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.
The document discusses the four primary types of tissues in the body: epithelial, connective, muscle, and nervous tissue. It provides details on the characteristics, locations, and functions of each type of tissue. It also describes the processes of tissue repair and regeneration.
Cardiac muscle consists of cross-striated cardiomyocytes that are joined end-to-end by specialized junctions called intercalated discs. These discs contain desmosomes and gap junctions. Desmosomes bind cells together while gap junctions allow action potentials to spread between cells, causing the heart to contract as a syncytium. Within intercalated discs are also Purkinje fibers, which are modified cardiac muscle cells that conduct electrical signals faster than normal cardiomyocytes. This allows for coordinated contraction of the heart.
1. Hemodynamic disorders involve changes in blood flow and pressure that can result in edema, hemorrhage, thrombosis, embolism, or shock.
2. Edema occurs when fluid moves from blood vessels into tissues, and can be caused by increased hydrostatic pressure, decreased plasma protein levels, lymphatic obstruction, or sodium retention.
3. Hemorrhage is the extravasation of blood from vessels, and can range from small petechiae to life-threatening hematomas depending on location and severity. Rapid or large blood losses can cause shock.
The document provides lecture notes on heart development. It discusses:
1. The heart develops from cardiogenic mesoderm and neural crest cells that migrate to the cardiogenic region.
2. The heart develops through 5 stages: specification of cardiac precursors, migration and fusion to form a heart tube, looping of the heart tube, chamber formation, and septation/valve formation.
3. The heart tube partitions internally through formation of septa to divide the atria, ventricles, and outflow tract into left and right sides. This completes the development of the four-chambered heart.
This document discusses hemodynamic disorders and their classification. It covers topics like hyperemia, hemorrhages, thrombosis, and edema. Hyperemia can be arterial from vasodilation or venous from impaired outflow. Hemorrhages are blood loss classified by size and site. Thrombosis involves inappropriate clotting within vessels. Edema is fluid accumulation in tissues. Organ-specific effects of disorders are also described.
The document discusses capillary function and structure. It notes that capillaries are the smallest blood vessels, connecting arterioles and venules. They allow for exchange of water, gases, nutrients, and waste through diffusion, filtration, and active transport. Capillaries come in three types - continuous, fenestrated, and sinusoidal - depending on the thickness of their endothelial lining and presence of gaps or pores to facilitate exchange. Tight junctions between endothelial cells help control permeability at different capillary beds.
This document discusses hemodynamic disturbances including edema, hyperemia and congestion, hemorrhage, thrombosis, infarction, and shock. It provides detailed information on edema, including the pathogenesis of different types such as cardiac, renal, pulmonary, hepatic, and cerebral edema. It also discusses hyperemia and congestion, explaining the differences between active and passive hyperemia. The effects of hemorrhage are outlined. Chronic venous congestion is described along with examples of congestion of the lungs and liver.
This document summarizes key concepts relating to cell injury, adaptation, and death. It discusses how cells respond to stress through reversible or irreversible injury, adaptation, or death. It also describes various types of cellular adaptation like hypertrophy, hyperplasia, atrophy, and metaplasia that cells undergo in response to stress. Additionally, it covers the mechanisms and morphological changes associated with different types of cell injury like necrosis and apoptosis.
The document discusses the four primary types of tissues in the body: epithelial, connective, muscle, and nervous tissue. It provides details on the characteristics, locations, and functions of each type of tissue. It also describes the processes of tissue repair and regeneration.
Cardiac muscle consists of cross-striated cardiomyocytes that are joined end-to-end by specialized junctions called intercalated discs. These discs contain desmosomes and gap junctions. Desmosomes bind cells together while gap junctions allow action potentials to spread between cells, causing the heart to contract as a syncytium. Within intercalated discs are also Purkinje fibers, which are modified cardiac muscle cells that conduct electrical signals faster than normal cardiomyocytes. This allows for coordinated contraction of the heart.
1. Hemodynamic disorders involve changes in blood flow and pressure that can result in edema, hemorrhage, thrombosis, embolism, or shock.
2. Edema occurs when fluid moves from blood vessels into tissues, and can be caused by increased hydrostatic pressure, decreased plasma protein levels, lymphatic obstruction, or sodium retention.
3. Hemorrhage is the extravasation of blood from vessels, and can range from small petechiae to life-threatening hematomas depending on location and severity. Rapid or large blood losses can cause shock.
The document provides lecture notes on heart development. It discusses:
1. The heart develops from cardiogenic mesoderm and neural crest cells that migrate to the cardiogenic region.
2. The heart develops through 5 stages: specification of cardiac precursors, migration and fusion to form a heart tube, looping of the heart tube, chamber formation, and septation/valve formation.
3. The heart tube partitions internally through formation of septa to divide the atria, ventricles, and outflow tract into left and right sides. This completes the development of the four-chambered heart.
This document discusses hemodynamic disorders and their classification. It covers topics like hyperemia, hemorrhages, thrombosis, and edema. Hyperemia can be arterial from vasodilation or venous from impaired outflow. Hemorrhages are blood loss classified by size and site. Thrombosis involves inappropriate clotting within vessels. Edema is fluid accumulation in tissues. Organ-specific effects of disorders are also described.
The document discusses capillary function and structure. It notes that capillaries are the smallest blood vessels, connecting arterioles and venules. They allow for exchange of water, gases, nutrients, and waste through diffusion, filtration, and active transport. Capillaries come in three types - continuous, fenestrated, and sinusoidal - depending on the thickness of their endothelial lining and presence of gaps or pores to facilitate exchange. Tight junctions between endothelial cells help control permeability at different capillary beds.
This document discusses hemodynamic disturbances including edema, hyperemia and congestion, hemorrhage, thrombosis, infarction, and shock. It provides detailed information on edema, including the pathogenesis of different types such as cardiac, renal, pulmonary, hepatic, and cerebral edema. It also discusses hyperemia and congestion, explaining the differences between active and passive hyperemia. The effects of hemorrhage are outlined. Chronic venous congestion is described along with examples of congestion of the lungs and liver.
This document summarizes key concepts relating to cell injury, adaptation, and death. It discusses how cells respond to stress through reversible or irreversible injury, adaptation, or death. It also describes various types of cellular adaptation like hypertrophy, hyperplasia, atrophy, and metaplasia that cells undergo in response to stress. Additionally, it covers the mechanisms and morphological changes associated with different types of cell injury like necrosis and apoptosis.
This document discusses cardiac output and the factors that affect it. It provides details on:
- Normal cardiac output values at rest and during activity.
- How the Frank-Starling mechanism and venous return primarily control cardiac output.
- Factors like metabolism, exercise, age, and body size that directly impact cardiac output.
- Pathologically high or low cardiac outputs and their underlying causes, including reduced peripheral resistance or issues with heart function.
- How cardiac output is measured and its relationship to venous return under normal conditions.
The document summarizes the anatomy of the anterior abdominal wall and groin region. It describes the layers that make up the abdominal wall from superficial to deep, including the skin, superficial fascia, deep fascia, muscles and rectus sheath. It discusses the contents and boundaries of the inguinal canal. It also outlines the structures contained within the femoral triangle in the groin, including the femoral artery and vein, nerves, and lymph nodes.
The skin is composed of three layers: the epidermis, dermis, and hypodermis. The epidermis is the outermost layer made up of stratified squamous epithelium. It contains no blood vessels and is divided into five sublayers - stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. The dermis lies below the epidermis and contains hair follicles, sweat glands, and blood vessels. It is divided into the papillary and reticular regions. The innermost layer, the hypodermis, is made up of loose connective tissue and stores fat.
The document discusses various types of embolism and thrombosis. It describes the Virschow triad of factors that can lead to thrombosis - endothelial injury, changes in blood flow, and hypercoagulability. It then examines different causes and outcomes of thrombosis and embolism in various parts of the body, such as pulmonary embolism from deep vein thrombosis, systemic embolism from cardiac sources, and amniotic fluid embolism during childbirth.
This document summarizes Starling's law of capillary exchange and the factors that influence fluid movement between capillaries and the interstitial space (Pc, Pi, πc, πi). It describes how small differences in these pressures normally result in equilibrium but how imbalances can cause edema. Specific causes of edema like increased hydrostatic pressure (heart failure), decreased oncotic pressure (liver disease), or increased permeability (burns) are explained. The role of the lymphatic system in maintaining fluid balance is also summarized.
The document provides an overview of the anatomy of the eye and ear. It describes the structures of the orbit, including the bones that make up its walls. It details the layers of the eyeball - fibrous, vascular and sensory layers - and identifies structures within each layer. These include the sclera, cornea, iris, choroid, ciliary body and retina. It also outlines the chambers of the eye and the extraocular muscles. For the ear, it identifies the external, middle and inner ear structures, such as the auricle, tympanic membrane, auditory ossicles, cochlea and vestibular system. It provides a brief overview of the nerves, blood supply and functions associated with
The document discusses the outcomes of acute inflammation and their morphological patterns. There are three potential outcomes of acute inflammation: 1) complete resolution, 2) healing by fibrosis, or 3) chronic inflammation. It also describes four main morphological patterns of acute inflammation: serous, fibrinous, suppurative (abscess formation), and ulcerative. Each pattern is associated with different clinical presentations and histological features.
it describes the microanatomy of skin and its appendages in a concise format. it will give the overview of the integumentary system of our body and largest organ of our body.
This document discusses several circulatory disorders including hyperemia, congestion, hemorrhage, and thrombosis. Hyperemia and congestion both involve increased blood volume in tissues but have different mechanisms. Hyperemia is an active process of arteriolar dilation while congestion is a passive process resulting from impaired venous outflow. Hemorrhage is defined as blood escaping from vessels, and can be classified by site, size, vessel type, and timing relative to trauma. Thrombosis is the formation of blood clots and can result from endothelial injury, abnormal blood flow like stasis or turbulence, or a hypercoagulable state of the blood.
The document discusses the structure and function of skin and fascia in the human body. It describes the layers of skin, including the epidermis and dermis, and conditions that can affect the skin like psoriasis, skin burns, and skin cancers. It also defines fascia as a fibrous tissue network beneath the skin that separates muscles, organs and tissues, allows muscle movement, and suspends organs. Specific types of fascia are described like the fascia lata in the lower limb.
The document discusses the anatomy and function of the heart. It describes the four chambers of the heart, including the left and right ventricles that pump blood to the lungs and body. It also discusses the causes and features of heart failure, which can occur when the heart is unable to pump sufficiently due to conditions that weaken it over time. Common causes include hypertension, heart attacks, and cardiac diseases. Features involve congestion in the lungs and other organs from blood backing up.
Purulent inflammation, also known as suppurative inflammation, results from bacterial infection and is characterized by large amounts of pus consisting of neutrophils, dead cells, and fluid. Abscesses form when pus accumulates in enclosed tissue spaces. Examples given include suppurative appendicitis, pyelonephritis, and purulent meningitis. Suppurative appendicitis specifically involves obstruction of the appendix leading to bacterial infection, swelling, and eventual rupture and abscess formation. Pyelonephritis is a urinary tract infection of the kidneys that can cause interstitial abscesses and suppuration if severe. Purulent meningitis is an infectious inflammation of the meninges often involving the brain and
The document summarizes the key steps in cardiac embryology:
1. The heart develops from mesoderm and appears in the third week as a linear heart tube that loops to the right.
2. Septa form to divide the heart into four chambers, with the atria separating in the fourth week and ventricles separating by the fifth week.
3. Valves develop from endocardial cushions that form in the atrioventricular canal and outflow tract.
4. The conducting system develops from pacemaker cells in the heart tube and sinus venosus.
The pelvic cavity is a bowl-shaped structure located below the abdominal cavity. It contains organs such as the urinary bladder, ovaries, uterus, rectum, and reproductive organs. In females, the pelvic cavity houses the ovaries, uterus, uterine tubes, vagina, and part of the rectum and urinary bladder. In males, the pelvic cavity contains the prostate, seminal vesicles, vas deferens, part of the rectum, and urinary bladder.
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.
Cell injury and death can occur through various mechanisms including hypoxia, physical or chemical insults, and microbial or immunological agents. The cellular response to injury depends on the cell type, extent, and type of injury. Initial responses include cellular adaptation, subcellular changes, or intracellular accumulations. Injury may result in reversible or irreversible cell damage and cell death. Irreversible injury is characterized by mitochondrial dysfunction and membrane damage, leading to necrosis or apoptosis. Different patterns of necrosis include coagulative, liquefactive, caseous, and gangrenous necrosis.
Intracellular accumulations ppt by dr usman nasirUsman Nasir
This document discusses intracellular accumulations, which occur due to metabolic derangements within cells. It defines intracellular accumulations and categorizes them as normal cellular constituents or abnormal endogenous or exogenous substances. Accumulations can occur in the cytoplasm or nucleus. The document then discusses the processes and sites of accumulations, including accumulation of lipids (resulting in steatosis), cholesterol, proteins, glycogen, and pigments. Specific diseases associated with accumulations of these substances are provided as examples.
1. An infarction is an area of ischemic necrosis in an organ resulting from reduced blood supply, usually due to arterial obstruction.
2. The main causes of infarction are thromboembolism and atherosclerosis, which interrupt arterial blood flow. This leads to localized tissue death from coagulative necrosis.
3. Pathologically, infarcts appear pale and wedge-shaped, with inflammation at the borders and eventual scar formation. Location and outcomes vary by organ, such as potentially lethal myocardial infarction or non-lethal splenic infarction.
Cardiac output refers to the volume of blood pumped by each ventricle per minute. It is determined by stroke volume, heart rate, preload, afterload, and peripheral resistance. Normal cardiac output is approximately 5 liters per minute. It can increase up to 600% in athletes due to enhanced cardiac reserve. Factors such as venous return, force of contraction, heart rate, and peripheral resistance maintain cardiac output within the body.
The cardiac conduction system is made up of four main structures that stimulate contraction of the heart muscle in a coordinated way. The sinoatrial node acts as the pacemaker and initiates electrical impulses throughout the heart. The atrioventricular node receives impulses from the atria and slows conduction to allow for proper atrial contraction before ventricular contraction. Impulses then travel through the atrioventricular bundle and Purkinje fibers to coordinate simultaneous contraction of the ventricles. An electrocardiogram is used to measure the electrical activity of the heart and detect any abnormalities.
The mitral valve develops between the 5th and 15th weeks of gestation. It consists of an annulus, two leaflets, chordae tendineae and papillary muscles. Rheumatic fever is a leading cause of mitral stenosis, which results from repeated bouts of inflammation damaging the mitral valve over time. Mitral stenosis causes elevated left atrial pressure and left atrial enlargement, often resulting in pulmonary hypertension. Echocardiography is the primary imaging method used to evaluate the mitral valve anatomy and measure the severity of mitral stenosis.
The CT images show a high-attenuation collection displacing the heart to the right, indicating hemopericardium or blood in the pericardial sac. Figure 3B further shows a brightly enhancing structure near a surgical clip on the distal posterior descending coronary artery, consistent with a pseudoaneurysm causing the hemorrhage. The findings are most consistent with hemopericardium developing several days after coronary bypass surgery.
This document discusses cardiac output and the factors that affect it. It provides details on:
- Normal cardiac output values at rest and during activity.
- How the Frank-Starling mechanism and venous return primarily control cardiac output.
- Factors like metabolism, exercise, age, and body size that directly impact cardiac output.
- Pathologically high or low cardiac outputs and their underlying causes, including reduced peripheral resistance or issues with heart function.
- How cardiac output is measured and its relationship to venous return under normal conditions.
The document summarizes the anatomy of the anterior abdominal wall and groin region. It describes the layers that make up the abdominal wall from superficial to deep, including the skin, superficial fascia, deep fascia, muscles and rectus sheath. It discusses the contents and boundaries of the inguinal canal. It also outlines the structures contained within the femoral triangle in the groin, including the femoral artery and vein, nerves, and lymph nodes.
The skin is composed of three layers: the epidermis, dermis, and hypodermis. The epidermis is the outermost layer made up of stratified squamous epithelium. It contains no blood vessels and is divided into five sublayers - stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. The dermis lies below the epidermis and contains hair follicles, sweat glands, and blood vessels. It is divided into the papillary and reticular regions. The innermost layer, the hypodermis, is made up of loose connective tissue and stores fat.
The document discusses various types of embolism and thrombosis. It describes the Virschow triad of factors that can lead to thrombosis - endothelial injury, changes in blood flow, and hypercoagulability. It then examines different causes and outcomes of thrombosis and embolism in various parts of the body, such as pulmonary embolism from deep vein thrombosis, systemic embolism from cardiac sources, and amniotic fluid embolism during childbirth.
This document summarizes Starling's law of capillary exchange and the factors that influence fluid movement between capillaries and the interstitial space (Pc, Pi, πc, πi). It describes how small differences in these pressures normally result in equilibrium but how imbalances can cause edema. Specific causes of edema like increased hydrostatic pressure (heart failure), decreased oncotic pressure (liver disease), or increased permeability (burns) are explained. The role of the lymphatic system in maintaining fluid balance is also summarized.
The document provides an overview of the anatomy of the eye and ear. It describes the structures of the orbit, including the bones that make up its walls. It details the layers of the eyeball - fibrous, vascular and sensory layers - and identifies structures within each layer. These include the sclera, cornea, iris, choroid, ciliary body and retina. It also outlines the chambers of the eye and the extraocular muscles. For the ear, it identifies the external, middle and inner ear structures, such as the auricle, tympanic membrane, auditory ossicles, cochlea and vestibular system. It provides a brief overview of the nerves, blood supply and functions associated with
The document discusses the outcomes of acute inflammation and their morphological patterns. There are three potential outcomes of acute inflammation: 1) complete resolution, 2) healing by fibrosis, or 3) chronic inflammation. It also describes four main morphological patterns of acute inflammation: serous, fibrinous, suppurative (abscess formation), and ulcerative. Each pattern is associated with different clinical presentations and histological features.
it describes the microanatomy of skin and its appendages in a concise format. it will give the overview of the integumentary system of our body and largest organ of our body.
This document discusses several circulatory disorders including hyperemia, congestion, hemorrhage, and thrombosis. Hyperemia and congestion both involve increased blood volume in tissues but have different mechanisms. Hyperemia is an active process of arteriolar dilation while congestion is a passive process resulting from impaired venous outflow. Hemorrhage is defined as blood escaping from vessels, and can be classified by site, size, vessel type, and timing relative to trauma. Thrombosis is the formation of blood clots and can result from endothelial injury, abnormal blood flow like stasis or turbulence, or a hypercoagulable state of the blood.
The document discusses the structure and function of skin and fascia in the human body. It describes the layers of skin, including the epidermis and dermis, and conditions that can affect the skin like psoriasis, skin burns, and skin cancers. It also defines fascia as a fibrous tissue network beneath the skin that separates muscles, organs and tissues, allows muscle movement, and suspends organs. Specific types of fascia are described like the fascia lata in the lower limb.
The document discusses the anatomy and function of the heart. It describes the four chambers of the heart, including the left and right ventricles that pump blood to the lungs and body. It also discusses the causes and features of heart failure, which can occur when the heart is unable to pump sufficiently due to conditions that weaken it over time. Common causes include hypertension, heart attacks, and cardiac diseases. Features involve congestion in the lungs and other organs from blood backing up.
Purulent inflammation, also known as suppurative inflammation, results from bacterial infection and is characterized by large amounts of pus consisting of neutrophils, dead cells, and fluid. Abscesses form when pus accumulates in enclosed tissue spaces. Examples given include suppurative appendicitis, pyelonephritis, and purulent meningitis. Suppurative appendicitis specifically involves obstruction of the appendix leading to bacterial infection, swelling, and eventual rupture and abscess formation. Pyelonephritis is a urinary tract infection of the kidneys that can cause interstitial abscesses and suppuration if severe. Purulent meningitis is an infectious inflammation of the meninges often involving the brain and
The document summarizes the key steps in cardiac embryology:
1. The heart develops from mesoderm and appears in the third week as a linear heart tube that loops to the right.
2. Septa form to divide the heart into four chambers, with the atria separating in the fourth week and ventricles separating by the fifth week.
3. Valves develop from endocardial cushions that form in the atrioventricular canal and outflow tract.
4. The conducting system develops from pacemaker cells in the heart tube and sinus venosus.
The pelvic cavity is a bowl-shaped structure located below the abdominal cavity. It contains organs such as the urinary bladder, ovaries, uterus, rectum, and reproductive organs. In females, the pelvic cavity houses the ovaries, uterus, uterine tubes, vagina, and part of the rectum and urinary bladder. In males, the pelvic cavity contains the prostate, seminal vesicles, vas deferens, part of the rectum, and urinary bladder.
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.
Cell injury and death can occur through various mechanisms including hypoxia, physical or chemical insults, and microbial or immunological agents. The cellular response to injury depends on the cell type, extent, and type of injury. Initial responses include cellular adaptation, subcellular changes, or intracellular accumulations. Injury may result in reversible or irreversible cell damage and cell death. Irreversible injury is characterized by mitochondrial dysfunction and membrane damage, leading to necrosis or apoptosis. Different patterns of necrosis include coagulative, liquefactive, caseous, and gangrenous necrosis.
Intracellular accumulations ppt by dr usman nasirUsman Nasir
This document discusses intracellular accumulations, which occur due to metabolic derangements within cells. It defines intracellular accumulations and categorizes them as normal cellular constituents or abnormal endogenous or exogenous substances. Accumulations can occur in the cytoplasm or nucleus. The document then discusses the processes and sites of accumulations, including accumulation of lipids (resulting in steatosis), cholesterol, proteins, glycogen, and pigments. Specific diseases associated with accumulations of these substances are provided as examples.
1. An infarction is an area of ischemic necrosis in an organ resulting from reduced blood supply, usually due to arterial obstruction.
2. The main causes of infarction are thromboembolism and atherosclerosis, which interrupt arterial blood flow. This leads to localized tissue death from coagulative necrosis.
3. Pathologically, infarcts appear pale and wedge-shaped, with inflammation at the borders and eventual scar formation. Location and outcomes vary by organ, such as potentially lethal myocardial infarction or non-lethal splenic infarction.
Cardiac output refers to the volume of blood pumped by each ventricle per minute. It is determined by stroke volume, heart rate, preload, afterload, and peripheral resistance. Normal cardiac output is approximately 5 liters per minute. It can increase up to 600% in athletes due to enhanced cardiac reserve. Factors such as venous return, force of contraction, heart rate, and peripheral resistance maintain cardiac output within the body.
The cardiac conduction system is made up of four main structures that stimulate contraction of the heart muscle in a coordinated way. The sinoatrial node acts as the pacemaker and initiates electrical impulses throughout the heart. The atrioventricular node receives impulses from the atria and slows conduction to allow for proper atrial contraction before ventricular contraction. Impulses then travel through the atrioventricular bundle and Purkinje fibers to coordinate simultaneous contraction of the ventricles. An electrocardiogram is used to measure the electrical activity of the heart and detect any abnormalities.
The mitral valve develops between the 5th and 15th weeks of gestation. It consists of an annulus, two leaflets, chordae tendineae and papillary muscles. Rheumatic fever is a leading cause of mitral stenosis, which results from repeated bouts of inflammation damaging the mitral valve over time. Mitral stenosis causes elevated left atrial pressure and left atrial enlargement, often resulting in pulmonary hypertension. Echocardiography is the primary imaging method used to evaluate the mitral valve anatomy and measure the severity of mitral stenosis.
The CT images show a high-attenuation collection displacing the heart to the right, indicating hemopericardium or blood in the pericardial sac. Figure 3B further shows a brightly enhancing structure near a surgical clip on the distal posterior descending coronary artery, consistent with a pseudoaneurysm causing the hemorrhage. The findings are most consistent with hemopericardium developing several days after coronary bypass surgery.
This document discusses constrictive pericarditis. It begins with definitions and mentions that constrictive pericarditis is the end stage of an inflammatory process involving the pericardium. Common causes in developed countries include idiopathic, postsurgical, or radiation injury, while tuberculosis is more common in developing countries. Over time, fibrosis and scarring of the pericardium develops, restricting heart filling. Clinical presentation involves signs of right heart failure like edema and ascites. Diagnosis involves identifying signs of restricted filling on imaging and hemodynamics. Treatment is surgical pericardiectomy except for transient cases.
The document discusses imaging of congenital heart diseases, describing the main types of defects such as atrial septal defects (ASD), ventricular septal defects (VSD), and patent ductus arteriosus (PDA). It provides details on the anatomy, classifications, imaging findings, and clinical presentations of each type of defect. Examples of echocardiograms and chest x-rays are shown to illustrate the imaging appearance of various congenital heart abnormalities.
The document describes a case of a 3-week-old infant referred for tachypnea. Chest x-ray showed cardiomegaly and normal pulmonary vascularity. Aortogram showed normal aorta but retrograde filling of the left coronary artery from collaterals, with the proximal left coronary draining into the pulmonary artery rather than the aorta. The most likely diagnosis is Bland-White-Garland Syndrome, a rare condition where one coronary artery, usually the left, originates from the pulmonary artery rather than the aorta.
The cardiovascular system consists of the heart and network of blood vessels that circulate blood throughout the body. The heart pumps blood in a continuous cycle called the cardiac cycle. Blood is carried away from the heart through arteries and returns to the heart through veins, passing through capillaries where nutrients and gases are exchanged. The cardiovascular system can be affected by congenital heart defects present from birth or conditions like heart failure that impair the heart's ability to pump effectively.
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.
The document provides information on cardiomyopathy including:
- Dilated cardiomyopathy is the most common type and causes the heart chambers to enlarge and the myocardium to weaken, reducing cardiac output. It can result from viral infections, alcohol toxicity, cancer treatments and genetic disorders.
- Hypertrophic cardiomyopathy causes thickening of the heart muscle walls, most often the septum. It can obstruct blood flow and cause chest pain, fainting and arrhythmias. Genetic factors and long-term pressure overload contribute to its development.
- Restrictive cardiomyopathy stiffens the heart muscle, impairing its ability to fill with blood. It is rare and can be caused by infiltrative diseases like amyloidosis
This document discusses various diseases of the pericardium, heart, and thoracic aorta as assessed through non-invasive imaging techniques. It covers conditions such as pericarditis, pericardial cysts, cardiac tumors including myxomas, angiosarcomas and lymphomas. Diseases of the thoracic aorta explored are aortic dissection, aneurysms, and rupture. Key imaging modalities discussed are echocardiography, CT, MRI, nuclear medicine scans.
This document contains information about hypertrophic obstructive cardiomyopathy (HOCM). It begins with an overview of HOCM, defining it as a genetic heart condition characterized by asymmetric left ventricular hypertrophy. It then discusses the pathophysiology of HOCM, focusing on left ventricular outflow tract obstruction, diastolic dysfunction, myocardial ischemia, and mitral regurgitation due to systolic anterior motion of the mitral valve. The document outlines clinical manifestations such as symptoms, physical exam findings, ECG and echocardiographic features, and complications. It concludes by covering treatment options for HOCM including medications, surgical septal myectomy via transaortic or transapical approaches, and other procedures like alcohol septal
The document discusses various hemodynamic disorders including hyperemia, congestion, thrombosis, embolism, and infarction. Hyperemia is an increased blood volume in tissue from vasodilation. Congestion is increased blood volume from impaired venous return. Thrombosis is the formation of a blood clot within vessels. An embolism occurs when a piece of thrombus or other material blocks a vessel. Infarction is tissue death from blocked arteries or veins.
The document discusses various hemodynamic disorders including hyperemia, congestion, thrombosis, embolism, and infarction. Hyperemia is an increased blood volume in tissue from vasodilation. Congestion is increased blood volume from impaired venous return. Thrombosis is the formation of a blood clot within vessels. An embolism occurs when a piece of thrombus or other material blocks a vessel. Infarction is tissue death from blocked arteries or veins.
1) Mitral regurgitation occurs when a portion of the left ventricular blood volume is directed backwards into the left atrium during systole instead of forwards through the aorta.
2) Causes of mitral regurgitation include myxomatous degeneration, rheumatic fever, hypertrophic cardiomyopathy, and regional wall motion abnormalities.
3) Cardiac MRI and CT are useful for evaluating mitral regurgitation through assessment of valve morphology, ventricular volumes and function, visualization of regurgitant jets, and quantification of regurgitant volumes. Phase contrast imaging allows for measurement of forward flow and calculation of regurgitant fraction.
This document contains several case studies in cardiology presented by Dr. Magdi Awad Sasi from the CCU department of Octoper Hospital in Benghazi, Libya.
The first case discusses a 55-year-old man presenting with chest pain and risk factors for cardiovascular disease. The most appropriate initial diagnostic procedure is listed as cardiac catheterization.
The second case involves a 35-year-old woman who died of pulmonary embolism, and upon autopsy was found to have mitral stenosis, likely due to previous rheumatic fever.
The third case describes a 74-year-old man found to have widening of the mediastinum and aortic insufficiency murmur, indicating
Fibroelastomas and rhabdomyomas are the most common benign cardiac tumors after myxomas. Myxomas typically originate in the left atrium and can cause obstruction of blood flow, embolic events, or valve dysfunction. Symptoms include dyspnea, palpitations, and constitutional symptoms. Diagnosis is made using echocardiography, CT, or MRI. Surgical excision is the treatment of choice and prognosis is generally good with low mortality rates.
1. Myocardial infarction occurs when blood flow decreases or stops to the heart muscle, depriving it of oxygen and causing cell death.
2. The ECG, blood tests of cardiac enzymes like troponin, and symptoms are used to diagnose a myocardial infarction.
3. Different coronary artery blockages can cause infarcts in specific heart regions, shown by distinct ST segment changes on ECG - inferior infarcts raise ST in II, III, AVF, etc.
This document presents two medical case studies involving imaging findings and diagnoses. The first case involves a woman with cough and dyspnea, and imaging shows a normal left lung but small right pulmonary artery and hypoplastic right lung. The most likely diagnosis is Swyer James Syndrome. The second case involves a woman with IV drug abuse presenting with fevers and leg pain, and imaging shows a filling defect across the iliac arteries. The most likely diagnosis is an embolism.
This document discusses various imaging approaches for evaluating acute chest pain and thoracic abnormalities. It begins by outlining how cardiac CT angiography can be used to assess coronary artery disease and causes of non-cardiac chest pain such as aortic disorders, pulmonary embolism, and other thoracic issues. Examples of CT and MRI images are provided to illustrate different pathologies. The document then focuses on specific conditions like aortic dissection, pulmonary embolism, pneumothorax, and pleural effusions. Imaging findings and diagnostic criteria for each condition are summarized.
This document discusses coronary artery disease and the abnormalities seen on echocardiography. It covers the pathophysiology of coronary syndromes and describes techniques for detecting wall motion abnormalities. It then details various complications that can occur with acute myocardial infarction such as pericardial effusions, infarct expansion, ventricular thrombi, and mitral regurgitation. Chronic complications of coronary artery disease discussed include left ventricular aneurysms, mural thrombi, and remodeling.
02 Disert. Mecanismo - Factores y receptores de Crecimientounab.patologia
El documento describe los mecanismos de los factores de crecimiento y sus receptores. Explica que los factores de crecimiento como el PDGF, EGF, TGF y FGF actúan como señalizadores químicos que modifican el crecimiento celular a través de la interacción con receptores como el EGFR, CSFR-1 y PDGFR. También menciona que muchos oncogenes codifican formas mutantes de estos receptores de superficie ligados al crecimiento celular y el desarrollo de tumores.
Este documento proporciona información sobre infecciones pulmonares como la tuberculosis y la neumonía. Resume las causas, síntomas y tratamientos de estas enfermedades, así como los tipos de micobacterias y bacterias que las causan. También describe brevemente otras infecciones como el SARS y la relación entre la tuberculosis y el VIH.
Este documento habla sobre las enfermedades pulmonares intersticiales como la asbestosis y la silicosis. La asbestosis es causada por la inhalación de fibras de asbesto y causa inflamación y cicatrización del tejido pulmonar, reduciendo la capacidad respiratoria. La silicosis es similar y es causada por la inhalación prolongada de polvo de sílice, pudiendo ser crónica, acelerada o aguda dependiendo de la exposición. Ambas enfermedades son irreversibles y su tratamiento se enfoca en controlar los
The document discusses the microscopic structure of the alveolar wall and lung anatomy. It describes the thin barrier between the alveolar air spaces and capillaries that allows for efficient gas exchange. It also mentions there are approximately 30 million alveoli in the human lung. Furthermore, it discusses factors that can disrupt the ventilation/perfusion ratio in the lungs such as areas with low oxygen and high carbon dioxide levels or reduced blood flow from embolisms.
Este documento describe diferentes tipos de vasculitis, enfermedades inflamatorias que afectan las paredes de los vasos sanguíneos. Explica las clasificaciones de las vasculitis según su patogénesis, incluyendo aquellas mediadas por autoinmunidad, infecciones, células u otros mecanismos. También detalla algunos síndromes específicos como la granulomatosis de Wegener, la poliarteritis nodosa y la enfermedad de Kawasaki, describiendo sus características clínicas y morfológicas
Este documento describe diferentes tipos de tumores vasculares benignos y malignos. Se describen hemangiomas benignos como hemangioma capilar y cavernoso. Se mencionan ectasias vasculares como nevus flammeus, arañas vasculares y telangiectasia hemorrágica hereditaria. Entre los tumores de grado intermedio se incluyen angiomatosis bacilar y los cuatro tipos de sarcoma de Kaposi. Los tumores malignos discutidos son angiosarcoma, hemangioendotelioma epiteloide y hemangiopericitoma. Finalmente
Este documento describe factores congénitos como cardiopatías congénitas. Explica que pueden ser de origen genético o causados por factores externos durante el embarazo. Las cardiopatías congénitas implican lesiones en las cámaras o válvulas del corazón. Se clasifican en cianóticas y no cianóticas. Algunas cardiopatías descritas son la transposición de las grandes arterias, la coartación de la aorta y su relación con el síndrome de Turner. El documento concluye que aunque las caus
The document discusses calcium, phosphate, and magnesium content and distribution in the human body. It also describes the physiological functions of calcium, including cellular functions like cell growth and division, and extracellular functions like mineralization and blood clotting. Calcium signaling is discussed, where calcium binds to and activates proteins like calmodulin and calcium ATPase pumps.
El documento describe las diferentes arritmias cardiacas, incluyendo sus causas, síntomas, diagnóstico y tratamiento. Define la arritmia cardiaca como cualquier alteración del ritmo o conducción del impulso cardiaco. Describe varios tipos como extrasístoles auriculares, taquicardia auricular paroxística, fibrilación y flúter auricular, síndrome de Wolf-Parkinson-White, extrasístoles ventriculares, taquicardia ventricular, fibrilación ventricular y bloqueo cardiaco. Explica que el diagnóstico inclu
El documento trata sobre la diabetes mellitus tipo 2. Explica que se debe a una resistencia a la insulina y una falla en la producción de insulina por el páncreas. Los principales factores de riesgo son la obesidad, la dieta alta en carbohidratos y la edad avanzada. Las complicaciones incluyen enfermedades cardíacas, daño ocular y neuropatía. El tratamiento involucra dieta, ejercicio y medicamentos para mejorar la sensibilidad a la insulina o estimular su producción.
La diabetes tipo 1 se caracteriza por la falta de producción de insulina debido a la destrucción de las células beta en el páncreas. Se diagnostica mediante niveles altos de glucosa en la sangre. Está causada por factores genéticos, autoinmunes y ambientales que desencadenan una respuesta autoinmune contra las células beta. Los síntomas incluyen cansancio, adelgazamiento, hambre y sed excesivas, orinar y beber mucho. El tratamiento consiste en la administración de insulina.
El documento describe el síndrome de Cushing, una afección causada por niveles excesivos de glucocorticoides como el cortisol. Las principales causas incluyen tumores en la hipófisis que secretan demasiada ACTH, tumores ectópicos que secretan ACTH, y tumores en las glándulas suprarrenales que producen cortisol de forma autónoma. El síndrome se caracteriza por hipertrofia bilateral de la corteza suprarrenal y síntomas como aumento de peso, diabetes y cambios en la piel.
La insuficiencia adrenal primaria u enfermedad de Addison es un déficit en la producción de cortisol causado por una falla en las glándulas suprarrenales. Los síntomas incluyen bajo peso, fatiga, hipotensión, aumento de apetito por sal y pigmentación intensa de la piel. Las causas más comunes son infecciones como tuberculosis o VIH, cánceres metastásicos y atrofia autoinmune de las glándulas suprarrenales.
The document discusses various endocrine diseases and disorders. It provides figures and diagrams showing the mechanisms and pathways of different endocrine glands like the pituitary, thyroid, adrenals and how diseases can disrupt the normal functioning of these glands and hormone production/regulation. Specific diseases covered include Graves' disease, hyperthyroidism, hypothyroidism, Cushing's syndrome, Addison's disease and disorders of the adrenal glands.
This document discusses several genes associated with hereditary cancer predisposition syndromes and their roles. It provides a table listing several cancer susceptibility genes including BRCA1, BRCA2, MEN1, RET, APC, and p53 and the cancers they predispose individuals to, such as breast and ovarian cancer, colon cancer, and Li-Fraumeni syndrome. The document also contains figures depicting cellular pathways involving tumor suppressor genes and oncogenes related to DNA repair, Wnt signaling, and growth factors.
El documento trata sobre varias proteínas relacionadas con la transducción de señales en procesos celulares como el crecimiento y la diferenciación. Explica cómo mutaciones en genes como RAS, BCR-ABL y BRAF afectan estas vías de señalización y pueden contribuir al desarrollo de cáncer. También describe otros mecanismos como las proteínas reguladoras del ciclo celular ciclinas y CDK, y su papel en la proliferación normal y anormal de las células.
Este documento describe los principales mediadores químicos de la inflamación como la histamina, serotonina, quinina, ácido araquidónico y sus derivados (prostaglandinas, tromboxano, prostaciclinas, leucotrienos). Explica sus funciones en la vasodilatación, permeabilidad vascular, dolor, fiebre y quimiotaxis durante la respuesta inflamatoria aguda y crónica.
01 Disert. Cascada del complemento y citoquinasunab.patologia
El documento describe las tres vías de la cascada del complemento (clásica, lectina y alternativa), los componentes proteicos involucrados en cada una, y sus efectos. Explica que la cascada del complemento conduce a la formación del complejo de ataque a la membrana, el cual genera poros que destruyen patógenos. También cubre brevemente las citoquinas, sus clases y mecanismos de acción.
An inflammation may be triggered by several mechanisms including noxious physical or chemical agents, accumulated metabolic products, immunologic or infectious tissue injury, or tissue necrosis. During an acute inflammation, there are hemodynamic changes like initial vasoconstriction followed by vasodilation increasing vascular permeability. This allows fluid and proteins to accumulate in tissues (edema) and neutrophils to migrate from blood vessels to the site of injury. Neutrophils play an important role by adhering to endothelial cells through a process involving selectins and integrins.
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.
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
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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).
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.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Novas diretrizes da OMS para os cuidados perinatais de mais qualidade
05 Cat. Cardiovascular I
1. Figure 12-1 Myocardium (cardiac muscle). A The histology of myocardium is shown, emphasizing the centrally-placed nuclei of the cardiac myocytes (arrowhead), intercalated discs (representing specialized end-to-end junctions of adjoining cells; highlighted by a double arrow) and the sarcomeric structure visible as cross-striations within myocytes. A capillary endothelial cell is indicated by an arrow. (Photomicrograph courtesy of Mark Flomenbaum, M.D., Ph.D., Office of the Chief Medical Examiner, New York City, NY.) B Electron microscopy of myocardium, showing myofibrillar (my) and mitochondrial (mi) architecture and the sarcolemmal membrane (s). Z bands are indicated by arrows. Bar = 1 μm. (Reproduced by permission from Vivaldi MT, et al. Triphenyltetrazolium staining of irreversible injury following coronary artery occlusion in rats. Am J Pathol 121:522, 1985. Copyright J.B. Lippincott, 1985.) The normal heart weight 250 to 300 g females and 300 to 350 g males. Thickness of the free wall of the right ventricle is 0.3 to 0.5 cm and that of the left ventricle 1.3 to 1.5 cm. Greater heart weight or ventricular thickness indicates hypertrophy, and an enlarged chamber size implies dilation . An increase in cardiac weight or size is termed cardiomegaly .
2. Figure 12-2 Aortic valve histology, shown as a low-magnification photomicrograph of cuspal cross-section in the systolic (nondistended) state, emphasizing three major layers (ventricularis [v], spongiosa [s], and fibrosa [f]). Superficial endothelial cells (arrow) and diffusely distributed deep interstitial cells are noted. The strength of the valve is predominantlyderived from the fibrosa, with its dense collagen (yellow) . This section highlights the dense, laminated elastic tissue in the ventricularis (double arrow) . The outflow surface is at top. (Reproduced by permission from Schoen FJ: Aortic valve structure-function correlations: Role of elastic fibers no longer a stretch of the imagination. J Heart Valve Dis 6:1, 1997.)
3. TABLE 12-1 -- Changes in the Aging Heart Increased cross-sectional luminal area Tortuosity Epicardial Coronary Arteries Lambl excrescences Buckling of mitral leaflets toward the left atrium Fibrous thickening of leaflets Mitral valve annular calcific deposits Aortic valve calcific deposits Valves Sigmoid-shaped ventricular septum Decreased left ventricular cavity size Increased left atrial cavity size Chambers
5. • Failure of the pump . In the most common circumstance, the cardiac muscle contracts weakly or inadequately, and the chambers cannot empty properly. In some conditions, however, the muscle cannot relax sufficiently to permit ventricular filling. • An obstruction to flow , owing to a lesion preventing valve opening or otherwise causing increased ventricular chamber pressure (e.g., aortic valvular stenosis, systemic hypertension, or aortic coarctation). The increased pressure overworks the chamber that pumps against the obstruction. • Regurgitant flow causes some of the output from each contraction to flow backward, adding a volume workload to each of the chambers, which must pump the extra blood (e.g., left ventricle in aortic regurgitation; left atrium and left ventricle in mitral regurgitation). • Disorders of cardiac conduction . Heart block or arrhythmias owing to uncoordinated generation of impulses (e.g., atrial or ventricular fibrillation) lead to nonuniform and inefficient contractions of the muscular walls. • Disruption of the continuity of the circulatory system that permits blood to escape (e.g., gunshot wound through the thoracic aorta).
6. • The Frank-Starling mechanism , in which the increased preload of dilation (thereby increasing cross-bridges within the sarcomeres) helps to sustain cardiac performance by enhancing contractility • Myocardial structural changes, including augmented muscle mass (hypertrophy) with or without cardiac chamber dilation , in which the mass of contractile tissue is augmented • Activation of neurohumoral systems , especially (1) release of the neurotransmitter norepinephrine by adrenergic cardiac nerves (which increases heart rate and augments myocardial contractility and vascular resistance), (2) activation of the renin-angiotensin-aldosterone system, and (3) release of atrial natriuretic peptide.
7. Figure 12-3 Left ventricular hypertrophy. A, Pressure hypertrophy due to left ventricular outflow obstruction. The left ventricle is on the lower right in this apical four-chamber view of the heart. B, Altered cardiac configuration in left ventricular hypertrophy without and with dilation, viewed in transverse heart sections. Compared with a normal heart ( center ), the pressurehypertrophied hearts ( left and in A ) have increased mass and a thick left ventricular wall, but the hypertrophied and dilated heart (right) has increased mass but a normal wall thickness. (Reproduced by permission from Edwards WD: Cardiac anatomy and examination of cardiac specimens. In Emmanouilides GC, Riemenschneider TA, Allen HD, Gutgesell HP (eds): Moss and Adams Heart Disease in Infants, Children, and Adolescents: Including the Fetus and Young Adults, 5th ed. Philadelphia, Williams and Wilkins, 1995, p. 86.)
8. Figure 12-4 Schematic representation of the sequence of events in cardiac hypertrophy and its progression to heart failure, emphasizing cellular and extracellular changes.
9. The most frequent causes of the major functional valvular lesions are as follows: • Aortic stenosis : calcification of anatomically normal and congenitally bicuspid aortic valves • Aortic insufficiency : dilation of the ascending aorta, related to hypertension and aging. • Mitral stenosis: rheumatic heart disease • Mitral insufficiency: myxomatous degeneration (mitral valve prolapse)
10. Figure 12-22 Calcific valvular degeneration. A, Calcific aortic stenosis of a previously normal valve having three cusps (viewed from aortic aspect). Nodular masses of calcium are heapedup within the sinuses of Valsalva (arrow) . Note that the commissures are not fused, as in postrheumatic aortic valve stenosis (see Fig. 12-24 E ). B, Calcific aortic stenosis occurring on a congenitally bicuspid valve. One cusp has a partial fusion at its center, called a raphe (arrow). C and D, Mitral annular calcification, with calcific nodules at the base (attachment margin) of the anterior mitral leaflet (arrows) . C, Left atrial view. D, Cut section of myocardium.
11. Figure 12-23 Myxomatous degeneration of the mitral valve. A, Long axis of left ventricle demonstrating hooding with prolapse of the posterior mitral leaflet into the left atrium (arrow) . The left ventricle is on right in this apical four-chamber view. (Courtesy of William D. Edwards, M.D., Mayo Clinic, Rochester, MN.) B, Opened valve, showing pronounced hooding of the posterior mitral leaflet with thrombotic plaques at sites of leaflet-left atrium contact (arrows). C , Opened valve with pronounced hooding from patient who died suddenly (double arrows) . Note also mitral annular calcification (arrowhead) .
12. Figure 12-12 Schematic representation of sequential progression of coronary artery lesion morphology, beginning with stable chronic plaque responsible for typical angina and leading to the various acute coronary syndromes. (Modified and redrawn from Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles. Philadelphia, W.B. Saunders Co., 1989, p. 63.)
13. Figure 12-11 Atherosclerotic plaque rupture. A, Plaque rupture without superimposed thrombus, in patient who died suddenly. B, Acute coronary thrombosis superimposed on an atherosclerotic plaque with focal disruption of the fibrous cap, triggering fatal myocardial infarction. C, Massive plaque rupture with superimposed thrombus, also triggering a fatal myocardial infarction (special stain highlighting fibrin in red). In both A and B, an arrow points to the site of plaque rupture. (B, reproduced from Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles. Philadelphia, W.B. Saunders, 1989, p. 61.)
14. Figure 12-13 Postmortem angiogram showing the posterior aspect of the heart of a patient who died during the evolution of acute myocardial infarction, demonstrating total occlusion of the distal right coronary artery by an acute thrombus (arrow) and a large zone of myocardial hypoperfusion involving the posterior left and right ventricles, as indicated by arrowheads, and having almost absent filling of capillaries, that is, less white. The heart has been fixed by coronary arterial perfusion with glutaraldehyde and cleared with methyl salicylate, followed by intracoronary injection of silicone polymer. Photograph courtesy of Lewis L. Lainey. (Reproduced by permission from Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles. Philadelphia, WB Saunders, 1989, p. 60.) TABLE 12-4 -- Approximate Time of Onset of Key Events in Ischemic Cardiac Myocytes ATP, adenosine triphosphate. >1 hr Microvascular injury 20–40 min Irreversible cell injury 40 min •• to 10% of normal 10 min •• to 50% of normal ATP reduced <2 min Loss of contractility Seconds Onset of ATP depletion Time Feature
15. Figure 12-14 Schematic representation of the progression of myocardial necrosis after coronary artery occlusion. Necrosis begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone. This entire region of myocardium (shaded) depends on the occluded vessel for perfusion and is the area at risk. Note that a very narrow zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion from the ventricle. The end result of the obstruction to blood flow is necrosis of the muscle that was dependent on perfusion from the coronary artery obstructed. Nearly the entire area at risk loses viability. The process is called myocardial infarction, and the region of necrotic muscle is a myocardial infarct .
16.
17. Figure 12-15 Acute myocardial infarct, predominantly of the posterolateral left ventricle, demonstrated histochemically by a lack of staining by the triphenyltetrazolium chloride (TTC) stain in areas of necrosis (arrow) . The staining defect is due to the enzyme leakage that follows cell death. Note the myocardial hemorrhage at one edge of the infarct that was associated with cardiac rupture, and the anterior scar (arrowhead) , indicative of old infarct. (Specimen the oriented with the posterior wall at the top.)
18. Figure 12-16 Microscopic features of myocardial infarction and its repair. A, One-day-old infarct showing coagulative necrosis along with wavy fibers (elongated and narrow), compared with adjacent normal fibers (at right). Widened spaces between the dead fibers contain edema fluid and scattered neutrophils. B, Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial infarction of 3 to 4 days' duration. C, Nearly complete removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days). D, Granulation tissue characterized by loose collagen and abundant capillaries. E, Well-healed myocardial infarct with replacement of the necrotic fibers by dense collagenous scar. A few residual cardiac muscle cells are present.
19. Grupo 1 Arritmias Grupo 2 Factores congénitos
20. Figure 12-5 Cardiac defects related to neural crest abnormalities. A, Biologic pathways for cardiac neural crest-related defects. B, Disease phenotypes. DORV, double-outlet right ventricle; TGA, transposition of the great arteries. (Reproduced by permission from Chien KR: Genomic circuits and the integrative biology of cardiac diseases. Nature 407:227, 2000.)
21. Figure 12-6 Schematic diagram of congenital left-to-right shunts. A, Atrial septal defect (ASD). B, Ventricular septal defect (VSD). With VSD the shunt is left-to-right, and the pressures are the same in both ventricles. Pressure hypertrophy of the right ventricle and volume hypertrophy of the left ventricle are generally present. C, Patent ductus arteriosus (PDA). D, Atrioventricular septal defect (AVSD). E, Large VSD with irreversible pulmonary hypertension. The shunt is right-to-left (shunt reversal). Volume hypertrophy and pressure hypertrophy of the right ventricle are present. Arrow indicates the direction of blood flow. The right ventricular pressure is now sufficient to yield a right-to-left shunt (Ao, aorta; LA, left atrium; LV, left ventricle; PT, pulmonary trunk; RA, right atrium; RV, right ventricle.)
22. Figure 12-7 Gross photograph of a ventricular septal defect (membranous type); defect denoted by arrow. (Courtesy of William D. Edwards, M.D., Mayo Clinic, Rochester, MN.)
23. Figure 12-8 Schematic diagram of the most important right-to-left shunts (cyanotic congenital heart disease) . A, Tetralogy of Fallot. Diagrammatic representation of anatomic variants, indicating that the direction of shunting across the VSD depends on the severity of the subpulmonary stenosis. Arrows indicate the direction of the blood flow. B, Transposition of the great vessels with and without VSD. (Ao, aorta; LA, left atrium; LV, left ventricle; PT, pulmonary trunk; RA, right atrium; RV, right ventricle.) (Courtesy of William D. Edwards, M.D., Mayo Clinic, Rochester, MN.)
24. Figure 12-9 Transposition of the great arteries. (Courtesy of William D. Edwards, M.D., Mayo Clinic, Rochester, MN.) Figure 12-10 Diagram showing coarctation of the aorta with and without PDA. (Ao, aorta; LA, left atrium; LV, left ventricle; PT, pulmonary trunk; RA, right atrium; RV, right ventricle; PDA, persistent ductus arteriosus.) (Courtesy of William D. Edwards, M.D., Mayo Clinic, Rochester, MN.)