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NSG 323 > HTN drugs > Flashcards

HTN drugs Flashcards

1
Q

SE of loop diuretics

A 
e- imbalances
hypotension
dehydration
postural hypotension
ototoxicity
increased risk of digoxin toxicity
increased uric acid-- gout pts
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2
Q

loop diuretics and lithium

A

lithium acts like a salt! it can cause a lithium toxicity if these are used together

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3
Q

thiazide diuretics onset

A

2 hrs, peaks in 4-6, lasts for 12

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4
Q

what is the most widely used diuretics

A

thiazides!

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5
Q

SE of thiazides

A 
e- imbalances
dehydration
hypovolemia
hyperglycemia (DM patients!)
increase uric acid
digoxin and Li toxicity
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6
Q

K sparing SE

A

hyperkalemia, watch for added K in diet

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7
Q

K sparing and ACE + ARBs

A

have d-d interactions related to potassium, with k sparing diuretics

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8
Q

typical order for K sparing

A

with another diuretic!

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9
Q

nursing considerations for diuretics

A

Hypokalemia (thiazide + loop)
hyperkalemia (k-sparing)
hydration status (daily weights, admin early in day)
NOT safe for pregnancy

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10
Q

Alpha 1 Adrenergic antagonists MOA

A

blocks the SNS action on arterioles and veins resulting in vasodilation

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11
Q

Alpha 1 is….

A

BLOOD VESSELS

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12
Q

SE of alpha 1 adrenergic antagonists

A

ortho hypo, 1st dose phenomena (don’t get up for 3 hours), reflex tachy (baroreceptor tachy), nasal congestion, inhibits ejaculation

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13
Q

alpha 2 agonist MOA

A

works on central nervous system in sympathetic OUTFLOW
alpha 2 is PREsynaptic.
causes norepi to accumulate in synapse. body recognizes it has enough and decreases synthesis of norepi.
results in vasodilation, decreased bp and decreased co

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14
Q

SE of alpha-2 agonist

A

dry mouth, sedation (will get better over time), rebound hypertension (if stopped abruptly)

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15
Q

BB types

A

beta 1– cardioselective

beta 2– cardio non selective

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16
Q

BB MOA

A

decreases HR, slows conduction through myocardium, decreases force of contraction
decreases peripheral vascular resistance over time
blocks beta1 on juxtaglomerular cells that release renin

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17
Q

BB SE

A

brady and AV heartblock, decrease CO (watch for falls), rebound cardiac excitation. may mask s/s of hypoglycemia in DM

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18
Q

common SE of bb

A

fatigue, drowsyness, dizzy, headache, sexual dysfunction

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19
Q

NSG considerations for BB

A

check BP and pulse, hold if less than 60
teach pt to wean off, not sudden
teach DM pts to monitor glucose more closely
s/s of HF

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20
Q

Alpha-beta blockers MOA

A

blocks alpha 1, beta 1&2
alpha blockade: dilation of arteriole and vein
beta blockade: decrease HR, contractility and conduction

21
Q

SE of alpha-beta blockers

A

brady, heart block, bronchocontriction, postural hypotension

22
Q

CCB MOA

A

works by inhibiting the influx of Ca, preventing muscular contraction. also vasodilation occurs

23
Q

CCB action on the heart (1)

A

normal Ca entry into the heart is positive ionotropic and has strong contraction.
CCB blocks Ca which decreases the contraction

24
Q

CCB action on the heart (2)

A

Normal Ca regulates the pace of the heart. BLOCKING Ca decreases the heart rate.

25
Q

CCB action on the heart (3)

A

AV node – excitability is controlled by the Ca influx. BLOCKING Ca decreases the conduction.

26
Q

CCB and BB

A

have the SAME effect on the heart. NO pts on them both at the same time! but nifedipine is ok!

27
Q

CCB dipines MOA

A

work primarily on b.v., vasodilation of arterioles and arteries, decreases BP

28
Q

SE of CCB dipines

A 
flushing, dizziness, peripheral edema, postural hypo, rash, gingival hypertrophy
reflex tachy (give BB to decrease this!)
29
Q

CCB non dipines effects

A

decrease contract, HR, and conduction

vasodilates, and increases coronary perfusion

30
Q

why is there no reflex tachy with nondipines?

A

the effects on the heart and the BV counterbalance one another!

31
Q

SE of CCBs nondip

A

constipation, dizziness, facial flushing, edema

can cause brady and heart blockand

32
Q

SE of CCBs nondip

A

constipation, dizziness, facial flushing, edema

can cause brady and heart block and heart failure

33
Q

NSG considerations for CCB

A

check pulse and BP
watch for reflex tachy
IV admin– tachy and hypo
no grapefruit juice

34
Q

what does aldersterone do in the body

A

promotes cardiac remodeling
initiates SNS activity
vascular fibrosis
disrupts baroreceptor activity

35
Q

what does angie do in the body

A

triggers release of Al from the adrenal cortex (hold on to water and sodium)
increases inflammation in the arteries
prothrombotic
increases insulin resistance at the tissues (hyperglycemia)
causes cardiac hypertrophy and vascular remodeling

36
Q

overview of benefits of ACE

A

treats HTN, post MI, HF, diabetes, prevents diabetic nephropathy, stroke and MI prevention

37
Q

ACE MOA for diabetic kidneys

A

decreases AT, vasodilation of the efferent arteriole, pressure in the glomerulus falls, slows the progression in CKD.

38
Q

what is recommended for DM pts as far as ACE goes

A

recommend all diabetics to be on an ACE even if BP is normal to protect the kidney from nephropathy

39
Q

ACE MOA

A

blocks the conversion of angie 1 to 2, resulting in vasodilation and decreased fluid volume
blocks aldosterone
increased bradykinin

40
Q

SE of ACE

A

dry cough, angioedema, 1st dose hypotension, and increased potassium

41
Q

ARBs MOA

A

angie gets made but blocked at receptors
potent vasodilator
prevents bad effects from AT2
blocks Al (but not as well)

42
Q

SE of ARB

A

decreased risk of cough

43
Q

Direct Renin inhibitors MOA

A

blocks the entire RAAS process

44
Q

SE of direct renin inhibitors

A

angioedema, cough, diarrhea

45
Q

direct vasodilators MOA (hydralazine)

A

causes direct relaxation of arteriolar smooth muscle

46
Q

SE of direct vasodilator (hydra)

A

reflex tachy (give BB), increases blood volume, SLE syndrome

47
Q

Direct vasodilator MOA nitro

A

causes venous and arteriolar dilation

48
Q

characteristics of nitroprusside

A

drug of choice for HTN emergencies, given continous IV, effects in seconds! don’t use for longer than 72 hours (toxic accumulation of thiocyanate)

49
Q

what do you give if blood volume increases while on nitroprusside?

A

lasix baby!

NSG 323 (12 decks)

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