Lecture 103 Mineral Metabolism Flashcards Preview

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Flashcards in Lecture 103 Mineral Metabolism Deck (16):

Explain how calcium gets into and out of the body and why extracellular fluid calcium concentration must be maintained at a tightly-controlled level.

short a: Calcium enters the body through the gut and exits via the kidney.


Describe the roles of the gut, kidney and bone in maintaining normal calcium levels.

short a: The bone is the major site for calcium storage in the body


Discuss how the parathyroid gland senses calcium levels in extracellular fluid. describe the receptor, describe it's effect

calcium sensing receptor (CaSR),
7 transmembrane GPCR, Ca2+ binds to extracellular domina which causes a change in the confirmation of CaSR, leads to phosphorylation of the intracellular tail which leads to more signaling to increase Ca2+ influx and inhibits PTH release (note normally Ca2+ influx causes exocytosis)


Discuss the effects of parathyroid hormone on bone and kidney. Describe the PTH receptor.

Parathyroid hormone has direct actions on bone to increase osteoclast-mediated bone
resorption. In the kidney PTH increases resorption of calcium and increases
excretion of phosphate. PTH receptor is a GPCR (7 transmembrane)


Discuss the synthesis of vitamin D and how it is regulated.

short a: Vitamin D is a steroid hormone whose synthesis begins with the actions of sunlight on the skin, and then continues in liver and then kidney where the active form is produced in response to PTH.


Discuss the effects of vitamin D on intestine, bone and kidney.

short a: Vitamin D acts through its intranuclear receptor to increase calcium absorption by the gut and kidney. In bone it provides calcium and phosphate for mineralization of bone matrix and promotes differentiation of osteoblasts.


What is the role of calcitonin? Does calcitonin play a large role in Ca2+ homeostasis?

It inhibits osteoclast-mediated bone resorption, thus lowering serum calcium.
No, in humans it appears to be of little importance, since removal of the thyroid gland has minimal effect on calcium homeostasis.


How does vitamin D deficiency present in children? How is this disease characterized?

rickets is characterized by delayed growth (due to inability to mineralize bone) and bowing of the legs. Muscles may be weak, making climbing stairs difficult. Rickets was common until the 1930’s in industrialized countries where air pollution limited children’s sunlight exposure. Without sunlight, vitamin D was not synthesized. Cod liver oil was discovered to be an excellent source of vitamin D in the early part of the 20th century, and was given to children to prevent rickets.


how is familial hypocalciuric hypercalcemia (FHH) characterized? what is it's pattern of transmission? what is the mutation?

it is an autosomal dominant disorder characterized by high serum calcium, high serum parathyroid hormone levels and low urinary calcium
FHH is caused by a mutation in the calcium-sensing receptor (CaSR) expressed on parathyroid and renal tubular cells. The mutation causes the CaSR to be less sensitive to extracellular calcium, so that when the calcium level is normal, the CaSR senses that the calcium level is too low. The result of this at the level of the parathyroids is that PTH is released when calcium is already normal or even mildly elevated. The result at the level of the kidney is that calcium is resorbed into the bloodstream even when calcium levels there are already normal or high. This disease usually has a benign course.


describe "hungry bones syndrome". how does it manifest? how it is treated?

low serum Ca2+, tingling around mouth, and hand or vocal cord tentany, abnormal cardiac conduction.
With an overactive parathyroid gland, the high PTH causes osteoclasts to resorb bone. In the areas where bone had been resorbed, osteoblasts came in and laid down new bone matrix. However, due to the actions of the high PTH levels on the bone, the bone matrix was never mineralized. After overactive parathyroid gland removal, the unmineralized (“hungry”) bone matrix is able to get the calcium and phosphate it needed, at the expense of serum calcium.
This condition responds well to supplemental calcium and vitamin D.


what is the normal Ca2+ serum levels?

normal 8.5- 10 mg/dl


what are the three forms of Ca2+?
name three places where phosphorus is found in the body?
where in the body is Magnesium found?

Ionized (free or unbound)
Protein bound (albumin and other proteins)
Complexed (to other ion;phosphate, citrate, carbonate)
14%-soft tissue
rest is in tissue to act at a enzyme co-factor


what is the role of extracellular Ca2+? intracellular Ca2+?

extracellular-excitation-contraction of heart and skeletal muscles
nervous system function
exocytosis, including hormone release
-second messenger
-intracellular trafficking
-muscle contraction


name the two regulators of mineral metabolism?

PTH and 1,25 dihydroxyvitamin D


where is PTH found? is the half-life short or long? what effect does this have?

Parathyroid hormone is released from the parathyroid cell when the cell-surface calcium-sensing receptor perceives extracellular calcium to be low.
half-life is very short (2-4 mins), allows for PTH levels (and thus Ca2+) to be tightly regulated


how is PTH production regulated?

Ca2+/Vit D levels via negative feedback
low Mg stimulate PTH release while high level stimulate it, however long term low Mg inhibits PTH release due to inhibition of exocytosis