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.
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
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
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
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.
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
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
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)
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.
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)
11
Q
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