UNBC Nursing 302 - Alterations in Musculoskeletal System PDF
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UNBC (University of Northern British Columbia)
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These lecture notes from UNBC Nursing 302 cover alterations in the musculoskeletal system. Topics include musculoskeletal injuries, fractures, healing, dislocations, support structures, and various other related issues.
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Alterations of Musculoskeletal Function Nursing 302 Musculo-Skeletal Injuries Fractures Fracture is a break in the continuity of a bone Classifications Complete or incomplete Greenstick Closed...
Alterations of Musculoskeletal Function Nursing 302 Musculo-Skeletal Injuries Fractures Fracture is a break in the continuity of a bone Classifications Complete or incomplete Greenstick Closed or open Torus Comminuted Bowing Linear Pathological Oblique Stress Spiral Fatigue Transverse Transchondral Fractures Fractures (Cont.) Healing Direct Most often occurs when surgical fixation is used to repair a broken bone Intramembranous bone formation No callus formation Indirect Most often observed when a fracture is treated with a cast or other nonsurgical method Intramembranous and endochondral bone formation Callus formation Remodelling of solid bone Bone Healing Callus Formation Fractures Manifestations Unnatural alignment, swelling, muscle spasm, tenderness, pain, impaired sensation, and decreased mobility Often transient numbness due to nerve trauma Treatment Immobilization Closed manipulation, traction, and open reduction Internal and external fixation Fractures (Cont.) Improper reduction or immobilization Nonunion, delayed union, and malunion Dislocation and Subluxation Dislocation Displacement of one or more bones in a joint Loss of contact between articular cartilage Subluxation Contact between articular surfaces is only partially lost Associated with fractures, muscle imbalance, rheumatoid arthritis, or other forms of joint instability Support Structures Strain Tearing or stretching to a tendon or muscle Sprain Tear or injury to a ligament Avulsion Complete separation of a tendon or ligament from its bony attachment site Support Structures (Cont.) Tendon and ligament injuries Usually lack sufficient strength to withstand some stress for 4 to 5 weeks after the injury Painful and are usually accompanied by soft tissue swelling, changes in tendon or ligament contour, and dislocation or subluxation of bones Rehabilitation is crucial to regaining good functional outcome Tendinopathy, Epicondylopathy, and Bursitis Tendinopathy Inflammation of a tendon Epicondylopathy Inflammation of a tendon where it attaches to a bone Tennis elbow (lateral epicondylitis) Golfer’s elbow (medial epicondylitis) Tendinopathy, Epicondylopathy, and Bursitis (Cont.) Bursitis Inflammation of a bursa Skin over bone, skin over muscle, and muscle and tendon over bone Inflammation caused by overuse or excessive pressure Epicondylopathy and Tendinopathy Muscle Strain Sudden, forced motion causing the muscle to become stretched beyond its normal capacity Can also involve the tendons Healing in three phases Destruction Repair Remodelling Muscle Strain (Cont.) Myositis ossificans Also called heterotopic ossification Late complication of local muscle injury Associated with burns, joint surgery, and trauma to the musculo-skeletal system or central nervous system Soft tissue calcification causes stiffness or deformity of an extremity Rhabdomyolysis Rapid breakdown of muscle that causes the release of intracellular contents, including the protein pigment myoglobin, into the extracellular space and bloodstream Can result in hyperkalemia, cardiac arrhythmia, or acute kidney failure Triad of manifestations Muscle pain Weakness Dark urine Rhabdomyolysis (Cont.) Diagnosed when CK level is five to ten times the upper limit of normal (about 1000 units/L) Kidney failure likely when CK reaches 15 000 units/L Preventing kidney failure and maintaining adequate urinary output are goals of treatment Compartment Syndrome Result of increased pressure within a muscle compartment Can be caused by any condition that disrupts the vascular supply to an extremity Muscle ischemia causes edema, rising compartment pressure, and tamponade that lead to muscle infarction and neural injury Compartment Syndrome (Cont.) “6 Ps” of compartment syndrome Volkmann ischemic contracture Diagnosis confirmed by measurement of intracompartmental pressure Surgical intervention indicated when pressure reaches 30 mm Hg Malignant Hyperthermia Hypermetabolic reaction to certain anaesthetics Mutation in the ryanodine receptor of skeletal muscle (RyR1) is responsible for the majority of cases Altered normal excitation-coupling process of muscle contraction Also causes hypermetabolism with extremely high body temperature, muscle rigidity, rhabdomyolysis, and death if not quickly treated with dantrolene infusion Pre-op evaluation is critical May be predicted with muscle-contracture test Osteoporosis Poorly mineralized bone and increased risk of fractures due to alterations in bone microarchitecture Old bone resorbed faster than new bone made Spontaneous fractures Osteoporosis (Cont.) Osteoporosis (Cont.) Potential causes Endocrine dysfunction Parathyroid hormone, cortisol, thyroid hormone, and growth hormone Medications Vitamin D deficiency Underlying diseases Low physical activity Abnormal BMI Fractures are the major complication Osteoporosis (Cont.) Postmenopausal osteoporosis Middle-aged and older women Estrogen deficiency and secondary causes Remodelling imbalance between the activity of osteoclasts and osteoblasts Osteoporosis (Cont.) Secondary osteoporosis Caused by other conditions Hormonal imbalances Medications Disease Regional osteoporosis Confined to a segment of the appendicular skeleton Associated with disuse May be transient Osteoporosis (Cont.) Glucocorticoid-induced osteoporosis Type of secondary osteoporosis Glucocorticoids improve osteoclast survival, which inhibits osteoblast formation and function Age-related bone loss Cause unclear Reduced physical activity is likely a factor Osteoporosis (Cont.) Osteoporosis (Cont.) Osteoporosis (Cont.) Kyphosis Osteoporosis (Cont.) Dual x-ray absorptiometry (DXA) Gold standard for detecting and monitoring osteoporosis Trabecular bone score (TBS) Evaluates pixel variations in the grey-level areas of lumbar spine images from DXA scans Enhanced predictions of fracture risk Osteomalacia Inadequate or delayed mineralization of osteoid Remodelling cycle proceeds through osteoid formation but calcification does not occur; the result is soft bones Pain, bone fractures, vertebral collapse, bone malformation Results from vitamin D deficiency Treatment varies by etiology Paget’s Disease Also called osteitis deformans Chronic accelerated remodelling of spongy bone and deposition of disorganized bone Enlarges and softens affected bones Mostly affects vertebrae, skull, sacrum, sternum, pelvis, and femur Often no symptoms Genetic and environmental factors Evaluation based on radiographic findings Osteomyelitis Bone infection often caused by bacteria, usually Staphylococcus aureus Hematogenous Pathogens carried through the bloodstream Cutaneous, sinus, ear, and dental infections Insidious onset Vague symptoms Fever, malaise, anorexia, weight loss, and pain Osteomyelitis (Cont.) Contiguous Infection spreads to an adjacent bone Open fractures, penetrating wounds, surgical procedures Manifested by signs and symptoms of soft tissue infection Low-grade fever, lymphadenopathy, local pain, and swelling Osteomyelitis (Cont.) Brodie abscesses Characterize subacute or chronic osteomyelitis Circumscribed lesions, usually in the ends of long bones Treatment Antibiotics, débridement, surgery, hyperbaric oxygen therapy Osteomyelitis (Cont.) Osteomyelitis (Cont.) Osteoarthritis Characterized by: Loss and damage of articular cartilage Inflammation New bone formation of joint margins Subchondral bone changes Variable degrees of mild synovitis Thickening of the joint capsule Prevalence increases with age Osteoarthritis (Cont.) Risk factors Increased age Joint trauma, long-term mechanical stress Obesity Osteoarthritis (Cont.) Characteristics Local areas of damage and loss of articular cartilage New bone formation of joint margins Subchondral bone changes Variable degrees of mild synovitis and thickening of the joint capsule Osteoarthritis (Cont.) Manifestations Pain (worsens with activity) Stiffness (diminishes with activity) Enlargement of the joint Tenderness Limited motion Muscle wasting Partial dislocation Deformity Osteoarthritis (Cont.) Conservative treatment Surgical treatment Exercise and weight loss Used to improve joint movement, correct deformity or malalignment, Pharmacological therapies or create a new joint with artificial Analgesics and anti- implants inflammatories Nutritional supplements Osteoarthritis (Cont.) Osteoarthritis (Cont.) Osteoarthritis (Cont.) Classic Inflammatory Joint Disease Inflammatory damage or destruction in the synovial membrane or articular cartilage Systemic signs of inflammation Infectious or noninfectious Rheumatoid Arthritis Inflammatory autoimmune joint disease Systemic autoimmune damage to connective tissue, primarily in the joints (synovial membrane) Similar symptoms to osteoarthritis Cause unknown; multifactorial with strong genetic predisposition Rheumatoid Arthritis (Cont.) Pathogenesis Three processes Neutrophils and other cells in the synovial fluid become activated. Inflammatory cytokines: tumour necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), interleukin-7 (IL-7), interleukin-21 (IL-21) induce enzymatic breakdown of cartilage and bone. T cells also interact with synovial fibroblasts through TNF-α, converting synovium into a thick, abnormal layer of granulation tissue (pannus). Rheumatoid Arthritis (Cont.) Insidious onset Systemic manifestations Inflammation, fever, fatigue, weakness, anorexia, weight loss, and generalized aching and stiffness Painful, tender, stiff joints Joint deformities Rheumatoid nodules Caplan’s syndrome Rheumatoid Arthritis (Cont.) Diagnosed by presence of autoantibodies (ACPA or RF) Early treatment with disease-modifying antirheumatic drugs Rheumatoid Arthritis (Cont.) Rheumatoid Arthritis (Cont.) Synovitis Ankylosing Spondylitis Group of inflammatory arthropathies known as spondyloarthropathies (SpA) Inflammatory joint disease of the spine or sacroiliac joints causing stiffening and fusion of the joints Systemic, autoimmune inflammatory disease Primary pathological site is the enthesis End result is fibrosis, ossification, and joint fusion Ankylosing Spondylitis (Cont.) Cause unknown, but there is a strong association with HLA-B27 antigen Begins with the inflammation of fibrocartilage, particularly in the vertebrae and sacroiliac joint Inflammatory cells infiltrate and erode fibrocartilage As repair begins, the scar tissue ossifies and calcifies; the joint eventually fuses Ankylosing Spondylitis (Cont.) Manifestations Early symptoms Low back pain that begins in early 20s and progresses over time Stiffness Pain Restricted motion Loss of normal lumbar curvature (lordosis) Increased concavity of upper spine (kyphosis) Ankylosing Spondylitis (Cont.) Sacroiliitis present on imaging Physiotherapy to maintain skeletal mobility and prevent the natural progression of contractures NSAIDs for pain Gout Syndrome caused by either overproduction or underexcretion of uric acid Manifests high levels of uric acid in the blood and other body fluids Occurs when the uric acid concentration increases to high enough levels to crystallize Gout (Cont.) Crystals deposit in connective tissues throughout the body When these crystals occur in the synovial fluid, the inflammation is known as gouty arthritis Linked to purine metabolism Gout (Cont.) Risk factors Male sex Increasing age High intake of alcohol, red meat, and fructose Medications Gout (Cont.) Manifestations Increase in serum urate concentration (hyperuricemia) Recurrent attacks of monoarticular arthritis (inflammation of a single joint) Deposits of monosodium urate monohydrate (tophi) in and around the joints Renal disease involving glomerular, tubular, and interstitial tissues and blood vessels Formation of renal stones Gout (Cont.) Clinical stages Asymptomatic hyperuricemia Acute gouty arthritis Tophaceous gout Gout (Cont.) Trauma is most common aggravating factor. Primary symptom is severe pain. Approximately 50% of the initial attacks occur in the metatarsophalangeal joint of the great toe. Other areas include the heel, ankle, instep of the foot, knee, wrist, or elbow. 1000 times more likely to develop renal stones than general population. Gout (Cont.) Manifestations of acute gouty attack Severe pain, especially at night Hot, red, tender joint Signs of systemic inflammation Increased sedimentation rate Fever Leukocytosis Gout (Cont.) Redrawn from Klippel, J.H., & Dieppe, P.A. (Eds.). (1998). Rheumatology (2nd ed.). St Louis, MO: Mosby.. Secondary Muscular Dysfunction Contractures Muscle fibre shortening without an action potential Caused by failure of the calcium pump, even with available ATP Stress-induced muscle tension Neck stiffness, back pain, and headache Associated with chronic anxiety Secondary Muscular Dysfunction (Cont.) Disuse atrophy Reduction in the normal size of muscle cells as a result of prolonged inactivity Bed rest Trauma (casting) Local nerve damage Prevention Isometric movements Passive lengthening exercises Fibromyalgia Chronic widespread diffuse joint pain, fatigue, and tender points Vague symptoms Increased sensitivity to touch Absence of inflammation Fatigue Sleep disturbances/nonrestorative sleep Anxiety and depression Fibromyalgia (Cont.) 80 to 90% of individuals affected are women, and the peak age is 30 to 50 years Inflammation may play a role CNS dysfunction Amplification of pain transmission and interpretation (central sensitization) Fibromyalgia (Cont.) Autoimmune disorders often coexist. Studies of genetic factors have implicated alterations in genes affecting serotonin, catecholamines, and dopamine. Fibromyalgia (Cont.) Manifestations Prominent symptom is diffuse, persistent (present more than 3 months) pain that is burning or gnawing in nature Only reliable finding on examination is the presence of multiple tender points; the pain often begins in one location, especially the neck and shoulders, but then becomes more generalized Profound fatigue Diagnosis Canadian Guidelines for the Diagnosis and Management of Fibromyalgia Syndrome contain specific criteria to aid accurate diagnosis Fibromyalgia (Cont.) Chronic Fatigue Syndrome Neuroimmunoendocrine disease Characterized by: Cognitive impairment Severe postexertional fatigue Unrefreshing sleep Decreased physical activity that affects daily functioning Diagnosis of exclusion Psychological and physiological involvement Muscle Membrane Abnormalities Myotonia Inherited diseases caused by alterations in skeletal muscle sodium and calcium ion channels Delayed relaxation after voluntary muscle contraction Periodic paralysis Characterized by episodes of flaccid weakness Usually hereditary Thyrotoxic hypokalemic Hyperkalemic Metabolic Muscle Diseases Endocrine disorders Systemic effects of hormonal imbalance overshadow muscular symptoms Diseases of energy metabolism McArdle’s disease Myophosphorylase deficiency Acid maltase deficiency Pompe’s disease Myoadenylate deaminase deficiency (MDD) Lipid deficiencies Inflammatory Muscle Diseases: Myositis Viral, bacterial, and parasitic myositis Tuberculosis and sarcoidosis Trichinellosis Toxoplasmosis Staphylococcus aureus Inflammatory Muscle Diseases: Myositis (Cont.) Polymyositis and dermatomyositis, and inclusion body myositis Idiopathic inflammatory myopathies Characterized by progressive, symmetrical proximal muscle weakness and myalgia that develop over weeks to months Associated with an increased risk of malignancy Muscle biopsy showing inflammatory cells grouped around blood vessels and atrophy of cells in muscle fascicles Treatment is immunosuppressive drugs Dermatomyositis From Habif, T.P. (1996). Clinical dermatology (3rd ed.). St Louis, MO: Mosby.. Toxic Myopathies Most common cause of toxic myopathy is alcohol abuse Acute attack of muscle weakness, pain, and swelling Chronic weakness in a drinker of long duration Necrosis of individual muscle fibres Other causes include lipid-lowering agents (fibrates and statins), antimalarial drugs, steroids, thiol derivatives, and narcotics Toxic Myopathies (Cont.) Manifestations: Acute muscle weakness Painless or severe pain if necrosis Most severe complication is rhabdomyolysis (acute muscle fibre necrosis with leakage of muscle protein into the bloodstream) that leads to myoglobinuria and acute kidney failure Bone Tumours May originate from bone cells, cartilage, fibrous tissue, marrow, or vascular tissue Osteogenic Chondrogenic Collagenic Myelogenic Bone Tumours (Cont.) Malignant bone tumours Increased nuclear/cytoplasmic ratio Irregular borders Excess chromatin Prominent nucleolus Increase in mitotic rate Bone Tumours (Cont.) Bone Tumours (Cont.) Patterns of bone destruction Geographical Moth-eaten Permeative Symptoms vague May be attributed to trauma, degenerative changes, or inflammation Bone Tumours (Cont.) Osteosarcoma Most common malignant bone-forming tumour Predominantly in persons under 20 years; occurs in 50- to 60-year-olds if they have a history of radiation therapy Tumours contain osteoid produced by anaplastic stromal cells Deposited as thick masses or “streamers” Located in the metaphyses of long bones 50% occur around the knees Osteosarcoma A, adapted from Bontrager, K.L., & Lampignanno, J.P. (Eds.). (2013). Textbook of radiographic positioning and related anatomy. St Louis, MO: Elsevier; B, from HaDuong, J.H., Martin, A.A., Skapek, S.X., et al. (2015). Pediatr Clin N Am, 62, 179–200. Bone Tumours Chondrosarcoma Cartilage-forming tumour Tumour of middle-aged and older adults Infiltrates trabeculae in spongy bone; frequent in the metaphyses or diaphysis of long bones Tumour expands and enlarges the bone Causes erosion of the cortex and can expand into the neighboring soft tissues Bone Tumours (Cont.) Fibrosarcoma Firm, fibrous mass of collagen, malignant fibroblasts, and osteoclast-like giant cells Usually affects metaphyses of the femur or tibia Metastasis to the lungs is common Bone Tumours (Cont.) Myelogenic tumours Giant cell tumour Causes extensive bone resorption because of the osteoclastic origin and RANKL overexpression Located in the epiphyses of the femur, tibia, radius, or humerus Has a slow, relentless growth rate Muscle Tumours Rhabdomyosarcoma Malignant tumour of striated muscle Highly malignant with rapid metastasis Usually muscles of the head, neck, and genitourinary tract Types Anaplastic Embryonal Alveolar