Acid-base homeostasis

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Acid-base homeostasis is the part of human homeostasis concerning the proper balance between acids and bases, in other words the pH. The body is very sensitive to its pH level. Outside the range of pH that is compatible with life, proteins are denatured and digested, enzymes lose their ability to function, and the body is unable to sustain itself.

Mechanism

The kidneys maintain acid-base homeostasis by regulating the pH of the blood plasma. Gains and losses of acid and base must be balanced. The study of the acid-base reactions in the body is acid base physiology.

Buffering agents

Any substance that can reversibly bind hydrogen ions is called a buffering agent. They function to impede any change in pH. Hydrogen ions are buffered by extracellular (e.g., bicarbonate, ammonia) and intracellular buffering agents (including proteins and phosphate).

Imbalance

Imbalance has several possible causes. An excess of acid is called acidosis and an excess in bases is called alkalosis. Acidosis is much more common than alkalosis. The imbalance is compensated by negative feedback to restore normal values. There are various renal responses to acidosis and alkalosis.

Causes

Sources of acid gain:

1. Carbon dioxide (since CO₂ and OH^-, hydroxide, form HCO₃^-, bicarbonate, and H⁺, a proton, in the presence of carbonic anhydrase)
2. Production of nonvolatile acids from the metabolism of proteins and other organic molecules
3. Loss of bicarbonate in faeces or urine
4. Intake of acids or acid precursors

Sources of acid loss:

1. Use of hydrogen ions in the metabolism of various organic anions
2. Loss of acid in the vomitus or urine

Response

Responses to acidosis:

1. Bicarbonate is added to the blood plasma by tubular cells.
   • Tubular cells reabsorb more bicarbonate from the tubular fluid.
   • Collecting duct cells secrete more hydrogen and generate more bicarbonate.
2. Ammoniagenesis leads to increased buffer formation (in the form of NH₃)

Responses to alkalosis:

1. Excretion of bicarbonate in urine.
   • This is caused by lowered rate of hydrogen ion secretion from the tubular epithelial cells.
   • This is also caused by lowered rates of glutamine metabolism and ammonia excretion.

See also

• Renal physiology

External links

• On-line text at AnaesthesiaMCQ.com
• Physiology at MCG 7/7ch12/7ch12lin
• Overview at kumc.edu
• Overview at mcgill.ca

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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