Reg of Plasma Potassium Flashcards
What is the most abundant IC cation? Why? What can IC K participate in? What is a normal range for EC K?
K (120 mM); use the Na-K ATPase;
specific cofactor for key cellular enzymes like pyruvate kinase, and participating in pH reg;
3.5-5 mM
What is the major determinant for cell membrane voltage difference? What is the main equation to determine membrane potential? Where is K concentration important? How does one maintain K balance?
K concentration gradient;
Nernst equation: Em = -RT/F ln [K]in/[K]out;
electrically excitable and unexcitable cells;
kidneys, which can increase or decrease K excretion to match increases or decreases in K consumption
How is hyperkalemia defined? What does this decrease and what happens to resting membrane potential? What are three consequences of hyperkalemia?
Increase in plasma K to > 5mM; decreases the K concentration gradient and resting membrane potential is depolarized;
muscle hyperexcitability, cardiac conduction problems, and metabolic acidosis because of effective K-H exchange
On the other hand, how is hypokalemia defined? What does this affect in terms of gradient and membrane potential? What are three consequences here?
<3.5 mM; increases outward K concentration gradient which hyperpolarizes the membrane potential;
Muscle hypoexcitability, arrhythmias (e.g. bradycardia) and metabolic alkalosis with more protons entering cell and potassium leaving (effective exchange)
How many mmol K is in the ECF? How about the amount present in muscle, liver, bone and RBC’s? How much does the colon excrete, and what is needed to maintain K balance in the body? How can K excretion be described in equation form?
65; 2600, 250, 300, 250;
just 10 mmole, meaning the kidney has to compensate and excrete more to adjust for variable increases and decreases in K levels in plasma;
Excretion (90 mmol) = Filtration (810) + Secretion (50) - Reabsorption (770)
What is the first line of defense against hyperkalemia? What can help promote this increased cellular uptake of K? Which cells DO NOT participate in uptake of K?
Who could be predisposed to hyperkalemia because of a deficiency of one of the mech’s listed?
Increased uptake/influx of K into cells mediated by Na/K ATPase;
Aldosterone (aldosterone receptor), insulin (with insulin receptor to activate GLUT4 receptors) and epi (increases cAMP);
RBC’s b/c of lack of nucleus;
diabetes mellitus with no insulin and therefore not as tolerant of K load
In the case of e.g. increased plasma H concentration, what happens to H? What would this H do to 2 particular things? What then is affected and what could be caused?
Increased cellular uptake of H into the cell; decreasing IC pH and inhibiting Na/K/2Cl transporter and the Na/K ATPase, affecting uptake of K into cells; this increases K efflux and could lead to HYPERKALEMIA!!!
In the case of low H in the plasma, what occurs with H inside cells? What would this allow for two particular things? What could then be affected?
H would move to EC fluid to compensate for alkalemia; this would disinhibit the Na/K/2Cl and Na/K ATPase and result in increased K influx; this could result in hypokalemia
When you give someone a K load, what happens to K levels in plasma? What is this effectively? How do you ultimately get rid of this K?
They go up, and over a couple hours normalize;
K buffering;
Get rid of the K by renal handling of it, with more excretion over several hours as K shifts from PLASMA to URINE
Where is K excretion regulated? How much is reabsorbed in prox tubule?
Distal nephron (could reabsorb or secrete K depending on K balance and K plasma levels); 80% (constitutively)
What are the two spots where K excretion is NOT regulated? How can you regulate it? Even with reabsorption of K, how could you still get hypokalemia? Given all the reabsorption in distal nephron of K, how much filtered load remains in urine proper?
Prox tubule (80%) and loop of Henle (TAL, 10%); at distal nephron by reabsorbing the 10% you have left, or not reabsorbing the 10% you have left and also secreting K in positive K balance; Chronic dietary K deficiency; 2%
In positive K balance, would there be reabsorption of K in distal nephron? What other action would occur in distal nephron in this state? How does this differ from Na? Ultimately, what levels of K can be excreted in the urine relative to the filtered load?
No; also have secretion of K into tubular fluid;
Na is NOT SECRETED ANYWHERE INTO TUBULAR FLUID!!!
10-150%!!! (Perhaps 20-180% secreted in distal nephron)
How is K reabsorbed in the proximal tubule? What are the two mech’s of reabsorption within the prox tubule? What is found on the basolateral membrane as it applies to K?
Paracellularly;
Entrained by water to move paracellularly in early prox tubule, or because of a more lumen positive transepi membrane voltage potential with more cations in the tubular fluid later on;
Na/K ATPase, and K channels and K-Cl transporters to move K back out of cell
In TAL, how is K reabsorbed? HOw much is reabsorbed? What mediates these two ways of reabsorption? What other ions can be driven in by one of these mechs?
Paracellular (50%) and transcellular (50%);
10% of that filtered;
lumen positive voltage difference due to K channels mediating efflux luminally and Cl channels on basolateral membrane, and presence of Na-K-Cl cotransporter;
Ca and Mg!!
In distal nephron, how is K transported? What happens within the cell and what else can be transported? Where does K go once in the cell? With K being reabsorbed at distal nephron to compensate for _______, what could occur?
Done transcellularly with active transport mediated by K/H ATPase (K in, H out);
Alkalinze cell and drive bicarb out of cell, moving Cl in;
Leaves at basolateral membrane by a K channel;
hypokalemia, you could have secondary metabolic alkalosis with more bicarb in plasma
