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MDTI > Small B Cell NHLs > Flashcards

Small B Cell NHLs Flashcards

1
Q

what are small B cell NHLs derived from?

A

mature B cells

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2
Q

is bone marrow involvement common in small B cell NHLs?

A

yes. lots of stage 4 disease (as well as liver/spleen involvement)

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3
Q

immunophenotypic profile for follicular lymphoma

A

CD19/20+ (mature B cell)
CD5- (not T cell)
kappa/lambda restricted
CD10+, BCL6+, BCL2+ (germinal center origin, but cells don’t apoptose)

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4
Q

immunophenotypic profile for CLL/SLL

A

CD19/20+ (mature B cell)
CD5+ (aberrant T cell marker)
kappa/lambda restricted
CD10-, BCL6-, BCL2+ (not from germinal center)

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5
Q

immunophenotypic profile for marginal zone lymphoma (MALT)

A

CD19/20+ (mature B cell)
CD5- (not T cell)
light chain restriction
CD10-, BCL6-, BCL2+ (not germinal center origin)
** no distinct immunophenotypic marker***

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6
Q

what is the most common NHL?

A

follicular lymphoma

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7
Q

what age group does follicular lymphoma affect?

A

middle age and older

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8
Q

morphology of follicular lymphoma

A

nodular neoplasm within lymph node. loss of mantle, polarity, tingible macrophages. complete loss of normal features. Contains centroblast & centrocytes.

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9
Q

growth of follicular lymphoma

A

indolent

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10
Q

clinical manifestation of follicular lymphoma

A

generalized lymphadenopathy, typically caught at stage 4 (disseminated) due to slow growth. spleen/liver involvement common with miliary lesions and painless splenomegaly. extra nodal involvement is uncommon.

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11
Q

prognosis of follicular lymphoma

A

incurable due to indolent growth (therapies target cell division). 7-9 year survival

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12
Q

current therapy for follicular lymphoma

A

observation, symptomatic relief, Rituxan, multiagent regiments (CHOP)

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13
Q

more severe follicular lymphoma

A

can transform into diffuse large b cell lymphoma. can occur after treatment and cuts survival to <1yr

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14
Q

derivation of follicular lymphoma

A

germinal center B cell

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15
Q

centrocytes

A

small cleaved, low grade germinal center b cells that can disseminate through the blood

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16
Q

centroblasts

A

large, transformed noncleaved germinal center B cells.

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17
Q

how to grade follicular lymphomas

A
  1. Cytology: centroblast count
  2. Extent of nodularity

(higher grades=higher centroblasts, diffuse nodules=more aggressive)

18
Q

bone marrow pattern in stage 4 follicular lymphoma

A

paratrabecular aggregates

19
Q

follicular lymphoma translocation

A

t(14;18). IgH-Bcl2=constitutive Bcl2 activity=no apoptosis

20
Q

Ki67 in follicular lymphoma

A

low. cells aren’t proliferating because they aren’t dying. Just accumulate instead.

21
Q

CLL/SLL derivation

A

unclear. either 1. mature B cells that just left marrow, haven’t encountered antigen, no TdT/CD34, with light chains or 2. B cells that encountered antigen in follicle and are chilling in the margin

22
Q

CLL/SLL stands for…

A

Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (circulating cells and solid masses)

23
Q

epidemiology of CLL/SLL

A

affects 60+ and males more than females. most common adult leukemia

24
Q

clinical features of CLL/SLL

A

usually asymptomatic, generalized lymphadenopathy, always stage 4, spleen&liver involvement, peripheral blood involvement (unlike FL), immune dysregulation (AIHA or thrombocytopenia) caused by normal B cells

25
Q

CLL/SLL prognosis

A

variable survival 4-6 years, easily transforms to prolymphocytic leukemia or undergoes Richter’s Transformation (both <1yr survival and resistant to treatment)

26
Q

Richter’s Transformation

A

transformation of CLL/SLL to diffuse large B cell lymphoma

27
Q

CLL/SLL morphology

A

diffuse sheet of small resting lymphocytes in lymph node with proliferation centers of larger transformed cells with more cytoplasm (pro lymphocytes or paraimmunoblasts). No follicle structure, effacement of architecture

28
Q

peripheral blood smear of CLL/SLL

A

lymphocytosis, smudge cells (disrupted white cells), spherocytes (autoimmune attack), nucleated RBCs, increased reticulocytes (polychromasia)

29
Q

CLL/SLL bone marrow involvement

A

nodular aggregates (or diffuse spread) in marrow away from trabecular in area of interstitium

30
Q

naive form of CLL/SLL

A

contains rearranged but unmutated Ig, pre-germinal center, Zap70+, aggressive form of the disease

31
Q

post germinal center form of CLL/SLL

A

contains rearranged and somatically hyper mutated Ig genes, has traversed GC. Zap70-, Indolent

32
Q

Marginal Zone Lymphoma origin

A

comes from ill defined area outside germinal center where B cells go after encountering antigen and either become memory or plasma B cells.

33
Q

three separate marginal zone lymphoma diseases

A

Nodal, Muscosal/Extranodal (MALT), Splenic

34
Q

MALT stands for…

A

extranodal marginal zone lymphoma of mucosa associated lymphoid tissue

35
Q

Cause of MALT

A

chronic inflammatory lesions (helicobacter, campylobacter, ect)

36
Q

MALT prognosis

A

indolent, but still can transform to diffuse large B cell lymphoma

37
Q

sites of MALT

A

Stomach, Small bowel, skin, orbit, Lung, Parotid, thryoid

38
Q

MALT morphology

A

abnormal germinal centers with expanded margins, and effacement of underlying architecture. small mature lymphocytes beyond margin, monocytoid b cells in margin, ample plasma cells

39
Q

consequence of increased plasma cells in MALT

A

can secrete a low level of Ig into serum and urine (paraprotein)

40
Q

main mechanism of MALT lymphomas

A

inhibit apoptosis/promote cell growth via NF-kB activation

41
Q

treatment of MALT

A

can treat underlying infections up to a certain point and neoplasm will regress. eventually cellular change will be independent of inflammatory stimulus and chemotherapy is required

MDTI (42 decks)

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