Phys Acid/base.txt

  1. What is the trademark of Conn's syndrome?
    • Hyperaldosteronism
    • Stimulated H-loss via H/K atpase
  2. What is Type I renal tubular acidosis?
    Inactive Na/H antiport (no angiotensin II)
  3. What is Type II renal tubular acidosis?
    inactive H-ATPase (lack of aldosterone)
  4. What is Type IV renal tubular acidosis?
    • No NH4+ because of hyperkalemia and no aldosterone
    • Also, the enzymes to break down glutamate are shot
  5. What state do volume contraction + Hypokalemia lead to?
  6. What pump is AngII in control of?
    Na/H exchanger
  7. What pumps is Aldo in charge of?
    • Na/K-ATPase = K secretion @ principal cells
    • H-ATPase = H secretion @ α intercalated cells
  8. What buffer does hypokalemia help activate?
  9. What is hypocholoremia's role in alkalosis?
    • The person has activated Aldo so there is high Na reabsorption
    • The Cl- can't be reabsorbed from lumen
    • Negative lumen = K and H secretion
    • K and H secretion = hypokalemia and alkalosis
  10. Is Conn's disease saline-resistant or saline-adaptive?
    • Saline-resistant
    • **due to tumor that performs hypersecretion of Aldo
Card Set
Phys Acid/base.txt
Phys Acid/base