Na/K/H2O Handling

Question 1

Equation for calculating serum osmolarity

Answer 1

SOsm = 2 x Na + (BUN/2.8) + (Glucose / 18)

Question 2

Normal sOsm

Answer 2

285 +/- 3 mOsm/kg

Question 3

Normal ECF K+

Answer 3

3.5 - 5.0 mM

Question 4

What is the main driving force for reabsorption of fluid from the renal interstitium into peritubular capillaries?

Answer 4

The oncotic pressure of the capillaries

Recall that the colloid pressure of the capillaries is high due to the presence of plasma proteins and the loss of fluid upstream via filtration

Question 5

What is the effect of tubular flow on sodium and water excretion?

Answer 5

Increased tubular flow decreases the amount of time that a reabsorbed substance has to interact with its epithelial transporter, thus increasing their excretion rates

Question 6

Is sweat hypertonic or hypotonic? And what are the implications of this?

Answer 6

Sweat is hypotonic; loss of hypotonic fluid causes the ECF to become hypertonic, activating the osmotic pathway in the hypothalamus for ADH synthesis and water retention

Question 7

Atrial Natriuretic Peptide (ANP)

Answer 7

A potent diuretic peptide produced by atrial cardiocytes in response to atrial distension; effects of ANP include:

Dilation of efferent and afferent arterioles - increases GFR and therefore excretion of Na+ and H2O through flow effects

Inhibition of ADH release in the hypothalamus as well as direct blockage of ADH action on tubules - increased water excretion

Decreased renin release and direct blockage of aldosterone action on tubules - increased Na+ excretion

Question 8

Normal ECF Na+

Answer 8

140 +/- 3 mEq/L

Question 9

Effect of aldosterone on K+ secretion

Answer 9

Increased ECF [K+] stimulates release of Aldosterone from the zona glomerulosa cells of the adrenal cortex; aldosterone increases the number of Na/K/ATPase pumps on the basolateral surface (step 1 effect) as well as the number of apical Na+ and K+ channels (step 2 effect)

Question 10

Effect of tubular flow on K+ secretion

Answer 10

Slow tubular flow inhibits secretion of K+ in tubular fluid by reducing its passive concentration gradient across the epithelial cell; in contrast, increased tubular flow increases the concentration gradient and promotes K+ secretion

Question 11

Why are loop diuretics K wasting?

Answer 11

Loop diuretics inhibit the Na/K/2Cl co-transporter in the ascending loop of Henle; this reduces the osmotic driving force for water reabsorption and thus more water remains in the tubule, causing increased tubular flow which increases K+ secretion via the flow effect

Question 12

K status in primary hyperaldosteronism

Answer 12

Aldosterone expands ECF volume and increases the filtration and tubular flow, causing increased K+ secretion

Question 13

K status in secondary hyperaldosteronism

Answer 13

Secondary hyperaldosteronism is due to decreased MAP (cardiac insufficiency, etc.)

Decreased MAP results in decreased GFR and decreased tubular flow causing a decrease in K+ secretion; this flow effect more than offsets the effect of aldosterone in increasing transporter number

Question 14

What is the effect of alkalosis on K levels?

Answer 14

Alkalosis increases K secretion (produces hypokalemia)

High pH causes a shift of K+ into cells from the ECF; this enhances the electrochemical gradient for K+ secretion via a step 2 effect

Apical membrane K+ channels are inhibited by increased [H+]; thus, alkalotic conditions allow greater flow of K+ from the cell into the tubule (step 2)

Question 15

What is the effect of acidosis on K+ levels?

Answer 15

Acidosis causes a shift of K+ from cells into the ECF and inhibits apical K+ channels, thereby causing increased retention of K+ (hyperkalemia)

Question 16

Effect of insulin on K+ levels

Answer 16

Increased ECF K+ causes insulin release from the pancrease; insulin stimulates the Na/K/ATPase, which packs K+ into cells

Question 17

Effect of catecholamines on K+

Answer 17

B2 adrenergic signaling drives K+ uptake into cells

Non-selective beta blockers (propanalol) prevent K+ movement into cells; selective Beta 1 blockers (metoprolol) do not affect K+ movement

Question 18

Causes of chronic hypokalemia

Answer 18

Renal Loss - Urine K > 20

Extra-renal Loss - Urine K < 20

Question 19

Hypokalemia - Clinical presentation & Treatment

Answer 19

Neuromuscular - weakness to paralysis
Cardiac - ECG abnormalities

Asymptomatic patients can be treated with correction of underlying cause and supportive care

Symptomatic patients (arrhythmia, paralysis, weakness) should receive IV replacement up to 40mEq/hour with ECG monitoring

Question 20

Hyperkalemia - Clinical presentation & Treatment

Answer 20

Neuromuscular abnormalities
ECG changes - peaked T waves, absent P waves; these changes are potentially lethal

Treatment: If ECG changes are present, give Calcium gluconate to stabilize the arrhythmia; meds to move K+ into cells (sodium bicarbonate, insulin), K+ exchange resin, hemodialysis

Question 21

What is ALWAYS the first test for hyperkalemia?

Answer 21

ECG

Question 22

Pseudohyperkalemia

Answer 22

Results from a difficult blood draw; tissue damage downstream from the tourniquet releases K+ and the high lab K+ is therefore an artifact

First, do ECG; then, repeat serum K+

Question 23

Causes of increased total body K+

Answer 23

Decreased renal K+ excretion; occurs in any condition that increases reabsorption of Na+ (i.e. congestive heart failure, pre-renal azotemia)

Question 24

Causes of hyperkalemia due to transcellular shift

Answer 24

Diabetes - no insulin to drive K+ into cells

Medications - non-selective beta blockers block the B2 receptor from mediating K+ uptake into the cell

Ischemia or tissue damage - i.e. rhabdomyolysis