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Pharm 1 > drug therapy for coronary heart disease > Flashcards

drug therapy for coronary heart disease Flashcards

1
Q

chronic coronary artery disease (CAD) reults from…

A

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

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2
Q

what is CAD

A

narroing or blockage of the coronary arteries, usually caused by atherosclerosis

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3
Q

what is atherosclerosis

A

-sometimes called hardening or clogging of the arteries
-is a buildup of cholesterol and fatty deposits (called plaques) on the inner walls of the arteries

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4
Q

describe how CAD works

A

plaque = decrease diameter of artery = macrophage increase to degrade plaque = plaque rupture = endothelium injury = platelet aggregation = thrombus = release chemical mediators thromboxane, serotonin, plt growth factor = vasoconstriction = further narrow coronary arteries = less o2 to tissue and worsen myocardial ischemia (reduced blood flow)

manifests as chest pain = BAD

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5
Q

what are some risk factors for developing CAD

A

-SMOKING
-hyperlipidemia
-hypertension
-obesity
-diabetes mellitus or prediabetes
-physical conditioning
-age
-ethnicity
-hisotry of preeclampsia in pregnancy
-genetics

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6
Q

risk factors for CAD

describe hyperlipidemia

A

-abnormal cholesterol levels
-high total cholesterol and low density lipoprotein cholesterol and low high-density lipoprotein cholesterol
-<40mg/dl

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7
Q

risk factors for CAD

describe obesity

A

->20% over ideal body weight
-abdominal obesity

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8
Q

risk factors for CAD

describe physical conditioning

A

<30mins of moderate intensity aerobic exercise less than 3 times weekly

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9
Q

risk factors for CAD

describe age

A

men > 45 years
women > 55 years

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10
Q

risk factors for CAD

describe genetics

A

-heart disease in father or brother <55 years
-heart disease in mother or sister <65 years

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11
Q

describe the clinical manifestation of CAD

A

-stable angina (i.e. classic, typical, exertional angina)
-variant angina

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12
Q

describe stable angina

A

-clinical expression of myocardial
-results when myocardial O2 demand is greater than the O2 supply to the heart muscle
-often results from exercise, physical exertion, elemental exposer to cold, emotions/stress

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13
Q

what are the signs and symptoms of stable angina

A

-substernal CP
-“squeezing”
-may radiate to jaw, neck, shoulders, arm (brief 5 minutes - O2 restoration helps)
-can have SOB, diaphoresis, N/V
-can be mistaken for arthritis pain/GI disturbances
-gender differences exist in symptom quality

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14
Q

what is the goal of treatment for stable angina

A

-relieve signs and symptoms
-then increase tolerance and quality of life

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15
Q

what is the treatment for stable angina

A

-thrombolytics and interventional therapies
-calcium channel blockers, beta blockers, and nitrates

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16
Q

describe variant angina

A

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

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17
Q

describe acute coronary syndrome (ACS)

A

-unstable angina (crescendo, rest or preinfarction angina)
-acute pain occurs at rest and lasts longer than 20 minutes
-can occur hours or days prior to acute myocardial infarction
-action = imperative
-time = tissue

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18
Q

what are the two types of MIs

A

-NSTEMI
-STEMI

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19
Q

what are some signs of myocardial infarction

A

subjective:
-sudden onset CP
-left arm pain (may or may not radiate)

objective:
-SOB
-diaphoresis, pale, cool skin
-ekg
-labs (creatine kinase and cardiac troponin 1 +troponin T)

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20
Q

describe NSTEMI

A

non ST elevate myocardial infarction

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21
Q

describe STEMI

A

greater then 20 minute persistent ST elevation on EKG

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22
Q

what labs are used to determine MI

A

-creatinine kinase
-cardiac troponin 1 and troponin T

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23
Q

describe cardiac kinase

A

-cardiac isoenzyme
-eleavated value indicates damage to skeletal, visceral, or cardiac muscle

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24
Q

describe cardiac troponin 1 and troponin T

A

biomarker of myocyte injury r/t MI

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25
Q

what are some nonpharmacologic management of CAD

A

-risk factor modification
-patient education
-revascularization, interventional procedures

26
Q

describe risk factor modification with CAD

A

lifestyle changes, medications
-obesity, stop smoking
-elevated triglycerides, cholesterol
-elevated BP, fasting glucose

27
Q

describe revascularization, interventional procedures r/t CAD

A

-cardiac catheterization
-coronary artery bypass graft
-intracoronary stent

28
Q

describe antianginal agents and give examples of types

A

-can be used alone or in combination with other heart meds or lifestyle changes
-nitrates, beta adrenergic blockers, calcium channel blockers

29
Q

what is the goal of antianginal agents

A

-improve O2 delivery or decrease consumption
-dilate blood vessels
-decrease cardiac workload

30
Q

what are nitrates and give examples

A

-potent vasodilators
-examples include nitroglycerin, isosorbide dinitrate, and isosorbide mononitrate

31
Q

whare are some therapeutic actions and indications of nitrates

A

-telax and dilate veins, arteries, and capillaries; increase bloodflow; lower systolic pressure
-relief of and prevention of angina pain
-decrease preload and afterload (allows more O2 to get to tissue)

32
Q

what are some adeverse effects of nitrates

A

-severe headache
-dizziness
-bradycardia
-syncope
-hypotension/orthostatic hypotension
-can see reflex tachycardia in response to hypotension (heart thinks it needs to speed up)

33
Q

what are the adverse effects of nitrates related to

A

-the hemodynamic changes are responsible for preload and afterload reducation and vasodilation

34
Q

how are nitrates administered

A

-may be SL (most common: 3 doses q 5min / while administering 3rd dose call 911 if at home)
-translingual spray
-transdermal patch
-topical ointment
-PO
-IV

35
Q

why is SL administration of nitrates preferred in emergency situations

A

avoids the first pass effect

36
Q

describe the absorbtion and half life of nitrates

A

-rapidly absorbed
-half life is 1-4 mins

37
Q

where are nitrates metabolized and excreted

A

-metabolized in liver
-excreted in urine

38
Q

what are some nursing implications r/t nitrates

A

-check vitals, especially BP prior to and after administration
-pay attention to pts presentation and watch for signs of MI
-teach about orthostatic hypotension and remind pt to keep nitrates with them

39
Q

what are some examples of beta adrenergic blockers

A

-atenolol
-metroprolol
-bisoprolol

these are all examples of cardo selective beta adrenergic blockers

40
Q

describe cardio selective beta adrenergic blockers

A

-20x more potent at blockig beta 1 receptors in the heart than they are at blocking beta 2 receptors
-less likely to cause bronchoconstriction compare to nonselctive beta adrenergic blockers

41
Q

describe the therapeutic actions and indications of beta adrenergic blockers

A

-decrease cardiac workload by slowing HR, decrease BP, and reduce contractility -> increase O2 to heart
-cornerstone daily tx for pts with angina
-tw of angina, HTN, prevention and tx post MI

42
Q

when should you take caution when giving beta adrenergic blockers

A

-2nd/3rd degree heart block
-cardiogenic shock
-severe bradycardia
-hypotension
-heart failure

43
Q

what is the black box warning for beta adrenergic blockers

A

remember DO NOT abruptly withdrawal medication, expecially in pts with CAD; slowly taper off med

44
Q

describe how beta adrenergic blockers interact with renal function

A

-well tolerated in patients with renal impairment
-may slow renal function decline

45
Q

gave an example of a calium channel blocker

A

nifedipine

46
Q

describe the theraputic actions and indications of calcium channel blockers

A

-inhibit the reflux of calcium entering through slow channels, producing vasodilation of the peripheral blood vessels and coronary arteries
-does not affect heart rate

47
Q

describe the pharmacokinetics of calcium channel blockers

A

-first pass metabolism in liver
-fecal and urinary excretion

48
Q

what are some adverse effects of calcium channel blockers and what may help reduce them

A

-hypotension
-flushing
-headache
-dizziness
-lower limb edema
-reflex tachycardia

-these appear to be dose related and the medication dose can be adjusted to help limit these effects

49
Q

what are the adverse effects of calium channel blockers related to

A

-vasodilation
-dosage

50
Q

describe the nursing implications related to calcium channel blockers

A

-chack vitals, especially BP prior to and after administration
-grapefruit juice will increase effects of med
-do not use with adrenergic stimulants (cocaine/ampethamines)
-will increase digoxin levels

51
Q

name some adjunctive antianginal drugs

A

-ranolazine
-dyslipidemic drugs
-antihypertensive drugs
-morphine
-antiplatelets

52
Q

describe ranolazine

A

-antiischemic metabolic modulator
-first line treatment for chronic angina

53
Q

what are some examples of dyslipidemic drugs

A

-atorvastatin
-cholesyramine
-niacin

54
Q

what are dyslipidemic drugs used for

A

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

55
Q

describe antihypertensive treatment as an adjunctive antianginal drug

A

-decrease peripheral vasular resistance can treat angina
-example: angiontensin converting enzyme (ACE) inhibitor

56
Q

describe morphine as an adjunctive antianginal drug

A

-opiod analgesic
-tx for pain and anxiety which decreases preload
-primary reliever of pain in post MI patients with unacceptable levels of pain

57
Q

what are some examples of antiplatelets given for antianginal effects

A

-aspirin (STANDARD)
-adenosine diphosphate (ADP) receptor antagonists
-glycoprotein (GP) IIb/IIa receptor antagonists

58
Q

describe aspirin as an antiplatelet

A

antiplatelet effect which at a lower dose effectovely suppress pletelet aggregation w/o affecting important endothelial function

59
Q

what is the goal of therapy with antianginal drugs

A

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

60
Q

describe tolerance of long acting nitrates

A

-develops with high dose, uninterrupted therapy
-decreases adverse effects and efficacy

61
Q

describe preventing tolerance stretegies for nitrates

A

-administer lowest effectove dose
-avoid long acting formas of nitrates
-only use long acting forms during waking hours

Pharm 1 (29 decks)

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