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brs (phase 1b) > (uro-renal) renal regulation of water & acid-base balance > Flashcards

(uro-renal) renal regulation of water & acid-base balance Flashcards

1
Q

what is osmolarity?

A

the concentration of osmotically active particles in solution

(quantitatively expressed is osmoles of solute per litre of solution)

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2
Q

what is the equation for osmolarity?

A

concentration x no. of dissociated particles

Osm/L OR mOsm/L

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3
Q

what are the units of osmolarity?

A

Osm/L OR mOsm/L

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4
Q

calculate the osmolarity for 100 mmol/L glucose and 100mmol/L NaCl

A

osmolarity for glucose

= 100 x 1 = 100 mOsm/L

(one dissociated particle)

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5
Q

calculate the osmolarity for 100mmol/L of NaCl

A

osmolarity for NaCl

= 100 x 2 = 200 mOsm/L

(two dissociated particles)

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6
Q

what is the driving force for osmosis?

A

oncotic pressure/osmotic pressure

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7
Q

what does the osmotic/oncotic pressure depend on?

A

directly proportional tot he number of solute particles

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8
Q

what is the total fluid volume?

A

approx 60% of body weight

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9
Q

describe the distribution of body fluid

A 
2/3 = intracellular
1/3 = extracellular

of the extracellular fluid

  • 1/4 = intravascular (plasma)
  • 3/4 = extravascular

of the extravascular

  • 95% = interstitial fluid
  • 5% = transcellular fluid
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10
Q

give an example of an intravascular fluid

A

plasma

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11
Q

give an example of an extravascular fluid

A

interstitial fluid

transcellular fluid (peritoneal fluid, CSF)

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12
Q

what are transcellular fluids?

A

fluid that fills up the spaces of chambers that are formed from the linings of epithelial cells

(CSF, peritoneal fluid)

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13
Q

what separates intracellular fluid from extracellular fluid?

A

cell membranes

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14
Q

water loss can either be regulated or unregulated - what are the four forms of unregulated water loss?

A

sweat

faeces

vomiting

evaporation from respiratory lining/skin

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15
Q

water loss can either be regulated or unregulated - what is the one form of regulated water loss?

A

renal urine production

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16
Q

what is positive water balance?

A

amount of water in the body is higher than what is required

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17
Q

what is negative water balance?

A

amount of water in the body is less than what is required

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18
Q

how do the kidneys respond to a positive water balance?

A

high water intake causes a positive water balance

= increased ECF volume
= reduced sodium concentration
= reduced plasma osmolarity
= production of hypo-osmolar urine
= osmolarity normalises as excess water is lost when the hypo-osmolar urine is excreted
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19
Q

how do the kidneys respond to a negative water balance?

A

low water intake causes a negative water balance

= reduced ECF volume
= increased sodium concentration
= increased plasma osmolarity
= production of hyperosmolar urine
= osmolarity normalises as as much water as possible is retained (+ more water is drank) when the hyperosmolar urine is excreted
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20
Q

besides hyper-osmotic urine production, what else causes the osmolarity to normalise in a negative water balance?

A

increased water intake due to thirst

+ combined w hyperosmolar urine production = normalises osmolarity

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21
Q

what is the structural functional unit of a kidney?

A

nephron

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22
Q

how much water is reabsorbed in the PCT?

A

67%

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23
Q

how much water is reabsorbed in the thin descending limb of the loop of Henle?

A

15%

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24
Q

what process does water reabsorption in the loop of Henle rely on?

A

osmosis (therefore, requires an osmotic gradient)

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25
Q

where in the loop of Henle can water be reabsorbed?

A

thin descending limb

but defo not in the thick ascending limb

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26
Q

where in the loop of Henle can salts (Na+, Cl-) be reabsorbed?

A

thick ascending limb

but defo not in the thin descending limb

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27
Q

what is an essential requirement for water reabsorption from the loop of Henle?

A

hyper-osmotic medullary interstitium

to created the osmotic gradient required for water reabsorption form the LOH and the collecting duct

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28
Q

explain the process by which water is reabsorbed from the loop of Henle

A

sodium and chloride are reabsorbed both actively and passively reabsorbed din the thick ascending limb

produce a hyperosmotic medullary interstitium

water follows osmotic gradient into the medullary interstitium (from the thin descending limb tubular cells via aquaporin channels)

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29
Q

how much water is reabsorbed in the collecting duct?

A

variable amounts

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30
Q

why is the amount of water reabsorbed in the collecting duct variable?

A

depends on vasopressin action which determines the number of aquaporin channels embedded in the tubular cell membranes to facilitate water reabsorption

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31
Q

explain the process of countercurrent multiplication in the loop of Henle

A

active salt reabsorption in the thick ascending limb causes the medullary interstitium to become hyperosmotic (reducing tubular fluid osmolarity)

water follows into the medullary interstitium from the thin descending limb due to the osmotic gradient (increasing tubular fluid osmolarity)

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32
Q

why is countercurrent multiplication called so?

A

countercurrent = fluid movement in opposite directions in the ascending and descending limbs

multiplication = process continues to repeat itself

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33
Q

what is the minimum, maximum and range of osmolarities in the loop of Henle?

A 
minimum = 300
maximum = 1200 (at tip of LOH)

= range due to repeated countercurrent multiplication cycles)

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34
Q

describe the osmolarity of the medullary interstitium as you do down the nephron

A

from the other medulla to the inner medullar

= becomes more hyperosmolar

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35
Q

what is the vasa recta?

A

series of blood vessels surrounding the loop of Henle in the renal medullary region

(responsible for oxygen and nutrient transport)

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36
Q

what are UT-A1 transporters?

A

urea transporters found on the apical membranes of the tubular cells in the collecting duct

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37
Q

what are UT-A3 transporters?

A

urea transporters found on the basolateral membranes of the tubular cells in the collecting duct

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38
Q

explain how urea recycling occurs in the nephron

A

urea take up into tubular cells from tubular fluid via UT-A1 transporters

urea transported into medullary interstitium via the UT-A3 transporters (increasing interstitial osmolarity)

then either

1) urea transported into the vas recta via UT-B1 transporters
2) urea transported back into the tubular fluid via UT-A2 transporters in the thin descending limb

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39
Q

where does the urea go after the medullary interstitium?

A

then either

1) urea transported into the vas recta via UT-B1 transporters
2) urea transported back into the tubular fluid via UT-A2 transporters in the thin descending limb

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40
Q

what is the maximum possible concentration of urea in the medullary interstitum?

A

600 mmol/L

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41
Q

what are UT-B1 receptors?

A

urea transporters found on the vasa recta

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42
Q

what are UT-A2 receptors?

A

urea transporters found on the thin descending limb of the loop of Henle

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43
Q

what is the purpose of urea recycling?

A

to increase medullary interstitium osmolarity for

1) urine concentration
2) because urea excretion requires less water (so less water loss)

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44
Q

differentiate between the vasa recta and the peritubular capillaries

A

both have the same function of nutrient transport

  • peritubular capillaries originate from the efferent arteriole and surround the renal cortex region mainly
  • vasa recta are specialised peritubular capillaries that supply the renal medulla
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45
Q

how does vasopressin affect urea recycling?

A

vaspressin increases UT-A1 and UT-A3 numbers so increases urea uptake into the medullary interstitium

= making it more hyper-osmotic

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46
Q

how many amino acids make up vasopressin?

A

nine

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47
Q

what is the main function of vasopressin?

A

concentrates the urine by increasing water reabsorption from the collecting duct

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48
Q

where is ADH produced?

A

hypothalamic magnocellular neurones in the supraoptic and paraventricular nucleus

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49
Q

where is ADH stored?

A

posterior pituitary gland

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50
Q

what is the normal plasma osmolality in a healthy adult?

A

275-290 mOsm/kg H2O

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51
Q

how is the fluctuation in osmolality detected?

A

osmoreceptors in the hypothalamus

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52
Q

what change in osmolality is required for detection by osmoreceptors?

A

approx 5-10%

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53
Q

which factors stimulate ADH production?

A

increased plasma osmolality

hypovolemia (decreased blood pressure)

nausea

angiotensin II

nicotine

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54
Q

which factors inhibit ADH production?

A

decrease plasma osmolality

hypervolemia (increased blood pressure)

ethanol

ANP (atrial natriuretic peptide)

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55
Q

which receptor does ADH act on in the collecting duct?

A

V2 receptor on the basolateral membrane of the tubular cells

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56
Q

what kind of receptors are V2 receptors?

A

G-protein coupled

57
Q

what are aquaporin 3 and aquaporin 4 channels?

A

water transporters on the basolateral membrane of the tubular collecting duct cells

58
Q

what does the activation of the V2 receptors cause?

A

stimulates activation of adenylate cyclase = converts ATP to cAMP

activates protein kinase A

stimulates the migration of aquaporin 2 channels into the apical membrane to facilitate water reabsorption

59
Q

what are aquaporin 2 channels and why are they important?

A

water transporters on the apical membrane of the tubular collecting duct cells

= facilitate water reabsorption from the tubular fluid

60
Q

which aquaporin channels does ADH act on?

A

aquaporin 2 & aquaporin 3

61
Q

what is diuresis?

A

increased dilute urine production

62
Q

what are the ADH levels in diuresis?

A

low or zero

63
Q

explain how diuresis occurs

A

-

64
Q

how low can urine osmolality actually get?

A

as low as 50 mOsm/L

65
Q

what is reabsorbed in the thin descending limb of the LOH?

A

water (passively)

66
Q

what is reabsorbed in the thick ascending limb of the LOH?

A

Na+, Cl- (actively in the inner medullary region and passively in the outer medullary region)

67
Q

describe the tubular fluid just at the end of the loop of Henle, prior to entering the collecting duct

A

hypoosmotic (due to ascending limb NaCl reabsorption)

68
Q

what happens in the DCT that contributes to diuresis?

A

increased active Na+, Cl- reabsorption

makes tubular fluid more hypoosmolar

69
Q

what happens in the collecting duct that contributes to diuresis?

A

increased Na+ reabsorption

70
Q

which transporter(s) is/are responsible for NaCl reabsorption in the thick ascending limb?

A

(basolateral) Na+-K+ ATPase, K+ - Cl- symporter

(apical) triple transporter

71
Q

which transporter(s) is/are responsible for NaCl reabsorption in the DCT?

A

(basolateral) Na+-K+ ATPase, K+ - Cl- symporter

(apical) Na+ - Cl- symporter

72
Q

in diuresis, why is water not reabsorbed in the DCT?

A

aquaporin 2 channels are absent in the DCT in diuresis

73
Q

which transporter(s) is/are responsible for Na reabsorption in the collecting duct?

A

(basolateral) Na+-K+ ATPase

(apical) Na+ channels

74
Q

in diuresis, despite the low ADH levels, why does some water reabsorption still occur in the collecting duct?

A

there are still some aquaporins present so water reabsorption can still take place in the absence of ADH

75
Q

what is antidiuresis?

A

production od low volumes of concentrated urine

76
Q

what are the ADH levels in antidiuresis?

A

high

77
Q

what three things does high ADH cause in antidiuresis?

A

(apical transporters)

thick ascending limb = triple transporter

DCT = Na+ - Cl- symporter

collecting duct = Na+ channels

78
Q

how high can urine osmolality actually get?

A

1200 mOsm/L

can produce as little as 0.5L of urine per day

79
Q

explain how antidiuresis occurs

A

-

80
Q

in anti-diuresis, why are large amounts of water reabsorbed in the DCT?

A

aquaporin 2 channels are present to facilitate water reabsorption

81
Q

in anti-diuresis, why are large amounts of water reabsorbed in the collecting duct?

A

there is a gradient in the medullary interstitium = gets more hyperosmolar as you progress from inner medulla to outer medulla, down the nephron

medullary hyperosmolarity stimulates more water reabsorption

82
Q

name three ADH-related clinical disorders

A

central diabetes insipidus

nephrogenic diabetes insipidus

syndrome of inappropriate ADH secretion (SIADH)

83
Q

what causes central diabetes insipidus?

A

decreased/negligent production and release of ADH

84
Q

what are the clinical features of central diabetes insipidus?

A

polydipsia
polyuria
(among others)

85
Q

what is the treatment for central diabetes insipidus?

A

external ADH administration

86
Q

what is SIADH?

A

syndrome of inappropriate ADH secretion

87
Q

what causes SIADH?

A

increased production and release of ADH

88
Q

what are the clinical features of SIADH?

A

hypervolemia
hyperosmolar urine production
hyponatraemia

89
Q

what is the treatment for SIADH?

A

non-peptide inhibitor of ADH receptor
(conivaptan & tolvaptan)

= prevents aquaporin channel facilitation of water reabsorption

90
Q

what is central/cranial diabetes insipidus?

A

impaired pituitary production of ADH leading to impaired water reabsorption in the renal collecting duct

(could be due to trauma or infection)

91
Q

what is nephrogenic diabetes insipidus?

A

impaired response to adequate ADH production due to damaged or mutant renal V2 receptors or aquaporin 2 channels

= leading to impaired water reabsorption from the renal collecting duct

92
Q

what causes nephrogenic diabetes insipidus?

A

less/mutant aquaporin 2 transporter

93
Q

what are the clinical features of nephrogenic diabetes insipidus?

A

polydipsia
polyuria
(among others)

94
Q

what is the treatment for nephrogenic diabetes insipidus?

A

thiazide diuretics + NSAIDs

diuretics reduce filtration rate at Bowman’s capsule so reduced volume of urine produced

95
Q

true or false: ADH regulates the number of aquaporin channels on both the apical and basolateral membranes of the principal cells

A

true

ADH can either upregulate/downregulate aquaporin 2 (apical) & aquaporin 3 (basolateral) channels

96
Q

true or false: the blood of a patient suffering from SIADH will slowly get more hyperosmotic

A

false

will become hypoosmotic as body conserves more water when not required

97
Q

how are most bases excreted?

A

base excretion in faeces

98
Q

how much metabolic acid is added to the body each day?

A

50-100 mEq/day

99
Q

which ion is essential for metabolic acid neutralisation?

A

baicrbonate ion (HCO3-)

100
Q

what is the ECF concentration of bicarbonate ions?

A

approx 350 mEq OR 24 mEq/L

101
Q

why are bicarbonate ions important in the body?

A

neutralise the metabolic acids produced daily to prevent acidosis or other acid-base disorders

102
Q

which enzyme catalyses the combination of carbon dioxide and water and what does this produce?

A

carbonic anhydrase

103
Q

what does carbonic acid dissociate into?

A

H+ ions

HCO3- ions

104
Q

what does the Henderson-Hasselbalch equation suggests about H+ ions and HCO3- ions?

A

[H+] = (24 x pCO2)/[HCO3-]

so the [H+] is directly proportional to the pCO2 = rises so H+ rises and falls so H+ fals

and the [H+] is inversely proportional to the [HCO3-] = rises so [H+] falls and falls so [H+ rises

105
Q

what kind of acid-base disorder results from a rise or fall in the PCO2?

A

respiratory

if pCO2 changes

106
Q

what kind of acid-base disorder results from a rise or fall in the [HCO3-]?

A

metabolic

if [HCO3-] changes

107
Q

how much of the bicarbonate in the tubular fluid is reabsorbed

A

approx 100% of the tubular fluid bicarbonate ions

108
Q

which transporters are responsible for bicarbonate ion reabsorption in the PCT tubular cells?

A

apical = H+ excretion

  • NHE3 (Na+-H+ antiporter)
  • H+ ATPase

basolateral = HCO3- reabsorption

  • Na+-K+ ATPase
  • NBC1 (Na+-HCO3- symporter)
109
Q

what are intercalated cells?

A

tubular cells involved in acid-base regulation

110
Q

what is the function of alpha intercalated cells?

A

H+ secretion

HCO3- reabsorption

111
Q

what is the function of beta intercalated cells?

A

HCO3- secretion

H+ reabsorption

112
Q

which transporters are responsible for bicarbonate ion reabsorption in the DCT and collecting duct tubular cells?

A

alpha intercalated cells

  • apical = H+ ATPase, H+-K+ ATPase
  • basolateral = Cl- - HCO3- antiporter

beta intercalated cells

  • apical = Cl- - HCO3- antiporter
  • basolateral = H+ ATPase

(swapped apical and basolateral in one cell to give arrangement for the other)

113
Q

what is glutamine important for in the PCT tubular cells?

A

glutamine produced two ammonium ions and one divalent ion

the divalent ion gives rise to two bicarbonate ions that are reabsorbed into the bloodstream

the ammonium ions are secreted into the tubular fluid via the Na+-H+ antiporter (substituted in place of H+)

114
Q

how do the ammonium ions leave the PCT tubular cells and enter the tubular fluid?

A

via the Na+ - H+ antiporter

115
Q

how are H+ ions secreted into the tubular fluid in the DCT and CD?

A

H+ ATPase

H+ - K+ ATPase

116
Q

explain how new bicarbonate ions are produced in the PCT tubule cells

A

glutamine produced two ammonium ions and one divalent ion

the divalent ion gives rise to two bicarbonate ions that are reabsorbed into the bloodstream

117
Q

why is it important that the ammonium ions produced in new bicarbonate ion formation is excreted from the tubular cells?

A

if reabsobed and not excreted, they would then travel to the liver and produce one urea molecule and one proton

the proton produced would need to be neutralised by the newly gained bicarbonate ions, nullifying the gain

118
Q

what are the two ways in which a net gain of bicarbonate ions is ensured in the tubular cells?

A
  • ensuring the secretion of ammonium ions in the PCT (which would otherwise form protons in the liver, that need to be neutralised)
  • providing non-bicarbonate buffers for H+ ion neutralisation in the DCT and CD
119
Q

explain how new bicarbonate ions are produced in the DCT and collecting duct tubule cells

A

carbonic acid dissociated to produce H+ ions and HCO3- ions

the bicarbonate ions are reabsorbed into the bloodstream

the remaining H+ ions, instead of being reabsorbed and needing to be neutralised by the newly gained bicarbonate ions, are secreted

the secreted H+ ions are neutralised by other non-bicarbonate buffers, such as phosphate (HPO42-)

120
Q

give an example of a non-bicarbonate buffer

A

HPO4(2-)

121
Q

what does glutamine produce in the PCT tubular cells?

A

two ammonium ions and one divalent ion (latter produced two bicarbonate ions)

122
Q

what happens to ammonia in the filtrate?

A

combines w a proton to form an ammonium ion to be excreted

123
Q

what are the characteristics of metabolic acidosis?

A

increased [HCO3-]

decreased pH

124
Q

what are the characteristics of metabolic alkalosis?

A

decreased [HCO3-]

increased pH

125
Q

what are the characteristics of respiratory acidosis?

A

increased pCO2

decreased pH

126
Q

what are the characteristics of respiratory alkalosis?

A

decreased pCO2

increased pH

127
Q

a problem in which parameter indicates a respiratory imbalance?

A

pCO2

128
Q

a problem in which parameter indicates a metabolic imbalance?

A

[HCO3-]

129
Q

what is the compensatory response to metabolic acidosis?

A

hyperventilation

increased HCO3- reabsorption and production

130
Q

what is the compensatory response to metabolic alkalosis?

A

hypoventilation

increased HCO3- excretion

131
Q

what is the compensatory response to respiratory acidosis?

A

acute = intracellular bufffering (H+ ions produced

chronic = increased HCO3- reabsoprtion and production

132
Q

what is the compensatory response to respiratory alkalosis?

A

acute = intracellular bufffering

chronic = reduced HCO3- reabsoprtion and production

133
Q

why is hyperventilation a compensatory mechanism?

A

hyperventilation
= pCO2 decreased
= reduced H+ ion due to reduced carbonic acid
= pH rises again

134
Q

why is hypoventilation a compensatory mechanism?

A

hypoventilation
= pCO2 increases
= increased H+ ion due to increased carbonic acid
= pH falls again

135
Q

what is intracellular buffering in acute respiratory acidosis?

A

carbon dioxide in the cell produces carbonic acid which dissociates into a proton ion and a bicarbonate ion

the proton ion is neutralised by cellular proteins and so there is a net gain of a bicarbonate ion (contributes to increased pH)

136
Q

what is intracellular buffering in acute respiratory alkalosis?

A

shifts the carbonic acid dissociation equation to the left so more carbonic acid is produced and fewer bicarbonate ions are produced

137
Q

identify the acid-base disorder through analysis of the patient’s data

pH = 7.2 (7.35-7.45)
[HCO3-] = 17 mEq/L (22-28)
pCO2 = 35 mmHg (35-35)
A

pH is reduced so acidosis

if respiratory = pCO2 should be higher BUT if metabolic = [HCO3-] should be lower, which it is so

= metabolic acidosis

138
Q

identify the acid-base disorder through analysis of the patient’s data

pH = 7.5 (7.35-7.45)
[HCO3-] = 17 mEq/L (22-28)
pCO2 = 35 mmHg (35-35)
A

pH is increased so alkalosis

if respiratory = pCO2 should fall, which it has BUT if metabolic = [HCO3-] should rise so

= respiratory alkalosis (w renal compensation)

brs (phase 1b) (71 decks)

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