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67 Cards in this Set
- Front
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factors in remembering things |
age--better when we are younger repetition and retrieval--things that are repeated exposed to activate learning mechanisms like LTP and snyaptogenesis emotion--high levels of emotion (good or bad) can enhance memory sleep--good, sufficient, restful sleep enhaces memory |
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brain damage |
the damage or death of neurons due to injury or other insult |
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necrosis |
1. accidental cell death 2, DOES NOT REQUIRE SIGNALING AND GENE EXPRESSION 3. cell swelling-which causes bursts 4. cell lyses (swells and bursts), spilling content 5. inflammation larger damage to cell |
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apoptosis |
1. "cell suicide"--very orderly 2. requires signaling and gene expression 3. cell shrinkage 4. cellfragnments into apoptotic bodies--like 5. clean pieces--no inflammation 6. smaller damage to cell |
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key points regarding necrosis and apoptosis |
1. necrosis represents immediate consequence and apoptosis secondary consequences 2. both represent continuum. some very damaged cells die by necrosis immediately and less damaged may die later in apoptosis 3. apoptosis occurs so that damaged cells not functioning normally don't adversely affect tissue function |
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causes of brain damage |
1. cerebrovascular disorders 2. brain tumors 3. physical trauma 4. infections 5. drugs and neurotoxins 6. neurodegenerative diseases |
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cerebrovascular disorders |
a group of brain dysfunctions related to diorders of the blood vessels supplying the brain |
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2 types of berebrovascular disorders causing brain injury |
aneurysms and cerebral hemorrhage thrombus and cerebrovascular occlusion |
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aneurysms and cerebral hemorrhage |
weakening of a blood vessel and if it bursts the seepage of blood into brain areas around it, caused by high blood pressure |
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thrombus and cerebrovascular occulusion |
blockage of a cerebral artery, often caused by atherosclerosis, a disease in which excess fats in the diet are deposited into blood vessels and blood clots form |
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mechanismsby which neurons die in cerebrovascular disorders |
1. crushing and compression of neurons by bleeding and hematoma (swelling mass of blood--clotted or unclotted) 2. ischemia |
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ischemia |
lack of blood (and thus O2 and glucose) delivery to "downstream" neurons causes both necrosis and apoptosis, occurs in both cerebral hemorrhage and cerebrovascular occlusion |
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hematoma |
causes death by necrosis, occurs in both cerebral hemorrhage only |
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how does ischemia cause death of neurons in necrosis |
energy defecit--lack of oxygen and glucose disrupts ato production, cells swell and burst whe pumps fail lactic acidosis--buildup of lactic acid from anaerobic metabolism poisons cells and causes pumps to fail |
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how does ischemia cause death of neurons in apoptosis |
oxidative stress glutamat excitotoxicity inflammation |
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exodative stress |
buildup of metabolic intermediates due to abnormal ATP production in the absense of oxygen that damage DNA, proteins, and membranes--causes the small damage if built up |
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glutamate excitoxicity |
hypoxic (lack of oxygen) neurons release excess amounts of the NT gultamate, which causes huge calcium influx into postsynaptic neurons, which triffers apoptosis |
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inflammation |
immune cells from necrosis can also accidently kill neurons by releasing substances that trigger apoptosis |
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brain tumors |
large, excessively proliferating masses of cells in the brain or spinal cord |
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main times of brain tumors |
glioma secondary mestastases primitive neuroectodermal tumor (PNET) meningloma |
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glioma |
glial cell tumor, very aggressive--rapidly growing, mostly found in adults |
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secondary metastases |
tumors that form elsewhere in the body and invade into the brain from the bloodstream, very aggressive, typically found in adults |
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PNET |
very aggressive tumor formed from neural stem cells in young children only |
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meningioma |
tumor of the meninges that grow outside the brain, typically very slow growing, typically found in adults |
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neural changes and brain tumors in necrosis |
compression due to tumor growth--crushes and kills neurons by necrosis, also causes neuronal misfiring |
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neural changes and brain tumors in necrosis and apoptosis |
compression of blood vessels due to tumor growth--occludes blood supply, can cause ischemia and death of neurons by necrosis and apoptosis tumor hijacking of blood supply of nutrients and oxygen |
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neural changes and brain tumors in apoptosis |
inflammation--immune cells attacking tumor release substances that cause neurons to die by apoptosis |
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traumatic brain injury (TBI) |
damage caused by a blow to the head |
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sources of injury in TBI |
1. coup 2. contrcoup 3. hematoma 4. edema |
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coup |
the inital or primary injury to the brain from the skill striking an object |
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contrcoup |
injury to the opposite part of the brain caused when the brain rebounds and slams into the other side of the skill |
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hematoma |
swelling mass of blood leaking into brain from torn blood vessels and pressing on brain tissue |
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edema |
swelling of brain tissue as a consequence of fluid accumulation in response to trauma |
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how do neurons die with TBI with necrosis |
primary brain injury--due to phsysical damage of neurons due to coup, contrcoup, hematoma and edma |
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how do neurons die with TBI with necrosis and apoptosis? |
compression of blood vessels due to hematoma decreased blood supply due to tearing of blood vessels |
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how do neurons die with TBI and apoptosis? |
inflammation glutamate excitotoxity |
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TBI vs concussion |
1. concussion milder form of TBI 2. in concussion, neurons typically injured more than death |
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infectious encephalitis |
infection of the brain by microorganisms |
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two main types of infectioius organisms causing encephalitis |
1. viruses 2. bacteria |
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4 examples of viral brain infections |
1. rabies 2. herpes simplex virus 3. polio 4. west nile virus |
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rabies |
infects through animal bites and moves into cns via infected sensory nerves |
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herpes simplex virus |
infects through breaks in skin and enters cns via infected sensory nerves |
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polio |
infect through GI tract and move and enters cns by infecting nerves of the gut, kills motor neurons |
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west nile virus |
infect through insect bite and enther cns via infected sensory nerves |
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neural changes in brain infections |
1. necrosis of neuronal cels by viral lysis or bacterial toxin 2. immune system tells infected neurons to die by apoptosis |
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drugs and neurotoxins |
destructions of neural tissue by ingested toxis substances |
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sources of common neurotoxic substances |
1. indutrial pollution--heavy metals like mercury, lead, or arsenic 2. synthetic drugs--moto, synthetic THC, K2, spice |
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neural changes caused by neurotoxins in necrosis |
necrosis of neuronal cells by the toxin |
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neural changes caused by neurotoxins in apoptosis |
inflammation--immune system may accidentally kill some neurons while cleaning out necrotic cells glutamate excitotoxicity--some neurotoxins trigger excitotoxicity |
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recovery from brain injury |
1. increased synaptic transmission 2. increased synaptogenesis 3. increased neurogenesis in key brain regions like the hippocampus 4. rehabilitation often involves activities which increase or strengthen these 5. recovery from brain injury is a form of learning |
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neurodegenerative diseases |
diseases that result in the progressive destruction of neurons |
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key points regarding neurodegenerative diseases |
1. not until late adulthood 2. progessive--get worse over time 3. no cure for them, only treat sympotoms 4. neurons typically die by apoptosis unlike other forms of brain damage |
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3 ex of neurodegenerative diseases |
1. huntington's disease 2. alzheimer's disease 3. parkinson's disease |
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huntington's disease |
1. degeneration and death of neurons predominantly in the basal ganglia and cortex 2. inherited or genetic disorder |
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symptoms of huntingtons's disease |
chorea, jerky movement dementia (decision making) anxiety, depression, blunted affect, egocentrism, and compulsive behavior |
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brain changes in huntingtons disease |
generalized and progressive brain atrophy, particularly in the cerebral cortex and basal ganglia |
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basal ganglia |
important in producing voluntary movement and inhibiting involuntary movement |
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neuropathological changes in huntington's disease |
huntington protein misfolds and creates inclusion bodies |
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inclusion bodies |
disrupt gene expression, calcium signaling, and mitochondrial function, and may also lead to apoptotic cell death bc normal huntington inhibit apoptosis |
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alzheimer's disease |
degeneration and death of neyrons preminantly in the limbic system and cerebral cortex |
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cause of alzheimer's disease |
unknown, but genetics, infection, head injury/TBI, high blood pressure and heart disease |
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symptoms of alzheimer's disease |
cognitive--dementia, defects in attention, impaired explicit memory, language difficulties (aphasia) emotional--depression, irritability, aggresion implicit memory motor--apraxia, difficulty putting together coordinating movements, danger of falling |
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brain changes in alzheimer's disease |
death of cholinergic neurons in the basal forebrain, important for attention death of neurons in the medial temporal corttex and hippocampus, memory consolidation and storage death of neurons in the prefrontal and other parts of the cortex and limbic system, working memory and emotion regulation |
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neuropathological changes in alzheimer's disease |
abnormal folding of amyloid protein with other protein called tau in neurofibrillary |
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parkinson's disease |
degeneration and death of dopaminergic neurons within the substantia nigra |
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parkinson's disease cause |
genetics, infections, pesticide/herbicide, exposure, trauma |
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sympotoms of parkinson's disease |
motor--tremor of head and exptremities, rigid and difficulty producing voluntary movements, slow movements (bradykinesia) cognitive--dementia or progressively impaired cognitive function (especially decision making) mental--depression |