Metabolic Alkalosis Flashcards Preview

Renal Block > Metabolic Alkalosis > Flashcards

Flashcards in Metabolic Alkalosis Deck (16):

1. Describe the role of the kidney in acid-base handling. What are the normal values for pH, H+, pCO2 and HCO3?

key role of kidney to regulate [H+] concentration at 40nM, major buffers include plasma HCO3, urine HPO4
pH 7.40 +/- 0.02
H+ 40+/- 2
pCO2 40 +/- 2
HCO3 24 +/- 2

it does this by HCO3- reabsorption of filtered HCO3 and generation of HCO3- via acid excretion (titratable acid H2PO4 and ammonium NH4+)


2. Recognize the factors that regulate kidney hydrogen excretion.

the proximal and distal tubule regulate Acid-base balance this is accomplished through the excretion of H+ to titratable acids and ammonium ions

4 factors that regulate renal H+ excretion are :
decreased pH
decreased plasma K
decreased effective circulating volume
increased aldosterone


3. Describe the underlying pathogenesis of metabolic alkalosis in the generation phase and the maintenance phase.

H+ loss
intracellular shift of H+
alkali administration
contraction alkalosis

ECV contraction
chloride depletion


4. Explain the diagnostic approach to metabolic alkalosis.

diagnosis hinges on urine Cl- (CHECK urine Cl-)

low Cl- is gastric losses, stool losses, diuretics, K+ depletion; treat with volume repletion and K+ replacement

normal Cl-: due to hyperaldosteronism, steroids, Barter or Cushing syndrome: treat cause, NaCl will not be effective


5. List the principles of therapy for metabolic alkalosis.

low Cl- is gastric losses, stool losses, diuretics, K+ depletion; treat with volume repletion and K+ replacement

normal Cl-: due to hyperaldosteronism, steroids, Barter or Cushing syndrome: treat cause, NaCl will not be effective


Where is the majority of bicarbonate reabsorbed and where is the bicarbonate generation occurring?

normally all HCO3- is reabsorbed in the PCT

bicarbonate is generated in the distal portion of the PCT and in the collecting ducts


Describe the process through which bicarbonate is reabsorbed.

hydrogen is secreted into the tubule and reacts with carbonic anhydrase there

water and CO2 are absorbed into the tubule and reacts with carbonic anhydrase in the tubule cell that produces bicarbonate to be exported into the interstitial space, and H+ goes back out to the tubule

H+ can be added to a titratable acid in in the collecting tubule or the PCT


How does ammonium excretion cause the removal of H+?

glutamine is absorbed by the proximal tubule and broken down to a a ketoglutarate and ammonium ions, a-ketogluterate is metabolized to bicarbonate ions which enter the interestitium , ammonium inks enter the lumen (this also promotes Na reabsorption)


How does decreased pH cause increased secretion of H+

PCT- increased synthesis and activity of Na/H exchange, increased ammonium production

in collecting tubules- increased H+-ATPase, insertion of cytoplasmic transporters and trapping of NH4+ in the lumen


How does effective circulating volume regulate the amount of H+ excreted?

RAAS prevents Na+ loss but also increased bicarbonate in PCT and producing hypkalemia which enhances m. alkalosis

aldosterone also directly stimulates H-ATPase pump and activates bicab reabsorption pump

ECV is also associated with decreased Cl-, K+ which independently increase H excretion


How does decreased K+ promote H+ excretion in kidney tubules cells?

K+ leaves cells, H+ enter cells and this intracellular acidosis will lead to HCO3- reabsorption, NH4+ excretion and enhanced m. alkalosis

REMEMBER: increased K+ associated with M. acidosis, decreased K+ associated with M. alkalosis


What conditions would lead to H+ in the urine or from the GI system?

urinary loss: diuretics, mineral corticoid excess, Bartter's and Gitelman's, post hypercapnia m. alk, hypercalcemia

digestive loss: gastric suctions (HCO3- produced by pancreas is unopposed), vomiting, diarrhea, chloride losing villous adenoma

note intracellular shift of H+ can be cause by hypokalemia and contraction alkalosis can be caused by loop diuretics


What is the effect of loop and thiazide diuretics on acid base balance?

cause more Na to reach the DCT and more fluid loss, increased aldosterone causes more exchange of Na for H
all leads to more acid secretion

Bartter and Gitelmans mimic a chronic overdose of diuretics


How do mineralocorticoid and Ca++ excess lead to alkalosis

mineralocorticoid excess: HTN, hypokalemia, m. alkalosis
Hypercalcemia: increased Ca, m. alkalosis, renal failure


Contrast early and late phase vomiting/gastric suctioning.

early phase: lots of bicarb lost in urine because bicarb is high in blood, Na and K follow HCO3- but Cl- is still reabsorbed

there is a switch from preserving pH to preserving volume

late phase, all HCO2- is reabsorbed now and hypovolemia becomes a problem, urine pH is down and urine Na, K and Cl- concentrations are down


Describe how M. alkalosis is maintained.

decreased ECV causes activation of RAAS, and overall leads to greater H+ (associated chloride depletion, hypokalemia independently increase H+)

aldosterone increases Na+ reabsorption with H+ and K+ excretion and directly stimulate H-ATPase pump and activation of the HCO3/Cl- pump

chloride depletion causes more distal reabsorption, and lest distal secretion of bicarb

low K+ leads to more H+ inside cells and more excretion