MSK Flashcards
osteo sarcoma
age group? area?
10-20 MC age
**METAPHYSEAL AREA OF LONG BONES**
EWING sarcoma
age? location?
5-25 y/o
**DIAPHYSES OF LONG BONES, ribs and flat bones**
osteoarthritis
what is this? where is it most common? what are the two types? what would you expect to see on a xray?
joint disease with protective cartilage on the ends of your bones wears down over time and subchondral bone wears down over time >40 yrs olds THINK ELDERLY, slow developing joint pain
early onset and late onset OA, erosive
hands, hips and knees most common
primary or secondary causes
joint enlargement, red swollen PIP, DIP, weakness and wasting of muscles around joint, deformities
xray: see narrowed asymetric joint space, with osteophyte formation, bony sclerosis
what is a osteophyte? what disease is this commonly seen in?
a bony outgrowth associated with the degeneration of cartilage at joints.
osteoarthritis
what are the characteristics associated with early osteoarthrits? (4 things)
1-2 years
morning stiffness lasting
they’re ok, they say they just keep going
red, prominent PIP, DIP joints with normal radiographs
what are the characteristics associated with late osteoarthritis?
AM stiffness lasting
mechanical stiffness that gets worse with movement, more pain the more they do
claim not to have the same strength they used to (opening jars/doors etc)
little evidence of inflammation
ABNORMAL RADIOGRAPHS
get less symptomatic in non-weight bearing joints AKA many patients have extreme hand deformities but are asymptomatic (once they are deformed they don’t hurt anymore)
what is the treatment options for osteoarthritis? (7 things)
joint conservation
exercise
weight loss
NSAIDs (caution with ulcers)
COX-2 inhibitor (safer for people with history of ulcers, but still need to watch for cardiac complications)
cartilage replacement (15-55)
total joint replacement
primary osteoarthritis is…..
idiopathic, arises spontaneously
secondary osteoarthritis can come from….
- posttraumatic
- congentiral deformation
- endocrinopathy
- neuropathic arthropathy
- padgets disease
- avascular necrosis
- skeletal hyperostosis DISH
what is the most common joint disorder in the US?
osteoarthritis
Osteoarthritis of the hip
what is this? what will you see on the xray? what is the “definitive cure”? what other surgical interventions can you do in younger patients?
degredation of articular cartilage, thickening of the subcondral bone
progressive hip pain that often complain of groin pain, “crunching” noises aka crepitus
xray osteophyte formation, decreased joint space, sunchondryl sclerosis and cysts
conservative: same as always
definitive cure: total hip arthroplasty THA (replace joint)
surgical: arthroscopic debridement, femoral head resurfacing in younger patients
osteoarthritis of the knee
what is this? what are four presentations you see with this? what is a possible muscle presentation? what is the gold standard for diagnosis? what are the conservative vs surgical treatment options?
degredation of the hyaline cartilage of the knee
pain is worse in AM, giving away or locking
joint hypertrophy, and tendernous at the joint line, possivle quadricept atrophy
gold standard: xray…see osteophyte formation, decreased joint space so bone on bone, sunchondral sclerosis
treatment: conservative normals plus cortisone injections and hyaluronic acid injections
surgical: knee arthroscopy, tibial/femoral osteotomy, total knee arthroplasty
what are the Early osteoarthritis presentations? (4)
1-2 years
morning stiffness lasting !!! “they’re ok, they just keep going!”
red, prominent DIP and PIP joint involvement
normal radiographs
osteoarthris…explain what happens in this…
normal bone programming
“cartilage scenescence”–we outlive our chondrocytes around 25-30 years old, it frays and falls apart and the chondrocytes become hypertrophic and grow larger, however they produce enzymes MMP and aggrecanases that break down the cartilage and act like growth plate cells where THEY MAKE MORE collagen 1 and 9, BONE THAN BREAK IT DOWN…CARTILAGE CAN’T REGROW SO YOU JUST GET INCREASED BONE GROWTH!!
“progressive loss of articular cartilage and reactive changes at the joint margins from bone rubbing on sunchondral bone rubbing on bone “behaves like a fracture” and stimulates chondrocyte hypertrophy and increased bone growth
what are the common presentations of late osteoarthritis? (5)
morning stiffness lasting
mechnical stiffness, gets worse with movement, more pain the more they do
not the same strength they used to (opening jars, turning handles)
abnormal radiographs! deformities obviously present, bone hypertrophies
get LESS symtomatic in non weight bearing joints, asymatic once they are deformed because they aren’t able to move them
what are the treatment options for someone with osteoporosis?
Not much…its a natural bone programming
Its “supposed” to happen
- joint conservation
- exercise low impact
- weight loss to relieve load on joints
NSAIDS and COX-2, total joint replacement, autologous cartilage implantation (not many people qualify)
what joints are most commonly effected by osteoarthritis?
PIP, DIP, hips, knees
infectious (septic) arthritis
how many joints does this involve? what joint is the most common? what is the most common agent? what are the four agents in children? what active people does this often effect and percent? what should you treat with until the cultures come back?
involves a single joint, most commonly the knee 90%
then hip, shoulder, anklet
Adults: S. aureus, streptococcus
children: Haemophilis influenzae, E. coli, pseudomonas, borrelia burgdoferi
- sexually activite individuals have increased risk from Neisseria gonnoreah 50%*
xray: may see gas in the joint space, arthrotomy and culture - treat until culture comes back: ceftrixaone, followed by 4 weeks of antibiotic after organism identified*
in infectious (septic) arthritis….what must you always do if the hip is involved?
arthrotomy….test it and see what it is!!
osteoporosis
what is this? who is it most common in? what is the nickname for this disease? what imaging type do you want to preform? what 3 presentations might you find on physical exam?
abnormal bone remodeling, decrease in the total volume of bone making it less dense, since less strong it leads to increased fractures!
imbalance between bone formation and reabsorption
most common in menopausal women
“silent disease”
presentation: height loss, kyphosis, severe cervical lordosis dowagers hump
Dexxa scan of spine and hip
what is an abnormal DEXA scan result that can indicate osteoporosis?
-2.5 and below
what are the treatment options for osteoporosis? (3)
- bisphosphonates: inhibits osteoclasts (jaw necrosis)
- HRT, estrogen, or progesterone (stroke, breast cancer)
- selective estrogen receptor modulator (serms)
what test should you do for herniated disk pulposa?
straight leg test
pain at
herniated nucleus pulposus
what happens in a herniation? where does this most commonly occur in the vertebrae and in the spinal cord? what will the 3 main symptoms be and what are 3 things a patient will get pain with that are normal things? what do you do for treatment?
this is when the nucleus pulposus, the soft gelatinous center is herniated posteriorally since this is where the annulus fibrosis is the weakest!!!
usually occurs in lumbar spine since takes the most load
see motor and sensory manifestation
- tingling, numbness, or burning pain (seen in sagital and axial MRI images)
- pain with coughing, sneezing, and laughing
RICE, NSAIDs, surgery
spinal stenosis
what is this caused by? what two conditions for the risk of stenosis increase with? what unique thing makes this better, and what makes this worse? what can you see the in the lumbar region? what will you see on the MRI? what can you do for treatments for this?
compression of nerves of spinal cord caused by narrowing of the spinal cord and foramen
commonly seen in spondylosis and degenerative arthritis
pain increases with walking or axial loading (leaning back), and decreases with leaning forward, flexion!
back and leg pain, soft tissue and thecal narrowing, can see loss of lumbar lordosis
TX: acetaminophen, weight reduction, pelvic tilt, abdominal exercises….last choice decompressive surgery
avascular necrosis
what causes the necrosis? how long can the cells survive? what is a unique sign that you will see? where does the pain present and what happens when the person rests? what are four surgical interventions you can do?
bone death from disruption of blood supply
osteocytes, blasts and clasts, die withing 24-48 hours of oxygen deprivation
reprofusion may regenerate bone growth
cresent sign: collapse of sunchondral bone
often seen pain in groin, thigh, buttock
pain typically decreases with rest
Treatment: NSAIDS, anticoagulants (heparin, coumadin etc) since can thin blood and help it get to the site if there is a clot!!
Surgical intervention: hip resurfacing, core depression, fibular bone graft, total hip arthroplasty
osteomyelitis
what is this and how does it present? what is the most common organism in this and what are the different potential organisms from adults to children? what can a xray show you? MRI? Labs? How long does this person need to be on antibiotics? what is commonly needed? what needs to be removed?
infection of the bone, bacterial, fungal
symtoms come from inflammatory response, pus inhibits blood flow, causing necrosis, if bacteria gets into the bone itself it can be difficult to eradicate
S. aureus most common in children and adult
Adults: S. pyogenes, Pseudomonas, E. coli
Children: Group B strep, E. coli, Streptococcus pyogenes, haemophilis influenzae
fever, chills, malaise, may have ulcer over effected area
xray:done destruction/hetertrophic bone formation
Labs: soft tissue involvement
6 weeks of antibiotic therapy required, can do hyperbaric chamber if not healing, debridement required in most cases and hardware removal, also amputation
where are the 3 most common locations for osteomyelitis in children?
femur, tibia, and humerus
aka the long bones
where are the three most common locations for osteomyelitis in adults?
vertebrae, maxilla, pelvis
scoliosis
what are the two general shapes of the spine you can see? what age group is this in and what gender? what are two unique indicators you can see? what do you see with the shoulder, iliac, scapula and flank? how do you describe the curve? what vertebrae is this most common in? what type of curvature is really rare?
lateral curvature of the spine in C or S shape, 3-18 years old!
cafe au lait spots and tufts of hair present=indicators
asymmetric in shoulder and iliac height, asymmetric scapula, flank decrease flexion
more common in girls during puberty growth spurt and cessation of spinal growth rate at are the greatest risk!
to measure the curvatue you look at the vertebrare at the apex of the curve and then describe relative to that
most common at T7-T8, left curvatures is rare!
what plane are the abnormalites in scoliosis found?
coronal
what are two things you can see on a xray in osteomyleitis?
late sequestra: dead bone surround granulation tissue
involucrum: (periseal new bone) make take several weeks to months to appeare
but careful when looking at xray…..visible changes on cray lag behind symptoms by 10 days
explain the 2 divisions of patients for scoliosis and what the treatment reccomendations are?
>20* curvatures: back brace and surgery consult
in scoliosis patients, when are increased xrays indicated? what is considered clinically significant for a curvature change using scolimeter?
>5* curvature change: increased xray
curve changes: >15% is signficant!!
what would you commonly see sacroilliacitis with?
ankylosing spondylitis
and bamboo spine
kyphosis
what vertebrae do you see this in? what other curvature typically accompanies this in the spine? what is the difference in treatments based on the degress of curvature in the spine?
increased curvature of thoracic vertebrae, commonly associated with scoliosis
rounded back appearance, usually accompanied by excessive lordosis
if 45-60* of curvature: PT and bending
if >60*: milwakee brace
surgery as last resort
what is the most common spinal deformity evaluated by a clinician?
idiopathic adolescent scoliosis
ankle sprain
what are the three types that can cause this and which ligaments are included in which types? what are the presents? what exam tests are important to do? what rule do you use to determine if a xray is needed? what is the treatment and what is one exception and how long do these patients need to be immobalized?
inversion injuries (90%), anterior talofibular (#1), calcaneofibular, posterior talofibular
eversion (10%), deltoid lig
lateral rotation (high ankle sprain): syndesmotic ligs, anterior tibiofibular joint, high ligs connect the tibia and fibula, pain with external rotation, pain just above the ankle squeeze test of tibia/fibula
point tender over lig, hypermobility with stress testing
anterior drawer tests
ottowa ankle rule to determine if xray is needed
Tx: conservative even if grade III, surgical repairs but is reserved for chronic instability, crutches 48-72 hours and brace, with syndesmotic sprain longer immobalization for 4-6 weeks
gout
what happens here? what do the crystal depositions look like? what is effected commonly as a strange presentation in most cases? what are the two ways these crystals accumulate and what are the percentages? what hardened structure can be found within joints of chronic gout? what labs do you do? what is diagnostic? what is the difference between the treatment for acute and chronic treatment?
most common form of inflammatory arthritis in m/w over 40
acute arthritis (usually at night) by sudden increase and deposition of uric acid crystals in the joint
great toe effected in 50% of cases, but can effect any joint in the body: ankles, knee, hands, wrists
cause: hyperuricemia, too much in circulation and in 90% of cases there isn’t enough secreted from the kidneys instead of overproduction (10%)
joints contain tophi, hardened nodules (chronic)
Labs: uric acid levels, may have elevated WBC, uric acid crystals in joints are diagnostic, xray to access joint damage
Acute TX: NSAIDS, colchicine
Chronic: Xanthine oxidase inhibitor, allopurinol (blocks production) or probenecid (increases uric acid excretion)
pseudogout
what is this caused by? what joint is the most commonly effected? what isn’t present that is seen in regular gout? where do you see the deposits? what do the crystals look like under the microscope?
acute inflammatory disease caused by calcium pyrophospate crystals
calcium pyrophosphate dihydrate disease
knees most commonly effected
*****no tophi present that differentiates from gout****
see calium deposits in the cartilage
aspiration see rod shapped crystals with blunt ends and befringement unlike gout
conservative and excision of chondrocalcinosis
adhesive capsulitis
what are 4 risk factors? what causes this? what imaging do you want to do? what is the reccomended treatment and how long can this take to be effective? what is last resort treatment? how do you make the diagnosis?
sedentary people, decreaed volume of the joint capsule and capsular contraction
“frozen shoulder”, insidious onset, gradual progression, pain at night
increased risk with: age, obesity, diabetic, middle aged women
there is a physical “block” preventing motion
xray: rule out other bony deformities
diagnosis is based on history and PE
treatment: NSAIDS and stretching, GH cortisone injection, takes patience since it can take up to a year to heal, manipulation under anesthesia as last chance
elbow dislocation
who is it common in? how does it happen? what must you access for? what do you treat with? what is important to do after reduction?
most common in children, 50% happen from sports
fall on outstrectched hand, 98% are posterior
arm held at side in splinted position, unwillingness to move elbow
obvious deformity, olecranon swelling
MUST access neurovascular structures, MUST perform POST reduction xray!!! two films!
treatment:
- reduction
- spint/cast 1-3 weeks
elbow gets very stiff very fast esp in kids, so want to initiate early ROM exercises to prevent flexion contracture
NSAIDS
lateral epicondylitis
what is a nickname for this condition? what muscles specifically does it effect? what does this person have a difficult time doing? what happens with pain and ROM? what are 5 treatment options? what is the last resort treatment and why?
“TENNIS ELBOW”, dengeneration/inflammation of the wrist extensor mechanism
LATERAL EPICONDYLE, DIFFICULTY LIFTING THINGS WHEN HAND IS PRONATED
involves the tendonous insertion of extensor carpi radialis brevis
tennis, golf, weight lifting
pain with repetitive extension and flexion
pain:
- radiate down the arm
- passive wrist flexion
3. active and resisted wrist extension
Treatment:
- eliminate aggrevating factors
- NSAIDS, ICE, HEAT
- tennis elbow strap
- cortisone injection, DONT INJECT TENDON
- surgical release/faciotomy if all else fails. only successful in 50% of people and longer than 6 months
olecranon bursitis
what are the two different causes? what is the difference in treatment between the two? what is the most common organism to cause it? what should you test? and for what two things?
inflammation of olecranon bursitis, can be from resting on the elbows a lot
usually quick onset
can be from infection: septic bursa
suspect infection if erythema and intense pain on palpation
send joint fluid for analysis: culture and crystal analysis
treatment for non infectious:
- padding/compression wrap, NSAIDS, heat, ice
- cortisone injection ***need to make sure 100% not infected if so***
treatment for infectious:
- treat cultured pathogens
- incision and drainage
most common organism is S. aureus
carpal tunnel syndrome
what happens? what causes the symptoms? what 4 special tests can you when diagnosing? what is the gold standard of care? what should you do first and for how long? describe the numbness pattern
most common nerve entrapement syndrome, median nerve under transverse carpal lig
pain and numbness in media distribution (pic), pain at night, weakness in thumb grip strength
tendernous and tingling at wrist and palmar area
Special tests:
Phalens test w/tingling after 1 min (I think of “flailing hands)
Tinel’s sign-taping over transverse lig produces tingling (I think tinel=tingle)
decreased 2 point sensation
electromyography/nerve conduction
gold standard: surgery, releases transverse lig, but first try night splint, NSAIDS for 4-6 weeks before surgery consult
DeQuervain’s disease
what is this caused by? who is it more common in? where do you see the localized pain, between what two things? what is 1 special test you want to do? what are the two treatment options?
extensor pollicus brevis and abductor pollicus longus act to abduct the thumb away from the hand in the radial plane, more common in women and diabetics
synovial/tendon sheath becomes inflammed from OVERUSE
pain over the CMP joint of first digit, trapezium and metacarpal of thumb
special test: finkelstein’s test (place thumbs inside of fist and ulnar deviate which causes pain!!)
tests: xray to rule out other things, labs for gout
treatment:
- NSAIDS, splint, cortisone injection, symptoms resolve in about a year
- fasciotomy of 1st dorsal compartment (not as common) but releases overlying lig
fibromyalgia
what is it? how long do you need to have it? what are the requirements? what are the 4 presentations? what are the 4 important things you need to rule out? what testing is ok? which arent? what should you NOT treat with? what are 4 potential medical treatments?
central pain syndrome, pain threshold disorder >3 months 6:1 females
increased activity in somatosensory cortex, posterior insula, and thalamus
allodynia (percieved pain when non, hugging), hyperplasia (aplified pain perception)
aggrevated by stress, lack of sleep, activity
- widespread muskulo pain
- sleep disturbance
- no objective physical findings
-
11/18 trigger points
* important to test deep tendon reflexes and sensation*
testing proceed with caution: NEED TO RULE OUT CELIAC DISEASE, IBS, VIT D DEF, HYPOTHYROIDISM
DO NOT ORDER RA/ANA
can order thyroid, electrolytes, vit D, ESR/CRP, Hep C, CPK
Don’t treat with: NSAIDS, narcotics
Treat with: Tricylic antipressants (help sleep), selective serotonin reuptake inhibitors (SSRIs), dual acting, lyrica neurontin but SO many side effects
what two exam tests are important for impingement/bursitis/tendonitis of the shoulder?
hawkins
Neers (impingement sign)
what does the medial meniscus look like? how much motion is allowed? what does it attach to?
Medial Meniscus
“C” shaped
attaches to tibia and MCL
2mm of motion
what is the shape of the lateral meniscus? how is it attached? how many mm of motion does it have?
Lateral meniscus
“o” shaped
loosely attached, decreasing risk for for injury
10 mm of motion as knee flexes
Reactive Arthritis (Reiter Syndrome)
what is this join infection caused by? what are the two most common routes a person can contract this? what are the 4 symtoms that are included as a part of this tetrad? what do you want to make sure you do? and what test will be negative? what do you treat with?
joint inflammation that presents after PREVIOUS INFECTIONs commonly from sexually transmitted or gastroenteritis
chlamydia urethritis most common pathogen
Tetrad presentation:
- urethritis (difficulty urinating,
2. conjunctivitis (eye inflammation)
3. olioarthritis (1-4 joints)
4. mucosal ulcers (oral, balantitis*peeling of skin on penis*, stomatitis *inflammation of the mouth)
5. keratoderma blennhoragicum rash/ulcers on bottom of feet
want to do a culture, will be RF NEGATIVE!
Treatment: NSAIDS, DMARDS antibiotics not really helpfuly even though infection!
developmental dysplasia of the hip (DDH)
4 dx?
tx goal?
3 tx and for what age group?
DX:
- barlow
- ortalani
- AP xray
- US at 6 weeks if female and breech
TX:
**goal is to keep the hip located so that the ligaments and bones have time to form and strengthen to hold it in place**
1. PAVLIK BRACE/harness
- use under 6 months for 8-12 weeks
- 90-95% successful
2. casting if older than 6 months
8-12 weeks
3. surgical reduction/fixation if older than 2 y/o
developmental dysplasia of hip (DDH)
3 causes?
which side MC? when present?
4 sxs
causes:
- generalized hip laxity
- complete hip dislocation
- acetabular abnormality
MC in left hip, present at birth
SXS:
1. initally asymptomatic
2. then with walking, limp and decreased leg length
3. asymetry of the skin folds
4. loss of adduction
slipped capital femoral epiphysis (SCFE)
what is this?
key fact?
age range?
5 potential causes?
slippage of the femoral epiphysis usually posteriorly
most common adolescent hip disorder, 8-16 y/o
causes:
- endocrine disease (GH, hypo/hyper thyroid)
- inflammation
- renal disease
- irradiation
- mechanical forces
slipped capital femoral epiphysis (SCFE)
6 sxs?
3 dx test? 2 findings?
SXS:
- acute or chronic
- pain with activity
- pain in hip, groin, knee
- limp
- decreased hip movement with INTERNAL ROTATION
- possible limb shortening
DX:
- AP and FROG LATERAL
- “fuzzy” irregularities on physis (growth plate)
- slipping at the physis
slipped capital femoral epiphysis (SCFE)
2 goals of tx?
1 tx option?
GOALS:
- stablize the epiphysis
- cause early closure of the physis
- surgical fixation
screw into the epiphysis
non weight bearing
WILL PROGRESS IF LEFT UNTREAED
osgood-schlatters disease
what is this and who do you find it in?
3 causes of this?
inflammation at the tibial tubercle apophysis during periods of growth/athletic children
MC in males!!!
CAUSES:
1. repetitive trauma/overuse
2. jumping/running
3. repetitive quadriceps use that pull on the insertion
osgood-schlatters disease
4 sxs of this?
dx?
3 tx?
SXS:
- gradual onset
- worsens with jumping, running, kneeling
- deformity at tibial tubercle with pt tender
- often bilateral
DX:
CLINICAL!!!
TX:
- symptomatic for several months
- resassurance
- rarely surgery for tibial tubercle excision
“nursemaids elbow” subluxation of the radial head
what is this?
what happens?
MC age?
3 sxs?
most common elbow injury in kids caused by increased joint laxity radial head is wedged in annular ligament
occurs in 2-3 years old MC
SXS:
- caused by forceful pronation/extension
- unwillingness to use arm
- arm held in extension by side
nursemaids elbow: sublaxation of the radicular head
2 dx?
tx 2?
DX:
- pain over the radial head
- xrays not helpful
TX:
- manipulation of the radial head with PRESSURE ON THE RADIAL HEAD WITH FORCE FLEX AND SOUPINATION
- cast for reccurent dislocations
GROWTH PLATE FRACTURES
SALTER HARRIS CLASSIFICATION
