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CNS Path Flashcards

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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
Complications of Tonsillar herniation
Brainstem compression (leads to death)
26
Types of cerebral oedema
Vasogenic Oedema Cytotoxic Oedema Interstitial Oedema
27
Definition and cause of Vasogenic oedema
Definition: - Fluid leaks into brain parenchyma because BBB is disrupted Cause: - Localised: Abscess, tumour, infarct - Generalised: Sepsis
28
Definition and cause of Cytotoxic oedema
Increased fluid as result of ischaemic injury Cause: Generalised ischaemia
29
Definition and cause of Interstitial oedema
Increased fluid in peri ventricular tissues Cause: Acute hydrocephalus
30
Rx of cerebral oedema
- Steroids if tumour related | - Surgical removal if haemorrhage
31
Type of infarcts in the circle of willis
Wedge shaped watershed infarcts
32
Place in brain most susceptible to infarction
Area between anterior and middle cerebral artery
33
Define stroke
Focal and/or global loss of cerebral function Lasting >24hrs
34
Define TIA
Transient Ischaemia Attack Focal loss of cerebral or ocular function lasting <24hrs
35
Timeline of macroscopic features of infarction (brain)
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
36
Timeline of microscopic features of infarction (brain)
0-12hrs - Red neurones - Oedema 12-48hrs - Inflammatory response - Neutrophil polymorphs 2-3w - Lots of microglia >3w - Reactive astrocytosis surrounding the infarction
37
Causes of Intracerebral haemorrhage 6
``` HTN Amyloid angiography Anticoagulants Tumours Vasculitis AV Malformation ```
38
Causes of Subarachnoid Haemorrhage 2
Berry aneurysm | AV malformation
39
Causes of HTN which cause Intracerebral Haemorrhage 5
Large vessel atherosclerosis Small vessel hyaline arteriolosclerosis Charcot-Bouchard Microaneurysms Lacunar Infarcts Slit Haemorrhages
40
Complications of lacunar infarcts
Accumulative effect to cause Multi-infarct dementia
41
What would cause bleeding into the ventricular system?
Intracerebral haemorrhage of the basal ganglia
42
Pathogenesis of amyloid angiography
Media of small penetrating vessels is replaced with amyloid This causes vessel wall weakening And increases the risk of rupture
43
In what diseases/aspects of life do you see amyloid angiography? 3
Alzheimer’s Down’s Syndrome Aging
44
Ix for amyloid angiography 2
Amyloid Immunological stain OR Congo-red stain (goes apple green under polarised light)
45
What is AV malformation?
Abnormal connections between arteries and veins Instead of joining via the capillary system, they just join up
46
Epi AV malformation
3rd-4th decade M>F
47
Complication of AV malformation
Rupture Intracerebral Haemorrhage SAH
48
Where do berry aneurysms occur?
Circle of Willis
49
RF for Berry aneursym 3
PCKD Neurofibromatosis Marfan’s
50
Causes of cardiac mural thrombi 3
MI Valve disease AF
51
Causes of embolic stroke
Cardiac mural thrombi Carotid atherosclerotic thromboembolism Ventricular septal defects (structural abnormality) Cardiac surgery Tumour, Fat, Gas, Atherosclerosis, foreign body, Infection, amniotic fluid
52
What % of brain tumours are mets?
50%
53
Most common origins of brain mets 4
Breast Prostate Lung GIT
54
Brain Tumour should be a differential Dx in ... 5
New onset epilepsy Hydrocephalus FNS Balance/Gait abnormalities Visual field defects
55
Complications of Brain tumours
``` Epillepsy, Hydrocephalus, FNS, Balance/gait abnormalities, Visual Field Defects ``` Raised ICP Brainstem compression
56
Ix of SOL
1. CT or MRI Confirm: 2. Brain biopsy (send to histology) 3. Brain smear (send to cytology)
57
How are brain tumours named?
According to the cells from which they are derived
58
Define Neuroblastoma
Tumour of neurones
59
Define Meningioma
Tumour of the meninges
60
Tumours of the Cranial Nerves
Schwannoma Neurofibroma
61
Define Gliomas
Tumours of Neuroglia: Astrocytoma Oligodendrocytoma Ependymoma
62
How are brain biopsies/smears graded?
1. Degree of nuclear atypia 2. Necrosis 3. Endothelial hyperplasia
63
Rx Brain tumour
1. Surgical Excision 2. Chemoradio 3. Proton beam
64
Weight of female adult brain
1250g
65
Weight of male adult brain
1400g
66
Gross features of cerebral atrophy
Narrowing (flattening) of gyri Widening of the sulci Compensatory enlargement of the centricular system
67
Which area of the brain suffers most neurodegeneration in Alzheimer’s disease?
Hippocampus
68
Which area of the brain suffers most neurodegeneration in parkinson’s disease?
Substantia Niagra
69
Epi Alzheimer’s
F>M 47% >85yo
70
Define neurodegeneration
Progressive neuronal degeneration and death
71
Define dementia
An acquired global impairment of intellect, reason and personality , without impaired consciousness
72
Gross appearance of an alzheimers brain 6
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
Microscopic features of Alzheimers disease 4
Tau-2 +ve Neurofibrillary tangles BA4-Amyloid Plaques - Senile (Neuritic) plaques Amyloid angiopathy Neuronal loss and reactive astrocytosis
74
Stain and colour of BA4- Amyloid Plaques
Sliver stain OR Congo-red stain —> apple green colour under polarised light
75
Where are BA4-Amyloid plaques deposited in alzheimers disease?
Mainly: - Hippocampus - Neocortex - But can be anywhere in the brain parenchyma
76
What cause the formation of BA4-Amyloid plaques?
Breakdown of the normal membrane protein APP (B-amyloid pre-cursor protein)
77
Stain used for Tau-2 +ve neurofibrillary tangles
Silver stain
78
Where are Tau-2 +ve neurofibrillary tangles deposited?
Cytoplasm of neurones
79
What do Tau-2 +ve neurofibrillary tangles look like?
- Bundles of filaments - Elongated - flame shaped
80
Pathogenesis of multi-infarct dementia
Chronic HTN causing: Lacunar infarcts - Presentation gets progressively worse with the accumulation of more infarcts
81
What disease is associated with Lewy Body Dementia?
Parkinsons
82
Epi of Vascular Muti-Infarct dementia
M>F
83
What parts of the brain are mainly involved in Vascular (Multi-infarct) dementia?
Cortex and basal ganglia
84
Epi of Pick’s Disease
Any age between 21-90
85
Gross features of Pick’s Disease
- Brain <1000g | - Selective atrophy of the temporal lobes and medial surface of the frontal lobes
86
What parts of the brain are involved in Pick’s disease
Temporal lobes Medial aspect of frontal lobes
87
Microscopic features of Pick’s disease
Neuronal Loss (in outer 3 layers of the cortex) Pick cells (swollen neurones)
88
Presentation of Pick’s Disease
Early onset of: - Fontal lobes: Behaviour and personality change - Temporal lobe: Language disturbance
89
Pathogenesis of Creutzfeldt Jakob Disease (CJD)
Prion disease usually acquired from beef resulting in transmissible spongiform encephalopathy
90
What is a Prion Disease?
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
Gross features of CJD
Brain usually looks normal
92
Microscopic features of CJD
- Spongiform transformation of the cerebral cortex - small vacuoles through the parenchyma - Numerous

Pathology (6 decks)

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