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Neurology > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

what are bridging veins

A

perforate through the arachnoid and dura, very delicate and can rupture in trauma

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2
Q

what are the types of glial cells and their functions

A

astrocytes- supporting structures in brain
oligodendrocytes- myelination
ependymal cells - ciliated cuboidal/ columnar epithelium that lines the ventricles
microglia- immune monitoring and antigen presentation

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3
Q

what can damage to nerve cells lead to

A

rapid necrosis with sudden acute functional failure

slow atrophy with gradually increasing dysfunction

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4
Q

what is nissl substance

A

material consisting of granular endoplasmic reticulum and ribosomes that occurs in nerve cell bodies and dendrites

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5
Q

what is acute neuronal injury/ red neurone

A 
occurs due to hypoxia/ ischaemia 
results in neuronal cell death 
-shrinking and angluation of nuclei 
-loss of the nucleolus 
-intensely red cytoplasm
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6
Q

what are the axonal responses to nerve injury

A

increased protein synthesis (cell body swells, enlarged nucleus)
chromatolysis (margination and loss of nissl substance)
degeneration of axon and myelin sheath distal to injury (wallerian degeneration)

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7
Q

what happens in neuronal atrophy (chronic degeneration)

A

shrunken, angulated and lost neurones, small dark nuclei, accumulation of lipofuscin pigment, reactive gliosis

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8
Q

what are sub cellular alterations (inclusions) cell damage

A

happen in neurodegenerative conditions

inclusions accumulate with ageing/ in viral infections

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9
Q

what type of damage are oligodendrocytes sensitive

A

oxidative damage

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10
Q

what cell type is damage in demyelinating disorders

A

oligodendrocyte

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11
Q

what does damage to the myelin sheath cause

A

reduced conduction and exposition of the axon

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12
Q

what do astrocytic processes do

A

envelop synaptic plates

wrap around vessels and capillaries within the brain (how they control BBB and cerebral blood flow)

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13
Q

what is the role of astrocytes

A

ionic, metabolic and nutritional homeostasis (do anaerobic glycolysis and give lactate to neurones. also moderate glutamate production)
work in conjunction with endothelium to maintain BBB
repair and scar formation (as no fibroblasts to do this)

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14
Q

what is gliosis

A

an astrocytic response that indicated CNS damage
astrocyte hyperplasia and hypertrophy
nucleus enlarges, becomes vesicular, nucleolus is prominent
cytoplasmic expansion

old lesions (equivalent to scarring)- meshwork of glial fibrils

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15
Q

what do ependymal cells provide a pathway for

A

ascending infection (line ventricles)

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16
Q

what are the possible causes of nervous system injury

A 
Hypoxia
Trauma
Toxic insult (exogenous and endogenous due to metabolic sustances within brain)
Metabolic abnormalities
Nutritional deficiencies
Infections
Genetic abnormalities
Ageing
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17
Q

what can cause CNS hypoxia

A

cerebral ischaemia, infarct, haemorrhage, trauma, cardiac arrest, cerebral palsy

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18
Q

how much of total body resting oxygen does the brain consume

A

20%

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19
Q

how much can cerebral blood flow increase to maintain oxygen consumptoms

A

only two fold

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20
Q

what happens after onset of ischaemia in the brain

A

mitochondria inhibit ATP synthesis

ATP reserves consumed within a few minutes

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21
Q

what is excitotoxicity

A

In context of energy failure- neuronal depolarisation causing glutamate release
At same time re uptake of glutamate by astrocytes is inhibited due to energy failure causing accumulation in synaptic space creating a glutamate store which leads to excitation of the post synaptic glutamate receptors= rapid accumulation of Ca in post synaptic neurone what causes;
protease activation
mictochondrial dysfunction
oxidative stress

these things are the main mediators of injury

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22
Q

what are the types of oedema

A

cytotoxic (pre morbid process, accumulation of Na and Cl in neurones moves water from interstitium into cell)

ionic (water goes into interstitium because of deficiency caused by cytoxic oedema)

vasogenic (large molecules like albumin enter interstitium from vessels (more marked swelling that ionic)

haemorragic (blood cells cross BBB if vessel damage bad enough)

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23
Q

what helps to maintain blood brain flow

A

autoregulatory mechanisms

dilatation and constriction of cerebral vessels

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24
Q

what is the definition of cerebrovascular disease

A

any abnormality of brain caused by a pathological process of blood vessels

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25
what are the main manifestations of cerebrovascular disease
brain ischaemia and infarction haemorrhages vascular malformations aneurysms
26
what is global hypoxic ischaemic damage
``` generalised reduction in blood flow/ oxygenation causes: -cardiac arrest -severe hypotension (hypovolaemic shock) -trauma ```
27
what is focal cerebral ischaemia and infarction
where the is restriction of blood flow to a localised area of the brain e.g. a vascular obstruction
28
what are the watershed areas
zone between two arterial territories | particular sensitive to loss of BP
29
what cell type is most sensitive to hypoxia in brain
neurones, especially in neocortex and hippocampus
30
a blood pressure below what leads to hypoperfusion in the brain
50 mmhg
31
what is a stroke
sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
32
what causes a infarction stroke
interuption of blood flow due to thrombosis or emboli
33
are men or women more likely to have an infarction stroke
men
34
what causes a thrombotic stroke
thrombosis in an atherosclerotic segment | mostly middle cerebral artery
35
what causes an embolic strole
from atheroma in internal carotid or aortic arch or heart
36
what are the rarer causes of cerebral infarction stroke
osteophytes compressing vertebral circulation, vasculitis, septal defects (e.g. left to right shunt creates emboli)
37
what are the risk factors for an infarction stroke
``` atheroma (intracranial -esp basilar- and extracranial- esp carotid and aorta) hypertension (risks atheroma and atherosclerosis) serum lipids, obesity, diet diabetes mellitus heart disease diseases of neck arteries drugs smoking septal defects ```
38
in a cerebral infarction what is the extent of damage determined by
arterial territory of the affected artery timescale of occlusion extend of collateral circulatory relief systemic perfusion pressure
39
what happens to the brain after 48hrs of an infarction
become gelatinous and friable
40
what is the most common cell type in area of damage after 2 days of an infarction
microglia
41
when does gliosis begin
after a week of infarction
42
when does a gliotic scar form
a few weeks after infarction
43
what is a haemorrhagic infarct
In the context of an infarct the BBB deteriorates | haemorhagic conversion happens
44
what happens if you thrombolyse an infarct too late
BBB will be damaged too much and will cause a haemorrhage
45
localise the vascular lesion: | contra‐lateral weakness or sensory loss. If dominant hemisphere, may be aphasia or apraxia
carotid artery disease
46
localise the vascular lesion: | weakness predominantly contralateral face and arm
middle cerebral artery
47
localise the vascular lesion: | weakness and sensory loss in contralateral leg
anterior cerebral artery
48
localise the vascular lesion: | vertigo, ataxia, dysarthria, and dysphasia
(brain stem syndromes) | vertebro-basilar artery disease
49
how does hypertension increase risks of stroke
accelerates atherosclerosis creates lacunes (CSF cavity in basal ganglia/ white matter- leads to lacuna infarcts) micro aneurysms (charcot bouchard) in small arteries (esp basal ganglia) fibrinoid necrosis of vessel walls if severe
50
what are the different consequences of HPTx in the brain
``` lacunar infarcts (atheroma, embolism in small penetrating vessels leads to occulsion (esp in basal ganglia) multi infarct dementia ruptured aneurysms and intracerebral haemorrhage hypertensive encephalopathy (in acute malignant hptx) (global cerebral oedema, tentorial and tonsilar herniation, petechiae and arteriolar fibrinodnecrosis) ```
51
what are lacunar infarcts
small lake like infarcts due to occulsion of small penetrating vessels particularly affect basal ganglia when multiple can contribute to multi infarct dementia
52
what is seen clinically in hypertensive encephalopathy
severe hypertension | symptoms of raised ICP
53
what is found pathologically in hypertensive encephalopathy
global cerebral oedema tentorial and tonsilar haemorrhages ateral fibrioid necrosis petechiae
54
what are the types of spnotaneous intracranial haemorrhage
intracerebral sub arachnoid haemorrhagic infarct
55
what are the types o traumatic intracranial haemorrhage
``` extra dural sub dural contusion (surface bruising) intracerebral sub arachnoid ```
56
what are the contributing factors to a intracerebral haemorrhage
Hypertension Aneurysms Systemic coagulation disorders Iatrogenic anticoagulation Vascular malformations Amyloid deposits (cerebral amyloid angiopathy) Open heart surgery Neoplasms Vasculitis (infectious and non‐infectious) causes of vascular injury/ disease - hptx - amyloid - diabetes - drugs, cocaine, alcoholism - vascullitis
57
where do intracerebral haemorrhages most commonly occur
basal ganglia thalamus cerebral white matter cerebellum
58
what usually surrounds an intracerebral haemorrhage and causes more damage
oedema adjecent tissue also softens can cause herniations
59
what happens in amyloid angiopathy
beta sheet of amyloid stick together, form a plaque and make vessels unable to respond to changes in BP= rupture = intracerebral haemorrhage
60
what does amyloid angiopathy happen in
Alzheimers and in old age
61
what types of vascular malfnormations cause intracranial haemorrhages
AVM cavernous angiomas venous angiomas capilary teleangectases
62
what else in brain can vascular malformations cause
headaches, seizures and focal neurological deficits
63
describe an anteriovenous malformation in the brain
``` abnormal tortuous vessels (conglomeration of arteries and veins) shunting from artery to vein which: -undergoes hypertrophy -is not compliant and ruptures easily -forms aneurysms- rupture ```
64
what is the most common cause of a subarachnoid haemorrhage
rupture of a saccular aneurysm (berry aneurysm) - 905 in ICA territory - 10% in vertebrobasilar
65
what causes a berry aneurysm
arise in aterial bifurcations arising from circle of willis acquired degenerative lesion due to chronic haemodynamic injury to the vessel associated with genetic PCKD and hormone abnormalities
66
what is seen pathologically after the rupture of a berry aneurysm
Intracerebral haematomas adjacent to aneurysms Infarcts of brain parenchyma may also develop – due to arterial spasm Mass effect of haematoma and features of raised ICP. Hydrocephalus: acute and chronic (accumulation of CSF as poor flow across surface)
67
what are the risk factor for a subarachnoid haemorrhage
(berry aneurysm) smoking hptx kidney disease
68
what is the clinical features of a sub arachnoid haemorrhage
``` severe headache vomiting loss of consciousness women> men survivors at risk of hydrocephalus ```

Neurology (35 decks)

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