Cardio Drugs - CLASSES/MECHANISMS Flashcards

1
Q

Hydralazine

A

Increases cGMP → smooth muscle relaxation

(arterioles > veins)

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2
Q

Nitroprusside

A

Short acting

Increases cGMP via direct release of NO

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3
Q

Fenoldopam

A

D1 receptor agonist → coronary, peripheral, renal, and splanchnic vasodilation

Decreases BP

Increases natriuresis

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4
Q

Ranolazine

A

Inhibits the late phase of sodium current → reducing diastolic wall tension and oxygen consumption

Does NOT affect HR or contractility

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5
Q

Milrinone

A

Selective PDE-3 inhibitor

Cardiomyocytes: Increases cAMP → Inccreases calcium influx → increases inotropy/chronotropy

Vascular smooth muscle: Increases cAMP → inhibition of MLCK → general vasodilation

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6
Q

Cholestyramine

A
  • *Bile acid resin:** Prevent intestinal reabsorption of
  • *bile acids** → liver must use CH to make more
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7
Q

Colestipol

A
  • *Bile acid resin:** Prevent intestinal reabsorption of
  • *bile acids** → liver must use CH to make more
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8
Q

Colesevelam

A
  • *Bile acid resin:** Prevent intestinal reabsorption of
  • *bile acids** → liver must use CH to make more
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9
Q

Ezetimibe

A

Prevent cholesterol absorption at
small intestine brush border

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10
Q

Gemfibrozil

A

Upregulate LPL → increases TG clearance

Activates PPAR-alpha → HDL synthesis

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11
Q

Bezafibrate

A

Upregulate LPL → increases TG clearance

Activates PPAR-alpha → HDL synthesis

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12
Q

Fenofibrate

A

Upregulate LPL → increases TG clearance

Activates PPAR-alpha → HDL synthesis

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13
Q

Niacin

A

Inhibits lipolysis (hormone sensitive lipase) in adipose tissue → reduces hepatic VLDL synthesis

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14
Q

Alirocumab

A

Inactivation of LDL-receptor degradation → increases amount of LDL removed from bloodstream

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15
Q

Evolocumab

A

Inactivation of LDL-receptor degradation → increases amount of LDL removed from bloodstream

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16
Q

Quinidine

A

Class IA antiarrhythmic

Increase AP duration

Increase ERP

Increase QT interval

Some K+ channel blocking effects

17
Q

Procainamide

A

Class IA antiarrhythmic

Increase AP duration

Increase ERP

Increase QT interval

Some K+ channel blocking effects

18
Q

Disopyramide

A

Class IA antiarrhythmic

Increase AP duration

Increase ERP

Increase QT interval

Some K+ channel blocking effects

19
Q

Lidocaine

A

Class IB antiarrhythmic

Decrease AP duration

Preferentially affect ischemic or depolarized
Purkinje and ventricular tissue

20
Q

Mexiletine

A

Class IB antiarrhythmic

Decrease AP duration

Preferentially affect ischemic or depolarized
Purkinje and ventricular tissue

21
Q

(Phenytoin)

A

Class IB antiarrhythmic

Decrease AP duration

Preferentially affect ischemic or depolarized
Purkinje and ventricular tissue

22
Q

Flecainide

A

Class IC antiarrhythmic

Significantly prolongs ERP in AV node
and accessory bypass tracts

No effect on ERP in Purkinje and ventricular tissue

23
Q

Propafenone

A

Class IC antiarrhythmic

Significantly prolongs ERP in AV node
and accessory bypass tracts

No effect on ERP in Purkinje and ventricular tissue

24
Q

Beta-blockers

A

Class II antiarrhythmic

Decrease SA and AV nodal activity by
decreasing cAMP and calcium currents

Suppress abnormal pacemakers by
decreasing slope of phase 4

AV node particularly sensitive → increases PR interval

25
Amiodarone
**Class III antiarrhythmic: K+ channel blocker** Increase AP duration Increase ERP Increase QT interval
26
Ibutilide
**Class III antiarrhythmic: K+ channel blocker** Increase AP duration Increase ERP Increase QT interval
27
Dofetilide
**Class III antiarrhythmic: K+ channel blocker** Increase AP duration Increase ERP Increase QT interval
28
Sotalol
**Class III antiarrhythmic: K+ channel blocker** Increase AP duration Increase ERP Increase QT interval (also a beta-blocker)
29
Verapamil, Diltiazem
**Class IV antiarrhythmics: CCBs** Decrease conduction velocity Increase ERP Increase PR interval
30
Adenosine
Increase K+ efflux from cells → hyperpolarizing cell and decrease calcium influx (inhibits L-type calcium channels) → decreasing AV node conduction
31
Mg2+
Effective in torsades and digoxin toxicity
32
Ivabradine
Selective inhibition of funny sodium channels → prolonging slow depolarization phase (phase 4) Decreases SA node firing **Negative chronotropic** effect **without inotropy** Reduces cardiac O2 requirement