Na/K/H2O Handling Flashcards
Equation for calculating serum osmolarity
SOsm = 2 x Na + (BUN/2.8) + (Glucose / 18)
Normal sOsm
285 +/- 3 mOsm/kg
Normal ECF K+
3.5 - 5.0 mM
What is the main driving force for reabsorption of fluid from the renal interstitium into peritubular capillaries?
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
What is the effect of tubular flow on sodium and water excretion?
Increased tubular flow decreases the amount of time that a reabsorbed substance has to interact with its epithelial transporter, thus increasing their excretion rates
Is sweat hypertonic or hypotonic? And what are the implications of this?
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
Atrial Natriuretic Peptide (ANP)
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
Normal ECF Na+
140 +/- 3 mEq/L
Effect of aldosterone on K+ secretion
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)
Effect of tubular flow on K+ secretion
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
Why are loop diuretics K wasting?
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
K status in primary hyperaldosteronism
Aldosterone expands ECF volume and increases the filtration and tubular flow, causing increased K+ secretion
K status in secondary hyperaldosteronism
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
What is the effect of alkalosis on K levels?
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)
What is the effect of acidosis on K+ levels?
Acidosis causes a shift of K+ from cells into the ECF and inhibits apical K+ channels, thereby causing increased retention of K+ (hyperkalemia)
Effect of insulin on K+ levels
Increased ECF K+ causes insulin release from the pancrease; insulin stimulates the Na/K/ATPase, which packs K+ into cells
Effect of catecholamines on K+
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
Causes of chronic hypokalemia
Renal Loss - Urine K > 20
Extra-renal Loss - Urine K < 20
Hypokalemia - Clinical presentation & Treatment
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
Hyperkalemia - Clinical presentation & Treatment
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
What is ALWAYS the first test for hyperkalemia?
ECG
Pseudohyperkalemia
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+
Causes of increased total body K+
Decreased renal K+ excretion; occurs in any condition that increases reabsorption of Na+ (i.e. congestive heart failure, pre-renal azotemia)
Causes of hyperkalemia due to transcellular shift
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
