Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hannah's Intersystem > Lymph Node Pathology > Flashcards

Lymph Node Pathology Flashcards

1
Q

List 3 examples of secondary lymphoid tissue

A

Lymph nodes
Spleen
MALT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some common sites of MALT?

A

Tonsils, adenoids
Along GIT
Airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the histological appearance of a naive B cell vs. an activated B cell

A

Naive: small, blue, not much cytoplasm
Activated: larger, different morphology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a primary follicle in the context of a lymph node?

A

A dense cellular aggregation composed of inactive small resting B cells (their condensed nuclear chromatin gives the follicle a blue colour)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a secondary follicle in the context of a lymph node?

A

Secondary follicles consist of a pale centre called the germinal centre, surrounded by a darker zone known as the mantle zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the structure of the mantle zone?

A

The mantle zone is made up of small resting B cells, the condensed nuclear chromatin producing the dark blue colour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the role and structure of the germinal centre?

A

The germinal centre is the site of B cell activation, clonal expansion and differentiation and consists of dividing B cells which are larger and paler than the small inactive lymphocytes of the marginal zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the structures found in a lymph node

A

External fibrous capsule: oval, well-circumscribed
Afferent and efferent veins and arteries, as well as the efferent lymphatic vessel: enter and leave at the hilum
Afferent lymphatics: enter around the outside of the node through the capsule, bring in APCs and Ag (which then travel through to the B and T cell areas)
Veins and arteries: form sinuses (cortical and inner medullary) which percolate through the node
B and T cell areas (cortex and paracortex respectively)
Inner medulla: with medullary sinuses and extensions of the B and (mostly) T cell areas called the medullary cords
Medullary cords: final differentiation into plasma cells occurs here (immunoblasts can be seen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens in a germinal centre and after?

A 
Following appropriate stimulation by APCs or Ag, naive B lymphocytes from the mantle zone undergo clonal expansion and differentiation into centroblasts, centrocytes then immunoblasts.
Somatic hypermutation and heavy chain class switching occur
From the GC, the activated B cells migrate to the medullary cords where they complete their differentiation into plasma cells (or some cells become memory B cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the paler areas within the GC?

A

Macrophages containing phagocytosed apoptotic cells (called tingible body macrophages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What other cells (besides B cells) are located within the GC?

A

FDCs

CD4 helper T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What conditions can cause a lymphadenopathy?

A

Reactive (inflammatory and infective): localised infection in the area of drainage, systemic infection (usually viral), non-infective systemic disease (e.g. RA, SLE), drugs
Neoplastic: lymphomas, leukaemic infiltration, metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When is a lymphadenopathy considered significant?

A

Dependent on age of patient and size of lymph nodes (generally cause for concern when <1-2cm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What histological features are seen in an acute non-specific lymphadenitis?

A

Neutrophil infiltration
Oedema
Follicular hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does an acute non-specific lymphadenitis present and what is the most common cause?

A

Nodes are large and painful

Usually caused by microbial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes pain in a lymphadenitis?

A

Lymph node capsule contains pain fibres which are stimulated when the capsule is stretched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 4 patterns of chronic non-specific lymphadenitis?

A 
Follicular hyperplasia
Paracortical
Sinus histiocytosis
Graulomatous inflammation
Mixed pattern
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What causes follicular hyperplasia in chronic non-specific lymphadenitis?

A

Stimuli that activate humoral immune responses (e.g. autoimmune disease, microbial infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What causes chronic paracortical lymphadenitis?

A

Stimuli that activate cellular immune responses (e.g. viral infections, certain drugs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What causes sinus histiocytosis?

A

Increase in macrophages in sinuses, caused by a non-specific stimulus (e.g. draining cancers, infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a more common cause of neoplastic lymphadenopathy: primary or secondary tumours?

A

Secondary

22
Q

What types of tumours readily metastasise to lymph nodes and which do not?

A

Many carcinomas, melanomas, germ cell tumours readily metastasise to lymph nodes
Sarcomas do not metastasise to nodes readily

23
Q

What is classification of neoplastic proliferations of haemopoietic and lymphoid tissues based on?

A

Cell lineage
Morphology
Immunophenotypic profiles +/- genetic abnormalities
Clinical features (to some extent)

24
Q

List 5 types of lymphoid neoplasms

A

Precursor B cell neoplasms
Precursor T cell neoplasms
Peripheral/mature B cell neoplasms
Peripheral/mature T cell and NK cell neoplasms
Hodgkin lymphoma (neoplasms of Reed Sternberg cells and their variants)

25
Q

List 3 types of myeloid neoplasms

A

AML and related neoplasms
Myelodysplastic syndromes
Myeloproliferative neoplasms e.g. CML

26
Q

What other types of haemopoietic and lymphoid tissue neoplasms are there besides lymphoid and myeloid?

A

Histiocytic and dendritic cell neoplasms

27
Q

What is the difference between a leukaemia and a lymphoma?

A

Based on cell type the neoplasm resembles and the relative involvement of bone marrow and peripheral blood vs. tissues (e.g. CLL vs. small lymphocytic lymphoma respectively)

28
Q

What is the universal B cell marker?

A

CD20

29
Q

What is the universal T cell marker?

A

CD3

30
Q

What is leukaemia?

A

Malignant neoplasm involving proliferation of haematolymphoid cells, mostly at a precursor stage, usually neoplastic cells spill over into blood +/- infiltrate other tissues

31
Q

What is the difference between an acute and a chronic leukaemia?

A

Acute: abnormal cells show features of blasts, abrupt clinical onset, aggressive if not treated, present with bleeding, infections and anaemia
Chronic: abnormal cells are more mature, more indolent course

32
Q

What is lymphoma?

A

Primary malignant neoplastic disease of lymphoid cells, mostly at a mature or post-bone marrow stage (peripheral)
Generally arise as more discrete masses in tissues outside of bone marrow but can involve bone marrow
No or minimal peripheral blood involvement

33
Q

What are the 2 main groups of lymphomas and what differentiates them?

A

Hodgkin lymphoma: nodal origin only

Non-Hodgkin lymphoma: nodal or extranodal origin

34
Q

List 4 risk factors for lymphoma

A

Immunosuppression/immunodeficiency: HIV, post-transplant, congenital immunodeficiency states
Some AI disease: Hashimoto’s thyroiditis
Infectious agents: EBV, H. pylori
Environmental: chemotherapy, radiation, chemical

35
Q

What is the characteristic chromosomal translocation in most follicular lymphomas and what is its effect?

A

t(14;18)
Juxtaposition of IgH locus on Ch 14 with BCL2 locus on Ch 18 results in overexpression of the BCL2 anti-apoptotic protein

36
Q

What is the characteristic chromosomal translocation in Burkitt’s lymphoma and what is its effect?

A

Part of Ch 8 with MYC oncogene is translocated to 1 of 3 Ig gene regions on other Chs, normally transcribed at a greater rate than MYC, leading to the over-expression of the c-MYC protein and therefore sustained growth promotion

37
Q

What is the role of EBV infection in promoting lymphoma?

A

Infects B lymphocytes but is kept within its latent phase but T cells
Loss of T cell immunity allow expression of viral proteins which can activate signalling pathways leading to polyclonal B cell proliferation and ultimately lymphoma

38
Q

What are the clinical features of lymphoma?

A

B symptoms: fever, night sweats, weight >10% from baseline in 6 months

39
Q

How is lymphoma diagnosed? What features are examined?

A

Most accurately using a tissue biopsy
Looking at morphology (architecture and cytological features), immunohistochemistry (using panel of antigenic markers), +/- flow cytometry and genetic studies

40
Q

What are the histological features of Hodgkin lymphoma?

A

Neoplastic cell referred to as Reed-Sternberg cell and variants
Neoplastic germinal centre B cells
Background of non-neoplastic lymphocytes and other inflammatory cells

41
Q

How does a Reed-Sternberg cell appear?

A

Large cell with abundant cytoplasm and a larger bilobate nucleus with prominent eosinophilic nucleoli

42
Q

When do many cases of Hodgkin lymphoma arise?

A

In young people (with a 2nd peak later in life)

43
Q

How many histological types of Hodgkin lymphoma are there?

A

5: 4 classical Hodgkin lymphomas and a nodular lymphocyte predominant type

44
Q

Where do Hodgkin lymphomas arise and spread to?

A

Initially enlargement of 1 LN group

May progress to involve adjacent LN groups and other lymphoid organs (e.g. spleen, bone marrow, liver)

45
Q

Where do non-Hodgkin lymphomas arise and spread to?

A

Usually arise in lymphoid organs (e.g. LNs), but many are “extranodal”

46
Q

Give examples of some extranodal origins of non-Hodgkin lymphomas

A

Thyroid in Hashimoto’s
Stomach in H. pylori gastritis
Other - e.g. brain, breast, lung, intestine

47
Q

What are the 2 main groups of non-Hodgkin lymphomas? Which is more common?

A 
B cell (85%)
T cell
48
Q

What is the most common B cell non-Hodgkin lymphoma?

A

Diffuse large B cell lymphoma

49
Q

Contrast diffuse large B cell lymphoma with follicular lymphoma histologically

A

Diffuse large B cell lymphoma: recapitulate GC or post-GC B cells (centroblasts and immunoblasts)
Follicular lymphoma: recapitulate differentiating B cells within a GC, forming nodules/follicles, but the predominant cell type shows features of centrocytes

50
Q

How is CLL differentiated from SLL?

A

Distinguished by presence/absence of lymphocytosis

Cells in both cases are mature-looking B lymphocytes of naive or memory cell type

51
Q

What pattern of CD markers is seen in follicular lymphoma?

A

Surface Ig +ive
B cell antigens (CD19, CD20, others)
CD10+, CD5-, CD43-

52
Q

What pattern of CD markers is seen in CLL/SLL?

A

Surface Ig weak
B cell antigens (CD19, CD20, others)
CD10-, CD5+, CD23+

Hannah's Intersystem (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions