10/4/2016 Challenges of Geriatric Patients Nurse Practitioners of - PDF document

10/4/2016 Challenges of Geriatric Patients Nurse Practitioners of Oregon 39 th Annual Education Conference DATE: October 14, 2016 PRESENTED BY: Laura M. Bryant, M.S.N., R.N. Director: Tuality Center for Geriatric Psychiatry AMYLOID PLAQUES Found in the spaces between the brain’s nerve cells. They consist largely of insoluble deposits of a toxic protein peptide: Beta-amyloid. Research has discovered that some people develop plaque with the aging process. The Alzheimer’s Dementia brain has many more plaques. It is still unknown if plaques cause Alzheimer’s Dementia or are a byproduct of the disease process. NEUROFIBRILLARY TANGLES Abnormal collections of twisted protein threads found inside nerve cells. Major component of tangles is a protein called Tau. 1

10/4/2016 TAU: Rhym es with WOW Found mostly in neurons, are proteins that stabilizes microtubules and are important in maintenance of cellular structure. In healing areas, tau is found in multiples areas of the body, organized in orderly parallel strands and helps food molecules travel along tracks. Tau can misfold or collapse into twisted strands called tangles, “tracks” then fall apart and disintegrate. (similar to prior protein-viral type illness. Note: TBI, concussions, CTE (chronic traumatic encephalopathy) The old versus the new Dementia(a catch all) verses neuropsychiatric neurocognitive disorder Dementia: senility, hardening of the arteries, senile dementia dates back to ancient Greek philosophers. 1906 Dr. Alois Alzheimer links symptoms of microscopic brain changes to his famous Auguste D. Case. He discovered: memory loss, unfounded suspicions about her family; found dramatic shrinkage and abnormal deposits in nerve cells. 1910 Alzheimer's disease named 1931 The electron microscope was invented 2

10/4/2016 1968 Development of cognitive measurement scale: Researchers develop the first validated measurement scale for assessing cognitive and functional decline in older adults 1974 National Institute of Aging Founded The primary federal agency supporting Alzheimer’s research. 1984 Beta-amyloid Identified A novel cerebrovascular amyloid protein Chief component of Alzheimer’s brain plaques Prime suspect in triggering nerve cell damage 1986 Discovered “Tau protein” 1987 First determinate gene identified. 1993 First Alzheimer’s risk factor gene identified APOE-e4 – Raises risk for disease but is not determinate who will develop the disease 2004 Initiative to establish standards for brain imaging. 2011 United States establishes the framework for a national strategic plan to coordinate responses including research, care and support ** The difficulty in diagnosing is that most testing can only be conclusive during autopsy. 3

10/4/2016 • Interference with ability to function at work or usual activities • Functional decline • No delirium or psychiatric disorder. • Cognitive impairment- history, mental status, neuro-psych testing • • Memory and Impaired Impaired Language  Common words Reasoning  safety  Spelling  Finances • Changes in behavior (mood  poor decisions agitation, apathy, sexualized  inability to do complex or behavior, profanity) • sequential activities Aggression • Impaired visuospatial ability • Executive function impaired (aren’t able to recognize faces, reasoning judgment and problem common objects, find things, solving (non-Amnesic) orient their clothes. • Alzheimer's Dementia: 50-70 % • Vascular Dementia: 25% • Dementia with Lewy Bodies: 15% • Frontotemporal Lobe Dementia: 5-8% • Creutzfeldt-Jakob disease • Huntington’s Disease • 20% of young onset • Alcohol related Dementia • Wernicke-Korsakoff syndrome • Parkinson’s Disease Dementia 4

10/4/2016 It is Progressive… Degenerative… Irreversible • Three General Stages • Mild (Early Stage) • Moderate (Middle Stage) • Severe (Late Stage) Longer course 1-10 (or 2-7, or 3-6?) The most prevalent brain cerebral atrophy (progressive loss of brain cells- entire brain or parts, reduced brain masses, shrinkage.) Causes of Alzheimer’s Dementia are unknown • There is a belief of genetic component 49%-79% But it is not a disease itself. It relates to a number of common symptoms. Symptoms progress, overlap, ebb some but mostly progressive. SYMPTOMS INCLUDE: • Short term memory loss • Decline in language • Disorientation • Mood swings • Loss of motivation • Inability to complete even the simple self care • Behavioral issues. 5

10/4/2016 MEDICATIONS: Mild to Moderate: Moderate to Severe: • • Rozadeyne Namenda • Excelon (regulating • Aricept glutamate/ too • Namenda much kills brain • cholinesterase cells.) inhibitors- prevent • may be used in breakdown of severe with Aricept. acetylcholine. MEDICATIONS Off label medications for more severe behavioral symptoms. Anti-psychotics: • Zyprexa • Seroquel • Risperidal Mood Stabilizers: • Depakote (Valproic Acid) Remember start low, go slow. Check Labs for Therapeutic Levels Ex: Depakote- valproic acid levels. General term used to describe symptoms related to decline in thinking skills, reasoning, planning, judgment and memory caused by conditions that block or reduce blood flow to the brain. CAUSES • Infarct in brain tissues: large or small • Long Time Chronic medical conditions that stress brain tissues • Hypertension • Heart Disease • COPD • Diabetes • High Cholesterol 6

10/4/2016 • Thorough medical history, including family history of dementia • CT Scans • Looks at brain structure • MRI Scans CT Atrophy • Look at structure and blood vessel abnormalities • Carotid Ultrasound • Looks at supply, structure and plaques • Neurospych and Cognitive testing MRI Atrophy FDA has not approved of any drugs specifically to treat symptoms of vascular dementia. However, utilization of medication for underlying conditions can be helpful Prescriptions for some Alzheimer’s medications can also help boost the level of brain cell messages Research is ongoing: Researchers at Harvard Stem Cell Institute at Massachusetts General Hospital in Boston have showed that by manipulating proteins in the hippocampus may result in stronger, more precise memories. Of course more research is needed, but it does sound promising! 7

10/4/2016 The 2 nd most common type of progressive, degenerative brain disorder An abnormal build-up of protein which form Lewy bodies –similar to Parkinson’s protein. They also have plaques/ tangles which affect men more. Patients suffer a progressive decline in mental ability includes symptoms of: Visual Hallucinations: • people • Shapes • Animals Movement disorders: • Parkinson’s • slowed movements • rigid muscles • Tremor • shuffling gait Poor Regulation of body functions: • Autonomic Nervous System • Blood Pressure • Pulse • Sweating • Gastro Intestinal Disturbances Cognitive problems: • Alzheimer’s dementia • Confusion • Poor attention • Visual/ Spatial problems 8

10/4/2016 Sleep Difficulty: • REM sleep disturbances in which people act out their dreams during sleep Fluctuating Attention: • Episodes of drowsiness • Long periods of staring off “into space” • Long naps during the day • Disorganized speech • Depression • Apathy • Severe Dementia • Aggression • Agitation • Increased risk of falls • Worsening Parkinson’s-like symptoms • Death on average of 8 years Medications: • Cholinesterase inhibitors Antipsychotics (off label): DO • Rivistigmine/ Exelon – may help NOT USE HALDOL. alertness, cognition and reduce • Consider: hallucinations • Sinemet and low dose • Side Effects: Seroquel • GI Upset • Zyprexa (Olanzapine) • Drooling/ Tearing • Risperdal (Risperidone) • Frequent Urination • Parkinson’s Medications: • Sinemet - May reduce rigid muscles, slow movements but increase confusion • Side Effects: • Hallucinations and Delusions 9