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What is the trademark of Conn's syndrome?
- Stimulated H-loss via H/K atpase
What is Type I renal tubular acidosis?
Inactive Na/H antiport (no angiotensin II)
What is Type II renal tubular acidosis?
inactive H-ATPase (lack of aldosterone)
What is Type IV renal tubular acidosis?
- No NH4+ because of hyperkalemia and no aldosterone
- Also, the enzymes to break down glutamate are shot
What state do volume contraction + Hypokalemia lead to?
What pump is AngII in control of?
What pumps is Aldo in charge of?
- Na/K-ATPase = K secretion @ principal cells
- H-ATPase = H secretion @ α intercalated cells
What buffer does hypokalemia help activate?
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
Is Conn's disease saline-resistant or saline-adaptive?
- **due to tumor that performs hypersecretion of Aldo
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