A few others (from looking at my notes):
Almost all of the osmotic pressure in extracellular fluids (ECF) is due to:
Na+ and Cl-
Important functions of sodium in the body.
Maintains ECF osmolarity (fluid balance)
Maintains ECF electroneutrality
Conducts action potentials in nerve/ muscle tissue (initiates skeletal muscle contractions)
Acid-base balance (sodium bicarbonate)
A. The renin-angiotensin-aldosterone mechanism:
B. ANP (atrial natriuretic peptide):
C. ADH (antidiuretic hormone):
No effect on Na+ (will cause dilutional hyponatremia, however)
ADH think WATER (PURE water without sodium, being retained):
ADH stimulates kidney tubule cells to become more permeable to water. In other words, ADH tells kidneys to "save the water!"
ADH increases blood volume (blood becomes "less thick") as urine output is decreased?.
ADH increases the permeability of the membrane to water and enhances free water reabsorption. Causes more water to be reabsorbed and returned to the circulation, making the blood more dilute (reduced osmolarity of the blood). The urine will then be more concentrated.
The name antidiuretic hormone (ADH) indicates that its effects are opposite those of diuretics.
Increased serum chloride equals increased serum sodium.
Increased serum chloride equals decreased serum bicarbonate (HCO3-).
Both hyponatremia and hypernatremia can cause:
LOC changes, confusion, seizures, coma
Electrolyte imbalances mainly the result of renal failure:
Hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia
Both hypokalemia and hyperkalemia can cause:
Skeletal muscle weakness, paralysis, lethal cardiac dysrhythmias, cardiac arrest
Medications contributing to hypokalemia:
Loop and thiazide diuretics (Lasix, Edecrin, HCTZ), laxatives and enemas (GoLitely, Kayexalate, Lactulose), corticosteroids, insulin
Medications contributing to hyperkalemia:
Potassium supplements (K-Dur), potassium salt substitutes, ACE inhibitors, Aldactone, Augmentin, "old" blood transfusions
A. The hormone insulin facilitates movement of K+ into cells.
B. Metabolic acidosis facilitates movement of K+ out of cells (metabolic acidosis = hyperkalemia; metabolic alkalosis = hypokalemia).
C. Severe exercise and cell trauma (including burns or excessive GI activity) move K+ into blood (out of cells), hyperkalemia.
D. Aldosterone increases tubular secretion of K+ into urine and thereby decreases serum potassium (This is why the potassium-sparing diruetic aldosterone, which is an aldosterone antagonist, can produce hyperkalemia).
E. Addison's disease has deficient production of aldosterone. The patient with Addison's is more likely to develop hyperkalemia.
F. Sammy has lost much fluid during his prolonged diarrhea. He is at risk for hypokalemia.
G. Cushing's syndrome decreases serum potassium (chronic steroid use will also decrease serum potassium, causing hypokalemia).
H. Loop diuretics (furosemide) cause serum potassium loss (hypokalemia).
What precautions are imperative in administration of IV fluids containing potassium?
Urinary output must be at least 30 ml/hr, IV site must be patent, proper dilution in IV fluid (20 mEq/250ml for peripheral IV site), no more than 20 mEq/hr, must be run on a pump, double check serum lab values, NEVER IV push!
Lethargy, leg cramps, muscle weakness, shallow respirations, irregular heart rate (dysrhythmias), hypoactive bowel sounds, nausea and vomiting, flat T waves on ECG
Cardiac (most important): peaked T wave, bradycardia, cardiac arrest
Mild hyperkalemia: hyperreflexia, muscle twitches
Severe hyperkalemia: numbness, weakness, paralysis
GI: increased peristalsis, abdominal cramping with diarrhea, vomiting
Tetany, positive Chvostek's and Trousseau's signs, paresthesias (tingling of lips and extremities), hyperreflexia, seizures, bleeding, increased peristalsis (diarrhea)
S/S Hypercalcemia (think malignancy, hyperparathyroidism, prolonged immobility)
Bone pain, fractures, kidney stones, polyuria, dehydration, blood clots, decreased peristalsis (constipation), hyporeflexia, confusion, lethargy, coma
Hypocalcemia = bleeding, hypercalcemia = blood clots
The effect of calcitonin is to lower serum calcium.
The effect of PTH is to raise serum calcium.
The effect of vitamin D is to raise serum calcium.
The effect of PTH is to lower serum phosphate.
The effect of vitamin D is to raise serum phosphate.
Hyperphosphatemia or hypophosphatemia.
A. Chronic use of antacids with aluminum or calcium that bind phosphate: hypophosphatemia
B. Alcoholism (with associated malnutrition): hypophosphatemia
C. Phosphate-containing enemas: hyperphosphatemia
D. Massive trauma: hyperphosphatemia
E. Renal failure: hyperphosphatemia