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RBC+erythropoiesis
Organisation of the Body
| Question | Answer |
|---|---|
| Physiological challenges of RBCs | Distribution of oxygen to from lungs to tissues Distribution of CO2 from tissues to lungs Switching mode appropriately Coping with the mammalian tidal lung Coping with the placenta Coping with high cellular turnover |
| Proportions of cells in the blood | Per ul of blood 250000 platelets 7000 white blood cells 5000000 red blood cells 95% of all blood cells are red |
| Haematocrit | Blood mixed with an anticoagulant e.g. heparin Centrifuged so separates based on sedimentation coefficient 50% is rbcs Rest is plasma Thin layer of buffy coat - wbcs |
| Why are red blood cells small and flexible | Average of 7.5 um wide and 2um thick Biconcave disc to increase SA:V Can pass through narrow capillaries - can stick together and deform to reduce blood viscosity and force on membranes No nucleus or large organelles |
| Haemoglobin | 750g per adult 6.5x10^8 molecules per rbc 2x alpha and 2x beta chains Heme prosthetic group containing Fe2+ 2.2g iron per adult (2/3 body iron) |
| Why do rbcs need reducing conditions | Fe2+ must not oxidise to Fe3+ when it binds to oxygen This would form methaemoglobin which is insoluble and cannot bind to oxygen |
| Erythrocyte membrane structure | Spectrin dimers underly the membrane Connected to the membrane by Band 3, Ankyrin and Protein 4.1R Contains enzymes for glycolysis Complexes contain antigens for A/B/O blood types (Duffy antigen) |
| Disadvantages of being anucleate | No further protein synthesis or repair - cells wear out so have a short lifespan of 120 days before being replaced Cells cant change proteins in new conditions - terminally differentiated and highly specialised Similarly true for platelets |
| Erythrocytes lack mitochondria | Very restricted metabolism - rely on substrate level phosphorylation and the pentose shunt Don't consume their oxygen Make enough ATP to pump ions Glycolytic intermediate 2,3-BPG shift O2 dissociation curve from HbO2 |
| Adaptation to oxygen carrying | Fe2+ is an oxygen carrier but must be protected against oxidation Arranged in heme groups to occupy binding sites Made soluble and properties determined by globin chains and their residues 4 proteins used to allow cooperativity Sequestered in rbcs |
| Enucleated erythrocytes | All mammals have enucleated erythrocytes Half the diameter - can move through tiny lung capillaries and maximises SA for exchange Also lightens the cell However, birds etc have large, nucleated oval shaped rbcs |
| Are all mammalian rbcs biconcave | No - camels have oval, enucleated rbcs |
| Faveolar lungs | Gas exchange occurs independently of air pumping Air is pumped by air sacs Gives a constant flow of air As capillaries are not squashed, they have thinner walls and a larger lumen, allowing for larger, nucleated rbcs |
| Superiority of gas exchange | Fish gills - counter current - blood O2 much higher than water Bird lung - cross current - blood O2 slightly higher than air Mammals - pool - blood cannot reach air O2 conc, so less efficient gas exchange |
| Mammalian air-blood barrier | Aerocytes and AT1 cells form the thin lining through which exchange occurs gCap function as stem cells The non-exchange side is thicker to support the alveoli |
| Stages of erythropoiesis | Phase 1 - generation of erythroid committed blast cells - due to EPO and IL3 Phase 2 - division and differentiation of erythroid progenitors Phase 3 - terminal maturation - marked by enucleation of reticulocytes |
| Control of erythropoiesis by Erythropoietin | Hypoxia due to decreased rbcs, low O2 or increased demand for O2 triggers kidney to release EPO This stimulated the red bone marrow to enhance erythropoiesis and increase rbc count This increases O2 carrying capacity of blood |
| How Oxygen inhibits Globin Transcription | Hypoxia inducible factor 1alpha is normally hydroxylated In low O2 this is not hydroxylated It forms dimers with HIF 1beta This acts as a transcription factor triggering EPO release |
| Summary of rbc turnover | Normally 10^6 rbcs produced per second Live for 120 days Phagocytosed by macrophages in liver and spleen Heme group converted to bilirubin and excreted Iron used to produce more Heme |
| What shortens rbc lifespan | Globinopathies Cytoskeletal abnormalities Hyperactive macrophages Auto-antibodies |
| Environmental effects on erythrocytes | Can normally maintain flow of ions in physiological conditions In hypotonic conditions water enters and leads to cell swelling and haemolysis Hypertonic conditions lead to crenation - the cytoskeleton is still present but the membrane collapses |
| Types of anaemia | Normocytic - normal rbc size - due to bleeding, bone marrow disorders etc Macrocytic - large rbcs - due to nutritional deficiency e.g. vitamin B12 or folate Microcytic - small rbcs- low haemocrit due to iron deficiency, high haemocrit due to thalassemia |
| Sickle cell anaemia | Beta globin mutations cause glutamic acid to be replaced by valine Causes aggregation of rbcs in low O2 High in malaria endemic regions as low O2 due to malarial infection leads to early sickling and removal of the infected cell before infection sets in |
| Hereditary spherocytosis | Caused by defects in anchoring of cytoskeleton to membrane Mutations in spectrin, ankyrin, Band 3 Leads to loss of membrane SA - micro spherocytosis Decreased rbc deformity and osmotic fragility Removal of abnormal cells Leads to splenomegaly |
| Potential future sources of rbcs | In vitro erythropoiesis Production of red blood cells from mesodermal cells Hard to achieve due to the complex nature of the process of producing rbcs |
| Viscosity of blood | Increases with decreased velocity Blood flow is slow in small vessels - viscosity can increase 10 times due to adherence of rbcs to each other (form rouleaux) and to vessel walls Shear forces no longer deform rbc - appear rigid |
| What increases the effect of increase in viscosity | If membrane is more rigid e.g. spectrin defect In aged erythrocytes If there are inclusions inside cells e.g. sickled cells |
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