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Blood > Haem 6 > Flashcards

Haem 6 Flashcards

1
Q

Differentiate normal and malignant haemopoiesis

A

Normal:
Polyclonal healthy/reactive

Malignant
Abnormal/clonal
Leukaemia (lymphoid,myeloid), myelodysplasia , myeloproliferative

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2
Q

Outline precursors to T cell, b cell, RBC, megakaryocyte/platelt, neutrophils, basophils, eosinophils and monocytes

A

Pre T, pre B, BFU-E, Meg-CFC, GM-CFC (granulocytes and monocytes),

  • CFC= colonony forming cells
  • BFU- E = erythroid burst-forming units
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3
Q

How to differntiate myeloblast and lymphoblast

A

Myeloblast small granues, nothing in lymphoblast

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4
Q

Outline the differentiaton of myeloblast into a neutrophil

A

Myeloblast –> promyelocyte –> myelocyte –> metamyelocyte –>band cell –> neutrophil

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5
Q

When would you see any myeloid precurosrs, not just neutrophils

A

In a myeloproliferative disease, e.g. chronic myeloid leukaemia incl. myeloblast

After chemotherapy when G-CSF given to increase formation of new granulocytes so lots of blasts in peripohery)

Sepsis (up to promyelocyte)

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6
Q

How is cell number controlled in productin of erythroid, lymphoid and myeloid cells

A

Haemopoiesis regulated by cytokines, chemokines and hormone…..

(so in infection, cytokines released could message the bone marrow that more neturophils required)

Erythroid- erythropoietin
Lymphoid- IL2
Myeloid- G-CSF and M-CSF (just monocyte)

Influence DIFFERENTIATION and PROLIFERATION

DNA directed differentiation and proliferation

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7
Q

Cell types found in bone marrow

A

Lymphoblasts

Myelpblast,promyeloblast,melocyte, metamyelocyte

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8
Q

How could WBC increase

A

Increase cell production:
Reactive (infection or inflammation)
Malignant (leukaemia or myeloproliferative)

Increase cell survival (failure of apoptosis –> acquired cancer causing mutations in lymphomas)

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9
Q

How could WBC decrease

A

Decreased cell production (impaired BM function, due to b12/folate deficiency OR BM failure- apalstic anaemia, post chemo, metastatic cancer, haematological cancer)

Or

Decreased cell survival (immune breakdown e.g. HIV)

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10
Q

Examples of normal (or reactive) with primary (malignant) haemopoiesis

A

Normal haemopoiesis:

  • Inflammation,
  • infection (parasitic),
  • increased cytokine production from distant tumour, (haemopoietc or non haemopoietic)

Abnormal haemopoiesis:

  • cancer of haemopoietic cells,
  • leukaemia (myeloid/lymphoid, chronic or acute)
  • myeloproliferative disorder
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11
Q

Genetic basis of CML

A

Fusion gene called BCR-ABL due to translocation of chromosome 9 and 22…

DNA damage occurs at early stage of differenation (at GM-CFC) so it leads to proliferation of many myeloid cell types (platelets, all white cells, etc)

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12
Q

How is a raised WCC investigated

CHECK

A 
BASICALLY: 
History and examination
Haemoglobin and platelet count 
Automated differential
Examine blood film

History and examination

Haemoglobin and platelet count (if low, could be because the immature cells produced in acute lymphoid leukaemia, for example, are suppressing platelet and red cell production because there are so many)

Automated differential (machine tells you about each type of blood cell….could be no differential if there are lots of blasts….. there could be lots of blasts because of malignancy OR because patient has been treated with G-CSF following chemotherapy to increase white cell count)

Examine blood film

Abnormality White cells only, or all 3 lineages (red cells/platelets/white cells)…. in malignancy usually only increase in ONE cell lineage, in reactivity increase in all the white cells (apart from CML, which also has all cells prolferating)

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

Mature cells only or mature and immature cells?

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13
Q

Causes of elevated WCC with:

increased by mature cells

increased mature +immature

Immatuure

A

Mature:

  • all lineages or only 1 of neutrophil, eos or baso –> reactive/infection
  • lymphocytes –> reactive (viral) or primary (chronic lymphocytic leukaemia)
Mature and immature: 
Neutrophils+
myelocytes+
basophils
?Chronic myeloid 
leukaemia
Immature: 
Blasts +
low Hb
low platelets
? Acute leukaemia
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14
Q

Neutrophil life span

A

2-3 days

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15
Q

T/F: neutrophils that are marginated are included in FBC

A

False

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16
Q

Cuase of neutrophilia which develops in minutes, hours, and days

A

mins: demargination (i.e. neutrophils stop going into tissues)
hours: early release from BM
days: increased production (X3 in inection)

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17
Q

How do neutrophils change in infection and CML

A

infectin: Neutrophilia >7.5x109/l
toxic granulation
vacuoles

CML: Neutrophilia (mature) and precursor cells (myelocytes), increase in monotcytes too… neutrophils don’t have toxic granules

18
Q

Common causes of neutrophilia

A
  1. Tissue inflammation (e.g.colitis, pancreatitis)
  2. Physical stress, adrenaline, CORTICOSTEROIDS
  3. Underlying neoplasia
    ie. Malignant neutrophilia:
    - myeloproliferative disorders like CML

SIN: Stress, inflammation, neoplasia

19
Q

Cuases of neutrophilia in infection

A

in localised and systemic acute bacterial, fungal, certain viral infections (less so)

20
Q

Which infections will not have neutrophilia

A

brucella, typhoid, many viral infections.

21
Q

Causes of eosinophilia

A
  1. -Reactive (parasitic infection; allergic disease e.g. asthma, rheumatoid, polyartertitis, pulmonary eosinopholia);
    - neoplasms inc. Hodgkin’s or T cell NHL;
    - hypereosinopshilic syndrome

Malignant:
Only one cause involing clonal process= Malignant chrnoic eosinopholic leukaemia (PDGFR fusion gene… fusion between FIP1L1 and PDGFR-a)

22
Q

When is monocytosis seen

A

Chronic infections and primary haematological disorders.

  • TB, brucella, typhoid
  • Viral; CMV, varicella zoster
  • Sarcoidosis
  • Chronic myelomonocytic leukaemia
23
Q

Causes of mature lymphocytosis

A

Mature

  • reactive to infection (EBV, CMV, toxoplasma),
  • autoimmune or inflammatory, sarcoidosis
  • underlying malignancy

primary disorder (CLL)

24
Q

What is 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.

Infectious mononucleosis, atypical cells

25
Q

What is more dangeorus monomorphic or pleomorphic lymphoytosis

A

monomorphic –> malignancy (clonal)

Pleomorphic –> reactive

26
Q

How can you distinguish between polyclonal and monoclonal lymphotcytosis

A

Immunophenotye (the antigens on the b cell surface)… in CLL they are CD5+

27
Q

State the cells in the myeloid lineage

A 
Monocyte 
Erythrocyte 
Dendritic cell 
Megakaryocyte 
Eosinophil 
Basophil 
Neutrophil 
Macrophage
28
Q

How can there be a loss of regulation of haemopoiesis

A

Normally controlled by homones etc and is DNA directed after this.

If DNA mutation at any point during differentiation, cells get survival advantage, stops being regulated by cytokines, replicates uncontrollable –> cancer.

29
Q

Define leukaemia

A

Malignant disease, when bone marrow produce increased number of immature (in the case of proliferative disorders) /abnormal (in the case of dysplastic disorders) leuocytes, leading to suppression of production of other blood cells like erythrocytes, granulocytes and platelets.

Can be myeloid or lymphoid

30
Q

Define lymphoma

A

Lymphoma typically more solid and found in lymph nodes etc

Leukaemia more often resulting in the increase of white cell count in the blood

31
Q

Differentiate reactive increase in whicte cell production vs malignant one with regard to the bone marrow

A

Normal infection (IE. reactive) –> differentiating cells in bone marrow stimulated and mature cells released into ciructilation

Hamatopoietic cancer (i.e. malignant), immature and mature cells released from the bone marrow

32
Q

Difference in white cell count with malignancy and reactive haemopoiesis

A

In maliginacy, usually just one white cell type increased as clonal process, whereas reactive usually all cell types increased (exception is CML, in which all granulocytes increased and monocytes too)

33
Q

Why is it important to see whether the increased WCC has mature white cells only or mature and immature cells

A

Mature and immature –> CML

Immature only- AML

34
Q

When might basophils be increased

A

Pox virus

35
Q

How would CLL vs ALL look on microscope

A

CLL- mature cells…. all have characteristic large nucleus and small cytoplasm as in typical lymphocytes.. all look same. Remember, may also look like this in autoimmune

ALL- much bigger, may contain nucleolus

36
Q

What type of infections could cause reactive lymphocytosis

A

EBV, CMV, toxoplasma

Infectious hep, rubella or herpes

37
Q

How to distinguish cause of lymphocytosis (e.g. is it reactive to underlying autoimmune disorder or CLL?)

A
  • Morphology (i.e. do they all look the same, if so CLL)
  • Immunophenotype (i.e. what surface molecules are they expressing, CLL ar CD5+)
  • Gene re-arrangement (if they are all derived from the same mother cell, they will have same TCR/immunoglobulin gene rearrangement, if they are different they will have different rearragnements…. use southern blot)….

also use light chain (if all they are polyclonal, there will be a mixture of kappa only and lamda only lymphocytes….. in monoclonal, thus CLL, they will all be kappa or all be lamda)

38
Q

What is aplastic anaemia

A

When there is damage to HSC so reduction in all cell types

39
Q

Differentiate myelodysplastic and myeloproliferative disease

A

Myelodysplastic is when cells cannot mature PROPERLY… instead they mature into something weird. Therefore you get a lot of dysfunctional cells. More symptoms arise as the number of dysfunctional cells increases compared to functional. If there is a mutation in these cells which stops them from maturing at all, then they cannot be released from the bone marrow, and it is now called acute myeloid leukaemia. (You would see a mixture of weird and normal cells in the peripheral circulation)

The difference between AML and myelodysplasia is that in AML the cells cannot mature at all (so you get lots of blasts) and in myelodysplasia they mature into something weird.

Myeloproliferative diseases occur when the normal cell type is produced, but just too much of it. So the maturation is normal, but the rate of proliferation is too high. There are 4 types…. 2 of which are chronic myeloid leukaemia and polycythaemia vera. (you would see immature cells in the peripheral circulation because rate of production is so high)

https://www.youtube.com/watch?v=hcuTspQc99s

This is a fantastic vid.

40
Q

What types of phagocyte would respond to the following types of lymphoma:

  1. Responds to all types of lymphoma
  2. Hodkin’s/Non Hodgkin’s
A
  1. neutrophil
  2. eosinophil (particularly hodgkins, and T-cell NHL). NB…. IL5 stimulates the production of eosinophils (can use antibody against this in treatment of these cancers)
41
Q

Causes of immature lymphocytosis

A

ALL

Blood (12 decks)

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