Renal Control of Acid-Base Balance Flashcards
(63 cards)
1
Q
Chemical buffers
-Function?
A
Minimize but don’t completely prevent pH changes caused by strong acid or base
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
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?
- pKa=6.8
A
As you add more HCl, the graph goes toward H2PO4 and a lower (more acidic) pH
-Opposite if you add NaOH (strong base)
4
Q
Two kinds of acid in the body?
A
- Volatile
- Fixed
5
Q
Volatile acid (only one)? -In chemical equilibrium with?
A
- Carbonic acid (H2CO3)
- In chemical equilibrium with CO2, a volatile gas
- H2CO3CO2 + H2O
6
Q
Volatile acid (only one)? -H2CO3 concentration in body fluids is controlled by?
A
Pulmonary ventilation
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
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
9
Q
2 metabolic sources of H+?
A
- Oxidative metabolism: CO2
- Non-volatile acids
10
Q
2 metabolic sources of H+
-Oxidative metabolism?
A
CO2 + H2OH2CO3H + HCO3
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
12
Q
3 lines of defense against pH changes?
A
- Chemical buffers
- Respiration
- Kidneys
13
Q
Major EC buffer
A
Bicarbonate system
14
Q
Bicarbonate system is the major EC buffer
-H2CO3 is in equilibrium with?
A
- HCO3
- CO2 and H2O
15
Q
Bicarbonate system is the major EC buffer
- Equilibrium between H2CO3 and HCO3 (pKa=?)
- Equation-pH= ?
A
pH = 3.8 + log [HCO3]/[H2CO3]
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]
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
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
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
20
Q
Response of bicarb system to strong acid figure
A
slide 18
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)
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
23
Q
Renal regulation of pH
- Most H is excreted in combination with urinary buffers
- Two types of urinary buffers?
A
- Titratable acid
- Ammonia
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
25
Types of urinary buffers
- Ammonia
- Generated by?
Generated by tubular epithelium
26
Total renal H excretion =?
H excretion = urinary excretion of titratable acid + ammonium -HCO3
27
Luminal pH along nephron
| -Acidification of the luminal fluid before it reaches the CD vs in the CD?
- 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
Collecting can secrete H or HCO3
| -2 different cell types?
Alpha and beta intercalated cells
29
Alpha intercalated cells
- Actively secrete H
| - H-ATPase
30
Beta intercalated cells
Secrete HCO3 to eliminate excess base
31
Acidification of urine begins in the PCT
| -Why is the acidification only slight in this segment?
Most of the H secreted by the PT is used to reabsorb filtered HCO3, so luminal pH falls only slightly in this segment
32
Tubular reabsorption of filtered HCO3
| -Effect of excretion of HCO3 compared to gaining H?
They have the same effects
| -Excretion of even a small amount of filtered HCO3 would acidify body fluids
33
Tubular reabsorption of filtered HCO3
| -In normal individuals?
Essentially all of filtered HCO3 must be recaptured
34
Tubular reabsorption of filtered HCO3
| -How does the kidney respond to a high arterial pH?
Incompletely reabsorbing HCO3
35
HCO3 reabsorption
- HCO3 is temporarily converted to?
- Process does not result in?
- Is it saturable?
- CO2
- Process does NOT result in net secretion of H
- It is saturable
36
HCO3 reabsorption
| -Ultimately dependent on?
Na-K ATPase
37
Excretion of H as titratable acid
| -most important buffer converted to a titratable acid?
Filtered HPO4 is the most important buffer converted to a titratable acid
38
Excretion of H as ammonium
- Two NH4 are generated by glutamine oxidation within the tubular epithelial cells
- Two HCO3 are produced by glutamine oxidation
39
Renal NH4 production/excretion is upregulated by?
Chronic acidemia
40
What happens in alkalemia?
The collecting ducts (beta intercalated cells) secrete HCO3
41
Factors controlling renal H secretion?
- 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
How does extensive use of diuretics lead to alkalemia?
- Extracellular volume contraction->RAAS->tubular secretion of H ion
- Potassium depletion->tubular secretion of H ion
43
How does extensive use of diuretics lead to alkalemia?
| -Increased tubular secretion of H ion leads to?
- Increased reabsorption of all filtered bicarb and contribution of new bicarb to blood
- Generation of metabolic alkalosis
44
Acidemia vs acidosis
Acidemia-a reduction in arterial pH below 7.35
Acidosis-any abnormal condition that produces acidemia
(alkalemia and alkalosis are the opposites)
45
Respiratory acidosis
Increased arterial PCO2 leads to increased H and HCO3
| -Opposite for respiratory alkalosis
46
Respiratory acidosis
- Increased arterial PCO2 leads to increased H and HCO3
- Renal response?
Increased H secretion restores extracellular pH, increases HCO3 further
-opposite for respiratory alkalosis
47
Metabolic acidosis
Low plasma pH (lowered ratio of HCO3 to PCO2)
48
Metabolic acidosis
| -Low plasma pH (lowered ratio of HCO3 to PCO2) due to?
- Gain of fixed acid in body fluids (ketone bodies, lactic acid)
- Loss of HCO3 (diarrhea)
- In either case HCO3 conc decreases
49
Metabolic acidosis
| -Respiratory compensation?
Increased ventilation (peripheral chemoreceptors)
50
Metabolic acidosis
| -Renal compensation?
increased H secretion and production of new HCO3
51
Chemical buffer systems
| -Mixture of?
Mixture of weak acid and its conjugate base in aqueous sol'n
52
Metabolic alkalosis
- Abnormally high plasma pH (increased ratio of HCO3)
| - HCO3 conc rises due to shift in carbonic anhydrase equilibrium toward HCO3
53
Metabolic alkalosis
| -Respiratory compensation?
Hypoventilation
54
Metabolic alkalosis
| -Renal compensation?
- Incomplete reabsorption of filtered HCO3
| - beta-intercalated cells excrete HCO3 to eliminate excess base
55
Davenport diagrams
slides 42-56
56
Anion gap
| -Used in differential diagnosis of?
Metabolic acidosis
57
- Anion gap equation?
| - Gap is comprised of?
- Anion gap = Na - (Cl + HCO3)
| - Gap is comprised of unmeasured anions including plasma albumin, phosphate, sulfate, citrate, lactate, ketoacids
58
Anion gap
- normal range?
- ***dependent on?***
- Normal range = 8-16 mEq/l
| - ***Method-dependent***
59
Anion gap is either normal or increased
| -Depends on?
Depends on the cause of the metabolic acidosis
60
Hyperchloremic acidosis
| -Anion gap?
- Anion gap is unchanged
| - Loss of HCO3 is matched by gain of Cl
61
Normochloremic acidosis
| -Anion gap?
- High anion gap acidosis
| - HCO3 is replaced by unmeasured anion (lactate, ketoacidosis, poisoning)
62
Mnemonic for causes of high anion gap acidosis?
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MUDPILES
Methanol
Uremia (chronic kidney failure)
Diabetic ketoacidosis
Propylene glycol
Iron/isoniazid
Lactic acidosis
Ethylene glycol
Salicylates (aspirin)
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63
Metabolic alkalosis
| -Abnormally high plasma pH (increased ratio of HCO3) due to?
- Excessive gain of strong base or HCO3 (alkali ingestion)
| - Excessive loss of fixed acid (loss of gastric acid through vomiting)
