Neuropathology 1: Cerebrovascular disease Flashcards

1
Q

Name the cellular components of the CNS.

A

Nerve cells (neurones)

Glial cells:
- Astrocytes
- Oligodendrocytes
- Ependymal cells

Microglia

Supporting structures:
- Connective tissue
- Meninges
- Blood vessels

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2
Q

What can damage to the nerve cells and/or their processes lead to?

A

Rapid necrosis with sudden acute functional failure (as seen in “stroke”)

Slow atrophy with gradually increasing dysfunction (as seen in age-related cerebral atrophy)

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3
Q

What is a nucleus and a ganglion?

A

Cluster of neurones in the CNS = nucleus

Cluster of neurones in the PNS = ganglion

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4
Q

Average size of neurone cell body?

A

10 to 50μm

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5
Q

Dendrite function?

A

Dendrites are short processes and have a large surface area for receiving signals from other neurons and pass it to the cell body.

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6
Q

Axon function?

A

The axon is the conducting region of the neuron and is responsible for generating and transmitting impulses typically away from the cell body.

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7
Q

What is the Nissl substance and it’s function?

A

Present in the cytoplasm of the cell body (soma) of nerve cells and is responsible for protein synthesis and cellular metabolism.

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8
Q

What is a “red neuron”?

A

Pathological finding in neurones (particularly of the CNS) that indicates acute neuronal injury and that’s followed by apoptosis or necrosis.

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9
Q

When is acute neuronal injury (“red neuron”) seen?

A
  • Occurs in the context of hypoxia/ischaemia.
  • Typically seen 12-24 hours after an irreversible “insult” to the cell i.e. ischaemic injury such as stroke.
  • Results in neuronal cell death
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10
Q

Histological appearance of acute neuronal injury (“red neuron”)?

A

Shrinking and angulation (non-rounded) nuclei.

Loss of nucleolus

Intensely red cytoplasm

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11
Q

Axonal responses to injury?

A

Increased protein synthesis -> cell body swelling, enlarged nucleolus

Chromatolysis – margination and loss of Nissl granules

Degeneration of axon and myelin sheath distal to injury

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12
Q

Simple neuronal atrophy (chronic degeneration features?

A

Shrunken, angulated and lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis

Functionally related neurones

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13
Q

Sub-cellular alterations – inclusions features?

A

Common in neurodegenerative
conditions, e.g. neurofibrillary tangles
in Alzheimer’s disease

Inclusions appear to accumulate with ageing

Also get inclusion in viral infections affecting the brain

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14
Q

Role of oligodendrocytes?

A

Wrap around axons to form myelin sheath in the CNS.

They are sensitive to oxidative damage.

Oligodendrocyte damage is a feature of demyelinating disorders i.e. Multiple Sclerosis and Guillian-Barre syndrome.

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15
Q

Role of astrocytes?

A

Ionic, metabolic and nutritional homeostasis

Work in conjunction with endothelial cells to maintain the blood brain barrier

The main cell involved in repair and scar formation given the lack of fibroblasts

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16
Q

Appearance and location of astrocytes?

A

Present throughout the CNS.

Star-shaped cells with multipolar cytoplasmic processes.

17
Q

What is an indicator of CNS injury shown by astrocyte hyperplasia and hypertrophy?

A

Gliosis

18
Q

Gliosis is a fibrous proliferation of glial cells in injured areas of the CNS. True/false?

A

True

19
Q

What are ependymal cells?

A

Lines the ventricular system

Limited reaction to injury

Infectious agents including viruses produces changes in ependymal cells

20
Q

What are microglia and their function?

A

Embryologically derived
Function as a macrophage system; phagocytosis

Response to Injury:
Microglia proliferate
Recruited through inflammatory mediators
Form aggregates around areas of necrotic and damaged tissues

21
Q

Causes of nervous system injury?

A

Hypoxia
Trauma
Toxic insult
Metabolic abnormalities
Nutritional deficiencies
Infections
Genetic abnormalities
Ageing

22
Q

What is the definition of stroke?

A

Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours.

23
Q

What is cause of a cerebral infarction?

A

Caused by interruption of cerebral blood flow due to thrombosis or emboli

24
Q

Peak incidence age of cerebral infarction?

A

> 70 years

25
Q

Risk factors for cerebral infarction?

A

Atheroma
- Intracranial vessels
- Extracranial vessels
Hypertension
- Risk factors for atheroma anywhere in intra and extracranial vessels
- Also causes changes in cerebral vessel walls
Serum lipids, obesity, diet
Diabetes mellitus
Heart disease
Disease of neck arteries
Drugs
Smoking
Septal defects

26
Q

What are lacunar infarcts?

A

Occlusion of small penetrating vessels – lenticulostriate branches