Lect 12 clin cases

Question 1

clinical presentation

• severe HA, muscle weakness
• BP 180/100
• pH= 7.5, bicarb = 36; PCO2 = 48; K = 2.0; K excretion = 1350; serum aldosterone increased; serum cortisol normal

Answer 1

• Conn syndrome
• hyperaldosteronism -> adrenal cortex secretes too much aldosterone due to tumor
  
  • not all adrenal steroids are elevated (cushing’s disease)
• HTN due to expansion of ECF
• partially compensated metabolic alkalosis

Question 2

why does conn’s syndrome cause metabolic alkalosis

Answer 2

• oversecretion of aldosterone causes increases Na+ retention (ECF expansion) and increased K+ secretion
• aldosterone stimulates H+-ATPase in distal tubule which increases the secretion of H+ and the return of HCO3- to plasma

Question 3

how is conn’s syndrome treated

Answer 3

• surgical removal of tumor
• aldosterone antagonist: spironolactone

Question 4

clinical presentation

• unconscious, urinates frequently, often thirsty
• breathing: deep and rapid
• BP 90/40; pulse 130/min
• K = 5.8; glucose = 500; bicarb = 6; pH = 7.25; PaCO2= 14
• anion gap 31

Answer 4

• type I diabetes -> low insulin -> formation of ketoacids which acidify blood and deplete HCO3-
• glucose acts as osmotic diuretic -> volume depletion
• partially compensated metabolic acidosis
• anion gap excessive due to ketoanions neutralizing HCO3-; Cl- does not increase
• hyperkalemia due to low insulin promotes K+ efflux from cells

Question 5

• pH = 7.51
• PaCO2=48
• bicarb = 37

Answer 5

partially compensated metabolic alkalosis

Question 6

volume contraction + hypokalemia ->

Answer 6

alkalosis

Question 7

how does volume contraction increase H+ loss

Answer 7

• activation of RAAS system
• angiotensin II stimulates Na+-H+ antiport in the proximal tubule and therefore HCO3- reabsorption
• aldosterone stimulates secretion of H+ via H+-ATPase from type A intercalated cells and K+ from principle cells

Question 8

treatment of contraction alkalosis

Answer 8

saline (NaCl or KCl) if saline responsive