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Semester 5 - Farmocology > Session 11 - Parkinsons > Flashcards

Session 11 - Parkinsons Flashcards

1
Q

Give four motor symptoms which characterise parkinson’s disease

A

Tremor
Rigidity
Bradykinesia
Postural Instability

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2
Q

Describe the tremor which occurs in parkinsons - What is it caused by?

A

 Low frequency rest tremor
 Abolished by movement
 Low dopamine and disturbance of other neurotransmitters

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3
Q

What two types of rigidity do you find in parkinsons?

A

Lead pipe rigiditiy/Cog-wheel

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4
Q

What type of rigidity do you not find in parkinsons and why?

A

Clasp knife

Sign of pyramidal disorder, which parkinsons is not.

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5
Q

What is rigidity caused by in parknson’s

A

Low dopamine and disturbance of other NTs

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6
Q

What is bradykinesia caused by in dopamine

A

Low dopamine

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7
Q

Give 6 non-motor manifestations of parkinson’s

A 
o	Mood changes
o	Pain
o	Cognitive change
o	Urinary symptoms
o	Sleep disorder
o	Sweating
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8
Q

What are two causes of parkinonism

A

o Idiopathic Parkinson’s Disease
o Dopamine blocking or depleting drugs
 Particularly antipsychotics

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9
Q

How is parkinson’s disease taken up?

A

Pre-synaptically by dopaminergic neurones

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10
Q

What are the two main pathologies which come in parkinsons?

A

Presence of neuronal inclusion called lewy bodies
Loss of dopaminergic neurones from pars compacta of the substantia nigra in the midbrain that project to the striatum of the basal ganglia

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11
Q

What are lewy bodies and how do they progress?

A

 Contain tangles of α-synuclein and ubiquitin

 Gradually become more widespread as the condition progresses, spreading from lower brainstem  Midbrain  Cortex

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12
Q

When do parkinson’s symptoms occur?

A

Once there is 50% cell loss

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13
Q

Outline the metabolic path of dopamine (before it and after)

A

L-Tyrosine -> L-Dopa -> Dopamine -> Noradrenaline -> Adrenaline

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14
Q

What converts L-dopa to dopamine?

A

DOPA decarboxylase

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15
Q

What is the main pharmacokinetic properterial difference between L-Dopa and Dopamine

A

L-dopa can.. Wait for it.. Cross the BBB :D :D :D :D !!! :D :D :D !!! :D :D :D :D

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16
Q

Name 6 drugs used in Parkinson’s treatment

A 
Levodopa (L-DOPA)
o	Dopamine receptor agonists
o	MAOI Type B inhibitors
o	COMT inhibitors
o	Anticholinergics
o	Amantadine
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17
Q

What is the route of admine of L-Dopa?

A

Oral

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18
Q

How much of an L-Dopa dosa reaches the brain

A

1%

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19
Q

What are indications for L-DOPA (1)

A

Parknsons

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20
Q

What is the mechanism of action for L-dopa

A

 L-DOPA is the immediate precursor of Dopamine and is able to penetrate the blood brain barrier to replenish the dopamine lost in the Neostriatum

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21
Q

Name four ADRs for L-dopa

A

 Nausea and vomiting
 Psychiatric side effects (Schizophrenia-like symptoms)
 Cardiovascular effects (hypotension)
 Dyskinesia

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22
Q

What kind of drug is L-dopa usually given with and why?

A

peripheral DOPA decarboxylase inhibitor (Sinemet, Madopar), reducing necessary dose, side effects and increase the amount of L-DOPA reaching the brain

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23
Q

Name a pharamocologically active substance which would increease breakdown of L-dopa

A

Vitamin B6

24
Q

What is the risk of using monoamine oxidase inhibitors as L-dopa adjuvants

A

Hypotensive crisis

25
Q

What do anti-psychotics do in parkinsons?

A

block dopamine receptors and parkinsonism is a side-effect

26
Q

Why do large doses of L-dopa have to be given?

A

 Extensive peripheral metabolism of L-DOPA means that large doses have to be given to produce therapeutic effects. These large doses are more likely to bring about adverse effects.

27
Q

What inhibits absorption of L-dopa

A

Large protein meals (compete with amino acids)

28
Q

How is L-dopa metabolised in the body?

A

 90% inactivated in intestinal wall by MAO and DOPA decarboxylase
 9% converted to dopamine in peripheral tissues
 1% crosses BBB to enter the CNS (competes with amino acids)

29
Q

Give two advantages of L-dopa

A

Highly efficacious

Low side effects

30
Q

Give two disadvantages of L-dopa

A

Precursor, needs enzyme conversion

- Long term loss of efficacy and development of involuntary movements

31
Q

Why would you use a dopamine receptor agonist?

A

 Used in combination with L-DOPA in an attempt to reduce it’s late adverse effects, or when it does not control symptoms

32
Q

Give three ADRs for dopamine agonists

A

 Sedation, hallucination, confusion
 Nausea
 Hypotension
 Psychiatric symptoms

33
Q

What is the most commonly used dopamine receptor agonist?

A

 Bromocriptine is most used

34
Q

What are the main psychiatric side-effects of dopamine receptor agonists

A

impulse control disorder – pathological gambling, compulsive shopping - Basically due to shit high dopamine

35
Q

Why is mech of action of monoamine oxidase inhibitor useful in parko?

A

 Selegiline selectively inhibits the MAOB enzyme in the brain that is normally responsible for the breakdown of dopamine. By inhibiting breakdown, the dose of L-DOPA is prolonged.

36
Q

Give three ADRs of MOA

A

 Selegiline selectively inhibits the MAOB enzyme in the brain that is normally responsible for the breakdown of dopamine. By inhibiting breakdown, the dose of L-DOPA is prolonged.

37
Q

What is a Catechol-O-methyl Transferase Inhibitors used for

A

 Adjunct to L-DOPA therapy to reduce end-dose ADRs

38
Q

Give a contra-indication for COMT?

A

Phaeochromcytoma - Can’t break down dat noradrenaline any more! So much adrenaline! Ahh!

39
Q

What is the mechanism of action of COMT

A

 Inhibits the enzyme COMT, which degrades L-dopa in the periphery. No therapeutic effect alone.
 Potentiates effects of L-dopa

40
Q

Give three ADRs for COMT

A

 Nausea and Vomiting
 Abdominal pain
 Diarrhoea

41
Q

What is the mech of action of anti-cholinergics in parko

A

 Antagonists at the muscarinic receptors that mediate striatal cholinergic excitation
 Acetylcholine -> Antagonistic effect on dopamine
 Main action in treatment of Parkinson’s disease is to reduce excessive striatal cholinergic activity

42
Q

What are the main ADRs of anti-cholinergics?

A

Alzheimers effects!
 CNS effects – Mild memory loss, acute confusional states
 Dry mouth and blurred vision (less common)

43
Q

Give two therapeutic notes for anticholinergics, in respect to withdrawal of therapy

A

 Termination of anticholinergic treatment should be gradual, as parkinsonism can worsen when these drugs are withdrawn
 Good for treating tremor, however has no effect on bradykinesia

44
Q

What does amatadine do and when is it used?

A

 Synergistic effect when used in conjunction with L-DOPA
 Stimulates neuronal dopamine release and inhibition of its reuptake
 Additional muscarinic blocking actions

45
Q

Give three ADRs of amantadine

A

 Anorexia
 Nausea
 Hallucinations

46
Q

How do you reduce side-effects of parkinsons?

A

Reduce L-dopa dose and add an adjuvant

47
Q

What is surgery used for in parko?

A

To remove lesions causing tremor and globus pallidus dysfunction

48
Q

What can you do to the subthalamic nucleus to treat parko?

A

Deep brain stim to relieve symptoms

49
Q

HOw does parko get worse

A

Over 15 year period
o Dyskinesia – 94% (writhing movement due to L-DOPA treatment)
o Falls – 81%
o Cognitive Decline – 84% (50% have hallucinations)
o Somnolence – 80%
o Swallowing Difficulty – 50%
o Severe Speech Problems – 27%

50
Q

What is myasthenia gravis? (3 main pathological things + bit that causes death)

A

o An autoimmune destruction of the end-plate ACh receptors
o Loss of junctional folds at the end-plate
o A widening of the synaptic cleft
The crisis point is when it affects respiratory muscles

51
Q

Give three presenting symptoms of myasthenia gravis

A

o Drooping eyelids
o Fatigability and sudden falling due to reduced ACh release
o Double vision

52
Q

When are symptoms of myasthenia gravis worse?

A

Effected by general state of health and emotion

53
Q

What is treatment for myasthenia gravis?

A

o Acetylcholinesterase inhibitors (e.g. Pyridostigmine)

 Prevent breakdown of Ach in synaptic cleft

54
Q

What are side-effects of Acetylcholinesterase inhibitors?

A

 Can cause muscarinic side effects (parallel those effects seen with excessive release of Ach)
 Miosis
 SSLUDGE Syndrome

55
Q

What is plasmapheresis used for in myasthenia gravis?

A

o Plasmapheresis
 Removes AchR antibodies and gives short term improvement
Immunosupression for long term treatment

56
Q

What is SSLUDGE syndrome?

A 
Muscarinic side effects
o	Salivation
o	Sweating
o	Lacrimation
o	Urinary Incontinence
o	Diarrhoea 
o	GI upset and hypermotility
o	Emesis

Semester 5 - Farmocology (27 decks)

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