Gomez CIS Flashcards
some causes of neutrophilia besides infection
MI, necrosis, acute stress, hypoxia, catecholamine or glucocorticoid administration
left shift
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
leukemoid reactions look like
chronic myelogenous leukemia
if it doesn’t look like that, it’s not a leukemoid reaction
how can you distinguish a leukemoid reaction from chronic myeloid leukemia?
- 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
red cells of different sizes
anisocytosis
hypersegmented neutrophil come from
B12 or folate deficiency
also chemotherapy
less lobes- seen in persistent bacterial infections, iron deficiency anemia and renal failure.
downey cell
reactive lymphocyte
most likely CD8+ cytotoxic T cell, not an infected B cell
are reactive atypical lymphocytes specific for infectious mono?
NO- activated lymphocytes may be seen with other viral infections and and in a lot of other reactive states
how to confirm mono?
heterophile antibodies (monospot) or IgM antibodies against EBV capsid antigen
what mimics mono?
CMV
distinguish neoplastic from reactive process
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
do we see philadelphia in other myeloproliferative disorders besides CML?
NO! in acute lymphoblastic, but NOT another myeloproliferative
where else can you get MALT besides gastric?
salivary, lacrimal
from autoimmune (e.g. Sjogren’s)
thyroid- hashimoto
no initial translocations, but eventually 11,18 (MALT 1) translocation
what is the name for lymphoid tissue invading the gland?
lymphoepithelial lesion
CML transitioning to AML, what testing do we want?
flow cytometry and cytogenetic studies
If these blasts are CD19, CD19, TDT+ and delta light chain restricted– this means lymphoid
primary criterion for a diagnosis of acute leukemia?
20% blasts in the blood or bone marrow
how would polycythemia vera present clinically
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
treatment options and prognosis of polycythemia vera?
phlebotomy +/- chemo
median survival with treatment is >10 years, 1 month without
possible final outcomes of polycythemia and how are they related to the form of therapy?
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
how to distinguish polycythemia vera from secondary erythrocytosis?
EPO levels high in secondary, low in vera
clinical manifestation of essential thrombocytosis?
hemorrhage, thrombosis –> erythromelalgia (intense, burning pain of hands or feet, erythema and skin warmth)
distinguish essential thrombocytosis from reactive thrombocytosis?
dx of exclusion. Must exclude all other reasons for a reactive thrombocytosis (bleeding, iron deficiency, infections, inflammation, paraneoplastic proliferations and other myeloproliferative disorders)
prognosis of essential thrombocytosis?
12-15 years, similar to that of age–matched controls (50-60 year olds)
anisocytosis with schistocytes, dacryocytes, what’s up?
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)
significance of auer rod?
these are blasts. fused neutrophil primary
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%
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
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
myelodysplastic syndromes distinguished from myeloproliferative disorders?
hematopoiesis in myeloproliferative disorders is effective, producing increased peripheral counts initially
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
