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Year 2 - BRS > 9.1 - Renal regulation of water and acid-base balance > Flashcards

9.1 - Renal regulation of water and acid-base balance Flashcards

1
Q

What is osmosis?

A

Flow of water from area of low solute concentration to area of high solute concentration across a semi-permeable membrane

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2
Q

What is the driving force for osmosis?

A

Osmotic (AKA oncotic) pressure - depends on the number of solute particles (not the size)

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3
Q

What is the difference between osmolarity and osmolality?

A
  • osmolarity - amount per L of solvent (calculated)
  • osmolality - amount per kg of solvent (measured)
  • in practice, they are very similar
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4
Q

How do you calculate osmolarity?

A

Osmolarity (Osm/L or mOsm/L) = concentration x no. of dissociated particles

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5
Q

Calculate the osmolarity for 100 mmol/L glucose and 100 mmol/L NaCl.

A
  • osmolarity for glucose = 100 x 1 = 100 mOsm/L
  • osmolarity for NaCl = 100 x 2 = 200 mOsm/L –> this is because NaCl’s dissociated particles is both Na+ and Cl-
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6
Q

What % of body weight is fluid?

A

60%

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7
Q

Describe the body’s fluid distribution in different compartments (in %).

A
  • 2/3 intracellular fluid
  • 1/3 extracellular fluid
    • 1/4 intravascular (plasma in bloodstream)
    • 3/4 extravascular:
    • 95% interstitial fluid (surrounds and bathes cells)
    • 5% transcellular fluid (including CSF, peritoneal fluid)
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8
Q

What are some ways of unregulated water loss? (4)

A
  • sweat
  • faeces
  • vomit
  • water evaporation from respiratory lining and skin
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9
Q

What is the regulated way of water loss?

A

Renal regulation - urine production (through positive and negative water balance)

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10
Q

Describe the steps for positive water balance.

A
  • high water intake
  • increases ECF volume –> lowers [Na+] –> lowers osmolarity
  • kidney produces large volume hypo-osmotic urine to lose water
  • osmolarity normalises
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11
Q

Describe the steps for negative water balance.

A
  • low water intake
  • lowers ECF volume –> increases [Na+] –> increases osmolarity
  • kidney produces small volume hyper-osmotic urine (compared to plasma)
  • osmolarity normalises
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12
Q

What happens in the PCT in terms of water (and sodium) reabsorption?

A

67% of water (and NaCl) is reabsorbed at PCT

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13
Q

What happens in the thin descending loop of Henle in terms of water/NaCl reabsorption?

A
  • 15% water passively reabsorbed (permeable to water)
  • NaCl is not reabsorbed (impermeable to NaCl)
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14
Q

What happens in the thin and thick ascending loop of Henle in terms of water/NaCl reabsorption?

A
  • thin ascending - NaCl passively reabsorbed
  • thick ascending - NaCl actively reabsorbed
  • water cannot be reabsorbed (impermeable to water)
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15
Q

What happens at the DCT and collecting duct in terms of water reabsorption?

A
  • variable amount of water reabsorbed depending on body’s needs
  • action of ADH kicks in to modulate aquaporin channels to vary amount of water reabsorption
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16
Q

How and why does water reabsorption occur passively in the kidney?

A
  • water is reabsorbed through the passive process of osmosis and requires a gradient
  • this is done as the body does not want to spend too much energy absorbing water
  • the medullary interstitium needs to be hyperosmotic for water reabsorption to occur from loop of Henle and collecting duct
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17
Q

What is the process of countercurrent multiplication?

A
  1. filtrate arrives at loop of Henle - isoosmotic with the plasma
  2. active salt reabsorption - thick ascending LoH
  3. passive water reabsorption - thin descending LoH
  4. process repeats again and again –> gradient down medulla
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18
Q

What is the detailed, step-by-step process of countercurrent multiplication?

A
  1. filtrate arrives at LoH at 300 mOsm/L = iso-osmotic with plasma
  2. active salt reabsorption in thick ascending LoH - salt into interstitium so osmolarity in tubular filtrate of ascending LoH decreases 300–>200 and medullary interstitium osmolarity rises 300–>400
  3. passive water reabsorption in descending LoH - since interstitium osmolarity is higher, water from descending loop moves into interstitium via osmosis to equilibrate the osmolarity = causes descending loop osmolarity to increase 300–>400
  4. repeat!! more filtrate arrives at descending loop (at 300 mOsm/L) and pushes rest of filtrate along loop, changing the osmolarities along the loop
  5. active salt reabsorption (thick ascending LoH) = increased osmolarity interstitium, decreased osmolarity ascending LoH
  6. passive water reabsorption (descending LoH) - water from descending loop into interstitium so descending osmolarity increases until it is equal to interstitium osmolarity
  7. gradient in medullary interstitium already developing from outer medulla to inner medulla
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19
Q

Why is the process called countercurrent multiplication?

A
  • countercurrent since filtrate flows in opposite directions in ascending and descending loops
  • multiplication since process repeats again and again to achieve a proper gradient down medulla
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20
Q

How does countercurrent multiplication help us?

A

Helps water passively reabsorb into body without spending a lot of energy

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21
Q

In collecting duct cells, what side does the basolateral cell membrane face?

A

The side with the blood capillaries

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22
Q

In collecting duct cells, what side does the apical cell membrane face?

A

The lumen of the collecting duct (the inside of the tube)

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23
Q

What is the vasa recta?

A

A series of blood capillaries that surround nephron mainly in medullary region

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24
Q

What happens to urea after being filtered through Bowman’s capsule (urea recycling mechanism)?

A
  1. travels through nephron and reaches collecting duct
  2. through UT-A1 and UT-A3 transporters, the urea is transported out into medullary interstitium (concentration of urea in interstitium can be has high as 600mmol/L)
  3. urea in interstitium can now either:
    - go into vasa recta through UT-B1 transporter which surrounds nephron so urea circulates medullary region (instead of leaving region - needed here to maintain concentration gradient)
    - go into descending LoH through UT-A2 transporter where it goes back through nephron and some exits collecting duct back into interstitium again (recycling)
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25
Q

What is the purpose of recycling urea?

A
  • increases interstitium osmolarity:
  • allows urine concentration to occur - as water moves from collecting duct into interstitium
  • urea excretion requires less water - when filtrate reaches inner medullary collecting duct it equilibrates with urea in inner medullary interstitium (as high as 600mmol/L, so concentration of urea in collecting duct could also go that high) = this urea then requires less water to excrete
  • both of these methods ultimately help us to conserve water in our body
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26
Q

What does vasopressin do to the urea recycling mechanism?

A

Vasopressin boosts UT-A1 and UT-A3 numbers - increases collecting duct permeability for urea to aid urea reabsorption and recycling

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27
Q

What is vasopressin?

A

Protein with length of 9 amino acids

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28
Q

What is the main function of vasopressin?

A

Promote water reabsorption from collecting duct

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29
Q

What are two other functions of vasopressin?

A
  • helps in urea reabsorption (boost UT-A1 and UT-A3)
  • helps in sodium reabsorption (increase Na+K+2Cl-, Na/Cl and Na+ transporters)
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30
Q

Where is vasopressin produced and stored?

A

Produced in hypothalamus by neurons in supraoptic and paraventricular nuclei, then stored in posterior pituitary

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31
Q

What factors stimulate ADH production and release? (5)

A
  • increase in plasma osmolarity
  • hypovolaemia
  • reduced blood pressure
  • angiotensin II
  • nicotine
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32
Q

What factors inhibit ADH production and release? (5)

A
  • reduction in plasma osmolarity
  • hypervolaemia
  • increased blood pressure
  • ethanol
  • atrial natriuretic peptide
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33
Q

What detects change in osmolarity to change ADH release?

A

Osmoreceptors

34
Q

What is plasma osmolality in a healthy adult?

A

275-290 mOsm/kg H2O

35
Q

How much of a change in blood pressure is needed for baroreceptors to detect it?

A

5-10% change, information transmitted to hypothalamus

36
Q

Describe how ADH works at the collecting duct.

A
  1. ADH binds to V2 receptor on basolateral membrane of principal cells of collecting duct
  2. this triggers G-protein mediated signal cascade in cell
  3. this activates protein kinase A
  4. this increases secretion of aquaporin 2 channels in vesicle-form which are inserted into apical cell membrane
  5. water then absorbed through aquaporin 2 into cell then through aquaporin 3 and 4 in basolateral membrane into blood vessel
  6. overall ADH up/downgrades both AQP2 (apical membrane) and AQP3 (basolateral membrane) numbers as required
37
Q

What is diuresis?

A

Increased excretion of dilute urine

38
Q

Describe the mechanism of diuresis in the nephron.

A
  1. little/no ADH
  2. blood filtered at Bowman’s capsule and filtrate enters nephron
  3. filtrate passes into PCT where 67% of water and 67% NaCl are reabsorbed into body
  4. isoosmotic fluid reaches descending LoH where water passively moves into interstitium
  5. fluid enters ascending LoH where NaCl is reabsorbed into interstitium leaving hypoosmotic fluid
  6. this hypoosmotic fluid enters DCT where AQP2 channels are absent since there is negligible ADH, but NaCl is actively reabsorbed again - makes fluid even more hypoosmotic
  7. hypoosmotic fluid enters collecting duct where more NaCl is reabsorbed
  8. when it reaches inner medullary region, some water is also reabsorbed since some aquaporins are always present and water moves via other pathways e.g. paracellularly between epithelial cells
  9. this leaves hypoosmotic fluid –> urine 50 mOsm/L vs 300 mOsm/L plasma
39
Q

At a cellular level, how is NaCl reabsorbed in thick ascending limb?

A
  1. Na+K+ATPase pumps Na+ into blood creating low [Na+] in cell
  2. through Na+K+2Cl- symporter, Na+ moves from high [Na+] in tubular fluid to low [Na+] in cell = releases energy, which K+ and Cl- use to get transported into cell
  3. once in cell, K+ and Cl- exit into blood through K+Cl- symporter (Cl- also leaves via Cl- channel, some K+ also recycled from apical membrane)
40
Q

At a cellular level, how is NaCl reabsorbed in the DCT?

A
  1. through Na+K+ATPase, Na+ pumped into blood
  2. NaCl enters cell from tubular filtrate through Na+Cl- symporter
  3. KCl leaves cell into blood via K+Cl- symporter (Cl- also leaves via Cl- channel)
41
Q

At a cellular level, how is NaCl reabsorbed in the collecting duct (principal cell)?

A

Through Na+ channels and Na+K+ATPase pump

42
Q

What is antidiuresis?

A

Concentrated urine excreted in low volumes - could be due to dehydration or disease

43
Q

Describe the mechanism of antidiuresis in the nephron.

A
  1. high amount of ADH
  2. blood filtered at Bowman’s capsule and filtrate enters nephron
  3. filtrate passes into PCT where 67% of water and 67% NaCl are reabsorbed into body
  4. isoosmotic fluid reaches descending LoH where water passively moves into interstitium
  5. fluid enters ascending LoH where NaCl is reabsorbed into interstitium leaving hypoosmotic fluid
  6. in DCT then collecting duct, NaCl is again actively reabsorbed
  7. in DCT and collecting duct, AQP2 are present so water is reabsorbed
  8. in collecting duct there is a gradient of osmolarity which increases as you go down = more water is reabsorbed from outer–>inner medullary regions
  9. by the time urine leaves kidneys, the osmolarity could be as high as 1200 mOsm/L, and urine volume as low as 500ml per day
44
Q

How does ADH support Na+ reabsorption? (3)

A
  • thick ascending limb: increased Na+K+2Cl- symporter
  • DCT: increased Na+Cl- symporter
  • collecting duct: increased Na+ channel
45
Q

What is AVP deficiency (central diabetes insipidus)?

A
  • decreased/negligent production and release of ADH
  • genetic or acquired due to e.g. infection or trauma
46
Q

What are the clinical features AVP deficiency? (2)

A
  • polyuria
  • polydipsia
47
Q

What is the treatment for AVP deficiency?

A

External ADH (desmopressin)

48
Q

What is AVP resistance (nephrogenic diabetes insipidus)?

A
  • correct amount of ADH produced but something wrong at collecting duct e.g:
  • fewer/mutant AQP2
  • mutant V2 receptors
49
Q

What are the clinical features AVP resistance? (2)

A
  • polyuria
  • polydipsia
50
Q

What is the treatment for AVP resistance?

A

Thiazide diuretics - reduce filtration rate at Bowman’s capsule so less blood filtered and less urine produced

51
Q

What is syndrome of inappropriate ADH secretion (SIADH)?

A

Increased production and release of ADH

52
Q

What are the clinical features of SIADH? (3)

A
  • hyperosmolar urine
  • hypervolaemia
  • hyponatraemia
53
Q

What is the treatment for SIADH?

A

Non-peptide inhibitor of ADH receptor (Conivaptan and Tolvaptan)

54
Q

How are acids and bases added to our body?

A

Through diet and metabolism

55
Q

What happens to the acids and bases in our body?

A
  • a lot of base is excreted in faeces
  • net addition of metabolic acid to our fluid compartments (50-100 mEq/day)
  • important to neutralise this excess metabolic acid or it will impact blood pH
56
Q

How is excess metabolic acid neutralised and what are some equations showing this?

A
  • by different buffer systems, mainly bicarbonate buffer system
  • this produces sodium salts + CO2 + water
  • H2SO4 + 2NaHCO3 <–> Na2SO4 + 2CO2 + 2H2O
  • HCl + NaHCO3 <–> NaCl + CO2 + H2O
57
Q

What is the role of the kidneys in acid-base neutralisation?

A
  • secretion and excretion of H+ (if body secretes more H+ than metabolic acids coming in = alkalosis, secretes less H+ = acidosis)
  • reabsorption of HCO3- (100%)
  • production of new HCO3-
58
Q

How much bicarbonate do we have in our ECF and why is this important?

A
  • ECF [HCO3-] = 350mEq OR 24mEq/L
  • if body continuously used HCO3- to neutralise metabolic acids without replenishing it, HCO3- would run out in a week
59
Q

What equation is most important in acid-base balancing?

A

CO2 + H2O <-(carbonic anhydrase)-> H2CO3 <–> H+ + HCO3-

(Highlights bicarbonate ion buffer system is unique and managed by both lungs through CO2 and kidneys through HCO3-)

60
Q

What is the Henderson-Hasselbalch equation?

A

pH = pK + log(HCO3- / alphaPCO2)

[H+] = (24xPCO2) / [HCO3-]

61
Q

What does the Henderson-Hasselbalch equation show?

A
  • the role that PCO2 and [HCO3-] plays on blood pH
  • if PCO2 rises, this increases [H+] –> acidosis, and if it falls it causes an alkalosis
  • inverse relationship of [H+] with [HCO3-] –> if [HCO3-] rises it causes alkalosis and if it falls acidosis
62
Q

What is an acid-base disorder due to changes in PCO2 called?

A

Respiratory disorder

63
Q

What is an acid-base disorder due to changes in [HCO3-] called?

A

Metabolic disorder

64
Q

How much HCO3- is reabsorbed in different parts of the nephron?

A
  • 80% in PCT
  • 10% in thick ascending LoH
  • 6% in DCT
  • 4% in collecting duct
  • (100% reabsorption)
65
Q

How is HCO3- reabsorbed at PCT?

A
  1. CO2 enters cell from tubular fluid by diffusion
  2. CO2 + H2O in presence of carbonic anhydrase to form H+ and HCO3-
  3. H+ can leave cell into tubular fluid through two methods:
    • Na+H+ antiporter (NHE3)- downward energy from Na+ travel into cell from tubular fluid, H+ moves into tubular fluid
    • H+ATPase pump (V-ATPase) - pumps H+ out
  4. HCO3- is reabsorbed from cell into blood through Na+HCO3- symporter (NBC1 - 1Na, 3HCO3)
  5. H+ that left cell into tubular fluid then reacts with HCO3- in fluid to form H2CO3 which splits into H2O and CO2, the CO2 of which moves back into the cell to repeat from step 1)
66
Q

How is HCO3- reabsorbed at thick ascending loop of Henle?

A

Very similar to reabsorption in PCT

67
Q

What do alpha intercalated cells do?

A

HCO3- reabsorption and H+ secretion

68
Q

What do beta intercalated cells do?

A

HCO3- secretion and H+ reabsorption

Think BETA = BYE BYE BICARBONATE

69
Q

How is HCO3- reabsorbed at alpha intercalated cells of DCT and collecting duct?

A
  1. H2O + CO2 –> H+ + HCO3-
  2. HCO3- moves into blood via Cl-HCO3- antiporter
  3. H+ moves into tubular fluid via H+ATPase pump and H+K+ATPase, where it combines with HCO3- to form H2CO3, which splits into H2O + CO2, the CO2 which diffuses back into cell to do step 1)
70
Q

How is HCO3- secreted (and H+ reabsorbed) at beta intercalated cells of DCT and collecting duct?

A
  1. H2O + CO2 –> H+ + HCO3-
  2. Cl-HCO3- antiporter secretes HCO3- into tubular fluid (to excrete in the case of alkalosis)
  3. H+ is reabsorbed into blood via H+ATPase pump
71
Q

How is new HCO3- produced at the PCT?

A
  1. one glutamine molecule gives 2 NH4+ molecules and 1 divalent ion (A2-) which gives rise to 2 HCO3-
  2. we do not want the 2 NH4+ to enter blood or they will go to liver and become NH3 + H+, which requires 1 HCO3- to neutralise and will nullify the effect of the 2 HCO3- produced from splitting glutamine
  3. the 2 NH4+ is excreted into tubular fluid through 2 methods:
    • Na+H+ antiporter (NH4+ substitutes in place of H+)
    • turns into NH3, moves into tubular fluid, combines with H+ –> NH4+ reformed
  4. NH4+ then excreted from body, leaving us with net gain of 2 HCO3-
72
Q

How is new HCO3- produced at DCT and collecting duct?

A
  • in alpha intercalated cell, when H+ is secreted into tubular fluid, instead of being neutralised by a HCO3- it is neutralised by a non-bicarbonate buffer (phosphate ion)
  • H+ + HPO42- –> H2PO4-
  • by using a non-bicarbonate buffer, the HCO3- that is produced in the alpha intercalated cell and reabsorbed into blood is a net gain of HCO3-
73
Q

How is metabolic acidosis characterised?

A

Decrease in [HCO3-] = decrease in pH

74
Q

What is the compensatory response to metabolic acidosis?

A
  • increased (hyper)ventilation kicks in first –> PCO2 down so [H+] down
  • increased [HCO3-] reabsorption and production to compensate
75
Q

How is metabolic alkalosis characterised?

A

Increase in [HCO3-] = increase in pH

76
Q

What is the compensatory response to metabolic alkalosis?

A
  • decreased ventilation which kicks in first –> PCO2 increases so H+ increases
  • increased [HCO3-] excretion to compensate
77
Q

How is respiratory acidosis characterised?

A

Increase in PCO2 = decrease in pH

78
Q

What is the compensatory response to respiratory acidosis?

A
  • acute - intracellular buffering - increased CO2 enters cell = increased H+ + HCO3-, H+ neutralised by cellular proteins = net gain of HCO3- = transported back into blood to increase pH
  • chronic - increased [HCO3-] reabsorption and production (along with increased H+ and NH4+ excretion)
79
Q

How is respiratory alkalosis characterised?

A

Decrease in PCO2 = increase in pH

80
Q

What is the compensatory response to respiratory alkalosis?

A
  • acute - intracellular buffering - shifting HCO3- buffer reaction towards more carbonic acid production so less HCO3- produced
  • chronic - reduced [HCO3-] reabsorption and production

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