pathophysiology Flashcards

autoimmunity: recognise the mechanisms of autoimmunity and how they apply to autoimmune rheumatic disease; recall major autoantibody systems which are used in the diagnosis and management of rheumatological disease

1
Q

key auto-antibodies in rheumatoid arthritis

A

rheumatoid factor, anti-cyclic citrullinated peptide antibody

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2
Q

key auto-antibodies in systemic lupus erythematosus

A

antinuclear antibodies, anti-double stranded DNA antibodies

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3
Q

key auto-antibodies in diffuse systemic sclerosis

A

anti-Scl-70 antibody

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4
Q

key auto-antibodies in limited systemic sclerosis

A

anti-centromere antibodies

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5
Q

key auto-antibodies in dermato/polymyositis

A

anti-tRNA transferase antibodies

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6
Q

key auto-antibodies in mixed (overlap) connective tissue disease

A

anti-U1-RNP antibodies

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7
Q

where are antinuclear antibodies present

A

all systemic lupus erythematosus cases, but not specific to it

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8
Q

what are anti-double stranded DNA antibodies specific for

A

specific for systemic lupus erythematosus

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9
Q

what does serum level of anti-double stranded DNA antibodies in systemic lupus erythematosus correlate with

A

disease activity, so can change over time

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10
Q

what are antinuclear antibodies reacting to

A

nuclear antigens

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11
Q

what happens if antinuclear antibodies test is positive

A

further tests will be performed to determine which type of antinuclear antibody it is, including anti-double stranded DNA antibodies and anti-Sm (both more specific to SLE)

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12
Q

what do patients with systemic lupus erythematosus commonly have low and high levels of during high disease activity

A

producing more immune complexes, so measure complement and antibody response: low complement levels (can see it declining as patient becomes more unwell as complement used up), high serum levels of anti-double stranded DNA antibodies (can see it rising as patient becomes more unwell)

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13
Q

pathogenesis of systemic lupus erythematosus

A

apoptosis leads to translocation of nuclear antigens to membrane surface -> impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens to immune cells (e.g. Sm) -> B cell autoimmunity -> tissue damage by antibody effector mechanisms e.g. complement activation and Fc receptor engagement

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