RBCs Flashcards
what are the 3 properties of red blood cells
- unique shape and deformability (membrane)
- allows gas exchange and movement through capillaries
- energy source (enzyme pathway)
- needs energy to keep Hb in reduced state and maintain osmotic equilibrium
- glycolysis
- HMP shunt - Haemoglobin
- gas exchange
what is the clinical implications of the haemoglobin properties of RBCs
- deficiency of iron = reduced production of haem resulting in low Hb (anaemia)
- Impaired production of globin chains results in low Hb (anaemia) = thalassemia
what is the clinical implications of the membrane properties of RBCs
abnormalities of the membrane can result in shortened lifespan of the red cell e.g. hereditary spherocytosis
what is the clinical implications of the enzyme pathway properties of RBCs
inherited defects in enzyme pathways leads to haemolysis (shortened red cell survival) e.g. G6DP enzyme deficiency
describe thalassaemia
Inherited mutation in beta or alpha chain so therefore globin affected and less haemoglobin present
erythroid development
- haemopoietic stem cell
- common myeloid progenitor
- early erythroid progenitor e.g. BFU-E and CFU-Es
- reticulocyte
- have RNA therefore measureable
- erythrocyte (mature RBC)
erythropoietin
regulates erythropoiesis
- is a glycoprotein, produced in the kidneys
- produced in response to low O2
- feedback loop
red cell destruction
- RBCs last 120 days
- cells less deformable, removed in spleen
- breakdown of RBC with release of HB
- globin chain reused
- haem
what is haem broken down to
iron -> transferrin -> bone marrow
protoporphyrin -> bilirubin -> liver -> bile (jaundice)
process of erythropoiesis and changes
takes 7-10 days
- Hb added
- complete loss of nucleus
- reticulocyte is extruded from marrow
- RNA lost => mature RBC
effects of EPO
increased O2 delivery
- increased BFU-E and CFU-E
- increased Hb synthesis
- decreased RBC maturation time
- increased reticulocyte release
factors impairing normal reticulocyte response
- deficiency of iron, B12, folate
- lack of EPO (renal disease)
- ineffective erythropoiesis
e. g. abnormal marrow function, thalassemia - chronic inflammation, malignancy
erythropoiesis during hypoxia
- is promoted by HIF-1 alpha and beta
- up regulates transferrin receptor = more iron into the red cell
- angiogenesis promoted
- glycolytic enzymes up-regulated to provide energy to RBC