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IM EOR > Ortho/Rheum -- 12% of EOR > Flashcards

Ortho/Rheum -- 12% of EOR Flashcards

1
Q

How is fibromyalgia diagnosed?

A

Clinical diagnosis

  • Labs will be normal
  • Chronic pain 3+ months
  • Tenderness in 11+ of 18 trigger points (must be bilateral, above and below waist)
  • Sleep studies will show no REM cycle
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2
Q

How is fibromyalgia treated?

A

Conservative measures:

  • Patient education
  • Sleep hygiene
  • Low impact aerobic exercise

Medical treatment:

  • TCAs (amitryptilline) = 1st line
  • SSNRI (duloxetine)
  • Pregabalin, esp useful for sleep symptoms
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3
Q

How do the presentations (not diagnostic findings) of gout and pseudogout differ?

A
  • Pseudogout usually in patients 60+ YO
  • Gout is usually found in a younger population than pseudogout
  • Pseudogout more likely to be found incidentally (asymptomatic) than gout – but clinically indistinguishable when symptomatic
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4
Q

Describe the color, polarity, and morphology of the findings on arthrocentesis in gout

A
  • Yellow (when parallel to polarizer)
  • Negatively bifrigent
  • Needle-shaped
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5
Q

Describe the color, polarity, and morphology of the findings on arthrocentesis in pseudogout

A
  • Blue (when parallel to polarizer)
  • Positively bifrigent
  • Rhomboid-shaped
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6
Q

What are the crystal compositions in gout and in pseudogout?

A

Gout: monosodium urate
Pseudogout: Ca pyrophosphae dehydrate

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7
Q

Punched out lesions and tophi are XR findings in what rheumatological condition?

A

Punched-out “rat-bite” lesions and tophi are associated with gout

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8
Q

What XR findings might be found in pseudogout?

A

Fine, linear calcifications of the cartilage

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9
Q

What kind of anti-hypertensive medication must be avoided in patients with gout?

A

Thiazide diuretics

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10
Q

What is the treatment for an acute gout attack?

A
  • NSAIDs – indomethacin TID is first line
  • Steroids if refractory or if renal dz precludes NSAID use
  • Colchicine can be used but has bad GI AEs
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11
Q

What is the treatment for chronic gout prophylaxis?

A
  • LSMs
  • Allopurinol – do NOT start during acute attack
  • Colchicine
  • Uricosuric drugs - probenecid, suulfinpyrazone – these are CIx w/renal dz
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12
Q

What is the very general pathophys of gout?

A

Uric acid accumulation and deposition in synovial fluid, 2/2 to:

    • Underexcretion from kidneys (renal dz, thiazides, ASA)
    • Overproduction due to increased cell turnover (chemo, cancer, hemolysis)
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13
Q

What is the tx for pseudogout?

A
  • Colchicine
  • NSAIDs are 1st line if 2+ joints involved
  • Steroids:
      • intraarticular if 1-2 joints
      • PO if 3+ joints
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14
Q

What is used for prophylaxis of pseudogout, when is it initiated, and what is the MOA?

A

Colchicine used for prophylaxis in pts with 3+ attacks per year

Colchicine inhibits microtubule assembly

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15
Q

What are some AEs associated with cochicine use?

A

Diarrhea and bone marrow suppression –> neutropenia

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16
Q

What drugs can cause/exacerbate gout?

A
  • ACEi’s
  • ARBs except losartan
  • ASA
  • Thiazide diuretics
  • Loop diuretics
  • Pyrazinamide
  • Ethambutol
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17
Q

What body systems are involved in polyarteritis nodosa? What body system is characteristically spared?

A 
Renal
GI
CNS
Dermatologic
\+ constitutional symptoms

Pulmonary vessels are generally not involved

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18
Q

50 YO male with hx of HTN, chronic Hep B, and Raynaud’s presents with vague symptoms of malaise and arthralgia, some fevers, neuropathy, and worsening pain after meals. What is this suspicious for and how is it treated?

A

Polyarteritis nodosa, treated with steroids +/- cyclophophamide if severe/refractory

In patients with Hep B, antiviral tx of hepatitis and possibly plasmapheresis

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19
Q

What viral illness is associated with polyarteritis nodosa?

A

Hep B and Hep C

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20
Q

What lab findings might be expected in a patient with polyarteritis nodosa?

A

Elevated ESR
Proteinurea
ANCA (-)

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21
Q

How is polyarteritis nodosa diagnosed?

A

Definitive diagnosis via biopsy - will show necrotizing medium vessel vasculitis without granulomas

Renal and/or mesenteric angiography will show microaneurysms with abrupt cut off of small arteries (“beading”)

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22
Q

What vessels are affected in polyarteritis nodosa?

A

Medium-sized vessels

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23
Q

Pt presents with symmetric, painless muscle weakness in proximal muscles evidenced by difficulty combing hair and rising from chair.

What is this suspicious for?

A

Polymyositis

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24
Q

Pt presents with symmetric, painless muscle weakness in proximal muscles evidenced by difficulty combing hair and rising from chair.

What lab findings might be expected for the likely diagnosis?

A 
Elevated Cr Kinase
Elevated aldolase
Elevated ESR, CRP, possible RF
Normocytic, normochronic anemia
Anti-Jo-1
Anti-signal recognition protein
\+ ANA
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25
Q

Pt presents with symmetric, painless muscle weakness in proximal muscles evidenced by difficulty combing hair and rising from chair.

What is the diagnostic test for the most likely diagnosis?

A

Muscle biopsy showing endomysial inflammation is definitive

Usually first step is electromyography

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26
Q

How is polymyositis treated?

A

High-dose corticosteroids are first line

Alternatives:

  • Methotrexate
  • IVIG
  • Mycophenolate
  • Azathioprine
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27
Q

What is one key characteristic that helps distinguish polymyositis from dermatomyositis?

A

Polymyositis is not associated with a rash

28
Q

What are two key characteristics that help distinguish polymyositis from polymyalgia rheumatica?

A

Polymyositis has loss of muscle strength and is painless

Polymyalgia rheumatica has normal muscle strength and is painful

29
Q

What are two lab findings that can help distinguish polymyositis from polymyalgia rheumatica?

A

Polymyositis has loss of strength and for that reason is associated with increased Cr kinase and increased aldolase

These will be normal in polymyalgia rheumatica

30
Q

What are some extramuscular/extraarticular findings in polymyositis?

A

Dysphagia
Low grade fever
Weight loss
Fatigue

31
Q

How do the presentations of polymyositis and polymyalgia rheumatica differ?

A

Polymyositis is painless and associated with muscle weakness

Polymyalgia rheumatica is painful but with no muscle weakness. It is also worse in the AM. There may be decreased active/passive ROM.

Both can have vague constitutional symptoms and both affect the proximal muscles

32
Q

What is the treatment for polymyalgia rheumatica?

A

Low-dose steroids

Methotrexate if refractory or if steroids are CIx’d

33
Q

What is the condition associated with the phrase “can’t pee, can’t see, can’t climb a tree” and what are the specific findings being described?

A

Reactive arthritis

Triad:

  • Urethritis/cervicitis/blanitis
  • Uveitis or conjunctivitis
  • Arthritis
34
Q

What is the work-up for reactive arthritis?

A

Arthrocentesis and negative cultures to r/o septic arthritis

Labs will show elevated WBCs, ESR
May see a normochromic anemia

35
Q

Reactive arthritis is a reaction to what, and what is the timeline?

A

Reaction to infection or inflammation elsewhere in the body

Often occurs 1-4 weeks after chlamydia or GI infection (salmonella, shigella, campy, or yersinia)

36
Q

What is the treatment for reactive arthritis?

A

NSAIDs are first line
Can use methotrexate or sulfasalazine 2nd line
Intraarticular steroids can be used

Antibiotics may be needed to clear the causative infection (not of the joint)

37
Q

What the the gene associated with reactive arthritis antibodies?

A

HLA-B27

38
Q

What are the genes associated with RA antibodies?

A

HLA-DRB 1 and 4

39
Q

What joints are characteristically affected and which are spared in RA?

A

Small joints are affected:

  • MCP
  • PIP
  • Wrist
  • MTP
  • Ankle

Spares the DIP joints!

40
Q

What kind of deformities may be seen in RA?

A
  • Ulnar deviation of the hand
  • Swan neck deformities
  • Boutonniere deformities
  • Rheumatoid nodules over bony prominences
41
Q

What is Felty syndrome?

A

RA +
Splenomegaly +
Neutropenia

42
Q

What is Caplan syndrome?

A

RA +
Pneumococoniosis +
Pulmonary nodules

43
Q

What joints of the spine might be affected in RA?

A

Cervical spine; may see C1-C2 subluxation

44
Q

What antibody may be positive in RA?

A

Anti-CCP is most specific

RF+ likely (sensitive, non-specific)

45
Q

What are characteristic XR findings associated with RA?

A 
Soft tissue swelling
Symmetric joint narrowing
Osteopenia
Bone and joint erosion
Joint subluxation

*XR may be normal in early disease

46
Q

What is the treatment for RA?

A 
DMARDs to slow progression
- Methotrexate
- Leflunomide
NSAIDs for immediate symptom control
Steroids are 2nd line for symptom control
47
Q

What is the MOA of methotrexate?

A

Folic antagonist

48
Q

What is the MOA of leflunomide?

A

T-cell inhibitor

49
Q

Describe the general pathophys of RA

A

Hyperplastic synovial tissue causes T-cell mediated joint destruction

50
Q

Patient presents with multiple dental caries complaining of dyspareunia. Parotid glands appear enlarged on PE. What is this suspicious for?

A

Sjogren syndrome

  • Dry eyes
  • Dry mouth ( –> cavities)
  • Vaginal dryness
  • Parotid gland enlargement
51
Q

What antibodies are associated with Sjogren syndrome?

A

antiSS-A (Ro)

antiSS-B (La)

52
Q

What is a Schirmer test?

A

Helps measure tear production:

  • Filter paper is placed on lower eyelid for 5 minutes
  • <5mm of wetting is positive, suggestive of Sjogren’s syndrome
53
Q

What is Rose Bengal stain used for?

A

Identifies corneal epithelium changes associated with Sjogren’s syndrome

54
Q

How is Sjogren’s syndrome treated, and what are some AEs of the treatment?

A

Cholinergic drugs: pilocarpine or cevimeline to help increase secretions.

AEs are SLUDD problems (salivation, lacrimation, urination, diaphoresis, diarrhea) as well as incontinence, n/v, blurred vision, and bradycardia

Other tx include artificial tears, increased fluid intake, sugar-free gum, artificial saliva, and fluoride

55
Q

Patients with Sjogren’s syndrome are at heightened risk for what other conditions?

A
  • Non-Hodgkin lymphoma
  • Pneumonitis
  • Interstitial nephritis

*If exposed to high antibody counts in utero, child has increased risk of congenital heart block

56
Q

What are the findings associated with limited scleroderma?

A
  • Tight, shiny, thickened skin of face, neck, and extremities distal to elbows/knees. Trunk is spared.

CREST:

  • Calcinosis cutis
  • Raynaud’s phenomenon
  • Esophageal motility disorder
  • Sclerodactyly
  • Telangiectasias
57
Q

What are the findings associated with diffuse sclerosis?

A

Tight, shiny, thickened skin involving distal body parts as well as trunk and proximal extremities.

+ Organ involvement:

  • Restrictive lung Dz (/Pulmonary HTN)
  • Pulmonary fibrosis
  • Myocardial fibrosis
58
Q

What is the classic triad of findings associated with SLE?

A

Malar rash
Joint pain
Fever

59
Q

Aside from the classic triad, what are some findings associated with SLE?

A 
Constitutional: Fevers, chills, fatigue, night sweats
CNS: HA, seizures, psychosis
Renal: Glomerulonephritis
Cardiopulm: Pericarditis, pleuritis
Other: Retinitis, oral ulcers, alopecia
60
Q

What are the antibodies associated with SLE?

A

ANA
Anti-dsDNA
Anti-Smith

May also see elevated antiphospholipid antibodies

61
Q

What are some (non-antibody) lab findings associated with SLE?

A
  • Pancytopenia
  • Anemia of chronic disease
  • Hemolytic anemia
  • Thrombocytopenia
62
Q

How is SLE disease progress monitored?

A

dsDNA antibodies

63
Q

What is the treatment protocol for SLE?

A

Mild disease, affecting skin, joints, and mucosa: Hydroxychloroquine +/- NSAIDs

Moderate disease: Add short-term steroid therapy

Severe (organ-threatening): High dose steroids or intermittent IV pulses of methylprednisolone +/- immunosuppresive agent (cyclophosphamide, mycophenolate, rituximab)

64
Q

How is scleroderma-associtated pulmonary fibrosis treated?

A

Cyclophosphamide

65
Q

What is the most sensitive antibody test for SLE?

A

Anti-Sm (Anti-dsDNA is ok but less sensitive)

66
Q

What disease is Anti-U1RNP associated with?

A

Anti-U1RNP antibody (anti-U1RNP) is generally known to be a serological marker for mixed connective tissue disease (MCTD), but can be detected also in patients with definite SSc or systemic lupus erythematosus (SLE)

67
Q

With what rheum dz is Hep B associated?

A

Polyarteritis nodosa

IM EOR (8 decks)

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