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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
Q

what are the main manifestations of cerebrovascular disease

A

brain ischaemia and infarction
haemorrhages
vascular malformations
aneurysms

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26
Q

what is global hypoxic ischaemic damage

A 
generalised reduction in blood flow/ oxygenation 
causes:
-cardiac arrest 
-severe hypotension (hypovolaemic shock)
-trauma
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27
Q

what is focal cerebral ischaemia and infarction

A

where the is restriction of blood flow to a localised area of the brain
e.g. a vascular obstruction

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28
Q

what are the watershed areas

A

zone between two arterial territories

particular sensitive to loss of BP

29
Q

what cell type is most sensitive to hypoxia in brain

A

neurones, especially in neocortex and hippocampus

30
Q

a blood pressure below what leads to hypoperfusion in the brain

A

50 mmhg

31
Q

what is a stroke

A

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

32
Q

what causes a infarction stroke

A

interuption of blood flow due to thrombosis or emboli

33
Q

are men or women more likely to have an infarction stroke

A

men

34
Q

what causes a thrombotic stroke

A

thrombosis in an atherosclerotic segment

mostly middle cerebral artery

35
Q

what causes an embolic strole

A

from atheroma in internal carotid or aortic arch or heart

36
Q

what are the rarer causes of cerebral infarction stroke

A

osteophytes compressing vertebral circulation, vasculitis, septal defects (e.g. left to right shunt creates emboli)

37
Q

what are the risk factors for an infarction stroke

A 
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
Q

in a cerebral infarction what is the extent of damage determined by

A

arterial territory of the affected artery
timescale of occlusion
extend of collateral circulatory relief
systemic perfusion pressure

39
Q

what happens to the brain after 48hrs of an infarction

A

become gelatinous and friable

40
Q

what is the most common cell type in area of damage after 2 days of an infarction

A

microglia

41
Q

when does gliosis begin

A

after a week of infarction

42
Q

when does a gliotic scar form

A

a few weeks after infarction

43
Q

what is a haemorrhagic infarct

A

In the context of an infarct the BBB deteriorates

haemorhagic conversion happens

44
Q

what happens if you thrombolyse an infarct too late

A

BBB will be damaged too much and will cause a haemorrhage

45
Q

localise the vascular lesion:

contra‐lateral weakness or sensory loss. If dominant hemisphere, may be aphasia or apraxia

A

carotid artery disease

46
Q

localise the vascular lesion:

weakness predominantly contralateral face and arm

A

middle cerebral artery

47
Q

localise the vascular lesion:

weakness and sensory loss in contralateral leg

A

anterior cerebral artery

48
Q

localise the vascular lesion:

vertigo, ataxia, dysarthria, and dysphasia

A

(brain stem syndromes)

vertebro-basilar artery disease

49
Q

how does hypertension increase risks of stroke

A

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
Q

what are the different consequences of HPTx in the brain

A 
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
Q

what are lacunar infarcts

A

small lake like infarcts due to occulsion of small penetrating vessels
particularly affect basal ganglia
when multiple can contribute to multi infarct dementia

52
Q

what is seen clinically in hypertensive encephalopathy

A

severe hypertension

symptoms of raised ICP

53
Q

what is found pathologically in hypertensive encephalopathy

A

global cerebral oedema
tentorial and tonsilar haemorrhages
ateral fibrioid necrosis
petechiae

54
Q

what are the types of spnotaneous intracranial haemorrhage

A

intracerebral
sub arachnoid
haemorrhagic infarct

55
Q

what are the types o traumatic intracranial haemorrhage

A 
extra dural 
sub dural 
contusion (surface bruising)
intracerebral 
sub arachnoid
56
Q

what are the contributing factors to a intracerebral haemorrhage

A

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
Q

where do intracerebral haemorrhages most commonly occur

A

basal ganglia
thalamus
cerebral white matter
cerebellum

58
Q

what usually surrounds an intracerebral haemorrhage and causes more damage

A

oedema
adjecent tissue also softens
can cause herniations

59
Q

what happens in amyloid angiopathy

A

beta sheet of amyloid stick together, form a plaque and make vessels unable to respond to changes in BP= rupture = intracerebral haemorrhage

60
Q

what does amyloid angiopathy happen in

A

Alzheimers and in old age

61
Q

what types of vascular malfnormations cause intracranial haemorrhages

A

AVM
cavernous angiomas
venous angiomas
capilary teleangectases

62
Q

what else in brain can vascular malformations cause

A

headaches, seizures and focal neurological deficits

63
Q

describe an anteriovenous malformation in the brain

A 
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
Q

what is the most common cause of a subarachnoid haemorrhage

A

rupture of a saccular aneurysm (berry aneurysm)

  • 905 in ICA territory
  • 10% in vertebrobasilar
65
Q

what causes a berry aneurysm

A

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
Q

what is seen pathologically after the rupture of a berry aneurysm

A

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
Q

what are the risk factor for a subarachnoid haemorrhage

A

(berry aneurysm)
smoking
hptx
kidney disease

68
Q

what is the clinical features of a sub arachnoid haemorrhage

A 
severe headache 
vomiting 
loss of consciousness 
women> men 
survivors at risk of hydrocephalus

Neurology (35 decks)

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