Hemostasis, bleeding, Shock.pptx
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Hemostasis is the complex process that limits blood loss from injured vessels. Blood coagulation tests help evaluate this process. Shock is defined as inadequate tissue perfusion resulting from failure to buffer against external forces, leading to organ and cellular dysfunction. The main types of shock are hypovolemic, cardiogenic, septic, neurogenic, traumatic, and obstructive shock.
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SHOCK
This document defines and classifies shock, discussing its pathogenesis and clinical features. It describes shock as a life-threatening condition characterized by reduced circulating blood volume and tissue perfusion. The document classifies shock into four main types - hypovolemic, cardiogenic, septic, and anaphylactic - and discusses their specific causes and pathophysiology. It also outlines the potential morbidities of shock including acute lung injury, kidney failure, liver dysfunction, and multi-organ failure.
Haemostasis
The document discusses the physiology of hemostasis, including:
- The essential components of hemostasis including platelet plug formation, coagulation pathways, and fibrinolysis.
- Conditions that can increase the risk of uncontrolled bleeding during surgery such as patient comorbidities, anticoagulant medications, hypothermia and acidosis.
- How achieving optimal hemostasis requires balancing procoagulant, anticoagulant, fibrinolytic and antifibrinolytic factors.
Introduction to Haemostasis
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.
Hemostasis and methods to control bleeding
The document discusses hemostasis and mechanisms of bleeding control. It describes how hemostasis involves vascular constriction, platelet plug formation, and blood clotting in response to vascular injury. Multiple mechanisms are involved in clot formation, including platelet adhesion and aggregation, thrombin conversion of fibrinogen to fibrin, and fibrin mesh contraction. A variety of techniques can be used to achieve hemostasis, including direct pressure, gauze packing, sutures, staples, cautery, and pharmacological agents.
Hemostasis
Hemostasis
Seminar Prepared by :-
Mohammed Saadi
Mohammed Musa
Hussein Jassam
Mahmoud Ahmed
Internal Medicine
College of Medicine - University of Kirkuk
CIRCULATORY DISTURBANCES OF OBSTRUCTIVE NATURE - THROMBOSIS
This document discusses thrombosis and thrombus formation. It defines thrombosis as the formation of a solid mass or thrombus in the circulation from blood components. It notes that thrombi can cause harmful effects like ischemic injury by decreasing blood flow or thromboembolism by breaking off and lodging in distant vessels. It describes the pathophysiology of thrombus formation including endothelial injury, altered blood flow, hypercoagulability, platelet activation, and coagulation system activation. It discusses different types of thrombi, their morphology, composition and distinguishing features. It also covers hypercoagulable states, causes of thrombosis, and the potential fates of thrombi.
Infarction
1) Infarction refers to the death of cells in a tissue due to an inadequate blood supply.
2) There are two main types of infarction - red and white - which are distinguished by their color and the type of tissue affected.
3) The development and severity of an infarction depends on factors like the anatomy of a tissue's blood supply, how quickly the blood flow is blocked, and the tissue's vulnerability to low oxygen levels.
CIRCULATORY DISTURBANCES OF OBSTRUCTIVE NATURE: THROMBOSIS
1. The document discusses hemodynamic disorders, thromboembolic disease, and shock. It covers topics such as thrombosis, thrombus formation, hypercoagulable states, and the fate of thrombi.
2. Thrombosis is the formation of a solid mass or thrombus in the circulatory system. Virchow's triad describes the key events in thrombus formation - endothelial injury, altered blood flow, and hypercoagulability.
3. Thrombus formation involves platelet activation at the site of injury, release of coagulation factors, and formation of a fibrin clot. Hypercoagulable states increase the risk of developing venous thrombosis.
Recommended
SHOCK
This document defines and classifies shock, discussing its pathogenesis and clinical features. It describes shock as a life-threatening condition characterized by reduced circulating blood volume and tissue perfusion. The document classifies shock into four main types - hypovolemic, cardiogenic, septic, and anaphylactic - and discusses their specific causes and pathophysiology. It also outlines the potential morbidities of shock including acute lung injury, kidney failure, liver dysfunction, and multi-organ failure.
Haemostasis
The document discusses the physiology of hemostasis, including:
- The essential components of hemostasis including platelet plug formation, coagulation pathways, and fibrinolysis.
- Conditions that can increase the risk of uncontrolled bleeding during surgery such as patient comorbidities, anticoagulant medications, hypothermia and acidosis.
- How achieving optimal hemostasis requires balancing procoagulant, anticoagulant, fibrinolytic and antifibrinolytic factors.
Introduction to Haemostasis
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.
Hemostasis and methods to control bleeding
The document discusses hemostasis and mechanisms of bleeding control. It describes how hemostasis involves vascular constriction, platelet plug formation, and blood clotting in response to vascular injury. Multiple mechanisms are involved in clot formation, including platelet adhesion and aggregation, thrombin conversion of fibrinogen to fibrin, and fibrin mesh contraction. A variety of techniques can be used to achieve hemostasis, including direct pressure, gauze packing, sutures, staples, cautery, and pharmacological agents.
Hemostasis
Hemostasis
Seminar Prepared by :-
Mohammed Saadi
Mohammed Musa
Hussein Jassam
Mahmoud Ahmed
Internal Medicine
College of Medicine - University of Kirkuk
CIRCULATORY DISTURBANCES OF OBSTRUCTIVE NATURE - THROMBOSIS
This document discusses thrombosis and thrombus formation. It defines thrombosis as the formation of a solid mass or thrombus in the circulation from blood components. It notes that thrombi can cause harmful effects like ischemic injury by decreasing blood flow or thromboembolism by breaking off and lodging in distant vessels. It describes the pathophysiology of thrombus formation including endothelial injury, altered blood flow, hypercoagulability, platelet activation, and coagulation system activation. It discusses different types of thrombi, their morphology, composition and distinguishing features. It also covers hypercoagulable states, causes of thrombosis, and the potential fates of thrombi.
Infarction
1) Infarction refers to the death of cells in a tissue due to an inadequate blood supply.
2) There are two main types of infarction - red and white - which are distinguished by their color and the type of tissue affected.
3) The development and severity of an infarction depends on factors like the anatomy of a tissue's blood supply, how quickly the blood flow is blocked, and the tissue's vulnerability to low oxygen levels.
CIRCULATORY DISTURBANCES OF OBSTRUCTIVE NATURE: THROMBOSIS
1. The document discusses hemodynamic disorders, thromboembolic disease, and shock. It covers topics such as thrombosis, thrombus formation, hypercoagulable states, and the fate of thrombi.
2. Thrombosis is the formation of a solid mass or thrombus in the circulatory system. Virchow's triad describes the key events in thrombus formation - endothelial injury, altered blood flow, and hypercoagulability.
3. Thrombus formation involves platelet activation at the site of injury, release of coagulation factors, and formation of a fibrin clot. Hypercoagulable states increase the risk of developing venous thrombosis.
hemostasis( coagulation)
Hemostasis is the regulated process that maintains blood in a liquid state within vessels but also forms clots to stop bleeding after vascular injury. It involves platelets, blood vessel walls, and coagulation/fibrinolytic systems. The hemostatic process begins with vasoconstriction and platelet plug formation before blood coagulation activates, forming fibrin to stabilize the platelet plug. Finally, fibrinolysis dissolves the clot. Tight regulation prevents inappropriate clotting within healthy vessels.
THROMBOSIS
Thrombosis is the formation of a blood clot or thrombus within a blood vessel. Virchow's triad describes the key factors that predispose to thrombosis: endothelial injury, altered blood flow, and hypercoagulability. Thrombosis occurs through platelet activation and aggregation, and activation of the coagulation cascade following vascular injury. Thrombi can cause ischemic injury by blocking blood flow or thromboembolism by dislodging and blocking vessels downstream. The fate of a thrombus includes resolution, organization, propagation or thromboembolism.
Mechanism of hemostasis copy
This document summarizes the mechanisms of hemostasis (prevention of blood loss), including vascular constriction, platelet plug formation, blood clot formation, and fibrinolysis. It describes the clotting factors and roles of calcium and platelets. Methods for controlling hemorrhage are discussed, including mechanical methods like direct pressure, ligation, and cauterization, as well as chemical/biological agents and radiological interventions. Supportive measures like fluid resuscitation and blood transfusion are also recommended.
Hemostasis of blood
Hemostasis is the process by which bleeding is stopped. It involves platelets, clotting factors, and the endothelium. When a blood vessel is injured, the processes of vascular constriction, platelet plug formation, fibrin formation, and fibrinolysis work together to form a blood clot. The extrinsic and intrinsic pathways activate coagulation factors that generate thrombin, which converts fibrinogen to fibrin to form the clot. Counterregulatory mechanisms then limit clotting and allow for clot resorption and tissue repair.
6.hemostasis
The document discusses management of intraoral bleeding during surgery. It covers hemostasis mechanisms, factors influencing surgical bleeding, adverse effects of bleeding, characteristics of ideal hemostatic agents, and various methods of hemostasis including mechanical, thermal, and chemical approaches. Common hemostatic agents discussed include adrenaline, bone wax, thrombin, gelfoam, and fibrin glue. Proper agent selection and application technique are important to control bleeding during oral surgery procedures.
Normal hemostasis
: Hemostasis is a complex process which causes the bleeding process to stop.
It refers to the process of keeping blood within a damaged blood vessel.
The endothelial cells of intact blood vessels prevent blood coagulation
Embolism
This document defines and describes different types of embolism. The most common type is thromboembolism, which occurs when a thrombus or part of a thrombus breaks off and is carried by the bloodstream. Pulmonary thromboembolism is a significant type that occurs when thrombi travel to the lungs and obstruct the pulmonary arteries. Other types include fat, air, gas and paradoxical embolisms. Air embolism can be venous, entering systemic veins during surgery or trauma, or arterial, entering the lungs during procedures like angiography. Decompression sickness is a form of gas embolism that affects divers or those exposed to changes in atmospheric pressure.
Hemostasis
Hemostasis is the process by which bleeding is stopped. It occurs in two steps: primary hemostasis involves platelet plug formation, while secondary hemostasis involves a blood clot forming due to coagulation. Platelets play a key role by adhering to damaged vessel walls, attracting more platelets to form a loose platelet plug which is strengthened when fibrin threads form during coagulation, constructing an unyielding plug. Coagulation is initiated through the intrinsic and extrinsic pathways which involve a cascade of coagulation factors ultimately forming thrombin to convert fibrinogen to fibrin for clot formation. Calcium ions are required for coagulation reactions to occur.
Thrombosis
Thrombosis is the formation of a blood clot or thrombus in the circulatory system. A thrombus forms when the normal balance between coagulation and fibrinolysis is disrupted, such as after an injury to the blood vessel wall. Virchow's triad describes the three main factors that contribute to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Thrombi can form in the heart, arteries, veins, or microcirculation and may cause complications like ischemic injury, thromboembolism, or organ infarction if left untreated. The fate of a thrombus depends on whether it is resolved by fibrinolysis, organized by the body, continues to grow, or embol
Lecture 10 (platelets and blood coagulations)
Hemostasis is the prevention of blood loss after an injury. It occurs through vascular constriction, platelet plug formation, blood coagulation, and fibrous tissue growth. Platelets are fragments of bone marrow cells that gather at injury sites. Coagulation involves activation of coagulation factors and the conversion of fibrinogen to fibrin fibers that trap platelets and cells to form clots. Clotting can lead to healing or dissolution. Conditions like vitamin K deficiency, hemophilia, or low platelets can cause excessive bleeding by interfering with coagulation factors or platelets. Blood thinners prevent harmful clots but increase bleeding risk. Tests assess coagulation times.
Bleeding and coagulation disorders hemostasis
1) Hemostasis is the process by which blood maintains its fluid state within vessels but also forms clots at sites of injury. It involves vasoconstriction, platelet plug formation, and coagulation cascade.
2) For blood not to clot normally in circulation, the endothelium prevents platelet adhesion, negatively charged particles repel clotting factors, circulation velocity must decrease for clotting, and natural anticoagulants and fibrinolysis are present.
3) Coagulation occurs through the intrinsic and extrinsic pathways activating prothrombin to thrombin which converts fibrinogen to fibrin threads forming a clot.
Management of intraoral bleeding
This document provides an overview of the management of intraoral bleeding. It begins with an introduction to blood and hemorrhage classification. It then discusses hemostasis, the coagulation cascade, laboratory tests for screening, and patient evaluation before surgery. The document covers local measures, drugs, dressings and other techniques for controlling bleeding, including ligation of vessels. It concludes with a discussion of the role of endothelium, platelets, and the coagulation cascade in normal hemostasis.
Local hemostatic agents(2)
(1) Hemostasis involves three synergistic factors - platelet plug formation, vasoconstriction, and fibrin clot formation. Secondary hemostasis specifically refers to the activation of the coagulation cascade and formation of a permanent fibrin plug.
(2) Surgical bleeding can be arterial, venous, or oozing and is influenced by patient factors like medications and coagulopathies as well as procedural factors. Excess bleeding can adversely impact the surgical field and patient.
(3) Methods to achieve hemostasis include mechanical methods like direct pressure, sutures and staples, and chemical methods like pharmacological agents and topical hemostatic agents. Topical agents can be passive, promoting cl
Embolism
1. Embolism occurs when a detached mass such as a blood clot, air bubble, or fat globule travels through the blood vessels and blocks circulation.
2. There are several types of embolism including pulmonary (lung), systemic, fat, marrow, air, and amniotic embolism.
3. Pulmonary embolism is a blockage in the pulmonary artery often caused by deep vein thrombosis, and it can lead to conditions like saddle embolism, paradoxical embolism, or cor pulmonale if left untreated.
Hemostasis
This document discusses hemostasis, the process by which bleeding is stopped. It describes the two main components: primary hemostasis involving platelet adhesion, aggregation, and plug formation; and secondary hemostasis where insoluble fibrin is generated through coagulation cascade reactions to strengthen the platelet plug. Key terms are defined, including hemostasis, thrombosis, hemorrhage, and coagulopathy. The roles of primary hemostasis, secondary hemostasis, the intrinsic pathway, extrinsic pathway, and common pathway in the coagulation cascade are explained.
Thrombosis
This document discusses thrombosis (blood clots) and its causes. There are three main factors that can lead to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Endothelial injury can result from physical trauma, infections, metabolic abnormalities, or high cholesterol. Changes in blood flow like stagnation can encourage clot formation. Hypercoagulability means an increased tendency to form clots, which can be primary issues with clotting factors or secondary causes like cancer, heart conditions, or prolonged bed rest. The document outlines many specific causes and consequences of thrombosis in greater detail.
thrombosis
This document discusses blood coagulation and thrombosis. It begins by defining coagulation as the process by which blood loses fluidity and becomes a jelly-like clot. It then describes the stages of clotting including formation of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin. The coagulation cascade and factors involved are also outlined. The document further discusses thrombosis, its causes including endothelial injury, alterations in blood flow, and hypercoagulability. Common sites of arterial and venous thrombi are compared. Oral health considerations and dental management of patients with bleeding disorders are summarized.
Hemostasis (COAGULATION)
INTRODUCTION TO HEMOSTASIS, PRIMARY AND SECONDARY HEMOSTASIS, LABORATORY TESTS THAT ASSESS PRIMARY HEMOSTASIS
Approach to bleeding
This document discusses the approach to evaluating and treating patients with bleeding disorders. It covers the basics of hemostasis, investigating the cause of bleeding through tests like coagulation studies and mixing tests, and treating bleeding through local measures, replacement therapy using blood components, or bypassing agents. The key is to determine if the bleeding is due to a platelet, vessel, or coagulation factor problem and then target replacement of the deficient component.
Pathology - Hemostasis
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.
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hemostasis( coagulation)
Hemostasis is the regulated process that maintains blood in a liquid state within vessels but also forms clots to stop bleeding after vascular injury. It involves platelets, blood vessel walls, and coagulation/fibrinolytic systems. The hemostatic process begins with vasoconstriction and platelet plug formation before blood coagulation activates, forming fibrin to stabilize the platelet plug. Finally, fibrinolysis dissolves the clot. Tight regulation prevents inappropriate clotting within healthy vessels.
THROMBOSIS
Thrombosis is the formation of a blood clot or thrombus within a blood vessel. Virchow's triad describes the key factors that predispose to thrombosis: endothelial injury, altered blood flow, and hypercoagulability. Thrombosis occurs through platelet activation and aggregation, and activation of the coagulation cascade following vascular injury. Thrombi can cause ischemic injury by blocking blood flow or thromboembolism by dislodging and blocking vessels downstream. The fate of a thrombus includes resolution, organization, propagation or thromboembolism.
Mechanism of hemostasis copy
This document summarizes the mechanisms of hemostasis (prevention of blood loss), including vascular constriction, platelet plug formation, blood clot formation, and fibrinolysis. It describes the clotting factors and roles of calcium and platelets. Methods for controlling hemorrhage are discussed, including mechanical methods like direct pressure, ligation, and cauterization, as well as chemical/biological agents and radiological interventions. Supportive measures like fluid resuscitation and blood transfusion are also recommended.
Hemostasis of blood
Hemostasis is the process by which bleeding is stopped. It involves platelets, clotting factors, and the endothelium. When a blood vessel is injured, the processes of vascular constriction, platelet plug formation, fibrin formation, and fibrinolysis work together to form a blood clot. The extrinsic and intrinsic pathways activate coagulation factors that generate thrombin, which converts fibrinogen to fibrin to form the clot. Counterregulatory mechanisms then limit clotting and allow for clot resorption and tissue repair.
6.hemostasis
The document discusses management of intraoral bleeding during surgery. It covers hemostasis mechanisms, factors influencing surgical bleeding, adverse effects of bleeding, characteristics of ideal hemostatic agents, and various methods of hemostasis including mechanical, thermal, and chemical approaches. Common hemostatic agents discussed include adrenaline, bone wax, thrombin, gelfoam, and fibrin glue. Proper agent selection and application technique are important to control bleeding during oral surgery procedures.
Normal hemostasis
: Hemostasis is a complex process which causes the bleeding process to stop.
It refers to the process of keeping blood within a damaged blood vessel.
The endothelial cells of intact blood vessels prevent blood coagulation
Embolism
This document defines and describes different types of embolism. The most common type is thromboembolism, which occurs when a thrombus or part of a thrombus breaks off and is carried by the bloodstream. Pulmonary thromboembolism is a significant type that occurs when thrombi travel to the lungs and obstruct the pulmonary arteries. Other types include fat, air, gas and paradoxical embolisms. Air embolism can be venous, entering systemic veins during surgery or trauma, or arterial, entering the lungs during procedures like angiography. Decompression sickness is a form of gas embolism that affects divers or those exposed to changes in atmospheric pressure.
Hemostasis
Hemostasis is the process by which bleeding is stopped. It occurs in two steps: primary hemostasis involves platelet plug formation, while secondary hemostasis involves a blood clot forming due to coagulation. Platelets play a key role by adhering to damaged vessel walls, attracting more platelets to form a loose platelet plug which is strengthened when fibrin threads form during coagulation, constructing an unyielding plug. Coagulation is initiated through the intrinsic and extrinsic pathways which involve a cascade of coagulation factors ultimately forming thrombin to convert fibrinogen to fibrin for clot formation. Calcium ions are required for coagulation reactions to occur.
Thrombosis
Thrombosis is the formation of a blood clot or thrombus in the circulatory system. A thrombus forms when the normal balance between coagulation and fibrinolysis is disrupted, such as after an injury to the blood vessel wall. Virchow's triad describes the three main factors that contribute to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Thrombi can form in the heart, arteries, veins, or microcirculation and may cause complications like ischemic injury, thromboembolism, or organ infarction if left untreated. The fate of a thrombus depends on whether it is resolved by fibrinolysis, organized by the body, continues to grow, or embol
Lecture 10 (platelets and blood coagulations)
Hemostasis is the prevention of blood loss after an injury. It occurs through vascular constriction, platelet plug formation, blood coagulation, and fibrous tissue growth. Platelets are fragments of bone marrow cells that gather at injury sites. Coagulation involves activation of coagulation factors and the conversion of fibrinogen to fibrin fibers that trap platelets and cells to form clots. Clotting can lead to healing or dissolution. Conditions like vitamin K deficiency, hemophilia, or low platelets can cause excessive bleeding by interfering with coagulation factors or platelets. Blood thinners prevent harmful clots but increase bleeding risk. Tests assess coagulation times.
Bleeding and coagulation disorders hemostasis
1) Hemostasis is the process by which blood maintains its fluid state within vessels but also forms clots at sites of injury. It involves vasoconstriction, platelet plug formation, and coagulation cascade.
2) For blood not to clot normally in circulation, the endothelium prevents platelet adhesion, negatively charged particles repel clotting factors, circulation velocity must decrease for clotting, and natural anticoagulants and fibrinolysis are present.
3) Coagulation occurs through the intrinsic and extrinsic pathways activating prothrombin to thrombin which converts fibrinogen to fibrin threads forming a clot.
Management of intraoral bleeding
This document provides an overview of the management of intraoral bleeding. It begins with an introduction to blood and hemorrhage classification. It then discusses hemostasis, the coagulation cascade, laboratory tests for screening, and patient evaluation before surgery. The document covers local measures, drugs, dressings and other techniques for controlling bleeding, including ligation of vessels. It concludes with a discussion of the role of endothelium, platelets, and the coagulation cascade in normal hemostasis.
Local hemostatic agents(2)
(1) Hemostasis involves three synergistic factors - platelet plug formation, vasoconstriction, and fibrin clot formation. Secondary hemostasis specifically refers to the activation of the coagulation cascade and formation of a permanent fibrin plug.
(2) Surgical bleeding can be arterial, venous, or oozing and is influenced by patient factors like medications and coagulopathies as well as procedural factors. Excess bleeding can adversely impact the surgical field and patient.
(3) Methods to achieve hemostasis include mechanical methods like direct pressure, sutures and staples, and chemical methods like pharmacological agents and topical hemostatic agents. Topical agents can be passive, promoting cl
Embolism
1. Embolism occurs when a detached mass such as a blood clot, air bubble, or fat globule travels through the blood vessels and blocks circulation.
2. There are several types of embolism including pulmonary (lung), systemic, fat, marrow, air, and amniotic embolism.
3. Pulmonary embolism is a blockage in the pulmonary artery often caused by deep vein thrombosis, and it can lead to conditions like saddle embolism, paradoxical embolism, or cor pulmonale if left untreated.
Hemostasis
This document discusses hemostasis, the process by which bleeding is stopped. It describes the two main components: primary hemostasis involving platelet adhesion, aggregation, and plug formation; and secondary hemostasis where insoluble fibrin is generated through coagulation cascade reactions to strengthen the platelet plug. Key terms are defined, including hemostasis, thrombosis, hemorrhage, and coagulopathy. The roles of primary hemostasis, secondary hemostasis, the intrinsic pathway, extrinsic pathway, and common pathway in the coagulation cascade are explained.
Thrombosis
This document discusses thrombosis (blood clots) and its causes. There are three main factors that can lead to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Endothelial injury can result from physical trauma, infections, metabolic abnormalities, or high cholesterol. Changes in blood flow like stagnation can encourage clot formation. Hypercoagulability means an increased tendency to form clots, which can be primary issues with clotting factors or secondary causes like cancer, heart conditions, or prolonged bed rest. The document outlines many specific causes and consequences of thrombosis in greater detail.
thrombosis
This document discusses blood coagulation and thrombosis. It begins by defining coagulation as the process by which blood loses fluidity and becomes a jelly-like clot. It then describes the stages of clotting including formation of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin. The coagulation cascade and factors involved are also outlined. The document further discusses thrombosis, its causes including endothelial injury, alterations in blood flow, and hypercoagulability. Common sites of arterial and venous thrombi are compared. Oral health considerations and dental management of patients with bleeding disorders are summarized.
Hemostasis (COAGULATION)
INTRODUCTION TO HEMOSTASIS, PRIMARY AND SECONDARY HEMOSTASIS, LABORATORY TESTS THAT ASSESS PRIMARY HEMOSTASIS
Approach to bleeding
This document discusses the approach to evaluating and treating patients with bleeding disorders. It covers the basics of hemostasis, investigating the cause of bleeding through tests like coagulation studies and mixing tests, and treating bleeding through local measures, replacement therapy using blood components, or bypassing agents. The key is to determine if the bleeding is due to a platelet, vessel, or coagulation factor problem and then target replacement of the deficient component.
Pathology - Hemostasis
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.
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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.
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