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Flashcards in diseases of K regulation Deck (22):

contributors to internal K balance

insulin, catecholamines and possibly aldosterone


How does insulin affect internal K balance

1) turns on Na/K pump which pumps 3 Na out of cell and 2 K into cell. 2)tuns on Na/H antiporter which transports Na into cell and H out of cell. The increased Na is then pumped out cell by Na/K pump, bringing K into cell


How do catecholamines affect internal K balance

Beta 2 agonist binds to Beta 2 receptor which then uses ATP to form cAMP. cAMP activates the Na/K pump, pumpning K from outside of the cell into the cell.


What is external K balance

anything you consume must be removed from the body to maintain a balance


How much of the filtered K is excreted



How much K is in the proximal tubule, descending limb, ascending limb, cortical collecting tubule, medullary collecting tubule

proximal tubule: 30-50% of filtered load. Descending lib: 120-140% of filtered load (due to K addition). Ascending limb: 15-20% of filtered load (due to K reabsorption). Cortical collecting tubule: 50% (K secretion). Medullary collecting tubule: 30% (K reabsorption)


Describe K movement in the cortical collecting tubule

epithelial Na channel (eNac) on apical side allows Na to move into the tubular cell. Na is then pumped out the basolateral membrane by Na/K pump which pumps K into the cell. Increased intracellular K is then secreted out of the cell via K channels on apical side.


What does aldosterone do

activates Na/K pump, Na channel or K channel and can eventually induce hypokalemia


Why is the mineralcorticoid receptor "promiscuous"

This receptor can bind to aldosterone as well as glucocorticoids such as cortisol. The receptor must be protected from these to prevent constant activation and hypokalemia.


Causes of hypokalemia

Transcellular shift (stress), decreased total body K (decreased intake or increased loss from GI or renal), or spurious (high WBC count )


Acute vs chronic hypokalemia

acute causes: cell shift seen in catecholamine excess (medications such as beta 2 agonist, or in stress such as asthma or alcohol withdrawal). Chronic causes: renal vs extrarenal loss of K. Extrarenal will have low urine K, renal will have high urine K


causes of extrarenal and renal hypokalemia

extrarenal: metabolic acidosis from diarrhea or decreased intake. Renal: metabolic alkalosis, low magnesium (nl pH) or metabolic acidosis (renal tubular acidosis)


consequences of hypokalemia

neuromuscular (weakness to paralysis of any muscles) and cardiac problems (EKG changes)


Treatment of hypokalemia due to asymptomatic metabolic acidosis

diarrhea or renal tubule acidosis: K citrate or K bicarbonate


Treatment of hypokalemia due to asymptomatic metabolic alkalosis/nl pH that is normotensive

KCl volume replacement


Treatment of hypokalemia due to asymptomatic metabolic alkalosis/nl pH that is hypertensive

K sparing diuretic


Treatment of hypokalemia that is symptomatic (arrhythmia, etc)

IV replacement of K up to 40mEq/hour. Continous ECG monitoring and serial serum K monitoring


Causes of hyperkalemia

decreased renal excretion, transcellular shift into ECF (DKA or hyperglycemia), or spurious (increased platelet count)


pseudohyperkalemia and first test to do

hyperkalemia in test tube but not in patient: do EKG FIRST and repeat serum K. If EKG is abnormal, treat for hyperkalemia This can occur from hemolysis, tough draaw, thrombocytosis


acute vs chronic hyperkalemia

acute: inadequate insulin response (ie diabetes), medications (beta blockers that are non selective), ischemic body part (rhabdomylosis, intestinal arterial insufficiency). Chronic: high dietary K intake is rarely sufficieny, must include a renal excretory defect. GFR usually not problem until <20mEq/L


consequences of hyperkalemia

neuromuscular and cardiac problems (peaked T waves, arrhythmias)


treatment of hyperkalemia

IF ECG changes: calcium gluconate, sodium bicarb, glucose and insulin, albuterol nebulizer, K exchange resin, hemodialysis. If no ECG changes: rule out spurious hyperkalemia