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70 Cards in this Set
- Front
- Back
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What is the normal potassium concentration in the ECF?
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4.2 mEq/L
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What is the normal potassium concentration in the ICF?
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140 mEq/L
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What happens if the plasma potassium rises by 3-4 mEq/L?
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Cardiac arrhythmias
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What is the normal K+ intake?
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100 mEq/day
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What is the normal K+ output in urine?
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92 mEq/day
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What is the normal K+ output in feces?
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8 mEq/day
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What percent of total body K is in cells? In ECF?
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In cells = 98%
In ECF = 2% |
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How much potassium can be in a typical single meal?
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50 mEq - almost as much as in the ECF!!
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What is very important that the body be able to do w/ K?
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Get it out of the ECF, so hyperkalemia and cardiac arrythmias don't occur.
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What is the regulation of body potassium primarily dependent on?
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Urinary excretion - only a small percent is via feces, most is in urine.
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What is the body's first line of defense against changes in ECF K concentration?
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Overflow into cells (hyperkal)
Outflow from cells (hypokalemia) |
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4 Factors that shift K+ into cells:
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-Insulin
-Aldosterone -B-adrenergic stimulation -Alkalosis |
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7 factors that shift K+ out of cells:
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-Insulin deficiency
-Aldosterone deficiency -alpha adrenergic stim -Acidosis -Cell lysis -Strenuous exercise -Increased ECF osmolarity |
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What normally happens when you eat a meal with 40 mEq of K?
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The ECF K conc stays constant as K shifts into the cells until the kidneys can eliminate the excess.
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What is one of the most important factors that decreases ECF K after a meal?
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Insulin - increases cell uptake
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What patients are prone to be hyperkalemic after a meal?
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Diabetes mellitus
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What is the syndrome of excess aldosterone?
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Conn's
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How does Conn's syndrome affect ECF potassium?
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There's too much aldosterone, so too much cell uptake, so hypokalemia
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How does Addison's disease affect ECF potassium?
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Not enough aldosterone, not enough cell uptake, not enough renal secretion; Hyperkalemia.
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What causes B-adrenergic stimulation?
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Epinephrine
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What does increased Epi cause?
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More uptake of K into cells
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What happens when you give B-blockers for HTN?
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Potassium fails to move into cells, so hyperkalemia
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Common B-blocker:
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Propanolol
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How does acidosis affect potassium levels? What is the mechanism?
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It decreases Na/K ATPase activity, so decreases cell uptake of K - hyperkalemia
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How does alkalosis affect potassium levels?
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Increases cell uptake of K so hypokalemia
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How would intense exercise kill a person?
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By the skeletal muscle release of K, if severe enough causing cardiac arrhythmia and sudden death.
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How does hyperosmolarity of ECF cause hyperkalemia?
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By decreasing water in the cell, it increases K, increasing its diffusion gradient to flow out, so increasing ECF K.
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What disease is common to have hyperosmolarity of plasma?
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Diabetes mellitus - due to large increases in plasma glucose.
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So 2 reasons for hyperkalemia in diabetes mellitus:
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-Decreased insulin (low cell uptake)
-Increased plasma osmolarity (high cell diffusion out) |
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How do you calculate the potassium filtration rate by the kidneys?
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GFR - Plasma conc
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How much potassium is filtered daily?
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180 L/day x 4.2 mEq/L = 756 mEq/day
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Where is potassium reabsorbed? How much of the filtered load?
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Proximal tubule - 65%
Asc Limb of LOH - 27% |
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How much of the filtered K load reaches the distal tubule?
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8%
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How much K is excreted in urine, why?
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12% - because 4% equivalent is secreted in the late distal tubule and collecting duct.
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What transporter is responsible for reabsorption in the thick ascending LOH? What is it a target of?
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Na/K/2Cl transporter - target of loop diuretics.
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What is the primary cause of daily variation in K excretion?
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The amt of secretion in the late distal tubule and collecting ducts.
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What cells secrete K there?
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Principle cells
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Is K always secreted by principle cells? Why/why not?
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No; it can be secreted or reabsorbed because the transporters are simply K channels.
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What happens to kidney processes when dietary K increases?
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More is secreted
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What happens when dietary K increases extremely?
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The secretion amount can be even higher than the glomerular filtration amount
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What happens when dietary K is significantly low?
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Net reabsorption instead of secretion
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So where does day-to-day regulation of K excretion occur?
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In the late distal and cortical collecting tubules - at the principle cells.
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What percent of cells in the late distal tubules and collecting ducts are Principle?
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90%
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What sets up the driving gradient for K secretion or reabsorption from principle cells?
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Na/K ATPase
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What regulates this Na/K ATPase?
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Aldosterone
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What are the 2 steps of K secretion by Principle cells?
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1. Uptake of K from ISF via Na/K ATPase
2. Diffusion from cell to kidney lumen via its very own special channel on the apical membrane. |
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What is the electrical negativity of the principle cells? Of the lumen?
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Cells = -70 mV
Lumen = -50 mV |
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3 Factors that control K secretion by Principle Cells:
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1. Activity of Na/K ATPase
2. Electrochemical gradient of K 3. Lumen membrane permeability |
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What happens to renal handling of K under conditions of severe depletion?
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Less is secreted, more gets reabsorbed.
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Where does the reabsorption increase occur in the nephron?
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-NOT at the normal sites for K reabsorption
-At the Intercalated cells |
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What transporter allows K reabsorption by intercalated cells?
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H/K ATPase
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Where is H/K ATPase located in intercalated cells?
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At the apical membrane
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Where does the H come from that is co-transported as K is reabsorbed?
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The carbonic anhydrase reaction that generates H+ for secretion.
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3 Principle factors that stimulate K secretion by principle cells:
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1. Increased plasma K
2. Increased Aldosterone 3. Increased Tubular flow rate |
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How does Acidosis affect K secretion?
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Chronic = increased excretion
Acute = decreased excretion |
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3 ways that Increased ECF K stimulates secretion:
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1. Stimulates NA/K ATPase so more pumped from ISF to cells
2. Increases diffusion gradient 3. Increases aldosterone secretion |
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Aldosterone acts on
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Na/K ATPase on the basolateral membrane of Principle cells
-Increased sodium reabsorption -Increased potassium secretion |
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Does Aldosterone ONLY affect NA/K ATPase?
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No; it also increases the luminal membrane K Permeability.
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How much can a 3 mEq/L increase in K plasma concentration increase aldosterone plasma conc?
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From 0 to 60 ng/100 mL - almost 10X!!
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How does increased tubular flow rate increase K secretion?
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It flushes it down and keeps the diffusion gradient high for secretion.
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What are 3 conditions in which tubular flow rate will be high?
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-Volume expansion
-High sodium intake -Diuretic drug treatment |
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When increased sodium intake stimulates high tubular flow rate, what will be the net effect on K excretion? Why?
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No change - because though K secretion is increased, Hi Na = Lo Aldosterone so net effect is no change.
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Why is the tubular flow rate mechanism for regulating K secretion important?
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Because if a patient IS having a high sodium intake, you don't want them to stop excreting K or else it would be bad for the heart.
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What will be the effect of low sodium intake on K handling?
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-Decreased tubular flowrate
-Incresed Aldosterone release -Net no change in K secretion |
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How does Acute acidosis affect K handling?
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Decreases secretion
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How does Acute acidosis decrease K secretion?
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H inhibits Na/K ATPase
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How does acute acidosis alter
-ICF K -ECF K |
ICF K decreases (no pumping in)
ECF K increases (accumulates) |
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How does chronic acidosis increase K secretion?
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By the increase in H+ secretion in the PROXIMAL tubule, it inhibits NaCl/H2O reabsorption; the tubular flow rate increases.
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Acute acidosis leads to
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Decreased K excretion
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Chronic acidosis leads to
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Increased K excretion
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