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Flashcards in Dementia Deck (45)
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1
Q
Delirium
A
1. A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment).

2. The disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day.

3. Theres a disturbance in cognition (e.g., memory deficit, disorientation, language, visuospatial ability, or perception).
2
Q
Types of dementia
A
-Alzheimer’s
-Frontotemporal
-Lewy Body
-Parkinson’s Vascular
-Huntington’s
-HIV
-Traumatic Brain Injury
-Prion Disease
3
Q
Dementia causes a progressive decline in intellectual functioning severe enough to _______
A
interfere with person’s normal daily activities and social relationships
4
Q
Dementia causes progressive declines in
A
-memory
-visual-spatial relationships
-performance of routine tasks
-language and communication skills
-abstract thinking
-ability to learn and carry out mathematical calculations
5
Q
2 categories of dementia
A
Reversible and Irreversible

*Individuals must have intensive medical physical to rule out reversible types of dementia
6
Q
Reversible causes of dementia
A
"DEMENTIA"
D-drugs, delirium
E-emotions (depression) & endocrine disorders
M-metabolic problems
E-eye & ear problems
N-nutritional disorders
T-tumors, toxicity, trauma to head
I-infections
A-alcohol, arteriosclerosis
7
Q
Irreversible causes of dementia
A
-Alzheimer’s
-Lewy Body Dementia
-Pick’s Disease (Frontotemperal Dementia)
-Parkinson’s
-Heady Injury
-Huntington’s Disease
-Jacob-Cruzefeldt Disease
8
Q
Alzheimer’s Dementia
A
-Insidious onset/gradual progression
-Memory & learning impairment, sometimes executive impairment
-Then perceptual-motor & language impairment
-Social cognition affected late in disease
-Gait disturbance, dysphagia, incontinence, myoclonus, seizures
-5% Diagnosed between around age 65, prevalence increases steeply, esp in 80s
-Mean survival 10yrs after diagnosis
9
Q
Alzheimer's dementia- About 0.1 % autosomal dominant inheritance, which have an onset before age
A
65
-This form of the disease is known as early onset familial Alzheimer's disease
10
Q
Alzheimer's dementia-
Most of autosomal dominant familial AD can be attributed to mutations in one of three genes:
A
-those encoding amyloid precursor protein (APP)
-those encoding presenilins 1 and 2

*Most mutations in the APP and presenilin genes increase the production of a small protein called Aβ42, which is the main component of senile plaques.
11
Q
Most cases of Alzheimer's disease do not exhibit
A
autosomal-dominant inheritance
12
Q
Alzheimer's dementia- environmental and genetic differences may act as risk factors. The best known genetic risk factor is the
A
inheritance of the ε4 allele of the apolipoprotein E
13
Q
know mini mental status exam
A
in other deck too
14
Q
Frontotemporal Dementia
A
-Encompasses Pick’s disease and several related illnesses.

-Insidious onset/gradual progression

-Reflect loss of frontal and temporal lobe function

-FT dementia accounts for 15% cases of dementia

-Higher proportion in individuals younger than 65

*Tau inclusions, pick bodies
15
Q
Symptoms of Frontotemporal Dementia
A
-Broad decline in insight
-Social skills, interpersonal conduct
-And executive functioning
-Mental rigidity
-Easily distractibility, labile affect and speech and language impairments
(echolalia and perseveration)
-Disinhibition
-Apathy
-Loss of sympathy/empathy
-Perseverative or compulsive behavior
-Hyperorality and diet changes
16
Q
Frontotemporal Dementia shows a prominent decline in ______, but a relative sparing of _________
A
-prominent decline in social cognition or executive abilities
-also decline in language ability, object naming, grammar
-Relative sparing of learning, memory, and perceptual-motor function
17
Q
Frontotemporal Dementia average age of onset is
A
53 years followed by fatal progression lasting less than 4 years
18
Q
Compared to Alzheimer’s disease, FT Dementia does not have impairments in
A
visual-spatial abilities – a function governed largely by the parietal lobes

-maintain their ability to copy a picture but not to draw one from their memory.
-do not lose their sense of direction, even in new surrounding
-do not manifest constructional apraxia
19
Q
FT shows prominent personality and behavioral disturbances accompanied by only relatively mild ________
A
memory impairment
20
Q
On CT/MRI, FT shows
A
-Frontal and anterior temporal lobes are atrophic. -Plaques and tangles are uncommon or absent

*Pick’s disease – neurons containing argentophilic (silver staining) inclusions (Pick bodies)
21
Q
FT has some gene mutations, 10% linked to mutant gene on _______
A
chromosome 17, which codes for tau (MAPT)
22
Q
Dementia with Lewy Bodies
A
-Cognitive decline, ≥1 yr prior to onset of parkinsonism features
-Fluctuating cognition w/ variations in attention/alertness (looks like delirium)
-Recurrent VH
-REM sleep behavior disorder
-Severe neuroleptic sensitivity (50%)
-Lewy bodies have greater distribution than in Parkinson’s
23
Q
Dementia with Lewy Bodies age
A
Older than 65

-sometimes initially diagnosed as alzheimer's
24
Q
Pathology of Dementia with Lewy Bodies age
A
-abundance of intracytoplasmic inclusions (lewy bodies) in cerebral cortex neurons that stain with alpha- synuclein antibodies
-Concentration of lewy bodies correlates with dementia
-Similar to Alzheimer’s disease, but older individuals with nonspecific cognitive deficits.
25
Q
Non-cognitive features of Dementia with Lewy Bodies (aka-S/S)
A
-characterized by mild extrapyramidal features, masked face, bradykinesia, and gait impairment.
-sudden unexpected changes in cognition, attentiveness and alertness; mimics episodes of delirium or toxic-metabolic encephalopathy
-Visual Hallucinations: detailed visions of people and animals, associated with lewy bodies in the temporal lobes
-Visual hallucinations also frequently develop in pts with advanced Alzheimer’s and Parkinson’s disease – but not at the onset of these illnesses
26
Q
About 50% of patients with Dementia with Lewy Bodies have REM sleep behavior disorder, which consists of
A
running, punching, and similar motions while asleep
27
Q
DLB is similar to extrapyramidal symptoms you see in Parkinson’s however DLB does not __________
A
repond to Parkinson’s treatment with L-dopa

-also pt will have visual hallucinations
28
Q
DLB pt with visual hallucination can be treated with
A
-antipsychotic agents
-dopamine blockers, readily produce pronounced extrapyramidal signs
-small amounts of antipsychotic agents can cause EPS (extrapyramidal symptoms)
29
Q
DLB treatment- what to give for cognitive function and visual hallucinations
A
Cholinesterase inhibitors stabilize or improve cognitive function and reduce visual hallucinations for several months
30
Q
DLB treatment- what will help REM sleep behavior disturbance
A
Long acting benzodiazepines, such as clonazepam, suppresses the REM sleep behavior disturbance
31
Q
Neurocognitive disorder due to Parkinson’s
A
-Established Parkinson’s Disease prior to cognitive decline
-Many diagnosed in their 60s, mild neurocognitive disorder occurs early but does not progress to major neurocognitive d/o until late
*Apathy, depressed/anxious mood, hallucinations/delusions, change of personality
*Lewy bodies present
32
Q
Vascular Dementia
A
-Clinically consistent with vascular etiology:
1. Onset of cognitive deficits is temporally related to cerebrovascular event
2. Evidence for decline is prominent in complex attention and frontal-executive tasks
3. Evidence of the presence of cerebrovascular disease
4. History, physical exam, and/or neuroimaging
5. Classically is acute stepwise decline in cognition
33
Q
Vascular Dementia risk factors
A
-HTN, DM, obesity, smoking, high cholesterol, high homocysteine levels
-Diagnosis: MRI/CT
34
Q
Med to give for Vascular Dementia
A
Because of frequent comorbidity of Alzheimer’s Disease, cholinesterase inhibitors provide symptomatic benefit in vascular dementia
35
Q
see comparative chart
A
slide 30, screen shot in folder
36
Q
Traumatic Brain Injury
A
-LOC, post-traumatic amnesia, disorientation, neurological signs

-Emotional and personality changes, physical sx (tinnitus, dizziness, fatigue)

-CT/MRI– not always, but may reveal petechial hemorrhages or evidence of contusion
37
Q
HIV
A
-Need documented infection with HIV

-25% of pts with HIV have mild neurocognitive D/O

-Risk: poor control of HIV

-CSF – high viral load; MRI- cortical thinning, ↓ brain volume, ↓ white matter
38
Q
Prion Disease
A
-Rapid progression; most common is Creutzfeldt-Jakob

-triad of dementia, myoclonus, and distinctive EEG patterns

-CSF: 14-3-3 protein and tau protein
-MRI: multifocal gray matter hyperintensities
39
Q
Huntington's
A
-CAG repeats on chromosome 4
-50% will develop dementia
-MRI- volume loss in basal ganglia
40
Q
Treatment for vascular dementia

KNOW!
A
-preventative measures: diet and exercise, control of HTN/DM, statins may slow progression

*Cholinesterase inhibitors (donepezil, rivastigmine, galantamine, tacrine); Increase Ach, modest improvement in memory and goal-directed thought

*NMDA antagonist - (Memantine); Protects neurons from excessive glutamate activity, which may be neurotoxic
41
Q
Psychosocial intervention:
A
Reduce stressors, education of caregivers, safety (assess driving, prevent wandering, reduce risk of falls)
42
Q
How to manage agitation
A
*All antipsychotics have a black box warning: Risk of increased mortality when used for dementia- related psychosis – deaths due to cardiac or infectious events*

-Antidepressants, cholinesterase inhibitors, non-pharmacologic (redirection, recreational therapy) antipsychotics, mood stabilizers, benzodiazepines
43
Q
Treatment for Lewy body dementia
A
use quetiapine or clozaril if need to use an antipsychotic
44
Q
Pseudodementia
A
-"Depression in old age”

-Depression occurs first, then neurocognitive deficits
Relatively abrupt onset

-Evaluation : MSE, neuropsychological testing - Lack of effort on part of the patient – “I don’t know”
45
Q
Treatment for psuedodementia
A
Improvement with antidepressant treatment