ANS Pharm: Dilators, PDEIs, Vasopressin Flashcards

1
Q
A
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2
Q

T/F:
Direct acting vasodilators relax arteries

A

True

without systemic or local constrictor mechanisms or Ca channels

VARY on effects on arteries, arterioles and veins

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3
Q

PDEIs cause smooth muscle relaxation where?

A
  • heart
  • lungs
  • genitals
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4
Q

PDEIs cause smooth muscle relaxation by increasing levels of

A

cAMP & cGMP

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5
Q

T/F:
Vasopressin is synthesized in the poserior pituitary

A

False
hypothalamus

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6
Q

When to use vasopressin

A

when catecholamines and fluids dont work

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7
Q

Goal BP when using direct vasodilators

A

below their baseline

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8
Q

NTG
Low dose vs high dose

A

low dose: venodilate; little effect on SVR

high dosE: arteriole dilation, ↓SVR, reflex tachycardia

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9
Q

Why is NTG first line for cardiac ischemia?

A
  • improves the balance of myocardial O2 supply and demand (direct coronary dilator + systemic effects)
  • dilates both normal & stenotic coronaries, preventing vasospasm
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10
Q

NTG cause severe hypoTN in these cases

A
  1. hypovolemia
  2. sildenafil (nitric oxide liberator)
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11
Q

NTG exerts its action via the liberation of ___, a vascular dilator.

A

nitric oxide

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12
Q

NTG is a nitric oxide ___.
Nipride is a nitric oxide ___.

A

NTG = liberator

Nipride = donor

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13
Q

NTG is used in MI but Nipride is not. Why?

A

Nipride = coronary steal

(redistribute blood away from ischemic tissue)

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14
Q

coronary steal

A

vessels to ischemic areas dilate to the max, so blood flow diverts to nonischemic tissue

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15
Q

NTG vs Nipride

which has more reflex tachycardia & why?

A

Nipride

more arteriole dilation

thus, nipride will also increase O2 consumption

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16
Q

How to treat reflex tachycardia from Nipride

A

B1B

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17
Q

Nipride Metabolism produces…

A
  • cyanide
  • binds to Hgb = methgb; binds to sulfur = thiocyanate
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18
Q

Nipride dose

A

MAX dose 500 mcg/kg
MAX rate 2 mcg/kg/min

Toxicity varies, thus maintain a high index of suspicion.

19
Q

T/F:
Hydralazine will not decrease preload.

A

True

it doesnt dilate venous capacitance vessels

decreases SVR but not preload

20
Q

T/F:
Use a B1B to treat reflex tachycardia from hydralazine

21
Q

HDZ produces vasodilation in …

A

cardiac, cerebral, splanchnic, and renal vasculature

decreases SVR but not preload

22
Q

Must give this direct vasodilator with a B1B

A

minoxidil

strong, direct vasodilation

23
Q

Why dont we use minoxidil for HTN anymore?

A
  • hypertrichosis (hair growth)
  • salt and water retention
  • pericardial effusion (rare)
24
Q

PDE
whats the difference between 3, 4 & 5?

A
  • 3: affects both
  • 4: cAMP
  • 5: cGMP
25
Q

PDEI agents by class

A
  • 3: milrinone, cilostazol
  • 4: roflumilast, apremilast, ibudilast
  • 5: sildenafil, tadalafil, vardenafil
26
Q

PDEIs location of action

A

3: both; dilate peripheral
4: ↑cAMP (airways, skin, immune)
5: ↑cGMP (lungs, penis)

27
Q

How do PDEIs affect the lungs?

A

3: airway smooth muscle relaxation
4: airway smooth muscle relaxation
5: pulm vasodilate & decrease pulm. artery pressure

28
Q

Why are PDE3s called inodilators?

A

increase inotropy and relax airway & vascular smooth muscle

milrinone, cilostazol

29
Q

PDE___ inhibitors vasodilate peripheralaly to treat intermittent claudication & prevent platelet aggregation (DVT prophylaxis)

A

3
milrinone, cilostazol

30
Q

PDE__ inhibitors may cause ventricular arrhythmias d/t increasing cAMP and Ca

31
Q

Ideal for weaning from cardiopulmonary bypass

A

milrinone

  • inotrope, A& V dilation
  • block platelet aggregation
  • decrease inflammation from the bypass
32
Q

milrinone is ___ x more potent than amrinone, replacing it.

33
Q

Nonspecific PDEIs

A

theophylline, methylxanthine

mild dilation of the airway smooth muscle and reduce inflammation

34
Q

Theophylline

A

increases the levels of cAMP in the airways

(asthma and COPD)

35
Q

vasopressin and oxytocin are similar _____

A

nonapeptides

36
Q

Vasopressin’s receptors

A

V1: SVR
V2: antidiuretic
V3: pituitary; modulate autocoids

autocoids: biological factors acting like “local” hormones

37
Q

How does GA & neuraxial anesthesia affect vasopressin?

A

decreases plasma [ ] of stress hormones, including vaso

so giving vaso can rapidly increase BP via V1

38
Q

Vasopressin dose

A

bolus (1 - 2 units)

infusion 0.01 - 0.1 unit/ minute

rapidly onsets and lasts 10 - 30 minutes.

39
Q

vasopressin
healthy vs SNS/RAAS dysfxn

A
  • healthy & conscious: little effect on BP due to reflex inhibition of efferent SNS
  • SNS or RAAS axis dysfunction: activates V1 receptors and may restore BP
40
Q

T/F:
In distributive shock, Vaso, neo and norepi are suitable options.

41
Q

Which receptors do our pressors affect?

42
Q

Which pressor is suitable for pulm HTN?

A

vasopressin

PVR = pulm vas resistance?

43
Q

PDE__ is useful in inflammatory states

44
Q
A

NTG

I guess both NTG and nipride are donors