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Pharmacology > HTN & Congestive Heart Failure > Flashcards

HTN & Congestive Heart Failure Flashcards

1
Q

ACE Inhibitors Meds

A

Captopril (PO)

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2
Q

Captopril Use

A

HTN, heart failure, DM nephropathy, MI

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3
Q

Captopril MOA

A
  • reduce levels of angiotensin II
  • increase levels of bradykinin
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4
Q

Captopril adverse effects

A
  • hyperkalemia
  • hypotension/orthostatic
  • teratogen
  • heart attack
  • cough
  • angioedema
  • reduced neutrophils + granulocytes
  • renal failure in pts. w/bilateral renal aa stenosis
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5
Q

Captopril interactions

A
  • diuretics, antihypertensives (hypotension)
  • drugs that raise K+ (hyperkalemia)
  • lithium accumulation
  • NSAIDs
  • taken w/digoxin can increase risk of hyperkalemia
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6
Q

Captopril implications

A
  • take first dose @bedtime to prevent orthostatic HOTN
  • educate on cough - notify prescriber
  • contraindicated w/pregnant + renal artery stenosis
  • monitor K, CBC, urine for protein
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7
Q

Angiotensin II Receptor Blockers (ARBs) meds

A

Irbesartan, Losartan

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8
Q

ARBs use

A

HTN, HF, DM nephropathy

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9
Q

ARBs MOA

A

block vasoconstriction effects of angiotensin II

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10
Q

ARBs adverse effects

A

angioedema, renal failure, fetal injury

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11
Q

ARBs implications

A

don’t cause cough or hyperkalemia

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12
Q

Direct Renin Inhibitors med

A

Aliskiren

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13
Q

Aliskiren use

A

HTN

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14
Q

Aliskiren MOA

A

binds to renin and inhibits conversion of angiotensinogen into angiotensin I

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15
Q

Aliskiren adverse effects

A

angioedema, cough, hyperkalemia, teratogenic, diarrhea

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16
Q

Aliskiren implications

A

avoid high fat meals with administration - affects absorption

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17
Q

Aldosterone antagonist meds

A

Eplerenone, spironolactone

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18
Q

Eplerenone, spironolactone use

A

HTN, HF

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19
Q

Eplerenone, spironolactone MOA

A

selective blockage of aldosterone receptors

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20
Q

Eplerenone, spironolactone adverse effects

A
  • hyperkalemia
  • drug binding w/receptors for other steroid hormones can cause gynecomastia, menstrual irregularities, impotence, hirsutism, deepening of voice
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21
Q

Eplerenone, spironolactone implications

A
  • monitor potassium
  • do not use in patients with renal disease or type 2 DM
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22
Q

Calcium channel blockers

A

lower BP and contractility

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23
Q

CCB use

A

HTN, angina pectoris, cardiac dysrhythmias

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24
Q

Verapamil, diltiazem work primarily on

A

arterioles and heart

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25
Q

Verapamil, diltiazem MOA

A
  • prevent calcium ions from entering heart mm cells and blood vessels
  • vasodilation, reduced arterial pressure, increased coronary perfusion
  • reduced force and HR
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26
Q

Verapamil, diltiazem adverse effects

A
  • constipation
  • bradycardia or AV block
  • result of vasodilation: dizzy, flushing, headache, peripheral edema
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27
Q

Verapamil, diltiazem implications

A
  • s/s of toxicity: severe hypotension, bradycardia, AV block, ventricular tachydysrhythmias
  • antidote is IV calcium gluconate
  • check HR and BP before giving
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28
Q

Amlodipine class

A

Dihydropyridines family of CCB

29
Q

Amlodipine MOA

A
  • blocks calcium channels in vascular smooth mm tissue
  • lowers BP, increase HR and contractility
30
Q

Amlodipine adverse effects

A

result of vasodilation: dizzy, flushing, headache, peripheral edema

31
Q

Amlodipine implications

A

peripheral edema is most common side effect of vasodilation

32
Q

Hydralazine use

A

essential HTN, HTN crisis, HF

32
Q

Hydralazine is a

A

vasodilator

33
Q

Hydralazine MOA

A

selective dilation of arterioles

34
Q

Hydralazine adverse effects

A

postural hypotension, reflex tachycardia, expansion of blood volume, systemic lupus erythematosus-like syndrome

35
Q

Hydralazine implications

A
  • symptoms may last 6months-year
  • stop drug if systemic lupus erythematous like syndrome occurs
36
Q

Nitroprusside is a

A

direct acting vasodilator

37
Q

Nitroprusside use

A

drug of choice for HTN crisis - potent and fast

38
Q

Nitroprusside MOA

A

causes venous and arteriolar dilation by increasing blood flow to the heart

39
Q

Nitroprusside adverse effects

A

excessive hypotension, cyanide poisoning

40
Q

Nitroprusside implications

A
  • monitor for thiocyanate toxicity by drawing cyanide levels
  • must check BP frequently
41
Q

Propranolol, metoprolol Use

A

MI, angina, HTN, hypertrophic cardiomyopathy, supraventricular arrythmias

42
Q

Propranolol, metoprolol adverse effects

A
  • hypotension, bradycardia, palpitations, hypoglycemia
  • non selective: n/v, bronchospasm, impotence
43
Q

Propranolol, metoprolol implications

A
  • avoid in asthma and COPD patients
  • monitor BP
44
Q

Clonidine Use

A

HTN

45
Q

Clonidine MOA

A

vasodilation, lower BP and CO

46
Q

Clonidine adverse effects

A

rebound hypertension, dry mouth, sedation

47
Q

Clonidine implications

A

monitor BP

48
Q

Nursing implications for ACE Inhibitors, ARBs, and Renin inhibitors

A
  • monitor BP closely for 2 hours after 1st dose
  • obtain WBC Q2weeks for first 3 months and monitor for neutropenia (mainly w/captopril)
  • target BP <140/90
  • instruct to lie down if hypotensive
  • warn about cough and to contact prescriber if present
  • avoid K supplements unless prescribed
  • warn woman of childbearing age
  • angioedema - if occurs, stop ACE inhibitors and NEVER take again
  • withdraw diuretics 1 week prior to starting ACE inhibitors
  • minimize NSAID use - decrease effectiveness
49
Q

Nursing implications for CCB

A
  • if baseline BP & HR to low, withhold med, document, and notify MD
  • contraindicated in pts with severe hypotension, sick sinus syndrome, and 2nd-3rd degree heart block
  • use with caution if taking digoxin or beta blockers
  • teach to self-monitor BP with goal of 140/90
  • inform about signs of heart block (slow HR, SOB, weight gain)
  • watch for ankle swelling
  • increase dietary fluid and fiber
  • swallow sustained-released tablets whole
50
Q

Nursing implications for BB

A
  • report signs of resp distress
  • check pulse daily
  • monitor BP regularly
  • warn about masked hypoglycemia
  • do not stop drug abruptly
  • take oral forms with meals for better absorption
  • antacids, barbiturates, anti-inflammatories, and rifampin can decrease effectiveness of BB
51
Q

Drugs to treat CHF

A

captopril, losartan, diuretics, propranolol, metoprolol, digoxin

52
Q

Thiazide diuretics

A

hydrochlorothiazide, moderate diuresis

53
Q

Loop diuretics

A

furosemide, profound diuresis, promote fluid loss even when GFR is low

54
Q

Potassium sparing diuretics

A

spironolactone, scant diuresis

55
Q

Diuretics MOA

A

promote excretion of water and electrolytes by the kidneys

56
Q

Diuretics adverse effects

A
  • hypotension
  • hyperkalemia (potassium-spring)
  • hypokalemia (loop and thiazide)
  • dysrhythmias when used with digoxin
57
Q

Diuretics implications

A

monitor potassium, take in the morning

58
Q

Digoxin class

A

Cardiac glycoside

59
Q

Digoxin MOA

A

increase contractility, decrease HR

60
Q

Digoxin Use

A

CHF, atrial tachycardia, atrial fibrillation

61
Q

Digoxin adverse effects

A

cardiac dysrhythmias, halos around eyes, n/v, bradycardia, hypokalemia

62
Q

Digoxin interactions

A
  • diuretics promote loss of potassium - increased risk of dysrhythmias and toxicity
  • ACE inhibitors/ARBs can increase potassium and decrease therapeutic responses to digoxin
63
Q

Digoxin contraindications

A
  • second or third degree heart block
  • caution with renal disease, hypothyroidism, hypokalemia
64
Q

Digoxin ranges

A
  • normal potassium: 3.5-5
  • therapeutic range: 0.5-2
  • > 2 is toxic
65
Q

Draw levels of digoxin

A

immediately before 1st dose or 4-10 hrs after it

66
Q

Signs of digoxin toxicity

A
  • anorexia, n/v, halos around eyes, bradycardia, heart block, dysrhythmias
  • hold medication and notify prescriber if concerned about toxicity
  • low potassium increases risk of toxicity
67
Q

If BPM is <60, digoxin

A

should be withheld, notify physician

68
Q

Digoxin patient education

A
  • avoid OTC
  • eat foods high in potassium
  • fresh and dry fruits, vegetables, potatoes

Pharmacology (9 decks)

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