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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
hypertension does what to the brain
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
pathology of hypertension and the brain
lacunar infarcts intracerebral haemorrhage and haematoma formation - ruptured aneurysms multi infarct dementia hypertensive encephalopathy
27
the myelin sheath in CNS is derived for what
oligo
28
primary demyelination secondary metabolic toxic
MS ``` central pontine myelinosis progressive multifocal leucoencephalopathy sub acute sclerosing panecncephalitis AIDS axonal degeneration ``` metabolic cyanide, CO, solvents
29
MS female:male what does it lead to brain and spinal cord what clinical features
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
MS aetiology
environmental genetic immune
31
MS morphology
external appearance of brain and spinal cord usually normal | cut surface - multiple areas of demyelination - plaques
32
MS plaques
well demarcated in white matter - acute lesions soft/pink and older firmer/pearly grey non anatomical distribution may act as SOL
33
types of MS plaques
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
acute MS plaques | chronic MS plaques
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
MS | main features of histology
demyelination inflammation gliosis
36
definition of dementia
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
is dementia part of ageing
NO | always pathological
38
primary and secondary dementia
primary (organic) - alzheimer's, levy body, hunting tons, picks secondary - other disorders resulting in secondary changes in the CNS
39
alzheimers age common? risks
5% >60 and 15% >80s usually sporadic may be familial, increased incidence with downs syndrome
40
progress of alzheimers
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
alzheimers disease macroscopic
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
alzheimers microscopic disease
intracytoplasmic neurofibrillary tangles (tau protein) Ab amyloid plaques amyloid antipathy extensive neuronal loss with astrocytosis
43
``` [amyloid] what accumulation? extracellular what polymerised what congo what 2 types EM ? ```
``` eosinophilic matrix beta pleated plate red AL or AA 10-12 nm fibrils ```
44
hallmarks of lewy body development of what fluctuation when
hallucinations and fluctuating levels of attention features of parkinson's disease in severity of condition on a day to day basis
45
dementia pathalogical features
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
``` huntingtons - what, age geentics clinical features symptoms dementia when ```
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
huntingtons microscopic appearance
loss of neurons in caudate nucleus and cerebral cortex accompanied by reactive fibrillary gliosis
48
picks disease is what
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
picks disease features
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
symptoms of picks disease timeline
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
multi infarct dementia is what
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
MID caused by what age M:W leads to what
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
difference between MID and alzheimers
abrupt onset stepwise progression hx of ht/stroke evidence of stroke will be seen on ST/MRI

Neurology (15 decks)

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