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Pathology - Y5 > Chronic Lymphocytic Leukaemia > Flashcards

Chronic Lymphocytic Leukaemia Flashcards

1
Q

What is the typical presentation of lymphoma?

A

Painless progressive lymphadenopathy

  • Palpable node
  • Extrinsic compression of any “tube”: e.g. Ureter, bile duct, large blood vessel, bowel, trachea, oesophagus

Infiltrate/impair an organ system

  • e.g. Skin rash, ocular and CNS, liver failure

Recurrent infections

Constitutional symptoms

Coincidental e.g. FBC, Imaging

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2
Q

What are the two broad classifications of B cell Non-Hodgkin’s Lymphoma?

A

Precursor B lymphoblastic leukaemia

Mature B lymphoblastic leukaemia

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3
Q

What are common types of B cell lymphoma?

A

Diffuse Large B-Cell Lymphoma (DLBCL)

Follicular NHL

CLL

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4
Q

What are the two broad classification of T cell lymphoma?

A

Precursor T lymphoblastic leukaemia or lymphoma (T-ALL)

Mature T and NK neoplasm

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5
Q

What are common types of T cell lymphoma?

A

PTCL

Anaplastic

Cutaneous

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6
Q

Summarise the epidemiology of Hodgkin’s 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
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7
Q

What are signs and symptoms associated with lymphoma?

A

Painless enlargement of lymph node/nodes.

May cause obstructive symptoms/signs

Constitutional symptoms:

  • Fever
  • Night sweats
  • Weight loss
  • Pruritis and rarely alcohol induced pain
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8
Q

What are the four types of classical Hodgkin’s Lymphoma?

A

Nodular sclerosing

Mixed cellularity

Lymphocyte rich

Lymphocyte depleted

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9
Q

What is the most common type of Hodgkin’s Lymphoma?

A

Nodular sclerosing

80%

Good prognosis

Causes the peak incidence in young women

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10
Q

Which Hodgkin’s Lymphoma are rare?

A

Lymphocyte rich: Rare - Good prognosis

Lymphocyte depleted: Rare - Poor Prognosis

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11
Q

How common is mixed cellularity Hodgkin’s Lymphoma?

A

17% - uncommon

Good prognosis

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12
Q

How is Hodgkin’s Lymphoma staged and why is this important?

A

Following pathological diagnosis of a lymph node biopsy patients are ‘staged’ this has prognostic significance and also may determine the best approach for therapy.

FDG-PET/CT scan

Consider biopsy of other site if possibly infiltrated e.g. liver

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13
Q

What is the staging for Hodgkin’s Lymphoma?

A

Stage:

  • I: One group of nodes
  • II: >1 group of nodes same side of the diaphragm
  • III: Nodes above and below the diaphragm
  • IV: Extra nodal spread

Suffix A if none of below, B if any of below

  • Fever
  • Unexplained Weight loss >10% in 6 months
  • Night sweats
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14
Q

What is the management for classical Hodgkin’s Lymphoma?

A

Combination chemotherapy - ABVD:

  • Adriamycin
  • Bleomycin
  • Vinblastine
  • DTIC

ABVD is given at 4-weekly intervals and is effective treatment. Preserves fertility (unlike MOPP the original chemo).

Can cause (long term):

  • Pulmonary fibrosis
  • Cardiomyopathy
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15
Q

How is chemotherapy administered in classical Hodgkin’s Lymphoma? What other management options are available?

A

Chemotherapy (essential for cure)

  • ABVD 2-6 cycles (depends: stage and interim response)
  • PET CT
  • Interim: After x2 cycles, response assessment
  • End of Treatment: Guides need for additional radiotherapy

n+/- Radiotherapy

Relapse (salvage chemotherapy)

High dose chemotherapy + Autologous PB stem cell transplant as support

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16
Q

Explain radiotherapy for classical Hodgkin’s Lymphoma.

A

Low/negligible risk of relapse

Risk of damage to normal tissue (collateral damage)

  • Ca breast (risk 1:4 after 25 years)
  • Leukaemia/mds (3%@10years)
  • Lung or skin cancer

Combined modality (chemo + radio) is the greatest risk of 2o malignancy

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17
Q

What is the prognosis of classical Hodgkin’s Lymphoma?

A

Older patients generally do less well as do those with lymphocyte-depleted histology.

Prognosis:

Cure rate ranges from 50-90%.

Over 80% of patients with stage I or II disease are cured

Only 50% of stage IV patients are cured

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18
Q

What is Non-Hodgkin’s Lymphoma?

A

Neoplastic proliferation of lymphoid cells.

Incidence rising 200/million population/year

Clinical course highly variable :

  • Fastest proliferating malignancy (Burkitt Lymphoma)
  • Indolent diseases (eg Follicular NHL with a possible 25 year survival)
  • Antibiotic responsive disease such as Gastric MALT
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19
Q

How is Non-Hodgkin’s Disease staged?

A

CT scan

PET scan (indicated in aggressive lymphomas)

BM biopsy

Lumbar puncture (if risk of CNS involvement)

20
Q

What are prognostic markers of Non-Hodgkin’s Lymphoma?

A

LDH

Performance status

HIV serology (if appropriate HTLV1 serology)

Hepatitis B serology (risk of reactivation if B cell depleting therapy given)

21
Q

What is the most common type of Non-Hodgkin’s Lymphoma?

A

Diffuse Large B Cell Lymphoma

(Followed by Follicular Lymphoma)

22
Q

Which types of Non-Hodgkin’s Lymphoma are classified by the WHO as being high grade and very aggressive?

A

Burkitt’s Lymphoma

T or B cell Lymphoblastic leukaemia/lymphoma

23
Q

Which types of Non-Hodgkin’s Lymphoma are classified by the WHO as being high grade and aggressive?

A

Diffuse Large B cell

Mantle cell

24
Q

Which types of Non-Hodgkin’s Lymphoma are classified by the WHO as being low grade and indolent?

A

Follicular

Small lymphocytic/CLL

Mucosa associated (MALT)

25
What is the predicted survival and curability of high grade, very aggressive forms of Non-Hodgkin's Lymphoma?
Weeks 2-5 (Without Rx) Curable
26
What is the predicted survival and curability of high grade, aggressive forms of Non-Hodgkin's Lymphoma?
Months 3-12 (Without Rx) Moderately curable
27
What is the predicted survival and curability of low grade, indolent forms of Non-Hodgkin's Lymphoma?
Years 10-15 Incurable (long remission)
28
How are very aggressive Non-Hodgkin's Lymphoma managed?
These are treated like acute leukaemia
29
What are the prognostic characteristics of DLBCL?
**IPI (International Prognostic Index):** * Age * Stage (Ann Arbor) * LDH * Extra-nodal disease sites * ECOG performance status
30
What is the treatment of DLBCL?
R-CHOP Rituximab - Anti-CD20 monoclonal antibody Combination therapy e.g. * Cyclophosphamide * Adriamycin * Vincristine * Prednisolone Aim of therapy is curative (overall approx 50%) **Relapse:** Autologous Stem Cell transplant salvage 25% of patients
31
What is Follicular NHL?
Associated with t(14;18) which results in over-expression of bcl2 an anti-apoptosis protein. FLIPI score (modified IPI) to stage. Incurable, median survival 12-15 years
32
What are extranodal marginal zone lymphomas?
Marginal zone NHL involving extra-nodal lymphoid tissue (e.g. Gastric mucosa-associated lymphoid tissue MALT/H.Pylori, Parotid MZL/Sjogren syndrome). * Comprise ~ 8% of all NHL * Chronic antigen stimulation; H.Pylori infection * Median age at presentation 55-60y Most commonly arise in stomach, usually present with epigastric pain, ulceration or bleeding. Usual presentation is Stage I[E]. Constitutional symptoms uncommon. H.Pylori eradication may cure 75% of patients.
33
What is Enteropathy Associated T-cell Lymphoma?
T cell NHL seen in patients with Coeliac disease Mature T cells (not precursor). Involving small intestine, jejunum and ileum. Has an aggressive (not indolent clinical course). Chronic antigen stimulation, triggered by gluten in a gluten sensitive individual. **Presentation & Clinical course:** * Abdominal pain, obstruction perforation, GI bleeding * Malabsorption * Systemic symptoms * Responds poorly to chemo generally fatal * Aim to prevent (strict adherence to Gluten free diet)
34
What is chronic lymphocytic leukaemia?
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
35
What are common laboratory features of CLL?
Lymphocytosis between 5 and 300 x 109/l Smear cells Normocytic normochromic anaemia Thrombocytopenia Bone marrow Lymphocytic replacement of normal marrow elements
36
What is the timecourse 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
37
What are prognostic features of CLL and how is it staged?
**Cell based prognostic factors:** * IgHV mutation status * CLL FISH cytogenetic panel * TP53 mutation status (Chromosome 17p del and/or TP53 point mutation) **Clinical staging systems:** * Binet or Rai (clinical staging) * CLL IPI score
38
What is the median survival of CLL?
* **Mutated:** 25 years * **Unmutated:** 8 years
39
What are clinical complications with CLL?
**Population of malignant (non functional) mature B cells+ hypogammaglobulinaemia:** Increased risk of infection **Proliferate within Bone marrow (efface):** Bone marrow failure **Circulate to nodes, spleen and blood:** Lymphadenopathy+/splenomegaly, lymphocytosis **Acquire further mutations:** Transform to high grade lymphoma; Richter Transformation (1% per year) **Disease of immune cells:** Auto-immune complications e.g. Immune haemolytic anaemia
40
How can sino-pulmonary infections in CLL be treated?
Early Rx with antibiotics Pneumocystis prophylaxis (may also require zoster ppx) Recurrent infection + IgG \< 5g/l \> IVIG replacement therapy
41
Which vaccinations should be offered to patients with CLL?
Pneumococcal Covid19 Seasonal flu **Avoid live vaccines**
42
Watch and wait is the preferred approach to CLL. When should treatment be given?
**Progressive lymphocytosis:** * \>50% Increase over 2 months * Lymphocyte doubling time \<6 months **Progressive marrow failure:** * Hb \< 100, platelets \<100, neutrophils \<1 **Massive or progressive lymphadenopathy/splenomegaly** **Systemic symptoms** **Autoimmune cytopenias (treat with immunosuppression not chemotherapy)**
43
What therapy can be offered for CLL patients?
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
44
Which BCR kinase can be used to treat CLL?
**Ibrutinib (BTK)** Idelalisib (PI3K)
45
Which BCL2 inhibitors can be used to treat CLL?
Venetoclax
46
Which experimental cell based therapies can be used to treat CLL?
Chimaeric Antigen Receptor T cells (CAR-T)
47
How does venetoclax work in CLL?
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).

Pathology - Y5 (59 decks)

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