Neuropathology 1: Cerebrovascular disease Flashcards
Name the cellular components of the CNS.
Nerve cells (neurones)
Glial cells:
- Astrocytes
- Oligodendrocytes
- Ependymal cells
Microglia
Supporting structures:
- Connective tissue
- Meninges
- Blood vessels
What can damage to the nerve cells and/or their processes lead to?
Rapid necrosis with sudden acute functional failure (as seen in “stroke”)
Slow atrophy with gradually increasing dysfunction (as seen in age-related cerebral atrophy)
What is a nucleus and a ganglion?
Cluster of neurones in the CNS = nucleus
Cluster of neurones in the PNS = ganglion
Average size of neurone cell body?
10 to 50μm
Dendrite function?
Dendrites are short processes and have a large surface area for receiving signals from other neurons and pass it to the cell body.
Axon function?
The axon is the conducting region of the neuron and is responsible for generating and transmitting impulses typically away from the cell body.
What is the Nissl substance and it’s function?
Present in the cytoplasm of the cell body (soma) of nerve cells and is responsible for protein synthesis and cellular metabolism.
What is a “red neuron”?
Pathological finding in neurones (particularly of the CNS) that indicates acute neuronal injury and that’s followed by apoptosis or necrosis.
When is acute neuronal injury (“red neuron”) seen?
- 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
Histological appearance of acute neuronal injury (“red neuron”)?
Shrinking and angulation (non-rounded) nuclei.
Loss of nucleolus
Intensely red cytoplasm
Axonal responses to injury?
Increased protein synthesis -> cell body swelling, enlarged nucleolus
Chromatolysis – margination and loss of Nissl granules
Degeneration of axon and myelin sheath distal to injury
Simple neuronal atrophy (chronic degeneration features?
Shrunken, angulated and lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis
Functionally related neurones
Sub-cellular alterations – inclusions features?
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
Role of oligodendrocytes?
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.
Role of astrocytes?
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
Appearance and location of astrocytes?
Present throughout the CNS.
Star-shaped cells with multipolar cytoplasmic processes.
What is an indicator of CNS injury shown by astrocyte hyperplasia and hypertrophy?
Gliosis
Gliosis is a fibrous proliferation of glial cells in injured areas of the CNS. True/false?
True
What are ependymal cells?
Lines the ventricular system
Limited reaction to injury
Infectious agents including viruses produces changes in ependymal cells
What are microglia and their function?
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
Causes of nervous system injury?
Hypoxia
Trauma
Toxic insult
Metabolic abnormalities
Nutritional deficiencies
Infections
Genetic abnormalities
Ageing
What is the definition of stroke?
Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours.
What is cause of a cerebral infarction?
Caused by interruption of cerebral blood flow due to thrombosis or emboli
Peak incidence age of cerebral infarction?
> 70 years
Risk factors for cerebral infarction?
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
What are lacunar infarcts?
Occlusion of small penetrating vessels – lenticulostriate branches
