This document discusses different types of embolisms including pulmonary thromboembolism, amniotic fluid embolism, fat embolism, and air embolism. It provides details on the pathogenesis, clinical features, risk factors, and consequences of each type. For pulmonary thromboembolism, it describes how clots form in veins and become dislodged, traveling to the lungs. It also compares thrombus and thromboembolism. For amniotic fluid embolism, it explains how amniotic debris enters the mother's blood during delivery and causes anaphylaxis-like reactions. Fat embolism most commonly occurs after bone fractures, when bone marrow fat enters the blood.
An embolus is a solid, liquid, or gaseous mass that breaks off and travels through the bloodstream, lodging in and blocking smaller blood vessels. Pulmonary embolisms originate from deep leg vein thrombi in 95% of cases and can cause infarction or blockage of lung tissue. Systemic embolisms originate from heart mural thrombi in 80% of cases and commonly impact the brain or lower extremities. Fat embolisms occur after bone fractures and burns, causing pulmonary insufficiency, neurological issues, and thrombocytopenia. Air embolisms enter the circulation through chest or obstetric injuries and can block major blood vessels. Amniotic fluid embolisms are a rare
An embolism occurs when a solid, liquid, or gas mass travels through the bloodstream and lodges in a blood vessel, blocking blood flow. There are several types of embolism including thromboembolism (blood clots), fat embolism, air embolism, septic embolism, and amniotic fluid embolism. Pulmonary thromboembolism is a common and potentially fatal condition where a blood clot forms in the deep veins and travels to the lungs. Fat embolism occurs after bone fractures and can lead to a serious condition called fat embolism syndrome. Amniotic fluid embolism is a rare but grave complication during childbirth with a high
Pathology of hemodynamic disorders part 2 nov 2017 Dr. Sufia HusainSufia Husain
This document discusses various types of hemodynamic disorders including embolism, infarction, and shock. It provides detailed information on different types of embolism such as pulmonary thromboembolism, systemic thromboembolism, fat embolism, air embolism, and amniotic fluid embolism. It also describes the stages of shock, associated pathophysiology and morphological changes in tissues during the different stages of shock.
Embolism is the obstruction of blood vessels by foreign material carried by the bloodstream called an embolus. The most common type is thromboembolism caused by blood clots. Embolisms can be classified by the material causing the obstruction (solid, liquid, gas), whether infected or not, and the source of the embolus (cardiac, arterial, venous, lymphatic). Pulmonary embolism is a serious and potentially fatal condition where blood clots block arteries in the lungs. Risk factors include immobilization, and clots most often originate from veins in the legs. Consequences can include sudden death, lung infarction, hemorrhage and chronic lung disease.
This document defines and describes different types of embolisms. It discusses pulmonary embolism which originates from deep vein thromboses. It also covers paradoxical embolism, fat embolism, air embolism, decompression sickness, amniotic fluid embolism, and hemorrhage. For each type, it provides details on causes, clinical presentations, and consequences.
An embolism occurs when a solid, liquid, or gas mass travels through the bloodstream and lodges in a blood vessel distant from its origin. Embolisms are classified based on their physical properties and source. Pulmonary embolisms involve blockages in the pulmonary arteries, often originating from deep leg veins or pelvic veins, while systemic embolisms block arterial circulation to organs. Specific types of embolisms include fat embolisms and marrow embolisms caused by trauma, and air embolisms which can result from injuries or medical procedures. Embolisms cause mechanical obstruction of blood vessels and biochemical injury depending on the composition and size of the obstructing material.
Edema can be caused by increased hydrostatic pressure, increased vascular permeability, decreased colloid osmotic pressure, decreased protein synthesis or increased protein loss, or lymphatic obstruction. The major mechanisms are increased hydrostatic pressure, as seen in congestive heart failure, or increased vascular permeability during inflammation. Edema fluid is usually a protein-poor transudate when caused by hydrostatic or oncotic pressure changes, but is a protein-rich exudate with inflammatory causes due to higher vascular permeability.
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.
An embolus is a solid, liquid, or gaseous mass that breaks off and travels through the bloodstream, lodging in and blocking smaller blood vessels. Pulmonary embolisms originate from deep leg vein thrombi in 95% of cases and can cause infarction or blockage of lung tissue. Systemic embolisms originate from heart mural thrombi in 80% of cases and commonly impact the brain or lower extremities. Fat embolisms occur after bone fractures and burns, causing pulmonary insufficiency, neurological issues, and thrombocytopenia. Air embolisms enter the circulation through chest or obstetric injuries and can block major blood vessels. Amniotic fluid embolisms are a rare
An embolism occurs when a solid, liquid, or gas mass travels through the bloodstream and lodges in a blood vessel, blocking blood flow. There are several types of embolism including thromboembolism (blood clots), fat embolism, air embolism, septic embolism, and amniotic fluid embolism. Pulmonary thromboembolism is a common and potentially fatal condition where a blood clot forms in the deep veins and travels to the lungs. Fat embolism occurs after bone fractures and can lead to a serious condition called fat embolism syndrome. Amniotic fluid embolism is a rare but grave complication during childbirth with a high
Pathology of hemodynamic disorders part 2 nov 2017 Dr. Sufia HusainSufia Husain
This document discusses various types of hemodynamic disorders including embolism, infarction, and shock. It provides detailed information on different types of embolism such as pulmonary thromboembolism, systemic thromboembolism, fat embolism, air embolism, and amniotic fluid embolism. It also describes the stages of shock, associated pathophysiology and morphological changes in tissues during the different stages of shock.
Embolism is the obstruction of blood vessels by foreign material carried by the bloodstream called an embolus. The most common type is thromboembolism caused by blood clots. Embolisms can be classified by the material causing the obstruction (solid, liquid, gas), whether infected or not, and the source of the embolus (cardiac, arterial, venous, lymphatic). Pulmonary embolism is a serious and potentially fatal condition where blood clots block arteries in the lungs. Risk factors include immobilization, and clots most often originate from veins in the legs. Consequences can include sudden death, lung infarction, hemorrhage and chronic lung disease.
This document defines and describes different types of embolisms. It discusses pulmonary embolism which originates from deep vein thromboses. It also covers paradoxical embolism, fat embolism, air embolism, decompression sickness, amniotic fluid embolism, and hemorrhage. For each type, it provides details on causes, clinical presentations, and consequences.
An embolism occurs when a solid, liquid, or gas mass travels through the bloodstream and lodges in a blood vessel distant from its origin. Embolisms are classified based on their physical properties and source. Pulmonary embolisms involve blockages in the pulmonary arteries, often originating from deep leg veins or pelvic veins, while systemic embolisms block arterial circulation to organs. Specific types of embolisms include fat embolisms and marrow embolisms caused by trauma, and air embolisms which can result from injuries or medical procedures. Embolisms cause mechanical obstruction of blood vessels and biochemical injury depending on the composition and size of the obstructing material.
Edema can be caused by increased hydrostatic pressure, increased vascular permeability, decreased colloid osmotic pressure, decreased protein synthesis or increased protein loss, or lymphatic obstruction. The major mechanisms are increased hydrostatic pressure, as seen in congestive heart failure, or increased vascular permeability during inflammation. Edema fluid is usually a protein-poor transudate when caused by hydrostatic or oncotic pressure changes, but is a protein-rich exudate with inflammatory causes due to higher vascular permeability.
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.
Embolism occurs when a solid, liquid, or gaseous mass travels through the bloodstream and lodges in a blood vessel distant from the site of origin. Embolisms are classified based on direction of travel and composition. Pulmonary embolisms involve the lungs while systemic embolisms affect other organs. Common causes of embolism include blood clots, fat droplets, air bubbles, and infectious materials. Symptoms vary depending on the size and location of the embolism but may include dyspnea, chest pain, and coughing. Diagnosis involves blood tests, imaging, and scans. Consequences depend on factors like vessel size and collateral blood flow.
This document summarizes embolic disorders that can occur during pregnancy, including venous thromboembolism, amniotic fluid embolism, and their causes, signs/symptoms, treatment, and complications. Venous thromboembolism is caused by Virchow's triad of endothelial damage, venous stasis, and hypercoagulability during pregnancy. It can lead to deep vein thrombosis and pulmonary embolism. Amniotic fluid embolism occurs when amniotic fluid enters the mother's bloodstream and causes respiratory distress, hypotension, and disseminated intravascular coagulation. Both conditions require emergency treatment and resuscitation to address complications like renal failure and death.
Pulmonary embolism (PE) refers to obstruction of the pulmonary artery or its branches, usually by blood clots originating from the deep veins of the lower extremities. PE is a common and potentially lethal condition, with many patients dying within hours of onset from blockage of blood flow to the lungs. The diagnosis of PE involves evaluating risk factors, performing physical exams, blood tests like D-dimer, and imaging tests like CT pulmonary angiography or ventilation-perfusion scans. Effective treatment requires identifying patients at high risk of complications or death.
1. Hemodynamic disorders involve changes in fluid balance, blood pressure, or vessel integrity that cause fluid to move between blood vessels and tissues. This can result in edema, hyperemia/congestion, hemorrhage, thrombosis, embolism, or infarction.
2. Edema is excess fluid in tissues, caused by increased pressure, reduced proteins, or lymphatic issues. Hyperemia is increased blood flow while congestion is decreased outflow. Hemorrhage occurs when vessels rupture. Thrombosis forms clots, which can embolize. Infarctions are areas of cell death from blocked arteries or veins.
3. Shock is a life-threatening drop in
This document discusses embolism, infarction, and their causes and classifications. It defines an embolism as a detached mass carried by the blood to distant sites, which can lodge and block vessels, causing tissue dysfunction. Emboli sources include thrombi, fat, air, debris. Embolisms are classified as pulmonary (95% from DVTs), systemic (sites include legs, brain, intestines, kidneys). Infarctions are areas of ischemic necrosis due to blood flow obstruction. They are classified as hemorrhagic, white, septic based on appearance and presence of infection. Infarcts are eventually replaced by scar tissue.
The document discusses different types of embolism. An embolism is a blockage of a blood vessel by an object that travels through the bloodstream. There are several types defined by the material causing the blockage (e.g. fat, air), origin (e.g. cardiac, arterial), and location (e.g. venous, pulmonary). Pulmonary embolism is a common and potentially fatal type where an embolism occurs in the pulmonary arteries. Risk factors, signs and symptoms, diagnostic tests, and treatment methods are described for pulmonary embolism specifically.
This document discusses different types of thromboembolism including pulmonary embolism, fat embolism, air embolism, and amniotic fluid embolism. It provides details on the definition, causes, risk factors, symptoms, diagnosis, treatment and prognosis of pulmonary embolism, which is the most common type of thromboembolism. The document also discusses the pathophysiology and mechanisms of the different embolism types.
1. Hemodynamic disorders involve changes in intravascular volume, pressure, or protein content that affect fluid movement across vessel walls and can cause edema, hyperemia, congestion, hemorrhage, thrombosis, embolism, infarction, or shock.
2. Edema is increased fluid in tissues, caused by increased hydrostatic pressure, reduced plasma proteins, lymphatic obstruction, sodium retention, or inflammation.
3. Thrombosis is inappropriate blood clot formation from endothelial injury, blood stasis, or hypercoagulability per Virchow's triad, and thrombi can embolize or organize.
4. Embolism occurs when a detached mass is
The document discusses various types of embolism and thrombosis. It describes the Virschow triad of factors that can lead to thrombosis - endothelial injury, changes in blood flow, and hypercoagulability. It then examines different causes and outcomes of thrombosis and embolism in various parts of the body, such as pulmonary embolism from deep vein thrombosis, systemic embolism from cardiac sources, and amniotic fluid embolism during childbirth.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
This document provides background information on fat embolism syndrome (FES). It discusses that FES has a high incidence in patients with major trauma and causes multi-organ inflammation if not diagnosed and treated swiftly. While the exact mechanisms are not fully understood, FES is thought to be triggered by the release of fat emboli from bone fractures that occlude blood vessels and cause pulmonary and systemic inflammation. The diagnosis is mainly clinical based on respiratory, skin and neurological symptoms following trauma. Supportive care is the primary treatment approach through oxygenation, ventilation and symptom management while efforts focus on prevention, early diagnosis and surgical stabilization of fractures.
Hemodynamic Disorders Question and Answersvasanthatpuram
This document discusses hemodynamic disorders and contains answers to 10 questions on related topics. It defines and classifies edema, discussing the etiopathogenesis and pathology of different types. It also discusses normal hemostasis mechanisms, Virchow's triad in thrombus formation, the morphology and fate of thrombi. Other topics addressed include heparin-induced thrombocytopenia, antiphospholipid antibody syndrome, types of embolism including Caisson disease, fat embolism, amniotic fluid embolism, the morphology of infarcts, and the definition, types, pathogenesis and morphological changes seen in shock.
EMBOLISM -a blockage in a blood vessel caused by a piece of material.pptxMeethuRappai1
This document summarizes thrombosis, embolism, and related topics. It discusses normal haemostasis and how thrombosis occurs due to endothelial injury, abnormal blood flow, hypercoagulability, and other factors. Thrombi can propagate, embolize, or dissolve. Embolism occurs when a detached mass is carried by the bloodstream, commonly causing pulmonary or systemic embolism. Specific types of embolism discussed are thromboembolism, fat embolism, air embolism, and amniotic fluid embolism.
This document discusses hemodynamic disorders including thrombosis, embolism, and hemorrhage. Thrombosis is the formation of a blood clot within a blood vessel. It can be caused by endothelial injury, changes in blood flow, changes in blood composition, or hypercoagulability. Embolism occurs when a mass travels through the bloodstream and blocks a vessel. Common types are thromboembolism, fat embolism, air embolism, and amniotic fluid embolism. Hemorrhage is the escape of blood from vessels. It can be external from sites like the skin or internal within body cavities. The effects of hemorrhage range from local homeostasis to systemic shock
1. The document discusses various vascular pathologies including hyperemia, congestion, thrombosis, embolism, and infarction.
2. It describes the morphology and causes of different types of hyperemia, congestion, thrombosis, pulmonary and non-pulmonary embolism, and hemorrhagic vs. white infarcts.
3. The roles of the endothelium, platelets, and coagulation cascade in thrombosis are examined, as are the potential fates of a thrombus and clinical effects of embolism.
Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel or heart chamber. There are three main types of thrombi based on composition and location. Thrombosis occurs due to endothelial injury, abnormal blood flow, and hypercoagulability. Thrombi form at sites of injury or turbulence in arteries and heart chambers, and at sites of stasis in veins. Microscopically, thrombi appear laminated with alternating pale and dark layers. Thrombosis can occur in any blood vessel and lead to complications such as embolism if parts of the thrombus break off.
EVASION OF APOPTOSIS powerpoint presentationJeenaRaj10
Tumor cells evade apoptosis through two major mechanisms: losing the function of the TP53 gene which regulates apoptosis, allowing cells to survive without regulation, or overexpressing anti-apoptotic BCL2 family members like BCL2 itself, protecting tumor cells from apoptosis and enabling survival and drug resistance. Mutations in genes involved in apoptosis pathways are common in cancers and help tumor cells resist programmed cell death.
This document discusses the limitless replicative potential of cancer cells. Normal cells have a limited ability to divide, typically 60-70 times, before reaching senescence. Cancer cells bypass this limitation through several factors. They evade senescence by accumulating genetic changes that deregulate cell cycle controls. They evade mitotic crisis, which is caused by telomere shortening, by expressing telomerase or using alternative lengthening of telomeres mechanisms. Cancer cells also have the property of self-renewal like stem cells, allowing them to perpetually replenish themselves through asymmetrical cell division producing more cancer stem cells.
Embolism occurs when a solid, liquid, or gaseous mass travels through the bloodstream and lodges in a blood vessel distant from the site of origin. Embolisms are classified based on direction of travel and composition. Pulmonary embolisms involve the lungs while systemic embolisms affect other organs. Common causes of embolism include blood clots, fat droplets, air bubbles, and infectious materials. Symptoms vary depending on the size and location of the embolism but may include dyspnea, chest pain, and coughing. Diagnosis involves blood tests, imaging, and scans. Consequences depend on factors like vessel size and collateral blood flow.
This document summarizes embolic disorders that can occur during pregnancy, including venous thromboembolism, amniotic fluid embolism, and their causes, signs/symptoms, treatment, and complications. Venous thromboembolism is caused by Virchow's triad of endothelial damage, venous stasis, and hypercoagulability during pregnancy. It can lead to deep vein thrombosis and pulmonary embolism. Amniotic fluid embolism occurs when amniotic fluid enters the mother's bloodstream and causes respiratory distress, hypotension, and disseminated intravascular coagulation. Both conditions require emergency treatment and resuscitation to address complications like renal failure and death.
Pulmonary embolism (PE) refers to obstruction of the pulmonary artery or its branches, usually by blood clots originating from the deep veins of the lower extremities. PE is a common and potentially lethal condition, with many patients dying within hours of onset from blockage of blood flow to the lungs. The diagnosis of PE involves evaluating risk factors, performing physical exams, blood tests like D-dimer, and imaging tests like CT pulmonary angiography or ventilation-perfusion scans. Effective treatment requires identifying patients at high risk of complications or death.
1. Hemodynamic disorders involve changes in fluid balance, blood pressure, or vessel integrity that cause fluid to move between blood vessels and tissues. This can result in edema, hyperemia/congestion, hemorrhage, thrombosis, embolism, or infarction.
2. Edema is excess fluid in tissues, caused by increased pressure, reduced proteins, or lymphatic issues. Hyperemia is increased blood flow while congestion is decreased outflow. Hemorrhage occurs when vessels rupture. Thrombosis forms clots, which can embolize. Infarctions are areas of cell death from blocked arteries or veins.
3. Shock is a life-threatening drop in
This document discusses embolism, infarction, and their causes and classifications. It defines an embolism as a detached mass carried by the blood to distant sites, which can lodge and block vessels, causing tissue dysfunction. Emboli sources include thrombi, fat, air, debris. Embolisms are classified as pulmonary (95% from DVTs), systemic (sites include legs, brain, intestines, kidneys). Infarctions are areas of ischemic necrosis due to blood flow obstruction. They are classified as hemorrhagic, white, septic based on appearance and presence of infection. Infarcts are eventually replaced by scar tissue.
The document discusses different types of embolism. An embolism is a blockage of a blood vessel by an object that travels through the bloodstream. There are several types defined by the material causing the blockage (e.g. fat, air), origin (e.g. cardiac, arterial), and location (e.g. venous, pulmonary). Pulmonary embolism is a common and potentially fatal type where an embolism occurs in the pulmonary arteries. Risk factors, signs and symptoms, diagnostic tests, and treatment methods are described for pulmonary embolism specifically.
This document discusses different types of thromboembolism including pulmonary embolism, fat embolism, air embolism, and amniotic fluid embolism. It provides details on the definition, causes, risk factors, symptoms, diagnosis, treatment and prognosis of pulmonary embolism, which is the most common type of thromboembolism. The document also discusses the pathophysiology and mechanisms of the different embolism types.
1. Hemodynamic disorders involve changes in intravascular volume, pressure, or protein content that affect fluid movement across vessel walls and can cause edema, hyperemia, congestion, hemorrhage, thrombosis, embolism, infarction, or shock.
2. Edema is increased fluid in tissues, caused by increased hydrostatic pressure, reduced plasma proteins, lymphatic obstruction, sodium retention, or inflammation.
3. Thrombosis is inappropriate blood clot formation from endothelial injury, blood stasis, or hypercoagulability per Virchow's triad, and thrombi can embolize or organize.
4. Embolism occurs when a detached mass is
The document discusses various types of embolism and thrombosis. It describes the Virschow triad of factors that can lead to thrombosis - endothelial injury, changes in blood flow, and hypercoagulability. It then examines different causes and outcomes of thrombosis and embolism in various parts of the body, such as pulmonary embolism from deep vein thrombosis, systemic embolism from cardiac sources, and amniotic fluid embolism during childbirth.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
This document provides background information on fat embolism syndrome (FES). It discusses that FES has a high incidence in patients with major trauma and causes multi-organ inflammation if not diagnosed and treated swiftly. While the exact mechanisms are not fully understood, FES is thought to be triggered by the release of fat emboli from bone fractures that occlude blood vessels and cause pulmonary and systemic inflammation. The diagnosis is mainly clinical based on respiratory, skin and neurological symptoms following trauma. Supportive care is the primary treatment approach through oxygenation, ventilation and symptom management while efforts focus on prevention, early diagnosis and surgical stabilization of fractures.
Hemodynamic Disorders Question and Answersvasanthatpuram
This document discusses hemodynamic disorders and contains answers to 10 questions on related topics. It defines and classifies edema, discussing the etiopathogenesis and pathology of different types. It also discusses normal hemostasis mechanisms, Virchow's triad in thrombus formation, the morphology and fate of thrombi. Other topics addressed include heparin-induced thrombocytopenia, antiphospholipid antibody syndrome, types of embolism including Caisson disease, fat embolism, amniotic fluid embolism, the morphology of infarcts, and the definition, types, pathogenesis and morphological changes seen in shock.
EMBOLISM -a blockage in a blood vessel caused by a piece of material.pptxMeethuRappai1
This document summarizes thrombosis, embolism, and related topics. It discusses normal haemostasis and how thrombosis occurs due to endothelial injury, abnormal blood flow, hypercoagulability, and other factors. Thrombi can propagate, embolize, or dissolve. Embolism occurs when a detached mass is carried by the bloodstream, commonly causing pulmonary or systemic embolism. Specific types of embolism discussed are thromboembolism, fat embolism, air embolism, and amniotic fluid embolism.
This document discusses hemodynamic disorders including thrombosis, embolism, and hemorrhage. Thrombosis is the formation of a blood clot within a blood vessel. It can be caused by endothelial injury, changes in blood flow, changes in blood composition, or hypercoagulability. Embolism occurs when a mass travels through the bloodstream and blocks a vessel. Common types are thromboembolism, fat embolism, air embolism, and amniotic fluid embolism. Hemorrhage is the escape of blood from vessels. It can be external from sites like the skin or internal within body cavities. The effects of hemorrhage range from local homeostasis to systemic shock
1. The document discusses various vascular pathologies including hyperemia, congestion, thrombosis, embolism, and infarction.
2. It describes the morphology and causes of different types of hyperemia, congestion, thrombosis, pulmonary and non-pulmonary embolism, and hemorrhagic vs. white infarcts.
3. The roles of the endothelium, platelets, and coagulation cascade in thrombosis are examined, as are the potential fates of a thrombus and clinical effects of embolism.
Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel or heart chamber. There are three main types of thrombi based on composition and location. Thrombosis occurs due to endothelial injury, abnormal blood flow, and hypercoagulability. Thrombi form at sites of injury or turbulence in arteries and heart chambers, and at sites of stasis in veins. Microscopically, thrombi appear laminated with alternating pale and dark layers. Thrombosis can occur in any blood vessel and lead to complications such as embolism if parts of the thrombus break off.
EVASION OF APOPTOSIS powerpoint presentationJeenaRaj10
Tumor cells evade apoptosis through two major mechanisms: losing the function of the TP53 gene which regulates apoptosis, allowing cells to survive without regulation, or overexpressing anti-apoptotic BCL2 family members like BCL2 itself, protecting tumor cells from apoptosis and enabling survival and drug resistance. Mutations in genes involved in apoptosis pathways are common in cancers and help tumor cells resist programmed cell death.
This document discusses the limitless replicative potential of cancer cells. Normal cells have a limited ability to divide, typically 60-70 times, before reaching senescence. Cancer cells bypass this limitation through several factors. They evade senescence by accumulating genetic changes that deregulate cell cycle controls. They evade mitotic crisis, which is caused by telomere shortening, by expressing telomerase or using alternative lengthening of telomeres mechanisms. Cancer cells also have the property of self-renewal like stem cells, allowing them to perpetually replenish themselves through asymmetrical cell division producing more cancer stem cells.
This document discusses angiogenesis, invasion, and metastasis of tumors. It describes how angiogenesis allows tumors to grow beyond 1-2mm by developing new blood vessels. The metastatic cascade is explained as a two-step process involving invasion of the extracellular matrix and vascular dissemination. Key factors and genetic alterations that influence angiogenesis and the various steps of invasion and metastasis are also outlined.
RED INFARCTS powerpoint presentation basicsJeenaRaj10
1) Red infarcts occur in tissues with dual blood supply, loose connective tissue, or venous outflow issues. They appear as sharply demarcated red or purple areas of necrosis.
2) Microscopically, red infarcts show ischemic coagulative necrosis within 4-12 hours. Acute inflammation infiltrates the area in the following days. Necrotic cells and blood are phagocytosed by macrophages.
3) Red infarcts can occur when blood flow is restored to a previously ischemic area, such as after an arterial blockage is treated. Affected organs include the lung, liver, intestine, and heart.
Factors influencing the development of an infarct.pptxJeenaRaj10
The document discusses factors that influence the development of an infarct. It explains that an infarct is caused by occlusion of the arterial supply or venous drainage of an area, ranging from tissue dysfunction to necrosis. Tissues with more connections like lungs and liver are less vulnerable due to dual blood supply. The rate of occlusion also influences outcomes, as slower occlusions allow for collateral vessel formation. Different tissues are more susceptible to hypoxic injury, with neurons vulnerable within minutes and fibroblasts only after hours of ischemia. Blood oxygen content additionally impacts infarct development.
Presentation1 powerpoint necrosis form of cell deathJeenaRaj10
Necrosis is the death of cells and living tissue. It can be caused by ischemia, physical or chemical agents, or immunological injury. There are several types of necrosis including coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Coagulative necrosis involves denaturation of proteins and enzymatic digestion of cells while preserving tissue architecture. Liquefactive necrosis causes tissue to become a liquid mass. Caseous necrosis is seen in tuberculosis and leaves tissue with a cheesy white appearance.
ORBITAL INFLAMMATION powerpoint presentationJeenaRaj10
The document discusses different types of orbital inflammation including preseptal cellulitis, orbital cellulitis, and cavernous sinus thrombosis. Preseptal cellulitis involves structures anterior to the orbital septum and causes swelling and redness of the eyelids but does not affect vision or eye movements. Orbital cellulitis is a purulent inflammation behind the orbital septum that can cause proptosis, restricted eye movements, and vision loss. Cavernous sinus thrombosis is a serious complication where infection and blood clots spread from the face or orbit to the cavernous sinus, which can lead to issues like paralysis of cranial nerves. Broad spectrum antibiotics, monitoring for complications, and surgical drainage may be
Pathology of Pneumonia POWERPOINT PRESENTATIONJeenaRaj10
This document provides information on pneumonia, including:
1. It describes the lung defense mechanisms against infection such as mucociliary clearance, phagocytosis by alveolar macrophages and neutrophils, and serum complement.
2. It classifies pneumonia based on etiology (infective, viral, bacterial, fungal, tuberculosis), morphology (lobar, bronchial, interstitial), duration (acute, chronic), and location (community-acquired, hospital-acquired). Common causative organisms are discussed for each type.
3. The pathogenesis of pneumonia is outlined as entry of microbes, followed by inflammation in the alveoli and surrounding tissues. Complications like abscesses and empy
NECROSIS AND APOPTOSIS POWERPOINT PRESENTATIONJeenaRaj10
This document discusses different types of cell death: necrosis, apoptosis, and necroptosis. Necrosis is unprogrammed cell death due to external factors like toxins or hypoxia. Apoptosis is programmed cell death that helps eliminate unwanted cells through activation of genes and enzymes. Necroptosis shares characteristics of both necrosis and apoptosis - it is caspase-independent cell death triggered by signaling pathways involving the kinases RIPK1 and RIPK3, which phosphorylate MLKL leading to plasma membrane disruption and cell rupture in a programmed manner. Necroptosis plays roles in processes like bone growth, diseases like pancreatitis, and host defense against viruses.
This document discusses various anticoagulants used in hematology. It defines anticoagulants as agents that prevent blood clot formation and lists their uses in preventing disorders caused by abnormal clots. The document describes characteristics anticoagulants must have for hematological examination and lists commonly used anticoagulants like EDTA, oxalates, sodium heparin, sodium citrate, and sodium fluoride/potassium oxalate mixture. Each anticoagulant is classified and their modes of action, concentrations, advantages and disadvantages are detailed.
Necrosis is irreversible injury and death of cells and living tissue. There are several patterns of necrosis that can occur in tissues including coagulative, liquefactive, and caseous necrosis. Coagulative necrosis involves the maintenance of cell outlines but loss of cellular details. The dead tissues remain in the body for a long period. Liquefactive necrosis results from the rapid dissolution of dead cells, often leading to abscess formation. Caseous necrosis converts dead tissue into a granular mass resembling cottage cheese, associated with tuberculosis lesions.
Necrosis is cell death in living tissue that can have various causes and appearances. There are several types of necrosis including coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Coagulative necrosis involves protein denaturation and enzymatic cell digestion that preserves tissue architecture. Liquefactive necrosis causes tissues to become a liquid mass. Caseous necrosis in tuberculosis infections leads to cheesy white tissue. Fat necrosis in the pancreas and breast appears chalky white.
This document provides an overview of gestational trophoblastic diseases (GTD), including their classification, histopathology, diagnosis, and management. Key points include:
1. GTD are classified by the WHO and include complete and partial hydatidiform moles, as well as benign and malignant trophoblastic lesions. Hydatidiform moles can develop into gestational trophoblastic neoplasia in a minority of cases.
2. Complete hydatidiform moles show diffuse hydropic changes of chorionic villi with abnormal trophoblastic hyperplasia, while partial moles have a mixture of normal and hydropic villi.
3. Malignant trophob
The immune system protects the body from infectious disease. Infectious disease is caused by pathogens like bacteria, viruses, fungi and parasites that invade the body. The immune system uses nonspecific defenses like skin, fever and inflammation that provide a fast response. It also uses specific defenses like white blood cells and antibodies that recognize and attack specific pathogens. B cells produce antibodies that mark pathogens for destruction by macrophages and killer T cells. Memory B cells provide faster immunity upon second exposure to the same pathogen through antibodies.
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3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
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Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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2. PULMONARY THROMBOEMBOLISM
• Fatal form of thromboembolism where occlusion of pulmonary
arterial tree occurs by thromboemboli
• Pulmonary emboli originates from deep vein thrombosis more
commonly
• Incidence – 100 – 200 cases/100,000 people in US
• Sex –more commonly seen in males than in females
3. PULMONARY THROMBOEMBOLISM
• Obstruction by thrombosis is uncommon but more commonly by thromboembolism
FEATURE PULMONARY THROMBUS PULMONARY
THROMBOEMBOLISM
Pathogenesis Locally formed Disseminated from thrombus
Location In small arteries and
branches
In major arteries and branches
Attachment to vessel
wall
Firmly adherent Loosely attached or lying freely
Gross appearance Head pale, tail red No distinct head and tail,
smooth surfaced which is dull
and dry
Microscopy Platelets and fibrin in layers.
Lines of zahn are seen
Mixed with blood clot.
Lines of zahn are rare
4. PULMONARY THROMBOEMBOLISM
Risk factors
• Stasis of venous blood and hypercoagulable state
Causes
• Most commonly seen in hospitalized and bed ridden patients
• Thrombi originating in large vein of lower legs (deep veins in
95% of thromboemboli)
• Less common sources
• Thrombus in the varicosities of superficial veins of legs
• Pelvic veins such as periprostatic, periovarian, uterine and
broad ligament veins
5. PULMONARY THROMBOEMBOLISM
• If the thrombus is large, it is impacted
• at the bifurcation of main pulmonary
artery - saddle thrombus
• In right ventricle
• Its out flow tract
6. PULMONARY THROMBOEMBOLISM
• Mostly large emboli is fragmented into
multiple small emboli which are impacted
in lower lobes of lungs
• Rarely paradoxical embolism occurs – by
passage of an embolus from right heart to
left heart through atrial or ventricular
septal defect
8. PULMONARY THROMBOEMBOLISM
CONSEQUENCES OF
PULMONARY
THROMBOEMBOLISM
Sudden death
Due to massive pulmonary
embolism or emboli
obstructing 60% or more
of pulm circulation
Acute
corpulmonale
Numerous small
emboli obstruct most
of the pulmonary
vessels
Right heart
failure
Pulmonary
infarct
Obstruction
of small
vessels
Pulmonary
hemorrhage
Obstruction of
terminal branches
(endarteries) leads to
central pulmonary
hemorrhage
Resolution
Pulmonary
hypertension
Chronic cor
pulmonale
Pulmonary
arteriosclerosis
Multiple small
emboli undergoing
organization rather
than resolution
Multiple emboli
9. AMNIOTIC FLUID EMBOLISM
• 5th most common cause of maternal mortality world wide
• Though incidence is 2 to 6 in 100,000 deliveries death rate is
80%
• AFE is rare obstetric complications in which amniotic fluid, hair,
fetal cells or other debris enters the maternal circulation
leading to cardiorespiratory failure
• Process is more similar to anaphylaxis than embolus
(anaphylactoid syndrome of pregnancy)
10. AMNIOTIC FLUID EMBOLISM
Common causes of amniotic fluid embolism
• Old age
• Trauma
• Abortion
• Caesarian section
• Instrumental delivery
11. AMNIOTIC FLUID EMBOLISM
Pathogenesis
• Cause is infusion of amniotic fluid or fetal tissue into maternal circulation via a tear in
the placental membranes or rupture of uterine veins
12. AMNIOTIC FLUID EMBOLISM
• Morbidity and mortality in amniotic fluid embolism is not because
of obstruction of pulmonary veins but is due to
• Components of amniotic fluid producing anaphylactic reaction
• Release of vasoactive substances result from degranulation of
mast cells releasing histamine and tryptase
• Biochemical activation of coagulation factors, components of
complement pathway
13. AMNIOTIC FLUID EMBOLISM
Amniotic fluid components
Amniotic fluid (biochemical mediators)
• Surfactant
• Endothelin
• Leukotriene C4 and D4
• IL – 1 and TNF – α
• Thromboxane A2
• Prostaglandins
• Arachidonic acid
• Thromboplastin
• Collagen and Tissue factor III
• Phospholipase A2
• PF III
Anaphylactic reaction with
multisystem involvement
Fetal components
• Lanugo hair
• Vernix caseosa
• Fetal squames
• Bile stained meconium
• Fetal gut mucin
• Trophoblasts
Mechanical obstruction
(minor effects)
14. AMNIOTIC FLUID EMBOLISM
Progression occurs in 2 phases (Cotton1996)
Phase I
Amniotic fluid and fetal cells in maternal circulation
Release of biochemical mediators
Pulmonary artery vasospasm
Pulmonary hypertension
Elevated right ventricular pressure
Hypoxia
Myocardial and pulmonary
capillary damage
Left heart failure
Acute respiratory
distress syndrome
15. AMNIOTIC FLUID EMBOLISM
Phase II Biochemical mediators
DIC
Activation of complement pathway and coagulation
factors
Hemorrhagic phase
Massive hemorrhage and uterine atony
16. AMNIOTIC FLUID EMBOLISM
Clinical features
• Characterized by severe dyspnea, cyanosis and
shock followed by neurologic impairment ranging
from headache to seizures, coma and by DIC
17. AMNIOTIC FLUID EMBOLISM
Findings at autopsy
• Presence of the following substances in pulmonary
microvasculature
• Squamous cells shed from fetal skin
• Lanugo hair
• Fat from vernix
• Mucin derived from the fetal respiratory or GIT
18. FAT EMBOLISM
• Refers to presence of microscopic fat globules (sometimes with
hematopoietic bone marrow) in the vasculature after the
fractures of long bones or rarely in the setting of soft tissue
trauma or burns
• Injuries rupture sinusoids in the marrow or small veinules
allowing marrow or adipose tissue to herniate into the vascular
spaces and travel into lung
21. FAT EMBOLISM
Non- traumatic causes
• Agglutination of chylomicrons and VLDL by high levels of plasma CRP
• Disease related
• Diabetes, acute pancreatitis, burns, SLE and sickle cell crisis
• Drug related
• Parenteral lipid infusion
• Procedure related
• Orthopedic surgery, liposuction
22. FAT EMBOLISM
Fat embolism syndrome –
• Term applied to the minority of
patients who become symptomatic
• Characterized by
• Pulmonary insufficiency
• Neurologic symptoms
• Anemia
• Thrombocytopenia
Fatal in 5 – 15% of cases
Hypoxemia
Neurological
abnormalities
Petechial rash
TRIAD OF FES
23. FAT EMBOLISM
• Platelets adhere to fat globules and subsequent
aggregation or splenic sequestration - leading to
thrombocytopenia
• RBCs adhere around fat globules and or subsequent
hemolysis – leading to anemia
• Rapid onset of thrombocytopenia –leads to petechial rash
which is useful diagnostic clue
24. FAT EMBOLISM
Pathogenesis
• Both mechanical obstruction and biochemical injury
Mechanical obstruction –
• Fat emboli with associated red cell and platelet aggregates can occlude the pulmonary
and cerebral microvasculature
Biochemical injury
• Release of free fatty acids from fat globules exacerbate the situation by Causing local
toxic injury to endothelium and platelet activation and granulocyte recruitment
• With release of free radicals, proteases and eicosanoid, more vascular damage occurs
25. FAT EMBOLISM
1 to 3 days after injury there is sudden onset of
• Tachypnea
• Dyspnea
• Tachycardia
• Irritability and restlessness
• Further progresses to delirium and coma
26. 3 types of fat embolism syndrome (Sevitts classification)
• Subclinical FES
• Non fulminant FES
• Fulminant FES
27. FAT EMBOLISM
Subclinical FES
• Occurs around 3 days after trauma
• Characterized by decreased PaO2, hemoglobin and
platelets
• No clinical signs and symptoms of respiratory
insufficiency
28. FAT EMBOLISM
Non fulminant FES
• Occurs at any time upto 6 days after trauma
• Clinical signs and symptoms are evident
• Petechiae, tachycardia, respiratory failure and signs of CNS
embolism
• Thrombocytopenia, anemia, coagulation abnormalities,
• Chest X-ray- pulmonary alveolar and interstitial opacities
30. FAT EMBOLISM
Fulminant FES
• Occurs suddenly and rapidly, progressing quickly to death with in few
hours of trauma
• Clinical features are acute respiratory failure, acute cor pulmonal and
neurological embolic changes
• These changes result in death of patient shortly after injury
31. FAT EMBOLISM
• Special techniques like frozen section and stains for fat are required to demonstrate fat as
lipids dissolve in paraffin embedded sections
32. AIR EMBOLISM
• Gas bubbles within the circulation
can coalesce to form frothy
masses that obstruct vascular flow
and cause distal ischemic injury
• Air embolism occurs when there is
communication between the
vasculature and outside air and
negative pressure gradient “sucks”
in air
33. AIR EMBOLISM
Causes
Surgical
• During neurosurgery in sitting position creating a gravitational gradient and air
enters into the cerebral circulation
• Introduced during laproscopy and obstetric procedures
Non-surgical
• During endovascular and interventional procedures
• During mechanical ventilation
• As a consequence to chest wall injury
• Scuba diving, contrast infusion CT scan, CPR
34. AIR EMBOLISM
• More than 100ml is necessary to produce clinical affect in pulmonary
vasculature
• 300 to 500ml of air at 100ml/sec introduced may be fatal
• Emboli trapped in pulmonary vasculature causes
• Perfusion blockage of down stream region
• Microemboli in capillaries causes intense inflammatory response with
release of cytokines that may injure alveoli
• Bubbles in CNS may have mental impairment and even sudden onset
of coma
35. AIR EMBOLISM
Venous air entrapment
Massive air emboli
Entrapment of air in Superior vena cava or
Right Atrium or Right Ventricle
Impedes flow through heart
Decreased cardiac output and
decreased blood pressure
Small air bubbles
36. AIR EMBOLISM
Venous air entrapment
Massive air emboli Small air bubbles
Air lodges in
pulmonary capillaries
Functional decrease in
capillary bed
Increased pulmonary
arterial pressure and
central venous pressure
Decreased cardiac output and
decreased blood pressure
Increased alveolar dead
space
Decreased PO2 and
increased PCO2
Abnormal air blood interface in
pulmonary arteries denatures plasma
proteins
Amorphous proteinaceous and
cellular debris created on cell
surface
Attracts and activates WBC
Injury to pulmonary capillary
cells and increased permeability
Alveolar flooding
Non-cardiogenic
pulmonary edema
37. AIR EMBOLISM
Decompression sickness
• Occurs when individual experiences
sudden decrease in atmospheric pressure
• People at risk are
• Scuba and deep sea divers
• Under water construction workers
38. AIR EMBOLISM
• In underwater partial pressure of nitrogen in breathing air is
higher
• Nitrogen is not used by body but it gets dissolved in tissues
• As the partial pressure increases more and more nitrogen is
dissolved in tissues
• When the pressure decreases, nitrogen in the tissues comes out
39. AIR EMBOLISM
Pathogenesis
• If the diver ascends too rapidly, nitrogen comes out of solution in the tissues
and blood
• Rapid formation of gas bubbles with in skeletal muscles and supporting
tissues in and about joints is responsible for painful conditions called “the
bends” as in 1880 it was noted in those afflicted characteristically arched
their backs in a marren reminiscent of then popular womens fashion pose
called Grecian bend (photo)
40. AIR EMBOLISM
• In the lungs, gas bubbles in vasculature causes
• Oedema
• Hemorrhage
• Focal atelectasis
• emphysema
Respiratory distress called chokes
41. AIR EMBOLISM
Caisson disease
• More chronic form of decompression sickness
• Named for the pressurized vessels used in bridge
construction
• Workers in these vessels suffered both acute and
chronic form of decompression sickness
42. AIR EMBOLISM
• Caisson disease
• Persistence of gas emboli in skeletal system leads to multiple foci of
ischemic necrosis
• Common sites – femoral head, tibia and humerus
• Treatment – patients are placed in chambers under sufficiently high
pressure to force the gas bubbles back into solution
• Subsequently slow decompression permits gradual resorption and
exhalation of gases which prevents obstructive bubbles from