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MSK #2 (Jones) [Selected Musculoskeletal Pathology- Dr. Jones] - Osteoporosis, Rickets, Ostetis Fibrosa Cystica, Renal Osteodystrophy
Terms in this set (14)
Estrogen deficiency plays a major role.
Decreased estrogen levels result in
increased secretion of IL-1, IL-6 and TNF
by blood monocytes and bone marrow cells. These cytokines are
potent stimulator of osteoclast
recruitment, differentiation and prolonged survival.
Compensatory osteoblastic activity can't keep up --> high turnover rate
Loss of bone most rapid from trabecular bone.
Vertebrae --> prominent trabecular component
-Back pain, shortening, dorsal kyphosis, cervical lordosis
Osteoblasts have reduced replication. Growth factors for osteoblasts lose their potency. End-result is skeleton populated by shitty, lazy osteoblasts.
Haversian systems are widened
What is the cellular difference between postmenopausal and senile osteoporosis?
Postmenopausal --> osteoclasts to blame
Senile --> osteoblasts to blame
What is required for Ca2+ absorption from the intestine?
Disorder in children in which deranged bone growth produces skeletal deformities. Vit D deficiency.
-Rachitic rosary (swollen costochondral jxn of ribs
-Bowing of arms and legs
-Thickened, irregular and lobulated epiphyseal plates
Disorder in adults; vit D deficiency --> bone that forms during the remodeling process is under-mineralized
-Osteopenic x-ray pattern
-Compression fractures and decrease in bone thickness
-Low serum ca2+ levels can stimulate secondary hyperparathyroidism (which makes the bone loss worse)
Factors the same in rickets and osteomalacia
-Defective mineralization of osteoid
-Increased unmineralized matrix
-Wide osteoid seams and a decrease in calcified bone
-Soft bones --> mineral composition is reduced to organic mineral composition
Primary vs Secondary
-Changes to anatomy known as
osteitis fibrous cystica
-Primary is worse on the skeleton
--? in cancellous bone osteoclasts create appearance of railroad tracks
-decreased done density
Widened Haversian Canals
What is a brown tumor?
Sequestered multinucleate macrophages and an in-growth of reparative fibrous tissue at micro fracture sites creates a mass. Brown color is result of the vascularity, hemorrhage, and hemosiderin deposition. Can undergo cystic degeneration.
Hallmarks of severe hyperparathyroidism
Generalized osteitis fibrosa cystica - von Recklinghausen disease of bone:
-Increased bone cells
-Cystic brown tumors
Collectively describes the skeletal changes due to renal disease:
1) Increased osteoclastic bone resorption mimicking osteitis fibrous cystica
2) Delayed matric mineralization (osteomalacia)
4) Growth retardation
Chronic renal failure has what effect on phosphate?
Phosphate retention and hyperphosphatemia. This, in turn, induces
because phosphate regulates PTH secretion (
increase serum phosphate --> increased PTH secretion
Why does renal damage cause hypocalcemia?
Because the kidneys are required to convert vitamin D into its active form. Renal hydroxyls, which accomplishes this task, is inhibited by high serum phosphate (doubly whammy).
What effect does renal damage have of levels of PTH?
PTH increases for a number of reasons:
3) Lack of vit D suppression
4) Decreased degradation and excretion of PTH
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