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38 Cards in this Set
- Front
- Back
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Importance of calcium
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tight jct maintenance
cell membrane stability enzyme activity stim-secretion coupling in nerves mm. contraction exocytosis blood coagulation |
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EC vs. IC calcium
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more calcium is EC
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importance of phosphate
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bone/teeth structural integrity
H+ buffer in plasma anion that balances magnesium and K+ vital to many enzyme pathways |
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body distribution of phosphate
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85% in skeleton, 6% in muscle, remainder in plasma and other tissues
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magnesium importance
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involved in neuromuscular transmission and acts as a cofactor in many enzyme reactions
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cortical vs. trabecular bone
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cortical is 80% of bone (tibia)
trabecular is 20% (vertebra) trabecular is more important in calcium homeostasis |
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females show more severe consequences of calcium homeostatic dysfunction due to
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25% less bone mass
accelerated bone loss after menopause |
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bone formation
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carried out by osteoblasts
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bone mineralization requires
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calcium, phosphate, and vit. D
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bone resorption
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carried out by osteoclasts
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bone resorption greatly exceeds formation after
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35 years of age
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vit D formation
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intestine (from diet) or skin, UV light --> Vit D3 --> liver --> 25-OH-D3 --> kidney --> 1,25-(OH)2-D3
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25-hydroxylation of vit. D3 increased by _____ and decreased by _____
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increased by PTH
decreased by Vit D |
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1-hydroxylation of 25-OH-D3 is decreased by
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elevated Calcium, phosphate, and vitamin D
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Vitamin D effects
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GI tract: increased absorption of calcium, phosphate, and magnesium; increased calcium binding proteins
Bone: increased mineralization of boney matrix; also increased resorption Parathyroid gland: decreased PTH synthesis |
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why does vitamin D cause bone resorption?
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paracrine signals from osteoblast activate osteoclasts
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PTH produced by
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cheif cells
some by oxyphil cells |
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effects of hypercalcemia on PTH
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decreased PTH synthesis, storage, release, and parathyroid size
Hypocalcemia has opposite effects |
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chronic hypomagnesmia and PTH
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can inhibit PTH synthesis and target tissue response
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PTH release increased by these drugs/hormones
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PDE inhibitors
epi dopamine histamine lithium thiazide diuretics |
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PTH decreased by
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alpha-adrenergic agonists
prostaglandins aluminum (antacids) |
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PTH metabolism
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mostly by liver, some in kidney
circulating half-life is 20-30 minutes |
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calcitonin made by
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parafollicular C cells
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calcitonin metabolism
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kidney
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calcitonin increased by
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increased calcium
food ingestion increased gastrin |
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calcitonin decreased by
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decreased calcium
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calcitonin effects
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inhibits bone resorption (escape from this occurs over time)
increases bone density decreases plasma phosphate |
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body's response to calcium deficiency
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increased PTH and vit D secretion leads to inflow of calcium; dispose of inflow of phosphate through renal excretion
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body's response to phosphate deficiency
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increases vit D3 secretion but not PTH
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osteomalacia and rickets
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inadequate mineralization
usually due to vit D def. |
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hyperparathyroidism symptoms
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decreased neuromuscular transmission
muscle weakness decreased GI motility poor mentation coma |
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hypoparathyroidism effects
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neuromuscular irritability as manifested by:
numbness and tingling tetany in hands and feet laryngeal muscle spasms |
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hypophosphatemia
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skeletal muscle weakness
cardiac/respiratory muscle dysfunction RBC membrane abnormalities abnormal bone formation |
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rickets
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bowing of extremities and chest wall collapse
mineralization defect and excess bone matrix low plasma calcium and phosphate elevated alkaline phosphatase elevated PTH |
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osteomalacia
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adults
pain, vertebral collapse, fractures along stress lines mineralization defect, excess bone matrix decreases plasma calcium and phosphate increases AP increases PTH |
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etiology of vitamin D def.
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dietary deficiency
liver disease GI disease insufficient sunlight |
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Vit D excess
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Calcium overabsorption in GI tract
increased bone resorption hypercalcemia, hypercalciuria kidney stones hyperphosphatemia decreased PTH |
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etiology of vit. D excess
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dietary excess
disorders causing excess PTH disease involving granuloma formation |
