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Cardio Step 1 > Pharmacology Part 1 > Flashcards

Pharmacology Part 1 Flashcards

1
Q

What is the therapy for essential hypertension?

A
  • Diuretics
  • ACE I
  • ARB
  • CCB
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2
Q

What is the therapy for CHF?

A
  • Diuretics
  • ACE I
  • ARB
  • Beta Blocker (compensated CHF)
  • K+ sparing diuretics
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3
Q

Beta blockers must be used cautiously in __________ and are contraindicated in ________

A

decompensated CHF, cardiogenic shock

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4
Q

What is the therapy for Diabetes Mellitus?

A
  • Diruetics
  • ACE I
  • ARB
  • CCB
  • Beta Blocker
  • Alpha Blocker
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5
Q

ACE Inhibitors are protective against what?

A

Diabetic nephropathy

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6
Q

What are the CCBs?

A

Nifedipine, verapamil, diltiazem, amlodipine

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7
Q

What is the mechanism of CCBs

A

Block voltage dependent L-type Ca Channels of Cardiac and smooth muscle and therby reduce muscle contractility

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8
Q

Name the order of Vascular smooth muscle CCBs

A

AND Vascular

A=N>D>V

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9
Q

Name the order of heart CCBs

A

AND Vascular backwards

V>D>N=A

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10
Q

What are the clinical uses of CCBs?

A 
Hypertension
Angina
Arrythmia (not nifedipine)
Prinzmetal's angina
Raynauds
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11
Q

What is the side effects of CCBs?

A 
Cardiac depression
AV block
peripheral edema
flushing
dizziness
constipation
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12
Q

What is the mechanism behind hydralazine?

A

Increased cGMP causes smooth muscle relaxation

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13
Q

Hydralazine vasodilates ______>_______ and thus causes _______ reduction

A

arterioles, veins, afterload

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14
Q

Hydralazine is used for what?

A

Severe hypertension

CHF

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15
Q

hydralazine is the first line therapy for ___________ with _______

A

hypertension in pregnancy, methyldopa

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16
Q

Hydralazine is coadministered with a ________ to prevent _______

A

Beta blocker

reflex tachycardia

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17
Q

Hydralazine side effects are what?

A 
Compensatory tachycardia
Fluid retention
Nausea
headache
angina
lupus-like syndrome
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18
Q

hydralazine is contraindicated in what?

A

Angina/CAD

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19
Q

What are the most common used drugs in malifnant hypertension?

A 
Nitroprusside
nicardipine
clevidipine
labetalol
fenoldopam
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20
Q

What is the mechanism of nitroprusside? and is it short or long acting?

A

Short acting and increases cGMP via direct release of NO

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21
Q

Nitroprusside can cause what and why?

A

Cyanide toxicity because it releases cyanide

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22
Q

What is the mechanism of fenoldopam?

A

Dopamine D1 agonist

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23
Q

Fenoldopam causes vasodilation where?

A

Coronary
peripheral
renal
splanchnic

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24
Q

Fenoldopam decreases ________ and increases ________

A

Blood Pressure, Natiuresis

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25
Q

What is the mechanism of nitroglycerin and isosorbide dinitrate?

A

Vasodilate by releasing NO in smooth muscle causing increase in cGMP and smooth muscle relaxation

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26
Q

Nitroglycerin and isosorbide dinitrate dilate ____ more than ______ and decrease______

A

veins, arteries, preload

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27
Q

What is the clinical use of nitroglycerin and isosorbide dinitrate

A

Angina, Pulmonary edema

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28
Q

What is the toxicity of nitroglycerin and isosorbide dinitrate?

A

Reflex tachycardia, hypotension, flushing, headache

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29
Q

What is Monday disease?

A

development of tolerance for the vasodilating action of nitroglycerin and isosorbide dinitrate during the work week and loss of tolerance over the weekend

30
Q

What does Monday disease results in upon reexposure to nitroglycerin and isosorbide dinitrate?

A

Tachycardia
Dizziness
Headache

31
Q

What is the goal of anti-anginal therapy?

A

Reduction go MVO2 by decreasing 1 or more of the determinants of MVO2

32
Q

What are the determinants of MVO2?

A

EDV, BP, HR, Contractility, Ejection Time

33
Q

Name the effects of nitrates on EDV, BP, Contractility, HR, ET, and MVO2

A 
Decrease EDV
Decrease BP
Increase Contractility (reflex)
Increase HR (reflex)
Decrease ET
Decrease MVO2
34
Q

Name the effects of Beta Blockers on EDV, BP, Contractility, HR, ET, and MVO2

A 
Increase EDV
Decrease BP
Decrease Contractility
Decrease HR
Increase ET
Decrease MVO2
35
Q

What is the effect of Nitrates + Beta blockers on EDV, BP, Contractility, HR, ET, and MVO2

A 
No effect/decrease EDV
Decrease BP
Little/no effect contractility
Decrease HR
Little/no effect ET
Very decrease MVO2
36
Q

CCB ______ is similar to nitrates in effect

A

Nifedipine

37
Q

CCB _______ is similar to Beta blockers in effect

A

Verapamil

38
Q

What are 2 partial beta agonists contradindicated in angina?

A

Pindolol

Acebutolol

39
Q

What type of drugs are the statins?

A

HMG-CoA reductase inhibitors

40
Q

What is the mechanism of action of the HMG-CoA reductase inhibitors?

A

Inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)

41
Q

What are the side effects of HMG-CoA reductase inhibitors?

A

Hepatotoxicity (increase LFTs)

Rhabdomyolysis

42
Q

Name the effects of HMG-CoA reductase inhibitors on LDL, HDL, and TG

A

3 times decease LDL
1 times increase HDL
1 times decrease TG

43
Q

What is the mechanism of action of Niacin (vitamin B3)?

A

Inhibits lipolysis in adipose tissue

Reduces hepatic VLDL secretion into circulation

44
Q

What are the side effects of Niacin?

A

Red flushed face
hyperglycemia
hyperuricemia

45
Q

With niacin, the red flushed face is decreased by what two things?

A

Aspirin

long-term use

46
Q

How does the hyperglycemia caused by Niacin present?

A

Acanthosis Nigricans

47
Q

How does the hyperuricemia caused by Niacin present?

A

Exacerbates gout

48
Q

Name the effects on LDL, HDL, and TG of Niacin

A

2 times decreases LDL
2 times increases HDL
1 time decreases TG

49
Q

Name 3 Bile acid resings

A

Cholestyramine
Colestipol
Colesevelam

50
Q

What is the mechanism of action of Bile acid resins?

A

Prevent intestinal absorption of BA and liver must use cholesterol to make more

51
Q

What are the side effects of bile acid resins that makes patients hate it?

A
  • Tastes bad
  • GI discomfort
  • Decreased absorption of fat-soluble vitamins
  • Cholesterol gallstones
52
Q

Name the effects on LDL, HDL, and TG of bile acid resins

A

2 times decrease in LDL
slight 1 times increase in HDL
slight 1 times increase in TG

53
Q

Name one cholesterol absorption blocker

A

Ezetimibe

54
Q

What is the mechanism of cholesterol absorption blockers?

A

Prevent cholesterol reabsorption at small intestine brush border

55
Q

What are the side effects of cholesterol absorption blockers?

A

increase in LFTs (rare)

Diarrhea

56
Q

Name the effects on LDL, HDL, and TG of Cholesterol absorption blockers

A

2 times decrease in LDL

no effect in HDL or TG

57
Q

Name 4 fibrates

A

Gemfibrozil
Clofibrate
Bezafibrate
fenofibrate

58
Q

What is the mechanism of action of Fibrates?

A

Upregulate LPL to increase TG clearance

59
Q

What are the side effects of fibrates?

A

Myositis
Hepatotoxicity (increased LFTs)
cholesterol gallstones

60
Q

Name the effects on LDL, HDL, and TG of fibrates

A

1 times decrease LDL
1 times increase HDL
3 times decrease TG

61
Q

What is the bioavailability, protein bound percent, and half life of Digoxin?

A

75% bioavailable
20-40% protein bound
40 hours

62
Q

How is digoxin excreted?

A

Urine

63
Q

What are the mechanisms of digoxin?

A
  1. Direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger increasing intracellular Ca and having a positive ionotropic effect
  2. Stimulates vagus nerve and decreases HR
64
Q

What is the clinical use of Digoxin?

A

CHF

Atrial Fibrilation

65
Q

Why is digoxin used in CHF?

A

Incrases contractility

66
Q

Why is digoxin used in Atrial Fibrillation?

A

Decreases conduction at the AV node and depresses SA node

67
Q

What are the cholinergic side effects of Digoxin?

A

Nausea
Vomitting
Diarrhea
Blurry yellow vision

68
Q

What are the ECG toxicities of Digoxin?

A 
Increased PR
Decreased QT
ST scooping
T wave inversion
Arrhythmia
AV block
69
Q

What is another toxicities of Digoxin?

A

Hyperkalemia, a poor prognostic indicator

70
Q

What are the factors predisposing to toxicity of Digoxin and why?

A
  • Renal Failure (decreased excretion)
  • Hypokalemia (permissive for digoxin binding at K site of NaK ATPase)
  • Quinidine (decreased Digoxin clearance and replaces digoxin from tissue binding sites)
71
Q

What is the antidote for Digoxin toxicity?

A
  • Slowly normalize K
  • Lidocaine
  • Cardiac pacer
  • Anti-digoxin Fab Fragments
  • Mg2+

Cardio Step 1 (14 decks)

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