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pharm exam 2 > drug therapy coronary heart disease > Flashcards

drug therapy coronary heart disease Flashcards

1
Q

chronic coronary artery disease (CAD) results from

A

damage to the intima (inner layer) of coronary arteries = build up of lipids and fiber in lumens

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2
Q

CAD is also known as

A

the narrowing or blockage of the coronary arteries, usually caused by arteriosclerosis

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3
Q

what is arteriosclerosis

A

hardening or clogging of the arteries; a build up cholesterol and fatty deposits (plaques) on the inner walls of the arteries

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4
Q

plaque in the arteries to what

A

decrease the diameter of the artery, increasing macrophage to degrade the plaque, resulting in the plaque rupturing = endothelium injury, aggrevates platelet = thrombus = release of chemical mediators thromboxane, serotonin, platelet regrowth = vasoconstriction = further narrowing coronary arteries, less oxygen to tissue and worsen myocardial ischemia (reduced blood flow)

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5
Q

symptom of coronary heart disease

A

chest pain, very very bad

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6
Q

risks factors for developing CAD

A

smoking, abnormal cholesterol level(hyperlipidemia), high BP, obesity, DM, little exercise, age (men>45, women>55), ethnicity, hx of preeclampsia, genetics(male<55, female<65)

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7
Q

CAD clinical manifestation

A

stable angina, variant angina

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8
Q

what is stable angina

A

classic, typical, exertion angina

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9
Q

what results from stable angina

A

when myocardial O2 demand is greater than the O2 supply to the heart muscle; from exercise, physical exertion elemental exposer to the cold emotion/stress

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10
Q

substernal chest pain (CP) is what; part of stable angina

A

squeezing, may radiate to jaw, neck, shoulders, arm (brief: 5 mins- O2 restoration helps)

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11
Q

signs of substerbal CP/ stable angina

A

SOB, diaphoresis, N/V, mistaken for arthritis pain/ GI disturbances, gender differences exist in symptom quality

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12
Q

treatment for stable angina

A

thrombolytics(lyse the clot) & interventional therapies; calcium channel blockers, beta blockers, nitrates (relieve s/sx), increase exercise tolerance and life, delay CAD progression

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13
Q

what Is variant angina

A

occurs at rest/ minimal exertion, occurs at same time of day, cyclic 3-6 months subsides

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14
Q

acute coronary syndrome (ACS)

A

unstable angina; acute pain occurs at rest and lasts longer than 20 mins; can occur hours/ days prior to acute myocardial infarction

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15
Q

2 types of myocardial infarcts (MI)

A

nstemi and stemi

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16
Q

nstemi MI

A

non ST elevate myocardial infarction

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17
Q

stemi MI

A

greater than 20 minute persistent ST elevation on ECG; very dangerous

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18
Q

labs for myocardial infarctions

A

creatine kinase: cardiac isoenzyme(shows damage to the heart); cardiac troponin 1 & troponin T: biomarker of myocyte injury(cell damage)

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19
Q

nonpharmacologic management of CAD

A

lifestyle changes & medications; obesity, stop smoking, patient education, interventional procedures (cardiac catheterization, coronary artery bypass graft, intracoronary stent)

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20
Q

antianginal agents used to

A

improve O2 delivery or decrease consumption; used alone of in combination with other cardiac medications

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21
Q

abtianginal agents will

A

dilate blood vessels, decrease cardiac workload

22
Q

types of antianginal agents

A

nitrates, beta adrenergic blockers, calcium channel blockers

23
Q

nitrates are

A

potent vasodilators

24
Q

examples of nitrates

A

nitroglycerin, isosorbide dinitrate

25
Q

therapeutic actions of nitrates

A

relax and dilate veins, arteries, and capillaries(systemic vascular dilatation): increase blood flow, lower systolic pressure; relief of and prevention of angina pain; decreases preload and after load

26
Q

adverse effects of nitrates

A

severe HA, dizziness, bradycardia, syncope, hypotension/ orthostatic

27
Q

what other symptom may you see with the use of nitrate

A

reflex tachycardia in response to hypotension (heart thinks it needs to speed up)

28
Q

how is nitrate given

A

may be SL(first pass effect with SL)(most common: 3 dose q 5 min/ while administering 3rd dose call 911 if at home), translingual spray, transdermal patch, topical ointment, PO, or IV

29
Q

the half of nitrate

A

rapidly absorbed/ half life = 1 to 4 minutes

30
Q

where is nitrate metabolized

A

in the liver, excreted in urine

31
Q

nursing considerations for nitrates

A

check vitals, BP prior and after administration (should see a drop)

32
Q

beta-adrenergic blockers examples

A

atenolol, metoprolol, bisoprolol (cardio selective)

33
Q

therapeutic actions of beta adrenergic blockers

A

decrease cardiac workload by slowing HR, decrease BP and reduce contractility(increase O2 to the heart), cornerstone daily med for patients with angina, decreases need for SL nitroglycerin for angina

34
Q

beta adrenergic blockers treats

A

angina, HTN, prophylaxis/ tx post MI

35
Q

caution of beta adrenergic blockers

A

in 2nd/3rd degree heart block, cariogenic shock, severe bradycardia, hypotension, heart failure

36
Q

black box warning on beta adrenergic blockers

A

do not stop abruptly, taper off; its well tolerates in patient with renal impairment/ may slow renal function decline

37
Q

example of calcium channel blockers

A

nifedipine

38
Q

therapeutic action of calcium channel blockers

A

inhibit the influx of calcium entering through slow channels, producing vasodilation of the peripheral blood vessels and coronary arteries (it does not affect the HR)

39
Q

pharmacokinetics of calcium channel blockers

A

first pass metabolism in the liver, fecal and urinary excretion

40
Q

adverse effects of calcium channel blockers

A

hypotension, flushing, HA, dizziness, lower limp edema, reflex tachycardia; dose related

41
Q

nursing considerations when using calcium channel blockers

A

check vitals, BP prior to and after administration (grapefruit juice will increase effect of medications/ do not use with adrenergic stimulants(cocaine), will increase digoxin levels

42
Q

adjunctive abtianginal drugs

A

ranolazine, dyslipiemic drugs, antihypertensive, morphine, anti platelets

43
Q

ranolazine is what

A

anti-ischemic metabolic modulator = first line tx for chronic angina

44
Q

dyslipidemic drugs do what

A

management of patients with major risk factors for atherosclerosis and vascular disorders (CAD, stroke, and peripheral arterial insufficiency)when lifestyle changes alone do not reduce blood lipids

45
Q

antihypertensive drugs do what

A

decrease peripheral vascular resistance can tx angina (ex. ACE inhibitors)

46
Q

morphine does what

A

helps pain/ anxiety, decreases preload; primary deliver in pain management in post MI in patients with unacceptable levels of pain

47
Q

antiplatelets examples/ do what

A

aspirin: at lower doses effectively suppress platelet aggregation w/o affecting important endothelial cell function; adenosine diphosphate (ADP) receptor antagonists: similar effects; glycoprotein (GP): inhibit platelet aggregation as well

48
Q

what is the purpose of giving thrombolytic agents following a stemi

A

is to dissolve thrombi and reestablish blood flow as quickly as possible, prevent or limit tissue damage, and maximize functional improvement. the antiplatelets are daily medication for prevention

49
Q

goals of therapy for antianginal drugs

A

relieve acute anginal pain, reduce number and severity of acute annginal attacks, improve exercise tolerance and life quality, delay progression of CAD, prevent MI and sudden cardiac death

50
Q

tolerance to long acting nitrate- antianginal drugs

A

develops with high dose, uninterrupted therapy; decrease adverse effects and efficacy

51
Q

preventing tolerance strategies: administer lowest effective dose and?

A

avoid ling acting forms of nitrates, only use long acting forms during waking hours

pharm exam 2 (8 decks)

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