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Path - Haem > Lymphoma 2 > Flashcards

Lymphoma 2 Flashcards

1
Q

how is lymphoma diagnosed and staged?

A
  1. lymph node biopsy & histology
  2. FDG-PET* or CT scan

+/-BM biopsy
+/-Lumbar puncture

  • fluorodeoxyglucose
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2
Q

what is the epideiology of HL?

A

Bimodal age incidence
Most common age 20-29, young women NS subtype
Second smaller peak affecting elderly >60 years old

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3
Q

What is always a worry in lymphoma?

A

Fatal hep b reactivaction!

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4
Q

what ar long teerm side effects of ABVD for HL?

A

Pulmonary fibrosis

cardiomyopathy - most deadly SE.

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5
Q

what is survival in HL?

A

Only 50% of stage IV patients are cured

s1-2: 80%

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6
Q

what is the treatment dilemma in HL?

A

Intensify therapy (chmo + radio): more cures & more secondary cancers

Reduce Therapy: less cures & less secondary cancer

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7
Q

how is nhl managed ?

A

A. histology

B. staging: pet/ct

C. prognostic markers: LDH/
HIV! - immunocompromise
Hep B - fatal reactivation risk
performance status

D. therapy:
Urgent chemotherapy ?
Monitor only {watch & wait} ?
Sub type specific eg Antibiotic eradication H.Pylori gastric MALT lymphoma) ?

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8
Q

what is median survival for burkitts lymphoma and t/b LL Without Rx?

A

Weeks 2-5

very aggressive

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9
Q

which are the indolent NHL?

A

Follicular NHL

Marginal zone lymphoma :
Gastric mucosa associated NHL (MALT lymphoma)
Thyroid (thyroiditis) Parotid (Sjogren’s)

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10
Q

what is the rx for DLBCL ?

A

R-CHOP (Rituximab-CHOP):
( 6-8 cycles - advanced. 3 if localised)

this is combination chemotherapy + antiCD20 rituximab

relpase: Autologous Stem Cell transplant salvage

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11
Q

how is folliculart NHL managed?

A

At presentation Watch and wait only treat “if clinically indicated”:
Nodal extrinsic compression: bowel, ureter, vena cava
Massive painful nodes,
recurrent infections

Treatment
combination Immuno-chemotherapy R-Bendamustine or R-COP

Treatment is not curative - cant cure

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12
Q

how is Enteropahy Associated T cell lymphoma (EATL) managed?

A

avoid gluten

poor response to chemo - fatal

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13
Q

what is Chronic Lymphocytic Leukaemia (CLL) ?

A

• Proliferation of mature CD5+ve/CD19+ve
B-lymphocytes

most common leukaemia in western world

also cd20, cd5 present on cell

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14
Q

the following findings are consistent with?

  • Lymphocytosis between 5 and 300 x 109/l
  • Smear cells
  • Normocytic normochromic anaemia
  • Thrombocytopenia
  • Bone marrow: will see Lymphocytic replacement of normal bone marrow elements
A

Chronic Lymphocytic Leukaemia (CLL)

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15
Q

what does the following mean :

Binet stage C, IgH unmutated, 17p del/p53mutated CLL

A

worse prognosis CLL

thesee are prognostic indicators

binet - clinical prognostic scoree

IgH - Immunoglobulin heavy chain gene mutation status:
Laboratory/malignant cell based prognostics. beter to be mutated

p53 & chromosome deletions - cytogenetic prosnotics

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16
Q

increased risk of infection - hypogammaglobulinaemeia
Richter transformation
WARM autoimmune haemolytic anaeemia

all togethr present in which leukaemia?

A

CLL

17
Q

what are complications of CLL?

how do we treat them?

A

Transformation to high grade lymphoma
{DLBCL subtype}

Richter’s syndrome: Treat as high grade lymphoma with R-CHOP

Acquired auto-immune haemolytic anaemia
rx: steroids

18
Q

how is CLL treated?

A

Prophylaxis:
Aciclovir
PCP prophylaxis for those receiving chemotherapy
IVIG is recommended for those with hypogammaglobulinemia and recurrent chest infections
Immunisation against pneumococcus, and seasonal flu
Avoid live vaccines (herpes zoster)

Watch and wait - unless contraindicated

Chemo - wont cure

Allogeneic SCT or CAR-T cells (chimaeric antigen receptor-T cells) - curative

19
Q

list some contraindications for watch and wait for CLL

A

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)

20
Q

why is TP53 status important in CLL?

A

if p53 is intact -> chemo + antiCD20

if there is 17p del/T p53 mutated CLL:

WONT respond to chemo

Need targeted therapy:

  1. BCR tyrosine Kinase Inhibitors
  2. BCL2 inhibitors
  3. Experimental Cell Based Therapies: CAR-T
21
Q

what is the risk of BCL2 inhibitor use in leukaemia?

A

tumour lysis syndrome

22
Q

how do Bcl2 inhibitors work

A

promote apoptosis

by blocking cells that regulate apoptosis

because the role of BCL2 (gene) is to make BCL2 proteins which have anti-apoptosis properties ->

they inhibit BAX/BAK at the mitochondria to stop apoptosis.

23
Q

how would you identify the cd cells present on lymphocytes?

on CLL?

A

immunophenotype - via flow cytometry

in CLL specifically use PERIPHERAL blood

24
Q

what is the role of FISH in CLL and leukaemias?

A

identifies chromosomal abnormalities eg mutations eeg

p53 deletions

25
Q

make sure to watch saved youtube videos on this

A

are very good!

26
Q

what is the richter transformation

A

when (B cell) CLL tranforms into DLBCL which has a very bad prognosis and is refractory to treatment

27
Q

what transformation can follicular lymphoma undergo?

A

can transform into DLBCL as well - bad prognosis

28
Q

what does t(14:18) mean and what will it result in?

A

translocation between chromosome 14 & 18.

found in Follicular lymphoma -> so there will be overexpression of BCL2 anti-apoptosis protein!

leading to cancer proliferation

29
Q

How does DLBCL present?

A

enlarging lymph node!

30
Q

what is most common cause of death in follicular lymphoma patients? why?

A

Infection - do to leukopenia!

in general there are cytopaenias:
anemia -> fatigue
thrombocytopaenia -> bleeding

31
Q

which factors are associated with poor prognosis in DLBCL?

A

Overall prognosis is months anyways but:

Age > 60y
serum LDH > normal
performance status 2-4
Ann Arbour stage III or IV
more than one extranodal site
32
Q

primary CNS Lymphomas (eg of the brain) are usually of which type?

A

DLBCL

33
Q

what translocation involves the IgH (immunoglobulin heavy chain) and Bcl-1 gene?

A

t(11:14)

IgH - 14
Bcl-1 aka cyclin D1 - 11

Mantle cell lymphoma

34
Q

drugs ending with ‘tinib’ are …?

A

tyrosine kinase inhibitors

35
Q

what are the biochemistry results in tumour lysis syndrome?

A

The P’s are high:

High Potassium, Phosphate,
High Uric acid

Low Ca2+

36
Q

what is the epidemiology of burkitt’s lymphoma?

A

Young boys most commonly affected

Associated with EBV & HIV - AIDs defining illness

Subsaharan africa

37
Q

List some AIDs defining malignancies

A

Most common - Kaposi sarcoma

  1. Burkitts lymphoma
  2. primary cns ;lymphoma
  3. cervical carcinoma

hence why if they have thesee - we test for HIV

38
Q

what are the 3 types of Burkitss lymphoma?

A

Endemic / African - lymphadenopathy + jaw sx

Sporadic - usa/eu -> lymphadenopathy + GIT mass /aorta’s sx

Immunodificiency related - HIV

39
Q

what chromosome have you noticed that all these lymphoma’s involve?

A

14 !! This is the IgH - Immunoglobulin heavy chain gene

Note that all these lymphomas involve chromosome 14 as the oncogenes arer moved near this promoter sequence!

Path - Haem (13 decks)

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