Rheum 2 (SLE, AS, Reactive, Psoriatic) Flashcards
What are ANA (anti-nuclear antibodies)
Protein antibodies that react against cellular nuclear material.
Found in 95% of patients with autoantibodies to nuclear material
Not specific to lupus
What type of ANA should you draw
IFA
**DO NOT DRAW DIRECT (ie. EIA) or ELISA–> very high false positive
When should you order an ANA?
- Confirmatory test- Help establish a diagnosis of a CT disease or autoimmune disease
- Exclude a disorder when findings are inconclusive
- Subclassify with an established diagnosis
SSA, SSB, anti-RNP - Monitor disease activity (Anti -double stranded DNA antibody levels in lupus nephritis)
Conditions with positive ANA
- SLE – 93%
- Sjogren’s Syndrome – 48%
- RA – 41%
- Hashimoto’s thyroiditis – 46%
- Primary biliary cirrhosis – 10-40%
- Autoimmune hepatitis – 63-91%
- HepC
- TB
- Mono
When should you draw ANA specific antibodies
1:160 titer
What diseases do the following ANA Ab suggest?
- Anti-dsDNA
- Anti-RNP (ribonuceloprotein)
- Anti-Sm (smith)
- Anti-dsDNA: SLE, monitor lupus nephritis
- Anti-RNP (ribonuceloprotein): Mixed CT dz
- Anti-Sm (smith): SLE, marker of dz
What diseases do the following ANA Ab suggest?
- Anti-SSA (Ro)
- Anti-SSB (La)
- Anti-Centromere (Scl-70)
- Anti-SSA (Ro): Sjogren’s syndrome, subacute cutaneous lupus, neonatal lupus
- Anti-SSB (La): Sjogren’s syndrome, SLE
- Anti-Centromere (Scl-70): scleroderma
Describe the use of ANA titers
The most dilute serum in which ANA is detected
Helpful to use as an adjunct to clinical evidence– Is less helpful if the clinical evidence is strong for an autoimmune disease
The presence of a titer alone is not diagnostic of the disease
In general, the higher the titer the more likely the disease exists and the more active it may be
Malar vs rosacea rash
Malar: spares nasal labial folds
Rosacea: can cross lines
*both have dry eyes
Risk factors of SLE
- F>M (8:1)–> but males have worse dz
- 20-30s
- nonwhite: white 3:1–> nonwhites have worse dz
- etiology unknown but possible genetic, hormonal, immunologic, environmental
Antibody formation with the creation of immune complexes which deposit in tissues–> complement cascade and immune activation
Affects virtually every organ
SLE
Describe the initial lab workup of SLE
- CBC
- CMP
- creatine kinase
- ESR, CRP
- UA
- 24 hr urine for creatinine clearance
- ANA
- ANA profile (anti-dsDNA)
- Anti-phospholipid Abs
- +/- C3, C4, CH50 (lupus nephritis)
What imaging could you get wtih SLE
Not routinely recommended unless specific concerns
- Pleuritic chest pain–> chest x-ray
- Renal impairment –> renal ultrasound
- Echocardiogram
Describe the ACR criteria for dx of SLE
4+ manifestations
- Malar rash
- Discoid rash
- photosensitivity
- oral ulcers (painless)
- polyarthritis (2+ peripheral joints w/o erosions, tenderness, swelling)
- Serositis (pleuritis, pericarditis)
- Renal (proteinuria 3+, cellular casts)
- Neurologic (seizure, psychosis w/o cause)
- Hematologic (anemia, leukopenia, thrombocytopenia)
- ANA titers >1:160
Common constitutional and mucocutaneous manifestations of SLE
Constitutional: Fatigue, fever, weight loss
Mucocutaneous: Alopecia, Raynaud’s, Subacute Cutaneous Lupus
Common MSK and Neurologic manifestations of SLE
Musculoskeletal: Avascular necrosis, myositis, joint laxity/disability
Neurologic: Cognitive dysfunction, stroke, peripheral neuropathy
Common CVP, hematologic, and manifestations of SLE
Cardiopulmonary: Acute pneumonitis, interstitial lung disease, myocarditis, PHTN
Hematologic: LAD
Gastrointestinal: Esophageal dysmotility, ascites, hepatitis
Vasculitis: Medium and small vessel
How do you monitor SLE with labs
Dependent on the patients disease activity (monitored by rheum)
- CRP and ESR may be normal during a flare or elevated when not flaring
1. CBC,
2. . ESR, CRP,
3. U/A, serum creatinine with eGFR,
4. anti-dsDNA,
5. C3 and C4
6. Kidney involvement -> spot urine protein and creatinine and serum albumin
Describe the tx of SLE
*No cure–> need to educate
1. Non-pharm: sun precautions/fluorescent lights–RIT dye, filters, SPF sunscreen, sun protective clothes
and exercise
2. NSAIDS
3. Antimalarials (hydroxychlorquine)
4. systemic steroids
5. Immunosuppresants (methotrexate)
*If pts are on these immunosupressants and come in with a sore throat, you need to start these patients on ABX sooner BC they are immunocompromised
SLE death is secondary to: a
- organ failure
2. infection secondary to immunosuppresion
SLE has an increased risk of what CA
- non-Hodgkin Lymphoma– B cell associated
Antibodies directed against either phospholipids or plasma proteins bound to phospholipids
Most of the antigens are involved in coagulation
Anti-phospholipid syndrome (APS)
What is the difference between primary APS and secondary APS
Primary: Presence of anti-phospholipid (aPL) in the setting of thrombosis
The other components of “CLOT” may be present
2/3 of clots are VENOUS; 1/3 are arterial
Secondary: Presence of aPL without manifestations or in conjunction with SLE
Up to 50% of SLE patients have one or more antiphospholipid antibodies