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y4 cancer care > Haematological Cancers > Flashcards

Haematological Cancers Flashcards

1
Q

Leukaemia is cancer of a particular line of stem cells in the bone marrow, causing unregulated production of a specific type of blood cell.

The types of leukaemia can be classified depending on how rapidly they progress (chronic is slow and acute is fast) and the cell line that is affected (myeloid or lymphoid) to make four main types:

A

Acute myeloid leukaemia (rapidly progressing cancer of the myeloid cell line)

Acute lymphoblastic leukaemia (rapidly progressing cancer of the lymphoid cell line)

Chronic myeloid leukaemia (slowly progressing cancer of the myeloid cell line)

Chronic lymphocytic leukaemia (slowly progressing cancer of the lymphoid cell line)

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2
Q

What patient group is most affected by leukaemia?

A

Most types of leukaemia occur in patients over 60-70. The exception is acute lymphoblastic leukaemia, which most commonly affects children under five years.

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3
Q

the most common leukaemia in children and is associated with Down syndrome =

A

ALL

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4
Q

leukaemia associated with warm haemolytic anaemia, Richter’s transformation and smudge cells =

A

CLL

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5
Q

leukaemia with three phases, including a long chronic phase, and is associated with the Philadelphia chromosome =

A

CML

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6
Q

leukaemia that may result in a transformation from a myeloproliferative disorder and is associated with Auer rods =

A

AML

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7
Q

What is the pathophysiology of leukaemia?

A

A genetic mutation in one of the precursor cells in the bone marrow leads to excessive production of a single type of abnormal white blood cell.

The excessive production of a single type of cell can suppress the other cell lines, causing the underproduction of different cell types. This can result in pancytopenia, which is a combination of low red blood cells (anaemia), white blood cells (leukopenia) and platelets (thrombocytopenia).

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8
Q

How may leukaemia present?

A

Fatigue
Fever
Lymphadenopathy
Hepatosplenomegaly
Pallor due to anaemia
Petechiae or bruising due to thrombocytopenia
Abnormal bleeding
Failure to thrive (children)

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9
Q

One key presenting feature of leukaemia is bleeding under the skin due to thrombocytopenia. Bleeding under the skin causes non-blanching lesions.

These lesions are called different things based on the size of the lesions:

A

Petechiae are less than 3mm and caused by burst capillaries
Purpura are 3 – 10mm
Ecchymosis is larger than 1cm

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10
Q

The top differentials for a non-blanching rash caused by bleeding under the skin are:

A

Leukaemia
Meningococcal septicaemia
Vasculitis
Henoch-Schönlein purpura (HSP)
Immune thrombocytopenic purpura (ITP)
Thrombotic thrombocytopenic purpura (TTP)
Traumatic or mechanical (e.g., severe vomiting)
Non-accidental injury

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11
Q

How can leukaemia be diagnosed?

A

FBC within 48 hours

Lactate dehydrogenase (often raised in leukaemia but is a very non-specific marker)

A blood film
Bone marrow biopsy
CT and PET scans for staging

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12
Q

Outline the options for obtaining a bone marrow biopsy

A

usually taken from the iliac crest
involves a local anaesthetic and a specialist needle

The options are aspiration or trephine:
Bone marrow aspiration = taking a liquid sample of cells from within the bone marrow

Bone marrow trephine = solid core sample of the bone marrow, provides a better assessment of the cells and structure

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13
Q

What is the pathophysiology of ALL?

A

Acute lymphoblastic leukaemia (ALL) affects one of the lymphocyte precursor cells, causing acute proliferation of a single type of lymphocyte, usually B-lymphocytes. Excessive accumulation of these cells replaces the other cell types in the bone marrow, leading to pancytopenia.

ALL most often affects children under five but can also affect older adults. It is more common with Down’s syndrome.

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14
Q

What is the pathophysiology of CLL? How does it present?

A

Chronic lymphocytic leukaemia is where there is slow proliferation of a single type of well-differentiated lymphocyte, usually B-lymphocytes.

It usually affects adults over 60 years of age.

It is often asymptomatic but can present with infections, anaemia, bleeding and weight loss.

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15
Q

How can CLL be investigated?

A

FBC:
* lymphocytosis
* anaemia: due to bone marrow replacement or autoimmune hemolytic anaemia (AIHA)
* thrombocytopenia: either due to bone marrow replacement or ITP

blood film: smudge cells

immunophenotyping is the key investigation

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16
Q

Give 4 complications of CLL

A

anaemia

hypogammaglobulinaemia leading to recurrent infections

warm autoimmune haemolytic anaemia in 10-15% of patients

transformation to high-grade lymphoma (Richter’s transformation)

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17
Q

What is Richter’s transformation?

A

when leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma. Patients often become unwell very suddenly

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18
Q

How does Richter’s transformation present?

A

lymph node swelling
fever without infection
weight loss
night sweats
nausea
abdominal pain

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19
Q

What are smear or smudge cells on blood film?

A

ruptured white blood cells that occur while preparing the blood film when the cells are aged or fragile. They are particularly associated with chronic lymphocytic leukaemia.

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20
Q

What are the 3 phases of CML?

A

Chronic phase
Accelerated phase
Blast phase

The chronic phase is often asymptomatic, and patients are diagnosed after an incidental finding of a raised WCC - can last several years before progressing.

The accelerated phase occurs when the abnormal blast cells take up a high proportion (10-20%) of the bone marrow and blood cells. In the accelerated phase, patients are more symptomatic and develop anaemia, thrombocytopenia and immunodeficiency.

The blast phase follows the accelerated phase and involves an even higher proportion (over 20%) of blast cells in the blood. The blast phase has severe symptoms and pancytopenia and is often fatal.

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21
Q

How may CML present?

A

Presentation (60-70 years)
anaemia: lethargy
weight loss and sweating are common
splenomegaly → abdo discomfort

On investigation:
an increase in granulocytes at different stages of maturation +/- thrombocytosis
decreased leukocyte alkaline phosphatase

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22
Q

How may CML be managed?

A

imatinib is now considered first-line treatment
- inhibitor of the tyrosine kinase associated with the BCR-ABL defect, very high response rate in chronic phase CML

hydroxyurea

interferon-alpha

allogenic bone marrow transplant

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23
Q

When does AML commonly present?

A

It can present at any age but normally presents from middle age onwards.

It can be the result of a transformation from a myeloproliferative disorder, such as polycythaemia rubra vera or myelofibrosis.

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24
Q

What may be found on blood film and bone marrow biopsy in AML?

A

high proportion of blast cells

Auer rods in the cytoplasm of blast cells are a characteristic finding

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25
Q

Give some poor prognostic features in AML

A

> 60 years
20% blasts after first course of chemo
cytogenetics: deletions of chromosome 5 or 7

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26
Q

What targeted therapies can be used to treat leukaemia?

A

Tyrosine kinase inhibitors (e.g., imantinib)

Monoclonal antibodies (e.g., rituximab, which targets B-cells)

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27
Q

Give some complications of chemotherapy

A

Failure to treat cancer
Stunted growth and development in children
Infections due to immunosuppression
Neurotoxicity
Cardiotoxicity
Infertility
Secondary malignancy
Tumour lysis syndrome

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28
Q

Lymphoma is a type of cancer affecting the lymphocytes inside the lymphatic system. Cancerous cells proliferate inside the lymph nodes, causing the lymph nodes to become abnormally large (lymphadenopathy).

What are the 2 main types?

A

Hodgkin’s lymphoma (a specific disease)

Non-Hodgkin’s lymphoma (which includes all other types)

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29
Q

Hodgkin’s lymphoma is the most common specific type of lymphoma. It has a bimodal age distribution with peaks around 20-25 and 80 years.

Risk factors for Hodgkin’s lymphoma include:

A

HIV
Epstein-Barr virus
Autoimmune conditions, such as rheumatoid arthritis and sarcoidosis
Family history

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30
Q

Non-Hodgkin’s lymphoma includes many types. A few notable ones are:

A

Diffuse large B cell lymphoma typically presents as a rapidly growing painless mass in older patients

Burkitt lymphoma is particularly associated with Epstein-Barr virus and HIV

MALT lymphoma affects the mucosa-associated lymphoid tissue, usually around the stomach

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31
Q

Risk factors for non-Hodgkin’s lymphoma include:

A

HIV
Epstein-Barr virus
Helicobacter pylori (H. pylori) infection is associated with MALT lymphoma
Hepatitis B or C infection
Exposure to pesticides
Exposure to trichloroethylene (a chemical with a variety of industrial uses)
Family history

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32
Q

How may lymphoma present?

A

Lymphadenopathy
The enlarged lymph nodes might be in the neck, axilla or inguinal region. They are characteristically non-tender and feel firm or rubbery.

Patients with Hodgkin’s lymphoma may experience lymph node pain after drinking alcohol

B symptoms refer to systemic symptoms of lymphoma:
Fever
Weight loss
Night sweats

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33
Q

What clinical findings may help to differentiate Hodgkins and non-Hodgkins lymphoma?

A

Lymphadenopathy in Hodgkin’s lymphoma can experience alcohol-induced pain in the node

‘B’ symptoms typically occur earlier in Hodgkin’s lymphoma and later in non-Hodgkin’s lymphoma

Extra-nodal disease is much more common in non-Hodgkin’s lymphoma than in Hodgkin’s lymphoma

34
Q

What extranodal disease may be present in Non-Hodgkin’s lymphoma?

A

gastric (dyspepsia, dysphagia, weight loss, abdominal pain), bone marrow (pancytopenia, bone pain), lungs, skin, central nervous system (nerve palsies)

35
Q

How may lymphoma be investigated?

A

Excisional lymph node biopsy is diagnostic

HIV test (often performed as this is a risk factor for non-Hodgkin’s lymphoma)
FBC and blood film
ESR (useful as a prognostic indicator)
LDH

CT, MRI, and PET scans may be used to help diagnose and stage the disease

36
Q

What is the characteristic finding from a biopsy of Hodgkin’s lymphoma?

A

Reed-Sternberg cells

They are large cancerous B lymphocytes with two nuclei and prominent nucleoli, giving them a cartoonish appearance of an owl face with large eyes.

37
Q

Investigation findings for Hodgkin’s lymphoma?

A

normocytic anaemia
may be multifactorial e.g. hypersplenism, bone marrow replacement by HL

eosinophilia
caused by the production of cytokines e.g. IL-5

LDH raised

lymph node biopsy
Reed-Sternberg cells are diagnostic

38
Q

What features suggest a poor prognosis of Hodgkin’s lymphoma?

A

B symptoms: weight loss > 10% in last 6 months, fever, night sweats

male

age > 45 years

stage IV disease

haemoglobin < 10.5 g/dl

lymphocyte count < 600/µl or < 8%

albumin < 40 g/l

white blood count > 15,000/µl

39
Q

The Lugano classification system is used for Hodgkin’s and non-Hodgkin’s lymphoma (replacing the older Ann Arbor system). It emphasises whether the affected nodes are above or below the diaphragm.

A simplified version is:

A

Stage 1: Confined to one node or group of nodes
Stage 2: In more than one group of nodes but on the same side of the diaphragm (either above or below)
Stage 3: Affects lymph nodes both above and below the diaphragm
Stage 4: Widespread involvement, including non-lymphatic organs, such as the lungs or liver

40
Q

How can Hodgkin’s lymphoma be managed?

A

chemotherapy and radiotherapy

Chemotherapy may result in infections, cognitive impairment, secondary cancers (e.g., leukaemia) and infertility.

Radiotherapy creates a risk of tissue fibrosis, secondary cancers and infertility.

41
Q

What chemotherapy regimes may be used in Hodgkin’s lymphoma?

A

ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine): considered the standard regime

BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone): alternative regime with better remission rates but higher toxicity

42
Q

What is the main risk to patients with treated Hodgkin’s lymphoma?

A

secondary malignancies are a risk, in particular solid tumours: breast and lung

43
Q

How can non-Hodgkin’s lymphoma be managed?

A

depends on the type and stage. It may involve:

Watchful waiting
Chemotherapy
Monoclonal antibodies (e.g., rituximab, which targets B cells)
Radiotherapy
Stem cell transplantation

44
Q

Give some complications of Non-Hodgkin’s lymphoma

A

Metastasis
Bone marrow infiltration causing anaemia, neutropenia or thrombocytopenia
Superior vena cava obstruction
Spinal cord compression
Complications related to treatment e.g. Side effects of chemotherapy

45
Q

What is the prognosis like for non-Hodgkin’s lymphoma?

A

Low-grade non-Hodgkin’s lymphoma has a better prognosis
High-grade non-Hodgkin’s lymphoma has a worse prognosis but a higher cure rate

46
Q

Burkitt’s lymphoma is a high-grade B-cell neoplasm. There are two major forms:

A

endemic (African) form: typically involves maxilla or mandible

sporadic form: abdominal (e.g. ileo-caecal) tumours are the most common form. More common in patients with HIV

47
Q

What are the microscopic findings of Burkitt’s lymphoma?

A

‘starry sky’ appearance: lymphocyte sheets interspersed with macrophages containing dead apoptotic tumour cells

48
Q

How can Burkitt’s lymphoma be managed?

A

Management is with chemotherapy. This tends to produce a rapid response which may cause ‘tumour lysis syndrome’.

Rasburicase is often given before the chemotherapy to reduce the risk of this occurring

49
Q

What is myeloma?

A

a type of cancer affecting the plasma cells in the bone marrow. Plasma cells are B lymphocytes that produce antibodies.

Cancer in a specific type of plasma cell results in the production of large quantities of a specific paraprotein (or M protein), which is an abnormal antibody.

50
Q

What is multiple myeloma?

A

where the myeloma affects multiple bone marrow areas in the body

51
Q

The CRAB mnemonic can be used to remember the four key features of myeloma:

A

C – Calcium (elevated)
R – Renal failure
A – Anaemia
B – Bone lesions and bone pain

52
Q

Anaemia is the most common complication of myeloma. Why does this occur?

A

Bone marrow infiltration by myeloma suppresses the other blood cell lines, leading to anaemia (low haemoglobin), leukopenia (low white blood cells) and thrombocytopenia (low platelets).

Anaemia in myeloma is normocytic and normochromic.

53
Q

What causes Myeloma bone disease?

A

cytokines released from abnormal plasma cells = increased osteoclast activity and suppressed osteoblast activity.

Osteoclasts absorb bone, and osteoblasts deposit bone. The metabolism of bone becomes imbalanced, with more bone being reabsorbed than constructed.

54
Q

Give some common sites of myeloma bone disease

A

skull, spine, long bones and ribs

55
Q

What are Plasmacytomas?

A

individual tumours formed by cancerous plasma cells. They can occur in the bones, replacing normal bone tissue, or in the soft tissues.

56
Q

Patients with myeloma often develop renal impairment, which can have various causes:

A

Paraproteins deposited in the kidneys
Hypercalcaemia affecting kidney function
Dehydration
Glomerulonephritis (inflammation around the glomerulus and nephron)
Medications used to treat the condition

57
Q

Plasma viscosity increases when more proteins are in the blood, such as the paraproteins found in myeloma.

Hyperviscosity syndrome is considered an emergency. It can cause many issues:

A

Bleeding (e.g., nosebleeds and bleeding gums)
Visual symptoms and eye changes (e.g., retinal haemorrhages)
Neurological complications (e.g., stroke)
Heart failure

58
Q

Give some risk factors for developing myeloma

A

Older age
Male
Black ethnic origin
Family history
Obesity

59
Q

The presenting features that should raise suspicion of myeloma include:

A

Persistent bone pain (e.g., spinal pain)
Pathological fractures
Hypercalcaemia
Anaemia
Renal impairment
Unexplained fatigue, weight loss, fever

60
Q

Other features of myeloma include:

A

amyloidosis e.g. macroglossia
carpal tunnel syndrome
neuropathy

61
Q

What lab investigations are indicated for myeloma?

A

FBC (anaemia or leukopenia in myeloma)
U&E (for renal impairment)
Calcium (raised in myeloma)
ESR (increased in myeloma)
Plasma viscosity (increased in myeloma)

Serum protein electrophoresis (to detect paraproteinaemia)

Serum-free light-chain assay (to detect abnormally abundant light chains)

Urine protein electrophoresis (to detect the Bence-Jones protein)

62
Q

What further investigations are indicated for myeloma?

A

Bone marrow biopsy is required to confirm the diagnosis and perform cytogenetic testing.

Imaging is used to assess for bone lesions. The order of preference is:

Whole-body MRI
Whole-body low-dose CT
Skeletal survey (x-ray images of the entire skeleton)

63
Q

Typical x-ray changes seen in patients with myeloma include:

A

Well-defined lytic lesions (described as looking “punched-out”)
Diffuse osteopenia
Abnormal fractures

Raindrop skull (sometimes called pepper pot skull) refers to multiple lytic lesions seen in the skull on an x-ray.

64
Q

How can myeloma be managed?

A

Treatment usually involves a combination of chemotherapy, which may include:

Bortezomib (a proteasome inhibitor)
Thalidomide
Dexamethasone

65
Q

High-dose chemotherapy followed by a stem cell transplant is an option for fitter patients with myeloma and may achieve a more extended period of remission.

Stem cell transplantation can be:

A

Autologous (using the person’s own stem cells)
Allogeneic (using stem cells from a healthy donor)

66
Q

Management of myeloma bone disease may involve:

A

Bisphosphonates to suppress osteoclast activity

Radiotherapy for bone lesions can improve bone pain

Orthopaedic surgery to stabilise bones (e.g., by inserting a prophylactic intramedullary rod) or treat fractures

Cement augmentation (injecting cement into vertebral fractures or lesions) to improve spine stability and pain

67
Q

There are many complications of myeloma and its treatment, including:

A

Infection
Bone pain
Fractures
Renal failure
Anaemia
Hypercalcaemia
Peripheral neuropathy
Spinal cord compression
Hyperviscosity syndrome
Venous thromboembolism

68
Q

Myeloproliferative disorders involve the uncontrolled proliferation of a single type of stem cell. They are considered a form of cancer occurring in the bone marrow, although they tend to develop and progress slowly. They have the potential to transform into acute myeloid leukaemia.

What are the 3 main disorders?

A

Primary myelofibrosis - haemopoetic stem cells
Polycythaemia vera - erythroid cells
Essential thrombocythaemia - megakaryocytes

69
Q

What gene mutation might be involved in myeloproliferative disorders?

A

JAK2. Treatment might involve JAK2 inhibitors, such as ruxolitinib.

70
Q

What is Myelofibrosis?

A

where the proliferation of a single cell line leads to bone marrow fibrosis, where bone marrow is replaced by scar tissue. This is in response to cytokines released from the proliferating cells e.g. fibroblast growth factor.

When the bone marrow is replaced with scar tissue, we see extramedullary haematopoiesis = hepatomegaly, splenomegaly, and portal hypertension.

71
Q

A blood film in myelofibrosis can show:

A

Teardrop-shaped red blood cells
Anisocytosis (varying sizes of red blood cells)
Blasts (immature red and white cells)

72
Q

How may myeloproliferative disorders present?

A

Initially, myeloproliferative disorders may be asymptomatic.

They can present with non-specific symptoms:

Fatigue
Weight loss
Night sweats
Fever

73
Q

Thrombosis is a common complication of polycythaemia and thrombocythaemia, leading to MI, stroke or VTE

Clinical signs of polycythaemia include:

A

Ruddy complexion (red face)
Conjunctival plethora (the opposite of conjunctival pallor)
Splenomegaly
Hypertension

74
Q

How can myeloproliferative disorders be diagnosed?

A

Bone marrow biopsy is required to confirm the diagnosis. Bone marrow aspiration may be “dry” with myelofibrosis, as the bone marrow has turned to scar tissue.

Testing for the JAK2, MPL and CALR genes can help with diagnosis and management.

75
Q

Management of primary myelofibrosis may involve:

A

No active treatment for mild disease with minimal symptoms

Supportive management of complications, such as anaemia, splenomegaly and portal hypertension

Chemotherapy (e.g., hydroxycarbamide) to help control the disease

Targeted therapies, such as JAK2 inhibitors (ruxolitinib)

Allogeneic stem cell transplantation (risky but potentially curative)

76
Q

Management of polycythaemia vera may involve:

A

Venesection to keep the haemoglobin in the normal range

Aspirin to reduce the risk of thrombus formation

Chemotherapy (typically hydroxycarbamide) to help control the disease

77
Q

Management of essential thrombocythaemia may involve:

A

Aspirin to reduce the risk of thrombus formation

Chemotherapy (typically hydroxycarbamide) to help control the disease

Anagrelide is a specialist platelet-lowering agent

78
Q

What is Myelodysplastic syndrome?

A

is a form of cancer caused by a mutation in the myeloid cells in the bone marrow, resulting in ineffective haematopoiesis

It has the potential to transform into acute myeloid leukaemia.

79
Q

How may Myelodysplastic syndrome present?

A

Patients may be asymptomatic. It may be diagnosed after incidental findings on a full blood count.

They may present with symptoms of:

Anaemia (fatigue, pallor or shortness of breath)
Neutropenia (frequent or severe infections)
Thrombocytopenia (bleeding and purpura)

80
Q

How may Myelodysplastic syndrome be investigated?

A

Full blood count will be abnormal. There may be blasts on the blood film.

Bone marrow biopsy is required to confirm the diagnosis.

81
Q

How may Myelodysplastic syndrome be managed?

A

Depending on the symptoms, risk of progression and overall prognosis, the treatment options are:

Watchful waiting
Supportive treatment (e.g., blood or platelet transfusions)
Erythropoietin (stimulates red blood cell production)
Granulocyte colony-stimulating factor (stimulates neutrophil production)
Chemotherapy and targeted therapies (e.g., lenalidomide)
Allogenic stem cell transplantation (risky but potentially curative)

82
Q

Myeloma without metastasis is characterised by what biochemical pattern?

A

high calcium, normal/high phosphate and normal alkaline phosphate

y4 cancer care (13 decks)

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