L4 Dementia Flashcards
(86 cards)
1
Q
What brain changes with aging are considered normal?
A
It’s not a clear cut from alzhemiers vs healthy aging
consider both structural and functional changes (both happen with aging and disease)
cognitive reserve generally decreases with age AND disease
2
Q
Structural changes of brain
A
- decrease in overall weight, 5-10%
- neuronal number loss is minimal, but decrease in size
- decreaed dendritic density, shorter branches
3
Q
Functional changes of brain
A
All decreasing…
* cognitive planning
* personality
* social behavior
* decision making
* short term memory
4
Q
Other changes within the brain
A
- white matter changes
- neurofibrillary tangles
- senile plaques
- changes in NT function (specific ones decreases with age, not all)
- impacted hippocampus
- reduced glucose metabolism
- change in communication between neuronal cells
- activated state of glial cells
5
Q
Accumulation of genetic damage throughout life
A
- damaged nuclear and mitochondrial DNA
- decreased capacity for DNA repair during aging
- Decreased functioning of proteins due to damage
- mitochondrial impairment
6
Q
Reduced Glucose Metabolism
A
- found in many brain regions, lots in temporal/parietal/motor cortex
- brain insulin resistance accelerates with aging
- Maintaining brain insulin sensitivity delays aging
7
Q
Change in communication between neuronal cells
A
decreased synaptic connections, increased inflammation, degenerated neurovascular units
8
Q
Activated state of glial cells
A
causes long term and chronic inflammation, which leads to cognitive impairments
9
Q
Dopamine
A
decreased within frontal cortex, hippocampus, basal ganglia
impacts body movement, motivation, mood, and memory
10
Q
Serotonin
A
decreased in frontal cortex, basal ganglia
impacts mood/behavior, sleep, appetite, memory
11
Q
Glutamate
A
decreased in motor cortex and basal ganglia
impacts learning and memory
12
Q
Neuroprotection is achieved by
A
exercise
continued cognitive challenge
low alcohol intake
13
Q
Risk factors for decreased brain function in older age
A
diabetes/insulin resistance
high cholesterol
HTN
stress
head trauma
sedentary activity
14
Q
Mini Cog
A
Step 1 - Three word registration
Step 2 - Clock Drawing
Step 3 - Three word recall
15
Q
Scoring for Mini-cog
A
one point for each word that is recalled without cueing
0 or 2 points –must draw clock correctly and place hands correctly for 11:10
16
Q
Can the mini-cog be used a diagnosis?
A
No
used to refer patients
quick screening tool, designed for assessment in early stages of dementia
17
Q
A mini-cog less than 3/5
A
validated for dementia screening
18
Q
Mini-cog score of 4/5
A
recommended when greater sensitivity is desired, may indicate need for further eval of cognitive status
19
Q
Anything less than ____ on mini-cog should be referred on
A
5
20
Q
Dementia
A
a syndrome of global intellectual decline
21
Q
DSM-4 Dementia
A
development of memory impairment with at least one of the following cognitive impairments: aphasia, apraxia, agnosia, disturbance of executive function. Deficits are severe enough to result in limitations of occupational or social function and represent a decline from prior level
22
Q
DSM-5 Dementia
A
the presence of memory impairment is not required, as some diseases have initial symptoms in other domains
23
Q
Alzheimer’s Disease pathology
A
- Global atrophy
- Inflammatory response
- Neurofibrillary tangles
- Senile plaques
24
Q
Atrophy in AD
A
occurs in the cerebral cortex, amygdala, and hippocampus due to neuronal cell death
25
Inflammation in AD
becomes excessive
Microglia (immune cells) in the brain become overactive and overproduce substances that produce death
26
Neurofibrillary tangles in AD
occurs intracellular
* tau protein helps provide structure that is necessary for cell function
* tau protein in AD becomes altered, collapses, and forms tangles, which results in decreased cell function
* earliest signs of disturbed nerve cell function are seen in synapses
27
Functions of tau protein
nerve sprouting which helps with self-repair
maintaining nutrient transport system essential for the cell to work and survive
28
Senile plaques
Happens extracellular
* abnormal cluster of amyloid protein frgaments that build up between cells and forms plaques
* can impact cell to cell communication
* might trigger inflammatory response
29
Mild Cognitive impairment
* cognitive impairment not severe enough to meet criteria for demenita
* preserved ADLs
* minimal impairment to complex IADLs
* most common deficits are memory, language, executive function, visuospatial function
* 10-15% will progress to alzhemiers each year
30
Onset of AD
typically insidious
* becomes apparent to others after pt has experienced an episode of stress
* early s/s: difficulty with intellectual tasks, forgetfulness, untidiness, confusion, errors in judgement
* short term memory becomes impaired
31
progression of AD
1. Short Term memory loss
2. Cognitive abilities impaired
3. Inability to perform IADLs
4. Long term memory loss
5. Communication loss
6. Inability to perform all other ADLs
highly variable from patient to patient, just a general pattern
32
Characteristics of Dementia
1. impairment in abstract thinking
2. impairment in judgement
3. personality change
4. motor unrest
5. gait disturbance
6. motor planning
7. reflex/tone changes
33
Impairment in abstract thinking
difficulty in defining words
inability to find similarities/differences
34
Impairment in judgement
unable to make plans
35
Personality changes
exaggeration of regular personality
paranoia/depression/anxiety
perseveration and confabulation
36
Motor unrest
pacing
wandering
unable to sit
37
Gait disturbance
balance problems
shuffling
freezing
38
Motor planning changes
apraxia (poor motor motor initiation)
agnosia (object recognition)
ataxia (motor incorrodination)
39
Reflex and tone changes
primitive reflex
myoclonic jerks
40
Dementia end stage indicators
limited vocabulary (<6 words)
no affect
non-ambulatory
can't sit up
swallowing difficulty
weight loss
bowel/bladder incontinence
recurrent infections
pressure wound development
41
Behavioral changes in AD
* repeating a word, question, activity
* exhibiting aggressive behaviors verbally or physically
* thinking suspicious thoughts
* having anxious or agitated feelings
* refusing help
* difficulty recognizing familiar people, places, or things
* wanting to leave
42
Behavioral changes are often seen in response to
physical discomfort
over-stimulation
unfamiliar surroundings
attempting to perform complex tasks
frustrating interactions
42
Screening...
used to determine if further testing is needed for a diagnosis
43
Staging...
is determining the severity or progression in someone who already has a diagnosis
43
Screening exams for AD
* MMSE--mini mental status exam
* SLUMS -- saint louis university mental status
* MoCA -- montreal cognitive assessment
* Clocks test
44
Staging exams
* FAST
* MMSE
* MoCA
* Allen Cognitive LEvels
45
Cut off score for alzheimers for MOCA
<26
46
Tests on the MoCA
1. Visuospatial/executive
2. Naming
3. Memory
4. Attention
5. Language
6. Abstraction
7. Delayed Recall
8. Orientation
47
Mini Mental State Exam (MMSE)
* used as a screening tool to identify the presence of cognitive decline or to stage dementia severity in older adults
* max score = 30
* positive for screening <24
48
Norms for staging with MMSE
< 24 = mild dementia
20-23 = mild dementia
10-19 = moderate dementia
0-9 = severe dementia
49
SLUMS norms (with hs education)
27-30 = normal
21-26 = mild neurocognitive disorder
1-20 = dementia
50
SLUMS norms (w/out hs education)
25-30 = normal
20-24 mild neurocognitive disorder
1-19 = dementia
51
Allen Cognitive Levels
* 6 main cognitive levels based on remaining abilities
* assess cognition by observing function
* allows for id of highest cognitive abilities to determine appropriate intervention strategies
* multiple assessments, including leather lacing and placemat test
52
Allen Cognitive Levels Names
Level 1 = automatic actions
Level 2 = postural actions
Level 3 = Manual actions
Level 4 = goal directed actions
Level 5 = Exploratory actions
Level 6 = Planned Actions
53
treatment for AD
* no treatment slows or stops the disease
* medications can slow symptoms for 6-12 mo for about 50% of pts
* also good to manage other medical processes
54
Cholinesterase inhibtors
* aricept, exelon, reminyl
* these degus prevent cholinesterase from destroying the depleting levels of acetylcholine.
* allows sufficient levels of ach to be present in NT junction
55
Rivastigmine
been found to improve behavioral and psychiatric s/s of dementia
brand name in exelon
56
Memantine hydrochloride
* namenda is the brand name
* excessive amounts of glutamate leaks out in the extracellular spaces, so glutamate tries to reuptake it. This becomes TOXIC
* blocks glutamate receptors and prevents re-uptake of excessive glutamate
57
Delirium
* clinical syndrome of confusion that may appear with structural changes in imaging
* has an abrupt onset but considered a temporary condition
* often occurs during hospital or ICU stays, and a good portion are preventable (30-40%)
58
Structural changes present with delirium
cortical atrophy
ventricular dilation
white matter lesions
s/s thought to be due to NT disturbances brought about elevated cortisol occurring with acute stress
59
S/S of delirium
disturbance in consciousness
hallucinations
cognitive impairment
inattention
drowsiness
inability to sleep
60
Criteria for delirium
1. Attention disturbance
2. Duration
3. Change in an additional cognitive domain not caused by NCD
4. Disturbances in 1/3 must not occur in context of a severely reduced level of arousal, like coma
61
Attention disturbance
reduced ability to direct, focus, sustain, and shift attention and orientation to the environment
62
Duration of delirium
hours to a few days
fluctuate in severity during course of a day, worse in evenings
63
Change in cognitive domain
memory deficit
language disturbance
perceptual disturbance
64
Delirium Causes
1. Medication
2. Surgery
3. Infections
4. Cardiac Illnesses
5. Metabolic disturbances
6. Neoplasms
7. Trauma
8. Substance abuse/withdrawal
9. Location change
65
Medication (causes of delirium)
alcohol
sedatives
anticonvulsants
antidepressants
antihypertensives
antiparkinsonism
corticosteroids
digitalis
66
Infections (causes of delirium)
upper respiratory infections
pneumonia
UTI
sepsis
67
Cardiac Illnesses ((causes of delirium)
atherosclerosis in neck and brain
CHF, MI, arrhythmias
68
Metabolic disturbances (causes of delirium)
liver/renal failure
fluid/electrolyte disturbances
hypoxia
69
Neoplasms (causes of delirium)
primary brain tumors
brain metastases
70
Trauma (causes of delirium)
post-operative delirium
burns
fractures
71
Predisposing factors for Delirium
* vision impairment without glasses available
* hearing impairment without hearing aids available
* functional mobility impairment
* cognitive impairment
* history of delirium
* multiple comorbid conditions
* physical restraint use
72
Prevention in hospital for delirium
* early mobility
* use of exercise
* proper hydration
* appropriate sensory stimulation (glasses, hearing aids)
* dentures
* sleep/wale cycle preservation
* provide cognitive orientation (family, objects, etc)
* hospital elder life program (prevention program)
73
Three versions of clinical presentation of delirium
Hyperactive (20%)
Hypoactive (20%)
Mixed (60%)
74
Hyperactive delirium
increased psychomotor activity, restlessness, rapid speech
75
Hypoactive Delirium
lethargy, slowed speech, apathy, decreased alertness
76
Mixed Delirium
shifts between hyperactive and hypoactive
77
Clinical Complications of delirium
* longer length of stay with worse physical and cognitive recovery
* continued dehydration/malnutrition
* falls
* aspiration pneumonia
* pressure ulcers
* joint cantractures
* deconditioning
* isolation
* increased 1 year mortality rate
* increased hospital readmission
* accelerated cognitive decline
78
Delirium vs dementia vs depression
Closely related
acute behavioral or mood change is suggestive of delirium
once medical contributors have been ruled out, depression can be ruled in if it is a more chronic low mood state. patients are less likely to self-report their cognitive problems
79
Onset (Delirium vs dementia vs depression)
Delirium: hours to days
Dementia: months to years
Depression: weeks to months
80
Mood Delirium vs dementia vs depression
Depression: low/apathetic
Delirium: fluctuates
Dementia: fluctuates
81
Course Delirium vs dementia vs depression
Depression: chronic
Delirium: acute
Dementia: chronic with deterioration over time
82
Self-awareness Delirium vs dementia vs depression
Depression: likely to be concerned about memory impairment
Delirium: may be aware of changes in cognition, fluctuates
Dementia: likely to hide or be unaware of cognitive deficits
83
ADLs and Delirium vs dementia vs depression
Dep: may neglect basic self care
Del: May be intact or impaired
Dem: may be intact early, impaired as disease progresses
84
IADLs Delirium vs dementia vs depression
Dep: may be intact or impaired
Del: may be intact or impaired
Dem: may be intact early, impaired before ADLs as disease progresses
