muscoloskeletal system dent · yprevention and treatment: yexercise ... yadulthood, trunk, limb...
TRANSCRIPT
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Musculoskeletal System
Jatuwit Howannapakorn M DJatuwit Howannapakorn, M.D.
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ContentsBonesBones
Developmental and acquired abnormalitiesOsteoporosisOsteoporosisRickets, osteomalacia, hyperparathyroidism, renal osteodystrophyy p yFractureOsteonecrosis (Avascular necrosis)( )InfectionsBone tumors and tumor-like lesions
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ContentsJointsJoints
Arthritis and osteoarthritisTumor and tumor-like lesions of jointsTumor and tumor like lesions of joints
Soft tissue tumors and tumor-like lesions
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Developmental & Acquired abnormalities in bone cells, matrix & structure
Dysostoses: localized problems in migration of mesenchymal Dysostoses: localized problems in migration of mesenchymal cells and their formation of condensations
Limited structure abnormalitiesMutation in transcription factors (Homeobox genes)
Dysplasia: mutations in regulators of skeletal organogenesisAffect bone and cartilage globallyMutation in cellular signaling and matrix components
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Defects in nuclear proteins and transcription factors
Failure of development of boneFailure of development of bone
Formation of extra bones (supernumerary)
F i f t di it ( d l )Fusion of two digits (syndactyly)
Development of long spider-like digits (arachnodactyly)
Failure closure of spinal column and skull (Craniorachischisis) MeningiomyeloceleMeningioencephalocele
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Defects in hormones and signal transduction
Achondroplasia:Achondroplasia:Major cause of dwarfismAutosomal dominant (80% new mutation)Autosomal dominant (80% new mutation)Point mutation of FGFR3
Thanatophoric dwarfism:Thanatophoric dwarfism:Most common lethal form of dwarfism1 in 20 000 live births1 in 20,000 live birthsMutation of FGFR3Shortening of limbs frontal bossing small chest cavity bell-Shortening of limbs, frontal bossing, small chest cavity, bellshaped abdomen
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Defects in extracellular structural proteins
Type 1 collagen diseases (osteogenic imperfecta)Type 1 collagen diseases (osteogenic imperfecta)Deficiency in the synthesis of type 1 collagenBone (too little bone), joint, eyes (blue sclerae), ears (hearing ( ) j y ( ) ( gloss), skin, teeth (dental imperfections)Four major subtypes:
T II f l i Type II: fatal in uteroType I: normal life span with increased fracture
Type 2, 10, and 11 collagen diseaseType 2, 10, and 11 collagen diseaseEarly destruction of joint (osteoarthritis)
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OsteoporosisIncreased porosity of skeleton resulting from reduced bone Increased porosity of skeleton resulting from reduced bone mass
Localized: disused osteoporosisLocalized: disused osteoporosisGeneralized: metabolic bone disease
Primary: Senile, postmenopausal, idiopathicy , p p , p
Secondary: Vit D deficiency, Steroids
Most common:Senile osteoporosispostmenopausal osteoporosis
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OsteoporosisPathogenesisPathogenesis
Age-related change:Osteoblast replication and biosynthesis ↓Osteoblast replication and biosynthesis ↓Low turnover variant
Reduced physical activity:Mechanical force ↓ bone remodeling ↓
Genetic factors:Type of Vitamin D receptor maximal peak mass
Body calcium nutritional state:C l i d fi i ↓ b Calcium deficiency ↓ bone mass
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OsteoporosisPathogenesisPathogenesis
Hormonal influences:Menopause ↓ estrogen ↑IL-1, IL-6, TNF from monocytes and bone Menopause ↓ estrogen ↑IL 1, IL 6, TNF from monocytes and bone marrow cells ↑osteoclast activity (30-40 yrs 35-50% bone loss)High turnover variant
↑ ↓Glucocorticoids ↑bone resorption & ↓bone formationBiphosphonate prevent bone loss
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OsteoporosisClinical course:Clinical course:
Veterbral fractures: thoracic and lumbar regions, painful
Multiple fractures loss of height lumbar lordosis and Multiple fractures loss of height, lumbar lordosis and kyphoscoliosis
Diagnosis:Diagnosis:30-40% bone loss detected by radiographsDual-energy absorption and quantitative CTDual energy absorption and quantitative CTBiopsy
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OsteoporosisPrevention and treatment:Prevention and treatment:
ExerciseCalcium and vitamin D intakeCalcium and vitamin D intakeEstrogen replacementBiphosphonateBiphosphonateRecombinant PTH
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Rickets and OsteomalaciaDefect in matrix mineralizationDefect in matrix mineralization
Lack of vitamin D or disturbance of its metabolism
Child “ i k ”Children “rickets”Skeletal deformities
d l “ l ”Adults “osteomalacia”Osteopenia fracture
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HyperparathyroidismPTH ↑osteoclastic activityPTH ↑osteoclastic activity
Osteitis fibrosa cystica (brown tumor)
Cli i l f tClinical features:Fracture, bone deformitiesJ i t i d d f tiJoint pain and dysfunction
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Renal OsteodystrophySkeletal changes of chronic renal disease:Skeletal changes of chronic renal disease:
High turnover osteodystrophy↑Osteoclastic bone resorption (osteoporosis)↑Osteoclastic bone resorption (osteoporosis)
Low turnover or aplastic disease↓Matrix mineralization (osteomalacia)
Pathogenesis:Vitamin D def. hypocalcemia PTH ↑ypHyperphosphatemia PTH ↑Metabolic acidosis bone resorption ↑pAluminum deposit bone mineralization ↓
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FracturesClassification:Classification:
Complete vs. incompleteClosed (simple) vs Opened (compound)Closed (simple) vs. Opened (compound)Comminuted (splintered)Displaced Displaced Pathologic fracture (underlying bone dis.)Stress fracture (repetitive loads)St ess actu e ( epet t ve oa s)
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FracturesReparative process:Reparative process:
1st week organizing hematoma (soft tissue callus, procallus)
2nd or 3rd week bony callus (cartilage and bone formation)y ( g )
Delayed healing: nonunionDisplaced, comminuted, compound fractures
Inadequate immobilization
Infections
C l i ↓ h h ↓ Vi i d f di b i l i ffi iCalcium↓, phophorus↓, Vitamin def. diabetics, vascular insufficiency
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Osteonecrosis (AVN)Ischemia infarctionIschemia infarction
Mechanisms:Vascular interruption (fracture)Vascular interruption (fracture)CorticosteroidsThrombosis and embolism (nitrogen bubbles dysbarism)Thrombosis and embolism (nitrogen bubbles, dysbarism)Vessel injury (vasculitis, radiation)
↑ Intraosseous pressure and vascular compression↑ Intraosseous pressure and vascular compressionVenous hypertension
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Osteonecrosis (AVN)Clinical course:Clinical course:
Subchondral infarcts chronic pain, 2nd osteoarthritisMedullary infarcts clinically silent painful collapseMedullary infarcts clinically silent, painful, collapse
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Infections—Osteomyelitis Pyogenic osteomyelitisPyogenic osteomyelitis
Bacterial infections: S. aureus (80-90%)S. aureus (80 90%)
E. coli, Pseudomonas, Klebsiella: IVDU, GU tract
Mixed organisms: fracture, direct spread
H. influenzae: neonatal period
Salmonella: sickle cell anemia
Spread hematogenous e tension from contiguous sites direct Spread: hematogenous, extension from contiguous sites, direct implantation
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Infections—OsteomyelitisPyogenic osteomyelitisPyogenic osteomyelitis
Sites:Neonate: Metaphysis, epiphysisNeonate: Metaphysis, epiphysis
Children: Metaphysis
Adult: Epiphysis, subchondral
Clinical course:Acute systemic illness, fever, malaise, leukocytosis, throbbing pain
X l i b d iX-ray: lytic bone destruction
Threatment: antibiotics and surgical drainage
5-25% chronic osteomyelitisy
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Infections—OsteomyelitisTuberculous osteomyelitisTuberculous osteomyelitis
1-3% of patients with pulmonary or extrapulmonary TB have osseous infectionHematogenous spread from visceral organs or direct extensionSpine infection (Pott disease): thoracic and lumbar vertebraep ( )More destructive and resistance to therapy than pyogenic osteomyelitis
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Bone tumors and Tumor-like lesionsHematopoietic (40%)Hematopoietic (40%)
Chondrogenic (22%)
O t i (19%)Osteogenic (19%)
Unnown origin (10%): giant cell tumor
Micellaneous:Fibrous and histiocyticVascularLipogenicNeurogenic
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Bone tumors and Tumor-like lesionsCharacteristic:Characteristic:
Osteosarcoma:Adolescence, metaphysis around the kneesAdolescence, metaphysis around the knees
ChondrosarcomaAdulthood, trunk, limb girdle, proximal long bones
Giant cell tumors and chondroblastoma:Epiphysis of long bones
Ewing sarcoma, osteofibrous dysplasia, adamantinomaDiaphysis
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Bone-forming tumorOsteoma:Osteoma:
skull, facial bonesMiddle-aged adultsMiddle aged adultsObstruction of sinuses, cosmetic problems
Osteoid osteoma osteoblastoma:Osteoid osteoma, osteoblastoma:Osteoid osteoma: <2 cm in size
Teens and twenties, femur, tibia, painful lesionTeens and twenties, femur, tibia, painful lesion
Osteoblastoma: >2 cm in sizeSpine, dull pain
X-ray: nidus
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Bone-forming tumorOsteosarcoma:Osteosarcoma:
Most common primary bone tumorAge: 75% (children <20 yo) 25% (elderly)Age: 75% (children, <20 yo) 25% (elderly)Secondary osteosarcoma: Paget disease, bone infarct, irradiationSites: metaphyseal region of long boneSites: metaphyseal region of long boneClinical: painful enlarging massX-ray: destructive, lytic and blastic mass with permeative ay: est uct ve, yt c a ast c ass w t pe eat ve margin, “Codman Triangle”Treatment: Chemotherapy, limb salvagepy g
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Cartilage-forming tumorOsteochondroma:Osteochondroma:
ExostosisSolitary and multiple (hereditary)Solitary and multiple (hereditary)Late adolescence and early adulthoodMetaphysis of long bonesMetaphysis of long bones
Clinical: slow-growing mass, can be painful, rare (<1%) chondrosarcoma
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Cartilage-forming tumorChondroma:Chondroma:
Intramedullary: enchondromaMetaphysis of short tubular bones of hands & feetMetaphysis of short tubular bones of hands & feet
Surface of bone: Subperiosteal or juxtacortical chondromaClinical: asymtomatic, painful, pathologic fracturey , p , p gX-ray: well-circumscribed oval lucencies (O ring sign)
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Cartilage-forming tumorChondrosarcoma:Chondrosarcoma:
Second most common malignant matrix-producing tumor of bonesAge 40 or olderMalignant transformation from enchondroma,
t h d h d bl tosteochondroma, chondroblastomaSites: central portions of skeleton, pelvis, shoulder, and ribsClinical: painful enlarging mass fractureClinical: painful enlarging mass, fractureX-ray: Destructive radiolucent massTreatment: Surgical excision, chemotherapyg py
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Fibrous and Fibro-osseous tumorsFibrous cortical defectFibrous cortical defect
30-50% of all children older than age 2 yearsEccentric in metaphysis of distal femur and proximal tibiaEccentric in metaphysis of distal femur and proximal tibiaSmall size, 0.5 cm in diameterSpontaneous resolutionSpontaneous resolution
Nonossifying fibromaLarge size tumor 5 to 6 cm in sizeLarge size tumor, 5 to 6 cm in sizeMay present with pathologic fracture
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Fibrous and Fibro-osseous tumorsFibrous dysplasiaFibrous dysplasia
Localized developmental arrestClinical pattern:Clinical pattern:
Single bone (Monostotic)
Multiple bones (Polyostotic)
Polyostotic disease with café au lait skin pigmentation and endocrine abnomalities (precocious puberty)
M t ti fib d l iMonostotic fibrous dysplasia:Early adolescence
Ribs, femur, tibia, jawbones, calvaria, humerus, , , j , ,
Enlargement and distortion of bone (craniofacial)
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Fibrous and Fibro-osseous tumorsFibrous dysplasiaFibrous dysplasia
Polyostotic fibrous dysplasia:Femur, skull, tibia, humerus, ribs, fibula, radius, ulna, mandible, Femur, skull, tibia, humerus, ribs, fibula, radius, ulna, mandible, vertebrae
Polyostotic fibrous dysplasia with café au lait skin pigmentation and endocrinopathies:
McCune-Albright syndrome
Sexual precocity hyperthyroidism pituitary adenomaSexual precocity, hyperthyroidism, pituitary adenoma
X-ray: ground glass appearanceTreatment: conservative surgeryTreatment: conservative surgery
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Metastatic diseaseAdults:Adults:
Prostate, breast, kidney, and lung
Children:Children:Neuroblastoma, Wilms tumor, osteosarcoma, Ewing sarcoma, rhabdomosarcomarhabdomosarcoma
X-ray:Multifocal or solitary (kidney thyroid)Multifocal or solitary (kidney, thyroid)
Lytic: Kidney, lung, GI and melanoma
Blastic: Prostate
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JointsOsteoarthritis:Osteoarthritis:
Degenerative joint diseaseProgressive erosion of articular cartilageProgressive erosion of articular cartilageIdiopathic (primary OA): aging phenomenonSecondary oateoarthritis (5%): diabetics ochronosis Secondary oateoarthritis (5%): diabetics, ochronosis, hemochromatosis, obesityWomen: knees and handsMen: hips
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OsteoarthritisPathogenesis:Pathogenesis:
Aging and mechanical effectsGenetic factors: high bone densityGenetic factors: high bone density
Clinical course:Primary OA: old age (>50 yr)Primary OA: old age (>50 yr)Secondary OA: younger age, underlying dis.Deep achy pain worsen with useDeep achy pain, worsen with useMorning stiffness, crepitus, limitation of movementNerve root compression (osteophytes)Nerve root compression (osteophytes)
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Rh t id th itiRheumatoid arthritisChronic systemic inflammatory disorder: skin blood vessels Chronic systemic inflammatory disorder: skin, blood vessels, heart, lungs, muscles, joints
Pathogenesis:Pathogenesis:Autoimmune disease: arthritogenic antigen CD4+ helper T cells inflammatory cytokinescells inflammatory cytokinesGenetic susceptibility: HLA-DR1*0401, *0404Antigens: unknowng
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Rh t id th itiRheumatoid arthritisClinical course:Clinical course:
50%, slow and insidious onset: malaise, fatigue, musculoskeletal pain, joint pain10% acute onset with sever symptomsSite: small joints > large joints: MCP, PIP, MTP, IP, wrists,
kl lb kankles, elbows, knees20%, partial or complete remission periodJoint destruction deformity: swan neck boutonniere of fingersJoint destruction, deformity: swan neck, boutonniere of fingersX-ray: juxta-articular osteopenia, bone erosion with narrowing of joint space
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Rh t id th itiRheumatoid arthritisLaboratory tests and Dx:Laboratory tests and Dx:
Serum rheumatoid factor (IgM to Fc portion): not specificSynovial fluid analysis: inflammatory exudatey y yClinical criteria: 4 criteria
Morning stiffnessA h i i i h j iArthritis in three or more jointsArthritis of typical hand jointsSymmetric arthritisRheumatoid nodulesSerum rheumatoid factorTypical radiographic changesTypical radiographic changes
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Rh t id th itiRheumatoid arthritisTreatment:Treatment:
Anti-inflammatory drugs (aspirin, NSAIDs)SteroidsSteroidsAnti-TNF antibody, soluble TNF receptor
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I f ti th itiInfectious arthritisSuppurative arthritis:Suppurative arthritis:
Bacteria: gonococcus, Staphylococcus, Strepcoccus, Haemophilus influenza, E. coli, salmonella, Pseudomonasp , . , ,Children <2 yr: H. InfluenzaeAdults: S. aureusYoung women: GonococcusSickle cell anemia: SamonellaPainful joint, fever, leukocytosisKnees, hip, shoulder, elbow, wristp
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G t d G t th itiGout and Gouty arthritisTransient attacks of arthritis initiated by crystallization of Transient attacks of arthritis initiated by crystallization of monosodium urates (needle shape, neg. birefringent) within jointsPathogenesis: hyperuricemia gout
Age: 20-30 yr after hyperuricemiaGenetic: Lesch-Nyhan syndromeHeavy alcohol consumptionOb itObesityDrugs: thiazidesLead toxicityLead toxicity
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G t d G t th itiGout and Gouty arthritisClinical course: four stagesClinical course: four stages
Asymptomatic hyperuricemia: puberty male or menopause womenAcute gouty arthritis: 50% MTP joint, ankles, heels, knees, wrists, fingers, elbowsgIntercritical goutChonic tophaceous gout: 12 years after first attackExtra-articular: atherosclerosis, hypertension, renal colic, gouty nephropathy
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P d tPseudogoutCalcium pyrophosphate crystal deposit disease (CPPD)Calcium pyrophosphate crystal deposit disease (CPPD)Age: over age 50Type: Idiopathic hereditary and secondary (joint damage Type: Idiopathic, hereditary and secondary (joint damage, hyperparathyroidism, hemochromatosis, hypomagnesemia, hypothyroidism)Clinical: aymptomatic, acute, sunacute, chronic arthritis of knees, wrists, elbows, shoulder, ankles
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T d T lik l iTumor and Tumor-like lesionsGanglion cysts:Ganglion cysts:
Size: 1 to 1.5 cm near joint capsule or tendonSite: wrists fingersSite: wrists, fingersEtiology: Cystic degeneration
Synovial cysts:Synovial cysts:Baker cyst of knees in RA patientsSynovial protrusion (diverticulum)Synovial protrusion (diverticulum)
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Soft tissue tumors and tumor-like lesions
Mesenchymal proliferations that occur in the extraskeletal Mesenchymal proliferations that occur in the extraskeletal, nonepithelial tissue
Classification: muscle fat fibrous vesels nervesClassification: muscle, fat, fibrous, vesels, nerves
Location: lower ext. (40%), upper ext. (20%), head&neck (10%) trunk&retroperitoneum (30%)(10%), trunk&retroperitoneum (30%)
Prognosis: histologic classification, grade I-III, Staging, superficial vs deep seatedsuperficial vs. deep-seated
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Fatty tumorsLipoma:Lipoma:
Most common soft tissue tumor of adultWell-encapsulated mass mature adipocytesWell encapsulated mass, mature adipocytesSoft, mobile, painless (exp. Angiolipoma)
Liposarcoma:Liposarcoma:Most common sarcoma of adult (40s-60s)Deep seat soft tisueDeep seat soft tisueWell-differentiated (indolent), myxoid (intermediate), round cell, pleomorphic (aggressive), p p ( gg )
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Fibrous tumors and tumor-like lesionsReeactive pseudosarcomtous proliferationsReeactive pseudosarcomtous proliferations
Nodular fasciitis, proliferative fasciitis, proliferative myositisMyositis ossificansMyositis ossificans
Fibromatoses:Superficial fibromatosis (palmar plantar penile)Superficial fibromatosis (palmar, plantar, penile)Deep-seated fibromatosis (desmoid tumors)
Fibrosarcoma:Fibrosarcoma:Aggressive tumors with recur and metastasis
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Fibrohistiocytic tumorsBenign fibrous histiocytoma (dermatofibroma):Benign fibrous histiocytoma (dermatofibroma):
Painless, slow growing tumor of dermis and subcutisAdequate treatment: simple excisionAdequate treatment: simple excision
Malignant fibrous hisiocytoma:Undifferentiated pleomorphic sarcomaUndifferentiated pleomorphic sarcomaDeep-seat soft tissue, superficial (atypical fibroxanthoma)Aggressive recur and metastasisAggressive, recur and metastasis
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Tumors of skeletal muscleRhabdomyoma:Rhabdomyoma:
Hamartomatous?Heart tongue external genitaliaHeart, tongue, external genitalia
Rhabdomyosarcoma:Most common soft tissue sarcoma of childhood and adolescenceMost common soft tissue sarcoma of childhood and adolescenceMost occur in head& neck or genitourinary tractType: embryonal alveolar pleomorphicType: embryonal, alveolar, pleomorphicAggressive tumor, also chemotherapy Rx
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Tumors of smooth muscleLeiomyoma:Leiomyoma:
Often arise in the uterusErector pili: skin nipples scrotum labiaErector pili: skin, nipples, scrotum, labiaSurgical removal
Leiomyosarcoma:Leiomyosarcoma:10 to 20% of soft tissue sarcomaAdult W>MAdult, W>M
Superficial or cutaneous lesion good prognosisDeep soft tissue local extension metastasisDeep soft tissue local extension, metastasis
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R fReferenceKumar Kabbas fausto: Robbins and Cotran Pathologic Basis Kumar, Kabbas, fausto: Robbins and Cotran Pathologic Basis of Disease: 7th ed
http://www pathguy com/lectures/bones htmhttp://www.pathguy.com/lectures/bones.htm