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Pharmacology N929 > Vasodilator Drugs > Flashcards

Vasodilator Drugs Flashcards

1
Q

nitric oxide properties, formation from, elimination, t1/2

A

endogenous, gas and acts as messenger
lipophilic, highly reactive and labile free radical (will not stay around for long since its so highly reactive)
formation: from L argon
elimination: oxidation to form NO(x) or nitrosylation of HGB
t1/2: a few seconds

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2
Q

NO MOA

A

acts on endothelium to vasodilate (used to be called endothelium relaxing factor or EDRF). increases cGMP which is how NO acts on smooth muscle

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3
Q

How is NO formed in body

A

formed from L arginine via NOS or NO synthase to make NO and L citrulline

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4
Q

nNOS

A

neuronal

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5
Q

inos

A

inducible (macrophage)

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6
Q

enos

A

endothelium

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7
Q

NO biological roles

A
  1. inhibit platelet aggregation (beneficial)
  2. cyto protection
  3. can inhibit cell adhesion to endothelium (protective)
  4. serves as neurotransmitter
  5. does have role in neuronal injury (harmful)
  6. inflammatory tissue injury (r/t free radical)
  7. vasodilators smooth muscle
  8. shock and hypotension
  9. cell proliferation
  10. immune cytotoxicity
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8
Q

NO intracellular**

A

acts on Ach, increase in intracellular Ca, activates eNOS–>L arginine–>NO which acts on ca channel then guanylate cyclase (which makes cGMP) to cause relaxation

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9
Q

Nitrovascular (NO donor) drugs

A

organic nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)
sodium nitroprusside
amyl nitrite
nitric oxide gas

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10
Q

Na Nitroprusside MOA

A

No release (spontaneously) resulting in activation of guanylate cyclase in vascular smooth muscle, formation of cGMP, vascular smooth muscle relaxation and vasodilation

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11
Q

Organic Nitrates MOA

A

require metabolism to release NO (S nitrosothiol and RNO2 involvement)

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12
Q

Sodium Nitroprusside Structure, metabolism

A

1 iron, 5 cyanide, 1 NO group
spontaneous breakdown to NO and cyanide (cyanide is direct acting peripheral vasodilator)
relaxation of arterial and venous smooth muscle
metabolism: cyanide combines with sulfur groups to form thiocyanate, undergoes renal excretion. so careful in impaired renal function

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13
Q

Sodium Nitroprusside onset, duration, t1/2, t1/2 of the metabolite, metabolism, excretion

A 
onset <2 minutes
duration 1-10 minutes
t1/2 2 minutes
t1/2 thiocyanate 2-7d
metabolism: renal excretion
excretion: some exhaled air, feces
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14
Q

Sodium nitroprusside Clinical Effects: CV, Renal, CNS, blood

A

CV: decrease arterial/venous pressure, decrease PVR, decrease after load, slight increase in HR. no significant effects on cardiac muscle
renal: vasodilation without significant change in GFR
CNS: increased CBF and ICP
blood: NO inhibits platelet aggregation

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15
Q

Sodium Nitroprusside Clinical Uses

A
  • HTN crisis: BP reduction to prevent/limit target organ damage
  • controlled hypotension during surgery: during anesthesia, to reduce bleeding when indicated
  • CHF: acute, decompensated
  • acute MI: to improve CO in LV failure, and low CO post MI. limited use due to coronary steal, altered BF results in division of blood away from ischemic areas
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16
Q

Sodium Nitroprusside Adverse Effects

A
  • profound hypotension
  • cyanide toxicity: often dose/duration related, but may occur at recommended doses. tissue anoxia, venous hyperoxemia, lactic acidosis, confusion, death,
  • metheglobinemia (>10% symptomatic)
  • thiocyanate accumulation (increased risk with prolonged infusion, neurotoxicity, hypothyroidism)
  • renal (increased creatinine)
  • high ICP, GI (nausea), HA, restlessness, flushing, dizziness, palpation
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17
Q

methemoglobinemia reversal agent

A

methylene blue

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18
Q

Sodium Nitroprusside: Drug Interactions

A

hypotensive drugs (negative inotropes, general anesthetics, circulatory depressants)

  • PDE5 inhibitors
  • soluble guanylate cyclase stimulators
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19
Q

Sodium Nitroprusside Stability

A

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

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20
Q

Sodium Nitroprusside Administration and considerations

A

IV infusion via infusion pump
diluted in 5% dextrose
shortest infusion duration possible to avoid toxicity, if reduction in BP not obtained within 10 minutes of max infusion rate, discontinue (r/t cyanide toxicity)
solution has faint brownish tint, if discolored then discard

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21
Q

Organic Nitrrates

A

nitroglycerin (glyceryl trinitrate)
isosorbide dinitrate
isosorbide mononitrate
amyl nitrite (rarely used)

22
Q

Nitroglycerin MOA

A

NO release through cellular metabolism via glutathione dependent pathway
requires thiols
NO released, stimulates guanylyl cyclase enzyme and forms cGMP
vascular smooth muscle relaxation and peripheral dilation

23
Q

nitroglycerin primary action, other actions, routes of administration

A

primary action: venous capacitance vessel dilation (versus arterial)
other actions: mildly dilate arteriolar resistance vessels, dilation of large coronary arteries
administered IV, SL, translingual spray, transdermal ointment

24
Q

Nitroglycerin preload and after load considerations

A

decreased preload, decreased MVO2 demand, modest decreased after load (related to arteriolar vessels), increased myocardial O2 supply in arteries.

25
Nitroglycerin CV, pulmonary, and other effects
decreased venous return, decreased end diastolic pressure, decreased CO, no change in SVR, increase in coronary BF to ischemic subendocardial areas (opposite of sodium nitroprusside). smooth muscle relaxation in bronchi, inhibits HPV inhibits platelet aggregation, smooth muscle relaxation to small GI tract
26
Nitroglycerin tolerance
after 8-10 hours, results in diminishing effectiveness. for PO and patch, have "off" period to recover metabolism enzymes
27
Nitroglycerin clinical uses
angina pectoris or prevention, SL (most commonly) HTN controlled hypotension during surgery NSTEMI acute MI HF, low output syndromes (decreases preload, relieves pulmonary edema)
28
Nitroglycerin Adverse Effects CNS, CV, hematologic, tolerance
CNS: throbbing HA and increased ICP CV: orthostatic hypotension, dizziness, syncope, reflex baroreceptor mediated tachycardia, flushing, vasodilation, venous pooling, decreased CO Hematologic: methemoglobinemia (rare and more unusual than for sodium nitroprusside) tolerance limits the use of nitrates
29
Nitroglycerin PK administration considerations, metabolism
large 1st pass (90%) following oral admin, give SL to avoid this. (isosorbide mononitrate and dinitrate avoid this as well) metabolized via liver through denigrated glutathione organic nitrate reductase to glyceryl denigrate and then mononitrate. "take nitrates off by glutathione"
30
Which organic nitrate can be given topical or transdermal
nitroglycerin
31
Nitroglycerin Drug Interactions
antihypertensive drugs-additive selective PDE5 inhibitors (adanafil, tadalafil, vardenafil, sildenafil) are an absolute contraindication. accumulation of cGMP via inhibiting breakdown guanylate cyclase stimulating drugs (stimulates enzyme that makes cGMP
32
Non Nitroglycerin Isosorbide Mononitrate, Dinitrate uses, absorption, DOA, metabolism, forms, dosing, contraindications
uses: for the prophylaxis of angina pectoris. alternative uses: heart failure in AA patients in combination with hydralazine absorption: well absorbed from GI tract duration of action: 6 hours metabolism: dinitrate metabolized to mononitrate form (t1/2 5 hours active metabolite), mononitrate metabolized by denigration to isosorbide to sorbitol-inactive -regular and ER forms need appropriate dosing intervals to allow for nitrate free periods and avoid tolerance avoid concomitant use with PDE5 inhibitor drugs toxicity similar to nitroglycerin
33
Phosphodiasterase Enzymes, role, classification
family of enzymes that break down cyclic nucleotides - regulate intracellular levels of 2nd messengers cAMP and cGMP - 11 major subfamilies that differ in localization and therapeutic targets
34
PDE inhibitors action and "older examples"
boost levels of cyclic nucleotides by preventing breakdown | older, nonselective PDE inhibitor drugs include caffeine and theophylline
35
PDE3 distribution, substrate it breaks down, function, clinical use of the inhibitor, drug example
distribution: broad, includes heart and vascular smooth muscle substrate: cAMP and cGMP function: cardiac contractility, platelet aggregation inhibitor clinical use: inotrope (+), peripheral vasodilator, limited for acute HF drug: amrinone, milrinone, (cilastazol for intermittent claudication)
36
PDE4 distribution, substrate it breaks down, function, clinical use of the inhibitor, drug example
distribution: broad, includes CV, neural, immune/inflammatory substrate: cAMP function: immune, inflammatory inhibitor clinical use: COPD, decreased inflammation and remodeling drug: roflumilast
37
PDE5 distribution, substrate it breaks down, function, clinical use of the inhibitor, drug example
broad, vascular smooth muscle especially erectile tissue, retina, lung substrate: cGMP function: vascular smooth muscle relaxation, esp erectile tissue, lung inhibitor clinical use: ED, pHTN drug: sildenafil, tadalafil, vardenafil
38
PDE5 Inhibitor MOA
nitric oxide reacts with guanylate cyclase to form cGMP which is usually broken down by PDE5
39
PDE3 Inhibitor MOA beta receptor example
beta receptor activation increases adenyl cyclase, cAMP. inhibiting PDE3 inhibits the breakdown of cAMP
40
milrinone MOA, effects, clinical uses, adverse effects, onset, t1/2, route of administration, metabolism, excretion
MOA: inhibits breakdown of cAMP effects: increases inotropy and cardiac contractility, vasodilation, little chronotropic activity clinical uses: acute HF, severe chronic HF, cardiogenic shock, heart transplant bridge or postop adverse effects: arrhythmias or hypotension onset IV: 5-15 minutes half life 3-6h route: IV only metabolism: >80% excretion: renal
41
role of aldosterone
increased sodium and water retention, potassium excretion. stimulated by AII
42
how is renin release stimulated
low blood pressure, low sodium, B1 receptor activation
43
what happens when AII acts on AT1 receptor
vasoconstriction, decreased renal BF and GFR, increased aldosterone secretion, remodeling
44
bradykinin and ACEI
ACEI inhibits breakdown of bradykinin, which is responsible for vasodilation, cough, angioedema
45
bradykinin t1/2, constitutive actions, inflammatory actions
endogenous peptide, t1/2 17 seconds constitutive actions: stimulates NO and prostacyclin formation to increase vasodilation vasodilation of heart, kidney, microvascular beds inflammatory actions: increases cap permeability
46
ACEI MOA, uses, clinical effects
MOA: block conversion of AI to AII, prevent vasoconstriction, aldosterone secretion, and Na/H2O retention used: HTN, CHF, mitral regurgitation, post MI, systolic HF, more effective in DM patients, delays progression of renal disease (diabetic neprhopathy) clinical effects: decreases BP, PVR, preload, after load, cardiac workload. does not result in reflex tachycardia. improves/prevents LV hypertrophy, remodeling. improves HF morbidity/mortality.
47
ACEI metabolism, elimination, route of administration, drug interactions, duration, 2 drugs for route 1, one drug for route 2
elanapril and ramipril are prodrugs metabolism: usually renal route of admin: usually PO except enalaprilat (IV) drug interactions: K sparing diuretics or K supplements DOA: long duration of decreased BP for the most part
48
ACEI SE's, CV, electrolyte, renal, inflammatory, fetal development, etc, contraindication
CV: hypotensive symptoms, syncope, first dose effect possible electrolyte: hyperkalemia, caution with potassium sparing diuretics and potassium supplements renal: decreased GFR, increased BUN and serum creatinine, renal dysfunction. contraindicated in bilateral renal artery stenosis inflammatory: dry cough r/t BKN, angioedema fetal development: teratogenic, contraindicated in pregnancy -neutropenia, agranylocytosis (captopril), proteinuria contraindications: renal artery stenosis
49
Angiotensin Receptor Antagonist (ARB) MOA, clinical effects, uses, metabolism, adverse effects, interactions, contraindication
MOA: competitive antagonist at AT1 receptor. blocks effects of angio mediated AT1 receptor. does not block breakdown of BKN, therefore do not have the cough and angioedema problem as often clinical effects and uses: HTN, CHF, mitral regurgitation, post MI, systolic HF, more effective in DM patients, delays progression of renal disease (diabetic neprhopathy) clinical effects: decreases BP, PVR, preload, after load, cardiac workload. does not result in reflex tachycardia. improves/prevents LV hypertrophy, remodeling. improves HF morbidity/mortality. metabolism: liver (CYP?) adverse effects: similar to ACEI interactions: K sparing diuretics and K supplements contraindication: renal artery stenosis, pregnancy
50
aldosterone antagonist MOA, effects, uses, metabolism, side effects, drug interactions, drug examples
MOA: competitive antagonist at mineralocorticoid receptor, blocks transcription of genes coding for Na+ channels. spironolactone off target effects include androgen, progesterone, receptor blocking effects: increased Na, H2O excretion, mild diuresis, increased K reabsorption uses: HTN, HF, K sparing diuresis, primary hyperaldosteronism, spironolactone off label includes acne, hirsutism, PCOS metabolism: spironolactone: hepatic. active metabolites canrenone and 7 alpha spironolactone. p-gp inhibitor. eplerenone: CYP3A4 se: hyperkalemia. spironolactone: broad, includes hepatic, renal, serious derm problems, GI, gynecomastia, menstrual irregularities, tumorigenic in animals drug interactions: other K sparing, K supplements, NSAID, eplerenone is a CYP3A4 inhibitor
51
hydralazine MOA, effects, first pass, bioavailability, t1/2, clinical uses, adverse effects, contraindication
MOA: release of NO from endothelial cells. effects: vasodilators arterioles, minimal venous effect, decreased SVR, DBP reduced more than SBP, increased HR SV CO extensive first pass bioavailability about 25% half life 1.5-3h clinical uses: HTN (usually with BB or diuretic), HF with reduced EF adverse effects: HA, nausea, palpitations, sweating, flushing, reflex tachycardia, tolerance, sodium and water retention, angina with EKG changes, lupus erythematous contraindication: CAD, mitral valve RH disease
52
minoxidil MOA, effects, oral absorption, peak effects, t1/2, clinical uses, adverse effects, warnings
MOA: directly relaxes arteriolar smooth muscle little effect on venous capacitance. increases efflux of K from vascular smooth muscle resulting in hyper polarization and vasodilation effects: dilates arterioles, not veins. use in hypertension (limited to later line therapy) 90% oral dose absorbed from GI tract peak effects 2-3h t1/2 4 hours 10% of drug recovered unchanged in urine clinical uses: HTN, later line therapy. usually in combo with BB or diuretic adverse effects: tachycardia, increased myocardial workload, palpitations, angina, na/fluid retention, edema, weight gain, hypertrichosis warnings: fluid retention, pericardial effusion/tamponade, rapid BP response, sinus tachycardia, elderly

Pharmacology N929 (11 decks)

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