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MS 2 - Unit 3 > Behavioral Science - dementias (combined lectures) > Flashcards

Behavioral Science - dementias (combined lectures) Flashcards

1
Q

What defines MCI vs normal aging?

A

MCI must have:
Memory complaint corroborated by an informant
Objective memory impairment for age and education
Preserved general cognition
Normal activities of daily living
Not demented

normal aging:
Difficulty retrieving words and names
Slower processing speed
Difficulty sustaining attention when faced with competing environmental stimuli
Learning something new takes a bigger effort
No functional impairment

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2
Q

DSM criteria for dementia (Neurocognitive Disorder):

A

1) decline in memory, complex attention, exec function, learning/memory, language, perceptual/motor, social cognition
2) Cognitive deficits must impact social and occupational function
3) Diagnosis must be made in the presence of intact sensory systems

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3
Q

two DSM5 suptypes of neurocognitive disorder

A

Meets 3 criteria (decline, social/ocupational impact, not due to focal neurological defecit in sensory systems)

MAJOR patient not capable of independent living
MINOR capable of independent living

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4
Q

When does early onset AD present? Late onset?

A

30 - 60 Yrs of age

>60

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5
Q

Is early onset AD usually sporadic or familial?

A

familial (older than 60, cases are much more likely to be sporadic)

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6
Q

What are the associated genetic mutations in early onset AD? Genetics (sex linked, autosomal, recessive, dominant)?

A

1- abnormal presenilin 2
14- abnormal presenilin 1
21- abnormal amyloid precursor protein

Autosomal dominant

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7
Q

What chromosome is APOE4 located on?

A

19

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8
Q

What is AD? How does it usually present clinically?

A

The most common cause of senile dementia.

presents with deficits in recent memory, progressing to global impairment of cognition.

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9
Q

What is a hallmark feature of AD suspected to account for clinical symptoms?

A

Neuronal and synaptic loss affecting cortical and some subcortical areas (e.g. nucleus basalis of Meynert).

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10
Q

Which type of neuron is thought to contribute to loss of cognitive function in AD?

A

cholanergic neurons

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11
Q

What enzymes is responsible for cleaving APP?

A

beta and gama secretase

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12
Q

What enzymes is responsible for cleaving APP?

A

beta and gama secretase

beta secretase is also called BACE1 (Beta-site APP Cleaving Enzyme 1)

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13
Q

A-beta deposits in cortical and leptomeningeal arteries and arterioles - disease?

A

cerebral amyloid angiopathy

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14
Q

development of abnormal proteinaceous (alpha-synuclein) cytoplasmic inclusions

A

Lewy bodies

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15
Q

what is Granulovacuolar degeneration (GVD) - what disease?

A

grainy deposits within neurons surrounded by a clear zone

AD (also lewey body dementia but LBD is often associated with AD hippocampal features)

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16
Q

what is Granulovacuolar degeneration (GVD) - what disease?

A

grainy deposits within neurons surrounded by a clear zone

AD (also lewey body dementia but LBD is often associated with AD hippocampal features)

Because of association with other dementias GVD and also Hirano bodies are not considered diagnostically important disease features

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17
Q

rapid or acute onset dementia, with especially rapid decline in the first few months - overlapping loss of cognitive and motor function, diffuse alpha-synuclein rich cytoplasmic inclusions throughout the brain (cortex and basal ganglia), sometimes cortical atrophy/ventriculomegaly, loss of Ach and DA neurons (in SN not VTA)

A

Lewy body dementia

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18
Q

Presinilin (what, where is it?)

A

component of gamma secretase complex (multimeric transmembrane protein complex responsible for cleaving the membraine associated region of amyloid precursor protein)

forms the catalytic/proteolytic site - mutations of presenlin 2 (chromasome 1) and preseilin 1 (chromasome 4) are involved in familial AD

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19
Q

Presinilin (what, where is it?)

A

component of gamma secretase complex (multimeric transmembrane protein complex responsible for cleaving the membraine associated region of amyloid precursor protein)

forms the catalytic/proteolytic site - mutations of presenlin 2 (chromasome 1) and preseilin 1 (chromasome 14) are involved in familial AD

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20
Q

1st and 2nd greatest risk factors for AD

A

Age, APOE4

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21
Q

Which APOE allele is thought to be protective against AD?

A

APOE 2

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22
Q

dense central core of compact amyloid, surrounded by a clear zone and a peripheral corona or halo consisting of non-compact amyloid and neurites, including axon terminals

A

neuritic/senile plaque

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23
Q

Apple-green birefringence of what stain under polarized light confirms presence of amyloid.

A

congo red

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24
Q

stain for neurofibrillary hyperphosphorylated tau tangles

A

silver

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25
Q

what is Tau? What is it’s function?

A

microtubule associated protein - stabilizes microtubules

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26
Q

How are neurofibrillary tangles formed?

A

hyperphosphorilation by microtubule associated kinases result in deassociation with MT fillament, MT depolimerization, and assemblage of hyperphosphorylated tau into paired helical filaments, which bundle to form neurofibrillary tangles

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27
Q

what are neuropil threads?

A

the dystrophic neurites at the periphery of neuritic plaques - major component is paired helical filaments of hyperphosphorylated tau

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28
Q

What are the gross features of Frontotemporal Lobar Degeneration as seen in frontotemporal dementia?

A

atrophy in the frontal lobe and temporal lobe of the brain, with sparing of the parietal and occipital lobes.

has so-called knife edge

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29
Q

what are the common accumulation products seen in frontotemporal lobular dengeneration/frontotemporal dementia?

A

*FTLD-Tau (Numerous tau containing neurons) Most common
*FTLD-TDP (TAR-DNA binding protein 43)
FTLD-FUS and other (less common)

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30
Q

Relative to AD what is the onset profile for FTD?

A

Earlier onset compared to AD

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31
Q

What are Pick bodies?

What diseases are they associated with?

Where are they seen?

A

intraneuronal inclusions of Tau

AD and FTD

Dentate gyrus of hippocampus

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32
Q

What are the stages of AD?

A

asympomatic, podromal (early, possible disease sympotms),

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33
Q

What are early cognitive symptoms of AD?

A

Trouble keeping appointments
Difficulty finding words
Misplacing objects

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34
Q

What are early functional symptoms?

A

Difficulty driving
Difficulty selecting clothes
Missing appointments
Problems at work

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35
Q

cognitive retardation from primary depression and dementia differ in that depressed patients usually

1
2
3

A

Demonstrate less motivation during cognitive testing

Express cognitive complaints that exceed measured deficits

Maintain language and motor skills

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36
Q

What are the indications for neuroimaging in a suspected demented patient?

1
2
3

A

Focal findings on exam

Rapid onset/decline

Falls, head trauma by history

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37
Q

What are 3 common features seen in both vascular dementia and AD?

A

Lacunar infarcts,

small vessel disease

white matter

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38
Q

Compared to AD, memory loss in FTD occurs earlier or later in the disease course?

A

later! (earlier onset in FTD and more rapid progression, but behavioral/emotional changes, not memory impairments, are not the initial clinical findings)

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39
Q

Are cholinesterase inhibitors useful for FTD?

A

no

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40
Q

What medication can help with behavioral control in FTD patients?

A

(anticonvulsants) Divalproex or valproic acid

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41
Q

Are SSRIs used for FTD?

A

yes - for irratability, depression, impulsive behaviors

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42
Q

Can atypical atipsychotics be used?

A

Yes, carefully

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43
Q

What are the most common pharmacologic treatments for AD?

A

Cholinergic therapy.

NMDA receptor antagonists

44
Q

Are current pharmacologic treatments disease modifying based on biomarkers (CSF-Tau Amyoid/FDG-PET?)?

A

no - for management of cognitive/behavioral symptoms symptoms

45
Q

Degeneration of ______ results in “Inwide-spread” of acetylchoiline deficiency in AD

A

the basal nucleus of Meynert

46
Q

memory deficits in AD are thought to be caused by_____?

A

Loss of Ach neurons

47
Q

Which class of agents and which drugs in particular are used to address consequences of degeneration in the basal nucleus of Meynert in AD?

A

anticholinergic agents

donepezil

rivastigmine

galantamine

48
Q

What drug is FDA approved for treatment of severe AD?

A

donepezil

  • AChE inhibitor - metabolized by CyP450
  • side effects are nausia, vomiting, sleep disturbance
49
Q

What neurodegenerative disease is memantine used for an why (pathophysiology of neuronal death/ drug MOA)?

A

AD - because loss of cholanergic neurons and symptoms cascade is thought to be caused by glutamatergic excitotoxicity

thinking is that excess glutamate signaling results in excess Ca 2+ influx into cytoplasm and activation of signalling pathways that lead to increased expression of phosphatases/kinases, which in turn disrupt microtubule stabiizing proteins and form intracellular filament aggregates that alter metabolic function and damage mitochondria triggering apoptosis

memantine is an NMDA receptor antagonist

50
Q

Can memantine be used alongside donepezil?

A

yes - combo of AChE blocker + NMDA blocker is most beneficial

51
Q

which antidepressants are used for AD?

A

sertraline and venlafaxine

52
Q

What anxiolytics are used for AD?

A

buspirone and lorazepam.

53
Q

what antipsychotics are used for AD?

A

risperidone and haloperidol

54
Q

Multi-infarct dementia

A

diffuse small infarctions that result from small vessel disease and lead to neuronal death and cognitive decline

feature of vascular dementia

55
Q

what are the common histologic features of vascular dementia?

A

diffuse lacunar infarcts caused by hypertension related small vessel pathology

white matter pathology

neuronal death

cerebral amyloid angiopathy

56
Q

What is a leukoencephalopathy? What type of dementia is it commonly associated with?

A

broad term that describes any disease that affects brain white matter (leuko = white)

common in vascular dementia

57
Q

What vessel branches are particularly susceptible to hypertensive small vessel pathology?

A

branchges of lenticulostriate arteries that supply basal ganglia and internal capsule

58
Q

what form of dementia can result from arteriosclerosis of small arteries?

A

subcortical dementia

59
Q

what are features of subcortical dementia

A

Cognitive slowing.
Impaired problem solving.
Visuospatial abnormalities.
Disturbances of mood and affect

60
Q

How common is vascular dementia relative to other dementias?

A

Most common after Alzheimer’s

61
Q

Progression of vascular dementia is usually _____

A

Step-wise - but can be abrupt after CVA

62
Q

what is a common association with vascular dementia?

A

cardiovascular risk factors - atherosclerosis, hypertension, hyperlipidemia, diabetes

63
Q

T/F “Mixed” dementia with AD or Lewy Body is not unusual

A

true

64
Q

T/F emotional lability (inapropriate ouburst of crying/laughing) is a common feature of subcortical vascular dementia

A

true

65
Q

T/F first line pharmacologic treatment for vascular dementia is anticholanergic agents

A

false! cholinesterase inhibitors are used to increase Ach

donepezil, glalantamine, rivastigmine

66
Q

T/F exercise (both physical and mental) is useful in treatment of vascular dementia

A

true

67
Q

T/F a “Mediterranean” diet is recommended for prevention/treatment of vascular dementia

A

true

68
Q

T/F focus of vascular dementia is control of cardiovascular risk factors

A

true

69
Q

what primary sporadic diseases are caused by intracellular missaccumulation of pre-synaptic protein alpha-synuclein?

A

parkinsons disease

lewy body dementia

70
Q

what is the site of apearance of lewy bodies in lewy body dementia vs parkinsons disease

A 
LBD = cortex
Parkinsons = SN
71
Q

What are the cardinal symptoms are parkinsons disease?

A 
resting tremor,
difficulty initiating movement (akinesia), slowed movement (bradykinesia), 
rigidity, 
shuffling gait
postural instability.
72
Q

parkinsons disease ever associated with dementia

A

yes, occasionally (probably underdiagnosed)

73
Q

Pallor of substantia nigra with degeneration and loss of pigmented dopaminergic neurons of substantia nigra pars compacta (SNpc) that contain eosinophilic inclusions called lewy bodies

what disease?

A

parkinsons

74
Q

palor of substantia nigra with degeneration or loss of substantia nigra pars compacta without lewy bodies is seen in what disease?

A

cortical basal degeneration or progressive cerebral palsy

75
Q

What are the 2 features necessary for making histologic diagnosis of parkinsons disease?

A

palor of substantia nigra

with lewy bodies!

76
Q

what is more common fronto temporal dementia or lewy body dementia?

A

lewy body dementia (3rd most common)

77
Q

T/F dual diagnosis of AD and LBD is possible

A

true

78
Q

T/F lewy body dementia can be associated with little or no atrophy

A

true

79
Q

What is a hallmark and distinctive feature of lewy body dementia?

A

visual hallucinations with significant cognative fluctuations from day to day

80
Q

T/F antypsychotic drugs are used to address conitive/behavioral fluctuations in LBD

A

False! antipsychotics are contraindicated due to increased sensitivity

81
Q

What drug is used to treat REM sleep disorder in LBD?

A

clonazepam

82
Q

what is the diagnostic criterion used to difference between LBD and PD?

A

uses time frame of appearance of parkinsonian symptoms

83
Q

Onset of dementia within 12 months of parkinsonism

A

LBD

84
Q

Onset of dementia more than 12 months after the diagnosis of PD

A

PD (w/ dementia)

85
Q

what is the Mini Mental Status Examination (MMSE)?

A

Standardized 30 point rating scale that SCREENS (does not diagnose) for dementia

86
Q

What factors can influence the MMSE results?

A

age, education, ethnicity

87
Q

T/F a higher number (1-30) indicates more severe cognitive impairment

A

False

low numbers are worse

88
Q

how is the MMSE result categorized?

A

normal
mild
moderate
severe

89
Q

MMSE of 20-10

A

possible moderate dementia

90
Q

What are early behavioral symptoms?

A

Subtle changes in personality
Social withdrawal
Depression

91
Q

MMSE score categorizing possible severe dementia

A
92
Q

Cognitively normal person’s MMSE score

A

30-27

93
Q

possible mild dementia MMSE score

A

30-20

94
Q

T/F MMSE scores can be used to discern the type of dementia

A

False - only severity

95
Q

What are the 5 categories of the MMSE?

A 
Orientation
Registration
Attention and Calculation
Recal
Language
96
Q

What is the MoCA?

A

Montreal cognitive assessment

Standardized 30 point rating scale
Screening tool … NOT a diagnostic tool
Not specific for dementia type
Scoring- can be impacted by age, education, ethnicity

97
Q

What is different about the MoCA and MMSE

A

Catagories and scoring

MoCA is more sensitive

98
Q

What are the catagories of the MoCA?

A 
Misuospatial/executive
naming
memory
attention
language
abstraction
delayed recal
orientation (optional)
99
Q

Is it possible to get a 30 on the MMSE and still have dementia?

A

yes (mild 30-20) – also test is NOT diagnostic

100
Q

What is the mini-cog? How is it performed? Interpreted?

A

stripped down version of MMSE

As Pt. to repeat 3 unrelated words (mushroom cannon flamingo)

then ask them to draw a clock showing a particular time

then ask to repeat words

Interpretation is subjective - if they have some difficulty on either they probably have some degree of cognitive impairment

101
Q

What is the scoring system on the MoCA?

A

Normal >26
Mild 18-26
Moderate 10-17
Severe

102
Q

What is included on the MoCA that is missing from MMSE?

A

assessment of executive function

103
Q

How does the MoCA assess working memory?

A

ask Pt. to repeat reverse number sequences

104
Q

What categories are functional assessment divided into?

A

ADLs - activities of daily living

IADLs - instrumental activities of daily living (allow people to engage with their environment and facilitate daily needs)

105
Q

ADL or IADL?

Dressing
Eating 
Ambulating 
Toileting
Hygiene
A

ADL

D
E
A
T
H
106
Q

ADL or IADL?

Shopping
Housekeeping
Accounting
Food Preparation
Transportation
A

IADL

S
H
A
F
T

MS 2 - Unit 3 (45 decks)

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