http://faculty.etsu.edu/currie/week8a.htm
This site wasn't so bad for basics, and it has links.
The biggest things to know about RBCs are: live 120 days, stored and clear in spleen, accumulate 2,3 DPG generated by Delhoff-Myer pathway to combat hypoxia by encouraging off-loading O2 from hemoglobin, microcytic anemia is caused by iron deficiency, macrocytic anemia is caused by folate or B12 deficiency (may be due to compromise in intrinsic factor production in stomach or terminal ileum absorption or part of WKS in alcoholics), biconcave disk increases surface area:volume to maximize diffusion capability and also allows easy compression to pass through small capillaries, are caught in fibrin to form clots, killed by bacterial hemolysins, erythropoiesis due to erythropoietin from kidney, which stimulates flat bone (adult) or long bone (infant) stimulation of RBC precursors, proerythroblasts become basophilic erythroblasts that make heterochromatophillic erythroblasts that make orthochromatophillic erythroblasts that lose their nucleus to become RBCs, one of only cell population in body without MHCI, a2b2 hemoglobin subunits as adults, a2y2 as babies, disorders include erythroblastosis fetalis (Rh- mother has consecutive Rh+ babies), conduct strictly anerobic metabolism, glycolysis makes principle nutrient glucose, produces pyruvate and then lactic acid, presence in urine indicates compromised ultrafiltration (unless menstruating), and they turn from blue to red when given oxygen according to Frank Netter.
