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Cerebrovascular Disease Flashcards

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
Q

where do embolic strokes usually originate from?

A

atheroma in internal carotid or aortic arch

emboli from heart due to AF

26
Q

what are risk factors for cerebral infarction?

A 
hypertension
serum lipids, obesity, diet
diabetes mellitus 
heart disease
drugs 
smoking
27
Q

what symptoms do patients often experience if they have a stroke due to carotid artery disease?

A

contra-lateral weakness / sensory loss

if dominant hemisphere, may be aphasia or apraxia

28
Q

what symptoms would usually indicate a middle cerebral artery stroke?

A

weakness in contralateral face and arm

29
Q

what symptoms would usually indicate an anterior cerebral artery stroke?

A

weakness and sensory loss in contralateral leg

30
Q

strokes in vertebro-basilar arteries can cause what symptoms?

A

vertigo
ataxia
dysarthria
dysphasia

31
Q

what is meant by vascular remodelling and how can this perpetuate a stroke?

A

accelerated atherosclerosis

arteriolosclerosis (thick, stiff vessel walls prone to rupture)

eventual fibrinoid necrosis of vessel walls

32
Q

where do micro aneurysms most commonly occur in the brain circulation?

A

branches of middle cerebral artery near the basal ganglia

33
Q

what is a lacunar infarct?

A

small “lake” like infarcts up to 15mm diameter

due to damage of lenticulostriate arteries in basal ganglia

34
Q

when can lacunar infarcts cause most damage?

A

if extends into internal capsule - can cause extensive motor weakness in face and limbs

35
Q

what are the hallmarks of hypertensive encephalopathy?

A

global cerebral oedema
tentorial and tonsillar herniation (due to raised ICP)
petechiae
anteriolar fibrinoid necrosis - high BP

36
Q

what are the clinical findings of hypertensive encephalopathy?

A

severe hypertension and symptoms of raised ICP

37
Q

where do most intracerebral haemorrhages occur?

A

most common - basal ganglia

thalamus, cerebral white matter and cerebellum

38
Q

how do intracerebral haemorrhages appear macroscopically?

A 
asymmetrical 
shifts and herniations of brain
well demarcated 
softening of adjacent tissue
surrounding oedema
39
Q

what vascular malformations can predispose to cerebrovascular disease?

A

arteriovenous malformations

cavernous / venous angiomas

40
Q

why do vascular malformations predispose to haemorrhage?

A

shunting from artery to vein = vein undergoes smooth muscle hypertrophy, vein is not compliant and ruptures easily

can also form aneurysms which rupture

41
Q

what normally causes a subarachnoid haemorrhage?

A

rupture of a saccular aneurysm (berry aneurysms)

42
Q

where do berry aneurysms normally occur?

A

internal carotid artery
vertebro-basilar circulation

*usually at arterial bifurcations

43
Q

what can be seen macroscopically around a berry aneurysm?

A

intracerebral haematomas next to aneurysms

infarcts of brain parenchyma - due to arterial spasm

haematoma may compress structures and cause features of raised ICP

44
Q

what are the risk factors for berry aneurysms?

A

smoking
hypertension
kidney disease

45
Q

what symptoms are usually experiences upon rupture of berry aneurysm?

A

severe headache
vomiting
LOC

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