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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
Q

How does L-DOPA act?

A
  • L-DOPA crosses the BBB&raquo_space; neurones.

- converted to DA in neurones and glia

26
Q

What is the main problem with L-DOPA?

A

Metabolised in the periphery&raquo_space; only 1% reaches brain.

-90% in intestine

27
Q

What is given with L-DOPA to prevent it being broken down, and how does it work?

A

Carbidopa.

  • inhibits DOPA decarboxylase
  • doesn’t pass BBB
28
Q

What are the main side effects of L-DOPA?

A
  • ‘On-off’ effect (worsening symptoms)
  • Nausea / anorexia
  • Dysknesias
  • Tachycardia
  • Hypotension
  • Insomnia
29
Q

What happens to the side effects of L-DOPA with time?

A

Increased side effects with time.

-partly due to increased dose

30
Q

How do MAO inhibitors reduce DA breakdown?

A

Mono-amine oxidase (MAO) breaks down DA to homovanillinic acid.
-inhibitors prevent this

31
Q

What is a commonly used MAO inhibitor?

A

Selegiline.

32
Q

How does Selegiline act?

A
  • MAOb inhibitor (CNS specific)
  • Increase DA in brain
  • Effective alone in early stages, ineffective later on
33
Q

Where are MAOa and MAOb located?

A

MAOa – periphery

MAOb – CNS

34
Q

How do COMT inhibitors reduce DA breakdown?

A

COMT breaks down L-DOPA (»3-O-methyl DOPA) and DA (»homovanillinic acid)
-inhibitors prevent this

35
Q

What are COMT inhibitors used for?

A

Patients with on-off symptoms.

36
Q

What COMT inhibitor was withdrawn due to adverse effects?

A

Tolcapone.

37
Q

How does amatidine act and when is it used?

A

Increases DA release.

-useful in early stages, but not generally used

38
Q

What are bromocriptine and peroglide?

A

Dopamine agonists.

-usually given towards end of disorder

39
Q

What are the selectivities of bromocriptine and peroglide?

A

Bromocriptine – D1 and D2.

Peroglide – D2 selective.

40
Q

What is the action of antimuscarinics?

A

Block muscarinic receptors.

  • most effective on tremor and drooling
  • used only in young with severe tremor
41
Q

How can surgery be used to treat Parkinson’s? (3)

A
  • Lesions
  • Implantable stimuli
  • Grafts
42
Q

What lesions can be used to treat Parkinson’s?

A
  • Motor thalamus (thalamotomy)
  • Globus pallidus (pallidotomy)
  • Subthalamus (subthalamotomy)
43
Q

Why are lesions used in Parkinson’s?

A

Can reduce motor symptoms; usually last resort.

44
Q

How does Huntington’s progress?

A

Gradual onset.

-death within 10-20 years

45
Q

What is the typical age of onset of Huntington’s?

A

30-50 years.

-younger&raquo_space; more severe

46
Q

What are the main symptoms of Huntington’s? (2)

A
  • Fidgeting / restlessness&raquo_space; chorea

- Irritability / moodiness&raquo_space; dementia

47
Q

What is chorea?

A

Jerky, involuntary movements.

48
Q

What is the general pathology of Huntington’s?

A

Selective cell loss in cerebral cortex and corpus striatum.

  • medium spiny neurones containing GABA and encephalin = 1st affected
  • altered NT levels
49
Q

What causes Huntington’s?

A

HEREDITARY – autosomal dominant

  • gene defect on chromosome 4 (4p16.3)
  • CAG repeate (polyglutamine)
50
Q

How is Huntington’s treated?

A

No cure.

-can control movement disorder: D2 antagonists, DA depletion

Yr2 Control - Term 2 and 3 (17 decks)

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