THIRST mechanism is very important!
Tight regulation of water balance is accomplished via the thirst mechanism and antidiuretic hormone (AVP). Both are crucial to maintaining a remarkably narrow range of plasma osmolarity of 282-298 mOsm/kg. Osmoregulation of AVP is mediated by osmoreceptors located in the anteromedial hypothalamus near the neurohypophyseal cell bodies in the supraoptic nucleus. These osmoreceptors are extremely sensitive to changes in osmotic pressure. For example a decrease in osmolarity of 1-2% suppresses AVP secretion to permit maximum water diuresis. Non-osmotic variables such as reductions in blood volume or arterial pressure can also effect AVP secretion. Nausea is also well known to be a potent stimulus for AVP secretion.
However, AVP secretion alone is not adequate to prevent dehydration and an intact thirst mechanism is vital for water homeostasis. Thirst is regulated by hypothalamic osmoreceptors that are sensitive to changes in effective osmotic pressure of body fluids. The osmotic threshold at which thirst mechanism is activated begins approximately 5 to 10 mOsm higher than the threshold for AVP release. These two systems work together to maintain plasma osmolality. With both systems intact, development of hypernatremia mostly occurs in patients who have lost their ability to maintain or increase free water intake, for example hospitalized patients and particularly the geriatric population. A much rarer cause of hypernatremia from decreased intake are adipsic disorders, where an alteration in the thirst mechanism prevents patients from taking in adequate free water despite elevations in plasma osmolarity.
Defects in ADH synthesis or secretion cause central diabetes insipidus(CDI) or in some instances a partial CDI. These patients are polyuric and cannot concentrate their urine but maintain normal serum osmolarity with drinking large amounts of water. The thirst mechanism is intact. These patients do relatively well till they physical cannot drink water or their access to free water is lost. Conversely, a lesion in the thirst center in the hypothalamus can lead to an abnormal or no thirst response to hyperosmolarity but a normal ADH response. A defect in osmoregulated thirst mechanism is termed hypodipsic or adipsic hypernatremia . It is frequently associated with defective ADH production as well, either a CDI or partial DI. Due to lack of thirst sense, patients with this condition may fail to drink spontaneously and are at risk of hypernatremia. This risk is compounded by the fact that many of them also have an ADH production defect.
Disorders characterized by adipsia are uncommon, but a significantly large number of cases have been now described in the literature. There are four main patterns of abnormal osmoregulatory function. Type A adipsia is characterized by an upward setting of the osmotic threshold for both thirst and vasopressin release, sometimes called essential hypernatremia. Type B adipsia is characterized by subnormal thirst and vasopressin responses to osmotic stimuli. This is due to partial destruction of the osmoreceptors. Complete destruction of these receptors is classified as type C adipsia and these patients have complete absences of ADH release and a lack of thirst mechanism. Type D is an extremely rare form that manifests as only a thirst mechanism failure with an intact ADH production. Some might term these adipsic disorders as thirst regulation failures with a partial CDI or complete CDI.
However, AVP secretion alone is not adequate to prevent dehydration and an intact thirst mechanism is vital for water homeostasis. Thirst is regulated by hypothalamic osmoreceptors that are sensitive to changes in effective osmotic pressure of body fluids. The osmotic threshold at which thirst mechanism is activated begins approximately 5 to 10 mOsm higher than the threshold for AVP release. These two systems work together to maintain plasma osmolality. With both systems intact, development of hypernatremia mostly occurs in patients who have lost their ability to maintain or increase free water intake, for example hospitalized patients and particularly the geriatric population. A much rarer cause of hypernatremia from decreased intake are adipsic disorders, where an alteration in the thirst mechanism prevents patients from taking in adequate free water despite elevations in plasma osmolarity.
Defects in ADH synthesis or secretion cause central diabetes insipidus(CDI) or in some instances a partial CDI. These patients are polyuric and cannot concentrate their urine but maintain normal serum osmolarity with drinking large amounts of water. The thirst mechanism is intact. These patients do relatively well till they physical cannot drink water or their access to free water is lost. Conversely, a lesion in the thirst center in the hypothalamus can lead to an abnormal or no thirst response to hyperosmolarity but a normal ADH response. A defect in osmoregulated thirst mechanism is termed hypodipsic or adipsic hypernatremia . It is frequently associated with defective ADH production as well, either a CDI or partial DI. Due to lack of thirst sense, patients with this condition may fail to drink spontaneously and are at risk of hypernatremia. This risk is compounded by the fact that many of them also have an ADH production defect.
Disorders characterized by adipsia are uncommon, but a significantly large number of cases have been now described in the literature. There are four main patterns of abnormal osmoregulatory function. Type A adipsia is characterized by an upward setting of the osmotic threshold for both thirst and vasopressin release, sometimes called essential hypernatremia. Type B adipsia is characterized by subnormal thirst and vasopressin responses to osmotic stimuli. This is due to partial destruction of the osmoreceptors. Complete destruction of these receptors is classified as type C adipsia and these patients have complete absences of ADH release and a lack of thirst mechanism. Type D is an extremely rare form that manifests as only a thirst mechanism failure with an intact ADH production. Some might term these adipsic disorders as thirst regulation failures with a partial CDI or complete CDI.
A nice review is listed below in this topic
http://www.ncbi.nlm.nih.gov/pubmed/17371462
http://www.ncbi.nlm.nih.gov/pubmed/6727142
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