Flashcards in White Blood Cell Disorders Deck (27):
Benign, exaggerated response to infection. Increased white count.
Cell that increases due to leukemoid reaction in appendicitis
Cell that increases due to leukemoid reaction in Whooping Cough (Bordetella Pertussis)
Cell that increases due to leukemoid reaction in cutaneous larva migrans
Immature bone marrow cells in peripheral blood. Can be due to fibrosis, metastatic breast cancer, sepsis, growth factor.
Condition where a certain white cell increases to more than 7000 due to infection, inflammation with necrosis, and drugs. Results in increased production of the cell and decreased margination.
Condition where a certain white cell decreases due to less than 1500. Can occur due to chemotherapy, aplastic anemia, immune destruction, septic shock. Results in decreased production of the cell and increased margination (destruction).
Condition where a certain white cell increases to more than 700. Can occur due to type I sensitivity, invasive helminths, hypocortisolism, neoplasms. Results in increased production (induced by interleukins) and increased tissue recruitment. Cell has a bilobed nucleus.
Condition where a certain white cell increases to more than 200. Usually from Chronic Myelogenous Leukemia. Can also be from other myeloproliferative neoplasms and and chronic kidney disease.
Proliferation of neoplastic cells, primarily in bone marrow and peripheral blood.
Proliferation of neoplastic cells, primarily in lymph nodes and extramedullary lymphoid tissue.
Disease class causing hypercellular bone marrow with effective hematopoesis-cytoses and cell proliferation
Myeloproliferative Neoplasms (MPN)
Disease class causing hypercellular bone marrow with ineffective hematopoesis-cytopenias, cell death.
Myelodysplastic Syndromes (MDS)
Myeloproliferative Neoplasm. BCR-ABL positive. Philadelphia chromosome. Immature myeloid cells. 40-60 years. Hepatosplenomegaly, fatigue, weakness, weight loss, anorexia. Leukocytosis, basophilia.
Chronic Myelogenous Leukemia
Rough way to calculate normal bone marrow cellularity
Has chronic phase (3 years), accelerated phase (1 year) and blast phase (acute leukemia). Treat with TKI (-tinibs). (BCR-ABL positive).
Chronic Myelogenous Leukemia
Increase in RBCs, granulocytes, platelets. JAK2 mutation.. Splenomegaly, hyperviscosity, gout, increased histamine. Increased RBC mass, decreased EPO, normal oxygen saturation, increased plasma volume. Most patients die of thrombotic events, can develop MDS or AML.
Rapid development of bone marrow fibrosis, extramedullary hematopoiesis. Teardrop cells. Leukoerythroblastic reaction. Splenomegaly, clusters of atypical megakaryocytes. Can have JAK2 mutation. Can progress to AML.
Myeloproliferative Disease. Proliferation of megakaryocytes, platelet count of over 450,000. Atypical platelet morphology-giant hypogranular platelets. Can have JAK2 mutation. Treat with alkylating agents or similar drugs to lower platelet count.
Hypercellular, dysplastic BM. Myeloblasts less than 20%. Elderly. Can progress to AML. Chromosomal abnormalities in 50% of cases (deletion of 5, 5q, 7, 7q). Ring sideroblasts. Treat with hypomethylating agents, allogenic stem cell transplant.
Greater than 20% blasts. Symptoms occur within weeks to months. Typically in adults. Large and uniform blasts, abundant cytoplasm, presence of Auer rods, myelodysplasia.
Acute Myeloblastic Leukemia (AML)
t(15;17). Needs acute tx, DIC, responds to ATRA, mutliple auer rods, disrupts retinoic acid receptor.
Acute Promyelocytic Leukemia- subset of AML
AML with favorable prognosis (3)
AML with unfavorable prognosis (1)
11q23 (MLL) rearrangements
Proliferative dendritic cells or macrophages. CD1a, langerin positive. Birbeck granules (tennis racket appearance), BRAF mutations.
Langerhans cell Histiocytosis
-Primary (genetic)=defects in perforin gene
-Secondary=From EBV, lymphomas
Very high ferritin, hypertriglyceridemia, hypofibrinogenemia, hemophagocytosis
Hemophagocytic lymphohistiocytosis/hemophagocytic syndrome