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BMS 615 Cardiovascular > Test 1: Wk2: Vasodialators - Salisbury > Flashcards

Test 1: Wk2: Vasodialators - Salisbury Flashcards

1
Q

BP =

A

TPR x CO

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2
Q

Arteriodilation ➡⬇TPR

Venodialation ➡⬇CO

A

both lead to ⬇BP

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3
Q

Vasodilators compensatory mechanisms

A

⬆HR and ⬆fluid retention

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4
Q

Ca channel blockers (2)

A

Dihydropyridines and non

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5
Q

Dihydropyridines (1)

A

amlodipine

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6
Q

non-Dihydropyridines (2)

A

verapamil and Diltiazem

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7
Q

K channel opener (1)

A

Minoxidil

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8
Q

Dopamine D1 Receptor Antagonist (1)

A

Fenoldopam

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9
Q

Guanylate Cyclase Activators (5)

A 
Nitroprusside 
Nitroglycerine 
Isosorbide Dinitrate 
Isosorbide Mononitrate 
Nitric Oxide
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10
Q

Phosphodiesterase inhibitors (2)

A

Sildenafil and Tadalafil

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11
Q

Ca Channel Blocker suffix

A

-dipine

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12
Q

All Ca channel blockers share what mechanisms

A

⬇Ca influx through voltage gated L type Ca Channels

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13
Q

Ca Channel Blockers targets (2)

A

blood vessels ion arterial system

heart

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14
Q

Vascular effects of Ca Channel Blockers

A

arteriodilation

⬇TPR➡⬇BP

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15
Q

are dihydropyridines stronger than non

A

yes, much stronger

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16
Q

Ca Channel Blockers Cardiac Effects

A

inhibit L-type Ca channels

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17
Q

Ca Channel Blockers inhibit what at the SA and AV nodes

A

phase 0 depol

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18
Q

Ca Channel Blockers inhibit what in cardiomyocytes

A

phase 2 action potential

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19
Q

Inhibition of L-type Ca channels leads to what 3 cardiac effects

A

⬇firing rate of SA node ➡⬇HR

⬇conduction velocity in AV node➡ block

⬇contractility of A and V muscles

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20
Q

Verapamil Diltiazem and Dihydropyridines cardiac effects

A

see chart

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21
Q

Ca Channel Blockers metabolized by

A

liver - hepatic metabolism

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22
Q

Ca Channel Blockers are effective through what administration

A

orally

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23
Q

Ca Channel Blockers uses

A

angina

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24
Q

Tx of angina

A

⬆ Coronary blood flow

⬇ MVO2 demand

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25
Q

how do Ca Channel Blockers ⬇ MVO2 demand

2 ways

A

⬇ afterload (all)

⬇ CO (verapamil and diltiazam)

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26
Q

what drug treats Supraventricular Tachyarrhythmias

A

verapmil - Ca Channel Blockers

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27
Q

how does verapamil treat Supraventricular Tachyarrhythmias (3 ways)

A

⬇ AV nodal conduction

control V and A flutter and A fib

⬇ PSVT

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28
Q

Ca Channel Blockers are used for — by — and —

A

hypertension
⬇ TPR
⬇ CO

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29
Q

which Ca Channel Blockers decrease CO

A

verapamil and diltiazem

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30
Q

Ca Channel Blockers adverse effects

A

see chart

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31
Q

Ca Channel Blockers contraindications (3)

A

avoid short term acting agents (Nifefipine)

Severe hepatic dysfunction

LV Dysfuntion

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32
Q

Short acting agents given with Ca Channel Blockers and increase

A

mortality and risk if MI

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33
Q

Ca Channel Blockers precautions (3)

A

Hypotension (all)

AV block (verapamil and diltiazem)

Sick sinus syndrome (verapamil and diltiazem)

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34
Q

Ca Channel Blockers drug interactions (4)

A

CYP3A4 inhibitors/ inducers

B blockers (verapamil diltiazem)

Digoxin (verapamil)

Antiarrhythmic drugs

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35
Q

Minoxidil is a

A

K channel opener

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36
Q

Minoxidil increases — efflux from vascular SM cells ➡ —➡ — ⬇ — ➡ ⬇—

A

Minoxidil increases K+ efflux from vascular SM cells ➡ hyperpol ➡ relaxation ⬇ TPR ➡ ⬇ BP

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37
Q

Minoxidil compensatory mechanism

A

increase HR CO and fluid accumulation

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38
Q

Minoxidil is a potent —

A

vasodilatior

39
Q

Minoxidil therapeutic uses (2)

A

refractory/malignant hypertension

alopecia

40
Q

Minoxidil adverse effects (4)

A

fluid retention

tachycardia

pericardial effusion/ cardiac tamponade

hypertrichosis

41
Q

Guanylyl Cyclase Activators mechanisms

A

activate GC
⬆ cGMP formation
⬆cGMP ➡ vasodilation

42
Q

Nitroprusside effects on arteriodilation and venodilation

A

they are balanced

43
Q

Nitroprusside Arteridilation ➡

A

⬇TPR➡⬇BP

44
Q

Nitroprusside venodilation ➡

A

⬇Preload➡ ⬇CO ➡⬇BP

45
Q

⬇BP ➡ Reflex ➡

A

⬆HR

46
Q

Nitroprusside overall effects

A

⬇TPR
⬇BP
⬇CO
⬆HR

47
Q

Nitroprusside t1/2 and onset

A

2min

immediate

48
Q

Nitroprusside administration

A

IV only

49
Q

— sensitivity with Nitroprusside

A

light

50
Q

Nitroprusside therapeutic uses (3)

A

hypertensive emergencies
CHF
MI

51
Q

Nitroprusside acute adverse effects

A

hypotension

52
Q

Nitroprusside chronic effects

A

CN- toxicity

53
Q

what can be given with Nitroprusside to reduce CN- toxicity

A

Thiosulfate

54
Q

Organic Nitrates (3)

A

Nitroglycerin
Longer acting
ISDN
ISMN

55
Q

Effects of Organic Nitrates are

A

dose related

56
Q

Organic Nitrates Low Dose

A

venodilation

see slide for more info

57
Q

Organic Nitrates High Dose

A

Venodilation
Arteriodilation
Reflex ⬆HR

58
Q

what Organic Nitrates have extensive first pass HM

A

nitroglycerin and ISDN

59
Q

what enzyme denitrations Organic Nitratesin HM

A

Glutathione-organic nitrate reductase

60
Q

what Organic Nitrates experience Vascular Metabolism

A

nitroglycerin

61
Q

how is nitroglycerin metabolized in vasulature

A

nitroglycerine ➡ ALDH2 ➡ NO

62
Q

Organic Nitrates tolerance

A

tx for >24 hrs

nitrate free period of 8-12 hrs

63
Q

nitroglycerin ointment dosing interval

A

3-4x day remove for 12 hr

64
Q

nitroglycerin patch dosing

A

1x daily remove for 12 hr

65
Q

ISDN oral sustained relase dosing

A

1-2x daily, 14hr tablet free interval

66
Q

ISMN

A

1x daily

67
Q

Organic Nitrates therapeutic uses (3)

A

angina

CHF

Acute MI

68
Q

Organic Nitrates adverse effects (2)

A

excessive hypotension

tolerance

69
Q

excessive hypotension effects

A

headache
tachycardia
orthostatic hypotension
angina

70
Q

Organic Nitrates with PDE5 inhibitors will result in

A

extreme hypotension

71
Q

Nitric oxide administration and t1/2

A

inhalation

very short

72
Q

nitrate and nitrite excreted in

A

urine

73
Q

Nitric oxide therapeutic uses

A

reverse hypoxic respiratory failure in neonates with pulmonary hypertension

74
Q

Nitric oxide adverse effects (2)

A

pulmonary edema

hypoxemia

75
Q

Hydralazine is a strong

A

arterial dialator

76
Q

Hydralazine therapeutic uses

A

CHF

Hypertension

77
Q

Hydralazine metabolism

A

hepatic and renal

78
Q

Hydralazine adverse effects (5)

A 
fluid retention
tachycardia 
headache
hypotension 
drug induced lupus-like syndrome
79
Q

antinuclear antibody positve is caused by what drug

A

hydralazine

80
Q

drug induced lupus-like syndrome risk factors

A

slow acetylates and female

81
Q

Fenoldopam is a

A

peripheral dopamine D1 receptor agonist

82
Q

Fenoldopam induces

A

systemic and renal arterial vasodilation

83
Q

Fenoldopam adminstration

A

IV - rapid acting 15-20 min

lasts 1-4 hrs

84
Q

Fenoldopam uses

A

hypertensive emergency

85
Q

Fenoldopam adverse effects (3)

A

hypersensitivity to sodium metabisulfate
tachycardia
hypotension

86
Q

PDE inhibitors (3)

A

sildenafil, tadalafil, verdenafil

87
Q

PDE Inhibitors inhibit — resulting in —

A

PDE type 5 resulting in ⬆ NO cGMP

88
Q

PDE Inhibitors relax SM in — and — resulting in — and —-

A

corpus cavernosum and lower urinary tract

erection and urination

89
Q

sildenafil, verdenafil, tadalafil time to peak conc.

A

1
1
1.5 hrs

90
Q

sildenafil, verdenafil, tadalafil t1/2

A

3-4

4-5

18

91
Q

sildenafil, verdenafil, tadalafil uses

A

erectile dysfunction

BPG - tadalafil

92
Q

sildenafil, verdenafil, tadalafil kinetics

A

orally

HM metabolized

93
Q

sildenafil, verdenafil, tadalafil adverse effects

A

hypotension

94
Q

sildenafil, verdenafil, tadalafil contraindications (4)

A

organic nitrates
a-blockers
CYP3A4 drugs
hepatic dysfunction

BMS 615 Cardiovascular (49 decks)

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