Parkinson pathophysiology and pharmacology Flashcards

1
Q

what age group does Parkinson’s disease generally occur more commonly in?

A

60yrs and over

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2
Q

what is young onset Parkinson’s disease?

A

when people younger than 40years old experience Parkinson’s disease

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3
Q

what is the average life expectancy of those with parkinsons?

A

7-14years post diagnosis

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4
Q

what is the most well-known symptom of Parkinson’s disease (PD)?

A

tremor

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5
Q

when is the tremor maximal?

A

when the patient is at rest - reduces when patient is moving or sleeping
-can be experienced in the later stages of the disease

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6
Q

what is bradykinaesia?

A

slowness of movement - so the patient experiences difficulty planning, initiating and executing movement.
-experienced in the early stages of the disease

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7
Q

what is rigidity?

A

stiffness and resistance to limb movement caused by increased muscle tone

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8
Q

two types of rigidity?

A
  1. uniform

2. cogwheel/ratchet

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9
Q

where does rigidity affect in early stages of the disease?

A

-the neck and shoulder muscles

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10
Q

what is the pathology of PD?

A
  • Degeneration of DAergic neurones of the nigrostriatal pathway
  • this causes a loss of dopamine transmission in the striatum
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11
Q

what is Parkinsonism?

A

Any condition with loss of striatal Dopamine transmission e.g.
pharmacological blockade, brain lesion etc

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12
Q

what are the four dopamine pathways in the brain?

A
  1. nigrostriatal
  2. mesolimbic
  3. mesocortical
  4. tuberoinfundibular
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13
Q

how is dopamine synthesised?

A

Tyrosine enters the neurone and tyrosine hydroxyls turns it to DOPA. Then DOPA becomes dopamine via DOPA decarboxylase.

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14
Q

why can’t we give dopamine itself as a drug?

A
  • coz it is polar so doesn’t cross membranes

- it is metabolised by MAO in the gut

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15
Q

what do we give to treat Parkinson’s?

A

L-DOPA which is a precursor to dopamine

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16
Q

what is the problem with giving L-DOPA?

A

it would get metabolised in periphery by amino acid decarboxylase present there so need to give high dose

17
Q

how do we overcome the L-DOPA metabolism?

A

give L-DOPA with a peripheral acting decarboxylase inhibitor e.g. carbidopa

18
Q

which monoamine oxidase metabolises dopamine

A

type b (MAOb)

19
Q

give an example of MAOB inhbitior

A

Selegiline

20
Q

what effect does D2 receptor have on adenylate cyclase

A

inhibits it

21
Q

what effect does D1 receptor have on adenylate cyclase

A

stimulates it

22
Q

give example of D2 receptor agonists and what do they do

A

bromocriptine
apomorphine
lisuride
inhbiit the striatal output neurone directly (so they mimic dopamine as dopamine has an inhbitory effect)

23
Q

anticholinergic drugs can also be given for PD, give examples

A

benztropine

benzhexol

24
Q

side effects of anticholinergic drugs are

A

confusion

anticholinergic effects

25
Q

what enzyme breaks down L-DOPA

A

COMT- catecholamine-o-methyl transferase
- so inhbiiting this enzyme helps to increase L-DOPA concentration. But can’t give this inhbitor alone, have to give with L-DP

26
Q

what is iatrogenic Parkinsonism

A

when the drugs given to block D2 receptors/ lower dopamine concentration and transmission, cause deficiency in dopamine and its action resulting in too low dopamine levels
- e.g. in schizophrenia we give D2 receptor agonists causing Parkinsonism