Lecture 18: Renal Control of Acid-Base Balance Flashcards

1
Q

Why is it important to keep the pH at 7.4?

A

pH changes affects protein structure and function

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2
Q

How do lungs maintain pH?

How do kidneys maintain pH?

A

Regulating PaCO2 levels levels via respiration (volatile acids)
Regulating [HCO3-] levels via excretion/resorption (fixed acids)

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3
Q

What is a buffer?

A

Sponge analogy - a molecule that soaks up as much H+ as it can so that blood doesn’t get too acidic/basic too easily

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4
Q

What are the important physiological buffers?

A

HCO3-
Hb
H2PO4-
NH4+

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5
Q

How does the ionic shift mechanism serve as a buffer?

A

If ICF or ECF has higher H+, exchange K+ across the membrane to normalize the pH while also balancing the positive charges

Example: If ICF is more acidic than the ECF. ECF gives 1 K+ to ICF in exchange for an H+ from ICF until they normalize.

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6
Q

What is the Henderson Hasselabalch equation?

A

pH = 6.1 + log (HCO3-)/0.03 pCO2

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7
Q

In the lungs, how can you “edit “ how much your pH changes?

A

Fasting breathing = bigger pH change

Directly proportional

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8
Q

Why is HCO3- reabsorbed? Where does this happen mostly?

A

HCO3- is the main buffer so body wants to keep it in the body
Most HCO3- reabsorbed at PCT

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9
Q

Explain how countercurrent multiplier results in concentrated urine

A
  • TAL permeable to NaCl not H2O > salt flows into interstitium
  • TDL permeable to H2O > water flows out to dilute the salt
  • remaining filtrate at TDL is now more concentrated
  • filtrate continues down to loop of Henle and reaches 1200 mOsm
  • moves up the TAL to be diluted as NaCl flows back out to repeat the process
  • H2O is reabsorbed at the CT/CD, leaving concentrated urine to be excreted out
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10
Q

What are 2 ways the body replenishes its supply of the HCO3- buffer?

A

Reabsorb and recycle HCO3- from filtrate at the PCT

Generate new HCO3- at collecting duct

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11
Q

How does HCO3- reabsorption happen at the PCT?

A
  • CO2 and H2O converted to HCO3- and H+ in PCT cell by CA
  • HCO3- transported to blood while H+ is brought out to the lumen by Na/H antiporter in exchange for Na+
  • H+ in lumen reacts with another HCO3- to form H2O and CO2 again, which is transported to PCT

And repeat

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12
Q

How is new HCO3- generated at the CD?

A
  • Intercalated cells at the CD converts CO2 + H2O into HCO3- and H+ using CA
  • HCO3- gets transported to blood for buffer use, H+ is transported to lumen and excreted to urine
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13
Q

What is the main problem with generating new HCO3- in the CD?

A

It dumps H+ in the lumen, and can get too acidic and damage the nephron

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14
Q

How does the body protect the nephron from acidic damage when generating new HCO3-?
Which one is largely used by the body? Why?

A
  • 2 ways: Use NH3+ and Titratable acids (phosphates) as buffers
  • Ammonia, since Glu is readily available in body whereas phosphates are limited supply
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15
Q

How does NH3 help the nephron “buffer” the lumen?

How do titratable acids “buffer” the lumen?

A

NH3 (made from Glu) and combine with H+ in the lumen to form NH4+
HPO4 filtered from blood into lumen and combines with H+ to form H2PO4

Both prevent accumulation of H+ in the lumen

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16
Q

Titratable acids and ammonium are responsible for _____ and ______ of total net acid excretion respectively

A

1/3

2/3

17
Q

renal tubular acidosis
Cause
Clinical

A

Kidneys unable to excrete H+ out to the lumen

Acidemia, normal AG, normal creatinine and no diarrhea (NAGMA)

18
Q

What is the defect in RTA type 1?

What condition is this associated with?

A

H+ excretion at the CD is impaired

Autoimmune disorders

19
Q

What is the defect in RTA Type 2?

What condition is this associated with?

A

Reabsorption of HCO3- at PCT impaired, leading to acid predominance
Fanconi’s syndrome (kids), multiple myeloma (adults), drug use

20
Q

What is the defect in RTA Type 4?

What condition is this associated with?

A
  • No aldosterone or response to aldosterone by kidneys = can’t get rid of K+ leading to hyperkalemia = depletes NH3 supply so you can’t properly buffer the lumen
  • Diabetic nephropathy, nephritis, drug use