Gomez CIS

Question 1

some causes of neutrophilia besides infection

Answer 1

MI, necrosis, acute stress, hypoxia, catecholamine or glucocorticoid administration

Question 2

left shift

Answer 2

if there are myeloblasts and a lot of immature forms, no question

if there are more than 3-5% band neutrophils, some people consider it to be a left shift

Question 3

leukemoid reactions look like

Answer 3

chronic myelogenous leukemia

if it doesn’t look like that, it’s not a leukemoid reaction

Question 4

how can you distinguish a leukemoid reaction from chronic myeloid leukemia?

Answer 4

• LAP (old version)
• could look for dohle bodies (more likely to be a leukemoid reaction)
• toxic granulation (inflammation)
• flow cytometry
• no clonality or BCR ABL mutation in a leukemoid reaction

CML may have basophilia and the patient may have splenomegaly
usually the left shift in CML is greater than in a leukemoid reaction

Question 5

red cells of different sizes

Answer 5

anisocytosis

Question 6

hypersegmented neutrophil come from

Answer 6

B12 or folate deficiency
also chemotherapy
less lobes- seen in persistent bacterial infections, iron deficiency anemia and renal failure.

Question 7

downey cell

Answer 7

reactive lymphocyte

most likely CD8+ cytotoxic T cell, not an infected B cell

Question 8

are reactive atypical lymphocytes specific for infectious mono?

Answer 8

NO- activated lymphocytes may be seen with other viral infections and and in a lot of other reactive states

Question 9

how to confirm mono?

Answer 9

heterophile antibodies (monospot) or IgM antibodies against EBV capsid antigen

Question 10

what mimics mono?

Answer 10

CMV

Question 11

distinguish neoplastic from reactive process

Answer 11

left shift in CML is greater than in a leukemoid reaction
CML may have basophilia and the pt may have splenomegaly
LAP score is low in CML
no clonality or BCR-ABL mutation in a leukemoid reaction

Question 12

do we see philadelphia in other myeloproliferative disorders besides CML?

Answer 12

NO! in acute lymphoblastic, but NOT another myeloproliferative

Question 13

where else can you get MALT besides gastric?

Answer 13

salivary, lacrimal

from autoimmune (e.g. Sjogren’s)

thyroid- hashimoto

no initial translocations, but eventually 11,18 (MALT 1) translocation

Question 14

what is the name for lymphoid tissue invading the gland?

Answer 14

lymphoepithelial lesion

Question 15

CML transitioning to AML, what testing do we want?

Answer 15

flow cytometry and cytogenetic studies

If these blasts are CD19, CD19, TDT+ and delta light chain restricted– this means lymphoid

Question 16

primary criterion for a diagnosis of acute leukemia?

Answer 16

20% blasts in the blood or bone marrow

Question 17

how would polycythemia vera present clinically

Answer 17

plethora, cyanosis, headaches, DVTs, strokes, MIs, GI infarcts, bleeding gums and nose bleeds, possible itching and peptic ulcers from basophilia, +/- splenommegaly. yperuricemia +/- gout. Granulocytosis, polycythemia, thrombocytosis, basophilia and possible monocytosis in the blood

Question 18

treatment options and prognosis of polycythemia vera?

Answer 18

phlebotomy +/- chemo

median survival with treatment is >10 years, 1 month without

Question 19

possible final outcomes of polycythemia and how are they related to the form of therapy?

Answer 19

worse with chemo– induce blast transformation earlier

spent phase in 15-20% of treated patients
blast phasse in 1-2% with phlebotomy alone
10-15% incidence of blast phase in those treated with alkylating agents or 32P

Question 20

how to distinguish polycythemia vera from secondary erythrocytosis?

Answer 20

EPO levels high in secondary, low in vera

Question 21

clinical manifestation of essential thrombocytosis?

Answer 21

hemorrhage, thrombosis –> erythromelalgia (intense, burning pain of hands or feet, erythema and skin warmth)

Question 22

distinguish essential thrombocytosis from reactive thrombocytosis?

Answer 22

dx of exclusion. Must exclude all other reasons for a reactive thrombocytosis (bleeding, iron deficiency, infections, inflammation, paraneoplastic proliferations and other myeloproliferative disorders)

Question 23

prognosis of essential thrombocytosis?

Answer 23

12-15 years, similar to that of age–matched controls (50-60 year olds)

Question 24

anisocytosis with schistocytes, dacryocytes, what’s up?

Answer 24

bone marrow fibrosis or

myelophthsic process (something is packing the marrow and these cells are squeezing through getting all bent out of shape)

need to do a bone marrow biopsy

could be primary meolofibrosis, bad prognosis. (3-5 years survival, 5-20% blast crisis)

Question 25

significance of auer rod?

Answer 25

these are blasts. fused neutrophil primary

Question 26

in a case of PML there were only 5% myeloblasts in the blood and 10% in teh bone marrow iwith the majority of the abnormal cells being promyelocytes. Does this mean that the patient does not meet the criteria for AML?

Answer 26

No– in APL the promyelocytes get to count towrard the 20%

Question 27

molecular abnormality associated with t(15,17)

Answer 27

PML/RARA fusion proteins block differentiation at promyelocyte stage. Pharmacologic doses of all trans retinoic acid overcome this block or arsenic trioxide can be used to degrade the fusion protein

Question 28

macrocytic anemia, dual RBC population, platelet count is mildly decreased and occasional hypogranular megathrombocytes are seen. What do we suspect?

Answer 28

myelodysplastic syndrome, should have bone marrow evaluation
dysplastic erythroid precursors, megaloblastoid maturation and dysplastic megakaryocytes are identified int eh bone marrow

Question 29

myelodysplastic syndromes distinguished from myeloproliferative disorders?

Answer 29

hematopoiesis in myeloproliferative disorders is effective, producing increased peripheral counts initially

Question 30

natural history of myelodysplastic syndromes, some complications?

Answer 30

varies widely

can have worsening cytopenias, rapidly progressive marrow failure, and trsnformation to AML that can all lead to death