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Department of medical physiology3rd week
Semester: winterStudy program: Dental medicineLecture: RNDr. Soňa Grešová, PhD.Department of medical physiologyFaculty of Medicine PJŠU
Department of medical physiology3rd week
1. Platelets – morfology, production, account, function
2. Blood clotting, haemocoagulation factors
3. Group antigens, blood transfusion
1. Prevention of Blood Clotting in the Normal Vascular System—Intravascular Anticoagulants
Endothelial Surface Factors
a) the smoothness of the endothelial cell surface-NO, PGI2 – inactivate receptors of Tr – againts aggregation,
- ADP adenosin diphosphatase – against adherence of Tr
b) glycocalyx- repels clotting factors and platelets, thereby preventing activation of
clotting
c) thrombomodulin which binds thrombin and activates a plasmaprotein, protein C
- anticoagulant by inactivating activated Factors V and VIII.
1. Prevention of Blood Clotting in the Normal Vascular System—Intravascular Anticoagulants
Antithrombin Action of Fibrin and Antithrombin III.• alpha-globulin called antithrombin III or antithrombin-heparin
cofactor
• Heparin combines with antithrombin III, the effectiveness of antithrombin III for removing thrombin increases
- anticoagulant by inactivating activated Thrombin and Factors XII, XI, X
and IX
Activation of Plasminogen to Form Plasmin• injured tissues and vascular endothelium release a powerful
activator called tissue plasminogen activator (t-PA)
1. Platelets – morfology, production, account, function
Platelets or thrombocytes are small colorless, non nucleated cells
Shape is spherical or rod shaped and become oval or disc shaped when inactivated
volume 6-9 fl (10-15 l)
average 2-4 µl
thickness 1µm
Platelets 150-350x109/l (150 000-300 000/mm3)
Lifespan 10 days
TROMBOCYTOSIS intense muscle work, altitude -hypoxia, dehydration, myeloproliferative disorders.
TROMBOCYTOPENIA – insufficient production, overbleeding<20.109l, functionless < 50.109l,
< microthrombocyts
> macrothrombocyts
Cell Lines in Blood Cell Formation (Hematopoiesis)
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.
1. Platelets –structure
Cell Membrane of Platelet
• It is 6 nm thick and contain lipids- phospholipids, cholesterol, glycolipids- Carbohydrates(glycocalyx)
• Glycopropteins -form a receptor for ADP and thrombin - receptors (glykoproteins): GP Ib – adherence;
GP IIb a GP IIIa - aggregation
• Phospholipids - accelerate clotting reactions. - form precursors for thromboxane A2
Cytoplasm • Tubular systemsDense tubular system- it is the main calcium storageOpened tubular system- it is creatived by numeorus invaginations and it is for
releasing of content from granules
• Fibrous structursSubmembrane filaments and mikrotubuls- they maintain the discoid shape and position of organels in
nonactive plateletsCytoplasmatic mikrofilaments- they are responsible for contraction at the releasing
granular content
1. Platelets –structure
Cytoplasm Proteins• The major proteins present are contractile proteins which are responsible for the
contraction of platelets:• Actin• Myosin• Thrombosthenin• Fibrin-stabilizing factor (PF XIII) : clotting factor• Platelet derived growth factor (PDGF) : helps repair damaged vascular walls.
Enzymes• The enzymes present are adenosine triphosphatase and the enzymes necessary
for the synthesis of prostaglandin.
Hormones• Adrenaline vascular and • Serotonin local tissue reactions• Histamine
1. Platelets –structure
Chemical substances: • Calcium ions• Mg- ions. • Adenosine triphosphate (ATP) • Adenosine diphosphate (ADP)
Cytoplasm Granules• α – granula- PF 1 – proaccelerin (f.V)- PF2 – β - thromboglobulin, which supports the transformation of
fibrinogen to fibrin- PF 3 – thromboplastic factor- PF 4 – antiheparine factor- PF 5 – platelet fibrinogen- factor of permeability, which increases permeability of the vessel wall• δ – granula (dense granules)- ADP and ATP- Ca2+ - Serotonine• λ- granula- they are lysosomes and contain the acidic hydrolases, glucuronidese, β-
galactosidase, elastase, colagenese and others
1. Platelets –structure
• PARTIPICIPATION ON HEMOSTATIC PROCESSES
- application of the mechanical and humoral action
• PARTICIPATION ON INFLAMMATORY PROCESSES
- realesing of platelet activating factor (PAF), which is mediator of inflammatory and alergic reactions
- activation of phospholipase A2 and production of the important inflammatory substances (prostaglandins, leucotriens, thromboxan)
1. Platelets –function
2. Blood clotting, haemocoagulationfactors
1. Vessel reactions in the place of damage
2. Platelet activitya) adhesion
b) change of the shape and
releasing reaction
c) aggregation
3. Haemocoagulation
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.
2. Blood clotting, haemocoagulationfactors
1. Vessel reactions in the place of damageVASOCONSTRICTION
REFLEX- it is allowed by the smooth muscle cell contraction as the
direct response of the vessel wall for damage- sympathetic mediates it and duration of this event is
some minutes or hours
HUMORAL- substances producing vasoconstriction are from platelets
mainly serotonine, but also substances as adrenaline, thromboxan A2, fibrinopeptids and fibronektine.
2. Platelet activity
- it consists in contact with collagen fibresthrough specific receptors on the platelet membrane (GP Ib) and with the certain binding places of the collagen molecule
a) adhesion:Negative influence: production of the instable prostacykline (PGI2), which is produced by
endothelial cells of the vessel wall
Positive influence: von Willebrand’s factor, thrombin, ADP
2. Blood clotting, haemocoagulationfactors
b) change of the shape and releasing reaction- platelets acquire the spheric shape- by the mechanism of the active contraction (presence of actin and myosin
in the cytoplasma) pseudopodia subendothelium fibres-bound are produced
SECRETION- ADP – stimulates the platelet aggregation - vonWillebrand’s factor – supports the platelet adhesion - fibronektin – supports the platelet adhesion- serotonin – supports the vasoconstriction- growth factor (PDGF – Platelet-derived Growth Factor) – mitogenic effect- thromboxan A2 – supports the vasoconstriction and platelet aggregation- PAF (Platelet Activating Factor) – activates not only next platelets but also
phagocytes
2. Blood clotting, haemocoagulationfactors
2. Blood clotting, haemocoagulationfactors
c) aggregation
- Primary phase of aggregation – aggregation is in progress after adhesion of the first platelet layer on the vessel wall. This phase is still reversible.
- binding of platelets by fibrinogen through fibrin receptors (GP IIb/IIIa)
COMPLEX of AGGREGATION: secondary phase of aggregation (irreversible).-binding between platelets and fibrinogen is stronger under influence of thrombospondine (protein from α-granules)
3. Haemocoagulation- Haemocoagulation factors
2. Blood clotting, haemocoagulation factors
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.
3. Haemocoagulation
a) Intrinsic pathway b) Extrinsic pathway
2. Blood clotting, haemocoagulationfactors
3. Haemocoagulation – a) Intrinsic pathway
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.
3. Haemocoagulation - Extrinsic pathway
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.
3. Haemocoagulation – Polymerization of fibrinogen
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.
3. Fibrinolysis
https://en.wikipedia.org/wiki/Carboxypeptidase_B2
Bleeding Time
• Duke’s Method
– Make a small incision or finger prick, and dab the end of the finger on a paper every 30 sec. until the bleeding stops.
– Count the number of the blots and divide by 2
– Normal bleeding time is 1 – 6 min.
– Abnormal bleeding time:
• Blood vessel defect, platelet defect, thrombocytopenia
Clotting Time
• To collect blood in a chemically clean glass test tube and then to tip the tube back and forth about every 30 seconds until the blood has clotted. By this method, the normal clotting time is 6 to 10 minutes
3. Group antigens, blood transfusion
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.
3. Group antigens, blood transfusion
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.
Copyright: Kujanik,S., & col. (1998). Practical lesson in physiology. Košice: Medical faculty UPJS.
Heredity of blood groups
Rh Blood Types
• Rh antigens are designated C,D, E, c, d, and e
• Rh positive (D antigen)
• Rh negative (person who does not have type D antigen)
Blood Type PathologyHemolytic Disease of the Newborn (Erythroblastosis Fetalis)
• the mother is Rh negative and the father Rh positive
• The baby has inherited the Rh-positive antigen from the father, and the mother develops anti-Rh agglutinins from exposure to the fetus’s Rh antigen
3. Principles of the blood transfusion
• plasma from donor cannot clott blood cells of recipient – give blood the same group, subgroup and Rh factor
1. Cross-matching2. Biological examination3. In the case negative reaction, the biological
examination repeat still 2x4. After the stopping of transfusion – to monitor
pacient 2-4 hours is needed