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Unit 4 SIGS cases 7-12
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Describe the bone marrow histopathologic changes in visceral leishmaniasis (reference pancytopenia)
amastigotes=Infected macrophages via reticuloendothelial->bone marrow suppression->Not good immune response->uncontrolled parasite dissemination->pancytopenia
PPSV23 - type vaccine, components, dosing
inactivated polysaccharide conjugate, 23 serotypes, T-cell independent to dependent, adults>65; ages 2-64 with conditions; 2 doses/5 years apart
Pathogenesis of CVID
Intrinsic B cell defects -> impaired differentiation -> no immunoglobulins
Describe the use of PPSV23 in diagnosis in CVID
determine if a lack of functional antibody; measuring serum levels of antibody, against vaccine antigens pneumococcal - CVID = low/absent antibody response
Differentiate between acquired and primary immune deficiency
Primary: result of genetic defects; Secondary: environmental factors - HIV
For CVID, what Immunoglobulin assay results are low - IgA, IgG, IgM? and what do low values mean?
low IgG, low IgA and/or low IgM levels; shortage of these antibodies makes it difficult for people with this disorder to fight off infections)
What is intravenous immunoglobulins (IVIg) treatment for CVID?
IVIg consists of monomeric IgG purified from pooled plasma from healthy donors; reduce inflammation + increase IgG
Characterize Leishmania infantum: structure, physiology, mode of transmission
nonflagellated protozoan in macrophage; reservoir dog->sandfly bite-> protozoa destroys macrophages->reticuloendothelial spread->damage spleen/liver/bone marrow
Describe the different forms of leishmaniasis
cutaneous-skin sores; mucocutaneous-nasal/oral mucosal ulcers; visceral-internal organs affected (spleen/liver/bone marrow)
Discuss why you do not use albendazole to treat cysticerci (calcified cysts) in a patient with seizures and no cerebral edema
Do not treat calcified cysts with antihelminith or corticosteroids but treat with antiepileptic to control the seizures
Explain how taeniasis and cysticercosis can be prevented.
treatment of human cases harboring adult T. solium (to reduce egg transmission); controlled disposal of human feces
Discuss the modes of transmission and life cycle of Taenia solium as they relate to cysticercosis and taeniasis.
host is man->intermediate pig->man has tapeworm->infects pig->man eats pig w/ mature larva->man ill eating eggs->inactive oncosphere->active oncosphere->cysts
Characterize Taenia solium, including structure, physiology, and epidemiology.
cestode, pork tapeworm; monoecious, hooklets on scolex, suckers; ingestion cysticerci in infected-undercooked pork; Latin America/Sub-Sahara Africa/India/Asia
Explain the significance of rouleaux, pancytopenia, elevated serum protein, calcium levels, and circulating plasma cells in the presentation of multiple myeloma.
extensive monoclonal B lymphocyte proliferation->stacks RBCs together; ->overrun bone marrow->anemia; ->osteoclasts increase->hypercalcemia; M-protein spikes
Discuss the indications/drug class of the VRd regimen (bortezomib, lenalidomide, and dexamethasone) for Multiple Myeloma (MM)
induction therapy for MM: Bortezomib-antineoplastic; Lenalidomide-immunomodulatory; dexamethasone-low dose gluccoctoricoid used w/ Lenalidomide
Explain the significance of the SPEP M-spike in the evaluation of multiple myeloma
A dense narrow band that is composed of a single class of immunoglobulins secreted by an abnormally expanded clone of plasma cells
Compare Hodgkin Lymphoma with Non-Hodgkin Lymphoma
Hodgkin: immunosuppresion+lymphs above diaphragm+Reed-Sternberg cells; Non-Hodgkin: Chromosomal/Autoimmune+Multiple lymphs+B-cell lineage
Describe the significance for PET-CT for the staging of malignancy.
Evaluate the spread of the cancer; Also see how successful the treatment is for the cancer.
Describe the Ann Arbor staging system used in staging Hodgkin lymphomas and the prognostic significance.
Hodgkin: contiguous lymph spread but NOT Non-Hodgkin; Ann Harbor I-IV (lymph spread increases+organ involved) + A (no b symptoms) B (yes B sympt)->IVB is worst
Explain the pathogenesis of EBV infection and how it relates to Hodgkin Lymphoma
EBV infects B lymphocytes->proliferate expression viral proteins->EBV-derived LMP-1->NF-kappaB & JAK/STAT->host cell proliferation/inhibit apoptosis by BCL2
use of TMP-SMX to treat Pneumocystis jirovecii; why is it an opportunistic infection in late HIV
inhibits dihydropteroate synthase+dihydrofolate reductase; PCP lacks ergosterol->antimycotic ineffective; Opportunistic infection in HIV CD4 low=AIDS defining
Discuss the laboratory tests that guide antiretroviral drug selection: HLA-B5701 & HIV resistance tests
Haplotype test: assessing the rate of HIV progression; genotype: drug resistance+correct therapy; HLA-B5701 don't use Abacavir drug
Identify the antiviral therapies for HIV and describe their site of action: Dolutegravir, Abacavir, Efavirenz
abacavir: NRTI-nucleoside reverse transcriptase inhibitor; dolutegravir: Integrase inhibitor; Efavirenz: NNRTI-Non-nucleoside reverse transcriptase inhibitors
Describe the effect HIV has on CD4+ T-cells.
HIV ->CD4 TH17 (activate neutrophils/protect mucoepithelium) is depleted->decrease CD4 T-> decrease TH1->not enough CD8T = infection + no control of infections


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