Gomez CIS Flashcards

1
Q

some causes of neutrophilia besides infection

A

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

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2
Q

left shift

A

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

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3
Q

leukemoid reactions look like

A

chronic myelogenous leukemia

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

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4
Q

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

A
  • 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

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5
Q

red cells of different sizes

A

anisocytosis

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6
Q

hypersegmented neutrophil come from

A

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

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7
Q

downey cell

A

reactive lymphocyte

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

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8
Q

are reactive atypical lymphocytes specific for infectious mono?

A

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

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9
Q

how to confirm mono?

A

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

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10
Q

what mimics mono?

A

CMV

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11
Q

distinguish neoplastic from reactive process

A

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

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12
Q

do we see philadelphia in other myeloproliferative disorders besides CML?

A

NO! in acute lymphoblastic, but NOT another myeloproliferative

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13
Q

where else can you get MALT besides gastric?

A

salivary, lacrimal

from autoimmune (e.g. Sjogren’s)

thyroid- hashimoto

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

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14
Q

what is the name for lymphoid tissue invading the gland?

A

lymphoepithelial lesion

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15
Q

CML transitioning to AML, what testing do we want?

A

flow cytometry and cytogenetic studies

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

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16
Q

primary criterion for a diagnosis of acute leukemia?

A

20% blasts in the blood or bone marrow

17
Q

how would polycythemia vera present clinically

A

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

18
Q

treatment options and prognosis of polycythemia vera?

A

phlebotomy +/- chemo

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

19
Q

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

A

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

20
Q

how to distinguish polycythemia vera from secondary erythrocytosis?

A

EPO levels high in secondary, low in vera

21
Q

clinical manifestation of essential thrombocytosis?

A

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

22
Q

distinguish essential thrombocytosis from reactive thrombocytosis?

A

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

23
Q

prognosis of essential thrombocytosis?

A

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

24
Q

anisocytosis with schistocytes, dacryocytes, what’s up?

A

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)

25
significance of auer rod?
these are blasts. fused neutrophil primary
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?
No-- in APL the promyelocytes get to count towrard the 20%
27
molecular abnormality associated with t(15,17)
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
28
macrocytic anemia, dual RBC population, platelet count is mildly decreased and occasional hypogranular megathrombocytes are seen. What do we suspect?
myelodysplastic syndrome, should have bone marrow evaluation dysplastic erythroid precursors, megaloblastoid maturation and dysplastic megakaryocytes are identified int eh bone marrow
29
myelodysplastic syndromes distinguished from myeloproliferative disorders?
hematopoiesis in myeloproliferative disorders is effective, producing increased peripheral counts initially
30
natural history of myelodysplastic syndromes, some complications?
varies widely | can have worsening cytopenias, rapidly progressive marrow failure, and trsnformation to AML that can all lead to death