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70 Cards in this Set

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