Neuropathology 1: CVD Flashcards

(49 cards)

1
Q

name the 3 types of glial cell

A

astrocytes - most prevalent
oligodendrocytes
ependymal cells

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2
Q

ependymal cells line..

A

the ventricular system

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3
Q

what is the pathological cellular response seen in stroke?

A

rapid necrosis with sudden acute functional failure

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4
Q

what kind of neuronal damage occurs as a result of hypoxia?

A

acute neuronal injury with irreversible shrinking and angulation of nuclei, loss of the nucleolus and a RED cytoplasm

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5
Q

when does acute neuronal injury occur in relation to the time of injury

A

12-24 hours after injury

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6
Q

name the axonal reaction to injury?

A

increased protein synthesis

degeneration of myelin sheath and axons distal to injury

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7
Q

what does chronic degeneration of a neuron look like?

A

shrunken, angulated and lost neurons
small dark nuclei
neuronal tissue replaced by reactive gliosis

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8
Q

small dark nuclei are an example of what damage?

A

chronic damage

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9
Q

what are inclusions? what are they common in?

A

subcellular alterations common in neurodegenerative conditions eg alzheimers and in aging

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10
Q

oligodendrocytes are sensitive to ___ damage

A

oxidative

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11
Q

damage to the myelin sheath poses what risks?

A

conduction reduced

axons exposed to injury

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12
Q

damage to what cells is a feature of demyelinating disorders

A

oligodendrocytes

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13
Q

star shaped cells with multipolar cytoplasmic processes describe….

A

astrocytes

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14
Q

what do the cytoplasmic processes of astrocytes do?

A

envelop synaptic plates

wrap around vessels and capillaries of the brain

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15
Q

what cells are responsible for reabsorbing and recycling glutamate?

A

astrocytes

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16
Q

what pathological process is the main indicator of CNS injury?

A

gliosis

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17
Q

describe gliosis

A

astrocyte hyperplasia and hypertrophy
prominent nucleolus
small dark nuclei

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18
Q

describe the role of M1 microglia

A

anti-inflammatory, phagocytic, for acute injury

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19
Q

describe the role of M2 microglia

A

pro-inflammatory, for chronic injury

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20
Q

which type of microglia is for chronic injury

21
Q

what happens to microglia when theyre injured?

A

they proliferate, are recruited via inflammatory mediators and form aggregates around necrotic tissue

22
Q

most common cause of nervous system injury?

23
Q

the brain consumes __ % of the body’s total oxygen

24
Q

describe the process of excitotoxicity

A

energy failure in the cell results in degradation of the mP -> glutamate released but not reabsorbed well -> severe excitation -> Ca excess

25
excess Ca as a result of excitotoxicity has what consequences?
oxidative stress apoptisis mitochondrial dysfunction protease activation
26
what happens in cytotoxic oedema? what can it lead to?
excess Na and Cl in the cell cause water to move into the cells across the BBB causing ionic oedema
27
vasogenic oedema occurs in what brain pathologies?
trauma, tumours, inflammation | encephalopathy
28
the brain receives __% of the cardiac output
15
29
global hypoxic ischaemic damage can occur in the context of...
generalised reduction in perfusion/oxygenation cardiac arrest severe hypotension
30
focal hypoxic ischaemic damage can occur in the context of...
vascular obstruction
31
what parts of the brain are more susceptible to ischaemic damage?
areas between arterial territories
32
neurons are more sensitive than glial cells to hypoxic ischaemic damage T or F
T, especially purkinje cells in the cerebellum
33
what kind of infarctive stroke is most common?
thrombotic
34
most common area for a thrombotic infarctive stroke
middle cerebral artery
35
where do cardioemboli tend to arise from?
internal carotids aorta heart
36
after 12-24hrs of cerebral infarction what does the brain look like microscopically?
red neurons, oedema
37
what becomes the predominant cell type -14 days after a cerebral infarction?
microglia
38
when does gliosis begin after a cerebral infarction
1 week
39
when does a gliotic scar appear after a cerebral infarction
after a few weeks
40
clinical presentation of a middle cerebral artery occlusion
weakness in contralateral face and arm
41
what is arteriolosclerosis
thicker, stiff, weaker arterioles
42
lacunar infarcts occur from occlusion of....
small penerating arteries
43
clinical presentation of hypertensive encephalopathy?
severely hypertensive | symptoms of raised ICP
44
pathological findings of hypertensive encephalopathy?
arteriolar fibrinoid necrosis petechiae tentorial and tonsillar herniation global cerebral oedema
45
what does amyloid do to BVs
thins their walls making them more likely to rupture
46
most likely area for an intracerebral haemorrhage
in basal ganglia
47
most common cause of subarachnoid haemorrhage?
berry aneurysm rupture
48
most common area of berry aneurysms?
around arterial bifurcations arising from the cirle of willis in territory of internal carotid
49
complications of subarachnoid haemorrhage
infarcts in brain parenchyma intracerebral haematomas hydrocephalus