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Pathology > CNS Path > Flashcards

CNS Path Flashcards

1
Q

Describe Neurones

A
  • Functional and structural unit of CNS
  • Transmit electrical impulses
  • Excitable cells
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2
Q

Describe Neuroglia

A
  • Non-excitable cells
  • Outnumber neurones 5:1
  • There are 2 types:
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3
Q

Describe macroglia

A
  • Macroglia are a Type of Neuroglia

-There are 3 types of macroglia
—> Oligodendrocytes, Astrocytes, Ependymal cells

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4
Q

Describe Oligodendrocytes

A

Produce Myelin

Type of macroglial cell

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5
Q

Describe astrocytes

A

Type of macroglial, neuroglial cell

Role:

  • Scar formation
  • Metabolism
  • Barrier function
  • Repair
  • Nutrients
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6
Q

Describe Ependymal cells

A

Line the brain ventricles

Type of macroglial neuroglial cells

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7
Q

Describe Microglia

A

CNS Macrophages

Fixed

Type of neuroglial cell

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8
Q

List the control centres in the brainstem

A 
1. Cardiac
2 Pulmonary
3. Urinary
4. Vomitting
5. Swallowing
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9
Q

What is the normal volume of CSF?

A

120 ml

Replaced 3-5 x/d

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10
Q

Causes of obstructive hydrocephalus

A

Tumours:

  • Of brainstem or posterior fossa
  • Papilloma of choroid plexus
  • Colloid cyst in 3rd ventricle

Blood: - SAH

Infection: - Meningitis

Congenital:

  • Chiari Malformalion
  • Dandy Walker syndrome
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11
Q

Describe Chiari malformation

A
  • Part of the cerebellum is pushed through the foramen magnum
  • Blocks flow of CSF through the foramen magnum
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12
Q

Describe Dandy Walker syndrome

A
  • Cerebellar hyperplasia and/or cyst formation

- Causes obstruction of CSF flow through the Foramen Magnum

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13
Q

Describe Hydrocephalus Ex Vacuo

A
  • Compensatory dilatation of the ventricles in dementia

- Due to loss of brain parenchyma

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14
Q

Normal composition of intracranial contents

A

Brain = 70%

CSF = 15%

Blood = 15%

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15
Q

At what level of CSF does compensation cease and ICP starts to increase?

A

15mmHg

200ml CSF

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16
Q

Causes of increased ICP

A

Tumour
Abscess
Infarction
Haemorrhage

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17
Q

Clinical features of Raised ICP

A 
HA
Vomitting
Confusion
FNS (Paralysis, Hemianopia, Dysphasia)
Depressed consciousness
Seizure
Papilloedema
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18
Q

Define papilloedema

A

Bilateral swollen optic discs

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19
Q

3 FNS

A

Hemianopia
Dysphasia
Paralysis

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20
Q

4 stages of raised ICP

A
  1. Spatial compensation
  2. Spatial compensation exhausted
    - ICP increases
    - SAP increases (Cushing response)
  3. Rapid increased ICP, decreased cerebral perfusion
  4. ICP=SAP (vasomotor paralysis)
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21
Q

What type of patients cope best with raised ICP?

A

Elderly

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22
Q

Mechanisms of spatial compensation in raised ICP

A
  • Flattening of gyri
  • Compression of ventricles
  • Lateral shift in midline structures
  • Internal herniation
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23
Q

Types of internal herniation

A

Supracallosal/ subfalcine
- Cingulate gyrus through Falx cerebri

Uncal Herniation
- Unci through tentorial incisure

Tonsillar Herniation
- Cerebellar tonsils through foramen magnum

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24
Q

Complications of uncal herniation and signs

A

CN3 compression

  • Ptosis
  • Eye deviated down and out
  • Abnormally dilated pupils

Posterior cerebral A aneurysm

Haemorrhage in midbrain and pons

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25
Q

Complications of Tonsillar herniation

A

Brainstem compression (leads to death)

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26
Q

Types of cerebral oedema

A

Vasogenic Oedema

Cytotoxic Oedema

Interstitial Oedema

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27
Q

Definition and cause of Vasogenic oedema

A

Definition:
- Fluid leaks into brain parenchyma because BBB is disrupted

Cause:

  • Localised: Abscess, tumour, infarct
  • Generalised: Sepsis
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28
Q

Definition and cause of Cytotoxic oedema

A

Increased fluid as result of ischaemic injury

Cause: Generalised ischaemia

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29
Q

Definition and cause of Interstitial oedema

A

Increased fluid in peri ventricular tissues

Cause: Acute hydrocephalus

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30
Q

Rx of cerebral oedema

A
  • Steroids if tumour related

- Surgical removal if haemorrhage

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31
Q

Type of infarcts in the circle of willis

A

Wedge shaped watershed infarcts

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32
Q

Place in brain most susceptible to infarction

A

Area between anterior and middle cerebral artery

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33
Q

Define stroke

A

Focal and/or global loss of cerebral function

Lasting >24hrs

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34
Q

Define TIA

A

Transient Ischaemia Attack

Focal loss of cerebral or ocular function lasting <24hrs

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35
Q

Timeline of macroscopic features of infarction (brain)

A

0-6hrs = nothing

6-48hrs

  • Tissue pale and swollen
  • Loss of margin between grey and white matter

2-10d
- Tissue is gelatinous and friable

10-14d
- Liquefactive necrosis

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36
Q

Timeline of microscopic features of infarction (brain)

A

0-12hrs

  • Red neurones
  • Oedema

12-48hrs

  • Inflammatory response
  • Neutrophil polymorphs

2-3w
- Lots of microglia

> 3w
- Reactive astrocytosis surrounding the infarction

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37
Q

Causes of Intracerebral haemorrhage

6

A 
HTN
Amyloid angiography
Anticoagulants
Tumours
Vasculitis
AV Malformation
38
Q

Causes of Subarachnoid Haemorrhage

2

A

Berry aneurysm

AV malformation

39
Q

Causes of HTN which cause Intracerebral Haemorrhage

5

A

Large vessel atherosclerosis

Small vessel hyaline arteriolosclerosis

Charcot-Bouchard Microaneurysms

Lacunar Infarcts

Slit Haemorrhages

40
Q

Complications of lacunar infarcts

A

Accumulative effect to cause Multi-infarct dementia

41
Q

What would cause bleeding into the ventricular system?

A

Intracerebral haemorrhage of the basal ganglia

42
Q

Pathogenesis of amyloid angiography

A

Media of small penetrating vessels is replaced with amyloid

This causes vessel wall weakening

And increases the risk of rupture

43
Q

In what diseases/aspects of life do you see amyloid angiography?

3

A

Alzheimer’s

Down’s Syndrome

Aging

44
Q

Ix for amyloid angiography

2

A

Amyloid Immunological stain

OR

Congo-red stain (goes apple green under polarised light)

45
Q

What is AV malformation?

A

Abnormal connections between arteries and veins

Instead of joining via the capillary system, they just join up

46
Q

Epi AV malformation

A

3rd-4th decade

M>F

47
Q

Complication of AV malformation

A

Rupture

Intracerebral Haemorrhage
SAH

48
Q

Where do berry aneurysms occur?

A

Circle of Willis

49
Q

RF for Berry aneursym

3

A

PCKD
Neurofibromatosis
Marfan’s

50
Q

Causes of cardiac mural thrombi

3

A

MI
Valve disease
AF

51
Q

Causes of embolic stroke

A

Cardiac mural thrombi

Carotid atherosclerotic thromboembolism

Ventricular septal defects (structural abnormality)

Cardiac surgery

Tumour, Fat, Gas, Atherosclerosis, foreign body, Infection, amniotic fluid

52
Q

What % of brain tumours are mets?

A

50%

53
Q

Most common origins of brain mets

4

A

Breast
Prostate
Lung
GIT

54
Q

Brain Tumour should be a differential Dx in …

5

A

New onset epilepsy

Hydrocephalus

FNS

Balance/Gait abnormalities

Visual field defects

55
Q

Complications of Brain tumours

A 
Epillepsy, 
Hydrocephalus, 
FNS, 
Balance/gait abnormalities, 
Visual Field Defects

Raised ICP
Brainstem compression

56
Q

Ix of SOL

A
  1. CT or MRI

Confirm:

  1. Brain biopsy (send to histology)
  2. Brain smear (send to cytology)
57
Q

How are brain tumours named?

A

According to the cells from which they are derived

58
Q

Define Neuroblastoma

A

Tumour of neurones

59
Q

Define Meningioma

A

Tumour of the meninges

60
Q

Tumours of the Cranial Nerves

A

Schwannoma

Neurofibroma

61
Q

Define Gliomas

A

Tumours of Neuroglia:

Astrocytoma
Oligodendrocytoma
Ependymoma

62
Q

How are brain biopsies/smears graded?

A
  1. Degree of nuclear atypia
  2. Necrosis
  3. Endothelial hyperplasia
63
Q

Rx Brain tumour

A
  1. Surgical Excision
  2. Chemoradio
  3. Proton beam
64
Q

Weight of female adult brain

A

1250g

65
Q

Weight of male adult brain

A

1400g

66
Q

Gross features of cerebral atrophy

A

Narrowing (flattening) of gyri

Widening of the sulci

Compensatory enlargement of the centricular system

67
Q

Which area of the brain suffers most neurodegeneration in Alzheimer’s disease?

A

Hippocampus

68
Q

Which area of the brain suffers most neurodegeneration in parkinson’s disease?

A

Substantia Niagra

69
Q

Epi Alzheimer’s

A

F>M

47% >85yo

70
Q

Define neurodegeneration

A

Progressive neuronal degeneration and death

71
Q

Define dementia

A

An acquired global impairment of intellect, reason and personality , without impaired consciousness

72
Q

Gross appearance of an alzheimers brain

6

A

Cerebral atrophy:

  • Brain weight <1000g
  • Atrophy is mostly in the frontal and parietal lobes
  • Hippocampal atrophy
  • Compensatory enlargement of ventricular system (Hydrocephalus ex vacuo)
  • Widening of sulci
  • Flattening of the gyri
73
Q

Microscopic features of Alzheimers disease

4

A

Tau-2 +ve Neurofibrillary tangles

BA4-Amyloid Plaques
- Senile (Neuritic) plaques

Amyloid angiopathy

Neuronal loss and reactive astrocytosis

74
Q

Stain and colour of BA4- Amyloid Plaques

A

Sliver stain

OR

Congo-red stain —> apple green colour under polarised light

75
Q

Where are BA4-Amyloid plaques deposited in alzheimers disease?

A

Mainly:

  • Hippocampus
  • Neocortex
  • But can be anywhere in the brain parenchyma
76
Q

What cause the formation of BA4-Amyloid plaques?

A

Breakdown of the normal membrane protein APP (B-amyloid pre-cursor protein)

77
Q

Stain used for Tau-2 +ve neurofibrillary tangles

A

Silver stain

78
Q

Where are Tau-2 +ve neurofibrillary tangles deposited?

A

Cytoplasm of neurones

79
Q

What do Tau-2 +ve neurofibrillary tangles look like?

A
  • Bundles of filaments
  • Elongated
  • flame shaped
80
Q

Pathogenesis of multi-infarct dementia

A

Chronic HTN causing:

Lacunar infarcts

  • Presentation gets progressively worse with the accumulation of more infarcts
81
Q

What disease is associated with Lewy Body Dementia?

A

Parkinsons

82
Q

Epi of Vascular Muti-Infarct dementia

A

M>F

83
Q

What parts of the brain are mainly involved in Vascular (Multi-infarct) dementia?

A

Cortex and basal ganglia

84
Q

Epi of Pick’s Disease

A

Any age between 21-90

85
Q

Gross features of Pick’s Disease

A
  • Brain <1000g

- Selective atrophy of the temporal lobes and medial surface of the frontal lobes

86
Q

What parts of the brain are involved in Pick’s disease

A

Temporal lobes

Medial aspect of frontal lobes

87
Q

Microscopic features of Pick’s disease

A

Neuronal Loss (in outer 3 layers of the cortex)

Pick cells (swollen neurones)

88
Q

Presentation of Pick’s Disease

A

Early onset of:

  • Fontal lobes: Behaviour and personality change
  • Temporal lobe: Language disturbance
89
Q

Pathogenesis of Creutzfeldt Jakob Disease (CJD)

A

Prion disease usually acquired from beef resulting in transmissible spongiform encephalopathy

90
Q

What is a Prion Disease?

A

Abnormal forms of normal neuronal cell proteins

They are produced following a mutation

They replicate and can be passed on by infection or inheritance

91
Q

Gross features of CJD

A

Brain usually looks normal

92
Q

Microscopic features of CJD

A
  • Spongiform transformation of the cerebral cortex
  • small vacuoles through the parenchyma
  • Numerous

Pathology (6 decks)

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