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Heart, Lungs and Blood > haematological cancer > Flashcards

haematological cancer Flashcards

1
Q

What is the difference between leukaemia and lymphoma?

A

Leukaemia is a liquid tumour that arises in the bone marrow and can spill into the blood, while lymphoma is a solid tumour that arises in the lymph nodes and may spread into bone marrow.

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2
Q

What is the aetiology of leukaemia?

A

Leukaemia is triggered by exposure to genetic modifiers and/or environmental modifiers that activate oncogenes, which are mutated genes that contribute to the development of cancer.

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3
Q

What are some examples of genetic modifiers that can trigger leukaemia?

A

Examples of genetic modifiers that can trigger leukaemia include mutations in tumour suppressor genes, chromosomal translocations, and gene fusions.

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4
Q

What are some examples of environmental modifiers that can trigger leukaemia?

A

Examples of environmental modifiers that can trigger leukaemia include exposure to radiation, chemotherapy, benzene, and other toxins.

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5
Q

What is the difference between lymphoid and myeloid leukaemia?

A

Lymphoid leukaemia arises from lymphocytes, while myeloid leukaemia arises from myeloid cells such as red blood cells, platelets, and white blood cells.

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6
Q

What is extra-nodal disease in lymphoma?

A

Extra-nodal disease in lymphoma refers to the involvement of other non-lymphatic tissues such as bone, adrenals, testicles, breast, renal, etc.

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7
Q

What is the difference between acute and chronic leukemia

A

Acute leukemia is the proliferation of immature cells, while chronic leukemia is the proliferation of mature cells.

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8
Q

What are the characteristics of acute leukemia?

A

Acute leukemia has a rapid onset, immature cells (blasts) in the blood/marrow, and can have a devastating course if left untreated. It is more common in younger patients.

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9
Q

What are the characteristics of chronic leukemia?

A

Chronic leukemia has a gradual onset, mature cells in the blood/marrow, and an indolent course. It is more common in older patients.

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10
Q

What is the difference between lymphoid and myeloid leukemia?

A

Lymphoid leukemia arises from cells in the lymphocyte line, while myeloid leukemia arises from cells in the granulocyte, monocyte, RBC, or megakaryocyte lines.

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11
Q

What are the symptoms of bone marrow failure in leukemia?

A

Bruising, bleeding (especially gums), petechiae, anemia (fatigue and breathlessness), and thrombocytopenia.

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12
Q

What kind of infections are common in leukemia?

A

Neutropenic (produce too few neutrophils), bacterial (chest infections, tonsillitis, or cellulitis), viral (ulcers and sores), and fungal (candida, disseminated e.g., fungal lung infections).

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13
Q

Which tissues can be affected by leukemia?

A

Enlargement of lymph nodes, spleen, liver, gums, nervous system, and testicles.

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14
Q

What is leukostasis?

A

A condition in which high levels of white blood cells in the blood can cause sludging of blood flow in small vessels, leading to organ damage or failure.

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15
Q

What are the complications of leukemia?

A

Lung infiltrates (breathlessness), cerebral vessel congestion (headache, confusion), retinal bleeds, kidney failure, and DIC (disseminated intravascular coagulation).

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16
Q

What are the initial steps in diagnosing Leukaemia?

A

History and Examination

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17
Q

What blood test is done to support the diagnosis of Leukaemia?

A

Blood Count

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18
Q

What can be observed through the process of Morphology in Leukaemia diagnosis?

A

Observing cells under the microscope to check for the presence of leukaemia cells.

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19
Q

What is the definitive test used for Leukaemia diagnosis?

A

Bone Marrow Biopsy

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20
Q

What can Genetic Testing tell us about Leukaemia?

A

Genetic testing in Leukaemia diagnosis can identify numeric or structural abnormalities, as well as micro-deletions or duplications. Additionally, Single Gene Disorders can be identified through gene panels using next-generation sequencing.

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21
Q

What is immunophenotyping and how does it work?

A

Immunophenotyping is a technique used to identify and classify blood cells based on the presence or absence of specific cell surface antigens. It works by using monoclonal antibodies that are labelled with fluorescent dyes and bind to specific antigens on the surface of cells. The labelled cells are then analyzed using a flow cytometer, which measures the amount of fluorescence emitted by each cell, allowing for the identification and classification of different types of blood cells.

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22
Q

What is flow cytometry and how is it used in immunophenotyping?

A

Flow cytometry is a technique used to measure physical and chemical characteristics of cells or particles in a fluid as they pass through a beam of light. It is used in immunophenotyping by allowing for the analysis of individual cells labeled with fluorescent dyes. A sample of cells is mixed with several different monoclonal antibodies labeled with different fluorescent dyes. The sample is then analyzed using a flow cytometer, which measures the amount of fluorescence emitted by each cell, allowing for the identification and classification of different types of blood cells based on their expression of specific cell surface antigens

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23
Q

What is acute lymphoblastic leukemia (ALL)?

A

ALL is the most common malignancy in childhood, characterized by the proliferation of immature lymphoid cells in the bone marrow and other organs.

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24
Q

What are some common presentations of ALL?

A

ALL may present with bone marrow involvement, bulky disease (such as mediastinal nodes), and may arise from either B cells or T cells.

25
Q

What is the risk of cerebro-spinal fluid (CSF) involvement in ALL?

A

ALL carries a risk of CSF involvement, meaning that the cancer may spread to the central nervous system.

26
Q

What is the significance of CSF analysis in ALL?

A

CSF analysis is important in the management of ALL, as it can detect the presence of cancer cells in the cerebro-spinal fluid, which can help guide treatment decisions.

27
Q

How is treatment directed at the CNS in ALL?

A

Treatment directed at the CNS in ALL may include intrathecal chemotherapy (administered directly into the cerebro-spinal fluid) or radiation therapy to the brain and spinal cord.

28
Q

What are some common clinical features of B cell ALL?

A

B cell ALL may present with bone marrow failure, a big spleen (splenomegaly), and is often characterized by the presence of specific markers on the surface of the cancer cells, such as CD10 and CD19.

29
Q

What are some common clinical features of T cell ALL?

A

T cell ALL typically affects teenage boys and may present with thoracic lymphadenopathy and mediastinal widening on chest X-ray. The cancer cells may also express low levels of certain markers, such as CD5 and CD7.

30
Q

How do B cell ALL and T cell ALL differ?

A

B cell ALL and T cell ALL differ in terms of the type of lymphoid cell that is affected. B cell ALL arises from immature B cells, while T cell ALL arises from immature T cells.

31
Q

How are B cell ALL and T cell ALL diagnosed?

A

B cell ALL and T cell ALL are typically diagnosed through a combination of blood tests, bone marrow biopsy, and immunophenotyping, which involves identifying specific markers on the surface of the cancer cells.

32
Q

What is the treatment for B cell ALL and T cell ALL?

A

Treatment for B cell ALL and T cell ALL typically involves a combination of chemotherapy and other therapies, such as radiation therapy or stem cell transplant, depending on the stage and extent of the disease.

33
Q

What are the diagnostic criteria for AML?

A

AML is diagnosed when there are 20% or more blasts (immature cells) in the bone marrow or on a blood film. It tends to occur more commonly in older patients, with a median age of 65.

34
Q

What are Auer rods and why are they significant in AML?

A

Auer rods are abnormal structures found in the cytoplasm of some AML cells. They are considered diagnostic for AML, as they are not found in other types of leukemia.

35
Q

What is the significance of myeloperoxidase-positive granules in AML?

A

Myeloperoxidase is an enzyme found in the granules of normal white blood cells, and its presence in the granules of AML cells can help support a diagnosis of AML.

36
Q

What is APL and how does it differ from other types of AML?

A

APL is a variant of AML that is associated with severe coagulopathy, meaning that it activates the clotting pathway and causes depletion of clotting factors. It is considered a hematological emergency.

37
Q

What is the specific treatment for APL?

A

The specific treatment for APL is all-trans-retinoic acid (ATRA), which causes the promyelocytes (immature cells) to differentiate into mature cells. Other therapies, such as chemotherapy and stem cell transplant, may also be used as part of the treatment plan.

38
Q

What factors should be considered when treating acute leukemia?

A

When treating acute leukemia, it is important to consider both patient factors (such as age, overall health, and previous medical history) and disease factors (such as disease stage and subtype).

39
Q

What is the difference between curative and palliative care for acute leukemia?

A

Curative care aims to cure the disease, while palliative care aims to manage symptoms and improve quality of life, but does not aim to cure the disease.

40
Q

What are some examples of supportive care measures for patients with acute leukemia?

A

Supportive care measures for patients with acute leukemia may include blood transfusions for anemia, platelet transfusions to prevent bleeding, correction of coagulation abnormalities (such as with fresh frozen plasma), hormone therapy to prevent menstruation, infection prophylaxis, and preservation of fertility through sperm or egg storage.

41
Q

What are some potential long-term effects of curative treatment for acute leukemia?

A

Curative treatment for acute leukemia may involve highly aggressive therapy over 6-12 months, with multiple prolonged hospital admissions. Potential long-term effects may include infertility, bone necrosis, and cardiac or neurological toxicity.

42
Q

What is the role of clinical trials in the treatment of acute leukemia?

A

Clinical trials, including early phase/experimental trials, may offer access to new therapies and treatment options for acute leukemia, and may be considered as an alternative to standard of care treatment.

43
Q

What are the main types of systemic anti-cancer therapy for acute leukemia?

A

The main types of systemic anti-cancer therapy for acute leukemia include chemotherapy, immunotherapy (such as monoclonal antibodies), and bone marrow transplantation. Radiotherapy may also be used in some cases.

44
Q

What are some potential risks associated with allogeneic transplantation?

A

Allogeneic transplantation carries significant risks, including graft failure, graft-versus-host disease (GvHD) affecting the skin, gut, and liver, infections, atypical viral reactivation, fertility issues, psychosocial issues, and burden of follow-up and morbidity. Relapse of the disease may also occur.

45
Q

What factors influence the prognosis in acute leukemia?

A

The prognosis in acute leukemia is influenced by factors such as the patient’s age, overall health, subtype and stage of the disease, and response to treatment. Other factors, such as genetic mutations and chromosomal abnormalities, may also play a role.

46
Q

What is the role of follow-up care in acute leukemia?

A

Follow-up care is important in acute leukemia to monitor for disease recurrence, manage side effects of treatment, and provide supportive care for the patient. Regular check-ups and monitoring of blood counts and other laboratory values may be necessary.

47
Q

What are some characteristic features of CLL?

A

CLL is typically seen in older patients (median age 70 years) and is characterized by the presence of abnormally high numbers of B lymphocytes in the blood and bone marrow. Lymphocyte count can exceed 5.0 x 10^9/L and may be very high (>100). Small/medium-sized lymphocytes are seen prominently on film and marrow, and smear cells can be seen on blood film.

48
Q

What are some common presentations of CLL?

A

CLL is often an incidental finding, with a high white blood cell count (WCC) on blood count being the most common initial presentation. Patients may be asymptomatic or present with generalized lymphadenopathy, splenomegaly, symptoms of anemia, autoimmune hemolytic anemia, bone marrow failure, and reduced immunoglobulins or white blood cell diversity.

49
Q

What are some special considerations when diagnosing and managing CLL?

A

CLL may be Coombs test (DAT) positive, indicating hemolysis, and is typically characterized by the presence of CD19+ B cell surface antigens. Genetic analysis can affect treatment decisions, and CLL may cross over with lymphoma or transform into a high-grade lymphoma. The term “CLL/SLL” may be used, and many patients may not require treatment initially, but should be monitored regularly.

50
Q

What are some laboratory findings that may be seen in patients with CLL and hemolysis?

A

Patients with CLL and hemolysis may show elevated levels of reticulocytes and bilirubin (unconjugated), as well as low levels of haptoglobin. Lactate dehydrogenase (LDH) levels may also be elevated.

51
Q

What are some characteristic features of CML?

A

CML typically affects older adults, with a peak incidence around 50 years of age. It is characterized by a mutation in a stem cell that affects the entire myeloid line, including granulocytes, monocytes, and megakaryocytes. CML has a slow course and is divided into three phases: chronic (<10% blasts), accelerated (10-20% blasts), and blast crisis (>20% blasts), which carries a worse prognosis.

52
Q

What are some common presentations of CML?

A

CML is often characterized by very high white blood cell counts, often exceeding 100 x 10^9/L, with all granulocyte lines and immature forms present. Patients may be asymptomatic, but can experience symptoms related to bone marrow failure, such as fatigue from anemia. Other symptoms may include splenomegaly (possibly massive), fever, sweats, weight loss, headaches, retinal bleeding, and priapism. CML is rare in young people (<19 years).

53
Q

How is CML diagnosed?

A

CML is typically diagnosed through blood tests, which may show a high white blood cell count with a left shift (immature cells), as well as a characteristic genetic abnormality called the Philadelphia chromosome. Bone marrow biopsy may also be performed to confirm the diagnosis and evaluate the extent of the disease.

54
Q

What is the treatment for CML?

A

The treatment for CML may include targeted therapy with tyrosine kinase inhibitors (TKIs), which can induce remission and prolong survival. Other treatments, such as chemotherapy, may be used in some cases. Allogeneic stem cell transplant may also be considered for some patients, particularly those in blast crisis.

55
Q

How is CML diagnosed?

A

CML is diagnosed through blood tests, which may show high white blood cell counts with a left shift (immature cells) and basophilia, as well as the presence of the Philadelphia chromosome, a genetic abnormality formed by the translocation of chromosomes 9 and 22. The disease is also characterized by the presence of myeloid cells.

56
Q

What are the different phases of CML?

A

CML is divided into three phases: chronic phase, accelerated phase, and blast crisis. The phases are defined by the percentage of blasts in the bone marrow, with chronic phase being characterized by less than 10% blasts, accelerated phase by 10-20% blasts, and blast crisis by more than 20% blasts. In some cases, CML may also transform to acute leukemia, either acute myeloid leukemia (AML) or acute lymphoblastic leukemia (ALL).

57
Q

What is the Philadelphia chromosome and its significance in CML?

A

The Philadelphia chromosome is a genetic abnormality formed by the translocation of chromosomes 9 and 22, resulting in the formation of a hybrid gene called BCR-ABL1. This gene produces a tyrosine kinase signaling protein that leads to the overproduction of myeloid cells, a hallmark of CML.

58
Q

What is the specific treatment for CML?

A

The specific treatment for CML is targeted therapy with tyrosine kinase inhibitors (TKIs), such as imatinib. TKIs can induce complete remission in about 70% of cases, and may be used in combination with other therapies such as chemotherapy or stem cell transplant in cases of blast crisis or accelerated phase.

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