Instructor: Self-study
Revised by: Sharee A. Wiggins, NP, MS(N), BC-GNP, BC-ANP
Edited by: Mary McDonald, MD
Reviewed by: Anne Walling, MB, ChB
Specific Learning Objectives
A. Introduction
Before reviewing the learning objectives and content, please take the following Pre-Test. You must do this before you can proceed with the module. The answers are given in the Post-Test that complete the module.
Please review the Objectives, Content material, and Cases before our class session. We will apply the tasks in the Skills Objectives to these cases, and you should think about them ahead of time.
B. Attitudes - the student will recognize that:
C. Knowledge - The student should be able to describe or explain:
D. Skills
E. Readings
Required Readings:
- Stalworth, M. & Sloane, P. D. Clinical implications of normal aging, (Chapter 2), 14-24. In, Ham, R. J., Sloane, P. D., Warshaw, G. A. Bernard, M. A., & Flaherty, E. (Eds.). Primary Care Geriatrics (5th Ed.) (2007). Mosby: St. Louis.
- Geriatric Review Syllabus (5th Ed.) Age-Related Physiologic Changes, pp. 10-23.
G. Cases
One of the stereotypes held by uninformed individuals about older adults is that “they” are all alike. This is rooted in ignorance. One of the tenets of geriatrics is that as people age they have increasing heterogeneity; they become more biologically unique. At a minimum, failure to recognize this principle interferes with providing quality medical care. On the other end of the spectrum, it could lead to harmful care. One example of this increasing heterogeneity is seen in the classic study, “Baltimore Longitudinal Study of Aging.” Repeated measures of creatinine clearance (CrCl) were obtained in volunteer subjects with no clinical evidence of renal disease. Of those participants, two-thirds had significant or small, but significant decreases in CrCl. However, one-third did not show any decrease. [Peterson, 1994; Lindeman and Shock, 1985].
Aging involves both intrinsic and extrinsic factors. Intrinsic factors are those specific features and processes that occur universally and cause irreversible cellular changes. Some challenge the view of aging as a gradual decline with irreversible losses, and note that there are some potentially modifiable factors (such as exercise) which can help compress morbidity into only the final years of life. Such a view supports the goal of increasing the number of years of functional capacity. The reality is that both views are applicable to modern geriatric medicine. Extrinsic aging involves factors such as lifestyle and environmental influence. The primary focus of this module is on intrinsic aging.
As we age there is a steady decline in physiologic reserves. Recovery takes longer and there is a reduced ability to compensate for illness or increased physiologic demands. Illnesses accumulate in number and severity. Physiologic decline plus disease results in excess morbidity and disability. Usual age-related changes can stack up against the hospitalized older adult and to existing burden. Students are encouraged to read the classic 1993 article by Morton C. Creditor, MD, “Hazards of Hospitalization of the Elderly,” Annals of Internal Medicine, 118(3), 219-223. It can be accessed online at: http://www.annals.org/cgi/content/full/118/3/219
Technically, we do not die from “old age.” We die from disease, which, if one lives long enough, is brought about by those irreversible cellular changes that permanently increase the probability of harmful consequences. “Old Age” was removed as a cause of death option for death certificates in 1951. [Hayflick; GSA, 2002]
Many of the most pronounced changes with aging are impaired responses to external stimuli, especially those mediated by a final calcium signal. Older persons have limited physiologic reserves. An alternative explanation is that older persons already employ some of their physiologic reserves just to maintain baseline homeostasis. There may be a price for persistent activation of the stress-response systems. Healthy older persons with higher systolic blood pressure, higher overnight cortisol and catecholamine secretion, and other evidence of activation of stress responses were more likely to have declines in cognitive or physical function during 3 years of follow-up.
With age, a number of changes occur in the eye anatomy. The periorbital tissues atrophy; the eyelids are more relaxed. Flaccidity of the lower lid may lead to ectropion (turns outward) or entropion (turns inward). Lacrimal gland function, tear production, and goblet cell function all decrease. Despite decreased tear production, periorbital tissue atrophy leads to displacement of the lacrimal punctum, which results in decreased drainage and a watering eye.
The conjunctiva atrophies and yellows. Corneal sensitivity to touch declines by 50% in advanced age. It also flattens, resulting in a one-third reduction in the amount of light into the eye. The iris becomes more rigid, yielding a smaller, more sluggishly responsive pupil. The lens yellows because of photo-oxidation of tryptophan in lens protein and an increased accumulation of insoluble protein in the center with the lens fibers.
Aqueous humor production decreases and the vitreous humor and body also shrink. Separation between the liquid and solid components may be manifest to the person as flashes of light. The retina becomes thinner because of a loss of neurons.
Presbyopia is an age-related vision change in which the distance needed to focus near objects increases. This is due to decreased lens elasticity and atrophy of the ciliary muscle. This process begins very slowly sometime during the fourth decade of life.
The older eye adapts more slowly to light change because the pupil is rigid, the lens is more opaque, and the retina less efficient. Alterations in the lens lead to significant increases in light scattering, which makes the older person much more sensitive to glare. After cataract removal, the glare threshold becomes normal.
Because of a decline in contrast sensitivity, older persons need increased contrast to discriminate between target and background. This factor should be taken into account in the design of living environments and in assessing medication self-administration difficulties.
The external auditory canal atrophies; its walls thin. Cerumen becomes drier and more tenacious, and thus has a greater tendency to form an impaction. Five distinct changes occur to varying degrees in the inner ear: loss of hair cells in the organ of Corti; loss of cochlear neurons; stiffening of the basilar membrane and calcification of the auditory mechanisms; thickening of the capillaries of the stria vascularis, which is the source of endolymph; and degeneration of spiral ligament. The sum of the changes is the loss of both high- and long-frequency audition. Hearing impairment affects 25% of persons age 65-74, and 50% of those 75-84. Despite 65% of persons > age 85 having impaired hearing, only 8% wear a hearing aid or other assistive listening device. [Ageworks; USC]
Clinical Tip: Your stethoscope can be used as both a speaking device (by you speaking into the diaphragm) and a listening device (with the earpieces in the patient’s ears).
The number of lingual papillae decrease with aging, but neurophysiologic responses are unaltered. The acuity of olfaction declines, and since taste is a combination of gustatory sense and smell, detection thresholds are increased by 50% by age 80, and recognition of familiar smells decreases by 15%.
The gums recede, exposing the tooth cementum, which is more prone to decay, and predisposing older persons to root caries. Enamel and dentin wear down, but the teeth maintain integrity in the absence of dental caries. Tooth loss is common, but not a normal age-related change. The primary etiology for loss of native teeth in the elderly is periodontal disease. Contrary to popular thought, the disease does not always have an oral hygiene etiology. The American Academy of Periodontology reports that research has revealed genetics may account for periodontal disease in up to 30% of the population. Further, despite aggressive oral hygiene, these individuals may be six times more likely to develop the disease.
The peripheral lung undergoes a number of anatomic changes, including an enlargement of alveolar ducts due to loss of elastic tissue that results in a decreased surface area for gas exchange. Airways in dependent portions of the lung sac close at higher volumes. The lower portions of the lung are better perfused at all ages, but higher closing volume with age increases ventilation perfusion mismatch and accounts for declining P02 with age.
Costochondral cartilage becomes calcified with age, and intercostal muscle contraction accounts for less chest expansion. By age 65 inspiration depends on abdominal muscles, which are only partially effective in opening airways in the seated or supine position. Full airway expansion occurs only in the upright (standing) position. In older persons cough is less vigorous. The number of cilia decrease with aging, and mucociliary clearance is slower and less effective. These age-related physiologic changes increase the risk of pulmonary infections in older adults.
Pulmonary function peaks at age 30, and this peak determines the likelihood of future compromise resulting from age-related changes. In nonsmoking men, forced vital capacity (FVC) decreases between 0.15 and 0.3 liters per decade. Forced expiratory volume in 1 second (FEV1) decreases by 0.2 to 0.3 liters per decade in nonsmoking men. In women changes are somewhat smaller and somewhat more gradual.
Total lung capacity (proportional to height) does not change significantly with age; however, with increasing age the residual volume (air left in the lung at the end of full expiration) increases because of higher closing volume. In young adults, residual volume accounts for 20% of total lung capacity; by age 60, residual volume increases to 35%. A simple colorized animation comparing representations of residual volume in younger vs. older lungs can be viewed at: http://www.ageworks.com/course_demo/513/module3/module3.htm#respiratory
Older adults have decreased responses to hypoxemia, hypercapnia, and mechanical loading. With exercise training many of these changes normalize; the implication is that central or peripheral receptor hyporesponsiveness is due to deconditioning, not an intrinsic change with aging.
The impact of changes in the cardiovascular system is minimal in a person at rest. However, the cardiac inotropic and chronotropic maximal and submaximal responses to catecholamine stimulation and to sympathetic nervous system stimulation are markedly impaired in the older person. Maximum heart rate declines with age. The formula, 220 minus age, estimates maximum heart rate in men and for women, 190 minus (0.8 x age). Older and younger persons require about the same cardiac output to perform a given level of work. In order to maintain cardiac output following stress or exertion, stroke volume is increased as a compensatory mechanism for reduced maximum heart rate. Recovery after exertion is markedly prolonged in the older persons. Cardiac murmurs are more common in older adults due to reduced compliance and calcification of cardiac valves.
Cardiovascular Changes with Age
UP
Down
No Effect
Heart Anatomy
Left ventricle muscle
X
Sinus node cells
X (by 90%)
Lipofuscin
X
Calcium deposition in valve
X
Electrophysiology
Intrinsic sinus rate
X
PR interval
X
Supraventricular and ventricular ectopy
X
Mechanical Function
Ejection Fraction
X
Resting Cardiac Output
X
Adrenergic Responses
Chronotropic
X
Inotropic
X
Recovery after exertion
X
Endocrinology
Atrial natriuretic peptide
X
- Blood-Pressure Regulation
Both systolic and diastolic blood pressures increase with age. Arterial compliance is reduced due to age-related changes such as fragmentation of elastin, increased collagen, subintimal calcification and thickening, and smooth muscle cell proliferation. Roughly 70% of hypertensive adults > age 60 have isolated systolic hypertension (ISH). ISH is most likely due to decreased arterial compliance. Compliance is also worsened by disease such as atherosclerosis. ISH – and the resulting widenend pulse pressure – is a greater risk factor for myocardial infarction, heart failure, and stroke, than diastolic blood pressure.
ß-Adrenergic-mediated vasodilation appears to be significantly impaired with age in the arterial tree but only modestly decreased in veins, and a-adrenergic vasocontriction is unaltered. Older patients, especially those with hypertension, are at higher risk for orthostatic hypotension.
- Clinical Implications:
- Orthostatic hypotension is an exam finding, not a disease
- It is defined as a decrease in systolic blood pressure (SBP) of 20 mg Hg or a drop of 10 mm Hg in diastolic blood pressure (DBP) within 3 minutes of standing
- The patient may or may not have any symptoms:
- Observed postural instability
- History of falls with position change
- Subjective report of feeling “dizzy,” lightheaded, weak, nauseated
- The presence or absence of symptoms should be documented
- Often, there will be a concurrent increase in heart rate as compensation for decreased stroke volume. This response can be dampened in the patient on beta-blocker therapy.
- Etiologies include medication side-effects, neurogenic and non-neurogenic etiologies
- Treatment is aimed at the underlying pathology or drug
- If the pathology cannot be corrected or the offending drug stopped or dose reduced, cautious and carefully justified drug treatments can be considered in symptomatic patients
- Nonsteroidal Anti-inflammatory drugs (NSAIDs) – blood volume expansion; risks of GI bleed and heart failure
- Fludrocortisone (Florinef ®) – blood volume expansion; numerous side effects
- Midodrine (ProAmatine ®) – vasoconstrictor; supine hypertension risk
Parotid salivary gland production decreases slightly. Chewing becomes less efficient. Swallowing is less coordinated, which increases risk of microaspiration, especially in the presence of dentures.
Anatomic changes in the esophagus include hypertrophy of the skeletal muscle at the upper third, thickening of the smooth-muscle layer along the lower two thirds, and a decrease in numbers of the myenteric ganglion cells that coordinate peristalsis. Secondary esophageal contractions appear to be greatly reduced.
Up to 30% of older adults have achlorhydria, which can result in insufficient intrinsic factor and pepsin to absorb B12 (pernicious anemia). After age 60, gastric ulcers are more common than duodenal ulcers. While helicobacter pylori is a major etiology in ulcer development, non-steroidal anti-inflammatory drugs (NSAIDs) are a major factor of both ulcer and GI bleed in older adults.
The absorption of calcium, iron, lactose, xylose, and vitamin D is decreased. Lactase levels decline, leading to intolerance of dairy products by many older people. The efficiency of calcium absorption from the gut lumen decreases because of decreased vitamin D receptors in the gut and decreased levels of circulating 1,25(OH)D.
With aging, anatomic changes in the large intestine include mucosal atrophy, cellular and structural abnormalities in the mucosal glands, hypertrophy of the muscularis mucosa, and atrophy of the muscularis externa. Diverticulosis (presence of outpouches in the intestinal wall called “diverticula”) increases with age. This is thought to be due to increased pressure and colon wall weakness. Functional changes include slowed transit, altered coordination of contraction, and an increase in opioid receptors that may predispose the older person to drug induced constipation.
Synthesis of vitamin-K-dependent clotting factors is decreased. The bile composition has a higher lithogenic index, which predisposes the older person to cholesterol gall-stone formation. In the liver, many drugs are metabolized more slowly by the cytochrome P-450 enzymes in older than in younger people. This decline in clearance may be due to an age-related reduction in liver mass that results in decreased hepatic metabolic capacity.
Age-related changes in the urinary bladder include reduced bladder elasticity, muscle tone, and capacity. Detrusor instability, and a weakened urinary sphincter are also consequences of aging.
The urinary system maintains fluid and electrolyte homeostasis remarkably well unless it is challenged. Between the ages of 30 and 80 years, renal mass decreases by 25% to 30%, and fat and fibrosis, in part, replace the functional parenchyma.
- Diffuse sclerosis of glomeruli proceeds at such a rate that 30% are destroyed by age 75.
- The basement membrane is thickened
- Patients have significant linear decreases in creatinine clearance with age (7.5 to 10 mL per minute per decade)
- It is important to recognize that even in the face of a “normal” creatinine clearance (CrCl) calculation, a reduction in CrCl does exist in frail older adults due to losses of lean muscle mass
Calculation of creatinine clearance in elderly:
Men: creatinine clearance (ml/min) =
140-age (years) X body weight (kg)
72 X serum creatinine (mg/dL)Women: men’s formula above x 85% (0.85)
- Impairment in excreting an acid load. The ability to maximally dilute urine and excrete a water load is impaired.
- The glucose threshold of the older kidney is lower.
- The renin-angiotensin system (RAS) is down-regulated such that there is a decreased renin response to volume depletion or salt restriction.
- Atrial natriuretic peptide (ANP) increases with age, further suppressing aldosterone release.
- Hydroxylation of vitamin D, is impaired with age, as is the metabolism of parathyroid hormone, calcitonin, and glucagon. The production of erythropoietin, however, appears to be unchanged with age.
Older people are at higher risk of volume depletion:
- Basal levels of antidiuretic hormone (ADH) are somewhat increased with age, yet basal serum sodium and basal osmolality are unchanged
- Reserves of body water are decreased because water constitutes a decreasing percentage of body mass with increasing age
- Central nervous system regulation of body fluids status is altered with aging. The older person has a decreased thirst drive, which may be mediated by decreased endogenous opioids (endorphins) or decreased responsiveness to them
- Maximum urine osmolality decreases and achievement of the maximally concentrated urine is delayed; thus, the volume of water excreted in the urine during water deprivation is higher
- The kidney's responsiveness to the renin-angiotensin-aldosterone pathway and atrial natriuretic peptide is impaired
- The number of very long nephrons that maximally concentrate urine decreases, and the interstitium around the loops of these long nephrons has a somewhat lower tonicity, which contributes to the propensity of the older person to develop dehydration
- It is much more difficult for older persons to excrete a fluid load, which also predisposes them to hyponatremia or even congestive heart failure.
Weight gain through age 60 is common, followed by decline thereafter. These changes are thought to be due to activity and intake changes rather than age-related physiology. However, body fat increases and redistributes, lean mass and total body water decrease. These are age-related changes which occur even in those who do not gain weight. Body fat and lean mass changes impact geriatric pharmacokinetics and creatinine clearance.
Overall, from age 30 to age 80, muscle mass decreases in relation to body weight by about 30% to 40%. From age 30 to age 80 a person’s strength of grip decreases 60%; however, activity plays an important mitigating role: assembly line workers who used their grip over their working life do not appear to lose any strength. Lower-extremity strength is lost at a relatively faster rate than upper-extremity strength, and is one of many contributions to increased fall risk in the elderly.
Though synaptic remodeling appears to occur at all ages, the stability of neuromuscular innervation is decreased with aging and synapses are eliminated. The contraction of the muscle is also altered. Examination of ankle dorsiflexion reveals a slower time to peak tension and a slower relaxation.
Skeletal muscle from older adults shows altered energetics. The decrease in enzyme activity of glycolytic enzymes is greater than that of oxidative enzymes. The diaphragm appears to be relatively resistant to these aging changes, underscoring the mitigating effect of activity.
By age 80, height loss of 2 inches is common. Changes in posture, normal age-related disc compression and increased hip and knee flexion all. Further height loss can occur with disease-related vertebral compression fractures associated with osteoporosis. Age-related changes include a reduction in bone density. In women, bone density losses accelerate during the post-menopausal years and osteopenia can become osteoporosis (Type I). Elderly men can also develop osteoporosis (Type II).
Osteoporosis principally represents increased resorption and defective formation of bone during remodeling. Type II osteoporosis (men and women) is felt to be the result of age-associated increases in parathyroid hormone levels, coupled with decreases in circulating levels of vitamin D, growth hormone, and insulin-like growth factors. These changes, along with a frequently decreased dietary intake of calcium, lead to decreased osteoblast functioning and inadequate bone formation.
The weight of the brain decreases significantly with normal aging. Cerebral blood flow decreases 20% and significant decrements in cerebral autoregulation occur. The age-related loss of neurons is not diffuse, and the most prominent losses tend to occur in the largest neurons. The subcortical regions, locus ceruleus and substantia nigra, appear to have large losses. In general, the density of dendritic connections of the remaining cortical neurons is decreased. In some areas, however, the dendritic connections may increase, perhaps as a result of chronic repatterning of the brain, invoked to compensate for cellular dropout. Neurons continue to form new synapses throughout the life span.
Lipofuscin appears to accumulate in certain areas of the brain, particularly in the hippocampus and frontal cortex, but the impact of lipofuscin on function is unknown. Myelin decreases, notably in the cortical white matter. Changes in brain enzymes, receptors, and neurotransmitters occur. These do not imply that changes in electrophysiology, thinking, or behavior occur.
Non-neurotransmitter enzymes decrease. For example, carbonic anhydrase, an important enzyme in detoxifying carbon dioxide, decreases with aging. Neurofibrillary tangles and senile plaques occur in certain areas of the brain in normal aging, but to a much smaller extent than in Alzheimer' s disease. Antibodies to paired helical filaments have identified nonamyloid plaques in Alzheimer's brains but not those of normal aged individuals. If this finding holds true, these lesions will clearly separate normal aging from Alzheimer's disease. Normal aging changes of slowed information processing and reaction time can impact ease of recall and mild forgetfulness. More significant changes are from disease rather than normal aging.
Spinal cord motor neurons are retained in large part to age 60. However, significant losses then seem to occur in the anterior horn cells. Finger and toe vibratory and tactile threshold decreases with age. Finger thermal threshold appears to increase with age. On exam, deep tendon reflexes (DTRs) may normally be diminished and Achilles’ response may even be absent. The critical feature is assessment of symmetry.
Changes in women
Estrogen production is markedly reduced (about 95%) and progesterone is also reduced. Testosterone and androstenedione production are reduced, as is the conversion by the ovary of adrenal androgens to testosterone and estrone.
Both the uterus and vagina atrophy. Vaginal walls become thinner and less elastic. Vaginal secretions are reduced, the pH increases, the microbial flora is altered, and vaginal lubrication is reduced both at baseline and during intercourse which can cause dyspareunia. In the breast, involution of glandular stromal and ductal tissue occurs as a result of estrogen deficiency. The acinar basement membrane is thicker, the lumina of the ducts are smaller, with cystic changes along the ducts, and fat tissue increases. The ligamentous support of the breast relaxes, and a loss of muscular tone results in an alteration in the breast contour.
Changes in Men
A gradual decline in male reproductive ability occurs; however, men do not have the total loss of reproductive ability that occurs in women. Sperm production decreases, and the sperm from older testes have an increased frequency of chromosomal abnormalities. The amount of total, free, and bioavailable testosterone decreases (about 35%). Because sex-hormone-binding globulin increases with age, the proportion of testosterone that is free decreases linearly with aging, probably as a consequence of a partial testicular failure. Benign prostatic hyperplasia (BPH) is present in about 90% of men by age 85. It is not clear whether this is a disease or an age-related change. BPH can lead to an increase in residual urine volume. Functionally, the volume of prostate secretions in ejaculate and in urine decreases. Erectile dysfunction (impotence), in which an erection cannot be achieved is experienced by 15% of men by the age of 65 and increases to 50% by age 80.
Older people have an increased susceptibility to hypothermia and hyperthermia. They have reduced muscle activity and less efficient shivering. Meal- or glucose-induced thermogenesis is also significantly decreased. They have impaired vasoconstrictor response to cooling by the skin arterioles, thus impeding ability to conserve heat. They have difficulty in discriminating temperature differences and often have a delayed perception of being cold, in comparison with younger people. Their skin vasodilatation response is impaired, greater threshold temperature is required to initiate sweating, and decreased sweat production occurs, both in response to heating and in response to cholinergic agonists.
The perception of being cold may also be an endocrine problem related to hypothyroidism disease which is common in older adults. Thyroid Stimulating Hormone (TSH) ultra assay and free T4 levels are needed for diagnosis. Another age-related endocrine change is impaired glucose homeostasis. This can result in an increase in serum glucose level in the presence of acute illness.
Afebrile response to infection is common in elderly persons. Up to 25% of patients who are clinically septic are afebrile. Older patients have a lower peak temperature in acute infectious illness, perhaps in part because of impaired thermal regulation, modified IL-1 and TNF-alpha responses, and hypothalamic alterations. One of the critical signs of infection in older adults – particularly frail elders – is a change in mental status. Temperature evaluation is not clinically reliable or useful in absent or low-febrile states.
The humoral antibody-mediated response appears to be significantly decreased with increasing age. Antibody response to vaccines is decreased.
The production of thymic hormones decreases and the mass of the thymus decreases by 90% from age 15 or 20 to age 75. This results in a decrease in the production of naive lymphocytes (i.e., those lymphocytes ready to respond to new challenges).
Total lymphocyte counts do not change with age. However, in the 3 years before death there appears to be a subtle, but significant, drop in circulating lymphocyte count. One study found that, during the year before death, TNF-alpha but not interleukin-1a appeared to increase.
Refer to Dermatology module.
Just a Routine Test
Mr. K is an active 90 year-old who is still working as a reporter for the local paper. He is in excellent health and takes no medications. He is scheduled for a follow up colonoscopy, since he had a benign polyp discovered three years ago. As part of the preparation the night before, he takes the routine "gallon of GoLytely" to clear his colon. He is found in the morning on the bathroom floor, groggy, with a laceration on his forehead. He doesn’t remember what happened. His BP is 120/80 lying down and 80/60 standing his pulse is 60 both lying and standing.
Questions:
When Renal Function Makes a Difference
Mrs. M is a 94 year old woman admitted to the hospital for fever and altered mental status. She lives in a nursing home and was found to be unresponsive and febrile this morning. She has an indwelling Foley catheter and her UA has numerous WBCs and bacteria. She is empirically covered for urosepsis with ticarcillin clavulanate but her blood cultures reveal enterococcus requiring use of aminoglycoside. Her serum creatinine is 0.7 mg/dl and her weight is 42 kg.
Questions:
American Academy of Periodontology, Available online at: http://www.perio.org/
American Geriatrics Society. Syllabus: Geriatric Medicine in Clinical Practice. Available online at: http://www.geriatricsyllabus.com/syllabus/main.jsp?cid=AGE
Bradley, J. G., & Davis, K. Orthostatic hypotension. American Family Physician; 2003; 68:2393-2398.
Franklin, S. S., Jacobs, M.J., Wong, N.D., L'Italien, G.J., & Lapuerta, P. Predominance of isolated systolic hypertension among middle-aged and elderly US hypertensives: Analysis based on National Health and Nutrition Examination Survey (NHANES) III. Hypertension; 2001; 37(3):869-74.
Hayflick, L. & Moody, H. R. (2002). Has anyone ever died of old age? Presentation at the 55th Annual Scientific Meeting of the Gerontological Society of America.
Lindeman, R. D., Tobin, J. & Shock, N. Longitudinal studies on rate of decline in renal function with age. Journal of the American Geriatrics Society; 1985; 33:278-285.
Peterson, M. (1994). Physical aspects of aging: Is there such a thing as “normal”? Geriatrics; 1994; 49(Feb):45-51.
Soltero, R. A., & Kujubu, D. A. How shall we manage isolated systolic hypertension in older adults? The Permanente Journal; 2003; 7(1):24-25.
Stalworth, M. & Sloane, P. D. Clinical implications of normal aging, (Chapter 2), 14-24. In, Ham, R. J., Sloane, P. D., Warshaw, G. A. Bernard, M. A., & Flaherty, E. (Eds.). Primary Care Geriatrics (5th Ed.) (2007). Mosby: St. Louis.
University of Southern California. Ageworks ®. Available online at: http://www.ageworks.com/
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The University of Kansas Medical Center