Coagulation or clotting is defined as the process in which blood loses its fluidity and becomes a jelly-like mass few minutes after it is shed out or collected in a container
This document summarizes blood coagulation and hemostasis. It discusses platelets, the platelet plug formation process, and the intrinsic and extrinsic pathways of blood coagulation. Disorders of coagulation covered include hemophilia A/B/C, von Willebrand disease, and purpura. Tests of hemostatic function like bleeding time, clotting time, and prothrombin time are also outlined. Anticoagulants like heparin and warfarin are briefly described.
Hemostasis is the process of preventing blood loss from broken blood vessels. It is achieved through three main mechanisms: vascular constriction, platelet plug formation, and blood coagulation. Vascular constriction occurs when smooth muscle contracts after vessel wall trauma. Platelets aggregate at the injury site to form a plug and provide clotting factors. Blood coagulation activates clotting factors through the extrinsic and intrinsic pathways, ultimately converting prothrombin to thrombin which converts fibrinogen to fibrin forming a clot. Clots are dissolved by plasmin which degrades fibrin, and several factors prevent excessive clotting.
the objectives from this ppt :-
1.Define haemostasis.
2.Describe the main mechanisms that prevent blood loss after an injury.
3.Describe role of platelets in haemostasis.
4.Outline the mechanism of platelet plug formation.
5.Describe the mechanisms of blood coagulation.
Diseases involving blood clotting factors can be inherited or acquired. The coagulation cascade involves several clotting factors that work together as enzymes to form a blood clot. Deficiencies or defects in these clotting factors can result in bleeding disorders. Some of the major clotting factor deficiencies include hemophilia A caused by factor VIII deficiency, hemophilia B caused by factor IX deficiency, von Willebrand disease caused by von Willebrand factor deficiency, and fibrinogen deficiencies that cause bleeding issues. Diagnostic tests evaluate clotting factor levels and clotting times. Treatment focuses on replacing the deficient clotting factor through blood products or concentrates.
This document summarizes blood coagulation and hemostasis. It discusses platelets, the platelet plug formation process, and the intrinsic and extrinsic pathways of blood coagulation. Disorders of coagulation covered include hemophilia A/B/C, von Willebrand disease, and purpura. Tests of hemostatic function like bleeding time, clotting time, and prothrombin time are also outlined. Anticoagulants like heparin and warfarin are briefly described.
Hemostasis is the process of preventing blood loss from broken blood vessels. It is achieved through three main mechanisms: vascular constriction, platelet plug formation, and blood coagulation. Vascular constriction occurs when smooth muscle contracts after vessel wall trauma. Platelets aggregate at the injury site to form a plug and provide clotting factors. Blood coagulation activates clotting factors through the extrinsic and intrinsic pathways, ultimately converting prothrombin to thrombin which converts fibrinogen to fibrin forming a clot. Clots are dissolved by plasmin which degrades fibrin, and several factors prevent excessive clotting.
the objectives from this ppt :-
1.Define haemostasis.
2.Describe the main mechanisms that prevent blood loss after an injury.
3.Describe role of platelets in haemostasis.
4.Outline the mechanism of platelet plug formation.
5.Describe the mechanisms of blood coagulation.
Diseases involving blood clotting factors can be inherited or acquired. The coagulation cascade involves several clotting factors that work together as enzymes to form a blood clot. Deficiencies or defects in these clotting factors can result in bleeding disorders. Some of the major clotting factor deficiencies include hemophilia A caused by factor VIII deficiency, hemophilia B caused by factor IX deficiency, von Willebrand disease caused by von Willebrand factor deficiency, and fibrinogen deficiencies that cause bleeding issues. Diagnostic tests evaluate clotting factor levels and clotting times. Treatment focuses on replacing the deficient clotting factor through blood products or concentrates.
This document discusses coagulation factors and blood clotting. It defines coagulation as the process where blood loses fluidity and forms a jelly-like clot. Thirteen coagulation factors are involved in a cascade of reactions to form a clot. The cascade involves the formation of prothrombin activator through the intrinsic and extrinsic pathways, followed by the conversion of prothrombin to thrombin and fibrinogen to fibrin. Deficiencies in specific factors can cause bleeding disorders like hemophilia. The clot then undergoes retraction and may be broken down through fibrinolysis.
Hemostasis occurs in three stages: vasoconstriction, platelet plug formation, and blood coagulation. Vasoconstriction decreases blood flow from damaged vessels. Platelets adhere to collagen at injury sites, forming a temporary platelet plug. Coagulation involves thrombin converting fibrinogen to fibrin, forming fibrin threads that strengthen the platelet plug and complete hemostasis. Blood coagulation is initiated through intrinsic and extrinsic pathways activating a cascade of clotting factors that ultimately generate thrombin. Thrombin then converts fibrinogen to fibrin to form a blood clot.
Blood Coagulation and Clotting Mechanism.pptxFarazaJaved
The document summarizes the process of blood coagulation. It discusses that coagulation occurs through a series of reactions activating clotting factors, which convert fibrinogen into fibrin forming a mesh that traps blood cells. The stages are formation of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin. Anticoagulants like heparin and warfarin prevent clotting by various mechanisms. Tests are used to detect disorders that cause excessive or insufficient clotting.
Plasma is the liquid component of blood that holds the blood cells in suspension. It makes up 55% of the blood's total volume and is mostly composed of water (92%) and dissolved proteins (8%). Plasma carries nutrients, hormones, carbon dioxide, and oxygen to tissues and transports waste products away from tissues. It plays a vital role in maintaining electrolyte balance and protects the body from infection. Plasma is separated from blood cells when a tube of blood is spun in a centrifuge.
Platelets are cell fragments produced by megakaryocytes in the bone marrow that help the body form blood clots to stop bleeding. They have no nucleus and an average lifespan of 8-9 days. Platelets attach to damaged blood vessel walls and release chemicals that attract more platelets to form a hemostatic plug to stop bleeding. Low platelet counts can cause excessive bleeding while high counts have few symptoms. Platelet counts are regulated by thrombopoietin and can be affected by disease, medications, and lifestyle factors.
The blood coagulation cascade involves three mechanisms to stop bleeding when blood vessels are damaged: vascular spasm, platelet plug formation, and blood clotting. Blood clotting is a complex series of enzymatic reactions that results in the formation of fibrin threads that trap blood cells to form a clot. There are two pathways - the intrinsic and extrinsic pathways - that activate clotting factors and ultimately convert prothrombin to thrombin which converts fibrinogen to fibrin. Anticoagulants like heparin and coumarins are used to delay the coagulation process in thromboembolic conditions.
This document discusses the structure, composition, functions, formation and lifespan of platelets. It provides details on platelets, including that they are the smallest blood cells, lack a nucleus, and function in hemostasis through adhesion, aggregation and clot formation. Platelets are formed from megakaryocytes in the bone marrow, have a lifespan of 8-12 days, and are destroyed by macrophages in the spleen.
Platelets play a key role in hemostasis through adhesion, activation, and aggregation at the site of vascular injury to form a platelet plug. The coagulation cascade then forms a blood clot through a series of coagulation factor activations. This process is regulated by anti-coagulation mechanisms including thrombomodulin and the fibrinolytic system. Abnormalities can cause excessive bleeding from issues like thrombocytopenia or vitamin K deficiency, or excessive clotting from conditions like deep vein thrombosis. Laboratory tests evaluate platelet count and function as well as coagulation factor levels.
The document summarizes the steps in blood coagulation (hemostasis). It involves platelets attaching to exposed collagen and releasing chemical signals that attract more platelets to form a platelet plug. The coagulation cascade then involves 12 clotting factors in a series of proteolytic reactions through the extrinsic and intrinsic pathways to ultimately form prothrombinase. Prothrombinase converts prothrombin to thrombin, which then converts fibrinogen to fibrin to form a clot in the common pathway. The clot is eventually dissolved by the enzyme plasmin through fibrinolysis.
Blood coagulation, also known as hemostasis, is the process by which blood changes from a liquid to a solid gel-like substance. It involves three stages: vasoconstriction, formation of a platelet plug, and coagulation of blood. When a blood vessel is injured, a series of reactions are initiated through the intrinsic and extrinsic pathways, ultimately resulting in a cross-linked fibrin mesh that traps blood cells to form a clot. Coagulation is tightly regulated by several mechanisms to prevent excessive clotting. Deficiencies or defects in the coagulation cascade can result in bleeding disorders.
The document discusses coagulation, hemostasis, and various bleeding disorders. It covers the process of coagulation including platelet adhesion, activation, and aggregation. It also discusses factors that promote coagulation as well as anticoagulant factors. Various bleeding disorders are described such as abnormalities of blood vessels, coagulation factors, platelets, and disseminated intravascular coagulation. Laboratory tests for evaluating coagulation are also mentioned.
This document discusses fibrinolysis, the process by which fibrin clots are broken down. It notes that plasminogen is activated to form plasmin, the main enzyme that degrades fibrin clots. Plasminogen activators such as tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) activate plasminogen on fibrin clot surfaces. Fibrin degradation products are formed that provide markers of fibrinolysis and inhibit thrombin. The process is regulated by inhibitors such as plasminogen activator inhibitor-1.
Hemostasis involves three main mechanisms: (1) vascular constriction to reduce blood flow from damaged vessels, (2) formation of a platelet plug to physically block blood loss from small cuts, and (3) formation of a blood clot through coagulation to seal larger vessel openings. Coagulation is initiated through both the intrinsic pathway, triggered by blood contact with exposed collagen, and the extrinsic pathway, triggered by tissue factor released from damaged cells. A complex cascade of coagulation factor activations ultimately leads to the generation of thrombin which converts fibrinogen to fibrin to form a clot.
Blood clotting is a process called coagulation where blood changes from a liquid to a solid gel-like state. It occurs through a cascade of biochemical reactions involving multiple clotting factors. Initially fibrinogen is converted to fibrin, which forms a mesh that entangles blood cells. Then the clot undergoes further changes to strengthen it. Precise regulation of coagulation prevents clotting inside healthy blood vessels but allows it to occur when vessels are damaged.
When blood is shed, it loses fluidity and forms a jelly-like clot within minutes through the coagulation process. Coagulation is important physiologically as it prevents further hemorrhaging by plugging bleeding vessels. Clotting occurs through a series of reactions involving prothrombin activators and factors in the intrinsic and extrinsic pathways. Deficiencies in factors like fibrinogen, prothrombin, or antihemophilic factor can cause bleeding disorders. Anticoagulants prevent coagulation and are used therapeutically or in blood banks.
I. Coagulation involves the transformation of blood from a liquid to a gel through a series of clotting factor reactions, forming a clot to prevent blood loss from injured vessels.
II. Coagulation occurs through the intrinsic and extrinsic pathways simultaneously. The extrinsic pathway is initiated by tissue injury while the intrinsic pathway is initiated by blood contact with collagen from an injured vessel.
III. Both pathways involve the formation of prothrombin activator which converts prothrombin to thrombin. Thrombin then catalyzes the conversion of fibrinogen to fibrin to form a mesh that traps platelets and cells, creating a clot and achieving hemostasis.
This document discusses erythropoiesis, the process of red blood cell formation. It covers the sites of hematopoiesis, blood cell precursors, the stages of erythropoiesis from pronormoblast to reticulocyte, and the factors that regulate and are necessary for erythropoiesis. Key factors discussed include erythropoietin, which stimulates red blood cell production; vitamin B12 and folic acid, which are required for DNA synthesis and cell maturation; and intrinsic factor, which is needed for vitamin B12 absorption.
The document summarizes blood clotting (coagulation). It identifies that there are 13 clotting factors involved in the process by which blood loses fluid and forms a jelly-like clot after leaving the body. The key steps are: 1) formation of a prothrombin activator, 2) conversion of prothrombin to thrombin, and 3) conversion of fibrinogen to fibrin to form the clot. The clotting factors work together in a cascade through positive feedback loops to activate thrombin and fibrinogen in the clotting process.
This document provides an introduction to haemostasis by Dr. Ibrahim Khider. It defines haemostasis as the process of stopping blood flow following injury to a blood vessel. There are three components involved - the extravascular tissues, blood vessels, and intravascular platelets and plasma proteins. Haemostasis occurs through primary, secondary, and tertiary processes. Primary haemostasis involves platelets forming a platelet plug at the site of injury within 3-5 minutes. Secondary haemostasis reinforces this plug with a fibrin clot formed from plasma coagulation factors, taking 5-10 minutes. Tertiary haemostasis involves fibrinolysis to remove the clot as healing occurs over 48-72 hours.
Blood coagulation is the process by which blood changes from a liquid to a gel-like mass. It involves several coagulation factors and occurs in three stages: formation of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin. The resulting blood clot traps platelets, red blood cells, and white blood cells. Over time, the clot retracts as platelets contract. Fibrinolysis then breaks down the clot. Coagulation ensures wounds are sealed but can become problematic if clots form inside blood vessels.
This document summarizes hemostasis, the process by which bleeding is stopped. It discusses the three components of hemostasis - extravascular, vascular, and intravascular. The normal hemostasis process involves platelet plug formation and fibrin clot formation via the coagulation cascade. Coagulation factors, platelets, and fibrinogen are involved. Hemostasis is balanced by natural anticoagulants. Genetic or acquired bleeding disorders can result from deficiencies in specific coagulation factors or platelets. Common disorders discussed include hemophilia A/B/C and von Willebrand disease.
This document discusses coagulation factors and blood clotting. It defines coagulation as the process where blood loses fluidity and forms a jelly-like clot. Thirteen coagulation factors are involved in a cascade of reactions to form a clot. The cascade involves the formation of prothrombin activator through the intrinsic and extrinsic pathways, followed by the conversion of prothrombin to thrombin and fibrinogen to fibrin. Deficiencies in specific factors can cause bleeding disorders like hemophilia. The clot then undergoes retraction and may be broken down through fibrinolysis.
Hemostasis occurs in three stages: vasoconstriction, platelet plug formation, and blood coagulation. Vasoconstriction decreases blood flow from damaged vessels. Platelets adhere to collagen at injury sites, forming a temporary platelet plug. Coagulation involves thrombin converting fibrinogen to fibrin, forming fibrin threads that strengthen the platelet plug and complete hemostasis. Blood coagulation is initiated through intrinsic and extrinsic pathways activating a cascade of clotting factors that ultimately generate thrombin. Thrombin then converts fibrinogen to fibrin to form a blood clot.
Blood Coagulation and Clotting Mechanism.pptxFarazaJaved
The document summarizes the process of blood coagulation. It discusses that coagulation occurs through a series of reactions activating clotting factors, which convert fibrinogen into fibrin forming a mesh that traps blood cells. The stages are formation of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin. Anticoagulants like heparin and warfarin prevent clotting by various mechanisms. Tests are used to detect disorders that cause excessive or insufficient clotting.
Plasma is the liquid component of blood that holds the blood cells in suspension. It makes up 55% of the blood's total volume and is mostly composed of water (92%) and dissolved proteins (8%). Plasma carries nutrients, hormones, carbon dioxide, and oxygen to tissues and transports waste products away from tissues. It plays a vital role in maintaining electrolyte balance and protects the body from infection. Plasma is separated from blood cells when a tube of blood is spun in a centrifuge.
Platelets are cell fragments produced by megakaryocytes in the bone marrow that help the body form blood clots to stop bleeding. They have no nucleus and an average lifespan of 8-9 days. Platelets attach to damaged blood vessel walls and release chemicals that attract more platelets to form a hemostatic plug to stop bleeding. Low platelet counts can cause excessive bleeding while high counts have few symptoms. Platelet counts are regulated by thrombopoietin and can be affected by disease, medications, and lifestyle factors.
The blood coagulation cascade involves three mechanisms to stop bleeding when blood vessels are damaged: vascular spasm, platelet plug formation, and blood clotting. Blood clotting is a complex series of enzymatic reactions that results in the formation of fibrin threads that trap blood cells to form a clot. There are two pathways - the intrinsic and extrinsic pathways - that activate clotting factors and ultimately convert prothrombin to thrombin which converts fibrinogen to fibrin. Anticoagulants like heparin and coumarins are used to delay the coagulation process in thromboembolic conditions.
This document discusses the structure, composition, functions, formation and lifespan of platelets. It provides details on platelets, including that they are the smallest blood cells, lack a nucleus, and function in hemostasis through adhesion, aggregation and clot formation. Platelets are formed from megakaryocytes in the bone marrow, have a lifespan of 8-12 days, and are destroyed by macrophages in the spleen.
Platelets play a key role in hemostasis through adhesion, activation, and aggregation at the site of vascular injury to form a platelet plug. The coagulation cascade then forms a blood clot through a series of coagulation factor activations. This process is regulated by anti-coagulation mechanisms including thrombomodulin and the fibrinolytic system. Abnormalities can cause excessive bleeding from issues like thrombocytopenia or vitamin K deficiency, or excessive clotting from conditions like deep vein thrombosis. Laboratory tests evaluate platelet count and function as well as coagulation factor levels.
The document summarizes the steps in blood coagulation (hemostasis). It involves platelets attaching to exposed collagen and releasing chemical signals that attract more platelets to form a platelet plug. The coagulation cascade then involves 12 clotting factors in a series of proteolytic reactions through the extrinsic and intrinsic pathways to ultimately form prothrombinase. Prothrombinase converts prothrombin to thrombin, which then converts fibrinogen to fibrin to form a clot in the common pathway. The clot is eventually dissolved by the enzyme plasmin through fibrinolysis.
Blood coagulation, also known as hemostasis, is the process by which blood changes from a liquid to a solid gel-like substance. It involves three stages: vasoconstriction, formation of a platelet plug, and coagulation of blood. When a blood vessel is injured, a series of reactions are initiated through the intrinsic and extrinsic pathways, ultimately resulting in a cross-linked fibrin mesh that traps blood cells to form a clot. Coagulation is tightly regulated by several mechanisms to prevent excessive clotting. Deficiencies or defects in the coagulation cascade can result in bleeding disorders.
The document discusses coagulation, hemostasis, and various bleeding disorders. It covers the process of coagulation including platelet adhesion, activation, and aggregation. It also discusses factors that promote coagulation as well as anticoagulant factors. Various bleeding disorders are described such as abnormalities of blood vessels, coagulation factors, platelets, and disseminated intravascular coagulation. Laboratory tests for evaluating coagulation are also mentioned.
This document discusses fibrinolysis, the process by which fibrin clots are broken down. It notes that plasminogen is activated to form plasmin, the main enzyme that degrades fibrin clots. Plasminogen activators such as tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) activate plasminogen on fibrin clot surfaces. Fibrin degradation products are formed that provide markers of fibrinolysis and inhibit thrombin. The process is regulated by inhibitors such as plasminogen activator inhibitor-1.
Hemostasis involves three main mechanisms: (1) vascular constriction to reduce blood flow from damaged vessels, (2) formation of a platelet plug to physically block blood loss from small cuts, and (3) formation of a blood clot through coagulation to seal larger vessel openings. Coagulation is initiated through both the intrinsic pathway, triggered by blood contact with exposed collagen, and the extrinsic pathway, triggered by tissue factor released from damaged cells. A complex cascade of coagulation factor activations ultimately leads to the generation of thrombin which converts fibrinogen to fibrin to form a clot.
Blood clotting is a process called coagulation where blood changes from a liquid to a solid gel-like state. It occurs through a cascade of biochemical reactions involving multiple clotting factors. Initially fibrinogen is converted to fibrin, which forms a mesh that entangles blood cells. Then the clot undergoes further changes to strengthen it. Precise regulation of coagulation prevents clotting inside healthy blood vessels but allows it to occur when vessels are damaged.
When blood is shed, it loses fluidity and forms a jelly-like clot within minutes through the coagulation process. Coagulation is important physiologically as it prevents further hemorrhaging by plugging bleeding vessels. Clotting occurs through a series of reactions involving prothrombin activators and factors in the intrinsic and extrinsic pathways. Deficiencies in factors like fibrinogen, prothrombin, or antihemophilic factor can cause bleeding disorders. Anticoagulants prevent coagulation and are used therapeutically or in blood banks.
I. Coagulation involves the transformation of blood from a liquid to a gel through a series of clotting factor reactions, forming a clot to prevent blood loss from injured vessels.
II. Coagulation occurs through the intrinsic and extrinsic pathways simultaneously. The extrinsic pathway is initiated by tissue injury while the intrinsic pathway is initiated by blood contact with collagen from an injured vessel.
III. Both pathways involve the formation of prothrombin activator which converts prothrombin to thrombin. Thrombin then catalyzes the conversion of fibrinogen to fibrin to form a mesh that traps platelets and cells, creating a clot and achieving hemostasis.
This document discusses erythropoiesis, the process of red blood cell formation. It covers the sites of hematopoiesis, blood cell precursors, the stages of erythropoiesis from pronormoblast to reticulocyte, and the factors that regulate and are necessary for erythropoiesis. Key factors discussed include erythropoietin, which stimulates red blood cell production; vitamin B12 and folic acid, which are required for DNA synthesis and cell maturation; and intrinsic factor, which is needed for vitamin B12 absorption.
The document summarizes blood clotting (coagulation). It identifies that there are 13 clotting factors involved in the process by which blood loses fluid and forms a jelly-like clot after leaving the body. The key steps are: 1) formation of a prothrombin activator, 2) conversion of prothrombin to thrombin, and 3) conversion of fibrinogen to fibrin to form the clot. The clotting factors work together in a cascade through positive feedback loops to activate thrombin and fibrinogen in the clotting process.
This document provides an introduction to haemostasis by Dr. Ibrahim Khider. It defines haemostasis as the process of stopping blood flow following injury to a blood vessel. There are three components involved - the extravascular tissues, blood vessels, and intravascular platelets and plasma proteins. Haemostasis occurs through primary, secondary, and tertiary processes. Primary haemostasis involves platelets forming a platelet plug at the site of injury within 3-5 minutes. Secondary haemostasis reinforces this plug with a fibrin clot formed from plasma coagulation factors, taking 5-10 minutes. Tertiary haemostasis involves fibrinolysis to remove the clot as healing occurs over 48-72 hours.
Blood coagulation is the process by which blood changes from a liquid to a gel-like mass. It involves several coagulation factors and occurs in three stages: formation of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin. The resulting blood clot traps platelets, red blood cells, and white blood cells. Over time, the clot retracts as platelets contract. Fibrinolysis then breaks down the clot. Coagulation ensures wounds are sealed but can become problematic if clots form inside blood vessels.
This document summarizes hemostasis, the process by which bleeding is stopped. It discusses the three components of hemostasis - extravascular, vascular, and intravascular. The normal hemostasis process involves platelet plug formation and fibrin clot formation via the coagulation cascade. Coagulation factors, platelets, and fibrinogen are involved. Hemostasis is balanced by natural anticoagulants. Genetic or acquired bleeding disorders can result from deficiencies in specific coagulation factors or platelets. Common disorders discussed include hemophilia A/B/C and von Willebrand disease.
The document summarizes the process of blood coagulation. It discusses that coagulation occurs through a series of reactions activating clotting factors, which leads to the formation of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin. Anticoagulants like heparin, warfarin, and citrates prevent coagulation by various mechanisms such as inhibiting thrombin or removing calcium from blood. Bleeding disorders occur when there are deficiencies in specific clotting factors.
This document discusses hemostasis in surgical patients. It begins by defining hemostasis as the state of fluid equilibrium within blood vessels. It then describes the two mechanisms of hemostasis - primary hemostasis involving vasoconstriction and platelet plug formation, and secondary hemostasis involving activation of the coagulation cascade and formation of a fibrin clot. The document outlines the coagulation cascade and its natural inhibitors. It discusses various defects of hemostasis, preoperative screening tests for bleeding risk, and strategies to achieve surgical hemostasis including direct pressure, cauterization, packing, topical hemostats, and fibrin glue.
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The document summarizes key aspects of haemostasis, the physiological process that stops bleeding from damaged blood vessels. It describes how haemostasis involves vascular constriction, platelet plug formation, and blood coagulation. Platelets, clotting factors in plasma, and vessel walls interact to seal leaks in blood vessels. Precise regulation of haemostasis is important for homeostasis, and excessive bleeding can result in death if not stopped.
phsiology of blood coagulation by dr chandbaby ansari.pdfAlfiaAnsari2
Hemostasis occurs in three stages: vasoconstriction, platelet plug formation, and coagulation. During vasoconstriction, blood vessels constrict to decrease blood loss. Platelets then adhere to collagen at the injury site and form a temporary platelet plug. Finally, fibrin threads form and attach to the platelet plug, blocking blood loss completely. Coagulation disorders like hemophilia can result from deficiencies in specific clotting factors and cause prolonged bleeding.
Hemostasis and coagulation of blood For M.Sc & Basic Medical Students by Pand...Pandian M
Blood coagulation
Mechanism of coagulation
STAGES OF HEMOSTASIS
Coagulation of blood
Factors involved in blood clotting
Enzyme cascade theory
Mechanisms for formation of prothrombin activator
Fibrinolysis
Anticlotting mechanism in the body
Applied physiology
The document discusses various blood disorders that affect red blood cells, including different types of anemia. It describes iron-deficiency anemia, which can be caused by low iron intake or blood loss. Anemia of chronic disease is common in people with kidney disease or other chronic illnesses. Pernicious anemia results from a vitamin B12 deficiency due to problems absorbing the vitamin. Aplastic anemia occurs when the bone marrow does not produce enough red blood cells or other blood cells.
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Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Hemostasis is the process by which bleeding is stopped. It involves three main mechanisms:
1. Vasoconstriction of blood vessels to reduce blood flow through the damaged vessel.
2. Formation of a platelet plug at the site of injury through platelet adhesion, activation, and aggregation. Chemicals released by platelets attract more platelets to form a temporary plug.
3. Coagulation cascade where prothrombin is converted to thrombin which then converts fibrinogen to fibrin, forming a mesh that strengthens the platelet plug.
Over time fibrin is broken down by plasmin in a process called fibrinolysis to remove the clot from the blood vessel. Together these processes
Coagulants and anticoagulants are used to control bleeding and clotting. Coagulants promote clotting while anticoagulants prevent clotting. Coagulants include thrombin and thromboplastin, which can be applied locally to control oozing of blood from small vessels. Transfusional coagulants include specific clotting factors administered to replace deficient factors. Nontransfusional coagulants include vitamin K, which is necessary for the production of several clotting factors in the liver.
This document discusses haemostasis and the mechanisms of blood coagulation. It describes that haemostasis occurs via 5 mechanisms: 1) vasoconstriction, 2) formation of a platelet plug, 3) formation of a blood clot through fibrin deposition, 4) clot retraction, and 5) repair of the damaged blood vessel. The coagulation cascade involves both the intrinsic and extrinsic pathways ultimately leading to thrombin activation and fibrin clot formation. Factors that affect coagulation include temperature, vessel damage, calcium levels, vitamin K, and anticoagulants like heparin and dicumarol. Disorders of haemostasis include purpura and haemophilia.
This document summarizes information about blood coagulation, blood groups, and related topics. It discusses hemostasis, the three stages of coagulation (formation of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin). It also describes blood clotting factors, tests for blood clotting like prothrombin time, and bleeding disorders like hemophilia. Additionally, it covers blood grouping systems like ABO and Rh, and provides guidance on dental management of patients with bleeding disorders.
The document discusses blood coagulation and factors involved. It explains that coagulation depends on a balance between procoagulant and anticoagulant factors. The intrinsic and extrinsic pathways activate thrombin which converts fibrinogen to fibrin to form a blood clot meshwork. Coagulation factors I through XIII are involved. Conditions that can cause excessive bleeding include vitamin K deficiency, hemophilia, and thrombocytopenia.
This document summarizes the process of hemostasis and coagulation. It begins with definitions of key terms like hemostasis, coagulation, and thrombosis. It then describes the three stages of hemostasis - vasoconstriction, platelet plug formation, and blood clot formation. The roles of platelets, thromboxane A2, and fibrin in coagulation are explained. Finally, it provides an overview of the intrinsic and extrinsic coagulation pathways and the role of calcium and vitamin K in blood clotting.
Blood coagulation cascade. Brief outline of blood clotting cascade with information on tests. Over view for medical laboratory scientist program and for ASCP certification test
Spleen, thymus Organs of the Lymphatic System Amen Ullah
The lymphatic system has both primary and secondary organs. The primary organs, where lymphocytes are generated, include the bone marrow and thymus gland. The bone marrow produces B lymphocytes and plasma cells, while the thymus gland helps mature T lymphocytes. The secondary organs, where adaptive immune responses are initiated, include the lymph nodes, spleen, and other mucosa-associated lymphatic tissues like Peyer's patches and tonsils. The spleen filters the blood and removes old red blood cells, bacteria, and foreign matter. The thymus gland plays a key role in developing T lymphocytes from childhood through adolescence.
Nervous control of blood vessels regulation of arterial pressureAmen Ullah
The main function of the circulatory system is to give local blood flow to the tissue. There arespecial need of the tissue which is:
delivery of oxygen to the tissue
delivery of nutrients to the tissue
removal of carbon dioxide from tissue
maintaining of normal concentration of ions
transform of hormones and other substance to tissue
The study of movement of blood through circulatory system.
cardiovascular system is Responsible for to pump the blood and to circulate it through different parts of the body.
It is essential for the maintenance of pressure and other physical factors within the blood vessels
Lymphatic system, Human Lymphatic systemAmen Ullah
Tissue fluid (interstitial fluid) that enters the lymphatic vessels.
larger particles that escape into tissue fluid can only be removed via lymphatic system.
Immunity is defined as the capacity of the body to resist pathogenic agents.
It is the ability of body to resist the entry of different types of foreign bodies like bacteria, virus, toxic substances, etc.
Humoral immunity is defined as the immunity mediated by antibodies, which are secreted by B lymphocytes.
B lymphocytes secrete the antibodies into the blood and lymph
Hemo: Referring to blood cells
Poiesis: “The development or production of”
The word Hemopoiesis refers to the production & development of all the blood cells
Factors responsible for erythropoiesis. Development and maturation of erythrocytes require mostly three types of factors
1. General factors 2. Maturation factors 3. Factors necessary for hemoglobin formation.
Cell-mediated immunity involves T lymphocytes, macrophages, and natural killer cells. It provides defense against viruses, fungi, and some bacteria through these cells, without involving antibodies. When antigens from invading microbes are presented on antigen-presenting cells like macrophages and dendritic cells, helper T cells are activated and stimulate cytotoxic T cells and B cells. Cytotoxic T cells then directly attack and destroy infected cells. Memory T cells also enhance future immune responses. Overall, cell-mediated immunity protects against intracellular pathogens through cellular immune responses.
Cardiac murmur is an abnormal heart sounds. can be heard with stethoscope or auscultation. the etiology of the cardiac murmur may be septal defect, valvular defects or vascular defects. the two main causes that lead to cardiac murmur, like stenosis and incompetence.
Arrhythmia is also known as irregular heart beats. If SA node is not the pacemaker, any other part of the heart such as atrial muscle, AV node and ventricular muscle becomes the pacemaker. the beats may be fast, slow or miss beats.
Blood (erythrocytes, leukocytes and platelets)Amen Ullah
Blood is a connective tissue composed of formed elements suspended in plasma. It functions to transport oxygen, nutrients, waste, hormones and more throughout the body. Blood is slightly alkaline with a pH between 7.35-7.45. It contains red blood cells which carry oxygen, white blood cells which protect against infection, platelets which help with clotting, and plasma which transports proteins, electrolytes and other substances. The composition and functions of these blood components were described in detail in the document.
Term and Definitions regarding microbiology, Pathogenicity and virulency, acute and chronic infection, primary and secondary infection, opportunistic infection.
This document discusses safe handling procedures for various chemicals commonly used in medical settings, including disinfectants, methyl methacrylate bone cement, chemotherapy drugs, and cytotoxic agents. It notes that gloves and eye protection should be worn when using disinfectants and other irritating chemicals. For methyl methacrylate, it recommends mixing it just before use with scavenging systems to collect vapors, as the vapors can be irritating and toxic. For chemotherapy drugs and other pharmaceuticals, it advises preparing and administering them carefully to minimize unnecessary exposures, and outlines specific procedures for intraperitoneal chemotherapy. Basic guidelines are provided for safely handling cytotoxic agents, including containment, protective equipment, washing hands after contact, and inc
The peripheral nervous system connects the central nervous system to the limbs and organs. It consists of the somatic nervous system, which controls voluntary movement, and the autonomic nervous system, which regulates involuntary functions. The autonomic nervous system has two divisions - the sympathetic nervous system, which activates the fight or flight response, and the parasympathetic nervous system, which promotes rest and digestion. Together these systems allow the nervous system to control and coordinate the body's activities.
Are you looking for a long-lasting solution to your missing tooth?
Dental implants are the most common type of method for replacing the missing tooth. Unlike dentures or bridges, implants are surgically placed in the jawbone. In layman’s terms, a dental implant is similar to the natural root of the tooth. It offers a stable foundation for the artificial tooth giving it the look, feel, and function similar to the natural tooth.
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
DECLARATION OF HELSINKI - History and principlesanaghabharat01
This SlideShare presentation provides a comprehensive overview of the Declaration of Helsinki, a foundational document outlining ethical guidelines for conducting medical research involving human subjects.
low birth weight presentation. Low birth weight (LBW) infant is defined as the one whose birth weight is less than 2500g irrespective of their gestational age. Premature birth and low birth weight(LBW) is still a serious problem in newborn. Causing high morbidity and mortality rate worldwide. The nursing care provide to low birth weight babies is crucial in promoting their overall health and development. Through careful assessment, diagnosis,, planning, and evaluation plays a vital role in ensuring these vulnerable infants receive the specialize care they need. In India every third of the infant weight less than 2500g.
Birth period, socioeconomical status, nutritional and intrauterine environment are the factors influencing low birth weight
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Co-Chairs, Val J. Lowe, MD, and Cyrus A. Raji, MD, PhD, prepared useful Practice Aids pertaining to Alzheimer’s disease for this CME/AAPA activity titled “Alzheimer’s Disease Case Conference: Gearing Up for the Expanding Role of Neuroradiology in Diagnosis and Treatment.” For the full presentation, downloadable Practice Aids, and complete CME/AAPA information, and to apply for credit, please visit us at https://bit.ly/3PvVY25. CME/AAPA credit will be available until June 28, 2025.
2. Coagulation
Coagulation or clotting is defined as the
process in which blood loses its fluidity and
becomes a jelly-like mass few minutes after it
is shed out or collected in a container.
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3. Factors involved in Blood Clotting
Factor I Fibrinogen
Factor II Prothrombin
Factor III Thromboplastin
(Tissue factor)
Factor IV Calcium
Factor V Labile factor
(Proaccelerin or accelerator
globulin)
Factor VI Presence has not
been proved
Factor VII Stable factor
Factor VIII Antihemophilic
factor (Antihemophilic
globulin)
Factor IX Christmas factor
Factor X Stuart-Prower
factor
Factor XI Plasma
thromboplastin antecedent
Factor XII Hageman factor
(Contact factor)
Factor XIII Fibrin-stabilizing
factor (Fibrinase).
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4. Stages of Blood Clotting
In general, blood clotting occurs in three
stages:
1. Formation of prothrombin activator
2. Conversion of prothrombin into thrombin
3. Conversion of fibrinogen into fibrin
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5. STAGE 1: Formation of Prothrombin
Activator
Thus, formation of prothrombin activator
occurs through two pathways:
i. Intrinsic pathway
ii. Extrinsic pathway.
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8. Blood Clot
Blood clot is defined as the mass of coagulated blood
which contains RBCs, WBCs and platelets entrapped in
fibrin meshwork. RBCs and WBCs are not necessary for
clotting process.
However, when clot is formed, these cells are trapped
in it along with platelets.
The trapped RBCs are responsible for the red color of
the clot.
The external blood clot is also called scab. It adheres
to the opening of damaged blood vessel and prevents
blood loss
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9. Clot Retraction
The process involving the contraction of blood
clot and oozing of serum is called clot
retraction (30-40 mints after).
Contractile proteins, namely actin, myosin and
thrombosthenin in the cytoplasm of platelets
are responsible for clot retraction
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10. Fibrinolysis
Lysis of blood clot inside the blood vessel is
called fibrinolysis.
It helps to remove the clot from lumen of the
blood vessel.
This process requires a substance called
plasmin or fibrinolysin.
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11. Anticoagulants
Substances which prevent or postpone
coagulation of blood are called anticoagulants.
1. Heparin
2. Coumarin Derivatives
3. EDTA
4. Oxalate Compounds
5. Citrates
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12. Thrombosis
Thrombosis or intravascular blood clotting refers to
coagulation of blood inside the blood vessels.
Normally, blood does not clot in the blood vessel because
of some factors which are already explained.
But some abnormal conditions cause thrombosis.
Causes of Thrombosis
1. Injury to blood vessels
2. Roughened endothelial lining
3. Sluggishness of blood flow
4. Agglutination of RBCs
5. Toxic thrombosis
6. Congenital absence of protein C
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13. Complications of Thrombosis
1. Thrombus
2. Embolism and embolus
3. Ischemia
4. Necrosis and infarction
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14. BLEEDING DISORDERS
Bleeding disorders are the conditions
characterized by
prolonged bleeding time or clotting time.
Bleeding disorders are of three types:
1. Hemophilia.
2. Purpura.
3. von Willebrand disease
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