clinical med musculoskeletal

hereditary disorders -- bad type 1 collagen ---> fragile bones

D, and also, lack of sunshine and malabsorption

• inadequate mineralization of bone matrix
• pigeon breast, lumbar lordosis, bowed-legs

there's no inital decrease in mass but decrease in density

ass. w hyperparathyroidism

early stage, osteitis fibrosa, osteitis fibrosa cystica "brown tumor"

bone tissue becomes soft and deformed as there's a resorption of the bone tissue and a replacement w cyst-like brown tumors and fibrous tissue

hits mandible and maxillary bones first, but goes everywhere

mosaic pattern of bone (misshapen bones) leading to unexplained fractures

inflam of bone due to an infectious organism, such as staphylococcus aureus

• 1 - hematogenous route - involves ends of long bones
• 2 - direct bone penetration - thru wounds, fractures, surgery

happens in pts w knock-knees or bowed-legs -- one side of epiphyseal plate grows faster than the other



usually hereditary, but forces like trauma near epiphysial plate may stim one side to grow faster

abnormal lateral curve of spine, usually affecting adolescent gals

abnormal anterioposterior curv of spine (old gals)

formation of granulation tissue callus at periphery of the post fracture hemorrhage clot

• differentiation of pluripotent cells into fibro and osteoblasts
• process moves from perphery toward center of fracture to resorb blood clot and provide deovascularization

reorganization and restoration

osteoid osteoma - benign, diaphyses of long bones (esp femur and tibia) in pts under 30

osteosarcoma - malignant, in femur tibia and humerus (mostly by the knee) --->early pain and metastases

both affect mostly folks <30 yo

endochondroma - benighn, usually in hands and feet of yong adults

chondrosarcoma - malignant, usually after 35 yo, involves pelvic bones, ribs, and vertebrae ... has better prognosis than does osteosarcoma

• in pts > 20 yo
• at end of long bones
• agressive malignant neoplasm featuring big multinucleated fibroblast-like cells

• rare malignant neoplasm
• occurs in older kids

• monoarticular disorder
• involves larger joints
• result of a bacterial infection

TB in intervertebral discs or joints

• most common disease of joints (esp wt bearing and interphalangeal jts)
• degenerative, not inflammatory
• caused by trauma or infection

nodular swelling seen in osteoarthritis

recurring attacks of acute arthritis due to precip of monosodium urate crystals creating inflammatory foci: tophi

• genetically determined myopathies with progressive atrophy and/or degen of muscle fibers
• ---> atrophy and loss of muscle fibers

• common
• x-linked recessive (boys get it, girls carry it)
• due to lack of dystrophin (a sarcolemmal protein that strenthens muscle cells)
• weakness starts at age 3, can't walk by age 10, death by age 20

involved muscles appear hypertrophied bc they're replaced by fibrofatty tissue - pseudohypertrophy

• x-linked recessive
• milder than Duchenne's - later onset, pts live normal lifespan, drugs (glucocoritcoids) can inccrease prodcution of dystrophin

• autosomal dominant
• 2 forms: a) from birth -real bad--->death soon
• b) adult form - weakness in face and hands, balndensess testicular atrophy, dementia

• Duchenne's - x-linked recessive, onset age 3, dead by age 20
• Becker's - x-linked recessive, appears around age 25, treatable
• Myotonic - autosomal dominant - if at birth, deadly. if as an adult, weakness

• autosomal dominant
• not lethal
• manifests during adolescnence

autosomal recessive, weaknedss in hips or shoulders leading to disability

• acquired autoimmune remitting desease
• antibodies attack the acetylcholine receptor of postsynaptic membrane of NMJ
• usually seen in females about 20 yo, starting w eye trouble

• myoglobin leaks out of skeletal muscles - result of overdoing a work out or getting a crush injury, electrical injury, heat stroke, motor seizure, or acute systemic viral illness (ex - the flu)
• myoglobin will appear in urine