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neurology > pathology III > Flashcards

pathology III Flashcards

1
Q

Dementia triad

A

Aphasia, apraxia, agnosia

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2
Q

What is apraxia

A

inability to perform preprogrammed motor tasks

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3
Q

What is agnosia?

A

inability to correctly interpret senses -cant recognize people, full bladder, pain

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4
Q

Presentation of parkinsons disease

A 
tremor
rigidity
akinesia (or bradykinsea)
postural instability
shuffling gait
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5
Q

Which drug contaminant presents similarly to parkinsons disease?

A

MPTP - metabolized to MPP+ which is toxic to substantial nigra

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6
Q

histological findings of parkinsons disease

A

loss of dopaminergic neurons of substantia nigra pars compacta AND lewy bodies

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7
Q

What are lewy bodies?

A

intracellular eosinophilic inclusion composed of alpha-synuclein seen in Parkinson disease

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8
Q

Cause of huntingtons disease

A

Autosomal dominant trinucleotide repeated (CAG) expansion gene on chromosome 4

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9
Q

Symptoms of huntingtons disease

A

chorea, athetosis, aggression, depression, dementia

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10
Q

pathophys of huntingtons

A

Increased dopamine, decreasd GABA and Ach

Neuronal death via NMDA-R binding and glutamate excitotoxicity

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11
Q

Gross findings in huntington disease

A

Atrophy of caudate and putamen with ex vacuo ventriculomegaly

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12
Q

Why do down syndrome patients have increased risk of Alzheimer disease?

A

APP is located on chromosome 21

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13
Q

ApoE2 is associated with..

A

DECREASED risk of the sporadic form of Alzheimers

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14
Q

ApoE4 is associated with…

A

INCREASED risk of the sporadic form of Alzheimers

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15
Q

What are the familial altered proteins seen in Alzheimers disease

A

APP, presenilin-1, presenilin-2

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16
Q

Gross findings of Alzheimers

A

widespread cortical atrophy especially in the hippocampus. Narrowing of gyri and widening of sucli

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17
Q

Histological findings of alzheimers

A

senile plaques in gray matter: extracellular B-amyloid core; may cause amyloid aniopathy ->intracranial hemorrhage
Neurofibrillary tangles: intracellular hyperphosphorylated tau protein

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18
Q

What are neurofibrillary tangles

A

intracellular hyperphosphorylated tau protein - insoluble cytoskeletal elements; number of tangles correlates with degree of dementia

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19
Q

frontotemporal dementia aka

A

picks disease

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20
Q

presentation of frontotemporal dementia

A

Early chagnes in personality and behaviour (behavioural variant) or aphasia

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21
Q

Gross findings of frontotemporal dementia

A

frontotemporal lobe degeneration

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22
Q

Histological findings of frontotemporal dementia

A

inclusions of hyperphosphoryalted tau (round pick bodies) or ubiquinated TDP-43

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23
Q

Lewy body dementia presentation

A

visual hallucinations, dementia with fluctuating cognition/alerntess, REM sleep behaviour disorder and parkinsonism

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24
Q

histological findings of lewy body dementia

A

intracellular lewy bodies primarily in cortex

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25
Q

vascular dementia presentation

A

multiple arterial infarcts or chronic ischemia lead to a stepwise decline in cognitive ability with late-onset memory impairment

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26
Q

MRI/CT findings of vascular dementia

A

multiple cortical and/or subcortical infarcts

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27
Q

Creutzfeldt-Jakob disease presentation

A

Rapidly progressive dementia with myoclonus and ataxia

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28
Q

What will you see on an EEG of Creutzfeldt-Jakob disease?

A

periodic sharp waves

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29
Q

What will you find in the CSF of someone with Creutzfeldt-Jakob disease?

A

increased 14-3-3 protein

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30
Q

gross findings of Creutzfeldt-Jakob disease?

A

spongiform cortex

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31
Q

histological findings of Creutzfeldt-Jakob disease?

A

Prions (PrPc->PrPsc sheet results in beta pleated sheet resistant to proteases)

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32
Q

Idiopathic intracranial hypertension aka

A

pseudotumour cerebri

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33
Q

risk factors for idiopathic intracranial hypertension

A

female, tetracyclines, obesity, vitamin A excess, danazol

34
Q

clinical findings of idiopathic intracranial hypertension

A

headache, tinnitus, diplopia, no change in mental status.

Impaired optic nerve axoplasmic flow - > papilloedema.
Enlarged blind spot and peripheral constriction.

Lumbar puncture with increased opening pressure that provides temporary relief of headaches

35
Q

treatment of idiopathic intracranial hypertension

A

weight loss, acetazolamide, invasive procedures for refractory cases (CSF shunt, optic nerve sheath fenestration surgery)

36
Q

What causes communicating hydrocephalus?

A

Decreased CSF uptake from arachnoid granulations (eg. arachnoid scarring post-meningitis)

37
Q

Presentation of communicating hydrocephalus

A

Increasd ICP, papilledema, herniation

38
Q

Presentation of normal pressure hydrocephalus

A

urinary incontenence, gait apraxia, cognitive dysfunction

39
Q

Treatment of normal pressure hydrocephalus

A

CSF shunt placement

40
Q

What causes normal pressure hydrocephalus?

A

Usually idiopathic, but expansion of the ventricles results in distortion of the fibers in the corona radiata

41
Q

What causes noncommunicating hydrocephalus?

A

structural blockage of CSF

42
Q

Ex vacuo ventriculomegaly presentation

A

Appearance of increased CSF on imaging but its ACTUALLY due to decreased brain tissue and neuronal atrophy

43
Q

Causes of ex vacuo ventriculomegaly

A

azheimers, advanced HIV, pick disease, huntington disease

44
Q

Presentation of aquaductal stenosis

A

enlarging head circumference

45
Q

Aquaductal stenosis cause

A

X-linked congenital narrowing

Can be from inflammation in utero

46
Q

What is multiple sclerosis?

A

autoimmune inflammation and demyelination of CNS with axonal damage

47
Q

Possible presentations of multiple sclerosis

A

Acute optic neuritis
Brain stem/cerebellar syndromes
Pyramidal tract demyelination
Spinal cord syndromes

48
Q

How does acute optic neuritis present?

A

painful unilateral vision loss associated with Marcus Gunn pupil

49
Q

How do spinal chord syndromes present?

A

electric shock-like sensations, neurogenic bladder, paraparesis, sensory manifestations

50
Q

Who is multiple sclerosis most common in?

A

Women aged 20 to 30 and farm from the equator

51
Q

Symptoms of multiple sclerosis may present with what?

A

increased body temp (hot back, exercise)

52
Q

findings in CSF of someone with multiple sclerosis

A

Increased IgG level and myelin basic protein

Oligoclonal bands - DIAGNOSITC

53
Q

What will be seen on MRI of someone with MS?

A

periventricular plaques and multiple white matter lesions disseminated in space and time

54
Q

Treatment of multiple sclerosis

A

Disease modifying therapies - B-interferon, glatiramer, natalizumab.
Treat acute flares with IV steroids.
Symptomatic treatment for neurogenic bladder, spasticity and pain

55
Q

What is cerebral amyloid angiopathy?

A

Recurrent hemorhagic strokes from B-amyloid deposits in artery walls (that make them weak and prone to rupture)

56
Q

Osmotic demyelination syndrome aka

A

Central pontine myelinosis

57
Q

Pathophys of osmotic demyelination syndrome?

A

massive axonal demylination in pontine white matter secondary to rapid osmotic changes - most commonly from correction of hyponatremia but can be from shifts of other osmolytes

58
Q

Presentation of osmotic demylination syndrome

A

acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness - causes locked in syndrome

59
Q

if you raise sodium too fast what happens?

A

osmotic demyelination syndrome

60
Q

if you decrease sodium too fast what happens?

A

cerebral edema/herniation

61
Q

most common type of acute inflammatory demyelinating polyradiculopathy

A

guillain-barre syndrome

62
Q

What cell type is destroyed in GBS?

A

Schwann cells

63
Q

Pathophys of GBS

A

autoimmune destruction of schwann cells via inflammation and demyelination of motor fibers, sensory fibers, peripheral nerves. Facilitated by molecular mimicry and triggered by inoculations or stress.

64
Q

GBS may be associated to which pathogen?

A

Campylobacter jejuni

65
Q

Presentation of GBS

A

symmetric ascending muscle weakness/paralysis and depression/absent distal tendon reflexes
Facial paralysis and respiratory failure common
May present with autonomic dysregulation (cardiac irregularities, hypertension, hypotension) or sensory abnormalities.

66
Q

CSF findings in GBS

A

increased protein with normal cell count (albuminocytologic dissociation)

67
Q

Treatment of GBS

A

respiratory support is critical until recovery. Disease-modifying treatment; plasmapheresis or IV immunoglobulins.

68
Q

Acute disseminated (postinfectious) encephalomyelitis pathophys

A

Multifocal inflammation and dyemylination after infection or vaccination

69
Q

Presentatino of acute disseminated (postinfectious) encephalomyelitis

A

rapidly progressive multifocal neurologic symptoms and latered mental status

70
Q

Charcot-Mari-Tooth disease aka

A

hereditary motor and sensory neuropathy

71
Q

Deformities seen in Charcot-Mari-Tooth disease?

A

pes cavus, hammer tow

72
Q

other symptoms seen in Charcot-Mari-Tooth disease?

A

foot drop/lower extremity weakness and sensory deficts

73
Q

What causes Charcot-Mari-Tooth disease?

A

Autosomal dominant disorder caused by defective production of proteins involved in peripheral nerves

74
Q

Most common type of Charcot-Mari-Tooth disease?

A

CMT1A

75
Q

Mutation in CMT1A?

A

PMP22 gene duplication

76
Q

What is progressive multifocal leukoencephalopathy?

A

demylination of CNS due to destruction of oligodendrocytes (from reactivation of JC virus)

77
Q

Which virus causes progressive multifocal leukoencephalopathy?

A

JC virus

78
Q

Which population gets progressive multifocal leukoencephalopathy?

A

aids patients with CD4 <200

79
Q

outlook of progressive multifocal leukoencephalopathy?

A

Rapidly progressive and usualyl fatal

80
Q

which brain areas are involved in progressive multifocal leukoencephalopathy?

A

parietal and occipital - visual symtpoms common

81
Q

which drug is associated with progressive multifocal leukoencephalopathy?

A

natalizumab

neurology (9 decks)

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