SLO1. DEFINITION AND CLASSIFICATION Alzheimers Disease, was discovered in 1906 by a German scientist named Alois Alzheimer. AD is a disease of the brain which is a progressive worsening and debilitating dementia that affects the mind and the intellect. Alzheimer's is not just a disease of old age. Early onset (also known as younger-onset) Alzheimer's affects people younger than age 65. Nearly 4% of the 5,4million Americans with Alzheimer's have early onset. Alzheimer's disease is different from normal aging. The symptoms of Alzheimers disease involve more than simple lapses in memory. People with Alzheimers experience difficulties in communicating, learning, thinking, and reasoning that can have an impact on a persons work and social and family life. Alzheimers is a disease that destroys brain cells which is not a normal part of aging. Alzheimer's disease causes brain changes that gradually get worse. It's the most common cause of dementia - a group of brain disorders that cause progressive loss of intellectual and social skills, severe enough to interfere with day-to-day life. In Alzheimer's disease, brain cells degenerate and die, causing a steady decline in memory and mental function. Alzheimerls disease (AD) is an age-related, non-reversible brain disorder that develops over a period of years. In healthy aging, most types of brain neurons are not lost in large numbers. In AD, however, where damage is widespread, many neurons stop functioning, lose connections with other neurons, and die because communication, metabolism, and repair are disrupted. At first, AD typically destroys neurons and their connections in parts of the brain that control memory, including the entorhinal cortex and the hippocampus. It later attacks areas in the cerebral cortex responsible for language and reasoning. Eventually, many other areas of the brain are damaged, and a person with AD becomes helpless and unresponsive to the outside world. There are three major hallmarks in the brain that are associated with the disease processes of AD: Amyloid plaques , which are made up of fragments of a protein called beta-amyloid peptide mixed with a collection of additional proteins, remnants of neurons, and bits and pieces of other nerve cells. Neurofibrillary tangles (NFTs) , found inside neurons, are abnormal collections of a protein called tau. Normal tau is required for healthy neurons. However, in AD, tau clumps together. As a result, neurons fail to function normally and eventually die. Loss of connections between neurons responsible for memory and learning . Neurons can't survive when they lose their connections to other neurons. As neurons die throughout the brain, the affected regions begin to atrophy, or shrink. By the final stage of AD, damage is widespread and brain tissue has shrunk significantly. Types of Alzheimers DiseaseThere are three known types of Alzheimer's disease. They include: Early-onset Alzheimers . This is a rare form of Alzheimers disease in which people are diagnosed with the disease before age 65. Less than 10% of all Alzheimers disease patients have this type. Because they experience premature aging, people with Down syndrome are particularly at risk for a form of early onset Alzheimers disease. Adults with Down syndrome are often in their mid- to late 40s or early 50s when symptoms first appear. Younger people who develop Alzheimers disease have more of the brain abnormalities that are associated with it. Early-onset Alzheimers appears to be linked with a genetic defect on chromosome 14, to which late-onset Alzheimers is not linked. A condition called myoclonus -- a form of muscle twitching and spasm -- is also more commonly seen in early-onset Alzheimers than in late-onset Alzheimers. Late-onset Alzheimers. This is the most common form of Alzheimers disease, accounting for about 90% of cases and usually occurring after age 65. Late-onset Alzheimers disease strikes almost half of all people over the age of 85 and may or may not be hereditary. Late-onset dementia is also called sporadic Alzheimers disease. Familial Alzheimers disease (FAD). This is a form of Alzheimers disease that is known to be entirely inherited. In affected families, members of at least two generations have had Alzheimers disease. FAD is extremely rare, accounting for less than 1% of all cases of Alzheimers disease. It has a much earlier onset (often in the 40s) and can be clearly seen to run in families.

Stadium demensia Alzheimer terbagi atas 3 stadium, yaitu : Stadium I (Mild AD)Berlangsung 2-4 tahun disebut stadium amnestik dengan gejala gangguan memori, berhitung dan aktifitas spontan menurun. Fungsi memori yang terganggu adalah memori baru atau lupa hal baru yang dialami Stadium II (Moderate AD)Berlangsung selama 2-10 tahun, dan disebutr stadium demensia. Gejalanya antara lain, Disorientasi gangguan bahasa (afasia), penderita mudah bingung, penurunan fungsi memori lebih berat sehingga penderita tak dapat melakukan kegiatan sampai selesai, tidak mengenal anggota keluarganya tidak ingat sudah melakukan suatu tindakan sehingga mengulanginya lagi. Dan ada gangguan visuospasial, menyebabkan penderita mudah tersesat dilingkungannya, depresi berat prevalensinya 15-20%, Stadium III (Severe AD)Stadium ini dicapai setelah penyakit berlangsung 6-12 tahun.Gejala klinisnya antara lain: Penderita menjadi vegetatif, tidak bergerak dan membisu, daya intelektual serta memori memburuk sehingga tidak mengenal keluarganya sendiri, tidak bisa mengendalikan buang air besar/ kecil, kegiatan sehari-hari membutuhkan bantuan orang lain,kematian terjadi akibat infeksi atau trauma. Mild Alzheimer's diseaseAlzheimer's disease is often first diagnosed in the mild, or early stage , when it becomes clear to family and doctors that a person is having significant trouble with memory and thinking.In the mild Alzheimer's stage, people may experience:- Memory loss for recent events.- Difficulty with problem solving, complex tasks and sound judgments.- Changes in personality.- Difficulty organizing and expressing thoughts.s increasingly challenging.- Getting lost or misplacing belongings. Moderate Alzheimer's diseaseDuring the moderate, or middle, Alzheimer's stage, people grow more confused and forgetful and begin to need help with daily activities and self-care.People with moderate Alzheimer's disease may:- Show increasingly poor judgment and deepening confusion.- Experience even greater memory loss. - Need help with some daily activities.- Undergo significant changes in personality and behavior. Severe Alzheimer's diseaseIn the severe, or late, stage of Alzheimer's, mental function continues to decline and the disease has a growing impact on movement and physical capabilities.In severe Alzheimer's, people generally:- Lose the ability to communicate coherently.- Require daily assistance with personal care. - Experience a decline in physical abilities.

2. EPIDEMIOLOGY An estimated 5.4 million Americans of all ages have Alzheimers disease in 2011. This figure includes 5.2 million people aged 65 and older and 200,000 individuals under age 65 who have younger-onset Alzheimers.

International statisticsPrevalence rates of AD similar to those in the United States have been reported in industrialized nations. The prevalence of dementia in subjects 65 years and older in North America is approximately 6-10%, with AD accounting for two-thirds of these cases. If milder cases are included, the prevalence rates do uble. Countries experiencing rapid increases in the elderly segments of their population have rates approaching those in the United States. AD has become nearly twice as prevalent as vascular dementia (VaD) in Korea, Japan, and China since transition in the early 1990s. American and European studies consistently reported AD to be more p revalent than VaD. They found a dementia prevalence rate among Chinese aged 50 years and older on the islet of Kin men for this age group of 11.2 per 1,000. AD accounted for 64.6% and VaD for 29.3%. These results, together with previous studies in Chinese populations, suggest that the rates of AD in the Chinese are low compared with those in whites. In Nigeria, the prevalence of dementia was low. Indian studies were contradictory, with both AD and VaD being more prevalent in different studies. -Age distribution for Alzheimer diseaseThe prevalence of AD increases with age. AD is most prevalent in individuals older than 60 years. Some forms of familial early-onset AD can appear as early as the third decade, but this represents a subgroup of the less than 10% of all familial cases of the disease.More than 90% of cases of AD are sporadic and occur in individuals older than 60 years. However, of interest, results of some studies of nonagenarians and centenarians suggest that the risk may decrease in individuals older than 90 years. If so, age is not an unqualified risk factor for the disease, but further stu dy of this matter is needed. -Sex distribution for Alzheimer diseaseAD affects both men and women; however, Plassman et al found the risk of developing AD to be significantly higher in women than in men, primarily due to women's higher life expectancy. -Prevalence of Alzheimer disease by raceAD and other dementias are more common in African Americans than in whites.In individuals age 65 and older, 7.8% of whites, 18.8% of African-Americans, and 20. 8% of Hispanics have AD or other dementias, and the prevalence of AD and other dementias is higher in older versus younger age groups.

3. ETHIOLOGY In the majority of cases, scientists do not yet know what causes Alzheimers disease. Most researchers agree that like other chronic conditions, Alzheimers disease results from multiple factors rather than a single cause. Biologically, the two key abnormalities seen are plaques - deposits of a protein fragment called beta-amyloid, and tangles - twisted strands of another protein, tau. In Alzheimers disease, the beta-amyloid accumulates in the brain either because of excess production of beta-amyloid or a decreased ability to dispose of it. The beta-amyloid fragments accumulate in microscopic plaques. Tangles are formed are formed when the protein tau twists into strands inside the dead brain cells. Scientists are not really certain what causes an individual to develop AD. In AD, changes in nerve endings and brain cells interfere with normal brain functions. Some scientists believe there may not even be a particular cause, but instead several factors that affect each person differently. These changes can be caused by: Genetic Influences: The presence of defective genes is known to increase a persons risk of developing AD, especially if there is a familial tendency of downs syndrome in the family. It has to do with the chromosome 21 defect gene, that makes a person predisposed to the disease of AD. Biochemical imbalance: A shortage of a vital chemical in the brain may contribute to AD. This chemical is known as amyloid. A defective protein: Some scientists believe that AD develops when a certain protein fails to maintain and protect the nerve cells. This protein is called apolipoprotein ( apoE) Everyone has this gene which helps carry cholesterol in the blood, however there is a scientific connection that it can contribute to some more predisposed for the risk of developing AD. A slow virus: Some scientists believe AD may be caused by a viral infection that takes years to develop fully. People do not catch it like other viruses. Factors such as stroke may make AD symptoms more severe. Some strokes can be prevented by treating high blood pressure. Stroke has a direct correlation on the brain, and can increase the chances of a person developing AD.4. RISK FACTORS

Risk factor

AgeHigh life expectancy. Normal aging process increases the risk of AD.

Positive family history Studies indicate that AD may be inheritable. Relatives with AD (i.e. parent or sibling) are at a risk for developing AD. Recent research has identified the presenilin 1 gene on chromosome 14 and the presenilin 2 gene on chromosome 1. Both genes appear to be strong indicators for Alzheimer Disease at an early age of onset (before the age of 65). Error! Bookmark not defined. Preliminary research has also found markers on chromosomes 9, 10 and 12 that might be linked to late-onset Alzheimer Disease (over the age of 65). Several research studies are underway collecting blood samples from people with Alzheimer Disease and their family members. These samples enable scientists to analyze DNA material within families with the intent of identifying genes that may be responsible for causing Alzheimer Disease.Error! Bookmark not defined.

Down SyndromeAlmost all individuals with Down syndrome over the age of 40 have changes to brain cells characteristic of Alzheimer Disease. In these individuals, dementia usually develops in 50's or 60's of age.

Head injurySome studies have shown that people who have had a head injury with loss of consciousness have an increased chance of developing Alzheimer disease. Research into the development of AD as a result of head injuries is ongoing.Error! Bookmark not defined. The increased risk is probably due to the upregulation of APP seen after brain trauma.

EducationSeveral studies have shown that people who have less than six years of formal education appear to have a higher risk of developing AD. Low education may reflect early experiences that were not beneficial to brain development. Higher education is thought to delay the onset of symptoms of Alzheimer Disease probably due to greater brain reserve or educational activities that may stimulate brain activity. Education as a protective factor requires more study to determine whether it is education that makes a difference or other factors related to it (e.g., income level).Error! Bookmark not defined.,Error! Bookmark not defined.

AluminumThe correlation between AD and aluminum is still under debate in the scientific community. Some studies have indicated that exposure to aluminum in drinking water may increase the chances of individuals developing Alzheimer Disease.Error! Bookmark not defined.

EstrogenResearch has been conducted on estrogen and its impact on various diseases, including AD. Current research indicates that combined estrogen therapy (estrogen plus progestin) in women over the age of 65 doubled their risk of developing Alzheimer Disease and Vascular Dementia, over a five-year period. Research continues to investigate the effects of estrogen-only therapy on cognition. Previous research has shown that women with Alzheimer Disease who were treated with estrogen showed no sign of improvement. Error! Bookmark not defined.,Error! Bookmark not defined.

Social, productive and Physical activityRecent data from the CSHA-2 (Canada Study for Health and Aging) show that regular physical activity was associated with reduced risk of AD. This information supports previous clinical trials showing exercise to benefit cognitive function. Identifying the protective effect of regular physical activity is an important finding since it may represent a relatively safe and available strategy to help prevent AD, as well as many other chronic conditions. The CSHA-2 recommends that further research still needs to be conducted in this area.Error! Bookmark not defined.

Comorbid diseasesHypertension, high cholesterol, diabetes mellitus and low estrogen may affect the development of AD. Co-morbid diseases that may affect the development of AD are being researched.Error! Bookmark not defined.,Error! Bookmark not defined.,Error! Bookmark not defined.

Other risk factors being studiedOther factors being investigated by researchers in relation to Alzheimer Disease include: Existing diseases or conditions that a person may have (such as heart disease, high cholesterol or high homocysteine levels in the blood) Toxins in the environment (such as fertilizers or pesticides) Antioxidants (such as vitamin E)Lifestyle choices (such as wine and coffee consumption, and diet)

5. PATOPHYSIOLOGY(di gambar hape) >> dr buku Shofi6. CLINICAL MANIFESTASIONS Common Changes in Mild AD Loses spark or zest for life does not start anything. Loses recent memory without a change in appearance or casual conversation. Loses judgment about money. Has difficulty with new learning and making new memories. Has trouble finding words may substitute or make up words that sound like or mean something like the forgotten word. May stop talking to avoid making mistakes. Has shorter attention span and less motivation to stay with an activity. Easily loses way going to familiar places. Resists change or new things. Has trouble organizing and thinking logically. Asks repetitive questions. Withdraws, loses interest, is irritable, not as sensitive to others' feelings, uncharacteristically angry when frustrated or tired. Won't make decisions. For example, when asked what she wants to eat, says "I'll have what she is having." Takes longer to do routine chores and becomes upset if rushed or if something unexpected happens. Forgets to pay, pays too much, or forgets how to pay may hand the checkout person a wallet instead of the correct amount of money. Forgets to eat, eats only one kind of food, or eats constantly. Loses or misplaces things by hiding them in odd places or forgets where things go, such as putting clothes in the dishwasher. Constantly checks, searches or hoards things of no value.

Common Changes in Moderate AD Changes in behavior, concern for appearance, hygiene, and sleep become more noticeable. Mixes up identity of people, such as thinking a son is a brother or that a wife is a stranger. Poor judgment creates safety issues when left alone may wander and risk exposure, poisoning, falls, selfneglect or exploitation. Has trouble recognizing familiar people and own objects; may take things that belong to others. Continuously repeats stories, favorite words, statements, or motions like tearing tissues. Has restless, repetitive movements in late afternoon or evening, such as pacing, trying doorknobs, fingering draperies. Cannot organize thoughts or follow logical explanations. Has trouble following written notes or completing tasks. Makes up stories to fill in gaps in memory. For example might say, "Mama will come for me when she gets off work." May be able to read but cannot formulate the correct response to a written request. May accuse, threaten, curse, fidget or behave inappropriately, such as kicking, hitting, biting, screaming or grabbing. May become sloppy or forget manners. May see, hear, smell, or taste things that are not there. May accuse spouse of an affair or family members of stealing. Naps frequently or awakens at night believing it is time to go to work. Has more difficulty positioning the body to use the toilet or sit in a chair. May think mirror image is following him or television story is happening to her. Needs help finding the toilet, using the shower, remembering to drink, and dressing for the weather or occasion. Exhibits inappropriate sexual behavior, such as mistaking another individual for a spouse. Forgets what is private behavior, and may disrobe or masturbate in public.

Common Changes in Severe AD Doesn't recognize self or close family. Speaks in gibberish, is mute, or is difficult to understand. May refuse to eat, chokes, or forgets to swallow. May repetitively cry out, pat or touch everything. Loses control of bowel and bladder. Loses weight and skin becomes thin and tears easily. May look uncomfortable or cry out when transferred or touched. Forgets how to walk or is too unsteady or weak to stand alone. May have seizures, frequent infections, falls. May groan, scream or mumble loudly. Sleeps more. Needs total assistance for all activities of daily living. *Adapted from Caring for People with Alzheimer's Disease: A Manual for Facility Staff (2nd edition), by Lisa P. Gwyther, 2001. Published by the American Health Care Association (1201 L Street, NW, Washington, DC 20005) and the Alzheimer's Association (919 N. Michigan Ave., Suite 1100, Chicago, IL 60611).

Early Signs finding it hard to remember things asking the same questions over and over having trouble paying bills or solving simple math problems getting lost losing things or putting them in odd places

Later signs forgetting how to brush your teeth or comb your hair being confused about time, people and places forgetting the names of common things suuch as desk, house, or apple. wandering away from home. Many other conditions such as drug interactions, reactions, depression, bacterial infections, kidney problems, and malnutrition can cause some of the same types of symptoms. Many of the secondary causes are treatable. A person with AD often feels a mixture of emotions.These include: Confusion: Many people with AD realize that something is wrong to them, and something is happening to their memory, or ability to function, but they are not sure what it is. Fear: Loss of memory and mental ability can make the world a very frightening place for these individuals. Anger: Many people feel angry about their loss of abilities and ask, Why is this happening to me? Frustration: No matter how hard people try, persons with AD just can not do all the things they used to do. Uncertainty: Because the symptoms and progress of AD vary so much, it is hard to know exactly what lies ahead for them. Grief/ Depression: Some people mourn the loss of their abilities and become increasingly depressed.

7. DIAGNOSTIC TEST & EXAMS Genetic testingResearchers have identified certain genes that increase the risk of developing Alzheimer's and other rare "deterministic" genes that directly cause Alzheimer's. Although genetic tests are available for some of these genes, health professionals do not currently recommend routine genetic testing for Alzheimer's disease.Risk genes: While there is a blood test for APOEe4, the strongest risk gene for Alzheimer's, this test is mainly used in clinical trials to identify people at higher risk of developing Alzheimer's. Carrying this gene mutation only indicates a greater risk; it does not indicate whether a person will develop Alzheimer's or whether a person has Alzheimer's. Genetic testing for APOEe4 is controversial and should only be undertaken after discussion with a physician or genetic counselor.Deterministic genes: Testing also is available for genes that cause autosomal dominant Alzheimer's disease (ADAD) or "familial Alzheimer's," a rare form of Alzheimer's that accounts for less than 5 percent of all cases. ADAD runs strongly in families and tends to begin earlier in life. Many people in these families do not wish to know their genetic status, but some get tested to learn whether they will eventually develop the disease. Some ADAD families have joined clinical studies to help researchers better understand Alzheimer's.

A new blood test called APOE (apolipoprotein E) genotyping has been used to identify individuals who carry the APOP4 gene. The presence of this gene increases a persons risk for AD and when the gene is present in a person with dementia, a diagnosis of AD is supported. This test is not recommended as a predictive test in individuals who do not have symptoms of cognitive impairment.

Neurological examDuring a neurological exam, the physician will closely evaluate the person for problems that may signal brain disorders other than Alzheimer's. The doctor will look for signs of small or large strokes, Parkinson's disease, brain tumors, fluid accumulation on the brain, and other illnesses that may impair memory or thinking.The physician will test: Reflexes Coordination, muscle tone and strength Eye movement Speech SensationNeurological testing: A patients brain functions can be tested in a number of ways. These tests would include: EEG ( electroencephalogram) CT Scan ( computerized tomography) MRI ( magnetic resonance imaging) Memory cards and evaluations Mental status testsMental status testing evaluates memory, ability to solve simple problems and other thinking skills. Such tests give an overall sense of whether a person: Is aware of symptoms Knows the date, time, and where he or she is Can remember a short list of words, follow instructions and do simple calculations

Psychological testing: A psychologist or psychiatrist determines a patients mental status by using a variety of testing, including the following: A full clinical interview Tests to determine memory loss and general mental health

The minimental state exam and the minicog test are two commonly used tests.

A. Minimental state exam (MMSE)During the MMSE, a health professional asks a patient a series of questions designed to test a range of everyday mental skills.Examples of questions include: Remember and repeat a few minutes later the names of three common objects (for instance, horse, flower, penny) State the year, season, day of the week and date Count backward from 100 by 7s or spell "world" backwards Name two familiar objects in the office as the examiner points to them Identify the location of the examiner's office (state, city, street address,floor) Repeat a common phrase or saying after the examiner Copy a picture of two interlocking shapes Follow a threepart instruction, such as: take a piece of paper in your right hand, fold it in half, and place it on the floor

The maximum MMSE score is 30 points. A score of 20 to 24 suggests mild dementia, 13 to 20 suggests moderate dementia, and less than 12 indicates severe dementia. On average, the MMSE score of a person with Alzheimer's declines about two to four points each year.

B. MinicogDuring the minicog, a person is asked to complete two tasks:1.Remember and a few minutes later repeat the names of three common objects2.Draw a face of a clock showing all 12 numbers in the right places and a time specified by the examiner

The results of this brief test can help a physician determine if further evaluation is needed.

C. Mood AssessmentIn addition to assessing mental status, the doctor will evaluate a person's sense of wellbeing to detect depression or other mood disorders that can causememory problems, loss of interest in life, and other symptoms that can overlap with dementia.

Brain imagingA standard medical workup for Alzheimer's disease often includes structural imaging with MRI or CT; these tests are primarily used to rule out other conditions that may cause symptoms similar to Alzheimer's but require different treatment. Structural imaging can reveal tumors, evidence of small or large strokes, damage from severe head trauma or a buildup of fluid in the brain.Imaging technologies have revolutionized our understanding of the structure and function of the living brain. Researchers are exploring whether the use of brain imaging may be expanded to play a more direct role in diagnosing Alzheimer's and detecting the disease early on.

8. MANAGEMENTCurrently, there is no cure or a way to prevent AD. Treatment modalities can improve the lives of some individuals with the disease. By the use of some medications it may make it easier to monitor and control some of the behavior seen with the progression of the disease progress.

Therapeutic options for Alzheimers disease :Non Pharmacologic therapyStimulation: Group activities, discussion groups, music therapy, multisensory stimulationPharmacologic therapyCholinesterase inhibitors (or cholinergics): Donepezil, rivastigmine, galantamineGlutamatergic agents: Memantine, D-cycloserineSelegilineHormone replacement therapy (estrogen)Anti-inflammatory drugs (NSAIDs)Antioxidant therapiesVitamin E Nootropic DrugsGinko BilobaNicergoline PiracetamTherapy for psychiatric symptoms : behavioural disturbances, mood disorders, agitation with dementia (e.g. delirium, depression, psychosis, insomnia, sundowning, aggression or anger, osteoarthritic pain)

TACRINE (cognex) and DONEPEZIL ( aricept) are prescription drugs that can help slow the development of mild or moderate AD in some cases. But be aware, there are no drugs that are without side effects. Anticholinesterase drug for example is Aricept.Anticholinesterase inhibitors are a class of drugs used to treat dementia associated with Alzheimer's disease. This class of drugs works by increasing the amount of a chemical called acetylcholine in the brain. This may reduce the symptoms of dementia associated with Alzheimer's disease but does not cure it. The safety of this drug during pregnancy or lactation in humans has not been established. therefore, usage in women who may become pregnant requires weighing the drug's potential benefit against its possible hazards to mother and child.Patients may develop "antocholinesterase insensitivity" for brief or prolonged periods. During these periods the patients should be carefully monitored and may need respiratory assistance. Dosages of antocholinesterase drugs should be reduced or withheld until patients again become sensitive to them.Side effects : Anticholinesterases cause a build up of ACh that results in potentiation of its effects at muscarinic receptors. This can cause bradycardia, miosis, GI upset, nausea, bronchospasm, increased bronchial secretions, sweating and salivation. For this reason an antimuscarinic such as glycopyrronium or atropine must be administered along with the anticholinesterase to minimise these effects.Other drugs, such as prescription tranquilizers and antidepressants, can help reduce anxiety, control outbursts and improve mood. By leveling out the dopamine and serotonin levels in the brain, it is believed to have a positive effect fro those with AD.

Some doctors have used vasodilators to help increase the blood flow to the brain, in an attempt to help relieve some symptoms. There is some evidence that suggests that inflammation in the brain may contribute to AD damage. Scientists believe that the use of NSAIDs (non steroidal antiinflammatory drugs) may help relieve some of the swelling, which in turn may improve symptoms. The use of NSAIDs do not slow down the disease progression, but may help make the person more comfortable with AD.

There has been research done regarding the use of Vitamin E, which has been said and documented that delay in progression may be as much as 7 months. Physical activity can help reduce anxiety and restlessness. A person should consult a health care provider before beginning an exercise program. A varied diet can keep resistance high and prevent;- Digestive problems- Dehydration- Malnutrition- Vitamin and mineral deficiencies

A positive attitude by both the patient and the families is an important part of treatment.

9. COMPLICATIONSOn average, people with Alzheimer's disease live four to six years after diagnosis, butsome survive as long as 20 years. Pneumonia is a common cause of death becauseimpaired swallowing allows food or beverages to enter the lungs, where they cancause an infection. Other common causes of death include complications from urinarytract infections and falls.

10. NURSING CARE1.Kerusakan memori b/d gangguan neurologis ditandai dengan penyakit yang diderita2.Konfusi kronis b/d penyakit Alzheimer ditandai dengan gangguan memori jangka panjang dan tdk terjadi perubahan tingkat kesadaran3.Defisit perawatan diri : berpakaian b/d gangguan neuromuskular ditandai dengan ketidakmampuan memilih pakaianchronic confusion r.f Alzheimers diseaseObjectivesOutcomesIntervetionRational

Altered interpretation and response to stimuli

No change on level of consciousnessAbility to execute complex mental processesAbility to identify person, place, timeAbility to choose between two or more alternativesAbility to cognitively retrieve and report previously stored informationProvision of a modified environment for the patient who is experiencing a chronic confusional state

Facilitating family participation in the emotional and physical care of patient.Obtain information about past and present patterns of behaviorMonitor cognitive functioning using a standardized assesment tool (eg. MMSE)Determine physical, social, and psychologic history of patient before the onset of confusion; usual habits and routinesMonitor nutrition and weightMonitor carefully for psychologic causes of increased confusion that may be acute and reversibleFamily teaching:Teach patient and significance others about patients medicationsExplain the effect of the patients illnessInclude family members in planning, providing, and evaluating care to the extent desireddCollaborative:Adminisster medicationsRefer to social services department for referral to day care programs, meals on wheel, respite care, and so forthProvide a low-stimulation environmentIdentify and remove potential dangers in environment for patientPlace identification bracelet on patientPrepare for interaction with eye contact and touch, as appropriate

dressing self-care deficit r.f cognitive impairment, neuromuscular impairment, perceptual impairmentObjectivesOutcomesInterventionRationa

Patient can dress independently,Choose clothes and obtain them from closet or drawersBe able to remove clothing, socks, and shoesAbility to dress selfChoosing, putting on, and removing clothes for a person who cannot do this for selfAssisting patient with clothesMonitor energy level and activity intoleranceMonitor for sensory, cognitive, or physical deficits that may make dressing difficult for the patientFamily/patient teaching:Demonstrate use of assistive devices and adaptive activitiesInstruct patient in alternative methods for dressingAccomodate cognitive deficits-help patient choose clothing that is loose fitting and easy to put onProvide patients clothes in accessible areaMaintain privacy while the patient is dressing

Impaired memory r.f neurological disturbancesObjectivesOutcomesInterventionsRational

Patient will accurately recall immediate, recent, and remote informationVerbalize being better able to rememberCognitive orientation : ability to identify person, place, and timeMemory: ability to cognitively retreive and report previously stored informationMemory training: facilitating of memoryAssess neurologic function to determine whether patient has memory loss only or also has problems, such as dementiaExplain to the patient that short-term memory loss frequently occurs with agingLabel items to increase recallDo not rearrange furniture in the room or the patients homeHelp the patient to relax in order to improve concentrationStimulate memory by repeating patients last expressed thought as appropriate

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O'Connor, Dominic. 2006. Pharmacology of Neuromuscular Blocking Drugs and anticholonesterase. http://www.anaesthesiauk.com/documents/PharmacologyNMBDsandAnticholinesterasesFinal.pdf accessed on December 5th 2011 at 9:56

Price, Sylvia A., Wilson, Lorraine M. 2006. PATOFISIOLOGI; Konsep Klinis Proses-Proses Penyakit. Edisi 6. Volume 2. Jakarta : Penerbit Buku Kedokteran EGC.Wilkinson, judith M. 2005. Prentice hall nursing diagnosis handbook with NOC Interventions and NOC outcomes. 8th ed. New jersey : pearson prentice hall