The science behind RA Flashcards

1
Q

Definition

A

Chronic, bilateral, symmetrical, polyarticular, inflammation of te joints.

, typically the knuckles amd proximal interphalyngeal joints.

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2
Q

Panus?

A

Rheumatoid synovitis, so inflammation of the synovium etc -> characterised by inflammatory cell infiltration, synoviocyte proliferation and neoangiogenesis.

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3
Q

Occurs in which joint in the back?

A

Facet joints (synovial joints within the back. Remember will present as bilateral. Can differentiate from axial spondylitis through if the patient can hyperextend their neck back the way.

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4
Q

Do we get seronegative and sero positive? Which antibodies do we expect to see?

A

Yes. Anti-CCP and potentially also RF in sero-postitive. Seronegative is a clinical diagnosis, and the prognosis is generally much better.

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5
Q

Rf is classically igm ->

A

attaches to fc part of iggg

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6
Q

What is Sjogren’s syndrome?

A

Dyrness of salivary glands, mucous membranes and places that produce fluids. Its another automimmune condition and is therefore associated with other autoimmune conditions such as RA and SLE.

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7
Q

Genetic susceptibilities and polymorphins

A

HLADRB1 (part of HLA-DR4): also CTLA4, c-REL, PTPN22 are all genetic susceptibilities.

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8
Q

What environmental factors can affect ra

A

SMOKING!! Viruses inc: E-Coli, Mycoplasma, periodontal gingivalis and gut microbiome.

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9
Q

What is citrillation ad how does it impact ra?

A

It is a normal process but if it goes wrong it is when we can get anti CCP antibodies.

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10
Q

Hoow do we know tha b cells are involved in pathogenesis in ra?

A

Because of the response to retinxunab -> targets the CD20+ on B cells specifically. May not be of use in sero negative because they aren’t producing their anti ccp antibodies and so the b cell lymphocytes will probably be less active and involved in the pathogenesis.

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11
Q

What are plasma cells?

A

They are what b cells differentiate into when they start producing large amounts of antibodies.

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12
Q

*Imbalance too much inflammation and not enough control of it
(TRregs)

A
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13
Q

What are the systemic effects that can be seen in ra? What causes them?

A

SO very heavily influenced by IL-6 and TNF alpha.
Uncontrolled chronic inflammation.
Vascular and cardiac: More phatty deposits, and altered lipid metabolism.
Liver -> anaemia of chronic disease (IL-6 increases hepacidin -> dyregulation of iron)
Lung -> interstitial disease/fibrosis
Brain -> fatigue and secondary fibromyalgia
Muscles -> Sarcopaenia
Bone -> Osteoporosis
Secondary Sjogren’s syndrome

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14
Q

What produces the proteases and what does it cause?

A

Synovcytes, especially when they are in their crazy stage. Causes degeneration of the articular cartilage.

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