Transport

Front 1

1. Where is most filtered water resorbed in kidney?
2. if inulin is 1.0 in the Bowman's space and is 3.0 in the PCT what does this mean?
3. ion that is the major driving force for water reabsorption?

Back 1

1. PCT - 2/3, same absorption for Na as well
2. that [ ] tripled, or only 1/3 of water is left
3. sodium Na

Front 2

1. Ion that is absorbed slower than water in PCT?
2. molecules absorbed faster than water in PCT
3. molecule added to urine to find amt water resorb?

Back 2

1. Chloride
2. Bicarbonate, glucose
3. Inulin - neither secreted nor resorbed

Front 3

1. what ions are absorbed in = [ ] to water?
2. ion that accounts for 90% of kidney O2 use?
3. in the PCT, is the peritubular side or the tubular lumen more negative (how much)
4. How is Na transported in the PCT?

Back 3

1. Na and K+
2. Sodium Na
3. Tubular side (-4 mV)
4. actively b/c charge is more (-) in the lumen and b/c it is in = [] on both sides

Front 4

1. In PCT, what is Na movement linked to going from lumen->cell?
2. movement of Na from cell to peritubular fluid is linked to?
3. which 1/2 of PCT does Cl resorption take place in

Back 4

1. symport w/ Glucose, amino acids, or phosphate, or antiport w/ H+
2. Na-K ATPase (3Na out /2K in) & symport of Na and HCO3-
3. second 1/2; and is both active and passive

Front 5

1. lumen->cell how is Cl moved?
2. energy for the process in 1 comes from?
3. How does Cl move from cell to peribular capill.
4. How does Na move from lumen to cell?

Back 5

1. antiport w/ a base such as formate, oxalate, OH-
2. Na/K ATPase on the peritubular side
3. via a K+-Cl- co transporter or selective Cl- channel
4. antiport w/ H+ - byproduct of Hbase dissociation in the cell, base- imp for Cl- resorption

Front 6

1. What are 2 substances absorbed through the tight jxns between PCT cells?
2. Why does Cl pass through the tight jxns?
3. Adaptation of PCT cells to allow for max water resorption?

Back 6

1. Na, Cl-
2. increasing tubular fluid [Cl] provides a gradient, Na follows the Cl-
3. lateral intercellular space, increases SA for Na/K ATPase pumps and water movement to capillary

Front 7

1. Why is fluid resorption favored in the PCT?
2. What "forces" change the backleak of NaCl and water from the intercellular space into the tubule?
3. effect on backleak if cap. hydrostatic P ^?

Back 7

1. low cap. hydrostatic pressure, high capillary oncotic pressure
2. Starling forces
3. backleak increases

Front 8

1. Where is the majority of potassium absorbed?
2. Is it active or passive? - can be secreted though
3. Urea comes from what?
4. What are plasma urea levels expressed as?

Back 8

1. PCT - 67% then TAL 20%
2. Passive, follows Na+ and water thru tight jxns
3. Protein metabolism
4. blood urea nitrogen BUN

Front 9

1. Mech. of urea resorption in proximal tubule?
2. Where is 99% of AA resorbe?
3. How is it moved?
4. Where is 99% of glucose resorbed? (by?)

Back 9

1. NaCl and H2O movement out of the tubule, urea becomes ^ [ ] so it also diffuses to lower [ ]
2. PCT, none is excreted normally
3. Cotransport w/ sodium, or by itself
4. PCT (SGLT2), coupled w/ Na resorption

Front 10

1. Differences between SGLT 1 and SGLT2
2. 2 types of cells in late DCT?
3. whichsecretes H+?
4. Is the DCT permeable to water?
5. What can intercalated cells resorb?

Back 10

1. SGLT1 can est. a much higher ratio of glucose
2. Principal cells (most) and intercalated cells
3. Intercalated
4. Nope
5. K+, can have net resorption in K+ depletion cases

Front 11

1. 2 main dif. between principal cells and other tubular cells?
This is where K+ is excreted in exchange for Na+, controlled by aldosterone

Back 11

1. a. potential difference across the luminal membrane is less than that across basolateral membrane & b. K+ is secreted rather than absorbed from lumen

Front 12

3 impacts of aldosterone on the DCT

Will get a rise in aldosterone in response to ^ K+ intake

Back 12

1. ^ basolateral membrane Na -K pump
2. ^ K permeability across luminal membrane
3. ^ Na+ permeability across luminal membrane

Front 13

1. impact of parathyroid hormone on Ca excretion
2. impact of PO4- on Ca excretion?
3. impact of low ECF on Ca?

Back 13

1. Decreases excretion, so ^ resorption
2. ^ PO4- is higher Ca resorption is
3. increases resorption

Front 14

1. Main location for Mg resorption?
2. impact of Mg, PTH, plasma Ca++ and ECF on excretion?

Back 14

1. TAL of Henle
2. Excretion decreased by low Mg, or ^ PTH or low plasma Ca++, low ECF

Front 15

1. Main location of PO4- reabsorption
2. impact of PTH, plasma POR-, and ECF volume on excretion
3. substance reabsorbed by carrier mediated active transport w/ a max rate?

Back 15

1. Proximal tubule
2. Excretion increased by high PTH, ^ PO4-, and ^ ECF volume
3. Glucose, AA, phosphate & sulfate

Front 16

1. What is splay in a glucose excretion graph
Reabsorption rate = filtered load - excretion rate = (GFR x Pconc) - (V x Uconc)

Back 16

1. curve in the graph where glucose is lost b/c the glucose transporter is saturated in some but not all nephrons

Front 17

1. What is osmotic diuresis?
2. 3 factors that may cause osmotic diuresis?

Back 17

1. Diuressis due to extra glucose in the renal tubule that holds water there, so more particles are retained as well as water
2. Excess of normally reabsorbed solute in renal tubule (glucose), OR presence of nonreabsorbed solute (mannitol) OR inhibition of solute resorption

Front 18

Substances secreted include - K+, H+, NH3, organic acids (urea), organic bases (thiamine) and foreign substances (PAH - Para-aminohippurate)

Back 18

...

Front 19

1. Where is para-aminohippurate excreted?

Back 19

1. in the proximal tubule by a carrier mediated mech., it is not resorbed