Class: Potassium disorder Flashcards
What is the major route by which potassium is eliminated from the body
Urine
What 3 things regulate K+ balance
Na/K ATPase
catecholamines
insulin
What happens to most filtered K+
Most of the filtered K is reabsorbed in the proximal tubule and loop of Henle
What do CD intercalated cells do with K+?
CD principal cells?
intercalated - reabsorb
principal cells - excrete
define normal, hyperkalemic, and severe hyperkalemic levels
normal = 3.5-5 hyper = > 5.5 severe = >6.5
What causes Pseudohypekalemia- (3) and a reason
hemolysis, leukocytosis, thrombocytosis (k released from these cells- serum value not plasma)
What is #1 reason fro hyperkalemia
renal failure
4 reasons for hyperkalemia (besides renal failure)
Metabolic acidosis
Hyperglycemia
tissue breakdown - most K+ is inside muscle cells
Hypoaldosteronism
Symptoms of hyperkalemia usually start at what level
> 6.5
2 Symptoms of hyperkalemia
Muscle weakness, paresthesias
Arrythmia
How does hyperkalemia cause arrythmia
High K concentration–> inactivation of sodium channels–> decreased excitability
EKG hyperkalemia sign
peaked T wave
What is resting mb potential with hyperkalemia
more positive (closer to threshold)
What does giving Calcium gluconate due to decrease arrythmias dt hyperkalemia
it raises threshold potential
hypokalemia and severe hypokalemia defined as
hypo = < 3.5 severe = < 2.5
Causes of Hypokalemia (5)
Alkalosis periodic paralysis hypothermia- causes shift into cells pseudohypokalemia- metabolically active cells take up K+ after blood drawn Hypomagnesemia
how does alkalosis cause hypokalemia
h ions released and move to the extracellular fluid to minimize the elevation in pH. To preserve electroneutrality, extracellular k enter the cells
Bartter Syndrome: MOA, result, inheritance pattern
AR, mimics loop diuretics to cuase hypokalemia and metabolic alkalosis
How does bartter syndrome present (3)
Presents early in life with
low BP
mental and growth retardation
Gittelman’s syndrome:
presents when, mimics what, result
presents later in life
mimics thiazides (Genetic defect of Na-Cl cotransporter in distal tubule)
result is hypokalemia and metabolic alkalosis
primary defect and urine pH in RTA type 1
impaired distal acidification, pH > 5.5
primary defect in RTA type 2
impaired proximal bicarbonate reabsorption, pH <5.5
primary defect in RTA type 4
decreased aldosterone secretion, pH <5.5
2 hypokalemia sx
Muscle Weakness and cardiac arrhythmia
