Metabolic alkalosis risk factors
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
Common risk factors in the development of Metabolic Alkalosis include Vomiting, Milk-alkali syndrome, Severe hypokalemia, Primary hyperaldosterinism, Cushing syndrome, Diuretics use and genetic disease for instances- Bartter and gitelman Disease.
Risk Factors
Risk Factors
- Common risk factors in the development of Metabolic Alkalosis include Vomiting, Milk-alkali syndrome, Severe hypokalemia, Primary hyperaldosterinism, Cushing syndrome, Diuretics use and genetic disease for instances- Bartter and Gitelman Disease.
Common Risk Factors
- Common risk factors in the development of Metabolic Alkalosis in patients who have conditions include:
- Vomiting (most commonly seen in pyloric stenosis), NG suction
- Diuretics: Loop and thiazide diuretics.
- Diarrhea
- Cystic fibrosis.[1]
- Dietary potassium depletion.[2]
- 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, nephroblastoma
- Mineralocorticoid excess due to primary decorticosterone excess (11 beta, 17 alpha hydroxylase deficiency), licorice(glycyrrhetinic acid) Closing
</ref>missing for<ref>tag - Chloride deficient infant formula.
- Villous adenoma[3]
- congenital chloride diarrhea[4]
- Bartter and Gitelman syndrome. [5]
- liddle syndrome</ref> [6]
- hemangiopericytoma
- Gastrocystoplasty [7]
- Post hypercapneic metabolic alkalosis.
References
References
- ↑ 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.
- ↑ Sabatini S (March 1996). “The cellular basis of metabolic alkalosis”. Kidney Int. 49 (3): 906–17. doi:10.1038/ki.1996.125. PMID 8648937.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
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