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FA17 Cardio 1 > HTN Drug Info + Tx > Flashcards

HTN Drug Info + Tx Flashcards

1
Q

First line HTN and late line TxofC

A

Thiazides
Calcium channel blockers
ACE
ARBs

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2
Q

Heart failure HTN tx

A

Ace inhibitor or ARB + beta blocker + diuretic + aldosterone antagonist

Try to get all four to lower mortality risk

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3
Q

Post-MI HTN tx

A

Beta blocker + ACE inhibitor or ARB

Try to get both

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4
Q

High coronary disease risk

HTN Tx

A

Beta blocker

ACE inhibitor or ARB

CCB or thiazides

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5
Q

Diabetes

HTN Tx

A

ACE inhibitor or ARB then CCB or thiazides

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6
Q

CKD HTN Tex

A

Ace inhibitor or ARB

Then CCB or thiazides

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7
Q

Recurrent stroke prevention HTN tx

A

Ace inhibitor or ARB

Then thiazides or CCB

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8
Q

Pregnancy and HTN tx options

A

NO ACE or ARB

Can use thiazides, CCB, or Beta blocker

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9
Q

If > 80 yrs w/risk of gout, urinary incontinence, SSRI rx or low serum Na

Avoid which ones?

A

No thiazides

Only ACE, CCB, ARB

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10
Q

Diuretics general classes

A

Thiazides

Loop

Potassium sparing

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11
Q

Diuretics general MOA

A

Decrease ability of kidneys to reabsorb water

Temporarily lower blood volume then it works to anti HTN

more effective when combined with ACEI/ARB

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12
Q

Thiazides

Dose and MOA

A

Dose in morning to avoid nocturia

Increased renal excretion of sodium, may vasodilator

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13
Q

Thiazides ADRs

A

Electrolyte abnormalities

Gout

Hyperglycemia (caution in DM)

Hypovolemia

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14
Q

specific electrolyte abnormalities associated with Thiazides

A

hyponatremia
hypokalemia
hypomagnesemia
hypercalcemia

contraction alkalosis

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15
Q

what should you do w/in 10-14 days of initiation on a thiazide

A

electrolyte panel

checks for hypokalemia and hyponatremia

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16
Q

loop diuretic dosage

A

dose in AM or afternoon

higher doses may be needed for decreased GFR (CKD pos), accustomed to med, or heart failure

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17
Q

loop diuretics ADRs

A

hyponatremia, hypokalemia, hypomagnesemia, hypOcalcemia
hyperuricemia
hyperglycemia

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18
Q

potassium sparing diuretics

A

Dose in AM or afternoon

weak so typically used as add on to prevent hypokalemia

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19
Q

ADRs potassium sparing diuretics

A

hyperkalemia (esp. in combo with ACE, ARB or K + supplement)

avoid in patients with DM or CKD

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20
Q

Aldosterone antagonists ADRs

A

hyperkalmia

avoid in CKD/DM

gynecomastia and impotence

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21
Q

ACE inhibitors TOC

A

HTN, CKD, and proteinuria

reduced morbidity and mortality in heart failure and recent MI

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22
Q

ACE I. MOA

A

blocks conversion of angiotensin II = vasodilation

blocks RAAS activation

inhibits bradykinin breakdown (vasodilation)

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23
Q

monitoring with ACE I

A

monitor serum K+ and Cr w/in 2 weeks of ignition or dose increasing

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24
Q

ACE I ADRs

A

dry cough (bc increased bradykinin)

angioedema

hyperkalemia

CI in pregnancy

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25
Q

ARBs MOA

A

block vasoconstriction effects of angiotensin II by blocking its receptor

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26
Q

ARBs CI

A

in pregnancy, history of ACEI ass. angioedema

must monitor renal status and K+ when starting

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27
Q

should you combine ACEI and ARB?

A

NO

it will reduce proteinuria but worsens renal outcomes

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28
Q

Direct Renin Inhibitor

A

inhibits conversion of angiotensinogen to angiotensin i

efficacy greater in combo with HCTZ

don’t use with ACEI/ARB

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29
Q

CCB

general MOA

A

inhibit influx of Ca across cardiac and smooth muscle cell membranes

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30
Q

Dihyropyridines MOA

A

block calcium channels in vasculature

potent arteriolar vasodilators

NO effect on AV nodal conduction

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31
Q

dihydropyridines ADR

A

baroreceptor mediated reflex tachycardia (potent vasodilation effects)

may cause or worsen peripheral edema

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32
Q

non dihydropyridines MOA

A

decrease HR by blocking SA and AV nodes

used to slow AV nodal conduction

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33
Q

non dihydropyridines SDR

A

bradycardia, AV block, systolic HF

decrease cardiac contractility and heart rate

dont use with beta blocker

constipation

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34
Q

CCB overdose

A

common

neurologic status may deteriorate quickly

prolonged PR interval and bradyarrhythmia

hyperglycemia

35
Q

B-1 receptors

A

heart, kidney

stimulation INCREASES HR, contractility, renin release

36
Q

B-2 receptors

A

lungs, liver, pancreas, arteriolar smooth muscle

stimulation causes bronchodilator and vasodilation

insulin secretion and glycogenolysis

37
Q

B-blockers MOA

A

bind to and block B1 receptors

reduced responsiveness to sympathetic activity

non-cardioselective or if given at high doses can get B2 if high enough

use in caution of asthma or COPD

38
Q

place in HTN treatment

B-blockers

A

not recommended first line except in cases of compelling cardiac indication (post MI or HF)

39
Q

B-blockers ADR

A

adverse effect on glucose metabolism and block recognition of hypoglycemia

precipitate heart block or bradyarrythmia

reduced sexual function, fatigue, reduced exercise tolerance

40
Q

types of B-blockers

A

cardioselective

non selective

intrinsic sympathomimetic activity

41
Q

non-selective B-blockers other indications

A

inhibit B1 and B2 receptors at all doses

migraine prophylaxis, essential tremor, portal HTN, thyrotoxicosis

42
Q

dosage of B-blockers

A

must be started low dose and dose titrated cautiously

should not be abruptly discontinued

43
Q

Mixed a1-b blockers MOA

A

block B receptors (decrease HR) and a1-r (peripheral vasodilation)

reduces mortality in its with systolic HF tx with diuretic and ACE inhibitor

44
Q

Mixed a1-b blockers ADR

A

lowers standing BP more than supine = orthostasis

additional blockage produces more hypotension

45
Q

Carvedilol (Coreg)

A

freq. used for BP in HF or DM

has less of an effect on glucose metabolism straight BB

46
Q

Labetolol (Trandate)

A

Freq. given IV pre to control BP when its cannot take their usual dose of oral BB

used in pregnancy

47
Q

a-1 blockers general use

A

not appropriate monotherapy for HTN

often used when both HTN and co-morbid BPH

48
Q

a-1 blockers MOA

A

vasodilation and BP lowering

block a-1 receptors on prostate

allowing for easier urine flow

49
Q

a-1 blockers dosage

A

dosed at bedtime

caution in elderly patients they have a greater tendency to develop orthostasis

50
Q

a-1 blockers ADRs

A

orthostatic hypotension

1st dose phenomenon

edema

51
Q

central A2 agonists MOA

A

stimulate A2 adrenergic in brain

reduces sympathetic outflow from CNS and increases vagal tone

52
Q

central A2 agonists ADRs

A

edema

abrupt discontinuation may cause rebound HTN

orthostatic hypotension

anticholinergic side effects

53
Q

Direct Arterial Vasodilators

A

Cause arterial smooth muscle relaxation and anti hypertension effects

HR neutral

Hydrazaline and Minoxidil

54
Q

Direct arterial vasodilators SDRs

A 
Sodium/water retention causing edema 
Angina
Reflex tachycardia 
`
Hydralazine - drug induced lupus
Minoxidil - excessive hair growth
55
Q

Pre-hypertension Tx

A

Trial of lifestyle management

56
Q

Stage I HTN tx

A

140-159/90-100

Single agent with close follow up, trial with lifestyle changes

57
Q

Stage II HTN tx

A

> 160/>100

Two agents with close follow up

58
Q

Treating African American HTN at any age

A

CCB and thiazides diuretics are more effective

ACE and ARBs are less effective but second line

59
Q

Treatment guidelines Caucasian non white

A

< 60 - ACE/ARBs followed by CCB

> 60 ACE/ARBs are still first line but slowly added, less aggressive BP target

60
Q

Pathophys of HTN Emergencies

A

Increased pressure autoregulation and abrupt rise in vascular resistance

Endothelial damage, local intravascular activation of clotting cascade, necrosis of vessels, and release more vasoconstriction — making BP worse

Left ventricle is unable to compensate for the acute rise = Left ventricular failure, pulmonary edema, and myocardial ischemia

61
Q

HTN crisis history

A

duration and severity

degree of control

medication history and compliance

presence of prev. end organ dysfunction

recent head injury, trauma

Pregnancy

62
Q

HTN crisis exam

BP measured

A

supine position and standing position to asses volume depletion

63
Q

end organ dysfunction exam

end organ dysfunction

A

eyes (retinal hemorrhage, exudate, papilledema)

CV (chest apin, jugular distention, cradles, dyspnea)

CNS (agitation, delirium, visual problems, seizures)

abdominal (masses or bruits noted)

64
Q

HTN crisis workup

A

serum chemistries

u/a

cbc

cardiac enzymes x 3

imaging

65
Q

HTN crisis

risks of lowering BP acutely

A

brain ischemia due to rapid BP drop

esp. in patients with long standing HTN, poorly controlled

therefore, reduce MAP no more than 10-20% over 1 hr using IV meds

66
Q

HTN emergency meds (6)

A

Sodium nitroprusside

Nicardipine hydrochloride

esmolol hydrochloride

nitroglycerin

hydrazine hydrochloride

labetalol hydrochloride

67
Q

sodium nitroprusside HTN use

avoid

A

increased ICP (head bleed or tumor)

CKD

68
Q

Nicardipine hydrochloride

HTN iris use

MC and avoid

A

MC: intercerebral hemorrhage

avoid: acute heart failure, coronary ischemia

69
Q

esmolol hydrochloride

MC

A

cardio causes, esp. peri-operative

B-blocker

70
Q

nitroglycerin

MC

A

MC: coronary ischemia, HF (vasodilation)

71
Q

hydrazine hydrochloride

mc

A

eclampsia

OK in pregnant patients

72
Q

labetalol hydrochloride

Avoid

A

actue HF

73
Q

cardiac complications in HTN

A

acute coronary syndrome

acute heart failure

74
Q

acute coronary symptoms in HTN crisis TX

A

beta blockers and nitroglycerin

thrombolytics are CI

75
Q

acute heart failure

cardiac complications HTN Crisis TX

A

loop diuretic IV administered first (fluid overload)

vasodilator (reduce after load)

avoid: Beta blockers, hydrazine

76
Q

HTN crisis sympathetic overactivity

occurs w/ + tx

A

cocaine toxicity, amphetamines

pheochromocytoma

severe autonomic dysfunction

tx: beta blocker

77
Q

acute ischemic stroke HTN crisis tx

A

let the BP rise ride unless >220 systolic

if they are going to give TPA, you do have to decrease BP

78
Q

acute aortic dissection crisis Tx

A

must rapidly lower SBP to 100-120 mm Hg within 20 min

use como of morphine + beta blocker _ vasodilators

79
Q

HTN acute intracerebral hemorrhage or subarachnoid hemorrhage

A

determine if ICP present

we have have issue with blood leaking - could make the bleeding worse or cause penumbra increase

80
Q

HTN in pregnancy

types

A

chronic HTN

pregnancy induced/gestational hen

preeclampsia

81
Q

chronic HTN pregnancy

A

> 140/90 before 20 weeks hesitation or pre pregnancy

HTN persists 12 weeks post partum

82
Q

gestational HTN

A

occurs after 20 weeks gestation without proteinuria

resolves by 12 weeks

83
Q

preeclampsia

A

high BP after 20 weeks WITH proteinuria

restricted activity, 1st pregnancy, multiple gestation

FA17 Cardio 1 (6 decks)

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