Cerebrovascular Disease NeuroPathology Flashcards
Rapid necrosis of nerve cells and/ortheirprocesses most commonly leads to what clinical picture?
suddenacutefunctionalfailure(“stroke”)
Slow atrophy of nerve cells and/ortheirprocesses most commonly leads to what clinical picture?
graduallyincreasingdysfunction(age- relatedcerebralatrophy)
How does acute neuronal injury appear microscopically?
- Shrunkenandangulated nuclei
- Lossofthenucleolus
- Intenselyredcytoplasm “RED NEURON”
At what stage are “RED NEURONS” normally seen microscopically?
- After hypoxia/ischaemia
- Typicallyvisible12-24hoursafteranirreversibleinsult (stroke)
- shows neuronal cell death
If an axon is severed, what occurs on either side of the damage?
- cellbodyswelling,enlargednucleolus
- Degenerationofaxonandmyelinsheathdistaltoinjury
What are the main functions of astrocytes?
- maintainthebloodbrain barrier
* Involvedinrepairand scarformation(due tolackof fibroblasts)
How do astrocytes usually respond to any CNS injury?
Gliosis => Astrocytehyperplasiaand hypertrophy
-indicatorofCNSinjury,regardlessofcause
How does old gliosis appear histologically?
- nuclei become smallanddark
- They lie inadensenetofprocesses(glialfibrils)
What type of damage are oligodendrocytes particularly susceptible to?
oxidativedamage
How do ependymal cells (which line ventricles) respond to CNS injury?
- Limitedreactiontoinjury
- disruption causes local proliferation of these cells =>smallirregularitiesontheventricularsurfaces”ependymalgranulations”
How do the microglia (macrophage-like cells) respond to CNS injury?
- proliferate
- Recruitedthroughinflammatorymediators
- Aggregate aroundnecroticanddamagedtissues
- M2 more acute, M1 - chronic
Why does the brain deteriorate so quickly once hypoxia and ischaemia occur?
- No O2 to create more ATP
- mitochondria inhibitATPsynthesis
=>ATPreserveis consumedwithinafewminutes
Why can excito-toxicity cause oxidative stress in neurones?
- excitatory signal depolarises neuon and releases glutamate
- lack of energy means astrocytes dont reuptake glutamate
- lots of glutamate in synapse causes lots of Ca2+ entry into post-synaptic terminal
=> mitochondrial dysfunction and oxidative stress
What are the main types of oedema in the brain?
Cytotoxicoedema - Na+/K+ channel dysfunction => cells retain Na+ and water
Ionic/osmotic oedema - water and Na+ from capillaries move into brain parenchymal extracellular space
Vasogenic oedema - BBB disrupted => leaking fluid from capillaries affects white matter
Haemorrhagic conversion - when RBCs cross BBB
What is meant by cerebrovascular disease?
- an abnormalityofbraincausedbyapathological processinbloodvessels
What are the 4 main components of cerebrovascular disease?
- Brainischaemiaandinfarction
- Haemorrhages
- Vascularmalformations
- Aneurysms