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acid-base balance (metabolic acidosis (overproduction of acid) (lactic…

- - - - inadequate oxygen delivery to tissues
      - ex: hypoxemia, low BP, extremely severe anemia
    - - inability of tissue to utilize oxygen
      - ex: thiamine deficiency, liver dysfunction, medications such as AZT, metformin
    - - bacteria in gut produce and metabolize D-lactic acid (SIBO)
  - - - methanol --> formic acid --> blindness
      - ethylene glycol --> oxalate --> renal failure
    - - difference between measured pOsm and calculated Posm (normally 5-10 mosm/L above calculated)
      - ethanol intoxication is the most common cause of an increased osmolar gap
      - a single molecule cannot contribute to both an osmolar gap and an anion gap
      - other toxins causing high anion gap metabolic acidosis are often associated with an increased osmolar gap (until the toxin is fully metabolized)
  - - - renal tubular acidosis (RTA)
        
        is the patient acidemic? check serum
        
        is the urine acidic? (pH < 5.5)
        
        is there buffer in the urine? check urine anion gap
        
        (+) anion gap = low NH4+ excretion or bicarb loss
        
        expected renal response to an acid load would be a (-) urine anion gap
        
        classification
        
        proximal (type II) RTA
        
        defect in HCO3- reabsoprtion (similar to the effects of acetazolamide)
        
        threshold for tubular bicarb reabsorption is lower --> low serum bicarb. If tubular bicarb is above threshold, you have bicarbonaturia and high urinary pH. If tubular bicarb level falls below threshold levels, reabsorption ensues --> low urine pH
        
        distal (type I) RTA
        
        defect in acid excretion (new HCO3- generation). Loss of bicarb day after day ("death by inches")
        
        distal hyperkalemic (type IV) RTA
        
        defect in acid excretion (ammoniagenesis, acid excretion)
        
        hyperkalemia inhibits ammonia production
        
        causes
        
        mineralocorticoid (aldosterone deficiency)
        
        primary
        
        4 more items...
        
        hyporeninemic hypoaldosteronism
        
        3 more items...
        
        mineralocorticoid (aldosterone) resistance (PHA-1, autosomal dominant)
        
        Distal tubule dysfunction
    - - diarrhea (most common)
- - - - lower filtration of bicarb leads to higher serum bicarb
    - - increased ATII
        
        sodium reabsoprtion increased in the PT, bicarb extruded on the basolateral side
      - increased aldo
        
        acts on intercalated alpha cell (H ATPase) - increased hydrogen secretion always for bicarb reabsorption
        
        also secretes potassium via the principal cell
        
        any process that increases aldo release will lead to maintenance of metabolic alkalosis in the right setting - a common abnormality associated with metabolic alkalosis is hypokalemia
      - two major components: proximal tubular bicarb reclamation and distal tubular bicarb generation. both ATII and aldo can act synergistically to increase serum bicarbonate mass
      - examples of maintenance
        
        use of diuretics leads to volume depletion --> ATII increases --> Na/H antiporter increases bicarb reclamation, GFR decreases and less bicarb is filtered
        
        volume depletion causes aldo release --> more NH4+ produced, bicarb generation increases
        
        hypokalemia ensures secondary to aldo action that more NH4+ is produced, bicarb generation increases, ICF is acidified
    - - proximal tubule: low serum K values causes K to move out of the cell to the interstitial fluid via exchange with a hydrogen ion. Glutamine metabolism leads to HCO3- production and NH3.
      - distal tubule: NH3 acts later as a receptor for hydrogen ion secretion. potassium-hydrogen exchanger --> H+ to the lumen and potassium moves into the alpha intercalated cell. this is how hypokalemia works to maintain alkalosis, because it allows for an increase in bicarbonate mass through this proton-K+ exchanger
    - - low luminal chloride concentration
      - increased chloride secretion with hydrogen
      - increased NH4+ production and bicarb generation
      - chloride mass relates to ECF! a low chloride mass can indicate volume contraction --> aldo release --> maintenance of alkalosis
  - - - GI causes
        
        vomiting
        
        villous adenoma
        
        congenital chloridorrhea
      - renal causes
        
        diuretics
        
        Bartters/Gitleman's
        
        non-absorbable anions
        
        post-hypercapnia
    - - primary hyperaldosteronism
      - Cushing's syndrome, licorice use, Liddle's syndrome
      - reninoma
      - congenital adrenal hyperplasia