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| Acidosis | |
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| General symptoms of acidosis. | |
| Pronunciation |
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| Specialty | Endocrinology |
Acidosis is a disorder when the bodily fluids contain excessive amounts of acid. It is the reverse of alkalosis, a state in which bodily fluids contain an excessive amount of base. Acidosis comes in two main forms: metabolic acidosis and respiratory acidosis. Respiratory acidosis is caused by insufficient carbon dioxide excretion from the lungs. Metabolic acidosis arises when the body produces acids more quickly than the kidneys can eliminate them, or when the kidneys or intestines remove too much alkali from the body.[2]
Signs and symptoms
[edit]Causes
[edit]Respiratory acidosis occurs when the lungs do not excrete enough CO2. Severe acute or chronic lung diseases like pneumonia or emphysema, as well as certain drugs that inhibit breathing when taken in excess, including general anesthetic medicines, can cause respiratory acidosis.[2]
Metabolic acidosis can result from acute kidney injury or chronic kidney disease (CKD), with the latter condition being the most frequent cause of chronic metabolic acidosis.[3] The most frequent causes of acute metabolic acidosis are lactic acidosis and diabetic ketoacidosis.[4] A less common cause of acute metabolic acidosis is alcoholic ketoacidosis, which is most frequently seen following a binge drinking episode. Metabolic acidosis is rarely caused by toxic alcohols, such as methanol, ethylene glycol, diethylene glycol, and propylene glycol.[5] When patients receive high intravenous dosages of benzodiazepines or other regularly used diluents, such as propylene glycol, it might result in lactic acidosis.[6] Fasting, especially if extended, can result in moderate ketoacidosis.[5]
The administration of drugs that are converted to hydrochloric acid can result in hyperkalemic hyperchloremic acidosis.[7] However, it is more commonly caused by problems with poor renal tubular acid and potassium excretion.[8][9] These conditions include tubular resistance to aldosterone,[8][9] hyporeninemic hypoaldosteronism,[9] adrenal insufficiency,[9] type 1 and type 2 pseudohypoaldosteronism,[10][11] and chronic kidney disease (CKD).[5]
Diarrhea is the most prevalent cause of hyperchloremic metabolic acidosis with low serum K+ level.[5]
Mechanism
[edit]Diagnosis
[edit]Classification
[edit]Treatment
[edit]Outlook
[edit]Epidemiology
[edit]See also
[edit]References
[edit]- ^ "Definition of ACIDOSIS". Merriam-Webster. 2023-10-23. Retrieved 2024-07-10.
- ^ a b Hansen-Flaschen, John (1998-07-20). "Acidosis". Encyclopedia Britannica. Retrieved 2024-07-10.
- ^ Kraut, Jeffrey A.; Kurtz, Ira (2005). "Metabolic Acidosis of CKD: Diagnosis, Clinical Characteristics, and Treatment". American Journal of Kidney Diseases. 45 (6). Elsevier BV: 978–993. doi:10.1053/j.ajkd.2005.03.003. ISSN 0272-6386.
- ^ Gabow, Patricia A.; Kaehny, William D.; Fennessey, Paul V.; Goodman, Stephen I.; Gross, Peter A.; Schrier, Robert W. (1980-10-09). "Diagnostic Importance of an Increased Serum Anion Gap". New England Journal of Medicine. 303 (15). Massachusetts Medical Society: 854–858. doi:10.1056/nejm198010093031505. ISSN 0028-4793.
- ^ a b c d Kraut, Jeffrey A.; Madias, Nicolaos E. (2010). "Metabolic acidosis: pathophysiology, diagnosis and management". Nature Reviews Nephrology. 6 (5): 274–285. doi:10.1038/nrneph.2010.33. ISSN 1759-5061.
- ^ Arbour, Richard; Esparis, Belen (2000). "Osmolar Gap Metabolic Acidosis in a 60-Year-Old Man Treated for Hypoxemic Respiratory Failure". Chest. 118 (2). Elsevier BV: 545–546. doi:10.1378/chest.118.2.545. ISSN 0012-3692.
- ^ Chan, J. C.; Asch, M. J.; Lin, S.; Hays, D. M. (1972-06-26). "Hyperalimentation with amino acid and casein hydrolysate solutions. Mechanism of acidosis". JAMA. 220 (13): 1700–1705. ISSN 0098-7484. PMID 4623985.
- ^ a b Karet, Fiona E. (2009). "Mechanisms in Hyperkalemic Renal Tubular Acidosis". Journal of the American Society of Nephrology. 20 (2). Ovid Technologies (Wolters Kluwer Health): 251–254. doi:10.1681/asn.2008020166. ISSN 1046-6673.
- ^ a b c d DuBose, Thomas D. (1997). "Hyperkalemic hyperchloremic metabolic acidosis: Pathophysiologic insights". Kidney International. 51 (2). Elsevier BV: 591–602. doi:10.1038/ki.1997.85. ISSN 0085-2538.
- ^ Chang, Sue S.; Grunder, Stefan; Hanukoglu, Aaron; Rösler, Ariel; Mathew, P.M.; Hanukoglu, Israel; Schild, Laurent; Lu, Yin; Shimkets, Richard A.; Nelson-Williams, Carol; Rossier, Bernard C.; Lifton, Richard P. (1996). "Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1". Nature Genetics. 12 (3). Springer Science and Business Media LLC: 248–253. doi:10.1038/ng0396-248. ISSN 1061-4036.
- ^ Xie, Jian; Craig, Leonard; Cobb, Melanie H.; Huang, Chou-Long (2006-05-09). "Role of with-no-lysine [K] kinases in the pathogenesis of Gordon's syndrome". Pediatric Nephrology. 21 (9). Springer Science and Business Media LLC: 1231–1236. doi:10.1007/s00467-006-0106-6. ISSN 0931-041X.