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77 Cards in this Set

  • Front
  • Back
Gene expression driving CLL
Abnormal CD5 expression on CD20+ B-cells
Gene mutation driving CML
bcr-abl fusion gene (anti-apoptotic + Tyr-kinase)
What mutation causes bcr-abl fusion protein?
t(9;22) Philadelphia chromosome
What % of marrow cells must be blasts to classify ACUTE diseas?
20%
Age of majority of AML cases
elderly; 80% of adult leukemias are AML
Where are Auer rods found?
in cytoplasm of blast cells of AML
Gene mutation causing APL
t(15;17) --> RAR-alpha + PML fusion gene
Treatment for APL
ATRA and chemo, arsenic trioxide
Age of majority of ALL cases
children, usually <6yo
Gene mutations driving ALL
- bcr-abl fusion protein

- 11q23 MLL gene

site of NEGATIVE central selection of T-cells
thymus medulla
site of POSITIVE central selection of T-cells
thymus cortex
location in lymph node for formation of germinal centres
cortex
location in lymph node for antigen stimulation
paracortex
antibodies in PRIMARY immune response
IgM
antibodies in SECONDARY immune response
IgA

IgG

role of T-cells in primary immune response
none; T-cell independent
role of T-cells in secondary immune response
activation of B-cells, Ig class switching

what is in the white pulp of the spleen?

lymphoid nodules

what is in the red pulp of the spleen?
sinusoids filled with blood
locations of MALT
- Waldeyer ring: naso/oropharynx, tonsils, adenoids

- Peyer's patches: ileum, appendix in GI tract

CD45+ cells
leukocytes; non-specific marker
CD20+ cells
mature B-cells; highly specific
CD19+ cells
B-cells; highly specific
bcl6 marker
B-cells in germinal centre
CD10+ cells
lymphoblastic B-cells in germinal centre
CD2+ cells
T-cells; highly specific
CD3+ cells
T-cells; highly specific
CD4+ cells
helper T-cells (Th1, Th2, Th17, etc)
CD8+ cells
cytotoxic T-cells
CD5+ cells
mostly T-cells
bcl2 marker
anti-apoptotic
CD15+, CD30+
Hodgkin's lymphoma (cHL)
CD34+ cells
stem cells
CD38+/CD138+
plasma B-cells (no other B-cell markers!)
Ki67 marker
proliferation
TdT+
lymphoblastic precursors
CD23+
follicular dendritic cells
CLL/SLL marker
acute, non-specific reactive lymphadenitis
bacterial infection causing neutrophilia
chronic, non-specific reactive lymphadenitis
follicular hyperplasia (B-cells)
paracortical/diffuse (T-cells)

sinus histiocytes

causes of follicular hyperplasia
rheumatoid arthritis

toxoplasmosis


early HIV

causes of paracortical/diffuse lymphadenitis
viral

drugs


dermatopathic

chronic, specific reactive lymphadenitis
granulomatous disease +/- abscesses
chronic, granulomatous lymphadenitis NO ABSCESSES
mycobacteria

fungi


sarcoidosis

chronic, granulomatous lymphadenitis WITH ABSCESSES
cat scratch disease (B. henselae bacteria)

tularemia

"popcorn cells" with exploded nuclei found in...
nodular-predominant Hodgkins lymphoma
Reed-Sternberg "owl eyes" cells found in...
classic Hodgkins lymphoma
Majority of B-lymphoblastic NHL manifest as...
ALL (acute lymphoblastic LEUKEMIA)

Majority of T-lymphoblastic NHL manifest as...

LBL (lymphoblastic LYMPHOMA)

Clinical signs of LBL
- mediastinal mass --> effusions

(since T-cell associated, in thymus)

clinical signs of ALL
- bleeding gums, bone pain

(since B-cell associated, and leukemic = blood phase)

Histology of LBL/ALL cells (3 Ms!)
- monomorphic

- monotonous


-medium-sized

LDH marker
sign of high cell turnover in leukemia/lymphoma (released when cells die)
CLL/SLL cell morphology
SMALL cells (duh), round/irregular shape

some larger prolymphocytes in nodes

origin of CLL/SLL
-naive B-cells (poorer prognosis)

-post-GC B-cells (better prognosis)

origin of follicular lymphoma
germinal centre B-cells
genetic mutation in follicular lymphoma
t(14;18) --> bcl2 anti-apoptotic protein + Ig heavy chain fusion protein

(prevents cells with lower affinity Abs from being destroyed)

Follicular lymphoma grade 1
0-5 centroblasts per high-power field
Follicular lymphoma grade 2
6-16 centroblasts per high-power field
follicular lymphoma grade 3a
>15 centroblasts per high-power field, some normal centrocytes remaining
follicular lymphoma grade 3b
>15 centroblasts per high-power field, with no remaining centrocytes

(MORE AGGRESSIVE)

DLBCL extranodal involvement sites
GI tract
DLBCL morphology
Diffuse

Large size (3-4x normal)
B-Cells

LBL markers
TdT+ (since precursor cells)
CD3+ (since T-cells)

+/- CD4, +/- CD8 expression varying based on stage of development

CLL/SLL markers

KEY:


CD23+ (follicular dendritic cells)


also:


CD5+ (abnormal expression in CLL)


CD20+ (since B-cell)

DLBCL markers
elevated LDH (indicates high turnover, since rapidly progressing disease)

elevated Ki67 (proliferation)




CD20+ (since B-cell)



plasma cell/multiple myeloma pathogenesis

(osteoclast activation by cytokines --> bone resorption --> lytic lesions & fractures)

plasma cell/multiple myeloma markers
CD138+ (plasma cell marker)

monoclonal lambda/kappa light chain


one heavy chain predominates

mycosis fungoides pathogenesis
plaque --> patch --> tumour
Leukemic "cousin" of Mycosis Fungoides
Sezary syndrome
Mycosis fungoides markers
CD3+

CD4+


CD8-


(T helper cell markers)

nodular predominant Hodgkins lymphoma markers
CD20+

CD45+


bcl6

classical Hodgkins lymphoma markers
CD15+

CD30+

NHL treatment (besides kicking the Sens' ass)
CHOP-R:

-cyclophosphamide


-hydroxydaunorubicin (adriamycin)


-oncovin (vincristine)


-prednisone


-rituximab

classic Hodgkins lymphoma treatment
ABVD:

-adriamycin


-bleomycin


-vinblastine


-dacarbazide




(or MOPP)

anti-CD20 monoclonal antibody therapy
rituximab
anti-CD30 monoclonal antibody therapy
brentuximab