pharma test 3 ch 12 and 17.txt

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  1. What is immunity and potential triggers
    The ability of the body to defend itself; infectious agents, foreign cells, abnormal cells
  2. Naturally acquired immunity
    acquired naturally via infection (chicken pox)
  3. Artifically acquired immunity
  4. Nonspecific (innate) immunity
    present at birth, providing immediate and general protection
  5. Specific (acquired) immunity
    effective in response to a foreign agent, develops in response to that agent and once established will respond to future exposures of that agent
  6. B cells
    produced in bone marrow, form antibodies, have immunoglobulins IgA, IgD, IgE, IgG, IgM
  7. T cells
    produced in bone marrow, mature in thymus, have subsets CD4+ and CD8+
  8. CD4+ cells
    T cells; class II histocompatibility molecules; essential for both cell and antibody related immunity
  9. CD8+ cells
    T cells; class I histocompatibility molecules; also cytotoxic T lymphocytes
  10. Two categories of histocompatibility molecules
    monozygotic (identical human twins, can accept tissue transplants from each other) and non-monozygotic (unique set of histocompatibility molecules, tissue transplants will provoke an immune response and could end up with transplant being rejected)
  11. Time course of nonspecific (innate) and specific (acquired) immunity
    innate - 12 hrs after infection acquired - up to 5 days after infection
  12. Six mechanisms in nonspecific (innate) immunity
    physical or chemical barriers (contain chemicals that destroy foreign invaders), phagocytosis (marophage eats other cell), natural killer cells (specialized leukocytes destroy abnormal cells), fever (stimulates phaocytes), interferon and inflammation
  13. Four processes of an inflammatory reaction
    redness, swelling, heat and pain
  14. Phases of wound healing
    haemostasis, inflammation, proliferation, remodelling
  15. When does regeneration and/or fibrosis happen?
    depends on the type of tissue damaged and the severity of the injury
  16. Three components of the lymphatic system
    vessels (transport lymph, lets immune cells pass in and out); nodes (produce and house lymphocytes and filter lymph) and organs (tonsils, thymus, etc)
  17. Two components of acquired immunity
    humoral (antibodies) and cell-mediated (activated lymphocytes)
  18. Humoral immunity
    B lymphocytes interact with antigen and become activated or they are transformed into plasma cells to produce antibodies
  19. Five immunoglobulins
    IgA (localized protection at mucosal surfaces); IgD (activates B lymphocytes); IgE (allergies); IgG (primary and secondary immune responses; neutralizes toxins, bacteria and viruses; crosses placenta) and IgM (protects newborns)
  20. Four types of T lymphocytes
    cytotoxic (killer cells), helper (increases activity of killer lymphocytes), suppressor (suppresses immune response) and memory (rapidly mobilized in response to second antigen encounter)
  21. Four types of hypersensitivity
    Type I (allergic reaction, anaphylaxis on subsequent exposure; 15-30 minute response time); Type II (Rh incompatibility; minutes-hours); Type III (immune complex disease; vasculitis, nephritis, arthus reaction, connective tissue diseases; 3-8 hours); Type IV (delayed type; antibodies are not involved unlike Types I - III; eczema; 48-72 bours)
  22. Four organ transplant types
    autograft (tissue grafted from one side to the other in same patient); isograft (tissue donated by identical twin); xenograft (tissue graft harvested from a different animal); allograft (tissue transplant from one human to another)
  23. Three types of anti-inflammatory medication
    analgesic (pain relieving); antipyretic (fever reducing); anticoagulant (inhibits platelet aggregation
  24. Asprin
    analgesic, antipyretic and anticoagulant ( do not reduce stiffness like NSAIDs)
  25. Acetaminophen and Ibuprofen
    analgesic and antipyretic
  26. Eight groups of NSAIDs (nonsteriodal anti-inflammatory drugs)
    salicylates (asprin), parachlorobenzoic acid derivatives (indomethacin), pyrazolone derivatives (phenylbutazone), proprionic derivatives (ibuprofen), fenamates (meclofenamic acid), oxicams (piroxicam), phenylacetic acids (diclofenac), some COX-2 inhibitors (Vioxx)
  27. Glucocorticosteroids (prednisone) fight inflammation by:
    decreasing cytokines, chemokines, adhesion molecules and inflammatory enzymes
  28. Osteoarthritis
    affects 86% of persons over 70, may start in 50's or 60's, results in deformation or mismatched joint surfaces; joint stiffness, pain in weight-bearing joint; may respond to local heat and analgesics early but late stage requires orthopedic or other interventions
  29. Rheumatoid arthritis
    between 30-70 years, mostly in women; joints inflamed, limited range of motion, progression leads to deformity; treat with asprin, NSAIDs, biologics and DEMARDs (disease modifying anti-rheumatic drugs)
  30. DEMARDs for RA
    immunosuppressive (methotrexate); antimalarial (Chloroquine); gold compounds (Auranofin); Chelator (Penicillamine); sulfa drugs (Sufasalazine); antihelmintic (levamisole)
  31. Biologics
    Three classes - white blood cell modulators, TNF (tumor necrosis factor) inhibitors, IL-6 (Interleukin-6) inhibitors
  32. Gout
    recurrent episodes or arthritis due to deposits of monosodium urate in joints and cartilate; treated with natural alkaloids, NSAIDs, uricosuric agents, xanthine oxidase inhibitors
  33. Autoimmunity
    immune system recognizes the difference between the individual's own tissues and those of invaders; develops antibodies to own tissues; lupus, scleroderma
  34. Four types of lupus
    Systemic (half organ threatening, half non-threatening), discoid (limited to skin of face, neck and scalp), drug-induced (only 4%, brought on by 70 different prescriptions)and neonatal (very rare, acquired from passage of maternal antibodies); mostly women

    • Scleroderma
    • autoimmune of connective tissue involving changes in blood vessels, skin, muscles and internal organs; two types - localized (reddish patches of skin, oval shaped, devoid of sweat glands and hair; also linear where it's a single line or band of thickened skin) and systemic (gradual in appearance on fingers, hands, face, lower arms & legs), mostly in women

    • CREST
    • systemic scleroderma; calcinosis, Raynoud's phenomenon, esophageal dysfuntion, sclerodactyly & telangiectasia

    • HIV
    • Human immunodeficiency virus; transmitted via contaminated body fluids

    • AIDS
    • acquired immunodeficiency virus; long latency period during which virus multiplies infecting and killing CD4 lymphocytes

    • Five characteristic traits of AIDS
    • destroys individual's immune system; increased susceptibility to infection; pandemic; HIV; transmitted via contaminated body fluids

    • Three diagnostic indicators of AIDS
    • presence of HIV antibodies; antibodies produced within first 3 months of infection; CD4 T-lymphocyte count less than 200

    • Treatment of AIDS
    • no cure, but medications may hinder HIV replication; goal is to prevent total distruction of immune system; highly active antiretroviral therapy (HAART)

    • Five classes of medications used to treat AIDS
    • non-nucleoside reverse transcriptase inhibitors (NNRTIs); nuceloside reverse transcriptase inhibitors (NRTIs); Protease inhibitors (PIs); Fusion inhibitors; integrase inhibitors

    • Active v. Passive immunity
    • active = exposure to disease or immunization; passive = natural (maternal antibodies) or vaccination against effects (immediate but no long term effects)
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pharma test 3 ch 12 and 17.txt
ch 12 and 17 pharma test 3
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