Haemotology- RBC Flashcards

1
Q

Explain Haemopoiesis, where it happens, from what cell, and the main 2 pathways

A

making of lymphoid and myeloid stem cells from haemopoietic stem cells (HSC) in bone marrow. HSC can self renew or differentiate.

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2
Q

Explain problems of high haemopoietic drive

A
  1. myeloproliferative disorder eg polycythemia= too many RBC, blood thickens and can clot.
  2. haemolysis
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3
Q

Requirements for erythropoiesis- Erythropoietin, where is it made and how does it work

A

EPO is a glycoprotein hormone made in the kidneys in response to hypoxia, stimulating RBC production

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4
Q

Requirements for erythropoiesis- Folate, where is it absorbed and when is it needed more average

A

Folic acid is absorbed in small intestine, large amount needed during pregnancy and sickle cell anaemia

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5
Q

Folate and B12 deficiency, what happens to cells and what problems does this cause

A

cells become macrocytic, can grow large but can’t divide, common in: megaloblastic anaemia, liver disease and ethanol toxicity.

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6
Q

Requirements for erythropoiesis- Iron, sources of iron, where it’s a absorbed

A

Fe2+ found in animals, Fe3+ found in non-haem foods and needs ascorbic acid/vitC for absorption. Absorbed in duodenum

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7
Q

Role of hepcidin and mechanism

A

hepcidin controls absorption and release of Iron. Hepcidin binds and degrades ferroportin, so less efflux of iron into blood and is instead stored as ferritin in cells. more eythropoiesis = less hepcidin. Hepcidin made more in inflammatory states = anaemia of chronic disease

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8
Q

Role of vitB12, where is it absorbed, what does it synthesise

A

alongside folate, needed for synthesis of thymine and dttp. 1. in stomach B12 cleaved by HCL and binds with intrinsic factor. 2. B12-IF binds to receptors in ileum. Deficiency caused by veganism, achlorhydria, low IF and coeliac

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9
Q

Erythrocyte destruction, what happens to haem, globin and iron

A

Iron returns to bone marrow, haem becomes bilarubin excreted in bile, globin becomes AA

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10
Q

RBC cell membrane, describe shape and structure

A

biconcave for manoeuvrability, lipid bilayer supported by protein cytoskeleton/transmembrane proteins which maintain shape and elasticity

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11
Q

Disruption of shape of RBC, what 2 problems can change the shape

A
  1. disruption of vertical linkages (spectrin)= spherocytosis, cytoplasm squeezes into smaller space, less flexible therefore haemolysis.
  2. horizontal linkage=hereditary elipocytosis
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12
Q

Nomenclature of RBC, different names for size, shape etc

A

hypochromia- large central pallor so low Hb conc and flatter
Polychromasia- blue tinge, young RBC, causes macrocytosis
Anisocytes- size
Poikilocytosis- shape

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13
Q

Problematic RBC, what cells are associated with problems and why

A

Target cells- more Hb in central pallor due to jaundice or liver disease
Sickle cells- crescent shaped, less soluble in deoxy form
RBC fragments- fragments, platelet rich blood clots, disseminated intravascular coagulation

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