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PTH

Endocrine

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

 



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