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Pharm > Vasodilators > Flashcards

Vasodilators Flashcards

1
Q

What is the first line treatment for HTN? Why?

A

thiazide diuretics

  • cheapest
  • fewest side effects
  • least complex dosing regimen
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2
Q

List the 4 sites where BP is controlled and how:

A
  1. arterioles (resistance)
  2. postcapillary venules (capacitance vessels)
  3. heart (altering pump output)
  4. kidney (regulating intravascular volume)
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3
Q

How do sympathoplegic agents decrease BP?

A
  • decrease SVR
  • inhibit cardiac function
  • increase venous pooling
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4
Q

How do direct vasodilators decrease BP?

A
  • relax vascular smooth muscle
  • dilating resistance vessels
  • increasing capacitance
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5
Q

How do angiotensin blockers lower BP?

A
  • decrease PVR
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6
Q

How do diuretics control BP?

A
  • deplete body of Na+
  • reduce blood volume
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7
Q

How is Ca2+ related to BP?

A
  • increased Ca2+ = vasoconstriction; BP up
  • decreased Ca2+ = vasodilation; BP down
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8
Q

Describe the 3 ways in which Ca2+ affects vessel diameter:

A

1) stimulates B2 receptor - Gs - adenylate cyclase - ^cAMP - decrease Ca2+
2) block A1 receptor - Gq - Phospholipase C - decrease Ca2+
3) nitric oxide - guanylate cyclase - cGMP - decrease Ca2+

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9
Q

Dose/onset/duration of Clevidipine:

A
  • dose: 1-2mg/hr
  • onset: 2-4 mins
  • duration: 5-15 mins
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10
Q

What is NOS?
What are its 2 forms?

A

NOS = nitric oxide synthase; when stimulated it takes L-argenine and makes nitric oxide

cNOS and iNOS

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11
Q

What is important to know about cNOS?

A
  • Ca2+ and calmodulin dependent
  • makes NO quickly but in small amounts
  • activated by blood shearing forces and NO-dependent vasodilator receptors
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12
Q

What is important to know about iNOS?

A

i = inflammation
- makes NO slowly but in large amounts
- activated by inflammation

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13
Q

What g-protein receptor is required for NO to move from cell to cell?

A

trick question - NO diffuses easily from cell to cell

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14
Q

What substances increase receptor-stimulated production of NO?

A
  • ACh
  • Substance P
  • Serotonin
  • Bradykinin
  • Thrombin
  • Stress
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15
Q

What makes NO have a short half-time?

A

it binds to heme-based proteins

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16
Q

Describe the physiologic effects of inhaled NO:

A
  • pulmonary vasodilator
  • will increase methemoglobin levels as NO combines with Hgb
17
Q

What can occur of inhaled NO is abruptly stopped?

A
  • arterial hypoxemia
  • pulmonary HTN
18
Q

MOA of sodium nitroprusside:

A
  • direct-acting, non-selective peripheral vasodilator
  • interacts with oxyhemoglobin - immediately dissociates to form methemoglobin, cyanide, and NO
  • through the NO pathway, cGMP inhibits Ca2+ entry into vascular smooth muscle and increases Ca2+ uptake by endoplasmic reticulum
  • relaxes arterial and venous smooth muscle –> reduced PVR and venous return
19
Q

Metabolism of sodium nitroprusside:

A
  • rapidly metabolized via uptake by RBCs
  • methemoglobin & cyanide released
  • cyanide converted to thiocyanate by rhondase
  • thiocyanate distributed in ECF and slowly eliminated by kidney
20
Q

What is important to know about rhondase?

A
  • temperature-specific (does not function during hypothermia)
  • specifically the enzymatic conversion of cyanide to thiocyanate
21
Q

Dose/onset/need-to-know for sodium nitroprusside:

A
  • dose: 0.3 - 10 mcg/kg/min
  • onset: immediate
  • needs to be protected from light
22
Q

Systemic effects of sodium nitroprusside:

A
  • CV: reflexive tachycardia, increased contractility, coronary steal
  • renal: decreased renal fxn, renin release
  • hepatic: none
  • cerebral: increased ICP
  • pulm: inhibits hypoxic pulmonary vasoconstriction
  • heme: inhibits PLT aggregation
23
Q

What is hypoxic pulmonary vasoconstriction?

A
  • local rxn that occurs in response to a reduction in alveolar oxygen tension
  • selectively increases the PVR in poorly ventilated areas to shut flow to better ventilated areas
  • begins within seconds, full effect in 15 mins
  • relevant during atelectasis & single-lung ventilation
24
Q

S/S of cyanide toxicity:

A
  • increased mixed venous O2
  • metabolic acidosis
  • CNS dysfxn
  • tachyphylaxis
  • cardiac arrhythmia
25
Q

Treatment for cyanide toxicity:

A
  • turn off sodium nitroprusside drip
  • 100% O2
  • give sodium bicarb
  • thiosulfate 150mg/kg
  • sodium nitrate
  • B12
  • methylene blue
26
Q

How does sodium nitrate treat cyanide toxicity?

A

binds 4 molecules of cyanide to methemoglobin to make a less toxic product

27
Q

How does thiosulfate treat cyanide toxicity?

A

turns cyanide to thiocyanate
(donates sulfur to rhondase)

28
Q

What is the treatment for thiocyanate toxicity?

A

dialysis

29
Q

MOA of nitroglycerine:

A
  • stimulates production of cGMP
  • needs a specific enzyme to generate NO
  • primarily acts on venous capacitance and large coronary arteries
30
Q

Through what routes is nitroglycerine available?

A

IV (specific tubing to avoid absorption of the drug into the tubing)
SL
*NO ORAL d/t 100% first pass metabolism**

31
Q

What is nitroglycerine used to treat?

A

angina & vasospasm

32
Q

What is important to know about isosorbide dinitrate?

A
  • not subject to 1st pass metab
  • used to treat angina pectoris
  • metabolite is more active (isosorbide MONOnitrate)
  • acute admin can cause orthostatic hypotension
33
Q

MOA of hydralazine:

A

directly dilates arteries but not veins

34
Q

SE of hydralazine:

A
  • HA
  • nausea
  • palpitations
  • sweating & flushing
  • lupus w/ long term use
35
Q

Do not use Hydralazine in what patient populations?

A

ischemic heart dz – the tachycardia and SNS stimulation may cause angina or ischemic arrhythmias

36
Q

MOA of Fenoldopam:

A
  • dopamine type 1 receptor agonist causing arterial dilation through increased cAMP
  • will increase renal BF
37
Q

Major adverse effect of Fenoldopam:

A

increased IOP

Pharm (19 decks)

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