ANS Pharm: Dilators, PDEIs, Vasopressin

Question 1

Answer 1

Question 2

T/F:
Direct acting vasodilators relax arteries

Answer 2

True

without systemic or local constrictor mechanisms or Ca channels

VARY on effects on arteries, arterioles and veins

Question 3

PDEIs cause smooth muscle relaxation where?

Answer 3

• heart
• lungs
• genitals

Question 4

PDEIs cause smooth muscle relaxation by increasing levels of

Answer 4

cAMP & cGMP

Question 5

T/F:
Vasopressin is synthesized in the poserior pituitary

Answer 5

False
hypothalamus

Question 6

When to use vasopressin

Answer 6

when catecholamines and fluids dont work

Question 7

Goal BP when using direct vasodilators

Answer 7

below their baseline

Question 8

NTG
Low dose vs high dose

Answer 8

low dose: venodilate; little effect on SVR

high dosE: arteriole dilation, ↓SVR, reflex tachycardia

Question 9

Why is NTG first line for cardiac ischemia?

Answer 9

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

Question 10

NTG cause severe hypoTN in these cases

Answer 10

1. hypovolemia
2. sildenafil (nitric oxide liberator)

Question 11

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

Answer 11

nitric oxide

Question 12

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

Answer 12

NTG = liberator

Nipride = donor

Question 13

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

Answer 13

Nipride = coronary steal

(redistribute blood away from ischemic tissue)

Question 14

coronary steal

Answer 14

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

Question 15

NTG vs Nipride

which has more reflex tachycardia & why?

Answer 15

Nipride

more arteriole dilation

thus, nipride will also increase O2 consumption

Question 16

How to treat reflex tachycardia from Nipride

Answer 16

B1B

Question 17

Nipride Metabolism produces…

Answer 17

• cyanide
• binds to Hgb = methgb; binds to sulfur = thiocyanate

Question 18

Nipride dose

Answer 18

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

Toxicity varies, thus maintain a high index of suspicion.

Question 19

T/F:
Hydralazine will not decrease preload.

Answer 19

True

it doesnt dilate venous capacitance vessels

decreases SVR but not preload

Question 20

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

Answer 20

True

Question 21

HDZ produces vasodilation in …

Answer 21

cardiac, cerebral, splanchnic, and renal vasculature

decreases SVR but not preload

Question 22

Must give this direct vasodilator with a B1B

Answer 22

minoxidil

strong, direct vasodilation

Question 23

Why dont we use minoxidil for HTN anymore?

Answer 23

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

Question 24

PDE
whats the difference between 3, 4 & 5?

Answer 24

• 3: affects both
• 4: cAMP
• 5: cGMP

Question 25

PDEI agents by class

Answer 25

* 3: milrinone, cilostazol * 4: roflumilast, apremilast, ibudilast * 5: sildenafil, tadalafil, vardenafil

Question 26

PDEIs location of action

Answer 26

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

Question 27

How do PDEIs affect the lungs?

Answer 27

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

Question 28

Why are PDE3s called inodilators?

Answer 28

increase inotropy and relax airway & vascular smooth muscle ## Footnote milrinone, cilostazol

Question 29

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

Answer 29

3 milrinone, cilostazol

Question 30

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

Answer 30

3

Question 31

Ideal for weaning from cardiopulmonary bypass

Answer 31

milrinone * inotrope, A& V dilation * block platelet aggregation * decrease inflammation from the bypass

Question 32

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

Answer 32

15-20

Question 33

Nonspecific PDEIs

Answer 33

theophylline, methylxanthine mild dilation of the airway smooth muscle and reduce inflammation

Question 34

Theophylline

Answer 34

increases the levels of cAMP in the airways (asthma and COPD)

Question 35

vasopressin and oxytocin are similar _____

Answer 35

nonapeptides

Question 36

Vasopressin's receptors

Answer 36

V1: SVR V2: antidiuretic V3: pituitary; modulate autocoids ## Footnote autocoids: biological factors acting like "local" hormones

Question 37

How does GA & neuraxial anesthesia affect vasopressin?

Answer 37

decreases plasma [ ] of stress hormones, including vaso so giving vaso can rapidly increase BP via V1

Question 38

Vasopressin dose

Answer 38

bolus (1 - 2 units) infusion 0.01 - 0.1 unit/ minute rapidly onsets and lasts 10 - 30 minutes.

Question 39

vasopressin healthy vs SNS/RAAS dysfxn

Answer 39

* 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

Question 40

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

Answer 40

true

Question 41

Which receptors do our pressors affect?

Answer 41

Question 42

Which pressor is suitable for pulm HTN?

Answer 42

vasopressin ## Footnote PVR = pulm vas resistance?

Question 43

PDE__ is useful in inflammatory states

Answer 43

4

Question 44

Answer 44

NTG I guess both NTG and nipride are donors