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Dr. Barr 2nd MSP

Dr. Barr's NYCC MSP 2nd exam

QuestionAnswer
When does septic arthritis occur, who gets it more often and why? Any age; infants and young children; immune systems not mature yet.
What organisms can get into the joints in septic arthritis and where does it lodge? S. aureus, H. influenza, Gonococcal infection in sexually active young adults; bacteria lodge in synovial membrane
What does inflammatory response in the synovial membrane promote and what is that? Pannus development: Joint is normally 1-5 cell layers thick, pannus is joint becoming thicker and thicker d/t hypertrophy.
Differentiate between acute and chronic septic arthritis. Acute form often progresses to maximum symptoms in 48 hours, irreversible damage occurs w/in 1 week and may -> chronic; chronic form w/o acute onset presents as smoldering chronic infection w/ recurring flares.
What does septic arthritis susually involve, what are the s/s and typical findings? Large joints; inflammatory signs, usually single joint; typically monoarthritic cond'n. Any monoarthritis should be thought of as infection until proven otherwise.
What are lab results w/ septic arthritis? Increased ESR, Alk PO4 normal, HLA B27 normal, RF normal, synovial biopsy is positive as is joint aspiration.
What is treatment of septic arthritis? Antibiotic therapy, aspiration to decompress the joint, irrigation of joint, decrease motion and weight bearing.
What is fungal arthritis normally found in association with and what other areas could it be found? A rare condition, usually complication of neoplastic Dz (low immune system); gym, woods, tropics
What is fungal arthritis associated with, what can it do, how is it Dx and Tx? Primary lung involvement or athlete's foot; highly destructive; in spine presents like Pott's; Dx by biopsy and Tx is difficult.
What are 4 classifications of bone neoplasia? 1. cysts (not neoplastic) 2. benign neoplasms 3. malignant neoplasms 4. miscellaneous diseases
Who usually gets a simple bone cyst and what is it? 3:1 males to females, typically in children up to 14 y/o, not a neoplasm, fluid filled cyst; aka unicameral or solitary bone cyst
What can cause a simple bone cyst? Secondary to trauma, Hematoma, Excess fluid accumulation, Lined w/ fibrous tissue
What does a simple bone cyst do, what is the MC site and s/s? Expands bone by fluid pressure that stimulates bone resorption; humerus or femur; asymptomatic until path. Fx, may feel hard palpable mass, rarely painful
What is a simple bone cyst composed of? Loose fibrous tissue, osteoclasts, macrophages, reactive bone
How is a simple bone cyst treated? Excision but if proteinaceous coat isn't removed it will recur.
What is an aneurysmal bone cyst? Not a neoplasm; cyst like cavity filled w/ blood; blood flow in and out of the cavity.
What is the gross appearance of an aneurysmal bone cyst? Externally appears smooth and enlarged w/ intact bone and periosteum, internally appears "sponge-like" w/ many cavities, septa b/w cavities are not elastic in nature
What are the cellular components of an aneurysmal bone cyst? Granulation tissue, giant cells, some trabeculae.
In reference to location where to aneurysmal and simple bone cysts usually lie? Aneurysmal: eccentric (off to side) Simple: eucentric (in center
What does an aneurysmal bone cyst do? Proliferation of vascular components, vascular and fluid (blood) pressure erodes bone, can get very large in size.
What are s/s of aneurysmal bone cyst and what is the treatment? >20 y/o; Pain and swelling, pathologic Fx, neurologic deficits; curettage and pack w/ bone chips, radiation therapy to damage the blood vessels if inoperable.
What is characteristic of benign bone neoplasms? None or minimal pain; geographic borders; well defined margins; intact, expanded or dense cortex; no periosteal response; no soft tissue destruction; slow growth; capsulated; short zone transition; well-defined cells; normal blood chemistry
What is characteristic of malignant bone neoplasms? Moderate to severe pain; motheaten appearance; poorly defined/ragged margins; disrupted cortex; spiky periosteal response; destruction of soft tissue; rapid growth; uncapsulated; wide or long zone of transition; poorly defined; abnormal blood chem.
What 4 characteristics of malignant bone neoplasms are visible on radiographs? Disrupted/destroyed cortex, Periosteal lifting, Soft tissue invasion, Long zone of transition
What cells can develop neoplasia in bone? Bone, cartilage, fibroblasts, blood cells, blood vessels
How do you differentiate bone neoplasias vs. infection and why? Bone neoplasias will not go through growth plates, discs, any cartilage b/c neoplasia needs blood supply; infections respect no tissue.
What is a primary bone tumor? Bone neoplasia that arises from cell lines normally found in bone and can be either benign or malignant.
What is a secondary bone tumor? A neoplastic process that arises outside the bone; ALWAYS IMPLIES METASTATIC Dz!
What are the 3 bone forming tumors? 1. Osteoma 2. Osteoid osteoma 3. Osteosarcoma
What is an osteoma and where is it commonly found? Densely sclerotic, well formed bony projections, little clinical significance; face, skull, sinuses, tibia
Who gets osteoid osteoma, what's the size and the classic pt. presentation? Males 2:1 ages 5-25; small in size always less than 2 cm in diameter, painful but benign, tumor area referred to as Nidus; Pain at night relieved by aspirin (NSAIDs not as effective)
Describe a Nidus in osteoid osteoma. Contains tiny trabecula and vascular overgrowth; lucent w/ sclerotic border; PGE2 (vasodilator) found at 12x normal levels; reactive bone form'n around nidus; Tx: wait until maturation then surgical excision
Where are osteoid osteomas normally found? Spine - neural arch Tibia Femur Diaphyseal or metaphyseal
What composes an osteosarcoma and what can it be? Osteoblasts, fibroblasts and chondroblasts; can be primary or secondary osteosarcoma.
Who normally presents with primary osteosarcoma, where are they commonly found and what are pt. presentations? Males over females, <20 y/o; found in ends of long bones 60% found around the knee; skeletally immature, pain, weakness, inflam. signs, swelling, decreased ROM
What is the radiographic presentation of primary osteosarcoma? Long zone of transition Disruption of cortex Periosteal reaction - Codman's triangle and sunburst appearance Invades neighboring soft tissue
What is the nature of primary osteosarcoma, where does mets usually occur and what is Tx? Aggressive tumor where by time it's Dx 20% have mets and 90% of pt. w/ mets will die; lungs, bones, brain; Surgery, chemotherapy, radiation therapy; 60% 5 year survival rate.
What can cause secondary osteosarcoma and what conditions can lead to it? Pre-existing bone pathology or carcinogenic influence in bone; radiation therapies, Paget's, chronic infections, HME.
Who gets secondary osteosarcoma and where are they commonly found? Males>females and >25 y/o, only 25% of all osteosarcoma are secondary; flat bones
What are the 4 chondromatous tumors in bone? 1. Osteochondroma 2. Hereditary Multiple Exostosis (HME) 3. Enchondroma 4. Chondrosarcoma
What is the most common benign bone neoplasia and what are the 3 presentations? Osteochondroma; Solitary (MC), Multiple (<6 bones involved), HME (scattered throughout skeleton); <1% of solitary form undergo malignant degeneration.
What are the 2 varieties of osteochondromas? 1. Sessile: broad base w/ cartilagenous cap covered by fibrous membrane 2. Pedunculated: stalk point away from joint space; both varieties can be found in same body
What is HME and who commonly gets it? Hereditary Multiple Exostosis; widespread multiple osteochondromas numbering 6-100s, familial Hx, males 3:1, painless lumpy joints
What can HME affect, what is Tx and will it undergo malignant degeneration? Growth plates (not always); surgical, most often for cosmetic reasons; up to 25% of HME pt may undergo malignant degeneration as osteosarcoma and chondrosarcoma.
What is enchondroma? Most common benign tumor of hand and foot, generally asymptomatic (til path. Fx), slow growing, mature cartilage, islands of cartilage left behind as bone grows, usually solitary lesions.
How does enchondroma look? Mass of cartilage enclosed by vascular, fibrous stroma, may show irregular calcification.
Who gets enchondroma and what is the multiple form called? M:F 2:1; Ollier's Dz
What is chondrosarcoma? Rare pathology of bone, develops very slowly over time, mets late in Dz process, malignant chondrocytes, necrosis, cystic change and hemorrhage.
What is the frequency of presentation of chondrosarcoma? 75% are primary chondrosarcomas: males 2:1 average 45 y/o; 25% are secondary chondrosarcomas from pre-existing bone condition such as paget's, HME, radiation
Where do chondrosarcomas usually occur? Ribs, shoulders, pelvic girdle
What is the gross appearance of chondrosarcoma? Translucent gray-white in color, mass of aberrant cartilage tissue, necrosis and cysts centrally, stippled calcifications present that may appear on radiographs
What is the clinical presentation and radiographic findings of chondrosarcoma? Soft tissue mass or Fx; Localized bone destruction, mottled areas of increased density, may expand bone, soft tissue mass, 50% stipled calcification.
What treatment is available for chondrosarcoma? Surgical removal of tumor; can mets to lung, liver, kidney and brain; 30-90% 5 year survival rate.
What are 3 fibrous tumors of bone? 1. Fibrous dysplasia 2. Fibrous cortical defect (FCD) 3. Fibrosarcoma
What is fibrous dysplasia and what does it contain? Focal, slowly expanding lesion; contains fibroblasts, collagen (type I), irregular trabeculae, cystic degeneration and slight hemorrhage.
Who is fibrous dysplasia commonly found in? Adults and children, <1% undergoes malignant degeneration
What are the 2 presentations of fibrous dysplasia? 1. Monostotic: 75% of patients, any age, femur, tibia, ribs and facial bones. 2. Polyostotic: Rare, more than half of skeleton affected
What are clinical presentations of monostotic fibrous dysplasia? Asymptomatic, bone may be enlarged or deformed, pathologic Fx
What are clinical presentations of polyostotic fibrous dysplasia? Deformity of bone, affecting siz and shape, Limb length discrepancies, Pathological Fx., Cafe au Lait spots
What are radiographic findings of fibrous dysplasia? Well defined, radiolucent lesion(s), enlargement of bone, ground glass matrix (haziness on x-ray)
What is fibrous cortical defect (FCD) including size and common locations? non-ossifying fibroma, fibroxanthoma (yellow), cortical lesion, likely not a neoplasm, common, 30-50% children >2 y/o; 0.5 - 5-6cm; tibia/fibula, femur
How does a fibrous cortical defect appear? Small area of bony cortex that is replaced by a well demarcated soft yellow-gray tissue; tissue is composed of fibroblasts and giant cells (macrophage), No new bone formation.
How does fibrous cortical defect present and what is treatment? Nocturnal leg pain, in rare cases pathologic Fx; No Tx, seem to resolve on own.
What is fibrosarcoma? Composed of primitive connective tissue and fibroblasts, sheets of malignant fibrous tissue, males>females age 30-40, develops slowly over time (not as slow as chondrosarcoma)
What are symptoms of fibrosarcoma? Local low grade pain and swelling that often refers to joint, duration of symptoms is about 2 years
How does fibrosarcoma appear on radiographs? cortex disappears, fibrous tissue, expansive; lytic cortical disruption more towards metaphysis (distal diaphysis)
How is fibrosarcoma treated and what will occur if it is untreated? Surgical removal, chemo and radiation; mets to lungs and lymph nodes.
What are the blood tumors of bone? 1. Giant cell tumor 2. Multiple myeloma
What is a giant cell tumor and who normally gets it? Uncommon tumor, monocytes and macrophages are cells of origin and are giant in size and multinucleated; 20-40 y/o, benign M:F 2:3, Aggressive M:F 3:2.
Where does giant cell tumor arise where does it extend to and what is the appearance on radiographs? W/in the metaphysis of tubular bones, large lesion extending into and filling the epiphysis, a solitary lytic lesion; Multiloculated "soap-bubble" appearance but not eccentric like aneurysmal bone cyst.
How do giant cell tumors appear, what do they consist of and what %s are bening and malignant? Multi-lobular; hemorrhage, cystic formation and yellow necrosis; benign 80-85%, malignant 25-20%
What are symptoms of a giant cell tumor? Non-specific local pain and tenderness, functional disability, pathologic fracture
What is the radiographic appearance of a giant cell tumor? Large expansile lesion of epiphysis surrounded by thinning cortex, tumor area is radiolucent w/ septa present.
What treatments are available for giant cell tumor? Surgery, drug therapy, radiation therapy
What is multiple myeloma? Malignant proliferation of plasma cells that infiltrate bone marrow, lesions small, appear osteolytic on x-ray.
Who gets multiple myeloma? Males>Females 2:1; 50-70 y/o; Hx of being farmers w/ exposure to pesticides; men's hair coloring?
What are the clinical findings of multiple myeloma? Amemia, osteopenia from deossification of bone, serum and urinary proteins produced w/ overproduction of immunoglobulins (Bence-Jones proteins), Renal Dz
What are symptoms of multiple myeloma? Pain is intermittent but becomes constant, pain worse during day and aggravated by activity and weight bearing, may come on quickly after strain or mild trauma, weight loss, cachexia, anemia, unexplained osteopenia
Where is multiple myeloma usually found? Vertebral body (MC), Skull and pelvis b/c hematopoesis occurs in these bones in older indiv.
What is the etiology of multiple myeloma, how do lesions appear? Unknown Et, small, round and lytic, termed punched out lesions; plain film is better for detection
What is treatment for multiple myeloma? Palliative, radiation and chemo, bone marrow transplantation, thalidomide, 90% of patients die w/in 3 years of Dx.
What are 2 miscellaneous pathologies that masquerade as primary bone tumors? 1. Hemangioma 2. Ewing's sarcoma
What is a hemangioma? Congenital vascular variant (overgrowth of vessels in bone but can be in other organs and skin), large thing walled blood vessels and siuses surrounded by bony trabeculae and reactive bone.
What are symptoms of hemantioma? Usually clinically silent, incidental finding, may have localized pain, muscle spasm and neurologic complaints but these are rare.
How does hemangioma look on film? Corduroy cloth appearance of vertebral bodies, coarse vertical striations separated by radiolucencies
What is Ewing's sarcoma in radiology reports? "Small, round, closely packed malignant cells"
What is Ewing's sarcoma and who gets it? A highly necrotic, aggressive tumor; possibly genetic link males:females 2:1; 5-30 y/o
Where would Ewing's sarcoma be located? Any bone but likes mid diaphysis of long bones and the pelvis; arises in medullary cavity and behaves like a primary malignant bone tumor.
How does the periosteum appear with Ewing's sarcoma? "onion skin" or layered appearance; behaves like a primary bone tumor with the classic 4 findings
How is Ewing's sarcoma treated? Surgery, radiation and chemo, 75% 5 year survival rate
What is Extraosseous Ewing's Sarcoma? Identical pathological description of tumor found outside the skeletal system w/ no bone involvement whatsoever.
What is the most common malignant tumor of bone? Metastatic Dz, most often comes from breast, lung, prostate and kidney
Where does metastatic disease arise from in males and females and what bones are most commonly affected? Females: breast; Males: prostate; vertebral bodies
How old is a patient usually when they present with metastatic Dz, what are other presentations and what is the quality of pain? 2nd half of life; weight loss and anemia; skeletal pain that is deep, achy, boring, constant and not relieved by rest.
What is the radiographic appearance of metastatic Dz? 75% osteoclastic (lytic), 15% Osteoblastic, 10% mixed blastic and lytic. "moth eaten" or "permeative" destruction is typical
What are characteristics of secondary bone tumors? No periosteal response, soft tissue mass is rare, lesions are small in size initially, do not expand bone, multiple sites of involvement.
Describe the synovial joint capsule. Skeletal ligaments bind bones together across joint space and blend w/ the fibrous capsule. Majority of these fibers run in the same direction and are composed of closely packed collagen fibers that allow little stretch.
What is the synovial membrane, what does it lack and what types of cells compose it? Lines all internal aspects of joint except the articular surface itself; lacks basement membrane and gap junctions; 1-5 cell layers thick, composed of A & B cells.
What are type A cells in synovium? Macrophages that contain lysosomal enzymes
What are type B cells in synovium? Type B cells are secretory and produce hyaluronic acid (part of synovial fluid).
How is the synovium arranged? In villi and microvilli, creating a very large surface area.
What is subsynovial tissue and how is it situated in joints? A loose vascularized areolar tissue (b/w capsule and membrane) in some joints the synovium is closely applied to the dense connective tissue of the joint capsule; in the knee joint the synovium overlies a fat pad posteriorly.
What is the function of the synovium? 1. Controls diffusion in and out of joint 2. Ingests debris 3. Secretes hyaluronate, immunoclobulins and lysosomal enzymes 4. Lubrication of joint by secreting synovial fluid 5. Subsynovial tissue is highly vascularized (caps)
What makes up the synovial fluid? Plasma filtrate and other secretions of synovium, should be clear, not turbid.
What does synovial fluid not contain? Fibrinogen so no clotting; shouldn't contain alpha-2 macroglobulin.
How is hyaluronate charged and what does this do for synovial fluid? Large and negatively charged w/ a high affinity to water, gives fluid its viscosity -> molecular sieve (keeps larger molecules away and allows small, soluble things through.
What is the function of articular cartilage? Absorb shock and lubricate surface of joint
Describe normal articular cartilage. Smooth, white, semirigid in appearance does not exceed 6mm in thickness (nutrition supply is diffusion don't want too thick)
What are the 5 histologic zones in articular cartilage? 1. Tangential zone 2. Transitional zone 3. Radial zone 4. Calcified zone 5. Subchondral bone plate
What is b/w the radial zone and the calcified zone and why is this significant? The tide mark or blue line: 1. Interface b/w mineralized and unmineralized cartilage. 2. Divides nutritional source for chondrocytes 3. Chondrocytes replicate and migrate up towards surface above line.
What is meant by dividing the nutritional source for chondrocytes? Above the blue line = diffusion Below the blue line = epiphyseal blood vessels. Below the line, chondrocytes will divide only if there is the appropriate chemical stimulus.
What makes up the articular cartilage's weight? Water comprises 68-78% and the remaining %s is type II collagen and proteoglycans, w/ trace amounts of lipids, phospholipids and lysozymes.
What do proteoglycans do for hyaline cartilage and what does disease do? Make up intercellualar matrix of hyaline cartilage and the nucleus pulposis; breakdown of proteoglycans in Dz (DJD, RA) leads to the loss of the capacity of cartilage to resist wear.
What do cracks do to cartilage? Cracks in cartilage begin on the surface and can extend deeper into the cartilage; we make it over our lifetime but after injury rate of synthesis is not enough to keep pace w/ needed repair. (pothole analogy)
What is Hilton's law? Every peripheral nerve supplying a muscle sends a branch to the joint moved by the muscle and to the skin overlying the joint.
What sort of nerve endings are in a joint? (4) 1. Encapsulated endings 2. GTOs 3. Pacinian corpuscles 4. Free nerve endings
What do encapsulated endings do as a nerve ending in a joint? Respond to mechanical stimuli such as pressure and stretch.
What do GTOs do as a nerve ending in a joint? A stretch receptor responding to the tension generated at the musculotendinous junction.
What do Pacinican Corpuscles do as a nerve ending in a joint? Respond to initiation and cesation of movement (acceleration and deceleration)
What do free nerve endings do as a nerve ending in a joint? Mediate pain.
What is bursae? Closed, flattened CT sacs that contain only enough fluid to moisten the walls of the sac. Deep lying bursae dev. before birth others around joints, subcutaneously, subtendinous or submuscular dev. d/t excessive friciton.
What is a tendon sheath? Fundamentally similar to bursae, tendon sheaths are complex tubes that wrap around a tendon. Mesotendons are variable but are gaps in the sheath that allow bvs to reach the tendon.
What does the tendon sheath consist of? 2 layers: a visceral layer closely applied to the tendon surface and a parietal or outer layer. These layers are separated by fluid produced by a synovial membrane that lines both layers (of sheath).
What are the characteristics of a non-inflammatory joint disease? 1. Asymmetrical loss of joint space across body b/c mechanical wear and tear. 2. Bone building at joint margins 3. Presence of osteophytes 4. Subchondral cysts (geode)
What are characteristics of an inflammatory joint disease? 1. Lytic changes 2. Symmetrical loss of joint space 3. Ligamentous laxity 4. Loss of architecture 5. Hyperemia 6. Ankylosis
What conditions are included in non-inflammatory joint disease? Degenerative Joint Disease Chondromalacia Patella Neuropathic Arthropathy
What is DJD? An inherently non-inflammatory disorder of synovial joints, characterized by deterioration of articular cartilage and by formation of new bone at the joint surfaces and margins. (bare area)
What are some facts about DJD? Most common form of joint disease in US. Seen in up to 95% of the population. Commonly seen as we age and most common to see in weight bearing joints. Cell changes can be seen as early as teens. More common in women and Native Americans
What causes DJD? Almost anything that can damage articular cartilage or the bone around a joint contributes to development of DJD
What factors promote DJD? Inherited poor cartilage, injury to cartilage, increased stiffness of subchondral bone.
What about genetics can cause DJD? Abnormal articular cartilage, fibrillin (type of collagen) present that can cause degenerative change.
How can an injury cause DJD? Anything that will result in damage to cartilage, commonly associated w/ trauma also associated w/ hypomobility -> Fibrillation occurs in cartilage.
What can happen w/ stiffening of subchondral bone? Microfractures, increased stiffness and thickening of subchondral bone (sclerosing), increased stress to cartilage. (can be d/t overuse, excessive stress...)
Degenerative events are a combination of ________ and __________ activity involving cartilage and bone. Degenerative and proliferative
What 4 things occur during degenerative events in DJD? 1. Loss of chondrocytes 2. Fat deposition around chondrocytes (esp. ones lost) 3. Presence of some matrix destroying proteases 4. Softening of cartilage
After the initial loss of chondrocytes, what degenerative events occur? (3) 1. Presence of fibrillation 2. Erosion of cartilage 3. Cartilage repair - mixed hyaline and fibrocartilage.
Describe the course of events that lead to a subchondral cyst. Loss of chondrocytes -> early cracking and fibrillation of cartilage -> bigger "hole" -> down to vascular bone -> fibrocartilagenous plug -> plug pops out -> bigger hole -> death of bone cells -> geode (subchondral cyst)
When does cartilage repair occur? Severe and deep cartilage injury stimulates formation of fibrocartilage but the injury must be down to vascularized bone to initiate formation.
Is fibrocartilage an ideal reparative material in DJD? No, b/c it imbibes water and is not the same as hyaline cartilage; just a patch (pothole)
When and where would new bone formation occur in DJD? At the joint margin = exophytic growth and in the subchondral bone = subjacent marrow; Occurs before, after or during the degenerative events.
Where and why do osteophytes occur during degenerative events of DJD? Protrude from margins of bone, contained w/in the joint capsule, development guided by mechanical forces on joint (stress), attempt at repair. Usually form east and west of joint.
What covers osteophytes? Fibrocartilage and fibrous tissue "cap"; in advanced DJD osteophytes can also undergo degenerative change.
What occurs in vertebrae w/ degeneration and where is weight shifted? Osteophytes result from a pulling on the annulus at the periosteal attachment (d/t narrowing discs); weight is shifted to the facets which gives further degenerative change at facet joints.
What will DJD never lead to? Ankylosis (fusion of bones); osteophytes can limit ROM but no fusion.
What can lead to eburnation and what is it? Subchondral bone proliferates, more often in areas of reduced cartilage, articular surfaces can be rubbed smooth, essentially polishing the bone causing death of osteocytes. Eburnation = mechanical process and subchondral sclerosing.
What are soft tissue changes with DJD? Synovial villus hypertrophy, capsular tears (uncommon), ligaments and menisci become frayed (b/c aberrant mechanical wear and tear)
What are clinical presentations of DJD? Aching in region of joint Worse w/ activity Relieved by rest Worse w/ prolonged rest Crepitus (grinding)
What are clinical findings w/ DJD? Decreased ROM, often not recognized by pt. May see local swelling but this is SECONDARY to DJD process Spinal cord symptoms Nerve root symptoms
Does joint degeneration always mean symptoms? Does not correlate w/ presence or absence of symptoms, except in severe lumbar, hip or knee DJD.
What will be found on films w/ DJD? (8) 1. Asymmetrical distribution 2. Non-uniform loss of joint space 3. Subchondral sclerosis 4. Subchondral cysts 5. Intra-articular loose bodies (joint mice) 6. Deformity 7. Joint subluxation (medical) 8. Vacuum sign (in spine)
What is vacuum sign? Discs dessicate and breakdown, nitrogen accumulates in disc space gives lucency in joint space that moves. (if anywhere other than spine something else other than DJD)
What does chondromalacia patella (CMP) mean? Cartilage softening disease
What would a patient with CMP complain of? Anterior knee pain; most overworked and imprecise dx of the knee; softening of cartilage is asymptomatic, b/c cartilage avascular softening can lead to issues.
What cartilage changes are observed in CMP? (3) 1. Softening of cartilage 2. fissuring of cartilage 3. fibrillation = excessive deposition of fibrillin in cartilage
What are causal theories of CMP? Inherent cartilage defect, abnormal contact w/ synovial membrane, loss of contact w/ articular cartilage (patella-femoral joint)
Describe the onset of chondromalacia patella. Age of onset 16-30 y/o, male=female, insidious onset w/o recent trauma, diffuse ache in one or both knees.
What is the pain like w/ chondromalacia patella and what other findings are there? Constant and worse w/ activity and stair climbing, squatting may be impossible, pt notices stiffness, grating sensation when load bearing, familial Hx of similar knee problems.
What is the onset of Sx of CMP frequently associated w/? Jogging or repetitive loading, immobilization, casting, improperly fitting appliances (pt purchased not doctor Rx), medial meniscectomy predisposes.
What is statistically associated w/ CMP? Abnormal function of extensor mechanism, functional incongruity, malalignment of lower extremity (adjust!), recurrent sublux./dislocation, patellar instability or damage.
What makes cartilage happy? Must have pressure (wnl) applied to it, too much/little leads to CMP and modifies calcification and vascularization of subchondral bone.
What other names does neuropathic arthropathy have? Neurotrophic Arthropathy, Neuroarthropathy, Charcot's joint
What must occur first for neuropathic arthropathy to develop? Neural damage!
What does a patient experience w/ neuropathic arthropathy? Premature and excessive traumatic degeneration resulting in severe destruction and instability.
What is the etiology of neuropathic arthropathy? 1. Congenital 2. Acquired: process/change occurred complications from type I diabetes, MS, chronic alcoholism, tertiary syphilis, syringomyelia 3. Iatrogenic (Dr. induced: long term therapy can -> negative effects)
What are clinical features of neuropathic arthropathy? usually seen in ankles and feet; altered gait; loss of DTR; insensitivity to pain; painless instability, joint enlargement, crepitus (liberating bone bits b/c smacking together)
What are radiographic features of neuropathic arthropathy? Not remarkable early but -> total loss of joint space; DJD (increased bone density and much subchondral sclerosing); Dislocation; Debris = "bag of bones" appearance
How is neuropathic arthropathy treated? Address primary pathology, supportive care and education; amputation usually results
What is rheumatoid arthritis? A systemic inflammatory disease that affects skin, blood vessels, heart, lungs, muscles and primarily joints.
What else is RA and what can it lead to? A non-suppurative proliferative synovitis that leads to destruction of articular cartilage and ankylosis of joints.
What are the 2 types of ankylosis of joints? 1. Fibrous 2. Bony
Who gets RA? Found in 1% of population; females:males = 3-5:1; Dx usually in 30s or 40s; cause is unknown, thought to be viral, autoimmune or genetic.
What happens during the course of RA? Course is highly unpredictable; 90% of patients have gradual onset; greatest damage occurs w/in the first 5 years of process; damage worse w/ older age of onset.
What is affected w/ RA? Generally affects smaller joints first and progresses to larger joints; hands, wrists and feet are most commonly involved (distal -> proximal); Can move to ankles, elbows, knees, hips and shoulders as Dz progresses.
Where in the spine is RA found and what sort of distribution is there? Most commonly in cervical spine (if there at all); extremity involvement usually has a symmetrical distribution.
How does RA begin and what occurs in the synovium? Begins as a non-distinct inflammation; synovium becomes edematous, thickened and hyperplastic.
What makes up the inflammatory infiltrate in RA and where to these cells deposit? Infiltrate: helper T-cells, plasma cells and macrophages; deposit in areolar tissue (subsynovial tissue in joint)
What covers portions of synovium in RA and what can this lead to? Fibrin covers portions of synovium, pieces of fibrin (rice bodies) float to joint space -> synovial membrane thickening and hypertrophy -> villi production and hypertrophy.
What do inflammatory cells stimulate in RA and what does this lead to? PGE2 stimulates osteoclastic activity -> juxta-articular erosion and breakdown, subchondral cysts (filled w/ pannus) and juxta-articular osteoporosis.
What is pannus in RA? The inflamed and hypertrophied synovial membrane.
What will the pannus in RA do? Fill the joint space (cover like cloak); produce proteases, elastases and collagenases (cause erosion); inhibit proteoglycan synthesis; stimulate production of fibroblasts.
When the pannus in RA stimulates production of fibroblasts what can happen? Fibrin over surface of pannus = uniform loss of joint space -> instability -> fibrous tissue in pannus -> fibrous ankylosis.
What immune complexes are present in RA patients? RA - IgG; autoimmunity to type II collagen; immune complexes found in synovial fluid, hyaline cartilage and fibrous tissue.
What does continued development of fibrous tissue in RA lead to? Fibrous pannus formation; tissue organizes into fibrous bands w/in the pannus -> fibrous ankylosis
How do synovial fluid and gross bones look w/ RA? Synovial fluid is turbid not clear and bones show bleeding b/c destruction is down in bone.
What else can be involved w/ RA? Tendons and ligaments and these can rupture b/c tendon sheaths can get synovial hypertrophy too.
How does a patient present w/ RA? Malaise, fatigue, low grade fever; non-localized musculoskeletal pain; eventually local pain, redness and swelling; stiffness during or after inactivity (pannus causing pain not activity; warm shower won't help)
What is found in 25% of patients w/ RA? Rheumatoid nodules usually seen w/ more severe disease and frequently found on elbows and forearms.
What are rheumatoid nodules? Areas of fibrous necrosis surrounded by lymphocytes and granulation tissue.
What causes "swan neck" and "boutonniere's" deformity? Muscular pulling (i.e. stronger extensors)
What else is seen in RA and more severe RA? Non-specific conjunctivitis; acute vasculitis
What do lab findings do for your diagnosis w/ RA? Support your diagnosis but do not conclusively determine diagnosis.
What are lab findings w/ RA? ESR is elevated Alk Phos levels normal Mild anemia Presence of RF is seropositive in 90% of patients (multiple antibodies, mainly IgM against IgG)
What are radiographic findings for RA? Bilaterally symetrical and periarticular soft tissue swelling -> uniform loss of joint space; juxta-articular osteopenia; "rat bite" lesion (erosion at margins); pseudocysts (filled w/ pannus)
What can cause "rat bite" lesions? Disuse, increase in PGE2 stimulates osteoclasts, hyperemia puts pressure on bone and causes resorption.
What can juvenile RA also be called? Still's Dz or juvenile arthritis
Who is affected w/ juvenile RA? <16 y/o
What occurs w/ juvenile RA? Inflammatory changes identical to adults, except you see less inflammation and less pannus formation.
What can Juvenile RA cause? Growth plate disturbances (can accelerate activity or cause premature fusion); can be mono, oligo or systemic arthritis; knees frequently involved (single joint involvement).
What may be seen in juvenile RA? fever, rash and organ enlargement; may involve strictly joints; 70-90% of patients undergo complete remission.
Created by: kabrown