BLOOD COAGULATION & HEMOSTASIS.pptx
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This document discusses the process of blood clot formation and prevention of blood loss. It describes that vascular constriction, platelet plug formation, and blood clotting close holes in veins. Platelets are formed from megakaryocytes, contain enzymes and glycoproteins, and adhere to collagen in damaged blood vessels to form platelet plugs. The clotting cascade involves the extrinsic and intrinsic pathways activating coagulation factors and converting prothrombin to thrombin and fibrinogen to fibrin to form a clot. Deficiencies in coagulation factors can cause bleeding disorders like hemophilia A, B, and C.
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Lymphocytes are spherical white blood cells that make up 20-45% of circulating white blood cells. They have a dark staining nucleus and thin rim of blue staining cytoplasm. Each lymphocyte recognizes a specific antigen. T lymphocytes can directly attack foreign cells, while B lymphocytes transform into plasma cells that secrete antibodies.
Hemostasis is the prevention of blood loss achieved through vascular constriction, formation of a platelet plug, and formation of a blood clot. When a blood vessel is cut, the smooth muscle contracts to reduce blood flow. Platelets aggregate at the site of injury to form a platelet plug. Blood coagulation involves the conversion of prothrombin to thrombin by prothrombin activ
Hemostasis rajiv kumar
Hemostasis is the biological process that controls bleeding at the site of injured blood vessels. It involves three key steps:
1) Platelet adhesion and activation forms a platelet plug to block blood loss.
2) Coagulation factors in the bloodstream form a fibrin clot over the platelet plug via the intrinsic and extrinsic pathways.
3) The fibrin clot is eventually dissolved by the fibrinolytic system to restore blood flow without risk of hemorrhage. Precise regulation of hemostasis maintains blood fluidity while enabling rapid clot formation in response to vessel injury.
Physiologulation
The document summarizes the physiology of blood coagulation, including the five main components (vessels, platelets, coagulation factors, inhibitors, fibrinolysis) and how they work together in a complex system. It describes platelet activation and aggregation to form a platelet plug, coagulation factors that amplify to form a fibrin mesh to strengthen the clot, and fibrinolysis to prevent excessive clotting and allow blood to flow again. A balance of these processes enables hemostasis to stop bleeding from injury while maintaining blood flow.
Physiologyof Coagulation
The document summarizes the physiology of blood coagulation, including the five main components (vessels, platelets, coagulation factors, inhibitors, fibrinolysis) and how they work together in a complex system. It describes platelet activation and aggregation to form a platelet plug, coagulation factors that amplify to form a fibrin mesh to strengthen the clot, and fibrinolysis to prevent excessive clotting and allow blood to flow again. A balance is needed between coagulation and anticoagulation/fibrinolysis to control clotting.
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The document summarizes the physiology of blood coagulation, including the five main components (vessels, platelets, coagulation factors, inhibitors, fibrinolysis) and how they work together in a complex system. It describes platelet activation and aggregation to form a platelet plug, followed by the coagulation cascade that forms a fibrin mesh to strengthen the clot. Fibrinolysis then acts to dissolve the clot once healing is complete to allow normal blood flow. The system is tightly regulated to balance clot formation and dissolution.
Hemostasis
Hemostasis is the process by which bleeding is stopped. It occurs via mechanical, chemical, and thermal means. Mechanical hemostasis involves direct pressure, gauze packing, and suturing or ligating cut blood vessels. Chemical hemostasis occurs via platelet plug formation and blood coagulation, while thermal hemostasis involves vasoconstriction to reduce blood flow to the site of injury. Together, these processes form a clot to seal the damaged vessel until tissue repair can take place.
Lecture 11 & 12 Clot
This document discusses platelets and the process of hemostasis. It notes that platelets form from megakaryocytes in the bone marrow, do not have nuclei, and play an important role in clotting. When platelets come into contact with collagen in damaged blood vessels, they swell, adhere to collagen, and secrete substances that activate nearby platelets, forming a platelet plug to stop bleeding. Blood coagulation further involves the conversion of prothrombin to thrombin and fibrinogen to fibrin fibers that trap platelets and blood cells to form a clot.
COAGULATION PROFILE.pptx
This document summarizes the process of hemostasis (blood clotting and dissolution). It discusses the key events in primary hemostasis involving platelet plug formation and secondary hemostasis involving the coagulation cascade and fibrin clot formation. It describes the clotting factors, coagulation pathways (extrinsic and intrinsic), and natural anticoagulants like heparin. Applied aspects such as causes of bleeding disorders and thromboembolic conditions are also covered at a high level.
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Hemostasis is the prevention of blood loss achieved through vascular constriction, formation of a platelet plug, and formation of a blood clot. When a blood vessel is cut, the smooth muscle contracts to reduce blood flow. Platelets aggregate at the site of injury to form a platelet plug. Blood coagulation involves the conversion of prothrombin to thrombin by prothrombin activ
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Hemostasis is the biological process that controls bleeding at the site of injured blood vessels. It involves three key steps:
1) Platelet adhesion and activation forms a platelet plug to block blood loss.
2) Coagulation factors in the bloodstream form a fibrin clot over the platelet plug via the intrinsic and extrinsic pathways.
3) The fibrin clot is eventually dissolved by the fibrinolytic system to restore blood flow without risk of hemorrhage. Precise regulation of hemostasis maintains blood fluidity while enabling rapid clot formation in response to vessel injury.
Physiologulation
The document summarizes the physiology of blood coagulation, including the five main components (vessels, platelets, coagulation factors, inhibitors, fibrinolysis) and how they work together in a complex system. It describes platelet activation and aggregation to form a platelet plug, coagulation factors that amplify to form a fibrin mesh to strengthen the clot, and fibrinolysis to prevent excessive clotting and allow blood to flow again. A balance of these processes enables hemostasis to stop bleeding from injury while maintaining blood flow.
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The document summarizes the physiology of blood coagulation, including the five main components (vessels, platelets, coagulation factors, inhibitors, fibrinolysis) and how they work together in a complex system. It describes platelet activation and aggregation to form a platelet plug, followed by the coagulation cascade that forms a fibrin mesh to strengthen the clot. Fibrinolysis then acts to dissolve the clot once healing is complete to allow normal blood flow. The system is tightly regulated to balance clot formation and dissolution.
Hemostasis
Hemostasis is the process by which bleeding is stopped. It occurs via mechanical, chemical, and thermal means. Mechanical hemostasis involves direct pressure, gauze packing, and suturing or ligating cut blood vessels. Chemical hemostasis occurs via platelet plug formation and blood coagulation, while thermal hemostasis involves vasoconstriction to reduce blood flow to the site of injury. Together, these processes form a clot to seal the damaged vessel until tissue repair can take place.
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This document discusses platelets and the process of hemostasis. It notes that platelets form from megakaryocytes in the bone marrow, do not have nuclei, and play an important role in clotting. When platelets come into contact with collagen in damaged blood vessels, they swell, adhere to collagen, and secrete substances that activate nearby platelets, forming a platelet plug to stop bleeding. Blood coagulation further involves the conversion of prothrombin to thrombin and fibrinogen to fibrin fibers that trap platelets and blood cells to form a clot.
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This document summarizes the process of hemostasis (blood clotting and dissolution). It discusses the key events in primary hemostasis involving platelet plug formation and secondary hemostasis involving the coagulation cascade and fibrin clot formation. It describes the clotting factors, coagulation pathways (extrinsic and intrinsic), and natural anticoagulants like heparin. Applied aspects such as causes of bleeding disorders and thromboembolic conditions are also covered at a high level.
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The document summarizes the process of blood clotting in three steps:
1) A complex cascade of chemical reactions forms prothrombin activator in response to blood vessel rupture or blood damage.
2) Prothrombin activator converts prothrombin into thrombin.
3) Thrombin converts fibrinogen into fibrin fibers that enmesh platelets and blood cells to form a clot.
platelets & hemostasis.pptx
This is the power point that explains about the blood and blood cells. Power point describes about the mechanism of coagulation and defense cells of our circulatory system.
Coagulation factors
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 .pptx
Platelets are disk-like cell fragments that originate from megakaryocytes and play a key role in hemostasis. When a blood vessel is damaged, platelets adhere to the site of injury and aggregate to form a platelet plug. This triggers the coagulation cascade, resulting in a fibrin clot that further strengthens the platelet plug. The clot then contracts through actin and myosin in the platelets. Over time, plasmin dissolves the clot through fibrinolysis, restoring blood flow in the vessel. A balance of pro-coagulant and anticoagulant factors normally maintains blood in a fluid state.
phsiology of blood coagulation by dr chandbaby ansari.pdf
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.
Platelets physiology
Hemostasis involves three key events to prevent blood loss from a ruptured blood vessel:
1) Vascular constriction occurs via pain signals and local vasoconstrictors to reduce blood flow.
2) Platelets form a plug by adhering to the ruptured vessel wall and releasing chemicals to activate more platelets.
3) A blood clot forms through the coagulation cascade, where thrombin converts fibrinogen to fibrin strands that reinforce the platelet plug. Together, the plug and clot seal the rupture.
Platelets physiology
Hemostasis is the prevention of blood loss from ruptured blood vessels. It involves three key events: 1) vascular constriction to reduce blood flow, 2) formation of a platelet plug to seal the rupture, and 3) formation of a blood clot through coagulation to reinforce the seal. Platelets adhere to collagen at the rupture site and aggregate, releasing chemicals to recruit more platelets until the plug is formed. Meanwhile, coagulation factors in the blood activate in a cascade, ultimately converting fibrinogen to fibrin fibers that strengthen the platelet plug and form a clot. The clot or plug then either organizes into fibrous tissue to permanently close the rupture or dissolves if no longer needed.
Platelets physiology
Hemostasis is the prevention of blood loss from ruptured blood vessels. It involves three key events: 1) vascular constriction to reduce blood flow, 2) formation of a platelet plug to seal the rupture, and 3) formation of a blood clot through coagulation to reinforce the seal. Platelets adhere to collagen at the rupture site and aggregate, releasing chemicals to recruit more platelets until the plug is formed. Meanwhile, coagulation factors in the blood activate in a cascade, ultimately converting fibrinogen to fibrin fibers that strengthen the platelet plug and form a clot. The clot or plug then either organizes into fibrous tissue to permanently close the rupture or dissolves if no longer needed.
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This document provides an overview of hemostasis (blood clotting). It discusses:
- The mechanisms of primary hemostasis mediated by platelets, including platelet adhesion, activation, release of granule contents, and aggregation.
- The process of secondary hemostasis (blood coagulation) mediated by coagulation proteins generating thrombin which converts fibrinogen to fibrin.
- Methods of achieving hemostasis including mechanical methods, electrosurgery, pharmacological agents, and topical hemostatic products.
platlets.pptx
1. Platelets are formed in the bone marrow from megakaryocytes and play a key role in hemostasis, the process of blood clotting.
2. When a blood vessel is injured, platelets adhere to the damaged vessel wall and release chemicals that attract more platelets to form a platelet plug.
3. The coagulation cascade is activated, involving clotting factors produced in the liver. This leads to the formation of a fibrin mesh that strengthens the platelet plug and forms a blood clot to seal the damaged vessel.
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The document describes the process of hemostasis, or stopping blood loss from damaged blood vessels. It occurs via vascular constriction, platelet plug formation, blood coagulation, and fibrous tissue growth. Blood coagulation involves the intrinsic and extrinsic pathways activating thrombin, which converts fibrinogen to fibrin to form a blood clot. The clot then retracts via platelets and fibroblasts may invade to permanently seal the break in the blood vessel.
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The document discusses hemostasis, the process by which bleeding is prevented after vascular injury. It describes the four main mechanisms: vasoconstriction, formation of a platelet plug, coagulation pathways, and fibrinolytic phase. Specifically, it details the roles of platelets, calcium ions, coagulation factors, fibrinogen and thrombin in forming a blood clot via the intrinsic and extrinsic coagulation pathways. It also discusses anticoagulants that prevent unnecessary clotting and plasmin which lyses blood clots.
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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.
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Platelets are cell fragments that help form blood clots to prevent or stop bleeding. They are produced through fragmentation of large bone marrow cells called megakaryocytes. Platelets contain granules with substances important for coagulation like fibrinogen and ADP. Platelets circulate freely but activate and aggregate at sites of injury to initiate clot formation through hemostasis, a process with 5 stages: vessel constriction, platelet plug formation, coagulation, clot retraction, and clot dissolution. Disorders can cause inappropriate clotting or bleeding due to problems with platelet or coagulation factor production, function, or clearance.
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This document discusses hemostasis, which is the biological process that controls bleeding at the site of injured blood vessels. It summarizes the key components and steps of hemostasis, including:
1. Vasoconstriction of injured blood vessels to reduce blood flow and platelet plug formation via adhesion and aggregation of platelets at the injury site.
2. Activation of the coagulation cascade through intrinsic and extrinsic pathways leading to thrombin generation and fibrin clot formation to strengthen the platelet plug.
3. Fibrinolysis by the plasminogen system which acts to dissolve clots when healing is complete to restore blood flow.
Normal haemostasis
This document discusses hemostasis, which is the biological process that controls bleeding at the site of injured blood vessels. It begins with an overview of hemostasis and its importance in maintaining blood fluidity and integrity of blood vessels. It then covers the components involved, including blood vessels, platelets, plasma coagulation factors, and the fibrinolytic system. The key stages and mechanisms of hemostasis are explained, including primary hemostasis mediated by platelets and secondary hemostasis involving the coagulation cascade and thrombin production. Inhibitors that regulate coagulation are also summarized.
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The document summarizes the process of blood clotting in three steps:
1) A complex cascade of chemical reactions forms prothrombin activator in response to blood vessel rupture or blood damage.
2) Prothrombin activator converts prothrombin into thrombin.
3) Thrombin converts fibrinogen into fibrin fibers that enmesh platelets and blood cells to form a clot.
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This is the power point that explains about the blood and blood cells. Power point describes about the mechanism of coagulation and defense cells of our circulatory system.
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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.
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Platelets are disk-like cell fragments that originate from megakaryocytes and play a key role in hemostasis. When a blood vessel is damaged, platelets adhere to the site of injury and aggregate to form a platelet plug. This triggers the coagulation cascade, resulting in a fibrin clot that further strengthens the platelet plug. The clot then contracts through actin and myosin in the platelets. Over time, plasmin dissolves the clot through fibrinolysis, restoring blood flow in the vessel. A balance of pro-coagulant and anticoagulant factors normally maintains blood in a fluid state.
phsiology of blood coagulation by dr chandbaby ansari.pdf
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.
Platelets physiology
Hemostasis involves three key events to prevent blood loss from a ruptured blood vessel:
1) Vascular constriction occurs via pain signals and local vasoconstrictors to reduce blood flow.
2) Platelets form a plug by adhering to the ruptured vessel wall and releasing chemicals to activate more platelets.
3) A blood clot forms through the coagulation cascade, where thrombin converts fibrinogen to fibrin strands that reinforce the platelet plug. Together, the plug and clot seal the rupture.
Platelets physiology
Hemostasis is the prevention of blood loss from ruptured blood vessels. It involves three key events: 1) vascular constriction to reduce blood flow, 2) formation of a platelet plug to seal the rupture, and 3) formation of a blood clot through coagulation to reinforce the seal. Platelets adhere to collagen at the rupture site and aggregate, releasing chemicals to recruit more platelets until the plug is formed. Meanwhile, coagulation factors in the blood activate in a cascade, ultimately converting fibrinogen to fibrin fibers that strengthen the platelet plug and form a clot. The clot or plug then either organizes into fibrous tissue to permanently close the rupture or dissolves if no longer needed.
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Hemostasis is the prevention of blood loss from ruptured blood vessels. It involves three key events: 1) vascular constriction to reduce blood flow, 2) formation of a platelet plug to seal the rupture, and 3) formation of a blood clot through coagulation to reinforce the seal. Platelets adhere to collagen at the rupture site and aggregate, releasing chemicals to recruit more platelets until the plug is formed. Meanwhile, coagulation factors in the blood activate in a cascade, ultimately converting fibrinogen to fibrin fibers that strengthen the platelet plug and form a clot. The clot or plug then either organizes into fibrous tissue to permanently close the rupture or dissolves if no longer needed.
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This document provides an overview of hemostasis (blood clotting). It discusses:
- The mechanisms of primary hemostasis mediated by platelets, including platelet adhesion, activation, release of granule contents, and aggregation.
- The process of secondary hemostasis (blood coagulation) mediated by coagulation proteins generating thrombin which converts fibrinogen to fibrin.
- Methods of achieving hemostasis including mechanical methods, electrosurgery, pharmacological agents, and topical hemostatic products.
platlets.pptx
1. Platelets are formed in the bone marrow from megakaryocytes and play a key role in hemostasis, the process of blood clotting.
2. When a blood vessel is injured, platelets adhere to the damaged vessel wall and release chemicals that attract more platelets to form a platelet plug.
3. The coagulation cascade is activated, involving clotting factors produced in the liver. This leads to the formation of a fibrin mesh that strengthens the platelet plug and forms a blood clot to seal the damaged vessel.
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The document describes the process of hemostasis, or stopping blood loss from damaged blood vessels. It occurs via vascular constriction, platelet plug formation, blood coagulation, and fibrous tissue growth. Blood coagulation involves the intrinsic and extrinsic pathways activating thrombin, which converts fibrinogen to fibrin to form a blood clot. The clot then retracts via platelets and fibroblasts may invade to permanently seal the break in the blood vessel.
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The document discusses hemostasis, the process by which bleeding is prevented after vascular injury. It describes the four main mechanisms: vasoconstriction, formation of a platelet plug, coagulation pathways, and fibrinolytic phase. Specifically, it details the roles of platelets, calcium ions, coagulation factors, fibrinogen and thrombin in forming a blood clot via the intrinsic and extrinsic coagulation pathways. It also discusses anticoagulants that prevent unnecessary clotting and plasmin which lyses blood clots.
Lecture 1 platelet and hemostasis
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.
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Platelets are cell fragments that help form blood clots to prevent or stop bleeding. They are produced through fragmentation of large bone marrow cells called megakaryocytes. Platelets contain granules with substances important for coagulation like fibrinogen and ADP. Platelets circulate freely but activate and aggregate at sites of injury to initiate clot formation through hemostasis, a process with 5 stages: vessel constriction, platelet plug formation, coagulation, clot retraction, and clot dissolution. Disorders can cause inappropriate clotting or bleeding due to problems with platelet or coagulation factor production, function, or clearance.
Normal haemostasis
This document discusses hemostasis, which is the biological process that controls bleeding at the site of injured blood vessels. It summarizes the key components and steps of hemostasis, including:
1. Vasoconstriction of injured blood vessels to reduce blood flow and platelet plug formation via adhesion and aggregation of platelets at the injury site.
2. Activation of the coagulation cascade through intrinsic and extrinsic pathways leading to thrombin generation and fibrin clot formation to strengthen the platelet plug.
3. Fibrinolysis by the plasminogen system which acts to dissolve clots when healing is complete to restore blood flow.
Normal haemostasis
This document discusses hemostasis, which is the biological process that controls bleeding at the site of injured blood vessels. It begins with an overview of hemostasis and its importance in maintaining blood fluidity and integrity of blood vessels. It then covers the components involved, including blood vessels, platelets, plasma coagulation factors, and the fibrinolytic system. The key stages and mechanisms of hemostasis are explained, including primary hemostasis mediated by platelets and secondary hemostasis involving the coagulation cascade and thrombin production. Inhibitors that regulate coagulation are also summarized.
Coagulation of blood and bleeding disorders
This presentation explains coagulation of blood and bleeding disorders, dental management of patient with bleeding disorders and bleeding gums
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Chapter wise All Notes of First year Basic Civil Engineering.pptx
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
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ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...
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Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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- 2. “Prevention of blood loss”
- 3. Vascular constriction Formation of platelet plug Blood clot formation Fibrous tissue organization to close the hole of veins.
- 4. Smooth muscle contraction to reduce blood flow after an injury or cut. 3 factors responsible for contraction. Nerve reflexes Autocoids from platelets or traumatized tissue Myogenic spasm
- 5. Thrombocytes Formed from megakaryocytes Anucleated 1,50000 – 300,000 / µl Actin myosin molecules & thrombosthenin Residual ER & golgi apparatus Enzyme system to synthesizeATP from ADP
- 6. Enzyme system to synthesize PGs. Fibrin stabilizing factor – form stable fibrin threads Growth factor Glycoprotein on surface Phospholipids Adenyl cyclase cAMP for further activation of platelets
- 7. Platelets in contact with collagen in damaged vessels Stick to collagen fibres Secretion of ADP & thromboxane A2 Increased number of activated platelets gathered to form platelet plug. Close small dents in vessel wall Fibrin threads
- 8. Clot – when blood looses its fluidity. Clot forms – 15 – 20 sec Activator substances – adheres to traumatized vessel Clot formed
- 11. CLOTTING FACTOR SYNONYMS Fibrinogen Factor I Prothrombin Factor II Tissue factor Factor III Calcium Factor IV Labile factor FactorV Accelerin FactorVII Antihemophillic factor FactorVIII Christmas factor Factor IX Stuart factor Factor X Plasma thromboplastin antecedent Factor XI Hageman factor Factor XII Fibrin stabilizing factor Factor XIII Prekallikrien Fletcher factor Kininogen HMWK
- 12. Clot Follows 2 ways. Invaded by fibroblasts Can be dissolved
- 13. Procoagulants Anticoagulants Formation of prothrombin activator Conversion of prothrombin to thrombin Conversion of fibrinogen to fibrin
- 14. Rate limiting step - formation of prothrombin activator. Calcium and prothrombin activator – convert prothrombin to thrombin Prothrombin – unstable protein Produced by liver Vitamin K – formation of prothrombin.
- 15. HMW high molecular weight Formed in liver Small leakage from capillary to interstitial fluid Pathological increase in permeability – abnormal coagulation. Thrombin form fibrin monomer. Thrombin – activation of fibrin stabilizing factor Covalent bond formation Formation of fibrin fibers
- 17. Extrinsic pathway Intrinsic pathway
- 18. Traumatized vessel release tissue factor . Factor III with factorVII act on factor X Factor Xa Factor Xa complexes with phospholipids & factorV . Prothrombin activator formed.
- 19. Trauma to blood or damage s platelets due to adherence to collagen. Activates factor XII. XIIa in presence of HMW kinogens & prekallikrien XI XIa IXa IXa +VIII Xa Xa + phospholipids +V prothrombin activator
- 21. Extraction of fluid after coagulation i.e. serum
- 22. Disseminated intravascular coagulation (DIC) Hemophilia Thrombocytopenia Purpura Thrombo embolic condition
- 23. HemophiliaA (VIII small component def.) Von willebrands disease (VIII large component def.) Hemophilia B (IX def) Hemophilia C (XI def.)