Metabolic alkalosis: Difference between revisions
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****Enhances Na reabsorption and K+/H+ secretion in renal tubule | ****Enhances Na reabsorption and K+/H+ secretion in renal tubule | ||
*****K/H+ secretion -> HCO3 generation | *****K/H+ secretion -> HCO3 generation | ||
******Resulting urine is alkaline with little chloride | ******Resulting urine is alkaline with little chloride | ||
*Chloride-Resistant | |||
**Excess mineralocorticoid activity leads to same cascade as above | |||
***However, excess mineralocorticoid is not a/w hypovolemia so urine chloride is generally normal | |||
==DDX== | ==DDX== |
Revision as of 02:58, 27 April 2011
Pathophysiology
- Chloride-Responsive
- Condition that produces chloride loss also tends to reduce extracellular volume
- Reduction in extracellular volume increases mineralocorticoid activity
- Enhances Na reabsorption and K+/H+ secretion in renal tubule
- K/H+ secretion -> HCO3 generation
- Resulting urine is alkaline with little chloride
- K/H+ secretion -> HCO3 generation
- Enhances Na reabsorption and K+/H+ secretion in renal tubule
- Reduction in extracellular volume increases mineralocorticoid activity
- Condition that produces chloride loss also tends to reduce extracellular volume
- Chloride-Resistant
- Excess mineralocorticoid activity leads to same cascade as above
- However, excess mineralocorticoid is not a/w hypovolemia so urine chloride is generally normal
- Excess mineralocorticoid activity leads to same cascade as above
DDX
- Chloride-Responsive (urine Cl < 20 mEq/L)
- Loss of gastric secretions
- vomiting
- NG suction
- bulemia
- Loss of colonic secretions
- congenital chloridorrhea
- villous adenoma
- Thiazides/loop after D/C
- Post hypercapnia
- Cystic fibrosis
- Loss of gastric secretions
- Chloride-resistant (urine Cl > 20 mEq/L)
- With HTN
- Primary hyperaldo
- adrenal adenoma
- bilateral adrenal
- hyperplasia
- adrenal carcinoma
- 11B-HSD2
- genetic, licorice
- chewing tobacco
- carbenoxolone
- CAH (11-Hydroxylase or 17-hydroxylase deficiency)
- Current diuretics + HTN
- Cushing syndrome
- Exogenous steroids
- Liddle syndrome
- Renovascular HTN
- Primary hyperaldo
- Without HTN
- Bartter syndrome^
- Gitelman syndrome^
- Severe K+ depletion
- Current thiazides/loop
- Hypomagnesemia
- With HTN
- Other causes
- Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
- Milk alkali syndrome
- Hypercalcemia
- Intravenous penicillin
- Refeeding alkalosis
- Massive blood transfusion
^ln children
Source
Emedicine, Tintinalli