Syndrome of inappropriate antidiuretic hormone pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The normal function of [[ADH]] on the [[kidney]]s is to control the amount of [[water]] reabsorbed by kidney [[nephron]]s. [[ADH]] acts in the distal portion of the [[renal tubule]] ([[ | The normal function of [[ADH|antidiuretic hormone (ADH)]] on the [[kidney]]s is to control the amount of [[water]] reabsorbed by kidney [[nephron]]s. [[ADH]] acts in the distal portion of the [[renal tubule]] ([[distal convoluted tubule]]) as well as on the [[collecting duct]] and causes the retention of [[water]]. Owing to the water retention, dilution of the [[blood]] and [[hyponatremia]] occurs. | ||
===Pathogenesis=== | |||
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*[[ADH]] is normally produced by the posterior [[pituitary]] gland. | *[[ADH]] is normally produced by the posterior [[pituitary]] gland. | ||
*In [[SIADH]], [[ADH]] level rises above the normal level. | *In [[SIADH]], [[ADH]] level rises above the normal level. | ||
*[[Aquaporins]] are localized on storage [[vesicles]] in the [[cytoplasm]] of the epithelial cells which make up the[[ collecting ducts]] of the [[kidneys]]. | *[[Aquaporins]] are localized on storage [[vesicles]] in the [[cytoplasm]] of the [[epithelial cells]] which make up the [[collecting ducts]] of the [[kidneys]]. | ||
*High[[ ADH]] level stimulates mass fusion of [[aquaporin]]-carrying storage vesicles with the[[ plasma membrane]]. | *High [[ADH]] level stimulates mass fusion of [[aquaporin]]-carrying storage vesicles with the [[plasma membrane]]. | ||
*High aquaporin density facilitates high diffusion of water across the [[plasma]] membrane. | *High [[aquaporin]] density facilitates high diffusion of water across the [[plasma]] membrane. | ||
* Excess [[water]] is reabsorbed from the [[nephrons]] and is returned to the [[blood]]. | *Excess [[water]] is reabsorbed from the [[nephrons]] and is returned to the [[blood]]. | ||
===Feedback inhibition=== | ===Feedback inhibition=== | ||
*Developmentally, Mammalian brain have evolved in times of [[water]] scarcity. | *Developmentally, Mammalian [[brain]] have evolved in times of [[water]] scarcity. | ||
*[[ADH]] is secreted to prevent water loss in the [[kidneys]]. | *[[ADH]] is secreted to prevent water loss in the [[kidneys]]. | ||
*When water is ingested, it is taken up into the circulation and results in a dilution of the [[Blood plasma|plasma]]. | *When water is ingested, it is taken up into the circulation and results in a dilution of the [[Blood plasma|plasma]]. | ||
*This dilution, otherwise described as a reduction in [[plasma osmolality]] is detected by [[osmoreceptor]]s in the [[hypothalamus]] of the [[brain]] | *This dilution, otherwise described as a reduction in [[plasma osmolality]] is detected by [[osmoreceptor]]s in the [[hypothalamus]] of the [[brain]]. Then, these switch off the release of [[ADH]]. | ||
*The decreasing concentration of ADH effectively inhibits the [[aquaporin]]s in the [[collecting ducts]] and [[distal convoluted tubule]]s in the [[nephron]]s of the [[kidney]]. | *The decreasing concentration of [[ADH]] effectively inhibits the [[aquaporin]]s in the [[collecting ducts]] and [[distal convoluted tubule]]s in the [[nephron]]s of the [[kidney]]. | ||
*This leads to less water | *This leads to less water reabsorption, thereby increasing [[urine]] output, decreasing urine osmolality, and increasing (normalization of) [[blood]] [[osmolality]]. | ||
In general, the plasma | *In general, the plasma [[sodium]] concentration is the primary osmotic determinant of [[AVP]] release. In [[SIADH]], there is non [[physiological]] secretion of [[AVP]]. There is enhanced water reabsorption, leading to dilutional [[hyponatremia]]. | ||
== Genetics== | == Genetics== | ||
*A [[mutation]] affecting the [[gene]] for the [[renal]] [[V2 receptor]] | |||
* A [[mutation]] affecting the [[gene]] for the [[renal]] V2 receptor | *[[Congenital]] [[nephrogenic diabetes insipidus]] is characterized by a [[resistance]] of the renal [[collecting duct]] to the action of the [[arginine vasopressin]] [[hormone]] responsible for the inability of the [[kidney]] to [[concentrate]] [[urine]]. | ||
*[[Congenital]][[ nephrogenic diabetes insipidus]] is characterized by a [[resistance]] of the renal [[collecting duct]] to the action of the [[arginine vasopressin]] [[hormone]] responsible for the inability of the[[ kidney]] to [[concentrate]] [[urine]]. | * Inactivating [[mutations]] of the [[V2 receptor]] gene leading to a loss of function of the mutated receptors are implicated in the [[X-linked]] form.<ref name="pmid22029026">{{cite journal |vauthors=Pillai BP, Unnikrishnan AG, Pavithran PV |title=Syndrome of inappropriate antidiuretic hormone secretion: Revisiting a classical endocrine disorder |journal=Indian J Endocrinol Metab |volume=15 Suppl 3 |issue= |pages=S208–15 |year=2011 |pmid=22029026 |pmc=3183532 |doi=10.4103/2230-8210.84870 |url=}}</ref> | ||
* Inactivating [[mutations]] of the | |||
<ref name="pmid22029026">{{cite journal |vauthors=Pillai BP, Unnikrishnan AG, Pavithran PV |title=Syndrome of inappropriate antidiuretic hormone secretion: Revisiting a classical endocrine disorder |journal=Indian J Endocrinol Metab |volume=15 Suppl 3 |issue= |pages=S208–15 |year=2011 |pmid=22029026 |pmc=3183532 |doi=10.4103/2230-8210.84870 |url=}}</ref> | |||
== Associated conditions== | == Associated conditions== | ||
[[SIADH]] is most commonly associated with: | *[[SIADH]] is most commonly associated with: | ||
* [[ Malignancies]] | ** [[Malignancies]] | ||
* [[CNS disease|Central nervous system disorders]] | ** [[CNS disease|Central nervous system disorders]] | ||
* [[Medications]] | ** [[Medications]] | ||
* [[ Pulmonary]] disorders | ** [[Pulmonary]] disorders | ||
== Gross pathology== | == Gross pathology== | ||
There are no [[gross]][[ pathology]] findings associated with [[SIADH]]. | There are no [[gross]] [[pathology]] findings associated with [[SIADH]]. | ||
== Microscopic pathology== | == Microscopic pathology== | ||
Revision as of 15:47, 11 October 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]
Overview
Syndrome of inappropriate antidiuretic hormone production (SIADH) is a condition in which the body develops an excess of water and a decrease in the concentration of electrolytes. SIADH may be caused by a central nervous system diseases, cancers, pulmonary diseases or some drugs.
Pathophysiology
The normal function of antidiuretic hormone (ADH) on the kidneys is to control the amount of water reabsorbed by kidney nephrons. ADH acts in the distal portion of the renal tubule (distal convoluted tubule) as well as on the collecting duct and causes the retention of water. Owing to the water retention, dilution of the blood and hyponatremia occurs.
Pathogenesis
| https://youtu.be/MR8BABoFTP8}} |
- ADH is normally produced by the posterior pituitary gland.
- In SIADH, ADH level rises above the normal level.
- Aquaporins are localized on storage vesicles in the cytoplasm of the epithelial cells which make up the collecting ducts of the kidneys.
- High ADH level stimulates mass fusion of aquaporin-carrying storage vesicles with the plasma membrane.
- High aquaporin density facilitates high diffusion of water across the plasma membrane.
- Excess water is reabsorbed from the nephrons and is returned to the blood.
Feedback inhibition
- Developmentally, Mammalian brain have evolved in times of water scarcity.
- ADH is secreted to prevent water loss in the kidneys.
- When water is ingested, it is taken up into the circulation and results in a dilution of the plasma.
- This dilution, otherwise described as a reduction in plasma osmolality is detected by osmoreceptors in the hypothalamus of the brain. Then, these switch off the release of ADH.
- The decreasing concentration of ADH effectively inhibits the aquaporins in the collecting ducts and distal convoluted tubules in the nephrons of the kidney.
- This leads to less water reabsorption, thereby increasing urine output, decreasing urine osmolality, and increasing (normalization of) blood osmolality.
- In general, the plasma sodium concentration is the primary osmotic determinant of AVP release. In SIADH, there is non physiological secretion of AVP. There is enhanced water reabsorption, leading to dilutional hyponatremia.
Genetics
- A mutation affecting the gene for the renal V2 receptor
- Congenital nephrogenic diabetes insipidus is characterized by a resistance of the renal collecting duct to the action of the arginine vasopressin hormone responsible for the inability of the kidney to concentrate urine.
- Inactivating mutations of the V2 receptor gene leading to a loss of function of the mutated receptors are implicated in the X-linked form.[1]
Associated conditions
- SIADH is most commonly associated with:
Gross pathology
There are no gross pathology findings associated with SIADH.
Microscopic pathology
There are no microscopic findings associated with SIADH.
References
- ↑ Pillai BP, Unnikrishnan AG, Pavithran PV (2011). "Syndrome of inappropriate antidiuretic hormone secretion: Revisiting a classical endocrine disorder". Indian J Endocrinol Metab. 15 Suppl 3: S208–15. doi:10.4103/2230-8210.84870. PMC 3183532. PMID 22029026.