CLINICAL USE OF DIURETICS

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CLINICAL USE OF DIURETICS
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PATHOGENESIS AND TREATMENT OF REFRACTORY EDEMA

• Determinants of diuretic response - site of
  action, antinatriuretic forces, fall in BP, rate
  of drug excretion
• excess sodium intake
• decreased or delayed intestinal absorption
• decreased drug entry into lumen
• increased distal reabsorption
• decreased loop sodium delivery (low GFR and/or
  enhanced proximal reabsorption

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Match the clinical setting with the preferred
diuretic

• Recurrent nehprolithiasis (Ca2)
• hepatic cirrhosis with ascites
• metabolic alkalosis in CHF
• hypercalcemia
• Hyponatremia due to SIADH

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Question

• The appropriate use of diuretics may induce or
  exacerbate effective circulating volume depletion
  in which of the following edematous states?
• CHF
• nephrotic syndrome
• renal failure
• hepatic cirrhosis and ascites

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Question

• What is the simplest way to detect this change?
• Measurement of urine Na concentration
• measurement of BUN
• estimation of JVP
• measurement of systemic BP

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CASE

• Previously well 45 YO male, acute onset of
  crushing CP and dyspnea. Medical eval confirms
  AMI and Pulm edema. Treated with O2 and diuretics
  he becomes edema free. Weight has fallen by 3 KG
  within 24 hours and his estimated JVP is less
  than 5 cm H2O. Now he is oliguric, urine Na lt 10.
  BUN increased from 10 to 28mg/dl.
• What are 2 most likely causes of oliguria and
  increase in BUN?
• Would a normal EF distinguish between these
  possibilities?
• Does low JVP exclude cardiac dysfunction?
• Is total ECF gt, , or lt normal?
• What modes of therapy might return BUN and urine
  output to normal?