Study

Unit 4 SIGS cases 1-6

  •   0%
  •  0     0     0

  • 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
  • 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
  • Explain how methotrexate relieves symptoms of rheumatoid arthritis
    mimics folate and blocks synthesis of tetrahydrofolate (inhibits dihydrofolate reductase)-> reduces pain & swelling
  • Relate the laboratory testing modalities utilized in the diagnosis and monitoring of systemic lupus erythematosus to its pathophysiology.
    + direct Coombs test: antibodies acting against RBC; renal biopsy: lupus nephritis management; autoantibodies: contribute to meeting diagnostic criteria
  • 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
  • Describe the signs/symptoms of cryptococcus neoformans infection and explain why flucytosine is used in combination with liposomal amphotericin B.
    Lungs: cough, SOB, CP, fever; Brain: headache, fever, N/V, neck pain, photosensitivity; synergistic for more aggressive treatment of cryptococcal meningitis
  • 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
  • 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
  • Discuss the use of hydroxychloroquine and glucocorticoids in treating auto-immune diseases.
    Hydroxy: May disrupt processing of auto-antigen engagement w/ T cells; Gluco: reduce synthesis inflamm. cytokines & upreg. synthesis of annexin A1
  • 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.
  • Describe the pathophysiology of acute HIV
    attachment (gp120, CD4r, CCR5) -> penetration -> uncoating -> reverse transcription -> integration of new vDNA -> transcription -> translation -> release
  • Characterize Borrelia burgdoferi (structure, physiology, epidemiology, mode of transmission).
    Spirochete, flagella, outer surface proteins (virulence factor), U.S., Canada, Europe;  Ixodes tick vector
  • Explain the benefits associated with folic acid supplementation during methotrexate therapy.
    Supplemental folic acid helps to alleviate the adverse effects of dihydrofolate reductase inhibition
  • 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
  • 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
  • Why are clavulanate and amoxicillin used to treat acute otitis media?
    Clavulanate is synergistic with amoxicillin to prevent degradation by beta-lactamase
  • Evaluate the pathogenesis and risk factors of autoimmune disease, including heritable and environmental factors. (SLE)
    genes & triggers -> anti-nuclear antibody, antigen-antibody complexes -> basement membrane -> complement cascade -> inflammation & hypocomplementemia
  • 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
  • Most common bacterial and viral pathogens causing acute otitis media in children?
    Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis 
  • Contrast the mechanisms of action and efficacies of liposomal amphotericin B, flucytosine, and fluconazole
    L. ampho B: binds ergosterol-> alter permeability; flucy: 5-FU-> FdUMP & FUTP-> inhibit DNA/RNA syn; flucon: inhibition of fungal CP450 decrease ergosterol syn.
  • 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 
  • Describe the CCR5 co-receptor tropism of certain HIV strains.
    tropism= gp120 complex binds CXCR4 (T cell infection only) OR CCR5 (T cell or macrophage infection) OR can bind both (dual tropism); assay determines type
  • Characterize the clinical presentation of SLE.
    increased anti-DNA antibodies, decreased complement levels, malar (butterfly) rash, alopecia, discoid rash (chronic, scaring), arthralgia, myalgia
  • 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