Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > Haematological cancer > Flashcards

Haematological cancer Flashcards

1
Q

Leukaemia : Definition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Leukaemia : Clinical features

A

Systemic sx
1 . Fatigue
2 . Fever

Interference with normal blood cell production;
1 . Anaemia

2 . Thrombocytopenia
* Non blanching lesions - Petechaei

Abnormal WBC
* Lymphadenopathy
* Weakened immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Leukaemia : Myeloid stem cells

A

Two main types of Haematopietic stem cells;
1. Myeloid stem cells
2. Lymphoid stem cells

Myeloid stem cells gives rise to a series of specialised cells;
1. Erythrocytes
2. Granulocytes: neutrophils, eosinophils, and basophils
3. Monocytes : Macrophages
4. Megakaryocytes : Platelets, Erythrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Myeloid Leukaemia : Types

A

Two main types of Myeloid Leukaemia
1. Acute Myeloid Leukaemia - aggressive, develops and progresses rapidly
2. Chronic Myeloid Leukaemia - chronic, develops slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Acute Myeloid Leukaemia : Definition

A

Neoplastic monoclonal proliferation of myeloblast stem cells which are precursors of myeloid blood cells, in the bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acute Myeloid Leukaemia : Pathophysiology

A

1 . Genetic and Molecular Abnormalities:

2 . Proliferation of Blast Cells:
* rapid proliferation of myeloblasts
* myeloblasts accumulate in the bone marrow, crowding out normal blood-forming cells

3 . Bone Marrow Infiltration:
excessive accumulation of myeloblasts in the bone marrow disrupts the normal hematopoietic process.

4 . Suppression of Normal Hematopoiesis:

5 . Circulation of Leukemic Cells:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute Myeloid Leukaemia : Risk factors

A
  • Age: Peak at 60
  • Previous Chemotherapy or Radiation:
  • Down’s syndrome
  • Environmental Exposures:- to Benzene
  • Myelodysplastic Syndromes (MDS):* transformation from a myeloproliferative disorder, such as polycythaemia ruby vera or myelofibrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute Myeloid Leukaemia :Clinical features

A
  1. Neutropenia - increased infections
  2. Anaemia
  3. Thrombocytopenia - low platelet, increased risk of bleeding
  4. Splenomegaly
  5. Bone pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute Myeloid Leukaemia : Diagnosis

A
  1. Blood smear : Myeloblasts - normally large cells, fine chromatin and prominent nucleoli
  2. Bone marrow biopsy -: increase in blast cells
  3. Histology : Auer rods
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Chronic myeloid leukaemia : Definition

A

CML is characterized by
* overproduction of partially mature myeloid cells
and
* presence of a specific genetic abnormality known as the Philadelphia chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Chronic myeloid leukaemia : Pathophysiology

A

1 . Chromosomal translocation which affects granulocytes

  • Translocation of chromosome 9 (ADL gene) and chromosome 22 (BCR gene)
  • results in Philidelphia chromosome 22.

2 . Fusion gene - BCR-ABL
* Translocation leads to a fusion gene called BCR-ABL which produced the BRC-ABL protein

3 . BCR-ABL protein acts to switch on tyrosine kinase activity

  • Leading to cell division of myeloid cells to be permanently switched on
  • Forcing myeloid cell proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CML : Clinical presentation

A
  1. Marked splenomegaly - abdominal discomfort
  2. Weightloss, sweating
  3. Anaemia - lethargy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chronic myeloid leukaemia : Ocurrence

Risk factors

A
  • Occurrence : 50-60 years
  • Risk factors : Benzene, radiation exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chronic myeloid leukaemia : Diagnosis

A
  1. Lab results : ***increased number of granulocytes - in different stages of maturation
  2. Bone marrow biopsy : hypercellularity of myeloid cells e.g. megakaryocytes
  3. Genetic testing : identify philidelphia chromosome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic myeloid leukaemia : Management

A
  1. Tyrosine kinase inhibitor - Imantinib - aiming to stop cell division caused by the BCR-ABL protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lymphoid stem cells : Definition

A

Two main types of Haematopietic stem cells;
1. Myeloid stem cells
2. Lymphoid stem cells

Lymphoid stem cells can mature into;
1. T cells
2. B cells
3. Natural Killer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Lymphoid Leukaemia : Definition

A

Neoplastic proliferation of a lymphoid stem cells (lymphoblasts) - precursor cell to T/B/Natural killer cells within the bone marrow

  • Usually effects one of the lymphocyte precursor cells, causing acute proliferation of a single type of lymphocyte
  • B cells most commonly affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lymphoid Leukaemia : Types

A
  1. Acute Lymphoid Leukaemia
  2. Chronic Lymphoid Leukaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Acute Lymphoid Leukaeimia : Types

A
  1. T- cell ALL : proliferation of T cell precursors
    Migrate to thymus or lymph nodes like normal T cells and cause these structures to enlarge.
  2. B-cell ALL : proliferation of B cell precursors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Acute Lymphoid Leukaeimia : Clinical features

A
  1. Fever
  2. Lymphadenopathy + hepatosplenomegaly
    * Thymus enlargement in T cell ALL - may present as mediastinal growth
  3. Anaemia/Neutropenia/Thrombocytopenia
  4. Neoplastic infiltration - bone pain, lymphadenopathy, palpable mass over the thymus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acute Lymphoid Leukaeimia : Occurence and Risk factors

A
  • Children < 5 years
  • Down’s syndrome - associated with Philidelphia chromosome (like Chronic Myeloid Leukaemia)
22
Q

Acute Lymphoid Leukaeimia : Diagnosis

A
  • Blood smear : lymphoblasts- smaller cells, coarse chromatin and small nucleoli
23
Q

Chronic lymphocytic leukaemia : Definition

A

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

24
Q

Chronic lymphocytic leukaemia : Pathophysiology

A
  1. Mutation in B cell pathway maturation
    * B cells to interfere with pathways of B cell receptor which activates tyrosine kinases this in turn;
    i) Prevents CLL cells maturing fully
    ii) Apoptosis is significantly delayed

2 . Leads to a build up of partially mature B cells in bone marrow

  1. > enter the bloodstream
    ->deposit mainly in lymphatic system—>lymphadenopathy (occasionallypainful)
25
Q

CLL - Clinical features

A
  1. Lymphocytosis
  2. Anorexia, weightloss
  3. Bleeding, infections
  4. Lymphadenopathy
26
Q

Chronic lymphocytic leukaemia : Diagnosis

A

Blood smear : ‘smudge’ cells -

immature B cells broken down during smear

Bloods : Lymphocytosis - low lymphocytes

27
Q

Chronic Leukaemia : Pathophysiology

A
  1. Partial maturation of cells
    * key distinction from acute leukaemia

Abnormal premature leukocytes don’t work as effectively which weakens the immune system.

28
Q

Leukaemia : Investigations

A

< 48 hours
Bloods;
1. FBC
2. Blood film
3. LDH - non specific marker of tissue damage

Investigations
4. Bone marrow Biopsy
5. CT and PET scan
6. Lymph node biopsy

29
Q

Leukaemia : Management

A
  1. Chemotherapy
  2. Targetted therapy
    * Tyrosine kinase inhibitors (e.g., ibrutinib)
    * Monoclonal antibodies (e.g., rituximab, which targets B-cells)
30
Q

Leukaemia : Complications of Chemotherapy

A

Infections due to immunosuppression
* Neurotoxicity
* Infertility
* Secondary malignancy
* Cardiotoxicity (heart damage)
* Tumour lysis syndrome

31
Q

Leukaemia : Tumor lysis syndrome

A

Tumour lysis syndrome results from chemicals released when cells are destroyed by chemotherapy, resulting in:
* High uric acid
* High potassium (hyperkalaemia)
* High phosphate
* Low calcium (as a result of high phosphate)

  1. Hyperuricaemia - AKI and uric acid stone } May require Allopurinol
  2. Hyperkalaemia : Cardiac Arrythmia
32
Q

Lymphoma : Definition

A

Lymphoma : 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

33
Q

Lymphoma : Types

A

two categories:
* Hodgkin’s lymphoma (a specific disease)
* Non-Hodgkin’s lymphoma (which includes all other types)

34
Q

Lymphoma : Clinical features

A

Lymphadenopathy is the key presenting symptom.
neck, axilla or inguinal region. T
non-tender and feel firm or rubbery.

Patients with Hodgkin’s lymphomamay experience lymph node pain after drinking alcohol.

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

35
Q

Lymphoma : Management

A

2 week cancer referral or within 48 hours for children if presenting with
Unexplained Lymphadenopathy or Splenomegaly

Typical criteria for urgent referral:
* Persistent (>6 weeks) lymphadenopathy
* One or more lymph nodes >2 cm in diameter
* Rapidly increasing lymphadenopathy
* Generalised lymphadenopathy
* Persistent and unexplained splenomegaly

36
Q

Hodgkin’s lymphoma

A

, is a type of lymphoma characterized by the abnormal proliferation of Reed-Sternberg cells which are large abnormal B cell lymphocytes found in the affected lymph nodes

  • Reed-Sternberg cells release excessive cytoskines causing inflammation and systemic symptoms such as fever and weight loss
37
Q

Hodgkin’s lymphoma : Occurrence

A

bimodal age distribution with peaks around 20-25 and 80 years.

38
Q

Hodgkin’s lymphoma : Risk factors

A

Risk factors for Hodgkin’s lymphoma include:
* HIV
* Epstein-Barr virus - can infect reed-sternberg cells and contribute to disease development
* Autoimmune conditions, such as rheumatoid arthritis and sarcoidosis
* Family history

39
Q

Hodgkin’s lymphoma : Clinical features

A
  • Non disseminated disease and systemic symptoms

1 . Lymphadenopathy which is:
* Painless
* Asymmetrical
Cervical nodes or mediastinal involvement in 60%
mediastinal lymphadenopathy : compress the airway and lead to dyspnoea, chest pain, and dry cough. It may also cause superior vena cava obstruction.

2 . Alcohol-induced pain at lymph node regions is a non-specific symptom

3 .B symptoms;
Fever >38ºC
Night sweats
Unintentional weight loss of >10% over 6 months

40
Q

Hodgkin’s Lymphoma : Diagnosis

A

Gold standard : Lymph node biopsy

  • Reed-Sternberg cells - large cancerous B lymphocytes with two nuclei and prominent nucleol
41
Q

Hodgkin’s Lymphoma : Management

A

First line : 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.

42
Q

Non-Hodgkin’s lymphoma : Types

A

1 . Diffuse large B cell lymphom } Most common form of aggressive NHL
typically presents as a** rapidly growing painless mass in older patients**
2 .Burkitt lymphoma is
particularly associated with Epstein-Barr virus and HIV
3 . MALT lymphoma
affects the mucosa-associated lymphoid tissue, usually around the stomach

43
Q

Non-Hodgkin’s lymphoma : Risk factors

A
  • HIV
  • Epstein-Barr virus
  • Helicobacter pylori (H. pylori) infection is associated with MALT lymphoma
  • Hepatitis B or C infection
  • Exposure to pesticides
44
Q

Non-Hodgkin’s lymphoma : Clinical presentation

A

Disseminated disease at presentation
1. Painless lymphadenopathy : cervical, axillary, inguinal, and femoral lymph nodes most commonly involvement
* SVC obstruction : SOB and facial oedema
* External biliary tree : Jaundice
* Ureters : Hydronephrosis
* Lymph system : Lymphoedema
2. Extranodal involvement
* Bone marrow : Pancytopenia
* Burkitt’s lymphoma : large abdominal mass and symptoms of bowel obstruction

45
Q

Non-Hodgkin’s lymphoma : Investigations

A
  1. Blood test : pancytopenia, U+Es (AKI), LDH elevated
  2. Screening : hepatitis B/C, HIV, HTLV-1
  3. CXR : mediastinal lymphadenopathy, pleural or pericardial effusions

Gold standard : Lymph node biosy

46
Q

Non-Hodgkin’s lymphoma : Management

A

Management of non-Hodgkin’s lymphoma depends on the type and stage. It may involve:

  • Watchful waiting if assymptomatic
  • Localised disease : Local radiotherapy
  • Monoclonal antibodies (e.g., rituximab, which targets B cells)
47
Q

Hodgkin’s vs Non Hodgkin’s : Clinical features

A

Hodgkin’s
1. Mature B cells - Reed Sternberg cells
2. Bimodal age distribution
3. Contiguous spread
4. Extranodal disease uncommon
5. Systemic symptoms common

Non Hodgkin’s
1. B or T cells affected, at various stages of maturation
1. More common with increasing age
1. Non-contiguous spread
1. Extranodal disease common
1. Systemic symptoms not common

48
Q

Plasma cells : Definition

A

Plasma cells are specialised B Lymphocyte cells which produce antibodies
* Formed following B cell activation after encounter an antigen
* Each type of plasma cell produces a specific antibody against a specific antigen

49
Q

Myeloma : Pathophysiology

A

1 . Abnormal Plasma Cell Proliferation
* Arises from a single abnormal plasma cell that undergoes uncontrolled proliferation
* Clonal expansion leads to the accumulation of malignant plasma cells in the bone marrow

2 . Abnormal excess antibody production
* Cloned Plasma cells produce identical monocloal antibodies - ‘Paraproteins’

3 .Renal Dysfunction: - Abnormal proteins produced by myeloma cells can accumulate in the kidneys

4 . Bone Marrow Infiltration:
myeloma cells in the bone marrow disrupts the normal hematopoietic function
anemia, leukopenia, and thrombocytopenia

5 . Bone Destruction:
Abnormal cells activate osteoclasts - bone destruction and the formation of lytic lesions

6 . Hypercalcemia:
* Bone destruction releases calcium into the bloodstream, leading to hypercalcemia.

50
Q

Myeloma : Blood findings

A

1 . full blood count: anaemia
Low WCC - high risk of infection
Low platelets : Bleeding

2 . Peripheral blood film: rouleaux formation
* Stacking of RBC due interaction with excess protein in the blood

3 . Urea and electrolytes: renal failure

4 . Bone profile: hypercalcaemia

51
Q

Myeloma : Diagnosis

A

1 . Protein electrophoresis

Serum : Raised concentrations of monoclonal IgA/IgG proteins
Urine : they are known as Bence Jones proteins

2 . Bone marrow aspiration
confirms the diagnosis if the number of plasma cells is significantly raised

3 . whole-body MRI - for lytic lesions
X-rays: ‘rain-drop skull’ (likened to the pattern rain forms after hitting a surface and splashing, where it leaves a random pattern of dark spots).

Haematology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions