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Leukemia
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Lymphomas
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Heme 2
| Question | Answer |
|---|---|
| Leukemia | -tumors that primarily involve bone marrow with spillage of neoplastic cells into the peripheral blood |
| Lymphomas | -tumors that produce masses in involved lymph nodes or other tissues |
| Plasma cell dyscrasias | -plasma cell tumors -usually present within the bones as discrete masses -cause systemic sx's |
| Understand that lymphoid neoplasms arise from transformed B cells and T cells. | -lymphoid neoplasms arise from a problem in differentiation of the normal life process of a B or T cell -more commonly B cells |
| Describe features common to the acute leukemias -pathophysiology | -path:block of differentiation-> accumulation of immature leukemic blasts in bone marrow->suppress function of normal hempoeitic stem cells |
| Describe features common to the acute leukemias -clinical | -abrupt, stormy onset -sx's related to depression of normal marrow function -bone pain and tenderness -generalized lymphadenopathy, spleenomegally, and hepatomegally -CNS manifestations |
| Describe features common to the acute leukemias -lab findings | -must identify blast forms in peripheral blood and bone marrow -WBC is variable -anemia almost always present -nuetropenia |
| chronic lymphocytic leukemia (CLL) | -most common leukemia of adults -identical to small lymphocitic lymphoma -both uncommon in Aisia -asymptomatic at presentation, easy fatigability, wt loss, anorexia, generalized lymphadenopathy and spleenomegally 50% of pts, hypogammaglobulinemia 50%, |
| multiple myeloma | -most common malignant plasma cell dyscrasias -multifocal lytic lesions thru skeletal systems -bone pain, recurrent infections (S. aureus, Strep pnuemoniae, E. coli), hyperviscosity syndrome, renal insufficiency |
| Hodgkin lymphoma | -ditinctive neoplastic giant cells (Reed-Sternberg) -systemic manifestations ->fever -sterotypical spread allows it to be treated differently than most lymphoid neoplasms -5 subtypes |
| Subtypes of Hodkin lymphoma | -nodular sclerosis -mixed cellularity -lymphocyte predominance -lymphocyte rich -lymphocyte depletion |
| acute myelogenous leukemia (AML) | -50 yo's -heterogenous -sx's caused by marrow failure(normal cells replaced by leukemic cells) -fatigue and pallor, abnormal bleeding, and infections |
| chronic myelogenous leukemia (CML) | -BCR-ABL fusion gene -onset is slow, sx's are non-specific (easy fatigue, weakness, wt loss) -dragging sensation in abdomen (extreme spleenomegally) -Ph chromosome differentiates from leukoid reaction -beging to resemble acute leukemia (blast crisis) |
| Signifigance of Reed-Sternberg cells in Hodgkins | -seperates it from non-Hodgkins -mixed with non-malignant inflammatory cells |
| general principles of the Ann Arbor classification system for staging of lymphomas | -I single lymph region or one organ -II two or more node regions on the same side of diaphragm/ limited contiguous extralymphatic organs -III node regions on both sides -IV multiple foci of one or more extralymphatic organs |
| Clinical features non-Hodgkin lymphoma | -more frequent involvement of multiple peripheral nodes -noncontigous spread - mesenteric nodes and Waldeyer ring commonly involved -extranodal involvement common |
| Clinical features Hodgkins lyymphoma | -more often localized to a single axial group of nodes (cervical, mediastium, para-aortic) -orderly spread by contiguity -mesenteric adn Waldeyer ring rarely involved -extranodal involvement uncommon |
| Clinical presentation of lymphomas | -painless enlargment of lymph nodes -fever -unexplained wt loss -pruritis -anemia |
| Clinical presentation of plasma cell dyscrasis | -bone pain -recurrent infections (S. aureus, S. pnuemonia, E. coli) -hyperviscosity (due to m protiens) -renal insufficiency |
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caplec