Haemotology- RBC Flashcards
Explain Haemopoiesis, where it happens, from what cell, and the main 2 pathways
making of lymphoid and myeloid stem cells from haemopoietic stem cells (HSC) in bone marrow. HSC can self renew or differentiate.
Explain problems of high haemopoietic drive
- myeloproliferative disorder eg polycythemia= too many RBC, blood thickens and can clot.
- haemolysis
Requirements for erythropoiesis- Erythropoietin, where is it made and how does it work
EPO is a glycoprotein hormone made in the kidneys in response to hypoxia, stimulating RBC production
Requirements for erythropoiesis- Folate, where is it absorbed and when is it needed more average
Folic acid is absorbed in small intestine, large amount needed during pregnancy and sickle cell anaemia
Folate and B12 deficiency, what happens to cells and what problems does this cause
cells become macrocytic, can grow large but can’t divide, common in: megaloblastic anaemia, liver disease and ethanol toxicity.
Requirements for erythropoiesis- Iron, sources of iron, where it’s a absorbed
Fe2+ found in animals, Fe3+ found in non-haem foods and needs ascorbic acid/vitC for absorption. Absorbed in duodenum
Role of hepcidin and mechanism
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
Role of vitB12, where is it absorbed, what does it synthesise
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
Erythrocyte destruction, what happens to haem, globin and iron
Iron returns to bone marrow, haem becomes bilarubin excreted in bile, globin becomes AA
RBC cell membrane, describe shape and structure
biconcave for manoeuvrability, lipid bilayer supported by protein cytoskeleton/transmembrane proteins which maintain shape and elasticity
Disruption of shape of RBC, what 2 problems can change the shape
- disruption of vertical linkages (spectrin)= spherocytosis, cytoplasm squeezes into smaller space, less flexible therefore haemolysis.
- horizontal linkage=hereditary elipocytosis
Nomenclature of RBC, different names for size, shape etc
hypochromia- large central pallor so low Hb conc and flatter
Polychromasia- blue tinge, young RBC, causes macrocytosis
Anisocytes- size
Poikilocytosis- shape
Problematic RBC, what cells are associated with problems and why
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