Leukemia, Lymphoma

Acute leukemia = die within short period if untreated and blast in BM or peripheral blood >20% WHO, or >30% FAB.

ALL, AML differences clinical feature (read MGH) and course different, but sometimes still difficult to distinguish, then will need specialized test like MPO, sudan stain, cytogenetics, immunophenotying for CD (refer to Essential Haem), but theres a hybrid leukemia (Essential 162)

NC, NC anemia, thrombocytopenia occur in ALL, AML, CLL (note in CML, theres frequently thrombocytosis instead)

Lymphadenopathy: more in ALL than AML, CLL 80% has this, not really a feature of CML

Splenomegaly: CML nearly always, usually massive, ALL may have moderate splenomegaly due to infiltration, monocytic AML (ie M5 in FAB classification) may have, CLL usu late stage has hepatosplenomegaly

Leukostasis: AML, CML blastic phase Leukemia vs lymphoma

CLL has lots of overlap with lymphoma, bx of LN in CLL actually shows low grade small lymphocytic lymphoma

But note lymphoma is malignant lymphocyte in primarily in LN, though it may have leukemic phase

Even if lymphoma infiltrated BM, it appears as lymphocytes infiltration instead of those blasts predominant pattern in leukemia

Now may think in chronic leukemia, theres accumulation of mature cell instead of blast, then how to differentiate? Thats why theres overlap between CLL and lymphoma

For lymphoma, think of the Ann Arbor system (more for HL), international prognostic index, B>T>NK, high vs low grade (NHL)

Some random detail points Infiltration gum? AML M5 (monocytic), Chronic myelomonocytic leukemia ALL CNS? Dx by lymphoblast in CSF, may present with meningeal syndrome (not specific for ALL, can also be used in any other meningeal irritation), CN palsy etc

ALL can have high, normal, low lymphocyte count (high is poor prognostic)

Only AML needs maintenance HTLV caused adult T-cell leukaemia/lymphoma EBVs role not well understood but 50% HL found it. MDS invariably turn into AML CML in the 3rd stage, ie blastic phase, 70% into AML, 30% into ALL. The blastic phase can develop in days to weeks (Essential 185)

CML is not = Ph positive! CML includes 6 different leukemia, though Ph positive is the most common (95%)

Ph chromosome means the abnormal shortened chromosome 22. In CML its t(9;22)(q34;q11), leading to production of a 210kDa TK, normal is 145kDa. In ALL, some may also have Ph chromosome (poor prognostic sign), but the Ph can have the same BCR breakpoint as in CML, can also have different breakpoint, leading to production of 190kDa TK instead.

Lymphoid organ in lymphoma? LN, spleen, tonsil, thymus, peyers patches, appendix

Hodgkin Lymphoma has bimodal peak, one in 30s, on in elderly. Non-hodgkin usu 60s.

Nodular sclerosis type of classical HL is the more common type (together with mixed cellularity type). NS HL more common in young women, featuring mediastinal involvementassociated pleural effusion and SVCO!

T-ALL also characteristically cause mediastinal mass thymus or mediastinal LN

CLL from antigen experienced, memory type B cell! No T cell

Dont forget the CLL monocloncal gammopathy in 5% patient!

LN in leukemia usu symmetrical, but in NHL asymmetrical. RS cell is clonal B cell.

Radiation related? Both ALL, AML may occur