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33 Cards in this Set
- Front
- Back
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Functions of Bones |
1 Movement of limbs, via mechanical support of muscles 2 Protection of the internal organs Ribs, skull 3 House bone marrow cells Medullary canal 4 Storage of calcium and phosphate salts |
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Facts to know about Bones |
1 Bones are living tissues Constantly change, based on stress (pressure and tension) Hypertrophy, deconditioning 2 Bones are not affected by autoimmune diseases 3 Joints are affected by autoimmune diseases Rheumatoid arthritis, lupus |
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sprain |
1 Injury to the ligamentous structures around a joint 2 Classified depending on amount of tissue damage First, second, third degree |
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Dislocations |
1 Complete loss of joint integrity with loss of anatomic relationships 2 Often significant ligamentous damage occurs 3 Subluxation: partial disruption of Anatomic relationship within the joint |
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Heterotopic Ossification |
1 Bone formation in muscle and other soft tissue areas 2 Occurs mostly after trauma 3 symptoms •May be asymptomatic •Pain and loss of motion •Edema, warmth, erythema, tenderness PT Gentle PROM-no forcible manipulation |
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Osteogenesis Imperfecta |
"defective bone formation" 1 Related to gene mutations encoding collagen type I 2 Collagen type I ●Widespread in the body ○Thin skin, defective heart valves, hearing problems, decrease tooth enamel ●Affects bones and connective tissue ●Clinical presentation depends on severity of disease |
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Osteomyelitis |
Inflammation of the bones caused by an infectious organism In children, infection occurs via the circulatory system Bacteria enters the metaphysis through arteries supplying nutrients to the bone Metaphysis very porous, so the infection Spreads easily and multiplies rapidly -forms pus-spreads to the to adjacent Portions of the epiphyses.
Pus filled cavities form - body attempts to wall off infection by producing reactive bone Bone deformities result, increasing predisposition to fractures Fractures heal poorly because of pus in the area In adults... usually result of puncture wound into bone, open fx, or respiratory/urinary tract infection. |
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Osteomyelitis Clinical Manifestations |
Vary between adults and children Pain Fever Local manifestations: edema, erythema, tenderness |
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Osteomyelitis Risk factors and Treatment |
Risk factors Chronic illness Surgical procedure to bone Open fracture Implanted orthopedic device Treatment Antibiotics Surgical drainage of pus Surgicar repair of defect |
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osteoporosis |
Most common metabolic bone disease It is a major public health threat for an estimated 44 million Americans Primarily a disease of older age But... can occur at any age ◆ 80% are female
Risk Factors •Gender •Race •Family history •Age •Low body weight •Early menopause •Low physical activity levels •Calcium and Vit D intake •alcohol, smoking, caffeine |
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Osteoporosis severity depends on... |
•Initial bone mass •Bone mass peaks at ages 25-35 °Then bone resorption>bone formation °PSS accelerated after menopause °Body size •Diet and lifestyle(intake of Vit D and calcium, ETOH, smoking) •Hormones(estrogen) •Age-related changes with metabolism |
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Osteoporosis primary and secondary |
●primary •Etiology unknown •Accounts for most cases •Disease of elderly •More women than men
●Secondary •Hormonal disturbances •Inadequate intake or malabsorption •lmmobilization •Drugs (anticonvulsants, anticoagulants) •Tumors (hormonal lesions, lesions that destroy the bone directly) |
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Osteoporosis Clinical Presentation |
●Symptoms can be nonspecific ●Fractures ○Head of femur. Distal radius, vertebrae, hips, ribs ○In vertebrae, usually anterior wedge or compression fracture ○Vertebral fractures cause: Dowager's hump ●Gradual height loss ●Protuberant lower abdomen ●Forward flexed posture ●Muscle spasms ●pain |
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Osteoporosis, Prevention, Diagnosis And Treatment. |
Prevention •85-90% of adult bone mass is acquired by age 18 in girls and 20 in boys •Tips •Intake of Vit. D and Calcium •Weight bearing and strengthening exercise •Avoid smoking and excessive alcohol Diagnosis •Bone mineral density testing X-rays to diagnose fractures
Treatment •No cure •Intervention to stop the Progression of bone loss •Medication •Exercise |
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Osteomalacia |
●"softening ot the bones" ●Deficiency of calcium, vitamin D and/or phosphate causes inadequate mineralization of bone matrix. ●Diagnosis difficult and delayed ●Most initially present with diffuse, generalized aching and fatigue ●Deformities of bones common ●Genu varum common because bones unable to carry body weight Thoracic kyphosis ●Fx |
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Page's disease |
Metabolic bone disease Etiology Unknown
Pathogenesis ●Initial stage: osteoclasts proliferate unrestrained ●Bone resorption rapid and osteoblasts cannot keep up Bone replaced with fibrous tissue ●Osteoblastic sclerotic phase ●Normal bone structure replaced by excessive unorganized new bone formation
Symptoms ●Asymptomatic ●Bone pain, arthritis, deformities, fractures ●Thickened cranial bones may compress CNs-> headaches, hearing loss, dizziness Treatment ●Meds to inhibit bone resorption and for pain reduction ●Goal is to induce full remission and prevent complications of the disease
PT ●symptomatic treatment ●Encourage regular exercise ●Fall prevention
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Fractures |
Defect in the continuity of a bone ●Types ●Traumatic ●Stress or fatigue ●pathologic °Insufficiency ●Simple-single fracture line Complete ●Extending through the entire thickness of the bones Incomplete ●Do not extend from one side to the other ●Displaced-bone has moved on either side of fracture ●Comminuted-multiple lines and fragments ●Open-skin is disrupted ●Closed-skin is not disrlipted ●Complicated-infected fx |
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Fractures healing and medication management |
Healing ●lmmobilization vs surgical repair ○Casting vs ORIF/THA/TKA ●Bone will begin to heal once the two side are compressed together immobilization of site ●Once healing has finished, restructuring will occur once mobilization has begun Depends on ●Nutritional status ●Infection Medical Management ●Open reduction internal fixation (ORIF) ●Total hip or knee arthroplasty ●casting ●Vertebral fractures :kyphoplasty, vertebroplasty Complications ●Malunion ●Delayed union ●Non union |
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Bone Tumors |
●Primary bone tumors ○Osteosarcoma(bone forming cells) ○Chondrosarcoma(cartilage cells) ○Ewing's sarcoma (primitive mesenchymal bone marrow cells)
●Secondary ○Metastases from breast, prostate, lung, kidneys, thyroid
●Medical Management ○Surgical resection ○Chemotherapy ○Radiation |
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Osteoarthritis (OA) |
●Degenerative joint disease(DJD) Usually only one side ●Most common joint disease ●Involves the entire synovial joint ●Develops under conditions that stress the joint surfaces ●Preferentially affects weight bearing joints ○Hips, knees, spine(vertebrae) ●Prevalence increases with age Etiology ●Active disease process with joint destruction and aberrant repair as a result of alterations in cellular function ●Multifactorial ○Includes genetics, nutrition, weight control, bone density, estrogen use, local biomechanical factors, previous injury
Pathogenesis ●Articular cartilage Softens, has surface defects, irregular thinning ●Decreased ability to attenuate load ●(+)inflammation ●Joint space narmwing ●Subchondral bone changes ○Sclerosis ○Osteophytes Signs and symptoms ●Joint pain(gradual onset, unilateral usually) ●Decreased strength and ROM ●Increased pain with weight bearing and activity ●Swelling localized to the joint ●Morning stiffness ○Lasts-30 minutes ●crepitus ●Locking of joint |
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Osteoarthritis (OA) Treatment |
●Decrease pain ●Improve function ●Slow disease progression
Treatment ●Medications ●Analgesics ●Topical analgesics ●NSAIDs ●Cox-2 inhibitors ●Supplements ○Chondroitin sulfate ○Glucosamine
●Viscosupplements ●Injectable ○glucocorticoids ●PT/OT ●Weight loss Surgical treatment ●Athroscopy ●Joint replacement ○Unicompartmental ○Total |
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Degenerative Disc Disease (DDD) Etiology |
Common musculoskeletal disease degenerative process in spine Peak in 40-50 y/o Etiology Age related changes Genetic inheritance Inadequate metabolite transport Repetitive external mechanical loading (Alteration of disc from prolonged sitting and heavy lifting) |
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Degenerative Disc Disease (DDD) Pathogenesis |
Same synovial process as in OA Intervertebral discs lose volume, shape and structure
Intervertebral disc looses height with age Decline in arterial supply to the periphery of the disc and impaired nutrient delivery · Affects cellular function Reduced cellular waste removal and increased lactic acid concentration Low pH compromises cellular metabolism Leads to cell death Repetitive external mechanical loading Repetitive external mechanical loading.Leads to fatigue failure of the matrix |
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Degenerative Disc Disease (DDD) Associated conditions |
Spinal stenosis Spinal canal narrows (leaning forward alleviates pressure extention increases pressure) Degenerative spondylolisthesis
Anterior slippage of one vertebrae on another Both cause compression of the spinal cord Further compromised if osteophytes are present
Some may not have any... But if they do... Both cause Low back pain Lower extremity pain and parasthesias Lower extremity weakness due to lack of innervation.stenosis Neurogenic claudicetion Symptoms Improve with flexion
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Degenerative Disc Disease DDD Treatment |
Goal Decrease pain Weight control Exercise core stabilization Less extension
Meds Lifestyle changes Aerobic conditioning physical therapy Surgery ●Laminectomy - increase space ●Discectomy- remove disc ●Fusion- fuse discEpidural- reduce pain ●Disc replacement- |
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Rheumatoid Arthritis(RA) |
Autoimmune disease inflammation/destruction at joint capsule Affects 1% of world population -2-3x more common in women Unknown etiology Chronic, systemic inflammatory disease Genetic and familial predisposition Environmental triggers Joint inflammation consequence of massive infiltration of immune cells into synovial fluid |
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Rheumatoid Arthritis (RA) Pathogenesis |
Primarily involves the synovial joints Begins as synovitis (thickening of synovial and edema)Leads to exudation of fluid and inflammatory cells Inflammation stimulates ingrowth of vessels and proliferation of synovial cells Pannus develops Covers articular surfaces like a sheet Rich in inflammatory cells that secrete Iytic enzymes cartilage is destroyed and erodes Me underlying bone Joints become immobilized Joint deformities result Synovial joint destruction and is bilateral |
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Rheumatoid Arthritis(RA) Clinical Presentation |
Course unpredictable, onset insidious •Some have acute onset of joint pain, swelling and redness •Morning stiffness(longer than OA) Over 1 hr •Chronic, symmetric inflammation of joints Typically small early involvement of hands and feetsystemic symptoms •Weakness and fatigue, malaise, low grade fever, Ioss of appetite •pathological lesions develop (25% of cases) •Rheumatoid nodules (fibrous tissue inflammatory cells) •Chronic inflammation of internal organs
Typical visible changes include •ulnar deviation of the fingers at the MCP joints hyperextension or hyperflexion of the MCP and PIPjoints •flexion contractures of the elbows •subluxation of the carpal bones and toes (cocked- up) |
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Rheumatoid Arthritis Treatment |
●Goal is to reduce pain, maintain mobility, minimize stiffness, edema and joint destruction ●Meds ●surgery ○synovectomy ○Total joint replacement |
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Gout |
"Acute, monoarticular, inllammatory arthritis" Characterized by hyperuricemia Decreased excretion via kidneys or Overproducuon of uric acid Primarily in joints, subcutaneous tissue, and kidneys Great toe, ankle, instep, knee, wrist, elbow, fingers Occurs primarily in middle age men Pathogenesis (First symptoms occur in tarsometatarsal joints of the big toe) Elevated blood uric acid levels enters the joint Hypersaturates the synovial fluid Uric crystals form and deposit in joints and periarticular connective tissue Provoke acute inflammation Tissue necrosis Mostly men with women in 10% and rarely in children. |
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Gout Clinical Features |
Acute ___ Cardinal signs of Inflammation Systemic symptoms(fever, tachycardia, exhaustion, Leukocytosis, chills) Chronic ___ Less Inflammation, less pain, more bone deformities Painless subcutaneous deposits of uric acid (tophi) Deposits of urates In Internal organs |
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Gout treatment |
Goal is to end acute attacks and prevent recurrent attacks NSAIDs Other meds Lifestyle changes Decrease uric acid Dietary changes Less alcohol. |
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Surgical interventions |
Total knee Arthroplasty (TKA) Total knee replacement Femoral component on tibial component Unicompartmental Knee Arthroplasty (UKA) One side of knee replaced(partial) Total hip Arthroplasty (THA) OPEN REDUCTION INTERNAL FIXATION.(ORIF) Surgery to repair broken bone Arthrodesis Surgical fusion with screws and plate Spine most common Can be ankle, knee, wrist Other lower quadrant surgeries Hip disarticulation high AK amputation near the hip joint Hemipelvectomy Removal of part of the pelvis Also high AK amputation. Lumbar Laminectomy Removal of lamia of the lumbar spine (Osteomyelitis) |
