Immune-Mediated Polyarthritis Flashcards
Polyarthropathy:
What hypersensitivities are associated with IMPA? Antigens?
- Type III - immune complex deposition
- Type II - antigen deposition or autoantibody formation
haptens (drugs), microbes, diets, tumors, self-antigens
What are the 4 classification of idiopathic IMPA?
- uncomplicated***
- reactive - infectious/inflammatory
- enteropathic - GI or hepatic disease
- neoplastic - outside joints
What breeds have a predisposition for developing Type I IMPA?
(uncomplicated)
sporting or large breeds, 2-6 y/o - GSD, Labs, Dobermans, Spaniels, Retrievers, Terriers, Poodles
What are 5 causes of Type II IMPA?
(infectious/inflammatory)
- endocarditis
- diskospondylitis
- pyelonephritis
- panreatitis
- chronic infections
What breeds are predisposed to developing non-erosive IMPA? What signs are associated?
- JUVENILE ONSET of AKITAS: neck and back pain, lymphadenopathy, meningitis
- SHAR-PEI FEVER: swollen hocks, amyloidosis
What breed is prone to developing polyarthritis-myositis? What sign is most commonly seen?
Spaniels
myalgia and muscle swelling —> bilaterally symmetrical atrophy and muscle contracture
What 2 breeds are predisposed to developing polyarthritis-meningitis? What sign is most commonly seen?
- Bernese Mountain dogs
- Boxers
cervical spinal pain
What drugs and vaccines can cause non-erosive IMPA?
DRUGS - sulfas, penicillins, cephalosporins, phenobarbarbital (Dobermans)
VACCINE - canine distemper virus, feline calicivirus
What is systemic lupus erythematosus (SLE)?
form of IMPA - multisystem, immune-mediated disease common in younger (2-4 y/o) GSDs, Shetland Sheepdogs, Irish Setters, OESD, Cocker Spaniels, Collies, and Poodles
What are 7 major signs of SLE?
- polyarthritis
- glomerulonephritis
- hemolytic anemia
- thrombocytopenia
- leukopenia
- skin lesions
- myositis
What are 4 minor signs of SLE?
- fever
- oral ulcerations
- lymphadenopathy
- CNS signs
What is erosive polyarthritis?
idiopathic Rheumatoid-like polyarthritis caused by the production of antibodies directed against IgA or IgM, which complexes within joint and Abs against collagen
- middle-ages, small breeds
What are 6 causes septic arthritis?
- bacterial - Staph, Sterp, Mycoplasma, Pasteurella, L-form, Bartonella
- fungal - Blasto, Coccidio, Crypto
- viral - distemper, calicivirus
- Leishmania
- Lyme
- Anaplasma phagocytophilium, Ehrlichia ewingii, RMSF
(usually only one joint affected)
What pattern on septic arthritis is associated with bacteremia?
a few, large proximal joints - shoulder, hip, elbow, stifle
- infection demonstrated within joints +/- blood or urine
What are the 5 most common presenting complaints in patients with polyarthritis?
- reluctance to walk, walking on eggshells, stiff gait, lameness, etc.
- pain localized to joints
- joint swelling common in carpi, tarsi, or stifles
- systemic: cyclic fever, lethargy, anorexia
- neck or back pain
What are radiographic signs of non-erosive and erosive polyarthritis?
NON-EROSIVE - joint or periarticular swelling
EROSIVE - subchondral bone destruction, irregular joint surfaces, narrowing of joint spaces, punched out lesions, luxation/subluxations
(can take 6 months to see changes!)
What are the 10 criteria for diagnosing erosive polyarthritis?
- stiffness
- pain on manipulation of at least one joint
- signs of arthritis for 3 months
- periarticular soft tissue swelling
- typical radiographic changes*
- inflammatory synovial fluid*
- symmetrical deformations of distal joints
- detection of RF in serum
- histological changes on synovium
- extra-articular symptoms, lymphadenopathy
(5 = probable, 7 = definitive)
How can rheumatoid factors be found when trying to diagnose erosive polyarthritis?
antibodies to IgA or IgM founf in synovial fluid or serum —> not specific or significant for idiopathic erosive PA
What 6 diagnostics are used to find underlying causes and determine treatment of polyarthritis?
- spinal radiographs - diskospondylitis
- thoracic radiographs - neoplasia, pneumonia
- abdominal ultrasounds - neoplasia, pancreatitis, pyelonephritis
- echocardiogram - vegetative lesion on valve (steroid can worsen!)
- blood cultures
- infectious disease testing - Bartonella
What diagnostic is used for SLE?
antinuclear antibodies —> tested for when IMPA is present with skin lesions, hemolytic anemia, thrombocytopenia, and/or glomerulonephritis
- false positive seen with infectious, inflammatory, or neoplastic disorders or drugs
What are LE cells?
phagocytized nuclear remnants, rarely seen but diagnostic of SLE
How are meningitis and myositis commonly seen with SLE/PA diagnosed?
MENINGITIS - CSF tap, serum IgA —> neutrophilic or mixed leukocytes pleocytosis
MYOSITIS - serum CK, EMG, muscle biopsy
What are the 3 aspects of treating erosive IMPA?
- treating underlying disease - reactive, Type II-VI; corticosteroids (contraindicated for infective endocarditis), removal of drugs, wait on vaccines
- analgesia - NSAIDs (if not on corticosteroids), opioids
- immunosuppression - Type I idiopathic, SLE, erosive PA, PA with meningitis and myositis
What primary immunosuppressives are recommended for erosive IMPA? What are 4 second line immunosuppressives?
Prednisone - 2 mg/kg/day
- Leflunomide*
- Cyclosporine*
- Mycophenolate
- Azathioprine
What 2 responses are expected with immunosuppressive treatment of erosive IMPA?
- improvement with pain and welling - within 7 days
- substantial decrease in WBCs in synovial fluid - repeat taps prior to tapering doses*, indicated in cases with relapse
When are patients in remission for erosive IMPA? How should drugs be changed at this point?
clinical signs and inflammation resolved/improved
- 2 weeks = taper slowing based on repeated joint taps, decreasing 25-50% every 2-4 weeks
- discontinue or acieve lowest effective dose that controls signs without excessive side effected (commonly reached by 6 months of therapy)
What is prognosis of IMPA like?
- good with Type I —> remission harder to achieve with Types II-IV
- poor long term with erosive PA —> rarely get off meds, commonly relapse with no response to therayp
- variable with SLE —> depinds on concurrent kidney disease and response to therapy
