Nycc Barr Exam 2 Spring 2011

Front 1

Question

Back 1

Answer

Front 2

When does septic arthritis occur, who gets it more often and why?

Back 2

Any age;

MORE FREQUENT INFANTS & CHILDREN d/t immune systems not mature yet.

Front 3

What organisms can get into the joints in septic arthritis and where does it lodge?

Back 3

STAPH & FLU & GONORRHEA (what a combo)

** bacteria lodge in synovial membrane

Front 4

Inflammatory response in the SYNOVIAL MEMBRANE is called a ________. Explain.

Back 4

PANNUS

Bacteria (STAPH/FLU/GONORRHEA) lodge in synovial membrane.

Joint is normally 1-5 cell layers thick, pannus is joint becoming thicker and thicker d/t HYPERTROPHY

Front 5

ACUTE vs. CHRONIC arthritis

Back 5

ACUTE: form often progresses to maximum symptoms in 48 hours, irreversible damage occurs w/in 1 week and may become chronic;

CHRONIC: form w/o acute onset presents as smoldering chronic infection w/ recurring flares.

Front 6

Joints of SEPTIC ARTHRITIS and what are the s/x and typical findings?

Back 6

LARGE JOINTs

MONOARTHRITIC (local)

INFECTION UNTIL PROVEN INNOCENT

Front 7

What are lab results w/ septic arthritis?

Back 7

Increased ESR, synovial biopsy is positive as is joint aspiration.

Alk PO4 normal, HLA B27 normal, RF normal,

Front 8

What is treatment of septic arthritis?

Back 8

Antibiotic therapy, aspiration to decompress the joint, irrigation of joint, decrease motion and weight bearing.

Front 9

What is fungal arthritis normally found in association with and what other areas could it be found?

Back 9

A rare condition, usually complication of neoplastic Dz (low immune system); gym, woods, tropics

Front 10

What is fungal arthritis associated with, what can it do, how is it Dx and Tx?

Back 10

Primary lung involvement or athlete's foot;
HIGHLY DESTRUCTIVE;

in spine presents like POTT'S DISEASE;

Dx by biopsy and Tx is difficult.

Front 11

What are 4 classifications of bone neoplasia?

Back 11

1. cysts (not neoplastic) 2. benign neoplasms 3. malignant neoplasms 4. miscellaneous diseases

Front 12

Who usually gets a simple bone cyst and what is it?

Not Test Question
(ntq)

Back 12

3:1 males to females
, typically in children up to 14 y/o,
not a neoplasm, fluid filled cyst;
aka UNICAMERAL or SINGLE-CHAMBERED bone cyst

Front 13

What can cause a simple bone cyst?

Back 13

UNICAMERAL
SIMPLE BONE CYST
Secondary to TRAUMA!
, Hematoma, Excess fluid accumulation, Lined w/ fibrous tissue

Front 14

What does a simple bone cyst do, what is the MC site and s/s?

Back 14

EXPANDS bone by FLUID PRESSURE that stimulates bone RESORPTION;
humerus or femur;
asymptomatic until path. Fx, may feel hard palpable mass, rarely painful

Front 15

What is a simple bone cyst composed of?

Back 15

Loose fibrous tissue,

osteoclasts, (gives lucent appearance)

macrophages,

reactive bone (thin cortex but Wolff's law to contain cyst)

Front 16

How is a simple bone cyst treated?

Back 16

Excision via CURETTE (a bladed melon baller for scraping) but if proteinaceous coat isn't removed it will recur.

Front 17

What is an aneurysmal bone cyst?

Back 17

Not a neoplasm; cyst like cavity filled w/ blood; blood flow in and out of the cavity. via FEEDER arteries that OVERWHELM the venous flow.
Sets up fluid pressure and creates a cyst.

Front 18

What is the gross appearance of an aneurysmal bone cyst?

Back 18

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

Front 19

What are the cellular components of an aneurysmal bone cyst?

Back 19

Granulation tissue, giant cells, some trabeculae.

Front 20

In reference to location where to aneurysmal and simple bone cysts usually lie?

Back 20

Aneurysmal: eccentric (off to side) Simple: eucentric (in center

Front 21

What does an aneurysmal bone cyst do?

Back 21

Proliferation of vascular components, vascular and fluid (blood) pressure erodes bone, can get very large in size.

Front 22

What are s/s of aneurysmal bone cyst and what is the treatment?

Back 22

>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.

Front 23

What is characteristic of benign bone neoplasms?

Back 23

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

Front 24

What is characteristic of malignant bone neoplasms?

Back 24

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.

Front 25

What 4 characteristics of malignant bone neoplasms are visible on radiographs?

Back 25

Disrupted/destroyed cortex, Periosteal lifting, Soft tissue invasion, Long zone of transition

Front 26

What cells can develop neoplasia in bone?

Back 26

Bone, cartilage, fibroblasts, blood cells, blood vessels

Front 27

How do you differentiate bone neoplasias vs. infection and why?

Back 27

Bone neoplasias will not go through growth plates, discs, any cartilage b/c neoplasia needs blood supply; infections respect no tissue.

Front 28

What is a primary bone tumor?

Back 28

Bone neoplasia that arises from cell lines normally found in bone and can be either benign or malignant.

Front 29

What is a secondary bone tumor?

Back 29

A neoplastic process that arises outside the bone; ALWAYS IMPLIES METASTATIC Dz!

Front 30

What are the 3 bone forming tumors?

Back 30

1. Osteoma 2. Osteoid osteoma 3. Osteosarcoma

Front 31

What is an osteoma and where is it commonly found?

Back 31

Densely sclerotic, well formed bony projections, little clinical significance; face, skull, sinuses, tibia

Front 32

Who gets osteoid osteoma, what's the size and the classic pt. presentation?

Back 32

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)

Front 33

Describe a Nidus in osteoid osteoma.

Back 33

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

Front 34

Where are osteoid osteomas normally found?

Back 34

Spine - neural arch Tibia Femur Diaphyseal or metaphyseal

Front 35

What composes an osteosarcoma and what can it be?

Back 35

Osteoblasts, fibroblasts and chondroblasts; can be primary or secondary osteosarcoma.

Front 36

Who normally presents with primary osteosarcoma, where are they commonly found and what are pt. presentations?

Back 36

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

Front 37

What is the radiographic presentation of primary osteosarcoma?

Back 37

Long zone of transition Disruption of cortex Periosteal reaction - Codman's triangle and sunburst appearance Invades neighboring soft tissue

Front 38

What is the nature of primary osteosarcoma, where does mets usually occur and what is Tx?

Back 38

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.

Front 39

What can cause secondary osteosarcoma and what conditions can lead to it?

Back 39

Pre-existing bone pathology or carcinogenic influence in bone; radiation therapies, Paget's, chronic infections, HME.

Front 40

Who gets secondary osteosarcoma and where are they commonly found?

Back 40

Males>females and >25 y/o, only 25% of all osteosarcoma are secondary; flat bones

Front 41

What are the 4 chondromatous tumors in bone?

Back 41

1. Osteochondroma 2. Hereditary Multiple Exostosis (HME) 3. Enchondroma 4. Chondrosarcoma

Front 42

What is the most common benign bone neoplasia and what are the 3 presentations?

Back 42

Osteochondroma; Solitary (MC), Multiple (<6 bones involved), HME (scattered throughout skeleton); <1% of solitary form undergo malignant degeneration.

Front 43

What are the 2 varieties of osteochondromas?

Back 43

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

Front 44

What is HME and who commonly gets it?

Back 44

Hereditary Multiple Exostosis; widespread multiple osteochondromas numbering 6-100s, familial Hx, males 3:1, painless lumpy joints

Front 45

What can HME affect, what is Tx and will it undergo malignant degeneration?

Back 45

Growth plates (not always); surgical, most often for cosmetic reasons; up to 25% of HME pt may undergo malignant degeneration as osteosarcoma and chondrosarcoma.

Front 46

What is enchondroma?

Back 46

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.

Front 47

How does enchondroma look?

Back 47

Mass of cartilage enclosed by vascular, fibrous stroma, may show irregular calcification.

Front 48

Who gets enchondroma and what is the multiple form called?

Back 48

M:F 2:1; Ollier's Dz

Front 49

What is chondrosarcoma?

Back 49

Rare pathology of bone, develops very slowly over time, mets late in Dz process, malignant chondrocytes, necrosis, cystic change and hemorrhage.

Front 50

What is the frequency of presentation of chondrosarcoma?

Back 50

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

Front 51

Where do chondrosarcomas usually occur?

Back 51

Ribs, shoulders, pelvic girdle

Front 52

What is the gross appearance of chondrosarcoma?

Back 52

Translucent gray-white in color, mass of aberrant cartilage tissue, necrosis and cysts centrally, stippled calcifications present that may appear on radiographs

Front 53

What is the clinical presentation and radiographic findings of chondrosarcoma?

Back 53

Soft tissue mass or Fx; Localized bone destruction, mottled areas of increased density, may expand bone, soft tissue mass, 50% stipled calcification.

Front 54

What treatment is available for chondrosarcoma?

Back 54

Surgical removal of tumor; can mets to lung, liver, kidney and brain; 30-90% 5 year survival rate.

Front 55

What are 3 fibrous tumors of bone?

Back 55

1. Fibrous dysplasia 2. Fibrous cortical defect (FCD) 3. Fibrosarcoma

Front 56

What is fibrous dysplasia and what does it contain?

Back 56

Focal, slowly expanding lesion; contains fibroblasts, collagen (type I), irregular trabeculae, cystic degeneration and slight hemorrhage.

Front 57

Who is fibrous dysplasia commonly found in?

Back 57

Adults and children, <1% undergoes malignant degeneration

Front 58

What are the 2 presentations of fibrous dysplasia?

Back 58

1. Monostotic: 75% of patients, any age, femur, tibia, ribs and facial bones. 2. Polyostotic: Rare, more than half of skeleton affected

Front 59

What are clinical presentations of monostotic fibrous dysplasia?

Back 59

Asymptomatic, bone may be enlarged or deformed, pathologic Fx

Front 60

What are clinical presentations of polyostotic fibrous dysplasia?

Back 60

Deformity of bone, affecting siz and shape, Limb length discrepancies, Pathological Fx., Cafe au Lait spots

Front 61

What are radiographic findings of fibrous dysplasia?

Back 61

Well defined, radiolucent lesion(s), enlargement of bone, ground glass matrix (haziness on x-ray)

Front 62

What is fibrous cortical defect (FCD) including size and common locations?

Back 62

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

Front 63

How does a fibrous cortical defect appear?

Back 63

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.

Front 64

How does fibrous cortical defect present and what is treatment?

Back 64

Nocturnal leg pain, in rare cases pathologic Fx; No Tx, seem to resolve on own.

Front 65

What is fibrosarcoma?

Back 65

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)

Front 66

What are symptoms of fibrosarcoma?

Back 66

Local low grade pain and swelling that often refers to joint, duration of symptoms is about 2 years

Front 67

How does fibrosarcoma appear on radiographs?

Back 67

cortex disappears, fibrous tissue, expansive; lytic cortical disruption more towards metaphysis (distal diaphysis)

Front 68

How is fibrosarcoma treated and what will occur if it is untreated?

Back 68

Surgical removal, chemo and radiation; mets to lungs and lymph nodes.

Front 69

What are the blood tumors of bone?

Back 69

1. Giant cell tumor 2. Multiple myeloma

Front 70

What is a giant cell tumor and who normally gets it?

Back 70

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.

Front 71

Where does giant cell tumor arise where does it extend to and what is the appearance on radiographs?

Back 71

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.

Front 72

How do giant cell tumors appear, what do they consist of and what %s are bening and malignant?

Back 72

Multi-lobular; hemorrhage, cystic formation and yellow necrosis; benign 80-85%, malignant 25-20%

Front 73

What are symptoms of a giant cell tumor?

Back 73

Non-specific local pain and tenderness, functional disability, pathologic fracture

Front 74

What is the radiographic appearance of a giant cell tumor?

Back 74

Large expansile lesion of epiphysis surrounded by thinning cortex, tumor area is radiolucent w/ septa present.

Front 75

What treatments are available for giant cell tumor?

Back 75

Surgery, drug therapy, radiation therapy

Front 76

What is multiple myeloma?

Back 76

Malignant proliferation of plasma cells that infiltrate bone marrow, lesions small, appear osteolytic on x-ray.

Front 77

Who gets multiple myeloma?

Back 77

Males>Females 2:1; 50-70 y/o; Hx of being farmers w/ exposure to pesticides; men's hair coloring?

Front 78

What are the clinical findings of multiple myeloma?

Back 78

Amemia, osteopenia from deossification of bone, serum and urinary proteins produced w/ overproduction of immunoglobulins (Bence-Jones proteins), Renal Dz

Front 79

What are symptoms of multiple myeloma?

Back 79

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

Front 80

Where is multiple myeloma usually found?

Back 80

Vertebral body (MC), Skull and pelvis b/c hematopoesis occurs in these bones in older indiv.

Front 81

What is the etiology of multiple myeloma, how do lesions appear?

Back 81

Unknown Et, small, round and lytic, termed punched out lesions; plain film is better for detection

Front 82

What is treatment for multiple myeloma?

Back 82

Palliative, radiation and chemo, bone marrow transplantation, thalidomide, 90% of patients die w/in 3 years of Dx.

Front 83

What are 2 miscellaneous pathologies that masquerade as primary bone tumors?

Back 83

1. Hemangioma 2. Ewing's sarcoma

Front 84

What is a hemangioma?

Back 84

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.

Front 85

What are symptoms of hemantioma?

Back 85

Usually clinically silent, incidental finding, may have localized pain, muscle spasm and neurologic complaints but these are rare.

Front 86

How does hemangioma look on film?

Back 86

Corduroy cloth appearance of vertebral bodies, coarse vertical striations separated by radiolucencies

Front 87

What is Ewing's sarcoma in radiology reports?

Back 87

"Small, round, closely packed malignant cells"

Front 88

What is Ewing's sarcoma and who gets it?

Back 88

A highly necrotic, aggressive tumor; possibly genetic link males:females 2:1; 5-30 y/o

Front 89

Where would Ewing's sarcoma be located?

Back 89

Any bone but likes mid diaphysis of long bones and the pelvis; arises in medullary cavity and behaves like a primary malignant bone tumor.

Front 90

How does the periosteum appear with Ewing's sarcoma?

Back 90

"onion skin" or layered appearance; behaves like a primary bone tumor with the classic 4 findings

Front 91

How is Ewing's sarcoma treated?

Back 91

Surgery, radiation and chemo, 75% 5 year survival rate

Front 92

What is Extraosseous Ewing's Sarcoma?

Back 92

Identical pathological description of tumor found outside the skeletal system w/ no bone involvement whatsoever.

Front 93

What is the most common malignant tumor of bone?

Back 93

Metastatic Dz, most often comes from breast, lung, prostate and kidney

Front 94

Where does metastatic disease arise from in males and females and what bones are most commonly affected?

Back 94

Females: breast; Males: prostate; vertebral bodies

Front 95

How old is a patient usually when they present with metastatic Dz, what are other presentations and what is the quality of pain?

Back 95

2nd half of life; weight loss and anemia; skeletal pain that is deep, achy, boring, constant and not relieved by rest.

Front 96

What is the radiographic appearance of metastatic Dz?

Back 96

75% osteoclastic (lytic), 15% Osteoblastic, 10% mixed blastic and lytic. "moth eaten" or "permeative" destruction is typical

Front 97

What are characteristics of secondary bone tumors?

Back 97

No periosteal response, soft tissue mass is rare, lesions are small in size initially, do not expand bone, multiple sites of involvement.

Front 98

Describe the synovial joint capsule.

Back 98

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.

Front 99

What is the synovial membrane, what does it lack and what types of cells compose it?

Back 99

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.

Front 100

What are type A cells in synovium?

Back 100

Macrophages that contain lysosomal enzymes

Front 101

What are type B cells in synovium?

Back 101

Type B cells are secretory and produce hyaluronic acid (part of synovial fluid).

Front 102

How is the synovium arranged?

Back 102

In villi and microvilli, creating a very large surface area.

Front 103

What is subsynovial tissue and how is it situated in joints?

Back 103

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.

Front 104

What is the function of the synovium?

Back 104

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)

Front 105

What makes up the synovial fluid?

Back 105

Plasma filtrate and other secretions of synovium, should be clear, not turbid.

Front 106

What does synovial fluid not contain?

Back 106

Fibrinogen so no clotting; shouldn't contain alpha-2 macroglobulin.

Front 107

How is hyaluronate charged and what does this do for synovial fluid?

Back 107

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.

Front 108

What is the function of articular cartilage?

Back 108

Absorb shock and lubricate surface of joint

Front 109

Describe normal articular cartilage.

Back 109

Smooth, white, semirigid in appearance does not exceed 6mm in thickness (nutrition supply is diffusion don't want too thick)

Front 110

What are the 5 histologic zones in articular cartilage?

Back 110

1. Tangential zone 2. Transitional zone 3. Radial zone 4. Calcified zone 5. Subchondral bone plate

Front 111

What is b/w the radial zone and the calcified zone and why is this significant?

Back 111

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.

Front 112

What is meant by dividing the nutritional source for chondrocytes?

Back 112

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.

Front 113

What makes up the articular cartilage's weight?

Back 113

Water comprises 68-78% and the remaining %s is type II collagen and proteoglycans, w/ trace amounts of lipids, phospholipids and lysozymes.

Front 114

What do proteoglycans do for hyaline cartilage and what does disease do?

Back 114

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.

Front 115

What do cracks do to cartilage?

Back 115

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)

Front 116

What is Hilton's law?

Back 116

Every peripheral nerve supplying a muscle sends a branch to the joint moved by the muscle and to the skin overlying the joint.

Front 117

What sort of nerve endings are in a joint? (4)

Back 117

1. Encapsulated endings 2. GTOs 3. Pacinian corpuscles 4. Free nerve endings

Front 118

What do encapsulated endings do as a nerve ending in a joint?

Back 118

Respond to mechanical stimuli such as pressure and stretch.

Front 119

What do GTOs do as a nerve ending in a joint?

Back 119

A stretch receptor responding to the tension generated at the musculotendinous junction.

Front 120

What do Pacinican Corpuscles do as a nerve ending in a joint?

Back 120

Respond to initiation and cesation of movement (acceleration and deceleration)

Front 121

What do free nerve endings do as a nerve ending in a joint?

Back 121

Mediate pain.

Front 122

What is bursae?

Back 122

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.

Front 123

What is a tendon sheath?

Back 123

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.

Front 124

What does the tendon sheath consist of?

Back 124

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).

Front 125

What are the characteristics of a non-inflammatory joint disease?

Back 125

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)

Front 126

What are characteristics of an inflammatory joint disease?

Back 126

1. Lytic changes 2. Symmetrical loss of joint space 3. Ligamentous laxity 4. Loss of architecture 5. Hyperemia 6. Ankylosis

Front 127

What conditions are included in non-inflammatory joint disease?

Back 127

Degenerative Joint Disease Chondromalacia Patella Neuropathic Arthropathy

Front 128

What is DJD?

Back 128

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)

Front 129

What are some facts about DJD?

Back 129

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

Front 130

What causes DJD?

Back 130

Almost anything that can damage articular cartilage or the bone around a joint contributes to development of DJD

Front 131

What factors promote DJD?

Back 131

Inherited poor cartilage, injury to cartilage, increased stiffness of subchondral bone.

Front 132

What about genetics can cause DJD?

Back 132

Abnormal articular cartilage, fibrillin (type of collagen) present that can cause degenerative change.

Front 133

How can an injury cause DJD?

Back 133

Anything that will result in damage to cartilage, commonly associated w/ trauma also associated w/ hypomobility -> Fibrillation occurs in cartilage.

Front 134

What can happen w/ stiffening of subchondral bone?

Back 134

Microfractures, increased stiffness and thickening of subchondral bone (sclerosing), increased stress to cartilage. (can be d/t overuse, excessive stress...)

Front 135

Degenerative events are a combination of ________ and __________ activity involving cartilage and bone.

Back 135

Degenerative and proliferative

Front 136

What 4 things occur during degenerative events in DJD?

Back 136

1. Loss of chondrocytes 2. Fat deposition around chondrocytes (esp. ones lost) 3. Presence of some matrix destroying proteases 4. Softening of cartilage

Front 137

After the initial loss of chondrocytes, what degenerative events occur? (3)

Back 137

1. Presence of fibrillation 2. Erosion of cartilage 3. Cartilage repair - mixed hyaline and fibrocartilage.

Front 138

Describe the course of events that lead to a subchondral cyst.

Back 138

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)

Front 139

When does cartilage repair occur?

Back 139

Severe and deep cartilage injury stimulates formation of fibrocartilage but the injury must be down to vascularized bone to initiate formation.

Front 140

Is fibrocartilage an ideal reparative material in DJD?

Back 140

No, b/c it imbibes water and is not the same as hyaline cartilage; just a patch (pothole)

Front 141

When and where would new bone formation occur in DJD?

Back 141

At the joint margin = exophytic growth and in the subchondral bone = subjacent marrow; Occurs before, after or during the degenerative events.

Front 142

Where and why do osteophytes occur during degenerative events of DJD?

Back 142

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.

Front 143

What covers osteophytes?

Back 143

Fibrocartilage and fibrous tissue "cap"; in advanced DJD osteophytes can also undergo degenerative change.

Front 144

What occurs in vertebrae w/ degeneration and where is weight shifted?

Back 144

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.

Front 145

What will DJD never lead to?

Back 145

Ankylosis (fusion of bones); osteophytes can limit ROM but no fusion.

Front 146

What can lead to eburnation and what is it?

Back 146

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.

Front 147

What are soft tissue changes with DJD?

Back 147

Synovial villus hypertrophy, capsular tears (uncommon), ligaments and menisci become frayed (b/c aberrant mechanical wear and tear)

Front 148

What are clinical presentations of DJD?

Back 148

Aching in region of joint Worse w/ activity Relieved by rest Worse w/ prolonged rest Crepitus (grinding)

Front 149

What are clinical findings w/ DJD?

Back 149

Decreased ROM, often not recognized by pt. May see local swelling but this is SECONDARY to DJD process Spinal cord symptoms Nerve root symptoms

Front 150

Does joint degeneration always mean symptoms?

Back 150

Does not correlate w/ presence or absence of symptoms, except in severe lumbar, hip or knee DJD.

Front 151

What will be found on films w/ DJD? (8)

Back 151

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)

Front 152

What is vacuum sign?

Back 152

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)

Front 153

What does chondromalacia patella (CMP) mean?

Back 153

Cartilage softening disease

Front 154

What would a patient with CMP complain of?

Back 154

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.

Front 155

What cartilage changes are observed in CMP? (3)

Back 155

1. Softening of cartilage 2. fissuring of cartilage 3. fibrillation = excessive deposition of fibrillin in cartilage

Front 156

What are causal theories of CMP?

Back 156

Inherent cartilage defect, abnormal contact w/ synovial membrane, loss of contact w/ articular cartilage (patella-femoral joint)

Front 157

Describe the onset of chondromalacia patella.

Back 157

Age of onset 16-30 y/o, male=female, insidious onset w/o recent trauma, diffuse ache in one or both knees.

Front 158

What is the pain like w/ chondromalacia patella and what other findings are there?

Back 158

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.

Front 159

What is the onset of Sx of CMP frequently associated w/?

Back 159

Jogging or repetitive loading, immobilization, casting, improperly fitting appliances (pt purchased not doctor Rx), medial meniscectomy predisposes.

Front 160

What is statistically associated w/ CMP?

Back 160

Abnormal function of extensor mechanism, functional incongruity, malalignment of lower extremity (adjust!), recurrent sublux./dislocation, patellar instability or damage.

Front 161

What makes cartilage happy?

Back 161

Must have pressure (wnl) applied to it, too much/little leads to CMP and modifies calcification and vascularization of subchondral bone.

Front 162

What other names does neuropathic arthropathy have?

Back 162

Neurotrophic Arthropathy, Neuroarthropathy, Charcot's joint

Front 163

What must occur first for neuropathic arthropathy to develop?

Back 163

Neural damage!

Front 164

What does a patient experience w/ neuropathic arthropathy?

Back 164

Premature and excessive traumatic degeneration resulting in severe destruction and instability.

Front 165

What is the etiology of neuropathic arthropathy?

Back 165

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)

Front 166

What are clinical features of neuropathic arthropathy?

Back 166

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)

Front 167

What are radiographic features of neuropathic arthropathy?

Back 167

Not remarkable early but -> total loss of joint space; DJD (increased bone density and much subchondral sclerosing); Dislocation; Debris = "bag of bones" appearance

Front 168

How is neuropathic arthropathy treated?

Back 168

Address primary pathology, supportive care and education; amputation usually results

Front 169

What is rheumatoid arthritis?

Back 169

A systemic inflammatory disease that affects skin, blood vessels, heart, lungs, muscles and primarily joints.

Front 170

What else is RA and what can it lead to?

Back 170

A non-suppurative proliferative synovitis that leads to destruction of articular cartilage and ankylosis of joints.

Front 171

What are the 2 types of ankylosis of joints?

Back 171

1. Fibrous 2. Bony

Front 172

Who gets RA?

Back 172

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.

Front 173

What happens during the course of RA?

Back 173

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.

Front 174

What is affected w/ RA?

Back 174

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.

Front 175

Where in the spine is RA found and what sort of distribution is there?

Back 175

Most commonly in cervical spine (if there at all); extremity involvement usually has a symmetrical distribution.

Front 176

How does RA begin and what occurs in the synovium?

Back 176

Begins as a non-distinct inflammation; synovium becomes edematous, thickened and hyperplastic.

Front 177

What makes up the inflammatory infiltrate in RA and where to these cells deposit?

Back 177

Infiltrate: helper T-cells, plasma cells and macrophages; deposit in areolar tissue (subsynovial tissue in joint)

Front 178

What covers portions of synovium in RA and what can this lead to?

Back 178

Fibrin covers portions of synovium, pieces of fibrin (rice bodies) float to joint space -> synovial membrane thickening and hypertrophy -> villi production and hypertrophy.

Front 179

What do inflammatory cells stimulate in RA and what does this lead to?

Back 179

PGE2 stimulates osteoclastic activity -> juxta-articular erosion and breakdown, subchondral cysts (filled w/ pannus) and juxta-articular osteoporosis.

Front 180

What is pannus in RA?

Back 180

The inflamed and hypertrophied synovial membrane.

Front 181

What will the pannus in RA do?

Back 181

Fill the joint space (cover like cloak); produce proteases, elastases and collagenases (cause erosion); inhibit proteoglycan synthesis; stimulate production of fibroblasts.

Front 182

When the pannus in RA stimulates production of fibroblasts what can happen?

Back 182

Fibrin over surface of pannus = uniform loss of joint space -> instability -> fibrous tissue in pannus -> fibrous ankylosis.

Front 183

What immune complexes are present in RA patients?

Back 183

RA - IgG; autoimmunity to type II collagen; immune complexes found in synovial fluid, hyaline cartilage and fibrous tissue.

Front 184

What does continued development of fibrous tissue in RA lead to?

Back 184

Fibrous pannus formation; tissue organizes into fibrous bands w/in the pannus -> fibrous ankylosis

Front 185

How do synovial fluid and gross bones look w/ RA?

Back 185

Synovial fluid is turbid not clear and bones show bleeding b/c destruction is down in bone.

Front 186

What else can be involved w/ RA?

Back 186

Tendons and ligaments and these can rupture b/c tendon sheaths can get synovial hypertrophy too.

Front 187

How does a patient present w/ RA?

Back 187

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)

Front 188

What is found in 25% of patients w/ RA?

Back 188

Rheumatoid nodules usually seen w/ more severe disease and frequently found on elbows and forearms.

Front 189

What are rheumatoid nodules?

Back 189

Areas of fibrous necrosis surrounded by lymphocytes and granulation tissue.

Front 190

What causes "swan neck" and "boutonniere's" deformity?

Back 190

Muscular pulling (i.e. stronger extensors)

Front 191

What else is seen in RA and more severe RA?

Back 191

Non-specific conjunctivitis; acute vasculitis

Front 192

What do lab findings do for your diagnosis w/ RA?

Back 192

Support your diagnosis but do not conclusively determine diagnosis.

Front 193

What are lab findings w/ RA?

Back 193

ESR is elevated Alk Phos levels normal Mild anemia Presence of RF is seropositive in 90% of patients (multiple antibodies, mainly IgM against IgG)

Front 194

What are radiographic findings for RA?

Back 194

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)

Front 195

What can cause "rat bite" lesions?

Back 195

Disuse, increase in PGE2 stimulates osteoclasts, hyperemia puts pressure on bone and causes resorption.

Front 196

What can juvenile RA also be called?

Back 196

Still's Dz or juvenile arthritis

Front 197

Who is affected w/ juvenile RA?

Back 197

<16 y/o

Front 198

What occurs w/ juvenile RA?

Back 198

Inflammatory changes identical to adults, except you see less inflammation and less pannus formation.

Front 199

What can Juvenile RA cause?

Back 199

Growth plate disturbances (can accelerate activity or cause premature fusion); can be mono, oligo or systemic arthritis; knees frequently involved (single joint involvement).

Front 200

What may be seen in juvenile RA?

Back 200

fever, rash and organ enlargement; may involve strictly joints; 70-90% of patients undergo complete remission.

Front 201

most highly destructive, hard to kill arthritis

Back 201

FUNGAL arthritis

treatment is highly toxic to liver

Front 202

a simple bone cyst is not a

Back 202

tumor. It is a fluid filled cyst.

Front 203

a simple bone cyst is secondary to __________

Back 203

TRAUMA like a hematoma (bleed inside a bone)

Front 204

What lines a simple bone cyst?

Back 204

cavity lined with PROTIENACEOUS COAT of FIBROUS TISSUE

Front 205

most common site of simple bone cyst

Back 205

HUMERUS

Front 206

Most common sites of simple bone cyst (2)

Back 206

HUMERUS (proximal)
&
FEMUR (lots of blood supply)

Front 207

simple cysts rarely ________ the bone.

Back 207

expand


75% of the time, they are not palpable

Front 208

Simple bone cysts are located ___________

Back 208

EUCYSTICALLY

and ergo, are prone to pathological fracture
(vs. aneurysmal bone cyst full of blood that is located eccentrically)

Front 209

When are simple bone cysts painful?

Back 209

when they break or fracture

Front 210

**note the _________location of simple bone cysts on radiographs. This is called EUCENTRIC

Back 210

centrally

Front 211

ABC

Back 211

Aneurysmal
Bone
Cyst

(blood)

Front 212

Which kind of cyst ALWAYS EXPANDS THE BONE?

Back 212

ABC! expands easy as 123! Simple as do-ray-me, ABC that's how easy bone expansion can be!

Aneurysmal
Bone
Cyst

Front 213

A big, expansile growth that looks like spongy trabecular radiolucency hanging off vertebrae neural arches (vs. vertebral bodies) is a?

Back 213

ABC
Aneurysmal
Bone
Cyst

"soap bubble appearance"

Front 214

soap bubble appearance

Back 214

common radiographic term for ABC

Front 215

What kind of cyst EXPANDS the bone, or HANGS off the bone and name?

Back 215

ABC

ECCENTRIC (hanging off, bulge on bone) But can you still trace the cortical line? Then it is intact.

Front 216

cortex looks eggshell thin and is eccentric with a soap-bubble appearance

Back 216

ABC
Aneurysmal
Bone Cyst

Front 217

in lab, decide whether lesion has qualities of _______ or _________

Back 217

benign or malignant

Front 218

on a radiograph, which cell line will have a BLASTIC appearance (vs. lytic)?

Back 218

BONE

What bone it's in determines what kind of tumor it is.

Front 219

Pain is associated with _________ problems.

Back 219

malignant


ie, benign doesn't normally hurt but malignancy pain is moderate to severe

Front 220

If a lesion likes a certain location, it is considered to be _____________

Back 220

geographic (a visible border)

ie, benign are geographic while malignant are moth-eaten or permeative

Front 221

definition as a feature

Back 221

well-defined vs. poorly defined
is benign vs. malignant

Front 222

Describe a benign cortex vs. malignant

Back 222

benign = intact/expanded/dense

malignant = disrupted/destroyed

Front 223

If the CORTEX IS INTACT, would the periosteum be lifted?

Back 223

NO!

Front 224

difference between benign and malignant periosteum

Back 224

benign is intact because nothing busted through whereas in neoplasia, it blows through as CODMAN'S TRIANGLE, SPICULES, LAMINATED (onion skin)

Front 225

soft tissue appearance of benign versus malignant

Back 225

in benign, no soft tissue invasion because periosteum not lifted and cortex not disrupted
BUT
will be with malignant conditions
SHEETS OF MALIGNANT TISSUE INVADING SURROUNDING TISSUE

Front 226

benign growth is ________

Back 226

slow

malignant is fast

Front 227

benign capsulation?

Back 227

yes, they are contained

malignant are uncontained

Front 228

Describe the ZONE OF TRANSITION in benign vs. malignant

Back 228

benign: short

malignant: long, difficult to determine where starts and stops

Front 229

malignant cells metastasize, benign

Back 229

do not

Front 230

describe cell fcn of benign vs. malignant

Back 230

benign tissue resembles same cell fcn of tissue of origin

malignant don't!

Front 231

lab findings of benign vs malignant

Back 231

benigh Normal

malignant Abnormal

Front 232

prognosis for benign and malignant

Back 232

good versus poor

Front 233

a neoplastic process arising OUTSIDE of bone

Back 233

SECONDARY bone tumors

Front 234

Secondary bone tumors always imply

Back 234

METASTASES

Front 235

What 3 mechanisms allow for metastases

Back 235

Hematogenous spread
direct extension
implantation

Front 236

describe an osteoma

Back 236

a bony bump of normal happy healthy bone cells that got kicked off and settled somewhere.
FACE SKULL SINUSES TIBIA
and Gardener's syndrome

Front 237

Gardener's syndrome

Back 237

multiple osteomas

Front 238

densely sclerotic
well-formed bony projections
little clinical significance

Back 238

OSTEOMA

cortices intact, periosteum not lifted, cortical line intact, contained by bone

Front 239

Is an osteoid osteoma benign or malignant?

Back 239

benign but PAINFUL

age GENDER location (Males age 5-25, spine-neural arch, tibia, diaphyseal or metaphyseal, femur)

Front 240

contains the tiny trabeculae and vascular overgrowth of an osteoid osteoma

Back 240

NIDUS

a tumor of VASCULAR OVERGROWTH containing PGE2 (vasodilator)

Front 241

What is found inside the nidus that causes the pain?

Back 241

PGE2 at 12x the normal level.
PGE2 is a vasodilator.
A nidus is closed so no room for vasodilation = pain

Front 242

classic patient presentation of osteoid osteoma

*board question and TEST question

Back 242

~young male
~pain at night due to PGE2
~relieved by aspirin as vasoconstricts

Front 243

treatment of osteoid osteoma

Back 243

wait until MATURATION then do surgical excision so when it actually is removed, it stays gone

Front 244

why does the board like to highlight the osteoid osteoma?

Back 244

found in the neural arch

of young males experiencing pain at night relieved by aspirin

Front 245

More stereotypical presentation of osteoid osteoma than neural arch?

Back 245

LONG bone

Front 246

CHRONIC arthritis has never presented with _____ ______.

Back 246

acute onset.

Front 247

Any ___________ should be thought of as an infection until proven otherwise.

Back 247

MONOARTHRITIC

Front 248

INFECTION of the joint space.

Back 248

SEPTIC ARTHRITIS

Front 249

HLA B27

Back 249

antigenic peptides (derived from self and non-self antigens) to T cells. HLA-B27 is strongly associated with ankylosing spondylitis (AS), and other associated inflammatory diseases referred to collectively as "spondyloarthritis".

Front 250

What is the only elevated lab result for SEPTIC ARTHRITIS?

Back 250

ESR (b/c it's an infection)

Also, synovial biopsy and joint aspiration are positive. All other findings normal labs.