Published Feb 13, 2006
CrystalClear75, BSN, RN
624 Posts
Hi,
We are learining the Endocrine system right now and my question is in regards to hyperparathyroidism and how bone resorption occurs, and fractures occur, but there is more calcium in the blood???? How could fractures occur when the parathyroid hormone secretes calcium and in this case as in hyperpara?? I'm also confused about resorption and reabsorption, thank you.
VickyRN, MSN, DNP, RN
49 Articles; 5,349 Posts
The body remains remarkably constant and balanced despite constantly changing external or internal environments. Homeostasis involves responses to stress (homeostatic mechanisms) to maintain a narrow range of conditions, thus sustaining life.
Homeostatic mechanisms are compensatory and self-regulating. They act by negative feedback to restore or preserve the optimum state by producing a change in the opposite direction – too much produces less, too little produces more. Negative feedback works in the body like a thermostat. If the temperature increases too far above the preset value, the thermostat turns off the heater to return the system to cooler temps. If the temperature drops too far, the thermostat in turns attempts to reverse this trend by turning on the heater.
STIMULUS (stressor): a change in the environment (internal or external). Any stimulus that disrupts the ‘steady state’ of homeostasis is a stress.
RESPONSE: compensates for, or cancels our the original stimulus. Once the original stressor has been compensated for, then the homeostatic mechanism turns itself off (is self-regulating).
Serum calcium level in the blood is maintained within a narrow range through the action of vitamin D and hormones (PTH and calcitonin).
A good example of a negative feedback system is the interplay involving parathyroid hormone, calcitonin, and bones. The parathyroid glands secrete parathyroid hormone when they "sense" blood calcium levels are below normal (9.0-10.5 mg/dL).
Bones serve as a large, dynamic reservoir of calcium that readily releases calcium when serum levels drop (the body's "calcium" bank). This helps maintain blood calcium levels within normal limits when calcium intake is inadequate. A chronically low calcium intake compromises bone integrity without affecting blood calcium levels.
Parathyroid hormone (PTH) increases serum Ca2+ levels by causing release of calcium from bones. PTH is secreted in response to decreased calcium levels. Breakdown of bone by osteoclasts is called resorption. (Just remember "clast" = "catastrophe" = breakdown [resorption] of bones = release of calcium; osteoBLASTS, on the other hand BUILD bones, and cause calcium from the blood to GO BACK INTO the bones. When you're REMODELING your house, you have to TEAR DOWN [osteoclasts], before you can BUILD BACK UP [osteoblasts]). The end result of PTH is INCREASED serum calcium
PTH also causes calcium reabsorption from kidney.
Calcitonin (from thyroid gland) decreases serum Ca2+ levels by causing the calcium to go back into the bones. It activates the osteoblasts. Calcitonin is secreted in response to an increase in calcium. The end result of calcitonin is DECREASE in serum calcium.
This, in a nutshell, is the way redistribution of calcium between bones and the blood works.
Vitamin D (Calcitriol) increases serum calcium level by facilitating absorption. It is necessary for the small intestine to absorb calcium. If you don’t have enough vitamin D, even if you have enough calcium, it will not be absorbed. Get vitamin D from sunshine or supplement. Vitamin D INCREASES serum calcium through increased absorption from the gut.
Hyperparathyroidism results in TOO MUCH parathyroid hormone = INCREASE in SERUM CALCIUM, DECREASED CALCIUM in BONES. This will disrupt homeostasis; the delicate negative feedback mechanism is not working properly. The narrow range of serum calcium will not be maintained properly (serum calcium will be increased above 10.5 mg/dL). The bones will become brittle through too much loss of calcium. They will break much more easily (pathologic fractures).
WOW Vicki, that made it totally clear, thank you!
My med surge book doesn't explain it THAT well. Okay, let me get this straight, when calcium levels fall, the parathyroid hormone is secreted in order to compensate for serum calcium and in turn it resorts to our bones for compensation or "homeostasis" so the serum calcium levels increase, cause this ONLY happens if the calcium is low. Then, Calcitonin comes along and says, "Hey, Don't take all of that bone(osteoclasts)" and tries to rebuild the bone's calcium(osteoblasts) which in turn, lowers serum calcium. Does that sound right? And I guess that's why things go out of wack cause it's kinda like an argument between the two. Does that make sense??
Okay, let me get this straight, when calcium levels fall, the parathyroid hormone is secreted in order to compensate for serum calcium and in turn it resorts to our bones for compensation or "homeostasis" so the serum calcium levels increase, cause this ONLY happens if the calcium is low.
This is correct :)
Then, Calcitonin comes along and says, "Hey, Don't take all of that bone(osteoclasts)" and tries to rebuild the bone's calcium(osteoblasts) which in turn, lowers serum calcium. Does that sound right? And I guess that's why things go out of wack cause it's kinda like an argument between the two. Does that make sense??
I'm trying to understand what you're saying here.... Calcitonin release is also a negative feedback mechanism, but it is released in response to HIGH blood calcium levels (above 10.5 mg/ dL). Calcitonin stimulates osteoblasts, which cause the calcium to leave the blood and go into the bones. This lowers serum calcium, until homeostasis (normal serum calcium levels) is attained. Then, the negative feedback mechanism turns off and stops calcitonin release from the thyroid gland.