Pathology of MSK non-tumor diseases Flashcards Preview

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Flashcards in Pathology of MSK non-tumor diseases Deck (17):

Osteogenesis imperfecta

-Pts have long arms relative to legs, multiple fractures in the legs from early life that healed improperly
-They have thin, weak tibias w/ little calcification (abnormal osteoid matrix)
-Usually is dominant (less severe) form
-Pts do not produce normal amount of osteoid so the bones (especially weight-bering ones) are susceptible to fractures
-Can also see blue sclera syndrome


Osteomyelitis 1

-Irregular lesion w/ sclerosis (encapsulation), suggests benign process
-Histologically see inflammatory cells (PMNs) eroding the bone
-Were recruited there due to an abscess from bacteria (usually staph aureus)


Osteomyelitis 2

-The bone is not viable, and is called sequestrum: necrotic bone detached from blood supply (looks dark)
-The new bone being formed around the lesion is the involucrum: body's attempt to make new bone around abscess (is the sclerotic region)
-Looks irregular and w/ pockets of bone formation
-Common complication: chronic suppurative osteomyelitis (draining sinuses btwn infected bone and skin), squamous cell CA and secondary amyloidosis


Pagets disease 1

-Pts (often men) usually over 40 have pain at site of lesion, w/ markedly elevated serum alk phos levels (w/o having other liver nzs or PTH elevated)
-Bone is thickened and deformed, a mix of sclerosis and lysis
-Can see cement (mosaic) lines: lines btwn resorbed and newly formed bone


Pagets disease 2

-There is normal calcification but abnormal resorption and production
-Variability in thickness of tabeculae
-Abnormal activity of both osteoclasts and osteoblasts, but osteoblast activity eventually is higher (phase 3), leading to thick bones and increases alk phos
-Phase 1: increased osteoclast activity
-Phase 2: mixed osteoclast and osteoblast activity both increased
-Complications: hemodynamic derrangement (due to hypervascular bone) and secondary osteosarcoma


Pott disease (TB infection of vertebrae)

-Pts have soft tissue lesions usually in the lower back, and are PPD positive (due to TB), often immunocompromised
-The mass is of lymph nodes and other soft tissue, there are granulomas of cartilaginous disks and collapsed vertebras
-Histologically, the masses contain lymphocytes and plasma cells, zones of degeneration (necrosis), some giant and epithelioid cells
-Positive for acid fast stain (TB), can culture and PCR for Dx


RA 1

-Chronic process of symmetrical joint destruction, 25% show rheumatoid nodules (subQ nodules on extensor surfaces)
-Joints are warm, tender, edematous, stiff
-There is pannus (fibrous outgrowth/thickening of synovium)
-The rheumatoid nodules show granulomas of chronic inflammation


RA 2

-Synovial fluid has high abundance of PMNs, which are drawn to the joint by chemokines/complement
-Chemokines released by plasma cells and lymphocytes, which are found in the joint tissue
-These are drawn to the joint due to the immune complexes formed from the RF-IgG complexes that are deposited in the joints (autoimmune) and phagocytosed by synoviocytes



-Leads to gradually progressive pain and limited range of motion in the affected joints (due to aging), NOT due to inflammation
-There can be deformities of subchondral bones (osteophytes indicating new bone formation), loss of articular cartilage and sclerosis
-The loss/fragmented articular cartilage also can lead to bone resorption
-Fibrocartilage shows uneven distribution of chondrocytes
-There is clefting/fraying and then loss of articular cartilage
-Some areas of thick bone, other areas of weak bone


Fibrous dysplasia 1

-Circumscribed uneven thinning of bone (ground glass appearance), progressive replacement of a localized area of bone by abnormal proliferation of fibrous tissue
-Middle of lesion is jelly-like substance (fibrous tissue + hemorrhage)
-Histologically there is osteoid getting calcified around edges, bone haphazardly formed but not at the stress lines (not lined by osteoblasts


Fibrous dysplasia 2

-Non-linear formation of bone, randomly organized into circles and semicircles (woven, not lamellar bone)
-Two types: monostotic (usually on ribs, causing deformities and pain/fracture) and polyostotic (usually affects face, also causing deformity and pain/fractures)
-The Rx is bone grafts
-Not a malignant process


Osteoporosis 1

-Decrease in total mass of bone with micro-architectural deterioration
-Ratio of mineralized:non-mineralized (osteoid) bone is normal
-Bone loss produces pain and increases chance of fracture
-Due to dysregulation of osteoclast formation/function via RANK pathway
-Very common, especially primary osteoporosis in elderly (resorption outpaces formation)


Osteoporosis 2

-Secondary osteoporosis: due to immobilization, drugs, malnutrition/absorption, or endocrine d/o
-Affects all bones in body, but pain primarily in weight bearing bones
-Ca, PO, alk phos values generally normal
-Histology: thinned cortical and trabecular bone (changes may be subtle, or very apparent)



-AKA rickets (when in children), structural abnormality of bone caused by defective mineralization of osteoid (osteoid is present in normal or increased amounts but not calcified)
-Due to lack of vit D (deficiency), which is required for mineralization of osteoid
-Rickets can cause deformities of bone and osteopenia, but osteomalacia only causes osteopenia (no deformities)
-Lab values: increased alk phos, decreased Ca, PO
-Histology: trabecular are characterized by peripheral "seams" of uncalcified osteoid


Gout 1

-Urate crystals are deposited in connective tissue, associated w/ increased uric acid in serum
-Primary: mainly elderly men w/ increased uric acid production, decreased uric acid excretion or both
-Secondary: rapid cell destruction releases uric acid (chemo), and decreased excretion (renal failure)
-Acute gouty arthritis: deposition of sodium urate crystals in synovial membrane


Gout 2

-Chronic tophaceous gout: deposition of large masses of urate crystals (tophi) in joints and soft tissues
-Histology of acute gouty arthritis: hyperplasia and acute inflammation of synovium, needle-shaped, elongate, birefringent crystals in fluid and WBCs
-Histology of chronic tophaceous gout: hyperplastic synovium with basophilic masses of crystals (tophi), chronic inflammation, and foreign body rxn around tophi


Achondroplasia, osteopetrosis, marfan syndrome

-Achondroplasia: mutation in fibroblast GF 3 (FGFR3) leads to defect in cartilage synthesis and failure of growth at epiphyseal plates (dwarfism)
-Osteopetrosis: defect in osteoclast reabsorption leading to dense, brittle bones. Causes limited marrow space
-Marfan's syndrome: mutation in fibrillin leads to tall stature, long finger, CV problems