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Path Exam 6 > Lymphoma > Flashcards

Lymphoma Flashcards

1
Q

What are the three areas where B cells are found within a lymph node?

A

Germinal Center: activated B cells proliferate
Mantle=Naive B cells
Margin=memory B cells

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2
Q

What is the differential if lymphadenopathy is present?

A

Reactive proliferation
Metastatic malignancy
Lymphoma

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3
Q

Reactive patterns of lymphadenopathy are _____

A

Reactive patterns in lymph node are benign

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4
Q

Patterns of reactive lymphadenopathy

A 
Follicular
Interfollicular
Sinusoidal
Mixed
Necrotizing
Granulomatous
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5
Q

What causes reactive lymphadenitis?

A

Response to an infection or cell debris or foreign material or antigen

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6
Q

What is a specific inflammatory pattern of lymph nodes?

A

Specific means that it is specific to a disease so you can look at the pattern and know the disease
Granulomatous lymphadenitis is specific to TB
Caseating Granulomas: TB, Cocci, other fungi
Noncaseating: Early TB, Sarcoidosis

If it isn’t specific, then it is either Acute or Chronic nonspecific

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7
Q

What is acute nonspecific localized lymphadenitis?

A

Localized means it is draining something locally

Example: pre-auricular nodes drain an infection in teeth, tonsils, etc

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8
Q

What is generalized acute nonspecific lymphadenitis?

A

In children, not adults
Enlarged lymph nodes throughout body
Reaction to a systemic viral infection or bacteremia

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9
Q

Acute Lymphadenitis clinically, morphologically, and diseases of each

A

Acute Lymphadenitis:
Clinical: enlarged, warm, red, and tender LN’s
Morph:
-Follicular Hyperplasia with necrosis and PMN’s
(pyogenic infection)
-Follicular Hyperplasia and suppurative granulomas
(Cat-Scratch–bartonella, Yersinia, Tularemia)

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10
Q

Mesenteric Lymphadenitis

A

Acute lymphadenitis of intrabdominal lymph nodes draining the intestines
Self-limited, symptoms like acute appendicitis
Often assoc. with enterocolitis from Yersinina Enterocolitica

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11
Q

Chronic nonspecific lymphadenitis clinical and morphological

A

Clinical: enlarged and non-tender
these are lymph nodes that have persisted for longer period of time than acute

Morphological:

  • Follicular Hyperplasia
  • Paracortical Hyperplasia
  • Sinus Histiocytosis
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12
Q

If pathologist says that a lymph node has hyperplasia, is it benign or malignant?

A

Hyperplasia is benign

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13
Q

Follicular hyperplasia characteristics and associated conditions

A

B cell proliferation causes prominent germinal centers and apoptotic bodies
Associated with early HIV and RA

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14
Q

Paracortical-Interfollicular Hyperplasia causing chronic nonspecific lymphadenitis characteristics and associated conditions

A

T-cell hyperplasia of immunoblasts with infiltrate of macrophages and eosinophils
Associated with viral infections: Mono (EBV), CMV, VZV
Also: vaccines and SLE

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15
Q

Sinus Histiocytosis causing chronic nonspecific lymphadenitis

A

Increase in macrophages in sinuses of LN
Benign LN’s, but often enlarged from draining breast, and colon cancer
May result from drainage of inflammatory foci

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16
Q

Mixed patterns of reactive LN hyperplasia

A

Follicular, interfollicular, sinus

Assoc. with Toxoplasmosis

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17
Q

What is a lymphoma?

A

Neoplastic monoclonal proliferations of lymphocytes that form a mass
All are malignant
Can be Indolent, Intermediate, Aggressive

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18
Q

Lymphoid neoplasm presentations

A

2/3 of lymphoid neoplasms present as tissue masses that can be nodal or extranodal
1/3 have leukemic presentations with symptoms related to bone marrow suppression

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19
Q

What types of cells make up a lymphoma and which are better or worse?

A

Lymphocytes:
B-cells= better
T-cells= worse
Nk cells= also bad

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20
Q

Lymphomas are often associated with what kind of immune system?

A

Lymphomas are often associated with immune abnormalities
More common in immunodeficient
Autoimmunity common

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21
Q

What happens to the immune system once someone develops a lymphoma?

A

Once a lymphoma starts, that rest of the immune system is suppressed

22
Q

What happens if neoplastic cells are injected into an individual? Where do they go?

A

Neoplastic cells act like the normal counterparts in many ways. If injected, the cells will migrate to the tissues where they are supposed to be.
Follicular Lymphoma cells home to germinal center
T-cell lymphoma cells home to the skin

23
Q

How is a lymphoma diagnosed?

A 
Biopsy is the only way
Features considered for diagnosis:
-Clinical Features of the disease
-Histology
-Immunophenotype
24
Q

How is clonality of a lymphoma determined?

A

Check for light chain Ig restriction
Normally there is a 50:50 distribution of kappa and lambda light chains, but when there is a monoclonal population the ratio will tip in one direction over another

25
What are the two main categories for the classification of a lymphoma?
Hodgkins and NonHodgkins lymphoma | NHL has many different types and is the most common
26
``` Follicular Lymphoma: Presentation Incidence Immunophenotype Mechanism ```
Presents as non-tender chronic lymphadenitis 40% of all lymphomas Middle age, M=F B-cells, markers: CD19, 20, 10 t(14;18) => over-expressed BCL2 => blocks apoptosis Resistant to chemotherapy
27
BCL-2 staining in normal lymph node vs in follicular lymphoma
In a normal lymph nodes, BCL2 is expressed in the marginal cells where we have memory B cells that we want to live forever In follicular lymphoma, the cells in the germinal center also stain for BCL2 indicating an abnormality
28
Follicular Lymphoma Morphology macroscopic and microscopic
Macro: LN's enlarged and often matted masses Micro: normal architecture of the node is effaced, follicles are everywhere and are filled with uniform cells
29
Follicular Lymphoma clinical aspects
Painless and often generalized lymphadenopathy Indolent progression, 7-9 year survival Treatment usually doesn't change survival Responds poorly to chemo, but rituximab (anti-CD20) can be used to control disease Transforms to aggressive large cell B lymphoma in 50% of cases => survival of 1 year
30
``` Diffuse Large B Cell Lymphoma: Presentation Features Markers Incidence Genetics Treatment ```
DLBCL is aggressive, causes a painless, localized mass that is extranodal (can be nodal) GI, skin, bone, CNS, Waldeyer's Ring All ages, but median age of 60 Most common aggressive lymphoma of adults B-cell markers CD19, 20, 10 BCL-6 most common, chromosome 3, represses factors that promote growth arrest and apoptosis in germinal centers (stops the factors that usually stop the cell growth and differentiation) Immunodeficiency associated–HIV, transplantation, elderly Neoplastic cells are EBV infected! Initial treatment is to restore immune function This is the end type for all B cell lymphomas (CLL and B lymphomas evolve into this) High mitotic rate, therefore responds well to Chemotherapy => 80% remission, 50% cured
31
What are the types of Burkitt Lymphoma?
African (endemic) Sporadic (nonendemic) HIV associated
32
Burkitt Lymphoma morphology
High mitotic index Diffuse, intermediate, uniform lymphs with apoptotic bodies forms a Starry Sky pattern Stars are the macrophages that have ingested the apoptotic bodies
33
What causes Burkitt Lymphoma?
MYC oncogene on chromosome 8 required usually t(8;14) puts Ig heavy chain promotor with MYC for upregulation of expression MYC: transcription regulator, increases aerobic glycolysis => increased growth
34
Burkitt Lymphoma clinical for the different types
African: 100% assoc. with EBV, extranodal, fasial, tends to be the mandible, leukemia unlikely HIV assoc.: 25% EBV assoc. Sporadic: USA, 15-20% EBV, more common in youth, causes 30% of childhood NHL
35
What is the fastest growing human tumor?
Burkitt Lymphoma
36
Where is sporadic Burkitt Lymphoma most often found in kids?
Ileocecal mass most common | Other visceral also possible: kidney, ovary, adrenal glands
37
How is Burkitt Lymphoma treated?
Though it is aggressive, it responds well to chemo and => cures in children and young adults, older adults more guarded prognosis
38
Mantle Cell Lymphoma
t(11;14) Cyclin D1 gene allows cell to progress through G1 –> S phase of cell cycle Late adulthood, painless LAD
39
What type of lymphoma is a MALToma?
Marginal Zone Lymphoma
40
MALToma/ Marginal Zone Lymphoma characteristics
Middle aged adults Marginal Zone is obviously nodal MALToma is extranodal: tends to arise from chronic inflammation and infection Remains localized for long periods before spreading systemically May regress if inciting agent removed
41
What diseases or conditions are assoc. with extranodal Marginal Zone Lymphoma?
Assoc. with autoimmune diseases: - Sjogren's syndrome (salivary glands) - Thyroid-Hashimoto's thyroiditis Chronic infection–H. pylori
42
What types of cells are involved with Marginal Zone Lymphoma?
Being marginal, they are memory B cells CD19,20
43
MALToma pathogenesis
Reactive polyclonal at first, transforms to monoclonal but B-cells still dependent on T cells so regression may still occur Acquisition of translocations of BCL10 or MALT1 result in growth factor independence Can transform into large B cell lymphoma
44
Fundamental difference between B and T cell lymphomas
T cell lymphomas are always diffuse | Only B cell lymphomas can cause a mass
45
General characteristics of Peripheral T-cell lymphoma unspecified
Most common T- cell lymphoma of adults Morphology: always diffuse, infiltrates of pleomorphic lymphs, reactive eosinophils, macrophages, prominent angiogenesis TdT negative, CD 2,3,5 positive, also CD4 or 8 Generalized lymphadenopathy, fever, weight loss, pruritis, eosinophilia all from cytokines that have been released Sometimes hard to tell this from an infection because of the eosinophils and the macrophages present
46
Anaplastic Large Cell Lymphoma
ALK gene (anaplastic large cell kinase) rearrangement present CD8+ T-cell; CD30 positive Morphology: large cells with horseshoe shaped nuclei and abundant cytoplasm resembles metastatic carcinoma, but that doesn't happen in kids This is a children and young adult type 80% cure with chemo Responds to ALK inhibitors
47
Large cells with horseshoe shaped nuclei that stain positive for ALK in a young person
Anaplastic Large Cell Lymphoma
48
Adult T-cell leukemia/lymphoma
Neoplasm of CD4 T-cells Caused by an HTLV-1 infection that is endemic to Japan, Africa, Caribbean. Causes Tax protein activation of NFKB Clinical: Skin involvement, also LN, liver, spleen and marrow Survival 3 months to 3 years T-cell morphology: multilobulated, cloverleaf nuclei
49
Mycosis Fungoides/Sezary Syndrome
2 manifestations of CD4 T-cell (SKIN HOMING) Morphology: cerebriform nuclei Name from doctors treating long-term what looked like a fungal infection but was actually the skin deposits of neoplastic T-cells Goes through phases: patch, red, exfoliative rash, plaque, then tumor After tumor phase it can spread to the lymph nodes and the bone marrow Microscope: Pautrier microabscesses = T-cells around dendritic cells in the skin, Sezary-Lutzner CD4 T-cells
50
What is Sezary Syndrom?
Red man exfoliative erythroderma, pruritic rash over body Has leukocytosis with large CD4 T-cells with cerebriform nuclei Occurs concurrently with Leukemia

Path Exam 6 (1 decks)

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