Pharm > Vasodilators > Flashcards

Vasodilators Flashcards

(37 cards)

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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:

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

What can occur of inhaled NO is abruptly stopped?

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A
  • arterial hypoxemia
  • pulmonary HTN
18
Q

MOA of sodium nitroprusside:

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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:

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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?

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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:

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

Systemic effects of sodium nitroprusside:

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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?

Study These Flashcards
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:

Study These Flashcards
A
  • increased mixed venous O2
  • metabolic acidosis
  • CNS dysfxn
  • tachyphylaxis
  • cardiac arrhythmia
25
Treatment for cyanide toxicity:
- turn off sodium nitroprusside drip - 100% O2 - give sodium bicarb - thiosulfate 150mg/kg - sodium nitrate - B12 - methylene blue
26
How does sodium nitrate treat cyanide toxicity?
binds 4 molecules of cyanide to methemoglobin to make a less toxic product
27
How does thiosulfate treat cyanide toxicity?
turns cyanide to thiocyanate (donates sulfur to rhondase)
28
What is the treatment for thiocyanate toxicity?
dialysis
29
MOA of nitroglycerine:
- stimulates production of cGMP - needs a specific enzyme to generate NO - primarily acts on venous capacitance and large coronary arteries
30
Through what routes is nitroglycerine available?
IV (specific tubing to avoid absorption of the drug into the tubing) SL *NO ORAL d/t 100% first pass metabolism**
31
What is nitroglycerine used to treat?
angina & vasospasm
32
What is important to know about isosorbide dinitrate?
- not subject to 1st pass metab - used to treat angina pectoris - metabolite is more active (isosorbide MONOnitrate) - acute admin can cause orthostatic hypotension
33
MOA of hydralazine:
directly dilates arteries but not veins
34
SE of hydralazine:
- HA - nausea - palpitations - sweating & flushing - lupus w/ long term use
35
Do not use Hydralazine in what patient populations?
ischemic heart dz -- the tachycardia and SNS stimulation may cause angina or ischemic arrhythmias
36
MOA of Fenoldopam:
- dopamine type 1 receptor agonist causing arterial dilation through increased cAMP - will increase renal BF
37
Major adverse effect of Fenoldopam:
increased IOP
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