urinary concentrating mechanisms Flashcards

1
Q

tubular osmolarity of proximal tubule

A

300mOsm/l

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2
Q

initial and final volume of fluid in proximal tubule

A

125ml/min

45ml/min

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3
Q

osmolarity definition

A

concentration of a solution expressed as the total number of solute particles per litre

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4
Q

tubular osmolarity in descending loop of Henle

A

1200 mOsm/L

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5
Q

tubular osmolarity in ascending limb + why

A

less than 300mOsm/L

extraction of salt decreases osmolarity

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6
Q

volume in loop of Henle + why

A

25ml/min due to loss of water

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7
Q

daily water intake + source

A

25000ml

fluid intake and food metabolism

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8
Q

daily loss of water + sources

A

1000ml- sweat, faeces, airways

remainder lost in urine

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9
Q

what is the default urine type produced?

A

dilute urine

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10
Q

diuresis definition

A

water loss

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11
Q

what happens during diuresis

A

large volumes of dilute hypotonic urine produced

20 litres a day

osmotic potential of 50mOsm/L

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12
Q

antidiuresis definition

A

water conservation

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13
Q

what happens during antidiuresis?

A

small volume of concentrated, hypertonic urine

0.5L a day

12000mOsm/L

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14
Q

important system in creating urine

A

countercurrent system

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15
Q

explain counter current system

A

loop of Henle acts as a countercurrent multiplier, as the different limbs have different permeabilities

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16
Q

explain descending limb movements

A

unregulated water permeability

water moves out of the tubule, leading to increased tubular osmolarity

17
Q

explain structure of ascending limb

A

composed of the thick and thin ascending limb- thin within medulla and then becomes thick in cortex

thick and thin refers to appearance of cells, not diameter

18
Q

explain permeability in thin ascending limb

A

high permeability of sodium- sodium reabsorbed - moves into interstitium

not permeable to water

19
Q

explain permeability in thick ascending limb

A

high permeability of sodium

not permeable to water

20
Q

explain stages of counter current multiplication

A
  1. Thick ascending limb actively transports sodium into the interstitium
  2. interstitial fluid then becomes hypertonic
  3. water leaves the permeable descending limb , increasing the osmolarity to 1200mosm/l
  4. sodium ions thus become more concentrated until they can passively diffuse out of the thin ascending limb, lowering the osmolarity
21
Q

gradient in cortico-papillary interstitium

A

greatest osmolarity near the bottom- least amount of water, greatest amount of sodium

22
Q

how is sodium absorbed by the thick ascending limb of the loop of Henle?

A

secondary active absorption

  1. basolateral sodium potassium ATPase creates inward sodium gradient
  2. one sodium, one potassium and two chlorides then move in via the apical NKCC channel down sodium’s electrochemical gradient
  3. apically, potassium then leaves down its conc gradient via a potassium leak channel
  4. chloride moves out basolaterally passively
23
Q

important molecule that increases hypertonicity

A

urea

24
Q

what percentage of inner medullary interstitial osmolarity is provided by urea?

A

50%

25
Q

explain movement of urea

A
  1. urea leaves the inner medullary collecting duct via the urea transporter
  2. increases the osmolarity of the interstitium so more water is reabsorbed
  3. urea passively moves bak into the loop of Henle, know as urea recycling
26
Q

explain counter current exchange in the vasa recta

A
  1. blood moves down descending limb, water leaves into the hypertonic interstitium
  2. sodium and other solutes diffuse into the blood down their concentration gradient
  3. ascending limb, water is drawn back into the vessels and the solutes move down their concentration gradient
27
Q

what is the net result of the counter current exchange in vasa recta?

A

water is excluded from interstitial fluid and salt is trapped in the interstitium

28
Q

how does water move out the descending limb?

A

via aquaporins

29
Q

different aquaporins + locations

A

AQP1- proximal tubule and descending limb cells

AQP2- apical membrane of collecting duct principal cells

AQP3/AQP4- basolateral membranes of collecting duct principals

30
Q

two different forms of expression of the channels explained

A

constitutively expressed- constant- AQP1, AQP3, AQP4

regulatively expressed- AQP2

31
Q

What regulates the expression of AQP2?

A

ADH, antidiuretic hormone, vasopressin

32
Q

where is ADH produced and secreted?

A

neuroendocrine cells of the neurohypophysis

in the supraoptic and paraventricular nuclei of the hypothalamus

33
Q

ADH function

A

causes the insertion of AQP II in the apical membrane of the principal cells of the collecting duct

increases the permeability of the collecting duct, resulting in more concentrated urine

34
Q

mechanism of ADH

A
  1. binds to V2 receptor on basolateral principle cells
  2. activates adenylate cyclase, producing cAMP and PKA
  3. vesicles containing AQP II phosphorylated resulting in their fusion
35
Q

other functions of ADH

A

activation of NK2CC

activation or urea transporter in inner medullary collecting duct cells

slow blood flow through vasa recta