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Specialized Pharmacology MN650 > Blood Pressure Meds > Flashcards

Blood Pressure Meds Flashcards

1
Q

Calcium has what effect on the myocardium?

A

a. Positive inotropic effects

b. increases force of contraction

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2
Q

Calcium is what effect on the sinoatrial node?

A

a. Increases spontaneous discharge, increasing HR

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3
Q

Calcium has what effect on the AV node/?

A

a. Causes firing

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4
Q

What effect do calcium channel blockers have on the myocardium?

A

a. Negative entropic effects

b. decreases the force of contraction

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5
Q

What effect do calcium channel blockers have on the SA and AV node?

A

a. Decreases excitability of the SA node

b. slows conductivity through AV node

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6
Q

What effects do calcium channel blockers have on the heart?

A

a. Reduces the force of contraction
b. slows heart rate
c. suppresses conduction through AV node

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7
Q

Name the calcium channel blocker drugs?

A

a. Verapamil
b. diltiazem
c. nifedipine

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8
Q

What is verapamil’s mechanism of action?

A

a. blocks calcium channels in blood vessels and in the heart

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9
Q

What is diltiazem mechanism of action?

A

a. blocks calcium channels in blood vessels and in the heart

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10
Q

What is nifedipine mechanism of action?

A

a. Blocks calcium channels in blood vessels

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11
Q

What are the indications for verapamil use?

A

a. angina pectoris
b. hypertension
c. cardiac dysrhythmias

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12
Q

Where is verapamil metabolized and excreted?

A

a. metabolized and eliminated by the liver

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13
Q

What are verapamil’s onset and peak times?

A

a. Onset : 30 minutes

b. Peak: within five hours

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14
Q

What are verapamil’s adverse effects?

A

a. Constipation
b. partial or complete AV block
c. Flushing
d. dizziness
e. gingival hyperplasia
f. peripheral edema

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15
Q

What are the negative effects of combining digoxin and verapamil?

A

a. Increased risk of AV block

b. digoxin toxicity

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16
Q

Why does digoxin toxicity occur when combed with verapamil?

A

a. Verapamil increases digoxin plasma levels

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17
Q

What drugs should not be given in combination with verapamil?

A

a. Digoxin and beta blockers

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18
Q

How does grapefruit juice affect calcium channel blockers?

A

a. It inhibits intestinal and hepatic metabolism , increasing their plasma levels

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19
Q

How does nifedipine cause an increase heart rate in contractility?

A

a. the immediate release form causes a rapid drop in BP, stimulating the sympathetic nervous system

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20
Q

Where is nifedipine metabolized and created?

A

a. By the kidneys in the urine

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21
Q

What are the indications for nifedipine use?

A

a. angina pectoris

b. hypertension

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22
Q

What are nifedipines adverse effects?

A

a. Constipation
b. Flushing
c. dizziness
d. gingival hyperplasia
e. peripheral edema

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23
Q

How to prevent reflex tachycardia caused by nifedipine use?

A

a. Combine with beta blocker

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24
Q

Hydralazine causes dilation of what vessels?

A

a. Arterioles

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25
Q

Minoxidil causes dilation of what vessels?

A

a. Arterioles

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26
Q

Nitroprussides cause dilation of what vessels?

A

a. Arterioles and veins

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27
Q

Hydralazine onset and duration after oral administration?

A

a. Onset: 45 minutes

b. Duration: 6 hrs

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28
Q

Hydralazine onset and duration after IV administration?

A

a. Onset: within 10 minutes

b. Duration: 2-4 hrs

29
Q

How is hydralazine metabolized?

A

a. inactivated by a metabolic process known as acetylation

b. will be inactivated quicker in some than others

30
Q

What are the indications for hydralazine use?

A

a. Hypertension

b. short term tx of heart failure (reduces afterload)

31
Q

What are the adverse effects of Hydralazine?

A

a. Reflex tachycardia
b. increased blood volume
c. systemic lupus erythematosus like syndrome

32
Q

What are the symptoms of systemic lupus erythematosus like syndrome?

A

a. Muscle and joint pain
b. fever
c. pericarditis

33
Q

What is the indication for Minoxidil ues?

A

a. Severe HTN unresponsive to other drugs

34
Q

What is the definition of primary hypertension?

A

a. Hypertension with no identifiable cause

35
Q

Systolic BP of 130 - 139 or diastolic of 80 - 89 is what type of hypertension?

A

a. Stage one hypertension

36
Q

Systolic BP ≥ 140 or diastolic ≥ 90 is what type of hypertension?

A

a. Stage two hypertension

37
Q

What factors influence cardiac output?

A

a. Heart rate
b. myocardial contractility
c. blood volume
d. venous return

38
Q

What are the three blood pressure regulatory systems?

A

a. Sympathetic nervous system
b. renin angiotensin aldosterone system
c. the kidneys

39
Q

Where are baroreceptors located?

A

a. The aortic arch and carotid sinus

40
Q

Where is renin released from?

A

a. Juxtaglomerular cells in the kidneys

41
Q

What is the action of renin?

A

a. Converts angiotensinogen to angiotensin I

42
Q

Describe the RAAS step wise process?

A

a. Kidney senses high BP
b. Renin released from kidneys
c. Renin converts Angiotensinogen to angiotensin I
d. Angiotensin converted ACE to angiotensin II
e. Angiotensin trigges aldosterone release

43
Q

What are the triggers for renin release?

A

a. Reduced renal blood flow
b. Reduced blood volume
c. Reduced BP
d. Activation of B1 receptors on kidneys

44
Q

What are the actions of angiontensin II?

A

a. Vasoconstriction = inc BP

b. Triggers aldosterone release

45
Q

Where is aldosterone released from?

A

a. Adrenal cortex

46
Q

What are the actions of aldosterone?

A

a. Na retention, water follows

b. Increases BP

47
Q

Where and how does Clonidine act to lower BP?

A

a. Acts in the brain stem

b. Suppresses sympathetic outflow

48
Q

What are the CV effects of Clonidine?

A

a. Decreased HR
b. Decreased myocardial contractility
c. Decreased BP (vasodilation)

49
Q

What is the mechanism of action of propranolol?

A

a. Non-selective B-adrenergic agonist

50
Q

Where are beta1 receptors located?

A

a. Heart
b. Kidneys
c. Fat cells

51
Q

What occurs with B1 receptor activation in the heart?

A

a. Increases SA, AV and ventricular muscle firing

52
Q

What occurs with B1 receptor activation kidneys?

A

a. Renin release, activating the RAAS

53
Q

What occurs with B1 receptor activation in Fat Cells?

A

a. Upregulates lipolysis

54
Q

What is metoprolol MOA?

A

a. Selective Beta-1 blocker

55
Q

What is metoprolol brand name?

A

a. Lopressor

56
Q

What is prazosin MOA?

A

a. Postsynaptic Alpha-1 adrenergic blocker

57
Q

Where are Alpha-1 receptors located?

A

a. Vascular smooth muscle

58
Q

What does Alpha-1 receptor activation cause?

A

a. Vasoconstriction

59
Q

Where and how does hydralazine reduce BP?

A

a. Vascular smooth muscle causing vasodilation

60
Q

What is clonidine MOA?

A

a. Alpha-2 blocker

b. Works in brain stem

61
Q

What is the preferred drug class for the initial treatment of HTN for a patient without any CI’s to other drugs?

A

a. Thiazide diuretic (HCTZ)

b. Works in brain stem

62
Q

What is the preferred drug class for the initial treatment of HTN for a patient with Heart Failure?

A

a. Diuretic
b. B-Blocker
c. ACEi
d. ARB
e. Aldosterone antagonist

63
Q

What is the preferred drug class for the initial treatment of HTN for a post MI patient?

A

a. B-blocker
b. ACEi
c. Aldosterone antagonist

64
Q

What is the preferred drug class for the initial treatment of HTN for a patient with high risk coronary disease?

A

a. Diuretic
b. B-blocker
c. ACEi
d. CCB

65
Q

What is the preferred drug class for the initial treatment of HTN for a patient with diabetes?

A

a. Diuretic
b. B-blocker
c. ACEi
d. ARB
e. CCB

66
Q

What is the preferred drug class for the initial treatment of HTN for a patient with chronic kidney disease?

A

a. ACEi

b. ARB

67
Q

What is the preferred drug class for the initial treatment of HTN for the prevention of recurrent stroke?

A

a. Diuretic

b. ACEi

68
Q

Which type of diuretic should be used in a patient with renal insufficiency?

A

a. Loop diuretics

69
Q

What class of drug is enalapril?

A

a. ACEi

Specialized Pharmacology MN650 (28 decks)

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