Rabu, 09 November 2011

ENGLISH TUTORIAL OF BLOCK 8


SCENARIO 5:
An eldery man recently has short memory. For example, every time he wants to read, he is always confused to find his glasses which he has put them on. When his grand children come to visit him, he cannot recognize them anymore. The man also said that he gets sleeping and urinating difficulties. After he was examined, the doctor that all of these are, probably, caused by aging process with geriatric symptoms. Other possibility is dementia.

GERONTOLOGY
Gerontology is the study of the aging processes and individuals as they grow from middle age through later life.
Gerontology  is the study of the social, psychological and biological aspects of aging. It is distinguished from geriatrics, which is the branch of medicine that studies the diseases of the elderly.
Gerontology followed by the sub-disciplines of:
1.     bio-gerontology: is the sub-field of gerontology concerned with the biological processes of aging. It involves interdisciplinary research on biological aging's causes, effects, and mechanisms.
2.    social gerontology: Social gerontology is a multi-disciplinary sub-field that specializes in studying or working with older adults.
Social gerontologists may have degrees or training in social work, nursing, psychology, sociology, demography, gerontology, or other social science disciplines. Social gerontologists are responsible for educating, researching, and advancing the broader causes of older people.
3.    medical gerontology: As with biogerontology, medical gerontology studies the biological causes and effects of aging.
4.    psycho gerontology
5.    anthropo gerontology
GERIATRIC
DEFINITION:
"Geriatrics" is medical practice that addresses the complex needs of older patients and emphasizes maintaining functional independence even in the presence of chronic disease. It requires an interdisciplinary approach - we will work with other physicians, nurses, social workers, occupational therapists and family members, in order to provide comprehensive care for these patients with multiple needs.
Geriatric is a combination between Medical Gerontology (Geriatric Medicine) and Socio Gerontology.
Geriatrics is a sub-specialty of internal medicine and family medicine that focuses on health care of elderly people.[1] It aims to promote health by preventing and treating diseases and disabilities in older adults. There is no set age at which patients may be under the care of a geriatrician, or physician who specializes in the care of elderly people. Rather, this decision is determined by the individual patient's needs, and the availability of a specialist.
Geriatrics is:
a.   the study of health and disease in later life
  1. the comprehensive health care of older persons and the well-being of their informal caregiver
Geriatrics, the care of aged people, differs from gerontology, which is the study of the aging process itself.
GERIATRIC MEDICINE
·         What kind of things that we learn in Geriatric Medicine?
The basic points are:
1. Study of aging
What is aging process?
2. The basic of clinical problems of the elderly
            a. Immobility
            b. Instability
            c. Intelectual Impairment
            d. Impairment of visison and hearing
            e. Isolation
            f. Inanition (Malnutrition)
            g. Irritable colon
            h. Incontinence Urine
            i. Infection
            j. Iatrogenesis
            k. Insomnia
            l. Immune deficiency
            m. Impotence
            n. Impecunity
3. The special features of disease in old age
4. organization & provision of medical, social, and voluntary services for old people.
AGING
DEFINITION:
In clinical, aging is a process that convert healthy adults into frail ones, with diminished reserve in most physiologycal systems and exponentially increasing vulnerability to most diseases and to death.
Aging is a summary term for a set of processes, which contribute to health deterioration and ultimately to death with the passage of time (calendar age).
In other words any process, which contributes to age-related decline in performance, productivity and health is a component of the aging process that deserves our attention and intervention.
You can think of aging as a group of processes responsible for such manifestations as increasing risk of  frailty, disability, morbidity (for age-related degenerative diseases in particular)  and ultimately increasing mortality rates.
the term "aging" refers to the biological process of growing older in a deleterious sense, what some authors call "senescence"
Senescence or biological aging is the change in the biology of an organism as it ages after its maturity. Such changes range from those affecting its cells and their function to those affecting the whole organism. There are a number of theories as to why senescence occurs; for example, some posit it is programmed by gene expression changes, others that it is the cumulative damage caused by biological processes.
AGE CATEGORY :
·         55-59 yr: initial of elderly (awal lanjut usia)
·         60-74 yr: elderly (lanjut usia)
·         75-90 yr: old (usia tua)
·         >90 yr: very old (usia sangat tua)
LIFE CYCLE:
Must be remembered!!!
Aging is already exist since the conception period, but in the initial of life, aging occurs coincided with the development process (that happen very fast), so that the aging process is covered. In a person with 30 years old, the growth and development process are stopped, so that the aging process start to appear in this age.
THEORIES OF AGING
How come we get old??
there are more than 200 theories that try to explain about aging process, but the experts support these
1.     The DNA and Genetic Theories
Pictured: KLEINSEK PhD., DONDon Kleinsek Ph.D.
Some scientists regard this as a Planned Obsolescence Theory because it focuses upon the encoded programming within our DNA. Our DNA is the blue-print of individual life obtained from our parents. It means we are born with a unique code and a predetermined tendency to certain types of physical and mental functioning that regulate the rate at which we age.
But this type of genetic clock can be greatly influenced with regard to its rate of timing. For example, DNA is easily oxidized and this damage can be accumulated from diet, lifestyle, toxins, pollution, radiation and other outside influences.
Thus, we each have the ability to accelerate DNA damage or slow it down.
One of the most recent theories regarding gene damage has been the Telomerase Theory of Aging. First discovered by scientists at the Geron Corporation, it is now understood that telomeres (the sequences of nucleic acids extending from the ends of chromosomes), shorten every time a cell divides. This shortening of telomeres is believed to lead to cellular damage due to the inability of the cell to duplicate itself correctly. Each time a cell divides it duplicates itself a little worse than the time before, thus this eventually leads to cellular dysfunction, aging and indeed death.
Further recent research by Don Kleinsek Ph.D., of GeriGene Inc. (one of the few genealogists looking for the genes involved with aging), indicates that telomeres can be repaired by the introduction of the relevant hormone. In other words telomeres and their subsequent processes affect each other. It may be possible, (once we know what each telomere is responsible for), to precisely introduce the necessary hormone and aid genetic repair, as well as the hormonal balance etc.
Another key element in rebuilding the disappearing telomeres is the enzyme telomerase, (an enzyme so-far only found in germ and cancer cells). Telomerase appears to repair and replace telomeres helping to re-regulate the clock that controls the life-span of dividing cells (see the Hayflick Limit Theory of Aging for further details).
In future protocols it may be possible to introduce telomerase. But right now we know that free radicals damage DNA (see the Free Radical Theory of Aging) and so does glycosylation (see the Cross-Linking Theory of Aging). Thus protocols for those two, as well as hormone replacement therapy may help prevent DNA damage.
2.    The Neuroendocrine Theory
Pictured: Ward Dean MD above, and Professor Vladimir Dilman below.Ward Dean
First proposed by Professor Vladimir Dilman and Ward Dean MD, this theory elaborates on wear and tear by focusing on the neuroendocrine system. This system is a complicated network of biochemicals that govern the release of hormones which are altered by the walnut sized gland called the hypothalamus located in the brain.
The hypothalamus controls various chain-reactions to instruct other organs and glands to release their hormones etc. The hypothalamus also responds to the body hormone levels as a guide to the overall hormonal activity.
But as we grow older the hypothalamus loses it precision regulatory ability and the receptors which uptake individual hormones become less sensitive to them. Accordingly, as we age the secretion of many hormones declines and their effectiveness (compared unit to unit) is also reduced due to the receptors down-grading.
These are some of the reasons that Dr. Dean recommends receptor resensitizers such as the bi-guanidine drug Metformin (which improves insulin sensitivity) and the eugeroic drug Modafinil (which improves noradrenaline sensitivity).
Professor Vladimir DilmanOne theory for the hypothalamus loss of regulation is that it is damaged by the hormone cortisol. Cortisol is produced from the adrenal glands (located on the kidneys) and cortisol is considered to be a dark-hormone responsible for stress. It is known to be one of the few hormones that increases with age.
If cortisol damages the hypothalamus, then over time it becomes a vicious cycle of continued hypothalamic damage, leading to an ever increasing degree of cortisol production and thus more hypothalamic damage. A catch-22 situation.
This damage could then lead to hormonal imbalance as the hypothalamus loses its ability to control the system. Such an argument demands the use of cortisol adjusters (such as DHEA, Gerovital-H3 ® or Phenytoin) to help slow down the cortisol accumulation.
http://www.antiaging-systems.com/resources/1/Dynamic/613/hypothalamus.gif
Dr. Dean also believes that the next-generation of hormone replacement therapy are the hypothalamus hormones (expected to be commercially available in the next few years). These types of natural supplements could present a whole new approach and concept to endocrine balance, control and improvement.
3.    The Free Radical Theory
Pictured: Denham Harman MDDenham Harman MD
This now very famous theory of aging was developed by Denham Harman MD at the University of Nebraska in 1956. The term free radical describes any molecule that has a free electron, and this property makes it react with healthy molecules in a destructive way.
Because the free radical molecule has an extra electron it creates an extra negative charge. This unbalanced energy makes the free radical bind itself to another balanced molecule as it tries to steal electrons. In so doing, the balanced molecule becomes unbalanced and thus a free radical itself. Perhaps a bit like bumper-cars crashing into each other at the Fair?
It is known that diet, lifestyle, drugs (e.g. tobacco and alcohol) and radiation etc., are all accelerators of free radical production within the body.
However, there is also natural production of free-radicals within the body. This is the result of the production of energy, particularly from the mitochondria (see the Mitochondrial Theory of Aging). The simple process of eating, drinking and breathing forms free-radicals from the energy production cycles, as the body produces the universal energy molecule Adenosine Triphosphate (ATP). Note; oxygen is a potent free-radical producer.
Free radicals are known to attack the structure of cell membranes, which then create metabolic waste products (see the Membrane Theory of Aging). Such toxic accumulations interfere with cell communication, disturb DNA, RNA and protein synthesis, lower energy levels and generally impede vital chemical processes.
Free radicals can however be transformed by free-radical scavengers (otherwise known as anti-oxidants). Particular anti-oxidants will bind to particular free radicals and help to stabilize them.
Free radicals come in a hierarchy (according to their potential for damage) with the hydroxyl-radical and the superoxide-radical at the top of the list. It is therefore necessary to take a cross-section of anti-oxidants in order for the process of elimination of the free radicals to occur, otherwise higher damage free radicals may be converted into a greater number of lower damage free radicals.
Such a broad cross-section of anti-oxidants includes substances such as beta carotene, vitamin C, grape seed extract, vitamin E and possibly also stronger substances such as Hydergine, Melatonin and Vinpocetine.
4.    The Membrane Theory of Aging
Pictured: Professor Imre Zs.-Nagy Professor Imre Zs.-Nagy
The membrane theory of aging was first described by Professor Imre Zs.-Nagy of Debrechen University, Hungary. According to this theory it is the age-related changes of the cells ability to transfer chemicals, heat and electrical processes that impair it.
As we grow older the cell membrane becomes less lipid (less watery and more solid). This impedes its efficiency to conduct normal function and in particular there is a toxic accumulation. This cellular toxin is referred to as lipofuscin and as we grow older lipofuscin deposits become more present in the brain, heart and lungs and also in the skin. Indeed some of the skin age-pigments referred to as liver or age-spots are composed of lipofuscin. It is known that Alzheimer Disease patients have much higher levels of lipofuscin deposits than compared to their healthy controls.
The cells declining efficiency also means that the essential and regular transfer of sodium and potassium is impaired, thus reducing communication. It is also believed that electrical and heat transfer is also impaired.
Professor Zs-Navy himself became involved in research to find substances that could aid in the removal of lipofuscin deposits and improve cellular lipidity and communication. The development was Centrophenoxine (Lucidril ®) which is perhaps the most efficient substance currently available; (interestingly, Professor Zs-Navy is currently working on an analogue). Other substances that have shown an ability to remove lipofuscin include DMAE and the amino-acids Acetyl-L-Carnitine and Carnosine.
5.    The Hayflick Limit Theory
Pictured: Dr. Leonard Hayflick Dr. Leonard Hayflick
The Hayflick Limit Theory of Aging (so called after its discoverer Dr. Leonard Hayflick) suggests that the human cell is limited in the number of times it can divide. Part of this theory may be affected by cell waste accumulation (which is described in the Membrane Theory of Aging).
Working with Dr. Moorehead in 1961, Dr. Hayflick theorized that the human cells ability to divide is limited to approximately 50-times, after which they simply stop dividing (and hence die).
He showed that nutrition has an effect on cells, with overfed cells dividing much faster than underfed cells. As cells divide to help repair and regenerate themselves we may consider that the DNA & Genetic Theory of Aging may play a role here. Maybe each time a cell divides it loses some blue-print information. Eventually (after 50-odd times of division) there is simply not enough DNA information available to complete any sort of division?
We also know that calorie restriction in animals significantly increases their life-span. In essence less fed animals live longer. Is this because they are subject to less free radical activity (see the Free Radical Theory of Aging) and therefore less cellular damage? Or is it that insulin and glucose damage (see the Cross-Linking Theory of Aging and the Neuroendocrine Theory of Aging for details) is less prevalent in them than in overfed animals?
The Hayflick Limit indicates the need to slow down the rate of cell division if we want to live long lives. Cell division can be slowed down by diet and lifestyle etc., but it is also surmised that cell-division can be improved with many of the protocols of the other aging theories described herein.
The use of ribonucleic acids (RNAs, the building-blocks of DNA), improve cell repair processes, enhance cellular capabilities and increase the maximum number of cell divisions in animals and vitro tests. Human clinical studies with RNA supplements such as NeyGeront ® and RN13 ® indicate that there are a number of biological, physiological and practical improvements for geriatric patients.
If laboratory results prove true also for the individual, then Carnosine will be another potent Hayflick Limit extender.
6.    The Mitochondrial Decline Theory
The mitochondria are the power producing organelles found in every cell of every organ. Their primary job is to create Adenosine Triphosphate (ATP) and they do so in the various energy cycles that involve nutrients such as Acetyl-L-Carnitine, CoQ10 (Idebenone), NADH and some B vitamins etc.
 is literally the life giving chemical because every movement, thought and action we make is generated from it. Yet very little ATP is literally the life giving chemical because every movement, thought and action we make is generated from it. Yet very little ATP can be stored in the body.
It is estimated that a 180 lb. man needs to generate an average of 80-90 lbs. of ATP daily! Under strenuous exercise the use of ATP may rise to as much as 1.1 lbs. per minute! But reserves of ATP are considered to be no more than 3-5 ounces, thus under those same strenuous exercise conditions that's approximately 8-seconds worth! Thus it becomes apparent that the mitochondria have to be very efficient and healthy, in order to produce a continuous supply of essential ATP for the necessary repair and regenerative process to occur.
Chemically speaking, under normal conditions the mitochondria are fiery furnaces and subject themselves to a lot of free radical damage (see the Free Radical Theory of Aging). They also lack most of the defenses found in other parts of the body, so as we age the mitochondria become less efficient, fewer in number and larger. Accordingly, ATP production declines.
As organs cannot borrow energy from one another, the efficiency of each organs mitochondria are essential to that particular organs repair processes and functions. If a particular organs mitochondria fail, then so does that organ (which of course can lead to death).
Enhancement and protection of the mitochondria is an essential part of preventing and slowing aging. Enhancement can be achieved with the above mention nutrients, as well as ATP supplements themselves. Protection may be afforded by a broad spectrum of anti-oxidants substances, as well as substances such as Idebenone and Pregnenolone.
Of particular use may be Acetyl-L-Carnitine and Hydergine, both of which have been proven in experiments to greatly improve the mitochondria condition of aged animals.
7.  The Cross-Linking Theory (Glycosylation Theory of Aging)
The Cross-Linking Theory of Aging is also referred to as the Glycosylation Theory of Aging. In this theory it is the binding of glucose (simple sugars) to protein, (a process that occurs under the presence of oxygen) that causes various problems.
Once this binding has occurred the protein becomes impaired and is unable to perform as efficiently. Living a longer life is going to lead to the increased possibility of oxygen meeting glucose and protein and known cross-linking disorders include senile cataract and the appearance of tough, leathery and yellow skin.
Indeed, you can see cross-linking in action now. Simply cut an apple in half and watch the oxygen in the air react with the glucose in the apple as it turns yellow and brown and eventually becomes tough.
Diabetes is often viewed as a form of accelerated aging and the age related imbalance of insulin and glucose tolerance leads to numerous problems; these have been called Syndrome X. In fact, diabetics have 2-3 times the numbers of cross-linked proteins when compared to their healthy counterparts.
The cross-linking of proteins may also be responsible for cardiac enlargement and the hardening of collagen, which may then lead to the increased susceptibility of a cardiac arrest.
Cross linked proteins have also been implicated in renal disorders.
It is also theorized that sugars binding to DNA may cause damage that leads to malformed cells and thus cancer.
The modern diet is of course a very sweet one and we are bombarded with simple sugars from soft drinks and processed foods etc. One obvious example to reduce the risk of cross-linking is to reduce sugar (and also simple carbohydrates) in ones diet. Some pharmacological interventions that could help reduce the carbohydrate/ starch/ glucose intake and affect, include Acarbose and Metformin.
But other supplements are also appearing that show great promise in the battle to prevent, slow and even break existing cross-links. Two of the most important at present are Aminoguanidine and the amino-acid Carnosine.
CHANGES IN AGING
1.       PHYSIOLOGICAL CHANGE

Physiological changes occur with aging in all organ systems. The cardiac output decreases, blood pressure increases and arteriosclerosis develops. The lungs show impaired gas exchange,  decrease in vital capacity and slower expiratory flow rates. The creatinine clearance decreases with age although the serum creatinine level remains relatively constant due to a proportionate age-related decrease in creatinine production. Functional'changes, largely related to altered motility patterns, occur in the gastrointestinal system with senescence, and atrophic gastritis and altered hepatic drug metabolism are common in the elderly. Progressive elevation of blood glucose occurs with age on a multifactorial basis and osteoporosis is frequently seen due 'to a linear decline in bone mass after the fourth decade. The epidermis of the skin atrophies with age and due to changes in collagen and elastin the skin loses its tone and elasticity. Lean body mass declines with ag'e and this is primarily due to loss and atrophy of muscle cells. Degenerative changes occur in many joints and this, combined with the loss of muscle mass, inhibits elderly patients locomotion. These changes with age have important practical implications for the clinical management of elderly patients: metabolism is altered, changes in response to commonly used drugs make different drug dosages necessary and there is need for rational preventive programs of diet and exercise in an effort to delay or reverse some of these changes.

NORMAL AGING affects all physiological processes. Subtle irreversible changes in the function of most organs can be shown to occur by the third and fourth decades of life, with progressive deterioration with age. The rapidity of the decline in function varies with the organ system under consideration but is relatively constant within a given system. Thus, the rate of aging is the same for a 45-year-old man as it is for an 85-year-old man; the difference is that by 85 years of age more agerelated changes have accumulated. An important concept not widely appreciated is the distinction that must be made between the normal attrition of function occurring in all persons with advancing age and the loss of function that marks the onset of pathological changes from one or more of the diseases encountered with increased prevalence in the older age group. Failure to recognize this difference can lead to progressive disability from treatable diseases in many cases.
In this review we will discuss some of the physiological changes that occur with aging in the cardiovascular, respiratory, renal, gastrointestinal, endocrine, skin and musculoskeletal systems and
their consequence for various therapeutic approaches in the day-to-day management of patients. We will concentrate mostly on changes that are of clinical importance and not discuss the increased incidence of such disorders as neoplasia that are well known to occur in all these systems.
The attrition of the neurological and immune systems with age are discussed in other sections of this issue.
Cardiovascular System
Heart
Cardiac output decreases linearly after the third decade at a rate of about 1 percent per year in
normal subjects otherwise free of cardiac disease. Due to the small decrease in surface area with
age the cardiac index falls at a slightly slower rate of 0.79 percent per year. The cardiac output
of an 80-year-old subject is approximately half that of a 20-year-old. The basis of this decrease
in cardiac function is unknown but may relate to one of several factors. First, senescent cardiac muscle has a decreased inotropic response to catecholamines, both endogenous and exogenous, and, perhaps of more clinical significance is a decreased response to cardiac glycosides. Second, with aging there is an associated increase in diastolic and systolic myocardial stiffness, perhaps due to increased interstitial fibrosis in the myocardium. Third, there is a progressive stiffening of arteries with age, particularly of the thoracic aorta, leading to an increased afterload of the heart. And finally, in autopsy studies as many as 78 percent of subjects older than 70 have been shown to have amyloid deposits in the myocardium, predominantly in the atria, but also in the ventricles and pulmonary vessels.' When amyloid is present in the ventricles and vessels it may lead to congestive failure, often with conduction defects. Cardiac amyloidosis may be a relative contraindication to treatment with digoxin since there appears to be an increased risk of arrhythmias.
GERIATRIC MEDICINE
Hypertension
A progressive increase in blood pressure after the first decade of life has long been regarded as
a normal consequence of aging and was the basis for ignoring the presence of hypertension in the
elderly. Only in the past decade or so have prospective studies provided evidence of the grave portents of hypertension for the older age group as well as the young and the potential preventive
value of early treatment. The elevation with age is more pronounced for systolic than diastolic pressure. When hypertension is defined as a systolic blood pressure of greater than 160 mm of mercury and simultaneously a diastolic of greater than 95 mm of mercury, approximately 16 percent of the general adult population is hypertensive but about 50 percent of those over age 65 are hypertensive. The Framingham Study clearly established that high blood pressure is a significant risk factor for stroke, coronary artery disease and congestive heart failure.6 Moreover, cardiovascular disease was a more frequent cause of death and morbidity in the hypertensive subjects older than 65 years of age than in the younger subjects. More recently the Hypertension Detection and Follow-up Program confirmed these findings and showed, as did the Veterans Administration Cooperative Study, that treatment was beneficial.7 All of these studies, as well as the European Working Party on High Blood Pressure in the Elderly, have shown that blood pressure in the elderly can be safely lowered when the antihypertensive therapy is chosen carefully and monitored regularly. The main question that needs to be answered at present is whether isolated systolic hypertension needs to be treated in elderly patients. Not enough data are yet available to answer this question and large-scale clinical trials are desperately needed. The discovery of nearly a dozen population isolates throughout the world among whom blood pressure does not increase with advancing age is provocative. In each isolate the culture had no access to added salt in the diet, suggesting an additional possible preventive approach that needs evaluation in our own culture.

Arteriosclerosis and Coronary Artery Disease
Thickening of the walls of arteries with hyperplasia of the intima, collagenization of the media and accumulation of calcium and phosphate in elastic fibers progressively occurs with aging. In addition, the lipid content of nonatherosclerotic portions of vessels increases, particularly of cholesterol Although none of these age-related changes has definitely been shown to be a precursor of arteriosclerosis, atherosclerosis clearly increases with aging. Raised fibrous plaques that contain lipid, atheromas, of the abdominal aorta increase linearly from onset at about age 20 to reach approximately 30 percent by -age 70. In general, atherosclerosis occurs earlier in the aorta and carotid arteries than in the coronary and cerebral arteries and peripheral vascular disease appears later. Myocardial infarction from coronary artery disease increases dramatically with age and although many risk factors are known, age itself is probably the most significant. Prevention at present is aimed at amelioration of the other factors, such as hypertension, obesity and cigarette smoking.

Respiratory System
Lung Volume
A linear decrease of vital capacity is found that amounts to a decrement of about 26 ml per year for men and 22 ml per year for women starting at age 20.'3 The total lung capacity remains constant, however, and thus the residual volume increases with age. The ratio of residual volume to total lung capacity (RV/TLC) is about 20 percent at age 20 and increases to 35 percent by age 60, with most of this increase in RV/TLC occurring after age 40.10 In most studies the functional residual capacity also increases, although not as rapidly as the residual volume.

Gas Exchange
Although alveolar oxygen tension remains constant with age, arterial oxygen pressure shows a progressive decrease, thus increasing the alveolararterial oxygen difference (A-a).0.9 Most of this
decrease in arterial oxygen pressure results from a mismatch of ventilation and perfusion. The elastic recoil of the lungs decreases with age and thus there is a greater tendency for airways to collapse. This is measured as an increase in "closing volume" which increases linearly above the age of 20. Airway closure occurs predominantly in the dependent zones of the lung and in the upright position this will result in a ventilationperfusion mismatch because more perfusion occurs in the lower lobes. Although an age-related decrease in carbon monoxide diffusing capacity has been shown, it is unclear whether this contributes to the reduction in arterial oxygen pressure.

Flow Rates
There is a 20 percent to 30 percent decrease in maximum voluntary ventilation, forced expiratory volume in one second, maximal expiratory flow rate and maximum midexpiratory flow during adult life. The basis for these changes is not known but again may relate to a decrease in the elastic recoil properties of the lung. This would result in both a decreased ability to generate normal expiratory pressures as well as increased resistance to expiration due to abnormally early airway collapse.

Infections
It is well known that elderly patients have a pronounced increase in incidence of pneumonia, both bacterial and viral, compared with younger persons. Although much of this may be due to a general depression of immune system function, other more specific factors may play a role. Pneumonia generally results from aspiration of oropharyngeal secretions and such aspiration appears more frequent in the elderly. Perhaps of even greater importance, the normal mechanical clearing of the tracheobronchial tree by the mucociliary apparatus is significantly slower in nonsmoking older persons than in their younger counterparts. Finally, due perhaps to poor oral hygiene, decreased flow of saliva or difficulty with swallowing, older persons have a higher rate of colonization of their oropharynx with Gram-negative bacilli than do younger persons.

Genitourinary System
Kidneys
A gradual decrease in the volume and weight of the kidneys occurs with aging so that by the ninth decade renal size is about 70 percent of that of the third decade. Moreover, there is a decline in the total number of glomeruli per kidney from about 1,000,000 below the age of 40 to about 700,000 by age 65.12 13 With the reduction in the number of glomeruli there is a concomitant age-related decrease in the creatinine clearance (C,.) and the decline is according to the following equation: C,., (ml/minute) = 135.0-0.84 X age (years).
The serum creatinine concentration, however, changes little with age.This is because of an age-related decrease in creatinine production due to a reduction in muscle cell mass that parallelsthe
decrease in glomerular filtration rate. This attrition in renal function has significant consequences for the clinical management of elderly patients. Thus, drugs such as aminoglycosides, digoxin, penicillin and tetracycline which are primarily cleared by glomerular filtration will have a prolonged half-life in an elderly person even when the dosage is modified through the standard use of the serum creatinine concentration. In fact, in one study the half-life of these drugs in older subjects with a normal serum creatinine concentration was about twice that in younger persons.'" Although the serum creatinine concentration does not change, there is a small but significant age-dependent increase in the blood urea nitrogen (BUN) concentration and the rate of rise is approximated by the following equation: BUN (mg/dl) = 7.56 + 0.119 X age.
This increase in the blood urea concentration is not always seen, however, since there is frequently
a decrease in the intake of protein as well. Tubular function also declines with aging. The maximal reabsorption of glucose follows a linear decrease such that the glucose threshold ranges from 130 to 310 mg/dl in elderly persons. Glycosuria may therefore be misleading in the diagnosis and management of diabetes mellitus in older persons. Both the concentrating and diluting ability of the kidneys also slowly deteriorates. This may contribute to the increased proclivity for dehydration and hyponatremia seen in older patients although excessive use of diuretics probably
plays a more major role. Interestingly, in the absence of congestive heart failure or urinary tract obstruction or infection, the nocturia of old age appears to be primarily of a central nonrenal origin due to a disturbance in the normal diurnal rhythm of excretion.

Bladder
Urinary incontinence has been found in 17 percent of men and 23 percent of women older than 65 years. In about half of the women and a fifth of the men this was due to stress incontinence alone. The capacity of the bladder decreases with age from about 500 to 600 ml for persons younger than 65 to 250 to 600 ml for those older than 65. Perhaps more important, in younger persons the sensation of needing to void occurs when the bladder is little more than half filled but in many who are older the sensation occurs much later or sometimes not at all, leading to overflow incontinence. These changes appear to be due more often to central nervous system disease than to bladder dysfunction.

Prostate
Enlargement of the prostate occurs in most older men; by age 80 more than 90 percent of men have symptomatic prostatic hyperplasia with varying degrees of bladder neck obstruction and urinary retention. Prostate surgery is required in 5 percent to 10 percent of all men at some time. Recently the cause of the hyperplasia has been more clearly defined; the concentration of dihydrotestosterone (DHT) increases in prostatic cells. The increase in the intraprostatic concentration of DHT is due to two age-related changes: an estrogen-mediated enhancement of androgen receptors on prostatic cells as well as a decrease in the intracellular catabolism of DHT. Future treatment of benign prostatic hyperplasia may be endocrinologic, aimed at reducing the intracellular concentration of DHT by competitive steroid antagonists.

Gastrointestinal System
Esophagus
Age-related changes of esophageal function, socalled presbyesophagus, are due primarily to disturbances of esophageal motility. The esophagus in an older person may have a decreased peristaltic response, an increased nonperistaltic response, a delayed transit time or a decreased relaxation of the lower sphincter on swallowing. The decrease in peristalsis and delay in transit time may lead to dysphagia with a voluntary curtailment of caloric consumption. Nonperistaltic contractions are found almost exclusively in the elderly. They occur in the lower two thirds of the
esophagus and are the cause of the "corkscrew" esophagus seen on barium swallow studies. Decreased relaxation of the lower esophageal sphincter on swallowing is the basis of achalasia and is more common in the elderly population.

Stomach
The incidence of atrophic gastritis increases significantly with age. In a Scandinavian study approximately 40 percent of apparently healthy subjects older than 65 had evidence of atrophic gastritis.2" At present, atrophic gastritis is divided into type A which is confined to the body and
fundus sparing the antrum and type B which is associated with atrophy of both antral and fundic glands. Both types increase in frequency with advancing years. Severe atrophic gastritis results
in achlorhydria, deficient intrinsic factor secretion, decreased pepsinogen production and, in type A, hypergastrinemia due to lack of acid inhibition of gastrin cell secretion. Type A atrophic gastritis appears to be an autoimmune disease, whereas type B may be due to local environmental factors such as chronic enterogastric bile reflux. Both types of atrophic gastritis are premalignant lesions.

Colon
A decrease in intestinal motility occurs with age. The colon becomes hypotonic, which leads to increased storage capacity, longer stool transit time and greater stool dehydration. These are all
etiologic factors in the chronic constipation that plagues the aged. Laxative abuse therefore results and is the most common cause of diarrhea in the elderly. A high-fiber diet is the treatment of choice and this can best be achieved by prescribing a diet rich in bran. Whether or not constipation is an etiologic factor in diverticulosis remains unclear but age certainly is. Diverticula are uncommon below the age of 40 but steadily increase thereafter until nearly 50 percent of those older than 80 have diverticulosis. Symptoms are present in only about 20 percent to 25 percent of those who are affected and severe disease with inflammation and bleeding occurs in a much smaller number.

Sphincter Control
Loss of control of the internal and external anal sphincters in the elderly in the presence of essentially normal cognitive function is a most emotionally traumatic and demeaning experience. The resulting fecal incontinence is one of the major causes for admission of many otherwise healthy persons to long-term care facilities. Recent studies have shown the cause to be a loss of tone of the external rectal sphincter. Biofeedback techniques allowed the regaining of sphincter and bowel control in as many as 70 percent of a group of patients studied.

Liver and Biliary Tract
The liver decreases in weight by as much as 20 percent after the age of 50 but perhaps because
of its large reserve capacity this attrition is not reflected by a decrease in the usual liver function
tests. Although tests of liver function show little or no change with age, a large number of drugs
such as diazepam and antipyrine are known to be metabolized more slowly by the liver in the elderly. This alteration in hepatic drug metabolism may be due to a decrease in the appearance, amount or distribution of the smooth endoplasmic reticulum. Biliary tract disease is unusual before
the third decade and the incidence of cholelithiasis increases greatly with age. In a large autopsy
series of subjects older than 70 years, 30 percent had gallstones and another 5 percent had previously had a cholecystectomy. In general, surgical operation is indicated in patients with gallstones, even if asymptomatic, since the risk of complications in an elderly patient is greater than the risk of operation.

Endocrine System
Glucose Homeostasis
Increasing age results in a progressive deterioration in the number and the function of insulinproducing beta cells. The capacity of these cells to recognize and respond to changes in glucose concentration is impaired. In elderly subjects a greater proportion of the insulin released into the circulation in response to a glucose challenge is in the form of the inactive precursor proinsulin than in their younger counterparts. Of perhaps even greater importance is the development of progressive peripheral insulin resistance with age. Compared with younger persons the elderly have a relative decrease in lean body mass with a relative increase in adiposity. Since little change in the total number of fat cells occurs with age, the increased adiposity appears due to an increase in fat cell size. In general, as adipocytes enlarge they turn down their insulin receptors. Thus, even in nonobese elderly persons there is peripheral insulin resistance due to increased size of adipocytes with a relative decrease in insulin receptors. The combination of abnormal beta cell function with peripheral insulin resistance leads to increased glucose intolerance in normal aged persons. Although diabetic ketoacidosis and lactic acidosis are uncommon in elderly diabetic persons, hyperosmolar nonketotic coma occurs with some frequency. As already discussed, there is a decrease in the renal concentrating function with age as well as a decrease in the maximal reabsorption of glucose. Thus, even mild hyperglycemia may lead to osmotic diuresis. This will cause further hyperglycemia and ultimately dehydration. The dehydration may lead to vascular insufficiency in elderly patients and they may become obtunded and refuse to drink; rapid progression to coma may then ensue. This syndrome is frequently precipitated or exacerbated by a myocardial infarction, pneumonia or urinary tract infection.

Osteoporosis
Osteoporosis is a skeletal disorder characterized by a decrease in bone mass which may result in
mechanical failure of the skeleton. The decrease in bone mass is an age-related phenomenon. Beginning in the fourth decade there is a linear decline in bone mass at a rate of about 10 percent
per decade for women and 5 percent per decade for men. Thus, by the eighth and ninth decades
30 percent to 50 percent of the skeletal mass may be lost. The decrease in bone mass is due to a
relative increase of bone resorption over formation but the basis of this is unknown. Hormonal factors certainly play a role since women are more susceptible than men and the rate of development of osteoporosis in women accelerates after menopause. Moreover, low-dose estrogen therapy can arrest or retard bone loss if begun shortly after the menopause.

Menopause
Nowhere are the development of age-related changes more apparent than in the human female
climacteric. Menopause occurs because of the disappearance of oocytes from the ovary through
ovulation and atresia. Little is understood about the process of ovarian atresia and whether it is due to primary ovarian failure or secondary to hypothalamic-pituitary changes. Several consequences of the menopause deserve mention. First is the vasomotor instability or hot flashes. Two thirds to three quarters of menopausal women will experience flushing, with 80 percent having the symptoms for longer than one year and 25 percent to 50 percent for more than five years. Changes in skin temperature, skin resistance, core temperature and pulse rate occur during the flush. Besides being a major disturbance while women are awake, the hot flashes may occur during sleep, leading to waking episodes. Insomnia with possible physiologic and psychologic disturbances may thus result. It is well known that arteriosclerotic cardiovascular disease is unusual in women before the menopause. The precise protective mechanism of ovarian function is not known, but premenopausal women have a higher ratio of high-density lipoproteins to low-density lipoproteins than do postmenopausal women. Osteoporosis with its relation to the menopause has already been discussed. Changes of the skin occur with age and the recent demonstration of estrogen receptors in the skin of mice suggests that estrogens could have direct effects on aging of the skin (see below).

Skin
Epidermis
Atrophy of the epidermis occurs with age and is most pronounced in exposed areas: face, neck, upper part of the chest, and extensor surface of the hands and forearms. In addition to the thinning of the epidermis there is notable flattening of the dermal epidermal junction wit effacement of both the dermal papillae and the epidermal reti pegs. The turnover rate of cells in the stratum corneum decreases with age and in persons older than 65 it takes 50 percent longer to reepithelialize blistered skin than in young adults. The decrease in epidermal cell growth and division occur with aging, a distinction between the attricausally contribute to the increase incidence tion in function of normal aging and pathological of decubitus ulcers in older patients.

Dermis
Dermal collagen becomes stiffer and less pliable with age; elastin is more cross-linked and has a
higher degree of calcification. These changes cause the skin to lose its tone and elasticity, resulting in sagging and wrinkling. An age-related decrease in the number of dermal blood vessels also develops. This relative ischemia of the skin may also play a pathogenetic role in the development of decubitus ulcers.

Musculoskeletal System
Muscle
The age-dependent decline in lean body mass is well known and is primarily due to loss and atrophy of muscle cells. Some muscles, such as the diaphragm, show few if any changes while others, such as the soleus, show pronounced infiltration by collagen and fat.:" Age-related changes also occur in the innervation of muscle but the exact pathologic process is not well understood. Although much of the decreased locomotion of elderly subjects is due to skeletal changes (see below), a substantial part is probably secondary to decreased muscle mass and function.

Skeletal
Degenerative joint disease occurs in 85 percent of persons older than 70 years of age and is a major cause of disability. It affects both the peripheral and axial skeleton and is characterized
by degeneration of cartilage, subchondral bone thickening and eburnation, and remodeling of bone with formation of marginal spurs and subarticular bone cysts. Due to its predilection for weight-bearing joints, wear-and-tear type mechanisms must be operative. When the degenerative changes are pronounced, pain can be severe, greatly limiting the activity status of an elderly patient. Fortunately, adequate drug and surgical treatments exist but old people are truly restricted by their joints.

Conclusion
We have briefly discussed some of the major changes that occur with age in several of the body
systems. Although it is tempting to regard many of the so-called diseases of the elderly as being the end stage of normal physiologic changes that occur with aging, a distinction between the attri tion in function of normal aging and pathological states must be clearly delineated. To do otherwise jeopardizes a patient's prospect for receiving preventive and remedial therapy.
2.       PSYCHOSOCIAL CHANGE


The aging process brings change. During our lifetime, many individual changes we undergo are psychological. Three particularly relevant areas of psychological change are: information processing, personality, and the myth of senility.
INFORMATION PROCESSING 
Reaction Time
REACTION TIME INCREASES WITH AGE. Reasons for this are difficult to isolate. The increases could be caused by a slowing of perception, transmission to the brain, decoding and recoding in the brain, transmission to the appropriate responding mechanism, an/or the mecanism of the response itself.
When time is a factor, age differences appear. This change might affect products in which rapid responses are required in order to accomplish a task (e.g., using an electric food processor). Most older persons need a longer period of time to react.
Reaction time is also correlated with the complexity of the task (e.g., operating a pushbutton door lock). If both age and complexity increase, then behavior becomes less efficient.
Since so many of today's routine activities are both complex and require rapid resposes, these factors may make the tasks harder for older people. If physical and/or health problems are not present, adaptation and practice offset age-related decrements.
Experience and usage can negate some reaction time loss. For example, on an assembly line, most older workers are able to keep production quotas because they are constantly utilizing skills, experiences, and behaviors which have been developed over the years.
 Intelligence
INTELLIGENCE ENDURES. It does not appear to change with age until quite late in the life span. Decrements that do appear seem to be more a factor of motivation, vocabulary, contemporary skills, and speed than they are a factor of age-related loss.
For example, old people may not be as highly motivated as younger people when taking tests. Older groups are usually at a disadvantage with younger groups when level of formal education and recency of contact with a testing environment are considered.
In general, speed decreases as age increases, and since most intelligence test are timed, this could affect overall scores. The vocabulary of older people is frequently limited and less contemporary than that of younger persons.
This is not due to lack  of intelligence, but rather to two educational differences—fewer years of formal education and fewer recent classroom experiences, which would expose tthe person to a situation that would build a more cntemporary vocabulary.
Designers need to take this vocabularly issue into account when designing complex tasks such as setting the timing sequence on appliances.
 Learning
AGE HAS LITTLE AFFECT ON LEARNING. It may take longer for an older person to learn something, but this illustrates, once again, that speed rather than ability differentiates older from younger learners.
Designers should note that for older people, retention is greatest for things which are both seen and heard (redundant cuing). Retention is next greatest for things which are heard, and lowest for things which are seen.
Designers may help older people by breaking complex tasks into simple, sequential sub-tasks, thus making learning easier.
Memory
Memory changes that accompany the aging process have a definite pattern. As people age, they tend to have more and more difficulty with short-term recall whereas long-term recall remains much more inact.
Reasons for this are unclear. It may be due to accumulated loss of neurons in the brain, but this is currently subject to debate.
Some researchers believe that social factors are responsible for memory loss, since the past, for many persons, may have been much more pleasant than the present. However, there is no general agreement in this matter either.
The programming of task sequences, such as found in pre-dialing features on many telephones, begins to address the problem of short-term recall.
 Problem-Solving
PROBLEM-SOLVING TECHNIQUES DIFFER WITH AGE. As age increases, we tend to solve problems differently from younger persons, Older people are much more reluctant to use trial-and-error beaviors than are younger people.
Prior to attempting a solution, most older people prefer to take time to "think through" the situation. Younger people are prone to use "trial and error" more quickly and more frequently. And while our reaction time increases with age and correlates with the comp[exity of a task, this increase is only measured in miliseconds..
This behvior could affect the manner in which older Americans use mechanical devices. Clear, easy-to-follow directions go a long way to encourage trial and error behavior and avoid intimidating older people.
 PERSONALITY

Aging does not affect us as a person — our personality remains fairly constant throughout our lifespan. Not only do we retain our individual differences, these differences become even more pronounced as we get older.
As we age, we generally become more and more like the person we were in our youth; a placid youngster becomes a more placid older person, a talkative teenager becomes a talkative older person, and a stubborn youngster carries the trait of stubbernness into old age. Still, wide variations have been observed, and it's difficult to make accurate predictions in this area.
Moreover, most people assume that when you get old it is "natural" to become forgetful and to lose contact with reality. This simply is not  true. While we may experience some difficulty with short-term memory as we get older, our long-term memory generally remains sound.
Except for gradual changes in our physical appearance and experiencing more physical problems, being "old" feels no different from how we feel now or when we were young.
In reality, an old person is a young person who has just lived longer.
Social Factors
SOCIETY IS CREATED FROM A CONSENSUS OF INDIVIDUALS.
These individuals, in turn, are influenced by the society in which they live. Thus, both Individuals and groups define and re-define our sense of self as we develop and as society changes. And society's view of "growing old" or being "old" is no exception to this process.
Our contemporary society is, in part, a product of the past. Past and present factors shape the society of tomorrow. Examining the social factors of today is similar to viewing a single frame of a motion picture.
Today's frame is a product of yesterday, but which now includes the largest number and percentage of older persons than ever before—more people age 65 and over are living today than have ever lived previously in all of recorded history.
These large numbers of older persons are a new phenomenon. Societies, world wide, are only beginning to learn how to accomodate age-related changes. To confound matters, contemporary society continues to feel the escalating effects of an aging baby-boom generation.
As a result of today's youth orientation and the increassed number of older persons, three issues present themselves. Gerontologists have named them agesim, gerontophobia, and retirement.
 Ageism
AGEISM REFERS TO DISCRIMINATION BASED ON AGE. This attitude arises because of age-related changes in appearance,  in beliefs, and in other behaviors—those characteristics which supposedly make older persons "different."
Agesim is seen in many contexts. It is insidious. It is also present in financial matters and employment. It is  demonstrated by our immediate asumption that slow drivers must be old. What's more, many older Americans, regardless of economic circumstances, find it extremely difficult to obtain loans, even for modest amoounts.
Finally, the need for legal protection as provided by the Age Discrimination in Employment Act (in effect for those age 40 and above) reflects the extent to which ageism permeates society.
 Gerontophobia
GERONTOPHOBIA IS THE FEAR OF OLD AGE, especially of growing old. This fear is a by-product of the high value contemporary society places on youth and productivity. It touches all facets of life, from physical appearance to the fear of death.
Since the dawn of human history people have sought the secret of immortality. We still search for that secret potion that will maintain our youth and keep us from aging. In his book, Age Wave, Ken Dychtwald identifies seven markers that can induce our phobia:
·         If young is good, then old is bad
·         If the young have it all, the old are losing it
·         If the young are creative, the old are dull
·         If the young are beautiful, then the old are unattractive
·         If the young are stimulating, then the old are boring
·         If the young are full of passion, then the old are beyond caring
·         If the children are tomorrow, the old represent yesterday
Each of us is constantly bombarded with incentives to to remain young and prolong our lives through medical breakthroughs. Unfortunately, this attitude has been internalized by many people — both old and young.
But, in the end, each of us will experience the aging process and, unless we die in our early years, we will continually grow older and struggle with the inevitable reality that our end is gradually approaching.
Retirement
RETIREMENT IS AN AMBIVALENT CONCEPT. It represents a reward for participation in the labor force. It also represents a mechanism to ensure turnover of the labor force, with younger workers moving into slots vacated by retirees.
On the one hand, each succeeding year the concept of retirement receives greater public support and approval as well as a transgenerational transfer of monies via the social secrity system.
On the other nand, retirement results in decreased income. It also leaves an older person with what some gerontologists describe as a "roleless role"—i.e., no alternative to the role, status, and significance of "employee" has yet evolved.
In a work-oriented society, this non-productive  status, along with society's youthemphasis, means that older people are at odds with contemporary norms in two resects: productivity and appearance! These factors contribute to the phenomena of agism and gerontophobia.
Many of the effects are obvious; others are quite subtile. All of us are guilty of ageism to some degree. Most of us suffer from gerontophobia. At the same time, we all experience the affects of the aging process, and we react to them.
Designers who are aware of and sensitive to these social phenomena are in a better position to advocate the development of accommodating products and environments.

3.
NUTRITION NEEDS CHANGE
Nutritional needs change throughout life. For the elderly, these changes may be related to normal aging processes, medical conditions, or lifestyles. Assessment of nutritional status is essential for preventing or maintaining a chronic disease and for healing. Knowing the causes of changing nutritional needs and dietary preferences is needed to understand a patient’s nutritional status. In order to meet the nutritional needs, consideration must be given to more than just diet.

Age-Related Changes and Nutrition
As people age, multiple changes occur that affect the nutritional status of an individual. Sacropenia, or the loss of lean muscle mass, can lead to a gain in body fat that may not be apparent by measuring body weight. It may be more noticeable by loss of strength, functional decline, and poor endurance. This loss also leads to reduced total body water content (Tabloski, 2006). Another common loss related to aging is changes in bone density, which can increase the risk for osteoporosis. Many changes occur throughout the digestive system. A decrease in saliva production— xerostomia—and changes in dentition alter the ability to chew and may lead to changes in food choices. There is a decrease in gastric acid secretion that can limit the absorption of iron and vitamin B12. Peristalsis is slower and constipation may be an issue because fluid intake is decreased. Appetite and thirst dysregulation also occur, leading to early satiety and a blunted thirst mechanism. Sensory changes affect the appetite in several ways. Vision loss makes shopping, preparing food, and even eating more difficult. Diminished taste and smell take away the appeal of many foods and may lead to preparing or consuming food that is no longer safe. Many other factors that are not necessarily part of the normal aging processes, but are often related to aging, create changes in appetite, what foods are chosen for meals, and the overall nutrition of the individual.
Sedentary lifestyle, social isolation, loneliness, or depression can lead to malnourishment. Medications can also change how nutrients are absorbed or how food tastes. Poverty and cognitive impairment are other issues that may affect eating habits and food choices.

Changes in Nutritional Needs
The overall nutritional requirements of the older adult do not change. What does change is the caloric intake. Because of the loss of lean muscle mass, the overall caloric intake requirement decreases while the need for other nutrients remains relatively unchanged. This makes eating nutrient-dense foods even more important for older adults. The nutrient requirements for older adults include increased intake of vitamins D, B12, and B6 and calcium. Of these, vitamin B12 is recommended exclusively to those over the age of 50 as a supplement because of the decreased absorption rate. Vitamin B12 deficiency can be responsible for depression, neurological disorders and macrocytic anemia. Protein is a nutrient that is often thought of as one to increase in aging. Unless the older adult requires additional protein for healing and strength, this is not necessarily the case. Because of the overall decrease in muscle mass, the recommended daily allowance does
not suggest increasing protein requirements in the elderly. Tufts University developed a Modified
MyPyramid for Older Adults that was published in the January 2008 issue of the Journal of Nutrition. This pyramid emphasizes eating nutrient-dense foods, the importance of fluid intake, and activities that may be typical of the older age group. The modified pyramid also suggests that supplements (for nutrients such as calcium and vitamins D and B12) may help people meeting their nutritional needs when food alone does not yield adequate amounts. More information on the Modified
Assessing Nutritional Status
A comprehensive assessment of nutritional status includes anthropometric measurements, laboratory values, physical exam, and patient history. Anthropometric measures include height, weight, body mass index, body fat measurement, muscle mass measurement, and body mass index. Laboratory values should include albumin, retinal-binding prealbumin, transferring, complete blood count, serum folate, vitamin B12, and cholesterol. A diet history is helpful if there is good 24-hour recall or a food record for 3 days leading up to the exam can be completed. The Hartford Foundation recommends the Mini Nutritional Assessment as a basic screening tool. This can be found on the Hartford Institute for Geriatric Nursing Web site (www.hartfordign.org) under “Try This.” There are other tools to assess areas that affect diet and nutrition including the Geriatric
Depression Scale, the Mini Mental Exam, and the Katz Index. Keep in mind that part of determining diet intake is the ability to obtain, prepare, and eat food. Knowing the financial status of the individual is also important in planning interventions. For communitydwelling seniors with limited support, these items may help explain the results found in the Mini Nutritional Assessment.

Conclusion
In order to understand the dietary needs of the older adult, it is important to know what the basic requirements of the healthy older adult are. A comprehensive assessment includes a lot more than just the basic nutritional assessment and should take into account the overall physical, mental, and psychosocial status of the person. This will lead to a better understanding of how to realistically meet the nutritional needs of the older adult.

DEMENTIA

Dementia facts*

*Dementia Facts Medically Edited by: Charles P. Davis, MD, PhD
  • Dementia is a term that describes a collection of symptoms that include decreased intellectual functioning that interferes with normal life functions and is usually used to describe people who have two or more major life functions impaired or lost such as memory, language, perception, judgment or reasoning; they may lose emotional and behavioral control, develop personality changes and have problem solving abilities reduced or lost.
  • There are different classification schemes for dementias roughly based (and with overlap) on observed problems; some frequently used are cortical (memory, language, thinking, social) , subcortical (emotions, movement, memory), progressive (cognitive abilities worsen over time), primary (results from a specific disease such as Alzheimer's disease and secondary (occurs because of disease or injury).
  • Alzheimer's disease (AD): is the most common cause of dementia in people over age 65 with cause possibly related to amyloid plaques and neurofibrillary tangles; almost all brain functions, including memory, movement, language, judgment, behavior, and abstract thinking, are eventually affected.
  • Vascular dementia: is the second most common cause of dementia caused by brain damage from cerebrovascular or cardiovascular problems (strokes) or other problems that inhibit vascular function; symptoms similar to AD but personality and emotions effected only late in the disease.
  • Lewy body dementia: is common and progressive where cells in the brain's cortex die and other contain abnormal structures (Lewy bodies); symptoms overlap with Alzheimer's disease but also include hallucinations, shuffling gait, and flexed posture with symptoms that may vary daily.
  • Frontotemporal dementia: is dementia linked to degeneration of nerve cells in the frontal and temporal brain lobes and some evidence for a genetic factor (many have a family history of the disease); symptoms in patients (usually ages 40 – 65) have judgment and social behavior problems such as stealing, neglecting responsibilities, increased appetite, compulsive behavior and eventual motor skill problems and memory loss.
  • HIV-associated dementia: is due to infection of the brain with HIV virus; symptoms include impaired memory, apathy, social withdrawal, and concentration problems.
  • Huntington's disease: is a heredity disorder caused by a faulty gene and children of a person with the disorder have a 50% chance of getting the disease; symptoms begin in 30-40 year old people with personality changes such as anxiety, depression and progress to show psychotic behavior severe dementia and chorea - involuntary jerky, arrhythmic movements of the body.
  • Dementia pugilistica: is also termed Boxer's syndrome, is due to traumatic injury (often repeatedly) to the brain; symptoms commonly are dementia and parkinsonism (tremors, gait abnormalities) and other changes depending where brain injury has happened.
  • Corticobasal degeneration: is a progressive nerve cell loss in multiple areas of the brain; symptoms begin at about age 60 on one side of the body and include poor coordination and rigidity with associated visual-spatial problems that can progress to memory loss, hesitant speech and dysphagia (difficulty swallowing).
  • Creutzfeldt-Jakob disease: is a rare disease that seems related to a gene mutation that causes rapid (death about one year after symptoms begin to develop) degenerative and fatal brain disease in people usually over 60 years old; personality changes and reduced coordination develop, rapidly followed by impaired judgment and vision and many patients develop a coma before they die.
  • Other rare hereditary dementias: – Most of these diseases develop in people between 50 – 60 years old and most have variable symptoms of poor reflexes, dementia, hallucinations, paralysis and most develop coma before death; some of the names of these diseases are Gerstmann-Straussler-Scheinker disease, familial British dementia, familial Danish dementia and fatal familial insomnia.
  • Secondary dementias: These dementias occur in patients with other disorders of movement such as Parkinson's disease or multiple sclerosis and may because by one or more problems listed above; these dementias may share symptoms with any of the above mentioned dementias but researchers are unsure if this is due to disease overlap or other causes.
  • Dementias in children: While infections, trauma and poisoning can lead to dementia in both children and adults, there are some dementias that are unique to children but may result in mental problems, seizures, reduction or loss of motor skills, blindness, neurodegeneration and death; many are inherited disorders such as Niemann-Pick disease, Batten disease, Lafora disease and mitochondrial abnormalities.
  • Other conditions that may cause dementia: Reactions to medications, endocrine and metabolic problems, nutritional deficiencies, infections, subdural hematomas, poisoning, brain tumors, anoxia (lack of oxygen), heart and lung problems.
  • What conditions are not dementia: Although these conditions may resemble some aspects of dementia, they have different causes, usually are treatable and have better outcomes; examples are depression, delirium, mild cognitive impairment and age-related cognitive decline.
  • Dementia causes: All causes of dementia result from death and damage of nerve cells in the brain; genetics and possibly the formation of different types of inclusions in the brain cells are likely the major causes, although some researchers suggest that certain inclusions may be only side effects of an underlying disorder.
  • Risk factors for dementia include advancing age, genetics (family history), smoking, alcohol use, atherosclerosis, high cholesterol, diabetes, high plasma homocysteine levels, mild cognitive impairment, Down syndrome
  • Dementia is diagnosed by using many methods such as patient's medical and family history, physical exam, neurological evaluations, cognitive and neuropsychological testing, CT's, MRI's and other brain scans, mental status exams, electroencephalograms, blood tests, psychiatric evaluations, and even some pre-symptomatic tests are available for some patients that may have a genetic link to dementia.
  • Most treatments for dementia will neither reverse or stop the disease; however, there are treatments and medications that may reduce the symptoms and slow the disease progression; they are tight glucose control by persons with diabetes, intellectual stimulating activities, lowering cholesterol and homocysteine levels, regular exercise, education, controlling inflammation of body tissues, using NSAID's and possibly other medications.

Introduction to Dementia

A woman in her early 50s was admitted to a hospital because of increasingly odd behavior. Her family reported that she had been showing memory problems and strong feelings of jealousy. She also had become disoriented at home and was hiding objects. During a doctor's examination, the woman was unable to remember her husband's name, the year, or how long she had been at the hospital. She could read but did not seem to understand what she read, and she stressed the words in an unusual way. She sometimes became agitated and seemed to have hallucinations and irrational fears.
This woman, known as Auguste D., was the first person reported to have the disease now known as Alzheimer's disease * (AD) after Alois Alzheimer, the German doctor who first described it. After Auguste D. died in 1906, doctors examined her brain and found that it appeared shrunken and contained several unusual features, including strange clumps of protein called plaques and tangled fibers inside the nerve cells. Memory impairments and other symptoms of dementia, which means "deprived of mind," had been described in older adults since ancient times. However, because Auguste D. began to show symptoms at a relatively early age, doctors did not think her disease could be related to what was then called "senile dementia. "The word senile is derived from a Latin term that means, roughly, "old age."
It is now clear that AD is a major cause of dementia in elderly people as well as in relatively young adults. Furthermore, we know that it is only one of many disorders that can lead to dementia. The U. S. Congress Office of Technology Assessment estimates that as many as 6.8 million people in the United States have dementia, and at least 1.8 million of those are severely affected. Studies in some communities have found that almost half of all people age 85 and older have some form of dementia. Although it is common in very elderly individuals, dementia is not a normal part of the aging process. Many people live into their 90s and even 100s without any symptoms of dementia.
Besides senile dementia, other terms often used to describe dementia include senility and organic brain syndrome. Senility and senile dementia are outdated terms that reflect the formerly widespread belief that dementia was a normal part of aging. Organic brain syndrome is a general term that refers to physical disorders (not psychiatric in origin) that impair mental functions.
Research in the last 30 years has led to a greatly improved understanding of what dementia is, who gets it, and how it develops and affects the brain. This work is beginning to pay off with better diagnostic techniques, improved treatments, and even potential ways of preventing these diseases.

What Is Dementia?

Dementia is not a specific disease. It is a descriptive term for a collection of symptoms that can be caused by a number of disorders that affect the brain. People with dementia have significantly impaired intellectual functioning that interferes with normal activities and relationships. They also lose their ability to solve problems and maintain emotional control, and they may experience personality changes and behavioral problems such as agitation, delusions, and hallucinations. While memory loss is a common symptom of dementia, memory loss by itself does not mean that a person has dementia. Doctors diagnose dementia only if two or more brain functions - such as memory, language skills, perception, or cognitive skills including reasoning and judgment - are significantly impaired without loss of consciousness.
There are many disorders that can cause dementia. Some, such as AD, lead to a progressive loss of mental functions. But other types of dementia can be halted or reversed with appropriate treatment.
With AD and many other types of dementia, disease processes cause many nerve cells to stop functioning, lose connections with other neurons, and die. In contrast, normal aging does not result in the loss of large numbers of neurons in the brain.

INSOMNIA IN ELDERLY
What is it?
  • Insomnia (in-som-nee-uh) is having trouble getting to sleep or staying asleep. Insomnia is also the feeling that you are not getting enough sleep. People over 65 years of age are more likely to have problems with sleep.
  •  
  • Adults need 7 1/2 to 8 hours of sleep each night. As people age their need for sleep actually stays the same or only decreases slightly (6 1/2 to 7 hours a night). Normal sleep happens in several stages. There are times in the night when you sleep lightly and do not dream. There are also periods of deep, dreamless sleep. Throughout the night you have several periods of active dreaming called REM (rapid eye movement) sleep. But, sleep patterns change as we grow older. The amount of time you spend in each type of sleep changes.

Overview

Elderly insomnia is a common complaint, both short term and long term (chronic). It is important to seek professional medical assistance to resolve the issue as it can lead to other health problems. Sleep is an important aspect of maintaining a healthy lifestyle as our bodies need time to rest and recover. A lack of sleep can also cause difficulties that are similar to symptoms of Alzheimer's disease: decreased response time, increased falls risk, decreased memory, attention and cognitive performance.
Changes in the sleep cycle that occur with age are one cause. Disturbed sleep may also be a symptom that reflects a more serious underlying medical concern. It may also accompany physical and emotional issues that are correctable or will resolve with time.

Causes

Insomnia is often a symptom of another health condition. It's important the health care professional looks for the underlying cause of the sleep problem and treats that condition.
The first task is usually to determine the duration of the insomnia: Short term (less than 3 weeks) or long-term (more than 3 weeks) problem. Then, determining the cause of the insomnia and treating the problem if possible.
If the problem remains, a non-pharmacologic treatment should be implemented.
Short-term elderly insomnia may be caused by acute stress, pain, environmental changes, medications, stimulants, or withdrawal of sedatives.
If the cause cannot be resolved with this method, doctors will typically treat with medication on a short-term basis.
Long-term elderly insomnia is more common. There are a wide variety of causes including:
  • Psychiatric disorders, such as conditioned insomnia
  • Alcohol and substance abuse
  • Depression and anxiety
  • Chronic pain
  • Nocturia
  • Many medical disorders such as congestive heart failure, hyperthyroidism, rheumatologic diseases, dementia, Parkinson's disease, chronic obstructive pulmonary disease (COPD), asthma, and gastroesophageal reflux disease (GERD).
The senior should be evaluated for these psychiatric and medical causes.
Depression is a common cause of elderly insomnia (most often resulting in early awakening) and is best treated with drugs that have sedative side effects.
Anxiety is the most common psychiatric common cause of elderly insomnia. These seniors experience difficulty falling asleep.

Non-Pharmacological Treatments

The first line of action for treating elderly insomnia should be non-pharmacological methods.
These methods include:
  • Sleep hygiene must be taught to the senior and his or her family.
  • Going to bed and waking up at the same time every day.
  • Help establish an evening routine for the senior to help them go to sleep.
  • Instruct the senior to avoid long periods of wakefulness in bed, and to not use the bed except for sleep and sex.
  • Instruct the patient to avoid napping.
  • Explain that exercise is important, but should be avoided close to bedtime.
  • Explain that caffeine, alcohol, and smoking should be avoided.
  • Stress management and relaxation therapy can also be helpful, especially if the senior is a worrier.
  • Many herbal treatments are also available although there is not strong evidence to support effectiveness.

Pharmacological Treatment Options

When medications are needed - after non-pharmacological options have been tried - those that have FDA indication for insomnia include barbiturates (pentobarbital, phenobarbital, secobarbital), benzodiazepines (quazepam [Doral], temazepam [Restoril], triazolam [Halcion]), zaleplon (Sonata), and zolpidem (Ambien).
Barbiturates are rarely used for elderly insomnia because they are dangerous, habit-forming, and have many CNS adverse effects including agitation, confusion, hyperkinesia, ataxia, nightmares, nervousness, hallucination, dizziness, and thinking abnormality.
Benzodiazepines are commonly used with adults. However, they are dangerous in the elderly. Elderly who take benzodiazepines are at an increased risk of serious adverse effects including oversedation, dizziness, weakness, unsteadiness, increased falls, mental confusion, dependence with withdrawal symptoms, lack of recall of events while on medication, amnesia, memory impairment, disorientation, nausea, change in appetite, headache, sleep disturbance, and agitation.
Zolpidem is a newer and safer treatment for short-term insomnia and should be used for 1-month-maximum. However, many seniors end up taking it for years. It can cause depression, behavioral changes, decreased respiratory function, dizziness, daytime drowsiness, drugged feelings, amnesia, diarrhea, headache, and nausea.
Zaleplon is the newest drug for short-term treatment of insomnia. It is very short-acting (2-4 hours). Zaleplon's adverse effects include drowsiness, dizziness, hallucination, tremor, vertigo, amnesia, paresthesia, depressed respiratory function, anorexia, and depersonalization. Zaleplon is useful for people who have an occasional problem falling asleep or waking up during the night, and for people who travel through time zones. However, these are not the usual complaints of the elderly.
Antihistamines are commonly used as treatment for elderly insomnia, though this is not an FDA indication. Diphenhydramine (Benadryl) is the active ingredient in over-the-counter sleep preparations such as Tylenol PM and others. Its use in the treatment of insomnia in the elderly is not recommended.

URINARY INCONTINENCE
Urinary incontinence is loss of bladder control. Symptoms can range from mild leaking to uncontrollable wetting. It can happen to anyone, but it becomes more common with age.
Most bladder control problems happen when muscles are too weak or too active. If the muscles that keep your bladder closed are weak, you may have accidents when you sneeze, laugh or lift a heavy object. This is stress incontinence. If bladder muscles become too active, you may feel a strong urge to go to the bathroom when you have little urine in your bladder. This is urge incontinence or overactive bladder. There are other causes of incontinence, such as prostate problems and nerve damage.
Treatment depends on the type of problem you have and what best fits your lifestyle. It may include simple exercises, medicines, special devices or procedures prescribed by your doctor, or surgery.

Background

Urinary incontinence is defined by the International Continence Society as the involuntary loss of urine that represents a hygienic or social problem to the individual.[1] Urinary incontinence can be thought of as a symptom as reported by the patient, as a sign that is demonstrable on examination, and as a disorder.
Urinary incontinence should not be thought of as a disease, because no specific etiology exists; most individual cases are likely multifactorial in nature. The etiologies of urinary incontinence are diverse and, in many cases, incompletely understood.
Patients with urinary incontinence should undergo a basic evaluation that includes a history, physical examination, and urinalysis (see Clinical). Additional information from a patient's voiding diary, cotton-swab test, cough stress test, measurement of postvoid residual (PVR) urine volume, cystoscopy, and urodynamic studies may be needed in selected patients (see Workup).
Videourodynamic studies are the criterion standard for the evaluation of an incontinent patient but are typically reserved to evaluate complex cases of stress urinary incontinence. Videourodynamic studies combine the radiographic findings of a voiding cystourethrogram and multichannel urodynamics. Go to Urodynamic Studies for Urinary Incontinence for more information on this topic.

Types of urinary incontinence

Four types of urinary incontinence are defined in the Clinical Practice Guideline issued by the Agency for Health Care Policy and Research: stress, urge, mixed, and overflow. Some authors include functional incontinence as a fifth type of incontinence.[2, 3, 4, 5]
Stress incontinence is characterized by urine leakage associated with increased abdominal pressure from laughing, sneezing, coughing, climbing stairs, or other physical stressors on the abdominal cavity and, thus, the bladder.[2, 6, 5] Urge urinary incontinence is involuntary leakage accompanied by or immediately preceded by urgency. Mixed urinary incontinence is a combination of stress and urge incontinence; it is marked by involuntary leakage associated with urgency and also with exertion, effort, sneezing or coughing.
Functional incontinence is the inability to hold urine due to reasons other than neuro-urologic and lower urinary tract dysfunction.
Other terms describing urinary incontinence are as follows:
  • Enuresis - Involuntary loss of urine
  • Nocturnal enuresis - Loss of urine occurring during sleep
  • Continuous urinary incontinence - Continuous leakage
Successful treatment of urinary incontinence must be tailored to the specific type of incontinence and its cause (see Treatment). The usual approaches are as follows:
  • Stress incontinence - Surgery, pelvic floor physiotherapy, anti-incontinence devices, and medication
  • Urge incontinence - Changes in diet, behavioral modification, pelvic-floor exercises, and/or medications and new forms of surgical intervention
  • Mixed incontinence - Anticholinergic drugs and surgery
  • Overflow incontinence - Catheterization regimen or diversion
  • Functional incontinence - Treatment of the underlying cause

Historical context

Urinary incontinence in women is not a recent medical and social phenomenon, but the relative importance attributed to urinary incontinence as a medical problem is increasing. Several factors responsible for the increased attention to incontinence can be cited.
First, women are more willing to talk openly about this disorder. Women are realizing that, in most cases, urinary incontinence is a treatable condition. Consequently, less embarrassment and fewer social stigmas are associated with the diagnosis.
Second, as the population ages, incontinence becomes a more frequent concern. Urinary incontinence often is the chief reason for institutionalization of elderly people.
Third, interest in urinary incontinence disorders within the medical community is surging. This increased interest is arising among basic scientists, clinical researchers, and clinicians. The subspecialties of urogynecology and female urology are emerging, and structured fellowships are in the credentialing process.
As a direct result of this increased interest, the public is becoming more aware of the problem and more active and educated about incontinence. Patient advocacy groups provide patients access to information, incontinence products, and physicians who have interest or special expertise in these disorders. In the last decade, funding opportunities for incontinence research have increased vastly. Subspecialty professional organizations and journals are now active.
Important contributions to the understanding of the structure and functioning of the lower urinary tract include an improved understanding of the anatomy and dynamic functioning of the pelvic floor and its contribution to continence. In addition, much study has been conducted to bolster the understanding of the neurophysiology of the bladder, urethra, and pelvic floor. Finally, interest in the diagnosis and treatment of incontinence is ongoing.
The discipline of urodynamic testing is a burgeoning field but remains in its scientific infancy. Techniques of dynamic imaging of the pelvic floor and lower urinary tract, along with electrophysiologic testing, hold much promise in improving the understanding of continence mechanisms and ensuring accurate diagnoses. Exciting advances in surgical, nonsurgical, and pharmacologic treatments for incontinence are reported commonly in the literature. The future ability of physicians to diagnose and treat urinary incontinence appears to be bright.
Still, much more progress is needed. An estimated 50-70% of women with urinary incontinence fail to seek medical evaluation and treatment because of social stigma. Only 5% of individuals who are incontinent and 2% of nursing home residents who are incontinent receive appropriate medical evaluation and treatment. Patients who are incontinent often cope with this condition for 6-9 years before seeking medical therapy.
In a 1997 survey of primary care physicians, about 40% reported that they sometimes, rarely, or never ask patients about incontinence. More than 40% of internists and family practitioners routinely recommended absorbent pads to their patients as a solution to incontinence disorders.[7] Continued education of the public and medical professionals is needed to improve the care rendered to individuals with urinary incontinence.
In 1989, the National Institutes of Health Consensus Development Conference estimated the annual cost of urinary incontinence in the United States to be $12.4 billion. Some experts believe that this is a conservative estimate. True costs can be difficult to estimate because many individuals do not come to the attention of medical specialists.
A 2009 survey of women in a managed care population found that the prevalence of undiagnosed urinary incontinence was 53% in the preceding year.[8] Some individuals pay out of pocket for adult incontinence undergarments, absorbable pads, skin care products, deodorants, and increased laundry expenses.
The psychosocial costs and morbidities are even more difficult to quantify. Embarrassment and depression are common. The affected individual may experience a decrease in social interactions, excursions out of the home, and sexual activity.
The psychosocial impact on at-home caregivers, spouses, or family members rarely is considered. Kelleher et al developed a questionnaire to assess the quality of life of women with incontinence.[9] This questionnaire has proven to be easy to use, valid, and reliable. This tool may be a valuable adjunct to pretherapy and posttherapy assessment, as well as valuable in comparing the quality of life impact of different urodynamic diagnoses.

 references:

and some lectures in 8 block.

kontributor: khofi khafizhah fatkhur
 

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