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clinical ad Flashcards

1
Q

what is dementia

A

an illness of brain resulting in impairments in multiple spheres of cognition

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2
Q

what is the #1 risk factor for dementia

A

age

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3
Q

T/F : dementia implies an etiology or diagnosis

A

FALSE

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4
Q

what are some diagnosis barriers for dementia

A
  • patient is typically unaware of symptoms
  • evaluation may be time consuming and not well compensated financially
  • belief that memory loss and cognitive decline are part of normal aging
  • belief by physicians and public that AD is not treatable
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5
Q

about how long is the delay between symptoms and diagnosis with AD

A

about 2 years

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6
Q

what’s the general path of symptoms that a patient with AD may experience as their disease progresses?

A

starts with cognitive symptoms, then diagnosis, then loss of function and independence, then behvaior issues, and then potential nursing home placement, then death

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7
Q

give an example of an ability that someone with a 20 MMSE score may start to lose or show signs of having difficulty with.

A

keeping appointments, using phone, obtaining meal or snack, traveling alone

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8
Q

most alzheimer’s patients die from what? what does not typically cause death with AD?

A
  • being bed-bound/bed sores
  • not typically caused by cognitive decline or mental impariments
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9
Q

what is the typical medical causes doctors rule out prior to diagnosing dementia?

A

alcoholic dementia, vitamin deficiencies, tumors, seizures, MS, infections, brain lesions

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10
Q

approximately what percent of the US population +65 is demented?

A

13.1 - 5.8million people

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11
Q

Decline in _____ causes someone to go from normal to mild cognitive impairment (MCI). Decline in _______ causes someone to go from MCI to dementia.

A
  1. cognition
  2. function
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12
Q

approximately what percent of the US population 65+ has MCI or dementia

A

29% - over 12 million people

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13
Q

AD8 screening is used to assess what? what kinds of questions are asked?

A

-used to assess cognitive impairment by asking family members questions as a checklist that identify if a person could have AD based on how many answers are NO to questions.

  • ex. “does your family member have trouble remembering appointments”
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14
Q

Montreal Cognitive Assessment is used for what?

A

a bedside cognitive screening where patients answer questions of a wide range to test cognitive function and is sensitive to early decline

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15
Q

what’s one downside to the Montreal Cognitive Assessment?

A

takes about 15 minutes so may be better to break up into pieces

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16
Q

the ROS identifies what main groups to assess dementia?

A

mood, behavior, psychosis, sleep, physical/motor skillsw

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17
Q

what are some common behaviors with dementia?

A
  • hallucinations/delusions
    -abusive/combative behavior
    -short term memory loss/repetition
  • wandering/pacing
  • agitation
  • wanting to go home
  • lethargy/lack of initiative
    -rummaging/hoarding
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18
Q

why is behavior a problem with ADRD?

A

memory is a part of the limbic symstem which is hit early and hard in every neurodegenerative disorder

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19
Q

how early can behavioral symptoms occur? depression? agitation?

A

-behavioral symptoms occur 3 years before diagnosis in 40%
-depression occurs 2 years before diagnosis in 60%
-agitation occurs 1 year before diagnosis in 80%

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20
Q

what differences do we see in hippocampal size in normal aging vs MCI vs AD at same age (75yr old) compared to a 25yr old

A
  • normal is slightly shrunk but not much
  • MCI is significantly shrunk but still has right shape
  • AD is warped and almost completed depleted
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21
Q

on a FDG-PET (fluorodeoxyglucose) what do we see different between normal and AD brain scans?

A

the normal scan lights up but the AD brain does not

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22
Q

what test is typically used to assess AD in the clinical setting?

A

Montreal Cognitive Assessment (MoCA)

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23
Q

how does an FDG-PET scan work

A

you are injected a sugary substance that your brain absorbs and activates various parts of the brain where high activity is

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24
Q

regular pet scans utilize what kind of substance to measure pathology in the brain?

A

radioactive compounds that bind to neurofibrillary tangles and plaques

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25
Q

can amyloid plaques be present in the brain and symptoms of AD not present themselves?

A

YES – plaques form years prior to any symptoms arising

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26
Q

what is the delay (years) between plaques appearing in HPC and AD diagnosis

A

15 years

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27
Q

what is one way csf is utilized in AD diagnosis

A

spinal taps can help to measure abnormal tau proteins in csf to diagnose AD

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28
Q

how are blood markers utilized in AD diagnosis

A

they measure for abnormal tau proteins in the blood

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29
Q

the Preclivity test using what to identify AD?

A

blood tests

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30
Q

which two tests can diagnose AD the earliest, and which two tests are only able to detect more severely progressed cases of AD?

A

earliest- amyloid imaging and CSF amyloid-beta 42 spinal tap
latest- cognitive performance tests and functional decline testing

31
Q

what takes someone from a prodromal phase to a dementia phase?

A

functional impairment

32
Q

describe the 6 step algorithm for dementia and what side steps are taken if signs are shown for alternate causes of symptoms

A
  1. memory complaint or other impetus for consult
  2. neuro exam with “bedside” cognitive eval (if shown normal complete neurophysch eval)
  3. medical with imaging and lab testing (if medically reversible cause of decline found treat as needed)
  4. establish diagnosis of dementia
  5. define type (use additional biomarkers to confirm diagnosis)
  6. treat type of dementia & related symptoms
33
Q

describe the 3 main identifiers in AD pathology and if/how they impact nerve cell

A

-neurofibrillary tangles - kill nerve cell inside out
-neuritic plaque - amyloid build up kills nerve cell from outside in
-cerebral atrophy

34
Q

describe the process of beta amyloid plaque formation in 3 steps

A
  1. APP (membrane-bound glycoprotein) serves as a growth factor in injury and repair but is the amyloid precursor
  2. APP normally cleaved by alpha-secretase and beta-secretase, but in AD gamma-secretase is active
  3. b-amylois is toxic to cells and accumulates in brain tissue as amyloid plaques
35
Q

describe how tau protein causes tangle formation in AD pathology

A

tau stabilizes microtubules, but when neuron is diseased, microtubules become destabilized and fall apart causing tangled clumps of hyperphosphorylated tau to float in the cell

36
Q

T/F : neurofibrillary degeneration spreads from nerve cell to nerve cell in all neurodegenerative diseases

A

true

37
Q

what was the significance of the study done by De calignon and Liu in 2012?

A

they added a promotor to abnormal tau to over-express it and better understand the pathology of how it worked in the hpc

38
Q

what are some main genetic markers that increase toxic amyloid in the brain?

A
  • APP
  • ApoE
  • PS1
  • PS2
39
Q

APP is linked to familial AD. what kind of genetic effect does it have and how is it passed thru generations

A

it is an autosomal dominant form of ad and it has a risk of 60% chance of developing AD for those who inherit it

40
Q

how early can AD arise in familial AD cases?

A

40s

41
Q

what is the gene that makes you more likely to develop AD

A

ApoE E4

42
Q

whats the chance difference between having one vs two copies of ApoE E4?

A

one copy -4x more likely than someone without a copy
two copy- 10x more likely than someone without a copy

43
Q

what are some other potential genetic markers that could impact AD risk outside of the normal pathology?

A
  • cholesterol - APOE, SORL1
  • inflammation - CR1, MS4A
  • synapse function - PICALM, BIN1
  • brain development - EPHA1
44
Q

what are the 4 main types of dementia? does someone only have just one in every case?

A

lewy body dementia, vascular dementia, frontotemporal dementia, and alzheimer’s - NO, majority of the time its a mixed bag of all of them

45
Q

which type of dementia is most prevalent of the 4?

A

AD - 60%

46
Q

what pathology do we see in vascular dementia

A

strokes

47
Q

what pathology do we see in frontotemporal dementia

A

tau accumulation tangles

48
Q

what pathology do we see in alzheimer’s

A

neurofibrillary tangles, and neuritic proteins

49
Q

what pathology do we see in lewy body dementia

A

lewy body bundles form

50
Q

frontotemporal dementia is associated with what main symptoms

A

loss of interpersonal skills and language issues

51
Q

ad is associated with what main symptoms

A

memory loss and slow progressing symptom appearance

52
Q

lewy body dementia is associated with what main symptoms

A

hallucinations and mild parkinsonism

53
Q

vascular dementia is associated with what main symptom

A

stroke

54
Q

what do we see in symptom category impact as the diseases of each types of dementia progress

A

they start out having higher prevalence in their specific areas, but by the end stages, all categories are equally as impactful

55
Q

T/F : QMP (quadruple misfolded proteins) are seen in stages prior to dementia

A

FALSE

56
Q

T/F : shared mechanisms can cause multiple neurodegenerative disease pathologies to be present in a patient

A

TRUE

57
Q

T/F : 1/5 of dementia patients have every form of dementia

A

TRUE

58
Q

the __(more/less)__ pathologies accumulated, the greater the risk and severity of cognitive decline

A

more

59
Q

final clinical stages of dementia present themselves in what symptom form

A

mute, fetal-like posture, bedridden, loss of ability to walk, rigidity, seizures, urinary and fecal incontinence

60
Q

AD is treated based on what?

A

main symptoms

61
Q

treating cognitive impairments as the main problem of AD can use what kinds of drugs?

A

cholinesterase inhibitors or memantine

62
Q

treating behavioral issues/psychiatric as the main problem of AD can use what kinds of drugs?

A

SSRI, antipsychotic, mood stabilizing anti-epileptic

63
Q

treating motor issues as the main problem of AD can use what kinds of drugs?

A

carbidopa levodopa, DA agonist

64
Q

what happens with acetylcholine production in severe stages of AD

A

production decreases

65
Q

how does the cholinergic pathway relate to dementia treatment

A

some cases can be treated via neurotransmitter replacement therapy in the cholinergic pathway to increase acetylcholine production

66
Q

memantine acts via ________ receptors found widespread through the _______

A

glutamate, cortex

67
Q

how does memantine work to enhance cognition?

A

it silences the background noise of receptors and neurotransmitters binding to all for the signal to be heard/identified for memory formation

68
Q

T/F : Treatments of AD can improve symptoms and longevity

A

FALSE - treatments currently can not impact longevity, all AD patients still die

69
Q

which treatment of the following improves symptoms most efficiently:

a. no treatment
b. AChEI’s
c. AChEI + memantine

A

C. AChEI + memantine

70
Q

what drug was pulled from the market despite being FDA approved and why?

A

ENGAGE and EMERGE was pulled bc no one would pay for it and it had 41% of subjects develop swelling/strokes/bleeding and 25% had worsening AD symptoms

71
Q

what drug was created at UK and impacts clinical outcomes currently? What is the downside of this medication

A

Lecanemab - only removes amyloid so for cases when amyloid isn’t the only pathology causing the disease progression

72
Q

lecanemab impacts CDR-SB which leads to potentially ________?

A

buying patients 1.5 more years of life for every 4 years of treatment

73
Q

how can antibodies catch amyloid and impact levels of risk?

A
  • they may recognize monomers - safest
  • they may recognize oligomers - increase risk but increase benefit
  • recognize plaque - highest risk but most likely to remove plaque
74
Q

amyloid from plaques impact blood vessels in what way?

A

they can clog vessels

ana 410G (8 decks)

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