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NRSG 220 > 9-14 STARRED FLASHCARDS > Flashcards

9-14 STARRED FLASHCARDS

1
Q

What are ACE inhibitors

A

first line agents in treatment of HTN and HF

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2
Q

How do ACE inhibitors work?

A

Block the conversion of angiotensin 1 to angiotensin 2

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3
Q

Where doe ace inhibitors act

A

in the lung (increases the potential for a cough)

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4
Q

What do ACE inhibitors actions result in

A

decrease in BP and PR
decrease in aldosterone secretion which reduces blood volume

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5
Q

What else do ACEI’s do?

A

Inhibit the breakdown of bradykinin

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6
Q

What can the accumulation of bradykinin cause

A

several ADEs effects of ACE inhibitor (cough for example)

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7
Q

Indications for ACE inhibitors

A

slow progression of HF
Lower mortality of recent acute MI
prophylaxis for adverse cardiac events
prevent or delay progression of renal disease and retinopathy of diabetics

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8
Q

ACE inhibitors contraindications

A

contraindicated in hyperkalemia
no pregnancy (major congenital defects)
caution with K+ sparing diuretics

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9
Q

What is the most serious ADE of ACEI

A

angioedema: rapid swelling of throat, face, larynx, tongue that can lead to airway obstruction

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10
Q

ACEI prototype drug

A

Lisinopril

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11
Q

ACEI therapeutic classification

A

antihypertensive

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12
Q

ACEI pharmacologic classification

A

ACE inhibitor

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13
Q

Therapeutic effects and uses for lisinopril

A

HF
HTN
Acute MI

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14
Q

Lisinopril MOA

A

Binds to and inhibits ACE action
decrease in serum angiotensin 2 reduces aldosterone, which results in less sodium and water retention

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15
Q

Lisinopril ADEs

A

Cough
Headahce
Dizziness
Orthostatic Hypotension

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16
Q

Lisinopril serious ADEs

A

Angioedema
Agranulocytosis
Hepatotoxicity

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17
Q

Lisinopril contraindications

A

pregnancy category D
angioedema
hyperkalemia
serious renal impairment

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18
Q

Lisnopril considerations

A

Check renal labs and K+ levels for hyperkalemia
monitor BP before administration and 30 min to 1 hour after

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19
Q

Lisinopril Drug Interactions NSAIDs

A

Decreased antihypertensive activity and worsened renal disease

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20
Q

Lisinopril drug interactions diuretics/other hypotensive

A

synergistic hypotensive action

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21
Q

lisnopril drug interactions potassium supplements, potassium sparing diuretics

A

Hyperkalemia

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22
Q

What pregnancy categories is lisinopril

A

Preg C first trimester
Preg D second and third trimester

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23
Q

Lisinopril treatment of OD

A

NS or vasopressor
Hemodialysis

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24
Q

ARBS indications

A

Same as for ACE inhibitors
Treat HTN and HF
Some approved to treat MI and prophylaxis of CVA
DO not cause cough
angioedema is less common

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25
Q

ARBs prototype

A

losartan

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26
Q

Losartan therapeutic classification

A

Antihypertensive

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27
Q

Losartan pharmacologic classification

A

Angiotensin 2 receptor blocker

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28
Q

Losartan therapeutic effects and uses

A

HTN
CVA prophylaxis
Prevention of diabetic nephropathy
Off label use for HF

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29
Q

Losartan MOA

A

selectively blocks angiotensin AT1 receptors, resulting in decreased BP
blockade prevents cardiac remodelling and deterioration of renal function in pts with DM

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30
Q

Losartan Drug interactions NSAIDs

A

decreased antihypertensive activity

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31
Q

Losartan drug interactions diuretics/other hypotensive

A

additive hypotensive action

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32
Q

Losartan drug interactions potassium supplements/potassium sparing diuretics

A

hyperkalemia

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33
Q

Losartan drug interactions alcohol

A

additive hypotensive effect

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34
Q

HTN damage on heart

A

hypertrophy, MI, HF

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35
Q

What to watch for with HTN heart damage

A

rapid weight gain (5lbs in 2/3days)
SOB
BLE edema

36
Q

HTN damage to eyes

A

Blindness - frequent eye checks

37
Q

HTN damage to the brain

A

Stroke - assess for speech changes, drooping face, one sided weakness

38
Q

HTN damage to kidneys

A

Kidney failure - watch for protein in the urine (micro and macro albuminuria)

39
Q

What is thiazide diuretic used for?

A

First line treatment option for HTN

40
Q

What is often required with thiazide diuretics?

A

multi-drug therapy

41
Q

What do thiazide diuretics do?

A

Decrease blood volume and decrease pressure

42
Q

Thiazide diuretics ADEs

A

dehydration
hyponatremia
hypokalemia (less with K+ sparing diuretics)
Nocturne (if taken too late in the day)
orthostatic hypotension

43
Q

what is a thiazide diuretic for HTN

A

hydrochlorothiazide

44
Q

What are potassium sparing diuretic examples

A

triameterene, spironolactone

45
Q

What are loop (high ceiling) diuretic examples

A

usually not used for HTN
furosemide, bumetanide = K+

46
Q

what do ACEI’s do?

A

cause vasodilation by reducing angiotensin 2
decrease aldosterone effects (which increases effectiveness of diuretics)
protect kidney

47
Q

Common ACEI agents?

A

enalapril, lisinopril, captopril

48
Q

ACEI ADEs

A

persistent cough
postural hypotension
hyperkalemis
angioedema

49
Q

What do ARBs do

A

inhibit effects of angiotensin 2
similar to ACEIs

50
Q

ARBS ADEs

A

hypotension
angioedema (rarer than with ACEI)
more expensive
no cough

51
Q

ARBs Drug

52
Q

What are beta adrenergic antagonists

A

nonspecific also causes bronchoconstriction

53
Q

Caution with what patients when using a BB

A

patients with asthma or HF

54
Q

What ADEs occur with BB

A

low doses uncommon

High doses:
fatigue, activity intolerance
erectile dysfunction
masks symptoms of hypoglycemia
clinical depression

55
Q

Actions of direct acting vasodilators

A

relax arterial smooth muscle directly = decrease in resistance and afterload
some also affect veins such as isosorbide denigrate (long acting nitrate) = decrease in preload

56
Q

Direct acting vasodilators ADEs

A

reflex tachycardia and hypotension
- compensatory increase in HR due to sudden drop in BP
fluid retention
can be minimized with beta blockers and diuretics

57
Q

Direct acting vasodilators agents

A

hydralazine, diazoxide, nitroprusside

58
Q

Direct acting vasodilatory prototype drug

A

Hydralazine

59
Q

Hydralazine therapeutic classification

A

antihypertensive

60
Q

hydralazine pharmacologic classification

A

direct vasodilator

61
Q

hydralazine uses

A

moderate-severe HTN
hypertensive emergencies
acute HF

62
Q

Hydralazine MOA

A

causes peripheral vasodilation
decreases PVR, HR and CO
decreases afterload
selective for arterioles

63
Q

Hydralazine considerations

A

Hx and PX
monitor lab tests for antinuclear antibody timer before and during therapy
monitor I&O
watch for ADEs
asses for rapid drop in BP and subsequent tachycardia

64
Q

Atorvastatin Considerations

A

obtain baseline lipid values
monitor LDL cholesterol levels
assess lipid lab tests within 2 to 4 weeks of initiation of therapy or change in dose
assess for signs of rhabdomyolysis or myopathies (generalized muscle pain/aches all over)
observe for digoxin toxicity
watch for hepatotoxicity (RUQ tenderness, stool changes, jaundice, bleeding/brusing, abd distension
no grapefruit juice
NO ALCOHOL

65
Q

Cholestyramine considerations

A

completely dissolve powder before administration
increase fluid intake
assess for early signs of hypoprothrombinemia
monitor lab tests for therapeutic effectiveness
consult prescriber to see if supplemental vitamins A and D and folic acid are required in LTC

66
Q

Gemfibrozil ADEs

A

abdominal cramping
D/V
Dyspepsia
headahce
dizziness
peripheral neuropathy
diminished libido

67
Q

Gemfibrozil serious ADEs

A

cholethiasis
anemia
eosinophilia
bleeding

68
Q

Gemfbrozil contraindications/precautions

A

gallbladder disease
serious liver impairment
renal impairment

69
Q

Gemfibrozil drug interactions with some statins

A

increased risk of myositis and rhabdomyolysis

70
Q

gembibriozil drug interactions with anticoagulants

A

increased risk of bleeding

71
Q

gemfibrozil drug interactions with antidiabetic agents

A

enhanced hypoglycemic effects

72
Q

Gemfibrozil considerations

A

monitor lab tests
consult prescriber if inadequate response after 3 months
educate pt drug will cause bloating and gas
watch for bleeding

73
Q

What does L sided HF indicate

A

Pulmonary edema

74
Q

what does R sided HF indicate

A

peripheral edema

75
Q

What is systolic failure

A

decreased contractility
decreased ejection fraction

76
Q

What id diastolic failure

A

decreased ventricular filing
normal ejection fraction

77
Q

HF considerations

A

ensure that pt monitor for dependent bilateral lower extremity (BLE) edema
worsening SOB or new onset
evaluate number of pillows needed to sleep at night or are they sleeping in a recliner
weight themselves everyday (same time same scale, same clothes)

78
Q

What weight gain should the patient call the HCP for

A

2lb in 1 day (realistically 5lbs in 2-3 days)

79
Q

What are cardiac glycosides used for

A

used in treating HF before ACE inhibitors
increase contractility (improve symptoms but do NOT improve mortality)
stabilize cardiac conduction abnormalities (so watch other antiarrhythmics
digitalization
dose gradually increased until tissues become saturated with medication and symptoms of HF diminish

80
Q

Digoxin ADE

A

General malaise
dizziness
headache
N/V
anorexia
visual disturbances (blurred or yellow vision think NCLEX)

81
Q

Digoxin serious ADEs

A

ventricular dysrhytmias
AV block
Atrial dysrhyhthmias
sinus bradycardia

82
Q

Organic nitrates mechanism

A

relax venous muscle which reduces preload = less work for the heart
relax arterial muscle which increases blood flow to myocardium

83
Q

Organic nitrates ADEs

A

hypotension
headache
tolerance

84
Q

What is nitric oxide

A

a cell signalling molecule and potent vasodilator

85
Q

Short acting Organic nitrates

A

stop angina attacks (like salbutamol for asthma)

86
Q

Long acting organic nitrates

A

prevent angina attacks (like salmeterol for asthma)

87
Q

Nitroglycerin MOA

A

at vascular smooth muscle, forms nitric oxide, which triggers a cascade resulting in release of calcium ions
relax both arterial and venous smooth muscle = less cardiac return (less preload)
dilates coronary arteries = increases O2 to the myocardium (cardiac muscles)

NRSG 220 (8 decks)

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