Kidney role in Acid/base bal Flashcards

1
Q

How does HCO3- prevent the continuous build up of 60meq of nonvolatile acid in the body?

A

“the twist”

  • You need high [ ]s of HCO3-
  • it converts nonvolatile(nongaseous) acid to a gaseous volatile form that can be ELIMINATED from ECF via respiration (CO2)
    (it acts more than just a buffer)
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2
Q

Where does most of the recapture of HCO3- take place?

A

Prox tubule - and is obligatory

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3
Q

Describe the process of how HCO3- is continuous replaced while maintaining electoneutrality?

A
  1. H+ is moved to lumen via H+/Na+ antiporter
  2. H+ binds to HCO3- → H2CO3
  3. H2CO3 is broken down via CA to H2O + CO2
  4. CO2 is transported into the cell via highly permeable membrane
  5. CO2 binds to H20 in the cell via CA→ H2CO3
  6. H2CO3 is broken down to H+ and HCO3-
  7. HCO3- is transferred out of the cell into the serosa via Na+/HCO3+ cotransporter
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4
Q

Which cells make HCO3-?

A

Intercalated cells (secrete H+ and HCO3-) in distal tubule

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5
Q

How do you not piss out acid with all of the H+ being moved to the lumen? (via Na/H+ antiporter and H+ pump?)

A

2 main buffering mechs:

  1. titratable acid
  2. ammonia trapping
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6
Q

titratable acid buffering mech

A

complexing H+ ion to a filtered anion (HPO42-)

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7
Q

Ammonia trapping buffering mech

A
  1. tubular cells break ↓ glutamine → ammonia (NH3)
  2. ammonia (NH3) readily diffuses through the apical membrane into tubule
  3. in Lumen, NH3 has very high affinity for H+ → NH4 +

(ammonia is now “trapped” with buffered H+)
- can be up/downregulated depending on H+ secretion

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8
Q

During metabolic acidosis, what happens to ammonia (NH3)?

A

Glutaminase is upregulated → more NH3 is made to buffer the increased secretion of H+

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9
Q

Is the process of HCO3- reabsorption neutral in terms of acid/base terms? What about Synthesis of HCO3-?

A

R: is neutral

S: not neutral - results in the elimination of acid in the urine

(note that R is a much larger process than S)

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10
Q

How is HCO3- R and secretion similar?

A

They both require apical secretion of H+ and basolateral movement of HCO3- into the ECF

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11
Q

Which takes priority, HCO3- reabsorption or Secretion?

A

reabsorption: its also a much larger process

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12
Q

What competitively inhibits HCO3- synthesis?

A

When the H+ in the lumen is used to convert HCO3- to CO2 + H2O.
This causes CO2 to go into the cell and ultimately result in H+ and HCO3- forming inside the cell.

This will inhibit the entry of CO2 from the serosa/blood and will compete for secretory and HCO3- extrusion transporters required for synth pathway.

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13
Q

Can synthesis take place with HCO3- in the tubular fluid?

A

No, only R will take place.
HCO3- synthesis can only occur after all the filtered load has been reabsorbed

  • usually only cells in the very distal parts of the tubule will end up synth HCO3-
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14
Q

What is the rate limiting for HCO3- homeostasis? What does this rate depend on?

A

Apical secretion of H+ and basolateral extrusion of bicarb

- rates depends on ECF pH and CO2 levels (they determine the # of transporters in the apical and basolateral membrane)

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15
Q

During metabolic imbalances, what two organ systems work together to deal with the threat?

A

Kidney and lungs

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16
Q

In the short term, how do the kidneys respond to respiratory acidosis? Long term?

A

Kidney responds to respiratory acidosis by increasing their excretion of H+ ions to counteract it.

Eventually . . . compensation is limited by increased filtered load of HCO3- that results
(thus in prolonged resp acidosis, one sees a partial renal compensation with elevated HCO3-)

17
Q

Hypokalemia will cause in alkalosis or acidosis?

A

Alkalosis

Hypokalemia induced shift of H+ into tubular cells results in inappropriately increased H+ secretion and urinary excretion → alkalosis

*the opp is also true, alkalosis leads to increased K+ and H+ excretion → hypokalemia

18
Q

Hyperkalemia will induce acidosis or alkalosis?

A

acidosis:

hyperkalemia reduces the rate of H+ secretion and subsequent excretion, and H+ is inappropriately retained in ECF