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Pharmacology II - CP > HTN/Dilators (Cardiovascular Part III) > Flashcards

HTN/Dilators (Cardiovascular Part III) Flashcards

1
Q

Nitric Oxide pharmacokinetics/background

A 
endogenous, gas messenger 
lipophilic, highly reactive
formed from L-arginine
1/2 life - few seconds
elimination - oxidation to form NOx, nitrosylation of hemoglobin
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2
Q

3 types of Nitric Oxide Synthase enzymes

A

nNOS - neuronal, iNOS- induceable (macrophage), eNOS (endothelium)

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3
Q

Protective biological roles of Nitric Oxide

A

neurotransmitter, immune cytotoxicity, inhibit platelet aggregation, cytoprotection, vasodilator smooth muscle relaxant, decrease cell adhesion, proliferation

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4
Q

Pathogenic biological roles of Nitric Oxide

A

inflammatory tissue injury, shock, hypotension, cell proliferation, neuronal injury

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5
Q

Nitric Oxide mediated vasodilation MOA

A

ACh stimulates formation of NO by increasing Ca++ influx and activating NOS, that converts L-arginine to NO that will go to the VSMC and increase cGMP causing relaxation/vasodilation of the smooth muscle

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6
Q

What are the organic nitrates?

A

nitroglycerin
isosorbide dinitrate
isosorbide mononitrate

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7
Q

mechanism of action of sodium nitroprusside

A

release NO spontaneously which increases cGMP and leads to vascular smooth muscle relaxation and dilation

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8
Q

mechanism of action of organic nitrates

A

go through metabolism to release NO, need thiols to convert to NO which will then increase cGMP and cause relaxation and dilation of VSMC

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9
Q

metabolism of sodium nitroprusside

A

spontaneous breakdown to NO and cyanide, the cyanide combines with sulfur groups to form thiocyanate and undergoes renal excretion

if builds up or have impaired renal function = cyanide toxicity

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10
Q

sodium nitroprusside pharmacokinetics

A

onset <2 mins
duration 1-10mins
half life 2 mins but half life of thiocyanate about 2-7 days
renal excretion but some as exhaled air or feces

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11
Q

sodium nitroprusside effects on cardiovascular

A

decrease arterial/venous pressure, decrease PVR, decrease afterload, slight increase in HR

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12
Q

sodium nitroprusside effects on renal, cns, and blood

A

renal: vasodilation w/o significant change in GFR
CNS: increase cerebral blood flow and intracranial pressure
blood: inhibits platelet aggregation

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13
Q

sodium nitroprusside uses

A

hypertensive crisis, controlled hypotension during surgery, congestive HF, acute MI

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14
Q

why does sodium nitroprusside have a limited use in acute MI treatment?

A

d/t coronary steal which alters blood flow resulting in diversion of blood away from the ischemic areas

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15
Q

sodium nitroprusside adverse effects

A

profound hypotension, cyanide toxicity, methemoglobinemia, thiocyanate accumulation, increased serum creatinine, HA, increased intracranial pressure, restlessness, flushing, dizziness, palpitation, nausea

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16
Q

s/s of cyanide toxicity

A

tissue anoxia, venous hyperoxemia, lactic acidosis, confusion, death

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17
Q

explain methemoglobinemia

A

some iron in hemoglobin is oxidized to ferric state with impaired oxygen affinity so there is a reduced o2 delivery to the tissues

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18
Q

what do we use to reverse methemoglobinemia?

A

methylene blue

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19
Q

what are drug interactions with sodium nitroprusside?

A

negative inotropes, general anesthetics, circulatory depressants, PDE-5 inhibitors (sildenafil), soluble guanylate cyclase stimulators (riociguat)

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20
Q

pearls about sodium nitroprusside

A

light and temperature sensitive (store at 20-25 degrees C, wrap aluminum around container)
deterioration = bluish color (normally brown tint)
diluted in D5%

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21
Q

primary action of nitroglycerin

A

venous capacitance vessel dilation (decreased preload, myocardial o2 demand)
mildly dilates arteriolar resistance vessels (modest decreased afterload)
large coronary artery dilation (increased supply)

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22
Q

nitroglycerin cardiovascular and pulmonary effects

A

decrease VR, decrease LVEDP/RVEDP, decrease CO, increase coronary blood flow to ischemic areas, bronchial dilation, inhibits HPV

23
Q

what is something we need to be mindful of with nitroglycerin?

A

can build tolerance, after about 8 hours = diminishing effectiveness

24
Q

clinical uses of nitroglycerin

A

angina (acute and prevention), hypertension, controlled hypotension during surgery, ACS, acute MI, heart failure

25
Q

nitroglycerin adverse effects

A

throbbing HA, increased ICP, orthostatic hypotension, dizziness, syncope, reflex tachycardia, flushing, vasodilation, venous pooling, decreased CO, methemoglobinemia (rare)

26
Q

nitroglycerin pharmacokinetics

A

large first pass effect after oral admin
metabolized in the liver
IV - immediate onset, 3-5 min duration
Spray or Sublingual - 1-3min onset, >25min duration
Oral ER- 60 min onset, 4-8hr duration
Topical - 15-30min onset, 7 hour duration
Transdermal- 30 min onset, 10-12hr duration

27
Q

drug interactions with nitroglycerin

A

antihypertensives (additive effect), PDE-5 inhibitors (ABSOLUTE CONTRAINDICATION- profound potentiation/hypotension), guanylate cyclase stimulating drugs

28
Q

what are isosorbide mononitrate and dinitrate used for?

A

prophylaxis angina pectoris, heart failure in Black patients in combo w/ hydralazine

29
Q

what do phosphodiesterase enzymes do?

A

regulate intracellular levels of 2nd messengers cAMP and cGMP

30
Q

what do PDE 5 Inhibitors do? (MOA)

A

blocks cGMP from breaking down to inactive GMP so it increases cGMP which leads to vasodilation/relaxation

31
Q

MOA of PDE 3 inhibitors?

A

increase cAMP by preventing cAMP converting to AMP

32
Q

Milrinone (PDE 3 inhibitor) pharmacokinetics and adverse effects

A

onset 5-15mins
half life 3-6 hours
majority not metabolized, >80% excreted renally unchanged

adverse effects: arrhythmias, hypotension

33
Q

Milrinone effects and clinical uses

A

increase contractility, vasodilation, little chronotropic activity

clinical uses: acute HF or severe chronic HF, cardiogenic shock, heart transplant bridge or post op

34
Q

Describe the renin angiotensin aldosterone system :-)

A

decreased BP is sensed and renin is released where it meets up with angiotensinogen and converts it to angiotensin I where that is converted into angiotensin II by angiotensin converting enzyme, angiotensin II will increase blood pressure and stimulate aldosterone release which will cause salt and water retention to also increase blood pressure

35
Q

If you block aldosterone what electrolyte abnormality would we be concerned about?

A

potassium

36
Q

What are AT1 receptors?

A

GPCRs/ang II receptors

lead to vasoconstriction, decrease renal blood flow and GFR, increase aldosterone, remodeling

37
Q

What drugs can inhibit the RAAS?

A

renin inhibitors, beta-1 adrenergic antagonists, angII antagonists (ARBs), ACE inhibitors, aldosterone antagonists

38
Q

how do ACE inhibitors work in terms of angiotensin?

A

block conversion of angI to angII (so decreased angII)
leading to vasodilation, decreased remodeling, decreased aldosterone, decreased sympathetic output, and increased natiuresis

39
Q

Another mechanism of ACE inhibitors

A

blocks bradykinin from breaking down (increased bradykinin)

can lead to vasodilation, cough, angioedema

40
Q

Bradykinin

A

endogenous peptide
1/2 life: 17 sec
stimulates NO and prostacyclin formation, vasodilation and increased capillary permeability

41
Q

What are ACE inhibitors first line therapy for ?

A

HTN, CHF, mitral regurgitation, more effective in patients with diabetes and delay progression of renal disease

42
Q

clinical effects of ACE inhibitors

A

decrease BP, PVR, preload, afterload, workload, improves/prevents hypertrophy
*does not result in reflex tachycardia

43
Q

ACE inhibitors pharmacokinetics

A

many are prodrugs and usually renally eliminated, usually used in combo with diuretics, interacts with K+ sparing diuretics and supplements, longer duration of action

44
Q

what do we worry about with ACE inhibitors? and common adverse effects

A

hypotension! (long duration of action)

hyperkalemia, renal dysfunction, dry cough, angioedema, fetal malformations

45
Q

why are ACE inhibitors contraindicated in patients with renal artery stenosis?

A

may develop renal failure d/t efferent arteriole vasoconstriction

46
Q

angiotensin blockers (ARBs) MOA

A

competitive antagonist at AT1 receptors, blocks effects of angII , does not block the breakdown of bradykinin

similar uses as ace inhibitors

47
Q

angiotensin blockers pharmacokinetics

A

avoid in sever renal and hepatic dysfunction, highly protein bound, some metabolized through CYP system

48
Q

Spironolactone (aldosterone antagonist) MOA and uses

A

competitive antagonist at mineralocorticoid receptors and prevent nuclear translocation and blocks transcription of genes coding for Na+ channels

increase Na and H2O excretion, diuresis, increase K+ reabsorption (HTN, HF, K+ sparing diuresis, hyperaldosteronism, acne, hirsutiusm)

49
Q

hydralazine (direct vasodilator) MOA, effects and uses

A

release of NO and inhibit Ca++ release from SR
vasodilates arterioles, minimal venous effect
decreased SVR and DBP, increase HR, SV, CO
used in HTN and HF

50
Q

hydralazine pharmacokinetics and adverse effects

A

extensive first pass, half life 1.5-3 hrs
A/E: HA, nausea, palpitations, sweating, flushing, reflex tachycardia, Na+ and H2O retention, angina
dont give in CAD and mitral valve disease

51
Q

Why is hydralazine given with a beta blocker and/or diuretic

A

because it can cause reflex tachycardia (beta blocker will prevent that) and Na+ and H2O retention (which the diuretic will prevent)

52
Q

minoxidil (direct vasodilator) MOA, effects, uses

A

directly relaxes the arteriolar smooth muscle, little effect on venous, increases efflux of K+ = hyperpolarization and vasodilation

dilates arterioles not veins
use in HTN usually in combo with diuretic and beta blocker

53
Q

minoxidil pharmacokinetics and adverse effects

A

peak 2-3 hours, half life 4 hours

A/E: tachycardia, increased workload, palpitations, angina, Na/H2O retention, edema, weight gain, hypertrichosis

54
Q

drugs commonly used for controlled hypotension

A

sodium nitroprusside (0.3-0.5 mcg/kg/min; dont exceed 2)
nitroglycerin (125-500 mcg/kg/min)
nicardipine (5 mcg/kg/min)
dexmeditomidine (0.2-0.7 mcg/kg/hr)

Pharmacology II - CP (12 decks)

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