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Flashcards in Autoimmune disease Deck (42)
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Outline the pathophysiology of immune mediated joint disease

- Failure of self-tolerance or alteration of self antigens so they are not recognised as self e.g. due to bacteria, drugs etc.
- Type III hypersensitivity reaction i.e. formation of immune complexes which deposit in synovial membrane


Outline the clinical presentation of immune-mediate polyarthritis

- Lethargy, stiffness, pyrexia
- Multisystemic signs e.g. depression, anorexia
- Joint palpatioin may show heat, swelling, crepitus, ligamentous laxity
- Polyarticular lameness
- May be waxing and waning, and shifting lameness
- May not appear lame if all limbs affected


What are the classifications of immune-mediated polyarthritis?

- Type I: idiopathic
- Type II: remote infection
- Type III: gastrointestinal disease
- Type IV: remote neoplasia


Explain how a type III hypersensitivity reaction leads to polyarthritis

- Deposition of complexes in synovium
- Leads to complement activation and inflammatory cell chemotaxis and cytokine release

- Leads to synovitis, inflammatory joint effusion, joint swelling and pain


You are suspicious of a case of immune mediated polyarthritis. Which tests would you use in order to work up this case and why?

- Synovial fluid analysis
- Radiography of joints if erosive suspected
- Urinalysis (rule out infection, assess glomerular damage)
- Screening for underlying disease with thoracic radiographs, abdominal ultrasound, +/- LN aspirates


What are the main methods required for the diagnosis of immune mediated polyarthritis?

Clinical signs and synovial fluid


Describe the typical results expected from synovial fluid in a case of immune mediated polyarthritis

- Increased volumes of turbid fluid from affected joints
- High numbers of non-degenerate, non-toxic neutrophils


Outline the radiographic appearance of non-erosive immune mediated polyarthritis on radiography

- Typically no bone abnormalities
- Joint effusions often seen but subtle


Outline the pathophysiology of erosive immune mediated polyarthritis

- Chronic synovitis leads to production of proliferative granulation tissue (pannus)
- Pannus invades articular cartilage, can erode subchondral bone
- Pannnus and inflamed synovium produce enzymes incl. proteases and collagenases leading to further joint destruction e.g. rheumatoid arthritis


In a case of immune mediated polyarthritis, what is the primary treatment?

Medical, following treatment of underlying cause if identified, using prednisolone initially (2-4mg/kg/day)


What drugs may be required as adjuncts to prednisolone in the treatment of IMPA?

- Azathioprine
- Ciclosporin (most popular)
- Cyclophosphamide (becoming less popular)
- leflunomide


What is the major side effect of cyclophosphamide?

Haemorrhagic cystitis


Briefly outline the use of leflunomide in the treatment of IMPA

- Newer drug, used in refractory cases
- Some evidence for usefulness


Compare the treatment of erosive and non-erosive IMPA

- Non-erosive typically easily treated with prednisolone alone, can add others if needed
- Erosive usually requires combination therapy


Outline the safety requirements for the use of drugs such as azathioprine and cyclophosphamide in the treatment of IMPA

- Cytotoxic, close monitoring required
- Cannot split tablets, but can send to lab for "repackaging"
- Must wear gloves


How is response to treatment for IMPA determined?

Mainly based on clinical signs, but can base decision on synovial fluid analysis cell counts


Outline a general approach to the management of a type I non-erosive IMPA

- Start on prednisolone 2-4mg/kg/day for 3 weeks
- At re-check, repeat synovial fluid testing to determine response (reduction in cell count)
- If poor response, add adjunctive drug or reassess diagnosis
- Taper pred over period of 3-6 months


What are the main risks related to repeated synoviocentesis in the monitoring of IMPA treatment?

- Risk of septic arthritis
- Risks of anaesthetic for each procedure


discuss the surgical treatment of IMPA

- High failure rates due to ongoing inflammation and effects of drugs on healing
- May need to stabilise cruciate deficient stifle
- Radical synovectomy may reduce production of inflammatory mediators


Compare the prognosis for erosive and non-erosive IMPA

- Non-erosive variable
- Erosive grave


What is the prevalence and prognosis for joint tumours in dogs and cats?

Uncommon and poor prognosis, usually malignant


Describe the commonly clinical presentation of joint tumours

Usually present with lameness affecting one limb only


Outline the pathogenesis of joint tumours

Are not tumours of the articular cartilage, are tumours of subchondral bone at articular margins that secondarily involve the joint


What is the most common joint tumour?

Synovial cell sarcoma


Give examples of less common joint tumours

- Rhabdomyosarcoma
- Myxoma/sarcoma
- Malignant fibrous histiocytoma
- Liposarcoma
- Undifferentiated sarcoma
- Melanoma
- Solitary plasmacytoma


What tests are required for the diagnosis of a joint tumour?

- Survey radiographs
- Immunohistochemistry
- Histopathology


Outline the radiographic appearance of a joint tumour

- Partially lobulated soft tissue mass adjacent to tendon sheath, joint or bursa
- Bone destruction in 10-45% of dogs, and >2 bones involved in 10%


Describe the radiographic appearance of bone destruction due to a joint tumour

- Smooth and well-delineated due to pressure necrosis from expansile mass
- Less distinctive ysis due to soft tissue infiltration of bone
- Bone destruction can appear as either permeative lysis or punctate bone loss


What method is used to diagnose synovial cell sarcomas specifically?

Cytokeratin immunohistochemistry


What method is used to diagnose histiocytic joint tumours specifically?

Cell morphology and CD18 immunohistochemistry