Unit 4 SIGS cases 7-12 | Baamboozle - Baamboozle

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