Potassium disorders Flashcards
(27 cards)
Functions of Potassium
- Regulation of neuromuscular excitability and muscle contraction
- Regulation of insulin secretion (low K inhibits secretion; high K stimulates insulin secretion)
Functions of Potassium
- Regulation of neuromuscular excitability and muscle contraction
- Regulation of insulin secretion (low K inhibits secretion; high K stimulates insulin secretion)
Alkalosis and K levels
Alkalosis causes H to move out and K into the cell –> potential hypokalemia
Alkalosis and K levels
Alkalosis causes H to move out and K into the cell –> potential hypokalemia
Acidosis and K levels
Acidosis causes H to move into the cell and K out
Acidosis and K levels
Acidosis causes H to move into the cell and K out
Diarrhea and K levels
There is a loss of K and HCO3 in the stool –> hypokalemia and metabolic acidosis
Diarrhea and K levels
There is a loss of K and HCO3 in the stool –> hypokalemia and metabolic acidosis
Drugs that commonly cause low K
MCC: Loop and thiazide diuretics
Also, Insulin and beta-2 agonists may shift K into the cell
Drugs that commonly cause low K
MCC: Loop and thiazide diuretics
Also, Insulin and beta-2 agonists may shift K into the cell
Clinical findings in hypokalemia
- Muscle weakness (due to changes in membrane potential)
- U waves on ECG
- Collecting tubules become refractory to ADH –> nephrogenic DI –> polyuria
- Tubule cells become distended with fluid (vacuolar nephropathy)
- Rhabdomyolysis (low K inhibits insulin –> decreased muscle glycogenesis)
Clinical findings in hypokalemia
- Muscle weakness (due to changes in membrane potential)
- U waves on ECG
- Collecting tubules become refractory to ADH –> nephrogenic DI –> polyuria
- Tubule cells become distended with fluid (vacuolar nephropathy)
- Rhabdomyolysis (low K inhibits insulin –> decreased muscle glycogenesis)
MCC of hyperkalemia
Renal failure
MCC of hyperkalemia
Renal failure
Pseudohyperkalemia
RBC hemolysis from difficult venipuncture
Pseudohyperkalemia
RBC hemolysis from difficult venipuncture
Clinical findings of hyperkalemia
- Ventricular arrhythmias
- Peaked T waves on ECG (due to accelerated depolarization of cardiac muscle)
- Muscle weakness (high K interferes with membrane excitability by partially depolarizing it)
Clinical findings of hyperkalemia
- Ventricular arrhythmias
- Peaked T waves on ECG (due to accelerated depolarization of cardiac muscle)
- Muscle weakness (high K interferes with membrane excitability by partially depolarizing it)
Functions of Potassium
- Regulation of neuromuscular excitability and muscle contraction
- Regulation of insulin secretion (low K inhibits secretion; high K stimulates insulin secretion)
Alkalosis and K levels
Alkalosis causes H to move out and K into the cell –> potential hypokalemia
Acidosis and K levels
Acidosis causes H to move into the cell and K out
Diarrhea and K levels
There is a loss of K and HCO3 in the stool –> hypokalemia and metabolic acidosis
Drugs that commonly cause low K
MCC: Loop and thiazide diuretics
Also, Insulin and beta-2 agonists may shift K into the cell
Clinical findings in hypokalemia
- Muscle weakness (due to changes in membrane potential)
- U waves on ECG
- Collecting tubules become refractory to ADH –> nephrogenic DI –> polyuria
- Tubule cells become distended with fluid (vacuolar nephropathy)
- Rhabdomyolysis (low K inhibits insulin –> decreased muscle glycogenesis)