antiHTN Flashcards

1
Q

HCTZ: class

A
  • thiazide diuretic
  • anti HTN
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2
Q

HCTZ: MOA

A
  • blocks the reabsorption of Na and Cl in the early DCT
    • retention of Na and Cl in the nephron causes water to be retained, so inc flow of urine
  • must have adequate kidney function/GFR to work
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3
Q

HCTZ: Indications

A
  • HTN
  • edema
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4
Q

HCTZ: SEs

A
  • hyponatremia
  • hypochloremia
  • dehydration
  • hypokalemia
  • hyperglycemia
  • hyperuricemia
  • inc LDL
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5
Q

HCTZ: nursing implications

A
  • evalute fluid and electrolyte levels
  • weigh patient
  • if K+ falls below 3.5, treat with K supplement or K sparing diuretics
    • eat K rich foods
  • measure uric acid levels
  • watch blood glucose levels
  • take in the morning
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6
Q

metoprolol: class

A
  • anti HTN
  • beta blocker
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7
Q

metoprolol: MOA

A
  • promotes selective blockade of beta 1 receptors in the heart
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8
Q

metoprolol: indications

A
  • HTN
  • angina
  • HF
    MI
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9
Q

metoprolol: SEs

A
  • fatigue
  • weakness
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10
Q

metoprolol: ADRs

A
  • bradycardia
  • heart block
  • HF (if used incautiously)
  • reduced CO
  • rebound cardiac excitement w/ abrupt withdrawal
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11
Q

metoprolol: nursing implications

A
  • contraindicated: bradycardia, AV heart block
  • caution in pts with HF
  • can be used more safely in asthmatic pts b/c selectively binds to beta 1
  • masks common signs of hypoglycemia so need to watch for fatigue, hunger, weakness
  • do not d/c abruptly
  • monitor BP and HR
  • stand up slowly due to possible orthostatic hypoTN
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12
Q

losartan: class

A
  • ARB
  • anti HTN
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13
Q

losartan: MOA

A
  • they block access of Ang II to its receptor
    • so cause dilation of arterioles and veins
  • dec release of aldosterone
  • inc excretion of Na and water
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14
Q

losartan: indication

A
  • HTN
  • HF
  • diabetic nephropathy
  • MI
  • stroke prevention
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15
Q

losartan: SEs

A
  • dizziness
  • hyperkalemia (b/c K sparing)
  • NO COUGH
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16
Q

losartan: ADRs

A
  • angioedema
  • fetal harm
  • renal failure
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17
Q

losartan: nursing implication

A
  • contraindicated in the 2nd and 3rd trimester of pregnancy, pts with bilateral renal A stenosis, hx of angioedema
  • can take w/ or w/o food
  • monitor BP, daily weights
  • monitor K+ levels
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18
Q

clonidine: class

A
  • centrally acting alpha 2 adrenergic agonist
  • anti HTN
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19
Q

clonidine: MOA

A
  • causes selective activation of alpha 2 receptors in the CNS
    • especially in the brainstem area assoc with autonomic regulation of the CV system
  • reduces sympathetic outflow to the blood vessels and to the heart
20
Q

clonidine: indications

A
  • HTN
  • severe pain
  • ADHD
  • uses under research: smoking cessation, opioid withdrawal, txing Tourette’s
21
Q

clonidine: SEs

A
  • drowsiness
  • xerostomia
  • constipation
  • CNS rxns: nightmares, vivd dreams, depression
22
Q

clonidine: ADRs

A
  • rebound HTN (w/ nervousness, tachycardia, sweating)
  • embryotoxic
  • abuse
23
Q

clonidine: nursing implications

A
  • avoid hazardous activity due to drowsiness
  • reduce xerostomia by chewing gum, drinking fluids
  • need to monitor BP
  • do not d/c abruptly to avoid rebound HTN
  • do not use in pregnant
  • take at bedtime
24
Q

nifedipine:class

A
  • dihydropyridine: calcium channel blocker (but only minimally in the heart unlike verapamil and diltizem)
25
Q

difference b/w verapamil and nifedipine

A
  • nifedipine produces only minimal blockade of calcium channels in the heart, so it can’t be used to tx dysrhythmias, does not cause cardiac suppression, and is less likely than verapamil to exacerbate preexisting cardiac disorders
  • nifedipine more likely to cause reflex tachycardia
  • nifedipine does not cause constipation
26
Q

nifedipine: MOA

A
  • blocks calcium channels in vascular SM, so it causes vasodilation in the peripheral arterioles–>lowers arterial pressure
  • calcium channel blcoakde in arteries and arterioles of heart inc coronary perfusion
  • activates baroreceptor reflex, so causes sympathetic stimulation of the heart, and contractile force/HR increase
    • only occurs with the immediate release formulation
27
Q

nifedipine: indications

A
  • angina pectoris
    • usually combined with a beta blocker to prevent reflex stimulation of the heart
    • when it acts on coronary vessels
  • essential HTN
    • only use SR formulation, b/c immediate release has been associated with an inc risk of MI
    • when it acts systemically
28
Q

nifedipine: SE

A
  • flushing
  • dizziness
  • headache
  • peripheral edema
  • gingival hyperplasia
  • chronic eczematous rash
  • **causes minimal blockage of Ca channels in the heart, so is not likely to exacerbate AV heart block, HF, bradycardia, or sick sinus syndrome, so nifedipine is preferred to verapamil for these pts
29
Q

nifedipine: ADRs

A
  • reflex tachycardia: inc O2 depmand and can inc pain in pts with angina
    • so should combine with a beta blocker to prevent this
  • hypotension
30
Q

nifedipine: nursing implications

A
  • inform pts about signs of edema
  • administer with a beta blocker to prevent reflex tachycardia
  • check BP, pulse, liver & kidney fcn before starting
  • monitor the serum levels of K+ if given with digoxin
31
Q

amlodipine: class

A
  • dihydropyridone: calcium channel blocker (but only minimally in the heart unlike verapamil and diltizem)
32
Q

amlodipine: MOA

A
  • selective blockade of Ca channels in blood vessles w/ minimal effects on the heart
33
Q

amlodipine: indications

A
  • essential HTN
  • angina pectoris
34
Q

amlodipine: SEs

A
  • peripheral and facial edema
  • flushing
  • dizziness
  • headache
  • eczematous rash
  • hypotension
35
Q

amlodipine: nursing implications

A
  • check BP, pulse, liver & kidney fcn before starting
36
Q

lisinopril: class

A
  • ACE inhibitors
  • anti HTN
37
Q

lisinopril: MOA

A
  • reduce levels of AngII thru inhibition of ACE
    • dilate blood vessels
    • reduce blood volume
    • prevent/reverse pathologic changes in the heart and blood vessels administered by Ang II and aldosterone
    • lower glomerular filtration pressure and cause slow development of renal injury
  • inc levels of bradykinin thru inhibition of kinase II
    • causes vasodilation
  • potassium sparing
38
Q

lisinopril: indications

A
  • HTN
    • especially malignant HTN and HTN secondary to renal arterial stenosis
    • essential HTN
  • HF
  • MI
  • diabetic and non-diabetic neuropathy
  • can also protect kidneys from damage–so can give to pt with diabetes
  • potassium sparing: good if someone on a potassium wasting drug
39
Q

lisinopril: SEs

A
  • first dose hypoTN: b/c lower Ang II–>vasodilation
  • hyperkalemia: b/c inhibition of Ang II–>inhibition of aldosterone
  • dizziness
40
Q

lisinopril: ADRs

A
  • renal failure, b/c Ang II will normally maintain glomerular filtration, so when we inhibit ACE and Ang II falls, then no urine production
  • fetal injury: hypoTN, hyperkalemia, skull hypoplasia, oliguria
    • during 2nd and 3rd trimester
  • angioedema: edema of tongue, glottis, lips, eyes, pharynx
  • cough: persistent, dry, nonproductive
    • when ACE gets degraded, you get bradykinin and if it builds up, then causes cough
41
Q

lisinopril: nursing implications

A
  • contraindicated in pts with bilateral renal stenosis
  • check BP after first hour on drug
    • take at bedtime if taking drug at home
  • shouldn’t take with NSAIDs b/c it will neutralize ACE, so will not lower BP like you want
  • monitor potassium
42
Q

furosemide: class

A
  • loop diuretic
43
Q

furosemide: MOA

A
  • acts in the thick segment of the ascending limb of Henle’s loop to block reabsorption of Na and Cl
    • by blocking solure reabsorption, furosemide prevents passive reabsorption of water (profound diuresis)
44
Q

furosemide: indications

A
  • reserved for situations that require rapid or massive mobilization of fluid
    • so should avoid the drug is less efficacious diuretis will suffice
  • pulmonary edema associated with CHF
  • edema of hepatic, cardiac, or renal origin that has been unresponsive to less efficacious diuretics
  • HTN that cannot be controlled with other diuretics
  • especially useful in patients with severe renal impairment, b/c (unlike thiazides) can promote renal diuresis when renal blood flow and GFR are low
45
Q

furosemide: SEs

A
  • hyponatremia
  • hypochloremia
  • hyperglycemia
  • hyperuricemia–>gout
  • reduces HDL, and raises LDL and triglycerides–>inc risk of coronary heart dz
46
Q

furosemide: ADRs

A
  • dehydration (dry mouth, thirst, oliguria)
    • can be anticipated by excessive loss of weight
    • can promote thrombosis and embolism: headache, pain in chest/calves/pelvis
  • HypoTN: due to loss of volume and relaxation of venous smooth muscle which reduces venous return to the heart
  • ototoxicity
  • maternal/fetal death, abortion
47
Q

furosemide: nursing implications

A
  • monitor weight loss (b/c can indicate dehydration)
  • monitor BP
    • and teach pt about symptoms of postural hypoTN (dizziness, lightheadedness)
  • contraindicated in pregnant patients
  • if taking once a day, take in the morning
    • if taking BID, then take at 8AM and 2PM
  • take with food if GI upset occurs
  • promote adherence by informing pt that meds will inc urine volume but effects will subside 6-8 hours after dosing
  • watch for signs and symptoms of hypokalemia
    • avoid K rich foods