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MSK > 11/17 > Flashcards

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
Q

Uric Acid Elimination

A

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
Q

Uric Acid Overproduction

A

Congenital Enzyme abnormalities like Lesch-Nyah Syndrome (HGPRT deficiency) and PRPP Synthetase overactivity

Lymphoproliferative diseases

Hemolysis

Psoriasis

Glycogen storage Disease

Ethanol, hypoxia

27
Q

Gout Stages

A
  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

  1. Intercritical Gout-
    Symptom free period between episodes of acute gout (can be months or years), if untreated then acute gouty arthritis becomes worse
  2. 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
Q

Acute Gout Treatment

A

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
Q

Chronic Gout Treatment

A

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
Q

Gout Meds

A

NSAIDS, steroids

Colchicine: inhibit microtubule

Probenecid: uricosuric

Allopurinol: inhibit xanthine oxidase

Febuxostat: inhibit xanthine oxidase

Pegylated uricase: breaks down uric acid

31
Q

CPPD

A

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
Q

CPPD Clinical

A

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
Q

Arthritis Epidemiology

A
  1. RA-
    1% of people, mainly white people, 3x more common in women

Risk factors: smoking, HLA-DR4 epitope, silica exposure

  1. JIA-
    More rare than RA
34
Q

JIA Subtypes

A

More heterogenous than RA, Associated with uveitis unlike RA

Oligoarticular, polyarticular, psoriatic arthritis, enthesitis related arthritis

Uveitis for oligoarthritis JIA

35
Q

RA and JIA Pathogenesis

A

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
Q

Felty’s Syndrome

A

Complication of RA in which patients develop splenomegaly and granulocytopenia

37
Q

Complications Unique to JIA

A
  1. Uveitis-
    Risk factors: female, younger, antinuclear antibodies positive

Can cause cataracts, glaucoma, visual impairment

Need ophthalmology screening every 3-12 months

  1. 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
Q

Clinical Features of JIA and RA

A

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
Q

Physical Exam for Arthritis

A

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
Q

Radiology for RA and JIA

A

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
Q

Treatments for JIA and RA

A

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
Q

Fibromyalgia

A

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
Q

Pain Medhanisms

A

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

  1. Neuropathic: peripheral nerve damage or entrapment, carpal/tarsal tunnel

Treat: peripheral (NSAIDs, opioid) and central (tricyclics antidepressants, neuroactive drugs) therapies

  1. Central (non-nociceptive): central disturbance in pain processing, fibromyalgia, IBS

Treat: tricyclics and neuroactive drugs
Behavioral factors more prominent

44
Q

Fibromyalgia Pain Processing

A

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
Q

Fibromyalgia Clinical

A

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
Q

Fibromyalgia Treatment

A
  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

  1. 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
Q

Rotator Cuff Tears

A

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
Q

Biceps Tear

A

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
Q

Per Major Tear

A

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
Q

AC Joint Injuries

A

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
Q

Shoulder Instability

A

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
Q

Shoulder Instability

A

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
Q

Glenohumeral DJD

A

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
Q

Lateral Epicondylitis

A

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
Q

Medial epicondylitis

A

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
Q

Compression Neuropathy

A 
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
Q

Carpal Tunnel

A

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
Q

Carpal Tunnel Tests

A

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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