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ALZHEIMER’S DISEASE: A Study of Alzheimer’s Disease Pathology and Nursing Management of Unmet Needs  By Jennifer Krueger, RN, BSN Alverno College, MSN.

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Presentation on theme: "ALZHEIMER’S DISEASE: A Study of Alzheimer’s Disease Pathology and Nursing Management of Unmet Needs  By Jennifer Krueger, RN, BSN Alverno College, MSN."— Presentation transcript:

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2 ALZHEIMER’S DISEASE: A Study of Alzheimer’s Disease Pathology and Nursing Management of Unmet Needs  By Jennifer Krueger, RN, BSN Alverno College, MSN 621 April 29, 2010

3 Click on the icon in the lower left corner of each slide to return to the Table of Contents page at any time. Only use the left or right arrows located in the upper right hand corner of each slide, to progress to the next slide or return to the previous slide. To navigate throughout this tutorial: Table of Contents (Unless specifically indicated, images were obtained from Microsoft Clipart, 2011)

4 CASE STUDY--Rosie Meet, Rosie! Rosie is 84 years old and lives with her daughter, son-in-law, and two grandchildren. She moved in with her daughter six months ago, after her husband passed away. While Rosie is in excellent physical health, her family has noticed some changes in her personality and decision- making skills. Throughout this tutorial, you will answer questions about Rosie as they relate to each section. When you come to a slide with Rosie’s picture, answer the question. Then click the forward arrow in the upper right corner of the slide to continue.

5 LEARNING OBJECTIVES:  Explain the basic pathology of Alzheimer’s Disease including the influence of stress, inflammation, aging and genetics.  Recognize challenging behavior as communication of unmet needs.  Identify nursing interventions that will influence/reduce challenging behaviors in patients with Alzheimer’s Disease.

6 TABLE OF CONTENTS Click on a box to find out more about each topic…

7 JUST THE FACTS Did You Know? Alzheimer’s Disease is the most common cause of dementia in older adults; 60-80% of all cases. (Omnicare, 2010) Approximately 13% of all persons older than 65 years old have Alzheimer’s Disease. (Omnicare, 2010) In 2008 5.2 million people were affected by Alzheimer’s Disease. (Omnicare, 2010) The risk of developing the disease increases with age, and approximately 50% of all people over the age 85 have Alzheimer’s Disease. ( Porth and Maftin, 2009) Currently, there are no specific diagnostic tests to diagnose Alzheimer’s Disease; diagnosis is made by excluding other possible causes of dementia symptoms. (Porth and Maftin, 2009)

8 JUST THE FACTS Did You Know? Weight of brain decreases. Neuron loss, mostly in the cortex in the superior temporal area. Neurons atrophy with changes in neurotransmission. Despite changes, cognitive abilities remain intact. Changes in personality or cognitive deficits are considered not normal in the older adult. Many times, plaques and tangles associated with Alzheimer’s Disease are found in older adults with no cognitive impairment. (Porth and Maftin, 2009) There are normal a changes in the brain, associated with aging…

9 JUST THE FACTS What Is Alzheimer’s Disease? A disease involving neuropathic and neurotransmitter changes. A disease causing cortical atrophy with loss of neurons particularly in the parietal and temporal lobes of the brain. A progressive disease leading to death within 8 to 10 years after diagnosis. Ranges in stages of very mild cognitive decline to very severe cognitive decline. (Image credit : Jannis Productions, Stacy Jannis. Picture used with permission from the Alzheimer’s Association) (Porth and Maftin, 2009) (Alzheimer’s Association, 2011)

10 JUST THE FACTS Stages Of Alzheimer’s Disease No Impairment. Person does not show any signs and symptoms to a medical professional or family members. Very Mild Cognitive Decline. Patient may feel like they have memory lapses, forgetting familiar words or objects. Family, friends and medical professionals do not detect any signs or symptoms. Mild Cognitive Decline (Early-stage). Family and friends may start noticing problems with name-finding, planning or organizing. A medical professional may detect problems with memory or concentration. Moderate Cognitive Decline (Mild or early-stage). A careful medical interview should be able to detect problems in several areas including, knowledge of current events, impaired ability to perform challenging mental arithmetic (counting backward from 75 by 7s), managing finances, memory of personal history, may be moody and withdrawn. Click on each stage to learn more…. (Stages are as defined by the Alzheimer’s Association) (Alzheimer’s Association, 2011) (Porth and Maftin, 2009)

11 JUST THE FACTS Stages Of Alzheimer’s Disease Moderately Severe Cognitive Decline (Moderate or mid-stage). Major gaps in memory and cognitive function. Will need some assistance with day to day activities. Will not remember address or phone numbers. Able to remember significant details about self and is usually able to use the toilet and feed self. Severe Cognitive Decline (Moderately severe or mid-stage). Memory continues to worsen. Significant changes in personality may emerge. Will need help with dressing, toileting; may be incontinent. Tends to wander or get lost. Very Severe Cognitive Decline (Severe or late-stage). Final stage of disease. Loses all ability to respond to their environment, including the ability to speak and control movement. Click on each stage to learn more….(Stages are as stated by the Alzheimer’s Association) (Alzheimer’s Association, 2011) (Porth and Maftin, 2009)

12 JUST THE FACTS Let’s Review! Two years ago, Rosie started to feel like she was forgetting simple things; birthdays, phone numbers and names of friends. Since moving in with her daughter, Rosie has been choosing inappropriate clothing for the season and is refusing to participate in her normal social activities. She seems moody at times and has been forgetting to take her daily medications. Rosie is most likely in what stage of Alzheimer’s Disease: Click on the correct shape below! Sorry, try again! Rosie’s cognitive ability is affected. Stage 1, is “No, Impairment”. Sorry, try again! Rosie’s impairment is not as severe as Stage 7. Sorry, try again! Rosie’s impairment is not as severe as Stage 5. You’re Correct! Rosie is most likely in the early stages of Alzheimer’s Disease.

13 PATHOPHYSIOLOGY Anatomy 101: The Brain Roll Over Each Lobe To Find Out! (Porth and Maftin, 2009) (Image credit: Alzheimer’s Disease Education and Referral Center, NIA. Picture used with permission from the Alzheimer’s Association) What area does what?

14 PATHOPHYSIOLOGY Anatomy 101: A Brain Cell Neuron: A brain cell affected by Alzheimer’s Disease Click on a box to label the parts of a neuron! Axon: The extension from the neuron cell body that takes information away from the cell body. Cell Body (S0ma): The part of the cell that contains the nucleus. Dendrite: Extensions from the neuron cell body that takes information to the cell body. The three main parts of a neuron: (Porth and Maftin, 2009)

15 PATHOPHYSIOLOGY Pathological Aspects The major pathological features of Alzheimer’s Disease are the presence of neuritic plaques, neurofibrillary tangles, and amyloid angiopathy. Click on a box to learn about each feature contributing to the progression of Alzheimer’s Disease. (Porth and Maftin, 2009)

16 PATHOPHYSIOLOGY Pathological Aspects Neuritic plaques are clusters of protein fragments, arranged around a central amyloid core. The most common type of deposits have fragment residues of 40-42 amino acids in length. Plaques are associated with degeneration of neurons at the synaptic junction, affecting cell to cell communication. As Alzheimer’s Disease progresses, plaque formation increases. (Porth and Maftin, 2009) (Wippolid, Carins, Vo, Holtzmann and Morris, 2007)

17 PATHOPHYSIOLOGY Pathological Aspects Are primarily composed of a protein called Tau wound around each other in a helical fashion. They are resistant to chemical or enzymatic breakdown and remain in brain tissue after the neuron dies. Tangles destroy cell transport systems leading to neuron death. Tangles have also been identified in other forms of dementia, although usually without plaque formation, as found in Alzheimer’s Disease. The relationship between tangles and plaques is not completely understood. (Alzheimer’s Association, 2011) (Lippens, Sillen, Landrieu, Amniai, Sibille, Babier, Leroy, Hanoulle & Wiersuzeski, 2007) (Wippolid, Garins, Vo, Holtzmann and Morris, 2007) (Porth and Maftin, 2009)

18 PATHOPHYSIOLOGY What About Tau? Tau protein is important in the structural stabilization of nerve cells, allowing transport of necessary proteins and enzyme-containing vesicles essential for cell maintenance and function. Tau is only present in neurons. Too much or too little Tau leads to neuronal dysfunction. If Tau collapses, as it does in Alzheimer’s Disease, it twists into helical strands becoming neruofibillary tangles. When tangles form, cells begin to die. (Alzheimer’s Association, 2011) (Lippens et al, 2007) (Wippolid et al, 2007)

19 PATHOPHYSIOLOGY Pathological Aspects There are many types of amyloid proteins present in the body; B-amyloid is unique to the brain. B-amyloid is a protein fragment that is snipped from a larger protein called Amyloid Precursor Protein (APP) which is associated with the cell membrane. APP processing can follow two pathways, benign and harmful. As the harmful pathway progresses, B-amyloid protein fragments start sticking together forming oligomers. Oligomers start to grow larger becoming protofibrils and fibrils; eventually other proteins and material are added forming neuritic plaques. (Menon and Lutsep, 2010) (Porth and Maftin, 2010) Click on each arrow below to progress the amyloid pathway to neuron death!

20 PATHOPHYSIOLOGY Pathological Aspects Click on the video to learn more ! (Retrieved from YouTube, 2011 and embedded with permission of the Alzheimer's Disease Education and Referral Center, a service of the National Institute on Aging, 2008). "

21 PATHOPHYSIOLOGY Pathological Aspects What does this all mean? Eventually, plaques and tangles spread to large portions of the brain causing severe atrophy and cortical damage. As plaques and tangles accumulate, neurons die. The cortex of the brain atrophies, initially damaging areas involved in thinking, planning and remembering. As the disease progresses, the parietal and temporal lobes of the brain are particularly affected; these areas are related to communication and interpretation of sensory input. (Alzheimer’s Association, 2011) (Porth and Maftin, 2009) Tangle and plaque involvement are represented by shaded blue areas. Images credit: Alzheimer’s Disease Education and Referral Center, NIA. Picture used with permission from the Alzheimer’s Association.)

22 PATHOPHYSIOLOGY Let’s Review! Sorry, try again! Confusion is a symptom of AD. Dehydration is not a major factor contributing to the progression of AD. You’re Correct! Neuritic plaques, neurofibrillary tangles and amyloid processing are the 3 major factors contributing to Alzheimer’s Disease. Sorry, try again! Of these three, only neuritic plaques is a factor contributing to AD. Sorry, try again! Falling is not a major factor contributing to the progression of a AD. Rosie has Stage 4 Alzheimer’s Disease. What three major factors contribute to the progression of her symptoms? A.Neurofibrillary tangles, confusion and dehydration. B. Neuritic plaques, neuron repair and synapse junctions. C.Neuritic plaques, neurofibrillary tangles and amyloid processing. D. Amyloid angiopathy, neuritic plaques and a history of falling.

23 PATHOPHYSIOLOGY Let’s Review! A.Neuritic plaques B.Amyloid Precursor Protein C. A-amyloid D. B-amyloid Inside Rosie’s brain, neurofibillary tangles are forming. Which protein fragment may be snipped from the larger APP, eventually leading to the formation of oligomers? Sorry, try again! Neuritic plaques are formed from clusters of protein fragments. Sorry, try again! Alpha amyloid is Not correct. Sorry, try again! Amyloid Precursor Protein is APP. You’re Correct! B-amyloid fragments may form oligomers that eventually form neuritic plaques, in people with AD.

24 IMMUNE AND STRESS RESPONSE Alzheimer’s Disease and the IMMUNE RESPONSE… What is the IMMUNE RESPONSE? (Porth and Maftin, 2009) “The collective response of cells and molecules of the Immune System” (Porth and Maftin, 2009). The Immune System includes: 1. Innate and Adaptive immunity (barriers to microbes/antigen recognition). 2. Cells ( Leukocytes, Lymphocytes, and Dendritic Cells). 3. Cytokines (Proteins that stimulate cells of the immune system to respond).

25 IMMUNE AND STRESS RESPONSE Alzheimer’s Disease and the IMMUNE RESPONSE An activated IMMUNE RESPONSE will begin the INFLAMMATORY PROCESS. There are two types of inflammatory process: Acute: Short in duration. Characterized by exudate seeping into tissues, heat, swelling, pain. Chronic : Long in duration, lasting days to years. Presence of WBC’s, fibrosis and tissue necrosis. (Porth and Maftin, 2009)

26 IMMUNE AND STRESS RESPONSE Alzheimer’s Disease and the IMMUNE RESPONSE…. The exact role the IMMUNE RESPONSE plays in AD is still uncertain; however it has been attracting attention in research in four ways: 1.As a first responder to initial pathological AD events. 2. Assisting in clearing of the toxic by-products of APP processing. 3. Provider of protection to neurons. 4. As a possible target for treatment strategies. (Cohen, 2009)

27 IMMUNE AND STRESS RESPONSE Alzheimer’s Disease and the IMMUNE RESPONSE Microglia are immune cells of the Central Nervous System (CNS). They are considered to be in a “resting state” until activated. Upon CNS injury, microglia are triggered from the substances released from the damaged tissue. Activated microglia release growth factors, anti-inflammatory factors, and protective substances (cytokines) to restore damaged tissue. Facts about “Microglia”; the first responders to initial Central Nervous System damage…. (University of Washington, 2008) Here

28 IMMUNE AND STRESS RESPONSE Alzheimer’s Disease and the IMMUNE RESPONSE Microglia immune response contributes to the progression of Alzheimer’s Disease, although exact contributions are not really known. In people with Alzheimer’s disease microglia are found in close association with B-amyloid. Microglia respond to abnormal APP processing by assisting in the clearing of toxic by-products. Their role in the CNS may be far more complex than previously appreciated. Microglia and Alzheimer’s Disease… (Cohen, 2009) (Mandrekar-Colucci and Landreth, 2010)

29 IMMUNE AND STRESS RESPONSE Alzheimer’s Disease and the STRESS RESPONSE What is the STRESS RESPONSE? Stress is a state of symptoms arising from the “coordinated activation of the neuroendocrine and immune system” (Porth and Maftin, 2009). It was first described by Hans Selye, an endocrinologist in the 1930’s. He called it the General Adaptation Syndrome (GAS). Activating the GAS releases hormones and neurotransmitters alerting the body to stressors. Adaptations are made within the body to return it to a balanced state. (Porth and Maftin, 2009)

30 IMMUNE AND STRESS RESPONSE Let’s Review! A. Neurons B.B-amyloid C. Monocyte D. Microglia Sorry, try again! Neurons are brain cells. Sorry, try again! Monocytes are white blood cells related to Microglia. Sorry, try again! B-amyloid is a protein fragment. You’re Correct! Microglia clear toxic by-products of APP processing. Which type of cell inside Rosie’s Central Nervous System clear toxic by-products of APP processing?

31 IMMUNE AND STRESS RESPONSE Let’s Review! A.Immune and Stress B.Digestive and Immune C. Skeletal and Stress D. Neurological and Respiratory Sorry, try again! This is not correct. Sorry, try again! This is not correct. Sorry, try again! This is not correct. You’re Correct! Although how, is not exactly known! Inside Rosie two complementary systems are triggered in the pathology of AD. Which two systems are involved?

32 GENETICALLY SPEAKING Early-Onset Late-Onset  Rare; only 5% of all people who have AD.  Develops in people ages 30-60 years old.  Some cases of early-onset AD are inherited; they are called Familial AD (FAD).  FAD is caused by gene mutations on specific chromosomes 21, 14, and 1.  These mutations form abnormal amyloid precursor protein (APP), causing increased amounts of B- amyloid.  If a person inherits either chromosomes, 21,14, or 1 they will almost always develop AD.  Most cases of AD are Late-Onset.  Develops after age 60.  Gene mutations found in early-onset are not found in late-onset.  A specific gene for late-onset has not been identified.  A pre-disposing genetic risk does exist related to, apolipoprotein E (APOE) gene, found on chromosome 19. Alzheimer’s and Genetics There are two types of Alzheimer’s Disease, early-onset and late onset; both have genetic links: (National Institute of Aging, 2008 )

33 GENETICALLY SPEAKING Genetic Research and Alzheimer’s Disease Research in AD genetics has intensified regarding questions related to “What makes the disease process begin?” and “What role do AD risk-factor genes interacting with other genes, lifestyle and/or environmental factors affect the risk of developing AD?” Focuses on prevention and treatments. Scientist believe four to seven more AD risk-factor genes exist and are working to discover them. A major goal is to develop accurate reliable screening tests; however they may never be able to predict with 100% accuracy. (National Institute of Aging, 2008)

34 GENETICALLY SPEAKING Let’s Review! A.Chromosome 21. B. APOE gene. C.Amyloid Precursor Protein (APP). D. Chromosome 1. Sorry, try again! Chromosome 21 is related to early-onset AD. Sorry, try again! APP is related to the formation of tangles found in both late & early-onset AD. Sorry, try again! Chromosome 1 is related to early-onset AD. You’re Correct! APOE gene has been identified as a risk factor gene related to late-onset AD. Rosie has late-onset Alzheimer’s Disease. What predisposing risk factor gene may have interacted with lifestyle and environmental factors increasing Rosie’s chances of developing Alzheimer’s Disease?

35 WHAT ARE CHALLENGING BEHAVIORS? “People only see what they are prepared to see….” (Ralph Waldo Emerson ThinkExist.com, 2011) Problem Behaviors Rosie’s has progressed to Stage 6 of Alzheimer’s Disease. She started to wander from home and became very verbally abusive. Her family was no longer able to care for her at home and placed her in a long-term care facility. Nursing staff has reported Rosie to be verbally abusive, fearful, and combative with bathing. She also continually calls out “ I want to go home!”. Challenging Behaviors What Do You See?

36 WHAT ARE CHALLENGING BEHAVIORS? What are typical CHALLENGING BEHAVIORS exhibited by people who have Alzheimer’s Disease? (Alzheimer’s Association,2011)

37 WHAT ARE CHALLENGING BEHAVIORS? In long-term care settings CHALLENGING BEHAVIORS might be exhibited… (Alzheimer’s Association,2011)

38 WHAT ARE CHALLENGING BEHAVIORS? Why do CHALLENGING BEHAVIORS occur? May be related to deterioration of brain due to disease pathology in areas that regulate impulse control, emotions and sensory processing. May be related to pain that can be felt, but not articulated or specifically identified. May be related to an underlying medical condition, like a urinary tract infection or pneumonia. May be related to side effects of medications. May be triggered by environmental conditions, for example lighting, noise or agitated behaviors of others. (Alzheimer’s Challenging Behavior Task Force, 2010) Click on the picture to find out!

39 WHAT ARE CHALLENGING BEHAVIORS? Whatever the source, a caregiver’s response may improve or make the behavior worse. In this way, “behaviors are best seen as a dynamic interaction between the person with dementia, the caregiver and the specific environment.” (Alzheimer’s Challenging Behavior Task Force, 2010)

40 WHAT ARE CHALLENGING BEHAVIORS? Let’s Review! A.Caregiver’s response to the bathing experience. B.Progression of AD affecting Rosie’s Parietal and Temporal lobes of her brain. C.Environment of shower room, including lighting, sounds and temperature. D. All of the above. Sorry, try again! This could be a contributing factor. Sorry, try again! This could be a contributing factor. Sorry, try again! This could be a contributing factor. You’re Correct! All of these factors could be influencing Rosie’s behavior. Since moving into the long-term care facility, Rosie’s challenging behavior of yelling and resisting bathing has worsened. What factors may be affecting her behavior?

41 NURSING MANAGEMENT OF UNMET NEEDS What are unmet needs? “When behavioral symptoms are unnoticed, dismissed or not understood as symptoms of unmet needs, the needs of the older person with dementia are missed…” (Kovach et al, 2006). Physical Needs: Pain, illness, hunger, thirst, constipation, fatigue, response to incontinence, side effects related to medications, impaired vision or hearing. Affective Needs: Intolerance of environmental stressors (overstimulation from noise, lighting, etc.), boredom, loneliness, balance of sensory-stimulating verses sensory-calming activities, meaningful human interaction. (Alzheimer’s Association, 2011) (Alzheimer’s Challenging Behaviors Task Force, 2010) (Kovach, C., Logan, B., Noonan, P., Schlidt, A., Smierz, J., Simpson, M., & Wells, T., 2006)

42 NURSING MANAGEMENT OF UNMET NEEDS “….failure to recognize behavior as symptoms leads to the under treatment of many needs.” (Kovach et al, 2006). What is YOUR response? Do you CONSISTENTLY DO A COMPLETE PHYSICAL ASSESSSMENT with anyone experiencing behavioral problems, especially when symptoms appear suddenly? Do you DISMISS BEHAVIOR SYMPTOMS, as “typical or normal behavior” for that person? Do you CONSIDER ENVIRONMENTAL STRESSORS OR PHYSICAL NEEDS WITH anyone experiencing behavior problems? Do you CONSIDER PERSONAL PREFERENCES with every activity? (What did the person enjoy/like prior to be moved to the facility? (Alzheimer’s Challenging Behavior Task Force, 2010) (Alzheimer’s Association, 2011) (Kovach et al, 2006)

43 NURSING MANAGEMENT OF UNMET NEEDS Possible BARRIERS…. (Alzheimer’s Challenging Behavior Task Force, 2010) (Simpson, Stevens, & Kovach, 2007)

44 NURSING MANAGEMENT OF UNMET NEEDS “It takes an average of 23 minutes to manage disruptive behaviors. Agitated behaviors are contagious, so it is advantageous to get them under control as soon as possible” (Alzheimer’s Challenging Behavior Task Force, 2010). To manage a CHALLENGING BEHAVIOR…. (Kovach et al, 2006) Assess for physical needs and intervene as necessary: Pain Thirst Physical illness Hunger Constipation Incontinence Vision Hearing

45 NURSING MANAGEMENT OF UNMET NEEDS “It takes an average of 23 minutes to manage disruptive behaviors. Agitated behaviors are contagious, so it is advantageous to get them under control as soon as possible” (Alzheimer’s Challenging Behavior Task Force, 2010). To manage a CHALLENGING BEHAVIOR…. (Kovach et al, 2006) Assess for affective needs and intervene as necessary: Environment (lighting, noise level, movement) Overstimulation/Understimulation Boredom Loneliness Need for human contact Fear New or different staff

46 NURSING MANAGEMENT OF UNMET NEEDS “It takes an average of 23 minutes to manage disruptive behaviors. Agitated behaviors are contagious, so it is advantageous to get them under control as soon as possible” (Alzheimer’s Challenging Behavior Task Force, 2010). To manage a CHALLENGING BEHAVIOR….adapt YOUR response: Stop the activity that could be contributing to the behavior. Try to distract with something enjoyable. Stay calm. Don’t argue. Respond to the emotions underlying the behavioral need. Ask yourself, “If safety is not an issue, can the behavior be accepted?” (Alzheimer’s Association, 2011) (Kovach et al, 2006)

47 NURSING MANAGEMENT OF UNMET NEEDS To manage a CHALLENGING BEHAVIOR…. Person-Centered Care: “Care provided according the residents’ needs, desires and preferences” (Alzheimer’s Challenging Behaviors Task Force, 2010). Adapting the environment by encouraging “a continuous process of listening, trying new things, seeing how they work and changing in an effort to individualize care” (Alzheimer’s Challenging Behaviors Task Force, 2010). “Person-Centered care seeks to maximize choice and autonomy, and thus can reduce the presence of challenging behaviors” (Alzheimer’s Challenging Behaviors Task Force, 2010). Likes to go to bed 22:30pm. Prefers waking up at 9:30. Does not like showers, baths only. Coffee, black, 2 sugars. Likes gardening, and quilting.

48 NURSING MANAGEMENT OF UNMET NEEDS Let’s Review! A.Ensure Rosie’s showering routine is designed around her preferences. B.Assess Rosie for physical needs, specifically pain. C.Stop the shower and stay calm. D. All of the above. Sorry, try again! You’re Correct! Assessing for pain, stopping the shower, staying calm and being person-centered may meet Rosie’s unmet needs. The next time Rosie becomes verbally abusive at her care-givers while being given a shower, the nurse should…

49 NURSING MANAGEMENT OF UNMET NEEDS Let’s Review! A.Call Rosie’s physician and ask them to increase the dosage of Rosie’s scheduled anti-psychotic. B.Plan to dismiss Rosie’s behavior as normal. C.Identify Rosie’s challenging behavior as an unmet need and be prepared to assess both physical and affective stressors. D. Insist with Rosie she needs to stop behaving this way. Sorry, try again! This should not be your first choice. Sorry, try again! By dismissing Rosie’s behavior as normal, you may miss an unmet need. Sorry, try again! Arguing with Rosie may make the situation worse. You’re Correct! Rosie’s challenging behavior may be related to an unmet need, like pain. As Rosie’s nurse, what can you do to affect Rosie’s possibility of exhibiting future, challenging behaviors?

50 REFERENCES Alzheimer’s Association. (2011). The challenging behaviors of Alzheimer’s disease. Portland, OR: Author. Alzheimer’s Association. (2011). Stages of Alzheimer’s disease. Retrieved from http://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp Alzheimer’s Association. (2011). Inside the brain: An interactive tour. Retrieved from http://www.alz.org/alzheimers_disease_4719.asp Alzheimer’s Challenging Behaviors Task Force (2010). Handcuffed. Milwaukee, WI: Author. Cohen, R. (2009). The role of the immune system in Alzheimer’s disease. Focus, The Journal of Lifelong Learning in Psychiatry, 7 (1), 28-35. Kovach, C., Logan, B., Noonan, P., Schlidt, A., Smierz, J., Simpson, M., & Wells, T., (2006). Effects of the serial trial intervention on discomfort and behavior of nursing home residents with dementia. American Journal of Alzheimer’s Disease and Other Dementias, 21 (3), 147-155. Lippens, G., Sillen, A., Landreau, I., Amniai, L., Sibille, N., Barbier, P., Leroy, A., Hanoulle, X., & Wieruszeski, J., ( 2007). Tau aggregation in Alzheimer’s disease. Prion, 1 (1), 21-25. Mandrekar-Colucci, S., Landreth, G., (2010). Microglia and inflammation in Alzheimer’s disease. CNS & Neurological Disorders Drug Targets, 9. Retrieved from http://www.biomedsearch.com/nih/Microglia-Inflammation-in-Alzheimers-Disease /20205644.html

51 REFERENCES Menon, R. and Lutsep, H. (2011). Cerebral amyloid angiopathy. Retrieved from http:// emedicine.medscape.com/article/1162720-overview. National Institute on Aging. (2008). Alzheimer’s disease genetics fact sheet (NIH Publication No. 08-6424). Washington, DC: U.S. Government Printing Office. National Institute on Aging. (2008). Inside the brain: Unraveling the mystery of Alzheimer’s disease. Retrieved from http://www.youtube.com/watch?v=NjgBnx1jVIU Omnicare. (2010). Geriatric pharmaceutical care guidelines. Covington, KY: Omnicare, Inc. Porth, C. and Matfin, G. (2009). Pathophysiology: Concepts of altered health states. Philadelphia, PA: Wolters Kluwer Health/ Lippencott Williams & Wilkins. Simpson, M., Stevens, P. & Kovach, C. (2007). Nurses’ experience with the clinical Application of a research-based nursing protocol in a long-term care setting. Journal of Clinical Nursing, 16, 1021-1028. Think Exist. (2011). Ralph Waldo Emerson. Think Exist.com. Retrieved from http://thinkexist.com/quotation/people_only_see_what_they_are_prepared_ to see/14514.html University of Washington. (2008). Microglia. Retrieved from http://faculty. Washington. edu/moeller/microglia.shtml

52 REFERENCES Wippolid, F., Carins, N., Vo, K., Holtzmann, D., & Morris, J., (2007). Neuropathology for the neuroradiologist: Plaques and tangles. American Journal of Neuroradiology 29 (1), 18-22.


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