Module 5: The Blood

Lesson 5: Hemostasis

Quá Trình Đông Cầm Máu

Nội dung bài học:
Mỗi bài học (lesson) bao gồm 4 phần chính: Thuật ngữ, Luyện Đọc, Luyện Nghe, và Bàn Luận.
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Dưới đây là danh sách những thuật ngữ Y khoa của module The Blood.
Khái quát được số lượng thuật ngữ sẽ xuất hiện trong bài đọc và nghe sẽ giúp bạn thoải mái tiêu thụ nội dung hơn. Sau khi hoàn thành nội dung đọc và nghe, bạn hãy quay lại đây và luyện tập (practice) để quen dần các thuật ngữ này. Đừng ép bản thân phải nhớ các thuật ngữ này vội vì bạn sẽ gặp và ôn lại danh sách này trong những bài học (lesson) khác của cùng một module.

Medical Terminology: The Blood

ABO blood group
blood-type classification based on the presence or absence of A and B glycoproteins on the erythrocyte membrane surface
clustering of cells into masses linked by antibodies
agranular leukocytes
leukocytes with few granules in their cytoplasm; specifically, monocytes, lymphocytes, and NK cells
most abundant plasma protein, accounting for most of the osmotic pressure of plasma
deficiency of red blood cells or hemoglobin
(also, immunoglobulins or gamma globulins) antigen-specific proteins produced by specialized B lymphocytes that protect the body by binding to foreign objects such as bacteria and viruses
substance such as heparin that opposes coagulation
anticoagulant that inactivates factor X and opposes the conversion of prothrombin (factor II) into thrombin in the common pathway
B lymphocytes
(also, B cells) lymphocytes that defend the body against specific pathogens and thereby provide specific immunity
granulocytes that stain with a basic (alkaline) stain and store histamine and heparin
yellowish bile pigment produced when iron is removed from heme and is further broken down into waste products
green bile pigment produced when the non-iron portion of heme is degraded into a waste product; converted to bilirubin in the liver
liquid connective tissue composed of formed elements—erythrocytes, leukocytes, and platelets—and a fluid extracellular matrix called plasma; component of the cardiovascular system
bone marrow biopsy
diagnostic test of a sample of red bone marrow
bone marrow transplant
treatment in which a donor’s healthy bone marrow with its stem cells replaces diseased or damaged bone marrow of a patient
localized bleeding under the skin due to damaged blood vessels
buffy coat
thin, pale layer of leukocytes and platelets that separates the erythrocytes from the plasma in a sample of centrifuged blood
compound of carbon dioxide and hemoglobin, and one of the ways in which carbon dioxide is carried in the blood
clotting factors
group of 12 identified substances active in coagulation
formation of a blood clot; part of the process of hemostasis
colony-stimulating factors (CSFs)
glycoproteins that trigger the proliferation and differentiation of myeloblasts into granular leukocytes (basophils, neutrophils, and eosinophils)
common pathway
final coagulation pathway activated either by the intrinsic or the extrinsic pathway, and ending in the formation of a blood clot
cross matching
blood test for identification of blood type using antibodies and small samples of blood
class of proteins that act as autocrine or paracrine signaling molecules; in the cardiovascular system, they stimulate the proliferation of progenitor cells and help to stimulate both nonspecific and specific resistance to disease
antimicrobial proteins released from neutrophils and macrophages that create openings in the plasma membranes to kill cells
molecule of hemoglobin without an oxygen molecule bound to it
(also, emigration) process by which leukocytes squeeze through adjacent cells in a blood vessel wall to enter tissues
thrombus that has broken free from the blood vessel wall and entered the circulation
(also, diapedesis) process by which leukocytes squeeze through adjacent cells in a blood vessel wall to enter tissues
granulocytes that stain with eosin; they release antihistamines and are especially active against parasitic worms
(also, red blood cell) mature myeloid blood cell that is composed mostly of hemoglobin and functions primarily in the transportation of oxygen and carbon dioxide
erythropoietin (EPO)
glycoprotein that triggers the bone marrow to produce RBCs; secreted by the kidney in response to low oxygen levels
extrinsic pathway
initial coagulation pathway that begins with tissue damage and results in the activation of the common pathway
protein-containing storage form of iron found in the bone marrow, liver, and spleen
insoluble, filamentous protein that forms the structure of a blood clot
plasma protein produced in the liver and involved in blood clotting
gradual degradation of a blood clot
formed elements
cellular components of blood; that is, erythrocytes, leukocytes, and platelets
heme-containing globular protein that is a constituent of hemoglobin
heterogeneous group of plasma proteins that includes transport proteins, clotting factors, immune proteins, and others
granular leukocytes
leukocytes with abundant granules in their cytoplasm; specifically, neutrophils, eosinophils, and basophils
(also, packed cell volume) volume percentage of erythrocytes in a sample of centrifuged blood
hematopoietic stem cell
type of pluripotent stem cell that gives rise to the formed elements of blood (hemocytoblast)
red, iron-containing pigment to which oxygen binds in hemoglobin
hematopoietic stem cell that gives rise to the formed elements of blood
oxygen-carrying compound in erythrocytes
destruction (lysis) of erythrocytes and the release of their hemoglobin into circulation
hemolytic disease of the newborn (HDN)
(also, erythroblastosis fetalis) disorder causing agglutination and hemolysis in an Rh+ fetus or newborn of an Rh− person
genetic disorder characterized by inadequate synthesis of clotting factors
production of the formed elements of blood
hemopoietic growth factors
chemical signals including erythropoietin, thrombopoietin, colony-stimulating factors, and interleukins that regulate the differentiation and proliferation of particular blood progenitor cells
excessive bleeding
protein-containing storage form of iron found in the bone marrow, liver, and spleen
physiological process by which bleeding ceases
short-acting anticoagulant stored in mast cells and released when tissues are injured, opposes prothrombin
below-normal level of oxygen saturation of blood (typically <95 percent)
(also, antibodies or gamma globulins) antigen-specific proteins produced by specialized B lymphocytes that protect the body by binding to foreign objects such as bacteria and viruses
signaling molecules that may function in hemopoiesis, inflammation, and specific immune responses
intrinsic pathway
initial coagulation pathway that begins with vascular damage or contact with foreign substances, and results in the activation of the common pathway
yellowing of the skin or whites of the eyes due to excess bilirubin in the blood
cancer involving leukocytes
(also, white blood cell) colorless, nucleated blood cell, the chief function of which is to protect the body from disease
excessive leukocyte proliferation
below-normal production of leukocytes
agranular leukocytes of the lymphoid stem cell line, many of which function in specific immunity
lymphoid stem cells
type of hematopoietic stem cells that gives rise to lymphocytes, including various T cells, B cells, and NK cells, all of which function in immunity
form of cancer in which masses of malignant T and/or B lymphocytes collect in lymph nodes, the spleen, the liver, and other tissues
digestive enzyme with bactericidal properties
phagocytic cell of the myeloid lineage; a matured monocyte
bone marrow cell that produces platelets
memory cell
type of B or T lymphocyte that forms after exposure to a pathogen
agranular leukocytes of the myeloid stem cell line that circulate in the bloodstream; tissue monocytes are macrophages
myeloid stem cells
type of hematopoietic stem cell that gives rise to some formed elements, including erythrocytes, megakaryocytes that produce platelets, and a myeloblast lineage that gives rise to monocytes and three forms of granular leukocytes (neutrophils, eosinophils, and basophils)
natural killer (NK) cells
cytotoxic lymphocytes capable of recognizing cells that do not express “self” proteins on their plasma membrane or that contain foreign or abnormal markers; provide generalized, nonspecific immunity
granulocytes that stain with a neutral dye and are the most numerous of the leukocytes; especially active against bacteria
molecule of hemoglobin to which oxygen is bound
packed cell volume (PCV)
(also, hematocrit) volume percentage of erythrocytes present in a sample of centrifuged blood
in blood, the liquid extracellular matrix composed mostly of water that circulates the formed elements and dissolved materials throughout the cardiovascular system
blood protein active in fibrinolysis
platelet plug
accumulation and adhesion of platelets at the site of blood vessel injury
(also, thrombocytes) one of the formed elements of blood that consists of cell fragments broken off from megakaryocytes
pluripotent stem cell
stem cell that derives from totipotent stem cells and is capable of differentiating into many, but not all, cell types
elevated level of hemoglobin, whether adaptive or pathological
having a lobed nucleus, as seen in some leukocytes
positive chemotaxis
process in which a cell is attracted to move in the direction of chemical stimuli
red blood cells (RBCs)
(also, erythrocytes) one of the formed elements of blood that transports oxygen
immature erythrocyte that may still contain fragments of organelles
Rh blood group
blood-type classification based on the presence or absence of the antigen Rh on the erythrocyte membrane surface
blood plasma that does not contain clotting factors
sickle cell disease
(also, sickle cell anemia) inherited blood disorder in which hemoglobin molecules are malformed, leading to the breakdown of RBCs that take on a characteristic sickle shape
T lymphocytes
(also, T cells) lymphocytes that provide cellular-level immunity by physically attacking foreign or diseased cells
inherited blood disorder in which maturation of RBCs does not proceed normally, leading to abnormal formation of hemoglobin and the destruction of RBCs
enzyme essential for the final steps in formation of a fibrin clot
platelets, one of the formed elements of blood that consists of cell fragments broken off from megakaryocytes
condition in which there are too few platelets, resulting in abnormal bleeding (hemophilia)
condition in which there are too many platelets, resulting in abnormal clotting (thrombosis)
hormone secreted by the liver and kidneys that prompts the development of megakaryocytes into thrombocytes (platelets)
excessive clot formation
aggregation of fibrin, platelets, and erythrocytes in an intact artery or vein
tissue factor
protein thromboplastin, which initiates the extrinsic pathway when released in response to tissue damage
totipotent stem cell
embryonic stem cell that is capable of differentiating into any and all cells of the body; enabling the full development of an organism
plasma protein that binds reversibly to iron and distributes it throughout the body
universal donor
individual with type O− blood
universal recipient
individual with type AB+ blood
vascular spasm
initial step in hemostasis, in which the smooth muscle in the walls of the ruptured or damaged blood vessel contracts
white blood cells (WBCs)
(also, leukocytes) one of the formed elements of blood that provides defense against disease agents and foreign materials
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Dưới đây là các bài văn nằm ở bên trái. Ở bên phải là các bài luyện tập (practice) để đánh giá khả năng đọc hiểu của bạn. Sẽ khó khăn trong thời gian đầu nếu vốn từ vựng của bạn còn hạn chế, đặc biệt là từ vựng Y khoa. Hãy kiên nhẫn và đọc nhiều nhất có kể, lượng kiến thức tích tụ dần sẽ giúp bạn đọc thoải mái hơn.
Platelets are key players in hemostasis, the process by which the body seals a ruptured blood vessel and prevents further loss of blood. Although rupture of larger vessels usually requires medical intervention, hemostasis is quite effective in dealing with small, simple wounds. There are three steps to the process: vascular spasm, the formation of a platelet plug, and coagulation (blood clotting). Failure of any of these steps will result in hemorrhage—excessive bleeding.
When a vessel is severed or punctured, or when the wall of a vessel is damaged, vascular spasm occurs. In vascular spasm, the smooth muscle in the walls of the vessel contracts dramatically. This smooth muscle has both circular layers; larger vessels also have longitudinal layers. The circular layers tend to constrict the flow of blood, whereas the longitudinal layers, when present, draw the vessel back into the surrounding tissue, often making it more difficult for a surgeon to locate, clamp, and tie off a severed vessel. The vascular spasm response is believed to be triggered by several chemicals called endothelins that are released by vessel-lining cells and by pain receptors in response to vessel injury. This phenomenon typically lasts for up to 30 minutes, although it can last for hours.
Plug In the second step, platelets, which normally float free in the plasma, encounter the area of vessel rupture with the exposed underlying connective tissue and collagenous fibers. The platelets begin to clump together, become spiked and sticky, and bind to the exposed collagen and endothelial lining. This process is assisted by a glycoprotein in the blood plasma called von Willebrand factor, which helps stabilize the growing platelet plug. As platelets collect, they simultaneously release chemicals from their granules into the plasma that further contribute to hemostasis. Among the substances released by the platelets are:

  • Adenosine diphosphate (ADP), which helps additional platelets to adhere to the injury site, reinforcing and expanding the platelet plug.
  • Serotonin, which maintains vasoconstriction.
  • Prostaglandins and phospholipids, which also maintain vasoconstriction and help to activate further clotting chemicals, as discussed next.

A platelet plug can temporarily seal a small opening in a blood vessel. Plug formation, in essence, buys the body time while more sophisticated and durable repairs are being made. In a similar manner, even modern naval warships still carry an assortment of wooden plugs to temporarily repair small breaches in their hulls until permanent repairs can be made.
Those more sophisticated and more durable repairs are collectively called coagulation, the formation of a blood clot. The process is sometimes characterized as a cascade, because one event prompts the next as in a multi-level waterfall. The result is the production of a gelatinous but robust clot made up of a mesh of fibrin—an insoluble filamentous protein derived from fibrinogen, the plasma protein introduced earlier—in which platelets and blood cells are trapped. Figure 1 summarizes the three steps of hemostasis.

A. Clotting Factors Involved in Coagulation

In the coagulation cascade, chemicals called clotting factors (or coagulation factors) prompt reactions that activate still more coagulation factors. The process is complex, but is initiated along two basic pathways:

  • The extrinsic pathway, which normally is triggered by trauma.
  • The intrinsic pathway, which begins in the bloodstream and is triggered by internal damage to the wall of the vessel.

Both of these merge into a third pathway, referred to as the common pathway (see Figure 1b). All three pathways are dependent upon the 12 known clotting factors, including Ca2+ and vitamin K (Table 1). Clotting factors are secreted primarily by the liver and the platelets. The liver requires the fat-soluble vitamin K to produce many of them. Vitamin K (along with biotin and folate) is somewhat unusual among vitamins in that it is not only consumed in the diet but is also synthesized by bacteria residing in the large intestine. The calcium ion, considered factor IV, is derived from the diet and from the breakdown of bone. Some recent evidence indicates that activation of various clotting factors occurs on specific receptor sites on the surfaces of platelets.

The 12 clotting factors are numbered I through XIII according to the order of their discovery. Factor VI was once believed to be a distinct clotting factor, but is now thought to be identical to factor V. Rather than renumber the other factors, factor VI was allowed to remain as a placeholder and also a reminder that knowledge changes over time.

B. Extrinsic Pathway

The quicker responding and more direct extrinsic pathway (also known as the tissue factor pathway) begins when damage occurs to the surrounding tissues, such as in a traumatic injury. Upon contact with blood plasma, the damaged extravascular cells, which are extrinsic to the bloodstream, release factor III (thromboplastin). Sequentially, Ca2+ then factor VII (proconvertin), which is activated by factor III, are added, forming an enzyme complex. This enzyme complex leads to activation of factor X (Stuart–Prower factor), which activates the common pathway discussed below. The events in the extrinsic pathway are completed in a matter of seconds.

C. Intrinsic Pathway

The intrinsic pathway (also known as the contact activation pathway) is longer and more complex. In this case, the factors involved are intrinsic to (present within) the bloodstream. The pathway can be prompted by damage to the tissues, resulting from internal factors such as arterial disease; however, it is most often initiated when factor XII (Hageman factor) comes into contact with foreign materials, such as when a blood sample is put into a glass test tube. Within the body, factor XII is typically activated when it encounters negatively charged molecules, such as inorganic polymers and phosphate produced earlier in the series of intrinsic pathway reactions. Factor XII sets off a series of reactions that in turn activates factor XI (antihemolytic factor C or plasma thromboplastin antecedent) then factor IX (antihemolytic factor B or plasma thromboplasmin). In the meantime, chemicals released by the platelets increase the rate of these activation reactions. Finally, factor VIII (antihemolytic factor A) from the platelets and endothelial cells combines with factor IX (antihemolytic factor B or plasma thromboplasmin) to form an enzyme complex that activates factor X (Stuart–Prower factor or thrombokinase), leading to the common pathway. The events in the intrinsic pathway are completed in a few minutes.

D. Common Pathway

Both the intrinsic and extrinsic pathways lead to the common pathway, in which fibrin is produced to seal off the vessel. Once factor X has been activated by either the intrinsic or extrinsic pathway, the enzyme prothrombinase converts factor II, the inactive enzyme prothrombin, into the active enzyme thrombin. (Note that if the enzyme thrombin were not normally in an inactive form, clots would form spontaneously, a condition not consistent with life.) Then, thrombin converts factor I, the soluble fibrinogen, into the insoluble fibrin protein strands. Factor XIII then stabilizes the fibrin clot.
The stabilized clot is acted upon by contractile proteins within the platelets. As these proteins contract, they pull on the fibrin threads, bringing the edges of the clot more tightly together, somewhat as we do when tightening loose shoelaces (see Figure 1a). This process also wrings out of the clot a small amount of fluid called serum, which is blood plasma without its clotting factors.

To restore normal blood flow as the vessel heals, the clot must eventually be removed. Fibrinolysis is the gradual degradation of the clot. Again, there is a fairly complicated series of reactions that involves factor XII and protein-catabolizing enzymes. During this process, the inactive protein plasminogen is converted into the active plasmin, which gradually breaks down the fibrin of the clot. Additionally, bradykinin, a vasodilator, is released, reversing the effects of the serotonin and prostaglandins from the platelets. This allows the smooth muscle in the walls of the vessels to relax and helps to restore the circulation.
An anticoagulant is any substance that opposes coagulation. Several circulating plasma anticoagulants play a role in limiting the coagulation process to the region of injury and restoring a normal, clot-free condition of blood. For instance, a cluster of proteins collectively referred to as the protein C system inactivates clotting factors involved in the intrinsic pathway. TFPI (tissue factor pathway inhibitor) inhibits the conversion of the inactive factor VII to the active form in the extrinsic pathway. Antithrombin inactivates factor X and opposes the conversion of prothrombin (factor II) to thrombin in the common pathway. And as noted earlier, basophils release heparin, a short-acting anticoagulant that also opposes prothrombin. Heparin is also found on the surfaces of cells lining the blood vessels. A pharmaceutical form of heparin is often administered therapeutically, for example, in surgical patients at risk for blood clots.
Either an insufficient or an excessive production of platelets can lead to severe disease or death. As discussed earlier, an insufficient number of platelets, called thrombocytopenia, typically results in the inability of blood to form clots. This can lead to excessive bleeding, even from minor wounds.

Another reason for failure of the blood to clot is the inadequate production of functional amounts of one or more clotting factors. This is the case in the genetic disorder hemophilia, which is actually a group of related disorders, the most common of which is hemophilia A, accounting for approximately 80 percent of cases. This disorder results in the inability to synthesize sufficient quantities of factor VIII. Hemophilia B is the second most common form, accounting for approximately 20 percent of cases. In this case, there is a deficiency of factor IX. Both of these defects are linked to the X chromosome and are typically passed from a healthy (carrier) female to their male offspring, since males are XY. Females would need to inherit a defective gene from each parent to manifest the disease, since they are XX. Patients with hemophilia bleed from even minor internal and external wounds, and leak blood into joint spaces after exercise and into urine and stool. Hemophilia C is a rare condition that is triggered by an autosomal (not sex) chromosome that renders factor XI nonfunctional. It is not a true recessive condition, since even individuals with a single copy of the mutant gene show a tendency to bleed. Regular infusions of clotting factors isolated from healthy donors can help prevent bleeding in hemophiliac patients. At some point, genetic therapy will become a viable option.

In contrast to the disorders characterized by coagulation failure is thrombocytosis, also mentioned earlier, a condition characterized by excessive numbers of platelets that increases the risk for excessive clot formation, a condition known as thrombosis. A thrombus (plural = thrombi) is an aggregation of platelets, erythrocytes, and even WBCs typically trapped within a mass of fibrin strands. While the formation of a clot is normal following the hemostatic mechanism just described, thrombi can form within an intact or only slightly damaged blood vessel. In a large vessel, a thrombus will adhere to the vessel wall and decrease the flow of blood, and is referred to as a mural thrombus. In a small vessel, it may actually totally block the flow of blood and is termed an occlusive thrombus. Thrombi are most commonly caused by vessel damage to the endothelial lining, which activates the clotting mechanism. These may include venous stasis, when blood in the veins, particularly in the legs, remains stationary for long periods. This is one of the dangers of long airplane flights in crowded conditions and may lead to deep vein thrombosis. Thrombophilia, also called hypercoagulation, is a condition in which there is a tendency to form thrombosis. This may be familial (genetic) or acquired. Acquired forms include the autoimmune disease lupus, immune reactions to heparin, polycythemia vera, thrombocytosis, sickle cell disease, pregnancy, and even obesity. A thrombus can seriously impede blood flow to or from a region and will cause a local increase in blood pressure. If flow is to be maintained, the heart will need to generate a greater pressure to overcome the resistance.

When a portion of a thrombus breaks free from the vessel wall and enters the circulation, it is referred to as an embolus. An embolus that is carried through the bloodstream can be large enough to block a vessel critical to a major organ. When it becomes trapped, an embolus is called an embolism. In the heart, brain, or lungs, an embolism may accordingly cause a heart attack, a stroke, or a pulmonary embolism. These are medical emergencies.

Among the many known biochemical activities of aspirin is its role as an anticoagulant. Aspirin (acetylsalicylic acid) is very effective at inhibiting the aggregation of platelets. It is routinely administered during a heart attack or stroke to reduce the adverse effects. Physicians sometimes recommend that patients at risk for cardiovascular disease take a low dose of aspirin on a daily basis as a preventive measure. However, aspirin can also lead to serious side effects, including increasing the risk of ulcers. A patient is well advised to consult a physician before beginning any aspirin regimen.

A class of drugs collectively known as thrombolytic agents can help speed up the degradation of an abnormal clot. If a thrombolytic agent is administered to a patient within 3 hours following a thrombotic stroke, the patient’s prognosis improves significantly. However, some strokes are not caused by thrombi, but by hemorrhage. Thus, the cause must be determined before treatment begins. Tissue plasminogen activator is an enzyme that catalyzes the conversion of plasminogen to plasmin, the primary enzyme that breaks down clots. It is released naturally by endothelial cells but is also used in clinical medicine. New research is progressing using compounds isolated from the venom of some species of snakes, particularly vipers and cobras, which may eventually have therapeutic value as thrombolytic agents.

OpenStax. (2022). Anatomy and Physiology 2e. Rice University. Retrieved June 15, 2023. ISBN-13: 978-1-711494-06-7 (Hardcover) ISBN-13: 978-1-711494-05-0 (Paperback) ISBN-13: 978-1-951693-42-8 (Digital). License: Attribution 4.0 International (CC BY 4.0). Access for free at

(a) An injury to a blood vessel initiates the process of hemostasis. Blood clotting involves three steps. First, vascular spasm constricts the flow of blood. Next, a platelet plug forms to temporarily seal small openings in the vessel. Coagulation then enables the repair of the vessel wall once the leakage of blood has stopped. (b) The synthesis of fibrin in blood clots involves either an intrinsic pathway or an extrinsic pathway, both of which lead to a common pathway. (credit a: Kevin MacKenzie)

Factor’s Number and NameType of moleculeSourcePathway(s)
I. FibrinogenPlasma proteinLiverCommon; converted into fibrin
II. ProthrombinPlasma proteinLiver*Common; converted into thrombin
III. Tissue thromboplastin or tissue factorLipoprotein mixtureDamaged cells and plateletsExtrinsic
IV. Calcium ionsInorganic ions in plasmaDiet, platelets, bone matrixEntire process
V. ProaccelerinPlasma proteinLiver, plateletsExtrinsic and intrinsic
VI. No name usedNot usedNot usedNot used
VII. ProconvertinPlasma proteinLiver *Extrinsic
VIII. Antihemolytic factor APlasma protein factorPlatelets and endothelial cellsIntrinsic; deficiency results in hemophilia A
IX. Antihemolytic factor B (plasma thromboplastin component)Plasma proteinLiver*Intrinsic; deficiency results in hemophilia B
X. Stuart–Prower factor (thrombokinase)ProteinLiver*Extrinsic and intrinsic
XI. Antihemolytic factor C (plasma thromboplastin antecedent)Plasma proteinLiverIntrinsic; deficiency results in hemophilia C
XII. Hageman factorPlasma proteinLiverIntrinsic; initiates clotting in vitro also activates plasmin
XIII. Fibrin-stabilizing factorPlasma proteinLiver, plateletsStabilizes fibrin; slows fibrinolysis

*Vitamin K required.

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Dưới đây là video và các luyện tập (practice) của bài này. Nghe là một kĩ năng khó, đặc biệt là khi chúng ta chưa quen nội dung và chưa có nhạy cảm ngôn ngữ. Nhưng cứ đi thật chậm và đừng bỏ cuộc.
Xem video và cảm nhận nội dung bài. Bạn có thể thả trôi, cảm nhận dòng chảy ngôn ngữ và không nhất thiết phải hiểu toàn bộ bài. Bên dưới là script để bạn khái quát nội dụng và tra từ mới.
  1. Hemostasis is the physiological process by which bleeding ceases.
  2. Hemostasis involves three basic steps: vascular spasm, the formation of a platelet plug, and coagulation.
  3. Coagulation occurs as clotting factors promote the formation of a fibrin clot.
  4. Fibrinolysis, on the other hand, is the process by which a clot is degraded in a healing vessel.
  5. Anticoagulants are substances that oppose coagulation.
  6. They are important in limiting the extent and duration of clotting.
  7. Inadequate clotting can result from too few platelets, or inadequate production of clotting factors, for instance, in the genetic disorder hemophilia.
  8. Excessive clotting, called thrombosis, can be caused by excessive numbers of platelets.
  9. A thrombus is a collection of fibrin, platelets, and erythrocytes that has accumulated along the lining of a blood vessel.
  10. Whereas an embolus is a thrombus that has broken free from the vessel wall and is circulating in the bloodstream.
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