Musculoskeletal Disorders in Adults and Children (Module 8) PDF

**Musculoskeletal Disorders in Adults and Children (Chapter 43, 44& 45 in 9^th^ ed. and 44, 45& 46^th^ 8thed)** **Physiology Review** -- Please review the structure and function of the musculoskeletal system with a focus on the following figures in Chapter 44 8th edition and chapter 43 in 9^th^ edi...

**Musculoskeletal Disorders in Adults and Children (Chapter 43, 44& 45 in 9^th^ ed. and 44, 45& 46^th^ 8thed)** **Physiology Review** -- Please review the structure and function of the musculoskeletal system with a focus on the following figures in Chapter 44 8th edition and chapter 43 in 9^th^ edition. Review the framework of the skeletal system. Be sure to know that the skeletal system protects soft tissues. And maintains them in their proper position while maintaining stability for the body. Review the figures that discuss - Cross sections of bones (epiphysis, metaphysis, diaphysis) - Main tissues of a joint - Types of joints. - The knee joint and synovium - Bone remodeling **Arthritis** - **Rheumatoid** - Pathology: - Much remains to be learned about the etiology of rheumatoid arthritis. It is thought that a bacterial or viral pathogen (e.g. Epstein-Barr virus or Helicobacter pylori), perhaps in combination with environmental factors like cigarette smoke, trigger an autoimmune response in synovial fluid of joints. Research indicates that there may be a genetic predisposition and stress may be a contributing factor. - The pathologic process starts as microvascular injury to the synovium. The small vessels become occluded and there is swelling of endothelial cells. Gaps develop between endothelial cells allowing inflammatory cells to migrate through them into the synovium. The synovium of a person with active rheumatoid arthritis is infiltrated with lymphocytes, macrophages, and T and B cell aggregates. These trigger swelling, pain, proliferation of cells in synovial lining and release of inflammatory mediators. - Proteins called cytokines are released. The dominant one is tumor necrosis factor (TNF). TNF stimulates production of other interleukins leading to a massive inflammatory response. TNF also inhibits bone formation, induces resorption, and stimulates secretion of enzymes that eat away cartilage. More tenderness, pain and swelling result. - As synovium gets larger it eventually forms tissue called pannus. Pannus attacks articular cartilage and then the soft subchondral bone that underlies it. The result is loss of function and deformity of the joint. - As the disease progresses pannus is gradually replaced by fibrous connective tissue that occludes the joint space. The fibrous tissue calcifies, causing immobility. - Risk Factors: - Females develop the disease more often than men (60-70%) - There is thought to be a genetic predisposition. - Age of onset usually between 40 and 60 years, although it can occur in childhood - Signs & Symptoms: - American College of Rheumatology lists 7 diagnostic criteria. Presence of 4 or more indicates rheumatoid arthritis 1. At least 1 hour of morning stiffness 2. Arthritis in 3 or more joints 3. Arthritis of hand joints 4. Symmetric swelling 5. Rheumatoid nodules 6. Presence of serum rheumatoid factor 7. Radiographic changes in hand or wrist joints - Extra-articular symptoms may include weight loss, neuropathy, scleritis, pericarditis, lymphadenopathy, and splenomegaly - Early clinical manifestations include fever, fatigue, weakness, anorexia, weight loss, generalized aching and stiffness. - Laboratory findings: - Elevated ESR (erythrocyte sedimentation rate) - Presence of rheumatoid factor - Anemia of chronic disease is common 8. cause inflammation and joint destruction - Prognosis: - About 10% of patients have long remissions. Most of those have presented with an acute onset of inflammatory polyarthritis. - The majority (65-70%) of patients have either fast or slow unrelenting progression of the disease with joint destruction and long-term disability. - The remaining patients have disease periods alternating with periods of partial or complete remission. - **Osteoarthritis - Inflammatory Joint Disease, Degenerative Joint Disease (DJD)** - Pathology: - The disease may be idiopathic (primary), secondary to trauma, or secondary to another disease. - Articular cartilage loss occurs through the enzymatic breakdown of the cartilage matrix: the proteoglycans, glycosaminoglycans, and collagen. It is the loss of proteoglycans that is the key to the OA process. Without the pumping action of the proteoglycans there is an increase of articular cartilage water content which leads to degeneration and loss of articular cartilage in synovial joints. The surface of the smooth cartilage surface softens, frays, and loses elasticity. Cartilage flakes off, and surface becomes thin. Deeper layers develop fissures. The cartilage may be entirely lost over some areas, exposing underlying bone. - Sclerosis (thickening and hardening) of underlying bone that is exposed. Cysts may develop, communicating with fissures. As pressure increases in cysts, they may break and release contents into synovial space. - Cartilage-coated osteophytes may grow outward, forming bone spurs (osteophytes). Parts of the spurs may break off, creating fragments (joint mice) in the synovial cavity. These irritate synovial membrane, causing synovitis and effusion. The result is enlargement and deformation of the joint, with limitation of movement. - Risk Factors: (The effects of these are additive and many people have several. - Age: over 40, incidence increases with age - Gender: incidence is the same, but women are more severely affected. Lack of estrogen in postmenopausal women is associated with more symptoms and more radiographic findings. - Genetics: 1. A genetic abnormality that causes changes in amino acids may be associated with cartilage deterioration. Also deficiencies in inhibitors of calcification leads to cartilage calcification causing loss of smooth cushion 2. Structural abnormalities, e.g. vargus/valgus, scoliosis, may cause unequal pressure distribution during weight-bearing activities and thus predispose to arthritis development. - Joint stress: 3. Obesity is a major risk factor. It increases the work of weight-bearing joints, particularly knees and hips. 4. Overuse injury, such as a cartilage tear, predisposes to degenerative changes. Repetitive motion increases joint wear. Jobs that involve extended standing, walking, lifting or knee bending pose risks for excessive joint wear. - Inflammation: inflammatory cells may release enzymes that digest cartilage cells. - Trauma leading to instability: injury to supporting structures or joint capsule. - Neurologic disorders: abnormal movements, positioning or weight-bearing. - Hematologic or endocrine disorders: bleeding into joints or disturbance of calcium metabolism. - Drugs: e.g. steroids that stimulate activity of collagen-digesting enzymes. - Signs & Symptoms: - Pain: Varies from dull and constant to sharp pain with joint movement and caused by poor cushioning of bone contact by excessively worn cartilage surfaces. Pain is relieved by rest. - Stiffness: usually seen in the morning and relieved by movement. - Crepitus: cracking sound with joint movement caused by changes in the synovial fluid and damaged cartilage that causes movement over irregular joint surfaces. - Swelling may be caused by excess synovial fluid in the knee. - Nodules in the joints of the fingers are common. - Tendonitis is common and may cause loss of flexibility. - Weight-bearing joints are often the first affected. **Ankylosing Spondylitis (AS)** - Chronic inflammatory joint disease of the spine and sacroiliac joints. The inflammatory process erodes the bone and repair leads to ossification of the disks, joints, and ligaments of the spinal column. Low back pain, stiffness, and restricted movement are clinical manifestations. AS has a strong association with HLA-B27. **Osteomyelitis** - Most often caused by bacteria: Staph. Aureus, group B strep, H. influenzae, and gram neg. bacteria. - Two routes of infection: Exogenous via a wound, surgical incision spreading the infection from the soft tissue to the bone. Second route is endogenous where a distant site of infection is carried by the blood to the bone (common in children). - Patho: initial infection provokes an intense inflammatory response, then the first stage walls off the infection where blood supply is blocked and abscess is formed. Second stage can result in bone necrosis. In children sinus tracts often form and the exudate escapes via the skin. In adults, pathological fx are often a complication. **Osteomalacia** - Called rickets in children which is rare in the US. - Incidence in adults is usually the elderly. - Most important contributing factor is vitamin D deficiency. - Patho: lack of vit. D causes low plasma calcium levels which increase PTH. PTH raises the plasma Ca. levels and increases phosphate renal clearance. Bones become spongy and are not able to mineralize properly with such low phosphate levels in the bone. **Osteoporosis** - Definition (WHO): Bone mass 2.5 standard deviations below the peak normal value for a young adult. - Pathology: - Bone is continuously going through a cyclic process of absorption and formation known as remodeling. Approximately 10 percent of a person's bone mass is being remodeled at any one point in time. This complex process is initiated by precursor osteoclasts that erode small remodeling sites (basic multicellular units) making little cavities (lacuna). The resulting erosion causes osteoblast precursors to be activated and they fill each of the eroded units with a collagen mesh. Calcium and phosphorus are then absorbed into the mesh to fill the lacuna. Osteoclast life is prolonged by the activation of RANK by RANKL. This longer survival of the osteoclast leads to an imbalance of more bone loss than bone replacement. - Video on the RANK/RANKL/OPG system (5mins) - Locally a number of hormones and growth factors regulate the microenvironment within bone remodeling occurs. These include the following cytokines: interleukins, tumor necrosis factor, and transforming growth factor. The reduction in estrogen that occurs during menopause may lead to an increase in osteoclast precursors as well as a reduction in cytokine production. This would create an imbalance in which bone resorption exceeds bone formation. Parathyroid hormone and vitamin D provide systematic regulation of bone metabolism. Age-related changes in the calcium-regulating parathyroid hormone may help protect bone or escalate its loss. - Between birth and age 30 bone formations exceeds absorption. Peak bone mass is achieved at about age 30 and there is a period of stability during which absorption and formation are in balance. Age-related bone loss then begins and is accelerated during the first 10 years after menopause. The onset of loss in the more metabolically active trabecular bone (vertebrae, pelvis, flat bones and ends of long bones) begins at least a decade before loss of cortical bone (shafts of long bones). Over a lifetime, women lose about 35% of their cortical bone and about 50% of trabecular bone. - Two mechanisms for pathology: - High turnover: Any condition that increases bone remodeling results in a net loss of bone. Reduced estrogen levels at menopause can trigger this. - Low turnover: There is a normal or decreased rate of remodeling accompanied by a decrease in bone formation. This type occurs in old age. - Types: - Type 1 primary: postmenopausal, caused by rapid drop in estrogen production at the time of menopause. Estrogen is essential for normal calcium absorption and incorporation into bone. Calcium and vitamin D deficient diet are contributing factors. - Type II primary: age-related or senile, occurs in both sexes over the age of 70. Results from a combination of factors: age-related gradual, slow decline in bone mass, age-related decline in vitamin D production, and development of intestinal vitamin D resistance. - Secondary: endocrine (hyperparathyroidism, GI disorders, neoplasms) or drug-related (alcoholism, corticosteroids, long-term use of aluminum-containing antacids, phenytoin, heparin). - Risk factors: - White or Asian. - Female. - Advancing age. - Positive family history. - Small skeletal frame. - Lifestyle factors: smoking, alcohol abuse, sedentary lifestyle, low calcium intake, high sodium or high protein diet, high caffeine intake (more than 2 cups coffee/day). - Very low body fat composition, such is that which sometimes occurs in competitive athletes, ballet dancers, or anorexic adolescents, may lead to hormonal abnormalities that can impair bone growth and cause osteoporosis. - Performance-enhancing drugs or steroid treatment increases risk for bone loss in both males and females. - Some medications, e.g. thyroid hormones, anticonvulsants, aluminum-containing antacids, diuretics, cholestyramine, and heparin increase the rate of bone loss. - Low testosterone levels in men. - Absence of menstrual periods in women. - Prolonged bed rest. - S/S: - Early symptoms: back pain, gradual decrease in height. - Later symptoms: kyphosis caused by vertebral collapse, pain and bone deformity, fractures are common as bones become weak and brittle. - Diagnostic tests: Dual-energy x-ray absorptiometry (DXA) is used to assess the spine, hip and/or wrist. Alternatively, the heel or hand may be used. Bone density is compared with standards for the patient\'s age, sex and size to obtain a Z-score. The T-score compares the patient to a healthy young adult of the same sex. A decrease of 1 standard deviation means that about 12% of bone mineral density has been lost and fracture risk is increased 1.5 to 3 times. Post-menopausal women should not have a T-score greater than 1 standard deviation below the mean. In other words, the T-score should be -1.00 or higher. A T-score of -1.00 to -2.5 indicates low bone mass (osteopenia). A T-score of -2.5 or lower indicates osteoporosis. **Paget disease**- (osteitis deformans) - Description: a state of increased metabolic activity of the bone; characterized by **abnormal and excessive bone remolding;** enlarges and softens the affected bones. - Pathology: - Excessive resorption of spongy bone. Bone marrow is replaced with extremely vascular fibrous tissue. Followed by abnormal new bone formation at an accelerated rate. Thickens and enlarges affected bones. - Bone assumes patchwork pattern with uneven lamellar structure. There are gaps in the bone tissue. This is not strong and predisposes to fractures. - Eventually there is \"burnout\", an inactive phase in which remodeling is decreased or absent. **Carpal Tunnel syndrome** - Probably the most common occupational injury. Office workers using computers are most commonly affected. - The problem may also occur as a result of a fracture of the arm, wrist, or hand. - Pathology: - Median nerve and flexor tendons of fingers pass through carpel tunnel, a relatively small space made up of carpel bones and transverse ligaments between flexor and abductor muscles. - Repetitive motion activities (greater than 8-9 repetitions per minute) create a situation where the wrist can\'t produce enough lubricating fluid. Friction without adequate lubrication leads to swelling and scaring. Pressure against the median nerve results. - S/S : - Compression of the nerve causes weakness, pain with opposition of the thumb, and burning, tingling, or aching, of palmar surface of thumb, index finger, middle finger and sometimes ring finger. Little finger spared. Pain may radiate to the forearm and the shoulder joint. - Pain is worse at night and may be an ache or tingling sensation. - Impaired 2 point discrimination. - There may be sensory loss and/or muscle weakness. - Progression: untreated, pressure leads to nerve and muscle atrophy (permanent damage) - Prevention: - Exercises before each work session and after breaks. - Keep wrist in neutral position. - Minimize repetitive movements, decrease speed. - Don\'t hold object in same way for an extended time. - Vary work activities. - Grip or lift with entire hand rather than just thumb and index finger. **Plantar-fasciitis (heel-spur)** - Pathology: - Inflammation of plantar fascia and attachment of Achilles tendon caused by repeatedly placing them under tension. - Starts as inflammation but, if untreated, areas of calcification can form. - Risk factors: - Often seen after a sudden increase in activity, e.g. new exercise program or change in work routine. - Overweight - Positive family history. - Flat feet. - Poor shoe support. - Signs & Symptoms: Heel pain and soreness, usually worse when first arising and often exacerbated the day after increased activity. **Gout** - Pathology: - Metabolic disorder that disrupts the body\'s control of uric acid production or excretion, causing high levels of uric acid in the blood (hyperuricemia) and in other body fluids (synovial fluid). At increased levels, uric acid crystallizes (monosodium urate crystals), forming precipitates that are deposited into the connective tissue. This causes acute, painful inflammation (gouty arthritis). - Tophus: chalky mass caused by chronic deposit of urates, can destroy joint and bone. Tophi can also be found in other areas, e.g. car cartilage, tendons, ligaments. Gout can occur as a secondary problem following administration of diuretics. Loop and thiazide diuretics decrease urate excretion by increasing net urate reabsorption; this can occur either by enhanced reabsorption or by reduced secretion. - Signs & symptoms: - Increased serum urate concentration (uricemia). - Recurrent attacks swelling, inflammation and pain, usually at joint of great toe. - Renal stones can be a complication. **Infections** - Toxic (suppurative) or Septic arthritis Pathology: - Bacterial infection within the joint space - Most common infecting organisms - Hemophilis influenzae, Neisseria gonorrheae, Salmonella, Staphylococcus aureus, Escherichia coli, Pseudomonas Mode of infection - Penetrating trauma or hematogenous - Signs & symptoms - Swollen, hot painful joint - Limited ROM - **Toxic general appearance** **Pediatric Disorders** Developmental Dysplasia (Dislocation) of the Hip (DDH) - Abnormal development of the proximal femur, acetabulum, or both. - Patho - the subluxed hip maintains contact with the acetabulum but is not well seated within the hip joint; typically the acetabulum is shallow or sloping rather than cup shaped. - S/S - asymmetry of gluteal thigh folds, leg length discrepancy, limitation of hip abduction, waddling gait, pain, positive Barlow, Ortolani, and/or Trendelenburg test. - TX - bracing, traction, casts, or combination of these. **Scoliosis** - a lateral curvature of the spine. - Pathology: disorder of asymmetrical growth, youngsters are at greatest risk during the adolescent growth spurt. - Risk factors: - Female - Positive family history - S/S: - Asymmetry of shoulder level. - Asymmetry of level of iliac crests. - Asymmetry of negative space between arms and sides of body - Asymmetry of skin folds of back and shoulder blades. - Asymmetry on forward bend. - Treatment - Mild curves: observation. - Mild-moderate: stabilization with brace plus exercises. - Severe: stabilization with surgery. **Legg Calve-Perthes Disease** - (coxa plana) - Avascular necrosis of the femoral head, usually a unilateral problem. - Patho: - The cause is unknown, possibly recurrent synovitis that increases intra-articular pressure and decreases blood supply. - Impaired blood supply to the joint cause's necrosis of the femoral head. - With time the femoral head will reform. - Risk factors: - Male - Age 4-11 years - S/S - Painless limp - Hip, thigh or knee pain - Limited abduction and internal rotation - Course of illness: - Self-limiting - May last 1-2 years - May predispose to degenerative disease later in life. - Tx: - Mild: rest and observation. - Moderate: anti-inflammatory agents and traction. - Severe: surgery. (Note: Adults may also develop avascular necrosis of the hip. Predisposing factors include trauma to the hip joint, alcohol abuse and systematic steroid use. The pathology is much the same: impairment of the blood supply, osteocyte death, resorption of dead bone, and replacement with new bone. However, adults are more likely to experience progressive disease. Treatment includes rest and removal of offending agents (alcohol, steroids). Surgical intervention, including bond grafting or hip replacement, may be required.) **Slipped Capital Femoral Epiphysis** - Pathology: - Displacement of the femoral head at the epiphysis. - Etiology unclear, thought to relate to hormonal changes that reduce mechanical integrity of growth plate. - Risk factors: - Male - Obesity - Puberty - Signs & Symptoms: - Painful limp - History of trauma (may be minor and forgotten) - Hip, knee or thigh pain - Limitation of external rotation - Altered gait - Management: - Mild-moderate: casting, fixation with pin - Severe: femoral osteotomy **Osgood-Schlatter disease** (a type of osteochondrosis) - Pathology: - Inflammation of the tibial tubercle at attachment of patellar tendon. - Tendonitis of the anterior patellar tendon resulting from overuse. - Adolescents are predisposed because differential growth of bone and soft tissue results in strong tendons with relatively weak attachments (prone to stress injury with overuse). - The problem is self-limiting but may take 6-24 months to completely resolve. - Risk factors: - Adolescent - Athletic participation - Signs & Symptoms: pain, swelling, tender to palpation, most severe with physical activity. A \"bump\" may appear and be tender where tendon is attached. - Treatment - - Rest, eliminate activities that are problematic for 3 weeks at least. - Anti-inflammatory agents. - May need splints or casting if severe. **Duchenne Muscular Dystrophy** Age of onset is about 3 years and occurs in males. Patho: X linked inherited disorder. The deletion of a DNA segment causes an absence of dystrophin which is required by the muscle. Loss of muscle fibers and muscle bulk are related to this lack of dystrophin. Fat and connective tissue accumulations occur in place of the muscle fiber. Clinical manifestations: Slow motor development, weakness, and muscle wasting. Muscles usually affected are the hips, shoulders, and quadriceps. Pulmonary complications occur related to severe scoliosis late in the disease.