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Renal Exam 2 > Renal Control of Acid-Base Balance > Flashcards

Renal Control of Acid-Base Balance Flashcards

1
Q

Chemical buffers

-Function?

A

Minimize but don’t completely prevent pH changes caused by strong acid or base

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2
Q

Ability (‘strength’) of buffer to minimize pH changes depends on?

A
  • Concentrations of buffer system components

- Nearness of buffer’s pKa to pH of sol’n

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3
Q

Example:

  • Phosphate buffer system-H2PO4 and HPO4+H
    • pKa=6.8
      - As you add more HCl which way does the graph/pH move?
A

As you add more HCl, the graph goes toward H2PO4 and a lower (more acidic) pH
-Opposite if you add NaOH (strong base)

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4
Q

Two kinds of acid in the body?

A
  • Volatile

- Fixed

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5
Q 
Volatile acid (only one)?
  -In chemical equilibrium with?
A
  • Carbonic acid (H2CO3)
  • In chemical equilibrium with CO2, a volatile gas
    • H2CO3CO2 + H2O
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6
Q 
Volatile acid (only one)?
  -H2CO3 concentration in body fluids is controlled by?
A

Pulmonary ventilation

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7
Q

Fixed acids

  • What are they?
  • Main difference between fixed and volatile acids?
A
  • Non-carbonic acids generated metabolically (e.g. sulfuric, phosphoric acids)
  • CANNOT be removed from body by ventilation
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8
Q

Fixed (non-volatile) acids

  • How are they removed from the body?
  • What eventually happens to them?
A
  • Internally neutralized by buffers in body fluids

- Ultimately excreted in urine

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9
Q

2 metabolic sources of H+?

A
  • Oxidative metabolism: CO2

- Non-volatile acids

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10
Q

2 metabolic sources of H+

-Oxidative metabolism?

A

CO2 + H2OH2CO3H + HCO3

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11
Q

2 metabolic sources of H+

-Nonvolatile acids?

A
  • Glycolysis-lactic acid
  • Incomplete oxidation of FA-ketone acids
  • Protein, nucleic acid, phospholipid metabolism: sulfuric, phosphoric, hydrochloric acids
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12
Q

3 lines of defense against pH changes?

A
  • Chemical buffers
  • Respiration
  • Kidneys
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13
Q

Major EC buffer

A

Bicarbonate system

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14
Q

Bicarbonate system is the major EC buffer

-H2CO3 is in equilibrium with?

A
  • HCO3

- CO2 and H2O

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15
Q

Bicarbonate system is the major EC buffer

  • Equilibrium between H2CO3 and HCO3 (pKa=?)
    • Equation-pH= ?
A

pH = 3.8 + log [HCO3]/[H2CO3]

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16
Q

Bicarbonate system is the major EC buffer

  • H2CO3 is also in equilibrium with CO2 and H2O
    • Equation?
A

pH = 6.1 + log [HCO3]/[CO2]

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17
Q

Bicarb buffer system cont.

  • How is CO2 concentration related to PCO2:
    • How does this change the equation?
    • Advantage?
A

For each mmHg PCO2 .03 mm CO2 is in sol’n

  • pH = 6.1 + log [HCO3]/[.03 x PCO2]
  • Advantage- [HCO3] and PCO2 are easily measured
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18
Q

Why is the bicarbonate system so powerful?

A
  • Components (HCO3 and CO2) are abundant

- Bicarbonate system is ‘open’; concentrations of HCO3 and CO2 are readily adjusted by respiration and renal function

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19
Q

Why is the bicarbonate system so powerful?

  • Components (HCO3 and CO2) are abundant
  • Bicarbonate system is ‘open’; concentrations of HCO3 and CO2 are readily adjusted by respiration and renal function
A

Oxidative metabolism->CO2->ventilation

Kidneys->HCO3->kidneys

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20
Q

Response of bicarb system to strong acid figure

A

slide 18

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21
Q

Renal regulation of pH (urine pH range 4.5-8)

-Renal response to excess acid?

A
  • All of filtered HCO3 is reabsorbed

- Additional H is secreted into lumen, excreted primarily as ammonium (NH4)

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22
Q

Renal regulation of pH

-Renal response to excess base?

A
  • Incomplete reabsorption of filtered HCO3
  • Decreased H secretion
  • Secretion of HCO3 in CD
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23
Q

Renal regulation of pH

  • Most H is excreted in combination with urinary buffers
    • Two types of urinary buffers?
A
  • Titratable acid

- Ammonia

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24
Q

Types of urinary buffers

  • Titratable acids
    • What are they?
    • Examples?
A
  • Conjugate bases of metabolic acids
    • Accept H in lumen
  • Examples-phosphate, creatinine, urate
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25
Q

Types of urinary buffers

  • Ammonia
    • Generated by?
A

Generated by tubular epithelium

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26
Q

Total renal H excretion =?

A

H excretion = urinary excretion of titratable acid + ammonium -HCO3

27
Q

Luminal pH along nephron

-Acidification of the luminal fluid before it reaches the CD vs in the CD?

A
  • Acidification of luminal fluid is rather modest (pH=6.7) before CD
  • In CD, fluid can be acidified to a pH as low as 4.5
28
Q

Collecting can secrete H or HCO3

-2 different cell types?

A

Alpha and beta intercalated cells

29
Q

Alpha intercalated cells

A
  • Actively secrete H

- H-ATPase

30
Q

Beta intercalated cells

A

Secrete HCO3 to eliminate excess base

31
Q

Acidification of urine begins in the PCT

-Why is the acidification only slight in this segment?

A

Most of the H secreted by the PT is used to reabsorb filtered HCO3, so luminal pH falls only slightly in this segment

32
Q

Tubular reabsorption of filtered HCO3

-Effect of excretion of HCO3 compared to gaining H?

A

They have the same effects

-Excretion of even a small amount of filtered HCO3 would acidify body fluids

33
Q

Tubular reabsorption of filtered HCO3

-In normal individuals?

A

Essentially all of filtered HCO3 must be recaptured

34
Q

Tubular reabsorption of filtered HCO3

-How does the kidney respond to a high arterial pH?

A

Incompletely reabsorbing HCO3

35
Q

HCO3 reabsorption

  • HCO3 is temporarily converted to?
  • Process does not result in?
  • Is it saturable?
A
  • CO2
  • Process does NOT result in net secretion of H
  • It is saturable
36
Q

HCO3 reabsorption

-Ultimately dependent on?

A

Na-K ATPase

37
Q

Excretion of H as titratable acid

-most important buffer converted to a titratable acid?

A

Filtered HPO4 is the most important buffer converted to a titratable acid

38
Q

Excretion of H as ammonium

A
  • Two NH4 are generated by glutamine oxidation within the tubular epithelial cells
  • Two HCO3 are produced by glutamine oxidation
39
Q

Renal NH4 production/excretion is upregulated by?

A

Chronic acidemia

40
Q

What happens in alkalemia?

A

The collecting ducts (beta intercalated cells) secrete HCO3

41
Q

Factors controlling renal H secretion?

A
  • Intracellular pH
  • Plasma PCO2
  • Carbonic anhydrase activity (affecting H and HCO3)
  • Na reabsorption (ECF volume changes due to angio/aldo)
  • Extracellular K conc
  • Aldosterone
42
Q

How does extensive use of diuretics lead to alkalemia?

A
  • Extracellular volume contraction->RAAS->tubular secretion of H ion
  • Potassium depletion->tubular secretion of H ion
43
Q

How does extensive use of diuretics lead to alkalemia?

-Increased tubular secretion of H ion leads to?

A
  • Increased reabsorption of all filtered bicarb and contribution of new bicarb to blood
  • Generation of metabolic alkalosis
44
Q

Acidemia vs acidosis

A

Acidemia-a reduction in arterial pH below 7.35

Acidosis-any abnormal condition that produces acidemia

(alkalemia and alkalosis are the opposites)

45
Q

Respiratory acidosis

A

Increased arterial PCO2 leads to increased H and HCO3

-Opposite for respiratory alkalosis

46
Q

Respiratory acidosis

  • Increased arterial PCO2 leads to increased H and HCO3
    • Renal response?
A

Increased H secretion restores extracellular pH, increases HCO3 further
-opposite for respiratory alkalosis

47
Q

Metabolic acidosis

A

Low plasma pH (lowered ratio of HCO3 to PCO2)

48
Q

Metabolic acidosis

-Low plasma pH (lowered ratio of HCO3 to PCO2) due to?

A
  • Gain of fixed acid in body fluids (ketone bodies, lactic acid)
  • Loss of HCO3 (diarrhea)
  • In either case HCO3 conc decreases
49
Q

Metabolic acidosis

-Respiratory compensation?

A

Increased ventilation (peripheral chemoreceptors)

50
Q

Metabolic acidosis

-Renal compensation?

A

increased H secretion and production of new HCO3

51
Q

Chemical buffer systems

-Mixture of?

A

Mixture of weak acid and its conjugate base in aqueous sol’n

52
Q

Metabolic alkalosis

A
  • Abnormally high plasma pH (increased ratio of HCO3)

- HCO3 conc rises due to shift in carbonic anhydrase equilibrium toward HCO3

53
Q

Metabolic alkalosis

-Respiratory compensation?

A

Hypoventilation

54
Q

Metabolic alkalosis

-Renal compensation?

A
  • Incomplete reabsorption of filtered HCO3

- beta-intercalated cells excrete HCO3 to eliminate excess base

55
Q

Davenport diagrams

A

slides 42-56

56
Q

Anion gap

-Used in differential diagnosis of?

A

Metabolic acidosis

57
Q
  • Anion gap equation?

- Gap is comprised of?

A
  • Anion gap = Na - (Cl + HCO3)

- Gap is comprised of unmeasured anions including plasma albumin, phosphate, sulfate, citrate, lactate, ketoacids

58
Q

Anion gap

  • normal range?
  • dependent on?
A
  • Normal range = 8-16 mEq/l

- Method-dependent

59
Q

Anion gap is either normal or increased

-Depends on?

A

Depends on the cause of the metabolic acidosis

60
Q

Hyperchloremic acidosis

-Anion gap?

A
  • Anion gap is unchanged

- Loss of HCO3 is matched by gain of Cl

61
Q

Normochloremic acidosis

-Anion gap?

A
  • High anion gap acidosis

- HCO3 is replaced by unmeasured anion (lactate, ketoacidosis, poisoning)

62
Q

Mnemonic for causes of high anion gap acidosis?

A 
MUDPILES
Methanol
Uremia (chronic kidney failure)
Diabetic ketoacidosis
Propylene glycol
Iron/isoniazid
Lactic acidosis
Ethylene glycol
Salicylates (aspirin)
63
Q

Metabolic alkalosis

-Abnormally high plasma pH (increased ratio of HCO3) due to?

A
  • Excessive gain of strong base or HCO3 (alkali ingestion)

- Excessive loss of fixed acid (loss of gastric acid through vomiting)

Renal Exam 2 (6 decks)

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