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Osha 3a > Paeds MSK > Flashcards

Paeds MSK Flashcards

1
Q

What is osteogenesis imperfecta?

A
  • AD condition
  • results in brittle bones susceptible to fracture
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2
Q

What is the pathophysiology of osteogenesis imperfecta?

A
  • genetic mutation
  • affects formation of collagen
  • needed for structure and function of bone, skin, tendons, connective tissue
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3
Q

How does osteogenesis imperfecta present?

A
  • recurrent and inappropriate fractures
  • hypermobility
  • blue/grey sclera
  • triangular face
  • dental problems
  • bone deformities
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4
Q

How is osteogenesis imperfecta investigated?

A
  • clinical diagnosis
  • X-Rays for fractures
  • normal bloods
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5
Q

How is osteogenesis imperfecta managed medically?

A
  • bisphosphonates
  • Vit D
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6
Q

How is osteogenesis imperfecta managed by the MDT?

A
  • physio and OT
  • ortho surgeons
  • specialist nurses
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7
Q

What is rickets?

A
  • defective bone mineralisation causes ‘soft’ and deformed bones
  • called osteomalacia in adults
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8
Q

What is the aetiology of rickets?

A
  • vit D deficiency (lack of sunlight or food)
  • calcium deficiency (dairy + green veg)
  • hereditary hypophosphataemic rickets
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9
Q

What are risk factors for rickets?

A
  • darker skin
  • low exposure to sunlight
  • cold climates
  • time indoors
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10
Q

How does rickets present?

A
  • lethargy
  • bone pain
  • poor growth
  • dental problems
  • muscle weakness
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11
Q

What bone deformities does rickets present with?

A
  • bowed legs
  • knock knees
  • rachitic rosary (costochondral junction swelling)
  • craniotabes (soft skull)
  • delayed teeth
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12
Q

How is rickets investigated?

A
  • serum 250hydroxyvitamin D >25nmol/L
  • raised ALP and PTH
  • low calcium and phosphate
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13
Q

What is the management of rickets?

A
  • Prevention (more likely if breastfed)
  • oral Vit D 400IU supplements for breastfeeding women and all children
  • ergocalciferol (vit D) if deficient
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14
Q

What is transient synovitis?

A
  • irritable hip
  • temporary irritation and inflammation in the synovial membrane
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15
Q

What is the epidemiology and aetiology of transient synovitis?

A
  • MC cause of hip pain in children aged 3-10
  • often associated with viral URTI: symptoms occur within a few weeks
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16
Q

What is the presentation of transient synovitis?

A
  • refusal to weight bear
  • limp
  • groin or hip pain
  • mild low grade temp
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17
Q

What is the management of transient synovitis?

A
  • exclude septic arthritis
  • symptomatic management
  • recovery within 1-2 weeks without long term effects
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18
Q

What is septic arthritis and what is the epidemiology?

A
  • infection inside a joint
  • MC in children <4 years
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19
Q

What bacteria cause septic arthritis?

A
  • S. aureus is MC
  • N. gonorrhoea (sexually active teens)
  • Group A strep (S. pyogenes)
  • H. influenzae
  • E. coli
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20
Q

What is the presentation of septic arthritis?

A
  • hot, red, swollen, painful joint
  • refusal to weight bear
  • affects single joint e.g. hip or knee
  • stiffness and reduced ROM
  • systemic symptoms: fever, lethargy, sepsis
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21
Q

What is the management for septic arthritis?

A
  • admit to hospital
  • joint aspiration before Abx: gram staining, MC&S
  • empirical IV Abx followed by specific Abx
  • surgical drainage and washout
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22
Q

What is osteomyelitis?

A
  • infection of the bone and bone marrow
  • typically in metaphysis of long bones
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23
Q

How can infection be introduced to bone in osteomyelitis?

A
  • open fracture or from blood
  • chronic osteomyelitis is slow growing and deep seated
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24
Q

What are risk factors for osteomyelitis?

A
  • males <10
  • open bone fracture
  • orthopaedic surgery
  • immunocompromised
  • sickle cell anaemia
  • HIV/TB
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25
Q

How does osteomyelitis present?

A
  • refusal to use limb or weight bear
  • pain
  • swelling
  • tenderness
  • systemic symptoms: fever
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26
Q

How is osteomyelitis investigated?

A
  • first line: X-Ray
  • GOLD: MRI
  • bloods + cultures
  • Bone marrow aspirate
27
Q

How is osteomyelitis managed?

A
  • extensive and prolonged Abx therapy
  • surgery for draining and debridement
28
Q

What is Perthes Disease?

A
  • disruption of blood flow to femoral head causing
  • avascular necrosis of bone
  • revascularisation and healing with bone remodelling as it heals
29
Q

What is the aetiology and epidemiology of Perthes disease?

A
  • idiopathic
  • MC boys 5-8y but can affect all children from 4-12
30
Q

What is the presentation of Perthes disease?

A
  • slow onset of pain in hip or groin
  • limp
  • restricted hip movement
  • referred knee pain
  • no history of trauma
31
Q

How is Perthes disease investigated?

A
  • X-Ray (may be normal)
  • bloods
  • technetium bone scan
  • MRI
32
Q

How is Perthes disease managed?

A
  • conservative to maintain position and alignment
  • reduce risk of damage or deformity to femoral head
  • bed rest, analgesia, crutches, traction
  • physio, X-Ray, surgery
33
Q

What is slipped femoral epiphysis?

A
  • head of femur dislocated along growth plate
34
Q

What is the epidemiology of slipped femoral epiphysis?

A
  • mc in males
  • aged 8-15
  • obese children
35
Q

How does slipped femoral epiphysis present?

A
  • adolescent, obese male undergoing growth spurt
  • painful limp
  • wanting to keep hip in external rotation with restricted internal rotation
  • hip, groin, knee or thigh pain
36
Q

How is slipped femoral epiphysis investigated?

A
  • 1st line: X-Ray
  • bloods normal
  • CT/MRI
37
Q

How is slipped femoral epiphysis managed?

A
  • surgery to return femoral head to correct position and fix in palce
38
Q

What is osgood-schlatter disease?

A
  • inflammation at tibial tuberosity where patellar ligament inserts
  • usually unilateral
39
Q

What is the epidemiology of osgood-schlatter disease?

A
  • males aged 10-15
  • common cause of anterior knee pain in adolescents
40
Q

What is the pathophysiology of osgood-schlatter disease?

A
  • patella tendon inserts into tibial tuberosity
  • stress from movement during growth causes inflammation
  • ligament pulls away tiny pieces of bone > new bone formation and calcification in response to injury
  • leads to tender bump > hard, non-tender as it heals
41
Q

How does osgood-schlatter disease present?

A
  • pain exacerbated by physical activity, kneeling and on extension
  • gradual onset of symptoms
  • palpable lump at tibial tuberosity
  • gradual onset
42
Q

How is osgood-schlatter disease managed?

A
  • NSAIDs
  • reduce physical activity
  • ice
  • stretching
43
Q

What is DDH?

A
  • structural abnormality in hips caused by abnormal development of fetal bones
  • leads to instability in hips and tendency for dislocation
44
Q

How is DDH recognised?

A
  • in newborn exam
  • child presents with hip asymmetry
  • reduced ROM in hip or limp
45
Q

What are risk factors for DDH?

A
  • 1º FHx
  • breech presentation from 36 weeks onwards
  • breech at birth if birth is after 28 weeks
46
Q

How is DDH screened for?

A
  • NIPE
  • different leg lengths
  • restricted hip abductionon one side
  • significant bilateral restriction in abduction
  • difference in knee level when hips flexed
  • clunking of hips on special testing
47
Q

What are the special tests for DDH?

A
  • Ortolani
  • Barlow
48
Q

How is DDH investigated?

A
  • USS
  • X-Ray
49
Q

How is DDH managed?

A
  • Pavlik harness if <6 mo
  • aims to keep femoral head in correct position
  • keeps hips flexed and abducted
  • may need surgery if harness fails or diagnosis >6 mo
50
Q

What is JIA?

A
  • autoimmune inflammation in joints
  • arthritis without any other cause
  • lasts more than 6 weeks in patient under 16
51
Q

What is the presentation of systemic JIA?

A
  • idiopathic inflammatory condition
  • subtle salmon pink rash
  • enlarged lymph nodes
  • high swinging fever
  • joint pain and inflammation
  • splenomegaly
  • muscle pain
52
Q

What are the results of investigations of systemic JIA?

A
  • ANA and RF negative
  • raised CRP, ESR, platelets
53
Q

How does polyarticular JIA present?

A
  • idiopathic inflammatory
  • 5 joints or more
  • symmetrical
  • affects small/large joints
  • minimal systemic symptoms: mild fever, anaemia, reduced growth
54
Q

What is a key complication of systemic JIA?

A
  • macrophage activation syndrome
  • massive inflammatory response
  • DIC, anaemia, bleeding, non-blanching rash
  • low ESR
55
Q

What results are found in investigation of polyarticular JIA?

A
  • mostly negative for RF
  • seropositive are older children and adolescents
56
Q

What is oligoarticular JIA?

A
  • involves 4 or less joints
  • aka pauciarticular JIA
57
Q

How does oligoarticular JIA present?

A
  • anterior uveitis
  • 4 or less joints
  • large joints e.g. knee or ankle
  • usually monoarthritis
58
Q

What is seen on investigation of oligoarticular JIA?

A
  • no systemic symptoms
  • normal/mildly elevated inflammatory markers
  • ANA positive
  • RF negative
59
Q

What is juvenile psoriatic arthritis?

A
  • seronegative inflammatory arthritis
  • symmetrical polyarthritis affecting small joints OR
  • asymmetrical arthritis affecting large joints
60
Q

How does juvenile psoriatic arthritis present?

A
  • plaques of psoriasis
  • pitting and onycholysis
  • dactylitis
  • enthesitis
61
Q

What is enthesitis-related arthritis?

A
  • more common in male children over 6 years
  • paeds version of seronegative spondyloarthropathies
  • most have HLA-B27 gene
62
Q

What is enthesitis?

A
  • inflammation at point where muscle inserts into bone
  • caused by trauma or autoimmune
63
Q

How does enthesitis-related arthritis present?

A
  • signs and symptoms of psoriasis and IBD
  • prone to anterior uveitis
64
Q

How is JIA managed?

A
  • NSAIDs
  • steroids - oral, IM or intra-articular
  • DMARDs e.g. methotrexate
  • biologics e.g. adalimumab

Osha 3a (14 decks)

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