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YEAR 1 - Physiology and Pharmacology (Anton) > 12. Body Fluids (TT) > Flashcards

12. Body Fluids (TT) Flashcards

1
Q

What organ is involved in acid-base homeostasis?

A

Kidneys (a lot of the material is related to chapter 11 of the spec)

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2
Q

What ion is involved in buffering blood pH?

A

Bicarbonate (HCO3-)

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3
Q

What is the bicarbonate ion concentration in plasma?

A

25mmol/L

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4
Q

How many moles of bicarbonate are filtered out into the tubular fluid by the kidneys each day?

A
  • 5mol
  • This is a very large amount compared to the 25mmol/L concentration of bicarbonate in the blood, implying that the kidneys must be reabsorbing a large amount of bicarbonate back into the blood.
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5
Q

What are the roles of the kidney in acid-base homeostasis of the blood?

A

The kidneys regulate HCO3- concentration by:

  1. Reabsorption of filtered HCO3- (back from the tubular fluid)
  2. Generation of new HCO3- (that has been used in buffering non-volatile acids)
  3. Distal tubular secretion of HCO3-
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6
Q

The kidneys are involved in reabsorption of HCO3- from the tubular fluid and in generation of new HCO3-. What process do these processes rely on?

A

H+ secretion into the tubular fluid

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7
Q

Where does each of the kidney’s three processes involved in maintaining acid-base homeostasis occur?

A
  • Reabsorption of filtered HCO3- -> Proximal tubule + Loop of Henle
  • Generation of new HCO3- -> Distal tubule + Collecting duct
  • Distal tubular secretion of HCO3- -> Distal tubule
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8
Q

What pH range do the kidneys attempt to maintain the blood at?

A

7.36-7.44

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9
Q

What are volatile acids? What are they produced by?

A

Volatile acids:

  • Carbon dioxide
  • Carried in blood as the potential acid H2CO3
  • Volatile means it can be excreted via the lungs
  • Produced by the metabolism
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10
Q

What are non-volatile acids? What are they produced by?

A
  • Acids produced by metabolism of amino acids and phopshate
  • They are essentially the blood acids that are not produced by CO2
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11
Q

How is CO2 (a volatile acid) carried in the blood?

A

As H2CO3.

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12
Q

What are non-volatile acids produced by and what is their production offset by?

A

Produced by the metabolism of:

  • Amino acids -> Cationic and sulphur containing
  • Phosphate

Offset by HCO3- production by the metabolism of:

  • Amino acids -> Anionic
  • Organic ions
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13
Q

What type of non-volatile acid is produced by the metabolism of:

  • Sulphur-containing amino acids
  • Cationic amino acids
  • Phosphate
A
  • Sulphur-containing amino acids -> H2SO4
  • Cationic amino acids -> HCl
  • Phosphate -> H2PO4-
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14
Q

Compare how metabolism of anionic and cationic amino acids affects non-volatile acid production.

A
  • Cationic -> Produce non-volatile acids
  • Anionic -> Produce HCO3- (offsetting non-volatile acid production)
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15
Q

After accounting for non-volatile acid formation and its offset by HCO3- production, what is the net non-volatile acid production?

A

70mmol/day (or mEq/day -> Milliequivalents)

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16
Q

What is a shorthand way of writing “non-volatile acids”?

A

NVAs

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17
Q

What must happen to NVAs and why?

A
  • They must be buffered and then excreted
  • This is done by reacting them with HCO3-
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18
Q

What is produced when a HCO3- reacts with an NVA?

A
  • Salt
  • Carbon dioxide
  • Water

For example:

HCl + NaHCO3 -> NaCl + CO2 + H2O

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19
Q

What type of buffer system is the HCO3-/CO2 buffer system that is used to buffer NVAs? Why?

A
  • It is an open system
  • This is because the products of the buffer reacting with the NVA are not confined to the body, since the CO2 produced can leave via the lungs
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20
Q

Write the Henderon-Hasselbalch equation.

A
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21
Q

Write the Henderson-Hasselbalch equation for the HCO3-/CO2.

A

pH = 6.1 + log([HCO3-]/0.03PCO2)

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22
Q

What two organs is the blood pH controlled by? How?

A
  • Kidneys -> Vary the HCO3- concentration
  • Lungs -> Excrete CO2 from the system

Since both HCO3- and CO2 are in the Henderson-Hasselbalch equation for the HCO3-/CO2 buffer system, these two organs control the blood pH.

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23
Q

How much NVA can 70mEq of HCO3- neutralise?

A

70mEq

H+ + HCO3- -> CO2 + H2O

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24
Q

What is the result of HCO3- reacting with NVAs and what is the response to this?

A
  • The blood becomes less acidic
  • But the HCO3- is gradually used up because the CO2 produced can be lost at the lungs
  • Therefore, the kidneys need to regenerate HCO3-
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25
Q

What is the driving force for reabsorption of filtered HCO3- from the tubular fluid and regeneration of new HCO3-?

A

H+ secretion into the tubular fluid.

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26
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).

27
Q

Is most H+ in the tubular fluid used to regenerate HCO3- or reabsorb it?

A

Reabsorb it.

28
Q

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

A

All along the renal tubule.

29
Q

Is all H+ in the tubular fluid used to reabsorb and regenerate new HCO3-? How is this controlled?

A
  • No, some is excreted
  • They are excreted mostly with urinary buffers
30
Q

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

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
31
Q

Draw the model for how H+ secretion into the renal tubule occurs.

A
  • CO2 and H2O react in epithelial cells, which is catalysed by carbonic anhydrase
  • HCO3- -> Pass across basolateral membrane into interstitial fluid and then blood
  • H+ -> Pass across apical membrane into the lumen

Depending on conditions in the renal tubule, this model can be used to both reabsorb bicarbonate ions, and to regenerate bicarbonate ions and excrete H+ in the urine.

32
Q

Describe where reabsorption HCO3- from the renal tubule occurs and the mechanism by which this happens.

A

In the proximal tubule mostly and loop of Henle (and somewhat in the distal tubule and collecting duct):

  • H+ ions are secreted into the tubular fluid by Na+/H+ exchange (due to large sodium gradient) and H+-ATPase
  • The H+ ions combine with HCO3- in the lumen to form carbonic acid
  • Carbonic acid (H2CO3) can dissociate into carbon dioxide and water under the action of carbonic anhydrase on the apical membrane
  • The CO2 can diffuse into the cell and react with water to reform H2CO3
  • Cytosolic carbonic anhydrase can reform HCO3- and H+
  • H+ can be returned to the lumen, restarting the process
  • HCO3- can move across the basolateral membrane into the interstitial fluid by:
    • HCO3-/Cl- exchanger
    • Na+/3HCO3- symporter (more important)
33
Q

By what transporters is H+ secreted into the renal tubule?

A
  • Mostly by the Na+/H+ exchanger, driven by a sodium gradient
  • Also by a H+-ATPase
34
Q

How is HCO3- moved across the basolateral membrane of epithelial cells in the renal tubule? What is usual about this?

A
  • HCO3-/Cl- exchanger
  • Na+/3HCO3- symporter (more important)

This is unusual because the symporter is moving sodium ions against their concentration gradient, which is why 3 bicarbonate ions are required per sodium.

35
Q

Describe where HCO3- is regenerated in the renal tubule and the mechanism by which this happens.

A

This happens mostly in the collecting duct and distal tubule. The mechanism is essentially the same as for HCO3- reabsorption, except no HCO3- is reabsorbed and there is no sodium-dependent processes:

  • H+ is secreted into the tubule by a H+-ATPase (with no help from the Na+/H+ exchanger since no sodium reabsorption is occuring at this point in the tubule)
  • In this case, however, H+ does not combine with HCO3-, since very little is present at this late point in the renal tubule
  • Instead, H+ is buffered by PO43- or by NH3 (or it acidifies the tubule fluid)
  • Inside the intercalated epithelial cells, cytosolic carbonic anhydrase forms HCO3- and H+ from water and CO2
  • This newly generated HCO3- can move across the basolateral membrane into the interstitial fluid by an HCO3-/Cl- exchanger
  • Na+/3HCO3- symporter is not involved because no sodium reabsorption is occuring at this point in the renal tubule

Note: The hydrogen isn’t really doing anything here, it is just being buffered.

36
Q

How much CO2 is used in HCO3- regeneration?

A

The same amount as was formed by the original reaction of the HCO3- with an NVA.

37
Q

In which cells does HCO3- regeneration take place?

A

Type A intercalated cells of the collecting duct (and distal tubule?)

38
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

39
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.

40
Q

What causes reabsorption of HCO3- in the early renal tubule and regeneration of HCO3- in the late renal tubule?

A
  • Firstly, HCO3- is all reabsorbed in the early renal tubule, so there is none left in the late tubule
  • Secondly, there is no sodium gradient across the epithelium in the late distal tubule (which is because there is no reabsorption of sodium here) and so the sodium-dependent processes do not occur.

Note: Ignore the middle part of the diagram.

41
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
42
Q

What are the main urinary buffers?

A
  • Phosphate
  • Ammonia
43
Q

Where does phosphate buffer come from, how much of it is available and how does it work as a urinary buffer?

A
  • Dietary in origin
  • So amount available is amount filtered minus that reabsorbed earlier in the tubule
  • Work by a two-step process:
    • H+ + PO43- -> HPO42-
    • H+ + HPO42- -> H2PO4-
44
Q

Where does ammonia buffer come from, how much of it is available and how does it work as a urinary buffer?

A
  • Synthesised within tubular cells from glutamine
  • Synthesis altered to reflect acid-base status: one of the main ways kidney responds to an acid load
  • H+ + NH3 -> NH4+
45
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
46
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-
47
Q

What happens to the products of ammoniagenesis in the proximal tubule cells?

A
  • Ammonia -> Diffuses across the apical membrane, before reacting with H+ ions to form ammonium
  • HCO3- -> Diffuses across the basolateral membrane
  • α-ketoglutarate -> Moves across the basolateral membrane via an exchanger that also brings PAH into the epithelial cell (PAH can be used as a marker of renal clearance)
48
Q

Describe the concept of diffusion trapping in the nephron.

A
  • After NH3 is synthesised in the epithelial cells of the proximal tubule, it diffuses into the lumen
  • The NH3 is converted to charged NH4+ using secreted H+
  • The pK is around 9, so at physiological pH the reaction is strongly to the right and there is lots of NH4+
  • This traps the ammonium in the lumen
  • As the luminal pH falls along the nephron, NH4+ is increasingly trapped

Some other points:

  • NH4+ may be generated from NH3 and H+ WITHIN tubule cells, then secreted by the Na+/H+ exchanger
49
Q

Where can ammonia be reabsorbed from the renal tubule after it is secreted there?

A
  • NH4+ may be reabsorbed in the TALH.
  • NH3 reforms in the more alkaline interstitial fluid, and diffuses back into the collecting duct where it is finally trapped by reacting it with H+.
  • It is then lost in the urine.
50
Q

Draw a graph to show bicarbonate reabsorption and excretion vary with plasma bicarbonate concentration.

A
51
Q

At what plasma bicarbonate concentration can the kidneys no longer reabsorb all of the bicarbonate from the tubular filtrate, so that some is excreted?

A

Around 20mmol/L

52
Q

Why are the kidneys not always able to reabsorb all of the bicarbonate from the tubular filtrate? What is the name for this?

A
  • Because the reabsorption is a carrier mediated process, meaning that there is a maximum rate of reabsorption possible
  • The maximum rate of reabsorption is the transport maxmimum (Tm)
53
Q

What is the general process that must be altered in order to change the rate of reabsorption of bicarbonate in the nephron?

A

H+ secretion into the lumen, because this is the driving force for the reabsorption of bicarbonate.

54
Q

How is H+ secretion into the lumen of the renal tubule (and therefore bicarbonate reabsorption) regulated?

A

H+ secretion is stimulated by:

  • Decreased plasma pH
  • Increased blood PCO2

This is due to:

  • In proximal tubule and TALH -> Upregulation of Na+/H+ exchanger
  • In collecting duct -> Insertion of H+-ATPase from vesicles

The result is that the Tm is changed and full reabsorption of bicarbonate is possible over a wider range of bicarbonate concentrations.

55
Q

Where does bicarbonate secretion into the renal tubule lumen happen?

A

Type B intercalated cells of the colleting duct

56
Q

Describe where and how secretion of bicarbonate into the renal tubule lumen occurs.

A

In the Type B intercalated cells of the collecting duct:

  • The same system is used as for regeneration of bicarbonate, except that the membrane proteins are reversed
  • The HCO3-/Cl- exchanger is on the apical membrane, while the H+-ATPase is on the basolateral membrane
  • Carbonic anhydrase converts water and CO2 into HCO3- and H+
  • However, this time the HCO3- moves into the tubule lumen, while H+ goes into the interstitial fluid (this is due to reversal of the membrane proteins)
57
Q

When is bicarbonate secretion into the renal tubule lumen useful?

A
  • In alkalosis
  • This is because H+ is moved into the interstitial fluid, meaning that the pH of the blood will drop
58
Q

Compare the location and reason for each of these processes occurring where they do:

  • Bicarbonate reabsorption
  • Bicarbonate regeneration
  • Bicarbonate secretion
A

Bicarbonate reabsorption:

  • Occurs most in the earliest part of the tubule -> PT, LOH
  • This is because there is enough bicarbonate in the lumen for this to happen, although the amount decreases along the tubule

Bicarbonate regeneration:

  • Occurs in the late parts of the tubule -> DT, CD
  • In type A intercalated cells
  • This happens because there is no bicarbonate left in the lumen, so it has to be generated by carbonic anhydrase in the epithelial cell
  • Allows response to acidosis

Bicarbonate regeneration:

  • Occurs in the late parts of the tubule -> DT, CD
  • In type B intercalated cells
  • This happens by the same process as bicarbonate regeneration, BUT the membrane proteins are on the opposite membranes, so bicarbonate is secreted into the tubule instead of the interstitial fluid
  • Allows response to alkalosis
59
Q

Describe and explain the relationship between potassium levels and pH.

A
  • Hyperkalaemia leads to acidosis
  • Acidosis also leads to hyperkalaemia
60
Q

Why does hyperkalaemia lead to acidosis?

A

Hyperkalaemia inhibits NH3 production and therefore H+ excretion (since NH3 is a urinary buffer that stops the urine becoming too acidic - CHECK THIS)

61
Q

Why does acidosis lead to hyperkalaemia?

A
  • Raised [H+] inhibits the basolateral Na+/K+-ATPase in the collecting duct and the apical membrane permeability to K+
  • This in turn reduces K+ secretion in the collecting duct
62
Q

What are the approximate daily intake values for sodium and potassium? [IMPORTANT]

A
  • Sodium = 2.4g
  • Potassium = 3g
63
Q

What are the 3 lines of defence against alkalosis/acidosis?

A
  • Buffers
  • Ventilatory mechanisms
  • Renal mechanisms
64
Q
A

YEAR 1 - Physiology and Pharmacology (Anton) (13 decks)

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