Rheumatoid Arthritis Flashcards

1
Q

What is RA?

A
  • Chronic, systemic disease
  • Inflammation of connective tissue in the diarthrodial (synovial) joints.
  • Typically with periods of remission and exacerbation.
  • Frequently accompanied by extra-articular manifestations.
  • It can occur at any time of life, but most people develop RA between the ages of 25 and 50.
  • One in 100 Canadians have RA, with women being affected 2 to 3 times more frequently than men.
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2
Q

Cause

A
  • Genetic predisposition appears to be important in the development of RA. For example, a higher occurrence of the disease has been noted in identical rather than fraternal twins.
  • However, having genes that are conducive to RA does not necessarily mean that you will develop the disease. Something is always needed to light the fire (trigger).
  • An autoimmune etiology is currently the most widely accepted
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3
Q

Behaviors

A

Joints

  • Specific articular involvement is manifested clinically by pain, stiffness, limitation of motion, and signs of inflammation (e.g., heat, swelling, tenderness)
  • Fatigue, weight loss and generalized stiffness may precede the onset of arthritic complaints
  • Joint symptoms occur symmetrically
  • Frequently affect the small joints of the hands and feet
  • Larger peripheral joints such as wrists, elbows, shoulders, knees, hips, ankles, and jaw may also be involved. The cervical spine may be affected, but the axial spine is generally spared
  • Most common - a slow onset of joint pain and stiffness starting in one joint and spreading to involve more joints over a period of weeks to months.
  • Joint stiffness after periods of inactivity.
  • Morning stiffness may last up to several hours or more, depending on disease activity.
  • Metacarpophalangeal (MCP) and Proximal interphalangeal (PIP) joints are typically swollen.
  • In early disease, the fingers may become spindle shaped from synovial hypertrophy and thickening of the joint capsule.
  • Joints become tender, painful, and warm to the touch.
  • Joint pain may increase with motion, vary in intensity, and may not be proportional to the degree of inflammation.
  • As disease activity progresses, inflammation and fibrosis of the joint capsule and supporting structures may lead to deformity and disability.
  • Atrophy of muscles and destruction of tendons around the joint cause one articular surface to slip past the other (subluxation).

Deformity

  • Ulnar drift, Boutonniere deformity, Swan neck deformity, Hallux valgus

Extra-articular manifestations

  • RA can affect nearly every system in the body
  • Three most common are rheumatoid nodules, Sjögren syndrome, and Felty syndrome
  • Rheumatoid nodules develop in up to 25% of all clients
  • Rheumatoid nodules appear subcutaneously as firm, non-tender, granuloma-type masses and are usually over the extensor surfaces of joints such as fingers and elbows
  • Nodules develop insidiously and can persist or regress spontaneously
  • RA - Complications
  • Flexion contractures and hand deformities cause diminished grasp strength and affect the client’s ability to perform self-care tasks.
  • Nodular myositis and muscle fibre degeneration can lead to pain similar to that of vascular insufficiency.
  • Cataract development and loss of vision can result from scleral nodules.
  • On the skin, nodules can ulcerate, similar to pressure sores.
  • Nodules on the vocal cords lead to progressive hoarseness.
  • Nodules in the vertebral bodies can cause bone destruction.
  • Carpal tunnel syndrome
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4
Q

Diagnositcs Studies

A
  • Positive Rheumatoid Factor (approx. 80% of clients)
  • Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) - general indicators of active inflammation
  • Synovial fluid analysis in early disease often shows a straw-coloured fluid with many fibrin flecks
  • White blood cell (WBC) count of synovial fluid is elevated (greater than 2.0 × 109/L)
  • Anti-CCP (anti-cyclic citrullinated peptide) antibody – specific marker
  • X-rays are not specifically diagnostic of RA, bone scans more useful
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5
Q

Disease-Modifying Anti-Rheumatic Drugs (DMARDs)

A

Therapeutic effect: DMARDs suppress inflammation and help to prevent damage to the joint - slows the disease process by modifying the immune system.

  • Prescribing DMARDs early on is important to prevent long-term damage.
  • Starts to work in approx. 6-8 weeks; however, some may take longer - up to 3-4 months.
  • While waiting for DMARDs to take effect, an additional medication such as a steroid or an NSAID may be prescribed to help control the symptoms.
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6
Q

Methotrexate

A
  • Inhibits DNA, RNA, protein synthesis
  • Usually the first drug of choice
  • Rapid anti-inflammatory effect - may be seen as early as 3 to 6 weeks
  • Given either as tablets or injection (once a week)
  • Side effects include bone marrow suppression and hepatotoxicity
  • Requires frequent laboratory monitoring, including CBC, hepatic and renal function
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7
Q

Hydroxychloroquine (Plaquenil)

Sulfasalazine (Salazopyrin)

A

Hydroxychloroquine (Plaquenil)

  • originally used to treat malaria
  • Suppresses formation of antigens
  • Given as a tablet, once or twice a day
  • Risk of ocular toxicity or ototoxicity

Sulfasalazine (Salazopyrin)

  • Blocks prostaglandin synthesis
  • Given as tablets, usually twice a day
  • May cause orange-yellow discoloration of urine or skin
  • Contraindicated for those allergic to sulfa
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8
Q

Gold Salds

A
  • Anti-inflammatory action and may decrease phagocytosis and lysosomal activity
  • Usually given in a weekly injection for five months, then biweekly or monthly to sustain the clinical effects.
  • Most common side effects are skin rashes, mouth ulcers, GI problems, particularly diarrhea, and renal toxicity
  • Parenteral - Myochrysine (gold sodium thiomalate)
  • Oral - Ridaura (Auranofin)
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9
Q

Biologics

A
  • Prevent/suppress inflammation that damages joints.
  • Biologics target molecules on cells of the immune system, joint, and the products that are secreted in the joint, all of which can cause inflammation and joint destruction.
  • Therapeutic effects may be quick (days to weeks) or may take 3-6 months.
  • There are several types of biologics, each of which targets a specific type of molecule involved in this process (tumor necrosis factor, interleukin-1, and cell surface molecules on T and B lymphocytes).
  • Patients who have had an unsatisfactory response to DMARDs, either alone or in combination with other arthritis medications, are usually good candidates for biologics.
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10
Q

TFN and Non TFN biologics

A

TNF biologics

  • Block the action of TNF (tumor necrosis factor)
  • Decreases inflammatory & immune response
  • Administered either by injection or by intravenous infusion.
  • Possible risks: injection site reaction, infusion reaction, infection
  • Etanercept (Enbrel), Infliximab (Remicade), Adalimumab (Humira)

Non-TNF biologics

  • Work via different mechanisms
  • Decreases inflammatory & immune response
  • Administered either by injection or by intravenous infusion.
  • Possible risks: injection site reaction, infusion reaction, infection
  • Anakinra (Kineret), Abatacept (Orencia), Rituximab (Rituxan)
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11
Q
A
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