When the kidneys generate 'new' HCO3-, what is the net effect?
Explanation
This question clarifies the crucial distinction between bicarbonate reabsorption (a 1-for-1 replacement) and the generation of new bicarbonate (a net gain for the body), which is essential for correcting acidosis.
Other questions
What is the normal concentration of hydrogen ions (H+) in the extracellular fluid, expressed in mEq/L?
Which of the three primary acid-base regulatory systems in the body is the slowest to respond to a change in H+ concentration?
What is the normal pH of venous blood and interstitial fluids?
The bicarbonate buffer system consists of a weak acid and a bicarbonate salt. What are these two components?
What is the pK of the phosphate buffer system, and why is this significant for its function in body fluids?
According to the Henderson-Hasselbalch equation, what is the effect of an increase in bicarbonate (HCO3-) concentration on the pH of the extracellular fluid?
In what two locations is the phosphate buffer system particularly important?
What percentage of the total chemical buffering of body fluids occurs inside the cells, primarily from intracellular proteins?
What is the isohydric principle regarding the body's buffer systems?
How much can doubling the normal alveolar ventilation rate raise the extracellular fluid pH?
What is the approximate efficiency of the respiratory mechanism for controlling H+ concentration in response to a metabolic disturbance?
How much nonvolatile acid does the body typically produce each day from the metabolism of proteins?
In which segments of the renal tubules does H+ secretion occur via secondary active transport coupled to sodium-hydrogen counter-transport?
What is the primary mechanism for H+ secretion in the intercalated cells of the late distal and collecting tubules?
What is the approximate minimal urine pH that can be achieved in normal kidneys?
What is the primary source of the ammonium ion (NH4+) that is used in the ammonia buffer system of the kidneys?
For each molecule of glutamine metabolized in the proximal tubules, how many NH4+ ions are secreted and how many HCO3- ions are reabsorbed?
What is the definition of 'titratable acid' in the context of quantifying renal acid-base excretion?
What is the most important stimulus for increasing H+ secretion by the tubules in acidosis?
What effect does hypokalemia (decreased plasma potassium concentration) have on renal H+ secretion?
An acidosis caused by a primary decrease in HCO3- concentration is termed what?
In a patient with severe chronic acidosis, what is the maximum amount of H+ that can be excreted in the urine per day, and what is the primary form of this excretion?
What is a common cause of metabolic acidosis characterized by the loss of large amounts of sodium bicarbonate into the feces?
What is the primary compensatory response to respiratory alkalosis?
In a clinical analysis of a simple acid-base disorder, what finding would be expected for a simple metabolic acidosis after partial respiratory compensation?
What is the normal range for the plasma anion gap?
Metabolic acidosis caused by diabetic ketoacidosis or lactic acidosis would be associated with which type of anion gap?
Why is the bicarbonate buffer system considered the most powerful extracellular buffer despite having a pK of 6.1, which is far from the normal blood pH of 7.4?
What is the overall buffering power of the respiratory system compared to all other chemical buffers in the extracellular fluid combined?
What is the term for a molecule that can release hydrogen ions in a solution?
Approximately how much bicarbonate (HCO3-) do the kidneys filter each day under normal conditions?
What percentage of HCO3- reabsorption occurs in the proximal tubule?
The reabsorption of filtered HCO3- from the renal tubules depends on its initial interaction with what substance in the tubular lumen?
In a situation of metabolic alkalosis, what is the renal response regarding H+ and HCO3-?
Under normal conditions, what percentage of the daily acid excretion is accounted for by the ammonia buffer system?
What is the primary abnormality in respiratory alkalosis?
What condition is a frequent cause of metabolic acidosis due to the formation of excess quantities of acetoacetic acid?
How does the administration of most diuretics (excluding carbonic anhydrase inhibitors) typically lead to metabolic alkalosis?
What is the first step in diagnosing a simple acid-base disorder from an arterial blood sample?
A patient has a low pH and a low plasma HCO3- concentration. What additional finding would confirm a diagnosis of simple metabolic acidosis with respiratory compensation?
The plasma anion gap is a diagnostic concept used to estimate the difference between what two groups?
What is hyperchloremic metabolic acidosis?
Why does extracellular fluid volume depletion tend to cause metabolic alkalosis?
Which of the following conditions is a cause of normal anion gap (hyperchloremic) metabolic acidosis?
When a strong acid like HCl is added to the bicarbonate buffer system, what is the immediate chemical result?
What is the primary role of the protein hemoglobin in acid-base balance?
If a person's arterial pH drops from 7.4 to 7.0 due to an acid infusion, what would be the approximate pH after the respiratory system compensates?
What is the net acid excretion by the kidneys calculated as?
In a case of respiratory acidosis, what is the primary derangement and what is the renal compensatory response?