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243 Cards in this Set
- Front
- Back
Septic arthritis occurs most frequently in __________
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Infants and young children
|
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What are the most common causes of septic arthritis?
|
Staph aureus, Haemophilius influenzae, Gonococcus spp.
|
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In septic arthritis bacteria lodge in the __________, sparking an __________ promoting __________ development
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No real membrane, inflammatory response, pannus
|
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How quickly does septic arthritis tend to progress?
|
Maximum symptoms within 48 hours, irreversible damage within one week
|
|
What are the signs and symptoms of septic arthritis?
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Inflammation of joint and decreased range of motion
|
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Septic arthritis tends to involve __________ joints and are __________-arthritic
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Large joints, mono-arthritic
|
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What are the laboratory results of septic arthritis?
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Increase ESR and joint aspiration, alk phos (acute = 0, chronic = mild increase), decrease in HLA B27 and RF
|
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Fungal arthritis is a rare and often a complication of __________, thus it affects the __________
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Neoplastic diseases, immunosuppressed
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Fungal arthritis is often associated with __________ or __________
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Primary lung fungal infection or athlete's foot
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Fugal arthritis of the spine presents like __________ since it is so __________
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Potts disease, destructive
|
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How is fungal arthritis treated?
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Strong drugs
|
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T or F? Cysts are non-neoplastic
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True
|
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Simple/______/______ bone cysts are a fluid filled cyst more common in __________ and lined with __________
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Unicameral/solitary, male, fibrous tissues
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Simple bone cysts are often secondary to __________?
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Trauma
|
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Why does bone reabsorption occur with a simple bone cyst?
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Expansion via fluid pressures
|
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What is the most common site for a simple bone cyst? When?
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Humerus and femur
14 years old |
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Simple bone cysts tend to be located how on a bone?
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Eucentric
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SBC's are __________ until fracture, and may be __________
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Asymptomatic/none painful, palpable
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Simple bone cysts are composed of __________
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Fibrous tissue, osteoclasts, macrophages, reactive bone
|
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How do you treat a simple bone cyst?
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Excise the protein lining to prevent recuration, replace with bone chips of healthy bone
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What is a cyst-like cavity filled with blood?
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Aneurysmal bone cysts
|
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What is the gross appearance of an aneurysmal bone cyst?
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Externally smooth with enlarged intact bone, internally cavernous with non-elastic septa (soap bubble)
|
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What are the cellular components of an aneursymal bone cyst?
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Granulation tissue, giant cells, minimal trabecular
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ABCs are __________ located and will __________
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Accentrically, expand greatly
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Aneurysmal bone cysts in vertebrae preference the __________
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Neural arch
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In an ABC, there is a proliferation of __________ whose pressure __________
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Vascular components, erodes/bulges bone
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An ABC may result in __________, __________, and __________
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Pain/swelling, fracture, neurological defects
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ABC usually onset __________ and occur __________ in males and females
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After age 20
Equally |
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How is an ABC treated?
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Scrape it out and bone pack; radiation if inoperable
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What are the cells that can develop into primary bone neoplasms?
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Bone, cartilage, fibroblasts, blood vessels, blood cells
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Neoplastic processes rarely cross __________ or __________, why?
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Growth plates or articulating cartilage
They're avascular areas |
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What type of bone tumor is always metatstatic?
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Secondary
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Osteoma's are densely __________ well formed __________ of __________ clinical significance
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Sclerotic, bony projections, little clinical significance
|
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What are the common locations of an osteoma?
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Face, scroll, sinuses, and tibia
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Multiple osteoma's with colon polyps is called?
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Gardner's syndrome
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Osteoid osteoma tends to affect whom?
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Males 5 - 25
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The osteoid osteoma tumor is referred to as a __________, which is _______ and less than _______ in size.
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Nidus, painful, 2 centimeters
|
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What does a nidus contain?
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Tiny trabecular a, vascular overgrowth and PGE2
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What is a nidus painful?
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PGE2 tells vessels to expand but they are compacted by the excessive bone
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How does a nidus appear on a radiograph?
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Tiny radiolucent center, radiodensity surrounding it due to reactive bone formation
|
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What is the classical presentation of osteoid osteoma?
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Pain at night, 18 year old male, relieved by aspirin/vasoconstrictive
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How is osteoid osteoma treated?
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Wait until maturity, and then surgically excise
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Where osteoid osteoma is most commonly located?
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Neural arches, tibia and femur (diaphysis or metaphysis)
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What is the rarely occurring osteosarcoma composed of?
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Osteoblasts, fibroblasts, and chondroblasts
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Where is a primary osteosarcoma most common?
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Males under 20, ends of long bone often around the knee
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What is the radiographic presentation of a primary osteosarcoma?
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Long transition, cortex disruption, periosteal lifting, and invasion of soft tissue
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What is the gross appearance of a primary osteosarcoma?
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Disorganized vasculature, local necrosis, no cortical line, excessive bony tissue
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Primary osteosarcoma is so aggressive that by diagnosis __% have metastasized, of which ___% die
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20%
90% |
|
How do you treat osteosarcoma
|
Surgery, chemo, radiation
(60%. Five year survival rate) |
|
What is a secondary osteosarcoma
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Sarcoma originating from another bone pathology or from a carcinogen
|
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Where is secondary osteosarcoma most common?
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Males 25 years or up, in flat bones
|
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What is the most common bone neoplasm and what are its three presentations?
|
Osteochondroma
SOLITARY, multiple, hereditary multiple exostosis (HME) |
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Osteochondroma presents with a bony __________ and a __________
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Exostosis, cartilage covered by fibrous membrane
|
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Which form of osteochondroma is least likely to become malignant?
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Solitary
|
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HME is more common in _______ and presents with _______ due to multiple osteochondromas
|
Men, painless lumpy joint
|
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HME may affect the __________
|
Growth plates
|
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How is HME treated? Why?
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Surgically
For cosmetic reasons, only 25% become malignant |
|
What is the most common benign tumor of the hand and foot?
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Encondroma
|
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What type of lesion is enchondroma typically?
|
Asymptomatic solitary
|
|
What is enchondroma?
|
Slow-growing mature cartilage enclosed by vascular stroma with irregular calcification
|
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What is left behind as the bone grows in enchondroma?
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Islands of cartilage
|
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Who more commonly gets enchondroma?
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Males
|
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What is the multiple form of enchodroma?
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Ollier's disease
|
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When may chondrosarcoma metastasize and what types of cell does it involve?
|
Late stage, chondrocytes
|
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What percent of chondrosarcoma are primary?
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75%
|
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Who most commonly gets primary chondrosarcoma?
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45 year old males
|
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Where in the body are chondrosarcoma's most common?
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Ribs, shoulder, and pelvic girdle
|
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What is the gross tissue appearance of chondrosarcoma?
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Translucent gray white mast with necrosis and cysts centrally
|
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What are the radiographic findings of chondrosarcoma?
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Localized bone destruction, random increase densities, expanded bone, ST mass, 50% have stippled calcification
|
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How is chondrosarcoma treated?
|
Surgery
|
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Where does chondrosarcoma tend to metastasize?
|
Lung, liver, kidney and the brain
|
|
What is the five year survival rate of chondrosarcoma?
|
30 - 90% dependent on where it's located
|
|
Why is drug and radiation therapy poorly effective for chondrosarcoma?
|
Both treatments attack fast dividing cells, chondrosarcoma is very slow growing
|
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Fibrous dysplasia is a __________ lesion, commonly of the __________, __________, __________ and __________ bones
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Slowly expanding focal lesion
Femur, tibia, ribs and facial bones |
|
Fibrous dysplasia contains what cellular components?
|
Fibroblasts, collagen, irregular trabeculae, cysts, and slight hemorrhage
|
|
Who gets fibrous dysplasia? What percent become malignant?
|
Adults and children
Less than 1% |
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Which is the most common form of fibrous dysplasia?
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Monostotic
|
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How does monostotic fibrous dysplasia clinically present?
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Typically asymptomatic, enlarged bone, pathological fracture
|
|
What is the clinical presentation of polyostotic fibrous dysplasia?
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Deformed shape and size of bone, limb length discrepancies, pathological fracture
|
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What are the radiographic findings of fibrous dysplasia?
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Well defined radiolucent lesions, enlarged bone, ground glass matrix
|
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Fibrous cortical defects aka __________, is common and effects __________
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Non-ossifying fibroma or fibroxanthoma
Children over 2 years |
|
True or False: Fibrous cortical defects is not a neoplasm
|
True
|
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Fibrous cortical defect tends to be ______cm lesions located in the __________, __________, or __________
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0.5 - 6cm
Tibia, fibula, femur |
|
What is the cellular appearance of a fibrous cortical defect?
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Well demarcated soft yellow/gray tissue comprised of fibroblasts and giant cells
|
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In fibrous cortical defect, there is no new __________, rather __________
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Bone formation, cortical replacement
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Fibrous cortical defects clinically present as __________, and rarely results in a __________
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Nocturnal leg pain
Pathological fracture |
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How is fibrous cortical defects treated?
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It's not
|
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Fibrosarcoma is composed of what?
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Primitive connective tissue, fibroblasts, sheets of malignant fibrous tissue
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Fibrosarcoma develops __________ overtime, most commonly in whom?
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Slowly
Males 30 to 40 years |
|
What are the signs/symptoms of fibrosarcoma?
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Two year duration of local low-grade pain and swelling, often referring to a joint
|
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How is fibrosarcoma treated and what happens if it is left untreated?
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Surgical removal
Metastasizes to the lungs and lymph nodes |
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What are the blood tumors of bone?
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Giant cell tumor and multiple myeloma
|
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The uncommon giant cell tumor involves __________ cells, of __________ origin
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Multinucleated, monocyte and macrophage origin
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Who gets benign giant cell tumors? Malignant giant cell tumors?
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Benign: females 20 to 40 years
Malignant: males 20 to 40 years |
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Giant cell tumors arise in the __________ and are __________ lesions extending into the epiphysis
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Metaphysis of tubular bone, large solitary lesion
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What is the cellular appearance of a giant cell tumor?
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Multi-lobar with areas of hemorrhage, cysts and yellow necrosis
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Giant cell tumors tend to be benign or malignant?
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Benign
|
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What are the signs and symptoms of giant cell tumor?
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Non-specific local pain/tenderness, functional disability, pathological fracture
|
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What is the radiographic appearance of giant cell tumor?
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Large radiolucent lesion of epiphysis, pinning cortex, septa, "soap bubble appearance"
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How are giant cell tumors treated?
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Standard (surgical, drugs, radiation)
|
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Multiple myeloma is a malignant proliferation of __________ that infiltrate __________
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Plasma cells
Bone marrow |
|
Describe the lesions associated with multiple myeloma
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1-5 mm lesions that appear osteolytic and round, "punched out" appearance
|
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Who commonly gets multiple myeloma?
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Males 50 - 70 years, farmers with pesticide exposure or men's hair coloring
|
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What are the clinical findings of multiple myeloma?
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Anemia, osteopenia, renal disease, increased immunoglobulins/serum and urinary proteins
|
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What is the pain related symptoms of multiple myeloma?
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Intermittent Px becoming continuous, worse at daytime/activity/weight-bearing, rapid onset post-trauma
|
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Multiple myeloma commonly occurs where?
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Vertebral body, skull, pelvis
|
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What is the etiology of multiple myeloma?
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Unknown
|
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How is multiple myeloma treated? Thus, what is the survival rate?
|
Most palliative, marrow transplant or thalidomide may also work
90% die in three years |
|
What pathologies may be confused with a primary bone tumor?
|
Hemangioma
Ewing's sarcoma |
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What are the non-pain related symptoms of multiple myeloma?
|
Weight loss, cachexia, anemia, unexplained osteopenia
|
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What is hemangioma?
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Congenital vascular variant with large thin walls and sinuses surrounded by trabeculae and reactive bone
|
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Hemangiomas are generally clinically __________, and presents with __________
|
Clinically silent
Localized pain, muscle spasm, neurological compromise |
|
In an x-ray, a hemangioma will have a __________ appearance of vertebral bodies
|
Striped/corduroy appearance
|
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Ewing's sarcoma is classically described as having __________
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Small, round closely packed cells
|
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Who MC gets Ewing's sarcoma?
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Males 5 to 30 years old
|
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A Ewing's sarcoma tumor is __________ necrotic and the disease may be __________
|
Highly necrotic
Genetic |
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Where does Ewings sarcoma like to occur?
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Any bone, prefers midshaft of long bones and pelvis, arises and medually cavity
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In an x-ray, Ewing's sarcoma has a __________ appearance
|
Periosteal "onionskin" appearance
|
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How is Ewing sarcoma treated? What is the survival rate?
|
Standard, 75% five year survival
|
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Extraosseous Ewing sarcoma has identical pathologies and descriptions of __________, but has no __________
|
Metastatic bone tumor, bone involvement
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________% of bone tumors are metastatic in origin
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70%
|
|
Malignant bone tumors tend to come from what locations?
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Breast, lung, prostate and kidney
|
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__________ spread is metastatic disease's favorite method
|
Hematogenous
|
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Most metastatic tumors in bone of females comes from where? In males?
|
Breast
Prostate |
|
What is the most common bone effected by metastatic disease?
|
Vertebrae
|
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Metastatic disease tends to occur when?
|
Second half of the life
|
|
What is the clinical presentation of metastatic disease?
|
Weight loss, anemia, skeletal pain, fever
|
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What is the quality of pain and metastatic disease?
|
Deep boring unrelieved by rest may worsen at night
|
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What is the radiographic appearance of metastatic disease?
|
Lytic (70%), blastic (15%), mixed (5%)
Moth eaten permeative |
|
Why many a bone become osteoblastic in metastatic disease?
|
Body's natural response to invasion of tissue
|
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How would the blood test appear with metastatic disease?
|
Increase in ESR, normal alk phos, anemia, decrease WBC
|
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What are the characteristics of a secondary bone tumor?
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No periosteal lift, rare st masses, small lesions, multi-site, structures not visualized, no bone expansion
|
|
How is metastatic disease treated? What is the prognosis?
|
Standard
Poor |
|
Ligaments are composed of __________ that allow for __________
|
Densely packed Type I collagen, little stretch
|
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The synovial membrane lines __________ except the __________
|
All internal aspects of a joint
Articular surface |
|
Why is the synovium not a true membrane?
|
No basement membrane or gap junction
|
|
Type A cells are __________
|
Macrophages
|
|
Type B cells are __________ and produce __________
|
Secretory
Hyaluronic acid |
|
What increases surface area of the synovium?
|
Villi and microvilli
|
|
What is sub-synovial tissue?
|
Loose highly vascularized areolar tissue
|
|
Where is the synovium in the knee?
|
Posteriorly overlying the fat pad
|
|
Synovial fluid is a __________
|
Plasma filtrate
|
|
Synovial fluids should not contain __________ and should appear __________
|
Fibrinogen and alpha-2 macroglobulin, clear
|
|
What allows for the proper viscosity of synovial fluid?
|
Hyaluronate is highly negative with a high water affinity
|
|
What is the importance of viscosity of synovial fluid?
|
Molecular sieve (forces debris away from joint surfaces and into macrophagic membrane)
|
|
Why is articular cartilage limited to 6mm thick?
|
Is diffusion dependent
|
|
Articular cartilage changes in thickness with stress/exercise due to __________, allowing for __________
|
Fluid absorption, better fits and better weight distribution
|
|
Which zones of cartilage are radio dense?
|
Calcified and subchondral
|
|
Where is the blueline/tide mark?
|
Between the radial and calcified zones
|
|
The blue line is the interface between what?
|
Cartilage and mineralized tissue
|
|
When do chondrocytes replicate and migrate above the tide mark? What about below?
|
All the time
Only with chemical stimulus (example: acromegaly) |
|
70 - 80% of articular cartilage weights is compromise of __________, the rest being __________ & __________
|
Water
Type II collagen and proteoglycans |
|
Proteoglycans make up the __________ and the __________
|
Intercellular matrix of hyaline, nucleus pulposis
|
|
What is Hilton's law?
|
Referred nerve pain due to joint disturbance
|
|
Encapsulated endings respond to __________ stimuli, such as __________ & __________
|
Mechanical stimuli
Pressure and stretch |
|
The golgi tendon organs respond to __________ at the __________
|
Tension
Musculotendinous junction |
|
Pacinian corpuscles respond to __________
|
Initiation and cessation of movement
|
|
Free nerve endings respond to __________
|
Pain
|
|
What is a bursae? When are they developed?
|
Closed sacs with moist walls
Fetal (deep bursae), jt/subcutaneous (friction response) |
|
Tendon sheaths are __________. What are the gaps called?
|
Complex tubes wrapping tendons
Mesotendons |
|
Tendon sheaths have a __________ lining both layers
|
Synovial membrane
|
|
Degenerative diseases are actually __________ diseases
|
Bone building
|
|
What is cartilage fibrillation?
|
Excess of deposition of fibrillin in cartilage
|
|
What are the general characteristics of non-inflammatory joint diseases?
|
Asymmetric, joint space loss, subchondral sclerosing, osteoclasts, mechanical pattern of wear
|
|
DJD aka __________, is a reactive pattern of joint tissues to __________
|
Osteoarthritis or osteoarthrosis, mechanical and biological factors
|
|
DJD most commonly affects what types of joint?
|
Synovial
|
|
Who has DJD? Where is it most often found?
|
95% of us, 40 - 50 year old men is most common
Older people in weight bearing joints |
|
Who most commonly gets moderate or severe DJD?
|
Women
|
|
What race has DJD more than anyone else?
|
Native Americans
|
|
What can cause cartilaginous damage and thus DJD?
|
Trauma, infection, repetitive use, heredity, immobility
|
|
Gravity leads to what type of osteoarthritis? Trauma?
|
Primary
Secondary |
|
What factors promote DJD?
|
Genetically poor cartilage, injury, increased stiffness of subchondral bone
|
|
What makes cartilage genetically poor?
|
Fibrillin
|
|
How does stiffening of subchondral bone occur in why will it promote DJD?
|
Stiffness causes increased stress to be transmitted into the cartilage
|
|
In DJD there is a loss of __________, and __________ & __________ of the cartilage
|
Chondrocytes, erosion, softening (fibrocartilage imbibs water)
|
|
In DJD, what is found around the chondrocytes
|
Matrix destroying proteases and fat
|
|
The cartilage repair of DJD is composed of __________
|
Hyaline (good), fibrocartilage (bad)
|
|
What is a subchondral cyst?
|
Subchondral fissure that balloons out with synovial fluid
|
|
When does fibrocartilage formation begin?
|
Injury to the vascularized bone
|
|
What would the blood test for DJD look like?
|
Normal, because it is a very slow process
|
|
In DJD, where is new bone formed?
|
Joint margins (eg. osteophytes) and subchondral bones (via subadjacent marrow)
|
|
Osteophytes are an attempt to __________ and are developmentally guided by __________
|
Repair and increase load surface
Mechanical forces |
|
What covers the surface of osteophytes?
|
Fibrocartilage and fibrous tissue
|
|
Vertebral osteophytes result from __________
|
Pulling of annulus at the periosteal attachment
|
|
Why are the facets commonly severely affected in vertebral DJD?
|
Disc degeneration shifts weight to the already degenerated facets
|
|
What is eburnation?
|
Articular surface polished causing death of osteophytes
|
|
What are the soft tissue changes of subchondral cyst? What is it also known as?
|
Synovial villus hypertrophy, capsular care, ligaments/menisci fray
Geode |
|
What is the clinical presentation of DJD?
|
Aching joint, worse with activity and prolonged rest, better with rest, DIPS and PIPs, doctor observes decreased range of motion
|
|
What common orientation is seen in the foot of a DJD patient?
|
Hallux valgus
|
|
What is a common secondary DJD process?
|
Localized swelling
|
|
What are the radiographic findings of DJD?
|
Asymmetrical, joint space loss, subchondral sclerosing, cysts, loose bodies, vacuum sign
|
|
Except in severe _____, ______ or ______ DJD, degeneration does not correlate with the presence of symptoms
|
Lumbar, hip, knee
|
|
What is a vacuum sign?
|
Common in spine, nitrogen gas from disc degeneration appears as radiolucent pockets
|
|
What is the "most overworked and imprecise diagnosis of the knee" associated with anterior knee pain
|
Chondromalacia patella
|
|
CMP has been used interchangeably with __________ of the knee
|
DJD
|
|
What are the cartilage changes in chondromalacia patella?
|
Softening, fissuring, and fibrillation
|
|
Softening of cartilage is or is not symptomatic?
|
IS NOT
|
|
What are the causal theories of chondromalacia patella?
|
Inherent cart defect, abnormal synovial membrane, loss of contact with articular cartilage
|
|
CMP occurs between __ - ___ years, equally between men and females, and has an __________ onset
|
16 - 30 years
Insidious without recent trauma |
|
Is chondromalacia patella a normal aging process?
|
Possible minor changes occur in everyone by 25 years and 50% show gross changes
|
|
Chondromalacia patella involves what signs/smptoms?
|
Diffuse fairly constant ache, worse with stairs anda ctivity, squatting impossible, overall stiffness, crepitus
|
|
The symptoms of CMP are associated with what 5 things?
|
Improper appliances (knee braces), immobilization/casts, repetitive loading and medial meniscetomy
|
|
What incidents are statistically associated with CMP?
|
Poor extensor mechanism, function incongruity, misaligned lower extremity, recurrent subluxation/dislocation, patellar instability
|
|
Too much or too little pressure leads to __________ and __________
|
CMP and changes in calcification and vascularization of subchondral bone
|
|
What is the best way to visualize CMP?
|
MRI
|
|
How may chondromalacia patella be treated?
|
Balance muscles, reduce tracking, cortisone, NSAIDS, cut 'er open
|
|
What is destructive articular disease secondary to neural damage?
|
Neuropathic arthopathy or Charcot's joint
|
|
In neuropathic arthropathy, the patient experience __________ degeneration resulting in __________
|
Premature and excessive traumatic
Severe destruction and instability |
|
What is the etiology of neuropathic arthropathy?
|
Congenital, acquired and latrogenic (doctor induced)
|
|
What may lead to acquired neuropathic arthropathy?
|
MS, syphilis, alcoholism, Type I diabetes, trauma
|
|
What are the clinical features of neuropathic arthropathy?
|
In ankles/feet, altered gait, loss of deep tendon reflex, insensitivity to pain, instability, joint enlargement
|
|
How quickly may neuropathic arthropathy form?
|
Weeks to years
|
|
What is the radiographic appearance of neuropathic arthopathy?
|
Initially insignificant
Later- DJD, dislocation, subchondral sclerosis, "bag of bones" debris appearance |
|
What are the 6 D's of neuropathic arthropathy?
|
Density, debris, destruction, dislocation, distention and degeneration
|
|
What are the characteristics of an inflammatory joint disease?
|
Lytic, symmetrical, erosion, of joint margins, ligamentous laxity, cysts
|
|
Rheumatoid arthritis is a __________ disease that affects the __________
|
Systemical inflammatory
Skin, blood, joints, muscle, heart, lungs |
|
Rheumatoid arthritis is not _______; it is a _______ synovitis leading to destruction of ____ & _______ of joints
|
Rheumatism, non-supperative proliferative, articular cartilage, ankylosis of joints
|
|
Who most commonly gets RA?
|
Females in their 30 - 40s
|
|
What is the etiology of RA?
|
Unknown, may be viral, genetic or autoimmune
|
|
RA is highly unpredictable or predictable? Although ___% have a _______ onset with the greatest damage occurring in _________
|
Unpredictable
90% Gradual First 5 years |
|
What joints are most commonly involved in RA? Where in the spine may it be found?
|
Smaller joints of extremities in a symmetrical distribution
Cervical |
|
RA Begins as what type of inflammation?
|
Non-distinct
|
|
What cells deposit in the areolar tissue of RA?
|
Inflammation (helper T cells, plasma cells and macrophages)
|
|
In RA, what occurs with the synovium?
|
Becomes edematous, thickens, and hyperplasia. Fibrin covers portions of it
|
|
IN RA, within the joint space there is __________ and __________
|
Villi production, rice bodies (fibrin pieces)
|
|
The inflammatory cell's PGE2 stimulates __________, thus leading to __________ and __________
|
Osteoclastic activity
Juxta-articular erosion and osteoporosis Subchondral cysts |
|
What is an inflamed and hypertrophied synovium?
|
Pannus
|
|
What does a pannus do?
|
Fill joint space
Produce protease, elastase, collagenase Decrease proteoglycans Increase fibroblasts Decreases ROM |
|
What is the immune response associated with RA?
|
Autoimmunity to type II collagen due to immune complex RA-IgG found in synovial fluid, hyaline, and fibrous tissue
|
|
At the end of RA, tissue is organized into __________ leading to __________, and possibly eventually __________.
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Fibrous bands within pannus, fibrous ankylosis, bony ankylosis
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What are the lab findings of RA?
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Increase ESR, normal alkaline phosphatase levels, mild anemia, rheumatoid factor
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Why is a bone scan a poor method of detecting RA?
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Although sensitive, poorly visualizes lytic changes
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In RA,there tends to be __________ deviation of the wrist, and __________ deviation of the fingers
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Radial
Ulnar |
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What % of RA patients are seropositive? What % of the normal population?
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90% of RA
5% of normal |
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What is the basic clinical presentation of RA?
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Malaise, fever, non-local pain --> becomes local, inflammation, stiffness with activity, conjunctivitis
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What is seen in severe RA?
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Rheumatoid nodules of the elbows/forearms, acute vasculitis
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What is a rheumatoid nodule?
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Areas of fibrous necrosis surrounded by lymphocytes and granulation tissue
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What are the radiographic findings of RA?
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Bilateral symmetrical, pseudocysts, "rat bite" lesion, uniform joint space loss, soft tissue swelling, osteoporosis
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Juvenile RA aka __________, occurs in people under _____, and appear identical to adult RA with the exception of __________
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Still's disease
16 years Less inflammation and pannus formation |
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What may juvenile RA do to the growth plate?
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Increase growth plate activity, or cause premature fusion
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Juvenile RA may be ____, _____ or _______ arthritis
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Mono, oligo or systemic
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What is the most commonly involved joint of juvenile RA? What may also occur in JRA?
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Knees
Fever, rash and organ enlargement |
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What percent of JRA patients undergo complete remission?
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70 - 90%
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