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Year 3 > MedEd chronic neuro > Flashcards

MedEd chronic neuro Flashcards

1
Q

what is MS

A

a chroninc inflammatory multifocal demyelinating disease of the CNS

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2
Q

what are RF for MS?

A

nordic origin/ living at high latitude
autoimmune disease
female gender

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3
Q

why are nordic people/those who live at high latitudes at risk for ms?

A

they get less vit D and vit D is protective of MS

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4
Q

what are the patterns of MS and which is most common

A

relapsing remitting is most common

there is also primary and secondary progressive

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5
Q

what are signs and symptoms of MS?

A 
optic neuritis
motor weakness
sensory disturbance 
faitgue 
hemiparesis 
lhermitte's sign- when they flex their leg forward they get an electric shock at the back of their neck
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6
Q

what sign is specific to MS, how do you ellicit it and what do you see?

A

lhermitte’s sign- when they flex their leg forward they get an electric shock at the back of their neck

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7
Q

how do you diagnose MS? what are the 3 catagories

A

absence of alternative diagnosis
dissemination in time
dissemination in space

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8
Q

what ix are done for MS? what will you see

A

hx
MRI with gadolinium contrast- old lesions are dark, new lesions are white
CSF- oligoclonal lesions in CSF but not in plasma
visually evoked potentials

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9
Q

what contrast is used in MRI for MS? why? what do you see?

A

gadolinium- it can show lesions over time
new lesions= white
old leasions= dark

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10
Q

what colour are old lesions on MRI in MS? explain why

A

dark- gadolinium leaks out of leaky capillaries so if there is an old lesion it won;t leak out as much

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11
Q

what colour are new lesions on MRI in MS? explain why

A

white- gadolinium leaks out of leaky capillaries so if there is an new lesion it leaks out a lot

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12
Q

what imaging is used in MS to see lesions?

A

MRI with gadolinium contrats

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13
Q

what is seen in csf in MS? where is this not seen?

A

oligoclonal bands

this is not seen in the serum

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14
Q

when you see an SBA about diagnosis of MS what should you think?

A

Which answer shows that there is both dissemination in time and in space?

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15
Q

what is MG?

A

autoantibodies against acetylcholine at neuromuscular jucntion

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16
Q

what antibodies are produced in MG?

A

anti acteylcholine

anti MuSK

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17
Q

what gland is often associated with MG?

A

thymus

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18
Q

who is more likely to get MG?

A

young women

old men

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19
Q

what are signs and symptoms for MG?

A 
ptosis
diplopia
dysathria
dysphagia
SOB
normal reflexes
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20
Q

what is the key defining feature about how muscles are affected in MG?

A

the more you use them the weaker they get

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21
Q

how do you differentiate MG from lambert eaton myasthenic syndrome?

A

there is hyperreflexia in LEMS but reflexes are normal in MG

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22
Q

what specific test can be done for MG, how is it done and what is seen?

A

simpson plus recovery test- you ask them to look up for 10 seconds then close thier eyes then open the eyes.

when they open the eyelids there will be ptosis in MG

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23
Q

what ix are done for MG? why are they done and what will you see?

A

bloods- anti acetyl and anti MuSK antibodies (these can be negative!!)
EMG- as you keep stimulating a nerve it will fire less and less as the condition is fatigueable
CT/MRI- to identify thymus involvement

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24
Q

what chronic neuro condition is the thymus associated with and involved in?

A

myasthenia gravis

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25
Q

what is MND?

A

build up of ubiquinated proteins in the cytoplasm causing muscle wasting and paralysis due to death os corticospinal tract

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26
Q

what is the prognosis of MND? how do people usually die?

A

3-4 years, due to resp failure

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27
Q

what are signs and symptoms of MND?

A 
progressive muscle weakness
dysphagia 
SOB
wasting of thenar muscles
wasting of tongue base
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28
Q

what is spared in MND?

A

oculumotor
sensory
autonomic function- no constipation etc

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29
Q

what are signs and symptoms of UMN lesions?

A 
spasticity 
hypereflexia
clonus
positive babinski's sign
paresis
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30
Q

what are signs and symptoms of LMN lesions?

A 
hypotonia
hyporeflexia
muscle atrophy
fasciculations and fibrillation
paresis
31
Q

what are the 3 types of parkinsonism? explain what they are

A

parkinsons disease
drug induced- symptoms of parkinsons disease but due to drugs not parkinsons disease pathophysiology
atypical parkinsonism- disorders that present like parkinsons disease but have different pathophysiolgy

32
Q

what is the pathophysiology behind parkisnons disease?

A

loss of dopaminergic neurones in the substantia nigra in the midbrain
misfolded alpha synuclein builds up
lewy bodies and lewy neurites

33
Q

where in the brain is the substantia nigra?

A

midbrain

34
Q

what are rf for parkinsons?

A

age
living in the countryside
genetic (fhx)

35
Q

what is the classic triad for parkinsons?

A

resting tremor
rigidity
bradykinesia

36
Q

what are the 6 ms of parkinsons?

A 
monotonous hypotnic speech
micrographia- small handwritting
march a petit pas- shuffling gait 
misery- depression
memory loss- dementia
hypomiMesis- lack of facial movement
37
Q

what type of rigidity is seen in parkinsons?

A

cogwheel

38
Q

how is huntigtons inheried?

A

autosomal dominant

39
Q

in what gene is there a mutation in huntingtons? what is the mutation?

A

HTT- expansion of CAG trinucleotide

40
Q

what is there atrophy of in the brain in huntingtons?

A

straitum

41
Q

what is the role of huntington for proteins?

A

It stabilises it and prevents apoptosis

42
Q

what are motor and cognitive symptoms of huntingtons?

A 
motor= chorea, athetosis, motor, dysphagia, ataxia 
cognitive= depression, personality change, lack of concentration, dementia
43
Q

what is the main motor symptom of huntingtons?

A

chorea

44
Q

what is the main ix for huntingtons?

A

CAG repeat testing

45
Q

how many CAG repeats do you need for huntingtons?

A

40 or more

46
Q

how does increasing cag repeats affect huntingtons?

A

higher cags= earlier onset and more severe disease

47
Q

what do you see on MRI in huntingtons?

A

straitum atrophy

48
Q

what is dementia?

A

severe loss of memory and other cognitive abilities leading to impaired daily function

49
Q

what are rf for dementia?

A 
increasing age
downs syndrome 
cardiovascular rf= hyperlipidaemia, hypertension
head trauma (sports eg heading the ball in football)
50
Q

what is pathophysiology in dementia?

A

build up of amyloid precursor protein
abnormal Abeta and gamma secretase is formed
extracellular amyloid plaques build up, intracellular neurofibrillary triangles made causing loss of neurones and synapses

51
Q

what is present intra v extracellularly in dementia and what does this cause?

A 
extracellular= amyloid plaques
intracellular= neurofibrillary triangles

both cause a loss in neurones and synapses

52
Q

what is protective of alzheimers?

A

exercise

education

53
Q

what are the 5 as of alzheimers?

A 
amnesia
anomia- cant name things (they know what a book is but they cant think of the word book when asked to say what it is)
apraxia- cant carry out normal tasks 
agnosia- cant recognise things 
aphasia- cant speak
54
Q

how is alzheimer’s diagnosed?

A

Clinically based on hx

55
Q

what would you see on csf in alzheimer’s?

A

high tau and low beta amyloid

56
Q

what ix might you do for alzheimers?

A

CT
MRI
PET

57
Q

what cognitive tests might be done for someone with alzheimers?

A

MMSE
addenbrooke’s cognitive assessment
MOCA

58
Q

what are signs and symptoms of frontotemporal dementia?

A 
personality change
disinhibition
overeating 
prefer sweet foods
emotional blunting 
relative preservation of memore
59
Q

in what type of dementia is there relative preservation of memory?

A

fronto temproal

60
Q

what is the pathophysiology behind vascular dementia?

A

tiny strokes and as the strokes occur it gets worse
affects small and medium vessels
this causes step wise progression

61
Q

what is progression of disease like in vascular dementia?

A

step wise progression

62
Q

what is another name for frontotemporal dementia?

A

picks disease

63
Q

what is picks disease?

A

fronto temporal dementia

64
Q

what is another name for MND?

A

ALS

65
Q

what is wernicke’s encephalopathy?

A

thiamine deficiency

66
Q

what are rf for wernicke’s encpehaloapthy?

A

alcoholism- decreases thiamine absorption and they eat less
malabsorption
bariatric surgery
dialysis- may dialyse the thiamine out

67
Q

what is there build up of in the brain in hepatic encephalopathy?

A

ammonia

68
Q

what is the triad for wernicke’s encephalopathy?

A

ataxia
eye signs
confusion

69
Q

what are signs and symptoms of wernickes encephalopathy?

A 
ataxia 
confusion
eye signs
alcoholism
malnourishment
70
Q

what are ix for wernickes encephalopathy?

A

Bloods- albumin, vit b1, LFTs
ECG
CT
neuropsychology- check if they are cinfused

71
Q

how serious is wernicke’s encephalopathy?

A

very it is a medical emergency and must be treated straight away

72
Q

what is korsakoff’s encephalopathy?

A

chronic wernicke’s encephalopathy

73
Q

how is korsakoff’s encephalopathy different to wernicke’s?

A

korsakoffs is chronic and there is no confusion

wernicke’s is acute and there is confusion

74
Q

what are signs and symptoms of korsakoff’s encephalopathy?

A

chronic and alert
amnesia and confabulation
irreversible

Year 3 (104 decks)

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