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Step 1 (Steffanie) > Cardio Pharm > Flashcards

Cardio Pharm Flashcards

1
Q

Where do dihydropyridine calcium channel blockers act?

A

On vascular smooth muscle

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2
Q

Where do non-dihydropyridine calcium channel blockers act?

A

On heart

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3
Q

Nimodipine use

A

Subarachnoid hemorrhage (prevents cerebral vasospasm)

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4
Q

Dihydropyridine clinical uses

A

HTN, angina, Raynaud phenomenon

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5
Q

Drugs used in hypertensive urgency or emergency

A

Nicardipine, Clevidipine, Fenoldopam, Labetalol, or Notroprusside

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6
Q

Non-dihydropyridine clinical uses

A

HTN, angina, atrial fibrillation/flutter

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7
Q

Adverse effects of non-dihydropyridines

A

Cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia

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8
Q

Adverse effects of dihydropyridines

A

Peripheral edema, flushing, dizziness

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9
Q

Mechanism of Hydralazine

A

Increase cGMP leading to smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction

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10
Q

Clinical uses of hydralazine

A

Severe HTN, HF,

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11
Q

Nitroprusside MOA

A

Increase cGMP via direct release of NO

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12
Q

MOA for Fenoldopam

A

Dopamine D1 receptor agonist - causes coronary, peripheral, renal, and splanchnic vasodilation. Decreases BP and increases natriuresis.

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13
Q

What are the adverse effects of nitrates?

A

Reflex tachycardia, hypotension, flushing, headache, “Monday disease”

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14
Q

When are nitrates contraindicated?

A

In right ventricular infarction

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15
Q

MOA for Ranolazine

A

Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. Does not affect HR or contractility

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16
Q

Clinical use of Ranolazine

A

Angina refractory to other medical therapies

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17
Q

Adverse effects of Ranolazine

A

Constipation, dizziness, headache, nausea, QT prolongation

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18
Q

MOA of Milrinone

A

Selective PDE-3 inhibitor.
In cardiomyocytes: Increase cAMP accumulation, leading to increase calcium influx, and increased inotropy and chronotropy.
In vascular smooth muscle: Increase cAMP accumulation, inhibition of MLCK activity, and general vasodilation

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19
Q

Adverse effects of Milrinone

A

Arrhythmias, hypotension

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20
Q

Name the HMG-CoA reductase inhibitors

A

Lovastatin, Pravastatin

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21
Q

MOA of Lovastatin, Pravastatin

A

Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor; decrease mortality in CAD patients

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22
Q

Adverse effects of HMG-CoA reductase inhibitors

A

Hepatotoxicity (increase LFTs), myopathy (when used with fibrates or niacin)

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23
Q

Name the bile acid resins

A

Cholestyramine, colestipol, colesevelam

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24
Q

MOA for bile acid resins

A

Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

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25
Q

MOA of Ezetimibe

A

Prevent cholesterol absorption at small intestine brush border

26
Q

MOA of Fibrates

A

Upregulate LPL leading to increased triglyceride clearance. Activates PPAR-alpha to induce HDL synthesis.

27
Q

Adverse effects of fibrates

A

Myopathy (increased risk with statins), cholesterol gallstones (via inhibition of cholesterol 7alpha-hydroxlase)

28
Q

MOA of Niacin

A

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

29
Q

Adverse effects of Niacin

A

Red, flushed face; hyperglycemia, hyperuricemia

30
Q

Name the PCSK9 inhibitors

A

Alirocumab, evolocumab

31
Q

MOA of PCSK9 inhibitors

A

Inactivation of LDL-receptor degradation, increasing amount of LDL removed from bloodstream

32
Q

Adverse effects of PCSK9 inhibitors

A

Myalgias, delirium, dementia, other neurocognitive effects

33
Q

MOA of Digoxin

A

Direct inhibition of Na+/K+ ATPase, leading to indirect inhibition of Na+/Ca2+ exchanger. Increased Ca2+ leads to positive inotropy. Also stimulates the vagus nerve leading to decreased HR.

34
Q

Clinical uses of Digoxin

A

HF (increase contractility); atrial fibrillation (decrease conduction at AV node and depression of SA node)

35
Q

Adverse effects of Digoxin

A

Cholinergic, hyperkalemia

36
Q

Antidote for Digoxin

A

Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

37
Q

Quinidine, Procainamide, Disopyramide are in which class of drugs?

A

Class 1A Antiarrhythmics

38
Q

MOA of class 1A antiarrhythmics

A

Increase AP duration, increase effective refractory period, increase QT interval, some potassium channel blocking effects

39
Q

Adverse effects of class 1A antiarrhythmics?

A

Cinchonism, reversible SLE-like syndrome, HF, thrombocytopenia, torsades de pointes

40
Q

Lidocaine, Mexiletine are in which class of drugs?

A

Class 1B Antiarrhythmics

41
Q

MOA of class 1B antiarrhythmics

A

Decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue

42
Q

Flecainide, Propafenone are in which class of drugs?

A

Class 1C Antiarrhythmics

43
Q

MOA of class 1C antiarrythmics

A

Prolongs ERP in AV node and accessory bypass tracts

44
Q

Adverse effects of class 1C antiarrhythmics

A

Pro-arrythmic, especially post MI

45
Q

What kind of drugs are class II antiarrhythmics?

A

Beta blockers

46
Q

MOA of class II antiarrythmics

A

Decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents. Suppress abnormal pacemakers by decreasing the slope of phase 4. Increase PR interval.

47
Q

How is beta blocker overdose treated?

A

With saline, atropine, glucagon

48
Q

What kind of drugs are class III antiarrhythmics?

A

Potassium channel blockers

49
Q

Amiodarone, Ibutilide, Dofetilide, Sotalol

A

Class III antiarrhythmics

50
Q

MOA of class III antiarrythmics

A

Increase AP duration, increase ERP, increase QT interval

51
Q

What is an adverse affect of class III antiarrythmics

A

Torsades de pointes

52
Q

Adverse effects of Amiodarone

A

Pulmonary fibrosis, hepatotoxicity, hypothyroidism or hyperthyroidism, acts as hapten, neurologic effects, constipation, cardiovascular effects

53
Q

What type of drugs are class IV antiarrhythmics?

A

Calcium channel blockers

54
Q

Verapamil, Diltiazem

A

Class IV antiarrhythmics

55
Q

MOA of class IV antiarrhythmics

A

Decrease conduction velocity, increase ERP, increase PR interval

56
Q

Adverse effects of class IV antiarrhythmics

A

Constipation, flushing, edema, cardiovascular effects

57
Q

Adenosine MOA

A

Increase K+ out of cells leading to hyperpolarization of the cell and decreased Ca2+ influx, decreasing AV node conduction

58
Q

Adverse effects of Adenosine

A

Flushing, hypotension, chest pain, sense of impending doom, bronchospasm

59
Q

How are torsades de pointes and digoxin toxicity treated?

A

Mg2+

60
Q

MOA of Ivabradine

A

Selective inhibition of funny sodium channels, prolonging slow depolarization phase (phase 4). Decreased SA node firing; negative chronotropic effect without inotropy. Reduces cardiac O2 requirement.

61
Q

When is Ivabradine used?

A

Chronic stable angina in pts who can’t take beta blockers. Chronic HF with reduced EF

Step 1 (Steffanie) (21 decks)

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