RS 14 95 de Me NT Ia

)
K
O
, O
M B
5
U T
I X
R E
I T
9
L
E E
D H
: T
4
T N
N I
E ”
A
M ,
1
E S
I
G A
A TI
S
N
T
A EN
M M
E
R
G
N
N D
I R
S E
R
U E
U TH
N O
“
, D
N EM
2
6 AN
R ,
E E
T S
P A
A E
H S
I
D
C
D
O S
T ’
S R
E E
T M
A I
L E
E H
R Z
( L
A
COGNITIVE PROBLEMS
Three most common in adults
Delirium—acute confusion
Dementia
Depression
Often associated with dementia and
delirium
2
DEMENTIA
Syndrome
Characterized by dysfunction or loss of:
Memory
Orientation
Attention
Language
Judgement
Reasoning
3
DEMENTIA
Other characteristics that can manifest
Personality changes
Behavioural problems such as:
Agitation
Delusions
Hallucinations
4
DEMENTIA
Problems disrupt individual’s
Work
Social responsibilities
Family responsibilities
Physicians usually diagnose when two
or more brain functions are significantly
impaired.
5
DEMENTIA
• Not a normal part of aging
• Affects about 500,000 Canadians
• ~100 causes of dementia
• Many patients with dementia have
Alzheimer’s disease (AD).
• Half of the patients in most long-term
care facilities have dementia.
6
ETIOLOGY AND PATHOPHYSIOLOGY
Due to treatable and nontreatable conditions
 The treatable conditions are potentially reversible
 Initially these conditions may be reversible.
 However, with prolonged exposure or disease,
irreversible changes may occur.
Two most common causes
 Neurodegenerative conditions - 60% to 80% of cases
 Vascular disorders
7
DEMENTIA
Vascular dementia
 Loss of cognitive function due to brain lesions
caused by cardiovascular disease
Ischemic lesions
Ischemic-hypoxic lesions
Hemorrhagic brain lesions
8
DEMENTIA
Vascular dementia (Cont.)
 Result of decreased blood supply from narrowing
and blocking of arteries that supply brain
 Can be caused by a single stroke or by multiple
strokes
9
DEMENTIA
Predisposed risks of dementia
 Smoking
 Cardiac dysrhythmias
 Hypertension
 Hypercholesterolemia
 Diabetes mellitus
 Coronary artery disease
 Metabolic syndrome
10
DEMENTIA
CLINICAL MANIFESTATIONS
Onset of dementia depends on cause.
Insidious and gradual
Abrupt
Vascular dementia tends to be abrupt or
progress in a stepwise pattern.
11
DEMENTIA
Cause of dementia difficult to

distinguish on the basis of
symptoms alone.
12
DEMENTIA
Acute or subacute pattern of change may be more
indicative of an infectious or metabolic change.
Metabolic changes include:
• encephalitis
• meningitis
• hypothyroidism
• and drug-related dementia.
13
DEMENTIA
Initial symptoms are related to changes in cognitive
function.
Family members often report to doctor
 Memory loss
 Mild disorientation
 Trouble with words and/or numbers
 Often it is a family member, in particular the spouse, who
reports the patient’s declining memory to the health care
provider.
A story about my Dad…
14
DEMENTIA
DIAGNOSTIC STUDIES
Focused on cause
 Reversible or nonreversible
Thoroughly evaluate patient history

 Medical
 Neurological
 Psychological
15
DEMENTIA
DIAGNOSTIC STUDIES
Physical examination to rule out
other medical conditions.
Screen for
Cobalamin (vitamin B12) deficiencies
Hypothyroidism
Possibly neurosyphilis
16
DEMENTIA
DIAGNOSTIC STUDIES
Mild cognitive impairment (MCI)
May be able to compensate, making
diagnoses difficult
About half of patients with MCI develop
dementia within 5 years
17
DEMENTIA
DIAGNOSTIC STUDIES
Mental status testing
Mini-Mental State Examination

 Commonly used tool
 Assesses cognitive functioning but does not
diagnose dementia
MOCA (Montreal Cognitive Assessment)
 Good sensitivity for diagnosing dementia
18
DEMENTIA
DIAGNOSTIC STUDIES
Depression often mistaken for
dementia and vice versa
Manifestations of depression, especially
in older adults
Sadness
Difficulty thinking and concentrating
19
DEMENTIA
DIAGNOSTIC STUDIES When dementia
Manifestations of depression and depression
occur together
 Fatigue (may occur in
 Apathy up to 40% of
 Feelings of despair patients with
dementia), the
 Inactivity intellectual
When the depression is severe, poor deterioration
can be extreme.
concentration and attention may result,
causing memory and functional impairment.
20
DEMENTIA
DIAGNOSTIC STUDIES
Computed tomography (CT)
Magnetic resonance imaging (MRI)
To characterize central nervous system
(CNS) changes:
 Single-photon emission computed tomography
(SPECT)
 Positron emission tomography (PET)
21
MILD COGNITIVE IMPAIRMENT
State of cognitive and functional ability below defined norms
that does not meet criteria for dementia.
Memory impaired but functions normally
• Symptoms are not severe enough to interfere with activities
of daily living.
• To the casual observer, an individual with MCI may seem
fairly normal. However, the person with MCI is often aware
of a significant change in memory, and family members
may observe changes in the individual’s abilities.
22
Characteristics
Memory complaint
Abnormal memory for age
Intact activities of daily living
Normal general cognitive functioning
23
10% to 20% of individuals >65
years old have MCI.
15% of those with MCI will

develop dementia.
24
Presently no widely accepted guidelines for treatment
 Insufficient evidence
 Research is being conducted.
Primary treatment consists of ongoing monitoring.
Research is being conducted to determine whether

patients would benefit from the medications used in
Alzheimer's Disease (acetylcholinesterase inhibitors).
25
ALZHEIMER’S DISEASE
• Chronic, progressive, degenerative disease of the brain.
• Most common form of dementia (about 63% of cases)
• It is estimated that 2.4% of people ages 65 to 74, and
nearly 34.5% of those over age 85, have AD.
• Ultimately, the disease is fatal, with death typically
occurring 4 to 6 years after diagnosis, although some
patients live for 20 years.
26
• Economic cost of care is high.
• Burden on patient, family, caregivers, and society as a
whole
• AD has been associated with lower socioeconomic status
and educational level and poor access to health care.
• Women are more likely than men to develop AD,
primarily because they live longer
27
• Exact cause is unknown.
• Age is most important risk factor.
• Familial Alzheimer’s disease
• Persons in whom a clear pattern of inheritance within
a family is established have familial Alzheimer’s
disease (FAD).
• FAD is associated with earlier onset (before 60 years
of age) and a more rapid disease course.
28
Changes in brain structure and function
Amyloid plaques
Neurofibrillary tangles
Loss of connections between cells and cell death
29
Fig. 62-1. Pathological changes in Alzheimer’s disease. A, Plaque with central amyloid core (white arrow) next to
a neurofibrillary tangle (black arrow) on the histological specimen from a brain autopsy. B, Schematic
representation of amyloid plaque and neurofibrillary tangle.
30
People develop some plaques in their brain
tissue.
In AD plaque is greater in certain parts.
 Clusters of insoluble plaque
β-Amyloid, other proteins, remnants of neurons,
non-nerve cells, and other cells
31
In AD, plaques in abnormal quantities
develop first in the parts of the brain used for
Memory
Cognitive function
Hippocampus (short term memory)
Eventually develops in the cerebral cortex
(language and reasoning)
32
Gradual loss of connections between
neurons
 Leads to damage and then death of neurons
 Affected parts of brain shrink.
Brain atrophy
Significant in final state of AD
33
Fig. 62-3. Effects of
Alzheimer’s disease
on the brain, shown
by positron emission
tomography (PET).
In PET, radioactive
fluorine is applied to
glucose
(fluorodeoxyglucose)a
nd the yellow areas
indicate
metabolically active
cells.
A, Normal brain.
B, Advanced AD,
recognized by
hypometabolism that
Indicates cell death in
many areas of the
brain.
EFFECT OF
ON THE BRAIN 34
GENETIC FACTORS
May play significant role in how the brain processes β
amyloid protein
 ↑ β-Amyloid protein  ↑ risk
First gene associated with AD

 Epsilon (E)-4 allele of apolipoprotein E (ApoE) gene on
chromosome 19
35
Researchers interested in link between
inflammation and AD
Theory suggests that formation of free radicals

damages neurons  loss of function
Oxidative damage leads to inflammation.
36
 Another area is focusing The management of
on the link between cardiovascular risk
cardiovascular disease and factors, such as high
cholesterol, diabetes
AD.
mellitus, high blood
 Common risk factors for pressure, and obesity,
heart disease are may help to avoid or
associated with increased delay cognitive decline
risk of AD.
37
• Pathological changes precede clinical
manifestations by 5 to 20 years.
• The Alzheimer’s Society has developed a list
of 10 warning signs.
• http://
www.alz.org/alzheimers_disease_10_signs_o
f_alzheimers.asp
38
Early Signs Early Signs
 Memory loss that affects job skills  Misplacing things
 Difficulty performing familiar tasks  Changes in mood or
 Problems with language behaviour
 Disorientation to time and place  Changes in
 Poor or ↓ judgement personality
 Problems with abstract thinking  Loss of initiative
39
Initial sign is subtle deterioration in memory.
Inevitably progresses to more profound

memory loss.
Manifestations easier to recognize when

family member or patient seeks medical help.
40
• Recent events and new
information cannot be
recalled. Behavioural manifestations of
AD (e.g., agitation,
• Behavioural manifestations aggression) result from
changes that take place within
are not intentional or the brain. They are neither
controllable because of intentional nor controllable by
the individual with the disease.
ongoing loss of neurons.
• Some develop psychotic
manifestations.
41
In AD that has progressed,
 Dysphasia (difficultly with language)
 Apraxia (difficulty with motor planning)
 Visual agnosia (difficulty recognizing objects)
 Dysgraphia (difficulty writing)
 Some long-term memory loss
 Wandering
42
Late stages
 Long-term memory loss
 Unable to communicate
 Cannot perform activities of daily living (ADLs)
 Patient may be unresponsive and incontinent,
requiring total care.
43
DIAGNOSTIC STUDIES
Diagnosis of exclusion
No single clinical test
Made once all other possible conditions
causing cognitive impairment have been
ruled out
44
DIAGNOSTIC STUDIES
Comprehensive patient evaluation
Complete health history
Physical examination
Neurological assessment
Mental status assessment
Laboratory tests
45
DIAGNOSTIC STUDIES
Brain imaging tests
CT MRI SPECT PET
Allow monitoring in early stages and treatment
response.
A CT or an MRI scan may show brain atrophy and enlarged
ventricles in the later stages of the disease, although this
finding occurs in other diseases and can also be seen in
persons without cognitive impairment.
46
DIAGNOSTIC STUDIES
PET
DIAGNOSTIC STUDIES
Neuropsychological testing can help document
degree of cognitive impairment.
 Mini-Mental State Examination (MMSE) is commonly
used, but does not diagnose dementia
 http://gem.rgp.toronto.on.ca/files/MMSE_Test%20(4).pdf
 MOCA (Montreal Cognitive Assessment) has better
sensitivity for detecting early dementia
 http://www.mocatest.org/paper-tests/moca-test-basic/
48
COLLABORATIVE CARE
No cure
Collaborative management aimed at:
 Improving or controlling decline in cognition
 Controlling undesirable behavioural manifestations
 Providing care for the caregiver
49
DRUG THERAPY
Cholinesterase inhibitors – donepezil
(Aricept), rivastigmine (Exelon), and
galantamine (Reminyl).
 Block cholinesterase, enzyme responsible for
breaking down acetylcholine
 Improve or stabilize cognitive decline but do not
cure or reverse
50
DRUG THERAPY
Cholinesterase inhibitors are recommended
for treatment of mild, moderate, and severe
dementia
 Improve or stabilize cognitive decline in some people
with AD
 Can enhance the patient’s functional abilities
DRUG THERAPY
Depression often treated with selective
serotonin reuptake inhibitors
May help with sleep problems
Antiseizure drugs
Manage behavioural problems
Stabilize mood
52
NURSING ASSESSMENT
Subjective data
 Past health history
 Medications
 Health perception
 Nutritional state
 Eliminating properly—incontinence
53
NURSING ASSESSMENT
Subjective data
 Activity-exercise habits and state
 Sleep-rest pattern
 Cognitive-perceptual state
54
NURSING ASSESSMENT
Objective data
 Dishevelled appearance
 Neurological
Early, middle, late
 Useful questions for the patient and informant are,
“When did you first notice the memory loss?” and
“How has the memory loss progressed since then?”
55
NURSING DIAGNOSES
• Impaired memory
• Self-care deficit
• Risk for injury
• Grief
• Wandering
56
PLANNING
Overall goals for patient
 Maintain functional ability as long as possible
 Maintain safe environment
 Personal care needs met
 Dignity maintained
57
PLANNING
Overall goals for caregiver of a patient
 Reduce caregiver stress
 Maintain personal, emotional, and physical health
 Cope with long-term effects associated with
caregiving
58
NURSING IMPLEMENTATION
• No known method to reduce risk of AD
• Antioxidants may be of benefit.
• Promote safety-physical activities, driving.
• Recognize and treat depression.
• Genetic testing - not performed on a regular basis.
• Early recognition and treatment important.
• Nurse should inform patients and family regarding early
warning signs.
59
ACUTE INTERVENTION
Diagnosis traumatic for patient and family
In the early stages of AD, patients are often aware that
their memory is faulty and do things to cover up or mask
the problem.
Patient often responds with
 Depression
 Denial
 Anxiety and fear
 Isolation
60
ACUTE INTERVENTION
Assess for depression and suicidal ideation.
Counselling and antidepressants may be

indicated.
Family members may be in denial, delaying

critical early care.
61
ACUTE INTERVENTION
Nurse should also assess family members and their
ability to cope and accept diagnosis.
Ongoing monitoring important
 Work in collaboration with patient’s caregiver.
 Teach caregiver how to manage care.
 **An important nursing responsibility is to work

collaboratively with the patient’s caregiver to manage clinical
manifestations effectively as they change over time.
62
ACUTE INTERVENTION
• AD patients subject to other
Patients with AD
health care problems. hospitalized in the acute
• Inability to communicate care setting will need to
be observed more
symptoms places responsibility on closely
caregivers and health care because of concerns for
professionals. safety, frequently
oriented to place and
• Hospitalization can precipitate a time, and given
worsening of disease or delirium. reassurance.
Another story…
63
AMBULATORY AND HOME CARE
Family members and friends care for most
AD patients in their homes.
Various facilities should be evaluated.

 Consider stage of AD patient when choosing.
 Nursing care intensifies over time.
64
BEHAVIOURAL PROBLEMS
Occur In 90% of AD Patients
These Problems Include:
 Repetitiveness  Agitation
 Delusions  Aggression
 Illusions  Altered sleep patterns
 Hallucinations  Wandering
 Resisting care
65
Behaviour is unpredictable.
Can be challenging for caregiver.
Behaviours are not intentional and are
difficult to control.
Often lead to placement in institutional
Settings.
66
Are a patient’s way of responding to
precipitating factors:
Pain
Frustration
Temperature extremes
Anxiety
67
Assess patient’s
 Physical status
 Environment
Reassure patient about his or her safety.
68
Nursing strategies to address difficult behaviours
 Redirection
 Distraction
 Reassurance
Do not threaten or restrain patient if frustrated.
Use of repetitive activities, songs, poems, music,
massage, aromas, or a favourite object can be
soothing to patients.
In the news….
http://www.cbc.ca/news/health/memory-care-centre-1.3265504
69
GROUP THINK
In Groups of 6
Discuss the video clip:
1. Do you agree or disagree with the techniques
illustrated?
2. How would you handle an encounter with a resistive
patient who believes they must exit the building?
3. Debrief….
AD patients can experience sundowning.
 Specific type of agitation
 Patient becomes more confused and agitated in late
afternoon or evening.
 Cause is unclear.
 Remain calm and avoid confrontation.
71
Nursing interventions: sundowning
 Create a quiet, calm environment.
 Maximize exposure to daylight.
 Evaluate medications.
 Limit naps and caffeine.
 Consult health care provider on drug therapy.
72
SAFETY
Risks
 Injury from falls
 Ingesting dangerous substances
 Wandering
 Injury to others and self
 Fire or burns
 Inability to respond to crisis
73
PAIN MANAGEMENT
Pain should be recognized and treated promptly.
Because of difficulties with oral and written language
associated with AD, patients may have difficulty
expressing physical complaints, including pain.
 Monitor patient’s response.

 Patients can have difficulty communicating complaints.
 May exhibit changes in behavior.
74
EATING/SWALLOWING DIFFICULTIES
Undernutrition problem in middle and late
stages
 Loss of interest in food
 Decreased ability to self-feed
Concern with this???
 Co-morbid conditions
75
INFECTION PREVENTION
Common
 Urinary tract infection
 Pneumonia
Ultimate cause of death in many AD patients
Manifestations need prompt evaluation and

treatment.
76
CAREGIVER SUPPORT
AD disrupts all aspects of personal and
family life.
Very stressful
Caregivers also exhibit adverse
consequences.
77
CAREGIVER SUPPORT
Work with caregiver to
 Assess stressors
 Identify coping strategies
 Find a support group
Local Alzheimer Society chapter
78
EVALUATION
Patient goals
 Functions at highest level of cognitive ability
 Performs self-care, bathing, dressing, and toileting
with assistance as needed
 Experiences no injury
 Uses assistive devices appropriately for ambulation
support
79
EVALUATION
Patient goals (Cont.)
 Uses effective coping strategies to manage grief
related to diagnosis of AD
 Verbalizes reality of health situation
 Remains in restricted area during ambulation and
activity
80

RS 14 95 de Me NT Ia

Caricato da

Informazioni sul documento

Titolo originale

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

RS 14 95 de Me NT Ia

Caricato da

Copyright:

Formati disponibili

)

Cause of dementia difficult to

A story about my Dad…

Thoroughly evaluate patient history

Mini-Mental State Examination

15% of those with MCI will

Research is being conducted to determine whether

First gene associated with AD

Theory suggests that formation of free radicals

Inevitably progresses to more profound

Manifestations easier to recognize when

Counselling and antidepressants may be

Family members may be in denial, delaying

 **An important nursing responsibility is to work

Various facilities should be evaluated.

Reassure patient about his or her safety.

 Monitor patient’s response.

Manifestations need prompt evaluation and

Potrebbero piacerti anche