Please confirm topic selection

Are you sure you want to trigger topic in your Anconeus AI algorithm?

Updated: Mar 8 2023

Acid-Base Disorders

  • Introduction
    • The kidneys play an important role in regulating the body's acid-base status via
      • HCO3 reabsorption
        • this is the major extracellular buffer and is thus why it is important to conserve HCO3
          • ~99.9% of filtered HCO3 is reabsorbed
            • the proximal convoluted tubule is the site where most of the filtered HCO3 is reabsorbed
        • Na+H+ exchanger secretes H+ into the tubular lumen and combines with filtered HCO3to form H2CO3
          • H2CO3 is converted into CO2 and H2O with the aid of brush border carbonic anhydrase
            • CO2 and H2O enters the proximal tubular cell to be converted into H2CO3 via intracellular carbonic anhydrase
              • H2CO3 becomed HCO3 and H+
                • H+ gets secreted by the Na+-H+ exchanger to reabsorb more HCO3
                  • there is no net secretion of H+ since it is being recycled
                  • angiotensin II stimulates the Na+-H+ exchanger which subsequently increases HCO3 reabsorption
                    • this explains contraction alkalosis
                • HCO3 gets transported into the blood via
                  • Na+-HCO3 cotransport
                  • Cl-HCO3 exchanger
          • excess of HCO3 exceeds HCO3 reabsorption capacity and results in HCO3excretion
          • arterial CO2 and renal compensation
            • not completely understood
            • respiratory acidosis
              • increased CO2 exposed to renal cells generates more H+ to be secreted by the Na+-H+ exchanger
                • this increases HCO3reabsorption
            • respiratory alkalosis
              • decreased CO2 exposed to renal cells decrease H+ secretion by the the Na+-H+ exchanger
                • this decreases HCO3 reabsorption
      • H+ excretion
        • H+ excretion is accompanied by new HCO3 synthesis and reabsorption
        • there are two mechanisms involved
          • excretion of titratable acid (e.g., urinary buffers such as inorganic phosphate)
            • this is accomplished by H+ATPase (which can be stimulated by aldosterone) and H+-K+ ATPase on α-intercalated cells of the late distal convoluted tubule and collecting ducts
              • H+ binds to HPO4-2 to form H2PO4 (the titratable acid)
                • every titratable acid that excreted results in the synthesis of HCO3
          • excretion of NH4+
            • proximal convoluted tubule
              • NH4+ is secreted via the Na+-H+ exchanger
                • glutamine is metabolized into glutamate and NH4+ by the enzyme glutaminase in the proximal convoluted tubular cells
                • NH3 is lipid soluble and diffuses from the tubular cell into the lumen because it is lipid soluble
                  • Na+-H+ exchanger secretes H+ which will bind to NH3 to form NH4+
                    • this is diffusion trapping
            • collecting duct
              • H+-ATPase and H+-K+ ATPase on α-intercalated cells secrete H+ to bind with NH3 and form NH4+
                • this is diffusion trapping
  • Acid-Base Disorders
    • Acidosis results in acidemia due to an increased serum H+ (decreased pH)
    • Alkalosis results in alkalemia due to a decreased serum H+ (increased pH)
    • These acid base disorders may be due to primary disturbances in HCO3 (metabolic) or arterial CO2 (PCO2) (respiratory)
      • the Hendersen-Hasselbalch equation shows that changes in HCO3 or PCO2 changes pH
        • pH = pKa + log ([HCO3-]/(0.03 * PCO2)
    • Metabolic acidosis
      • due to a decrease in HCO3
        • either because of increased H+ or loss of HCO3
    • Metabolic alkalosis
      • due to an increase in HCO3
    • Respiratory acidosis
      • due to an increase in CO2
        • secondary to hypoventilation (which retains CO2)
    • Respiratory alkalosis
      • due to a decrease in CO2
        • secondary to hyperventilation
    • Winter's formula
      • determines expected respiratory compensation in response to metabolic acidosis
      • PCO2 = 1.5 (HCO3-) + 8 +/- 2
        • if actual PCO2 is greater than expected PCO2 → also has a primary respiratory acidosis
        • if actual PCO2 is less than expected PCO2 → also has a primary respiratory alkalosis
      • Acid-Base Disorders
      • Acid-Base Disorder
      • pH
      • PCO2
      • [HCO3-]
      • Compensatory Response
      • Metabolic acidosis
      • (primary disturbance)
      • Hyperventilation
      • Metabolic alkalosis 
      • (primary disturbance)
      • Hypoventilation
      • Respiratory acidosis
      • (primary disturbance)
      • ↑ renal HCO3- reabsorption
      • Respiratory alkalosis
      • (primary disturbance)
      • ↓ renal HCO3- reabsorption
1 of 0
1 of 5
Private Note

Attach Treatment Poll
Treatment poll is required to gain more useful feedback from members.
Please enter Question Text
Please enter at least 2 unique options
Please enter at least 2 unique options
Please enter at least 2 unique options