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blood (physiology)
Blood (physiology), blood is composed of 91%-92% water and 8%-9% solute. Normal whole blood: 1.050-1.060. The more red blood cells, the greater the specific gravity; Plasma: 1.025-1.092 The more hemoglobin, the greater the specific gravity. ; Red blood cells: 1.090-1.092 Proportional to hemoglobin.
Edited at 2023-09-27 01:11:38
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blood (physiology)
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- Outline
blood
Overview of blood physiology
blood composition
plasma
Water 91%-92%
Solute 8%-9%
plasma proteins
albumin
produced by liver
globulin
Mainly produced by the liver
α1-globulin
α2-globulin
beta-globulin
Mainly produced by plasma cells
γ-globulin
fibrinogen
Function: Form plasma colloid osmotic pressure, maintain the relatively long half-life of certain hormones in plasma, transport substances, buffer changes in H, participate in blood coagulation, anticoagulation, fibrinolysis, defense and other physiological processes, resist pathogenic microorganisms, nutrition
The difference between serum and plasma is that serum lacks fibrinogen and some consumed coagulation factors.
gas
electrolyte
Na ,K ,Ca etc.
Other organic matter
hormone
metabolic tail products
organic nutrients
blood cells
Red blood cells (about 99% of blood cells)
leukocyte
platelets
Hematocrit: The percentage of blood cells in whole blood
Normal male: 0.4-05 Normal female: 0.37-0.48
Physical and chemical properties of blood
specific gravity of blood
Normal human whole blood: 1.050-1.060. The more red blood cells, the greater the specific gravity. Plasma: 1.025-1.092 The more hemoglobin, the greater the specific gravity Red blood cells: 1.090-1.092 is proportional to hemoglobin
blood viscosity
Derived from friction between molecules or particles within a liquid
Whole blood: 4-5 Plasma: 1.6-2.4
Mainly depends on hematocrit and plasma protein content
plasma osmolarity
Osmosis: the movement of water molecules from a solution of low concentration into a solution of high concentration
Osmotic pressure: The additional pressure exerted above the surface of a solution to prevent osmosis from occurring.
Essence: the ability of solute particles and retaining water molecules in a solution
Depends on the number of solute particles per unit volume of solution
composition
Crystal osmotic pressure: 298.5mOsm/(kg.H2O)
Crystal substances: inorganic salts, glucose, urea, etc., main source: NaCl
Function: Maintain water balance inside and outside cells and maintain the normal shape of red blood cells.
Colloidal osmotic pressure: 1.5mOsm/(kg.H2O
Colloidal substances: plasma proteins, mainly albumin
Function: Maintain water balance inside and outside blood vessels and maintain adequate blood volume in blood vessels
Plasma pH
Normal person: 7.35-7.45
Blood cell physiology (few test points, can be ignored)
Red blood cell physiology
Shape: Nucleusless, double concave disc shape, diameter 7-8um,
Quantity: Most among blood cells
Male: (4.0～5.5)×1012/L Female: (3.5～5.0)×1012/L
Anemia: The number of red blood cells or hemoglobin concentration in the blood is lower than the normal minimum
Physiological properties
Plastic deformability
Definition: Normal red blood cells have the ability to deform under the action of external force, mainly due to their biconcave disc shape.
Meaning: Allows red blood cells to pass through small capillaries
Influencing factors: surface area to volume ratio; viscosity of red blood cell contents; elasticity of red blood cell membranes
suspension stability
Definition: When an erythrocyte sedimentation tube containing anticoagulated blood is placed vertically, the characteristic that red blood cells can be suspended relatively stably in the plasma is called suspension stability.
Erythrocyte sedimentation rate (ESR): The sedimentation speed of red blood cells is usually expressed by the distance that red blood cells sink at the end of the first hour. It is called the erythrocyte sedimentation rate, or erythrocyte sedimentation rate for short. The greater the ESR, the weaker the suspension stability.
Stacking of red blood cells: Multiple red blood cells attach to each other quickly with concave surfaces, forming a "string of money" shape, which can accelerate erythrocyte sedimentation rate
Promote stacking: fibrinogen, globulin, cholesterol, inflammatory factors
Inhibition of concatenation: albumin, lecithin
Osmotic fragility
Definition: The characteristic of red blood cells swelling and rupturing in hypotonic saline solution is called erythrocyte osmotic fragility, or fragility for short. Red blood cells have a certain degree of resistance to hypotonic saline solutions, with low resistance and high osmotic fragility.
Influencing factors: aging RBC> newly mature RBC; hereditary spherocytosis> normal RBC
function of red blood cells
Transporting O2 and CO2: 98.5% of the oxygen in the blood is combined with hemoglobin to form oxyhemoglobin. CO2 in the blood mainly exists in the form of bicarbonate and carbamoyl hemoglobin.
Involved in buffering blood pH and clearance of immune complexes
production of red blood cells
Substances required for the production of red blood cells
Essential raw materials for red blood cell synthesis: iron and protein
Iron deficiency causing iron deficiency anemia (hypochromic microcytic anemia)
Substances required for red blood cell maturation: folic acid and vitamin B12
Folic acid and vitamin B12 deficiencies cause megaloblastic anemia (large cell anemia)
Regulation of erythropoiesis
Main regulator: Erythropoietin
Function: hypoxia → kidney → EPO → bone marrow → stimulate erythroid-committed progenitor cells in the bone marrow to produce red blood cells and enter the blood. Tissue hypoxia is a physiological stimulus that promotes EPO secretion
Renal anemia may occur due to insufficient EPO due to kidney disease
Other regulators
Androgens: increase the concentration of EPO in plasma
Thyroid hormones, adrenocortical hormones, growth hormone, etc. can change tissue requirements for oxygen and indirectly promote red blood cell production.
destruction of red blood cells
The average life span of normal human red blood cells is 120 days
Aged red blood cells have reduced deformability and increased fragility
Extravascular destruction: 90% of senescent red blood cells are phagocytized by macrophages in the spleen, bone marrow, and liver
Intravascular destruction: 10% of senescent red blood cells are damaged by mechanical impact in blood vessels
Hypersplenism can cause hemolytic anemia
White blood cell physiology
Quantity: Different periods and different states vary, mainly 10 to the 9th power
Classification
neutrophils
monocytes
eosinophils
basophils
Lymphocytes
Platelet Physiology
Shape: Platelets are small in size, have no nuclei, are slightly convex on both sides, and have a disc shape with a diameter of 2 to 3 μm.
Quantity: Normal platelet quantity: (100~300)×109/L
Function
(1) Platelets help maintain the integrity of blood vessel walls (2) Platelets are helpful in repairing damaged blood vessels (3) Participate in hemostasis and coagulation
Physiological properties
1. Platelet adhesion: The adhesion between platelets and non-platelet surfaces is called platelet adhesion. vWF is the bridge between platelets adhering to collagen fibers.
2. Platelet release: The phenomenon in which platelets discharge substances stored in dense bodies, α-granules or lysosomes after being stimulated.
Dense bodies: ADP, ATP, 5-hydroxytryptamine (5-HT), Ca2+
α-granules: β-platelet globulin, platelet factor 4, vWF, various coagulation factors (fibrinogen, coagulation factor V), thrombospondin, PDGF, etc.
Platelets can also instantly synthesize and release thromboxane A2 (TXA2). TXA2 has strong platelet aggregation and vasoconstriction effects. Aspirin can inhibit cyclooxygenase and inhibit the synthesis of TXA2.
3. Platelet aggregation: Platelets adhere to each other, and platelets aggregate to form platelet hemostatic plugs.
Participating substances: fibrinogen, Ca2+ and GPⅡ/Ⅲa on platelet membrane
Activators: ADP, epinephrine, 5-hydroxytryptamine, histamine, collagen, thrombin, TXA2, etc.
Inhibitors: prostacyclin (PGI2) and NO
4. Platelet contraction causes blood clots to retract and serum to precipitate
5. Platelet adsorption: The surface of platelets can adsorb a variety of coagulation factors in plasma, and adsorption increases the concentration of local coagulation factors.
Production: Platelets are broken off from mature megakaryocytes in the bone marrow.
Regulation: Thrombopoietin (TPO) is the most important physiological regulator of platelet production. It is mainly produced by the liver and is the cytokine with the strongest effect on stimulating the proliferation and differentiation of megakaryocyte progenitor cells.
Physiological hemostasis
Concept: Under normal circumstances, bleeding caused by damage to small blood vessels will stop on its own within a few minutes.
Bleeding time: reflects the physiological hemostatic function status. For normal people, it should not exceed 9 minutes (template method).
basic process
vasoconstriction
Injury stimulates reflexive contraction of blood vessels Vascular wall injury causes vascular myogenic contraction Platelets and endothelial cells release vasoconstrictor substances 5-HT, TXA2, endothelin, etc.
Platelets stop thrombus formation
Platelets adhere to the damaged site (identification) → release aggregation agents (ADP, TXA2, etc.) → more platelets adhere to each other and aggregate on the collagen exposed under the endothelium → form platelet hemostatic thrombus → preliminary hemostasis (primary hemostasis)
blood clotting
Vascular damage → activation of coagulation system → fibrin formation → blood clot formation → permanent hemostasis (secondary hemostasis)
Concept: The process in which blood changes from a flowing liquid state to an immobile gel state.
Blood coagulation is a complex protein enzymatic process involving coagulation factors. It is an important link in physiological hemostasis.
Essence: The process of changing soluble fibrinogen in the blood into insoluble fibrin
Coagulation factors: Substances in plasma and tissues that directly participate in blood coagulation
(1) Except for FIV, which is Ca2+, the other coagulation factors are proteins. (2) FⅡ, FⅦ, FⅨ, FⅩ, FⅪ, FⅫ, FⅩⅢ and prekallikrein are all serine proteases and exist in the form of zymogens (3) FⅢ, FⅤ, FⅧ and HK (polymer kininogen) are cofactors (4) Except for FIII, other coagulation factors are present in fresh plasma. (5) The production of FⅡ, FⅦ, FⅨ, and FⅩ requires the participation of vitamin K
blood coagulation process
Formation of prothrombinase complex
prothrombinase complex FⅩa generated by the endogenous and extrinsic coagulation pathways can form an FⅩa-FⅤa-Ca2-phospholipid complex with FⅤa on the surface of the phospholipid membrane in the presence of Ca2, that is, the prothrombinase complex. , thereby activating prothrombin
(1) Intrinsic coagulation pathway: The intrinsic coagulation pathway (intrinsic pathway) means that all factors involved in coagulation come from blood, usually due to the interaction between blood and negatively charged foreign body surfaces (such as glass, clay, sulfate, collagen, etc. ) activated by contact Initiation factor: Factor XII Hemophilia: Type A and B (deficiency of VIII and IX respectively)
Extrinsic coagulation pathway: The coagulation process initiated by the exposure of tissue factor (TF) from outside the blood to the blood is called the extrinsic pathway, also known as the tissue factor pathway. pathway) Initiation factor: Factor III
activation of thrombin
thrombin function
Conversion of fibrinogen into fibrin monomer
Activate FⅩⅢ to generate FⅩⅢa. Under the action of Ca2+, FⅩⅢa causes fibrin monomers to polymerize with each other, forming a water-insoluble cross-linked fibrin polymer clot.
Activate FⅤ, FⅧ and FⅪ to form a positive feedback mechanism of the coagulation process
Activate platelets. In unactivated platelets, negatively charged phospholipids (such as phosphatidylserine, etc.) are present on the inner surface of the membrane
Fibrin production
Physiological coagulation mechanism in vivo-extrinsic pathway plays a key role
Factor III is the initiator of physiological coagulation
Factor III is "anchored" to the cell membrane, limiting coagulation to the local area (the site of damaged blood vessels)
The complex of factor III and FVIIa can directly activate FIX and strengthen the intrinsic coagulation pathway.
Negative regulation of blood coagulation
Anticoagulant effect of vascular endothelium
The vascular endothelium is intact, has no activating effect on factor XII and platelets, and the blood coagulation process is not easy to initiate.
Rapid blood flow and dilution make platelets and coagulation factors less likely to aggregate
The anticoagulant system in plasma acts against blood coagulation
①Heparan sulfate proteoglycan (has heparin-like effect); ②Synthesize and secrete tissue factor pathway inhibitor (TFPI) and antithrombin; ③ Thrombin regulatory protein is expressed on the membrane and participates in the inactivation of FVa and FVIIIa through the protein C system.
Synthetic and secreted tissue plasminogen activator (t-PA) promotes fibrinolysis
Fibrin adsorption, blood flow dilution, and monocyte-macrophage phagocytosis
Physiological anticoagulant substances
Serine protease inhibitors: antithrombin (antithrombin III) is the most important, inactivating IIа, Ⅸа, Ⅹа, Ⅺа, Ⅻа
Protein C system: Protein C, thrombin regulatory protein (TM), etc., inactivate Ⅷа and Ⅴа, which can prevent the coagulation process from extending to surrounding normal blood vessels.
Tissue factor pathway inhibitor (TFPI): negative feedback inhibition of the extrinsic coagulation pathway
Heparin: enhances antithrombin activity
Clinical application
(1) Warm saline gauze compression to stop bleeding - promote coagulation (2) Cool down or increase the smoothness of the surface of foreign objects - anticoagulation (3) Remove Ca2 from plasma - anticoagulation (4) Vitamin K antagonists (such as warfarin) (5) Heparin
Dissolution of fibrin
Concept: The process in which thrombus (fibrin) is degraded and liquefied under the action of plasmin, also called fibrinolysis.
The components of the fibrinolytic system: plasminogen (referred to as plasminogen), fibrinolytic enzyme (referred to as plasmin), plasminogen activator and fibrinolysis inhibitor
stage of fibrinolysis
activation of plasminogen
plasminogen activator
Tissue-type activator is synthesized and released by endothelial cells of small blood vessels.
Urokinase-type activator is mainly produced by renal blood vessels and collecting duct epithelial cells
Depends on XII activators such as factor XIIa and kallikrein.
Degradation of fibrin (or fibrinogen)
Product: FDP
fibrinolysis inhibitor
Anti-plasmin, can inactivate plasmin
Plasminogen activator inhibitor, which inhibits the activation of plasminogen
physiological significance
It mainly prevents thrombosis, ensures smooth blood flow, and facilitates the regeneration and repair of damaged tissue.
Blood type and blood transfusion principles
ABO blood type
Blood type: usually refers to the type of specific antigen on the red blood cell membrane
Red blood cell agglutination: If two different types of blood are mixed, red blood cells clump into clusters. (antigen-antibody reaction)
ABO blood type: classified based on whether the red blood cell membrane contains A antigen or B antigen
Rh blood type: classified based on whether the red blood cell membrane contains D antigen
Rh negative: red blood cells do not contain D antigen on their membranes
Rh positive: contains D antigen on the red blood cell membrane
Transfusion reaction: After an Rh-negative person receives Rh-positive blood for the first time, a transfusion reaction generally does not occur, but antibodies against Rh antigens are produced; when Rh-positive blood is transfused again, the transfused red blood cells will be destroyed and hemolysis will occur.
Mother-infant blood group incompatibility: The antibodies of the Rh blood group system are mainly IgG, which have smaller molecules and can pass through the placenta. Therefore, when an Rh-negative mother gives birth to an Rh-positive fetus, the red blood cells or D antigen of the Rh-positive fetus can enter the mother's body during delivery, causing the mother's body to produce anti-D antibodies. If an Rh-positive fetus is conceived again, the anti-D antibodies in the mother can enter the fetus and cause hemolysis of the newborn, and even cause fetal death. If a Rh-negative mother gives birth to her first child, specific anti-D immune globulin is promptly infused to neutralize the D antigen entering the mother's body to avoid sensitization of the Rh-negative mother and prevent neonatal hemolysis in the second pregnancy. .
Blood transfusion principle
blood group identification
Cross-match test: Even if a blood transfusion is performed between people with the same blood type, a cross-match test must be performed before the transfusion. The mixing of the donor's red blood cells and the recipient's serum is called the primary cross-match; the mixing of the recipient's red blood cells and the donor's serum is called the secondary cross-match.
Judgment based on the results of the cross-match blood test: If there is no agglutination reaction on both sides, it means that the blood match is consistent, and blood transfusion can be performed; if the primary side agglutinates, it means that the blood match is incompatible, and blood transfusion is prohibited; if there is no agglutination on the primary side, it is said that the secondary side is agglutinated. If the blood matching is basically consistent, only a small amount of blood can be transfused slowly and the blood should be closely observed for transfusion reactions.