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Blood groups and Hemostasis. Dpt. Of Normal, Pathological and Clinical Physiology. Blood groups. blood transfusion often resulted in agglutination and hemolysis , often led to death (renal shock)

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blood groups and hemostasis

Blood groups and Hemostasis

Dpt. Of Normal, Pathological and Clinical Physiology

blood groups
Blood groups
  • blood transfusion often resulted in agglutination and hemolysis, often led to death (renal shock)
  • antibodies in the plasma of one blood react with antigens on the surface of the red cells of another blood
  • more than 30 commonly occurring antigens
  • hundreds of rare antigens
  • two particular groups of antigens: AB0 and Rh systems are immunogenic enough to cause hemagglutination
ab0 system history



actual nomenclature













AB0 system - history
ab0 system
AB0 system
  • four groups: A, B, AB, 0
  • two (3) agglutinogens = antigens on the surface of RBC
  • two agglutinins = antibodies present in the plasma
  • agglutinogens = glycoprotein, oligosaccharides having different carbohydrate at their endings

A – N-acetylgalactosamin

B – galactose

H – fucosotransferasa

ab0 agglutinogens
AB0 agglutinogens
  • determined by two genes, one on each of two paired chromosomes
  • 0 is functionless gene; O = “ohne”
  • A gene determines A group; B gene determines B group
  • codominancy:
  • blood type A: genotype AA, A0
  • blood type B: genotype BB, B0
  • blood type AB: genotype AB
  • blood type 0: genotype 00 (or hh “Bombay” + either AA, AO, BB, BO, or AB)

+ Hh or HH

ab0 agglutinogens6
AB0 agglutinogens
  • antigen H forms the antigen-carrying molecule
  • subtypes of A antigen A1…A6, different immunogenity
  • detectable in 4weeks old embryo
  • during labor, 20-30% of the immunogenity in adult (> 18 years)
ab0 agglutinins
AB0 agglutinins
  • antibodies present in the plasma
  • γ-globulins, IgGand IgM molecules (pentamers, not diffusing trough the placenta)
  • not present immediately after birth
  • produced in 2-8 months after birth by plasma cells (specialized B-cells, stimulated by similar oligosaccharides often expressed in the nature – food, intestinal bacterias)
  • highest titer around at 10 years of age
  • antibodies against the AB0type not present in the blood
  • group A  antibodies anti-B
  • group B  antibodies anti-A
  • group AB  no antibodies
  • group 0  antibodies anti-A and anti-B
frequencies of the different blood types
Frequencies of the different blood types
  • differ according to geographic and time locations
  • group A: Atlantic population and Eskimos (60%)
  • group B: east-south Asia, India (40%)
  • group 0: America'sIndians (100%)
  • the Czech Rep.: A-42 %, 0-32 %, B-18 %, AB-8 %
  • white people: A-47 %, 0-41 %, B-9 %, AB-3 %
  • universal donor, universal acceptor - antigens
  • autotransfusion
rh system ii
Rh system II
  • Landsteiner 1940
  • C, D, E antigens (D is most immunogenic)
  • 85 % white people Rh+, 99 % Asians Rh+, African black 100 % Rh+
  • clinical importance:
      • blood transfusion
      • pregnancy: mother Rh negative and fetus Rh positive, antibodies diffuse trough the placenta (erythroblastosis fetalis, new-born hemolysis, kernicterus, jaundice)

in both cases the exposition to the antigen is needed first (sensitization), because anti-Rh antibodies are NOT normally produced – Rh antigen is not often present in the nature

other systems
Other systems
  • MNSs: very low immunogens, normally no natural antibodies in blood occur, Landsteiner 1927
  • P system: Landsteiner, low immunogens ( 80% people); subtypes
  • Kell, Duffy, Kidd, Lutheran, Diego
  • three mechanisms:
  • vascular spasm
  • formation of a platelet plug
  • blood coagulation
  • neural: nervous reflexes induces by activation of pain fibers, local myogenic spasm
  • humoral: thromboxan A2andserotoninand other substances produced by activated platelets
  • vasoconstriction itself stops the bleeding in vessels as large as a. radialis (under ideal circumstances / i.e. crushed, not cut)
  • lasts for minutes or even hours
  • do not have nuclei, oval discs 2-4 mm, half-life 4-8days
  • megakaryocytes (1000-5000 platelets)
  • 150 – 300.000 per 1 microliter
  • platelets cytoplasm contains:
    • actin and myosin and thrombosthenin (platelet contraction)
    • vesicles containing Ca2+ , serotonin, ADP
    • enzymes that synthesize prostaglandins
    • a-granules: PDGF, coagulating factors, von Willebrandt factor (adhesion)
    • lysozomy
  • platelets membrane contains large amount of phospholipids
platelets function
platelets function
  • adhesion, collagen: vonWillebrandt Factor released from endothel
  • activation: swelling, irregular forms, pseudopods, release of serotonin, vWF, tromboxan A2, ADP  activation of other platletes
  • aggregation: stimulated by trombin, tromboxan A2, vWF, fibrinogen

 platelet plug (loose, then fibrin threads form an unyielding plug)

closing the minute ruptures

(small vessels, many times per day, petechiae)

t h rombopoetin
  • produced bythe liver,little in kidney
  • receptors in plasma membrane of stem cells and megakaryocytes andplatelets (regulation)
  • constant production, regulation by the number of platelets / the more platelets  the more T bound to them  less T act on stem cells and megakaryocytes
  • liver diseases  bleeding (together with lower production of clotting factors)
clotting pathways
clotting pathways
  • the sense is to form fibrinmonomers and then polymers = fibrin fibers (threads) within few seconds (and pesence of Ca2+)
  • fibrin is formed by activated thrombin  all activators of prothrombin are called trombokinases (tissue and plasmatic trk)


extrinsic pathway


clotting factors proenzymes
clotting factors - proenzymes

* vitamin K dependent

clotting pathway common
clotting pathway – common

X Þ Xa: activated either by intrisic or extrinsic pathway

II Þ IIa: protrombin, trombin

XIII Þ XIIIa I Þ Ia:fibrinogenfibrin




clotting pathway – intrinsicsubmucosis, phospholipids released from platelets

XII Þ XIIa: catalyzed by kalikrein a kininogen, activated by negative charges (glass, collagen)

XI Þ XIa: activated by XIIa

IX Þ IXa: activated byXIa

X Þ Xa

1 – 6 minutes



clotting pathway – extrinsictissue, lipoproteins

VII Þ VIIa: activated by tissue factor III(thromboplastin) which is released from damaged tissues

X Þ Xa: activated byVIIa

10 seconds, explosive

(VIIaactivatesIXof intrinsic pathway as well)

anticlotting mechanisms
anticlotting mechanisms
  • endothelial smoothness, glycocalyx (mucopolysaccharide repelling the factors) and thrombomodulin (protein binding thrombin)
  • fibrin itself remove thrombin from the blood
  • catching of activated factors by liver
  • consumption of activated factors
  • antithrombin III: proteases inhibitor, its binding is facilitated by heparin

 no activation of IX, X, XI, XII

  • heparin – polysaccharide released from mast cells and basophils
  • thrombomodulin (endotelial wall) catalyzesactivation of protein C by thrombin
  • activated protein C (APC)
      • inactivates VIII
      • inactivates V
      • activates tissue plasminogen activator (TPA)
  • TPA catalyzesactivation of plasminogen to form plasmin, plasmin causes lysis of the clot
  • alteplase (recombinant), streptokinase, urokinase
  • heparin (+ antithrombin III)
  • citrate, oxalate (bind Ca2+)
  • coumarin, warfarin (inhibition of vitamin K)
excessive bleeding
excessive bleeding
  • failure of blood clotting (coagulopathy)
    • hematoms, joint bleeding
  • platelets failure thrombocytopathy
    • petechiae
  • vessels defects
    • petechiae
innate coagulopathy
innate coagulopathy
  • abnormality or deficiency of one of the clotting factors
  • hemophilia A, classic h.
    • defect of VIII (3 subunits, defect of the clotting factor)
    • transmitted genetically, X chromosome, males
    • hemophilic arthropathy, muscle bleeding in legs
    • 1 z 10000 born males
  • von Willebrandt disease: defect of VIII, all subunits impaired (vW factor, antigen factor and clotting factor)
  • hemophilia B: defect of IX
  • other disorders when impaired factors I, II, V, VII, X, XIII
  • deficiency of XI almost without any clinical signs
acquired coagulopthies
acquired coagulopthies
  • liver diseases (cirrhosis) – deficiency of all factors
  • heparin
  • deficiency of vitamin K
  • DIC
    • sepsis, leukemia, AB0 incompatibility
defects of platelets
defects of platelets
  • trombocytopenia: aplasia (radiation), hypovitaminosis B12, sequestration
  • trombocytopathy: acetylsalicylic acid (inhibition of COX Þ suppresses synthesis of thromboxan A2 and secretion of ADP
defekty c v
Defekty cév
  • von Willebrandtova choroba: defekt endotelu, chybí vWF Þ porucha adheze, nedostatek VIII (vWF je jeho přenašeč)
  • skorbut
  • vrozené defekty pojiva: Rendu-Osler, Henoch-Schönlein