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Mechanisms of Cerebral Injury

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Answer
show Brain accounts for 20% of body oxygen consumption Depletion of oxygen occurs within 10 sec of cessation of blood flow Conversion to anaerobic metabolism occurs within 2-4 minutes ATP supplies exhausted within 4-5 minutes  
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Hypoxia   show
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show Severe or total loss of blood supply Can be to the entire brain (cardiac arrest) or to a focal area (stroke) Small focal areas have advantage of collateral circulation Global or Focal  
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show if 1 vessel is blocked due to a stroke, cells that are further away, but close to another blood vessel can get blood supply from other vessel feeding area nearby. It’s getting a lower pressure of blood, but it’s getting some.  
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show Blood flow inadequate to meet the metabolic needs of the entire brain Cardiac arrests, shock, or severe dysrhythmias Failure of Na/K ATPase pump causes neuronal edema Calcium influx causes release of intracellular digestive enzymes  
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Global Ischemia (cont)   show
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Excitotoxicity Amino Acids   show
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show NMDA-subtype of glutamate receptors, opens and allows sodium and calcium to enter the cell-results in prolonged action potentials, swelling iontropic receptor which allows na and ca to passively move into cell– edema & prolonged action potential  
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Excitotoxicity Calcium   show
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Excitotoxicity excess Glutamate   show
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Excess Glutamate and O2   show
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show Return of oxygen to ischemic cells can lead to oxygen free fradical formation, and allows inflammatory cells to enter the ischemic area  
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show Leads to lipid peroxidation of the cell membrane, which activates the arachadonic acid cascade, leading to more free radical formation  
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Reperfusion Injury   show
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show Calcium channel blocker that is preferential for cerebral blood vessels. Approved for prophylaxis vs brain injury after intracranial aneurysm rupture Being investigated for prevention of some of the deleterious effects of excess glutamate/excitotoxicity  
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Intracranial Pressure   show
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Intracrania Pressure s/s   show
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show Bradycardia, hypertension (with widening pulse pressure), and irregular respiratory pattern Pulse pressure: difference between sys and diastole– so systolic will raise and diastolic won’t  
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Monroe-Kellie's Hypothesis   show
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Modified Monroe-Kellie Hypothesis   show
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Cerebral Perfusion Pressure (CPP)   show
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Artificially raise Blood Pressure   show
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Brain Herniation General   show
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show Falx Cerebri: between hemispheres Tentorium Cerebelli: above cerebellum  
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show Cingulate Herniation (subfalcine herniation): Cingulate gyrus beneath the falx cerebri. Greatest danger from compression of blood vessels  
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show Uncal Herniation (transtentorial herniation): : Medial aspect of temporal lobe protrudes over the tentorial edge. Ipsilateral pupil dilatation. Can interfere with RAS Ipsilateral: pupil dilated with ICP, they maybe have herniation of that side  
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show Central Herniation: Downward displacement of hemispheres, basal ganglia, diencephalon and midbrain through tentorial incisura. Slowly dilating pupils  
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show Tonsillar Herniation: Cereballar tonsils through foramen magnum, compression of medulla. Less common but high mortality in short period of time. See changes in HR, BP, constricted pupils, ataxic breathing.  
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Cerebral Edema   show
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Institial Cerebral Edema   show
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Vasogenic Edema   show
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show Increase in fluid matter in intracellular space, mostly gray matter. Caused by water intoxication, severe ischemia, hypoxia, acidosis, and brain trauma. Cause: water intox, dilutional hyponatremia  
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show Corticosteroid therapy for localized edema (such as inflammation around a tumor). Controversial in use of generalized edema Unsure of mechanism of action, but appears to stabilize the cell membrane and scavenger free radicals  
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Mannitol (Osmitrol)   show
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show Apendymals: coriod plexus in 2 lateral vent & will travel down into 3rd vent, thru aqueduct into 4th vent & has openings that allow it to free float down spinal cord & around the brain  
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Noncommunicating Hydrocephalus   show
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Communicating Hydrocephalus   show
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