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Parkinson's Disease Flashcards

1
Q

4 cardinal clinical features of parkinson’s disease:

A
  • tremor
  • cogwheel rigidity
  • bradykinesia
  • postural abnormalities
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2
Q

Clinical Features of Parkinson’s Disease:

A
  • tremor
  • cogwheel rigidity
  • bradykinesia
  • postural abnormalities
  • unilateral at onset
  • reduced arm swing
  • shuffling, festinating gait
  • falls
  • micrographia
  • non-motor symptoms: anosmia,
    constipation, abnormal dreams,
    urinary symptoms
  • neuro-psych symptoms: anxiety,
    depression, psychosis and
    dementia
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3
Q

Diagramatic Representation of Symptoms and Signs in Idiopathic Parkinson’s Disease:

A

insert diagram

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4
Q

What are the basal ganglia?

A

An area of the fore and midbrain known to be involved in control of movement and motor learning

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5
Q

Main components of the basal ganglia:

A
  • caudate nucleus
  • putamen
  • globus pallidus

also substantia nigra and subthalamic nucleus have an anatomical and functional relationship shared with neostriatum

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6
Q

Neuroanatomy-basal Ganglia:

A

insert diagram

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7
Q

What is the primary afferent source of the basal ganglia?

A

From the cerebral cortex (somatosensory and primary motor cortex)

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8
Q

Direct and Indirect Pathways of Basal Ganglia:

A

insert diagram

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9
Q

Incidence of Parkinson’s Disease:
- females
- age
- males

A
  • 37.6 per 100,000
  • increases with age
  • 61.2 per 100,000
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10
Q

Parkinson’s Disease: Pathophysiology:

A
  • loss of dopamine containing
    neurons of the Pars Compacta of
    the Substantia Nigra
  • neurons lose dark melanin
    granules with a concurrent loss of
    dopamine in nigrostriatal
    pathways and neostriatum
  • definitive diagnosis would require
    identification of alpha synuclein
    within lewy bodies
  • lewy bodies present in surviving
    neurons only in substantia nigra;
    which is the differentiating feature
    between dementia with lewy
    bodies and parkinson’s disease
  • clinical signs and symptoms are
    seen after 70-80% nigral neurons
    and corresponding granules and
    dopamine are lost
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11
Q

Parkinson’s Disease: Aetiology:

A
  • unknown
  • genetics (15% of patients have
    familial hereditary parkinson’s)
  • environmental toxins
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12
Q

Parkinson’s Disease: Genes:

A
  • SNCA = responsible for alpha
    synuclein production; deposited in
    clumps in Lewy bodies
  • PARK2 = makes protein parkin,
    which has a role in cell breakdown
    and recycling proteins
  • PARK7 = found in rare early-onset
    Parkinson’s Disease, protect
    against mitochondrial stress
  • PINK1, LRRK2
  • Autosomal Dominant or Recessive
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13
Q

Neuropathology:

A

(affects gut as well)

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14
Q

Parkinson’s Disease forms part of a spectrum of disorders associated with lewy bodies.

What is the difference between a patient with “Parkinson’s Disease with Dementia” and a patient with “Dementia with Lewy Bodies”?

A
  • Parkinson’s Disease with
    Dementia will have the onset of
    Parkinson’s disease/parkinsonism
    first and dementia AT LEAST A
    YEAR AFTER
  • Dementia with Lewy Bodies will
    have parkinsonism and then
    dementia occurring WITHIN A YEAR
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15
Q

Lewy Body Dementia:

A
  • often presents with cognitive
    impairment
  • visual hallucinations are common
  • fluctuates
  • lewy bodies found sub-cortically
    and cerebral cortex
  • anti-parkinsonian treatments
    make the hallucinations worse
  • and the neuroleptics make the
    extra-pyramidal symptoms
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16
Q

Parkinson’s Disease: Treatment Overview:

A
  • pharmacological
  • therapy: physio, Tai Chi, pilates
  • surgical: deep brain stimulation
  • supportive: social prescribers
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17
Q

Core Drug: L-Dopa: Mechanism of Action:

A
  • passes through BBB as a pre-
    cursor of dopamine
  • converted to dopamine in the
    brain
  • replenishes the lost dopamine in
    the neostriatum
  • used to treat Parkinson’s Disease
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18
Q

In the UK Gold-standard pharmacological treatment for Parkinson’s Disease?

A
  • L-dopa

and one of the following:

  • carbidopa
  • benserazide
  • co-careldopa (L-dopa + carbidopa)
  • co-beneldopa (L-dopa +
    benserazide)
19
Q

Carbidopa and Benserazide are

A

dopamine-decarboxylase inhibitors

inhibits the peripheral conversion of L-dopa to dopamine

increases the amount of L-dopa available to brain tissue

20
Q

Core Drug: L-dopa: Side Effects:

A
  • initially very well tolerated and
    effective
  • low dosage and slow
  • nausea, GI side effects
  • postural hypotension
  • long term complications after 7-8
    years:
    - motor fluctuations
    - dyskinesias-hyperkinetic
    involuntary movements
  • neuro-psychiatric complications:
    - confusion
    - hallucinations
    - psychosis
21
Q

Core Drug: L-dopa: Drug Class:

A

Anti-parkinsonians
Dopamine precursor

22
Q

Core Drug: Ropinirole: Drug Class:

A

Anti-parkinsonians
Dopamine Agonist

23
Q

Core Drug: Ropinirole: Mechanism of Action:

A
  • direct stimulation of dopaminergic
    receptors
  • increased production of dopamine
24
Q

Core Drug: Ropinirole: Side Effects:

A
  • postural hypotension (more)
  • more GI side effects
  • dopamine dysregulation
    syndrome/impulse control
    disorder: gambling, hypersexuality
    warn patient and relatives
  • excessive daytime sleepiness:
    DVLA
25
Q

What is the first line anti-parkinsonian drug for Parkinson’s patients under 60?

A

Ropinirole
takes longer to get to a therapeutic dose

causes less tardive dyskinesias (less long term side effects) but more when initially started

26
Q

Core Drug: Rasgiline: Drug Class:

A

Anti-parkinsonians
MAO-B inhibitor (monoamine oxidase B)

27
Q

Core Drug: Rasgiline: Mechanism of Action:

A
  • selective inhibitor of Monoamine
    Oxidase B (MAO-B)
  • blocks dopamine metabolism in
    the CNS
  • used in early disease; prolongs
    time before l-dopa or dopamine
    agonist required
  • adjunctive to L-dopa to prevent
    end of dose deterioration; when L-
    dopa effects stop lasting till the
    next dose
28
Q

Core Drug: Rasgiline: Side Effects:

A
  • abdominal pain
  • depression
  • sleep disorders
  • vomiting
29
Q

Core Drug: Entacapone: Drug Class:

A

Anti-parkinsonians
Catechol-o-methyltransferase inhibitors (COMT inhibitors)

30
Q

Core Drug: Entacapone: Mechanism of Action:

A
  • inhibits catechol-o-
    methyltransferase (COMT) enzyme
  • blocks dopamine metabolism
  • extends benefits of L-dopa
31
Q

Deep Brain Stimulation:

A
  • used for complex/late stage
    parkinson’s disease
  • electrodes implanted into globus
    pallidus or subthalamic nuclei
  • used to treat motor symptoms
  • indicated in on/off fluctuations or
    L-dopa induced dyskinesias
  • long lasting

to be eligible more than 30% of day must be spent in dyskinesia

Side Effects: executive function, verbal fluency decreases, apathy

32
Q

Core Drug: Entacapone: Side Effects:

A
  • abdominal pain
  • confusion
  • GI side effects
  • dizziness
  • dry mouth
  • vomiting
33
Q

What main treatments throughout different stages of parkinson’s disease?

A
  • early = dopamine agonist =
    rasgillne
  • mid = L-dopa
  • late = deep brain stimulation or
    apomorphine
34
Q

Late Stage Complex Parkinson’s Disease and Apomorphine:

A
  • dopamine agonist
  • subcutaneous injection
  • used wit L-dopa
  • lasts 40mins
  • sudden and unpredicatable
    changes in symptoms
  • dyskinesia
  • off period not controlled by other
    drugs

side effects: sleepy, hallucinations, impulse behaviours, hypotension,
cardiac disorders

35
Q

Complex Stage Parkinson’s Disease and Duodopa:

A
  • gel form of levodopa
  • directly delivered via a tube into
    the intestine
  • fewer motor fluctuation
  • overall improved quality of life
36
Q

Other Parkinsonian Syndromes: MSA, PSP:

A
  • Multiple System Atrophy (MSA):
    • early falls
    • autonomic, cerebellar,
      parkinsonian variant
    • immunecytochemistry
      demonstrating alpha synuclein
      inclusions in the glia
  • Progressive Supranuclear Palsy
    (PSP):
    - early falls
    - failure of vertical eye
    movements
    - dysarthria
    - tau pathology showing
    neurofibrillary tangles within
    neurons
37
Q

Tic Disorders:

A
  • sudden, stereotyped movements
    or sounds which occur at irregular
    intervals
  • linked to increased dopaminergic
    activity in basal ganglia
    - abnormality in the cortico-
    striato-thalamocortical circuits
    - disinhibition of excitatory
    neurons in thalamus resulting
    in hyperexcitability of cortical
    motor areas

associated with basal ganglia dysfunction

38
Q

Gilles de la Tourette’s Syndrome:

A
  • presents in childhood age 7+
  • more common in males x4
  • motor tics in cranial/orbital region
  • vocal tics
  • associated with ADHD, OCD
39
Q

Is chorea, dystonia, tremors, tics and myoclonus bradykinetic disorder?

A

Hyperkinetic
all suppressable slightly
due to increased dopaminergic activity in basal ganglia

parkinsons is bradykinetic

40
Q

Chorea:

A
  • hyperkinetic
  • increased dopaminergic activity in
    basal ganglia
  • rapid, irregular, involuntary dance
    like movements that flow
    randomly from one body region to
    another

most common form is huntington’s disease

41
Q

Huntington’s Disease:

A
  • progressive disorder
  • presents with either psychiatric or
    neurological symptoms
  • autosomal dominant
  • key to diagnosis is family history
  • expanded trinucleotide (CAG)
    repeat on chromosome 4, coding
    for huntington protein
  • whole genome sequency
  • atrophy of caudate nucleus,
    putamen, globus pallidus and a
    degree of cerebral atrophy
42
Q

Apart from genetic causes, what are other causes of chorea?

A
  • vascular
  • systemic lupus erythematosus
  • auto-immune encephalitis
  • toxoplasmosis
43
Q

Dystonia:

A
  • abnormal twisting posture often
    facial
  • may be associated with jerky
    tremor
  • pathophysiology not fully
    understood: PET scans suggest
    abnormal activity in motor cortex
  • abnormal dopaminergic activity in
    basal ganglia supported by:
    • dystonia caused by blocked
      dopamine receptors
    • some are levodopa induced
44
Q

Hyperkinetic movement disorder treatments: (core drugs)

A
  • dopamine receptor blocking
    agents = typical antipsychotics =
    core drugs: Haloperidol,
    Chlorpromazine
  • Core Drugs: atypical anti-
    psychotics: Clozapine,
    Olanzapine, Aripiprazole

NSB (50 decks)

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