Endocrine
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| Axial skeleton: | 15 % of skel mass; verts, pelvis, skull; majority of cancellous bone (most of Ca efflux from this); 80 % of metabolic activity
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| Appendicular Skeleton | 85 % of skel mass; long bones; majority of cortical bone; 20 % of metabolic activity
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| Hypercalcemia S/S | serum Ca >10.5 mg/dL; altered mentation, N/V; polyuria, polydipsia, stones
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| Hypercalcemia pathogenesis | accel bone resorption by osteoclasts (PTH, 1,25 (OH)D, IL-1, IL-6, TNF-alpha); enhanced GI absorption of Ca (vit D); hypercalcemia represents eclipsed renal capacity to excrete Ca load ( ie, hypercalciuria also present)
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| Hypercalcemia: causes | inc skeleton resorption (primary hyperPTH; malig); inc GI absorption (milk-alk syn); both inc skel resorp & GI absorption (granulomatous: sarcoid, TB, fungal)
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| Primary hyperPTH mnemonic | Bones, stones, moans & groans
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| Primary hyperPTH evolving clin spectrum | more recently, less about stones & bone dz, more asymptomatic
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| Hypercalcemia: nonpharm tx | Tx underlying cause; enhance calciuresis: Fluids (2-3 L / day po for mild; IV saline for severe / Ca > 13); loop diuretics (only after volume repletion); furosemide
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| Hypercalcemia: Pharm tx: Inhibit osteoclastic resorption: | Bisphosphonates (pamidronate IV; zoledronic acid for malig-related hyperCa). Calcitonin (transient benefit d/t tachyphylaxis). Cinacalcet. Lastline: plicamycin, gallium nitrate
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| Hypercalcemia: Pharm tx: Inhibit osteoclast resorption/reduce GI absorption: | Glucocorticoids (prednisone; solumedrol)
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| Chvostek sx = | twitching of face and upper lip in response to tapping inferior to TMJ joint
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| Trousseau sx = | inflate BP cuff, leave it there; pt gets carpal spasm
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| If suspect pt is hypocalcemic, measure 1,25-D? | No; measure 25-OH D
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| Acute Hypocalcemia S/S | tetany, twitching, paresthesia; Chvostek sx; Trousseau sx; seizures; laryngo or bronchospasm; long QT; arrhythmia; hypotension
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| Chronic Hypocalcemia S/S | ectopic calcification (basal ganglia); EPS; parkinsonism; dementia; cataracts; abnml teeth; dry skin
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| Most common cause of hypocalcemia | surgically induced hypoPTH
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| Hypocalcemia Tx | Vit D (25 OH D deficiency): Calcium (2000-4000 mg/day); ergocalciferol / cholecalciferol if 25 OH D deficient; Calcitriol if 25 OH D sufficient
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| Osteomalacia = | Defective bone matrix mineralization d/t: inadequate Ca & phosphorus; deficient mineralizn mechm in presence of normal Ca / phosphorus
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| Osteomalacia in childhood is: | rickets
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| Osteomalacia symptoms | diffuse bone pain (esp pelvis), waddling gait, mx weakness, fractures & pseudofractures (Looser’s zones) of long bones, ribs, pelvis
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| Osteomalacia: causes | Vitamin D disorders; Hypophosphatemia (inherited disorders); Mineralization disorders
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| Osteomalacia: Tx | Vitamin D (25 OH D def): Ca (1500-2000 mg/day); ergocalciferol (D2-Drisdol) cholecalciferol (D3); Calcitriol (for hypophosphatemic osteomalacia)
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| Pagets Disease = | Localized disorder of bone remodeling
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| Pagets Dz: initiating lesion is: | inc bone resorption (giant multicellular osteoclasts); bone formation and mineralization is normal, though of irregular woven type
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| Pagets Dz: most commonly affects: | pelvis, femur, spine, skull and tibia
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| Pagets Dz: Sx | pain, bowing, fracture, HA, hearing loss; elevated alk phos (hallmark); bone turnover markers often elevated
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| Pagets Dz: Tx | Inhibit osteoclast resorption/ bone formation: bisphosphonates; calcitonin
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| Storage form of vitamin D = | 25-hydroxyvitamin D (hydroxycholecalciferol OR calcidiol)
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| Active form of vitamin D = | 1,25-dihydroxyvitamin D (1,25-dihydroxycholecalciferol OR calcitriol)
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| Calcidiol is stored in ___ cells | fat cells (fat soluble vitamin)
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| 25-hydroxyvitamin is converted by PTH or decreased phosphate level into: | calcitriol (occurs in kidney)
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| Patients on steroid tx (esp longterm) should also be on: | vitamin D
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| Vitamin D conversion / activation pathway | 7-dehydrocholesterol + UVB -> cholecalciferol (D3) -> converted to 25-hydroxyvitamin D (Calcidiol) in Liver -> converted to 1,25-dihydroxyvitamin D (Calcitriol) in Kidney.
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| Primary hyperPTH etiologies | PTh adenoma most common. Rarely diffuse hyperplasia. MEN syndrome. 20% of pts on lithium.
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| Secondary hyperPTH is caused by: | Ca & vitamin D deficiency, or skeletal resistance to PTH
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| HypoPTH etiologies | Usually post-thyroid or PTH surgery. May be autoimmune or 2/2 hypomagnesemia.
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| HypoPTH labs (diagnostic triad) | Low Ca (corrected for albumin), low PO4, low PTH
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| hypoparathyroid labs | Low serum & urine ca, PTH, Mg; high PO4, nl alk phos
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| hypoparathyroid imaging | CT/MRI: dense bones & basal ganglia calcifications; xray: bone mineral density at L-spine
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| PTH labs | can measure Ca, PO4, Mg, PTH directly; Alk phos assoc w/osteocyte activity (higher in growing kids, M>F, or mets)
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