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Step 1 Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

CCBs on vascular smooth muscle

A

amlopdipine=nifedipine>diltiazem>verapamil

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2
Q

CCBs on heart

A

verapamil>diltiazem>amlodipine=nifedipine

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3
Q

Strongest CCB on heart

A

verpamail [verapamil=ventricle]

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4
Q

CCB for SAH

A

nimodipine

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5
Q

Prinzmetal’s angina tx

A

dihydropyridine CCB (except nimodipine)

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6
Q

hydralazine MOA

A

increase cGMP to inc. smooth muscle relaxation, dilates arterioles>veins

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7
Q

hydralazine clinical use

A

First-line therapy for HTN in pregnancy with methyldopa, severe HTN

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8
Q

hydralazine toxicity

A

use beta-blocker to prevent reflex tachycardia.

fluid retention, lupus-like syndrome

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9
Q

CCB MOA

A

block voltage-dependent L-type calcium channels on cardiac and smooth muscle

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10
Q

Nitroprusside

A

Short acting; inc. cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide)

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11
Q

Fenoldopam

A

DA D1 receptor agonist: coronary, peripheral, renal, and splanchnic vasodilation. Dec. BP and inc. natriuresis.

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12
Q

Nitroglycerin, isosorbide dinitrate MOA

A

inc. NO in vascular smooth muscle leading to increase in cGMP and smooth muscle relaxation. Dilate veins»arteries, dec. preload

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13
Q

NTG, isosorbide clinical use

A

angina, ACS, pulm. edema

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14
Q

NTG, isosorbide toxicity

A

Reflex tachycardia (treat with beta-blockers), hypotension, flushing, HA, “monday disease” in industrial exposure

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15
Q

fact: nifedipine is similar to ntirates in effect; verapamil is similar to beta-blockers in effect

A

.

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16
Q

what beta-blockers contraindicated in angina

A

pindolol and acebutolol: partial beta-agonists

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17
Q

statins MOA

A

block HMG-CoA reduction to mevalonate

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18
Q

statins side effects

A

Hepatotoxicity (inc. LFTs), rhabdo (esp. with fibrate and niacin use)

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19
Q

niacin clinical effects

A

dec. ldl and inc. hdl a decent amount, slight dec. in TGs

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20
Q

niacin MOA

A

inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

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21
Q

niacin side effects

A

red, flushed face
Hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)

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22
Q

bile acid resins example

A

cholestyramine, colestipol, colesevelam

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23
Q

bile acid resin side effects

A

inc. TGs, tastes bad, GI discomfort, fat-soluble vitamin deficiencies, cholesterol gallstones

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24
Q

cholesterol absorption blocker name

A

Ezetimibe

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25
Q

ezetimibe side effects

A

rare inc. LFTs, diarrhea

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26
Q

fibrates main effect

A

lower TGs

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27
Q

fibrates MOA

A

upregulate LPL to inc. TG clearance

Activates PPAR-alpha to induce HDL synthesis

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28
Q

fibrates toxicity

A

myositis (inc. risk with concurrent statins), hepatotoxicity (inc. LFTs), chol. gallstones (esp. with concurrent bile acid resins)

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29
Q

cardiac glycosides MOA

A

direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger which increases ICF Ca.
Also stimulates vagus nerve.

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30
Q

drug contraindications to digoxin

A

verapamil, amiodarone, quinidine (decrease digoxin cleraance; displaces digoxin from tissue-binding sites)

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31
Q

factors that predispose to digoxin toxicity

A

hypokalemia (because digoxin binds at K+ binding site) on Na/K ATPase

32
Q

digoxin ECG

A

inc. PR, dec. QT, ST scooping, T-wave inversion, arrhthmia, AV block

33
Q

digoxin toxicity

A

cholinergic with blurry yellow vision (Van Gogh eyes), hyperkalemia

34
Q

digoxin antidote

A

slowly normalize K, cardiac pacer, anti-digoxin Fab fragment, Mg2+

35
Q

Class I antiarrhythmics are ALL

A

Na+ channel blockers

36
Q

Class II antiarrhythmics are ALL

A

Beta-blockers

37
Q

Class III antiarrhythmics are ALL

A

K+ channel blockers

38
Q

Class IV antiarrhythmics are ALL

A

CCBs

39
Q

General Class I facts

A

slow or block conduction especially in depolarized cells. Dec. slop of phase 0 depolarization and inc. threshold for firing in abnormal pacemaker cells. Are state dependent (depress tissue that is frequently depolarized)

40
Q

Class I toxicity is induced by what

A

hyperkalemia inc. toxicity for all Class I drugs

41
Q

What are the Class IA drugs

A

Quinidine, Procainamide, Disopyramide [The Queen Proclaims Diso’s pyramid]

42
Q

Class IA MOA

A

inc. Ap duration, inc. effective refractory period, inc. QT interval

43
Q

Class IA clinical use

A

Artial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

44
Q

Class IA toxicities

A

Cinchonism: quinidine
SLE-like: procainamide
HF: disopyramide
Thrombocytopenia, torsades from inc. QT

45
Q

Class IB drugs names

A

Lidocaine, mexiletine (phenytoin also acts as IB)

46
Q

Class IB MOA

A

dec. AP duration. affect ischemic or depolarized purkinje and ventricular tissue.

47
Q

Class IB use

A

acute ventricular arrhthmias (especially post-MI), digitalis induced arrhthmias. [IB is Best post-MI]

48
Q

Class IB toxicity

A

CNS stimulation/depression, CV depression

49
Q

Class IC names

A

Flecainide, Propafenone “Can I have Fries, Please]

50
Q

Class IC MOA

A

Significantly prolongs refractory period in AV node.

No effect on AP duration.

51
Q

Class IC use

A

SVTs, including a. fib. Last resort in refractory VT.

52
Q

Class IC toxicity

A

Proarrhythmic, especially post-MI. [IC is contraindicated in structural and ischemic heart disease]

53
Q

How do the Class I drugs affect AP

A

IA: prolongs it, medium phase 0 slope decrease
IB: shortens it, little phase 0 slope decrease
IC: no change, large phase 0 slope decrease (like a triangle)

54
Q

Beta-blockers MOA

A

decrease SA and AV nodal activity by dec. cAMP, dec. Ca2+ currents. Suppress abnormal pacemakers by dec. slop of phase 4.
AV node is sensitive, inc. PR interval.

55
Q

Beta-blockers use

A

SVT, slowing ventricular rate during a. fib and a. flutter (rate control)?

56
Q

What is used for rhythm control???

A

?????

57
Q

Beta-blockers toxicity

A

Metoprolol: dysplipidemia
Propranolol: vasospasm in Prinzmetal’s
Cocaine users: risk of unpoopsed alpha receptor agonist activity

58
Q

beta-blockers toxicity antidote

A

glucagon

59
Q

beta-blockers AP graph

A

slow phase 4 depolarization of pacemaker cells and prolong repolarization

60
Q

Class III names

A

Amiodarone, Ibutilide, Dofetilide, Sotalol [Class III gives you AIDS]

61
Q

Class III MOA

A

inc. AP duration, inc. ERP. Last line of drugs used. Inc. QT interval.

62
Q

Class III use

A

a. fib/flutter, ventricular tachy (amiodarone, sotalol)

63
Q

Class III toxicities

A

Sotalol: torsades, excessive beta blockade
ibutilide: torsades
Amiodarone: a full list

64
Q

Amiodarone toxicity

A

Pulm. fibrosis, hepatotoxicity, hypothyroid/hyperthyroid, corneal deposits, blue/gray skin deposits with photodermatitis, nerulogic effects, constipation, CV effects (brady, AV block, CHF)

65
Q

Amiodarone labs to check and overarching effects

A

Check PFTs, LFTs, and TFTs when using it

It has Class I, II, III, and IV effects and alters the lipid membrane

66
Q

Class IV names

A

Verapamil, diltiazem (v for ventricle)

67
Q

Class IV MOA

A

dec. conduction velocity, inc. ERP, inc. PR

68
Q

Class IV use

A

prevent nodal arrhythmias (SVT), rate control in a. fib

69
Q

CCBs toxicity

A

constipation, flushing, edema, CV effects

70
Q

CCBs AP graph

A

Slow rise of action potential and prolong repolarization at AV node

71
Q

Adenosine MOA

A

inc. K+ out of cells to hyperpolarize the cell and dec. calcium current.

72
Q

Adenosine toxicity

A

flushing, hypotension, CP.

73
Q

How to block adenosine

A

theophylline and caffeine.

74
Q

Mg2+ in CV medicine

A

Used in torsades and digoxin toxicity

75
Q

Theophylline MOA

A

Adenosine antagonist and competitive nonselective phosphodiesterase inhibitor

Step 1 Pharmacology (17 decks)

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