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Systemic Pathology > Lymphoreticular Pathology > Flashcards

Lymphoreticular Pathology Flashcards

1
Q

Site for production of lymphocytes
What could this be

A

Primary lymphocytes

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2
Q

Are sites where lymphocytes encounter Ags and undergo Ag-driven proliferation and differentiation – lymph nodes, spleen, Peyer’s patches
Where could this be

A

Secondary lymphocytes

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3
Q

What is another name for secondary lymphocytes

A

Peripheral lymphocytes

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4
Q

What are tertiary lymphocytes

A

Tertiary lymphoid organs are acquired lymphoid tissues in the stomach, skin, respiratory and reproductive tracts in response to infection

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5
Q

The paracortex is mainly populated by

A

The paracortex is mainly populated by T-cells responsible for Cellular Mediated Immunity (CMI). Expansion of the paracortex is an indication of CMI response

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6
Q

The cortex is populated by

A

The cortex is organised into follicles and is populated by B-cells, which participate in humoral immune response

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7
Q

What do activates T cells express

A

Activated T-cells express HLA-DR and IL-2R (CD25), and differentiate into TH-1 or TH-2 cells, depending on the nature of the Ag.

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8
Q

70% of T-cells are CD4+ helper cells, intermingled with relatively sparse CD8+ T-cells.
True or false

A

True

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9
Q

What does the medulla contain

A

The medulla, close to the hilum consists of cords and sinuses. Medullary cords contain transformed lymphoid cells and plasma cells.

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10
Q

How do lymphocytes enter into circulation

A

Lymphocytes from the circulation enter into the node thru specialised vessels – high endothelial venules in the paracortex.

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11
Q

Follicles in the newborn have germinal centres – 1o follicles, consisting mainly of mature, naïve B-cells.
True or false

A

False
Follicles in the newborn have germinal centers

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12
Q

How are secondary follicles formed

A

Secondary follicles are formed as a result of antigenic stimulation, and are characterised by the presence of germinal centres.

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13
Q

What do germinal centers of follicles consist of

A

The germinal centres consist of B-cells (Follicular centre cells)
- centroblasts (large non-cleaved cells)
- centrocytes (small cleaved cells)
- large cleaved
- small non-cleaved cells
- tingible body macrophages
- follicular dendritic cells

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14
Q

Most often is secondary to bacterial infection. Common in axillary, inguinal nodes from infections in extremities.
●Cervical nodes may be enlarged in infections of the teeth and tonsils.
●Bacteraemia and viral infections may lead to acute generalised LAP.
●Grossly LN is enlarged, oedematous and reddish. Rarely poses a diagnostic problem.
●Micro-enlargement of follicles and germinal centre, suppuration, neutrophil infiltration.
What condition could this be

A

Acute lymphadenitis

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15
Q

What are some characteristics of lymph nodes in chronic reactions

A

Usually they are non tender because node enlargement occur over time
NB
Chronic immune reaction can promote the appearance of organized immune cells in nonlymphoid tissue
- H Pylori gastritis, aggregate mucosa lymphocytes simulates payers patches
- Rheumatoid arthritis, B cell follicles appear in the inflamed Synovium

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16
Q

Seen in TB.
●Suppurative granulomatous LAP is seen in LGV and cat scratch disease.
●LGV = STD caused by Chlamydia trachomatis (L1, L2 and L3).
●Characterised by stellate abscesses, buboes and +ve Frei test.
What condition could this be

A

Granulomatous lymphadenitis

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17
Q

What is follicular hyperplasia

A

Follicular enlargement due to widening of the GC –seen in Rheumathoid arthritis, toxoplasmosis, measles, AIDS.

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18
Q

What causes paracortical expansion

A

Increased stimulation by T-cells. Seen in viral infections, pertusis, infectious mononucleosis.

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19
Q

What are some reactive states of

A

Sinus histiocytosis/hyperplasia
Dermatopathic lymphadenopathy
Lipomelanic reticulosis

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20
Q

What is sinus histiocytosis/hyperplasia

A

Distension of medullary sinuses by histiocytes. In nodes draining areas of inflammation and neoplasia e.g axilla LN in breast cancer.

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21
Q

Where are dermatopathic lymphadenopathy seen in

A

Seen in nodes draining areas of chronic dermatitis, Seen in psoriasis, mycosis fungoides, etc
Sometimes it may be seen in the absence of dermatitis.

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22
Q

Histology shows infiltrate of lymphocytes containing melanin and neutral fats
What could this be

A

Lipomelanic reticulosis

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23
Q

a febrile illness first described in Japanese children and now seen in other places.
●Characterised by fever, conjunctivitis, skin rash, pharyngitis and cervical LAP. 40% of patients also have arthritis.
What could this be

A

Kawasaki disease

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24
Q

What are some drugs which could induce LAPs

A

Anticonvulsants-dipheny-hydantoin and carbamazepin (Tegretol). Characterized by fever, rash, eosinophilia, splenomegaly, follicular hyperplasia.

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25
Q

A febrile disease of children and young adults.
●There is bilateral cervical LAP, Some patients have immune deficiency
What could this be

A

Sinus histiocytosis with massive lymphadenopathy (SHML) (Rosai-Dorfman syndrome)

26
Q

A necrotising histiocytic lymphadenitis
Self-limited, SLE-like disease affecting cervical LN of young individuals.
What condition could this be

A

Kikuchi’s disease

27
Q

What are some characteristics of an AIDs-related LAP

A

Persistent generalised LAP is seen in 60% of HIV / AIDS patients. Lymph nodes in HIV show a spectrum of changes:
- Severe follicular hyperplasia
- Regressive follicular hyperplasia
- Follicular involution, progressing to
lymphocyte depletion. Helper T-cells are reduced and suppressor T-cells are increased in the germinal centres.

The changes correspond to clinical progression from early asymptomatic HIV infection to AIDS.
●LNs may also show malignant lesions such as Kaposi sarcoma, HL, NHL.
●Progressively transformed germinal centre (PTGC) – Most often affects the cervical LN of young males. Very few cases evolve into NLPHL.

28
Q

What are lymphomas

A

Lymphomas are tumours of the immune system and majority are of B-cell origin.
●Lymphomas constitute a major cause of lymphadenopathy, morbidity + mortality; they may be nodal or extranodal.
●Based on the presence or absence of the Reed-Sternberg cell, lymphomas are classified into Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL)

29
Q

What are the classification of lymphomas based on the presence and absence of Reed-Sternberg cell

A

Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL)

30
Q

●First described by Thomas Hodgkin in 1832 while serving as a curator at Guy’s hospital.
● HL is mainly a nodal disease.
●It has a predetermined mode of spread.
●It arises from a lymph node or a chain of nodes and spreads to anatomically contiguous chain.
●Years of controversy on the nature of HL.
●Majority of cells in HL are non neoplastic inflammatory cells within which are R-S cells and variants.
What condition could this be

A

Hodgkin lymphoma

31
Q

Who proved that RS cells are clonally related malignant lymphoid B-cell

A

Kuppers et al (1994) proved beyond doubt that Hodgkin and R-S cells are clonally-related malignant lymphoid B-cell. The name therefore changed from HD to HL

32
Q

First described by Sternberg and Dorothy Reed is a tumour giant cell 20-30mm in diam. It has two nuclei or a bilobed nucleus, each measuring 12-18mm in diam. Each nucleus has a nucleolus, which is typically eosinophilic, with a clear zone around it, giving an owl eye appearance.
What cell is this

A

The classical Reed-Sternberg cell

33
Q

What are other cells associated with classical Reed-Sternberg cell

A

Other cells : Lacunar cell, Lymphocytic and Histiocytic (popcorn) cell, Hodgkin cell

34
Q

What is Hodgkin’s lymphoma

A

HL is a tumour of germinal centre B-cell with non-productive Ig gene rearrangements, representing failed attempts at B-cell Ab production. Under normal circumstances, such cells undergo apoptosis in the germinal centre, and the mechanisms by which H-RS cell escape cell death have been unravelled

35
Q

What is the characteristic giant cell in HL and NLPHL respectively

A

The characteristic giant cell in HL is H-RS cell and in NLPHL L and H cell.

36
Q

H-RS cells express proteins found in other cell lines but not CD20 and ………

A

CD79a

37
Q

What do L and H cells express

A

L and H cells express CD20 and Bcl-6 typical of GC B-cells.

38
Q

At what stage does NLPHL arise

A

NLPHL arises at GC stage of B-cell maturation.

39
Q

What are other factors which could cause Hogkin’s lymphoma

A

Environmental (viral infection) and genetic factors are also important.
The risk of concordance for HL in monozygotic twins is 100, compared to dizygotic twins with no increased risk.

40
Q

What is the role of HBV in HL

A

EBV contributes to oncogenesis in HL.
●The risk of developing HL is 3x higher in those with history of IM.
●~ 50% HL in developed world is EBV +ve.
●Transforming ability of EBV mainly through LMPs
LMP1 mimics constitutively active CD40R, a signaling pathway leading to NFKB activation in Ag-activated B-cell.
LMP2 shuts down BCR expression, prevents activation but also mimics BCR
Both LMP1 and LMP2 may activate NFKB with upregulation of anti-apoptotic genes
Upregulation inhibits Fas signaling pathway enabling pre-apoptotic H-RS cells to survive negative selection.
●However, only ~ 50% of CHL are EBV +ve.
●There must be additional transforming events in EBV –ve cases

41
Q

Most common subtype of HL in Europeans
●Common in young women below the age of 40, and has a predilection for mediastinal lymph nodes.
●Characterised by presence of lacunar cells.
●Has a nodular pattern with fibrous bands separating nodules.
●Diffuse areas, areas of necrosis may also be seen.

Lacunar cells are many, H-RS cells are very few.
●Background shows inflammatory cells, palisaded histiocytes resembling granulomas.
●Graded (Grades 1 and 2) based on the number and atypia of R-S cells.
Grade 2 tumours show increased rate of relapse, shorter survival, worse response to initial therapy and worse prognosis than NS-1.
What could this be

A

Nodular sclerosis

42
Q

Occurs at a younger age group in underdeveloped countries compared with those in industrialised nations. Among Caucasians it is more common in older males.
●The stroma shows plasma cells, eosinophils and histiocytes.
●Tumour cells are EBV+ in over 60% of cases.
What condition could this be

A

Mixed cellularity

43
Q

Entity has undergone attrition with the use of IHC.
●Cases previously diagnosed as LD were actually anaplastic carcinomas or high grade NHLs.
●LD occurs in older patients, in HIV +ve individuals and in developing countries.
●It is aggressive but probably curable.
What could this be

A

Lymphocyte depletion

44
Q

hese are cases of classical HD with a background infiltrate of predominantly lymphocytes, rare or no eosinophils. Generally not common, and is uncommon before 40 years. EBV negative.
What could this be

A

Lymphocyte-rich CHL

45
Q

Has a nodular growth pattern. It differs in so many respects (morphology, immunophenotype, clinically) from classical HL.
●However, it resembles HL more than it resembles NHL.
What condition could this be

A

NLPHL

46
Q

The neoplastic R-S cells are v. scarce.
●An indolent disease with a tendency to be localized, also responds to local Rx.
●Immunophenotype: CD45+. EMA +, CD15 and CD 30 –ve; +ve for B-cell- associated Ags - CD20, BCL6.
●Some cases may evolve from progressively transformed germinal centers.
What condition could this be

A

NLPHD

47
Q

How is Hodgkin lymphoma staged

A

I – A single lymph node or a single extralymphatic organ
●II- 2 or more groups of lymph nodes on the same side of diaphragm or localized involvement of an extralymphatics organ or site(IIE)
●III- Lymph nodes on different side of diaphragm without or with involvement of an extralymphatic organ or site (IIIE)
●IV- Diffuse involvement of 1 or more extralymphatic organs or sites with or without lymphatic involvement

48
Q

What are some differences between HL and NHL

A

Unlike HL:
It has a haphazard mode of spread.
It commonly involves extranodal sites.
It has a leukaemic phase.

49
Q

What is NHL

A

Driving this continual reclassification are:
●New data on the biology of lymphomas.
●Uncertainty as to what is important in the accurate classification of lymphomas (is it morphology, immunophenotype, genotype, clinical behaviour, something else?).
●NHL may be nodular or diffuse. Nodular NHLs are more common in adults and they have a better prognosis than diffuse type.
●In children NHLs are commonly extra nodal, diffuse and high grade

NHL may be low, interm. or high grade.
●Low grade NHLs e.g SLL (CLL in bone marrow) are indolent, but incurable. Leukaemic phase is common with low grade NHL than with high grade.
●Some intermediate grade lymphoma have aggressive rate of growth but are potentially curable using CHOP chemoRx.(cyclophosphamide, hydroxydau-norubicin, oncovin and prednisolone)

High grade NHLs (Burkitt lymphoblastic lymphoma) are the most common types in children. Prognosis in adults is unfavorable; in children a cure rate of 80-90% could be achieved.
●NHL is more common in males. The incidence and mortality is increasing from HIV-infected population.

50
Q

What is the etiology of NHL

A

The search for the etiology of NHL is partially successful.
●Congenital and acquired immune deficiency states are the best recognized risk factors for developing NHL.
●The association between gastric marginal zone lymphoma and H. pylori infection is well known.
●EBV and adult T-cell leukaemia/lymphoma virus are recognised causes of some types of NHL.

However, the etiology of the majority of NHL remains unknown.
●Excessive exposure to sunlight and electromagnetic fields are thought to play a role. Attention is also being focused on the role of: herbicides, pesticides, contamination of ground and surface water by nitrites from fertilisers, hepatitis C virus infection as well as occupational exposure to some solvents used in hairdressing. Exposure to petrochemicals is a risk factor for developing NHL.

51
Q

●B cell acute lymphoblastic leukaemia/lymphoma
●T Cell acute lymphoblastic Leukaemia/lymphoma
What condition could this be

A

Lymphoid leukemia

52
Q

What are some examples of NHL from a matured B cell origin

A

Burkitt lymphoma
2.Diffuse large B cell lymphoma
3.Extranodal marginal B cell lymphoma
4.Follicular lymphoma
5.Hairy cell leukaemia
6.Multiple myeloma/solitary plasmacytoma
7.Small lymphocytic lymphoma/ chronic lymphocytic leukaemia

53
Q

What are some examples of NHL from a mature T cell origin

A

Adult T cell leukaemia/lymphoma
2.Peripheral T cell lymphoma
3.Anaplastic large cell lymphoma
4.Extra nodal NK/T Cell lymphoma
5.Mycosis fungoides/Sazary syndrome
6.Large granular lymphocytic leukaemia

54
Q

First described by Dennis Burkitt, a surgeon in Uganda in 1958.
●The most common malignant tumour in children in most of tropical Africa and the fastest-growing tumour known.
●Usually extra nodal, highly aggressive with a possibility of cure.
●Endemic form, which occurs in Africa involves the jaw or abdominal organs.
●Sporadic form, seen in older children and adults present with intra-abdominal mass.
What condition could this be

A

Burkitt lymphoma

55
Q

What is the epidemiology of Burkitt lymphoma

A

The geographic distribution of BL in high incidence areas is governed by two parameters: temperature and humidity.
●BL is common in tropical areas where the mean monthly temperature is over 60oF (15.5oC) and the relative humidity is high.
●The BL belt is within lat. 10-15o N and S of the equator.
●Rare in highland areas >1550m above sea level; unknown in dry arid areas with rainfall <50 cm per year
It is unknown in cold areas with diurnal temperatures <16oC.
●It is rare < 2 years and > 15 years; the peak incidence is 5-9 years.
●Boys are affected twice as often as girls.
●It is rare among the higher socio-economic group of Africans in endemic areas

56
Q

What is the etiology of BL

A

Circumstantial evidence links EBV with BL. EBV is transmitted by saliva. It infects B-cells, nasopharyngeal epithelium and is ubiquitous, worldwide.
●In 100% of cases of endemic BL, tumour cells carry EBV genome and express EBV-encoded antigens.
●EBV infects B-cells by binding to complement receptor type 2 (CR2, CD21). The spectrum of sequelae to EBV infection is wide and viral replication is controlled by humoral and T-cell immune reaction in most cases.

T-cell immunity is required for the control of EBV infection.
●Individuals with deficiency in T-cell mediated immunity are susceptible to uncontrolled, widely-disseminated and lethal acute EBV infection.
●Malaria infection is known to cause T-cell immunodeficiency, and this association may be the link between EBV infection and BL.
●Only 20% of sporadic BL, seen in other parts of the world carry the EBV genome.

oth endemic and sporadic BL have translocation of c-myc oncogene from chr 8 to chr 14 in the Ig Heavy chain; in a minority of cases Ig λ, chr 8 to chr 22 or Ig к chr 2 to chr 8. This leads to deregulation of c-myc, causing proliferation without differentiation.
●The M:F ratio for sporadic BL is 5:1.
●Peripheral LAP is very rare in endemic BL, whereas it is seen in 10% of cases of sporadic BL.

57
Q

What are the clinical presentations of Burkitts lymphoma

A

Jaw mass in 75% of cases; the maxilla is more often affected than the mandible.
●Abdominal mass in 60% of cases; ascites is frequent.
●CNS disease (30% of cases) manifests as paraplegia, multiple cranial nerve paralysis or malignant pleiocytosis.
●Other organs: thyroid, testes, breast, ovaries.

58
Q

What are the histological findings of Burkitt lymphoma

A

Histology shows monomorphic sheets of lymphoblasts within which are scattered macrophages with phagocytosed debris, giving the classical “starry sky” appearance.

59
Q

How is Burkitt lymphoma treated

A

Chemotherapy CHOP
●Lasix given to ensure urine output of 100-150ml/hour
●Xanthine oxydase inhibitor (Allopirinol) started at least 24 hours before chemoRx to offset anticipated hyperuricaemia.

Relapse: 2 patterns:
Early relapse within 3 months of chemoRx, at original site.
Late relapse > 3 months of chemoRx, at new sites, frequent CNS involvement.

60
Q

What is the staging for Burkitt lymphoma

A

Stage A – Single extra-abdominal mass.
●Stage B – Multiple extra-abdominal Mass.
●Stage C – Abdominal mass with or
without facial tumour.
Stage D – Abdominal mass with sites of tumour other than facial or bone marrow.
Stage AR – Abdominal mass with > 90% of tumour resected.

Systemic Pathology (17 decks)

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