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Hypertension Flashcards

1
Q

normal BP

A

<80

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2
Q

pre hypertension

A

120-139/80-89

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3
Q

stage I HTN

A

140-159/90-99

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4
Q

stage II HTN

A

> 160/>100

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5
Q

which drugs can cause secondary HTN

A

corticosteroids, anorexiants/decongestants, thyroid hormone excess, OCPs, NSAIDs/COX-2, occasionally TCA’s and venlafaxine, excessive licorice

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6
Q

goal BP- no diabetes, no kidney diseases

A

<140/90

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7
Q

goal BP- diabetes or kidney disease

A

<130/80

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8
Q

first choice patient with stage I HTN without compelling indications

A

Thiazide

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9
Q

first choice for patient with stage II HTN without compelling indications

A

2 drug combo: ACEI, ARB, BB, or CCB

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10
Q

first choice HTN tx pt has heart failure

A

ACEI plus BB

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11
Q

first choice HTN tx pt has CAD

A

ACEI plus BB

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12
Q

first choice HTN tx pt has diabetes

A

ACEI or ARB

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13
Q

first choice HTN tx pt has CKD

A

ACEI or ARB

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14
Q

first choice HTN tx pt has recurrent stroke

A

ACEI plus thiazide

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15
Q

first choice HTN tx pt has isolated systolic HTN

A

thiazide

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16
Q

what does excessive body sodium do in the body

A

increases vascular resistance (increases vessel rigidity, fluid retention, and epi and norepi release

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17
Q

this diuretic has a potent diuretic effect but low hypertensive effect

A

furosemide

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18
Q

this class inhibits luminal NaCl transport in the distal tubule of the kidney

A

thiazide

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19
Q

short term effects: sodium and water excretion (decreases plasma volume)

A

HCTZ

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20
Q

long term effects: decrease peripheral vascular resistance

A

HCTZ

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21
Q

this class loses efficacy as renal function declines, not generally used if creat clearance is <30 mL/min

A

thiazide diuretics

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22
Q

can use this class for HTN, CHF, nephrogenic diabetes insipidus, and to prevent kidney stones due to hypercalciuria

A

thiazide diuretics

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23
Q

Adverse effects: HYPOkalemia, hyperuricemia, hypomagnesemia, impaired carb tolerance, and HYPERglycemia

A

thiazide

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24
Q

this class changes urine ionic content: increases the loss of Na, K, and water

A

thiazide

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25
Q

adverse effects: hyperlipidemia, hyponatremia (our goal), allergies, weakness, fatigue, parasthesias, impotence, photosensitivity

A

thiazide

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26
Q

this drug is usually combined with loop diuretics for patients with HF who are refractory to loop diuretics alone (given 30 min before lasix)

A

metolazone

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27
Q

this drug requires close monitoring, can cause volume depletion and hypokalemia

A

metolazone

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28
Q

this class acts on the ascending LOH at the chloride pump (can potentially cause a 25-30% reduction in Na content of urine)

A

loops

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29
Q

this class is the most potent diuretic. can be used on pts with renal insufficiency that have failed thiazide

A

loops

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30
Q

this class can increase renal blood flow. Can relieve pulmonary congestion, decrease LV filling pressures before diuresis occurs

A

loops

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31
Q

class causes changes in urine ionic content: increases loss of Na, K ,water, and calcium

A

loops

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32
Q

this class is used for edema (heart failure), hypercalcemia, hyperkalemia, and acute renal failure

A

loops

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33
Q

adverse effects include: hyperuricemia, hyperglycemia, hypovolemia, hypotension, potassium and magnesium depletion, allergic reactions, and ototoxicity

A

loops

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34
Q

this drug is a synthetic steroid antagonist of aldosterone. It inhibits Na resorption and K secretion in collecting tubules

A

spironolactone

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35
Q

this drug is effective as an antiHTN, but limited use due to hyperkalemia

A

spironolactone

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36
Q

Can be used to treat primary and secondary aldosteronism. Also, it can blunt the potassium wasting tendencies of other diuretics

A

spironolactone

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37
Q

Adverse effects include gynocomastia, menstrual irregularities, hyperkalemia, and hyperchloremic metabolic acidosis

A

spironolactone

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38
Q

this drug directly inhibits sodium flux through the ion channels of the collecting tubule

A

triamterene

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39
Q

therapeutic uses: blunt K wasting tendencies of other diuretics, HTN. It is a weak diuretic alone, and is usually combined with thiazides

A

triamterene

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40
Q

adverse effects include hyperkalemia, hyperchloremic metabolic acidosis, and kidney stones

A

triamterene

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41
Q

all diuretics interact with this class of drug

A

NSAIDs

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42
Q

cholestyramine and sucralfate decrease the absorption of this diuretic

A

furosemide (loop)

43
Q

Drug interactions include ACE I, digoxin, and diabetic medications

A

loop and thiazide diuretics

44
Q

potassium sparing diuretics interact with this drug class

45
Q

this class blocks the conversion of angiotensin I to angiotensin II, resulting in vasodilation of vascular smooth muscle

46
Q

this class reduces PVR without a reflexive increase in CO, HR, or contractility

47
Q

this class stimulates the synthesis of vasodilatory prostaglandins. It decreases aldosterone, H20, and Na retention. Inhibits breakdown of bradykinin

48
Q

DO NOT USE in pregnancy or renovascular HTN

49
Q

Adverse effects: dry cough, altered taste, rashes, fever, hyperkalemia, elevations in SCr and BUN, hypotension and first dose syncope, and angioedema

50
Q

this class blocks the angiotensin II receptors competitively inhibiting angiotensin II binding to AT1 receptors. Blocks pressor and aldosterone-releasing effects causing vasodilation and decreased PVR

A

Angiotensin II antagonists

51
Q

this class inhibits angiotensin II generated from all pathways, but DO NOT stimulate the synthesis of vasodilatory compounds

52
Q

This class is indicated for HTN and CHF. It is renal protective in patients with DM and may be considered first line

53
Q

DO not use in pregnancy or renal artery stenosis

54
Q

ADRs: rash, altered taste, hyperkalemia, elevated SCr BUN

55
Q

this ARB reduces uric acid

56
Q

this class causes reduction in HR, contractility, BP, and suppresses sympathetic nervous system activity

A

Beta blockers

57
Q

therapeutic uses include ischemic heart disease, heart failure, dysrhythmias, and HTN

58
Q

this class of BB shows partial agonist activity- less reduction in resting HR, CO, and BP

A

intrinsic sympathomimetic activity (ISA)

59
Q

contraindications include severe asthma, severe bradycardia, heart block, and overt HF

60
Q

Adverse effects include fatigue, lethargy, insomnia, depression, bronchoconstriction, cold extremities, sexual dysfunction, decrease HDL increase LDL, bradycardia. Abrupt withdrawal may precipitate MI

61
Q

block the inward movement of Ca by binding to L-type calcium, resulting in smooth muscle relaxation and arteriolar dilation

62
Q

Therapeutic effects include coronary and peripheral vasodilation, negative inotropic and chronotropic effects. Alleviate coronary vasospasm

63
Q

Used in HTN, ischemic heart disease, and dysrhythmias

A

CCB (dysrhythmias are non-dihydropyridinies only)

64
Q

this drug is indicated for angina, HTN, supraventricular tachyarrhythmias, and migraines. Effects both cardiac and vascular smooth muscle

65
Q

this CCB effects cardiac and vascular smooth muscle but has less negative inotropic effects than verapamil, so fewer SEs

66
Q

these CCBs have a great affinity for vascular cells IN THE PERIPHERY and does not effect cardiac contractility

A

dihydropyridines

67
Q

these CCBs are beneficial for decreasing PVR but may induce reflex tachycardia

A

dihydropyridines

68
Q

second generation dyhydropyridines- very effective and widely used

A

amlodipine and felodipine

69
Q

this class of CCB can cause hypotension, dizziness and peripheral edema

A

dihydropyridines

70
Q

this class of CCB can cause hypotension, dizziness, constipation, bradycardia, and exacerbation of HF

A

non-dihydropyridines

71
Q

these drugs have no effect on blood sugar or lipids

72
Q

this class is contraindicated in hypotension and immediate release in CV indications in adult pts due to cardiac ischemia

A

dihydropyridines

73
Q

this class is contraindicated in severe bradycardia, hypotension, heart block, or overt HF. Careful in patients taking beta blockers (can cause AV block or heart failure)

A

non-dihydropyridines

74
Q

this drug increases plasma digoxin levels

75
Q

this class lowers MAP by causing relaxation of both arterial and venous smooth muscle. Causes minimal changes in CO, renal blood flow, and GFR

A

alpha 1 receptor antagonists

76
Q

this class is primarily used for BPH. Not used much for HTN (inferior to diuretics, postural hypotension, and first dose syncope)

A

alpha 1 receptor antagonists

77
Q

caution in pts with poorly controlled angina w/o beta blocker and incontinence

A

alpha 1 receptor antagonists

78
Q

ADRs: first dose syncope, dizziness, HA, postural hypotension, weakness, nausea, palpitations

A

alpha 1 receptor antagonists

79
Q

alpha 2 agonist- causes inhibition of NE causing vasodilation. reduce activity of vasomotor center in the brian (reduced symp activity, vasodilation)

80
Q

this drug does not decrease renal BF or GFR- agent of choice for pts with chronic renal disease

81
Q

Indicated in HTN, drug withdrawl, and side effects associated with neuroleptics

82
Q

ADRs: dry mouth, sedation, depression, hypotension, sexual dysfunction, urinary retention, constipation, and dizziness. ABRUPT withdrawal can cause severe HTN

83
Q

analogue of levodopa- gets converted to methylnorepinepherine centrally decreases adrenergic outflow from the CNS. (acts as an alpha 2 agonist to decrease symp outflow)

A

methyldopa

84
Q

agent of choice in HTN pts with chronic renal disease and pregnancy

A

methyldopa

85
Q

this class directly acts on vascular smooth muscle, primary arterioles to decrease tone. Involves a decrease in calcium entry and mobilization of intracellular calcium stores

A

hydralazine

86
Q

this is used for moderate to severe HTN- needs to be given with diuretic acid and a sympatholytic drug

A

hydralazine

87
Q

ADRs include HA, nausea, anorexia, palpitations. Higher doses produce high incidence of symptoms that resemble lupus erythematosus

A

hydralazine

88
Q

this class can be used as monotherapy or combo with diuretics or ARBs

89
Q

this class inhibits generation of angiotensin I- preventing the formation of angiotensin II and reducing activation of all AT receptors

90
Q

this drug does not inhibit bradykinin breakdown like ACEI

91
Q

contraindicated in pregnancy- risk of fetal death or injury. DC ASAP (cat C in first trimester, D in second and third)

92
Q

ADRs include angioedema, diarrhea, HA, cough, and an increase in SrCr

93
Q

competitive inhibitor of CYP3A4. Interacts with atorvastatin and ketoconazole. Decreased efficacy of furosemide

94
Q

DOC for HTN in pregnancy

A

methyldopa or labetalol (hydralazine if IV)

95
Q

isolated systolic HTN

A

SBP > 140, DBP <90

96
Q

goal treatment of iso systolic HTN

97
Q

DOC iso systolic HTN

A

thiazide diuretic

98
Q

severely elevated BP without end organ damage

A

hypertensive urgency

99
Q

severely elevated BP associated with acute and ongoing organ damage in the brain, kidneys, heart, eyes, or vascular system. (end organ damage; DBP usually >/= 130)

A

hypertensive emergency

100
Q

Treat hypertensive urgency

A

(hours to days) clonidine, captopril, labetolol

101
Q

treat hypertensive emergency

A

(minutes to hours) IV nitroprusside

102
Q

this is a prodrug that decompensates to NO, causing vasodilation. Dilates both arteries AND veins (reduced TPR and venous return)

A

nitroprusside

103
Q

this drug has an immediate onset of action (1-2 minutes). Can cause HA, dizziness, nausea, and palpitations

A

nitroprusside

104
Q

metab of this drug results in cyanide production. Can administer thiosulfate to counteract

A

nitroprusside

Pharmacy (22 decks)

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