ATHEROSCLEROSIS & IHD.ppt
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Atherosclerosis is characterized by fatty plaques or atheromas that form within arteries. Over time, these plaques can narrow or block arteries, restricting blood flow. This restricted blood flow can lead to myocardial infarction (MI), commonly known as a heart attack. During an MI, part of the heart muscle dies due to an inadequate blood supply. The degree and location of damage depends on which coronary artery is blocked and for how long. MIs can cause permanent damage and weakening of the heart muscle if not promptly treated. Chronic ischemia from long-term reduced blood flow can also cause scarring of heart muscle over many years.
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Cardiac pathology
Ischemic heart disease, resulting from impaired blood supply to the heart, is currently the leading cause of cardiovascular disease death worldwide. It refers to conditions including angina, heart attack, chronic heart disease, heart failure and sudden cardiac death. The most common cause is coronary artery atherosclerosis and thrombosis, usually resulting from plaque rupture or erosion in the arteries. Vulnerable plaques are prone to rupture due to characteristics like a thin fibrous cap and large lipid core, exposing thrombogenic materials and narrowing the artery. Timely reopening of the blocked artery is crucial to limiting heart muscle damage from lack of blood flow.
IHD - TA L2.pptx
The document provides information on ischemic heart disease (IHD), including:
1) IHD is caused by inadequate blood supply to the heart muscle and can be due to blockages in the coronary arteries from atherosclerosis or other causes like vasospasm.
2) IHD can present as stable angina, unstable angina, myocardial infarction, or heart failure. A myocardial infarction occurs when prolonged ischemia causes death of heart muscle tissue.
3) The pathology of a myocardial infarction involves plaque rupture, thrombus formation, and complete blockage of blood flow leading to irreversible damage to heart muscle within minutes to hours.
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ISCHEMIC HEART DISEASE.pptx
Ischemic heart disease (IHD) is caused by an imbalance between the heart's blood supply and oxygen demand, usually due to atherosclerotic narrowing of the coronary arteries. This leads to myocardial ischemia and can result in angina, myocardial infarction (MI), or heart failure. MI occurs when ischemia is severe or prolonged enough to cause cardiac cell death. It is typically caused by coronary artery thrombosis due to atherosclerotic plaque rupture. MI can damage heart muscle and lead to complications like arrhythmias, heart failure, or cardiac rupture. Reperfusion through procedures like angioplasty aims to limit damage but can paradoxically worsen injury through reperfusion injury mechanisms.
2. ISCHEMIC HEART DISEASE.pptx
Ischemic heart disease (IHD) is caused by reduced blood flow to the heart muscle and usually results from plaque buildup in the coronary arteries. This leads to not enough oxygen reaching the heart muscle. The main manifestations of IHD include angina pectoris (chest pain), myocardial infarction (heart attack), and sudden cardiac death. A heart attack occurs when a plaque ruptures and causes a blood clot that completely blocks blood flow, causing heart cell death. Reperfusion through procedures like angioplasty can limit damage but also cause additional injury. Complications from a heart attack include heart failure, arrhythmias, and cardiac rupture.
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Ischemic heart disease, resulting from impaired blood supply to the heart, is currently the leading cause of cardiovascular disease death worldwide. It refers to conditions including angina, heart attack, chronic heart disease, heart failure and sudden cardiac death. The most common cause is coronary artery atherosclerosis and thrombosis, usually resulting from plaque rupture or erosion in the arteries. Vulnerable plaques are prone to rupture due to characteristics like a thin fibrous cap and large lipid core, exposing thrombogenic materials and narrowing the artery. Timely reopening of the blocked artery is crucial to limiting heart muscle damage from lack of blood flow.
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1) IHD is caused by inadequate blood supply to the heart muscle and can be due to blockages in the coronary arteries from atherosclerosis or other causes like vasospasm.
2) IHD can present as stable angina, unstable angina, myocardial infarction, or heart failure. A myocardial infarction occurs when prolonged ischemia causes death of heart muscle tissue.
3) The pathology of a myocardial infarction involves plaque rupture, thrombus formation, and complete blockage of blood flow leading to irreversible damage to heart muscle within minutes to hours.
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ISCHEMIC HEART DISEASE.pptx
Ischemic heart disease (IHD) is caused by an imbalance between the heart's blood supply and oxygen demand, usually due to atherosclerotic narrowing of the coronary arteries. This leads to myocardial ischemia and can result in angina, myocardial infarction (MI), or heart failure. MI occurs when ischemia is severe or prolonged enough to cause cardiac cell death. It is typically caused by coronary artery thrombosis due to atherosclerotic plaque rupture. MI can damage heart muscle and lead to complications like arrhythmias, heart failure, or cardiac rupture. Reperfusion through procedures like angioplasty aims to limit damage but can paradoxically worsen injury through reperfusion injury mechanisms.
2. ISCHEMIC HEART DISEASE.pptx
Ischemic heart disease (IHD) is caused by reduced blood flow to the heart muscle and usually results from plaque buildup in the coronary arteries. This leads to not enough oxygen reaching the heart muscle. The main manifestations of IHD include angina pectoris (chest pain), myocardial infarction (heart attack), and sudden cardiac death. A heart attack occurs when a plaque ruptures and causes a blood clot that completely blocks blood flow, causing heart cell death. Reperfusion through procedures like angioplasty can limit damage but also cause additional injury. Complications from a heart attack include heart failure, arrhythmias, and cardiac rupture.
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The document discusses atherosclerosis, which is a disease characterized by endothelial dysfunction, vascular inflammation, and the buildup of lipids and other materials within the inner layer of arterial walls. This buildup forms atherosclerotic plaques that protrude into the arterial lumen. Major risk factors for atherosclerosis include increasing age, male gender, family history, genetic abnormalities, hyperlipidemia, hypertension, cigarette smoking, and diabetes. The consequences of atherosclerosis include heart attacks, strokes, aortic aneurysms, and peripheral vascular disease. Prevention involves lifestyle changes while treatment focuses on controlling risk factors and surgical interventions if needed.
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Discussion #1The diagnosis consistent with John’s history and .docx
Discussion #1
The diagnosis consistent with John’s history and physical exam is a type of acute coronary syndrome known as myocardial infarction (MI), specifically a ST-elevation myocardial infarction (STEMI). A MI results from an interruption or complete obstruction in bloodflow through the coronary arteries for a prolonged period of time by a thrombus, which leads to the death of heart muscle cells (myocyte necrosis) (McCance & Huether, 2014). Atherosclerotic CAD, coronary spasms, and/or coronary artery embolisms are all possible causes of a MI.
A MI can be subdivided into two categories: STEMI and non-STEMI. This depends on where the infarction occurs. If the thrombus breaks apart before complete death of the tissue distant from the site results, it will only affect the subendocardium, and be termed a Non-STEMI. On a ECG, a non-STEMI (subendocardial MI) will present itself with inverted T waves and ST depression. Although the less severe of the two type of MI, non-STEMI patients are at risk of recurrent clot formation on the disrupted plaque and require intervention. Transmural infractions (STEMIs) occur when a clot is permanently lodged in the vessel and affects the endocardium all the way through to the epicardium (McCance & Huether, 2014). Marked ST elevation will be visible on the ECG of a STEMI patient and immediate intervention is required to restore coronary bloodflow.
When atherosclerotic plaque builds up in the coronary arteries, it can be disrupted by means of ulceration or rupture. This occurs “because of shear forces, inflammation with release of multiple inflammatory mediators, secretion of macrophage-derived degradative enzymes, and apoptosis of cells at the edges of the lesions” (McCance & Huether, 2014, p. 1156). When the plaque is disrupted, the clotting cascade is activated due to the exposed vessel wall and platelets aggregate to the site forming a thrombus and causing obstruction of the vessel. Vessel obstruction is further exacerbated when thromboxane A2 and endothelin, vasoconstrictors, are realeased during the process (McCance & Huether, 2014). This ischemic injury can lead to infarction of the heart muscle.
Angina pectoris is the term used to describe chest pain that is often caused by myocardial ischemia (a lack of blood supply to the heart). The pain is the result of lactic acid accumulation irritating nerve fibers in the myocardium (McCance & Huether, 2014). Silent ischemia is a lack of bloodflow, and therefore oxygen, to the heart that does not produce pain, and is commonly experienced in individuals with mental stress, women, and diabetics. “Myocardial ischemia also can result from other causes of decreased blood and oxygen delivery to the myocardium, such as coronary spasm, hypotension, dysrhythmias, and decreased oxygen-carrying capacity of the blood (anemia, hypoxemia)” (McCance & Huether, 2014, p. 1153).
Over 400,000 annual deaths in the U.S. are related to sudden cardiac death (Sara, Eleid, Gulati, & Holm.
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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.
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Aneurysm
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Myocardial infarction occurs when blood flow to the heart is blocked, causing heart muscle tissue to die. This is usually due to a buildup of plaque in the coronary arteries. There are different types of myocardial infarction defined by location and pathology. The pathophysiology involves plaque rupture triggering blood clot formation that blocks an artery, causing ischemia and cell death. This damages the heart muscle and can impair heart function. Diagnosis involves ECG and blood tests to detect cardiac enzymes released during cell death. Treatment goals to limit damage include restoring blood flow and preventing further clotting.
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This document discusses the pathogenesis of atherosclerosis. It begins with a brief history of atherosclerosis and then discusses the structure of the normal artery and endothelial cells. It describes the response to injury hypothesis for the initiation and progression of atherosclerotic lesions. It discusses complications of atherosclerosis including plaque rupture and thrombosis. It concludes by discussing risk factors for atherosclerosis such as smoking, hypertension, hyperlipidemia, and metabolic syndrome.
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Atherosclerosis is a disease characterized by the buildup of fatty plaques in the inner walls of arteries. Over time, plaque accumulates and narrows the arteries. This restricts blood flow and can lead to complications like heart attacks and strokes. The plaques are made up of fat, cholesterol, calcium and other substances found in the blood. They form when cholesterol builds up and white blood cells try to repair the damaged lining of the artery. Major risk factors include age, male sex, family history, high blood pressure, high cholesterol, diabetes and smoking. Lifestyle changes like quitting smoking, exercising and eating a healthy diet can help reduce risk.
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Pathology of blood vessels
This document summarizes pathology of blood vessels. It begins by describing the normal structure of arteries, veins and capillaries. It then discusses the cells that make up blood vessel walls and their response to injury, which can lead to intimal thickening. It also briefly mentions some congenital vessel anomalies. The majority of the document focuses on arteriosclerosis and its subtype, atherosclerosis - describing the morphology, risk factors, pathogenesis, natural history and approaches for prevention. It concludes by outlining hypertensive vascular disease, its causes and pathogenesis.
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The document discusses atherosclerosis, which is a disease characterized by endothelial dysfunction, vascular inflammation, and the buildup of lipids and other materials within the inner layer of arterial walls. This buildup forms atherosclerotic plaques that protrude into the arterial lumen. Major risk factors for atherosclerosis include increasing age, male gender, family history, genetic abnormalities, hyperlipidemia, hypertension, cigarette smoking, and diabetes. The consequences of atherosclerosis include heart attacks, strokes, aortic aneurysms, and peripheral vascular disease. Prevention involves lifestyle changes while treatment focuses on controlling risk factors and surgical interventions if needed.
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Discussion #1
The diagnosis consistent with John’s history and physical exam is a type of acute coronary syndrome known as myocardial infarction (MI), specifically a ST-elevation myocardial infarction (STEMI). A MI results from an interruption or complete obstruction in bloodflow through the coronary arteries for a prolonged period of time by a thrombus, which leads to the death of heart muscle cells (myocyte necrosis) (McCance & Huether, 2014). Atherosclerotic CAD, coronary spasms, and/or coronary artery embolisms are all possible causes of a MI.
A MI can be subdivided into two categories: STEMI and non-STEMI. This depends on where the infarction occurs. If the thrombus breaks apart before complete death of the tissue distant from the site results, it will only affect the subendocardium, and be termed a Non-STEMI. On a ECG, a non-STEMI (subendocardial MI) will present itself with inverted T waves and ST depression. Although the less severe of the two type of MI, non-STEMI patients are at risk of recurrent clot formation on the disrupted plaque and require intervention. Transmural infractions (STEMIs) occur when a clot is permanently lodged in the vessel and affects the endocardium all the way through to the epicardium (McCance & Huether, 2014). Marked ST elevation will be visible on the ECG of a STEMI patient and immediate intervention is required to restore coronary bloodflow.
When atherosclerotic plaque builds up in the coronary arteries, it can be disrupted by means of ulceration or rupture. This occurs “because of shear forces, inflammation with release of multiple inflammatory mediators, secretion of macrophage-derived degradative enzymes, and apoptosis of cells at the edges of the lesions” (McCance & Huether, 2014, p. 1156). When the plaque is disrupted, the clotting cascade is activated due to the exposed vessel wall and platelets aggregate to the site forming a thrombus and causing obstruction of the vessel. Vessel obstruction is further exacerbated when thromboxane A2 and endothelin, vasoconstrictors, are realeased during the process (McCance & Huether, 2014). This ischemic injury can lead to infarction of the heart muscle.
Angina pectoris is the term used to describe chest pain that is often caused by myocardial ischemia (a lack of blood supply to the heart). The pain is the result of lactic acid accumulation irritating nerve fibers in the myocardium (McCance & Huether, 2014). Silent ischemia is a lack of bloodflow, and therefore oxygen, to the heart that does not produce pain, and is commonly experienced in individuals with mental stress, women, and diabetics. “Myocardial ischemia also can result from other causes of decreased blood and oxygen delivery to the myocardium, such as coronary spasm, hypotension, dysrhythmias, and decreased oxygen-carrying capacity of the blood (anemia, hypoxemia)” (McCance & Huether, 2014, p. 1153).
Over 400,000 annual deaths in the U.S. are related to sudden cardiac death (Sara, Eleid, Gulati, & Holm.
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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.
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PATHOPHYSIOLOGY OF CARDIOPULMONARY DISEASE
Three components of cardiac diseases
1- diseases affecting heart muscles
2- diseases affecting heart valves
3- defects of the cardiac nervous system
Disease affecting cardiac muscle
Coronary artery disease
Myocardial infarct
Pericarditis
Congestive heart failure
Aneurysm
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Myocardial infarction occurs when blood flow to the heart is blocked, causing heart muscle tissue to die. This is usually due to a buildup of plaque in the coronary arteries. There are different types of myocardial infarction defined by location and pathology. The pathophysiology involves plaque rupture triggering blood clot formation that blocks an artery, causing ischemia and cell death. This damages the heart muscle and can impair heart function. Diagnosis involves ECG and blood tests to detect cardiac enzymes released during cell death. Treatment goals to limit damage include restoring blood flow and preventing further clotting.
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This document discusses the pathogenesis of atherosclerosis. It begins with a brief history of atherosclerosis and then discusses the structure of the normal artery and endothelial cells. It describes the response to injury hypothesis for the initiation and progression of atherosclerotic lesions. It discusses complications of atherosclerosis including plaque rupture and thrombosis. It concludes by discussing risk factors for atherosclerosis such as smoking, hypertension, hyperlipidemia, and metabolic syndrome.
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Atherosclerosis is a disease characterized by the buildup of fatty plaques in the inner walls of arteries. Over time, plaque accumulates and narrows the arteries. This restricts blood flow and can lead to complications like heart attacks and strokes. The plaques are made up of fat, cholesterol, calcium and other substances found in the blood. They form when cholesterol builds up and white blood cells try to repair the damaged lining of the artery. Major risk factors include age, male sex, family history, high blood pressure, high cholesterol, diabetes and smoking. Lifestyle changes like quitting smoking, exercising and eating a healthy diet can help reduce risk.
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This document provides an overview of ischemic heart disease. It defines ischemic heart disease as a set of clinical conditions caused by a sudden reduction in blood flow to the heart. The main types discussed are angina pectoris, NSTEMI, and STEMI. The document discusses the pathogenesis of atherosclerosis and myocardial injury. It also covers the clinical presentation, diagnosis, and complications of stable angina, unstable angina, NSTEMI, STEMI, and ischemic reperfusion injury. Chronic ischemic heart disease and various cardiac biomarkers are also summarized.
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CHRONIC MYELOBLASTIC LEUKEMIA.ppt
This document discusses chronic myeloid leukemia (CML), a myeloproliferative disorder originating from stem cells characterized by the Philadelphia chromosome. The key points are:
CML is caused by the BCR-ABL fusion gene resulting from a translocation between chromosomes 9 and 22, which encodes for uncontrolled tyrosine kinase activity. This leads to increased proliferation of myeloid cells.
CML progresses through three phases: chronic, accelerated, and blastic (acute) phases as the disease becomes more aggressive and chemotherapy-resistant over time.
Diagnosis involves blood tests showing leukocytosis with immature cells, elevated LDH and basophils, and bone marrow biopsy demonstrating hypercellularity and myeloid hyper
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1) Acute lymphoblastic leukemia (ALL) is a cancer of the lymphoid line of white blood cells. It is primarily a disease of children and is the most common malignant disease in children.
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This document discusses peripheral smear preparation and increased white blood cell counts (leucocytosis). It describes the different types of white blood cells (WBCs) - granulocytes like neutrophils, eosinophils and basophils, and non-granulocytes like lymphocytes and monocytes. It then focuses on lymphocytosis, which is an increase in lymphocytes, and can be either absolute or relative. Some common causes of lymphocytosis include various viral and bacterial infections as well as some cancers like leukemia. The document also covers eosinophilia, which is a rise in eosinophils, and lists various pathological causes like parasite infections, allergic reactions, and pulmonary and skin conditions.
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The ABO blood group system is one of the most important blood group systems for transfusions. It is determined by the ABO gene which has three alleles - IA, IB, and i - that encode for the A, B, and O antigens, respectively. The ABO blood types are determined by which alleles are present: IAIA or IAi produce type A blood, IBIB or IBi produce type B, IAIB produces AB, and ii produces O. The Rh system, specifically the D antigen, is the second most important blood group and sensitization to the D antigen in Rh-negative pregnant women can cause hemolytic disease of the newborn if not prevented.
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Amyloidosis refers to deposits of abnormal protein fibers called amyloid in tissues and organs. There are two major types - AL amyloidosis associated with immunoglobulin light chains from plasma cell disorders, and AA amyloidosis associated with chronic inflammatory conditions. Amyloidosis can be systemic, affecting multiple organs, or localized to a single organ. On microscopy, amyloid stains pink with hematoxylin and eosin and exhibits green birefringence under polarized light with Congo red staining. However, immunostaining is needed to determine the subtype of amyloid protein involved. Systemic amyloidosis can involve the kidneys, liver, spleen, heart and cause organ dysfunction.
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This document discusses rheumatic heart disease, defining it as a post-streptococcal inflammatory disease affecting the heart, joints, nervous system and skin. It most commonly affects children ages 5-15. The disease is more common in low socioeconomic groups and causes damage through lesions in the heart tissue known as Aschoff nodules. These nodules progress through exudative, proliferative and fibrotic stages, ultimately causing scarring of the heart valves and tissues if left untreated. The mitral valve is most often affected, followed by the aortic valve.
BPH.pptx
Benign prostatic hyperplasia (BPH) is a noncancerous enlargement of the prostate gland that is common in men over 50 years of age. It results from proliferation of both epithelial and stromal cells in the prostate transition zone, forming nodules that can compress the urethra. BPH often causes obstructive symptoms like hesitancy, weak urinary stream, and incomplete emptying of the bladder. Diagnosis is typically made through a physical exam and medical history, with severity assessed using the International Prostate Symptom Score questionnaire. Microscopically, BPH nodules are composed of hyperplastic glands and stroma within well-demarcated areas that compress the ure
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Fatty liver is characterized by the appearance of fat in the cytoplasm of liver cells. It often occurs because the liver plays a key role in fat metabolism. Fatty liver has many potential causes including obesity, diabetes, malnutrition, alcohol abuse, medications, and other illnesses. Microscopically, lipid vacuoles of varying sizes are seen within hepatocytes, sometimes clustered around the nucleus or towards the cell periphery. Special stains can be used to identify fat deposits in liver tissue samples.
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blood grouping.ppt
This document discusses immunohematology and blood grouping techniques. It explains that immunohematology applies immunology principles to study red blood cell antigens and antibodies in blood. The most important blood group systems are ABO and Rh, which are determined using agglutination reactions between red blood cell antigens and their corresponding antibodies. The document then describes the procedures for performing the slide and tube methods of ABO blood grouping and Rh typing, including preparation of reagents and blood samples, performing the tests, and interpreting the results.
Urinalysis and its importance.pptx
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- 1. ATHEROSCLEROSIS AND MYOCARDIAL INFARCTION Dr Ravi Shrivastava
- 2. DEFINITION Atherosclerosis It is characterised by fibrofatty plaques or atheromas. It is an thickening and hardening of large and medium-sized muscular arteries, primarily due to involvement of tunica intima and The term atherosclerosis is derived from athero-(meaning porridge) referring to the soft lipid-rich material in the centre of atheroma, and sclerosis (scarring) referring to connective tissue in the plaques.
- 3. ATHEROSCLEROSIS (ATH) Intimal lesions called atheromas (fibrofatty plaques) that weaken the muscular media, protrude into vessel lumen Atheromatous plaques- a raised lesion with a soft, Yelllow, grumous core of lipid (cholesterol and cholesterol esters ) covered by a fibrous cap.
- 4. MAJOR COMPONENTS OF PLAQUE Cells (SMC, macrophages and other WBC) ECM (collagen, elastin, and PGs) Lipid = Cholesterol (Intra/extracellular) (Often calcification)
- 8. INITIATION OF FATTY STREAK
- 9. FATTY STREAK
- 12. CONSEQUENCES OF PLAQUE FORMATION Generalized Narrowing/Occlusion Rupture Emboli Leading to specific problems: Myocardial and cerebral infarcts Aortic aneurysms Peripheral vascular disease
- 13. GROSS APPEARANCE Affected vessels will show raised yellowish white lesions. Cut section shows firm fibrous cap(sclerosis) and a central core composed of yellow white soft material
- 14. MICROSCOPIC FEATURES Lesion is composed of afibrous cap and a necrotic core. The superficial part of the fibrous cap is composed of smooth muscle cells,dense connective tissue and components of extracellular matrix. The cellular area under the fibrous cap is composed of macrophages,lymphocytes and lipid laiden foam cells
- 16. IHD and MI
- 17. Ischaemic heart disease (IHD) Defined as acute or chronic form of cardiac disability arising from imbalance between the myocardial supply and demand for oxygenated blood. Since narrowing or obstruction of the coronary arterial system is the most common cause of myocardial anoxia. The alternate term ‘coronary artery disease (CAD)’ is used synonymously with IHD.
- 18. ETIOPATHOGENESIS IHD is invariably caused by disease affecting the coronary arteries, the most prevalent being atherosclerosis accounting for more than 90% cases, while other causes are responsible for less than 10% cases of IHD. Therefore, it is convenient to consider the etiology of IHD under three broad headings: i. Coronary atherosclerosis ii. Superadded changes in coronary atherosclerosis iii. Non-atherosclerotic causes
- 19. III. NON-ATHEROSCLEROTIC CAUSES Several other coronary lesions may cause IHD in less than 10% of cases. 1. Vasospasm 2. Stenosis of coronary ostia 3. Arteritis Various types 4. Embolism 5. Thrombotic diseases 6. Trauma 7. Aneurysms 8. Compression
- 20. ACUTE MYOCARDIAL INFARCTION Acute myocardial infarction (MI) is the most important and feared consequence of coronary artery disease. Many patients may die within the first few hours of the onset, while remainder suffer from effects of impaired cardiac function. A significant factor that may prevent or diminish the myocardial damage is the development of collateral circulation through anastomotic channels over a period of time. A regular and well-planned exercise programme encourages good collateral circulation and improved
- 21. 5. Transmural versus subendocardial infarcts There are some differences in the pathogenesis of the transmural infarcts involving the full thickness of ventricular wall and the subendocardial (laminar) infarcts affecting the inner subendocardial one-third to half. (1/3 to1/2)
- 24. MORPHOLOGIC FEATURES The gross and microscopic changes in the myocardial infarction vary according to the age of the infarct and are therefore described sequentially in the Table. From 0-6 hours to 4th week changes
- 27. CHRONIC ISCHAEMIC HEART DISEASE Chronic ischaemic heart disease, ischaemic cardiomyopathy or myocardial fibrosis, are the terms used for focal or diffuse fibrosis in the myocardium characteristically found in elderly patients of progressive IHD. Such small areas of fibrous scarring are commonly found in the heart of patients who have history of episodes of angina and attacks of MI some years back.
- 28. ETIOPATHOGENESIS In majority of cases, coronary atherosclerosis causes progressive ischaemic myocardial damage and replacement by myocardial fibrosis. A small percentage of cases may result from other causes such as emboli, coronary arteritis and myocarditis.
- 30. THANK YOU