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PathY5 > CLL and quiz > Flashcards

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
Q

What is MALT lymphomagenesis?

A

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

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26
Q

How do you treat gastric MALT?

A

Omep 20mg/Clarith 500mg/amox 1gm bd
Repeat breath test at 2 months
Repeat endoscopy every 6 months for 1st 2years then annually

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27
Q

How good is gastric MALT treatment?

A

Durable remission in 75% of patients
response may be delayed until 1yr
If fails eradication therapy then may require chemotherapy

28
Q

Who gets CLL?

A
  • 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
Q

What are the lab findings of CLL?

A
  • 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
Q

What is the diagnostic algorithm for CLL?

A 
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
Q

What are the prognostic factors of CLL?

A

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
Q

How do you determine clinical stage?

A

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
Q

How does IgH gene mutation status affect survival?

A

Mutated: 25 yrs
Unmutated: 8 years

34
Q 
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 
A) 111
B) 133
C) 114
D) 79
E) 32
35
Q

Why do CLL patients have increased risk of infection and bone marrow failure?

A

Malignant (non functional) mature B cells+ hypogammaglobulinaemia

Proliferate within Bone marrow (efface)

36
Q

What complications may occur in CLL?

A

Lymphadenopathy+/splenomegaly, lymphocytosis

Transform to high grade lymphoma

Auto-immune complications e.g. haemolytic anaemia

37
Q

What are is the treatment of CLL?

A

Suportive treatment
Vaccination
Anti-infective prophylaxis and treatment

Specific scenarios
Auto-immune cytopaenias
High grade (Richter) transformation

Leukaemia directed treatment
Tailored to patient

38
Q

How do you do prophylactic treatment of infections in CLL?

A

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
Q

How to you treat autoimmune phenomena?

A

Steroids

Rituximab

40
Q

If CLL transforms to high grade lymphoma what is it called?

A

Richter’s syndrome

41
Q

What is the indication for more than watch and wait?

A 
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
Q

What is first line therapy for TP53 intact disease

A

Young patient:

FCR
Fludarabine Cyclophosphamide Rituximab (anti CD20 moab)
Rituximab-Bendamustine

Obinutuzumab (anti CD20) +Chlorambucil

Older patients:
Supportive care only

43
Q

How do you manage high risk cases of CLL?

A

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
Q

What are some treatment options in CLL?

A

BCR Kinase Inhibitors
Ibrutinib (BTK)
idelalisib (PI3K)

BCL2 inhibitors
Venetoclax

Experimental Cell Based Therapies
Chimaeric Antigen Receptor T cells (CAR-T)

45
Q

What is the presentation of lymphoma?

A

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
Q

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

A

NOT TRUE: Chronic EBV is linked to adult leukaemia and lymphoma

EBV is not linked to leukaemia

47
Q

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

A

NOT TRUE: Follicular NHL: BCR-ABL1

All the other answers include the immunoglobulin gene which is important in B cell lymphomas

48
Q

Lymph node biopsy: Reed Sternberg Cells are present with a background of chronic inflammatory cells and eosinophils: what is the report outcome?

A

Hodgkins lymphoma

49
Q

What is the epidemiology of Hodgkin Lymphoma?

A

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
Q

What are the symptoms of Hodgkins lymphoma?

A

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
Q

What is nodular sclerosing Hodgkins lymphoma?

A

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
Q

What do bad coeliacs get?

A

Enteropahy Associated T cell lymphoma (EATL)

53
Q

What is EATL?

A

mature T cells (not precursor)
Involving small intestine Jejunum and Ileum
Has an aggressive (not indolent clinical course)

54
Q

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

A

Follicular lymphoma

Is an indolent lymphoma and Gastric MALT can be cured with antibiotics/ eradication therapy (HPylori)

55
Q

cHL PET CT shows disease involving mediastinum spleen and liver. What Ann Arbor Stage?

A

Stage 4 (liver is not lymphatic)

56
Q

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

A

Follicular lymphoma

Is an indolent lymphoma and Gastric MALT can be cured with antibiotics/ eradication therapy (HPylori)

57
Q

22 year old female with cHL, mediastinal mass- what is the most likely subtype?

A

Nodular sclerosis

58
Q

What is the natural history of CLL?

A

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
Q

How does venetoclax work?

A

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
Q

What is CLL therapy?

A

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
Q

What’s the worse toxicity for the direct treatments?

A

financial lmao, like tens of thousands of pounds

62
Q

What is CLL therapy?

A

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
Q

What’s the worse toxicity for the direct treatments?

A

financial lmao, like tens of thousands

64
Q

CLL: who has the worst prognosis?

IgHV mutated, TP53 wt
IgHV mutated, TP53 mutated
IgHV unmutated, TP53 wt
IgHV unmutated, TP53 mutated

A

IgHV unmutated, TP53 mutated

65
Q

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

A

Blocks BCL2 protein

PathY5 (98 decks)

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