Renal Handling of K, Ca, PO4 3- Flashcards
Normal K+ levels
Why is deviation dangerous?
3.6 to 5.2mEq/L– deviaition is cause for alarm because the resting membrane potential of excitibility cells critically dpends on Extracellular K+
Elevated extracellular K+ depolarizes cells while low K+ levels will hyperpolarize cells.
What percent of K+ is outside? WHy? What happens if this inscrease
2%- by the collective operation of the Na-K-ATPase in cells around the body.
vigorous exercise may acutely damage some muscle cells and this may dump extra K+ into the extracelullular compartment. A quick shift of K+ into skeletal muscle (body wide) can and does “buffer” this type of K+ disturbance.
What two hormones regulate K+ shift? And when?
What else regulates K+ movement between intra and extracelluar
INsulin (after meal) and Epi (fast after trauma or exercise). Both of these hormones promote K+ uptake in muscle by stimulating the Na-K-ATPase activity.
Also K+ intra and extracellular movement is controlled by pH. When acidosis K+ moves out of the cell and alklasis does the opposite. — reasons still debated
What is the prodominant means of K+ excretion?
Urine– although a small amount is lost through feces and urine.
Example what happens to buffer K+ rises
1 K+ load causes a sudden rise
- Theres a fast movement of K+ into cells– serves as an immediate storage so ec K+ isn’t too high
- Overtime (8-14 hours later) there is anincrease in excretion of K+
How much of Potassium (k+) is fillered?
Freely Filtered
PT- 80% - paracellular passive through tight junctions
Thick Ascening Loop of Henle- 10%- Na-k-2CL
Distal and CD- VARIES- this is what is important for body’s regulation (although medullary CD is always associated with net K+ reabsoprtion)
What part of the nephron vaires in K+ absorption/Secretion?
What happens when low dietary intake?
High Dietary intake of K+?
When low dietary intake- distal nephron has small K+ reabsoption (2% of the 10% remaining in filtrate) and then 6% at the medullary CD so only 2% is excreted. (Note that the distal nephron does very little to conserve K+ but active in getting rid of it– high dietary intak)
High intake
- 20-160% of the load is secreted (mainly in the cortical CD)! (10-150% of the filtered amoutn can be excreted- because the secretion makes up for all the early reabsoption in the nephron)
2, Medullary CD still reabsorbs even when K+ is high
In the CD there is both absorption and secretio in the CD? How does this happen?
The principle cells mediate K+ secretion. – since secretion can be so large this is the key modulatory in K+ excretion amounts.
The intercalated cells mediate K+ reabsortpion
Explain the process of secretion of K+ at the cortical CD
On the principle cells!!
- Active Na/K at BL membrane (can be inhibited by ouabin)
- Passive diffusion of K+ into lumen at apical– this K+ is bought in by the BL Na/K+ pump
- There is also K+ channels in the BL so K+ can leak back out.– but little does because of the electrical gradient across the epithelium– more negative towards Apical
How can K+ net secretion be altered
remmeber at the COrtical CD on principle cells
- Closig apical K+ channels so then K+ would leave through BL K+ channels– opposite true as well
- Close apical Na channels- this would reduce the Na/K Pump so less K+ avliable to enter the apical K+ channel
- Abnormally low K+ levels would limit K+ avliable for the Na/K pump so less secretion. High plasma would od the oppotiste.
- Higher than normal tubular K+ woudl redue the electrochemical gradient so there would be a reducton in secretion. Remember this graident is what makes K+ go throught he apical channel into lumen and not the BL chanell back to interstitum.
K+ affects which hormone? How
Aldoesterone! High plasma K+ triggers Aldosterone release. which promotes the opening of apical K_ channels allowing for more secretion. Secretion changes proportionally to aldosterone. Aldosterone also increase Na/K ATPase operation.
Explain tubular flow rate affect on K+ secretio
increased tubular flow (or increased urine formation rate) promotes K+ secretion. Consequently, the increased urine flow associated with extracellular volume expansion leads to
increased K+ secretion
When tubular flow rate is low, the K+ moving out of the
principle cell into the tubular lumen has time to accumulate, slowing further K+ movement out of the cell. When tubular flow rate is high, the K+ moving out of the principle cell is swept away, promoting further K+ movement out of the cell.
Aldosterone has impacts on wht two ions? Why doesn’t that cause probelsm
Na (reabsorption) and K+ (secretion)
High NaCL would lead to high BP so we would reduce aldosterone circulating. Aldosterone promotes Na+ reabsotpin and K+ secretion. so reudcing aldosterone alsosterone will increase Na+ excretion and K+ retention. However, the increased GFR and tubular flow rate (associated with increased blood volume and BP) will promote K+ secretion. The net result is that K+ remains relatively unchanged while the excess Na+ is excreted.
What is a diuretic
An agent that increase urin volume and reduces EC fluid volume. This is usually accomplished by promoting Na+ and H2O excretion. However, the tubular flow dependence of K+ secretion can generate an unwanted side effect of diuretic use. The unwanted side effect is increased K+ excretion.
K+ excretind diuretics- normally act upstream of CD
K sparing- act on CD
When does GI Ca/phophate absorption exceed excretion
When is there a net loss in Ca2+
Growth and pregnancy
In osteoporosis patients, urinary loss of Ca2+ and phosphate can
exceed their gain.
