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CLL and quiz Flashcards

1
Q

When are Reed Steenberg cells present?

A

Classical Hodgkin Lymphoma

NLPHL

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2
Q

What is Non-Hodgkins Lymphoma?

A

Neoplastic proliferation of lymphoid cells.

Originates in lymphoid tissue (lymph nodes, bone marrow, spleen)

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3
Q

What is the incidence of NHL?

A

Fastest growing human cancer (Burkitt Lymphoma)

Indolent diseases with a 25 year survival

Incidence rising 200/million population/year

Antibiotic responsive disease such as Gastric MALT

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4
Q

What is the presentation of NHL?

A

Painless lymphadenopathy
Compression symptoms
B symptoms

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5
Q

How do you classify biopsies for NHL?

A

WHO classification of Lymphoma subtype

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6
Q

How do you diagnose and stage NHL?

A

CT scan
PET scan (indicated in aggressive lymphomas)
BM biopsy
Lumbar puncture (if risk of CNS involvement )

Histological diagnosis

Blood tests (LDH, albumin, kidney/BM function, HIV/ HepB/ HTLV1)

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7
Q

What tests give prognostic markers for NHL?

A

LDH
Performance status
HIV serology (if appropriate HTLV1 serology)
Hepatitis B serology (risk of reactivation if B cell depleting therapy given

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8
Q

What therapy would you give someone who has NHL?

A

Urgent chemotherapy
Monitor only
Antibiotic eradication (H.Pylori gastric MALT lymphoma)

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9
Q

Which cancers are high grade?

A

V aggressive
Burkitts lymphoma
T/B cell lymphoblastic leukaemia/ lymphoma

Aggressive
Diffuse large B cell
Mantle

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10
Q

What are the low grade blood cancers?

A 
Follicular
Small lymphocytic (CLL)
Mucosa Associated (MALT)
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11
Q

What is the median survival for very aggressive, aggressive and indolent NHL?

A

V. Aggressive: 2-5 weeks
Aggressive: 3-12 months
Indolent: 10-15 years

BUT the chances of cure are the highest in the most aggressive tumours.

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12
Q

How do you manage V Aggressive NHL?

A

These are treated on acute leukaemia type chemotherapy protocols (not discussed further)

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13
Q

What is DLBCL?

A 
Diffuse large B cell (DLBCL)
Aggressive B cell NHL
30-40% of all NHL
Prognosis and treatment determined by
Precise histological diagnosis
Anatomical stage
IPI (International Prognostic Index)
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14
Q

What is the DLBCL International Prognostic Index?

A 
Age > 60y
serum LDH > normal
performance status 2-4
stage III or IV
more than one extranodal site
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15
Q

What is the 5 year predicted survival by number of risk factors?

A

0-1: 73%
2: 51%
3: 43%
4-5: 26%

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16
Q

How is DLBCL treated?

A

Treated by x 6-8 cycles of R-CHOP (Rituximab-CHOP)

combination chemotherapy using a mixture of drugs usually including an anthracycline (e.g. doxorubicin).

R is Immunotherapy using the anti CD20 monoclonal antibody Rituximab

Aim of therapy is curative (overall approx 50%)

Relapse: Autologous Stem Cell transplant salvage 25% of patients

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17
Q

How do you give combination drugs in DLBCL?

A

Cyclophosphamide 750 mg/m2 i.v. D1
Adriamycin 50 mg/m2 i.v. D1
Vincristine 1.4 mg/m2 i.v. D1
Prednisolone 40 mg/m2 p.o. D1‑D5

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18
Q

What is follicular NHL?

A

Indolent lymphoma
35% of NHL
Associated with t(14;18) which results in over-expression of bcl2 an anti-apoptosis protein
FLIPI score (modified IPI)
Incurable, median survival 12-15 years
May require 2-3 different chemotherapy schedules over the 12-15 year period

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19
Q

Why is follicular NHL benign?

A

Incurable

variable/long natural history

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20
Q

What is the treatment of follicular NHL?

A

Watch and wait
Treatment:
- Immunochemotherapy R CVP
- Maintenance Rituximab

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21
Q

What is a MALT lymphoma?

A

Is a Marginal zone NHL involving extranodal lymphoid tissue (ie mucosa-associated lymphoid tissue MALT)

Comprise ~ 8% of all NHL

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22
Q

What chronic antigen stimulation may result in MALT lymphoma?

A

Sjogrens syndrome ; parotid lymphoma (MZL)
H.Pylori ; Gastric MALT lymphoma (MZL)
Hashimoto’s Thyroid; Thyroid (MZL)
Lachrymal gland (?Psittaci infection)

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23
Q

What is the median age of presentation of MALT lymphoma?

A

55-60y

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24
Q

What are the symptoms of MALT lymphoma?

A

Most commonly arise in stomach, usually present with dyspepsia or epigastric pain
Usual presentation is Stage I[E] (Extra-nodal site)
‘B’-symptoms uncommon

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25
What is MALT lymphomagenesis?
Chronic gastritis Caused by H.Pylori infection Proliferation polyclonal Antigen specific B cells Antigen dependent Transformed B-cell clone Antibiotic Sensitive MALT Antigen independent Transformed B cells -> Antibiotic insensitive MALT
26
How do you treat gastric MALT?
Omep 20mg/Clarith 500mg/amox 1gm bd Repeat breath test at 2 months Repeat endoscopy every 6 months for 1st 2years then annually
27
How good is gastric MALT treatment?
Durable remission in 75% of patients response may be delayed until 1yr If fails eradication therapy then may require chemotherapy
28
Who gets CLL?
* Proliferation of mature B-lymphocytes * Commonest leukaemia in the western world Caucasian UK incidence 4.2/100,000/year Age at presentation median 72 (10% aged <55yrs) Relatives x7 increased incidence
29
What are the lab findings of CLL?
* Lymphocytosis between 5 and 300 x 109/l * Smear cells in peripheral blood * Normocytic normochromic anaemia * Thrombocytopenia * Bone marrow Lymphocytic replacement of normal marrow elements
30
What is the diagnostic algorithm for CLL?
``` Immature lymphoblasts ( TdT positive) Think Acute Lymphoblastic Leukaemia (ALL) ``` Small mature lymphocytes +smear cells (need immunophenotype) + Mature B cells CD5 +ve = Mantle cell lymphoma Small mature lymphocytes +smear cells (need immunophenotype) + Mature B cells CD5 +ve + Immunophenotype CLL score 4-5/5 = CLL
31
What are the prognostic factors of CLL?
Clinical (quantify the burden of malignant cells) Rai staging Binet staging Laboratory/malignant cell based CD38 expression bad prognosis Cytogenetics (FISH panel) Immunglobulin gene mutation status IgH mutated IgH unmutated
32
How do you determine clinical stage?
A= <3 Lymphoid areas, 60% patients, 12y survival B= >3 Lymphoid areas, 30% of patients, 5y survivial C= Hb <100 g/l, Platelets <100x109/l, 10% patients, 2y survival
33
How does IgH gene mutation status affect survival?
Mutated: 25 yrs Unmutated: 8 years
34
``` What is the median survival in months of patients who have: A) Normal Karyotype B) Deletion of 13q C) Trisomy 12 D) Deletion of 11q (ATM) E) Deletion of 17p (TP53) ```
``` A) 111 B) 133 C) 114 D) 79 E) 32 ```
35
Why do CLL patients have increased risk of infection and bone marrow failure?
Malignant (non functional) mature B cells+ hypogammaglobulinaemia Proliferate within Bone marrow (efface)
36
What complications may occur in CLL?
Lymphadenopathy+/splenomegaly, lymphocytosis Transform to high grade lymphoma Auto-immune complications e.g. haemolytic anaemia
37
What are is the treatment of CLL?
Suportive treatment Vaccination Anti-infective prophylaxis and treatment Specific scenarios Auto-immune cytopaenias High grade (Richter) transformation Leukaemia directed treatment Tailored to patient
38
How do you do prophylactic treatment of infections in CLL?
Aciclovir PCP prophylaxis for those receiving fludarabine or alemtuzumab (Campath) IVIG is recommended for those with hypogammaglobulinemia and recurrent bacterial infections Immunisation against pneumococcus, and seasonal flu
39
How to you treat autoimmune phenomena?
Steroids | Rituximab
40
If CLL transforms to high grade lymphoma what is it called?
Richter's syndrome
41
What is the indication for more than watch and wait?
``` Watch and wait unless Progressive lymphocytosis lymphocyte doubling time <6 months Progressive marrow failure Hb < 100, platelets <100, neutrophils <1 Massive or progressive lymphadenopathy/splenomegaly Systemic symptoms (B symptoms) Autoimmune cytopenias (treat with steroids) ```
42
What is first line therapy for TP53 intact disease
Young patient: FCR Fludarabine Cyclophosphamide Rituximab (anti CD20 moab) Rituximab-Bendamustine Obinutuzumab (anti CD20) +Chlorambucil Older patients: Supportive care only
43
How do you manage high risk cases of CLL?
How to manage high risk cases Patients with TP53/17p deleted CLL 1st Line Refractory disease or early relapse (<24 months) Patients failed 2 lines of chemotherapy New agents Ibrutinib (Bruton Tyrosine Kinase Inhibitor) Venetoclax (anti Bcl2 oral agent)
44
What are some treatment options in CLL?
BCR Kinase Inhibitors Ibrutinib (BTK) idelalisib (PI3K) BCL2 inhibitors Venetoclax Experimental Cell Based Therapies Chimaeric Antigen Receptor T cells (CAR-T)
45
What is the presentation of lymphoma?
Painless progressive lymphadenopathy Palpable node Extrinsic compression of any “tube” Eg Ureter, Bile duct, large blood vessel, bowel, trachea, oesophagus Infiltrate/impair an organ system E.g. skin rash, ocular&CNS, liver failure Recurrent infections Constitutional symptoms Coincidental e.g. FBC, Imaging
46
Which of these are NOT true? Marginal Zone Lymphoma of the parotid is linked to Sjogrens Syndrome MALT lymphoma of the stomach is linked to H Pylori Ciclosporin therapy is linked to increased EBV which can cause lymphoma Chronic EBV is linked to adult leukaemia and lymphoma
NOT TRUE: Chronic EBV is linked to adult leukaemia and lymphoma EBV is not linked to leukaemia
47
In certain NHL subtypes, chromosome translocations involving a proto-oncogene are seen. Which statement is NOT true? Follicular NHL: IgH -BCL2 Mantle Cell Lymphoma: IgH-Cyclin D1 Follicular NHL: BCR-ABL1 Burkitt Lymphoma: IgH- cMYC
NOT TRUE: Follicular NHL: BCR-ABL1 All the other answers include the immunoglobulin gene which is important in B cell lymphomas
48
Lymph node biopsy: Reed Sternberg Cells are present with a background of chronic inflammatory cells and eosinophils: what is the report outcome?
Hodgkins lymphoma
49
What is the epidemiology of Hodgkin Lymphoma?
1% of all cancer, 3:100,000 population HL is more common in males than females. Bimodal age incidence Most common age 20-29, young women NS subtype Second smaller peak affecting elderly >60 years old
50
What are the symptoms of Hodgkins lymphoma?
Painless enlargement of lymph node/nodes. May cause obstructive symptoms/signs Constitutional symptoms; (the B symptoms 1)fever, 2) night sweats 3) weight loss . Pruritis and rarely alcohol induced pain
51
What is nodular sclerosing Hodgkins lymphoma?
Young women(>men) 20-29 years Neck nodes and mediastinal mass(may be massive and compress SVC or trachea) May have B symptoms Needs a Tissue diagnosis
52
What do bad coeliacs get?
Enteropahy Associated T cell lymphoma (EATL)
53
What is EATL?
mature T cells (not precursor) Involving small intestine Jejunum and Ileum Has an aggressive (not indolent clinical course)
54
NHL: Monitoring only is appropriate for asymptomatic small volume disease in this lymphoma sub type: Burkitt Gastric MALT Follicular lymphoma Diffuse large B cell lymphoma
Follicular lymphoma Is an indolent lymphoma and Gastric MALT can be cured with antibiotics/ eradication therapy (HPylori)
55
cHL PET CT shows disease involving mediastinum spleen and liver. What Ann Arbor Stage?
Stage 4 (liver is not lymphatic)
56
NHL: Monitoring only is appropriate for asymptomatic small volume disease in this lymphoma sub type: Burkitt Gastric MALT Follicular lymphoma Diffuse large B cell lymphoma
Follicular lymphoma Is an indolent lymphoma and Gastric MALT can be cured with antibiotics/ eradication therapy (HPylori)
57
22 year old female with cHL, mediastinal mass- what is the most likely subtype?
Nodular sclerosis
58
What is the natural history of CLL?
Highly variable natural history Initially 5-10 years good health until progression to a 2-3 year terminal phase Rapid progression to death within 2-3 years In a disorder of elderly 1/3 never progress 1/3 Progress, respond to CLL Rx (death from unrelated disorder) 1/3 Progress, require multiple lines of Rx, refractory disease, death from CLL
59
How does venetoclax work?
Orally active Bcl 2 inhibitor, permits apoptosis of CLL cells In high risk CLL p53 mutated 85% response and maintained at greater than 1 year Main risk is Tumour lysis syndrome when initiating therapy (potentially fatal)
60
What is CLL therapy?
Combination Immuno-chemotherapy (being superseded by targeted Rx) Targeted Therapy BTK inhibitor BCL2 inhibitor Cellular therapy only for relapsed high risk cases Allogeneic SCT CAR-T therapy
61
What's the worse toxicity for the direct treatments?
financial lmao, like tens of thousands of pounds
62
What is CLL therapy?
Combination Immuno-chemotherapy (being superseded by targeted Rx) Targeted Therapy BTK inhibitor BCL2 inhibitor Cellular therapy only for relapsed high risk cases Allogeneic SCT CAR-T therapy
63
What's the worse toxicity for the direct treatments?
financial lmao, like tens of thousands
64
CLL: who has the worst prognosis? IgHV mutated, TP53 wt IgHV mutated, TP53 mutated IgHV unmutated, TP53 wt IgHV unmutated, TP53 mutated
IgHV unmutated, TP53 mutated
65
How does venetoclax work? Blocks BCL2 protein Targets CD20 antigen on B cells inhibits TP53 protein Irreverisbly binds to BTK (Bruton Tyrosine Kinase) PD1 ligand inhibitor
Blocks BCL2 protein

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