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Haematology > Red blood cells > Flashcards

Red blood cells Flashcards

1
Q

What is Haemopoiesis?

A

The formation of development of blood cells

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2
Q

What two abilities do Haemopoietic stem cells have?

A

Self renewal so the pool is not depleted

Differentiate into mature progeny

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3
Q

What are the sites of haemopoiesis in the fetus?

A

Yolk site - generation of HSC

Liver - HSC expansion

Bone marrow - develops late, main site in adults

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4
Q

How is Haemopoiesis regulated, what can happen if this is disturbed?

A

Number of genes, transcription factors, growth factors and microenvironment. Distruption can disturb balance of proliferation and differentiation which can lead to leukaemia or bone marrow failure.

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5
Q

How do Glycoprotein hormones regulate proliferation and differentiation of HSCs?

A

Act as Haemopoietic growth factors. Bind to cell surface receptors.

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6
Q

Which growth factors control granulocyte and monocyte production?

A

G-CSF (granulocyte-colony stimulating factor)

and G-M CSF (Both granulocyte and monocyte) These can be injected after chemo

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7
Q

What is Thromopoietin?

A

Thrombopoietin is a glycoprotein hormone produced by the liver and kidney which regulates the production of platelets. It stimulates the production and differentiation of megakaryocytes

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8
Q

How is a erythrocyte created?

A

Common myeloid progenitor to proerythroblast to erythroblasts to erythrocyte.

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9
Q

Why may there be red blood cells seen with nuclei?

A

If some have been released prematurely due to large demand

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10
Q

What is Polychromasia?

A

Polychromasia is the presentation of multicolored red blood cells in a blood smear test. It’s an indication of red blood cells being released prematurely from bone marrow during formation.

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11
Q

What is required for erythropoiesis?

A

Iron
Folate
Vitamin B12
Erythropoietin

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12
Q

What is Microcytic Anaemia caused by?

A

Iron Deficiency

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13
Q

What is Macrocytic Anaemia caused by?

A

B12/ folate deficiency

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14
Q

When is Erythropoietin synthesized?

A

It is a glycoprotein growth protein made in the kidney in response to hypoxia - stimulates bone marrow to produce more red blood cells

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15
Q

What two functions does Iron have?

A

Oxygen transport in Haemoglobin

Mitochondrial proteins cofactor. Used in DNA cell cycle and apoptosis

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16
Q

Where is Iron absorbed in the body?

A

Duodenum

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17
Q

Which Iron is derived from animals and most easily absorbed?

A

Ferrous form Fe2+, Haem Iron

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18
Q

Which Iron requires action of reducing substances?

A

Non-Haem Iron, Ferric Fe3+

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19
Q

What is excess iron potentially toxic to?

A

Liver and heart

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20
Q

What happens to Hepcidin levels when Erythrocyte requirement increases?

A

Levels decrease as synthesis is suppressed by erythropoietic activity. Allowing more Fe absorption

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21
Q

What is ferroportin?

A

Ferroportin is a transmembrane protein that transports iron from the inside of a cell to the outside of the cell. Increases Iron absorption.

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22
Q

How is High Storage Iron controlled so Iron isn’t effluxed from enterocyte?

A

Hepcidin synthesis increases and binds to ferroportin, degrading it.
Prevents efflux of Iron and so it is lost alongside the gut being shedded.

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23
Q

What is Anaemia of Chronic disease?

A

Hepcidin production is increases in inflammatory states. reduced irons supply.

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24
Q

What are the 4 DNA precursors?

A

dATP dTTP dCTP dGTP

25
Q

What is dTTP required for? And what does dTTP require for itself?

A

VB12 and folate needed for dTTP synthesis.

dTTP required for Thymidine.

26
Q

What does deficiency of Folate and VB12 do?

A

Leads to macrocytes due to megaloblastic erythropoiesis. Which is a lack of DNA to divide but cell continues to grow.

27
Q

What does B12 bind to in the stomach?

A

Binds to Intrinsic factor (IF)

28
Q

Where is IF made?

A

Intrinsic factor made in the gastric parietal cells.

29
Q

Where does B12-IF bind in the Small Intestine?

A

Binds to receptors in the Ileium.

30
Q

What is Pernicious Anaemia?

A

Inadequate secretion of IF ( Autoimmune disorder )

B12 anaemia

31
Q

When do Folic Acid requirements increase?

A

During pregnancy and Increased red cell production e.g. sickle cell anaemia

32
Q

How are erythrocytes destroyed? Where does the Iron go?

A

Phagocytic cells of the spleen ( macrophages )

Iron returns to bone marrow

33
Q

What is the r.b.c membrane made up of?

A

Lipid bilayer supported by protein cytoskeleton and has transmembrane proteins.

34
Q

What causes Hereditary Spherocytosis?

A

Autosomal Dominant - Disruption of vertical linkages in membrane (ankyrin/spectrin)

35
Q

What are Spherocytes?

A

Spherical cells, regular outline and lack of central pallor.

36
Q

What causes Hereditary Elliptocytosis?

A

Disruption of horizontal linkages in membrane.

37
Q

What are Elliptocytes?

A

Hyperchromic with lack of central pallor

Oval shaped

38
Q

What is the structure of haemoglobin?

A

tetramer : made of 4 subunits

Each subunit made of a globin chain ( 2 alpha 2 beta ) bound to a haem group

39
Q

What does a Haem group consist of?

A

Ferrous Iron ion Fe2+

held in a porphyrin ring

40
Q

How does haemoglobin differ at birth?

A

Fetal Haemoglobin ( Haemoglobin F ) has 2 alpha, and 2 gamma chains. ( Around week 3 Gamma levels go down and Beta increases )

41
Q

Which factors cause left shift on the Oxygen Hb dissociation curve?

A 
Decreased temperature
Decreased 2,3 DPG
Decreased [ H+ ]
CO
HbF

(Gives up O2 less readily, more affinity)

42
Q

What factors cause right shift on the Oxygen Hb dissociation curve?

What is this called?

A 
Increased CO2 levels
Increased [ H+ ]
Increased 2,3 DPG
Increased Temperature
Hb S
Decreased affinity for O2

Bohr’s effect

43
Q

What does G6PD deficiency do to red blood cells?

A

To become vulnerable to oxidant damage. causing intravascular haemolysis - hemolytic anaemia

44
Q

What is 2,3-DPG?

A

Allosteric effector produced by rapaport-Leubering shuttle

Binds to beta-globin chain

45
Q

Genetics behind G6PD deficiency?

A

X linked inheritance. Gene is on X chromosome so affects hemizygous males. Occasionally homozygous females.

46
Q

What are Irregularly contracted cells?

A

Seen in intravascular haemolysis

lack central pallor, and the hemoglobin appears condensed and irregularly distributed in the red blood cell. … They are larger than mature red cells, and are bluish in colour.

47
Q

What are heinz bodies?

A

Denatured Haemoglobin forms round inclusions known as heinz boides. Detectable by tests

48
Q

What may be the causes of of microcytosis?

A

Defect in Haem synthesis
(Iron deficiency, Anemia of Chronic disease)

Defect in globin synthesis (thalassaemia)
Can be defect in the alpha chain synthesis (alpha thalassaema)
or beta chain synthesis (Beta thalassaemia)

49
Q

What types may macrocytes be?

A

Round macrocytes
Oval macrocytes
polychromatic macrocytes

50
Q

What may be some causes of macrocytosis?

A

Lack of V B12 or folic acid - megaloblastic anaemia

Liver disease and ethanol toxicity

Haemolysis- polychromasia

preganancy

51
Q

What is hypochromia? Why does it occur?

A

Cells have larger area. of central pallor - lower Hb content and concentration and flatter cell

often microcytic too
seen in iron defiency and thalassaemia

52
Q

What does it mean for a r.b.c to be polychromatic?

A

Indicates the cell is young.

increased blue tinge to the cytoplasm

larger than normal - polychromasia is one of the causes of macrocytosis

53
Q

What are immature red blood cells called? (can be found in bone marrow and peripheral blood)

why might they have increased levels?

A

Reticulocytes

In response to bleeding or cell destruction, high altitude

normal levels is 0.5-1.5% in blood

54
Q

How to stain for reticulocytes?

A

methylene blue stains RNA content

55
Q

What is Anisocytosis?

A

Red cells showing. more variation in size than is normal.

(e.g. seen in px with Fe deficiency recieving replacement therapy

56
Q

What is Poikilocytosis?

A

Red cells showing. more variation in shape than is normal.

57
Q

What are the characteristics of target cells?

A

Accumulation of Hb in the centre of central pallor

occur in:
obstructive jaundice
liver disease
haemoglobinpathies
hyposplenism
sickle cell
58
Q

Why do Sickle cells become crescent shaped?

A

Polymerisation of Hb S which when deoxygenated is less soluble than Hb A.

Occurs when one or two copies of abnormal Beta globin gene (Beta S) are inherited

Haematology (7 decks)

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