Week 5 Flashcards
clinical presentation of rheumatoid arthritis
• Inflammation of joints, tendons, bursae; symmetric distribution
• Early morning joint stiffness lasting more than 1 hours that eases with physical activity
• First joints to get it — small joints of hands, feet
Wrists, MCP, PIP joints, sometimes DIP
complications and adverse effects of chronic glucocorticoid use.
susceptibility to infections; acute adrenal insufficiency (with increased stress from infection, surgery, or trauma); cushingoid state (moonface, buffalo hump, central obesity).
autoimmune response inducing the development of rheumatoid arthritis
- genetics + environment (cigarette smoke)
- citrullination of argining to citrulline in DNA encoding Type II collagen which becomes an antigen and is presented by APC’s to T helper cells whcih activate B cells making autoantibodies against self antigens
pathogenesis of RA
- CD4+ T cells become activated by antigen-presenting cells (APCs) through interactions between the T cell receptor and class II major histocompatibility complex (MHC)-peptide antigen (signal 1) with co-stimulation through the CD28-CD80/86 pathway, as well as other pathways
- CD4+ THcells in turn activate B cells, some of which are destined to differentiate into autoantibody-producing plasma cells.
- mmune complexes, possibly comprised of rheumatoid factors (RFs) and anti–cyclic citrullinated peptides (CCP) antibodies, may form inside the joint, activating the complement pathway and amplifying inflammation.
- In RA, bone formation is inhibited through the Wnt pathway, presumably due to the action of elevated levels of DKK-1.
- In addition to inhibiting bone formation, TNF-α stimulates osteoclastogenesis
NSAIDS
- adjunct for analgesic, anti-inflammatory
- COX1,2 inhibitors
- Chronic use»_space; gastritis, peptic ulcer disease, impaired renal function
GLUCOCORTICOIDS
- First, low-moderate doses to get rapid disease control before effective DMARD therapy (takes weeks/months)
- 1-2 week bursts for management of acute disease flares
- Chronic administration – low dose (5-10mg/d of prednisone or equivalent) – in those with poor response to DMARD therapy
- But prednisone causes osteoporosis and other long-term complications; Use bisphosphonate to prevent osteoporosis in those gettig 5mg/d or more of prednisone for >3months
DMARDs
- hydroxychloroquine, sulfasalazine, methotrexate, and leflunomide;
- they exhibit a delayed onset of action of approximately 6–12 weeks
how rheumatoid arthritis may lead to irreversible, debilitating joint damage
RA affects synovial tissue and underlying cartilage and bone
rationale for administering influenza and pneumococcal conjugate vaccine in patients with rheumatoid arthritis
about to put this patient on immunosuppressive drugs so you want to be sure they are fully vaccinated before doing so. They will be prone to infection with these meds, so it’s just a precaution.
CRITERIA FOR THE CLASSIFICATION OF GLOBAL FUNCTIONAL STATUS IN RHEUMATOID ARTHRITIS
- Class I Completely able to perform usual activities of daily living (self-care, vocational, and avocational)
- Class II Able to perform usual self-care and vocational activities, but limited in avocational activities
- Class III Able to perform usual self-care activities, but limited in vocational and avocational activities
- Class IV Limited in ability to perform usual self-care, vocational, and avocational activities
RA vs OA
RA: autoimmune disorder, symmetric joints affected, morning stiffness, bone eroision, swan neck/boutonniere/ulnar deviation
OA: mechanical degeneration, weight bearing joints affected, stiffness with overuse, herberden and bouchard nodes
clinical manifestations of SLE
- Musculoskeletal symptoms: arthritis, myalgia
- Mucocutaneous manifestations: Erythematous rash on cheeks and bridge of nose (malar rash) lasting days to weeks, Discoid scaly erythematous plaques on scalp, face, and neck
- Kidney: renal disease is usually present
- Vascular manifestations: raynauds, DVT
- Pulmonary involvement
- GI involvement
- Cardiac involvement: pericarditis, myocarditis
- Hematologic: anemia, thrombocytopenia, leukopenia
mmunopathology of SLE-induced anemia
-Autoantibodies directly react to human antigens, immune complexes are deposited in tissue and blood vessels, and the complement cascade is activated, which results in inflammation and organ damage.
risk factors for developing SLE
- Age: between ages 15 and 44 years;
- Sex: females
- Genetics: Evidence of familial susceptibility
- Ethnicity/race: More common and more severe in African American
significance of hypocomplementemia in the pathophysiology of SLE
- Engulfment of apoptotic cells via complement prevents a prominent inflammatory response from occurring
- inability of macrophages to clear apoptotic cells effectively is associated with an increased display of apoptotic cell debris on the surfaces of dendritic cells, where it may be presented to autoreactive lymphocytes
