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RS > Session 5: Control of plasma pH > Flashcards

Session 5: Control of plasma pH Flashcards

1
Q

Normal pH range of blood plasma

A

7.35-7.45

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2
Q

What is a blood plasma pH below its range called?

A

Acidaemia

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3
Q

What is a blood plasma above its range called?

A

Alkalaemia

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4
Q

Explain the effects of alkalaemia.

A

It reduces the solubility of Ca2+ which means that free Ca2+ leaves the ECF and binds to bone and proteins.

This leads to the classic symptoms of hypocalcaemia.

These include paraesthesia and tetany.

At 7.55 mortality rate is 45%

At 7.65 mortality rate is 80%

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5
Q

Explain the effects of acidaemia

A

Increased H+ concentrations affects enzyme function by denaturing proteins. This leads to effects on muscle contractility, glycolysis and hepatic function.

It also leads to potassium movement out of the cells leading to hyperkalaemia which can be fatal as it can lead to arrhythmia etc.

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6
Q

The H+ concentration in ECF is very low so just a very small change in amounts of acid would change pH drastically.

Why is this not the case?

A

Because H+ ions are buffered by binding to various sites.

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7
Q

What is the most important ECF buffer for H+ ions?

A

The carbon dioxide/hydrogen carbonate system.

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8
Q

Explain the CO2/HCO3- buffer system.

A

Dissolved CO2 reacts with water to form H+ and HCO3-

The pH depends on how much CO2 reacts to form H+.

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9
Q

The ratio depends of HCO3- concentration to pCO2 (which in its way leads to CO2 concentration).

How is the pCO2 controlled?

A

By the lungs

Hyperventilating decreases pCO2

Hypoventilating increases pCO2

This is controlled by chemoreceptors

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10
Q

How is the HCO3- controlled?

A

Largely created by reactions in the red cells but whose concentration is controlled by the kidneys.

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11
Q

What disturbs the pCO2?

A

Respiratory disease

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12
Q

What disturbs the HCO3- concentration?

A

Metabolic or kidney disease

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13
Q

Briefly explain how the kidneys control pH.

A

Recovery of bicarbonate

Active secretion of H+

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14
Q

What is the normal range of pCO2 in the arterial blood?

A

4.7-6.0

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15
Q

Where is HCO3- filtered?

A

At the glomerulus

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16
Q

Where is HCO3- reabsorbed?

A

Mostly in the PCT (80%)

Up to 15% of HCO3- is also absorbed in the thick ascending limb of the loop of Henle.

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17
Q

Explain the basic renal control of HCO3-.

A

In the tubular cells CO2 and water react to form H+ and HCO3-. This is a reversible reaction.

However the H+ and HCO3- are transported out. H+ in exchange for Na+ to end up in the lumen of the tubule.

HCO3- is transported into the blood along with Na+.

The H+ that ends up in the lumen makes the ultrafiltrate acidic and it doesn’t want to be. The H+ therefore binds to HCO3- in the lumen of the tubule and produces H2O and CO2. H2O and CO2 can freely diffuse into the tubular cell again in order to provide more to the reaction creating more H+ and HCO3- again.

This allows HCO3- to be reabsorbed again.

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18
Q

Explain the buffering system and HCO3- reabsorption in the distal convoluted tubule.

A

HCO3- absorption and H+ excretion in the distal tubule through its intercalated cells.

Here H+ is actively secreted via a H+-ATPase. This is because the Na+ gradient is insufficient to drive H+ out of the cell. Also not a lot of HCO3- is still available in the DCT lumen so little CO2 will enter the cell to react with water and produce more H+ and HCO3-.

So H+ will need another buffer which is HPO42- which becomes more effective as the pHof the ultrafiltrate falls.

HPO24- reacts with H+ to create H2PO4-

The active secretion of H+ leads to more H+ to be created in the CO2/HCO3- reaction.

HCO3- is transported into the capillary in exchange for Cl-.

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19
Q

The total buffering capacity of phosphate and the other weak acids is limited by the amount filtered. Replacement of any further HCO3- needs to take place by a mechanism within the kidney.

What is this mechanism?

A

Excretion of ammonium ions by the production of the amino acid glutamine.

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20
Q

Explain the glutamine reaction and its purpose.

A

Glutamine is converted into NH4+ and alpha-ketoglutarate.

The alpha-ketoglutarate is the converted into two HCO3-. The HCO3- is transported into the capillaries along with Na+.

The ammonium is converted into NH3 and H+.

The NH3 can freely diffuse into the lumen of the proximal convoluted tubule. In the lumen the ammonia NH3 will react with H+ to produce NH4+.

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21
Q

Why is acid excretion important?

A

To keep HCO3- concentrations normal.

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22
Q

Explain how acidosis leads to hyperkalaemia.

A

Potassium ions move out of cells

Decreased potassium excretion in distal nephron

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23
Q

Explain how alkalosis leads to hypokalaemia.

A

Potassium ions move into cells

Enchance excretion of potassium in distal nephron.

24
Q

Explain acid base disturbances and potassium in hyperkalaemia.

A

Hyperkalaemia makes the intracellular pH of tubular cells more alkaline.

This leads to H+ moving out of the cells. This leads to HCO3- excretion and metabolic acidosis.

25
Q

Explain acid base disturbances and potassium in hypokalaemia.

A

Makes the intracellular pH of tubular cells more acidic.

H+ ions move into the cells and this favours H+ excretion and HCO3- recovery. This leads to metabolic alkalosis.

26
Q

What happens in hypoventilation to pCO2?

A

Hypercapnia (increased pCO2)

27
Q

What happens to plasma pH due to hypercapnia?

A

Plasma pH decreases

28
Q

What is respiratory acidaemia and what are is pCO2, HCO3- and pH in it?

A

When pCO2 rises due to hypoventilation or other lung disease where you can’t expirate correctly.

High pCO2.

Normal HCO3-

Low pH

29
Q

What is respiratory alkalaemia and what are the levels of pCO2, HCO3- and pH in it?

A

Due to hyperventilation leading to hypocapnia which is a fall in pCO2.

The hypocapnia (fall in pCO2) leads to a rise in pH.

HCO3- stays the same.

30
Q

How is respiratory acidosis compensated?

A

Kidneys increase HCO3- concentration.

31
Q

How is respiratory alkalosis compensated?

A

By the kidneys by decreasing HCO3-.

32
Q

How long does it take for the compensation mechanism by the kidneys?

A

Around 2-3 days

33
Q

What is compensated respiratory acidosis characterised by?

A

High pCO2

Raised HCO3- conc

Relatively normal pH

34
Q

What is compensated respiratory alkalosis characterised by?

A

Low pCO2

Low HCO3- conc.

Relatively normal pH

35
Q

Explain metabolic acidosis.

A

Tissue produce acid which reacts with HCO3- which removes it.

Leads to a fall in HCO3-. This leads to a fall in pH.

36
Q

What is metabolic acidosis initially characterised by?

A

Normal pCO2

Low HCO3- conc

Low pH

37
Q

Explain the compensatory mechanism in metabolic acidosis.

A

Peripheral chemoreceptors in the carotid bodies detect the pH drop. This leads to an increase in ventilation -> hyperventilation to lower pCO2.

38
Q

What is compensated metabolic acidosis characterised by?

A

Low HCO3-

Lowered pCO2

Nearer normal pH

39
Q

What is metabolic alkalosis characterised by?

A

Normal pCO2

Raised HCO3-

Increased pH

40
Q

Explain the compensatory mechanism of metabolic alkalosis.

A

Cannot be easily corrected by decreased ventilation since that would lead to hypoxia.

Instead a rise in pH of tubular cells leads to a fall in H+ excretion and a reduction in HCO3- recovery.

41
Q

Explain the anion gap.

A

The difference between measured cations and anions.

(Na+ + K+) - (Cl- + HCO3-)

42
Q

What is the anion gap normally?

A

10-18 mmol/l

43
Q

When is the anion gap increased?

A

If HCO3- is replaced by other anions

44
Q

Conditions leading to respiratory acidosis.

A

Type 2 respiratory failure like severe COPD, severe asthma, drug overdose or neuromuscular disease where pO2 is low and pCO2 is high.

45
Q

Conditions leading to respiratory alkalosis.

A

Hyperventilation due to e.g. panic attacks and/or anxiety. Low pCO2 and a rise in pH.

Hyperventilation in response to long-term hypoxia in type 1 respiratory failure.

46
Q

Conditions leading to metabolic acidosis with an increased anion gap.

A

Keto-acidosis like diabetes

Lactic acidosis like exercising to exhaustion or poor tissue perfusion.

Uraemic acidosis in advanced renal failure with reduced acid secretion, build up of phosphate, sulphate and urate in blood.

47
Q

When in metabolic acidosis can the anion gap be normal?

A

If anion gap is normal HCO3- is replaced by Cl-.

48
Q

Conditions leading to metabolic acidosis with a normal anion gap.

A

Renal tubular acidosis where there are problems with transport mechanisms in the tubules.

Severe persistent diarrhoea leading to metabolic acidosis due to loss of HCO3- which is replaced by Cl-

49
Q

Explain the potassium concentrations in metabolic acidosis due to diabetic ketoacidosis.

A

Usually acidosis leads to hyperkalaemia.

However in diabetic ketoacidosis there may be a total body depletion of K+.

Initially K+ moves out of the cells due to the acidosis and the lack of insulin. However the osmotic diuresis leads to K+ being lost in urine.

Then giving insulin to these patients makes K+ move into cells again and can lead to hypokalaemia instead.

50
Q

Conditions leading to metabolic alkalosis.

A

HCO3- is retained in place of Cl-.

Severe prolonged vomiting leading to loss of H+ as the stomach is a major site of H+ secretion and also HCO3- production.

Potassium depletion and mineralcorticoid excess.

Loop diuretics and thiazides

51
Q

Explain how metabolic alkalosis is corrected in persistent vomiting.

A

HCO3- increase after persisting vomiting as H+ is excreted and more HCO3-.

Rise in pH of tubular cells leads to fall in H+ excretion and reduction in HCO3- recovery.

52
Q

Why might there be a problem with the compensation of metabolic alkalosis due to peristent vomiting.

A

If there is also volume depletion the capacity to lose HCO3- is reduced because of high rate of Na+ recovery to retain water.

Recovering Na+ favours H+ excretion and HCO3- recovery.

53
Q

If pCO2 is not normal, HCO3- conc is normal and pH has changed in the opposite direction to pCO2.

What will it be?

A

Respiratory alkalosis or acidosis

54
Q

If HCO3- is not normal, pCO2 is normal and pH has changed in the same direction as HCO3-.

What is it?

A

Metabolic acidosis/alkalosis

55
Q
A

RS (28 decks)

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