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Renal (Year 2 GM) > Acid Base Balance > Flashcards

Acid Base Balance Flashcards

1
Q

What is the normal pH of arterialized blood?

A

7.4

Free [H+] = 40 x 10-9 moles/l or 40 x 10-6 mmoles/l

Only free H+ ions contribute to pH

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2
Q

How does concentration of H+ compare to the concentration of other plasma constituents?

A

Other plasma constituents are present in mmoles eg Na+, K+, Cl-, glucose etc. So [H+] is one millioneth that of other plasma constituents.

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3
Q

What is the equation for respiratory acid?

A
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4
Q

Why isn’t the formation of carbonic acid a net contributor to increase acid?

A

Any increase in production results in increase in ventilation

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5
Q

What are the sources of metabolic acid?

A

Inorganic - S-containing amino acids - H2SO4 and phosphoric acid is produced from phospholipids

Organic acids - fatty acids, lactic acid

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6
Q

What is the henderson hasselnach equation?

A

Defines pH in terms of the ratio of [A-]/[HA]

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7
Q

What is the most important exctracellular buffer?

A

Bicarbonate

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8
Q

What determines the amount of H2CO3?

A

The amount of CO2 dissolved in plasma

Solubility of CO2 and PCO2

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9
Q

What is the solubility of H2CO3 in blood at 37 degrees celcius?

A

0.03 mmoles/l/mmHg

OR

0.225 mmoles/l/kPa

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10
Q

How do you calculcate the concentration of H2CO3 in the blood?

A

Use the solubility of CO2 in blood multiplied by the the pressure of PCO2

The ratio of bicarbonate to H2CO3 is 20:1 - so the concentration of bicarbonate will be 20 times greater

24 mmoles/l is described as the standard bicarbonate

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11
Q

What is the range of pH compatible with life?

A

7.0 - 7.6

Average pH is 7.4

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12
Q

What is the effect of adding H+ to the bicarbonate position?

A

Drives the reaction to the right (the side which favours more production of water and carbon dioxide)

Some of the additional H+ ions are removed from solution and therfore the change in pH is reduced

Ventillation also serves to remove CO2 and water from the RHS of the equation - respiration increases the buffering capacity and H+ ions are prevented from contributing to the pH

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13
Q

What happens to the bicarbonate equation when there is a decrease in H+ ions?

A

Ventilation is decreased and CO2 increases

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14
Q

Which organ is responsible for H+ elimination from the body?

A

By the kidneys - this excretion is coupled to the regulation of plasma bicarbonate

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15
Q

What are other buffers in the ECF?

A
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16
Q

What are the primary intracellular buffers?

A

Proteins

Organic and inorganic phosphates

In erythrocytes - haemoglobin

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17
Q

How does regulation of ICF pH alter the plasma electrolytes?

A

Buffering of H+ ions by ICF buffers 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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18
Q

In acidosis what is the movement of potssium?

A

Out of cells into the plasma

Causes depolarisation of excitable tissues

Causes ventricular fibrillation and death

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19
Q

Where in the body is an additional store of buffer?

A

Bone carbonate

In chronic acid loads (renal failure) - it results in the wasting of bones

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20
Q

What percentage of metabolic acid is buffered in the plasma?

A

43% (primarily with HCO3)

57% in cells

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21
Q

How is the respiratory acid buffered?

A

97% of buffering occurs within the cells - haemoglobin is particularly important - rest with plasma proteins

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22
Q

What is the equation to show how pH is related to renal regulation and respiratory regulation?

A
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23
Q

How does the kidney regulate bicarbonate?

A

It reabsorbs filtered HCO3

It generates new HCO3

(both these processes depend on active H+ secretion from the tubule cells into the lumen)

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24
Q

What are the mechanisms for reabsorption of bicarbonate?

A

a) Active H+secretion from the tubule cells
b) coupled to passive Na+ reabsorption
c) filtered HCO3- reacts with the secreted H+ to form H2CO3. In the presence of carbonic anhydrase on the luminal membrane - CO2 and H2O
d) CO2 is freely permeable and enters the cell
e) Within the cell, CO2 - H2CO3 in the presence of carbonic anhydrase (present in all tubule cells) which then dissociates to form H+ and HCO3- f) The H+ ions are the source of the secreted H+
g) The HCO3- ions pass into the peritubular capillaries with Na+
h) Bulk of HCO3- reabsorption occurs in the proximal tubule >90%

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25
Q

What is the minimum and maximum urine pH in humans?

A

Minimum = 4.5 - 5.0

Maximum = 8.0

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26
Q

Usually net production of 50 - 100 mmoles H+ per day - this would result in a pH of 1 in the urine - stinging! - why isn’t this the case?

A

Several weak acids and bases act as buffers. Most is done by dibasic phosphate, HPO42--, also uric acid and creatinine.

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

Generates net HCO3 and excretes H+

Only used for acid loads

27
Q

What is the process of titratable acidity?

A

The dibasic phosphate is present in the lumen of the tubule - Na2 HPO4. One sodium is reabsorbed in exchange for secreted H+. This monobasic phosphate removes H+ from the body.

CO2 from the blood enters the tubule cells and forms H+ and HCO3-. The H+ formed here is the source of H+ that is exchanged for sodium in the previous step. HCO3 - here re enters the blood

the process occurs primarily 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

28
Q

What is the process of titratable acidity dependant on?

A

Dependant on PCO2 of the blood

29
Q

What are the two noteable features of titratable acidity?

A

Generates new bicarbonate

Excretes H+

30
Q

How is ammonium produced?

A

Deamination of amino acids, primarily gluatmine - by the action of renal glutaminase within the renal tubule cells

31
Q

Which is lipid soluble NH3 or NH4+?

A

NH3 is lipid soluble

NH4+ is not

32
Q

What is the movement of NH3?

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)

33
Q

What is the source of H+ in ammonium excretion?

A

CO2 from the blood

34
Q

Where is the ammonium/sodium exchanger?

A

In the proximal tubule

35
Q

Ammonium excretion without the ammonium/sodium exchanger

A
36
Q

Ammonium excretion with the ammonium/sodim transporter

A
37
Q

What is the activity of renal glutaminase when intracellular pH falls?

A

Renal glutaminase activity increases and therefore more ammonium is produced and excreted

This results in net excretion of H+ and generation of new HCO3-

This ability to augment ammonium productio nis the main adaptive mechanism of the kidney to acid loads

38
Q

How many mmoles are a day are lost as NH4+ ?

A

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

39
Q

What is the delay of the ability to augment the production of NH4+?

A

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

It also takes time to switch off the ability to make NH4+ when there is excess of alkali.

40
Q

What results in respiratory acidosis?

A

Decreased ventilation (retention of CO2)

Increase in PCO2

41
Q

What are the causes of respiratory acidosis?

A

Acute: drugs which depress the medullary respiratory centres, such as barbiturates and opiates.

Obstructions of major airways.

Chronic: lung disease eg bronchitis, emphysema, asthma.

42
Q

What is the response to respiratory acidosis?

A

Need to increase bicarbonate concentration (increase reabsorption and generation)

Excrete H+

Renal glutaminase is stimulated by the drop in pH (serves to increase ammonia) but this response takes time

The increase in PCO2 increases the ability to reabsorb it (CO2 in the plasma is needed to regenerate H+ (In the proximal tubule cell) that is used to reabsorb HCO3- from the renal tubule

43
Q

In compensated respiratory acidosis what are the blood gases and pH like?

A

Blood gases remain abnormal

pH is normalised so long as renal function is sound

Only restoration of normal ventilation can remove the primary disturbance

44
Q

What is the mechanism of respiratory alkalosis?

A

Fall in PCO2

Increased ventillation and CO2 blow off

45
Q

What are causes of respiratory alkalosis?

A

Acute: voluntary hyperventilation, aspirin, first ascent to altitude

Chronic: long term residence at altitude, decreases PO2 to < 60mmHg (8kPa) stimulates peripheral chemoreceptors to increase ventilation.

46
Q

What is the way we protect pH during respiratory alkalosis?

A

We reabsorb less bicarbonate

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.

Ventilation must be normalised to correct the disturbance

47
Q

What type of breathing is stimulated in metabolic acidosis?

A

Increase in ventilation depth rather than rate - reaching a maximum of 30 litres per minute rather than 5-6 litres per minute

Kussmaul breathing 0 seen in renal failure or diabetic ketoacidosis - very severe

48
Q

How does kussmaul breathing present a problem for the kidneys?

A

Kidneys use CO2 to free up hydrogen ions - these hydrogen ions are used to reabsorb bicarbonate and are sometimes excreted (titratable acidity and ammonium excretion)

Respiratory compensation however lowers the PCO2 to protect the pH

However: the amount of H+ secreted is less than normal due to decrease in PCO2. The bicarbonate is reduced moreso. A smaller fraction of H+ is needed for HCO3 reabsorption - greater proportion is available for excretion in the form of titratable acid and ammonium

49
Q

Summary of the order of the body’s response when there is metabolic acidosis

A

ECF and ICF buffer

Respiratory compensation

Renal compensation (takes a while to reach maximum activity - renal glutaminase is responsible for deamination - increasing H + excretion and HCO3 reabsorption)

Metabolic alkalosis

50
Q

What are the causes of metabolic alkalosis?

A
  1. Increase in H+ ion loss- vomiting loss of gastric secretions
  2. ­ renal H+ loss- aldosterone excess, excess liquorice ingestion
  3. Excess administration of HCO3- is unlikely to produce a metabolic alkalosis in subjects with normal renal function, but may do so if renal function impaired.
  4. 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.
51
Q

How is metabolic alkalosis corrected?

A

Too much H+ for HCO3 to reabsorb - even in th presence of increased PCO2 - excess is lost in the urine - respiratory compensation delays renal correction but protects the pH

52
Q

Summary of Acid/Base Disorders

A
53
Q

What is blood pH defined as?

A

The ratio of bicarbonate to PCO2

Therefore a decrease in pH is caused by either a decrease in HCO3-

OR

Increased PCO2

An increase in pH (alkalosis)

is CAUSED by either:

increased HCO3+

Or

decreased PCO2

54
Q

How does the decrease in pH compare between acute exposure to los PCO2 and Chronic exposure to PCO2?

A

Acute: Large decrease in pH

Chronic: Small decrease in pH (NH3 production is fully turned on)

55
Q

In the case where a patient has a haemorrhage and also has metabolic acidosis (diabetic ketoacidosis) and respiratory acidosis (chronic bronchitis) what should you do?

A

High acidity causes hyperkalaemia because hydrogen ions are buffered intracellularly in exchange for potassium ions - danger of centricular fibrillation

(cells soak up hydrogen and expel potassium)

TREATMENT:

  1. Insulin or increase glucose if non-diabetic, stimulates cellular uptake of potassim - make sure not to overcompensate and cause hypokalaemia
  2. Calcium resonium - exchanges calcium ions for potassium ions
  3. Calcium gluconate (iv) - decreases the excitability of the heart and stabilizes cardiac muscle cell membranes
56
Q

Whar are the effects on the blood after episodes of severe vomiting?

A

Loss of sodium chloride and water - hypovolaemia

Loss of HCL - metabolic acidosis

57
Q

In metabolic alkalosis as a result of vomiting - what is the effect of hypovolaemia on aldosterone, sodium and H+?

A

Stimulates aldosterone - increases sodium reabsorption in the distal tubule

Main exchange for sodium is hydrogen (chlorine is low due to loss of NaCl from vomiting)

Respiratory compensation is said to exacerbate metabolic alkalosis

Restoration of volume takes precedence over correction of metabolic alkalosis

58
Q

Why do you become alkalotic in vomiting and diarrhoea (cause of metabolic acidosis)?

A

Decrease in ECF volume results in aldosterone production and results in ‘contraction alkalosis’

Alkalosis is corrected by giving sodium chloride and restoring volume

59
Q

Why does liquorice cause metabolic alkalosis?

A

Contains glycyrrhizic acid - very similar to aldosterone

60
Q

What is the anion gap?

A

The difference between the sum of the principle cations (sodium and potassium) and the principle anions in the plasma (Chlorine and HCO3-)

Normally 14-18 mmoles/l

61
Q

How does the anion gap change in metabolic acidosis?

A

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.

62
Q

When does the anion gap stay the same in acidosis and when does it change?

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. Chloride is included in the principle anions.

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

These are not included in the principle anions so the gap between cations and anions increases

63
Q
A

Renal (Year 2 GM) (28 decks)

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