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Handout – REVIEW SISTEM GERAK Oleh : dr.

Zainuri Sabta Nugraha

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Zainuri Sabta Nugraha 2 |Page .Handout – REVIEW SISTEM GERAK Oleh : dr.

Handout – REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha 3 |Page .

Handout – REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha 4 |Page .

often high-grade and requiring adjunctive chemo (chondromsarcoma is just surgical Tx).Nerve sheath cell  neurofibroma / schwannoma  MPNST . cellularity. intraspinal seeding.Smooth muscle  leimyoma  leiomyosarcoma . and rhabdomyosarcoma in kids. can see bacterial colonies. chronic OM w/ draining sinus. loss of articular cartilage. bone-bone contact w/o intervening cartilage). ↑sarcoma risk w/ radiation. expand and compress surrounding tissue  pseudocapsule. presence of glandular cells = metastatic - Multiple Myeloma – multifocal destructive bone lesions. and extravasated 5 |Page . ↑granularity. inflammatory cells. rapidly-growing mass that may regress. solitary.e. joint mice (pieces of cartilage in joint space). juxtaarticular erosions. bimodal age distribution (fist peek in teens).Sarcomas grow quickly.Handout – REVIEW SISTEM GERAK Oleh : dr. ↑PMN’s. glassy blue appearance. intermediate grade treated the same as high-grade (w/ adjunctive chemo) Nodular Fasciitis – volar aspect of forearm. and radiation all ↑risk. skull). axial location (vertebrae. sarcomas spread hematogenously to lung. necrosis. and sclerotic phases overlap. Wilm’s. ↑vascularity. sources include prostate (multiple lytic lesions w/ sclerosis). lytic. most commonly due to Staph aureus. environmental factors.Gout – acute arthritis or chronic tophaceous gout. Ewing’s sarcoma). lymphatic / vascular spread. can see calcification and necrosis. osteosarcoma. exaggeration of synovium w/ proliferation of lining cells. thickening of trabecular bone. path requires >90% tumor necrosis to say that chemo was effective - Chondrosarcoma – neoplastic cartilage. can see fibroblasts. Ewing’s.Fibroblast  fibroma  fibrosarcoma . eburnation (ivory-like polishing of bone ends.Endothelium  hemangioma  angiosarcoma . benign tumors. true capsule exists in benign lesions. liver. mesenchymal mucin. 2nd most common malignant matrix-producing bone tumor. histiocytes and giant cells trying to surround and wall off crystals . breast. vascular / nerve invasion.Adipocyte  lipoma  liposarcoma . ↑vascularity. genetics. MDM2 overexpression. punched-out defects w/ intense proliferation of plasma cells - Rheumatoid arthritis – perivascular infiltrates. need Bx andculture to rule out cancer (i. neuroblastoma. BV proliferation  procallus /bony callus formation and mineralization  organization of bony trabecular orienting along stress lines - Osteomyelitis – Can have abscess. subchondral cysts. or new bone growtharound devitalized bone (involucrum).Skeletal muscle  rhabdomyoma  rhabdomyosarcoma . mosaic pattern in lamellar bone which is thickened. can see clefts - . prosthesis. lymphedema . ribs. mixed. most common primary malignant tumor (besides MM and lymphoma). ↑cellularity and multiple nuclei in lacunae - Metatstatic disease in bone – most common skeletal malignancy via direct extension. mitotic activity.Grading – based on pleiomorphism. organizing fibrin deposition. necrotic bone (sequestrum). pt more prone to fracture and ↑risk of osteogenic sarcoma - Osteosarcoma – malignant cells making bone matrx. irregular tortoise shell patterns of bone deposition (lamellae in multipledirections). pannus. and bone whereas carcinomas spread via lymphatics. pt > 40 YO and male. ankylosis. empty lacunae (dead osteocytes). osteophytes. kidney. and lung. and suppurative inflammation w/ PMN infiltrate - Paget’s Disease – probably due to paramyovirus. common occurs around the knee (lots of bone mass). Zainuri Sabta Nugraha MUSCULOSKELETAL PATHOLOGY Fracture – hematoma  activation of osteoprogenitor cells. intense lymphocytic infiltrate - Degenerative joint disease – fibrillation of articular surface. can be due to Rb mutation.

fluffy periostitis. cut out. spinal erosions syndesmophytes (bridging osteophytes)  fusion (Bamboo spine). less symmetrical vs.Liposarcoma – not due to malignant transformation of lipoma. effusion widens joint space Soft Tissues – Reiter’s produces swelling of entire digit (sausage digit). tumor is hemorrhagic and necrotic. asymmetric involvement in other joints. caparl joints. OA preserves bone mineralization. normal mineralization. normal bone mineralization. normal mineralization - Reiter’s – similar to PA but involves feet and SI joints (bilateral but not symmetrical). Cartilage. can be confused w/ sarcoma (high cellular w/ mitotic figures). fusiform soft tissue swelling. PIP.PA – joint space irregular  erosions covering entire joint.Lipoma – most common soft tissue tumor in adults. erosions are sharply circumscribed w/ overhanging edges Tumors Aggressive – poorly defined margins. several joints involved in one digit (sausage digit). distal radial-ulnar joint. symmetrical involvement. normal fat . ulnar drift. bizarre. encapsulated. marginal erosions. sclerosis. fluffy periostitis near involved joint (new bone growth). DIP. involves great toe MTP. will see myxoid stroma. Zainuri Sabta Nugraha RBC’s. non-marginal erosions and tophi  asymmetrical lumps and bumps. “hair-onend” appearance. Soft Tissue Bone – inflammatory arthritis  periarticular / generalized osteopenia. found in extremities and retroperitonuem. late bony changes. fluffy periostitis (spicules coming off margin) . Ewing’s sarcoma. RA. PIP. no osteophytes (inflammation prevents bone growth). assess mineralization in mid-shaft of metacarpal bones - Cartilage – inflammatory arthritis causes early erosions in bare areas of bone within joint not covered by articular cartilage. periosteal reaction (i. narrowing in almost all arthritis - OA – joint space narrowing. myxoid is most common type. sharplycircumscribed erosions away from the joint) PA – classic = symmetrical involvement of DIP. width of joint space indirect measure of articular cartilage. generalized soft tissue sweeling in PA and Reiter’s. periarticular / diffuse osteopenia.Malignant Fibrous Histiocytoma – large unencapsulate mass in retroperitoneum or extremity. marginal erosions in bare areas. subluxations . focal swelling in RA and gout (tophi – lumpy-bumpy soft tissue swelling. protrusions of osteophytes but no erosions. periarticular swelling.e.Handout – REVIEW SISTEM GERAK Oleh : dr. spine pseudoarthrosies (fracture through fused spine  pain and neurological deficits)  - Gout – cystal-induced arthropathy. can have subcondral cysts RA – MCP.AS – symmetrical SI joint inflammation  erosions  fusion. storiform-pleiomorphic pattern (multinucleated cells. reactive condition . fine branching vascular network. and lipoblasts in various stages of differentiation MUSCULOSKELETAL IMAGING Arthritis ABC’s of Arthritis – Alignment. uniform joint space narrowing (entire joint inflamed). fine lines coming off bone indicating aggressive growth). common = pauciarticular distribution of erosive changes. Bone. swirling growth pattern) . often ASx. no marginsseen w/ permeative pattern (most aggressive) 6 |Page . 1st CMC. pauciarticular w/ several joints involved. also affects hips / knees. fusion across severely affected joints.

soft tissue extension. calcified soft tissue mass. ACL. lateral / medial meniscus Infection. femoral head in superior-lateral position. looks like small balls - Osteosarcoma – MRI to assess intra and extraosseous extent of disease. posterior spinal line (most important). permeates bone.Handout – REVIEW SISTEM GERAK Oleh : dr. proximal humerus. femur. flocculent. sitting position. L/R oblique views. or rings-and-arcs. involve proximal femur / pelvis Paget’s Disease – paramyxovirus. fallen fragments in cyst for Dx. absent or mature periosteal (arrested thickening of bone) reaction Bone matrix – solid. may resolve over time or use CT-guided RF ablation Trauma C-Spine – lateral. seen in falls w/ outstretched arms and elbow pain. shoulder.e.Child abuse – corner fracture (periosteum ripping away bone fragment  bleeding /cloaking thickens and calcifies w/ repetitive trauma. MRI better shows margins - Simple Bone Cyst – common in children. common in elderly. NSAIDs). frequently expansile. assess alignment w/ anterior spinal line (not reliable in elderly w/ osteophytes). cloud-like or ivory (most dense). need MRI to assess bone involvement for limb-sparing surgery Chrondrosarcoma – involves pelvis. and Systemic Bone Diseases 7 |Page . found in older pt. tibia. seen in young males in diving accidents Odontoid Fx – hard to find. benign bone-forming lesion. fat pad displaced due to hemarthrosis. Metabolic. posterior rib fracture. NOF). knee driven posteriorly. thickened trabeculae and ↑width of bone. mono or polyostotic. due to hyperextension or mixed mechanism Anterior shoulder dislocation – goes down and medial. can be non-displaced. Zainuri Sabta Nugraha Nonaggressive – well defined margins (i. lateral view allows visualization of prevertebral soft tissues (swelling suggests bone injury). can be painful (use ASA. odontoid. AP. grey homogenous matrix (ground glass). may need surgery - Fibrous dysplasia – unknown cause. can see irregular calcifications typical of cartilage matrix Ewing’s Sarcoma – highly aggressive. after relocation can see impaction fracture on lateral humeral head (Hill-Sachs deformity suggests prior dislocation) Acetabular fracture – seen in MVA. pushing femoral head out posteriorly Radial head fracture – subtle. ill-defined margins. take another xray 7-10 days later to better see fracture . can produce fractures or degenerate into sarcoma. seen in kids / young adult males. no bony matrix or periosteal reaction. ASx until fracture (malignant lesions usually painful). can see intra-articular fragment of bone in acetabulum (remove or get early arthritis). hair-on-end / sunburst reaction due to pushing out into soft tissue and periosteum can’t contain reaction. adjacent intense sclerotic bone formation despite small size of lesion. uncontrolled local bone metabolism Osteoid Osteoma – small. cartilage ossifies around periphery. subdural hematoma and SAH due to shaken baby Knee – best seen w/ MRI – PCL. non-displaced. spinolaminar line (junction of lamina at base of spinous process) Hangman’s Fx – usually hyperextension w/ massive prevertebral soft tissue swelling Jefferson Fx – break in C1 ring due to axial load pushing C2 up and displacing fragments laterally. expansile w/ sharp margins. use fat-pad sign (joint effusion good sign of occult fracture. multiple fractures of different ages. due to calcification of osteoid Carilage matrix – stippled. can be exuberant and mimic bone forming tumor). ↑density inside and outside of bone. fluid filled mass pushing outward. usually ASx.

Capsule – variable thickness.Muscles / tendons have most of stress distribution. renal rickets in kids. best seen w/ MRI Sickle Cell Disease – can result in osteonecrosis due to stasis of blood. component of joint fluid and cartilage . provides support . fibroblastderived (Type B). basis for immune activation and autoimmunity). ability to allow water to leave w/ compression and reabsorb water w/ relief of pressure = resiliency. Zainuri Sabta Nugraha OM (osteomyelitis) – acute presents w/ subperiosteal abscess + elevation of periosteum. controlled by TIMPs (slow cartilage degradation) Scleroderma – too much CT accumulating .Injury – chondrocytes ↑matrix production. but not as much Type II collagen production Osteoarthritis 8 |Page . stabilized by link proteins (all components made by chondrocytes) PG’s found in other CT types. see subperiosteal resorption w/ fuzzy bone margins (see in margins of middle phalanges) Osteonecrosis – bone infarction and death. highly vascular w/ lypmhatics and nerves.↓chondroitan sulfate (↓water retention).Handout – REVIEW SISTEM GERAK Oleh : dr. Aggregan is the primary PG PG (proteoglikan) – protein core filament. heparin. periosteal reaction simulating infection Neuroblastoma – mets to bone widening of skull sutures - - CARTILAGE PHYSIOLOGY AND OSTEOARTHRITIS . spreads to involve disc destruction of disc  narrowing of disc space Renal Osteodystrophy – hyperPTH  bone resoprtion at many sites inducing osteoporosis and osteosclerosis. common in femoral head. collagen comes up in arcs from bone in triple helix (if dysfunctional or modified collagen. all under metabolic control (cytokines / GF’s). infarcts in femoral head. neural input important (reflexes prepare joints for stress) . keratan. lining cells are source of nutrients for chondrocytes (on subchondral bone plate which is avascular) . smaller PG aggregates.e. cartilage matrix has slow turnover. h-shaped deformities due to central compression of vertebral bodies Leukemia – lytic lesions.Cartilage structure – 70% water. constant production and metabolism . ↓nutrient supply. mast cells. shorter HA. immature periosteal reaction mimics tumor. chondrocytes at bottom of cartilage generate matrix (lots of PG’s). pressure forces water off sulfate groups.Matrix metabolism changes w/ age . dendritic cells. early destruction of femoral cortex. cannot produce large amounts of matrix MMP – degradation of CT structures.Atypical osteoarthritis – due to neurological system that is not intact. contains hyaluronan. not efficient. PG’s attached non-covalently to HA.Synovial fluid – primary metabolic supply for cartilage. can lead to osteoarthritis) Type II collagen most common in cartilage. lubricin. and synovial lining cells . both are sulfated which attract water. GAG’s stuck as side chains (i.Synovial Lining Cells – monocyte-derived (Type A. can track along the bone  soft tissue sinuses  dense sclerotic reaction. water reattaches w/o pressure. cloacae (tracks in bone) Vertebral disc space infection – starts in vertebral endplate. chondrocytes at bottom of cartilage plate inactive but respond w/ disease. pt w/ DM / peripheral neuropathy at risk  aggressive arthritis especially in legs . chondroitin also a side chain).Joint = capsule w/ synovial fluid inside (from synovial lining cells) . make HA. metabolic supply ↓ w/ age.Synovial Lining – covers all areas within joint except cartilage. lack of fine position sense. possibly leading to arthritis . chronic OM – walled-off area w/ persistent infection / low grade inflammation. often ligamentous.Lubrication via hyaluronic acid (long sugar). comprise 20% of cartilage volume Chondrocytes gets nutrients from synovial fluid.

aging / hereditary Management – progressive exercise to ↑function. also need to determine if joint is truly affected or if adjacent tissues / structures are affected Normal joint fluid <200 WBC. Tetracycline (↓MMP activity) Surgery – arthroscopy (trim cartilage / ligaments). neither NSAIDs nor Tylenol affect disease progression COX2 Inhibitors – pain relief equivalent to older NSAIDs. >2. 3x/week. etc. also female sex. minimal morning / inactivity stiffness (<20 min).000 Chronic polyarthritis – can be RA. joint replacement - - - - RHEUMATOID ARTHRITIS Morning stiffness >1 hour (any inflammatory arthritis. can be mistaken for RA until other organs involved). previous trauma. hands almost always involved. hypoPO4.000. most functional effect). marginal osteophytes (uneven. often added to NSAID or acetaminophen regimens (combining small / multiple doses of several meds can treat OA while avoiding SE’s) Codeine / Oxycodone (narcotic analgesics) – can induce tolerance. renal. endurance. don’t avoid exercise / weight loss as treatment. hypothyroidism. osteotomy. trauma. DM neuropathy. spondyloarthropathies (akylosing spondylitis. 2nd line – NSAID. can cause constipation or rash. foot (MTP of first toe) Does NOT involve – ankle. ↓ROM (crepitus on passive ROM). CMC – base of thumb. NM dysfunction (neuropathy disrupts joint mechanics  accelerated OA). Rheumatoid factor in 80% but not specific Need to determine if there is inflammation when pt presents w/ joint pain  look for warmth. lumbar / cervical spine. eventually get cartilage / bone erosion in hand / feet Rhematoid nodules in 30% but specific. Zainuri Sabta Nugraha Imaging – interspace narrowing. PIP –Bouchard’s nodes. intra-articular agents / lavage. Reiter’s Syndrome). vs. neuropathic joints. elbow. structural / osteoarthritis) Polyarthritis – at least three joint areas. systemic rheumatic diseases (systemic vasculitis has arthritis. metabolic disorders OA features progressive cartilage loss. pain related to use. most common in hand. hypertrophied bone edges) Locations – knee. gout. overuse. symmetry typical No imaging abnormalities early. MCP (except in thumb). hypoMg. erythema.. 3rd line – arthroscopy. strength (↓falling risk) Strengthening exercise – low-impact. 1st line – Tylenol. ↓GI toxicity. misalignment Affects cartilage in weight-bearing joints. worse during the day. but can have renal toxicity and edema Tramadol (codeine) – affects opioid and 5HT pathways. worsening CHF. hip. midfoot usually spared Underlying disease associated w/ OA and CPPD – hemochromatosis. psoriatic arthritis.↓inflammation. NM disease. then knee and hip involvement Hip – subchondral sclerosis  loss of joint space  pain radiating down medial leg (vs. subchondral cysts. subchondral sclerosis (thickening of bone plate beneath cartilage). bony enlargement of joints (not inflammation. osteoarthritis 200-2. no effect on platelets. bowel immotility. predisposing metabolic disease (CPPD – pseudogout) OA secondary to DM neuropathy – MTP 2-5 also involved. juvenile chronic arthritis. swelling. hereditary factors. opioids. septic arthritis can have WBC > 100. hands (DIP – Heberden’s nodes. trauma. continuous (15-30 min). morning stiffness. wrist. shoulder Women – higher incidence. bursitis – lateral leg pain) Ankle OA suggests another process is also at work – i. hyperPTH. DIP most common. use generic and low-dose first. pain relief comparable to NSAID w/ less toxicity NSAID . SE include GI. prevent ↓ in joint space).000 can be RA. obesity (affects legs). marginal osteophytes. creates better joint alignment and slows OA progression Acetominophen – first line therapy. total joint replacement Summary – make sure pain is joint-related.e.Handout – REVIEW SISTEM GERAK Oleh : dr. which is spongy) Age is biggest factor (idiopathic). avoided by adding Propoxyphene or Tylenol 3 (w/ codeine) in ↓doses to other regimens Topical anesthetic – Capsaicin–containing drugs for Sx relief Intra-articular Tx – steroids or HA (not as commonly used) Other Tx – glucosamine (Sx benefit. subchondral thickening. joint instability. and psoriatic arthritis 9 |Page . SLE. edema.

periarticular demineralization (OA has reactive bone and sclerosis in response to ↓cartilage). Tx that remove T cells in joint not effective. PIP of hands (vs. DIP in hyperextension Mallet deformity – d/t tendon slippage. joint lining cells. joint space normal. large erosions. cartilage has been eroded. osteoclast promoting cytokines) which is precursor to true erosion Later in disease . synovial pannus eating into bone Erosions occur on bone side first.e. T cell clones can transfer disease to another host) No identified antigen that uniformly elicits T cells response in RA. OA – DIP. macs. w/ psoriatic skin rashes and nail abnormalities. dendritic cells. rare reactive bone formation. extensor tendons slip to volar side to all tendons work to flex the finger Early in RA – bones are normal.Handout – REVIEW SISTEM GERAK Oleh : dr. functions like LN in RA. thumb base - - - - - RA in feet – hard to examine. can see pronounced interosseous muscle atrophy. not just due to arthritis but also tendon slippage Boutonniere deformity – PIP in flexion. cervical spine (L/S spine in OA. associated w/ specific MHC alleles (T cell function important in RA pathogenesis. eventually get hallux valgus deformity (toes point outward). associated w/ autoAB production. elbows (OA can also affect knees) RA also involves ankles. T cells quickly repopulate w/ more aggressive clones Metaplasia of joint lining into lymphoid organ  immune cells. PIP. pt walking on metatarsal heads. painful  toe subluxation. express CD5. requires surgery w/ complex fusion to restore anatomic position of foot Some erosion evident in MTP early on. OA in hands – RA has more prominent early soft tissue swelling. base of thumb) RA can also involve large joints like knees. ulnar deviation of fingers (subluxation under metacarpal heads) along with radial deviation at the wrist Patients can have OA w/ RA – abnormalities in DIP as well as PIP and MCP Lumpy swelling of tendon sheaths (tenosynovium lining tendons). toe contracture (weight-bearing pad under MTP slips forward. not all RF+ pt have RA ↑T lymphocytes and ↑APC’s to activate T cells in joint fluid. feet.↓joint space. possible to have immune mediated events that reflect infection elsewhere Reiter’s Syndrome and reactive arthritis – clear link between infection elsewhere (i. also ↑monocyte / macs. MCP. TMJ. local steroid injections. surgery Swan neck deformity – hyperextension at PIP  DIP passively pulled into flexion contracture. pannus can attach directly to bare areas w/o having to go through cartilage first Can also see tendon rupture due to tenosynovitis and rubbing against eroded bone . gaps of erosion in bone cortex eventually no cartilage space left. shoulders. some osteopenia near the joint only (local effect of cytokines like IL-1. Sjogren’s Syndrome). but RA can occur in pt w/ agammaglobulinemia (so autoAB’s are not necessary for RA) Rheumatoid factor = AB against immunoglobulin (usually IgM). Rheumatoid factor and other autoAB’s made in joint.RA – wrist. more severe joint deformity. MCP. interactions between these and T cells.RA vs. also progressive flattening and eversion of foot . fibroblasts eroding cartilage all contribute to disease 10 | P a g e . more erosions (rare in OA except for collapsed cysts). thickening of synovial lining cells and fibroblast layer B-cells are a small but significant proportion of synovial lining cells. TNF. accumulation not random (some clones are dominant). GI) and development of arthritis RA did not exist before contact between Old and New World (environmental factors) ↑Lymphocytes in RA synovial fluid. very uncomfortable and limit hand function Wrist swelling  carpal tunnel syndrome (median nerve compression)  atrophy of thenar muscles and sensory losses (can become permanent). both have joint narrowing (cartilage damaged in both directions) . chronic lung / liver disease. inflammation of DIP (sauage digit in every finger) Hands in RA – later. bare areas of bone lack cartilage. OA DIP. articular cartilage only present on weight-bearing surface of bone. lower spine and sacral ileitis in spondyloarthropathies). PIP swelling. larynx Psoriatic arthritis – affects hands. hip. little soft tissue swelling. more common in women No evidence that infection present in RA joint. PIP. Zainuri Sabta Nugraha RA involves wrists. treat w/ splinting. PIP. ulceration) Swelling / deformity in ankles are seen along w/ Achilles and extensor tendon involvement. swell under other conditions. and cartilage all together. progresses so toes no longer associate w/ appropriate metatarsal RA from early to late adulthood (30-60). antigen for RF is Fc portion of IgG. AB’s alone can create immune complexes. but present in many other diseases (endocarditis.

also make inflammatory PG’s. shoulder. can originate at foot. knee. Zainuri Sabta Nugraha Inflammatory leukocytes adhere to luminal side of epithelium  cognate cell-cell interactions (specific receptorligand) or secreted cytokines acting locally TNF from synovial monocyte / mac  autocrine feedback to mac to make IL-1  IL-1 / TNF activate synovial fibroblasts  transformed to make cartilage-degrading proteases instead of joint lubricant. other proteases Ligamentous Strains Grade I – intact structurally. . functional way.Metatarsus adductus – turning-in of foot in 0-18 months.Handout – REVIEW SISTEM GERAK Oleh : dr. need subluxation or dislocation to significantly injure ligament . prevent re-injury (correct underlying biomechanical factors. corticosteroid injections. microscopic disruption Grade II – partial tear w/ laxity. functional progression of activity (reestablish motor skills). spontaneously resolves in 80%. compression. retroversion / anteversion (outward proximally) In-Toeing – common. ice. start CV conditioning as early as possible. arachadonic acid metabolites.↑proprioception w/ balance agility drills . closed chain exercises helpful and shouldn’t be painful. surgery . or hip . cytokines.Recovery Phase –need 60% ROM to enter this phase. ↑TNF / IL-1 in joint can enter systemic circulation constitutional Sx Therapy targets – y-IFN (Th1 cytokine).PE – joint swelling in proportion to degree of injury. relative rest.Dx – x-rays for Grade II / III or severe trauma. most spontaneously improve. injury occurs when there is motion in abnormal plane or excessive motion in normal plane. IL-17 (activates synovial fibroblasts). compression wraps. ankle (gold standard) - Principle of Rehabilitation Acute Phase . can also use NSAID. fibula in front of medial malleolus) - 11 | P a g e . stress radiographs for determining endpoint in ankles. definite endpoint Grade III – complete disruption w/o endpoint (flail joint). elevation). chemokines TNF acts on endothelium to ↑adhesion molecules for leukocytes. MRI for knee. monocytes respond to ODF (osteoclast differentiating factor) and turn to osteoclasts (accelerated 100x w/ TNF and IL-1) which attack bone after fibroblast degradation of cartilage Cytokines  T cell activation. tenderness over ligamentous attachments. reactive O2 species. education) MUSCULOSKELETAL GROWTH AND DEVELOPMENT Torsional Deformities of Lower Limbs Torsion – twisting in reference to tibia. MMP. defined by transmalleolar axis (movement of fibular with respect to medial aspect of distal tibia /medial malleolus if extreme.Maintenance Phase – return to activity in progressive. ↓pH in joint and at cartilage-pannus junction. internal / external Version – twisting in reference to femur. IL-15 (T-cell GF). splinting / bracing. ecchymosis. requires surgical repair . can treat w/ casting or rarely surgery . other mediators – PG.Ligaments stabilize joints by allowing movement in only certain planes.Avoid steroids in Achilles and patellar tendons (risk of rupture) .Internal tibial torsion – 6-18 months. ↑endurance w/ ↑reps / ↓resistance. want to keep as active as possible unless bone is fractured. restricted AROM and PROM . NO. need ↑muscle strength (start w/ isometric  isotonic / isokinetic). limited to forefoot.↓pain / inflammation (PRICE – protection. ROM can be restored passively or actively. no laxity.

Bowlegs (Genu Varum) – inward angulation with respect to midline (angle made by femur and tibia opens inward). lower limb. Stage IV disease can result in fusion of bones Rickets – widened growth plates on x-ray . and alk. rotation of femoral head with respect to femoral condyles (i. red flag for CP or myelodysplasia. Barlow – flex hip to 90o. improves spontaneously Angular Deformities of Lower Limbs Valgus – deviation / angulation away from midline Varus – deviation / angulation towards midline .Calcaneovalgus foot – foot is excessively dorsiflexed to the leg and turned outward.In-toeing can also be cause by clubfoot (entire foot involved). children start bowlegged  normal  knock-knee  normal . continuum of subtle findings subluxation dislocation Mechanical factors often responsible – small space (common in firstborns). breech presentation (legs adducted). can be physiologic. first-born and female. or metaphyseal chondroplasia . both AP and lateral.External rotary contractures of hip – 0-18 months. abduct hip w/ Pavlik harness. no sex 12 | P a g e .External tibial torsion – uncommon. improves spontaneously within a few weeks after birth. free range but limited range of motion. sacral dimple. to assess alignment Labs – rule out renal rickets. breech. PO4. flex hip to 90o. adduct past midline. left hip more involved (left leg adducted commonly in utero) DDH often presents w/ torticollis (head tilting / rotation) and metatarsus adductus (both mechanical problems). infant needs to be relaxed. Zainuri Sabta Nugraha Femoral anteversion – 3-9 years. caused by Blount’s Disease (growth plate abnormality – uneven growth of proximal tibial epiphysis. get Ca. phos. rickets. gout and pseudogout are very treatable. USN allows visualization of cartilage but may be too sensitive PE – should be part of every well-baby exam. Vit. localize angulation. femoral head rotated vertically away from plane of condyles) .PE – need to see if there is laxity about knee joint.Physiologic Bowing – 15o normal in infants. legs move to neutral position by 18-24 months. seen in ages 3-5. Levels . more growth laterally). gently push posteriorly to dislocate Tx (0-6 months) – reduce femoral head into acetabulum. x-rays unreliable. occur in overweight kids and those who are early walkers. D. x-rays are otherwise normal. foot and postural deformities) Newborn to 2 months – Ortolani and Barlow tests most reliable. pt has feet straight forward but knees inward.e. packaging problem .Infantile Blount’s Disease – can’t make Dx until 2 years old. family Hx) and Minor (limited hip abduction. Orolani .stabilize pelvis. not problematic even if it persists. no arthritis or functional problems. DDH more common in females (estrogen effect) Hip at Risk – Major (abnormal clinical exam. usually normal growth. track w/ Salenius and Vankka chart. x-ray show excessive beaking on medial side of proximal tibia  depression of medial plateau. and foot on same film. neurologic problems (cerebral palsy) Out-toeing – less frequent than in-toeing . knees pointed straight ahead but feet turned outward .Handout – REVIEW SISTEM GERAK Oleh : dr.Radiographic – XR of whole hip. metabolic bone disease. bone dysplasia Developmental Dysplasia of the Hip Not always seen at birth. pt tends to have internal tibial torsion. make sure harness isn’t too tight  avascular necrosis of femoral head Crystalline Arthropathies bias Crystals build up in joint space and cause inflammation. the abduct and lift towards socket (can catch hip dislocations or subluxations which then relocate). usually normal developmental variation. also test motion of all lower limb joints. but can be caused by renal osteodystrophy.Knock Knees (Genu Valgum) – outward angulation. assess alignment . atavistic first toe (overactive abductor hallucis only).

and extremely tender joint Resolves in 3-10 days even w/o Tx. no hydronephrosis evident for several weeks. but NOT gouty arthritis Partial HGPRT Deficiency – 1% of normal enzyme activity can avoid mental retardation (but still abnormal basal ganglia).Handout – REVIEW SISTEM GERAK Oleh : dr. pt w/ ↑↑uric acid should get allopurinol . compulsive self-mutilation. ankle. RA. toxins (EtOH. most pt have MTP involvement of big toe Dx – urate crystals found inside WBC’s in the affected joint. but host response is excessive. no stones . rarely found in shoulder Pseudogout – calcium pyrophosphate crystals (CPPD) Hydroxyapatite – Dx requires EM and alozerine red. hot pain in a red. swollen. atherosclerosis. superactive PRPP synthetase. mono). Pb). x-ray has punched-out lesions w/ overhanging edges (↑bone growth) - Causes of Hyperuricemia Decreased Excretion (90%) – Dehydration / starvation / ketosis (post-up pt are NPO. usually monoarticular Deep. most common crystalline disease. CPPD. mental retardation. WBC’s can’t destroy crystals. tissue trauma during surgery releases purines.Acute uric acid nephropathy – crystalline arthropathies can lead to simultaneous. more common in pt undergoing induction chemo for leukemia / lymphoma (get allopurinol w/ chemo) . gouty renal disease. associated w/ obesity.consistently <13 (most pt w/ gout are at 8-9). stabbing. but many SE’s. rarely affects other joints). often at night. Zainuri Sabta Nugraha Gout – monosodium urate crystals (from uric acid). myeloproliferative disorders (lymphoma. psoriasis Complete HGPRT Deficiency – Lesch-Nyhan Syndrome uric acid overproduction. degeneratie. inflammation. leukemia. uric acid crystals present in urine.Calculi – 90% of pt w/ kidney stones have calcium stones. midfoot. most pt have hyperuricemia. EtOH. bilateral. traumatic. post-op. early onset and severe arthritis gout / renal disease Acute Gout Crystals in WBC  intense inflammatory reaction (crystals themselves aren’t harmful. and others Renal Disease with Gout Urate nephropathy – pt w/ hyperuricemia can get kidney damage but only if uric acid . low-dose ASA). but 15% have normal uric acid during gout attack (but hyperuricemia for many years before attack). rarely affects fingers but can coexist in OA Heberden’s nodes in DIP. HGPRT deficiency. hypothyroidism Increased Production (10%) – EtOH (2 beers can trigger gout attack). engulf and release inflammatory mediators severe inflammatory arthritis). amyloid. knee. DM. but also other toes. ↑uric acid w/ purine salvage pathways).Gout can co-exist w/ OA. rare to find uric acid stones but many calcium stones form around a small uric acid crystal. acute illness (mono). heel. hyperlipidemia. warm.Gout can present as acute gouty arthritis or chronic tophaceous gout. minor trauma or ↑activity can trigger episode - 13 | P a g e . ↓uric acid helps to prevent calcium stones in pts w/ recurrent stones Acute Gouty Arthritis Abrupt onset. HTN. don’t need to use for every pt w/ ↑uric acid (only ~15% actually have gout) .pregnancy.G6PD deficiency. microscopic obstruction of kidneys from excess uric acid crystals. self-limited nature of attacks. neoplastic (rarest) . negative associations – SLE. drugs (diuretics. dialysis . common in shoulder (“Milwaukee”) Calcium Oxalate – seen in pts on dialysis Dx categories – infections.evident on USN or CT. microcephaly. renal abnormality (tubular disorders). crystals alone in a joint can’t cause gout Unexplained features – initiation of attack.ASx Hyperuricemia – allopurinol used to ↓uric acid production. joint distribution (big toe most common. septic arthritis.

6 mg bid . liver) ORTHOPEDIC SURGERY • Hip = ball and socket. heal easily if aligned properly Angulation – described by where apex of fracture is pointing Open fracture is surgical emergency. grade 2 (1-10 cm). within joints are facets. Greenstick fracture in children since bones pliable enough to allow partial breakage  stuck in bent position (requires complete refracture to set bone). gout has needleshaped uric acid crystals inside WBC that appear yellow.Allopurinol DDI’s – azathioprine (competitive inhibitor of enzyme affected by allopurinol). highly vascular). will often require 25 years of allopurinol to get resolution of severe tophi . uricosurics CI’ed (renal insufficiency w/ creatinine clearance <80. grade 1 (<1cm hole. uric acid overexcretion).Handout – REVIEW SISTEM GERAK Oleh : dr. thrombocytopenia . joint fluid aspirate under polarized light. Zainuri Sabta Nugraha Dx – clinical findings. the more urgently it needs repair. i. grade 3 (>10 cm. positive response to gout therapies. risk for chronic OM. can cause irreversible aplastic anemia on first dose o Intra Articular steroids / NSAIDs – don’t work well unless given very early in an attack o Narcotics – usually ineffective for pain relief . no longer in contact w/ articular surface. neuropathy. SE – N/V/D.Diet .Long-term anti-hyperuricemic treatment o ↑Frequency of gout attacks during establishment of long-term control. ↓mobility Treatment o First choice – indomethacin 35-30 mg qid tapering over five days o Colchicine 0. MCP / TMP = hinge. pt w/ lots of attacks or tophi (large uric acid conglomerates) should get long-term therapy to protect kidneys. described with respect to direction of distal part of joint - - 14 | P a g e . need to use prophylactic doses to try to ↓attacks during long-term therapy induction o Allopurinol 300 mg PO qd to ↓uric acid production o Sulfinpyrazone 100 mg titrated or probenecid 500 mg qd-bid – uricosurics (↑uric acid excretion. discs. pathological fracture) Comminuted fracture has multiple pieces. difficult dosing. pseudogout.90% will have another attack within 5 years of first attack. traumatic arthritis. buckle fracture in children since bones soft enough to allow crushing instead of breaking. urine uric acid > 13. sickle cell anemia. radial head fracture can be treated w/ sling but femur / displaced / scaphoid fractures and polytrauma require surgery Dislocation – components of joint have come apart. then max 0. classic radiographs Diagnostic arthrocentesis – aspirate joint fluid. RA. cartilage at articular surface avascular (poor response to injury) Open (“compound”) fracture = hole in skin. clean).Prophylaxis – indomethacin 25 mg qd-bid. view using multiple polarizing lenses. IV colchicines are dangerous but used as one-time dose post-op o Butazolidin – rarely used. muscle disease.Indications for allopurinol – tophi. epiphysis (variable vascularity). the closer a bone is to the center of body. OA.6 mg TID over the next week (most pt get significant SE after 8th pill). use only if gout is due to ↓excretion. metaphysic (trabecular area. dirty) Simple fractures – oblique (most common) or transverse (straight across bone. physis (growth plate in children). apalstic anemia.6 mg one tablet / hr. don’t use drugs if excretion <900 mg / 24 hours or kidney stones will form) .↓high purine foods (brain. skin reactions. colchicine 0. renal stones (any type). kidney.Colchicine – from a plant. chemotherapy induction . bony infarct Complications – quality of life issues pain. OM. pseudogout has rhomboid crystals that are blue DDx of 1st MTP toe inflammation – gout. myelosuppression. mecaptopurine . cyclosporine.e. heart. AC / SC = fibrous. knee is complex joint w/ changing rotational axis Long bones – diaphysis (cortical bone. rare unless bone already weakened. sub-talar = saddle. often have 5-6 attack the following year. menisci. auxiliary joints. Salter fracture = physeal fracture. max 12 tablets in first day. highly vascular). butterfly fragment is fracture element w/ threepoint bend (+/twist).

produce ECM proteins (collagen I and osteocalcin). shoulder pulled in. anterolateral pain radiating down the arm. produces AP (needed for mineralization. subscapularis) Biceps tendonitis – distal rupture (lump closer to shoulder. passive ROM = active ROM (but decreased). septic joints. ↑pressure  BV’s and nerves compressed 6 P’s of compartment syndrome – pain out of proportion to injury. less structurally resistant. treat w/ RICE (rest. red. DISH Pediatric issues – OM. seizure can cause posterior dislocation (stronger back muscles) Subluxation – joint has come apart but components still intact. sealed contact area w/ bone acidic environment. club feet. commonly due to overuse. AC separation. lysosomal enzymes. pt does well w/ arthroscopic surgery (rotator cuff = supra/infraspinatus. hip injury can cause knee pain). emergent. muscles compartmentalized by fascia to ↑power. peritendon. chronic pain more common Adhesive capsulitis – fibrosis of capsule. can be post-surgery. elevation) Sprains / Strains – grade 1 (pain but still functional). incomplete process once over 20-30 (bone resorbed > bone replaced) 15 | P a g e . left behind in bone as osteocytes to maintain function OC – multi-nucleated giant cells from hematopoietic precursors. TNF-α. should wash out joint if pus suspected (insidious onset of warm. teres minor. swelling can exceed potential space  bone / fascia not pliable. broken clavicle).Handout – REVIEW SISTEM GERAK Oleh : dr. fractures that attenuate skin or neurovascular structures Septic joints can be post-trauma or dental procedure w/ prosthetic joint. pain to passive stretch Tendonitis / bursitis – inflammation of tendon. fascia is taut bruising. pallor (↓perfusion. injury. can reattach tendon to radial tuberosity. MI. Tx w/ strengthening of rotator cuff. prone to fracture w/ ↓Ca or osteoid OB – from CT progenitors. compression. trabecular bone is loosely connected mesh. restores supination). strain = response to force Neuropathies – sciatica (low back pain). insertion. used as serum marker for OB activity). carpal tunnel syndrome (most common mononeuropathy in upper extremity). stress = force. anti-inflammatory meds. some dislocations. PROM >> AROM. ankylosing spondylitis. mediate bone resorption. bleeding. painful arc. chronic condition in elderly. IL-6. passive ROM > active ROM but still movement painful Shoulder impingement – rotator cuff tendons pinched under acromion  compression of bursa. pinched nerve (consider referred Sx – i. pressure. paresthesia below injury. on outside of most long bones. stimulated by IL-1.e. Tx w/ therapy to stretch shoulder Shoulder arthritis – bone spurs inhibit movement. lateral • - - - METABOLIC BONE DISEASE ECM of bone = osteoid (cross-linked Type I collage) and mineral crystals laid down over osteoid by osteoblasts Cortical / laminar bone is thick. pulselessness (too late). if untreated can lead to joint degeneration. pt has insidious pain and stiffness. painful. too late). or overlying bursa. kyphosis. all treated w/ RICE Spinal deformities – scoliosis. migrate into bone before beginning resorption Ongoing bone remodeling – OC breakdown for 7-10 days OB bone reformation for 3 months. usually gradual onset w/ night pain (but not awakening). complete turnover of bone every few years. Zainuri Sabta Nugraha Most shoulder dislocations are anterior occurring during external rotation. rest Rotator cuff tear – limits voluntary motion of shoulder. DDH. painful. less common Ortho emergencies – open fractures. proximal rupture (lump closer to elbow). regulated by TGF. capsule extends around metaphysic). and swollen joint) Compartment syndrome – occurs after injury. impinged tendon weakens  humeral head drops  impingement worsens. grade 2 (↓function). more common in children (rich vascular supply. or due to other coexisting diseases. infections are common in children Acute shoulder pain is atypical (probably traumatic. grade 3 (no function). resistant to fracture. ice.β and IGF1. obturator nerve runs down medial compartment from hip  knee.

pt should have adequate Ca / Vit. women need supplemental Ca pre-menopause (1 g/day). five-year period of accelerated loss in post-menopausal women w/o HRT. Hb. not as potent as estrogen but still ↑blood stasis (thrombosis) Bisphosphonates – aledronate / risedronate potent inhibitors of OC. carotene. avoid hypogonadism in younger pt. ↑bone density. should give 800 units Gonadal steroid replacement . seen in astronauts Osteoporosis 15-25% of women will sustain OP fracture at some point.5 SD below mean for healthy young individuals.↓OC activity. high risk w/ hypothalamic amenorrhea (hyperPRL or exercise-induced). possible erosive esophagitis w/ bleeding. used as 3rd or 4th line agent Any pt on GC for >1 week will have OP. immobilization (bed rest) ↑resorption and ↓formation. D receptor. ↓fracture risk.D. remaining bone normal. can occur w/ minimal trauma. cholesterol (malabsorption). ↓fracture risk by 50%.↓OC activity. thin body (obesity ↑mechanical loading of bones). +family Hx. cancer (multiple myeloma) Prevention – adequate Ca intake. white / asian (black females have same risk as white men). poorly assess w/ x-ray. start concurrently Osteomalacia / Rickets Case – resection of 15 feet of SI due to Crohn’s. fair skin.D. sustained ↑ in bone density. young women should get 500 mg/day (i. max bone density in mid-20’s. ↓PO4. slows bone loss but doesn’t restore bone (unlike bisphosphonates). but resume normal rate of loss afterwards Fracture threshold = certain amount of bone to maintain integrity. replace hormones in men w/ testosterone deficiency and deficient pre-menopausal women Raloxifene – SERM. OC markers are pyridinoline crosslinks and N-telopeptide (part of Type I collagen after degradation). need bone densitometry (DEXA) which measure bone thickness. reported as T-score (i. need to take w/ full glass of water. Ca low / normal.0 worse than -3. available as nasal spray or injection. ↑hot flashes. density given as g/cm2. albumin. most pt w/ OP are hypgonadal). weight-bearing exercise Tx – most important is to prevent falls Calcium / Vitamin D – RDA for Vitamin D is 400 units / day. smoking. erve compression. can provide pain control for acute fracture.) End-stage disease – marked dorsal kyphosis. GC excess from steroid therapy or Cushing’s Early OP is ASx unless there is fracture. -4. no food or supine position for 30 minutes (now available as one pill /week) Calcitonin . SE include N/V. zero Vit. hyperPTH and hyperTH ↑OC activity. osteomalacia. vertebral compressions most common along w/ hip and wrist fractures (↑trabecular bone). chronic muscle pain Dx – bone density more than 2. steady loss of bone after. loss of lumbar lordosis. infection. can cause arthritis. effective Tx and prevention.e. OB’s active in OP but can’t keep up w/ resorption. no trophic effect on breast / uterus. long-term estrogen ↑bone mass and ↓fracture risk. ↑osteoid seams (unmineralized osteoid) - - - - 16 | P a g e . bisphosphonates can reverse / slow GC-induced OP. one Tums).0) Bone markers – OB releases AP and osteocalcin (less available but more sensitive). etc. ↑AP. Cushing’s ↓OB activity.Handout – REVIEW SISTEM GERAK Oleh : dr. estrogen probably as effective as bisphosphonates. markers useful for following response to Tx Osteopenia – caused by hypogonadism (both men / women. Zainuri Sabta Nugraha Mechanical loading is stimulus for bone formation. everyone falls below threshold if they live long enough Risk factors – polymorphism in Vit. death rate from hip fracture is 10% (PE.e. flushing. 10% of men .OP = ↓bone mass. seen in post-menopause w/o HRT.

renal failure. causes bone deformities. nerve compression.Handout – REVIEW SISTEM GERAK Oleh : dr. Paget’s Disease ↑Bone turnover. ↑bone resorption  exuberant compensatory increase on bone formation  thick / abnormal bones w/ ↑bone density Most pt ASx. nerve compression. ↑PTH. then x-ray involved areas Tx only if symptomatic w/ pain. ↓Vit. ↑risk of osteogenic sarcoma Dx . PTH not adequate  ↓serum Ca Patient presents w/ bone pain and pathologic fractures. can also be caused by malabsorption.D deficiency (inadequate intake / sunlight) or resistance. bisphosphoates more potent than calcitonin 17 | P a g e . phosphaturia (renal Ca absorption and PO4 excretion). arthritis. arthritis. bone scan determines extent of disease. give Vitamin D if deficient. and hypoPO4  inadequate bone mineralization  osteopenia  if severe. osteomalacia is inadequate bone mineralization in adults Most commonly due to Vit. thought to be widening of space around nutrient arteries Children – bowing of legs w/ weight-bearing deformation. can have marked deformation of arms and legs. deformity. severe liver disease. not ↓Ca. tumors. possible late ↓Ca Pseudofracture – fractures only go halfway through bone. Zainuri Sabta Nugraha - - Osteomalacia can be due to malabsorption. ↓bone density.↑AP and characteristic radiologic appearance. XLR hypoPO4. possible Sx include bone pain / deformity. children also short Tx – treat underlying disorder. or PO4 binders. fat soluble vitamins often first manifestation Generalized bone pain in absence of fractions (never seen in OP) Rickets in children. prone to fractures. leads to PO4 deficiency. possibly due to viral infection.D  ↓Ca absorption from GI  secondary hyperPTH  serum Ca normalized at the cost of increased bone resorption. hypoPO4. also get rachitic rosary (↑costochondral joint junction w/ bulging). if severe. Al and F also inhibit bone mineralization in high amounts Bone disease caused by ↓PO4. ↑AP from compensatory OB activity. give active form w/ renal dz. hereditary syndrome Second major cause is PO4 deficiency secondary to renal tubular disease.

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