This document discusses cardiac disorders and atherosclerosis. It begins by outlining the objectives of reviewing cardiac anatomy and physiology, coronary circulation, the conduction system of the heart, factors regulating stroke volume, and atherosclerosis. It then provides details on the location and chambers of the heart, blood flow through the heart, the conducting system, coronary circulation, the anatomy of blood vessels, lipoproteins, atherosclerosis versus arteriosclerosis, risk factors for coronary artery disease, and major constitutional and acquired risk factors.
This document provides an outline and introduction for a 15-hour course on cardiovascular pathology. It begins with an outline of topics to be covered, including the heart, arteries, veins, and investigations. It then provides details on the anatomy and physiology of the cardiovascular system and mechanisms of cardiovascular disease. Key topics summarized include the structure and function of the heart, cardiac output, laws of the cardiovascular system, mechanisms of cardiovascular disease, and common investigations like imaging, electrocardiograms, and diagnostic tests.
Lecture 7 diseases of the vascular system - Pathology Areej Abu Hanieh
This document discusses diseases of the vascular system. It begins by introducing arterial diseases such as atherosclerosis, which is the most common and involves the deposition of lipid plaques in artery walls. Aneurysms are localized swellings in artery walls that can be caused by atherosclerosis or other factors like hypertension. Vasospastic conditions like Raynaud's disease involve vasoconstriction of small blood vessels. The document also covers diseases of the veins such as varicose veins, chronic venous insufficiency, and venous thromboses. Deep vein thromboses in particular can be dangerous if pieces of the clot break off and travel to the lungs (pulmonary embolism).
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.
- Hemangioma is a benign tumor of blood vessels characterized by increased and abnormal blood vessels. Cavernous hemangioma involves large, dilated vascular channels in the liver. It arises from endothelial cells and can cause abdominal pain from compression.
- Coronary artery atherosclerosis involves plaques with necrotic cores, cholesterol, and inflammatory cells that can rupture and cause thrombosis, potentially leading to myocardial infarction.
- Aortic aneurysm is an abnormal dilation of the aorta that can contain thrombi and cause emboli in the lungs through fragmentation. Medial calcification or Monckeberg's sclerosis involves calcification of medium arteries and can cause hypertension.
This document discusses arteriosclerosis and atherosclerosis. It defines arteriosclerosis as the thickening, hardening, and loss of elasticity of artery walls. Atherosclerosis is a specific form of arteriosclerosis characterized by the buildup of fatty plaques on artery walls. Risk factors for atherosclerosis include age, gender, genetics, hyperlipidemia, hypertension, and diabetes. The pathogenesis of atherosclerosis involves endothelial injury, smooth muscle cell proliferation, and accumulation of macrophages and lipids in the artery wall to form atherosclerotic plaques. Treatment options discussed are medications, angioplasty, stenting, and bypass surgery. The document also discusses venous disease and varicose veins, symptoms, and treatment methods
This document discusses vascular diseases including atherosclerosis and hypertension. It provides detailed diagrams and descriptions of:
1. The progression of atherosclerotic lesions from fatty streaks to complicated plaques that can obstruct blood vessels.
2. The response-to-injury hypothesis of how atherosclerosis develops from initial endothelial damage and accumulation of inflammatory cells and lipids.
3. Types of hypertension including essential hypertension thought to be caused by genetic and environmental factors that increase cardiac output and peripheral resistance.
4. Specific genetic mutations and pathways involved in inherited forms of hypertension affecting sodium reabsorption and the renin-angiotensin system.
This document provides an outline and introduction for a 15-hour course on cardiovascular pathology. It begins with an outline of topics to be covered, including the heart, arteries, veins, and investigations. It then provides details on the anatomy and physiology of the cardiovascular system and mechanisms of cardiovascular disease. Key topics summarized include the structure and function of the heart, cardiac output, laws of the cardiovascular system, mechanisms of cardiovascular disease, and common investigations like imaging, electrocardiograms, and diagnostic tests.
Lecture 7 diseases of the vascular system - Pathology Areej Abu Hanieh
This document discusses diseases of the vascular system. It begins by introducing arterial diseases such as atherosclerosis, which is the most common and involves the deposition of lipid plaques in artery walls. Aneurysms are localized swellings in artery walls that can be caused by atherosclerosis or other factors like hypertension. Vasospastic conditions like Raynaud's disease involve vasoconstriction of small blood vessels. The document also covers diseases of the veins such as varicose veins, chronic venous insufficiency, and venous thromboses. Deep vein thromboses in particular can be dangerous if pieces of the clot break off and travel to the lungs (pulmonary embolism).
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.
- Hemangioma is a benign tumor of blood vessels characterized by increased and abnormal blood vessels. Cavernous hemangioma involves large, dilated vascular channels in the liver. It arises from endothelial cells and can cause abdominal pain from compression.
- Coronary artery atherosclerosis involves plaques with necrotic cores, cholesterol, and inflammatory cells that can rupture and cause thrombosis, potentially leading to myocardial infarction.
- Aortic aneurysm is an abnormal dilation of the aorta that can contain thrombi and cause emboli in the lungs through fragmentation. Medial calcification or Monckeberg's sclerosis involves calcification of medium arteries and can cause hypertension.
This document discusses arteriosclerosis and atherosclerosis. It defines arteriosclerosis as the thickening, hardening, and loss of elasticity of artery walls. Atherosclerosis is a specific form of arteriosclerosis characterized by the buildup of fatty plaques on artery walls. Risk factors for atherosclerosis include age, gender, genetics, hyperlipidemia, hypertension, and diabetes. The pathogenesis of atherosclerosis involves endothelial injury, smooth muscle cell proliferation, and accumulation of macrophages and lipids in the artery wall to form atherosclerotic plaques. Treatment options discussed are medications, angioplasty, stenting, and bypass surgery. The document also discusses venous disease and varicose veins, symptoms, and treatment methods
This document discusses vascular diseases including atherosclerosis and hypertension. It provides detailed diagrams and descriptions of:
1. The progression of atherosclerotic lesions from fatty streaks to complicated plaques that can obstruct blood vessels.
2. The response-to-injury hypothesis of how atherosclerosis develops from initial endothelial damage and accumulation of inflammatory cells and lipids.
3. Types of hypertension including essential hypertension thought to be caused by genetic and environmental factors that increase cardiac output and peripheral resistance.
4. Specific genetic mutations and pathways involved in inherited forms of hypertension affecting sodium reabsorption and the renin-angiotensin system.
1. The document discusses atherosclerosis and ischemic heart disease. Atherosclerosis is a disease of large and medium arteries characterized by plaque buildup within the artery wall.
2. Risk factors for atherosclerosis include age, gender, family history, hyperlipidemia, hypertension, smoking, and diabetes. Grossly, plaques appear white to yellow and firm or soft. Microscopically, plaques contain macrophages, foam cells, cholesterol, and calcium.
3. Ischemic heart disease is caused by an imbalance between myocardial oxygen supply and demand. Myocardial infarction results from coronary artery occlusion and causes heart muscle cell death. On gross exam, infarcts appear yellow or hemorrhagic
This document summarizes various cardiac pathologies. It discusses problems related to inadequate cardiac output such as leaks in the cardiovascular system, irregular heart rhythms, obstructions to blood flow, and valve problems. Congenital heart diseases are also examined, noting they result from mixing of oxygenated and unoxygenated blood and can be caused by genetic or environmental factors like infections. Specific congenital defects like atrial septal defects and tetralogy of Fallot are described. Other cardiac conditions reviewed include ischemic heart disease, hypertension, cardiomyopathy, pericardial diseases, infective endocarditis, and rheumatic fever.
The document discusses the cardiovascular system and provides information about diseases of blood vessels and the heart. It covers topics like arteriosclerosis, atherosclerosis, aneurysms, vasculitis, and tumors of blood vessels. For diseases of the heart, it mentions mechanisms of cardiac dysfunction like pump failure, outflow obstruction, regurgitant flow, conduction defects, and disruption of circulation. Risk factors for atherosclerosis include age, sex, genetics, hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis of atherosclerosis involves chronic endothelial injury and inflammation.
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.
Vasculitis refers to inflammatory diseases involving blood vessels. This document discusses several types of vasculitis including:
- Buerger's disease (thromboangiitis obliterans), which causes inflammation and thrombosis of small and medium arteries in smokers.
- Polyarteritis nodosa, a systemic vasculitis of small and medium arteries typically involving the kidneys and viscera.
- Giant cell arteritis, which causes inflammation of large and medium arteries in the head, especially the temporal arteries, in older individuals.
- Takayasu arteritis, a rare vasculitis causing fibrous thickening of the aortic arch and narrowing of great vessel origins.
The document discusses various congenital cardiac defects including:
1) Ventricular septal defects which allow left-to-right shunting of blood and can cause pressure/volume changes in the ventricles.
2) Transposition of the great arteries where the aorta arises from the right ventricle and pulmonary artery from the left ventricle, causing right-to-left shunting.
3) Tetralogy of Fallot, a condition characterized by four defects that cause deoxygenated blood to bypass the lungs and mix with oxygenated blood.
This document provides information about atherosclerosis, including its definition, locations where it commonly occurs, complications that can arise, risk factors, pathogenesis, and histological features. It defines atherosclerosis as a hardening and loss of elasticity of arterial walls. The most common sites are the abdominal aorta, iliac arteries, coronary arteries, and carotid arteries. Complications include myocardial infarction, stroke, aneurysm formation, and gangrene. Major risk factors include hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis involves response to endothelial injury from various insults, resulting in inflammation and deposition of lipids in the arterial wall.
Cardiovascular disease is caused by conditions that affect the heart and blood vessels such as coronary heart disease, thrombosis, heart attacks, and strokes. The main causes are atherosclerosis, where plaque builds up in the arteries, and hypertension, or high blood pressure. Risk factors for cardiovascular disease include unhealthy eating, smoking, lack of exercise, obesity, diabetes, and high cholesterol.
This document provides an overview of atherosclerosis (ATH), including its definition, most common sites of occurrence, characteristic lesions, risk factors, pathogenesis, and complications. It defines ATH as a hardening and loss of elasticity of arterial walls. Key points include: ATH is a chronic inflammatory response initiated by endothelial injury; lipoproteins such as LDL accumulate in the arterial wall and undergo oxidation, promoting inflammation; risk factors include age, genetics, hypertension, hyperlipidemia, smoking, and diabetes. Complications involve reduced blood flow leading to ischemia of vital organs.
FULL HYPERMEDIA INTERACTIVE VERSION
OPEN / DOWNLOAD FULL LIVE HYPERMEDIA PRESENTATION
http://www.scribd.com/doc/106694518/IVMS-CV-Cardiovascular-PathologyPresentation
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.
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.
The heart is a muscle about the size of a fist located behind the breastbone. It pumps blood through the body through two coronary arteries that encircle the heart. Coronary artery disease occurs when fatty deposits build up in the arteries and reduce blood flow, which can lead to chest pain, heart attacks, or heart failure. Risk factors for coronary artery disease include age, family history, smoking, high blood pressure, high cholesterol, obesity, and diabetes. Treatment depends on the severity of disease but may include lifestyle changes, medications, procedures like angioplasty to open blocked arteries, or bypass surgery.
This document discusses various types of heart disease, including myocarditis, arrhythmia, cardiac failure, ischemic heart disease, and myocardial infarction. It provides details on:
- Causes of myocarditis including various infectious and non-infectious agents
- Classification of myocarditis and cardiac failure based on factors like duration, etiology, and location of failure
- Symptoms of cardiac failure like shortness of breath, fatigue, and edema
- Causes, symptoms, and signs of arrhythmias, ischemic heart disease, and myocardial infarction
- Types of arrhythmias based on the cardiac function affected - automatism, conductivity, excitability, or contractility
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.
This document provides information about various cardiovascular pathology cases for medical students. It includes questions and descriptions of thrombus, organizing thrombus, atherosclerosis, lung and spleen infarction, mesenteric artery occlusion, aortic dissection, myocardial infarction, and jars containing specimens of lung infarction, bowel infarction, early and advanced atherosclerosis, aortic dissection, left ventricular hypertrophy, and old myocardial infarction. Students are asked to identify features, causes, and complications represented in the images and specimens.
The document discusses several cardiovascular pathologies including congenital disorders like hemophilia and defects of the interventricular septum. Hemophilia is an inherited bleeding disorder caused by deficiencies in clotting factors VIII or IX. Symptoms include bleeding into joints and prolonged bleeding. Interventricular septal defects are openings in the wall between the ventricles that can cause murmurs. The document also covers traumatic reticuloperitonitis in cattle which is caused by sharp objects piercing the reticulum and pericardium, causing inflammation and fluid buildup. Myocarditis, or heart muscle inflammation, has various infectious causes like certain viruses in various animal species.
Arteries are blood vessels that carry blood away from the heart. This blood is normally oxygenated, exceptions made for the pulmonary and umbilical arteries
The cardiovascular system includes the heart, blood vessels, and blood. The heart pumps blood through the blood vessels, supplying oxygen and nutrients to tissues and removing waste. The document defines the components of the cardiovascular system, including blood, heart chambers and valves, arteries, veins, and capillaries. It also describes diseases that can affect the heart such as coronary artery disease, heart attacks, and congestive heart failure.
The document summarizes the cardiovascular system, including the circulatory and lymphatic systems. It describes the heart, blood vessels, blood flow through pulmonary and systemic circulation. It also discusses common diseases like atherosclerosis, heart attack, angina, and their diagnosis and treatment. The circulatory system functions to transport blood throughout the body, while the lymphatic system transports lymph and maintains fluid balance.
1. The document discusses atherosclerosis and ischemic heart disease. Atherosclerosis is a disease of large and medium arteries characterized by plaque buildup within the artery wall.
2. Risk factors for atherosclerosis include age, gender, family history, hyperlipidemia, hypertension, smoking, and diabetes. Grossly, plaques appear white to yellow and firm or soft. Microscopically, plaques contain macrophages, foam cells, cholesterol, and calcium.
3. Ischemic heart disease is caused by an imbalance between myocardial oxygen supply and demand. Myocardial infarction results from coronary artery occlusion and causes heart muscle cell death. On gross exam, infarcts appear yellow or hemorrhagic
This document summarizes various cardiac pathologies. It discusses problems related to inadequate cardiac output such as leaks in the cardiovascular system, irregular heart rhythms, obstructions to blood flow, and valve problems. Congenital heart diseases are also examined, noting they result from mixing of oxygenated and unoxygenated blood and can be caused by genetic or environmental factors like infections. Specific congenital defects like atrial septal defects and tetralogy of Fallot are described. Other cardiac conditions reviewed include ischemic heart disease, hypertension, cardiomyopathy, pericardial diseases, infective endocarditis, and rheumatic fever.
The document discusses the cardiovascular system and provides information about diseases of blood vessels and the heart. It covers topics like arteriosclerosis, atherosclerosis, aneurysms, vasculitis, and tumors of blood vessels. For diseases of the heart, it mentions mechanisms of cardiac dysfunction like pump failure, outflow obstruction, regurgitant flow, conduction defects, and disruption of circulation. Risk factors for atherosclerosis include age, sex, genetics, hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis of atherosclerosis involves chronic endothelial injury and inflammation.
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.
Vasculitis refers to inflammatory diseases involving blood vessels. This document discusses several types of vasculitis including:
- Buerger's disease (thromboangiitis obliterans), which causes inflammation and thrombosis of small and medium arteries in smokers.
- Polyarteritis nodosa, a systemic vasculitis of small and medium arteries typically involving the kidneys and viscera.
- Giant cell arteritis, which causes inflammation of large and medium arteries in the head, especially the temporal arteries, in older individuals.
- Takayasu arteritis, a rare vasculitis causing fibrous thickening of the aortic arch and narrowing of great vessel origins.
The document discusses various congenital cardiac defects including:
1) Ventricular septal defects which allow left-to-right shunting of blood and can cause pressure/volume changes in the ventricles.
2) Transposition of the great arteries where the aorta arises from the right ventricle and pulmonary artery from the left ventricle, causing right-to-left shunting.
3) Tetralogy of Fallot, a condition characterized by four defects that cause deoxygenated blood to bypass the lungs and mix with oxygenated blood.
This document provides information about atherosclerosis, including its definition, locations where it commonly occurs, complications that can arise, risk factors, pathogenesis, and histological features. It defines atherosclerosis as a hardening and loss of elasticity of arterial walls. The most common sites are the abdominal aorta, iliac arteries, coronary arteries, and carotid arteries. Complications include myocardial infarction, stroke, aneurysm formation, and gangrene. Major risk factors include hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis involves response to endothelial injury from various insults, resulting in inflammation and deposition of lipids in the arterial wall.
Cardiovascular disease is caused by conditions that affect the heart and blood vessels such as coronary heart disease, thrombosis, heart attacks, and strokes. The main causes are atherosclerosis, where plaque builds up in the arteries, and hypertension, or high blood pressure. Risk factors for cardiovascular disease include unhealthy eating, smoking, lack of exercise, obesity, diabetes, and high cholesterol.
This document provides an overview of atherosclerosis (ATH), including its definition, most common sites of occurrence, characteristic lesions, risk factors, pathogenesis, and complications. It defines ATH as a hardening and loss of elasticity of arterial walls. Key points include: ATH is a chronic inflammatory response initiated by endothelial injury; lipoproteins such as LDL accumulate in the arterial wall and undergo oxidation, promoting inflammation; risk factors include age, genetics, hypertension, hyperlipidemia, smoking, and diabetes. Complications involve reduced blood flow leading to ischemia of vital organs.
FULL HYPERMEDIA INTERACTIVE VERSION
OPEN / DOWNLOAD FULL LIVE HYPERMEDIA PRESENTATION
http://www.scribd.com/doc/106694518/IVMS-CV-Cardiovascular-PathologyPresentation
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.
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.
The heart is a muscle about the size of a fist located behind the breastbone. It pumps blood through the body through two coronary arteries that encircle the heart. Coronary artery disease occurs when fatty deposits build up in the arteries and reduce blood flow, which can lead to chest pain, heart attacks, or heart failure. Risk factors for coronary artery disease include age, family history, smoking, high blood pressure, high cholesterol, obesity, and diabetes. Treatment depends on the severity of disease but may include lifestyle changes, medications, procedures like angioplasty to open blocked arteries, or bypass surgery.
This document discusses various types of heart disease, including myocarditis, arrhythmia, cardiac failure, ischemic heart disease, and myocardial infarction. It provides details on:
- Causes of myocarditis including various infectious and non-infectious agents
- Classification of myocarditis and cardiac failure based on factors like duration, etiology, and location of failure
- Symptoms of cardiac failure like shortness of breath, fatigue, and edema
- Causes, symptoms, and signs of arrhythmias, ischemic heart disease, and myocardial infarction
- Types of arrhythmias based on the cardiac function affected - automatism, conductivity, excitability, or contractility
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.
This document provides information about various cardiovascular pathology cases for medical students. It includes questions and descriptions of thrombus, organizing thrombus, atherosclerosis, lung and spleen infarction, mesenteric artery occlusion, aortic dissection, myocardial infarction, and jars containing specimens of lung infarction, bowel infarction, early and advanced atherosclerosis, aortic dissection, left ventricular hypertrophy, and old myocardial infarction. Students are asked to identify features, causes, and complications represented in the images and specimens.
The document discusses several cardiovascular pathologies including congenital disorders like hemophilia and defects of the interventricular septum. Hemophilia is an inherited bleeding disorder caused by deficiencies in clotting factors VIII or IX. Symptoms include bleeding into joints and prolonged bleeding. Interventricular septal defects are openings in the wall between the ventricles that can cause murmurs. The document also covers traumatic reticuloperitonitis in cattle which is caused by sharp objects piercing the reticulum and pericardium, causing inflammation and fluid buildup. Myocarditis, or heart muscle inflammation, has various infectious causes like certain viruses in various animal species.
Arteries are blood vessels that carry blood away from the heart. This blood is normally oxygenated, exceptions made for the pulmonary and umbilical arteries
The cardiovascular system includes the heart, blood vessels, and blood. The heart pumps blood through the blood vessels, supplying oxygen and nutrients to tissues and removing waste. The document defines the components of the cardiovascular system, including blood, heart chambers and valves, arteries, veins, and capillaries. It also describes diseases that can affect the heart such as coronary artery disease, heart attacks, and congestive heart failure.
The document summarizes the cardiovascular system, including the circulatory and lymphatic systems. It describes the heart, blood vessels, blood flow through pulmonary and systemic circulation. It also discusses common diseases like atherosclerosis, heart attack, angina, and their diagnosis and treatment. The circulatory system functions to transport blood throughout the body, while the lymphatic system transports lymph and maintains fluid balance.
This document summarizes vascular pathology and diseases of blood vessels. It describes the normal structure of blood vessels and the three layers - intima, media, and adventitia. It then discusses different types of arteries and veins as well as blood flow. Various vascular disorders are outlined including atherosclerosis, aneurysms, vasculitis, and problems with veins and lymphatics. The major risk factors for atherosclerosis are identified as age, male gender, family history, hyperlipidemia, hypertension, smoking, and diabetes. The characteristic lesions of atherosclerosis including fatty streaks and fibrous plaques are described. Complications such as plaque rupture, thrombosis, and aneurysm formation are also summarized.
Circulatory system of head and neck BY DR. C. P. ARYA (B.Sc. B.D.S.; M.D.S.;...DR. C. P. ARYA
The document discusses the circulatory system of the head and neck, including key arteries and structures:
- The common carotid artery divides into the external and internal carotid arteries, with the external supplying blood to the face and neck and the internal supplying the brain.
- Important structures along the carotid arteries include the carotid body, which detects changes in blood gases, and the carotid sinus, a baroreceptor site.
- Branches of the external carotid artery include the superior thyroid artery and branches that supply the face and pharynx. The internal carotid artery branches further within the skull to supply the brain.
The cardiovascular system includes the heart and blood vessels. The heart has four chambers and pumps oxygenated blood received from the lungs into the main artery (aorta) and deoxygenated blood received from the body into the pulmonary artery to be sent to the lungs. Blood flows through two circulations - systemic circulation where blood is pumped from the heart to the body and pulmonary circulation where blood travels from the heart to the lungs to be oxygenated. The circulatory system transports nutrients, oxygen, carbon dioxide and waste through arteries, veins and capillaries to keep the body functioning properly.
The circulatory system, also known as the cardiovascular system, moves substances to and from cells and helps regulate body temperature and pH. It consists of the heart, blood, and blood vessels. The heart begins beating around 21 days after conception at a rate near the mother's, which then accelerates over the first month. Blood vessels include arteries, which carry blood away from the heart, veins, which carry blood toward the heart, and capillaries, which connect arterioles and venules and closely interact with tissues. Deoxygenated blood returns to the heart through the superior and inferior vena cavae and is pumped through the pulmonary and systemic circuits to be oxygenated in the lungs before being distributed to the body
The document describes the structure and function of blood vessels, including arteries, veins, and capillaries. It discusses the layers of the vessel walls (tunica intima, media, and adventitia), and how features like elastic fibers, smooth muscle cells, and valves aid in blood flow and pressure regulation. Key differences are that arteries have thick muscular walls to handle high pressure blood from the heart and maintain flow, while veins have thin walls and valves to prevent backflow of low pressure blood back to the heart. Capillaries are only one cell thick to enable maximum exchange of materials between blood and tissues. The document also covers atherosclerosis and its obstruction of blood flow.
Circulatory system of human being its structure function types and comparison...Nabeel805998
It includes a comprehensive description of circulatory system, its structure function and types.
It also includes diagrammatic representation of various parts circuits and working of human circulation.
This document provides an overview of the embryological development and anatomy of arteries and veins in the head and neck region. It discusses the formation of blood and aortic arches in early embryonic development. It then describes the course, branches, and clinical relevance of major arteries like the common carotid artery, external carotid artery, internal carotid artery, and branches including the lingual, facial, and superior thyroid arteries. It also briefly outlines the structure and differences between arteries, veins, and capillaries.
This document summarizes arteriosclerosis and atherosclerosis. It discusses the pathogenesis and risk factors of atherosclerosis, including endothelial injury, smooth muscle cell proliferation, the role of blood monocytes and hyperlipidemia. It describes the progression of atherosclerotic plaques and the major symptoms of atherosclerosis, which include heart attacks and strokes. Tests for diagnosis and treatments such as medications, angioplasty, stenting and bypass surgery are outlined. Prevention of atherosclerotic vascular disease through controlling risk factors is also discussed. The document concludes with information on venous disease, insufficiency, classification, symptoms, evaluation and treatments like compression, sclerotherapy and surgery.
This document summarizes information about atherosclerosis and coronary artery disease. It discusses the structure and function of the heart, how coronary arteries supply the heart with blood, and what happens in atherosclerosis when fatty deposits build up in the arteries. The document outlines risk factors for coronary artery disease like high blood pressure, smoking, obesity, and lack of physical activity. It describes potential signs and symptoms of the disease including chest pain, shortness of breath, and heart attack. Finally, it provides an overview of treatment options for coronary artery disease such as lifestyle changes, medications, stenting, angioplasty, and bypass surgery.
This document provides an overview of the circulatory system, including its components and functions. It describes that blood is composed of plasma, proteins, formed elements, and transports oxygen, nutrients, and waste. It also summarizes the structures and roles of the heart, blood vessels (arteries, veins, capillaries), and different types of circulation (systemic, pulmonary, coronary, hepatic portal).
Atherosclerosis is a condition where arteries thicken due to plaque buildup. It develops when cholesterol and other fatty substances build up in artery walls. This restricts blood flow and can cause blood clots if plaques rupture. Risk factors include high cholesterol, smoking, diabetes, and obesity. Diagnosis involves tests like angiograms, stress tests, CT scans, and ultrasounds. Treatment focuses on lifestyle changes and medications to control risk factors and slow progression, while procedures like angioplasty and stenting are used to open blocked arteries.
Coronary artery disease is one of the most common and serious effects of aging where fatty deposits build up in the walls of blood vessels and narrow the passageway for blood flow. Over time, this condition called atherosclerosis can lead to a blockage of the coronary arteries and a heart attack. The heart is a muscle that pumps blood through the lungs and body to provide oxygen and nutrients. The coronary arteries supply blood to the heart muscle itself. Risk factors for coronary artery disease include high blood pressure, high cholesterol, smoking, obesity, and lack of physical activity. Treatment options depend on the severity of blockages and may include lifestyle changes, medications, angioplasty, stenting, or bypass surgery.
Atherosclerosis is a disease where fatty deposits build up in the arteries and restrict blood flow. It is the leading cause of heart attacks and occurs when cholesterol builds up on the inner walls of the arteries that supply the heart. Over time, this buildup narrows the arteries and reduces blood flow. If a blocked artery completely closes off, it can cause a heart attack. Risk factors include high blood pressure, smoking, obesity, lack of exercise, diabetes, and high cholesterol. Treatment options depend on the severity and can include lifestyle changes, medications, angioplasty, stents, or bypass surgery to reroute blood flow around blocked arteries.
Chapter 37- Circulatory and Respiratory SystemsMary Beth Smith
The circulatory system transports blood throughout the body via the heart and blood vessels. The heart has four chambers and uses valves to pump oxygenated blood from the lungs and deoxygenated blood to the lungs. Blood flows through arteries, capillaries, and veins. The respiratory system exchanges gases through the nose, pharynx, trachea, bronchi, and alveoli in the lungs. Breathing is controlled by the medulla oblongata and diaphragm. Smoking damages lungs and increases risk of diseases like cancer, emphysema, and bronchitis.
The circulatory system transports blood throughout the body via the heart and blood vessels. The heart has four chambers and uses valves to pump oxygenated blood from the lungs and deoxygenated blood to the lungs. Blood flows through arteries, capillaries, and veins. The respiratory system exchanges gases through the nose, pharynx, trachea, bronchi, and alveoli in the lungs. Breathing is controlled by the medulla oblongata and diaphragm. Smoking damages lungs and increases risk of diseases like cancer, emphysema, and bronchitis.
The document provides an overview of the human cardiovascular system. It describes the structure and function of the heart, including the layers of the heart wall, valves, conduction system, and heart sounds. It discusses the role of arteries, veins, and capillaries in circulating blood throughout the body and exchanging gases and nutrients at the tissue level. It also covers cardiac cycle, heart rate regulation by the autonomic nervous system, effects of ions like potassium and calcium on heart function, and factors influencing blood pressure.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
2. Objectives
Review the A & P of the heart
Review the following structure that support the cardiac
metabolism i.e.
Coronary circulation ( collateral arteries)
Heart action i.e. conduction system ,myocardial contraction
and relaxation
Briefly discuss the normal function of lipoprotein
List the vessels most commonly effected by
atherosclerosis.
List the risk factors in atherosclerosis.
Describe the possible mechanism involved in the
development of atherosclerosis.
Explain the physiological changes in patients with
ischemic heart diseases
2
8. Conducting System of Heart
Groups of autorhythmic cells are found at the:
Sinoatrial node – located near the opening of the SVC.
Atrioventricular node – located in the inferior interatrial
septum near the tricuspid orifice.
Atrioventricular bundle – found in the superior
interventricular septum.
Right and left bundle branches – travel through the
interventricular septum to the apex of the heart.
Purkinje fibers – cells that wind their way throughout the
ventricles.
8
11. Factors regulating stroke volume
Stroke volume is regulated by the three factors.
Preload
Afterload
Myocardial contractility
12. Factors regulating stroke volume
Preload:
Reflects the loading conditions of the ventricle at the
end of diastole, just before the onset of systole.
Volume of blood stretching the myocardial muscle at
end of diastole, also known as end-diastolic volume
Within certain limits if the end-diastolic volume or
preload increases, the stoke volume also increases.
13. Factors regulating stroke volume
Afterload:
The force that the contracting heart muscle must
generate to eject blood from the filled heart.
Increased peripheral vascular resistance(PVR)
increases the afterload and decreases stroke volume
14. Factors regulating SV.
Myocardial contractility
The ability of the contractile cells of the heart muscle to
contract effectively
Depends on the availability of ATP and Calcium ions
and the integrity of heart muscles itself.
The more effective the heart muscles contract,
greater the blood ejected from the heart.
16. Coronary circulation
The left and the right coronary artries, arise from the
coronary sinus of aorta just above the aortic valve.
The left coronary artery supplies blood flow to the
anterior and left lateral portions of the LV.
The left main coronary artery divides into the left
anterior descending and circumflex branches.
The left anterior descending artery supply the LV, the
anterior portion of the interventricular septum and the
anterior papillary muscle of the LV
The circumflex artery supply the left lateral wall of the
LV.
16
17. Coronary circulation
The right coronary artery supply most of the right
ventricle and the posterior part of the LV.
Posterior descending artery, a branch of the right
coronary artery supplies the posterior portion of the
heart, interventricular septum, sinoatrial (SA) and
atrioventricular (AV) nodes, and posterior papillary
muscle.
Beside main branches of coronary arteries there are
smaller arteries that form collateral circulation.
With gradual occlusion of the larger vessels, the
smaller collateral vessels increase in size and provide
alternative channels for blood flow. 17
18. A & P of blood vessels:
18
A & P of blood vessels
19. Tunica interna: (the inner most coat)
Consists of a layer of simple squamous epithelium
called endothelium, a basement membrane and a layer
of elastic connective tissue called the internal elastic
lamina.
The endothelial is a continuous layer and line the
entire cardiovascular system.
The tunica interna is closest to the lumen, the hollow
center through which blood flow.
19
20. Tunica media: (The middle coat)
It is usually the thickest layer
This layer consists of elastic fibers (smooth
muscle) that extend circularly( in ring)
around the lumen.
Due to there plentiful elastic fibers the wall
of arteries easily stretch and expend without
tearing in response to small increase in
pressure.
Tunica externa: ( the external coat)
It is composed mainly of elastic and collagen
fibers
20
21. Lipoprotein:
Particles found in plasma that transport lipids
including cholesterol
Lipoprotein classes
Chylomicrons: take lipids from small intestine
through lymph cells
Very low density lipoproteins (VLDL)
Intermediate density lipoproteins (IDL)
Low density lipoproteins (LDL)
High density lipoproteins (HDL)
21
22. Function of lipoprotein::
Chylomicrons transport dietary triglycerides and cholesterol
absorbed by intestinal epithelia.
LDL and HDL transport both dietary and endogenous
cholesterol in the plasma.
LDL is the main transporter of cholesterol and makes up
more than half of the total lipoprotein in plasma.
LDL bind to macrophages and form foam cell.
HDL causes reverse transport of cholesterol, it carry
cholesterol away from the artery and it removes lipid from
atherosclerotic plaque and transport it to liver for excretion
in bile.
Increase HDL decrease the rate of IHD.
22
24. Arteriosclerosis vs
Atherosclerosis
Arteriosclerosis – natural changes in the intimal
layer, connective tissue and diameter of the artery
resulting in thickening & hardening of the arterial
walls.
Atherosclerosis – pathologic phenomenon occurring
in the coronary (thus causing coronary artery disease),
carotid, iliac, and femoral arteries as well as the aorta.
Atherosclerosis is a specific form of arteriosclerosis
affecting primarily the intima (the innermost layer) of
large and medium-sized arteries and is characterized by
the presence of fibro-fatty plaques or atheromas.
25. Atherosclerosis
An atheroma consists mainly of macrophages cells or
debris, containing lipids (cholesterol and fatty acids),
calcium and a variable amount of fibrous connective
tissue (collagens, proteoglycans).
The term atherosclerosis is derived from “athero”
referring to “a paste” the soft lipid-rich material and
“sclerosis” or scarring is referred to “hardness” denotes
the formation of fibro fatty lesions in the intimal lining of
arteries.
26. Atherosclerosis
Most commonly affected arteries by atherosclerosis
include large & medium sized arteries like aorta,
coronary, popliteal and cerebral arteries.
Major complications that result from ischemia due to
atherosclerosis include myocardial infarction leading to
heart attacks & cerebral infarction leading to strokes.
Less common complications include peripheral vascular
disease, aneurysmal dilatation due to weakened arterial
wall and chronic ischemic heart disease.
28. Carotid artery disease.
This happens when plaque builds up in the carotid
arteries. These arteries supply oxygen-rich blood to your
brain.
When blood flow to the brain is reduced or blocked, it
can lead to stroke.
Peripheral arterial disease (PAD).
This occurs when plaque builds up in the major arteries
that supply oxygen-rich blood to the legs, arms, and
pelvis.
When blood flow to these parts of the body is reduced
or blocked, it can lead to numbness, pain, and
sometimes dangerous infections 28
29. Risk Factors for CAD
29
Uncontrollable/non modifiable
•Sex: Heart disease occurs three times more often in
men than in premenopausal women
•Hereditary: Family history of coronary heart disease
•Genetic factors
•Race: higher incidence of heart disease in African
Americans than in Caucasians
•Increasing age
30. Risk Factors for CAD
30
Controllable/ modifiable
•High blood cholesterol level
•Cigarette smoking, tobacco use
•Hypertension
•Diabetes mellitus
•Lack of estrogen in women
•Physical inactivity
•Obesity
31. Major Constitutional Risk Factors
AGE
Atherosclerosis is an age-related disease.
Clinically significant lesions are found
with increasing age.
Fully-developed atheromatous plaques
usually appear in 40s and beyond.
Evidence in support comes from the high
death rate from IHD in this age group.
32. Major Constitutional Risk Factors
SEX
Incidence and severity of atherosclerosis is more in
men than in women.
Prevalence of atherosclerotic IHD is about three times
higher in men than in women.
Lower incidence of IHD in women, especially in
premenopausal age is probably due to high levels of
estrogens & high-density lipo- proteins, both of which
have anti-atherogenic influence.
33. Major Constitutional Risk Factors
GENETIC FACTORS
Hereditary genetic derangements of lipoprotein metabolism
predispose the individuals to high blood lipid level.
FAMILIAL AND RACIAL FACTORS
Familial predisposition to atherosclerosis may be related to other
risk factors like diabetes, hypertension and hyperlipoproteinemia.
Racial differences too exist. Blacks have less severe
atherosclerosis than Whites.
34. Major Acquired Risk Factors
HYPERLIPIDAEMIA
Hypercholesterolemia has directly
proportionate relationship with
atherosclerosis & IHD because:
The atherosclerotic plaques contain cholesterol
largely derived from the lipoproteins in the blood.
Individuals with hypercholesterolemia have
increased risk of developing atherosclerosis and IHD.
Individuals with hypercholesterolemia have higher
death rates (mortality)from IHD.
Dietary control & administration of cholesterol-
lowering drugs have beneficial effect on reducing the
risk of IHD.
35. Major Acquired Risk Factors
HYPERLIPIDAEMIA CONT…
An elevation of serum cholesterol levels above 260mg/dl
in men and women between 30 and 50 years of age has
three times higher risk of developing IHD as compared to
people with normal serum cholesterol levels (140-200
mg/dl).
Low-density lipoproteins (LDL) is richest in cholesterol
and has maximum association with atherosclerosis. HDL
is protective good cholesterol against atherosclerosis.
Diet rich in saturated fats e.g., eggs, meat, milk, butter etc,
raises the plasma cholesterol level while diet rich in poly-
unsaturated fats and omega-3 fatty acids e.g., fish, fish oils
etc lowers its level.
36. Major Acquired Risk Factors
HYPERTENSION
Hypertension causes mechanical injury to the arterial
wall due to increased blood pressure leading to
atherosclerotic IHD and cerebrovascular disease.
Endothelial injury due to persistent high B.P leads to
plaque formation.
A systolic pressure of over 160 mmHg or a diastolic
pressure of over 95 mmHg leads to 5 times higher risk
of developing IHD than in people with normal B.P.
(140/90 mmHg or less).
37. Major Acquired Risk Factors
SMOKING
Cigarette smoking is associated with higher risk of
atherosclerosis, IHD and sudden cardiac death.
Increased risk is due to the accumulation of carbon
monoxide in the blood that produces carboxy-
hemoglobin and eventually hypoxia in the arterial wall
favoring atherosclerosis.
Smoking also promotes atherosclerosis by increased
platelet adhesiveness, raised endothelial permeability,
sympathetic nervous system stimulation by nicotine.
38. Major Acquired Risk Factors
DIABETES MELLITUS
Atherosclerosis develops at an early age in people with
both insulin-dependent & non-insulin dependent diabetes
mellitus.
The risk of cerebrovascular disease is high and frequency
to develop gangrene of foot is about 100 times increased.
Causes of increased severity of atherosclerosis with DM
are complex & include increased aggregation of platelets,
increased LDL and decreased HDL.
39. Minor Risk Factors
1. Higher incidence of atherosclerosis in developed countries is
primarily because of environmental influences.
2. Obesity: Risk is increased if a person is overweight by 20%
or more.
3. Use of exogenous hormones (e.g. oral contraceptives) by
women or endogenous estrogen deficiency e.g., in post-
menopausal women leads to increased risk.
4. Physical inactivity and lack of exercise increase the risk
5. Stressful life style led by aggressiveness, a sense of urgency
& over-ambitiousness is associated with the risk of IHD.
40. Minor Risk Factors
6. Infections particularly clamydia pneumonia and viruses
such as herpes virus and cytomegalovirus increases
coronary atherosclerotic lesions.
7. Moderate consumption of alcohol has slightly beneficial
effect by causing vasodilatation.
However persistent consumption of alcohol in large
quantities causes more damage. The direct toxic effect
of alcohol results in fat deposition in the liver that
becomes a constant source of low-grade asymptomatic
fat emboli. Fat emboli become hydrolyzed to free fatty
acids, which cause endothelial cells damage.
41. Mechanism of development of atherosclerosis
Endothelial injury by (Agents such as smoking, elevated
LDL levels, immune mechanisms, and mechanical stress
associated with hypertension)
Monocytes attach to endothelium, penetrate to sub-
endothelial spaces and converted to macrophages
Activated macrophages release free radicals that oxidize
LDL
Oxidized LDL is toxic to the endothelium, causing
endothelial loss and exposure of the sub-endothelial
tissue to blood components.
This leads to platelet adhesion and aggregation
and fibrin deposition.
41
42. Mechanism of development of atherosclerosis
Platelets and activated macrophages release various
factors that leads to proliferation of smooth muscle cells
and deposition of extracellular matrix( collagen and
elastic fibers).
Activated macrophages also ingest oxidized LDL to
become foam cells.
The necrotic foam cells release lipids to form a lipid
core.
Fatty streaks and proliferated smooth muscles form
fibrous plaque
A fatty streak consists of lipid-containing foam cells in
the arterial wall just beneath the endothelium.
43. Mechanism of development of atherosclerosis
Endothelial necrosis and luminal narrowing occurs
Sometimes Plaque is ulcerated or ruptures, more
platelet aggregation occurs that leads to thrombus
formation.
Rupture, ulceration, or erosion of an unstable or
vulnerable fibrous cap may lead to hemorrhage into
the plaque or thrombotic occlusion of the vessel
lumen.
Occlusion or narrowing of the vessel may then lead
to ischemic heart diseases or myocardial infarction.
47. Ischemic Heart Disease
o Leading cause of death in industrialized countries
o Leads to angina, myocardial infarction, sudden
cardiac death, and chronic heart failure
o It results from coronary arteries atherosclerosis
o Narrowing and hardening of the arteries leads to
imbalance between supply and demand of blood
for cardiac muscles = Ischemia.
o Ischemia is either detected by a symptom
(angina) or indirectly by electrocardiogram and
other non-invasive (e.g. echo) & invasive
diagnostic techniques (e.g. cardiac enzymes).
49. Myocardial Ischemia
Ischemia is inadequate blood flow to a tissue or part
of the body.
Myocardial ischemia occurs when the blood flow
demands of the heart muscles exceed the blood supplied
by the coronary arteries.
Pathophysiology of Myocardial Ischemia
Under resting conditions, myocardial oxygen supply
and delivery of nutrients through the coronary arteries
should match the metabolic requirements of the heart.
When the metabolic needs of the heart increase, the
coronary blood flow must increase accordingly.
50. With age and progressive occlusion
of coronary arteries, smaller
collateral vessels may begin to
carry a greater proportion of blood
and thus provide an alternate means
of perfusion for an area of
myocardium.
These collateral blood vessels may
run parallel to the larger coronary
arteries & be connected to other
small coronary vessels by vascular
connections called anastomoses.
Pathophysiology of Myocardial
Ischemia
51. Development of collateral circulation may
reduce or delay the occurrence of
symptoms from myocardial ischemia until
the blockage is very progressed.
The presence of extensively developed
collateral circulation might also explain
why many older individuals often survive
serious heart attacks, while younger
individuals have not yet developed
collateral circulation, often do not.
Pathophysiology of Myocardial
Ischemia
52. Symptoms of Coronary Artery
Disease
Most common symptom is Angina Pectoris
also known as chest discomfort.
Quality - "squeezing," "grip like," "pressure like,"
"suffocating" and "heavy”; or a "discomfort" but not
"pain." Angina is almost never sharp or stabbing,
and usually does not change with position or
respiration.
Duration - angina episode is typically minutes in
duration. Feeling discomfort or a dull ache lasting
for hours is rarely angina.
53
53. Angina
Angina is a symptom of a condition called
myocardial ischemia
Other symptoms that can occur with coronary artery
disease include:
Decrease peripheral pulse
Nausea and vomiting
Fainting
Sweating
Cool extremities
Shortness of breath
54
55. Angina Pectoris
Usually substernal, but radiation to the neck, jaw,
epigastrium, or arms can occur.
Pain above the mandible, below the epigastrium, or
localized to a small area over the left lateral chest is
rarely angina.
Provocation - angina is generally precipitated by
exertion or emotional stress and commonly relieved
by rest. Sublingual nitroglycerin also relieves
angina, usually within 30 seconds to several minutes.
56
57. Ischemia
Ischemia is most likely to occur when the heart
demands extra oxygen. This is most common during
one or more of the four E’s:
• Exertion (activity)
• Eating
• Excitement
• Exposure to cold
58
58. Myocardial Ischemia
Types of angina
Stable Angina Pectoris
Unstable Angina
Prinzmetal’s or Variant angina
(coronary spasm)
59
59. Stable Angina Pectoris
A type of angina brought on by an imbalance between
the heart’s need for oxygen-rich blood and the amount
available.
Episodic chest pain
Stress or exertion
Fix atherosclerotic plaque (75%)
Crushing, squeezing, suffocating, sub sternal sensation
Pain intensity increase at onset and end of attack
It is relieved by rest and/or oral medications
(nitroglycerin)
60
60. Unstable Angina
When a change in status of angina occurs (e.g. new
onset; angina of increasing severity, duration or
frequency; or angina occurring at rest for the first
time). feel more severe, or last longer.
Unstable angina is usually triggered by minor
injury to atherosclerotic plaque.
Plaque disruption may occur with or with out
thrombosis, it increase the degree of coronary
artery obstruction
61
61. Additionally there is a release of vasoconstricting
factors i.e thromboxane, serotonine, and platelet
derived growth factors from platelets that
aggregate at the site of injury.
These platelets factors contribute even at rest the
episode of reduce coronary blood flow.
Close observation and intensive therapy is
required; more serious clinical situation as may be
a precursor of MI.
62
62. Prinzmetal’s Angina/Variant angina
(or coronary spasm)
Variant angina are first describe by prinzmetal
in 1959.
A coronary artery can go into spasm,
disrupting blood flow to the heart muscle
(ischemia).
The hallmark is ST segment elevation on the
ECG during angina attack.
Usually associated with fixed atherosclerotic
lesion, but not always.
63
63. This type of angina is not common usually occurs
at rest (often at night), and episodes are frequently
associated with ventricular arrhythmias.
The mechanism of coronary vasospasm is
unclear.
It has been suggested that it may result from
hyper active sympathetic nervous system response
from a defect in handling of calcium in vascular
smooth muscle and reduces production of
prostaglandin I2.
64
66. Pain is caused by :
Build up of lactic acid or abnormal stretching of
the ischemic myocardium irritates myocardial
nerve fibers.
Afferent sympathetic fibers enter the spinal cord
from levels C3 to T4 accounting for the variety of
locations and radiation pattern of anginal pain.
Dysrhythmias occurs in severe pain
67
69. Myocardial Infarction:
Myocardial Infarction (MI) is the condition of
irreversible necrosis of heart muscle that results
from prolonged ischemia or may be defined as
Ischemic death of myocardium.
Prolonged Ischemia longer than 30-45 minutes
causes irreversible cellular damage and muscle
death or necrosis.
70
70. Myocardial infarction is the medical term for heart
attack.
Heart attack means there has been death of heart
cells.
This is the result of a complete blockage of one of
the blood vessels that feeds the heart muscle
(coronary artery).
Cell death does not occur immediately once the
artery is blocked. It takes several minutes to start
the injury process and this continues for several
hours unless the artery is opened, restoring blood
flow.
71
71. Cardiac muscle requires about 1.3 ml of oxygen
per 100 gm of muscle tissue per minute just to
remain alive.
At resting state normally left ventricle receive
8 ml of blood per 100 gm of tissue.
If there is 15-30% of normal resting coronary
blood flow the muscle will not die.
72
72. Site of MI
Anterior MI-involves the anterior wall of the left
ventricle.
Other sites of infarction are:
Inferior
Posterior
Lateral (anterolateral)
Septal ( Anteroseptal)
73
73. Anterior wall infarctions result from lesions in
the left coronary anterior artery.
Inferior wall infarction results of right coronary
artery lesions.
Anterioseptal result from left anterior
descending.
Lateral MI involves circumflex and Lt anterior
descending.
Posterior wall infarction results from Rt.
Coronary artery and circumflex.
74
74. Are there different types of heart
attacks?
The location of the blockage, the length of time the
blockage persisted and the amount of damage will
determine the type of heart attack that occurs.
75
75. Types of Heart Attacks
Pathologically there are two patterns of MI:
Transmural (Q wave infarction)
Subendocardial (non Q wave infarction)
76
76. Q-wave MI
A MI or heart attack that is caused by a prolonged
period of blocked blood supply.
A large area of the heart muscle is affected, causing
changes on the ECG as well as chemical markers in the
blood.
Involves the entire depth of the ventricular wall.
77
77. Non-Q-wave MI
A MI or heart attack that does not cause changes
on the electrocardiogram (ECG) however, chemical
markers in the blood indicate that damage has
occurred to the heart muscle.
78
78. Symptoms of a Heart Attack
Chest pain or discomfort in the center of the chest;
a “squeezing,” heaviness” or “crushing” feeling that
lasts for more than a few minutes or goes away and
comes back.
Fullness, indigestion, or choking feeling (may feel like
“heartburn”)
• Nausea or vomiting
• Light-headedness
• Extreme weakness or anxiety
• Rapid or irregular heart beats
79
80. Cardiac markers:
Cardiac markers are proteins that leak out of
injured myocardial cells through their
damaged cell membranes into the
bloodstream.
Until the 1980s, the enzymes SGOT and LDH
were used to assess cardiac injury.
Now, the markers most widely used in
detection of MI are MB subtype of the enzyme
creatine kinase, and cardiac troponins T and I
as they are more specific for myocardial injury.
81
81. The cardiac troponins T and I which are
released within 4–6 hours of an attack of MI
and remain elevated for up to 2 weeks, have
nearly complete tissue specificity and are now
the preferred markers for assessing myocardial
damage.
Elevated troponins in the setting of chest pain
may accurately predict a high likelihood of a
myocardial infarction in the near future.
New markers such as glycogen phosphorylase
isoenzyme BB are under investigation.
82
82. Treatment of myocardial ischemia and the resulting
angina can involve two strategies:
1. Increase coronary blood flow by dilating coronary
arteries.
2. Reduce cardiac workload by reducing heart rate
and/or force of contraction.
Rationale for the Treatment of Myocardial Ischemia
Treatment of Myocardial
Ischemia
83. The treatment regimen may include:
1. Non-pharmacologic treatment
2. Pharmacologic therapies.
Treatment of myocardial ischemia:
Pacing of physical activity.
Avoidance of stress (emotional, physiologic,
cold).
Reduction of risk factors for ischemic heart
disease, (hyperlipidemia, obesity,
hypertension, diabetes, smoking, etc.)
Non-pharmacologic Treatment
Treatment of Myocardial
Ischemia
84. Mechanism of Action
Dilate coronary arteries and increase myocardial
blood flow.
Dilate peripheral arteries and reduce afterload.
Dilate peripheral veins and reduce preload.
Examples
Amyl nitrate, nitroglycerine, isosorbide dinitrite
Pharmacologic Treatment
Treatment of Myocardial
Ischemia
Nitrates
85. Mechanism of action
Block myocardial β-adrenergic receptors.
Reduce heart rate and cardiac output (reduced myocardial
workload and oxygen demand).
Examples of β-Adrenergic Receptor Antagonists
May be selective β1 (atenolol), or
Nonselective β1 and β2 blockers (propranolol)
Pharmacologic Treatment
β-Adrenergic Blockers
Treatment of Myocardial
Ischemia
86. Mechanism of action
Block calcium channels in vascular smooth muscles.
Dilate coronary arteries and increase myocardial blood flow.
Dilate peripheral arteries and reduce afterload.
Examples
Dihydropyridines (nifedipine), verapamil, diltiazem
Dihydropyridines have greater specificity for
relaxing vascular smooth muscle.
Calcium Channel Blockers
Treatment of Myocardial
Ischemia
87. Mechanism
Prevent platelet aggregation.
Used for prophylaxis of blood clots
particularly in unstable angina.
Aspirin
Surgical Treatment
Coronary Angioplasty
Uses a balloon catheter to open occluded blood
vessels
Usually performed under local anesthesia
Use of metal “stents” in opened vessel reduces rate of
occlusion
Metal Stent
Treatment Cont…
88. Treatment of Myocardial
Ischemia
Coronary artery bypass graft
Revascularization procedure in which a blood vessel
is taken from elsewhere in the body & surgically
sutured around a blocked coronary artery.
May involve multiple (one to five) blood vessels.
Re-occlusion of transplanted vessel is possible.
Surgical Treatment
89. 5. β -Blockers: Reduce the effect of catecholamine release
on
the myocardium, reduce heart rate and myocardial work.
6. Pain management: Sublingual nitroglycerin, morphine if
necessary.
7. Antiarrhythmic drugs: To treat and prevent a number of
potentially life-threatening arrhythmias that might arise
following a myocardial infarction.
8. ACE inhibitors: the negative effects of vasoconstriction
and salt and water retention on the myocardium.
Treatment for myocardial
infarction
Myocardial Infarction
90. 1. Streptokinase: Derived from β -hemolytic streptococcus
bacteria; involved in the activation of plasmin.
2. Anistreplase (APSAC): Complex of human lys-
plasminogen and streptokinase.
3. Urokinase: Endogenous human enzyme that converts
plasminogen to active plasmin
4. Routes of administration: Intravenous for all of the
above.
5. Major unwanted effects: Internal bleeding,
gastrointestinal bleeding, stroke, allergic reactions
Myocardial Infarction
Thrombolytic Agents Used Clinically
91. 1. Sublingual nitroglycerin: A potent vasodilator
of coronary arteries, also dilates peripheral
arteries & veins to reduce preload and afterload
on the heart.
2. Morphine sulfate: Powerful opioid analgesic
that also provides a degree of sedation &
vasodilatation.
Although the opioid analgesics have little effect on
the myocardium, they are powerful respiratory
depressants.
Myocardial Infarction
Pain Management in Myocardial Infarction
92. Inhibits the cyclo-oxygenase pathway for the
synthesis of prostaglandins, prostacyclins &
thromboxanes.
Inhibits aggregation of platelets and is effective in
reducing myocardial infarction, stroke and
mortality in high-risk patients.
Myocardial Infarction
Aspirin
93. Key terms
Cardiac tamponade: Excessive pressure that
develops from the accumulation of fluid in the
pericardium.
Pericarditis: Inflammation of the pericardium.
Stroke volume: Volume of blood ejected from
each ventricle per beat.
Myocardial Infarction
94. 1. Danish MI. Short text book of pathology. 4th
edition;
2010. Johar Publications, Karachi-Pakistan.
2. Emanuel Rubin & John L. Farber, Essential Pathology,
Philadelphia, 1990.
3. Kumar, Vinay; Abbas, Abul K; Aster, Jon. (2009).
Robbins & Cotran pathologic basis of diseases (8th ed.).
St. Louis, Mo: Elsevier Saunders. ISBN 1-4160-3121-9.
3. Porth CM. Pathophysiology: Concepts of altered Health
States. 7th
edition; 2005. Lippincott Williams & Wilkins.
Reference
s
Editor's Notes
Cholesterol is carried in the blood attached to proteins called lipoproteins. HDL or good cholesterol can move LDL cholesterol from the blood to the liver to be broken down and disposed of as waste. HDL cholesterol is referred to as good cholesterol because it reduces the level of cholesterol in the blood.
Hereditary means that it is in your genes & cannot be prevented but familial means that it runs in your family. For example if your mother has a heart attack or diabetes because of her diet and lifestyle then because you are in her family with her same diet then you could too have a heart attack or diabetes but if you change your lifestyle and eat better you wont. So hereditary is genes and can’t be prevented but familial can be avoided.
It is widely known that cigarette smoking is a major environmental risk factor for atherosclerosis. Gene/environment interaction has also been demonstrated in this regard. Indeed, a synergistic effect between cigarette smoking & genetic carrier state increases the risk of atherosclerosis to a large extent.
Oral contraceptives increase the risk for venous thrombosis and pulmonary embolism, particularly if associated with confounding factors such as genetic predisposition, smoking, hypertension or obesity.
Estrogen is a vasodilator, its deficiency will predispose to atherosclerosis.
An anastomosis is the reconnection of two streams that previously branched out, such as blood vessels or leaf veins.
The exercise stress test is used to provide information about how the heart responds to exertion. It usually involves walking on a treadmill or pedaling a stationary bike at increasing levels of difficulty, while your electrocardiogram, heart rate, and blood pressure are monitored.
Nuclear Imaging is a technique for producing images of various body parts using small amounts of radioactive tracers. After administration (orally, intravenously of as inhalation) of the tracer, images of the body part are obtained with a gamma camera, which helps physicians in diagnosing conditions. Nuclear imaging uses low doses of radioactive substances (e.g. Tritium or Iodine). Using special detection equipment, the radioactive substances can be traced in the body to see where and when they concentrate.
The saphenous vein, the internal mammary artery or the radial artery can be used as grafts. Saphenous vein is the most commonly used conduit. There are several reasons for this, it has relatively large diameter, it is technically easy to use, it is plentiful and therefore can be used to perform multiple grafts, it is long and can reach any coronary artery.
Urokinase is a thrombolytic enzyme predominantly formed in the kidney and excreted in the urine
Histidine-rich glycoprotein (HRG) and plasmin inhibitor are two plasma proteins that form reversible complexes with the
lysine-binding sites of plasminogen