Metabolism acids

Changes that follow the primary disorder and attempt to restore the blood pH to normal are referred to as compensatory changes. It should be stressed that compensation never normalizes the pH. Because all metabolic acid-base disorders are chronic and the normal respiratory system can quickly alter the PaC02, essentially all metabolic disorders are accompanied by some degree of respiratory compensation.3 Similarly, chronic respiratory acid-base disorders are typically accompanied by attempts at metabolic compensation.4,5 However, with acute respiratory acid-base disorders there is insufficient time for the metabolic pathways to compensate significantly.6 As such, acute respiratory derangements are essentially uncompensated. 

Normally everything is in balance. The lungs have the numerator (pC02), and the kidneys have the denominator ([HCO 3]). The amount of C02 produced by metabolism is balanced by the amount of C02 blown off by the lungs and let go by the kidney. It s the same way with the other metabolic acids—they leave the body as C02 or they are excreted by the kidneys. If everything always stayed in balance, you wouldn t have to learn all this—but as usual it doesn t, and you do. 

It will be apparent that in the absence of a buffer the production of carbon dioxide and metabolic acids would result a change in pH with all of the implied problems that... 

The pH is maintained, therefore, in that a reduction in [HC03 ] is countered by a corresponding decrease in [H2CO3]. The increase in metabolic acid is compensated by a corresponding increase in CO2. 

Human blood plasma normally has a pH close to 7.4. Should the pH-regulating mechanisms fail or be overwhelmed, as may happen in severe uncontrolled diabetes when an overproduction of metabolic acids causes acidosis, the pH of the blood can fall to 6.8 or below, leading to irreparable cell damage and death. In other diseases the pH may rise to lethal levels. 

Tin metabolic acidosis (p. 652) there is an increase in glutamine processing by the kidneys. Not all the excess NH4 thus produced is released into the bloodstream or converted to urea some is excreted directly into the urine. In the kidney, the NH% forms salts with metabolic acids, facilitating their removal in the urine. Bicarbonate produced by the decarboxylation of a-lcetoglutarate in the citric acid cycle can also serve as a buffer in blood plasma. Taken together, these effects of glutamine metabolism in the kidney tend to counteract acidosis. ... 

Boric Acid Boric oxide, [CAS 1303-86-21, B2O3, is acidic, It exists in two forms, a glassy form obtained by high temperature dehydration of boric acid, and crystalline form obtained by slow heating of metabolic acid. 

As shown in Figure 17.9, esters of sulfuric acid exist in which either one or both of the ionizable H atoms are replaced by hydrocarbon substituents, such as the methyl group. Replacement of one H yields an acid ester, and replacement of both yields an ester. Metabolically, acid ester sulfates are synthesized in phase II reactions to produce water-soluble products of xenobiotic compounds (such as phenol) that are readily eliminated from the body (see Section 7.4). 

Electrolyte balance Mineral balance Metal metabolism Acid-base balance Fluid balance Hematologic Mouth Teeth... 

Absorption Spectra of the Metabolic Acids of Penicillium charlesii and Their Relationship to the Absorption Spectrum of Ascorbic Acid, R. W. Herbert and E. L. Hirst, Biochem. /., 29, 1881 (1935). 

Plots of alkalinty versus Tqo2 and Ca " " versus alkalinity demonstrate conclusively the occurrence of metabolic dissolution. However, they do not show the ratio of the rates of dissolution and carbon oxidation well. The reason is that calcite dissolution is rapid relative to organic matter oxidation. Therefore, pore waters that have become undersaturated due to oxic metabolism re-equilibrate with sedimentary calcite very rapidly. The sedimentary layer in which the release of metabolic acids is not matched by dissolution is expected to be thin, so that the slope... 

Ono K, Nagano O, Ohta Y, Kosaka F. Neuromuscular effects of respiratory and metabolic acid-base changes in vitro with and without nondepolarizing muscle relaxants. Anesthesiology 1990 73(4) 710-16. 

Hypoventilation causes retention of C02 by the lungs, which can lead to a respiratory acidosis. Hyperventilation can cause a respiratory alkalosis. Metabolic acidosis can result from accumulation of metabolic acids (lactic acid or the ketone bodies p-hydroxybutyric acid and acetoacetic acid), or ingestion of acids or compounds that are metabolized to acids (methanol, ethylene glycol). Metabolic alkalosis is due to increased HC03, which is accompanied by an increased pH. Acid-base disturbances lead to compensatory responses that attempt to restore normal pH. For example, a metabolic acidosis causes hyperventilation and the release of C02, which tends to lower the pH. During metabolic acidosis, the kidneys excrete NH4+, which contains H+ buffered by ammonia. 

Ammonia is released into the urine, where it buffers the hydrogen ions produced by phosphoric acid, sulfuric acid (produced from cysteine), and various metabolic acids (e.g., lactic acid and the ketone bodies, ace-toacetic acid and P-hydroxybutyric acid). 

Many holistically-minded health experts consider cancer an effect of deep imbalances in the body, not a disease. These imbalances are caused by metabolic acids that build up in the blood and are released into cells, tissues, and organs. 

Most metabolic acid-base disorders develop slowly, within hours in diabetic ketoacidosis and months or even years in chronic renal disease. The respiratory system responds immediately to a change in acid-base status, but several hours maybe required for the response to become maximal. The maximum response is not attained until both the central and peripheral chemoreceptors are fully stimulated. For example, in the early stages of metabolic acidosis, plasma pH decreases, but because H ions equilibrate rather slowly across the blood-brain barrier, the pH in CSF remains nearly normal. However, because peripheral chemoreceptors are stimulated by the decreased plasma pH, hyperventilation occurs, and plasma PCO2 decreases. When this occurs, the PCO2 of the CSF decreases immediately because CO2 equilibrates rapidly across the blood-brain barrier, leading to a rise in the pH of the CSF. This will inhibit the central chemoreceptors. But as plasma bicarbonate gradually falls because of acidosis, bicarbonate concentration and pH in the CSF wih also fall over several hours. At this point, stimulation of respiration becomes maximal as both the central and peripheral chemoreceptors are maximally stimulated. 

Abnormalities of acid-base status of the blood are always accompanied by characteristic changes in electrolyte concentrations in the plasma, especially in metabolic acid-base disorders. Hydrogen ions cannot accumulate without concomitant accumulation of anions, such as CL or lactate, or without exchange for cations, such as or NaL Consequently, electrolyte composition of blood serum or plasma is often determined along with measurements of blood gases and pH and to assess acid-base disturbances. 

Under normal conditions, the liver provides 80% or more of the glucose produced in the body. During prolonged starvation, however, this proportion decreases, while that synthesized in the kidney increases to nearly half of the total, possibly in response to a need for NH3 to neutralize the metabolic acids eliminated in the urine in increased amounts (Chapter 22). 

As with the metabolic acid-base disturbances, there are two cardinal respiratory acid-base disturbances respiratory acidosis and respiratory alkalosis. These disorders are generated by a primary alteration in carbon dioxide excretion, which changes the concentration of carbon dioxide, and therefore the carbonic acid concentration in body fluids. A primary reduction in PaC02 causes a rise in pH (respiratory alkalosis), and a primary increase in PaC02 causes a decrease in pH (respiratory acidosis). Unlike the metabolic disturbances, for which respiratory compensation is rapid, metabolic compensation for the respiratory disturbances is slow. Hence these disturbances can be further divided into acute disorders, with a duration of minutes to hours that is too short for metabolic compensation to have occurred, and chronic disorders, that have been present long enough for metabolic compensation to be complete. 

In the conditions discussed above (diabetic ketoacidosis, lactic acidosis, uremia, and ingestion of salicylate, ethylene glycol, or methanol) metabolic acidosis is associated with an increased anion gap. In the face of excess metabolic acids, bicarbonate is depleted in the process of buffering excess hydrogen ions. Provided that the renal functions is normal, the kidney attempts to compensate by secreting an acid urine and retaining bicarbonate. 

Renal tubular acidosis can be classified into two main types, type I and type II, which are hereditary (11). Renal tubular acidosis can also result from accumulation of waste products, including a variety of metabolic acids in uremia. Another type of renal tubular acidosis, type IV, is due to hyporeninemic hypoaldostero-nism. Hypoaldosteronism appears to be secondary to the inability of the kidney to... 

Metabolic acid-base disorders are those which directly cause a change in the bicarbonate concentration. Examples incluile diabetes mcliitus. where altered intemiediary metabolism in the absence of insulin cau.ses a build up of hydrogen ion from the ioni/ation of aceloacetic and P-hydroxybutyric acids, or loss of bicarbonate from the extracellular Iluid. e.g. from a duodenal fistula. 

Primary problems with hydrogen ion production or excretion are reflected in the IHCO,"] and these are called metabolic acid-base disorders. 

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