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Pharm extra > Anti parkinsonian drugs > Flashcards

Anti parkinsonian drugs Flashcards

1
Q

what is dopmamine

A

monoamine neurotransmitter,

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2
Q

describe dopamine metabolism

A

Tyrosine - L-DOPA - Dopamine

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3
Q

what enzymes are involved in dopamine metabolism

A

Tyrosine Hydroxylase (TH)

DOPA Decarboxylase (DD)

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4
Q

what trnasporters transport dopamine from the synapse and into
cells

A

Dopamine Transporter (DAT)

Noradrenaline/Norepinephrine Transporter (NET)

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5
Q

where are these transporters found

A

dopaminergic neurones and glial cells

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6
Q

what metabolises monamines

A

Monoamine Oxidases:
A - all monamines
B - specific for dopamine

Catechol-0-Methyltransferase
- catecholamines

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7
Q

what are the dopaminergic pathways of the brain

A

Mesolimbic pathway
Mesocortical pathway
Nigrostriatal pathway
Tuberoinfundibular pathway

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8
Q

describe the mesolimbic pathway

A

starts in VTA to NAcc - Euphoria

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9
Q

In which conditions is the mesolimbic pathway disrupted in

A

addiction and schizophrenia

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10
Q

describe the mesocortical pathway

A

starts in VTA - cerebral cortex (frontal lobe)

controls executive and behavioural functions

problem in schizoids

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11
Q

describe the nigrostriatal pathway

A

starts in Substansia nigra pc - striatum

coordinates motor movement

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12
Q

what part of the striatum is the NAcc in

A

ventral striatum

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13
Q

describe the tuberoinfundibulnar pathway

A

from Arcuate nucleus - median eminence

(connects hypothalamus to pituitary

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14
Q

what are some affects that having too much prolactin would cause

A

Galactorrhoea, Ammenorhoea, loss of libido

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15
Q

describe the epidemiology of Parkinson’s

A

1-2% of individuals over 60

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16
Q

5% of cases are due to what mutation in….

A

certain genes SNCA, LRRK2, Parkin

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17
Q

categorise the symptomology of Parkinson’s

A

Motor
Autonomic
Neuropsychiatric

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18
Q

what are the motor symptoms of Parkinson’s

A 
Lead pipe rigidity
Bradykinesia
Resting tremor
postural instability
parkinsonian gait
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19
Q

describe the parkinsonian gait

A

loss of arm swing, shuffling steps

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20
Q

what are the autonomic symptoms of Parkinson’s

A

anosmia
postural hypotension
constipation

21
Q

neuropsychiatric symptoms of Parkinson’s

A

sleep disorders
Depression
Irritability

22
Q

describe the pathology of Parkinson’s

A

loss of dopaminergic neurones in substantia nigra pc

23
Q

what % loss of neurones do u need before motor symptoms appear

A

80%

24
Q

what do you see on the post mortem of a Parkinson’s patient

A

Lewy bodies (protein aggregates in cell bodies)

Lewy neurites (protein aggregates in cell axons)

25
Q

what are these protein aggregates made off

A

alpha-synuclein and ubiquitin

26
Q

categorise the treatment for Parkinson’s

A

replace the dopamine - L-DOPA or agonist)

reduce the breakdown on dopamine (MAO inhibitor)

27
Q

what is L-DOPA also known as

A

Levodopa

28
Q

why is L-DOPA the preferred choice of dopamine replacement

A

TH is rate limiting enzyme

Rapidly converted to DA by DOPA-D

can cross BBB

29
Q

what does peripheral breakdown of L-DOPA cause

A

Nausea and vomiting

30
Q

long term side effects of Levodopa

A

dyskinesias & ‘on-off’ effects. NOT disease-modifying

31
Q

what adjuncts are often given with levodopa therapy

A

DOPA decarboxylase inhibitors: Carbidopa & Benserazide

COMT inhibitors: Entacapone & Tolcapone

32
Q

how do the DOPA-D inhibitors work

A

Do not cross BBB - prevent peripheral breakdown of levodopa

Reduce required levodopa dosage

33
Q

how do the COMT inhibitors work

A

increase amount of levodopa in the brain

34
Q

which receptors does dopamine act on

A

D1,5(Gs linked) or

D2-4 (Gi-linked) receptors

35
Q

what are the dopamine agonists divided into

A

(potent D2 rc agonists):

Ergot derivatives:

Non-ergot derivatives:

36
Q

what problems are ergot derivatives associated with

A

Associated with cardiac fibrosis

37
Q

give examples of ergot derivative’s

A

Bromocriptine, Carbergoline and Pergolide.

38
Q

give examples of non ergot derivative’s

A

Ropinirole and Rotigatine

39
Q

Side-effects of Dopamine Agonists

A

Nausea

Vomiting

Hallucinations

Impulse Control Disorders (e.g. pathological gambling)

Psychosis

Raynaud’s Phenomenon

40
Q

L-DOPA vs Dopamine Agonists which is better

A

L-DOPA = more effective, gold standard + less side effect

41
Q

how do MonoAmine Oxidase B Inhibitors help

A

Not as effective as L-DOPA

useful in combination with L-DOPA to reduce doses

used to delay the time which a patient starts
L-DOPA

42
Q

give an example of MAO-B inhibitor

A

Selegiline

43
Q

give an example of Catechol-O-MethylTransferase Inhibitors

are these a good treatment

A

Entacapone , Tolcapone

NOT liscenced as monotherapy

44
Q

categorise Schizophrenia Symptomology

A

Positive symptoms:
↑ Mesolimbic dopaminergic activity

Negative symptoms:
↓ Mesocortical dopaminergic activity

45
Q

+ve symptoms in schizophrenia

A

Hallucinations: Auditory & visual

Delusions: Paranoia

Thought disorder: Denial about oneself

46
Q

-ve symptoms in schizophrenia

A

Affective flattening: lack of emotion

Alogia: lack of speech

Avolition/ apathy: loss of motivation

47
Q

Schizophrenia – Who Gets It?

A

1% of population & has genetic influences

Onset : 15-35 years (YOUNG)

Higher incidence in ethnic minorities (eg Afro-Caribbean

immigrants)
- Second Generation Specifically

48
Q

what is the basis of schizophrenia pharmacology

A

The Anti-Psychotics are antagonists

Pharm extra (6 decks)

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