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Pharm II > (04-05-17) Cardiovascular Drugs > Flashcards

(04-05-17) Cardiovascular Drugs Flashcards

1
Q

underlying defect is a failure in the regulation of vascular resistance

A

hypertension

*defined as TWO BP readings of at least 140/90 separated by 2 minutes on 2 or more visits

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2
Q

what is systolic BP

A

pressure at peak of left ventricular contraction

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3
Q

what is diastolic BP?

A

resting resistance of the arterial system

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4
Q

what is the prevalence of HTN?

A

20-30% of all adults (more than 50 mill)

-1 in 4 pts in teh US have HTN

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5
Q

what % of pts with HTN are not being treated?

A

46.4%

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6
Q

what % of the pts that are being treated for HTN are adequately controlled?

A

49%

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7
Q

compromises 90-95% HTN pts

  • precise etiology is unknown
  • older pts
A

primary HTN

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8
Q

other 5-10% of pts with HTN

  • there is some underlying condition
  • often younger pts
  • –renal, endocrine, neurologic disorders
A

secondary HTN

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9
Q

what are the #’s for normal HTN?

A

less than 120 / less than 80

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10
Q

what are the #’s for pre-HTN?

A

120-139 / 80-89

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11
Q

what are the #’s for stage one HTN?

A

140-159 / 90-99

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12
Q

what are the #’s for stage two HTN?

A

greater than 60 / greater than 100

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13
Q

what is considered an URGENCY with HTN?

A
  • systolic is greater than 180

- diastolic is greater than 110

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14
Q

what is considered an EMERGENCY?

A
  • same as with urgency but now with evidence of end-organ damage
  • -confusion
  • -chest pain
  • -renal failure
  • -visual changes
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15
Q

what are the benefits of treatment of HTN?

A
  • reduces incidence of stroke
  • dec MI
  • dec CHF
  • reduciton of 12mm HG in SBP for ppl instage 1 HTN over a 10 year period in prevention of 1 death in 11 pts treated
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16
Q

what are the goals of tx of HTN?

A
  • limit end-organ damage
  • most adults less than 140/99 mmHG
  • diabetes or renal disease less than 130/80 mmHg
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17
Q

what are the ways to treat HTN?

A
  • ALWAYS start with lifestyle modifications (weight loss, red sodium, aerobic exercise, dec alcohol intake, stop smoking)
  • MOST pts require pharmacologic treatment
  • MOST require more than one agent to achieve goals
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18
Q

what are the 5 common anti-hypertensive groups?

A
  • diuretics
  • adrenergic agents
  • CCBs
  • ACEIs
  • ARBs
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19
Q

what are the steps to treating HTN pharmacologically?

A
  1. diuretic, beta blocker, ACEI/CCB. Thiazide is preferred
  2. after 1-3 months, inc the dose, add a different class, or substitute another drug
  3. add a 3rd drug, discontinue the 2nd drug, and substitute another
  4. add a 3rd and 4th drug
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20
Q

what is the mechanism of thiazide diuretics?

A
  • dec CO (by reducing plasma volume)

- dec peripheral resistance (red Na-Ca exchange)

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21
Q

where do thiazide diuretics work?

A

distal convoluted tubule

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22
Q

what are the adverse effects of thiazide diuretics?

A
  • hypokalemia (tired, lethargic, weakness)
  • xerostomia
  • anorexia

*all bc it basically drains your system of water

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23
Q

why are loop diuretics considered the “strong cousin” of thiazide diuretics?

A

bc they act the same way just in a different part of the body

  • ASCENDING LOOP OF HENLE
  • inhibits reabsorption of Na with concurrent loss of fluids
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24
Q

what is the most commonly used loop diuretic?

A

furosemide (lasix)

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25
Q

what are the adverse reactions of loop diuretics?

A
  • hypokalemia
  • hyperuricemia
  • mostly used in pts with CHF
  • can also be used if rapid diuresis is desired
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26
Q

-diuretics involvoing “potassium -catching” ability

A

potassium sparing diuretics

*used as adjunctive therapy with other drugs

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27
Q

what pt populationare potassium sparing diuretics good for?

A

pts concerned about UNWANTED HYPOKALEMIA

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28
Q

what is the mechanism of potassium sparing diuretics?

A
  • competitive ANTAGONISTS compete with aldosterone

- directly block Na channels

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29
Q

where do potassium sparing diuretics work ?

A

DCT and collecting duct

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30
Q

what are the adverse reactions of potassium sparing diuretics?

A
  • hyperkalemia

- arrhythmia

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31
Q

what are the receptors for the adrenergic agents for HTN?

A
  • alpha 1 = inc BP
  • alpha 2 = stimulation inhibits norepi
  • beta 1 = inc HR and contraction
  • beta 2 = inc contraciton and CO (not as strong as beta 1)
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32
Q

what are the medication mechanisms for adrenergic agents of HTN?

A
  • alpha 2 agonists
  • alpha 1 antagonists
  • non-selective beta 1 and beta 2 antagonists
  • beta 1 antagonists
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33
Q

what is the mechanism of alpha 1 antagonists?

A
  • block receptors in arteries and veins therefore relaxing smooth muscle associated with these
  • not typically used drug for HTN, can use in CONJUNCTION with BPH
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34
Q

what are the side effects of alpha 1 antagonists?

A

postural hypotension

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35
Q

what is the mechanism of alpha 2 agonists?

A
  • inhibition action of epi and norepi
  • leads to vessel dilation
  • NOT FIRST LINE, usually 3rd or 4th
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36
Q

what are the side effects of alpha 2 agonists?

A

drowsiness, sedation

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37
Q

why do beta blockers help asthema?

A

bc they lead to bronchial dilation

38
Q

what pts are NON-SELECTIVE beta blockers bad for?

A

pts with reactive airway disease

39
Q

what pts are SELECTIVE (B1 only) good for?

A

-ischemic heart disease pts and MI

-

40
Q

what is the disadvantage to selective B1 blockers?

A
  • hypotention

- bradycardia

41
Q
  • these drugs have the suffix -dipine

- used to treat HTN and other cardiac conditions such as arrhythmias and angina

A

Calcium channel blockers

42
Q

what is the mechanism for calcium channel blocker?

A
  • inhibit the movement of calcium into cardiac cells

- produces vasodilation and reduces afterload

43
Q

how does the CCB, dihydropyridine work?

A

reduce vascular resistance = dilation

44
Q

how does the CCB, NON-dihydropyridine work?

A

reduce myocardial O2 demand = treat angina

45
Q

what are the adverse reactions of CCB?

A
  • gingival overgrowth
  • excessive HYPOtension (dizziness, syncope)
  • nausea and vomitting
  • bradycardia
46
Q

what is the mechanism of ACE inhibitors?

A

block conversion of angiotensin I to II in order to reduce BP

47
Q

where do ACE inhibitors work?

A

KIDNEY

-the renin-angiotension system

48
Q

what are the adverse effects of angiotension converting enzyme inhibitors

A
  • hypotension (dizziness and syncope)
  • URI - dry cough
  • N&V
  • lichenoid oral lesions
  • avoid NSAIDS during drug action
49
Q

what is the mechanism of angiotension receptor blockers?

A

attach to the angiotension II receptor and block the effect of angiotension II

50
Q

what is the prototype of angiotension receptor blockers?

A

losartan (cozaar)

51
Q

what are the adverse reactions of angiotension receptor blockers>

A

ARBs are more specific than ACEIs and expected to have FEWER adverse reactions

-can include: dizziness, fatigue, insomnia, headache, URI, diharrea, angioedema

52
Q

what are the most common meds for each of the treatments of HTN?

A
  • thiazide = HCTZ
  • ACEI = lisinopril
  • Beta-blockers = metoprolol
  • CCBs = amlodipine
53
Q

what is the cut off for BP reading for tx in the CCC

for EMERGENCIES

A

less than 180/110

54
Q

how does the med plavix (clopidogrel) work after MI and stent placement?

A
  • anti-platelet that inc bleeding time
  • prevents fibrinogen binding and dec platelet aggregation and adhesion
  • platelet turn around is 5-9 days
55
Q

how does the med plendil (felodipine) work after MI and stent placement?

A
  • CCB
  • produces relaxation of coronoary smooth muscle and vasodilation
  • inc myocardial oxygen delivery
56
Q

how does the med nitrostat work after MI and stent placement?

A
  • nitroglycerine - peripheral vasodilator

- dec workload of the heart

57
Q

what meds would a pt be on if they have a bare metal stent?

A

-aspirin and plavix for a month after procedure

58
Q

how does a drug eluting stent work?

A
  • stent witha drug to block cell proliferation

- possibly dec stent re-stenosis

59
Q

how do you prevent re-stenosis for a bare metal stent

A

-dual platelet therapy for at least a month (ideally for a year)

60
Q

how do you prevent re-stenosis for a drug eluting stent?

A

-dual platelet therapy for at least 6 months, ideally for a year

61
Q

mismatch between O2 needs of the heart and delivery of O2 to the heart
-relieved by O2, rest, and vasodilators

A

angina

62
Q

what is the treatment of angina?

A
  • stop procedure
  • position upright (trendellenburg if SBP less than 100)
  • 100% O2
  • sublingual nitro 0.4 mg
  • morphine for pain relief
63
Q

what are the best anti-anginal drugs?

A
  • nitro (by far most common)
  • CCBs
  • B-adrenergic blocking agents
64
Q

how does the most common anti-anginal drug nitro work?

A
  • vasodilator
  • activates guanyly cyclase and inc cGMP producing relaxation of vascular smooth muscle
  • reduces workload of the heart, also reduces O2 needs
65
Q

what are the adverse reactions of nitro?

A
  • severe headaches
  • flushing, hypotension, light-headedness, syncope
  • burning/tingling
66
Q

ischemia leading to death of myocardial tissue

-NOT RELIEVED by O2, rest, and vasodilators

A

MI

*GET PT TO HOSPITAL

67
Q

complex disease proces by which heart is unable to fill with or eject blood to meet bodily needs

  • ischemic heart disease
  • valvular heart disease
  • hypertension
A

CHF

68
Q

what side of the heart is responsible for systemic heart failure?

A

right

69
Q

what side of the heart is responsible for pulmonary congestion?

A

left

70
Q

what are the classes for CHF?

A
  1. symptomatic only with greater than normal activity
  2. symptomatic only with ordinary activity
  3. symptomatic with minimal activity
  4. symptomatic at rest
71
Q

what is the number one treatment option for CHF?

A

digoxin

*still not considered first line therapy though

72
Q

what is the mechanism of digoxin in the treatment of CHF?

A
  • inc force and strength of contraction of the myocardium
  • allows the heart to do more work without inc the use of O2
  • the heart becomes more efficient, and CO inc
73
Q

what are the adverse reactions fo digoxin?

A

narrow therapeutic index so slight changes can lead to bad things

  • arrythmias
  • visual changes
  • N&V
  • headaches
74
Q

what are the first line therapy for CHF>

A

ACEIs

75
Q

occurs when multiple areas within the atria depolarize, causing a quivering of the atrium. AV node sporadically reacts leading to rate in the 180s

A

atrial filibration

*quivering of the heart allows for thrombus formation

76
Q

what is the inc in risk of CVA in pts with atrial filibration?

A

7x

77
Q

how do antiarrhytic agents work?

A

depressing parts of the heart that are beating abnormally

  • dec velocity of depolarization
  • dec propagation
  • inhibit aberrant impulse propagation
78
Q

what are the adverse rxns of antiarrhythmic agents?

A
  • these have a NARROW THERAPEUTIC INDEX so they are difficult to manage
  • only used for pts with arrhymias that prevent the proper functioning of the heart
79
Q

elevations in cholesterol and/or triglycerides and is associated with the development of arteriosclerosis

A

hyperlipidemia

80
Q

what is the first line of defense when it comes to hyperlipidemia>

A

lifestyle changes

  • inc exercise
  • dec saturated fat in diet
  • dec cholesterol from the diet
81
Q

what are the drugs that are included in antihyperlipidemics?

A
  • HMG CoA reductase inhibitors (STATINS)
  • inhibitors of intestinal absorption of cholesterol
  • gemfibrozil
  • niacin
82
Q

how do the “statin” drugs work?

A

lower cholesterol levels by inhibiting HMG CoA reductase, the rate limiting enzyme in cholesterol synthesis

83
Q

what are the adverse effects of “statins”

A
  • GI complaints
  • muscle pain
  • skin rash
  • CAN INC ANTICOAGULANT EFFECTS OF WARFARIN
84
Q

what is ezetimibe (zetia)?

A

-inhibitors of intestinal absorption of cholesterol

85
Q

what are the adverse reactions of zetia?

A
  • fatigue
  • abdominal pain
  • diarrhea
86
Q

how does gemfibrozil (lopid) work?

A
  • used when triglycerides are elevated
  • incs lipolysis of trigylcerides, decreasing lipolysis in adipose tissue, and inhibiting secretion of VLDLs from the liver
87
Q

what are the adverse rxns of gemfibrozil?

A
  • promote gallstone formation

- taste preversion and hyperglycemia

88
Q

what % of ppl with aortic stenosis will die if valve is not replaced in 3 years?

A

75%

89
Q

what is the treatment of aortic stenosis?

A

coumadin

90
Q
  • commonly used for pts with sick sinus syndrome
  • tx for long-term bradycardia
  • can be used for atrium, ventricle, or both
A

pacemaker

91
Q

how do Implated Cardiovascular Defilibrators (ICDs) work?

A

provide a shock wihthin 15 seconds of sensing a dysrhythmia

Pharm II (16 decks)

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