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Rheumatology > Testing for Rheum > Flashcards

Testing for Rheum Flashcards

1
Q

How are dxs made for rheum disorders?

A
  • based upon criteria for classification of various rheum disorders:
    clinical features (h and p)
    lab/radiographic findings
  • dx tests don’t make the dx (they help confirm)
  • dx tests modify the probability that a particular disorder is present
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2
Q

What is sensitivity?

A
  • proportion of pts w/ positive test who have the disease - so a negative test will effectively rule out the disease
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3
Q

What is specificity?

A
  • proportion of pts w/ negative test who don’t have the disease - so positive test will effectively rule in disease
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4
Q

How do you screen for autoimmune disease?

A
  • primarily by H and P
  • increase your pretest probability by asking ?s that support the dx of inflammatory arthropathy or systemic rheumatic disease
  • look for clues on physical exam
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5
Q

When should you order serologic testing?

A
  • You should have a compelling reason to order rheum eval tests
  • assist in confirming a specific dx (high index of clinical suspicion)
  • formulate appropriate management
  • eval/monitor disease activity
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6
Q

What are acute phase reactants?

A

proteins synthesized by the liver and induced by:

  • inflammation: infections, autoimmune disorders, neoplasms
  • tissue injury/necrosis: trauma, infarction
  • parallels chronic inflammation, goes up and down w/ inflammation
  • monitors disease activity
  • not DX!
    examples:
  • coag proteins (I, II) fibrinogen levels inc, platelets inc
  • CRP
  • complement components (C3, C4, B)
  • many others: fibronectin, transport proteins (Hp, Transferrin, Ceruloplasmin)
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7
Q

What is the ESR?

A
  • the distance at which erythrocytes have settled in a vertical column of anticoag blood in an hour (mm/hr)
  • in an inflammatory state: positively charged acute phase proteins neutralize negative charges and allow RBC to aggregate
  • now RBC fall at a diff rate, and a further distance - increased ESR
  • indirect measurement of serum APR concentrastion, particularly fibrinogen
  • influenced by size, shape, number of RBCs (ESR is increased in anemia)
  • as a pt’s condition changes the ESR changes relatively slowly
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8
Q

When would the ESR be increased?

A
  • w/ age, slightly higher in women, preg, diabetes, renal failure, malignancy, tissue damage (MI, CVA)
  • both ESR and CRP elevated in obesity: due at least in part to IL-6 secretion by adipose tissue
  • acute phase reactants
  • paraproteins
  • anemia (fewer cells, less repellent forces)
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9
Q

Normal values for ESR?

A
  • male: less than 17mm/hr
  • female: less than 25mm/hr
  • kids: less than 10mm/hr
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10
Q

Elevated ESR remains an impt dx criterion for which 2 rheumatic conditions?

A
  • polymyalgia rheumatica: greater than 40 mm/hr

- GCA: greater tahn 90mm/hr

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11
Q

Uses of ESR in other rheum diseases?

A
  • limited utility for differentiating inflammatory jt disease from noninflammatory jt disease: nondx
  • not reqd for dx of RA: good hx and physical far more sig than ESR in establishing the dx, but ESR can be helpful in monitoring disease activity
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12
Q

What is CRP?

A
  • acute phase protein produced by the liver:
    produced in response to inflammation:
    infections, long term chronic inflammatory illness
  • enhances complement binding and phagocytosis
  • acute increases w/in 6 hrs, peaks at 48 hrs
  • 2 types of tests:
    standard CRP
    High-sensitivity CRP (hs-CRP)
  • less sensitive than ESR to irrelevant factors (age, gender, anemia)
  • responds more quickly
  • more expensive, may not be available, don’t always know how to interpret
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13
Q

Normal values of of CRP?

A
  • in adults: less than 1 mg/L
  • low grade inflammation: 1-10 mg/L
  • systemic inflammation is greater than 10 mg/L
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14
Q

Use of ESR and CRP in rheum?

A
  • nonspecific indicators of inflammation
  • not useful as screening tests for rheumatic diseases
  • can’t differentiate one disease from another
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15
Q

What is the Rheumatoid Factor? Sensitivity? Specificity?

A
  • an auto-ab directed against Fc portion of IgG
  • sensitivity: 80% in pts w/ RA
  • specificity: 80-90%
  • prevalence of RA: 0.5-3%
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16
Q

What are other conditions that cause a positive Rheumatoif factor?

A
  • SLE
  • scleroderma
  • Sjogren syndrome
  • cryoglobulinemia
  • infections: Hep, TB, SBE, Syphilis, parasitic disease, viral (mono)
  • pulm diseases (sarcoidosis)
  • malignancy
  • thus RF isn’t dx for RA on its own, testing is most useful when there is a moderate level of suspicion for RA
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17
Q

What is the post test probablity?

A
  • the probability that the pt has a disease given a positive test result
    (should only get test if you have a high pretest probability)
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18
Q

Why does clinical impression count the most in dx RA?

A
  • up to 30% of pts w/ RA are RF negative early in the disease
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19
Q

Normal value of RF?

A
  • measured as a titer

- less than 1:80 is negative

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20
Q

What is the classificaiton criteria of RA?

A
  • need a total score of at least 6
  • number and site of involved jts (synovitis)
    2-10 large jts = 1 pt
    1-3 small jts = 2 pts
    4-10 small jts = 3 pts
    more than 10 jts = 5 pts
  • serological abnormality (RF or anti-ccp ab):
    low positive (above ULN)= 2 pts
    high positive (over 3x the ULN)= 3 pts
  • elevated acute phase response (ESR or CRP) above the ULN= 1 pt
  • sx duration at least 6 wks = 1 pt
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21
Q

What does RF correlate w/ in pts w/ established RA?

A
  • correlates w/ severe articular disease and extra-articular manifestations
  • once test is positive there is no value in re-testing: RF doesn’t change w/ disease activity
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22
Q

Use of RF?

A
  • it isn’t dx for RA

- the test’s utility is greatest when there is a moderate pre-test probability of disease

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23
Q

What is the Anti-CCP? Use?

A
  • citrulline ab, CCP abs
  • ab directed against citrullinated peptide residues present w/ inflammtory sites
  • mostly assoc w/ RA, sensitivity equivalent to RF
  • greater specificity than RF, useful when RF is negative
  • may be detected in healthy people yrs b/f onset of RA
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24
Q

What is an ANA?

A
  • autoabs directed at nuclear ags (or contents of cell nucleus)
  • ANAs are serologic hallmarks of systemic autoimmune disease
  • provide further dx and prognostic data concerning pts who have minimal sxs or who have clinical features of more than 1 autoimmune disease
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25
Q

Use of ANA?

A
  • help establish a dx in a pt w/ clinical features suggestive of an autoimmune or corrective tissue disorder
  • to exclude such disorders in pts w/ few or uncertain clinical findings
  • to subclassify a pt w/ est dx of an autoimmune or CT disease
  • to monitor disease activity (ex: anti ds-DNA ab levels in lupus nephritis)
26
Q

Positive ANA is seen in what diseases?

A
  • Systemic autoimmune disease
  • organ specific immune diseases (hashiomotos, graves, autoimmune hepatitis)
  • variety of infections: mono, hep c, HIV, SBE
  • normal individuals - false positives are generally low titers and more commonly seen in women and the elderly
  • therefore their presence doesn’t mandate the presence of illness
27
Q

Sensitivities of positive ANA for particular autoimmune diseases?

A 
- SLE: 93%
almost all pts w/ SLE have positive ANA, but this test isn't specific for SLE
- mixed CT disease: 93%
- scleroderma: 85%
- drug induced lupus: 100%
28
Q

What are non-rheumatic conditions causing positive ANA?

A
  • normal individuals: females over males, increasign age, relatives of pts w/ rheumatic disease, pregnancy
  • hepatic disease: chronic active hepatitis
  • pulm: idiopathic pulm fibrosis
  • chronic infections
  • malignancies: lymphoma, leukemia, melanoma, solid tumors (ovary, breast, lung, kidney)
  • heme disorders: ITP, autoimmune hemolytic anemai
  • drug induced
  • misc: autoimmune thyroiditis, type 1 DM
29
Q

ANA abs seen in normal pop?

A
  • ANA 1:40 - almost 32% of normals
  • 1:80 - seen in almost 13%
  • 1:160 seen in almost 5%
  • 1:320 seen in almost 3%
  • no set titer that can distinguish b/t those w/ and w/o SLE
  • positive ANAs are commonly found in the normal pop
  • for higher titers patterns of ANA may be given:
    homogenous, speckled, nucleolar, rim but staining patterns aren’t specific and not reliable for dx diff diseases
30
Q

Criteria for classification of SLE?

A
  • malar rash
  • discoid rash
  • photosensitivity
  • oral ulcers
  • arthritis
  • serositis
  • neuro disorders
  • renal disorder: proteinuria or Casts
  • heme:
    HA w/ reticulocytosis or
    leukopenia or
    lymphocytopenia or
    thrombocytopenia
  • immunologic disorder:
    antiphospholipid ab or
    abnormal titer of anti-nDNA or
    anti-Sm (smith ag) or
    confirmed false + STS (VDRL)
  • ANA (abn titer)
  • dx is made when any 4 or more of these manifestations are present, either serially or simulateously
31
Q

When should an ANA be ordered?

A
  • when your pre-test probability for lupus is moderate (should have at least 3/11 criteria b/f ordering ANA)
  • not recommened as random screening test
  • not useful to dx other conditions but may support clinical dx
32
Q

Once the ANA is positive, does it serve a purpose?

A
  • no utility in disease monitoring
  • there is no need to repeat it
  • specific autoab tests possess dx significance in the right clincal setting
33
Q

Diff types of ANAs?

A
  • defined by their target ag
  • including ds-DNA
  • individual nuclear histones
  • RNA protein complexes
  • some of these abs are relatively specific for a particular disease or for specific clincal manifestations in pts w/ SLE
34
Q

Use of Anti-dsDNA?

A
  • specific for SLE (60-70%)
  • single stranded nonspecific
  • farr assay preferable to ELISA
  • may fluctuate w/ disease activity (may use to monitor disease)
35
Q

Use of Anti-Sm?

A
  • highly speciifc for SLE (but not sensitive)
36
Q

Use of ACA?

A
  • anti-centromere ab (ACA): assoc w/ CREST, and scleroderma
37
Q

Use of anti-topoisomerase I (Scl-70)?

A
  • assoc w/ diffuse scleroderma
38
Q

Use of Anti-Ro (SS-A) and La (SS-B)?

A
  • assoc w/ sjogrens
  • can be seen in SLE
  • may be assoc w/ neonatal heart block in babies of mothers w/ this ab
39
Q

Use of Anti-U1 snRNP?

A
  • nonspecific
  • part of criteria for mixed CT disease (MCTD)
  • may be seen in other systemic rheumatic diseases
40
Q

Use of Anti-Jo-1 (anti-histydl-tRNA synthestase)?

A
  • specific for myositis assoc w/ interstitial lung disease

- raynauds

41
Q

General Utility of ANA?

A
  • not recommended as a screening test

- greatest utility for dx of lupus w/ moderate pre-test probability

42
Q

What are serum complements? Levels assoc w/ certain rheum diseases?

A
  • not an ab test, but very useful for monitoring disease activity in SLE

low C3 and C4:

  • reflect consumption of complement
  • demonstrates active SLE
  • usually caused by presence of immune complexes in SLE
  • seen in some forms of vasculitis
43
Q

What are Antineutrophil cytoplasmic abs (ANCA)?

A
  • group of abs mainly of IgG type directed against Ags in cytoplasm of neutrophil granulocytes and monocytes
  • seen on immunofluoresscence as:
    perinuclear staining: P-ANCA
    cytoplasmic staining: C-ANCA
44
Q

ANCA is most strongly assoc w/ what?

A
  • vasculitis
  • c-ANCA (PR3): wegner’s granulomatosis microscopic polyangiitis
  • p-ANCA (MPO): churg-strauss vasculitis
45
Q

Utility of ANCA?

A
  • ANCA alone isn’t dx for vasculitis

- if not ANCA positive - consider dx other than vasculitis

46
Q

What is HLA-B27? Normal frequency?

A
  • class I MHC product
  • alpha chain
  • beta-2 microglobulin
  • normal frequency:
    caucasians 6-10%
    african americans 4%
    native americans 13%
47
Q

HLA-B27 syndromes?

A
  • ankylosing spondylitis: over 90%
  • reactive arthritis (Reiter’s syndrome): over 80%
  • enteropathic spondylitis: 75%
  • psoriatic spondylitis: 50%
48
Q

Use of HLA-B27?

A
  • sensitivity 95% for pts w/ ankylosing spondylitis
  • present in 5-8% general pop
  • incidence of disease: 0.5-1.0%
  • HLA-B27 of no value in dx typical back pain pt
  • not reqd to confirm a clinical and radiologic dx of ankylosing spondylitis
49
Q

How do you dx Ankylosing spondylitis?

A
  • clinical evidence - inflammatory back pain of insidious onset, worse in morning, better w/ exercise and NSAIDs
  • radiographic evidence (looks like bamboo on x-ray - has syndesmophyte formation)
  • HLA-B27 positive
50
Q

Relative CIs, and complications of arthrocentesis?

A 
- relative CIs:
overlying skin infections
bleeding diathesis
- complications:
infection
bleeding
cartilage injury
vasovagal episode
51
Q

Studies from an arthrocentesis?

A
  • appearance: color, turbidity, viscosity, quantity
  • cell counts: leukocyte, erythrocyte, diff cell counts, morphologic study
  • culture: aerobic, anaerobic
  • protein
  • glucose
  • mucin clot

special studies:

  • RF
  • ANA
  • complement
  • enzymes
  • exam for crystals
  • immunoglobulins
52
Q

Normal levels of uric acid? Critical value?

A
  • by-product of purine (adenine, guanin) catabolism:
    men 4-8.5 mg/dL
    women 2.7-7.3 mg/dL
    critical value: greater than 12.0 mg/dL
53
Q

2 mechanisms of hyperuricemia?

A

increased production:

  • dietary purines (Meat, yeast/beer, beans)
  • endogenous purine synthesis (cancers)
  • tissue nucleic acid breakdown (chemo, hemolysis)

decreased excetion (75% renal):

  • renal failure
  • inhibition of tubular urate secretion (competitive anion excess: keto-/lactic acidosis)
  • enhanced tubular rate reabsorption (diuretics, insulin resistance, dehydration)
54
Q

Drugs that effect uric acid levels?

A

increased by:

  • low dose ASA
  • ETOH
  • caffeine
  • vitamin C

decreased by:

  • high dose ASA
  • estrogens
  • corticosteroids
55
Q

What is the clinical significance of elevated uric acid?

A
  • gout
  • asx hyperuricemia: occurence 10% of adult men
  • renal impairment
  • toxemia of pregnancy (increased catabolism of purines = increased uric acid)
  • conditions assoc w/ increased production
56
Q

What is gout?

A
  • jt pain w/ swelling and erythema
  • deposition of sodium urate crystals in jts and tissues: synovial fluid analysis shows neg birefringent needle-shaped crystals
  • repeated attacks lead to destruction of tissues and severe arthritic like malformations
  • uric acid can be normal in 30% of acute gout attacks
57
Q

What is CREST syndrome? What tests can be used to help dx this?

A
  • C: calcinosis
  • R: raynauds
  • E: esophageal dysmotility
  • S: sclerodactyly
  • T: telangiectasia
  • ANA: 70-90% positive
  • anti-centromere AB:
    70-85% sensitivity
    very specific for CREST syndrome
58
Q

What is Systemic sclerosis (scleroderma)? Tests used to help dx?

A
  • characterized by fxnl and structural abnormalities of small blood vessels, fibrosis of skin and organs, and autoabs
  • eosinophilia: 100%
  • ANA: 70-90%:
    anti-Scl70: 30-70%
    nucleolar: 40-70%
  • RF: 30%
59
Q

What is Sjogren’s syndrome? Tests used to help dx?

A
  • characterized by diminished lacrimal and salivary gland secretion (sicca syndrome). Pt presents w/ fatigue, dry eyes and mouth
  • Anti-Ro (SS-A): 90%
  • Anti-La (SS-B): 60%
60
Q

What are MCTD? Tests used to help dx?

A
  • is a syndrome of overlapping disease manifestations w/ features of: RA, SLE, scleroderma, and polymyositis
  • low titer ANA
  • nuclear RNP abs: over 95%
61
Q

What are myositis disorders? Tests?

A 
- dermatomyositis: 
inflammatory myopathy w/ cutaneous lesions, muscle pain and weakness
- ANA screening: 40-60% positive
- Anti-PM-Scl: 10%
- increased CPK/Aldolase enzymes 
Polymyositis: characterized by progressive muscle pain and weakness
ANA screening 40-60% 
anti-PM-Scl: 50%
62
Q

Are serologic tests for rheum diseases dx?

A
  • no supportive, not dx

Rheumatology (8 decks)

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