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N929 Pharmacology > Week 3 Pharmacology Flashcards > Flashcards

Week 3 Pharmacology Flashcards

(126 cards)

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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
Cyanide toxicity
``` often dose/duration related tissue anoxia venous hyperoxemia (tissue cannot extract O2) lactic acidosis confusion death ```
26
Thiocyanate accumulation
increase risk with prolonged infusion; renal impairment neurotoxicity, including... tinnitus, miosis, hyperreflexia hypothyroidism (d/t impaired iodine uptake)
27
Organic Nitrates
Nitroglycerin (glyceryl trinitrate) isosorbide dinitrate isosorbide mononitrate amyl nitrite (not used)
28
MOA of Nitroglycerin
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
29
Actions of Nitroglycerin
venous capacitance vessles mildly dilate arteriolar resistance vessels dilation of large coronary arteries administered IV SL translingual spray transdermal ointment
30
Major Effects of Nitroglycerin
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)
31
Cardiovascular application of nitroglycerin
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)
32
Other applications of Nitroglycerin
smooth muscle relaxation in bronchi, GI tract- small | inhibits platelet aggregation
33
Pulmonary application of Nitroglycerin
bronchial dilation | inhibits HPV
34
Tolerance of Nitroglycerin
after 8-10 hours, results in diminishing effects
35
Cautions of Nitroglycerin
volume depletion, hypotension, bradycardia or tachycardia, constrictive pericarditis, aortic/mitral stenosis, inferior wall MI and RT ventricular involvement
36
Clinical Uses of Nitroglycerin
``` angina hypertension (peri-op, HTN emergencies, post operative HTN) controlled hypotension during surgery Non-ST segment elevation ACD Acute MI HF, Low output syndromes ```
37
Why use nitroglycerin in Low Output Syndromes
decreases preload, relieves pulmonary edema
38
Adverse Effects of Nitroglycerin
throbbing headache, increased ICP, orthostatic hypotension, dizziness, syncope, reflex tachycardia, flushing, vasodilation, venous pooling, decreased CO, methemoglobinemia, limitation of the use of nitrates
39
Pharmacokinetics of Nitroglycerin
large first pass following oral administration | metabolized in the liver
40
Duration of IV Nitroglycerin
3-5 minutes
41
Onset of sublingual Nitroglycerin
1-3 minutes
42
Duration of sublingual Nitroglycerin
> 25 minutes
43
Onset of topical Nitroglycerin
15-30 minutes
44
Duration of topical Nitroglycerin
7 hours
45
Onset of transdermal Nitroglycerin
about 30 minutes
46
Duration of Nitroglycerin
10-12 hours
47
Onset of Oral Isosorbide Dinitrate
about 60 minutes
48
Duration of Oral Isosorbide Dinitrate
up to 8 hours
49
Onset of Oral Isosorbide mononitrate (reg + extended)
30-45 minutes
50
Duration of Oral Isosorbide Mononitrate
greater then 6 hours
51
Duration of Extended release Oral Isosorbide mononitrate
12 to 24 hours
52
Drug Interactions with Nitroglycerinn
``` antihypertensive drugs (additive effects) selective PDE5 inihibitor drugs guanylate cyclase stimulating drugs ```
53
Phosphodiesterase Enzymes
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
Inhibitors
boost levels of cyclic nucleotides by preventing breakdown
55
Older non-selective drugs that INHIBIT PDE
caffeine, theophylline
56
Body Distribution of PDE3
broad includes heart and vascular smooth muscle
57
Body Distribution of PDE4
broad includes CV, neural, immune/inflammatory
58
Body Distribution of PDE5
broad | vascular smooth muscle, especially erectile tissue, retina, lung
59
Substrate of PDE3
cAMP | cGMP
60
Substrate of PDE4
cAMP
61
Substrate of PDE5
cGMP
62
Function of PDE3
cardiac contractility | platelet aggregation
63
Function of PDE4
Immune, inflammatory
64
Function of PDE5
vascular smooth muscle relax (erectile tissue, lung)
65
Inhibitor Clinical Use of PDE3 (milrinone, amrinone)
intotrope, peripheral vasodilator | limited for acute HF
66
Inhibitor Clinical Use of PDE3 (cilastazol)
intermittent claudication | helps with exercise
67
Inhibitor Clinical Use of PDE4
roflumilast | COPD- decreases inflammation, decreases remodeling
68
inhibitor of clinical Use of PDE5
Sildenafil tadalafil vardenafil erectile dysfunction, pulmonary hypertension
69
MOA of Milrnone
inhibits breakdown of cAMP
70
Effects of Milrnone
inotropic increases cardiac contractility vasodilation little chronotropic activity
71
Clinical uses of Milrnone
acute heart failure or severe chronic HF cardiogenic shock heart transplant bridge or post-op
72
Adverse effects of Milrnone
arrhythmias | hypotension
73
PK of Milrnone (Onset, 1/2 life, administration, metabolism)
5-15 minutes 3-6hours parental only majority not metabolized > 80% excreted renally unchanged
74
Angiotensin 2
stimualtion of aldosterone secretion | constriction of Vascular smooth muscle
75
Aldosterone
increased water and sodium retention
76
Renin
secreted by JG apparatus vasoconstriction and sodium retention formed/secreted from JG cells release stimulated decrease BP or Na, B1 receptor activation
77
goal of renin
maintain tissue perfusion through increase extracellular fluid volume
78
RAAS is synergistic with
SNS by increasing the release of NE from SN terminals
79
Renin activates what to cleave angiotensinogen to angiotensin 1
protease
80
ACE
broad protease action forms ang2 from ang1 metabolism of BKN to inactive form located in membrane of EC cells
81
Angiotensin 2
``` vasoconstriction (AT1 receptor) aldosterone secretion (AT1 receptors) increase ADH, increase proximal tubule Na resorbption ```
82
Aldosterone
steroid, adrenal cortex regulates gene expression, increase Na reabsorption H20 retained, K excreted
83
ATI1 Receptor
``` regulation of blood pressure regulation of body fluid balance vasoconstriction inflammation platelet aggregation/adhesion reactive oxygen species production proliferation hypertropy fibrosis ```
84
B1 adrenegric receptor antagonist (metoprolol)
antagonize sympathetic stimulation of beta 1 receptor JGC
85
Bradykinin
``` endogenous substance 1/2 life is 17 seconds stimulates NO and prostacyclin formation vasodilation (heart, kidney, microvascular beds) increases capillary permeability ```
86
ACE inhibitor Drug list
``` captopril benazepril enalapril fosinopril lisinopril moexipril perindopril quinapril ramipril trandorapril ```
87
MOA of ACE inhibitors
block conversion of angiotensin 1 to angiotensin 2 prevent vasoconstriction prevent aldosterone secretion, decrease sodium and water retention
88
First line therapy of ACE Inhibitors
HTN, CHF, Mitral regurgitation
89
ACE inhibitors are
more effective in DM patients | delay progression of renal disease
90
Clinical Effects of ACE Inhibitors
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
Common clinical uses for ACE inhibitors
HTN post MI Systolic HF diabetic nephropathy
92
Drug interactions of ACE inhibitors
K sparing diuretcis | K supplements
93
Cardiovascular AE's of ACE Inhibitors
``` hypotensive symptoms (syncope) 1st dose effect ```
94
Electrolyte AE's of ACE Inhibitors
increase K
95
Renal AE's of ACE Inhibitors
decrease GFR adn increase BUN and serum Cr, renal dysfunction contraindicated in bilateral renal artery stenosis
96
inflammatory AE's of ACE Inhibitors
vasodilation cough angioedema
97
Fetal Development AE's of ACE Inhibitors
contraindicated | fetal malformations- teratogenic
98
Mnemonic for AE's of ACE Inhibitors
``` 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
Angiotensin receptor blockers
``` azilsartan candesartan eprosartan irbesartan losartan olmesartan telmisartan valsartan ```
100
MOA of Angiotensin Receptor Blockers
competitive antagonist @ AT1 receptor blocks effects of Ang 2 mediated by AT1 receptor does not block breakdown of BKN
101
PK of ARbs
metabolism CYP2C9- losartan, irbesartan
102
Drug INteractions with ARBs
K sparing diuretics | K supplements
103
Contraindications of ARBS
renal artery stenosis | pregnancy
104
ARBs vs ACEis
no difference in HTN, total mortality, CV morbidity, mortality ARBs slightly more tolerable d/t less cough Higher quality data in ACEi
105
Aldosterone Antagonist
spironolactone | eplernone
106
Mechanism of action for Aldosterone Antagonist
competitive antagonist at mineralocorticoid rec prevent nuclear translocation of receptor blocks transcription of genes coding for Na channels
107
MOA of spirolactone
off target effects include androgen, progesterone receptor blocking
108
Effects of Aldosterone Antagonist
increase Na, H20 excretion, mild diuresis | increase K reabsorption
109
Uses of Aldosterone Antagonist
HTN, HF | K sparing hyperaldosterism
110
PK of Spirolactone
hepatic | active metabolites
111
Pk of eplernone
CYP3A4
112
AE of Aldosterone Antagonist
hyperkalemia
113
AE of Spirolactone
hepatic, renal, serious derm (SJ, TEN) GI gynecomastia, menstral irregularities
114
Drug interactions of Aldosterone Antagonist
other K sparing drugs (ACEi, ARBs) K supplements NSAID increase renal risk
115
MOA of hydralazine
release NO from endothelial cells | inhibition of calcium release from SR?
116
Effects of hydralazine
``` vasodilates arterioles minimal venous effect decreased SVR DBP reduced > SBP increase HR, stroke volume, cardiac output ```
117
PK of hydralazine
extensive first pass bioavailability ~25% half life 1.5-3hours
118
Clinical Uses of hydralazine
HTN- used with BB and diuretic | HF- reduced EF
119
AE of hydralazine
headache, nausea, palpitations, sweating, flushing, reflex tachycardia tolerance, sodium/h20 retention angina wiht EKG changes lupus erythematosus (reversible)
120
Contraindications of hydralazine
CAD, mitral valve RH disease
121
MOA of Minoxidil
directly relaxes the arteriolar smooth muscle, no venous effect increases the efflux of potassium from vascular smooth muscle resulting in hyperpolarization and vasodilation
122
Effects of Minoxidil
dilates arterioles, not veins | used in hypertension
123
PK of Minoxidil
90% oral dose absorbed from GI tract peak effect 2-3 hours half life- 4 hours 10% of drug recovered unchanged in urine
124
Clinical uses of Minoxidil
HTN
125
Adverse effects of Minoxidil
tachycardia, increase MVO2, palpitations, angina, sodium fluid retention edema weight gain hypertrichosis
126
Warnings of Minoxidil
``` fluid retention pericardial effusion/tamponade rapid BP response sinus tachycardia elderly ```

N929 Pharmacology (16 decks)

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