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MUSCULOSKELETAL FUNCTION
Characteristics
Axial skeleton includes skull, thorax, vertebral column Appendicular skeleton consists of upper/lower extremities, shoulder, hip Two types of connective tissue are included: cartilage and bone Both include living cells, nonliving intercellular protein fibers and amorphous ground substance Tissue cells secrete and maintain intercellular substances, e.g. calcium salts Collagen(tensile strength) and elastin(stretch)
Cartilage
Firm but flexible connective tissue consisting of cells and intercellular fibers embedded in amorphous gel-like material; smooth, resilient surface and weight-bearing Essential for growth before and after birth Postnatal, cartilage plays a role in growth of long bones and persists as articular cartilage Elastic(ear),hyaline(most abundant,epiphyseal plates), fibrocartilage(intervertebral discs)
Bone
Intercellular matrix impregnated with inorganic calcium salts Organic matter 1/3 Inorganic salts 2/3 Can take up lead and antibiotics Cancellous(spongy) Compact(cortical)
Osteogenic Cells
Found in periosteum, endosteum, epiphyseal plate of growing bone Active during normal growth, during fracture healing, replacement of worn-out bone tissue Both periosteum and endosteum contribute to growth and remodeling of bone and are necessary for repair
Bone Cells
Osteoblasts
Bone building cells are responsible for formation of bone matrix Two stages include ossification and calcification Secrete alkaline phosphatase
Osteocytes
Mature bone cells actively involved in maintaining the bony matrix
Osteoclasts
Responsible for the resorption of bone matrix and release of calcium and phosphate from bone
Classification of Bones
Long(arm), short(ankle), flat(skull), irregular(jaw) Bone marrow occupies medullary cavity of long bones and cancellous bone in vertebrae, ribs, sternum and pelvis; composition varies with age and site Red bone marrow contains developing RBC, gradually replaced with . . . Yellow bone marrow composed of adipose tissues Red persists in vertebrae, ribs, sternum and ilia
Diarthroidial Joints
Little movement, sacroiliac Hinge, interphalangeal Many planes-hip Frequently affected by rheumatic disorders Articular cartilage is hyaline and heals slowly(diffusion)
Blood supply to synovial membrane rich healing and repair rapid and complete; innervated only by autonomic fibers, relatively free of pain fibers local anesthesia As a rule, each joint of an extremity in innervated by all the peripheral nerves that cross the articulation referral of pain from one joint to another Synovial membrane can form closed sacs that are not part of joint-bursae. Prevents friction on tendon. Bunion is inflamed bursa of metatarsophalaneal joint of great toe
Knee Injuries
Subject to abnormal twisting and compression Menisci are C-shaped plates of fibrocartilage superimposed on condyles of tibia and femur; stabilize, lubricate and load bear Cruciate ligament secures femur to tibia in crossed position. Controls flexion and lateral rotation. ACL is weaker-often injured. Immediately disabling Patellar subluxation and dislocation
Hip Injuries
Ball/socket joint in which femoral head articulates deeply in acetabulum; vascular anatomy of femoral head is critical - viability of femoral head may lead to avascualar necrosis. Fractures
Major public health problem; falls most common cause Categorized by location; 90% are femoral neck and intertrochanteric fractures Location important to blood flow
Fractures
Sudden injury Fatigue or stress Pathological (10-15% of patients with metastatic disease Classified according to location, type, and direction or pattern of fracture line (see figure 42-5)
HEMATOMA FORMATION
Hematoma facilitates the formation of the fibrin meshwork that seals off fracture site and serves as a framework for the influx of inflammatory cells, fibroblasts, and new capillary buds.
Fibrocartilaginous cartilage converted to bony callus. Newly formed osteoblasts first deposit bone on outer surface of bone and then move toward fracture site. Begins 3-4 weeks after injury. USUALLY SAFE TO REMOVE CAST
REMODELING Dead portions of bone are removed by osteoclasts and compact bone replaces spongy bone; reorganization of mineralized bone occurs along lines of mechanical stress. Resembles original unbroken bone but thickened area remains as evidence of healed fracture.
Fat Embolism
FES refers to a constellation of clinical manifestations resulting from fat droplets in small blood vessels of lung or other organs after a long bone fracture or other major trauma. Released from bone marrow or adipose tissue at fracture site into venous system; rare Respiratory failure, cerebral dysfunction and skin petechiae(does not blanch); symptoms within a few hours to 3-4 days. Initial findings subtle change in behavior and disorientation Stabilize fractures early
Osteomyelitis
Acute or chronic infection Direct contamination, seeding through bloodstream(hematogenous), vascular insufficiency Staphylococcus most commonproduces a collagen binding adhesion molecule allowing it to adhere to connective tissue elements of bone and ability to internalize and survive in osteoblasts making the microorganism resistant to antibiotics Sequestrum-infected dead bone separated from living bone
Osteonecrosis
Death of bone segment caused by interruption of blood supply to marrow, medullary bone, or cortex; proximal femur, distal femur and proximal humerus Common complicating disorder of sickle cell disease, steroid therapy(5-25%), and hip surgery Results from ischemia but mechanisms vary; steroids unclear may increase intraosseous pressure with vascular compression, sickle cell thrombosis
Neoplasms
Benign include osteoma, chrondroma, osteochrondroma, and giant cell Osteosarcoma-peak during teens, bones with maximum growth velocity;localized pain and swelling Ewings sarcoma Metastatic-skeletal metastases are most common malignancy of osseous tissue:spine, femur, pelvis, ribs, sternum, humerus, skull Breast, lung, prostate, kidney and thyroid are most common. 50% of bone must be destroyed before lesion is visible on plain radiograph
Osteoporosis
Classified as primary(postmenapausal women or elderly) or secondary(endocrine or genetic disorder) Enhanced bone resorption relative to bone formation; varies with age, sex, nutritional status and genetic predisposition Maximal bone mass achieved at 30; loss is 1%/year in menopausal women; AA less prone than caucasians/Asians Greatest losses occur in areas containing abundant cancellous bone such as spine and femoral neck Alcohol is a direct inhibitor of osteoblasts and may also inhibit calcium absorption. Prolonged use of medication that increases calcium excretion such as antacids and anticonvulsants Premature and low birth weight infants at risk Female athletes- poor nutrition, amenorrhea, estrogen lack
Osteoporosis
Changes occur in the diaphysis and metaphysis of the bone; diameter of bone enlarges causing the outer supporting cortex to thin; resembles porcelain vase First manifestations are pain accompanied by skeletal fractures-vertebral compression, hip, pelvis, humerus Fractures represent end stage of disease Wedging and collapse of vertebrae causes height loss and kyphosis(hump) Monitor with bone mass density studies Prevention and early detection critical:Regular exercise and 1500 mg calcium in post menopausal women
Rheumatoid Arthritis
Systemic inflammatory disease that attacks joints by producing proliferative synovitis that leads to destruction of articular cartilage and underlying bone 0.3-1.5% of population; women 2-3X Cause not established; genetic predisposition and immunologically mediated Pathogenesis is an aberrant immune response that leads to synovial inflammation and destruction of joint architecture May be initiated by activation of CD+4 helper T cells, release of cytokines and antibody formation 70-80% have rheumatoid factor (RF) autoantibody Joint and extra-articular manifestations
Osteoarthritis(OA)
-Formerly DJD; most prevalent form and leading cause of disability and pain in elderly -Primary or secondary -Progressive loss of articular cartilage and synovitis result from inflammation caused when cartilage attempts to repair itself -Creates osteophytes or spurs which cause joint pain, stiffness, and loss of motion
Pathogenesis of OA
Resides in the homeostatic mechanism that maintains the articular cartilage Plays two roles: (1) smooth weight bearing surface and (2) transmits the load down to the bone dissipating mechanical stress Composition and mechanical properties of cartilage are changed Chemical messengers such as cytokines stimulate production and release of proteases that are destructive to joint structure, more injury results and repair mechanism is inadequate; portions become completely eroded and synovial membrane inflammation
Ankylosing Spondylitis, Gout, and Osteomalacia will not be covered on the exam