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Internal Medicine EOR > Orthopedics and Rheumatology > Flashcards

Orthopedics and Rheumatology Flashcards

1
Q

What is fibromyalgia?

A

a common condition characterized by widespread pain in joints, muscles, tendons, and other soft tissues

  • the cause of the disorder is unknown, physical or emotional trauma may play a role
  • three months of widespread pain at 11 of 18 tender sites
  • DX is clinical
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2
Q

What is the tx of fibromyalgia?

A

treat with tricyclics (TCAs) - cymbalta, SSRIs, neurontin, and exercise
-pregabalin (lyrica) is the only drug FDA approved to treat fibromyalgia

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3
Q

What is the American College of Rheumatology criteria for the classification of fibromyalgia?

A
  • widespread pain for at least 3 months, defined as the presence of all of the following:
  • pain on the right and left sides of the body
  • pain above and below the waist (including shoulder and buttock pain)
  • pain in the axial skeleton (cervical, thoracic, or lumbar spine; anterior chest)
  • pain on palpation with a 4-kg force in 11 of the following 18 sites (9 bilateral sites, for a total of 18 sites):
  • occiput: at the insertions of one or more of the following muscles: trapezius, sternocleidomastoid, splenius capitis, semispinalis capitis
  • low cervical: at the anterior aspect of the interspaces between the transverse processes of C5 to C7
  • trapezius: at the midpoint of the upper border
  • supraspinatus: above the scapular spine near the medial border
  • second rib: just lateral to the second costochondral junctions
  • lateral epicondyle: 2 cm distal to the lateral epicondyle
  • gluteal: at the upper outer quadrant of the buttocks at the anterior edge of the gluteus maximus muscle
  • greater trochanter: posterior to the greater trochanteric prominence
  • knee: at the medial fat pad proximal to the joint line
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4
Q

What is gout?

A

involves the accumulation of uric acid in the soft tissue of joints and bone

  • altered purine metabolism and sodium urate crystal precipitation into the synovial fluid, M>W (9:1) until menopause (1:1)
  • usually young, >30 yo, asymmetric; great toe; tophi
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5
Q

What are the s/s of gout?

A

MC = podagra (attack of MTP of the great toe) (70% of cases); pain, swelling, redness, exquisite tenderness
-in chronic gout = tophi

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6
Q

How is the dx of gout made?

A

diagnosis is by arthrocentesis - rod-shaped negatively birefringent

  • serum uric acid level > 8 (not diagnostic)
  • imaging: small, punched out lesions on XR = high likelihood diagnosis
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7
Q

What is the tx for gout?

A

lifestyle: elevation, rest, decrease purines (meats, beer, seafood, alcohol) weight loss, increase protein, limit alcohol
- pharm NSAIDs = drug of choice (indomethacin tid); colchicine = effective but bad GI s/e; steroid injections for those who can’t take NSAIDs, oral pred if other meds not tolerated
- thiazide diuretics and aspirin should be avoided
- the management between acute attacks: colchicine, allopurinol
- don’t start someone on allopurinol in an acute attack

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8
Q

What is pseudogout?

A

usually > 60 yo; large joints, lower extremity, no tophi

-similar gout symptoms

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9
Q

How is pseudogout dx?

A

rhomboid-shaped calcium pyrophosphate crystals - positively birefringent
-XR shows fine, linear calcification in cartilage

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10
Q

What is the tx of pseudogout?

A

NSAIDs, colchicine, intra-articular steroid injections

-colchicine = prophylaxis, NSAIDs = acute attack

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11
Q

What is polyarteritis nodosa?

A

a blood vessel disease characterized by inflammation of small and medium-sized arteries (vasculitis), which can restrict blood flow and damage vital organs and tissues

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12
Q

What are the characteristics of polyarteritis nodosa?

A
  • most common in middle-aged men in their 40-50;s
  • associated with Hepatitis B and C - increased microaneurysms with aneurysmal rupture leading to hemorrhage and thrombosis as well as organ ischemia or infarction
  • damage to affected artery = hypertension, aneurysm, thrombosis, necrosis
  • renal: HTN 2/2 increased renin production (may progress to renal failure)
  • constitutional: fevers, myalgias, arthritis
  • CNS: neuropathy, amaurosis fugax, peripheral neuropathy
  • Dermatologic: livedo reticularis, purpura, ulcers, gangrene
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13
Q

How is polyarteritis dx?

A

required confirmation with either a tissue biopsy or angiogram

  • biopsy demonstrates necrotizing arteritis or arteriography showing the typical aneurysms in medium-sized arteries
  • increased ESR, most common in middle age men of 45 years old
  • classic PAN is ANCA negative (P-ANCA positive in <20% cases)
  • renal or mesenteric angiography: microaneurysms with abrupt cut-offs of small arteries)
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14
Q

What is the tx of polyarteritis?

A

steroids (prednisone) +/- cyclophosphamide if refractory

-plasmapheresis in patients with hepatitis B virus

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15
Q

What is polymyalgia rheumatica?

A

is an idiopathic inflammatory condition AFFECTING THE JOINTS causing PAINFUL synovitis, bursitis, and tenosynovitis - aching STIFFNESS of PROXIMAL JOINTS (shoulder, hip, neck) in patients > 50 years old

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16
Q

What are the characteristics of polymyalgia rheumatica?

A

-PMR is closely related to giant cell arteritis (temporal arteritis)
-joint pain versus muscle pain in polymyositis
-STIFFINESS versus the weakness of polymyositis
ESR is markedly elevated (usually > 50)
-temporal arteritis is confirmed by TEMPORAL ARTERY BIOPSY

17
Q

How is polymyalgia rheumatica tx?

A

patient respond quickly to low-dose corticosteroid therapy, which may be required for up to 2 years and slowly tapered
-methotrexate may also be used

18
Q

What is polymyositis?

A

a chronic, idiopathic inflammatory DISEASE OF THE MUSCLE causing symmetrical, proximal, PAINLESS (versus polymyalgia rheumatica) muscle weakness

  • i.e quadriceps femoris
  • different from dermatomyositis which is characterized by inflammatory and degenerative changes in the skin and muscles
  • differentiate from Polymyalgia Rheumatica (PMR) by lack of pain which causes stiff joints usually of the shoulder, hip, and neck
19
Q

How is polymyositis dx?

A

diagnosis of PM/DM involves a physical examination of muscle strength, blood tests for muscle enzymes, electrical tests of muscle and nerves and is confirmed by muscle biopsy

  • increased enzymes: increased aldolase, creatine kinase; increased ESR (+) muscle biopsy, abnormal EMG
  • (+) ANTI-JO 1 Ab: myositis-specific antibody-associated with interstitial lung fibrosis
  • “mechanical hands” hyperkeratotic cracked hands with a dirty appearance
  • (+) Anti-SRP Ab: signal recognition particle Ab
  • (+) Anti-Mi-2 Ab: specific for dermatomyositis
  • muscle biopsy: endomysial involvement with PM
20
Q

What is the tx for polymyositis?

A

corticosteroids and sometimes other immunosuppressants (methotrexate/azathioprine)

21
Q

What is reactive arthritis (Reiter syndrome)?

A

autoimmune response to infection in another part of the body (Chlamydia +/- gonorrhea MC)

  1. asymmetric inflammatory arthritis
  2. conjunctivitis, uveitis, urethritis, and arthritis (can’t see, can’t pee, can’t climb a tree)
    - most commonly seen in Chlamydia (+/- gonorrhea and GI infections such as salmonella, Shigella, Campylobacter, Yersinia)
  3. Diagnosed by a history of infection, clinical exam, positive HLA-B27 (80%)
22
Q

What is the tx for reactive arthritis (Reiter syndrome)?

A

NSAIDs are the mainstay of therapy, antibiotics to treat the infection that triggered the disease (Chlamydia)

23
Q

What is rheumatoid arthritis?

A

MORNING JOINT STIFFNESS > 30 minutes after initiating movement and improves later in the day (vs OA which gets worse throughout the day and if morning stiffness is present will be <30 minutes)

  1. prodrome of constitutional symptoms including fevers, fatigue, weight loss, and anorexia
  2. Small joint stiffness (MCP, wrist, PIP, knee, MTP, shoulder, ankle) worse with rest
  3. symmetric arthritis: swollen, tender, and boggy joint
    a. boutonniere deformity: flexion at PIP, hyperextension of DIP
    b. swan neck deformity: flexion at DIP with joint hyperextension at PIP
    c. ulnar deviation at MCP joint
    d. Rheumatoid nodules
24
Q

What are the diagnostic studies for rheumatoid arthritis?

A
  1. (+) Rheumatoid factor (sensitive but not specific); increased CRP and ESR
  2. (+) anti-citrullinated peptide antibodies (most specific for RA)
25
Q

What is the tx for rheumatoid arthritis?

A

Prompt initiation of DMARDs

  • methotrexate - methotrexate (MTX) is the cornerstone for therapy for RA and is effective as monotherapy for many patients
  • Hydroxychlorquine (Plaquenil) - hydroxychloroquine (HCQ) may be added to a number of traditional DMARDs, including MTX, to improved response, HCQ is less effective as monotherapy
  • Sulfasalazine - sulfasalazine (SSZ) is often used in combination with HCQ and MTX as part of the so-called “triple therapy” regimen, when used in this combination, response rates may rival those seen with biologic DMARDs
  • Leflunomide - LEF is effective as monotherapy for both RA and spondyloarthritis, and therefore may be a good choice when the clinical diagnosis is less clear, diarrhea is a common side effect, however, and may limit its use
  • other - other drugs with a much more limited role, due to the more effective and/or safer agents that are available including azathioprine, gold, and cyclosporine
  • NSAIDs for pain control and low dose corticosteroids
  • Biologic agents - the development of biologic agents represents an advance in the treatment of RA comparable to the introduction of glucocorticoids
  • the cytokines interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha both mediate inflammation and bone resorption in RA
  • agents that inhibit B-cell function, T cell function, and the actions of proinflammatory cytokines (eg, the human recombinant IL-1 receptor antagonist, anakinra, and anti-TNF-alpha agents including entanercept, infliximab, and adalimumab) are all used for the treatment of RA
26
Q

What is sjogren syndrome?

A

a relatively common chronic, autoimmune, systemic, inflammatory disorder of unknown cause attacking the exocrine glands

27
Q

What are the characteristics of Sjogren syndrome?

A

characterized by dryness of the mouth, eyes, and other mucous membranes due to lymphocytic infiltration of the exocrine gland and secondary gland dysfunction

  • salivary glands - xerostomia (dry mouth)
  • lacrimal glands - dry eyes (keratoconjunctivitis sicca)
  • parotid enlargement
28
Q

How is Sjogren syndrome dx?

A

ANA (especially anti-SS-A (RO) and anti-SS-B (La)

  • (+) Rheumatoid factor (RF)
  • (+) schirmer test (<5 mm lacrimation in 5 min)
29
Q

What is the tx for Sjogren syndrome?

A

treat with artificial tears, pilocarpine (cholinergic) for xerostomia

  • pilocarpine: a cholinergic drug that increased lacrimation and salivation (side effects include diaphoresis, flushing, sweating, bradycardia, diarrhea, N/V, incontinence and blurred vision)
  • cevimeline: stimulates muscarinic cholinergic receptors
30
Q

What is systemic lupus erythematosus?

A

triad of join pain + fever + malar (butterfly rash) - fixed erythematous rash on cheeks and bridge of nose sparing nasolabial folds

  • (+) anti-nuclear Ab (ANA): ANA best initial test (not specific)
  • (+) anti-double-stranded DNA and Anti-Smith ab: 100% specific for SLE (not sensitive)
31
Q

How do you dx systemic lupus erythematous?

A

4 or more of the following 11 criteria met

  • malar rash (butterfly rash)
  • discoid rash (chronic, can scar)
  • photosensitivity (other rashes from sun exposure)
  • mucosal involvement (ulcers, mouth, and nose)
  • serositis (pleuritis, pericarditis)
  • joint arthritis (2 or more)
  • renal disorders (abnormal urine protein, diffuse glomerulonephritis)
  • neurologic disorders (anemia, thrombocytopenia, leukopenia)
  • ANA
  • other antibodies: Anti Smith, Anti-dsDNA, Anti-phospholipid (Anticardiolipin, lupus anticoagulant, Anti-B2 glycoprotein)
32
Q

What is the tx for systemic lupus erythematous?

A

manage with sun protection, hydroxychloroquine (for skin lesions), NSAIDs or acetaminophen for arthritis
-pulse dose steroids; cytotoxic drugs (methotrexate, cyclophosphamide)

33
Q

What is systemic sclerosis (scleroderma)?

A

systemic connective tissue disorder causing thickened skin (sclerodctyly), lung, heart, kidney, and GI tract

  • tight, shiny, thickened skin due to fibrous collagen buildup
  • limited cutaneous systemic sclerosis “CREST SYNDROME” - calcinosis cutis, Raynaud’s phenomenon, esophageal motility disorder, sclerodactyly (claw hand), telangiectasis)
  • affects the face, neck as well as distal to the elbow and knees
  • Raynaud’s phenomenon (60-70%) - worsens with smoking, gold, emotional stress, CCBs are the treatment of choice
  • Diffuse cutaneous systemic sclerosis - skin thickening of the trunk and proximal extremities
34
Q

What are the laboratory studies specific to scleroderma?

A
  • (+) ANTI-CENTROMERE AB: associated with limited crest disease and better prognosis
  • (+) ANTI-ACL-70 AB: associated with diffuse disease and multiple organ involvement (+) ANA
35
Q

What is the tx for systemic sclerosis (scleroderma)?

A

acute management with DMARDs and steroids

-treat Raynaud’s with vasodilators (CCBs and prostacyclin)

Internal Medicine EOR (10 decks)

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