Brainscape's Knowledge GenomeTM

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


See full index

1. NEUROPHARMACOLOGY > drug names (L4-8) > Flashcards

drug names (L4-8) Flashcards

1
Q

hemicholinium 3

A

cholinergic transmission at neuromuscular junction:
synthesis step is initiatied by the reuptake of choline. which is Na+ dependent
this is blocked by hemicholiniom 3 (blocks the pump - so twitches in the muscles will fade away since there is not ACh being synthesised)
(not used clinically)

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

vesicamol

A

cholinergic transmission at neuromuscular junction:
storage step - Uptake and storage of ACh in synaptic vesicles is inhibited by vesamicol
(not used clinically)
Pump can be inhibited by vesamicol. Slowly will develop a block of the muscle twitches because no ACh is pumped into vesicles

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

Tetrodotoxin (TTX)

A

cholinergic transmission at neuromuscular junction:
release step - Tetrodotoxin (TTX) blocks voltage-gated Na+ channels
(no action potential – no release)

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

conatoxins

A

cholinergic transmission at neuromuscular junction:
release step - P/Q & N-type voltage-gated
Ca2+ channels are blocked by conatoxins
(no Ca2+ influx – no release)

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

Botulinum toxin

A

cholinergic transmission at neuromuscular junction:
release step - Botulinum toxin blocks vesicle fusion – no release
inhibits the fusion process - toxin will destroy the proteins involved in the fusion of vesicles
Causes paralysis

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

Dendrotoxins

A

cholinergic transmission at neuromuscular junction:
release step - Dendrotoxins block voltage-gated K+ channels (more Ca2+ influx – more release)
AP doesn’t repolarise, prolonged depolarization, more CA influx, constant neurotransmitter release

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

Ziconotide

A

Ziconotide acts as a selective N-type voltage-gated calcium channel blocker.

Given via the intrathecal route for the management of severe pain (directly through the spinal cord)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

clinical uses of Botulinum toxin

A

muscular spasms are resistant to other treatments
Give injection of botulinum toxin to prevent activity of neuromuscular junction there
children with cerebral palsy and this toxin can be used as treatment as well
overactivation of the neuromuscular junction could cause drooling or sweating

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

α-latrotoxin

A

black widow spider venom

With α-LTX - huge amount of release of neurotrans, muscles spams (black widow spider overcomes its prey like this)

After - stops the endocytosis process, so vesicle membranes are not taken back, no more vesicles produced, desensitisation of receptors of presynaptic membrane, paralysis

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

nerve gases or neostigmine (different drugs, same effect)

A

Drugs that inhibit AChE, anticholinesterases (eg nerve gases, neostigmine) increase the concentration and effects of ACh -can lead to muscle spasms

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

Tubocurarine

A

found in vines of amazons, effective antagonist of receptors at neuromuscular junction, competitive antagonist
so if you increase the conc of ACh by inhibiting the enzyme that breaks it down, you can overcome the effect of tubocurarine

arrow poison – kills prey by respiratory paralysis
clinical side effects – decreased BP due to ganglion block & resultant vasodilatation

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

alpha bungarotoxin

A

Non depolarising because they are antagonists and block the receptors (like alpha bungarotoxin, found in the taiwanese snake, it binds to the same place as acetylcholine so should be competitive with tubocurarine, but it sticks covalently to the binding site so it cannot come off)

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

Vecuronium and rocuronium

A

used clinically because during an operation, we dont want muscle twitches. used for anaesthetics (safer because used at low doses)
Very rapid onsets, so for urgent surgeries
Reversed by anticholinesterases by poisoning it

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

suxamethonium

A

depolarising blocker - agonist
used clinically
rapid onset of paralysis
short duration – broken down by plasmacholinesterases
tracheal intubation, electroconvulsive therapy
BUT
side effects include:
bradycardia (decreased heart rate) due to M2 mAChR activation in heart
K+ release in trauma (eg burns) – cardiac dysrhythmias & cardiac arrest
prolonged paralysis (2hr+) in 1:3500 people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

κ-bungarotoxin

A

irreversible (like α-bungarotoxin at NMJ)

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

trimethaphan

A

competitive antagonist

occasionally used in surgery for controlled hypotension & hypertensive crises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hexamethonium & tubocurarine

A

non competitive-open channel blockers
(drug sits in channel like plug in a bottle)
(compare with tubocurarine at NMJ-competitive)

hexamethonium used to reduce blood pressure
tubocurarine blocks the binding site of ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

nicotine & lobeline

A

ACh nicotinic receptor (nAChR) agonists
Lobeline - selective for ganglionic & chromaffin cell nAChR

repeatedly stimulate receptors
inactivate voltage-gated Na+ channels
desensitise nAChR receptors

not broken down by AChE
not used clinically as ganglion blockers – but nicotine (and varenicline - α4β2 nAChR) for tobacco addiction…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ganglionic non-depolarising blockers (antagonists)

A

κ-bungarotoxin
trimethaphan
hexamethonium
tubocurarine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Depolarising blockers (agonists)

A

nicotine
lobeline
suxamethonium

21
Q

parasympathomimetics

A

called parasympathomimetics because they mimic the physiological effects of the parasympathetic nervous system

carbachol
pilocarpine
cevimeline
bethanechol

22
Q

parasympatholytics

A

called parasympatholytic because they oppose the effects of the parasympathetic nervous system

23
Q

physotigmine

A

From the Calabar Bean aka “The Ordeal Bean”
First anticholinesterases found
1st clinical use:
1877 for glaucoma

24
Q

clinical uses of neostigmine

A

reversal of neuromuscular paralysis

25
Q

clinical uses of Edrophonium

A

diagnosis of myasthenia gravis

26
Q

clinical uses of Neostigmine & pyridostigmine

A

treatment of myasthenia gravis

27
Q

clinical uses of Physostigmine & ecothiopate

A

treatment of glaucoma (previously)

28
Q

clinical uses of Donepezil (Aricept), Galantamine, Rivastigmine

A

Alzheimer’s Disease

29
Q

physiological effects of neostigmine, edrophonium, neostigmine, pyridostigmine, phsostigmine, ecotigmine, ecothiopate, donepezil, galantamine and rivastimine

A

due to ↑↑↑ACh activity at autonomic NEJ, NMJ & CNS

↑ secretion: salivary, lacrimal,
bronchial, GI glands

↑ peristaltic activity
(stimulant laxatives)

🕆 NMJ: depolarisation block

🕆 bronchoconstriction

🕆 bradycardia and hypotension

🕆 CNS - convulsions, respiratory failure, unconsciousness, death

30
Q

atropine

A

counteract effects of excessive ACh M stimulation
it is a possible treatment for nerve agent intoxication
M3 receptors are found on the lumen of blood vessels, circulation of acetylcholine is stimulating M3, leads to vasodilation
increasing heart rate

also counteracts effects of excessive mach stimulation

31
Q

reversal of organophosphate nerve agent effects (name the 3 compounds for this)

A

ATROPINE
counteract effects of excessive mACh stimulation

OXIMES
eg pralidoxime (2-PAM)
antidote to nerve agent
reactivate the AChE
But…ageing….

VALIUM
for seizures

32
Q

organophosphate working as insecticides

A

Organophosphate insecticides can give rise to some bad symptoms
Because sulfur group replaces the oxygen group in malathion insecticides
Very effective against insects because they have oxidase that converts S to O which kills them (we are less efficient at that process)

33
Q

monoamine oxidase

MAO

A

inhibitors used for depression

34
Q

catechol-o-methyl transferase (COMT)

A

inhibitors used for parkinsons disease to increase the dopamine levels in the brain

35
Q

aldehyde dehydrogenase (ADH)

A

??

36
Q

α-methylparatyrosine

A

was used in treating pheochromocytoma, a tumour of chromaffin cells in adrenal medulla. This will release a lot of adrenaline or noradrenaline, heart beats fast, high blood pressure etc

37
Q

antabuse effects (2)

A
  • Dopamine b hydroxylase affected by antabuse. so antabuse inhibits the conversion of dopamine into noradrenaline
  • Primary target of it is another enzyme that degrades alcohol (acetyldehydrogenase), so it causes accumulation of toxic compounds in our body after taking alcohol.
38
Q

tyramine

A

(it’s an indirectly acting sympathomimetics)
stimulates NA release
Competes with NA for NET
Displaces NA from vesicle

CHEESE REACTION
Tyramine in food (red wine, cheese, yogurt) metabolised by MAO
Some antidepressants (Phenelzine) inhibit MAO
Combining both can lead to “Cheese Reaction” & hypertensive crisis

39
Q

noradrenaline (NA)

A

Arousal/wakefulness/alertness - forebrain
Mood - amygdala/hippocampus
Control of pain – spinal cord
Blood pressure/autonomic function - hypothalamus & NTS

40
Q

dopamine (DA)

A

Nigrostriatal system - motor control
Mesolimbic/mesocortical systems - behaviour / mood
Tuberohypophyseal system - endocrine control

41
Q

serotonin (5-HT)

A
  • sleep, wakefulness and mood
  • feeding behaviour
  • control of sensory transmission (especially pain pathways)
42
Q

MDMA effect on monoamine uptake

A

COMPETES WITH SEROTONIN

MDMA has preferential action on serotonin both at the level of the transporter (MDMA is taken up by the serotonin transporter) and interferes with VMAT
this results in an efflux of serotonin from the inside to outside of the cell - you get an accumulation of serotonin outside of the cell

43
Q

cocaine effect on monoamine uptake

A

Cocaine has a preferential action at the dopamine transporter, which results in the accumulation of dopamine in the extracellular space (affects dopamine transporter and others too)

it blocks the transporter and doesn’t allow anything through

44
Q

amphetamine effect on monoamine uptake

A

Amphetamine targets noradrenaline/norepinephrine transporter. it enters the cell using it. Can also affect the vesicular monoamine transporter.
It also inhibits MAO, monoamine oxidase (enzyme that breaks down the monoamine) so inhibiting s MAO will allow the release of more monoamine in the synaptic cleft to prolong the effects of amphetamine

45
Q

stimulant properties of amphetamines

A 
MAIN EFFECTS
increased motor activity
euphoria and excitement
insomnia
anorexia
  • Effects are due mainly to increased levels of monoamines in the synaptic cleft.
  • Amphetamines induce strong psychological dependence.
  • Amphetamine psychosis can occur with prolonged use and resembles symptoms of schizophrenia
46
Q

clinical uses of amphetamines

A
  • Attention deficit hyperactivity disorder (ADHD)
    Adderall- 2.5 or 5 mg once or twice per day
    Ritalin - < 60 mg /day
  • Narcolepsy
    Adderall- 5 mg to 60 mg per day in divided doses
    Ritalin - < 60 mg /day
  • Obesity
    Methedrine - 5 mg tablet before each meal as it suppresses the appetite
47
Q

stimulant properties of cocaine

A

MAIN EFFECTS
Increased motor activity
Euphoria, excitement and garrulousness
Increased peripheral sympathetic NS activity (↑BP, ↑HR)

  • Effects are due mainly to increased levels of monoamines (especially dopamine) in the synaptic cleft.
  • Shorter lasting effects compared to amph.
  • Causes strong psychological dependence.
48
Q

modafinil effects

A

MAIN EFFECTS
Increased wakefulness and vigilance
Suggested to improve cognitive performance (likely through increased wakefulness)

  • Binds with low affinity to DAT and to NET
  • Has additional actions at a variety of NT systems (5-HT, glutamate)
  • Low abuse potential (no high or euphoria)

1. NEUROPHARMACOLOGY (8 decks)

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