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Urinary System > Acid-Base Balance > Flashcards

Acid-Base Balance Flashcards

1
Q

Metabolic reactions are very sensitive to the pH of the fluid in which they occur, what does this relate to?

A

The high reactivity of H+ ions with Pr- which causes changes in configuration and function, especially in enzymes

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2
Q

Why is the pH of the ECF very closely regulated?

A

Because acid/base disturbances lead to lots of metabolic disturbances

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3
Q

What is the normal pH and free H+ ion concentration of arterialised blood?

A

pH 7.4

Free H+ ion concentration 40 x 10^-9 moles/l or 40 x 10^-6 mmoles

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4
Q

What ions contribute to pH?

A

Only free H+ ions

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5
Q

What are the sources of H+ ions?

A

Respiratory acid

Metabolic acid

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6
Q

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

A

Because any increase in production causes an increase in ventilation, problems occur when lung function is impaired

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7
Q

What is the equation for respiratory acid production?

A

CO2 + H2O H2CO2 H+ + HCO3-

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8
Q

How is metabolic acid produced?

A

Via metabolism or inorganic and organic acids

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9
Q

What is the oxidation of organic anions a major source of?

A

Alkali

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10
Q

What is the function of a buffer?

A

To minimise the changes in pH when H+ ions are added or removed

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11
Q

What is the Henderson-Hasselbach equation?

A

pH = pK + log [A-] / [HA]

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12
Q

What is the most important extracellular buffer system?

A

The bicarbonate buffer system,

H2CO3 H+ + HCO3-

pH = pK + log⁡ [HCO3-] / [H2CO3]

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13
Q

What is the Henderson-Hasselbach equation for a pH of 7.4 and a pK of 6.1, for the bicarbonate buffer system?

A

7.4 = 6.1 + log [HCO3-] / [H2CO3]

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14
Q

What does the quantity of carbonic acid depend on?

A

The amount of CO2 dissolved in the plasma, which depends on the solubility of CO2 and Pco2

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15
Q

What is the solubility of CO2 in blood at 37 degrees?

A

0.03mmoles/l/mmHg PCO2

or

0.225 mmoles/l/kPa PCO2

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16
Q

What is the normal value of PCO2?

A

40mmHg or 5.3 kPa

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17
Q

At a normal PCO2, what is the value of [H2CO3]?

A

40 x 0.03mmoles/l
or
5.3 x 0.225 mmoles/l

= 1.2 mmoles/l

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18
Q

What is the normal value of [HCO3-]?

A

24mmoles/l

Normal range 22-26

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19
Q

How does the bicarbonate system work as a buffer?

A

An increase in ECF H+ ion concentration drives the reaction to the right, so that some of the additional H+ ions are removed from solution and so any change in pH is reduced

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20
Q

What happens in an ordinary budder system?

A

As H+ increases and drives reaction to the right, the increase in products would begin to push the reaction back to reach a new equilibrium position where only some of the additional H+ ions are buffered

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21
Q

What greatly increases the buffering capacity of the bicarbonate?

A

Ventilation is increased and CO2 is decreased so the reaction is pulled to the right, greatly increasing the buffering capacity of the bicarbonate

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22
Q

When is the aim of the acid/base balance met?

A

Once arterial pH has been protected

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23
Q

How is H+ eliminated from the body?

A

By the kidneys

Excretion coupled to the regulation of plasma [HCO3-]

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24
Q

What are the other buffers in the ECF?

A

Plasma proteins

Dibasic phosphate

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25
Q

What are the primary intracellular buffers?

A

Proteins
Organic and inorganic phosphates
Haemoglobin

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26
Q

Buffering of H+ ions by ICF buffers causes changes in what?

A

Plasma electrolytes

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27
Q

To maintain electrochemical neutrality, the movement of H+ must be accompanied by what?

A

Cl-

or

exchanged for a cation K+

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28
Q

In acidosis, the movement of K+ out of cells into plasma can cause what?

A

Hyperkalaemia

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29
Q

What does hyperkalaemia cause?

A

Depolarisation of excitable tissues, leading to ventricular fibrillation and death

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30
Q

What provides an additional store of buffer? When is this important?

A

Bone carbonate

Important in chronic acid loads, as in chronic renal failure there is wasting of the bones

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31
Q

What is the loading of H+ from the diet?

A

50-100 mmoles per day

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32
Q

If H+ ions were present as free ions in total body water, what pH would they cause?

A

1.2-2.4

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33
Q

When does arterial pH remain normal?

A

As long as the lungs and kidneys are working

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34
Q

What percentage of metabolic acid is buffered in the plasma?

A

43% buffered in plasma

57% buffered in cells

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35
Q

What percentage of buffering occurs in the cells?

A

97% of buffering occurs within the cells, the rest occurs with plasma proteins

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36
Q

How does the kidney regulate [HCO3-]?

A

Reabsorbing filtered HCO3-
Generating new HCO3-

Both of these processes depend on active H+ ion secretion from the tubule cells into the lumen

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37
Q

What is the mechanism for the reabsorption off 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 -> CO2 and H2O
CO2 is freely permeable and enters the cell -> H2O in the presence of carbonic anhydrase which then dissociates to form H+ and HCO3-
H+ ions are the source of secreted H+
HCO3- ions pass into the peritubular capillaries with Na+

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38
Q

Where does the bulk of HCO3- reabsorption occur?

A

In the proximal tubule (> 90%)

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39
Q

What is the normal GFR value?

A

180l/day

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40
Q

What is the minimum urine pH in humans?

A

4.5-5

Maximum is around 8

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41
Q

What is the net production of H+ per day?

A

50-100 mmoles

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42
Q

What molecules are responsible for most buffering?

A

Dibasic phosphate
Uric acid
Creatinine

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43
Q

Why is the formation of titratable acidity important?

A

It generates new HCO3- and excretes H+

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44
Q

Where is Na2HPO4?

A

In the lumen - one Na+ is reabsorbed in exchange for secreted H+

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45
Q

What is the source of new HCO3-?

A

Indirectly CO2 from the blood - enters tubule cells, combining with water to form carbonic acid in the presence of carbonic anhydrase

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46
Q

Carbonic anhydrase dissociates to yield what?

A

H+ which is used for secretion and new HCO3-

47
Q

What happens to phosphate ions not reabsorbed by the proximal tubule Tm?

A

They become greatly concentrated in the distal tubule because of removal of up to 95% of the initial filtrate

48
Q

Ammonium excretion is a major adaptive response to what?

A

An acid load - generates new HCO3- and excretes H+

49
Q

What is the basis for the mechanism of ammonium excretion?

A

NH3 is lipid soluble, NH4+ is not

50
Q

How is NH3 produced?

A

By deamination of amino acids, primarily glutamine, by the action of renal glutaminase within the renal tubule cells

51
Q

What happens when NH3 moves out into the tubule lumen?

A

It combines with secreted H+ ions to form NH4+, which then combines with Cl- ions to form NH4Cl

52
Q

How is NH4Cl excreted?

A

Via the distal tubule mechanism

53
Q

What is the source of secreted H+?

A

CO2 from the blood

54
Q

What exchanger is there in the proximal tubule?

A

NH4+/Na+ exchanger - NH4+ ions formed within the cells pass out into the lumen

55
Q

What is the activity of renal glutaminase dependent on?

A

pH

56
Q

What effect does a fall in intracellular pH have on renal glutaminase?

A

When intracellular pH falls there is an increase in renal glutaminase and therefore more NH4+ produced and excreted

57
Q

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

A

The ability to augment NH4+ production

58
Q

Why does it take 4-5 to reach maximum effect of ammonium excretion?

A

Because of the requirements of increased protein synthesis

59
Q

How much H+ can be lost as NH4+ in severe acidosis?

A

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

60
Q

When does a change in pH occur?

A

If respiratory or renal function is abnormal, or any acid/base load overwhelms the body, a change in pH occurs
Decreased pH - acidosis
Increased pH - alkalosis

61
Q

What disorders affect PCO2?

A

Respiratory

62
Q

What disorders affect [HCO3-]?

A

Renal

63
Q

Why does the pH fall in respiratory acidosis?

A

Due to a respiratory change - so PCO2 must have increased

Respiratory acidosis results from reduced ventilation and therefore retention of CO2

64
Q

What are the acute causes of respiratory acidosis?

A

Drugs which depress the medullary respiratory centres e.g. barbiturates and opiates, obstruction of major airways

65
Q

What are the chronic causes of respiratory acidosis?

A

Lung disease e.g. bronchitis, emphysema, asthma

Response is to protect pH and so increase [HCO3-]

66
Q

Acid conditions stimulate what?

A

Glutaminase - so more NH3 is produced

67
Q

What is the effect of respiratory acidosis on PCO2, H+ and HCO3-?

A

PCO2 increased
This causes increased secretion of H+ and increased HCO3-

Increased PCO2 also increases the ability to reabsorb HCO3-

68
Q

What can be done to remove the primary disturbance causing respiratory acidosis?

What does this mean in chronic respiratory acidosis?

A

Only restoration of normal ventilation can remove the primary disturbance

Although the renal compensation to increase HCO3- protects the pH, it does not correct the original disturbance

This means that in chronic respiratory acidosis e.g. bronchitis, blood gas values are never normalised
The underlying disease process prevents the correction of ventilation

69
Q

Patients with lung disease will always have aberrant PCO2 and [HCO3-], but when will pH be maintained at a level compatible with life?

A

As long as kidney function is not impaired

70
Q

What is respiratory alkalosis due to?

A

A fall in PCO2

This can only occur through increased ventilation and CO2 blow-off (alveolar hyperventilation)

71
Q

What are the acute causes of respiratory alkalosis?

A

Voluntary hyperventilation
Aspirin
First ascent to altitude

72
Q

What are the chronic causes of respiratory acidosis?

A

Long-term residence at altitude

Decreased PO2 to < 60 mmHg (8kPa) which stimulates peripheral chemoreceptors to increase ventilation

73
Q

How are alkaline conditions dealt with?

A

HCO3- resorptive mechanism

If PCO2 decreases, less H+ is available for secretion, so less of the filtered load of HCO3- is reabsorbed so HCO3- is lost in the urine

74
Q

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

A

Ventilation must be normalised

75
Q

What is metabolic acidosis due to?

A

Decreased [HCO3-], either due to an increased buffering of H+ or due to direct loss of HCO3-

76
Q

What must be done to protect the pH in metabolic acidosis?

A

PCO2 must be decreased

77
Q

What are the causes of metabolic acidosis?

A

Increased H+ production, as in ketoacidosis or lactic acidosis
Failure to excrete normal dietary load of H+ as in renal failure
Loss of HCO3- as in diarrhoea i.e. failure to reabsorb intestinal HCO3-

78
Q

Metabolic acidosis stimulates ventilation so that

A

PCO2 falls

79
Q

In what way is ventilation increased in metabolic acidosis?

A

In depth rather than in rate - this may be very striking, reaching a maximum of 30 L/min (compared to the normal 5-6 L/min) when the arterial pH falls to 7.0

80
Q

What is Kussmaul breathing an established clinical sign of?

A

Renal failure or diabetic ketoacidosis

81
Q

How do the kidneys normally correct the disturbance caused by metabolic acidosis?

A

By restoring [HCO3-] and getting rid of H+ ions

82
Q

What is the source of H+ ions in metabolic acidosis?

A

The source of H+ ions is the carbonic acid from CO2, but the respiratory compensation lowers the PCO2 to protect the pH

83
Q

Compensations for acid/base disturbances are always in what direction?

A

Always in the same direction as the initial disturbance i.e. increased CO2 -> increased carbonic acid

84
Q

What would complete compensation remove?

A

The drive to correct the original disturbance

85
Q

What is the survival value of compensation?

A

If there was no pressure to correct the original disturbance, a further perturbation may push the system so far that the compensation can no longer be effective

86
Q

Why is the total amount o H+ secreted by the renal tubule in metabolic acidosis less than normal?

A

Because of the decrease in PCO2

87
Q

Why is a smaller fraction of total H+ needed for HCO3- reabsorption (and therefore a greater proportion is available for excretion) in metabolic acidosis?

A

Because the plasma [HCO3-] and the filtered load of [HCO3-] is reduced to an even greater extent

88
Q

What effect does decreased H+ secretion have on HCO3-?

A

HCO3- reabsorption greatly decreased

Increase in new HCO3- generated

89
Q

What effect does increased metabolic H+ within the body have?

A

Immediate buffering in the ECF and then ICF

Respiratory compensation within minutes

90
Q

Why does renal correction of metabolic acidosis take longer to develop the full response to increased H+ excretion and to generate new HCO3-?

A

Because renal glutaminase takes 4-5 days to reach maximum

91
Q

What does respiratory compensation delay?

A

Renal correction, but protects the pH which is more important

92
Q

What needs to happen in metabolic alkalosis to protect the pH?

A

[HCO3-] has to increase and PCO2 increase

93
Q

What are the causes of metabolic alkalosis?

A

Increased H+ ion loss e.g. vomiting, loss of gastric secretions
Increased renal H+ loss e.g. aldosterone excess, excess liquorice ingestion
Excess administration of HCO3- in patients with impaired renal function (unlikely to cause metabolic alkalosis in patients with normal renal function)
Massive blood transfusions, at least 8 units required to have this effect

94
Q

In metabolic alkalosis, the greatly increased filtered load of HCO3- exceeds what?

A

The level of H+ secretion to reabsorb it, even in the presence of increased PCO2

95
Q

For a given increase in PCO2, is there a smaller decrease in pH in chronic or acute respiratory acidosis?

A

Chronic respiratory acidosis

96
Q

How long does NH3 production take to be fully turned on?

A

4-5 days to be fully turned on, so initially [HCO3-] can only be raised by titratable acid

97
Q

When do acid/base disturbance not occur in isolation?

A

Acid/base disturbances do not occur in isolation in otherwise healthy individuals

98
Q

What should be considered in diabetic patients with ketoacidosis?

A

Badly controlled diabetes (metabolic acidosis)

99
Q

What kind of acid/base disturbance is likely in a patient who is a long-term smoker and has chronic bronchitis?

A

Respiratory acidosis

100
Q

What kind of acid/base disturbance is likely in a patient with a haemorrhage?

A

Lactic acidosis (combined metabolic and respirator acidosis)

101
Q

What does high acidity also cause, other than acidosis?

A

Hyperkalaemia as H+ ions are buffered intracellularly in exchange for K+ ions - danger of ventricular fibrillation

102
Q

What is the treatment of hyperkalaemia?

A

Insulin if diabetic, glucose if non-diabetic (stimulates cellular uptake of K+)

Calcium resonium either orally or rectally - exchanges Ca2+ ions for K+ ions

Ca gluconate (IV) - reduces excitability of the heart and stabilised the cardiac muscle membranes

103
Q

What effect does vomiting have on acid/base balance?

A

Loss of NaCl and H2O causes hypovolaemia
Loss of HCl causes metabolic alkalosis
Hypovolaemia stimulates aldosterone to increase distal tubule Na+ reabsorption
Respiratory compensation for metabolic alkalosis helps drive H+ secretion and exacerbates metabolic alkalosis by adding more HCO3- to the plasma

104
Q

Under conditions of avid Na+ reabsorption, what is the main ion exchanged for Na+?

A

H+

105
Q

What takes precedence over the correction of metabolic alkalosis following vomiting?

A

Restoration of volume

106
Q

What will giving a patient NaCl following vomiting achieve?

A

Restoration of volume, alkalosis will be corrected

107
Q

What happens to acid/base balance in vomiting and diarrhoea?

A

The patient becomes alkalotic despite acid and alkaline loss, because the decreased ECF volume causes an increase in aldosterone resulting in contraction alkalosis

108
Q

How does excess liquorice ingestion cause metabolic alkalosis?

A

It contains glycyrrhizic acid which is very similar to aldosterone - causes contraction alkalosis

109
Q

The anion gap is the difference between the sum of the principle cations (Na+ and K+) and the principle anions in the plasma (Cl- and HCO3-), what is the normal value of this?

A

14-18mmoles/l

110
Q

Why can it be useful to measure the anion hap in metabolic acidosis?

A

It can help determine the cause of 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
If the acidosis is due to e.g. 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 the anion gap
In lactic or diabetic acidosis, the reduction in bicarbonate is made up by other anions such as lactate, and so the anion gap is increased

111
Q

What is used to measure real plasma flow?

A

The organic anion para-amino-hippuric (PAH) acid

112
Q

How is PAH filtered?

A

Freely filtered at the glomerulus, and then PAH remaining in the plasma is actively secreted into the tubule
> 90% of plasma is cleared of its PAH content in one transit of the kidney

113
Q

What is PAH clearance a measurement of?

A

All the plasma flowing through the kidneys at a given time - renal plasma flow, 660ml/min

Urinary System (22 decks)

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