Handout REVIEW SISTEM GERAK Oleh : dr.

Zainuri Sabta Nugraha

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha

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

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha

RBCs, can be confused w/ sarcoma (high cellular w/ mitotic figures), reactive condition - Malignant Fibrous Histiocytoma large unencapsulate mass in retroperitoneum or extremity, tumor is hemorrhagic and necrotic, storiform-pleiomorphic pattern (multinucleated cells, swirling growth pattern) - Lipoma most common soft tissue tumor in adults, often ASx, encapsulated, normal fat - Liposarcoma not due to malignant transformation of lipoma, found in extremities and retroperitonuem, myxoid is most common type, will see myxoid stroma, fine branching vascular network, and lipoblasts in various stages of differentiation

MUSCULOSKELETAL IMAGING Arthritis

ABCs of Arthritis Alignment, Bone, Cartilage, Soft Tissue Bone inflammatory arthritis periarticular / generalized osteopenia; OA preserves bone mineralization; 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, width of joint space indirect measure of articular cartilage, narrowing in almost all arthritis

OA joint space narrowing, sclerosis, protrusions of osteophytes but no erosions, DIP, PIP, 1st CMC, ulnar drift, normal mineralization, can have subcondral cysts RA MCP, PIP, caparl joints, distal radial-ulnar joint, marginal erosions in bare areas, uniform joint space narrowing (entire joint inflamed), no osteophytes (inflammation prevents bone growth), symmetrical involvement, periarticular / diffuse osteopenia, periarticular swelling, subluxations - PA joint space irregular erosions covering entire joint, effusion widens joint space Soft Tissues Reiters produces swelling of entire digit (sausage digit), generalized soft tissue sweeling in PA and Reiters, focal swelling in RA and gout (tophi lumpy-bumpy soft tissue swelling; cut out, sharplycircumscribed erosions away from the joint) PA classic = symmetrical involvement of DIP, common = pauciarticular distribution of erosive changes, less symmetrical vs. RA, several joints involved in one digit (sausage digit), marginal erosions, fluffy periostitis near involved joint (new bone growth), fusiform soft tissue swelling, fusion across severely affected joints, normal mineralization

Reiters similar to PA but involves feet and SI joints (bilateral but not symmetrical), pauciarticular w/ several joints involved, fluffy periostitis (spicules coming off margin) - AS symmetrical SI joint inflammation erosions fusion, also affects hips / knees, spinal erosions syndesmophytes (bridging osteophytes) fusion (Bamboo spine); fluffy periostitis, spine pseudoarthrosies (fracture through fused spine pain and neurological deficits)

Gout cystal-induced arthropathy, involves great toe MTP, asymmetric involvement in other joints, bizarre,

non-marginal erosions and tophi asymmetrical lumps and bumps, normal bone mineralization, late bony changes; erosions are sharply circumscribed w/ overhanging edges

Tumors
Aggressive poorly defined margins, periosteal reaction (i.e. Ewings sarcoma, hair-onend appearance, fine lines coming off bone indicating aggressive growth), no marginsseen w/ permeative pattern (most aggressive)

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha Nonaggressive well defined margins (i.e. NOF), absent or mature periosteal (arrested thickening of bone) reaction Bone matrix solid, cloud-like or ivory (most dense), due to calcification of osteoid Carilage matrix stippled, flocculent, or rings-and-arcs, cartilage ossifies around periphery, looks like small

balls

Osteosarcoma MRI to assess intra and extraosseous extent of disease, density inside and outside of bone, calcified soft tissue mass, need MRI to assess bone involvement for limb-sparing surgery Chrondrosarcoma involves pelvis, femur, tibia, shoulder, found in older pt, can see irregular calcifications typical of cartilage matrix Ewings Sarcoma highly aggressive, ill-defined margins, permeates bone, hair-on-end / sunburst reaction due to pushing out into soft tissue and periosteum cant contain reaction, soft tissue extension, MRI better shows margins

Simple Bone Cyst common in children, proximal humerus, expansile w/ sharp margins, no bony matrix or periosteal reaction, fluid filled mass pushing outward, ASx until fracture (malignant lesions usually painful), fallen fragments in cyst for Dx, may need surgery

Fibrous dysplasia unknown cause, mono or polyostotic, grey homogenous matrix (ground glass), frequently expansile, involve proximal femur / pelvis Pagets Disease paramyxovirus, common in elderly, usually ASx, can produce fractures or degenerate into sarcoma, thickened trabeculae and width of bone, uncontrolled local bone metabolism Osteoid Osteoma small, benign bone-forming lesion, adjacent intense sclerotic bone formation despite small size of lesion, seen in kids / young adult males, can be painful (use ASA, NSAIDs), may resolve over time or use CT-guided RF ablation

Trauma
C-Spine lateral, AP, odontoid, L/R oblique views, lateral view allows visualization of prevertebral soft tissues (swelling suggests bone injury), assess alignment w/ anterior spinal line (not reliable in elderly w/ osteophytes), posterior spinal line (most important), spinolaminar line (junction of lamina at base of spinous process) Hangmans 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, seen in young males in diving accidents Odontoid Fx hard to find, non-displaced, due to hyperextension or mixed mechanism Anterior shoulder dislocation goes down and medial, after relocation can see impaction fracture on lateral humeral head (Hill-Sachs deformity suggests prior dislocation) Acetabular fracture seen in MVA, femoral head in superior-lateral position, can see intra-articular fragment of bone in acetabulum (remove or get early arthritis), sitting position, knee driven posteriorly, pushing femoral head out posteriorly Radial head fracture subtle, use fat-pad sign (joint effusion good sign of occult fracture, fat pad displaced due to hemarthrosis, seen in falls w/ outstretched arms and elbow pain, can be non-displaced, take another xray 7-10 days later to better see fracture - Child abuse corner fracture (periosteum ripping away bone fragment bleeding /cloaking thickens and calcifies w/ repetitive trauma, can be exuberant and mimic bone forming tumor), posterior rib fracture, multiple fractures of different ages, subdural hematoma and SAH due to shaken baby Knee best seen w/ MRI PCL, ACL, lateral / medial meniscus

Infection, Metabolic, and Systemic Bone Diseases

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha OM (osteomyelitis) acute presents w/ subperiosteal abscess + elevation of periosteum, early destruction of femoral cortex, immature periosteal reaction mimics tumor; chronic OM walled-off area w/ persistent infection / low grade inflammation, can track along the bone soft tissue sinuses dense sclerotic reaction, cloacae (tracks in bone) Vertebral disc space infection starts in vertebral endplate, spreads to involve disc destruction of disc narrowing of disc space Renal Osteodystrophy hyperPTH bone resoprtion at many sites inducing osteoporosis and osteosclerosis, renal rickets in kids, see subperiosteal resorption w/ fuzzy bone margins (see in margins of middle phalanges) Osteonecrosis bone infarction and death, common in femoral head, best seen w/ MRI Sickle Cell Disease can result in osteonecrosis due to stasis of blood, infarcts in femoral head, h-shaped deformities due to central compression of vertebral bodies Leukemia lytic lesions, periosteal reaction simulating infection Neuroblastoma mets to bone widening of skull sutures

CARTILAGE PHYSIOLOGY AND OSTEOARTHRITIS

- Joint = capsule w/ synovial fluid inside (from synovial lining cells) - Capsule variable thickness, often ligamentous, provides support - Synovial Lining covers all areas within joint except cartilage, highly vascular w/ lypmhatics and nerves, contains hyaluronan, lubricin, and synovial lining cells - Synovial Lining Cells monocyte-derived (Type A, basis for immune activation and autoimmunity), fibroblastderived (Type B), dendritic cells, mast cells; lining cells are source of nutrients for chondrocytes (on subchondral bone plate which is avascular) - Muscles / tendons have most of stress distribution, neural input important (reflexes prepare joints for stress) - Atypical osteoarthritis due to neurological system that is not intact, lack of fine position sense, pt w/ DM / peripheral neuropathy at risk aggressive arthritis especially in legs - Synovial fluid primary metabolic supply for cartilage, not efficient, cartilage matrix has slow turnover, chondrocytes at bottom of cartilage plate inactive but respond w/ disease, metabolic supply w/ age, possibly leading to arthritis - Lubrication via hyaluronic acid (long sugar), component of joint fluid and cartilage - Cartilage structure 70% water, ability to allow water to leave w/ compression and reabsorb water w/ relief of pressure = resiliency, chondrocytes at bottom of cartilage generate matrix (lots of PGs), collagen comes up in arcs from bone in triple helix (if dysfunctional or modified collagen, can lead to osteoarthritis) Type II collagen most common in cartilage, Aggregan is the primary PG PG (proteoglikan) protein core filament, GAGs stuck as side chains (i.e. heparin, keratan, both are sulfated which attract water; chondroitin also a side chain), pressure forces water off sulfate groups, water reattaches w/o pressure, PGs attached non-covalently to HA, stabilized by link proteins (all components made by chondrocytes) PGs found in other CT types, comprise 20% of cartilage volume Chondrocytes gets nutrients from synovial fluid, make HA, all under metabolic control (cytokines / GFs), constant production and metabolism - Matrix metabolism changes w/ age - chondroitan sulfate (water retention), smaller PG aggregates, shorter HA, nutrient supply, cannot produce large amounts of matrix MMP degradation of CT structures, controlled by TIMPs (slow cartilage degradation) Scleroderma too much CT accumulating - Injury chondrocytes matrix production, but not as much Type II collagen production

Osteoarthritis
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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha Imaging interspace narrowing, marginal osteophytes, subchondral sclerosis (thickening of bone plate beneath cartilage), subchondral cysts, misalignment Affects cartilage in weight-bearing joints, pain related to use, worse during the day, minimal morning / inactivity stiffness (<20 min), ROM (crepitus on passive ROM), joint instability, bony enlargement of joints (not inflammation, which is spongy) Age is biggest factor (idiopathic), also female sex, obesity (affects legs), hereditary factors, trauma, NM dysfunction (neuropathy disrupts joint mechanics accelerated OA), metabolic disorders OA features progressive cartilage loss, subchondral thickening, marginal osteophytes (uneven, hypertrophied bone edges) Locations knee, hip, lumbar / cervical spine, hands (DIP Heberdens nodes, PIP Bouchards nodes, CMC base of thumb, most common in hand, most functional effect), foot (MTP of first toe) Does NOT involve ankle, MCP (except in thumb), wrist, elbow, shoulder Women higher incidence, DIP most common, then knee and hip involvement Hip subchondral sclerosis loss of joint space pain radiating down medial leg (vs. bursitis lateral leg pain) Ankle OA suggests another process is also at work i.e. DM neuropathy, NM disease, previous trauma, overuse, predisposing metabolic disease (CPPD pseudogout) OA secondary to DM neuropathy MTP 2-5 also involved, midfoot usually spared Underlying disease associated w/ OA and CPPD hemochromatosis, hyperPTH, hypothyroidism, hypoPO4, hypoMg, neuropathic joints, trauma, aging / hereditary Management progressive exercise to function, endurance, strength (falling risk) Strengthening exercise low-impact, continuous (15-30 min), 3x/week, creates better joint alignment and slows OA progression Acetominophen first line therapy, pain relief comparable to NSAID w/ less toxicity NSAID - inflammation, SE include GI, renal, worsening CHF, edema; use generic and low-dose first, neither NSAIDs nor Tylenol affect disease progression COX2 Inhibitors pain relief equivalent to older NSAIDs, GI toxicity, no effect on platelets, but can have renal toxicity and edema Tramadol (codeine) affects opioid and 5HT pathways, can cause constipation or rash, often added to NSAID or acetaminophen regimens (combining small / multiple doses of several meds can treat OA while avoiding SEs) Codeine / Oxycodone (narcotic analgesics) can induce tolerance, bowel immotility, avoided by adding Propoxyphene or Tylenol 3 (w/ codeine) in doses to other regimens Topical anesthetic Capsaicincontaining drugs for Sx relief Intra-articular Tx steroids or HA (not as commonly used) Other Tx glucosamine (Sx benefit, prevent in joint space), Tetracycline (MMP activity) Surgery arthroscopy (trim cartilage / ligaments), total joint replacement Summary make sure pain is joint-related, dont avoid exercise / weight loss as treatment, 1st line Tylenol, 2nd line NSAID, intra-articular agents / lavage, opioids, 3rd line arthroscopy, osteotomy, joint replacement

RHEUMATOID ARTHRITIS
Morning stiffness >1 hour (any inflammatory arthritis, vs. structural / osteoarthritis) Polyarthritis at least three joint areas, hands almost always involved, symmetry typical No imaging abnormalities early, eventually get cartilage / bone erosion in hand / feet Rhematoid nodules in 30% but specific, Rheumatoid factor in 80% but not specific Need to determine if there is inflammation when pt presents w/ joint pain look for warmth, morning stiffness, erythema, swelling, also need to determine if joint is truly affected or if adjacent tissues / structures are affected Normal joint fluid <200 WBC, osteoarthritis 200-2,000, >2,000 can be RA, psoriatic arthritis, gout, SLE, etc.; septic arthritis can have WBC > 100,000 Chronic polyarthritis can be RA, juvenile chronic arthritis, systemic rheumatic diseases (systemic vasculitis has arthritis, can be mistaken for RA until other organs involved), spondyloarthropathies (akylosing spondylitis, Reiters Syndrome), and psoriatic arthritis

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha

RA involves wrists, MCP, PIP of hands (vs. OA DIP, PIP, base of thumb) RA can also involve large joints like knees, shoulders, elbows (OA can also affect knees) RA also involves ankles, feet, hip, cervical spine (L/S spine in OA, lower spine and sacral ileitis in spondyloarthropathies), TMJ, larynx Psoriatic arthritis affects hands, w/ psoriatic skin rashes and nail abnormalities, inflammation of DIP (sauage digit in every finger) Hands in RA later, can see pronounced interosseous muscle atrophy, PIP swelling, 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), very uncomfortable and limit hand function Wrist swelling carpal tunnel syndrome (median nerve compression) atrophy of thenar muscles and sensory losses (can become permanent), treat w/ splinting, local steroid injections, surgery Swan neck deformity hyperextension at PIP DIP passively pulled into flexion contracture, not just due to arthritis but also tendon slippage Boutonniere deformity PIP in flexion, DIP in hyperextension Mallet deformity d/t tendon slippage, extensor tendons slip to volar side to all tendons work to flex the finger Early in RA bones are normal, joint space normal, little soft tissue swelling, some osteopenia near the joint only (local effect of cytokines like IL-1, TNF, osteoclast promoting cytokines) which is precursor to true erosion Later in disease - joint space, cartilage has been eroded, gaps of erosion in bone cortex eventually no cartilage space left, large erosions, synovial pannus eating into bone Erosions occur on bone side first, articular cartilage only present on weight-bearing surface of bone, bare areas of bone lack cartilage, 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 - RA vs. OA in hands RA has more prominent early soft tissue swelling, periarticular demineralization (OA has reactive bone and sclerosis in response to cartilage), more erosions (rare in OA except for collapsed cysts), rare reactive bone formation, more severe joint deformity, both have joint narrowing (cartilage damaged in both directions) - RA wrist, MCP, PIP; OA DIP, PIP, thumb base

RA in feet hard to examine, swell under other conditions, eventually get hallux valgus deformity (toes point outward), toe contracture (weight-bearing pad under MTP slips forward, pt walking on metatarsal heads, painful toe subluxation, ulceration) Swelling / deformity in ankles are seen along w/ Achilles and extensor tendon involvement, also progressive flattening and eversion of foot , requires surgery w/ complex fusion to restore anatomic position of foot Some erosion evident in MTP early on, progresses so toes no longer associate w/ appropriate metatarsal RA from early to late adulthood (30-60), more common in women No evidence that infection present in RA joint, possible to have immune mediated events that reflect infection elsewhere Reiters Syndrome and reactive arthritis clear link between infection elsewhere (i.e. GI) and development of arthritis RA did not exist before contact between Old and New World (environmental factors) Lymphocytes in RA synovial fluid, also monocyte / macs, thickening of synovial lining cells and fibroblast layer B-cells are a small but significant proportion of synovial lining cells, express CD5, associated w/ autoAB production, Rheumatoid factor and other autoABs made in joint, functions like LN in RA, but RA can occur in pt w/ agammaglobulinemia (so autoABs are not necessary for RA) Rheumatoid factor = AB against immunoglobulin (usually IgM), antigen for RF is Fc portion of IgG, ABs alone can create immune complexes, but present in many other diseases (endocarditis, chronic lung / liver disease, Sjogrens Syndrome), not all RF+ pt have RA T lymphocytes and APCs to activate T cells in joint fluid, accumulation not random (some clones are dominant), associated w/ specific MHC alleles (T cell function important in RA pathogenesis, T cell clones can transfer disease to another host) No identified antigen that uniformly elicits T cells response in RA, Tx that remove T cells in joint not effective, T cells quickly repopulate w/ more aggressive clones Metaplasia of joint lining into lymphoid organ immune cells, joint lining cells, and cartilage all together; interactions between these and T cells, dendritic cells, macs, fibroblasts eroding cartilage all contribute to disease

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Handout REVIEW SISTEM GERAK Oleh : dr. 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, also make inflammatory PGs, cytokines, chemokines TNF acts on endothelium to adhesion molecules for leukocytes, 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, TNF / IL-1 in joint can enter systemic circulation constitutional Sx Therapy targets y-IFN (Th1 cytokine), IL-15 (T-cell GF), IL-17 (activates synovial fibroblasts); other mediators PG, arachadonic acid metabolites, MMP, NO, pH in joint and at cartilage-pannus junction, reactive O2 species, other proteases

Ligamentous Strains
Grade I intact structurally, no laxity, microscopic disruption Grade II partial tear w/ laxity, definite endpoint Grade III complete disruption w/o endpoint (flail joint), requires surgical repair - Ligaments stabilize joints by allowing movement in only certain planes, injury occurs when there is motion in abnormal plane or excessive motion in normal plane, need subluxation or dislocation to significantly injure ligament - PE joint swelling in proportion to degree of injury, ecchymosis, tenderness over ligamentous attachments, restricted AROM and PROM - Dx x-rays for Grade II / III or severe trauma, stress radiographs for determining endpoint in ankles, MRI for knee, shoulder, ankle (gold standard) -

Principle of Rehabilitation Acute Phase - pain / inflammation (PRICE protection, relative rest, ice, compression, elevation), want to keep as active as possible unless bone is fractured, can also use NSAID, corticosteroid injections, splinting / bracing, compression wraps, surgery - Avoid steroids in Achilles and patellar tendons (risk of rupture) - Recovery Phase need 60% ROM to enter this phase, ROM can be restored passively or actively, need muscle strength (start w/ isometric isotonic / isokinetic), closed chain exercises helpful and shouldnt be painful, endurance w/ reps / resistance, - proprioception w/ balance agility drills - Maintenance Phase return to activity in progressive, functional way, start CV conditioning as early as possible, functional progression of activity (reestablish motor skills), prevent re-injury (correct underlying biomechanical factors, education)

MUSCULOSKELETAL GROWTH AND DEVELOPMENT

Torsional Deformities of Lower Limbs
Torsion twisting in reference to tibia, internal / external Version twisting in reference to femur, retroversion / anteversion (outward proximally) In-Toeing common, can originate at foot, knee, or hip - Metatarsus adductus turning-in of foot in 0-18 months, limited to forefoot, spontaneously resolves in 80%, can treat w/ casting or rarely surgery - Internal tibial torsion 6-18 months, most spontaneously improve, defined by transmalleolar axis (movement of fibular with respect to medial aspect of distal tibia /medial malleolus if extreme, fibula in front of medial malleolus) -

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha Femoral anteversion 3-9 years, usually normal growth, pt has feet straight forward but knees inward, not problematic even if it persists, no arthritis or functional problems, rotation of femoral head with respect to femoral condyles (i.e. femoral head rotated vertically away from plane of condyles) - In-toeing can also be cause by clubfoot (entire foot involved), atavistic first toe (overactive abductor hallucis only), neurologic problems (cerebral palsy) Out-toeing less frequent than in-toeing - Calcaneovalgus foot foot is excessively dorsiflexed to the leg and turned outward, improves spontaneously within a few weeks after birth, packaging problem - External tibial torsion uncommon, red flag for CP or myelodysplasia, knees pointed straight ahead but feet turned outward - External rotary contractures of hip 0-18 months, improves spontaneously Angular Deformities of Lower Limbs Valgus deviation / angulation away from midline Varus deviation / angulation towards midline - PE need to see if there is laxity about knee joint, also test motion of all lower limb joints, localize angulation, assess alignment - Radiographic XR of whole hip, lower limb, and foot on same film, both AP and lateral, to assess alignment Labs rule out renal rickets, get Ca, PO4, Vit. D, and alk. phos. Levels - Bowlegs (Genu Varum) inward angulation with respect to midline (angle made by femur and tibia opens inward), can be physiologic, caused by Blounts Disease (growth plate abnormality uneven growth of proximal tibial epiphysis, more growth laterally), rickets, or metaphyseal chondroplasia - Physiologic Bowing 15o normal in infants, legs move to neutral position by 18-24 months, x-rays are otherwise normal, track w/ Salenius and Vankka chart, children start bowlegged normal knock-knee normal - Infantile Blounts Disease cant make Dx until 2 years old, occur in overweight kids and those who are early walkers, pt tends to have internal tibial torsion, x-ray show excessive beaking on medial side of proximal tibia depression of medial plateau, Stage IV disease can result in fusion of bones Rickets widened growth plates on x-ray - Knock Knees (Genu Valgum) outward angulation, seen in ages 3-5, usually normal developmental variation, but can be caused by renal osteodystrophy, metabolic bone disease, bone dysplasia

Developmental Dysplasia of the Hip Not always seen at birth, continuum of subtle findings subluxation dislocation Mechanical factors often responsible small space (common in firstborns), breech presentation (legs adducted), left hip more involved (left leg adducted commonly in utero) DDH often presents w/ torticollis (head tilting / rotation) and metatarsus adductus (both mechanical problems), DDH more common in females (estrogen effect) Hip at Risk Major (abnormal clinical exam, breech, first-born and female, family Hx) and Minor (limited hip abduction, sacral dimple, foot and postural deformities) Newborn to 2 months Ortolani and Barlow tests most reliable, x-rays unreliable, USN allows visualization of cartilage but may be too sensitive PE should be part of every well-baby exam, infant needs to be relaxed, Orolani - stabilize pelvis, flex hip to 90o, adduct past midline, the abduct and lift towards socket (can catch hip dislocations or subluxations which then relocate); Barlow flex hip to 90o, gently push posteriorly to dislocate Tx (0-6 months) reduce femoral head into acetabulum, abduct hip w/ Pavlik harness, free range but limited range of motion, make sure harness isnt too tight avascular necrosis of femoral head

Crystalline Arthropathies
bias Crystals build up in joint space and cause inflammation, gout and pseudogout are very treatable, no sex

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha Gout monosodium urate crystals (from uric acid), most common crystalline disease, rarely found in shoulder Pseudogout calcium pyrophosphate crystals (CPPD) Hydroxyapatite Dx requires EM and alozerine red, common in shoulder (Milwaukee) Calcium Oxalate seen in pts on dialysis Dx categories infections, inflammation, degeneratie, traumatic, neoplastic (rarest) - ASx Hyperuricemia allopurinol used to uric acid production, but many SEs, dont need to use for every pt w/ uric acid (only ~15% actually have gout) - Gout can present as acute gouty arthritis or chronic tophaceous gout; associated w/ obesity, DM, hyperlipidemia, HTN, atherosclerosis, EtOH, acute illness (mono),pregnancy, post-op; negative associations SLE, RA, amyloid, dialysis - Gout can co-exist w/ OA, CPPD, septic arthritis, and others Renal Disease with Gout Urate nephropathy pt w/ hyperuricemia can get kidney damage but only if uric acid - consistently <13 (most pt w/ gout are at 8-9), pt w/ uric acid should get allopurinol - Acute uric acid nephropathy crystalline arthropathies can lead to simultaneous, bilateral, microscopic obstruction of kidneys from excess uric acid crystals, no stones - evident on USN or CT, no hydronephrosis evident for several weeks, more common in pt undergoing induction chemo for leukemia / lymphoma (get allopurinol w/ chemo) - Calculi 90% of pt w/ kidney stones have calcium stones, rare to find uric acid stones but many calcium stones form around a small uric acid crystal, uric acid helps to prevent calcium stones in pts w/ recurrent stones

Acute Gouty Arthritis

Abrupt onset, often at night, usually monoarticular Deep, stabbing, hot pain in a red, warm, swollen, and extremely tender joint Resolves in 3-10 days even w/o Tx, most pt have MTP involvement of big toe Dx urate crystals found inside WBCs in the affected joint, most pt have hyperuricemia, but 15% have normal uric acid during gout attack (but hyperuricemia for many years before attack), 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, tissue trauma during surgery releases purines, uric acid w/ purine salvage pathways), renal abnormality (tubular disorders), drugs (diuretics, low-dose ASA), toxins (EtOH, Pb), hypothyroidism Increased Production (10%) EtOH (2 beers can trigger gout attack), HGPRT deficiency,G6PD deficiency, superactive PRPP synthetase, myeloproliferative disorders (lymphoma, leukemia, mono), psoriasis Complete HGPRT Deficiency Lesch-Nyhan Syndrome uric acid overproduction, mental retardation, microcephaly, compulsive self-mutilation, gouty renal disease, uric acid crystals present in urine, but NOT gouty arthritis Partial HGPRT Deficiency 1% of normal enzyme activity can avoid mental retardation (but still abnormal basal ganglia), early onset and severe arthritis gout / renal disease

Acute Gout
Crystals in WBC intense inflammatory reaction (crystals themselves arent harmful, but host response is excessive, WBCs cant destroy crystals, engulf and release inflammatory mediators severe inflammatory arthritis), crystals alone in a joint cant cause gout Unexplained features initiation of attack, self-limited nature of attacks, joint distribution (big toe most common, but also other toes, midfoot, heel, ankle, knee; rarely affects fingers but can coexist in OA Heberdens nodes in DIP; rarely affects other joints), minor trauma or activity can trigger episode

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha Dx clinical findings, joint fluid aspirate under polarized light, positive response to gout therapies, classic radiographs Diagnostic arthrocentesis aspirate joint fluid, view using multiple polarizing lenses, gout has needleshaped uric acid crystals inside WBC that appear yellow; pseudogout has rhomboid crystals that are blue DDx of 1st MTP toe inflammation gout, pseudogout, RA, OA, traumatic arthritis, sickle cell anemia, OM, bony infarct Complications quality of life issues pain, mobility

Treatment
o First choice indomethacin 35-30 mg qid tapering over five days o Colchicine 0.6 mg one tablet / hr, max 12 tablets in first day, then max 0.6 mg TID over the next week (most pt get significant SE after 8th pill), IV colchicines are dangerous but used as one-time dose post-op o Butazolidin rarely used, can cause irreversible aplastic anemia on first dose o Intra Articular steroids / NSAIDs dont work well unless given very early in an attack o Narcotics usually ineffective for pain relief - Prophylaxis indomethacin 25 mg qd-bid, colchicine 0.6 mg bid - Long-term anti-hyperuricemic treatment o Frequency of gout attacks during establishment of long-term control, 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, use only if gout is due to excretion, dont use drugs if excretion <900 mg / 24 hours or kidney stones will form) - 90% will have another attack within 5 years of first attack, often have 5-6 attack the following year, pt w/ lots of attacks or tophi (large uric acid conglomerates) should get long-term therapy to protect kidneys, will often require 25 years of allopurinol to get resolution of severe tophi - Colchicine from a plant, difficult dosing, SE N/V/D, skin reactions, myelosuppression, muscle disease, neuropathy, apalstic anemia, thrombocytopenia - Indications for allopurinol tophi, uricosurics CIed (renal insufficiency w/ creatinine clearance <80, urine uric acid > 13, uric acid overexcretion), renal stones (any type), chemotherapy induction - Allopurinol DDIs azathioprine (competitive inhibitor of enzyme affected by allopurinol), cyclosporine, mecaptopurine - Diet - high purine foods (brain, heart, kidney, liver)

ORTHOPEDIC SURGERY

Hip = ball and socket, MCP / TMP = hinge, AC / SC = fibrous, sub-talar = saddle; within joints are facets, auxiliary joints, discs, menisci; knee is complex joint w/ changing rotational axis Long bones diaphysis (cortical bone, highly vascular), metaphysic (trabecular area, highly vascular), physis (growth plate in children), epiphysis (variable vascularity), cartilage at articular surface avascular (poor response to injury) Open (compound) fracture = hole in skin, grade 1 (<1cm hole, clean), grade 2 (1-10 cm), grade 3 (>10 cm, dirty) Simple fractures oblique (most common) or transverse (straight across bone, rare unless bone already weakened, i.e. pathological fracture) Comminuted fracture has multiple pieces, butterfly fragment is fracture element w/ threepoint bend (+/twist), buckle fracture in children since bones soft enough to allow crushing instead of breaking, Greenstick fracture in children since bones pliable enough to allow partial breakage stuck in bent position (requires complete refracture to set bone), Salter fracture = physeal fracture, heal easily if aligned properly Angulation described by where apex of fracture is pointing Open fracture is surgical emergency, risk for chronic OM, the closer a bone is to the center of body, the more urgently it needs repair; radial head fracture can be treated w/ sling but femur / displaced / scaphoid fractures and polytrauma require surgery Dislocation components of joint have come apart, no longer in contact w/ articular surface, described with respect to direction of distal part of joint

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

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha Mechanical loading is stimulus for bone formation, immobilization (bed rest) resorption and formation, seen in astronauts Osteoporosis 15-25% of women will sustain OP fracture at some point, 10% of men - OP = bone mass, remaining bone normal, max bone density in mid-20s, steady loss of bone after, five-year period of accelerated loss in post-menopausal women w/o HRT, but resume normal rate of loss afterwards Fracture threshold = certain amount of bone to maintain integrity, everyone falls below threshold if they live long enough Risk factors polymorphism in Vit. D receptor, +family Hx, thin body (obesity mechanical loading of bones), fair skin, smoking, white / asian (black females have same risk as white men), GC excess from steroid therapy or Cushings Early OP is ASx unless there is fracture, can occur w/ minimal trauma, vertebral compressions most common along w/ hip and wrist fractures (trabecular bone), death rate from hip fracture is 10% (PE, infection, etc.) End-stage disease marked dorsal kyphosis, loss of lumbar lordosis, can cause arthritis, erve compression, chronic muscle pain Dx bone density more than 2.5 SD below mean for healthy young individuals, poorly assess w/ x-ray, need bone densitometry (DEXA) which measure bone thickness, density given as g/cm2, reported as T-score (i.e. -4.0 worse than -3.0) Bone markers OB releases AP and osteocalcin (less available but more sensitive), OBs active in OP but cant keep up w/ resorption, OC markers are pyridinoline crosslinks and N-telopeptide (part of Type I collagen after degradation), markers useful for following response to Tx Osteopenia caused by hypogonadism (both men / women, seen in post-menopause w/o HRT, most pt w/ OP are hypgonadal), hyperPTH and hyperTH OC activity, Cushings OB activity, osteomalacia, cancer (multiple myeloma) Prevention adequate Ca intake, women need supplemental Ca pre-menopause (1 g/day), young women should get 500 mg/day (i.e. one Tums); avoid hypogonadism in younger pt, high risk w/ hypothalamic amenorrhea (hyperPRL or exercise-induced); weight-bearing exercise Tx most important is to prevent falls Calcium / Vitamin D RDA for Vitamin D is 400 units / day, should give 800 units Gonadal steroid replacement - OC activity, effective Tx and prevention, estrogen probably as effective as bisphosphonates, long-term estrogen bone mass and fracture risk, replace hormones in men w/ testosterone deficiency and deficient pre-menopausal women Raloxifene SERM, bone density, fracture risk, no trophic effect on breast / uterus, hot flashes, not as potent as estrogen but still blood stasis (thrombosis) Bisphosphonates aledronate / risedronate potent inhibitors of OC, sustained in bone density, fracture risk by 50%, possible erosive esophagitis w/ bleeding, need to take w/ full glass of water, no food or supine position for 30 minutes (now available as one pill /week) Calcitonin - OC activity, slows bone loss but doesnt restore bone (unlike bisphosphonates), available as nasal spray or injection, can provide pain control for acute fracture, SE include N/V, flushing; used as 3rd or 4th line agent Any pt on GC for >1 week will have OP, pt should have adequate Ca / Vit.D, bisphosphonates can reverse / slow GC-induced OP, start concurrently Osteomalacia / Rickets Case resection of 15 feet of SI due to Crohns, Ca low / normal, PO4, albumin, Hb, carotene, cholesterol (malabsorption), AP, zero Vit.D, osteoid seams (unmineralized osteoid)

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Handout REVIEW SISTEM GERAK Oleh : dr. Zainuri Sabta Nugraha

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

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