9344401
Description
Flashcards by Amelia Claire, updated more than 1 year ago
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Created by Amelia Claire
almost 7 years ago
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| Question | Answer |
| osteoarthritis | not inflammatory, degenerative joint disease progressive loss of cartilage from the joints progression from bone to thinning cartilage and destruction. can affect any joints. treatment = lifestyle, analgesics, surgery, patient centred, individual |
| drugs for osteoarthritis | paracetamol NSAIDs corticosteroids heat/ice capsaicin topical formulation hyaluronic acid opioids lidocaine patches glucosamine and chondroitin may slow progression of joint disease - try for 8 weeks and determine if pain reduced. |
| rheumatoid arthritis | inflammatory cause not fully understood, but is an atypical immune response whereby immune system attacks joints leading to damage considered chronic autoimmune disease - appears mainly in digits (poor blood supply?)( inflammation of synovial membrane, leukocyte infiltration (macrophages, neutrophils, T&B lymphocytes, plasma cells and cytokines - IL-1, TNF alpha and IL-6) |
| pro inflammatory mediators | following cytokines TNF-alpha (trimeric structure) IL-1 IL-6 |
| anti-inflammatory mediators | following cytokines TGF-Beta IL-10 |
| Dugs for RA (analgesics) | NSAIDs Paracetamol Codeine (analgesics) |
| disease modifying agents (DMARDs) | synthetic and biological glucocorticoids administered to control the disease rather than just manage symptoms of pain |
| synthetic DMARDs | methotrexate sulphasalazine hydroxycholroquine leflunomide |
| methotrexate | synthetic DMARD folic acid antagonist inhibits DNA synthesis and cell replication by competitively inhibiting conversion of folic acid to dominic acid, with cytotoxic, immunosuppressive and anti-inflammatory action. MOA: competitively inhibits dihydrofolate reductase (DHFR) an enzyme that precipitates synthesis to the active form of folate, needed for the synthesis of nucleotides. methotrexate decreases circulating purine and pyrimidine, making them less available for DNA and RNA synthesis which may affect immune cell proliferation and cytokine expression. |
| sulfasalazine | pro-drug synthetic DMARD used in churns, exact MOA unknown, local anti-inflammatory action. |
| hydroxychloroquine | synthetic DMARD OG antimalarial increases pH of lysosomes from 4-6 causes decreased intracellular processing, glycosylation and secretion of proteins, with many immunological and non-immunologic consequences. these effects are believed to be the cause of decreased immune cell functioning, such as reduced chemotaxis, phagocytosis and superoxide production by neutrophils. |
| leflunomide | synthetic DMARD competitie inhibitor of dihydroorotate dehydrogenase (rate limiting enzyme in de novo synthesis of pyrimidines) hence reduces lymphocyte proliferation specific for activated T lymphocytes. |
| biological DMARDs | monoclonal antibodies to TNFalpha: infliximab, adalimumab soluble receptor decoy for TNFalpha: (TNFalpha agonist) etanercept receptor antagonist to IL-1 anakinra (cytokine modulator = neutralises IL-1) monoclonal antibody to CD20 rituximab |
| infliximab | binds to TNF alpha to inhibit its activity TNF alpha is a cytokine involved in inflammatory and immune responses and the pathogenesis of RA, psoriasis and IBD |
| adalimumab | binds to TNF alpha to inhibit its activity TNF alpha is a cytokine involved in inflammatory and immune responses and the pathogenesis of RA, psoriasis and IBD |
| Etanercept | TNF alpha antagonist - binds to TNF alpha and inhibits its actions |
| Anakinra | cytokine modulator, recombinant form of an human interleukin 1 (IL-1) receptor antagonist - neutralises activity of IL-1, which is involved in the inflammatory response |
| rituximab | depletes B- lymphocytes, may suppress inflammatory activity by reducing B-lymphocyte induced T-Cell activation and resulting cytokine production. induces the apoptosis of B-Cells |
| all about TNF alpha Tumor Necrosis Factor | TNF alpha is a potent pro-inflammatory cytokine, mainly produced by monocytes. it is a major contributor to the inflammatory and destructive changes that occur in RA. a blockade of TNFalpha results in the reduction in a number of other pro-inflammatory cytokines, (IL-1, IL-6 and IL-8) |
| destructive effects of TNFalpha in joints in RA | bone erosion, swelling, joint space narrowing, bone resorption and cartilage degradation |
| Receptor Antagonist to IL-1 (IL-1RA) | recombinant human IL-1 is a receptor antagonist and prevents IL01 from binding to it's receptor, it decreases IL-1 mediated activity IL-1RA is a member of the Interleukin 1 cytokine family. it is secreted by various types of cells, including immune, epithelial and adipose cells. |
| other immunomodulatory and cytotoxic agents | azathioprine and cyclosporin A additional drugs sometimes used -> high potential for toxicity, typically these drugs are used for extra-articular, life threatening manifestations of RA, such as vasculitis Corticosteroids via injection for systemic effect |
| Gout | gout is related to arthritis; it is peripheral resulting from deposition of sodium rate crystals in one or more joints linked to metabolic disorder (hypercuricemia) which is an excess of uric acid that deposits in the joints, lactate builds in synovial joints and this decreases pH leading to rate crystallisation there is an immune reaction to the crystals, activation of complement and kinin systems, accumulation of neutrophils and chemotactic mediators |
| gout treatment targets | dietary restriction of exogenous purines (meats) xanthine oxidase inhibitors acton the endogenous purines. recombinant uricase acts on the body's urate pool, and uricosuric agents act on renal tubules |
| acute pharmacological treatment of gout | NSAIDs and paracetamol, but not aspirin, as aspirin competes with uric acid for exretion colchicine - destabilises microtubules and hinders their polymerisation, affecting immune cell's division and movement corticosteroids (intra-articular and short term only) |
| chronic treatment of gout | allopurinol (pro-drug) alloxantlhine inhibits xanthine oxidase, reducing production of uric acid |
| prophylactic treatment of gout | probenecid (uricosuric drug) inhibits the tubular reabsorption of urate, increasing the urinary excretion of uric acid and decreasing soluble urate levels |
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