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AP0509 Component 2 Exam > Haematopoiesis and Anaemias > Flashcards

Haematopoiesis and Anaemias Flashcards

1
Q

Main function of red blood cells (erythrocytes)

A
  • transports O2 and CO2
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2
Q

Main function of neutrophils

A
  • phagocytose and destroy invading bacteria
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3
Q

Main function of eosinophils

A
  • destroy larger parasites and modulate allergic inflammatory responses
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4
Q

Main function of basophils

A
  • release histamine (and in some species serotonin) in certain immune reactions
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5
Q

Main function of monocytes

A
  • become tissue macrophages, which phagocytose and digest invading microorganisms and foreign bodies
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6
Q

Main function of B cells

A
  • make antibodies
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7
Q

Main function of T cells

A
  • kill virus-infected cells and regulate activities of other leucocytes
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8
Q

Main function of natural killer (NK) cells

A
  • kill virus-infected cells and some tumour cells
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9
Q

Main function of platelets

A
  • initiate blood clotting
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10
Q

Wright’s stain

A
  • Histological stain that differentiates blood cells
  • Eosin bind to basic compounds like proteins in cytoplasm and methylene blue; converting ferric iron in Hb to ferrous iron
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11
Q

Stem Cell Theory of Haematopoiesis

A
  • All cells derived from a pool of stem cells that are self-renewing
  • Pluripotential & multipotential stem cells give rise to committed stem cells for each cell line
  • Committed stem cells have receptors for specific growth factors
  • Respond to stimulation by division & maturation (precursor cell stages) into end-stage cells
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12
Q

Progenitor and precursor cells

A
  • unspecialized or exhibits partial characteristics of specialized cells, but can produce more than one type of specialized cell type
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13
Q

Cell differentiation definitions

A
  • TOTIPOTENT; form all cells including extraembryonic and placental cells
  • PLURIPOTENT; give rise to all cell types
  • MULTIPOTENT; give rise to more than one cell type but limited
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14
Q

What can multipotent stem cell (MSC) differentiate to?

A
  • Colony Forming Unit-Granulocyte, Erythrocyte, Monocyte, Megaokaryocyte (CFU-GEMM); myeloid cell line - late RBC’s, platelets, granulocytes and monocytes
  • Lymphoid stem cell (lymphoid cell line – later lymphocytes and natural killer cells)
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15
Q

Haemopoietic stem cells (HSC)

A
  • HSC are multi-potent stem cells that occur at a

frequency of 1:5000 in bone marrow

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16
Q

Timeline of development of blood cells

A
  • 3 wk : formation of blood islands from yolk sac
  • 6 wk : liver becomes hematopoietic organ
  • 6-8 wk : spleen (until 8th month)
  • ~20wk : bone marrow (life-long)
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17
Q

What is meant by stem cell niche?

A
  • a specific site (microenvironment) in adult tissues where stem cells reside
    and undergo renewal and differentiation
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18
Q

What are the 2 haematopoietic niches in bone marrow?

A
  • Osteoblastic niche at the endosteal surface

- Vascular niche involving sinusoidal blood vessels

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19
Q

What is the osteoblastic niche?

A
  • maintains quiescence and harbours the Long Term-HSC
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20
Q

What is the vascular niche?

A
  • supports proliferation, differentiation and mobilization (transendothelial migration) of Short Term-HSC to blood stream in response to physiological demands and act as back up outside the BM for HSC during times of BM stress
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21
Q

Intrinsic v Extrinsic factors controlling haematopoiesis

A
  • Cell fate determination is governed by interactions between extrinsic and intrinsic factors
  • Soluble growth factors (extrinsic)
  • Transcription factors (intrinsic)
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22
Q

Sequence of erythropoiesis

A
  • proerythroblast
  • basophilic erythroblast
  • polychromatophilic erythroblast
  • orthochromatophilic erythroblast
  • reticulocyte
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23
Q

Proerythroblast

A
  • First cell committed to RBC
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24
Q

Basophilic erythroblast

A
  • nucleus becomes smaller

- cytoplasm becomes more basophilic due to the presence of ribosomes

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25
Q

polychromatophilic erythroblast

A
  • produce more haemoglobin

- cytoplasm starts to take up both basophilic and eosinophilic stains

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26
Q

orthochromatophilic erythroblast

A
  • extrudes nucleus
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27
Q

reticulocyte

A
  • cytoplasm containing reticular networks of polyribosomes

- Enters circulation

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28
Q

transcription factors in erythropoiesis

A
  • regulate stem cell survival (e.g. GATA2) or involved in differentiation (e.g. GATA1 – myeloid differentiation)
  • can interact to reinforce one programme which may suppress that of another lineage and can induce protein synthesis associated with a specific lineage
29
Q

soluble factors in erythropoiesis

A
  • act locally or systemically

- May cause proliferation, stimulate differentiation, maturation, prevent apoptosis and affect function

30
Q

Erythropoietin

A
  • hormone produced in peritubular fibroblast like cells
  • anti-apoptotic
  • levels increase with decrease in Hb
31
Q

Red Blood Cell metabolism

A
  • Red blood cells function without a nucleus and mitochondria
  • Only nucleated RBC; normoblasts (RBC precursor) and megaloblasts which appear in megaloblastic anaemia
  • No nucleus; enhances flexibility, restricts size, increasing O2
    carrying capacity
  • Reduced life span
32
Q

Pentose Phosphate Pathway

A
  • Generates reduced NAD i.e. NADPH
  • NADPH generates reduced glutathione (anti-oxidant)
  • Generation of reduced glutathione stimulates glucose metabolism
  • help prevent oxidative stress
  • to reduce the oxidated form of glutathione
  • keep haemaglobin in ferrous state (Fe2+ allow O2 binding)
33
Q

Methemoglobin reductase pathway

A
  • Maintains iron in Fe2+ state
34
Q

Leubering Rapaport Bypass

A
  • 2,3-DPG regulates O2 carrying capacity and release
35
Q

Lactic acid fermentation

A
  • Produces NAD+ and ATP
36
Q

How do red blood cells make ATP?

A
  • EMBDEN MEYERHOF PATHWAY
  • glycolysis of glucose to pyruvate forming ATP and NADH
  • lactic acid fermentation on pyruvate forming ATP, NAD+, lactate
37
Q

Causes of anaemia

A
  • decrease in production
  • increase in destruction
  • blood loss
38
Q

WHO definition of anaemia

A
  • < 13g/dL (men)
  • <12g/dL (women)
  • <11g/dL if pregnant
39
Q

Classification of anaemias

A
  • by film appearance/morphology

- by cause (underlying morphology)

40
Q

Diagnosis of anaemia

A
  • Physical examination
  • Full blood count
  • Reticulocyte count; decreased in states of decreased production, Increased in destruction of red blood cells
  • Bone marrow biopsy
41
Q

RBC Assessment

A
  • Number – Done by automated counters
  • Size - Large, normal size, or small; all same size versus variable sizes (anisocytosis). Mean volume
  • Shape - Normal biconcave disc, versus spherocytes, versus oddly shaped cells (poikilocytosis)
  • Color - Generally an artifact of size of cell
42
Q

Normocytic anaemia

A
  • Normal size RBC – reduced number
43
Q

Haemolytic anaemia

A
  • RBC destroyed faster than being synthesised
44
Q

Normochromic/normocytic (NN) anaemia classification

A
  • reduction in Hb and RBC counts
  • normal mean corpuscular volume (MCV), mean corpuscular Hb (MCH) and mean corpuscular Hb concentration (MCHC).
  • Due to bleeding from internal or external injury.
  • Due to bone marrow failure.
  • Many haemolytic anaemias.
45
Q

Macrocytic (normochromic) (MN) anaemia classification

A
  • MCV of > 100 fl and a normal MCHC. Cells are much larger but the cellular [Hb] is normal.
  • Megaloblastic anaemias
  • certain haemolytic anaemias.
46
Q

Microcytic (hypochromic) (MH) anaemia classification

A
  • MCV of < 85 fl and an MCHC of < 30 g/dl.
  • Iron deficiency anaemia (most common)
  • Sideroblastic anaemias (impaired haem synthesis)
  • Thalassaemia syndromes (impaired globin synthesis)
47
Q

Red blood cell aplasia

A
  • erythroblasts; reduced or increased
  • Pure RBC aplasia (PRBCA) most common due to reduced erythroblasts
  • Congenital, most common DIAMOND-BLACKFAN ANAEMIA (congenital hypoplastic anaemia), ribosomal protein genes
  • Myelodysplastic syndrome-excessive fibroblast growth
48
Q

Acquired PRBCA

A
  • Causes; Primary or secondary
  • infections; virus e.g. HIV, bacteria e.g. staphylococcal
  • Solid and haematological tumours
  • Autoimmune disease
  • Drugs and chemical
49
Q

Treatments of aplastic anaemia

A
  • transfusions
  • corticosteroids
  • bone marrow transplant
50
Q

Macrocytic (megaloblastic) anaemia

A
  • disorder of DNA synthesis, cells undergo incorrect division
  • B12 and/or folate deficiency
  • dietary or due to malabsorption
  • decrease in Hb, increase in mean corpuscular volume
  • classical anaemia symptoms plus neurological symptoms
  • other rapidly dividing cells (skin GI mucosa, hair follicles etc.) also affected
51
Q

Anaemia of chronic disease

A
  • normochromic/normocytic (i.e normal cells in reduced numbers)
  • mechanism unclear; often seen in malignant disease, chronic inflammation and chronic infection
  • only cured by treating underlying cause
52
Q

Chronic renal failure

A
  • reduced production of erythroid precursors
  • caused by lack of EPO production (by kidneys)
  • normal cells produced but in greatly reduced number
  • normochromic normocytic anaemia
53
Q

Polycythemia vera

A
  • increase in all blood cells
  • causes: unknown mutation in stem cells and JAK2, increased sensitivity to EPO (erythropoietin)
  • symptoms: headaches, dizziness, flushed complexion, increased blood viscosity, number of RBCs increased for no other reason
54
Q

Erythemia

A
  • increase in red blood cells

- phlebotomy is most common treatment

55
Q

Haemolytic anaemia

A
  • results from increased rate of RBC destruction
  • RBC are removed extravascularly by macrophages of reticuloendothelial system in marrow, liver and spleen
  • increased haemolysis: symptoms of anaemia, splenomegaly due to increased workload
56
Q

How doesn’t shortened lifespan always lead to anaemia?

A
  • bone marrow can increase production 6-8 fold
  • maintains normal Hb level
  • marrow will exhibit hyperplasia
  • “compensated haemolytic disease” for haemolytic disorders with reticulocytosis, but no anaemia
57
Q

Classifying haemolytic anaemia

A
  • intrinsic or extrinsic: is problem within RBCs themselves (membrane, enzymes, globin) or outside (physical, chemical, mechanical, drugs)?
  • intravascular or extravascular: site of production - important for diagnosis
  • acquired or inherited
58
Q

Intravascular haemolysis

A
  • RBCs destroyed in circulation
  • released Hb in plasma
  • can be immune mediated e.g. blood group incompatibility
  • iron containing compounds in blood can cause damage
  • Free Hb can bind haptoglobin, can reduce haptoglobin levels
59
Q

Extravascular haemolysis

A
  • premature destruction of RBCs in spleen/bone marrow
  • RBC removed by macrophages
  • Haem breakdown in macrophage generates bilirubin
  • bilirubin released and bound onto albumin to liver for conjugation and excretion in bile
  • rise in unconjugated bilirubin
  • jaundice
60
Q

Evidence of increased haemolysis

A
  • damaged RBCs: destroyed released into plasma, osmotic fragility, sickle cells, red cell fragments
  • biochemical indicators: bilirubin, haptoglobin, breakdown products
  • haemoglobinuria (high Hb in urine) and often linked with haemolytic anaemia
  • increased erythropoiesis: reticulocytosis, erythroid hyperplasia
61
Q

Acquired (extrinsic) anaemia

A
  • immune: autoimmune, HDN, incompatible transfusion, drug induced
  • non-immune: mechanical, chemical, infection, burns, toxins
62
Q

Inherited (intrinsic) anaemia

A
  • membrane defects: e.g. spherocytosis
  • globin defects e.g. sickle
  • enzyme defects e.g. G6PD deficiency
63
Q

RBC Membrane defects in haemolytic anaemia

A
  • hereditary spherocytosis; skeletal membrane and lipid bilayer protein interactions, spherical, loss of flexibility
  • hereditary elliptocytosis; oval and elliptoid, protein deficiency
  • paroxysmal nocturnal haemoglobinuria; mutation in PIG-A, defect in GPI, cells sensitive to complement
64
Q

Hereditary spherocytosis/elliptocytosis

A
  • abnormal membrane construction
  • RBCs are unusual shape and rigid
  • readily removed by spleen
  • morphology: spherocytes/elliptocytes, reticulocytosis, RBCs smaller than usual
  • responds to splenectomy
65
Q

Globin abnormalities e.g. sickle cell

A
  • defective Hb produced: caused by single amino acid substitution on beta-chain of molecule
  • during sickle crises (infection, low O2 tension etc.) Hb becomes rigid: cells distort lifespan 10-12 days
66
Q

Mechanical part of extrinsic haemolytic anaemias

A
  • RBCs damaged/destroyed by mechanical process
  • prosthetic heart valves, laying down of fibrin strands, marching, long-distance running
  • lab findings: film shows fragments
67
Q

Chemical/physical part of extrinsic haemolytic anaemias

A
  • RBCs damaged directly
  • Burns victims: heat over 47oC cremates cells
  • lead poisoning: direct toxic effect on RBCs
  • damaged cells removed by spleen (haemolysis)
68
Q

Immune-mediated haemolysis

A
  • antibodies react with RBCs and cause destruction
  • causes include incompatible blood transfusion, autoantibodies e.g. lupus, drug reactions
  • RBCs May show autoagglutination on film
  • can be extravascular
69
Q

Infection of extrinsic haemolytic anaemias

A
  • RBCs removed as spleen defects intracellular infection e.g. malaria
  • organism conducts life-span within RBC

AP0509 Component 2 Exam (21 decks)

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