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17 Cards in this Set
- Front
- Back
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global ischemia
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cessation of blood flow to the entire brain
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global ischemia damage time frame
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less than 4 mins--no obvious damage following reperfusion
4-15 mins--death of specific neuronal populations greater than 15 mins--necrosis occurs in brain greater than 30 mins--large scale necrosis of brain |
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what is delayed neuronal death
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vulnerable neurons die b/w 24-72 hours following reperfusion
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hypothermia
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most effective treatmen of global ischemic brain damage; decreases damaging reactions in brain tissue
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main cause of ischemic damage
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loss of ATP
ATP is zero by 4 mins loss of ATP causes cessation of all ATP dependent processes in the brain the most important being sodium/potassium atpase (ionic equilibrium) |
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consequence of disrupting state of neuronal cells
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ions begin to equilibrate and ion gradients are lost
this results in net depolarization |
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ions that mediate necrosis during ischemia
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if ischemia persists for greater than 20 mins, sodium influx causes cell swelling, lysis and death
less than 20mins, calcium influx causes the necrosis |
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what is excitotoxicity
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influx of sodium and calcium during ischemia causes release of neurotransmitters, which further causes depolarization
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damages that occurs w/ reperfusion
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free radical production when oxygen is returned
protein synthesis is inhibited overproduction of NO--contributes to further free radical damage massive changes in gene transcription activation of apoptosis |
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flow metabolism coupling
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increase in neuronal activity leads to increase in local blood flow
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what is the OGI
oxygen-glucose index |
ratio of oxygen to glucose use
normal valus is 5.5 meaning that 5.5 molecules of oxygen are consumed for every 1 carbon of glucose utilized |
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how does OGI change when neuronal activity (and blood flow) increases
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OGI decreases to about 4
SO MORE GLUCOSE THAN OXYGEN IS BEING CONSUMED so arteria-venous oxygen difference will be less in active brain regions deoxyhemoglobin levels will be less in active brain regions |
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how does functional magnetic resonance imaging work
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based on decrease in deoxyhemoglobin that occurs in active brain regions
so in active brain regions, fMRI signal will increase |
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extrinsic mechanism of cerebral blood flow autoregulation
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baroreceptor relex--increase in MAP leads to vasodilation and decrease in MAP leads to vasoconstriction (via increase in sympathetic tone)
cerebral ischemic response--when pressure falls below 50mmgHg, CNS stimulates cardiovascular system to increase HR and CO cushing reflex--increase intracranial pressure will cause MAP to increase, therefore increase in blood flow |
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intrinsic mechanism of cerebral blood flow autoregulation
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arterial CO2--hypercapnia (vasodilation); hypocapnia (vasocontriction)
potassium ion adenosine nitric oxide arachidonate hydrogen all are vasodilators |
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neurogenic autoregulation
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nitregic innnervation--postganglionic nerves innervating cerebral arteries; produces NO, which relaxes smooth muscles cholinergic--vasodilation via NO production
adrenergic--norepinephrine causes NO release, therefore vasodilation |
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myogenic autoregulation
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stretch of smooth muscles causes muscle to contract
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