Arteriosclerosis 5 5-2014 lect 3
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This document discusses arteriosclerosis and atherosclerosis. It defines arteriosclerosis as hardening of the arteries, and identifies three patterns: small artery disease; calcification in aging muscular arteries; and atherosclerosis. Atherosclerosis is caused by fatty lesions called atheromas that protrude into arteries. Risk factors for atherosclerosis include age, gender, genetics, hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis involves endothelial injury, lipoprotein accumulation, monocyte recruitment, and smooth muscle cell proliferation. Morphologically, atherosclerosis begins as fatty streaks and progresses to atheromatous plaques containing lipids, cells, and extracellular matrix.
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Atherosclerosis pathology mbbs
The document discusses atherosclerosis and its risk factors and various hypotheses about its pathogenesis. It describes the roles of oxidized LDL, macrophages, and endothelial cells in driving atherosclerosis. It outlines the progression from fatty streaks to more advanced atheromatous plaques and complicated lesions. Fatty streaks are the earliest subclinical lesions while atherosclerosis refers to lesions that are clinically significant. Complications can arise from processes like calcification, ulceration, rupture, hemorrhage, and thrombosis.
Atherosclerosis
1. Atherosclerosis is a condition where arteries become narrowed and hardened due to plaque buildup in the artery wall.
2. Major risk factors include dyslipidemia, hypertension, diabetes, and smoking, which can cause endothelial injury and initiate a response involving smooth muscle cell proliferation and monocyte infiltration.
3. Plaque is made up of fat, cholesterol, calcium, and other substances and can progressively worsen over time, potentially leading to complications like heart attacks or strokes if plaques rupture or thrombosis occurs.
Embolism
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.
Odema
This document provides an overview of edema, including its definition, types, pathogenesis, and examples of important types of edema. Edema is defined as the abnormal accumulation of free fluid in interstitial tissue spaces or body cavities. It can be localized to an organ or limb, or generalized throughout the body. The pathogenesis of edema involves mechanisms that interfere with fluid balance, plasma oncotic pressure, capillary hydrostatic pressure, lymphatic flow, and sodium and water retention. Examples of important types of edema discussed include renal edema, cardiac edema, pulmonary edema, cerebral edema, hepatic edema, nutritional edema, and myxoedema.
Atherosclerosis
Atherosclerosis is triggered by injury to endothelial cells caused by physical trauma, hypertension, turbulent blood flow, free radicals from smoking or pollution, hyperlipidemia, homocysteinemia, or hyperglycemia from diabetes. This injury causes an inflammatory response and increased permeability, allowing monocytes and LDL to enter the arterial wall. Monocytes become lipid-laden foam cells, which accumulate and recruit smooth muscle cells to form fatty streaks. Over time, fatty streaks progress to atheromas containing lipid and smooth muscle, which can rupture and cause thrombosis leading to heart attacks or strokes.
Atherosclerosis morphology
description of gross and microscopic morphology of an atherosclerotic lesion, includes fatty streak, simple plaque and fatty plaque.
Haemodynamic disoders
The document discusses various hemodynamic disorders including edema, hemorrhage, thrombosis, embolism, and shock. It defines each condition and describes their mechanisms and presentations. Edema is an accumulation of fluid in tissues and can be caused by increased hydrostatic pressure, decreased oncotic pressure, lymphatic obstruction, or sodium retention. Hemorrhage is the leakage of blood from vessels, while thrombosis is the formation of a clot within vessels. Embolism occurs when a clot or other material travels through the bloodstream and blocks a vessel in another part of the body.
Atherosclerosis
Atherosclerosis is a disease where plaque builds up inside arteries. It is caused by risk factors like high cholesterol, hypertension, smoking, and diabetes. The plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, the plaque hardens and narrows the arteries. This limits blood flow and can lead to heart attacks, strokes, or other serious health problems if a plaque ruptures or a blood clot forms. The pathophysiology of atherosclerosis involves endothelial injury triggering a reaction and inflammation response, accumulation of macrophages in the arteries, and formation of foam cells which contribute to the growth of plaque over time.
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Atherosclerosis pathology mbbs
The document discusses atherosclerosis and its risk factors and various hypotheses about its pathogenesis. It describes the roles of oxidized LDL, macrophages, and endothelial cells in driving atherosclerosis. It outlines the progression from fatty streaks to more advanced atheromatous plaques and complicated lesions. Fatty streaks are the earliest subclinical lesions while atherosclerosis refers to lesions that are clinically significant. Complications can arise from processes like calcification, ulceration, rupture, hemorrhage, and thrombosis.
Atherosclerosis
1. Atherosclerosis is a condition where arteries become narrowed and hardened due to plaque buildup in the artery wall.
2. Major risk factors include dyslipidemia, hypertension, diabetes, and smoking, which can cause endothelial injury and initiate a response involving smooth muscle cell proliferation and monocyte infiltration.
3. Plaque is made up of fat, cholesterol, calcium, and other substances and can progressively worsen over time, potentially leading to complications like heart attacks or strokes if plaques rupture or thrombosis occurs.
Embolism
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.
Odema
This document provides an overview of edema, including its definition, types, pathogenesis, and examples of important types of edema. Edema is defined as the abnormal accumulation of free fluid in interstitial tissue spaces or body cavities. It can be localized to an organ or limb, or generalized throughout the body. The pathogenesis of edema involves mechanisms that interfere with fluid balance, plasma oncotic pressure, capillary hydrostatic pressure, lymphatic flow, and sodium and water retention. Examples of important types of edema discussed include renal edema, cardiac edema, pulmonary edema, cerebral edema, hepatic edema, nutritional edema, and myxoedema.
Atherosclerosis
Atherosclerosis is triggered by injury to endothelial cells caused by physical trauma, hypertension, turbulent blood flow, free radicals from smoking or pollution, hyperlipidemia, homocysteinemia, or hyperglycemia from diabetes. This injury causes an inflammatory response and increased permeability, allowing monocytes and LDL to enter the arterial wall. Monocytes become lipid-laden foam cells, which accumulate and recruit smooth muscle cells to form fatty streaks. Over time, fatty streaks progress to atheromas containing lipid and smooth muscle, which can rupture and cause thrombosis leading to heart attacks or strokes.
Atherosclerosis morphology
description of gross and microscopic morphology of an atherosclerotic lesion, includes fatty streak, simple plaque and fatty plaque.
Haemodynamic disoders
The document discusses various hemodynamic disorders including edema, hemorrhage, thrombosis, embolism, and shock. It defines each condition and describes their mechanisms and presentations. Edema is an accumulation of fluid in tissues and can be caused by increased hydrostatic pressure, decreased oncotic pressure, lymphatic obstruction, or sodium retention. Hemorrhage is the leakage of blood from vessels, while thrombosis is the formation of a clot within vessels. Embolism occurs when a clot or other material travels through the bloodstream and blocks a vessel in another part of the body.
Atherosclerosis
Atherosclerosis is a disease where plaque builds up inside arteries. It is caused by risk factors like high cholesterol, hypertension, smoking, and diabetes. The plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, the plaque hardens and narrows the arteries. This limits blood flow and can lead to heart attacks, strokes, or other serious health problems if a plaque ruptures or a blood clot forms. The pathophysiology of atherosclerosis involves endothelial injury triggering a reaction and inflammation response, accumulation of macrophages in the arteries, and formation of foam cells which contribute to the growth of plaque over time.
Atherosclerosis
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Artherosclerosis
Arteriosclerosis, also known as atherosclerosis, is a chronic inflammatory condition of the arteries that begins in childhood. It involves both elastic and muscular arteries systemically and segmentally. Risk factors include hypercholesterolemia, hyperlipidemia, smoking, hypertension, diabetes, sedentary lifestyle, obesity, and family history. It develops as a chronic inflammatory response to endothelial injury caused by interactions between modified lipoproteins, macrophages, T-lymphocytes, and normal arterial wall constituents. Over time, this can lead to plaque formation, arterial narrowing, reduced blood flow, increased blood pressure, and complications like ischemia and gangrene. Treatment focuses on risk factor modification through lifestyle changes and medication, while advanced cases
Pathology ofbloodandlymphaticvessels
The document discusses pathology of blood and lymphatic vessels. It describes the three main cellular components of vessel walls: endothelial cells, smooth muscle cells, and pericytes. Endothelial injury is critical for thrombus formation, atherosclerosis, and effects of hypertension. Endothelial dysfunction and activation are terms used to describe changes in endothelial cells in response to stimuli. Vascular injury ultimately results in intimal thickening. The document also discusses diseases of arteries including atherosclerosis, hypertensive vascular disease, inflammatory vasculitides, and others.
CVS pathology 2- atherosclerosis 2019, sufia husain
Atherosclerosis is a disease characterized by the buildup of fatty plaques in the inner walls of arteries. Over time, plaque accumulates and narrows the arteries. This restricts blood flow and can lead to complications like heart attacks and strokes. The plaques are made up of fat, cholesterol, calcium and other substances found in the blood. They form when cholesterol builds up and white blood cells try to repair the damaged lining of the artery. Major risk factors include age, male sex, family history, high blood pressure, high cholesterol, diabetes and smoking. Lifestyle changes like quitting smoking, exercising and eating a healthy diet can help reduce risk.
Blood vessel pathology
1. The document discusses the anatomy and pathology of blood vessels, including different types of arteries, veins, and capillaries.
2. It covers various vascular diseases like atherosclerosis, hypertension, and Buerger's disease. Atherosclerosis causes over half of deaths in western world and risk increases significantly between ages 40-60.
3. Hypertension is a major risk factor for ischemic heart disease and cerebrovascular accidents, with over 60% increased risk for IHD and 50% of hypertensive patients dying of heart or kidney disease.
Cardiac pathology
Ischemic heart disease, resulting from impaired blood supply to the heart, is currently the leading cause of cardiovascular disease death worldwide. It refers to conditions including angina, heart attack, chronic heart disease, heart failure and sudden cardiac death. The most common cause is coronary artery atherosclerosis and thrombosis, usually resulting from plaque rupture or erosion in the arteries. Vulnerable plaques are prone to rupture due to characteristics like a thin fibrous cap and large lipid core, exposing thrombogenic materials and narrowing the artery. Timely reopening of the blocked artery is crucial to limiting heart muscle damage from lack of blood flow.
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This document provides an overview of thromboembolism and its pathology. It discusses the Virchow triad of factors that predispose to thrombosis - endothelial injury, abnormal blood flow, and hypercoagulability. The key components and processes of thrombogenesis are described. Risk factors for deep vein thrombosis and the pathology of pulmonary embolism are also reviewed. The student is expected to understand the basic pathology of thrombogenesis and identify risk factors for thrombosis.
Atherosclerosis3
This document discusses the pathogenesis of atherosclerosis. It begins with a brief history of atherosclerosis and then discusses the structure of the normal artery and endothelial cells. It describes the response to injury hypothesis for the initiation and progression of atherosclerotic lesions. It discusses complications of atherosclerosis including plaque rupture and thrombosis. It concludes by discussing risk factors for atherosclerosis such as smoking, hypertension, hyperlipidemia, and metabolic syndrome.
Embolism
This document defines and describes different types of embolism. The most common type is thromboembolism, which occurs when a thrombus or part of a thrombus breaks off and is carried by the bloodstream. Pulmonary thromboembolism is a significant type that occurs when thrombi travel to the lungs and obstruct the pulmonary arteries. Other types include fat, air, gas and paradoxical embolisms. Air embolism can be venous, entering systemic veins during surgery or trauma, or arterial, entering the lungs during procedures like angiography. Decompression sickness is a form of gas embolism that affects divers or those exposed to changes in atmospheric pressure.
The vascular biology of atherosclerosis
Atherosclerosis begins with the accumulation of oxidized LDL particles in the arterial intima. This triggers an inflammatory response characterized by the recruitment and retention of monocytes and T cells. Monocytes take up oxidized LDL and become lipid-laden foam cells. Smooth muscle cells also migrate from the media and proliferate in the intima, secreting extracellular matrix. Over time, a complex atherosclerotic plaque develops containing foam cells, smooth muscle cells, extracellular matrix, microvessels, and areas of hemorrhage and thrombosis. The plaque can rupture, leading to clinical events such as heart attack or stroke.
Pathology of hemodynamic disorders Part 1 nov 2017 Sufia Husain
This document provides an overview of hemodynamic disorders including edema, hyperemia, congestion, hemorrhage, thrombosis, and infarction. It begins by defining edema and its various types. It then discusses hyperemia and congestion, distinguishing between the active process of hyperemia and the passive process of congestion. The document outlines the causes, pathogenesis and morphology of thrombosis. It also discusses endothelial injury, abnormal blood flow, and hypercoagulable states as they relate to the development of thrombosis. Specific conditions that can lead to endothelial dysfunction and abnormal blood flow are highlighted.
Diseases of blood vessels
This document discusses diseases of blood vessels including Monckeberg's arteriosclerosis, aneurysms, and tumors of blood vessels. Monckeberg's arteriosclerosis involves calcium deposition in the media of large and medium arteries. Aneurysms are abnormal dilations of blood vessels that can be classified based on composition, shape, location, and pathogenesis. Common types include atherosclerotic, syphilitic, dissecting, and berry aneurysms. Tumors of blood vessels include benign hemangiomas as well as intermediate and malignant tumors such as hemangioendotheliomas and angiosarcomas.
Atherosclerosis
Atherosclerosis is a disease affecting large arteries characterized by plaque buildup in the vessel wall containing lipids, inflammatory cells, and smooth muscle cells. It is caused by multiple risk factors like hyperlipidemia, smoking, hypertension, and diabetes. Symptoms vary depending on location and severity of blockages, and may include leg pain with walking, non-healing wounds, or gangrene. Treatment involves lifestyle changes, medications, and procedures like angioplasty or bypass surgery to improve blood flow.
Shock
This document defines and classifies shock. Shock is characterized by inadequate perfusion of cells and tissues due to reduced circulating blood volume and blood pressure. Shock is classified as hypovolemic (caused by blood or plasma loss), cardiogenic (caused by heart disease), septic (caused by infection), or other types like traumatic or neurogenic shock. The pathophysiology of each type is described. Hypovolemic shock results from blood or fluid loss, cardiogenic shock from reduced cardiac output, and septic shock from activation of the immune system and inflammatory response to infection. Shock progresses through compensated, decompensated, and irreversible stages as the body attempts but fails to maintain adequate perfusion of vital
Atherosclerosis - Pathogenesis
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The document contains 16 multiple choice questions testing knowledge of hemodynamic and thrombosis related topics. The questions cover causes of edema, sites of thrombosis formation, mechanisms of pulmonary embolism and congestive heart failure edema, characteristics of venous thrombosis and infarction, and definitions relating to thrombosis pathology. Key areas addressed include causes of generalized edema, predisposing factors for thrombosis, mechanisms of edema in heart failure, common sites of thrombus origin and venous thrombosis.
Pathology of hemodynamic disorders part 2 nov 2017 Dr. Sufia 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.
Diseases of vessels
Vascular disorders can affect arteries and veins in various ways. The document discusses several types of vascular disorders including:
1. Atherosclerosis is a buildup of plaque in the arteries which can restrict blood flow and cause complications like heart attacks and strokes.
2. Vasculitis refers to inflammation of blood vessels which has various immune-mediated forms that can affect large, medium, or small vessels.
3. Aneurysms are abnormal dilations of blood vessels or the heart that can be true or pseudo in nature and occur in different locations.
1. edema; hemodynamic disorders
The document discusses hemodynamic disorders including edema, hyperemia, hemorrhage, hemostasis, thrombosis, embolism, and infarction. Edema is defined as increased fluid in the interstitial tissue spaces and can be caused by increased hydrostatic pressure, decreased oncotic pressure, sodium retention, or inflammation. Treatment for edema focuses on reducing sodium intake, using diuretics to increase sodium excretion, and aldosterone antagonists.
Thrombosis complete
The document discusses thrombosis and thrombus formation. It defines thrombosis as the formation of a solid blood clot within the circulatory system. A thrombus is the blood clot itself. The key points covered include:
- Virchow's triad predisposes to clotting via endothelial injury, altered blood flow, and hypercoagulability.
- Platelets play a central role by adhering to injuries, releasing activation factors, and aggregating.
- The coagulation cascade is activated via intrinsic and extrinsic pathways ultimately forming fibrin.
- Stasis and turbulence promote clotting by slowing blood flow and pushing platelets to vessel walls.
- Hypercoag
Atherosclerosis and arteriosclerosis .pdf
1. Atherosclerosis is the accumulation of inflammatory cells, lipids, and connective tissue in the intima of large and medium arteries, forming fibroinflammatory plaques known as atheromas.
2. It develops over decades as a response to endothelial injury from risk factors like hypercholesterolemia and hypertension.
3. Complicated plaques can rupture, causing thrombosis, embolism, and occlusion of vessels, leading to complications like myocardial infarction.
Arteriosclerosis 6
Arteriosclerosis is a thickening and loss of elasticity of arterial walls that can occur in three patterns: atherosclerosis, Mönckeberg medial calcific sclerosis, and arteriolosclerosis. Atherosclerosis involves the buildup of fatty plaques in arteries due to risk factors like hyperlipidemia, hypertension, smoking, and diabetes. Over time, plaques can rupture, limiting blood flow and risking heart attack or stroke. Arteriolosclerosis affects small arteries and arterioles, presenting as either hyaline or hyperplastic thickening of vessel walls that reduces blood flow and can cause organ damage.
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Arteriosclerosis, also known as atherosclerosis, is a chronic inflammatory condition of the arteries that begins in childhood. It involves both elastic and muscular arteries systemically and segmentally. Risk factors include hypercholesterolemia, hyperlipidemia, smoking, hypertension, diabetes, sedentary lifestyle, obesity, and family history. It develops as a chronic inflammatory response to endothelial injury caused by interactions between modified lipoproteins, macrophages, T-lymphocytes, and normal arterial wall constituents. Over time, this can lead to plaque formation, arterial narrowing, reduced blood flow, increased blood pressure, and complications like ischemia and gangrene. Treatment focuses on risk factor modification through lifestyle changes and medication, while advanced cases
Pathology ofbloodandlymphaticvessels
The document discusses pathology of blood and lymphatic vessels. It describes the three main cellular components of vessel walls: endothelial cells, smooth muscle cells, and pericytes. Endothelial injury is critical for thrombus formation, atherosclerosis, and effects of hypertension. Endothelial dysfunction and activation are terms used to describe changes in endothelial cells in response to stimuli. Vascular injury ultimately results in intimal thickening. The document also discusses diseases of arteries including atherosclerosis, hypertensive vascular disease, inflammatory vasculitides, and others.
CVS pathology 2- atherosclerosis 2019, sufia husain
Atherosclerosis is a disease characterized by the buildup of fatty plaques in the inner walls of arteries. Over time, plaque accumulates and narrows the arteries. This restricts blood flow and can lead to complications like heart attacks and strokes. The plaques are made up of fat, cholesterol, calcium and other substances found in the blood. They form when cholesterol builds up and white blood cells try to repair the damaged lining of the artery. Major risk factors include age, male sex, family history, high blood pressure, high cholesterol, diabetes and smoking. Lifestyle changes like quitting smoking, exercising and eating a healthy diet can help reduce risk.
Blood vessel pathology
1. The document discusses the anatomy and pathology of blood vessels, including different types of arteries, veins, and capillaries.
2. It covers various vascular diseases like atherosclerosis, hypertension, and Buerger's disease. Atherosclerosis causes over half of deaths in western world and risk increases significantly between ages 40-60.
3. Hypertension is a major risk factor for ischemic heart disease and cerebrovascular accidents, with over 60% increased risk for IHD and 50% of hypertensive patients dying of heart or kidney disease.
Cardiac pathology
Ischemic heart disease, resulting from impaired blood supply to the heart, is currently the leading cause of cardiovascular disease death worldwide. It refers to conditions including angina, heart attack, chronic heart disease, heart failure and sudden cardiac death. The most common cause is coronary artery atherosclerosis and thrombosis, usually resulting from plaque rupture or erosion in the arteries. Vulnerable plaques are prone to rupture due to characteristics like a thin fibrous cap and large lipid core, exposing thrombogenic materials and narrowing the artery. Timely reopening of the blocked artery is crucial to limiting heart muscle damage from lack of blood flow.
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Atherosclerosis3
This document discusses the pathogenesis of atherosclerosis. It begins with a brief history of atherosclerosis and then discusses the structure of the normal artery and endothelial cells. It describes the response to injury hypothesis for the initiation and progression of atherosclerotic lesions. It discusses complications of atherosclerosis including plaque rupture and thrombosis. It concludes by discussing risk factors for atherosclerosis such as smoking, hypertension, hyperlipidemia, and metabolic syndrome.
Embolism
This document defines and describes different types of embolism. The most common type is thromboembolism, which occurs when a thrombus or part of a thrombus breaks off and is carried by the bloodstream. Pulmonary thromboembolism is a significant type that occurs when thrombi travel to the lungs and obstruct the pulmonary arteries. Other types include fat, air, gas and paradoxical embolisms. Air embolism can be venous, entering systemic veins during surgery or trauma, or arterial, entering the lungs during procedures like angiography. Decompression sickness is a form of gas embolism that affects divers or those exposed to changes in atmospheric pressure.
The vascular biology of atherosclerosis
Atherosclerosis begins with the accumulation of oxidized LDL particles in the arterial intima. This triggers an inflammatory response characterized by the recruitment and retention of monocytes and T cells. Monocytes take up oxidized LDL and become lipid-laden foam cells. Smooth muscle cells also migrate from the media and proliferate in the intima, secreting extracellular matrix. Over time, a complex atherosclerotic plaque develops containing foam cells, smooth muscle cells, extracellular matrix, microvessels, and areas of hemorrhage and thrombosis. The plaque can rupture, leading to clinical events such as heart attack or stroke.
Pathology of hemodynamic disorders Part 1 nov 2017 Sufia Husain
This document provides an overview of hemodynamic disorders including edema, hyperemia, congestion, hemorrhage, thrombosis, and infarction. It begins by defining edema and its various types. It then discusses hyperemia and congestion, distinguishing between the active process of hyperemia and the passive process of congestion. The document outlines the causes, pathogenesis and morphology of thrombosis. It also discusses endothelial injury, abnormal blood flow, and hypercoagulable states as they relate to the development of thrombosis. Specific conditions that can lead to endothelial dysfunction and abnormal blood flow are highlighted.
Diseases of blood vessels
This document discusses diseases of blood vessels including Monckeberg's arteriosclerosis, aneurysms, and tumors of blood vessels. Monckeberg's arteriosclerosis involves calcium deposition in the media of large and medium arteries. Aneurysms are abnormal dilations of blood vessels that can be classified based on composition, shape, location, and pathogenesis. Common types include atherosclerotic, syphilitic, dissecting, and berry aneurysms. Tumors of blood vessels include benign hemangiomas as well as intermediate and malignant tumors such as hemangioendotheliomas and angiosarcomas.
Atherosclerosis
Atherosclerosis is a disease affecting large arteries characterized by plaque buildup in the vessel wall containing lipids, inflammatory cells, and smooth muscle cells. It is caused by multiple risk factors like hyperlipidemia, smoking, hypertension, and diabetes. Symptoms vary depending on location and severity of blockages, and may include leg pain with walking, non-healing wounds, or gangrene. Treatment involves lifestyle changes, medications, and procedures like angioplasty or bypass surgery to improve blood flow.
Shock
This document defines and classifies shock. Shock is characterized by inadequate perfusion of cells and tissues due to reduced circulating blood volume and blood pressure. Shock is classified as hypovolemic (caused by blood or plasma loss), cardiogenic (caused by heart disease), septic (caused by infection), or other types like traumatic or neurogenic shock. The pathophysiology of each type is described. Hypovolemic shock results from blood or fluid loss, cardiogenic shock from reduced cardiac output, and septic shock from activation of the immune system and inflammatory response to infection. Shock progresses through compensated, decompensated, and irreversible stages as the body attempts but fails to maintain adequate perfusion of vital
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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.
Diseases of vessels
Vascular disorders can affect arteries and veins in various ways. The document discusses several types of vascular disorders including:
1. Atherosclerosis is a buildup of plaque in the arteries which can restrict blood flow and cause complications like heart attacks and strokes.
2. Vasculitis refers to inflammation of blood vessels which has various immune-mediated forms that can affect large, medium, or small vessels.
3. Aneurysms are abnormal dilations of blood vessels or the heart that can be true or pseudo in nature and occur in different locations.
1. edema; hemodynamic disorders
The document discusses hemodynamic disorders including edema, hyperemia, hemorrhage, hemostasis, thrombosis, embolism, and infarction. Edema is defined as increased fluid in the interstitial tissue spaces and can be caused by increased hydrostatic pressure, decreased oncotic pressure, sodium retention, or inflammation. Treatment for edema focuses on reducing sodium intake, using diuretics to increase sodium excretion, and aldosterone antagonists.
Thrombosis complete
The document discusses thrombosis and thrombus formation. It defines thrombosis as the formation of a solid blood clot within the circulatory system. A thrombus is the blood clot itself. The key points covered include:
- Virchow's triad predisposes to clotting via endothelial injury, altered blood flow, and hypercoagulability.
- Platelets play a central role by adhering to injuries, releasing activation factors, and aggregating.
- The coagulation cascade is activated via intrinsic and extrinsic pathways ultimately forming fibrin.
- Stasis and turbulence promote clotting by slowing blood flow and pushing platelets to vessel walls.
- Hypercoag
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Atherosclerosis and arteriosclerosis .pdf
1. Atherosclerosis is the accumulation of inflammatory cells, lipids, and connective tissue in the intima of large and medium arteries, forming fibroinflammatory plaques known as atheromas.
2. It develops over decades as a response to endothelial injury from risk factors like hypercholesterolemia and hypertension.
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Atherosclerosis is a disease where plaque builds up inside arteries. It is a chronic inflammatory response causing a build-up of fat, cholesterol, and other substances in the arteries. This build-up is called atheroma or plaque. Common sites of atherosclerosis are the abdominal aorta, coronary arteries, and carotid arteries. Risk factors include high LDL cholesterol and low HDL cholesterol. The current hypothesis is that it is initiated by endothelial dysfunction allowing inflammation and migration of cells into the artery wall where they proliferate and accumulate lipids over time, forming plaque. If plaque ruptures, it can cause heart attack or stroke by blocking blood flow.
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Atherosclerosis is a disease where plaque builds up inside arteries. It is a chronic inflammatory response causing a build-up of fat, cholesterol, and other substances in the arteries. This build-up is called atheroma or plaque. Common sites of atherosclerosis are the abdominal aorta, coronary arteries, and carotid arteries. Risk factors include high LDL cholesterol and low HDL cholesterol. The current hypothesis is that it is initiated by endothelial dysfunction allowing inflammation and migration of cells into the artery wall where they proliferate and accumulate lipids over time, forming plaque. If plaque ruptures, it can cause heart attack or stroke by blocking blood flow.
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Atherosclerosis is the hardening and narrowing of arteries caused by plaque buildup within the arterial wall. Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and narrows the arteries. There are three main types of atherosclerotic lesions: fatty streaks consisting of lipid-filled foam cells, fibrous plaques made of extracellular lipid and connective tissue, and complicated lesions with features like hemorrhage and ulceration. Risk factors for atherosclerosis include diabetes, hyperlipidemia, smoking, and hypertension. Genetic factors can also influence a person's risk by impacting lipid metabolism, coagulation, blood pressure regulation, and other
Atherosclerosis
Atherosclerosis - Definition - Risk Factors - Lesser and Non Quantitated risk factors - Arterial wall - The development of Atherosclerosis - Many Features of the injury Hypothesis - The process of Atherogenesis - Pathogenesis in short - Morphology of Atheroma - Components of Atheromatous Plaque (MP) - Complications and clinical significance - Cardiovascular risk and its assessment.
pathology of Atherosclerosis, dissection and aneurysm copy
Based on the information provided about Mr. Gamal:
- CT angiography would likely reveal an abdominal aortic aneurysm, showing markedly increased aortic diameter below the renal arteries.
- The most probable cause in his case is atherosclerosis, given his risk factors of diabetes, hypertension, smoking history and hyperlipidemia.
- His risk factors are diabetes, hypertension, smoking history, obesity (BMI of 30), and hyperlipidemia.
- His condition would be classified as an atherosclerotic abdominal aortic aneurysm.
- Possible complications include rupture of the aneurysm, thrombosis/embolism, compression of adjacent structures, or occlusion of branches supplying organs like the kidneys or intestines
Pathology of blood vessels
This document summarizes pathology of blood vessels. It begins by describing the normal structure of arteries, veins and capillaries. It then discusses the cells that make up blood vessel walls and their response to injury, which can lead to intimal thickening. It also briefly mentions some congenital vessel anomalies. The majority of the document focuses on arteriosclerosis and its subtype, atherosclerosis - describing the morphology, risk factors, pathogenesis, natural history and approaches for prevention. It concludes by outlining hypertensive vascular disease, its causes and pathogenesis.
Atherosclerosis Slideshare Pathology Ppt Notes
This document summarizes atherosclerosis and its pathogenesis. It defines key terms like arteriosclerosis, atherosclerosis, and atherogenesis. It describes the major locations where atherosclerosis occurs and risk factors like dyslipidemia, hypertension, smoking, age, and family history. Symptoms include chest pain and shortness of breath. The pathogenesis involves two main hypotheses: 1) the reaction-to-injury hypothesis where endothelial injury leads to intimal proliferation and foam cell formation, and 2) the monoclonal hypothesis where smooth muscle cell proliferation is the primary event. Overall it provides an overview of atherosclerosis, its terminology, risk factors, symptoms, and pathogenic mechanisms.
WUP Pathology of BLOOD VESSELS in philippines .pptx
pathology of vascular system for medical students in asian counties such as Philippines. The chapter is seen in Robbins Pathologic bases of disease
acute coronary syndrome
Acute coronary syndrome (ACS) occurs when a plaque in the coronary arteries ruptures or erodes, restricting blood flow. Plaque forms over time as LDL cholesterol builds up in artery walls due to risk factors like smoking, diabetes, and hypertension. The plaque contains an inflammatory necrotic core covered by a fibrous cap. Rupture occurs when the cap thins, exposing the core and triggering a clot. Medications treat ACS by lowering cholesterol and inflammation to stabilize plaques and prevent clots.
Aneurysms & dissection
An aneurysm is an abnormal dilation of a blood vessel or heart. True aneurysms involve an intact but thinned wall, while false aneurysms involve a defect in the wall. Aneurysms are usually caused by atherosclerosis or hypertension and can rupture catastrophically. Arterial dissection occurs when blood enters the arterial wall, dissecting between layers. The main types are abdominal aortic aneurysms and thoracic aortic aneurysms. Unruptured aneurysms are generally managed surgically while ruptured aneurysms have high mortality.
PATHOLOGY - Arteriosclerosis
Arteriosclerosis is the hardening and narrowing of arteries due to plaque buildup. The three main types are arteriolosclerosis (small arteries), Monckeberg medial sclerosis (calcification of muscular arteries), and atherosclerosis (most common). Atherosclerosis features atheromas that protrude into the vessel lumen. Risk factors like age, gender, genetics, hyperlipidemia, hypertension, smoking, and diabetes accelerate atherosclerosis. Inflammation and infection also contribute to plaque formation and rupture, which can cause acute issues like heart attack or stroke.
Vulnerable plaque
The document discusses vulnerable plaques and patients. It defines vulnerable plaque as a plaque susceptible to rupture. Research has shown that ruptured thin-cap fibroatheromas (TCFAs) are the most common underlying plaque morphology in cardiac deaths. The goal is to identify vulnerable plaques in stable patients to prevent events like heart attack and sudden cardiac death. A vulnerable plaque is typically characterized by a thin fibrous cap, large lipid core, and inflammation. Identifying high-risk features in plaques can help determine which patients are vulnerable.
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pathology of Atherosclerosis, dissection and aneurysm copy
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Repair 2017
Tissue repair occurs through two main processes: regeneration and scar formation. Regeneration involves the proliferation of residual cells to replace damaged tissue. Some tissues like skin and liver can regenerate fully. Scar formation involves the deposition of connective tissue when regeneration is not possible. This involves granulation tissue formation, fibronectin production, collagenization, and scar maturation. Cell proliferation in repair is regulated by growth factors and the extracellular matrix plays a key role in wound healing and scar formation.
Repair 2
This document discusses the process of wound healing through first and second intention. It begins by outlining the steps of healing by first intention for clean surgical incisions, including clot formation, re-epithelialization across the wound by day 3, and collagen deposition and scar maturation over subsequent weeks. Healing by second intention for wounds with separated edges involves more granulation tissue formation and wound contraction to reduce the gap between tissue edges. Complications can arise from deficient or excessive scar formation, including dehiscence, ulceration, hypertrophic scarring, and contractures.
Repair and healing_1
Tissue repair occurs through two main processes: regeneration and scar formation. Regeneration involves the proliferation of residual cells to replace damaged tissue. Some tissues like skin and liver can regenerate fully. Scar formation involves the deposition of connective tissue when regeneration is not possible. This involves granulation tissue formation, fibronectin production, collagenization, and scar maturation. Cell proliferation in repair is regulated by growth factors and the extracellular matrix plays a key role in wound healing and scar formation.
Infarction
Infarction is defined as an area of necrosis due to decreased blood flow. It can be hemorrhagic or anemic, red or white. Cardiac biomarkers such as troponin T and I, creatine kinase (CK-MB), and myoglobin are released from damaged heart muscle and can help evaluate myocardial injury. These biomarkers have characteristic rise and fall patterns. Renal failure can alter the diagnostic accuracy of cardiac biomarkers. Treatment of acute myocardial infarction focuses on restoring normal blood flow and salvaging heart muscle.
Neoplasia 120107095645-phpapp01
Cancer arises from uncontrolled cell growth and spread of abnormal cells. It is not a single disease but many disorders that differ in causes and responses to treatment. Some cancers like Hodgkin's lymphoma are curable, while others like pancreatic cancer are usually fatal. Understanding the molecular basis and causes of cancer has led to declines in cancer mortality in recent decades. Neoplasia refers to abnormal cell growth, and tumors can be benign or malignant. Benign tumors are self-limited and do not spread, while malignant tumors invade nearby tissue and metastasize. Cancers are classified based on the cell type of origin, such as carcinomas arising from epithelial cells and sarcomas from connective tissue cells.
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This document discusses cellular responses to stress and noxious stimuli. It describes how cells maintain homeostasis through adaptations like hypertrophy, hyperplasia, and atrophy in response to physiological changes. If stresses exceed adaptive responses, cells undergo injury which can initially be reversible but lead to irreversible injury and cell death if the stress persists. The document outlines different types of cell death including necrosis, apoptosis, and autophagy, and discusses how cellular derangements and metabolic issues can also contribute to cell injury over time.
Cell injury reversible injury lecture 5
Cells can become rapidly nonfunctional after injury, though the damage may be reversible. Prolonged injury can lead to irreversible damage and cell death. Under the microscope, reversible injury shows cellular swelling and fatty change, while necrosis appears glassy and homogeneous as proteins and RNA denature. Necrotic cells release enzymes and can be detected in blood earlier than microscopic changes appear.
Cell injury metaplasia l autosaved]
Metaplasia is a reversible change where one differentiated cell type is replaced by another. The most common epithelial metaplasia is the replacement of columnar cells with squamous cells. Stones in excretory ducts can lead to squamous metaplasia by replacing the normal columnar epithelium with stratified squamous epithelium. Prolonged influences that cause metaplasia can initiate cancer if the metaplastic epithelium undergoes malignant transformation.
Cell injury causes and overview of cell injury and cell death lect 4 jan 2020
Cell injury occurs when cells are stressed beyond their ability to adapt or are exposed to damaging agents. Injury can progress from a reversible to an irreversible stage, ultimately leading to cell death. The hallmarks of reversible injury include reduced ATP production, cellular swelling, and alterations to organelles. With continued damage, injury becomes irreversible and the cell dies through necrosis or apoptosis. Hypoxia is the most common cause of cell injury, as it reduces aerobic respiration. Other causes include physical and chemical agents, infections, immunological reactions, genetic factors, and nutritional imbalances.
Cell adaptations dec 2019 lect 2
Metaplasia is the replacement of one adult cell type with another adult cell type. It is typically irreversible (c) and describes the underlying pathology of Barrett's oesophagus (d), where the normal squamous epithelium of the lower esophagus is replaced by columnar epithelium resembling intestinal epithelium. Metaplasia is not an increase in cell number or size (e) and does not preserve mucus secretion or be caused by B12 deficiency (a,b).
Cell adaptation 31dec 2019 lect 3
1. Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferations may eventually arise. Patients with hyperplasia are at increased risk for developing cancer.
2. Hyperplasia is the result of growth factor-driven proliferation of mature cells and increased output of new cells from tissue stem cells.
3. Metaplasia is a reversible change where one cell type replaces another. It results from the reprogramming of stem cells or undifferentiated mesenchymal cells, causing them to differentiate along a new pathway in response to environmental signals.
Cell injury apoptosis lect 08jan 2020
Apoptosis is a tightly regulated and genetically programmed form of cell death where cells activate enzymes to degrade their own nuclear DNA and proteins. Cells undergoing apoptosis break into fragments called apoptotic bodies that are phagocytosed without eliciting inflammation. Apoptosis eliminates damaged or unneeded cells and plays an important role in development, tissue homeostasis, and the removal of infected or abnormal cells. It involves cell shrinkage, chromatin condensation, blebbing of the cell membrane, and the formation of apoptotic bodies that are phagocytosed without inflammatory response.
Cell injury necrosis lect 6 jan 2020
This document discusses various patterns of tissue necrosis seen microscopically:
- Coagulative necrosis preserves tissue architecture for days as cells are slowly removed by phagocytosis. It can result from ischemia.
- Liquefactive necrosis digests dead cells into a liquid mass due to bacterial or fungal infection stimulating leukocytes. Pus results.
- Specific types of necrosis include caseous, fat, fibrinoid, and those seen in conditions like gangrene and myocardial infarction.
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This document defines and discusses different types of aneurysms. It begins by defining a true aneurysm as an abnormal dilation of a blood vessel or heart that involves an attenuated but intact arterial wall. It then discusses classifications of aneurysms by shape and size. The document goes on to explain the pathogenesis of aneurysms, focusing on processes that compromise the structure or function of vascular wall connective tissue. It provides details on abdominal aortic aneurysms, thoracic aortic aneurysms, and aortic dissection.
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Arteriosclerosis 5 5-2014 lect 3
- 2. ARTERIOSCLEROSIS BY DR ABDUL AZIZ SHAIKH MBBS,M.PHIL(HISTOPATHOLOGY) LUMHS JAMSHORO
- 4. Arteriosclerosis means hardening of the arteries. It reflects arterial wall thickening and loss of elasticity. Three patterns. a) Arteriosclerosis affects small arteries and arterioles and cause ischemic injury.
- 5. b)Mönckeberg medial sclerosis is calcific deposits in muscular arteries in old age. c)Atheroclerossis: Greek word for gruel and hardening.
- 6. ATHEROSCLEROSIS •It is caused by intimal lesions called atheromas that protude into vessel lumens. •An atheromatous plaque consists of a raised lesion with soft yellow, grumous core of lipid(mainly cholesterol and cholesterol esters) covered by a white fibrous cap.
- 8. ATHEROSCLEROSIS •They cause obstruction of blood flow, can rupture leading to catastrophic vessel thrombosis, weakens media leads to aneurysm formation.
- 9. EPIDEMIOLOGY Constitutional risk factors in IHD: a) Age: Old age b) Gender: Females protected in pre menopausal age. c) Genetics: Family History
- 10. CONTINUED Modified risk Factors: a) Hyperlipidemia: Hypercholestrolemia, LDL is bad cholesterol. b) Hypertension: Both systolic and diastolic c) Cigarette smoking d) Diabetes Mellitus
- 11. CONTINUED Additional risk factors: a) Inflammation: Increased CRP b) Hyperhomocystinemia c) Metabolic syndrome: Associated with insulin resistance d) Lipoprotein (a) is an altered form of LDL e) Factors affecting hemostasis: Elevated levels of plasminogen activator inhibitor 1. Thrombin and platelet derived factors. f) Type A Personality persons
- 14. PATHOGENESIS •Response-to-injury hypothesis: According to this, atherosclerosis is a chronic inflammatory and healing response of arterial wall to endothelial injury. •Lesion progression occurs through the interaction of modified lipoproteins, monocyte-derived macrophage, and T lymphocytes with the normal cellular constituents arterial wall.
- 15. CONTINUED Following Pathologic events occur: a) Endothelial injury, which causes increased vascular peremeability, leukocyte adhesion and thrombosis. b) Accumulation of lipoproteins(mainly LDL) in the vessel wall. c) Monocyte adhesion to endothelium, followed by migration into intima and transformation into macrophages and foam cells. d) Platelet adhesion
- 16. CONTINUED e) Factor release from activated platelets, macrophages and vascular wall cells inducing smooth muscle cell recruitment. f) Smooth muscle cell proliferation and ECM production. g) Lipid accumulation both extracellular and within cells(macrophages and smooth muscles)
- 25. MORPHOLOGY • Fatty streaks: Fatty streaks are the earliest lesion in atherosclerosis. They are composed of lipid filled foamy macrophages. These lesions don’t cause any flow disturbane. • Atherosclerotic plaque: The key processes in atherosclerosis are intimal thickening and lipid accumulation. • Atheromatous plaque impinge on the lumen of artery and grossly appear white to yellow; superimposed thrombus over ulcerated plaques is red-brown.
- 27. CONTINUED Plaques vary from 0.3 to 1.5cm in diameter but can coalese to form large masses. Atherosclerotic plaques have three principle components. i. Cells, including smooth muscle cells, macrophages and T-cells. ii. ECM including collagen, elastic fibers, and proteoglycans and iii. Intracellular and extra cellular lipid.
- 31. CONTINUED Atherosclerotic plaques are susceptible to the following clinically important changes. i. Rupture, ulceration or erosin-leads to thrombosis ii. Haemorrhage into a plaque. iii. Atheroembolism. iv. Aneurysm formation.
- 38. JAZAKALLAH