Musculoskeletal Key Concept PDF

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Musculoskeletal Key Concept Chapter 44 Bone remodeling  Bone-remodeling units  Repair of microscopic injuries and maintenance of bone integrity  Phases: o Activation of the remodeling cycle o Resorption o Formation of new bone (secondary bone) o Takes 4–6 months Joint capsule  Connective tissue covers the ends of the bones where they meet in the joint.  Is richly supplied with nerves, blood vessels, and lymphatic vessels. Glycoproteins  Are carbohydrate-protein complexes of bone.  Control collagen interactions that lead to fibril formation.  Play a role in calcification. Work function of a muscle  To accomplish work Types of muscle contraction  Excitation o Is the spread of action potential from the nerve terminal to the neuromuscular junction o Initiates an electrical impulse; muscle fiber action potential. Triggers voltage-sensitive receptors in the t-tubule wall, opening RyR channels and releasing calcium Coupling o Release of calcium leaves actin free to bind with myosin. o

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Contraction o Thin filament, actin, then slides toward the thick filament, myosin, forming a crossbridge that causes muscle to shorten (sliding-filament theory, now called the crossbridge theory). o “All or nothing” principle applies.

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Relaxation o Cross-bridge detaches, and a sarcomere lengthens as calcium is pumped back into the sarcoplasmic reticulum.

Structures of the bone  Compact bone o Also called cortical bone o 85% of the skeleton

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Solid and extremely strong Haversian system Haversian canal, lamellae, lacunae, osteocyte, and canaliculi

Spongy bone o Also called cancellous bone o 15% of the skeleton o Filled with red bone marrow o Lack Haversian system o Trabeculae: Plates or bars

Sharpey fibers  A matrix of connective tissue consisting of bundles of strong predominantly type I collagen fibers connecting periosteum to bone. Epiphyseal plate  In a child, epiphysis is separated from metaphysis by a cartilaginous growth plate; after puberty, the epiphyseal plate calcifies and the epiphysis and metaphysis merge. Stages of bone healing  Hematoma formation o Clot forms.  Procallus formation o Produces granulation tissue.  Callus formation o Forms membranous or woven bone.  Callus replacement o Replaces the callus with lamellar bone or trabecular bone.  Remodeling o Periosteal and endosteal surfaces are remodeled to the size and shape of the bone before the injury. Joint types: Diarthrosis, synchondosis, gomphosis  Synarthrosis o Immoveable  Diarthrosis o Freely moveable  Amphiarthrosis o Slightly moveable Muscle contraction: ions, process  Ryanodine receptors (RyRs): Primary ion channels that control calcium release in muscles o RyR1: Skeletal muscle o RyR2: Cardiac muscle o RyR3: Diaphragm, smooth muscle, and brain Volkmann canals  Any of the small channels in the bone that transmit blood vessels from the periosteum into the bone and that communicate with the haversian canals

Synovial fluid: types of cells, movement of synovial fluid  Superfiltrated plasma fluid.  Lubricates the joint surfaces and nourishes the pad of the articular cartilage.  Contains free-floating synovial cells and various leukocytes that phagocytize joint debris and microorganisms. Articular cartilage  The smooth, white tissue that covers the ends of bones where they come together to form joints o It allows the bones to glide over each other with very little friction Muscle fiber types  Each muscle fiber is a single muscle cell o Surrounded by a membrane capable of excitation and impulse propagation  Myofibrils o Functional units of contractions  White muscle (type II fibers): Fast  Red muscle (type I fibers): Slow  Sarcoplasm o Cytoplasm of the muscle cell  Sarcotubular system o Transverse tubules o Sarcoplasmic reticulum  Sarcomere o Portion of myofibril o Composed of proteins actin, myosin, titin, and nebulin Osteocytes/osteoclasts  Osteocytes o Bone maintenance  Develop dendritic processes that extend to either the bone surface or the bone’s vascular space.  Help maintain bone by signaling osteoblasts and osteoclasts to form and resorb bone.  Are located in the lacuna.  Coordinate osteoblast and osteoclast functions.  Respond to parathyroid hormone.  Osteoclasts o Bone resorption  Are large, multinucleated cells.  Contain lysosomes filled with hydrolytic enzymes.  Have microvilli called ruffled borders.  Are located in Howship lacunae.  Are attached to integrins by podosomes (helps bind to bone)  Osteoclasts loosen from bone surface.  Osteoclasts become inactive and rest.

Chapter 45 Fracture types  Complete: Bone is broken all the way through.  Incomplete: Bone is damaged but still in one piece. o Closed or simple (complete or incomplete): Skin is intact. o Open or compound (complete or incomplete): Skin is broken.  Comminuted o Bone breaks into more than two fragments.  Linear o Fracture runs parallel to the long axis of the bone.  Oblique o Fracture of the shaft of the bone is slanted.  Spiral o Encircles the bone.  Transverse o Occurs straight across the bone.  Greenstick o Perforates one cortex and splinters the spongy bone.  Torus o Cortex buckles but does not break.  Bowing o Longitudinal force is applied to a bone.  Pathologic o Break occurs at the site of a preexisting abnormality.  Stress o Fatigue and insufficiency o Transchondral Joint dislocations  Temporary displacement of bone from its joint Tendon: injury, function Bone loss: menopause, age-related  Markedly increased bone resorption leads to the initial fall in bonemineral density.  With increasing age, there is also a significant reduction in boneformation. Inflammatory Joint Disease  RA Osteoporosis: types  Perimenopausal  Iatrogenic  Regional

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Postmenopausal Glucocorticoid-induced

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Age-related bone loss

Myoglobinuria: Crush syndrome  A medical condition characterized by major shock and kidney failure after a crushing injury to skeletal muscle.  Rhabdomyolysis o Life-threatening complication of severe muscle trauma with muscle cell loss  Crush syndrome vs. crush injuries  Compartment syndromes o Rapid breakdown of muscle that causes the release of intracellular contents  Protein pigment myoglobin into extracellular space and bloodstream o Classic triad  Muscle pain, weakness, and dark urine (from myoglobin) o Treatment  Rapid intravenous hydration: To maintain adequate kidney flow  Hyperkalemia: May require temporary hemodialysis. Osteomyelitis  Is usually caused by a Staphylococcus aureus infection.  Is often outside the body (exogenous); can be from a bloodborne (endogenous) infection.  Infection spreads under the periosteum and along the bone shaft or into the bone marrow. o In adults: Affects the cortex o Sequestra: Sections of dead bone from periosteal separation o Involucrum: Periosteal new bone  Acute vs. subacute vs. chronic  Clinical manifestations o Acute and chronic inflammation, fever, pain, necrotic bone  Treatment o Antibiotics, débridement, surgery, hyperbaric oxygen therapy Osteosarcoma  38% of bone tumors  Predominant in adolescents and young adults; occurs in seniors with a history of radiation therapy  Contain masses of osteoids: Bone-forming tumors o Streamers: Noncalcified bone matrix and callus  Location: In the metaphyses of the long bones o 50% occur around the knees  Clinical manifestations o Pain and swelling  Treatment o Systemic chemotherapy and surgery

Joint disease/stiffness  Arthritis OA  Common age-related disorder of synovial joints  Inflammatory joint disease  Loss of articular cartilage, sclerosis of underlying bone, and formation of bone spurs (osteophytes)  Also called degenerative joint disease.   

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Incidence increases with age Local areas of damage and loss of articular cartilage, new bone formation of joint margins, and thickening of joint capsule Clinical manifestations o Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity o Joint swelling in the fingers: Heberden and Bouchard nodes o Joint effusion: Exudate or blood entering the joint Treatment o Rest of involved joint until inflammation subsides o Aerobic exercise and range-of-motion exercise o Cane, braces, walker o Weight loss, if obese o Balanced diet o Analgesic and antiinflammatory drug o Magnetic bracelets and acupuncture o Intraarticular injection of high-molecular-weight viscosupplements, particularly hyaluronic acid o Surgery: Joint replacement

Ankylosing spondylitis  Chronic inflammatory joint disease of the spine or sacroiliac joints, causing stiffening and fusion of the joints  Unknown cause but strong association with human leukocyte antigen B27 (HLA-B27)  Affects peripheral joints of appendicular skeleton.  Clinical manifestations o Low back pain, stiffness, pain, and restricted motion, o Loss of normal lumbar curvature  Kyphosis o Chest pain/restricted chest movement o Fibrotic changes to organs Gout   

Is a metabolic disorder that disrupts the body’s control of uric acid production or excretion. o Exhibits high levels of uric acid in the blood and other body fluids. Occurs when the uric acid concentration increases to high enough levels to crystallize. Crystals deposit in connective tissues throughout the body.

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o If prolonged in joints: Gouty arthritis o Tophi: Small, white visible nodules Related to purine metabolism Causes o Purine synthesis or breakdown is accelerated. o Poor uric acid secretion in the kidneys Mechanisms for crystal deposition o Low body temperatures o Decreased albumin or glycosaminoglycan levels o Changes in ion concentration and pH o Trauma Primary vs. secondary Clinical stages o Asymptomatic hyperuricemia  Urate level is high with no symptoms. Acute gouty arthritis o Attacks develop. Tophaceous gout o Urate crystal deposits (tophi) appear in cartilage, synovial membranes, tendons, and soft tissues. Clinical manifestations o Pain in the great toe (usually, but not always): Worse at night o Increase in serum urate concentration: Hyperuricemia o Recurrent attacks of monoarticular arthritis: Inflammation of a single joint o Deposits of monosodium urate monohydrate (tophi) in and around the joints o Renal disease, involving glomerular, tubular, and interstitial tissues and blood vessels o Formation of renal stones Treatment o Pharmacological/nonpharmacological o Avoidance of weightbearing o Weight reduction o Avoidance of alcohol o Dietary changes

Fibromyalgia  Chronic widespread joint and muscle pain, fatigue, and tender points  Link between inflammatory process and FM  WPI and SSI for diagnosis o WPI of at least 7 and SSI of at least 5 o WPI of 3–6 and SSI of at least 9  Clinical manifestations o Vague symptoms o Increased sensitivity to touch, absence of inflammation, fatigue, nonrestorative sleep, depression, anxiety

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Treatment o Medications that improve sleep and vitamin D supplementation: May be helpful o Pregabalin o Combination of modalities, including education, medication, exercise, and cognitivebehavioral therapy

Rheumatoid arthritis  Rheumatoid arthritis (RA): Inflammatory joint disease  Systemic autoimmune destruction to synovial membrane and joints  Presence of rheumatoid factors (RFs): RA or RF test o Antibodies (immunoglobulin G [IgG] and IgM) against antibodies; sometimes IgA  Joint fluid with inflammatory exudate  Rupture of cyst or synovial joint  Clinical manifestations o Symmetric joint swelling, joint deformities o Systemic manifestations of inflammation o Rheumatoid nodules in organs o Caplan syndrome

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o Painful, tender, stiff joints Treatment o Disease-modifying antirheumatic drugs (DMARDs) such as methotrexate (MTX, first line), azathioprine, sulfasalazine, hydroxychloroquine, leflunomide, and cyclosporine o Biological DMARDs (bDMARDs): Medications affect specific processes in the development of RA, such as TNF. o Education o Nonsteroidal antiinflammatory drugs (NSAIDs), glucocorticoids, intraarticular steroid injections o Physical and occupational therapy with therapeutic exercise and use of assistive devices o

Surgery: Synovectomy or joint replacement

Chapter 46 Creatinine: total muscle mass  Between birth and maturity, muscle nuclei in the body increase 14 times in boys and 10 times in girls.  Composition and size of muscles vary with age. o Growth in length occurs at the ends of muscles. o Increase in length is accompanied by an increase in the number of nuclei in the fibers. o Muscle fibers increase in diameter as the fibrils become more numerous. o Fibrils themselves do not increase in diameter.  Infants o Muscle: Approximately 25% of the total body weight (40% in adults) is in muscle. o Majority of weight: Is in the axial musculature (55% in an adult’s lower limbs).

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Respiratory and facial muscles are well developed at birth.  For breathing and sucking Other muscle groups, such as the pelvic muscles, take several years to develop.

Bone growth: physeal plate  Until adult stature is achieved, bone growth occurs at the physeal plate through endochondral ossification.  Bone is being constantly destroyed and re-formed.  Epiphyseal closure o Unites the metaphysis and the epiphysis. o Occurs earlier in girls than in boys because of earlier puberty in girls. Skeletal deformities of the newborn: hip  Developmental dysplasia of the hip o Formerly: Congenital dislocation of the hip o Abnormality of the proximal femur, acetabulum, or both o Risk factors  Family history, female, metatarsus adductus, torticollis, oligohydramnios, first pregnancy, breech presentation o Subluxated or dislocated or acetabular dysplasia o Clinical manifestations  Asymmetry of gluteal or thigh folds  Limb length discrepancy: Galeazzi sign  Limitation of hip abduction  Positive Ortolani sign: Hip dislocated but reducible  Positive Barlow maneuver: Hip reduced but dislocatable  Positive Trendelenburg gait: Waddling  Pain: Very late o Treatment  The earlier the treatment is begun—usually before 1 year of age—the better the result.  In children younger than 4 months of age: Pavlik harness  Up to 12 months of age: Closed reduction (without opening the joint), followed by spica or body casting for up to 3 months  After 12 months of age: Surgical intervention, including opening the joint and cutting and realigning the femur and/or acetabulum  As the child ages: Failure of good outcomes  Up to 70% of children treated surgically after 3 years of age develop early osteoarthritis Congenital skeletal defects  Syndactyly

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o Webbing of the fingers o Fusion of the soft tissues of the fingers o Complex syndactyly: Also includes fusion of the bones and nails Vestigial tabs o Extra digit

Osteogenesis imperfecta  “Brittle bone” disease  Defect in bone and/or vessel collagen production  Sillence classification o Types I through IV, based on severity  Results in osteoporosis, increased rate of fractures, bony deformation, triangular facies, vascular weakness, blue sclera, poor dentition  Treatment o Prompt fracture care, careful handling and positioning, telescoping rods, bisphosphonate therapy, genetic counseling Vitamin related bone deformities  Rickets Scoliosis: structural  Curvature associated with vertebral rotation  Skeletal abnormalities, neuromuscular disease, trauma, extraspinal contractures, bone infections of the vertebrae, metabolic bone disorders, joint disease, and tumors Juvenile idiopathic arthritis  Juvenile idiopathic arthritis (JIA): Childhood form of rheumatoid arthritis  Basic pathophysiology: Same as adult form  One difference: Mode of onset o Fewer than five joints: Pauciarticular arthritis o More than five joints: Polyarticular arthritis o Systemic: Still disease Differences in JIA and adult rheumatoid arthritis (RA) o Large joints are affected. o Spinal changes include subluxation and ankylosis of the cervical spine. o Joint pain is not as severe. o Antinuclear antibody test is positive. o Chronic uveitis is common. o Rheumatoid factor is seldom detected. o Rheumatoid nodules are common in the heart, lungs, eyes, and other organs. o Is positive for cyclic citrullinated peptide antibody. o Treatment: Supportive, biologics Osteochondrosis  Avascular diseases of the bone; insufficient blood supply to growing bones o Several types  Osgood-Schlatter (tibial tubercle) 

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 Sinding-Larsen-Johansson (distal patellar pole)  Panner (radial head)  Kohler (navicular bone of the foot)  Sever (calcaneus) Activity-related pain of the affected region that improves with rest Treatment  Antiinflammatory medications  Modification of activities and even immobilization  Reparative correction by revascularization

Rickets  Disorder causing mineralization failure, “soft” bones, and skeletal deformity  Causes o Insufficient vitamin D o Insensitivity to vitamin D o Renal wasting of vitamin D o Inability to absorb calcium or vitamin D in the gut  Clinical Manifestations o Short stature o Bowing of the limbs with hypotonia and muscle weakness  Treatment o Calcium, phosphorus, and vitamin D levels must be optimized before surgical intervention Osgood-Schlatter disease  Tendinitis of the anterior patellar tendon and osteochondrosis of the tubercle of the tibia  Mild tendinitis to a complete separation of the anterior extension of the tibial epiphysis  Clinical manifestations o Pain and swelling in the affected area, becoming prominent and tender to direct pressure, especially after physical activity  Treatment o Restriction from strenuous physical activity: 4–8 weeks o If pain relief is not achieved: Cast or brace o Return to unrestricted athletic participation: Another 8 weeks Cerebral palsy: Diagnosis  Nonprogressive disorder of movement and posture caused by injury or malformation of developing CNS.  Disease patterns o Hemiplegia, diplegia, quadriplegia  Clinical manifestations o Motor milestones are not met  Treatment o No cure: Multidisciplinary approach; surgery

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Physical and occupational therapies, orthotics, spasticity reduction (selected dorsal rhizotomy, baclofen), botulinum-A (Botox) toxin injections

Osteosarcoma  Originates from bone-producing mesenchymal cells.  Makes osteoid tissue.  Deletion of genetic material on the long arm of chromosome 13  Most occurring between 10 and 18 years of age  Clinical manifestations o Pain  Treatment o Surgery and multiagent chemotherapy o Radiation Osteomyelitis  Infection in the bone o Is often associated with septic arthritis because an infant’s bone has blood vessels that perforate the growth plate. o Begins as a bloody abscess in the metaphysis of the bone.  Vertebrae may be involved in adolescents and adults. o These age groups are affected less often than younger populations.  Infection spreads under the periosteum and along the bone shaft or into the bone marrow. o Sequestra  Sections of dead bone from periosteal separation o Involucrum  Periosteal new bone o Secondary septic arthritis  Pus of ruptured joint causes inflammation  Clinical manifestations o Infants  Fever and failure to move the affected limb (pseudoparalysis) o Children  Fever and systemic signs of toxicity  Swelling, fever, tenderness, and decreasing ability to bear weight on or move the affected area  Onset can be abrupt. o Adolescents o Back pain for several weeks: May be the only complaint. 

Treatment o Intravenous (IV) antibiotics or, in highly reliable children and families, a combination of IV and oral antibiotics for 6 weeks o Drainage and margination of bone: For abscess o Immobilization: Pain control

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If a joint is infected (septic arthritis): It is a surgical emergency: Lysozymes released from the involved neutrophils cause damage to the articular cartilage.

Ewing sarcoma  Malignant round cell tumor of...