloblastic anemia (triamterene)
Glucose intolerance in DM (amiloride)
Increased BUN (amiloride)
Leg cramps (triamerene)
```
97
"-pril" (mechanism)
Blocks ACEi at the active site
| Inhibits bradykinin degradation
98
"-pril" (3 uses)
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
"-pril" (side effects)
```
"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
Aliskiren (mechanism)
Renin inhibitor
101
Aliskiren (side effects)
Don't use if pregnant, hyperkalemia
| Headache/diarrhea
102
"-sartan" (side effect)
Fetal renal damage
| Less cough than ACEi b/c doesn't inhibit bradykinin degradation (so use in pts who can't tolerate ACEi)
103
"-rinone" (mechanism)
Inamrinone, Milrinone
Phosphodiesterase inhibitors --> increases cAMP --> increases Ca2+ flow into cardiac myocytes --> increases contractility and CO
104
"-rinone" (use)
Acute exacerbation of HF (IV only)
105
"-rinone" (side effect)
Arrhythmias
| Vasodilation! (from increased cAMP) -> limited use in hypotensive pts
106
Indapamide (mechanism)
Thiazide diuretics
107
Iloprost (mechanism and 2 uses)
```
PGI2 analog (longer HL)
For Raynaud's phenomenon (peripheral vascular diseases), MI
```
108
Alprostadil (mechanism and 2 uses)
PGE1 analog
| Used as vasolidator for neonates, erectile dysfx
109
"-statin" (use)
Lipid-lowering drug (high LDL as main indication)
110
Drugs for SVTs (A fib/flutter) and Vtach control
(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
Omega-3 fatty acids (mechanism, use, and side effect)
Lower TG synthesis (but not as well as fibrates)
Antihyperlipidemic (high TG as main indication)
Side effect: nausea
112
Magnesium sulfate (use)
Tx of TdP
