Kidney 3

Question 1

What concentration of waste products are we obligated to remove each day?

Answer 1

600mosm

Question 2

What is the maximum concentration of urine we can possibly produce?

Answer 2

1400mosm/L

Question 3

What volume of water loss are we obligated to lose even in extreme water deprivation?

Answer 3

0.44L/day

Question 4

What is a urine output of less than 0.44L/day called?

Answer 4

Oliguria

Question 5

What definition is given to dilute urine?

Answer 5

Osmolarity <300mosm/L (that of plasma)

Question 6

What is a normal urine output?

Answer 6

1-2L/day

Question 7

What is a urine output of >2.5L/day called?

Answer 7

Polyuria

Question 8

Wha is the term given to the rate of clearance of all osmotically active particles?

Answer 8

The osmolar clearance

Question 9

What is the formula for osmolar clearance?

Answer 9

Clearance (osmolar) = (U(osm) x V) / (P(osm))

NB: V = urine flow rate

Question 10

What is free water clearance?

Answer 10

The volume of blood plasma that is cleared of solute free water per unit time.

Question 11

What is the free water clearance formula?

Answer 11

Clearance (water) = V - clearance(osmolar)

NB: V = urine flow rate

Question 12

What would a free water clearance > 0 mean?

Answer 12

Hypo-osmotic, dilute urine

Question 13

What would a free water clearance < 0 mean?

Answer 13

Hyper-osmotic, concentrated urine

Question 14

What receptors monitor the osmolarity and where are they located?

Answer 14

Osmoreceptors near the hypothalamus

Question 15

In which X3 specific locations are the osmoreceptors in the hypothalamus found?

Answer 15

1) OVLT = organum vasculosum lamina terminalis
2) MPN = median preoptic nucleus
3) SFO = sub-fornical organ

Question 16

Where do the osmoreceptors signal to when they detect changes in plasma osmolarity?

Answer 16

To the paraventricular and supraoptic nuclei in the hypothalamus

Question 17

what do the paraventricular and supraoptic nuclei in the hypothalamus do when triggered by the osmoreceptors?

Answer 17

They produce and secrete ADH into the blood stream via the posterior pituitary, which travels in the blood to the kidneys and stimulated the expression of AQP2 water channels in the collecting ducts to increase water reabsorption. This is done via stimulation of V2 GPCR receptors which increase levels of cAMP.

Question 18

What is the plasma half life of ADH?

Answer 18

10-20 mins

Question 19

Where are the osmoreceptors for thirst located?

NB: they are NOT located in the same nucleus as those for ADH

Answer 19

In the pre-lateral nuclei

Question 20

Other than osmolarity, what other things can alter the release of ADH?

These all require difference percentage changes to trigger ADH release, which requires the most and least percentage change to mount an ADH release response?

Answer 20

Blood pressure and blood volume

Osmolarity = smallest % change requires
Blood volume
Blood pressure = largest % change required

Question 21

Explain diabetes insipidus.

Answer 21

• Not linked to diabetes mellitus
• is an ADH related condition
• symptoms same as diabetes mellitus
• for one of X2 reasons there is no ADH mediated increase in AQP2 expression in the collecting ducts

Question 22

What are the X2 types of diabetes insipidus?

What is the malfunction in each of these types?

Answer 22

1) neurogenic = no ADH secretion at all

2) neonrogenic = improper kidney response to ADH (still secreted but no/ reduced effect)

Question 23

What happens to potassium at the renal corpuscle?

Answer 23

It is freely filtered

Question 24

How much potassium is reabsorbed overall?

Answer 24

95%

Question 25

How much potassium is reabsorbed at the PCT?

How is this achieved?

Answer 25

65%

It follows the movement of Na and H2O via passive diffusion between cells, as there are no transporters for K on the luminal membrane in the PCT.

Question 26

How much potassium is reabsorbed at the thick ascending limb?

How is this achieved?

Answer 26

30%

By the Na/K/Cl co-transporters that are also important for Na reabsorption here

Question 27

How much potassium is reabsorbed at the DCT?

How is this achieved?

Answer 27

5%

Via intercalated cells (type A) (same as those found in the collecting duct) which use a K/H exchanger

Question 28

How much potassium is reabsorbed at the collecting duct?

How is this achieved?

Answer 28

There are X2 types of cells here

1) principal cells = which were good for Na reabsorption = actually secrete K!!
2) type A intercalated cells = same as those used for K reabsorption in the DCT via K/H antiporters in the luminal surface

Question 29

In terms of K secretion in the collecting duct principal cells, what are the X3 types of channels which secrete K?

Answer 29

1) ROMK = renal outer medullary K channels
2) BK = big conductance K channels (calcium activated)
3) K/Cl co-transporters

Question 30

Which outweighs which in the collecting duct:

Principal cell secretion of K or type A intercalated cell K reabsorption?

Answer 30

Principal cell K secretion

Question 31

What affects the principal cell secretion or K?

Answer 31

Aldosterone stimulates all the channels

Question 32

What can excess insulin cause?

Answer 32

Hypokalaemia

Question 33

How does the K sparing diuretic spironolactone work?

Answer 33

Inhibits aldosterone acting on the principal cells therefore reduced K secretion

Question 34

How does the K sparing diuretic amiloride work?

Answer 34

Inhibits principle cell Na channels therefore reduces K secretion

Question 35

What are the treatment steps for hyperkalaemia?

Answer 35

1) calcium to antagonise K effect on heart (decreases RMP therefore increasing the stimulus needed to initiate an AP)
2) give insulin sliding scale to shift K into the cells (exploiting the excess insulin effect seen in hypokalaemia)
3) give loop diuretics to increase K excretion (thiazide/furosemide)