deck_2052836

Question 1

AML with good prognosis

Answer 1

t(8:21)Inv(16)T(15:17)

Question 2

MDS Clinical

Answer 2

50-80 yo.Weakness, infections, bleeding, or assymptomatic9-29 month survival30% progression to AMLTreatment:SupportiveHypomethylating agents - Decitabine, AzacitidineSCT

Question 3

Myelodysplastic syndromes

Answer 3

Blasts

Question 4

Leukemoid Rxn

Answer 4

50-80 or 90K LeukocytesNeutrophils, lymphocytes, or eosinophilsCauses:*Perforating appendicitis(neut)*Bordatella (lymphocytes) - Whooping cough*Cutaneous larval migrans- Eosinophilia

Question 5

Neutropenia

Answer 5

dfdff

Question 6

AML Inv(16)

Answer 6

Granulocytic and monocytic AML Extramedullary involvemenFAVORABLE PROGNOSIS

Question 7

AML with T(8:21)

Answer 7

Granulocytic AML with a few auer rodsFAVORABLE PROGNOSIS

Question 9

AML t(15:17)

Answer 9

Acute promyelocytic leukemiahypergranular progmyelocytes with auer rodsLeukopenia with DIC Treat with ATRA (screwed up RA signaling)FAVORABLE PROGNOSIS

Question 10

Polycythema Vera

Answer 10

JAK mutationIncreased RBC mass, Leukocytosis, thrombocytosisDecreased EPOBM fibrosis and hypercellularity in late diseaseSplenomegaly, thrombosis, gout, histamine

Question 11

Benign WBC disorders

Answer 11

Leukemoid reactionLeukoerythroblastic reactionNeutrophiliaNeutropeniaEosinophiliaBasophilia

Question 13

Hemophagocytic lymphohistocytosis

Answer 13

Primary: defects in perforin geneSecondary: EBV and Lymphoma associated*Hypertriglyceridemia, hypofibrinogenemia, hemophagocytosisFEVER

Question 14

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

Answer 14

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

Question 16

AML with MDS changes

Answer 16

Monosomy 5, 7POOR PROGNOSIS

Question 17

add last

Answer 17

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Question 18

CML t(9:22)

Answer 18

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)

Question 19

ALL

Answer 19

Common in children(75% of childhood cancers) though 50% are adultsM>F*small blasts*High N/C*Absent or scant nucleoli

Question 20

Neutrophilia

Answer 20

Neutrohils >7k*Infection*Sterile inflam and necrosis (MI)*Drugs- ie. lithium, steroids, catecholaminesIncreased production or decreased margination

Question 21

Eosinophilia

Answer 21

>.7k eosin*Asthma/allergy*parasitic*addisons/hypercortisol*Hodgkins lymphomaIncreased recruitment or production via leukotriene stimulation

Question 22

Basophilia

Answer 22

>.2K*CML*CKD

Question 23

Test obey dcj ghjk gjh. V

Answer 23

Gfjhgjhg fishy dying ghfjhgjh nbn.

Question 24

add last

Answer 24

fghgfhh

Question 25

my card1

Answer 25

my card2

Question 26

0 AML

Answer 26

*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)

Question 27

Langerhans cell histocytosis

Answer 27

CD1a langerin positive*Tennis racket BIRBECK GRANULLESBRAF MUTATIONS

Question 28

MPNs

Answer 28

CMLPolycythema VeraPMF (primary myelofibrosis)Essential Thrombocythemia

Question 29

AML 11q23

Answer 29

MLLmonocytic hyperleukocytosisINTERMEDIATE TO POOR PROGNOSIS

Question 30

Essential Thrombocythemia

Answer 30

Jak2 mutation>450K atypical plateletsHypercellular BM with abnormal megakayocytesGiant hypogranular plateletsBleeding, splenomegalu12-15 year survival- treat with alkylating agents

Question 31

PMF

Answer 31

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

Question 32

AML clinical presentation

Answer 32

*Cytopenia- weakness, fatigue, petechiae, infectionsSometimes:Orgaonmegalylymphadenopathyextramedullary infiltrationrare coagulopathy

Question 33

Leukoerythroblastic RXN

Answer 33

Immature BM cells in peripheral bloodInfiltration of BM- Mets, BM fibrosisStress- Sepsis or GF stressi.e. Myeloblasts and nucleated RBCS

Question 34

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

Answer 34

why si it impotannt that when iron binds to oxygen that this is a tempoary

Question 35

new

Answer 35

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