Alzheimer's and dementia

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Alzheimer's and dementia
2013-12-09 17:11:00
3220 final exam fall
3220 final exam fall
Show Answers:

  1. what is most likely to cause dementia
    Alzheimer's Dx
  2. what percentage of adults over age 65 have dementia?
  3. what do you associate with early Alzheimer's Dx?
    forgetting recent event
  4. progression of Alzheimer's Dx: early phase
    • slow, but relentless
    • short term memory loss, leading to confusion, getting lost, disorientation with the familiar 
    • as the disease progresses, it lead to poor judgement and personality changes [caused by actual changed in the brain and not from the reaction of memory loss]
    • behavioral problems such as wandring, agitation, sundowning
  5. progression of Alzheimer's: late phase
    • a lot of damage in the brain
    • unable to do self-care, loss of ADLs, incontinence, loss of identity, recognition, communication 
    • death [4-8 years, but as long as 20 yr, from onset]
  6. Sun-downing
    these are the people you want to watch more carefully because their acting disoriented or different and up and around when everybody is sleeping. Tends to happen at or around the time of sunset, it’s related to diurnal rhythms and the persons personality changes -> disorientation, agitation. They found that exposure to sunlight during the daytime tends to keep the person on a schedule and sleeping at night between.
  7. who is at risk for Alzheimer's
    • ageing: over 65 yr old [but less than 15% of those over 65 have dementia]
    • family history: esp. early onset type [as early as 40 yrs]
    • maybes?: female gender [they live longer], head injury, lower educational level, smoking, high apoE4 [transport cholesterol], high homocystine [related to cardiovascular Dx]
  8. Alzheimer's diagnosis: how do you know?
    • first, tests for dementia: mini-cognition, more extensiv, then 
    • deficits in at least TWO cognitive areas
    • cognitive changes are progressive 
    • disease exclusion: between 40-90 yrs old, examination, imaging for/to rule out other causes
    • after death: smaller brain, atrophy, microscopic changes [plaques and tangles]
  9. what causes Alzheimer's? three features
    • degeneration of neurons, neural death
    • neuritic plagues
    • neurofibrillary tangles inside neurons
  10. neuronal degeneration
    • location: hippocampus first, then to cerebral cortex
    • memory first, then language, then other functions [emotional and personality changes]
    • part of what's going on is this reduced cholinergic transmission [Ach] within the brain [a lack of Ach response ]
  11. neutritic plaques
    • beta amyloid [protein fragment] with neuron parts from neuritic plaques in brain
    • beta amyloid is in high concentration in Alzheimer's Dx, and is neurotoxic [release free radicals, kill hippocampus called, dec. circulation, opens calcium channels to neurons at a toxic level, etc.]
    • but not so toxic to younger brains
  12. neurofinrillary tangles, and tau
    • tau forms bridges between microtubules inside neurons to stabilize them 
    • in Alzheimer's Dx, tau becomes helical, causing tangles of microtubles in neurons
  13. Apolipoprotein E4
    bind to beta amyloid [causes plaques]
  14. endoplasmic reticulum-associated binding protein [ERAP]
    works with beta amyloid
  15. homoncysteine
    high levels inc. Alzheimer's Dx risk, related to atherosclerosis, dec. it with folate, vit B6 and B12
  16. how can AD be treated
    • no cure
    • inhibit cholinesterase
    • NMDA receptor antagonist 
    • treat associated symptoms
    • Vit E - did not work
    • Selegiline - did not work 
    • NSAIDs - seems to help when detected early
  17. why inhibit cholinesterase?
    • cholinesterase breaks down Ach
    • which is low in Alzheimer patients
  18. which effect increased Ach would most limit use of cholinesterase inhibitors in certain patients?
    • bronchconstriction 
    • - people who already have resp problems
    • it also causes bradycardia and weight loss
    • rapid progression of symptoms if medication is discontinued
  19. cholinesterase inhibitor drug interaction with cholinergic receptor blockers
    • first generation antihistamines [benadryl]
    • tricyclic antidepressants 
    • conventional antipsychotics [can cause drugs not to work as they should]
  20. how would blocking cholinergic receptors affect cholinesterase inhibitors
    • it will keep them from having any good affect
    • If you block the place where Ach would normally plug into to cause its affect, your going to end up not having good effect from your cholinesterase inhibitors
  21. should cholinesterase inhibitors be used with cholinergic receptor blockers in patients with Alzheimer's Dx?
  22. Common cholinesterase inhibitors
    • Donepezil [Aricept]: best tolerated, only required once a day, broken down by P450 enzyme so avoid grapefruit 
    • Rivastigmine [Exelon]: causes irreverable inhibition of cholinesterase which gives a longer effect, no P450 enzyme issue
    • Galantamine [Razadyne, Reminyl]: 
    • Tacrine [Cognex]: first approved, but likely to cause liver injury. last choice drug
  23. Memantidine [Nameda]
    • NMDA [N-methyl-d-aspartate] receptor antagonist
    • newest class of drugs for AD
    • only used in advanced part of AD
    • better tolerated then the cholinesterase inhibitors, few SE
    • helps learning and memory
    • effect: moderates the major exitatory neurotransmitter in the brain, glutamate
    • blocks glutamate receptors on membrane at low glutamate concentrations, but not high concentrations
  24. how does glutamate cause "learning"?
    • surge of glutamate allows quick short influx of calcium into the neuron = learning
    • if glutamate constantly leaks, nor surge occurs, and calcium constantly would inc. in neurons - no learning occur and neuron damage
  25. NSAIDs and Alzheimer's
    • if you take NSAIDs for two years, low or high dose, AND
    • if it is two years before Alzheimer's Dx symptoms start, then 
    • 80% dec. in AD onset will occur
    • we have to predict AD in order to do this
    • aspirin does not work as well to prevent AD
    • not dose dependent, so not anti-inflammatory
  26. not so effective drugs for AD
    • vit E: does not work and affects clotting
    • ginko biloba: be aware, it also affects clotting factor = less clotting time
    • estrogen: can make AD worse
    • atypical antipsychotics: helps psych symptoms in pt. who already have AD, might = more deaths though
    • SSRIs: work well for depression
  27. American Academy of Neurology guidelines, 2001 on Vitamin E therapy for AD
    they recommended trying Vit. E therapy, although no evidence has been shown