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.
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 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.
Dr. Radhwan Hazem Alkhashab discusses coagulation disorders and hemostasis. Normal hemostasis requires a balance between procoagulant and anticoagulant pathways. Coagulation studies are used to evaluate abnormal bleeding/thrombosis, assist with anticoagulation management, and help with massive transfusion resuscitation. The physiology of hemostasis involves platelets, vascular endothelium, and coagulation factors. Damage exposes tissue which activates platelets and coagulation pathways to form clots. Inherited bleeding disorders include von Willebrand disease and hemophilia A/B.
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.
Coagulant & AntiCoagulant Haemostasis (arrest of blood loss) and blood coagulation involve complex interaction between the injury vessel wall, platelets and coagulation factors
PC of Blood and Blood forming agents.pdfRAMDAS BHAT
This document provides an overview of drugs acting on blood and blood forming agents. It discusses coagulants that promote coagulation like calcium salts and vitamin K. It also discusses anticoagulants that prevent coagulation, including heparin, low molecular weight heparins, direct thrombin inhibitors, factor Xa inhibitors, and vitamin K antagonists like warfarin. The document provides details on the mechanisms of coagulation, platelet function, fibrinolysis, and conditions requiring treatment with coagulants or anticoagulants.
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.
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.
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 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.
Dr. Radhwan Hazem Alkhashab discusses coagulation disorders and hemostasis. Normal hemostasis requires a balance between procoagulant and anticoagulant pathways. Coagulation studies are used to evaluate abnormal bleeding/thrombosis, assist with anticoagulation management, and help with massive transfusion resuscitation. The physiology of hemostasis involves platelets, vascular endothelium, and coagulation factors. Damage exposes tissue which activates platelets and coagulation pathways to form clots. Inherited bleeding disorders include von Willebrand disease and hemophilia A/B.
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.
Coagulant & AntiCoagulant Haemostasis (arrest of blood loss) and blood coagulation involve complex interaction between the injury vessel wall, platelets and coagulation factors
PC of Blood and Blood forming agents.pdfRAMDAS BHAT
This document provides an overview of drugs acting on blood and blood forming agents. It discusses coagulants that promote coagulation like calcium salts and vitamin K. It also discusses anticoagulants that prevent coagulation, including heparin, low molecular weight heparins, direct thrombin inhibitors, factor Xa inhibitors, and vitamin K antagonists like warfarin. The document provides details on the mechanisms of coagulation, platelet function, fibrinolysis, and conditions requiring treatment with coagulants or anticoagulants.
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.
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.
The seminar presentation covered hemostasis and approaches to bleeding disorders in pediatrics. It discussed the pathophysiology, clinical features, laboratory findings and management of idiopathic thrombocytopenic purpura, Von Willebrand's disease, and hemophilia. It provided an overview of hemostasis and the coagulation cascade, approaches to evaluating a child with bleeding, and specifics on selected bleeding disorders. The presentation included descriptions of laboratory tests used to evaluate coagulation factors and identify bleeding disorders.
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.
The document discusses coagulation and disseminated intravascular coagulation (DIC). It begins by explaining the three stages of hemostasis: vascular spasm, primary hemostasis involving platelet plug formation, and secondary hemostasis involving fibrin strand formation. It then details the coagulation cascade and its four phases: initiation, amplification, propagation, and clot stabilization. The document concludes by covering the causes, mechanisms, clinical manifestations, diagnosis, differential diagnosis, and treatment of DIC.
Introduction-to-Blood-Coagulation2
Blood coagulation, also known as clotting, is a crucial process that prevents excessive bleeding when a blood vessel is injured. Let me break it down for you:
Primary Hemostasis:
The initial stage involves blood vessel constriction (vasoconstriction) and platelet aggregation at the site of vessel injury. Platelets are small blood cells that play a key role in clot formation.
When a blood vessel is damaged, platelets adhere to the exposed collagen fibers in the vessel wall, forming a temporary plug.
Secondary Hemostasis (Coagulation):
This stage is where the actual clotting process occurs.
Coagulation factors, which are proteins in the blood, interact to form a stable clot. There are 13 principal coagulation factors (designated with Roman numerals I to XIII).
Coagulation can be initiated through two separate pathways:
Extrinsic Pathway:
Activated in response to a protein called tissue factor, which is expressed by cells external to blood vessels.
Tissue factor activates factor VII, leading to a cascade of reactions that ultimately produce factor X.
Intrinsic Pathway:
Activated by injury within a blood vessel.
Begins with the activation of factor XII (Hageman factor) when blood circulates over injured internal vessel surfaces.
Components of the intrinsic pathway can also be activated by the extrinsic pathway.
Both pathways converge to produce factor X, which marks the beginning of the common pathway of coagulation.
Factor X then leads to the formation of a fibrin clot, which stabilizes the platelet plug.
Fibrin is a protein that forms a mesh-like structure, trapping blood cells and reinforcing the clot12.
#deepaayu #samglobaluniversity #SAMGlobalUniversity #Blood
Hemostasis is the arrest of bleeding from an injured blood vessel. It occurs naturally through vasoconstriction, platelet plug formation, and coagulation cascades, but can also be controlled surgically. The body forms a clot to stop bleeding but also uses fibrinolysis to prevent excessive clotting. Hemostasis can be evaluated through history, exam, and lab tests like platelet count, prothrombin time, and partial thromboplastin time to check primary and secondary hemostasis.
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
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.
Blood coagulation is a complex process involving multiple coagulation factors that work together in a cascade to ultimately convert fibrinogen into fibrin to form a blood clot. There are two pathways (intrinsic and extrinsic) that lead to the formation of thrombin, which then converts fibrinogen into fibrin. Some bleeding disorders result from deficiencies in specific coagulation factors, such as Hemophilia A and B due to Factor VIII and IX deficiencies. Von Willebrand disease is caused by a defect in von Willebrand factor which is involved in platelet function. Coagulation tests evaluate different parts of the coagulation cascade to identify deficiencies.
Bleeding disorders are caused by abnormalities in hemostasis and coagulation, characterized by spontaneous or trauma-induced skin or mucosal bleeding from capillaries. The process of hemostasis involves platelet plug formation and coagulation reactions resulting in fibrin formation to stop bleeding. Disorders can involve abnormalities of platelets, blood vessels, or coagulation factors, leading to excessive bleeding from sites like the skin, joints, muscles or body cavities. Diagnosis involves tests like aPTT, PT, and platelet counts to assess the coagulation pathways and pinpoint the cause of bleeding.
Bleeding disorders are caused by abnormalities in hemostasis and coagulation, characterized by skin or mucous membrane bleeding from small blood vessels. The bleeding is usually spontaneous or from minor trauma. Hemostasis involves platelet plug formation and the coagulation cascade, which produces fibrin. Testing such as aPTT, PT, fibrinogen levels, and platelet counts are used to assess coagulation function and identify the cause of bleeding disorders. Treatment depends on the underlying cause, such as replacing deficient clotting factors.
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.
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.
This document discusses hemostasis, the process by which bleeding is stopped. It describes the three main stages of hemostasis: vasoconstriction, platelet plug formation, and blood clotting. When a blood vessel is injured, vasoconstriction occurs to reduce blood loss. Then, platelets adhere to the injury site and aggregate to form a temporary platelet plug. Finally, fibrin threads are produced and attach to the platelet plug to completely seal the break in the blood vessel. The coagulation cascade involves multiple clotting factors that activate one another in a chain reaction to ultimately produce a fibrin clot.
The document summarizes the clotting mechanism and anticoagulants. It describes how hemostasis involves primary hemostasis through platelet plug formation and secondary hemostasis via the coagulation cascade. The coagulation cascade consists of the intrinsic and extrinsic pathways that converge at the activation of factor X and lead to thrombin generation and fibrin clot formation. Anticoagulants like heparin and warfarin inhibit factors in the coagulation cascade. Laboratory tests are used to evaluate hemostasis and identify deficiencies.
The document discusses recent advances in antithrombotic therapy. It describes the components of thrombus, types of thrombosis, and pathological conditions like stroke and myocardial infarction. Newer antithrombotic agents discussed include direct factor Xa inhibitors, tissue factor inhibitors, and platelet receptor antagonists. These target specific coagulation factors, platelet activation pathways, and inflammation to reduce thrombus formation. However, traditional agents like heparin, coumarins and aspirin remain standard treatments due to side effects and costs of newer drugs. Continued research is needed to develop safer, more effective antithrombotics.
The document discusses recent advances in antithrombotic therapy. It describes the components of thrombus, types of thrombosis, and pathological conditions like stroke and myocardial infarction. Newer antithrombotic agents discussed include direct factor Xa inhibitors, tissue factor inhibitors, and platelet P-selectin inhibitors. These target specific components of the coagulation cascade and inflammatory processes in thrombosis. While promising, currently no single new agent has replaced standards like heparin, warfarin, and aspirin due to limitations like side effects or cost. Continued research is needed to develop safer, more effective antithrombotic drugs.
The document discusses recent advances in antithrombotic therapy. It describes the components of thrombus, types of thrombosis, and pathological conditions like stroke and myocardial infarction. Newer antithrombotic agents discussed include direct factor Xa inhibitors, tissue factor inhibitors, and platelet inhibitors that target receptors like P-selectin, GPVI collagen receptor, and ADP receptors. While these new agents show promise, conventional treatments like heparin, coumarins and aspirin remain standard of care due to side effects and costs of newer therapies. Continued research is needed to develop safer, more effective antithrombotic drugs.
This document provides an overview of basic wound closure and knot tying techniques. It discusses common suture materials including absorbable, non-absorbable, natural, synthetic, monofilament and multifilament sutures. It also reviews wound closure techniques such as simple, mattress and subcuticular sutures. Finally, it demonstrates how to tie a basic two-hand square knot for wound closure.
The seminar presentation covered hemostasis and approaches to bleeding disorders in pediatrics. It discussed the pathophysiology, clinical features, laboratory findings and management of idiopathic thrombocytopenic purpura, Von Willebrand's disease, and hemophilia. It provided an overview of hemostasis and the coagulation cascade, approaches to evaluating a child with bleeding, and specifics on selected bleeding disorders. The presentation included descriptions of laboratory tests used to evaluate coagulation factors and identify bleeding disorders.
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.
The document discusses coagulation and disseminated intravascular coagulation (DIC). It begins by explaining the three stages of hemostasis: vascular spasm, primary hemostasis involving platelet plug formation, and secondary hemostasis involving fibrin strand formation. It then details the coagulation cascade and its four phases: initiation, amplification, propagation, and clot stabilization. The document concludes by covering the causes, mechanisms, clinical manifestations, diagnosis, differential diagnosis, and treatment of DIC.
Introduction-to-Blood-Coagulation2
Blood coagulation, also known as clotting, is a crucial process that prevents excessive bleeding when a blood vessel is injured. Let me break it down for you:
Primary Hemostasis:
The initial stage involves blood vessel constriction (vasoconstriction) and platelet aggregation at the site of vessel injury. Platelets are small blood cells that play a key role in clot formation.
When a blood vessel is damaged, platelets adhere to the exposed collagen fibers in the vessel wall, forming a temporary plug.
Secondary Hemostasis (Coagulation):
This stage is where the actual clotting process occurs.
Coagulation factors, which are proteins in the blood, interact to form a stable clot. There are 13 principal coagulation factors (designated with Roman numerals I to XIII).
Coagulation can be initiated through two separate pathways:
Extrinsic Pathway:
Activated in response to a protein called tissue factor, which is expressed by cells external to blood vessels.
Tissue factor activates factor VII, leading to a cascade of reactions that ultimately produce factor X.
Intrinsic Pathway:
Activated by injury within a blood vessel.
Begins with the activation of factor XII (Hageman factor) when blood circulates over injured internal vessel surfaces.
Components of the intrinsic pathway can also be activated by the extrinsic pathway.
Both pathways converge to produce factor X, which marks the beginning of the common pathway of coagulation.
Factor X then leads to the formation of a fibrin clot, which stabilizes the platelet plug.
Fibrin is a protein that forms a mesh-like structure, trapping blood cells and reinforcing the clot12.
#deepaayu #samglobaluniversity #SAMGlobalUniversity #Blood
Hemostasis is the arrest of bleeding from an injured blood vessel. It occurs naturally through vasoconstriction, platelet plug formation, and coagulation cascades, but can also be controlled surgically. The body forms a clot to stop bleeding but also uses fibrinolysis to prevent excessive clotting. Hemostasis can be evaluated through history, exam, and lab tests like platelet count, prothrombin time, and partial thromboplastin time to check primary and secondary hemostasis.
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
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.
Blood coagulation is a complex process involving multiple coagulation factors that work together in a cascade to ultimately convert fibrinogen into fibrin to form a blood clot. There are two pathways (intrinsic and extrinsic) that lead to the formation of thrombin, which then converts fibrinogen into fibrin. Some bleeding disorders result from deficiencies in specific coagulation factors, such as Hemophilia A and B due to Factor VIII and IX deficiencies. Von Willebrand disease is caused by a defect in von Willebrand factor which is involved in platelet function. Coagulation tests evaluate different parts of the coagulation cascade to identify deficiencies.
Bleeding disorders are caused by abnormalities in hemostasis and coagulation, characterized by spontaneous or trauma-induced skin or mucosal bleeding from capillaries. The process of hemostasis involves platelet plug formation and coagulation reactions resulting in fibrin formation to stop bleeding. Disorders can involve abnormalities of platelets, blood vessels, or coagulation factors, leading to excessive bleeding from sites like the skin, joints, muscles or body cavities. Diagnosis involves tests like aPTT, PT, and platelet counts to assess the coagulation pathways and pinpoint the cause of bleeding.
Bleeding disorders are caused by abnormalities in hemostasis and coagulation, characterized by skin or mucous membrane bleeding from small blood vessels. The bleeding is usually spontaneous or from minor trauma. Hemostasis involves platelet plug formation and the coagulation cascade, which produces fibrin. Testing such as aPTT, PT, fibrinogen levels, and platelet counts are used to assess coagulation function and identify the cause of bleeding disorders. Treatment depends on the underlying cause, such as replacing deficient clotting factors.
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.
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.
This document discusses hemostasis, the process by which bleeding is stopped. It describes the three main stages of hemostasis: vasoconstriction, platelet plug formation, and blood clotting. When a blood vessel is injured, vasoconstriction occurs to reduce blood loss. Then, platelets adhere to the injury site and aggregate to form a temporary platelet plug. Finally, fibrin threads are produced and attach to the platelet plug to completely seal the break in the blood vessel. The coagulation cascade involves multiple clotting factors that activate one another in a chain reaction to ultimately produce a fibrin clot.
The document summarizes the clotting mechanism and anticoagulants. It describes how hemostasis involves primary hemostasis through platelet plug formation and secondary hemostasis via the coagulation cascade. The coagulation cascade consists of the intrinsic and extrinsic pathways that converge at the activation of factor X and lead to thrombin generation and fibrin clot formation. Anticoagulants like heparin and warfarin inhibit factors in the coagulation cascade. Laboratory tests are used to evaluate hemostasis and identify deficiencies.
The document discusses recent advances in antithrombotic therapy. It describes the components of thrombus, types of thrombosis, and pathological conditions like stroke and myocardial infarction. Newer antithrombotic agents discussed include direct factor Xa inhibitors, tissue factor inhibitors, and platelet receptor antagonists. These target specific coagulation factors, platelet activation pathways, and inflammation to reduce thrombus formation. However, traditional agents like heparin, coumarins and aspirin remain standard treatments due to side effects and costs of newer drugs. Continued research is needed to develop safer, more effective antithrombotics.
The document discusses recent advances in antithrombotic therapy. It describes the components of thrombus, types of thrombosis, and pathological conditions like stroke and myocardial infarction. Newer antithrombotic agents discussed include direct factor Xa inhibitors, tissue factor inhibitors, and platelet P-selectin inhibitors. These target specific components of the coagulation cascade and inflammatory processes in thrombosis. While promising, currently no single new agent has replaced standards like heparin, warfarin, and aspirin due to limitations like side effects or cost. Continued research is needed to develop safer, more effective antithrombotic drugs.
The document discusses recent advances in antithrombotic therapy. It describes the components of thrombus, types of thrombosis, and pathological conditions like stroke and myocardial infarction. Newer antithrombotic agents discussed include direct factor Xa inhibitors, tissue factor inhibitors, and platelet inhibitors that target receptors like P-selectin, GPVI collagen receptor, and ADP receptors. While these new agents show promise, conventional treatments like heparin, coumarins and aspirin remain standard of care due to side effects and costs of newer therapies. Continued research is needed to develop safer, more effective antithrombotic drugs.
This document provides an overview of basic wound closure and knot tying techniques. It discusses common suture materials including absorbable, non-absorbable, natural, synthetic, monofilament and multifilament sutures. It also reviews wound closure techniques such as simple, mattress and subcuticular sutures. Finally, it demonstrates how to tie a basic two-hand square knot for wound closure.
This document discusses antepartum haemorrhage (APH), defined as bleeding from the genital tract between 28 weeks of pregnancy and onset of labor. The main causes of APH discussed are placenta praevia, placental abruption, local causes, and undetermined origin. Placenta praevia is when the placenta implants in the lower uterine segment, and is classified into four grades based on how close it is to the cervix. Placental abruption is the premature separation of a normally implanted placenta, which can lead to hemorrhage, fetal hypoxia, and maternal shock. Management of placenta praevia and abruption focus on early delivery, usually by
Postpartum haemorrhage is a leading cause of maternal mortality. It is defined as bleeding over 500ml after childbirth. The main causes are an atonic uterus, retained placenta or tissue, and tears. Risk factors include advanced maternal age, previous bleeding, and multiple gestation. Rapid evaluation and treatment is critical to prevent shock. Initial management includes IV fluids, uterotonic drugs, massage, and identifying the cause. For an atonic uterus, oxytocin is first-line treatment followed by ergometrine or misoprostol if needed. For retained placenta, controlled cord traction and manual removal are attempted. Secondary PPH occurs after 24 hours and is usually due to infection.
The document discusses congenital anomalies (birth defects) that can occur during fetal development. It defines congenital anomalies as structural abnormalities present at birth, which can be caused by genetic factors like chromosomal abnormalities or gene mutations, or environmental factors like infections, radiation, chemicals, and maternal diseases during pregnancy. The most common types of abnormalities are malformations affecting organ formation, disruptions of formed structures, and deformations from mechanical forces. Prenatal screening techniques like ultrasound and tests of maternal serum can detect some anomalies, while invasive tests on amniotic fluid or placenta like amniocentesis or CVS allow for chromosomal analysis. Fetal therapy during pregnancy may help treat some conditions.
Atropine sulfate is a medication used to treat nerve agent and pesticide poisonings, slow heart rates, and decrease saliva production during surgery. It works by blocking the effects of acetylcholine in the nervous system. Atropine sulfate is available in injection, tablet, ophthalmic ointment, and ophthalmic solution forms. It can be administered through the mouth, intravenously, intramuscularly, or rectally. Adverse effects include dry mouth, blurred vision, increased heart rate, and difficulty urinating. Nurses monitor patients for side effects and educate them on proper administration and storage of atropine sulfate.
Lipoma is the most common soft tissue tumor arising from yellow fat. It presents as a mobile, lobular mass that is non-tender and has a semi-fluctuant consistency. On examination, the mass can slip under the examining fingers, known as the "slip sign". Lipomas most commonly occur just under the skin, but can also develop in various deep locations like intermuscularly, intra-articularly, or retroperitoneally. While lipomas are usually benign and can be excised with clear margins, liposarcomas are rare malignant versions that require wide excision and potentially adjuvant therapies.
This document discusses hypertension, including its definition, causes, types, pathophysiology, clinical manifestations, and management. It defines hypertension as a persistent blood pressure above 140/90 mmHg. The main types are primary (essential) hypertension, which has no known cause and accounts for 90-95% of cases, and secondary hypertension caused by other conditions. Risk factors for primary hypertension include age, family history, race, obesity, diet, stress, and certain medications. The pathophysiology involves dysfunction of the body's blood pressure control systems and increased peripheral resistance. Clinical signs may include headaches, dizziness, and vision changes. Management involves lifestyle changes, medications like diuretics, beta-blockers, and calcium channel
This document provides information about diabetes mellitus (DM), including the different types of DM, their causes, symptoms, risk factors, and diagnostic tests. It discusses the main types of DM: type 1 DM which results from autoimmune destruction of insulin-producing beta cells; type 2 DM which involves insulin resistance and relative lack of insulin; and gestational DM which occurs during pregnancy. Other less common types like maturity onset diabetes of the young (MODY) and neonatal DM are also mentioned. The tests used to diagnose the different types include the A1C test, fasting blood glucose test, and oral glucose tolerance test. Treatment involves healthy eating, physical activity, medication as needed, and monitoring of blood sugar levels.
Cerebral palsy is a disorder of movement and posture caused by non-progressive damage to the developing brain, which can occur during pregnancy, birth, or early childhood. The main types are spastic, which causes increased muscle tone and stiffness; dystonic, characterized by involuntary movements; and ataxic, with lack of coordination. Cerebral palsy results in difficulties with motor skills, movement, muscle tone, reflexes, posture, and balance. Early intervention with a multidisciplinary team including physical therapists, occupational therapists, and doctors can help improve development and prevent complications.
This document discusses acute diarrheal disease, including its definition, classification, risk factors, clinical features, evaluation, and management. It defines acute diarrhea as three or more loose stools per day. It classifies diarrhea based on pathogens, duration, and mechanism. Risk factors include young age, immune deficiency, malnutrition, and exposure to unsanitary conditions. Clinical assessment involves classifying the illness, assessing hydration and nutritional status, and looking for comorbidities. Management involves fluid replacement, zinc supplementation, continued feeding, and antibiotics in some cases. The principles of rehydration therapy are outlined depending on the level of dehydration.
A complete blood count provides important information about red blood cells, white blood cells, and platelets. It can help screen for disorders and monitor treatment. Abnormal results for red blood cells, white blood cells, or platelets can indicate conditions like anemia, infection, leukemia, or liver disease. The specific cell counts and values help doctors further characterize any abnormalities found on a complete blood count.
This document discusses urinalysis and urine formation. It provides details on:
- Urine is formed by the kidneys through filtration, reabsorption, and secretion processes in the nephrons.
- A urinalysis examines the physical, chemical, and microscopic properties of urine and can detect various metabolic and infectious diseases.
- Urine output is evaluated to assess fluid balance and kidney function, with normal output being 500-2500 mL per day. Polyuria and oliguria can indicate various physiological and pathological conditions.
The document provides an outline of a lecture on the endocrine system. It discusses the key endocrine glands including the pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, and pineal gland. For each gland, it describes the location, cell types, hormones produced, and basic functions of the hormones. The hypothalamic-pituitary relationships that regulate many endocrine glands are also summarized.
The document provides an overview of the digestive system, including its main functions and components. The digestive system consists of the alimentary canal and digestive glands. The alimentary canal runs from the mouth to the anus and includes the mouth, pharynx, esophagus, stomach, small intestine, and large intestine. Each part has specific structures and functions related to ingestion, digestion, absorption, and elimination of food.
Hydrocele is a collection of fluid around one or both testicles, causing swelling of the scrotum or groin area. It commonly occurs in men over 40. There are two types: noncommunicating, where the fluid sac closes but the body doesn't absorb the fluid; and communicating, where the sac doesn't close completely, allowing fluid to flow in and out. Symptoms include swelling of the scrotum, pain, redness, and a feeling of pressure at the base of the penis. Diagnosis involves physical examination, transillumination to identify structures beneath the skin, and ultrasound to check for fluid presence. Treatment options include surgery, needle aspiration, or sclerotherapy to reduce reaccumulation of
This document discusses various nail abnormalities including brittle or crumbly nails which can be caused by aging, water/chemical exposure, fungal infection, lichen planus, thyroid disorders or psoriasis. Discolored nails are also covered, such as yellow nails from fungus or psoriasis. Loose nails can result from injury, infection or conditions like amyloidosis. Koilonychia causes indented spoon-shaped nails due to iron deficiency or other issues. Clubbing refers to unusually curved fingertips/nails associated with lung or heart conditions. Various other abnormalities like pitting, Beau's lines, Muehrcke's lines, and splinter hemorrhages are also summarized along with their potential causes.
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Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
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
Pengantar Penggunaan Flutter - Dart programming language1.pptx
4. Heamostasis.pptx
1. Dr Fouad Al-Khalli .
Heamostasis
The Haemostasis is the arrest (stoppage) of
bleeding, either by the physiological properties of
vasoconstriction and coagulation, or by surgical
means.
Physiological haemostatic mechanism are most
effective in dealing with injuries in small vessels;
arterioles, capillaries and venules, which are the
most common source of bleeding in everyday
life.
In contrast, the bleeding from a medium or large
artery is not usually controllable by the body.
2. Dr Fouad Al-Khalli .
Continue of Haemostasis:
The haemostatic system consists of;
- platelets,
- clotting factors in the plasma and
- vessels walls.
These components of the system interact to seal
leaks in the blood vessels.
Haemostasis is very important to the
maintenance of homeostasis.
If bleeding is not stopped, excessive blood loss from
a cut or torn vessel can result in a positive-feedback
cycle, consisting of ever-decreasing blood volume
and blood pressure, which disrupts homeostasis and
results in death.
3. Dr Fouad Al-Khalli .
Formed in the bone marrow from the magakaryocytes.
It production is under the control of a hormone thrombopoietin
( formed mainly in the liver).
Life span of platelets (half-life of 4 days) = 7 -10 days.
Count = 250 000 per mm³(µl) (♂170 – 360 x 10³, ♀180 – 400 x 10³).
Diameter = 1-2 µm (some may reach 4 µ).
Have a ring of microtubules around their periphery and an
extensively invaginated membrane with an intricated (complex)
canalicular system in contact with extracellular fluid.
Platelets Granules:
1. Dense granules: contain nonprotein substances; ADP, serotonin, and
other adenine nucleotides.
2. α-granules: contain proteins other than the hydrolases in the
lysosomes, which are: von Willebrand’s factor, Clotting factors,
Platelet-derived growth factor.
Thrombocytes
4. Dr Fouad Al-Khalli .
Steps of Heamostasis
From: Saladin: Anatomy & Physiology, 3rd ed.,2003.
5. Dr Fouad Al-Khalli .
Haemostatic Mechanisms
The steps of haemostasis that help prevent excessive
blood loss:
1-Vascular spasm,
2- platelet plug formation, and
3- blood coagulation can cause heamostasis.
1. Vascular Spasm: An immediate but temporary
constriction of a blood vessel resulting from contraction
of smooth muscle within the wall of the vessel. This
constriction can close small vessels completely and
stop the flow of blood through them.
• Chemicals also produce vascular spasm. For example,
during platelet plug formation, platelets release
thromboxanes, and endothelial cells release the peptide
endothelin.
6. Dr Fouad Al-Khalli .
Continue of Haemostatic Mechanisms:
2. Platelet plug formation:
• It is an accumulation of platelets that can seal up small tears in
blood vessels.
• Small tears occurs in the smaller vessels and capillaries
many times each day, and platelet plug formation quickly
closes them.
• The formation of platelet plug is a series of steps, many of
which take place simultaneously:
- platelets adhesion.
- platelet release reaction.
- platelet aggregation.
The activated platelets also display particular
phospholipids, called platelet factor III (PFIII) which is
important in clot-formation.
7. Dr Fouad Al-Khalli .
Platelets Mediated Haemostasis
vWF = von Willebrand’s
factor = F VIII.
PDGF= platelet derived
growth factor
TXA2 = Thromboxane A2
PAF = platelet-activating
factor
(Release)
Continue of :Haemostatic Mechanisms:
From; Color Atlas of Physiology.5th Int.ed.2006.
Secretion
5
4
3
2
1
8. Dr Fouad Al-Khalli .
Platelet Release Reaction:
Collagen exposure or thrombin action stimulate the
release of platelet granule which contents;
ADP
Serotonin
Prostaglandins
von Willebrand factor (vWF); which also secreted by
endothelial cells.
Lysosomal enzymes
Heparin antagonizing factor (platelet factor 4).
*PAF (Plasma platelet activating factor) activates
phospholypase C and deacyl-glycerol which convert
Arachidonic acid to Thromboxan A2.
* PAF: is secreted by neutrophiles and monocytes.
Continue of Haemostatic Mechanisms:
9. Dr Fouad Al-Khalli .
Collagen + thrombin
Prostaglandins synthesis
Thromboxan A₂
Lowers platelet cAMP
Starts release reaction
Vascular endothelial cells
Release of prostocyclin
Increased level of cAMP
Inhibition
of the release reaction
and aggregation of
platelets.
Platelet Release Reaction
Continue of Haemostatic Mechanisms:
Activation Inhibition
10. Dr Fouad Al-Khalli .
3. Coagulation:
• Coagulation (clotting = a clot formation) of the blood is
the last but most effective defense against bleeding.
• Coagulation is one of the most complex processes
in the body, involving over 30 chemical reactions.
• It is, a transformation of a plasma protein into a solid
gel (a clot = thrombus), which consisting mainly of a
protein polymer known as fibrin.
• Clotting occurs locally around the original platelet
plug and is the dominant haemostatic defense.
• Its function is to support and reinforce the platelet
plug and to solidify blood that remains in the wound
channel.
Continue of Haemostatic Mechanisms:
11. Dr Fouad Al-Khalli .
Factor Name Function Pathway
I = Fibrinogen Converted to fibrin Common
II = Prothrombin Converted to thrombin (enzyme) Common
III = Tissue thromboplastin Cofactor Extrinsic
IV = Calcium ions (Ca⁺⁺ ) Cofactor Intrinsic, extrinsic,
and common
V = Proaccelerin Cofactor Common
VII*= Proconvertin Enzyme Extrinsic
VIII = Antihemophilic factor A Cofactor Intrinsic
IX = Plasma thromboplastin component:
(Christmas factor), AHF-B. Enzyme Intrinsic
X = Stuart - Prower factor Enzyme Common
XI = Plasma thromboplastin antecedent:
Enzyme Intrinsic
XII = Hageman factor Enzyme Intrinsic
XIII = Fibrin stabilizing factor Enzyme Common
*Factor VI is no longer referenced; it is now believed to be the same substance
as activated factor V.
Clotting Factors
Continue of Haemostatic Mechanisms:
12. Dr Fouad Al-Khalli .
XIII
XIIIa
Fibrinogen Fibrin
monomer
Thrombin
Endothelial damage and
exposure of collagen
Tissue injury and exposure
of tissue thromboplastin (III)
XII XIIa
XI XIa
IX IXa
X Xa
VIIa VII
Fibrin
polymer
Prothrombin
Ca²⁺
Ca²⁺, PF3
Va, PF3, Ca²⁺
VIIIa, PF3, Ca²⁺
Intrinsic Pathway Extrinsic Pathway
The Clot Formation (Coagulation)
Intrinsic pathway
Extrinsic pathway
Common pathway
Ca²⁺
Common
pathway
13. Dr Fouad Al-Khalli .
Platelets
Fibrin
network
Trapped red
blood cells
Blood Clot
Blood clot consists of
fibrin fibers that trap red
blood cells, platelets and
fluid.
From: Seeley et al., Anatomy and Physiology, 8th ed., 2008.
14. Dr Fouad Al-Khalli .
Physiological Limitation of Blood coagulation
1. Liberation of certain plasma inhibitors:
Antithrombin III: it is a circulating plasma protein ( a
protease inhibitor ) which bind to serine protease in the
coagulation system. This binding is activated by Heparin, so the
antithrombin III binds to, and inhibits factors II, VII, IX, Xa, and XI.
2. Fibrinolytic System:
Endothelial Thrombomodulin is thrombin-binding protein forming
a complex which acts as anticoagulant:
Thrombomodulin + thrombin
Protein C Active protein C*
Inactivate VIIIa Inactivate Va
Plasminogen Plasmin
(Plasmin has a very strong fibrinolytic effect.)
3. Removal and dilution of the activated factors by blood.
* TPA= tissue
plasminogen
activator
15. Dr Fouad Al-Khalli .
Inhibition of Blood Clotting System
From Color Atlas of Pathophysiology- Thieme.
TFPI
TFPI = tissue factor pathway inhibitor
Extrinsic
Pathway
Intrinsic
Pathway
Antithrombin
III
Heparin
Thrombin
Protein
C
16. Dr Fouad Al-Khalli .
TFPI
Antithrombin
III Heparin
Inhibition of Blood Clotting System
*
* Thrombin also play a
role in inactivation of
factor Va and VIIIa.
See next plat.
Modifid from Color Atlas of Physiology: 5th ed., 2003.
TFPI = tissue factor pathway inhibitor.
17. Dr Fouad Al-Khalli .
Thrombin first bind to a thrombin
receptor, (thrombomodulin), on
endothelial cells.
Then activates protein C, which
inactivates clotting factors VIIIa and
Va
This binding also eliminates
thrombin’s procoagulant effects.
Inactivation of factors VIIIa and Va
From: Vander et al.: Human Physiology: 9th ed., 2004.
Procoagulant:
1. Cleaves fibrinogen to fibrin
2. Activates clotting factors XI, VIII, V, and XIII
3. Stimulates platelet activation
Anticoagulant:
Thrombin indirectly inactivates factors VIIIa and Va via protein C.
Actions of Thrombin
18. Dr Fouad Al-Khalli .
Plasminogen
Plasma kallikrein
Urokinase
Streptokinase*
Staphylokinase*
Tissue plasminogen
activator
Plasmin
Fibrin mesh-work
Soluble
fibrinopeptides
α₂-Antiplasmin
Tranexamic acid*
Basic Fibrinolytic System
And Plasminogen activators
From Color Atlas of Pathophysiology. Int. ed. 2006.
* = drugs
19. Dr Fouad Al-Khalli .
Anticlotting Role of Endothelial Cells
Action Result
1. Normally provide an intact barrier
between the blood and subendothelial
connective tissue factor.
Platelet aggregation and the formation of
tissue factor–VIIa complexes are not
triggered.
2. Synthesize and release PGI₂ and nitric
oxide.
These inhibit platelet activation and
aggregation.
3. Secrete tissue factor pathway
inhibitor (TFPI).
Inhibits the ability of tissue factor–factor VIIa
complexes to generate factor Xa.
4. Bind thrombin (via thrombomodulin),
which then activates protein C.
Active protein C inactivates clotting factors
VIIIa and Va.
5. Display heparin molecules on the
surfaces of their plasma membranes.
Heparin binds antithrombin III, and this
molecule then inactivates thrombin and
several other clotting factors.
6. Secrete tissue plasminogen
activator.
Tissue plasminogen activator catalyzes the
formation of plasmin, which dissolves clots.
20. Dr Fouad Al-Khalli .
Liver
Synthesizes
Bile salts
Clotting
factors
Bile salts in
bile
In GIT
Absorption of vit . K
Vit. K in the blood Clotting factors
In the blood
Role of Liver in Clotting
From: Vander et al.: Human Physiology: 9th ed., 2004.
Factor
II, VII, IX,
and X.
21. Dr Fouad Al-Khalli .
Anticoagulants
In Vitro:
1. Calcium precipitators:
- Na citrate (non toxic).
- Ammonium oxalate (toxic).
- EDTA (ethylene diamine tetraacetic acid)
2. Prevention of platelet aggregation:-
Smooth wall surface by coating the wall by
silicone oil, or paraffin oil (silicone or paraffin
coated test tubes).
3. Addition of anticoagulant: as heparin.
22. Dr Fouad Al-Khalli .
In Vivo:
1. Heparin: The mucoprotein naturally produced by mast
cells and granulocytes, acts as cofactor for the action
of antithrombin III, and so facilitates its anticoagulant
effects. The clotting factors that are inhibited are the
active forms of factors II, IX, X, XI, and XII. Heparin
also inhibits platelets function.
2. The coumarin drugs (Warfarin and Decomarol):
Interferes with the action of vit. K, and prevents it from
taking part in the synthesis of prothrombin (II), VII, IX,
and X in the liver. has the same action.
3. Aspirin: Inhibits the aggregation of the platelets by
inhibiting the platelet thromboxan A2 formation.
4. Streptokinase and Urokinase; which are activators of
plasminogen to plasmin.
Continue of: Anticoagulants
23. Dr Fouad Al-Khalli .
Intravascular
thrombosis
The causes Abnormalities of Haemostasis
From: Color Atlas of Pathophysiology : 2000. Theime
1
2
3
4
1.Defect in clotting mechanism.
2.Disorders of platelets.
3.Defect of blood vessels.
4.Intravascular thrombus forming.
24. Dr Fouad Al-Khalli .
Continue of Abnormalities of Haemostasis
1. Defect in clotting mechanism:
a) Acquired:
Lack of Vit. K leads to decreased factor II, VII, IX and
X, as in obstructive jaundice.
b) Hereditary: (Haemophilias):
Congenital disease, transmitted by female but only
male suffers from it (as an X chromosome linked
recessive trait by clinically unaffected female carriers
to males):
- Haemophilia A : absence of factor VIII – 85%
- Haemophilia B : absence of factor IX - 14 15%
- Haemophilia C : absence of factor XI - rare ??.
The most common bleeding sites are the muscles and the large joints of the leg, the latter
becoming markedly deformed with time (hemophilic arthropathy).
25. Dr Fouad Al-Khalli .
2. Disorders of Platelets:
a) Decrease of platelet number:
Thrombocytopenia ; as in purpura which
leads to easy bruisbility (blue and black
spots on the skin).
b) Defective platelets: normal count but
defective: as in: Thrombocytopathia =
thrombostaenia purpura.
3. Defect of the Blood Vessels:
Vascular purpuras as in typhus and typhoid.
Continue of Abnormalities of Haemostasis
26. Dr Fouad Al-Khalli .
Continue of Abnormalities of Haemostasis
4. Intravascular Thrombosis:
a) Abnormalities of Blood Vessels:
- Atherosclerosis, Trauma, Loss of venous tone (e.g.,
varicosities).
b) Abnormalities in Blood Flow:
- stasis; as in pregnancy and neoplasia.
- hyperviscosity; as in polycythaemia vera .
- turbulences; as in coarctation of the aorta.
c) Abnormalities of the Blood:
- Increased platelets count; as in thrombocythemia.
- Hypercoagulable states; as in increased activation
of clotting factors ( operation; ↑ activity of clotting F.
and ↓ activity of fibrinolysis).
27. Dr Fouad Al-Khalli .
Haemostatic Tests
1.Quick Test:
- Plasma is transiently made incoagulable with
substances that form complex with Ca² (citrate,
oxalate, or EDTA = ethylenediaminetetraacetic acid).
- An excessive amount of Ca² and tissue
thrombokinase are then added and a resulting
clotting time is compared with serial dilutions
of normal plasma.
28. Dr Fouad Al-Khalli .
2. Partial Thromboplastin Time (PTT):
- Kephalin, kaolin (substances for contraction
activation) and Ca² are added to the citrated
plasma and time until clotting is measured
( NV = 25 -38sec.).
3. Plasma Thrombin Time:
- Thrombin is added to the citrated plasma
and the clotting time is measured (NV= 18 –
22 sec).
4. Bleeding Time: normal = < 5 min.
5. Platelets Count: NV 250 000 per µl
Continue of Haemostatic Tests
29. Dr Fouad Al-Khalli .
Interpretation of Clotting Test Results
From Color Atlas of Pathophysiology. Int. ed. 2006.
PTT= Partial thromboplastin time.
HMK= Heigh molecular weight kininogen.