deck_2052836 Flashcards
AML with good prognosis
t(8:21)Inv(16)T(15:17)
MDS Clinical
50-80 yo.Weakness, infections, bleeding, or assymptomatic9-29 month survival30% progression to AMLTreatment:SupportiveHypomethylating agents - Decitabine, AzacitidineSCT
Myelodysplastic syndromes
Blasts
Leukemoid Rxn
50-80 or 90K LeukocytesNeutrophils, lymphocytes, or eosinophilsCauses:*Perforating appendicitis(neut)*Bordatella (lymphocytes) - Whooping cough*Cutaneous larval migrans- Eosinophilia
Neutropenia
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AML Inv(16)
Granulocytic and monocytic AML Extramedullary involvemenFAVORABLE PROGNOSIS
AML with T(8:21)
Granulocytic AML with a few auer rodsFAVORABLE PROGNOSIS
AML t(15:17)
Acute promyelocytic leukemiahypergranular progmyelocytes with auer rodsLeukopenia with DIC Treat with ATRA (screwed up RA signaling)FAVORABLE PROGNOSIS
Polycythema Vera
JAK mutationIncreased RBC mass, Leukocytosis, thrombocytosisDecreased EPOBM fibrosis and hypercellularity in late diseaseSplenomegaly, thrombosis, gout, histamine
Benign WBC disorders
Leukemoid reactionLeukoerythroblastic reactionNeutrophiliaNeutropeniaEosinophiliaBasophilia
Hemophagocytic lymphohistocytosis
Primary: defects in perforin geneSecondary: EBV and Lymphoma associated*Hypertriglyceridemia, hypofibrinogenemia, hemophagocytosisFEVER
What contributions from the Extrinsic and Intrinsic Pathways help form the enzyme complex necessary to begin the Common Pathway?Hdb jdjs jdhgdh hda. Factors VIII and IX from the Extrinsic Pathway; Factor VII from the Intrinsic Pathway b. Factor III from the Extrinsic Pathway; Factor XII from the Intrinsic Pathwayc. Factor VII from the Extrinsic Pathway; Factors VIII and IX from the Intrinsic Pathwayd. none of the above
What contributions from the Extrinsic and Intrinsic Pathways help form the enzyme complex necessary to begin the Common Pathway?a. Factors VIII and IX from the Extrinsic Pathway; Factor VII from the Intrinsic Pathway b. Factor III from the Extrinsic Pathway; Factor XII from the Intrinsic Pathwayc. Factor VII from the Extrinsic Pathway; Factors VIII and IX from the Intrinsic Pathwayd. none of the above
AML with MDS changes
Monosomy 5, 7POOR PROGNOSIS
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CML t(9:22)
40-60 YOHepatosplenomegaly with weakness, weight loss, anorexiaWBC increased (100K): Mature Myeloid cells present with left shiftBM- Granulocytic hyperplasiat(9:22) BCR-ABL fusion “philadelphia chromosome”Chronic phase-3 years, accelerated 1 yr, then AML or ALLConstitutive TK activity - treat with TKi - DASATINIB, IMATINIB (gleevec)
ALL
Common in children(75% of childhood cancers) though 50% are adultsM>F*small blasts*High N/C*Absent or scant nucleoli
Neutrophilia
Neutrohils >7k*Infection*Sterile inflam and necrosis (MI)*Drugs- ie. lithium, steroids, catecholaminesIncreased production or decreased margination
Eosinophilia
>.7k eosin*Asthma/allergy*parasitic*addisons/hypercortisol*Hodgkins lymphomaIncreased recruitment or production via leukotriene stimulation
Basophilia
>.2K*CML*CKD
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0 AML
*course of weeks to months*Adults age 60*25% long term survival (poor prognosis overall) *large uniform blasts (>20% in BM or PB)*fine chromatin with many nucleoli*Cytoplams with granules*Auer rods!!!*myelodysplasiaTest with MPE or NSE enzyme assay (blue granules and bright red cytoplasm respectively)
Langerhans cell histocytosis
CD1a langerin positive*Tennis racket BIRBECK GRANULLESBRAF MUTATIONS
MPNs
CMLPolycythema VeraPMF (primary myelofibrosis)Essential Thrombocythemia
AML 11q23
MLLmonocytic hyperleukocytosisINTERMEDIATE TO POOR PROGNOSIS
Essential Thrombocythemia
Jak2 mutation>450K atypical plateletsHypercellular BM with abnormal megakayocytesGiant hypogranular plateletsBleeding, splenomegalu12-15 year survival- treat with alkylating agents
PMF
Primary myelofibrosisTEARDROP RBCsLeukoerythroblastic rxn - Immature cess in peripheral bloodJak/MPL mutationBM fibrosis and Megakaryocyte atypia*Splenomegaly with portal HTN,*Splenic infarct and reactive left pleural effusion10 years in prefribrotic then 3-7 in fibrotic stages5-30% get AML *BM failure*Throbosis*Portal HTN*HF
AML clinical presentation
*Cytopenia- weakness, fatigue, petechiae, infectionsSometimes:Orgaonmegalylymphadenopathyextramedullary infiltrationrare coagulopathy
Leukoerythroblastic RXN
Immature BM cells in peripheral bloodInfiltration of BM- Mets, BM fibrosisStress- Sepsis or GF stressi.e. Myeloblasts and nucleated RBCS
Why is it important that when iron binds to oxygen that this is a temporary and reversible interaction?a. because the hemoglobin can then be fully saturatedb. because the oxygen needs to dissociate into tissuesc. because RBCs consume some of the oxygen they carryd. because carbon dioxide binds to the ironmolecule simultaneously
why si it impotannt that when iron binds to oxygen that this is a tempoary
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