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Pediatrics > musculoskeletal disorders > Flashcards

musculoskeletal disorders Flashcards

1
Q

Juvenile idiopathic arthritis

A
  • JIA is not a single disease, as the rterm includes all forms of childhood arthritis
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2
Q

three systems used to diagnose and classify childhood arthritis

A
  • American college of Rheumatology criteria for JIA
  • European League against rheumatism criteria for JIA
  • international league of associations for rheumatology criteria for JIA
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3
Q

diagnosis of JIA

A
  • defined as persistent arthritis lasting at least 6 weeks in one or more joints in a child younger than 16 years of age when all other cuases are eliminated
  • etiology- genetic predisposition with external trigger
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4
Q

Systemic JIA

A
  • 4-17% cases
  • M=F onset throughout childhood
  • spiking fever 1-2 times/day for at least 2 weeks. fever typically accompanied by an evanescent rash on trunk or limbs
  • systemic signs: pleuritic, pericarditid, myocarditis, hepatosplenomegaly, lymphadenopathy
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5
Q

polyarticular JIA

A
  • RF positive: onset 2-4 and 6 to 12
    RF neg: onset late childhood or adolescence
  • arthritis in 5 or more joints: symmetrical. affecting both large and small joints. joints are swollen and warm but rarely red
    -rheumatoid nodules on elbows, tibial crests and fingers. less common in RF negative
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6
Q

Oligoarticular JIA

A
  • 27-56% of children with JIA
  • onset in early childhood peak at 2-4 years
  • female> male
  • low grade inflammation in 4 or fewer joints
  • joints are swollen and may be warm
  • systemic signs unusual
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7
Q

Primary clinical manifestation

A
  • joint swelling, pain, and stiffness
    -morning stiffness
  • muscle atrophy, weakness poor muscle endurance
  • ## systemic manifestation
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8
Q

secondary clinical manifestation

A
  • limited joint motion; soft tissue contracture
  • fatigue
  • decreased aerobic capacity
  • growth abnormalities
  • osteopenia; osteoporosis
  • difficulties with ADL
  • participation restriction
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9
Q

medical management

- NSAIDS

A
  • most widely used first line therapy
  • -naproxen, tolmetin and ibuprofen at emost common
  • reduce fever, pain and inflammation, but do not alter the course of the disease
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10
Q

medical management

- methotrexate

A
  • most common disease modifying antirheumatic drug
  • prescribed to children with poly and systemic JIA
  • weekly oral administration
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11
Q

goal of pharmacologic therapy

A
  • control arthritis; preventing joint erosion

- manage extra articular manifestation

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12
Q

PT intervention in acute phase

A
  • maintaining and preserving joint function
  • RICE- avoid heat, US and diathermy
  • splinting
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13
Q

PT intervention in subacute and chronic

A
  • restoration and compensation of cuntion and activities

- balance rest and exercise

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14
Q

aerobic fitness prescription

A
  • 2x/week for 45-60 mins of moderate to vigorous intensity
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15
Q

resistance training prescription

A
  • 2x week. light weights with 2-3 sets to 10-15 reps
  • use isometrics with acute joint inflammation
  • progress to concentric and eccentric as inflammation subsides
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16
Q

athrogryposis multiplex congenital defined

A
  • a non-progressive neuromuscular syndrome present at birth that is characterized by severe joint contractures, muscle weakness and fibrosis
  • prescence of contractures in 2 or more body areas

-children bright and motivated

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17
Q

Forms of AMC

A
  • amyoplasia 43% lack of muscle formation or development
  • contrcatures syndrome 35%
  • distal asrthogryposis 7%
18
Q

AMC etiology

A
  • lack of fetal movement
  • associated with neurogenic and myopathic diorders
  • decr amniotic fluid, especially in 3rd trimester, may inhibit freedom of movement in utero
19
Q

factor implicated in AMC are

A
  • hyperthermia of the fetus
  • prenatal virus
  • fetal vascular compromise
  • septum of the uteru
  • decr amniotic fluid
  • gene deformity
  • muscle and/or connective tissue development abnormalities
  • CNS or SC malformation
20
Q

AMC type 1

A
  • Jacknifed 55%
  • flexed with dislocated hips, extended knees,clubfeet, internally rotated shoulder flexed elbows and flexed and ulnarly deviated wrists
21
Q

AMC type 2

A
  • frog legs 45%
  • the second pattern present with abducted, internally rotated hips , flexed knees, clubfeet, internally rotated shoulder, extended elbows flexed and ulnarly deviated writs
22
Q

DEvelopment, strength and mobility infancy Type 1

A
  • stretching of hip flexors and prone positioning
  • roll or scooting on bottom as primary means of floor mobility
  • delays in ability to attain independent sitting
  • typically able to stand when placed well before they can pull to stand
  • usually begin to walk with assistance, and assistive device and LE orthotics around 18 months
23
Q

DEvel3opment strength and mobility Type 2

A
  • more positioning options due to hip and knee flexion
  • -may have difficulty with prone to elbow extension contrcatures making it difficult to prop
  • slower in attaining rolling but faster in sitting and scooting compared to type 1
  • depending on strength and amount of bracing required to stand, these children may be unable to independently transition from floor to stand
24
Q

standing for AMC

A
  • standing is very important during years 1 and 2
  • families encouraged to start standing ~6 months
  • initiate in a standing frame
  • floor to stand activities do not usually emerge until the child is securely ambulating
25
Q

stretching and splinting infancy

A
  • stetching programs are imperative in addressing primary imairments of AMC
  • -3-5 sets/ day with 3-5 reps each set, hold 20-30 sec
  • thermodynamic splints adjusted every 4-6 wks
  • AFOs for clubfeet mus have calcaneus aligned in neutral worn 22hr/day
26
Q

knee contractures addressed early by

A

using splinting and stretching
-first 3-4 months, splint worn up to 20 hr/day

extension contrcatures- anterior thermoplastic knee flexion splints

flexion contractures- posterior extension splints

older infants use splints for appropriate activities

27
Q

osteogenesis imperfect OI

A

-brittle bones disease, characterized by lax joints, weak muscles and diffuse osteoporosis

28
Q

classification of OI

A
  • silence and danks classified 4 genetic types of OI

-has been expanded to 8 types
first 4 usually autosomal dominant

-defect in Type 1 collage. types 5-8 do not have type 1 collagen defect

29
Q

Type 1 OI

A
  • mild to moderate bone fragility with a few to several fractures
  • little or no bone malformation
  • most frcatures occur before puberty
  • normal birth height/weight
  • muscle weakness
  • joint laxity
  • flat feet
  • dislocations and sprains
  • avg life expectancy
  • associated with blue sclera, triangle face, and hearing loss beginning in 0s or 30s
30
Q

Type 2 OI

A
  • perinatal lethal
    -extreme bone fragility and delay of ossification of skull and facial bones
    -long bones are crumbled
    -infants are small with short, curved , deformed extremities
    -
31
Q

Type 3 OI

A
  • usually autosomal dominant, but rare recessive cases
  • severe with progressive deformity of the long bones, skull and psine
  • -results in short stature
  • severe bone fragility
  • several dozen to hundreds of fractures
  • blue sclera at birth, lessens with age
32
Q

Type 4 OI

A
  • mild to moderate deformity
  • short stature after birth
  • sclera normal
  • dentionogenesis imperfect is common (teeth)
  • hearing loss variable
  • prohnosis for ambulation is excellent
33
Q

type 5 OI

A
  • autosomal dominant
  • hypertrophic calcification of fractures and surgical osteotomies
  • may have calcification of interosseous membranes of radius and ulna leading to limitation of supination/pronation
  • 5% of the moderate to severe cases of OI
34
Q

type 6 OI

A
  • autosomal recessive and extremely rare

- moderate to severe deformity but with normal teetch and sclera

35
Q

type 7 OI

A

autosomal recessive and associated with gene defect that affects translation of collagen

  • normal sclera and dentin
  • moderate to severe bone fragility and shortening of humerus and femur
36
Q

type 8 OI

A
  • autosomal recessive and caused by mutations of genes that affect translation of collagen with mutation in cartilage protein
  • normal sclera , flattened long bones, slender ribs, small to normal head size
  • growth deficiency for those that survive to teen years
37
Q

diagnosis of OI

A
  • based on clinical manifestation and skin biopsy that looks at collagen
  • the collagen defect determined what type of OI
  • x-rays and bone scans show evidence of multiple old fractures and skeletal deformities
38
Q

medical management o fOI

A

no cure

  • use of biosphonates
  • whole body vibration
  • internal fixation with intramedullary rods
39
Q

intervention positions for OI

A

sidelying- supported by towel rolls

prone- start with child on caregiver. adv to towel roll ow soft wedge

supine- provide support for arms. hips should be in neutral position with knees over a roll

position should not be changed frequently and should not restrict spontaneous movement

40
Q

intervention for infancy of OI

A
  • often scoot on bottom befor ecrawling
  • difficulty with transitions in and out of sitting due to short extremities
  • pull to sit contraindicated
  • pt should support at trunk/pelvis, never with hands on the legs
  • never use baby walker or jumping seats

Pediatrics (19 decks)

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