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Neurology > Neuropathology* > Flashcards

Neuropathology* Flashcards

1
Q

Dura is what
arachnoid
pia mater

A

tough fibrous bridges crevices attached to skull

delicate sealed bag for CSF bridges crevices

delicate dips into crevices

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2
Q

Cellular components of the CNS

A 
nerve cells (neurones)
glial cells (astrocytes, oligo, epyndema)
blood vessels 
microglia 
connective tissue - meninges
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3
Q

how can the cells of the CNS be damaged

A 
lack of oxygen 
trauma 
toxic insult
metabolic abnormailites
nutritional deficiencies
infections
ageing 
genetic abnormalities
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4
Q

neuronal responses to injury/diseases

A

acute neuronal injury
simple neuronal atrophy
sub cellular alterations
axonal reaction

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5
Q

hypoxic damage to the CNS - which cells are more venerable and why

A

neurones

can’t use anaerobic glycolysis

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6
Q

what is axonal reaction

A

a reaction within the cell body that is associated with axonal injury

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7
Q

axonal injury

A 
increased RNA and protein synthesis 
swelling of cell body 
peripheral displacement of nucleus 
enlargement of nucleolus
central chromatolysis
anterograde degeneration of axon occurs distal to site of injury
breakdown of myelin sheath
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8
Q

astrocyte reaction to injury

A

reaction that leads to cell death or degeneration

gliosis

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9
Q

gliosis

A

astrocytes undergo hyperplasia and hypertrophy
nucleus enlarges becomes vesicular and the nucleolus is prominent
cytoplasmic expansion
only lesions - nuclei become small and dark and lie in a dense net or processes (glial fibrils)

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10
Q

oligo response to injury

A

limited

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11
Q

ependymal reaction

A

limited
disruption can lead to proliferation of sub-ependymal astrocytes to produce small irregularities on ventricular surface - epenedymal granulations

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12
Q

microglia respond to injury how

A

proliferating
developing elongated nuclei (rod cells)
forming aggregates about small foci of tissue necrosis (microglial nodules)
congregate around portions of dying neurones (neuronophagia)

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13
Q

how much CO does the brain receive
how much oxygen does the brain use
what kind of metabolism does the brain require
what mechanism maintains blood flow at a constant rate

A

15%
20%
active aerobic metabolism of glucose
auto regulatory mechanisms

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14
Q

damage to the anterior cerebral artery leads to what lobe dysfunction and what symptoms

A

frontal lobe dysfunction

contralateral sensory loss in foot and leg
paresis of arm and foot, relative sparing of thigh and face

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15
Q

middle cerebral artery damage

A 
dominant V non dom
hemiparesis
hemisensory loss
aphasia/dysphasia 
apraxia
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16
Q

vertebro basilar supplies what

A

brain stem
cerebellum
occipital lobe

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17
Q

damage to vertebra basilar leading to dysfunction in brain stem, occipital lobe

A

mid brain - webers syndrome
pons - medial and lateral inferior pontine syndromes
medulla - lateral medullary syndrome

homonymous hemi with sparing of the macula

cerebellum - ataxia, nystagmus, intention tremor, pendular reflexes

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18
Q

in hypo ischemia damage which cell are more vulnerable

what areas can be seen

A

nuerons more than glial
some groups of neurons more than others

water shed areas - border zone between two major arteries - both supply this area

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19
Q

definition of cerebra vascular disease “stroke”

A

sudden disturbance of cerebral function of vascular origin that causes death or lasts 24 hours

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20
Q

cerebral infarction is caused by what

A

local interruption of cerebral blood flow due to thrombosis or emboli

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21
Q 
cerebral infarction at 4-12 hours
15-20
24-36
36-48
day 3
1-2 weeks
months
A

brain may appear normal

ischeamic neuronal changes develop, defined margin between ischaemic and normal brain

inflam reaction, extravasation of RBCs, activation of astrocytes and microglia

necrosis area visible macroscopically, becomes swollen and softer than surrounding tissue

macrophages infiltrate area

liquefaction of tissue and gliosis

cavitation and completion of glial scar

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22
Q

subarachnoid haemorrhage types

A

spontaneous - most common cause if rupture of an aneurysm 90% which arise as arterial bifurcation in territory of internal carotid rather and 10% in vertebra basilar circulation

traumatic

23
Q

morphology of a subarachnoid haemmorhage

A

rupture of berry aneurysm - bleeding into subarachnoid space
may get intracerebral haematomas adjacent to anneuryms
infarcts of brain parenchyma may also develop due to arterial spasm - mass effect of haematoma and raised ICP

24
Q

clinical features of a SAH

prognosis

A

abrupt onset
severe headache, vom, LOC
no history of repceipitating factor
50% die within several days of onset

25
Q

hypertension does what to the brain

A

increased amount of atheroma
hyaline arteriosclerosis
micro aneurysms
altered response of cerebral blood vessels to chronic hypertension with a shift of the auto regulatory curve to the right

26
Q

pathology of hypertension and the brain

A

lacunar infarcts
intracerebral haemorrhage and haematoma formation - ruptured aneurysms
multi infarct dementia
hypertensive encephalopathy

27
Q

the myelin sheath in CNS is derived for what

A

oligo

28
Q

primary demyelination
secondary
metabolic
toxic

A

MS

central pontine myelinosis
progressive multifocal leucoencephalopathy
sub acute sclerosing panecncephalitis
AIDS
axonal degeneration

metabolic

cyanide, CO, solvents

29
Q

MS female:male
what does it lead to
brain and spinal cord what
clinical features

A

2:1
episodes of neurological deficit separated by time

brain and spinal cord lesions disseminated in both time and space

acute or insidious, variable distribution

30
Q

MS aetiology

A

environmental
genetic
immune

31
Q

MS morphology

A

external appearance of brain and spinal cord usually normal

cut surface - multiple areas of demyelination - plaques

32
Q

MS plaques

A

well demarcated in white matter - acute lesions soft/pink and older firmer/pearly grey
non anatomical distribution
may act as SOL

33
Q

types of MS plaques

A

acute active - evidence of ongoing myelin breakdown w inflam cells. small lesions often centred around veins

chronic (inactive) plaques [inactive plaques] -centre contains little or no myelin. astrocyte proliferation and gliosis are prominent

chronic active plaques

shadow plaques - border between normal and affected white matter is not clearly defined

34
Q

acute MS plaques

chronic MS plaques

A

demyelinated plaques are yellow/brown with an ill defined edge which blends into surrounding white matter

well demarcated brown/grey lesions in white matter, classically situated around lateral ventricles

35
Q

MS

main features of histology

A

demyelination
inflammation
gliosis

36
Q

definition of dementia

A

impairment of previously acquired occupational or social functioning due to development of acquired and persistent memory impairment associated with impairment of intellectual function in the presence of normal consciousness

37
Q

is dementia part of ageing

A

NO

always pathological

38
Q

primary and secondary dementia

A

primary (organic) - alzheimer’s, levy body, hunting tons, picks

secondary - other disorders resulting in secondary changes in the CNS

39
Q

alzheimers
age
common?
risks

A

5% >60 and 15% >80s
usually sporadic
may be familial, increased incidence with downs syndrome

40
Q

progress of alzheimers

A

insidious impairment of higher intellectual function with alterations in mood and behaviour
later - progressive disorientation, memory loss, aphasia indicate severe cortisol dysfunction
can result in profound disability, muteness and immobility

41
Q

alzheimers disease macroscopic

A

decreased size and weight of brain
widening of sulci
narrowing of gyro
compensatory dilataton ventricles, secondary hydrocephalus
frontal, parietal and temporal lobes affected
brainstem and cerebellum normal

42
Q

alzheimers microscopic disease

A

intracytoplasmic neurofibrillary tangles (tau protein)
Ab amyloid plaques
amyloid antipathy
extensive neuronal loss with astrocytosis

43
Q 
[amyloid]
what accumulation?
extracellular what
polymerised what 
congo what
2 types
EM ?
A 
eosinophilic
matrix
beta pleated plate
red
AL or AA
10-12 nm fibrils
44
Q

hallmarks of lewy body
development of what
fluctuation when

A

hallucinations and fluctuating levels of attention
features of parkinson’s disease
in severity of condition on a day to day basis

45
Q

dementia pathalogical features

A

degeneration of the substantia nigra
remaining nerve cells contain lewy bodies
degeneration of the cortical areas of the brain
degeneration of the cortical areas with formation of cortical lewy bodies which can be detected by immunochemical staining for the protein ubiquitin

46
Q 
huntingtons - what, age
geentics 
clinical features
symptoms 
dementia when
A

neuropsychiatric, 35-50
autosomal dom inheritence
emotional, cognitive and motor disturbances
chorea, myoclonus, clumsiness, slurred speech, depression, irritability and apathy

develop dementia later on

47
Q

huntingtons microscopic appearance

A

loss of neurons in caudate nucleus and cerebral cortex accompanied by reactive fibrillary gliosis

48
Q

picks disease is what

A

progressive dementia occurring in middle life (50-60s) characterised by slowly progressing changes in character and social deterioration leading to impairment of intellect, memory and language

49
Q

picks disease features

A

extreme atrophy of cerebral cortex in frontal and temporal lobes
brain weight <1kg
neuronal loss and astrocytosis
picks cells and intracytoplasmic inflammation inclusions known as picks bodies

50
Q

symptoms of picks disease

timeline

A

personality and behavioural changes
speech and communication problems
changes in eating habits
reduced attention span

may last between 2-10 years, mean length is 7 years

51
Q

multi infarct dementia is what

A

disorder involving a deterioration in mental functioning due to changes of damage to the brain tissue from hypoxia or anoxia as a result of multiple blood clots within the blood vessels supplying the brain

52
Q

MID caused by what
age
M:W
leads to what

A

successive multiple cerebral infarcts - dementia results when a sufficient area of the brain is damaged

> 60 but also seen in middle aged hypertensives

M>W

sufferers have insight -> depression and anxiety

53
Q

difference between MID and alzheimers

A

abrupt onset
stepwise progression
hx of ht/stroke
evidence of stroke will be seen on ST/MRI

Neurology (15 decks)

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