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Medicine - Blood

A mind map about blood in Chapter 3 of Physiology, including blood composition and physical and chemical properties, blood cell physiology, physiological hemostasis, etc.

Edited at 2023-12-07 13:45:42

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Medicine - Blood

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Outline

blood

Blood composition and physical and chemical properties

blood

plasma

Light yellow translucent liquid

Water 91%~92%

small molecule substances

electrolyte

Nutrients

metabolite

hormone

protein

Albumin content is highest

globulin

produced by liver

fibrinogen

blood cells

leukocyte

platelets

red blood cells

Refers to total body blood volume

Physical and chemical properties of blood

blood color

Mainly depends on the amount of hemoglobin in red blood cells

blood relative density

The relative density of normal human blood is 1.050~1.060 The relative density of plasma is 1.025~1.030, depending on the plasma protein content The relative density of red blood cells is 1.090~1.092, depending on the hemoglobin content in red blood cells

blood viscosity

Whole blood 4-5

Plasma 1.6-2.4

plasma osmolality

The ability of solute molecules in a solution to attract and retain water molecules Proportional to the number of solutes and independent of solute type and particle size

Normal plasma osmotic pressure is 300mmol/L

crystal osmotic pressure

The electrolyte production in plasma (Na⁺ and Cl⁺) accounts for more than 99% of the total plasma osmotic pressure. The crystalline osmotic pressure of plasma and tissue fluid is basically the same.

Maintain water balance inside and outside cells and normal cell shape and volume

colloid osmotic pressure

Formed by colloidal substances in plasma (plasma proteins, mainly albumin), albumin has a small molecular weight and a large number of molecules.

Maintain water balance inside and outside blood vessels and normal circulating blood volume

isotonic solution

Solutions whose osmotic pressure is equal to that of plasma, such as 1.9% urea; 2% NaHCO₃; 5% glucose; 0.9% NaCl

Hypotonic solution: red blood cells absorb water and rupture

Hypertonic solution: Red blood cells lose water and shrink

isotonic solution

The osmotic pressure formed by the solutes in the solution that cannot freely pass through the red blood cell membrane is equal to the osmotic pressure within the red blood cells. For example, 0.9% NaCl is an isotonic solution. Although 1.9% urea is isotonic with plasma and is an isotonic solution, it can freely pass through red blood cells and cause hemolysis, so it is not an isotonic solution.

blood pH

7.35~3.45

Plasma pH mainly depends on the ratio of NaHCO₃/H₂CO₃ in plasma

blood cell physiology

Physiological properties of red blood cells

Osmotic fragility

The characteristic of red blood cells swelling and rupturing in hypotonic solutions is called erythrocyte osmotic fragility.

c (NaCl) drops to 0.42%, some red blood cells begin to rupture and hemolysis occurs c (NaCl) drops to 0.35%, and all red blood cells undergo hemolysis

Red blood cells have certain resistance to hypotonic solutions. The resistance to hypotonic solutions decreases and the osmotic fragility of red blood cells increases.

suspension stability

Normally, red blood cells sink slowly, indicating that red blood cells can be suspended in the blood more stably. Biconcave disc-shaped red blood cells have a larger surface area to volume ratio, resulting in greater friction between red blood cells and plasma. Prevent red blood cells from sinking

Erythrocyte sedimentation rate ESR (erythrocyte sedimentation rate): Let the anticoagulated blood sedimentation tube stand still, and the sedimentation rate of the red blood cells is expressed by the distance the red blood cells have sunk at the end of the first hour.

The higher the erythrocyte sedimentation rate, the lower the suspension stability.

The main factors affecting the suspension stability of red blood cells: changes in plasma components. Albumin and lecithin in plasma inhibit concatenation; globulin, fibrinogen, and cholesterol promote concatenation.

Plastic deformability

Normal red blood cells have the ability to deform under the action of external force. After the external force is removed, the deformed red blood cells return to a double-concave disk.

All related to the biconcave disc shape of red blood cells

Erythropoiesis raw materials

Protein and iron are important basic raw materials for the production of hemoglobin Folic acid and vitamin B₁₂ are essential substances for the maturation of red blood cells

The conversion of folic acid requires the participation of vitamin B₁₂, and the absorption of vitamin B₁₂ requires the participation of intrinsic factors produced by gastric mucosal parietal cells. Lack of any one of them can cause megaloblastic anemia.

Regulation of erythropoiesis

Erythropoietin (EPO)

Main factors regulating erythropoiesis

Promote the proliferation and differentiation of late erythroid progenitor cells

Accelerate proliferation of young RBCs

Accelerates the release of reticulocytes from bone marrow

sex hormones

androgens

Indirectly stimulates bone marrow and promotes RBC production

Promote EPO production in the liver (adult men have more red blood cells than adult women)

Estrogen

Small doses reduce the response of red blood cells to EPO; large doses inhibit EPO production

Physiological hemostasis

Physiological hemostatic process

Under normal circumstances, bleeding caused by damage to small blood vessels stops on its own after a period of time, which is called physiological hemostasis.

Damaged blood vessels constrict

Platelets stop thrombus formation

blood clotting

clotting factor

Usually exists as an inactive zymogen

Except for IV, which is Ca²⁺, the other coagulation factors are proteins, and most of them have the function of proteolytic enzymes.

Except for factor III (tissue factor), all other coagulation factors are present in plasma.

The synthesis of factors Ⅱ (prothrombin), Ⅶ (proconvertin), Ⅸ (plasma thrombokinase), and Ⅹ (stuart-power factor) in the liver requires the participation of vitamin K, and is called a vitamin K-dependent coagulation factor.

V (proaccelerin) and VIII (antihemophilic factor) speed up coagulation by 10 million times

blood clotting process

①Prothrombin activator formation

Intrinsic coagulation pathway (all coagulation factors are present in the blood)

When coagulation factor XII (contact factor) comes into contact with the surface of a negatively charged foreign body, it is activated especially under the action of collagen fibers to form ₐ, which can activate prekallikrein into kininase, which in turn activates factor A large amount of ₫ₐ is produced, ₐₐ activates factor ₪ (plasma thromboplastin precursor) to form ₪ₐ, platelets are also activated in large quantities, and platelet phospholipids are released;

Ⅺₐ activates factor IX (plasma thromboplastin) with the participation of Ca²⁺. IXₐ forms a complex with VIII, platelet phospholipid (PL) and Ca²⁺, which cooperatively activates factor The function of ⁺ is to connect ₪ₐ and ₩ to the phospholipid surface. Factor Ⅷ accelerates the activation of factor ₐ by factor ₐₐ 200,000 times.

Lack of factor VIII impairs the intrinsic coagulation pathway, and minor trauma can cause bleeding, which is clinically called hemophilia A. Lack of factor XI, the activation of factor X in the intrinsic coagulation pathway is blocked, and the blood is not easy to coagulate, which is called hemophilia B

Extrinsic coagulation pathway (tissue factor (III) is involved in the coagulation process)

In the case of tissue damage or blood vessel rupture, the coagulation reaction caused by the contact of extravascular coagulation factor III (tissue factor) with blood. Coagulation factor III is a lipoprotein complex that is widely present in extravascular tissues

After trauma and bleeding, factor III enters blood vessels and forms a complex with factor VII (proconvertin) and Ca²⁺ in plasma to activate factor X. ₦ₐ is a protease that hydrolyzes factor X and activates it. Ca²⁺ functions to connect ₦ₐ and

Both the intrinsic coagulation pathway and the extrinsic coagulation pathway ultimately activate factor X and enter the common coagulation process.

②Prothrombin activation

Prothrombin (factor II) is rapidly activated into thrombin under the action of prothrombin activator

Thrombin function: ① Convert fibrinogen into fibrin monomer ② Activate factor XIII (fibrin stabilizing factor) to generate ₩ₐ Provides a phospholipid surface for the coagulation process

③Fibrin formation

Thrombin can rapidly catalyze the conversion of fibrinogen into fibrin monomers

Under the action of Ca²⁺, thrombin activates factor VIII, which converts fibrinogen monomers into solid insoluble fibrin polymers. Fibrin polymers form a network that traps red blood cells and forms a blood clot.

Anticoagulation and fibrinolysis

anticoagulation mechanism of blood

Anticoagulant effect of vascular endothelium: Vascular endothelium has anticoagulant and antiplatelet effects

Physiological anticoagulant substances

Antithrombin III: a protease inhibitor secreted by liver cells and vascular endothelial cells; Combines with thrombin to inactivate factors VII, IX, X, XI, and XII to achieve anticoagulant effect; When combined with heparin, the anticoagulant effect increases 2000 times

Heparin: synthesized by mast cells It has almost no anticoagulant properties. After combining with antithrombin, it increases its affinity with thrombin and enhances antithrombin activity.

Protein C system: Activated protein C inhibits the action of factor Xₐ and promotes fibrinolysis by inactivating Vₐ and VIII

Tissue factor pathway inhibitor: produced by vascular endothelium, directly inhibits the activity of Xₐ, in the presence of Ca²⁺, inactivates factor VIII and tissue factor complex, inhibiting the extrinsic coagulation pathway

fibrinolysis (fibrinolysis)

Prevent thrombosis

plasminogen activation

vasoactivator

tissue activator

coagulation factor XII-dependent activator

Degradation of fibrinolytic proteins

fibrinolysis inhibitor

Under normal circumstances, plasma plasmin does not play a role

Blood types and transfusions

ABO blood group system

Type A has A agglutinogen and anti-B antibodies

Type B has B agglutinogen and anti-A antibodies

Type AB has AB agglutinogen, neither anti-A antibodies nor anti-B antibodies

Type O does not have AB agglutinogen and is anti-A and anti-B

Natural antibodies are IgM antibodies, which have a large molecular weight and cannot pass through the placenta.

Rh blood group system

Those with D agglutinogen on the surface of red blood cells are called Rh positive; those without D agglutinogen are called Rh negative.

No natural antibodies against Rh exist in human serum

Antibodies of the Rh blood group system are mainly IgG, which have a small molecular weight and can pass through the placenta. When an Rh-negative mother gives birth to an Rh-positive fetus for the first time, there are no antibodies in the mother's body. Rh-positive fetal red blood cells enter the mother's body. The mother's body produces antibodies slowly, and neonatal hemolysis does not occur in the first child. If an Rh-negative mother becomes pregnant with an Rh-positive fetus again, the anti-Rh antibodies in the mother will pass through the placenta and enter the fetus, causing hemolysis of the newborn.

crossmatch test

Primary side: Serum coordination test between donor red blood cells and recipient serum

If agglutination reaction occurs on the primary side, the blood is incompatible and blood transfusion cannot be performed; There is no blood on the primary side, but there is on the secondary side. The blood matching is basically consistent, and a small amount of blood is transfused slowly.

Hematocrit: The percentage of blood cells occupied by the volume of blood 40% to 50% for adult men; 37% to 48% for adult women; 55% for newborns