Path 4 Flashcards
Stress Fracture
bone fractures after repeated extra stress
Incomplete Fracture
bone is cracked, but not broken into two pieces
ex: greenstick fracture to childs long bone
Closed Fracture
overlying tissues are intact
Compound Fracture
“Open” “complicated”
-the bacteria have a route from the surface to the bone, bone can stick out
Multifragmented Fracture
“comminuted”
-the bone is broken into several pieces
Complex Fracture
ends of the bone fragments have done serious damage to the surrounding tissue
Pathologic Fracture
intrinsic disease of the bone, force would not have broken normal bone
ex: osteoporosis, cancer, osteogenesis imperfects
Skull Fracture
- flat bone
- not depressed, not displaced
Callus Formation
1st: bleeding and formation of blood clot (dead bone b/c devascularization at edges of fracture)
2nd: recruitment & neovascularization, neutrophils, fibroblasts organize
3rd: ingrowth of osteocytes & new or woven bone formation, cartilage produced at surface of callus
4th: after many months, continued remodeling of bone with reduction of callus over time until complete healing
Fibrous Nonunion
-pathological bone healing where fractured bones are not closely aligned with each other to form callus and to continue the remodeling process to make a perfectly healed bone
How do we repair a fracture?
metal devices, plates, nails, screws
Osteonecrosis
- spongy bone can be infarcted easily wherever it has an end-artery pattern of vascularization & the artery is compromised. Near convex surfaces of joints, feared result is detachment of the articular cartilage
- overlying cartilage & synovium/joint space will be spared. Infarction & necrosis in the shaft is more difficult b/c of collateral circulation - usually trauma
Osteonecrosis of Femoral Head related to?
- sickle cell disease
- decompression sickness
- femoral neck fracture/dislocation
- alcohol abuse/glucocorticoid use
Osteonecrosis in Sickle Cell
- Sickle is most common inherited blood disorder in US
- more than 70,000 people have it
- 1 in 500 AA
- 8% AA are carriers
- 2 million have trait
- 1 in 12 AA has trait
- multiple painful bone infarcts resulting in osteonecrosis
- **hypercellular marrow that interferes with blood low in the marrow and can lead to infarct and necrosis
Osteomyelitis
bone infection
- often by pyogenic organisms (any can be)
- hematogenous spread(kids 2-5y/o), contiguous spread, or in patients with vascular insufficiency (poor wound healing)
no organism identified in 50%
Risk Factors in Osteomyelitis
-presence of foreign materials, diabetes, orthopedic surgery, adjacent infection, peripheral vascular disease, sickle cell disease, congenital phagocyte function defect
Pyogenic Osteomyelitis
begins in metaphysis and can spread hematogenously
- staph in 80-90%
- mixed bacteria in trauma/surgery
- Salmonella - Sickle Cell
Tuberculous Osteomyelitis
Pott disease, vertebrae
Syphilitic Osteomyelitis
neonates, saddle nose, saber shins
Squamous cell carcinoma in Osteomyelitis
-develop in bone or sinus tract of long standing chronic osteomyelitis
Involucrum
Subperiosteal shell of viable new bone, surrounding reactive bone
Sequestrum
Inner native necrotic cortex, remaining fragment inside involucrum
Osteomyelitis Micrograph of Dead Bone
- lots of polymorphoneclear leukocytes
- fibrin and old blood
- bony spicule have no osteocytes in lacunae-dead bone
- no lymphocytes present
Osteomyelitis in Diabetes
-ulceration & necrosis
Pott Disease
“tuberculous spondylitis”
- oldest demonstrated disease
- infection of vertebral bodies(spondylitis) and joint spaces (spondylarthritis)
Syphilis
- spirochete “Treponema palidum”
- late disease affects skeletal system
Primary Syphilis
- sexual contact with infectious lesions on a person with syphilis
- 10-90 days after initial exposure, skin lesion appears at point of contact (genitalia)
Secondary Syphilis
1-6 months ofter primary
Tertiary Syphilis
1-10 years after primary
Congenital Syphilis
“saber shin”
-anterior deformity of the tibia due to periostits and an inflammatory reaction at the outside bony cortex
“saddle nose” -destruction of nasal bone
-result of transmission from a mother to her fetus
Osteoarthritis
- degenerative joint disease, characterized by joint cartilage breakdown causing painful and stiff joints
- “inflammation of joints” causes disability
- no cure
- only strikes one joint - stress like hip, back, knee, hand
- painful use of joint, painful periods after use, joint discomfort after weather changes, swelling, stiffness, bony lumps in hands/fingers, decreased flexibility
Bony Growth in Osteoarthritis
- result of body’s attempt to repair the joint
- body makes it more difficult with the addition of these bony growths
Risk Factors for Osteoarthritis
- female gender
- age >45y/o
- joint injuries
- obesity
- diseases that cause malformation/disfigurement of bone structure
- weakened quads
- other arthritis
Rheumatoid Arthritis Pathology
-severe ulnar deviation with subluxation (incomplete luxation or dislocation
“swan-neck” abnormality
-small joints affected first (hands/feet) followed by wrists, elbows, ankles, knees
Rheumatoid Nodule
-occur in 20% of patients
-acellular center of eosinophilic material “fibrinoid”
surrounded by palisaded histiocytes and other cells, maybe with a rim of granulation tissue
-occur anywhere-extensor surfaces, pericardium, aortic valve (rare), lung perenchyma
Pannus
“membrane of granulation tissue”
forms in RA
-after years, can proliferate and contribute to joint destruction, spreads over and erodes articular cartilage and bone leading to fibrosis of joint
What do urate crystals look like under microscope?
Needle shaped, under parallel polarized light YELLOW
What do Calcium Phosphate Crystals look like under microscope?
-polarize yellow when Perpendicular to long axis of crystals
Pigmented Villonodular Synovitis
- localized, destructive lesion within a single joint (knee), with proliferation of synovium, hemosiderin pigmentation, and destruction of joint.
- clonal
- excision is usually curative - may recur
