Jan9 M1-Potassium Homeostasis

Question 1

where K is located in the body

Answer 1

98% in the cells

Question 2

why K evels are tightly regulated

Answer 2

ICF vs ECF K difference dictates membrane excitability

Question 3

membrane excitability in hyperK vs hypoK and consequences

Answer 3

hyperK: depolarization (cells closer to AP threshold)
hypoK: hyperpolarization cells further from AP threshold)
Reason: K rushes out of the cell at depolarization so if high K outside, feel already depolarized a bit

Question 4

main consequence of K problems and problem where it’s more common

Answer 4

arrhythmias. more in hyperK

Question 5

why hyperK associated with decreased membrane excitability

Answer 5

because after causing depol, K inactives the Na channels

Question 6

consequence of hyperK on muscles and the heart

Answer 6

muscle weakness, cramping, paralysis, rhabdomyolysis

heart: arrhythmias (potentially fatal)

Question 7

characteristics of hyperK and hypoK on ECG

Answer 7

hyperK: pointy T waves
hypoK: U waves

Question 8

normal K intake and body stores and urine output daily

Answer 8

100 mmol/day
50 mmol/kg (3500 mmol)
100 mmol/day in the urine

Question 9

2 organs responsible for K excretion and relative importance

Answer 9

colon: less 10% K excretion
kidneys: 90% K excretion

Question 10

plasma K

Answer 10

4 mmol/L

Question 11

high K foods

Answer 11

bananas, oranges, potatoes with skin, coconut water, electrolyte drinks, meat, yogurt, fish, legumes, leafy greens

Question 12

short term vs long term mechanisms of K handling

Answer 12

short term: shift it in the cells

long term: excreted by the kidneys

Question 13

1st mechanism of K shifting

Answer 13

insulin release from pancreas (stimulated by higher ECF K and glucose if present)

Question 14

K shifts in what cells mostly and why

Answer 14

liver and skeletal muscle cells because is where K is highest in the body

Question 15

how K is shifted in skeletal muscle and liver cells by insulin’s effect

Answer 15

Insulin stimulates Na-K ATPase for K uptake

Question 16

2nd mechanism for K shifting and when it is stimulated

Answer 16

beta-adrenergic stimulus from E and NE that act on Na-K ATPase

Question 17

NE and E: where are they released from during exercise

Answer 17

from SS nerves and the adrenal medulla

Question 18

how to treat hyperkalemia

Answer 18

insulin and salbutamol

Question 19

aldo also acts on the Na-K ATPase but in what cells?

Answer 19

PCT and CT/CD

Question 20

K handling in the nephron (by %)

Answer 20

PCT (80%) and loop (20%)
DCT: secreted
CT (CCD): secreted

Question 21

aldosterone acts where

Answer 21

late DCT and CT (CCD)

Question 22

K in the PCT

Answer 22

passive reabso via K channels (follows Na and water). Note: Na-K ATPase (baso)

Question 23

K in the loop of Henle

Answer 23

IN TAL**: Na-K-2Cl transporter takes these in and ROMK (renal outer medullary channel) excretes K (note: Na-K ATPase present (baso))

Question 24

What cells handle secretion in the CCD and what channels are there

Answer 24

principal cells. Na-K ATPase, ENac for Na, ROMK for K

Question 25

aldo function in the CCD (3)

Answer 25

binds aldoR (intially cytosolic), TF that makes ENac and ROMK. ENac lets Na in which makes an electrical gradient for K to go out via ROMK
Revs up the Na-K ATPase

Question 26

stimuli for aldo production (2)

Answer 26

-RAAS (decreased flow to AA)

increase in plasma K -acts on adrenals to make them release aldo

Question 27

states favoring K excretion

Answer 27

• volume contraction (more Na reabso = more K out)
• diuretics (same)
• alkalosis (increases ENac and ROMK activity)

Question 28

what cells are responsible for a greater K excretion in alkalosis and how

Answer 28

alpha intercalated. base in cell so H+ stays in cell so H+ K+ exchanger works less (to take H out and bring K in) so more K out

Question 29

stuff that can cause hyperK and hypoK

Answer 29

hyperK: renal failure (reduced distal Na delivery)
hypoK: diuretics, volume contraction

Question 30

how K excreted in hypovolemia given that much less Na reaches the CCD (avid reabso of Na in PCT)

Answer 30

hypovolemia stimulates RAAS so aldo still acts to secrete K (in PCT and CCD)

Question 31

how aldo senses Na and K (how adrenals know when to secrete aldo)

Answer 31

Na via baroreceptors in the AA (kidney): RAAS

K via plasma conc of K (sensed in adrenals)

Question 32

how does a high salt diet affect K secretion

Answer 32

No rise in K secretion bc the high Na turns off aldo (turns off RAAS) so less ENac channels to begin with