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Systems: Urinary AB > Acid Base Balance > Flashcards

Acid Base Balance Flashcards

1
Q

What are metabolic reactions sensitive to?

A

pH of the fluid in which they occur

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2
Q

Why are metabolic reactions sensitive to pH?

A

It is due to the high reactivity of the H ions with Pr which can cause changes in configuration and function leading to metabolic disturbance

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3
Q

What is pH very closely related to?

A

ECF

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4
Q

What is the normal pH of arterialised blood?

A
  • pH 7.4

- Equal to free [H+] of 40 x 10^-9 moles/l or 40 x 10^-6 mmoles/l.

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5
Q

What is the only thing that contributes to pH?

A

Free H ions

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6
Q

What produces H ions?

A

The body

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7
Q

How does the levels of H in the blood compare to other plasma constituents?

A

It is one millionth of other constituents

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8
Q

What are the potential sources of H?

A
  • Respiratory acid

- Metabolic acid

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9
Q

Why is carbonic acid not normally a net contributor to increased acid?

A

An increase in production usually increases ventilation

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10
Q

When does a build up of respiratory acid occur?

A

When lung function is impaired

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11
Q

What is the major source of alkali?

A

Oxidation of organic anions such as citrate

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12
Q

How is metabolic acid gained via inorganic acids?

A

S-containing amino acids

H2SO4 and phosphoric acid is produced from phospholipids

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13
Q

How is metabolic acid gained via organic acids?

A
  • Fatty acids, lactic acids

- On a normal diet, there is a net gain to the body of 50-100 mmoles H per day

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14
Q

What do buffers do?

A

Minimise changes in pH when H ions are added or removed

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15
Q

What does the Henderson-Hasselbach equation equal?

A

It defines the pH in terms of the ratio of [A]/[HA] NOT the absolute amounts

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16
Q

What is the Henderson Hasselbach equation?

A

pH=pK+ log ( [A]/[HA])

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17
Q

What is the most important extracellular buffer?

A

Bicarbonate buffer system

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18
Q

What does the quantity of H2CO3 depend on?

A

The amount of CO2 dissolved in plasma which depends on solubility of CO2 AND Pco2

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19
Q

What is the normal pCO2 and ranges?

A
  • Normal 5.3kPa (40mmHg)

- Range 4.8-5.9 (36-44)

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20
Q

What is the normal bicarbonate and ranges?

A
  • Normal 24mmoles/l

- Range 22-26

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21
Q

What is the normal pH and ranges?

A
  • Normal 7.4

- Range 7.37-7.43

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22
Q

What is a simplified version of the Henderson-Hasselbach equation?

A

pH= [HCO3]/PCO2

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23
Q

How is the basic mechanism of the bicarbonate buffer system evident?

A
  • As ECF increases, H drives the reaction to the right, so that some of the additional increased H ions are removed from solution and a change in pH is reduced.
  • In an ordinary buffer system the increase in products would push the reaction back to a new equilibrium where only some of the additional H ions are buffered
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24
Q

How does bicarbonate prevent H from contributing to the pH?

A

H has NOT been eliminated from the body. Instead the HCO3- has buffered the H+ and the respiratory compensation has greatly increased the buffering capacity so that free H+ions are prevented from contributing to the pH.

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25
Q

How is H eliminated from the body?

A

Elimination of H+ from the body is by the kidneys and this excretion is coupled to the regulation of plasma [HCO3-]

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26
Q

What other buffers are there in the ECF?

A

Plasma proteins
Pr+ H HPr

Dibasic phosphate to monobasic phosphate
HPO4+H H2PO4

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27
Q

What are primary intracellular buffers?

A

Primary intracellular buffers are proteins, organic and inorganic phosphates and, in the erythrocytes, haemoglobin

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28
Q

What does buffering of H ions by ICF buffers cause?

A

They cause changes in plasma electrolytes, since to maintain electrochemical neutrality, movement of H+ must be accompanied by Cl- as in red cells or exchanged for a cation, K+ .

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29
Q

How does acidosis lead to death?

A

In acidosis, the movement of K+ out of cells into plasma can cause hyperkalaemia which cause depolarization of excitable tissues leading to ventricular fibrillation and death.

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30
Q

What does bone carbonate provide?

A

An additional store of buffer

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31
Q

When is bone carbonate very important?

A

In chronic acid loads such as chronic renal failure which leads to wasting of bones

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32
Q

When does arterial pH remain remarkably constant?

A

When the lungs and kidneys are working normally

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33
Q

What happens to H gained through diet?

A

H is buffered until the kidneys can excrete it

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34
Q

What buffering occurs for metabolic acid?

A

43% buffered in plasma, primarily with HCO3 57% in cells

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35
Q

How does the kidney regulate [HCO3]?

A
  • By reabsorbing filtered HCO3

- By generating new HCO3

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36
Q

What does regulation of [HCO3] by the kidney depend on?

A

Active H ion secretion from the tubule cells into the lumen

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37
Q

Describe the mechanism for the reabsorption of HCO3.

A
  • Active H secretion from the tubule cells coupled to passive Na reabsorption
  • Filtered HCO3 reacts with the secreted H to form H2CO3. In the presence of carbonic anhydrase on the luminal membrane forming CO2 and H2O
  • CO2 is freely permeable and enters the cell
  • Within the cell CO2 reacts in the presence of carbonic anhydrase (present in all tubule cells) to from H2CO3 which then dissociates to form H and HCO3
  • The H ions are the source of the secreted H
  • The HCO3 ions pass into the peritubular capillaries with Na
  • Bulk of HCO3 reabsorption occurs in the proximal tubule >90%
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38
Q

What is the importance of HCO3 reabsorption?

A

HCO3 must be reabsorbed as failure to do so would mean that H would be added to the ECF

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39
Q

When is there no excretion of H ions?

A

During HCO3 reabsorption

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40
Q

Why is it efficient to convert HCO3 to CO2?

A

Although the HCO3- reabsorbed is not the same ion as was filtered, the net effect is the same. HCO3- is a large charged molecule, by converting it to CO2 it is much easier to save this valuable buffer.

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41
Q

What is the minimum urine pH in humans?

A

4.5-5

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42
Q

What is the maximum urine pH in humans?

A

8

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43
Q

What is the usual net production of H per day?

A

50-100 mmoles

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44
Q

What would happen is H ions were free in urine?

A

pH would be very low and result in stinging hence why H is buffered in urine

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45
Q

What acts as buffers?

A

Several weak acids and bases act as buffers. Most is done by dibasic phosphate, HPO4, also uric acid and creatinine.

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46
Q

Why is the process of buffering urine called titratable acidity?

A

The process is called “titratable acidity” because its extent is measured by the amount of NaOH needed to titrate urine pH back to 7.4 for a 24hour urine sample.

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47
Q

What is the importance of the formation of titratable acidity?

A

It generate new HCO3 and excretes H

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48
Q

What is titratable acidtiy only used for?

A

Acid loads

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49
Q

What is the process of titratable acidity dependent on?

A

Pco2 of the blood

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50
Q

Describe the process of titratable acidity.

A
  • Na2HPO4 in the lumen. One Na+ is reabsorbed in exchange for secreted H+. This monobasic phosphate removes H+ from the body.
  • The source of the new HCO3- is indirectly CO2 from the blood. It enters the tubule cells, combining with H2O to form carbonic acid, in the presence of carbonic anhydrase, which then dissociates to yield H+, used for secretion, and new HCO3- , which passes with Na+ into the peritubular capillaries.
  • Occurs principally in the distal tubule. This is where, phosphate ions, not reabsorbed by the proximal tubule Tm mechanism, become greatly concentrated because of removal of up to 95% of the initial filtrate.
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51
Q

What is the site of formation of titratable acidity?

A

Distal tubule

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52
Q

Why is the distal tubule the site of titratable acidity?

A

Because un-reabsorbed dibasic phosphate becomes highly concentrated by the removal of volume of filtrate.

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53
Q

What does a major adaptive response to an acid load cause?

A

Generation of new HCO3 and excretion of H

54
Q

What is the basis of the mechanism of ammonium excretion?

A

NH3 is lipid soluble. NH4 is not. This differential solubility is basis for mechanism

55
Q

How is NH3 produced?

A

NH3 is produced by deamination of amino acids, primarily glutamine, by the action of renal glutaminase within the renal tubule cells

56
Q

What happens to NH3 once it is formed?

A

NH3 moves out into the tubule lumen, where it combines with secreted H+ ions to form NH4+ which combines with Cl- ions (from NaCl) to form NH4Cl which is excreted. (Distal tubule mechanism)

57
Q

What is the source of secreted H ions in ammonium excretion?

A

CO2 from the blood

58
Q

What happens to new formed HCO3 in ammonium excretion?

A

The new HCO3- passes with Na+ ions into the peritubular capillaries

59
Q

What exchanger is there in the proximal tubule which allows NH4 ions formed within cells to pass out into the lumen?

A

NH4/Na exchanger

60
Q

What is renal glutaminase exquisitely dependent on?

A

pH

61
Q

What happens to renal glutaminase activity when intracellular pH falls?

A

There is an increase in renal glutaminase activity and therefore more NH4 is produced and excreted

62
Q

What is the main adaptive response of the kidney to acid loads?

A

The ability to augment NH4+ production

63
Q

How long does it take kidney augmentation of NH4 production to reach maximal effect?

A

It takes 4-5 days to reach maximal effect because of the requirements of increased protein synthesis.

64
Q

How can the amount of H lost ad NH4 differ?

A

Normally only 30-50 mmoles H+ per day are lost as NH4+ , but this can increase to 250 mmoles/l in the presence of severe acidosis

65
Q

How quickly can the ability to make NH4 be switched off when there is excess alkali?

A

It takes time

66
Q

When does a change in pH occur?

A

If renal or respiratory function is abnormal, or any acid or base load overwhelms the body, a change in pH occurs.

67
Q

What is a decreased pH known as?

A

Acidosis

68
Q

What is an increased pH known as?

A

Alkalosis

69
Q

What do respiratory disorders affect?

A

Pco2

70
Q

What do renal disorders affect?

A

[HCO3]

71
Q

What is respiratory acidosis?

A

pH has fallen and it is due to a respiratory change, so Pco2 must have increased. Respiratory acidosis results from reduced ventilation and therefore retention of CO2.

72
Q

What acute causes of respiratory acidosis are there?

A
  • Drugs which depress the medullary respiratory centres, such as barbiturates and opiates.
  • Obstructions of major airways
73
Q

What chronic causes of respiratory acidosis are there?

A

Lung disease e.g.

  • Bronchitis
  • Emphysema
  • Asthma
74
Q

What is the response to respiratory acidosis?

A

Need to protect pH so need to increase [HCO3]

75
Q

How is [HCO3] increased in respiratory acidosis?

A
  • The increased Pco2 will lead to increased secretion of H+ and increased HCO3. Acid conditions stimulate renal glutaminase so get more NH3 produced, BUT, it takes time.
  • So there is increased generation of new HCO3- as well as increased reabsorption, because having generated more HCO3- , the increased Pco2 will also increase the ability to reabsorb it.
76
Q

What is the problem with renal compensation to increase HCO3 in respiratory acidosis?

A

It protects the pH, it does not correct the original disturbance

77
Q

What is the only way to ‘cure’ respiratory acidosis?

A

Only restoration of normal ventilation can remove the primary disturbance.

78
Q

Why do blood gas values never normalise in chronic respiratory acidosis?

A
  • The underlying disease process prevents the correction of ventilation, but because the kidney maintains high [HCO3], the pH is protected
  • Patients with lung disease will always have aberrant Pco2 and [HCO3-], but as long as kidney function is not impaired pH can be maintained at a level compatible with life.
79
Q

When do problems arise for patients with lung disease?

A

When they develop renal dysfunction

80
Q

What is respiratory alkalosis?

A

Alkalosis of respiratory origin so must be due to a fall in Pco2 and this can only occur through increased ventilation and CO2 blow-off

81
Q

What are acute causes of respiratory alkalosis?

A
  • Voluntary hyperventilation
  • Aspirin
  • First ascent to altitude
82
Q

What are chronic causes of respiratory alkalosis?

A

Long term residence at altitude,

-Decreased Po2 to <60mmHg (8kPa) stimulates peripheral chemoreceptors to increase ventilation.

83
Q

What should happen to protect pH in respiratory alkalosis?

A

[HCO3] should decrease

84
Q

How are alkaline conditions dealt with?

A

By the HCO3- reabsorptive mechanism.

85
Q

What must be normalised to correct the disturbance in respiratory alkalosis?

A

Ventilation

86
Q

What is the HCO3 reabsorptive mechanism in the correction of respiratory alkalosis?

A

If decreased Pco2 , less H+ is available for secretion, therefore less of the filtered load of HCO3- is reabsorbed so HCO3- is lost in the urine

87
Q

What is metabolic acidosis?

A
  • An acidosis of metabolic origin must be due to a decreased[HCO3-].
  • So decreased [HCO3], either due to increased buffering of H+ or direct loss of HCO3
88
Q

What must happen to protect pH in metabolic acidosis?

A

-Pco2 must be decreased

89
Q

What are the causes of metabolic acidosis?

A
  • H+ production, as in ketoacidosis of a diabetic (acetoacetic acid, B-hydroxybutyric acid) or in lactic acidosis.
  • Failure to excrete the normal dietary load of H+ as in renal failure.
  • Loss of HCO3- as in diarrhoea ie failure to reabsorb intestinal HCO3- .
90
Q

What is Kussmaul breathing an established clinical sign of?

A

Renal failure or diabetic ketoacidosis

91
Q

What is Kussmaul breathing?

A
  • Degree of hyperventilation.
  • Increase in ventilation depth rather than rate, which may be very striking, reaching a maximum of 30 l/min cf normal 5-6 l/min when the arterial pH falls to 7.0.
92
Q

What does metabolic acidosis stimulate?

A

Ventilation so that PCco2 will fall

93
Q

How do the kidneys normally correct metabolic acidosis?

A

Normally the kidneys correct the disturbance by restoring [HCO3-] and getting rid of H+ ions.

94
Q

What is the problem with the kidneys correcting metabolic acidosis?

A

Source of H+ ions is the carbonic acid from CO2, but the respiratory compensation lowers the Pco2 to protect the pH

95
Q

What would complete compensation of disturbance do?

A

Complete compensation would remove the drive to correct the original disturbance. Survival value of this is that if there were no pressure to correct initial disturbance, a further perturbation may push the system so far that compensation can no longer be effective.

96
Q

In the correction of metabolic acidosis, how do the kidneys get around the fact that there is less Pco2?

A

Because of the decreased Pco2, the total amount of H+ secreted by the renal tubule will be less than normal BUT because the plasma [HCO3-] and therefore filtered load of HCO3- is reduced to an even greater extent , a smaller fraction of total H+ is needed for HCO3- reabsorption and therefore a greater proportion is available for excretion in the form of titratable acid and NH4+.

97
Q

What is very important in the correction of metabolic acidosis?

A

Time

98
Q

What does increased metabolic H within the body lead to?

A
  • Immediate buffering in ECF and then ICF.
  • Respiratory compensation within minutes.
  • Renal correction of the disturbance takes longer to develop the full response to increase H+ excretion and generate new HCO3- because renal glutaminase takes 4-5 days to reach maximum. As HCO3- starts to increase , respiratory compensation begins to wear off until eventually get rid of all excess H+ .
99
Q

What is the disadvantage of respiratory compensation in metabolic disturbance?

A

So, respiratory compensation delays the renal correction, but protects the pH, much more important.

100
Q

What is metabolic alkalosis?

A

[HCO3-] must have increased and Pco2 will increase to protect the pH

101
Q

What are the causes of metabolic alkalosis?

A
  • Increased H+ ion loss- vomiting loss of gastric secretions
  • Increased renal H+ loss- aldosterone excess, excess liquorice ingestion
  • Excess administration of HCO3 in those with renal impairment
  • Massive blood transfusions
102
Q

Why can massive blood transfusions cause metabolic alkalsosis?

A

Massive blood transfusions can lead to metabolic alkalosis because bank blood contains citrate to prevent coagulation, which is converted to HCO3-, but need at least 8 units to have this effect.

103
Q

How is excess HCO3 lost in metabolic alkalosis?

A

In the urine

104
Q

What is the primary disturbance in respiratory acidosis?

A

Increased Pco2

105
Q

What is the primary disturbance in respiratory alkalosis?

A

Decreased Pco2

106
Q

What is the primary disturbance in metabolic acidosis?

A

Decreased HCO3

107
Q

What is the primary disturbance in metabolic alkalosis?

A

Increased HCO3

108
Q

What is the compensation in respiratory acidosis?

A

Increased [HCO3]

109
Q

What is the compensation in respiratory alkalosis?

A

Decreased [HCO3]

110
Q

What is the compensation in metabolic acidosis?

A

Decreased Pco2

111
Q

What is the compensation in metabolic alkalosis?

A

Increased Pco2

112
Q

What happens to the pH in respiratory acidosis?

A

Decreased

113
Q

What happens to the pH in respiratory alkalosis?

A

Increased

114
Q

What happens to the pH in metabolic acidosis?

A

Decreased

115
Q

What happens to the pH in metabolic alkalosis?

A

Increased

116
Q

What happens to H ion in respiratory acidosis?

A

Increased

117
Q

What happens to H ion in respiratory alkalosis?

A

Decreased

118
Q

What happens to H ion in metabolic acidosis?

A

Increased

119
Q

What happens to H ion in metabolic alkalosis?

A

Decreased

120
Q

What is a decrease in pH caused by?

A

Either
Decreased HCO3
or
Increased Pco2

121
Q

What is an increase in pH caused by?

A

Either
Increased HCO3
or
Decreased Pco2

122
Q

How does the decrease in pH differ between chronic and acute respiratory acidosis?

A

For a given increase in Pco2, there is a smaller decrease in pH in chronic respiratory acidosis than in acute respiratory acidosis

123
Q

Why is there a small decrease in pH for chronic respiratory acidosis compared to acute?

A

Answer lies in mechanisms used to raise [HCO3-]. NH3 production takes 4-5 days to be fully turned on. So initially can only raise [HCO3-] by titratable acid, so limited. With time, can use NH3 production which has a considerable capacity to raise [HCO3-].

124
Q

Why can high acidity lead to ventricular fibrillation?

A

High acidity will cause Hyperkalaemia as H+ ions are buffered intracellularly in exchange for K+ ions

125
Q

When there is ECF volume deficit and acid/base disturbance what happens?

A

Restoration of volume takes precedence over acid/base disturbance

126
Q

Why can excess ingestion of liquorice cause metabolic alkalosis?

A

Liquorice contains glycyrrhizic acid, which is very similar to aldosterone

127
Q

Why does alkalosis occur in vomiting/diarrhoea even though acid and alkali are lost?

A

Decreased ECF, increases aldosterone which causes contraction alkalosis

128
Q

What is the anion gap?

A
  • The difference between the sum of the principal cations (Na+ and K+) and the principal anions in the plasma (Cl- and HCO3).
  • Normally 14-18mmoles/L
129
Q

What can the anion gap be useful to measure?

A

It can be useful to measure the anion gap in metabolic acidosis.
There are 2 patterns of metabolic acidosis in terms of anion gap, in one there is no change from normal and in the other the anion gap increases.

130
Q

When is there no change in the anion gap in metabolic acidosis?

A

If the acidosis is due for example to a loss of bicarbonate from the gut, then the reduction of bicarbonate is compensated by an increase in chloride and so there is no change in anion gap.

131
Q

When does the anion gap increase in metabolic acidosis?

A

However in eg lactic or diabetic acidosis, the reduction in bicarbonate is made up by other anions such as lactate, acetoacetate, -OH butyrate and so the anion gap is increased.

Systems: Urinary AB (26 decks)

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