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Physiology > acid base > Flashcards

acid base Flashcards

1
Q

According to the Henderson Hasselbach equation, raising __ or lowering __ would increase pH.

A

Raising HCO3- or lowering pCO2

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2
Q
A

Uncompensated metabolic acidosis = Moving down along a pCO2 diagonal to a lower bicarbonate

Uncompensated respiratory acidosis = Moving from one pCO2 diagonal to a higher pCO2 diagonal

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3
Q

What are the two types of acid loads?

A

CO2 = respiratory acidosis

Nonvolatile acids = metabolic acidosis

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4
Q

Causes of metabolic acidosis (nonvolatile acids)

A
  • Exogenous acid loads
    • Salicylate, methanol, ethylene glycol
  • Excess endogenous acid production
    • Ketoacids, lactic acid
  • Decreased renal excretion of normal endogenous acids
    • Renal failure
  • Loss of alkali
    • GI losses (e.g. diarrhea), urine losses (e.g. proximal tubular acidosis)
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5
Q

Alkali loads

A
  • Excess CO2 removal = respiratory alkalosis
  • Nonvolataile alkali = metabolic alkalosis
    • Exogenous alkali
      • NaHCO3 administration
    • Loss of acid
      • GI losses (e.g. gastric fluid)
      • Excess urine H+ losses
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6
Q

A small increase in pCO2 will immediately cause

A

an immediate change in the cerebral interstitial pH that will activate chemoreceptors –> hyperventilation to blow off CO2

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7
Q

Increase in nonvolatile acids or a decrease in [HCO3-] will cause..

A

a slower ventilatory response because it takes longer for nonvolatile acids and HCO3- to cross the BBB to reach central chemoreceptors

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8
Q

The ventilatory response to metabolic acid-base disturbances is not achieved for ___

A

12-24 hours!

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9
Q

Does urine have bicarbonate in it?

A

Nope.

70-80% of filtered bicarb is reabsorbed at the proximal tubule

The rest is reabsorbed at teh more distal segments

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10
Q

What are the 2 ways kidneys regulate HCO3- concentration?

A
  • Reabsorption of HCO3-
  • Generation of new HCO3-
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11
Q

How does the kidney produce additional HCO3- beyond what was filtered at the glomerulus?

A

It excretes acid (titratable acid and ammonium), generating bicarb in the process.

Net acid excretion = Amt of bicarb regeneration

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12
Q

The kidney excretes titratable acid and ammonium to regenerate bicarb.

What is titratable acid?

A

Protons coupled to urinary buffers like phosphate

The nephron can’t excrete free protons that well.

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13
Q

Under normal conditions, the amt of titratable acid excreted is ____ at the amt of ammonium excreted.

Under acidic conditions, which one gets excreted more?

A

Normal: it’s about half&half

Acidic: Way more NH4+ is excreted

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14
Q

What is the equation of net acid excretion in the urine?

A

Net acid excretion =

titratable acid + ammonium - urinary bicarbonate

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15
Q

Recall how HCO3- is reabsorbed at the proximal tubule

A
  • Na,H exchanger on the apical membrane sends out H+ into the lumen, which combines with HCO3- to form H2CO3
  • Carbonic anhydrase turns it into CO2 + H2O
  • CO2 enters the proximal tubule cell, where another carbonic anhydrase combines it with OH- to reform HCO3-​
  • An Na,HCO3-​ exchanger on the basolateral side sends both Na+ and HCO3-​ out into the blood.
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16
Q

What drives the Na,H exchanger on the apical side?

A

The basolateral Na,K+ ATPase keeps [Na+] in the cell low –> driving force to take in Na+ and send out H+

17
Q

How is proximal tubule bicarbonate reabsorption regulated?

A

pH

peritubular bicarbonate

extracellular volume status

hormones

18
Q

pH & bicarbonate reabsorption

A

Factors that decrease intracellular pH increase the amt of H+ available for secretion –> allosterically enhance the Na,H-exchanger to promote reabsorption.

  • Ex) Increased pCO2 will decrease pH
  • Ex) Chronic K+ depletion will decrease pH
  • Chronic acidosis may also increase the # of apical Na,H-exchangers and basolateral Na,HCO3- transporters in the proximal tubule.
19
Q

Peritubular bicarbonate & HCO3- reabsorption

A

Decreased peritubular HCO3- will increase reabsorption

20
Q

Extracellular volume status & proximal bicarbonate reabsorption

A

Increased ECFV will inhibit HCO3- reabsorption

Decreased ECFV will promote reabsorption

(just think starling forces)

21
Q

Hormones that influence HCO3- reabsorption:

Adrenergic agonists

Angiotensin II

Parathyroid hormone

Glucocorticoids

A

Adrenergic agonists & Angiotensin II activate the apical Na/H exchanger. (Maintains metabolic alkalosis during volume or Cl- depletion)

Parathyroid hormone decreases reabsorption (though hypercalcemia increases it)

Glucocorticoids are involved in chronic adaptation to acidosis through the Na/H exchanger.

22
Q

While the distal tubule isn’t as good at secretingH+ and reabsorbing HCO3- as the proximal tubule, it can generate a large transepithelial pH gradient because of its ____.

This is used to drive HCO3- reabsorption

A

H+ ATPase & H,K-ATPase both secrete H+ to drive HCO3- reabsorption

23
Q

How does H+ secretion cause HCO3- generation in an intercalated cell of the collecting tubule?

A
  • H+ secretion via H+ ATPase and H-K ATPase lowers intracellular [H+]
    • These H+ will combine with an ion like phosphate to form a tiratable acid in the urine like H2PO4-
  • This drives the carbonic anhydrase reaction to keep splitting up H2CO3 into H+ and new HCO3-
  • New HCO3- gets reabsorbed via the HCO3-/Cl exchanger
25
Q

Bicarbonate secretion would only occur if you have

A

metabolic alkalosis

26
Q

What stimulates H+ secretion at the collecting tubule?

A
  • Increased Na+ reabsorption –> negative lumen voltage drives H+ ATPase to secrete more H+ into the lumen
  • Increased mineralocorticoids
  • K+ depletion
27
Q

Why is there a minimal urine pH achievable in urine?

A

The elctrogenic H+ATPase is sensitive to luminal pH - the amt of H+ it can excrete as titratable acid depends on how much urinary buffer is available.

28
Q

Most ammonia at physiologicla pH exists as

29
Q

Metabolism of ____ forms one HCO3- for every NH4+ excreted

30
Q

Which part of the kidney is responsible for most ammonia production?

A

proximal tubule

31
Q

What factors alter ammonia production?

A
  • Acidosis increases NH3 production
  • Hyperkalemia suppresses NH3 production
  • Hormones
32
Q

Pathway of ammonia in the nephron

A
  1. Produced in the proximal tubule
    1. Glutaminase breaks glutamine into NH4+
    2. Na,H-exchanger drives NH4+’s breakdown into H and NH3, which will diffuse into the lumen
  2. Reabsorbed at the thick ascending limb
    1. Na-K-2Cl cotransporter sometimes uses NH4+ insead of K+
  3. Secreted via diffusion at the collecting tubule​
33
Q

Lactic acid and keotacid production are decreased by

34
Q

How do the kidneys respond to metabolic acidosis?

A

Lowered HCO3- in the plasma means less is getting filtered -> kidney increases bicarbonate reabsorption & generation

Low pH, glucorticoids, mineral corticoids, distal delivery of non-reabsorbable anions –> H+ secretion into the urine

35
Q

What might prevent HCO3- excretion in metabolic alkalosis?

A

ECFV depletion will

  • decrease GFR
  • Increase prox tubule bicarb reabsorption
  • Release angiotensin & mineralcorticoids
    • Mineral corticoids stimulate H+ secretion
  • Cl- depletion
  • K+ depletion -> stimulates H+ secretion

Physiology (42 decks)

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