Nervous system pathology overview Flashcards

1
Q

What are the 4 main types of tissue of the CNS?

A

Neurones
Glial cells
Migroglia
Supporting cells

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2
Q

What are the 4 glial cells?

A
  • Astrocytes
  • Oligodendrocytes
  • Schwann cells (not CNS)
  • Ependymal cells
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3
Q

What are the main supporting structures of the CNS?

A
  • Connective tissue
  • Meninges
  • Blood vessels
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4
Q

What are the functions of astrocytes?

A

Structural support
Repair (In CNS injury)
Regulation of the BBB

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5
Q

What are the functions of oligodendrocytes?

A

Myelination of neurones within the CNS
Structural support of the CNS
Delivery of nutrients to neurone axons

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6
Q

What are the functions of the ependymal cells?

A

Line the brain ventricles and central canal
Produce and circulate CSF

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7
Q

What are microglia?

A

Macrophages of the CNS

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8
Q

What are the 2 main types of microglia?

A
  • M1 - Pro-inflammatory
  • M2 - Clean up of debris and pathogens
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9
Q

What main structures are found within the cell body of a neurone?

A

Nucleus
Nucleolus
Nissl substance

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10
Q

What is the Nissl substance?

A

A specialised form of RER found in neurones to produce the high amount of protein required for the neurone to function

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11
Q

What are some causes of acute irreversible neuronal injury?

A

Hypoxia
Ischaemia

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12
Q

What will histology show in acute irreversible neuronal injury?

A
  • Red cytoplasm neurones
  • Shrunken, angulated nuclei
  • Loss of the nucleoli
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13
Q

Describe the histology of axonal damage

A

Increase protein synthesis so cell body swells, nucleus grows, Nissl substance breaks down (Chromatolysis) and the distal axon degenerated (Wallerian degeneration)

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14
Q

How does axonal damage differ between the CNS and PNS?

A

In the CNS, the myelin sheath degenerates due to oxidative stress on the oligodendrocytes

In the PNS, the myelin sheath is preserved, forming a neural tube to afford some generation

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15
Q

Describe the histopathology of neuronal atrophy

A

Shrunken and reduced number of neurones
Reactive gliosis/glial scar
Lipofuscin pigment

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16
Q

What is lipofuscin pigment?

A

This is the “wear and tear” pigment, acting as the cellular equivalent to rust
It is a granular yellow brown pigment occurring in proteins, lipids and highly oxidised metals in response to atrophy

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17
Q

What is reactive gliosis?

A

An early response to CNS injury in which astrocytes proliferate to contain and repair the damage

18
Q

Describe the histopathology of reactive gliosis

A
  • Hyperplasia and hypertrophy
  • Nuclear enlargement and prominent nucleolus
  • Cytoplasmic expansion
19
Q

What is late gliosis?

A

This is the formation of a glial scar following CNS injury

20
Q

What are the positives of glial scar formation?

A

It can shield the healthy tissue and isolate the injured area, preventing the spread of inflammation

21
Q

What are the negatives of glial scar formation?

A

It can be a barrier to healing, blocking axonal regeneration and preventing injured neurones from reconnecting

22
Q

What are the histological features of a glial scar?

A
  • Small, dark nuclei
  • Dense net of processes (glial fibrils)
23
Q

What is excitotoxicity?

A

This is a major mechanism involved in acute neuronal injury

Glutamate acts as a fuel for uncontrolled Ca2+ entry, activating proteases and disrupting mitochondrial function

This causes oxidative stress, damaging cellular components

24
Q

What is cytotoxic oedema?

A

Oedema occurring when dying cells begin to take up water as ions move in (There is no swelling as there is no increase in brain volume)

25
Q

What diseases can cause cytotoxic oedema?

A

Hypothermia
Reye’s syndrome
Intoxication

26
Q

What is vasogenic oedema?

A

A condition in which partial oedema of the BBB causes flooding a proteins and therefore water into the brain

27
Q

What are some causes of demyelination?

A
  • Autoimmune attacks (MS)
  • Genetic factors
  • Acquired (Trauma, infection, toxins)
28
Q

What are some examples of primary demyelinating disorders?

A

Multiple sclerosis
Post-infections autoimmune disorders

29
Q

What are some examples of post-infectious autoimmune disorder that can cause demyelination?

A

Acute disseminated encephalomyelitis
Acute haemorrhagic leukoencephalitis

30
Q

What is acute disseminated encephalomyelitis?

A

A self-limiting post-infectious autoimmune disorder resulting in a mild “Power cut” like period, commonly affecting children

31
Q

What is acute haemorrhagic leukoencephalitis?

A

A post-infectious autoimmune disorder, which can be rapidly fatal “Lightning strike”, commonly affecting adults

32
Q

What are some types of secondary demyelinating disorders?

A

Viral
Metabolic
Toxic

33
Q

What is a viral secondary demyelinating disorder?

A

JC virus, causing progressive multifocal leukoencephalopathy

34
Q

What is a metabolic secondary demyelinating disorder?

A

Central pontine myelinosis

35
Q

Describe the pathophysiology of central pontine myelinosis

A
  • Sodium controls movement of water
  • Rapid administration of IV NaCl in hyponatraemia can cause an increase in sodium in the blood, and therefore an increase in sodium in the brain
  • Water is therefore drawn out of the cells to the Na+ in the brain causing demyelination
  • This primarily affects the pons
36
Q

What are some toxic causes of demyelination?

A

CO
Organic solvents
Cyanide

37
Q

What are the 3 types of plaques found in MS?

A

Active plaques (Active battlefield)
Inactive plaques (Scorched battlefield)
Shadow plaques (Healing of landscape)

38
Q

Describe the histopathology of active plaques in MS

A

Immune cells are active attacking white matter causing
ongoing demyelination

39
Q

Describe the histopathology of inactive plaques in MS

A
  • Immune cell attack ceased but gliosis takes over (scarring)
  • Little myeline remaining and reduced oligodendrocyte
    numbers
40
Q

Describe the histopathology of shadow plaques in MS

A
  • Areas of remyelination, lesions become less defined hence “shadow”
  • Myeline sheath is thinner and more fragile