3.5 White Blood Cells Flashcards

1
Q

Which white blood cells are produced from the common myeloid progenitor?

A

Granulocytes – neutrophils, basophils and eosinophils

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2
Q

What is the difference between monocytes and macrophages?

A

Monocytes migrate to tissues where they develop into macrophages

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3
Q

What are the main functions of neutrophils?

A

Chemotaxis and pathogen phagocytosis

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4
Q

What do neutrophils have?

A

Segmented (lobulated) nuclei

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5
Q

What granulocyte is this and why?

A

Basophil

Granules containing heparin, histamine and proteases

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6
Q

What are the main functions of basophils?

A

Mediation of type 1 hypersensitivity reactions, releasing histamine and leukotrienes

Modulation of inflammatory responses, releasing heparin and proteases

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7
Q

What is the main function of eosinophils?

A

Phagocytosis and defense against parasitic infection

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8
Q

What granulocyte is this and why?

A

Eosinophil

Bilobed nucleus and pink granules

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9
Q

What is a 2nd function of eosinophils?

A

Regulation of type 1 hypersensitivity reactions

Inactivates histamines and leukotrienes released by basophils and mast cells

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10
Q

What is left shift?

A

Presence of non-segmented neutrophil precursors due to increased bone marrow output

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11
Q

How many lobes is normal for a neutrophil?

A

3-5

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12
Q

What is it called when there are more than 5 lobes in a neutrophil?

A

Hypersegmented neutrophil

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13
Q

What are the steps of chemotaxis?

A

MARDi MP

Migration 
Adhesion
Rolling
Diapediesis
Migration
Phagocytosis
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14
Q

What is diapedesis?

A

When white blood cells migrate across the blood vessel wall

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15
Q

What is contained within the granules of basophils?

A

Heparin, histamine and proteolytic enzymes

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16
Q

What do monocytes do?

A

Phagocytose microorganisms coated in antibody and complement
Phagocytose bacteria and fungi
Present antigens to lymphoid cells

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17
Q

How are macrophages related to iron?

A

They store and release iron

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18
Q

What white blood cells are derived from the common lymphoid progenitor?

A

T cell, B cells and NK cells

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19
Q

Where and how do B lymphocytes develop?

A

Originate in bone marrow and foetal liver

Develop in the bone marrow and differentiate into plasma cells involving Ig light and heavy chain gene rearrangement

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20
Q

How do B cells mature?

A

After being exposed to antigens in lymphoid tissue

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21
Q

What do B cells do once mature?

A

Recognise non-self antigens which triggers production of specific Ig’s and antibodies (cell mediated immunity)

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22
Q

What are T cells involved in?

A

Cell mediated immunity

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23
Q

How are T cells developed?

A

Foetal lymphocyte progenitors migrate from the liver to the thymus to develop

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24
Q

What do NK Cells do?

A

Part of innate immunity

Kill tumour and virus infected cells

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25
Q

What is leukocytosis?

A

To many white blood cells of any type

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26
Q

What are transient and persistent leukocytosis caused by respectively?

A

Transient – infections
Persistent – leukemia

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27
Q

What is meant by neutrophilia, basophilia and eosinophillia?

A

Too many of each type of white blood cell

28
Q

What is leukopenia?

A

Too little of any type of white blood cell

29
Q

What is the most abundant type of white blood cell?

A

Neutrophils

30
Q

What can cause neutrophilia? (NIICE PreT)

A

Neoplasm
Infection
Inflammation
Corticosteroids
Exercise
Pregnancy
Tissue damage

31
Q

How does exercise increase the number of neutrophils?

A

Exercise causes a rapid shift of neutrophils from marginated pool to circulating pool

32
Q

What might neutrophilia be accompanied with?

A

Left shift (increase in non-segmented neutrophil precursors) and toxic changes

33
Q

What is toxic granulation of neutrophils?

A

Heavy coarse granulation of neutrophils

34
Q

What causes neutropenia? (BRAID)

A

Benign ethnic neutropenia (people of African descent)
Radiotherapy
Autoimmune disorders
Infections (severe viral and bacterial)
Drugs (chemotherapy)

35
Q

What is considered a low neutrophil count?

A

<0.5 x 10^9/L

36
Q

What is lymphocytosis?

A

Too many lymphocytes

37
Q

How to recognize lymphocytosis from a blood film?

A

Atypical lymphocytes (e.g. in Epstein Barr Virus infection)
Basophillic cytoplasm
Scalloped margins of WBC

38
Q

What condition in children causes lymphocytosis?

A

Whopping cough

39
Q

What causes lymphopenia?

A

HIV infection
Chemotherapy
Radiotherapy
Corticosteroids

40
Q

What causes monocytosis?

A

Infection or chronic inflammation

41
Q

What causes eosinophilia?

A

Allergy, parasitic infection, asthma, eczema

Can also occur in leukemia

42
Q

What causes basophillia?

A

Usually in leukemia, otherwise uncommon

43
Q

A 6-year old child is diagnosed with acute lymphoblastic leukaemia. The doctor warns the parents that their child is more susceptible to infections. Why is this the case?

A

Bone marrow is infiltrated with lymphoblasts, impairing haemopoiesis

44
Q

How do macrophages form?

A

Common myeloid progenitor → monocytes → migrate to tissue → macrophages

45
Q

Which white blood cell stores and releases iron?

A

Macrophages

46
Q

What do B lymphocytes mature into?

A

Plasma cells which secrete antibodies

47
Q

What is meant by reactive or secondary changes?

A

When a normal or healthy bone marrow responds to an external stimulus such as infection, inflammation or infarction

48
Q

What is a primary blood cell disorder?

A

The leukocyte count or morphology is abnormal due to acquired somatic DNA damage affecting a haematopoietic precursor cell

This gives rise to blood cancers such as leukaemia, lymphoma, myeloma or myeloproliferative disorders

49
Q

When might toxic granulation be seen?

A

During pregnancy

50
Q

What causes chronic myeloid leukaemia?

A

Translocation occurs between ABL1 gene on chromosome 9 and BCR gene on chromosome 22

Chromosome 22 now has BCR-ABL1, becoming a philadelphia chromosome

Results in uncontrolled tyrosine kinase activity

51
Q

Why does the fusion gene BCR-ABL1 cause CML?

A

The fusion protein has constitutive tyrosine kinase activity which drives autonomous blood cell proliferation

52
Q

What happens to the spleen in CML?

A

Enlarged (splenomegaly)

53
Q

How is CML treated?

A

Tyrosine kinase inhibitors

54
Q

What cells are increased in CML?

A

All granulocytes and their precursors

55
Q

What causes too many monocytes?

A

Infection (particularly chronic bacterial infection) or chronic inflammation

56
Q

What might lymphocytes due to a viral infection look like?

A

Intensely basophilic cytoplasm, scalloped margins and hugging of the surrounding red blood cells

57
Q

What cell type is characteristic of chronic lymphocytic leukaemia?

A

Smudge cells

58
Q

What are some haematological features of acute lymphoblastic leukaemia?

A

Leukocytosis with lymphoblasts in the blood
Normocytic, normochromic anaemia
Neutropenia
Thrombocytopenia (low platelet count)
Replacement of normal bone marrow cells by lymphoblasts

59
Q

Why might a child with acute lymphoblastic leukaemia have bruising and be pale?

A

Bruising is due to thrombocytopenia

Paleness is due to anaemia

Both occur due to the replacement of normal bone marrow cells with infiltrating lymphoblasts

60
Q

What are the treatment options for ALL?

A
Supportive
Red cells
Platelets
Antibiotics
Systemic chemotherapy
Intrathecal chemotherapy
61
Q

What are clinical features of leukemia due to accumulation of abnormal cells?

A

Leukocytosis
Bone pain in acute leukemia
Splenomegaly, hepatomegaly, lymphadenopathy, thymic enlargement
Skin infiltration

62
Q

What are clinical features of leukemia due to the metabolic effects of leukemic cell proliferation?

A

Hyperuricaemia and renal failure
Weight loss
Low grade fever
Sweating

63
Q

What are clinical features of leukemia due to abnormal haemopoiesis?

A

Fatigue, pallor, breathlessness (anaemia)

Fever, other features of infection (neutropenia)

Brusing, petechiae, bleeding (thrombocytopenia)

64
Q

Mutations in what genes usually cause acute myeloid leukaemia?

A

Mutations in transcription factors for multiple genes causing profoundly disturbed cell behaviour

65
Q

What does acute myeloid leukemia result in?

A

Reduced haemopoiesis