Hyponatremia pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Sodium is the main cation in the extracellular fluid; thus the plasma concentration of sodium is determinant of serum osmolality. Hyponatremia represents as an excess of water relative to total body sodium, arising as a result of impaired water excretion by the kidneys or the depletion of sodium in excess of water. Tonicity is the most important factor | |||
<table class="wikitable"> | Hypotonic (dilutional) hyponatraemia is classified by the extracellular volume status into hypo-, eu- and hyper-volemic hyponatremia.<table class="wikitable"> | ||
<tr class="v-firstrow"><th>Term</th><th>Definitions<ref name="Laczi-2008">{{Cite journal | last1 = Laczi | first1 = F. | title = [Etiology, diagnostics and therapy of hyponatremias]. | journal = Orv Hetil | volume = 149 | issue = 29 | pages = 1347-54 | month = Jul | year = 2008 | doi = 10.1556/OH.2008.28409 | PMID = 18617466 }}</ref><ref name="Douglas-2006">{{Cite journal | last1 = Douglas | first1 = I. | title = Hyponatremia: why it matters, how it presents, how we can manage it. | journal = Cleve Clin J Med | volume = 73 Suppl 3 | issue = | pages = S4-12 | month = Sep | year = 2006 | doi = | PMID = 16970147 }}</ref><ref name="Verbalis-2013">{{Cite journal | last1 = Verbalis | first1 = JG. | last2 = Goldsmith | first2 = SR. | last3 = Greenberg | first3 = A. | last4 = Korzelius | first4 = C. | last5 = Schrier | first5 = RW. | last6 = Sterns | first6 = RH. | last7 = Thompson | first7 = CJ. | title = Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. | journal = Am J Med | volume = 126 | issue = 10 Suppl 1 | pages = S1-42 | month = Oct | year = 2013 | doi = 10.1016/j.amjmed.2013.07.006 | PMID = 24074529 }}</ref></th></tr> | <tr class="v-firstrow"><th>Term</th><th>Definitions<ref name="Laczi-2008">{{Cite journal | last1 = Laczi | first1 = F. | title = [Etiology, diagnostics and therapy of hyponatremias]. | journal = Orv Hetil | volume = 149 | issue = 29 | pages = 1347-54 | month = Jul | year = 2008 | doi = 10.1556/OH.2008.28409 | PMID = 18617466 }}</ref><ref name="Douglas-2006">{{Cite journal | last1 = Douglas | first1 = I. | title = Hyponatremia: why it matters, how it presents, how we can manage it. | journal = Cleve Clin J Med | volume = 73 Suppl 3 | issue = | pages = S4-12 | month = Sep | year = 2006 | doi = | PMID = 16970147 }}</ref><ref name="Verbalis-2013">{{Cite journal | last1 = Verbalis | first1 = JG. | last2 = Goldsmith | first2 = SR. | last3 = Greenberg | first3 = A. | last4 = Korzelius | first4 = C. | last5 = Schrier | first5 = RW. | last6 = Sterns | first6 = RH. | last7 = Thompson | first7 = CJ. | title = Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. | journal = Am J Med | volume = 126 | issue = 10 Suppl 1 | pages = S1-42 | month = Oct | year = 2013 | doi = 10.1016/j.amjmed.2013.07.006 | PMID = 24074529 }}</ref></th></tr> | ||
<tr><td>[[Hyponatremia]]</td><td>Hyponatremia is defined as a serum sodium concentration < 135 mEq/L.</td></tr> | <tr><td>[[Hyponatremia]]</td><td>Hyponatremia is defined as a serum sodium concentration < 135 mEq/L.</td></tr> |
Revision as of 19:06, 20 April 2018
Hyponatremia Microchapters |
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Hyponatremia pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Saeedeh Kowsarnia M.D.[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Sodium is the main cation in the extracellular fluid; thus the plasma concentration of sodium is determinant of serum osmolality. Hyponatremia represents as an excess of water relative to total body sodium, arising as a result of impaired water excretion by the kidneys or the depletion of sodium in excess of water. Tonicity is the most important factor
Hypotonic (dilutional) hyponatraemia is classified by the extracellular volume status into hypo-, eu- and hyper-volemic hyponatremia.
Term | Definitions[1][2][3] |
---|---|
Hyponatremia | Hyponatremia is defined as a serum sodium concentration < 135 mEq/L. |
Hypotonic hyponatremia | Hyponatremia with low osmolality (hypotonic hyponatremia) is defined as hyponatremia with a serum osmolality below 280 mOsm/kg. |
Hypertonic hyponatremia | Hyponatremia with high osmolality (hypertonic hyponatremia) is defined as hyponatremia with a serum osmolality greater than 295 mOsm/kg. |
Isotonic hyponatremia | Hyponatremia with normal osmolality (Isotonic hyponatremia) is defined as hyponatremia with a serum osmolality ranging between 280-295 mOsm/kg. |
Hyponatremia based on ECF volume | |
Hypovolemic hyponatremia | Hyponatremia plus decreased extracellular cellular fluid volume. Usually diagnosed by history and physical examinationshowing water depletion plus spot urine sodium <20 to 30 mmol/L, unless kidney is the source of sodium loss. |
Euvolemic hyponatremia | Hyponatremia plus normal extracellular cellular fluid volume. Majority of cases are of this type. Usually diagnosed by spot urine sodium ≥ 20 to 30 mmol/L, unless secondarily sodium depleted. |
Hypervolemia hyponatremia | Hyponatremia plus increased extracellular cellular fluid volume. Usually diagnosed by history and physical examinationshowing water retention plus spot urine sodium <20 to 30 mmol/L |
Pathogenesis
- The exact pathogenesis of [disease name] is not fully understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Laczi, F. (2008). "[Etiology, diagnostics and therapy of hyponatremias]". Orv Hetil. 149 (29): 1347–54. doi:10.1556/OH.2008.28409. PMID 18617466. Unknown parameter
|month=
ignored (help) - ↑ Douglas, I. (2006). "Hyponatremia: why it matters, how it presents, how we can manage it". Cleve Clin J Med. 73 Suppl 3: S4–12. PMID 16970147. Unknown parameter
|month=
ignored (help) - ↑ Verbalis, JG.; Goldsmith, SR.; Greenberg, A.; Korzelius, C.; Schrier, RW.; Sterns, RH.; Thompson, CJ. (2013). "Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations". Am J Med. 126 (10 Suppl 1): S1–42. doi:10.1016/j.amjmed.2013.07.006. PMID 24074529. Unknown parameter
|month=
ignored (help)