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Neurology - professional - batt > Cerebrovascular disease > Flashcards

Cerebrovascular disease Flashcards

1
Q

What are to modes of response that nerve cell/ their processes have to injury?

A

rapid necrosis with sudden acute functional failure or slow atrophy with gradually increasing dysfunction

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2
Q

When does acute neuronal injury occur?

A

after hypoxia/ischaemia

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3
Q

When is acute neuronal injury visible after an injury to the cell?

A

12-24 hours

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4
Q

What is seen in acute neuronal injury?

A

shrinking and angulation of nuclei; loss of the nucleolus and intensely red cytoplasm

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5
Q

What is Wallerian degeneration?

A

antegrade degeneration of axona and myelin sheath distal to injury

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6
Q

What happens to the cell body when there is damage to the axon?

A

increased protein synthesis causing cell body swelling and an enlarged nucleolus; chromatolysis- migration and loss of Nissl granules

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7
Q

When does simple neuronal atrophy occur?

A

with chronic degradation eg in MS or Alzheimers

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8
Q

What is seen cellularly with simple neuronal atrophy?

A

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

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9
Q

What are common examples of inclusions in neurones?

A

can accumulate with age; common in neurodegenerative conditions eg neurofibrillary tangles in Alzheimers and in viral infections

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10
Q

What is a difference between the metabolism of astrocytes and neurones?

A

astrocytes carry out anaeriobic glycolysis

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11
Q

What is the main cell involved in repair and scar formation in the brain?

A

astrocytes

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12
Q

What is the most important indicator of CNS injury?

A

gliosis

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13
Q

What occurs in gliosis?

A

astorpcyte hyperplasia nad hypertrophy; get enlarged vesicular nuclei with prominent nucleoli; cytoplasmic expansion with extension of ramifying processes

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14
Q

How do old gliotic lesions appear?

A

nuclei become small and dakr and lie in a dense net of glial fibrils

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15
Q

How are Schwann cells involved with axonal loss in the PNS?

A

Schwann cells can assist the regrowth of axons through organising a neural tube

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16
Q

What type of damage are oligodendrocytes sensitive to?

A

oxidative damage

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17
Q

What does disruption of ependymal cells lead to?

A

a local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulation

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18
Q

What are the two typees of microglial cell?

A

M1 and M2

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19
Q

What is the function of M1 microglial cells?

A

pro-inflammatory, more chronic

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20
Q

what is the function of M2 microglial cells?

A

anti-inflammatory, phagocytic and moreacute

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21
Q

What is thought to be large reason the brain has such high energy demands?

A

neuronal membrane sodium/potassium ATPases for APs

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22
Q

What is the maximum that cerebral blood flow can increase to maintain oxygen delivery?

A

twofold

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23
Q

Why are neurones so vulnerable CNS cells?

A

metabolically dependent on oxidative phosphorylation

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24
Q

What happens to the neurone with hypoxia nad hypoglycaemia and therefore energy failure?

A

there is neuronal depolarisation and astrocyte reuptake is inhibited so there is a glutamate soterm and excitation

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25
Q

What does a glutamate storm lead to?

A

influx of calcium into the cell which results in protease activation; mitochondrial dysfunction; oxidative stress; apoptosis and necrosis

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26
Q

What happens in cytotoxic oedmea?

A

osmotically active extracellular ions eg sodiu mand clhoride move into dying cells

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27
Q

What does cytotoxic oedema lead to?

A

ionic and vasogenic oedema

28
Q

What causes ionic oedema?

A

because of cytotoxic oedema, the extracellular space is relatively devoid of sodium so sodium crosses the BBB, driving chloride entry and water

29
Q

What causes vasogenic oedema?

A

when there is deterioration and breakdown of the BBB albumin passes into the axtracellular space bringing water- not RBCs

30
Q

What is haemorrhagic conversion?

A

when integrity of the BBB is completely lost and blood enters the extracellular space

31
Q

What parts of the brain does the anterior cerebral artery sjupply?

A

media frontal and parietal lobes

32
Q

What areas does the middle cerebral artery supply?

A

the lateral frontal and temporal lobes

33
Q

Where does the posterior cerebral artery supply?

A

the occipital lobe

34
Q

What would be affected by a blockage in the anterior cerebral artery?

A

trunk legs sensory and motor abnormalities; frontal lobe dysfunction and higher cognitive dysfunction

35
Q

What would be affected by a blockage in the middle cerebral artery?

A

major bulk of the sensory and motor cortices would be affected

36
Q

What is global hypoxic ischaemia damage?

A

systemic compromise to circulation which cannot be compensated for by CNS autoregulation

37
Q

What is focal ischaemia?

A

restriction of blood flow to a localised area of the brain

38
Q

What are watershed areas?

A

zone between 2 arterial territories

39
Q

Which areas of the brain are most sensitive to global hypoxic ischaemic damage?

A

watershed areas

40
Q

Which neurones are most sensitive within the brain?

A

those within neocortex; hippocampus and purkinje cells of the cerebellum

41
Q

What is the most common area for thrombosis in the cerebral bloodsupply?

A

middle cerebral artery

42
Q

What is seen between 12-24 hours after cerebral infarction?

A

pale soft and swollen with illdefined margin between injured and normal brain; red neuron; cytotoxic and vasogenic oedema with generalised cell swelling

43
Q

What is seen 24-48 horus post infarction?

A

increasing neutrophils; extravasation of RBCs and activation of astrocytes and microglia

44
Q

What is seen 2-14 days post infarction?

A

brain is gelatinous and friable; oedeam demarcates lesion; microglia become predominant cell type; myelin breakdown; reactive gliosis

45
Q

What is seen several months post-infarction?

A

increasing liquification; eventual cavity lined by dark grey tissue; ongoing phagocytosis brings cavitation and surroung gliotic scar

46
Q

What is a gliotic scar characterised by?

A

astrocytes with abundant fine cytoplasmic processes

47
Q

What are the two causes of a haemorrhagic infarct?

A

haemorrhagic conversion and ischaemia; reperfusion results in haemorrhage thorugh damaged vessels

48
Q

What symtpoms are seen with middle cerebral artery lesions?

A

weakness predominantly contralateral face and arm

49
Q

What symptoms are seen with anterior cerebral artery lesions?

A

weakness and sensory loss in contralateral leg

50
Q

What symptoms are seen with vertebro-basilar artery disease?

A

vertigo; ataxia; dysarthrai and dysphagia- brainstemsyndrome

51
Q

What is name of the micro-aneurysms that develop with chronic hypertension?

A

Charcot-Bouchard

52
Q

Where are Charcot-Bouchard lesions often found?

A

in small MCA branches most commonly within the basal ganglia

53
Q

What are lacunar infarcts?

A

infarcts of deep cerebral white matter; basal ganglia or pons from a single small penetrating vessel

54
Q

What do lots of lacunar infarcts lead to?

A

multi-infarct dementia

55
Q

What are the causes of spontaneous intracranial haemorrhage?

A

intracerebral haemorrhage; sub-arachnoid haemorrhage and haemorrhagic infarct

56
Q

What is an important risk factor in spontaneous haemorrhage?

A

HT

57
Q

What are contributing factors to intracerbral haemorrhage?

A

aneurysm; systemic coagulation disorder; vascular malformation; amyloid deposits; vasculitis; neoplasm

58
Q

How does amyloid angiopathy lead to haemorrhage?

A

deposition of protein leads to vessels becoming less compliant and more likley to rupture and lead to a lobar intracerebral haemorrhage

59
Q

What are the most common vascular malformations leading to haemorrhage?

A

AV malformations; cavrnous angioma

60
Q

As well as bleeding what else are AV malformations implicated in?

A

are SOLs which can lead to focal neuro deficits; seizrues and headaches

61
Q

Where are AVMs most commonly founjd?

A

in cerebral hemispheres in MCA territory

62
Q

What is the most common cause of a subarachnoid haemorrhage?

A

rupture of a saccular aneurysm eg Berry

63
Q

Where are the majority of subarachnoid haemoorhages?

A

in the territory of the ICA, at arterial bifurctions

64
Q

What happens due to the mass effecti nthe ubsarachnoid space?

A

CSF is obstructed leading to hydrocephalus

65
Q

What are the symtpoms of subarachnoid haemorrhahge ?

A

severe headache; vomiting and LOC; meningeal signs

Neurology - professional - batt (40 decks)

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