Mixed Phase: osteoblastic activity and bone formation.
Osteosclerotic Phase: Finally an apparent exhaustion of cellular activity.
Increased rik for development of what?
Diagnosis: initially radiographic, then check for elevated levels of urinary hydroxyproline (increased bone resorption) and serum alkaline phosphatase (increased bone apposition).
Tx: Calcitonin, bisphosphonates, analgesics for bone pain.
Increased risk for development of sarcomas (especially osteosarcoma).
Hyperparathyroidism: what is it?
What does PTH do?
Inappropriate secretion of PTH
PTH plays a central role in calcium homeostasis via it's effects on: Osteoclast activation, increased calcium resorption by the kidneys, and increased synthesis of vitamin D in the kidneys resulting in increased calcium absorption from the gut.
Net result: Elevation in serum calcium level.
What's primary and secondary hyperparathyroidism?
Primary: due to parathyroid hyperplasia (95%), adenoma or carcinoma. Important cause of hypercalcemia.
Secondary: Due to renal failure (most common cause), leads to poor calcium retention and altered vitamin D metabolism. It's caused by any condition associated with a chronic depression in the serum calcium level. Low serum calcium level leads to compensatory over activity of the parathyroids.
What clinical manifestations has been traditionally associated with primary hyperparathyroidism?
painful bones, renal stones, abdominal groans and psychic moans.
What is the treatment for primary and secondary hyperparathyroidism (they're different)
Primary: Remove affected gland/tumor
Secondary: Renal transplant, Vitamin D supplementation.
What is it?
what is it's main cause?
What are it's three normal pathways of spreading?
Infection spreading through the medullary spaces of bone causing inflammation of the bone and marrow.
Usually a bacterial infection.
1. Hematogenous spread (esp. Staph Aureus)
2. Direct extension from soft tissues
3. Direct traumatic introduction (implantation following compound fractures or surgery)
What's the treatment of osteomyelitis?
Ill-defined areas of radiolucency develop and may be intermixed with radiopaque sequestra.
Non-vital bone (sequestrum) surrounded by rim of new bone (involucrum).
Tx: drainage, antibiotics, surgical debridement.
Fibrous dysplasia: what is it?
who does it affect?
Replacement of normal bone by fibrous CT and abnormal bony trabeculae.
Affects adolescents and young adults.
"Chinese characters" mix of cellular fibrous CT intermixed with elongated trabeculae of immature woven bone. Looks like ground glass.
Monostotic fibrous dysplasia?
Polyostotic fibrous dysplasia without endocrine involvement?
Polyostotic fibrous dysplasia in association with endocrinopathies?
Monostotic fibrous dysplasia: involves a single bone. 70% of cases. Childhood.
Polystotic fibrous dysplasia without endocrine involvement: (Jaffe Syndrome): multiple bones affected. Involvement is unilateral. craniofacial bones. Cafe-au-lait pigments.
Polyostotic fibrous dysplasia with endocrinopathies (McCune-Albright syndrome): least common 3%. Cafe-au-lait spots and endocrine abnormalities.