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Clin haem > Hodgkin & Non-hodgkin lymphoma > Flashcards

Hodgkin & Non-hodgkin lymphoma Flashcards

1
Q

What prognosis of stage 1-2 disease of HL is favourable?

A
  • no large mediastinal lymphadenopathy
  • ESR < 50 without B symptoms
  • ESR < 30 with B symptoms
  • Age ≤ 50 years
  • 1-3 lymph nodes involved
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2
Q

What prognosis of stage 1-2 disease of HL is unfavourable?

A
  • large mediastinal lymphadenopathy
  • ESR ≥ 50 without B symptoms
  • ESR ≤ 30 with B symptoms
  • 4 or more lymph node sites involved
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3
Q

What are the classical Hodgkin lymphoma types?

A
  • nodular sclerosing
  • lymphocyte rich
  • mixed cellularity
  • lymphocyte depleted
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4
Q

what’s the other type of Hodgkin lymphoma that’s not classical?

A

Nodular lymphocyte predominant

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5
Q

what is the most widely used regime for early-stage disease?

A

2 courses of ABVD chemotherapy followed by 20 Gy radiotherapy to the involved field.
note: if lymph nodes are not bulky omit radiotherapy and do 3 courses of ABVD chemo

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6
Q

if early-stage disease is unfavourable what is the regime?

A

treat with 4 to 6 courses of ABVD followed by 30 Gy radiotherapy for bulky disease
note: or the first 2 cycles can be replaced by BEACOPP

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7
Q

what is the regime used for advanced stage disease?

A

6 courses of ABVD are most widely used
or BEACOPP can be used but it’s more toxic

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8
Q

Subsequent radiotherapy is given if residual nodes are more than 1.5 cm diameter, or smaller but remain PET positive. T or F.

A

True

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9
Q

What drug is used alternatively to bleomycin since bleomycin causes pulmonary toxicity?

A

anti-CD30 monoclonal antibody conjugate Brentuximab (Adecertis).
new regime called AAVD
note: but it can cause febrile neutropenia and it’s more costly

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10
Q

Hodgkin cells stain with CD30 and CD15, but are usually negative for B-cell antigen expression such as CD10, CD19 or CD20. T or F.

A

True

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11
Q

PET/CT is widely used after the first two cycles of ABVD and if there is residual active disease, treatment might be switched to more intensive chemotherapy such as BEACOPP. T or F.

A

True

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12
Q

Inflammatory disease can cause a false positive PET scan. T or F.

A

True

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13
Q

What is the treatment plan for relapsed cases?

A
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14
Q

What are the late effects of Hodgkin lymphoma and its treatment?

A
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15
Q

What is Hodgkin Lymphoma?

A
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16
Q

What are the clinical features of Hodgkin lymphoma?

A
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17
Q

What are the haematological and biochemical findings of Hodgkin lymphoma?

A
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18
Q

How do you diagnose Hodgkin lymphoma?

A
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19
Q

Nodular sclerosis?

A
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20
Q

Lymphocyte rich?

A
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21
Q

Mixed cellularity?

A
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22
Q

Lymphocyte depleted?

A
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23
Q

what’s the difference between Hodgkins and non-hodgkins lymphoma?

A

Hodgkins has nodal involvement and non-hodgkins has nodal and extranodal involvement

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24
Q

what’s the difference between low grade and high grade lymphomas?

A

low grade disorders are relatively indolent, respond well to treatment but are difficult to cure.
while high grade disorders are aggressive and need urgent treatment but are more often curable

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25
Q

what are the lab investigations/ findings in NHL? hint: 7

A
  • there may be anaemia, neutropenia or thromobocytopenia
  • lymphoma cells may be found in peripheral blood in some pts
  • trephine biopsy for staging; PET scan shows marrow uptake or if cytopenias are present
  • serum LDH is raised (prognostic marker)
  • elevation of uric acid may occur
  • there may be a paraprotein (Ig electrophoresis)
  • HIV status should be tested; can influence prognosis in some subtypes like Burkitts
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26
Q

what are the clinical features of NHL?

A
  • superficial lymphadenopathy (painless)
  • constitutional symptoms: fever, night sweats, weight loss
  • oropharyngeal involvement: sore throat, obstructed breathing
  • symptoms dues to anaemia, infections due to neutropenia or purpura with thrombocytopenia
  • abdominal disease: liver & spleen often enlarged
  • other organs involved: skin, brain, testis or thyroid
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27
Q

which NHL subtype can HIV positivity influence prognosis in?

A

Burkitt lymphoma

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28
Q

what is the general principle of treatment for NHL?

A

usually combination of chemotherapy drugs with a monoclonal antibody directed against the tumour cell

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29
Q

what are the low-grade Hodgkin lymphomas?

A
  • small lymphocytic lymphoma
  • lymphoplasmacytoid lymphoma/Waldentrom macroglobulinaemia
  • marginal zone lymphomas
  • follicular lymphoma
  • mantle cell lymphoma
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30
Q

what is small lymphocytic lymphoma?

A

same morphology and immunophenotype as B-CLL but with <5x10^9/L peripheral blood B cells and no cytopenias

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31
Q

Hyperviscosity syndrome is a common complication of IgM paraproteinemia. T or F.

A

True
note: IgM paraprotein increases blood viscosity more than equivalent concentrations of IgG or IgA; seen in lymphoplasmacytoid lymphoma/Waldenstrom macroglobulinaemia

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32
Q

where do marginal zone lymphomas arise from?

A

the marginal zone of B cell germinal follicles of lymph nodes, spleen or mucosa (MALT)
note: its classified based on where it comes from

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33
Q

Gastric MALT lymphoma is the most common form of the MALT lymphomas and is preceded by what kind of infection?

A

Helicobacter pylori

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34
Q

what is the hallmark of follicular lymphoma?

A

t(14;18) involving the BCL2 gene which results in the over expression of BCL2 protein

35
Q

what’s the function of BCL2?

A

it prevents cells from undergoing apoptosis and increases the lifespan of malignant B cells

36
Q

The cells of follicular lymphoma are typically positive for which markers?

A

CD10, CD19, CD20, BCL2 and BCL6

37
Q

where are mantle cell lymphomas derived from?

A

pre-germinal centre cells localised in primary follicles or in the mantle region of secondary follicles

38
Q

MCL has a characteristic phenotype of what?

A

CD19+ and CD5+ (Like CLL)
CD22+ and CD23-

39
Q

Presence of which translocation is required for diagnosis of MCL?

A

t(11;14)

40
Q

In MCL, a specific translocation juxtaposes the cyclin D1 gene (CCND1) to the immunoglobulin heavy-chain gene, and leads to decreased expression of cyclin D. T or F.

A

Falses
it leads to increased expression of cyclin D which alters cell cycle behaviour
note: the translocation is t(11;14)

41
Q

What type of B cells are in MCL and MZL?

A

naive B cells and memory B cells respectively

42
Q

what are the high grade NHL?

A
  • diffuse large B cell lymphomas
  • primary central nervous system lymphoma
  • primary mediastinal B cell lymphoma
  • Burkitt lymphoma
  • lymphoblastic lymphoma
43
Q

what’s the definitive investigation done in non-hodgkins?

A

whole lymph node excision biopsy or more usually core needle biopsy of lymph node or of other involved tissue

44
Q

translocation found in follicular lymphoma?

A

t(8;18)

45
Q

translocation found in mantle cell lymphoma?

A

t(11;14)

46
Q

translocation found in Burkitt lymphoma?

A

t(8;14)

47
Q

translocation found in anapaestic large cell lymphoma?

A

t(2;5)

48
Q

which mutation is found in lymphoplasmacytic lymphoma?

A

MYD88

49
Q

oral agents that block activity of the BTK or PI3Kδ proteins are used for?

A

B cell chronic lymphocytic lymphoma
note: BTK inhibitors=ibrutinib & PI3K inhibitors= idelalisib

50
Q

which drug inhibits BCL-2 activity?

A

venetoclax
note: which is useful in DLBCL

51
Q

(CAR)-T cells developed against specific B-cell-associated targets (like CD19) are used for what?

A

replaced or refractory patients with some subtypes of lymphoma

52
Q

In the 85% of cases of NHL that are of B-cell origin, antibodies against CD20 have proven of great benefit. T or F.

A

True

53
Q

Which monoclonal antibody drug is used against CD20?

A

Rituximab

54
Q

Which monoclonal antibody drug is used against CD30?

A

Brentuximab
note: used for anaplastic large cell lymphoma & other NHL

55
Q

Acute hyper viscosity syndrome is treated with what?

A

repeated plasmapheresis until the underlying disease can be brought under control
note: can be used to relieve symptoms of lymphoplasmacytic lymphoma

56
Q

Marginal zone lymphomas are thought to occur in response to an antigen or inflammation. T or F.

A

True
- the cells acquire secondary genetic damage that leads to lymphoma

57
Q

In MZL, molecular tests show point mutations involving which pathway?

A

NF-κB pathway

58
Q

what is the median age of onset for follicular lymphoma?

A

60 years

59
Q

Those with disseminated (stage II–IV) disease in follicular lymphoma are generally treated in the absence of symptoms. T or F.

A

False
- not treated until complications occur (watch and wait)

60
Q

how is follicular lymphoma treated?

A

therapy is usually rituximab, either alone or in combination with chemotherapy (B-R or R-CVP or R-CHOP); or it can be combined with Ibrutinib (BTK inhibitor)

61
Q

what are the 2 major subtypes of mantle cell lymphoma?

A

one type involving lymph nodes and extra nodal sites and the other a leukaemic non-nodal subtype

62
Q

what is the characteristic cell pattern seen in mantle cell lymphoma?

A

deformed pattern of small lymphocytes with angular nuclei (centrocytes)

63
Q

clinical presentation of the classical type of MCL?

A

lymphadenopathy

64
Q

clinical presentation of the leukaemia type of MCL?

A

systemic symptoms and bone marrow and splenic disease

65
Q

the nodal type of MCL tends to be more aggressive with high expression of?

A

Ki67

66
Q

current treatment regime for MCL?

A
  • chemotherapy, like R-CHOP
  • Ibrutinib is effective
  • SCT
  • maintenance with rituximab
67
Q

Histologically, the biopsy of DLBCL shows what?

A

large neoplastic cells with prominent nucleoli

68
Q

DLBCL is subdivided into which subtypes?

A

germinal center (GCB) and activated B cell (ABC)
note: they stain with antibodies to BCL6 and CD19 or MUM1

69
Q

what’s the clinical presentation of DLBCL?

A

rapidly progressive lymphadenopathy which may also involve the bone marrow, GIT, brain, spinal cord, kidneys, etc

70
Q

what is the most common cytogenetic changes in DLBCL?

A

involve the IGH locus on chromosome 14 and the BCL6 gene at chromosome 3q27

71
Q

Double expressor or double hit DLBCL aberrantly express which gene mutations?

A

both MYC and either BCL-2 or BCL-6

72
Q

the mainstay of treatment for DLBCL is?

A

rituximab in combination with CHOP

73
Q

Endemic Burkitt lymphoma is seen is which areas?

A

in areas with chronic malaria exposure

74
Q

Burkitt lymphoma is associated with what kind of infection?

A

EBV infection

75
Q

which gene mutation is over-expressed in Burkitt lymphoma?

A

the MYC oncogene is overexpressed because it is translocated to an immunoglobulin gene, usually the heavy-chain locus t(8;14)

76
Q

what is the typical presentation in Burkitt lymphoma?

A

usually a child, presenting with massive lymphadenopathy, often of the jaw

77
Q

what does the histological picture of Burkitt lymphoma look like?

A
  • very high proliferative index of over 95%
  • shows sheets of lymphoblasts and starry sky tingible body macrophages
78
Q

what are the types of T cell non-hodgkin lymphoma?

A
  • peripheral T cell non-hodgkin lymphoma unspecified
  • angioimmunoblastic lymphadenopathy
  • mycosis fungoides
  • sezary syndrome
  • adult T cell leukaemia/lymphoma
  • enteropathy-associated T-cell lymphoma
  • anaplastic large cell lymphoma
  • extranodal NK/T cell lymphoma
79
Q

what is mycoses fungicides?

A

a chronic cutaneous T-cell lymphoma that presents with severe pruritus and psoriasis-like eczematoid skin lesions (can later become plaques and ulcerated tumours)

80
Q

what is seen in Sezary syndrome?

A

there is dermatitis and generalised erythroderma, but also lymphadenopathy and circulating T-lymphoma cells

81
Q

Anaplastic large cell lymphoma is usually associated with the t(2;5)(p23;q35) translocation which leads to the overexpression of which gene?

A

overexpression of ALK

82
Q

how is anaplastic large cell lymphoma treated?

A
  • Crizotinib (ALK inhibitor)
  • Brentuximab (cuz its also CD30+)
83
Q

Cattleman disease may in some subtypes progress to a B-cell lymphoma. T or F.

A

True

84
Q

The multicentric form of castleman disease is most common in subjects with what kind of infection?

A

HIV infection (when the cells contain HHV8)

Clin haem (9 decks)

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