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Peds Patho > Ortho > Flashcards

Ortho Flashcards

1
Q

how can the idea of a crooked young tree be applied to orthopedics?

A

a crooked young tree–like a deformed young child–can be helped to grow straight by applying appropriate forces

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2
Q

what is morphogenesis?

A

the formation of all tissues and organs

–gives rise to structures appropriate to their position w/in the embryo

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3
Q

morphogenesis relies on…

A

certain cellular activities

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4
Q

when are arm/leg buds present?

A

~ 4 weeks

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5
Q

when are fingers and toes evident?

A

by the end of week 8

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6
Q

how do bones w/in the limb form?

A

by endochondral ossification

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7
Q

what is endochondral ossification?

A

the replacement of cartilage w/bone

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8
Q

when does endochondral ossification occur?

A

weeks 5-12

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9
Q

when is the ossification center present in all bones?

A

by week 10

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10
Q

when are fingernails and toenails present?

A

by week 10

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11
Q

what happens by week 10?

A

1) ossification centers are present in all bones

2) fingernails and toenails are present

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12
Q

how can limb patterning go wrong?

A

errors in the pathways that control limb patterning

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13
Q

what is the occurrence of limb deficiences?

A

3 to 8 per 1000 live births

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14
Q

do limb deficiencies occur with other deficiencies?

A

yes: 50%
(errors in the pathways controlling limb patterning are often assoc. w/defects in the development of other organ systems w/in the embryo)

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15
Q

most commonly affected organ systems, along w/limbs (in terms of deficiencies) ?

A

GI tract, heart, CNS, GU tract

–> WHY? theory: development at the same time or all are patterned by the same developmental signaling pathway

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16
Q

VACTERL Association

A 
Vertebral anomalies
Anal atresia
Cardiac anomalies
TE tracheoesophageal fistula
Renal anomalies
Limb abnormalities (mostly upper)
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17
Q

what is bone?

A
  • -a structure AND an organ
  • -provides rigid framework/protection
  • -act as levers
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18
Q

bone contains…

A

hemopoietic tissue for production of:

erythrocytes, granular leukocytes, & platelets

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19
Q

bone acts as a reservoir for:

A
  • -calcium
  • -phosphorus
  • -sodium
  • -magnesium
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20
Q

what is responsible for long & short bone formation?

A

endochondral ossification (cartilage becomes replaced w/bone)

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21
Q

what is responsible for longitudinal growth?

A

epiphyseal cartilage of long bone

  • -located b/t epiphysis & metaphysis
  • -aka “growth plate”
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22
Q

what is bone formation?

A

–an ongoing process of breakdown & build-up

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23
Q

what alters the size & shape of bone?

A

partial resorption of preformed bone tissue & simultaneous deposition of new bone
(bones constantly remodeling!)

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24
Q

what distinguishes peds from adult orthopedics?

A

Growth!

includes tissues, organs…

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25
Q

how many calories are required for growth in a kid & adult?

A

Kid: 110 calories/kg
Adult: 40 calories/kg

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26
Q

how much protein is required for growth in a kid & adult?

A

Kid: 2 gram/kg/day
Adult: 1 gram/kg/day

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27
Q

from birth, how much will parts of body grow?

ht, wt, femur, tibia, spine

A
  • -ht will increase 350%
  • -wt will increase 20-fold
  • -femur & tibia will triple in length
  • -spine will double in length
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28
Q

how do bones grow?

A

–in length and width!

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29
Q

how does remodeling work?

A

via simultaneous:

1) osteoblastic deposition
2) osteoclastic resorption

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30
Q

a period of growth will have more of what form of remodeling?

A

osteoblastic deposition

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31
Q

how do we classify bones?

A
  • -Long bones
  • -short bones
  • -flat bones
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32
Q

are growth plates uniform?

A

no! diff. bones grow @ diff. rates!

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33
Q

what may contribute to our understanding of peds orthopedics?

A

cartilage may have its own individual growth patterns

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34
Q

an embryonic limb has its basic structure at what length?

A

by about 1 cm

–could continue to grow but is controlled by something

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35
Q

how are peds bones diff. from adults’?

A

– less mineralized
– have > vascular supply
(adult bones: break. kid bones: tend to BEND before they break.)
–more strain in children than adults
–greater energy absorption before failure/fracture

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36
Q

Salter Harris classification:

A

1) Separated/Straight across
2) Above physis or Away from joint
3) Lower (below physis, in epiphysis)
4) TE (thru everything) –> all 3 layers
5) Rammed (crushed physis)

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37
Q

will a salter harris 1 fracture show on x-ray?

A

won’t show on x-ray for 10 days

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38
Q

why is dx of fracture more diffcult in peds?

A

bc of lack of ossification

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39
Q

w/ type 3/4 fractures, we worry about:

A

growth arrest –> grows right through the growth plate

type 5 can also have a growth arrest, but less likely

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40
Q

5 fractures unique to children:

A

1) Torus “buckle” fracture
2) Physeal fractures
3) Greenstick
4) Bowing
5) Avulsion

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41
Q

Torus “buckle” fracture

A

dented, but intact

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42
Q

greenstick fracture

A

bends & cracks but doesn’t break into pieces

bend on one side, break on the other

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43
Q

avulsion

A

piece of bone pops off

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44
Q

management of fracture

A

–assess, pain control, stabilize, antibiotics if open, refer, x-rays (at least 2 views. if oblique is available, always take it!! esp. w/elbow)

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45
Q

fractures suggestive of abuse?

A

spiral, esp. of lower extremities in non-walking child, or humeral
–BUT, in tibia esp..can see NOT d/t abuse–foot stuck in seatbelt, etc.

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46
Q

little kids and break

A

actually have overgrowth after break!

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47
Q

blasts

A

=bone-forming

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48
Q

bone remodeling

A

a lifelong process where mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed (a process called ossification or new bone formation)
–these processes also control the reshaping or replacement of bone following injuries like fractures

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49
Q

compartment syndrome

A
  • -happens when pressure w/in the myofascial compartment increases to point where circulation is compromised (from swelling or bleeding that occurs w/in a compartment)
  • -> ischemia –> necrosis
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50
Q

patho of compartment syndrome?

A
  • -fascia is v. thick & dense–holds pressure in
  • -> compresses vessels –> risk ischemia
  • -tissue is actually compromised ; damage to soft tissue increases intracompartmental pressure –> closing venules
  • -arterial inflow increases press. to the point that arterioles close; ischemia sets in
51
Q

sign of increased intracompartmental pressure

A

edema or hematoma

52
Q

is ischemia reversible?

A

if > 6 hrs, may be irreversible

  • -Volkmann’s ischemic contracture
  • -permanent nerve dysfunction
  • -amputation
53
Q

Volkmann’s ischemic contracture

A
  • -a deformity of the hand, fingers, and wrist caused by injury to the muscles of the forearm
  • -occurs when there is a lack of blood flow (ischemia) to the forearm
  • -Trauma to the arm, including a crush injury or fracture, can lead to swelling that presses on blood vessels and can decrease blood flow to the arm.
54
Q

compartment syndrome occurs mostly in:

A

–tibia & forearm fractures

55
Q

5 P’s of compartment syndrome:

or any fracture

A

1) Pain
2) Pulse (lessness)
3) Pallor
4) Paresthesia
5) Paralysis

56
Q

w/paresthesia, always:

A

compare to other side!

kid may say they can’t move it–but could really be d/t pain

57
Q

toxic synovitis is us. in what age?

A

3-8 yrs

58
Q

classic position of osteomyelitis? why?

A
  • -flexion, abduction, & external rotation
  • *maximizes capsular volume**
  • -comfortable in this position
59
Q

osteomyelitis

A

an acute or chronic inflammatory process of the bone & its structures secondary to infection w/pyogenic organisms

  • -50% in preschool-aged children
  • -may be localized or spread through periosteum, cortex, marrow, and cancellous tissue
60
Q

biggest cause of osteomyelitis?

A

staph aureus

61
Q

septic arthritis

A

joint is infected

62
Q

usual origin of bone infections in children?

A

hematogenous (through the blood)

..b/c of rich vascular supply in their growing bones, can often get infection this way

63
Q

where do hematogenous organisms tend to start the infection?

A

in the metaphyseal ends of the long bones

  • -bc of sluggish circulation in the metaphyseal capillary loops
  • -then: osteoblasts die & osteoclasts take over
64
Q

body produces what in response to toxins/bacterial antigens w/osteomyelitis?

A

interleukin-1 is produced by macrophages

–> inflam. cells migrate under physis –> increase thrombosis –> reduces child’s ability to fight infection!

65
Q

physis

A

growth plate

66
Q

longterm consequences of osteomyselitis in infants?

A

devastating for rest of life–always playing “catch up”

67
Q

signs of osteomyelitis?

A
  • -painful focal swelling w/cardinal signs of inflammation
  • -may be able to elicit point tenderness over bone
  • -movements of adjoining joint may be restricted d/t joint involvement or soft tissue inflamm.
68
Q

what should you consider in differential for osteomyelitis?

A
  • -cellulitis, subcutaneous abscess, fractures, bone tumors
  • -in newborns/infants it may present as pseudoparalysis: also consider CNS disease, cerebral hemorrhage, trauma, child abuse
69
Q

tx of osteomyelitis:

A
  • -consult ortho & ID
  • -initiate antibiotic tx AFTER getting blood/aspirates for culture
  • -preferred: nafcillin, vancomycin, clindamycin, cefazolin
  • *DON’T start antibiotics in prim. care setting if you suspect septic joint or osteomyelitis
70
Q

osteomyelitis labs

A

acute infection:

  • -ESR, CRP high initially
  • -white cell count high
71
Q

6 lower limb deformities:

A

1) proximal femoral focal deficiency
2) fibular/tibial hemimelia
3) hemihypertrophy
4) leg length discrepancy
5) clubfoot
6) genu valgum & varus

72
Q

PFFD: proximal femoral focal deficiency

A

aka: congenital short femur
- -1 in 50,000 live births
- -options: amputation & leg lengthening (2-4 needed)

73
Q

fibular/tibial hemimelia

A

–congenital absence or deficiency of tibia or fibula

74
Q

tibial hemimelia

A

–autosomal dominant
–ABSENCE of tibia –> reconstruction difficult
(no extensor mechanism)

75
Q

fibular hemimelia

A
  • -not assoc. w/genetic pattern
  • -can be assoc. w/: ball & socket ankle joint, absent lateral rays of the foot, hypoplasia of femoral condyles, tarsal coalition & clubfoot
76
Q

rays

A

toes

77
Q

hemihypertrophy

A
  • -one side grows larger than the other
  • -assoc. w/embryonal cancers, includ. Wilm’s tumors
    • -> do screening u.s. of kidney q 3 mos until age 6
    • -> fetal alpha protein tests q 6 mos until age 6-7
  • -seen in Beckwith-Wiedemann syndrome (renal tumors)
78
Q

common causes of hemihypertrophy

A
  • -port wine stains

- -vascular anomalies

79
Q

3 other syndromes hemihypertrophy is found in:

A

1) Klippel-Trenaunay-Weber: port wine stains, varicose veins
2) McCune-Albright: premature puberty, large cafe-au-laits
3) Jaffe-Campanacci (cafe au lait spots; NOFs)

80
Q

leg length discrepancy manifests as:

A

painless limp

81
Q

when is leg length discrepancy corrected?

A

usually not unless > 1.5-2 cm

82
Q

leg length discrepancy can be d/t:

A
  • -hemihypertrophy
  • -hemimelia
  • -or just bc that’s how your body is built!
83
Q

also see w/leg length discrepancy:

A
  • -1 hip higher than the other

- -can have compensatory scoliosis

84
Q

clubfoot

A 
CAVE:
Cavus: v. high arch
Adductus
Varus: hind foot (heel)
Equinus: pointed down
85
Q

clubfoot tx:

A
  • -ponsetti casting (4-8 weekly casts)
    • +/- Achilles lengthening
    • boots & bar until age 4
      • -> wear 20-24 hrs/day at first; then nights & naps; then nights
  • *30-40% risk of recurrence
86
Q

genu valgum

A

“knock knee”

  • -overgrowth on medial side of growth plate
  • -unknown cause
  • -tx: growth modulation or osteotomy if deformity is signficant
87
Q

growth modulation

A

used in tx of genu valgum

–“tether” side growing the fastest on either side of growth plate

88
Q

genu varum & Blount’s Disease

A
  • -bowing of knees

- -physiologic is normal until age 2-3 yrs

89
Q

genu varum & Blount’s Disease: when to refer?

A

refer to ortho if older than 3 or it appears to be worsening

90
Q

why do we see Late-onset Blount’s?

A

adolescents w/rapid weight gain: if not tx’d, will have pain d/t bones rubbing together, by age 30

91
Q

osteogenesis imperfecta

A

aka “brittle bone disease”

  • -congenital bone fragility caused by mutations in genes that code for type 1 collagen
    • -> have less collagen than normal or poorer quality collagen
  • -Types 1-4; mildest to most severe
92
Q

genes that code for type 1 collagen:

A

COL1A1, COL1A2 –> 90% of mutations

93
Q

w. OI Type 1, you can see:

A

blue sclera!!

  • -dental problems, premature deafness
  • -fractures may occur for first time at later age: when child starts to walk
  • -less frequent after puberty then more later in life (osteoporosis)
  • -scoliosis/kyphosis in 20% of cases
94
Q

OI Type II

A
  • -v. short, v. bowed limbs
  • -babies born w/dwarfism, blue sclera
  • -us. fatal at birth, may live several mos.
  • -multiple fractures; long bones short & crumpled
95
Q

OI Type III

A
  • -sclera blue but fade over years; white in adulthd.
  • -dentinogenesis imperfecta common
  • -bowing of limbs w/growth; multiple fractures later in life, d/t micro-fractures
  • *barrel-shaped chest**, pectus carinatum deformity
  • -radiograph= “popcorn bones”
  • -affected children become wheelchair-bound, non-ambulatory
96
Q

when do you see popcorn bones on radiograph?

A

Type III OI

97
Q

OI Type IV

A
  • -white sclera, moderate bone fragility & deformity
  • -axial skeleton involvement (kyphoscoliosis) common
  • -dentinogenesis imperfecta
  • *almost always have dental issues
98
Q

Type V OI

A
  • -moderate in severity
  • -similar to type IV
  • *dominantly inherited & accts. for 5% of moderate-severe OI cases
99
Q

Type VI OI

A
  • -extremely rare
  • -sim. to type IV in appear/sx
  • -bone pain
  • -bit more difficult to dx
100
Q

6 assessment points for OI:

A

1) rare: 1 in every 12-15,000 live births
2) fractures that recur
3) bone pain
4) ligamentous laxity & joint hypermobility
5) wormian bones skull 60% of pts
6) blue sclerae

101
Q

OI tx:

A

1) Biphosphinates (Pamidronate, etc)
- -> incr. cortical thickness
2) GH: stimulate osteoblast function
3) gene therapy
4) surgical interventions
5) physiotherapy

102
Q

DDH risk factors (4):

A

1) female
2) first born
3) feet first (breech)
4) family hx

103
Q

assessment for DDH:

A

1) Barlow: roll hip out of socket
2) Ortolani: push back into place
- -> “clunk” = positive Ortolani

104
Q

galeazzi sign for DDH

A

is level of knees “off?”

ileum/acetab <60 degree angle = shallow

105
Q

management of DDH

A
  • -early reduction beneficial for remodeling
  • -Pavlik harness up to 3 mos. (legs in frog position!)
  • -closed/open reduction & spica cast (if not enough progress w/harness: 12 wks in cast, change once at 6 wks)
106
Q

scoliosis

A

lateral curvature of the spine w/minimum Cobb angle of >/equal to 10 degrees

107
Q

4 types of scoliosis:

A

1) idiopathic: w/out assoc. disease/anomalies
2) congenital–underlying anomaly
3) neuromuscular
4) other

108
Q

idiopathic scoliosis: infantile

A
  • -birth-3 mos.
  • -boys more than girls
  • -us. L thoracic curve pattern
  • -RVAD >20 degrees –> prone to progression
  • -Mehta casting: cycle for 1 yr: wear 2 mos, off 2 weeks
109
Q

RVAD

A

rib vertebral angle difference

110
Q

idiopathic scoliosis: early onset

A
  • -3-10 yrs
  • -girls more than boys
  • -higher risk of progression (have a ton of growth left!)
111
Q

idiopathic scoliosis: adolescent (AIS)

A
  • -girls more than boys, 4:1
  • -higher w/ + family hx
  • -us. no pain (if pain, r/o other causes)
  • -9 to young adulthd.
112
Q

most common form of scoliosis?

A

AIS
& best prognosis!
tx begins w/observation only; often curvature won’t worsen

113
Q

surgical intervention for AIS when…?

A

50 degree or > Cobb angle

114
Q

Scoli Score

A
  • -an AIS prognostic test
  • -for mild curve, 10-25 degrees
  • -takes into acct. the Cobb angle at time of test
  • -risk of progression to 40 degrees
115
Q

congenital scoliosis

A
  • -newborns or young infants
  • -cause = abnormal development
  • -occurs when vertebrae fail to form properly, create extra segments, or fuse togeth. during fetal develop.
  • -high rate of other deformities w/it
  • -tx = observation to surgery, depend. on curvature
116
Q

3 causes of congenital scoliosis:

A

vertebrae:

1) fails to form
2) forms extra segment
3) doesn’t separate

117
Q

common assoc. defect w/congenital scoliosis?

A

absent or fused ribs

  • -also anomalies of GU tract, cardiac
  • *Cardiac, uro consults!!
118
Q

tx for congenital scoliosis?

A
  • -curves tend to be more rigid than in idiopathic –> resistant to correction
  • -curve progression unpredictable –> need frequent f/u’s!!
  • *Always send for: echo, renal u.s.
119
Q

surgical intervention for congenital scoliosis?

A

–remove extra vertebrae/ fusion
–growing rod/VEPTR, attach. to spine, ribs, or pelvis
w/missing rib, rib prosthesis compliments scoliosis surgery: maintains chest space where there are fused or missing ribs
–> allows room for heart & lung develop.

120
Q

VEPTR

A

vertical, expandable, titanium rib

121
Q

neuromuscular scoliosis can be d/t:

A
  • -CP
  • -SMA 1 & 2
  • -muscular dystrophies (DMD, Becker’s, congenital)
122
Q

neurogenic scoliosis

A

d/t traumatic brain injury

123
Q

goal w/CP and scoliosis?

A

get them balanced–seated evenly, with head above

124
Q

what happens to ribs w/SMA?

A

ribs just droop–tiny lung space (d/t “parsol effect” of ribs)

Peds Patho (8 decks)

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