Lymphadenopathy

Question 1

When looking at histology at lymph node what is the biggest marker of neoplasia?

Answer 1

– Loss of Architecture, if you don’t see distinct follicles and other structures, then increased chances of it being neoplasia.

Question 2

What are different clinical symptoms of reactive vs neoplastic lymphadenopathy?

Answer 2

Reactive: Fast growth, painful, systemic symptoms (fever, etc.) and usually mobile.
Neoplastic: Slow growing over time, nontender, no other associated symptoms, location of uncommon LAD

Question 3

What scenerio might a patient have reactive follicular hyperplasia that is non-neoplastic?

Answer 3

Autoimmune Disorder
HIV
Toxoplasmosis

Question 4

When would the paracortical region of the lymph node be hyperplastic, not associated with neoplasm?

Answer 4

EBV
CMV
Herpes
(Viruses, since.. T-cells)

Question 5

A middle aged man with presents with progressive lymphadenopathy throughout his body over the past 6 months. Painless LAD with mild spenlomegaly.

Answer 5

Follicular Lymphoma

Question 6

What would histology find in follicular lymphoma patient lymph node biopsy?

Answer 6

Follicular Hyperplasia – more numerous follicules and decreases paracortical space.

Question 7

What would be the most common surface markers of Follicular lymphoma?

Answer 7

CD10 – usually found on B-cells
CD19/CD20 – mature B-cells
Negative CD5 (T-cells)
Negative CD23 (Naive Mantle Cells)

Question 8

What is the therapy for progressive follicular lymphoma?

Answer 8

Anti-CD20 Therapy

– Rituximab – Causes Complement, CD8 killing, and Apoptosis of CD20 expressing cells.

Question 9

If a patient with follicular lymphoma for many years suddenly notices a rapid increase in size of my lymph nodes, what is most likely responsible?

Answer 9

Follicular Lymphoma has a high rate of transformation into a more aggressive form.

• • Diffuse Large B-cell Lymphoma
• • Burkitt Lymphoma

Question 10

What is the common mutation associated with follicular lymphoma?

Answer 10

– t(14,18) where IgH fuses with BCL-2 (anti-apoptosis), thus harder for the cell to induce apoptosis when damaged because there is alot being produced.

Question 11

How can you differentiate between Burkitt and Large B-cell Lymphoma?

Answer 11

Both of them are positive for CD19/CD20, but Burkitt will additionally have CD10

Question 12

What kind of lymphoma frequent arises from mucosal lymphoid tissue that slowly develops over time?

Answer 12

Lymphoma arising from Margin of Follicle
– Extranodal Marginal Zone Lymphoma –
(Usually in MALToma)
– t(11,18) MALT1-IAP2 fusion

Question 13

What is the common mutation in mantle cell lymphoma?

Answer 13

t(11,14) – cyclinD-IgH fusion

Allow cell cycle progression

Question 14

What translocation and gene action is common associated with “Starry Night” histology?

Answer 14

Translocations involving c-MYC and an immunoglobulin loci

– t(8,14) or t(2,8) or (8,22)

Question 15

What is a common antigenic marker of Mantle cell lymphoma to differentiate it from others?

Answer 15

Mantle Cell = CD5+ CD23-

CLL/SLL = CD5+ and CD23+

Question 16

What differentiates Follicular and Marginal Zone Lymphomas?

Answer 16

Follicular = CD10+
Marginal = CD10-

Question 17

What lymphoma is most common associated with EBV outside of the US?

Answer 17

Burkitt Lymphoma - most commonly

Extranodal NK/T-cell lymphoma

Question 18

What are the EBV proteins EBNA1/LMP2 responsible for?

Answer 18

Induces the B-cells to move into the germinal center and proliferate without antigen recognition.

Question 19

What commonly keeps the EBV infected cells under control?

Answer 19

Cytotoxic T-cells, thus immune compromised individuals can have re-activation of EBV

Question 20

Who commonly is infected with EBV and what can be a marker of acute EBV infection?

Answer 20

Most people are infected in developing countries, less people in developed countries.

• • Downey Cells (expanded CD8+ T-cells)
• • Heterophile antibody expression by B-cells

Question 21

When can you detect anti-EBNA antibodies in the serum?

Answer 21

Usually takes the body significant amount of time to get the EBV infection under control and would not be observed until 3-5 months later.

Question 22

How can EBV contribute to oncogenesis?

Answer 22

• Direct Transformation, EBV genes cause overexpression of certain genes/unstable genome. Can increase the risk of a translocation.
• Chronic Inflammation / Bystander Cells get induced

Question 23

If you find an ALK gene rearrangement, what might be the lympoma you are dealing with?

Answer 23

Anaplastic Large Cell Lymphoma

– t(2,5) tyrosine kinase receptor activation

Question 24

What patient populations are common found with EBV associated Burkitt Lymphoma?

Answer 24

• • EBV-endemic areas

- - Immunosuppressed individuals

Question 25

What are the common differences between Hodgkins and Non-Hodgkins lymphomas?

Answer 25

Hodgkins – usually localized to a single lymph node and spreads one by one over time, does not spread outside the lymph nodes or into marrow. Non-Hodgkin is all the opposite involving multiple nodes.

Question 26

What is a key histological find for Hodgkin’s Lymphoma?

Answer 26

Reed Sternberg Cells

– B-cell lineage

Question 27

What do Reed Sternberg Cells look like histologically?

Answer 27

• Large Size
• Binucleation
• “Owl’s Eye”
• B-lineage neoplastic cells

Question 28

What are the surface antigenic marker differences between Hodgkins and Nonhodgkins?

Answer 28

Hodgkins – CD15+ CD30+ (Think lower number with younger people)
NonHodgkins – CD20+ CD45+ (Higher number, older people)

Question 29

What are the clinical differences between Hodgkins and Nonhodgkins?

Answer 29

Hodgkins – Mediastinal Mass, moderately aggressive

NonHodgkins – Cervical / Axillary nodes, slow growing

Question 30

What are the histological differences between Hodgkins and Nonhodgkins?

Answer 30

Hodgkins – Reed Sternberg Cells

Non — Popcorn Cells / Nodular