11/17 Flashcards
Tumor History
- Soft tissue-
How long has mass been there, is it growing, painful, other masses, any trauma - Bone-
Pain with activity or constant, unproportional pain to injury, growing mass
Bone radiographs for tumors
Need plain X-rays before more specialized imaging
Malignant: cortical destruction/endosteal erosion, surrounding soft tissue mass, periosteal reaction, ill defined borders
Benign has opposite of each, fractures can happen in either situation
Fixed to underlying bone suggests bone tumor rather than soft tissue tumor, painless growing mass suggests soft tissue instead of bone tumor
PET 3 Uses
- Prebiopsy determination of grade correlated with histologic grade
- Evaluation of response to neo-adjuvant chemotherapy highly correlated with histological necrosis
- Screen for local or distant recurrence
Worrisome Features for Malignancy in Bone and Soft Tissue Tumors- H&P Summary
History: enlarging mass
Physical exam: size larger than 5 cm, location deep to fascia, consistency more firm than muscle, fixed to adjacent structures
Radiographic: destructive pattern on X-ray, heterogenous signal on MRI
Exostosis
Displaced nest of physeal cartilage, grows into stalk off side of bone
Painless mass, remove via surgery if cause mechanical pain or growing after puberty
Chondroma or Enchondroma
Benign cartilage nest located inside bone, can fracture due to thinning of cortex
Can see hereditary forms
Commonly seen in fingers/toes
Fibrous cortical defect or Non-ossifying fibroma
Bone tumor in kids, seen in eccentric location in bone
Normally have ossification as age, so observe
Classic Appareance:
Osteoid Osteoma
In the cortex
Pain at night that responds to anti-inflammatories
Resolves over time as the child matures
Has a central nidus, best seen on CT
Treated with radio frequency ablation
3 Common Types of Bone Sarcoma
- Osteosarcoma-
Pain and swelling, in kids, around knee
Aggressive appearance on imaging, treated with surgery and chemotherapy, decent 5 year survival
Bone forming destructive lesion that extends outside cortex
Histology: Pleomorphic Cells, mitotic figures, malignant osteoid
Treated with removal of involved bone and reconstruction
- Chondrosarcoma-
Seen in patients 30-50s, pain and swelling, treated with surgical resection
Stippled calcification that extends outside bone, looks kinda like cloud of gas
Histology: Looks like cartilage but too cellular to be benign, atypical and binucleation are common for chondrocytes
- Ewing Sarcoma-
In kids, pain and swelling, can mimic infection, treated with surgery and chemotherapy
Diaphyseal location and periosteal reaction (onion-skinning)
Small round blue cell tumor, cytogenics shows 11:22 translocation
Surgically remove the affected bone
Metastatic carcinoma sites
Axial more than appendicular, vertebral bodies more than posterior elements
Lumbar then thoracic, cervical, sacrum
Compression fracture of spine is common presentation of metastatic disease
Proximal more than distal
Breast, prostate, thyroid
Goals for Surgical Treatment of metastatic Disease: Stabilize bone Maintain function Improve pain Establish histologic diagnosis
Characteristics of Soft Tissue Malignancies
Tumor greater than 5 cm, tumor deep to fascia, rapid growth, more firm than muscle
Painless
Benign soft tissue masses are the opposite but are also mobile
Monoarticular Arthritis
An acute monoarticular and inflammatory arthritis is infection until proven otherwise, need synovial fluid examination to exclude infection
- Acute-
Bacterial or viral infection, crystal induced arthritis, hemorrhagic effusion - Chronic-
Fungal/mycobacterial/Lyme Infection, osteoarthritis, foreign body synovitis, pigmented villonodular synovitis, malignancy
Distribution of Joint Involvement in Arthritis Types
DIP Joints: osteoarthritis, psoriasis Arthritis
PIP Joints: osteoarthritis, psoriasis Arthritis, RA, JIA
MCP Joints: RA, JIA
CMC Joints: osteoarthritis
Synovial Fluid
Secreted by joint tissues containing synoviocytes and fibroblasts
High levels of hyaluronic acid
Function: lubricates Joints, transports nutritional substances to joints
Characteristics: clear or pale yellow, viscous, doesn’t clot, low volume
When infected: less viscous since hyaluronic acid breaks down, opaque or translucent
Differential for Non-inflammatory Synovial Fluid
WBCs less than 2,000
Osteoarthritis, endocrine disorder, avascular necrosis
Amyloidosis, neuropathic Arthritis (Charcot joint), Metabolic Disorders like alkaptoniria
Differential for Inflammatory Synovial Fluid
WBC between 2-75k
Inflammatory arthritis: rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, reactive arthritis, ankylosing spondylitis
Crystal Induced Arthritis: gout, calcium lyrophosphate deposition disease (CPPD)
Septic joints may appear in this range
Differential for Hemorrhagic Synovial Fluid
Clotting Disorders like hemophilia or anticoagulants
Trauma
Pigmented villonodular synovitis
Auto-antibodies in Arthritis
Rheumatoid Factor: antibody to IgG, common in patients with RA, small percent of JIA, worse prognosis
Anti-cyclic citrullinated peptide antibody: antibody to citrullinated proteins, 80% of RA, worse prognosis
Anti-nuclear antibody: antibody to nuclear contents, in JIA p, increased risk of uveitis, helpful to diagnose other conditions like lupus
Mechanical vs. Inflammatory Arthritis
Mechanical: minimal morning stiffness, symptoms, worse with activity, symptoms improve with rest
Inflammatory: morning stiffness longer than 30 minutes, symptoms worse with inactivity and improve with activity
Osteoarthritis
Structural or functional failure of a joint due to loss of cartilage and other joint tissues which is evident on radiographs and causes discomfort or decreased function
Super common in old people, affects everyone equally
Primary/idiopathic: no predisposing condition, often associated with aging
Secondary: affects young people, trauma, inflammatory arthritis, crystal arthropathy, infection, metabolic disorders
Effects of Aging on Joint Tissue
Oxidative stress and damage
Decreased levels of GFs and the body’s responsiveness
Increased formation of advanced glycation end products
Reduced hydration and increased collagen cleavage
Increased calcification of matrix
OA Clinical
Activity related pain becomes rest pain and then night pain with instability
Symptoms improve with rest and little morning stiffness
One or few joints, asymmetric, pain and/or loss of ROM, crepitus
Bony enlargement of a joint: Bouchard Nodes at PIP, Heberden Nodes at DIP
Common locations: CMC, PIP, DIP, hip, knee, foot, cervical/lumbar spine
Non pharmacological OA Management
Weight loss, lifestyle modification, PT, OT
Use cane/splint/brace, Tai chi, other physical exercise
Osteoarthritis Therapies
- Capsaicin- topical
Induces release and depletes neuron stores of substance P (pain signaling molecule)
Irritant to eye, can causes pain
- NSAID- oral or topical
Inhibits prostaglandin synthesis
Gastritis, Hypertension, potential MI, renal insufficiency
- Acetaminophen- oral
Impacts prostaglandin synthesis and blocks pain impulse generation
Liver toxicity
- Tramadol- oral
Opioid agonist
Constipation, sedation
- Glucocorticoids- Intraarticular
Multiple immunosuppressive effects
Injection risks: pain, infection, injury to nerve or ligament
- Hyaluronic Acid- Intraarticular
Provides additional volume, viscosity and cushion to joint space
Injection risks
Uric Acid Elimination
Under excretion of uric acid most common cause of hyperuricemia
No uricase in human tissue so can’t degrade but can excrete
- GI tract-
Enters intestine passively, 1/3 irate elimination, intestinal bacteria can degrade - Kidney-
Secrete only small amount that passes through kidneys, 2/3 of irate elimination, URAT 1 and Glut9 are irate transporters in tubule
Causes- renal insufficiency, diuretics, low dose aspirin, hypertension, ketoacidosis, cyclosporine
Estrogen is uricosuric so premenopausal women less likely to get gout
Uric Acid Overproduction
Congenital Enzyme abnormalities like Lesch-Nyah Syndrome (HGPRT deficiency) and PRPP Synthetase overactivity
Lymphoproliferative diseases
Hemolysis
Psoriasis
Glycogen storage Disease
Ethanol, hypoxia
Gout Stages
- Classical Acute Gout-
Acute onset with one or a few joints, podagra or great metatarsalphalangeal joint is common, will resolve without treatment
Triggers: surgery, alcohol, increased dietary purines, fluctuations in uric acid levels
- Intercritical Gout-
Symptom free period between episodes of acute gout (can be months or years), if untreated then acute gouty arthritis becomes worse - Chronic Tophaceous Gout-
Tophi are deposits of irate crystals in tissue
Common tophi sites: synovium, subchondral bone, olecranon bursae, infrapatellar tendon, Achilles’ tendon, ear pinnae
Frequent acute gouty arthritis, bone destruction and degenerative arthritis, polyarthropathy
Acute Gout Treatment
NDAIDS, Colchicine, intraarticular steroids, systemic steroids, analgesia
Acute gout will go away without treatment
Bad Foods: alcohol, shellfish, organ meats, purine rich foods, fructose
Good foods: fruits like cherries, dairy
Allopurinol can change gout levels and cause transient flare
Chronic Gout Treatment
Want uric acid levels below 6 mg/dL
Reduce uric acid production: allopurinol, febuxostat
Increased renal uric acid excretion: Probenicid (Losartan)
Breakdown uric acid: pegylated uricase
Gout Meds
NSAIDS, steroids
Colchicine: inhibit microtubule
Probenecid: uricosuric
Allopurinol: inhibit xanthine oxidase
Febuxostat: inhibit xanthine oxidase
Pegylated uricase: breaks down uric acid
CPPD
Influenced by ambient calcium, magnesium, pH, matrix composition
Autosomal Dominant CPPD: mutations in ANKH gene that encodes a PP transporter
Most common joints: knee, shoulder, wrist, pubic symphysis
Conditions associated with CPPD-
Hyperparathyroidism, hypothyroidism, chronic renal insufficiency, too little magnesium and phosphate, too much iron, lymphoproliferative disorders
CPPD Clinical
Crystals appear as rhomboids and are positively birefringent
(Gout is needle shaped and negatively birefringent)
Treatment-
Reduce inflammation, no preventative treatment
For acute: reduce symptoms, treat any associated triggering illnesses
NSAIDs, colchicine (not as effective as with gout), steroids, analgesics, sometimes methotrexate or hydroxychloroquine
Radiology: thin white line in gray cartilage of joint
Arthritis Epidemiology
- RA-
1% of people, mainly white people, 3x more common in women
Risk factors: smoking, HLA-DR4 epitope, silica exposure
- JIA-
More rare than RA
JIA Subtypes
More heterogenous than RA, Associated with uveitis unlike RA
Oligoarticular, polyarticular, psoriatic arthritis, enthesitis related arthritis
Uveitis for oligoarthritis JIA
RA and JIA Pathogenesis
Abnormal Inflammation: TNF and IL-6 upregulated, B and T cells dysregulated
Angiogenesis in the synovium, synovial pannus so abnormal extra layer of synovial
Activated fibroblasts to contribute to proliferation of the synovium, activated osteoclasts erode away bone, proteases damage and deplete cartilage
Felty’s Syndrome
Complication of RA in which patients develop splenomegaly and granulocytopenia
Complications Unique to JIA
- Uveitis-
Risk factors: female, younger, antinuclear antibodies positive
Can cause cataracts, glaucoma, visual impairment
Need ophthalmology screening every 3-12 months
- Limb Length disparity-
Leg with arthritis often longer due to inflammation mediated hyperemia of the growth plate
Micrognathia from involvement of the temporomandibular joints so undersized jaw
Clinical Features of JIA and RA
JIA-
Systemic Onset: Daily fever with high temps in morning, evanescent rash that comes and goes with fever, enlarged spleen or liver, serous membrane inflammation like pericardial effusion
Lab studies of onset: Leukocytosis, elevated EST and CRP, high ferritin, usually don’t have the specific antibodies
Physical Exam for Arthritis
Patient with RA or polyarticular JIA will have symmetric arthritis
Oligoarticular JIA will have asymmetric pattern
Look for swelling, loss of ROM, rheumatoid nodules
Radiology for RA and JIA
Periarticular Arthritis
Erosions: loss of cortex of bone, common in MCP, PIP, MTP, and ulnar styloids
Joint space narrowing
Subluxation of joint: cervical instability with problems with atlas and dens
MRI and ultrasound may be better bu5 start with X-ray
Can easily see ulnar deviation of fingers
Treatments for JIA and RA
NSAIDs and glucocorticoids
Disease modifying anti-rheumatic drugs (DMARDs)-
Hydroxychloroquine: inhibits TLR 7 and 9 signaling
Sulfasalazine: unknown mechanism
Methotrexate: inhibits dihydrofolate reductase
Leflunomide: inhibits dihydroorotate dehydrogenase
Biologics- Anti TNF agents
Rituximab (antibody against CD20), not JIA
Anakinra (IL-1 receptor antagonist), not for JIA
Abatacept (T cell costimulatory inhibitor, CD80)
Tocilizumab (IL-6 receptor antagonist)
Etanercept and adalimumab only for polyarticular JIA
Fibromyalgia
Chronic condition with unknown etiology with widespread musculoskeletal pain unexplained
Presents with sleep problems, cognitive dysfunction, and fatigue
Etiology: women more than men, every race equally likely
Less likely in kids but usually present when 11-15 and in white people
Pain Medhanisms
Pressure, heat, or chemical like bradykinin activate nociceptive receptors, A fibers (thick myelinated, fast) and C fibers (unmyelinated, slow) send signal to dorsal horn of spinal cord, goes to thalamus/brainstem to frontal lobe, limbic system, insula, and somatosensory cortex
Chronic Pain Mechanisms-
1. Peripheral (nociceptive): inflammation or mechanical pain, RA
Treat: NSAIDs, steroids, opioids
Behavioral factors minor
- Neuropathic: peripheral nerve damage or entrapment, carpal/tarsal tunnel
Treat: peripheral (NSAIDs, opioid) and central (tricyclics antidepressants, neuroactive drugs) therapies
- Central (non-nociceptive): central disturbance in pain processing, fibromyalgia, IBS
Treat: tricyclics and neuroactive drugs
Behavioral factors more prominent
Fibromyalgia Pain Processing
Have higher levels of chemicals in CSF that increase pain and lower levels of those that decrease pain (except opioid)
Detect pain at lower threshold, unregulated opioid receptors, increased activity in CNS pain sensing areas
fMRI: have different areas of brain activated by pain stimulus compared to normal controls
Orthostatic hypotension, higher HR and variability in HR
Chronic pain, widespread to both sides of body
Gets worse from exercise, weather, stress/anxiety
Fibromyalgia Clinical
Physical Exam-
Normal but hyperalgesia, diffuse tender points, and allodynia (pain for normally not painful stuff)
Tender points: scoring system with 11, need less for kids
Occipital, trapezius, gluteal, greater trochanter, knee, second rib, supraspinatus, lateral epicondyle of humerus
Differential diagnosis: need to exclude autoimmune, endocrine, hematologist disorders, and much more
No lab test is diagnostic but excludes other disorders
Symptoms: headaches, brain fog, TMJ disorders, IBS, constitutional problems, loss of balance, non cardiac chest pain, nondermal parathesis
Fibromyalgia Treatment
- Education-
Info about the disease, provide resources, try to include family, discuss expectations - Nonpharmacological-
Sleep hygiene, exercise, cognitive behavioral therapy
Multidisciplinary team often needed
- Pharmacological- one reduces symptoms by 30% so need combos and with nonpharmacological
Tricyclics antidepressants: amitriptyline, nortriotyline Muscle relaxant: cyclobenzaprine SRIs: duloxetine, milnacipran GABA agonists: gabapentin, pregabalin Other analgesics: Tylenol, NSAIDs
Avoid narcotics
Rotator Cuff Tears
Degenerative in nature, cause pain that is worse with overhead activities, night pain
Supraspinatus tendon most commonly injured, Problem lifting arm
Tendons insert in greater tubercle of humerus and provide stability to it
Often have PROM but lack AROM, weak forward elevation and lateral rotation
X-rays are ok but MRI the gold standard
PT for impingement and degenerative tears, only surgery if fail
Acute tears from trauma need immediate surgery or irreparable
Biceps Tear
Long head rupture is often degenerative, issues if problems with RTC
Distal biceps rupture during eccentric contraction while lifting, traumatic, rare in women
LHB rupture will have muscle sit inferiorly like Popeye
Long head rupture doesn’t affect strength, distal rupture will have supination weakness
Treatment-
LHB: conservative, rest, no surgery
Distal: surgery if want to be active, less active don’t have surgery and accept weakness
Distal needs surgery soon or have permanent supination loss, both always keep their Popeye appearance
Per Major Tear
Often guys have eccentric overload injury while benching, eternal head tears from lateral aspect of bicipital groove
Feel pop, see bruising and deformity as it retracts from humerus to ball up in chest
ROM intact, internal strength may be limited
Get surgery urgently, permanent deformity and loss of ROM/strength if missed/wait too long for surgery
AC Joint Injuries
Direct blow like in sports or bikers
Prominent distal clavicle if torn, clavicle will be elevated if coracoclavicular ligaments are torn should have normal ROM and strength but pain
Treatment is conservative with rest, only surgery if patient still has pain with conservative care
Cosmetic ramification
Shoulder Instability
Anterior dislocation: contact sports or traumatic fall, most common, when abducted and externally rotated
Posterior dislocation: less common, electrocution, seizures, MVA
Loss of AROM/PROM due to mechanical block of HH until reduce
Check NV status, esp. axillary nerve
Get 3 X-ray views including axillary so don’t miss posterior dislocation
Bankart Lesion: Tear of the anterior/inferior labrum during anterior dislocation, very common
Patients 40+ prone to sustaining RTC tear (esp. subscapularis)
Young people have bankart tear, old people have RTC tear if additional trauma
Treatment-
Immediate: NV exam and X-rays, reduce, redo NV exam, place in sling and rehab when comfortable
Need axillary X-ray
- Under 20 yo have high rate of recurrent dislocations
- Over 40 yo have low recurrent dislocations but additional tears, fix RTC urgently if torn but not as likely as subscapularis, do rehab
Shoulder Instability
Standard liftoff: move hand from b hind back, subscapularis
Belly press: hands on belly and make elbows out, subscapularis
Anterior apprehension: make shoulder abducted and externally rotated, anterior Instability if fear HH pop out
Relocation test: do anterior apprehension Test, shoulder feel better if push HH back into the joint
Glenohumeral DJD
Can get arthritis years after fracture or dislocation, less common than hip/knee arthritis
ROM is fine but may be slightly limited due to pain but RTC work
May do shoulder replacement if really bad
Lateral Epicondylitis
Tennis elbow
Tendinosis of the extensor Carpi Radialis brevis at its origin, no inflammatory cells, angiofibroblastic dysplasia
Arm pain worse with repetitive activity, mainly older people, men and women equally likely
Treatment: conservative, PT, corticosteroid, counterforce brace, surgery for debridement of pathologic tissue if symptomatic for a year
Medial epicondylitis
Golfer’s elbow
Tendinosis of the pronator teres and flexor Carpi radialis
Pain worsened by activity esp. wrist flexion/pronation
Treatment the same as lateral epicondylitis
Compression Neuropathy
Pathophysiology- Ischemia or impaired venous return Intraneural edema Decreased axoplasmic transport Membrane instability Fibrosis
Risk factors: female, endocrine problems, rheumatoid arthritis, gout, old, fat, alcoholic, occupational
Carpal Tunnel
Numbness/tingling with activity and at night, hand/wrist/forearm pain, weakness, drop things
Pain when hand is flexed
Thenar muscle wasting
Sensory testing: monofilament and vibration
Diagnostic: nerve conduction study (motor/sensory latency) and EMG
Carpal Tunnel Tests
Median Nerve Compression Test: putting pressure on the median nerve will reproduce symptoms
Tinel’s Test: tapping on the median nerve will reproduce symptoms
Phalen’s Test: maximal flexion of the wrist will place pressure on the median nerve and reproduce symptoms
