<prompt> Metabolic alkalosis is seen in all except -Thiazide diuretic therapyProlonged vomitingUretero-sigmoidostomyCushings disease  <response>: Causes of Metabolic Alkalosis I. Exogenous HCO3-loads A. Acute alkali administration B. Milk-alkali syndrome II. Effective ECFV contraction, normotension, K deficiency, and secondary hyperreninemic hyperaldosteronism A. Gastrointestinal origin 1. Vomiting 2. Gastric aspiration 3. Congenital chloridorrhea 4. Villous adenoma B. Renal origin 1. Diuretics 2. Posthypercapnic state 3. Hypercalcemiahypoparathyroidism 4. Recovery from lactic acidosis or ketoacidosis 5. Nonreabsorbable anions including penicillin, carbenicillin 6. Mg2 deficiency 7. K depletion 8. Baters syndrome loss of function mutations of transpoers and ion channels in TALH 9. Gitelmans syndrome loss of function mutation in Na-Cl-cotranspoer in DCT III. ECFV expansion, hypeension, K deficiency, and mineralocoicoid excess A. High renin 1. Renal aery stenosis 2. Accelerated hypeension 3. Renin-secreting tumor 4. Estrogen therapy B. Low renin 1. Primary aldosteronism a. Adenoma b. Hyperplasia c. Carcinoma 2. Adrenal enzyme defects a. 11b-Hydroxylase deficiency b. 17a-Hydroxylase deficiency 3. Cushings syndrome or disease 4. Other a. Licorice b. Carbenoxolone c. Chewers tobacco IV. Gain-of-function mutation of renal sodium channel with ECFV expansion, hypeension, K deficiency, and hyporeninemic-hypoaldosteronism A. Liddles syndrome Ref: Harrisons principles of internal medicine 19E, pg 321 