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Diseases of the Musculoskeletal System Chapter 37.

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Presentation on theme: "Diseases of the Musculoskeletal System Chapter 37."— Presentation transcript:

1 Diseases of the Musculoskeletal System Chapter 37

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6 Skeletal Skeletal trauma/fractures –Incidence Young males and older adults Tibia, clavicle, lower humerus (young persons) Hands, feet -- workplace accidents Upper femur, upper humerus, vertebrae, pelvis (elderly) –Osteoporosis –Diff types (complete/incomplete, open/closed) Incomplete -- bones of children –Flexible –Growing Stress w/ repeated stress (ex athletics) –Fatigue –Insufficiency (weight bearing bones)

7 - Pathophysiology Healing similar to soft-tissue injuries stages –No scar tissue Periosteum, blood vessels disrupted Bleeding  clot form = n (hematoma) Stages –Hematoma –Procallus form = n »Intense inflammatory response »Fibroblasts, collagen, growth factors, osteoblasts impt –Callus »Hardened membr (woven bone) –Remodeling »Osteoclasts;  original shape »Resorption unneeded callus

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9 –Clinical Signs/symptoms –Impaired function –Unnatural alignment; possible rotation, angulation –Swelling –Tenderness –Severe pain (trauma, muscle spasm) Stress fractures -- pain with accelerated remodeling –Relieved by rest –Treatment Realign to normal position (manipulation, traction) Surgery –Prosthesis, screw, plate, etc., possible Splints, casts

10 Metabolic bone disease (Osteoporosis) –remodeling imbalance favors bone resorption –Incidence Common disorder of bone metabolism Heredity evidence in women –Fracture due to bone weakness Common -- vertebrae, distal radius, proximal femur Fractures after trauma Compression fractures (esp vertebral) –Non-symptomatic until indicated by fracture

11 –Pathophysiology Age  –Bone resorption exceeding bone growth –  Net bone mass loss –More rapid in women »Exaggerated at menopause »Type I (Postmenopausal) –Type II C both sexes over age 70 »Neck, hip, humerus, tibia May involve postaglandins, interleukins, various growth factors that affect osteoclasts Estrogen decr w/ menopause  incr = d risk –Estrogen inhibits bone resorption –Also in young, female athletes »Training  decr = d estrogen »Found decr = d bone mass, incr’d fractures

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13 –Clinical Pain Bone deformity Fractures Vertebral collapse  hunchback, decr = d height –Treatment C slow rate of Ca, bone loss Incr dietary Ca Vit D  incr intestinal abs = n Ca Regular, moderate exercise Hormone treatment (estrogen, progesterone) Reduce risk of falls

14 Bone tumors –Common secondary tumor site Primary often prostate, breast, thyroid, lung, kidney Access through blood Often axial skeleton (not skull), proximal femur, humerus May induce bone breakdown or bone growth

15 –Primary tumors less common Actively growing bone Pain early indication May  bone weakening Pressure  adjacent bone deformed by abnormal remodeling Metastasis often to lung Most more in males than females –About 1/3 primary tumors benign Ex: osteoma of skull and osteoid osteoma of long bone Ex: chondroblastoma –Arises in cartilage of epiphyses of arm, leg bones –Rare

16 –Malignant bone tumors Osteogenic sarcoma (=osteosarcoma) most common –Usually age years –Knee often –Common metastasis  lung –Previous metastasis by time of diagnosis  poor prognosis –Now better chemotherapy (80% 5 yr recovery rate) –Surgery often Chondrosarcoma –Usually age yrs –Slow-growing –May break through bone surface –Interior of pelvis, ribs, prox femur, humerus –Surgical excision

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18 Diseases of the Joints Osteoarthritis = Degenerative Joint Disease –Incidence Most common joint disease in US Incr = s w/ age –Age most affected –> 75 yrs -- 85% affected –Pathophysiology Articular cartilage becomes thin, irregular, frayed –Probably enz breakdown of cartilage  Cracks, fissures in articular cartilage –Fill w/ synovial fluid

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20 –Pathophys (cont’d) Penetrates to underlying bone w/ progression –May  fluid-filled cysts –Bone forms around cysts –May  microfractures Fibrocartilage plugs form for repair –Activyt  plugs stripped away, then reformed, then restripped –  Smooth bone surface Fibrocartilage fragments may react at synovial membr surface –  inflamm response C > repair –  decr = d movement Cells in synovial membr may dev into osteoblasts –  form = n bone spurs at joint –  pain, decr = d movement

21 –Degeneration Mostly at larger weight-bearing joints (also fingers) Related to –Wear-and-tear OR –Biochem defect in joint cartilage OR –Excessive loading (malformed joint, postural defect, obesity) OR –Genetic –Clinical Joint aches, stiffness –Incr w/ activity; diminish w/ rest Progression w/ age Loss of mobility if hip, knee affected –Therapy limited Analgesics for pain Reduce obvious stresses Surgical removal of bone spurs or artificial joint replacement

22 Rheumatoid arthritis C systemic disease involving joints –Incidence About 1% adult pop = n affected 3 female: 1 male Age of onset usually (but also infancy  90's) May be due to –Infection –Autoimmune disorder –Genetic predisposition

23 –Get immune-mediated destruction of joints Environmental stimulus  immune response to Ag If predisposed, Ab = s transform to A rheumatoid (Rfs) Rfs complex in blood, synovial fluid  inflamm response at joint Inflamm mediators breakdown joint tissue  joint tissue destroyed

24 –Get pattern of chronic inflamm = n Incr = d number of cells in synovium  Thickening of synovium (maybe after cartilage destroyed by inflamm = n process) Thickened synovium covers adjacent joint surfaces –Over time may enlarge, fill joint space –In late stage = ankylosis = fused joint Causes swelling; stiffness; pain Swelling also due to incr = d exudate in synovial membr –Joint deformities  Loss of joint motion  Muscular atrophy

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26 –Sytemic effects variable Generalized weakness, malaise Rheumatoid nodules form –Focal subcu swelling –Elbow, heel, dorsal surface of head; also internal –Made of macrophages, lymphocytes, collagen, cell debris –Typically painless Rheumatoid vasculitis common –Systemic inflamm = n of blood vessels –May involve pericardium, pleural effusion –Therapy C no cure; can’t reverse destruction of structures Relieve pain, reduce swelling (antiinflammatories) Reduce stress Strengthen assoc = d muscles Replace severely effected joints

27 Diseases of Skeletal Muscle Disuse atrophy –Pathologic reduction in size of muscle fibers Follows prolonged bed rest, trauma, nerve damage –Muscle strength decr = s from baseline About 3% per day –To prevent Frequent isometric muscle contractions Passive lengthening exercise –If no reuse in 1 year, regen = n muscle fibers impaired

28 Fibromyalgia –Chronic musculoskel syndrome –Get diffuse chronic pain, tenderness w/ no inflamm = n, fatigue 9 common points in body (neck, shoulders, hips, knees) Profound fatigue May  depression Also migraine, irritable bowel disease common –Incidence Mostly women Peak age = yrs Increases w/ age

29 –Probably several causes virus, Phys/emotional trauma, emotional trauma, medication –Found metab alterations in muscle May  pain, fatigue –Also found diff blood flow to thalamus May C > chronic stress response –Treatment Antiinflammatories (not very effective) CNS active agents somewhat helpful

30 Muscle Strains –Gen’l term for muscle damage –Seen after traumatic, sports injuries Sudden, forced motion Muscle becomes stretched beyond normal length May include wounds –Often involves tendon also –May include hemorrhage, inflamm = n –Muscle cells usually regenerate in up to 6 weeks –Treatment Ice relieves swelling Analgesics Alternating heat/cold if more severe form Surgery, immobilization if tearing, bleeding

31 Musculoskeletal Disorders May accompany fractures, dislocations Ligament = fibrous connective tissue band joining joint –Needed to support bones, joints Strain = tear in tendon –May be due to major trauma –Also spontaneous w/ corticosteroid admin, rheumatoid arthritis, lupus

32 –Common sites Tendons of hands, feet Knee Upper arm - w/ lifting excess wt Thigh Ankle Heel - w/ forced flexion Sprain = tear in ligament –Common sites Wrist Ankle Elbow Knee

33 –Avulsion = total sep = n tendon/ligament from bone Due to abnormal stress Young athletes (sprinters, hurdlers, runners) –Pathophysiology Tearing  inflamm response Exudate torn ends Macrophages, fibroblasts Repair –Collagen form = n random, then organized –Vascular fibrous tissue fuses new, old tissues –Healing tendon separates from surrounding soft tissue –Can = t support strong pull for 4-5 weeks

34 Clinical –Pain C sharp, localized –Soft-tissue swelling –Joint swelling –Flexion deformities –If in extremities, motion affected Treatment –Suture tendon/ligament –Tendon/ligament grafting


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