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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
Q

What are the two main categories for the classification of a lymphoma?

A

Hodgkins and NonHodgkins lymphoma

NHL has many different types and is the most common

26
Q 
Follicular Lymphoma:
Presentation
Incidence
Immunophenotype
Mechanism
A

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
Q

BCL-2 staining in normal lymph node vs in follicular lymphoma

A

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
Q

Follicular Lymphoma Morphology macroscopic and microscopic

A

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
Q

Follicular Lymphoma clinical aspects

A

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
Q 
Diffuse Large B Cell Lymphoma:
Presentation
Features
Markers
Incidence
Genetics
Treatment
A

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
Q

What are the types of Burkitt Lymphoma?

A

African (endemic)
Sporadic (nonendemic)
HIV associated

32
Q

Burkitt Lymphoma morphology

A

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
Q

What causes Burkitt Lymphoma?

A

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
Q

Burkitt Lymphoma clinical for the different types

A

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
Q

What is the fastest growing human tumor?

A

Burkitt Lymphoma

36
Q

Where is sporadic Burkitt Lymphoma most often found in kids?

A

Ileocecal mass most common

Other visceral also possible: kidney, ovary, adrenal glands

37
Q

How is Burkitt Lymphoma treated?

A

Though it is aggressive, it responds well to chemo and => cures in children and young adults, older adults more guarded prognosis

38
Q

Mantle Cell Lymphoma

A

t(11;14) Cyclin D1 gene allows cell to progress through G1 –> S phase of cell cycle
Late adulthood, painless LAD

39
Q

What type of lymphoma is a MALToma?

A

Marginal Zone Lymphoma

40
Q

MALToma/ Marginal Zone Lymphoma characteristics

A

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
Q

What diseases or conditions are assoc. with extranodal Marginal Zone Lymphoma?

A

Assoc. with autoimmune diseases:

  • Sjogren’s syndrome (salivary glands)
  • Thyroid-Hashimoto’s thyroiditis

Chronic infection–H. pylori

42
Q

What types of cells are involved with Marginal Zone Lymphoma?

A

Being marginal, they are memory B cells CD19,20

43
Q

MALToma pathogenesis

A

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
Q

Fundamental difference between B and T cell lymphomas

A

T cell lymphomas are always diffuse

Only B cell lymphomas can cause a mass

45
Q

General characteristics of Peripheral T-cell lymphoma unspecified

A

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
Q

Anaplastic Large Cell Lymphoma

A

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
Q

Large cells with horseshoe shaped nuclei that stain positive for ALK in a young person

A

Anaplastic Large Cell Lymphoma

48
Q

Adult T-cell leukemia/lymphoma

A

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
Q

Mycosis Fungoides/Sezary Syndrome

A

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
Q

What is Sezary Syndrom?

A

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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