Musculoskeletal System Review of Anatomy and Physiology PDF
Document Details
Uploaded by BreathtakingFactorial2901
Southwestern University PHINMA
Tags
Summary
This document is a review of the musculoskeletal system, covering anatomy, physiology, and various laboratory and diagnostic findings. It details the roles of bones, joints, cartilages, and muscles in the body's structure and function. It also discusses clinical correlations for better understanding of diseases and treatments.
Full Transcript
LESSON TITLE: MUSCULOSKELETAL SYSTEM REVIEW OF ANATOMY AND PHYSIOLOGY, LABORATORY AND DIAGNOSTIC FINDINGS, ARTHRITIS: OSTEOARTHRITIS, RHEUMATOID ARTHRITIS, GOUTY ARTHRITIS AND SEPTIC ARTHRITIS Anatomy and Physiology The musculoskeletal system consists of bones, muscles, cartilage, tendons, ligament...
LESSON TITLE: MUSCULOSKELETAL SYSTEM REVIEW OF ANATOMY AND PHYSIOLOGY, LABORATORY AND DIAGNOSTIC FINDINGS, ARTHRITIS: OSTEOARTHRITIS, RHEUMATOID ARTHRITIS, GOUTY ARTHRITIS AND SEPTIC ARTHRITIS Anatomy and Physiology The musculoskeletal system consists of bones, muscles, cartilage, tendons, ligaments, and other connective tissues that support the body's structure and enable movement. This system is vital for providing form, stability, and movement and plays roles in mineral storage, hematopoiesis, and protection of internal organs. 1. Components of the Musculoskeletal System A. Bones Structure: Rigid organs composed of osseous tissue, bone marrow, nerves, and blood vessels. Function: o Support: Provides the framework of the body. o Protection: Shields vital organs (e.g., skull protects the brain). o Movement: Serves as levers for muscles. o Mineral Storage: Reservoir for calcium and phosphorus. o Hematopoiesis: Blood cell production in the bone marrow. Bones support body weight and allow resistance during physical activity, maintaining homeostasis of minerals crucial for nerve and muscle function. B. Joints Structure: Articulations where bones meet. Types: o Synarthrosis: Immovable joints (e.g., skull sutures). o Amphiarthrosis: Slightly movable joints (e.g., pubic symphysis). o Diarthrosis (Synovial Joints): Freely movable joints (e.g., knee, hip). Function: Facilitates movement and provides mechanical support. Joints ensure a range of motion and distribute load to prevent wear and tear on bones. C. Cartilage Structure: Flexible connective tissue composed of chondrocytes. Types: o Hyaline Cartilage: Reduces friction (e.g., ends of long bones). o Elastic Cartilage: Provides flexibility (e.g., external ear). o Fibrocartilage: Resists compression (e.g., intervertebral discs). Function: Acts as a cushion and structural component in joints and other parts. Prevents bone erosion and distributes stress during weight-bearing activities. D. Muscles Structure: Composed of muscle fibers bundled into fascicles. Types: o Skeletal Muscle: Voluntary, striated; enables movement. o Smooth Muscle: Involuntary, non-striated; found in internal organs. o Cardiac Muscle: Involuntary, striated; unique to the heart. Function: o Movement: Contraction and relaxation generate force. o Posture: Maintain body position. o Heat Production: Thermogenesis during muscle activity. Muscles convert chemical energy (ATP) into mechanical energy for movement, aiding circulation and maintaining posture. ATP (adenosine triphosphate) is the primary energy currency of cells, and it plays a vital role in the musculoskeletal system, particularly in muscle contraction and relaxation. Key functions: 1. Muscle Contraction: Myosin-Actin Interaction: Muscle contraction occurs through the interaction of two proteins: actin and myosin. Myosin heads (part of the myosin protein) bind to actin filaments, forming cross-bridges. This binding and the subsequent "power stroke" (where the myosin head pulls the actin filament) require ATP. ATP Hydrolysis: ATP is hydrolyzed (broken down) into ADP (adenosine diphosphate) and inorganic phosphate (Pi), releasing energy. This energy fuels the movement of the myosin head, causing the muscle to contract. Breaking the Cross-Bridge: ATP is also needed to break the cross-bridge between myosin and actin, allowing the muscle to relax. When ATP binds to the myosin head, it detaches from the actin filament, allowing the muscle to lengthen. 2. Muscle Relaxation: Calcium Ion Transport: Muscle relaxation also depends on ATP. After contraction, calcium ions (which trigger muscle contraction) need to be pumped back into the sarcoplasmic reticulum (SR), a storage compartment within muscle cells. This active transport of calcium ions requires ATP. 3. Maintaining Muscle Tone: Even at rest, muscles maintain a certain level of tension called muscle tone. This requires ongoing ATP use to maintain a low level of muscle fiber activity. ATP Regeneration: Since the amount of ATP stored in muscles is limited, it needs to be constantly regenerated. There are three main ways this happens: Creatine Phosphate: This provides a quick burst of energy by transferring a phosphate group to ADP to form ATP. This system is used for short, intense activities. Anaerobic Glycolysis: This breaks down glucose to produce ATP without oxygen. It's faster than aerobic respiration but produces less ATP and leads to lactic acid buildup. Aerobic Respiration: This uses oxygen to break down glucose and other fuels to produce a large amount of ATP. This is the primary energy source for sustained muscle activity. In summary, ATP is essential for all aspects of muscle function, from contraction and relaxation to maintaining muscle tone. Without a constant supply of ATP, muscles would be unable to function properly. E. Tendons and Ligaments Tendons: Connect muscle to bone; transmit force for movement. Ligaments: Connect bone to bone; stabilize joints. These structures provide mechanical strength and elasticity, ensuring joint integrity and efficient force transmission. 2. Musculoskeletal Physiology A. Bone Remodeling Process: Continuous cycle of bone resorption (osteoclasts) and formation (osteoblasts). Purpose: o Adapt to stress (e.g., weight-bearing activities). o Repair microdamage. o Maintain mineral balance. Ensures bones remain strong and responsive to physical demands. B. Muscle Contraction Mechanism: Sliding filament theory: 1. Excitation: Neural signal triggers calcium release in muscle cells. 2. Coupling: Calcium binds to troponin, exposing active sites on actin. 3. Contraction: Myosin heads bind to actin, pulling filaments for muscle shortening. 4. Relaxation: ATP restores myosin to resting state. Effective contraction depends on calcium, ATP, and intact neuromuscular signaling for precise movement and posture. C. Joint Function Synovial Fluid: Lubricates joints, reduces friction, and nourishes cartilage. Load Distribution: Joints absorb and distribute mechanical forces. Prevents joint degeneration and ensures smooth movement during activities. D. Integration with Other Systems Nervous System: Controls voluntary and reflexive muscle contractions. Cardiovascular System: Supplies oxygen and nutrients, removes waste. Endocrine System: Regulates bone metabolism (e.g., parathyroid hormone, calcitonin). Coordination among systems ensures efficiency in movement, repair, and homeostasis. 3. Clinical Correlation Fractures: Bone stress exceeding strength; indicates a balance disruption in remodeling. Osteoporosis: Decreased bone density; highlights importance of calcium and hormonal regulation. Arthritis: Joint inflammation or degeneration; underscores the significance of cartilage health. Muscle Atrophy: Loss of muscle mass from disuse; emphasizes the need for regular activity. Understanding anatomy and physiology aids in diagnosing and managing musculoskeletal disorders, promoting optimal function and quality of life. Synopsis: The musculoskeletal system is essential for movement, support, and protection, integrating various components that work together harmoniously. Knowledge of its anatomy and physiology, with clinical implications, underpins effective prevention, assessment, and treatment of musculoskeletal conditions. Laboratory and Diagnostic Findings in the Musculoskeletal System The musculoskeletal system's assessment involves laboratory tests and imaging studies that evaluate bone, muscle, joint, and connective tissue health. These findings aid in diagnosing disorders, monitoring disease progression, and evaluating treatment efficacy. 1. Laboratory Tests A. Serum Calcium Normal Range: 8.5–10.2 mg/dL Significance: o Elevated levels (hypercalcemia): May indicate hyperparathyroidism, bone metastasis, or prolonged immobility. o Decreased levels (hypocalcemia): Associated with osteoporosis, osteomalacia, or vitamin D deficiency. Calcium is critical for bone mineralization, and abnormalities reflect metabolic or structural bone conditions. B. Serum Phosphorus Normal Range: 2.5–4.5 mg/dL Significance: o Elevated levels: Often seen in chronic kidney disease, affecting bone turnover. o Decreased levels: Linked to osteomalacia or malnutrition. Phosphorus works with calcium to maintain bone strength; imbalances disrupt skeletal integrity. C. Alkaline Phosphatase (ALP) Normal Range: 44–147 IU/L (varies with age and lab) Significance: o Elevated levels: Indicate increased bone turnover, such as in Paget’s disease, fractures, or bone tumors. o Decreased levels: Rare but may occur in malnutrition. ALP is produced by osteoblasts during bone formation, making it a marker of bone activity. D. Vitamin D (25-Hydroxyvitamin D) Normal Range: 20–50 ng/mL Significance: o Deficiency: Causes osteomalacia in adults and rickets in children. o Excess: May lead to hypercalcemia and associated complications. Vitamin D is essential for calcium and phosphorus absorption, influencing bone health. E. Creatine Kinase (CK) Normal Range: 20–200 U/L Significance: o Elevated levels: Suggest muscle damage, as seen in myositis, rhabdomyolysis, or muscular dystrophy. CK is released when muscle tissue is damaged, serving as a marker for muscle pathology. F. Rheumatoid Factor (RF) and Anti-Cyclic Citrullinated Peptide (Anti-CCP) Significance: o Positive RF or Anti-CCP: Indicates autoimmune diseases like rheumatoid arthritis (RA). These antibodies target joint tissues, aiding in diagnosing inflammatory arthritis. G. Uric Acid Normal Range: 2.4–6.0 mg/dL (women), 3.4–7.0 mg/dL (men) Significance: o Elevated levels: Associated with gout, causing joint inflammation due to uric acid crystal deposition. Uric acid monitoring helps identify and manage gout. H. Erythrocyte Sedimentation Rate (ESR) and C - reactive protein (CRP) Significance: o Elevated levels: Indicate inflammation, seen in conditions like RA, lupus, or osteomyelitis. These markers assess systemic inflammation, guiding the evaluation of musculoskeletal infections and autoimmune diseases. 2. Diagnostic Imaging Studies A. X-Ray Purpose: Visualizes bone structure, alignment, fractures, and joint abnormalities. Findings: o Fractures: Discontinuity in bone structure. o Osteoarthritis: Joint space narrowing, osteophytes. Provides a baseline assessment for bone and joint integrity. B. Dual-Energy X-Ray Absorptiometry (DEXA) Purpose: Measures bone mineral density (BMD). Findings: o Low BMD: Indicates osteoporosis or osteopenia. Aids in fracture risk prediction and monitoring treatment efficacy. C. Magnetic Resonance Imaging (MRI) Purpose: Detailed visualization of soft tissues, cartilage, ligaments, and bone marrow. Findings: o Herniated discs, ligament tears, or bone marrow edema. Useful for diagnosing soft tissue injuries and early bone changes not seen on X-ray. D. Computed Tomography (CT) Purpose: Provides detailed cross-sectional images of bones and joints. Findings: o Complex fractures or bone tumors. Offers superior detail compared to X-rays for complex anatomical regions. E. Bone Scan Purpose: Detects metabolic activity in bones using a radioactive tracer. Findings: o Increased uptake: Seen in fractures, tumors, or infections. o Decreased uptake: Indicates avascular necrosis. Sensitive for detecting bone pathologies before structural changes are visible. F. Ultrasound Purpose: Assesses soft tissues, synovial fluid, and tendons. Findings: o Effusion in joints or tendon tears. Non-invasive and safe for diagnosing joint and soft tissue conditions. 3. Diagnostic Procedures A. Arthrocentesis Purpose: Aspiration of synovial fluid from a joint. Findings: o Cloudy fluid with elevated WBCs: Indicates infection or inflammation (e.g., septic arthritis). o Crystals in fluid: Suggest gout or pseudogout. Directly assesses joint inflammation or infection. B. Electromyography (EMG) Purpose: Evaluates electrical activity of muscles. Findings: o Abnormal signals: Indicate nerve or muscle disorders (e.g., myopathy, neuropathy). Differentiates between muscular and neural causes of weakness. C. Biopsy Purpose: Sample of bone, muscle, or joint tissue for histological analysis. Findings: o Abnormal cells: Suggest malignancy or infections like tuberculosis. Confirms diagnosis of certain musculoskeletal diseases. D. Joint or Bone Biopsy Purpose: Identify infections, cancers, or metabolic bone diseases. Provides definitive diagnosis when imaging and labs are inconclusive. Synopsis: Laboratory and diagnostic findings are crucial for evaluating musculoskeletal health. Tests like serum calcium and ALP provide insights into bone metabolism, while imaging studies such as MRI and X-rays identify structural and soft tissue abnormalities. Understanding these findings helps clinicians diagnose conditions, monitor treatment responses, and guide patient care. OSTEOARTHRITIS Osteoarthritis (OA), also known as degenerative joint disease or osteoarthrosis (even though inflammation may be present), is the most common and most frequently disabling of the joint disorders. OA occurs most often in weight-bearing joints (hips, knees, cervical and lumbar spine), and may also involve the proximal and distal finger joints. Classifications 1. Primary (idiopathic) With no prior event or disease related to the OA. 2. Secondary Resulting from previous joint injury or inflammatory disease. Risk Factors 1. Increased age 2. Between 50 to 60 years of age 3. Genetic 4. Previous joint damage 5. Congenital and developmental disorders of the hip: congenital subluxation–dislocation of the hip, acetabular dysplasia, Legg- Calvé-Perthes disease, and slipped capital femoral epiphysis 6. Obesity 7. Repetitive use (occupational or recreational) Clinical Manifestations 1. Primary manifestations: pain, stiffness, and functional impairment Pain - caused by an inflamed synovium, stretching of the joint capsule or ligaments, irritation of nerve endings in the periosteum over osteophytes (bone spurs), trabecular microfracture, intraosseous hypertension, bursitis, tendinitis, and muscle spasm. Stiffness - most commonly experienced in the morning or after awakening, usually lasts less than 30 minutes and decreases with movement. Functional impairment - results from pain on movement and limited motion caused by structural changes in the joints. 2. Painful bony nodes when inflamed Assessment and Diagnostic Findings 1. Tender and enlarged joints 2. X-ray - progressive loss of the joint cartilage Medical Management 1. Weight reduction 2. Prevention of injuries 3. Perinatal screening for congenital hip disease 4. Use of heat, joint rest and avoidance of joint overuse, orthotic devices (splints, braces) 5. Isometric and postural exercises, and aerobic exercise 6. Massage, yoga, or music therapy 7. Pulsed electromagnetic fields, or Transcutaneous electrical nerve stimulation (TENS) 8. Occupational and physical therapy 9. Herbal and dietary supplements 10. Acupuncture, acupressure, wearing copper bracelets or magnets, and participation in T’ai chi 11. Pharmacologic Therapy a. Initial analgesic therapy: Acetaminophen b. Other analgesics: NSAIDs, COX-2 enzyme blockers, Opioids, Intra-articular corticosteroids, Topical analgesic agents such as Capsaicin (Capsin, Zostrix), or Methylsalicylate c. Glucosamine and Chondroitin – modify cartilage structure d. Intra-articular Viscosupplementation (hyaluronates) – supplements the viscous properties of synovial fluid Surgical Management 1. Osteotomy 2. Arthroplasty Nursing Management Pain management and optimal functional ability are major goals of nursing intervention. 1. Advise the patient to reduce weight and to exercise (walking). 2. Refer the patient for physical therapy or to an exercise program. 3. Encourage the patient to use canes or other assistive devices for ambulation. 4. Provide adequate pain management. Osteoarthritis (OA) Osteoarthritis is the most common form of arthritis, characterized by the progressive degeneration of articular cartilage, subchondral bone remodeling, and synovial inflammation, leading to joint pain, stiffness, and functional impairment. 1. Anatomy and Physiology Anatomy of Joints Joints are the sites where two or more bones meet, allowing for movement and providing support. Articular cartilage: Covers the ends of bones, reducing friction and distributing load. Synovial membrane: Produces synovial fluid for lubrication and nourishment. Subchondral bone: Lies beneath the cartilage and absorbs shock. Ligaments and muscles: Stabilize the joint and aid in movement. Physiology Healthy cartilage undergoes continuous remodeling, maintaining a balance between degradation and repair. Chondrocytes, the primary cartilage cells, regulate extracellular matrix (ECM) turnover by producing collagen and proteoglycans. Understanding normal joint anatomy and physiology provides insight into the structural and functional changes that occur in OA. 2. Pathophysiology 1. Cartilage Breakdown: o Mechanical stress and aging lead to chondrocyte dysfunction. o Increased production of matrix-degrading enzymes (e.g., matrix metalloproteinases) degrades collagen and proteoglycans. 2. Subchondral Bone Remodeling: o Bone becomes sclerotic and forms osteophytes (bone spurs) to stabilize the joint. 3. Synovial Inflammation: o Low-grade inflammation in the synovium produces cytokines (e.g., IL-1, TNF-α), accelerating cartilage degradation. 4. Joint Space Narrowing: o Loss of cartilage and abnormal bone remodeling reduce joint space, impairing movement. Pathophysiological changes explain the progressive nature of OA and its clinical manifestations, guiding treatment strategies. 3. Risk Factors 1. Aging: o Reduced cartilage repair with age predisposes to degeneration. 2. Obesity: o Increased weight exerts excess mechanical stress on weight-bearing joints. 3. Joint Injury: o Trauma or repetitive use accelerates cartilage wear. 4. Genetics: o Family history increases susceptibility due to inherited structural abnormalities. 5. Gender: o Women, particularly postmenopausal, have higher rates due to hormonal changes affecting bone density. Identifying risk factors helps in early detection and implementation of preventive measures. 4. Signs and Symptoms 1. Pain: o Worsens with activity, improves with rest due to cartilage loss exposing nerve endings in subchondral bone. 2. Stiffness: o Morning stiffness (