Health Dictionary
Reliable, easy-to-read patient information on common medical conditions β written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Metabolic alkalosis risk factors
Introduction
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
- β Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-JΓ€ggi C, Bianchetti MG (1995). “Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis”. Am J Nephrol. 15 (3): 245β50. doi:10.1159/000168839. PMIDΒ 7618650.
- β Sabatini S (March 1996). “The cellular basis of metabolic alkalosis”. Kidney Int. 49 (3): 906β17. doi:10.1038/ki.1996.125. PMIDΒ 8648937.
- β Babior BM (October 1966). “Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances”. Am J Med. 41 (4): 615β21. doi:10.1016/0002-9343(66)90223-3. PMIDΒ 5927076.
- β HΓΆglund 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): 316β9. doi:10.1038/ng1196-316. PMIDΒ 8896562.
- β Kurtz I (October 1998). “Molecular pathogenesis of Bartter’s and Gitelman’s syndromes”. Kidney Int. 54 (4): 1396β410. doi:10.1046/j.1523-1755.1998.00124.x. PMIDΒ 9767561.
- β Warnock DG (January 1998). “Liddle syndrome: an autosomal dominant form of human hypertension”. Kidney Int. 53 (1): 18β24. doi:10.1046/j.1523-1755.1998.00728.x. PMIDΒ 9452995.
- β 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): 546β9. doi:10.1097/00005392-199508000-00066. PMIDΒ 7609133.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]