Jan9 M1-Potassium Homeostasis Flashcards
where K is located in the body
98% in the cells
why K evels are tightly regulated
ICF vs ECF K difference dictates membrane excitability
membrane excitability in hyperK vs hypoK and consequences
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
main consequence of K problems and problem where it’s more common
arrhythmias. more in hyperK
why hyperK associated with decreased membrane excitability
because after causing depol, K inactives the Na channels
consequence of hyperK on muscles and the heart
muscle weakness, cramping, paralysis, rhabdomyolysis
heart: arrhythmias (potentially fatal)
characteristics of hyperK and hypoK on ECG
hyperK: pointy T waves
hypoK: U waves
normal K intake and body stores and urine output daily
100 mmol/day
50 mmol/kg (3500 mmol)
100 mmol/day in the urine
2 organs responsible for K excretion and relative importance
colon: less 10% K excretion
kidneys: 90% K excretion
plasma K
4 mmol/L
high K foods
bananas, oranges, potatoes with skin, coconut water, electrolyte drinks, meat, yogurt, fish, legumes, leafy greens
short term vs long term mechanisms of K handling
short term: shift it in the cells
long term: excreted by the kidneys
1st mechanism of K shifting
insulin release from pancreas (stimulated by higher ECF K and glucose if present)
K shifts in what cells mostly and why
liver and skeletal muscle cells because is where K is highest in the body
how K is shifted in skeletal muscle and liver cells by insulin’s effect
Insulin stimulates Na-K ATPase for K uptake
2nd mechanism for K shifting and when it is stimulated
beta-adrenergic stimulus from E and NE that act on Na-K ATPase
NE and E: where are they released from during exercise
from SS nerves and the adrenal medulla
how to treat hyperkalemia
insulin and salbutamol
aldo also acts on the Na-K ATPase but in what cells?
PCT and CT/CD
K handling in the nephron (by %)
PCT (80%) and loop (20%)
DCT: secreted
CT (CCD): secreted
aldosterone acts where
late DCT and CT (CCD)
K in the PCT
passive reabso via K channels (follows Na and water). Note: Na-K ATPase (baso)
K in the loop of Henle
IN TAL**: Na-K-2Cl transporter takes these in and ROMK (renal outer medullary channel) excretes K (note: Na-K ATPase present (baso))
What cells handle secretion in the CCD and what channels are there
principal cells. Na-K ATPase, ENac for Na, ROMK for K
aldo function in the CCD (3)
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
stimuli for aldo production (2)
-RAAS (decreased flow to AA)
increase in plasma K -acts on adrenals to make them release aldo
states favoring K excretion
- volume contraction (more Na reabso = more K out)
- diuretics (same)
- alkalosis (increases ENac and ROMK activity)
what cells are responsible for a greater K excretion in alkalosis and how
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
stuff that can cause hyperK and hypoK
hyperK: renal failure (reduced distal Na delivery)
hypoK: diuretics, volume contraction
how K excreted in hypovolemia given that much less Na reaches the CCD (avid reabso of Na in PCT)
hypovolemia stimulates RAAS so aldo still acts to secrete K (in PCT and CCD)
how aldo senses Na and K (how adrenals know when to secrete aldo)
Na via baroreceptors in the AA (kidney): RAAS
K via plasma conc of K (sensed in adrenals)
how does a high salt diet affect K secretion
No rise in K secretion bc the high Na turns off aldo (turns off RAAS) so less ENac channels to begin with
