Wondershare EdrawMind
MindMap Gallery Physiology-blood summary mind map
- 23
- 1
Physiology-blood summary mind map
An article about physiology-blood summary mind map, including the composition of blood Metabolism and characteristics of red blood cells, white blood cells, and plasma, The processes and characteristics of coagulation and hemostasis, etc. Hope this helps!
Edited at 2023-12-01 18:03:56
- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
- Plant asexual reproduction
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
- Reproductive development of animals
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
Physiology-blood summary mind map
- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
- Plant asexual reproduction
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
- Reproductive development of animals
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
- Recommended to you
- Outline
Blood (Part 2)
Physiological hemostasis
definition
Under normal circumstances, bleeding caused by damage to small blood vessels will stop on its own within a few minutes.
Bleeding time and clotting time
出血时间
小针刺破耳垂或指尖,使血液自然流出,再测定出的出血持续时间
反映毛细血管壁和血小板止血功能
凝血时间
指血液离开血管，在体外发生凝固的时间
测定内源性凝血途径中各种凝血因子是否缺乏，功能是否正常，或者是否有抗凝物质增多
process
Damaged small blood vessels constrict
① Injurious stimulation reflexively causes blood vessels to constrict; ②Injury to the blood vessel wall causes local vascular myogenic contraction; ③Platelets adhering to the injured area release vasoconstrictor substances such as 5-HT and TXA₂, causing vasoconstriction
Platelets stop thrombus formation (Primary hemostasis/preliminary hemostasis)
For details, see the physiological characteristics of platelets above.
①After vascular injury, Plt recognizes and adheres to subendothelial collagen ②Plt releases ADP.TXA₂, and Plt irreversibly aggregates and adsorbs ③Platelets stop thrombus formation
blood clotting (Second stage hemostasis/effective hemostasis)
See blood coagulation below for details.
Damage to blood vessels activates the coagulation system, converts fibrinogen in the plasma into insoluble fibrin thrombus, and causes local fibrous tissue proliferation.
Phase 1: Platelet aggregation → loose hemostatic plug Phase II: Fibrin and platelet aggregation → firm hemostatic thrombus
blood clotting
clotting factor
One thousand yuan, two blood clots, three exceptions The fourth is calcium, the fifth is volatile, and the eighth is blood-resistant. Depend on VK: Son’s wife is king 2 7 9 10 Being consumed: Love me all your life 13 2 5 8 Unstable: My dad 5 8
type
Only FIV is not a protein, but a calcium ion
FVI is activated factor V, which is factor Va
Except for factor IV, none are normally active
FII, VII, IX and
Existence part
Only FIII is not in plasma, but in tissues
synthetic parts
FⅢ.Ⅳ.Ⅴ is not synthesized in liver cells
ⅢSynthesized in vascular endothelial cells IV is calcium ion and does not need to be synthesized Ⅴ is synthesized in vascular endothelial cells and platelets
All other factors can be synthesized in the liver, among which FⅡ.Ⅶ.Ⅸ.Ⅹ is synthesized with the participation of vitamin K, also known as vitamin K-dependent coagulation factors.
People with liver dysfunction are prone to bleeding
effect
FⅡ.Ⅳ.Ⅶ.Ⅸ.Ⅹ.Ⅺ.Ⅻ and prekallikrein are both serine proteases
Hydrolyze specific peptide chains → activate them
FⅢ.Ⅳ.Ⅴ.Ⅷ and high molecular kininogen are cofactors
Accelerate the catalytic efficiency of serine proteases
Most unstable
FⅤ,Ⅷ(most unstable)
It is consumed
FⅡ.Ⅴ.Ⅷ.ⅩⅢ
coagulation pathway
initiation factor
Exogenous: FIII
Endogenous: FⅫ
Endogenous specific
FⅧ.Ⅸ.Ⅻ.Ⅺ
common intersection
FⅩ
coagulation process
prothrombinase complex/ Thromboplastin formation
Activate F10
endogenous coagulation pathway
F10 is gradually activated by coagulation factors in the plasma
F12 foreign matter→F12a
Precleavage Kallikrein PK, PK→kallikrein KK
KK positive feedback activates F12 and generates F12a
F12a activates F11,F11→F11a
In the presence of Ca²⁺, F11a activates F9
F9→F9a
F9a F8a Phospholipid Ca²⁺ forms F10 enzyme complex (intrinsic pathway factor X enzyme complex)
F9a is not only the receptor of F10, it has an activating effect on F10 (F8a can accelerate the reaction as a cofactor), and it can also activate F7 through positive feedback.
Activate F10,F10→F10a
exogenous coagulation pathway
Relying on F3 released from extravascular tissues to participate in the activation of F10
F3/tissue factor TF is both a receptor for F7 and a cofactor that promotes activation of F10a by F7a.
A small amount of F7 in the body is in an activated state (F7a), and F7a can activate F7, forming a positive feedback
F3 F7a Ca²⁺ forms the F7a-tissue factor complex (Extrinsic Pathway Factor X Enzyme Complex))
Activate F9
F9→F9a
Activate F10
F10→F10a
The role of F10a
F7 can also form a complex and activate F10, but the effect is poor
F10a F5 phospholipid Ca²⁺ forms F5a-F10a-Ca²⁺-phospholipid complex (prothrombinase complex)
F5a is a cofactor of F10a
I take calcium tablets
Activate prothrombin, F2→F2a
F10a can activate F7→F7a, forming positive feedback
Thrombin F2a generation
Activate F13,F13→F13a
Positive feedback
Activate F2 (function > thromboplastin)
Activate F5.8.11 to promote positive feedback
Activate platelets, increase phospholipids, and promote the synthesis of prothrombin enzyme complex
Directly or indirectly activates the protein C system
It can directly or indirectly inactivate F5a.F8a, thereby restricting the coagulation process and limiting the coagulation process to the injured site.
Activate F1
fibrin production
Fibrin monomer formation
Under the action of thrombin F2a, fibrinogen F1 loses peptide segment A.B and forms fibrin monomer F1a.
Polymerization of fibrin monomers
Peptide segments A and B are released, exposing the complementary region, and the monomers polymerize from here.
Fibrin cross-linking
Under the action of F13a and calcium ions, polymerized fibrin Become a stable cross-linked fibrin polymer
serum
1 to 2 hours after blood coagulation, the platelets in the blood clot are activated, causing the blood clot to retract, releasing a light yellow liquid called serum.
Some coagulation factors are consumed during the coagulation process, so the difference between serum and plasma is that the former lacks fibrinogen and coagulation factors such as F2, F5, F8, and F13, but also adds a small amount of substances released by platelets during the coagulation process.
examine
APTT/CT
definition
Add activated partial thromboplastin/clotting time reagent to the test plasma and Ca2, the time required for plasma coagulation
significance
intrinsic coagulation system screening test
normal value
35～45s
Difference＞10s
extend
Deficiency of intrinsic pathway-related coagulation factors
Lack of F12, 8, 9
Fibrin activation pathway related factor deficiency
F10, 5, 2, 1 lacking
Fibrinolytic hyperactivity
shorten
hypercoagulable state
PT
definition
Ca2 and tissue factor/tissue thromboplastin are added to the tested plasma, and the time for plasma coagulation
significance
extrinsic coagulation system screening test
normal value
12±1s
Difference>3s
extend
Extrinsic pathway-related coagulation factor deficiency
Lack of F3 and 7
Fibrin activation pathway related factor deficiency
F10, 5, 2, 1 lacking
Fibrinolytic hyperactivity
shorten
hypercoagulable state
TT
definition
The time required for fibrin filaments to begin to appear when thrombin solution is added to the tested plasma
significance
fibrinogen screening test
normal
16-18s
Difference>3s
extend
F1 lacks
Fibrinolytic hyperactivity
Related diseases
Thrombocytopenia
Reduction in quantity (mostly caused by immune factors, drugs, etc.)
hereditary platelet disorders
Platelets cannot stick to each other to form clots
hemophilia
Lack of vWF → Platelets cannot adhere to injured vessel walls → Von Willebrand disease
Lack of F8/9a/F11a→Hemophilia A/B/C
disseminated intravascular coagulation
Due to excessive coagulation, coagulation factors are consumed in large amounts
Regulation of coagulation
Anticoagulant effect of vascular endothelium
Prevent the spread of blood coagulation reaction
barrier effect
Normal vascular endothelium serves as a barrier to prevent coagulation factors and platelets from coming into contact with subendothelial components, thus preventing activation of the coagulation system and platelet activation.
anticoagulant effect
Physiological anticoagulants such as heparan sulfate proteoglycan, thromboplastin-secreting tissue factor pathway inhibitor TFPI, and antithrombin exist on the vascular endothelium.
Inhibits Plt aggregation
Vascular endothelium can release prostacyclin PGI2 and NO can inhibit Plt aggregation
Promote fibrinolysis
Vascular endothelial cells can secrete tissue plasminogen activator (t-PA) to promote fibrinolysis and ensure smooth blood vessels.
Fibrin adsorption, blood flow dilution and phagocytosis by mononuclear phagocytes
Adsorption
90% of the thrombin formed during the coagulation process can be adsorbed by fibrin, which not only helps to accelerate the local coagulation reaction, but also prevents thrombin from spreading to the surroundings.
dilution
Activated coagulation factors that enter the circulation and can be diluted by blood
Devour
Activated coagulation factors can be inactivated by anticoagulant substances in plasma and phagocytosed by monocytes and macrophages.
Physiological anticoagulant substances
serine protease inhibitor
include
Antithrombin, heparin cofactor I, C1 inhibitor, α1 antitrypsin, α2-antiplasmin, α3-macroglobulin
antithrombin
来自
由肝细胞和血管内皮细胞分泌
作用
是最重要的抑制物
能与内源性凝血途径产生的凝血酶F2a、F9a、F10a、F11a F12a分子活性中心的丝氨酸残基结合而抑制其活性
Responsible for inactivating 60%~70% of thrombin
在缺乏肝素的情况下，经常与内皮细胞表面的硫酸乙酰肝素结合扩大抗凝效果 (但不明显，作用依旧很弱)，结合肝素后，抗凝作用增加2000倍
Heparin cofactor II
Inactivate 30% thrombin
Protein C system
Protein C (PC), protein S (PS)
Protein C
from
Synthesized by the liver, its synthesis requires the participation of VitK
Vitamin K dependent protein
effect
Thrombin and TM form a complex at a ratio of 1:1, cleave PC, and form activated PC (APC). APC uses PS as a cofactor to inactivate F5a and F8a.
Thereby inhibiting the activation of F10 and prothrombin, thereby preventing the coagulation process from extending to surrounding normal blood vessels.
Stimulate the release of plasminogen activator, enhance plasmin activity, and promote fibrin degradation
Protein S
effect
Is a cofactor of protein C
Enhance protein C hydrolysis and inactivation of F8a and F5a
ThrombomodulinTM
Thrombin receptor on the surface of vascular endothelial cells
protein C inhibitor
tissue factor pathway inhibitor TFPI
from
vascular endothelial cells
effect
It is a specific inhibitor of the extrinsic coagulation pathway and is the main physiological anticoagulant substance. TFPI can bind to F10a and F7-tissue factor complexes and inhibit their activity (only after binding to F10 can the complex be combined)
It binds to F10 to make it allosteric, and then forms a tetramer with the complex for inactivation, exerting a negative feedback effect on inhibiting the extrinsic coagulation pathway.
heparin
from
Acidic mucopolysaccharides produced by mast cells and basophils
effect
Anticoagulant both internally and externally
Enhance the effect of antithrombin
Heparin binds to AT, causing AT configuration changes and exposing the active center. Allosteric AT combines with factor Xa or thrombin at a ratio of 1:1 to form a complex, causing the inactivation of the above two serine proteases.
Heparin itself has anticoagulant effect, but in the absence of antithrombin, the anticoagulant effect of heparin is very weak
Can promote the release of tissue factor pathway inhibitor (TFPI) and inhibit the coagulation process
In vivo effects > In vitro effects
Inhibit platelet adhesion, aggregation and release reactions
other factors
Promote coagulation
Warm saline gauze compression to stop bleeding
Gauze is a foreign body that can activate F12 and platelets. Appropriate heating can accelerate the enzymatic reaction in the coagulation process.
Within a certain range, temperature ↑, thrombin activity ↑, accelerate coagulation
Vitamin K
Participates in the synthesis of coagulation factors and has indirect effects on accelerating coagulation and hemostasis.
Anticoagulation
Contact surface roughness
The blood flows faster and the lining of blood vessels is smooth and intact, making it more difficult for blood to clot.
wooden stick stirring
Stirring removes fibrin to produce defibrinated blood that never coagulates, but does not preserve red blood cells
Sodium citrate, ammonium oxalate and potassium oxalate
By binding to Ca, it removes free plasma Ca and plays an anticoagulant effect.
heparin
Inhibit thrombin activity
dicoumarol
Competitively inhibits vitamin K and inhibits the synthesis of Vk-dependent coagulation factors
No synthesis in vitro → no anticoagulant effect in vitro
VK antagonists (such as warfarin)
Inhibits the synthesis of vitamin K-dependent coagulation factors such as F2, F7, F9, and F10
Genetically engineered plasminogen activator
anticoagulants
Dissolution of fibrin
composition
Plasminogen(PLG)
A serine protease synthesized primarily by the liver and also found in eosinophils
plasminogen activator
Tissue plasminogen activator (t-PA)
The main plasminogen activator in the human body, mainly synthesized in endothelial cells
Urokinase plasminogen activator (u-PA)/urokinase (UK)
The main forms are pro-urokinase (pro-UK) and double-chain urokinase-type plasminogen activator
other
FXIIa, kallikrein
plasmin related inhibitor
Mainly include α2-plasmin inhibitor (α2-PI), α1 antitrypsin (α1-AT) and α2-antiplasmin (α2-AP), etc.
It has the effect of inhibiting t-PA, plasmin, etc.
process
activation of plasminogen
Plasminogen is converted to plasmin by plasmin activator
Degradation of fibrin and fibrinogen
Plasmin has poor specificity. In addition to F1 and F1a, it can also hydrolyze F2, 5, 8, 10, 12, etc.
Plasmin hydrolyzes fibrin and fibrinogen into many soluble small peptides (Fibrin degradation product FDP)
Fibrin degradation products generally no longer coagulate and some even have anticoagulant effects.
blood type
definition
Types of specific antigens/agglutinants on the red blood cell membrane
red blood cell agglutination
definition
When specific proteins (agglutinogens/antigens) on red blood cells meet the same type of antibodies (lectins) in the serum of different individuals of the same animal, the red blood cells aggregate into clumps, which is an immune phenomenon accompanied by hemolysis (essentially an antigen-antibody reaction )
Taxonomy
There are no natural antibodies (IgM, impermeable to the placenta) in newborns in the early stage, but immune antibodies (IgG, impermeable to the placenta) can be obtained from the mother and fetus. The antibody content of newborns is 1/3 of that of adults.
Gene → Glycosyltransferase → Antigen oligosaccharide chain composition → Blood type
ABO blood group system
Mainly natural antibodies IgM
Type A blood: contains A agglutinogen/antigen on the red blood cell membrane and anti-B agglutinin/antibody in the serum
Blood type B: contains B antigen on the red blood cell membrane and anti-A antibodies in the serum
Type O blood: The red blood cell membrane does not contain A.B antigen (contains H antigen), and the serum contains anti-A.B antibodies.
Type AB: Contains A and B antigens on the red blood cell membrane, but does not contain A.B antibodies in the serum
Rh blood group system
antigen
There are six antigens C, D, and E on the human RBC membrane. D antigen has the strongest antigenicity
If D antigen is present, it is Rh; if there is no D antigen, it is Rh-
Antibody
Natural antibodies do not exist, Immune antibodies are mainly IgG
When Rh RBCs enter the body of an Rh- person, anti-Rh antibodies are produced through humoral immunity, and Rh RBCs enter again, triggering an immune response (hemolytic anemia of newborns)
Blood transfusion principle
Homotype blood transfusion (best)
Prevent hemolytic reaction caused by blood type incompatibility
Cross matching before blood transfusion
The principle is that the donor's RBCs are not agglutinated by the recipient's plasma.
main side
Donor red blood cells Recipient serum
secondary side
Recipient red blood cells Donor serum
in principle
If there is no agglutination on both primary and secondary sides, the blood match is compatible and blood transfusion is possible.
There is agglutination on the main side and the blood type is not suitable, so blood transfusion is not possible.
There is agglutination on the secondary side but not on the primary side. Blood transfusion can be done in emergency situations, but the blood transfusion should not be too fast or too much, and the situation should be closely observed.
law
Use anti-A/anti-B antibodies to detect the presence of A/B antigens on red blood cells
Use red blood cells of known blood type to detect the presence of anti-A/B antibodies in serum
Blood (Part 1)
blood
composition
Plasma 55%
plasma proteins
The biggest difference from tissue fluid
divided into
albumin/albumin
40-48g/L
It is a material for tissue repair and growth, and is the main determinant of plasma colloid osmotic pressure (the highest content). Binding to lipids and cholesterol facilitates their transportation
globulin
Normal white/globulin ratio: 1.5-2.5
肝病时，白蛋白由肝脏合成→白蛋白↓ 免疫活跃→球蛋白↑
15-30g/L
Divided into three categories: α, β and γ. γ globulins are almost all immune antibodies, called immunoglobulins, and are divided into five types: IgM/A/E/G/D (IgG is the most common)
fibrinogen
7-10g/L
Participates in the blood coagulation reaction and is eventually transformed into fibrin filaments under the catalysis of thrombin, etc. Traps red blood cells, forms clots, and plays a role in hemostasis and coagulation.
Blood cells 45%
red blood cellsRBC
Most, accounting for 99%
Normal male: 4.0-5.5×10^12/L
Normal female: 3.5-5.0×10^12/L
PlateletsPlt
Normal: 100-300×10⁹/L
white blood cellsWBC
Minimum, normal: 4.0×10⁹/L
Physical and chemical properties
Hematocrit
definition
Volume percentage of blood cells in blood
Reflects the relative concentration of blood cells and plasma
normal value
40-50% for men, 37-48% for women
Specific gravity (mass density)
definition
The ratio of the density of the substance to the density of water
normal value
Whole blood specific gravity 1.050-1.060
Depends on the number of blood cells
Plasma specific gravity 1.025-1.030
Depends on plasma protein concentration
Red blood cell specific gravity 1.090-1.092
Depends on the concentration of hemoglobin in red blood cells
viscosity
definition
It comes from the friction between molecules and particles inside the liquid, that is, internal friction
normal value
Take water as 1
The relative viscosity of whole blood is 4.0-5.0
Depends on hematocrit (volume ratio of blood cells in blood volume)
The relative viscosity of plasma is 1.6-2.4
Depends on plasma protein content
whole blood cells Plasma to see plasma protein
plasma osmolarity
definition
Refers to the ability of a solution to drive water molecules from the low concentration side through the semipermeable membrane into the high concentration side.
composition
Crystal osmotic pressure 98.5%
Plasma osmolarity is determined by crystalloid osmolality/NaCl concentration
definition
80% of the osmotic pressure formed by crystalline substances comes from NaCl
numerical value
298.7mmol/L or 766.7KPa
significance
interstitial fluid crystallographic osmotic pressure
Maintain water balance inside and outside cells
Colloidal osmotic pressure 1.5%
definition
75-80% of the osmotic pressure formed by protein comes from albumin
numerical value
1.3mmol/L or 3.3KPa
significance
colloid osmotic pressure of plasma
Maintain water balance inside and outside capillaries and maintain plasma volume
Decreased plasma protein will cause interstitial fluid to remain in the interstitial space and cause edema.
normal value
280-310mmol/L
The total osmotic pressure of intracellular fluid and tissue fluid in the body is the same
总渗透压：组织液=血浆=细胞内液
晶体渗透压：组织液＞血浆＞细胞内液(钠泵不断泵钠)
胶体渗透压：组织液＜血浆＜细胞内液(细胞内蛋白质多)
Equivalent to 0.9% NaCl solution or 5% glucose solution (isotonic liquid)
red blood cells
quantity
male
Red blood cell count 4.0～5.5×10^12/L Hemoglobin concentration Hb: 120～160g/L
female
Red blood cell count 3.5～5.0×10^12/L Hemoglobin concentration Hb: 110~150g/L, pregnant women <100g/L
shape
Double convex disc type
Give red blood cells a larger surface area to volume ratio
No nucleus, no mitochondria
Maintaining shape requires energy, and glycolysis is the only way to gain energy.
characteristic
Plastic deformability
definition
It is easy to deform under the action of external force and can recover after the external force is removed.
Influencing factors
The surface area/volume ratio determines the deformation and is proportional to the
RBC’s bi-concave disc shape increases surface area
suspension stability
definition
suspension stability
The friction between red blood cells and plasma resists sinking, making red blood cells evenly suspended in the plasma and not easy to sink.
Erythrocyte sedimentation rate ESR
Opposite of suspension stability
The distance RBC sinks in 1 hour in a static anticoagulated blood test tube
Influencing factors
Globulin, fibrinogen↑
Negatively charged, red blood cells are positively charged, attracting each other
Cholesterol ↑
Cholesterol promotes RBC aggregation
Red blood cell stack↑→surface area/volume ratio↓→friction↓
sink quickly
Albumin, lecithin↑
Negatively charged, mutually repulsive with red blood cells↑
Red blood cell stack↓→surface area/volume ratio↑→friction↑
sink slowly
Note
The influencing factors are not in the red blood cells themselves It lies in the changes in plasma composition
Put red blood cells with slow erythrocyte sedimentation rate into the plasma of a person with fast erythrocyte sedimentation rate → fast erythrocyte sedimentation rate
Red blood cells with fast erythrocyte sedimentation rate are put into the plasma of a person with slow erythrocyte sedimentation rate → slow erythrocyte sedimentation rate
Osmotic brittleness/brittleness
The worse the denaturation ability, the higher the brittleness and the easier it is to break.
definition
The ability of red blood cells to swell and rupture in hypotonic solutions
Isotonic 0.9% solution, maintains normal size and shape
In hypotonic sodium chloride solution, red blood cells swell into a spherical shape. At 0.32%, they swell and rupture.
Influencing factors
type
Aged red blood cells have weak resistance and high fragility
Reticulocytes and immature red blood cells are highly resistant and less fragile
Phospholipids/cholesterol
Bilayer, phospholipid↑→glycoprotein↑
Phospholipids↑→Fluidity, Toughness↑→Brittleness↓
Surface area/volume ratio (double concave dish)
Value↓(spherical RBC)→brittleness↑
Selective permeability of membranes
Water, oxygen, carbon dioxide and urea can pass freely,
Glucose, amino acids, and negative ions Cl⁻/HCO₃⁻ are easier to pass through.
Positive ions²⁺ have a hard time passing through
metabolism
synthesis
place
Adult: bone marrow, only
raw material
Protein and Iron (Basic Ingredients)
Important raw material for the synthesis of hemoglobin
Iron deficiency leading to dystrophic anemia/hypochromic microcytic anemia
Vitamin B₁₂, folic acid (maturation factor)
Participate in DNA synthesis (Important coenzyme)
Lack of VB₁₂/folic acid leads to DNA synthesis disorder, resulting in abnormal nuclear development, slowed down division of young red blood cells, imbalanced nuclear and cytoplasmic development, and increased red blood cell volume (megaloblastic anemia).
intrinsic factor
Participates in vitamin B₁₂ reabsorption
Gastrectomy (secretion of intrinsic factor)
Terminal ileum resection (reabsorption site)
Vitamin B₁₂ deficiency
Other substances
Amino acids. Other vitamins (VB6.B2.C.E) and trace elements (copper, manganese, cobalt and zinc)
generative regulation
Late erythroid progenitor cells are mainly regulated by EPO due to the dense presence of erythropoietin (EPO) receptors. Early erythroid progenitor cells are less affected by EPO due to sparse EPO receptors and are mainly regulated by cytokines.
Early days
Cytokines
Stem cell factor (SCF), interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF)
Stimulates the proliferation and development of early erythroid progenitor cells (BFU-E) into late erythroid progenitor cells (CFU-E)
Blast Boost Activator (BPA)
Promote the proliferation of early erythroid progenitor cells
Transforming growth factor beta, interferon gamma and tumor necrosis factor, etc.
It can inhibit the proliferation of early erythroid progenitor cells and negatively regulate the production of red blood cells.
later stage
Erythropoietin EPO
from
Interstitial cells (fibroblasts, endothelial cells) around renal cortex tubules
Renal failure → renal anemia
Function
Mainly acts on late erythroid progenitor cells
Promote the production, development and hemoglobin synthesis of red blood cells
Promotes the release of mature red blood cells into the blood
adjust
Red blood cells↓
Renal hypoxia (atmospheric oxygen partial pressure ↓ tissue blood flow ↓ hemoglobin oxygen affinity ↑ tissue oxygen consumption ↑) → EPO synthesis ↑ → red blood cells ↑
CO₂ retention does not necessarily mean hypoxia
Thyroid hormones, adrenaline and growth hormone, etc.
Change tissue demand for oxygen, resulting in tissue hypoxia
sex hormones
Androgens promote, estrogen suppresses
Male red blood cells > Female
destroy
The normal life span of red blood cells is 120 days
way
Extravascular destruction 90%
parts
spleen, bone marrow, liver
Aged red blood cells are an important source of bilirubin
mechanism
Aged red blood cells have reduced deformability and increased fragility, making it difficult for them to pass through tiny pores. Therefore, they are easily retained in the spleen and bone marrow and are phagocytosed by macrophages.
10% intravascular damage
mechanism
Aging RBCs are damaged by mechanical shock in blood vessels
Note
The hemoglobin in the plasma is too high and is excreted by the kidneys, forming hemoglobinuria.
leukocyte
quantity
4.0～10×10⁹/L
Classification
granular leukocytes
Neutral particles 50~70%
parts
blood, bone marrow
Features
Active deformation motility, high chemotaxis, and strong phagocytosis ability
Function
Phagocytosis
The most important phagocyte
Lysosomal enzymes phagocytose pathogenic microorganisms, tissue fragments, and other foreign matter
Acute purulent inflammation, significantly increased number of effector cells that are the first to arrive at the inflammatory site
Can phagocytose and eliminate aging red blood cells and antigen-antibody complexes, etc.
Eosinophils 0.5-5%
parts
organize
Features
Has phagocytic ability but no bactericidal ability (no lysozyme)
There are diurnal fluctuations, decreasing in the early morning and increasing at midnight.
Function
Limiting the role of basophils and mast cells in type I/immediate allergic reactions
Involved in the immune response to worms
Increased allergic diseases or parasitic diseases
Basophilic granules 0 to 1%
parts
blood
Features
It does not have phagocytic ability and is mainly involved in hypersensitive allergic reactions and parasite immune responses.
effect
Contains a variety of biologically active substances
Histamine, allergic slow response cells
Cause allergic reaction symptoms such as asthma and urticaria
Eotaxin A
Attract eosinophils to aggregate to limit the role of basophils in allergic reactions
heparin
Anticoagulation
agranular leukocytes
Monocytes 3~8%
parts
blood
Features
Exists in the bloodstream, stays in the blood for 10 to 20 hours and then migrates into tissues to develop into macrophages. Together they are called the monocyte-macrophage system and play a defensive role.
effect
late stage inflammatory cells
Swallow more bacteria and more foreign matter
Synthesize and release a variety of cytokines
Such as colony-stimulating factor (CSF)), interleukins (IL-1, IL-3, IL-6), Tumor necrosis factor (TNF-α), interferon (INF-α, INF-β), participate in the regulation of other cell activities
Strong ability to kill tumors and virus-infected cells
Efficiently process and present antigens
Participate in the activation of specific immune functions of lymphocytes
Lymphocytes 20~40%
parts
blood, tissue fluid, lymph
Classification
T lymphocytes
Differentiates from hematopoietic stem cells in the bone marrow and migrates to the thymus to mature
Long life, from several months to more than a year
B lymphocytes
Differentiates from hematopoietic stem cells in the bone marrow and stays in the bone marrow to mature.
Life span is short, usually 3 to 5 days
Function
Participate in immune response
T lymphocytes
Directly phagocytose problem cells → cellular immunity
B lymphocytes
Secrete antibodies in the body and bind to antigen → humoral immunity
NK cells
natural immunity
Physiological properties
Leukocyte extravasation
Extend pseudopods to perform deformation movements. With this movement, white blood cells can pass through the blood vessel wall.
Lymphocytes move without pseudopods
Chemotaxis
Has the tendency to migrate towards certain chemicals, including bacterial toxins, cells or cell degradation products, antigen-antibody complexes and some cytokines
Chemicals that attract white blood cells are called chemokines
Phagocytosis
selective
正常细胞表面光滑,其表面存在可以排斥吞噬的保护性蛋白,故不易被吞噬
坏死的组织和外源性颗粒,因缺乏相应的保护机制而易被吞噬
在特异性抗体和某些补体的激活产物调理下, 白细胞对外源性异物的识别和吞噬作用加强
The process of surrounding foreign matter and swallowing it into the cytoplasm
Secrete a variety of cytokines
Interleukin (IL), interferon (IFN), tumor necrosis factor (TNF), and colony-stimulating factor participate in the regulation of inflammation and the immune system through autocrine or paracrine
platelets
quantity
Normal adult is 100~300×10⁹/L
Physiological properties
Adhesion (positioning)
condition
Platelet membrane glycoprotein GPIb/IV/V complex
receptor
Deficiency → giant platelet syndrome
vW
Bridge (connecting collagen fibers to GPIb)
Deficiency → von Willebrand disease
Subendothelial components (collagen fibers)
damaged subendothelial component
process
Vascular endothelial injury → Exposure of collagen fibers → Platelets adhere to collagen fibers → Adsorption of coagulation factors → Formation of thromboplastin activator → Formation of soft thrombus
Release (call friends)
definition
After Plt is stimulated, it is the process of expelling substances stored in dense bodies, α-granules, and lysosomes. The release of substances can promote further activation and aggregation of Plt, and accelerate hemostasis.
discharge substances
expel original substances
dense body
ADP, ATP, 5-hydroxytryptamine (5-HT), Ca²⁺
α-granules
β-platelet globulin, platelet factor 4 (PF4), vWF, fibrinogen, Coagulation factor V, thrombospondin, platelet-derived growth factor PDGF, etc.
lysosome
Temporarily synthesize and release
Thromboxane A2 (TXA₂)
process
Release platelet factors → promote fibrin formation → network blood cells → expand thrombus
Aggregation (platelet adhesion)
definition
Platelets stick to each other and aggregate into aggregates
Platelet membrane glycoprotein GPIIb/IIIa complex, Connected to each other via fibrinogen, Ca²⁺
phase
first gathering phase
Occurs rapidly and can also depolymerize quickly → reversible aggregation
second gathering phase
Occurs slowly, cannot depolymerize → irreversible aggregation
Influencing factors
Polymerizer
Physiological
ADP. Thrombin
Low concentration first aggregation Medium concentration first and then second high concentration second aggregation
Subendothelial collagen exposure
irreversible
Epinephrine, 5-HT, histamine, TXA₂, etc.
irreversible
pathological
Bacteria, viruses, immune complexes, drugs, etc.
inhibitor
prostaglandin PGI2, nitric oxide NO
aspirin
Aspirin inhibits cyclooxygenase COX synthesis→ Inhibits the conversion of arachidonic acid into PGG2, PGI2→TXA2↓
shrink
process
Under the action of ²⁺, the contractile protein of platelets causes the blood clot to retract → solid thrombus
Contractile proteins: actin, myosin, microtubules and related proteins
Adsorption
Adsorbs coagulation factors in plasma to facilitate blood coagulation
definition
Coagulation factors (FⅠ, Ⅴ, Ⅺ, ⅩⅢ) can be adsorbed on the surface of platelets
significance
Increase local coagulation factor concentration ↑→ to accelerate blood coagulation and physiological hemostasis
Function
Helps maintain the integrity of blood vessel walls (vascular endothelial cells)
Platelets can adhere and fuse into the vascular endothelium, thus maintaining the integrity of the vascular endothelium → When the platelet count drops to 50×10⁹/L, the capillary fragility increases and bleeding is easy (blood spots)
Platelets can release vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF), which are beneficial to the repair of damaged blood vessels.
Participate in physiological hemostasis
Is central to the process of hemostasis
Participate in blood coagulation
A small number of platelets are needed for coagulation, and platelets have little effect on coagulation.
Contains a variety of coagulation factors
PF3 provides a place for coagulation reaction, PF2 promotes the conversion of fibrinogen into fibrin monomer, and PF4 is used against heparin.
Participate in the fibrinolytic process
It has both promoting and inhibiting effects on fibrinolysis.