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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
what is the range for basophilia?
Basophil count> 0.1x109/l
26
what is monocytosis?
Increased numbers of monocytes
27
when is monocytosis seen?
- Monocyte count does rise alongside neutrophils in infection - Systemic lupus erythamatosus (SLE) - Rheumatoid arthritis - Protozoal infections
28
what is lymphocytosis?
increased number of lymphocytes - 3.0x10^9/l
29
when is a raised lymphocyte count seen?
in healthy children
30
when is lymphocytosis seen?
- Infectious mononucleosis-glandular fever - Whooping cough - Viral infections - Measles - Mumps - HIV - TB
31
what is lymphocytopaenia?
decreased number of lymphocytes
32
when can lymphocytoaenia be seen?
Viral infections-HIV Drugs Bone marrow failure
33
how is glandular fever spread?
through saliva
34
what causes glandular fever?
Epstein Barr virus (EBV)
35
what are the symptoms of glandular fever?
``` Lymphadenopathy Sore throat Stiff neck Rash Lethargy Malaise Headaches Dry cough Mild/severe fever ```
36
what leads to the diagnosis of glandular fever?
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
37
what is the treatment for glandular fever?
``` Usually non required Will recover in 4-6 weeks Corticosteroids in severe cases Sometimes antibiotics Streptococcal infection ```
38
what is haemopoietic malignancy?
Clonal disease | Derived from one single cell in the bone marrow undergoing genetic alteration
39
what % of malignant diseases are haemopoietic malignancy?
7%
40
what are the groups of haemopoietic lineage when classifying haematological malignancy?
Myeloid neoplasms | Lymphoid neoplasms
41
what is acute leukaemia?
Associated with stem cells or early progenitors
42
what happens during acute leukaemia?
Increased rate of proliferation Reduced apoptosis Accumulation of early haemopoietic cells in bone marrow (Blast cells
43
what is the prognosis for acute leukaemia?
Immediate treatment- fatal if untreated
44
what is chronic leukaemia?
associated with mature cells
45
which has the faster progression acute leukaemia or chronic leukaemia?
Acute leukaemia - Aggressive disease/faster progression
46
what are the classifications of acute myeloid leukaemia?
M0 M1 M2
47
what are the classifications of acute lymphoblastic leukaemia?
L1 L2 L3
48
what is used in the WHO classification of leukaemia?
``` Morphology Cytogenetics Immunophenotyping Genotype Considers biology behind the disease Prognosis and treatment ```
49
what are symptoms of leukaemia?
``` Pallor Lethargy Pharyngitis Recurrent infections Easy bruising Pyrexia Night sweats Bone pain Flu-like symptoms Lymphadenopathy Hepatomegaly Asymptomatic-chance finding ```
50
why does bone marrow failure occurs during leukaemia?
due to accumulation of malignant cells
51
what are some clinical features of leukaemia?
``` Opportunist infections Candida Psuedomonas aeruginosa Anaemia Thrombocytopaenia Bleeding gums petichiae Disseminated intravascular coagulation (DIC) Gum hypertrophy Skin involvement ```
52
what does the diagnosis of acute leukaemia include?
- > 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
what is the most common form of leukaemia?
acute myeloid leukaemia
54
what is the median age of onset for acute myeloid leukaemia?
65 years
55
what has an influence on the prognosis of acute myeloid leukaemia?
Cytogenetics have a significant influence on prognosis | Initial response to treatment influences prognosis
56
how is acute myeloid leukaemia classified?
by specific gene type
57
how many AML patients have karyotype abnormalities?
60%
58
what gene mutations are associated with acute myeloid leukaemia?
FLT3 | CEBPA
59
what are the 6 main groups of acute myeloid leukaemia?
``` AML-undifferentiated AML without maturation AML with maturation Acute promyelocytic leukaemia Acute myelomonocytic leukaemia Acute megakaryoblastic leukaemia ```
60
what does a full blood count of an AML patient show?
Low or high WBC Low haemoglobin Low platelets Blast cells
61
what is seen in the lab findings of AML?
Test for DIC usually positive | Bone marrow biopsy shows hypercellular marrow
62
what are blasts classified by using in AML?
Immunophenotyping Immunofluorescence staining Molecular analysis- karyotyping or RT-PCR
63
what is the specific therapy for acute myeloid leukaemia?
``` chemotherapy Myelotoxic drugs Severe marrow failure Targeted therapies FLT3 inhibitors ATRA- all-trans Retinoic Acid ```
64
what is the general supportive therapy for acute myeloid leukaemia?
Fresh frozen plasma Clotting factors Platelet transfusions
65
what happens during acute promyelocytic leukaemia (APML)?
Maturation arrest at promyelocyte stage of development occurs
66
what genetic mutation is present in APML?
Most cases show presence of t(15;17) mutation | PML/RARA fusion gene
67
how is APML treated?
- Targeted treatment to disassociate the fusion protein Allows cells to mature - Transformed from a near universally fatal disease
68
what is the prognosis of APML?
- 95% survival at 5 years
69
what do most APML patients present with?
Most patients with APL present with pancytopenia. Low WBC, RBC and platelets 10-30% of patients present with raised WBC’s.
70
how does APML differ from AML in patient presentation?
most patients of APML present with coagulopathy
71
what is chronic myeloid leukaemia?
Clonal disorder of a pluripotent stem cell
72
what is seen in chromic myeloid leukaemia in terms of genes?
Presence of Philadelphia chromosome (Ph chromosome) | t(9;22) (q34;q11) translocation
73
what are the clinical features of CML?
- occurs in either sex - 40-60 years - no predisposing factors - insidious onset - vague symptoms
74
what are the symptoms of CML?
Weight loss, night sweats lassitude | Features of anaemia
75
what symptoms are seen in advanced stages of CML?
Bruising and bleeding Petichiae Ecchymosis
76
what are the lab findings of CML?
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
what are the 3 phases of CML?
- chronic phase - accelerated phase - blastic transformation
78
what happens in the chronic phase of CML?
90% present in chronic phase | 2-3 years
79
what occurs in the accelerated phase of CML?
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
what happens during plastic transformation phase of CML?
``` >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
how is the chronic phase of CML treated?
Imatinib (Glivec) 400mg daily Inhibitor of BCR-ABL1 Protein Good response in almost all patients Bone marrow transplant-imatinib failures
82
how can the accelerated and blastic phase of CML be treated?
``` May be in this stage for several months Less easy to control New chromosome abnormalities Treat as AML/ALL Resistance to treatment common ```
83
what is acute lymphoblastic leukaemia (ALL)?
a malignant disorder of the B lymphoid progenitor cells
84
how is acute lymphoblastic leukaemia classified into its groups?
by immunophenotyping
85
who does ALL affect?
Affects children and adults with a peak prevalence between age 2-5 years.
86
what is the cause of acute lymphoblastic leukaemia?
``` cause is unknown - possibly: - Mutations in stem cells - Mutations in cancer-related genes - Environmental factors ```
87
when is increased risk of ALL seen?
Down syndrome Fanconi’s anaemia Family history of autoimmune disease
88
what are the clinical features of ALL?
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
what % of ALL patients have abnormal blood counts?
90%
90
what is seen in the abnormal blood count of ALL patients?
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
what are the blood film features of B-Acute lymphoblastic leukaemia?
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
why is knowing the genetic subtype important?
an important guide to treatment protocol and prognosis
93
how is ALL treated in children?
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
what happens in the treatment of ALL in adults?
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
what is the peak age of prevalence for Chronic Lymphoblastic leukaemia (CLL)?
60-80
96
which cells does CLL effect?
mature lymphocytes
97
what happens during CLL?
Cells accumulate in blood, bone marrow, spleen, liver, lymph nodes
98
what are the clinical features of CLL?
``` Asymptomatic Anaemia Bruising Splenomegaly Recurrent infection Symmetrical enlargement of cervical, inguinal and axillary lymphnodes Enlarged tonsils ```
99
what is seen in the lab findings of CLL?
``` Lymphocytosis >5x109/l B cells CD19+, weak CD20+ and CD5+ Normochromic/normocytic anaemia Thrombocytopaenia Auto-immune haemolysis Reduced serum immunoglobulins ```
100
what happens to the appearance of lymphocytes in CLL?
lymphocytes appear morphologically mature and homogenous, with dense nuclear chromatin and little cytoplasm
101
what are the prognostic factors of CLL?
Can live for >20 years after diagnosis.
102
what are the cytogenetic abnormalities associated with CLL?
Cytogenetic abnormalities Deletion 13q14, 11q23, 6q21 Trisomy 12 Structural abnormalities of 17p and p53gene
103
what are the treatments for CLL?
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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