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Aneesha Flashcards BRS 2 > Renal regulation of water and acid base balance > Flashcards

Renal regulation of water and acid base balance Flashcards

1
Q

Define osmosis

A

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

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2
Q

What is the driving force behind osmosis?

A

Osmotic/ oncotic pressure which depends on number (NOT SIZE) of solute particles

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3
Q

How do we calculate osmolarity?

A

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

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4
Q

How much of body weight is fluid?

A

60%

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5
Q

Describe the body’s fluid distribution in different compartments

A

2/3 intracellular fluid (ICF)

1/3 extracellular fluid (ECF)
Of this,
-1/4 is intravascular (plasma in bloodstream)
-3/4 is extravascular. of this
-95% is interstitial fluid - (that surrounds and bathes cells)
- 5% of this is transcellular fluid (including cerebrospinal fluid, peritoneal fluid)- very important though

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6
Q

What are the 2 broad categories by which water loss occurs?

A

Regulated
Unregulated

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7
Q

What are ways of unregulated water loss?

A

Sweat
Water evaporation from respiratory lining and skin
Faeces
Vomit

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8
Q

What is the regulated way of losing water?

A

Renal regulation through urine production

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9
Q

What are the 2 types of water balance involved in renal regulation?

A

Positive water balance
Negative water balance

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10
Q
  • Describe the steps for positive water balance
A

High water intake → increases ECF volume (that is the first place water goes when it enters body) → lowers Na+ conc → lowers osmolarity → kidney produces hypoosmotic urine to lose water → osmolarity of ECF normalises

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11
Q

Describe the steps for negative water balance

A

Low water intake → lowers ECF volume → increases Na+ conc → increases osmolarity → leads to hyperosmotic urine production (compared to plasma) → osmolarity of ECF normalises

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12
Q

How much water is reabsorbed at the PCT?

A

67%

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13
Q

What substances are reabsorbed in the descending limb of the loop of Henle?
Does this occur actively or passively?

A
  • Water passively reabsorbed (15%)
  • NaCl isn’t reabsorbed
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14
Q

What substances are reabsorbed in the ascending limb of the loop of Henle?
Does this occur actively or passively?

A
  • NaCl is reabsorbed passively in the thin ascending limb
  • NaCl is also reabsorbed actively in the thick ascending limb
  • Water can’t be reabsorbed
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15
Q

What substances are reabsorbed in the DCT and collecting duct?
How is this mediated?

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

When it comes to water reabsorption from kidney, how and why is it done passively?

A

Water is reabsorbed from the kidney through the passive process of osmosis.
This requires a gradient.
Therefore the medullary interstitium needs to be hyperosmolar to allow the passive reabsorption of water from the loop of Henle and collecting duct.
This occurs because the body doesn’t want to expend too much energy on water reabsorption

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17
Q
  • Describe how the process of countercurrent multiplication works in steps
A

Filtrate arrives at loop of Henle at 300 mOsm/L which is isoosmotic with the plasma (300 mOsm/L too)

2) Active salt reabsorption occurs- in the thick ascending loop, salt is actively reabsorbed into interstitium so osmolarity in tubular filtrate of ascending loop decreases 300 → 200 and medullary interstitium osmolarity rises 300 → 400 because salt is being added

3) Passive water reabsorption occurs- since interstitium osmolarity is higher, water from descending loop moves into interstitium through osmosis to equilibrate the osmolarity- this causes descending loop osmolarity to increase 300 → 400

These 2 steps above basically repeat themselves over and over again now:

4) More filtrate arrives at descending loop (at 300 mOsm/L) and pushes rest of filtrate along loop which changes up the osmolarities along the loop

5) Active salt reabsorption occurs- salt gets reabsorbed from thick ascending loop which increases osmolarity of interstitium and osmolarity in ascending loop falls

6) Passive water reabsorption occurs- water flows out from descending limb into interstitium so descending loop osmolarity increases til its = to interstitium osmolarity

Gradient in medullary interstitium already developing from outer medulla to inner medulla

This process repeats again and again (hence multiplication process) to achieve a proper gradient down medulla

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18
Q

Where does the term counter current come from in counter current multiplication?

A

because filtrate flows in opposite directions in ascending and descending loops of Henle

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19
Q

Which side does the basolateral cell membrane face in the collecting ducts?

A

The side with the blood capillaries

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20
Q

What side does the apical cell membrane face in the collecting ducts?

A

The lumen of the collecting duct (inside the tube)

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21
Q

What is the vasa recta?

A

A series of blood capillaries surrounding the nephron mainly in the medullary region

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22
Q

What happens to urea after being filtered through Bowman’s capsule?

A

Urea is transported through the nephron and reaches the collecting duct.

At the collecting duct it is tranpported into the medullary interstitium via UT-A1 (apical cell membrane) and UT-A3 (basolateral cell membrane) transporters- the concentration of urea in the medullary interstitium can be as high as 600mmol/L)

Urea in the interstitium can now either:
1. Be transported into the vasa recta via UT-B1 transporters. This surrounds nephron and therefore urea circulates in the medullary region
2. Be transported back into the descending limb of the loop of Henle via UT-A2 transporters where it goes back through nephron and some exits collecting duct back into interstitium again (recycling)

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23
Q

What is the purpose of the recycling of urea?

A

To increase interstitium osmolarity which
1. Allows concentration of urine water moves from collecting duct into interstitium (as osmolarity in interstitium is higher)
2. Allows excretion of urea with less water - this is because when filtrate reaches inner medullary collecting duct it equilibrates with urea in inner medullary interstitium (which could be as high as 600 mmol/L so conc of urea in collecting duct could also go up to as high as this)- 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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24
Q

How does vasopressin help urea recycling?

A

Helps to boost UT-A1 and UT-A3 numbers to increase collecting ducts permeability to urea to aid in urea reabsorption

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25
Q

What is the structure of vasopressin?

A

Protein hormone with length of 9 amino acids

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26
Q

What is the
a) main function
b) two other functions in the kidney
of vasopressin?

A

a) promotes water reabsorption at the collecting duct
b) helps in urea reabsorption, helps in sodium reabsorption

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27
Q

What is the
a) main function
b) two other functions in the kidney
of vasopressin?

A

a) promotes water reabsorption at the collecting duct
b) helps in urea reabsorption, helps in sodium reabsorption

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28
Q

Where is vasopressin
a) produced
b) stored?

A

a) In the hypothalamus by neurones in the supraoptic and paraventricular nuclei
b) in posterior pituitary in storage granules

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29
Q

How does plasma osmolarity affect ADH production and release?

A

An increase in plasma osmolarity is detected by osmoreceptors in the hypothalamus (are sensitive to even 2-3% change) and this stimulates increased ADH production and release which leads to a reaction cascade and increased export of aquaporin 2 to collecting duct membrane to increase water reabsorption

Decrease in plasma osmolarity inhibits ADH production and release to keep aquaporin channels internalised because we have excess fluid in plasma which we want to lose

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30
Q

What is plasma osmolarity in a healthy adult?

A

275-290 mOsm/kg H2O

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31
Q

How does hypovolemia affect ADH production and release?

A

low blood volume → decreases blood pressure → detected by baroreceptors → info transmitted to hypothalamus → body wants to conserve fluid so this stimulates ADH production and release to open aquaporins to reabsorb water

32
Q

How does hypervolemia affect ADH production and release?

A

Hypervolemia means high blood volume → increases blood pressure → detected by baroreceptors → info transmitted to hypothalamus → body wants to get rid of excess fluid so inhibits ADH release to keep aquaporins closed to lose water

33
Q

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

A

5-10%

34
Q

What factors other than increased plasma osmolarity and hypovolemia stimulate ADH production and release?

A
  • Nicotine
  • Nausea
  • Angiotensin II
35
Q

What factors other than decreased plasma osmolarity and hypervolemia inhibit ADH production and release?

A
  • Ethanol
  • Atrial natriuretic peptide
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 cell membrane into blood vessel

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 for diuresis occurring in the nephron

A

1) ADH amount is 0 or small

2) Blood filtered at Bowman’s capsule and filtrate enters nephron

3) Filtrate passes into PCT where 67% of water and 67% of NaCl are reabsorbed into body

4) Isoosmotic fluid reaches descending limb of loop of Henle where water passively moves into interstitium

5) Fluid enters ascending limb of loop of Henle where NaCl is reabsorbed into interstitium leaving hypoosmotic fluid

6) This hypoosmotic fluid enters DCT where AQP2 channels are absent since there’s negligible ADH, however NaCl is actively reabsorbed again- this makes the 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 the fluid even more hypoosmolar to create urine at 50 mOsm/L compared to plasma which is 300 mOsm/L

39
Q
  • At a cellular level how is NaCl reabsorbed in thick ascending limb?
A

1) Na+ K+ ATPase pump pumps Na+ into blood creating low conc of Na+ in cell

2) Through Na+ K+ 2Cl- symporter, Na+ moves from region of high Na+ (in tubular fluid) to low Na+ in cell which releases energy which K+ and Cl- use to get transported through this symporter into the cell

3) Once in cell K+ and Cl- then exit cell into blood through K+ Cl- symporter

40
Q

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

A

1) Through Na+ K+ ATPase pump, Na+ is pumped into blood

2) NaCl enters cell from tubular filtrate through Na+ Cl- symporter

3) KCl leaves cell into blood via K+ Cl- symporter

41
Q

At a cellular level how is Na+ reabsorbed in collecting duct?

A

Through Na+ channels and Na+ K+ ATPase pump

42
Q

What is antidiuresis? What could cause it?

A

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

43
Q

Describe the mechanism for antidiuresis occurring in the nephron

A

1) There is a high amount of ADH

2) Fluid filtered through Bowman’s then passes through PCT where 67% water and 67% NaCl is reabsorbed leaving isosmotic fluid

3) Water moves out of fluid in descending limb and NaCl moves out of fluid in ascending limb of loop of Henle leaving hypoosmolar fluid

4) In DCT then collecting duct NaCl is again actively reabsorbed

5) In DCT and collecting duct, AQP2 are present so water is reabsorbed

6) In collecting duct there is a gradient of osmolarity which increases as you go down it meaning more and more water is reabsorbed into interstitium from outer medullary to inner medullary regions

7) 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

What does ADH do in terms of Na+ reabsorption?

A

Supports it in:

  • Thick ascending limb- increased Na+ K+ 2Cl- symporters
  • DCT- increased Na+ Cl- symporters
  • Collecting duct- increased Na+ channels
45
Q

Cause of central diabetes insipidus?

A

Decreased/ negligent production and release of ADH
Can be congenital or acquired e.g. due to trauma, infection

46
Q

Clinical features of central diabetes insipidus?

A
  • Polyuria- large urine volume
  • Polydipsia- thirst
47
Q

Treatment for central diabetes insipidus?

A

External ADH

48
Q

What causes nephrogenic diabetes insipidus?

A

correct amount of ADH is produced but something goes wrong at the collecting duct
a) fewer/ mutant AQP2
b)mutant V2 receptors

49
Q

Clinical features of nephrogenic diabetes insipidus?

A

polyuria
polydipsia

50
Q

Treatment for nephrogenic diabetes insipidus?

A
  • Thiazide diuretics
  • NSAIDs
51
Q

Cause of SIADH?

A

Increased production and release of ADH

52
Q

Clinical features of SIADH?

A
  • Hyperosmolar urine
  • Hypervolemia
  • Hyponatremia
53
Q

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 that are added to our body in our body?

A
  • A lot of base is excreted in faeces
  • There is however a net addition of metabolic acid to our fluid compartments (50-100 mEq/day): need to neutralise this so it doesn’t affect blood pH
56
Q

How is excess metabolic acid neutralised?

A
  • By different buffer systems, mainly by bicarbonate buffer system
  • This produces sodium salts and CO2
57
Q

How much bicarbonate do we have in ECF compartment?
Why is this important?

A

350mEq or 24mEq/L
If the body just continuously used bicarbonate to neutralise metabolic acids without replenishing it, the bicarbonate would run out in 4-7 days

58
Q

How do kidneys make sure HCO3- isn’t exhausted?

A
  • Helps with secretion and excretion H+ → there is a fine balance because if body secretes more H+ than metabolic acids coming in, there will be an alkalosis and if less H+ is secreted then acidosis will occur
  • Reabsorption of 100% of HCO3-
  • Production of new HCO3-
59
Q

what is the carbonic anhydrase reaction?

A
60
Q

What 2 organs are involved in the bicarbonate ion buffer system?

A

lungs (through CO2) and kidneys (through HCO3-)

61
Q

What does the Henderson-Hasselbalch equation help us study?

A
  • The role that PCO2 and conc of HCO3- plays on blood pH
  • It shows that if PCO2 rises in body, this increases H+ ion conc causing acidosis and if it falls it causes an alkalosis
  • It also shows inverse relationship of H+ conc with HCO3- conc → if HCO3- rises it’ll cause alkalosis and if it falls it’ll cause an 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- conc called?

A

Metabolic disorder

64
Q

How much HCO3- is reabsorbed in nephron at different areas?

A
  • 80% in PCT
  • 10% in loop of Henle
  • 6% in DCT
  • 4% in collecting duct
65
Q

Describe how HCO3- is reabsorbed at PCT

A

1) CO2 enters cell from tubular fluid by diffusion

2) CO2 reacts with H2O in presence of carbonic anhydrase to make H+ and HCO3-

3) H+ can leave cell into tubular fluid through 2 methods:

  • Through Na+ H+ antiporter- using downward energy from Na+ travel into cell from tubular fluid, H+ moves into tubular fluid
  • Through H+ ATPase pump which pumps H+ ion

4) HCO3- from the reaction is reabsorbed from cell into blood through Na+ HCO3- symporter

5) The H+ that left the 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 cell to start from step 1) with the main final step being the HCO3- leaving cell into blood

66
Q

Describe how HCO3- is reabsorbed at ascending limb of loop of Henle

A

Very similar to PCT

67
Q

Describe how HCO3- is reabsorbed at DCT and collecting duct

A

At alpha intercalated cell:

1) H2O + CO2 leads to H+ and HCO3-

2) 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 and CO2, the CO2 of which diffuses back into cell to do step 1)

3) HCO3- moves into blood via Cl- HCO3- antiporter

At beta intercalated cell:

1) H2O + CO2 leads to H+ and HCO3-

2) Cl- HCO3- antiporter secretes HCO3- into tubular fluid (to excrete in the case of alkalosis in body due to excess HCO3-)

3) H+ is absorbed back into blood via H+ ATPase pump

68
Q

Function of alpha intercalated cell?

A

HCO3- reabsorption and H+ secretion

69
Q

Function of beta intercalated cell?

A

HCO3- secretion and H+ reabsorption

70
Q

Describe how new HCO3- is produced at PCT

A

1) 1 glutamine molecules gives 2 NH4+ molecules and 1 divalent ion (A2-) which gives rise to 2 HCO3-

2) The 2 NH4+ is excreted into tubular fluid through 2 methods:

  • Through Na+ H+ antiporter (NH4+ substitutes in place of H+)
  • Turns into NH3 and moves into tubular fluid where it combines with a H+ to form NH4+ again

3) NH4+ then excreted from body leaving us with a net gain of 2 HCO3-

71
Q

why do we not want the 2 ammonia ions produced from glutamine in PCT to enter blood?

A

If it does, it will go to liver and be split into NH3 and H+, the H+ of which will require 1 HCO3- to neutralise it, which will nullify the effect of the 2 HCO3- we just produced from splitting the glutamine

72
Q

Describe how new HCO3- is 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’s neutralised by a non-bicarbonate buffer- a 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- conc leading to decrease in pH

74
Q

What is the compensatory response for metabolic acidosis?

A
  • Increased (hyper)ventilation which kicks in first → PCO2 goes down so H+ conc goes down
  • Increased HCO3- conc reabsorption and production to compensate for decrease in conc
75
Q

How is metabolic alkalosis characterised?

What is the compensatory response?

A

Increased HCO3- conc leading to increased pH

  • Decreased (hypo)ventilation which kicks in first → PCO2 goes up so H+ conc goes up
  • Increased HCO3- conc excretion to compensate for increase in conc
76
Q

How is respiratory acidosis characterised?

How is this compensated?

A

Increased PCO2 leading to lower pH

  • Acute- increased CO2 enters cells where it reacts with H2O in presence of carbonic anhydrase to produce a H+ and a HCO3- and the H+ is neutralised by cellular proteins so there’s a net gain of HCO3- which is transported back into blood to help with increasing pH
  • Chronic- increased HCO3- reabsorption and production in kidney along with increased H+ and NH4+ ion excretion to help normalise pH
77
Q

How is respiratory alkalosis characterised?

How is this compensated?

A

Decreased PCO2 leading to higher pH

  • Acute- shifting bicarbonate buffer reaction towards more carbonic acid production so less HCO3- produced
  • Chronic- decreased HCO3- reabsorption and production in kidney to normalise pH

Aneesha Flashcards BRS 2 (47 decks)

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