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11. Urinary > 6. Control of Acid Base and Potassium Concentration > Flashcards

6. Control of Acid Base and Potassium Concentration Flashcards

1
Q

What is the normal range of plasma pH?

A

7.38-7.46

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2
Q

What is the normal range of plasma [H+]?

A

37-43mmol/L

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3
Q

Where are the results of acidaemia severe?

A

When pH drops below 7.1

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4
Q

When are the results of acidaemia life threatening?

A

When pH drops below 7.0

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5
Q

What are the results of acidaemia?

A

Reduced enzyme function, reduced cardiac and skeletal muscle contractility, reduced glycolysis, reduced hepatic function, increased plasma potassium.

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6
Q

What is the effect of alkalaemia?

A

Reduced solubility of calcium salts, free Ca2+ leaves the ECF, binding to bone and proteins, so hypocalcaemia and increased excitability of nerves.

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7
Q

What happens with pH >7.45?

A

Paresthesia, and tetany - uncontrolled muscle contractions.

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8
Q

What is the mortality risk with pH > 7.55?

A

45%

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9
Q

What is the mortality risk with pH > 7.65?

A

80%

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10
Q

How are major changes in pH from small [H+] changes prevented?

A

With buffering of H+ ions.

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11
Q

What is the important buffering system of H+?

A

Carbon dioxide/ hydrogen carbonate system.

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12
Q

What determines the extent of the H+ reaction with CO2 in buffering?

A

The ratio of pCO2 of the plasma to [HCO3-].

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13
Q

What organ controls pCO2 of the plasma?

A

The lungs.

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14
Q

What organ controls [HCO3-] of the plasma?

A

The kidneys.

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15
Q

What is the normal ratio of pCO2:[HCO3-]?

A

20:1.

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16
Q

How can pH be calculated from pCO2 and [HCO3-]?

A

pH = 6.1 + log ([HCO3-]/(pCO2 x 0.23)).

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17
Q

What is the mechanism of respiratory alkalaemia?

A

Hyperventilation leads to hypocapnia so the ratio is altered, more H+ is buffered, and pH rises.

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18
Q

What is the mechanism of respiratory acidaemia?

A

Hypoventilation leads to hypercapnia so the ratio is altered, less H+ are buffered, and the pH decreases.

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19
Q

Generally, how is respiratory acidaemia or alkalaemia compensated for?

A

Changes in [HCO3-] by the kidney from variable excretion and production.

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20
Q

How is respiratory acidaemia compensated for?

A

If pCO2 rises, [HCO3-] rises proportionally to restore pH as the kidneys excrete less and produce more.

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21
Q

How is respiratory alkalaemia compensated for?

A

If pCO2 falls, [HCO3-] falls proportionally to restore pH as the kidneys excrete more and produce less.

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22
Q

What is the mechanism behind metabolic acidosis?

A

Metabolically produced H+ ions react with HCO3- to make CO2 in the venous blood. The CO2 is breathed out through the lungs and there is a proportional reduction of [HCO3-]. This alters the ratio, less H+ is buffered, and pH decreases.

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23
Q

What is the mechanism behind metabolic alkalosis?

A

If plasma [HCO3-] rises, e.g. from persistent vomiting, the ratio will be faltered, relatively more H+ is buffered, and pH increases.

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24
Q

What can cause a metabolic increase in [HCO3-]?

A

Persistent vomiting.

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25
Q

Generally, how is metabolic acidosis or alkalosis compensated for?

A

pCO2 is altered by the lungs to balance the ratio and restore pH. Changes in plasma pH drive changes in pCO2 by the peripheral chemoreceptors.

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26
Q

How is metabolic acidosis compensated for?

A

If [HCO3-] falls, pCO2 is lowered proportionally by increasing ventilation.

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27
Q

How is metabolic alkalosis partially compensated for?

A

If [HCO3-] rises, pCO2 is slightly raised by reducing ventilation to a point.

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28
Q

What will the following arterial blood gas results be for respiratory acidaemia: pH, pCO2, [HCO3-], pO2?

A

pH low, pCO2 high, [HCO3-] normal, pO2 low.

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29
Q

What will the following arterial blood gas results be for partially/fully compensated respiratory acidaemia: pH, pCO2, [HCO3-], pO2?

A

pH low or normal, pCO2 high, [HCO3-] high, pO2 low.

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30
Q

What will the following arterial blood gas results be for respiratory alkalaemia: pH, pCO2, [HCO3-], pO2?

A

pH high, pCO2 low, [HCO3-] normal, pO2 normal or high.

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31
Q

What will the following arterial blood gas results be for partially/fully compensated respiratory alkalaemia: pH, pCO2, [HCO3-], pO2?

A

pH high or normal, pCO2 low, [HCO3-] low, pO2 high.

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32
Q

What will the following arterial blood gas results be for metabolic acidosis: pH, pCO2, [HCO3-], pO2, anion gap?

A

pH low, pCO2 normal, [HCO3-] low, pO2 normal, anion gap high.

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33
Q

What will the following arterial blood gas results be for partially/fully compensated metabolic acidosis: pH, pCO2, [HCO3-], pO2, anion gap?

A

pH low or normal, pCO2 low, [HCO3-] low, pO2 high or normal, anion gap high.

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34
Q

What will the following arterial blood gas results be for metabolic alkalosis: pH, pCO2, [HCO3-], pO2?

A

pH high, pCO2 normal, [HCO3-] high, pO2 normal.

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35
Q

What will the following arterial blood gas results be for partially/fully compensated alkalosis: pH, pCO2, [HCO3-], pO2?

A

pH high or normal, pCO2 high, [HCO3-] high, pO2 low or normal.

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36
Q

Where is a large fraction of HCO3- reabsorbed?

A

In the proximal convoluted tubule.

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37
Q

How is HCO3- reabsorbed in the PCT?

A

3Na2KATPase sets up a Na+ concentration gradient in PCT cells, H+ ions are pumped out of the apical membrane up their concentration gradient in exchange for the inward movement of Na+ down its concentration gradient. The H+ reacts with the filtered HCO3- to produce CO2 which enters the cell and reacts with water to produce H+ ions. The H+ is exported, recreating HCO3-, which crosses the basolateral membrane to enter the plasma.

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38
Q

Where is filtered HCO3- reabsorbed in the kidney?

A

80-90% in the PCT, up to 15% in the thick ascending limb of the loop of Henle.

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39
Q

How is H+ excreted in the distal convoluted tubule?

A

H+ is pumped across the apical membrane by H+-ATPase.

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40
Q

Why does H+ need to be actively transported in excretion in the distal convoluted tubule?

A

Because most HCO3- as been recovered and the Na+ gradient is insufficient to drive H+ secretion.

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41
Q

What happens to K+ when H+ is exported in the distal convoluted tubule?

A

K+ is absorbed into the blood.

42
Q

How is blood pH linked to K+?

A

As H+ is exported, K+ is absorbed in the blood. So lots of H+ exported, means lots of K+ absorbed.

43
Q

What is the minimum pH of the urine?

A

4.5

44
Q

How is H+ buffered in the urine?

A

There is no HCO3-, so instead it is buffered by phosphate. The rest of H+ in the urine is attached to ammonia as ammonium.

45
Q

What is meant by phosphate being a titratable acid?

A

It can freely gain H+ ions in an acid/base reaction.

46
Q

What K+ level is metabolic acidosis associated with?

A

Hyperkalaemia.

47
Q

Why is metabolic acidosis associated with hyperkalaemia?

A

As [K+] rises, the kidney’s ability to reabsorb and create HCO3- is reduced. Hyperkalaemia makes intracellular pH alkaline, favouring HCO3- excretion.

48
Q

How is metabolic alkalosis associated with hypokalaemia?

A

Hypokalaemia makes intracellular pH acidic so favours H+ excretion and HCO3- recovery.

49
Q

Why does [HCO3-] increase after persistent vomiting?

A

The kidneys try to compensate for the dehydration, so can’t excrete HCO3-. This means HCO3- and Na+ recovery is favoured to increase osmolarity of the plasma to increase movement of water in.

50
Q

How does the body respond to [HCO3-] increases after persistent vomiting?

A

It stops actively secreting H+, as this would worsen metabolic alkalosis.

51
Q

What is the effect of H+ stopping secretion on K+ reabsorption?

A

It stops K+ reabsorption.

52
Q

When does metabolic acidosis occur?

A

If there is excess metabolic production of acids, acids are ingested, HCO3- is lost, or there is a problem with the renal excretion of acid.

53
Q

What is the anion gap?

A

The difference between the sum of the measured concentrations of Na+ and K+ and the sum of the measured concentrations of Cl- and HCO3-.

54
Q

When does the anion gap increase?

A

When HCP3- is replaced in the plasma by another anion not included in the calculation, e.g. with excess acid production.

55
Q

Why does metabolic acidosis from renal excretion of H+ not result in an anion gap change?

A

The [HCO3-] is changed directly without replacement by an unmeasured ion, so the gap doesn’t change.

56
Q

What is the plasma [K+] range?

A

3.5-5.3mmol/L

57
Q

Why is high [K+] inside the cell essential?

A

Maintains cell volume, regulated intracellular pH, controls cell-enzyme function, DNA/protein synthesis, cell growth.

58
Q

Why is low [K+] outside the cell necessary?

A

To maintain the steep K+ ion gradient responsible for the membrane potential of excitable and non-excitable cells.

59
Q

How does increased ECF [K+] affect the cell membrane?

A

It depolarises the cell membrane.

60
Q

How does reduced ECF [K+] affect the cell membrane.

A

It hyperpolarises the cell membrane.

61
Q

What metabolic disturbance result from extremely low extracellular [K+]?

A

Inability of the kidney to form concentrated urine, a tendency to develop metabolic alkalosis, large enhancement of renal ammonium excretion.

62
Q

What homeostatic mechanism keep the ECF [K+] tightly controlled?

A

External and internal balance.

63
Q

Which cells secrete K+ in the DCT and collecting duct?

A

Principal cells.

64
Q

How is K+ secretion powered in the DCT and collecting duct?

A

It is a passive process driven by the electro-chemical gradient for K+ between the principal cell and the lumen.

65
Q

Through which channel is Na+ reabsorbed in the DCT and collecting duct?

A

ENaC.

66
Q

What tubular factors affect K+ secretion by principal cell?

A

Aldosterone, ECF [K+], acid base status.

67
Q

Which luminal factors affect K+ secretion by principal cells?

A

Increased distal tubular flow rate means more K+ loss, increased Na+ delivery to distal tubule means more K+ loss.

68
Q

How does aldosterone affect the channels in the basolateral and apical membranes?

A

Basolateral - increased transcription of Na-K-ATPase.

Apical - increases transcription of ENaC and K+ channels.

69
Q

What is the overall result of aldosterone on K+ excretion?

A

Increases it.

70
Q

How does [K+] affect aldosterone secretion?

A

Increased K+ stimulates aldosterone secretion.

71
Q

How does acidaemia affect secretion of K+?

A

It decreases [K+] in principal cells and therefore decreases secretion.

72
Q

How does alkalaemia affect secretion of K+?

A

It increased [K+] in principal cells and therefore increases secretion.

73
Q

How is K+ absorbed in the DCT and collecting duct via intercalated cells?

A

In an active process that is mediated by H+-K+-ATPase in the apical membrane.

74
Q

What is the external balance of K+?

A

It regulates the total body K+ content which depends on dietary intake and excretion. It controls K+ long-term by varying excretion.

75
Q

What is the internal balance of K+?

A

It regulates K+ movement between ECF and ICF in moment to moment control.

76
Q

How does internal balance respond to increased ECF/plasma [K+]?

A

Need to move K+ into ICF so more Na-K-ATPase active.

77
Q

How does internal balance response to decreased ECF/plasma [K+]?

A

Need to move K+ into ECF so more K+ channels active.

78
Q

How does insulin cause K+ to move intracellularly?

A

K+ in splanchnic blood stimulates insulin secretion from the pancreas. Insulin increases the amount of Na-K-ATPase so there is uptake of K+.

79
Q

How do catecholamines (B2 agonists) cause K+ to move intracellularly?

A

B2 adrenoceptors stimulate Na-K-ATPase. Exercise and trauma increases K+ exit from the cells and increased catecholamine help offset ECF [K+] rise.

80
Q

How does aldosterone cause K+ to move intracellularly?

A

It is a steroid hormone that increases transcription of Na-K-ATPase in the basolateral membrane and ENaC/K+ channels in the apical membrane. This gives increased K+ excretion.

81
Q

How does exercise cause K+ to move extracellularly?

A

Skeletal muscle contraction releases K+, the increase is proportional to the intensity of the exercise. Uptake of K+ by non-contracting tissues prevents hyperkalaemia.

82
Q

How does cell lysis cause K+ to move extracellularly?

A

K+ is released from the ICF to the ECF in cell lysis.

83
Q

What can cause cell lysis?

A

Trauma to skeletal muscle, intravascular haemolysis, and cancer chemotherapy.

84
Q

How does plasma hyperosmolarity cause K+ to move extracellularly?

A

Increased plasma osmolarity causes water to move from ICF to ECF by osmosis. [K+] increases in ICF and then K+ moves down gradient.

85
Q

How does hypokalaemia affect cardiac cells?

A

It hyperpolarises them so more fast Na+ channels are available in active form and the heart is more excitable.

86
Q

How does hyperkalaemia affect cardiac cells?

A

It depolarises them as more fast Na+ channels stay inactive and the heart is less excitable.

87
Q

What are the external balance problems that cause hypokalaemia?

A

Inadequate intake, excessive loss - diarrhoea/ vomiting, diuretic drugs/ osmotic diuresis, high aldosterone.

88
Q

What are the internal balance problems that cause hypokalaemia?

A

Shift of potassium ECF -> ICF from alkalosis.

89
Q

What are the GI clinical features of hypokalaemia?

A

Neuromuscular dysfunction so paralytic ileus.

90
Q

What are the skeletal muscle clinical features of hypokalemia?

A

Neuromuscular dysfunction so muscle weakness.

91
Q

What are the renal clinical features of hypokalaemia?

A

Dysfunction of collecting duct cells so unresponsive to ADH and nephrogenic diabetes.

92
Q

How is hypokalaemia treated?

A

Treat cause, K+ replacement either IV or oral, if from high aldosterone - K+ sparing diuretics (block aldosterone), K+ sparing (amiloride), and aldosterone antagonists (spironolactone).

93
Q

What are the ECG changes of hypokalaemia?

A

ST depression, shallow T wave, and prominent U wave.

94
Q

What are the external balance problems causing hyperkalaemia?

A

Inadequate renal excretion, acute kidney injury, chronic kidney injury, reduced mineralocorticoid effect (drugs which reduce aldosterone action, adrenal insufficiency).

95
Q

What are the internal balance problems causing hyperkalamia?

A

Shifts of K+ from ICF -> ECF from acidaemia and cell lysis.

96
Q

What are the GI clinical features of hyperkalaemia?

A

Neuromuscular dysfunction so paralytic ileus.

97
Q

What are the ECG changes with serum [K+] of 6.5-7mmol/L?

A

Tall, peaked T waves.

98
Q

What are the ECG changes with serum [K+] of 8mmol/L?

A

Prolonged PR interval, tall T waves, ST segment depression.

99
Q

What are the ECF changes with serum [K+] of 9mmol/L?

A

Widened QRS interval.

100
Q

What are the ECF changes with serum [K+] of 10mmol/L?

A

Ventricular fibrillation.

101
Q

What are the emergency treatments of hyperkalaemia?

A

Reduce K+ effect on heart with IV calcium gluconate, shift K+ into ICF via IV glucose and insulin, dialysis.

102
Q

What are the longer term treatments of hyperkalaemia?

A

Remove excess K+ wit dialysis or oral K+ binding resins to bind K+ in the gut, reduce intake, and treat cause.

11. Urinary (12 decks)

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