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RENAL PHYSIOLOGY > Acid Base Balance > Flashcards

Acid Base Balance Flashcards

1
Q

Why is ECF pH regulation so important?

A

H+ is very reactive, changes in pH cause changes in metabolic reactions

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2
Q

What is the normal blood pH?

A

7.4

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3
Q

Which ions contribute to pH?

A

FREE H+

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4
Q

What is the typical concentration of free H+?

A

40x10^-9

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5
Q

What are the sources of acid?

A

Respiratory Acid Metabolic acid

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6
Q

How is respiratory acid produced?

A

CO2 + H2O = H2CO3 = H+ + HCO3-

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7
Q

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

A

Usually ↑acid = ↑ventilation

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8
Q

What are the sources of metabolic acid?

A

Inorganic acids Organic acids

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9
Q

What are the sources of inorganic acids?

A

S-containing amino acids (H2SO4) Phospholipids (Phosphoric acids)

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10
Q

What are the sources of organic acids?

A

Fatty acids Lactic acids

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11
Q

What is the normal daily net gain of acid?

A

50-100mmoles H+/day

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12
Q

What is the source of alkali?

A

Oxidation of organic anions i.e citrate

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13
Q

Carbonic acid dissociates into what?

A

H+ + HCO3-

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14
Q

What is the role of buffers?

A

Minimise pH changes when H+ ions are removed

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15
Q

What is the Henderson-Hasselbalch equation?

A

pH defined in ratio of acid to base pH = pK + log([A-]/[HA])

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16
Q

What is the most important extracellular buffer?

A

Bicarbonate buffer system

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17
Q

What is the pK of bicarbonate?

A

6.1

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18
Q

What is the ratio of bicarbonate to carbonic acid in normal blood pH?

A

20:1

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19
Q

The quantity of H2CO3 depends on what?

A

CO2 in plasma Solubility/partial pressure of CO2

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20
Q

What is the normal [HCO3-] in man?

A

24mmoles/L (22-26)

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21
Q

What is the normal pCO2 in man?

A

40mmHg (36-44)

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22
Q

Why does the increased levels of H2O and CO2 due to carbonic acid dissociation not cause equilibrium and increased H+?

A

The CO2 is exhaled

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23
Q

What is the net effect of respiratory compensation of increased acid?

A

The dissociation is driven to the right and more able to act as a buffer

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24
Q

Decreased [H+] will lead to what?

A

Decreased ventilation, increased CO2

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25
Q

[HCO3-] is regulated where?

A

Renal system

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26
Q

PCO2 is regulated where?

A

Respiratory system

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27
Q

What are the ECF buffers?

A

HCO3- Plasma proteins Dibasic phosphate

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28
Q

How do plasma proteins buffer acid?

A

Pr- + H+ = HPr

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29
Q

How does Dibasic phosphate buffer acid?

A

HPO42- + H+ « H2PO4- (monobasic phosphate)

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30
Q

What are the primary intracellular buffers?

A

Proteins

Organic/inorganic phosphates

Haemoglobin

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31
Q

How is movement of H+ kept electrochemically neutral?

A

Exchange for K+

Or

Accompany with Cl-

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32
Q

How does acidosis cause ventricular fibrillation?

A

Movement of K+ out of cells causes Hyperkalemia

Depolarisation of excitable dissues –> VFib

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33
Q

Where is the additional store of acid buffer?

A

Bone

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34
Q

How does chronic renal failure lead to bone wasting?

A

The additional store of carbonate (bones) is broken down to free it

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35
Q

Acidosis leads to what change in the blood?

A

Hyperkalemia

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36
Q

Where is metabolic acid buffered?

A

43% in plasma

57% in cells

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37
Q

Where is respiratory acid buffered?

A

97% in cells (Hb and plasma proteins)

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38
Q

How does the kidney regulate [HCO3-]?

A

Reabsorption of HCO3-

Generation of new HCO3-

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39
Q

Where is new HCO3- generated?

A

Kidneys

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40
Q

Secretion of H+ from tubule cells is coupled with what?

A

Passive Na+ reabsorption

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41
Q

What is the mechanism for HCO3- reabsorption?

A

H+ filtered out (Na+ reabsorbed)

H+ and HCO3- forms H2O + CO2 in presence of carbionic anhydrase on luminal membrane

CO2 taken up and form back into H+ and HCO3- in presence of carbionic anhydrase

HCO3- passes back into the peritubular capillaries with Na+

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42
Q

What enzyme assists with HCO3- dissociation?

A

Carbonic anhydrase

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43
Q

What is the source of secreted H+?

A

H+ released by the dissociation of H2CO3

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44
Q

Where does the bulk of HCO3- reabsorption take place?

A

Proximal tubule (>90%)

45
Q

Where is carbonic anhydrase located?

A

All tubule cells

Luminal membrane of tubule

46
Q

How much H+ is excreted in HCO3- reabsorption?

A

None

47
Q

What would be the result of failure to reabsorb intestinal bicarbonate?

A

Metabolic Acidosis

48
Q

What are the minimum and maximum pH of urine in humans?

A

4.5-5 (minimum)

8 (maximum)

49
Q

What are the acid buffers in urine?

A

Dibasic phosphate

Uric acid

Creatinine

50
Q

What is titratable acidity?

A

The amount of NaOH needed to titrate urine pH back to 7.4 for a 24hr urine sample

51
Q

What is the indirect source of new HCO3-?

A

CO2 in blood

52
Q

How does blood CO2 form new HCO3-?

A

CO2 enters tubule cells, combines with H2O = carbonic acid

This yields H+ and (new) HCO3-

Passes into capillaries with Na+

(in presence of carbonic anhydrase)

53
Q

Formation of new HCO3- takes place where? Why?

A

Distal tubule

Phosphate ions become highly concentrated here (exhausted Tm mechanism)

54
Q

What is the fate of produced when the distal tubule produces HCO3-?

A

Exchanged for Na+ (Na2HPO4)

Bound to phosphate (HPO42-)

Excreted as H2PO4-

55
Q

What is the source of CO2 for production of new bicarbonate?

A

Blood (dependent on PCO2)

56
Q

Why is [PO4] high in the distal tubule?

A

Because what isnt absorbed in the proximal tubule is concentrated in the loop of Henle

57
Q

What is the purpose of ammonium excretion?

A

Adaptive response to acid loads

Generated HCO3- and H+

58
Q

What is the solubility of ammonia?

A

Lipid soluble

59
Q

Why is Ammonium used for responding to acid loads?

A

Because Ammonium is NOT lipid soluble

60
Q

Where is ammonia produced in the body?

A

Deamination of amino acids - glutamine

61
Q

How is Ammonia produced?

A

Deamination of glutamine by renal glutaminase within renal tubule cells

62
Q

What is the mechanism of H+ secretion via ammonium?

A

NH3 passes into tubule

Combines with H+ to form NH4+

NH4+ + Cl- = NH4Cl

NH4Cl is excreted

63
Q

What is the source of secreted CO2 in ammonium excretion?

A

CO2 from the blood (reforms H+ and HCO3-)

64
Q

How does ammonium enter the proximal tubule?

A

Presence of NH4+/Na+ exchangers in the proximal tubule

65
Q

Glutamine reductase acting on glutamine forms what?

A

Glutamate

66
Q

How does ammonium enter the tubule in the distal tubule?

A

Passive flow of lipid soluble NH3 into the tubule

67
Q

Where is the ammonium/sodium antitransporter located?

A

Brush border membrane of the proximal tubule

68
Q

Renal glutaminase is dependent on what?

A

pH

pH↓ = ↑glutaminase activity

Leading to greated NH4+ excretion

69
Q

How long does it take for the kidney to respond to increased acid loads by ammonium excretion? Why?

A

4-5 days

Slow rate of increased protein (glutamine) synthesis

70
Q

How much H+ is lost per day via ammonium excretion?

A

30-50mmoles

(up to 250 in severe acidosis)

71
Q

What are the main mechanisms of renal H+ excretion?

A

Ammonium

Phosphate

Bicarbonate

72
Q

What are the causes of acute respiratory acidosis?

A

Obstruction of airways

Drugs which depress medullary centres
(Barbiturates, opiates)

73
Q

What are the causes of chronic respiratory acidosis?

A

Chronic lung disease:
Bronchitis, emphysema, asthma

74
Q

What change in [HCO3-] is seen in chronic respiratory acidosis?

A

Increased bicarbonate

75
Q

Renal compensation only serves to correct what?

A

pH level of blood - not the disturbance

76
Q

What are the causes of acute respiratory alkalosis?

A

Hyperventilation

Aspirin

First ascent to altitude

77
Q

What are the cause of chronic respiratory alkalosis?

A

Long term high altitude

PO2 <60mmHg

78
Q

How does bicarbonate respond to high pH?

A

Decreased [HCO3-]

79
Q

What is the net effect in urine in a ↓PCO2?

A

Less HCO3- reabsorption, leading to HCO3- excretion

80
Q

What is metabolic acidosis?

A

Decreased [HCO3-]

81
Q

What are the causes of metabolic acidosis?

A

Increased H+ production: Diabetic ketoacidosis, lactic acidosis

Failure to excrete normal dietary load of H+ in renal failure

Loss of HCO3- in diarrhoea

82
Q

Increased ventilation due to metabolic acidosis presents how?

A

Kussmaul breathing

83
Q

Kussmaul breathing is a sign of what?

A

Arterial pH <7

Renal failure

Diabetic ketoacidosis

84
Q

How is blood pH defined?

A

[HCO3-]/PCO2

85
Q

What are the responses to increased metabolic H+ in the body?

A

Immediate: ECF/ICF buffering

Minutes: Respiratory compensation

Hours/days: Generation of HCO3-, stimulation of renal glutaminase

86
Q

What is metabolic alkalosis?

A

↑[HCO3-] causing increased PCO2 to protect the pH

87
Q

What are the causes of metabolic alkalosis?

A

H+ loss due to vomiting

Renal H+ due to aldosterone excess, liquorice

Excess HCO3- administration in impaired renal function

Massive blood transfusions (8+ units)

88
Q

How do massive blood transfusions lead to metabolic alkalosis?

A

Blood banks add citrate to prevent coagulation - converted to HCO3-

89
Q

How does excess HCO3- lead to alkalosis?

A

Filtered load of HCO3- exceeds secreted H+ needed to reabsorb it

90
Q

How does respiratory compensation cause a delay in renal correction of metabolic acidosis?

A

In order to protect pH, ventilation decreases to blow off less CO2 and increase acidity

But blowing off CO2 means the kidney can’t use the H+ to reabsorb the excess HCO3-

91
Q

What is the primary disturbance in respiratory acidosis?

A

Increased PCO2

92
Q

What is the primary disturbance in respiratory alkalosis?

A

Decreased PCO2

93
Q

What is the primary disturbance in metabolic acidosis?

A

Decreased [HCO3-]

94
Q

What is the primary disturbance in metabolic alkalosis?

A

Increased [HCO3-]

95
Q

An increase in pH is caused by what?

A

Increased HCO3-

Or

Decreased PCO2

96
Q

A decrease in pH is caused by what?

A

Decreased HCO3-

Or

Increased PCO2

97
Q

How do pH changes relative to PCO2 differ in chronic vs acute respiratory acidosis?

A

Chronic acidosis - increase in PCO2 has a smaller decrease in pH

Acute acidosis - increase in PCO2 has a larger decrease in pH

98
Q

Why do PCO2 changes cause smaller changes in blood pH in chronic acidosis?

A

Because after 4-5 days, NH3 production will have increased and is able to act as a buffer

99
Q

How does haemorrhage cause lactic acidosis?

A

Loss of blood = ↓perfusion of tissues = ↓Aerobic respiration = Lactic acid production

100
Q

How does severe acidosis lead to kyperkalemia?

A

H+ ions are buffered intracellularly in exchange for K+ ions

101
Q

How would a patient in severe acidosis leading to hyperkalemia be treated?

A

Insulin (uptake of K+)

Calcium resonium (exchange Ca2+ for K+)

Ca gluconate (decrease heart excitability)

102
Q

When managing severe acidosis, what levels should be monitored?

A

ph, HCO3-, etc

POTASSIUM (risk of hypokalemia)

103
Q

How would severe vomiting affect acid/base levels?

A

Loss of NaCl/H2O –> hypovolaemia

Loss of HCl –> metabolic alkalosis

104
Q

How would vomiting causing hypovolaemia worsen the metabolic alkalosis?

A

Hypovolemia would stimulate aldosterone production

Aldosterone would cause distal tubule exchange of Na+ for H+, leading to further loss of H+

Additional loss of K+

105
Q

How does excess liquorice affect the acid/base balance?

A

Contains glycyrrhizic acid, acts like aldosterone

Causes more H+ secretion leading to metabolic alkalosis

106
Q

What is the anion gap?

A

Difference between sum of principal cations (Na+, K+)
and principal anions (Cl-, HCO3-)

107
Q

What is a normal anion gap?

A

16mmoles/L (14-18)

108
Q

How does acidosis due to loss of bicarbonate affect the anion gap?

A

No change in anion gap, loss of HCO3- is compensated by increasing Cl-

109
Q

How does acidosis due to lactic/diabetic acidosis affect the anion gap?

A

Reduction in bicarbonate made up for with lactate, acetoacetate, B-OH butyrate

So anion gap

RENAL PHYSIOLOGY (10 decks)

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