Every white cell disorder from HEM13 (MPNs), HEM14 (MDS and acute leukemia), HEM19 (lymphoma) and HEM27 (WBC lab) on one page: where each sits by lineage and tempo, the driver lesion behind it, how to work it up, and how the diseases transform into, mimic and complicate each other.
Rows are the lineage (decided by flow cytometry markers). Columns are the tempo: mature cells growing slowly, mature cells growing fast, or blasts piling up behind a maturation block. Dashed chips sit in more than one box, usually because the disease changes over time. Select any disorder to see its essentials and everything it connects to; connected disorders light up on the map.
Every white cell neoplasm is one cell that took one kind of hit. Select a disorder to reveal its driver lesion, how that lesion produces the disease, and its flowchart from the lecture notes. Select a group question to reveal the group summary.
The same routine runs through all four lectures: reactive or neoplastic, then lineage and maturity, then the specific entity, then the specimen and tests that prove it. Each step has the matching flowcharts from the lecture notes.
Pick a kind of relationship. Use Focus on to see only the links for one disorder. Select any name to jump to it on the map.
Each card shows the answer a question wants you to jump to. Decide why it's wrong, then reveal the catch.
| Topic | In-house | Boards / standard | On the exam |
|---|---|---|---|
| ET platelet threshold | >600 × 10⁹/L (HEM13) | ≥450 × 10⁹/L (WHO) | 600k on in-house items; 450k on boards |
| CALR gene name | "Calretinin" (HEM13) | Calreticulin (calretinin is a mesothelioma marker) | Use calreticulin |
| Most common NHL | Follicular, "in the U.S." (HEM19) | DLBCL overall; follicular = most common indolent | Match the wording of the question |
| ALL hypodiploidy | "Intermediate" in one place, "unfavorable" in another (HEM14) | Near-haploid/<44 chromosomes = unfavorable | Hyperdiploid good, hypodiploid bad |
| Hodgkin PD-L1 gene | "Chromosome 2" (HEM19 slide) | 9p24.1 amplification | Know the concept: PD-L1 ↑ → immune evasion |
| Marginal zone CD43 | Negative (HEM27 grid) vs weak (HEM19) | Positive in a subset | Key on CD5− and CD10− |
| PV survival | ≈10 years with treatment | Often longer today | Answer ≈10 y in-house |
Filtered by the lecture highlight above.
| Disorder | Lectures | Markers / look | Genetics | Course | Clinches it |
|---|
Answer before you open each one.
Lymphoid blast crisis (≈30% of blast crises; ≈60% are myeloid). The BCR-ABL translocation arose in a pluripotent stem cell above the myeloid/lymphoid split.
MDS → AML arising from MDS. Blasts <20% with dysplasia, then ≥20%. Monosomy 7 in an older patient = unfavorable, worse than de novo AML with a balanced translocation.
BCR-ABL (FISH/PCR): negative in the leukemoid reaction, positive in CML. The LAP score is high in the reactive patient and low in CML.
Richter transformation to DLBCL (≈10% of CLL). Follicular lymphoma (30–50%, often with MYC), MALT lymphoma and NLPHL can also transform to DLBCL.
CD23 (CLL+, mantle−) and cyclin D1 (mantle+, CLL−). CLL/SLL survives a median of 4–6 years and is often watched; mantle cell (t(11;14)) is the worst of the small-cell lymphomas at 3–5 years.
MALT lymphoma → H. pylori eradication (antigen-driven, can regress). t(11;18) API2-MALT1 predicts resistance.
Not multiple myeloma. CD4+ T cells with clover-leaf nuclei = ATLL from HTLV-1 (Tax). Both cause hypercalcemia with lytic lesions.
Therapy-related MDS/AML: alkylating agents → −5/−7 after 5–10 years (topoisomerase II inhibitors → 11q23 after 1–3 years). It progresses to AML faster and has a poor prognosis. Other late effects: breast cancer, cardiac disease, pulmonary fibrosis.