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11/17 Flashcards

1
Q

Tumor History

A
  1. Soft tissue-
    How long has mass been there, is it growing, painful, other masses, any trauma
  2. Bone-
    Pain with activity or constant, unproportional pain to injury, growing mass
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2
Q

Bone radiographs for tumors

A

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

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3
Q

PET 3 Uses

A
  1. Prebiopsy determination of grade correlated with histologic grade
  2. Evaluation of response to neo-adjuvant chemotherapy highly correlated with histological necrosis
  3. Screen for local or distant recurrence
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4
Q

Worrisome Features for Malignancy in Bone and Soft Tissue Tumors- H&P Summary

A

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

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5
Q

Exostosis

A

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

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6
Q

Chondroma or Enchondroma

A

Benign cartilage nest located inside bone, can fracture due to thinning of cortex

Can see hereditary forms

Commonly seen in fingers/toes

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7
Q

Fibrous cortical defect or Non-ossifying fibroma

A

Bone tumor in kids, seen in eccentric location in bone

Normally have ossification as age, so observe

Classic Appareance:

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8
Q

Osteoid Osteoma

A

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

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9
Q

3 Common Types of Bone Sarcoma

A
  1. 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

  1. 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

  1. 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

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10
Q

Metastatic carcinoma sites

A

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
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11
Q

Characteristics of Soft Tissue Malignancies

A

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

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12
Q

Monoarticular Arthritis

A

An acute monoarticular and inflammatory arthritis is infection until proven otherwise, need synovial fluid examination to exclude infection

  1. Acute-
    Bacterial or viral infection, crystal induced arthritis, hemorrhagic effusion
  2. Chronic-
    Fungal/mycobacterial/Lyme Infection, osteoarthritis, foreign body synovitis, pigmented villonodular synovitis, malignancy
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13
Q

Distribution of Joint Involvement in Arthritis Types

A

DIP Joints: osteoarthritis, psoriasis Arthritis

PIP Joints: osteoarthritis, psoriasis Arthritis, RA, JIA

MCP Joints: RA, JIA

CMC Joints: osteoarthritis

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14
Q

Synovial Fluid

A

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

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15
Q

Differential for Non-inflammatory Synovial Fluid

A

WBCs less than 2,000

Osteoarthritis, endocrine disorder, avascular necrosis

Amyloidosis, neuropathic Arthritis (Charcot joint), Metabolic Disorders like alkaptoniria

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16
Q

Differential for Inflammatory Synovial Fluid

A

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

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17
Q

Differential for Hemorrhagic Synovial Fluid

A

Clotting Disorders like hemophilia or anticoagulants

Trauma

Pigmented villonodular synovitis

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18
Q

Auto-antibodies in Arthritis

A

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

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19
Q

Mechanical vs. Inflammatory Arthritis

A

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

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20
Q

Osteoarthritis

A

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

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21
Q

Effects of Aging on Joint Tissue

A

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

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22
Q

OA Clinical

A

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

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23
Q

Non pharmacological OA Management

A

Weight loss, lifestyle modification, PT, OT

Use cane/splint/brace, Tai chi, other physical exercise

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24
Q

Osteoarthritis Therapies

A
  1. Capsaicin- topical
    Induces release and depletes neuron stores of substance P (pain signaling molecule)

Irritant to eye, can causes pain

  1. NSAID- oral or topical
    Inhibits prostaglandin synthesis

Gastritis, Hypertension, potential MI, renal insufficiency

  1. Acetaminophen- oral
    Impacts prostaglandin synthesis and blocks pain impulse generation

Liver toxicity

  1. Tramadol- oral
    Opioid agonist

Constipation, sedation

  1. Glucocorticoids- Intraarticular
    Multiple immunosuppressive effects

Injection risks: pain, infection, injury to nerve or ligament

  1. Hyaluronic Acid- Intraarticular
    Provides additional volume, viscosity and cushion to joint space
    Injection risks
25
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 1. GI tract- Enters intestine passively, 1/3 irate elimination, intestinal bacteria can degrade 2. 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
26
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
27
Gout Stages
1. 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 2. Intercritical Gout- Symptom free period between episodes of acute gout (can be months or years), if untreated then acute gouty arthritis becomes worse 3. 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
28
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
29
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
30
Gout Meds
NSAIDS, steroids Colchicine: inhibit microtubule Probenecid: uricosuric Allopurinol: inhibit xanthine oxidase Febuxostat: inhibit xanthine oxidase Pegylated uricase: breaks down uric acid
31
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
32
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
33
Arthritis Epidemiology
1. RA- 1% of people, mainly white people, 3x more common in women Risk factors: smoking, HLA-DR4 epitope, silica exposure 2. JIA- More rare than RA
34
JIA Subtypes
More heterogenous than RA, Associated with uveitis unlike RA Oligoarticular, polyarticular, psoriatic arthritis, enthesitis related arthritis Uveitis for oligoarthritis JIA
35
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
36
Felty’s Syndrome
Complication of RA in which patients develop splenomegaly and granulocytopenia
37
Complications Unique to JIA
1. Uveitis- Risk factors: female, younger, antinuclear antibodies positive Can cause cataracts, glaucoma, visual impairment Need ophthalmology screening every 3-12 months 2. 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
38
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
39
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
40
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
41
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
42
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
43
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 2. Neuropathic: peripheral nerve damage or entrapment, carpal/tarsal tunnel Treat: peripheral (NSAIDs, opioid) and central (tricyclics antidepressants, neuroactive drugs) therapies 3. Central (non-nociceptive): central disturbance in pain processing, fibromyalgia, IBS Treat: tricyclics and neuroactive drugs Behavioral factors more prominent
44
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
45
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
46
Fibromyalgia Treatment
1. Education- Info about the disease, provide resources, try to include family, discuss expectations 2. Nonpharmacological- Sleep hygiene, exercise, cognitive behavioral therapy Multidisciplinary team often needed 3. 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
47
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
48
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
49
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
50
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
51
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 1. Under 20 yo have high rate of recurrent dislocations 2. Over 40 yo have low recurrent dislocations but additional tears, fix RTC urgently if torn but not as likely as subscapularis, do rehab
52
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
53
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
54
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
55
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
56
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
57
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
58
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

MSK (17 decks)

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