HTN drugs

Question 1

SE of loop diuretics

Answer 1

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

Question 2

loop diuretics and lithium

Answer 2

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

Question 3

thiazide diuretics onset

Answer 3

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

Question 4

what is the most widely used diuretics

Answer 4

thiazides!

Question 5

SE of thiazides

Answer 5

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

Question 6

K sparing SE

Answer 6

hyperkalemia, watch for added K in diet

Question 7

K sparing and ACE + ARBs

Answer 7

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

Question 8

typical order for K sparing

Answer 8

with another diuretic!

Question 9

nursing considerations for diuretics

Answer 9

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

Question 10

Alpha 1 Adrenergic antagonists MOA

Answer 10

blocks the SNS action on arterioles and veins resulting in vasodilation

Question 11

Alpha 1 is….

Answer 11

BLOOD VESSELS

Question 12

SE of alpha 1 adrenergic antagonists

Answer 12

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

Question 13

alpha 2 agonist MOA

Answer 13

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

Question 14

SE of alpha-2 agonist

Answer 14

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

Question 15

BB types

Answer 15

beta 1– cardioselective

beta 2– cardio non selective

Question 16

BB MOA

Answer 16

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

Question 17

BB SE

Answer 17

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

Question 18

common SE of bb

Answer 18

fatigue, drowsyness, dizzy, headache, sexual dysfunction

Question 19

NSG considerations for BB

Answer 19

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

Question 20

Alpha-beta blockers MOA

Answer 20

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

Question 21

SE of alpha-beta blockers

Answer 21

brady, heart block, bronchocontriction, postural hypotension

Question 22

CCB MOA

Answer 22

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

Question 23

CCB action on the heart (1)

Answer 23

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

Question 24

CCB action on the heart (2)

Answer 24

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

Question 25

CCB action on the heart (3)

Answer 25

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

Question 26

CCB and BB

Answer 26

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

Question 27

CCB dipines MOA

Answer 27

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

Question 28

SE of CCB dipines

Answer 28

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

Question 29

CCB non dipines effects

Answer 29

decrease contract, HR, and conduction | vasodilates, and increases coronary perfusion

Question 30

why is there no reflex tachy with nondipines?

Answer 30

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

Question 31

SE of CCBs nondip

Answer 31

constipation, dizziness, facial flushing, edema | can cause brady and heart blockand

Question 32

SE of CCBs nondip

Answer 32

constipation, dizziness, facial flushing, edema | can cause brady and heart block and heart failure

Question 33

NSG considerations for CCB

Answer 33

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

Question 34

what does aldersterone do in the body

Answer 34

promotes cardiac remodeling initiates SNS activity vascular fibrosis disrupts baroreceptor activity

Question 35

what does angie do in the body

Answer 35

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

Question 36

overview of benefits of ACE

Answer 36

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

Question 37

ACE MOA for diabetic kidneys

Answer 37

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

Question 38

what is recommended for DM pts as far as ACE goes

Answer 38

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

Question 39

ACE MOA

Answer 39

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

Question 40

SE of ACE

Answer 40

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

Question 41

ARBs MOA

Answer 41

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

Question 42

SE of ARB

Answer 42

decreased risk of cough

Question 43

Direct Renin inhibitors MOA

Answer 43

blocks the entire RAAS process

Question 44

SE of direct renin inhibitors

Answer 44

angioedema, cough, diarrhea

Question 45

direct vasodilators MOA (hydralazine)

Answer 45

causes direct relaxation of arteriolar smooth muscle

Question 46

SE of direct vasodilator (hydra)

Answer 46

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

Question 47

Direct vasodilator MOA nitro

Answer 47

causes venous and arteriolar dilation

Question 48

characteristics of nitroprusside

Answer 48

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

Question 49

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

Answer 49

lasix baby!