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Neurology > Parkinsons, Huntington, ALS > Flashcards

Parkinsons, Huntington, ALS Flashcards

1
Q

What is the biggest risk factor in development of Parkinson’s diease?

A
  • Age
  • 1st degree relative
  • M > W
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2
Q

What are the most common clinical findings for Parkinson’s Disease?

A
  • Resting Tremor - pill rolling / Chin Tremor <– unique
  • Increases resistance to passive movement - Rigidity
  • Slow movements / Decreased arm swing - bradykinesia
  • Dragging of one leg or foot – imbalanced gait
  • Masked facial expression
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3
Q

What are nonmotor early signs of Parkinson’s Disease?

A
  • REM Sleep Behavior disorder

- Loss of Smell

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4
Q

What is a characteristic finding in histology for Parkinson’s Disease?

A
  • Loss of Substandia Nigra

- Lewy Bodies w/ Alpha Synuclein inside

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5
Q

What are common gene mutations found in Parkinson’s disease?

A
  • Parkin Gene – younger onset typicallly

- Alpha-Synuclein mutation – accumulates in Lewy Bodies

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6
Q

What is the confirmatory test for Parkinson’s Disease?

A
  • Responds to L-Dopa (or Dopa-angonists)
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7
Q

What disorder also is found to have Lewy Bodies and loss of substania nigra, but different clinical presentation?

A

Lewy Body Dementia

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8
Q

How are Parkinson’s and Lewy Body Dementia different?

A
  • Lewy Body Dementia has earlier onset of dementia compared to Parkinson’s usually within a year or two from onset of Parkinsonian symptoms / fluctuating cognition. Parkinson’s patient’s don’t develop dementia until many years into the disease.
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9
Q

What is typically the first line therapy for parkinson’s diease?

A

Dopamine Receptor Agonists - restore function of the indirect pathway to release inhibition of thalamas

  • Pramipexole
  • Ropinerole
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10
Q

If a patient is being given Pramipexole and Ropinerole, what do they do?

A

D2 Agonists – induces striatum to release GABA to Globus Palladus Externa – allowing release of inhibition of thalamas by subthalamic nucleus

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11
Q

What drug is used for Parkinson’s Disease when the typical treatments have failed, or for immediate therapy of an attack?

A

Apomorphine – D4 Agonist

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12
Q

What are the most common side effects of Dopamine Agonists?

A
  • sudden sleep attacks

- CNS toxicity with confusion / disorientation / too much movement

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13
Q

What patient population would typically get L-DOPA over Dopamine Agonists?

A
  • Older patients with Parkinson’s
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14
Q

What is an advantage of Dopamine Agonists over L-DOPA?

A
  • longer half lives
  • effectiveness does not decline over time
  • less oxidative damage from dopamine degradation
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15
Q

What is the common drug administered with L-Dopa?

A
  • Carbidopa - peripheral inhibitor of L-AAAD and does not cross the blood brain barrier
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16
Q

How does co-administering Carbidopa help with L-Dopa?

A

– increases half life in order of the dopamine to get into the CNS and fill up the vesicles

17
Q

What is the difference between Carbidopa and Entacapone?

A

Carbidopa – blocks peripheral L-AAAD

Entacapone – blocks peripheral COMT

18
Q

How are Tolcapone and Entacapone different?

A

Both inhibit COMT
Tolcapone – inhibits both peripheral and CNS COMT
- limits peripheral side effects of dopamine and increases half life
- Hepatotoxicity – must monitor
Entacapone – only inhibits peripheral COMT to help with side effects mostly

19
Q

What must be monitored when a patient is on Apomorphine?

A
  • can develop a Prolonged QT
20
Q

How can MAO Inhibitors help with Parkinson’s disease?

A
  • increases dopamine half-life in the body
  • decreases oxidative stressers from the breakdown
    • Can be used with L-Dopa in progressed disease
21
Q

What is a complication with using MAO inhibitors?

A
    • Tyramine builds up from random foods, which is usually broken down in the liver by MAO
    • Tyramine acts like NE causing sympathetic symptoms
    • Serotonin Syndrome – hyperthermia, agitation
22
Q

What do Selegiline and Rasagiline do?

A
  • MAO Inhibitors
  • irreversible
  • can be used at first diagnosis of Parkinson’s
23
Q

What can be used for Parkinson’s, if the patient has Glaucoma or Psychosis (contraindication for dopamine therapy)?

A

Anticholinergic Drugs (3rd line therapy)

  • Trihexyphenidyl
  • Benztropine
24
Q

What effects do Trihexyphenidyl and Benztropine have on Parkinson’s?

A
  • Since cholinergic neurons induce release of GABA to the globus palladus externa – preventing subthalamic inhibition
  • if you inhibit cholinergics, then can reduce subthalamic activation (on inhibiting thalamas)
25
Q

How can Amantadine help with Parkinson’s disease?

A
  • increases dopamine release from synapse
  • mild anti-cholinergic
  • blocks NMDA receptors
26
Q

When is Amantadine most commonly used?>

A

Given with L-Dopa when its effectiveness is wearing down and Amantadine can help the effects of it, but also diminishes over time as well

27
Q

If a patient has progressive chorea with several family members who have had similar symptoms, but ended up committing suicide, what might be the condition?

A

Huntington’s Disease

  • autodominant
  • chorea - too much movement
  • develop dementia over time and depression
28
Q

What is most characteristic genetic finding with Huntington’s Disease?

A
  • Huntingtin Gene mutation
29
Q

What is the finding of “Anticipation” within families with Huntinington’s diease consistent with?

A

Number of CAG repeats within the gene

– the most the repeats the earlier onset of the disease

30
Q

How does Huntington’s disease affect the basal ganglia?

A
  • Loss of Cholinergic Neurons in the Striatum -
    Thus, unable to inhibit the Globus Palladus Externa from constantly inhibiting the subthalamic nucleus (not allowing it to stop thalamus activation)
  • Unregulated Movement!
31
Q

What is the therapeutic solution to Huntington’s Disease?

A

Treat the Symptoms

  • Antidepressant – Fluoxetine
  • Tetrabenzine – inhibits VMAT from filling vessicles, so can help with the overactive basal ganglia
32
Q

If a patient notices that he has progressive weakness in his upper extremities, new onset difficulties with his vision and swallowing. What might be the most concerning diagnosis?

A

Amyotrophic Lateral Sclerosis

33
Q

What is the best treatment option for ALS?

A
  • Riluzole – can prolong life by a few months

- inhibits NMDA channels

34
Q

What are common symptoms associated with ALS?

A
  • LMN degradation – muscle atrophy, fasiculations
  • UMN degradation – loss of reflexes
  • CNS degradation – cranial nerves
35
Q

What are typical genetic and histologic findings with ALS?

A

Familial - Superoxide Dismutase Mutation

  • Accumulation of TDP-43
  • Atrophy of anterior spinal roots
  • degradation of multiple tracts in the spinal cord

Neurology (11 decks)

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