Metabolic alkalosis classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]
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:
- Chloride depletion or Gastrointestinal loss of hydrogen
- GI loss: Vomiting (most commonly seen in pyloric stenosis), NG suction , Zollinger-ellison syndrome, Bulimia.[2]
- Diuretics: Loop and thiazide diuretics.
- Diarrhea: Villous adenoma[3], congenital chloride diarrhea[4]
- Cystic fibrosis.[5]
- Chloride deficient infant formula.
- Gastrocystoplasty [6]
- Post hypercapneic metabolic alkalosis.
- Potassium depletion or Mineralocorticoids excess or Renal loss of hydrogen
- Dietary potassium depletion.[7]
- Primary hyperaldosteronism: Conn syndrome or adenoma, hyperplasia, carcinoma, renin or glucocorticoid responsive.
- Secondary hyperaldosteronism: Reno vascular hypertension, edema (cirrhosis, heart failure, nephrotic syndrome), juxtaglomerular cell(renin producing) tumor, renal cell carcinoma, hemangiopericytoma, nephroblastoma
- Mineralocorticoid excess due to primary decorticosterone excess (11 beta, 17 alpha hydroxylase deficiency), licorice(glycyrrhetinic acid), liddle syndrome.[8] [9]
- Bartter and Gitelman syndrome. [10]
- Laxative
- Reduced Glomerular filtration rate
- ECF volume depletion/ Volume contraction
- Hypovolemia or massive diuresis with loop diuretics.
- Miscellanous
- Hypercalcemia due to Milk-alkali syndrome or bone metastasis.
- Massive blood transfusion.
- Acetate containing colloid sollution.
- Exogenous alkali admintration.
- Combined antacid and cation exchange resin administration.
- Sodium penicillins.
References
References
- ↑ “Metabolic Alkalosis – Jeffrey M. Rimmer, F. John Gennari, 1987”.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Sabatini S (March 1996). “The cellular basis of metabolic alkalosis”. Kidney Int. 49 (3): 906–17. doi:10.1038/ki.1996.125. PMID 8648937.
- ↑ 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.
- ↑ 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.
- ↑ 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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