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Pharmacotherapy 1 > 2- Adrenergics > Flashcards

2- Adrenergics Flashcards

1
Q

Describe the major steps in catecholamine synthesis and metabolism.

A

-import tyrosine –hydroxylase–>
dopa –decarboylase–>
dopamine –> import into vessicle –> –methyltransferase–> NE

NE released into synapse. Take back up and recycled or broken down by MAO.

NE ==>
–MAO–> aldehyde reductase –> COMT adds methyl to catechol –> alcohol dehydrogenase, aldehydedehydrogenase
==> vanilyllmandelic acid = VMA

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2
Q

Where are alpha1, alpha2, and beta1 and beta2 receptors?

A

alpha1=vascular smooth muscle, arteries, salivary glands, skin, sweat stress, radial iris

alpha2=CV control center of brain, gastric secretions

beta1=heart, kidneys

beta2=lungs, arteries in skeletal muscle, uterus (preg), ciliary epithelium

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3
Q

What signalling is activated at alpha1 receptors?

A

Gq–> Ca2+ and PKC

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4
Q

Which direct-acting adrenergic receptor agonists act on alpha1 receptors?

What can these agents be used for?

A

phenylephrine (Neosynephrine)
methoxamine (Vasoxyl)
Oxymetazoline (Visine)

vasoconstriction: incr BP, decongestants

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5
Q

Which direct-acting adrenergic receptor agnists acton alpha2 receptors?

What can these agents be used for?

A 
clonidine (Catapres)
methyldopa (Aldomet)
Guanabenz (Wytensin)
Guanfacine (Tenex)
Tizanidine (Zanaflex)

these affec the CV control center of brain…turn off symp NS

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6
Q

What signalling is activated at alpha2 receptors?

A

Gi –> reduce cAMP-dep PK activity, open K channels

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7
Q

Which direct-acting adrenergic receptor agonists are non-selective for beta receptors (activate both beta1 and beta2)?

A

isoproterenol (Isuprel)

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8
Q

Which direct-acting adrenergic receptor agonists are selective for beta1 receptors?

A

dobutamine (Dobutrex)

Dopamine (Intropin)

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9
Q

Which direct-acting adrenergic receptor agonists are selective for beta2 receptors?

A 
terbutaline (Brethine, Bricanyl)
metaproterenol (Metprel, Alupent)
albuterol (Proventil, Ventolin)
salmeterol (Serevent)
ritodrine (Yutopar)
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10
Q

What signalling pathway do beta receptors activate?

A

Gs ==> increase cAMP-dep PK activity

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11
Q

Who does NE interact with the G-protein active site to produce a response?

A

catechol h-bonds with serines

the positive amine is stabilized by anionic aspartate

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12
Q

What are the three main characteristics of adrenergic agonists?

A

amine
alpha and beta carbons (alkyl chain)
catechol

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13
Q

Describe how alterations to the amine of an adrenergic receptor agonist affect its activity/selectivity.

A

increase in size of alkyl substituents increases beta-receptor activity ; beta2 receptor selective drugs tend to have larger amine head groups. –> also MAO resistance

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14
Q

How do alpha substitutions on the alkyl chain of an adrenergic receptor agonist affect its activity/selectivity?

A
  1. block oxidation by MAO
  2. increase lipophilicity (incr CNS act)
  3. reduce direct agonist activity at both alpha and beta adrenergic receptors
  4. alter receptor selectivity: alpha2>alpha1, beta2>beta1
  5. introduces chiral center (s-preferred)
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15
Q

How do beta substitutions on the alkyl chain of an adrenergic receptor agonist affect its activity/selectivity?

A

a. direct agonists possess beta-hydroxyl group
b. enhances uptake and storage in vesicles
c. introduces chiral center (R-preferred)

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16
Q

How do alterations of the aromatic rings of an adrenergic receptor agonist affect its activity/selectivity?

A

a. 3 and 4 positions most important
b. reduced susceptibility to COMT (incr oral BA)
c. removal of OH incr lipophilicity
d. replace catechol (3,4) w resorcinol (2, 4) to incr beta2 R selecivity

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17
Q

What are the two S/A relationships that allow us to drive beta2 selectivity?

A
  1. bulky head group on amine
  2. replace catechol w resorcinol

this is favorable for design f bronchodilators w/o activity on heart

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18
Q

Describe the effect of NE on HR and BP.

A

sel for a1 and B1

alpha1 - vasoconstrict –> INCR BP

beta1 –> expect incr HR but baroreceptors –> decr HR

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19
Q

Describe the effect of Epi on HR and BP.

A

sel for a1, B1, B2

a1 - vasoconstrict –> incr BP
beta2 –> musculoskeletal vasodilation –> decr BP –> NO NET CHANGE IN BP

beta1 –> incr HR

20
Q

Describe the effects of isoproterenol on HR and BP.

A

sel for beta1, beta2

beta2 - vasodilation –> decr BP
beta1 - incr HR (also baroreceptor reflex)

21
Q

describe the effects of phenylephrine on HR and BP.

A

sel for a1

a1 – vasoconstrict –> incr BP
baroreceptors decr HR

can be used acutely as a vasopressor and for some arrythmias.

22
Q

Describe NE as a direct-acting adrenergic receptor agonist.

What are its use and clinical considerations?

A

alpha and beta1 agonist
substrate for MAO and COMT
PE admin

use: pressor

Nabisulfite used in prep to prevent ox

23
Q

Describe Epi as a direct-acting adrenergic receptor agonist.

What are its use and clinical considerations?

A

potent a, B1, B2 ag
substrate for MAO and COMT
PE admin
Nabisulife antiox

Uses: anaphylaxis, glaucoma, in comb w local anesthetics

24
Q

Describe phenylephrine as a direct-acting adrenergic receptor agonist.
What are its use and clinical considerations?

A

potent a1 ag
substrate for MAO
admin PE, po, local

uses: mydriasis w/o cycloplegia
glaucoma
nasal decongestant

25
Q

Describe the S/A of 2-aralkylimidazolines.

A

substituted aromatic ringe + metylene or aminoe + five-membered dibasic ring –> very basic

these compounds exist in ionized form at physiologic pH

26
Q

Describe 2-aralkylimidazolines as a direct-acting adrenergic receptor agonist. List them.
What are its use and clinical considerations?

A

naphazoline (Privine)
tetrahydrozolnie (Visine)
oxymetazoline (Afrin, Visine)

partial agonists at alpha Rs

  • admin local/top to promote vasoconstriction
    use: nasal and ophtalmic decongestants

tachyphylaxis/desensitization

27
Q

Describe clonidine as a direct-acting adrenergic receptor agonist.
Describe S/A.

What are its use and clinical considerations?

A

sel alpha2 R ag –> act CV center in nucleus of solitary tract –> reduce sympathetic tone
(phenyliminio)imidazoline

basicity of guanidine is decr’d d/t dichlorophenyl rings –> can cross BBB

admin: po, PE, TD

Uses: HTN, opiate withdrawl

28
Q

What are the effects of alpha2 mediated reduction in sympathetic tone?

A

decr B1, a1 act
decr HR/contractility
decr renin
decr vasoconstriction

==> decr BP

29
Q

Describe open-ring imidazolides as a direct-acting adrenergic receptor agonist.
List them.
Describe S/A.

What are its use and clinical considerations?

A

bridge to guanidine decr pKa so non-ionized at physio pH

guanabenz (Wytensin)–short half life ~2
guanfacine (Tenex, Intuiv)

admin po

Uses: HTN, ADHD (guanfacine)

30
Q

What are the uses of apraclonidine (Iopidine) and tizanidine (Zanaflex)?

A

glauma

muscle spasticity

31
Q

What are the adverse effects of alpha2-adrenergic R ag?

A

sedation
Na and water retention (RAAS act)
dry mouth
withdrawl syndrme (rebound HTN, tachycardia)–> taper to dc

32
Q

Describe isoproterenol as a direct acting adrenergic receptor agonist.
What are its uses and clinical considerations?

A

non-sel beta r ag

metab by phase II and COMT (not MAO)

effects: bronchodil and incr CO
admin: po, PE, inhaled
uses: asthma, COPD, cardiostimulant

33
Q

Describe resorcinol derivatives as a direct acting adrenergic receptor agonists. List them
What are their uses and clinical considerations?

A

metaproterenol (Alupent, Metaprel)
terbutaline (Brianyl, Brethine)

sel B2 R ag

–> bronchodil
(card effect at high doses)

no metab by MAO or COMT; longer doa than isoproterenol

Uses: asthma, COPD
terbutaline as tocolytic

34
Q

What is the fxn of a tocolytic?

A

prevent premature labor

35
Q

Describe meta hydroxylmethyl derivatives as a direct acting adrenergic receptor agonists. List them
What are their uses and clinical considerations?

A

albuterol
levalbuterol
salmeterol

sel beta2 R ag
–> bronchodil (card at high dose)

no metab by MAO or COMT, longer doa than isoproterenol

use: asthma, COPD

36
Q

Which are the long-acting beta-receptor agonists?

Describe moa and use.

A

salmeterol
formoterol

sel B2
not met’d by MAO or COMT

DPI or MDI
uses: asthma, COPD (not acute asthma Sx)

37
Q

Describe the moa of dobutamine as a direct-acting adrenergic receptor agonist. Describe it’s uses.

A 
dopamine-deriv
racemic mix
(+)-B1 ag; a1 antag
(-)-a1 ag
NET: incr inotropic effect w little chronotropic effect

metab by COMT
admin PE

USe: acute HF, shock

38
Q

What is the moa of indirect-acting sympathomimetics?

List them.

A

promote release of NE via reverse action of plasma membrane transporter.

amphetamine
pseduoephedrine
ephedrine
phenylpropanolamine 
tyramine
39
Q

What are the clinical uses of indirect-acting sympathomimetics?

A

amphetamines: ADHD, narcolepsy, anorexiant
others: nasal decongestants

40
Q

Compare and contrast the activity of (-)-Ephedrine and (+)- Pseduoephredrine

A

ephredrine has R config at beta-OH and S at alpha carbon for direct ag activity at adrenergic R

pseudoephredrine is S,S. S configuration of beta-OH reduces agonist activity-major mechanism is via reversal of the transporter

41
Q

What is the chemical difference between pseudoephedrine and meth?

A

beta hydroxyl (S-config) converted to H after rxn with Li and NH4+

more hydrophobic–get CNS activation

42
Q

How are cocaine and antidepressants indirect-acting sympathomimetics? i.e. moa

A

block reuptake transporters on presynaptic neuron, incr amt of NT in synapse

43
Q

How do MAO inhibitors act as indirect sympathomimetics?

A

decrease amt of NE that is broken down, incr amt of NE available to be secreted into synapse

44
Q

Coadministration of MAOI with other indirect-acting sympathomimetics can lead to what complication?

A

hypertensive crisis

45
Q

What are examples of MAOIs?

A

phenelzine

selegiline

Pharmacotherapy 1 (26 decks)

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