Submitted to: Asst. Prof.

Kathleah Caluscusan
Submitted by: Catherine Perez
Submitted on: March 6, 2015

Alzheimers disease

This is the most common form of dementia among people over age 65 years old. (Black &
Hokanson, 2009)
It is a chronic, progressive, degenerative, disease of the brain. It is the most common form of
dementia, accounting approximately 60% to 80% of all cases of dementia. AD is named after
Alois Alzheimer, a German physician who in 1906 described changes in the brain tissue of a 51
year old woman who died of an unusual illness
It is estimated that 5% of people ages 65 to 74 and nearly 50% of those age 85 have AD. Most
patients live 8 to 10 years after being diagnosed, although some live for 20 years. The burden on
the patient, family, caregiver, and society as a whole is staggering.
The incidence of AD is higher in African Americans and Hispanic Americans. It is associated
with lower socioeconomic status and educational level and poor access to health care. Women
are more likely than men to develop AD, because they live longer.
Pathophysiology
The exact etiology is unknown. Age is the most important risk factor. However, AD is a disease
that destroys brain cells, which is not normal part of aging. Small percent of people younger than
60 y/o will develop AD. This is referred to as early-onset. AD in individuals after 60 y/o is called
late-onset.
Persons in whom a clear pattern of inheritance within a family is established are said to have
familial Alzheimers disease. Other cases in which no familial connection can be made are
termed as sporadic. FAD is associated with early-onset and more rapid disease.
Genetic factors are also linked to AD. At least five chromosomes (1, 12, 14, 19 and 21) are
involved in some forms of familial AD. Four genetic loci have also been identified as
contributing to AD, including amyloid precursor gene, presenilin 1 gene, presenilin 2 gene, and
apolipoprotein E gene on chromosome 19. (Black & Hokanson, 2009)
Characteristics findings of AD relate to changes in brains structure and function.
1. Amyloid plaques
2. Neurofibrillary tangles
3. Loss of connections between cells and cell death
As part of aging, people develop some plaques in brain tissue, but in AD there are more plaques
in certain parts of brain. These plaques consist of clusters of insoluble deposits of protein called
B-amyloid, other proteins, remnants of neurons, non-nerve cells such as microglia (cells that
surround and digest damage cells or foreign substances) and other cells such as astrocytes Bamyloid is cleaved from amyloid precursor protein (APP), which is associated with the cell
membrane. Plaques develop in first in areas of the brain used for memory and cognitive function,
including the hippocampus (important in forming and storing short-term memory). AD attacks
the cerebral cortex, especially the areas responsible for language and reasoning.
Neurofibrillary tangles are abnormal collections of twisted protein threads inside nerve cells. The
main component is a protein called tau. Tau protein provides support for intracellular structure
through their support of microtubules. They hold the microtubules together like railroad ties hold
railroad tracks together. In AD, Tau protein is altered and as a result the microtubules twist
together in a helical fashion. This forms the neurofibrillary tangles in the neurons with AD.

Plaques and neurofibrillary tangles are not unique to patients with AD or dementia. They are also
found in the brains of individuals without evidence of cognitive impairment. However there are
more plentiful in the brains of AD individuals.
The gradual loss of connection between neurons leads to damage and then death of the neurons.
Affected parts of the brain begin to shrink in a process called brain atrophy. By the final state,
brain tissue shrunk significantly.
(Lewis, Heitkemper, Dirksen, O'Brien, & Linda, 2008)
Assessment
An initial sign: subtle deterioration in memory
Inevitably this progresses to more profound memory loss that interferes with the patients ability
to function. As the disease progresses, manifestations are more easily noticed and become
serious enough to cause people with AD or their family members to seek medical help. Recent
events and new information cannot be recalled. Personal hygiene deteriorates, as does the ability
to concentrate and maintain attention. Ongoing loss of neurons in AD can cause a person to act in
altered or unpredictable ways. Behavioral manifestations (e.g. agitation) result from changes that
take place within the brain. They are neither intentional nor controllable by the individual with
the disease. Some develop psychotic manifestations (e.g. delusions, illusions, hallucinations)
With progression of AD, additional cognitive impairments are noted.
Dysphasia difficulty comprehending language and oral communication
Apraxia inability to manipulate objects or perform purposeful acts
Visual agnosia inability to recognize objects by sight
Dysgraphia difficulty communicating via writing
Eventually long-term memories cannot be recalled, and patient loses the ability to recognize
family members and friends. Other problems include aggression and tendency to wander.
Later in the disease, ability to communicate and to perform activities of daily living is lost. In
final stage, patient is unresponsive and incontinent and requires total care.
(Lewis, Heitkemper, Dirksen, O'Brien, & Linda, 2008)
Diagnostic Studies
Diagnosis is primarily a diagnosis of exclusion. No single clinical test can be used to diagnose
AD. In patients with cognitive impairment, there is increased emphasis on early and careful
evaluation.
A complete patient evaluation includes complete health history, physical examination, neurologic
and mental status assessment and laboratory tests. CT or MRI scan show brain atrophy and
enlarge ventricles in the later stage, although this finding occurs in the disease and can also be
seen in persons without cognitive impairment. Newer techniques include SPECT, magnetic
resonance spectroscopy (MRS) and PET allow detection of changes early as well as monitoring
of treatment response.
Neuropsychologic testing with tools such as the Mini-Mental State Examination can help
document the degree of cognitive impairment.

(Lewis, Heitkemper, Dirksen, O'Brien, & Linda, 2008)

Autopsy is the definitive diagnosis of AD.
(Hragrove-Huttel, 2005)
Nursing Diagnoses and expected outcomes
Disturbed thought processes related to effects of dementia as evidenced by loss of memory and
other cognitive deficits

The client will function at highest level of cognitive ability

Self-care deficit (bathing, dressing, toileting) related to memory deficits and neuromuscular
impairment as evidenced by inability to independently and appropriately bathe, dress or toilet

The client will perform self-care bathing, dressing, and toileting with assistance as
needed

Risk for injury related to impaired judgment, possible gait instability, muscle weakness and
sensory/perceptual alterations

The client will experience no injury and use assistive devices appropriately for
ambulation support

Wandering related to disease process as evidenced by getting lost numerous times a day and
patients statement of I dont know where I am

The client will remain in restricted area during ambulation and activity

(Lewis, Heitkemper, Dirksen, O'Brien, & Linda, 2008)

Nursing intervention
Nursing care is focused on decreasing clinical manifestations, preventing harm and supporting
patient and caregiver throughout disease process
Supporting Cognitive function
1. Provide a calm, predictable environment to minimize confusion and disorientation
2. Help patient feel a sense of security with a quiet, pleasant manner; clear, simple
explanations; and use of memory aids and cues
Promoting Physical Safety
1. Provide a safe environment (whether at home or in the hospital) to allow patient to move
about as freely as possible and relieve familys worry about safety
2. Prevent falls and other accidents by removing obvious hazards and providing adequate
lighting; install handrails in the home
3. Prohibit driving
4. Allow smoking only with supervision
5. Reduce wandering behavior with gentle persuasion and distraction. Supervise all
activities outside the home to protect patient. As needed, secure doors leading from the
house. Ensure that patient wears an identification bracelet or neck chain.
6. Avoid restraints because they may increase agitation
Promoting Independence in Self-Care Activities

1. Simplify daily activities into short achievable steps so that patient feels a sense of
accomplishment
2. Maintain patients personal dignity and autonomy
3. Encourage patient to make choices when appropriate and to participate in self-care
activities as much as possible.
Reducing anxiety and agitation
1. Provide emotional support to reinforce a positive self-image
(Johnson, 2010)
Collaborative
1. Cholinesterase inhibitors are used in the treatment of mild to moderate dementia. They
block cholinesterase, the enzyme responsible for breakdown of acetylcholine in the
synaptic cleft
a. donepezil (Aricept)
b. rivastigmine (Exelon)
c. galantamine (Razadyne)
2. Memantine (Namenda) is used for the treatment of the middle to late stages of AD. It
appears to protect the brains nerve cells against excess amounts of glutamate, which is
released in large amounts by cells damaged by AD. The attachment of glutamate to Nmethyl-D-aspartate (NMDA) receptors permits calcium to flow freely into the cell, which
will lead to cell degeneration. Memantine may prevent this destructive sequence by
blocking the action of glutamate.
3. Conventional Antipsychotic drugs used to manage acute episodes of agitation, aggressive
behavior and psychosis. However, this is associated with side effects including
extrapyramidal symptoms and anticholinergic activity, especially in older adults
a. haloperidol (Haldol)
4. Atypical Antipsychotic used more commonly for behavioral management of AD.
a. risperidone (Risperidal)
b. olanzapine (Zyprexa)
c. quetiapine (Seroquel)
5. Selective serotonin reuptake inhibitors (SSRIs) used to treat depression
a. fluoxetine (Prozac)
b. sertraline (Zoloft)
c. fluvoxamine (Luvox)
d. citalopram (Celexa)
6. Antidepressants help with problems related to sleep. However this may result in
hypotension
a. trazodone (Desyrel)
7. Antiseizure drugs used to manage behavioral problems. These drugs act as mood
stablizers
a. valproic acid (Depakene)
b. carbamazepine (Tegretol)
(Lewis, Heitkemper, Dirksen, O'Brien, & Linda, 2008)
Bibliography
Black, J. M., & Hokanson, H. J. (2009). Medical-Surgical Nursing: Clinical
Management for Positive Outcomes 8th ed. St. Louis, Missouri: Saunders
ELsevier.

Hragrove-Huttel, R. A. (2005). Medical-Surgical Nursing 4th ed. PA: Lippincott

Williams & Wilkins.
Johnson, J. Y. (2010). Brunner & Suddarth's textbook of medical-surgical nursing
12th ed. Philadelphia: Wolters, Kluwer/Lippincott, WIlliams & Wilkins.
Lewis, S. L., Heitkemper, M. M., Dirksen, S. R., O'Brien, P. G., & Linda, B. (2008).
Medical-Surgical Nursing: Assessment and Management of Clinical Problems
7th ed. Singapore: Mosby.