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Unit 2 Flashcards

1
Q

What is lymphadenopathy?

A

Enlarged lymph nodes

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2
Q

What does painful LAD signify?

A

Acute infection

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3
Q

What does painless LAD signify?

A

Chronic inflammation, metastatic carcinoma, or lymphoma

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4
Q

What are the three small cell lymphomas?

A

(1) Follicular
(2) Mantle
(3) Marginal

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5
Q

Follicular lymphoma

A 
Neoplastic small B cells 
CD20+
Follicle-like nodules in cortex AND medulla
Mostly adults (~60 years) 
Germinal B-cell markers: CD10, BCL6
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6
Q

What do follicular lymphoma B-cells have that reactive germinal cell center B-cells (follicular hyperplasia) do not have?

A

Neoplastic cells have BCL2 (no apoptosis), whereas normal cells do not (want apoptosis)

Reactive have TINGIBLE BODY MACROPHAGES, whereas lymphoma cells do not

Neoplastic follicles are homogenous; reactive follicles have light/dark zones

Follicles through entire lymph node in neoplasia (not just cortex), and no other structures

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7
Q

What is the gene translocation in follicular lymphoma?

A

t(14;18)
Ig heavy chain (IGH) + BCL2

Ig heavy chain is obviously heavily expressed in B cells, so BCL2 (when translocated) becomes over-expressed

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8
Q

What does BCL2 do?

A

Main function: stabilizes mitochondrial membrane. Prohibits Cytochrome C from leaking from mitchondria into cytoplasm –> blocks apoptosis

In the follicle of the lymph node, where there are developing B cells, you want apoptosis!

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9
Q

Mantle cell lymphoma

A

Neoplastic small B cells
CD20+
Mantle zone of lymph node
Mostly adults (~60 years)

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10
Q

What is the gene translocation in mantle cell lymphoma?

A

t(11;14)
Cyclin D1 on Chr 11 translocates to Ig heavy chain locus on Chr 14

Overexpression of cyclin D1 promotes G1/S transition in cell cycle

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11
Q

Burkitt Lymphoma

A

Neoplastic intermediate B cells
CD20+
Associated with EBV
Classically presents as an extranodal mass in child or YA

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12
Q

Endemic Burkitt Lymphoma

A

Malarial belt of Africa
In jaw
4-7 years of age

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13
Q

Sporadic Burkitt Lymphoma

A 
Mostly children or YA
Ileocecal  area (abdomen)
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14
Q

What genetic causes drive Burkitt Lymphoma development?

A

t(8;14)
Translocations of c-myc on Chr 8

Overexpression of c-myc oncogene promotes cell growth

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15
Q

What does Burkitt Lymphoma look like on histology?

A

Starry skies :)

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16
Q

How is Hodgkin Lymphoma different from NHL?

A

NHL: large mass of malignant cells
Hodgkin: rare neoplastic Reed-Sternberg cells

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17
Q

What do Reed-Sternberg cells do and cause?

A

Secrete cytokines that draw in other inflammatory cells, which then results in production of a mass

Cytokines –> ‘B’ symptoms (fevers, chills, night sweats) –> also attract lymphocytes, plasma cells, macs, and eos

May lead to fibrosis

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18
Q

Describe Reed-Sternberg cells

A

Large B cell
Multilobed nuclei and prominent nucleoli (“owl eyes”)
CD15+ and CD30+

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19
Q

Nodular sclerosis HL

A

Classical presentation: enlarging cervical neck/mediastinal LN in a YA, usually female

Lymph node is divided by broad bands of fibrosis

RS cells sit in big open spaces = lacunar cells

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20
Q

Mixed cellularity CHL

A

More often on or below both sides of the diaphragm

On histology, RS cells + mixed cells in background –> abundant eosinophils (IL-5)

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21
Q

Lymphocyte rich CHL

A

Nodular growth pattern
Classic RS cells very rare
Best prognosis

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22
Q

Lymphocyte depleted CHL

A

Least frequent subtype (~1%)
Paucity of lymphocytes
Numerous RS cells, which appear bizarre
Worst prognosis :(

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23
Q

Plasma cell neoplasm

A

Clonal proliferation of plasma cells
Express one Ig or protein
Mostly bone marrow, but also elsewhere

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24
Q

What are two germinal B cell markers?

A

BCL6 and CD10

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25
Plasma cell myeloma (multiple myeloma)
Bone marrow-based M protein in serum/urine Clinical features: bone pain in the back or extremities (osteoporosis) Radiologic features: lytic bone lesions, osteoporosis, fractures
26
What is an M protein?
A monoclonal protein --> a polypeptide subunit of the Ab | Can be detected in urine
27
What is the definition of an acute leukemia?
A neoplastic proliferation of blasts Defined as an accumulation of >20% blasts in the bone marrow
28
What is the hallmark of a lymphoblast?
(+) for TdT in the nucleus TdT = DNA polymerase
29
What is the classic hallmark of a myeloblast?
Presence of myeloperoxidase (MPO) Cytoplasm --> can crystallize into an AUER ROD
30
Describe ALL
Acute lymphoblastic leukemia +TdT 75% in kids <6 yrs Associated with Down Syndrome (after the age of 5)
31
Describe (in-depth) the subclassifications of ALL
B-ALL: 80-85% of cases of ALL Typical ALL of childhood T-ALL: Around 25% of cases More frequently in adolescent and YA Often presents as a mediastinal mass (thymus region)
32
What markers do B-ALL cells express?
CD19 and CD22 Usually do not express CD20 or surface Ig (mature markers)
33
What are the 3 common cytogenetic abnormalities seen in B-ALL, and what are the age groups associated with them?
t(12;21) 25% of childhood B-ALL Very favorable prognosis t(9;22) --> BCR-ABL1 (p190 breakpoint instead of p210 in CML --> Ph+ ALL) 25% of adult ALL (more common in adults) Worst prognosis translocation of 11q23 --> MLL Neonates & young infants Poor prognosis
34
What are the surface cell markers of T-ALL?
CD3 and CD7
35
What is the full name of T-ALL? And why?
T acute lymphoblastic lymphoma Lymphoma because the cells are forming a mass ("-oma") in the mediastinum. Leukemia = they're floating around.
36
What are prognostic factors in ALL?
``` Worse prognosis: Infant (10 yo) Very high WBC count T-lymphoblastic Hypodiploidy (<46) Slow response to Rx Min. residual disease ``` Better prognosis: 1-10 yo B-lymphoblastic Hyperdiploidy (51-65)
37
Describe AML
Acute myeloid leukemia Elderly (~65) **AUER RODS (from MPO)**
38
What are the cytogenetic classifications of AML? What are the typical patient ages and prognoses?
t(8;21) Younger patients Relatively good prognosis inv(16) or t(16;16) Younger patients Relatively good prognosis t(15;17) --> PML-RARA aka acute promyelocytic leukemia (APL) t(1;22) Mostly seen in infants with Down Syndrome Relatively good prognosis ``` Abnormalities of 11q23 --> MLL Poor prognosis (similar to cases of ALL with abnormalities of MLL) ```
39
What is MLL?
Mixed lineage leukemia
40
Why is APL important?
Acute promyelocytic leukemia Abnormal promyelocytes predominate instead of blasts Important because: (1) The gene fusion fuses retinoic acid receptor-alpha (RARA) gene to another gene. RARA is needed for differentiation of promyelocytes. Fused protein = block in differentiation. However, block can be overcome with high doses of all-trans retinoic acid (ATRA) + arsenic salts --> give 'em Vitamin A (ATRA), not chemotherapy! (2) Sometimes --> DIC :(((( (b/c of Auer rods)
41
What is a myelodysplastic syndrome?
Cytopenias with hypercellular bone marrow (basically, pre-leukemia) Abnormal maturation with increased IMMATURE CELLS (blasts) - but 20% blasts)
42
What are the two main categories of therapy-related AML? What is their prognosis?
Alkylating agents or radiation 2-8 years later Usually progresses to AML via an MDS stage Whole or partial losses of Chr 5 and/or 7 Topoisomerase inhibitors 1-2 years later de novo AML rearrangement of MLL gene (11q23) All have very poor prognosis
43
What are 3 molecular markers currently used to predict prognosis in patients with AML? Which one trumps the other two?
****1. FLT3****** Prognosis: POOR 2. Nucleophosmin-1 (NPM1) mutation Prognosis: GOOD 3. CEBPA mutation Prognosis: GOOD (#2 & #3 = as long as #1 is absent)
44
Describe CLL
Chronic lymphocytic leukemia Neoplastic proliferation of naive B cells Cells co-express CD5 and CD20 (CD5 normally on T cells) Negative for CD10 (not germinally-derived) Smudge cells
45
What is SLL?
Small lymphocytic lymphoma Occurs when CLL spreads to lymph nodes --> generalized lymphadenopathy
46
What is a myeloproliferative neoplasm?
A neoplastic proliferation of MATURE myeloid cells (megakaryocytes, monocytes, RBCs, and granulocytes) Causes an increase in errybody. However, named based on predominant cell.
47
What are some complications of MPNs?
(1) Increased risk for hyperuricemia and gout (2) Progression to marrow fibrosis (3) Transformation to acute leukemia
48
Describe CML
Chronic myeloid leukemia Increase in *granulocytes* --> leukocytosis. Markedly hypercellular bone marrow. BCR-ABL1 gene transfusion! (p210) Tyrosine-kinase inhibitors (TKIs) (like imatinib) have dramatically improved prognosis = 5-year overall survival rates around 80-85%
49
What are 2 reasons for hepatosplenomegaly frequently seen in MPNs?
(1) Sequestration of extra blood cells | 2) Extramedullary hematopoiesis --> blood cells are made in liver (like they were in fetal stage
50
Describe polycythemia vera
Neoplastic proliferation of mature myeloid cells, especially RBCs Associated with JAK2 mutation Most serious complication are arterial or venous thrombosis
51
Which thromboses should raise the suspicious of PV?
Mesenteric vein, portal vein, or splenic vein
52
What are the phases of PV?
(1) Polycythemic phase = increased blood counts (2) Spent phase = extensive marrow fibrosis with corresponding fall in blood counts
53
What is Budd-Chiari Syndrome?
Thrombosis in/occlusion of the hepatic vein Classically presents as abdominal pain, ascites, and liver enlargement (#1 cause of this = PV)
54
Treatment of PV?
Phlebotomy 2nd line: hydroxyurea
55
Essential Thrombocythemia
Persistent thrombocytosis JAK2 mutations present in 50% of cases Increased risk of bleeding (if they don't work at all) and/or thrombosis (if there are too many & they all work)
56
What is a sign of essential thrombocythemia on histology?
Clusters of very large megakaryocytes
57
Primary Myelofibrosis (PMF)
Megakaryocytic hyperplasia (and, to lesser extent, granulocytic), but NO RBCs JAK2 mutations in 50% of cases Results in marrow fibrosis --> extramedullary hematopoiesis in spleen --> splenomegaly Leukoerythroblastosis = more immature cells in the blood (both red and white), b/c forced out from spleen
58
What type of cells occur on a smear in myelofibrosis?
Tear drop cells (dacrocytes) | Small # of RBCs in fibrotic marrow have to squeeze to get out
59
What type of cytopenia is suspicious for MDS (myelodysplastic syndrome)?
Persistent cytopenia in 2+ lineages in a patient of advanced age
60
What are four possible causes of secondary myelodysplasia that might mimic MDS?
1. Vitamin deficiency (B12, folate, etc.) 2. Toxin exposure (e.g., heavy metals) 3. Exposure to certain drugs 4. Viral infections
61
What are 3 viruses known to have oncogenic effects in some types of lymphomas?
(1) Epstein-Barr virus (EBV): Some cases of classical Hodgkin lymphoma, some cases of Burkitt lymphoma, some other B cell non-Hodgkin lymphomas (2) Human T cell leukemia virus-1 (HTLV-1): Causative factor in adult T cell leukemia/lymphoma (ATLL) (3) Kaposi sarcoma herpesvirus/Human herpesvirus-8 (KSV/HHV-8): Primary effusion lymphoma
62
Contrast the incidence of leukemias & lymphomas in children vs. adults
In childhood: Leukemia is the most common childhood cancer by type. Lymphoma is the third most common childhood cancer by type. In adults: Non-Hodgkin’s lymphoma is 7th most common Leukemia is 10th most common

Blood & Lymph (2 decks)

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