Applied Neuropharmacology Flashcards

1
Q

how could you use pharmacological intervention to reduce synaptic transmission?

A
> block Na channels
> increase transmitter uptake
> block release of machinery
> increase breakdown of the transmitter
> block voltage gated Ca channels
> inhibit synthesis and packaging of neurotransmitter
> activate presynaptic inhibitory receptors
> block postsynaptic receptors
> block voltage gated Ca channels
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2
Q

what pharmacological intervention could increase synaptic transmission?

A

> block uptake of transmitter
block breakdown of transmitter
potentiate the effects of the transmitter on the receptor
activate postsynaptic receptors with an antagonist
increase synthesis and packaging of neurotransmitter

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3
Q

name 6 types of neurotransmitters

A
> acetylcholine
> monoamines
> amino acids
> purines
> neuropeptides
> NO
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4
Q

name three monoamines

A

> noradrenaline
dopamine
serotonin

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5
Q

name some neuropeptides

A

> endorphins
CCK
substance P

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6
Q

what is the anatomical distribution of dopamine in the brain?

A

> brainstem
basal ganglia
limbic system and frontal cortex

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7
Q

what are the physiological functions affected by dopamine?

A

> vomiting
voluntary movement
emotions and reward

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8
Q

what is the pathophysiology of parkinsons?

A

> degeneration of the dopamine in the substantia nigra

> dopamine deficiency in the basal ganglia

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9
Q

describe dopamine synthesis

A
glycine
alanine
phenylalanine
tyrosine
DOPA
dopamine
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10
Q

how is dopamine synthesis modulated in vivo

A

> dopamine does not cross the blood brain barrier so cannot just be given
the enzyme that converts DOPA into dopamine is blocked outside the BBB
DOPA crosses the BBB and is converted into dopamine

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11
Q

why can dopamine produce many and different effects in different brain regions?

A

as there are 5 subtypes of metabotropic receptors that do different things and are expressed in different parts of the brain

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12
Q

what is dopamine broken down into?

A

homovanillic acid

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13
Q

what are the key enzymes in dopamine breakdown?

A

> MAO-B

> COMT

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14
Q

what are the two intermediate substances in dopamine breakdown?

A

> dihydroxyphenylacetic acid

> 3-methoxytryptamine

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15
Q

name a dopamine precursor drug

A

levodopa

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16
Q

what are the two types of dopamine agonists?

A

> ergots
non-ergots
apomorphine

17
Q

what drugs improve the symptoms of parkinsons?

A

> levodopa

> dopamine agonists

18
Q

why are ergots no longer used to treat parkinsons?

A

they stimulate the receptors of fibroblasts so there is fibrosis of lungs and peritoneum

19
Q

what enzyme inhibitors are there that affect dopamine?

A

> peripheral AAAD inhibitors
MAOB inhibitors
COMT inhibitors

20
Q

what are the advantages of peripheral AAAD inhibitors?

A

> decrease peripheral side effects of levodopa

> allows a greater proportion of the oral dose to reach the CNS

21
Q

what are the effects of MAOB and COMT inhibitors?

A

> decrease metabolism of dopamine

> increases the effectiveness of levodopa

22
Q

what can dopaminergic drugs worsen or cause?

A

> nausea
vomiting
psychosis
impulsivity/abnormal behaviours

23
Q

what do dopaminergic drugs not help?

A

> dysarthria
balance
cognition

24
Q

what can dopamine antagonists improve?

A

> nausea
vomiting
psychosis

25
Q

what can dopamine antagonists cause or worsen?

A

parkinsons

26
Q

is the area postrema (vomiting centre) functionally inside or outside the BBB?

A

outside

27
Q

can domperidone, a dopamine antagonist be used to treat nausea in a patient with parkinsons?

A

yes as it does not cross the blood brain barrier

28
Q

domperidone is an anti-emeic. what has this drug permitted the use of in parkinsons?

A

apomorphine which is a powerful emetic

29
Q

what is dyskinesias?

A

abnormal involuntary movements

30
Q

what can cause dyskinesias?

A

dopaminergic drugs

31
Q

what are the effects of long term dopamine antagonists?

A

> parkinsonism

> tardive dyskinesias (by continually blocking the dopamine centre it could be sensitised)

32
Q

what are selective serotonin reuptake inhibitors used as?

A

antidepressants

33
Q

what are triptans used to treat?

A

migraine

34
Q

what are GABA agonists?

A

anti-epilepsy drugs

35
Q

what are noradrenaline reuptake blockers used as?

A

antidepressants

36
Q

what are MAO inhibitors used as?

A

antidepressants