Flashcards in Urine concentration/dilution Deck (38):
Where is ammonium converted to urea?
How do we measure [urea] in the US?
BUN = mg/dL
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
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
What produces NH4 in the body?
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
What is significant about the loop of henle as far as transporters go?
Has active urea transporters
What happens to the [urea] as you move from the proximal tubule to the end of the loop of henle?
The amount of urea reabsorbed by the collecting duct is dependent on what? Why?
[ADH], since ADH activates a urea transporter
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
To produce concentrated urine the kidney needs what two things?
ADH and a hyperosmotic renal medulla
The loops of Henle act as what (as far as countercurrent exchange goes)?
The vasa recta act as what (as far as countercurrent exchange goes)?
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
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
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
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
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.
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.
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
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
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
What is the MOA of ADH?
Adds aquaporins to the collecting duct via V2 receptor and G protein
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
What is diabetes insipidus? (2)
Either a lesion in the hypothalamus (central DI) or a problem with recruitment of aquaporins (nephrogenic DI)
What are the factors that control ADH release?
BP via baroreceptors
Volume via Atrial stretch receptors
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.
Which generates a stronger ADH response, a change in blood osmolality or volume?
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
What are the two drugs discussed in class that increase ADH?
What is the one drug discussed in class that decreases ADH?
Above what plasma osmolality does the thirst response kick in? What causes this to occur?
280 mOsm/kg H2O
Caused by plasma AVP (ADH)
What is the relationship between plasma osmolality and [ADH]
What is the relationship between blood volume and [ADH]
What is the effect on angiotensin II as far as thirst goes?
Increases via stimulating the hypothalamus
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
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