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Erythropoiesis {Location, Activation Source)
Occurs in bone marrow
Stimulates by EPO (produced in the kidney)
Life span is 120 days
Stages: stem cell → common myeloid progenitor cells (CMP)→ erythroblasts → reticulocytes

Senescene of RBC {Causes, Markers}
Aging of RBC due to:
Oxidative stress: becomes damage and can no longer synthesize proteins
Deform: has to change shape to enter capillary
Senescene Markers
Flip of surface that expose phosphatidylserine (signal macrophages)
Bind to proteins band 3 that forms clusters and signal for it to be removed
The loss of sialic acid (DON’T EAT ME) signal due to wear and tear
Reticuloendothelial System (RES) / Mononuclear Phagocyte System (MPS)
Breakdown of damaged RBC by macrophages
Occurs in
Spleen: primary site known as RBC graveyard
Liver: via Kupffer cells
Bone marrow
Hemoglobin Breakdown
Globin Chains break down as amino acid and reuse in protein synthesis
Heme groups split into ferric iron and protoporphyrin ring
Fe2+ transports by transferrin to BM to store in ferritin or hemosiderin
Protoporphyrin rings are converted into biliverdin → unconjugated bilirubin → bind with albumin to become conjugated → excrete in bile → intestines
Hepcidin
A hormone produced by liver that regulate metabolism of iron by inhibiting ferroportin
Increased during inflammation, this can leads to anemia
Ferroportin
A protein that export iron to the bloodstream from macrophages (recycled iron) & enterocytes (absorbed dietary iron from intestine)