Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
110 Cards in this Set
- Front
- Back
Isolated DIP pattern?
|
Psoriatic Arthritis
|
|
DIP, PIP, 1st CMC pattern?
|
OA
|
|
PIP, MCP, wrist pattern
|
RA
|
|
Sternoclavicular pattern
|
Septic arthritis from IV Drug Abuse
|
|
Sausage toes pattern
|
Reactive(Reiters) Arthritis, Psoriatic Arthritis, Enteropathic Arthritis
|
|
Heel tendonitis pattern
|
Reactive, Psoriatic, or Enteropathic Arthritis
|
|
1st MTP joint (Podagra) Pattern
|
Gout, OA
|
|
Perarticular (ankles) pattern
|
Sarcoid
|
|
Excruciating pain pattern
|
Gout, Septic arthritis, acute rheumatic fever.
|
|
For which diseases is ESR very sensitive?
|
Vasculitis and Polymyalgia rheumatica
|
|
What does the RF serology test for?
|
The presence of an IgM directed against an IgG in the synovial fluid. Remember 20% of RA patients are RF negative.
|
|
Patients with RF+ serum are more at risk for developing?
|
nodules, joint erosions, vasculitis, and other extra-articular manifestations of RA
|
|
Which antibody has the highest disease specficity for RA?
|
anti-CCP, antibody to citrulline epitopes.
|
|
How are ANAs detected?
|
LE cell prep, damage cell, incubate in whole anti-coagulated blood, and look for phagocytic cells that have ingested nuclear material.
|
|
Are spondyloarthropathies usually RFpositive or negative?
|
usually sero-negative
|
|
is JRA RF+/-?
|
Rf+
|
|
Which antibodies are seen in a higher percentage in the elderly?
|
ANA
|
|
Which antibodies reflect disease activity?
|
Complement, dsDNA
|
|
Which antibody does not reflect disease activity?
|
ANA, antiSmith
|
|
What does a serum uric acid evaluate?
|
The effectiveness of uricosuric agent or allopurinol.
|
|
What is the diagnostic utility of HLA B27 in rheumatic disorders?
|
It does not have strong diagnostic value. While 90% of AS patients are B27 positive, there are many people in society (9% total) that don't have AS but are B27 positive.
|
|
Centromere antibody is associated with which disease?
|
Scleroderma, associated with CREST syndrome. More pulmonary, less renal involvement.
|
|
Topoisomerase is associated with which disease?
|
Diffuse scleroderma
|
|
Jo-1 antibody is associated with which disease?
|
Polymyositis, especially sever disease with interstitial pulmonary fibrosis.
|
|
ssA and ssB are associated with which disorders?
|
Connective Tissue disorders like Sjogrens and SLE.
|
|
Histone antibody is associated with which disorder?
|
Drug-induced Lupus
|
|
Which autoantibodies are associated with fetal heart blocks?
|
ssA and ssB
|
|
Which autoantibody is associated with Drug-Induced Lupus?
|
antihistone
|
|
Which autoantibody is associated with Keratoconjunctivitis Sicca?
|
ssA and ssB (connective tissue disorder)
|
|
Which disorder is associated with severe renal involvement?
|
anti-dsDNA
|
|
Which autoantibody is associated with a self-limiting disease?
|
antihistone, drug induced lupus
|
|
How is Type 1 synovial fluid distinguished?
|
(0-10,000 WBC) It is non-inflammatory, with high viscosity, 90% glucose, and generally clear except for trauma related blood. Seen in OA, structural problems, trauma.
|
|
How is Type 2 synovial fluid distinguished?
|
(5,000-25,000 WBC) Slightly turbid, monos and polys, medium viscosity with 80-90% glucose content. Examples are SLE, Enteropathic arthritis, amyloid
|
|
How is Type 3 synovial fluid distinguished?
|
(25,000-75,000 WBC) More polys than monos, slightly more turbid appearance with low viscosity, and very low glucose. Common in RA, Sarcoid, Reiters.
|
|
How is Type 4 synovial fluid distinguished?
|
(more than 50,000 WBC) PMNs only, Turbid appearance, very low viscosity, very low glucose content, seem in CPPD, Gout, GC and non GC bacterial septic joints.
|
|
If a patient has chronic inflammation in a joint but the cultures are negative, what should the next step be?
|
Get synovial tissue by biopsy or do an arthroscopy.
|
|
What is the work up for monoarthritis?
|
First always cultures and crystals. If negative do a biopsy. Xrays early to rule out destructive process.
|
|
What are the basic clinical features of AS?
|
inflammatory back pain, bilateral sacroilitis, peripheral arthritis. Male predominant. Extra-articular features are uveitis, aortic regurgitation, apical TB-like lung disease, Cauda Equina Syndrome, spinal fractures
|
|
What is the goal of treatment for AS?
|
Preserve functional position and ROM with therapy, use NSAIDs and Cox-2 inhibitors like Celebrex for pain and stiffness.
|
|
What is the classical triad for Reiter's Syndrome?
|
Conjunctivitis, Urethritis, and Arthritis. The arthritis is asymmetric, oligoarticular, and mostly in the lower extremity. Sausage toes. Can be preceded by Bacillary dysentery. Common mucocutaenous lesions are painless oral ulcers, Keratoderma Blennorrhagica, Circinate Balanitis(glans penis) and Nail changes
|
|
Characteristics of psoriatic arthritis?
|
psoriatic rash, usually on the knee, precedes the arthritic involvement. Closely associated with nail pits. There are five different patterns of presentation. Same treatment as RA. anti-TNF therapy can treat psoriasis and arthritis (also methotrexate.)
|
|
Explain the relationship of Peripheral arthritis with IBD?
|
The onset is acute, painful, asymmetric and involves just a couple big LE joints. It is self-limiting and correlates with UC or Chrons attacks. No HLA-B27 association.
|
|
Explain the relationship between axial arthritis and IBD.
|
Similar to ankylosing spondylitis, no correlation with bowel disease activity, and there is a 50% B27 association.
|
|
Why is routine testing for B27 not done for spondyloarthropathies?
|
Because there would be such a high number of false positives, not a good screening tool, only used with difficult patients when you are in doubt of diagnosis.
|
|
Radiographic findings for AS?
|
Bamboo Spine, motheaten appearance of SI joints
|
|
What are the features of Non GC bacterial infection of a joint?
|
Fever and joint pain. The knee is most common, accompanied by peripheral blood leukocytosis
|
|
What is the most common causative organism of Non GC bacterial infection in joint?
|
S. Aureus
|
|
What is the mechanism of anemia in SLE patients?
|
decreased RBC production from systemic inflammation (anemia of chronic disease)
|
|
How do ANA molecules attach human cells?
|
Cannot penetrate viable cells, They are not likely to cause damage by just binding to nuclear antigens inside cells.
|
|
What kind of molecule is an anti-smith antibody?
|
ribonucleoprotein
|
|
Which environmental factors increase expression of SLE?
|
women of childbearing age, sun exposure, genetic predisposition
|
|
Which antibodies are positive in SLE?
|
ANA, dsDNA, LE for nuclear antigens are the most prevalent, less prevalent are anti-smith, anti-ssA, anti-ssB, and anti-RNP
|
|
Which antibodies in SLE are associated with photosensitivity and subacute lupus?
|
anti-ssA
|
|
Which antibodies for SLE correlate with disease activity?
|
anti-dsDNA
|
|
What is one of the most important causes of death in SLE?
|
infection. you have to exclude the possibility of infection prior to therapy.
|
|
How is arthritis treated in SLE?
|
NSAIDS, Cox-2 agents, DMARDs
|
|
How are dermatological conditions of SLE treated?
|
topical steroids, but more severe disease can be treated with hydrochloroquine. Sun exposure should be avoided.
|
|
Which hematologic concerns are prevalent in SLE?
|
Anemia of chronic disease, thromboembolic disease from circulating lupus anticoagulants.
|
|
What kind of ventilatory defect is present in SLE?
|
restrictive ventilatory defect
|
|
What is the most common pulmonary manifestation of SLE?
|
pleuritis +/- effusion. Also seen are ILD, Pulmonary HTN, diaphragmatic dysfunction, and acute lupus pneumonitis(dramatic, life threatening)
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
What is the most important prognostic factor in SLE?
|
kidney involvement, lupus nephritis. present in over 50% of patients. occurs within the first few years of diagnosis, detected by proteinuria. causes HTN. A renal biopsy is invasive and expensive, and should be done thoughtfully.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (severe) proliferative glomerulonephritis
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (severe) proliferative glomerulonephritis
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (severe) proliferative glomerulonephritis
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (severe) proliferative glomerulonephritis
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (severe) proliferative glomerulonephritis
|
|
What does chronicty indicate?
|
the extent of activity and extent of chronic damage in the kidneys in SLE. Low levels can be treated well with steroids, but higher levels cannot be treated well regardless of tx.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
What does chronicty indicate?
|
the extent of activity and extent of chronic damage in the kidneys in SLE. Low levels can be treated well with steroids, but higher levels cannot be treated well regardless of tx.
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (severe) proliferative glomerulonephritis
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (severe) proliferative glomerulonephritis
|
|
Which renal histology types have good prognosis in SLE?
|
mesangial glomerulonephropathy, mid proliferative glomerulonephritis, and membranous glomerulopathy.
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (severe) proliferative glomerulonephritis
|
|
What does chronicty indicate?
|
the extent of activity and extent of chronic damage in the kidneys in SLE. Low levels can be treated well with steroids, but higher levels cannot be treated well regardless of tx.
|
|
What does chronicty indicate?
|
the extent of activity and extent of chronic damage in the kidneys in SLE. Low levels can be treated well with steroids, but higher levels cannot be treated well regardless of tx.
|
|
What does chronicty indicate?
|
the extent of activity and extent of chronic damage in the kidneys in SLE. Low levels can be treated well with steroids, but higher levels cannot be treated well regardless of tx.
|
|
Most important prognostic factor in SLE?
|
Renal involvement, lupus nephritis is in over 50% of patients, occurs within the first few years of diagnosis, detected by proteinuria.
|
|
Which renal histology types have good prognosis in SLE?
|
Mesangial, midproliferative, and membranous GN
|
|
Which renal histology types have poor prognosis in SLE?
|
Diffuse (Severe) Proliferative GN
|
|
What does chronicity indicate?
|
Extent and severity of renal involvement in SLE. Low levels can be treated with steroids, but high levels are difficult to manage with any medication.
|
|
When should a patient with lupus nephritis be treated with cytotoxic drugs?
|
When they can't be treated with steroids. Use azathioprine or cyclophosphamide.
|