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Clinical Pharmacology & Intro to Prescribing > Session 13: Neurology > Flashcards

Session 13: Neurology Flashcards

1
Q

Clinical features of parkinsonism.

A

Tremor

Rigidity

Bradykinesia

Postural instability

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2
Q

Non-motor manifestations of PD

A

Mood changes

Pain

Cognitive changes

Urinary symptoms

Sleep disorder

Sweating

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3
Q

Features of parkinson down the line after 15 year follow up.

A

Dyskinesia

Falls

Cognitive decline

Somnolence

Swallowing difficulties

Severe speech problems

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4
Q

DDx of idiopathic parkinson’s disease.

A

Drug induced parkinsonism

Vascular parkinsonism

Progressive supranuclear palsy

Multiple systems atrophy

Corticobasal degeneration

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5
Q

Pathophysiologt of IPD.

A

Neurodegeneration with Lewy bodies present.

There is a loss of pigment of the substantia nigra (50% loss leads to symptoms)

There is an increased turnover and and upregulation of receptors.

Reduction of dopamine

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6
Q

Explain the catecholamine synthesis pathway of dopamine.

A

L-Tyrosine -> L-DOPA - (DOPA decarboxylase) > Dopamine -> Noradrenaline -> Adrenaline

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7
Q

Explain the dopamine degradation.

A

Dopamine is converted to an acetic acid or 3-MT via monoamine oxidase (MAO) or catechol-O-methyl transferase (COMT).

These products are then converted into homovanillic acid by MAO or COMT again.

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8
Q

Explain the transport of neurotransmitters.

A

Synthesis of neurotransmitters and formation of vesicles happen in the soma of the neuron. They are then transported down the axon to the presynaptic terminal.

An action potential then causes calcium to enter the presynaptic terminal and there is a release of neurotransmitters as calcium binds to the vesicles.

NT attaches to a receptor and either excites or inhibits.

NT dissociates and is either degraded or taken up again by the synaptic cleft and recycled.

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9
Q

Give an example of a scan used in IPD.

A

DAT scan

It records the presynaptic uptake and will be abnormal in PD.

However it is not diagnostic.

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10
Q

Why is Parkinson’s not treated with dopamine?

A

Because dopamine cannot cross the blood-brain barrier.

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11
Q

Give examples of drugs used in Parkinson’s.

A

Levodopa (L-DOPA)

Dopamine receptor agonists

MAOI type B inhibitors

COMT inhibitors

Anticholinergics

Amantidine

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12
Q

How does levodopa rely on the dopaminergic cell in the substantia nigra?

A

Levodopa must be taken up by the dopaminergic cells in order to be converted into dopamine.

This means that fewer remaining cells -> less reliable effect of levodopa and motor symptoms will become less sedated.

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13
Q

Pharmacokinetics of levodopa.

A

Oral admin

Absorbed by active transport and 90% of it is inactivated in the intestinal wall. This is by MAO and dopa decarboxylase.

Half-life of 2 hours meaning there is a short dose interval and fluctuations in blood levels and symptoms.

9% converted to dopamine in peripheral tissues by DOPA decarboxylase (AADC)

This means that less then 1% will enter the CNS.

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14
Q

If less than 1% of levodopa will enter the CNS, how is it effective?

A

Because you also give a DOPA decarboxylase inhibitor (AADCi) with the levodopa.

The DOPA decarboxylase inhibitor cannot pass the BBB so it only inhibits the conversion of levodopa to dopamine in the periphery and not in the CNS.

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15
Q

Give examples of DOPA decarboxylase inhibitors.

A

Usually come in a combination with the levodopa such as co-careldopa (Sinemet) and co-beneldopa (Madopar)

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16
Q

Benefits of combination therapy of levodopa and DOPA decarboxylase inhibitor.

A

Reduced dose required

Reduced side effects

Increased levodopa reaching the brain

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17
Q

Advantages of L-DOPA

A

Highly efficacious and low side effects.

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18
Q

Give ADRs of levodopa.

A

Nausea and anorexia as it targets the vomiting centres

Hypotension

Psychosis

Tachycardia

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19
Q

Disadvantages of levodopa

A

Needs enzyme conversion to be active

Long term effects as the levodopa will start to wear off.

There is a loss of efficacy as the dopaminergic neurones will die.

There are involuntary movements and motor complications.

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20
Q

Give examples of motor complications of long term levodopa administration.

A

On/off freezing in place

Dyskinesias

Dystonia

Freezing

21
Q

DDIs of levodopa

A

Vitamin B6 increases peripheral breakdown of levodopa.

When administered with MAOIs there is a risk of hypertensive crisis.

Many antipsychotic drugs block dopamine receptors and parkinsonism is a side effect.

22
Q

Give examples of dopamine receptor agonists.

A

Non-ergo such as ropinirole and pramipexole

23
Q

When are dopamine receptor agonists used?

A

As de novo therapy or as an add on therapy.

24
Q

Advantages of dopamine receptor agonists.

A

Direct acting

Less dyskinesias and motor complications

Possible neuroprotection

25
Q

Disadvantages of dopamine receptor agonists.

A

Less efficacy than L-DOPA

Impulse control disorders might manifest

More psychiatric side-effects

Expensive

26
Q

Give examples of impulse control disorders that might manifest as side effects of dopamine receptor agonists.

A

Pathological gambling

Hypersexuality

Compulsive shopping

Desire to increase the dosage due to ‘rewarding nature of drug’.

Punding

27
Q

Give ADRs of dopamine receptor agonists.

A

Sedation

Hallucinations

Confusion

Nausea

Hypotension

28
Q

Explain the action of monoamine oxidase B inhibitors (MAOis)

A

Monoamine oxidase B metabolises dopamine.

This means that an inhibitor will enhance dopamine.

29
Q

Give examples of monoamine oxidase B inhibitors.

A

Selegiline

Rasagaline

30
Q

Can MAO inhibitors be used alone?

A

Yes they can

They prolong the action of levodopa and smooths out motor response.

It may also be neuroprotective.

31
Q

Explain the mechanism of action of COMT inhibitors.

A

Reduce the peripheral breakdown of L-DOPA to 3-O-methyldopa.

This is important as 3-O-methyldopa will compete with L-DOPA active transport into CNS.

Less 3-O-methyldopa means more L-DOPA can cross the BBB.

32
Q

Give examples of COMT inhibitors.

A

Entacapone which doesn’t cross the BBB

Tolcapone which crosses the BBB but main effect is peripheral

33
Q

Can COMT inhibitors be given alone?

A

No, they are no therapeutic effect alone

34
Q

When are COMT-inhibitors given then?

A

In combination with L dopa and peripheral dopa decarboxilase inibitor (Stalevo)

35
Q

Advantages of COMT inhibitors.

A

They have an L-DOPA sparing effect and prolongs the motor response to L-DOPA and reduces the symptoms of wearing off.

36
Q

Explain why anticholinergics might be used in IPD.

A

May have an antagonistic effect to dopamine.

37
Q

Advantages of anticholinergics in IPD.

A

Treats the tremor and don’t act via the dopamine systems.

38
Q

Disadvantages of anticholinergics in treatement of IPD.

A

No effect on bradykinesia

Side effects such as confusion, drowsiness and other anticholinergic side effects.

39
Q

Explain mechanism of action of amantadine.

A

Uncertain but possible enhanced dopamine release and anticholinergic NDMA inhibition.

It is not really used anymore

40
Q

If all medications fail, what is suggested as the next intervention?

A

Apomorphine or surgery such as deep brain stimulation.

41
Q

Clinical features of myasthenia gravis.

A

Fluctuating, fatigueable, weakness of the skeletal muscles.

The most common presentation is of the extraocular muscles.

There is also bulbar involvement leading to dysphagia, dysphonia and dysarthria.

Limb weakness

Respiratory muscle involvement.

42
Q

Give examples of drugs affecting the neuromuscular transmission that will exacerbate Myasthenia gravis.

A

Aminoglycosides

Beta-blockers, CCBs, quinidine and procainamide.

Chloroquine and penicillamine

Succinylcholine

Magnesium

ACE inhibitors

43
Q

Complications of myasthenia gravis.

A

Acute exacerbation -> myasthenic crisis

Overtreatment -> cholinergic crisis

44
Q

Explain the action of ACh esterase inhibitors.

A

Enhance the neuromuscular transmission by inhibiting the breakdown of acetylcholine.

This happens in both skeletal and smooth muscle.

45
Q

Explain cholinergic crisis.

A

If an excess dose is taken which can happen in MG because as they take the medication they might feel better and want to take more.

An excess dose can cause a depolarising block.

46
Q

Give examples of ACh esterase inhibitors.

A

Pyridostigmine taken orally

Neostigmine take oral or IV

47
Q

Cholinergic side effects of pyridostigmine.

A

SSLUDGE

Salivation

Sweating

Lacrimation

Urinary incontinence

Diarrhoea

GI Upset and hypermotility

Emesis

48
Q
A

Clinical Pharmacology & Intro to Prescribing (24 decks)

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