Cerebrovascular Disease Flashcards
(45 cards)
rapid necrosis of nerve cells and/or their processes most commonly leads to what clinical picture?
sudden acute functional (stroke)
slow atrophy of nerve cells and/or their processes most commonly leads to what clinical picture?
gradually increasing dysfunction (age related cerebral atrophy)
how does acute neuronal injury appear microscopically?
shrunken and angulated nuclei
loss of nucleolus
intensely red cytoplasm - “red neurone”
at what stage are red neurones normally seen microscopically?
after hypoxia / ischaemia
typically visible 12-24 hrs after irreversible insult (stroke)
shows neuronal cell death
if an axon is severed, what occurs in either side of damage?
cell body swelling, enlarged nucleolus
degeneration of axon and myelin sheath distal to injury
what are the main functions of astrocytes?
maintain the BBB
involved in repair and scar formation (due to lack of fibroblasts)
how do astrocytes usually respond to CNS injury?
gliosis = astrocyte hyperplasia and hypertrophy
this is indicator of CNS injury, regardless of cause
how does old gliosis appear histologically?
nuclei become small and dark
they lie in a dense net of processes (glial fibrils)
what type of damage are oligodendrocytes particularly susceptible to?
oxidative damage
how do ependymal cells (which line ventricles) respond to CNS injury?
limited reaction to injury
disruption causes local proliferation of these cells - small irregularities on the ventricular surfaces “ependymal granulations”
how do the microglia (macrophage like cells) respond to CNS injury?
proliferate
recruited through inflammatory mediators
aggregate around necrotic and damaged tissues
M2 more acute, M1 - chronic
why does the brain deteriorate so quickly once hypoxia and ischaemia occur?
no O2 to create more ATP
mitochondria inhibit ATP synthesis so reserve is consumed within few mins
why can excito-toxicity cause oxidative stress in neurones?
excitatory signal depolarises neurone and releases glutamate
lack of energy means astrocytes don’t reuptake glutamate
loss of glutamate in synapse causes lots Ca2+ entry into post-synaptic terminal = mitochondrial dysfunction and oxidative stress
what are the 4 main types of oedema in the brain?
cytotoxic oedema
ionic/osmotic oedema
vasogenic oedema
haemorrhagic conversion
what causes cytotoxic oedema?
Na+/K+ channel dysfunction -> cells retain Na+ and water
what causes ionic/osmotic oedema?
water and Na+ from capillaries move into brain parenchymal extracellular space
what causes vasogenic oedema?
BBB disrupted -> leaking fluid from capillaries affect white matter
what causes haemorrhagic conversion?
when RBCs cross BBB
what is meant by cerebrovascular disease?
an abnormality of brain caused by pathological process in blood vessels
what are the 4 main components of cerebrovascular disease?
brain ischaemia and infarction
haemorrhages
vascular malformations
aneurysms
what would cause a global hypoxia and ischaemic damage to the brain as opposed to focal area of ischaemia?
cardiac arrest and severe hypotension (trauma with hypovolaemic shock)
focal = vascular obstruction
what is the definition of a stroke?
sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
what gender and age are most common for stroke to occur?
peak incidence is >70yrs
men > women
strokes caused by atherosclerotic thrombus are most common in which artery of cerebrum?
middle cerebral artery or its branches