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Block 8 week 5 > Dementia and alzheimer disease-aziz > Flashcards

Dementia and alzheimer disease-aziz Flashcards

1
Q

Most of your preceptions and sensations happen in the (Blank) of your brain and most of your actions happen in the (blank) of your brain

A

back

front

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2
Q

What is more complex. the primary areas or association areas?

A

association areas

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3
Q

What do the primary areas do?

What do asociation areas do?

A
  • they determine what they want done

- figure out how to make the action happen

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4
Q

What is the primary area that is damaged in alzheimers?

A

temporal lobe

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5
Q

If you lose where brocas area is on the right side what will you lose?

A

emotional speech

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6
Q

Where does degredation occur in alzheimers?

A

prefrontal cortex and temporal lobe

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7
Q

What areas of the basal ganglia that are important for emotion and cognition?

A

Caudate

Nucleus accumbens

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8
Q

What neurotransmitter is important for the basal forebrain and the pontomesencephalic region?
Where do they project to?
What are the receptor types and what is their main action?

A

acetylcholine

basal forebrain-> cerebral cortex
pontomesencephalic region-> thalamus, cerebellum, pons, medulla

muscarinic and nicotinic

Neuromodulation

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9
Q

What neurotransmitter is important for LTP?

A

glutamate

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10
Q

What receptor type is important for synaptic plasticity?

Major exctiatory receptor?

A

NMDA

AMPA/kainate

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11
Q

Where do you find the cell bodies of neurons that produce dopamine?
Where do they project to?

A

midbrain: substantia nigra, pars compacta, ventral tegmental area
- striatum, prefrontal cortex, limbic cortex, nucleus accumbens, amygdala

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12
Q

What are all the neurotransmitters involved in neuromodulation?

A 
norepinephrine
dopamine
serotonin
histamine (excitatory only)
Peptides
acetylcholine
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13
Q

Where is the location of the cell bodies of neurons that produce norepinephrine?
Where do they project to?
Main actions?

A

-sympathetic ganglia
-pons: locus ceruleus and lateral tegmental area
smooth muscle, cardiac muscle, enter CNS
-sympathetic functions, neuromodulation

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14
Q

Where is the location of the cell bdies of neurons that produce serotonin?
Where do they project to?
What is their main action?

A

midbrain and pons: raphe nuclei

  • entire CNS
  • neuromodulation
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15
Q

Where is the location of the cell bodies of neurons that produce histamine?
Where do they project to?
What is their main action?

A

hypothalamus: tuberomammillary nucleus
midbrain: reticular formation
- entire brain
- excitatory neuromodulation

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16
Q

What is the location of the cell bodies of glycine?

WHere do you find cell bodies of neurons that produce peptides?

A
  • spinal cord (possibly brainstem and retina)

- entire CNS

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17
Q

What are all the components of executive function?

A

Working memory, mental flexibility, inhibition, fluency, abstract reasoning

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18
Q

What are all the cognitive domains in the neurocognitive assessment?

A
  • Memory (episodic)
  • Attention
  • Executive function
  • Language
  • Visuospatial abilities
  • Behavior assessment
  • Functional status
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19
Q

What test is the most sensitive for cognitive screening?

What test is the least sensitive for cognitive screening?

A

MOCA (montreal cognitive assessment)

Animal naming and Modified Blessed

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20
Q

What test is the most specific for cognitive screening?

A

ANT and Memory Phrase and Animal naming (ANT)

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21
Q

What test is the least specific for cognitive screening?

A

MMSE

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22
Q

What cognitive test screening takes the longest? Takes the shortest amount of time?

A

MOCA

Clock drawing

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23
Q

What is mild cognitive impairment?

A

-cognitive impairment that doesn’t interfere with activities of daily living and is not severe enough to meet criteria of dementia

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24
Q

About (blank) of patients with MCI eventually convert to dementia by 6 years.

A

80%

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25
Q

What are the risk factors for progression?

A

Apo E allele carrier, poor performance on semantic cueing memory test, reduced hippocampal volumes.

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26
Q

What are normal aging issues?

A

multi-tasking problems, time problems, difficulty coming up with words

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27
Q

What are single domain issues?

A

issues in one aspect of cognition or personality

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28
Q

What differentiates mild cognitive impairment from dementia?

A

A: functional status. With mild cognitive impairment you have a larger than normal deficit in cognition but you are still functional

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29
Q

What is dementia?

A

progressive deterioration of cognitive function, that results in impairment of social and occupational skills

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30
Q

Dementia is usually caused by relentless brain tissue loss due to (Blank)

A

multiple degenerative processes

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31
Q

If you have Rapid degeneration of cognitive processes this is called (Blank) …can take hours to months. This is opposed to dementia which is slow degeneration (takes years)

A

Delirium

32
Q

The hallmark sign of dementia is (blank)

A

neuronal loss

33
Q

What are some types of dementia (neurodegenerative)?

A
  • Alzheimer dementia
  • Dementia with Lewy bodies
  • Frontotemporal dementia
  • Vascular dementia
  • Parkinson DIsease Dementia
  • Corticobasalar degeneration
  • Normal pressure hydrocephalus
34
Q

Dementia is a cognitive decline whereas alzheimers is a type of (blank)

A

cognitive decline (i.e memory decline)

35
Q

What are the risk factors for Alzheimer Dementia?

A
  • Age
  • Female sex
  • Low level of education
  • Down syndrome
  • Head trauma
  • ApoE e4
  • Genetic: APP, PS-1, PS-2
36
Q

In the CSF of an alzheimers patient, what will be high amounts in the CSF? What will be in low amounts?

A

Tau

Amyloid beta

37
Q

What does a brain look like in advanced Alzheimers?

A

HELLA atrophied!!!!!

38
Q

What are symptoms of alzheimers?

A
  • memory loss that disrupts daily life
  • challenges in planning or solving problems
  • difficulty completely familiar tasks at home, at work, or at leisure
  • confusion with time or place
  • trouble understanding visual images and spatial relationships
  • new problems with words in speaking or writing
  • misplacing things and losing the ability to retrace steps
  • decreased or poor judgement
  • withdrawal from work or social activities
  • changes in mood and personality, including apathy and depression
39
Q

What are the domains affected in alzheimers from most affected to least?

A

Memory> language> executive> visuospatial> behavioral

40
Q

What is the DSM IV diagnostic criteria for alzheimers disease?

A
  • impaired memory
  • one of the following cognitive disturbances: Aphasia, apraxia, agnosia, disturbed exec function
  • cognitive abnormalities must represent change from a previous higher level of function, be progressive and impair function
  • gradual onset and continued decline
  • not present exclusively during delirium
41
Q

What are the initial tests you want to perform on a patient you suspect has dementia?

A
  • CBC
  • CMP
  • Serum B12
  • Thyroid function test
  • Non contrast CT or MRI
  • depression screening
42
Q

What TESTS should you not give your patients that you suspect have dementia?

A
  • Syphilis screening
  • EEG
  • Lumbar puncture (w/ some exceptions: mets, CNS infection, hydrocephalus, <55 yo, unusual dementia)
  • Linear or volumetric MR or CT (for hippocampal atrophy)
  • SPECT
  • APO e4 genotyping
43
Q

THere is insufficient evidence to support/refute what three things?

A
  • PET
  • Genetic markers for AD
  • CSF or other biomarkers for AD
44
Q

SO whats the deal with APoE-e4?

A

its a huge risk factor for AD, but nobody cares

45
Q

What are the three phases of Alzheimers?

A
  • Pre-symptomatic or preclincal phase (changes in biomarkers)
  • symptomatic, pre-dementia phase- MCI (mild cognitive impairment)
  • dementia phase (insidious onset
46
Q

What phase of alzheimers is this:
Insidious onset over months to years with a clear-cut history of progression of cognitive decline, usually obtained from informant

A

dementia phase

47
Q

If you have mild cog impairment what stage of alzheimers are you in?

A

Symptomatic, pre-dementia phase

48
Q

What are markers for amyloid beta accumulation?

A

CSF Aβ1-42

PET amyloid imaging

49
Q

What are markers of neuronal injury or neurodegeneration?

A

Molecular markers of neuronal injury: CSF phosphrylated tau and total tau.
Imaging markers of synaptic dysfunction
Imaging markers of neuronal loss and atrophy

50
Q

What is in high amounts during the preclinical alzheimersstage/

A

amyloid and synaptic dysfunction

51
Q

What is in high amounts during mild cognitive impairment?

A
  • synaptic dysfunction
  • amyloid B accumulation
  • abnormal brain structures present
52
Q

What is in high amounts during dementia?

A
  • synaptic dysfunction
  • amyloid B accumulation
  • abnormal brain structures present
  • Clinical function abnormal
53
Q

What are all the components in helping a dementia patient?

A
  • home care
  • institutionalized care
  • hospital care
  • clinic care
  • community care
54
Q

WHat are some dementia complications?

A 
Inadequate nutrition. 
Reduced hygiene. 
Difficulty taking medications. 
Deterioration of emotional health. 
Difficulty communicating. 
Delusions and hallucinations. 
Sleep difficulties..
Personal safety challenges.
55
Q

What are the drugs used to treat dementia?

A 
Cholinesterase inhibitors
-Donepezil (aricept)
-Galantamine (Reminyl)
-Rivastigamine (Exelon)
NMDA inhibitor
-Memantine.
56
Q

What are the SEs of cholinesterase inhibitors?

A
  • Nausea
  • vomiting
  • diarrhea
  • vivid dreams
57
Q

What are the SEs of memantine?

A
  • Confusion
  • headaches
  • dizziness
58
Q

Alzheimers dementia is associated with decreased (blank) activity. What breaks this neurotransmitter down? So what class of drug slows down the breakdown of this and helps to slow down alzheimers?

A

cholinergic

  • acetylcholinesterase
  • cholinesterase inhibitors
59
Q

What is the glutamate hypothesis?

A

When glutamate producing neurons die they release a ton of glutamate causing NMDA activation and excitotoxicity and thus neuron death

60
Q

What is the MOA of memantine and why is it awesome for tx in MODERATE to SEVERE dementia? Why isnt it used a lot?

A

NMDA inhibitor thus reducing chance of excitotoxicity

SE such as dizziness, confusion, headache, constipation and has similiar effects to placebo

61
Q

How do you prevent dementia?

A 
Primary Prevention
Secondary prevention
Diet
Physical Exercise
Intellectual  activities
Management of CVD risk factors
62
Q

What is the best prevention for Alzheimers?

A

Viewing the brain as a highly vascular organ, and taking vascular protection measures are probably the best prevention

63
Q

What kind of diet and exercise do you want to utilize to prevent alzheimers?

A 
Exercise (walk >2 miles/day)
High fish/DHA, low sat. fat
Green tea
Red wine, modest alcohol
Mediterranean diet
64
Q

Median survival time in years from dementia onset to death = in females? In males ? Overall?

A

Female=4.6
Males=4.1
Overall=4.5 years

65
Q 
Median survival time in years from dementia onset to death = 
Age based: 
65-69 yo =?10.7 years
70-79 yo=? 	5.4 years
80-89 yo	=?4.3 years
>89 yo =?	    3.8 years
A 
Age based: 
65-69 yo =10.7 years
70-79 yo 	=5.4 years
80-89 yo	=4.3 years
>89 yo=  3.8 years
66
Q

What is this:

Heterogenous group of disorders that display involvement of frontal and anterior temporal structures.

A

Frontotemporal Dementia/Degeneration

67
Q

What are the Frontotermporal Dementia/Degeneration subtypes?

A 
Behavioral variant Frotntotemporal Dementia (bvFTD)
Semantic variants (SV)
Progressive NonFluent Aphasia (PNFA)
68
Q

What is this:

agrammatism, speech apraxia, and word finding difficulties. Speech effortful, slow and sometimes telegraphic.

A

Progressive NonFluent aphasia (PNFA)

69
Q

What is this:
fluent, effortless, and grammatically correct, but word finding difficulty = empty speech, naming deficits and loss of word knowledge.

A

Semantic Variant (SV)

70
Q

What is this:

lack of insight, hyperorality, apathy, irritability, disinhibition, lack of empathy, rudeness

A

Behavioral variant Frontotemporal Dementia (bvFTD)

71
Q

What genetic chromosomes are involved in frontotemporal dementia?
What is the pathology behind it?

A

17,9

Tauopathy, TDP-43 proteinopathy

72
Q

What is the clinical spectrum of vascular dementia?

A
  • multiple ischemic infarcts
  • single strategic infarction (caudate, hippocampal, paramedian thalamic, rt parietal lobe)
  • cerebral hemorrhage
  • extensive microvascular disease
  • hereditary vascular disease
  • hypoperfusion injury
  • vasculitis and other angiopathies
73
Q

What are some common single strategic infarcts that can cause vascular dementia?

A

Caudate nucleus, Hippocampi, paramedian thalami, Rt. Parietal lobe.

74
Q

What are some common extensive microvascular diseases that can cause vascular dementia?

A

Lacunar state, Binswanger’s disease

75
Q

What are soe common hereditary vascular diseases that can cause vascular dementia?

A

CADASIL, MELAS, Fabry’s disease.

76
Q

What are the core features of dementia with lewy bodies?

A
  • Fluctuating cognition or alertness
  • Recurrent visual hallucinations
  • Spontaneous motor symptoms of parkinsonism
77
Q

What are the supportive features of dementia with lewy bodies?
What does the MRI look like?
What is the pathology?

A

Supportive features:

  • repeated falls,
  • syncope or transient LOC, -delusions,
  • neuroleptic sensitivity
  • hallucinations of other modalities,
  • REM sleep behavior disorders,
  • depression

MRI: Normal or whole brain atrophy

Pathology: Lewy Bodies.

Block 8 week 5 (9 decks)

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