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45 Cards in this Set
- Front
- Back
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What are the connective tissue pathologies? |
Classic Ehlers-Danlos syndrome Pediatric Lupus Juvenile Idiopathic Arthritis Hemophilia |
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Etiology and Pathology of EDS |
Etiology: Autosomal dominant inheritance most common Pathology: Abnormal collagen Type V |
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EDS BF&S impairments |
•DevelopmentalDelay •Hyperextensibility of the skin & joints •Scarring •Hernias •Easybruising •Musclehypotonia •Structuralcardiac abnormalities |
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EDS activity and Participation restrictions |
•Needto avoid physical activities that put bones and joints at risk •Mayencounter social stigma •Maylimit choice of hobby or activities as isometric and strenuous weight-bearingexercise must be avoided |
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EDS - Potential Interventions |
•Childand family education to minimize injury •Strengtheningand fitness programs to reduce injuries (Avoid contact sports & rough-houseplay) •Painmanagement as needed •Assistivedevices and functional training as needed |
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Etiology and Pathology of JIA |
Etiology: May be genetic/environmental, autoimmune related to inc interleukin 1 Pathology: Joint inflammation, joint synovium proliferates --> pannus --> erodes cartilage 7 bone Joint adhesions and osteophytes |
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JIA BS&F impairments |
•Systemiconset •Oligoarthritis: 20% have chronic iritiswhich may lead to blindness •Rheumatoidfactor – negative polyarticularonset: bilateral knees, wrists &ankles •Rheumatoidfactor - positive polyarticularonset All have a degree of ROM limitations& joint space narrowing &/or destruction. |
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JIA activity and participation instructions |
May limit mobility and self care activities May impair hand writing |
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JIA potential Interventions |
•Child& Family Education •ROM •Strengthening& fitness programs •Painmanagement (NSAIDS) •Environmental& lifestyle modifications •Splinting •Assistivedevice & mobility aid selection |
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Etiology and Pathology of Hemophilia |
•Etiology: Defect in gene on X chromosome; incidence 1per 5,000 live male births •Pathology: Missing protein (clotting factor) requiredfor blood clotting |
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Hemophilia BS&F impairemnts |
-Joint destruction,leading to prematurearthritis andchronic pain -Muscle disuseatrophy -Potential nervecompression -If bleeding occursin the brain, sensory,motor, orcognitive impairmentsmaydevelop; if thebleeding is severe,death may result |
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Hemophilia potential activity and participation restrictions |
Pain may lead to diminished interaction with peers and absencefrom work/school. Functionallimitations due to pain and joint swelling. |
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What are the bony disorders |
•ArthrogryposisMultiplex Congenita (AMC) •BlountDisease •Legg-Calvé-PerthesDisease •Slippedcapital epiphysis •Scurvy •Rickets •OsteogenesisImperfecta (OI) |
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Etiology of AMC |
Congenital: -Suspect teratogens -Lack of in uteromovement -In utero muscle atrophy caused by muscle disease, virus, or maternalfever -Insufficient room due to lack of amniotic fluid or abnormally shapeduterus. |
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Pathology of AMC |
•Deficitin the motor unit leads to severe fetal weakness •Fetalimmobility leads to hypoplasticjoint development & contractures |
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AMC BF&S impairments |
•Characteristicimpairment is joint contractures. •Hipdislocations/subluxations •Decreasedjaw and tongue ROM •Tubularlimbs, lacking normal joint creases •Diminishedmass and muscle strength |
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AMC activity and participation limitations |
•Mobilitydifficulties •DiminishedADL skills such as dressing and toileting •Poorgrasp and feeding or speech difficulties •Limitedplay and activity •Cognition is typical |
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AMC potential interventions |
•Surgery •Stretchingand Splinting/Casting •Orthotics •Adaptingenvironment •Assistivetechnology for mobility & communication |
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Etiology and Pathology of Blount disease (Tibia Vara) |
Etiology: -Infantile: obese children who walked before age 1 -Juvenile: most common in obese African-Americanteenagers Pathology: -Compression of proximal tibial physes that inhibits normal endochondral growth |
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Blount Disease BS&F impairments |
Lateral bowing of the tibia Medial Knee Instability |
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Blount disease activity and participation limitations |
Pain Knee instability Progressive joint degeneration Cosmesis |
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Blount disease potential interventions |
Postsurgical ambulation training Splinting as needed |
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Etiology for Legg-Calve-Perthes Disease |
•Unclear •Numerousassociated factors include later birth presentation, increasing parental age,ADHD •Higherincidence in lower SES, urban areas leads to hypothesis of nutrition. |
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Pathology for Legg-Calve-Perthes Disease |
•Unclear •Currenttheory: vascular disruption leading toaseptic necrosis of proximal femur •Systemiccomponent suspected because epiphyseal changes have been noted in the nonproblematicjoints; blood content abnormalities |
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Legg-Calve-Perthes BF&S impairments |
•Limpcaused by pain or weak abductor muscles •Frequentlypositive Trendelenburg sign •LimitedROM in hip abduction & internal rotation •Painin hip or groin with activity •Maybe referred knee pain |
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Legg-Calve-Perthes activity and participation limitations |
Pain can limit play & ADLs Limp |
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Legg-Calve-Perthes Interventions |
-Child/Family education -ROM program -Ambulation training post surgery --Proximal varus derotational osteotomy of the femur -Positioning Devices |
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Etiology of Slipped Capital Femoral Epiphysis |
Unclear -2.5:1 male-female ratio -Higher incidence in african americans -Local trauma in 25% of cases -Inflammation may weaken physeal plate -Endocrine/hormone imbalance -Delayed skeletal maturity -Obesity -Hereditary |
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Pathology of Slipped Capital Femoral Epiphysis |
Posterior displacement of the capital femoral epiphysis from femoral neck through a weakened physis |
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Slipped Capital Femoral Epiphysis BF&S impairments |
-Antalgic limp -Groin pain or referred AM thigh and knee -ER posturing -Dec hip flexion, abd, and IR -Leg moves into ER when flexed. |
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Slipped Capital Femoral Epiphysis activity and participation limitations |
Pain may limit activities Long term degenerative changes |
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Slipped Capital Femoral Epiphysis interventions |
-Child and family education -ROM program -Positioning program -Postsurgical ambulation training |
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Describe a epiphyseal fracture |
Fracture goes through the growth plate. Can cause growth arrest in a childs bone See Salter Harris Classification |
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What is a greenstick fracture |
Occur in long bones when a force applied to one side of the bone breaks. Cause angular deformity |
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Etiology of Osteogenesis Imperfecta |
Dominant heritable genetic disorder Collagen defect, bone fragility, and frequent fracture |
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Pathology of Osteogenesis Imperfecta |
-Defects in type 1 collagen -Increased bone turnover -Sequelaeinclude shore stature, scoliosis, poor tooth formation, deafness, blue sclera,translucent skin, osteoporosis, and ligamentous laxity. |
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Review slide 38 |
Types of OI |
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Osteogenesis Imperfecta BF&S Impairments |
Propensity for fractures and deformities Severe scoliosis may impair cardiorespiratory status |
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Osteogenesis Imperfecta activity and participation limitations |
Fragility with play and ADLs Deformities may diminish ADL skills and mobility |
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Osteogenesis Imperfecta potential interventions |
•Childand family education •ROMprogram •Strengtheningand fitness programs •Developmentalstimulation •Functionaltraining •Behavioralmodification to reduce injury •Splintingand ambulation aid selection |
