STEPTRACKERHEMATOLOGY + ONCOLOGY | PATHOLOGY | HIGH-YIELD REVIEW

Myelodysplastic Syndromes & Lymphadenopathy

A crowded marrow that makes bad cells, and how to read an enlarged lymph node — reactive or malignant.

FOCUS ON
In MDS the marrow is full but the blood is empty (ineffective hematopoiesis). Look for dysplastic cells and blasts below 20%. Know pseudo-Pelger-Huët cells, 5q− (lenalidomide), and progression to AML. For nodes, the reactive pattern (follicular, paracortical, sinus, granulomatous) points to the cause. Reactive follicles are BCL2⁻; follicular lymphoma is BCL2⁺.
TOPIC
DETAIL
MECHANISM
CLUE
MDS — definition
Clonal stem-cell disorder: cytopenias + dysplasia + blasts < 20% (≥ 20% = AML).
Cells die in the marrow before release (ineffective hematopoiesis)
Older adults; prior chemo/radiation, benzene, smoking
MDS — morphology
Pseudo-Pelger-Huët (bilobed) neutrophils, hypogranular neutrophils, ring sideroblasts, megaloblastoid RBC precursors, micromegakaryocytes.
Usually hypercellular marrow
Macrocytic anemia often
MDS — genetics
del(5q): older women, macrocytic anemia, normal/high platelets · SF3B1: ring sideroblasts · monosomy 7, TP53: poor.
Clonal mutations accumulate
5q− responds to lenalidomide
MDS — course & treatment
~1/3 progress to AML; infections and bleeding cause most deaths.
Transfusions, hypomethylating agents (azacitidine, decitabine), lenalidomide, stem cell transplant
Rising blasts = transformation
Node — general clues
Tender: acute infection. Painless, hard, fixed: carcinoma. Painless, rubbery: lymphoma.
Location points to the drainage area
Left supraclavicular (Virchow) → abdominal/gastric cancer
Follicular hyperplasia
B-cell zone
More and larger germinal centers, varied in size, with tingible-body macrophages.
B-cell stimulation
RA, early HIV, syphilis, toxoplasmosis
Paracortical hyperplasia
T-cell zone
Expanded interfollicular T-cell areas with immunoblasts.
T-cell stimulation
Viral infection (EBV), phenytoin, vaccination
Sinus histiocytosis
Sinuses packed with macrophages.
Draining tumor or debris
Nodes draining a carcinoma
Granulomatous lymphadenitis
Granulomas within the node.
Th1 response
TB, sarcoidosis, fungi, cat-scratch (stellate abscesses)

Mechanism — ineffective hematopoiesis

Clonal stem cellMutations
→
Dysplastic precursorsFull marrow
→
Die in marrowApoptosis
→
CytopeniasEmpty blood
→
More mutations→ AML

Reactive hyperplasia vs follicular lymphoma

FEATURE
REACTIVE
FOLLICULAR LYMPHOMA
Architecture
Preserved; follicles in cortex
Effaced; back-to-back follicles
Follicle size
Variable
Uniform
Tingible-body macrophages
Present
Absent
Zonation (polarity)
Present
Lost
BCL2 in germinal centers
Negative
Positive
Light chains
Polyclonal κ and λ
Monoclonal

How it's tested

COMMON CONFUSIONBlasts decide the label: below 20% is MDS, at or above 20% is AML.
THE TRAPNormal germinal centers do not express BCL2 because their cells are meant to die if they don't fit. BCL2⁺ follicles mean follicular lymphoma.
YOUR APPROACHCytopenias + cellular marrow + dysplasia → MDS → count blasts → check 5q. For nodes: tenderness, location, then the histologic zone that's expanded.

If you see… think…

70-year-old, pancytopenia, hypercellular marrow, 8% blasts → MDS
Bilobed, hyposegmented neutrophils → pseudo-Pelger-Huët (MDS)
Older woman, macrocytic anemia, normal platelets, del(5q) → 5q− MDS — lenalidomide
MDS with blasts rising to 25% → AML transformation
Cytopenias years after chemotherapy → therapy-related MDS
Hard left supraclavicular node + weight loss → gastric carcinoma (Virchow node)
Teen with sore throat, tender neck nodes, atypical lymphocytes → paracortical hyperplasia (EBV)
Axillary node with stellate microabscesses after kitten scratch → Bartonella
Back-to-back BCL2⁺ follicles → follicular lymphoma
Lymphadenopathy on phenytoin → drug-induced reactive hyperplasia