Lecture 4: Renal Physiology: Glomerular and tubular function 2 Flashcards Preview

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Flashcards in Lecture 4: Renal Physiology: Glomerular and tubular function 2 Deck (16):

Is the LOH actually an adaptation?

Bird and reptiles of dray lands have LOH --> concentrate their urine --> extract/hold maximum amount of water


What are some quantitative features of urine in regards to the LOH

Concentration: 50 - 1200 mOsm/kg water
- dilute urine when drinking lots of water - concentrates when in desert/drunk
Volume: 0.5 - 20L per day
Note: must always be generating atleast Some urine --> meed to remove nitrogenous waste


What are the different LOH types in the nephron?

1. Short loop
2. Long loop nephrons


What is the functions of tight junctions in relation to the salt gradient?

Tight "tight" junctions are important --> stop sale moving down its gradient --> allows gradient to build outside of cell --> H2O stays inside of urine


Short Loop nephrons Single effect

290 --> 310 mOsm/L (change of 20 mOsm gradient)
Thick ascending limb
1. Na2ClK channel pumps into cell
2. NaKATPase pumps once Na out into ECF at a time --> single effect
3. K recycles back into tubule vis ROMK (Renal Outer Medulla K channel)
4. HYPERtonic ECF
Note: Water tight Tight junctions
Note: NKCC2 is the target of the diuretic Furosemide


Proportion of salt in TAL

1/3 of salt remains in TAL --> transfer of ions still occurs --> allows GFR to remain constant


What drug targets the Na2ClK channel?



Countercurrent Multiplication

TAL pushes salt out into ECF --> Decrease in TAL osmo and Increase in ECF osmolaity --> Water comes out of opposing TDL --> Increased Osmolality inside TDL
1. Fluid w. gradient of salt
2. ECF has salt gradient
- increased salt in interstitium due to transporter
- increased water removed by TDL
- increased salt concentration in TCL due to H2O removal
MULTIPLICATION: stronger and stronger gradient created --> as more and more H2O is removed from TDL of LOH --> Increased osmolality entering the TAL
- Counter current multiplication --> forms NaCl gradient in Outer medulla
Start: Normal Tissue osmolality 300mOsm --> Finish: 600mOsm at bottom of LOH


Where is water extracted from in the outer medulla?

1. Thin Descending Limb
2. Collecting Duct


Where does the water go which is secreted from the tubules into the ECF (in order to avoid volume overload)

Vasa recta (forms parallel rays from near medullary boundary)
- functions via carrying blood in the opposite direction to fluid flow in the tubules --> Countercurrent flow occurs --> avoids "wash out"
- Descending vasa recta = H2O out and Ascending vasa recta = H2O rebasorbed into BV from TDL --> avoids dilution of salt concentration gradient --> Na+ remains concentrated outside of the urinary filtrate --> keeps gradient


What is the main function of the Vasa recta

Vasa recta excrete water in descending limb --> Vasa recta reabsorbs water in its Ascending limb from CD and TDL --> high H2O available for reabsorption --> no large fluid volume in tubules following Na --> No increased blood pressure --> no increased flow rate --> no decreased reabsorption of Na+ --> not "wash out" of urine --> salt can be reabsorbed by TAL --> keeps salt concentration gradient within tubule


When can wash out not be avoided?

Deregulation of Renal Auto-regulation --> increased BP --> dilution/washout of salt --> cannot concentrate urine


What effect does flow rate have on transfer?

Slow blood flow = low transfer
High blood flow = washout => less able to equilibrate Na and H2O (Salt stays in ECF and isnt reabsorbed in TAL)


What occurs at the Early DCT?

apically: NaCl cotransporter
Basolateral: NaKATPase
Water tight tight junctions
- allows NaCl to be taken from urine + water to stay in tubule --> diluting segment (along w. TAL)
NaCl targeted by thiazide diuretics (used to treat hypertension/heart failure)
NaCl mutation --> Glittleman's syndrome --> hypokalemic metabolic alkalosis --> + hypocalciuric and hypomagnesmic


What is a drug that targets NaCl channel in Early DCT

Thiazide diuretics
-treats hypertension and heart failure


What is the mutation of NaCl channel called?

Glitteman's syndrome --> wasting of Na and Cl being peed out
1. hypokalemic metabolic alkalosis
2. hypocalciuric and hypomagnesmic