Download White Blood Cells Disorders Questions And Answers 2023/2024 and more Exams Nursing in PDF only on Docsity!
White Blood Cells Disorders Questions And Answers 2023/
1.nonneoplastic
2.results most commonly from decreased of granulocytes
3.most common form:neutropenia(agranulocytosis:granulocytes are significantly decreased) - ANS- Leukopenia
1.nonneoplastic
2.associated with rare congenital immunodeficiency,HIV infection - ANS-Lymphopenia
1.nonneoplastic
2.usually due to inflammatory states caused by microbial or nonmicrobial stimuli
3.neutrophilic,eosinophilic,basophilic,monocytic,lymphocytic - ANS-Reactive leukocytosis
1.Reactive leukocytosis
2.caused by Epstein-Barr virus - ANS-Infectious mononucleosis
1.nonneoplastic
2.triggered by infections and nonmicrobial stimuli
3.inflammation of lymph nodes
4.proliferation of immune cells
5.might be acute or chronic - ANS-Reactive lymphadenitis
1.reactive lymphadenitis
2.self limited
3.caused by Bartonella henselae
4.childhood disease - ANS-Cat scratch disease
1.viral infection or other proinflammatory stimuli trigger activation of macrophages throughout the body
2.macrophages are activated due to prolonged cytokines release from cytotoxic T cells(it remains engaged with targeted cells)
3.macrophages results in release of additional proinflammatory cytokines=>systemic inflammation - ANS-Hemophagocytic Histiocytosis
1.Acute lymphoblastic leukemia/lymphoma
2.About 85% of ALL are B-ALLs
3.B-ALL:manifest as childhood acute leukemias
T-ALL:manifest as adolescent thymus lymphomas
4.Pathogenesis:Many chromosomal aberrations in ALL dysregulate the expression and function of transcription factors that are required for the normal differentiation of B and T cell progenitors.
T-ALL: gain of function mutation of NOtCH
B-ALL:loss of function mutation of PAX
However,mutations in transcription factor genes are not sufficient to produce ALL,aberrations that drive cell growth(Mutation that increaseRAS signaling)
5.Morphology:marrow is hypercellular and packed with lymphoblasts,high mitosis rate,anemia,neutropenia
6.Genetics:
Childhood preB commonly have hyperdiploidy with (12,21) translocation of ETV6 and Runx1 fusion genes
Adult preB-All is 25% due to (9,22) translocation that leads to ABL and BCR fusion genes
7.immunophenot - ANS-Precursor B cell and T cell neoplasms
1.pathogenesis:CLL/SLL is an indolent,slowly growing tumor in which tumor cell survival is most important;CLL/SLL cells contain high levels of BCL2 protein;CLL/SLL also causes immune dysregulation by suppressing normal B cell functions resulting in hypogammaglobulinemia
the sites of chronic infection(H.Pylori gastritis).In case of H.pylori-associated gastric marginal zone lymphoma,eradication of H.Pyloriwith antibiotics often leads to regression of tumor cells,which depend on inflammatory cytokines secreted by H.pyloric-specific T cells for their growth and survival.Based on these observations,it is supposed that a B cell clone emerges that depends on antigen-stimulated T helper cells for signals that drive survival and growth.As further clon - ANS-Extranodal marginal zone lymphoma
1.the most common type of of NHL(50% of NHL in adults)
2.Pathogenesis:about one third of of large diffuse B cell lymphomas have rearrangements of the BCL gene,and even higher fraction of tumors have activating point mutations in the BCl6 promoter.Both aberrations lead to increased levels of BCl6 protein,an important transcriptional regulator of gene expression in germinal center B cells.Another 30% of tumors have a (14,18) translocation involving BCL gene that results in overexpression of BCl2 protein.The remaining tumors have other diverse driver mutations,such as translocations involving MYC gene.
3.immunophenotype:CD20,surface IgM/IgG;CD10,bCL2 variably expressed
4.Subtypes of DLBL
A.EBV associated diffuse lBL
B.Kaposi sarcoma herpesvirus
C.Mediastinal large B cell lymphoma
5.Clinical features:Patients typically present with a rapidly enlarging,often symptomatic mass at one or several sites.Extranodal p - ANS-Diffuse large B cell lymphoma
1.Burkkit lymphoma is endemic in parts of Africa and occurs sporadically in other geographic areas,including the US
2.Pathogenesis:Burkett lymphoma is highly associated with translocations involving the MYC gene on chromosome 8 that result in overexpression of the MYC transcription factor.Most translocations fuse MYC with IgH gene on chromosome 14,but variant transloctaions involving the kappa or lambda light chain loci also are observed.
3.In most endemic cases and 20% of sporadic cases,the tumor cells are latently infected with EBV.
4.Morphology:VERY HIGH rates of proliferation and apoptosis
5.immunophenotype:CD20,surface IgM,germinal center CD10 and BCl
6.clinical feautures:both the endemic and non- endemic form affect young adults and mainly children.Endemic tumors:maxillary and mandibular masses;Non-endemic tumors:abdominal tumors.Burkkit lymphoma is highly aggressive. - ANS-Burkkit lymphoma
1.These B cell proliferations contain neoplastic plasma cells that virtually always secrete a monoclonal immunoglobulin or immunoglobulin fragment,which serve as tumor markers
2.M monoclonal protein identified in the blood
3.Terms used to describe the abnormal immunoglobulins associated with plasma cell neoplasms include monoclonal gammopathy,dysproteinemia,and paraproteinemia.These proteins are associated with several clinicopathologic entities
A.Multiple myeloma(plasma cell myeloma):usually presents as tumorous masses scattered throughout the skeletal system.
B.Monoclonal gammopathy of undetermined significance is applied to patients whithout signs or symptoms who have small to moderately large M components in their blood.MGUS is common in elderly and and has a low but constant rate of transforming to a symptomatic monoclonal gammopathy,most often multiple myeloma
C.Primary or immunocyte-associated amyloi - ANS-Plasma cell neoplasms and related entities
1.The median age at diagnosis is 70 years
2.It principally involves the bone marrow and usually is associated with lytic lesions throughout the skeletal system
3.The most frequent M protein produced by myeloma cells is IgG followed by IgA.In the remaining cases,the plasma cells only produce kappa or lambda light chains.Because free light chains are small in size,they are also excreted in the urine,where they are referred to as Bence Jones proteins.In many cases,the malignant plasma cells secrete both complete immunoglobulins and free light chains and thus produce both M proteins and Bence Jones proteins.
4.Pathogenesis:Myeloma often has chromosomal translocations that fuse IgH locus on chromosome 14 to oncogenes such as cyclin D1 and cyclin D3 genes.Proliferation of myeloma cells is also supported by the cytokine IL6,which is produced by fibroblasts and macrophages in the bone marrow stroma.Multiple myeloma has a nu - ANS-Multiple myeloma
1.A B cell neoplasm of older adults
