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Antibodies bind to circulating antigens in blood and body fluids resulting in the formation of immune complexes that deposit in tissues and vessel walls. These immune complexes activate complement and neutrophils resulting in tissue destruction.

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Joints
Not organ specific
Most commonly result in a vasculitis in the skin, kidney, or lungs

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Collagen, Immunoglobulin G (Ig G)

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Also type 4 mechanism of hypersensitivity

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Also type 4 mechanism of hypersensitivity

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Cell mediated reaction: T1 helper cells produce interferon gamma resulting in the activation of macrophages and T cytotoxic cells that attack the target cell through the release of destructive enzymes.

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Genetics (60% risk)

Susceptibility genes (ex. HLA-DR81)

Epigenetic modifications

Non-Genetic Risk Factors (40% of risk)

Smoking

Microbiota

Female sex

Western diet (high intake of pre-packaged food, red/ processed meat, high sugar drinks, etc.)

Ethnic factors (non-Hispanic African Americans at increased risk)

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Clinical Manifestation: appear gradually over a period of weeks or months

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Clinical Manifestation: appear gradually over a period of weeks or months

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fever

fatigue

weakness

anorexia

weight loss

generalized aching

stiffness

Due to joint inflammation, some may experience loss of mobility

Loss in joint motion can lead to atrophy of the surrounding muscles and joint deformities
Can cause joint deformities in:

fingers

feet

contractures of knees and hips

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Antibodies bind to circulating antigens in the blood or body fluids, form immune complexes
Immune complexes are then deposited in vascular tissues or vessel walls
Complexes activate the complement cascade through C1 and generate fragments, including C5a (chemotactic for neutrophils- migrate to inflamed area and attach to the IgG) and C3b (in the immune complexes)
Neutrophils attempt to phagocytose the tissue (unsuccessfully) and release degradative enzymes that destroy healthy tissues
Two major subtypes: presence or absence of ACPA's

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NSAIDs

Glucocorticoids

Intra-articular steroid injections

Physical/occupational therapy along with therapeutic exercise

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https://www.youtube.com/watch?v=r8PjxvR6Dqw

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Rheumatoid Arthritis Nursing NCLEX Lecture: Symptoms, Treatment, Interventions, Medications

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Osteoclast generation resulting in bone destruction, the hallmark of RA. Inflammation can spread to the articular cartilage, fibrous joint capsule, bone, and surrounding ligaments and tendons, causing pain, joint deformity, and loss of function

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synovium in normal joints: thin delicate linking that serves as an important source of nutrients for cartilage and produces lubricant for joints
synovial lining is hypertrophied, 8-10 cells thick (typically 1-3 cells thick) --> invades and erodes cartilage and bone
subintimal area of synovium typically has very few cells, but with RA is heavily infiltrated with T and B lymphocytes, macrophages and mononuclear cells --> accompanied by angiogenesis