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Flashcards in Urine concentration/dilution Deck (38):
1

Where is ammonium converted to urea?

Liver

2

How do we measure [urea] in the US?

BUN = mg/dL

3

Why is it that on a short term basis, urea excretion may not match the production rate?

Urea is needed in the regulation of water

4

What happens to urea in the proximal tubule? Loop of henle?

50% Reabsorbed in the proximal tubule

About same amount as above secreted in the loop of henle

5

What produces NH4 in the body?

Protein catabolism

6

Why do we reabsorb urea in the proximal tubule and collecting duct, only to secrete a very similar amount in the loop of henle?

Helps to create a hyperosmotic area in the renal medulla

7

What is significant about the loop of henle as far as transporters go?

Has active urea transporters

8

What happens to the [urea] as you move from the proximal tubule to the end of the loop of henle?

increases

9

The amount of urea reabsorbed by the collecting duct is dependent on what? Why?

[ADH], since ADH activates a urea transporter

10

About 40% of the urea that was filtered is excreted. Where did the rest go?

•~10% enters the vasa recta
•~50% enters the loops of Henle

11

To produce concentrated urine the kidney needs what two things?

ADH and a hyperosmotic renal medulla

12

The loops of Henle act as what (as far as countercurrent exchange goes)?

Countercurrent multipliers

13

The vasa recta act as what (as far as countercurrent exchange goes)?

Countercurrent exchangers

14

What are the relative permeabilities to water of the thin descending loop, thin ascending loop, and thick ascending loop?

Thin descending loop is permeable

Thin and thick ascending are not permeable

15

What is occurring in the thick limb of the tubule?

secondary active transport to move Na+ and C1- out of the tubule and K+ back in

16

The thick limb (which is impermeable to water) pumps Na and Cl out in exchange for a K in. What is the consequence of this?

K+ movement inwards causes the lumen to become positively charged, forcing cations out of the lumen, and diluting the filtrate

17

What is Bartter syndrome?

A genetic disease in which Na reabsorption in the thick limb is impaired, (d/t loss of Barttin protein) leading to a chronic loss of Na, Mg, as well as metabolic acidosis

18

The greater the length of the loop of Henle, the (BLANK) the osmolality that can be reached at the tip of the medulla.

The greater the length of the loop of Henle, the GREATER the osmolality that can be reached at the tip of the medulla.

19

Juxtamedullary nephrons have longer loops of Henle and spread the gradient over a longer distance. What is the effect of this?

The greater the length of the loop of Henle, the greater the osmolality that can be reached at the tip of the medulla.

20

What is the overall effect of the nephron countercurrent exchanger? (this is a longer answer probably not suitable for a notecard, but whatevs)

High osmolality of the interstitium allows water from new filtrate to flow into the interstitium, causing hyperosmolality of the filtrate.

Since the filtrate is hyperosmotic to plasma, ions tend to flow out after it leaves the descending limb, but water is prevented from following d/t the walls of the ascending loop. Thus we can remove water from the remaining filtrate in the collecting duct easily d/t this high osmolality of the interstitium

21

Too much blood flowing through the kidney medulla could wash out the gradient. How is this prevented? (2)

1. Minimal blood entering the peritubular capillaries
2. Countercurrent in the vasa recta

22

What is the countercurrent utilized by the vasa recta?

1. As blood travels down, lose water, gain ions
2. As blood goes up, lose ions, gain water

23

What is the MOA of ADH?

Adds aquaporins to the collecting duct via V2 receptor and G protein

24

What is the osmolality of the filtrate at each of the major areas in the nephron (assume Proximal tubule = 1) [descending, ascending, collecting duct]

Descending = 1 or slightly >1

Ascending = <>1 if ADH present

25

What is diabetes insipidus? (2)

Either a lesion in the hypothalamus (central DI) or a problem with recruitment of aquaporins (nephrogenic DI)

26

What are the factors that control ADH release?

BP via baroreceptors

Volume via Atrial stretch receptors

27

Baroreceptors fire in response to what? Where does this signal go? What does this cause?

Fire in response to increased BP.

Goes to NTS.

Less firing causes ADH release and v.v.

28

Which generates a stronger ADH response, a change in blood osmolality or volume?

osmolality

29

What happens to baroreceptors in pts who are confined to a bed?

there is a gradual shift of fluid from the legs to the abdomen, thorax and head. This would increase venous return to the heart and raise the blood pressure in the atria.

Thus increase urine excretion

30

What are the two drugs discussed in class that increase ADH?

1. Morphine
2. Nicotine

31

What is the one drug discussed in class that decreases ADH?

Ethanol

32

Above what plasma osmolality does the thirst response kick in? What causes this to occur?

280 mOsm/kg H2O

Caused by plasma AVP (ADH)

33

What is the relationship between plasma osmolality and [ADH]

Linear

34

What is the relationship between blood volume and [ADH]

Parabolic (kinda)

35

What is the effect on angiotensin II as far as thirst goes?

Increases via stimulating the hypothalamus

36

Why do people with a high protein diet have an increased ability to concentrate their urine?

Increases urea deposition in the medullary interstitium means there is a higher osmolarity gradient

37

Why do patients with Barrett's syndrome end up with hypomagnesemia and hypokalemia?

Cannot transport Mg or other ions if the Na gradient is not established

38

What does dehydration do to the rate of sympathetic nerve firing?

Increases (don't know how)