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Step 1 cardiology > Pharmacology > Flashcards

Pharmacology Flashcards

(59 cards)

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1
Q

Primary HTN tx

A

thiazide diuretics, ACE inhibitors, ARB, dihydropyridine Ca channel blockers

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2
Q

HTN w/ HF tx

A

diuretics, ACEI, ARBs, BB (compensated HF), aldosterone antagonists

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3
Q

what must be used cautiously in decompensated HF and are contraindicated in cardiogenic shock?

A

BB

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4
Q

HTN w/ DM

A

ACEI, ARBS, Ca channel blockers, thiazide diuretics, BB

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5
Q

what are protective against diabetic nephropathy?

A

ACEI, ARBs

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6
Q

HTN w/ pregnancy

A

hydralazine, labetalol, methyldopa, nifedipine

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7
Q

dihydropyridine Ca channel blockers

A

act on vasc SM

amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

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8
Q

non-dihydropyridine Ca channel blockers

A

act on heart

diltiazem, verapamil

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9
Q

Ca channel blocker MOA

A

block voltage-dependent L-type ca channels on cardiac and SM –> dec. muscle contractility

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10
Q

Ca channel blockers potency order on Vasc SM

A

amlodipine=nifedipine > diltiazem > verapamil

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11
Q

Ca channel blockers potency order on Heart

A

verapamil > diltiazem > amlodipine = nifedipine

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12
Q

dihydropyridines use

A

HTN, angina (incl. Prinzmetal), Raynaud’s

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13
Q

nimodipine use

A

subarachnoid heme (prevents cerebral vasospasm)

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14
Q

clevidipine use

A

HTN, angina, atrial fib/flutter

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15
Q

non-dihydropyridine ca channel blocker ADR

A

cardiac depression, AV block, hyperprolactinemia, constipation

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16
Q

dihydropyridine ca channel blocker ADR

A

peripheral edema, flushing, dizziness, gingival hyperplasia

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17
Q

Hydralazine MOA

A

inc cGMP –> smooth muscle relaxation.

vasodilates arterioles > veins

afterload reduction

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18
Q

Hydralazine use

A

acute severe HTN; HF (w/ organic nitrate)

Safe in pregnancy

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19
Q

Hydralazine codrug

A

BB to prevent reflex tachycardia

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20
Q

Hydralazine ADR

A

compensatory tachycardia, fluid retention, HA, angina, lupus-like syndrome

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21
Q

Hydralazine contraindications

A

pts with angina/CAD

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22
Q

HTN emergency

A

clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside

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23
Q

Nitroprusside MOA

A

short acting; inc cGMP via direct rls of NO

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24
Q

Nitroprusside toxicity

25
Fenoldopam MOA
D1 agonist, coronary, peripheral, renal, and splanchnic vasodilation dec. BP, inc. natriuresis PO anti-HTN
26
Fenoldopam ADR
hypotension, tachycardia
27
Nitrates list
nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
28
Nitrates MOA
vasodilate by inc NO in vasc SM --> inc in cGMP and SM relaxation. Dilates veins >> arteries. Dec preload
29
Nitrates use
angina, acute coronary syndrome, pulmonary edema
30
Nitrates ADR
reflex tachycardia (tx with BB), hypotension, flushing, HA , "Monday dx" in industrial exposure
31
Monday Disease
development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend --> tachycardia, dizziness, HA upon reexposure
32
antianginal therapy
goal is reduction of myocardial O2 consumption by dec 1 or more of the determinants of MVO2: end diastolic volume, BP, HR, contractility
33
Nitrates MVO2 effects
Decreased: end diastolic volume, BP, ejection time, No change: contractility Increased: HR (reflex response)
34
BB MVO2 effects
Decreased: BP, contractility, HR No change: end diastolic volume increased: ejection time
35
Nitrates+ BB MVO2 effects
greatly decreased: MVO2 decreased: BP no change: end diastolic volume, contractility, HR, ejection time
36
what partial B-agonists are contraindicated in angina/
pindolol and acebutolol
37
Ranolazine MOA
inhibits late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. doesn't affect HR or contractility
38
ranolazine use
angina refractory to other medical therapies
39
ranolazine ADR
constipation, dizziness, HA, nausea, QT prolongation
40
HMG-CoA reductase inhibitor MOA
inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor
41
HMG-CoA reductase inhibitor use
severe dec. in LDL, dec. in triglycerides increase in HDL dec mortality in CAD
42
HMG-CoA reductase inhibitor ADR
hepatotoxicity, myopathy (esp. when used w/ fibrates or niacin)
43
Bile acid resins MOA
cholestyramine, colestipol, colesevelam prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
44
Bile acid resins effect
moderate decrease in LDL, slight inc in HDL/triglycerides
45
Bile acid resins ADR
GI upset, dec absorption of other drugs and fat-soluble vitamins
46
Ezetimibe MOA
prevent cholesterol absorption at SI brush border
47
Ezetimibe effect
moderate dec in LDL; no change in HDL/trigylcerides
48
Ezetimibe ADR
rare inc in LFTs, diarrhea
49
Fibrates MOA
Gemfibrozil, Bezafibrate, fenofibrate upregulate LPL--> inc TG clearance activates PPAR-a to induce HDL synthesis
50
Fibrates effect
severe dec in triglycerides; dec LDL; inc in HDL
51
Fibrates ADR
myopathy (inc risk w/ statins); cholesterol gallstones
52
Niacin (vit B3) MOA
``` inhibits lipolysis (hormone-sensitive) in adipose tissue; reduces hepatic VLDL synthesis ```
53
Niacin ADR
red flushed face (tx w/ prophylactic NSAIDS) Hyperglycemia Hyperuricemia
54
Niacin effect
moderate dec in LDL moderate inc in HDL dec in triglycerides
55
Digoxin (cardiac glycoside) MOA
direct inhibition of Na/K ATPase --> indirect inhibition of Na/Ca exchanger. inc Ca --> positive inotropy. Stimulates vagus nerve --> dec HR
56
Digoxin use
``` HF (inc contractility) atrial fibrillation (dec conduction at AV node and depression of SA node) ```
57
Digoxin ADR
Cholinergic, blurry yellow vision, AV block
58
Factors predisposing to Digoxin toxicity
renal failure, hypokalemia, drugs that displace digoxin from tissue binding sites, dec clearance (verapamil, amiodarone, quinidine)
59
Digoxin antidotes
slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2

Step 1 cardiology (2 decks)

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