Ion regulation_acid/base

Question 1

K+ handling in different nephron segments

Answer 1

Most reabsorbed in PT
some in TAL via NKCC
**Physiological control exerted in CD principle cells where K is either secreted or reabsorbed

Question 2

factors that affect K secretion

Answer 2

1) ECF K
2) Na reabs–>more neg TEPD—>more K in
3) Luminal flow rate —>inc K secretion
4) ECF pH: More H+ out=more K in
5) Aldosterone —>+more K out

Question 3

osmotic diuretics

Answer 3

e.g. mannitol
inhibit reabsorption of water and therefore water esp in the PCT

increase flow—>wash out K concentration—>inc K secretion—>Hypokalemia

Question 4

Carbonic Anhydrase inhibitors

Answer 4

e.g. acetazolamide
inhibit NaHCO3- reabsorption
back up CA reaction—>decrease H/Na exchanger –>increase luminal Na–>diuresis

can cause altitude sickness

Question 5

Loop diuretics

Answer 5

Furosemide (Lasix, bumetanide (bumex)
inhibit NKCC by competing with Cl
increase RBF—>dissipates high solute conc–>decreased water reabs TDL and mCD

cause hypokalemia
Increased excretion of Ca and Mg (hypocalcemia and hypomagnesemia)

**can increase renin due to lower blood volume

Question 6

Thiazide diuretics

Answer 6

e.g. hydrocholorthiazide
act on DCT
inhibit Na Cl co-transport—>increase Na and Cl excretion (and K)

Question 7

Potassium sparing diuretics

Answer 7

inhibit Na reabs, K secretion

often used in combination with other diuretics that increase K secretion

e.g. Triamerene and spironolacetone (block ald)

Question 8

Effects of H+ on free Ca

Answer 8

acidemia =increased H= increased free Ca –> hypercalcemia

alkalemia=low H+= decreased free Ca–> hypocalcemia

Question 9

PTH function

Answer 9

1) release Ca from bone
2) activates Vit D—>increase Ca reabs from kidney
3) increased Ca reabs from Gi

Question 10

Ca regulation in nepron

Answer 10

most is reabs in the PCT
major site or regulation is in DCT where PTH and Vit D can act

transcellular reabs in the TAL and PCT due to positive TEPD

Question 11

Phosphate handling in the nephron

Answer 11

Mostly done in the PCT with the same Na/X co-transporter

**saturable (has Tm)

PTH lowers Tm—>more Pi is excreted

Question 12

Renal handling of Mg

Answer 12

the bulk of Mg is reabsorbed in the TAL by paracellular movement

Question 13

Causes of hyperkalemia

Answer 13

Acidosis
Low Na diet (less negative TEPD)
Hypoaldosteronism (Addisons)

Question 14

Causes of hypokalemia

Answer 14

Alkalosis
Hyperaldosteronism (Conn’s)
diuretics

Question 15

physiological effects of hyperkalemia

Answer 15

lower AP threshold
increased T wave, prolonged PR
moves K into cells

Question 16

physiological effects of hypokalemia

Answer 16

increased AP threshold
low T wave, increased U wave
moves K out of the

Question 17

Renal response to exs acid

Answer 17

all HCO3 is reabsorbed

Increased H+ secretion—>increased excretion as NH4

Question 18

Renal response to exs base

Answer 18

incomplete reabs of HCO3-
decreased H+ secretion
secretion of HCO3- in CD by Beta cells

Question 19

Total H+ excretion

Answer 19

= ex of titratable acids+ ammonium - HCO3-

Question 20

handling of H+ in the nephron

Answer 20

Most H+ is secreted in the PCT in order to reabs more HCO3- (but no real net loss of H+)
the major place for adjustment of H+ ions is the CD (can highly acidify the urine)

Question 21

handling of HCO3- in the nephron

Answer 21

in the PCT combines with H+ —>CO2 via CA—>reenters cell—>HCO3—->reabs thru Na/HCO3- symporter (SATURABLE)

Almost completely reab in PCT

Question 22

factors controlling H+

Answer 22

1) Intracellular pH (decrease—>inc H secretion)
2) Plasma CO2
3) CA activity (if inhibited—>acidosis)
4) Na reabs (increased Na reabs—>increased H+ excretion thru antiporter)
5) ECF K (hypokalemia–>increased K reabs—>increased H+ secretion)
6. Aldosterone

Question 23

Metabolic acidosis

Answer 23

Dec pH either from increased acids, loss of HCO3- (diarrhea)

• –>increased RR
• —>increased H+ secretion, production of new HCO3-

Question 24

Metabolic alkalosis

Answer 24

high plasma pH from gain of base, or loss of acid (vomiting)

—>decreased RR
—>decreased HCO3- reabs
B cells secrete HCO3-

Question 25

hyperchloremic acidosis

Answer 25

type of metabolic acidosis
A.G. is unchanged
loss of HCO3- is matched by gain of Cl-

Question 26

High anion gap acidosis

Answer 26

HCO3- is replaced by unmeasured anion (lactate, ketoacidosis)

anion gap>18