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Haematology basic science Flashcards

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1
Q

What is the difference between plasma and serum?

A

Plasma: liquid in blood
Serum: plasma without fibrinogens (contains all blood proteins not used in coag. and all electrolytes, abodies, hormones. Includes drugs/microorganisms)

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2
Q

What is haematopoeisis? Where does this take place in: embryo/birth/child/adult?

A

Production of blood cells from relatively small pool of pluripotent stem cells.

Embryo: yolk sac then liver and 3rd-7th month in the spleen

Birth: mostly bone marrow, liver and spleen when needed

Child: no. of active sites in bone marrow decreases but still retains ability for haematopoeisis

Adult: bone marrow of skull/ribs/sternum/pelvis/proximal femur

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3
Q

What is a pluripotent stem cell? what is a ‘blast cell’?

A

they have the ability to form all adult cell types.

Blast cell: nucleated precursor cells

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4
Q 
What is the haemtopoetic tree? 
What is:
Eyrthropoesis
Thrombopoeisis
Lymphopoeisis
Myelopoeisis
Granulopoeisis
A

This is a schematic representation of haematopoeisis showing stem cells to progenitor cells to precursor cells to mature cells then cell death.

Erythropoesis: RBC
Thrombopoeisis: Platelets
Lymphopoeisis: Lymphocytes
Myelopoeisis: granulocytes and monocytes
Granulopoeisis: granulocytes
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5
Q

What 3 things do stem cells have to do to produce blood cells?

A

proliferation
differentiation - commit to lineage and mature (acquire and lose functional properties) before apoptosis
self renew

(they sit at the top of the tree and divider slowly and slef replicate, they occasionally drop down to multipotent progenitors)

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6
Q

describe the granulopoeisis of neutrophils

A

Stem cell to multipotent progenitors to common myeloid progenitor then:

myeloblast (common myeloid progenitor) - promyelocyte - myelocyte - metomyelocyte - band forms - neutrophils

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7
Q

Describe erythropoeisis and where do RBC precursors get their iron from? what is a reticulocyte?

A

Stem cell to multipotent progenitors to common myeloid progenitor then:

pro-normoblast - early normoblast - intermediate normoblast - late normoblast - reticulocyte (polychromasia) - mature RBC (eyrthrocyte)

(bone marrow macrophages give iron to RBC precursors)

Reticulocyte: red cells that have just left the bone marrow and still contain RNA, they stain a deeper red/purple and cause a polychromatic blood film

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8
Q

Describe how platelets are formed?

A

they bud off megakaryocytes and take the cytoplasm with them

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9
Q

What are granulocytes?

A

Cells that contain granules: eosinophils/basophils/neutrophils

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10
Q

Describe the function of neutrophils:
lifespan in circulation
what do they work to do?
What type of infection do they increase in?

A

polymorph cells

  • short life span in circulation then transit to tissues
  • phagocytose: kill with granule contents and then die in the process
  • attract other cells
  • increase in body stress e.g. infection/trauma/infarction
  • increase in bacterial infection
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11
Q

What do eosinophils look like? what is their role?

A

bilobed with bright orange/red granules

-parasitic infection/allergic rxns

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12
Q

what do basophils look like? is their few or many in the circulation? what is their role?

A

Infrequent in circulation - large deep purple granules

-circulating version of tissue mast cell (histamine) which mediates hypersensitivity rxns and Fc receptors bind IgE

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13
Q

What are monocytes? what do they look like? what is their role?

A

circulating version of macrophages

  • large single nucleus with pale blue cytoplasm often vacuolated
  • circulate for one week then enter tissues = macrophages (longer life than neutrophils)
  • attract other cells
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14
Q

What do lymphocytes look like when non-activated vs when activated? what are the three types of lymphocytes and what are their roles?

A

Non-activated: mature cells with small condensed nucleus and rim of cytoplasm

Activated (atypical): large, plentiful blue cytoplasm surrounding neighbouring cells, nucleus more ‘open’ structure

B cells - abody producing (autoimmune and bacterial infections)
T cells - cell mediated immunity/regulatory function/viral infections
NK cells - antiviral cells and tumour

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15
Q

What are the 4 ways of identifying stem cells or early committed precursors of blood cells? how can mature cells be assessed 3?

A

Stem cells:
Immunophenotyping: the expression profile of proteins on the cell surface (using immunofluorescence)
Cytochemistry: biochemistry of cells
Bioassay: culture in-vitro and they will show progeny in different growth conditions
Animal models

Mature cells:

  • FBC
  • morphological assessment
  • immunophenotyping but not usually required.
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16
Q

what are the 4 ways of examining the haematopoeitic system?

A

Peripheral blood: FBC/blood film
Bone marrow: aspiration and biopsy
Specialised tests of bone marrow
look at other sites relevant to blood production e.g. splenomegaly/hepatomegaly

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17
Q

What is the lifespan of:

  • RBC
  • neutrophils
  • platelets
A

RBC: 120 days
Neutrophils: 7-8hours
Platelets: 7-10 days

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18
Q

Bone marrow:
what are the 3 compartments?
what are trabeculae?
what is endosteum, what is special about the blood supply??

A

3 compartments:

  • cellular: haemopoetic stem cells and non-haemopoeitic cells
  • Acellular: connective tissue matrix (collagen and fibronectin)
  • blood supply

Trabeculae are minute projections of bone found throught the metaphysis which causes lots of cells to be close to bone

endosteum in the interface between bone and bone marrow and is covered in bone lining cells (osteoblasts/clasts) and there is a rich supply of arterioles and sinusoids near the endosteum

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19
Q

Blood supply of bone marrow:

  • how is the passage of cells in/out circulation regulated? what is the endothelium like here?
  • is there capillaries?
A
  • Arteries feed into sinusoids which regulate passage of cells in/out circulation (don’t feed into capillaries)
  • The endothelium of sinusoids is fenestrated (holes in actual endothelial cells not gaps between to allow cells in and out)
  • no capillaries
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20
Q 
How are:
-neutrophils
-megakaryocytes
-RBCs 
released from marrow
Study These Flashcards
A

Neutrophils:
-actively migrate towards sinusoids

Megakaryocytes:
-fenestrate endothelial cell with cytoplasmic processes and release platelets directly into circulation

RBCs:
-sinusoidal dilatation and increase the blood flow

21
Q

what is the difference between red and yellow bone marrow?

Study These Flashcards
A

Red: haemopoeitically active (decreases with age)
Yellow: fatty and inactive (increases with age)

22
Q

what is the myeloid:eyrthroid ration referring to? what is this usually?

Study These Flashcards
A

Neutrophils and precursors : nucleated RBC precursors

1.5-3.3 : 1

This can change e.g reverse in haemolysis via compensatory respons

23
Q

what 3 factors regulate haemopoeisis?

Study These Flashcards
A

Complex interplay of ‘random’ events and microenvironmental precursors:

  • activation lineage specific transcription factors
  • chemical influences including cytokines from immediate and distant microenv.
  • location in the marrow itself seems to be important
24
Q

What is a bone marrow niche? give an example

Study These Flashcards
A

certain areas of bone marrow release certain factors to influence the maturity of cells:
-anatomical sites where HSC reside and renew
(HSC outside the niche don’t self renew or differentiate)

e.g. erythroid proliferation occurs around ‘nurse’ macrophages in the form of islands

25
why do RBC's need ATP?
RBC ion balance and cell volume are actively regulated by energy-dependant sodium/potassium pump (Na+/K+ ATPases)
26
How do RBC's synthesise ATP? what does this yield?
Anaerobic glycolysis - because they have no mitochondria | -this yields 4ATP and 2NADH but uses 2ATP so net yield = 2ATP and 2NADH
27
How is iron kept in a Fe2+ (ferrous) state?
NADH from glycolysis helps keep iron in Fe2+ state | -methaemoglobin (HbFe3+) cannot bind O2
28
What is the 'hexose monophosphat shunt'? (AKA pentose phosphate pathway)
This is the pathway by which some glucose is metabolised through in the RBC: - it produces NADPH which is required for maintenance of adequate levels of reduced glutathione - rate limiting enzyme is G6PD
29
Why is glutathione important for RBCs?
Glutathione helps protect against the toxic effects of reactive oxygen species (free radicals) (Reduced) glutathione is essential to detoxify hydrogen peroxide (H2O2), the primary intermediate in oxidative damage In RBCs, lack of reduced glutathione (e.g. as a consequence of glucose 6-phosphate dehydrogenase insufficiency and hence NADPH deficiency) can lead to cell damage (prevents the build up of hydrogen peroxide and minimises oxidative stress) (02 -> 02. -> H202 -> H20)
30
What is an important bi-product of glycolysis in the RBC which releases oxygen from haemoglobin? what happens to the production of this in anaemia or at high altitude?
2,3 bisphosphoglycerate (2,3 BPG) | -in anaemia or at high altitude synthesis of this increases
31
How is the affinity for 2,3BPG different in foetal haemoglobin compared to adult haemoglobin? How does this affect oxygen carrying capacity?
Foetal Hb has a higher affinity for O2 than adult HbF has lower affinity for 2,3, BPG than does HbA This facilitates the transfer of O2 from the mother to the foetus (it holds onto it's oxygen more)
32
What three ways is carbon dioxide transported first to the left side of the heart and then to the lungs?
1: physically dissolved in solution (PCO2) 10% 2: Bound to Hb 30% 3: as bicarbonate ion -HC03 60% (this is facilitated by carbonic anhydrase, a RBC enzyme)
33
Where do B cells and T cells mature? what happens once they have matured?
B cells - bone marrow T cells - thymus They mature and then travel to secondary lymphoid organs: - lymph nodes - spleen - tonsils - epithelio-lymphoid tissues - bone marrow
34
What are the main functions of the spleen?
- filter circulatory fluid - house immune cells - removes fragile RBCs
35
what are the main functions of lymph nodes?
- filter circulatory fluid | - house immune cells
36
In the lymph node where do: -B cells -Plasma cells reside?
B cells - assoc. with follicles and germinal centres, interfollicular Plasma cells - medulla
37
What are the causes for lymphadenopathy?
Local inflammation = local lymphadenopathy - infection - trauma Systemic inflammation = generalised lymphadenopathy - infection - auto-immune Malignancy - haematological/metastases Others: sarcoid/castlemans disease
38
What is lymphangitis?
superficial infection and red lines extend from inflamed region
39
Spleen: what is the difference between the white and red pulp of the spleen? What is the blood supply?
White pulp - lymphocytes (T cells) - periarteriolar lymphoid sheath which is expanded by lymphoid follicles - Ag reaches white pulp, APC's in white pulp present Ag = T cell and B cell response Red pulp - sinusoid and cords - sinusoids have fenestrated endothelium - cords contain macrophages, fibroblasts, cells in transit Blood enters spleen, goes through white pulp and then goes through red pulp where most old/diseased cells are removed Spleen = very vascular and rupture (trauma/diseased spleen) is a surgical emergency -splenic artery and vein
40
What are 5 causes of splenomegaly?
Infection: TB/EBV/Typhoid/Malaria/brucellosis/...others Congestion: portal hypertension/heart failure Inflammatory: SLE/Rheumatoid Storage diseases: Gauchers/niemann picks Haematological disease: myeloproliferative disorders/lymphoma/leukaemia/haemolytic anaemia/ITP (it is a site of extramedullary haematopoeisis in marrow failure)
41
Following splenectomy what infections is the patient susceptable to? How is this prevented?
Infections: - pneumococcus - haemophilus - meningococcus - Capnocytophaga canimorsus Prevention: - vaccination - prophylactic penicillin V
42
Hypersplenism: - clinical features - triad
Clinical features: - dragging sensation in LUQ - Pain if infarction - Discomfort on eating Triad: 1 - splenomegaly 2 - fall in 1+ of components of blood (the spleen traps and stores blood cells) 3 - correction of cytopenia by splenectomy
43
Hyposplenism: causes what is seen on blood film? What is seen clinically?
Causes: - splenectomy most commonly - coeliac (atrophy) - sickle cell - sarcoid - iatrogenic features on blood film mainly from red pulp function: howell-jolly bodies and other RBC abnormalities Clinical features from immunodeficiency
44
What chains make up immunoglobulins? which types of immunoglobulins are monomers/dimers/pentamers?
2 heavy and 2 light chains Monomers: IgD, IgE, IgG Dimers: IgA Pentamer: IgM
45
Describe how B cell development allows many combinations of the gene code for their heavy and light chains to be produced?
1. B-cells are produced and develop in the bone marrow 2. They contain certain genes responsible for coding for heavy and light chains of immunoglobulin, within these genes there is ‘variable’ areas: VDJ - a. Early in development the variable areas in the genes for light and heavy chains gene segments are removed and recombined = VDJ recombination 3. This means that each B-cell produced has a slightly different gene code for the heavy and light chains of the immunoglobulin they can produce 4. If this causes the immunoglobulin to bind to any ‘self’ antigens, these B-cells are removed 5. Then immature B-cells (who haven’t met their antigen) leave the bone marrow ready to meet their target
46
Which type of antibody is made and expressed by B cells?
IgM
47
What happens to the immature B cells once they have left the bone marrow?
1. The immature or ‘naïve’ 1. B-cells travel to the follicle germinal centre of the lymph node 2. They wait to come into contact with their antigen 3. If they do, they identify the antigen and then improve the ‘fit’ of the antibody they produce to the antigen (by somatic mutation) 4. The best ‘fit’ then goes on to differentiate and proliferate as a plasma cell and produce antibody, or a B-memory cell 5. The worse ‘fits’ are deleted.
48
How come the antibodies produced by B-cells in response to antigen is polyclonal?
♦ This natural response to antigen produces polyclonal antibodies. On 1 antigen there will be many ‘epitopes’ or areas that antibody can bind to – so different B-cells will be able to react to different areas of the antigen and this will therefore produce different antibodies. o Each B-cell will produce exactly the same antibody o However lots of B-cells will be activated as they will be complementary to different areas of the antigen o So lots of B-cells will be activated and therefore lots of antibodies will be made. o Different antibodies are from different B-cell lineages
49
What causes a polyclonal increase in immunoglobulins?
ν Infection ν Autoimmune ν Malignancy- reaction of the host to the malignant clone ν Liver disease

Haematology (19 decks)

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