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Neurology > Neuropathology 1 > Flashcards

Neuropathology 1 Flashcards

1
Q

Where are schwann cells found?

A

PNS

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2
Q

Where are oligodendrocytes found?

A

CNS

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3
Q

Primary demyelinating disease

A

MS

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4
Q

Secondary demyelinating disease?

A
  • Central pontine myelinosis
  • Progressive multifocal leucoencephalopathy (inborn)
  • Sub-acute sclerosing panencephalitis
  • AIDS
  • Axonal degeneration
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5
Q

Secondary demyelinating disease resulting from alcoholism/malnutrition/hyponatremia?

A

Central pontine myelinosis

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6
Q

What are shadow plaques?

A

Plaques when they’re completely demyelinated

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7
Q

Main histological features of MS?

A

Demyelination
Inflammation
Gliosis

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8
Q

Main histological features of MS?

A
  • Demyelination
  • Inflammation
  • Gliosis
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9
Q

What does the ependyma do?

A

Lines the ventricular system

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10
Q

Function of microglia?

A

Resident macrophages of the brain and CNS. They are the first and main form of immune defence in the CNS

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11
Q

Name 3 types of glial cell

A

Oligodendrocytes
Microglia
Ependyma

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12
Q

How can cells in the CNS become damaged?

A 
Hypoxia
Trauma
Nutritional deficiency
Toxic insult
Metabolic abnormalities
Ageing
Infections
Genetic abnormalities
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13
Q

What is an axonal reaction?

A

A reaction within the cell body that is associated with axonal injury

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14
Q

Glial cells are derived from which layer?

A

The neuroectoderm

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15
Q

These cells are phagocytic, respond to inflammation like microphages

A

Microglia

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16
Q

A reaction within the CELL BODY that is associated with axonal injury

A

Axonal reaction

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17
Q

What happens when neurones become damaged due to hypoxia

A

Glutamate receptors become activated and this results in uncontrolled calcium entry into the cell

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18
Q

Response to axonal injury

A
  • increased RNA and protein synthesis
  • swelling of cell body
  • peripheral displacement of nucleus
  • enlargement of nucleolus
  • central chromatolysis
  • anterograde degeneration of axon occurs distal to site of injury
  • breakdown of myelin sheath
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19
Q

Most important histopathological indicator of CNS injury

A

Gliosis

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20
Q

What happens to astrocytes in gliosis

A

Astrocytes undergo hyperplasia and hypertrophy

21
Q

In gliosis, what happens to the nucleus?

A

Nucleus enlarges and becomes vesicular

The nucleolus is prominent

22
Q

What happens to the cytoplasm in gliosis?

A

The cytoplasm expands and the ramifying process extend

23
Q

What happens if you disrupt ependymal cells?

A

The sub-epithelial ependymal astrocytes proliferate and this forms small irregularities on the ventricular surfaces

  • these are called ependymal granulations
24
Q

Infectious agents including virus could produce changes in which type of cell?

A

Ependymal cells

25
Q

If injury occurs, what cell would you find elongated nuclei (rod cells) in?

A

Microglia

26
Q

What is neuronophagia?

A

When tonnes of microglia congregate around portions of dying neurons

27
Q

What are microglial nodules?

A

Microglia that have congregated around small foci of tissue necrosis

28
Q

What is apraxia?

A

Inability to perform purposeful actions

29
Q

Damage to anterior cerebral artery

A

Frontal lobe dysfunction
Contralateral sensory loss in lower limb and foot
Paresis of foot and arm (thigh and face generally spared)

30
Q

Damage to middle cerebral artery

A

Hemiparesis
Hemisensory loss
Aphasia/dysphasia
Apraxia

31
Q

Which arteries supply the brainstem, cerebellum and occipital lobe?

A

The vertebrobasilar arteries

32
Q

What is Weber’s syndrome?

A

Ipsilateral IIIrd nerve palsy

Contralateral hemiparesis/hemiplegia

33
Q

Damage to which part of the brain could cause Webers syndrom?

A

Midbrain

34
Q

Damage to which part of the brain could cause medial and lateral pontine syndrome?

A

Pons

35
Q

Damage to which part of the brain could cause lateral medullary syndrome?

A

Medulla

36
Q

Damage to the occipital lobe presents as _____

A

Homonymous hemianopia with macular sparing

37
Q

How does damage to the cerebellum present?

A

Ataxia
Nystagmous
Intention tremor
Pendular reflexes

38
Q

Which is more vulnerable to hypoxic-ischemic damage: neurons or glial cells?

A

Neurons are more vulnerable than glial cells

39
Q

Definition of stroke

A

A sudden disturbance of CEREBRAL FUNCTION of VASCULAR ORIGIN that causes death or lasts over 24 hours

40
Q

What happens 4-12 hours after cerebral infarction?

A

4-12 hours: brain may appear normal

41
Q

What happens 15-20 hours after cerebral infarction?

A

Ischemic neuronal changes develop, defined margin between ischemic and normal brain

42
Q

What happens 24-36 hours after cerebral infarction?

A

Inflammatory reaction
Extravastation of red blood cells
Activation of astrocytes and microglia

43
Q

What happens 36-48 hours after cerebral infarction?

A

Necrotic area visible macroscopically

Becomes swollen and softer than surrounding tissue

44
Q

When do macrophages infiltrate into the infarction area?

A

Day 3

45
Q

What happens 1-2 weeks after cerebral infarction?

A

Liquefacation of tissue and gliosis

46
Q

Where do 90% of subarachnoid haemorrhages occur?

A

Arterial bifurcations in the territory of the internal carotid artery

(10% in the vertebro-basilar circulation)

47
Q

90 % of lacunar infarcts are associated with what?

A

hypertension

48
Q

Hypertension is particularly associated with this type of infarct

A

Lacunar infarcts

Neurology (56 decks)

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