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25 Cards in this Set
- Front
- Back
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What are the three hormones that act on calcium and phosphate and what is their net effect?
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PTH: increase Ca, Decrease PO4
Vit.D: increase Ca, increase PO4 Calcitonin: decrease Ca, decrease PO4 |
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What makes PTH? What stimulates PTH production?
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Chief cells in the Parathyroid
stimulator: low calcium inhibitor: Vitamin D |
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What makes Calcitonin and where? What stimulates/inhibits calcitonin?
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Parafollicular cells of the Thyroid Gland. Made as a preprohormone.
stimulates: high calcium, gastrin |
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What is the most active form of Vitamin D and how do we get it?
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Calcitrol. You either take in through the GI from your diet, or synthesize it from cholesterol via 25-hydroxylase in the liver to make Vit.D.
Calcitrol, the most active form, is made in the Kidney by 1-hydroxylase. You get the 1,25-dihydroxy form. |
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How do you regulate the active form of Vitamin D?
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stimulation/inhibition of 1-hydroxylase
(controls level of 1,25-dihydroxy-Vit.D) 24,25-dihydroxy is the less active form, made when calcium is low. |
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Where is Vitamin D stored?
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It is lipid-like, stored in fats with a long half life.
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What are the three types of bone cells, where are they found, and what are they each derived from?
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- osteoblasts come from osteoprogenitors, and live on the bone surface building bone.
- osteocytes come from osteoblasts, are inside the bone to form structure. - osteoclasts come from stem cells, and are on the bone surface ready to fuck shit up. |
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How to osteoblasts form bone?
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- osteoblast secretes collagen
- collagen forms osteoid array - osteoblast makes alkaline phosphatase, making PO4. - Calcium phosphate precipitates out - bicarbonate and OH make hydroxyapatite to form bone mineral - the mineral surrounding the bone converts it to an osteocyte. |
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What is osteolysis?
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Calcium moving in and out of the bone via fluid-filled canaliculi
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What is collagenase? How much action does it have?
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What osteocytes use to break down bone and resorb calcium into the serum.
Babies conduct 100% bone turnover in a year, adults 18%! Necessary for bone strength. |
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PTH is the most important regulator of calcium. What is its effect on the kidney, bone, and GI?
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Kidney: increases reabsorption of calcium, decrease absorption of phosphate. Increase 1,25-Vit.D production.
Bone: stimulate osteolysis - stimulate osteoclasts - inhibit collagen production by osteoblasts GI: increase absorption of calcium and phosphate. |
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What will happen to urine calcium levels with PTH action?
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You will see it decrease
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How is calcium homeostasis affected by thyroidectomy?
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It isn't! Calcitonin is produced by Chief cells in the PARAthyroid.
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What are calcitonin's effects?
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- decrease osteolysis
- decrease bone resorption - increase bone formation |
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What stimulates production of 1,25-Vit.D?
What are its effects on the GI, bone and kidney? |
low PO4 or low Calcium
GI: increase calcium and phosphate reabsorption bone: synergize with PTH to increase bone resorption kidney: increase calcium and phosphate reabsorption, inhibits 1-hydroxylase activity |
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Out of the 3: kidney, bone and GI, which has the most pronounced and immediate effects on calcium/PO4 homeostasis?
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Kidney: rapid but small range
Bone: slow but wide range, long action GI: slow, small range |
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What is the mechanism of action for the 3 bone hormones?
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PTH & Calcitonin act through cAMP membrane receptors, changing permeability to calcium.
1,25-Vit.D binds nuclear receptors to induce mRNA including Calcium Binding Protein in GI and Kidney. |
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Differentiate Hypercalcemia from Hypocalcemia
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Hypercalcemia:
- neuromuscular weakness - CNA impairment - calcium precipitation in bones, kidney, joints - GI disturbance (constipation) HyPOcalcemia: - neuromuscular hyperexcitability (Chovstek sign, Trousseu's sign) - Parathesia (pins and needles) - hyperventilation - convulsions |
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Hyperparathyroidism
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parathyroid tumor
- leads to hypercalcemia, kidney stones (hypercalcuria), bone demineralization - disease "osteitis cystica" BONE CYSTS secondary hyperparathyroidism: kidney failure (chronically low calcium levels overstimulate production of PTH) |
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HyPOparathyroidism
PseudoHYPOparathyroidism |
usually due to accidental surgical removal of Parathyroid with thyroid. or autoimmune or chronically low Magnesium levels.
get hypocalcemia PseudohypoPTH: High PTH levels but symptoms of hyPO-PTH - due to PTH receptor defect. |
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Vitamin D poisoning results
Vit D deficiency |
Vit D poisoning = hypercalcemia
Vit D deficiency = RICKETS in children, OSTEOMALACIA in adults. low calcium accretion in bone. Can be caused by no Vit D receptors, no Vit production or absorption in kidneys or GI, GI surgery, or living in the dark. |
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Osteoperosis
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Matrix and mineral are lost. Common in post-menopausal women. Treat with exercise, calcium intake, estrogen replacement therapy. Fosamax biphosphonate, Tamoxifen (estrogenic bone properties)
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How can malignancy lead to Hypercalcemia?
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PTH secreting tumors stimulate osteoclast activity and get bone resorption, excess Vit D.
Tx: biphosphonates, PTH Sx, withhold Vit D. |
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What is Paget's disease?
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osteitis deformans - bone remodeling disorder.
- increased osteoclastic activity early, late increased osteoblast activity - nerves get trapped in abnormal ways in the bone Tx: biphosphonates |
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What are the drug treatments for osteoperosis?
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ERT/HRT: reduced risk of fractures
SERMs/Tamoxifen: agonist on bone Biphosphonates |
