diseases of K regulation

Question 1

contributors to internal K balance

Answer 1

insulin, catecholamines and possibly aldosterone

Question 2

How does insulin affect internal K balance

Answer 2

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

Question 3

How do catecholamines affect internal K balance

Answer 3

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.

Question 4

What is external K balance

Answer 4

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

Question 5

How much of the filtered K is excreted

Answer 5

50%

Question 6

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

Answer 6

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)

Question 7

Describe K movement in the cortical collecting tubule

Answer 7

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.

Question 8

What does aldosterone do

Answer 8

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

Question 9

Why is the mineralcorticoid receptor “promiscuous”

Answer 9

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.

Question 10

Causes of hypokalemia

Answer 10

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

Question 11

Acute vs chronic hypokalemia

Answer 11

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

Question 12

causes of extrarenal and renal hypokalemia

Answer 12

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

Question 13

consequences of hypokalemia

Answer 13

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

Question 14

Treatment of hypokalemia due to asymptomatic metabolic acidosis

Answer 14

diarrhea or renal tubule acidosis: K citrate or K bicarbonate

Question 15

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

Answer 15

KCl volume replacement

Question 16

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

Answer 16

K sparing diuretic

Question 17

Treatment of hypokalemia that is symptomatic (arrhythmia, etc)

Answer 17

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

Question 18

Causes of hyperkalemia

Answer 18

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

Question 19

pseudohyperkalemia and first test to do

Answer 19

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

Question 20

acute vs chronic hyperkalemia

Answer 20

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

Question 21

consequences of hyperkalemia

Answer 21

neuromuscular and cardiac problems (peaked T waves, arrhythmias)

Question 22

treatment of hyperkalemia

Answer 22

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