5. Regulation of water balance Flashcards

1
Q

Describe how number of dissolved particles effects osmolarity

A

The greater the number of dissolved particles, the greater the osmolarity

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2
Q

What would happen if we didn’t get rid of the excess volume, excess water and excess salt?

A

Excess Volume: oedema + increase in BP
Excess Water: cells swell
Excess Salt: cells shrink

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3
Q

What are the normal ranges for plasma osmolarity and urine osmolarity?

A

Plasma: 285-295 mosmol/L
Urine: 50-1200 mosmol/L

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4
Q

What is the most abundant component of plasma and ECF?

A

Water

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5
Q

What is the most prevalent solute of plasma and ECF?

A

Na+

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6
Q

What is used to regulate plasma osmolarity?

A

Water balance

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7
Q

What determines ECF volume?

A

Salt concentration (because water follows salt)

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8
Q

What is the main fluid compartment?

A

Intracellular: 65%

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9
Q

What are the different routes of getting rid of water? How much is removed via each of these methods per day?

A

Skin/sweat: 450 mL
Faeces: 100 ml
Respiration: 350 ml
URINE: 1500 ml = variable and regulatable

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10
Q

Describe the movement of water

A

Water flows across a semi permeable membrane from a region of low osmolarity to a region of high osmolarity

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11
Q

What is the consequence of regulation of water and salt balance being interrelated?

A

If we increase salt we have to increase water, which increases volume
If we decrease salt we have to decrease water, which decreases the volume

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12
Q

How much excess water and salt do we consume per day?

A

20-25%

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13
Q

Which region of the nephron is impermeable to water?

A

Ascending limb of loop of henle

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14
Q

How much water is reabsorbed?

A

99%

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15
Q

What determines an animals ability to produce concentrated urine?

A

Medulla to cortex ratio

Large medulla to cortex ratio can make highly concentrated urine

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16
Q

What needs to be created for water to be drawn out of the tubules and into the interstitium?

A

Hyperosmolar Region of interstitial fluid

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17
Q

Describe how much water is reabsorbed in each of the different parts of the nephron.

A

70% in the PCT
10% in the loop of Henle
Amount reabsorbed in the collecting duct varies

18
Q

Describe the osmolarity gradient in the interstitium.

A
Lowest osmolarity (around the same as plasma) in the cortex
Highest osmolarity in the inner medulla
19
Q

What does the shape of the loop of henle allow?

A

Countercurrent system
Descending limb: water exits
Ascending limb: Na+ exits

20
Q

What is the approximate gradient between the ascending loop of Henle and the interstitium?

A

200 mosmol/L

21
Q

What else accounts for the hyperosmolarity of the interstitial space?

A

UREA

22
Q

Which parts of the nephron are permeable to urea? How does this set up a circulation of urea?

A

Bottom of the CD (inner medullary collecting duct)
Bottom of the descending limb of the loop of Henle
The upper part of the CD is permeable to water so concentration of urea increases as it passes down the CD.
The urea moves out into interstitial space (down the concentration gradient) and then passes into the loop of Henle and recirculates.

23
Q

Where are the urea transporters: A1, A2, A3 and B1 found?

A

UT-A1: tubular side of the CD cells
UT-A2: thin descending limb of the loop of Henle
UT-A3: basolateral membrane of CD cells
UT-B1: vasa recta

24
Q

What do Point mutations in UT-A2 result in?

A

Reduced BP

25
Q

What does loss of function mutations in UT-B result in?

A

Reduction in urine concentrating ability

26
Q

Does length of loop of henle determine how concentrated urine can be made?

A

No.

The extent of activity of the transport system does.

27
Q

What supplies blood to the cells in the loop of henle and CD?

A

Vasa recta

28
Q

Describe the permeability of vasa recta

A

Permeable to water and solutes.

29
Q

How do you prevent the vasa recta from washing out the countercurrent gradient?

A

Vasa recta passes along the same path as the loop of Henle
As blood descends it loses water and gains salt
As blood ascends it absorbs water and loses salt
Allows delivery of O2 and nutrients without disrupting the countercurrent gradient.

30
Q

What does ADH bind to?

A

V2 receptors on basolateral membrane of Principal cells in the CD

31
Q

What is ADH also known as?

A

Vasopressin

Antidiuretic hormone

32
Q

Where is ADH synthesised and what kind of hormone is it?

A

Synthesised in hypothalamus
Peptide hormone
Packaged into granules

33
Q

Where is ADH secreted from?

A

Posterior pituitary (neurohypophysis)

34
Q

Which transport channels does ADH stimulate?

A

Aquaporin 2: more move to the apical surface, increasing water permeability and increasing water reabsorption
UT-A1 and UT-A3: increases membrane localisation of these in CCD, this stimulates urea transport from the IMCD into the interstitial tissue and thin ascending limb of the loop of Henle.

35
Q

What triggers ADH release?

A

Increase in plasma osmolarity detected by osmoreceptors in hypothalamus (>300mosmol/L)
Large drop in BP detected by baroreceptors/ stretch receptors

36
Q

What inhibits ADH release? and what does this lead to?

A

Ethanol

leads to dehydration as urine volume increases

37
Q

Describe the response to high water load

A
Decrease plasma osmolarity 
Detected by hypothalamic osmoreceptors
Decreases ADH release
Decreases permeability of CD to water
Increases urine flow rate
Increased fluid loss raises plasma osmolarity
38
Q

Describe the response to dehydration

A

Increase plasma osmolarity
Detected by hypothalamic osmoreceptors
Increases ADH release
Increases permeability of CD to water
Decreases urine flow rate
Decreased fluid loss lowers plasma osmolarity
Increased thirst and water intake lowers plasma osmolarity

39
Q

What keeps plasma osmolarity in a normal range and determines urine output and water balance?

A

Feedback control via ADH

40
Q

State 3 issues that can cause problems with water balance. Which disease involves these 3 issues and what are the symptoms?

A

Absent ADH
No detection of ADH (mutant receptor)
No response to the ADH signal (mutant aquaporin 2)
Diabetes Insipidus: polyuria and polydipsia