Chapter 10: Metabolic Acid-Base Disorders Flashcards

1
Q

Describe the proposed pathogenesis of a hyperchloremic metabolic acidosis caused by small bowel diarrhea.

A

Increased delivery of small intestinal contents to the colon overwhelms the reabsorptive properties of the colon. These small intestinal are generally rich in bicarbonate from alkaline pancreatic and biliary secretions as well as from secretion of bicarbonate in the ileum in exchange for chloride. The loss of these contents then causes a loss of bicarbonate in excess of chloride. As a side note, this can also cause enough volume loss to compromise perfusion and create a metabolic acidosis, making this a mixed acidosis process.

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2
Q

What part of the renal tubules is affected in type 2 renal tubular acidosis?

A

Proximal renal tubule. Type 1 renal tubule acidosis is caused by dysfunction of the distal renal tubules.

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3
Q

How do you diagnosis distal renal tubule acidosis?

A

Increased urine pH (>6.0) in the presence of systemic acidosis after ruling out urinary tract infection by urease-positive organisms (Proteus, Staph. Aureus).
You can also do an ammonium chloride tolerance test. This is performed by orally administering ammonium chloride (NH4Cl) at 0.2 g/kg, then monitor urine pH every hour for 5 hours. The urine pH should decrease to at least 5.16 if the animal does not have renal tubule acidosis. However, it can (and likely will) also cause a systemic acidosis.

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4
Q

Impaired hydrogen ion secretion in the collecting ducts is consistent with which type of renal tubule acidosis?

A

Type 1 (distal RTA)

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5
Q

Reduced renal reabsorption of bicarbonate is consistent with which type of renal tubule acidosis?

A

Type 2 (proximal RTA)

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6
Q

What other urinary abnormality can help to support a diagnosis of proximal (type 2) renal tubule acidosis?

A

Glucosuria

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7
Q

Patients with Fanconi syndrome have defects in what biochemical parameters due to their renal tubular disease?

A

Glucose, phosphate, potassium, sodium, uric acid, and amino acid reabsorption

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8
Q

How do carbonic anhydrase inhibitors cause metabolic acidosis? What other electrolyte can they cause derangements in?

A

They cause decreased bicarbonate reabsorption by noncompetitive inhibition of the luminal and cellular carbonic anhydrase.
Hypokalemia can occur from increased sodium delivery to the distal nephron that then gets reabsorbed in exchange for potassium (potassium is wasted in urine).

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9
Q

How does ammonium chloride cause metabolic acidosis?

A

NH4+ is converted in the liver to urea and H+. This causes the acidosis. The delivery of chloride in this compound contributes to the hyperchloremic metabolic acidosis (normal anion gap). As a side note, metabolism of cationic amino acids (lysine, arginine, histidine) have a similar mechanism without the addition of chloride.

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10
Q

What type of fluid is most likely to cause a dilution acidosis with a normal anion gap?

A

0.9% sodium chloride. The lack of buffer in this solution dilutes the serum bicarbonate, and the addition of chloride can cause further loss of bicarbonate in exchange for the chloride to maintain electroneutrality and contribute to the hyperchloremic metabolic acidosis (normal anion gap).

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11
Q

List two ways aldosterone helps limit metabolic acidosis.

A
  1. Increased sodium reabsorption increases luminal negative to allow for increased hydrogen ion secretion
  2. Directly stimulate H+ secretion by increasing luminal hydrogen-ATPase in the medullary collecting duct
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