TMU 题-blood
TMU 题-blood
TMU 题-blood
TMU 题-blood
TMU 题-blood
TMU 题-blood
TMU 题-blood
TMU 题-blood
TMU 题-blood
Overview
Coagulation is a cascade of plasma clotting factors (mostly liver-made; II, VII, IX, X are vitamin-K-dependent) needing Ca²⁺ and a platelet phospholipid surface. Two initiating pathways converge on a common pathway.
Intrinsic pathway
Triggered by contact with a damaged (collagen) surface: factor XII → XI → IX → VIII.
Extrinsic pathway
Triggered by tissue factor (III) released from injured tissue + factor VII (faster).
Common pathway
Both routes activate factor X → Xa. Xa converts prothrombin (II) into thrombin (IIa). Thrombin converts fibrinogen (I) into fibrin; factor XIII cross-links the fibrin into a stable clot that traps platelets and cells.
Total
Total plasma osmotic pressure ≈ 313 mOsm and depends on the NUMBER of solute particles, not their nature. It has two components:
Crystalloid osmotic pressure
Generated by electrolytes (mainly NaCl) — small and numerous, so it is the LARGE component (~99%). Because these solutes are kept out of cells by the membrane, crystalloid OP governs water movement across the cell membrane and so maintains cell volume / intra- vs extra-cellular water balance.
Colloid osmotic pressure
Generated by plasma proteins, chiefly albumin — large and few, so it is SMALL (~25 mmHg). Because proteins cannot cross the capillary wall, colloid OP governs water movement across the capillary wall and maintains the plasma vs interstitial fluid balance.
Significance
A fall in colloid OP (low albumin — liver/renal disease, malnutrition) → fluid leaks into the interstitium → oedema.
Morphology
Biconcave, anucleate disc (~7–8 µm), no organelles, packed with haemoglobin; large surface-area:volume ratio favours gas exchange and deformability; lifespan ~120 days.
Plastic deformation
Red cells deform to squeeze through capillaries and splenic sinusoid pores <1 µm.
Osmotic fragility
Sensitivity to osmotic change: in HYPOtonic solution the cell swells and bursts (haemolysis); in HYPERtonic it shrinks (crenation). Normal haemolysis begins at ~0.42–0.45% NaCl and is complete at ~0.30–0.33% NaCl.
Suspension stability (ESR)
Red cells stay evenly suspended in plasma; the ESR measures how fast they settle in 1 h (♂ 0–15, ♀ 0–20 mm/h). Rouleaux formation (↑fibrinogen/globulins) raises the ESR.
Site and stages
Red cells arise in red bone marrow from a pluripotent haematopoietic stem cell → proerythroblast → normoblast → reticulocyte → erythrocyte (fetal sequence: yolk sac → liver/spleen → marrow).
Raw materials and maturation factors
- Iron + protein → build haemoglobin; deficiency → microcytic hypochromic anaemia.
- Vitamin B₁₂ + folic acid → DNA synthesis/nuclear maturation; deficiency → megaloblastic anaemia. B₁₂ absorption needs gastric intrinsic factor.
Regulation
Chiefly by erythropoietin (EPO) from the kidney: low blood O₂ (hypoxia) → ↑EPO → ↑proerythroblast production and faster maturation — a negative-feedback loop. Androgen, thyroid hormone and growth hormone also stimulate it.
ABO antigens and antibodies
- Group A: A antigen on red cells, anti-B in plasma.
- Group B: B antigen, anti-A.
- Group AB: A and B antigens, no antibody — universal recipient.
- Group O: no antigen, both anti-A and anti-B — universal-donor red cell.
Transfusion reaction
If a recipient's antibody meets the matching donor antigen → agglutination and haemolysis of the transfused red cells.
Principles
Give ABO- and Rh-identical blood; always cross-match before transfusion. The Rh(D) system matters because an Rh-negative recipient can be sensitised to form anti-D, important in transfusion and in haemolytic disease of the newborn (prevented by anti-D immunoglobulin).