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Year 2 - MCD - Haematology > Abnormal Chite Cell Count > Flashcards

Abnormal Chite Cell Count Flashcards

1
Q

Pancytopenia

A

all lineages reduced

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2
Q

When might myeloid precursors be found in the blood?

A
  • in sepsis

- in patient that are given G-CSF

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3
Q

How is the production of RBCs, lymphoid and myeloid cells controlled?

A

RBC - erythropoietin
lymphoid - IL2
myeloid: G-CSF or M-CSF

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4
Q

Eosinophilia

A
  • very common in general population

-

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5
Q

Normal / reactive eosinophilia

A
  • stimulated by: inflammation, infection (e.g. parasitic), increased cytokine production (distant tumor, paraneoplastic syndrome, haematopoietic to non-haematopoietic)
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6
Q

How does leukaemia usually present with regards to cell amounts?

A
  • leukocytosis

- anemia and thrombopenia

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7
Q

How does leukaemia usually present with regards to cell amounts?

A
  • leukocytosis

- anemia and thrombopenia

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8
Q

Causes of Neutrophilia

A
  • Infection
  • Tissue inflammation (e.g.colitis, pancreatitis)
  • Physical stress, adrenaline, corticosteroids
  • underlying neoplasia
  • Malignant neutrophilia: myeloproliferative disorders or
    CML
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9
Q

Neutrophilia in infections

A
  • Localised and systemic infections
  • acute bacterial, fungal, certain viral infections
  • Some infections characteristically do not produce a neutrophilia e.g. brucella, typhoid, many viral infections
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10
Q

Causes of reactive eosinophilia

A
  • Parasitic infestation
  • Allergic diseases e.g. asthma, rheumatoid, polyarteritis,pulmonary eosinophilia.
  • Neoplasms, esp. Hodgkin’s, T-cell NHL
  • Hypereosinophilic syndrome
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11
Q

Causes of malignant eosinophilia

A
  • Malignant chronic eosinophilic Leukemia (PDGFR fusion gene)
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12
Q

When would a patient present with 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)
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13
Q

Causes of reactive lymphocytosis

A
  • Infection
  • > EBV, CMV, Toxoplasma
  • > infectious hepatitis, rubella, herpes infections
  • smokers can have lymphocytosis
  • Autoimmune disorders
  • neoplasia
  • sarcoidosis
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14
Q

Causes of reactive lymphocytosis

A
  • Infection
  • > EBV, CMV, Toxoplasma
  • > infectious hepatitis, rubella, herpes infections
  • smokers can have lymphocytosis
  • Autoimmune disorders (but might also haven lymphopenia)
  • neoplasia
  • sarcoidosis
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15
Q

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.
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16
Q

Normal haematopoiesis

A

Polyclonal healthy / reactive

  • normal marrow
  • reactive marrow
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17
Q

Malignant haematopoiesis

A

Abnormal / clonal

- leukemia (l/m), myelodysplasia, myeloproliferative

18
Q

Which cells are normally found in the marrow?

A
  • lymphoblasts
  • myeloblasts
  • promyelocytes
  • myelocytes
  • metamyelocytes
19
Q

Which cells are normally found in the peripheral blood?

A
  • T-lymphocytes
  • B- lymphocytes
  • NK-cells
  • Granulocytes (E, B, N)
  • monocytes
20
Q

What mechanisms cause leukocytosis?

A

Increased Cell Production:

  • Reactive (Infection, Inflammation)
  • Malignant (Leukaemia, myeloproliferative)

Increased Cell Survival:
- Failure of apoptosis (eg acquired cancer causing mutations in some lymphomas)

21
Q

What mechanisms cause Leukipenia?

A

Decreased Cell Production:

  • Impaired BM function (B12 or folate deficiency -> sometimes vegans have lower levels of Leuks due to deficiencies)
  • BM failure (aplastic anaemia, post chemotherapy, metastatic cancer, haematological cancer)

Decreased Cell Survival:
- immune breakdown

22
Q

malignant (primary) eosinophilia

A
  • cancers of haematopoietic cells
  • leukemia (m or l, a or c)
  • myeloproliferative disorders)
23
Q

What would you expect the result of a blood film to be in CML?

A
  • very high WBC count

- film would show every stage of white cell maturation

24
Q

How to investigate a raised WCC? (1)

A
  • History and examination
  • Hb and platelet count
  • Automated differential
  • Examine blood film
25
Q

How to investigate a raised WCC? (2)

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?
26
Q

What usually differentiates cancer from a reactive condition?

A
  • Usually: in cancer there will be clones identical to mother cell, abnormality of 1 particular cell type.
    All types suggests a reactive condiiton.
  • also in cancer you would probably have thrombopenia and anaemia / erythropenia
27
Q

Neutrophils - location, lifespan, circulation

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)
28
Q

How fast can neutrophilia develop?

A
  • minutes > demargination
  • hours > early release from BM
  • days > increased production (x3 in infection)
29
Q

What is margination of neutrophils?

A

Margination refers to the prolonged transit of neutrophils through specific organs, which results in discrete intravascular (marginated) pools; these can be found within the spleen, liver, bone marrow and, more controversially, the lung.

30
Q

How can you differentiate between reactive and malignant eosinophilia?

A

reactive: no changes in the eosinophil
malignant: abnormalities in granule distribution, cells look abnormal; also look for the PDGFR mutation

31
Q

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)
32
Q

Lymphocytosis

A

Mature cells:

  • reactive to onfection
  • primary disorder

Immature cells:
- primary disorder (leukemia/lymphoma)

33
Q

How do mature and immature lymphocytes differ in appearance?

A

M: small cell with a high nucleus to cytoplasm ratio, compact and dark chromatin

-> CLL or autoimmune/inflammatory disease

IM: high nucleocytoplasmic ratio but more cytopplasm than mature cells, larger cells, nucleolus in the nucleus -> blasts, immature cells.

-> ALL

34
Q

How to see if lymphocytosis of mature cells is primary or reactive?

A

=> thorough examination of the blood film

  • Secondary (reactive); polyclonal response to infection, chronic inflammation, or underlying malignancy.
  • Primary; monoclonal lymphoid proliferation e.g. CLL
35
Q

When would you expect to see a reactive lymphocytosis?

A

Infection:

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

Autoimmune disorders
neoplasia
sarcoidosis

36
Q

Mononucleosis syndrome

A
  • abnormal lymphocytes
  • Very big lymohocytes with a blastic appearance,
  • Secondary to EBV: other cell linneages are not affected
  • In leukemia you would have anaemia and throbocytopenia
37
Q

What key points would you look at to distinguish causes of lymphocytosis?

A

Morphology
Immunophenotype
Gene re-arragement

38
Q

Light chains in normal conditions and in malignancy?

A

Normal: similar amount of kappa and lambda

Malignant lymohocytosis: the malignant clone will have only one type of light chains.

39
Q

Evaluating lymphocytosis through 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

40
Q

Look at PP and patient cases in presentation slides

A

:)

Year 2 - MCD - Haematology (11 decks)

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