risk factors of stroke and pathophysiology Flashcards
risk factors
hypertension history (50%), current smoker(20%), waist to hip ratio(25`%), diet, physical activity, alcohol, stress, cardiac causes, ratio of ApoB to ApoA (25%)
why does haemorrhage happen
history of hypertension (60-70%), amyloid (15-20%), excess alcohol, hypocholesterolaemia, haemhorrhagic transformation
what is more damaging- ischeamic or haemorrhagic stroke
haemorrhagic, more likely to be dependent on others on daily living or death. over 50% of patients after ischaemic stroke can be independent
penumbra
ischemic brain tissue that has just enough energy to survive for a short time but not enough to communicate and function.
why is time important in ischaemic stroke
every minute in which a large vessel ischaemic stroke is untreated the average patients loses 1.9 million neurons, 13.8 billion synapses as 12km of aonal fibres. need to work fast to save as much brain as possible
how ischaemic stroke occurs
results from the failure of cerebral blood flow to a part of the brain. can be transient (TIA), results in varying degrees of hypoxia and hypoglycaemia
hypoxia development in ischaemic stroke
hypoxia stresses the metabolic machinery of brain cells which malfunction but are still alive especially in the penumbra, if prolonged the hypoxia becomes anoxia, which results in infarction and this is a completed stroke. from here further damage can result from oedema from water causing cells to swell and burst and is depending on the size and location of stroke or whether there is secondary haemorrhage into the stroke
how can oedema affect the brain
squashes areas of the brain as it swells and moves the midline, can be treated sometimes by removing section of skull to allow swelling outwards and improve mortality
ischeamic cascade
brain cells lose ability to produce ATP due to inadequate blood supply, cells in affected area switch to anerobic metabolism which leads to less production of ATP, releases lactic acid which is an irritant and has potential to destroy cells by disruption of the normal acid-base balance in brain. ATP reliant ion transport pump fails and membrane becomes depolarised, influx of calcium, efflux of potassium, intracellular calcium levels too high and trigger release of glutamate, stimulates AMPA receptors and calcium permeable NMDA receptors so more calcium influx, overexcites cells and activates proteases, lipases and free radicals- excitotoxity
excitotoxicity
cell membrane broken down by phospholipases, becomes more permeable and allows ions and harmful chemicals into cell, mitochondria break down, releasing tons and apoptotic factors into cell, cells undergo apoptosis, cells die through necrosis then release glutamate and toxic chemicals into the environment which poisons and overexcites neurones. loss of vascular structural integrity results in breakdown of the BBB and contributes to cerebral oedema