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Geriatrics > Cognitive Disorders of Aging > Flashcards

Cognitive Disorders of Aging Flashcards

1
Q

what functions decrease as a result of neurocognitive disorders of aging?

A
  • sensory - sight, hearing, smelling, tasting, proprioception
  • motor - walking, talking, dancing, exercise
  • memory - short term, long term, memory recall
  • cognitive - speech, learning, reading, writing
  • behavior and emotions
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2
Q

describe healthy brain function

A
  • 10 B neurons, each neuron joins a network of other neurons to coordinate different functions
  • these functions require an immense amount of energy and oxygen (when something goes wrong in one of these networks, immediate or progressive loss of function occurs due to neuronal death)
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3
Q

describe aging and memory

A
  • minor short term memory los, losing or misplacing items, occasional forgetfulness, forgetting details
  • dementias - loss of memory and other mental abilities severe enough to interfere with daily life (cause physical changes in the brain)
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4
Q

what are 7 types of dementias?

A
  • alzheimer’s disease
  • vascular dementia
  • mixed dementia
  • lewy body dementia
  • hungington’s disease
  • creutzfeldt-jakob disease
  • frontotemporal dementia
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5
Q

describe alzheimer’s disease

A
  • alois alzheimer was first to describe “pre-senile” dementia
  • characterized by problems in memory, thinking, and behavior great enough to interfere with daily life
  • considered a progressive, degenerative disease that worsens over time
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6
Q

describe how alzheimer’s disease worsens over time

A
  • early stage = mild memory loss

- late stage = loss of ability to converse and respond to their environment

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7
Q

what is the average lifespan after initial symptom presentation of a patient with alzheimer’s disease?

A

about 8 years, but can range from 4-20 years depending on age and general health

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8
Q

what are the neurological findings of alzheimer’s disease?

A

loss of neurons leads to atrophy of the cortical structure of the brain in the affected regions

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9
Q

what are the histological findings of alzheimer’s disease?

A
  • presence of dense amyloid plaques primarily composed of insoluble beta-amyloid peptides and cellular material around neurons
  • presence of neurofibrillary tangles composed of aggregations of microtubule associated tau proteins that accumulate inside the neurons itself
  • lewy bodies
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10
Q

what are the biochemical findings of alzheimer’s disease related to amyloid precursor protein?

A
  • amyloid precursor protein (APP) is a transmembrane protein involved in neuron growth, survival, and post injury repair
  • APP is cleaved, beta- and gamma-secretase into smaller pieces
  • beta amyloid fragments of this protein begin to clump together forming plaques
  • inhibition of enzyme function and glucose utilization by neurons is also observed
  • apoptosis is triggered = neuronal loss = cortical atrophy
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11
Q

what are the biochemical findings of alzheimer’s disease related to neurofibrillary tangles?

A
  • microtubules (components of the neuronal cytoskeleton) are stabilized by phosphorylated tau proteins
  • tau proteins are hyper-phosphorylated, thereby creating clumps or “tangles”
  • this causes microtubules to fall apart, thereby losing the cell’s nutrient transport system, and the cell dies
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12
Q

T or F:

most people develop plaques and tangles as they age, but alzheimer’s disease patients develop a much larger amount

A

true

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13
Q

___ is the most common cause of dementia and represents ___% of all dementia cases

A
  • alzheimer’s

- 60-80%

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14
Q

what is the greatest known risk factor for alzheimer’s disease?

A

age (but can happen in younger people as well)

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15
Q

alzheimer’s disease is the ___ largest cause of death in the US

A

6th

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16
Q

___ is caused by inadequate blood flow to the brain which results in localized hypoxia and eventual neuronal death

A

vascular dementia

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17
Q

hypoxia that results from vascular dementia causes varying degrees of cognitive impairment, which can range from mild to severe. what are some of these impairments?

A
  • memory loss, problems thinking, problems solving, reasoning, speech, word recall, etc.
  • confusion, disorientation, attention problems, vision problems, etc.
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18
Q

what are the typical symptoms of vascular dementia?

A

they vary widely depending on affected brain area

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19
Q

what are the risk factors for vascular dementia?

A
  • advancing age, smoking, cariovascular disease (HTN, hypercholesteremia, etc.), diabetes, lack of exercise, obesity, and alcohol consumption
  • same for heart disease
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20
Q

what is the treatment and prevention for vascular dementia?

A
  • addressing risk factors

- some alzheimer’s drugs may help

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21
Q

what is the cause of lewy body dementia?

A
  • unknown

- does not appear to have any association with familial or genetic inheritance

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22
Q

how is lewy body dementia diagnosed?

A

through autopsy (post mortem)

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23
Q

what is the “hallmark” of lewy body dementia?

A
  • lewy bodies present in histological samples
  • alpha-synuclein protein is present but its function is unknown
  • present in other dementias including parkinson’s disease and alzheimer’s
  • destroys brain cells and gets worse over time
  • limits lifespan
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24
Q

what are the symptoms of lewy body dementia?

A
  • changes in cognitive ability (thinking and reasoning)
  • confusion and varying alertness
  • memory problems
  • changes in posture and balance
  • autonomic system disturbences
  • visual hallucinations
  • delusions
  • trouble interpreting visual information
  • acting out dreams, sometimes violently (REM sleep disorder)
25
Q

what is the treatment for lewy body dementia?

A
  • address symptoms
  • antipsychotic drugs - can cause serious side effects in 50% of patients
  • antidepressants - SSRIs
  • clonazepam - REM sleep disorder
26
Q

mixed dementia typically includes characteristics of what other three dementias?

A
  • alzheimers disease, vascular dementia, and lewy body dementia
  • plaques, lewy bodies, and vascular changes (blood clots)
27
Q

T or F:

symptoms of mixed dementia are indistinguishable from other types of dementia

A

true

28
Q

when is mixed dementia usually diagnosed?

A

post mortem

29
Q

what are the drugs used to treat mixed dementia?

A

no specific drugs for treating mixed dementia are FDA approved

30
Q

huntington’s disease is a brain disorder that causes changes in the central brain that affect movement, thinking, and mood, and is caused by a single defective gene in ___

A

chromosome 4

31
Q

describe the defective gene in chromosome 4 that causes huntington’s disease

A
  • the gene codes for a protein huntingtin, which when damaged, causes brain changes that lead to the phenotype observed
  • normally, this protein contains 17-20 repetitions of a chemical code, but in huntington’s, this protein contains more than 40 repetitions
  • the more repeats, the sooner the onset of symptoms and the faster the progression of the disease
32
Q

when do symptoms of huntington’s disease develop?

A

between age 30-50 but can appear as early as 2 and late as 80

33
Q

how can huntington’s disease be diagnosed?

A
  • a genetic test is available to diagnose this disease

- diagnostic tests essentially measure the # of repetitions

34
Q

is there a cure for huntington’s disease?

A

no

35
Q

what is the treatment for huntington’s disease?

A
  • antipsychotics for involuntary muscle movements and SSRIs for anxiety and depression
  • several possible treatments are being investigated
  • gene silencing (stops production of mutant protein)
  • neuronal replacement (stem cells help repair damaged neurons)
36
Q

___ is a type of dementia caused by a prion protein found int he body that folds into an abnormal shape and causes similar prion proteins to do the same in the brain

A

creutzfeldt-jakob disease

37
Q

___ are known as “infectious proteins” that can cause normally folded proteins to misfold

A

prions

38
Q

describe creutzfeldt-jakob disease

A
  • similar to bovine spongiform encephalopathy in cows
  • fast moving disease that causes dementia that gets worse very quickly
  • rare but extremely fatal, as 90% of patients die within one year of diagnosis
  • can be passed on by exposure to infected brain or spinal tissue
39
Q

what are the sources of infection of creutzfeldt-jakob disease?

A
  • medical procedures involving instruments used in neurosurgery, growth hormone from human sources, or certain transplanted human tissues
  • consumption of BSE infected beef can cause a variant of CJD
40
Q

what is the best diagnostic instrument for creutzfeldt-jakob disease?

A

rapid symtpom progression

41
Q

is there a cure for creutzfeldt-jakob disease?

A

no

42
Q

what is the cause of frontotemporal dementia?

A

inherited with no apparent risk factors

43
Q

describe frontotemporal dementia

A
  • neuronal damage leads to functional losses associated with the frontal and temporal regions of the brain
  • progressive deterioration of behavior and personality, language, muscle, and motor function
  • there are approximately 6 subtypes/variations of this disease
44
Q

describe the behavior variant of frontotemporal dementia

A
  • severe changes in personality

- nerve cell loss in areas that control conduct, judgement, empathy, and foresight

45
Q

describe primary progressive aphasia associated with frontotemporal dementia

A
  • semantic variant - patient loses ability to understand or formulate words in a spoken sentence
  • non-fluent or agrammatic variant - patient speech is hesitant, labored, or devoid of grammar
46
Q

what 3 characteristics of frontotemporal dementia affect muscles?

A
  • amyotrophic lateral sclerosis (ALS) - muscle weakness and wasting, effects the motor neurons
  • corticobasal syndrome - loss of coordination and stiffening of arms and legs
  • progressive supranuclear palsy - muscle stiffness, difficulty walking, changes in posture
47
Q

what two main types of medications are used to treat neurocognitive disorders?

A
  • cholinesterase inhibitors treat the symptoms but not the source of the disease
  • glutamine regulators
48
Q

describe how cholinesterase inhibitors are used to treat symptoms of neurocognitive disorders

A
  • acetylcholine is a NT involved in learning and memory
  • cholinesterase inhibitors prevent acetylcholine from being broken down
  • this allows transmission of this chemical between the associated neuronal network to continue
  • reduce memory related symptoms
49
Q

describe how glutamate regulators are used to treat neurocognitive disorders

A
  • glutamate is involved in information processing

- improves mental function and ability to perform activities

50
Q

what specific medications are used to treat mild to moderate alzheimers? what is the method of action?

A
  • exelon, aricept, razadyne

- inhibits acetylcholine breakdown

51
Q

what specific medications are used to treat moderate to severe alzheimer’s? what functions do they improve?

A
  • namenda, namenda/namzaric

- improves memory, attention, reason, language, and task performance

52
Q

in the dental management of patients with neurocognitive disorders, patient assessment should be directed toward ___

A

understanding the nature, severity, control, and stability of the disease

53
Q

what are some disease-related oral complications of patients with neurocognitive disorders?

A
  • poor oral hygiene due to decreased ability to perform simple tasks
  • increased xerostomia (polypharmacy) - caries
  • periodontal disease
  • candidiasis
  • increased risk for aspiration pneumonia
54
Q

treatment planning for patients with neurocognitive disorders should be focused on ___

A

preventing oral disease

  • complex tx should be done before moderate to severe stage of dementia
  • maintain dental status and minimize deterioration in severe alzheimers
  • removable appliances may need to be excluded from tx plan of severe alzheimer’s patients due to risk of self injury
55
Q

according to the sparks study, ___ may be a risk factor for alzheimer’s disease

A

periodontitis

56
Q

the kamer study found an association between periodontal disease and an increased load of ___

A

beta amyloid plaques

57
Q

the kamer study hypothesized that periodontally produced ___ may travel into the brain through neural pathways that connect the oral cavity directly to the brain, and that some perio-related microorganisms can invade neural tissue

A

cytokines

58
Q

in relation to the kamer study, treponema species are closely related to t. pallidum (syphillus) which have been shown to enter the brain and induce what 3 things in patients with syphillus?

A
  • chronic inflammation
  • cortical atrophy
  • amyloid depositions

Geriatrics (4 decks)

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