Unit 4 SIGS cases 1-6 | Baamboozle - Baamboozle | The Most Fun Classroom Games!

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

Describe the pathophysiology of acute HIV

attachment (gp120, CD4r, CCR5) -> penetration -> uncoating -> reverse transcription -> integration of new vDNA -> transcription -> translation -> release

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

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.

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

Characterize the clinical presentation of SLE.

increased anti-DNA antibodies, decreased complement levels, malar (butterfly) rash, alopecia, discoid rash (chronic, scaring), arthralgia, myalgia

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

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

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

Explain the benefits associated with folic acid supplementation during methotrexate therapy.

Supplemental folic acid helps to alleviate the adverse effects of dihydrofolate reductase inhibition

Explain how methotrexate relieves symptoms of rheumatoid arthritis

mimics folate and blocks synthesis of tetrahydrofolate (inhibits dihydrofolate reductase)-> reduces pain & swelling

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 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.

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

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

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

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

Characterize Borrelia burgdoferi (structure, physiology, epidemiology, mode of transmission).

Spirochete, flagella, outer surface proteins (virulence factor), U.S., Canada, Europe; Ixodes tick vector

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

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

Why are clavulanate and amoxicillin used to treat acute otitis media?

Clavulanate is synergistic with amoxicillin to prevent degradation by beta-lactamase

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

Most common bacterial and viral pathogens causing acute otitis media in children?

Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis