Cerebrovascular Disease Flashcards

(45 cards)

1
Q

rapid necrosis of nerve cells and/or their processes most commonly leads to what clinical picture?

A

sudden acute functional (stroke)

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2
Q

slow atrophy of nerve cells and/or their processes most commonly leads to what clinical picture?

A

gradually increasing dysfunction (age related cerebral atrophy)

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3
Q

how does acute neuronal injury appear microscopically?

A

shrunken and angulated nuclei
loss of nucleolus
intensely red cytoplasm - “red neurone”

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4
Q

at what stage are red neurones normally seen microscopically?

A

after hypoxia / ischaemia
typically visible 12-24 hrs after irreversible insult (stroke)
shows neuronal cell death

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5
Q

if an axon is severed, what occurs in either side of damage?

A

cell body swelling, enlarged nucleolus

degeneration of axon and myelin sheath distal to injury

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6
Q

what are the main functions of astrocytes?

A

maintain the BBB

involved in repair and scar formation (due to lack of fibroblasts)

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7
Q

how do astrocytes usually respond to CNS injury?

A

gliosis = astrocyte hyperplasia and hypertrophy

this is indicator of CNS injury, regardless of cause

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8
Q

how does old gliosis appear histologically?

A

nuclei become small and dark

they lie in a dense net of processes (glial fibrils)

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9
Q

what type of damage are oligodendrocytes particularly susceptible to?

A

oxidative damage

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10
Q

how do ependymal cells (which line ventricles) respond to CNS injury?

A

limited reaction to injury

disruption causes local proliferation of these cells - small irregularities on the ventricular surfaces “ependymal granulations”

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11
Q

how do the microglia (macrophage like cells) respond to CNS injury?

A

proliferate
recruited through inflammatory mediators
aggregate around necrotic and damaged tissues
M2 more acute, M1 - chronic

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12
Q

why does the brain deteriorate so quickly once hypoxia and ischaemia occur?

A

no O2 to create more ATP

mitochondria inhibit ATP synthesis so reserve is consumed within few mins

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13
Q

why can excito-toxicity cause oxidative stress in neurones?

A

excitatory signal depolarises neurone and releases glutamate

lack of energy means astrocytes don’t reuptake glutamate

loss of glutamate in synapse causes lots Ca2+ entry into post-synaptic terminal = mitochondrial dysfunction and oxidative stress

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14
Q

what are the 4 main types of oedema in the brain?

A

cytotoxic oedema
ionic/osmotic oedema
vasogenic oedema
haemorrhagic conversion

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15
Q

what causes cytotoxic oedema?

A

Na+/K+ channel dysfunction -> cells retain Na+ and water

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16
Q

what causes ionic/osmotic oedema?

A

water and Na+ from capillaries move into brain parenchymal extracellular space

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17
Q

what causes vasogenic oedema?

A

BBB disrupted -> leaking fluid from capillaries affect white matter

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18
Q

what causes haemorrhagic conversion?

A

when RBCs cross BBB

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19
Q

what is meant by cerebrovascular disease?

A

an abnormality of brain caused by pathological process in blood vessels

20
Q

what are the 4 main components of cerebrovascular disease?

A

brain ischaemia and infarction
haemorrhages
vascular malformations
aneurysms

21
Q

what would cause a global hypoxia and ischaemic damage to the brain as opposed to focal area of ischaemia?

A

cardiac arrest and severe hypotension (trauma with hypovolaemic shock)

focal = vascular obstruction

22
Q

what is the definition of a stroke?

A

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

23
Q

what gender and age are most common for stroke to occur?

A

peak incidence is >70yrs

men > women

24
Q

strokes caused by atherosclerotic thrombus are most common in which artery of cerebrum?

A

middle cerebral artery or its branches

25
where do embolic strokes usually originate from?
atheroma in internal carotid or aortic arch | emboli from heart due to AF
26
what are risk factors for cerebral infarction?
``` hypertension serum lipids, obesity, diet diabetes mellitus heart disease drugs smoking ```
27
what symptoms do patients often experience if they have a stroke due to carotid artery disease?
contra-lateral weakness / sensory loss if dominant hemisphere, may be aphasia or apraxia
28
what symptoms would usually indicate a middle cerebral artery stroke?
weakness in contralateral face and arm
29
what symptoms would usually indicate an anterior cerebral artery stroke?
weakness and sensory loss in contralateral leg
30
strokes in vertebro-basilar arteries can cause what symptoms?
vertigo ataxia dysarthria dysphasia
31
what is meant by vascular remodelling and how can this perpetuate a stroke?
accelerated atherosclerosis arteriolosclerosis (thick, stiff vessel walls prone to rupture) eventual fibrinoid necrosis of vessel walls
32
where do micro aneurysms most commonly occur in the brain circulation?
branches of middle cerebral artery near the basal ganglia
33
what is a lacunar infarct?
small "lake" like infarcts up to 15mm diameter | due to damage of lenticulostriate arteries in basal ganglia
34
when can lacunar infarcts cause most damage?
if extends into internal capsule - can cause extensive motor weakness in face and limbs
35
what are the hallmarks of hypertensive encephalopathy?
global cerebral oedema tentorial and tonsillar herniation (due to raised ICP) petechiae anteriolar fibrinoid necrosis - high BP
36
what are the clinical findings of hypertensive encephalopathy?
severe hypertension and symptoms of raised ICP
37
where do most intracerebral haemorrhages occur?
most common - basal ganglia thalamus, cerebral white matter and cerebellum
38
how do intracerebral haemorrhages appear macroscopically?
``` asymmetrical shifts and herniations of brain well demarcated softening of adjacent tissue surrounding oedema ```
39
what vascular malformations can predispose to cerebrovascular disease?
arteriovenous malformations | cavernous / venous angiomas
40
why do vascular malformations predispose to haemorrhage?
shunting from artery to vein = vein undergoes smooth muscle hypertrophy, vein is not compliant and ruptures easily can also form aneurysms which rupture
41
what normally causes a subarachnoid haemorrhage?
rupture of a saccular aneurysm (berry aneurysms)
42
where do berry aneurysms normally occur?
internal carotid artery vertebro-basilar circulation *usually at arterial bifurcations
43
what can be seen macroscopically around a berry aneurysm?
intracerebral haematomas next to aneurysms infarcts of brain parenchyma - due to arterial spasm haematoma may compress structures and cause features of raised ICP
44
what are the risk factors for berry aneurysms?
smoking hypertension kidney disease
45
what symptoms are usually experiences upon rupture of berry aneurysm?
severe headache vomiting LOC