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2=Neurobiology > L3. Parkinson's disease > Flashcards

L3. Parkinson's disease Flashcards

1
Q

what does the incidence of PD increase with

A

age

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2
Q

3 main features of PD

A

resting tremor
muscle ridigity
bradykinesia

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3
Q

what is the most common 1st sxs of PD

A

bradykinesia

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4
Q

4 other clinical feautures of PD

A
  1. postural instability
  2. depression
  3. autonomic NS dysfunction
  4. decreased cognitive impairment
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5
Q

give a few examples of autonomic dysfunction

A

impaired GI motility, bladder dysfunction, sialorrhoea, excessive head and neck sweating, orthostatic hypertension

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6
Q

give a few examples of decreased cognitive impairment

A

impaired visual-spatial perception and attendtion, slowness in motor tasks, impaired concentration, dementation

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7
Q

which part of the brain is involved in PD

A

substantia nigra

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8
Q

normal function of substantia nigra

A

allows smooth movements - regulation of posture and muscle tone

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9
Q

what is present in the substantia nigra in PD

A

lewy bodies and lewy neurites

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10
Q

what neurones are located in the substantia nigra?

A

dopamine

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11
Q

what is degraded in PD

A

substantia nigra

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12
Q

3 pathophysiological causes of PD

A
  1. loss of >80% dopamine
  2. loss of dopamine receptors in nigrostriatal pathway
  3. increase in acetylcholine in striatum
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13
Q

describe 4 steps in dopamine stimulation in a healthy individual

A
  1. DA stimulates basal ganglia
  2. basal ganglia has dampening effect on reticular formation - reducing unneccesary movements.Ach reduced
  3. rReticular formation sends motor info to spinal cord
  4. controlled smooth movement
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14
Q

describe 4 steps in dopamine stimulation in a person with PD

A
  1. lack of DA - basal ganglia not stimulated
  2. increase in ACh - inhibits smooth movement and dampening effect of RF
  3. info not sent to RG and therefore not sent to spinal cord
  4. increased muscle tension and tremor
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15
Q

what is parkinsonism

A

umbrella term used to describe conditions which have similar sxs to PD

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16
Q

what is the cause of PD

A

idiopathic

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17
Q

what 3 drugs can cause PD like sxs?

A

anti-psychotic drugs block DA receptors
MPTP
rotenone (pesticide)

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18
Q

what 5 things can cause secondary parkinsonism?

A
  1. drugs
  2. toxins
  3. neoplasms/strokes
  4. other neuronal system degenerations
  5. genetics
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19
Q

which 4 drugs can cause secondary parkinsonism?

A
  1. antipsychotics
  2. anti-emetics
  3. methyl-dopa (Anti-hypertensive)
  4. reserpine
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20
Q

what 2 toxins can cause secondary parkinsonism?

A

MPTP

carbon monoxide poisoning

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21
Q

strokes in what region of the brain can cause secondary parkinsonism?

A

nigrostriatal pathway

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22
Q

other neuronal system degenerations which can cause secondary parkinsonism?

A
  1. wilson’s disease - copper in brain
  2. progressive supranuclear palsy
  3. multiple-system atrophy
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23
Q

what is the only technique to differentiate PD and parkinsonism?

A

DAT scan (DA transporter scan)

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24
Q

what does the DAT scan image?

A

presynaptic DA transporter

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25
Q

2 approaches to treatment of PD

A

dopamine and ACh

26
Q

physiology of DA approach to treatment

A

increase DA conc in nigrostriatal system

27
Q

physiology of Ach approach to treatment

A

decrease influence of ACh in striatum

28
Q

4 drugs used in DA approach

A
  1. MAO inhibitors
  2. L-dopa
  3. dopamine agonists
  4. COMPT inhibitors
29
Q

2 drugs used in Ach approach

A
  1. anti-muscarinics

2. amantadine

30
Q

how does levo-dopa work?

A

it is a precursor for DA

31
Q

why are peripheral decarboxylase inhibitors used with L-dopa?

A

can use lower L-dopa dose - decrease side effects; nausea and vomiting

32
Q

3 acute side effects of L-dopa

A
  1. hallucinations
  2. confusion
  3. dyskinesias
33
Q

chronic side effect of L-dopa

A

benefits of the drug decline after 5 years - PD sxs reoccur

34
Q

L-dopa can lead to the on-off effect. what is this?

A

as the drug has a short half-life, sxs reappear before taking the next dose

35
Q

treatment for on-off effect

A

using modified release preparations (gel)

36
Q

name for L-dopa + benserazide

A

Co-beneldopa

37
Q

name for L-dopa + carbidopa

A

Co-careldopa

38
Q

what are Co-beneldopa and Co-careldopa examples of ? which is this used in combo with?

A

PDI.

L-dopa

39
Q

how does DA agonist work to treat PD?

A

stimulates D1 and D2 receptors

40
Q

name 5 sxs of dopamine agonists

A
  1. nausea
  2. vomiting
  3. hallucinations
  4. narcolepsy
  5. confusion
  6. paranoia
  7. postural hypotension
  8. peripheral swelling
41
Q

name 1 example of dopamine agonist

A 
brocriptine 
pergolide 
pramipexol
ropinirole
cabergoline 
apomorphine
42
Q

physiology of MAO inhibitors

A

inhibit MAO - which normally would break down DA. causing increase of DA in the synapse

43
Q

1 example of MAO inhibitors

A

Selegiline

Rasagiline

44
Q

what does COMPT inhibitors stand for?

A

catechol-o-methyl transferase inhibitors

45
Q

physiology of COMPT inhibitors

A

prevent breakdown of L-dopa and DA

46
Q

when are COMPT inhibitors used?

A

only in combo with L-dopa - used in advanced stages of the disease

47
Q

1 example of COMPT inhibitor

A

entacopone

tolcapone

48
Q

how do anti-muscarinic drugs work

A

block muscarinic receptors in striatum

49
Q

what are anti-muscarinics useful in treating?

A

tremor

50
Q

drug interactions of anti-muscarinincs

A

increase side effects of tricyclics

51
Q

1 example of anti-muscarinincc

A

benzhexol
benztropine
procyclidine
orphenadrine

52
Q

physiology of amantadine

A

increases release of DA

53
Q

2 side effects of amantadine

A
  1. confusion

2. tolerance may develop

54
Q

describe 3 steps in syntheiss of DA

A
  1. tyrosine
  2. DOPA
  3. DA
55
Q

in the substantia nigra - why is DA not converted into NA?

A

the enzyme required is not present

56
Q

2 moleucles which DA can be metabolised into

A

DOPAC and HVA

57
Q

why may mild PD be left untreated/delayed treatment?

A

delay the use of L-dopa; to delay onset of its side effects

58
Q

what 2 other neurological disorders are seen in PD?

A

depression and dementia

59
Q

treatment for depression + PD

A

tricyclics or SSRIs

60
Q

treatment for dementia + PD

A

reduce PD treatment dose -use clozapine

61
Q

why can a vaccine which attacks alpha-synuclein be useful in treating PD?

A

alpha-synuclein is present in lewy bodies

62
Q

what can glial cell line-derived neurotrophic factor possibly do?

A

stimulate growth of cells which are lost during PD

2=Neurobiology (6 decks)

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