Porth's Essentials of Pathophysiology, 4e

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Integrative Body Functions

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serum sodium and osmolality levels. 10 The inability to perceive and respond to thirst is compounded in elderly persons who have had a stroke and may be further influenced by confusion, sensory deficits, and motor disturbances. Polydipsia. Polydipsia, or excessive thirst, is nor- mal when it accompanies conditions of water deficit, but abnormal when it results in excess water intake. Increased thirst and drinking behavior can be classified into two categories: (1) inappropriate or false thirst that occurs despite normal levels of body water and serum osmolality, and (2) compulsive water drinking. Inappropriate or excessive thirst may persist despite adequate hydration. It is a common complaint in per- sons with congestive heart failure and chronic kidney disease. Although the cause of thirst in these people is unclear, it may result from increased angiotensin II lev- els. Thirst is also a common complaint in those with dry mouth caused by decreased salivary function or treatment with drugs with an anticholinergic action (e.g., antihistamines, atropine) that lead to decreased salivary flow. Psychogenic polydipsia involves compulsive water drinking and is usually seen in persons with psychiat- ric disorders, most commonly schizophrenia. Persons with the disorder drink large amounts of water and excrete large amounts of urine. The cause of exces- sive water drinking in these persons is uncertain. It has been suggested that it may share the same pathology as the psychosis because persons with the disorder often increase their water drinking during periods of exac- erbation of their psychotic symptoms. 11 The condition may be compounded by antipsychotic medications that increase ADH levels and interfere with water excretion by the kidneys. Cigarette smoking, which is common among persons with psychiatric disorders, also stimu- lates ADH secretion. Excessive water ingestion coupled with impaired water excretion (or rapid ingestion at a rate that exceeds renal excretion) in persons with psy- chogenic polydipsia can lead to water intoxication (see section on hyponatremia). Treatment usually consists of water restriction and behavioral measures aimed at decreasing water consumption. Measurements of body weight can be used to provide an estimate of water consumption. 12 The antidiuretic hormone, also known as vasopres- sin , controls the reabsorption of water by the kid- neys. 1,2,7 Antidiuretic hormone is a small peptide, nine amino acids in length, that is synthesized by cells in the supraoptic and paraventricular nuclei of the hypothalamus and then transported along a neu- ral pathway (i.e., hypothalamic-hypophysial tract) to the posterior pituitary gland, where it is stored. When the supraoptic and paraventricular nuclei in the hypo- thalamus are stimulated by increased serum osmolal- ity or other factors, nerve impulses travel down the Antidiuretic Hormone and Disorders of Antidiuretic Hormone

hypothalamic-hypophyseal tract to the posterior pitu- itary gland, causing the stored ADH to be released into the circulation (see Fig. 8-7). As with thirst, ADH levels are controlled by ECF volume and osmolality. Osmoreceptors in the hypo- thalamus sense changes in ECF osmolality and stimu- late the production and release of ADH (see Fig. 8-7). A small increase in serum osmolality of 1% is suffi- cient to cause ADH release. 7 Stretch receptors that are sensitive to changes in blood pressure and the effec- tive circulating volume also contribute to the regula- tion of ADH release (i.e., nonosmotic ADH secretion). A blood volume decrease of 5% to 10% produces a maximal increase in ADH levels. 7 As with many other homeostatic mechanisms, acute conditions pro- duce greater changes in ADH levels than do chronic conditions. Antidiuretic hormone exerts its effects through vaso- pressin receptors located in the collecting tubules of the kidney. In the presence of ADH, highly permeable water channels called aquaporins are inserted into the tubu- lar membrane. The increased water permeability allows water from the urine filtrate to be reabsorbed into the blood, making the urine more concentrated (see under- standing urine concentration, Chapter 24). The abnormal synthesis and release of ADH occurs in a number of stress situations including severe pain, nausea, trauma, surgery, certain anesthetic agents, and some narcotics (e.g., morphine and meperidine). Among other drugs that affect ADH are nicotine, which stim- ulates its release, and alcohol, which inhibits it. Two important conditions that alter ADH levels are diabetes insipidus and the syndrome of inappropriate secretion of ADH. Diabetes Insipidus. Diabetes insipidus (DI) is caused by a deficiency of ADH or a decreased renal response to ADH. 13 Persons with DI are unable to concentrate their urine during periods of water restriction and they excrete large volumes of urine, usually 3 to 20 L/ day, depending on the degree of ADH deficiency or renal insensitivity to ADH. This large urine output is accompanied by excessive thirst. As long as the thirst mechanism is normal and fluid is readily available, there is little or no alteration in the fluid levels of per- sons with DI. The danger arises when the condition develops in someone who is unable to communicate the need for water or is unable to secure the needed water. In such cases, inadequate fluid intake rapidly leads to increased serum osmolality and hypertonic dehydration. There are two types of DI: neurogenic or central DI, which occurs because of a defect in the synthesis or release of ADH, and nephrogenic DI, which occurs because the kidneys do not respond to ADH. 13–16 Most cases of neurogenic DI are caused by inflamma- tory, autoimmune, or vascular diseases that affect the hypothalamic-neurohypophyseal system, with less than 10% attributed to heritary forms of the disorder. In neurogenic DI, loss of 80% of ADH-secretory neurons is necessary before polyuria becomes evident. 14 Most

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