Parkinson's Disease & Movement Disorders (Exam V) Flashcards

1
Q

What symptom is the hallmark of Parkinson’s disease?

A
  • Tremor at rest (rhythmic movement around a joint)
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2
Q

What is Chorea?

A
  • Muscle jerking in various areas
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3
Q

What is ballismus?

A
  • Violent abnormal movements
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4
Q

What is essential tremor?
What is this indicative of?

A
  • Tremor occurring with movement
  • Not Parkinson’s, brain lesion, EtOH, etc.
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5
Q

What is Athetosis?
Is this indicative of Parkinson’s disease?

A
  • Slow, writhing movement
  • Not typical of Parkinson’s
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6
Q

What is dystonia?

A
  • Abnormal posture w/ no movement.
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7
Q

What are Tics?

A
  • Single, repetitive movements (especially facial)
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8
Q

What is choreathetosis?

A
  • Combination of jerking & flowing movements of both chorea & athetosis (dystonia can be present as well)
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9
Q

What are possible causes of choreathetosis?

A
  • Trauma
  • Chore Gravidarum
  • Tumors
  • Cerebral Palsy
  • Huntington’s
  • Kernicterus (↑ bilirubin)
  • Ataxia Telangectasia
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10
Q

What collection of neurons regulates motor activities?

A
  • Basal Ganglia/Nuclei
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11
Q

Communication from the motor cortex to the thalamus goes through the _____ ______.

A

Basal Ganglia

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12
Q

What specific area of the basal ganglia is damaged in Parkinson’s Disease?

A
  • Pars Compacta (in Substantia Nigra)
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13
Q

What is the normal pathway of motor movement?

A
  1. Dopamine release from Pars Compacta
  2. Striatum activated
  3. Direct pathway with GABA & Sub P
  4. GABA & Sub P inhibit basal ganglia
  5. Basal Ganglia → GABA inhibits Thalamus
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14
Q

How does Parkinson’s disease differ from the normal pathway of motor movement?

A
  1. No Dopamine from Pars Compacta
  2. Dopamine-Striatum pathway bypassed
  3. Alternate pathway with glutamate activates basal ganglia.
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15
Q

What is TRAP in relation to Parkinson’s Disease?

A
  • Tremor
  • Rigidity
  • Akinesia
  • Posture
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16
Q

Does coginitive decline occur with Parkinson’s disease?

A

Yes, eventually.

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17
Q

What environmental factors protect against Parkinson’s Disease?

A
  • Cigarettes
  • Coffee
  • Anti-inflammatories
  • Uric Acid
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18
Q

What environmental factors increase risk of developing Parkinson’s disease?

A
  • Lead & Manganese exposure
  • Vitamin D deficiency
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19
Q

What genetic component is often present in Parkinson’s patients?
What percentage of Parkinson’s patients have this?

A
  • SNCA - α-Synuclein
  • 10-15%
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20
Q

Do Parkinson’s tremors start all over the body?

A

No, they usually start on one side.

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21
Q

What is Akinesia?

A
  • Loss or impairment in power of voluntary movement.
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22
Q

What drug is given as firstline treatment for Parkinson’s?
Why this drug?

A
  • Levo-dopa (dopamine precursor)
  • Able to cross BBB unlike dopamine
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23
Q

What are Lewy Bodies?
What diseases have these present?

A
  • Misfolded proteins
  • Mad-Cow, Parkinson’s, Alzheimer’s, Multiple System Atrophy
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24
Q

What occupation’s have an increased risk of developing Parkinson’s?

A
  • Healthcare
  • Teaching
  • Farming
25
Q

What non-occupational risk factors exist for Parkinson’s Disease?

A
  • > 60yo
  • Hereditary
  • Males
  • Herbicides/Pesticides
26
Q

What are the treatments for Parkinson’s?

A
  • Exercise
  • Levo-Dopa
  • CNS antimuscarinics
27
Q

What drugs should be avoided when one has Parkinson’s Disease?

A
  • D2 Antagonists (Haldol, etc.)
  • MPTP (destroys dopaminergic neurons)
28
Q

Where is MPTP found?

A
  • Illicit synthetic opioids (causes drug-induced Parkinson’s)
29
Q

How much of L-Dopa crosses the BBB?
Can this be increased? With what? How much?

A
  • 1-3%
  • With Carbidopa (10% uptake of Levo-dopa)
30
Q

How does carbidopa work?

A
  • Inhibits Dopa-Decarboxylase from forming dopamine peripherally (thus saving Levo-dopa for the CNS)
31
Q

Is Levo-dopa a treatment or a cure for Parkinson’s?

A
  • Treatment, effective for a period of time before more neurons degrade.
32
Q

What adverse effects can be seen from levodopa?

A
  • Delusions
  • Dyskinesias - Choreathetosis (too much dopamine)
33
Q

What drug treats delusions associated with levodopa administration?

A
  • Pimavanserin - antipsychotic (inverse agonist of 5-HT2A) suppresses signaling to visual cortex.
34
Q

What is the On-Off Phenomenon with Levo-dopa?
When does it occur?

A
  • Increased mobility followed by marked akinesia.
  • Associated with long-term use.
35
Q

What drug interactions exist for Levodopa?

A
  • Vitamin B6 & MAOI’s
36
Q

What contraindications exist for Levodopa?

A
  • Psychosis (↑ dopamine signalling)
  • Glaucoma
  • Melanoma (L-dopa feeds these tumors)
37
Q

How is L-Dopa broken down peripherally?
What drug inhibits this?

A
  • COMT
  • Entacapone & Tolcapone
38
Q

What monoamine oxidase is specific for dopamine?
What drug can prevent the breakdown of Dopamine in the CNS by inhibiting MAOB?

A
  • MAO-B
  • Selegiline
39
Q

What MAOI’s can be paired with Levo-dopa?

A
  • Selegiline
  • Rasagiline
40
Q

What dopamine agonist is useful for “off” periods from levodopa & relief of akinesia?

A
  • Apomorphine
41
Q

What antiviral agent has antiparkinson’s effects?

A
  • Amantadine
42
Q

What is the most common movement disorder?
What is the treatment?

A
  • Essential tremor (β1 receptor dysfunction) tremor with movement
  • βblockers
43
Q

What is benign hereditary chorea?
What is the treatment?

A
  • Chorea in childhood with no progression and no dementia.
  • Tetrabenazine (↓ Dopamine)
44
Q

What is Tardive Dyskinesia?
What is the most common cause?

A
  • Repetitive, involuntary movements.
  • Anti-psychotic drugs.
45
Q

What is Muscular Dystrophy?
What occurs with these disorders?

A
  • Group of muscle disorders of childhood.
  • Progessive degeneration of muscle fibers.
46
Q

What is the most common & severe muscular dystrophy disorder?
How is it inherited?

A
  • Duchenne’s Muscular Dystrophy (most severe)
  • X-linked dystrophin gene absent - passed by mother to sons
47
Q

What sign is seen with children who have Duchenne’s MD?

A
  • Gower’s Sign - using hands to pushing on legs to stand.
48
Q

What treatment exist for Duchenne’s MD?
What is the life expectancy?

A
  • Corticosteroids, β2 agonists, & orthopedic braces.
  • 20’s
49
Q

What characterizes Cerebral Palsy?
What is the usual cause?

A
  • Non-progressive motor disorder of the CNS.
  • Birth Trauma (or hemmorhage, anoxia, &/or infection)
50
Q

When does Huntington’s disease normally occur?
Is this disease autosomal dominant or recessive?

A
  • age 30 - 40
  • Dominant
51
Q

What characterizes the pathophysiology of Huntington’s disease?

A
  • GABA reduced in the basal ganglia
  • Reduction in ChAT (Choline Acetyltranferase)
  • Excess Dopamine
52
Q

What symptoms are seen with Huntington’s disease?

A
  • Progressive loss of muscular control
  • Chorea
  • Dementia
53
Q

What treatments are there for Huntington’s disease?

A
  • Tetrabenazine = ↓ excess dopamine
  • Dopamine Receptor blockers (ex. Haldol)
54
Q

What characterizes ALS?
When does death occur?

A
  • Loss of motor neurons
  • 2-6 years after diagnosis
55
Q

What are the treatments for Lou Gehrig’s disease?

A
  • Riluzole - Na⁺ channel blocker (specific for damaged neurons)
  • Edaravone - antioxidant.
56
Q

What two anatomical changes are seen in Alzheimer’s disease?

A
  • Neurofibrillary tangles inside the neuron
  • Amyloid plaques outside the neuron
57
Q

What palliative treatments are available for Alzheimer’s disease?

A
  • CNS AChE inhibitors (Tacrine & Rivastigmine) ( ↑ACh at synapse)
  • NMDAr Antagonist (Memantine)
58
Q

What are the treatment’s for restless leg syndrome?

A
  • Dopamine agonists
  • Gabapentin
  • Benzodiazepines
  • Clonazepam