May 2, 2016 - SG11 - Abnormal Serum Potassium

Question 1

TTKG Calculation

Answer 1

TTKG = ( Urine K⁺ / Serum K⁺ ) / ( Urine Osm / Serum Osm )

Question 2

Factors Influencing Potassium Movement

Answer 2

Beta-2 agonists - increase the efficiency of the Na/K ATPase by phosphorylating it which brings more potassium into the cell and therefore leads to hypokalemia.

Alpha-2 agonists - decreases the efficiency of the Na/K ATPase by dephosphorylating it which develops hyperkalemia.

Insulin - increases the efficiency of NHE1 which is a Na/H antiporter. More sodium enters the cell which can feed the Na/K ATPase, thereby bringing more potassium into the cell and leading to hypokalemia.

Digoxin - acts as a competitive inhibitor for K+ and therefore less enters the cell, resulting in hyperkalemia

Cell Lysis - ruptured cells leak potassium and results in hyperkalemia

New Cells - require potassium and suck it up, resulting in hypokalemia

Question 3

Treatment of Hypokalemia

Answer 3

ECG to make sure this is not an emergency - if so, give IV potassium at a rate of 1 mmol/minute.

Low potassium leads to a lower potential inside the cell which takes it longer to repolarize after an action potential.

Question 4

Crystals and AKI

Answer 4

Crystals building up inside the kidney such as uric acid crystals or calcium phosphate crystals can cause the kidneys to be plugged or damaged. Can result in blood and protein in the urine.

Question 5

Treatment of Hyperkalemia

Answer 5

Give IV calcium

Give insulin and glucose

Give salbutamol (beta-2 agonist)

Give diuretics (that aren’t K-sparing)

Reduce intake

Give potassium chelators

Question 6

Fluid Retention and Potassium

Answer 6

With dehydrated states the body is trying to retain sodium and cannot effectively excrete potassium. Also, it is holding onto chloride really well too. Potassium cannot effectively leave the principal cell.