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FHB - Pulmonary & Renal - Exam 2 > Renal - Hydrogen Ion Excretion - Lecture 10 > Flashcards

Renal - Hydrogen Ion Excretion - Lecture 10 Flashcards

1
Q

How is both the reabsorption of the filtered HCO3- and the excretion of nonvolatile acids achieved?

A

Via secretion of H+ by nephrons

  • secreted H+ serves to reabsorb the filtered load of HCO3-
  • urine acidity is usually 50 to 100 mEq of H+ –> urine is slightly acidic
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2
Q

Because the kidneys cannot excrete urine more acidic than pH of 4 to 4.5, how is the secretion of H+ achieved?

A

To secrete sufficient acid, a buffer like phosphate is used

or even creatinine, which has a less important role than Pi

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3
Q

What are the various urinary buffers for H+ called?

A

Titratable Acids

  • excretion of H+ as a titratable acid is INSUFFICIENT to balance the daily nonvolatile acid load
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4
Q

Because the excretion of H+ as a titratable acid is INSUFFICIENT to balance the daily nonvolatile acid load, what other important mechanism contributed to the maintenance of acid-base balance in the kidney?

A

Via synthesis and excretion of NH4+ (ammonium)

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5
Q

Is the majority of HCO3-

  1. Filtered
  2. Excreted
  3. Secreted
  4. Reabsorbed

Where?

A

REABSORBED!

  • in the proximal tubule (80%)
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6
Q

What reaction predominates in the Proximal tubule? What enzyme is vital to this reaction?

A

CO2 HYDRATION REACTION:
[HCO3- + H+ –> H2CO3 –> (CA) –> H2O + CO2]

The presence of Carbonic Anhydrase in the brush border

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7
Q

Why is the net secretion of H+ in the PT very low?

A

net secretion of H+ is very low due to neutralization reaction of H+ with HCO3 - during bicarbonate ion “recycling” or reabsorption

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8
Q

What mechanisms facilitate reabsorption in the PT? (2 transporters)

A
  1. Apical H+ - ATPase (out)
  2. Apical Na/H (out) Antiporter

H+ moves out in both cases!

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9
Q

What reactions predominate in the Distal Tubule and Collecting Duct for H+?

Is the net secretion of H+ in this area high or low? How is this achieved?

A
  1. Phosphate and Ammonium ion reactions
    - no Carbonic Anhydrase here
    - low HCO3-
  2. Net secretion of H+ is HIGH due to proton pumping, buffered by phosphate and ion trapping as ammonium
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10
Q

Describe what occurs in DISTAL Renal Tubular Acidosis (Type I-RTA)

2 reasons

A
  1. Failure of distal nephron to secrete H+ !!!! (H+ remains in the plasma)
  2. Increased Back leaking of H+ or H+ pump failure (decreased plasma pH)
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11
Q

Describe what occurs in PROXIMAL Renal Tubular Acidosis (Type II-RTA)

2 reasons

A

REMEMBER** proximal is type 2 even tho proximal tubule comes 1st

  1. Failure of proximal nephron to recycle H+ due to low CARBONIC ANHYDRASE
  2. Decreased HCO3- reabsorption (low plasma pH = acidic)
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12
Q

Why does 80% of Reabsorption of filtered bicarbonate occur in the PROXIMAL TUBULE? (3)

A
  1. High Carbonic Anhydrase Activity
  2. Apical H+ - ATPase
  3. Basolateral Cl- / HCO3- Antiporter (HCO3- pumped out into the blood, Cl- pumped into the cell)
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13
Q

Why does 20% of Reabsorption of filtered bicarbonate occur in the Distal Tubule and Cortical Collecting Duct? (4)

A
  1. Low Carbonic Anhydrase Concentration (bad)
  2. Apical H+-ATPase
  3. Apical K+/H - ATPase
  4. Basolateral Cl-/HCO3 - Antiporter
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14
Q

The plasma HCO3 - concentration is regulated near what value for HCO3-?

A

Renal Plasma Threshold!

- important in regulating plasma [HCO3-]

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15
Q

What cells secrete HCO3-?

When do they facilitate the secretion of HCO3- and what mechanisms due they utilize to achieve this?

A

Collecting Duct!

  1. Basolateral H+-ATPase that pushes H+ back into the blood
  2. Apical Cl/HCO3- antiporter (cl in, HCO3 out)
    - BOTH ACTIVATED in states of metabolic alkalosis
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16
Q

What 7 factors regulate HCO3- reabsorption?

A
  1. GFR
  2. Na balance
  3. Systemic Acid-Base Balance
  4. Aldosterone
  5. Arterial [K+]
  6. Arterial [Cl-]
  7. Extracellular Fluid Volume
17
Q

How does GFR regulate HCO3- reabsorption? Which mechanism is important for this?

A
  1. Reabsorption rate of HCO3- is matched to changes in filtered load of HCO3- by GT BALANCE!
18
Q

How does Na Balance regulate HCO3- reabsorption?

What happens to HCO3- reabsorption when you retain Na?
Lose Na?

A
  1. Apical Na/H Antiporter is important for HCO3- reabsorption (Na into cell, H+ out into TF!! - binds to NH4+ in the Tubular Fluid)
  2. Retain Na –> volume expansion and positive Na balance –> HCO3- reabsorption goes down (antiproton functioning less)
  3. Lose Na –> volume contraction and negative Na balance –> HCO3- reabsorption goes up!
19
Q

How does Systemic acid/base balance regulate HCO3- reabsorption?

  1. In metabolic/respiratory acidosis
  2. In metabolic/respiratory alkalosis
A
  1. senses decrease in pH
    - respiratory acidosis = increase in PaCO2
    - metabolic acidosis = decrease in plasma HCO3-

a) Increase acidification of ICF –> increased insertion of apical H-ATPase -> increased H+ secretion and increased HCO3- reabsorption

  1. Senses Increase in pH:
    - respiratory alkalosis = decrease in PaCO2
    - metabolic alkalosis = increase in plasma HCO3-

b) decreased acidification of ICF –> decreased insertion of apical H-ATPase -> decreased H+ secretion and decreased HCO3- reabsorption

20
Q

How does Aldosterone regulate HCO3- reabsorption?

  1. 2 cases of increased aldosterone and its affect of H+ secretion (state where and which cells)
  2. One case of decreased aldosterone
A
  1. a) Increased aldosterone –> increased secretion of H+ in intercalated cells of CD

b) increased aldosterone –> increased Na reabsorption by principal cells of CD
- -> increased Negativity of LUMEN of Tubule
- -> increased H+ secretion (indirect affect of Na reabsorption)

  1. Decreased aldosterone –> decreased H+ secretion in intercalated cells of CD
21
Q

How does Arterial [K+] regulate HCO3- reabsorption?

  1. Increased
    - what is the pH of urine
    - what is the pH of the extracellular fluid
    - is this hyperkalemia or hypokalemia?
  2. Decreased
    - what is the pH of urine
    - what is the pH of the extracellular fluid
    - is this hyperkalemia or hypokalemia?
A
  1. Increased arterial K+ :
    - increased basolateral K-H exchange (K into cell, H+ into the plasma)
    - -> extracellular acidosis with an ALKALINE urine –> hyperkalemic metabolic acidosis
  2. Decreased Arterial K+ :
    - DECREASED basolateral K-H exchange (K into cell, H+ into the plasma)
    ( K remains in the plasma since concentration is low to begin with, H+ is not pumped out of the
  • extracellular alkalosis with an ACIDIC urine
    = hypokalemic metabolic ALKALOSIS
22
Q

How does Arterial [Cl-] regulate HCO3- reabsorption?

  1. Increased [Cl-]
  2. Decreased [Cl-]
A
  1. Increased [Cl-]
    - decreased HCO3- reabsorption
  2. Decreased [Cl-]
    - increased HCO3- reabsorption
  • maintains plasma electroneutrality since both compete for the same cations in tubular fluid
  • little change in anion gap
23
Q

What is the equation for the anion gap?

A

[A-] = [Na+] - [HCO3-] - [Cl-]

24
Q

How does changing the ECF affect HCO3-?

A

expansion of ECF inhibits HCO3- reabsorption due to dilution of plasma [HCO3-]

25
Q

What is the urine pH for

  1. Vegetarian diets
  2. Sulfur containing amino Acid Diets

What is the minimal urinary pH?

What is the source of urinary free H+?

A
  1. pH= 8 or higher
  2. pH = 5-6 (forms H2SO4)
  3. minimal pH is about 4.4
    - impressive ability of distal nephron to secrete H+ against a strong acid gradient before back leaking occurs
    • fixed acids
      titratable acids
      - NOT CARBONIC ACID!!
26
Q

Carbonic Acid is a source of urinary free H+. True or False? Why?

A

FALSE!

  • it readily becomes CO2 and diffuses back into the blood
27
Q

Because secreted H+ combines with HPO4- to form H2PO4-, how does this prevent back diffusion?

A

Negatively charged ion is LIPID INSOLUBLE therefor no back diffusion will occur

28
Q

What types of acids are the following and which functions best as a Titratable acid. Why?

  1. H2SO4
  2. H2PO4-
  3. NH4+
A
  1. H2SO4 –> Sulfuric Acid is a strong acid
  2. H2PO4–> pH lies mostly within the urinary pH range (4-7)
  3. NH4+ –> ammonium is a weak acid
29
Q

What is the pK of NH3/NH4+?

What is NH3 produced from?

A
  1. 3

- metabolism of amino acids

30
Q

Of the two, which is freely permeable and which is impermeable and why?

  1. NH3
  2. NH4+
A
  1. NH3
    - freely permeably
  2. NH4+
    - lipid impermeable because it is CHARGED
    - formation of NH4+ keeps the concentration of NH3 LOW!
31
Q
  1. When is the formation of NH4+ enhanced?
  2. What compound production is increased?
  3. What does this permit the secretion of into TUBULAR FLUID?
A
  1. Chronic Acidosis
  2. NH3 production increases
  3. Permits the secretion of additional H+ load into tubular fluid at ph levels equivalent to normal
32
Q

Describe the steps of chronic acidosis.

A
  1. Increased production rate of renal NH3

2. Increased secretion of additional H+ into tubular fluid (adaptation_

33
Q

For each molecule of NH4+ excreted into urine, what is reabsorbed to ECF?

A

HCO3-!

-“new”

34
Q

Where is NH4+ first secreted?
Where is it reabsorbed?
Where is it secreted again?

A
  1. Secreted in the Proximal tubule, and HCO3- is reabsorbed into the blood
  2. Reabsorbed in the THICK ASCENDING LIMB of the Loop of Henle and accumulates in the medullary interstitial
  3. Secreted by COLLECTING duct via nonionic diffusion and diffusion trapping and NH4+ antiprotons

FHB - Pulmonary & Renal - Exam 2 (21 decks)

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