Alzheimer’s disease

Introduction:
Approximately 10% of all persons over the age of 70 years have significant memory loss, and in more than half, the
cause is Alzheimer’s disease (AD) s. AD can manifest as young as the third decade, but it is the most common cause
of dementia in the elderly. Patients most often present with an insidious loss of episodic memory followed by a slowly
progressive dementia that evolves over years. In typical amnestic AD, brain imaging reveals atrophy that begins in the
medial temporal lobes before spreading to lateral and medial parietal and temporal lobes and lateral frontal cortex.
Microscopically, there are neuritic plaques containing amyloid beta (Aβ), neurofibrillary tangles (NFTs) composed of
hyperphosphorylated tau filaments, and Aβ accumulation of in blood vessel walls in cortex and leptomeninges. The
identification of causative mutations and susceptibility genes for AD has provided a foundation for rapid progress in
understanding the biological basis of the disorder. The major genetic risk for AD is apolipoprotein ε4 (Apo ε4).
Carrying one Ε4 allele increases the risk for AD by 2- to 3-fold, whereas two alleles increase the risk 16-fold.

History:
 In November 1906, at a German psychiatrists meeting, Alois Alzheimer presented the pathological
findings on a brain of a 56 y.o. woman who died after a progressive dementia
 The Case Auguste Deter , This 51 y.o. woman was admitted to Frankfort hospital in 1901 for progressive
dementia.
 She was under the care of Dr. Alzheimer until her death in 1906. He did an autopsy, examined her brain
& described the typical abnormalities of what would be called later Alzheimer’s disease.
 This case did not prompt any reaction until Kraepelin, in 1910, referred to it as “Alzheimer’s Disease”
(presenile dementia) in the 8th edition of his psychiatry book
 1962: Corselis: presenile & senile dementias have the same pathological abnormalities 1983:Coyle et al:
Acetylcholine deficit in the cortex
 1995: The first gene abnormalities in familial Alzheimer disease are identified (Presenilin 1 & 2)

Definition:
Alzheimer’s disease, or senile dementia of the Alzheimer’s type, is a chronic, progressive, and degenerative
brain disorder that is accompanied by profound effects on memory, cognition, and ability for self-care.

Alzheimer’s disease is one of the most feared disorders of modern times because of its catastrophic
consequences for the patient, family, and caregivers, who are faced with many crucial end-of-life decisions.

AD is a complex brain disorder caused by a combination of various factors that may include genetics,
neurotransmitter changes, vascular abnormalities, stress hormones, circadian changes, head trauma, and the
presence of seizure disorders.

Research article:
In India, more than 4 million people have some form of dementia. Worldwide, at least 44 million people are
living with dementia, making the disease a global health crisis that must be addressed.

Incidence of Alzheimer’s disease in India: A 10 years follow-up study

Objective

To determine overall and age -specific incidence rates of Alzheimer’s disease (AD) in a southern Indian
province, Kerala
A 10-year (2001–2011) prospective epidemiologic study of community residing subjects aged ≥55 years at
enrollment. The catchment area included four urban and semi-urban regions of Trivandrum city in Kerala,
India, was selected to provide a range of demographic and socioeconomic representation. Cognitive and
functional ability screening were done at baseline and 24-month follow-up assessments. Consensus
diagnostic procedures were done using the Diagnostic and Statistical Manual of Mental Disorders, 4th
edition (DSM-IV), and the National Institute of Neurological and Communicative Disorders and Stroke–
Alzheimer’s Disease and Related Disorders Association (NINDS-ADRDA) criteria for the diagnosis of
dementia and AD.

The incidence of AD in southern India is not as low as that found in northern India. Nevertheless, it is still
lower than that of the average incidence rates of AD reported in Europe and North America. This could
possibly suggest the presence of underlying protective factors, or the absence of certain risk factors. The
frequency of the APOE4 allele, a well recognized risk factor for AD is reported to be low in the Indian
population in general, with regional differences. The frequency of the APOE4 allele is lower in the north
and central Indian populations compared with the US population.

Risk Factors
With the exception of cases of Alzheimer’s caused by genetic abnormalities, experts believe that Alzheimer’s, like
other common chronic diseases, develops as a result of multiple factors rather than a single cause.

Age, Family History and the Apolipoprotein E (APOE)-e4 Gene The greatest risk factors for late-onset Alzheimer’s
are older age,29-30 having a family history of Alzheimer’s31-34 and carrying the APOE-e4 gene.

1. Age

Age is the greatest of these three risk factors, with the vast majority of people with Alzheimer’s dementia
being age 65 or older. The percentage of people with Alzheimer’s dementia increases dramatically with age:
3 percent of people age 65-74, 17 percent of people age 75-84 and 32 percent of people age 85 or older have
Alzheimer’s dementia.

2. Family History

A family history of Alzheimer’s is not necessary for an individual to develop the disease. However,
individuals who have a parent, brother or sister with Alzheimer’s are more likely to develop the disease than
those who do not have a first-degree relative with Alzheimer’s. Those who have more than one first-degree
relative with Alzheimer’s are at even higher risk.

3. APOE-e4 Gene

The APOE gene provides the blueprint for a protein that transports cholesterol in the bloodstream. Everyone
inherits one of three forms of the APOE gene — e2, e3 or e4 — from each parent. The e3 form is the most
common. The e4 form is the next most common, and the e2 form is the least common

Others risk factors:

1. Down syndrome
2. Head injury: Some studies have shown a link between Alzheimer's disease and a major head injury.
3. High cholesterol levels and high blood pressure may also raise the risk.
4. Depression
5. Alcohol
6. Diabetes mellitus type 2
7. Obesity and lack of physical activity
Types:
AD can be classified into two types:

1. Familial or early onset AD

Familial AD is rare, accounting for less than 10% of all cases, and is frequently associated with genetic
mutations. It occurs in middle- aged adults. If family members have at least one other relative with AD, then
there is a familial component, which nonspecifically includes both environmental triggers and genetic
determinants.

2. Sporadic or late-onset AD:

Majority of Alzheimer's cases are late-onset, affecting people older than 65 years of age. The exact genetic
trigger is not yet identified.

Pathophysiology

Figure 1: Pathophysiology of alzheimer’s disease

 Specific neuropathologic and biochemical changes are found in patients with AD. These include
neurofibrillary tangles (tangled masses of nonfunctioning neurons) and senile or neuritic plaques
(deposits of amyloid protein, part of a larger protein called amyloid precursor protein in the brain).
 The neuronal damage occurs primarily in the cerebral cortex and results in decreased brain size. Similar
changes are found in the normal brain tissue of older adults, but to a lesser extent.
 Cells that use the neurotransmitter acetylcholine are principally affected by AD.
 At the biochemical level, the enzyme active in producing acetylcholine, which is specifically involved in
memory processing, is decreased.
Scientists have been studying complex neurodegenerative diseases such as AD and have focused on two key
issues: whether a gene might influence a person’s overall risk of developing the disease, and whether a gene
might influence some particular aspect of a person’s risk, such as the age at which the disease begins (age at
onset). There are genetic differences in early-onset and late-onset forms of AD.

Researchers are conducting tests to explain what predisposes people to develop the plaques and
neurofibrillary tangles that can be seen at autopsy in the brains of patients with AD. Understanding the
complex ways in which aging and genetic and nongenetic factors affect brain cells over time, eventually
leading to AD, continues to increase. Researchers have discovered how amyloid plaques form and cause
neuronal death, the possible relationship between various forms of tau protein and impaired function, the
roles of inflammation and oxidative stress, and the contribution of brain infarctions to the disease

Stages of Alzheimer’s disease

Stage 1: No Impairment

During this stage, Alzheimer’s is not detectable and no memory problems or other symptoms of dementia
are evident.

Stage 2: Very Mild Decline

The person may notice minor memory problems or lose things around the house, although not to the point
where the memory loss can easily be distinguished from normal age-related memory loss. The person will
still do well on memory tests and the disease is unlikely to be detected by loved ones or physicians.

Stage 3: Mild Decline

At this stage, the family members and friends of the person may begin to notice cognitive problems.
Performance on memory tests are affected and physicians will be able to detect impaired cognitive function.

People in stage 3 will have difficulty in many areas including:

 Finding the right word during conversations

 Organizing and planning
 Remembering names of new acquaintances
 People with stage three Alzheimer’s may also frequently lose personal possessions, including valuables.

Stage 4: Moderate Decline

In stage four of Alzheimer’s, clear-cut symptoms of the disease are apparent. People with stage four of
Alzheimer’s:

 Have difficulty with simple arithmetic

 Have poor short-term memory (may not recall what they ate for breakfast, for example)
 Inability to manage finance and pay bills
 May forget details about their life histories

Stage 5: Moderately Severe Decline

During the fifth stage of Alzheimer’s, people begin to need help with many day-to-day activities. People in
stage five of the disease may experience:

 Difficulty dressing appropriately

 Inability to recall simple details about themselves such as their own phone number
 Significant confusion

On the other hand, people in stage five maintain functionality. They typically can still bathe and toilet
independently. They also usually still know their family members and some detail about their personal
histories, especially their childhood and youth.

Stage 6: Severe Decline

People with the sixth stage of Alzheimer’s need constant supervision and frequently require professional
care. Symptoms include:

 Confusion or unawareness of environment and surroundings

 Inability to recognize faces except for the closest friends and relatives
 Inability to remember most details of personal history
 Loss of bladder and bowel control
 Major personality changes and potential behavior problems
 The need for assistance with activities of daily living such as toileting and bathing
 Wandering

Stages 7: Very Severe Decline

Stage seven is the final stage of Alzheimer’s. Because the disease is a terminal illness, people in stage seven
are nearing death. In stage seven of the disease, people lose the ability to communicate or respond to their
environment. While they may still be able to utter words and phrases, they have no insight into their
condition and need assistance with all activities of daily living. In the final stages of Alzheimer’s, people
may lose their ability to swallow.

Clinical Manifestations
 The cognitive changes of AD tend to follow a characteristic pattern, beginning with memory impairment
and progressing to language and visuospatial deficits.
 Yet, approximately 20% of patients with AD present with nonmemory complaints such as word-finding,
organizational, or navigational difficulty.
 In other patients, upstream visual processing dysfunction (referred to as posterior cortical atrophy
syndrome) or a progressive “logopenic” aphasia are the primary manifestations of AD for years before
progressing to involve memory and other cognitive domains. Still other patients may present with an
asymmetric akineticrigid-dystonic (“corticobasal”) syndrome or a dysexecutive “frontal variant” of AD.
 In the early stages of AD, forgetfulness and subtle memory loss occur.
 Patients may experience small difficulties in work or social activities but have adequate cognitive
function to compensate for the loss and continue to function independently.
 With further progression of AD, the deficits can no longer be concealed. Forgetfulness is manifested in
many daily actions; patients may lose their ability to recognize familiar faces, places, and objects, and
they may become lost in a familiar environment. They may repeat the same stories because they forget
that they have already told them.
 Trying to reason with people with AD and using reality orientation only increase their anxiety without
increasing function.
 Conversation becomes difficult, and word-finding difficulties occur. The ability to formulate concepts
and think abstractly disappears; for example, a patient can interpret a proverb only in concrete terms.
 Patients are often unable to recognize the consequences of their actions and therefore exhibit impulsive
behavior.
 Patients have difficulty with everyday activities, such as operating simple appliances and handling
money. Personality changes are also usually evident. Patients may become depressed, suspicious,
paranoid, hostile, and even combative.
 Progression of the disease intensifies the symptoms: speaking skills deteriorate to nonsense syllables,
agitation and physical activity increase, and patients may wander at night.
 Eventually, assistance is needed for most ADLs, including eating and toileting, because dysphagia and
incontinence develop. The terminal stage, in which patients are usually immobile and require total care,
may last months or years.
 Occasionally, patients may recognize family members or caregivers. Death occurs as a result of
complications such as pneumonia, malnutrition, or dehydration.
 Mild Cognitive Impairment (MCI): A Potential Precursor to Alzheimer’s and Other Dementias
 MCI is a condition in which an individual has mild but measurable changes in thinking abilities that are
noticeable to the person affected and to family members and friends, but the individual is still able to
carry out everyday activities.
 Approximately 15 percent to 20 percent of people age 65 or older have MCI. People with MCI,
especially MCI involving memory problems, are more likely to develop Alzheimer’s or other dementias
than people without MCI.
 A systematic review of 32 studies found that an average of 32 percent of individuals with MCI
developed Alzheimer’s dementia within 5 years’ follow-up. A Meta analysis of 41 studies found that
among individuals with MCI who were tracked for 5 years or longer, an average of 38 percent developed
dementia. Identifying which individuals with MCI are more likely to develop Alzheimer’s or other
dementias is a major goal of current research.

Assessment and Diagnostic Findings

A definitive diagnosis of AD can be made only at autopsy, but an accurate clinical diagnosis can be made in
about 90% of cases. The most important goal is to rule out other causes of dementia or reversible causes of
confusion, such as other types of dementia, depression, delirium, alcohol or drug abuse, or inappropriate
drug dosage or drug toxicity.

 AD is a diagnosis of exclusion, and a diagnosis of probable AD is made when the medical history,
physical examination, and laboratory tests have excluded all known causes of other dementias.
 The health history—including medical history, family history, social and cultural history, and
medication history— and the physical examination, including functional and mental health status, are
essential to the diagnosis of probable AD.
 Diagnostic tests, including complete blood count, chemistry profile, and vitamin B12 and thyroid
hormone levels, as well as screening with electroencephalography, computed tomography (CT),
magnetic resonance imaging (MRI), and examination of the cerebrospinal fluid may all refute or support
a diagnosis of probable AD.
 Depression can closely mimic early-stage AD and coexists in many patients. Therefore, assessing the
patient for underlying depression is important to rule this out. Tests such as the MMSE are useful for
screening (Borson, Scanlan, Watanabe, et al., 2005).
 Both CT and MRI of the brain are useful for excluding hematoma, brain tumor, stroke, normal-pressure
hydrocephalus, and atrophy but are not reliable in making a definitive diagnosis of AD.
 Infections and physiologic disturbances, such as hypothyroidism, Parkinson’s disease, and vitamin B12
deficiency, can cause cognitive impairment that may be misdiagnosed as AD. Biochemical abnormalities
can be excluded through examination of the blood and cerebrospinal fluid.
 PET can also be used to detect the presence of fibrillar amyloid in the brain.
 Electroencephalogram (EEG) is normal or shows nonspecific slowing; prolonged EEG can be used to
seek out intermittent nonconvulsive seizures.
 Routine spinal fluid examination is also normal.Cerebrospinal fluid (CSF) Aβ42 level is reduced,
whereas the tau protein is elevated, but the test characteristics of these assays still make interpretation
challenging in individual patients.

Genetic considerations:
Several genes play an important role in the pathogenesis of AD. One is the APP gene on chromosome 21.
Adults with trisomy 21 (Down’s syndrome) consistently develop the typical neuropathologic hallmarks of
AD if they survive beyond age 40 years, and many develop a progressive dementia superimposed on their
baseline mental retardation. The extra dose of the APP gene on chromosome 21 is the initiating cause of AD
in adult Down’s syndrome and results in excess cerebral amyloid production. Supporting this hypothesis,
some families with early age-of-onset familial AD (FAD) have point mutations in APP. Investigation of
large families with multigenerational FAD led to the discovery of two additional AD-causing genes, the
presenilins. Presenilin-1 (PS-1) is on chromosome 14 and encodes a protein called S182. Mutations in this
gene cause an early-age-of-onset AD, with onset before the age of 60 and often before age 50, transmitted in
an autosomal dominant, highly penetrant fashion.

Medical Management
 The primary goal is to manage the cognitive and behavioral symptoms. There is no cure and no way to
slow the progression of the disease.
 The cholinesterase inhibitors (CEIs) donepezil hydrochloride (Aricept), rivastigmine tartrate (Exelon),
galantamine hydrobromide (Razadyne [formerly known as Reminyl]),( Donepezil (target dose, 10 mg
daily), rivastigmine (target dose, 6 mg twice daily or 9.5-mg patch daily), galantamine (target dose 24
mg daily, extended-release), and memantine (target dose, 10 mg twice daily)) and tacrine (Cognex)
enhance acetylcholine uptake in the brain, thus maintaining memory skills for a period of time; these
medications are used for mild to moderate symptoms. Due to hepatotoxicity, tacrine is no longer used.
Dose escalations for each of these medications must be carried out over 4–6 weeks to minimize side
effects.
 Donepezil and the newest medication memantine (Namenda), a receptor agonist, can be used for
management of moderate to severe symptoms. Cognitive ability may improve within 6 to 12 months of
therapy, but cessation of the medications results in disease progression and cognitive decline.
 It is recommended that treatment continue at least through the moderate stage of the illness.
Combination of a CEI with memantine may be useful for mild to moderate cognitive symptoms.
 Behavioral problems such as agitation and psychosis can be managed by behavioral and psychosocial
therapies.
 Associated depression and behavioral problems can also be treated pharmacologically if other
interventions fail.
 Because symptoms change over time, all patients with AD who take medications should be reevaluated
routinely, and the nurse should document and report both positive and negative responses to
medications.
 Mild to moderate depression is common in the early stages of AD and may respond to antidepressants or
cholinesterase inhibitors. Selective serotonin reuptake inhibitors (SSRIs) are commonly used due to their
low anticholinergic side effects (for example, escitalopram, and target dose 5–10 mg daily). Seizures can
be treated with levetiracetam unless the patient had a different regimen that was effective prior to the
onset of AD. Agitation, insomnia, hallucinations, and belligerence are especially troublesome
 characteristics of some AD patients, and these behaviors can lead to nursing home placement. The newer
generation of atypical antipsychotics, such as risperidone, quetiapine, and olanzapine, are being used in
low doses to treat these neuropsychiatric symptoms.

The management of AD is challenging and gratifying despite the absence of a cure or a robust
pharmacologic treatment. The primary focus is on long-term amelioration of associated behavioral and
neurologic problems, as well as providing caregiver support.
Building rapport with the patient, family members, and other caregivers is essential to successful
management.
In the early stages of AD, memory aids such as notebooks and posted daily reminders can be helpful.
Family members should emphasize activities that are pleasant while curtailing those that increase stress on
the patient.
Kitchens, bathrooms, stairways, and bedrooms need to be made safe, and eventually patients will need to
stop driving. Loss of independence and change of environment may worsen confusion, agitation, and anger.
Communication and repeated calm reassurance are necessary. Caregiver “burnout” is common, often
resulting in nursing home placement of the patient or new health problems for the caregiver. Respite breaks
for the caregiver help to maintain a successful long-term therapeutic milieu. Use of adult day care centers
can be helpful.
Nursing Management
Nurses play an important role in the recognition of dementia, particularly in hospitalized elderly, by
assessing for signs (eg, repeating or asking the same thing over and over, getting lost) during the nursing
admission assessment (Maslow & Mezey, 2008). Nursing interventions for dementia are aimed at promoting
patient function and independence for as long as possible. Other important goals include promoting the
patient’s physical safety, promoting independence in self-care activities, reducing anxiety and agitation,
improving communication, providing for socialization and intimacy, promoting adequate nutrition,
promoting balanced activity and rest, and supporting and educating family caregivers.
Nursing diagnoses:
1. Disturbed Thought Processes related to progressive dementia as evidenced by disorientation to time and
place, loss of short-term memory, inability to concentrate, and periods of agitation.
2. Disturbed sensory perception related to alzheimer’s disease progression, transmission and/or integration
of neurologic disease or deficit, chronic illness aging as evidenced by disorientation to time, place,
person, or events, change in sensory acuity, altered abstraction or conceptualization, changes in problem
solving abilities
3. Chronic Confusion related to Dementia as evidenced by Decreased ability to interpret one’s
environment, Decreased capacity for thought, Memory impairment
4. Impaired verbal communication related to alzheimer’s disease as evidenced by confusion, anxiety,
restlessness, disorientation to person, place, time and circumstance, agitation, flight of ideas, repetitive
speech, inability to speak [properly], stuttering, slurring, impaired articulation, difficulty with phonation,
inability to name words, inability to identify objects, difficulty comprehending communication,
difficulty forming words or sentences, aphonia, dyslalia, dysarthria, inappropriate verbalizations,
aphasia, dysphasia, apraxia, dyslexia.
5. Impaired physical mobility related to alzheimer’s disease progression, dementia, inability to bear weight,
poor nutrition, perceptual impairment, cognitive impairment, as evidenced by weakness, inability to
move at will, bear weight, immobility, gait disturbances, balance and coordination deficits, difficulty
turning
6. Disturbed sleep pattern related to alzheimer’s disease progression, depression, confusion, boredom,
environmental stimuli, obstructive sleep apnea as evidenced by interrupted sleep, difficulty falling
asleep, awakening early, fatigue, lethargy, irritability, insomnia
7. Imbalanced Nutrition: Less Than Body Requirement related to dysphagia secondary to neurological
disorder.
8. Self- care deficit (grooming and dressing related to difficulty in completing tasks/ loss of previous
capabilities as evidenced by forgetfulness, inability to recall previous tasks, presence of urinary
incontinence, Difficulty articulating needs.
9. Social isolation related to chronic confusion, disease progression, agitation, combativeness as evidenced
by uncommunicative, withdrawn.
10. Compromised family coping related to chronic illness, progression of the disease that exhausts the
caregiver or family unit, progressive dependence of the patient on the family as evidenced by fatigue,
anxiety, stress, social isolation, financial insecurity, expression of inadequate understanding of crisis and
patient’s responses to health problems and necessary supportive behaviors
11. Risk for injury related to disorientation to time and place confusion (wandering at night) forgetfulness
and increased memory loss presence of motor disturbance i.e. apraxia

These nursing interventions apply to all patients with dementia, regardless of cause.
Maintaining thought process:
 Assess patient’s ability for thought processing every shift. Observe patient for cognitive functioning,
memory changes, disorientation, difficulty with communication, or changes in thinking patterns.
 Assess the level of cognitive disorders such as change to orientation to people, places and times, range,
attention, thinking skills
 Assess patient’s ability to cope with events, interests in surroundings and activity, motivation, and
changes in memory pattern.
 Orient patient to environment as needed, if patient’s short term memory is intact. Using of calendars,
radio, newspapers, television and so forth, are also appropriate.
 Assess patient for sensory deprivation, concurrent use of CNS drugs, poor nutrition, dehydration,
infection, or other concomitant disease processes.
 Label drawers; use written reminders notes, pictures, or color-coding articles to assist patients.
 Provide opportunity for social interaction, but to do not force interaction.
Supporting Cognitive Function:
 Assess patient for reversible or irreversible dementia, causes, ability to interpret environment,
intellectual thought processes, memory loss, disturbances with orientation, behavior, and socialization.
 As the patient’s cognitive ability declines, family members must provide more and more assistance and
supervision.
 A calm, predictable environment helps people with dementia interpret their surroundings and activities.
 Environmental stimuli are limited, and a regular routine is established. A quiet, pleasant manner of
speaking, clear and simple explanations, and use of memory aids and cues help minimize confusion and
disorientation and give patients a sense of security.
 Prominently displayed clocks and calendars may enhance orientation to time.
 Color-coding the doorway may help patients who have difficulty locating their room.
 Active participation may help patients maintain cognitive, functional, and social interaction abilities for
a longer period.
 Physical activity and communication have also been demonstrated to slow some of the cognitive decline
of AD.
Improving Communication.
 To promote the patient’s interpretation of messages, the nurse should remain unhurried and reduce
noises and distractions.
 Use of clear, easy-to understand sentences to convey messages is essential because patients frequently
forget the meaning of words or have difficulty organizing and expressing thoughts.
 In the earlier stages of dementia, lists and simple written instructions that serve as reminders may be
helpful.
 In later stages, the patient may be able to point to an object or use nonverbal language to communicate.
 Tactile stimuli, such as hugs or hand pats, are usually interpreted as signs of affection, concern, and
security.
Improving physical mobility:
 Assess patient’s functional ability for mobility and note changes.
 Assess patient’s degree of cognitive impairment and ability to follow commands, and adapt interventions
as needed.
 Provide patients with enough time to perform mobility related assignment. Use simple instructions.
 Provide range of motion exercises every shift. Encourage active range of motion exercises.
 Assist patient with walking if at all possible, utilizing sufficient help. A one or two-person pivot transfer
utilizing a transfer belt can be used if patient has weight-bearing ability.
 Use mechanical lift for patients who cannot bear weight, and help them out of bed at least daily.
 Instruct family regarding ROM exercises, methods of transferring patients from bed to wheelchair, and
turning at routine intervals.
Improving sleep pattern:
 Assess patient’s sleep patterns and changes, naps, and frequency, amount of activity, sedentary status,
number and time of awakenings during night, and patient’s complaints of fatigue apathy, lethargy, and
impotence.
 Assess patient for complaints or signs of pain, dyspnea, nocturia or cramps.
 Ensure environment is quiet, well-ventilated, absence of odor, and has comfortable temperature.
 Provide ritualistic procedures of warm drink, extra covers, clean linens, or warm baths prior to bedtime.
 Instruct family regarding Sundowning syndrome, methods of coping, and possibility of changing their
sleeping cycle to match that of the patient’s once discharged.
Promoting Adequate Nutrition:
 Mealtime can be a pleasant social occasion or a time of upset and distress, and it should be kept simple
and calm, without confrontations.
 Patients prefer familiar foods that look appetizing and taste good. To avoid any “playing” with food, one
dish is offered at a time.
 Food is cut into small pieces to prevent choking. Liquids may be easier to swallow if they are converted
to gelatin. Hot food and beverages are served warm, and the temperature of the foods should be checked
to prevent burns.
 When lack of coordination interferes with self-feeding, adaptive equipment is helpful. Some patients
may do well eating with a spoon or with their fingers.
 If this is the case, an apron or a smock, rather than a bib, is used to protect clothing. As deficits progress,
it may become necessary to feed the patient.
 Forgetfulness, disinterest, dental problems, lack of coordination, overstimulation, and choking all serve
as barriers to good nutrition and hydration.

Promoting Independence in Self-Care Activities:
 Pathophysiologic changes in the brain make it difficult for people with AD to maintain physical
independence.
 Patients should be assisted to remain functionally independent for as long as possible.
 Simplify daily activities by organizing them into short, achievable steps so that the patient experiences a
sense of accomplishment.
 Frequently, occupational therapists can suggest ways to simplify tasks or recommend adaptive
equipment.
 Direct patient supervision is sometimes necessary, but maintaining personal dignity and autonomy is
important for people with AD, who should be encouraged to make choices when appropriate and to
participate in self-care activities as much as possible.
Reducing Anxiety and Agitation:
 Despite profound cognitive losses, patients are sometimes aware of their diminishing abilities. Patients
need constant emotional support that reinforces a positive self-image.
 When loss of skills occurs, goals are adjusted to fit the patient’s declining ability. The environment
should be kept familiar and noise-free.
 Excitement and confusion can be upsetting and may precipitate a combative, agitated state known as a
catastrophic reaction (overreaction to excessive stimulation).
 The patient may respond by screaming, crying, or becoming abusive (physically or verbally); this may
be the patient’s only way of expressing an inability to cope with the environment.
 When this occurs, it is important to remain calm and unhurried.
 Forcing the patient to proceed with the activity only increases the agitation. It is better to postpone the
activity until later, even to another day.
 Frequently, the patient quickly forgets what triggered the reaction. Measures such as moving to a
familiar environment, listening to music, stroking, rocking, or distraction may quiet the patient.
Structuring activity is also helpful.
 Becoming familiar with a particular patient’s predicted responses to certain stressors helps caregivers
avoid similar situations.
Providing for Socialization and Intimacy Needs:
 Because socialization with friends can be comforting, visits, letters, and phone calls are encouraged.
 Visits should be brief and no stressful; limiting visitors to one or two at a time helps reduce
overstimulation.
 Recreation is important, and people with dementia are encouraged to participate in simple activities.
 Realistic goals for activities that provide satisfaction are appropriate. Hobbies and activities such as
walking, exercising, and socializing can improve the quality of life.
 Spouses should be encouraged to talk about any sexual concerns, and sexual counseling may be
necessary. Simple expressions of love, such as touching and holding, are often meaningful.
Improving family coping:
 Assess family’s knowledge of patient’s disease and erratic behaviors, and possible violent reactions.
 Assess for level of family’s fatigue, reduced social exposure of family, feelings about role reversal in
caring for patient and increasing demands of patient.
 Provide for opportunity for family to express concerns and lack of control of situation
 Assist in defining problem and use of techniques to cope and solve problems.
 Assist family to identify patient’s reactions and behaviors and reasons for them.
 Instruct family and demonstrate time-saving, energy-conserving techniques to be used to assist patient.
 Instruct family regarding community resources available for AD, their families, as well as utilization of
respite care.
Promoting Physical Safety:
 A safe home and hospital environment allows the patient to move about as freely as possible and relieves
the family of constant worry about safety.
 To prevent falls and other injuries, all obvious hazards are removed and hand rails are installed in the
home.
 A hazard free environment allows the patient maximum independence and a sense of autonomy.
Adequate lighting, especially in halls, stairs, and bathrooms, is necessary.
 Nightlights are helpful, particularly if the patient has increased confusion at night (sundowning). Driving
is prohibited, and smoking is allowed only with supervision.
 The patient may have a short attention span and be forgetful. Wandering behavior can often be reduced
by gentle persuasion or distraction.
 Restraints should be avoided because they increase agitation. Doors leading from the house must be
secured.
 Outside the home, all activities must be supervised to protect the patient, and the patient should wear an
identification bracelet or neck chain in case of separation from the caregiver.
Supporting Home and Community-Based Care:
 The emotional burden on the families of patients with all types of dementia is enormous. The physical
health of the patient is often very stable, and the mental degeneration is gradual.
 Family members may cling to the hope that the diagnosis is incorrect and that their relative will improve
with greater effort. Family members are faced with numerous difficult decisions (eg, when the patient
should stop driving, when to assume responsibility for the patient’s financial affairs).
 Aggression and hostility exhibited by the patient are often misunderstood by families or caregivers, who
feel unappreciated, frustrated, and angry. Feelings of guilt, nervousness, and worry contribute to
caregiver fatigue, depression, and family dysfunction.
 Neglect or abuse of the patient can occur, and this has been documented in home situations as well as in
institutions. If neglect or abuse of any kind—including physical, emotional, sexual, or financial abuse—
is suspected, the local adult protective services agency must be notified. The role of the nurse is to report
the suspected abuse, not to prove it.

Preventive measures:
 Given the growing population of elderly people and the concomitant increase in prevalence of Alzheimer
disease (AD), family physicians should be aware of strategies that could delay or prevent onset of AD.
 There is no evidence that screening for AD in the general population is effective, but among patients at
higher risk, such as those with a family history of AD who are concerned about AD and those
complaining of memory problems, cognitive testing should be considered.
 Patients presenting with memory difficulties who test positive for mild cognitive impairment are at
increased risk of developing AD at a rate of about 10% annually. Neuroimaging has shown some
 structural markers, but they are not specific enough to be useful. Certain genetic defects have a higher
predictive value for AD, but the value is still too low for screening the general population.
 There is good evidence that blood pressure control could prevent development of AD and that estrogens
do not reduce the incidence of AD. Observational studies suggest that a healthy diet, exercise, new
learning experiences, and cholesterol control help prevent AD.
 Two diets that have been studied and may be beneficial are the DASH (Dietary Approaches to Stop
Hypertension) diet and the Mediterranean diet. The DASH diet emphasizes vegetables, fruits and fat-free
or low-fat dairy products; includes whole grains, fish, poultry, beans, seeds, nuts and vegetable oils; and
limits sodium, sweets, sugary beverages and red meats. A Mediterranean diet includes relatively little
red meat and emphasizes whole grains, fruits and vegetables, fish and shellfish, and nuts, olive oil and
other healthy fats.

Conclusions:

Although the human and societal cost of AD is staggering, there is hope that earlier and better diagnosis,
increased knowledge of its natural history with support of the patient and family throughout the disease
stages, effective symptomatic drugs, and potentially effective disease modification strategies will have a
dramatic impact on the number of persons affected in the future, and the quality of life of persons currently
affected. The fast pace of research and development in AD is unique in neurological history, and should lead
to a better future for aging populations.

References:
 Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L. 1., Jameson, J. L., & Loscalzo, J. (2015).
Harrison's principles of internal medicine (19th edition.). New York: McGraw Hill Education page
no.2598-2603.
 Hinkle, J. L. (2014). Brunner & Suddarth's textbook of medical-surgical nursing (Edition 13.).
Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; page no. 217-220.
 Incidence of Alzheimer’s disease in India: A 10 years follow-up study retrieved from:
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553547/)
Name of the institution: College of nursing, ILBS

Title of seminar topic: Alzheimer’s disease

Subject: Clinical Speciality -1

Name of the supervisor: Ms. Madhavi verma

Group: M.Sc. nursing 1st year

Date and Time:

AV aids:

General objective: The group will be able to understand the Alzheimer’s disease is and how the disease
progresses.

Specific objectives: After the completion of this topic group will be able to;

 Identify current understanding of the complex interacting processes that lead to AD and dementia.
 Identify the challenges faced by individuals diagnosed with Alzheimer’s disease.
 Describe the stages of Alzheimer’s disease.
 Describe, in overview, the processes involved in identifying, evaluating and caring for individuals with
cognitive impairment, AD.
 Demonstrate understanding of pathogenesis, treatment, and outcome of the disease processes
 Recognize the role of nurses in care of people with Alzheimer’s disease.
 SEMINAR ON
ALZHEIMER’S
DISEASE

SUBMITTED TO: SUBMITTED BY:

Ms. MADHAVI VERMA DEEPIKA BIST

READER

CON, ILBS
INDEX
M.Sc. NURSING 1ST YEAR

DATE OF SUBMISSION:
S. NO. CONTENT PAGE
NO.

1. Introduction, history and definition 1

2. Research article 1,2

3. Risk factors 2

4. Types 3

5. Pathophysiology 3-4

6. Stages of Alzheimer’s disease 4-5

7. Clinical manifestations 5-6

8. Assessment and diagnostic findings 6-7

9. Genetic consideration 7

10. Medical management 7-8

11. Nursing management 8-11

12. Preventive measures 11

13. Conclusion 12