Pediatrics 5th year, 10th lecture/part two (Dr. Adnan)

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The lecture has been given on Feb. 10th, 2011 by Dr. Adnan.

The lecture has been given on Feb. 10th, 2011 by Dr. Adnan.

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  • 1. Renal Tubular acidosis Dr. Adnan MH Hamawandi Professor of Pediatrics College of Medicine University of Sulaimany
  • 2. Normal acid-base homeostasis
    • Acid base balance is maintained by pulmonary excretion of carbon dioxide plus the renal excretion of excess hydrogen ions. Acute changes in acid base status are prevented by the body’s buffer system. The most important of these in the ECF is bicarbonate because it is plentiful, can be conserved and generated by the kidney, and links the lungs and kidneys by carbonic acid dissociation:
    • CO 2 + H 2 O H 2 CO 3 H + + HCO - 3
    • The growing child excretes approximately 1-3mEq/kg daily. Most of this net acid is derived from dietary protein. The kidney excretes net acid by acidifying the urine via the following mechanisms: 1. Reclaiming all filtered bicarbonate. 2. Excreting urinary anions which combine with hydrogen ions to form titratable acid. 3. producing ammonia in Proximal RT cells(NH 4) .
  • 3. Assessing acid base status
    • Measuring a patient’s serum electrolytes, blood PH, and blood gases provides the data for determining acid-base status. 1. serum electrolyte levels provide the total carbon dioxide and permit calculation of the anion gap. A- The total carbon dioxide is almost identical to the serum HCO - 3 plus small contribution of dissolved CO 2 and H 2 CO 3 . B- Anion gap : Serum Na + – ( Cl - + Total CO 2 ) is normally 16-24 in infants 12-20 in older children. A large anion gap means there is an excess of one or more unmeasured anions like lactate or acetoacetate. 2. Blood PH indicates the net acid-base status and identifies acidemia (PH<7.35) or alkalemia (PH>7.45). The blood PH may be within the normal range in acid-base disorders if there is compensation for the primary disturbance or if there is a
  • 4. Assessing acid base status
    • mixed disorder. Reasonable estimates of the PH change expected in an uncompensated, primary acid-base disturbance are as follows: A- For every change in arterial partial pressure of carbon dioxide(PaCO 2 ) of 10mmHg, the PH will change inversely by 0.08. B- For every change in serum HCO 3 - of 10mmol/L, the PH will change 0.15. C- In situations in which the expected changes are not observed, there is either a mixed acid-base disturbance or compensation (or both). 3. Arterial blood gas analysis provides (PaCO 2 ) that allows assessment of pulmonary ventilation. It also provides the amount of buffer base excess or deficit which is calculated by determining how much of a change in PH cannot be explained by a change in PaCO 2 . The base excess (or deficit) equals 0.67 multiplied by the multiple of 0.01 PH unit unexplained by the PaCO 2 . The base deficit can be used to estimate the total bicarbonate deficit using the following formula:
    • (base deficit) x (body weight in kg.) x (0.3)
  • 5. Renal Tubular Acidosis
    • These are heterogeneous group of disorders, all of which are characterized by hyperchloremic metabolic acidosis and tubular dysfunction , but usually not by renal insufficiency. Children with RTA may have growth failure and episodes of vomiting and dehydration
  • 6. Distal Renal tubular Acidosis (Type I)
    • Is characterized by failure of the distal renal tubules to secrete the 1-3 mEq /kg/day of dietary acid (hydrogen ion) necessary to maintain acid-base homeostasis.
    • The urine cannot be maximally acidified and new bicarbonate cannot be generated.
    • Chronic positive hydrogen ion imbalance results in buffering by bone. This leads to increased skeletal calcium resorption, hypercalciuria, and increased risk of nephrocalcinosis and stones.
  • 7. Proximal Renal Tubular Acidosis (Type II)
    • Is characterized by decreased proximal tubular resorption of bicarbonate. A reduction in the normally variable renal threshold of bicarbonate causes a marked bicarbonate leak, which disappears when serum bicarbonate falls below the threshold level (e.g. to 15mEq/L). The defect may be isolated or may occur with other proximal tubular abnormalities, such as glycosuria, aminoaciduria, phosphaturia or kaliuria. Diffuse proximal tubular dysfunction is termed Fanconi’s syndrome.
  • 8. Type IV renal tubular acidosis
    • Includes a group of disorders, all of which are characterized by defects in distal tubular hydrogen ion and potassium secretion, leading to hyperchloremic metabolic acidosis and hyperkalemia.