Erythrocytes & Hemostasis – Quick Review
Erythropoiesis
- Red blood cells (RBCs) formed in red bone marrow.
- Stimulated by erythropoietin (EPO) released mainly by kidneys in response to blood O_2 levels.
RBC Turnover & Recycling
- Lifespan: 100!–!120 days.
- No protein synthesis → loss of elasticity → cannot self-repair.
- Spleen screens and removes aged, rigid cells; macrophages destroy them.
- Iron & globin recycled; part of heme → bile → feces.
- Key lab indices: RBC count, hematocrit, hemoglobin.
RBC Disorders
- Balance of production vs. destruction critical.
Anemia (deficiency)
- Etiologies
- Blood loss.
- ↓ Production (hypoplastic/aplastic): nutrient lack, ↓EPO (renal failure), marrow damage (mutations, autoimmune, toxins, drugs, radiation, idiopathic).
- ↑ Destruction (hemolytic):
- Inherited: intrinsic RBC defects (e.g., abnormal hemoglobin).
- Acquired: toxins, drugs, autoimmune, infections, overactive spleen, transfusion mismatch.
- Consequences: hypoxemia → weakness, confusion; severe → organ failure, life-threatening.
Polycythemia (excess)
- Primary: polycythemia vera (myeloproliferative cancer).
- Secondary: chronic hypoxia → ↑EPO (smoking, pollution, emphysema, high altitude, intense training).
- Effects: ↑ blood volume/viscosity & BP → thrombosis (MI, stroke, PE); ↑ cardiac workload → heart failure.
Hemostasis
Physiological stoppage of bleeding; three sequential steps.
1. Vasoconstriction
- Immediate smooth-muscle contraction at injury.
- Sustained by humoral vasoconstrictors (e.g., 5-hydroxytryptamine).
2. Temporary Hemostatic (Platelet) Plug
- Platelet adhesion to exposed collagen/endothelium → swell, pseudopodia, degranulation.
- Release ADP & thromboxane A_2 → activate & recruit more platelets → aggregation.
- Platelet Activating Factor (from neutrophils/monocytes) amplifies aggregation.
- Prostacyclin limits plug spread.
- Low-dose aspirin blocks thromboxane A_2 synthesis → inhibits aggregation.
3. Definitive Hemostatic Clot
- Platelet plug triggers intrinsic pathway → prothrombin activator → fibrin formation → stable clot.