Sympathomimetics part 2

Question 1

NOREPI is __ to epi at β1, very little β2 actions.
Potent α1 producing intense vasoconstriction in arterial and venous vascular beds

Because is has ver little B2 = no bronchodilating effects!

Answer 1

equal

Question 2

Norepi Increases BP by increasing __ , May trigger the baroreceptor reflex, increased __ can elicit a reflex bradycardia.

Answer 2

SVR

SVR

Question 3

NE released during stress in brain stem’s __ ___, which is the origin of most NE pathways in the brain.
Noradrenergic neurons project from __ __ to the cerebral cortex, limbic system, and spinal cord.

Answer 3

Locus ceruleus

Locus ceruleus

Question 4

NE is a catecholamine & phenethylamine derivative.

Stereoisomer - we use the dextro or levo form?

Answer 4

LEVOphed

Question 5

NE is synthesized in adrenal medulla from the amino acid __, then oxidated to __, then de-carboxylated to __

Answer 5

tyrosine
L-DOPA
Dopamine

Question 6

NE action is followed by signal termination - either by degradation of NE or by NE uptake by surrounding cells.

Answer 6

degradation OR uptake

Question 7

What are the two major urinary metabolites of catecholamine metabolism?

Answer 7

VMA and MOPEG

Zach rode his mopeg to the vma’s to get an award for the best skiing wreck of the winter break.

Question 8

Again, does NE activate B2?

Answer 8

No, no bronchodilating properties

Question 9

Again, how do NE increase BP?

Answer 9

Alpha 1 and 2 agonist causing increased SVR

Question 10

Dopamine is a Phenethylamine derivative that is released by hypothalamus, stimulates the __.

Answer 10

Stimulates the CTZ

Question 11

Of all the dopamine receptors, only d1 and d_ have clinical significance

Answer 11

d1 and d2

Question 12

D1receptor works post synaptically to __

Answer 12

vasodilation of renal, mesenteric, coronary, and cerebral blood vessels

Question 13

D2 receptor works pre synaptically to __

Answer 13

inhibits the release of NE, (post-synaptic) weak vasoconstriction

Question 14

Dopamine acts @
β1 receptors with 3-10mcg/kg/min doses,
α1 @ >10mcg/kg/min doses

Answer 14

A portion of dopamine’s + inotrope effect is from release of endogenous NE (indirect actions!)

Question 15

“Renal Dose Dopamine” 1-3 mcg/kg/min implies dopamine only works at kidneys at this level

Answer 15

NOT TRUE

Question 16

Dopamine inactivated by reuptake via dopamine transporter DAT

Answer 16

Enzymatic breakdown by catechol-O-methyl transferase (COMT) and monoamine oxidase (MAO) contributes to ending dopamine effects.

Dopamine may also simply diffuse away from the synapse, and help to regulate blood pressure

Question 17

Dopamine doses

Answer 17

2 to 5 μg/kg/min:
binds D1 receptors, dilating blood vessels, increasing blood flow to renal, mesenteric, and coronary arteries
5 to 10 μg/kg/min:
Positive inotropic and chronotropic effects via increased β1 receptor activation. Used in patients with shock or heart failure to increase CO & BP.
10 to 20 μg/kg/min:
Dopamine causes vasoconstriction, increases SVR, and increases BP through α1 receptor activation.

Question 18

ISOPROTERENOL is the Most potent activator of β adrenergic receptors due to substitution of isopropyl group at terminal amine of the beta-phenylethylamine

Answer 18

Has no α effects – no increases in SBP directly, increased SBP indirectly from greater CO

Question 19

ISOPROTERENOL is used for greater HR, increased myocardial contractility, cardiac automaticity, bronchodilation, reductions in PVR

Answer 19

Use with post heart transplant patients due to de-innervation of the orthotopic heart transplant
Primary use is for bradycardia & heart block.
Isoproterenol causes + chrontropic, dromotropic, & inotropic effects (β1).
Isoproterenol activates all β receptors – not always desirable

Question 20

Isoproterenol Uses/ Contraindications

Answer 20

Resistant bradyarrhythmias when pacing is not available
Pharmacologic pacing for torsade de pointes (polymorphic ventricular tachycardia)
Contraindications - angina, pre-existing arrhythmias, tachycardia or AV block caused by cardiac glycoside intoxication. Ventricular arrhythmias due to AV nodal block.
Usual effective dose 0.2-2 mcg/kg/minute

Question 21

Dobutamine- direct stimulation B1 receptors.

Answer 21

Dobutamine not as useful in ischemic heart disease because it may increase HR, potentially increasing myocardial oxygen demand

Question 22

DOBUTAMINE Selective β1 adrenergic agonist used to improve cardiac output

Answer 22

+ dromotrope… be careful with atrial fibrillation as HR may markedly increase.

Question 23

Dobutamine is given as a racemic mixture of both + & - isomers.

Answer 23

The + isomer is a potent β1 agonist

The – isomer is an α1 agonist.

Question 24

Dobutamine Dosing

Answer 24

rates typically 2-10 mcg/kg/min

Question 25

PHENYLEPHRINE Synthetic non-catecholamine Principally α1 direct effect with only a small part via indirect release of NE Minimal if any β effect

Answer 25

Venoconstriction > arterial constriction differing only by lacking a 4-hydroxyl group on the benzene ring from epi

Question 26

Phenylephrine may impair LV global function when given rapidly to anesthetized patients (1mcg/kg)

Answer 26

Can be used to treat PSVT (500mcg bolus)

Question 27

Dexmedetomidine - Like clonidine, agonist of α2 - adrenergic receptors in the brain.

Answer 27

imidazole compound

Question 28

Dexmedetomidine has no absolute contraindications but ---

Answer 28

Caution with boluses due to peripheral α2 -receptor stimulation with resulting hypertension and bradycardia

Question 29

EPHEDRINE - Indirect acting synthetic noncatecholamine

Answer 29

Stimulates α and β adrenergic receptors | Endogenous release of NE (indirect) and direct stimulation of adrenergic receptors

Question 30

takes 250X an ephedrine dose to equal an epi dose

Answer 30

good to know

Question 31

Vasopressin stored in the posterior pituitary for release into the bloodstream or directly into the brain

Answer 31

Not an adrenergic agent Works on Three arginine vasopressin receptor types CRNA’s should like AVPR1A best!