Calcium Basics Flashcards
calcium - overview & functions
*functions: bone formation, muscle contraction, blood clotting
*main source of calcium = diet (milk, cheese, veggies, etc)
*intake balanced through feces & urine loss
*stored primarily in bone, some in ICF, some in ECF
calcium states
*calcium is stored in bones, intracellular fluid, and extracellular fluid
*calcium in the ECF (aka serum calcium) is what carries out body functions
*serum calcium exists in 3 forms:
1. free calcium (ACTIVE form; about 50%) → ionized serum calcium
2. bound to proteins (esp. albumin) = ~45% (NOT active)
3. bound to anions ~5%
effects of albumin of serum calcium
*normal albumin state (4g/dL) = normal total calcium, normal free (ionized) calcium
*low albumin state = normal total calcium, high free calcium
*high albumin state = normal total calcium, low free calcium
corrected calcium equation & explanation (based on albumin)
*remember that free (aka ionized) serum calcium is what actually carries out the functions of calcium
*either too much or too little free calcium causes problems
*whenever a pt’s albumin is higher or lower than 4, we correct the calcium to make sure we have an accurate assessment of the calcium levels
equation: corrected Ca = (0.8 x [4.0 - patient’s albumin] + serum Ca level)
corrected calcium equation
corrected Ca = (0.8 x [4.0 - patient’s albumin] + serum Ca level)
effects of pH on calcium
*in acidemia, extra hydrogen ions bind to negatively charged albumin binding sites; albumin binds less positively charged Ca2+ → higher free (ionized) calcium
*in alkalemia, fewer hydrogen ions to bind negatively charged albumin binding sites; albumin binds more positively charged Ca2+ → lower free (ionized) calcium
*therefore, in acidotic/alkalotic states, check an ionized (free) calcium level
phosphorous - overview
*functions: muscle contraction, cell metabolism (the “P” in ATP), oxygen release from RBCs
*stored primarily in bone, some in ICF, tiny bit in ECF
*NOT protein bound (no need to calculate a correction for albumin levels)
*dietary source
*intake balanced by urine loss alone
hormones that play a role in calcium regulation
- PTH (parathyroid hormone) → results in increased serum Ca2+
- calcitriol (Vitamin D) → results in increased serum Ca2+
- calcitonin → “tones down” serum calcium (decreases Ca2+)
parathyroid glands - function
*trigger: LOW free/ionized Ca2+
*mechanism: secrete PTH → increased bone resorption to release Ca2+ and increased Ca2+ reabsorption from urine
*effect: INCREASE SERUM CALCIUM and decreased serum phosphorous
parathyroid hormone - effects
- direct effect on bone: stimulates osteoclasts → increased bone resorption to release Ca2+; also releases phosphorous
- direct effect on kidney: increased calcium reabsorption from urine; promotes phosphate excretion in urine (phosphate-trashing hormone)
- indirect effect on GI tract: increased Ca2+ absorption from gut but increasing calcitriol formation
- stimulates conversion of 25-OH(D) to 1,25(OH)2D by the kidneys → increased calcitriol
recall: PTH is released in response to low serum calcium, and it results in increased serum calcium and decreased serum phosphorous
calcitriol / vitamin D - overview
*calcitriol (1,25-dihydroxyvitamin D) is the metabolically active form of vitamin D
*liver stores vitamin D or converts it to 25-hydroxyvitamin D
KIDNEYS convert 25-hydroxyvitamin D to calcitriol (1,25-dihydroxyvitamin D) via 1-alpha-hydroxylase; *PTH stimulates this conversion
conversion to calcitriol by the kidneys
*KIDNEYS convert 25-hydroxyvitamin D to calcitriol (1,25-dihydroxyvitamin D) via 1-alpha-hydroxylase
*PTH stimulates this conversion
calcitriol - effects
- small intestine (most critical effect): increased Ca2+ and phosphorous absorption
- bone: increases bone osteoclast activity to release Ca2+ and phosphorous
- kidneys: increases Ca2+ and phosphorous reabsorption in proximal tubules
overall: increases serum calcium and increases serum phosphorous
mechanism: low vitamin D → secondary hyperparathyroidism
*low vitamin D = low calcitriol = low calcium and low phosphorous due to decreased gut reabsorption
*body compensates by increasing PTH → urinary excretion of phosphorus
*result: secondary hyperparathyroidism (high PTH, normal/low calcium, low phosphorous)
calcitonin - effects
*calcitonin TONES DOWN calcium (results in decreased serum calcium)
*released from parafollicular cells of the thyroid (aka C-cells)
*opposes PTH resorptive effects on bone osteoclasts → PROMOTES BONE FORMATION
*inhibits renal reabsorption of calcium