C3.2 Stroke Flashcards
what are the 2 main types of stroke
- ischaemic (~85%)
due to thrombosis of a major cerebral artery (lack of blood flow:Oz & glucose delivery) - haemorrhagic (~15%)
due to rupture of a cerebral artery. - bleed in brain
2 types of haemorrhagic = intracerebral and subarachnoid
Explain Transient Ischaemic Attack (TIA)
short episode of focal ischaemia without permanent infarction. This can highlight potential risk of stroke
what happens to the brain after stroke
Immediately after a stroke the brain becomes infarcted: (loss of blood flow in the specific area of damage) and cannot be recovered.
The area of the brain immediately adjacent to this (the penumbra) is subject to reduced blood flow and can also become damaged. Rapid treatment is needed.
Name some Mediators of cellular damage in ischaemia
▪ Glutamate - excitatory ▪ Calcium - 2nd messenger ▪ Neuroinflammation ▪ Free radicals Imbalance or altered levels can lead to cell damage
describe glutamate in stroke
impaired signalling/uptake and excitotoxicity
increased intracellular Ca = Ca dependent release of glutamate + loss Na gradient = decreased glutamate reuptake
increased extracellular glutamate = excessive glutamate receptor activation
= Glutamate mediated cell death
(+ Excessive activation of AMPA and NMDA receptors = increased intracellular Na & Ca. Excess intracellular Na = loss of ionic homeostasis, cell swelling and lysis)
describe problem of increase in intracellular Ca
Increase in intracellular Ca results in increases in kinase activity/ damage to cell, DNA, proteins, increased inflammatory signalling inside the cell, increases proteases activity leading to cytoskeletal damage
A number of pathophysiology mechanisms all due to increased intracellular Ca
what his increased after cerebral ischaemia
Neuroinflammation is increased
- E.g. the increased release of cytokine TNFa can increase infarct size after stroke. Inhibition of TNFa is shown to decrease infarct size after experimental stroke.
