pathophysiology test 4 AD

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185962
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pathophysiology test 4 AD
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2012-12-04 00:00:59
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alzheimers
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alzheimers
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  1. prevalence of AD
    approx 6M
  2. is early or late onset of AD more common
    late, often sporadic 70%, >65
  3. onset of familial AD
    rare (<5%), onset < 40
  4. 3 susceptibility genes for AD
    • amyoid presursor protein APP
    • presenilin I & II
    • Apo E4
  5. 5 morphological atrophy's of AD
    • diffuse cortical atrophy
    • increase ventricular volume
    • atrophy of gyri
    • enlargement of sulci
    • hippocampal atrophy
  6. 3 imaging techniques for AD & explain
    FDG - reveals metabolic deficits by assessing glucose utilisation rate

    Pittsburgh Compound B - radiotracer for imaging amyloid paques by positron emission tomography

    In Vivo human imaging - imaging for amyloid deposits by positron emission tomography (PET)
  7. cognitive changes in AD
    gradual decline in memory, cognition and function
  8. a complication from AD
    weight loss - may be due to infection, wandering, problems eating
  9. 7 cognitive and functional declines in AD
    • decrease new memory acquisition
    • aphasia - decrease language
    • apraxia - decrease performing sequential motor tasks
    • anosognosia - pt unaware of his/her own difficulties
    • navigational difficulties
    • sleep difficulties
    • shuffling gait in some pts, but w/o the tremor of PD
  10. five stages of AD
    • MCI
    • early
    • middle
    • late
    • end-stage
  11. give the order of top 3 impairments from AD
    • memory
    • language
    • visuospatial
  12. 3 factors of MCI in AD
    • syndromic designation
    • categorizes pts with cognitive complaints, but insufficient to warrant a syndromic diagnosis of dementia
    • 10% to 15% chance/yr of AD
  13. 3 main histopathology of AD
    • amyloid plaques
    • neurofibrillary tangles
    • Abeta42 amyloid in arterial walls of cerebral blood vessels
  14. what are neurofibrillary tangles of AD
    highly phosphorylated tau protein
  15. 3 characteristics of amyloid plaques
    • senile plaques with Abeta amyloid
    • smaller soluble oligomers are receiving more attention as the possible more toxic moiety
    • oligomers accumulate to form plaques
  16. In AD which 2 neurotransmitters do you have a progressive loss of
    • cholinergic neurons
    • principal cortical neurons
  17. in AD what enzyme and receptor do you have progressive loss of
    • acetylcholinesterase
    • nicotinic acetylcholine receptors
  18. what are the 2 molecular changes in plaques in AD
    • amyloid precursor protein
    • presenilin I & II
  19. what toxin results from cleaving beta-secretase
    Abeta 42
  20. give the steps of APP cleavage
    • alpha or beta secretase cleavage
    • beta secretase cleavage by gamma-secretase to Abeta 42(toxic) or A beta 40 (nontoxic)
    • alpha secretase cleaved by gamma secretase to P3 (nontoxic)
  21. 6 treatable causes of dementia to rule out
    • brain tumors
    • thyroid disease
    • vitamin deficiencies
    • drug & Rx toxicities
    • chronic infection
    • severe depression (pseudodementia)

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