• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/10

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

10 Cards in this Set

  • Front
  • Back

Distribution of K in body

>98% in cells


Only 3.5-5 mM in ECF


- low [K] -> vasoconstriction et vice versa


Main determinant of cell V


Required for cell fx's & growth


Required for RMP

Internal K balance

Determined by Na/K-ATPase


- EC K(M, K) ~ 1mM -> saturated


- IC K(M, Na) ~ cell lvl -> IC [Na] affects [K]!

Role of insulin in K balance

-> ↑ K uptake:




- ↑ Na/K-ATPase activity


- ↑ glucose uptake -> G6P -> Na/Pi co-transport required ->


- ↑ Na/H exchanger activity ->


=>> ↑[Na](ic) -> Na/K-ATPase stimulated

Role of exercise/catecholamines in K balance

AP -> Na in, then K out -> ↑[Na](ic) -> N/Kase stimulated; BUT


Na in < K out -> much more K lost than can be regained =>


K -> T tubules & circulation => catecholamines:


- pre-exercise: epinephrine -> β-R -> ↑ N/Kase -> K uptake


- post-exercise: norepinephrine -> α-R -> ↓ N/Kase -> K loss from muscle

Role of A-B balance in K balance

~ each H entering cell is replaced by K leaving -> electroneutrality


- mostly during gain/loss of HCl (not organic acids / CO2)




=> K depletion -> IC acidosis, et vice versa

Role of plasma osmolality in K balance

Plasma hyperosmolality -> cell shrinkage -> ↑[K](ic) -> K leaks -> hyperkalemia


- vice versa: hypotonicity, swelling (diabetes mellitus - glucose is effective osmolyte)

External K balance

Regulation of renal/GI K excretion


K is present in most food


-> K mostly excreted, not too necessary to conserve

K transport along nephron

PT: 2/3 K reabsorbed, passive paracellular


Mediated by solvent drag & lumen + voltage (2nd half)


ALH: thin - K secreted, passive (high medullary [K])


thick - most K reabsorbed again


=> cortico-papillary gradient -| back leak from CD in medulla


DT & CD: cortical - principal cells (Na X K secretion) > α-type intercalated cells (H X K reabsorption)


basal N/Kase: 3Na/2K -> Na reabsorbed > K secreted -> lumen '-' charge -> furhter luminal K channel secretion


medullary CD - only reabsorption: passive & luminal H/Kase

K secretion regulation

Takes place predominantly in late DT & CCD


Plasma [K] -> (↑ aldosterone) -> ↑ K secretion (directly)


↑ rate of Na reabsorption in CCD -> ↑ K secretion (coupled)


[Cl-] (wrt/ other anios) in tubular fluid -> ↑ K reabsorption (w/ Cl-)


↑ Luminal flow rate -> ↑ K secretion (passive & signaling via cilia)


↑ ADH -> ↑ K secretion (water & K secretion uncoupled)


↑ pH -> K secretion

TTKG (Trans-Tubular K Gradient)

- Extrapolates driving F for K secretion by correcting for H2O reabsorption


- Determines if inappropriate response to hyperkalemia is due to kidney fx




TTKG = [U(K)/P(K)] / [U(osm)/P(osm)]