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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
ezetimibe side effects
rare inc. LFTs, diarrhea
26
fibrates main effect
lower TGs
27
fibrates MOA
upregulate LPL to inc. TG clearance | Activates PPAR-alpha to induce HDL synthesis
28
fibrates toxicity
myositis (inc. risk with concurrent statins), hepatotoxicity (inc. LFTs), chol. gallstones (esp. with concurrent bile acid resins)
29
cardiac glycosides MOA
direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger which increases ICF Ca. Also stimulates vagus nerve.
30
drug contraindications to digoxin
verapamil, amiodarone, quinidine (decrease digoxin cleraance; displaces digoxin from tissue-binding sites)
31
factors that predispose to digoxin toxicity
hypokalemia (because digoxin binds at K+ binding site) on Na/K ATPase
32
digoxin ECG
inc. PR, dec. QT, ST scooping, T-wave inversion, arrhthmia, AV block
33
digoxin toxicity
cholinergic with blurry yellow vision (Van Gogh eyes), hyperkalemia
34
digoxin antidote
slowly normalize K, cardiac pacer, anti-digoxin Fab fragment, Mg2+
35
Class I antiarrhythmics are ALL
Na+ channel blockers
36
Class II antiarrhythmics are ALL
Beta-blockers
37
Class III antiarrhythmics are ALL
K+ channel blockers
38
Class IV antiarrhythmics are ALL
CCBs
39
General Class I facts
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
Class I toxicity is induced by what
hyperkalemia inc. toxicity for all Class I drugs
41
What are the Class IA drugs
Quinidine, Procainamide, Disopyramide [The Queen Proclaims Diso's pyramid]
42
Class IA MOA
inc. Ap duration, inc. effective refractory period, inc. QT interval
43
Class IA clinical use
Artial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT
44
Class IA toxicities
Cinchonism: quinidine SLE-like: procainamide HF: disopyramide Thrombocytopenia, torsades from inc. QT
45
Class IB drugs names
Lidocaine, mexiletine (phenytoin also acts as IB)
46
Class IB MOA
dec. AP duration. affect ischemic or depolarized purkinje and ventricular tissue.
47
Class IB use
acute ventricular arrhthmias (especially post-MI), digitalis induced arrhthmias. [IB is Best post-MI]
48
Class IB toxicity
CNS stimulation/depression, CV depression
49
Class IC names
Flecainide, Propafenone "Can I have Fries, Please]
50
Class IC MOA
Significantly prolongs refractory period in AV node. | No effect on AP duration.
51
Class IC use
SVTs, including a. fib. Last resort in refractory VT.
52
Class IC toxicity
Proarrhythmic, especially post-MI. [IC is contraindicated in structural and ischemic heart disease]
53
How do the Class I drugs affect AP
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
Beta-blockers MOA
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
Beta-blockers use
SVT, slowing ventricular rate during a. fib and a. flutter (rate control)?
56
What is used for rhythm control???
?????
57
Beta-blockers toxicity
Metoprolol: dysplipidemia Propranolol: vasospasm in Prinzmetal's Cocaine users: risk of unpoopsed alpha receptor agonist activity
58
beta-blockers toxicity antidote
glucagon
59
beta-blockers AP graph
slow phase 4 depolarization of pacemaker cells and prolong repolarization
60
Class III names
Amiodarone, Ibutilide, Dofetilide, Sotalol [Class III gives you AIDS]
61
Class III MOA
inc. AP duration, inc. ERP. Last line of drugs used. Inc. QT interval.
62
Class III use
a. fib/flutter, ventricular tachy (amiodarone, sotalol)
63
Class III toxicities
Sotalol: torsades, excessive beta blockade ibutilide: torsades Amiodarone: a full list
64
Amiodarone toxicity
Pulm. fibrosis, hepatotoxicity, hypothyroid/hyperthyroid, corneal deposits, blue/gray skin deposits with photodermatitis, nerulogic effects, constipation, CV effects (brady, AV block, CHF)
65
Amiodarone labs to check and overarching effects
Check PFTs, LFTs, and TFTs when using it | It has Class I, II, III, and IV effects and alters the lipid membrane
66
Class IV names
Verapamil, diltiazem (v for ventricle)
67
Class IV MOA
dec. conduction velocity, inc. ERP, inc. PR
68
Class IV use
prevent nodal arrhythmias (SVT), rate control in a. fib
69
CCBs toxicity
constipation, flushing, edema, CV effects
70
CCBs AP graph
Slow rise of action potential and prolong repolarization at AV node
71
Adenosine MOA
inc. K+ out of cells to hyperpolarize the cell and dec. calcium current.
72
Adenosine toxicity
flushing, hypotension, CP.
73
How to block adenosine
theophylline and caffeine.
74
Mg2+ in CV medicine
Used in torsades and digoxin toxicity
75
Theophylline MOA
Adenosine antagonist and competitive nonselective phosphodiesterase inhibitor

Step 1 Pharmacology (17 decks)

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