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CNS II > Parkinson/Dementia TBL > Flashcards

Parkinson/Dementia TBL Flashcards

(PH-1) Describe rationale for and the mechanism of action of L-dopa and L-dopa plus carbidopa in the treatment of Parkinson disease, list their side effects, and describe the motor fluctuations observed in patients receiving these medications (PH-2) List the prototype indirectly-acting dopamine agonists used in the treatment of Parkinson disease, describe their mechanism of action, and list their major side effects (PH-3) List the prototype MAO and COMT inhibitors used in the treatment of Park

1
Q

MOA of Levadopa

A

converted to dopamine by DOPA decarboxylase

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2
Q

Why can’t dopamine just be given?

A

dopamine has low bioavailability and cannot cross BBB

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3
Q

enzyme that converts Levadopa to dopamine

A

DOPA decarboxylase

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4
Q

reason for giving carbidopa with levadopa

A

inhibits DOPA decarboxylase in the periphery, reducing side effects, increasing plasma half-life of levadopa

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4
Q

main effect of levadopa

A

reduces bradykinesia

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5
Q

dope dependant effects of Levadopa

A

GI problems, postural hypotension and rarely heart problems

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6
Q

main frequent side effects of Levadopa

A

dyskinesias (chorea, ballismus, myclonus, tics, tremor) anxiety, agitation, delusions, depression

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7
Q

conditions for which levadopa is contraindicated

A

hx of psychosis

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8
Q

bromocriptine class

A

partial D2 agonist

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9
Q

pramipexole class

A

partial D2 agonist

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10
Q

ropoinirole class

A

partial D2 agonist

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11
Q

most common movement SE in levadopa

A

choreoathosis of face and distal extremities

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12
Q

apomorphone

A

partial D2 agonist

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13
Q

bromocriptine use

A

pts refractory or cannot tolerate lavedopa

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14
Q

SE of bromocriptine

A

postural hypotension, arrythmias, dyskinesias, mental status changes

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15
Q

first line drugs in early onset PD

A

pramipexole, ropinirole

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16
Q

SE of pramipexole, ropinirole

A

Anorexia, n/v, dyskinesias, sleepiness and fatiuge

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17
Q

drug that should be reduced in renal dysfunction

A

pramipexole

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18
Q

drug taht may interact with caffiene and warfarin

A

ropinirole

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19
Q

drug with D3 affinity

A

pramipexole

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20
Q

subQ injectable PD drug

A

apomorphine

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21
Q

temporary relief of “off periods:

A

apomorphine

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22
Q

PD drug causing severe nausea

A

apomorphine

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23
Q

PD drug that only is effective for a few weeks

A

amantadine

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24
Q

PD drug causing lace like face rash

A

amantadine

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25
Q

PD drug that can cause acute toxic psychosis

A

amantadine

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26
Q

seleglinine MOA

A

increases dopamine, by inhibiting MAO B - which metabolizes dopamine to NE and serotonin

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27
Q

metabolizes dopamine to NE and Serotonin

A

MAO B

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28
Q

used as adjunct to levaopa or alone in new pts

A

seleglinine

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29
Q

SE of seleglinine

A

insomnia, GI issue,

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30
Q

PD drug that can cause serotinin syndrome

A

selegiline

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31
Q

bad serious drug interaction with selegiline

A

meperidine

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32
Q

COMT inhibitors

A

entacapone and tolcapone

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33
Q

adjunct to levadopa to improve “on-time”

A

COMT inhibitors

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34
Q

SE of COMT inhibitors

A

dyskinesia, GI distress and postural hypotension, orange urine

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35
Q

increases liver enzymes and can cause actute liver failure

A

tolcapone

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36
Q

MOA of antimuscarinic drugs in PD

A

decrease exititory cholinergic neurons in striatum by blocking muscarinic receptors

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37
Q

antimuscarinic PD drugs

A

benzotropine, trihexyphenidyl

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38
Q

SE of antimuscarinic PD drugs

A

drowsiness, inattention, confusion, hallucinations, atropine like effetcs

39
Q

PD drugs that increase tardive dyskinesias form AP drugs

A

antimuscarinic PD drugs

40
Q

Alzeheimer cholinesterase inhibitor drugs (3)

A

donepezil, rivastigmine, galantamine

41
Q

SE of Alzeheimer cholinesterase inhibitor drugs

A

n/v, diarrhea, vomiting, anorexia, weight loss

42
Q

reason for Alzeheimer cholinesterase inhibitor drugs

A

to address defict of ACh in brain

43
Q

MOA of menantine

A

blocks NMDA receptor that binds glu

44
Q

use of menantine

A

moderate to severe Alzheimer’s

45
Q

drug class to use in treating depression in alzheimer’s

A

SSRI

46
Q

cardinal features of PD

A

tremor at rest , bradykinesia, rigidity

47
Q

late feature of PD

A

postureal instability

48
Q

motions to clicially observe bradykinesia

A

finger tapping, hand gripping, pronation/supination hand movements, heel ot toe tapping

49
Q

main way to distinguish movement sx in PD from others

A

PD usually begins one sided and remains stronger on that side as it procedes bilateraly

50
Q

test for rigidity

A

pasivly manipulating the limbs

51
Q

test of postural rigidity

A

“pull test”

52
Q

PD sx least responsive to dopaminergic therapies

A

postural instability

53
Q

nonmotor sx of PD

A

dementia, psychosis, hallucinatiions, mood disorders, sleep problems, autonomic dysfunction, pain and sensory disturbances

54
Q

nonmotor sx of PD that can predict mortality

A

congnitive dysfunction and mortality

55
Q

PD sx that can predict onset of dementia

A

older age, severity of motor sx, hallucinations, depression, FMX of dementia

56
Q

type of dementia in PD

A

subcortical

57
Q

sx of subcortical dementia

A

psychomotor retardation, memory difficulty, alterned personality

58
Q

dementia normally found in alzheimer’s but not PD

A

aphasia/apraxia

59
Q

main neuropathologic finding in PD

A

lewy bodies, as well as amyloid plaques.neurofibrillary tangles

60
Q

ddx of PD when motor and dementia sx occur at onset

A

lewy body dementia

61
Q

imaging study that should be done in suspected PD

A

MRI to rule out structural abnormalities

62
Q

dx criteria of PD

A

bradykinesia and either tremor and/or rigidity. response to dopaminergic therapy, rest tremor and asymetric sx

63
Q

non drug thereapy for PD

A

exercise, speech therapy, nutrition counseling

64
Q

histoligic findings in Alzheiners

A

Beta - amyloid plaques and neurofibrillary tangles

65
Q

protein found in CSF of alzheimer’s pts

A

tau

66
Q

genetic polymorphism in alzeheimer’s

A

APOE on chromosome19

67
Q

diognostic criteria of Alzheimer’s

A

1) short-term memory impairment,
2) one or more of:
- aphasia
- apraxia
- agnosia
- disturbance in executive functionin
3) gradual onset and continuing cognitive decline
4) not due to another underlining disease

68
Q

age determining early.late onset alzheimer’s

A

65

69
Q

sx of Lewy body dementia

A

parkinsonion sx, dementia, visual hallucinations, rapid course

70
Q

histologic finding in Lewy body dementia

A

eosinophilic inclusion bodies in cerebral cortex and brainstem

71
Q

drugs NOT to give in Lewy Body dementia

A

conventional Anti-psychotics

72
Q

histopathology of frontotemporal dementia

A

tau-positive inclusions

73
Q

sx of frontotemporal dementia

A

disinhibtion and shallow effect OR early and progressive loss of expressive launguage and severe naming difficulties

74
Q

sx of huntingtons

A

psych - depression, anxiety, irritability, hallucinations, delusions. Physical sx of chorea

75
Q

sx of CJD

A

rapidly progressing dementia with severe cerebellar/extrapyramidal signs and myoclonus

76
Q

type of CJD with longer course

A

vCJD

77
Q

medical conditions that can mimic dementia

A

diseases of basal ganglia, cerebellum degeneration, encephalitis, MS, Wilson’s disease, neuronal storage disease

78
Q

treatable causes of demantia

A

vascular disorders, normal pressure hydrocephalus, infections, metabolic disorders, nutritional disorders

79
Q

imaging findings in dementia

A

cortical atrophy and enlarged ventricles

80
Q

score on MMSE suggestive of imparment

A

25/30

81
Q

score on MMSE definitive for impairment

A

20/30

82
Q

early behavioral stages of dementia sx

A

sugtle change in personality, decrease in interests, apathy and labile emotions, slight loss of high performance function

83
Q

middle behavioral stages of dementia sx

A

early changes more pronounced, possible psychosis, poor insight

84
Q

advanced sx of dementia

A

imability to perform tasks of daily living, incontenince, extreme emotional lability, inability to recognize friends and relatives

85
Q

end stage of dementia sx

A

mute and unresponsive, death within a year

86
Q

noncog sx of dementia

A

hallucinations and dementia, depression,

87
Q

ddx to lead to depression rather than dementia

A

recent weight loss, worsening sleep, crying, self-deprecating comments, social withdrawal, psychomotor agitation and negativism

88
Q

imagint that can be used to identify type of dementia

A

PET

89
Q

PET findings in alzheimer’s

A

temporal and parietal hypometabolism

90
Q

drug used for younger PD pts

A

Ropinerole, pramipexole

91
Q

addition to L-dopa when it starts not to work as well

A

entacapone

92
Q

how many substantia nigra neurons need to be lost to have PD sx

A

80%

93
Q

Ropinirole acts mainly on

A

the post-synaptic neurons in the indirect nigrostriatal pathway

94
Q

PD drug acting mainly in the periphery

A

entacapone

CNS II (25 decks)

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