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N929 Pharmacology > Week 3 Pharmacology Flashcards > Flashcards

Week 3 Pharmacology Flashcards

1
Q

Background of Nitric Oxide

A

endogenous, gas messenger
lipophilic, highly reactive and labile free radical
forms from L-arginine
elimiated by oxidation to form Nox, nitrosylation of hemoglobin
half life is a few seconds

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2
Q

Pathogenic Biological Roles of Nitric Oxide

A

Neuronal Injury (NMDA)
Cell proliferation
shock (hypotension)
inflammatory tissue injury

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3
Q

Protective Biological Roles of Nitric Oxide

A 
NT
Immune Cytotoxicity
Inhibit Platelet agreggation
Cyto-protection
Vasodilator Smooth muscle relaxant
Decreases cell adhesion and proliferation
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4
Q

Nitrovasodilator Drugs

A 
NO- Donor
organic nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)
sodium nitroprusside
amyl nitrite
nitric oxide gas
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5
Q

Mechanism of Action of Sodium Nitroprusside & Organic Nitrates

A

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

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6
Q

What do organic nitrates require to release NO

A

metabolism

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7
Q

Sodium Nitroprusside

A

complex of 1 iron, 5 cyanide and 1 NO group
spontaneous breakdown to NO and cynaide
Direct acting peripheral vasodilator
relaxation of arterial and venous smooth muscle

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8
Q

Metabolism of Sodium Nitroprusside

A

cyanide combines with sulfur groups to form thiocyanate undergoes renal excretion

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9
Q

Onset of Sodium Nitroprusside

A

less then 2 minutes

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10
Q

Duration of Sodium Nitroprusside

A

1-10 minutes

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11
Q

Half life of Nitroprusside

A

about 2 minutes

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12
Q

Half life of thiocyanate

A

2-7 days

Increased with impaired renal function

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13
Q

Excretion of Sodium Nitroprusside

A

renal excretion as metabolites (thiocyanate) some exhaled air, feces

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14
Q

Cardiovascular Clinical Effects of Sodium Nitroprusside

A 
decrease arterial and venous pressure
decreases peripheral vascular resistance
decrease in afterload 
slight increase in HR
lacks significant effects on nonvascular smooth muscle and cardiac muscle
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15
Q

Renal Clinical Effects of Sodium Nitroprusside

A

vasodilation without significant change in GFR

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16
Q

CNS Clinical effects of Sodium Nitroprusside

A

increase in CBF and intracranial pressure

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17
Q

Blood Clinical effects of Sodium Nitroprusside

A

Decreases platelet aggregation (NO)

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18
Q

Clinical Uses of Sodium Nitroprusside

A

Hypertensive Crisis
Controlled Hypotension during surgery
Congestive Heart Failure (Acute and decompensated)
Acute Myocardial MI

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19
Q

During surgery how does sodium nitroprusside help?

A

reduces bleeding when inidicated

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20
Q

What does SNP do during acute myocardial MI?

A

improves cardiac output in LV failure & low CO post MI

limited use due to coronary steal- altered BF results in diversion of blood away from ischemic areas

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21
Q

Adverse effects of SNP?

A 
profound hypotension
cyanide toxicity
methemoglobinemia
thiocyanate accumulation
renal
increase in intracranial pressure, GI, headache, restlessness, flushing, dizziness, palpitation
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22
Q

Drug interactions of SNP

A 
negative inotropes
GA
Circualtory depressants
Phosphodiesterase type 5 inhibitors
soluble guanylate cyclase stimulators
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23
Q

Stability of SNP

A

unstable
light and temperature sensitive
protect from light and store at 20-25C
deterioration results in change to blueish color
wrap container with aluminium foil or other opaque material

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24
Q

Administration of SNP

A

IV infusion
Diluted in 5% Dextrose
shortest infusion duration possible to avoid toxicity- if not reduced within 10 mintues @ max infusion move on
solution has faint brownish tint, if discolored discard

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25
Q

Cyanide toxicity

A 
often dose/duration related
tissue anoxia
venous hyperoxemia (tissue cannot extract O2)
lactic acidosis
confusion death
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26
Q

Thiocyanate accumulation

A

increase risk with prolonged infusion; renal impairment
neurotoxicity, including… tinnitus, miosis, hyperreflexia
hypothyroidism (d/t impaired iodine uptake)

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27
Q

Organic Nitrates

A

Nitroglycerin (glyceryl trinitrate)
isosorbide dinitrate
isosorbide mononitrate
amyl nitrite (not used)

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28
Q

MOA of Nitroglycerin

A

No release through cellular metabolism (Glutathione-depedent pathway)
requires thiols
NO released, stimulates GC and formation of cGMP
vascular smooth msucle relaxation and peripheral vasodilation

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29
Q

Actions of Nitroglycerin

A

venous capacitance vessles
mildly dilate arteriolar resistance vessels
dilation of large coronary arteries
administered IV SL translingual spray transdermal ointment

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30
Q

Major Effects of Nitroglycerin

A

dilation of venous capacitance vessels that decreases preloand and MVO2 demand
arteriolar resistance vessels (mild) causes small decrease in afterload, decrease MVO2 demand
Myocardial arteries (increases MVO2 supply)

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31
Q

Cardiovascular application of nitroglycerin

A

decreases venous return, decrease L and R ventricular end diastolic pressure
decreases CO
no change in SVR
increase in coronary BF to ischemic subendocardial areas (opposite SNP)

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32
Q

Other applications of Nitroglycerin

A

smooth muscle relaxation in bronchi, GI tract- small

inhibits platelet aggregation

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33
Q

Pulmonary application of Nitroglycerin

A

bronchial dilation

inhibits HPV

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34
Q

Tolerance of Nitroglycerin

A

after 8-10 hours, results in diminishing effects

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35
Q

Cautions of Nitroglycerin

A

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

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36
Q

Clinical Uses of Nitroglycerin

A 
angina
hypertension (peri-op, HTN emergencies, post operative HTN)
controlled hypotension during surgery
Non-ST segment elevation ACD
Acute MI
HF, Low output syndromes
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37
Q

Why use nitroglycerin in Low Output Syndromes

A

decreases preload, relieves pulmonary edema

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38
Q

Adverse Effects of Nitroglycerin

A

throbbing headache, increased ICP, orthostatic hypotension, dizziness, syncope, reflex tachycardia, flushing, vasodilation, venous pooling, decreased CO, methemoglobinemia, limitation of the use of nitrates

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39
Q

Pharmacokinetics of Nitroglycerin

A

large first pass following oral administration

metabolized in the liver

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40
Q

Duration of IV Nitroglycerin

A

3-5 minutes

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41
Q

Onset of sublingual Nitroglycerin

A

1-3 minutes

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42
Q

Duration of sublingual Nitroglycerin

A

> 25 minutes

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43
Q

Onset of topical Nitroglycerin

A

15-30 minutes

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44
Q

Duration of topical Nitroglycerin

A

7 hours

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45
Q

Onset of transdermal Nitroglycerin

A

about 30 minutes

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46
Q

Duration of Nitroglycerin

A

10-12 hours

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47
Q

Onset of Oral Isosorbide Dinitrate

A

about 60 minutes

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48
Q

Duration of Oral Isosorbide Dinitrate

A

up to 8 hours

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49
Q

Onset of Oral Isosorbide mononitrate (reg + extended)

A

30-45 minutes

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50
Q

Duration of Oral Isosorbide Mononitrate

A

greater then 6 hours

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51
Q

Duration of Extended release Oral Isosorbide mononitrate

A

12 to 24 hours

52
Q

Drug Interactions with Nitroglycerinn

A 
antihypertensive drugs (additive effects)
selective PDE5 inihibitor drugs
guanylate cyclase stimulating drugs
53
Q

Phosphodiesterase Enzymes

A

family of enzymes that breakdown cyclic nucleotides
regulate intracellular levels of 2nd messanger cAMP and cGMP
11 major subfamilies that differ in localization, potential therapeutic targets

54
Q

Inhibitors

A

boost levels of cyclic nucleotides by preventing breakdown

55
Q

Older non-selective drugs that INHIBIT PDE

A

caffeine, theophylline

56
Q

Body Distribution of PDE3

A

broad includes heart and vascular smooth muscle

57
Q

Body Distribution of PDE4

A

broad includes CV, neural, immune/inflammatory

58
Q

Body Distribution of PDE5

A

broad

vascular smooth muscle, especially erectile tissue, retina, lung

59
Q

Substrate of PDE3

A

cAMP

cGMP

60
Q

Substrate of PDE4

A

cAMP

61
Q

Substrate of PDE5

A

cGMP

62
Q

Function of PDE3

A

cardiac contractility

platelet aggregation

63
Q

Function of PDE4

A

Immune, inflammatory

64
Q

Function of PDE5

A

vascular smooth muscle relax (erectile tissue, lung)

65
Q

Inhibitor Clinical Use of PDE3 (milrinone, amrinone)

A

intotrope, peripheral vasodilator

limited for acute HF

66
Q

Inhibitor Clinical Use of PDE3 (cilastazol)

A

intermittent claudication

helps with exercise

67
Q

Inhibitor Clinical Use of PDE4

A

roflumilast

COPD- decreases inflammation, decreases remodeling

68
Q

inhibitor of clinical Use of PDE5

A

Sildenafil
tadalafil
vardenafil
erectile dysfunction, pulmonary hypertension

69
Q

MOA of Milrnone

A

inhibits breakdown of cAMP

70
Q

Effects of Milrnone

A

inotropic increases cardiac contractility
vasodilation
little chronotropic activity

71
Q

Clinical uses of Milrnone

A

acute heart failure or severe chronic HF
cardiogenic shock
heart transplant bridge or post-op

72
Q

Adverse effects of Milrnone

A

arrhythmias

hypotension

73
Q

PK of Milrnone (Onset, 1/2 life, administration, metabolism)

A

5-15 minutes
3-6hours
parental only
majority not metabolized > 80% excreted renally unchanged

74
Q

Angiotensin 2

A

stimualtion of aldosterone secretion

constriction of Vascular smooth muscle

75
Q

Aldosterone

A

increased water and sodium retention

76
Q

Renin

A

secreted by JG apparatus
vasoconstriction and sodium retention
formed/secreted from JG cells
release stimulated decrease BP or Na, B1 receptor activation

77
Q

goal of renin

A

maintain tissue perfusion through increase extracellular fluid volume

78
Q

RAAS is synergistic with

A

SNS by increasing the release of NE from SN terminals

79
Q

Renin activates what to cleave angiotensinogen to angiotensin 1

A

protease

80
Q

ACE

A

broad protease action forms ang2 from ang1
metabolism of BKN to inactive form
located in membrane of EC cells

81
Q

Angiotensin 2

A 
vasoconstriction (AT1 receptor)
aldosterone secretion (AT1 receptors)
increase ADH, increase proximal tubule Na resorbption
82
Q

Aldosterone

A

steroid, adrenal cortex
regulates gene expression, increase Na reabsorption
H20 retained, K excreted

83
Q

ATI1 Receptor

A 
regulation of blood pressure
regulation of body fluid balance
vasoconstriction
inflammation
platelet aggregation/adhesion
reactive oxygen species production
proliferation
hypertropy
fibrosis
84
Q

B1 adrenegric receptor antagonist (metoprolol)

A

antagonize sympathetic stimulation of beta 1 receptor JGC

85
Q

Bradykinin

A 
endogenous substance
1/2 life is 17 seconds
stimulates NO and prostacyclin formation
vasodilation (heart, kidney, microvascular beds)
increases capillary permeability
86
Q

ACE inhibitor Drug list

A 
captopril
benazepril
enalapril
fosinopril
lisinopril
moexipril
perindopril
quinapril
ramipril
trandorapril
87
Q

MOA of ACE inhibitors

A

block conversion of angiotensin 1 to angiotensin 2
prevent vasoconstriction
prevent aldosterone secretion, decrease sodium and water retention

88
Q

First line therapy of ACE Inhibitors

A

HTN, CHF, Mitral regurgitation

89
Q

ACE inhibitors are

A

more effective in DM patients

delay progression of renal disease

90
Q

Clinical Effects of ACE Inhibitors

A

decrease BP, peripheral vascular resistance
decrease preload, afterload
decrease cardiac workload
do not result in reflex tachycardia
improves/presents LV hypertropy, remodeling
improves morbidity/mortality HF
diabetic nephropathy-delays progression (improves renal hemodynamics)

91
Q

Common clinical uses for ACE inhibitors

A

HTN post MI Systolic HF diabetic nephropathy

92
Q

Drug interactions of ACE inhibitors

A

K sparing diuretcis

K supplements

93
Q

Cardiovascular AE’s of ACE Inhibitors

A 
hypotensive symptoms (syncope)
1st dose effect
94
Q

Electrolyte AE’s of ACE Inhibitors

A

increase K

95
Q

Renal AE’s of ACE Inhibitors

A

decrease GFR adn increase BUN and serum Cr, renal dysfunction
contraindicated in bilateral renal artery stenosis

96
Q

inflammatory AE’s of ACE Inhibitors

A

vasodilation
cough
angioedema

97
Q

Fetal Development AE’s of ACE Inhibitors

A

contraindicated

fetal malformations- teratogenic

98
Q

Mnemonic for AE’s of ACE Inhibitors

A 
CAPTOPRIL
cough/ c1 esterase deficiency
angioedema/agranulocytosis
proteinuria/potassium excess
taste change
orthrostatic hypotension
pregnancy contraindication
renal artery stenosis contraindications
increases renin
leuopenia/liver toxicity
99
Q

Angiotensin receptor blockers

A 
azilsartan
candesartan
eprosartan
irbesartan
losartan
olmesartan
telmisartan
valsartan
100
Q

MOA of Angiotensin Receptor Blockers

A

competitive antagonist @ AT1 receptor
blocks effects of Ang 2 mediated by AT1 receptor
does not block breakdown of BKN

101
Q

PK of ARbs

A

metabolism CYP2C9- losartan, irbesartan

102
Q

Drug INteractions with ARBs

A

K sparing diuretics

K supplements

103
Q

Contraindications of ARBS

A

renal artery stenosis

pregnancy

104
Q

ARBs vs ACEis

A

no difference in HTN, total mortality, CV morbidity, mortality
ARBs slightly more tolerable d/t less cough
Higher quality data in ACEi

105
Q

Aldosterone Antagonist

A

spironolactone

eplernone

106
Q

Mechanism of action for Aldosterone Antagonist

A

competitive antagonist at mineralocorticoid rec
prevent nuclear translocation of receptor
blocks transcription of genes coding for Na channels

107
Q

MOA of spirolactone

A

off target effects include androgen, progesterone receptor blocking

108
Q

Effects of Aldosterone Antagonist

A

increase Na, H20 excretion, mild diuresis

increase K reabsorption

109
Q

Uses of Aldosterone Antagonist

A

HTN, HF

K sparing hyperaldosterism

110
Q

PK of Spirolactone

A

hepatic

active metabolites

111
Q

Pk of eplernone

A

CYP3A4

112
Q

AE of Aldosterone Antagonist

A

hyperkalemia

113
Q

AE of Spirolactone

A

hepatic, renal, serious derm (SJ, TEN) GI gynecomastia, menstral irregularities

114
Q

Drug interactions of Aldosterone Antagonist

A

other K sparing drugs (ACEi, ARBs)
K supplements
NSAID increase renal risk

115
Q

MOA of hydralazine

A

release NO from endothelial cells

inhibition of calcium release from SR?

116
Q

Effects of hydralazine

A 
vasodilates arterioles
minimal venous effect
decreased SVR
DBP reduced > SBP
increase HR, stroke volume, cardiac output
117
Q

PK of hydralazine

A

extensive first pass
bioavailability ~25%
half life 1.5-3hours

118
Q

Clinical Uses of hydralazine

A

HTN- used with BB and diuretic

HF- reduced EF

119
Q

AE of hydralazine

A

headache, nausea, palpitations, sweating, flushing, reflex tachycardia tolerance,
sodium/h20 retention
angina wiht EKG changes
lupus erythematosus (reversible)

120
Q

Contraindications of hydralazine

A

CAD, mitral valve RH disease

121
Q

MOA of Minoxidil

A

directly relaxes the arteriolar smooth muscle, no venous effect
increases the efflux of potassium from vascular smooth muscle resulting in hyperpolarization and vasodilation

122
Q

Effects of Minoxidil

A

dilates arterioles, not veins

used in hypertension

123
Q

PK of Minoxidil

A

90% oral dose absorbed from GI tract
peak effect 2-3 hours
half life- 4 hours
10% of drug recovered unchanged in urine

124
Q

Clinical uses of Minoxidil

A

HTN

125
Q

Adverse effects of Minoxidil

A

tachycardia, increase MVO2, palpitations, angina, sodium fluid retention edema
weight gain
hypertrichosis

126
Q

Warnings of Minoxidil

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

N929 Pharmacology (16 decks)

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