Musculoskeletal Disorders in Adults and Children 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...

**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 Longitudinal section of long bone (tibia) showing cancellous and compact bone. **FIG. 43.6 Types of Joints** Cartilaginous (amphiarthrodial) joints, which are slightly movable, include: (A) a synchondrosis that attaches ribs to costal cartilage; (B) a symphysis that connects vertebrae; and (C) the symphysis that connects the two pubic bones. Fibrous (synarthrodial) joints, which are immovable, include (D) the syndesmosis between the tibia and fibula; (E) sutures that connect the skull bones; and the gomphosis (not shown), which holds teeth in their sockets. The synovial joints include (F) the spheroid type at the shoulder; (G) the hinge type at the elbow; (H) the gliding joints of the hand; and (I) the ball and socket (hip). **[Bone Structure]** Cortical or Compact Bone (85%) - Also called cortical bone - Solid & extremely strong - Haversian system - Haversian canal, lamellae, lacunae, osteocyte, & canaliculi Spongy Bone (15%) - Also called cancellous bone - Filled with red bone marrow - Lack Haversian system - Trabeculae: Plates or bars - Axial Skeleton -- 80 bones - Skull, vertebrae, vertebral column, and thorax - Appendicular Skeleton -- 126 bones - Upper/lower extremities, shoulder girdle, pelvic girdle **[RANK/RANKL/OPG System]** **Osteoclasts:** responsible for bone resorption - "C" - Chewing of bone -- think of chewing the mineral contents and the organic matrix & make room for new bone to be formed - This is where the osteoblasts fill in the lacunae - To do this, they need RANKL - Osteoclasts have a receptor for RANK; you need to **Osteoblasts:** responsible for new osteoid matrix - This is the primary bone-producing cell - Osteoblasts are active on the outer surface of bones, where they form a single layer of cells - Mature osteoblasts produce inorganic calcium phosphate \> which converts to hydroxyapatite \> mature osteoblasts also produce an organic matrix that is composed mainly of type I collagen - Once this process is complete, osteoblasts deposit new bone in response to the bone resorbed by osteoclasts. - Response to PTH and produce osteocalcin when stimulated by 1,25-dihydroxy-vitamin D3 - Initiate new bone formation by their synthesis of osteoid (nonmineralized bone matrix) \*\*Osteoclasts & osteoblasts work in balance\*\* **Osteocytes:** mature osteoblast maintain nutrition & waste exchange - The most abundant cells in the bone; it is within a space in the hardened bone matrix called a **lacuna** - Osteocytes are transformed osteoblasts that have been trapped or surrounded in osteoid as it hardens d/t minerals that enter during calcification - **It is the final differentiation stage for an osteoblast** - Functions: (1) Acting as mechanoreceptors (responds to changes in weightbearing or other stressors on the bone) & synthesizing certain matrix molecules (resulting in bone remodeling), (2) controlling osteoblast differentiation and production of growth factors, (3) maintaining bone homeostasis, (4) key regulators of both bone formation and bone resorption, and (5) help concentrate nutrients in the matrix. **RANK:** prolongs osteoclast survival; a receptor on osteoclasts **RANKL:** increases bone resorption; this is a protein that is expressed on osteoblasts Links up with RANK & activate osteoclast to chew away at the bone **OPG:** reduces the number of RANK/RANKL binding -- which reduces bone resorption -- made by osteoblasts - Inhibits RANKL - Role: act as a decoy receptor for RANKL by binding to RANKL - Prevents RANK from binding to RANKL, thus inhibiting osteoclast formation & activity, which helps prevent excessive bone breakdown - Estrogen stimulates OPG. This is why there is excessive osteoclast activity at postmenopausal stage. +-----------------------------------+-----------------------------------+ | **Structural Element** | **Function** | +===================================+===================================+ | Osteoblasts | - Synthesizes collagen & | | | proteoglycans | | | | | | - Synthesizes osteoid, which | | | initiates new bone formation | | | | | | - Mineralizes osteoid matrix | | | | | | - Produces receptor activator | | | of nuclear factor-kb ligand | | | (RANKL), which stimulates | | | osteoclast resorption of bone | | | | | | - Produces osteoprotegerin | | | (OPG), which inhibits | | | osteoclast formation by | | | binding to RANKL | +-----------------------------------+-----------------------------------+ | Osteoclasts | - Resorbs bone | | | | | | - Plays a major role in bone | | | homeostasis | +-----------------------------------+-----------------------------------+ | Osteocytes | - Transform osteoblasts trapped | | | in osteoid | | | | | | - Signals both osteoblasts & | | | osteoclasts | | | | | | - Maintains bone homeostasis | | | | | | - Synthesizes new bone matrix | | | | | | - Initiates osteoclast function | | | | | | - Possesses mechanosensory | | | receptors to reduce or | | | augment bone mass | | | | | | - Produces sclerostin (SOST), | | | which inhibits bone growth | +-----------------------------------+-----------------------------------+ | **Bone Matrix** | | +-----------------------------------+-----------------------------------+ | Proteoglycans | - Controls transport of ionized | | | materials through matrix | +-----------------------------------+-----------------------------------+ | **Glycoproteins** | | +-----------------------------------+-----------------------------------+ | Osteocalcin | - Vitamin K-dependent protein | | | present in bone | | | | | | - Inhibits calcium phosphate | | | precipitation (attracts | | | calcium ions to incorporate | | | into hydroxyapatite crystals) | | | | | | - Serum osteocalcin is a | | | sensitive marker of bone | | | formation | +-----------------------------------+-----------------------------------+ | Minerals | | +-----------------------------------+-----------------------------------+ | Calcium | - Crystallizes, providing bone | | | rigidity & compressive | | | strength | +-----------------------------------+-----------------------------------+ | Phosphate | - Balance of organic & | | | inorganic phosphate required | | | for proper bone | | | mineralization | | | | | | - Regulates Vitamin D, | | | promoting mineralization | +-----------------------------------+-----------------------------------+ | **Vitamins** | | +-----------------------------------+-----------------------------------+ | Vitamin D | - Assists with differentiation | | | & mineralization of | | | osteoblasts | +-----------------------------------+-----------------------------------+ | Vitamin K | - Increases bone calcification | | | | | | - Reduces serum osteocalcin | +-----------------------------------+-----------------------------------+ | Insulin-Like Growth Factor (IGF) | | +-----------------------------------+-----------------------------------+ | Osteoprotegerin (OPG) | - Inhibits bone | | | remodeling/resorption | | | | | | - Produced by several cells, | | | including osteoblasts | | | | | | - This is a decoy receptor for | | | RANKL (it binds to RANKL, | | | therefore inhibiting | | | RANK/RANKL interactions and | | | suppressing osteoclast | | | formation and bone | | | resorption) | | | | | | - May directly interfere with | | | ability of osteoclasts' | | | podosomes to attach to bone | | | matrix | +-----------------------------------+-----------------------------------+ | Receptor activator of nuclear | - Stimulates differentiation of | | factor-kB (RANK) | osteoclast precursors | | | | | | - Activates mature osteoclasts | +-----------------------------------+-----------------------------------+ | Receptor activator of nuclear | - Promotes osteoclast | | factor-kb ligand (RANKL) | differentiation/activation | | | | | | - Inhibits osteoclast apoptosis | +-----------------------------------+-----------------------------------+ **[Osteoporosis]** - Multifactorial disorder associated w/ low bone mass & enhanced skeletal fragility - Risk factors: genetics, smoking, older age, low BMI - Secondary causes: chronic steroid therapy, diabetes, RA, celiac disease, & more - Patho: imbalance in RANK/RANKL/OPG system which favors bone resorption, such as: - Reduced estrogen levels: INCREASED bone remodeling resulting in net loss of bone - Old age: normal or DECREASED rate of remodeling & decrease in bone formation - Peak bone performance ends at age 30 -- increased bone breakdown occurs afterwards compared to reformation of bone **[PTH/Calcitonin]** - The parathyroid hormone is a regulator of calcium and phosphorate levels in the blood. Why? - Parathyroid hormone works on a negative feedback loop. Whenever there is an increased serum ionized calcium levels -- your body inhibits the PTH. If there is decreased calcium levels -- your body will stimulate the PTH. - PTH binds to receptors on osteoblasts \> cytokines are released (RANKL & macrophage colony stimulating factors) \> RANKL is going to cause a breakdown \> formation of osteoclasts that breakdown bone \> release of calcium & phosphorus into the blood \> phosphorus is going to bind to calcium in the blood to reduce the amount of available free calcium - The PTH will try & fix this: PTH binds to the principal cells on the tubules of the kidneys \> the body will reabsorb calcium by excreting phosphorus \> calcium absorbed into the bloodstream & free to be used in cellular processes - PTH helps convert the precursor of Vitamin D (calciferol or D3) - In summary, the PTH increases serum calcium levels by triggering the release of calcium from the bone & increasing the reabsorption of calcium in the intestines with the help of Vitamin D, thus conserving calcium in the kidneys while excreting phosphorus in the urine. - Conversely, Calcitonin moves calcium INTO the bone & thereby decreasing serum calcium levels. +-----------------------+-----------------------+-----------------------+ | **Feature** | **Calcitonin** | **Parathyroid Hormone | | | | (PTH)** | +=======================+=======================+=======================+ | Source Gland | Thyroid gland | Parathyroid gland | | | (C-cells) | | +-----------------------+-----------------------+-----------------------+ | Primary Function | Decreases blood | Increases blood | | | calcium levels | calcium levels | +-----------------------+-----------------------+-----------------------+ | Mechanisms of Action | -Inhibits osteoclast | -Stimulates | | | activity (bone | osteoclast activity | | | breakdown) | (bone breakdown) | | | | | | | -Increases calcium | -Increases calcium | | | excretion by the | reabsorption by the | | | kidneys\ | kidneys | | | -Decreases calcium | | | | absorption in the | -Increases calcium | | | intestines | absorption in the | | | | intestines | | | | (indirectly through | | | | vitamin D activation) | +-----------------------+-----------------------+-----------------------+ | Overall Effect on | LOWERS blood calcium | RAISES blood calcium | | Calciumm | | | +-----------------------+-----------------------+-----------------------+ | Role in Calcium | Fine-tuning calcium | Major regulator of | | Homeostasis | levels, particularly | calcium levels | | | after meals | | +-----------------------+-----------------------+-----------------------+ | Clinical Significance | -Used as a medication | -Elevated levels | | | for hypercalcemia | indicate | | | | hyperparathyroidism | | | -Marker for medullary | | | | thyroid CA | -Low levels indicate | | | | hypoparathyroidism | | | | | | | | -Used as a medication | | | | for osteoporosis | +-----------------------+-----------------------+-----------------------+ - PTH works on the bone, kidneys, and intestines **[Osteoarthritis (OA)]** - OA is primarily a disease of cartilage (predominantly Type 2 collagen, proteoglycans and glycosaminoglycans) - Focal degenerative disorder of synovial joints, primarily affecting articular cartilage & sub-condylar bone - Develops due to an imbalance b/w destruction & synthesis of articular cartilage - Proteoglycans are one of the main components of cartilage; normally they bind water and provide basis for absorbing high compressive loads - **In OA, proteoglycans are dysfunctional, leading to imbalance of articular cartilage water content** - Pain, stiffness, enlargement of the joints, limited ROM is the typical clinical presentation **[Rheumatoid Arthritis (RA)]** - Chronic autoimmune disease characterized by joint inflammation and extra-articular manifestations - Autoantibodies most common: Rheumatoid Factor (RF) and anti-citrullinated protein antibodies (ACPA) - These are specific to RA, but not sensitive - Inflammatory pathway: proliferation of synovial cells in joints -- pannus formation -- cartilage destruction & periarticular bony erosions = deformities & loss of function **[Ankylosing Spondylitis (AS)]** - Form of arthritis that primarily affects the spine - Causes inflammation of the vertebra leading to severe, chronic pain and discomfort - If advanced, inflammation leads to ankyloses, or new bone formation within the spine, causing them to fuse together and become immobile - Hallmark feature: involvement of the sacroiliac (SI) joints **[Osteomalacia]** - Deficiency of vitamin D lowers the absorption of calcium from the intestines - Mineralization is inadequate or delayed - Bone formation progresses to osteoid formation, but calcification does not occur; result is soft bones - Clinical manifestations : pain, bone fractures, vertebral collapse, bone malformation, waddling gait, facial deformities, knock nees **[Arthritis]** **\*Exam: Understand the complications of rheumatoid 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. **FIGURE Emerging Model of Pathogenesis of Rheumatoid Arthritis** Rheumatoid arthritis is an autoimmune disease of a genetically susceptible host triggered by an unknown antigenic agent. Chronic autoimmune reaction with activation of CD4+ helper T cells and possibly other lymphocytes and the local release of inflammatory cytokines and mediators eventually destroy the joint. T cells stimulate cells in the joint to produce cytokines that are key mediators of synovial damage. Apparently immune complex deposition also plays a role. Tumor necrosis factor *(TNF)* and interleukin-1 *(IL-1),* as well as some other cytokines, stimulate synovial cells to proliferate and produce other mediators of inflammation, such as prostaglandin E~2~ *(PGE~2~),* matrix metalloproteinases, and enzymes, which all contribute to destruction of cartilage. Activated T cells and synovial fibroblasts also produce receptor activator of nuclear factor κβ ligand *(RANKL),* which activates the osteoclasts and promotes bone destruction. Pannus is a mass of synovium and synovial stroma with inflammatory cells, granulation tissue, and fibroblasts that grows over the articular surface and causes its destruction. - 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. **FIGURE Rheumatoid Arthritis** A, Schematic view of the joint lesion. B, Advanced rheumatoid arthritis involving femur. There is prominent proliferation of synovium and almost complete destruction of overlying articular cartilage.  - 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)** **\*Exam: Understand the complications of osteoarthritis** - 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 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)** **\*Exam: Know the description of 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** **\*Exam: Patho of 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** **\*Exam: Understand the patho of 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) - Osteoblast (the cells that help form new bone) -- RANK Ligand is a protein that is expressed by osteoblasts - RANK is a protein expressed on Osteoclasts (receptor sites) - Osteoprotegerin (OPG), another protein secreted by osteoblasts, is a natural inhibitor of RANK Ligand and plays a role in regulating bone resorption. - The binding of RANK Ligand to RANK is essential for osteoclast formation, function, and survival. - In postmenopausal women, as estrogen declines, RANK Ligand secretion increases. - Elevated RANK Ligand levels lead to increased osteoclast formation, function, and survival - Greater osteoclast activity increases bone loss, weakens bone architecture, and can ultimately lead to fracture - Locally several 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 (remember this is d/t RANK Ligand secretion increases) - 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)** **\*Exam: Know the description of Paget disease** - 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 affected. - The problem may also occur because 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** **\*Exam: Patho of 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. **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 joints - 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)** **\*Exam: Know the description of Legg-Calves-Perthes disease** - 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)** **\*Exam: Know the description of osgood-schlatter disease** - 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.