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NRSG 220 > 9-14 STARRED FLASHCARDS > Flashcards

9-14 STARRED FLASHCARDS

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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
ARBs prototype
losartan
26
Losartan therapeutic classification
Antihypertensive
27
Losartan pharmacologic classification
Angiotensin 2 receptor blocker
28
Losartan therapeutic effects and uses
HTN CVA prophylaxis Prevention of diabetic nephropathy Off label use for HF
29
Losartan MOA
selectively blocks angiotensin AT1 receptors, resulting in decreased BP blockade prevents cardiac remodelling and deterioration of renal function in pts with DM
30
Losartan Drug interactions NSAIDs
decreased antihypertensive activity
31
Losartan drug interactions diuretics/other hypotensive
additive hypotensive action
32
Losartan drug interactions potassium supplements/potassium sparing diuretics
hyperkalemia
33
Losartan drug interactions alcohol
additive hypotensive effect
34
HTN damage on heart
hypertrophy, MI, HF
35
What to watch for with HTN heart damage
rapid weight gain (5lbs in 2/3days) SOB BLE edema
36
HTN damage to eyes
Blindness - frequent eye checks
37
HTN damage to the brain
Stroke - assess for speech changes, drooping face, one sided weakness
38
HTN damage to kidneys
Kidney failure - watch for protein in the urine (micro and macro albuminuria)
39
What is thiazide diuretic used for?
First line treatment option for HTN
40
What is often required with thiazide diuretics?
multi-drug therapy
41
What do thiazide diuretics do?
Decrease blood volume and decrease pressure
42
Thiazide diuretics ADEs
dehydration hyponatremia hypokalemia (less with K+ sparing diuretics) Nocturne (if taken too late in the day) orthostatic hypotension
43
what is a thiazide diuretic for HTN
hydrochlorothiazide
44
What are potassium sparing diuretic examples
triameterene, spironolactone
45
What are loop (high ceiling) diuretic examples
usually not used for HTN furosemide, bumetanide = K+
46
what do ACEI's do?
cause vasodilation by reducing angiotensin 2 decrease aldosterone effects (which increases effectiveness of diuretics) protect kidney
47
Common ACEI agents?
enalapril, lisinopril, captopril
48
ACEI ADEs
persistent cough postural hypotension hyperkalemis angioedema
49
What do ARBs do
inhibit effects of angiotensin 2 similar to ACEIs
50
ARBS ADEs
hypotension angioedema (rarer than with ACEI) more expensive no cough
51
ARBs Drug
Losartan
52
What are beta adrenergic antagonists
nonspecific also causes bronchoconstriction
53
Caution with what patients when using a BB
patients with asthma or HF
54
What ADEs occur with BB
low doses uncommon High doses: fatigue, activity intolerance erectile dysfunction masks symptoms of hypoglycemia clinical depression
55
Actions of direct acting vasodilators
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
Direct acting vasodilators ADEs
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
Direct acting vasodilators agents
hydralazine, diazoxide, nitroprusside
58
Direct acting vasodilatory prototype drug
Hydralazine
59
Hydralazine therapeutic classification
antihypertensive
60
hydralazine pharmacologic classification
direct vasodilator
61
hydralazine uses
moderate-severe HTN hypertensive emergencies acute HF
62
Hydralazine MOA
causes peripheral vasodilation decreases PVR, HR and CO decreases afterload selective for arterioles
63
Hydralazine considerations
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
Atorvastatin Considerations
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
Cholestyramine considerations
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
Gemfibrozil ADEs
abdominal cramping D/V Dyspepsia headahce dizziness peripheral neuropathy diminished libido
67
Gemfibrozil serious ADEs
cholethiasis anemia eosinophilia bleeding
68
Gemfbrozil contraindications/precautions
gallbladder disease serious liver impairment renal impairment
69
Gemfibrozil drug interactions with some statins
increased risk of myositis and rhabdomyolysis
70
gembibriozil drug interactions with anticoagulants
increased risk of bleeding
71
gemfibrozil drug interactions with antidiabetic agents
enhanced hypoglycemic effects
72
Gemfibrozil considerations
monitor lab tests consult prescriber if inadequate response after 3 months educate pt drug will cause bloating and gas watch for bleeding
73
What does L sided HF indicate
Pulmonary edema
74
what does R sided HF indicate
peripheral edema
75
What is systolic failure
decreased contractility decreased ejection fraction
76
What id diastolic failure
decreased ventricular filing normal ejection fraction
77
HF considerations
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
What weight gain should the patient call the HCP for
2lb in 1 day (realistically 5lbs in 2-3 days)
79
What are cardiac glycosides used for
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
Digoxin ADE
General malaise dizziness headache N/V anorexia visual disturbances (blurred or yellow vision think NCLEX)
81
Digoxin serious ADEs
ventricular dysrhytmias AV block Atrial dysrhyhthmias sinus bradycardia
82
Organic nitrates mechanism
relax venous muscle which reduces preload = less work for the heart relax arterial muscle which increases blood flow to myocardium
83
Organic nitrates ADEs
hypotension headache tolerance
84
What is nitric oxide
a cell signalling molecule and potent vasodilator
85
Short acting Organic nitrates
stop angina attacks (like salbutamol for asthma)
86
Long acting organic nitrates
prevent angina attacks (like salmeterol for asthma)
87
Nitroglycerin MOA
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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