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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
ARBs MOA
block vasoconstriction effects of angiotensin II by blocking its receptor
26
ARBs CI
in pregnancy, history of ACEI ass. angioedema must monitor renal status and K+ when starting
27
should you combine ACEI and ARB?
NO it will reduce proteinuria but worsens renal outcomes
28
Direct Renin Inhibitor
inhibits conversion of angiotensinogen to angiotensin i efficacy greater in combo with HCTZ don't use with ACEI/ARB
29
CCB general MOA
inhibit influx of Ca across cardiac and smooth muscle cell membranes
30
Dihyropyridines MOA
block calcium channels in vasculature potent arteriolar vasodilators NO effect on AV nodal conduction
31
dihydropyridines ADR
baroreceptor mediated reflex tachycardia (potent vasodilation effects) may cause or worsen peripheral edema
32
non dihydropyridines MOA
decrease HR by blocking SA and AV nodes used to slow AV nodal conduction
33
non dihydropyridines SDR
bradycardia, AV block, systolic HF decrease cardiac contractility and heart rate dont use with beta blocker constipation
34
CCB overdose
common neurologic status may deteriorate quickly prolonged PR interval and bradyarrhythmia hyperglycemia
35
B-1 receptors
heart, kidney stimulation INCREASES HR, contractility, renin release
36
B-2 receptors
lungs, liver, pancreas, arteriolar smooth muscle stimulation causes bronchodilator and vasodilation insulin secretion and glycogenolysis
37
B-blockers MOA
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
place in HTN treatment B-blockers
not recommended first line except in cases of compelling cardiac indication (post MI or HF)
39
B-blockers ADR
adverse effect on glucose metabolism and block recognition of hypoglycemia precipitate heart block or bradyarrythmia reduced sexual function, fatigue, reduced exercise tolerance
40
types of B-blockers
cardioselective non selective intrinsic sympathomimetic activity
41
non-selective B-blockers other indications
inhibit B1 and B2 receptors at all doses migraine prophylaxis, essential tremor, portal HTN, thyrotoxicosis
42
dosage of B-blockers
must be started low dose and dose titrated cautiously should not be abruptly discontinued
43
Mixed a1-b blockers MOA
block B receptors (decrease HR) and a1-r (peripheral vasodilation) reduces mortality in its with systolic HF tx with diuretic and ACE inhibitor
44
Mixed a1-b blockers ADR
lowers standing BP more than supine = orthostasis additional blockage produces more hypotension
45
Carvedilol (Coreg)
freq. used for BP in HF or DM has less of an effect on glucose metabolism straight BB
46
Labetolol (Trandate)
Freq. given IV pre to control BP when its cannot take their usual dose of oral BB used in pregnancy
47
a-1 blockers general use
not appropriate monotherapy for HTN often used when both HTN and co-morbid BPH
48
a-1 blockers MOA
vasodilation and BP lowering block a-1 receptors on prostate allowing for easier urine flow
49
a-1 blockers dosage
dosed at bedtime caution in elderly patients they have a greater tendency to develop orthostasis
50
a-1 blockers ADRs
orthostatic hypotension 1st dose phenomenon edema
51
central A2 agonists MOA
stimulate A2 adrenergic in brain reduces sympathetic outflow from CNS and increases vagal tone
52
central A2 agonists ADRs
edema abrupt discontinuation may cause rebound HTN orthostatic hypotension anticholinergic side effects
53
Direct Arterial Vasodilators
Cause arterial smooth muscle relaxation and anti hypertension effects HR neutral Hydrazaline and Minoxidil
54
Direct arterial vasodilators SDRs
``` Sodium/water retention causing edema Angina Reflex tachycardia ` Hydralazine - drug induced lupus Minoxidil - excessive hair growth ```
55
Pre-hypertension Tx
Trial of lifestyle management
56
Stage I HTN tx
140-159/90-100 Single agent with close follow up, trial with lifestyle changes
57
Stage II HTN tx
>160/>100 Two agents with close follow up
58
Treating African American HTN at any age
CCB and thiazides diuretics are more effective ACE and ARBs are less effective but second line
59
Treatment guidelines Caucasian non white
< 60 - ACE/ARBs followed by CCB >60 ACE/ARBs are still first line but slowly added, less aggressive BP target
60
Pathophys of HTN Emergencies
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
HTN crisis history
duration and severity degree of control medication history and compliance presence of prev. end organ dysfunction recent head injury, trauma Pregnancy
62
HTN crisis exam BP measured
supine position and standing position to asses volume depletion
63
end organ dysfunction exam end organ dysfunction
eyes (retinal hemorrhage, exudate, papilledema) CV (chest apin, jugular distention, cradles, dyspnea) CNS (agitation, delirium, visual problems, seizures) abdominal (masses or bruits noted)
64
HTN crisis workup
serum chemistries u/a cbc cardiac enzymes x 3 imaging
65
HTN crisis risks of lowering BP acutely
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
HTN emergency meds (6)
Sodium nitroprusside Nicardipine hydrochloride esmolol hydrochloride nitroglycerin hydrazine hydrochloride labetalol hydrochloride
67
sodium nitroprusside HTN use avoid
increased ICP (head bleed or tumor) CKD
68
Nicardipine hydrochloride HTN iris use MC and avoid
MC: intercerebral hemorrhage avoid: acute heart failure, coronary ischemia
69
esmolol hydrochloride MC
cardio causes, esp. peri-operative B-blocker
70
nitroglycerin MC
MC: coronary ischemia, HF (vasodilation)
71
hydrazine hydrochloride mc
eclampsia OK in pregnant patients
72
labetalol hydrochloride Avoid
actue HF
73
cardiac complications in HTN
acute coronary syndrome acute heart failure
74
acute coronary symptoms in HTN crisis TX
beta blockers and nitroglycerin thrombolytics are CI
75
acute heart failure cardiac complications HTN Crisis TX
loop diuretic IV administered first (fluid overload) vasodilator (reduce after load) avoid: Beta blockers, hydrazine
76
HTN crisis sympathetic overactivity occurs w/ + tx
cocaine toxicity, amphetamines pheochromocytoma severe autonomic dysfunction tx: beta blocker
77
acute ischemic stroke HTN crisis tx
let the BP rise ride unless >220 systolic if they are going to give TPA, you do have to decrease BP
78
acute aortic dissection crisis Tx
must rapidly lower SBP to 100-120 mm Hg within 20 min use como of morphine + beta blocker _ vasodilators
79
HTN acute intracerebral hemorrhage or subarachnoid hemorrhage
determine if ICP present we have have issue with blood leaking - could make the bleeding worse or cause penumbra increase
80
HTN in pregnancy types
chronic HTN pregnancy induced/gestational hen preeclampsia
81
chronic HTN pregnancy
>140/90 before 20 weeks hesitation or pre pregnancy HTN persists 12 weeks post partum
82
gestational HTN
occurs after 20 weeks gestation without proteinuria resolves by 12 weeks
83
preeclampsia
high BP after 20 weeks WITH proteinuria restricted activity, 1st pregnancy, multiple gestation

FA17 Cardio 1 (6 decks)

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