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Clinical Pharmacology, Therapeutics & Principles of Prescribing > Clinical Pharmacology of Parkinson's Disease & Myasthenia Gravis > Flashcards

Clinical Pharmacology of Parkinson's Disease & Myasthenia Gravis Flashcards

1
Q

List some of the clinical features of Parkinsonism

A

Tremor

Rigidity

Bradykinesia

Postural instability

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2
Q

What is the difference between clasp-knife, lead-pipe and cog-wheel signs?

What type of neurological signs do each indicate?

A

Clasp-knife: spasticity- initial resistance followed by sudden release (UMN sign)

Lead-pipe: continuous rigidity when moving (Parkinsonism)

Cog-wheel: intermitent rigidity when moving (Parkinsonism)

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3
Q

List some non motor manifestations of Parkinsonism

A

Mood changes

Pain

Cognitive change

Urinary symptoms

Sleep disorder

Sweating

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4
Q

Explain the prognosis of PD by using 15 year follow up %s

A

Dyskinesia- 94%

Cognitive Decline- 84%

Falls- 81% Somnolence- 80%

Difficulty swallowing- 50%

Severe speech problems- 27%

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5
Q

What features need to be present to diagnose idiopathic parkinsons disease?

A

Clinical features

Exclusion of other causes of Parkinsonism

Response to treatment

Structural neurology imaging is normal

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6
Q

Where are the cell bodies of dopaminergic neurones found?

A

In the substantia nigra of the basal ganglia

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7
Q

What effect does dopaminergic neurone stimulation have on the neostriatium in “normal” circumstances?

A

Inhibitory effect on ACh production

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8
Q

How does loss of dopaminergic neurons in the substantia nigra lead to impaired mobility (as in Parkinsonism)?

A

Loss of dopaminergic neurons

Loss of inhibiton of Ach production in the neostratum

Stimulation of motor cortex and spinal cord

Leads to problems starting and planning movement

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9
Q

L-DOPA is generated from _________ by the enzyme, ______________

A

L-Tyrosine

Tyrosine hydroxylase

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10
Q

L-DOPA is converted to what by DOPA decarboxylase?

A

Dopamine

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11
Q

Dopamine is converted to what using dopamine B-hydroxlase?

This can then be converted by further enzymatic action to what?

A

Noradrenaline

Adrenaline

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12
Q

What are the 6 classes of drugs that can be used in the treatment of idopathic PD?

A

Levodopa

Dopamine receptor agonists

MAOI type B inhibitors COMT inibitors

Anticholinergics Amantidine

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13
Q

Why can we not just use dopamine in the treatment of IPD?

A

It does not cross the BBB whereas L-DOPA can cross via active transport

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14
Q

Why is treatment with L-DOPA less effective with advancing IPD?

A

L-DOPA must be taken up by dopaminergic neurons in the substantia nigra to be converted to dopamine

The less cells there are here, the less reliable L-DOPAs effects

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15
Q

How is Levodopa administered?

A

Orally

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16
Q

How is Levodopa absorbed?

A

By active transport

In competition with amino acids (no high protein meals with it)

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17
Q

What is the half life of Levodopa?

What does this mean in relation to administration?

A

2 hours

Should be given in short dose intervals

Fluctuations in blood levels and symptoms

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18
Q

How can we prevent Levodopa from being converted to dopamine in the peripheral tissues?

Give three reasons why we would want to prevent peripheral dopamine production

A

Use in combination with a peripheral DOPA decarboxylase inhibitor

  1. Reduce the required dose of L-DOPA
  2. Reduced side effects
  3. Increased L-DOPA reaching the CNS
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19
Q

Give two examples of L-DOPA formulations that are used to treat IPD?

A

Co-careldopa (Sinemet)

Co-beneldopa (Madopar)

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20
Q

What are some advantages of L-DOPA over other classes of drugs used to treat IPD?

A

Highly efficacious

Low side effects

21
Q

List some of the side effects of L-DOPA

A

Nausea

Anorexia

Hypotension

Psychosis

Tachycardia

22
Q

Give some disadvantages of L-DOPA compared to other IPD therapy

A

It is a precursor- requires enzymatic conversion

In the long-term: loss of efficacy involuntary movements and motor complications

23
Q

_______ increases peripheral breakdown of L-DOPA

A

Pyridoxine (Vitamin B6)

24
Q

What is the risk when combining MAOIs with L-DOPA?

A

Hypertensive crisis

25
Q

Dopamine receptor agonists can be separated into which categories?

A

Ergot derived

Non-ergot derived

Patches

Subcutaneous

26
Q

Give some examples of ergot-derived dopamine receptor agonists

A

Bromocryptine

Pergolide

Cabergoline

27
Q

Give some examples of non ergot-derived dopamine receptor agonists

A

Ropinirole

Pramipexole

28
Q

List some advantages of Dopamine Receptor Agonists compared to other treatments for IPD

A

Direct acting

Less motor complications

Possible neuroprotection

29
Q

List some disadvantages of Dopamine Receptor Agonists compared to other treatments for IPD

A

Less efficacy than L-DOPA

Impulse control disorders

More psychiatric side effects

Expensive

30
Q

List some side effects of Dopamine Receptor Agonists

A

Sedation

Hallucinations

Confusion

Nausea

Hypotension

Impulse control disorders

31
Q

What is the method of action of Monoamine oxidase B inhibitors?

A

MAOB inhibits the metabolism of dopamine to enhance the effects of dopamine

32
Q

Give some examples of MAOB inhibitors

A

Selegiline

Rasaglaine

33
Q

List some of the advantages of MAOB inhibitors for the treatment if IPD over other treatment methods

A

Can be used alone

Can be used with L-DOPA to prolong its action

Smooths out the motor response

May be neuroprotective

34
Q

What is the mechanism of action of COMT inhibitors in the treatment of IPD?

A

Inhibition of catechol-O-methyl Transferase

Reduce the breakdown of L-DOPA in the peripheral as the product of this breakdown competes with L-DOPA transport into the CNS

NOT USED ALONE

35
Q

What use to COMT inhibitors have in the treatment of IPD?

A

Used as an “add on” as they have a L-DOPA sparing effect

It prolongs the motor response to L-DOPA

(reduces symptoms of “wearing off”)

36
Q

Give some disadvantages of Anticholinergics in the treatment of IPD

A

No effect on bradykinesia

Generally poorly tolerated

Side effects: confustion, drowsiness, anticholinergic side effects

Not much place for these in the treatment of PD

37
Q

What is the mechanism of action of Amantadine?

When is it used in the treatmne if PD?

A

The mechanism of action is uncertain

Possible enhanced dopamine release

It isn’t!!!!! Used for fatigue in MS

38
Q

Surgery can be of high value in selected cases of IPD, which patients would make good candidates for surgery?

A

Dopamine responsive patients

Significant side effects with L-DOPA

No psychiatric illness

39
Q

What is Myasthenia Gravis?

A

An autoimmune condition in which antibodies are produced against ACh receptors at the neuromuscular junction

40
Q

What is the main presenting symptom of myasthenia gravis?

Where is this most commonly seen?

A

Fluctuating, FATIGUABLE, weakness of skeletal muscle

Most common in the extraocular muscles: causing PTOSIS and DIPLOPIA

41
Q

How might a patient with bulbar involvement myasthenia gravis present?

A

Dysphagia

Dysphonia

Dysarthria

42
Q

Describe the pattern of limb weakness seen in myasthenia gravis

A

Proximal and symmetric

43
Q

Which kind of drugs exacerbate myasthenia gravis?

A

Drugs affecting NMJ transmission:

Aminoglycosides, beta blockers, CCBs, ACE inhibitors, Magnesium

44
Q

Give examples of some of the complications of myasthenia gravis

A

Acute exacerbation–> Myasthenic crisis

Overtreatment–> Cholinergic crisis (depolarising block)

45
Q

What is the main way to therapeutically manage myasthenia gravis?

Give an example

How is this administered?

A

Acetylcholinerase inhibitors e.g. Pyridostigmine

Orally

46
Q

What is the onset, peak and duration of Pyridostigmine?

What is the relevance of these in relation to timing of taking medication?

A

Onset: 30 minutes

Peak: 60-120 minutes

Duration: 3-6 hours

Needs to be given 30-40 minutes before mealtimes (otherwise risk of aspiration)

Needs to be given regularly (TDS initially can go up to 6 times a day)

47
Q

What are the antimusclarinic side effects of acetylcholinesterase inhibitors?

What is the mneumonic used to remember these?

A

Salivation

Sweating

Lacrimation

Urinary incontinence

Diarrhoea

GI upset and hypermotility

Emesis

“SSLUDGE”

48
Q
A

Clinical Pharmacology, Therapeutics & Principles of Prescribing (22 decks)

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