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Y5 Haematology > Lymphoma > Flashcards

Lymphoma Flashcards

1
Q

What percentage of lymphoma is Hodgkins, and Non-Hodgkins?

A 
Hodgkins = 20%
Non-Hodgkins = 80%
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2
Q

Clinical Presentation of Hodgkins Lymphoma

A

Assymetrical painless lymphadenopathy +/- obstructive/mass effect symptoms +/- constitutional symptoms (weight loss, fever, night sweats, pruritis, fatigue.
Pel-Ebstein Fever seen in minority. Can rarely get pain in affected nodes after alcohol.

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3
Q

Epidemiology of Hodgkins Lymphoma

A

M>F; bimodal age incidence (20-29 and >60)

EBV associated

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4
Q

Investigations for Hodgkins Lymphoma, how is it diagnosed?

A

CT/PET
Tissue Diagnosis: LN or BM biopsy - cell stain with CD15 & CD30 –> Reed-Sternberg cell on a background of lymphocytes and reactive cells
Definitive diagnosis = LN biopsy, Staged using PET/CT

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5
Q

What are the characteristics of a Reed Sternberg Cell?

In what percentage of cases are the RS cells found to be infected with EBV?

A 
large size (20–50 micrometres), abundant, amphophilic, finely granular/homogeneous cytoplasm; two mirror-image nuclei (owl eyes) each with an eosinophilic nucleolus and a thick nuclear membrane. 
50% of cases cells are infected with EBV
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6
Q

What are the subtypes of HL? What is the most common subtype and what are the prognoses for each?

A

Nodular sclerosing - most common, 80%, good prog.
Mixed cellularity - 17%, good prog
Lymphocyte Rich - rare, good prog
Lymphocyte depleted - rare, poor prog
Nodular Lymphocyte predominant - not classical HL, 5%, (disorder of the elderly, multiple recurrences)

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7
Q

Stages of Hodgkin’s Lymphoma

A

Stage 1 - one LN region (can include spleen)
Stage 2 - 2 + LN regions on the same side of the diaphragm
Stage 3 - 2+ LN regions on opposite sides of the diaphragm
Stage 4 - extranodal sites (liver, BM)
A: no constitutional symptoms B: Constitutional symptoms

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8
Q

Treatment for Hodgkins Lymphoma

A
  1. Combination Chemotherapy - ABVD: Adriamycin, Bleomycin, Vinblastine and Decarbazine; 2-4 cycles in stage 1/2, 6-8 cycle in stage 3/4
  2. Radiotherapy - used at end of chemo in bulky areas
  3. Intensive chemo and autologous SCT - for relapsed patients
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9
Q

Prognosis of Hodgkins Lymphoma

A

Generally v. good: 50-90% cured
50% for stage 4
Worse prog. in older patients and patients with lymphocyte depleted histology.

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10
Q

Describe the process of Autologous SCT, its advantages and when it is used.

A

Autologous = patients own SCs are harvested and frozen.
Enables high dose chemo +/- radiotherapy to eradicate malignant cells at the cost of partial or even complete bone marrow ablation. Frozen SCs are then reintroduced into patient.
Used: multiple myeloma and lymphoma, particularly with relapse, less used in leukaemia
Advantages: no graft host disease (GVHD) risk and lower risk of infection

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11
Q

Describe the process of Allogenic SCT, its risks and when it is used.

A

Allogenic = HLA-matched donor SCs are harvested
Patients own BM is completely eradicated by high-does chemo +/- radiotherapy. Donor Scs are introduced to colonise ‘empty’ BM
Used: Leukaemia
Risks: GVHD, opportunistic infections, infertility and secondary malignancies

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12
Q

How is Non-Hodgkins Lymphoma staged (investigation and classification system)?
Name 2 prognostic markers in NHL.

A

Ix: CT/PET, BM biopsy, LP
Classification: same as Hodgkins Lymphoma
Prognostic Markers: LDH, Performance status

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13
Q

Name 2 long term side effects of chemotherapy treatment for HL.

A

Pulmonary Fibrosis

Cardiomyopathy

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14
Q

What is Non Hodgkins Lymphoma?

A

Neoplastic proliferation of lymphoid cells. Originates in lymphoid tissue (lymph nodes, bone marrow, spleen).
No Reed Sternberg cells on biopsy.
Can have a B or T cell lineage/

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15
Q

Presentation of Non Hodgkin Lymphoma

A

Painless Lymphadenopathy, compression symptoms, B/constitutional symptoms (weight loss, fever, low grade fever, night sweats, pruritis, fatigue)

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16
Q

What are the 3 ways of classifying NHL?

A
  1. Mature or Immature
  2. Histology: High Grade (Very Aggressive, Aggressive), Low Grade (Indolent)
  3. Lineage: B or T cell
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17
Q

What are the main T-cell lymphomas? (NHL’s with T cell lineage)

A 
Anaplastic large cell lymphoma
Peripheral T cell Lymphoma 
Adult T cell leukaemia/lymphoma
Enteropathy-associated T cell lymphoma (EATL)
Cutaneous T cell Lymphoma
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18
Q

What are the main B cell Lymphomas?

A 
Burkitt's
Diffuse Large B-Cell (DLBC)
Mantle cell Lymphoma
Follicular
Mucosal Associated Lymphoid Tissue (MALT)
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19
Q 
Diffuse Large B cell Lymphoma
Low Grade/High Grade
B/T cell
% of NHL
Epidemiology
A

Aggressive (High Grade) B cell NHL
30-40% of all NHL
Epi: Middle aged and elderly

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20
Q

What mixture of drugs is used in R-CHOP (chemotherapy regimen)?

A

Rituximab, Cyclophosphamide, Adriamycin, Vincristine, Prednisolone

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21
Q

Follicular NHL
Low Grade/High Grade
B/T cell
% of NHL

A

Indolent/Low Grade B cell NHL

35% of NHL

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22
Q

What genetic mutation is associated with Follicular NHL? What is the physiological result of this mutation?

A

t(14:18) translocation, results in over expression of bcl2, an anti-apoptosis protein

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23
Q 
MALT
Low Grade/High Grade 
B/T cell
% of NHL
Epidemiology
A

Indolent/Low Grade B Cell NHL
(Marginal zone NHL involving extranodal lymphoid tissue)
8% of NHL
Epi: 55-60yo

24
Q

What causes MALT? What disease is it associated with?

A

Chronic antigen stimulation
H.pylori –> gastric MALT lymphoma
Sjorgen’s syndrome –> parotid MZL (Marginal Zone Lymphoma)
Hashimotos Thyroiditis –> Thyroid MZL

25
Q

Mantle Cell Lymphoma
Low/High Grade
B/T cell
Epidemiology

A

Aggressive (High Grade) B cell NHL (disseminated at presentation)
Epi: Middle Aged, M>F

26
Q

What are the 3 types of Burkitt’s lymphoma?

A

Endemic, Sporadic, Immuno-deficiency

27
Q

What is the genetic mutation associated with Burkitt’s lymphoma? How is this expressed?

A

t(8;14) translocation

c-myc oncogene overexpression

28
Q

Stereotypical histology of Burkitt’s Lymphoma.

A

Starry Sky appearance

29
Q

What is the treatment for Burkitt’s Lymphoma?

A

Chemotherapy: Rituximab + Leukaemia protocol

SCT

30
Q

Stereotypical histology of Diffuse Large B-cell Lymphoma.

A

Sheets of large lymphoid cells

31
Q

Stereotypical histology of Mantle Cell Lymphoma.

A

Angular nuclei

32
Q

Stereotypical histology of Follicular Lymphoma.

A

Follicular pattern, nodular appearance

33
Q

Which type(s) of Burkitt’s lymphoma is/are associated with EBV?

A

Endemic and Sporadic

34
Q

Which type(s) of lymphoma has a characteristic jaw involvement and abdominal masses?

A

Endemic Burkitt’s Lymphoma

35
Q

Which type of lymphoma is most often seen in HIV /post transplant patients?

A

Immuno-deficiency Burkitts Lymphoma

36
Q

What genetic mutation is commonly seen in Mantle Cell Lymphoma? How does this mutation present physiologically?

A

t(11;14) translocation

Cyclin D1 deregulation

37
Q

Treatment and Prognosis for Mantle Cell Lymphoma

A

Rx: R-CHOP, Auto-SCT for relapse
Prog: 3-5 years

38
Q

Treatment and Management of Gastric MALT Stage I-II disease

A

Treat the cause!
Eradication therapy: Omep 20mg/Clarith 500mg/amox 1gm BD
Repeat breath test at 2 months
Repeat endoscopy every 6 months for 1st 2 years, then annually

39
Q

Treatment and Prognosis for Follicular Lymphoma

A

Rx: Watch and wait, only treat if clinically indicated (compression/painful nodes) with R-CVP chemo
Prog: mostly incurable, med survival = 12-15 years

40
Q

Treatment for Diffuse Large B Cell Lymphoma

A

Rx: Rituximab-CHOP, Auto SCT for relapse

41
Q

What is the most common clinical presentation of MALT Lymphomas?

A

Dyspepsia or epigastric pain - MALT most commonly arises in the stomach

42
Q

What genetic mutation in MALT is predictive of poor response eradication therapy?

A

t(11;18) translocation = API2-MLT fusion gene

43
Q

Where do most Lymphoma chromosomal translocations occur and why? What oncogenes are commonly involved?

A

Most often translocations involve the Ig locus, because the Ig promoter is highly active in B cells.
Oncogenes: bc12, bc16, Myc, CyclinD1

44
Q

What 3 components of the lymphocyte ‘lifestyle’ make it particularly susceptible to genetic mutation?

A
  1. Rapid Cell proliferation in immune response
  2. Dependent on apoptosis (90% of normal cells die) to ensure antibody specificity
  3. DNA molecules are cut and rejoined & undergo deliberate point mutation to generate Ig and T cell receptor diversity
45
Q

Which diseases are each of these translocations associated with?

a. t(8;14)
b. t(11;14)
c. t(14;18)

A

a. Burkitt’s Lymphoma
b. Mantle Cell Lymphoma
c. Follicular Lymphoma

46
Q

Which diseases are each of these translocations associated with?

d. t(2;5)
e. t(9;22)
f. t(11;18)

A

a. Anaplastic Large Cell Lymphoma
b. (Philidelphia Chromosome!)CML & AML - realise this shouldn’t really be in Lymphoma!
c. MALT

47
Q

Which Lymphoma is associated with longstanding Coeliac disease?

A

Enteropathy-associated T cell Lymphoma (EATL)

48
Q

How are T cell Lymphomas treated?

A

Alemtuzumab (anti-CD52)

49
Q

Which Lymphoma is associated with mycosis fungoides?

A

Cutaneous T cell Lymphoma

50
Q

Which T cell Lymphomas are considered High Grade/Aggressive?

A

Anaplastic large cell lymphoma
Peripheral T-Cell Lymphoma
Adult T cell Leukaemia/Lymphoma

51
Q

What genetic mutation is seen in Anaplastic large cell lymphoma? What protein expression results?

A

t(2;5)

ALK-1 protein expression

52
Q 
Who (stereotypically) gets: 
1. Anaplastic large cell lymphoma
2. Peripheral T cell Lymphoma
3. Adult T cell Lymphoma
(Age/Nationality)
A
  1. Children and young adults
  2. Middle aged and elderly
  3. Caribbean and Japanese
53
Q

What is believed to be the cause of Adult T cell Leukaemia/Lymphoma?

A

Human T cell Leukaemia/Lymphotrophic virus type 1 (HTLV-1)

54
Q

What protein does Rituximab target?

A

Rituximab is monoclonal antibody again the protein CD20 (primarily found on the surface of B cells)

55
Q

Histology of Anaplastic Large cell Lymphoma

A

Large ‘epithelioid’ lymphocytes that express CD30 and T cell markers.

Y5 Haematology (10 decks)

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