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3C week 1- intro to neuro and opthal > neuropathology > Flashcards

neuropathology Flashcards

1
Q

what structure is contained within the internal capsule

A

cortical spinal tract

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2
Q

why are neurons highly sensitive cells (destruction)

A

they have a high metabolic demand and so are sensitive to metabolic changes

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3
Q

can mature neurons undergo cell division

A

no

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4
Q

what is gliosis

A

proliferation of astrocytes (in response to injury)

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5
Q

function of astrocytes (2)

A

preserve CSF barriers, gliosis

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6
Q

role of oligodendrogytes

A

myelination

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7
Q

role of empendymal cells

A

help csf movement via use of cillia

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8
Q

role of microglia

A

immune system (turn into mobile phagocytes)

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9
Q

where are the most sensitive cells in the brain

A

pyramidal cells in CA1 (hipp.)

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10
Q

what type of cells are commonly seen in the cerebellum

A

purkinje cells

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11
Q

when might laminar necrosis occur

A

when there is damage to layers III,V,VI of the neo cortex

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12
Q

what is cerebral vascular disease

A

a neurological defecit due to cerebrovascular compromise

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13
Q

what causes the majority of cerebral vascular disease

A

ischaemia (85%)

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14
Q

what are the 2 most common causes of global hypoxia

A

severe hypotension; cardiac arrest

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15
Q

what type of necrosis is seen in ischaemic stroke

A

liquefactive necrosis

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16
Q

what are red neurons

A

eosinophillic neurons that are dying (degredation of nucelus and nissel bodies) as a result of ischemia

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17
Q

6 most common causes of intercerebral haemorrhages

A
  1. hypertension
  2. cerebral amyloid angiopathy
  3. saccular aneursms
  4. vascular malformations
  5. tumours
  6. vasculitis
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18
Q

what 4 brain areas are the most common for ICH to occurwhen due to HTN

A
  1. putamen
  2. thalamus
  3. cerebellum
  4. pons
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19
Q

what are the layers surroudning the brain (inner to out - 7)

A
  1. pia mater
  2. arachnoid mater
  3. dura mater
  4. bone
  5. periosteum
  6. aponeurosis
  7. skin
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20
Q

after passing under what structure does the anterior middle meningeal artery split

A

pterion

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21
Q

what is the pterion

A

junction between the frontal, parietal, greater sphenoid and squeamous temporal bone

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22
Q

why is the pterion clinically significant (2)

A

is is the weakest point in the skull => easy to fracture which can cause a bleed in the MMA and lead to epidural haemorrhage

also may be an acess point during surgery

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23
Q

epidural vs subdural haematoma

A

epi - does not cross suture line, suually associated w pterion skull fracture
sub - crosses suture line, may involve venous blood

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24
Q

what 4 type of haemorrhages can arise from traumatic vascular injury

A
  1. extradural
  2. subdural
  3. subarachnoid
  4. intraparenchymal
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25
Q

what are coup and contrecoup injuries

A

injuries that arise from the head hitting a surface hard causing forces to be trasmitted through the brain (coup) and then for the brain to rebound off the other side of the skull (contrecoup)

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26
Q

what injury is commonly seen in motor vehicle accidents

A

diffuse axonal injury

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27
Q

how does diffuse axonal injury occur

A

cerebrum pivots around the brainstem which causes the axons to stretch

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28
Q

what does the stretching of axons in diffuse axonal injury cause

A

stretched axons causes changes in the axonal cytoskeleton such as compacting microtubules; fast axonal flow is also halted

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29
Q

what common injury is a type of diffuse axonal injury

A

concussion - a mild non permaent axonal injury

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30
Q

what do axons release iin response to injury

A

BAPP

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31
Q

what is brain herniation

A

displacement of the brain due to mass effect

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32
Q

what is tonsillar herniation

A

displacement of the cerebellar tonsils into the foramen magnum compressing the brainstem causing cardio-respiratory arrest

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33
Q

what is subfalcine herniation

A

displacement of the cingulate gyrus compressing the ACA and causing infarction

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34
Q

what is uncal herniation and what can it lead to (3)

A

displacement of the temporal lobe uncus
can lead to:
1. CN III compression
2. PCA compression
3. Paramedian artery rupture (brainstem haemorrhages)

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35
Q

what cells myelinate the CNS and PNS

A

CNS - oligodendrocytes
PNS - schwaann

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36
Q

what is the most common demyelinating disorder

A

multiple sclerosis (see DM)

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37
Q

what syndrome is related to MS but occurs in the PNS

A

Guillain-Barre syndrome

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38
Q

what to myelin plaque look like in the brain

A

irregular, sharply demarcated plaques

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39
Q

what is the most severe consquence of measles

A

subacute sclerosing panencephalitis (long latency period)

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40
Q

what is progressive multifocal leukoencephalopathy

A

rapidly progressing destruction of oligodendrocytes arising from an infection (JC virus) to these cells; the virus is generally harmless unless immunocomprimised

41
Q

what is central pontine myelinolysis

A

destruction of myeling arising due to the rapid correction of a Na+ defecit (e.g.in severely malnoursished ppl) - this will lead to dehydration of the brain cells

42
Q

what causes leukodystrophies

A

mutations in the myelin producing enzymes

43
Q

what is an example of a leukodystrophy

A

adrenoleukodystrophy (ALD)

44
Q

how can ALD be tested for

A

looking for the presence of long chain fatty acids in the blood

45
Q

what is the most common leukodystrophy

A

metachromatic leukodystrophy - accumulation of fats in oligodendrocytes due to malfunction of enzyme

46
Q

why are acquired metabolic/toxic brain disorders common

A

due to the high metabolic demand of the brain

47
Q

what effect can B12 deficiency have on the CNS

A

subacute combined degeneration of the spinal chord

48
Q

what defines a NDD and what are the 3 main function impacted in these characters of diseases

A

progressive loss of neurological function characterised by neuronal loss and protein accumulation
1. dementia
2. loss of motor control
3. paralysis

49
Q

what is hydrocephalus ex vacuole

A

shrinking of brain matter (thinning of gyri and widening of sulci seen)

50
Q

what are the 4 pathological feature seen in AD

A
  1. TAU neurofibrillary tangles
  2. senile plaques (β-amyloid)
  3. granular vacuole degeneration
  4. cerebral amyloidangiopathy (can lead to ICH)
51
Q

what is the normal function of TAU

A

microtubule association protein that stabilizes neuronal microtubules (this is lost in AD)

52
Q

what is the second most common cause of dementia

A

vascular dementia

53
Q

what can cause vascular dementia to arise (4)

A

arises from a multifocal infarction due to:
hypertension
atherosclerosis
vasculitis

54
Q

what is pick’s disease

A

AKA Frontal-temporal dementia ->a tauopathy that results in frontal degeneration (with temporal/parietal sparing)

55
Q

pick’s disease presentation

A

behavioural and language symptoms arising early which eventually progress to dementia

56
Q

what is normal pressure hydrocephalus

A

ventricular enlargement without increased CSF pressure due to blockage of the normal flow of CSF through the spine and brain

57
Q

3 symptoms of normal pressure hydrocephalus

A

3Ws:
Wet (incontinence)
Wobbly (gait disturbance)
Wacky (dementia)

58
Q

how is normal pressure hydrocephalus treated

A

ventriculoperitoneal shunts

59
Q

what are the 4 secondary disease targets that can result in neuronal death

A
  1. gene transcription (TF activation, histone activation etc.)
  2. axonal function (fast/slow transport)
  3. synaptic transmission (NT storage/release, receptor levels)
  4. survivial (apoptosis)
60
Q

4 ways infection can reach the CNS

A
  1. haematological spread
  2. infection via local spread (from sinuses, teeth, bone etc.)
  3. peripheral nerves (rabies, herpes zoester etc.)
  4. direct implantation from trauma
61
Q

what layer of the brain is involved in bacterial meningitis

A

leptomininges (subarachnoid space)

62
Q

3 types of meningitis

A

acute pyrogenic (bacterial)
aseptic (viral)
chronic (TB etc.)

63
Q

how does bacterial meningitis usually arise

A

Haematogenous dissemination of bacteria

64
Q

which bacteria are commonly responsible for bacterial meningitis
(2)

A

strep. pneumoniae
Neisseria meningitidis

65
Q

what might a brain abcess present as

A

headache; focal neurological defecit

66
Q

what causes cerebral oedema in a brain abcess

A

increased vascular permeability

67
Q

what is viral encephalitis accompanied by

A

viral meningitis (aseptic meningitis can occur alone)

68
Q

what cells become involved in viral encephalitis

A

neurones and glial cells

69
Q

4 most common primary tumours that spread to the brain

A

lung
breast
kidney
melanoma

70
Q

where do adult primary brain tumour usually arise

A

supratentorially

71
Q

what are the 3 most common primary brain tumours in adults

A

glioblastoma; meningionma; schwannoma

72
Q

what are the 3 most common primary brain tumours in children

A

pliocytic astrocytoma; ependymoma; medulloblastoma

73
Q

characteristic finding on a scan for glioblastoma

A

butterfly lesion - arises in the cerebral hemisphere and crosses the corpus callosum

74
Q

what cells surround a glioblastoma

A

pleomorphic astrocytes surround areas of necrosis with endothelial cell proliferation

75
Q

what is the most common benign brain tumour in adults and where is it derived from

A

meningioma; derived from arachnoid cells

76
Q

what might a meningioma present with

A

seizures

77
Q

meningioma pathology

A

whorled pattern with pasammoma bodies

78
Q

what nerve do schwannomas affect the most and what do they present with

A

CN VIII (vestibulocochlear), usually at the cerebellopontine angle - presents with deafness and tinnitus

79
Q

what are bilateral schwannomas associated with

A

neurofibromatosis type 2

80
Q

schwannoma pathology

A

spindle cell tumour with antoniA and antoni B areas (s100 +ve)

81
Q

how do oligodendrogliomas appear

A

calcified tumour in the white matter of the frontal lobe

82
Q

how might oligodendrogliomas present

A

seizures

83
Q

oligodendrogliomas pathology

A

“fried egg” cells on biopsy with areas of calcification

84
Q

what is the most common primary brain tumour in children

A

pilocytic astrocytoma (benign tumour)

85
Q

what are the 3 most common areas for a pilocytic astrocytoma to arise

A

cerebellum; optic nerve/chiasm; hypothalamic region

86
Q

pilocytic astrocytoma presentation

A

symptoms lasting several months; symptoms relating to the focal defecit depending on where the tumour is

87
Q

pilocytic astrocytoma pathology (2)

A
  1. cystic lesion with a mural nodule;
  2. thick eoisinophilic astrocytic processes (rosenthal fibres) with eosinophilic granular bodies
88
Q

what are 2 characteristic cells of pilocytic astrocytoma

A

1.rosenthal fibres;
2. hair-like projection

89
Q

how is a pilocytic astrocytoma treated

A

cerebellum - resection + chemo + radiatino
optic/hypothalamic - chemo + radiation

90
Q

what is a medulloblastoma

A

a malignant tumor derived from the granular cells of the cerebellum

91
Q

why is molecular subtyping important

A

determines outcome

92
Q

medulloblastoma pathology (2)

A

1.malignant small round blue cells
2. homer-wright rosettes

93
Q

how does a medulloblastoma spread

A

Rapid spreading via the CSF

94
Q

what is an ependymoma

A

malignant tumour of ependymal cells; usually arises in the 4th ventricle and can block the flow of CSF (resulting in hydrocephalus)

95
Q

ependymoma pathology

A

perivascular (around the bvs) pesuedo-rosettes

96
Q

what is a craniopharyngioma

A

a benign tumour which arises from the epithelial remnants of rathke’s pouche

97
Q

where is a craniopharyngioma found and what structure can it compress

A

above the piturity; it can compress the optic chiasm

98
Q

what symptom can craniopharyngioma cause due to compression of the optic chiasm

A

bitemporal hemianopia

3C week 1- intro to neuro and opthal (6 decks)

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