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Unit 4 SIGS cases 1-6

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    Unit 4 SIGS cases 1-6 SSOs / WFAs
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  • Most common bacterial and viral pathogens causing acute otitis media in children?
    Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis 
  •  15
  • Diagnostic tests to differentiate and identify bacterial and viral causes of acute otitis media.
    oxidase, catalse, nitrate reduction, butyrate esterase, Blood/chocolate agar, gram stain
  •  15
  • Why are clavulanate and amoxicillin used to treat acute otitis media?
    Clavulanate is synergistic with amoxicillin to prevent degradation by beta-lactamase
  •  15
  • Name OMT techniques to treat acute otitis media and state why this is effective.
    Galbreath, auricular drainage, lymphatic pump; Promotes drainage of lymph to decrease pathogen proliferation
  •  15
  • Describe the signs and symptoms of Lyme disease.
    1. erythema migrains (target rash), flu-like symptoms 2.  bilateral Bell's palsy, AV nodal block 3. arthritis , encephalopathy 
  •  15
  • Characterize Borrelia burgdoferi (structure, physiology, epidemiology, mode of transmission).
    Spirochete, flagella, outer surface proteins (virulence factor), U.S., Canada, Europe;  Ixodes tick vector
  •  15
  • Explain the pathogenesis of infection with Borrelia burgdoferi and Lyme-disease causing organisms.
    Infected Ixodes Tick bite-> binding of OspC to plasminogen-> if bite lasts 36-72+ hrs, spread via bloodstream->Early stage-> Early disseminated--> Late stage
  •  15
  • Describe and justify the two-tiered serologic testing for diagnosing Lyme Disease
    EIA or IFA -> (positive) -> IgM and IgG Western blot (30- days) OR IgG Western Blot (30+ days); cross reaction --> false positive
  •  15
  • Explain the delayed onset of symptoms following exposure to Toxicodendron species.
    Due to the time that it takes to activate and recruit T cells to the site
  •  15
  • Explain how the immune response induces skin changes (vesicles and bullae) in type IV hypersensitivity reactions.
    activated T lymphocytes-> (1) release cytokines, inflammation & macrophage activation (2) T cell-mediated cytotoxicity -> ROStissue damage-> skin changes
  •  15
  • Discuss the role of haptens, including urushiol, in the immune response (priming of T cells).
    Small, enter skin -> bind self-proteins -> Langerhans recognizes & goes to lymph-> MHC-II binds -> TH1 release IL2 -> release IFN -> macrophage -> inflammation
  •  15
  • Explain why antihistamines are NOT an effective treatment for Toxicodendron dermatitis.
    The itching is not caused by histamine release; the itching sensation is due to other granules that are released.
  •  15
  • Characterize the serologic workup for rheumatoid arthritis
    RF= IgM rheumatoid antibody binds modified IgG; ACPA= anti-citrullinated peptide antibodies; ESR= correlates w/ disease activity; CRP= objective measure
  •  15
  • Explain how methotrexate relieves symptoms of rheumatoid arthritis
    mimics folate and blocks synthesis of tetrahydrofolate (inhibits dihydrofolate reductase)-> reduces pain & swelling
  •  15
  • Explain the benefits associated with folic acid supplementation during methotrexate therapy.
    Supplemental folic acid helps to alleviate the adverse effects of dihydrofolate reductase inhibition
  •  15
  • Describe the clinical presentation of rheumatoid arthritis. 
    Swelling and pain in MCP and PIP (DIPs are preserved); morning stiffness 30+ minutes; symmetrical; positive rheumatoid factor, elevated ESR and CRP
  •  15