11.4 Introduction to Haematologic Malignancies Flashcards

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1
Q

What is leukaemia?

A

Malignant process involving excess of clonal white blood cells

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2
Q

Acute vs chronic leukaemia

A

Excess:

Acute: immature cells; “blasts”
Chronic: end-stage cells

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3
Q

Leukaemia vs lymphoma

A

Leukemia: affects circulating WBCs
Lymphoma: localised to lymph nodes

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4
Q

What is the incidence of haematological malignancies in adults?

A

20%

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5
Q

List some risk factors for haematological malignancies

A
  • Smoking
  • Genetic abnormalities
  • Family history
  • Exposure to carcinogens/radiation
  • Viral infections (e.g. Epstein Barr Virus)
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6
Q

Indolent vs aggressive lymphoma; which is curable, and which is incurable?

A

Indolent: slow cellular accumulation (incurable)
Aggressive: rapid cellular division (curable)

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7
Q

Why is the term “metastasis” not commonly used in the context of lyphoma or leukaemia?

A
  • Lymphocytes usually migrate around the body
  • Therefore, the movement of these cells is not metastasis, but regular movement
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8
Q

“Infiltrate” vs “involved with” in terms of haematological malignancies

A

Infiltrate: a cancerous lymphocyte has moved to an area where it does not belong (e.g. lymph node cell in skin)
Involved with: cancerous lymphocyte in an area that it is local to

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9
Q

What percentage of cells in the peripheral blood/bone marrow must be blast cells for a diagnosis of acute lymphoblastic leukaemia?

A

> =20%

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10
Q

What structure(s) differentiate between hodgkins and non-hodgkins lymphoma?

A

Reed-Sternberg cell (multinucleated giant cell made of lymphocytes)

Hodgkins has one, non-hodgkins doesn’t.

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11
Q

Which type of lymphocytes does hodgkin’s lymphoma affect? Therefore, is it acute or chronic?

A
  • Affects B lymphocytes (mature)
  • Therefore, it is chronic
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12
Q

List cancers in B cells, T cells, and NK cells in order from most to least common

A
  • B Cells (85%)
  • T Cells (15%)
  • NK Cells (<1%)
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13
Q

How are indolent haematological malignancies most commonly found?

A
  • Incidentally
  • They are found on routine blood tests, or when imaging
  • After all, if they are not causing the patients any symptoms (since the cells are slow replicating), how would we notice them?
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14
Q

How can lymphoma cause splenomegaly?

A
  • Lymphocytes are homed to the spleen
  • As they rapidly proliferate, the spleen is enlarged
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15
Q

What are some signs of aggressive lymphoma?

A
  • Rapidly enlarging lymphadenopathy
  • High cell turnover = high LDH
  • Bone marrow infiltration would cause anaemia, thrombocytopaenia, neutropaenia
  • Constituional symptoms (explained on another card)
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16
Q

Is bone pain more common in lymphoma or multiple myeloma?

A

Myeloma

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17
Q

What are constitutional B symptoms?

A
  • Fever (>38.3°C)
  • Drenching night sweats
  • Weight loss (>10% body weight over few months) -> intentional or unintentional
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18
Q

What is the most common form of lymphoma?

A

Diffuse large B cell lymphoma (DLBCL)

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19
Q

Is DLBCL aggressive or indolent?

A

Aggressive

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20
Q

Typical blood work results for DLBCL

A
  • Mild anaemia
  • LDH 450
21
Q

What scans are performed in patients with suspected lymphoma? Why?

A
  • PET scan: activity in tissues
  • CT scan: anatomy
22
Q

Nodal vs extranodal blood/lymph cancers

A

Nodal: Isolated within lymph nodes and spleen
Extranodal: Anything outside of this

23
Q

Ann arbor staging classifies the spread of lyphoma. What are stage 1, 2, 3, and 4?

A

Stage 1: 1 site of disease
Stage 2: 2+ site on same side of diaphragm
Stage 3: Disease on both sides of diaphragm
Stage 4: Widespread involvement of extralymphoid sites

24
Q

Explain the concept of sanctuary sites. Where are these sites located?

A

Sanctuary sites are areas where it is difficult for anti-cancer drugs to penetrate due to barriers. These include the brain, the eyes, and the testes

25
Q

What factors influence the prognosis in cancer (particularly lymphoma?)

A

What kind of damage has it done?:
- LDH (how aggressive?)
- Cytopenia?
- What stage?
- Extranodal sites?
Patient related factors:
- Age?
- Comorbidities?
- Organ function?
- Frailty/disability?
Response to treatment:
- Depth of response
- Minimal residual disease
- Relapse time?

26
Q

Why do we systemic therapy (like chemotherapy) for lymphoma?

A
  • It is considered systemic
  • We can’t cut it out, because these cells can exist all throughout the body
27
Q

Rituximab cancer therapy mechanism. What other mechanisms can monoclonal antibodies use to kill haematologic malignancies?

A
  • Monoclonal antibody for CD20; which is a B cell surface marker
  • Causes immune destruction/removal of cancerous cells, or you can attach radioactive particles/chemotherapy that kill the cell once engulfed

There are other monoclonal antibodies. Not just this one.

28
Q

Describe CAR-T cancer therapy

A
  • Take out patient’s T cells
  • Engineer them to kill cancer
  • Put them back in
  • KABOOM
29
Q

Describe the genetics behind Follicular Lymphoma

A
  • Translocation of antiapoptotic gene from chromosome 14-18
  • Moved next to highly-expressed immunoglobulin gene
  • Enhanced activity, leads to overproliferation
30
Q

Describe the role of Reed-Sternberg cells in Hodgkin’s Lymphoma

A
  • They command the rest of the immune system in such a way that drives the disease
  • The actual amount of cancer burden is very low
31
Q

What are the two most common age groups for Hodgkin’s

A
  • Young adults (20-24)
  • Older adults (80+)
32
Q

What is the most common cause of death in patients with hodgkin’s lymphoma?

A

Second malignancy

33
Q

What are some common comorbidities that arise alongside T cell lymphoma?

A
  • Shingles
  • Cold sores
  • Urticaria
34
Q

Chornic Lymphocytic Leukaemia can be reclassified as a lymphoma. What is it called then?

A

Small lymphocytic lymphoma (SLL)

35
Q

Mutated vs unmutated Chronic Lymphocytic Leukaemia. Which generally requires therapy, and which doesn’t

A

Mutated: Memory B Cells
Unmutated: Naive B Cells

36
Q

Most common way of finding Chronic Lymphocytic Leukaemia (CLL)?

A

Incidental findings on CBC

37
Q

Presenting symptoms of chronic lymphocytic leukaemia

A
  • Recurrent infections
  • Constitutional symptoms
  • Splenomegaly, adenopathy
  • Rashes
38
Q

Describe the three stages of Binet CLL staging

A

Stage A: No anaemia, no thrombocytopenia, <3 lymph node areas
Stage B: No anaemia/thrombocytopenia, >3 lymph node areas
Stage C: Anaemia, thrombocytopenia, any number of lymph sites

39
Q

What is hypogammaglobulinaemia?

A

Reduced serum antibody levels

40
Q

Describe multiple myeloma, including cell of origin

A
  • Cancer of plasma cells in bone marrow
  • Decreases production of other cells, and causes bone pain
41
Q

Describe the 2 mechanisms by which plasma cells can decrease haematopoiesis in multiple myeloma

A
  1. Crowding out
  2. Communicating with microenvironment to reduce haematopoiesis
42
Q

Do the hyperproduced antibodies in multiple myeloma even work?

A

Nope. Not good.

43
Q

Which two antibody isotypes are most commonly mutated in multiple myeloma?

A
  • IgG (2/3)
  • IgA (1/3)
44
Q

Peripheral blood findings in myliple myeloma

A

Presence of circulating plasma cells

45
Q

Bone marrow aspirate findings of multiple myeloma

A

Large presence of plasma cells

46
Q

Explain the CRAB pnemonic for multiple myeloma features

A
  • Calcium high
  • Renal insufficiency
  • Anemia
  • Bone lytic lesions, bone pain
47
Q

How does multiple myeloma cause renal failure?

A
  • Abnormal antibodies have toxic effect on distal tubule
  • Can block nephrons entirely
48
Q

What is MGUS? Does it always lead to myeloma?

A
  • Monocllonal gammopathy of undetermined significance
  • Will not always leads to cancer
49
Q
A