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Sophie - Applied Physiology & Pharmacology Year 2 > 51.5 Acid-Base Balance > Flashcards

51.5 Acid-Base Balance Flashcards

1
Q

What does acid-base balance refer to?

A

The processes that maintain the hydrogen ion concentration of body fluids within its normal limits

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2
Q

What are the three main factors that determine pH?

A
  1. Difference between total conc of strong cations (e.g. Na+) and total conc of strong anions (e.g. Cl-)
  2. Quantity and pKa of weak acids present (e.g. phosphate ions or ionisable groups on proteins)
  3. Partial pressure of CO2
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3
Q

What are the 3 pH maintenance mechanisms?

A

1: Ventilatory mechanisms

2: Buffers

3: Renal mechanisms

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4
Q

What is the main EC buffer?

A

Bicarbonate

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5
Q

What is the Henderson-Hasselbach equation?

A
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6
Q

Are buffers short or long term? Why?

A

Temporary measure
*Limited
*Act in a timescale of seconds

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7
Q

What are the IC buffers?

A

Haemoglobin, other proteins, phosphate.

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8
Q

What is the ventilatory maintenance mechanism?

A

Acidotic –> hyperventilation (increase CO2 removal -> decrease blood pH)
Alkalotic –> hypoventilation
Generally greater response to acidosis (don’t want to stop breathing)

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9
Q

How is the pH of blood sensed?

A

By chemoreceptors in the carotid body in the aortic arch and by central chemoreceptors in the medulla. Send signal via glossopharyngeal nerve to respiratory centres in medulla –> in/decreased firing down phrenic nerve to diaphragm/ intercostal nerve to intercostal muscles depending.
less firing if less acidic.

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10
Q

What are the chemoreceptors sensitive to?

A

CO2 and directly to pH (increased non-volatile acids)

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11
Q

What is the timescale of the ventilatory mechanism?

A

Minutes (5-15)

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12
Q

What is the renal mechanism? What is the timescale?

A

Hours to weeks
Adjust resorption/ secretion/ regeneration of bicarbonate and H+

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13
Q

What are the 3 steps of pH maintenance that happen in the kidney?

A
  1. Reabsorbing filtered load of bicarbonate
  2. Excretion of non-volatile acids into tubule
  3. Helps regenerate bicarbonate that has been buffering non-volatile acids in blood.
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14
Q

Where and how is the filtered load of bicarbonate reabsorbed?

A
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15
Q

What do type A intercalated cells facilitate?

A

Type a intercalated cells facilitate the elimination of acids and regeneration of bicarbonate.

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16
Q

What happens in type A intercalated cells?

A

*CO2 hydrated by CA: CO2 + H20 –> HCO3- + H+
* HCO3- exits via basolateral membrane into blood (recovered)
* H+ secreted by ATPase into lumen where it is buffered by urinary buffers (phosphate + ammonia) trapping it in the urine where it can be excreted.

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17
Q

By what 2 processes is bicarbonate regenrated?

A

*Regeneration of bicarbonate in type A intercalated cells when CO2 is hydrated by CA.
*During production of ammonia in the proximal tubule

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18
Q

What is the role of Type B intercalated cells?

A

*Bicarbonate secretion (apical membrane has bicarbonate/Cl exchangers)

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19
Q

What happens to type B intercalated cells in alkalosis?

A

*Can increase the number of transporters

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20
Q

What are the two types of pH disturbances?

A

Respiratory and metabolic

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21
Q

What causes metabolic acidosis? (1)

A

Increased amounts of non-volatile acids

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22
Q

What causes metabolic alkalosis? (1)

A

Increased amounts of non-volatile bases

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23
Q

What causes respiratory acidosis? (1)

A

Failure to remove CO2 from the blood (alveolar hypoventilation)

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24
Q

What causes respiratory alkalosis? (1)

A

Fall in plasma pCO2 (alveolar hyperventilation)

25
Q

What is the list of causes for metabolic acidosis?

A
  • Endogenous acid loading (diabetic ketoacidosis)
  • Exogenous acid loading (methanol ingestion)
  • Loss of base from gut (diarrhoea)
  • Impaired renal acid secretion (renal tubular acidosis)
26
Q

What is the list of causes for metabolic alkalosis?

A
  • Loss of gastric juice (vomiting)
  • Excessive base ingestion
  • Aldosterone excess (increased salt retention, so increased bicarbonate reabsorption and acid excretion)
  • Alkaline diuresis therapy (for drug poisoning)
27
Q

What is the list of causes for respiratory acidosis?

A
  • Impaired ventilation, due to obstruction (asthma, COPD)
  • Impaired gas exchange (V/Q mismatch)
  • Decreased respiratory drive (drugs)
  • Inhalation of CO2
  • Neuromuscular problems (difficult to breathe)
28
Q

What is the list of causes for respiratory alkalosis?

A
  • Hypoxia
  • Increased respiratory drive (cerebrovascular disease)
  • Hepatic failure (stimulates respiration)
  • Drugs, poisons
29
Q

What is the summary for two single values each causing respiratory or metabolic pH disturbances?

A

Respiratory: pCO2
Metabolic: HCO3-

30
Q

What are volatile acids? Give examples.

A

Acids that can be lost to the air so are removed by the lungs

  • CO2, acetone
31
Q

What is the anion gap? What can it tell us?

A

Whether metabolic acidosis is due to increased acid or decreased bicarbonate.
Na+ = K+ - Cl- - HCO3-
Acidosis with a high anion gap indicates more acid in blood than normal (>12)
If the anion gap is normal, indicates metabolic acidosis is due to bicarbonate loss.

32
Q

What can cause a large anion gap? (>20mmol/L)

A
  • Lactate
  • Ketones
  • Toxins
  • Renal failure
33
Q

What can cause a small anion gap? (<7mmol/L)

A

Low albumin

34
Q

What are non-volatile bases? Give examples.

A

Bases produced from sources other than CO2 and not excreted by the lungs

  • such as glutamate, aspartate, citrate, acetate
35
Q

What are non-volatile acids? Give examples.

A

Acids produced from sources other than CO2 and not excreted by the lungs

  • such as lactic acid, acetoacetic acid, β-hydroxybutyrate

(think metabolism)

36
Q

What are some pathological consequences of pH becoming too high/alkaline?

A

7.5 - Tetany (low Ca2+), fainting (low cerebral blood flow)
7.6 - Hypokalaemia, cardiac dysrhythmias
7.7 - Haemoloysis
7.8 - Death

37
Q

What are some pathological consequences of pH becoming too low/acidic?

A

7.3 - Hyperkalaemia
7.2 - Reduced cardiac contractility
7.1 - Bone resorption
7.0 - Cerebral palsy in newborn
6.9 - Death

38
Q

What are the four steps of physiological changes when pH decreases from 7.4 to 7.35?

A
  • Hyperventilation
  • Systemic vasodilation
  • Pulmonary vasoconstriction
  • Renal ammoniagenesis
39
Q

What are the four steps of physiological changes when pH increases from 7.4 to 7.45?

A
  • Hypoventilation
  • Systemic vasoconstriction
  • Pulmonary vasodilation
  • Renal bicarbonate secretion
40
Q

What is the normal range of arterial blood pH?

A

7.35-7.45

41
Q

When faced with alkaline challenge (such as vomiting), how does the kidney respond?

A
  • Decreases net acid excretion - reduces excretion rates of titratable acid and NH4+
  • So less new HCO3- formed
42
Q

What are Davenport diagrams?

A
  • Plots of [HCO3-] against pH at different PCO2 values
  • They allow us to see the effects of different metabolic disturbances
43
Q

How do each type of acidosis and alkalosis appear on a Davenport diagram?

A
44
Q

Show on a Davenport diagram how each type of acidosis and alkalosis is corrected. How fast does this happen?

A
  • Metabolic disturbances are corrected by respiratory changes -> This is FAST
  • Respiratory disturbances are corrected by metabolic changes -> This is SLOW
45
Q

Describe how you can interpret blood gases to identify the various types of alkalosis and acidosis.

A
  1. Check the pH to see if it is acidosis or alkalosis
  2. Check to see if this can be explained by the pCO2 level
    • If yes, then it is respiratory acidosis/alkalosis
    • If not, then it is metabolic acidosis/alkalosis
46
Q

Give the normal values for arterial and venous blood for these:

  • pH
  • PCO2
  • PO2
  • HCO3-
  • Base excess
A
47
Q

What is base excess and why is it important?

[IMPORTANT]

A
  • There may be situations where there is both a respiratory acidosis AND metabolic acidosis simultaneously
  • In these situations, the metabolic acidosis will only be revealed once the respiratory acidosis is corrected
  • In these situations, the base excess is a way of identifying this right at the start
  • How it is done:
    • “Ventilate” a sample of blood
    • Titrate to assess the acidity
    • Base excess is a measure of this
48
Q

What are the consequences of chronic acidosis and alkalosis?

[IMPORTANT]

A

Chronic acidosis:

  • Loss of bone density -> Due to acid buffering
  • Muscle wastage -> Due to increased protein catabolism Acid buffering leads to loss of bone density, resulting in an increased risk of bone fractures

Chronic alkalosis:

  • Neuromuscular irritability + Tetany
  • Abnormal heart rhythms (usually due to accompanying electrolyte abnormalities such as low levels of potassium in the blood)
49
Q

What is the total amount of H+ that must be secreted into the tubular fluid per day by the kidneys?

A
  • 4320mEq/day is needed to recovered filtered HCO3-
  • 70mEq/day is needed to regenerate HCO3- that was used in buffering NVAs

So the total is 4390mEq/day (equal to 4390mmol/day).

50
Q

Where does H+ secretion into the tubular fluid occur? [IMPORTANT]

A

All along the renal tubule.

51
Q

What are the roles of the different segments of the nephron in acid-base homeostasis?

A
  • Glomerulus
    • Involved in filtering out almost all HCO3- from the blood
  • Proximal tubule
    • Involved in 80% of HCO3- reabsorption into the blood
    • Not really involved in HCO3- regeneration
    • Ammoniagenesis (ammonia is used as a urinary buffer)
  • Loop of Henle
    • Involved in 15% of HCO3- reabsorption into the blood
  • Distal tubule and collecting duct
    • Residual HCO3- recovery
    • Involved in HCO3- regeneration
52
Q

What determines the fate of H+ when it is secreted into the renal tubule?

A
  • If the H+ reacts with filtered HCO3-, the bicarbonate is reabsorbed (4.3mol day-1)
  • If the H+ reacts with a urinary buffer, it is excreted. This is used in regenerating bicarbonate. (70mmol day-1)
53
Q

What can mutations in transport proteins involved in the reabsorption and regeneration of HCO3- in the tubule, as well as in carbonic anhydrase, result in?

A

Renal tubular acidosis -> This is acidosis of the plasma, NOT the tubular fluid

54
Q

How much H+ is generated in the regeneration of HCO3- in type A intercalated cells of the collecting duct and distal tubule?

A

Equivalent to the amount of NVA buffered by HCO3- in the plasma.

55
Q

Describe the location and mechanism for ammoniagenesis. [IMPORTANT]

A

Occurs in the cells of the proximal tubule:

  • Glutamine is converted to glutamic acid by glutaminase
  • Glutamic acid is converted to α-ketoglutaric acid by glutamate dehydrogenase
  • Both of these steps yield: 1 NH3 and 1 HCO3-
56
Q

What are urinary buffers?

A
  • Buffers other than HCO3- that are found in the renal tubule
  • They react with the H+ that is secreted into the renal tubule lumen at the collecting duct and distal tubule
  • They are used to allow large amounts of free H+ secretion into the tubular fluid without unsustainable drops in urinary pH
57
Q

Describe how ammoniagenesis is involved in acid-base balance. Where does it occur? [IMPORTANT]

A
  • Ammoniagenesis is upregulated when plasma pH is acidic
  • It occurs in proximal tubule cells
58
Q

How does the renal tubule respond to acidosis?

A
  • Acidosis leads to insertion of H+-ATPase into the apical membrane of the renal tubule cells, leading to increased H+secretion into the tubule.
  • This is done by cytoskeletal-driven fusion of subapical vesicles.
59
Q

What is the difference between respiratory and renal regulation of acid-base balance?

A

Respiratory - quick.
* induced by action of chemoreceptor on medullary respiratory centres
*acidosis - accelerated breathing
Renal - long-term
*altering bicarbonate flux.

Sophie - Applied Physiology & Pharmacology Year 2 (32 decks)

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