S5) Acid Base Balance Flashcards

1
Q

What is alkalaemia?

A

Alkalaemia is a plasma pH greater than 7.45

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2
Q

What is acidaemia?

A

Acidaemia is a plasma pH less than 7.35

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3
Q

Which conditions can arise from alkalaemia?

A
  • Paraesthesia
  • Tetany
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4
Q

Why does alkalaemia lead to paraesthesia and tetany?

A
  • Free calcium is lowered by causing Ca2+ to come out of solution
  • This increases neuronal excitability
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5
Q

Describe the mortality associated with alkalaemia

A
  • 45% mortality - pH rises to 7.55
  • 80% mortality - pH rises to 7.65
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6
Q

Describe the effect of acidaemia on excitability in the body

A
  • Increases plasma [K+]
  • Affects excitability (particularly cardiac muscle) which causes arrhythmias
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7
Q

Describe the effect of acidaemia on enzymes

A
  • Increasing [H+] affects many enzymes and denatures proteins
  • This affects muscle contractility, glycolysis, hepatic function
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8
Q

Describe the mortality associated with acidaemia

A
  • Severe effects – below pH 7.1
  • Life threatening – below pH 7.0
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9
Q

pCO2 is determined by respiration.

Identify the factors which disturb and control pCO2

A
  • Controlled by chemoreceptors
  • Disturbed by respiratory disease
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10
Q

[HCO3-] is determined by the kidneys.

Identify the factors which disturb and control [HCO3-]

A
  • Controlled by the kidney
  • Disturbed by metabolic and renal disease
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11
Q

Why does metabolic acid not deplete hydrogen carbonate?

A
  • The kidneys recover all filtered HCO3-
  • PCT makes HCO3- from AA, putting NH4+ into urine
  • DCT makes HCO3- from CO2 and H2O (H+ is buffered by phosphate and ammonia in the urine)
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12
Q

Describe the renal control of hydrogen carbonate

A
  • HCO3- filtered at the glomerulus & recovered in PCT
  • H+ excretion linked to Na+ entry in PCT
  • H+ reacts with HCO3- (lumen) to form CO2 which enters cell and is converted back to HCO3- which enters ECF
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13
Q

Describe the role of glutamine in the creation of hydrogen carbonate in th PCT

A
  • Glutamine breaks down and forms α-ketoglutarate
  • HCO3- and ammonium are produced
  • HCO3- enters ECF and NH4+ enters lumen (urine)
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14
Q

Describe the renal control of hydrogen carbonate in the distal tubule and collecting duct

A
  • DCT and CD also actively secrete H+
  • H+ buffered by ammonia and phosphate to produce NH4+ and H2PO4- which are excreted
  • HCO3- now can enter plasma
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15
Q

Excretion of ammonium is the major adaptive response to an increased acid load.

Describe the role of ammonium in the renal control of HCO3-

A

NH4+ ⇒ NH3 + H+

  • NH3 freely moves into lumen and throughout interstitium
  • H+ actively pumped into lumen in DCT and CT
  • H+ combines with NH3 to form NH4+ (trapped in lumen)
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16
Q

What is the pH of urine?

A

The minimum pH of urine is 4.5

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17
Q

How much acid is secreted per day and why?

A
  • Total acid excretion = 50 – 100mmol H+ per day
  • Needed to keep normal [HCO3-]
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18
Q

Explain how acidosis leads to hyperkalaemia

A
  • K+ move out of cells
  • Decreased K+ excretion in distal nephron
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19
Q

Explain how alkalosis leads to hypokalaemia

A
  • K+ move into cells
  • Enhanced excretion of K+ in distal nephron
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20
Q

Explain how hyperkalaemia can lead to metabolic acidosis

A
  • Hyperkalaemia makes pHi of tubular cells more alkaline
  • H+ move out of the cells which favours HCO3- excretion
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21
Q

Explain how hypokalaemia can lead to metabolic alkalosis

A
  • Hypokalaemia makes pHi of tubular cells more acidic
  • H+ move into the cells which favours H+ excretion and HCO3- recovery
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22
Q

How does hypoventilation lead to respiratory acidosis (acidaemia)?

A
  • Hypoventilation → hypercapnia (pCO2 rises)
  • Hypercapnia → fall in plasma pH
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23
Q

Identify 3 factors which characterise respiratory acidosis

A
  • High pCO2
  • Normal HCO3-
  • Low pH
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24
Q

How does hyperventilation lead to respiratory alkalosis (alkalaemia)?

A
  • Hyperventilation → hypocapnia (fall in pCO2)
  • Hypocapnia → rise in pH
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25
Q

Identify 3 factors which characterise respiratory alkalosis

A
  • Low pCO2
  • Normal HCO3-
  • Raised pH
26
Q

How do kidneys compensate for respiratory acidosis?

A

The kidneys increase [HCO3-] to compensate for respiratory acidosis

27
Q

How do kidneys compensate for respiratory alkalosis?

A

The kidneys decrease [HCO3-] to compensate for respiratory alkalosis

28
Q

Identify 3 factors which characterise compensated respiratory acidosis

A
  • High pCO2
  • Raised [HCO3-]
  • Relatively normal pH
29
Q

Identify 3 factors which characterise compensated respiratory alkalosis

A
  • Low pCO2
  • Lowered [HCO3-]
  • Relatively normal pH
30
Q

What is the anion gap?

A

The anion gap is the difference between measured cations and anions

([Na+] + [K+]) – ([Cl-] + [HCO3-])

31
Q

What is the normal value for the anion gap and why?

A

Normally 10 – 18 mmol.l-1 due to other anions that are not measured

32
Q

How can the anion gap be increased?

A

Increased if HCO3- is replaced by other anions:

E.g. If a metabolic acid (such as lactic acid) reacts with HCO3- the anion of the acid replaces HCO3-

33
Q

In renal causes of acidosis, the anion gap will be unchanged.

Why?

A

Not making enough HCO3- but this is replaced by Cl-

34
Q

In terms of the anion gap, identify 2 factors which characterise metabolic acidosis

A
  • Increased anion gap if HCO3- is replaced by another organic anion from an acid
  • Normal anion gap if HCO3- replaced by Cl-
35
Q

Explain how carotid bodies compensate for metabolic acidosis

A
  • Peripheral chemoreceptor (carotid bodies) detect pH drop
  • Ventilation is stimulated which leads to a decrease in pCO2
36
Q

Identify 3 factors which characterise compensated metabolic acidosis

A
  • Low HCO3-
  • Lowered pCO2
  • Nearer normal pH
37
Q

What is observed in Type II Respiratory Failure?

A
  • Low pO2 and high pCO2
  • Alveoli cannot be properly ventilated
38
Q

Identify 4 clinical conditions in Type II respiratory failure which lead to respiratory acidosis

A
  • Severe COPD
  • Severe asthma
  • Drug overdose
  • Neuromuscular disease
39
Q

How can respiratory acidosis be compensated for?

A

Increase [HCO3-]

40
Q

What is observed in Type I Respiratory Failure (hyperventilation in response to long term hypoxia)?

A

Low pCO2 with initial rise in pH

41
Q

Identify 2 clinical conditions in Type I respiratory failure which cause respiratory alkalosis

A
  • Chronic hyperventilation
  • Anxiety/panic attacks
42
Q

How can respiratory alkalosis be compensated for?

A

Decrease [HCO3-]

43
Q

Identify and describe 3 clinical conditions which can cause metabolic acidosis

A
  • Keto-acidosis: seen in diabetes
  • Lactic acidosis: exercising to exhaustion leading to poor tissue perfusion
  • Uraemic acidosis: advanced renal failure leading to reduced acid secretion & build up of plasma phosphate, sulphate, urate
44
Q

Identify 2 clinical conditions which lead to metabolic acidosis with a normal anion gap

A
  • Renal tubular acidosis
  • Severe persistent diarrhoea
45
Q

Renal tubular acidosis involves problems with transport mechanisms in the tubules.

Identify and describe its 2 forms

A
  • Type 1 RTA (distal) involves the inability to pump out H+
  • Type 2 RTA (proximal) involves problems with HCO3- reabsorption
46
Q

Identify 3 clinical states which lead to metabolic alkalosis

A
  • Severe prolonged vomiting (loss of H+ from stomach)
  • Potassium depletion
  • Mineralocorticoid excess
47
Q

Certain diuretics can also cause metabolic alkalosis.

Identify 2

A
  • Loop diuretic
  • Thiazide diuretic
48
Q

What process is occuring in the following:

Abnormal pCO2, normal [HCO3-] and pH has changed in opposite direction to pCO2

A

Respiratory acidosis / alkalosis

49
Q

What process is occurring in the following:

Abnormal [HCO3-], normal pCO2 and pH has changed in the same direction as [HCO3-]

A

Metabolic acidosis / alkalosis

50
Q

What process is occurring in the following:

High pCO2, raised [HCO3-] and pH is relatively normal

A

Compensated respiratory acidosis

51
Q

What process is occurring in the following:

Low [HCO3-], low pCO2 and pH is relatively normal

A

Compensated respiratory alkalosis / compensated metabolic acidosis (check anion gap)

52
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.22 (7.35 - 7.45)
  • pCO2 = 8.1 (4.7 - 6.0)
  • HCO3- = 24 (22 - 26)
  • pO2 = 8.9 (9.3 - 13.3)
A

Uncompensated respiratory acidosis

53
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.22 (7.35 - 7.45)
  • pCO2 = 4.5 (4.7 - 6.0)
  • HCO3- = 13 (22 - 26)
  • pO2 = 12.4 (9.3 - 13.3)
A

Partially compensated metabolic acidosis

54
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.46 (7.35 - 7.45)
  • pCO2 = 3.3 (4.7 - 6.0)
  • HCO3- = 17 (22 - 26)
  • pO2 = 13.3 (9.3 - 13.3)
A

Partially compensated respiratory alkalosis

55
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.22 (7.35 - 7.45)
  • pCO2 = 4.8 (4.7 - 6.0)
  • HCO3- = 14 (22 - 26)
  • pO2 = 11.8 (9.3 - 13.3)
A

Uncompensated metabolic acidosis

56
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.28 (7.35 - 7.45)
  • pCO2 = 8.6 (4.7 - 6.0)
  • HCO3- = 30 (22 - 26)
  • pO2 = 8.6 (9.3 - 13.3)
A

Partially compensated respiratory acidosis

57
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.46 (7.35 - 7.45)
  • pCO2 = 5.6 (4.7 - 6.0)
  • HCO3- = 29 (22 - 26)
  • pO2 = 10.1 (9.3 - 13.3)
A

Uncompensated metabolic alkalosis

58
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.35 (7.35 - 7.45)
  • pCO2 = 7 (4.7 - 6.0)
  • HCO3- = 28 (22 - 26)
  • pO2 = 8.6 (9.3 - 13.3)
A

Fully compensated respiratory acidosis

59
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.35 (7.35 - 7.45)
  • pCO2 = 4.1 (4.7 - 6.0)
  • HCO3- = 17 (22 - 26)
  • pO2 = 13.0 (9.3 - 13.3)
A

Fully compensated metabolic acidosis

60
Q

Describe the form of acidosis/alkalosis happening in the patient:

  • pH = 7.5 (7.35 - 7.45)
  • pCO2 = 4.5 (4.7 - 6.0)
  • HCO3- = 26 (22 - 26)
  • pO2 = 13.0 (9.3 - 13.3)
A

Uncompensated respiratory alkalosis