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Body metabolic acidosis, the aforementioned set of regulatory agencies will play a compensatory regulation. Such as to maintain the pH value within the normal range called compensatory metabolic acidosis, pH value was lower than the normal limit of decompensated metabolic acidosis.
1. Buffer extracellular fluid extracellular acidosis [H increased, immediate reaction buffer. The buffer base in the largest number of HCO3-in this example, the reaction is as follows:
H + HCO3- H2CO3 H2O + CO2
CO2 by breathing to enhance the discharge, HCO3-reduced.
2. Respiratory compensation [H increases, the stimulation of medullary respiratory center, carotid body and aortic body chemoreceptors, causing breathing to deepen faster, increase alveolar ventilation, discharge more CO 3. Extracellular ion exchange H into the cell, K out to the cell. H-ion cells with the buffer substance in the Pr-, HPO4 =, Hb-binding and so are buffered. H also cation exchange with bone buffering.
4. Kidneys of non-compensatory metabolic acidosis caused by renal dysfunction, who, by renal compensation. Row of three forms of renal acid are enhanced.
(1) row of H increased, HCO3-reabsorption strengthen: acidosis, renal tubular epithelial cells increased carbonic anhydrase activity, generating an increase in H and HCO3-, H secretion into the lumen, Na and HCO3-exchange accompanied by the re-absorption. Obviously this is a row of acid base security process.
(2) NH4 excretion increased: acid


osis, renal tubular epithelial cells increased NH3, NH3 may be produced at this time of substrate, such as easy access to the mitochondrial glutamine metabolism in sake. NH3 diffusion into the lumen, combined with H generated NH4, combined with anion from the urine. This is the main form of renal row of H, so the compensatory role of big. This process is accompanied by an increase in NaHCO3 reabsorption.
(3) increase in titratable acid excretion: renal tubular acidosis, increased secretion of epithelial cells in H, can form more acid phosphate.
Na2HPO4 H NH2PO4 + Na (discharge) (with HCO3-reabsorption)
Na2HPO4 and more with a H discharge, but also have increased reabsorption of sodium bicarbonate. Na2HPO4 that is, the amount of titratable acid.
Decompensated metabolic acidosis, acid-base balance of the index to reflect changes as follows:AG AG is not measured by an increase of negative ions increased
No increase in negative ions were not determined not to increase BG
Acetazolamide causes metabolic acidosis mechanism
13:22 Type: Web Abstract Kai Wen Education
Acetazolamide led to the mechanism of metabolic acidosis in patients taking a carbonic anhydrase inhibitor acetazolamide urine after NaCl, water, HCO3-excretion increased, and metabolic acidosis. Analysis of the patients with metabolic acidosis is due to:
A. increase in tubular K-H exchange
B. Na exchange for a reduced renal tubular H
C. proximal tubule reabsorption increased K
D. decreased glomerular filtration rate
E. decreased renal tubular reabsorption of Na
Answers and Analysis: The problem selected B.
Acetazolamide inhibition of proximal tubule reabsorption of HCO3 85, due to combination of Na and HCO3 excretion, thereby reducing the proximal convoluted tubule Na reabsorption. Reabsorption of Na and H are coupled, that is H-Na exchange, Na reabsorption decreased, the H-Na exchange weakened.
But the main reason is the inhibition of proximal tubule reabsorption of HCO3, the body consumes stored HCO3, lead to high chloride acidosis. Statement: Any manuscript type "original" all text, pictures, and audio and video releases, both Kai Wen education network, without the site license agreement, any media, websites and individuals shall not be reproduced or otherwise be published, rights reserved.
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Anion gap can be divided into two types of normal and increased.First, the normal anion gap metabolic acidosis(A) of the renal loss of bicarbonate lost : proximal renal tubular acidosis, as HC0 3 - the maximum width value of the decrease in absorption may be normal 260mmol / L down to 150 ~ 200mmol / L; dilution acidosis, blood volume expansion, the proximal renal tubular reabsorption of HC0 3 - reduction; use of carbonic brother inhibitor, with primary hyperparathyroidism decreased reabsorption of phosphate; extrarenal loss: diarrhea, intestinal fistula, biliary fistula , pancreatic fistula, intestinal obstruction, intestinal decompression, and other ureteral anastomosis of the sigmoid colon caused by digestion is lost.(B) barriers lead to renal bicarbonate generation high acidosis: gradient defect distal renal tubular acidosis type, secretion of H return to blood flow, leading to high potassium chloride acidosis; of low renin acidosis and retention of low potassium of aldosterone diuretics such as triamterene, spironolactone, etc., inhibit the distal tubule Na reabsorption, K and H excretion decreased, leading to high potassium chloride acidosis; voltage-dependent renal tubular acidosis, leading to hyperkalemia of renal tubular acidosis.(C) an increase in acid intake by mouth, intravenous, parenteral nutrition intake of ammonium chloride, isotonic saline, etc. too much.Second, increased anion gap metabolic acidosis(A) of the inorganic acid excretion to reduce acute and chronic renal failure caused by sulfate, phosphate retention.(B) formation of organic acids have increased over ketones, such as diabetes, fasting, starvation, severe dehydration, alcoholism, etc.; produce too much lactic acid, such as shock, hypoxia, diabetes, severe liver disease, severe burns , violent activities, biguanides such as oral hypoglycemic agents; Others, such as high fever, severe infection, trauma, burns and other catabolic hyperthyroidism, excessive intake of potassium and so on.(C) excessive intake of organic acids such as lactic acid, methanol, ethylene glycol and so on.


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