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Year 2 neuro exam 1 > Path XII > Flashcards

Path XII Flashcards

1
Q

synucleinopathy

A

parkinsons

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2
Q

lewy bodies

A

fibrils of insoluble polymers of alpha synuclein deposited in neuronal body and form lamellated eosinophilic cytoplasmic inclusions (lewy bodies)

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3
Q

lewy bodies are also found in what cells

A

astrocytes and oligodendrocytes

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4
Q

aggregates in parkinsons

A

alpha synuclein

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5
Q

lewy bodies cause what

A

neuronal degeneration and death

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6
Q

lewy bodies are found where in brain

A

all throughout

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7
Q

black color of substantia nigra can come from what

A

melanin in catecholaminergic cells

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8
Q

melanin granule color in lewy body

A

red brown

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9
Q

what stain would be + in substantia nigra neurons

A

GFAP for gliosis

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10
Q

second most common cause of dementia (not AD)

A

diffuse lewy body disease

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11
Q

diffuse lewy body disease combines what

A

dementia and parkinsonism

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12
Q

diffuse lewy body disease presentation

A

fluctuating attention and cognition and visual hallucinations
depression, sleep disorder and autonomic dysfunction

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13
Q

motor manifestations in diffuse lewy body disease

A

bradykinesia, rigidity, and less frequently tremor… may appear later

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14
Q

brain in diffuse lewy body disease

A

not atrophic

small inconspicuous lewy bodies in neocortex, limbic system and brainstem

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15
Q

circuits involved in multiple system atrophy MSA

A

1: striatonigral circuit (parkinsonism)
2: olivopontocerebellar circuit (ataxia)
3: autonomic nervous system including central elements (orthostatic hypotension as prominent component)

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16
Q

steele gray color of putamen

A

multiple system atrophy

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17
Q

are there lewy bodies in substantia nigra in multiple system atrophy

A

no

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18
Q

huntingtons

A

fatal autosomal dominant condition beings in 4th-5th decade of life

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19
Q

characterization of huntingtons

A

behavioral changes, chorea, dementia

Sx begin before age 20

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20
Q

areas affected by huntington

A

caudate and putamen

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21
Q

IHC stain for huntingonts

A

huntington protein or ubiquitin

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22
Q

aggregations in huntingtons

A

abnormal huntington protein (with ubiquitin)

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23
Q

aggregated huntington can cause what

A

taken up by neurons and suggests prion like spread from one neuron to another

24
Q

trineucleotide repeat disorder in huntingtons

A

CAG

increased glutamine

25
Q

gene for huntington

A

4p16.3 encodes protein huntingtin

more than 35 CAG copies assoc with disease

26
Q

type of transmission of CAG in huntingtons

A

paternal transmission

“anticipation” inc risk earlier onset in upcoming generations

27
Q

polyglutamine or polyQ

A

HD

because inc CAG which encodes glutamine or “Q”

28
Q

3 mechanisms of unstable repeats cause disease

A

loss of function from transcription silencing
toxic gain of function from alterations of protein structure
toxic gain of function mediated by mRNA like fragile X tremor ataxia syndrome

29
Q

gross image of HD brain

A

large ventricles and atrophy of caudate nuclei

30
Q

Tx HD

A

dopamine antagonists

genetic screening

31
Q

structure implicated in HD

A

degeneration GABA neurons of striatum-caudate nucleus

32
Q

hemibalismus affects what structure

A

subthalamic nucleus

contralateral hemorrhagic damage

33
Q

characteristics hemiballismus

A

violent, flinging movements usually involving an entire arm on one side

34
Q

chorea, dance like gait, athetosis, personality changes

A

HD

35
Q 
pill rolling tremor at rest
bradykinesia
masked facies
small movements
cogwheel rigidity
A

PD

36
Q

ALS affects what motor neurons

A

UMN and LMN

37
Q

LMN loss causes what

A

mm weakness, atrophy and fasciculations

38
Q

UMN involvement causes what

A

spasticity, clonus, hyperactive DTR and babinski sign

39
Q

when does dementia occur in ALS

A

onset or later

40
Q

what type ALS has worse prognosis

A

progressive bulbar palsy

41
Q

ALS patients die from

A

respiratory paralysis usually within 2-3 years Sx

42
Q

Dx ALS based on

A

clinical and electrodiagnositc findings and muscle biopsy

43
Q

Where does the degeneration in ALS occur

A

anterior horns and motor nuclei of brain stem

44
Q

what nuclei are specifically affected in ALS

A

hypoglossal nuclei, oculomotor, trochlear and abducens
medulla
open space at top where 4th ventricle is

45
Q

etiology of ALS

A

prion like spread misfolded proteins SOD-1 and TDP-43

46
Q

how do motor neurons die in ALS

A

wallerian degeneration with secondary gliosis

47
Q

Dx ALS

A

clinical: progression of weakness over mo

needle electromyography and nerve conduction studies

48
Q

3 groups ataxia

A

friedreichs ataxia
spinocerebellar ataxia
cerebellar ataxia

49
Q

friedreichs ataxia

A

autosomal recessive
GAA repeats on frataxin gene
spasticity weakness, sensory neurpathy, cardiomyopathy

50
Q

friedrichs ataxia seen in what age group

A

young kids <10

51
Q

death in friedrichs ataxia

A

CHF and arrhythmias

52
Q

spinocerebellar ataxias

A

autosomal dominant ataxias caused by CAG repeats on multiple chromosomal loci

53
Q

cerebellar ataxias

A

diverse group of sporadic diseases that cause cerebellar degeneration and degeneration of other anatomical systems

54
Q

friedreichs ataxia is what type disease

A

degenerative. not demyelinating

55
Q

what causes cerebellar ataxia in friedreichs

A

loss of sensory ganaglion cells and degeneration of axons in peripheral nerves, dorsal roots and posterior columns deprives cerebellum of sensory input

Year 2 neuro exam 1 (23 decks)

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