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MSK2 > Autoimmune disease > Flashcards

Autoimmune disease Flashcards

Immune mediated joint disease,

1
Q

Outline the pathophysiology of immune mediated joint disease

A
  • 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
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2
Q

Outline the clinical presentation of immune-mediate polyarthritis

A
  • 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
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3
Q

What are the classifications of immune-mediated polyarthritis?

A
  • Type I: idiopathic
  • Type II: remote infection
  • Type III: gastrointestinal disease
  • Type IV: remote neoplasia
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4
Q

Explain how a type III hypersensitivity reaction leads to polyarthritis

A
  • 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
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5
Q

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

A
  • 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
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6
Q

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

A

Clinical signs and synovial fluid

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7
Q

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

A
  • Increased volumes of turbid fluid from affected joints

- High numbers of non-degenerate, non-toxic neutrophils

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8
Q

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

A
  • Typically no bone abnormalities

- Joint effusions often seen but subtle

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9
Q

Outline the pathophysiology of erosive immune mediated polyarthritis

A
  • 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
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10
Q

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

A

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

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11
Q

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

A
  • Azathioprine
  • Ciclosporin (most popular)
  • Cyclophosphamide (becoming less popular)
  • leflunomide
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12
Q

What is the major side effect of cyclophosphamide?

A

Haemorrhagic cystitis

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13
Q

Briefly outline the use of leflunomide in the treatment of IMPA

A
  • Newer drug, used in refractory cases

- Some evidence for usefulness

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14
Q

Compare the treatment of erosive and non-erosive IMPA

A
  • Non-erosive typically easily treated with prednisolone alone, can add others if needed
  • Erosive usually requires combination therapy
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15
Q

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

A
  • Cytotoxic, close monitoring required
  • Cannot split tablets, but can send to lab for “repackaging”
  • Must wear gloves
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16
Q

How is response to treatment for IMPA determined?

A

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

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17
Q

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

A
  • 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
18
Q

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

A
  • Risk of septic arthritis

- Risks of anaesthetic for each procedure

19
Q

discuss the surgical treatment of IMPA

A
  • 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
20
Q

Compare the prognosis for erosive and non-erosive IMPA

A
  • Non-erosive variable

- Erosive grave

21
Q

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

A

Uncommon and poor prognosis, usually malignant

22
Q

Describe the commonly clinical presentation of joint tumours

A

Usually present with lameness affecting one limb only

23
Q

Outline the pathogenesis of joint tumours

A

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

24
Q

What is the most common joint tumour?

A

Synovial cell sarcoma

25
Q

Give examples of less common joint tumours

A
  • FSA
  • Rhabdomyosarcoma
  • Myxoma/sarcoma
  • Malignant fibrous histiocytoma
  • Liposarcoma
  • OSA
  • Undifferentiated sarcoma
  • MCT
  • SCC
  • Melanoma
  • Solitary plasmacytoma
26
Q

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

A
  • Survey radiographs
  • Immunohistochemistry
  • Histopathology
27
Q

Outline the radiographic appearance of a joint tumour

A
  • 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%
28
Q

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

A
  • 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
29
Q

What method is used to diagnose synovial cell sarcomas specifically?

A

Cytokeratin immunohistochemistry

30
Q

What method is used to diagnose histiocytic joint tumours specifically?

A

Cell morphology and CD18 immunohistochemistry

31
Q

What method is used to diagnose synovial myxomas?

A

Histologic pattern

32
Q

What method is used to diagnose malignant fibrous histiocytoma?

A

Actin

33
Q

Outline the pathophysiology of synovial cell sarcomas

A
  • Malignant tumour from mesenchyal cells within tenosynovial tissue of joints, bursa, tendon sheath
  • Mets to regional LNs and lungs, 32% mets at diagnosis
34
Q

Which sites are most commonly affected by synovial cell sarcomas?

A
  • Stifle most common

- then elbow, shoulder antebrachiocarpal, talocrural and hip joints

35
Q

Describe the histological appearance of synovial cell sarcomas

A
  • 2 cell populations: epitheliod or spindle

- Histological subclassifications of either monophasic or biphasic (both cell types)

36
Q

Describe the signalment of synovial cell sarcomas

A
  • Mean age 6-8 years
  • Males slightly more
  • Flat coated retriever and Golden Retriever predisposed
37
Q

What is the treatment for synovial cell sarcoma?

A

Limb amputation (role of chemo unknown)

38
Q

Outline the prognosis for synovial cell sarcomas with and without treatment

A
  • Overall MST 455days-17mo
  • No treatment MST 93 days
  • Mets reduce MST (<6mo v 46-48mo)
39
Q

What are the prognostic factors for synovial cell sarcomas?

A
  • Clinical stage
  • Surgical dose
  • Histologic grade
  • Positive cytokeratin staining
40
Q

What are the features of a T3, N0, M1 synovial cell sarcoma?

A
  • T3: tumour invading bone and joints
  • N0: no evidence of regonal lymph node involvement
  • M1: evidence of distant metastasis
41
Q

Outline equine immune mediate polyarthritis

A
  • rarely reported
  • Synovitis with IgG complex deposition in foals reported
  • EHV-4 implicated
  • Associated with strep, rhodococcus
  • Most due to systemic infection
42
Q

Outline crystal based arthritis in dogs and cats

A
  • Very rare
  • Deposition of crystal in and around joints causing inflammation, pain
  • Not true gout
  • Periarticualr and synovial deposits of calcium phosphate or pyrophosphate

MSK2 (29 decks)

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