Diseases of Aging PDF

DISEASES OF AGING  Diseases of Aging In a man's middle years there is scarcely a part of the body he would hesitate to turn over to the proper authorities. -E.B. White DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Diseas...

DISEASES OF AGING  Diseases of Aging In a man's middle years there is scarcely a part of the body he would hesitate to turn over to the proper authorities. -E.B. White DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Diseases of Aging Heart and Cerebrovascular disease Diabetes Mellitus Neurodegenerative disease Alzheimer’s Disease Parkinson’s DiseaseCancer - ? Cancer Arthritis Osteoporosis DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Age-related changes in the heart Size and number of cardiac muscle cells decreases, replaced by fibrous tissue. Increase in fat deposits on the surface of the heart. Endocardium thickens. Calcification of heart valves (30% of people over 75). Characteristic electrocardiogram (EKG) changes. Perhaps due to fibroses in conductive fibers. Systolic/diastolic blood pressures tend to increase: 120/80mmHg -> 130/90mmHg. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Age-related changes in the heart Reduced maximum oxygen consumption. Decreases by 30, 40% reduction by 65 yrs. Resting and maximum heart rate decrease. Cardiac output (blood pumped per minute) declines 1% per year after age 20, down 50% by age 80. Cardiac reserve declines with age. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Heart and Cerebrovascular Disease Complex diseases with a common origin: Blood vessel disfunction DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Blood vessel changes Reduction of elasticity in vessel walls (20 ->70yrs, 50% decrease). Reduction in eleastin protein content, replaced by collagen. Elastin calcifies. These changes can narrow arteries and increase peripheral resistance. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Atherosclerosis and Arterosclerosis Atherosclerosis: plaques, deposits on the inner surface of arteries. Plaque deposit is progressive: plaques get larger and more numerous. Consist of: lipid, protein, and immune cells. As plaques develop, they calcify. Leads to Arteriosclerosis, hardening of the arteries, which can lead to further damage. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Fatty Arteries Normal Coronary Atherosclerotic Artery Artery Photos: Klatt, Edward C., WebPath.com DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Pathogenesis of Atherosclerosis Endothelial Dysfunction Injury to the endothelium is the primary event Mechanical, tissue hypoxia, aging, etc. Impair endothelial protection Decrease in plasminogen activators, heparan sulphate, prostacyclin DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Pathogenesis of Atherosclerosis If the endothelium is damaged it no longer serves as a barrier. LDL cholesterol passes into the intima (internal layer of the vessel) and accumulates and modified (oxidized) by free radicals Attracts monocytes and is ingested by macrophages Key step is attraction of monocytes and T lymphocytes by TNF and MCP released by injured endothelium. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Pathogenesis of Atherosclerosis Monocytes migrate to subendothelial space where they become macrophages. Foam cells secrete PDGF, IL-1, TGF, TNF which activate SM cells to migrate and proliferate and deposit connective tissue. Foam cells also release TNF which is highly thrombogenic. Gives rise to overlying thrombus formation DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024 Atherosclerosis  Hypertension Caused by: aging changes of the vessels, atherosclerosis, arteriosclerosis, high sodium. Effects: heart attack, heart failure, kidney damage, blood vessel rupture (hemorrhage stroke). DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Coronary artery disease Ischemic heart disease: Occluded arteries->insufficient blood flow->ischemic heart attack. Plaques can trap blood platelets, cause a blood clot (thrombus). Heart disease is progressive and has positive feedback cycle. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024 Introduction: Hypertension Hypertension, or high blood pressure, is a treatable chronic disease. People who have hypertension have more stress placed on their circulatory systems than people without high blood pressure. Latest estimates are that more than 50 million Americans suffer from hypertension. Hypertension contributes to death from heart disease and kidney disease. HYPERTENSION Bringing blood pressure to an acceptable level does not mean the disease has gene away; it only means that the disease has been brought under control, and this control must be continued. HOW DO PEOPLE KNOW THEY HAVE HYPERTENSION? Hypertension has been called "the silent killer" because it gives no warning. In the early stages of this disease, there often are no symptoms. As the disease develops, people may complain of headaches, vision changes, or problems with their urinary output. If they would consult a physician at this point in their disease, permanent damage to a vital organ could be avoided. Some people with high blood pressure do not seek help until they have severe problems. By that time, permanent damage to vital organs is common You have a higher risk of hypertension if you: Have a family history of hypertension, heart disease, or kidney disease. Smoke cigarettes.. Are overweight Use a lot of salt in your diet Are African-American Eat a large amount of saturated fats CAUSES AND TREATMENT OF HYPERTENSlON Many conditions seem to cause hypertension,and some causes are still unknown. Research scientists are investigating diet, heredity, birth control pills, kidney infections and chemicals as possible causes of this chronic disease. An individualized treatment plan is developed by a physician after a thorough medical examination. Treatment may consist of a combination of diet, medication and exercise. Your Role as a Homemaker/Home Health Aide Follow the plan of care for your client. Support your client in complying with his medication plan, diet, and exercise. Report to your supervisor any deviation from the care plan. Assist the client with incorporating his treatment into his usual daily routine. Because he will always be on some treatment for this disease, it. is important ' that the treatment become a regular part of his day. Your Role as a Homemaker/Home Health Aide Listen to your client. If he has questions about hypertension and/or his treat. ment, answer him honestly. If you do not know the answer, call your supervisor and be sure that the client receives his answers. Be observant for possible side effects from the medication. Depending on the drug and the client, side effects range from a stuffy nose to muscle cramps, weakness, nightmares, and impotence. Your Role as a Homemaker/Home Health Aide Careful observations and objective, timely reporting of these and other symptoms will result in a treatment plan the client can live with the rest of his life. If the client starts taking any medications, including nonprescription drugs, report this to your supervisor. Introduction to Myocardial Infarction Heart attack is a general term that describes sudden damage to the heart. There are many medical reasons people have heart attacks, but they all have the same results. A decrease in the blood supply to the heart eventually leads to heart muscle damage and possibly permanent tissue death. Introduction to Myocardial Infarction The word infarct means “death of tissue due to lack of blood.” The word myocardial refers to heart muscle. So a myocardial infarction, or MI is really the death of part of the heart due to a blockage in a blood vessel. If the blood vessel involved is a small one and only a small amount of heart muscle is affected this may be called a minor or small heart attack. Introduction to Myocardial Infarction If the blood vessel involved is a large one and a large portion of the heart is damaged, it is often called a massive heart attack. The ultimate recovery of the injured heart depends on the location of the MI within the heart; presence of atherosclerosis; age. sex; and the health history of the individual. ARTERIOSCLEROSIS Arteriosclerosis is hardening of arteries and leads to a decrease in the blood supply, to body tissue due to a thickening of vessel walls. Atherosclerosis is a form of arteriosclerosis that takes place in several steps: A fatty streak develops in the vessel. A fibrous plaque develops on top of the fatty streak. Depending on the size of this plaque, the vessel remains open or becomes completely obstructed. Sometimes, a clot develops in the, same spot as the fibrous plaque. Introduction to Myocardial Infarction If atherosclerosis is discovered and treated after the first stage. The condition is reversible. However once a vessel is completely blocked by plaque it usually remains that way. SIGNS AND SYMPTOMS or A HEART ATTACK The following signs and symptoms may appear in your client or in a member of the family. Call for emergency help immediately and keep the client quiet and warm until help arrives. 1. Chest pain that may or may not radiate to the arm or jaw. 2.Wet clammy skin 3.Weak and/or rapid pulse rate 4.Pale color 5.Low blood pressure 6.Shortness of breath 7. Nausea SIGNS AND SYMPTOMS or A HEART ATTACK The single best way to prevent or minimize permanent damage to the heart is to get help at a hospital as soon as possible. Every minute is important! Your Role as a Homemaker /Home Health Aide After hospitalization, your client will return with an individualized plan of care based on: The type of heart attack he had. His recovery up to that point. His home situation. His prognosis. Your Role as a Homemaker /Home Health Aide Allow him as large a part in his care as his activity level permits. The plan of care you will receive from your supervisor will include instructions about: Activity restrictions Diet restrictions Medications Emotional support PACEMAKERS A pacemaker is an electrical device placed either in the left or right upper chest under the skin. The job of this device is to regulate the heart rhythm. A pacemaker can be temporary or permanent. THREE TYPES OF PEACEMAKER Fixed-rate. Stimulation rate is fixed usually between 60 and 70 beats per minute. This is used only if the heart is totally dependent on electrical stimulation and is only used temporarily. It is rarely seen in the home. Syn c h ro n o u s. Sti mu l ati o n o cc u rs after a predetermined lack of the heart’s own activity. This type is not seen often in the home. ' Demand. When the heartbeat falls below a predetermined rate, the pacemaker takes over. This is the most common type. lntroduction: Angina Angina is a brief, temporary pain or heaviness in the chest that results from lack of oxygen to the heart. Usually after resting and medication, the client no longer experiences discomfort. An episode may be brought on by stress or physical activity. Angina differs from person to person. Changes in your client's angina signal a change in his cardiac status and should be reported to your supervisor immediately. CAUSES OF ANGINA Angina is caused by narrowing of the coronary arteries that bring oxygen to the heart. As these vessels narrow, the amount of oxygen decreases, causing pain and discomfort. This is not a heart attack or myocardial infarction because it is a temporary condition. However, if angina is allowed to continue without treatment, the sufferer could have a heart attack, and sustain permanent damage to the heart. You have a higher risk of angina if you: Have high blood pressure Have high blood cholesterol Smoke cigarettes Are overweight Have high stress levels. TREATMENT There is no sure cure for angina. Most people with the disease, however, learn to live productive and meaningful lives. The aim of all treatment is to increase the flow of blood and oxygen to the heart. This is accomplished in several ways. TREATMENT Medication. The physician will prescribe a regime of medication to help the client and decrease his pain. The medication will be individualized for his particular condition a n d s h o u l d n o t b e a l t e re d w i t h o u t consulting the doctor. Control of risk factors. The client may be put on a weight-reducing diet, told to decrease his use of cigarettes, and advised to decrease his stress. TREATMENT These alterations in lifestyle are difficult, and the client and his family will need a great deal of encouragement and support to reach the goal. Surg e ry. I f this tre atriie nt has b e e n recommended by a physician and your client or his family have questions, report this to your supervisor immediately so that questions can be answered. Introduction: Diabetes When the body cannot change carbohydrates (sugars and starches) into energy because of an imbalance of insulin, the result is the chronic disease ' known as diabetes mellitus. The pancreas usually produces insan on a feed back mechanism. When the body needs insulin following a meal or when extra energy is needed, the pancreas is alerted and it pumps extra insan into the bloodstream. If, however, the body needs insulin and none is pro du ced; sta rc h es a n d su ga rs ca n n o t be converted into energy and absorbed by the cells. Sugar remains in the bloodstream and is eventually excreted in the urine as waste. SIGNS AND SYMPTOMS OF DIABETES MELLITUS Fatigue, tiredness Loss of weight Sores heal poorly and slowly High blood sugar Sugar in the urine Frequent and large amounts of urine Excessive thirst Poor vision Inflammation of the vagina TYPES OF DM There are two types of diabetes. Type I results in the person having to take insulin. Type II diabetes, the pancreas produces some insulin, but not enough for normal body function. In this type of diabetes, the person may take oral medications or just regulate his diet. Because a diabetic has a regulated amount of insulin in his body, his food intake must be regulated also. TYPES OF DM If the amount of food is greater than the amount of insulin available, there will be too much unmetabolized sugar left in the, blood. If the amount of insulin is greater than the amount of food available, there will not be any carbohydrates for the insulin to metabolize, and this will cause other problems. TYPES OF DM Diabetes can be controlled, but never cured. A diabetic must maintain a special diet and must sometimes take medication by mouth or insulin by injection forever. A person with diabetes can live a full and productive life if he keeps to a diet and a medication schedule. Diagnosis of this disease can be made only by a physician following laboratory tests. DIABETIC COMA AND INSULIN SHOCK Be alert for signs and symptoms of diabetic coma and insulin shock or insulin reaction, and follow the emergency procedure for your client). Signs and Symptoms of Diabetic Coma (Hyperglycemia! High-Blood-Sugar Diabetic Ketoacidosis) Diabetic coma (ketoacidosis) occurs when the blood has too many carbohydrates and not enough insulin to metabolize it. The symptoms include: DIABETIC COMA AND INSULIN SHOCK Air hunger; heavy, labored breathing; increased respiration Loss of appetite Dulled senses Nausea and/or vomiting Weakness Abdominal pains or discomfort Generalized aches DIABETIC COMA AND INSULIN SHOCK Increased thirst and parched tongue Sweet or fruity odor of the breath Flushed dry skin Increased urination Soft eyeballs Upon examination. large amounts of sugar and ketones In the urine and high blood sugar  Aging of the Central Nervous System Cell loss Brain weight increases to age 30, declines by 10% by 90 yrs of age. Due to this Ventricles enlarge. Gyri become smaller, sulci between them enlarge. Grey and white matter reduced. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  The Neuron DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  The Neuron: the brain’s basic functional unit Soma Dendrites Myelin Sheath Axon Axon Terminals DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Aging of the Central Nervous System Neuronal function decline Rate of conduction along axons declines, due to loss of myelin. Synapses time increases. Reduced levels of synapse enzymes, receptors, etc. Reduced numbers of dendrites and dendritic spines (in some areas o the brain). Cellular changes: Lipofuscin deposits. Decrease in dark staining cytoplasmic Nissl bodies. Glia: 10 times more glial cells than neurons In some areas, glial numbers increase, in other areas they decrease. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Neurodegeneration Involved in disorders like Alzheimer’s, Huntington’s, Parkinson’s. Also involved in neuromuscular diseases like ALS or Lou Gehrig’s disease. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Alzheimer’s Disease Neurodegenerative disease causing progressive memory & language loss Associated with deposition of amyloid protein (APP) in CNS and neurofibrillary tangles (NFTs). NFTs associated with mutations to Tau proteins that stabilize microtubules. Mutations to PS-1 and PS-2 (presenelin genes) give rise to early onset disease. Mutation to apolipoprotein E gives rise to late onset. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Neurofibrillary Tangles in Alzheimer’s Disease From http://www.rnw.nl/health/html/brain.html  Neuronal Plaques in Alzheimer’s Disease From http://www.rnw.nl/health/html/brain.html  Plaques and neurofibrillary tangles From Department of Pathology, Virginia Commonwealth University  Alzheimer’s Disease http://abdellab.sunderland.ac.uk/lectures/Neurodegeneration/ References/Brain_Neurons_AD_Normal.html Amyloid precursor protein (APP) is membrane protein that sits in the membrane and extends outward. It is though to be important for neuronal growth, survival, and repair. Enzymes cut the APP into fragments, the most important of which for AD is called b-amyloid (beta-amyloid) or Aß. Beta-amyloid is “sticky” so the fragments cling together along with other material outside of the cell, forming the plaques seen in the AD brain. Alzheimer’s pathogenesis Rate of Aß accumulation and aggregation determined by: Genotype, production of amyloid peptide, tau, presenilin proteins. Efficiency of degradation of Aß. Levels of plasmin (cleavage product of plasminogen). DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Amyloid Hypothesis The trigger for alzheimer’s disease is the A-beta peptide, and the accumulation of this peptide in the form of plaques is the initiating molecular event. The plaques trigger an inflammatory response, neuronal cell death, and gradual cognitive decline. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is caused by an imbalance between A-beta production and A-beta clearance. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  The History of Parkinson’s Disease Parkinson’s Disease (PD) was first described by James Parkinson in 1817(1) He noted ‘Involuntary tremulous motion’ ‘A propensity to bend forwards’ ‘The senses and intellect are intact’ 40 years later Charcot named Parkinson’s Disease DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  Parkinson’s disease Progressive neurodegenerative disease Incidence: 1 in 200 over the age of 55. Clinical descriptions: Useless contractions of the skeletal muscles causing muscle rigidity and tremors. Resting tremor, muscular rigidity, bradykinesia, and postural instability. 20%DR.ofFELIPE patients develop Alzheimer’s A. MERANO,RN disease. Faculty, CEFI College of Nursing – First Semester 2024  Parkinson’s disease Pathologic features: Loss of dopaminergic neurons in the substantia nigra (SN). Presence of Lewy bodies, intracellular inclusions, in surviving neurons in various areas of the brain, particularly the SN. Leads to reduced production of dopamine Reduced dopamine levels leads to striatal dopamine deficiency and development of PD symptoms. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024  The role of dopamine Dopamine acts to oppose acetylcholine Dopamine inhibitory Acetylchloline excitatory Depletion in dopamine results in hypokinetic disorders such as PD DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024 -synuclein pathology: abnormal neuronal and glial inclusions and processes  Lewy body disease Mutations in -synuclein can lead to either mendelian Parkinson’s or Lewy body dementia. Triplication of -synuclein leads to disease onset in the 30’s. Normal genetic variability: people with higher expressing alleles have a higher risk of sporadic disease. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024 Models of Parkinson’s disease 6-OHDA: neurotransmitter analogue depletes noradrenergic stores in nerve endings -> reduces dopamine levels. produces free-radicals -> apoptosis. MPTP: a contaminant that can result from sloppy synthesis of MPPP, a street analog of the opioid meperidine (Demerol). Taken up by domaminergic neurons -> free radicals -> apoptosis. -synuclein overexpression -> inhibits MAPK signaling -> induces apoptosis. DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024 Models of Parkinson’s disease Transgenic mice that expressed wildtype -synuclein w/ platelet-derived growth factor-beta gene promoter (pan- neuronal) Progressive accumulation of -synuclein and ubiquitin- immunoreactive inclusions in neurons in the neocortex, hippocampus, and substantia nigra. Ultrastructural analysis shows electron-dense intranuclear deposits and cytoplasmic inclusions. These alterations were associated with loss of dopaminergic terminals in the basal ganglia and with motor impairments. Masliah et al., 2000 DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024 Models of Parkinson’s disease Transgenic flys that expressed wildtype and pathogenic a-synuclein (pan-neuronal). Observed: adult-onset loss of dopaminergic neurons, filamentous intraneuronal inclusions containing alpha-synuclein reminiscent of Lewy bodies, and locomotor dysfunction. One pathogenic mutation esp. bad. All produced premature loss of climbing ability. Feany and Bender, 2000 DR. FELIPE A. MERANO,RN Faculty, CEFI College of Nursing – First Semester 2024 Protein deposits lead to neurodegeneration  Alzheimer’s disease Relationship between age, Amyloid Beta (Αβ)42 accumulation, normal aging, Mild cognitive impairment (MCI), and Alzheimer’s disease (AD). Typically, the Αβ42 levels in the brains of AD patients are 1,000-10,000-fold higher than in the brains of normal controls. Thank you for Listening Check your SILID for Assignment