Pharm Exam 2 Heart Drugs

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129 Terms

1
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what are the three factors responsible for hypertension?

cardiac output, peripheral resistance, blood volume

2
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what determines cardiac output?

stroke volume and heart rate

3
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what does increase blood volume do to BP?

increases it

4
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what affects blood volume?

fluid loss/retention

5
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what raises BP?

epinephrine and norepinephrine injections, antidiuertic hormone

6
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what is the primary homostatic mechanism for controlling BP?

renin-angiotensin-aldosterone system

7
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what is true of primary hypertension?

there is no identifiable cause

8
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what can cause secondary hypertension?

cushing’s, hyperthyroidism, chronic renal disease and certain drugs

9
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what does untreated hypertension affect?

the heart, brain, kidneys and retina

10
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what are some non-pharmacological methods to control hypertension?

limit alcohol intake, restrict sodium, reduce saturated fat and cholesterol, increase fruit and veg intake, increase aerobic physical activity, stop tobacco use, reduce stress and maintain a good weight

11
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what is the first line of defense for pharmacologic management for hypertension?

diuretics, ACE inhibitors, ARBs, direct renin inhibitors, calcium channel blockers

12
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what is the second line of defense for pharmacologic management for hypertension?

Beta-adrenegeric receptor blockers, alpha-1-adrenegric receptor, alpha-2-adrenergic agonists, direct-acting vasodilators, peripherally acting adrengic neuron blockers

13
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what is the main way diuretics work to manage hypertension?

increase urinary flow — increase excretion of water and sodium — reduces blood volume and cardiac workload

14
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what do diuretics reduce?

edema and pulmonary congestion

15
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what type of hypertension can diuretics manage?

mild to moderate

16
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what are the types of diuretics?

potassium-sparing, thiazide and thiazide-like, loop/high-ceiling

17
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what is crucial to monitor with diuretics?

renal function, electrolyte level, gout, blood glucose and BUN, sodium intake, weight loss, fatigue and muscle cramps

18
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non-potassium-sparing diuretics may cause what?

orthostatic hypotension and photosensitivity

19
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what needs to be evaluated when using non-potassium sparing diuretics for hypertension?

laboratory electrolyte values, potassium levels, daily weights

intake and output assessment of edema and signs of fluid overload

20
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what are side effects of non-potassium-sparing diuretics?

hypokalemia, hypomagnesemia, hypocalcemia

21
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what population are non-potassium-sparing diuretics contraindicated for?

pregnant and lactating women

those with history of gout or kidney stones

22
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what should be monitoring points for thiazide-like diuretics?

blood glucose and uric acid levels, potassium loss

23
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what conditions are contraindicated for use of thiazide-like diuretics?

pregnancy and lactation, systemic lupus and those using digoxin

24
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what needs to be monitored with loop diuretics?

severe potassium loss, hypokalemia, hypotension, hearing loss, glucose and uric acid levels

25
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what is the specific calcium channel blocker drug?

nifedipine

26
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what does nifedipine (calcium channel blocker) treat?

hypertension and other cardiovascular disease

27
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how does nifedipine calcium channel blocker work?

blocks calcium ion channels which causes vasodilation and decreases BP

28
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what conditions is nifediphrine used for?

HTN, angina and arrhythmias

29
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what are the adverse effects of nifedipine?

dizziness, edema, headache, flushing

30
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what do calcium channel blockers target?

some target channels in arterioles and other affect cardiac muscle

31
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what needs to be monitored in patients taking calcium channel blockers?

heart rate and BP

signs of heart failure and reflex tachycardia

history of heart dysrhythmias and pregnancy

32
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what should patients avoid when taking calcium channel blockers?

avoid drinking grapefruit juice

33
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what is the specific ACE inhibitor we talked about?

enalapril

34
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what does ACE stand for?

angitensin-converting-enzyme

35
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what do ACE inhibitors affect?

renin-angiotension system

36
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how do ACE inhibitors (enlalpril) work?

blocks the effects of angiotensin II (vasodilation occurs) — lowers peripheral resistance — decreases blood volume

37
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what are ACE (enlapril) used for?

HTN, HF and diabetic neuropathy

38
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what needs to be monitored with ACE inhibitors?

vitals, hypotension, angioedema, hypokalemia, cough, neutropenia, dizziness, light headedness

39
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when do ACE (enalapril) inhibitors need to be avoided?

during pregnancy category D

40
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what is the HTN beta-adrenegeic blocker discussed?

metoprolol

41
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what does metoprolol (beta blocker HTN) do?

decreases heart rate and contractility by blocking beta1 receptors in juxtaglomerular apparatus — inhibits secretion or renin — reduces cardiac output and lowers systemic BP

42
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what conditions is metoprolol (beta blocker) used for?

HTN, post MI and heart failure

43
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what is the mechanism of action for metoprolol?

block cardiac action of sympathetic nervous system to slow heart rate and BP, reducing workload of heart

44
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what type of effect does metroprolol have?

inotropic

45
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what are adverse effects of metoprolol?

fluid retention, worsening of heart failure, fatigue, hypotension, bradycardia,

46
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what needs to be monitored when taking metroprolol?

heart and glucose

47
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can you stop taking metoprolol abruptly?

no

48
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what else should be monitored with metoprolol (beta blocker)?

worsening symptoms, liver function/hepatic toxicity, blood pressure/pulse

49
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what do alpha-1 adrenergic antagonists (doxazosin) do?

block sympathetic receptors in arterioles

second line drug used in comb with diuretics

50
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what do alpha 2- adrenergic antagonists do?

decrease outflow of sympathetic nerve impulses from the CNS to heart and arterioles

51
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what are the monitoring points for alpha adrenergic antagonists?

vital signs

heart block and rebound hypertension

blood glucose for diabetics

52
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what direct vasodilators was discussed?

hydralazine

53
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what does hydralazine cause?

vasodilation by direct relaxation of arterial smooth muscle

54
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what are direct vasodilators only used for?

severe hypertension and hypertension crisis

55
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what are the serious adverse effects of hydralazine?

reflex tachycardia, sodium and fluid retention

56
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what are direct vasodilators contraindicated for?

Hypersensitivity, coronary artery disease
Rheumatic mitral valve disease, cerebrovascular disease
Renal insufficiency, systemic lupus erythematosus

57
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what are the monitoring points for direct vasodilators?

V/S, ECG and pulse ox

58
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direct vasodilators, specifically hydralazine, what can be an adverse effect?

lupus like syndrome

59
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what needs to be monitored with IV diazoxide (direct vasodilator)?

sodium and water output

60
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what needs to be monitored with use of minoxidil (Loniten) (direct vaso)?

orthostatic hypotension

61
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what can a nitroprusside IV (direct vaso) be used for?

hypertensive emergencies during labor and delivery to lower blood pressure instantaneously

62
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what is the drug choice ACE inhibitor for heart failure?

lisinoprill

63
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what does lisinopril do?

reduce afterload and increases cardiac output

64
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how does lisinopril work?

enhance excretion of sodium and water — lowers peripheral resistance and reduces blood volume — decreases BP

65
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in order to increase the survival of MI what are patients given?

captopril or lisinopril

66
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what are the adverse effects of lisinopril?

first does hypotension, cough, hyperkalemia, renal failure

67
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what needs to be monitored when taking lisinopril?

CBC, hypotension, impaired kidney function, hyperkalemia, autoimmune, sodium and potassium restrictions

68
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what should you not us with lisinopril?

other medications, OTCs, herbals and vitamins

69
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what are ARBs?

angiotensin 2 receptor blockers

70
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what do ARBs act similar to?

ACE inhibitors, block angiotension 2

71
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what are ARBs used for?

patients who are unable to tolerate adverse effects of ACE inhibitors

72
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what needs to be monitored in patients taking ARBs?

hyperkalemia, K+, renal function

73
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what type of drug is digoxin?

cardiac glycoside

74
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what does digoxin do?

increases force of heartbeat and slows heart rate

75
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what is the MOA for digoxin?

inhibt Na+/K+ ATPase and increase calcium

76
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what is digoxin used for?

heart failure and Afib to improve cardiac output

77
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what is the primary use of digoxin?

increase contractility or strength or myocardial contraction

78
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what are the adverse effects of digoxin?

neutropenia, dysrhythmias, digitalis toxicity = visual halos, arrhythmias

79
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what is true of digoxin?

second line treatment of HF and narrow therapeutic range

80
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what needs to be monitored with digoxin?

ventricular dysrhythmias, renal function, drug interactions, pulse rate, weigh gain and digoxin levels

81
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what can increase the risk of dogoxin toxcicity?

gensing

82
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what can decrease the affects of digoxin?

antidiarrheals and antacids

83
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what should patients taking digoxin eat?

foods high in potassium

84
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what type of drug is milrinone?

phosphodiestaerase inhibitor

85
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what is the mechanism of action for milrinone?

block enzyme phosphodiesterase in cardiac and smooth muscle which increases cAMP, calcium and contractility and cardiac output

86
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what does milrinone cause?

positive inotropic response and vasodialation

87
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what does milrinone increase and decrease?

increases contractility and decreases afterload

88
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what is milrinone used for?

short term therapy for acute HF

89
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what are the adverse effects of milrinone?

hypokalemia, hypotension, ventricular dysrhythmias

90
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what are the monitoring points and report points for milrinone?

hypotension, renal impairments, ventricular dysrhythmias, irregular or rapid heart rate, fever of 101 or higher or increase in chest pain

91
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what is coronary artery disease?

narrowing or occlusion of a coronary artery leading to myocardial ischemia, one of th eleading causes of death

92
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what is angina pectrois?

acute chest pain due to insufficent oxygen to myocardium

93
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what is stable angina?

fairly predictable frequency, intensity and duration, relieved by rest

94
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what is an unstable angina?

episodes occur more frequently, more intensly and during periods of rest

95
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what is vasospastic angina?

caused by spasms of coronary arteries

96
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what is silent angina?

occurs in absence of angina pain

97
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what are non-pharmacological management for angina?

lifestyle changes (tobacco, diet, booze, exercise)

percutaneous coronary intervention

coronary artery bypass graft for severe cases

98
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what is the goal of pharmacological intervention for angina?

to reduce intensity and frequency of episodes and improve exercise tolerance

99
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what are the two categories of pharmocalogic aids for angina?

those that terminate acute episodes and those that decrease frequency

100
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how do drugs for angina reduce myocardial demand?

slow heart rate, reduce preload, reduce contractility, lower blood pressure