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SGUL - Physiology 1 > Acid Base Balance > Flashcards

Acid Base Balance Flashcards

1
Q

Why should the pH be kept constant in the body?

A
  • Enzymes function at a particular pH within a narrow range
  • Enzymes have a huge number of functions around the body
  • Abnormal pH can result in disturbances in a wide range of body systems.
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2
Q

What is the result of an abnormal pH?

A
  • Abnormal respiratory and cardiac functions
  • Derangements in blood clotting and drug metabolism
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3
Q

How does the metabolism of carbohydrates and fats produce acid?

A

CO2 + H2O = H2CO3 (volatile acid), which is reversible with H+ and HCO3-
- CO2 doesn’t usually result in an increase in H+ in the plasma - excreted from the body via the lungs
- H2CO3 produced is known as a volatile acid.

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4
Q

How does protein metabolism produce acid?

A
  • Generates non-volatile (fixed) acids.
    Examples:
  • S-containing amino acids (such as cysteine and methionine) make H2SO4
  • lysine, arginine and histidine make HCl
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5
Q

Why do non-volatile acids from metabolism need to be removed quickly?

A

Otherwise there will be a net gain of H+

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6
Q

What are the 3 mechanisms that compensate for the disturbances in body pH?

A
  • the ICF and ECF buffering systems
  • the respiratory system adjustment of ECF PCO2
  • the renal adjustment of ECG [HCO3-]
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7
Q

What is the first line of defense against changes in body pH?

A
  • Intracellular and extracellular buffer systems.
  • Participate in accordance with their pKa and their quantity.
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8
Q

What is a particularly important buffer system? Why is it important?

A

CO2-HCO3- buffer system
- CO2 and HCO3-, can be regulated independantly

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9
Q

What is the second mechanism against changes in body pH?

A

Respiratory system that regulates the plasma PCO2

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10
Q

How does the respiratory system respond to changes in pH?

A

Controls the excretion or retention of metabolically produced CO2

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11
Q

What is the third mechanism against changes in body pH?

A

Kidneys

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12
Q

How do kidneys respond to changes in pH?

A
  • Regulates excretion or retention of HCO3-
  • Regulates the regeneration of HCO3-
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13
Q

What is a buffer?

A

Solution that minimises the change in [H+]

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14
Q

What are the advantages of the CO2-HCO3- buffering system? PART 1

A
  • CO2 and HCO3- can be regulated independently.
  • Excretion or retention of CO2 is controlled by the lung
  • Reabsorption and regeneration of HCO3- is controlled by the kidney.
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15
Q

What are the advantages of the CO2-HCO3- buffering system? PART 2

A
  • Readily available supply of CO2 from cellular metabolism.
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16
Q

Why are other mechanisms apart from buffering needed for pH maintenance? PART 1

A
  • Buffers are present in limited quantities.
  • As the buffer capacity is used, less is available to control pH.
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17
Q

Why are other mechanisms apart from buffering needed for pH maintenance? PART 2

A
  • Other mechanisms needed to eliminate the excess H+ or base which caused the change in pH and to restore the buffer capacity to normal.
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18
Q

What does the Henderson-Hasselbalch equation describe?

A
  • Derivation of pH as a measure of acidity in biological and chemical systems, using pKa
  • Estimating the pH of a buffer solution and finding the equilibrium pH in acid-base reactions.
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19
Q

What is concentration of dissolved CO2 in plasma proportional to?

A

Partial pressure of CO2

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20
Q

What is the proportionality constant for plasma at 37 °C?

A

0.03

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21
Q

What are the primary renal mechanisms involved in the renal control of acid-base levels?

A
  • reabsorption and secretion of HCO3-
  • formation of HCO3-
  • secretion of [H+] into tubular fluid
  • buffer systems within the tubule that react with the secreted [H+]
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22
Q

Describe the movement of bicarbonate in the kidneys.

A
  • Bicarbonate ions are freely filtered by the glomeruli.
  • Daily filtered load of bicarbonate is 4500 mmol
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23
Q

What would happen if some of this bicarbonate is excreted through urine?

A

Stores of this buffer would quickly reduce

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24
Q

What prevents the loss of bicarbonate by excretion?

A

Avid tubular reabsorption of bicarbonate ions

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25
Q

Describe the renal control of [H+] and [HCO3-]. PART 1

A
  • Filtered HCO3- combines with H+ to form carbonic acid
  • Carbonic acid dissociates to form CO2 and H2O this is catalyzed by carbonic anhydrase
  • CO2 crosses into the tubular cell down a gradient
  • Kidney tubule cells form carbonic acid (H2CO3) from CO2 and water using carbonic anhydrase
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26
Q

Describe the renal control of [H+] and [HCO3-]. PART 2

A
  • The carbonic acid then dissociates into HCO3- and H+
  • Na+ moving down its concentration gradient from the tubular fluid into the cell provides energy for the secondary active secretion of H+ into the tubule lumen.
  • ATP provides energy for the primary active secretion of H+ from the cell into the lumen.
  • With each H+ that is secreted, one HCO3- enters the blood accompanied by Na+.
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27
Q

When are new HCO3- ions generated?

A

When H+ derived from the intracellular H2CO3 is secreted into the tubule and buffered in the tubular fluid by a non-bicarbonate buffer.

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28
Q

What are the effects of carbonic anhydrase inhibitors?

A
  • Inhibit the formation of H+ for the acidification of the tubular fluid.
  • Reabsorption of HCO3- is inhibited
  • Causes acidosis and loss of Na+
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29
Q

Describe the regeneration of bicarbonate. PART 1

A
  • Concentration of bicarbonate in the tubular fluid is equivalent to that of plasma.
  • If the bicarbonate were not reabsorbed, the buffering capacity of the blood would rapidly be depleted.
  • Reabsorption occurs in PCT
30
Q

Describe the regeneration of bicarbonate. PART 2

A
  • Filtered bicarbonate combines with secreted hydrogen ions forming carbonic acid.
  • Carbonic acid then dissociates to form CO2 and water - catalysed by carbonic anhydrase, which is present in the luminal brush border of the proximal tubular cells
31
Q

Describe the regeneration of bicarbonate. PART 3

A
  • CO2 readily crosses into the tubular cell down a concentration gradient.
  • Inside the cell, the CO2 recombines with the water, again under the influence of of carbonic anhydrase, to form carbonic acid.
  • The carbonic acid further dissociates to bicarbonate and hydrogen ions.
  • The bicarbonate passes back into the blood stream, whilst the H+ passes back into the tubular fluid in exchange for sodium.
32
Q

Describe the acidification of urine. PART 1

A
  • H+-ATPase pump becomes more important in the later part of the nephron in allowing H+ to be secreted against a substantial [H+] gradient.
  • Secretion of H+ is rate limiting and the pH can fall to as low as 4.5 in the collecting duct when the maximal rates of H+ secretion are achieved.
  • At this pH, the rate of H+ back diffusion equals the rate of H+ secretion. Urine becomes acidified
33
Q

Outline the role of the collecting tubule in urine acidification.

A
  • Bicarbonate concentration of the tubular fluid reaching the collecting tubule is low
  • Proton secretion can reduce the tubular fluid pH substantially.
  • Phosphate and ammonia are titrated and acid is formed for excretion.
34
Q

How can the amount of H+ secreted during HCO3- regeneration be estimated?

A

Measuring the amount of NaOH required to titrate the urine back to pH 7.4

35
Q

Describe phosphate as a buffer. PART 1

A
  • Poor buffers in the ECF because they are low in concentration.
  • Filtered at the glomerulus and the filtered load of phosphate exceeds its reabsorptive Tm, so the excess phosphate becomes concentrated in its progress along the tubule. - Good buffer in tubular fluid
  • Large amount reabsorbed in the proximal tubules, so it is not present in very high quantities.
36
Q

Describe phosphate as a buffer. PART 2

A
  • pK is 6.8, close to the pH of the filtrate
  • Acceptance of a proton still leaves it with one negative charge.
  • Remains lipid-insoluble and cannot diffuse back into the blood carrying protons with it.
37
Q

Where are the largest amounts of carbonic anhydrase found?

A

Intercalated cells of the distal tubule and the collecting duct

38
Q

Where is there no carbonic anhydrase?

A

Luminal brush border

39
Q

What transporter protein is used for bicarbonate transport?

A

Secondary active Cl-HCO3- exchanger.

40
Q

What does the regeneration of HCO3- occur by?

A

Secretion of H+ that reacts with nonbicarbonate buffers present in the glomerular filtrate.

41
Q

Describe ammonia as another buffer. PART 1

A
  • Ammonium ions are produced in several tubular segments from glutamine, which enters the tubular epithelial cells by an active mechanism.
  • 2 NH4 and 2 HCO3- molecules are produced from each glutamine molecule.
  • Glutamine is metabolised to NH3 and an α-ketoglutarate ion, which is further metabolised to CO2 and H2O.
42
Q

Describe ammonia as another buffer. PART 2

A
  • Hydrated to form H+ and HCO3- by carbonic anhydrase.
  • H+ combines with the NH3, forming NH4+, which is secreted into the lumen by a sodium-driven secondary active antiporter.
43
Q

List the three stages of urine buffering and the reinforcement of plasma bicarbonate concentration.

A
  • reabsorption of bicarbonate
  • formation of titratable acid phosphate
  • ammonia secretion which creates new bicarbonate
44
Q

Describe the role of the respiratory system.

A
  • Regulated by the H+ concentration of the CSF (cerebrospinal fluid) in the chemosensitive area of the medulla.
  • Chemosensitive area doesn’t respond to plasma H+ directly because of the inability of charged ions to cross the blood-brain barrier.
  • CO2, however, can cross the barrier and then be hydrated to form H2CO3, which dissociates to produce H+ and HCO3-.
45
Q

What is the result of an elevated plasma PCO2?

A
  • Decreased CSF pH
  • Stimulates pulmonary ventilation
  • Increases respiratory excretion of CO2 - decreases the PCO2
  • Returns ECF pH towards the normal range of 7.35 to 7.45.
  • Opposite for decreased PCO2
46
Q

Where are peripheral chemoreceptors found?

A
  • Aortic arch
  • Carotid bodies
47
Q

How do chemoreceptors respond to decreased plasma pH?

A

Stimulating respiratory excretion of CO2

48
Q

How is pH regulated in red blood cells? PART 1

A
  • CO2 equilibrates rapidly across the RBC membrane.
  • In the RBC the high concentration of carbonic anhydrase facilitates the reaction of CO2 with H2O.
49
Q

How is pH regulated in red blood cells? PART 2

A
  • Dissociation of H2CO3 to HCO3- and H+
  • Buffering of H+ by haemoglobin
  • Subsequent exchange of HCO3- for CL- has a direct effect on the ECF HCO3- and PCO2 levels, and therefore on pH.
50
Q

Describe metabolic acidosis.

A

Low pH as a result of increased ECF [H+] or decreased ECF [HCO3-].

51
Q

What is metabolic acidosis caused by? For each cause, briefly state how acidosis is induced.

A
  • severe sepsis or shock, producing lactic acid
  • uncontrolled diabetes - overproduction of 3-OH-butyric acid and other ketoacids
  • diarrhoea, leading to the loss of HCO3- from the GI tract
52
Q

Describe integrated renal and pulmonary compensation for metabolic acidosis. PART 1

A
  • In the ECF/ICF buffering system, the [HCO3-] falls as it is used to mop up the H+.
  • Rise in [H+]/decreased pH stimulates respiration by acting on the peripheral chemoreceptors to cause hyperventilation and expel more CO2.
  • Respiratory compensation allows the pH to return towards normal because the ratio of HCO3 to CO2 rises.
53
Q

Describe integrated renal and pulmonary compensation for metabolic acidosis. PART 2

A
  • Buffering and hyperventilation are not fully effective in preventing a rise in [H+]
  • [H+] remains raised throughout the body.
  • Renal compensation for metabolic acidosis involves the maximal conservation of filtered HCO3- and the increased regeneration of new bicarbonate.
  • Kidney stimulates H+ secretion to increase HCO3- reabsorption.
54
Q

Describe integrated renal and pulmonary compensation for metabolic acidosis. PART 3

A
  • Over days, the kidney (except in renal failure) may be able to correct the disturbance by excreting the excess H+.
  • Plasma [H+] returns to normal and ventilation is also normalised.
  • Ammonium secretion also plays a major role in renal generation of new HCO3-.
55
Q

Describe metabolic alkalosis.

A
  • Alkaline urine with bicarbonate in it.
    → Increase in ECF HCO3-
    → Decrease in ECF H+
56
Q

How do diuretics such as frusemide and thiazide contribute to alkalosis?

A
  • Inhibit carbonic anhydrase
  • Interfere with reabsorption of chloride and sodium in the renal tubules.
  • Urinary losses of chloride exceed those of bicarbonate.
  • Also volume-depleted (increasing aldosterone levels) and have a low dietary chloride intake (‘salt restricted’ diet).
57
Q

What condition is common in alkalosis patients?

A

Hypokalaemia

58
Q

Describe the integrated renal and pulmonary compensation for metabolic alkalosis. PART 1

A
  • H+ in the blood is used up in trying to reduce an increase in bicarbonate ions, and the fall in H+ reduces the stimulation of peripheral chemoreceptors
  • Ventilation is reduced
  • Less CO2 is expelled, so [CO2] rises.
59
Q

Describe the integrated renal and pulmonary compensation for metabolic alkalosis. PART 2

A
  • More H+ is generated and [HCO3-] rises further.
  • pH returns to normal because the ratio of HCO3-:CO2 falls towards normal.
60
Q

How do the kidneys help remove the inhibitory effect on ventilation?

A
  • Rise in pH in the tubule cells reduces H+ secretion and HCO3- reabsorption
  • Allows the plasma [H+] to rise and correct the plasma HCO3-
61
Q

What is it about plasma that controls pH?

A

→ Presence of buffers that are effective in vivo

62
Q

What is the equation for the bicarbonate system?

A

→ H+ + HCO3- ⇌ H2CO3 ⇌ CO2 + H2O

63
Q

What is the equation for the phosphate system?

A

→ H+ + HPO4 2- ⇌ H2PO4-

64
Q

What is pK?

A

→ The equilibrium point of a buffer
→ Where it most strongly resists changes in pH

65
Q

Which buffer is theoretically better and why?

A

→ Phosphate
→because the PK lies within the body pH ranges

66
Q

What are the 2 ways H+ gets into urine?

A

→ H+ ATPase
→ while Na+ moves in H+ moves out

67
Q

What happens to the HCO3- in tubular cells?

A

→ diffuses out and goes back into blood
→ Via a symporter with Na+ ions

68
Q

Where is most HCO3- reabsorbed?

A

→ 85-90% at the proximal tubule

69
Q

What can bicarbonate reabsorption also be stimulated by?

A

→ angiotensin II

70
Q

What is the pH like in the DCT and why?

A

→H+ ATPase pumps out the H+
→ DCT has a lower pH
→ HCO3- is low because it has been reabsorbed and H+ needs to react with other buffers

71
Q

What is the fate of H+ with phosphate in intercalated cells?

A
  • Carbonic acid dissociates into H+ and HCO3-
  • H+ is secreted via ATPase (aldosterone sensitive)
  • Reacts with phosphate andbecomes H2PO4-
  • Excreted into urine
  • HCO3- reabsorbed with a HCO3- / Cl antiporter
72
Q

What is metabolic alkalosis caused by?

A

→ Excessive diuretic use
→ Vomiting - loss of H+
→ Antacids
→ Hypokalemia

SGUL - Physiology 1 (68 decks)

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