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
activation of collecting duct ENaC, ROMK, H+ATPase, and H/K ATPase causes
due to
- hypokalemia and chloride depletion
- primary/secondary hyperaldosteronism or mimics of aldosteronism
relationship between plasma potassium and bicarbonate reabsorption
- as plasma potassium increases, HCO3 reabsorbed goes down
HCO3 reabsorption rises with what K+ levels
- low
secondary stimulation of collecting duct ion transport due to which syndromes
- Cl depletion syndrome
- renal Cl losses
- Alkali intake or administration
Cl depletion syndromes have what BP
- BP normal or low
extra-renal losses of Cl with secondary renal K losses due to
- vomiting, nasogastric drainage
- congenital chloridorrhea
- high volume ileostomy drainage
- cystic fibrosis
- some villous adenomas
VCICV
alkali intake or administration due to
- kidney failure
- dietary Cl- restriction
BP of appparent or for real mineralocorticoid excess syndromes
- high
conditions of apparent mineralcortcoid excess syndrome
- liddle
- 11-hydroxysteroid dehydrogenase inhibition or deficiency
conditions of mineralocorticoid excess syndromes
- primary aldosteronism
- glucocorticoid remediable aldosteronism
- Cushing syndrome
- congenital adrenal hyperplasia
- renin secreting tumors or renal artery stenosis
- fludrocortisone
PGCRFC
please get cush real fucking cool
how loop and thiazide diuretics cause metabolic alkalosis
- loss of Na+ and Cl- in urine
- decrease ECF volume
- activate SNS and RAAS
- secondary hyperaldosteronism
- ENaC activation (which reabsorbs Na)
- negative charge in cortical collecting duct
- loss of H+ (due to AGII and Aldo) and K+(due to Aldo) in urine
- hypokalemia metabolic alkalosis
what is natruiresis
- excretion of sodium in the urine
what mechanisms result in aldosterone escape
- pressure natriuresis
- atrial natriuretic peptide
- down regulation of NaCl in DCT
