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Yr2 Control - Term 2 and 3 > Drug Treatments of Movement Disorders > Flashcards

Drug Treatments of Movement Disorders Flashcards

1
Q

What are the main features of neurodegenerative disorders? (3)

A
  • Loss of neurons
  • Progressive
  • Irreversible (cannot regenerate neurons)
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2
Q

When was Parkinson’s first described, and what were the main features?

A

1817.

  • ‘shaking palsy
  • akinetic-rigid syndrome
  • extrapyramidal disorder
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3
Q

How does Parkinson’s progress?

A

Slowly; usually die within 10-15 years.

-death usually due to bronchopneumonia / sepsis

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4
Q

What is remission, and how common is it in Parkinson’s?

A

Disappearance of signs.

-rare, and only lasts for seconds/minutes

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5
Q

What are the main symptoms of Parkinson’s? (6)

A
  • Tremor (4-7Hz)
  • Rigidity (increased tone)
  • Slurred speech
  • Akinesia
  • Decreased blinking
  • Postural changes (stoop, shuffling)
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6
Q

What are the unusual ways to describe some of the symptoms of Parkinson’s?

A

TREMOR – ‘pill rolling’
RIGIDITY - ‘lead piping limbs’
DECREASED BLINKING – ‘serpentine stare’
POSTURAL CHANGES – ‘telegraph pole falls’

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7
Q

What is akinesia?

A

Difficulty initiating voluntary movements.

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8
Q

What is the general pathology of Parkinson’s?

A
  • Loss of neruones in substantia nigra
  • Lewy body accumulation (eosinophilic proteins in cells)
  • Loss of nigro-subtantia inhibitory-excitatory pathway
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9
Q

What type of neurones are affected by Parkinson’s?

A

Dopaminergic neurones.

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10
Q

What causes Parkinson’s?

A

Unknown cause.

-idiopathic

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11
Q

What disorders are associated with Parkinson’s? (3)

A
  • Drug-induced (iatrogenic)
  • MPTP-induced (amphetamine-related)
  • Post-encephalitic
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12
Q

What are the 2 pathways affected by Parkinson’s?

A

Indirect and direct.

-both involve dopamine (D1/D2)

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13
Q

What is the direct pathway?

A

D1-mediated.

-signals from striatum

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14
Q

What is the indirect pathway?

A

D2-mediated.

-signals from striatum

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15
Q

What is the abbreviation of dopamine?

A

DA.

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16
Q

What are the general mechanisms of Parkinson’s treatment? (2)

A
  • Increase DA activity

- Decrease Ach activity

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17
Q

How is DA activity increased? (4)

A
  • Replace DA
  • Decrease DA breakdown
  • Increase DA release
  • DA agonists
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18
Q

What drug is used to replace DA?

A

L-DOPA.

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19
Q

What drugs are used to decrease DA breakdown? (2)

A
  • MAO inhibitors

- COMT inhibitors

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20
Q

What drug is used to increase DA release?

A

Amantidine.

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21
Q

What drugs are used as DA agonists? (2)

A
  • Bromocriptine

- Pergolide

22
Q

What class of drugs decrease Ach activity?

A

Antimuscarinics.

-benzhexol, orphenadrine

23
Q

What is the 1st line treatment for Parkinson’s?

A
  • L-DOPA

- MAO / COMT inhibitors

24
Q

How does L-DOPA increase dopamine levels?

A

L-DOPA is a precursor for dopamine.

-DOPA decarboxylase converts it

25
How does L-DOPA act?
- L-DOPA crosses the BBB >> neurones. | - converted to DA in neurones and glia
26
What is the main problem with L-DOPA?
Metabolised in the periphery >> only 1% reaches brain. | -90% in intestine
27
What is given with L-DOPA to prevent it being broken down, and how does it work?
Carbidopa. - inhibits DOPA decarboxylase - doesn’t pass BBB
28
What are the main side effects of L-DOPA?
- ‘On-off’ effect (worsening symptoms) - Nausea / anorexia - Dysknesias - Tachycardia - Hypotension - Insomnia
29
What happens to the side effects of L-DOPA with time?
Increased side effects with time. | -partly due to increased dose
30
How do MAO inhibitors reduce DA breakdown?
Mono-amine oxidase (MAO) breaks down DA to homovanillinic acid. -inhibitors prevent this
31
What is a commonly used MAO inhibitor?
Selegiline.
32
How does Selegiline act?
- MAOb inhibitor (CNS specific) - Increase DA in brain - Effective alone in early stages, ineffective later on
33
Where are MAOa and MAOb located?
MAOa – periphery | MAOb – CNS
34
How do COMT inhibitors reduce DA breakdown?
COMT breaks down L-DOPA (>>3-O-methyl DOPA) and DA (>>homovanillinic acid) -inhibitors prevent this
35
What are COMT inhibitors used for?
Patients with on-off symptoms.
36
What COMT inhibitor was withdrawn due to adverse effects?
Tolcapone.
37
How does amatidine act and when is it used?
Increases DA release. | -useful in early stages, but not generally used
38
What are bromocriptine and peroglide?
Dopamine agonists. | -usually given towards end of disorder
39
What are the selectivities of bromocriptine and peroglide?
Bromocriptine – D1 and D2. | Peroglide – D2 selective.
40
What is the action of antimuscarinics?
Block muscarinic receptors. - most effective on tremor and drooling - used only in young with severe tremor
41
How can surgery be used to treat Parkinson’s? (3)
- Lesions - Implantable stimuli - Grafts
42
What lesions can be used to treat Parkinson’s?
- Motor thalamus (thalamotomy) - Globus pallidus (pallidotomy) - Subthalamus (subthalamotomy)
43
Why are lesions used in Parkinson's?
Can reduce motor symptoms; usually last resort.
44
How does Huntington’s progress?
Gradual onset. | -death within 10-20 years
45
What is the typical age of onset of Huntington’s?
30-50 years. | -younger >> more severe
46
What are the main symptoms of Huntington’s? (2)
- Fidgeting / restlessness >> chorea | - Irritability / moodiness >> dementia
47
What is chorea?
Jerky, involuntary movements.
48
What is the general pathology of Huntington’s?
Selective cell loss in cerebral cortex and corpus striatum. - medium spiny neurones containing GABA and encephalin = 1st affected - altered NT levels
49
What causes Huntington’s?
HEREDITARY – autosomal dominant - gene defect on chromosome 4 (4p16.3) - CAG repeate (polyglutamine)
50
How is Huntington’s treated?
No cure. | -can control movement disorder: D2 antagonists, DA depletion

Yr2 Control - Term 2 and 3 (17 decks)

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