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N929 Pharmacology II > Cardiovascular agents lecture III > Flashcards

Cardiovascular agents lecture III Flashcards

1
Q

Nitric oxide is

A

endogenous, lipophilic, highly reactive, and a free radical

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2
Q

Elimination half time of nitric oxide is

A

a few seconds; it does not stay around for long!

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3
Q

Nitric oxide is eliminated via

A

oxidized to form NO

terminates its action

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4
Q

Endothelin derived relaxing factor is

A

also known as nitric oxide and it increases CAMP

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5
Q

Nitric oxide is formed from

A

arginine by NOS

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6
Q

nNOS is found in

A

the neuronal tissue

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7
Q

iNOS is found in

A

macrophages

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8
Q

eNOS is found in

A

endothelium & is what we’re most concerned with

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9
Q

Nitric oxide can be (biological roles)

A

protective or pathogenic

our focus is on the vasodilator role

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10
Q

Mechanism of action of nitric oxide:

A

nitric oxide forms from arginine and that goes into smooth muscle cell and stimulates guanylyl cyclase
that forms cyclic GMP which results in relaxation

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11
Q

Nitrovasodilator (NO donor) drugs include

A

organic nitrates- nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
Sodium nitroprusside
amyl nitrite
nitric oxide gas-used in neonates or pulmonary hypertension

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12
Q

The mechanism of action of organic nitrates is similar to nitroprusside but

A

-it requires metabolism to release NO; depends on the availability of the other components needed for metabolism

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13
Q

The mechanism of action of sodium nitroprusside

A

NO release resulting in activation of GC in vascular smooth muscle, formation of cGMP, vascular smooth muscle relaxation and vasodilation

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14
Q

The tolerance effect is typically seen in

A

organic nitrates because it needs the metabolism step to release nitric oxide and if you run out of enzymes to metabolize the drug is unable to work

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15
Q

Sodium nitroprusside works by

A

spontaneous breakdown to NO & cyanide causing relaxation of arterial and venous smooth muscle

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16
Q

Sodium nitroprusside is metabolized via

A

cyanide combines with sulfur groups to form thiocyanate; then undergoes renal excretion

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17
Q

What is the half-life of sodium nitroprusside versus thiocyanate?

A

sodium nitroprusside- 2 minutes

half-life thiocyanate- 2-7 days (increased with impaired renal function)

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18
Q

The onset of action and duration of sodium nitroprusside is

A

onset <2 minutes

duration 1-10 minutes

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19
Q

The renal effects of sodium nitroprusside includes

A

vasodilation without significant changes in GFR

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20
Q

The CNS effects of sodium nitroprusside include

A

increased cerebral blood flow and ICP

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21
Q

The blood effects of sodium nitroprusside include

A

inhibits platelet aggregation

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22
Q

The cardiovascular effects of sodium nitroprusside include

A

decreased arterial/venous pressure, decreased peripheral vascular resistance, decreased afterload (in HF or MI- CO may increase due to decreased afterload), slight increase in HR
LACKS significant effects on nonvascular smooth muscle and cardiac muscle

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23
Q

Sodium nitroprusside is used for:

A

hypertensive crisis= BP reduction to prevent/limit target organ damage
controlled hypotension during surgery- to reduce bleeding when indicated
CHF-acute, decompensated
Acute MI- to improve CO in LV failure and low CO post MI

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24
Q

Sodium nitroprusside has limited use in acute MI due to

A

coronary steal- altered blood flow results in diversion of blood away from ischemic areas

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25
Q

Sodium nitroprusside has limited clinical uses because

A

it is short acting and very unstable

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26
Q

Adverse effects of sodium nitroprusside include

A

profound hypotension, cyanide toxicity, methemoglobinemia, thiocyanate accumulation, increased serum creatinine (transient), increased ICP, HA, nausea, restlessness, flushing, dizziness, palpitation

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27
Q

Cyanide toxicity and sodium nitroprusside

A

often dose/duration related but can occur at recommended doses, tissue anoxia, lactic acidosis, confusion, death, venous hyperoxemia- tissues cannot extract oxygen

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28
Q

Sodium nitroprusside and methemoglobinemia

A

iron in hemoglobin is oxidized to iron with impaired oxygen affinity, reduced O2 delivery to tissues (hypoxia); metHb >10% symptomatic

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29
Q

Methemoglobinemia should be considered as differential diagnosis in patients with

A

impaired oxygenation despite adequate cardiac output and arterial oxygenation

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30
Q

The reversal agent of methemoglobinemia is

A

methylene blue

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31
Q

Thiocyanate accumulation can cause

A

hypothyroidism due to impaired iodine uptake
neurotoxicity, including tinnitus, miosis, and hyperreflexia
increased risk w/ prolonged infusion & renal impairment

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32
Q

Sodium nitroprusside interacts with

A

hypotensive drugs including negative inotropes, general anesthetics and circulatory depressants
phosphodiesterase type 5 inhibitors (i.e. sildenafil)
soluble guanylate cyclase stimulators
will see a large drop in BP with these drugs

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33
Q

Sodium nitroprusside stability

A

unstable
sensitive to light and temperature
needs to be wrapped with opaque material
results in discoloration of fluid

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34
Q

When administering sodium nitroprusside,

A

must be shortest infusion duration possible to avoid toxicity, if reduction in BP not obtained within 10 minutes @ max infusion rate then it needs to be discontinued

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35
Q

The mechanism of action of nitroglycerin includes

A

NO release through cellular metabolism- glutathione- dependent pathway
requires thiols
when NO is released it stimulates guanylyl cyclase and formation of cGMP causing vascular smooth muscle relaxation and peripheral vasodilation

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36
Q

The primary action of nitroglycerin is at

A

venous capacitance vessels

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37
Q

Sites of action of nitroglycerin include

A

primary at venous capacitance vessels
mildly dilates arteriolar resistance vessels
dilation of large coronary arteries

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38
Q

Nitroglycerin’s action at the myocardial arteries causes

A

increased myocardial O2 supply

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39
Q

Nitroglycerin’s action at the arteriolar resistance vessels causes

A

modest decrease in afterload and decreased myocardial O2 demand

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40
Q

Nitroglycerin’s action at the venous capacitance vessels causes

A

decreased preload

decreased myocardial O2 demand

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41
Q

Nitroglycerin’s effect on the CV system includes

A

decreased venous return; decrease L & R ventricular end diastolic pressure, decreased CO, no change in SVR, increased coronary blood flow

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42
Q

Nitroglycerin’s pulmonary effects include

A

bronchial dilation and inhibition of hypoxic pulmonary vasoconstriction

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43
Q

Tolerance to nitroglycerin results

A

after 8-10 hours and diminishes effectiveness

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44
Q

Nitroglycerin should be used with caution in

A

volume depletion, hypotension, bradycardia or tachycardia, constrictive pericarditis, aortic/mitral stenosis, inferior wall MI and right ventricular involvement

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45
Q

Effects of nitroglycerin on blood

A

inhibits platelet aggregation

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46
Q

Clinical uses of nitroglycerin include

A

angina, hypertension (perioperative HTN, hypertensive emergencies, postop hypertension), controlled hypotension during surgery, NSTEMI, acute MI (limits damage), HF-low output syndromes

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47
Q

Nitroglycerin is used in HF and low output syndromes because

A

it decreases preload and relieves pulmonary edema

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48
Q

Nitroglycerin is used in angina because

A

it reduces myocardial oxygen requirements

venodilation decreases venous return to the heart which reduced RVEDP and LVEDP

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49
Q

Adverse CNS effects of nitroglycerin include

A

throbbing HA & increased ICP

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50
Q

Adverse CV effects of nitroglycerin include

A

orthostatic hypotension, dizziness, syncope, flushing, reflex tachycardia (baroreceptor), vasodilation, venous pooling, decreased CO

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51
Q

Hematologic adverse effects of nitroglycerin include

A

methemoglobinemia (rare)

52
Q

Nitroglycerin is not given orally because

A

it has a large first-pass effect of 90%

53
Q

Nitroglycerin is metabolized via the

A

liver-denitrated by glutathione-organic nitrate reductase to glyceryl dinitrate and then mononitrate

54
Q

Nitroglycerin has drug interactions with

A

antihypertensive drugs-additive effects
selective PDE-5 inhibitor drugs (avanafil, sildenafil)
Guanylate cyclase stimulating drugs
anything that is working to increase cGMP will have potentiation

55
Q

Nitroglycerin and selective PDE-5 inhibitor drugs

A

absolute contraindication
profound potentiation
possible life-threatening hypotension and/or hemodynamic compromise
accumulation of cGMP by inhibiting its breakdown

56
Q

Isosorbide mononitrate and dinitrate are used for

A

prevention of angina
used for HF in black patients in combination with hydralazine
can be given PO

57
Q

Isosorbide mononitrate and dinitrate should not be given to patients using

A

PDE5 inhibitor drugs

58
Q

Phosphodiesterase enzymes are

A

a family of enzymes that breakdown cyclic nucleotides

regulate intracellular levels of 2nd messengers cAMP & cGMP

59
Q

Phosphodiesterase enzyme inhibitors work by

A

boosting levels of cyclic nucleotides by preventing breakdown

60
Q

Non-selective drugs that inhibit PDE include

A

caffeine and theophylline

61
Q

The mechanism of action of PDE5 inhibitors is

A

cyclic GMP is boosted resulting in vasodilation

62
Q

PDE5 acts on

A

vascular smooth muscles to relax (specifically erectile tissue & the lung)

63
Q

PDE5 is used clinically for

A

erectile dysfunction & pulmonary hypertension

64
Q

PDE5 drugs include

A

sildenafil, tadalafil, vardenafil

65
Q

PDE5 is selective for

66
Q

PDE4 is selective for

67
Q

PDE4 functions via the

A

immune & inflammatory systems

68
Q

PDE4 is used clinically for

A

COPD to decrease inflammation and decrease remodeling

69
Q

PDE4 drugs include

A

roflumilast

70
Q

PDE3 drugs include

A

amrinone, milrinone, and cilastazol

71
Q

PDE3 drugs are used clinically as

A

positive inotropes, peripheral vasodilator, limited for acute HF
intermittent claudication-cilastozol

72
Q

PDE3 drugs are selective for

A

cAMP & cGMP

73
Q

PDE3 drugs function at

A

cardiac contractility and platelet aggregation

74
Q

The mechanism of action of milrinone is

A

inhibits breakdown of cAMP

75
Q

Milrinone is clinically used for

A

acute HF or severe chronic HF
cardiogenic shock
heart transplant bridge or postop

76
Q

Milrinone causes effects at

A

inotropy–> increased cardiac contractility
vasodilation
little chronotropic activity

77
Q

Adverse effects of milrinone include

A

arrhythmias & hypotension

78
Q

The onset, half-life and metabolism of milrinone

A

onset: 5-15 minutes (IV)
half-life: 3-6 hours
majority not metabolized; >80% excreted renally unchanged

79
Q

Describe the renin angiotensin system

A

renin converts angiotensinogen to angiotensin I
converting enzyme turns angiotensin I to angiotensin II
Angiotensin II stimulates aldosterone secretion which increases water and sodium retention and increases preload
Angiotensin II also causes constriction of vascular smooth muscle which increases afterload

80
Q

Renin is secreted by

A

the JG apparatus

81
Q

Renin causes

A

vasoconstriction and sodium retention

82
Q

The RAAS is synergistic with

A

the SNS by increasing the resistance of noradrenaline from the sympathetic nerve terminals

83
Q

Renin release is stimulated by

A

decreased blood pressure, Na+, beta 1 receptor activation

84
Q

Angiotensin converting enzyme is located

A

in the membrane of endothelial cells
forms Ang II from Ang I
metabolism of bradykinin to inactive form

85
Q

Aldosterone causes

A

increased sodium reabsorption, water retention, and secretes K+

86
Q

Angiotensin II causes

A

potent vasoconstriction via the AT1 receptor

aldosterone secretion at the AT1 receptor

87
Q

What drug can block the increased heart rate and release of renin?

A

metoprolol because it blocks the beta 1 in the heart and beta 2 in the kidneys

88
Q

Blocking aldosterone causes

A

hyperkalemia

89
Q

Angiotensin II works on the

A

AT1 receptor

90
Q

ACE inhibitors work at

A

AT1 receptors

mediates hypertrophy which is why it is used in HF

91
Q

The RAAS system can be blocked via

A

ACEI, Renin inhibitors, ARBs, beta blockers, and aldosterone inhibitors

92
Q

ACEI cause a decrease in

A

angiotensin II and an increase in bradykinin

93
Q

ACEI increase bradykinin which causes

A

vasodilation, cough, and angioedema

94
Q

ACEI decreases angiotensin II which causes

A

vasodilation, decreased remodeling, decreased sympathetic output, increase natiuresis, and decreased aldosterone (decreased Na+/H2O retention, increased K+ retenetion)

95
Q

ACEI drugs have the suffix of

A

“pril”

96
Q

Bradykinin causes

A

NO & prostacyclin formation leading to vasodilation (heart, kidney, microvascular beds)
inflammatory actions–> increased capillary permeability

97
Q

ACE-I drugs MOA

A

block the conversion of AngI to Ang II
prevent vasoconstriction
prevent aldosterone secretion, decreasing Na & water retention

98
Q

ACE-I drugs treat

A

HTN, CHF, post MI, diabetic neuropathy, & mitral regurgitation (first line therapy)
more effective in DM pts
delay progression of renal disease

99
Q

Clinical effects of ACE-I include

A

decreased BP, peripheral vascular resistance
decreased preload, afterload
decreased cardiac workload
does not result in reflex tachycardia
improves/prevents LV hypertrophy, remodeling
improves morbidity/mortality HF
diabetic neuropathy delays progression (improves renal hemodynamics)

100
Q

ACE-I has drug interactions with

A

K+ sparing diuretics and K+ supplements

101
Q

ACE-I drugs tend to be

A

pro-drugs meaning they are inactive until metabolism step forms active metabolism

102
Q

Contraindications for ACE-I include

A

renal artery stenosis as they may develop renal failure due to efferent arteriole constriction
contraindicated in pregnancy

103
Q

ACE-I adverse effects include

A

hypotensive symptoms, syncope, “1st dose effect” possible
hyperkalemia
decreased GFR, increased BUN & serum creat., renal dysfunction
dry cough (5-20%) bradykinin related
angioedema-bradykinin related
fetal malformations- teratogenic

104
Q

ARBs suffix

A

‘sartan’

105
Q

Captopril side effects:

A 
Cough
Angioedema/ agranulocytosis
Proteinuira/potassium excess
taste change
orthostatic hypotension
pregnancy (contraindication)
renal artery stenosis (contraindication)
increases renin
liver toxicity/ leukopenia
106
Q

ARBs have interactions with

A

K+ sparing diuretics ad K+ supplements

107
Q

ARBs are contraindicated in

A

renal artery stenosis and pregnancy

108
Q

Adverse effects of ARBs include

A

similar to ACEI

less frequent cough & angioedema

109
Q

Clinical effects and uses of ARBs are

A

similar to ACEi

110
Q

ARBs mechanism of action

A

competitive antagonist @ AT1 receptor
blocks effects of ang II mediated by At1 receptor
does not block breakdown of BKN- thus BKN does not accumulate

111
Q

Differences between ACEi and ARBs

A

no difference between efficacy in HTN
ARBs slight more tolerable, less likely to be discontinued
ACEi have been around longer so higher quality of data

112
Q

Aldosterone antagonist includes

A

spironolactone, eplerenone

113
Q

Mechanism of action of aldosterone antagonist

A

competitive antagonist at mineralocorticoid receptor (kidney but also heart, blood vessels, and brain)
prevent nuclear translocation of receptor
blocks transcription of genes coding for Na+ channels

114
Q

Effects of aldosterone antagonists include

A

increased sodium, H2O excretion, mild diuresis

Increased K+ reabsorption

115
Q

Uses of aldosterone antagonist include

A

HTN, HF, K+ sparing diuresis, hyperaldosteronism,

spironolactone- off label- acne, PCOS, hirsutism

116
Q

Adverse effects of aldosterone antagonists include

A

hyperkalemia

spironolactone– broad; includes hepatic, renal, serious derm, GI, menstrual irregularities

117
Q

Drug interactions with aldosterone antagonists include

A

other K+ sparing (ACEI, ARBs, etc.)
K+ supplements
NSAIDs (increased renal risks)

118
Q

The mechanism of action of hydralazine

A

release of NO from endothelial cells

inhibition of Ca release from SR

119
Q

The effects of hydralazine include

A

vasodilates arterioles, minimal venous effect, decreased SVR, DBP reduced» SBP, increases HR, SV & CO

120
Q

Clinical uses of hydralazine include

A

hypertension-usually in combo w/ beta blocker & diuretic (to limit SNS effects)
HF= reduced EF

121
Q

Adverse effects of hydralazine include

A

HA, nausea, palpitations, sweating, flushing, reflex tachycardia, tolerance/tachyphylaxis, sodium and H2O retention, angina with EKG changes, lupus (reversible)

122
Q

Hydralazine is contraindicated in

A

CAD, mitral valve, RH disease

123
Q

The mechanism of action of minoxidil is

A

directly relaxes the arteriolar smooth muscle little effect on venous capacitance
increases the efflux of K+ from VSM resulting in hyperpolarization and vasodilation

124
Q

Effects of minoxidil include

A

dilates arterioles, not veins

use in hypertension (limited to later-line therapy due to risk-benefit profile)

125
Q

Clinical uses of minoxidil include

A

hypertension-later line therapy

usually in combination with beta blocker & diuretic (to limit SNS effects)

126
Q

Adverse effects of minoxidil include

A 
tachycardia, increased myocardial workload
palpitations, angina
sodium/fluid retention, edema
weight gain
hypertrichosis
127
Q

Warnings with minoxidil include

A

fluid retention, pericardial effusion/tamponade, rapid BP response, sinus tachycardia, elderly

N929 Pharmacology II (16 decks)

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