8 - Renal Potassium and Acid-Base Handling Flashcards
Where is the body’s potassium located?
Approximately 98% of body’s potassium is within the cells.
2% is in ECF where the concentration is 4 mEq/L, this is tightly regulated.
What is normal daily potassium intake? What is that per meal and what effect would that have on EC K concentration?
About 100 mEq/day, which is 33 per meal.
An increase in 33 mEq/L in the 14 L ECF would increase EC K from 4 to 6.4 mEq/L which would cause hyperkalemia.
What are the first signs of hyperkalemia in cardiac tissue? What do further increases lead to?
Tall, thin T waves.
Further increases lead to prolonged PR intervals, depressed ST segments, and lengthened QRS interval.
When ECF is ~10 mEq/L K+, ventricles begin to fibrillate.
How does the body prevent hyperkalemia from occuring? What causes this to occur?
By increasing cellular uptake of K.
Insulin, aldosterone, and b-adrenergic stimulation all increase cellular K+ uptake by stimulating Na/K ATPase pump.
What are factors that increase extracellular potassium?
Insulin deficiency, aldosterone deficiency, alpha adrenergic stimulation, acidosis, and increased plasma osmolarity.
How is K+ handled by the kidneys? How much of the filtered K+ from the kidney is excreted under normal to high intake?
It it freely filtered.
15-80% of the filtered load is excreted in urine.
How much K+ is reabsorbed in the PT and loop of henle under normal/high intake?
What happens to K+ in the CD?
60% reabsorbed by paracellular diffusion in the PT
20-30% in the loop of henle by the Na/K/2Cl transporter
Secreted in the principal cells of the CD via BK and ROMK channels.
How does excretion of K+ change during potassium depletion? How does filtration change and how does PT and thick ascending loop handling change?
Final excretion is about 1% of the filtered load.
K+ is still freely filtered and handled the same way in the PT and thick ascending loop of henle.
How does renal potassium handling differ under depleted conditions?
Difference is in the distal tubule and CD.
Instead of net secretion of K+ by principal cells, there is a reabsorption of K+ in the distal segments by the intercalated cells of the CD.
What are factors that increase potassium secretion?
- Increased ECF potassium concentration - stimulated Na/K ATPase in principal cells, increased potassium gradient, increased aldosterone
- Increased aldosterone
- Increased tubular flow rate (increased Na+ delivery)
- Acidosis (acute) - inhibits K+ excretion
- Acidosis (chronic)- stimulates K+ excretion
How is K+ secretion in the late distal tubule and collecting duct regulated?
Feedback loop.
Increase in plasma K+ increases aldosterone, which increases K+ secretion in the cortical CD, which increases K+ excretion.
What are five ways that elevation of aldosterone increase potassium excretion?
- Increasing Na/K ATPase in basal membrane
- Increased expression of ENaC in apical membrane
- Elevating SGK1 which increases ENaC expression
- Stimulating CAP1 which activate ENaC
- Stimulating permeability of apical membrane to K+
What are the two things that control potassium excretion rate?
Aldosterone and ECF potassium.
What is Addison’s disease and what does it cause?
Lack of aldosterone due to adrenal insufficiency.
Loss of sodium, accumulation of potassium.
What is Conn’s syndrome and what does it cause?
Aldosterone excess due to adrenal tumors.
Sodium retention and potassium depletion.
