Unit 3 - Formative 9 D2

Front 1

Most common site for BM biopsy

Back 1

Posterior Superior Iliac crest

Front 2

Flow Cytometry

Back 2

Forward scatter info on cell size
Side scatter: info on granularity

Front 3

Reactive Leukopenia

Back 3

lp secondary to a disorder (infection, inflammation, autoimmune, drugs, chemicals, etc)

You see neutropenia and lymphopenia but NOT MO, EO, or BA

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Isolated neutropenia

Back 4

Bacterial Infection

Front 5

Isolated lymphopenia

Back 5

Viral infection (HIV, EBV, etc)

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Back 6

Reative Lymphocytes

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Back 7

Aplastic anemia; BM not able to produce sufficient new cells to replenish blood cells; results in pancytopenia

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Myelodysplasia

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Ineffective hematopoiesis and subsequent pancytopenia; ringed siderblasts often present

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Back 9

Dysplasia of myelodysplasia in BM

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Back 10

Dohle Body (lower right blue area)

Note granulations - lysozymes to kill bacteria

Vacuoles indicate phagocytic activity

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Back 11

Monocyte

Isolated monocytosis indicates chronic infection

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Eosinophil

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Back 13

Esosinophil

Front 14

Back 14

Basophil

Front 15

Isolated eosinophilia

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Allergic and hypersensitivity reactions

Front 16

Isolated basophilia

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Chronic Myelogenous Leukemia

Front 17

Acute Leukemia

Back 17

Short time course; rapidly diving immature cells

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Chronic Leukemia

Back 18

Long time course of disease; rapidly diving mature cells

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Back 19

Myeloblasts in AML; delicate chromatin, prominent nucleoli and fine azurophilic granules in the cytoplasm

CD34 and Cd33 markers of the same blasts

Front 20

Acute Myelongeous Leukemia

Back 20

BM accumulation of immature myeloid cells

Common in ADULTS

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Back 21

Auer Rod; diagnostic of AML

Front 22

Acute Lymphoblastic/Lymphoid Leukemia

Back 22

Malignant neoplasms of the hematopoietic precursor cells of lymphoblasts

Common in CHILDREN

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AML vs ALL

Back 23

ALL affects lymphocytic cells
AML affects myeloid cells

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Back 24

Lymphoblasts in ALL

Condensed nuclear chromatin, small nucleoli, scant agranular cytoplasm

Express Tdt and CD22; CD10 and CD19

Front 25

CML morphology

Back 25

Type of myeloproliferative disorder; Proliferation of granulocytes and platelets

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Polycythemia vera

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Type of myeloproliferative disorder; proliferation of RBC and paltelets

Front 27

Essential thrombocytosis

Back 27

Type of myeloproliferative disorder; Proliferation of megakaryocytes

Front 28

Primary myelofibrosis

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Type of myeloproliferative disorder; proliferation of fibroblasts, granulocytes & megakaryocytes

Front 29

Philadelphia Chromosome

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t(9;22); BCR-ABL in 90-95% of cases in CML

Front 30

Gleevec and CML

Back 30

Philadelphia chromosome (bcr-abl) constitutively activates tyrosine kinase; gleevec binds to TK active site as a competitive inhibitor

Front 31

How can you acquire resistance to Gleevec?

Back 31

additional mutations in bcr-abl protein = reduced gleevec binding

or amplification of the bcr-abl gene locus

Front 32

Pathogenetics of Polycythemia Vera

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Mutations in JAK2 Tyrosine Kinase lead to constitutive kinase activity

Front 33

JAK-STAT signaling (this is how EPO stimulates erythropoisesis)

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JAKs cross phorphorylate -> STATS bind and are phorphorylated -> STATS dimerize and become transcription factors in nucleus

Front 34

CP of CML

Back 34

Strokes, headaches, weakness due to thickened blood (immature myeloid cell proliferation)

Front 35

CP of Polycythemia Vera

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Strokes, headaches, weakness due to thickened blood (immature myeloid cell proliferation)

Front 36

CP of essential thrombocytosis

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Episodes of bleeding/fibrosis

Front 37

CP of primary myelofibrosis

Back 37

Marked thrombycytosis

Front 38

Back 38

CBC from a pt with CML; note the large buffy coat

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Back 39

BM from pt w chronic CML; note the hypercellular marrow

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Back 40

PB from pt with CML

Note increased WBC as well as presence of a full range of myeloid maturation

Front 41

Chediak Higashi Mutation

Back 41

LYST gene; unable to transport materials into lysosomes

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Back 42

Chediak-Higashi Syndrome associated with albinism

Neutropenia most common presentation; recurrent, life threatening infections in various organs

Front 43

Chronic Granulomatous Disease of Childhood

Back 43

CGD; phagoytes can't form superoxide radical and thus can't kill bacteria

Front 44

Myeloperoxidase Deficiency (MPOD)

Back 44

MPO found in azurophilic granules of neutrophils and lysomes of monocytes; MPO converts H202 and Cl into hypochlorus acid (bleach) to kill bacteria

Ability to kill fungi completely absent so pts present more often with candida infections

Front 45

Fungal Infections in Diabetics

Back 45

Myeloperoxidase Deficiency (MPOD)

Front 46

"Neutrophils Like Making Everything Better Except Pus"

Seven differentiated formed elements present in blood

Back 46

Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils

Erythrocytes
Platelets

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Back 47

Reticulocytes; immature RBC in peripheral blood

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Back 48

Eosinophil

Antimicrobial function, protects against helminthic and protozoan infection

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Back 49

Megakaryote; produce platelets

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Back 50

Bone Marrow Graphic

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Back 51

Note the myeloid commited precursors

Granulocyte macrophage CFU
Eosinophil CFU
Basophil CFU
Megakaryocyte CFU
Erythroid CFU

Front 52

Note two commited precursors from lymphoid stem cell

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Commited Precursors

Front 53

Erythroid Differentiation

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Erythroid Differentiation

Front 54

Granulocyte Differentiation

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Granulocyte Differentiation

Front 55

Immature Myeloid Algorithm

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Immature Myeloid Algorithm