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Pharmacology quiz 1 > Questions > Flashcards

Questions Flashcards

1
Q

JNC normal BP

A

< 120 and < 80

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1
Q

JNC PreHTN

A

120-139 or 80-89

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1
Q

JNC Stage 1 HTN

A

140-159 or 90-99

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2
Q

JNC Stage 2 HTN

A

>160 or >100

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3
Q

How should you treat stage 1 HTN?

A

Thiazide

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4
Q

How should you treat stage 2 HTN?

A

Thiazide + ACEi

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5
Q

What is target BP for HTN treatment?

A

< 140/90

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6
Q

Name risk factors associated with HTN

A

Male, smoker, glucose 102-125, obesity, FH, age (men > 65), dyslipidemia

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7
Q

How to treat african americans with HTN

A

CCB and diuretic

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8
Q

How to treat pregnant women with HTN

A

methyldopa, BB, vasodilators

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9
Q

How to treat children/adolescents with HTN

A

lower doses, same drugs as adults

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10
Q

JNC recommendations for combination choice

A

BP >20/10 above treatment goal, includes a diuretic, caution in elderly - combinations can mask side effects

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11
Q

How does hexamethonium work?

A

block Ach at nicotinic receptors at sympathetic and parasympathetic autonomic ganglia, reduce arteriolar and vasomotor tone, can paralyze you = DIE!

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12
Q

Name the effects of the ganglionic blockade

A

Sympathetic: arterioles and veins, Parasympathetic: heart, GI tract, bladder

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13
Q

How does reserpine work?

A

NT reuptake blockade - can lead to sedation, tremors - only used in 3rd world countries

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14
Q

How does guanethidine work?

A

inhibits NE release - can cause HOTN - GONE!

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15
Q

What do alpha-1 receptors mediate?

A

vasoconstriction

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16
Q

What do Beta-1 receptors mediate?

A

tachycardia (BB work here)

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17
Q

What do Beta-2 receptors mediate?

A

vasodilation, bronchodilation

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18
Q

How can BP be affected by the SNS?

A

Blocking beta-1 receptors, blocking peripheral alpha-1 receptors, triggering central alpha-2 receptors

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19
Q

What happens after blocking beta-1 receptors?

A

reduce HR and renin release

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20
Q

What happens after blocking peripheral alpha-1 receptors?

A

vasodilation, decreased peripheral resistance

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21
Q

What happens when you trigger central aplhpa-2 receptors?

A

reduce sympathetic outflow of heart

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22
Q

How do BB work?

A

reduce renin, decrease beta-1 activation = decreased CO

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23
Q

Who do you use BB in?

A

younger pts, pts with cardiac disease

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24
Q

Are BB effective at primary prevention of HTN?

A

No

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25
Q

How are BB excreted/metabolized?

A

Renally (adjust if CrCl <35), Hepatic - first pass effect with oral drugs

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26
Q

What are side effects of BB?

A

can penetrate BBB - lethargy, confusion, nightmares, bradycardia, hypotension, AV conduction block, bronchoconstriction, hypoglycemia, increased LDL, decreased HDL

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27
Q

Name the 3 BB you need to know

A

Metoprolol ER (Lopressor), Carvedilol (Coreg), Nebivolol (Bystolic)

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28
Q

Name a non-selective BB

A

Propanolol

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29
Q

Name a selective BB

A

Metoprolol

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30
Q

Name a BB that aids in alpha-1 blockade

A

Labetolol. Carvedilol

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31
Q

Name a BB that will increase NO levels

A

Nebivolol

32
Q

What is the MOA for alpha blockers

A

reduce peripheral resistance

33
Q

What is the body’s response to HOTN?

A

increased HR, CO, fluid retention, reflex tacycardia

34
Q

ADR for alpha blockers

A

first dose syncope, peripheral edema, non-selective can cause urinary incontinence, HA, nasal congestion

35
Q

Who would use alpha-blockers?

A

younger pts

36
Q

What is the class drug for alpha blockers?

A

Doxazosin (cardura)

37
Q

What is an alternative use for alpha blockers?

A

BPH

38
Q

How do alpha stimulants work?

A

???

39
Q

What alpha stimulant can be used as a tablet or patch?

A

Clonidine - ADHD, psychosis, RLS, ulcerative colitis, tha shakes from addiction

40
Q

Side effects of alpha stimulants

A

dry mouth, bradycardia, orthostatic HOTN, sedation, abrupt withdrawal can cause HTN crisis

41
Q

Name the 3 alpha stimulants

A

Clonidine, Catapres TTS, methyldopa

42
Q

What is the MOA for direct vasodilators?

A

increase NO levels

43
Q

Side effects for direct vasodilators

A

the usual + pericarditis –> tamponade, increased O2 demand –> exacerbate angina, some sodium and water retention

44
Q

When can you prescribe a direct vasodilator?

A

when 3 anti-hypertensives including a diuretic have failed

45
Q

What are the direct vasodilators you need to know?

A

Minoxidil AKA rogaine, hydralazine

46
Q

How does hydralazine work?

A

open K channels causing increased NO

47
Q

Side effects of hydralazine

A

reflex tachycardia - give with BB, HA, lupus like syndrome, short half life so frequent dosing

48
Q

What is a hypertensive emergency?

A

>220/140

49
Q

What is a hypertensive urgency?

A

>180/110

50
Q

Which anti-hypertensive drug contains cyanide?

A

sodium nitroprusside

51
Q

What is target therapy for hypertensive emergency and urgency?

A

30% below their current number - reduced risk of stroke

52
Q

What are the effects of CCB?

A

vasodilation, decreased contractility

53
Q

What are the 3 classes of CCB?

A

Dihydropyridines, phenylalkylamines, benzothiazepine

54
Q

Name a drug from each class of CCB.

A

Dihydropyridine: Amlodipine, Nicardipine, Phenylalkylamine: Verapamine, Benzothiazepine: Diltiazem

55
Q

Name 2 CCBs that are once a day

A

Amlodipine, Felodipine

56
Q

Which CCB is shown to decrease mortality?

A

Amlodipine

57
Q

Which CCB is used to treat hypertensive emergency?

A

Nicardipine

58
Q

Which CCB most effects cardiac contractility?

A

verapamil

59
Q

Which CCB most effects HTN?

A

nicardipine

60
Q

Which CCB most effects both HTN and cardiac contractility?

A

Diltiazem

61
Q

Which CCBs have vasular side effects?

A

dihydropyridines (amlodipine)

62
Q

Which CCBs have side effects on cardiac contractility?

A

non-dyhydropyridines

63
Q

Can you use CCB in mild-moderate renal failure?

A

yes

64
Q

What is a major disadvantage of CCB?

A

many drug interactions: BB: additive effects, CYP3A4 inhibitors increase CCB

65
Q

What is the MOA of ACEi?

A

decreased AngII and increased bradykinin = vasodilation

66
Q

Which anti-hypertensive decreases NSAID effects?

A

ACEi - increased prostaglandins

67
Q

Name 3 ACEi

A

Lisinopril, Captopril, Ramipril

68
Q

T or F: decreased mortality is a class effect of ACEi

A

TRUE

69
Q

Who cannot use ACEi?

A

pregnant women, people with bilateral renal artery stenosis, previous angioedema

70
Q

Name a short acting ACEi

A

captopril

71
Q

Name 2 long-acting ACEi

A

Lisinopril, Ramipril

72
Q

Name an injectable ACEi

A

Enalaprilat

73
Q

Most common side effects of ACEi

A

cough, hyperkalemia, renal impairment

74
Q

What is the MOA of ARBs?

A

block AngII binding to receptors

75
Q

Name 2 ARBs

A

Losartan, valsartan

76
Q

What are advantages of ARBs?

A

once a day dosing, can treat diabetic nephropathy, less dry cough, can be interchanged for HTN or HF

77
Q

What are disadvantages of ARBs?

A

Bradykinin levels fall = less vasodilation, no injectable forms

78
Q

What is the MOA for renin antagonists?

A

Aliskiren has negative effects on renin, blocks angiotensinogen to AngI

79
Q

Who should use renin antagonsists?

A

patients who benefit from ACEi or ARBs and are now refractory

80
Q

Give 3 combination therapies for HTN

A

ACEi + thiazide, ARB + thiazide, ARB + CCB

Pharmacology quiz 1 (2 decks)

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