Neuropathology Flashcards

1
Q

Describe the two types of microglia cells; M1 and M2

A
M1 = pro- inflammatory, chronic 
M2= anti-inflammatory, phagocytic, acute
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2
Q

What is gliosis?

A

An indicator of CNS injury

Astrocyte hyperplasia and hypertrophy

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3
Q

What is chromatolysis?

A

Margination and loss of Nissl granules

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4
Q

What is wallerian degeneration?

A

Degeneration of the axon and myelin sheath distal to the site of injury

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5
Q

The brain receives what % of CO?

A

The brain receives 15% of CO and uses 20% of the total body oxygen consumption

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6
Q

What is meant by ‘excitotoxicity’?

A

Energy failure in the cell

Pathological process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters

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7
Q

Describe cytotoxic oedema and its causes

A

More water in the cell (ICP is not raised)

Intoxication/ severe hypothermia

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8
Q

Describe ionic oedema and its causes

A

AKA osmotic oedema

Hyponatraemia/ excess water intake/ SIADH

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9
Q

Causes of vasogenic oedema

A

Trauma/ tumours/ inflammation/ infection/ hypertension/ encephalopathy

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10
Q

Infarcts in the brain most commonly affect which artery territory?

A

MCA (middle cerebral artery)

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11
Q

What are ‘watershed areas’ and why are these particularly sensitive to infarcts?

A

Watershed areas are the zones between two arterial territories

They are sensitive to infarcts as they are distant from the heart and therefore not very well supplied

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12
Q

Some neurones are more sensitive than others to infarction. Give two examples.

A

Neurons in the neocortex and hippocampus

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13
Q

Describe the differences between global and focal infarctions

A

Global infarctions involve a generalised reduction in blood flow/ oxygenation. Examples include severe hypotension and cardiac arrests.

Focal infarctions involve restriction to blood flow in a localised area of the brain due to vascular obstruction.

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14
Q

What would the brain look like 12-24 hours after a stroke?

A

Pale, soft and swollen
Red neurons
Oedema
Neutrophils

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15
Q

What would the brain look like months after a stroke?

A

Liquified
Cavities form which are lined by dark grey tissue
Gliotic scar formation

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16
Q

What are the two mechanisms for haemorrhage?

A

Disruption of the BBB

Haemorrhagic conversion

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17
Q

Neglect syndrome indicates damage to which side of the brain?

A

Right side

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18
Q

Aphasia/dysphasia indicates damage to which side of the brain?

A

Left side

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19
Q

How would a vascular lesion in the middle cerebral artery present?

A

Weakness of the contralateral face and arm

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20
Q

How would a vascular lesion in the anterior cerebral artery present?

A

Weakness and sensory loss in the contralateral leg

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21
Q

How would a vascular lesion in the vertebra-basilar artery system present?

A

Vertigo, ataxia, dysarthria and dysphagia

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22
Q

What are lacunae?

A

Lacunar infarcts

  • Small infarcts in deep parts of the brain
  • many are incidental findings (not that significant)
  • multiple lacunar infarcts can contribute to multiple infarct dementia
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23
Q

What is a charcot-bouchard aneurysm?

A

These are micro-aneurysms occurring in small vessels

Occur mostly in the MCA branches in the basal ganglia

Rupture causes intracerebral haemorrhage

24
Q

What is amyloid angiopathy and when does this occur?

A

Amyloid angiopathy involves the deposition of amyloid in vessels, causing them to become less compliant

Can lead to rupture causing intracerebral haemorrhage

This is an age-related process and occurs in alzheimer’s

25
Q

Describe arteriovenous malformations

A

These are abnormal torturous vessels which involve shunting from artery to vein

The vein undergoes smooth muscle hypertrophy, becomes less compliant and ruptures easily

Most AVMs occur in the MCA territory

They are the most common congenital vascular malformation

26
Q

Describe the two following primary demyelinating disorders;
Acute disseminated encephalomyelitis (ADEM)

Acute haemorrhage leukoencephalitis (AHL)

A

ADEM

  • self limiting - low mortality
  • occurs in children
  • autoimmune

AHL

  • fatal - high mortality
  • occurs in adults
  • high mortality
27
Q

Give some examples of primary demyelinating disorders

A

MS
ADEM
AHL

28
Q

Give some examples of secondary demyelinating disorders

A

(PML) Progressive multifocal leukoencephalopathy - (Viral disease)

Central pontine myelinosis (over rapid correction of hyponatraemia)

Toxic insults e.g with cyanide or CO

29
Q

Is MS a white matter or grey matter disease?

A

MS is a white matter disease as this is the part of the brain which is myelinated

30
Q

Describe the appearance of the plaques which you get in MS

A

Well circumscribed, well demarcated plaques with a glassy/ translucent appearance

31
Q

Describe the differences between active and inactive plaques in MS

A

Active plaques

  • ongoing demyelination
  • microglial cells
  • plaques are yellow/brown with an ill defined edge (blends into the white matter)

Inactive plaques

  • glosis predominates
  • well demarcated grey/brown lesions in the white matter - classically located in the lateral ventricles
32
Q

Which neurodegenerative diseases are associated with the basal ganglia and brainstem?

A

Parkinson’s and Huntington’s

33
Q

Which condition is most associated with cortical atrophy?

A

Dementia

34
Q

What are some of the pathological features of alzheimer’s?

A

Amyloid angiopathy

Atrophy - compensatory widening of the ventricles (2ndry hydrocephalus)

Neuronal loss

Neurofibrillary tangles

Neuritic plaques

35
Q

What are some of the pathological features of Lewy body dementia?

A

Loss of pigmented lesions causes pallor in the substantial nigra

Reactive gliosis

Lewy bodies

36
Q

What are some of the pathological features of huntington’s?

A

Atrophy of the basal ganglia

Reduction in the size of the caudate nucleus

Cortical atrophy

37
Q

What are some of the pathological features of front-temporal dementia?

A

Extreme atrophy of the frontal lobe

Pick’s cells

38
Q

Where is CSF produced and absorbed?

A

CSF is produced by the choroid plexus in the lateral and fourth ventricles

CSF is absorbed by the arachnoid granulations

39
Q

What are some of the causes of raised ICP?

A

Increased CSF

SOL

Oedema

Increased venous volume

40
Q

What are some of the effects of raised ICP on the brain?

A

Intracranial shifts and herniations “cloning”

Midline shift

Pressure on cranial nerves

Impaired blood flow

41
Q

What are some of the clinical signs of raised ICP?

A

Papilloedema

Headache

Neck stiffness

N&V

42
Q

Describe a sulfalcine herniation

A

Expansion of the cerebral hemisphere displaces the cingulate gyrus under the falx cerebri

43
Q

Describe a tectorial herniation

A

Medial aspect of the temporal lobe herniates over the tentorium cerebelli

44
Q

Describe a cerebellar herniation

A

Displacement of the cerebellar tonsils through the foramen magnum

45
Q

What are the 3 causes of hydrocephalus?

A

Obstruction to CSF flow

Decreased reabsorption of CSF

Overproduction of CSF

46
Q

What is the difference between communicating and non-communicating (obstructive) hydrocephalus?

A

Obstructive (non-communicating)

  • Due to a structural pathology outwith the ventricular system blocking the flow of CSF
  • Dilatation of the ventricular system is seen superior to site of obstruction
  • Causes include: tumours, haemorrhage, aqueduct stenosis and arnold chiari malformations

Non-obstructive (communicating)

  • Due to an imbalance of CSF production and absorption (referred to as communicating as it is a problem within the ventricular system)
  • E.g chord plexus tumours cause increased CSF production (v.rare)
  • E.g meningitis or post-haemorrhage cause failure of reabsorption at the arachnoid granulations
47
Q

What is meant by the term ‘Hydrocephalus Ex Vacuo’?

A

Occurs when there is damage to the brain caused by stroke or injury, causing a shrinkage of the brain

Although there is more CSF than usual, the CSF pressure itself is normal.

48
Q

Give examples of space occupying lesions

A

Tumours
Abscesses
Haematomas
Localised brain swelling

49
Q

What is the most common type of brain tumour in children?

A

Medullobastoma

50
Q

Where do most tumours arise in relation to the tentorium cerebelli in children vs adults?

A

Most tumours arise below the tentorium cerebelli in children and above the tentorium cerebelli in adults

51
Q

What is the most common cause of brain tumours?

A

Metastasis
(much more common than primary bone tumours)

Mets from; breast, lung, kidney, thyroid and colon

52
Q

What is the most common type of tumour in adults?

A

Astrocytoma

53
Q

What are some possible causes of abscesses in the brain?

A

Local extension e.g from mastoiditis

Direct implantation of infectious agents e.g from skull fractures and penetrating injuries

Haematogenous spread from infections elsewhere

54
Q

How would a brain abscess be investigated and managed?

A

Diagnosis; CT/ MRI +aspiration for culture

Management; aspiration and antibiotics

55
Q

Why are the frontal and temporal lobes at greater risk of contusions?

A

The undersurface of the lobes have sharp bony prominences causing them to be at increased risk of contusions and lacerations

56
Q

What is meant by coup and contracoup?

A

Coup are surface contusions/ lacerations occurring at the point of impact

Contracoup occur at the opposite side from the point of impact and are often worse than coup injuries