Metabolic alkalosis: Difference between revisions

Revision as of 05:12, 14 March 2011

DDX

Chloride-responsive (urine Cl < 20 mEq/L)
1. Loss of gastric secretions
  1. vomiting
  2. NG suction
  3. bulemia
2. Loss of colonic secretions
  1. congenital chloridorrhea
  2. villous adenoma
3. Thiazides/loop after D/C
4. Post hypercapnia
5. Cystic fibrosis
Chloride-resistant (urine Cl > 20 mEq/L)
1. With HTN
  1. Primary hyperaldo
    1. adrenal adenoma
    2. bilateral adrenal
    3. hyperplasia
    4. adrenal carcinoma
  2. 11B-HSD2
    1. genetic, licorice
    2. chewing tobacco
    3. carbenoxolone
  3. CAH (11-Hydroxylase or 17-hydroxylase deficiency)
  4. Current diuretics + HTN
  5. Cushing syndrome
  6. Exogenous steroids
  7. Liddle syndrome
  8. Renovascular HTN
2. Without HTN
  1. Bartter syndrome^
  2. Gitelman syndrome^
  3. Severe K+ depletion
  4. Current thiazides/loop
  5. Hypomagnesemia
Other causes
1. Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
2. Milk alkali syndrome
3. Hypercalcemia
4. Intravenous penicillin
5. Refeeding alkalosis
6. Massive blood transfusion

^ln children

Source

2/21/06 DONALDSON (adapted from emedicine)

Authors:

@@ Line 1: / Line 1: @@
 ==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
+#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
+##Without HTN
+###Bartter syndrome^
+###Gitelman syndrome^
+###Severe K+ depletion
+###Current thiazides/loop
+###Hypomagnesemia
+#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
-I. Chloride-responsive (urine Cl < 20 mEq/L)
-) Loss of gastric secretions
-          a) vomiting
-          b) NG suction
-          c) bulemia
-) Loss of colonic secretions
-          a) congenital chloridorrhea
-          b) villous adenoma
-) Thiazides/loop after D/C
-) Post hypercapnia
-) Cystic fibrosis
-II. Chloride-resistant (urine Cl > 20 mEq/L)
-) With HTN
-          a) Primary hyperaldo
-               i. adrenal adenoma
-               ii. bilateral adrenal
-               iii. hyperplasia
-               iv. adrenal carcinoma
-          b) 11B-HSD2
-               i. genetic, licorice
-               ii. chewing tobacco
-               iii. carbenoxolone
-          c) CAH (11-Hydroxylase or 17-hydroxylase deficiency)
-          d) Current diuretics + HTN
-          e) Cushing syndrome
-          f) Exogenous steroids
-          g) Liddle syndrome
-          h) Renovascular HTN
-) Without HTN
-          a) Bartter syndrome*
-          b) Gitelman syndrome*
-          c) Severe K+ depletion
-          d) Current thiazides/loop
-          e) Hypomagnesemia
-III. 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 ==
 /21/06 DONALDSON (adapted from emedicine)
 [[Category:FEN]]