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Metabolic alkalosis classification

Introduction

Overview

Overview

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

Classification

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

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.

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