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BRS 1b > 7.1 Renal regulation of water and acid-base balance > Flashcards

7.1 Renal regulation of water and acid-base balance Flashcards

- different renal processes regulating water balance - role of vasopressin in urine production and excretion - the role of kidney in maintaining the body's acid base balance - different renal-regulation associated clinical disorders

1
Q

What the simplified version of the henserson-hasselbalch equation?

A

[H+] = (24*PCO2)/[HCO3-]

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2
Q

Where are the osmoreceptors?

A

Hypothalamus

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3
Q

What are the 5 functions of the kidney?

A

excretion of metabolic products e.g. urea
excretion of foreign substances e.g. drugs
homeostasis of body fluids, electrolytes & acid base balance
regulates blood pressure
secretes hormones (erythropoietin, renin)

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4
Q

What are the 3 types of passive transport that take place in the kidney?

A

diffusion
osmosis
electrical gradient difference

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5
Q

What are the 2 types of passive transport that take place in the kidney?

A 
primary active (ATPase pump, endocytosis)
secondary active (symport, antiport)
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6
Q

What is secondary active transport?

A

Movement of one solute along its electrochemical gradient which provides energy for the other solute to move against it

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7
Q

How is osmolarity calculated?

A

concentration x number of dissociated particles
mOsm/L

e.g. 100mmol/ L of NaCl
= 100 x 2
= 200 mOsm/L

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8
Q

Calculate the osmolarity for 100 mmol/L of glucose

A

100 mOsm/L

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9
Q

What % of your body weight is total fluid volume?

A

60%

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10
Q

What are the two main fluid compartments, what % of your total fluid volume are they?

A

extracellular fluid 33%

intracellular fluid 66%

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11
Q

What is the extracellular fluid made of?

A

25% - intravascular (plasma)

75% - extravascular (95% interstitial fluid, 5% transcellular fluid)

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12
Q

What is an example of transcellular fluid?

A

CSF

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13
Q

What are the two types of water loss?

A

unregulated

regulated

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14
Q

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

A

sweat
feces
vomit
water evaporation from respiratory lining and skin

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15
Q

What is regulated water loss?

A

renal regulation - urine production

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16
Q

What are the two types of water balance?

A

positive water balance

negative water balance

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17
Q

What positive water balance?

A

high water intake
increases the ECF volume
decreases Na+
decreases osmolarity

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18
Q

How do the kidneys correct positive water balance?

A

hyperosmotic urine (compared to plasma)

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19
Q

What is negative water balance?

A

low water balance
this causes ECF volume to decrease
increasing the concentration of Na+
increasing osmolarity

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20
Q

How do the kidneys correct negative water balance?

A

hyperosmotic urine production (compared to plasma)

and trigger thirst

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21
Q

Where is most water reabsorbed in the kidney?

A

PCT (~67%)

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22
Q

What % of water is reabsorbed in the loop of Henle?

A

15%

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23
Q

What is reabsorbed in the ascending limb of the loop of Henle?

A

NaCl

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24
Q

How is NaCl reabsorbed in the ascending limb of the loop of henle?

A

thin: passively
thick: actively

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25
Q

What happens in the descending limb of the loop of henle?

A

water is passively reabsorbed

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26
Q

Why is it significant that water is reabsorbed passively?

A

a gradient is therefore required so,

the medullary interstitium needs to be hyperosmotic

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27
Q

Why is NaCl transported into an out of in the loop of henle?

A

to maintain the so the medullary interstitium is hyperosmotic so more water reabsorption can occur

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28
Q

How much water is reabsorbed in the PCT and collecting duct?

A

variable depending of the body’s need and activation of the aquaporin 2 channels activated by vasopressin

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29
Q

Why is water passively reabsorbed?

A

so the body does not have to spend a lot of energy

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30
Q

What does counter current multiplication do in the kidneys?

A

highest osmolarity at bottom of loop of henle;

maintains gradient so water can move out of urine by osmosis

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31
Q

What is the vasa recta?

A

series of capillaries around the nephron, supply blood to the medulla

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32
Q

What transporter facilitate the recycling of urea out from the collecting duct into the medullary interstitium

A

UT-A1

UT-A3

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33
Q

What is the concentration of urea in the medullary interstitim

A

up to 600 mmol/L

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34
Q

What membrane does the UT-A1 transporter allow urea to cross?

A

apical cell membrane of collecting duct

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35
Q

What membrane does the UT-A3 transporter allow urea to cross?

A

basolateral cell membrane

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36
Q

Once urea has reached the medullary interstitium, what are the two places it can go?

A

Vasa recta

Thin descending limb

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37
Q

What transporter facilitates the movement of urea from the medullary interstitium into the vasa recta?

A

UT-B1

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38
Q

What transporter facilitates the movement of urea from the medullary interstitium into the thin descending limb?

A

UT-A2

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39
Q

What is the purpose of urea recycling from the collecting duct into the thin descending limb?

A

to increase the osmolarity of the interstitium

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40
Q

Urea recycling causes an increase in the osmolarity of the interstitium, what two purposes does this serve?

A

urine concentration occurs

urea excretion requires less water

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41
Q

How does urea recycling mean that urea excretion requires less water?

A

is the concentration of urea outside the collecting duct is high (up to 600 mmol/L) then the concentration of urea excreted in the urine can also be this high, meaning less water will have to be dragged along with it

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42
Q

Which urea transporters does vasopressin increase the expression of?

A

UT-A1
UT-A3

–> remember increases the concentration of urine

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43
Q

When intravenous fluids are given, what is the first fluid compartment it enters?

A

extracellular fluid compartment

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44
Q

Which compound, NaCl or Urea is responsible for generating a hyperosmotic medullary interstitium?

A

both

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45
Q

What type of hormone is vasopressin?

A

peptide hormone (9 aa)

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46
Q

Where is vasopressin produced?

A

Hypothalamus, from neurones in supraoptic and paraventricular nuclei

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47
Q

Where is vasopressin stored?

A

posterior pituitary

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48
Q

What is the primary function of vasopressin?

A

promotes water reabsorption from the collecting duct

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49
Q

What would a high plasma osmolarity cause in terms of ADH?

A

stimulate ADH production and release

opens up aquaporin channels

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50
Q

What would happen if plasma osmolarity decreased?

A

inhibition of ADH production and release

51
Q

What is hypovolemia?

A

decreased volume of circulating blood in the body

52
Q

What % change of circulating blood volume is required for stimulation/inhibition of ADH receptors?

A

5-10%

53
Q

What receptors detect the change in circulating blood volume?

A

baroreceptors

54
Q

What are the 5 factors that stimulate ADH production and release?

A 
increased plasma osmolarity
hypovolaemia (low blood pressure)
nausea
angiotensin II
nicotine
55
Q

What are the 4 factors that inhibition ADH production and release?

A

decreased plasma osmolarity
hypervolaemia (high blood pressure)
ethanol
atrial natriuretic peptide

56
Q

describe the mechanism of action of ADH?

A
  1. ADH binds to the V2 receptors on the basolateral membrane of a principle cell
  2. This triggers a G protein mediated signalling cascade
  3. This activates protein kinase A
  4. Which increases the secretion of aquaporin-2 channels
  5. These AP2 channels are transported to and inserted in the apical membrane
  6. Through these channels allow more water to be reabsorbed by thr PCT
57
Q

What AQP receptors can ADH increase and decrease as required?

A

AQP2 on the apical membrane

AQP3 on the basolateral membrane

58
Q

Explain Na+ reabsorption into the blood in the thick ascending limb

A

Na - K ATPase pump (pumps out Na into the blood)
Low conc. of Na+ in the cell
Na+ K 2Cl symporter, transports sodium into the cell down its gradient.
This releases energy used to transports K and Cl into the cell
K and Cl are then transported into the blood by the K and Cl symporter
K used by Na - K ATPase pump to transport Na into the blood

59
Q

In terms of osmolarity, when urine enters the descending limb it is..

A

isosmotic

60
Q

In terms of osmolarity, when urine enters the descending limb it is..

A

hypoosmotic

61
Q

What substances move in out out in the DCT?

A

Na - active

Cl - active

62
Q

What substances move in or out in the collecting duct?

A 
Na Cl (active) - outer medulla
Water - inner medulla
63
Q

What osmolarity is urine?

A

50 mOsm/L

64
Q

What osmolarity is plasma?

A

~ 300 mOsm/L

65
Q

What is antidiuresis?

A

concentrated urine in low volume excretion

66
Q

What happens in antidiuresis?

A

ADH –> high
ADH supports Na reabsorption in:
- Thick ascending limb: Na+-K+-2Cl-
- Distal Convoluted tubule: Na+ - Cl- symporter
- Collecting duct: Na+ channel
by increasing the number of symporters and channels

67
Q

What happens to water reabsorbtion in anti-diuresis?

A

DCT - water reabsorption

CD- water reabsorption in inner and outer medulla

68
Q

What could the osmolarity of urine be in anti-diuresis

A

1200 mOsm/L

69
Q

What are 3 ADH related clinical disorders?

A
  • central diabetes insipidus
  • syndrome of inappropriate ADH secretion (SIADH)
  • nephrogenic diabetes insipidus
70
Q

What is the cause of central diabetes insipidus?

A

decreased/negligent production and release of ADH

71
Q

What is the cause of SIADH?

A

increased production and release of ADH

72
Q

What is the cause of nephrogenic diabetes insipidus?

A

less/mutant AQP2
mutant V2 receptor
(normal amount of ADH produced)

73
Q

What are the clinical features of central diabetes insipidus?

A

polyuria

polydipsia

74
Q

What are the clinical features of SIADH?

A

hyperosmolar urine
hypervolaemia
hyponatraemia

75
Q

What are the clinical features of nephrogenic diabetes insipidus?

A

polyuria

polydipsia

76
Q

What is the treatment for central diabetes insipidus?

A

external ADH

77
Q

What is the treatment for SIADH?

A

non-peptide inhibitor of ADH receptor

conivaptan & tolvaptan

78
Q

What is the treatment for nephrogenic diabetes insipidus?

A

thiazide diuretics and NSAIDs

79
Q

What do thiazide diuretics do?

A

reduce filtration rate at bowman’s capsule so less urine produced

80
Q

Does ADH regulate the number of aquaporin channels on the apical or basolateral membrane?

A

both

81
Q

What will the blood be in SIADH?

A

hypoosmotic - as holding onto a lot of water when it doesnt need to

82
Q

What will the blood be in SIADH?

A

hypoosmotic - as holding onto a lot of water when it doesnt need to

83
Q

What two things introduce acids and bases into our body?

A

diet

metabolism

84
Q

What is the primary was bases are excreted from the body?

A

faeces

85
Q

Because most of the bases are removed in faeces, what does this leave us with

A

net addition of metabolic acid

86
Q

Why is it important to remove this net addition of metabolic acid?

A

so it does not affect the blood pH

87
Q

What is the primary way metabolic acids are neutralised?

A

bicarbonate buffer system

88
Q

What is the problem with the bicarbonate buffer system?

A

if it isnt replenished it will run out.

89
Q

What is the role of the kidneys in metabolic acid neutralisation?

A

secretion and excretion of H+
reabsorption of HCO3- (almost 100%)
production of new HCO3-

90
Q

What is the equation showing the bicarbonate ion as a buffer?

A

carbon dioxide + water <–carbonic anhydrase–> H+ + bicarbonate (HCO3-)

91
Q

What organs manage the bicarbonate buffer system?

A

lungs

kidney

92
Q

What happens to H+ if PCO2 increases?

A

[H+] also increases

93
Q

If changes in H+ are caused by fluctuations in PCO2, what type of acid base disorder is it?

A

respiratory

94
Q

If changes in H+ are caused by fluctuations in [HCO3-] , what type of acid base disorder is it?

A

metabolic

95
Q

Where is most bicarbonate ions reabsorbed ?

A

PCT

96
Q

What are the two ways the H+ ion can exit the cell and enter the tubular fluid?

A

Na+ H+ antiporter

H+ ATPase pump

97
Q

How is bicarbonate reabsorbed into the blood in the PCT?

A

Na+ HCO3- symporter

98
Q

Where are the intercalating cells?

A

DCT and collecting duct

99
Q

What are the two types of intercalated cells?

A

a and b

100
Q

What is the function of the a intercalated cell?

A

HCO3- reabsorption

H+ secretion

101
Q

What is the function of the b intercalated cell?

A

HCO3- secretion

H+ reabsorption

102
Q

Which intercalated cell is more commonly used?

A

a, for reabsorption of bicarbonate

b is used if body is getting alkali

103
Q

What transporter is used to move HCO3- ions out of the intercalated cell into the blood (a), or tubular fluid (b)

A

Cl-HCO3- antiporter

104
Q

Why do we have two types of intercalated cells?

A

to manage the acid base balance in the body

105
Q

Where are new bicarbonate ions produced?

A

PCT

106
Q

What molecule is bicarbonate created from in the PCT, and what other products are made?

A

Glutamine –> 2ammonium + 2 bicarbonate

107
Q

When bicarbonate is produced in the PCT, why is it important that the ammonium is removed and not sent to the liver?

A

In the liver it will become 2 urea and a proton which will require neutralisation by a bicarbonate ion, nullifying its production

108
Q

What is done with the ammonium byproduct in the PCT?

A

excreted in the urine

109
Q

What are the two ways in which ammonium is removed from the cells in the PCT and into the tubular fluid?

A 
Na+ H+ antiporter (with NH4+ ion substituting with H+)
become ammonia (NH3) gas and diffuse out into the tubular fluid where it will bind with an H+ and become NH4+
110
Q

How is bicarbonate produced in the DCT and collecting duct.

A

In the a intercalated cells,
when H+ is transported into the tubular fluid, instead of being neutralised by a bicarbonate, it can be neutralised by a phosphate ion (phosphate buffer system) so the bicarbonate made in the cell and enters the blood is a net gain

111
Q

What are the four acid base imbalances?

A

metabolic acidosis
metabolic alkalosis
respiratory acidosis
respiratory alkalosis

112
Q

What are the characteristics of metabolic acidosis?

A

low [HCO3-], low pH

113
Q

What are the characteristics of metabolic alkalosis?

A

increased [HCO3-]

increased pH

114
Q

What are the characteristics of respiratory acidosis?

A

increased pCO2

decreased pH

115
Q

What are the characteristics of respiratory alkalosis?

A

decreased pCO2

increased pH

116
Q

What is the compensatory response for metabolic acidosis?

A

increased ventilation

increased [HCO3-] reabsorption and production

117
Q

What affect does hyperventilation have on PCO2?

A

hyperventilation = decreased PCO2

118
Q

What is the compensatory response for metabolic alkalosis?

A

decreased ventilation

increase [HCO3-] excretion

119
Q

What is the compensatory response for respiratory acidosis?

A

acute: intracellular buffering (so inc. CO2 enters the cells and gets turned into H+ and HCO3- by carbonic anhydrase, H+ neutralised by cell proteins so net +1 bicarbonate)
chronic: increased [HCO3-] reabsorption and production, increased excretion of H+ and NH4+

120
Q

What is the compensatory response for respiratory alkalosis?

A

acute: intracellular buffering (shift equation to more carbonic acid side, so less bicarbonate produced)
chronic: decreased [HCO3-] reabsorption and production

121
Q

pH= 7.2 [HCO3-] = 17mEq/L pco2 = 35mmHg

A

metabolic acidosis

122
Q

pH=7.5, [HCO3-] = 17mEq/L, PCO2= 35mmHg

A

respiratory alkalosis

123
Q

What is normal range of [HCO3-]?

A

23-30 mEq/L (24)

124
Q

What is normal range of PCO2?

A

35 to 45 mmHg

4.7 - 6.0 kPa

BRS 1b (25 decks)

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