fluid Osmolarity/ADH Flashcards
how is body fluid osmolarity regulated? (2)
by a process called Osmoregulation!
even small changes in plasma osmolarity result in hormonal changes that alter water uptake by kidney and stimulate thirst!
where in the nephron does the hormonal regulation of plasma osmolarity occur?
Late distsl tubule and collecting duct!
where in the hypothalmus is thirst regulated
what is is sensitive too?
Pre-optic area
raised plasma osmotic p. and reduced ECF
when is the thrist mechanism set?
only when the level of dehydrdation exceeds the kidney capacity to regulate it
what is ADH/ vasopressin?
where on the kidney does it act?
acts in late distal tubule and collecting duct> allows water reabsorption and regulates plasma osmolarity!
inserts Aquaporin channels into apical/luminal side
water filitered in kidney can then leave via tubule back to plasma
what happens if ADH levels r low?
little water is resbsoed
water stays in tubule>
DILUTE URINE (water dieuris)
changes in plasma osmolarity is corrected by altering TOTAL AMOUNT OF WATER (solvent)
NOT by changes in solute!!!!
ok
Which 2 physiological mechanisms exist to help maintain plasma osmolality?
- Thirst /drinking behaviour
- ADH release
Which of the two physiological mechanisms that control plasma osmolality is its first line of defence?
thirst only occurs if the situation is bad enough that ADH hormone cannot handle it alone.
functions of ADH
How would you describe the osmolarity of glomerular filtrate (tubular fluid) as it reaches the top of the ascending limb of the loop of Henle compared to plasma?
Hypo‐osmotic compared to plasma
(more dilute)
bc in this region water cant leave, so it diluted the tubule
Fluid entering the DCT has low osmolality of 100 mOsm/Kg
how would you describe the Interstitial Osmolarity changes that occur from the cortex to the papillary region of the kidney?
Increase osmotic gradient as you move deeper into the kidney parenchyma
How does this corticomedullary concentration gradient allow the kidney to produce concentrated urine?
Under the influence of ADH, aquaporins in the collecting duct are inserted.
water is drawn out of the filtrate through the aquaporin channels, due to the high osmolarity of the interstitium.
What role does urea play in the kidney? how is it transported?
ADH allows urea recycling from the collecting duct
it moves through the Aquaporin channels along with water
Urea accumulates in the interstitium and aids in increasing the interstitial concentration “1200”
therefore increasing the kidneys ability to produce hyperosmotic urine.(concentrated)
Explain why water leaving the descending limb of the loop of Henle and the collecting duct does not dilute the concentration of the interstitial fluid thus destroying the concentration gradient.
Because of the vasa recta
In the nephron, where is the site of glucose reabsorption?
What has happened to the total volume of filtrate by the end of the proximal tubule??
isotonic (same)
bc water and solutes r both leaving
we have to handle WATER if we wanna change osmolarity,
cuz if we handle salt, weyre only gunna change the Volume
so if u see a patient with a there plasma osmolaraity changing, what we r seeing is a patient who is manifesting a disorder in the way they handle water!
it not that theyre not handling Na properly!
If Water intake < water excretion = plasma osmolarity ____
Water intake > than water excretion = plasma osmolarity ____
Water intake < water excretion = plasma osmolarity ↑
Water intake > than water excretion = plasma osmolarity ↓
where r osmorecpeters located?
how do osmorecepters sense changes in plasma osmolarity?
they have fenestrated leaky endothelium & r exposed directly to systemic circulation (on plasma side of Blood brain barrier)
what structure lies close to the OVLT? what is the significance of this?
Cells of the supra optic nucleus lie close to OVLT
so oslmolarity and BV r being monitered all the time simultaneously!
so there is a feeding from the OVLT from the barorecepter,
so if barorecpeters sense BV is down, there is a drive to release ADH and therefore increase BP
a change in 1% in plasma osmolarity is sufficient to release ADH!
olaaaa
water is saved
Notice that ADH never goes down to zero!
so ADH not an all or nothing response!
weyre ALWAYS secreting a little bit of ADH all the time
Osmotic v Haemodynamic
when BV is significantly low, the body will cope with a low osmolarity
come back to it alaa!
what is the stimulus for thirst?
Large deficits in water
when u sit there and ur just like oooh. im thirsty..ur already 10% over ur normal range of osmolarity
(ur kidney in the background has already tried to correct that but has failed to do so)
the analogue if thirst is craving salt!
cooool
when we drink water, the water goes throught the GI ba3daaaayn gets reabdorbed.
so how do we know when to stop drinking?
thist behaviour is switched off by the active drinking!
ADH effects
Promblems w/ ADH secretion
Central diabetes insipidus
damage to the pituitary gland or hypothalamus. This damage disrupts the normal production, storage and release of ADH.
Nephrogenic diabetes insipidus
defect in the kidney tubules — This defect makes your kidneys unable to properly respond to ADH.
consequences of untreated DI
Severe dehydration
high Na levels (hyoernatremia)
reduce consciousness
coma & death
Treatment
Give Vasopressin (ADH) spray > for nephrogenic
oral spray> for central
what is term used to describe excessive release of ADH from the PP gland or another source
how do patients present?
Syndrome of inappropriate antidiuretic hormone secretion or SIADH
dilutional hyponutremia!>> too much water reabsorbes is diluting the Na concentration in the plasma!
Location of Aquaporins!
explain the Aquapoirns channels sensitive to ADH
ADH allows insertion of AQ 2 on the apical side
AQ 4 >> always at the door!> its always at the basolateral side
bs AQ 2 in apical side, is ony there under the influence of ADH
so if we have no ADH> we have little expression of AQ 2 on luminal side.
why do we need a high medullary intersitial concentration gradient?
which nephron is important in making this?
this will provide us with an osmotic gradient that will pull water out of the cells to be reabsorbed!
Juxta medullary nephrons!
basically is its more concentrated>> more water will want to come out of nephron> causing concentrated urine!
what r the requirement for forming concentrated urine?
& urea helps as well!
those with kidney transplant>> will pee 6-7 liters of urine!
why is this so?
bc that medullary concentration gradient isn’t there yet.. it takes a while to develop!
bc they have no way in forming concentrated urine!
what is process by which medually interstium fluid becomes hyperosmotic?
via Counter Current mechanism
how the counter current mechanism able to do what it does?
it depends on the special anatomical arrangments of the
loops of Henle and Vasa recta!
what r the major factors that contribute to the build up of solute concetration in the renal medulla?
- -Na-K-Cl cotransporter out in thick ascending limb
- active transport of ions from collecting ducts to meduallry interstitium
- diffusion of Urea
what r the special characteristics of the loop of henle that cause solutes to be trapped in the renal medulla?
- Na-K-CL cotranporter
- thick ascending is impermeabke to water> so solutes leaving r not followed by water
what allows water to move out the descending loop of Henle?
it is absolutly dependent on the concentration gradient
which is established by the action of the NA-K-2CL tranporters in the ascending limb!
what allows us to reach very high Medullary interstitium osmolarity int he deepest parts of the nephron?
UREA recycling!
when it moves out of the nephron, it concentrates the interstium!>
moves through AQ channels>> so its dependent on ADH
we have this gradient created by the NA-K-2CL channels, which is AIDED by the recycling of urea
giving us a stratifed vertical gradient!
how much is the Medullary interstitium at the papillae?
hyperosmotic up to 1200 mOsm/Kg at papilla
alaa understanfd the counter current mechanism
What is an effective osmole?
that in the kidney it can have an osmotic effect
Urea NORMALLY doesnt have an osmotic efect in any other tissue in the body,
BUT it DOES have an Osmotic effect in the kidney!
and it will increase the osmalarity and encourage water to move out!
explain Recycling of urea
- Urea reabsorption from medullary CD
- (Cortical CD cells are impermeable to urea)
- Moves into interstitium> makes it more concentrated> then recycled back into the loop
- works only under the influence of ADH
function of VASA RECTA
they work along side with the counter-current multiplier, to prevent the meduallry interstiutium from being dissapated!
w/ out the vasa recta, the solutes that were pumped into the renal medulla by the counter-current sys, would be rapidly dissipated
oh no
how is the vasa recta orientated with the loop of henle
what r 2 special feautres of vasa recta help to presevre the medually osmotic gradient?
runs opposite to it!
1) sluggish slow blood flow> helps minimize solute loss, delivers nutrients
2) hair pin configuration of vasa recta ( acts as an exchanger)
describe how the vasa recta preserves the medullar concentration gradient?
how is everything being transported in and out of the Vasa recta?
Diffusion
pic alaa
Kideny goes through all this just to maintain the meduallry osmotic gradient!
wtf why the fuss? who cares?
bc w/ out this gradient made (1200mmos/L)
we r not able to raise the concentration of the URINE above 300 mmos/L
as a result u wont be able to conserve water when u r dehydrated!
its the hyperosmotic gradient we created in the medullary interstitium is what is gunna allow water to move into the interstiutm and into the blood during times of DEHYDRATION!
