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Haematology > Abnormal white cell count > Flashcards

Abnormal white cell count Flashcards

1
Q

What is meant by pancytopenia

A

All blood cell lineages reduced

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2
Q

What is meant by haemopoiesis

A

Haemopoiesis: production of blood cells in Marrow

Creation of mature blood cells

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3
Q

Describe normal haemopoiesis

A

Normal haemopoiesis (polyclonal healthy/ reactive)
Normal marrow
Reactive marrow - very active bone marrow- in response to infection or inflammation for example.

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4
Q

Describe malignant haemopoiesis

A 
Malignant haemopoiesis (abnormal/clonal)
Leukaemia (lymphoid,myeloid), myelodysplasia, myeloproliferative

Malignant- cancer cells divide from mother cells- same features as mother cells- clonality- fundamental feature of cancer- helps distinguish process from a benign condition

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5
Q

Outline the cell lines that the haemopoietic stem cells can differentiate into

A 
HSCs -- Pre T- T cell
HSC- Pre- B- B cell
HSC- Meg-CFC- Megakaryocyte/platelet
HSC- GM-CFC- Granulocytes and Monocytes
HSC- BFU-E- RBCs

§ HSCs can differentiate into many cell lines.
o BFU-E = Blast Forming Unit Erythrocyte.

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6
Q

What are the granulocytes

A

Granulocytes (neutrophils, basophils and eosinophils)

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7
Q

Describe the key properties of haemopoietic stem cells

A

Capacity for self-renewal

Multi-potent

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8
Q

Which cells come under the myeloid cells

A 
Erythrocytes 
Neutrophils 
Basophils 
Eosinophils 
Monocytes 
Macrophages 
Megakaryocytes 
Dendritic Cells
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9
Q

What is the lymphoid lineage

A

Lymphoid cells are lymphocytes = T cells, B cells and NK cells

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10
Q

What is important to remember about the differentiation and maturation of blood cell lineages

A

Different stages of maturation- normally exclusively seen in the bone marrow
Normal- should only see mature cells in the peripheral blood

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11
Q

Describe two circumstances in which we may see immature cells in the peripheral blood

A

GCSF – growth hormone (daily injection in cancer patients to recover neutrophils after chemotherapy)
Following single injection- will see lots of different myeloid precursors

Sepsis- bone marrow tries to compensate for stressful situation- releases lots of myeloid precursors- typically immature white cells and nucleated red cells- presence together- leucoerythroblastic picture- important to recognise- indicates patient is septic or that the bone marrow is infiltrated by a tumour

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12
Q

Outline the normal steps of differentiation to a mature neutrophil

A

myeloblast > promyelocyte > myelocyte > metamyelocyte (> neutrophil)

First 4 steps occur in the bone marrow
Hence only mature neutrophils should be seen in the peripheral blood.

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13
Q

Describe how the appearance of white cells changes as they develop.

A

They become smaller and their cytoplasm becomes clearer.

Will also develop a multi-lobed nucleus.

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14
Q

Describe the chemicals that influence differentiation and proliferation

A

Cytokines influence differentiation and proliferation

o RBCs – EPO.
o Lymphoid cells – IL-2.
o Myeloid cells – G-CSF, M-CSF.

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15
Q

What can affect these regulating cytokine signals

A

DNA directed differentiation and proliferation
§ DNA damage in cancer can affect these regulating signals and lead to the cancer proliferation.
o Leukaemia – malignant process in primary lymphoid organs.
o Lymphoma/Leukaemia – lymphatic cell tumours in tissue/blood.
o Myeloma – disease of bone marrow.

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16
Q

What can be given to patients with renal impairment to help manage the anaemia

A

Renal impairment- defective EPO- can treat with recombinant EPO- which improves the anaemia

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17
Q

Describe the two main groups of white cells and their overall function

A

White cells consist of two main groups:
Phagocytes; including monocytes and granulocytes, the subtypes of the latter including neutrophils basophils and eosinophils
Immunocytes; which consist of T and B lymphocytes. These cell types will react in response to different stimuli.
Both cell groups are present throughout body tissues and play a central role in the response to infection mediated via phagocytosis and soluble proteins of the immunoglobulin and complement system.

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18
Q

What do cells of the lymphoid lineage differentiate from

A

Lymphoblasts

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19
Q

What do the phagocytic cells differentiate from

A

Myeloid lineages

Myeloblasts
Promyelocytes
Myelocytes
Metamyelocytes

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20
Q

What is the key difference between the lymphoid tissue and peripheral blood

A

Lymphoid tissue vs peripheral blood: only mature cells in blood, mix of immature and mature cells in tissue

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21
Q

Broadly speaking, what two things can result in a leucocytosis

A

Increased white blood cell production

Increased white blood cell survival

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22
Q

Describe how an increased white blood cell production can lead to a leucocytosis

A

Reactive (essentially, a normal physiological response)
Infection (sepsis)
Inflammation

Malignant
Leukaemia
myeloproliferative
Clone of abnormal cells- acquired mutation that allows them to proliferate uncontrollably – malignant

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23
Q

What is the difference in the type of white blood cell seen in the peripheral blood of someone with an infection/inflammation (reactive) and someone with a malignancy (primary)?

A

Reactive – only mature white blood cells (to respond to the infection or inflammation)
Primary – mature AND immature white blood cells present

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24
Q

Describe how increased cell survival can cause a leucocytosis

A

Failure of apoptosis (eg acquired cancer causing mutations in some lymphomas

Mutations in onco-suppressor genes- allows the cells to proliferate uncontrollably

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25
Q

Broadly speaking, what two things can result in a leucoocytopenia

A

Decreased white blood cell production

Decreased White blood cell survival

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26
Q

Describe how a decreased white blood cell production can lead to a leucocytopenia

A 
Impaired BM function
B12 or Folate deficiency
BM failure
Aplastic anaemia
Post chemotherapy
Metastatic cancer
Haematological cancer
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27
Q

Where is B12 of folate deficiency particualry common

A

Vegans

Can generally result in a pancytopenia

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28
Q

Describe how a decreased cell survival can lead to a leukocytopenia

A

Immune breakdown

Auto-antibodies against immune cells- many connective tissue disorders- but also in Autoimmune diseases.

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29
Q

Describe a reactive eosinophilia

A

Inflammation
Infection (usually parasitic- but any infection can increase eosinophil count)
Increased cytokine production (pan-neoplastic effect of some tumours):
-Distant tumour
-Haemopoietic or non haemopoietic

Eosinophils will retain normal morphology
Usually associated with other white cell abnormalities- monocytosis and neutrophilia
Rarely associated with symptoms

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30
Q

Describe pan-neoplasms that can cause a reactive esopinophilia

A

Important to investigate
Isolated tumours and hemopoietic cancers- Hodgking’s lymphoma

Release cytokines which trigger eosinophil production and proliferation.

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31
Q

Describe primary (malignant) eosinophilia

A 
AbnormalHaemopoiesis
(autonomous cell growth)
Cancers of haemopoietic cells
Leukaemia:
-Myeloid or lymphoid
-Chronic or acute

Myeloproliferative disorders

All myeloproliferative disorders- characterised by eosinophilia

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32
Q

Where does the mutation occur in CML and describe the consequences of this mutation

A

Mutation at early stage of haematopoiesis- instead of apoptosis- increased proliferation of cells in granulocytic lineage and platelets and monocytes
Very high white cell count
Blood film- will show every stage of white cell maturation

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33
Q

Summarise the first stages in investigating a leucocytosis

A

History and examination
Haemoglobin and platelet count
Automated differential (% and absolute number of each WC type)
Examine blood film

34
Q

Describe why examination and history are so important

A

History- want to see if patient is symptomatic or not- leucocytosis can sometimes be a incidenta finding- patient asymptomatic- smoking- mild leuckocytosis in general population- common to see reactive lymphocytosis or neutrophilia
Ask for recent travel history- eosinophilia- knowing patient been in African area with G.I symptoms- indicated parasitic infection

On examination- focus on lymphadenothy and hepatosplenomegaly- underying lymho- or myeloprolierative disorder

35
Q

Describe why it is important to look at Hb and platelet counts

A

Look at what happens to Hb and platelets

Isolated neutrophilia less concerning than combination with low Hb and raised white cell count

Mild neutrophilia- which is long-lasting and not associated with symptoms- likely to be reactive

Rarely with a patient with a low Hb, thrombocytopenia and raised WBC count- not something to be worried about- usually typical presentation of leukaemia

36
Q

Describe the importance of the automated differential

A

If you get no differential- machine cannot recognise what the cells are- GCSF injection (myeloid precursors which the machine cannot characterise) or presence of malignant condition
When an elevated WBC is identified it is necessary to first look at the automated differential. Is the leucocytosis due to an elevation of a particular cell type i.e. an increase in one cell type only e.g. a lymphocytosis, a neutrophilia or an eosinophilia, or alternatively an increase in all cell types.

37
Q

Summarise the other key stages in investigating a leucocytosis

A

Abnormality White cells only, or all 3 lineages (red cells/platelets/white cells) ?

White cells 1 cell type only, or all lineages? (e.g. neuts/eos/monocytes/lymphocytes)

Mature cells only or mature and immature cells?

38
Q

Describe the importance of checking whether the abnormality is white blood cells only or all blood cell lineages

A

Can tell you what the disease is caused by

Raised WBC, raised HB and platelet count- myeloproliferative disorder

Malignant- only one type of white cell lineage increased – cancer is a clonal process- mother cell generated lots of daughter cells which are identical to the mother cell
Thus the abnormality of one particular cells

Chronic Lymphocytic Leukaemia - increased number of lymphocytes- but rarely any increase in myeloid cell lines

39
Q

Describe the importance of checking whether the abnormality is in one white cell lineage only or others (myeloid/lymphoid)

A

Reactive- all types involved- one exception- CML- patients can have increase in all white cells- lots of white cells- of all different myeloid precursors- eosinophils, basophils (otherwise rarely seen in blood), to be sure of CML > AML –look for presence of eosinophilia.

Can tell you more about cause (reactive or malignant)

40
Q

Describe the usefulness in checking whether the cells are mature cells only, or a mixture of mature and immature

A

Mature or immature- doens’t do much in distinguishing reactive from malignant- in CLL- all mature cells but malignant but in CML- both mature and immature cells.

41
Q

Describe the potential causes of a leucocytosis where only mature cells are present

A

Lymphocytes
Reactive(viral) or primary
(chronic lymphocytic leukaemia

All lineages
or only one
neuts, eos, baso– reactive/infection

42
Q

Describe the potential causes of a leucocytosis where only immature cells are present

A

Blasts +
low Hb
low platelets
? Acute leukaemia

43
Q

Describe the potential causes of a leucocytosis where a mixture of mature and immature cells are present

A 
Neutrophils+
myelocytes+
basophils
?Chronic myeloid 
leukaemia
44
Q

What are the normal ranges of the different parameters

A 
a. Hb 
120-160 g/L 
b. Platelets 
150-400 x 109/L 
c. WCC 
4-11 x 109/L 
d. Neutrophils 
2.5-7.5 x 109/L 
e. Lymphocytes 
1.5-3.5 x 109/L 
f. Monocytes 
0.2-0.8 x 109/L 
g. Eosinophils 
0.04-0.44 x 109/L 
h. Basophils 
0.01-0.1 x 109/L
45
Q

What can an abnormal WCC be due to

A

§ Abnormal WCC can be caused by:
o Phagocytes – neutrophils, eosinophils and monocytes.
o Immune cells – lymphocytes (infection or CML).

46
Q

Describe the key features of neutrophils

A

Present in BM, blood and tissues
Life span 2-3 days in tissues (hours in PB)
50% circulating neutrophils are marginated (not counted in FBC)

47
Q

What is the difference between the circulating pool and marginated pool of neutrophils

A

Some neutrophils represent circulating pool- but others are margianted (adhere to endothelial cells and migrate into different tissues)
Balance between circulating and marginated pool- can change in minutes- stress- need more neutrophils- marginated pool can be switched into circulating- so neutrophilia can be developed in minutes

48
Q

Outline the time frames in which neutrophilia can develop

A

§ Neutrophilia can develop in:
o Minutes – demargination.
o Hours – early release from BM – i.e. sepsis.
o Days – increased production – i.e. x3 in infection.

49
Q

Describe the features of neutrophils in the peripheral blood when caused by infection

A

Neutrophilia >7.5x109/l
toxic granulation
vacuoles

Infection- abnormal neutrophils- white spots in cytoplasm (vacuoles)- abnormal distribution of granules-

Neutrophils in leukaemia do not have granules and do not look toxic.

50
Q

Describe the features of neutrophils in the peripheral blood when caused by leukaemia

A

Chronic leukaemia
Chronic myeloid leukaemia
Neutrophilia and
Precursor cells (myelocytes

CML- lose different stages of myeloid differentiation
Band cells- neutrophils with non-segmented nuclei.

51
Q

What else would be present in the blood film of someone with leukaemia that would not be present in someone with an infection?

A

Myelocytes and metamyelocytes – these precursors would not be found in the peripheral blood of someone responding to infection

52
Q

What are the different causes of neutrophilia

A

Infection
Tissue inflammation (e.g.colitis, pancreatitis)
Physical stress, adrenaline, corticosteroids
underlying neoplasia

Malignant neutrophilia
myeloproliferative disorders
CML

53
Q

Which infections may result in a neutrophilia

A

Localised and systemic infections

acute bacterial, fungal, certain viral infections

54
Q

Which infections will not produce a neutrophilia

A

Some infections characteristically do not produce a neutrophilia e.g. brucella, typhoid, many viral infections.

55
Q

Describe the causes of a reactive eosinophilia

A

1 Reactive
Parasitic infestation
Allergic diseases e.g. asthma, rheumatoid, polyarteritis,pulmonary eosinophilia.
Neoplasms, esp. Hodgkin’s, T-cell NHL- may make IL-5
Hypereosinophilic syndrome- heart damage- >1.5 – need to treat patients to prevent organ damage- regardless of underlying cause

Drugs also an important cause

 Hodgkin’s disease will show up on x-ray with increased mediastinal mass and there will be increased IL-5 secretion (stimulates reactive).
 You can also get a mutation in GM-CFC.
Malignancy- leucoerythroblastic picture- abnormal granules

56
Q

Describe a cause of a malignant eosinophilia

A

Malignant Chronic Eosinophilic Leukaemia (PDGFR fusion gene)

mutation in alpha or beta gene
very rare

57
Q

Describe monocytosis

A 
Rare but seen in certain chronic infections and primary haematological disorders
TB, brucella, typhoid
Viral; CMV, varicella zoster
Sarcoidosis
Chronic myelomonocytic leukaemia (MDS)
58
Q

Summarise the different causes of neutropholia

A

Bacterial - infection

Auto-immune
Tissue necrosis — inflammation

All types of neoplasia (cells not part of malignant population)

59
Q

Summarise the different causes of an eosinophilia

A

parasitic- infection

Allergic
(asthma, atopy, drug reactions)- inflammation

Hodgkin’s
NHL– neoplasia (cells not part of malignant population)

60
Q

What is an infectious cause of a basophilia

A

Pox virus

61
Q

What is an infectious cause of mono

A

Chronic (TB,

Brucella)

62
Q

Summarise the different causes of lymphocytosis

A

Mature or immature cells
If mature is it :
reactive to infection
primary disorder (CLL)

If immature it is:
primary disorder (leukaemia/lymphoma)
63
Q

Compare different blood films in lymphocytosis

A

 LEFT picture:
o Cells are like each other – oligoclonal expansion.
o Could be CLL (Chronic Lymphocytic Leukaemia) or autoimmune conditions.

 RIGHT picture:
o Immature lymphoblasts are much larger and you can see a nucleolus which shows immaturity.
o This is acute lymphoblastic leukaemia.
nuclei will be pinker

64
Q

When we see mature cells in a lymphocytosis how can we easily distinguish between reactive and primary causes

A

Is it primary or reactive ?
Secondary (reactive); polyclonal response to infection, chronic inflammation, or underlying malignancy.
Primary; monoclonal lymphoid proliferation e.g. CLL

65
Q

What will be seen in mononucleosis syndrome

A

“atypical lymphocyte”

Mononucleosis syndrome

Night time sweating, fatigue

Leukaemia- other lineages affectesd
nucleosis- not much change in other lineages

66
Q

Describe the key features of glandular fever

A

 Shows a reactive-looking lymphocyte that looks like an immature lymphocyte seen in acute lymphoblastic leukaemia BUT these lymphocytes tend to have RBCs clump them and they are jagged and are not self-clumped.
 High WCC with reactive-looking lymphocytes shows glandular fever.

67
Q

Describe the pathogenesis of glandular fever

A

EBV infection of B-lymphocytes via CD21 receptor
Infected B-cell proliferates and expresses EBV associated antigens
Cytotoxic T-lymphocyte response
acute infection resolved resulting in lifelong sub-clinical infection.

Cytokines from t-cells result in symtpoms

68
Q

Describe lymphocytosis in elderly patients

A 
Elderly patients with lymphocytosis
mature lymphocytes (may be smear cells)
differential: reactive to underlying auto immune disorder or chronic lymphocytic leukaemia

How can you distinguish?
Morphology
Immunophenotype
Gene re-arragement

69
Q

Describe how we can evaluate lymphocytosis using (B cell) light chain restriction

A

 Polyclonal expansion – involve more than one mother cell and so the light chains express both kappa and lambda.
o This is indicative of a response to infection.
 Monoclonal expansion – all antibodies are from ONE mother cell and this is indicative of a cancer

70
Q

Describe how we can evaluate lymphocytosis using gene rearrangement

A

Imuunoglobulin genes (Ig) and T cell receptor (TCR) genes undergo recombination in antigen stimulated B cells or T cells.

With primary monoclonal proliferation all daughter cells carry identical configuration of Ig, or TCR gene. This can be detected by Southern Blot analysis

71
Q

What should we do when looking at an abnormal white cell count

A

Look at all aspects of FBC
Look at automated differential
Look at blood film

72
Q

Likely causes of eosinophila in patient with recent travel history

A 
Parasitic infestation (schistosomiasis)
Underlying lymphoma (HL or T NHL)
allergic autoimmune disorder (asthma/urticaria)
73
Q

Describe case 2

A

 Cells are mature – nucleoli cannot be seen.
 Cells are very like each other – monoclonal expansion.
o Could be reactive – viral or TB.
o Primary/monoclonal – CLL.
 Further tests show there is light chain restriction (kappa restriction) so this is most likely CLL.

Lymphoma- need lymph node biopsy- BM and blood normal

Peripheral blood immunophenotype for light chain and ig, TCR type

74
Q

Describe case 3

A

 Cells are immature as they are irregular and have nucleoli.
 Most likely acute lymphoblastic leukaemia.

75
Q

Describe case 4

A

 You can see neutrophils and neutrophil precursors.
 Toxic granules cannot also be seen which should be seen in infection.
 Basophils and myelocytes can also be seen.
 There has been an expansion of the myeloid cells so this is CML.

76
Q

What else can cause an eosinophilia

A

Pulmonary eosinophilia.

Hodgkin’s disease, a cancer of the lymphatic system which may produce a reactive eosinophilia.

77
Q

Describe the response to a pyogenic bacterial infection

A

Increase in cell numbers: Infection by pyogenic bacteria will result in tissue damage and the production and release of a range of inflammatory cytokines. Amongst these may be factors such as granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) that will stimulate granulocyte and monocyte production by the bone marrow. More importantly in the acute response there will be the early release from the BM of less mature cells.

This will result in an increase in the circulating granulocyte count and a left shifted appearance in the peripheral blood.

Chemotaxis: The phagocytes will circulate in the peripheral blood, at the site of infection they will move out of the circulation and into the tissues moving to the site of inflammation in response to chemotactic factors.

Phagocytosis: The neutrophils and monocytes will encounter foreign material that has been opsonised by immunoglobulin or complement. Using their Fc and C3b receptors they are able to recognise and phagocytose the foreign material.

Killing and digestion: Ingested material will be killed within the phagocytic vacuoles by both oxidative and non-oxidative mechanisms.

78
Q

Describe the context of a lymphocytosis

A

When a lymphocytosis is identified in a FBC the blood film must be examined for the presence of:

A typical / reactive lymphocytesseenin mononucleosis syndromes.
Immediate response to acute stress (e.g. heart attack or other severe pain).
Small lymphocytes and smudge cells seen in chronic lymphocytic leukaemia.
Primitive blasts seen in acute lymphoblastic leukaemia.

79
Q

Describe reactive lymphocytosis

A

Infection
EBV, CMV, Toxoplasma
infectious hepatitis, rubella, herpes infections

Autoimmune disorders
neoplasia
sarcoidosis

80
Q

What are the causes of a reactive lymphocytosis

A

Infection
EBV, CMV, Toxoplasma
infectious hepatitis, rubella, herpes infections

Autoimmune disorders
neoplasia
sarcoidosis

Haematology (11 decks)

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