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Neuropathology Flashcards

(60 cards)

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1
Q

Histological changes in Alzheimer’s?

A 
Neuronal loss in cortex and hippocampus
Synaptic loss
Granulovascular degeneration
Senile plaques
Neurofibrillary tangles
Hirano bodies
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2
Q

What is granulovascular degeneration?

A

Small vacuoles with central granules in cytoplasm of neurons - particularly in temporal lobes

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3
Q

What cleaves beta A4?

A

Cleaved from amyloid-beta precursor protein by beta and gamma-secretases

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4
Q

How are neuritic plaques visualized?

A

Neurites visualized with silver stains.

May be seen as an eosinophilic mass on haematoxylin and eosin stains.

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5
Q

Diseases in which neuritic plaques are seen?

A

Normal ageing

Downs

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6
Q

What are neurofibrillary tangles composed of?

A

Cytoskeletal elements - primarily abnormally phosphorylated tau protein.

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7
Q

What stimulates formation of abnormal tau?

A

Beta A4 peptide interacts with cholinergic receptors, stimulating abnormal hyperphosphorylation of tau.

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8
Q

How can hyperphosphorylated tau be visualised?

A

Staining with antibody to abnormal tau

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9
Q

Which conditions do neurofibrillary tangles occur in?

A 
Alzheimers
Downs
Dementia pugilistica (punch-drunk syndrome)
Parinkson-dementia complex of Guam
Hallervorden-Spatz disease
Normal elderly
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10
Q

Structure of Hirano bodies?

A

Rod-shaped eosinophilic bodies n cytoplasm of neurons

Intracellular aggregates of actin and actin-associated proteins

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11
Q

Pathology of cerebral amyloid angiopathy?

A

Accumulation of A beta in walls of blood vessels, particularly arteries and arterioles in cerebral cortex overlying leptomeninges

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12
Q

What % of the elderly have Cerebral amyloid angiopathy?

A

30%

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13
Q

What % of patients with Alzheimer’s have Cerebral Amyloid Angiopathy?

A

90%

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14
Q

Relation between tangles and cognitive decline

A

Increase in number and distribution

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15
Q

Best neuropathological correlate of decline?

A

Number of synapses

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16
Q

Marker for synapses?

A

Antibody to synaptophysin, a protein found in presynaptic endings

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17
Q

What is Binswanger’s Disease?

A

Subcortical vascular dementia/subcortical arteriosclerotic encephalopathy
Many small infarctions of what matter that spares cortical regions.
Co-exists with Alzheimer’s-type changes

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18
Q

Histology of Lewy bodies?

A

Weakly eosinphilic
Spherical
Cytoplasmic inclusions

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19
Q

Correlation between number of Lewy bodies and cognitive decline?

A

None

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20
Q

What can we use to identify Lewy body?

A

Antibody to protease ubiquitin

Staining with alpha-synuclein antibodies

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21
Q

What do lewy bodies contain?

A

Accumulations of alpha-synuclein

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22
Q

What does alpha-synuclein do?

A

Accelerates reuptake of dopamine in neurons; this dopamine overload may be toxic

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23
Q

Where does microvacuolation occur in Lewy Body Dementia?

A

Microvacuolation of cerebral cortex, mainly in medial temporal region.

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24
Q

Name some tauopathies?

A

Alzheimers
Picks
Progressive supranuclear palsy
Corticobasal degenerations

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25
Name some synucleopathies?
Parkinsons Lewy Body Dementia Multisystem atrophy
26
Most common type of frontotemporal dementia?
Frontal lobe degeneration
27
Characteristics of Picks disease?
Prepronderance of atrophy in frontotemporal regions
28
What are Pick cells?
Abnormal swollen oval-shaped neuronal cells with loss of Nissl's substance and peripherally displaced nucleus
29
Most common form of CJD?
Sporadic
30
What is variant CJD related to?
Bovine spongiform encephalopathy
31
Which gene encodes prion protein?
On chromosome 20
32
What does PrPSc do?
Protease-resistant Accumulates in CNS Triggers conversion of normal PrPc to PrPSc
33
How can PrPSc be identified?
Immunoperoxidase staining
34
Pathology in vCJD?
Marked accumulation of prion protein | Plaques are florid
35
What protein is found in CSF in CJD
14-3-3
36
In which type of CJD are the EEG changes lacking?
Familial
37
In which type of CJD are 14-3-3 proteins absent?
Familial - <50%
38
Which phenotype of codon 129 at PrP is present in CJD?
M/M phenotype
39
What % of people with sporadic CJD have M/M phenotype?
73%
40
What % of people with variant CJD have M/M phenotype?
100%
41
Most supportive diagnostic test for CJD?
MRI
42
Which type of MRI most shows pulvinar sign?
FLAIR sequences of MRI
43
EEG signs in classic CJD?
Triphasic, sharp waves
44
Major HIV receptors?
CD4 | CD8
45
Source of CNS infection in HIV?
Infected CD4+ T cells and monocytes
46
Most commonly infected neurocells of HIV-1?
Perivascular macrophage and microglia
47
Which factors cause demyelination of oligodendrocytes?
Tumour necrosis factor
48
Which factors are neurotoxic and cause apoptosis of neuronal cells?
Platelet activating factor Quinolinic acid Nitric oxide Some metabolites of arachidonic acid
49
Most common psychiatric presentation in AIDs?
HIV-related dementia | Depression
50
What % of HIV-infected patients present with psychosis?
10%
51
Which tissue volume is reduced in schizophrenia
Thalamus | Temporolimbic structures including hippocampus, amygdala and parahyppocampal gyrus
52
What happens to basal ganglia in schizophrenia?
Reduced volume, particularly in preneuroleptic area in catatonic patients. Enlargement due to classic neuroleptics - reversed by atypicals
53
What is Heschl's gyrus?
Primary auditory cortex
54
Neuronal density in schizophrenia?
Increased, may relate o observed decrease in neuronal size, with decreased dendritic arborisation and decreased neuropil compartment.
55
Any cell number or size change in schizophrenia?
Reduced numbers and size in affecting neurons in hippocampus and DLPFC
56
Pathological changes of Wernickes?
Degenerative changes including gliosis, small haemorrhages in third ventricle and aqueduct and cerebellar atrophy
57
Where is small haemorrhage seen in Wernickes?
Mamillary bodies Hypothalamus Mediodorsal thalamic nucleus
58
Cell count changes in autism?
Lower Purkinje cell count
59
Neocortex changes in Autism?
Inconsistent changes - increased cortical volume possibly related to reduced pruning
60
Pathological changes in Autism?
Hypoplasia of cerebellar vemis and cerebellar hemispheres

Psychiatry (10 decks)

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