Immune-Mediated Polyarthritis Flashcards

1
Q

Polyarthropathy:

A
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2
Q

What hypersensitivities are associated with IMPA? Antigens?

A
  • Type III - immune complex deposition
  • Type II - antigen deposition or autoantibody formation

haptens (drugs), microbes, diets, tumors, self-antigens

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3
Q

What are the 4 classification of idiopathic IMPA?

A
  1. uncomplicated***
  2. reactive - infectious/inflammatory
  3. enteropathic - GI or hepatic disease
  4. neoplastic - outside joints
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4
Q

What breeds have a predisposition for developing Type I IMPA?

A

(uncomplicated)

sporting or large breeds, 2-6 y/o - GSD, Labs, Dobermans, Spaniels, Retrievers, Terriers, Poodles

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5
Q

What are 5 causes of Type II IMPA?

A

(infectious/inflammatory)

  1. endocarditis
  2. diskospondylitis
  3. pyelonephritis
  4. panreatitis
  5. chronic infections
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6
Q

What breeds are predisposed to developing non-erosive IMPA? What signs are associated?

A
  • JUVENILE ONSET of AKITAS: neck and back pain, lymphadenopathy, meningitis
  • SHAR-PEI FEVER: swollen hocks, amyloidosis
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7
Q

What breed is prone to developing polyarthritis-myositis? What sign is most commonly seen?

A

Spaniels

myalgia and muscle swelling —> bilaterally symmetrical atrophy and muscle contracture

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8
Q

What 2 breeds are predisposed to developing polyarthritis-meningitis? What sign is most commonly seen?

A
  1. Bernese Mountain dogs
  2. Boxers

cervical spinal pain

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9
Q

What drugs and vaccines can cause non-erosive IMPA?

A

DRUGS - sulfas, penicillins, cephalosporins, phenobarbarbital (Dobermans)

VACCINE - canine distemper virus, feline calicivirus

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10
Q

What is systemic lupus erythematosus (SLE)?

A

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

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11
Q

What are 7 major signs of SLE?

A
  1. polyarthritis
  2. glomerulonephritis
  3. hemolytic anemia
  4. thrombocytopenia
  5. leukopenia
  6. skin lesions
  7. myositis
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12
Q

What are 4 minor signs of SLE?

A
  1. fever
  2. oral ulcerations
  3. lymphadenopathy
  4. CNS signs
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13
Q

What is erosive polyarthritis?

A

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
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14
Q

What are 6 causes septic arthritis?

A
  1. bacterial - Staph, Sterp, Mycoplasma, Pasteurella, L-form, Bartonella
  2. fungal - Blasto, Coccidio, Crypto
  3. viral - distemper, calicivirus
  4. Leishmania
  5. Lyme
  6. Anaplasma phagocytophilium, Ehrlichia ewingii, RMSF

(usually only one joint affected)

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15
Q

What pattern on septic arthritis is associated with bacteremia?

A

a few, large proximal joints - shoulder, hip, elbow, stifle

  • infection demonstrated within joints +/- blood or urine
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16
Q

What are the 5 most common presenting complaints in patients with polyarthritis?

A
  1. reluctance to walk, walking on eggshells, stiff gait, lameness, etc.
  2. pain localized to joints
  3. joint swelling common in carpi, tarsi, or stifles
  4. systemic: cyclic fever, lethargy, anorexia
  5. neck or back pain
17
Q

What are radiographic signs of non-erosive and erosive polyarthritis?

A

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!)

18
Q

What are the 10 criteria for diagnosing erosive polyarthritis?

A
  1. stiffness
  2. pain on manipulation of at least one joint
  3. signs of arthritis for 3 months
  4. periarticular soft tissue swelling
  5. typical radiographic changes*
  6. inflammatory synovial fluid*
  7. symmetrical deformations of distal joints
  8. detection of RF in serum
  9. histological changes on synovium
  10. extra-articular symptoms, lymphadenopathy

(5 = probable, 7 = definitive)

19
Q

How can rheumatoid factors be found when trying to diagnose erosive polyarthritis?

A

antibodies to IgA or IgM founf in synovial fluid or serum —> not specific or significant for idiopathic erosive PA

20
Q

What 6 diagnostics are used to find underlying causes and determine treatment of polyarthritis?

A
  1. spinal radiographs - diskospondylitis
  2. thoracic radiographs - neoplasia, pneumonia
  3. abdominal ultrasounds - neoplasia, pancreatitis, pyelonephritis
  4. echocardiogram - vegetative lesion on valve (steroid can worsen!)
  5. blood cultures
  6. infectious disease testing - Bartonella
21
Q

What diagnostic is used for SLE?

A

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
22
Q

What are LE cells?

A

phagocytized nuclear remnants, rarely seen but diagnostic of SLE

23
Q

How are meningitis and myositis commonly seen with SLE/PA diagnosed?

A

MENINGITIS - CSF tap, serum IgA —> neutrophilic or mixed leukocytes pleocytosis

MYOSITIS - serum CK, EMG, muscle biopsy

24
Q

What are the 3 aspects of treating erosive IMPA?

A
  1. treating underlying disease - reactive, Type II-VI; corticosteroids (contraindicated for infective endocarditis), removal of drugs, wait on vaccines
  2. analgesia - NSAIDs (if not on corticosteroids), opioids
  3. immunosuppression - Type I idiopathic, SLE, erosive PA, PA with meningitis and myositis
25
Q

What primary immunosuppressives are recommended for erosive IMPA? What are 4 second line immunosuppressives?

A

Prednisone - 2 mg/kg/day

  1. Leflunomide*
  2. Cyclosporine*
  3. Mycophenolate
  4. Azathioprine
26
Q

What 2 responses are expected with immunosuppressive treatment of erosive IMPA?

A
  1. improvement with pain and welling - within 7 days
  2. substantial decrease in WBCs in synovial fluid - repeat taps prior to tapering doses*, indicated in cases with relapse
27
Q

When are patients in remission for erosive IMPA? How should drugs be changed at this point?

A

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)
28
Q

What is prognosis of IMPA like?

A
  • 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