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{{Metabolic alkalosis}}
{{Metabolic alkalosis}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{MMT}}
==Overview==
==Overview==
There is no established system for the classification of [disease name].
Metabolic Alkalosis can be classified according to pathophysiology, etiology and chloride responsiveness or urinary chloride concentration.


OR
==Classification==
 
*1.The following classification of Metabolic Alkalosis is based on Pathophysiology<ref name="urlMetabolic Alkalosis - Jeffrey M. Rimmer, F. John Gennari, 1987">{{cite web |url=https://doi.org/10.1177%2F088506668700200304 |title=Metabolic Alkalosis - Jeffrey M. Rimmer, F. John Gennari, 1987 |format= |work= |accessdate=}}</ref>:
[Disease name] may be classified according to [classification method] into [number] subtypes/groups: [group1], [group2], [group3], and [group4].
 
OR
 
[Disease name] may be classified into [large number > 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3].
[Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].
 
OR
 
Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.
 
OR
 
If the staging system involves specific and characteristic findings and features:
According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].
 
OR
 
The staging of [malignancy name] is based on the [staging system].


OR
{{Family tree/start}}
{{Family tree | | | | A01 | | | |A01= Metabolic Alkalosis}}
{{Family tree | | | | |!| | | | | }}
{{Family tree | | | | B01 | | | |B01= Stimulation on Collecting Duct}}
{{Family tree | |,|-|-|^|-|-|.| | }}
{{Family tree | C01 | | | | C02 |C01= Primary stimulation by Mineralocorticoid Excess causing HTN: •Congenital Adrenal Hyperplasia <br>•Cushing Syndrome <br>•Primary aldosteronism <br>•Renin Secreting tumors <br>•Medications(Fluoroprednisolone, Fludrocortisone) <br>•Liddle Syndrome <br>•11 beta hydroxysteroid dehydrogenase deficiency | C02= Secondary Stimulation by Chloride depletion causing normal or low blood pressure: •Vomiting <br>•NG tube intubation <br>•Congenital Chloridorrhea <br>•Ileostomy <br>•Cystic fibrosis <br>•Diuretics <br>•Bartter syndrome <br>•Gitelman syndrome <br>•Hypokalemia}}
{{Family tree/end}}


There is no established system for the staging of [malignancy name].
*2.The classification based on etiologies are following:
 
==Classification==


*There is no established system for the classification of [disease name].
*'''[[Chloride]] depletion''' o[[Gastrointestinal|r '''Gastrointestinal''']] '''loss of [[hydrogen]]'''
OR
**[[Gastrointestinal tract|GI]] loss: [[Vomiting]] (most commonly seen in [[pyloric stenosis]]), [[Nasogastric tube|NG suction]] , [[Zollinger-Ellison syndrome|Zollinger-ellison]] syndrome, [[Bulimia nervosa|Bulimia]].<ref name="pmid1928424">{{cite journal |vauthors=Galla JH, Gifford JD, Luke RG, Rome L |title=Adaptations to chloride-depletion alkalosis |journal=Am J Physiol |volume=261 |issue=4 Pt 2 |pages=R771–81 |date=October 1991 |pmid=1928424 |doi=10.1152/ajpregu.1991.261.4.R771 |url=}}</ref>
*[Disease name] may be classified according to [classification method] into [number] subtypes/groups:  
**[[Diuretic|Diuretics]]: [[Loop diuretic|Loop]] and [[thiazide diuretics]].
**[Group1]
**[[Diarrhea]]: [[Villous adenoma]]<ref name="pmid5927076">{{cite journal |vauthors=Babior BM |title=Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances |journal=Am J Med |volume=41 |issue=4 |pages=615–21 |date=October 1966 |pmid=5927076 |doi=10.1016/0002-9343(66)90223-3 |url=}}</ref>, [[congenital chloride diarrhea]]<ref name="pmid8896562">{{cite journal |vauthors=Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J |title=Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea |journal=Nat Genet |volume=14 |issue=3 |pages=316–9 |date=November 1996 |pmid=8896562 |doi=10.1038/ng1196-316 |url=}}</ref>
**[Group2]
**[[Cystic fibrosis]].<ref name="pmid7618650">{{cite journal |vauthors=Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG |title=Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis |journal=Am J Nephrol |volume=15 |issue=3 |pages=245–50 |date=1995 |pmid=7618650 |doi=10.1159/000168839 |url=}}</ref>
**[Group3]
**[[Chloride]] deficient [[Infant formula|infant formula.]]
**[Group4]
**Gastrocystoplasty <ref name="pmid7609133">{{cite journal |vauthors=Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI |title=Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty |journal=J Urol |volume=154 |issue=2 Pt 1 |pages=546–9 |date=August 1995 |pmid=7609133 |doi=10.1097/00005392-199508000-00066 |url=}}</ref>
OR
**Post hypercapneic [[metabolic alkalosis]].
*[Disease name] may be classified into [large number > 6] subtypes based on:
*'''[[Potassium]] depletion''' or '''[[Mineralocorticoids]] excess''' or '''[[Renal]] loss of [[hydrogen]]'''
**[Classification method 1]
**Dietary [[potassium]] depletion.<ref name="pmid8648937">{{cite journal |vauthors=Sabatini S |title=The cellular basis of metabolic alkalosis |journal=Kidney Int |volume=49 |issue=3 |pages=906–17 |date=March 1996 |pmid=8648937 |doi=10.1038/ki.1996.125 |url=}}</ref>
**[Classification method 2]
**[[Primary Hyperaldosteronism|Primary hyperaldosteronism]]: [[Conn syndrome]] or [[adenoma]], [[hyperplasia]], [[carcinoma]], [[renin]] or [[glucocorticoid]] responsive.
**[Classification method 3]
**[[Secondary hyperaldosteronism]]: [[Renovascular hypertension|Reno vascular hypertension]], [[edema]] ([[cirrhosis]], [[heart failure]], [[Nephrotic syndrome|nephrotic syndrome)]], [[Juxtaglomerular apparatus|juxtaglomerular cell]]([[Renin-secreting tumors|renin producing) tumor]], [[renal cell carcinoma]], [[hemangiopericytoma]], [[nephroblastoma]]
*[Disease name] may be classified into several subtypes based on:  
**[[Mineralocorticoid]] excess due to primary decorticosterone excess ([[11β-hydroxylase deficiency|11 beta]], [[17 alpha-hydroxylase deficiency|17 alpha hydroxylase deficienc]]<nowiki/>y), [[licorice]]([[glycyrrhetinic acid]]), [[Liddle's syndrome|liddle syndrome]].<ref name="pmid1731223">{{cite journal |vauthors=Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM |title=A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension |journal=Nature |volume=355 |issue=6357 |pages=262–5 |date=January 1992 |pmid=1731223 |doi=10.1038/355262a0 |url=}}</ref> <ref name="pmid9452995">{{cite journal |vauthors=Warnock DG |title=Liddle syndrome: an autosomal dominant form of human hypertension |journal=Kidney Int |volume=53 |issue=1 |pages=18–24 |date=January 1998 |pmid=9452995 |doi=10.1046/j.1523-1755.1998.00728.x |url=}}</ref>
**[Classification method 1]
**[[Bartter syndrome|Bartter]] and [[Gitelman syndrome]]. <ref name="pmid9767561">{{cite journal |vauthors=Kurtz I |title=Molecular pathogenesis of Bartter's and Gitelman's syndromes |journal=Kidney Int |volume=54 |issue=4 |pages=1396–410 |date=October 1998 |pmid=9767561 |doi=10.1046/j.1523-1755.1998.00124.x |url=}}</ref>
**[Classification method 2]
**[[Laxative]]
**[Classification method 3]
*'''Reduced [[Glomerular filtration rate]]'''
OR
**[[Chronic kidney disease]]
*Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.
*'''[[Extracellular fluid|ECF volume]] depletion/ [[Volume depletion|Volume contraction]]'''
OR
**[[Hypovolemia]] or [[Diuresis|massive diuresis]] with [[loop diuretics]].
*If the staging system involves specific and characteristic findings and features:
*'''Miscellanous'''
*According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].
**[[Hypercalcemia]] due to [[Milk-alkali syndrome]] or [[bone metastasis]].
OR
**Massive [[blood transfusion]].
*The staging of [malignancy name] is based on the [staging system].
**[[Acetate]] containing [[Colloid|colloid sollution]].
OR
**[[Exogenous]] [[alkali]] admintration.
*There is no established system for the staging of [malignancy name].
**Combined [[antacid]] and cation exchange resin administration.
**Sodium [[Penicillin|penicillins]].


==References==
==References==

Latest revision as of 05:27, 20 January 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]

Overview

Metabolic Alkalosis can be classified according to pathophysiology, etiology and chloride responsiveness or urinary chloride concentration.

Classification

  • 1.The following classification of Metabolic Alkalosis is based on Pathophysiology[1]:
 
 
 
Metabolic Alkalosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stimulation on Collecting Duct
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Primary stimulation by Mineralocorticoid Excess causing HTN: •Congenital Adrenal Hyperplasia
•Cushing Syndrome
•Primary aldosteronism
•Renin Secreting tumors
•Medications(Fluoroprednisolone, Fludrocortisone)
•Liddle Syndrome
•11 beta hydroxysteroid dehydrogenase deficiency
 
 
 
Secondary Stimulation by Chloride depletion causing normal or low blood pressure: •Vomiting
•NG tube intubation
•Congenital Chloridorrhea
•Ileostomy
•Cystic fibrosis
•Diuretics
•Bartter syndrome
•Gitelman syndrome
•Hypokalemia
  • 2.The classification based on etiologies are following:

References

  1. ↑ "Metabolic Alkalosis - Jeffrey M. Rimmer, F. John Gennari, 1987".
  2. ↑ Galla JH, Gifford JD, Luke RG, Rome L (October 1991). "Adaptations to chloride-depletion alkalosis". Am J Physiol. 261 (4 Pt 2): R771–81. doi:10.1152/ajpregu.1991.261.4.R771. PMID 1928424.
  3. ↑ Babior BM (October 1966). "Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances". Am J Med. 41 (4): 615–21. doi:10.1016/0002-9343(66)90223-3. PMID 5927076.
  4. ↑ Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J (November 1996). "Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea". Nat Genet. 14 (3): 316–9. doi:10.1038/ng1196-316. PMID 8896562.
  5. ↑ Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG (1995). "Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis". Am J Nephrol. 15 (3): 245–50. doi:10.1159/000168839. PMID 7618650.
  6. ↑ Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI (August 1995). "Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty". J Urol. 154 (2 Pt 1): 546–9. doi:10.1097/00005392-199508000-00066. PMID 7609133.
  7. ↑ Sabatini S (March 1996). "The cellular basis of metabolic alkalosis". Kidney Int. 49 (3): 906–17. doi:10.1038/ki.1996.125. PMID 8648937.
  8. ↑ Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM (January 1992). "A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension". Nature. 355 (6357): 262–5. doi:10.1038/355262a0. PMID 1731223.
  9. ↑ Warnock DG (January 1998). "Liddle syndrome: an autosomal dominant form of human hypertension". Kidney Int. 53 (1): 18–24. doi:10.1046/j.1523-1755.1998.00728.x. PMID 9452995.
  10. ↑ Kurtz I (October 1998). "Molecular pathogenesis of Bartter's and Gitelman's syndromes". Kidney Int. 54 (4): 1396–410. doi:10.1046/j.1523-1755.1998.00124.x. PMID 9767561.

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