The document discusses several cardiovascular pathophysiologies including diseases of the arteries, veins, heart, and heart failure. It describes atherosclerosis as a form of arteriosclerosis caused by lipid accumulation in the arterial wall. Hypertension is classified as primary or secondary and can lead to complications like left ventricular hypertrophy. Coronary artery disease results from atherosclerosis narrowing the coronary arteries and can cause myocardial ischemia or infarction. Heart failure can be systolic or diastolic depending on whether contractility or filling is impaired.
This document summarizes cardiovascular anatomy and physiology. It describes the structure of the heart including the chambers and valves. It explains blood flow through the pulmonary and systemic circulations. It discusses the electrical conduction system of the heart including the sinoatrial node, atrioventricular node, and Purkinje fibers. It also covers cardiac muscle cell structure, the cardiac cycle, and regulation of heart rate and rhythm.
The document discusses various cardiovascular diseases and disorders. It covers topics like arteriosclerosis, atherosclerosis, hypertension, aneurysms, peripheral artery disease, coronary artery disease, myocardial infarction, cardiomyopathies, valvular dysfunction, infective endocarditis, heart failure, and dysrhythmias. For each topic, it provides details on pathogenesis, risk factors, symptoms, and progression. The document aims to provide an overview of alterations in cardiovascular function and related diseases of the arteries, veins, heart wall, and heart rhythm.
This document provides an overview of hypertension including: prevalence in the US, blood pressure regulation mechanisms, stages of hypertension, hypertensive crises, pathophysiology, risk factors, target organ damage, diagnostic evaluations, and treatment regimens. It discusses the role of the kidneys, endothelium, baroreceptors, and RAAS system in blood pressure regulation. It also reviews epidemiological data on hypertension prevalence among different racial groups.
Heparin is a muco polysaccharide found in mast cells that is the strongest acid in the body. It is a powerful anticoagulant that activates antithrombin III to inhibit coagulation factors. Heparin is not effective when taken orally and can cause hematomas if taken intramuscularly, so it is usually administered intravenously or subcutaneously. Potential side effects of heparin include bleeding, hypersensitivity, thrombocytopenia, alopecia, and osteoporosis. Low molecular weight heparins like enoxaparin have a more favorable pharmacokinetic profile, lower risk of side effects, and mainly inhibit factor Xa rather than thrombin.
Heparin is a glycosaminoglycan found in mast cells that acts as an anticoagulant by catalyzing the inhibition of coagulation factors like thrombin and factor Xa by antithrombin. It is commonly extracted from pig intestines or cow lungs. Low molecular weight heparins produced by fractionation have a higher affinity for inhibiting factor Xa over thrombin. Heparin is used to prevent and treat deep vein thrombosis and pulmonary embolism and in other conditions like myocardial infarction and unstable angina. Adverse effects include heparin-induced thrombocytopenia and osteoporosis with prolonged use.
Heparin is an anticoagulant used to prevent and treat blood clots. It works by interacting with antithrombin to accelerate the inhibition of enzymes involved in clot formation. Heparin can be unfractionated or low molecular weight and is derived from animal tissues, administered intravenously or subcutaneously, and has a short half-life of 1.5 hours. Its indications include treating and preventing deep vein thrombosis, pulmonary embolism, and arterial clots. Common adverse effects include bleeding risks and hematologic issues.
Anticoagulants are substances that prevent blood from clotting by suppressing clotting factors. There are two main types: heparin and vitamin K antagonists like warfarin. Anticoagulants are important for embalming as they help keep blood in a liquid state, allowing for drainage and preventing blockages during the embalming process. Kelquestrol D3 is an example of an anticoagulant fluid used in embalming to maintain blood fluidity and condition water used in the process. Anticoagulants are a key component of arterial fluids but do not dissolve existing clots.
This document discusses coagulants and anticoagulants. It describes how thrombosis occurs via venous and arterial pathways and the process of hemostasis. Coagulation involves a balance between procoagulants and anticoagulants. Common coagulation factors and pathways are outlined. Vitamin K and other coagulants like fibrinogen and antihemophilic factor are discussed. Anticoagulants include heparins, oral anticoagulants like warfarin, and other agents. Mechanisms, uses, and adverse effects of various coagulants and anticoagulants are summarized.
This document summarizes cardiovascular anatomy and physiology. It describes the structure of the heart including the chambers and valves. It explains blood flow through the pulmonary and systemic circulations. It discusses the electrical conduction system of the heart including the sinoatrial node, atrioventricular node, and Purkinje fibers. It also covers cardiac muscle cell structure, the cardiac cycle, and regulation of heart rate and rhythm.
The document discusses various cardiovascular diseases and disorders. It covers topics like arteriosclerosis, atherosclerosis, hypertension, aneurysms, peripheral artery disease, coronary artery disease, myocardial infarction, cardiomyopathies, valvular dysfunction, infective endocarditis, heart failure, and dysrhythmias. For each topic, it provides details on pathogenesis, risk factors, symptoms, and progression. The document aims to provide an overview of alterations in cardiovascular function and related diseases of the arteries, veins, heart wall, and heart rhythm.
This document provides an overview of hypertension including: prevalence in the US, blood pressure regulation mechanisms, stages of hypertension, hypertensive crises, pathophysiology, risk factors, target organ damage, diagnostic evaluations, and treatment regimens. It discusses the role of the kidneys, endothelium, baroreceptors, and RAAS system in blood pressure regulation. It also reviews epidemiological data on hypertension prevalence among different racial groups.
Heparin is a muco polysaccharide found in mast cells that is the strongest acid in the body. It is a powerful anticoagulant that activates antithrombin III to inhibit coagulation factors. Heparin is not effective when taken orally and can cause hematomas if taken intramuscularly, so it is usually administered intravenously or subcutaneously. Potential side effects of heparin include bleeding, hypersensitivity, thrombocytopenia, alopecia, and osteoporosis. Low molecular weight heparins like enoxaparin have a more favorable pharmacokinetic profile, lower risk of side effects, and mainly inhibit factor Xa rather than thrombin.
Heparin is a glycosaminoglycan found in mast cells that acts as an anticoagulant by catalyzing the inhibition of coagulation factors like thrombin and factor Xa by antithrombin. It is commonly extracted from pig intestines or cow lungs. Low molecular weight heparins produced by fractionation have a higher affinity for inhibiting factor Xa over thrombin. Heparin is used to prevent and treat deep vein thrombosis and pulmonary embolism and in other conditions like myocardial infarction and unstable angina. Adverse effects include heparin-induced thrombocytopenia and osteoporosis with prolonged use.
Heparin is an anticoagulant used to prevent and treat blood clots. It works by interacting with antithrombin to accelerate the inhibition of enzymes involved in clot formation. Heparin can be unfractionated or low molecular weight and is derived from animal tissues, administered intravenously or subcutaneously, and has a short half-life of 1.5 hours. Its indications include treating and preventing deep vein thrombosis, pulmonary embolism, and arterial clots. Common adverse effects include bleeding risks and hematologic issues.
Anticoagulants are substances that prevent blood from clotting by suppressing clotting factors. There are two main types: heparin and vitamin K antagonists like warfarin. Anticoagulants are important for embalming as they help keep blood in a liquid state, allowing for drainage and preventing blockages during the embalming process. Kelquestrol D3 is an example of an anticoagulant fluid used in embalming to maintain blood fluidity and condition water used in the process. Anticoagulants are a key component of arterial fluids but do not dissolve existing clots.
This document discusses coagulants and anticoagulants. It describes how thrombosis occurs via venous and arterial pathways and the process of hemostasis. Coagulation involves a balance between procoagulants and anticoagulants. Common coagulation factors and pathways are outlined. Vitamin K and other coagulants like fibrinogen and antihemophilic factor are discussed. Anticoagulants include heparins, oral anticoagulants like warfarin, and other agents. Mechanisms, uses, and adverse effects of various coagulants and anticoagulants are summarized.
This document summarizes drugs used to treat three blood dysfunctions: thrombosis, bleeding, and anemia. It discusses anticoagulant and thrombolytic drugs used to treat thrombosis. Anticoagulants like heparin and warfarin prevent clotting through different mechanisms. Heparin enhances antithrombin inhibition of coagulation factors. Warfarin inhibits vitamin K-dependent clotting factor synthesis. Thrombolytics like plasmin dissolve clots by activating plasminogen. The document also covers the mechanisms, uses, and toxicities of various anticoagulant and thrombolytic drugs.
This document provides an overview of anticoagulants. It discusses the history of anticoagulant development beginning in the late 19th century. Common anticoagulants used for blood collection and storage are described, including their mechanisms of action and uses. EDTA, citrate, and heparin are highlighted. The coagulation cascade and numbered coagulation factors are also summarized. Changes that occur in stored blood over time are reviewed at both the physical and biochemical levels. Finally, therapeutic uses of anticoagulants like heparin and warfarin are mentioned.
Hypertensive disorders are common and serious conditions seen in obstetrics. They include gestational hypertension, preeclampsia, eclampsia, and chronic hypertension with or without superimposed preeclampsia. Preeclampsia is defined as new hypertension and proteinuria after 20 weeks of gestation. It is caused by reduced placental perfusion leading to release of anti-angiogenic factors from the placenta that cause maternal endothelial dysfunction. Complications include organ damage, seizures, and death. Treatment involves blood pressure control, delivery once the fetus is mature, and magnesium sulfate to prevent seizures in severe preeclampsia and eclampsia.
Hypertension, or high blood pressure, has been documented as far back as 2600 BC. It was not until the early 18th century that methods for measuring blood pressure were developed. Blood pressure is determined by cardiac output and systemic vascular resistance. Sustained elevated blood pressure is defined as hypertension. Primary hypertension has no identifiable cause, while secondary hypertension is caused by an underlying condition. Lifestyle modifications and medication are used to treat hypertension and reduce complications like heart disease, stroke, and kidney damage. Accurate measurement and long-term management require a collaborative approach between patients and healthcare providers.
This document provides an overview of cardiovascular diseases. It begins with an introduction noting that CVD is a leading cause of death globally and in India. It then outlines the contents to be covered, which include diagnoses, causes, and specific conditions like hypertension, coronary artery disease, angina pectoris, and more. The document discusses examining patients for cardiovascular issues through taking a history and performing a physical exam of things like vital signs, pulse, heart sounds and murmurs. It lists various potential causes of cardiovascular disease including issues with the myocardium, endocardium, pericardium, and congenital abnormalities.
Hypertension is defined as a systolic blood pressure of 140 mm Hg or higher or a diastolic blood pressure of 90 mm Hg or higher. About 1 billion people worldwide and 1 in 3 Americans have hypertension. Hypertension directly increases the risk of cardiovascular disease. Prehypertension is defined as a systolic blood pressure of 120-139 mm Hg or a diastolic blood pressure of 80-89 mm Hg. The main factors that influence blood pressure are cardiac output, systemic vascular resistance, and fluid volume control by the kidneys. Hypertension can lead to damage of the heart, brain, kidneys, eyes, and vasculature if not properly treated.
This document discusses hypertension, or high blood pressure. It notes that hypertension affects around 50 million people in the US. The main types are primary hypertension, which has no known cause, and secondary hypertension, which is caused by another disease like kidney disease. Risk factors for hypertension include genetics, family history, obesity, stress, alcohol, sodium, tobacco, and age. Untreated hypertension can lead to heart attack, stroke, kidney failure, and vision loss. African Americans have a higher risk than other populations. Treatment involves lifestyle changes and medication, with the goal of controlling blood pressure.
This document summarizes various cardiovascular diseases and disorders. It describes diseases of the veins like varicose veins, chronic venous insufficiency, and deep vein thrombosis. It also discusses diseases of arteries and veins including primary and secondary hypertension, aneurysms, atherosclerosis, and peripheral artery disease. Coronary artery disease and myocardial infarction are explained in detail. Finally, disorders of the heart wall like pericarditis, cardiomyopathies, and valvular dysfunctions are outlined.
This document summarizes various cardiovascular diseases and disorders. It describes diseases of the veins like varicose veins, chronic venous insufficiency, and deep vein thrombosis. It also discusses diseases of arteries and veins including primary and secondary hypertension, aneurysms, atherosclerosis, and peripheral artery disease. Coronary artery disease and myocardial infarction are explained in detail. Finally, disorders of the heart wall like pericarditis, cardiomyopathies, and valvular dysfunctions are outlined.
This document discusses several types of congenital and acquired cardiovascular defects that can occur in children. It describes common congenital defects such as ventricular septal defects, tetralogy of Fallot, and transposition of the great arteries. It also discusses acquired conditions like Kawasaki disease and hypertension. For each type of defect or condition, it provides details on manifestations, risk factors, diagnostic criteria and treatments when available. The goal is to comprehensively cover alterations in cardiovascular function that pediatric nurses should understand.
This document outlines the structure and function of blood vessels and diseases that affect them. It discusses the layers of blood vessels including the intima, media, and adventitia, and how these layers vary between arteries, veins, capillaries and lymphatics. Key vascular diseases covered include congenital anomalies, arteriosclerosis, hypertensive vascular disease, atherosclerosis, aneurysms, and vasculitides. Atherosclerosis is discussed in depth, outlining the pathogenesis involving endothelial injury, inflammation, and lipid accumulation leading to fatty streaks and atheroma formation.
The document discusses diseases of the cardiovascular system, focusing on diseases of arteries and veins. It describes atherosclerosis as a hardening and thickening of arteries due to plaque buildup. Other artery diseases discussed include arteriosclerosis, medial sclerosis, endarteritis obliterans, and arteritis. Aneurysms, which are local artery dilations, are also covered. Finally, the document touches on varicose veins, phlebitis, and venous thrombosis as common diseases of veins.
Blood coagulation, Embolism, Ischaemia and Infarction [Autosaved].pptxSam Edeson
This document provides an overview of blood coagulation and related processes including thrombosis, embolism, ischemia, and infarction. It defines these terms and describes the key points of coagulation, risk factors for thrombosis, outcomes of thrombi, types of embolism, signs of ischemia, causes of ischemia/infarction, and classifications of infarcts. The document aims to explain the fine interplay between coagulation and fibrinolytic systems in hemostasis and the cascade of events that can lead to reduced blood flow and tissue damage.
Lecture 11 disturbances of body fluids and electrolytesGreen-book
This document discusses ischemia, thrombosis, embolism, and infarction. It defines these terms and describes their causes and pathogenesis. Ischemia is a decrease in oxygenated blood flow to tissue, usually due to vessel constriction or blockage. Thrombosis is the formation of a blood clot within a blood vessel. Embolism occurs when a piece of a thrombus or other material breaks off and is carried by the bloodstream. Infarction refers to the tissue death caused by obstruction of an artery and loss of blood supply. The document provides detailed explanations of the mechanisms, predisposing factors, pathological features, and clinical implications of these disturbances of body fluids and electrolytes.
Are localized abnormal dilations of arteries.
Result due to weakening of the vessel wall.
Have the tendency to rupture.
Law of Laplace: states that as the diameter of aneurysm increases the wall stress increases : further enlargement and rupture is inevitable.
Aneurysms are classified by:
Location ( e.g abdominal aortic aneurysm)
Etiology (e.g. syphlitic aneurysm)
Shape (e.g. fusiform , saccular)
This document discusses several inherited diseases including sickle cell disease, hemophilia, muscular dystrophy, cystic fibrosis, and Huntington's disease. Sickle cell disease is caused by a mutation that causes red blood cells to take on an abnormal sickle shape, leading to anemia and organ damage. Hemophilia is a bleeding disorder caused by deficiencies in clotting factors VIII or IX that is inherited in an X-linked recessive pattern. Muscular dystrophy encompasses genetic diseases that cause progressive muscle weakness and loss of muscle mass through defective muscle proteins. Cystic fibrosis is caused by a gene mutation that causes thick, sticky mucus to build up in the lungs and digestive system. Huntington's disease is an inherited
The document discusses avascular necrosis (AVN), also known as osteonecrosis, which is the death of bone tissue due to a lack of blood supply. It provides details on:
- The main causes of AVN including trauma, alcoholism, steroid use, decompression sickness, and blood disorders.
- The pathology and progression of AVN, from initial bone cell death, to bone repair attempts, to structural failure and collapse if left untreated.
- Clinical signs and symptoms including pain that worsens with activity and improved with rest, limited range of motion, and characteristic findings on x-rays such as patchy demineralization and sclerosis.
- Staging of AVN
The document summarizes normal hemostasis and various bleeding disorders. It describes the three stages of normal coagulation as primary hemostasis involving platelets, secondary hemostasis involving clotting factors, and tertiary hemostasis involving fibrin formation and resolution. Causes of bleeding disorders include vessel wall abnormalities, platelet deficiencies or dysfunctions, and clotting factor derangements. Specific disorders discussed include immune thrombocytopenic purpura, hemophilia, von Willebrand disease, and thrombotic thrombocytopenic purpura. Tests used to evaluate bleeding disorders and clinical manifestations of different disorders are also summarized.
1. The document discusses various hemodynamic and circulatory disorders that can disrupt homeostasis, including fluid imbalances and disturbances that can lead to hemorrhage, hyperemia, congestion, edema, thrombosis, and embolism.
2. It defines different types of hemorrhage and edema, and explains the pathophysiology of thrombosis, noting key factors like endothelial injury, changes in blood flow, and hypercoagulability.
3. The morphology and locations of arterial thrombi, venous thrombi, and thrombi on heart valves are described, along with various underlying causes.
This document discusses bone marrow diseases, including malignant infiltration, secondary marrow hyperplasia, and lysosomal storage diseases. Specific diseases covered include multiple myeloma, leukemia, sickle cell anemia, thalassemia, Gaucher's disease, and Niemann-Pick disease. For each, the document discusses incidence, radiographic manifestations, and differential diagnosis. Radiographic findings include bone marrow hyperplasia, osteopenia, bone infarcts, vertebral compression fractures, and organomegaly of the spleen and liver. The goal is to understand the disease processes and radiologic presentations to aid in successful patient management.
This document summarizes drugs used to treat three blood dysfunctions: thrombosis, bleeding, and anemia. It discusses anticoagulant and thrombolytic drugs used to treat thrombosis. Anticoagulants like heparin and warfarin prevent clotting through different mechanisms. Heparin enhances antithrombin inhibition of coagulation factors. Warfarin inhibits vitamin K-dependent clotting factor synthesis. Thrombolytics like plasmin dissolve clots by activating plasminogen. The document also covers the mechanisms, uses, and toxicities of various anticoagulant and thrombolytic drugs.
This document provides an overview of anticoagulants. It discusses the history of anticoagulant development beginning in the late 19th century. Common anticoagulants used for blood collection and storage are described, including their mechanisms of action and uses. EDTA, citrate, and heparin are highlighted. The coagulation cascade and numbered coagulation factors are also summarized. Changes that occur in stored blood over time are reviewed at both the physical and biochemical levels. Finally, therapeutic uses of anticoagulants like heparin and warfarin are mentioned.
Hypertensive disorders are common and serious conditions seen in obstetrics. They include gestational hypertension, preeclampsia, eclampsia, and chronic hypertension with or without superimposed preeclampsia. Preeclampsia is defined as new hypertension and proteinuria after 20 weeks of gestation. It is caused by reduced placental perfusion leading to release of anti-angiogenic factors from the placenta that cause maternal endothelial dysfunction. Complications include organ damage, seizures, and death. Treatment involves blood pressure control, delivery once the fetus is mature, and magnesium sulfate to prevent seizures in severe preeclampsia and eclampsia.
Hypertension, or high blood pressure, has been documented as far back as 2600 BC. It was not until the early 18th century that methods for measuring blood pressure were developed. Blood pressure is determined by cardiac output and systemic vascular resistance. Sustained elevated blood pressure is defined as hypertension. Primary hypertension has no identifiable cause, while secondary hypertension is caused by an underlying condition. Lifestyle modifications and medication are used to treat hypertension and reduce complications like heart disease, stroke, and kidney damage. Accurate measurement and long-term management require a collaborative approach between patients and healthcare providers.
This document provides an overview of cardiovascular diseases. It begins with an introduction noting that CVD is a leading cause of death globally and in India. It then outlines the contents to be covered, which include diagnoses, causes, and specific conditions like hypertension, coronary artery disease, angina pectoris, and more. The document discusses examining patients for cardiovascular issues through taking a history and performing a physical exam of things like vital signs, pulse, heart sounds and murmurs. It lists various potential causes of cardiovascular disease including issues with the myocardium, endocardium, pericardium, and congenital abnormalities.
Hypertension is defined as a systolic blood pressure of 140 mm Hg or higher or a diastolic blood pressure of 90 mm Hg or higher. About 1 billion people worldwide and 1 in 3 Americans have hypertension. Hypertension directly increases the risk of cardiovascular disease. Prehypertension is defined as a systolic blood pressure of 120-139 mm Hg or a diastolic blood pressure of 80-89 mm Hg. The main factors that influence blood pressure are cardiac output, systemic vascular resistance, and fluid volume control by the kidneys. Hypertension can lead to damage of the heart, brain, kidneys, eyes, and vasculature if not properly treated.
This document discusses hypertension, or high blood pressure. It notes that hypertension affects around 50 million people in the US. The main types are primary hypertension, which has no known cause, and secondary hypertension, which is caused by another disease like kidney disease. Risk factors for hypertension include genetics, family history, obesity, stress, alcohol, sodium, tobacco, and age. Untreated hypertension can lead to heart attack, stroke, kidney failure, and vision loss. African Americans have a higher risk than other populations. Treatment involves lifestyle changes and medication, with the goal of controlling blood pressure.
This document summarizes various cardiovascular diseases and disorders. It describes diseases of the veins like varicose veins, chronic venous insufficiency, and deep vein thrombosis. It also discusses diseases of arteries and veins including primary and secondary hypertension, aneurysms, atherosclerosis, and peripheral artery disease. Coronary artery disease and myocardial infarction are explained in detail. Finally, disorders of the heart wall like pericarditis, cardiomyopathies, and valvular dysfunctions are outlined.
This document summarizes various cardiovascular diseases and disorders. It describes diseases of the veins like varicose veins, chronic venous insufficiency, and deep vein thrombosis. It also discusses diseases of arteries and veins including primary and secondary hypertension, aneurysms, atherosclerosis, and peripheral artery disease. Coronary artery disease and myocardial infarction are explained in detail. Finally, disorders of the heart wall like pericarditis, cardiomyopathies, and valvular dysfunctions are outlined.
This document discusses several types of congenital and acquired cardiovascular defects that can occur in children. It describes common congenital defects such as ventricular septal defects, tetralogy of Fallot, and transposition of the great arteries. It also discusses acquired conditions like Kawasaki disease and hypertension. For each type of defect or condition, it provides details on manifestations, risk factors, diagnostic criteria and treatments when available. The goal is to comprehensively cover alterations in cardiovascular function that pediatric nurses should understand.
This document outlines the structure and function of blood vessels and diseases that affect them. It discusses the layers of blood vessels including the intima, media, and adventitia, and how these layers vary between arteries, veins, capillaries and lymphatics. Key vascular diseases covered include congenital anomalies, arteriosclerosis, hypertensive vascular disease, atherosclerosis, aneurysms, and vasculitides. Atherosclerosis is discussed in depth, outlining the pathogenesis involving endothelial injury, inflammation, and lipid accumulation leading to fatty streaks and atheroma formation.
The document discusses diseases of the cardiovascular system, focusing on diseases of arteries and veins. It describes atherosclerosis as a hardening and thickening of arteries due to plaque buildup. Other artery diseases discussed include arteriosclerosis, medial sclerosis, endarteritis obliterans, and arteritis. Aneurysms, which are local artery dilations, are also covered. Finally, the document touches on varicose veins, phlebitis, and venous thrombosis as common diseases of veins.
Blood coagulation, Embolism, Ischaemia and Infarction [Autosaved].pptxSam Edeson
This document provides an overview of blood coagulation and related processes including thrombosis, embolism, ischemia, and infarction. It defines these terms and describes the key points of coagulation, risk factors for thrombosis, outcomes of thrombi, types of embolism, signs of ischemia, causes of ischemia/infarction, and classifications of infarcts. The document aims to explain the fine interplay between coagulation and fibrinolytic systems in hemostasis and the cascade of events that can lead to reduced blood flow and tissue damage.
Lecture 11 disturbances of body fluids and electrolytesGreen-book
This document discusses ischemia, thrombosis, embolism, and infarction. It defines these terms and describes their causes and pathogenesis. Ischemia is a decrease in oxygenated blood flow to tissue, usually due to vessel constriction or blockage. Thrombosis is the formation of a blood clot within a blood vessel. Embolism occurs when a piece of a thrombus or other material breaks off and is carried by the bloodstream. Infarction refers to the tissue death caused by obstruction of an artery and loss of blood supply. The document provides detailed explanations of the mechanisms, predisposing factors, pathological features, and clinical implications of these disturbances of body fluids and electrolytes.
Are localized abnormal dilations of arteries.
Result due to weakening of the vessel wall.
Have the tendency to rupture.
Law of Laplace: states that as the diameter of aneurysm increases the wall stress increases : further enlargement and rupture is inevitable.
Aneurysms are classified by:
Location ( e.g abdominal aortic aneurysm)
Etiology (e.g. syphlitic aneurysm)
Shape (e.g. fusiform , saccular)
This document discusses several inherited diseases including sickle cell disease, hemophilia, muscular dystrophy, cystic fibrosis, and Huntington's disease. Sickle cell disease is caused by a mutation that causes red blood cells to take on an abnormal sickle shape, leading to anemia and organ damage. Hemophilia is a bleeding disorder caused by deficiencies in clotting factors VIII or IX that is inherited in an X-linked recessive pattern. Muscular dystrophy encompasses genetic diseases that cause progressive muscle weakness and loss of muscle mass through defective muscle proteins. Cystic fibrosis is caused by a gene mutation that causes thick, sticky mucus to build up in the lungs and digestive system. Huntington's disease is an inherited
The document discusses avascular necrosis (AVN), also known as osteonecrosis, which is the death of bone tissue due to a lack of blood supply. It provides details on:
- The main causes of AVN including trauma, alcoholism, steroid use, decompression sickness, and blood disorders.
- The pathology and progression of AVN, from initial bone cell death, to bone repair attempts, to structural failure and collapse if left untreated.
- Clinical signs and symptoms including pain that worsens with activity and improved with rest, limited range of motion, and characteristic findings on x-rays such as patchy demineralization and sclerosis.
- Staging of AVN
The document summarizes normal hemostasis and various bleeding disorders. It describes the three stages of normal coagulation as primary hemostasis involving platelets, secondary hemostasis involving clotting factors, and tertiary hemostasis involving fibrin formation and resolution. Causes of bleeding disorders include vessel wall abnormalities, platelet deficiencies or dysfunctions, and clotting factor derangements. Specific disorders discussed include immune thrombocytopenic purpura, hemophilia, von Willebrand disease, and thrombotic thrombocytopenic purpura. Tests used to evaluate bleeding disorders and clinical manifestations of different disorders are also summarized.
1. The document discusses various hemodynamic and circulatory disorders that can disrupt homeostasis, including fluid imbalances and disturbances that can lead to hemorrhage, hyperemia, congestion, edema, thrombosis, and embolism.
2. It defines different types of hemorrhage and edema, and explains the pathophysiology of thrombosis, noting key factors like endothelial injury, changes in blood flow, and hypercoagulability.
3. The morphology and locations of arterial thrombi, venous thrombi, and thrombi on heart valves are described, along with various underlying causes.
This document discusses bone marrow diseases, including malignant infiltration, secondary marrow hyperplasia, and lysosomal storage diseases. Specific diseases covered include multiple myeloma, leukemia, sickle cell anemia, thalassemia, Gaucher's disease, and Niemann-Pick disease. For each, the document discusses incidence, radiographic manifestations, and differential diagnosis. Radiographic findings include bone marrow hyperplasia, osteopenia, bone infarcts, vertebral compression fractures, and organomegaly of the spleen and liver. The goal is to understand the disease processes and radiologic presentations to aid in successful patient management.
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.
Chronic venous insufficiency (CVI) refers to functional changes that may occur in the lower extremity due to persistent elevation of venous pressures, most commonly resulting from venous reflux due to faulty valve function. CVI affects about 7% of the population and prevalence of venous leg ulcers ranges from 1% to 2%. Diagnosis involves clinical examination showing signs such as varicose veins, edema, skin changes, as well as noninvasive testing including venous duplex imaging and air plethysmography and invasive testing such as contrast venography. Pathophysiology involves retrograde blood flow due to valve incompetence leading to increased hydrostatic pressures, edema, skin changes, and ulceration through mechanisms such as venous microangiop
Diseases involving blood vessels of the kidneyessamramdan
1) Nearly all renal diseases secondarily involve the renal blood vessels, with the main diseases affecting the kidneys' blood vessels being benign nephrosclerosis, malignant nephrosclerosis, and thrombotic microangiopathies.
2) Benign nephrosclerosis is characterized by hyaline thickening of small arteries and arterioles causing ischemic atrophy, while malignant nephrosclerosis features hyperplastic "onion skin" thickening of arterioles and fibrinoid necrosis.
3) Thrombotic microangiopathies include hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, characterized by microangiopathic hemolytic anemia
Acute lymphocytic leukemia (ALL) is an abnormal growth of lymphocyte precursors in the bone marrow. It results in the accumulation of immature white blood cells in the bloodstream and tissues, which can lead to organ malfunction. Symptoms include fever, bruising, difficulty breathing, anemia, and fast heart rate. Diagnosis involves tests such as bone marrow aspiration and biopsy, blood counts, and lumbar puncture. Treatment consists of chemotherapy, radiation therapy, blood transfusions, and stem cell or bone marrow transplants, with nursing focused on managing complications and providing support.
Hemodynamic disorders med- 2011, final iiدكتور مريض
1. Thrombosis is the formation of a blood clot (thrombus) within the circulatory system of a living organism. It is caused by endothelial injury, changes in blood flow, and hypercoagulability according to Virchow's triad.
2. Thrombi form in arteries and veins, and can cause obstruction, ischemia, infarction, or embolization if parts break off. Common sites are the legs, lungs, heart, and brain.
3. Embolism occurs when a thrombus or other mass travels through the bloodstream and blocks a vessel in another part of the body, potentially causing infarction or sepsis. Pulmonary embolism from deep leg vein
This document discusses the classification and treatment of vascular anomalies. It begins by classifying vascular tumors and malformations, distinguishing between high-flow and low-flow lesions. For vascular tumors, it describes hemangiomas and their treatment with beta-blockers. For high-flow malformations, it discusses arteriovenous malformations and their endovascular embolization. For low-flow malformations, it covers venous and lymphatic malformations and sclerotherapy treatments. It emphasizes the need for a multidisciplinary approach and notes limited available data. It provides contact information for Emory's developing vascular anomalies clinic.
The document provides information on examining the thorax and lungs, including:
1. Identifying important anatomical landmarks of the thorax such as the sternal angle and 12th rib.
2. Recognizing the lobes of the right and left lungs and their locations.
3. Performing a thorough respiratory exam involving inspection, palpation, percussion, and auscultation of the chest to identify any abnormalities.
4. Understanding common respiratory symptoms, signs, and their clinical significance for evaluating patients.
This document outlines cognitive and clinical objectives for assessing patients by organ system during an advanced practice health assessment. It includes objectives for general survey and vital signs, skin/hair/nails, head and neck, and thorax/lungs. The cognitive objectives describe the important concepts to understand, while the clinical objectives list the specific skills and techniques students should demonstrate, such as taking a patient history and performing a physical exam of each body system.
1. The document describes the three layers of skin (epidermis, dermis, subcutaneous tissue), their structures, and functions.
2. It lists 5 functions of skin: homeostasis, boundary for body fluids, protection, temperature regulation, and vitamin D synthesis. Hair, nails and glands are skin appendages.
3. Three types of glands are described - sebaceous, eccrine and apocrine - with their locations and secretions. Central and peripheral cyanosis are distinguished based on oxygen levels in arterial blood.
The document outlines the anatomy and examination of the head and neck region. It describes the bones, muscles, nerves, blood vessels and structures of the eyes, ears, nose, mouth, throat and neck. Key points include identifying the cranial nerves involved in vision and hearing, describing visual field defects and causes of abnormal eye movements. Examination techniques are covered such as visual acuity tests, otoscopy, lymph node palpation and assessment of the thyroid gland. The overall goal is to teach students to obtain a relevant history and perform a complete physical exam of the head and neck.
1. The document defines key cardiovascular terms like systole, diastole, and describes the location of important cardiac structures underneath the chest wall.
2. It explains the structure and function of the atrioventricular and semilunar valves, and their role in the formation of heart sounds S1 and S2.
3. The normal pulse, effects of inspiration on heart rate, and blood flow through the heart during diastole and systole are described.
This document provides guidelines for conducting a general survey and measuring vital signs during a patient exam. It includes instructions for assessing a patient's general appearance, measuring their blood pressure, heart rate, respiratory rate, and temperature. Normal and abnormal ranges are provided for blood pressure, with recommendations to recheck high or inconsistent readings. Factors that can affect blood pressure measurements, like cuff size and position, are also outlined.
This document provides information on performing a general survey and measuring vital signs. It describes aspects to observe in a general patient survey, such as appearance, posture, and gait. It then discusses the importance of measuring weight, height, temperature, blood pressure, heart rate, rhythm, and respiratory rate as vital signs. For each vital sign, it explains the proper technique for measurement and provides normal ranges. It also describes abnormalities that may be observed, such as orthostatic hypotension or irregular pulses.
The document outlines key anatomical landmarks of the thorax and lungs including the locations of the lung apices, bases, and fissures. It also describes common symptoms of respiratory conditions such as dyspnea, wheezing, cough, and characteristics of sputum including color, amount, and smell which can provide clues to underlying conditions.
This document summarizes notes about a midterm exam on hair, skin, and nails. It covers several topics: conducting a health history by asking open-ended questions; counseling on common skin cancers like basal cell carcinoma, squamous cell carcinoma, and melanoma - the most lethal type; risk factors for melanoma; and classifying primary skin lesions. Key points include that half of melanomas are found by patients themselves and the HARMM model for melanoma risk assessment considers history, age, regular checkups, moles changing, and male gender.
This document provides guidelines for conducting a general survey and measuring vital signs during a patient exam. It includes instructions for assessing a patient's general appearance, measuring their blood pressure, heart rate, respiratory rate, and temperature. Normal and abnormal ranges are provided for blood pressure, with recommendations to recheck high or inconsistent readings. Factors that can affect blood pressure measurements, like cuff size and position, are also outlined.
The document summarizes cellular structures and functions. It identifies the five chief cellular functions as movement, conductivity, metabolic absorption, secretion, and excretion. It then describes the structures and functions of key cellular organelles like the nucleus, ribosomes, endoplasmic reticulum, Golgi apparatus, lysosomes, and mitochondria. It also discusses plasma membrane structure and functions such as transport, protection, and cell communication.
The document defines key terms related to infection and host-pathogen interactions. It describes the process by which bacteria, viruses, and fungi cause infection, including how they evade host defenses. Clinical manifestations of infection result from direct microbial effects as well as the host inflammatory response, commonly including fever. A variety of microbes are capable of infecting the HEENT, respiratory, and GU tracts.
Cell injury and death can occur through various mechanisms including hypoxic injury, chemical injury, and free radical damage. Specific types of cell changes include atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia which have distinct morphological features and adaptive advantages or disadvantages. Necrosis can occur through various pathological processes including coagulative, liquefactive, caseous, and gangrenous necrosis each with characteristic tissue involvement and mechanisms of cellular damage. Systemic manifestations of cell injury include fever, increased heart rate, leukocytosis, pain, and presence of cellular enzymes in extracellular fluid.
The document summarizes cellular structures and functions. It identifies the five chief cellular functions as movement, conductivity, metabolic absorption, secretion, and excretion. It then describes the structures and functions of key cellular organelles like the nucleus, ribosomes, endoplasmic reticulum, Golgi apparatus, lysosomes, and mitochondria. It also discusses plasma membrane structure and functions such as transport, protection, and cell communication.
Cell injury and death can occur through various mechanisms including hypoxic injury, chemical injury, and free radical damage. Specific types of cell changes include atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia which have distinct morphological features and adaptive advantages or disadvantages. Necrosis can occur through various pathological processes including coagulative, liquefactive, caseous, and gangrenous necrosis each with characteristic tissue involvement and mechanisms of cellular damage. Systemic manifestations of cell injury include fever, increased heart rate, leukocytosis, pain, and presence of cellular enzymes in extracellular fluid.
The document summarizes key cellular structures and functions:
1. It identifies the five main cellular functions as movement, conductivity, metabolic absorption, secretion, and excretion.
2. It describes the structures and functions of key organelles including the nucleus, ribosomes, endoplasmic reticulum, Golgi apparatus, lysosomes, and mitochondria.
3. It explains several mechanisms of cellular transport and communication including diffusion, osmosis, active transport, receptors, and junctions between cells.
The document summarizes cellular structures and functions. It identifies the five chief cellular functions as movement, conductivity, metabolic absorption, secretion, and excretion. It then describes the structures and functions of key cellular organelles including the nucleus, ribosomes, endoplasmic reticulum, Golgi apparatus, lysosomes, and mitochondria. It also discusses plasma membrane structure and functions such as transport, protection, and cell communication.
The document discusses the structure and function of the pulmonary system. It describes the major structures including the airways, blood vessels, chest wall, and lungs. It explains that the lungs are made up of lobes, segments, and lobules from the branching airways. The document also discusses the conducting airways, gas exchange airways, respiratory mucosa, pulmonary and bronchial circulation, pulmonary lymphatic system, chest wall and pleura, and the main functions of the pulmonary system including gas exchange, pH maintenance, and temperature regulation.
The document summarizes the structure and function of the pulmonary system. It describes the major components including the airways, blood vessels, lungs, and chest wall. It then discusses the conducting airways and gas exchange regions of the lungs. Finally, it explains the mechanics of breathing including ventilation, elastic recoil, compliance, and airway resistance.
This document discusses neurological pathophysiology, including seizures, alterations in cognition, Alzheimer's disease, and cerebral hemodynamics. It defines seizures and their classifications, describes the pathophysiology of seizures involving neuronal firing and spreading. It also discusses various types of alterations in cognition like agnosia, dysphasia, acute confusional states, dementia, and Alzheimer's disease focusing on pathogenesis. Finally, it explains concepts of cerebral hemodynamics including cerebral blood flow, intracranial pressure, cerebral edema, and their effects on brain function.
Which means 5% is due to: renal (renal artery stenosis) and hyperaldosteronism. \n
AWESOME!!\n
Pheochromocytoma - very rare. Causes head aches and sweating. \nRenal vascular disease - triggar RAA system. \n
“lower the pressure, the better, as long as it is not symptomatic”.\n
ALWAYS start with life style modification. \nIf not at goal, then look at drugs. \nBeta blockers and diaretics as long as they are not opposed to them.\nIf diabetic, then use ACE inhibitors.\nSometimes ACEi don’t work as well as Ca channel blockers in AA.\n
acute corronary syndrom, Marfan’s with aneurism, AAA, worry about dissection through vessel wall. \n
Pain secondary to ischemia. \nUsually seen in youn men who smoke cigarrettes. \nTx - sessations, vasodilators\n
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May be due to decreased release of vasodilation chemicals. \nImmune complex, type III\nTips of fingers, top of phylanges. Can happen more with stress. \nWhite, blue, then red. \n\n
Can become painful and lower extremity edema. Can cause hyperpigmentation and ulceration due to venus stasis. \n
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Number one Killer in us Men and Women.\n\n
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Silent MI - diabete. Based on secondary neuropathy. No sensation of chest pain. \nWomen present with atypical presentations: tierd, vague abdominal pain, be sensitive.\nVessels decrease by 50% before symptoms. \nStart with exercise induced pain. \n
Some women will just have back pain. \nEcho’s and stress tests\nACE Inhib - actually prevents remodelling that predispose heart to “floppy sloppy”.\n\n
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Q-wave - with full-thickness (transmurral).\nBlood must be blocked for 20 minutes or more. \nDysrhythmia is the most common complication resulting from an MI. \nThen remodeling, then heart failure. \n
Myosite might be stunned for a couple days. \n
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Inflammation makes exudate. \nIf infectious, then cells like PMN’s will come in. \nTampanad - enough fluid to cause contraction on heart. \nFever, Chest pain that increases when lying down!!! Slight ST segment elevation with no Q. --> acute pericarditis. \n
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SUDDEN DEATH - \n
Dilated: viral, pregnancy, drugs and etoh.\nHypertrophic: valve regurg, fatigue, dry cough at night, \nRestrictive: least common. \n\nTx - diuretics, ACEi, \n
If it occurs during diastole, it is most likely a pathologic murmur.\n
Egophany - A to E changes. Sign of consolidation. \n
Balooning at leaflett’s. \nLate systolic murmer is a back-flow murmur. \n
Usually staph, need anti bact with dental.\nLess rheumatic, more drug use.\nUnexplaned feaver and new murmur. MOST IMPORTANT signs. \nCould become emboli, bacteremic, autoimmune predisposition. \n
Takes a long time for IV-antibiotics \n
RIght sidded - due to lung disease, core pulmonaly,\nIf bad enough, can lead to left sided. \nLeft sided - due to systemic HTN, Mitral stenosis, \n