Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro_Week1 > 9- CNS pharmacology > Flashcards

9- CNS pharmacology Flashcards

1
Q

Describe mechanisms alter activity in ANS

Compare and contrast with selectivity of action/clinical uses

A

1) synthesis/storage/release =
no clinical utility;
lesser selectivity
altering affects potentially all synapses

2) metabolism of NTM
inhib NT degradation enzymes (AChE inhib and MAOI)
moderate utility in therapeutics
block reuptake –> prolong NT in synapse –> incr postsyn

3) postsyn receptor stim or block
GREATEST CLINICAL UTILITY b/c most selective (specific agonists and antagonists allow for selectivity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which mechanism byw hich drugs alter activity in ANS has greatest clinical utility

A

postsyn receptor stim or block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List the steps in synth, storage, release, and inactiv of ACh

Fwd rxn catalyzed
Backward rxnc atalyzed by

A

Acetyl-CoA + Choline ACh + CoA

Fwd catalyzed by CAT
Backward catalyzed by AChE

ACh then transport into vesicles by ACh transporter

After Ca2+ release, ACh vesicles fuse with presynap membrane and exocytose contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Botulinum toxin

1) mech
2) causes
3) uses

A

inhib ACh release at excitatory NMJ by cleaving synaptobrevin

flaccid paralysis

used in cholinergic hyperactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tetanus toxin

1) mech
2) causes

A

inhib ACh release at inhib NMJ by cleaving synaptobrevin

tetany

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Black Widow spider venom

mech

A

stim ACh release by incr excessive vesicle clumping and “explosive release”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Achesterase inhib
mechansims

drug names

A

incr ACh activity in synapse and at receptor

physostigmine
donepezil
neostigmine
edrophonium
organophsophates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cholinergic receptors
Difference btwn nAChR and mAChR

Where found?

A

nicotinic = ANS ganglia (SNS and PNS preganglionic)
muscle type nAChR found in NMJ

muscarinic = postsyn terminal of postganglionic parasymp
also on sweat glands (SNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cholinergic receptors
Difference btwn nAChR and mAChr

signal transduction

A

nAChR = ligand gated ion channel or ionotropic

muscarinic = GPCRs or metabotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Significance of presynaptic vs. postsynaptic cholinergic receptros

what type of receptors for each usu

A

presynap = pass messages sent by CNS to PNS (usu ionotropic for propagation)

postsynp = muscarinic receptors for affecting response from an end organ target (usu metabotropic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Muscarinic cholinergic drugs

Pharm actions of direct acting muscarinic agonists

A

effect simil to physiological stim of PNS
(incr salivation, miosis, accomodation, incr urinary and GI motility)

also vasodilation, decr periph resistance d/t NO and MRs on endothelial cells

incr sweating

DUMBBELSS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Consequences of overdose on muscarinic agonists

Treatment

A

SLUDGE

tx = atropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Muscarinic cholinergic drugs
Acetylcholine
Pharm action

A

short half life –> not good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Muscarinic cholinergic drugs
Behtanechol
mechanism

use

A

4’ amino acholine ester
can’t cross BBB
resistant to AChE

urinary retention (post op)
paralytic ileus (non-obstructive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Muscarinic cholinergic drugs Pilocarpine
Mechanism

Use

A

3’ amino alkyloid
crosses BBB

miosis for cataract surgery;
glaucoma
dx xerostomia (dry mouth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Charged 4’ compounds that can’t cross BBB

name drugs

A

Bethanechol

Acetylcholine

17
Q

lipid soluble 3’ alkyloid can cross BBB

name drugs

A

pilocarpine

18
Q

Muscarinic antagonists
Atropine
mech

use

A

3’ amine that crosses BBB

ER treatment of mushroom poison
AChE inhibitor toxicity
severe bradycardia
asthma attack unresponsive to beta agonists
Parkinson's disease
Extrapyramidal effects of antipsych
19
Q

Muscarinic antagonists
Scopolamine

mech

use

A

3’ amine that crosses BBB

MORE CNS depression and vestib suppression than atropine
preanesthetic
motion sickness

20
Q

Muscarinic antagonists

mech

use

A

3’ amine that crosses BBB

causes mydriasis and cycloplegia (paralysis of accommodation)
6 hrs

21
Q

AChE inhibitors

pharmacologic actions

why do they affect both muscarinic and nicotinic cholinergic transmission

A

inhib of AChE hydrolysis of ACh –> prolong ACh action

because ACh active at both muscarinic and nicotinic AChR

22
Q 
Reversible AChE (useful or not?)
Name of drugs
A

Useful

Physostigmine
Donepezil
Neostimine
Edrophonium

23
Q 
Irreversible AChE (useful or not)
Name of drugs
A

toxic

organophosphates

24
Q

Adrenergic neurotransmission

Synthesis from Tyrosine to epinephrine

A

Tyr –> L dopa via Tyr Hydroxylase

L dopa –> DA via DA decarboxylase

DA –> NE via DA beta hydroxylase

NE –> E via PNMT

25
Q

Adrenergic neurotransmission

Drugs and their targets

A

Alpha methyl tyrosine
Alpha methyldopa

both inhib Tyr hydroxylase

26
Q

Adrenergic neurotransmission

Storage of dopamine?

Drug targets

A

VMAT transports DA into vesicles (then convert to NE)

Reserpine inhib VMAT, decr DA, decr NE

27
Q

Adrenergic neurotransmission

Mech of release of NE?

A

after Ca2+ release, NE fuse with presynap and exocytose into cleft

28
Q

Adrenergic neurotransmission

inactivation

A

terminated by reuptake into neuron using (DA = DAT; NE = NET)

degrade after uptake into neuron or by liver (catecholamines escape circulation) via MAO A or MAOB or COMT

29
Q

NT that are degraded by
MAO A
MAO B

A

NE; serotonin, tyramine

DA

30
Q

Drug targets of MAO A nad B

A

Phenelzine = irrev inhib of MAO A and MAO B

Selegiline = irrev inhib of MAO B

31
Q

Interaction btwn adrenergic with receptor

A

NE bind adrenergic R on postsyn membrane

32
Q

Distinguish btwn
direct acting
indirect acting

adrenergic agonists

A

direct = bind directly to target receptors and elicits same effect as NT (most therapeutics)

indirect = drug effect on processing of NT –> incr NT (usu incr storage and release) (displace endogenous NE into cytoplasm after uptake by VMAT)

or inhib of NT reuptake from synapse

33
Q

Oral effectiveness of adrenergic agonist incr with

A

1) non-catechols = no 3,4-hydroxy group on rings) since not substrate for COMT in liver
2) has methyl group on alpha carbon of phenylethylamine to protect from MAO in liver

ex = ephedrine, amphetamine

34
Q

Distribution of adrenergic agonist

ability to enter CNS incr with ___

A

drugs with no hydroxyl group on phenyl ring so more lipophilic (ephedrine, amphetamine)

35
Q

Duration of action of adrenergic agonist

half life is incr by ___

A

same factors that protect drug from COMT or MAO metab

36
Q

Adrenergic antagonists

mode of action for sympatholytic vs receptor blocker

A

sympatholytic = interfere with adrenergic presynaptically (decr specificity)

receptor blocker = block SNS stim by combine with adrenergic receptor at postganglionic symp
(better utility than sympatholytic)

37
Q

describe how an agonist of α2 adrenergic receptors can have antagonistic effects on the SNS.

A

CNS = stim of alpha2 (postsyn) in brain stem vasomotor center –> decr peripheral SNS activity

SNS = stim peripheral alpha2 (presynap)–> decr NE release from symp neurons

Neuro_Week1 (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions