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Block 8 Week 5 Colt > Movement Disorders - Rothrock > Flashcards

Movement Disorders - Rothrock Flashcards

1
Q

Which pyramidal tract is involved in motor?

A

corticospinal tract

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2
Q

What are the extrapyramidal motor tracts.

A 
Basal ganglia
cerebellar
vestibulospinal
rubrospinal
"Mollaret's Triangle"
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3
Q

Parkinsonism is when ACh levels are far greater than (blank) levels

A

dopamine

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4
Q

Choreoathetosis is when Dopamine levels are far greater than (blank) levels

A

ACh

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5
Q

PD is a loss of dopaminergic neurons in the (blank) tract

A

nigrostriatal

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6
Q

PD leads to a shortage of DA in which circuit?

A

extrapyramidal motor cicrcuit

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7
Q

t/F: parkinsonism is the same thing as PD

A

false

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8
Q

What part of the substantia nigra is the primary victim of PD?

A

pars compacta

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9
Q

Where do the fibers of the pars compacta project?

A

to the corpus striatum which is made up of the caudate and putamen

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10
Q

what is the avg. age of onset of PD?

A

55 years

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11
Q

how does PD affect the sexes?

A

male:female 3:2

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12
Q

what percent of the nigrastriatal neurons are lost before the motor signs of parkinson’s emerge?

A

60-80%

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13
Q

what are the potential causes of PD?

A
  1. idiopathic
  2. genetic
  3. environ. toxins
  4. diet
  5. multiple causes
  6. alpha synuclein lewy bodies
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14
Q

what type of ACh receptors are overactivated in PD?

A

mACh which leads to increased GABA release

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15
Q

What is the acronym for the clincal signs of parkinsonism?

A

Tremor
Rigidity
Akinesia (or bradykinesia)
Postural changes (loss of righting reflex, stooped posture)

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16
Q

What is PD characterized by posturally?

A

stooped posture, EXAGGERATED FLEXION

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17
Q

What are the ancillary features of PD?

A 
sialorrhea (drooling)
micrographia
hypophonic speech with decreased inflection
slow thinking
subcortical dementia
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18
Q

Is PD characterized by symmetrical or asymmetrical movement?

A

asymmetrical

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19
Q

what are the drugs that increase DA levels?

A
  1. levodopa
  2. MAO-B inhibitors (rasagiline/Azilect)
  3. COMT inhibitors (entacapone/Comtan aka carbidopa)
  4. DM receptor agonists (Requip)
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20
Q

What is the other treatment option for PD that is not increasing DA levels?

A

anti-ACh

anitmuscarinics (Artane)

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21
Q

what is the most robust therapeutic for PD?

A

levodopa

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22
Q

How does levodopa enter the brain?

A

via the L-amino transporter

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23
Q

Can actual dopamine cross the BBB?

A

noooope

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24
Q

what is the issue with levodopa half life?

A

short; end-of-dose effect is common; peak-dose effect leads to hyperkinesia

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25
Q

What enzyme converts levodopa to Da?

A

L-amino acid decarboxylase (DOPA decarboxylase)

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26
Q

Where in the body is DOPA decarboxylase found?

A

peripheral tissue and in the brain!

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27
Q

Because of the presence of DOPA decarb’ase in the periphery, what do we give with L-DOPA and why?

A

carbidopa, a DOPA decarb’ase inhibitor that DOES NOT CROSS THE BBB to increase effective dose of L-DOPA reaching the brain

28
Q

what are the SE of levodopa?

A

N/V
orthostatic hypotension
hallucinations and distorted thinking
dyskinesias, fixed dystonias, choreoathetosis

29
Q

Amantadine promotes DA release from the…

A

substantia nigra

30
Q

In what severity of PD do you use amantadine?

A

early/mild cases of PD

31
Q

which DA increasing drug shows tachyphylaxis?

A

Amantadine; effects are short lived

32
Q

What are the SE of amantadine?

A

restlessness, insomnia, agitation
hallucinations and confusion
livedo reticularis (lacy purple skin discoloration)

33
Q

How do MAO-B inhibitors work?

A

inhibit DA metabolism; good for early/mild PD; use with levodopa/carbidopa for adv. PD

34
Q

What are the SE of MAO-B inhibitors?

A

confusion, hallucinations
Enhance DA SE (GI distress, dyskinesia) when taken with levodopa
Serotonin syndrome in pts taking SSRIs

35
Q

T/F: COMT is only found in the brain

A

false; found in brain and peripheral tissues

36
Q

What is the action of COMT?

A

converts levodopa to 3-O-methyldopa which competes with levodopa for transport into the brain

37
Q

T/F: COMT inhibitors can be used as monotherapy

A

false; used as adjunctive with levodopa

38
Q

Where do the COMT inhibitors work?

A

in the periphery so the levodopa can make it to the brain

39
Q

What are the SE of COMT inhibitors?

A

N/V
Urine discoloration (orange, red, brown, or black)
sleep disturbance

40
Q

DA receptor agonists activate which DA receptor?

A

D2 receptors

41
Q

What is the plus of using a DA receptor agonist over levodopa?

A

provider a smoother and more continuous receptor activation and rarely cause dyskinesia

42
Q

T/f: D2 agonists require functional DA neurons

A

false; that’s why they are good in adv. PD where there are few DA neurons!!

43
Q

T/F: D2 agonists can be used as monotherapy

A

true; in early cases of PD

44
Q

what’s the plus for using D2 agonists with levodopa?

A

decrease the “off” period and decreases the dose requirement

45
Q

What are the side effects of D2 receptor agonists?

A 
Dizziness and hallucinations
Impulse control disorders 
Hypotension 
Insomnia 
Nausea
46
Q

What completely unrelated dz are D2 agonists also indicated for?

A

restless leg lol

47
Q

which D2 agonist is a ergot alkaloid?

A

Parlodel

48
Q

Which D2 receptor agonist is used to treat neuroleptic malignant syndrome?

A

Parlodel

49
Q

What are the clinical signs of NMS?

A

rigidity, tremulousness, fever, autonomic instability (BP), agitation>delirium>coma

50
Q

plasma (blank) is elevated due to rhabdomyolysis from NMS

A

plasma CPK

51
Q

T/F: NMS progresses rapidly and requires aggressive tx

A

true

52
Q

What causes NMS?

A

typical antipsychotics like butyrophenones, phenothiazines, and promethazine
ALSO atypical antipsychotics

53
Q

mACh receptor agonists may improve tremor in early PD but have little effect on (blank and blank)

A

rigidity and bradykinesia

54
Q

What are the side effects of mACh receptor agonists?

A

dry mouth
urinary retention
confusion and memory impairment
(think opposite of SLUDGE syndrome)

55
Q

what is the treatment strategy for PD in pts younger than 65?

A
  1. more emphasis on long-term considerations
  2. start with D2 agonist
  3. add levodopa/carbidopa when agonist no longer sufficient
56
Q

What is the treatment strategy for older pts with PD?

A
  1. emphasis on providing symptomatic relief w/ few SE

2. use levodopa/carbidopa

57
Q

T/F: pts that only have mild tremor can go on anti-mACh monotherapy

A

true

58
Q

deep brain stimulation targets which two brain structures?

A

subthalamic nucleus and globus pallidus internus

59
Q

what is the target Sx for deep brain stim?

A

tremor; DBS less likely to help balance and gait
excessive off time
DA-responsiveness
Sig. dyskinesia with current meds

60
Q

t/F: initial trial of levodopa/carbidopa can be used to help confirm a PD Dx

A

true

61
Q

What drugs are the preferable initial rx?

A

D2 agonist and MAO-B inhibitors; especially in younger pts

62
Q

T/f: COMT inhibitors can be used in monotherapy

A

false; use w/ levodopa

63
Q

What are the signs of Progressive supranuclear palsy?

A 
impaired eye movements (vertical) -- doll's eye
axial rigidity
mild, slowly progressing dementia
dysphagia
refractory to PD meds
64
Q

Describe a physiologic tremor

A

Action tremor:

symmetric, high freq/low ampl; may involve speech; worse w/ fatigue, caffeine, exposure to cold; better w/ alcohol

65
Q

Describe an essential tremor

A

may involve the head; autosomal dom inheritance

66
Q

describe the parkinsonian resting tremor?

A

asymmetric, low freq/high amplitude; tends to spare speech and head

Block 8 Week 5 Colt (12 decks)

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