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132 Cards in this Set

  • Front
  • Back
cervical osteoarthritis: signs & symptoms
restricted motion,
radicular symptoms, numbness/tingling (NT)
recurrent “kink in neck” or “slept wrong”
HNP: general signs & symptoms
limited ROM,
radicular symptoms
Reason for HNP symptoms
nerve compression or irritation
Symptoms that diagnose C4/5 HNP
C5 nerve root:
- deltoid weakness
- not much numbness/tingling
- shoulder pain
Symptoms that diagnose C5/6 HNP
C6 nerve root
- biceps weakness
- wrist extensor weakness
- numbness/tingling along radial aspect
Symptoms that diagnose C6/7 HNP
C7 nerve root
- triceps weakness
- finger extensor weakness
- numbeness/tingling along dorsal middle finger
Symptoms that diagnose C7/T1 HNP
T1 nerve root
- grip strength week
- numbness/tingling along little finger
Conservative treatment options for cervical HNP
rest, cervical collar, traction
NSAIDs or steroids
epidural injections
Surgical treatment options for cervical HNP
discectomy +/- fusion
Stenosis: definition
narrowing of canal or foramen
Stenosis: causes
3 types cervical fracture
flexion (most common)
6 types of cervical orthopedic pathology
brachial plexopathy
Shoulder joints involved in OA
gleno-humeral joint
acromial-clavicular joint (AC)
Impingement in shoulder: definition
anything that narrows subacromial space (< 7mm on MRI)
Causes of subacromial impingement
- subacromial spur, clavicular spur
- coraco-acromial ligament thickening or calcification
- hypertrophy of the rotator cuff
- loose body
- fracture (greater tuberosity)
- Os acromiale (ossicles on anterior portion of acromion)
- 2° instability
Shoulder joint impingement: signs & symptoms
rotator cuff irritation, tear;
Shoulder joint impingement: conservative treatment
- rest,
- subacromial injection
- PT (strengthen lower parts rotator cuff to keep humoral head down in joint)
Shoulder joint impingement: surgical treatment
subacromial decompression:
- arthroscopic or open +/- rotator cuff repair
- correct instability
2 types of shoulder tears
traumatic or degenerative

Traumatic/degnerative shoulder tears: locations
rotator cuff
Biceps tears: types
SLAP tear (superior labrum, anterior to posterior)
biceps instability
Shoulder fractures: locations
Types of shoulder orthopedic pathologies
Calcific tendonitis
Thoracic outlet syndrome
Reflex sympathetic dystrophy
Elbow instability: types
- ulnar/humeral
- radial head - often in young children
- Monteggia fracture
--- fx of ulna displaces radial head
--- in older children
Elbow fractures: locations
radial head
distal humerus (supracondylar)
2 syndromes 2* impingement of Median nerve
Anterior Interosseus nerve
Carpal Tunnel Syndrome
anterior interosseus nerve
- what
- where
largest branch of median nerve
passes btw 2 heads of pronator teres
Impingement of anterior interosseus nerve
impairment of
- flexor pollicis longus,
- flexor digitorum profundus,
- pronator quadratus

abnormal pinch
Most common neuropathy in upper extremity
carpal tunnel syndrome
Where is Posterior Interosseus Nerve
Arcade of Frohse
btw 2 heads of supinator
Symptoms of posterior interosseus nerve impingement
motor involvement only; no sensory
Ulnar Tunnel Syndrome
- basic presentation
- location of nerve
cubital tunnel – funny bone area
btw flexor carpi ulnaris muscle heads
increased stretch with elbow flexion
mimics tenous elbow but with NT in small & ring fingers
snapping ulnar nerve
ulnar nerve subluxation
Hand/wrist ganglion
anywhere associated with joint
tendon usu. involved
synovial fluid – can be aspirated, but will recur
usu. cosmetic
Hand/wrist ganglion: locations
wrist most common (90%)
tendon related (filled with synovial fluid)
Gangion treatments (rate of occurrence)
aspiration - 50% recurrence
surfical excision – 5-10% recurrence
Trigger finger
- definition
- signs & symptoms
- treatment
tenosynovitis: inflammation of synovium that surrounds tendon

s/s: pain, swelling, pain moving finger or sticking

Tx: cortisone
- surgery to release eyelit - recurrent surgeries weaken muscle
Why is healing of scaphoid fractures slow?

F/U recommendations
blood supply distal to proximal

F/U 3-4 weeks s/p initial (-) Xray
2 causes of wrist instability
- SLAC wrist (Scapho-lunate advanced collapse)

- chronic untreated scaphoid fracture or scapholunate dissociation
--- dissociation causes “gap-toothed sign”
--- can be corrected with fusion or bone grafting
3 types of lumbar orthopedic pathology
lumbar fracture: treatment options
balloon w/ cement to allow fx site to elevate
gross sign on hip fracture
unilateral leg shortening
orthopedic pathology characteristic of hip joint over other locations
avascular necrosis
2* temporary or permament loss of blood supply to femoral head
Knee instability: types
ACL (most common)
multiligament (usu. trauma related)
Meniscus injury
Meniscal tear
- degenerative
- buckethandle
- horizontal cleavage
- radial

Discoid meniscus
Causes of patellar instability
may be multifactoria
hip anteversion
tight lateral retinaculum
lax medial retinaculum OR lax patellofemoral ligament
patella alta
hypoplastic trochlea
connective tissue disorder (Ehlers Danlos, Marfans, etc)
elevated Q angle indicates...?
mechanical etiology of patellar instability
Osteoarthritis in the knee: locations
Articular cartilage damage in the knee: causes
osteochondral defect (OCD) – area bare of cartilage, exposed bone
bone bruise
Bakers cyst usually indicates what?
pathology on back of knee joint, e.g.: meniscal tear
Pigmented Villonodulal Synovitis
thickened hypertrophy of synovium
Tendon ruptures of knee:
- which ones?
- treatment
patellar tendon, quad tendon
Tx: immediate surgery
LisFranc's injury
dislocation of LisFranc’s joint (btw 1st & 2nd metatarsal joint)
Plantar fasciitis
- etiology
- signs & symptoms
- treatment
usu. 2° inadequate arch support
pain can flair in morning b/c of toe flexion during sleep
Tx: orthotics, esp. splint during sleep
- etiology
- signs & symptoms
- treatment
most commonly S. aureus
Tx: percutaneous drainage or surgical I&D
I.V. ABS x6 weeks
- type of bone
- function
Diaphysis - cortical - stability
- type of bone
- function
Metaphysis - cancellous - cushioning
Cortical bone structure
comprised of osteons (Haversian systems)
osteons communicate w/ medullary cavity by Volkmann’s canals
Haversian system
- osteon w/ central haversian canal
- central canal contains cells, vessels, nerves
- Volksmann’s canal connects osteons
Cancellous bone structure
trabecular or spongy bone
bony struts (trabeculae) oriented in direction of greatest stress
3 mechanisms of bone formation
cutting cones
intramembranous (periosteal) bone formation
endochondral bone formation
Cutting cones
primarily a mechanism to remodel bone
osteoclasts at the front of the cutting cone remove bone
trailing osteoblasts lay down new bone
intramembranous (periosteal) bone formation
long bone grows in width
osteoblasts differentiate directly from preosteoblasts & lay down seams of osteoid
does NOT involve cartilage anlage (precursor)
endochondral bone formation
long bone grows in length
osteoblasts line cartilage precursor
chondrocytes hypertrophy, degerate & calcify (area of decreased O2)
vascular invasion of cartilage occurs, followed by ossification (increased O2 tension)
bone healing: 2 prerequisites
blood supply
mechanical stability
blood supply in long bones: 3 sources
nutrient artery (intramedullary)
nutrient artery (intramedullary)
normally major blood supply for diaphyseal cortex (80-85%)
enters long bone via nutrient foramen
forms medullary arteries up and down bone
periosteal vessels
arise from capillary-rich periosteum
normally supply outer 15-20% of cortex
can supply much greater proportion cortex if medullary blood supply injured
metaphyseal vessels
arise from periarticular vessels
penetrate the thin cortex in metaphyseal region
anastamose with medullary blood supply in adults (in children, physis interrupts)
Normal bone blood supply pattern
Fractured bone blood supply pattern
endosteal/medullary: internal --> external

periosteal/external: external --> internal
Mechanical stability in bone healing
early stability promotes revascularization
after 1st mo., loading & interfragmentary motion promotes greater callus formation
mechanical load & small displacements @fx site stimulate healing
inadequate stabilization may result in excessive deformation at fx site
2° interruption of tissue differentiation into bone (soft callus)
over-stabilization reduces periosteal bone formation (hard callus)
3 stages of bone healing
Repair step of bone healing
periosteal callus forms along periphery of fx site
– intramembranous ossification initiated by preosteoblasts
intramedullary callus forms in center of fx site
– endochondral ossification at site of fx hematoma
callus formation
Remodelling step of bone healing
woven bone gradually converted to lamellar bone
medullary cavity reconstituted
bone restructured in response to stress & strain (Wolff’s Law)
Direct bone healing
occurs when no motion at fx site (i.e.: rigid internal fixation)
NOT involve formation of fx callus
(1) cutting cone formed, crosses fx site
(2) osteobasts deposit lamellar bone behind osteoclasts – form 2° osteon
(3) gradually, fx healed by formation of numerous 2° osteons

slow process – months to years (av. 18 months)
direct bone healing: contact healing
direct contact btw fx ends

allows healing to begin w/ lamellar bone immediately
direct bone healing: gap healing
gaps > 200-500 μm primarily filled w/ woven bone
- subsequently remodeled into lamellar bone
- larger gaps healed by indirect bone healing
Indirect (secondary) bone healing
occurs when fx not rigidly fixed (more naturally occuring)
bridging periosteal (soft) callus+ medullary (hard) callus re-est structural continuity
callus subsequently undergoes endochondral ossification
process fairly rapid: 6 – 12 weeks
Transforming Growth Factor (TGF)
superfamily of growth factors
promotes prolif, diff’n mesenchymal precursors for osteoblasts, osteoclasts, chondrocytes
- stimulates endochondral and intramembranous bone formation
- induces synthesis of cartilage-specific proteoglycans & type II collagen
- type II collagen occurs w/ 2° components of healing
- stimulates collagen synthesis by osteoblasts
Bone Morphogenic Proteins (BMP)
Osteoinductive proteins initially isolated from demineralized bone matrix
BMP that induces cell differentiation
BMP-3 (osteogenin) – v. potent inducer of mesenchymal tissue diff’n into bone
BMPs that promote endochondral ossification
BMP-2 and BMP-7 induce in segmental defects
BMPs that regulate extracellular matrix production
BMP-1 cleaves C-terminus of procollagens I, II, III
Fibroblast Growth Factors (FGF)
acidic form (FGF-1) & basic form (FGF-2)
increase proliferation of chondrocytes and osteoblasts
enhance callus formation
FGF-2 stimulates angiogenesis
Platelet-Derived Growth Factor (PDGF)
dimer of products of 2 genes, PDGF-A & PDGF-B
stimulates bone cell growth
increase type I collagen synthesis by increasing number of osteoblasts
PDGF-BB stimulates bone resorption by increasing number of osteoclasts
Insulin-like Growth Factor
stimulates bone collagen and matrix synthesis
stimulates replication of osteoblasts
inhibits bone collagen degradation
Interleukins important in bone healing
IL-1 stimulates bone resorption
IL-1 & IL-6 synthesized w/ decreased estrogen
Cytokines important in bone RESORPTION
Cytokines needed for bone resorption & formation
Cytokines important in bone FORMATION
Prostaglandin E: role in bone healing
stimulate osteoblastic bone formation;
inhibit activity of isolated osteoclasts
Leukotrienes: role in bone healing
stimulate bone formation;
enhance capacity isolated osteoclasts form Howship lacunae
Hormones that influence bone healing
- stimulates fx healing thru receptor mediated mechanism
- modulates release of specific inhibitor IL-1

Thryroid hormones
- Thyroxine & triiodothryonine stimulate osteoclastic bone resorption

- inhibit Ca2+ absorption from the gut
- causes increased PTH --> increased osteoclastic bone resorption
Local anatomic factors that influence healing
Soft tissue injury
Interruption of local bloody supply
Interposition of soft tissue at fx site
bone death cause by radiation, thermal or chemical burns, or infection
Systemic factors that cause problems with bone healing
- causes reduced activity and proliferation of osteochondral cells
- decreased callus formation

- cigarette smoke inhibits osteoblasts
- nicotine causes vasoconstriction diminishing blood flow at fx site

Diabetes Mellitus
- associated with collagen defects including:
--- decreased collagen content
--- defective cross linking
--- alterations in collagen sub-type ratios
Role of EM field in bone healing
Wolff's Law
in vitro bone deformation --> piezoelectric currents & streaming potentials

Wolff’s Law
– bone responds to mechanical stress
-- needs (-) charge for bone healing

Exogenous EM fields may stimulate mech. loading & stimulate bone repair

clinical efficacy v. controversial
Types of clinical EM devices for bone healing
direct electrical current
capacitively coupled electric fields
pulsed EM fields (PEMF)
Fragility fractures
caused by fall of standing height or less
osteoporosis – most common cause
33-50% of women will get in life time
15-33% of men
likelihood increases with ag
Vitamin D3 deficiency
deficiency common with age
lack of sunlight
deficiency  osteomalacia
very common in nursing homes
may interfere with fx healing
Vitamin D3 dosages
Young: 400 IU/day
Older: 600-800 IU/day maintenance
if deficient: 50,000 IU/week
Lab test to diagnose vitamin D deficiency
1,25 OH Vit D level
Prevalence of metabolic and vitamin D deficiencies in bone healing problems
84% all people with problems healing have metabolic or endocrine abnormalities

64% - vit. D deficiency
Anatomy unique to skeletally immature bones
order: epiphysis, physis, metaphysis, diaphysis
physis – growth plate
periosteum – thicker, osteogenic, attaches firmly at periphery of physes
bone – more pourus, ductile
Periosteum in children
more readily elevated from diaphysis and metaphysis than in adults
often intact on concave (compression) side of the injury
- may be helpful as a hinge for reduction
- promote rapid healing
periosteal new bone

contributes to remodeling
Physeal anatomy: gross
secondary centers of ossification
primary ossification

center – diaphyseal
secondary ossification
centers – epiphyseal
occur at different

stages of development
girls earlier than boys
Physeal anatomy: histologic zones
reserve zone – matrix production
proliferative zone = cellular proliferation, longitudinal growth
hypertrophic zone
- subdivided into maturation, degeneration, provisional calcification
- location of most pediatric fractures
Physeal anatomy: vasculature
medullary arteries do not anastamose – interrupted by physis

about-face of arteries provides area of turbulence in which bacteria can get stuck
Examination of injured child
assess location of deformity or tenderness
carefully assess and document specifically: distal neurologic and circulatory function
radiographic evaulation – xrays
xray evaluation of child bony injury
at least 2 orthogonal views (front/back or 2 sides)
include joint above and below fracture
understand normal ossification patterns – comparison radiographs rarely needed
Fractures common only in immature skeletons
physeal injuries – “weak link”
buckle or torus fracture (crushed end)
plastic deformation
greenstick fracture
buckle or torus fracture (crushed end)
compression failure
usu. at metaphyseal/diaphyseal junction
plastic deformation
microscopic failure in bending
permanent deformity can result
forearm, fibula common
greenstick fracture
bending mechanism
failure on tension side
incomplete fracture – plastic deformation on compression side
may need to complete fracture to realign
Salter-Harris Classification for pediatric fractures
Type I -
Type II -
Type III -
Type IV -
Type V -
Type I – through physis
Type II – through physis & metaphysis - **most common
Type III – through physis & epiphysis
Type IV – through metaphysis, physis, epiphysis
Type V – crush injury to entire physis
Type I & II Salter Harris fractures: treatment
closed redution, immobilization
exceptions: proximal femur, distal femur
Type III & IV Salter Harris fractures: treatment
intraarticular and physeal step-off
needs anatomic reduction
may need ORIF
Physeal fractures
traditionally believed to occur primarily through zone of hypertrophy
some fractures may traverse more than one zone
growth disturbance/arrest potentially related to site of fx w/in physeal zones, disruption vascularity
Fracture tx in children – general principles
children heal faster
need less immobilization time
stiffness of adjacent joints less likely
restore lenth, alignment, rotation when possible
keep residual angulation as small as poss., using closed tx methods
closed treatment of peds fractures: general principles
molded casts, cast changes, cast wedging, etc.
achieve adequate anesthesia/analgesia/relaxation
local or regional anesthesia, conscious sedation or general anesthesia
exceptions to closed methods: Salter III, IV; multitrauma
closed treatment of peds fractures: methods
gentle reduction of physeal injuries – traction 1st, adequate relaxation
use well molded casts/splints
use immobilizatio method on day of injury that will last entire course of tx
consider likelihood of postreduction swelling
repeat xrays q 7d - doc. mntn of acceptable position until early bone healing
reduction principles in pediatric fractures
in gen, do not remanipulate physeal fx after 5-7 days (risk further damage)
metaphyseal/diaphyseal fx can be remanip’d w/ analgesia < 3wks s/p injury
immobilization time in pediatric fractures
physeal injuries heal in half time of nonphyseal injuries
healing time dependent on fx, location, displacement
stiffness from immobilization rare – ergo, err toward more time in cast
Open treatment of pediatric fractures
respect and protect growth cartilage
adequate visualization (resect periosteum, metaphyseal bone if needed)
keep fixation in metaphysis/epiphysis if possible when much growth φ remains
use smooth K-wires if need to cross physis
* displaced intra-articular fx will not remodel – anatomic reduction mandatory
Complications of fractures in children
limb length discrepancy
physeal arrest
nonunion (rare)
Remodeling of children’s fractures
occurs by physeal and periosteal growth changes
greater in younger children
greater if near a rapidly growing physis
remodelling in children's fractures not as reliable in which cases?
midshaft angulation
older children
large angulation (>20-30°)
rotational deformity will not remodel
**intraarticular deformity will not remodel
remodeling in child fractures more likely if...?
2 years or more growth remaining
fx near end of bone
angulation in plane of movement of adjacent joint
primary sequella of growth arrest 2* to limb fracture in children
limb length deficiency
partial cessation of longitudinal growth: 2 outcomes
angular deformity if peripheral
progressive shortening if central
physes susceptible to growth arrest
- why?
- where?
large cross sectional area
large growth potential
complex geometric anatomy
distal femur, distal tibial, proximal tibial, distal radius
growth arrest/growth slowdown lines
aka: transverse lines of Park, Harris lines
occur after fractures or stress (e.g.: chemotherapy)
~ lifelines in tree trunk
result from temporary slowsown of normal longitudinal browth
thickened osseous plate in metaphysis
radiodense on xray
appear 6-12 weeks after fx
should be parallel to physis – indicates no growth disruption
angling of growth slowdown lines suggests what?

follow up:
if angled or point to physis, suspect physeal bar
imaging physeal bar
tomograms/CT scans
map bar to determine location, extent