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Haematology > WBC in health and disease > Flashcards

WBC in health and disease Flashcards

1
Q

what are the 2 groups WBCs are classified into?

A
  • polymorphonuclear cells (PMN)

- Lymphocytes

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2
Q

what are WBCs responsible for?

A
  • WBC are responsible for the consequences of mismatched blood
  • Responsible for graft v host disease following transplantation
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3
Q

what are polymorphonuclear cells called?

A

granulocytes

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4
Q

what are the 3 types of PMNs?

A

Neutrophil
Basophil
Eosinophil

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5
Q

how are monocytes produced?

A

granulopoiesis

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6
Q

where are neutrophils produced?

A

in bone marrow

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7
Q

what % of blood leukocytes are neutrophils?

A

40-80%

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8
Q

where are neutrophils present?

A

in blood and tissue

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9
Q

what is humoral immunity?

A

production of antibodies

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10
Q

what is cell mediated immunity?

A
  • Specific elimination of micro-organisms by cells of the immune system
  • Production of cytotoxic cells
  • Release cytokines that enhance activity of cells such as NK cells and macrophages (tissue lymphocytes)
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11
Q

what is the function of lymphocyte?

A

Have unique ability to recognise antigens

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12
Q

what is the lifespan of lymphocytes?

A

2-3 days

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13
Q

what are non malignant haematological disease of WBCs?

A
  • Quantitative WBC disorders
    Increased numbers
    Low numbers
  • Morphological abnormalities
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14
Q

what are malignant haematological diseases of WBCs?

A

leukaemia
lymphoma
myeloma

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15
Q

what are the benign WBC disorders that result in an increased level?

A 
Neutrophilia
Eosinophilia
Basophilia
Lymphocytosis
Monocytosis
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16
Q

what are the benign WBC disorders that result in a decreased level?

A

Neutropaenia

Lymphocytopaenia

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17
Q

what is neutrophilia?

A
  • neutrophil increase due to severe infection
  • > 7.5x109/l
  • Immature neutrophils
  • Toxic granulation
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18
Q

what is neutropaenia?

A

Neutrophil count <2x109/l

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19
Q

what can cause neutropenia?

A

drug induced - after chemo
post viral/bacterial infection
hereditary

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20
Q

what are symptoms of severe neutropaenia?

A 
Infections of the mouth and throat
Ulceration of the skin
Septicaemia
Opportunist pathogenic infections:
Staph epidermidus
Gram negative organisms of bowel.
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21
Q

what happens when neutrophil count <0.5x109/l?

A

patient may be considered for isolation

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22
Q

what can cause eosinophilia?

A

Parasitic infections
Allergic disease
Skin diseases
Drugs

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23
Q

what can cause basophilia?

A

Mixodema
Smallpox
Chickenpox
Ulcerative colitis

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24
Q

what is the range for eosinophilia?

A

Eosinophil count >0.4x109/l

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25
Q

what is the range for basophilia?

A

Basophil count> 0.1x109/l

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26
Q

what is monocytosis?

A

Increased numbers of monocytes

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27
Q

when is monocytosis seen?

A
  • Monocyte count does rise alongside neutrophils in infection
  • Systemic lupus erythamatosus (SLE)
  • Rheumatoid arthritis
  • Protozoal infections
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28
Q

what is lymphocytosis?

A

increased number of lymphocytes - 3.0x10^9/l

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29
Q

when is a raised lymphocyte count seen?

A

in healthy children

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30
Q

when is lymphocytosis seen?

A
  • Infectious mononucleosis-glandular fever
  • Whooping cough
  • Viral infections
  • Measles
  • Mumps
  • HIV
  • TB
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31
Q

what is lymphocytopaenia?

A

decreased number of lymphocytes

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32
Q

when can lymphocytoaenia be seen?

A

Viral infections-HIV
Drugs
Bone marrow failure

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33
Q

how is glandular fever spread?

A

through saliva

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34
Q

what causes glandular fever?

A

Epstein Barr virus (EBV)

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35
Q

what are the symptoms of glandular fever?

A 
Lymphadenopathy
Sore throat
Stiff neck
Rash
Lethargy
Malaise
Headaches
Dry cough
Mild/severe fever
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36
Q

what leads to the diagnosis of glandular fever?

A

Moderate raised WBC (10-20 x109/l)
Absolute lymphocytosis
Atypical lymphocytes seen in peripheral blood
Heterophile antibodies found in serum in high titres
Paul Bunnel antibodies
Positive monospot test
Presence of EBV

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37
Q

what is the treatment for glandular fever?

A 
Usually non required
Will recover in 4-6 weeks
Corticosteroids in severe cases
Sometimes antibiotics
Streptococcal infection
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38
Q

what is haemopoietic malignancy?

A

Clonal disease

Derived from one single cell in the bone marrow undergoing genetic alteration

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39
Q

what % of malignant diseases are haemopoietic malignancy?

A

7%

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40
Q

what are the groups of haemopoietic lineage when classifying haematological malignancy?

A

Myeloid neoplasms

Lymphoid neoplasms

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41
Q

what is acute leukaemia?

A

Associated with stem cells or early progenitors

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42
Q

what happens during acute leukaemia?

A

Increased rate of proliferation
Reduced apoptosis
Accumulation of early haemopoietic cells in bone marrow (Blast cells

43
Q

what is the prognosis for acute leukaemia?

A

Immediate treatment- fatal if untreated

44
Q

what is chronic leukaemia?

A

associated with mature cells

45
Q

which has the faster progression acute leukaemia or chronic leukaemia?

A

Acute leukaemia - Aggressive disease/faster progression

46
Q

what are the classifications of acute myeloid leukaemia?

A

M0
M1
M2

47
Q

what are the classifications of acute lymphoblastic leukaemia?

A

L1
L2
L3

48
Q

what is used in the WHO classification of leukaemia?

A 
Morphology
Cytogenetics
Immunophenotyping
Genotype
Considers biology behind the disease
Prognosis and treatment
49
Q

what are symptoms of leukaemia?

A 
Pallor
Lethargy
Pharyngitis
Recurrent infections
Easy bruising
Pyrexia
Night sweats
Bone pain
Flu-like symptoms
Lymphadenopathy
Hepatomegaly
Asymptomatic-chance finding
50
Q

why does bone marrow failure occurs during leukaemia?

A

due to accumulation of malignant cells

51
Q

what are some clinical features of leukaemia?

A 
Opportunist infections
Candida
Psuedomonas aeruginosa
Anaemia
Thrombocytopaenia
Bleeding gums
petichiae
Disseminated intravascular coagulation (DIC)
Gum hypertrophy
Skin involvement
52
Q

what does the diagnosis of acute leukaemia include?

A
  • > 20% blast cells in blood or bone marrow at clinical presentation
  • Lineage determined by microscopy (morphology)
  • Immunophenotyping (flow cytometry)
  • Cytogenetic and molecular analysis
  • Cytochemistry is used less frequently
  • Karyotyping
53
Q

what is the most common form of leukaemia?

A

acute myeloid leukaemia

54
Q

what is the median age of onset for acute myeloid leukaemia?

A

65 years

55
Q

what has an influence on the prognosis of acute myeloid leukaemia?

A

Cytogenetics have a significant influence on prognosis

Initial response to treatment influences prognosis

56
Q

how is acute myeloid leukaemia classified?

A

by specific gene type

57
Q

how many AML patients have karyotype abnormalities?

A

60%

58
Q

what gene mutations are associated with acute myeloid leukaemia?

A

FLT3

CEBPA

59
Q

what are the 6 main groups of acute myeloid leukaemia?

A 
AML-undifferentiated
AML without maturation
AML with maturation
Acute promyelocytic leukaemia
Acute myelomonocytic leukaemia
Acute megakaryoblastic leukaemia
60
Q

what does a full blood count of an AML patient show?

A

Low or high WBC
Low haemoglobin
Low platelets
Blast cells

61
Q

what is seen in the lab findings of AML?

A

Test for DIC usually positive

Bone marrow biopsy shows hypercellular marrow

62
Q

what are blasts classified by using in AML?

A

Immunophenotyping
Immunofluorescence staining
Molecular analysis- karyotyping or RT-PCR

63
Q

what is the specific therapy for acute myeloid leukaemia?

A 
chemotherapy 
Myelotoxic drugs 
Severe marrow failure
Targeted therapies
FLT3 inhibitors
ATRA- all-trans Retinoic Acid
64
Q

what is the general supportive therapy for acute myeloid leukaemia?

A

Fresh frozen plasma
Clotting factors
Platelet transfusions

65
Q

what happens during acute promyelocytic leukaemia (APML)?

A

Maturation arrest at promyelocyte stage of development occurs

66
Q

what genetic mutation is present in APML?

A

Most cases show presence of t(15;17) mutation

PML/RARAfusion gene

67
Q

how is APML treated?

A
  • Targeted treatment to disassociate the fusion protein
    Allows cells to mature
  • Transformed from a near universally fatal disease
68
Q

what is the prognosis of APML?

A
  • 95% survival at 5 years
69
Q

what do most APML patients present with?

A

Most patients with APL present with pancytopenia.
Low WBC, RBC and platelets
10-30% of patients present with raised WBC’s.

70
Q

how does APML differ from AML in patient presentation?

A

most patients of APML present with coagulopathy

71
Q

what is chronic myeloid leukaemia?

A

Clonal disorder of a pluripotent stem cell

72
Q

what is seen in chromic myeloid leukaemia in terms of genes?

A

Presence of Philadelphia chromosome (Ph chromosome)

t(9;22) (q34;q11) translocation

73
Q

what are the clinical features of CML?

A
  • occurs in either sex
  • 40-60 years
  • no predisposing factors
  • insidious onset
  • vague symptoms
74
Q

what are the symptoms of CML?

A

Weight loss, night sweats lassitude

Features of anaemia

75
Q

what symptoms are seen in advanced stages of CML?

A

Bruising and bleeding
Petichiae
Ecchymosis

76
Q

what are the lab findings of CML?

A

Leucocytosis > 50x109/l
Complete spectrum of myeloid cells
↑circulating basophils
Normochromic/normocytic anaemia
Platelet count increased, normal or decreased
Hypercelluar bone marrow
BCR-ABL1 can be demonstrated in 98% of cases

77
Q

what are the 3 phases of CML?

A
  • chronic phase
  • accelerated phase
  • blastic transformation
78
Q

what happens in the chronic phase of CML?

A

90% present in chronic phase

2-3 years

79
Q

what occurs in the accelerated phase of CML?

A

Emergence of discreet blast cell population
Rising leucocyte count during adequate treatment
Platelet count <100, or >1000 x 109/l
Haemoglobin <8.0g/dl
>10% blasts in peripheral blood
>20% basophils and eosinophils in peripheral blood
Difficult to treat

80
Q

what happens during plastic transformation phase of CML?

A 
>30% blasts in the blood or bone marrow.
Marked anaemia and thrombocytopenia
Transform into:
AML – poor prognosis, survival <1year
ALL – poor prognosis, survival 1-2 years
81
Q

how is the chronic phase of CML treated?

A

Imatinib (Glivec) 400mg daily
Inhibitor of BCR-ABL1 Protein
Good response in almost all patients
Bone marrow transplant-imatinib failures

82
Q

how can the accelerated and blastic phase of CML be treated?

A 
May be in this stage for several months
Less easy to control
New chromosome abnormalities
Treat as AML/ALL
Resistance to treatment common
83
Q

what is acute lymphoblastic leukaemia (ALL)?

A

a malignant disorder of the B lymphoid progenitor cells

84
Q

how is acute lymphoblastic leukaemia classified into its groups?

A

by immunophenotyping

85
Q

who does ALL affect?

A

Affects children and adults with a peak prevalence between age 2-5 years.

86
Q

what is the cause of acute lymphoblastic leukaemia?

A 
cause is unknown -
possibly:
- Mutations in stem cells
- Mutations in cancer-related genes
- Environmental factors
87
Q

when is increased risk of ALL seen?

A

Down syndrome
Fanconi’s anaemia
Family history of autoimmune disease

88
Q

what are the clinical features of ALL?

A

Very diverse findings-associated with BM failure

Lethargy/weakness/paleness- due to anaemia

Petechia (capillary haemorrhaging) or bruising –due to thrombocytopenia (low platelets)

Joint pain is a common feature in children

89
Q

what % of ALL patients have abnormal blood counts?

A

90%

90
Q

what is seen in the abnormal blood count of ALL patients?

A

Anaemia- Mild to severe
Platelets- <100 in 75% of cases, <10 in 15%
WBC – 50% of cases have abnormal WBC, 10% have very high WBC

91
Q

what are the blood film features of B-Acute lymphoblastic leukaemia?

A

Blasts are twice the size of a red blood cell

Sparse cytoplasm

Nucleus generally round or oval, occasionally have indented nucleus

Homogenous chromatin

Occasional nucleoli

Vacuoles often present

92
Q

why is knowing the genetic subtype important?

A

an important guide to treatment protocol and prognosis

93
Q

how is ALL treated in children?

A

Chemotherapy
Induce remission
>90% in children
80-90% in adults

Radiotherapy
Risk adjusted
Guided by age, gender and WBC at presentation

Maintenance therapy
2-3 years
SCT if relapse occurs

94
Q

what happens in the treatment of ALL in adults?

A

Proved challenging
Relapse common
<40% free of leukaemia after 5 years
5% in over 70’s

Supportive treatment
Therapy for resultant bone marrow failure

95
Q

what is the peak age of prevalence for Chronic Lymphoblastic leukaemia (CLL)?

A

60-80

96
Q

which cells does CLL effect?

A

mature lymphocytes

97
Q

what happens during CLL?

A

Cells accumulate in blood, bone marrow, spleen, liver, lymph nodes

98
Q

what are the clinical features of CLL?

A 
Asymptomatic
Anaemia
Bruising
Splenomegaly
Recurrent infection
Symmetrical enlargement of cervical, inguinal and axillary lymphnodes
Enlarged tonsils
99
Q

what is seen in the lab findings of CLL?

A 
Lymphocytosis
>5x109/l
B cells CD19+, weak CD20+ and CD5+ 
Normochromic/normocytic anaemia
Thrombocytopaenia
Auto-immune haemolysis
Reduced serum immunoglobulins
100
Q

what happens to the appearance of lymphocytes in CLL?

A

lymphocytes appear morphologically mature and homogenous, with dense nuclear chromatin and little cytoplasm

101
Q

what are the prognostic factors of CLL?

A

Can live for >20 years after diagnosis.

102
Q

what are the cytogenetic abnormalities associated with CLL?

A

Cytogenetic abnormalities
Deletion 13q14, 11q23, 6q21
Trisomy 12
Structural abnormalities of 17p and p53gene

103
Q

what are the treatments for CLL?

A

many never need therapy
radiotherapy
combination chemotherapy
Chlorambucil- alkylating agent, used for very old or unfit patients
Campath- monoclonal antibody therapy- used for poor prognosis patients with p53 deletion.
cyclosporin
splenectomy

Haematology (7 decks)

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