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Therapeutics > Lecture 7: Indirect-acting Sympathomimetics > Flashcards

Lecture 7: Indirect-acting Sympathomimetics Flashcards

1
Q

Indirect-acting sympathomimetics

A

-promote release of NE (dopamine)
-reverse action of plasma membrane transporter (NET and DAT)

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2
Q

types of indirect-acting sympathomimetics

A

-amphetamine
-pseudoephedrine
-ephedrine
-tyramine

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3
Q

indirect sympathomimetic uses

A

-amphetamines: ADHD, narcolepsy, anorexiant
-others: nasal congestant

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4
Q

Structures

A

structures

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5
Q

Amphetamine use

A

-narcolepsy
-ADHD
-also used as appetite suppressant

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6
Q

Amphetamine problems

A

-anorexia
-poor growth
-sleep disturbances
-jitteriness

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7
Q

Toxic dose of Amphetamine

A

-INcrease BP, HR via NE signaling
-potential for stroke, arrhythmia, MI, sudden death
-agitation, confusion, addiction

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8
Q

Amphetamine also releases

A

-dopamine
=CNS effects

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9
Q

Phentermine/Topiramate

A

-weight loss
-Phen: sympathomimetic
-Topir: antiepileptic
-avoid: HTN, heart disease, pregnancy (birth defects)

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10
Q
  • Ephedrine and + Pseudoephedrine
A

-indirect sympathomimetics
-alkaloid obtained from stems of ephedra
-also found in mahuand

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11
Q

D–Ephedrine structure

A

-desired R config at B-OH and S config at a carbon
-direct a and B agonist activity at receptors

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12
Q

L-+-pseudoephedrine

A

-SS diasteromer
-S config of B-OH
-REDUCES agonist activity
-major mech is via reversal of transporter

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13
Q

Pseudoephedrine use

A

-nasal congestion

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14
Q

Ephedrine use

A

-DIRECT a B effects
-banned as weight loss supplement bc BP, stroke, death

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15
Q

Ephedra

A

-combo of ephedrine and pseudoephedrine enatiomers

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16
Q

Problems with pseudo/ephedrine

A

-increase BP
-increase HR
-via NE signaling from SNS

17
Q

Pseudo/ephedrine warning

A

-do not use if taking MAO-inhibitor
-can be used to make meth

18
Q

Indirect sympathomimetics vs NE and Epi

A

-indirect are ORALLY active
-due to methyl substitution that blocks oxidation by MAO

19
Q

MAO inhibitors

A

-indirect-acting sympathomimetic
-decrease breakdown of tyramine
=bolus release of NE
-could lead to HTN crisis

20
Q

MAO inhibitor medications

A

-phenelzine (antidepressant)
-selegiline
-

21
Q

Tyramine

A

-indirect sympathomimetic in meats and cheese
-digested by MAO

22
Q

other indirect sympathomimetics

A

-amphetamine
-methylphenidate
-pseudoephridrine

23
Q

NET blockers

A

-norepineephrine reuptake inhibitors
-cocaine, methylphenidate
-tricyclic antidepressants

24
Q

Cocaine action

A

-block NET and DAT
-decrease uptake
-enhance NE signaling by keeping more transmitter in synaptic cleft

25
Q

Cocaine clinical use

A

-local anesthetic
-sodium channel blocker
-nasal mucosa and vasoconstriction

26
Q

Cocaine side effects

A

-increase BP and HR
-potential for stroke, MI, death
-euphoria, alertness, arrousal, addiction

27
Q

Methylphenidate

A

-NET and DAT inhibitor
-riatlin

28
Q

methylphenidate action

A

-block NE and DA reuptake transporters from transporting monoamines from synaptic cleft back to pre-synaptic terminal
=enhance NE and DA signaling

29
Q

Methylphenidate use

A

-ADHD
-narcolepsy

30
Q

Methylphenidate problems

A

-similar to amphetamine
-priapism (prolonged erection)
-addictive potential via enhanced DA signaling

31
Q

Atomoxetine action

A

-NET inhibitor
-enhance NE levels

32
Q

Atomoxetine clinical use

A

-ADHD

-not controlled, not a stimulant

33
Q

Atomoxetine problems

A

-suicide
-priapism
-take longer/maybe not as effective as stimulants

34
Q

Non-stimulants for ADHD

A

-guanfacine (a2 agonist)
-clonidine (a2 agonist)
-atomoxetine (NET inhibitor)

35
Q

Stimulants for ADHD

A

-amphetamine
-methylphenidate

Therapeutics (78 decks)

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