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17 - CPT and Prescribing > 12 - Neurological Disorders > Flashcards

12 - Neurological Disorders Flashcards

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1
Q

What are some clinical features of Parkinsonism?

A

Motor: resting/pill rolling tremor, bradykinesia, rigidity, postural instability, shuffling gait

Non-motor: mood changes (depression), cognitive change, urinary symptoms, sleep disorders, sweating, pain

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2
Q

After 15 years, what clinical features will patients with PD have during follow up?

A
  • Dyskinesia (94%) (secondary to LDopa treatment)
  • Falls (81%)
  • Cognitive decline (84%)
  • Somnolence (80%)
  • Swallowing difficulties (50%)
  • Severe speech problems (27%)
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3
Q

How do you make a diagnosis of idiopathic Parkinson’s Disease?

A
  • Clinical features
  • Exclude other causes of Parkinsonism
  • Response to treatment
  • Normal structural neuro-imaging e.g PET
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4
Q

What are some non-idiopathic causes of Parkinsonism?

A
  • Drug induced
  • Vascular
  • Progressive supranuclear
  • Corticobasal degeneration
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5
Q

What is the pathology of idiopathic parkinson’s disease?

A
  • When over 50% loss of pigment this is when symptoms occur
  • Lewy body deposition in pars compacta of substantia nigra causes neurodegeneration
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6
Q

How is the basal ganglia circuit affected in Parkinson’s disease?

A
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7
Q

How is dopamine synthesised and degraded?

A
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8
Q

What are the six different classes of drugs used to treat IPD?

A
  • Levodopa (L-DOPA)
  • Dopamine receptor agonists
  • MAOI type B inhibitors
  • COMT inhibitors
  • Anticholinergics
  • Amantidine
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9
Q

Why is L-DOPA used to treat IPD instead of Dopamine?

A

- Dopamine receptor agonists

  • It is given orally and must be taken up by dopaminergic cells in the substantia nigra to be converted to dopamine
  • Given up to 5 times a day as short half life of 2 hours
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10
Q

How is L-Dopa absorbed when taken orally?

A

Don’t eat big protein meals with Levodopa as there will be more competition for absorption

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11
Q

What is L-Dopa administered with?

A

- Peripheral DOPA decarboxylase inhibitor (co-careldopa/co-beneldopa)

  • Reduces the dose required, reduces side effects and increases amount of L-Dopa reaching the brain
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12
Q

What are the advantages and disadvantages of using L-Dopa in IPD?

A

+ Highly efficacious

+ Low side effects (e.g nausea, vomiting, hypotension, tachycardia, psychosis)

  • Needs enzyme conversion
  • Involunrary movements
  • Loses efficacy as disease progresses as loss of neurones
  • Motor complications e.g freezing, dystonia
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13
Q

What DDIs does L-Dopa have?

A

- Pyridoxine (Vit B6): increases peripheral breakdown of L-DOPA

- MAOIs: risk hypertensive crisis

- Antipsychotic drugs: lead to parkinsonism (block dopamine receptors)

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14
Q

What are some different subtypes of dopamine receptor agonists and give some examples in each subtype?

A
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15
Q

What are the advantages and disadvantages of using dopamine receptor agonists as treatment for IPD?

A

+ direct acting

+ less motor complications/dyskinesias

+ possible neuroprotection

  • less efficacy than L-Dopa
  • impulse control disorders
  • more psychiatric side effects
  • expensive
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16
Q

What are some impulse control disorders? (a.k.a dopaine dysregulation syndrome)

A
  • Pathological gambling
  • Hypersexuality
  • Compulsive shopping
  • Desire to increase dosage
  • Punding
17
Q

What are some of the side effects of dopamine receptor agonists?

A
  • Impulse control disorders
  • Hallucinations
  • Confusion
  • Hypotension
  • Sedation
  • Nausea
18
Q

What is the mechanism of action of monoamine oxidase B inhibitors and give some examples of this class of drugs?

A
    • Inhibits metabolism of dopamine* by MAO
  • Prolongs action of L-DOPA
  • Smooths out motor response

- Selegiline

- Rasagaline

19
Q

How do COMT inhibitors work to treat IPD and what is an example of this class of drug?

A

- Entacapone

- Reduce peripheral breakdown of L-DOPA to 3-O-methyldopa (3-O-methyldopa competes with L-DOPA for active transport into CNS)

  • Prolongs motor response to L-DOPA so reduces symptoms of wearing off
  • No therapeutic effect alone, need to be given as Stalevo with carbidopa and levodopa
20
Q

How are anticholinergics used to treat IPD and what are some examples of these types of drugs?

A

- Acetyl choline may have antagonistics effects on dopamine

  • Minor role in treatment of PD
  • Orphenadrine
  • Procyclidine
21
Q

What are the advantages and disadvantages of using anti-cholinergics to treat Parkinson’s disease?

A

+ Treats tremor

+ Not acting via dopamine systems

  • No effect on bradykinesia
  • Side effects like confusion, drowsiness, usual anticholinergic side effects (urinary retention, dry mouth etc)
22
Q

What is the MOA of Amantadine in the treatment of IPD?

A

Unknown but possibly:

  • Enhanced dopamine release
  • Anticholinergic NMDA inhibition

DOPAMINE RECEPTOR AGONIST

23
Q

What are the disadvantages of amantadine?

A
  • Poorly effective
  • Few side effects
  • Little effect on tremor
24
Q

Apart from pharmacology, what else can we do to help the treatment of IPD?

A

Deep brain stimulation stereotactically in the subthalamic nucleus

25
Q

What are the differences in the post synaptic membrane of a normal neuromuscular junction with that of one in myasthenia gravis?

A

Autoimmune disease not neurodegenerative

26
Q

How does myasthenia gravis present?

A

- Extraocular muscles – commonest presentation

- Bulbar involvement – dysphagia, dysphonia, dysarthria

- Limb weakness – proximal symmetric

- Respiratory muscle involvement - e.g tired when walking stairs

FLUCTUATING FATIGUABLE WEAKNESS OF SKELETAL MUSCLE

27
Q

What are some classes of drugs that can exacerbate a patient’s myasthenia gravis?

A
  • Aminoglycosides
  • Beta-blockers
  • CCBs
  • Quinidine
  • ACE inhibitors

BE CAREFUL WHEN PRESCRIBING TO MG PATIENTS

28
Q

What are the complications of Myasthenia gravis?

A

- Acute exacerbation – Myasthenic crisis

- Overtreatment – cholinergic crisis

29
Q

What is the acute therapeutic management of Myasthenia gravis?

A

Acetylcholinesterase inhibitors – enhance neuromuscular transmission at skeletal and smooth muscle by stopping breakdown of Ach at NMJ

  • Pyridostigmine (oral)
  • Neostigmine (oral/IV)
30
Q

Why may pyridostigmine be used over neostigmine?

A
  • Although has quicker action and duration of 4 hours it has more significant cholinergic side effects
31
Q

What are cholinergic side effects?

A
  • Miosis

- SSLUDGE syndrome: salivation, sweating, lacrimation, urinary incontinence, diarrhea, GI upset and hypermotility, emesis

32
Q

What are the three parts of treating a patient with PD?

A
  • Neuroprotection e.g L-Dopa
  • Symptomatic treatment
  • Surgery
33
Q

Apart from AchEi’s, how can myasthenia gravis be pharmacologically treated?

A
  • Immunoglobulins IV to help a crisis
  • Azathioprine to be steroid sparing
  • Corticosteroids to decrease immune response
  • Plasmapheresis
34
Q

What antiemetic would you not give to a patient with Parkinson’s?

A
  • Metoclopramide as it is a dopamine d2 antagonist working all over the body so will affect the CNS
  • Give domperidone instead as only acts on D2 receptors in the gut, not the CTZ as cannot cross BBB

17 - CPT and Prescribing (25 decks)

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