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ESA 5 - Nervous System > Introduction to Neuropathology > Flashcards

Introduction to Neuropathology Flashcards

1
Q

What commensal organisms are present in the CNS?

A

None - it is normally sterile

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2
Q

How might microorganisms gain entry to the CNS?

A
  • Direct spread
  • Blood-bourne
  • Iatrogenic
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3
Q

GIve two examples of where infection might spread to the CNS by direct spread

A
  • Middle ear infection
  • Base of skull fracture
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4
Q

How are patients with a basal skull fracture managed?

A

Aseptically, with prophylactic antibiotics

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5
Q

What infections might spread to the CNS by the blood bourne route?

A
  • Sepsis
  • Infective endocarditis
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6
Q

How does infective endocarditis spread to the CNS?

A

An emboli from the infected heart valves travels to the brain

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7
Q

What are the iatrogenic causes of CNS infection?

A
  • V-P shunt
  • Surgery
  • Lumbar puncture
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8
Q

What is meningitis?

A

Inflammation of the leptomeninges

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9
Q

How does meningitis spread?

A

In the blood

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10
Q

Does meningitis present with septicaemia?

A

Can present with or without

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11
Q

What is essential in meningitis?

A

Prompt diagnosis and treatment

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12
Q

What are the causative organisms of meningitis in neonates?

A
  • E.coli
  • L. monocytogenes
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13
Q

What are the causative organisms of meningitis in 2-5 year olds?

A

H. influenzae type B

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14
Q

What are the causative organisms of meningitis in 5-30 year olds?

A

N. Meningitidis

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15
Q

What are the causative organisms of meningitis in people over 30 years?

A

S. pneumoniae

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16
Q

What organism causes chronic meningitis?

A

M. tuberculosis

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17
Q

What are the features of chronic meningitis?

A
  • Granulomatous inflammation
  • Fibrosis of meninges
  • Nerve entrapment
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18
Q

What are the local complications of meningitis?

A
  • Death
  • Cerebral infarction
  • Cerebral abscess
  • Subdural empyema
  • Epilepsy
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19
Q

How does meningitis cause death?

A

Swelling leads to raised intracranial pressure, leading to death

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20
Q

What does cerebral infarction in meningitis lead to?

A

Neurological deficit

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21
Q

When do systemic complications of meningitis occur?

A

If it is associated with septicaemia

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22
Q

Is encephalitis caused by viruses or bacteria?

A

Classically viral

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23
Q

What is affected in encephalitis?

A

The parenchyma, not the meninges

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24
Q

What does the virus cause in encephalitis?

A

Neuronal cell death

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25
Q

What is neuronal cell death in encephalitis characterised by?

A

Inclusion bodies

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26
Q

What causes temporal lobe encephalitis?

A

Herpes virus

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27
Q

What causes spinal cord motor neurones encephalitis?

A

Polio

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28
Q

What causes brain stem encephalitis?

A

Rabies

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29
Q

What kind of inflammatory reaction can cause encephalitis?

A

Lymphocytic

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30
Q

What is a prion?

A

A protein that is a normla constituent of the synapse, but of unkown function

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31
Q

How can mutated PrP (prion protein) be obtained?

A
  • Sporadic
  • Familial
  • Ingested
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32
Q

What effect does mutated PrP have?

A

It interacts with normal PrP to undergo post translocation conformational change

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33
Q

What is the result of PrPSC being extremely structurally stable?

A

It accumulates and aggregates

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34
Q

What is the result of the accumulation and aggregation of PRPSC?

A

Causes neuronal death and ‘holes’ in grey matter

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35
Q

What kind of neuropathology are caused by prions?

A

Spongiform encephalopathies

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36
Q

Give two examples of human spongiform encephalopathies

A
  • Kuru
  • Variety Creutzfeld-Jacob disease (vCJD)
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37
Q

Is vCJD different from classical CJD?

A

Yes

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38
Q

What is unique about each case of vCJD?

A

It has a unique genetic prion sequence

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39
Q

What supports the association between vCJD and BSE?

A

Strong laboratory and epidemiological evidence

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40
Q

How long does vCJD incubate for?

A

15+ years

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41
Q

What is the difficulty of eradicating vCJD?

A

Prions are not eradicated by traditional sterilisation

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42
Q

What is the difference between classic CJD and vCJD in terms of median age of death?

A
  • Classic = 68 years
  • Variant = 28 years
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43
Q

What is the difference between classic CJD and vCJD in terms of median duration of illness?

A
  • Classic = 4-5 months
  • Variant = 13-14 months
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44
Q

What are the clinical signs and symptoms of classic CJD?

A

Dementia and early neurologic signs

45
Q

What are the clinical signs and symptoms of vCJD?

A
  • Prominent psychiatric/behavioural symptoms
  • Painful dyesthesiasis
  • Delayed neurologic signs
46
Q

What is the difference between classic CJD and vCJD in terms of the electroencephalogram presentation?

A

With classic CJD, periodic sharp waves on the electroencephalogram are often present. With vCJD, these are often absent

47
Q

What is the difference between classic CJD and vCJD in terms of the presence of ‘florid plaques’ on neuropathology?

A

In classic CJD, they are rare or absent. In vCJD, they are present in large numbers

48
Q

What is the difference between classic CJD and vCJD in terms of immunohistochemical analysis of brain tissue?

A

In classic CJD, there is variable accumulation. In vCJD, there is marked accumulation of protease-resistance prion protein

49
Q

What is the difference between classic CJD and vCJD in terms of the presence of agent in the lymphoid tissue?

A

In classic CJD, it is not readily detected. In variant CJD, it is readily detected

50
Q

What criteria of infections do prion diseases not fulfill?

A
  • The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms
  • The microorganism must be isolated from a diseased organism, and grown in pure culture
  • The cultured microorganism should cause a disease when introduced into a healthy organism
  • The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being indentical to the original specific causative agent
51
Q

What is dementia defined as?

A

Acquired global impairment of intellect, reason, and personality, without impairment of consciousness

52
Q

What are the types of dementia?

A
  • Alzheimer’s
  • Vascular dementia
  • Lewy body
  • Picks disease
53
Q

What % of cases of dementia are caused by Alzheimer’s?

A
  • 50%
54
Q

What is Alzheimer’s disease?

A

A disease characterised by exaggerated ageing process

55
Q

What is the pathological process in Alzheimers disease?

A

There is a loss of cortical neurones due to increased neural damage, leading to decreased brain weight and cortical atrophy

56
Q

What can cause neuronal damage in Alzheimers?

A
  • Neurofibrillary tangles
  • Senile plaques
57
Q

What are neurofibrillary tangles?

A

Intracellular twisted filaments of Tau protein

58
Q

What does Tau normally do?

A

Binds and stabilises microtubules

59
Q

What happens to Tau in Alzheimers?

A

It gets hyperphosphorylated

60
Q

What are senile plaques?

A

Foci of enlarged axons, synaptic terminals, and dendrites with amyloid deposition in vessels in the centre of the plaque

61
Q

What condition can predispose to Alzheimers?

A

Down’s syndrome - leads to early onset AD

62
Q

What mutations can predipose to Alzheimers?

A

3 mutations on chromosome 21;

  • Amyloid precursor protein (APP) gene
  • Presenilin (PS) genes 1 and 2, which code for components of secretase enzyme
63
Q

Why does mutation of PS genes 1 and 2 lead to Alzheimers?

A

It leads to incomplete breakdown of APP, and amyloid deposition

64
Q

What is the normal intracranial pressure (ICP)?

A

0-10mmHg

65
Q

When might ICP be increased physiologically?

A

During coughing and straining - increase to 20mmHg

66
Q

When is a rise in ICP significant?

A

If the increase in maintaned for several minutes

67
Q

What is employed to maintain a normal ICP?

A

Compensation mechanisms

68
Q

What are the compensation mechanisms aiming to reduce ICP?

A
  • Reduced blood volume
  • Reduced CSF volume
  • Brain atrophy
69
Q

At what ICP can vascular mechanisms maintain cerebral blood flow?

A

<60mmHg

70
Q

What does an expanding lesion in the brain cause?

A
  • Deformation or destruction of the brain around the lesion
  • Displacement of the midline structures, leading to loss of symmetry
  • Brain shift resulting in herniation
71
Q

What is a hernia?

A

A protrusion of an organ or part of an organ through a wall that normally contains it

72
Q

What are the types of brain herniation?

A
  • Subfalcine
  • Tentorial
  • Tonsilar
73
Q

Do subfalcine haemorrhages occur on the same side, or the opposite side, of the mass?

A

Same side

74
Q

What happens in a subfalcine herniation?

A

The cingulate gyrus is pushed under the gree edge of the falx cerebri

75
Q

What does a subfalcine herniation cause?

A

Ischaemia of the medial parts of the frontal and parietal lobe and corpus callosum due to compression of the anterior cerebral artery, leading to infarction

76
Q

What happens in a tentorial herniation?

A

The uncus/medial part of the parahippocampal gyrus herniate through the tentorial notch

77
Q

What does a tentorial herniation cause?

A
  • Damage to the oculomotor nerve on the same side
  • Occlusion of blood flow in the posterior cerebral and superior cerebellar arteries
78
Q

Why is a tentorial herniation frequently fatal?

A

Because of secondary haemorrhage into the brainstem, leading to duret haemorrhage

79
Q

Where is tentorial herniation a common mode of death?

A

In those with large brain tumours and intracranial haemorrhage

80
Q

What happens in a tonsillar herniation?

A

Cerebellar tonsils are pushed into the foramen magnum, compressing the brainstem

81
Q

What origin to benign CNS tumours have?

A

Meningeal origin

82
Q

What is a benign tumour of the meninges called?

A

Meningioma

83
Q

What is the origin of malignant CNS tumours?

A

Astrocytes

84
Q

What are malignant tumours of astrocytes called?

A

Astrocytomas

85
Q

How do astrocytomas progress?

A

They spread along the nerve tracts, and through the subarachnoid space

86
Q

How do astrocytomas often present?

A

WIth a spinal secondary

87
Q

Give three examples of other CNS tumours

A
  • Neurofibromas
  • Ependyomas
  • Neuronal tumours, e.g. medullobastoma
88
Q

What is the most common form of CNS tumour

A

Metastasis from other tissues

89
Q

What is a stroke?

A

A sudden event producing a disturbance of CNS function due to vascular disease

90
Q

What do the clinical features of strokes depend on?

A

Site and type of lesion

91
Q

What are the categories of strokes?

A
  • Cerebral infarction (85%)
  • Cerebral haemorrhage (15%)
92
Q

What risk factors are related to stroke?

A
  • Hyperlipidaemia
  • Hypertension
  • Diabetes mellitus
93
Q

What are the potential pathogenesis’ of stroke?

A
  • Embolism (most common)
  • Thrombosis
94
Q

What can cause embolisms leading to strokes?

A
  • Atrial fibrillation
  • Mural thrombus
  • Atheromatous debris from carotid atheroma
  • Thrombus over ruptured atheromatous plaque
  • Aneurysm
95
Q

What are the types of infarct in stroke?

A
  • Regional
  • Lacuna
96
Q

What is a regional infarct?

A

One that originates from a named cerebral artery, or carotid

97
Q

What is a lacuna infarct?

A

An infarct that is less than 1cm

98
Q

What are lacuna infarcts associated with?

A

Hypertension

99
Q

Where do lacuna infarcts commonly affect?

A

Basal ganglia

100
Q

What causes cerebral haemorrhages?

A

They are spontaneous, i.e. non-traumatic

101
Q

What are the types of cerebral haemorrhages?

A
  • Intracerebral (10% of all strokes)
  • Subarachnoid haemorrhages (5% of all strokes)
102
Q

What are intracranial haemorrhages associated with?

A

Hypertensive vessel damage

103
Q

What are Charcot-Bouchard aneurysms?

A

Aneurysms that occur in small blood vessels, which are a common cause of intracerebral haemorrhage

104
Q

What can predispose to intracerebral haemorrhages?

A

Deposition of amyloid around cerebral vessels in the elderly

105
Q

How do intracerebral haemorrhages cause brain pathology?

A

They produce a space occupying lesion, causing RICP

106
Q

What happens in subarachnoid haemorrhages?

A

There is rupture of ‘berry’ aneurysms

107
Q

What are the risk factors for subarachnoid haemorrhages?

A
  • Male sex
  • Hypertension
  • Atheroma
  • Links to other diseases
108
Q

Where are subarachnoid haemorrhages sited?

A

At branching points in the Circle of Willis

109
Q

What are the symptoms of subarachnoid haemorrhages?

A
  • Sudden severe headache
  • Sentinel headache
  • Loss of consciousness
  • Often instantly fatal*

ESA 5 - Nervous System (18 decks)

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