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Pathophysiology of Aging

From Zisook S, Downs NS. J Clin Psych 1998 59(sLLppl 4) 80-91 data from Dorgan CA, editor. Statistical record of health and medicine. New York International Thompson Publishing Co 1995. [Pg.376]

Placed in the context of response to drugs it is most useful to discuss age-related physiological changes [Pg.376]

FIGURE 24.1 Age-related impairment in cognitive function as defined by six or more errors in the Mini-Mental Status Exam. (Data from Robins LN, Regier DA, editors. Psychiatric disorders in America the Epidemiolgic Catchment Area Study. New York The Eree Press 1991.) [Pg.376]

The observed pharmacodynamic response is the result of extent of drug exposure determined by drug pharmacokinetics (Table 24.2) and sensitivity [Pg.376]


Young RW Pathophysiology of age-related macular degeneration. Surv Ophthalmol 1987 31 291. [Pg.642]

Lindeman RD. Overview Renal physiology and pathophysiology of aging. Am J Kidney Dis 1990 26 275-82. [Pg.387]

A pressure sore is also called a decubitus ulcer and bed sore. A classification system for pressure sores is presented in Table 47-5. Many factors are thought to predispose patients to the formation of pressure ulcers paralysis, paresis, immobilization, malnutrition, anemia, infection, and advanced age. Four factors thought to be most critical to their formation are pressure, shearing forces, friction, and moisture however, there is still debate as to the exact pathophysiology of pressure sore formation. The areas of highest pressure are generated over the bony prominences. [Pg.531]

Until recently, little attention had been paid to nicotinic mechanisms in explaining either the pathophysiology or treatment of AD. Patients with AD have a marked reduction in cortical nicotinic cholinergic receptor binding compared with that of age-matched control subjects (Aubert et al. 1992 Flynn and Mash 1986 Whitehouse et al. 1986). Psychiatrically healthy elderly subjects show an age-related decline in cortical nicotinic binding (Flynn and Mash 1986). [Pg.567]

Giorgio, S., Alessia, L., LUcilla, P., Daniele, T., and Francesso, A. (2006). Treatment of Alzheimer s disease From pharmacology to a better understanding of disease pathophysiology. Mech. Ageing Dev. 127,148-157. [Pg.69]

Acute reduction in renal perfusion is considered important in the pathophysiology of contrast agent-induced nephrotoxicity. Color-coded duplex sonography has been used in assessing intrarenal vascular resistance in 10 patients (mean age 51 years) after intravenous injection of 100 ml of the low-osmolar contrast medium iopamidol (iodine 300 mg/ml) (182). The resistive index was measured at 1-minute intervals over 10 minutes after injection in each patient. There was a statistically significant rise in resistive index at 2, 3, 4, and 5 minutes after injection, mean values 0.74, 0.75, 0.72, and 0.75... [Pg.1870]

Auto-oxidation of catecholamines also leads to formation of the polymeric pigment neuromelanin that increases with age and is responsible for the dark coloration of DA-pro-ducing cells in the substantia nigra and the norepinephrine neurons of the locus coeruleus (42). A physiological role for this polymer is not established, and there is no evidence to support its involvement either in normal loss of DA neurons with aging or in the pathophysiology of PD. [Pg.716]


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