LEUKAEMIAS AND LYMPHOMAS Flashcards

(72 cards)

1
Q

Name the different types of white blood cells

A
  1. Eosinophil
  2. Basophil
  3. Neutrophil
  4. Plasma cell
  5. B cell
  6. T cell
  7. NK cell
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2
Q

What are red cells made from

A

HEAMATOPOIETIC cells that differentiate into MYERLOID stem cells
then red cells

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3
Q

What are platelets made from

A

HEAMATOPOIETIC cells that differentiate into MYERLOID stem cells
then platelets

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4
Q

What are eosinophils made from

A

HEAMATOPOIETIC cells that differentiate into MYOBLASTS then GRANULOCYTES then basophils

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5
Q

What are basophils made from

A

HEAMATOPOIETIC cells that differentiate into MYOBLASTS then GRANULOCYTES then eosinophils

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6
Q

What are neutrophils made from

A

HEAMATOPOIETIC cells that differentiate into MYOBLASTS then GRANULOCYTES then neutrophils

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7
Q

What Are B cells made from

A

HEAMATOPOIETIC cells that differentiate into LYMPHOBLASTS then B cells

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8
Q

What Are T cells made from

A

HEAMATOPOIETIC cells that differentiate into LYMPHOBLASTS then T cells

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9
Q

What Are NK cells made from

A

HEAMATOPOIETIC cells that differentiate into LYMPHOBLASTS then NK cells

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10
Q

What can B cells differentiate into

A

Plasma cells

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11
Q

Name the 2 main types of leukemias

A
  1. Early myeloid

2. Lymphoid

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12
Q

What is acute leukemias

A

Early myeloid or lymphoid precursors accumulating in the bone marrow, blood and other bodily tissues

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13
Q

What is acute leukemias likely due to

A

Single genetic mutation in a population of early progenitor cells

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14
Q

Name the 2 main subtypes of leukaemia

A
  1. Acute myeloid leukaemia (AML)

2. Acute lymphoid leukemias (ALL)

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15
Q

How do we further classify leukemias

A

Based on the morphology of the malignant cells involved

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16
Q

Name three recognised classified subgroup of acute myeloid leukaemia

A
  1. AML with recurrent genetic abnormalities
  2. AML with multilineage dysplasia
  3. AML not otherwise categorised
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17
Q

Describe the clinical features of acute myeloid leukaemia

A
  1. Presents as ‘acute marrow failure’: anaemia, infections, easy bruising, bleeding
  2. orofacial infections
  3. Organ infiltration may occur
  4. May see infiltration of the gingivea
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18
Q

Give examples of orofacial infection seen in acute leukaemias

A

staphylococcal skin infections and oral candidosis

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19
Q

What can infiltration of the gingiva lead to

A

Significant gingival hypertrophy

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20
Q

How can we diagnose acute myeloid leukaemia

A
  1. Full blood count and blood film
  2. Bone marrow sampling
  3. Can utilise PCR
  4. surface antigen expression
  5. Immunofluorescence techniques
  6. Cytogenetics
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21
Q

Why do we take a full blood count and blood film to diagnose acute myeloid leukaemia

A

Helps show the morphology of the cancerous cells

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22
Q

What can Cytogenetics show us

A

reveal specific abnormalities in the genes which is useful for prognoSIS

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23
Q

Give signs of a poor prognosis

A

1, Increasing age

  1. High WCC
  2. Male gender
  3. Certain cytogenetic abnormalities
  4. Poor response to treatment
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24
Q

How do we manage acute myeloid leukaemia

A
  1. Induction therapy

2. Consolidation

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25
What is the aim of induction therapy
Get the patient into remission
26
What happens in consolation
Cycles of chemotherapy
27
What is the survival rate of acute myeloid leukaemia
30-60% at 5 years
28
How can we manage acute lymphoid leukemias
1. Induction 2. Consolation 3. Prophylaxis via intrathecal methotrexate and cranial irradiation 4. Maintenance chemo
29
Name the 2 main types of chronic leukaemia
1. Chronic Lymphoid Leukaemias (CLL) | 2. Chronic Myeloid Leukaemias (CML)
30
What can chronic lymphoid leukemias be divided into
B cell and T cell forms
31
In whom is chronic lymphoid leukemia more common in
The elderly
32
What is Chronic Lymphoid Leukaemia characterised by
Accumulation of the lymphocytes in the blood, marrow, spleen and lymph nodes
33
What can a full blood count of a patient with chronic lymphoid leukemia show
lymphocytosis, anaemia and thrombtopenia
34
What is chronic myeloid leukaemia characterised by
Increasing white cell count and splenomegaly
35
How common is chronic myeloid leukaemia
1 in 100,000
36
What is the peak incident age for chronic myeloid leukaemia
50-60 years
37
What are the clinical features of chronic leukaemia split into
3 PHASES: 1. Chronic 2. Accelerated 3. Blast crisis
38
Give some clinical features of the chronic phase of chronic leukemias
1. lethargy, 2. frequent infections, 3. easy bleeding, 4. feeling full without eating 5. hyperviscosity may lead to visual disturbances
39
Give some clinical features of the accelerated phase of chronic leukemias
1. pyrexia, 2. poor appetite, 3, weight loss, 4. generally unwell patient
40
What happens in the blast crisis of chronic leukemias
patients convert to acute leukaemia and become generally very unwell, spleen enlarges and their symptoms worsen
41
What is another term for the blast crisis phase of chronic leukemias
acute phase
42
Give some oral manifestations of leukaemia we should look out for
1. General pallor of the oral mucosae (underlying anaemia) 2. Gingival bleeding 3. Intraoral petechiae and eechymosis 4. Hyperplasia of the gingivae 5. Mucosal ulceration 6. Oral infections 7. cervical lymphadenopathy 8. Severe mucositis 9. Xerostomia 10. Trismus
43
Name the 2 types of lymphoma
1. Hodgkin’s | 2. Non-Hodgkin’s (NHL)
44
Ho common is Hodgkin’s lymphoma
3 in 100,000 incidences
45
What is the age incidence of Hodgkin’s lymphoma
incidence at young adults around 20 years old and then later in life (higher in men)
46
What are the clinical features of Hodgkin’s lymphoma
1. Mostly involves painlessly enlarging lymph nodes 2. Spleen involved in 30% 3. 1/3 patients have “B-symptoms”
47
What are B symptoms
1. Fever 2. Drenching in night sweats 3. Weight loss
48
How can we diagnose Hodgkin’s lymphoma
1. Tissue sampling of enlarged node 2. Bone marrow sampling 3. CT scanning 4. Histological exam
49
What can a tissue example of a patient with Hodgkin’s lymphoma show
Can reveal the type of Hodgkin’s lymphoma
50
Name the different types of Hodgkin’s lymphoma
1. Modular sclerosing 2. Lymphocyte predominant 3. Mixed cellularity 4. Lymphocyte depleted
51
How is the stage of Hodgkin’s lymphoma determines
Bone marrow sampling and CT scanning
52
What system do we use to classify Hodgkin’s lymphoma
Ann Arbor Staging system
53
How does the Ann Arbor Staging system stage Hodgkin’s lymphoma
stage I which is local disease well contained to stage IV which is diffuse disease with extralymphatic sites affected
54
What does a histological exam of Hodgkin’s lymphoma show
reveals the presence of “Reed Sternberg Cells”
55
What are “Reed Sternberg Cells”
giant cells derived from B cells considered to be crippled germinal centre B cells
56
Name one of the most common causes of caner mortality in young adults
Non-Hodgkin’s lymphoma
57
What does the incidence of Non-Hodgkin’s lymphoma increase with
Increases with age and is more predominant in males
58
Name the most common type of Non-Hodgkin’s lymphoma
Follicular form
59
What are the clinical features of Non-Hodgkin’s lymphoma based on
Based on a spectrum from low grade to high grade
60
What is the median survival for low grade Non-Hodgkin’s lymphoma
8years
61
What is the median survival for high grade Non-Hodgkin’s lymphoma
3 years
62
Name the most common repenting symptom of Non-Hodgkin’s lymphoma
Superficial lymphadenopathy
63
List some orofacial manifestations of lymphoma
1. Facial asymmmetry 2. visible neck swellings 3. Tooth displacement 4. Pain and paraesthesia 5. Ulceration of the lesion 6. Cervical lymphadenopathy 7. Trismus
64
How do we manage low grade Non-Hodgkin’s lymphoma
1. Watch and wait 2. Local radiotherapy 3. Chemotherapy and monoclonal antibody therapy
65
How do we manage High grade Non-Hodgkin’s lymphoma
Combination chemotherapy e.g. R-CHOP protocol (many exist)
66
How do we manage relapsed Non-Hodgkin’s lymphoma
Consider autologous stem cell transplant (PBSCT)
67
What can happen in patients who have undergone an allogenic transplant to treat their haematological malignancy
Can develop graft versus host disease
68
What is graft versus host disease
This is where the donated bone marrow or stem cells (the “graft”) attack the patient’s own cells.
69
What can graft versus host disease cause
Can cause a significant degree of non-relapse related morbidity and mortality to patients.
70
Name the 2 main types of graft versus host disease
Acute or chronic
71
Name the most commonly affected site in graft versus host disease
Skin, gut or liver | In the head and neck, the oral mucosa and the salivary glands may be targeted
72
List some oral affects of chronic graft versus host disease
1. Lip/oral cancers 2. Drug-induced gingival overgrowth 3. OHL (oral hairy leukoplakia) 4. Recurrent or persistent oral infections 5. Oral lichenoid lesions 6. Mucositis/oral ulceration 7. Xerostomia 8. Perioral fibrosis 9. Dysgeusia