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Morning Report > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Illness script: 27-year-old otherwise healthy woman presented with unilateral vision loss

  • sudden
  • central vision loss
  • painless, no eye redness
  • decreasing smelling sensation, otherwise no systemic symptoms
  • MRI, MRA, MRV negative
  • opthalmology exam showed macular edema, beading of retinal veins, retinal hemorrhage and 1+ keratocytes
A

Dx: Ocular sarcoidosis (with retinal vasculitis and posterior uveitis)

DDx:

Central retinal artery occlusion

Optic neuritis (multiple sclerosis, or isolated)

Posterior uveitis (syphilis)

Large vessel vasculitis

Retinal detachment

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2
Q

Ocular sarcoidosis

A

Occurs in 20-25% of patients with sarcoidosis, and can usually be identified at disease presentation. Thus it is important to have an ophthalmic evaluation when sarcoidosis is diagnosed (particularly for uveitis and/or glaucoma).

Can involve orbit, anterior and posterior segments of the eye, conjunctiva, lacrimal glands, and extraocular muscles.

In a series of 81 patients in ophthalmology clinic:

  • 40% uveitis
  • 30% keratoconjunctivitis sicca
  • 15% adnexal (eyelid or conjunctival) granulomas
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3
Q

Retinal vasculitis associated with sarcoidosis

A

Findings: retinal periphlebitis*, diffuse capillary leakage, retinal neovascularization, vitreous inflammation, choroidal granulomas, and optic nerve disease

*described as “resembling candle wax drippings”

  • a finding considered by some to be pathognomonic of sarcoidosis
  • primarily occurs around the vein and rarely occurs around arteries, which differentiates sarcoidosis from Behçet’s syndrome
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4
Q

Uvea anatomy

A

Anterior uveitis

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5
Q

What are the diagnostic criteria for SLE?

A

Need the presence of 4/11 criteria, 85% sensitivity and 95% specificity.

S Serositis/Pleuritis/Perciarditis

O Oral ulcer, usually painless

A Arthritis; non-erosive, 2+ peripheral joints

P Photosensitivity

B Blood; anemia, thrombocytopenia

R Renal (proteinuria, 0.5 g/day)

A ANA positivity

I Immunologic (Anti-DS DNA, Anti-Smith, APLS AB)

N Neuro; cerebritis, seizures, psychosis

M Malar Rash

D Discoid Rash

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6
Q

What are the lab abnormalities associated with SLE? What auto-antibodies?

A

During an active flare patients have low complement levels (C3 and C4) due to immune complex deposition causing complement activation and consumption. There will also be an elevated ESR and CRP.

  • ANA – screening test, 95% sensitivity
  • Anti-dsDNA – high specificity, sensitivity 70%, level fluctuates with disease activity
  • Anti-Smith – most specific, only 30-40% sensitivity
  • Anti-SSA (Ro) or Anti-SSB (La) – present in 15% of patients with SLE and other connective tissue disorders such as Sjogren’s syndrome
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7
Q

What is the anti-body that is positive in drug induced lupus?

A

Anti-Histone AB

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8
Q

How do you treat mild SLE disease?

A

Hydroxychloroquine/chloroquine +/- NSAIDs +/- short-term low dose prednisone (<7.5 mg/day)

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9
Q

How do you treat moderate SLE disease?

A

Hydroxychloroquine/chloroquine +/- short-term prednisone 5-15 mg + often need steroid-sparing agent immunosuppressive agent (i.e. azathioprine or methotrexate)

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10
Q

How do you treat severe life threatening SLE disease?

A

Induction therapy followed by maintenance therapy; agents such as mycophenolate, cyclophosphamide, or rituximab often used, often get short course of IV steroids

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11
Q

What is the clinical presentation of gout?

A
  • Acute onset <24 hrs
  • Severe pain, redness, warmth, swelling
    • Fever may be present
    • Leukocytosis, elevated ESR, CRP
    • Plain film may show subcortical bone cysts
    • Acute serum uric acid not helpful in diagnosis
  • Often lower extremity – 1st MTP = podagra
  • 80% monoarticular
  • Rarely axial joints
  • Resolves within days
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12
Q

When should an arthrocentesis be performed? What should you send?

A
  • Indications for arthrocentesis:
    • Any new joint effusion or sign of inflammation within a joint
    • Rule out acute septic arthritis
    • Confirmation of presence of crystals
  • Order cell count, gram stain/culture, crystals
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13
Q

What are general cut off values for WBC in synovial fluid that indicates inflammatory vs non-inflammatory?

A

WBC cut off of 2000 cells can help differentiate non-inflammatory from inflammatory.

Non-Inflammatory causes; OA, trauma, avascular necrosis

WBC > 2000 think inflammatory etiologies

  • Inflammatory
    • Gout/pseudogout, RA, spondyloarthritis, lupus, lyme
  • Septic – often WBC >50,000, >75% PMNs
    • LR increases with increasing WBC
    • Can have WBC <25,000 with Neisseria, immunocompromised
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14
Q

What type of cyrstals do you expect to see in gout?

A

Monosodium urate crystals

  • Needle shaped, negatively birefringent
  • Appear bright against dark background when two polarizing filters are crossed
  • Appear yellow or blue depending on orientation of the analyzer
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15
Q

What type of crystals do you see in pseudogout?

A
  • Calcium pyrophosphate dihydrate crystals
    • Rhomboid or rectangular
    • Weak positive birefringence – blue
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16
Q

How do you treat gout acutely?

A
  • Prednisone 30mg PO
    • Treat for duration of flare – usually 5-7 days
  • NSAIDs – Naproxen 500mg PO BID or indomethacin 50mg PO TID
    • OK for younger patients without renal, CV or GI disease
  • Colchicine – loading dose 1.8mg PO in first 24hrs, then 0.6mg PO daily or BID
    • Cannot use in severe renal or hepatic dysfunction
  • Intra-articular injection of corticosteroid
    • Must rule out infection first
    • Good for involvement of only 1-2 joints, or if patient is NPO
17
Q

What are the indications for maintenance therapy for gout?

A
  • Aimed at reducing number of recurrences
  • Always use concomitant lifestyle modifications
  • Indicated for multiple recurrent attacks
    • Imaging suggestive of joint destruction or tophi
    • Renal disease w/GFR<60
  • Goal to lower uric acid <6 mg/dL
  • Typically wait two weeks after a flare to start maintenance
  • Acute urate lowering therapy can perhaps precipitate flare
18
Q

What do you use for gout prophylaxis?

A
  • Allopurinol – start at 100mg PO daily
    • Xanthine-oxidase inhibitor
    • HLA-B5801+ increased risk of cutaneous necrosis
    • Febuxostat 40mg daily is an alternative – more $$$
  • Probenecid – 250mg PO BID
    • Promotes uric acid excretion
    • Use in patients with low urinary excretion of uric acid in the setting of high serum uric acid
    • Avoid with history uric acid nephrolithiasis
19
Q

When do you perform a renal biopsy in SLE?

A
  • Kidney biopsy
    • Proteinuria >500mg/day
    • Active urine sediment (hematuria, cellular casts)
    • Rising Cr
    • Any other sign of renal involvement
20
Q

What is the pathogenesis of microscopic polyangitis?

A
  • Immune-mediated disorder in which tissue injury results from an initiating inflammatory event (unknown) and a highly specific immune response.
  • Often associated with anti neutrophil cytoplasmic autoantibodies aka ANCA which destroy WBCs leading blood vessel damage
21
Q

What is the Chapel Hill Consensus Conference Criteria to diagnose MPA?

A
  • Small vessel vasculitis (arterioles, capillaries, venules)
  • Necrotizing vasculitis, with few or no immune deposits
  • Necrotizing glomerulonephritis is very common. Pulmonary capillaritis often occurs.
  • Granulomatous inflammation is absent (as opposed to GPA)
22
Q

What is the clinical presentation and what are the clinical feature of MPA?

A
  • Most commonly in older adults, both sexes affected equally
  • Most common symptoms:
    • Kidney inflammation (80%)
      • Asymptomatic hematuria
      • A rise in serum creatinine occurring over days or weeks with hematuria and cellular casts. Rapidly rising serum creatinine with hematuria, hypertension, and edema is a medical emergency that requires urgent therapy
      • Variable degree of proteinuria that is usually subnephrotic
      • Rapidly progressive glomerulonephritis
  • Weight loss (>70%)
  • Skin lesions (60%)
  • Nerve damage (peripheral nerves) (60%)
  • Fevers (55%)
  • Pulmonary
    • Pulmonary: Pulmonary fibrosis, PAH, airway or parenchymal involvement leading to cough, hemoptysis, effusions
    • Skin: purpura involving the lower extremities that may be accompanied by focal necrosis and ulceration
23
Q

How do you diagnose MPA?

A
  • MPA is an ANCA associated vasculitis associated with MPO-ANCA, remember GPA is associated with PR3-ANCA
  • Other labs are non specific for MPA but done to exclude other diseases or determine extent of disease involvement
    • Leukocytosis, thrombocytosis (>400K/microL), High ESR/CRP, normochromic, normocytic anemia common
    • ANA, anti GBM-Ab, C3/C4, Hepatitis, HIV, Tb to exclude other causes
  • Pursue a biopsy of a presumed actie site of disease to make a tissue diagnose.
24
Q

What is sarcoidosis? What is the cause of sarcoidosis?

A

Sarcoidosis is non-caseating granulomas that are predominantly found in the lungs and hilar lymph nodes. The etiology is unknown but is thought to be due to a variety of environmental exposures.

25
Q

What is the epidemiology of sarcoidosis?

A

More common in African Americans than caucasians, female:male predominance is 2:1, most common in ages 25 to 35.

26
Q

What are the different stages of pulmonary sarcoidosis?

A

◦Stage 1-bilateral hilar lymphadenopathy
◦Stage 2-bilateral hilar lymphadenopathy with infiltration
◦Stage 3-infiltration alone
◦Stage 4-fibrotic bands, bullae, hilar retraction, bronchiectasis

27
Q

What are some of the extra-pulmonary manifestations of sarcoidosis?

A
  1. Cutaneous; erythema nodosum
  2. Cardiac; patchy granulomas that cause cardiomopathy or conduction abnormalities
  3. Neurologic; cranial nerve palsies, headache, weakness, seizures
  4. Opthalmic; anterior uveitis
  5. Renal; hypercalcemia, hypercalcuria
28
Q

What is the treatment for sarcoidosis?

A

Glucocorticoids

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