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4th yr- CMS- Medicine > LEUKAEMIAS AND LYMPHOMAS > Flashcards

LEUKAEMIAS AND LYMPHOMAS Flashcards

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
Q

What is the aim of induction therapy

A

Get the patient into remission

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26
Q

What happens in consolation

A

Cycles of chemotherapy

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27
Q

What is the survival rate of acute myeloid leukaemia

A

30-60% at 5 years

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28
Q

How can we manage acute lymphoid leukemias

A
  1. Induction
  2. Consolation
  3. Prophylaxis via intrathecal methotrexate and cranial irradiation
  4. Maintenance chemo
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29
Q

Name the 2 main types of chronic leukaemia

A
  1. Chronic Lymphoid Leukaemias (CLL)

2. Chronic Myeloid Leukaemias (CML)

30
Q

What can chronic lymphoid leukemias be divided into

A

B cell and T cell forms

31
Q

In whom is chronic lymphoid leukemia more common in

A

The elderly

32
Q

What is Chronic Lymphoid Leukaemia characterised by

A

Accumulation of the lymphocytes in the blood, marrow, spleen and lymph nodes

33
Q

What can a full blood count of a patient with chronic lymphoid leukemia show

A

lymphocytosis, anaemia and thrombtopenia

34
Q

What is chronic myeloid leukaemia characterised by

A

Increasing white cell count and splenomegaly

35
Q

How common is chronic myeloid leukaemia

A

1 in 100,000

36
Q

What is the peak incident age for chronic myeloid leukaemia

A

50-60 years

37
Q

What are the clinical features of chronic leukaemia split into

A

3 PHASES:

  1. Chronic
  2. Accelerated
  3. Blast crisis
38
Q

Give some clinical features of the chronic phase of chronic leukemias

A
  1. lethargy,
  2. frequent infections,
  3. easy bleeding,
  4. feeling full without eating
  5. hyperviscosity may lead to visual disturbances
39
Q

Give some clinical features of the accelerated phase of chronic leukemias

A
  1. pyrexia,
  2. poor appetite,
    3, weight loss,
  3. generally unwell patient
40
Q

What happens in the blast crisis of chronic leukemias

A

patients convert to acute leukaemia and become generally very unwell, spleen enlarges and their symptoms worsen

41
Q

What is another term for the blast crisis phase of chronic leukemias

A

acute phase

42
Q

Give some oral manifestations of leukaemia we should look out for

A
  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
Q

Name the 2 types of lymphoma

A
  1. Hodgkin’s

2. Non-Hodgkin’s (NHL)

44
Q

Ho common is Hodgkin’s lymphoma

A

3 in 100,000 incidences

45
Q

What is the age incidence of Hodgkin’s lymphoma

A

incidence at young adults around 20 years old and then later in life (higher in men)

46
Q

What are the clinical features of Hodgkin’s lymphoma

A
  1. Mostly involves painlessly enlarging lymph nodes
  2. Spleen involved in 30%
  3. 1/3 patients have “B-symptoms”
47
Q

What are B symptoms

A
  1. Fever
  2. Drenching in night sweats
  3. Weight loss
48
Q

How can we diagnose Hodgkin’s lymphoma

A
  1. Tissue sampling of enlarged node
  2. Bone marrow sampling
  3. CT scanning
  4. Histological exam
49
Q

What can a tissue example of a patient with Hodgkin’s lymphoma show

A

Can reveal the type of Hodgkin’s lymphoma

50
Q

Name the different types of Hodgkin’s lymphoma

A
  1. Modular sclerosing
  2. Lymphocyte predominant
  3. Mixed cellularity
  4. Lymphocyte depleted
51
Q

How is the stage of Hodgkin’s lymphoma determines

A

Bone marrow sampling and CT scanning

52
Q

What system do we use to classify Hodgkin’s lymphoma

A

Ann Arbor Staging system

53
Q

How does the Ann Arbor Staging system stage Hodgkin’s lymphoma

A

stage I which is local disease well contained to stage IV which is diffuse disease with extralymphatic sites affected

54
Q

What does a histological exam of Hodgkin’s lymphoma show

A

reveals the presence of “Reed Sternberg Cells”

55
Q

What are “Reed Sternberg Cells”

A

giant cells derived from B cells considered to be crippled germinal centre B cells

56
Q

Name one of the most common causes of caner mortality in young adults

A

Non-Hodgkin’s lymphoma

57
Q

What does the incidence of Non-Hodgkin’s lymphoma increase with

A

Increases with age and is more predominant in males

58
Q

Name the most common type of Non-Hodgkin’s lymphoma

A

Follicular form

59
Q

What are the clinical features of Non-Hodgkin’s lymphoma based on

A

Based on a spectrum from low grade to high grade

60
Q

What is the median survival for low grade Non-Hodgkin’s lymphoma

61
Q

What is the median survival for high grade Non-Hodgkin’s lymphoma

62
Q

Name the most common repenting symptom of Non-Hodgkin’s lymphoma

A

Superficial lymphadenopathy

63
Q

List some orofacial manifestations of lymphoma

A
  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
Q

How do we manage low grade Non-Hodgkin’s lymphoma

A
  1. Watch and wait
  2. Local radiotherapy
  3. Chemotherapy and monoclonal antibody therapy
65
Q

How do we manage High grade Non-Hodgkin’s lymphoma

A

Combination chemotherapy e.g. R-CHOP protocol (many exist)

66
Q

How do we manage relapsed Non-Hodgkin’s lymphoma

A

Consider autologous stem cell transplant (PBSCT)

67
Q

What can happen in patients who have undergone an allogenic transplant to treat their haematological malignancy

A

Can develop graft versus host disease

68
Q

What is graft versus host disease

A

This is where the donated bone marrow or stem cells (the “graft”) attack the patient’s own cells.

69
Q

What can graft versus host disease cause

A

Can cause a significant degree of non-relapse related morbidity and mortality to patients.

70
Q

Name the 2 main types of graft versus host disease

A

Acute or chronic

71
Q

Name the most commonly affected site in graft versus host disease

A

Skin, gut or liver

In the head and neck, the oral mucosa and the salivary glands may be targeted

72
Q

List some oral affects of chronic graft versus host disease

A
  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

4th yr- CMS- Medicine (14 decks)

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