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CNS > Degenerative disease of the central nervous system > Flashcards

Degenerative disease of the central nervous system Flashcards

1
Q

what is the requirments for dementia

A

progressive, multiple domains of cogntiv fuction
loss of acquired skills and interference in occupation and society

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2
Q

what are the main types of late onset dementia - 65years plus

A

alzheimers - 55%
vascular - 20%
lewy body - 20%
other - 5%

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3
Q

what are the main signs of young onset demitia

A

alzheimers - 33%
vascular - 15%
frontotemporal - 15%
other - 33%

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4
Q

uncommon cuaes of demita

A

toxic - alchol
genetic - huntingtons
infection - hiv, cjd
inflammatory - ms

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5
Q

what are some treatable causes of dementia

A

b12 deficenties
endocrein - thryoid disease
infective - hiv syphilliis

tumour
hydrocephalus - is normal pressure
psedudodementia

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6
Q

main examinato for demai

A

cogative, neuroglica, vasucalr

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7
Q

infestaigaion for demetnai

A

ct, bloods, mri
csf, eeg, geetics

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8
Q

what screening tools can be used for dementai

A

mini mental
montreal

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9
Q

what are the ementail domians of dementia

A

memory, attention, languate, vistuospian, behvoru, emiotial ,e exentuive fucnit, apraxia, agnosias

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10
Q

main cluses in tup eof demtain of speed

A

speed fast ,- cjd
stepwize progseion - vasualr

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11
Q

what would you suspect if there is abnormal movemtn in demiea

A

huntiongtons

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12
Q

alzheimers is invovle dn what pathology

A

b amyloid plaques and neurofibrillary tangles

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13
Q

risk factor for alzheimers

A

genetic and enviromental

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14
Q

genees assoicated with alzymers

A

apoe, app, psen1, psen2

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15
Q

what are the clincal signs of dementia

A

memory distubances
languae and visuospacial problems
persoanly preserved until later

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16
Q

what are the patholgoy associated with frontal temporal dementia

A

tau - protein

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17
Q

how to detect tau protiens

A

in csf

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18
Q

what is the changes seen in frontalotempral dementai

A

dysphagia, memory changes, eating habits change,
good visospacl / memory, until later

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19
Q

what is the signs seen in dematia with lewy bodies

A

visulospatial and executive funciton decline
prominetn fluctuation
parkionsn and visual hallionsums

20
Q

what are lewy bodies made up of

A

a synuclein - these produce dopamine

21
Q

pharamlocil treatemtn for dementia

A

insomia treatment
behvioru - with antipycotiscs
depression

22
Q

what are the specific treatments for alzymers

A

cholinesterase inhibtor
- donepezil , rivastmien, galatamine
nmda angagoinss , mematine

23
Q

treatment for frontal temproal or vasuclar dementa

A

no

24
Q

what is requried for diganosis of parkingons

A

bradykinseas, rigidity, tremour, postural instabily - unsteadiness/ falls

25
Q

what are the main cuase of parkinos patholgy

A

dompaine loss
lewys bodies

26
Q

cuaes of parkinosn

A

drug induced - dopammine antagoins
idopathic
vascualr
parkinsons plus

27
Q

what are parkinsons plus syndomes

A

parkions with muliple system - demtia or yee problems
atropy or progesive suprnucler palsy - dyspahga , vision, palsy

28
Q

genes that are risk factor for parkons

A

lrrk2, parkin, gba

29
Q

when does tremor occur in parkinons

A

when the perons is at rest, ie not when arms are up

30
Q

what are the non motor signs of parkisinson

A

rem sleep behaviour disorder
autonomic dysfuciotn - urinary , bowel, sexual
neuropatic - hallucination , cogantive
depression, fatique pain

31
Q

what it the first nucleur effectd by parkins

A

putamen

32
Q

second nuclur effected by parkions

A

caudate

33
Q

treatmen for parkinson

A

levodopa
comt inhitors
Dopamine agonists
Monoamine oxidase-B inhibitors

34
Q

what is levodopa compined with

A

periphal decarboxylase ihitor to stop it being metabolised before reaching the rbain

35
Q

exmaples of periphalr decarboxylase inhibotr

A

carbidopa dn benserazide

36
Q

what is the sid eeffect of levodpa

A

dyskinase - exxcessive motr movemtns

37
Q

what are comt inhitors

A

They prent comt from metabolise levodopa in the body and the brian

38
Q

role of dopamine atnagoists

A

mimic dopaine adn stimaaltes domapine recpotrs

39
Q

downs side of dopamine agonsi

A

pulmonary firbosis

40
Q

examples of dopamine agonsi

A

bromocriptine, pergolide, cabergoline

41
Q

role of monoamine oxidase-B inhtor

A

block monoamine oxidase-B enzymes increasing circulating dopaimne

42
Q

examplesof monoamine oxidase b inhitors

A

selegilrine
rasagiline

43
Q

later complicaitn of parkins

A

hallunciation, impulse contorl
balance issues
demia - 50% after 10 years
gait freezing
swallowing issues

44
Q

neurosugy fo rpaksinon

A

deep brain stimulation

45
Q
A

CNS (36 decks)

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