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\u4e8b\u5b9f\u4e0a\u3059\u3079\u3066\u306e\u5668\u5b98\u7cfb\u306f\u3001\u8001\u5316\u306b\u95a2\u9023\u3059\u308b\u7279\u5b9a\u306e\u751f\u7406\u5b66\u7684\u5909\u5316\u306b\u95a2\u4e0e\u3057\u3066\u3044\u308b\u3002\u7d2f\u7a4d\u7684\u306b\u3001\u7d30\u80de\u306e\u30bf\u30fc\u30f3\u30aa\u30fc\u30d0\u30fc\u306e\u55aa\u5931\u3001\u7c98\u819c\u306e\u6a5f\u80fd\u4f4e\u4e0b\u3001\u60aa\u6db2\u8cea\u304a\u3088\u3073\u9aa8\u683c\u7b4b\u91cf\u306e\u7121\u99c4\u3001\u8840\u7ba1\u30b3\u30f3\u30d7\u30e9\u30a4\u30a2\u30f3\u30b9\u306e\u5897\u52a0\u30a2\u30c6\u30ed\u30fc\u30e0\u786c\u5316\u6027\u4f4e\u4e0b\u3001\u304a\u3088\u3073\u8133\u840e\u7e2e\u306f\u3059\u3079\u3066\u3001\u8001\u5316\u306b\u898b\u3089\u308c\u308b\u69d8\u3005\u306a\u5909\u5316\u306b\u5bc4\u4e0e\u3059\u308b\u3002\u8001\u5316\u306e\u6b63\u5e38\u306a\u904e\u7a0b\u3068\u3001\u75be\u60a3\u306e\u8a2d\u5b9a\u3067\u8d77\u3053\u308b\u75c5\u7406\u5909\u5316\u3092\u533a\u5225\u3059\u308b\u3053\u3068\u306f\u4e0d\u53ef\u6b20\u3067\u3042\u308b\u304c\u3001\u88dc\u511f\u6a5f\u69cb\u306e\u6e1b\u5c11\u307e\u305f\u306f\u5168\u640d\u5931\u306e\u305f\u3081\u306b\u8457\u3057\u304f\u629c\u672c\u7684\u3067\u3042\u308b\u3002<\/p>\n Specifically, some of the many changes which occur are listed by organ system below.<\/p>\n Neurological<\/b><\/p>\n Abnormal compensatory mechanisms predispose individuals to neurodegeneration and dementia, Parkinson disease, and overall cerebral atrophy are observable in aging individuals.[7]<\/a><\/p>\n Gastrointestinal<\/b><\/p>\n Changes in taste and smell, altered gut motility, and intestinal microbiota abnormalities can lead to age-related anorexia and subsequent caloric and\/or nutritional deficiency. The weakening of smooth muscle in the intestinal tract can promote the development of diverticular disease and can play a role in bowel obstructions or constipation. Decreased metabolic activity, specifically in the liver, can lead to alterations in drug metabolism.[8]<\/a><\/p>\n Renal<\/b><\/p>\n Aging leads to a reduced number of functional glomeruli and an increased prevalence of sclerotic changes within the glomeruli or renal vasculature. Additionally, there is a normal decrease in GFR observed in advanced age, but this places the elderly at much higher risk for complications in the event that they develop chronic or acute kidney disease, as they have less functional glomeruli as a result of normal aging physiology.[9]<\/a><\/p>\n Cardiovascular<\/b><\/p>\n Aging lowers the threshold for cardiovascular disease development. This is mostly due to a loss of cardioprotective and compensatory mechanisms that otherwise help to prevent the development of serious cardiac disease. For example, vascular stiffening, increased left ventricular wall thickness, myocardial fibrosis, calcification of valves and their related structures, as well as decreased aerobic tolerance and increase of problematic cardiomyocyte remodeling all potentially increase risks for cardiovascular diseases with aging.[10]<\/a><\/p>\n Respiratory<\/b><\/p>\n Age-related changes in the respiratory system primarily center upon the loss of elasticity and decrease in chest wall compliance leading to increased work of breathing, as well as increased residual volume and functional residual capacity. Additionally, decreased strength and function of respiratory muscles is observable. All of these changes drop an aging patient\u2019s threshold in compensating for an acute illness or respiratory failure.[11]<\/a><\/p>\n Endocrine<\/b><\/p>\n Age-related decline in endocrine function can yield various effects within the realm of metabolic and hormonal control in aging populations. Thyroxin and triiodothyronine secretion decrease, resulting in overall decreased metabolic activity, circadian rhythms become altered, and patients are prone to reduced REM sleep. Alterations in glucose metabolism and, specifically, insulin secretion develop with age, promoting the development of diabetes mellitus in the elderly. Specific sex-linked endocrine function is impaired or altered with age as well. Women typically experience menopause in their sixth decade of life, which is accompanied by an increased risk of cardiovascular disease, loss of bone mass, and atrophy of estrogen-responsive tissue.[12]<\/a><\/p>\n<\/div>\n The process of aging is well understood to be part of the natural progression of the human life cycle. Simply by virtue of cellular degradation combined with the loss of biosynthetic and cellular repair mechanisms that might have compensated for this degradation in our youth, aging is a chronic and unavoidable state that we will eventually all enter.<\/p>\n<\/div>\n On a cellular level, aging is believed to result from a variety of factors related to cellular senescence. The overarching notion is that human cells can only replicate a finite number of times before they become senescent. Previous research in this field has shown that as a cell divides, telomeres on the DNA strand become gradually shortened.[13]<\/a>\u00a0The mechanism by which this occurs can be summarized by understanding that the telomeres appear to serve a chromosome-protective role. As the telomere length decreases, so too are the protective qualities of the proteins, which normally at the distal ends of the telomere and allow DNA repair enzymes to recognize telomeres amongst sites of DNA damage. As a result, the loss of telomere length and concomitant loss of these protective proteins exposes the ends of the chromosomes to damage by DNA repair enzymes.[14]<\/a>\u00a0This process is compounded by DNA repair complex-mediated activation of transcription factor p53, which, in conjunction with cyclin-dependent kinase inhibitor p21, can result in subsequent senescence of cells and, ultimately, cessation of their metabolic and replicative functions.[15]<\/a><\/p>\n<\/div>\n Tests relevant to aging and its associated physiology are system and patient or pathology-specific. For example, in an elderly patient with confusion or alterations in neurological status, it might be valuable to administer the mini-mental state examination (MMSE) or, whereas in a patient of 20 years old with similar symptoms, the underlying pathology is likely, not due to dementia as it would be in the elderly patient, so different testing would be necessary.[16]<\/a>\u00a0Additionally, in patients with advanced age, certain routine screening tools or tests require implementation due to the unique set of health concerns experienced at older ages. For example, men should receive digital rectal exams for prostate cancer screening; women mammography for breast cancer screening, and annual colonoscopies are a great screening tool to exclude colon cancer in men and women alike. The purpose of such screening tools is to discover disease as early as possible in its clinical course and identify unhealthy lifestyles and behaviors for which the patient can then receive counseling.[17]<\/a>\u00a0Such tools are especially valuable in such an aging population as it is well understood that disease risk increases with age.<\/p>\n<\/div>\n Three distinct processes can reasonably explain the pathophysiology underlying the aging process:<\/p>\n Production of Free Radicals<\/b><\/p>\n Free radicals are well known in the biochemical world as a normal byproduct of healthy physiology in well-regulated, relatively small amounts. They exist as a molecule with a single, unpaired valence electron, rendering them highly reactive in the presence of other substances as they attempt to interact with other substances in an effort to obtain additional valence electrons and balance the electron configuration.[18]<\/a>\u00a0The exact underlying mechanisms underlying the downstream adverse effects of free radical generation and subsequent interaction with cellular components is beyond the scope of this paper, but it bears mentioning that free radicals can denature proteins, destroy membrane lipids, nucleic acids, and certain organelles such as lysosomes and proteasomes.[19]<\/a>\u00a0The importance of understanding free radical or reactive oxygen species-derived degenerative changes is that the belief is that accumulated cellular damage via these molecules will\u2014in time\u2014cumulatively overwhelm the cell\u2019s damage repair mechanisms, leading to the eventual physiologic collapse of first, the cell, then the whole organism.[18]<\/a><\/p>\n Glycation<\/b><\/p>\n Advanced glycosylation end-products form when reactions occur between aldehyde groups of reducing sugars and amino groups of proteins. The formation of these metabolic products occurs in a fashion dependent on elevated blood glucose.[20]<\/a>\u00a0In aging individuals, glycemic control becomes less regulated, and glucose tolerance can undergo significant alteration. The predominance of advanced glycosylation end-products can result in such abnormalities as vascular fibrosis, thickened basement membranes, impaired lipid metabolism, and reduced collagenous elasticity. Furthermore, advanced glycosylation end-products are associated with the induction of inflammatory responses, resulting in the release of inflammatory substances and reactive oxygen species, causing further tissue damage.[18]<\/a><\/p>\n Reduced Regenerative Capacity<\/b><\/p>\n In healthy individuals, a balance exists between one cell\u2019s apoptosis and the maturation and healthy development of another cell that essentially takes the place of the first. Researchers believe that mechanisms within the cell cycle control both the programmed death of a senescent cell but also signal externally to other cells the need for the development of a new, healthy cell to backfill whatever metabolic demands the senescent cell might have been meeting. The progression between stages in the cell cycle is controlled by regulatory proteins, whose function demonstrably declines in senescent cells compared to younger, healthy cells. The ability of these protein-derived signaling pathways to communicate the need for cell regeneration and maturation in the healthy, young cells seems to be reduced in the aging process, while the pro-apoptotic pathway signaling mechanisms continue to function, leading to a net decline in functional, healthy cells.[18]<\/a><\/p>\n<\/div>\n The aging process is a natural phenomenon that occurs due to a variety of loosely understood mechanisms. Via a combination of telomeric shortening, which triggers pro-apoptotic pathways when sensed in the cell cycle, which subsequently triggers inflammatory mediators and the release of damaging reactive oxygen species, our bodies and their ability to maintain physiologic homeostasis degrade with time. Moreover, so too does the body's ability to regenerate or reproduce healthy cells and tissues as we age. The aging process brings with it phenotypical changes that clinicians must understand and consider when caring for aging patients.<\/p>\n It is essential to recognize that aging involves a great deal of interplay between lifestyle and genetics. An individual who maintains a healthy lifestyle, has access to adequate, routine medical care and screenings, and enters into late adulthood with a clean bill of health will experience a vastly different aging process than someone who is sedentary, makes poor diet and lifestyle choices, and has lived with chronic disease before and upon entry into late adulthood.<\/p>\n Aging is relevant to clinical care and management because it often implies underlying derangements of normal physiology. As an example, this article mentioned earlier that urinary tract infections are more common in the elderly. Some patients may experience an increased frequency of falls due to the weakness imposed by their urinary tract infection or their bladder urgency forcing them to attempt to hurriedly make it to a toilet. Clinicians must remain vigilant of the manifestations of disease in aging, and likewise, the presentation of physiologic derangements that pose a potential risk to health, like falls and urinary tract infections.[21]<\/a>\u00a0Aging, although a normal aspect of typical physiology, does incur some manifestations of physiologic derangement that clinicians should learn to interpret in context.<\/p>\n<\/div>\n\u7d39\u4ecb<\/h2>\n
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