Bone Pathology Flashcards
Vitamin D Life
skin and diet-> blood -> liver -> Vitamin D (OH)1-> kidney -> Vitamin D (OH)2
In summary, for healthy bone
Ca, P (diet)
Vit D (diet, skin synthesis)
gut (absorbing Ca, P, Vit D)
kidney (makes Vit D (OH)2, resorbs/excretes Ca, P)
parathyroids (master gland for Ca, bone metabolism)
bone healing complications
Mal-alignment: deformed healing
Non-union / mal-union / pseudoarthrosis
Osteomyelitis (compound fractures)
Growth disturbance (epiphyseal plate injury in children)
Arthritis (if fracture affects articular surface)
Fat embolism syndrome (within several days of fx)
Immobilization complications
- Thrombophlebitis/thromboembolism
- Osteoporosis of immobilized bone
causes for osteopenia
osteopenia: Generalized decrease in bone mineralization
osteoporosis, osteomalacia, malignancy, rare hereditory diseases
Pathological fracture
fracture through diseased bone—usually refers to fracture through tumorous or tumor-like bone
best osteoporosis prevention
maximize peak bone mass (teens/young adults)
encourage weight-bearing exercise and Ca supplementation
strong predictor of osteoporosis risk
Maternal hip fracture:
Baseline labs: to exclude secondary causes of osteoporosis/osteopenia
serum Ca, P, alkaline phosphatase, 250H – Vit D, TSH, sometimes PTH (renal insufficiency or malabsorption)
Most anti-osteoporosis meds
inhibit bone resorption
Biochemical serum markers of bone formation and resorption:
currently NOT sufficiently standardized or studied to provide meaningful diagnostic or therapeutic guidance
PRIMARY HYPERPARATHYROIDISM
Hypercalcemia due to primary hyperplasia or NEOPLASTIC enlargement of parathyroid glands
Spectrum of bony changes due to variable degrees of osteoclastic bone resorption—ranging from subtle subperiosteal cortical erosions to diffuse osteoporosis to tumor-like skeletal change (osteitis fibrosa cystica/”Brown tumor”)
Favors resorption of cortical bone over trabecular bone
Pathology: osteoclastic bone resorption/peritrabecular fibrosis = osteitis fibrosa
Some complications:
Fractures
Constitutional symptoms; metabolic impairment of kidneys; muscle weakness; neuropsychiatric syndromes (all direct effects of Ca++)
Renal stone disease
NOTE: Secondary hyperparathyroidism (renal disease) may also produce gross skeletal change.
OSTEOMALACIA
Definition: decreased bone mineralization with excess osteoid (wide osteoid seams)
Due to interference with calcium, phosphate, or vitamin D metabolism: diagnostic challenge—what’s causing the interference?
Radiologically appears osteopenic (like osteoporosis)
May present with diffuse skeletal pain (without fracture)
Associations:
Environmental: classic childhood rickets
Poor diet; sun exposure in northern latitudes
Intestinal malabsorption—commonest cause of Vit D deficiency in USA
Liver or renal disease (impaired hydroxylation of Vit D)
Rare congenital/inborn errors of metabolism
-Deficient Vit D hydroxylation
-Renal tubular phosphate leak
-End organ resistance to Vit D (OH)2
OSTEOMYELITIS
“Primary” mode of acquisition: hematogenous spread to bone from often occult source elsewhere
“Secondary” mode of acquisition: spread to bone from adjacent contiguous infection (joint infection/other soft tissue infection)
“Direct” infection: e.g., compound fractures allowing direct injection of common bacteria onto raw fracture surfaces; orthopedic procedures ± prosthetic devices