Step 1 Hematology High Yield

Front 1

t(9;22)

Back 1

CML

Front 2

t(8;14)

Back 2

Burkitt's lymphoma

Front 3

t(14;18)

Back 3

Follicular lymphoma

Front 4

t(15;17)

Back 4

AML (type M3)

Front 5

t(11;22)

Back 5

Ewing's sarcoma

Front 6

t(11;14)

Back 6

Mantle cell lymphoma

Front 7

c-myc activation

Back 7

Burkitt's lymphoma, t(8;14). C-myc causes cell proliferation (vs. bcl-2 which is anti-apoptotic; or bcl-1 (Mantle) which is a cell cycle protein, and therefore proliferative rather than just anti-apoptotic)

Front 8

What are two ways by which cells can proliferate?

Back 8

Stimulate proliferation (c-myc in Burkitt's, blc-1 in mantle cell), or inhibit apoptosis (bcl-2 in follicular lymphoma), or both (bcr-abl in CML)

Front 9

bcl-2 activation

Back 9

Follicular lymphoma, t(14;18)

Front 10

bcr-abl hybrid

Back 10

CML, t(9;22), Philadelphia chromosome. Increased cell division and inhibition of apoptosis.

Front 11

This disease is responsive to all-trans retinoic acid (ATRA), which removes the differentiation block.

Back 11

AML (type M3)

Front 12

This is due to a differentiation block, and this is due to out of control proliferation.

Back 12

Acute Myelogenous Leukemia is due to a differentiation block, thus immature forms predominate. Chronic myelogenous leukemia is due to out of control proliferation (bcr-abl hybrid protein), so high numbers of all forms, mature and immature, are seen.

Front 13

Leukemia in a person < 15 yo

Back 13

ALL

Front 14

Leukemia in a person ~60 yo

Back 14

AML

Front 15

Leukemia in a person 30-60 yo

Back 15

CML

Front 16

Leukemia in a person > 60 yo

Back 16

CLL

Front 17

Auer bodies are located in the cytoplasm of these cell types

Back 17

Granulocytes and myeloblasts
(in AML M3)

Front 18

Auer bodies (rods) are seen in this disease

Back 18

Acute promyelocytic leukemia (AML M3)

Front 19

Treatment of this leukemia can cause DIC

Back 19

Treatment of AML M3 with ATRA can cause release of Auer rods, precipitating DIC

Front 20

How to differentiate CML from a leukemoid reaction

Back 20

Leukocyte alkaline phosphatase. It's going to be high in a leukemoid reaction, but low in CML. Alkaline phosphatase is produced by normal PMNs, but not neoplastic PMNs.

Front 21

Leukemoid reaction

Back 21

Benign but exaggerated response to infection; increased WBC with left shift (80% bands). PMNs in perforated appendicitis, lymphocytes in whooping cough, and eosinophils in cutaneous larva migrans. Common in children, who will respond to an infection with a 30,000 WBC whereas an adult might respond with an increase to 15,000 WBC.

Front 22

General findings in leukemia.

Back 22

Bone marrow infiltration causing marrow failure which leads to: anemia (low RBCs), infection (low WBCs), hemorrhage (low plts).

Front 23

This leukemia may spread to the CNS and testes

Back 23

ALL

Front 24

This leukemia has TdT+ cells

Back 24

ALL (TdT is a marker of pre-T and pre-B cells)

Front 25

This leukemia is the most responsive to therapy

Back 25

ALL

Front 26

These leukemias are "blastic"

Back 26

The acute leukemias: acute lymphoblastic and acute myeloblastic. Acute leukemias are caused by a differentiation block, so there is a proliferation of immature (blast) cells

Front 27

Smudge cells are seen on the blood smear of this leukemia

Back 27

CLL

Front 28

This leukemia is associated with warm antibody (IgG) autoimmune hemolytic anemia

Back 28

CLL

Front 29

This leukemia is basically the same as this lymphoma

Back 29

CLL=SLL (small lymphocytic lymphoma)

Front 30

The Philadelphia chromosome causes proliferation of this cell type

Back 30

Myeloid stem cells

Front 31

This leukemia presents with increased PMNs, metamyelocytes, and basophils

Back 31

CML

Front 32

What is a "blast crisis"?

Back 32

Transformation of CML to AML (2/3) or ALL (1/3). Due to a differentiation block transposed on the increased proliferation. Increased proliferation of CML means that there are more opportunities for the cells to mutate into AML or ALL, which are characterized by differentiation blocks.

Front 33

Imatinib is used to treat this disease

Back 33

CML. Imatinib is anti-bcr-abl Ig

Front 34

This disease stains TRAP positive (tartrate-resistant acid phosphatase)

Back 34

Hairy cell leukemia

Front 35

This disease is a mature B-cell tumor seen in the elderly

Back 35

Hairy cell leukemia

Front 36

This disease is characterized by defective cells that express S-100 and CD1a

Back 36

Histiocytosis X
(proliferative disorder of Langerhans/dendritic cells from the monocyte lineage)

Front 37

Birbeck granules

Back 37

"Tennis rackets" on EM

Front 38

Birbeck granules are characteristic of this proliferative disorder

Back 38

Langerhans cell histiocytosis ("Histiocytosis X")

Front 39

These are older terms for histiocytosis X

Back 39

Letterer-Siwe disease, Hand-Schuller-Christian disease, eosinophilic granuloma

Front 40

This is the only myeloproliferative disorder that does not feature a JAK2 mutation

Back 40

CML
(it features a Philadelphia t[9;22] mutation)

Front 41

These are the four myeloproliferative disorders

Back 41

Polycythemia vera (high RBC, WBC, plt)
Essential thrombocytosis (high plt)
Myelofibrosis (low RBC, variable WBC, variable plt)
CML (low RBC, high WBC, high plt)

Front 42

This disease results in fibrotic obliteration of the bone marrow

Back 42

Myelofibrosis (a myeloproliferative disorder characterized by decreased RBC)

Front 43

This gene is involved in hematopoietic growth factor signaling

Back 43

JAK2