High Yield 5 Flashcards
What is calcific tendonitis?
Calcium deposits within tendon
Pain related to impingement, inflammation, and increased intratendinous pressure from the calcific deposit
Sx + physical for calcific tendonitis
Hx
Localized pain
Gradual, atraumatic
Worse at night
Physical
Pain worse with AROM compared to PROM
Ix + management calcific tendonitis
XR + US show calcium deposits
Management
Often resolves spontaneously within 3-6mo
NSAIDs, steroid inj
Shockwave therapy
Therapeutic US
Heat
What is CRPS?
Complex regional pain syndrome
Severe, continuing pain, disproportionate to any inciting event
Manifested by four clinical characteristics: based on Budapest criteria:
Intense pain
Vasomotor disturbances (temp or color changes)
Sudomotor (sweat glands) disturbances, as increased sweating or clammy skin
Motor or trophic changes (tremor, decreased ROM, weakness + hair, nail or skin changes)
RF for CRPS
Females
40-70S
Upper limb more common
Most report a triggering event (eg #, surgery, sprain)
Sx of CRPS
Progressive pain
Burning, throbbing
Sensitivity to cold, touch
Functional limitation
Physical for CRPS
Allodynia
Eedema
Color or temp changes
Thickening of skin
Joint contractures
Abnormal hair growth
Ix for CRPS
Sympathetic nerve blockage (lumbar block for lower extremity or stellate ganglion block for upper extremity)
Labs to exclude other systemic causes: CBC, ESR, fasting glucose, calcium, T4, TSH
Bone scan can show increased uptake
XRs can be initially normal then show patchy subchondral osteopenia + bone demineralization
Management of CRPS
Bisphosphonates
Short course steroids
Sympathetic nerve blockade
TCAs for pain relief
Gabapentin
Ketamine
Acupuncture
Physical therapy - Tactile desensitization, strengthening
Transcutaneous electrical nerve stimulation can be beneficial.
Behavioral management
Relaxation techniques
Stress management
Mirror therapy
Aerobic exercise
Somatosensory rehabilitation
What are the Spondyloarthropathies?
Ankylosing spondylitis (AS).
Reactive arthritis (ReA).
Psoriatic arthritis (PsA).
Arthritis associated with inflammatory bowel disease (IBD).
Juvenile onset spondyloarthritis.
Undifferentiated spondyloarthropathy (USpA)
RF for spondyloarthropathy
Male
Caucasian
Unprotected sex
Positive family history
ReA is significantly increased in persons with HIV.
More common in patients who were not breast fed
HLA-B27
RF for OA
Age
Fam hx
Obesity
Females
Joint injury
Impact sports
Abnormal biomechanics
Sx of OA
Insidious pain over years
Crepitus
Grinding
Stiffness <30mins after immobilization
Physical for OA (general, knees, hands, hips)
Joint line tenderness is common in hands and knees.
Joints may have crepitus, decreased range of motion (ROM), effusion, and atrophy of surrounding muscles.
In knees, involved compartments can include medial (most common), patellofemoral, and/or lateral, so accurate palpation is important. Effusion and trace joint warmth are common in acute flares.
In hands, may see nodules in the DIP and PIP joints, termed Heberden and Bouchard nodes, respectively
In hips, decreased and painful internal rotation are early signs, and tenderness over the anterior joint line is a later finding.
XR findings for OA generally, and XR views for thumb, hands, shoulder, knee + hip
X-ray characteristics include osteophytes, joint space narrowing, subchondral sclerosis, and cyst formation
Thumb CMC joint: true AP (Robert) view of the thumb, wrist AP, and oblique
Hands: AP and lateral
Shoulder: true glenohumeral AP (Grashey) view most sensitive
Knee: Weight-bearing AP in 20 to 45 degrees of flexion (Rosenberg view) is most sensitive and accurate for the medial and lateral compartments. Supine lateral and sunrise or merchant views are best for patellofemoral compartment.
Hip: Weight-bearing anteroposterior (AP) films are most sensitive.
Management of OA
Education
Set reasonable expectations on outcome (pain reduction, increased function, not cure).
Modification of activities to minimize pain and risk of joint trauma
Importance of nonpharmacologic therapies
Weight loss
Exercise
Aquatic and low-impact land-based aerobic exercise, strength training, and ROM exercise
Mood + sleep management
Meds
Topical NSAIDs
Oral NSAIDs
Duloxetine
Injections
PRP
Viscosupplementation with hyaluronate
Steroid inj - usually lasts 2-4 wks. Max 4 inj per year
Possible stem cell inj
Surgery
When “bone on bone”
Debridement or osteotomy
Joint replacement
Other
Bracing
Heat/ ice
TENS
RMT
Acupuncture
Walking aids
What should be discouraged in management of OA?
Glucosamine supplements
Visco supplements
Opioids
Repeat steroid injections
Arthroscopy
What is osteochondritis dissecans?
Osteonecrosis of a fragment of subchondral bone + cartilage, which can break off and cause pain, swelling + joint dysfunction
What are the common places osteochondritis dissecans affects?
Knee (lateral aspect of medial femoral condyle)
Ankle (talar dome)
Elbow (humeral capitellum)
RF for osteochondritis dissecans
Typically 12-19y/o
Boys more common
OCD in one joint is a RF for contralateral joint
Sports involving jumping, pivoting, cutting movements
Sports with repetitive loading of the elbows, such as baseball and gymnastics, are specific risk factors for OCD of the elbow.
Sx of osteochondritis dissecans
Vague, insidious, poorly localized pain
Can have swelling + stiffness
Can have locking/ catching sensation
Hx of ankle sprain, not responding to therapy 4-6 wks after injury
Physical for osteochondritis dissecans
Decreased or painful ROM
Joint line tenderness
Wilson’s sign - flex the knee to 90 deg, internally rotate the tibia and extend the knee slowly, watching for a painful response and pain is then relieved by external rotation
Ix for osteochondritis dissecans
XR
Characteristic appearance on x-ray is a well-circumscribed lucent defect in subchondral bone that may or may not contain an internal bone density
MRI
Arthroscopy is gold standard
DDx for osteochondritis dissecans
Fracture
Ligamentous or cartilage injury
Tendinosis
Inflammatory arthropathy
Mechanical issue (i.e., patellofemoral pain syndrome)
Juvenile: apophyseal injury
Adult: osteoarthritis
Management + RTP of osteochondritis dissecans
If asymptomatic, incidental finding = monitor until radiographic healing
If symptomatic, stable (not displaced): relative rest, non wt bearing if lower limb, consider bracing or casting, physio for strengthening
If symptomatic, unstable (displaced lesion) or failed conservative management: refer to ortho for fixation/ debridement/ microfracture
Refer all adults to ortho
RTP
3-4mo
DDx for hypermobility
Ehlers-Danlos syndrome classic type
Marfan syndrome
Osteogenesis imperfecta
Loeys-Dietz syndrome
Ankylosing spondylitis
Rheumatoid arthritis
Fibromyalgia
Multiple sclerosis
Amyotrophic lateral sclerosis
Autonomic polyneuropathies
Myopathy
Chronic fatigue syndrome
Management of hypermobility
PT
OT
Splints, orthotics
RF for hypermobility
Females
Children + teens
Conditions associated w/ hypermobility
Recurrent joint subluxation and dislocation
Pes planus
Chronic pain
Anxiety and depression
Gastroesophageal reflux disease (GERD)
Irritable bowel syndrome (IBS)
Syncope
Orthostatic hypotension
What is osteoporosis?
Systemic disorder characterized by decreased bone mass and microarchitectural deterioration of bone leading to bone fragility and increased susceptibility to fractures of the hip, spine, and wrist
What is osteopenia vs osteoporosis?
Osteopenia (low bone mass):
Bone mineral density (BMD) defined as T-score between −1.0 and −2.5 standard deviation (SD) below the mean of a young adult reference population on dual energy x-ray absorptiometry (DEXA) scan
Osteoporosis (decreased bone mass):
BMD T-score ≤2.5 SD below the mean of a young adult reference population
Types of osteoporosis
Primary: age-related (postmenopausal estrogen deficiency, age-related vitamin D deficiency)
Secondary: (drug or concurrent medical condition etiology)
Hx + Ix for osteoporosis
Hx
Low trauma #
Height loss
Investigations
DEXA
T + L spine to evaluate for #
Management of osteoporosis
Bisphosphonates
Inhibit osteoblast + osteoclast activity
SE: N/V, abdo pain, esophagitis, osteonecrosis of jaw
OR denosumab
Exercise + balance therapy
Repeat BMD q2yrs
Prevention of osteoporosis
Identify + treat secondary causes
Vit D + calcium supplement
RF for osteoporosis
Female sex
Parental history of osteoporotic hip fracture
Personal history of fracture
Age 65 yr or older
Low body weight
Diet low in calcium; low in vitamins C, D, and K; and decreased copper, manganese, and zinc mineral content
Estrogen deficiency: postmenopausal or premenopausal secondary to over exercising and/or eating disorder
Sedentary lifestyle, lack of weight-bearing exercise
History of falls
Female athlete triad: low energy availability (EA) (with or without disordered eating), menstrual dysfunction, low BMD
Medications: glucocorticoids, anticonvulsants, cancer chemo drugs, thyroid replacement drugs, proton pump inhibitors (PPIs)
Excessive alcohol
Smoking
Other diseases: diabetes, hyperparathyroidism, hyperthyroidism, multiple myeloma, rheumatoid arthritis
Impaired absorption of calcium, phosphate, and vitamin D from the gastrointestinal (GI) tract, as in inflammatory bowel disease, gastrectomy, celiac disease, jejunoileal bypass, or pancreatic insufficiency
What is myofascial pain syndrome?
Myofascial trigger points are “knots” in muscle that cause pain
MPS is >1 MTP
Sx + physical for myofascial pain syndrome
Hx
Vague, persistent or intermittent pain
Can be uni or bilateral
Physical criteria for diagnosis
Palpation of taut band
Tender in taut band
Reproduction of index pain w/ sustained pressure on MTP
RF for myofascial pain syndrome
Poor posture
Overuse
Repetitive motion
Deconditioned muscle
Prolonged sitting
Management of myofascial pain syndrome
Address biomechanical factors
Dry needling, trigger point inj, acupuncture
Sx + physical exam for fibromyalgia
Sx
Widespread, symmetrical pain
Poor sleep, fatigue
Associated w/ myofascial pain
Exam
Tenderness in multiple soft tissue locations
What is a stress #?
Damage d/t repetitive loading that exceeds healing capacity
Can range from mild periosteal reaction to displaced #
What are low vs high risk stress #?
Low risk = pelvic, femoral shaft, posteromedial tibia, fibula, metatarsal shafts, cuboid, calcaneus, and cuneiform
High risk = femoral neck (FNSF), anterior tibial shaft (ATSF), patella, medial malleolus, 2nd metatarsal base, proximal 5th metatarsal, sesamoids, tarsal navicular, and talus
RF for stress #
Female gender
Female body mass index (BMI) <19
Late menarche ≥15 yr
Prior SF
Extreme pes cavus or planus
>5 degrees knee valgus/external rotation (ER)
Inadequate caloric intake
Excessive caffeine, alcohol, or tobacco use
Amenorrhea/oligomenorrhea
Osteopenia
Chronic corticosteroid use
Rapid increase in training volume
Recreational runners >25 miles per week
Poor footwear
Running on hard surfaces
Low 25-hydroxyvitamin D
Low testosterone (males)
Sx of stress #
Insidious pain w/ repetitive activity
Pain at rest
Ask about RF, nutrition, steroid use, menses
Physical for stress #
Direct bony tenderness +/- edema
Tender “N” spot (dorsal central third of the navicular bone between the anterior tibial and hallucis longus tendons) suggestive of SF
Calcaneal squeeze test: simultaneous pressure on the medial and lateral aspects of calcaneus, pain suggestive of SF
Fulcrum test: pain at the site with bending the long bone over a table edge or examiner’s leg or forearm; useful for tibial and FSSF
Log roll test: Passive internal rotation (IR)/ER of the thigh elicits groin pain in an FNSF.
Patellar-pubic percussion test: Place stethoscope on the ipsilateral pubic tubercle and percuss the ipsilateral patella or use a tuning fork; the sound is reduced on the side in which an FNSF is present.
Flamingo test: Patient stands on the affected side. A positive test is indicated by pain in the location of the SF; useful for FNSF, FSSF, lower leg, and sacral SF
Tuning fork test: pain when applying a 128-Hz tuning fork over the site of suspected SF; useful for tibia and fibula SFs
Ix for stress #
XR, repeat in 2-3 wks if normal
Lucency or callus formation visible
Bone scan
MRI is gold standard
Labs: vitamin D, CBC, chem 7, calcium, TSH, albumin, prealbumin, phosphate, and parathyroid hormone
Females with menstrual dysfunction: FSH, LH, estradiol, testosterone, HCG
Dexamethasone suppression test if excess cortisol suspected
DDx for stress #
Muscle strain/tendinopathy
Fasciitis/periostitis
Exertional compartment syndrome
Nerve/artery entrapment
Bone tumor
FNSF may mimic adductor or hip flexor strain.
ATSF can be confused with shin splints.
Medial tibial SF can mimic anserine bursitis.
Management of stress # (general)
Relative rest
Cast/ boot/ crutches to ensure pain free rest
Compression boot for tibial SF
NSAIDs
Refer to ortho for high risk SF
Shock wave therapy
FU q2-4 wks
Nutrition:
Adequate calories, protein, and carbohydrates for age; body type and sport
Daily calcium 2,000 mg and vitamin D 800 IU
50,000 IU vitamin D weekly ×12 if deficient
Complications of stress #
Complete fracture, delayed union, nonunion, avascular necrosis
Prevention of stress #
Adequate calories and nutrition
1,500 to 2,000 mg calcium and 800 IU vitamin D per day
Screen for female athlete triad.
Padded insoles and orthotics (military recruits)
Replace footwear after 6 mo or 300 miles.
Limit training increase to 10% per week (intensity, duration, frequency).
Sport that causes stress fracture of coracoid process
Trapshooting
Sport that causes stress fracture of Scapula
Running with hand weights
Sport that causes stress fracture of humerus
Throwing, racket sports
Sport that causes stress fracture of olecranon
Throwing, pitching
Sport that causes stress fracture of ulna
Racket sports, gymnastics, volleyball, swimming, wheelchair sports
Sport that causes stress fracture of Pars interarticularis
Gymnastics, ballet, cricket fast bowling, volleyball, spring board diving
Sport that causes stress fracture of Pubic ramus, femur
Distance running, ballet
Sport that causes stress fracture of Tibia
Running
Sport that causes stress fracture of fibula
Running, ballet, aerobics
Sport that causes stress fracture of Medial malleolus
Running, basketball
Sport that causes stress fracture of talus
Pole vaulting
Sport that causes stress fracture of navicular
Sprinting, mid distance running, handling, long jump, triple jump, football
Sport that causes stress fracture of base of second metatarsal
Ballet
Sport that causes stress fracture of 5th metatarsal
Tennis, ballet
Sport that causes stress fracture of Sesamoid bone
Running, ballet, basketball, skating
Management of femoral neck stress fracture
Bed rest for one week then gradual weight-bearing if non-displaced, if displaced needs surgical fixation
Management of anterior tibia fracture
Non-weightbearing on crutches for six weeks or screw fixation
Management of medial malleolus stress fracture
Non-wt bearing cast immobilisation for six weeks or surgical fixation
Management of talus stress fracture
Non-wt bearing cast immobilisation for six weeks or surgical fixation
Management of navicular stress fracture
Non-weight bearing cast immobilisation for six weeks or surgical fixation
Management of base of 5th metatarsal stress fracture
Cast immobilisation
Management of base of 2nd metatarsal stress fracture
Non-wt bearing x2 wks then partial wt bearing x2 wks
Management of sesamoid stress fracture
Non wt bearing x4 wks
What is myositis ossificans?
A localized heterotopic ossification that develops in muscle from physical trauma
Anterior muscle groups of the thigh and arm are most frequently affected but may occur at any site
Osteoblasts proliferate inappropriately in a healing muscle hematoma and lay down bone over a period of weeks to months.
Bone maturation usually takes 6 to 12 mo to complete.
Once ossification takes place, little can be done to accelerate the resorptive process, which may take months to years.
Average duration of symptoms related to myositis ossificans (MO) is 1.1 yr.
RF for myositis ossificans
Contact sports
Application of heat or massage to injury site
Premature return to activity
Reduced range of motion of injured muscle
Previous muscle injury
Delay in treatment >3 days
Adjacent joint effusion
Sx of myositis ossificans
Pain, stiffness, weakness, decreased muscle mass
Night pain
Signs of MO present 2-3wks post injury - presents as unresponsive to treatment
Physical for myositis ossificans
Initially, may palpate a doughy mass at 1 to 2 wk that gradually becomes indurated
Persistent tenderness to palpation with local edema that fails to resolve
Reduced range of motion that worsens 2 to 3 wk after injury
Ix for myositis ossificans
US detects calcifications within 2 wks of injury
XR detects calcifications within 3-4 wks of injury
Bone scan will show if it is fully developed
DDx for myositis ossificans
Muscle contusion
Muscle or tendon tear
Fracture
Malignant neoplasm: osteosarcoma, lymphoma, or rhabdomyosarcoma
Compartment syndrome
Abscess
Rhabdomyolysis
Management of myositis ossificans
Self limiting
RICE
Non painful passive stretching + strengthening
Shock wave therapy
RTP usually 3-6mo
Sx can persist for >1yr
Prevention of myositis ossificans when contusion occurs
Immobilize muscle in slight tension (i.e. slightly flexed knee for quad injury) for 24 hrs
Rest, ice, compression, elevation
Avoid soft tissue therapy in firt 24hrs
NSAIDs
What primary cancers metastasize to bone?
Lung, breast, prostate ϲaոϲеr, and multiple myеlοma
What imaging to use for ?lytic lesion?
Bone scan
In multiple myeloma, whole body MRI often used
Types of Benign bone tumors
Osteoid Osteoma
Osteoblastoma
Enchondroma
Chondroblastoma
Giant Cell Tumor of Bone
Osteochondroma
Fibrous Dysplasia
Aneurysmal Bone Cyst
Types of malignant bone tumors
Osteosarcoma
Chondrosarcoma
Ewing Sarcoma
Malignant Fibrous Histiocytoma of Bone
Fibrosarcoma of Bone
Multiple Myeloma
Lymphoma of Bone
Metastatic Bone Disease
Types of benign soft tissue tumors
Lipomas
Hemangiomas
Schwannomas and Neurofibromas
Fibromas
Leiomyomas
Myxomas
types of malignant soft tissue tumor
Desmoid Tumors (Aggressive Fibromatosis)
Giant Cell Tumor of Tendon Sheath
Pigmented Villonodular Synovitis (PVNS)
Liposarcoma
Rhabdomyosarcoma
Leiomyosarcoma
Synovial Sarcoma
Angiosarcoma
Malignant Peripheral Nerve Sheath Tumor (MPNST)
Fibrosarcoma
Epithelioid Sarcoma
Undifferentiated Pleomorphic Sarcoma (UPS)
What is gout?
Inflammatory deposition of monosodium urate crystals
Stages of gout
Acute phase: inflammatory monarthritis; resolves within several days to just over a week
Interval phase: The patient is asymptomatic.
Chronic phase: intermittent repeated flairs of monarticular or polyarticular gout and soft tissue deposition of tophi
Common joints affected by gout
1st metatarsophalangeal (MTP) joint (most common site of initial presentation; also known as podagra), olecranon, ankle, wrist, knee, tarsal joints, and interphalangeal joints of the hand
RF for gout
Male
Dehydration
Pacific islander
Excessive alcohol intake (especially beer and liquor)
Hypertension and cardiovascular disease
Chronic diuretic use (thiazide and loop)
Organ transplant recipients treated with calcineurin inhibitors
Recent surgery
Hyperuricemic state (from either overproduction or underexcretion of uric acid)
Rapid changes in uric acid level
Diets high in purine-containing products
Diets low in dairy or high in meat or fish
Sx + physical for gout + signs of tophi
Severely painful, erythematous, and swollen joint (noninfectious monarthritis)
Pain at its max at 24-48 hrs
Physical
Gout:
Swelling, erythema, warmth, and tenderness of affected joint
80% of flares involve a single joint (1st MTP, knee, ankle, and other joints).
Sometimes overlying skin can be erythematous and desquamated, resembling cellulitis.
Tophi:
Subcutaneous nodules (resembling rheumatoid arthritis) or a bulky mass overlying a joint
± Tenderness or erythema of tophi
Aspirated tophi contents appear as white pasty or chalky material.
Ix for gout
Labs: CBC, CRP, uric acid (can be normal)
Joint aspirate
Gout: needle-shaped, negatively birefringent monosodium urate crystals are seen under polarized light microscopy.
CPPD (pseudogout): rhomboid-shaped crystals with weakly positive birefringence
DDx for gout
Pseudogout
Rheumatoid arthritis
Septic arthritis
Osteoarthritis
Reactive arthritis
Osteomyelitis
Malignancy
Joint trauma
Management of gout
NSAIDs (naproxen 500mg BID or indomethacin 50mg TID) x3-10 days
Oral prednisone 40mg x2-3 days then taper
Intra-articular steroid injections
Colchicine 0.6mg BID
Prevention of gout
Minimize alcohol
Minimize meat + seafood
Increase dairy
Minimize diuretic use
Urate lowering meds
Indications for preventative meds in gout, + when to start
Recurrent or disabling gout attacks (specifically >2 gout attacks per year).
Persistent tophi.
Joint damage noted on imaging.
Uric acid nephropathy or nephrolithiasis
Wait 2-6 wks after acute attack
Allopurinol 100mg, titrate up to target uric acid <6
Febuxostat is alternative for those w/ renal failure
What is pseudogout?
Calcium pyrophosphate deposition disease (CPPD)
RF for pseudogout
Gout (20% may be hyperuricemic)
Hemochromatosis
Hypothyroidism
Trauma
Osteoarthritis
Hyperparathyroidism
Hemosiderosis
Hypophosphatasia
Hypomagnesemia
Aging
Amyloidosis
Sx of pseudogout
Acute joint swelling in one or more joints with previous episodes involving the same joint (characteristic of crystal arthropathies)
The most common joint is the knee, followed by the wrist, shoulder, and hip.
May be severe and associated with malaise and fever
Period of previous episodes (typically several days to weeks)
Patients often are symptom-free between attacks.
Physical for pseudogout
Warmth
Edema/effusion
Tender
Limited range of motion
Ix for pseudogout
Synovial fluid microscopy
weakly positive birefringent rhomboidal-shaped crystals
XRs show calcium deposition
Once dx, check calcium, magnesium, thyroid-stimulating hormone, ferritin, transferrin, iron, phosphorus, and alkaline phosphatase levels
DDx for pseudogout
Gout (can coexist)
Septic arthritis (can coexist)
Rheumatoid arthritis
Osteoarthritis
Trauma (hemarthrosis)
Human leukocyte antigen B27–related peripheral arthritis (psoriatic arthritis, ankylosing spondylitis, reactive arthritis)
Management of pseudogout
Joint aspiration
Intra-articular steroid inj
Joint rest, splinting
NSAIDs
Colchicine 2nd line
Prevention of pseudogout
Colchicine 0.6mg BID for recurrent attacks
Sx + hx qs for rheumatoid arthritis
Polyarthritis most commonly affecting the joints of the wrist, the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of the hands, and the metatarsophalangeal (MTP) joints of the feet
Warmth, swelling, tenderness
Stiffness in AM >1 hr, improves w/ activity
Progression to joint destruction and deformities (ulnar deviation at MCPs, volar subluxation at MCPs and wrists, swan-neck, and/or boutonnière deformities of fingers)
Constitutional symptoms are very common (e.g., low-grade fever, fatigue, myalgia, weight loss)
Extra-articular manifestations: anemia, rheumatoid nodules (20–30%), pleuritis, pericarditis, entrapment neuropathies (carpal tunnel syndrome), episcleritis and scleritis (<1%), splenomegaly, renal disease, interstitial lung fibrosis, pericarditis, interstitial lung disease, vasculitis, Sjögren syndrome, Felty syndrome (rheumatoid arthritis [RA], splenomegaly, neutropenia)
RF for rheumatoid arthritis
Female gender (Pregnancy and oral contraceptive use may be protective.)
Nulliparity
Family history (identical twins 3 to 4 times more likely to share disease than fraternal twins)
Human leukocyte antigen (HLA)-DR4 (also tend to have more severe disease)
Cigarette smoking
Silica or asbestos exposure
Electrical workers
Wood workers
Physical for rheumatoid arthritis
Examine joints thoroughly for synovitis (warmth, swelling, tenderness, erythema).
Look for deformities (swan-neck, boutonnières, ulnar deviation of digits/wrists, volar subluxation at MCP or wrist)
Nail fold infarcts
Splinter hemorrhages
Rheumatoid nodules
Splenomegaly
Pericardial rub
Pleural effusions
Ix for rheumatoid arthritis
Joint fluid exam
10,000 white blood cells (WBCs) with neutrophilic predominance characteristic but nondiagnostic
RF positive in 80%
Anti-CCP
Low Hb, high leuks, high platelets, low albumin, high ALP
XR
Erosions or bony decalcification
CT or MRI
DDx for rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Osteoarthritis (typically involves distal interphalangeals, knees, hips)
Reactive arthritis
Lyme disease
Gout
Pseudogout
Polymyalgia rheumatica
Hypothyroidism
Hypertrophic osteoarthropathy
Colitis
Ankylosing spondylitis
Management of rheumatoid arthritis
Education, relative rest, exercise, PT, OT, CBT
Strength training + aerobic exercise
Fish oil
Limit CV RF
DMARDs
Methotrexate - works within 4 wks
not to take in pregnancy
monitor for hematologic, hepatic, or pulmonary side effects
use folic acid supplementation 1 mg daily with methotrexate
If fails, combine therapy with other DMARDs (methotrexate + sulfasalazine + hydroxychloroquine) or a biologic agent with or without methotrexate
Sulfasalazine
Hydroxychloroquine
Minocycline
Azathioprine
TNFi - etanercept, infliximab
Steroids
Complications of rheumatoid arthritis
Increased risk of CV disease + stroke
Increased risk of infection
Increased risk of lymphoma
What features suggest an inflammatory disorder?
Insidious onset
Prolonged stiffness after rest
Pain worse at night.
Improvement with motor activity
Fever, weight loss.
Raised to CRP
Good response to NSAIDs
Differential diagnosis for atraumatic single swollen joint
Septic arthritis, gout, pseudo gout, Lyme disease, reactive or psoriatic arthritis, osteoarthritis, malignancy (synovial sarcoma), rheumatoid arthritis, sarcoidosis, haemophilia
Differential diagnosis for atraumatic polyarthritis (pain + swelling)
Rheumatoid arthritis, viral arthritis (EBV, parvo virus), psoriatic or reactive arthritis, inflammatory osteoarthritis, SLE, rheumatic fever, haemachromatosis, Sjögren’s syndrome
Differential diagnosis for polyarthralgia (joint pain without swelling)
Drug induced (quinolones, acyclovir, vitamin A, beta blockers, statins)
Viral infection, thyroid disease, parathyroid disease, PMR, inflammatory myositis, leukaemia, depression, somatisation, fibromyalgia
What is the work up for Lyme disease?
Enzyme immunoassay and Western blot.
Hx qs for syncope
Before: events leading up to syncope, prodrome
Lightheadedness, nausea, tunnel vision
During exertion (?cardiac) or after (?non cardiac)
During
LOC time
After
Mental state - groggy (?non cardiac) vs alert (?cardiac)
r/o seizure (tongue biting, jerking, incontinence)
Fam hx
Physical on sideline for syncope
Check BP both arms
Consider rectal temp
Full neuro eval
Glucose
Physical in office for syncope
Orthostatic vitals
Cardiac exam - standing, supine + supine w/ valsalva
Neuro exam
Ix for syncope
ECG
Labs - CBC, TSH, glucose
Echo
Holter
Stress testing
DDx for syncope
Cardiac causes (usually occurs during exertion):
Anomalous coronary artery
Arrythmogenic right ventricular cardiomyopathy (ARVC)
Brugada syndrome
Catecholaminergic polymorphic ventricular tachycardia (CPVT)
Coronary artery disease
HCM
LQTS
Myocarditis
Right ventricular outflow tract ventricular tachycardia
Severe aortic valve stenosis
Non cardiac causes (usually after or not related to exertion)
Drug abuse
Heat stroke
Hypoglycemia
Hyponatremia
Orthostatic hypotension
Seizure
Vasovagal syncope
Prevention of syncope
Education regarding warm up + cool down
Proper nutrition + hydration
Appropriate clothing
What is rhabdomyolysis?
Breakdown + necrosis of skeletal muscle w/ release of CK + myoglobin
Combination of myoglobinuria, hypovolemia, and aciduria may lead to acute renal disease Can be result of trauma/crush injury or as a result of training error where exertion persists beyond the point of fatigue (exertional rhabdomyolysis [ER]), often due to novel activity
RF for rhabdomyolysis
Sudden increase in exercise intensity and repetitive muscular loading
Inadequate conditioning
Poor hydration
Exercise in high heat or humidity
Stimulant and supplement use (phentermine, creatine)
High body mass
High-risk medication or drug use (cocaine, amphetamines, alcohol, nonsteroidal anti-inflammatory drugs [NSAIDs], antihistamines, statins, etc.)
Ongoing infection/exercise while febrile
Sickle cell trait
Heritable muscle enzyme deficiencies
Sx of rhabdomyolysis
Muscle pain, weakness, dark urine
Fever, tachycardia, nausea
Malaise
Physical for rhabdomyolysis
Muscle tenderness, swelling, weakness
Hypovolemic state
Decreased urine output
Ix for rhabdomyolysis (initially + once resolved)
CK 5-10 times upper limit of normal
UA - positive for heme but absent RBCs suggested myoglobinuria
Other labs: CBC, K+, Na+, Ph, uric acid, Ca
Once rhabdo is resolved, to determine if genetically causes, do forearm ischemic test
Obtain baseline ammonia and lactic acid levels.
Inflate sphygmomanometer to >200 mm Hg.
Patient performs hand-grip exercises to fatigue.
Cuff is removed and serial blood tests are drawn.
Minimal or no rise in lactic acid suggests carbohydrate metabolism disorder or McArdle disease.
Delayed rise or no rise in the ammonia level suggests myoadenylate deaminase deficiency.
Normal rise in ammonia and lactic acid levels suggests the presence of a disorder of lipid metabolism.
Muscle biopsy + genetic testing if ?underlying genetic condition
DDx for rhabdomyolysis
Muscle strain
Delayed onset muscle soreness
Muscle infection
Sickle cell crisis
Nontraumatic myopathies
Hypercalcemia/hyperparathyroidism
Hypo/hyperthyroidism
Management of rhabdomyolysis
Aggressive fluid resus w/ isotonic saline
Bicarb administration
Treat underlying cause
Complications (early + late) of rhabdomyolysis
Early complications:
Hyperkalemia
Hypocalcemia
Cardiac arrhythmia
Cardiac arrest
Compartment syndrome
Late complications (past 12 hr):
ARF with oliguria
Hypercalcemia
Disseminated intravascular coagulation
Compartment syndrome
Sx of hypoglycemia + glucose reading
Sweating, HA, tremor, hunger, altered LOC
<3.6
Management of hypoglycemia
glucose gel in buccal mucosa or glucagon 1mg IM
If sx resolve w/ glucagon, give long acting carb and monitor glucose frequently
Prevention of hypoglycemia w/ exercise
Inform diabetic athletes about signs of hypoglycemia
Have 15g of sugar when exercising (1.5 cup fruit juice)
Check blood sugar before + after exercise
Warm up for 15 mins before intense exercise
Consider reducing insulin dose prior to exercise
What is REDS?
Dietary intake is insufficient for energy expenditure (problematic low energy availability)
Hx qs to ask for REDS
Diet
Food restriction
Menstruation
Irregular menses
Delayed onset of menses
Exercise
Excessive exercise beyond recommended amount
Reduced performance
Injuries
Hx of stress #
Exercising while injured
Recurrent injuries
Prolonged recovery
Mental health
Body image
Fear of weight gain
Life stressors
Low mood
Other sx
Persistent fatigue
Cold intolerance
Constipation
Hair loss, dry skin
Physical for REDS
Ht, wt, BMI
Orthostatic vitals
Hair, skin, nails
Thyroid exam
Cardiac exam
Consider pelvic exam if amenorrhea
Ix for REDS
Labs - CBC, lytes, iron, TSH, LH + FSH (low or normal), estrogen (low), prolactin (normal), cortisol (mildly elevated)
PT
DEXA if stress #
DDx for REDS
Pregnancy
Pituitary disease
Hyperthyroidism
Hypogonadism
Hyperparathyroidism
Primary ovarian insufficiency
Polycystic ovarian syndrome
Adrenal dysfunction
Autoimmune disease
Anabolic steroid use/abuse
Excess glucocorticoid administration
Malabsorption syndromes
RF for REDS
Low self esteem
Tendency towards perfectionism
Sports that promote leanness (gymnastics, figure skating, ballet, diving, swimming, XC running)
Veggie
Early sport specific training
Prolonged exercise periods
Dieting
Management of REDS
Education
Increase energy intake
Reduce exercise
Energy rich supplement
Address underlying mental health dx (CBT, antidepressants for comorbid anxiety/ depression)
Calcium 1500mg/ day
Vit D 1000 IU/ day
Activity modification recommendations + home exercises
Rest days
High impact loading + resistance training to support BMD
Referrals
RD
Sports psychologist
S+C
Complications of REDS
Infertility
Decreased BMD
Iron deficiency
Increased risk of illness + injury
Stress #
Depression + anxiety
Decreased strength + endurance
Decreased concentration + coordinati
Prevention of REDS
Education on RED-S, healthy eating
Reduce emphasis on weight
Promote that good performance doesn’t necessarily mean a healthy athlete
Screen for RED-S in PPE
What qs to ask in infertility/ abnormal menses?
Menstrual hx
Cycle length
LMP
Age of menarche
Frequency + duration of menses
Past irregularity
Prev pregnancies
Sexual activity
Contraception
PMH
Training
Overtraining
Diet
Eating disorders
Calcium intake
Injuries
Stress #
Androgen excess, abnormal thyroid, pituitary disorders:
Hair growth, acne
Temp intolerance, palps, bowel changes, tremor, mood changes, skin
HA, galactorrhea
Changes in weight
Psychosocial stressors
Meds + drugs
Physical for infertility/ abnormal menses
BP, HR
Ht, wt, body fat %
Skin + hair
Thyroid exam
Pelvic exam
Ix for infertility/ abnormal menses
bHCG
TSH, T4
FSH, LH
Prolactin, total + free testosterone, estrogen
Pelvic US
Head MRI for ?pituitary tumor
Male factors
DDx for infertility/ abnormal menses
Hypothalamic dysfunction:
Functional hypothalamic amenorrhea:
Energy deficiency–related amenorrhea secondary to excessive exercise, weight loss, disordered eating
Primary gonadotropin-releasing hormone (GnRH) deficiency:
Congenital disorders such as Kallmann syndrome
Secondary/acquired GnRH deficiency:
Traumatic brain injury, brain tumor
Physiologic:
Pregnancy
Hormonal contraception
Menopause
Pituitary dysfunction:
Hyperprolactinemia
Prolactinoma
Cushing syndrome
Empty sella syndrome
Sheehan syndrome
Autoimmune disease
Medications
Anatomic abnormality/outflow tract obstruction:
Congenital: müllerian agenesis, imperforate hymen, transverse vaginal septum, androgen insensitivity
Acquired: Asherman syndrome
Primary ovarian insufficiency:
Congenital: gonadal dysgenesis, Turner syndrome
Acquired: ovarian neoplasm, ovarian destruction secondary to medications, radiation, autoimmune disorder
Other endocrine gland dysfunction:
Thyroid dysfunction
Polycystic ovary syndrome (PCOS)
Adrenal dysfunction
Management of infertility
Chart cycle, intercourse, training
Functional hypothalamic amenorrhea
Reduce training
Increase body wt
Calcium + vit D
What is oligomenorrhea?
Menstrual cycles >35 days, no perceptible s
What is amenorrhea?
No menstrual cycle >3mo
What is primary amenorrhea?
> 15 y/o no periodW
What is PARmed-X?
screening tool to identify high risk pregnancy (prior spontaneous abortion, placenta previa, spotting, incompetent cervix, triplets, medical conditions)
provides prescription exercise program in pregnancy
What advice can you give for exercise during pregnancy?
Avoid exercise lying on back from 16 wks onwards
Avoid exercise in warm or humid conditions
Avoid breath holding exercise
Avoid contact sport or sport w/ high risk of falling
What are Warning signs to stop exercise in pregnancy?
Vaginal bleeding
Dyspnea prior to exertion
Dizziness
Headache
Chest pain
Muscle weakness
Calf pain or swelling
Preterm labor
Decreased fetal movements
Amniotic fluid leakage
What are Absolute CI to exercise in pregnancy?
Incompetent cervix
Intrauterine growth restriction (IUGR)
Multiple gestations (more than triplets)
Persistent 2nd- or 3rd-trimester bleeding
Placenta previa after 25 to 28 wk of gestation
Preeclampsia
Pregnancy-induced hypertension (HTN)
Premature labor during current or prior pregnancy
Premature rupture of membranes
Risk of premature labor
What are common MSK issues in pregnancy?
Carpal tunnel syndrome
De Quervain tenosynovitis
Lower back + pelvic pain
Femoral head osteonecrosis
Usually occurs late in pregnancy or after delivery
Sx: antalgic gait, pain at rest, painful ROM
Rx: restricted wt bearing, avoid surgery til after delivery
Transient osteoporosis
Sx: antalgic gait, pain w/ activity but not at rest, usually 3rd trimester
Rx: protected wt bearing
What are the best forms of exercise during pregnancy?
Swimming
Stationary cycling
Weight training
Walking
Positive effects of exercise during pregnancy
potential risk reduction for development of GDM, pregnancy-induced HTN, and preeclampsia
a decrease in postpartum depression symptoms
decreased incidence of urinary incontinence
Sx of altitude sickness + onset
usually onset within 12-24hrs and self limited
Nausea
Light-headedness
Headache
Insomnia
Anorexia
Malaise
Fatigue
Weakness
Impaired memory
Inability to focus or concentrate
Sx + onset of HAPE
Symptoms of AMS may present initially and then progress 2 to 5 days after ascent to dyspnea on exertion and/or dyspnea at rest:
Persistent cough, progressing to pink, foamy sputum
Chest tightness
Fatigue
Muscle weakness
Sx of HACE
HACE:
Ataxia
Confusion
Headache
Vomiting
Disorientation
Irrational behavior
Auditory or visual hallucination
Lethargy
Altered level of consciousness
Unconsciousness or coma within 24 hr after the onset of ataxia
RF for altitude sickness
Rapid ascent
Sleeping at altitude >2,000 m; exceeding >500 m/day sleeping altitude above 2,500 m
Lack of acclimatization
Young age
Strenuous exertion at high altitude
Previous history and/or individual susceptibility to altitude illness
Obesity
Chronic obstructive pulmonary disease, sickle cell disease, uncompensated congestive heart failure, or pulmonary hypertension
Signs of AMS on exam
usually normal, potentially tachy or bradycardic
Signs of HAPE on exam
Breathlessness at rest
Cyanosis
Crackles in right middle lobe are typical but can be anywhere in the lung field.
Tachycardia
Tachypnea
Low-grade fever
Orthopnea
Signs of HACE on exam
Inability to perform activities such as dressing or eating
Truncal ataxia demonstrated by poor heel-toe walking
Mental status changes
Occasionally focal neurologic deficits
Funduscopic examination can demonstrate papilledema and retinal hemorrhages
DDx of AMS
Dehydration
Exhaustion
Viral syndrome
Gastroenteritis
Hangover
Hypothermia
Carbon monoxide exposure
Hyponatremia
Seizures or focal neurologic deficits are uncommon.
DDx of HAPE
Pneumonia
Asthma
Pulmonary embolism
Congestive heart failure
Myocardial infarction
Fever >101°F, chills, or mucopurulent sputum are typically absent
DDx of HACE
In addition to AMS differential:
Cerebrovascular accident
Alcohol intoxication
Brain tumor
Central nervous system (CNS) infection (e.g., meningitis)
Acute psychosis/delirium
General management of altitude sickness
Descent to a lower altitude is the mainstay of treatment for any HAI.
Low-intensity descent of at least 500 m is recommended.
Avoid further ascent until symptoms resolve.
Supplemental oxygen 2 to 4 L/min if available
Portable hyperbaric if unable to descend
Meds in altitude sickness - prevention + management - doses, and which are banned by WADA
Prevention:
ibuprofen (AMS)
Acetazolamide (diamox) - lowers blood pH, increasing minute ventilation + oxygenation - Banned by WADA
Dexamethasone - banned
Budesonide
Nifedipine - Adversely affects performance but not banned, used to prevent or treat HAPE
Treatment:
ibuprofen, tylenol, ondansetron for sx
Dexamethasone
Prevention of altitude sickness
Graded ascent
If travel to destination >2500m, spend 1 night in intermediate elevation
Do not ascend >500m a day
Rest day every 1000m gained
High carb diet
Adequate hydration
Sleep hygiene at altitude
More arousals, increased periodic breathing
Environment should be quiet + dark, comfortable temp
Avoid caffeine, nicotine, alcohol
Late afternoon/ evening exercise
Light bedtime snack
Aggressively manage jet lag
RF for decompression sickness
Inexperience
Fatigue
Hypovolemia/dehydration
Poor physical conditioning
Obesity
PFO
Atrial septal defect (ASD)
Panic or anxiety while diving
Rapid ascent from depth
Holding breath during ascent
Omitted decompression stops
Flying <24hrs after diving
Inadequate rest between dives
Hx qs for decompression sickness
Get info from dive computer + buddy
Details of dive (depth, time, deco stops)
Sx of arterial gas embolism
LOC, wheezing, blood in ear, decreased reflexes, weakness or paralysis, chest pain, irregular breathing, vomiting, hemoptysis, vision changes, headache, unilateral motor changes, Gate changes, vertigo, confusion
Physical for decompression sickness
General manifestations of gas deposition in the CNS may mimic a transient ischemic attack (TIA), cerebrovascular accident (CVA), or seizure (epilepsy): manifest by confusion, personality changes, altered level of consciousness, delirium, numbness, weakness, aphasia, paresthesias, rapidly ascending paraplegia, or paralysis.
Bubble formation in the inner ear can cause tinnitus (ringing sensation), sensorineural hearing loss, and dysequilibrium, with associated nausea, vomiting, ataxia and nystagmus (the staggers).
Joints may exhibit erythema and edema of periarticular surfaces, vague soreness, muscle weakness or fatigue, and pain with movement.
Gas deposition in soft tissues may manifest as urticaria, mottled skin rash (cutis marmorata), or subcutaneous emphysema.
Management of decompression sickness
100% O2 via non rebreathe mask
Hyperbaric O2 chamber
Echo to check for PFO once well
Causes of tiredness in an athlete
Poor sleep, social factors, over training, and adequate carb intake, timing of carb intake, and adequate protein intake, inadequate hydration
Iron deficiency, viral illness (mono), asthma, sinusitis, depression, anxiety, prescription Med, alcohol alcohol, PCOS, hypo thyroidism, diabetes, chronic fatigue syndrome, coeliac, eating disorders, malignancy, adrenal disease, renal disease, cardiac disease, HIV, hepatitis, malaria, pregnancy, postconcussion, SLE etc
What is functional overreaching?
Increased training leading to a temporary performance reduction, with improved performance after rest. Last days two weeks, causes acute fatigue and then positive adaptation.
What is non-functional overreaching?
Intense training leading to longer performance reduction but with full recovery after rest, accompanied by psychological or neuro endocrinological symptoms, last weeks to months
What is overtraining syndrome?
Intense training over months leading to reduced performance, severe psych, neuro, endocrinological symptoms
Sx + hx qs for overtraining
Decreased performance, fatigue
Training
Current training intensity, frequency
Non training stressors
Finances
Relationships
School
Sleep
Diet
Menses
Physical for overtraining
Vitals
HEENT to r/o infection inc mono
Neck + thyroid exam
Chest auscultation
Abdo exam for splenomegaly
Neurological exam
DDx for overtraining
Major depression or other psychological disorder
Disordered eating pattern
Organic disease (mononucleosis or other infections, hypothyroidism, anemia)
Drug abuse
Nutritional deficiencies
Concussion
Management of overtraining
Team approach
Rest
Sleep
Nutrition
Counselling
Prevention of overtraining
Daily training logs
Proper coaching
Rest days
Maximise sleep
Proper nutrition
Hx qs + sx of exercise induced bronchoconstriction
Wheezing, coughing, SOB, chest tightness
Usually within 15 mins of onset of exertion
Recovery within 90 mins of completion
Personal or fam hx of asthma
RF sports for exercise induced bronchoconstriction
Cold weather sports
Sports w/ long duration of high intensity exercise (running, cycling, soccer, rugby)
Physical for exercise induced bronchoconstriction
Cardiac + resp exam
Ix for exercise induced bronchoconstriction
Gold standard is eucapnic voluntary hyperapnea testing
PFTs w/ salbutamol for reversibility
If neg, do pre + post exercise
Inhaled mannitol testing - fall in FEV1 >15% from baseline is diagnostic
DDx for exercise induced bronchoconstriction
Asthma with exercise exacerbation
Vocal cord dysfunction (VCD)
Exercise-induced hyperventilation
Restrictive lung disease
Cystic fibrosis
Coronary artery disease
Congenital/acquired heart defects
Arrhythmias
Congestive heart failure
Cardiomyopathy
GERD
Anxiety
Management + future prevention of exercise induced bronchoconstriction
Ventolin 2-4 puffs before exercise, repeat during exercise PRN
If no response or needing it daily, add montelukast 10mg PO 2hrs before exercise or ICS
Prevention in future
Warm up
Interval training with rests during to allow a refractory period
Avoid triggers (cold)
Breathe through nose (more humid)
Sx of MI
CP, SOB, pre-syncope
N/V
Ix for MI
Cardiac markers, lytes, coag, CXR, ECG
Management of MI
Support ABCs
Aspirin 325mg
Oxygen if low sats
Nitro SL or spray - unless inferior MI
IV access
Morphine IV if discomfort not relieved by nitro spray
Time from onset <12 hrs - reperfusion (PCI within 90 mins, fibrinolysis within 30 mins)
Time from onset >12 hrs - start nitro or heparin
ECG findings for STEMI + NSTEMI
ST elevation, new LBBB (STEMI)
NSTEMI - ST depression, T wave investion
What is HOCM?
Asymmetric LV hypertrophy
Autosomal dominant
Primary cause of sudden cardiac death in <35 y/o
RF for HOCM
Fam hx of sudden cardiac death
12-30 y/o
Prior hx of syncope
Abnormal BP response to exercise
Acute sx of HOCM
Collapse
Brief sz like activity after collapse
Hx qs to ask in HOCM - in clinic
Unexplained syncope
Exertional chest pain or palps
Dyspnea out of proportion to exertion
Fam hx: sudden cardiac death, hypertrophic cardiomyopathy, Marfans
Physical for HOCM
Usually normal exam
If murmur present, usually midsystolic + heard midleft sternal border
Worrisome if rising from squatting to standing or performing valsalva worsens the murmur
Ix + ECG findings for HOCM
If genotype positive but phenotype neg, should have ECG, echo + exam annually for kids + q5yrs for adults
ECG
LVH findings - markedly increased voltages in precordial leads
Increased voltage
Repolarization abnormalities
Prominent deep Q waves in left precordial leads, ischemic ST changes in 90% of cases
T wave inversion, ST depression in infero-lateral leads, prominent dagger life septal Q waves in lateral leads (V4-6) and inferior leads (II, III, aVF)
Echo - LVH, LV outflow obstruction
Genetic testing
Exercise stress testing for symptomatic pts
DDx of SCD
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Congenital coronary artery anomalies
arrhythmogenic right ventricular cardiomyopathy
myocarditis
Marfans
Congenital aortic stenosis
Mitral valve prolapse
ion channel disorders like long QT, short Qt, Brugada, WPW, catecholaminergic polymorphic ventricular tachycardia
Cocaine, amphetamines
Hypo or hyperkalemia
Hypo or hyperthermia
Trauma (direct blow at critical time in rhythm (during ascending part of T wave) to precordium = commotio cordis) - causes VFib, most common in young boys during sports
Management (acute + longterm) of SCD
Acute
CPR
AED
Rapid cooling (induced hypothermia) after VF arrest
Long term
Implantable defib
Meds - usually BB
Ablation or myomectomy
Disqualified from all competitive sports except low dynamic intensity
Triggers for fatal arrhythmias during exercise
Surges in catecholamine levels
Dehydration
Electrolyte imbalances
Increased platelet aggregation
Evaluation of an athlete w/ condition that cause SCD
History of symptoms, particularly with exertion
Family history of symptoms and sudden death.
Examine
ECG
Echo
What is a Osteoid Osteoma?
A small, benign, painful tumor usually affecting long bones; more common in young adults.
What is a Osteoblastoma?
benign
Similar to osteoid osteoma but larger and less painful; often found in the spine.
What is a Enchondroma?
A benign cartilage tumor that typically occurs in the small bones of hands and feet.
What is a Chondroblastoma?
A rare, benign cartilage tumor usually found in the ends of long bones in adolescents.
What is a Giant Cell Tumor of Bone?
Locally aggressive but benign tumor; often arises near the knee in young adults.
What is a Osteochondroma?
The most common benign bone tumor, often found near growth plates; it may present as a painless bony outgrowth.
What is a Desmoid Tumor?
(Aggressive Fibromatosis): Non-metastatic but can be locally invasive; often involve deep muscles and fascia.
What is a Giant Cell Tumor of Tendon Sheath?
A slow-growing malignant tumor, usually around the fingers or hands, that can recur locally.
What is a Liposarcoma?
A malignant tumor of fat tissue, which can vary in aggressiveness.
What is a Rhabdomyosarcoma?
malignant tumor, Originates in skeletal muscle; common in children and young adults.
What is a Leiomyosarcoma?
Arises from smooth muscle; often affects the uterus, abdomen, or blood vessels. malignant
What is a Angiosarcoma?
A malignant tumor from blood vessels; can occur anywhere, including the skin and soft tissues.
What is a Malignant Peripheral Nerve Sheath Tumor (MPNST)?
Often associated with neurofibromatosis type 1 (NF1); aggressive with potential for recurrence.
What is a Fibrosarcoma?
Originates from fibrous tissue; generally affects deep tissues of limbs or trunk. malignant
What is a Schwannomas and Neurofibromas?
benign Tumors from peripheral nerves; associated with neurofibromatosis.
What is a Fibromas?
benign Connective tissue tumors, including fibromatosis (e.g., palmar fibromatosis or Dupuytren’s contracture).
What is a Leiomyoma?
benign Tumors from smooth muscle; common in uterine tissue but also found in other soft tissues.
What is a Myxoma?
benign Soft tissue tumors with a gelatinous appearance, often arising from connective tissue.
What is a Osteosarcoma?
malignant The most common primary bone cancer; typically occurs in the metaphysis of long bones (e.g., around the knee) in teenagers and young adults.
What is a Chondrosarcoma?
malignant
A cartilage-producing tumor; commonly found in the pelvis, femur, and shoulder, and often affects older adults.
What is a Ewing Sarcoma?
A highly aggressive tumor seen in children and young adults; often arises in the pelvis, femur, or chest wall.
What is Multiple Myeloma?
A cancer of plasma cells that often causes multiple lesions in bones; most common in older adults.
What is a Lymphoma of Bone?
rare malignant tumor
can appear as a primary tumor in the bone or as part of a systemic lymphoma.
