7. Acid Base Regulation Flashcards

1
Q

What is an acid and a base?

A
  • Acid - a substance that can release H+ ions in solution

* Base - a substance than can accept H+ ions in solution

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2
Q

What is a buffer?

A

A substance which can release or accept H+ ions in solution, resulting in minimal changes to pH

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3
Q

What is the normal plasma [H+] and corresponding pH?

A
  • [H+] = 40nmol/l
  • pH = 7.4
  • Normal range - 7.34-7.45
  • Range compatible with life - 6.8-7.8
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4
Q

What is the urine pH range?

A

pH4.0-8.5

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5
Q

What controls the pH of urine?

A
  • Dissociation of hydrogen bicarbonate

* Involves carbonic anhydrase

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6
Q

Why is the control of pH in the body important?

A
  • Metabolic reactions are sensitive to pH

* H+ ions change the shapes of proteins, including enzymes

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7
Q

What is the principle buffer in blood and intracellular fluid?

A
  • Blood - H2CO3 <=> H+ + HCO3-

* ICF - H2PO4 <=> H+ + HPO42-

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8
Q

How much of the H+/OH- load is buffered in cells in metabolic acidosis/alkalosis?

A
  • Metabolic acidosis - 80-85% of acid load is buffered in cells
  • Metabolic alkalosis - 30-35% of OH- load is buffered in cells
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9
Q

How much of the H+/OH- load is buffered in cells in respiratory acidosis/alkalosis?

A

All buffering is intracellular

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10
Q

What happens to H2SO4 and HCL produced in metabolism?

A
  • They don’t circulate as free acids, but are immediately buffered in the ECF by HCO3-
  • H2SO4 + 2NaHCO3 => Na2SO4 + 2H2CO3 => 2H2O + CO2
  • HCl + NaHCO3 => NaCl + H2O + CO2
  • Minimise increase in H+, but excess must be excreted to prevent progressive depletion of HCO3-
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11
Q

What are the sources of H+ in the body?

A
  • Physiological - carbohydrates, fats, arginine etc.
  • Pathological - hypoxia, diabetes, ketoacids
  • Volatile acids - derived from metabolism of carbohydrates and fats, results in CO2 production lost in respiration
  • Non-volatile acids - derived from metabolism of proteins, results in H+, excreted by kidneys
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12
Q

How much acid do kidneys excrete?

A

50-100mmol of non-carbonic acids per day

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13
Q

Outline renal kidney H+ excretion?

A
  • All bicarbonate filtered into urine is reabsorbed
  • Secreted H+ are excreted with filtered buffers (phosphates + creatinine) or manufactured buffers (ammonia, from glutamine in PCT)
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14
Q

What are the primary and secondary mechanisms to increase H+ secretion?

A
  • Primary - decrease plasma bicarbonate concentration & increase PaCO2
  • Secondary - increase filtered load of bicarbonate, decrease ECF volume, increase angiotensin II, increase aldosterone, hypokalaemia
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15
Q

What are the primary and secondary mechanisms to decrease H+ secretion?

A
  • Primary - increase plasma bicarbonate concentration & decrease PaCO2
  • Secondary - decrease filtered load of bicarbonate, increase ECF volume, decrease aldosterone, hyperkalaemia
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16
Q

Summarise the reabsorption of bicarbonate

A
  • 80% reabsorbed in the PCT
  • Remaining absorbed in (thick) ascending limb
  • Net reabsorption of 1 filtered Na+ and 1HCO3-
17
Q

Why and how is bicarbonate reformed?

A
  • Formed as bicarbonate is lost during buffering of non-volatile acids
  • In the liver, amino acids => glutamine + urea
  • Glutamine => ammonium ions + α-ketoglutarate in the kidney
  • α-ketoglutarate => bicarbonate
18
Q

Outline ammonium excretion

A
  • Ability to excrete H+ as ammonium - adds degree of flexibility to renal acid-base regulation
  • NH3 produced in tubular cells predominantly from glutamine
  • Some excess NH3 diffuses into lumen
  • Excreted H+ combines with NH3 to form NH4+
19
Q

What causes metabolic acidosis and how is it compensated?

A

• Low plasma pH and HCO3-
- addition of non-volatile acids
- loss of non-volatile alkalis
- failure to reabsorb sufficient HCO3-
• Respiratory compensation - raised ventilation
• Renal compensation - excretion of net acid increases

20
Q

What causes metabolic alkalosis and how is it compensated?

A

• Raised plasma pH and HCO3-
- loss of non-volatile acid
- raised aldosterone
• Respiratory compensation - reduced ventilation
• Renal compensation - excretion of excess HCO3-

21
Q

What causes respiratory acidosis and how is it compensated?

A
• Low plasma pH and high pCO2
- reduced alveolar ventilation
- impaired gas diffusion
• Renal compensation 
- increased HCO3- reabsorption and NH4+ secretion (several days)
- acute phase: cellular buffering
22
Q

What causes respiratory alkalosis and how is it compensated?

A
• Raised plasma pH and reduced pCO2
- increased alveolar ventilation
• Renal compensation
- decreased HCO3- reabsorption and NH4+ secretion (several days)
- acute phase: cellular buffering