patho MS (musculoskeletal)

Overuse and athletic (not fractures)..
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• Rotator cuff injury is among the most common causes of shoulder pain.

• Rotator cuff tendinopathy almost always represents chronic injury to the supraspinatus (abduction) and/or infraspinatus

• Tears occur primarily in the supraspinatus tendon.

• Sports injuries due to overuse and subluxation of the glenohumeral joint are most common in adolescents and young adults
knee injuries (ACL injuries, meniscal injuries- acute and chronic, MCL and LCL injuries, paterllar dislocations)ACL injuries occur with sudden deceleration with a rotational maneuver, usually without contact. - (Any athlete sport can cause this) Acute meniscal injuries occur with a twisting motion on the weight-bearing knee. Chronic meniscal tears occur from mechanical grinding of osteophytes on the meniscus in older patients with osteoarthritis. Medial collateral and lateral collateral injuries occur from valgus and varus stress, respectively. Patellar dislocations occur from direct contact or a sudden change of direction.ankle injuries (most common, what does the mechanism involve and what ligaments are damaged)• Ankle sprains most common injury to ankle • The mechanism of most ankle sprains involves *inversion and damages the lateral ligaments.* (roll ankle outward)healing process in soft tissue• Repair is accomplished by fibroblasts from the inner tendon sheath (not as vascular as a bone so take longer to heal) • Capillaries infiltrate the injured area during the initial healing process • Formation of the long collagen bundlestreatment of these athletic and overuse injuries (prevention, acute injury management, and chronic management- why might an MRI be needed)• Prevention: • Don't be a week-end warrior • Ergonomical work area • Neuromuscular training, warm-up, stretching, strengthening, plyometrics & agility exercise • Maintain a healthy weight* • Acute injury management • RICE, NSAIDS, Tylenol (rest, ice, compression, elevation) • X-rays if indicated • Chronic management • Activity modification • PT • Braces • Ongoing Tylenol & NSAIDs • Knee & Shoulder injuries: referral to surgeon, typically evaluated with MRI*- because soft tissue of ligaments etc doesn't show up on an xrayTraumatic injuries, compression syndrome and rhabdomyolysis..Signs and symptoms of these things• Pain • Tenderness at the site of bone disruption • Swelling • Loss of function • Deformity of the affected part • Abnormal mobilitysoft tissue injuries (contusion, hematoma, laceration)• Contusion= An injury to soft tissue that results from direct trauma and is usually caused by striking a body part against a hard object • Hematoma =A large area of local hemorrhage • Laceration= An injury in which the skin is torn or its continuity is disruptedfractures (traumatic and complications, open fractures, stress fractures)• Traumatic fracture = Disruption or break in the bone from force, often also includes damage to vascular structures, nerves & soft tissue • Complications: arterial injuries, nerve injuries, compartment syndromes, VTE, fat embolism • Open fracture = Direct communication between the fracture & outside environment • Stress fracture= Bone breaks due to repeated tensile or compressive stressespediatric signs of abuse and what do we do as providers to catch this and help"Corner" metaphyseal fractures Transverse tibial fractures are the most common Fractures at multiple stages of healing= Associated with child abuse, but osteogenesis imperfecta must be ruled out Early consultation with child protective services thorough historyolder adults- most common joint with problemsHip fractures substantially increase the risk of major morbidity and death in older patients. Men and women over the age of 60 with distal radius fractures are more than five times as likely to have a hip fracture within 1 year.healing fractures- direct• Most often occurs when surgical fixation is used to repair a broken bone • Intramembranous bone formation • No callus formationhealing fractures- indirect• Most often observed when a fracture is treated with a cast or other nonsurgical method • Intramembranous and endochondral bone formation • Callus formation • Remodeling of solid bone5 stages of bone healing and factors that impede the processFive Stages of Bone Healing 1) Hematoma formation 2) Cellular proliferation 3) Callus formation 4) Ossification 5) Remodeling Factors that impede this process: Patient's age; Current medications; Debilitating diseases; Local stress around the fracture site; Circulatory problems; Coagulation disorders; Poor nutritiontreatment of fractures• Three objectives for treatment of fractures: 1) Reduction of the fracture • Closed manipulation or surgical reduction 2) Immobilization • Immobilization through the use of external devices 3) Preservation and restoration of the function • Therapyrhabdomylosis is what, caused by, can result in whatRapid breakdown of muscle that causes the release of intracellular contents, including the protein pigment myoglobin, into the extracellular space and bloodstream Caused by: trauma or muscle compression, drugs, infections, & others Can result in hyperkalemia, cardiac arrhythmia, or acute renal failuremanifestations and how to diagnose rabdo, main complication• *Muscle pain & weakness* • *Dark urine (red to brown)* • Fever, malaise, tachycardia, and GI symptoms may also be present Diagnosed when CK level 5-10 times upper limit of normal Renal failure likely when CK reaches 15,000 units/L Preventing kidney failure and maintaining adequate urinary output are goals of treatmentcompartment syndrome results from what, what results, what can cause itResult of increased pressure within a muscle compartment - exceeds the perfusion pressure of the tissue Cellular anoxia = muscle ischemia causes edema, rising compartment pressure, and tamponade that lead to muscle infarction and neural injury Can be caused by any condition that disrupts the vascular supply to an extremity • fractures, crush injuries, SIRS, infection, rhabdo, birth injury, prolonged immobilization, snakebitesmanifestations and what do we do urgently for compartment syndrome, how to confirm diagnosis, when is surgery indicated, treated with whatManifests with pain, paresthesia, pallor, diminished pulse, worsening symptoms with passive stretching; upper extremity, Volkmann ischemic contracture STAT surgery consult • Diagnosis can be confirmed by measurement of intracompartmental pressure • Surgical intervention indicated when pressure reaches 30 mm Hg Treated with extremity fasciotomyInflammatory over reactions..Systemic autoimmune rheumatic diseases are what, what do they share• A group of chronic disorders characterized by diffuse inflammatory lesions and degenerative changes in connective tissue • These disorders share similar clinical features and may affect many of the same organsRheumatoid arthritis (RA) patient or inflammatory arthritis presents howI just hurt in the mornings, it's crazy I feel 90 years old when I wake up! = how it might present= RA or Inflammatory Arthritissigns and symptoms of RA, associated with what, systemic manifestations, local, characterized by what, may involve what• *Insidious (GRADUAL) onset of pain, stiffness, & swelling of multiple joints= polyarticular* • Associated with extra-articular as well as articular manifestations • Systemic manifestations such as fatigue, anorexia, weight loss, and generalized aching and stiffness. • Local tenderness from pressure applied on the joint or by pain on moving the join • Anemia, fatigue, subcutaneous ("rheumatoid") nodules, pleuropericarditis, neuropathy, episcleritis, scleritis, splenomegaly, Sjögren's syndrome, vasculitis, and renal disease • Characterized by exacerbations and remissions • May involve only a few joints for brief durations, or it may become relentlessly progressive and debilitatingRA diagnosis , what do we draw and what are these checking for• Rheumatoid factor - autoantibodies* (moderate specific, can be positive and something else is going on) - could be lupus, Sjogren's syndrome, malaria, rubella, vaccinations can cause a positive result • Anti-citrullinated peptide antibodies (ACPA)* • Anti-cyclic citrullinated peptides (CCP)* • Sedimentation rate (ESR) and C- reactive protein (CRP) ESR and CRP= immune reactions, extra proteins in our blood= inflammatory process going oncause and patho of RA• Genetic & Environmental • MHC gene involved, along with many other genes • Repeated activation of *innate immunity* • Loads joints with APC's - T-cells & B-cells respond (antigen presenting cells in the joint spaces, presenting to the adaptive immune system, T and B cells respond and create more immune response) begins to break down cartilage in the bone • Macrophages & complement activation also play a critical role.three processes of RA= what do we see that is abnormal• Neutrophils and other cells in the synovial fluid become activated • Inflammatory cytokines: tumor 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)*treatment of RA- meds and non meds, prevent what, labs• STOP inflammation!!= • Diagnose promptly, refer quickly. • Nonpharmacologic measures= • patient education, psychosocial interventions, and physical and occupational therapy (chronic disease- will have for rest of their life) • DMARDs - disease-modifying antirheumatic drug • Consider holding for infection! • CBC, ESR, CRP, Liver & kidney function, Baseline eye exams, TB testing, Screening for hepatitis B & C Prevent infection- we will be suppressing the immune system - rule out TB and hepatitis, will have to collaborate with her specialist, but she can get really sick with something like an URI from being immune suppressedmy toddler has weird fevers and i think her arms hurt her!JIA (Juvenille idiopathic arthritis) Systemic Juvenile Idiopathic Arthritis (formerly known as juvenile RA)JIA is what, what happens, what is present, type of disorder, how do you get it• A chronic disease characterized by synovitis • Synovial fluid accumulation and synovial thickening tumor-like expansion of inflamed synovial tissue, pannus Pannus -- proliferation of synoviocytes and invasion of the synovial tissue by inflammatory cells, including lymphocytes, macrophages, and dendritic cells, recruited from the peripheral circulation • As with most autoimmune disorders, interactions among genetic factors, immune mechanisms, and environmental exposuresrisks (age, race) , manifestations- what do we really have to watch for , and treatment of JIA• Risks= Peak onset 1-3 years of age, with more girls affected, then another peak at 8- 10 years of age with more boys affected. Caucasian • Manifestations= Fever - 98% Arthritis - 88% (8% w/ monoarthritis, 45% w/ oligoarthritis, & 47% w/ polyarthritis) Rash - 81% Lymphadenopathy - 31% Lab abnormalities -- granulocyte predominant leukocytosis, elevated acute-phase reactants including thrombocytosis, and hyperferritinemia Stunted growth also may occur* • Influence epiphyseal growth by stimulating growth of the affected • Treatment= • NSAIDS • Glucocorticoidssystemic lupus erythematosus (SLE) is what, what type of hypersensitivity, what happens in the body, can do what to tissues and how, what can trigger it, who is it more common in- race and sex• B-cell hyperreactivity (stage III hypersensitivity) • Formation of autoantibodies and immune complexes • Increased production of antibodies against self (autoantibodies) and non-self antigens • Can directly damage tissues or combine with corresponding antigens to form tissue-damaging *immune complexes*- make immune complexes and deposits elsewhere- kidneys etc Antinuclear antibodies Other antibodies Platelets Coagulation factors Red blood cell surface antigens • Remember immune complexes in stage III hypersensitivity, macrophages destroy the kidney • Can be triggered by drugs as well. • Hormonal influence (estrogen, progesterone, much more common in females, but males have worse prognosis) • African American > Caucasianmanifestations of SLE• Constitutional symptoms, such as fatigue, fever, and weight loss • Arthritis and arthralgias occur in over 90% of patients • Comorbid: • Cardiac disease = pericardial effusions • Renal disease= ESRD • GI symptoms (can be related to treatment) • Pulmonary= ILD • Neuropsych • Heme - higher risk for blood clots/thrombosis Can affect every organ system Hair loss, oral lesions, sesntiive to sun, joint pain/swelling, pericarditis symptomstesting and treatment of SLE• Testing= • CBC, UA, BMP • antinuclear antibodies (ANA; and if positive, other specific autoantibodies, such as anti-double-stranded DNA [anti-dsDNA] and anti-Smith [anti-Sm]), antiphospholipid antibodies, C3 and C4 or CH50 complement levels, erythrocyte sedimentation rate (ESR) and/or C-reactive protein (CRP) levels, and the urine protein-to-creatinine ratio. • Treatment = Nonpharmacological • sun protection, diet and nutrition, exercise, smoking cessation, maintenance of appropriate immunizations, treatment of comorbid conditions, avoidance of certain medications, and pregnancy and contraception counseling • Antimalarial (inhibits neutrophils & chemotaxis)manifestations of children with SLE• Constitutional symptoms= • Fever, malaise, anorexia, weight loss • Affects their growth & development** • Symptoms of the integumentary, musculoskeletal, central nervous, cardiac, pulmonary, and hematopoietic systems are similar to those of adults. • Endocrine abnormalities include: • Cushing syndrome from long-term corticosteroid use. • Autoimmune thyroiditis.cause and patho of fibromyalgia (what plays a role, brain scan?• CNS dysfunction • Amplification of pain transmission and interpretation (central sensitization) • Exaggerated pain response to experimental pain stimulus, altered structural and neurotransmitter function, and changes in resting-state functional connectivity • Sleep, mood, and cognitive disturbances, as well as stress-related factors involving the autonomic nervous system (ANS), each contribute to the central nervous system hyperirritability • *Genetic and environmental factors* likely interact to promote a state of chronic central and peripheral nervous system hyperirritability. • Studies of genetic factors have implicated alterations in genes affecting serotonin, catecholamines, and dopamine Brain scans show changes with fibromanifestations of fibro (how is the pain described, presentation, who is most affected)• Chronic widespread diffuse joint pain, fatigue, and *tender points* • Manifestations= Vague symptoms, increased sensitivity to touch, absence of clinical inflammation, sleep disturbances/nonrestorative sleep, & Anxiety and depression Prominent symptom of fibromyalgia is *diffuse, chronic (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 • 80% to 90% of individuals affected are women, and the peak age is 30 to 50 years*diagnosis of fibro• Axial pain, left- and right-sided pain, and upper and lower segment pain; and a symptom severity (SS) score • SS score includes symptoms such as fatigue, waking unrefreshed, and cognitive difficulty • CBC, CMP, inflammatory markers to rule out other diseases. Rule everything else out before diagnosis, don't have a cure or even good meds availabletreatment of fibro• Education= • Good sleep hygiene, treating comorbid mood disorders, weight reduction in overweight patients, aerobic cardiovascular training • Medications= • Antidepressants & related drugs • PT, CBT, referrals to multidisciplinary teamchronic fatigue syndrome (CFS) is also known as, what type of disease• Also known as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) • Neuro immune-endocrine disease: • complicated disease characterized by unexplained, persistent, and relapsing fatigue • Proposed etiology: infection, immune dysfunction, endocrine-metabolic, depressiondiagnosis of chronic fatigue syndrome• Diagnosis difficult, Characterized by: Post-exertional malaise (prolonged exacerbation of symptoms after physical, cognitive, or orthostatic exertion or stress) Unrefreshing sleep after sleeping many hours Cognitive impairment, exacerbated by exertion or stress Orthostatic intolerance • Diagnosis of exclusionCFS management• Psychologic and physiologic involvement • Supportive & treat symptoms and comorbid conditions • sleep disorders, pain, depression and anxiety, memory and concentration difficulties, and dizziness and lightheadedness.My back just always hurts..Anklyosing spondylitis (AS)AS is what, what area is affected, end result is what• Group of inflammatory arthropathies known as spondyloarthropathies (SpA) • Inflammatory joint disease of the spine or *sacroiliac joints causing stiffening and fusion of the joints* • End result is fibrosis, ossification, and joint fusionmanifestations of AS (comorbid conditions, when does it begin, what does the back look like)• 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) • Sacroiliitis present on imaging • Comorbid: heel pain, dactylitis, uveitis, IBD, psoriasis. Another disease of enraged and hyperactive immune system- therefore have comorbid conditions Dactylitis- sausage finger- enlarged fingercause and patho of AS (specific antigen, specfic body system)• Complex interaction between: -axial skeleton and its entheses -peripheral joints -genetics -immune systems including the cytokines -bowel -MHC, human leukocyte antigen *HLA-B27 antigen* plays a role -Cyclooxygenases (COX), tumor necrosis factor (TNF)-alpha, and interleukin (IL) 17 play a large role Bone changes from inflammation Begins with the inflammation of fibrocartilage, particularly in the vertebrae and sacroiliac joint Inflammatory cells infiltrate and erode fibrocartilage Reparative process via the mesenchymal cells & new bone formation Scar tissue ossifies and calcifies; the joint eventually fuses Bowel gut health contributes*tests and treatment of AS = prognosis• Labs & Diagnostic Testing= HLA-B27 is present in 85 to 95 percent of Caucasian patients with AS Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) X-rays, MRIs Not as high of a genetic marker in blacks, doesn't mean they don't have it but not as high of a chance of being there • Treatment= Physical therapy to maintain skeletal mobility and prevent the natural progression of contractures NSAIDs for pain Good prognosis but causes quality of life things- chronic issuegouty arthritis patho• Hyperuricemia (all about too much uric acid) absolute or relative impairment of renal and gut urate excretion and/or overproduction of urate leads to monosodium urate (MSU) crystal deposition • Neutrophil recruitment to the joint innate immune system-mediated inflammation and include activation of monocytes/macrophages, mast cells, endothelial cells, and dendritic cells) and of the NOD-like receptor protein 3 inflammasome, which leads to IL 1*. Release of IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and additional proinflammatory molecules also supports MSU crystal-induced inflammation. • Phagocytosis of MSU crystals by neutrophils= • respiratory burst and release of lysosomal enzymes, superoxide anion, leukotriene B4, and IL-1 and additional cytokines and chemokine • Severe articular and periarticular *inflammationmanifestations of acute gout attacks and triggers of gout, onset when, what area of body, reoccuring attacks?• Manifestations of acute attacks= • Monoarticular, with severe pain, redness, swelling and disability - can extend beyond the joint (one joint) • Triggers = • Alcohol consumption, including beer, spirits, and wine • Trauma, surgery, starvation, fatty foods and other dietary triggers (meat, seafood), dehydration, ingestion of drugs affecting (raising or lowering) serum urate concentrations • Obesity • Onset nocturnal • Lower extremity involvement (1st metatarsophalangeal) or knee (great toe- classic presentation) • Recurrent attacks with resolution between attackscomplications of gout• Complications: -Tophi or the accumulation of crystalline deposits in articular surfaces, bones, soft tissue, and cartilage -Gouty nephropathy or renal impairment -Uric acid kidney stones -Hyperuricemia: purines turn into uric acid, can get from diet and purine synthesistesting- what is the gold standard and treatment for gout- more common in who, work on what• Testing = • Uric acid levels, BMP • Joint aspiration * gold standard • Treatment = • Termination and prevention of the acute attacks of gouty arthritis • NSAIDs, glucocorticoids • Joint injections Relapsing disease, used to be called the kings disease because only kinds had access to the foods, wine, etc WORK ON PREVENTION*, more prevalent in males = avoid triggersMore zebra rheumatological disorders..Systemic sclerosis- Scleroderma is what kind of disease, what is most commonly involved, manifestations, how do we treat, prognosis• Autoimmune disease of *connective tissue characterized by excessive collagen deposition in the skin and internal organs*- skin involvement very common • Skin involvement - thickening & hardening • Clinical features Hardening of the skin (scleroderma) is limited to the hands and face. Calcinosis (calcium deposits in the subcutaneous tissue that erupt through the skin) Sclerodactyly (localized scleroderma of the fingers) Telangiectasia Raynaud phenomenon Esophageal dysmotility Pulmonary vascular disease/PAH & ILD Kidney damage • Reverse inflammation or vasoconstriction *Poor prognosis*reactive arthritis (formerly known as what, is a form of what, hen does it happen)(formerly known as Reiter Syndrome) form of spondylarthritis Arthritis that follows infection • Preceding infection* • Peripheral arthritis (often the knees); enthesitis (inflammation at ligaments, tendons, joint capsule); dactylitis; low back pain • Extra-articular symptoms such as uveitis, bowel inflammation, carditis, GUsymptoms of reactive arthritis, common infections, how do we treat, remission"Can't see, can't pee, can't climb a tree" (knee and back pain, cant see and chlyamdia - cant pee) Develops in a genetically susceptible host after a bacterial infection due to *Chlamydia trachomatis or other infections (Salmonella, Shigella, Yersinia, or Campylobacter in the gastrointestinal tract) Treat the infection; treat the inflammation Majority of patients are in remission at 6-12 monthspsoriatic arthritis is what, who does it occur in, can be where, what are signs, what is the patho similar too• Inflammatory arthritis • may occur in up to 30 percent of patients with psoriasis • Can be peripheral, axial, or both • Nail pits and onycholysis* • Uveitis and conjunctivitis & pitting edema also common • Patho is quite similar RA (hyperactive B cells, B cells make auto antibodies and deposit in joints)treatment for psoriatic artritis• drug therapy • physical and occupational therapy, exercise, prescription of orthotics, and education regarding the disease and about joint protection, disease management, and proper use of medicationgiant cell arteritis (GCA) and Polymyalgia rhematica patho• Patho is similar: • Associated with specific alleles of HLA/MHC DR4; T-helper cells/ T-reg cells (lots of T helper cells and not a lot of T reg cells- help police so immune system doesn't get over active) • Inflammation with tissue or vascular destructionssymptoms of GCA• Constitutional symptoms= • Malaise, fatigue, fever, weight loss, cough, sore throat • Manifestations related to vascular involvement • Ischemic optic neuropathy ( can cause blindless) • Claudication of jaw or arm • Diagnostic testing: temporal artery biopsysymptoms of PMR• aching and morning stiffness about the shoulders, hip girdle, and neck • elevated acute phase reactants (eg, ESR and/or CRP) • prompt response to glucocorticoids Bilateral neck, torso, shoulders, hips, thigh- worse in the morningmyositis is what, what can it cause, characterized by waht, associated with waht, muscle biopsy, treatment is whatInflammatory Muscle Diseases: Myositis • Viral myositis- • Can cause rhabdo • Polymyositis and dermatomyositis, and inclusion-body myositis Idiopathic inflammatory myopathies Characterized by progressive, symmetric 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 = muscle biopsy to diagnosis Treatment is immunosuppressive drugsOsteomyelitis, bone cancers, osteoporosisosteomyelitis is what, acute, chronic• Origin of bone infections • Microorganisms introduced during injury, introduced during operative procedures or from the blood stream • Acute= • Dull pain at the involved site, with or without movement • Tenderness, warmth, erythema, and swelling • Fevers/rigors • Chronic= Intermittent flares of pain and swelling The hallmark infected dead bone, a sequestrum, that has separated from the living bone. All inflammatory processes of bone, excluding those in rheumatic diseases that are caused by microorganisms. Usually occurs in adults.actions of micro-organisms localized in the bone in osteomyelitis and treatment• Actions of Microorganisms Localized in Bone= Proliferate Produce cell death Spread within the bone shaft Incite a chronic inflammatory response with further destruction of bone • Treatment= • Antibiotics, debridement, surgery, hyperbaric oxygen therapyosteonecrosis also called what, what is it, how is it different to OM, what causes itOsteonecrosis (Avascular necrosis of bone) - lack of blood supply to the bone, not related to OM • Causes • Mechanical disruption of blood vessels • Thrombosis and embolism • Vessel injury • Increased intraosseous pressureblood flow in osteonecrosis and symptoms• Blood Flow Interconnecting plexus Outer cortex receives supply form surrounding blood vessels. Some sites have limited collateral circulation; interruption flow affects significant amount of bone tissue. • Symptoms = • Can be asymptomatic or symptomatic with paindiagnosis and treatment of osteonecrosis• Diagnostic testing= • X-ray of the site, could also consider MRI if high suspicion • Treatment= • depends on the underlying pathologic process. • short-term immobilization, nonsteroidal anti-inflammatory drugs, exercises, and limitation in weight bearing are used. • Surgery, osteonecrosis of the knee or hip often leads to total joint replacement.pediatric pearl- Legg Calve PErthes (is what, presents how, age)Pediatric pearl: Legg-Calve-Perthes = avascular necrosis of the hip, presets with hip pain or a limp between the ages 3 & 12 years.juvenile osteochondrosis (idiopathic avascular necrosis) is what, types,• One or more growth ossification centers undergoes a period of degeneration, necrosis, or inactivity that is followed by regeneration and usually deformity • Legg-Calvé-Perthes disease • Osgood-Schlatter disease • Slipped capital femoral epiphysisblood supply in juvenile osteocondrosis• Decrease blood supply • Trauma • Change in clotting sensitivity • Vascular injury • Genetic predisposition • Involves areas of significant tensile or compressive stressLegg Calve perthes disease is what, causes what, type of disease, more common in who, what leads to it, what makes it worse and what makes it better• Interrupted blood supply to the femoral head • Causes epiphyseal necrosis or degeneration of the head of the femur • Self-limiting disease • More common in boys • Injury or trauma precedes onset in approximately 30% to 50% of cases • Pain is usually aggravated by activity and relieved by rest and administration of anti-inflammatoriesclinical manifestations of legg calve perthes disease and management• Clinical manifestations = Spasm on rotation of hip • Limited internal rotation or abduction of hip • Trendelenburg gait • Clinical management= • Anti-inflammatories • Serial radiographs • Surgeryosgood schlatter disease is what, how common, manifestations, managementTendinitis of the anterior patellar tendon and osteochondrosis of the tubercle of the tibia One of the most common ailments in children involved in sports Clinical manifestations= • Pain • Swelling Clinical management= • Restricted activity; usually 4-8 weeks • Cast or knee immobilizer Severs disease—heel bonesymptoms and signs of bone tumors , where do bone tumors originate• Symptoms= • Pain • Presence of a mass • Impairment of function Bone tumors originate in the mesoderm (either the fibroblast or reticulum of the mesoderm)benign vs malignant tumors• Characteristics of Benign Tumors (Osteoma, Chondroma, Osteochondroma, & Giant cell tumor)= • Limited to the confines of the bone • Well-demarcated edges • Surrounded by a thin rim of sclerotic bone • Characteristics of Malignant Bone Tumors (Osteosarcoma, Ewing Sarcoma, Chondrosarcoma)= • Tend to be ill defined • Lack sharp borders • Extend beyond the confines of the bonosteochrondroma is what kind of tumor, how does it occur, how do you get it, when can you see/feel it*benign bone tumor* • Can occur as a solitary lesion • Inherited syndrome of hereditary multiple exostoses • Exostoses occur throughout the skeleton • Painful, palpable mass when traumatizednon-ossifying fibroma is what, how common, how to treat*benign bone tumor* • Sharply demarcated, cortically based lesions of fibrocytes • Nearly 30% of all children have at least one • Observational treatmentosteosarcoma is what, how common, where does it originate, linked to what, type of tumor and where does it extend*malignant bone tumor* Most common malignant bone tumor in childhood (peaks in adolescent and then >65 years of age) Originates in mesenchymal cells* Linked to deletion of genetic material on the long arm of chromosome 13 and oncogene src Bulky tumor extending into a soft tissue massmanifestations and management of osteosacromaClinical manifestations = Night pain, swelling, warmth, and redness • Cough, dyspnea, and chest pain if lung metastasis Clinical management = Graded according to malignancy • Surgery and chemotherapyEwing sarcoma is what kind of tumor, what is unique about it, what chromosomes are abnormal, penetration of what, metastasis*malignant bone tumor* • Most lethal childhood bone tumor • Translocation of chromosomes 11 and 22 • Penetrates the bone to form soft tissue mass • Metastasizes to nearly every organmanifestations and management of ewing sarcoma• Clinical manifestations= Pain that increases in severity Fever Malaise Anorexia • Clinical management = Radiation and chemotherapy • Surgical debridement • Long-term effects from therapymetastatic bone cancer characterisitcsMetastatic lesions are seen most often in the spine, femur, pelvis, ribs, sternum, proximal humerus, and skull. Tumors that frequently spread to the skeletal system are those of the breast, lung, prostate, kidney, and thyroid.metastatic bone cancer treatment• Preventing pathologic fractures • Promoting survival with maximum functioning • Allowing the person to maintain as much mobility and pain control as possible • Chemotherapy • Irradiation • Surgical stabilizationosteoporosis (OP) and bone patho...major infleunces on equilibrium of bone tissue• Mechanical stress • Calcium and phosphate levels in the extracellular fluid • Hormones and local growth factors • Cytokinestypes of bone remodeling• Osteoblasts and osteoclasts in homeostatic balance in normal tissue • RANK/RANKL • Osteoprotegerin • Structural remodeling= • Involves deposition of new bone on the outer aspect of the shaft at the same time that bone is resorbed from the inner aspect of the shaft • Internal remodeling= • Largely involves the replacement of trabecular bone, continuous during adulthoodcauses and patho of osteopenia and osteoporosis• Osteopenia= • Reduction in bone mass greater than expected for age, race, or sex • Osteoporosis= • Low bone mass, microarchitectural disruption, and skeletal fragility • Causes= -Decrease in bone formation, inadequate bone mineralization, excessive bone deossification -Intrinsic bone dysfunction: mitochondria dysfunction, oxidative stress, declining autophagy, DNA damage, osteoprogenitor and osteocyte senescence -Extrinsic mechanisms: age-related changes in other organs, such as ovaries, innate immune system.signs and symptoms of osteoporosis, risks, what do we measure• Asymptomatic frequently, until fractures occurs • Fragility fracture, particularly at the spine, hip, wrist, humerus, rib, and pelvis • Occur spontaneously or with minor trauma • Bone density measurement= • T-score that is 2.5 SD below young adult • T-score that is 1-2.5 below young adult = osteopenia • Those at risk: • Advancing age, previous facture, glucocorticoid use, low body weight, parental hx of hip fracture, cigarette smoker, RA. Fragility fracture- small event causes a fracture, minor injury causes a fracturediagnosis and treatment of OP• Diagnosis = • BMD assessment • Dual-energy x-ray absorptiometry (DXA) of the spine and hip • Treatment= • Prevention: = • Regular exercise and adequate calcium intake are important factors in preventing osteoporosis Weight-bearing exercises such as walking, jogging, rowing, and weight lifting are important in the maintenance of bone mass Drug treatment= • Anabolic agents • Antiresorptive agentsosteomalacia is what, what does not occur, symptomsA generalized bone condition in which inadequate mineralization of bone results from a calcium or phosphate deficiency, or both Remodeling cycle proceeds through osteoid formation but calcification does not occur; the result is soft bones • Pain, bone fractures, vertebral collapse, bone malformationrickets is what• A disorder of vitamin D deficiency, inadequate calcium absorption, and impaired mineralization of bone in childrenpaget disease is what kind of bone diease, what happens, symptoms, characterized by what, mostly affects where, how do we evaluateOsteoclast disorder, accelerated rate of bone remodeling A progressive skeletal disorder that involves excessive bone destruction and repair; often asymptomatic If people have symptoms—pain and deformities in affected areas and a heightened risk of fracture Characterized by increasing structural changes of the long bones, spine, pelvis, and cranium • Mostly affects vertebrae, skull, sacrum, sternum, pelvis, & femur • Evaluation based on radiographic findingsbone system across the life span..development of the skeletal system- develops from where, when,• Develops from the mesodermal and neural crest cells of the developing embryo • *4th week*: development of the vertebrae of the axial skeleton •* Late in 4th week*: the paddle-shaped *limb buds of the lower extremities make their appearance • *9th week*: ossification begins with the appearance of ossification centers in the lower thoracic and upper lumbar vertebrae.congenital deformities (mild and major limb malformations)• *Mild limb deformities* (relatively common) • Syndactyly: simple webbing of the fingers or toes • Polydactyly: the presence of an extra digit • Absence of a bone such as the phalanx, rib, or clavicle • *Major limb malformations* (relatively rare) • Joint contractures and dislocations • Absence of entire bones, joints, or limbslower extremity positional deformities summary- metatarsus adductus, calcavenvaulgus feet= these are all what, and why do they happen• Metatarsus adductus= medial deviation of the forefoot while the hindfoot remains neutral. • Calcaneovalgus feet= hyper dorsiflexion of the foot with the abduction of the forefoot • Positional clubfoot • Internal and external tibial torsion = In-toeing, out-toeing • Physiologic genu varum = physiologic bowing These normally go away with time** = THESE ARE BENIGN Baby's may not get the movement they need in utero- can be positionalcongenital clubfootCongenital clubfoot- more severe than positional clubfoot- developed abnormal sublaxation of talo clavicularnavicular joint, underdevelopment of soft tissues of medial side of foot = need manipulation and castingdevelopmental dysplasia of the hip (DDH) when do we check for this, what happens, how does the hip presentcheck on a well baby exam • Abnormality of the hip that can affect the femur, acetabulum, or both • The hip can present as subluxated, dislocated, or acetabular dysplasiamanifestations pf DDH• Asymmetry of skinfolds at groin crease • Galeazzi sign • Limitation of hip abduction • Positive Ortolani sign • Positive Barlow signhow do we get DDH, risk factors, and management of DDH• Either idiopathic or teratologic (secondary to another disorder) • Risk factors= • Female sex • Oligohydramnios (too little/decreased amniotic fluid) • Positive family history • Breech presentation • Clinical management= • Pavlik harness • Closed reduction with spica casting • Surgery • Outcome becomes poorer with age NEED TO CATCH EARLY- outcomes worse if not caughtosteogenesis imperfecta is what, defect of what, manifestations• "Brittle bone disease" • Defect in type I collagen production* • Bone and vessel collagen • Clinical manifestations= Osteopenia, Increased rate of fractures, Bone deformity (bowing) Abnormality in hip development that leads to a wide spectrum of hip problems in infants and children Type III- Short stature and Blue sclera and poor dentition Aortic aneurysmosteogensis imperfecta management (surgical and medical)• Surgical = • Intramedullary or telescoping rod placement • Medical= • Increased calcium and vitamin D • Biphosphateswhat is scoliosis and types• Lateral deviation of the spinal column that may or may not include rotation or deformity of the vertebrae • Types: • Congenital scoliosis: caused by disturbances in vertebral development during the 6th to 8th week of embryologic development • Neuromuscular scoliosis: develops from neuropathic or myopathic diseases • *Idiopathic scoliosis: structural spinal curvature for which no cause has been established= Includes the common scoliosis often monitored in adolescents Idiopathic- happens in adolescents/teensMuscular dystrophies are what• Group of inherited disorders that cause *progressive muscle fiber loss* • The muscular dystrophies cause weakness, mostly of the voluntary musclesduchenne muscular dystrophy- DMD- how do we get it, who does it affect more, how common, caused by what,• Most common of the muscular dystrophies • X-linked = • Generally, affects boys (girls are carriers) • Caused by mutations in the dystrophin gene= • Dystrophin maintains the structural integrity of the cytoskeleton Can affect cardiac muscle toobecker muscular dystrophy is caused by what, when does it present, life expectancy compared to DMD• Caused by alterations of the same dystrophin gene and protein as seen in DMD • Presents later in life than DMD • Longer life expectancyaging and the bones (what happens to the bones, bone remodeling)• Bone loss • Less dense, less strong, more brittle • Bone remodel time is lengthenejoints as we age (cartilage, range of motion) and muscles are we age (muscle mass and strength, oxygen intake, meatbolic rate, body mass)• Joints = • Cartilage becomes more rigid, fragile, susceptible to fraying • Decreased range of motion • Muscles= • Sarcopenia (muscle breakdown) • Decrease in muscle mass and strength • Reduced oxygen intake, basal metabolic rate, and lean body masssymptoms of osteoarthritis and locaiton, how is RA different than OA• Symptoms= Joint pain, stiffness, and locomotor restriction Present in just one or a few joints in a middle-age or older person As disease progresses: Limitation of motion, joint instability, deformity • Location= • knees, hips, finger interphalangeal joints, first carpometacarpal (CMC) joints, first metatarsophalangeal (MTP) joints, and apophyseal (facet) joints of the lower cervical and lower lumbar spine RA= symmetrical, OA= not symmetricalsecondary OAhas a known underlying cause such as= • congenital or acquired defects of joint structures, trauma, metabolic disorders, or inflammatory diseases.OA patho- formerly known as what, progressive what, what thickens, smyptoms of OA - triggered by what, how is it different than RA• Formerly considered to be simply a degenerative "wear and tear" process, actually called Degenerative Joint Disease • Some argue OA should also be considered a systemic rather than focal MS disease A progressive loss of articular cartilage *Thickening of subchondral bone* • Osteophytes • Bone spurs Synovitis & synovial hypertrophy - but different immune cells than RA • Felt trigger are DAMPs* (in RA it's the B cells, in OA it's the DAMPS, RA is autoantibodies, OA is damaged pathways) Soft tissue damage • ligaments, the joint capsule, and, in the knee, the menisci Symptoms of OA= Bouchard and Heberden nodes), deformity of jointtesting and treatment for OA - goals• Testing= • X-rays • Goals: minimize pain, optimize function, and beneficially modify the process of joint damage • Nonpharmacological, *weight loss (10% total reduction = 50% reduction in pain), exercise, walking aids • Pharmacological, NSAIDs • Surgery (joint replacements)previous contentstudy anemia and immuneZOOM REVIEW...hip dysplasia (what is a main symptom, when would we pick up on it)6-month well child exam Check for hip dysplasia - usually would have caught before 6 months Waddling gait and shorter leg* at birth = we should have picked this up way before 6 monthsdad has RA- what does this mean for baby, JIA vs. RADad has RA= I'm worried the baby is going to get juvenile or RA= it could be genetic Arthritis's is polygenetic- not a single gene- more than one involved and environment/epigenetics involved that can make a difference for the baby Baby may have an increased risk but it's very difficult to predict Juvenile arthritis vs. RA= larger joints affected with juvenile; pain is less significant (kids are resilient)other things besides hip dysplasia that are on the newborn screenDuchenne's muscular dystrophy osteogenesis imperfectaduchennes muscular dystrophy, what happens, and what is impacted, what does it end up in, prognosisDuchenne's muscular dystrophy gene= muscle fiber loss, dystrophin is impacted, dystrophin maintains cytoskeleton, anchors muscle fibers to the basement membrane- if we lose dystrophin, we have muscular breakdown = results in muscular weakness, poor prognosis, end up in wheelchairs= significantly impaired mobilityosteogenesis imperfecta is what, what is abnormal, what is the baby more prone to, what to educate onbrittle bones from a defect in collagen synthesis = not making collagen of bones- have to educate the parents that the child needs more calcium, vitamin D, careful handling baby= baby is more prone to fracturesPaget's disease - how do you get it and what is a huge risk factoron new born screening too- not a single gene, first degree relative= much greater risk= *both genetic and environmental influences= 15 to 40% of people that have Paget disease have a FIRST DEGREE RELATIVE WITH THE DISEASE*mom is tired, has gained weight, pain everywhere and not sleeping well= what does she have, what tells us this, how is it different than CFS, lupus, to treat fibro, prognosis of fibroTender points on body= upper back, shoulders Answer is fibromyalgia Fibro vs. chronic fatigue= tender points in fibromyalgia, infection usually before chronic fatigue = see a triggering event, fibro does not have a triggering event Lupus= antigens against our self To treat fibro= sleep hygiene, meds, CBT, weight loss, exercise Fibro = prognosis is chronic condition, wide range of how severe it can bedad has pain in both wrists and hands, sometimes even knees, worse in the mornings= what does he have, what labs would we check, what is this in one sentence, what is unique abbout this lab, treatment for this, high levels of what immunoglobin*ANA high, sed rate through the roof, rheumatoid factor is positive Immune system attacking own joints Rheumatoid factor= B cells are making antibodies or immunoglobins, IgM autoantibody is what rheumatoid factor is measuring We can get false positive rheumatoid factor = TB, leprosy, parasitic infections (from traveling etc), sarcoidosis= HIGH LEVELS OF IgM Releasing things and macrophages and phagocytic activity in the joint space- MASSSIVE inflammatory destruction in the joint Treatment: DMARDs, steroids to simmer down inflammation, immune suppressionRA vs. ASRA more common in females, ankylosing spondylitis= more common in males = autoimmune inflammatory condition that attacks the Sacroiliac joints = loose natural curvature of spine AS inflammation of fibrocartilage in the spine = *SI joints*- loose lower curvature15 yaer old that injured self during soccor game - what do we need to find out, sprain vs. strain, dislocation involved what, top 5 diagnosis, what is the most severe- and our first worry*how did it happen/describe the mechanism of injury* = history is very important, can you bear weight, did you feel it pop Turn and twisting and I did hear it pop Sprain= ligament Strain= muscle Dislocation= patella ACL tear, patellar dislocation, Meniscal tear, fracture, bone contusions = top 5 Fracture is the most severe = number one priority= he's 15 so we worry about growth plate fractures* this is the first priority of concernligament tear needs what, loose body- how will they complain, how do we treat his knee injury, when would we suspect a loose body, what is essential to prevent another injuryLigament tear= HAVE TO HVE AN MRI, XRAY cant see soft tissues structures He needs RICE= NSaids block COX pathway which blocks prostaglandins LOOSE BODY= they will complain of sharp, intermittent pain ACL is repaired, he comes back 6 months later= it locks up and hurts and then goes away= CONCERN FOR A LOOSE BODY and getting caught in a crevis intermittently To prevent another knee injury= MAKE SURE THEY ARE WARMING UP/Stretching, NEUROMUSCULAR AND PROPRIOCEPTIVE TRAINING- straining muscles around it to protect knee , decreases ACL tears if you get this trainingbone cancers- when would we suspect osteosarcoma, legg pathe disease, how to check for scoliosis and ewing sarcoma- how is it differentWant to also rule out weird growths on bones, because of osteosarcoma- we get these on femurs, PALPABLE MASS ON FEMUR= osteosarcoma in this age Hip pain in this patient= legg calve perthes disease= avascular necrosis of the hip, decrease blood supply to femoral head = keep them off the hip, degeneration of the femur head Bend over and touch toes= checking for scoliosis Ewing sarcoma= BONE MARROW and breaks through the bone- big soft tissue massgrandma has right knee and hip pain, 53 year old and overweight= what does she have, what do we need to rule out, what is the patho of this disease, how is it different than RA, treatment- what specfically is very important, what would be an incorrect statementOA, need to rule out septic arthritis and osteomyelitis OA= loss of articular cartilage, degenerative disease, slower than RA, wear and tear and progressively loose articular cartilage, still get immune response from the wear and tear, this articular cartilage is damaged= so immune system attempts to repair and get bone spurs (built up calcifications) Pain worsens with activity= OA NEEDS TO LOOSE Weight, PT, knee and hip replacements if bad enough Treat with pain medicines= *we want her pain under control to continue exercising- take Tylenol or a PPI and Advil and treat pain so you can continue to work with PT and loose weight" If she says- I cant use those pain medications it will mask what's going on with my body= this is incorrect- this is the wrong answergrandpa has R shoulder pain after falling on- what are the possible diagnosis, what do we needFractures, tear or rotator cuff injury, dislocation of joint, sublaxation (slips out), contusion We need IMAGING= need Xrays at first to rule out fracture, then we need an MRI= for the soft tissues PTgreat gandma with insidious back pain, white women worse with activity, had covid and long term use of inhalers, previous heavy smoker= what do we need to check for what, how does their back look, what are her risk factors, what is important to check, what will help to build bone strength, what is the patho*Want a bone scan to check for osteoporosis, spine X rays Significant lordosis and some kyphosis X rays= severe Fractured back from coughing from covid and has OP Female, smoker, post menopausal age, low weight, steroids, = risk factors for OP VIT D deficiency= poor bone strength Weight bearing exercises to help build bones Osteoporosis is= reduction in bone mass, decreased bone mineral density= increased risk for fracture Imbalance of formation and reabsorption of bone*comorbid conditions with OP- who is at high risk for this, rickets, osteoclasts vs blasts,Comorbid conditions common with OP= vit D deficiency (CKD patients at risk for vit D def and OP), and also eating disorders (young females with this- high risk for OP early in their life) Rickets= Vit D deficiency and calcium malabsorption, bones are brittle and under-minieralized Reabsorption and formation of new bones- osteoclasts and blasts Blasts= bone builders, synthesize collagen and control mineralization Clasts= remodeling of the bone, reabsorptionwhat are we most worried about in OP patients and what jointWorried about falls with this OP patient= HIP FRACTURES- are the most concerning joint with falls *Hip fractures= mobility and balance issues = medications and vision problems (macular degeneration), Parkinson's, = so try to prevent thesered flags of a spinal fracture, another term for adult ricketsRed flags of a spinal fracture= older population, direct trauma Another term for adult rickets= osteomalacia*- softening of the adult bone, like an adult rickets because not enough calcium and vit D, vit D is critical in our bone formationgreat grandpa with toe pain- labs to order and what would you expect to be highi, what does he have and what is the patho of this, what causes the fever, does this only present in the toe, what can hapen short term and long term, to treat short term and long term, to treat and long term, what do we tell him to change as far as his lifestyleRight big toe felt like it was on fire Labs to order= CBC- WBC is high, uric acid high Gout= hyperuricemia= not execrating enough or over production of urate, genetic and environmental, crystal deposits in joints and immune system sees abnormal crystals and neutrophils try to phagocytosis and we can inflammatory response Interleukin 6 - causing fever Does gout always present in the toe? = no, can have it in ankle, knees Could get urate kidney stones, but long term- the prognosis if we don't take care of the gout= can have chronic joint issues/destruction= deformities etc and tophi To treat= meds decrease inflammation, steroids, NSAIDs, colchicine Long term we give uric acid blockers= cherry juice and allopurinol Stop drinking, minimize meat consumption, weight loss (obesity= more inflammation)what do we need to avoid if kidneys not working wellNSAIDS = on the final