Lect 14: Regulating Plasma K+ Flashcards Preview

Unit 7 - Repro & Renal Physiology > Lect 14: Regulating Plasma K+ > Flashcards

Flashcards in Lect 14: Regulating Plasma K+ Deck (39)
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Extracellular K is tightly regulated in the plasma in a normal range of

3.5 - 5 mM but it is the outwardly directed K gradient. Na is low inside the cell and K is low outside of the cell


Why is K+ important?

that K+ gradient across the cell membrane is the major determinant of the potential or voltage difference across the cell membrane in both electrically excitable and unexcitable cells....certain tissues need these currents for the excitability (such a s cardiac tissue, neurons etc.


What organ maintains K+ balance?

the balance is maintained by the renal handing of K by the kidneys which increase or decrease K excretion to match increases and decreases in K+ consumption


the positive charge carried by the movement of the cation, K+ across the cell membrane may arise from passive, protein-mediated transport, or simple diffusion

The positive charge carried out of the cell by K current through membrane channels is the dominant ionic current determining the inside-negative cell membrane potential difference....for a certain K+ conc, the potential difference across the cell membrane (-60mV) is very close to the K+ equilibrium potential


Hyperkalemia - increased k+ conc in plasma (>5)

decreases the magnitude of the outwardly directed K+ conc gradient, decreasing the contribution of the gradient to the cell membrane potential--> less negative potential difference in both excitable and non-excitable cells


What happens to cells/organs as a result of hyperkalemia

when hyperkalemia occurs in excitable cells, electrical signaling is or impulse propagation is disturbed and may cause hyperexcitable muscle contraction, in heart-->uncontrolled muscle spasm-->cardiac arrest


Which type of acidosis can be cause by hyperkalemia?

metabolic acidosis because of the effective exchange of intracellular H+ for extracellular K+ across cell membranes, which adds acid (H+) to the plasma - more K+ want to go into the cell, so more H+ will come out.


Hypokalemia - decrease in plasma K+ so more K+ will want to flow out of the cell (outward gradient increased). What happens to the inside negative potential? difference?

it goes up because more K+ is leaving the cell


How would hypokalemia affect excitable organs?

it would weaken muscle contraction (muscle hypoexcitability) --> if this happens in the lungs, they won't get adequately perfused and you would go into respiratory failure


Which kind of metabolic syndrome could hypokalemia?

METABOLIC ALKALOSIS - because as K+ is rushing out of the cell, H+ are rushing back into the cell and less is around int he blood so you drop H+ conc and you get alkalosis


External K+ balance

since K consumption is variable, the kidney must increase or decrease excrete of it accordingly...in order tot keep the plasma ECF constant

kidneys and feces...colon excretes 10% of ingested K+


Internal K+ balance

is regulated by the Na/K ATPase...keeps plasma K+ in balance....needs to be maintained because 1% shift in intracellular K+ would increase plasma [K+] by 50%


Increased uptake of K+ into cells is the first line of defense against hyperkalemia

plasma levels of K rises because of the food we eat and it could be from their release of diseased or injured cells. To compensate for this, the cell sequesters it inside. Upregulating Na/K ATPase synthesis.
-->insulin, epinephrine and aldosterone promote an increased cellular uptake of K+ and a shift from EC fluid into cells.


Why do diabetics have to watch their K intake

RBC do not have a nuclsus and therefore cannot upregulate synthesis of Na/K ATPase to protect it from hyperkalemia. So the dysregulation of insulin release and circulating levels of insulin in poorly conteolled diabetes mellitus may compromise the tolerance of diabetic patients to a K+ load and predispose them to hyperkalemia


Acidemia inhibits the Na/K ATPase and the Na/K/2Cl co-transporter causing loss of K+ from cells, resulting in hyperkalemia

acidosis - lots of H+ in blood will want to push H+ into cells and cause K+ to rush out of cells causing hyperkalemia.

alkalosis - not enough H+ in the blood so H+ rush out of the cell and K+ rushes in....causing hypokalemia


Acidemia---> hyperkalemia

When H+ conc is high outside of the cell, it gets pumped into the cell. The intracellular conc of H+ now increases, inhibiting the Na/K ATPase and the Na/K/2Cl co-transporter. This decreases K+ uptake into the cell via both transporters, which decreases intracellular K as well as increases exctracellular K possibly causing hyperkalemia

---opposite is true


Decreased cellular uptake of H+ and efflux of H+ will occur when plasma H+ conc decreases.

The resulting decrease in intracellular H+ conc dis-inhibits or stimulates the Na/K ATPase as well as the Na/K/2Cl co-transporter. This dis-inhibition or stimulation increases K+ uptake into the cell via the Na/K/ATPase and the Na/K/Cl co-transporter, which both increases intracellular K+ as well as decreases extracellular K+ possibly causing hypokalemia


If you inject a person with a bolus of K+ their plasma conc will increase initially but then it will decrease. The first line of defense against hyperkalemia is to

increase its uptake into cells. The increase is detected by a change in membrane potential within minutes! By 1) release of aldosterone from the adrenal cortex 2) release of epinephrine from the adrenal medulla 3) release of insulin from the pancreas. They completely mitigate the rise in K+ within an hour...so it is buffered


Reabsorption of K+ in the kidney in the proximal tubule is constitutive (80%) and LH (10%)

So the fraction of K+ filtered does not change when the plasma K+ conc is increased or decreased, whether or not you have hypo or hyperkalemia


It is the distal nephron (late distal tubule and cortical collecting duct) that reabsorbs K+ and secretes it,.

Reabsorption or secretion depends on the plasma conc. if plasma conc is below normal it will be reabsorbed; if it is above normal then it will be secreted


How do you handle K+ when dietary intake is low and K balance is negative?

When K+ balance is negative (too little in diet), increased K+ reabsorption in the distal tubule restores K balance.

==>despite a compensating increase in K+ reabsorption, hypokalemia may result from chronic dietary K+ deficiency.


K+ excretion is regulated either by
1. INCREASING K+ REABSORPTION from the remaining 10% of filtered K+ entering the distal nephron, which decreases K+ excretion when in negative K+ balance

2. by DECREASING REABSORPTION from the remaining 10% of filtered K entering the distal nephron
3. secreting additional K+ into the tubular fluid of the distal nephron, both of which increase K excretion when in positive K+ balance


Handling K+ when intake is too much

secretion by the distal nephron increases...it may increase to levels sufficient 10 - 150% of the filtered load. The compensatory increase in k+ excretion results from a decrease in K+ reabsorptoin as well as from a secretion of K+ into the distal nephron


Which two segments are K+ excretion not regulated?

proximal tubule and loop of Henle


K+ reabsorption in the proximal tubule

==> occurs by solvent drag and by passive electro-diffusion


In the early proximal tubule

active transcellular Na (SODIUM) transport resulting from uptake across the lumen and efflux across the basolateral membrane drives net fluid reabsorption by osmosis transcellularly and via a paracellular pathway between cells.

A flow of K+ is entrained in the flow of fluid between cells driven by osmosis and is described as a process of solvent drag. K is dragged from the TF into the interstitial fluid


In the LATE proximal tubule

transepithelial voltage changes from lumen negative to lumen positive and this provides an electrical driving force "pushing" movement of K+ through the paracellular pathway. Simple electro-diffusion describes the process of paracellular transfer of K+ in the late proximal tubule `


K+ Absorption the Thick AL occurs by both transcellular and paracellular transport

Paracellular pathway: a lumen positive voltage difference across the tubule epithlium drives K+ passively through the paracellular pathway by diffusion. The positive charge is made from K+ channels effluxing it out. The negative charge on the basoalateral side is made by Cl- being pumped out and this draws K+ into the interstitium


K+ Absorption the Thick AL occurs by both transcellular and paracellular transport

Transcellular Transport: transporters
Lumenal transporters: Na-K-2Cl co-transporter gets these thing uptaken into the cell
Basolateral: ion-specific efflux (Na/K ATPase and Cl and K+ channels


The presence of K+ channels in the lumen mediates efflux of a small amount of intracellular K back into the TF, which together with Cl efflux across the basolateral membrane

generates a lumen positive potential difference across the TAL tubular epithelium. The lumen positive potential difference also seves as a driving force for K, Na, Ca and Mg reabsorption across the TAL epithelium