Acid Base Disorders 2 Flashcards
Differential diagnosis of metabolic alkalosis
- Bartter Syndrome
- Aldosteronism
- NG suction
- Gitelman Syndrome
- Excess Akalai (antacids)
- Renin
- Emesis
- Diuretics
increased serum HCO3 in metabolic alkalosis due to
- GI hydrogen loss
- renal hydrogen loss
metabolic consequences of metabolic alkalosis
- hypercarbia
- hypoxemia
- hypocalcemia
- hypokalemia
two phases of metabolic alkalosis
- generation phase
- maintenance phase
generation phase of metabolic alkalosis - loss of gastric acids
- loss of HCl, Na and H2O from stomach and generation of Na and HCO3
- reabsorb filtered chloride (prefer reabsorb Cl over HCO3) due to onset of hypovolemia and loss of excess HCO3 in urine with sodium and potassium
what would rapidly restore the situation to baseline in generation phase of metabolic alkalosis
- renal excretion of alkali or retention of acid
maintenance phase of metabolic alkalosis - clinically evidence only when the elevated _________ concentration persists
requires impairment of
- serum bicarbonate
- requires impairment of renal excretion of bicarbonate
causes of impaired renal bicarbonate excretion in metabolic alkalosis
- kidney failure
- secondary stimulation of collecting duct ion transport
- primary stimulation of collecting duct ion transport
maintenance phase of metabolic alkalosis linked to - loss of gastric acids
- chloride depletion
- hypokalemia
- greater degree of hypovolemia so enhanced reabsorption of filtered NaCl and all of the excess HCO3
- increase in aldosterone which excretes more H+ in collecting duct
- aciduria
maintenance phase of metabolic alkalosis- secondary stimulation of collecting duct ion transport due to
- extra-renal losses of Cl with secondary renal K losses
- renal Cl losses with secondary K losses
renal Cl loses with secondary K loses due to
- chloruretic diuretic drugs
- recovery from chronic hypercapnia
- inactivating mutation of Cl- linked Na+ cotransporters (Bartter and Gitelman syndromes)
maintenance phase of metabolic alkalosis - primary stimulation of collecting duct ion transport due to
- mineralocorticoid induced or apparently mineralocorticoid excess syndromes
- activating mutations of ENaC or signal pathway
up regulation of proximal tubule Na+/H+ exchanger and H+ ATPase results in
- increased HCO3- reabsorption
- pump more hydrogen out which will absorb more HCO3 and bring it into the cell
impairment of LOH Na/K/2Cl results in
what causes this
- increased Na+ delivery to distal nephron
- loop diuretics
- Bartter syndrome
impairment of early distal tubule Na/Cl transporter and late distal tubule HCO3/CL exchanger results in
what causes this
- increased Na+ delivery to distal nephron
- thiazide diuretics
- Gitelman syndrome