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4TH YEAR - CPTP > Parkinson's/Epilepsy > Flashcards

Parkinson's/Epilepsy Flashcards

1
Q

How is Parkinson’s diagnosed?

A

Bradykinesia +1 of:

  • 4-6 Hz tremor
  • Mucular rigidity
  • Postural instability

ASSYMETRICAL

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2
Q

If these symptoms are bilateral, how does this change the diagnosis?

A

More likely to be SECONDARY PARKINSONISM caused by drugs (e.g. neuroleptics, antiemetics), CVD, infections etc

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3
Q

Name some non-motor symptoms of parkinson

A
  • REM behaviour disorder (acting out dreams) and other sleep disorders
  • Reduction in olfactory function (ANOSMIA IN 90%!!!!)
  • Depression/anxiety/hallucinations
  • Parasthesia
  • Fatigue
  • Sexual dysfunction
  • Bladder dysfunction
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4
Q

If you see a patient with rapid onset parkinsonism and dementia, what is the most likely diagnosis?

A

Lewy Body Dementia

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5
Q

What is Parkinson’s Disease?

A

A progressive neurodegenerative disease with two main features:

  1. Loss of pigmented dopaminergic neurons in the substantia nigra
  2. Increase in Lewy Bodies
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6
Q

Name some other relevant motor features of PD

A

Dysphagia

Dysarthria

Hypersalivation

Blurred vision

Micrographia

Dystonia

Stooped posture

Shuffling gate

Freezing

Festinant

FALLS

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7
Q

What does festinant mean?

A

Having short stride and quickened gait

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8
Q

What is a parkinson plus syndrome?

A

A group of syndromes that exhibit the same symptoms as parkinsons but with additional features:

  • Multiple system atrophy
  • Corticobasal degeneration
  • Progressive supranuclear palsy
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9
Q

What are the typical pre-motor symptoms?

A
  • Impaired olfaction
  • REM behaviour disorder
  • Depression
  • Constipation
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10
Q

What imaging technique is used in parkinson diagnosis?

A

SPECT - measures loflupane (DaTSCAN) uptake in presynaptic dopamine transporters

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11
Q

What does a DaTSCAN look like in a PD patient?

A

More like .. than the usual “

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12
Q

What are the pros and cons of DaTSCANS?

A

PRO - high sensitivity and specificity

CON - expensive

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13
Q

Describe the onset and progression of PD

A

Insidious onset (latent period can be up to 3 decades)

Long clinical course (10-30 years)

Incurable, decreased life expectancy

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14
Q

Name the 7 classes of drugs used to treat PD?

A
  • L-dopa (give with decarboxylase inhibitor)
  • Dopamine agonists
  • MAOB inhibitors
  • COMPT inhibitors
  • Amantadine
  • Anticholinergics
  • Oestrogen
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15
Q

Name two examples of L-Dopa with decarboxylase inhibitor

A

Madopar, Sinemet

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16
Q

Name two examples of MAOB inhibitors

A

Selegiline, Rasagiline

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17
Q

Name three examples of dopamine agonists

A

Ropinirole, Pramipexole, Rotigotine, Apomorphine

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18
Q

How do L-Dopa and decarboxylase inhibitors work?

A

L-dopa is converted to dopamine in the brain

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19
Q

How do COMT inhibitors work, and what is an example?

A

Entacapone They stop L-dopa from being converted to 3-0 methydopa (must be used alongside)

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20
Q

How do MAOB inhibitors work?

A

They stop dopamine from being converted to its inactive metabolite

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21
Q

Which of the drug treatments is best for symptom control?

A

L-dopa, however it has motor complications, unlike the others

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22
Q

Why is L-Dopa used in older patients and dopamine agonists used in younger ones?

A

L-dopa is the best for symptomatic treatment but DAs are best in delaying onset of motor complications

Also DA causes orthostatic hypotension, which could contribute to falls in the elderly

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23
Q

Which members of the MDT are involved in Parkinsons care?

A

PD nurse specialist, physiotherapy, occupational therapy, SALT, support groups

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24
Q

What drug is primarily used in early PD?

A

MAOB inhibitors (best at stopping progression of disease, but not that good at symptom control)

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25
Q

What medications should be stopped when prescribing for PD?

A

Dopamine-blocking agents:

  • Neuroleptics
  • Antiemetics
  • Sodium valproate
  • CCBs
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26
Q

If a PD patient starts experiencing hallucinations from their meds, what can be given to them?

A

Quetiapine

27
Q

How does Amantadine work?

A

Stimulates release of dopamine

28
Q

What is the pharmacology of L-Dopa?

A
  • Absorbed from small bowel
  • Motor symptoms improve 20-70%
29
Q

What are the short term side effects of L-Dopa?

A

GI - nausea, vomiting, decreased appetite

Psychiatric - confusion, hallucinations, delusions

Cardiovascular - postural hypotension

Sleep disorders - somnolence, insomnia, vivid dream/ nightmares

30
Q

What are the long term side effects of L-Dopa?

A

DYSKINESIAS - Abnormal involuntary movements

RESPONSE FLUCTUATIONS - end-of-dose deterioration and unpredictable on/off switching

PSYCHIATRIC - confusion, hallucinations

31
Q

What is the pharmacology of Dopamine agonists?

A
  • Act directly on D1/D2 postsynaptic receptors in the striatum
32
Q

Which dopamine agonists are administered by which routes?

A

Ropinirole - oral

Rotigotine - transdermal

Subcutaneous - apomorphine

33
Q

What are the side effects of dopamine agonists?

A
  • Nausea, vomiting, loss of appetite
  • Postural hypotension
  • Confusion, hallucinations
  • Somnolence
  • Impulse control disorders (hypersexuality, gambling etc)
34
Q

What is the pharmacology of MOAB inhibitors?

A
  • Irreversible inhibitors
  • Decrease dopamine breakdown so that there is more in the synaptic cleft

NB - in practice these are rarely used alone as they have a weak clinical effect

35
Q

What are the side effects of MOAB inhibitors?

A

Nausea, vomiting, confusion

36
Q

What is an important drug interaction to be aware of in reference to MOAB inhibitors?

A

Interact with anti-depressants –> SEROTONIN SYNDROME

37
Q

What is the pharmacology of COMT inhibitors?

A

Inhibit COMT so that more levodopa is available to cross the BBB

38
Q

What are the side effects of COMT inhibitors?

A

Nausea, vomiting, confusion

DIARRHOEA AND DISCOLOURATION OF BODY FLUIDS

Increased dyskinesias

39
Q

What is the pharmacology of amantadine?

A

Antiviral, NMDA receptor antagonist causing increased release of dopamine

40
Q

When is amantadine used?

A

In the later stages of disease to treat dyskinesias (however do not use in the elderly as it causes confusion)

41
Q

What are the side effects of amantadine?

A
  • Confusion
  • Halluciantions, pscyhosis
  • Livedo reticularis (skin condition)
  • Ankle oedema
42
Q

What is the pharmacology of anticholinergics?

A

Decrease the effects of relative ACh excess, that occurs due to dopaminergic deficiency

43
Q

What are the side effects of anticholinergics?

A

Cognitive impairment

Dry mouth, blurred vision, constipation, urinary retention, dizziness

44
Q

When are anticholinergics used?

A

In the young, to combat tremor

45
Q

What are the future PD treatments?

A
  • Fetal mesencephalic dopamine cell implantation
  • Intraputaminal glial cell line derived neutrophilic factor
46
Q

What drug is first line for generalised epilepsy?

A

Men: Sodium Valproate (2nd lamotrigine)

Women: Lamotrigine (less teratogenic)

47
Q

What drug is first line for focal epilepsy?

A

Carbamazepine and Lamotrigine (better tolerated)

48
Q

Which members of the MDT are involved in the care of a patient with epilepsy?

A

Epileptologists, neurosurgeons, nurses, EEG technicians, psychiatrists, social workers, DVLA, pharmacologists

49
Q

What drug is first line for generalised absence seizures?

A

Ethosuximide

50
Q

What are the size effects of carbamazepine, phenytoin and lamotrigine?

A

Tiredness, double vision, steadiness, RASH

51
Q

What are the side effects of sodium valproate?

A

Weight gain

Tremor

Parkinsonism

Teratogenicity

52
Q

What are the side effects of topiramate?

A

Weight loss, behavioural changes, paraesthesia, kidney stones

53
Q

What are the side effects of levetiracetam?

A

Tiredness, dizziness, aggresion

54
Q

Which AEDs are enzyme inducers of the OCP?

A

Carbamazepine (anything -epine) Phennytoin Topiramate

55
Q

Which AEDs are metabolised by the liver and which renally?

A

If in doubt, CP450

Renal - Gabapentin, Levetiracetam

56
Q

What are the indications for monitoring AEDs?

A
  • As guide to dosing
  • To check compliance
  • Toxic symptoms
  • To monitor interactions
  • During pregnancy
  • Learning disabilities
57
Q

How is status epilepticus treated?

A

ABCDE

Hospital - IV lorazepam

GP - rectal diazepam

Kids - buccal midazelam

If these fail, give phenytoin, phenobarbital or transfer to ITU

At 30 min do bloods to see if there is an underlying cause

At 60 mins admit to ICU for continuous monitoring

58
Q

Why do you sometimes get:

a) raised GGT
b) hyponatremia

when being treated with carbamazepine, and what is the consequence?

A

a) this is because carbamazepine is an enzyme induce, you can continue with treatment but monitor
b) as a consequence of SIADH - if symptomatic should discontinue treatment

59
Q

Why does carbamazepine require dose adjustment as you continue treatment?

A

It is an AUTO-INDUCER - as treatment goes on it induces its own metabolism, so you will need to increase the dose

60
Q

What are the symptoms of carbamazepine toxicity? How should it be managed?

A

Nystagmus Ataxia Increased seizure frequency

THESE ARE DUE TO CEREBELLAR TOXICITY

Activated charcoal and supportive care

61
Q

What anti epileptic should be used in pregnancy?

A

Carbamazepine

(sodium valproate associated with neural tube defects)

62
Q

What antiepileptic should be used in lactation?

A

Most of the older ones are safe!

63
Q

What is delirium tremens?

A

Acute alcohol withdrawal with agitation, fever, confusion, hallucinations, tonic clonic seizure

Usually occurs after 8hrs with a peak at day 2 and recovery at day 5

64
Q

How is delirium tremens treated?

A

Chlordiazepoxide oral

4TH YEAR - CPTP (19 decks)

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