Metabolic alkalosis classification: Difference between revisions
Jump to navigation
Jump to search
| (One intermediate revision by the same user not shown) | |||
| Line 7: | Line 7: | ||
==Classification== | ==Classification== | ||
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>: | *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>: | ||
{{Family tree/start}} | {{Family tree/start}} | ||
| Line 16: | Line 16: | ||
{{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 | 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}} | {{Family tree/end}} | ||
*2.The classification based on etiologies are following: | |||
*'''[[Chloride]] depletion''' o[[Gastrointestinal|r '''Gastrointestinal''']] '''loss of [[hydrogen]]''' | |||
**[[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> | |||
**[[Diuretic|Diuretics]]: [[Loop diuretic|Loop]] and [[thiazide diuretics]]. | |||
**[[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> | |||
**[[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> | |||
**[[Chloride]] deficient [[Infant formula|infant formula.]] | |||
**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> | |||
**Post hypercapneic [[metabolic alkalosis]]. | |||
*'''[[Potassium]] depletion''' or '''[[Mineralocorticoids]] excess''' or '''[[Renal]] loss of [[hydrogen]]''' | |||
**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> | |||
**[[Primary Hyperaldosteronism|Primary hyperaldosteronism]]: [[Conn syndrome]] or [[adenoma]], [[hyperplasia]], [[carcinoma]], [[renin]] or [[glucocorticoid]] responsive. | |||
**[[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]] | |||
**[[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> | |||
**[[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> | |||
**[[Laxative]] | |||
*'''Reduced [[Glomerular filtration rate]]''' | |||
**[[Chronic kidney disease]] | |||
*'''[[Extracellular fluid|ECF volume]] depletion/ [[Volume depletion|Volume contraction]]''' | |||
**[[Hypovolemia]] or [[Diuresis|massive diuresis]] with [[loop diuretics]]. | |||
*'''Miscellanous''' | |||
**[[Hypercalcemia]] due to [[Milk-alkali syndrome]] or [[bone metastasis]]. | |||
**Massive [[blood transfusion]]. | |||
**[[Acetate]] containing [[Colloid|colloid sollution]]. | |||
**[[Exogenous]] [[alkali]] admintration. | |||
**Combined [[antacid]] and cation exchange resin administration. | |||
**Sodium [[Penicillin|penicillins]]. | |||
==References== | ==References== | ||
Latest revision as of 05:27, 20 January 2021
|
Metabolic alkalosis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Metabolic alkalosis classification On the Web |
|
American Roentgen Ray Society Images of Metabolic alkalosis classification |
|
Risk calculators and risk factors for 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
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:
- 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
- ↑ "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.