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Haematology > Haematological malignancies > Flashcards

Haematological malignancies Flashcards

1
Q

What is myeloma?

A

Cancer of the differentiated B lymphocytes (plasma cells)

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2
Q

How does myeloma lead to progressive bone marrow failure?

A

Malignant plasma cells accumulate in the bone marrow

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3
Q

What are monoclonal paraproteins in myeloma?

A

The excess of certain types of immunoglobulins from the malignant plasma cells

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4
Q

What are the percentages for the monoclonal paraproteins produced in myeloma?

A
  • IgG (55%)
  • IgA (20%)
  • Rarely IgM and IgD
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5
Q

Why are people with myeloma more susceptible to infections?

A

Besides the excess of one type of immunoglobulin, other immunoglobulin levels are low resulting in immunoparesis

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6
Q

Give some clinical presentations of myeloma

A
  • Old age
  • Calcium elevated
  • Renal failure
  • Anaemia
  • Bone lytic lesion - back pain
  • Recurrent bacterial infections due to neutropenia
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7
Q

What is the acronym used to remember most clinical presentations of myeloma?

A

OLD CRAB

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8
Q

Why does kidney failure occur in myeloma?

A

There is nephrotic syndrome due to immunoglobulin precipitation and deposition in all organs, but especially kidneys

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9
Q

How would you diagnose myeloma?

A
  • Bloods
  • U+Es
  • Bence-Jones protein in urine
  • Plain X-ray
  • Serum and urine electrophoresis
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10
Q

What might you see in bloods taken in myeloma?

A
  • Normocytic normochromic anaemia
  • Raised ESR
  • Rouleaux formation on blood film
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11
Q

What is ESR?

A

Erythrocyte sedimentation rate = how quickly RBCs settle, faster may indicate inflammation

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12
Q

What is Rouleaux formation?

A

Stacks/aggregation of RBCs seen on myeloma blood films

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13
Q

What might you see in U+Es taken in myeloma?

A
  • High calcium

* High alkaline phosphatase

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14
Q

What might you see on an X-ray taken in myeloma?

A

• Lytic ‘punched out’ lesions
- Pepper-pot skull, vertebral collapse
• Osteoporosis

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15
Q

What is a prognostic indicator in myeloma?

A

The presence of B2-microglobulin in serum and urine electrophoresis

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16
Q

What are the diagnostic requirements for myeloma?

A
  • Monoclonal protein band in serum or urine
  • Increased plasma cells on bone marrow biopsy
  • Hypercalcaemia/renal failure/anaemia
  • Bone lesions on skeletal survey
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17
Q

How would you treat myeloma?

A
  • Analgesia for bone pain
  • Bisphosphonate (e.g. zolendronate) to reduce fracture rates and bone pain
  • Anaemia corrected with RBC transfusion and erythropoietin can be used
  • Rehydration and ensuring adequate fluid intake of 3L/day
  • Renal dialysis for acute renal failure
  • Quickly treat infections with broad spectrum antibiotics
  • Chemotherapy
  • Stem cell transplant
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18
Q

Why should you avoid NSAIDs in myeloma?

A

They increase the risk of renal failure

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19
Q

What chemotherapy might be used to treat myeloma?

A
  • CTD (Cyclophosphamide, Thalidomide, Dexamethasone) – for less fit people, max 8 cycles
  • VAD (Vincristine, Adriamycin and Dexamethasone) – for fitter people, max 6 cycles
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20
Q

What is the peak age for myeloma?

A

70 years old

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21
Q

Does myeloma affect Afro-Caribbeans or Caucasians more?

A

Afro-Caribbeans

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22
Q

What are the 4 main subtypes of leukaemia?

A
  • Acute lymphoblastic leukaemia (ALL)
  • Acute myeloid leukaemia (AML)
  • Chronic myeloid leukaemia (CML)
  • Chronic lymphocytic leukaemia (CLL)
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23
Q

What is leukaemia?

A

The presence of rapidly proliferating immature blast blood cells in the bone marrow that are non-functional

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24
Q

What is the pathophysiology of leukaemia?

A
  1. Making rapidly dividing, non-functional leukaemia cells wastes energy
  2. Leukamia cells take up food and space in the bone marrow reducing normal cell growth
  3. Fewer functioning blood cells are producted
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25
Q

What is acute lymphoblastic leukaemia (ALL)?

A

Malignancy of immature lymphoid cells which give rise to T and B cells

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26
Q

What is the pathophysiology of ALL?

A

B or T lymphocyte cell lines are affected by arresting their maturation and promoting uncontrolled proliferation of immature blast cells (myeloblasts or lymphoblasts)

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27
Q

Give the 6 areas of infiltration/failure which cause ALL symptoms

A
  1. Marrow failure
  2. Bone marrow infiltration
  3. Liver/spleen infiltration
  4. Node infiltration
  5. CNS infiltration
  6. Mediastinum infiltration
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28
Q

Give some clinical presentations of ALL

A 
• Anaemia
- breathlessness, fatigue, angina, claudication
• Low WCC
- infection, fever and mouth ulcers
• Bleeding
• Bone pain
• Hepatosplenomegaly
• Lymphadenopathy
• Headache and cranial nerve palsies
• Mediastinal masses with SVC obstruction
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29
Q

How would you diagnose ALL?

A
  • FBC and blood film
  • CXR and CT
  • Lumbar puncture
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30
Q

What might you see on an ALL FBC and blood film?

A
  • High WCC

* Blast cells on film and in bone marrow

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31
Q

What would you look for on a CXR and CT scan in ALL?

A

Mediastinal and abdominal lymphadenopathy

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32
Q

Why would you do a lumbar punture in ALL?

A

To look for CNS involvement

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33
Q

How would you treat ALL?

A
  • Blood and platelet transfusions
  • Prophylactic antivirals, antibacterials and antifungals
  • Allopurinol
  • IV fluids – insert a Hickman line to easily take bloods and administer drugs
  • Chemotherapy
  • Marrow transplant
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34
Q

What is the peak age for ALL?

A

2-4 yrs - commonest childhood cancer

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35
Q

What is the commonest acute leukaemia in adults?

A

Acute myeloid leukaemia

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36
Q

What is acute myeloid leukaemia (AML)?

A

The neoplastic proliferation of blast cells derived from marrow myeloid elements (myeloblasts)

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37
Q

What do myeloblast cells give rise to?

A
  • Basophils
  • Neutrophils
  • Eosinophils
  • Monocytes
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38
Q

What do lymphoblast cells give rise to?

A
  • B lymphocytes
  • T lymphocytes
  • Natural killer cells
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39
Q

Give some clinical presentations of AML

A
  • Anaemia
  • Infection
  • Bleeding
  • Hepatomegaly
  • Splenomegaly
  • Gum hypertrophy
  • DIC in a subtype where thromboplastin is released
40
Q

How would you diagnose AML?

A
  • WCC is often raised, but can be normal or even low

* May be few blast cells in the peripheral blood so diagnosis depend on bone marrow biopsy

41
Q

How would you differentiate between ALL and AML?

A

Microscopy, immunophenotyping and molecular methods

42
Q

What are some complications of AML?

A

Infection leading to septicaemia since common organisms may present oddly

43
Q

How would you treat AML?

A
  • Blood and platelet transfusions
  • Prophylactic antivirals, antibacterials and antifungals
  • Allopurinol
  • IV fluids – insert a Hickman line to easily take bloods and administer drugs
  • Chemotherapy
  • Marrow transplant
44
Q

What is the peak age of CML?

A

40-60yrs

45
Q

What percentage of people with CML have the Philadephia chromosome?

A

> 80%

46
Q

What is the Philadephia chromosome?

A

A chromosome abnormality causing CML where there is a fusion gene BCR/ABL on chromosome 22, which has tyrosine kinase activity

47
Q

What is chronic myeloid leukaemia (CML)?

A

Uncontrolled proliferation of myeloid cells

48
Q

Give some clinical presentations of CML

A
  • Symptomatic anaemia e.g. shortness of breath
  • Abdominal discomfort due to splenomegaly
  • Weight loss
  • Tiredness
  • Pallor
  • Fever and sweats in the absence of infection
  • May be features of gout due to purine breakdown
  • May be bleeding due to platelet dysfunction
49
Q

How would you diagnose CML?

A
  • Blood count

* Bone marrow aspirate

50
Q

What would you see in the blood count in CML?

A
  • Very high WCC with whole spectrum of myeloid cells
  • Low Hb (normochromic and normocytic)
  • Platelets are low, normal or raised
51
Q

What would you see in the bone marrow aspirate in CML?

A

Hypercellular (increased cells)

52
Q

How would you treat CML?

A
  • Stem cell transplant

* Oral Imatinib – specific BCR/ABL tyrosine kinase inhibitor

53
Q

What is the most common leukaemia?

A

Chronic lymphocytic leukaemia

54
Q

What is chronic lymphocytic leukaemia (CLL)?

A

The accumulation of mature B cells that have escaped programmed cell death and undergone cell-cycle arrest

55
Q

What are the clinical presentation of CLL?

A
  • Often asymptomatic, found on routine FBC
  • May be anaemic or infection prone
  • If it is severe, weight loss, sweats and anorexia may occur
  • Hepatosplenomegaly
  • Enlarged, rubbery, non-tender nodes
56
Q

How would you diagnose CLL?

A
  • Blood count

* Blood film

57
Q

What would you see in the blood count in CLL?

A
  • Raised WCC with very high lymphocytes

* Normal or low Hb

58
Q

What might you see on the blood film in CLL?

A

Smudge cells may be seen in vitro

59
Q

Give some complications of CLL

A
  • Autoimmune haemolysis
  • Increased infection risk due to hypogammaglobulinaemia (low IgG) - especially herpes zoster
  • Marrow failure
60
Q

Describe the progression of CLL

A
  • Many stay stable for years and may even regress
  • Death is often due to complication of infection
  • May transform into aggressive lymphoma = Richter’s syndrome
  • Prognosis is ‘rule of 3s’
61
Q

What is the ‘rule of 3s’ progression?

A
  • 1/3 will never progress
  • 1/3 progress slowly
  • 1/3 progress actively
62
Q

How would you treat CLL?

A
  • Blood transfusions
  • Human IV immunoglobulins
  • Chemotherapy
  • Radiotherapy
  • Possibly try stem cell transplant
63
Q

What is lymphoma?

A

Disorders caused by malignant proliferations of lymphocytes

64
Q

What are the 2 main types of lymphoma?

A

Hodgkin’s lymphoma and Non-Hodgkin’s lymphoma

65
Q

What is the key difference in differentiating between the 2 types of lymphoma?

A

HL has Reed-Sternberg cells (or varients) and NHL doesn’t

66
Q

What are the 4 main causes of lymphoma?

A
  • Primary immunodeficiency
  • Secondary immunodeficiency
  • Infection
  • Autoimmune disorders
67
Q

Give 2 examples of primary immunodeficiency causes of lymphoma

A
  1. Ataxia telangiectasia

2. Wiscott-Aldrich syndrome

68
Q

Give 2 examples of secondary immunodeficiency causes of lymphoma

A
  1. HIV

2. Transplant recipients

69
Q

Give 3 examples of infection causes of lymphoma

A
  1. Epstein-Barr Virus (EBV)
  2. Human T-lymphotropic virus
  3. Helicobacter pylori
70
Q

Give an example of an autoimmune cause of lymphoma

A

Systemic lupus erythematosus (SLE)

71
Q

What are the peak ages of incidence of Hodgkin’s lymphoma?

A
  • Teenagers: 13-19yrs

* The elderly: >65yrs

72
Q

What are the 2 divisions of Hodgkin’s lymphoma

A
  • Classical Hodgkin’s lymphoma (cHL)

* Nodular lymphocyte predominant Hodgkin’s lymphoma (NLPHL)

73
Q

What is the key difference in differentiating between the 2 types of Hodgkin’s lymphoma?

A
  • cHL is 90-95% of cases and has the Reed-Sternberg cell

* NLPHL has the Reed-Sternberg varient ‘popcorn’ cell

74
Q

Give 5 risk factors for Hodgkin’s lymphoma

A
  1. Affected sibling
  2. EBV (glandular fever)
  3. SLE
  4. Obesity
  5. Post-transplant
75
Q

What are the clinical presentation for Hodgkin’s lymphoma?

A
  • ‘Rubbery’ painless cervical lymphadenopathy
  • Sometimes a cough occurs due to mediastinal lymphadenopathy
  • Generalised disease e.g. hepatosplenomegaly
  • Constitutional B symptoms
76
Q

State the 3 main constitutional B symptoms

A
  • Weight loss
  • Fever
  • Night sweats
77
Q

Give 6 emergency presentations of Hodgkin’s lymphoma

A
  • Infection
  • Dyspnoea
  • Blackouts
  • Sensation of fullness in the head
  • Facial oedema
  • Superior vena cava obstruction with increased jugular venous pressure (JVP)
78
Q

What is the classification system used for lymphomas?

A

The Ann Arbor classification

79
Q

What are the stages in the Ann Arbor classification?

A
  1. Confined to a single lymph node region
  2. Involvement of two or more nodal areas on the same side of the diaphragm
  3. Involvement of nodes on both sides of the diaphragm
  4. Spread beyond lymph nodes
    • Each stage is either A or B:
    - A = no systemic symptoms other than puritus (severe skin itching)
    - B = presence of B symptoms
80
Q

How would you treat Hodgkin’s lymphoma?

A

• Stages I-A to II-A (with less than 3 areas involved) = Short course of ABVD chemo followed by radiotherapy
• Stages II-A to IV-B (with more than 3 areas involved) =
Longer course of ABVD chemo

81
Q

What is combination chemotherapy ABVD?

A
  • Adriamycin
  • Bleomycin
  • Vinblastine
  • Dacarbazine
82
Q

What are some complications of radiotherapy treatment?

A

May increase risk of 2nd malignancies – solid tumours especially lung, breast, melanoma, stomach, sarcoma and thyroid

83
Q

What are some complications of chemotherapy treatment?

A
  • Myelosuppression
  • Nausea
  • Alopecia
  • Infection
  • Infertility
84
Q

Is the majority of Non-Hodgkin’s lymphoma of B cell or T cell origin?

A

B cell origin (80%)

85
Q

What are the 4 areas of clinical presentation for Non-Hodgkin’s lymphoma?

A
  1. Nodal disease
  2. Extranodal disease
  3. Systemic B symptoms
  4. Pancytopenia
86
Q

What might be a symptom of nodal disease in Non-Hodgkin’s lymphoma?

A

Superficial lymphadenopathy (majority have this)

87
Q

What might be affected in extranodal disease in Non-Hodgkin’s lymphoma?

A
  • Skin (especially T-cell lymphomas)
  • Oropharynx
  • Gut
  • Small bowel
  • Bone
  • CNS,
  • Lungs
88
Q

What might occur due to pancytopenia in Non-Hodgkin’s lymphoma?

A
  • Anaemia
  • Infection
  • Bleeding
89
Q

What is the cmmonest type of Hodgkin’s lymphoma?

A

Diffuse large B-cell lymphoma [DLBCL]

90
Q

How might you diagnose Hodgkin’s lymphoma?

A

CT/MRI of chest abdomen and pelvis for staging

91
Q

How might you diagnose Non-Hodgkin’s lymphoma?

A
  • Lymph node excision or bone marrow biopsy – no Reed-Sternberg cells
  • CT/MRI of chest, abdomen and pelvis for staging (Ann Arbor)
  • Immunophenotyping
  • Cytogenetics
92
Q

How might you treat low grade Non-Hodgkin’s lymphoma?

A
  • None may be required

* Radiotherapy may be curative in localised disease

93
Q

How might you treat high grade Non-Hodgkin’s lymphoma?

A
  • Early: 3 months R-CHOP regimen with radiotherapy

* Late: 6 month R-CHOP regimen with radiotherapy

94
Q

What is the R-CHOP regimen treatment for Non-Hodgkin’s lymphoma?

A
  • Rituximab
  • Cyclophosphamide
  • Hydroxy-daunorbicin
  • Oncovin (= brand name for Vicristine)
  • Prednisolone
95
Q

What is Rituximab and what does it target?

A
  • A monoclonal antibody with minimal side effects

* Targets CD20 expressed of B cell surface

Haematology (5 decks)

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