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Psychiatry > Neuropathology > Flashcards

Neuropathology Flashcards

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
Q

Name some synucleopathies?

A

Parkinsons
Lewy Body Dementia
Multisystem atrophy

26
Q

Most common type of frontotemporal dementia?

A

Frontal lobe degeneration

27
Q

Characteristics of Picks disease?

A

Prepronderance of atrophy in frontotemporal regions

28
Q

What are Pick cells?

A

Abnormal swollen oval-shaped neuronal cells with loss of Nissl’s substance and peripherally displaced nucleus

29
Q

Most common form of CJD?

A

Sporadic

30
Q

What is variant CJD related to?

A

Bovine spongiform encephalopathy

31
Q

Which gene encodes prion protein?

A

On chromosome 20

32
Q

What does PrPSc do?

A

Protease-resistant
Accumulates in CNS
Triggers conversion of normal PrPc to PrPSc

33
Q

How can PrPSc be identified?

A

Immunoperoxidase staining

34
Q

Pathology in vCJD?

A

Marked accumulation of prion protein

Plaques are florid

35
Q

What protein is found in CSF in CJD

A

14-3-3

36
Q

In which type of CJD are the EEG changes lacking?

A

Familial

37
Q

In which type of CJD are 14-3-3 proteins absent?

A

Familial - <50%

38
Q

Which phenotype of codon 129 at PrP is present in CJD?

A

M/M phenotype

39
Q

What % of people with sporadic CJD have M/M phenotype?

A

73%

40
Q

What % of people with variant CJD have M/M phenotype?

A

100%

41
Q

Most supportive diagnostic test for CJD?

A

MRI

42
Q

Which type of MRI most shows pulvinar sign?

A

FLAIR sequences of MRI

43
Q

EEG signs in classic CJD?

A

Triphasic, sharp waves

44
Q

Major HIV receptors?

A

CD4

CD8

45
Q

Source of CNS infection in HIV?

A

Infected CD4+ T cells and monocytes

46
Q

Most commonly infected neurocells of HIV-1?

A

Perivascular macrophage and microglia

47
Q

Which factors cause demyelination of oligodendrocytes?

A

Tumour necrosis factor

48
Q

Which factors are neurotoxic and cause apoptosis of neuronal cells?

A

Platelet activating factor
Quinolinic acid
Nitric oxide
Some metabolites of arachidonic acid

49
Q

Most common psychiatric presentation in AIDs?

A

HIV-related dementia

Depression

50
Q

What % of HIV-infected patients present with psychosis?

A

10%

51
Q

Which tissue volume is reduced in schizophrenia

A

Thalamus

Temporolimbic structures including hippocampus, amygdala and parahyppocampal gyrus

52
Q

What happens to basal ganglia in schizophrenia?

A

Reduced volume, particularly in preneuroleptic area in catatonic patients.
Enlargement due to classic neuroleptics - reversed by atypicals

53
Q

What is Heschl’s gyrus?

A

Primary auditory cortex

54
Q

Neuronal density in schizophrenia?

A

Increased, may relate o observed decrease in neuronal size, with decreased dendritic arborisation and decreased neuropil compartment.

55
Q

Any cell number or size change in schizophrenia?

A

Reduced numbers and size in affecting neurons in hippocampus and DLPFC

56
Q

Pathological changes of Wernickes?

A

Degenerative changes including gliosis, small haemorrhages in third ventricle and aqueduct and cerebellar atrophy

57
Q

Where is small haemorrhage seen in Wernickes?

A

Mamillary bodies
Hypothalamus
Mediodorsal thalamic nucleus

58
Q

Cell count changes in autism?

A

Lower Purkinje cell count

59
Q

Neocortex changes in Autism?

A

Inconsistent changes - increased cortical volume possibly related to reduced pruning

60
Q

Pathological changes in Autism?

A

Hypoplasia of cerebellar vemis and cerebellar hemispheres

Psychiatry (10 decks)

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