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1B Urology and Renal Medicine > Renal regulation of water and acid-base balance > Flashcards

Renal regulation of water and acid-base balance Flashcards

1
Q

what is osmotic pressure proportional to?

A

no. solute particles but not dependant on size of the solute particles

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2
Q

how do you calculate osmolarity?

A

osmolarity= concentration x no. dissociated particules

= Osm/L or mOsm/L

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3
Q

what is the osmolarity for 100mmol/L NaCl?

A

100x2= 200mOsm/L

dissociated into Na and Cl

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4
Q

what is the distribution of body fluid?

A

1/3 extracellular

extracellular= plasma, interstitial fluid, transcellular fluid ( CSF, peritoneal fluid)

2/3 intracellular fluid

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5
Q

what are the process of unregulated water loss?

A

sweat

feces

vomit

water evaporation from respiratory lining and skin

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6
Q

how does regulated water loss occur?

A

renal regulation- urine production

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7
Q

what occur on positive water balance?

A

high water intake -> increase ECF volume, decrease Na conc -> decrease osmolarity

hypoosmotic urine production

osmolarity normalises

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8
Q

how does negative water balance stabalise?

A

low water intake -> low ECF volume, Increased Na conc -> increase osmolarity

hyperosmotic urine production

osmolarity normalises

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9
Q

how does water reabsorption occur?

A

water reabsorbed through passive osmosis so requires a gradient

medullary interstitium needs to be hyperosmotic for water reabsorption from Loop of Henle and collecting duct

cannot absorb water in ascending loop of Henle

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10
Q

what is countercurrent multiplication?

A

passive gradient created from active salt reabsorption and passive water reabsorption in LOH that allows water to flow out of collecting duct

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11
Q

how does urea recycling occur?

A

2 urea transporters in CD

urea enters interstitium increasing osmolarity and enters LOH

this helps water reabsorption so increasing urine concentration and urea excretion requires less water

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12
Q

what are the urea transporter

A

UT-A1 and UT-A3 on collecting duct

UT-A2 on LOH for reabsorption

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13
Q

what is the orle of vasopressin in water reabsorption?

A

promote water reabsorption from collecting duct

boots UT-A1 and UT-A3 numbers

this increases urea recycling and decreases water loss

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14
Q

what is vasopressin /ADH made up of?

A

protein (length of 9 amino acids)

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15
Q

where is vasopressin produced?

A

hypothalamus (neurons in supraoptic & paraventricular nuclei)

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16
Q

where is vasopressin stored?

A

posterior pituitary

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17
Q

what factors are stimulatory on ADH production and release?

A

increased plasma osmolarity

decreased blood pressure/ hypovolemia ( 5-19% change required for detection by baroreceptors- info transferred to hypothalamus)

nause

angiotensin II

nicotine

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18
Q

what factors are inhibitory for ADH production and release?

A

decreased plasma osmolarity

hypervolemia/ increased blood pressure

ethanol

atrial natriuretic peptide

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19
Q

what is the mechanism of action of ADH?

A

ADH binds V2 receptor on basolateral membrane of renal collecting duct

activates G protein which stimulates adenylate cyclase to convert ATP to cAMP

this stimulates protein kinase A which causes AQP2 channels to migrate and fuse with the apical cell membrane

also regulates number of AQP3 on basolateral membrane

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20
Q

what happens during diuresis?

A

increased excretion of dilute urine

at the beginning of the LOH the filtrate is isosmotic

NaCl is actively absorbed in the thick ascending limb LOH creating hypoosmotic fluid

there is low/zero ADH present so there are less AQP2 channels in DCT so lower water reabsorption but continuing salt reabsorption

further salt is reabsorbed in the CD along with some water (transcellular pathways and small amounts AQP)

this causes increased excretion of dilute urine

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21
Q

how is NaCl reabsorbed in the thick ascending limb of LOH?

A
  • NaK+ATPase pump uses ATP to pump in 2 K+ and out 3Na+
  • this creates low sodium within the cell
  • using this gradient the sodium from tubular fluid enters cell using Na+K+2CL- symporter (triple transporter)
  • K+ and Cl- leave the cell via KCl symporter and is reabsorbed by the blood
  • K+ is recycled
  • this allow overall for NaCL to be reabsorbed by the blood
22
Q

what is the difference in NaCl reabsorption between DCT and thick ascending limb LOH?

A

there is no K+ recycling

Na+Cl- symporter instead of triple transporter

23
Q

how is sodium reabsorbed in the collecting duct?

A

using principle cell

NaKATPase pump moves 3 Na+ out of the cell using ATP to ADP + Pi

Na+ is transported into the cell via Na channels - this increases Na+ to be transported out to the blood

24
Q

what happens during antidiuresis?

A

low volumes of concentrated urine

ADH levels high which increases AQP channels

ADH also boost number of following transporters:

  1. thick ascending limb- Na+K+Cl- symporter
  2. DCT- Na+Cl- symporter
  3. CD- Na+ Channel

hypoosmotic fluid reaches DCT- ADH high so increase AQP2 channels in DCT, cortical CD and medullary CD

in CD also uses countercurrent gradient to absorb more water

this increases the concentration of urine- up to 1200mOsm/L and. vol as low as 0.5L/day

25
Q

what is the causes of central diabetes insipidus?

A

deceased/ negligent production and release of ADH

26
Q

what is the cause of nephrogenic diabetes insipidus?

A

less/mutant AQP2

mutant V2 receptor

27
Q

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

A

increased production and release of ADH

28
Q

what are the clinical features of diabetes insipidus?

A

polyuria

polydipsia

29
Q

what are the clinical features of SIADH?

A

hyperosmolar urine

hypervolemia

hyponatremia

30
Q

what is the treatment for central diabetes insipidus?

A

enternal ADH

31
Q

what is the treatment for nephrogenic DI?

A

thiazide diuretics + NSAIDS

32
Q

what is the treatment for SIADH?

A

non-peptide inhibitor of ADH receptor

( conivaptan & tolvaptan)

33
Q

what is the role of the kidneys?

A

secretion & excretion H+

reabsorption of HCO3-

production of new HCO3-

34
Q

by what equation does bicarbonate neutralise H2SO4 and HCl?

35
Q

how is a new addition of metabolic acid created?

36
Q

what is the role of bicarbonate ions

A

act as buffer

regulated by kidneys and lungs

CO2 + H20 H2CO3 H+ +HCO3-

first conversion via carbonic anhydrase

37
Q

what is the Henderson-hasselbalch equation?

38
Q

where is bicarbonate ion reabsorbed?

A

80% PCT

10% thick ascending LOH

6% DCT

4% Medullary CD

39
Q

if there is a change in Pco2 what is the acid base disorder due to

A

respiratory system

40
Q

if there is a change in HCO3- conc, what is the acid base disorder due to?

A

metabolic disordere

41
Q

how are bicarbonate ions reabsorbed in PCT?

A
  1. Na+K+ ATPase removes 3Na+ from the cell and brings 2K+ in
  2. H+ and HCO3- are converted from H20 and CO2 inside the cell
  3. H+ acts on 2 mechanisms
    1. Na+H+ antiporter (NHE3)
      1. uses the downhill energy released by sodium to transport the proton into tubular fluid
    2. H+ATPase pump (V-ATPase)
      1. pumps proton out into tubular fluid
  4. bicarbonate leaves via Na+HCO3- symporter (NBC1)
    1. enters blood
  5. the H+ in tubular fluid conbines with HCO3- to form H20 and CO2 via carbonic anhydrase (via H2CO3) and enters the cell again via diffusion
  6. this process allows bicarbonate from tubular fluid to be reabsorbed
42
Q

how are bicarbonate ions reabsorbed in DCT and CD?

A
  1. 2 cells used here
    1. alpha intercalated cells
    2. beta intercalated cells
  2. alpha intercalated cells:
    1. pump out H+ into tubular fluid by H+ATPase and H+K+ATPase pump
    2. bicarbonate leaves cell into blood by CL-HCO3- antiporter
  3. beta intercalated cells (less important as causes loss bicarb)
    1. Cl-HCO3- antiporter present on apical membrane to move bicarbonate into tubular fluid
    2. H+ pumped into blood by H+ATPase pump
43
Q

what is the role of alpha intercalated cells?

A

HCO3- reabsorption

H+ secretion

44
Q

what is the role of beta intercalated cells?

A

HCO3- secretion and H+ reabsorption

important in alkalasis- want to lose the extra bicarbonates

45
Q

how are new bicarbonate ions produced in PCT?

A
  1. via amoniogenesis
  2. glutamine produces 2NH4+ and A(2-)
  3. A2- gives 2 molecules of bicarbonate (reabsorbed by blood)
  4. ammonia ions excreted by body (or would be converted to urea and proton by liver- proton need to be bonded to bicarbonate to no new net gain of bicarbonate )
    1. transported to tubuar fluid by:
    2. Na+H+ antiporter (NHE3)
    3. diffusion as NH3 gas
      1. NH3 bings with H+ to form NH4+ which is excreted by kidney
46
Q

how are new bicarbonate ions produced in DCT and CD?

A
  1. via alpha intercalated cells H+ are pumped into tubular fluid
  2. H+ react with HPO42- in tubular fluid (phosphate buffer)
  3. form H2PO4- which is excreted
  4. as this buffer is no a bicarbonate the original bicarbonate produced from H2) and Co2 in principle cell can be transported to blood by Cl-HCO3- antiporter as new bicarbonate
47
Q

what acid-base disorder is characterized by:

low HCO3-

low pH

what is the compensatory mechanism?

A

metabolic acidosis

compensation:

  1. increased ventilation
  2. increased HCO3- reabsorption and production
48
Q

what acid base disorder is chacterised by high HCO3- and high pH:

what is the compensation?

A

metabolic alkalosis

compensation:

  1. hypoventilation
  2. increased HCO3- excretion
49
Q

what acid-base disorder is characterised by high Pco2 and low pH?

what is the compensation?

A

respiratory acidosis

compensation

acute: intracellular buffering
chronic: HCO30 reabsorption and production

50
Q

what acid base disorder is characterised by low Pco2 and high pH?

what is the compensation

A

respiratory alkalosis

acute: intracellular buffering
chronic: decreased HCO3- reabsorption and production

1B Urology and Renal Medicine (6 decks)

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