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Neurology > Neuropathology I > Flashcards

Neuropathology I Flashcards

1
Q

What are the cellular components of the CNS?

A

Nerve cells, microglia, glial cells and supporting structures

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2
Q

What are some examples of glial cells?

A

Astrocytes, oligodendrocytes, ependymal cells

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3
Q

What are some supporting structures of the CNS?

A

Connective tissue, meninges, blood vessels

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4
Q

What are some causes of CNS injury?

A

Hypoxia, trauma, toxic insult, metabolic abnormalities, nutritional deficiencies, infections, genetic abnormalities, ageing

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5
Q

What can damage to nerve cells or their processes lead to?

A

Rapid necrosis with sudden acute functional failure

Slow atrophy with gradually increasing dysfunction

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6
Q

What causes acute neuronal injury?

A

Hypoxia or ischaemia = results in neuronal death

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7
Q

When does acute neuronal injury become visible?

A

Typically 12-24hrs after an irreversible insult to the cell

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8
Q

What are the features of acute neuronal injury?

A

Shrinking and angulation of nuclei
Loss of nucleus
Intensely red cytoplasm

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9
Q

What are some examples of axonal reactions?

A

Increased protein synthesis leading to cell body swelling and enlarged nucleolus
Chromatolysis
Inclusions

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10
Q

What is chromatolysis?

A

Margination and loss of Nissl granules

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11
Q

What are some features of axonal inclusions?

A

Common in neurodegenerative conditions
Accumulate with ageing
Can occur in viral infections

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12
Q

What is the appearance of astrocytes?

A

Star shaped with multipolar cytoplasmic processes = present throughout CNS

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13
Q

What are some features of astrocytic processes?

A

Envelop synaptic plates

Wrap around vessels and capillaries within the brain

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14
Q

What is the function of astrocytes?

A

Repair and scar formation

Work with endothelial cells to maintain BBB

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15
Q

What is the most important histopathological indicator of CNS injury?

A

Gliosis = astrocyte hyperplasia and hypertrophy, with cytoplasmic expansion and extension of ramifying processes

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16
Q

What happens to the nucleus of the astrocyte in gliosis?

A

Enlarges = becomes vesicular with prominent nucleolus

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17
Q

How do old gliotic lesions appear?

A

Nuclei become small and dark, and lie in a dense net of glial fibrils

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18
Q

What forms the myelin sheath?

A

Oligodendrocytes = wrap around axons

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19
Q

How do oligodendrocytes react to injury?

A

Limited reaction = demyelination and apoptosis

Sensitive to oxidative damage

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20
Q

Where are ependymal cells found?

A

Line the ventricular system = infectious agents produce changes in these cells

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21
Q

What is disruption of ependymal cells associated with?

A

Local proliferation of sub-ependymal astrocytes = produces ependymal granulations

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22
Q

What is the function of microglia?

A

Function as macrophages = embryologically derived

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23
Q

How do microglia respond to injury?

A

Microglia proliferate and are recruited through inflammatory mediators = form aggregates around areas of necrosis and tissue damage

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24
Q

How are microglia important mediators of acute nervous system injury?

A 
M2 = anti-inflammatory, phagocytic, more acute
M1 = pro-inflammatory, more chronic
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25
Q

What is the most important baseline cause of neuronal injury?

A

Hypoxia = cerebral ischaemia, infarct, haemorrhage, cerebral palsy, cardiac arrest

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26
Q

How much of the body’s resting oxygen does the brain consume?

A

20% = cerebral blood flow can only increase twofold to maintain oxygen delivery

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27
Q

What does onset of ischaemia cause the mitochondria to do?

A

Causes mitochondrial inhibition of ATP synthesis = leads to ATP reserves being consumed in minutes

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28
Q

What are the different kinds of oedema?

A

Cytotoxic, ionic, vasogenic and haemorrhagic conversion

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29
Q

What are some causes of cytotoxic oedema?

A

Intoxication, Reye’s and severe hypothermia

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30
Q

What causes ionic oedema?

A

Also called osmotic oedema = hyponatraemia and excess water intake

31
Q

What is the most important kind of oedema?

A

Vasogenic = caused by trauma, tumours, inflammation, infection or hypertensive encephalopathy

32
Q

What is the definition of cerebrovascular disease?

A

Any abnormality of the brain caused by a pathological process in blood vessels

33
Q

What is the epidemiology of cerebrovascular disease?

A

3rd commonest cause of death

Commonest cause of adult disability

34
Q

What are the different kinds of cerebrovascular disease?

A

Brain ischaemia and infarction, haemorrhages, vascular malformations, aneurysms

35
Q

What are the two types of cerebral ischaemia?

A

Global or focal (vascular obstruction)

36
Q

What is global hypoxic ischaemic damage?

A

Generalised reduction in cerebral perfusion = autoregulatory mechanisms cannot compensate

37
Q

What are the causes of global hypoxic ischaemic damage?

A

Cardiac arrest, shock/severe hypotension, trauma

38
Q

What areas are particularly sensitive to global hypoxic ischaemic damage?

A

Watershed areas = zone between two arterial territories

39
Q

What cell types are most sensitive to global hypoxic ischaemic damage?

A

Neurons more sensitive than glial cells = neurons of neurocortex and hippocampus are most sensitive

40
Q

What does severe ischaemia in global hypoxia ischaemic damage lead to?

A

Pan-necrosis

41
Q

What is a stroke?

A

Sudden disturbance of cerebral function of vascular origin

42
Q

What causes a cerebral infarction?

A

Interruption of cerebral blood flow due to thrombosis or emboli

43
Q

What is the epidemiology of cerebral infarction?

A

Peak incidence age >70

More common in men

44
Q

What are the two types of cerebral infarctions?

A 
Thrombotic = usually middle cerebral artery territory
Embolic = from atheroma in internal carotid or aortic arch
45
Q

What are the risk factors for cerebral infarctions?

A

Atheroma, hypertension, obesity, diabetes, heart disease, disease of neck arteries, drugs, smoking

46
Q

What changes can be seen up to 24hrs after a cerebral infarction?

A 
0-12hrs = little change visible
12-24hrs = pale soft and swollen with ill defined margin between injured and normal brain, red neuron and oedema with generalised cell swelling
47
Q

What changes can be seen 24-48hrs after a cerebral infarction?

A

Pale soft and swollen with ill defined margin between injured and normal brain, increasing neutrophils and extravasation of RBC, activation of astrocytes/microglia

48
Q

What changes occur 2-14 days after a cerebral infarction?

A

Brain becomes gelatinous and friable, reduction in surrounding tissue oedema, microglia become predominant cell type, reactive gliosis begins from week 1

49
Q

What changes occur several months after a cerebral infarction?

A

Increasing liquefication, cavity with dark grey tissue lining, ongoing phagocytosis brings increasing cavitation and surrounding gliotic scar formation

50
Q

What occurs in haemorrhagic infarcts?

A

BBB disruption and haemorrhagic conversion

51
Q

What is thrombolysis?

A

Occlusion of a vessel with reperfusion and leakage through a damaged capillary bed following lysis of the embolus

52
Q

What symptoms occur if there is a lesion of the carotid artery?

A

Contralateral weakness or sensory loss, if dominant hemisphere there may be aphasia or apraxia

53
Q

What symptoms occur if there is a lesion in the middle cerebral artery?

A

Weakness = predominantly contralateral face and arm

54
Q

What symptoms occur if there is a lesion of the anterior cerebral artery?

A

Weakness and sensory loss in the contralateral leg

55
Q

What symptoms occur if there is a lesion in the vertebro-basilar artery?

A

Vertigo, ataxia, dysarthria, dysphagia

56
Q

What features occur in hypertension?

A

Accelerated atherosclerosis, lacunes, hyaline atherosclerosis, micro-aneurysms

57
Q

What are the consequences of atherosclerosis?

A

Lacunar infarcts, multi-infarct dementia, hypertensive encephalopathy, ruptured aneurysms and intra-cerebral haemorrhage

58
Q

What are the types of spontaneous intracranial haemorrhages?

A

Intracerebral, subarachnoid or due to haemorrhagic infarct

59
Q

What are some causes of traumatic intracranial haemorrhage?

A

Extra/subdural haematoma, contusion, intracerebral or subarachnoid haemorrhage

60
Q

What are the contributing factors to an intracerebral haemorrhage occurring?

A

Hypertension, aneurysms, coagulation disorders, vascular malformations, amyloid deposits, open heart surgery, neoplasms, vasculitis

61
Q

What are the most common sites for intracerebral haemorrhages?

A

Basal ganglia, thalamus, cerebral white matter or cerebellum

62
Q

What are the features of an intracerebral haemorrhage?

A

Asymmetrical distortion, herniations and shifts, well demarcated intraparenchymal haematomas, sofetning of adjacent tissue, surrounding oedema

63
Q

What are some vascular malformations that can cause major bleeds?

A

Arteriovenous malformations and cavernous angiomas

64
Q

What are some vascular malformations which rarely bleed?

A

Venous angiomas and capillary telangectases

65
Q

What additional symptoms can vascular malformations cause?

A

Seizures, headaches and focal neurological deficits

66
Q

What are some features of arteriovenous malformations?

A

Abnormal tortuous vessels shunting from artery to vein = undergo smooth muscle hypertrophy, non-compliant and rupture easily, form aneurysms

67
Q

What are the two types of subarachnoid haemorrhage?

A

Spontaneous or traumatic

68
Q

What is the most common cause of a subarachnoid haemorrhage?

A

Ruptured berry aneurysm = 90% in territory of ICA, other 10% in territory of vertebro-basilar circulation

69
Q

Where do subarachnoid haemorrhages arise?

A

At arterial bifurcations = blood enters subarachnoid space

70
Q

What are some features of subarachnoid haemorrhages?

A

Intracerebral haematomas adjacent to aneurysms

Infarcts of brain parenchyma

71
Q

What are the risk factors for subarachnoid haematomas?

A

Smoking, hypertension and kidney disease

72
Q

What are the clinical features of subarachnoid haemorrhages?

A

Abrupt onset and no history of precipitating factor
Severe headache and loss of consciousness
Vomiting

73
Q

What is the prognosis of a subarachnoid haemorrhage?

A

50% die within several days of onset

Survivors are at risk of hydrocephalus

Neurology (48 decks)

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