Review of Musculoskeletal System
Chapter 36
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Skeletal System
• Function:
– Protection – Hematopoiesis – Mineral homeostasis • Calcium • Phosphorus • Carbonate • Magnesium
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Structure
• Bone is a connective tissue:
– Matrix • Collagen fibers for flexibility and tensile strength • Calcium for rigidity • Hydroxyapatite Ca5(PO4)3OH
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• Cells:
– Osteoblast
• Form organic components of matrix
– Osteocyte – Osteoblasts
• • • • • From monocytes Secrete citric and lactic acids Collagenases and other enzymes Stimulated by PTH Inhibited by Calcitonin
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Types of Bone
• Dense or Compact (85%)
– Osteon (Haversian System) – Central (Haversian) canal – Lamellae – Lacunae with osteocytes – Canaliculi
• Spongy (cancellous) bone (15%)
– trabeculae
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Periosteum
• Outer layer is dense, irregular CT with nerves and blood vessels • Inner layer
– Osteoblasts – Anchored to bone by collagen fibers that penetrate into bone
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Bone Formation
• Endochondral ossification
– Inside hyaline cartilage – Most bones
• Intramembranous ossification
– Forms directly inside membranes – Bones of skull
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Growth
• Lengthening of bones at epiphyseal plate
– Grows from cartilage
• Forms epiphyseal line when done growing • Undergoing constant remodeling
– Adaptation to stress – Healing
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Skeleton
• 206 bones • Axial skeleton
– Skull and hyoid – Vertebral column – Ribs and sternum
• Appendicular skeleton
– Shoulder girdle – Pelvic girdle
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Classification
• Long bones: – Diaphysis – Epiphysis – Metaphysis – Medullary cavity – Endosteum
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Classification cont.
• • • • • Short bones Flat bones Irregular bones Sesamoid bones Wormian bones
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Joints
• Degree of movement – Synarthrosis – immovable joint – Amphiarthrosis – slightly movable joint – Diarthrosis – freely movable joint
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• Synovial joints – Joint capsule • Fibrous CT • Tendons and ligaments • Nerves, blood and lymph vessels – Synovial membrane • Loose fibrous CT • Many blood vessels – good repair – Joint (synovial) Cavity
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• Synovial fluid – Plasma filtrate – Synovial cells and leukocytes phagocytize debris and microbes • Articular cartilage – Reduce friction – Distribute force
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Bone Pathophysiology
• Inherited conditions:
– Osteogenesis imperfecta • Inherited defect in collagen synthesis • Osteopenia and brittle bones • Often- defective tooth formation, blue sclera, faulty hearing • Inheritance can be dominant, recessive or by new mutation • Several degrees of severity
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• Achondroplasia
– Involves a defect in normal cartilage development – Epiphyseal plates close early in long bones; individual has short arms and legs, but normal spine and skull – Dominant inheritance, but frequent new mutations – Other organs develop normally – Individuals live a normal lifespan
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Acquired disorders
• Osteoporosis – “porous bone”
– Most common metabolic bone disease in North America – Can be attributed to genetics, diet or hormones – Most osteoporosis is idiopathic osteoporosis – Bone loss due to an identifiable cause is secondary osteoporosis – Bone tissue is mineralized normally, but over time the structural integrity of bone is lost and it becomes thinner and weaker, and more prone to fractures.
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• Key features: bone fracture and the associated pain. • WHO defines osteoporosis by bone density:
– Normal bone > 833 mg/cm2 – Osteopenia 833 to 648 mg/cm2 – Osteoporosis < 648 mg/cm2
• Can be generalized, involving major portions of the axial skeleton • Can be regional, involving one segment of the appendicular skeleton
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• Remodeling is constant
– Teen years more bone is laid down than reabsorbed – Peak bone mass or maximum density reached at around 30 years of age – After age 30, bone is reabsorbed faster than it is laid down – In women, bone loss is most rapid in the first years after menopause, but continues throughout postmenopausal years – Est. 55% of people over 50 have osteoporosis or low bone mass.
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• Men also lose bone density, but start out with more bone mass so takes longer. • By age 90 about 17% of males have had a hip fracture, vs. 32 % of females • Vertebral fractures also occur → kyphosis • Most common in whites, but affects all races. • African Americans have about half the fracture rates of whites (higher peak bone mass)
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Risk factors
• • • • • • • • • Family history White race Increased age Female sex Small stature Fair or pale skin Thin build Early menopause (natural or surgical) Late menarche
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Risk factors cont.
• • • • • • • • • • Nulliparity Obesity Weight below a healthy range Acidosis Low dietary calcium and vitamin D High caffeine intake Sedentary life style Smoker Excessive alcohol consumption Liver, kidney disease, rheumatoid arthritis, etc.
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• Often progresses silently for decades until fracture occurs • Bones can fracture spontaneously • Most severe in spine, wrist and hips • Estrogens and androgens may be factors in both sexes
– Testosterone is converted into estrogen in peripheral tissues and decreases bone loss
• Rapid bone loss is osteoclast mediated • Slow bone loss is osteoblast mediated
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Clinical manifestations
• • • • Pain and bone deformity Kyphosis caused by vertebral collapse Fractures of long bones Fatal complications include fat or pulmonary embolism, pneumonia, hemorrhage and shock • 20 % die as a result of surgical complications
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Treatment
• No known cure • Slow bone loss and promote bone deposition • Calcium and vitamin D supplements • Calcitonin • Hormone replacement therapy • Biophosphates – inhibit osteoclasts • Dual x-ray absorptiometry for diagnosis • PREVENTION
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Prevention
• Intake of calcium, vitamin D, magnesium and possibly boron • Regular, weight-bearing exercise • Avoid tobacco and glucocorticoids • No alcoholism • Hormone replacement? • Parathyroid hormone? • Testosterone for men and possibly women
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Rickets and Osteomalacia
• Inadequate mineral deposition in essentially normal organic matrix • Softened bone:
– Subject to malformation and distortion –pain
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Rickets
• Dietary vitamin D deficiency causes inadequate mineralization of the developing skeleton in infants and children • Rarely seen in Western nations
– Poverty – Ignorance
• Bones are soft and easily deformed • Tendency to fractures • Therapy: supply vitamin D and calcium
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Osteomalacia
• Rarely due to vitamin D deficiency • Usually GI malabsorption, renal defect or chronic kidney or liver diseases. • Elderly often affected due to inadequate diet or lack of outdoor activity • May accompany and complicate osteoporosis.
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Joint Disorders
• Osteoarthritis
– Most common joint disease in North America – Minimal inflammatory component – Differentiated from inflammatory disease by:
• Absence of synovial membrane inflammation • Lack of systemic signs and symptoms • Normal synovial fluid
– Much of the pain and loss of mobility associated with aging.
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Osteoarthritis
• Incidence increases with age: 85% of people age 65 have some joint degeneration • Incidence similar, but women more severely affected • Exceptional stress on joints: gymnasts, etc. • Biochemical defect in cartilage • Malformed joint, obesity and postural defects • Genetic component • Torn ACL or meniscectomy
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Osteoarthritis
• When associated with known risk factors it is secondary OA • No risk factors – idiopathic OA • Pathological characteristics:
– Erosion of the articular cartilage – Sclerosis of subchondral bone – Formation of bone spurs or osteophytes
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Osteoarthritis
• Begins in articular cartilage
– Yellow-grey or brownish gray – Thin, irregular, frayed – Cracks or fissures develop (fibrillation) – Fluid filled cysts may form – Microfractures of subchondral bone – Formation of fibrocartilage repair plugs – Bone surface exposed – Bone responds by becoming dense and hard
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Osteoarthritis
• Synovial membrane is indirectly affected
– Fragments of fibrocartilage cause inflammation –pain – Fibrous repair of joint capsule restricts motion – Osteophytes form – pain and loss of motion • Joint mice
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Osteoarthritis
• Affects one or more weight-bearing joints
– Hand, wrist, lower cervical spine, lumbar spine and sacroiliac, hip, knees, ankles, feet
• Aches and stiffness
– Symptoms increase with activity; diminish with rest
• Usually no swelling or redness of adjacent tissues • Sometimes nocturnal pain – may be referred
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Osteoarthritis
Primary signs and symptoms of joint disease are: pain, stiffness, enlargement or swelling, tenderness, limited range of motion, muscle wasting, partial dislocation, and deformity
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Osteoarthritis
• Evaluation made through clinical assessment and radiologic studies, CT scan, arthroscopy and MRI • Treatment: • Glucosamine may decrease pain and slow or stop progression – 1500 mg/day • Chondroitin sulfate – questionable absorption
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Osteoarthritis
• Analgesics and antiinflammatory drugs • Range of motion exercises • Reduce aggravating factors
– Weight loss – Use of cane, crutches or walker
• Surgical removal of bone spurs • Replacement of joint
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Rheumatoid Arthritis
• Systemic disease with prominent involvement of the joints • Inflammatory joint disease characterized by:
– Inflammatory damage in the synovial membrane or articular cartilage – Systemic signs of inflammation: fever, leukocytosis, malaise, anorexia, hyperfibrinogenemia)
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Rheumatoid Arthritis
• Systemic autoimmune disease that causes chronic inflammation of connective tissue • Initially affects synovial membrane • Later articular cartilage, joint capsule, ligaments and tendons, and bone • Affects joints of hands, wrists, ankles, and feet, but shoulders, hips and cervical spine may also be involved • Systemic effects on heart, kidney, lungs, skin and other organs
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Rheumatoid Arthritis
• • • • • • • • • Mild to severe Destroys and distorts joints Reduces life expectancy Remission and exacerbation 1 – 2% of adult population Women : men = 3:1 Onset usually in 20’s or 30’s Symptoms lessen during pregnancy Seasonal variation
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Rheumatoid Arthritis
• Idiopathic disease • Immune-mediated destruction of joints • Rheumatoid factors (IgM and IgG) target blood cells and synovial membranes forming antigen-antibody complexes • Genetic predisposition • Possibly bacterial or viral infection (Epstein-Barr)
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Rheumatoid Arthritis
• Chronic inflammation of synovial membrane • Cellular proliferation and damage to the microcirculation • Synovial membrane becomes irregular • Swelling, stiffness and pain • Cartilage and bone destruction • Ankylosis or fusing of joint • Ligaments and tendons also affected
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Rheumatoid Arthritis
• Systemic effects:
– Generalized weakness and malaise – Up to 35% develop granulomas called rheumatoid nodules – Systemic inflammation of blood vessels – rheumatoid vasculitis – Serous membranes may be affected
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Rheumatoid Arthritis
• Evaluation :
– Physical examination – X-ray – Serologic tests for rheumatoid factor and circulating antigen-antibody complexes
• No cure
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Rheumatoid Arthritis
• Therapy: • Relieve pain and swelling and retain as much joint function as possible • Resting the joint, or binding or splinting • Use of hot and cold packs • Diet high in calories and vitamins • Strengthening of associated muscles
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Rheumatoid Arthritis
• Drug therapy:
– Methotrexate – Antimalarial drugs and immunosuppression
• Surgical
– Synovectomy – Correction of deformities – Joint replacement
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