Phys Acid/base.txt

What is the trademark of Conn's syndrome?
- Hyperaldosteronism
- 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?

Alkalosis
What pump is AngII in control of?

Na/H exchanger
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?

NH₄⁺
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?
- Saline-resistant
- **due to tumor that performs hypersecretion of Aldo

Author

kepling

77662

Card Set

Phys Acid/base.txt

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Phys Acid/base

Updated

2011-04-06T01:13:44Z

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