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Z Year 2 BRS URO > Renal Regulation of water and acid base balance > Flashcards

Renal Regulation of water and acid base balance Flashcards

1
Q

What is osmolarity? How do you calculate it?

A

Concentration x No. of dissociated particles

= Osm/L OR mOsm/L

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2
Q

What is osmotic pressure directly proportional to?

A

number of solute particles

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3
Q

How much fluid is in the body?

A

total fluid volume = around 60% of body weight

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4
Q

What is a 1/3 of the fluid in the body?

A

Extracellular

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5
Q

What is 2/3 of the fluid in the body?

A

Intracellular

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6
Q

What is the distribution of extracellular fluid?

A
  • 3/4: 95% interstitial fluid and 5% tranacellluar fluid

- 1/4 intravascular (plasma)

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7
Q

What makes up unregulated water loss?

A
  • Sweat
  • Feces
  • Vomit
  • Water evaporation from respiratory lining and skin
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8
Q

What makes up regulated water loss?

A

-Renal regulation (urine production)

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9
Q

How does renal regulation act in positive water balance?

A
  1. High water intake
  2. Increase ECF volume
  3. Decrease conc of na+ and Decrease osmolatity
  4. Hypoosmotic urine production
  5. Osmolarity normalizes
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10
Q

How does renal regulation act in negative water balance?

A
  1. Low water intake
  2. Decreased ECF volume, increased Na+ conc and increase osmolarity
  3. Hyperosmotic urine production
  4. Osmolarity normalizes
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11
Q

Why is there a gradient for water reabsorption?

A

reabsorbed through the passive process of osmosis

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12
Q

What are the conditions in the medullary interstitium and why?

A
  • needs to be hyperosmotic

- for water reabsorption to occur from the Loop of Henle and Collecting duct

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13
Q

What is vasopressin / ADH?

A

protein (length of 9 amino acids)

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14
Q

What is the main function of ADH / vasopressin?

A

promote absoprtion from collecting duct

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15
Q

Where is ADH / vasopressin produced?

A

Hypothalamus (neurons in supraoptic and paraventricular nuclei)

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16
Q

Where is ADH / vasopressin stored?

A

posterior pituitary

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17
Q

What is plasma osmolarity usually?

A

275-290 mOsm/kg H2O (healthy adult)

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18
Q

What is needed for detection of plasma osmolarity by baroreceptors?

A

5-10% change required for detection by baroreceptors; information transmitted to hypothalamus

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19
Q

What is fluctuation of plasma osmolarity detected by?

A

osmoreceptors in the hypothalamus

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20
Q

What are the stimulatory factors influencing ADH production and release?

A
  1. Increased plasma osmolarity
  2. Hypovolemia (decreased BP
  3. Nausea
  4. Angiotensin II
  5. Nicotine
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21
Q

What are the inhibitory factors influencing ADH production and release?

A
  1. Decreased plasma osmolarity
  2. hypervolemia (increased BP)
  3. Ethanol
  4. Atrial natriuretic peptide
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22
Q

How does ADH support Na+ reabsorption and where when ADH is high?

A
  • Thick ascending limb: ↑Na+ - K+ - 2Cl- symporter
  • Distal convoluted tubule: ↑Na+ - Cl- symporter
  • Collecting duct: ↑Na+ channel
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23
Q

What is the cause of central diabetes insipidus?

A

Decreased/negligent production and release of ADH

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24
Q

What are the clinical features of central diabetes insipidus?

A
  • Polyuria

* Polydipsia

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25
Q

What is the treatment of central diabetes insipidus?

A

external ADH

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26
Q

What is the cause of syndrome of inappropriate ADH secretion (SIADH)?

A

Increased production and release of ADH

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27
Q

What are the clinical features of syndrome of inappropriate ADH secretion (SIADH)?

A
  • Hyperosmolar urine
  • Hypervolemia
  • Hyponatremia
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28
Q

What is the treatment of syndrome of inappropriate ADH secretion (SIADH)?

A

Non-peptide inhibitor of ADH receptor

conivaptan & tolvaptan

29
Q

What is the cause of nephrogenic diabetes insipidus?

A
  1. Less/mutant AQP2

2. Mutant V2 receptor

30
Q

What are the clinical features of nephrogenic diabetes insipidus?

A
  • Polyuria

* Polydipsia

31
Q

What is the treatment of nephrogenic diabetes insipidus?

A

thiazide diuretics + NSAIDs

32
Q

What is the role of the kidneys in acid base balance?

A
  1. Secretion and excretion of H+
  2. Reabsoprtion of HCO3-
  3. Production of new HCO3-
33
Q

What is the ⍺-Intercalated cell responsible for?

A
  1. HCO3- reabsorption

2. H+ secretion

34
Q

What is the β-Intercalated cell responsible for?

A
  1. HCO3- secretion

2. H+ reabsorption

35
Q

What are the characteristics of metabolic acidosis?

A
  1. Decreased [HCO3-]

2. Decreased pH

36
Q

What is the compensatory response to metabolic acidosis?

A
  1. Increased ventilation

2. Increased [HCO3-] reabsorption and production

37
Q

What are the characteristics of metabolic alkalosis?

A
  1. Increased [HCO3-]

2. Increased pH

38
Q

What is the compensatory response to metabolic alkalosis?

A
  1. Decreased ventilation

2. Increased [HCO3-] excretion

39
Q

What are the characteristics of respiratory acidosis?

A
  1. Increased PCO2

2. Decreased pH

40
Q

What is the compensatory response to respiratory acidosis?

A
  1. Acute: intracellular buffering

2. Chronic: increased [HCO3-] reabsorption and production

41
Q

What are the characteristics of respiratory alkalosis?

A
  1. Decreased PCO2

2. Increase pH

42
Q

What is the compensatory response to respiratory alkalosis?

A
  1. Acute: intracellular buffering

2. Chronic: decreased [HCO3-] reabsorption and production

43
Q

How much water is reabsorbed in proximal convoluted tubule?

A

67% and 67% NaCL

44
Q

What does fluid first enter?

A

ECF not ICF

45
Q

What happens in ascending loop of Henle?

A
  • not absorbed water

- Na+ Cl- is passively absorbed in thin portion and actively in thick portion

46
Q

What happens in descending loop of Henle?

A
  • water is being passively reabsorbed

- Na+Cl- is not being reabsorbed

47
Q

What helps to create the gradient in the medullary interstitium?

A

urea and salt

48
Q

How is urea reabsorbed in the collecting duct?

A
  1. UT-A1 on apical cell membrane

2. UT-A3 on basolateral cell membran

49
Q

How is the interstitium osmoloarity increased by urea?

A
  • using UT a3 and Ut a1 urea pumped out into interstituim

- increasing the interstitium osmolarity

50
Q

What happens to this urea?

A
  1. reabsorbed by vasa recta (UT-B1)

2. Into loop of Henle (thin descending limb) (UT-A2)

51
Q

Why is urea recycling important?

A
  • helps in water reabsorption (urine concentration occurs)

- Urea excretion requires less water

52
Q

What does vasopressin do in urea recycling?

A

can increase no. of UT-A1 and UT-A3 - so increase permeability of collecting duct to Urea

53
Q

How does ADH work?

A
  1. ADH has arrived through blood vessel to principal cell
  2. Binds to V2 receptor
  3. G protein signalling cascade activated which results in activation of protein kinase A
  4. Protein kinase A increases the secretion of aquaporin 2 channels (AQP2) in vesicle form which is then transferred to the apical cell membrane and then these AQP2 are inserted into the apical cell membrane
  5. When water arrives here (lumen) it is reabsorbed though these channels AQP2 and then AQP4/AQP3 channel
54
Q

What can ADH do to the AQP channels?

A

can up or down regulate AQP2 and AQP3 numbers as required in both basolateral and apical cell membrane

55
Q

How is NaCl reabsorbed in the. thick asceding limb?

A
  1. Na+-K+ ATPase Pump actively pumps out 3 Na+ and pumps in 2 K+
  2. so inside cell low Na+ and so Na+ from fluid enters and then K+ and Cl- leave the cell by K+ Cl- symporter and reabsorbed by blood
56
Q

What is diuresis?

A

increased dilute urine excretion

57
Q

When is there diuresis?

A

low ADH

58
Q

What does the zero or small about of ADH mean for water?

A

No AQP2 channel so none reabsorbed in dct but some in collecting duct reabsorbed and because lots of salt reabsorption but very little water reabsorption

59
Q

What is antidiuresis?

A

concentrated urine in low volume excretion

60
Q

What are the levels of ADH in antidiuresis?

A

high

61
Q

How is base excreted and how is this combatted?

A
  1. A lot of base excreted through feaces
  2. lots of metabolic acid and this is neutralised by bicarbonate
  3. CO2 released by lungs and acids released by kidneys
62
Q

Where is HCO3- reabsorbed?

A
  1. 80% in pct
  2. 10% in thick ascending loop
  3. 6% in dct
  4. 4% in collecting duct
63
Q

How is the bicarbonate ion reabsorbed in the proximal convoluted tubule?

A
  1. CO2 enters cell by diffusion and by action of carbonic anhydrase produces HCO3- and H+
  2. H+ enters tubular fluid by Na+ and H+ anti porter (NHE3) and by the H+ ATPase pump (V-ATPase)
  3. HCO3- leaves the cell by Na+ HCO3- symporter which then enters blood
  4. So HCO3- from tubular fluid gets absorbed into blood
64
Q

How is the bicarbonate ion reabsorbed in the dct and ct by the alpha intercalated cell?

A
  • H+ reabsorbed into tubular fluid by H+ ATPase and H+-K+ ATPase
  • HCO3- leaves cell by Cl- HCO3- anti porter.
65
Q

How is the bicarbonate ion reabsorbed in the dct and ct by the beta intercalated cell?

A
  1. HCO3- leaves cell at apical membrane with Cl- HCO3- anti porter so HCO3- goes into tubular fluid
  2. H+ pumped into blood by H+ ATPase pump
    (mostly in alkalosis)
66
Q

How is new bicarbonate ion produced in the pct?

A
  1. Glutamine produces 2NH4+ and one A2- which gives 2 molecules of HCO3- which is reabsorbed by the blood
  2. NH4+ needs to be excreted by kidneys into tubular fluid by Na+ H+ anti porter (NHE3), diffusion by NH3 gas and once it reaches the tubular fluid it is protonated to form NH4+
67
Q

How is new bicarbonate ion produced in the dct?

A
  1. H+ pumped out (by alpha intercalated cell) is neutralised by buffer (which is NOT bicarbonate) and then this ion is then secreted out
  2. From carbonic anhydrase the H+ is pumped out into tubular fluid and neutralised the HCO3- goes into blood and is effectively a new HCO3- ion
68
Q

What happens to CO2 level when increasing ventilation?

A

decreases CO2 level

Z Year 2 BRS URO (5 decks)

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