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2020 MHS Physio Unit 2 > urine dilution and concentration > Flashcards

urine dilution and concentration Flashcards

1
Q

what is the physiological range in humans for urine concentration?

A
  1. intake exceeds loss
    1. balance is positive
    2. osmolality od body fluids decreases
    3. compensatory mech
      1. excretion of dilute urine
      2. large volume of hyposmotic urine is produced
  2. inttake is less than losses
    1. balance is negative
    2. osmolality of body fluids increases
    3. compensatory mech
      1. excretion of concentrated urine

normal conditions rangle from 50-1200mOsm/L

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2
Q

describe th conditions:

  1. intake exceeds water loss
  2. intake is less than water loss
A
  1. intake exceeds loss
    1. balance is positive
    2. osmolality od body fluids decreases
    3. compensatory mech
      1. excretion of dilute urine
      2. large volume of hyposmotic urine is produced
  2. inttake is less than losses
    1. balance is negative
    2. osmolality of body fluids increases
    3. compensatory mech
      1. excretion of concentrated urine

normal conditions rangle from 50-1200mOsm/L

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3
Q

why doesn’t osmolarity change very much?

A

diuresis-removal of water from the kidney

water moves between ICF and ECF to compensate. In the case of hydration, cells swell.

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4
Q

What location is under hormone control for water reabsorption?

A
  1. Glomerulus=100mOsm/L
  2. PT
    1. reabsorbs large quantity of solutes and waer followed by osmosis leaving osmolarity unchanged
  3. tDLH
    1. highly permeable to water, only. interstitial oSm increases with increasing depth into medulla. Water responds by moving out of the tubule an dfiltrate equiliberates to outside oSm.
  4. TAL/early DT
    1. activly reabsorbs solute but is impermeable to water. Dropping oSm to 100osm/L
  5. late DT/CCT/CCD
    1. water permeability is hormonolly driviventhese section and in the most extreme diuresis highly limited yielding urine osmolarity down to 50mOsm/L
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5
Q

desceibe the nephrons section and their involvment in H2O reabsorption (general)

A
  1. Glomerulus=100mOsm/L
  2. PT
    1. reabsorbs large quantity of solutes and waer followed by osmosis leaving osmolarity unchanged
  3. tDLH
    1. highly permeable to water, only. interstitial oSm increases with increasing depth into medulla. Water responds by moving out of the tubule an dfiltrate equiliberates to outside oSm.
  4. TAL/early DT
    1. activly reabsorbs solute but is impermeable to water. Dropping oSm to 100osm/L
  5. late DT/CCT/CCD
    1. water permeability is hormonolly driviventhese section and in the most extreme diuresis highly limited yielding urine osmolarity down to 50mOsm/L
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6
Q

describe uring concentration (anti diuresis)

A
  1. under negative water balance, water is conserved by renal reabsoprtion
  2. inconctrast with diuresis
    1. DCT/CCT/collecting duct
      1. permeable to water.
      2. can concentrate urine to 1200mOsm
  3. water in this section moves by osmosis in response to interstitial osmolarity which in the deep medulaa can reach 1200mOsm
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7
Q

what are the only organs regulating body water?

A

kidney and sense of thirst

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8
Q

describe the water osmolarity through the nephron. how do diruesis and anti-diuresis play into this structure?

A
  1. PT-isoosmotic
  2. loop of henle-increasing
  3. decreasing after

diuresis

  1. lack of water reabsorption result in hypoosmotic urein
    1. in the distal convoluted tubule
    2. collecting duct tubule
    3. and collecting duct

antidiuresis

  1. water permability leads to hyperosmotic urine in the
    1. distal tubule
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9
Q

ADH is released from and acts where?

A

ADH

  1. stimulation
    1. most effective
      1. increase in osmolarity
      2. detected by osmoreceptors in the hypothalmus
    2. least effective
      1. decrease in blood pressure
  2. fast action
    1. minutes plasma ADH rises several folds
    2. short half life
  3. action
    1. released from the paraventricular cells in pituitary then to the hypothalmus.
    2. ADH binds to the V2 (G protein, AC) receptor in the priciple cells of the distal collecting tubule and collecting duct
    3. this induces premade AQP2 insertion into the apical side of the cells, and transcription of more AQP2.
      1. decreasing ADH->withdrawl of AQP2 into vesicles
  4. note
    1. basolateral membrane contains non-ADH dependent aquaporin isoforms
      1. AQP3 and AQP4
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10
Q

which hormone responds to high osmolarity and is the fastest responding in generating anti-diuresis.

A

ADH

  1. stimulation
    1. most effective
      1. increase in osmolarity
      2. detected by osmoreceptors in the hypothalmus
    2. least effective
      1. decrease in blood pressure
  2. fast action
    1. minutes plasma ADH rises several folds
    2. short half life
  3. action
    1. released from the paraventricular cells in pituitary then to the hypothalmus.
    2. ADH binds to the V2 (G protein, AC) receptor in the priciple cells of the distal collecting tubule and collecting duct
    3. this induces premade AQP2 insertion into the apical side of the cells, and transcription of more AQP2.
      1. decreasing ADH->withdrawl of AQP2 into vesicles
  4. note
    1. basolateral membrane contains non-ADH dependent aquaporin isoforms
      1. AQP3 and AQP4
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11
Q

descreibe the mechanism of ADH

A

ADH

  1. stimulation
    1. most effective
      1. increase in osmolarity
      2. detected by osmoreceptors in the hypothalmus
    2. least effective
      1. decrease in blood pressure
  2. fast action
    1. minutes plasma ADH rises several folds
    2. short half life
  3. action
    1. released from the paraventricular cells in pituitary then to the hypothalmus.
    2. ADH binds to the V2 (G protein, AC) receptor in the priciple cells of the distal collecting tubule and collecting duct
    3. this induces premade AQP2 insertion into the apical side of the cells, and transcription of more AQP2.
      1. decreasing ADH->withdrawl of AQP2 into vesicles
  4. note
    1. basolateral membrane contains non-ADH dependent aquaporin isoforms
      1. AQP3 and AQP4
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12
Q

Is ADH an all or non hormone ?

A

ADH

  1. osmoarilty
    1. proportional to osmolarity of ECF
  2. BP
    1. inversely proportional to blood volume
      2.
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13
Q

compare osmolarity-bp with respect to ADH

A

ADH

  1. osmoarilty
    1. proportional to osmolarity of ECF
  2. BP
    1. inversely proportional to blood volume
      2.
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14
Q

increase ADH leads to an increase in what channel and where?

A

AQP2 in the apical principal cells of the distal tubule in the nephron

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15
Q

permeable to only water

A

permeability differences assist with reabsorption of water

  1. tDLH
    1. permeable to only water
  2. tALH
    1. permeable ot solute bu not water
  3. TAL
    1. permeable to solute but not water

the key to water handeling is the counter current arrangment of the loop of henle

  • filtrate flows in the opposite direction within the two limbs
    • desceing and ascending
    • allowing limbs to differ in terms of water and solut permeability
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16
Q

permeable to only solutes-2 locations

A

permeability differences assist with reabsorption of water

  1. tDLH
    1. permeable to only water
  2. tALH
    1. permeable ot solute bu not water
  3. TAL
    1. permeable to solute but not water

the key to water handeling is the counter current arrangment of the loop of henle

  • filtrate flows in the opposite direction within the two limbs
    • desceing and ascending
    • allowing limbs to differ in terms of water and solut permeability
17
Q

is key to water handling in the nephron?

A

permeability differences assist with reabsorption of water

  1. tDLH
    1. permeable to only water
  2. tALH
    1. permeable ot solute bu not water
  3. TAL
    1. permeable to solute but not water

the key to water handeling is the counter current arrangment of the loop of henle

  • filtrate flows in the opposite direction within the two limbs
    • desceing and ascending
    • allowing limbs to differ in terms of water and solut permeability
18
Q

what two limbs differ in solubility. explain

A

permeability differences assist with reabsorption of water

  1. tDLH
    1. permeable to only water
  2. tALH
    1. permeable ot solute bu not water
  3. TAL
    1. permeable to solute but not water

the key to water handeling is the counter current arrangment of the loop of henle

  • filtrate flows in the opposite direction within the two limbs
    • desceing and ascending
    • allowing limbs to differ in terms of water and solut permeability
19
Q

with the single effect in play how can the multiplication of the sigle effect act to increase the tubule reabsorption?

A
  1. DLH/ALH
    1. 300mOsm/L
  2. tALH impermeable to water

single effect

  1. NKCC2 generates transepithelial 200mOsm/L gradient
  2. with no water from the lumen of ALH into interstium
  3. increases osmolarity to 400mOsm/L
  4. effect
    1. instant equiliberates
      1. with tDLH is permeable to water

multiplication of the “single effect” by counter current flow

  1. isosmotic fluid enters the top of the tDLH and equiliberates with the interstitium
    1. diminishes tha transepithelial gradient to 100mOsm/L
  2. hyperosmotic fluid flows into the bottom of the tALH
    1. no transepithelial gradient at this level
  3. hypoosmotic fluid at the top of the TAL flows toward the cortex
20
Q

describe the single effect in creating an osmotic gradient

A
  1. DLH/ALH
    1. 300mOsm/L
  2. tALH impermeable to water

single effect

  1. NKCC2 generates transepithelial 200mOsm/L gradient
  2. with no water from the lumen of ALH into interstium
  3. increases osmolarity to 400mOsm/L
  4. effect
    1. instant equiliberates
      1. with tDLH is permeable to water
21
Q

describe sodium movement in the NaCl

A

NaCl reabsorption in tALH and TAL

  1. in tALH NaCl movement is passive via paracellular route
  2. in TAL its active with movement into the cell mediated by NKCC2 transporter
  3. NKCC2 can power a 200mOsm gradient max
22
Q

where is the movement of Na via NKCC2

A

NaCl reabsorption in tALH and TAL

  1. in tALH NaCl movement is passive via paracellular route
  2. in TAL its active with movement into the cell mediated by NKCC2 transporter
  3. NKCC2 can power a 200mOsm gradient max
23
Q

what hormone plays a role in Urea reuptake? how?

A
  1. Na and Cl reabsorption drives medullary up to 600mOsm
  2. additional osmolarity increase comes from Urea
    1. urea is produced from amino acid catabolism by the liver
    2. Freely filtered
    3. passivly reabsorbed from CCT
  3. secretion of urea to reach higher concentrations in the tuble compared to the plasma
  4. ADH results in insertion of urea transporter in medullary collecting duct that facilitetes diffusion
  5. greater the concetration of urin=greater [urea] in filtrate in collecting tubules ->more urea that moves back in to the extracellular space and cycles back in the loop of henele
24
Q

what happens when there is a greater [urea] in the CCT?

A
  1. Na and Cl reabsorption drives medullary up to 600mOsm
  2. additional osmolarity increase comes from Urea
    1. urea is produced from amino acid catabolism by the liver
    2. Freely filtered
    3. passivly reabsorbed from CCT
  3. secretion of urea to reach higher concentrations in the tuble compared to the plasma
  4. ADH results in insertion of urea transporter in medullary collecting duct that facilitetes diffusion
  5. greater the concetration of urin=greater [urea] in filtrate in collecting tubules ->more urea that moves back in to the extracellular space and cycles back in the loop of henele
25
Q

describe the % of urea found in the following locations

  1. PCT
  2. tDLH
  3. tALH
  4. CCD
A
  1. Na and Cl reabsorption drives medullary up to 600mOsm
  2. additional osmolarity increase comes from Urea
    1. urea is produced from amino acid catabolism by the liver
    2. Freely filtered
    3. passivly reabsorbed from CCT
  3. secretion of urea to reach higher concentrations in the tuble compared to the plasma
  4. ADH results in insertion of urea transporter in medullary collecting duct that facilitetes diffusion
  5. greater the concetration of urin=greater [urea] in filtrate in collecting tubules ->more urea that moves back in to the extracellular space and cycles back in the loop of henele
26
Q

which nephrons make a greater contribution to the interstitial gradient?

A
  1. juxtamedullary nephrons loop of henle goes further into the medulla than the cortical ones.
  2. juxtamedullary nephron make a greater contribution to the intertitial gradient
  3. they both fuse to make a common collecting duct, allowing water to absorbed from both during anti-diuressi
27
Q

They both act to absorb water during anti-diuresis.

A
  1. juxtamedullary nephrons loop of henle goes further into the medulla than the cortical ones.
  2. juxtamedullary nephron make a greater contribution to the intertitial gradient
  3. they both fuse to make a common collecting duct, allowing water to absorbed from both during anti-diuressi
28
Q

given the counter current arrangemtn of the vasa recta and the loop of henle, how does water get delivered to the restof the circulatory system?

A

starlings equation- increasing the amount of water interstitially leads to a greater pressure and the water goes into the capillary where it is taken up

osmolarity trapping is possible due to the architecture of the kidney:

  1. isolation from other structures
  2. low blood flow to the medulla
  3. counter current geometry
29
Q

Why doesnt the blood on the ascending side of the vasarecta wash out the graient generated by the interstitum?

A

osmolarity trapping is possible due to the architecture of the kidney:

  1. isolation from other structures
  2. low blood flow to the medulla
    1. ​flow in the vasa recta cannot be extreme and some of the solutes are recycled between descending and ascending limbs of the capillary loop
    2. in steady state condition, the gradient is stable and solute + water is continually drawn out of the medulla
  3. counter current geometry

2020 MHS Physio Unit 2 (9 decks)

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