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CPR-2 > Lecture 3: RAAS- Antihypertensives > Flashcards

Lecture 3: RAAS- Antihypertensives Flashcards

1
Q

Which commonly used drugs have been associated with the induction of HTN?

A

Oral contraceptives

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2
Q

Angiotensin II formed from RAAS is a potent _________.

A

Angiotensin II formed from RAAS is a potent vasoconstrictor.

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3
Q

Angiotensin II acts to increase what 2 things?

A

1) Total peripheral resistance
2) Extracellular fluid volume

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4
Q

What 3 things are stimulated by angiotensin II?

A
  1. Stimulates thirst
  2. Aldosterone secretion (causes retention of Na+)
  3. ADH secretion (retention of H2O)
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5
Q

What is the MOA of Captopril?

A
  • Competitive inhibitor of ACE
  • Prevents conversion of angiotensin I —> angiotensin II
  • Increases plasma renin and decreases aldosterone secretion = lower BP
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6
Q

Why is enalapril significant?

A

Is a prodrug, w/ active form being enalaprilat

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7
Q

What are ACE inhibitors used for clinically?

A
  • HTN, can combo w/ thiazide or loop diuretic
  • Acute HTN (urgency/emergency)
  • HF w/ reduced ejection fraction
  • Diabetic nephropathy
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8
Q

What are the adverse effects associated w/ ACE inhibitors?

Which AE is the reason most people stop taking the drug and what is a potentially deadly AE?

A
  • Cough = #1 reason people stop taking
  • Hypotension, HA, drowsiness
  • Angioedema = can be fatal
  • Loss of/altered taste
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9
Q

ACE inhibitor drugs have what suffix?

A

-pril

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10
Q

What is the MOA of the -sartans?

A

- Competitive nonpeptide angiotensin II receptor antagonist

  • Blocks the vasocontrictor and aldosterone-secreting effects
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11
Q

What is the clinical application of the -sartans (i.e., losartan)?

A
  • Diabetic nephropathy w/ ↑ Scr and proteinuria
  • HTN, alone or in combo
  • Heart failure if intolerant of ACE inhibitors
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12
Q

What is the big advantage of the -sartans for HTN and other clinical applications?

A

Doesn’t produce as much of a cough as the ACE inhibitors so is better tolerated

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13
Q

What is the significance of Valsartan and Candesartan?

A
  • Valsartan = is NOT a prodrug requring activation
  • Candesartan = has irreversible binding of the angiotensin II receptor
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14
Q

Which drug is often used in people w/ heart failure that are intolerant to ACE inhibitors (i.e., too much cough)?

A

Losartan

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15
Q

Which drug used for the tx of HTN is a direct renin inhibitor?

A

Aliskiren

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16
Q

What are the effects of Aliskiren?

A

Direct renin inhibitor –> blocks conversion of angiotensinogen to angiotensin I

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17
Q

What is the clinical application of Aliskiren?

How often is it used?

A
  • Tx of HTN, alone or in combo w/ others
  • New, expensive, no obvious benefits, some evidence of increased risk of AE’s
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18
Q

What are some of the AE’s associated w/ Aliskiren?

A
  • Skin rash
  • Diarrhea
  • >300% increase in creatine phosphokinase (1%)
  • Hyperkalemia, especially if combined or pt has renal dysf. or DM
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19
Q

You should NOT use a β-blocker, like propranolol, in patients with what 2 disorders?

A

1) Asthma
2) Diabetes

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20
Q

Which drugs work well in combo when treating an African American for HTN?

A
  • Diuretics and Ca2+ channel blockers
  • β-blockers, ACE inhibitors and ARBS work well when added to diuretic, but NOT as monotherapy
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21
Q

Which HTN drugs should not be given to sexually active girls?

A
  • ACE inhibitors
  • ARBs
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22
Q

Which drug used for HTN is contraindicated throughout pregnancy?

A

ACE inhibitors

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23
Q

What is the effect of drugs that interfer with Angiotensin II on pts with bilateral renal stenosis and pts with diabetes?

A
  • Can precipitate renal failure in pts w/ bilateral renal stenosis
  • Can help preserve renal function in diabetics
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24
Q

What type of HTN is associated with unilateral renal artery stenosis?

A

Angiotensin II-dependent HTN

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25
Q

How can reducing salt help hypertension?

A

limits fluid retention

increases Na-retaining receptors –> drugs work better too

26
Q

What were the first drugs though of to control htn?

AEs?

A

alpha blockers

phentolamine –> short half life, long hypotensive episodes, orthostatic hypoT, tachycardia and arrhythmias

phenoxybenzamine –> non-competitive antagonist; similar to phentolamine + miosis

27
Q

When phentolamine and phenoxybenzamine didn’t work to control htn, what was the next class of drugs created and how did they work?

A

alpha-1 selective blockers (ozins)

ALLHAT data show they increase risk of HF and stroke

cause retrograde ejaculation

now used to tx BPH

28
Q

What is clonidine?

A

alpha-2 adrenergic agonist that can cross the BBB –> reduces overall sympathetic tone

Used to tx htn, ADHD, tourettes

IV admin causes transient incr in BP

AE: drowsiness, xerostomia, *rebound htn if dose is missed*

29
Q

What is alpha-methyldopa’s MOA and its use?

A

alpha-2 receptor agonist

drug of choice for gestational htn

can cause positive coombs test and SLE-like sx

30
Q

What is hexamethonium’s MOA, use, and AEs?

A

blocks nicotinic receptors of both SNS and PSNS

used to lower BP, best if inj 3-4x/day

AEs from disruptions of PSNS and SNS:

PSNS –> higher resting HR and BP and opposite of SLUDGEM

SNS –> difficult to maintain CO/BP when upright

31
Q

MOA, use and AEs of reserpine

A

MOA: blocks VMAT so NE can’t get into synaptic vesicles

oldest/least effect sympatholytic

AEs: crosses BBB –> severe depression/suicidal ideation

32
Q

MOA, use, and AEs of guanethidine

A

displaces NE from synaptic vesicles –> lowers CO, TPR, RBF, and GFR

used for tx of htn beginnning in 1960

AEs: severe orthostatic hypotension

BP slowly increases during day

33
Q

Why are beta-blockers contraindicated if there is peripheral vascular dz?

A

cause cold extremities, esp in infants

34
Q

What is the difference btw atenelol and metoprolol?

A

both selective B1 blockers

metoprolol has a shorter half-life than atenelol but available in XR, more lipid soluble, so more likely to cause adverse CNS effects

35
Q

What is bisoprolol noted for?

A

has highest beta1-selectivity

36
Q

What does phenylephrine do and how does it affect BP?

A

alpha1 agonist

raises blood pressure substantially

37
Q

Why aren’t beta blockers used as the first choice tx for HTN?

A

doesn’t prevent MI, HF, or death as well as other therapies

significan’t higher incidence of stroke than other therapies

38
Q

How do ACE inh affect GFR?

A

decreases GFR by decreasing resistance in efferent arterioles

this means serum creatinine increases even though ACEIs preserve kidny fxn in hyperfiltering diabetics

<30% incr likely ok

39
Q

What is significant about valsartan?

A

not a prodrug

40
Q

What are the off-label uses of nifedipine (2)?

A

hypertensive emergency in pregnancy

pulmonary htn

41
Q

What are the AEs of nifedipine?

A

flushing, peripheral edema, headache

palpitations

gingival hyperplasia

42
Q

Why is amlodipine so widely used for HTN?

A

long 1/2 life of 30-50 hrs

43
Q

What is hydralazine?

A

direct vasodilator of arterioles

exact mechanism unknown

*used for htn in pregnancy

can cause drug-induced lupus-like syn

44
Q

What are the 3 direct vasodilators to know, and what vessels do they work on?

A

hydralazine - arterioles

nitroprusside - venous and arterioles

monoxidil - arterioles

45
Q

What is the use of nitroprusside?

A

directly dilates veins and arterioles

used for management of htn crisis and HF

half life is only abt 2 min, can be used to dial up or down bp fast

46
Q

How does the blockade of RAS affect bilateral renal A stenosis?

A

reduced arterial pressure only after volume depletion

may lower GFR

47
Q

What does plasma renin look like in bilateral and unilateral renal stenosis?

A

bilateral - normal or low

unilateral - elevated

48
Q

Do you perform renal revascularization in pts w/ renal A stenosis or atherosclerotic dz?

A

from ASTRAL and CORAL trials: restoring vessel patency fails to materially recover kidney fxn

no better than ACEIs and statins

49
Q

What are primary agents to tx htn?

A

thiazide diuretics

ACE inhibitors

ARBs

CCBs

50
Q

What are secondary agents to tx htn?

A

loop diuretics

K+ sparing diuretics

beta blockers

direct renin inhibitors

alpha-1 blockers

central alpha-2 agonists

direct vasodilators

51
Q

What is your first line tx for htn w/ stable ischemic heart dz?

A

beta blockers –> if goal not met add dihydropyridine CCBs, thiazide diuretics, and or MRAs as needed

52
Q

How do you tx htn in pts w/ chronic kidney dz?

A

if no albuminuria - usual first line meds

if albuminuria –> ACE inhibitors or ARBs if intolerant

53
Q

What do you do if a pt has an ischemic stroke and high BP, but doesn’t qualify for thrombolysis?

A

BP 220/110 or less –> htn tx within first 48-72 hrs is ineffective to prevent death, only tx after neurological stability

BP over 220/110 –> lower BP 155 during first 24 hrs

54
Q

What do you do if someone had a stroke more than 72 hrs ago and is stable neurologically but has htn?

A

initiate hypertensive tx unless 140/90 or below and not previously hypertensive

55
Q

How do you treat htn in black adults?

A

initial tx should include a thiazide diuretic or CCB

2+ agents are recommended bc usually AAs have decreased renin - need diff drug than ACEIs and ARBs

56
Q

What drugs are used to tx htn in pregnancy?

A

alpha-methyldopa

difedipine

labetalol

(never ACEIs, ARBs, or direct renin inh)

57
Q

What diuretic is preferred by clinicians as a primary tx for htn?

A

chlorthalidone

58
Q

What beta blocker also causes NO-induced vasodilation?

A

nebivolol

59
Q

What is generally true about unlateral renovascular htn?

A

kidney damage is irreversible

60
Q

If someone has a stroke and HTN, what do you do?

A

lower w/ IV infusion if systolic > 220, but don’t let it get below 140

CPR-2 (28 decks)

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