Miscellaneous Flashcards
Myeloid cells in EMH of spleen
Can look immature for some reason
Primary follicles
BCL2+ CD10-
Remember that BCL2 is normally a ____ marker
T cell
Early “precursor” to progressive transformation of germinal center
Follicle lysis
Normal distribution of B cells in lymph node
Within germinal center, mantle zone, and marginal zone
Intrasinusoidal pattern of lymphoma within node
ALCL ALK+ DLBCL
Difference in AML blasts vs MDS blasts
In AML they are often CD34 and CD117 negative In MDS they are often positive
Can see circulating polyclonal plasma cells in…
Angioimmunoblastic T cell lymphoma Superbug infection HIV *Also can see few clonal circulating plasma cells in myeloma, not an outright plasma cell leukema*
Lesson to learn about flow…
Do NOT make your morphologic impression based on flow! -Case called “T cell lymphoproliferative process” by flow was actually a DLBCL (miscalled a PTCL by outside client based on flow) -Case with flow showing “increased CD4+/CD57+ coexpression, can be seen in nodular LP HL” by flow is actually a T-cell/histiocyte rich large B cell lymphoma (miscalled NLPHL by outside)
Evan’s Syndrome
-An autoimmune disease in which an individual’s antibodies attack their own red blood cells and platelets -Both of these events may occur simultaneously or one may follow on from the other -Combination of autoimmune hemolytic anemia (DAT+) and idiopathic thrombocytopenic purpura
TAR Syndrome
Thrombocytopenia-Absent Radius Syndrome: -rare genetic disorder that is characterized by the absence of the radius bone in the forearm, and a dramatically reduced platelet count -may occur as a part of the 1q21.1 deletion syndrome -other findings may include heart problems, kidney problems, knee joint problems, lactose intolerance and thumb hypoplasia
Rules for karyotype clonality
Loss= 3 cells Gain= 2 cells Structural= 2 cells
Rules for separated 138+ plasma cells FISH
≥8 total cells for 1F1G1R ≥5 total cells for all the readers (not a %) for everything else (p.s. these are arbitrary cutoffs)
Commonly rearranged chromosomes in hematolymphoid neoplasms
chromosomes 1 and 6 (this is why we have the MYB FISH- not to look at the gene rather to look at chromosome 6)
ATM gene
DNA repair gene
Location of BCL-6 gene
chromosome 3q27
TdT
can be expressed on immature myeloid cells in addition to immature lymphoid cells
Burkitt
shows a loss of normal infiltrating lymphocytes, unlike DLBCL
BCL2+
unlikely to be Burkitt
MYH9 disorders
1. May-Hegglin Anomaly:
- AD mutation in this gene leading to Dohle leukocyte inclusions (in granulocytes only) with macrothrombocytopenia (usually requires no tx, unless severe)
- MHA is also a feature of the Alport syndrome (hereditary nephritis with sensorineural hearing loss)
2.Sebastian, Fechtner, Epstein syndromes:
- related syndromes with macrothrombocytopenia and leukocyte inclusions
- also feature deafness, nephritis, and/or cataracts
BCL2 IHC interpretation
weaker in B cell lymphomas compared to adjacent normal T cell expression
Interstitial lymphoid aggregate
If perivascular, interstitital- very good sign it is reactive
Monocytic AML with hemophagocytosis
t(8;16)
Flow findings in APL
- side scatter usually increased (unlike monoblastic AML)
- CD33 usually very tight cluster (not a smear)
- CD11b, CD11c, CD15 negative
- in hypogranular APL: pCD34, pCD15 with negative CD2, CD56
- Note: variant APL such as t(11;17) may be more monocytic, more hypogranular
Monoblastic AML
often associated with MLL
less strong side scatter than APL
CD123
plasmacytoid dendritic cells
hairy cell leukemia
basophils
increased plasma cells
normal aging
MGUS
viral (HIV)
autoimmune
Assessing Fe stores
If 1-2 histiocytes contain iron, then can say decreased (or absent)
If a lot, you can also say increased
Otherwise, say present
ATRA syndrome
potentially life-threatening complication observed in patients with acute promyelocytic leukemia(APML) and first thought to be specifically associated with all-trans retinoic acid (ATRA) (also known as tretinoin) treatment.[1] Subsequently it was recognized that so-called RAS appeared in APML patients who had been treated with another highly efficacious drug, arsenic trioxide, and yet did not appear in patients treated with tretinoin for other disorders. These facts and others support the notion that RAS depends on the presence of the malignant promyelocytes. This has led to the growing deprecation of the term ‘retinoic acid syndrome’ and to an increasing use of the term differentiation syndrome to signify this APML treatment complication
The syndrome is characterized by dyspnea, fever, weight gain, hypotension, and pulmonary infiltrates. This is effectively treated by givingdexamethasone and holding ATRA (or arsenic trioxide) in severe cases.
PRES
Posterior reversible encephalopathy syndrome (PRES), also known as reversible posterior leukoencephalopathy syndrome (RPLS), is a syndrome characterized byheadache, confusion, seizures and visual loss. It may occur due to a number of causes, predominantly malignant hypertension, eclampsia and some medical treatments (immunosuppresion). Onmagnetic resonance imaging (MRI) of the brain, areas of edema (swelling) are seen.
Blastic plasmacytoid dendritic cells
CD13, CD33, very bright HLA-DR, TdT (~30%), TCL1 in some
TdT in AML
Usually in M0
CD43
Burkitt (almost all)
Threshold for BCL6 staining and BCL2 staining
~30%
Threshold for BCL2 staining and MYC staining
??? (not 30%)
Starry Sky Appearance
T-lymphoblastic lymphoma!
NOT just Burkitt (any highly proliferative lymphoma can look like this)
Flow findings for resting vs activated T lymphocytes
Resting: HLA-DR-, CD25-
Activated: HLA-DR+, CD25+
Lymphoid Aggregates
Small Lymphocytes: nuclei almost touching one another
Large Cell Lymphoma & Plasma Cells: more cytoplasm between cells
Hemepath Cytology
- If you see 2 distinct populations- you may be more worried (especially if the patient is young and has LAD (eg Hodgkin)
- If you see small cells transitioning to large cells with medium sized cells, then more likely to be reactive (eg EBV)
Flow of normal germinal center B cells
bright CD20
HLA-DR
FMC-7
Pitfall when looking for myelofibrosis
Previous biopsy site (consider if the fibrosis is not diffuse, rather an isolated focus)
CD99
HPC
Ewings
ALL
Anaplastic meningioma
Merkel cell CA
Synovial Sarc
ET-like CML
A small % of CML will present like ET, showing only thrombocytosis
CALR mutations
In/dels (NOT point mutations)
Megaloblastoid erythroblasts
glycophorin
e-cadherin
Megakaryocyte stains
CD61 and CD42
MPNs reported in children
ET and CML
Hypermutation Testing
- Somatic hypermutation happens in V region: sequence V and compare (if it all looks the same, then it is not hypermutated)
- Sometimes in FL this can happen inthe J region, which messes up primer attachment to J (in these cases will see t(14;18) but not IgH rearrangment; if add kappa then increase sensitivity from 80% to 90%)
Primary DLBCL of Liver
Very deadly, survival < 6 mos?
Parafollicular CLL
know it exists
BCL2 in nodal marginal zone lymphoma
positive? negative in reactive?
Lymphoid depleted LN
HIV node
“Monocytic/Histiocytic Proliferation”
*BE CAREFUL with this dx! Whenever a myeloid sarcoma does not express the CD43 or MPO, don’t immediately go down this monocytic route! Often it is something else (and benign!!)
2 examples I’ve seen: giant cell poor tenosynovial giant cell tumor (?desmin pos? synovium is modified monocytic cells), lymphoid depleted “burnt out” HIV lymphadenitis
