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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.

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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

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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

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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

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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

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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:

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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.
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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
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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
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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

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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
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12
Q

CML : Clinical presentation

A
  1. Marked splenomegaly - abdominal discomfort
  2. Weightloss, sweating
  3. Anaemia - lethargy
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13
Q

Chronic myeloid leukaemia : Ocurrence

Risk factors

A
  • Occurrence : 50-60 years
  • Risk factors : Benzene, radiation exposure
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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
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15
Q

Chronic myeloid leukaemia : Management

A
  1. Tyrosine kinase inhibitor - Imantinib - aiming to stop cell division caused by the BCR-ABL protein
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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

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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
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18
Q

Lymphoid Leukaemia : Types

A
  1. Acute Lymphoid Leukaemia
  2. Chronic Lymphoid Leukaemia
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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
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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
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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
CLL - Clinical features
1. Lymphocytosis 2. Anorexia, weightloss 3. Bleeding, infections 4. Lymphadenopathy
26
Chronic lymphocytic leukaemia : Diagnosis
Blood smear : ‘smudge’ cells - immature B cells broken down during smear Bloods : Lymphocytosis - low lymphocytes
27
Chronic Leukaemia : Pathophysiology
1. Partial maturation of cells * key distinction from acute leukaemia ***Abnormal premature leukocytes don’t work as effectively which weakens the immune system.***
28
Leukaemia : Investigations
**< 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
Leukaemia : Management
1. Chemotherapy 2. Targetted therapy * Tyrosine kinase inhibitors (e.g., ibrutinib) * Monoclonal antibodies (e.g., rituximab, which targets B-cells)
30
Leukaemia : Complications of Chemotherapy
Infections due to immunosuppression * Neurotoxicity * Infertility * Secondary malignancy * Cardiotoxicity (heart damage) * **Tumour lysis syndrome**
31
Leukaemia : Tumor lysis syndrome
*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
Lymphoma : Definition
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
Lymphoma : Types
two categories: * ***Hodgkin’s lymphoma*** (a specific disease) * ***Non-Hodgkin’s lymphoma*** (which includes all other types)
34
Lymphoma : Clinical features
**Lymphadenopathy** is the key presenting symptom. neck, axilla or inguinal region. T ***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
35
Lymphoma : Management
**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
Hodgkin's lymphoma
, 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
Hodgkin's lymphoma : Occurrence
*bimodal age distribution* with peaks around **20-25** and **80 years**.
38
Hodgkin's lymphoma : Risk factors
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
Hodgkin's lymphoma : Clinical features
* **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
Hodgkin's Lymphoma : Diagnosis
Gold standard : Lymph node biopsy * **Reed-Sternberg cells** - large cancerous B lymphocytes with two nuclei and prominent nucleol
41
Hodgkin's Lymphoma : Management
**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
Non-Hodgkin's lymphoma : Types
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
Non-Hodgkin's lymphoma : Risk factors
* HIV * Epstein-Barr virus * Helicobacter pylori (H. pylori) infection is associated with MALT lymphoma * Hepatitis B or C infection * Exposure to pesticides
44
Non-Hodgkin's lymphoma : Clinical presentation
**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
Non-Hodgkin's lymphoma : Investigations
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
Non-Hodgkin's lymphoma : Management
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
Hodgkin's vs Non Hodgkin's : Clinical features
**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
Plasma cells : Definition
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
Myeloma : Pathophysiology
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
Myeloma : Blood findings
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
Myeloma : Diagnosis
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)

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