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"...a major reorganization of the text, offers an interdisciplinary focus, with special information on nursing care, pharmacy issues, patient & family education, palliative care, and end-of-life care."
Differentiating between normal aging and successful aging is useful. Normal aging refers to the common complex of diseases and impairments that characterize many of the elderly. However, persons age very differently: some acquire diseases and impairments, and others seem to escape specific diseases altogether and are said to have died of old age. The latter may maintain an active healthy life until death.
Successful (healthy) aging refers to a process by which deleterious effects are minimized, preserving function until senescence makes continued life impossible. Persons who age successfully avoid experiencing many of the unwanted features of aging. For example, they may avoid near-total tooth loss, which used to be (and is in some societies) usual and universal among the elderly. The elderly may be able to avoid the complications of vascular disease, even while the circulatory system continues to age, by controlling blood glucose levels and body fat percentage.
The concept of successful aging is thataging is not necessarily accompanied by debilitating disease and disability. Although the percentage of persons > 65 and the proportion of the elderly > 85 have both increased -in the USA, the percentage of elderly persons residing in nursing homes has decreased (to 5.2%). Similarly, the percentage of persons aged 75 to 84 who report disabilities has decreased (to < 30% ), as has the percentage of persons with debilitating disease. Although there may be alternative explanations for these changes in health stat -s, one viable explanation is an increase in the proportion of persons who are aging successfully.
Disease vs. aging: In both aging and senescence, many physiologic functions decline, but normal decline is not usually considered the same as disease. The distinction between normal decline and disease is often but not always clear and may be due only to statistical distribution. Glucose intolerance is considered normal aging, but diabetes is considered a disease, although a very common one. The incidence and prevalence of type 11 diabetes increase with age, so that among persons > 75 years of age, > 10% have diabetes. Cognitive decline is nearly universal with advanced age and is considered normal aging; however, cognitive decline consistent with dementia, although common in late life, is considered a disease. Alzheimer's disease is a pathologic process distinct from normal aging, a conclusion supported by analysis of brain tissue at autopsy.
The average life span of Americans has been increasing dramatically since the industrial revolution. However, most of the gains resulted from decreasing childhood mortality. The maximum life span, generally determined to be about 125 years for women and somewhat shorter for men, has changed little in recorded history, although some experts suggest that it may be slowly increasing.
Several factors influence longevity. One is heredity. Heredity primarily influences whether an individual will contract a disease. Inheriting a propensity to hypercholesterolemia is likely to result in a short life, whereas inheriting genes that protect against heart disease and cancer helps ensure a long life. Medical treatment contributes to increased survival after diseases are contracted, especially when diseases (eg, infectious diseases, cancer) are curable. Another important influence on longevity is lifestyle; avoiding smoking, maintaining a healthy weight and diet, and exercising appropriately help people avoid disease. Exposure to environmental toxins can shorten life span even among people with the most robust genetic makeup.
CELLULAR AND MOLECULAR AGING
Cells lose their ability to divide over time unless they become cancerous. This limit to cellular replicative capacity (Hayflick's limit or phenomenon) can be demonstrated in fibroblasts removed from the umbilical cord of newborns and cultured in vitro. The fibroblasts divide only until they are dense enough to contact each other-a phenomenon called contact inhibition. If diluted, the fibroblasts divide again until maximum density is reached. This process can be repeated; however, after about 50 divisions, the fibroblasts stop dividing regardless of their density. Hayflick's limit is thought to reflect in vivo processes; fibroblasts removed from elderly persons tend to divide fewer times. Studies have shown that the loss of replicative capacity does not depend on the total amount of time cells are cultured (chronologic age) but on the number of divisions (biologic age).
When cells divide so many times that they cannot divide again, they enlarge and exist for some time before gradually dying. Such cells differ in morphology and function from young cells that are still dividing and from young cells whose division has been arrested by experimental manipulation.
One biologic mechanism for Hayflick's limit is now understood. Telomeres are stretches of DNA at the end of chromosomes that serve as handles by which chromosomes are moved during the telophase of meiosis. Telomeres are irreversibly shortened each time a cell divides. When the telomeres become too short, the cell can no longer divide.
In transformed (eg, cancerous) cells, the enzyme telomerase lengthens telomeres after telophase. The telomeres of transformed cells do not shorten after each division, and thus the cells become immortal, dividing far beyond Hayflick's limit. Normal postmitotic cells (except for fetal and germ cells) express telomerase in very small amounts, and their telomeres become shorter after each cell division.
The relevance of Hayflick's limit to senescence of the whole organism is unclear. Although some cells (eg, intestinal epithelial cells, skin fibroblasts) divide more or less continuously throughout life, they are unlikely to approach the limit of 50 divisions. Even if they did, the cells most likely to cause functional failure during senescence are probably those that divide very little (immune and endocrine cells) or not at all (neurons and muscle cells). Furthermore, senescence in metazoans composed entirely of postmitotic cells is just as predictable and robust as that in metazoans containing mitotic cells.
Mechanisms other than telomerase shortening may be involved in senescence. For example, messenger RNA (mRNA) transferred from senescent cells into young cells stops cell division in the young cells. The mRNA acts as a gerontogene (a gene mutation that increases life span), whose function may resemble that of a tumor suppressor gene (eg, p53). Mutations in p53 lead to uncontrolled cell division, cancer, and often death of the organism. Mutations in gerontogenes extend the number of divisions in cells.
Necrosis and apoptosis: Cell death may occur by necrosis or apoptosis. Necrosis is due to physical or chemical insults (eg, metabolic inhibition, ischemia) that overwhelm normal cellular processes and make the cell nonviable. In necrosis, loss of ion gradients across the cell membrane leads to an influx of calcium and other ions, which triggers proteolysis and rupture of organelle membranes. Necrosis is a purely entropic phenomenon due to loss of the cell's ability to transform external energy.
In contrast, apoptosis is a highly regulated, orderly process by which a cell essentially commits suicide; usually, the stimulus for apoptosis is a physiologic signal or a very mild insult. A defining feature of apoptosis is the fragmentation of the cell's DNA, produced by a regulated activation of deoxyribonuclease. However, several other biochemical processes that also lead to cell death are simultaneously induced. Apoptosis is essential for normal development and remodeling.
Apoptosis has been implicated in several age-related diseases, including Alzheimer's disease. Whether age-related cell death is due primarily to necrosis or to apoptosis affects whether aging is considered the result of entropic processes (if due primarily to necrosis) or of relatively simpler, more regulated processes (if due primarily to apoptosis)...
1. Biology of Aging.
3. History and Physical Examination.
4. Comprehensive Geriatric Assessment.
5. Prevention of Disease and Disability.
6. Clinical Pharmacology.
7. Geriatric Interdisciplinary Terms.
9. Geriatric Social Work.
11. Continuity of Care: Integration of Services.
12. Quality of Life and therapeutic Objectives.
13. Care of the Dying Patient.
14. Legal and Ethical Issues.
15. Social Issues.
16. Managed Care.
17. Health Care Funding.
Section 2: Falls, Fractures, and Injury.
19. Chronic Dizziness and Postural Instability.
21. Gait Disorders.
23. The Elderly Driver.
Section 3: Surgery and Rehabilitation.
25. Preoperative Evaluation.
26. Perioperative Care.
27. Anesthesia Considerations.
29. Rehabilitation for Specific Problems.
30. Occupational Therapy.
Section 4: Psychiatric Disorders.
32. Aging and Mental Health.
34. Anxiety Disorders.
35. Somatoform Disorders.
36. Psychotic Disorders.
37. Substance Abuse and Dependence.
Section 5: Delirium and Dementia.
38. Mental Status Examination.
41. Behavior Disorders in Dementia.
Section 6: Neurologic Disorders.
42. Aging and the Nervous System.
45. Speech Disorders.
46. Movement Disorders.
47. Sleep Disorders.
Section 7: Musculoskeletal Disorders.
48. Aging and the Musculoskeletal System.
49. Metabolic Bone Disease.
50. Nonmetabolic Bone Disease.
51. Local Joint, Tendon, and Bursa Disorders.
52. Rheumatic Diseases.
53. Vasculitic Syndromes.
54. Muscular Disorders.
55. Hand Disorders.
56. Foot Disorders.
Section 8: Metabolic and Endocrine Disorders.
57. Disorders of Water and Electrolyte Balance.
58. Disorders of Mineral Metabolism.
59. Disorders of Acid-Base Metabolism.
60. Vitamin and Trace Mineral Disorders.
61. Protein-Energy Undernutrition.
63. Lipoprotein Disorders.
64. Disorders of Carbohydrate Metabolism.
65. Thyroid Disorders.
66. Hormonal Supplementation.
67. Hyperthermia and Hypothermia.
Section 9: Hematologic Disorders and Cancer.
68. Aging and the Blood.
70. Hypercoagulability and Anticoagulation.
71. Chronic Myeloid Disorders.
73. Hematologic Malignancies.
Section 10: Pulmonary Disorders.
75. Aging and the Lungs.
76. Pulmonary Infections.
77. Pulmonary Embolism.
78. Chronic Obstructive Pulmonary Disease.
79. Respiratory Failure.
80. Interstitial Lung Diseases.
81. Lung Cancer.
82. Pulmonary Rehabilitation.
Section 11: Cardiovascular Disorders.
83. Aging and the Cardiovascular System.
84. Diagnostic Evaluation.
88. Coronary Artery Disease.
89. Valvular Heart Disease.
90. Infective Endocarditis.
91. Arrhythmias and Conduction Disturbances.
92. Heart Failure and Cardiomyopathy.
93. Peripheral Arterial Disease.
94. Peripheral Venous Disease.
96. Cardiovascular Surgery and Percutaneous Interventional Techniques.
Section 12: Kidney and Urinary Tract Disorders.
97. Aging and the Kidney.
98. Renal Disorders.
99. Urinary Incontinence.
100. Urinary Tract Infections.
101. Urinary Tract Tumors.
Section 13: Gastrointestinal Disorders.
102. Aging and the Gastrointestinal Tract.
103. Endoscopic Gastrointestinal Procedures.
104. Dental and Oral Disorders.
105. Esophageal Disorders.
106. Gastric Disorders.
107. Lower Gastrointestinal Tract Disorders.
108. Liver and Biliary Disorders.
109. Anorectal Disorders.
110. Constipation, Diarrhea, and Fecal Incontinence.
112. Acute Abdomen and Surgical Gastroenterology.
113. Gastrointestinal Tumors.
Section 14: Men's and Women's Health Issues.
115. Sexual Dysfunction in Men.
116. Sexual Dysfunction in Women.
117. Male Genital Disorders.
118. Female Genital Disorders.
120. Estrogen Replacement Therapy.
121. Breast Cancer.
Section 15: Dermatologic and Sensory Organ Disorders.
122. Aging and the Skin.
123. Common Skin Disorders.
124. Pressure Sores.
125. Skin Cancer.
126. Aging and the Eye.
127. Ocular Disorders.
128. Hearing Loss.
129. Ear Disorder.
130. Nose and Throat Disorders.
Section 16: Infectious Disease.
131. Aging and the Immune System.
133. Antimicrobial Drugs.
134. Human Immunodeficiency Virus Infection.
I. Laboratory Values.
II. Weights and Measures.
III. Trade Names of Some Commonly Used Drugs.
IV. Resources List.
Barnes & Noble.com: Can you tell us a bit about your background?
Mark Beers: I am a physician trained in internal medicine and geriatrics. I went to medical school at the University of Vermont and was a house officer at Tufts New England Medical Center and the Mount Sinai Hospital in New York City. I completed a geriatrics fellowship at Harvard Medical School. Prior to joining Merck seven years ago as the associate editor of the Merck Manuals, I was on the faculty at UCLA. My research has been in the field of medication use in the elderly.
B&N.com: In addition to editing The Merck Manual of Geriatrics you are also one of the primary editors of The Merck Manual, 17th Edition. What do you see as your chief motivator when working on these references?
MB: I have had a long-held interest in medical education. The original Merck Manual, now in its 17th edition, has a 100-year history of providing the finest-quality clinically useful information for doctors and other health professionals. Editing this book has been a joyful way of helping these professionals provide the best care to their patients.
The Merck Manual of Geriatrics is somewhat different, providing focused information about care of older adults. It is written for a broader audience, including not only health professionals but also all those involved in the care of older adults. While not expressly written for a lay audience, many laypeople have found it very useful.
The Merck Manual Home Edition is written for laypeople. In that book we have tried to translate the complex language of medical care into plain English, providing every person with the information he or she needs and wants to know about the practice of medicine.
B&N.com: What is the biggest challenge of editing a book like The Merck Manual of Geriatrics?
MB: Geriatric care is complex, in part because older people are complex and in part because providing care to older people requires the expertise of many kinds of professionals. In this edition we have tried to tie together those complexities and needs through a multidisciplinary approach. To the best of our knowledge, no medical textbook of geriatrics has attempted to do this before. It was a struggle, and we hope we have succeeded.
B&N.com: Can you describe some of the differences -- whether scope, content, or structure -- between the first edition and this new third edition?
MB: There are few similarities between the first and third editions of The Merck Manual of Geriatrics. The field of geriatrics has progressed enormously, and the new edition contains large amounts of information that was not available a decade ago. The third edition is also far more focused on medical issues relevant to the elderly and the specifics of those medical issues to the health of older people than previous editions. In addition, we have added much more about approaches to care, including setting goals and caring for dying patients.
We are now able to give more information about drug problems in the elderly and the underlying pathology of many of the diseases of aging. Importantly, this newest edition takes a multidisciplinary approach, providing specific information to doctors, nurses, pharmacists, therapists, social workers, and lay caregivers.
B&N.com: What changes or advances in the treatment for the elderly do you think will happen, or hope will happen, within the next ten years?
MB: It is always dangerous to predict. Nonetheless, I think that we can expect to develop better treatments for depression and pain in the elderly and maybe even for some causes of frailty and muscle weakness.
We are learning more about the causes and potential treatments for Alzheimer's disease and remain hopeful of major breakthroughs in this decade. The study of medication problems in the elderly has blossomed in this country, and we can expect more information that will help us use all medications wisely in older adults.
B&N.com: Do you have an interest in any particular health problems or issues?
MB: I have two special areas of interest. The first is medication problems in general and the ways to get doctors to use medications more appropriately in the elderly. The second is the vexing problem of behavior disorders in elderly people with dementia.
B&N.com: Would you please recommend two or three medical books (besides the Merck Manuals!) that you would like to recommend as your favorites or that have impressed you recently?
MB: My favorite medical text, other than the Merck Manuals, is Harrison's Principles of Internal Medicine. It is the first one I read as a medical student, and I have continued to rely on it.
I am particularly fond of a book for caregivers of people with dementia called The 36-Hour Day. I recommend it often.
Just to round out the list in the nonmedical area, James Joyce's Ulysses is a book I read parts of yearly and straight through every few years. Writing doesn't get any better than that! I will also admit happily that I reread Alice in Wonderland every year, too, and have about a dozen different printings in my collection.