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pharmacology > drugs for angina, MI and CVA > Flashcards

drugs for angina, MI and CVA Flashcards

1
Q

what is atherossclerosis

A

this is when the arterial blood supply is compromised due to narrowing and the cardiovascular and cerebrovascular supply becomes impaired

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2
Q

what are deprived of nutrients with atherosclerosis since blood and cerebral vascular flow are impaired

A

heart brain and other organs

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3
Q

angina pectoris, acute MI and cerebral vascular accident are all results of what

A

atherosclerosis and poor blood supply

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4
Q

endothelial injury and inflammation result in what cells migrating

A

immune cells to the site of injury

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5
Q

when are tight junctions between cells loosened

A

when there is endothelial injury

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6
Q

what is going to go into the tight junstions of cells if they are loosned

A

LDL

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7
Q

what are foam cells

A

this is when macrophages engulf oxdized LDL

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8
Q

when t-lymphocytes secrete cytokines inducing smooth muscle migration, what happens to blood vessel elasticity and responsiveness

A

impiares bloof vessel elasticity and responsiveness to stimuli

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9
Q

angina pectrois is what kind of issue

A

it is a demand issue

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10
Q

what is angina pectoris

A

this is acute chest pain arising from inadequate oxygen supply to the myocardium

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11
Q

what is characterized by a steady, intense pain that is sometimes accompanies by a crushing, constricting sensation

A

angina pectoris

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12
Q

your patient comes in with pain radiating across the left shoulder, down the left arm, they are pallor, SOB, and sweating - what do you suspect is happening

A

the patient is experiencing angina pectoris

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13
Q

what might a female patient with angina pectoris experience

A

nausea, abdominal pain

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14
Q

stable angina

A

predicatble frquency, duration and intensity, not associated with myocardial damage

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15
Q

unstable angina - intensity, variable period, frequency

A

variable intensity, occurs during period of rest, inceased frequncy

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16
Q

what is associated with an increased risk of MI

A

unstable angina

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17
Q

non-pharmacological interventions for stable angina

A

limit alcohol, foods high in cholestoroal, control hyperlipidemia, control hypertension, regular exercise, control blood glucose

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18
Q

limit alcohol, foods high in cholestoroal, control hyperlipidemia, control hypertension, regular exercise, control blood glucose

A

non-pharmacological interventions for stable angina

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19
Q

what is the goal of drug therapy

A

slow HR, reduce force of cardiac contraction, dilate veins, dilate arterioles

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20
Q

what is the first line therapy for stable angina

A

nitrates

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21
Q

what do nitrates do

A

they facilitate the formation of nitric acid, a potent dialator for smooth muscle

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22
Q

nitrate; what does the dilation of smooth muscle allow for; blood flow

A

decreased the amount of blood returning to the heart, CO, workload, O2 demand

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23
Q

decreases the amount of blood returning to the heart, CO, workload, O2 demand

A

nitrate

24
Q

nitrates; what does the dilation of arterial smooth muscle do to blood flow and oxygen supply

A

increases blood flow and improves oxygen supply to the myocardium

25
Q

what is the protocol for taking nitrate

A

rest, take drug and wait 5 min, if no imporvement take another dose wait 5 min

26
Q

what is the maximum dose for nitrates

A

3 doses in 15 minutes

27
Q

how should you withdrawl a patient off of nitrate

A

slowly to prevent risk of MI

28
Q

adverse effects for nitrates

A

all rt vasodilation and decrease in blood flow - headache, dizziness weakness, hypotension, relfex tachycardia

29
Q

your patient recently had angina, and is experiencing a headache and hypotension. they ask why this is happening - why

A

because there is vasodilation and decreased blood flow

30
Q

when should you be cautious when giving nitrates

A

wiht pt with hypotension, hypovolemia

31
Q

what drug interactions are there for nitrates

A

treatment for ED, alcohol

32
Q

why dont you want your patient to take nitrates when they are on ED medications and drinking alcohol

A

because they both cause vasodliation, so could lead to hypotension

33
Q

beta adrenergic antagonists are first line therapy for what- angina pectoris

A

first like therapy for chrinic stable angina

34
Q

hwo to beta adrenergic antagonists work

A

they work to reduce the cardiac workload, which slows the HR and reduces contractilitiy

35
Q

what works to reduce cardiac workload, slows HR and contractibility

A

beta adrenergic antagonists

36
Q

when should you be careful when usings beta adrenergeric antogonists (4)

A

asthma, COPD, depression and diabetes

37
Q

adverse effects of beta adrenergic antagonists - think weakness

A

fatigue, weakness, bradycardia, hypotension, sleep distubrances

38
Q

how should you take a patient off of beta adrenergic antagonist drugs

A

reduce the does over 1-2 weeks

39
Q

why arent calcium channel blockers firts line therapy for angina?

A

because they can cause low bp

40
Q

calcium channel blockers are used for the prevention of what angina, and in clients whom cannot tolerate what

A

the prevention of chronic stable angina in clients who cannot tolerate beta blockers

41
Q

what causes decreased myocardial demand, relax arteriolar smooth muscle lowering BP and decreasing afterload, and decreases heart rate

A

calcium channel blockers

42
Q

adverse effects of CCB

A

dizziness, lightheadedness, fatigue, bradycardia, flushing, nausea

43
Q

what should you monitor for with someone taking ccb

A

hypotension, and reflex tachycardia

44
Q

why should grapefruit juice be avoided when on ccb

A

because it will increase the ccb levels

45
Q

what is myocardial infarction a result of what disease

A

result of advanced coronary artery disease

46
Q

what happens when a coronary artery is occluded

A

MI and necrosis

47
Q

what are the goals of MI therapy

A

reduce myocardial oxygen demand

restore blood supplt to the damaged myocardium

48
Q

thrombolytics - MI

A

restore blood supply to the damamged myocardium

49
Q

nitrates, beta blockers, ACE inhibitors - are used to prevent what demand?????

A

to reduce myocardial oxyegn demand and to prevent further infarction

50
Q

what is used to control or prevent MI-associated dysrhythmias

A

beat blockers

51
Q

what is used to reduce post-MI mortality

A

aspirin, beta-blockers, ace inhibitors, statins

52
Q

how do we manage severe pain and anxiety of MI

A

opiates

53
Q

warning signs of stroke

A

paralysis on one side, vision issues, dizziness, speech problems, headache

54
Q

true or false

80% of strokes are thrombotic and 20% are hemorrhagic

A

trie

55
Q

how can we pharmacologically treat thrombotic CVA

A

thrombolytics

pharmacology (26 decks)

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