This document discusses cardiac hepatopathy, which is liver damage caused by underlying cardiac disorders. It can manifest as congestive hepatopathy from chronic passive venous congestion, or acute cardiogenic liver injury from acute cardiocirculatory failure. Congestive hepatopathy is characterized histologically by necrosis in zone 3 of the liver and presents with elevated cholestasis markers. Acute cardiogenic liver injury shows striking elevations in transaminases and presents necrosis primarily in zone 3 as well. Both forms of cardiac hepatopathy carry prognostic implications and their treatment involves managing the underlying heart condition.
Renal hypertension is high blood pressure caused by kidney disease. It can be caused by renal stenosis where the renal arteries narrow, decreasing blood flow to the kidneys, or chronic glomerulonephritis where inflammation damages the glomeruli. This causes increased renal vascular resistance and decreased glomerular filtration, stimulating the renin-angiotensin system which increases blood pressure. Investigations include blood and urine tests, ultrasound, CT scan, and biopsy. Treatments depend on the cause but may include angioplasty, stenting, medications, or controlling blood pressure and protein intake.
This document provides an overview of heart failure, including its definition, epidemiology, prognosis, terminology, classification, etiology, pathogenesis, neurohormonal mechanisms, approach to diagnosis, and imaging techniques. Some key points include:
- Heart failure is defined as a clinical syndrome resulting from structural or functional impairment of ventricular filling or ejection of blood.
- It is a growing problem worldwide with increased prevalence with age. Prognosis remains poor with 30-40% of patients dying within 1 year of diagnosis.
- Pathogenesis involves neurohormonal activation of the sympathetic nervous system and renin-angiotensin system as compensatory mechanisms which eventually contribute to disease progression.
- Diagnosis involves
The document discusses hypertension and its effects on the kidney. It begins by defining normal blood pressure regulation and the role of the kidney in long-term blood pressure control. It then discusses the epidemiology of hypertension globally and in various countries. The document also covers the epidemiology of chronic kidney disease, how hypertension affects the kidney and can lead to hypertensive nephropathy, and how chronic kidney disease in turn affects blood pressure. It concludes by outlining blood pressure targets and treatment strategies for patients with hypertension and chronic kidney disease.
This document defines renal artery stenosis and discusses its causes and pathophysiology. Renal artery stenosis occurs when blood flow to the kidneys is reduced due to narrowing of the renal arteries, which can activate the renin-angiotensin-aldosterone system and cause hypertension. The main causes are atherosclerosis and fibromuscular dysplasia. Renal artery stenosis can lead to ischemic nephropathy and reduced kidney function over time if left untreated. Diagnosis involves demonstrating both the vascular lesion and RAAS activation.
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can result from conditions that weaken the heart muscle such as coronary artery disease or hypertension.
The document defines heart failure and describes its prevalence increasing with age and being higher in males than females aged 40-75. Symptoms of left ventricular failure include breathing difficulties, cough, and leg swelling while right ventricular failure symptoms include abdominal swelling and pain.
Signs include elevated jugular venous pressure, lung crackles, edema, hepatomegaly, and murmurs. Precipitating factors include infection, medications, thyroid issues, and arrhythmias. Diagnostic tests include chest x-ray, echocardiogram
Diagnosis of Pulmonary Embolism is often difficult. This presentation highlights step-wise and practical approach to the diagnosis of PE in short and precise fashion.
The document discusses the treatment of heart failure in patients with chronic kidney disease. It notes that CKD is a common comorbidity in heart failure patients and that the coexistence of the two conditions increases health risks. The main treatments discussed are:
1. ACE inhibitors and ARBs to improve ventricular function, though they can worsen kidney function. Close monitoring of kidney function and electrolytes is needed.
2. Beta blockers like bisoprolol and carvedilol to improve ventricular function, though they can cause hypotension and kidney dysfunction.
3. Aldosterone antagonists to reduce heart failure worsening and increase survival, though they can cause hyperkalemia and worsen kidney function.
The document provides information on congestive cardiac failure (CCF), including:
1. CCF occurs when the heart cannot pump enough blood to meet the body's needs, causing fluid buildup in tissues.
2. Risk factors include age, hypertension, diabetes, smoking, and coronary artery disease. Symptoms include shortness of breath, fatigue, and swelling.
3. Diagnosis involves medical history, physical exam, chest X-ray, echocardiogram and blood tests. Treatment focuses on lifestyle changes, medications, procedures and managing underlying causes.
Renal hypertension is high blood pressure caused by kidney disease. It can be caused by renal stenosis where the renal arteries narrow, decreasing blood flow to the kidneys, or chronic glomerulonephritis where inflammation damages the glomeruli. This causes increased renal vascular resistance and decreased glomerular filtration, stimulating the renin-angiotensin system which increases blood pressure. Investigations include blood and urine tests, ultrasound, CT scan, and biopsy. Treatments depend on the cause but may include angioplasty, stenting, medications, or controlling blood pressure and protein intake.
This document provides an overview of heart failure, including its definition, epidemiology, prognosis, terminology, classification, etiology, pathogenesis, neurohormonal mechanisms, approach to diagnosis, and imaging techniques. Some key points include:
- Heart failure is defined as a clinical syndrome resulting from structural or functional impairment of ventricular filling or ejection of blood.
- It is a growing problem worldwide with increased prevalence with age. Prognosis remains poor with 30-40% of patients dying within 1 year of diagnosis.
- Pathogenesis involves neurohormonal activation of the sympathetic nervous system and renin-angiotensin system as compensatory mechanisms which eventually contribute to disease progression.
- Diagnosis involves
The document discusses hypertension and its effects on the kidney. It begins by defining normal blood pressure regulation and the role of the kidney in long-term blood pressure control. It then discusses the epidemiology of hypertension globally and in various countries. The document also covers the epidemiology of chronic kidney disease, how hypertension affects the kidney and can lead to hypertensive nephropathy, and how chronic kidney disease in turn affects blood pressure. It concludes by outlining blood pressure targets and treatment strategies for patients with hypertension and chronic kidney disease.
This document defines renal artery stenosis and discusses its causes and pathophysiology. Renal artery stenosis occurs when blood flow to the kidneys is reduced due to narrowing of the renal arteries, which can activate the renin-angiotensin-aldosterone system and cause hypertension. The main causes are atherosclerosis and fibromuscular dysplasia. Renal artery stenosis can lead to ischemic nephropathy and reduced kidney function over time if left untreated. Diagnosis involves demonstrating both the vascular lesion and RAAS activation.
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can result from conditions that weaken the heart muscle such as coronary artery disease or hypertension.
The document defines heart failure and describes its prevalence increasing with age and being higher in males than females aged 40-75. Symptoms of left ventricular failure include breathing difficulties, cough, and leg swelling while right ventricular failure symptoms include abdominal swelling and pain.
Signs include elevated jugular venous pressure, lung crackles, edema, hepatomegaly, and murmurs. Precipitating factors include infection, medications, thyroid issues, and arrhythmias. Diagnostic tests include chest x-ray, echocardiogram
Diagnosis of Pulmonary Embolism is often difficult. This presentation highlights step-wise and practical approach to the diagnosis of PE in short and precise fashion.
The document discusses the treatment of heart failure in patients with chronic kidney disease. It notes that CKD is a common comorbidity in heart failure patients and that the coexistence of the two conditions increases health risks. The main treatments discussed are:
1. ACE inhibitors and ARBs to improve ventricular function, though they can worsen kidney function. Close monitoring of kidney function and electrolytes is needed.
2. Beta blockers like bisoprolol and carvedilol to improve ventricular function, though they can cause hypotension and kidney dysfunction.
3. Aldosterone antagonists to reduce heart failure worsening and increase survival, though they can cause hyperkalemia and worsen kidney function.
The document provides information on congestive cardiac failure (CCF), including:
1. CCF occurs when the heart cannot pump enough blood to meet the body's needs, causing fluid buildup in tissues.
2. Risk factors include age, hypertension, diabetes, smoking, and coronary artery disease. Symptoms include shortness of breath, fatigue, and swelling.
3. Diagnosis involves medical history, physical exam, chest X-ray, echocardiogram and blood tests. Treatment focuses on lifestyle changes, medications, procedures and managing underlying causes.
A review of Hypertrophic cardiomyopathy. Ideal for Cardiology Fellows and Internal Medicine Residents. Draws figures and information from review articles published on the subject as well as classical teaching books.
The patient with chronic liver disease presents a range of potential challenges when a severe intercurrent illness occurs or major surgery is required. Even well-compensated liver cirrhosis in high functioning patients renders such individuals vulnerable to a myriad of problems when physiological stressors occur. Severe acute liver failure is another clearly defined sydrome in which extremely rapid and complex multiple organ failure typically ensues. Whilst intensivists are familiar and adept with the management of other major organ failure, new acute liver failure or decompensated chronic liver disease is particularly difficult to manage due to the inherent breadth of roles that the liver has in maintaining health as well as the current lack of comprehensive support therapies other than organ transplantation. While effective artificial life-supports for severe respiratory, cardiac or renal failure are available in the intensive care setting, support for over liver failure is less straightforward. The failing liver inevitably and rapidly impact on every other organ system, necessitating a systematic and comprehensive approach when planning patient care.
As with any dynamic and complex disease process, management is optimised when major clinical problems are anticipated and the detrimental impact is mitigated by the timely application of effective interventions. For patients with severe acute liver failure, a knowledge of the cause, disease trajectory, severity of organ failure as well as early interventions to prevent cerebral oedema are likely to improve outcomes. Specific treatments such as temperature management, respiratory support, osmotherapy and blood purification may be readily applied and reduce the risk of poor outcomes. In the setting of decompensated chronic liver disease, identifying reversible causes of deterioration and proactively managing the resulting predictable problems will ensure the best chance for recovery or stabilisation until subsequent transplantation. The majority of patients can be effectively managed in non-transplant centres, however it is also essential to identify those patients for whom orthotopic liver transplantation is the best or only option for survival. Early discussion with a transplant centre may assist intensivists in deciding who should be transferred and guide the timing of retrieval.
This document discusses renal vascular diseases, focusing on hypertensive vascular disease and its effects on the kidneys. It describes benign nephrosclerosis, which involves mild vascular changes and scarring of the kidneys, and malignant nephrosclerosis, a more severe form seen in accelerated hypertension. Benign nephrosclerosis may cause mild symptoms and rarely kidney failure, while malignant nephrosclerosis is life-threatening and usually leads to kidney failure or death within a year if untreated.
Portal hypertension is defined as elevated hepatic venous pressure gradient over 5mmHg caused by increased resistance to blood flow in the liver and increased blood flow to the portal vein. It commonly results from cirrhosis and causes complications like variceal bleeding, ascites, and hepatic encephalopathy. Ascites develops from increased portal pressure causing fluid retention. Spontaneous bacterial peritonitis is a common infection of ascitic fluid. Hepatorenal syndrome is a type of kidney failure seen in advanced liver disease. Treatment focuses on managing the underlying cause, complications, and symptoms.
This document discusses kidney failure caused by hypertension. It begins by defining blood pressure and the stages of hypertension. It then explains how high blood pressure can damage the kidneys over time by restricting blood flow. Specifically, it describes how narrowing of the renal arteries from conditions like atherosclerosis and fibromuscular dysplasia can lead to renal hypertension. Left untreated, this causes further kidney damage through activation of the renin-angiotensin system and fluid retention, eventually leading to kidney failure and the need for dialysis or transplantation. The document outlines symptoms, diagnostic tests, prevention methods like controlling blood pressure, and treatments including medications and revascularization.
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Cardiorenal syndrome (CRS) refers to conditions where acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. CRS is classified into 5 subtypes depending on whether cardiac or renal dysfunction occurs first, and whether it is acute or chronic. Type 1 involves acute cardiac dysfunction leading to acute kidney injury. Type 2 involves chronic cardiac dysfunction resulting in worsening chronic kidney disease. Type 3 involves acute kidney injury leading to cardiac issues. Type 4 involves chronic kidney disease contributing to cardiac problems. Type 5 involves secondary cardiac and renal dysfunction due to another systemic condition. Early diagnosis and treatment individualized to the CRS subtype is important for improving survival.
Management of liver failure in general intensive careDr fakhir Raza
The document provides guidance on the management of acute liver failure and cirrhotic patients in the intensive care unit. It recommends:
1) Treating extrahepatic organ failure early and preventing aggravating factors to reduce morbidity and mortality in acute liver failure patients.
2) Initiating N-acetylcysteine therapy for all acute liver failure patients regardless of etiology to improve outcomes.
3) Consulting a liver transplant center to discuss further investigations or transplant evaluation if initial tests are negative for acute liver failure patients.
Portopulmonary hypertension and hepatopulmonary syndrome1Samiaa Sadek
This document defines and describes porto-pulmonary hypertension (POPH) and hepatopulmonary syndrome (HPS), two pulmonary vascular complications that can arise from liver disease and portal hypertension. POPH is characterized by elevated pulmonary artery pressure and resistance, while HPS involves pulmonary vasodilation and intrapulmonary shunting leading to hypoxemia. The document covers diagnostic criteria and evaluations, pathophysiology, treatment options including liver transplantation, and prognosis for each condition.
This document provides an overview of cardiac failure/congestive heart failure. It begins with an introduction and objectives. It then reviews heart anatomy and physiology, including the structure of the heart, conducting system, heart sounds, and ECG. It defines cardiac failure and discusses epidemiology, causes, pathophysiology, clinical manifestations, classifications, diagnostic process, medical management, and complications. Nursing management is also addressed using the nursing process approach.
This document discusses the pathophysiology of heart failure. It describes how heart failure can result from abnormalities in systolic or diastolic cardiac function. In heart failure with reduced ejection fraction (HFrEF), the left ventricle contracts poorly and cannot adequately pump blood. In heart failure with preserved ejection fraction (HFpEF), left ventricular filling is impaired. Both types result in inadequate blood flow and organ congestion. The document discusses neurohormonal changes, organ dysfunction, and other compensatory mechanisms involved in heart failure.
Heart failure occurs when the heart is unable to pump sufficiently to meet the body's needs. It can be systolic, caused by the ventricles' inability to contract properly, or diastolic, caused by the ventricles' inability to relax and fill normally. Symptoms depend on whether the left or right ventricle is affected. Management involves risk factor control, lifestyle changes, diuretics, ACE inhibitors, beta blockers, and sometimes surgical procedures like defibrillators or transplantation for severe cases.
Congestive heart failure (CHF), also known as heart failure, is a condition where the heart muscle is unable to pump sufficiently to maintain blood flow to meet the body's needs. It is classified by the New York Heart Association system from Class I (no symptoms) to Class IV (symptoms at rest). The American College of Cardiology/American Heart Association categorizes heart failure into four stages from asymptomatic structural heart disease to end-stage disease. Common causes include ischemic heart disease, hypertension, diabetes and obesity. Symptoms vary depending on whether the left or right side of the heart is affected but may include shortness of breath, fatigue, swelling and coughing. Diagnosis involves imaging, blood tests and physical exams.
Heart failure is a clinical syndrome that develops when –
The heart can not maintain adequate output
or
Can do so only at the expense of elevated ventricular filling pressure
The document provides an overview of cardiomyopathies including definitions, classifications, presentations, evaluations, and treatments. It discusses the main types - dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. For dilated cardiomyopathy, it describes the etiologies, clinical features, investigations, and treatments. It notes dilated cardiomyopathy is the most common cardiomyopathic phenotype and often a final common pathway of cardiac injuries. For hypertrophic cardiomyopathy, it discusses the pathophysiology, clinical manifestations, investigations, and treatments including the use of beta-blockers and surgical procedures. For restrictive cardiomyopathy, it lists possible causes and notes the hallmark is abnormal diastolic function with excessive ventricular wall rig
This document provides an overview of drugs for congestive heart failure. It defines heart failure as the heart's inability to pump sufficient blood to meet the body's needs. Causes include diseases like atherosclerosis, heart attacks, and hypertension. Signs and symptoms include dyspnea, fatigue, edema, and confusion. Angiotensin receptor blockers work by competitively blocking angiotensin II receptors, reducing blood pressure, afterload, and remodeling of the left ventricle. Common drug classes discussed are ACE inhibitors, ARBs, diuretics, beta-blockers, and aldosterone antagonists. Stages of heart failure and appropriate therapies are also covered.
AKI is characterized by a sudden impairment of kidney function resulting in the retention of waste products normally cleared by the kidneys. It is diagnosed by an increase in BUN/creatinine and/or decrease in urine output. AKI can range from asymptomatic lab abnormalities to life-threatening complications. Common causes include ischemia, nephrotoxins, sepsis, surgery, and obstruction of urine flow. A careful history, physical exam, urine analysis, and consideration of potential causes are used to diagnose the type and severity of AKI.
Journal of Gastroenterology, Liver & Pancreatic diseases is an open access, peer reviewed, scholarly journal dedicated to publish articles covering all areas of Gastroenterology, Liver & Pancreas.
The journal aims to promote latest information and provide a forum for doctors, researchers, physicians, and healthcare professionals to find most recent advances in the areas of Gastroenterology, Liver & Pancreas. Journal of Gastroenterology, Liver & Pancreatic diseases accepts research articles, reviews, mini reviews, case reports and rapid communication covering all aspects of Gastroenterology, Liver & Pancreas.
Journal of Gastroenterology, Liver & Pancreatic diseases strongly supports the scientific up gradation and fortification in related scientific research community by enhancing access to peer reviewed scientific literary works. Austin Publishing Group also brings universally peer reviewed journals under one roof thereby promoting knowledge sharing, mutual promotion of multidisciplinary science.
This document provides an overview of hypersensitivity and its classification. It discusses the four main types of hypersensitivity: Type I is anaphylactic and mediated by IgE antibodies, examples include anaphylaxis and atopy. Type II involves IgG antibodies causing blood transfusion reactions, hemolytic disease of newborn, and drug-induced hemolysis. Type III hypersensitivity involves immune complex deposition that can cause localized or generalized tissue damage. Type IV is cell-mediated and causes delayed reactions like tuberculin reactions and contact dermatitis. It provides details on the mechanisms, features, and examples of each type of hypersensitivity reaction.
Este documento trata sobre la geografía y el medio ambiente. Explica que la geografía describe y representa gráficamente la Tierra, mientras que el medio ambiente se refiere a las relaciones entre los humanos y la Tierra. También define el medio ambiente como todo aquello que nos influye y sobre lo que podemos actuar. Finalmente, señala que la ecología estudia a los seres vivos, su ambiente y cómo las interacciones entre organismos y ambiente afectan sus propiedades.
A review of Hypertrophic cardiomyopathy. Ideal for Cardiology Fellows and Internal Medicine Residents. Draws figures and information from review articles published on the subject as well as classical teaching books.
The patient with chronic liver disease presents a range of potential challenges when a severe intercurrent illness occurs or major surgery is required. Even well-compensated liver cirrhosis in high functioning patients renders such individuals vulnerable to a myriad of problems when physiological stressors occur. Severe acute liver failure is another clearly defined sydrome in which extremely rapid and complex multiple organ failure typically ensues. Whilst intensivists are familiar and adept with the management of other major organ failure, new acute liver failure or decompensated chronic liver disease is particularly difficult to manage due to the inherent breadth of roles that the liver has in maintaining health as well as the current lack of comprehensive support therapies other than organ transplantation. While effective artificial life-supports for severe respiratory, cardiac or renal failure are available in the intensive care setting, support for over liver failure is less straightforward. The failing liver inevitably and rapidly impact on every other organ system, necessitating a systematic and comprehensive approach when planning patient care.
As with any dynamic and complex disease process, management is optimised when major clinical problems are anticipated and the detrimental impact is mitigated by the timely application of effective interventions. For patients with severe acute liver failure, a knowledge of the cause, disease trajectory, severity of organ failure as well as early interventions to prevent cerebral oedema are likely to improve outcomes. Specific treatments such as temperature management, respiratory support, osmotherapy and blood purification may be readily applied and reduce the risk of poor outcomes. In the setting of decompensated chronic liver disease, identifying reversible causes of deterioration and proactively managing the resulting predictable problems will ensure the best chance for recovery or stabilisation until subsequent transplantation. The majority of patients can be effectively managed in non-transplant centres, however it is also essential to identify those patients for whom orthotopic liver transplantation is the best or only option for survival. Early discussion with a transplant centre may assist intensivists in deciding who should be transferred and guide the timing of retrieval.
This document discusses renal vascular diseases, focusing on hypertensive vascular disease and its effects on the kidneys. It describes benign nephrosclerosis, which involves mild vascular changes and scarring of the kidneys, and malignant nephrosclerosis, a more severe form seen in accelerated hypertension. Benign nephrosclerosis may cause mild symptoms and rarely kidney failure, while malignant nephrosclerosis is life-threatening and usually leads to kidney failure or death within a year if untreated.
Portal hypertension is defined as elevated hepatic venous pressure gradient over 5mmHg caused by increased resistance to blood flow in the liver and increased blood flow to the portal vein. It commonly results from cirrhosis and causes complications like variceal bleeding, ascites, and hepatic encephalopathy. Ascites develops from increased portal pressure causing fluid retention. Spontaneous bacterial peritonitis is a common infection of ascitic fluid. Hepatorenal syndrome is a type of kidney failure seen in advanced liver disease. Treatment focuses on managing the underlying cause, complications, and symptoms.
This document discusses kidney failure caused by hypertension. It begins by defining blood pressure and the stages of hypertension. It then explains how high blood pressure can damage the kidneys over time by restricting blood flow. Specifically, it describes how narrowing of the renal arteries from conditions like atherosclerosis and fibromuscular dysplasia can lead to renal hypertension. Left untreated, this causes further kidney damage through activation of the renin-angiotensin system and fluid retention, eventually leading to kidney failure and the need for dialysis or transplantation. The document outlines symptoms, diagnostic tests, prevention methods like controlling blood pressure, and treatments including medications and revascularization.
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Cardiorenal syndrome (CRS) refers to conditions where acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. CRS is classified into 5 subtypes depending on whether cardiac or renal dysfunction occurs first, and whether it is acute or chronic. Type 1 involves acute cardiac dysfunction leading to acute kidney injury. Type 2 involves chronic cardiac dysfunction resulting in worsening chronic kidney disease. Type 3 involves acute kidney injury leading to cardiac issues. Type 4 involves chronic kidney disease contributing to cardiac problems. Type 5 involves secondary cardiac and renal dysfunction due to another systemic condition. Early diagnosis and treatment individualized to the CRS subtype is important for improving survival.
Management of liver failure in general intensive careDr fakhir Raza
The document provides guidance on the management of acute liver failure and cirrhotic patients in the intensive care unit. It recommends:
1) Treating extrahepatic organ failure early and preventing aggravating factors to reduce morbidity and mortality in acute liver failure patients.
2) Initiating N-acetylcysteine therapy for all acute liver failure patients regardless of etiology to improve outcomes.
3) Consulting a liver transplant center to discuss further investigations or transplant evaluation if initial tests are negative for acute liver failure patients.
Portopulmonary hypertension and hepatopulmonary syndrome1Samiaa Sadek
This document defines and describes porto-pulmonary hypertension (POPH) and hepatopulmonary syndrome (HPS), two pulmonary vascular complications that can arise from liver disease and portal hypertension. POPH is characterized by elevated pulmonary artery pressure and resistance, while HPS involves pulmonary vasodilation and intrapulmonary shunting leading to hypoxemia. The document covers diagnostic criteria and evaluations, pathophysiology, treatment options including liver transplantation, and prognosis for each condition.
This document provides an overview of cardiac failure/congestive heart failure. It begins with an introduction and objectives. It then reviews heart anatomy and physiology, including the structure of the heart, conducting system, heart sounds, and ECG. It defines cardiac failure and discusses epidemiology, causes, pathophysiology, clinical manifestations, classifications, diagnostic process, medical management, and complications. Nursing management is also addressed using the nursing process approach.
This document discusses the pathophysiology of heart failure. It describes how heart failure can result from abnormalities in systolic or diastolic cardiac function. In heart failure with reduced ejection fraction (HFrEF), the left ventricle contracts poorly and cannot adequately pump blood. In heart failure with preserved ejection fraction (HFpEF), left ventricular filling is impaired. Both types result in inadequate blood flow and organ congestion. The document discusses neurohormonal changes, organ dysfunction, and other compensatory mechanisms involved in heart failure.
Heart failure occurs when the heart is unable to pump sufficiently to meet the body's needs. It can be systolic, caused by the ventricles' inability to contract properly, or diastolic, caused by the ventricles' inability to relax and fill normally. Symptoms depend on whether the left or right ventricle is affected. Management involves risk factor control, lifestyle changes, diuretics, ACE inhibitors, beta blockers, and sometimes surgical procedures like defibrillators or transplantation for severe cases.
Congestive heart failure (CHF), also known as heart failure, is a condition where the heart muscle is unable to pump sufficiently to maintain blood flow to meet the body's needs. It is classified by the New York Heart Association system from Class I (no symptoms) to Class IV (symptoms at rest). The American College of Cardiology/American Heart Association categorizes heart failure into four stages from asymptomatic structural heart disease to end-stage disease. Common causes include ischemic heart disease, hypertension, diabetes and obesity. Symptoms vary depending on whether the left or right side of the heart is affected but may include shortness of breath, fatigue, swelling and coughing. Diagnosis involves imaging, blood tests and physical exams.
Heart failure is a clinical syndrome that develops when –
The heart can not maintain adequate output
or
Can do so only at the expense of elevated ventricular filling pressure
The document provides an overview of cardiomyopathies including definitions, classifications, presentations, evaluations, and treatments. It discusses the main types - dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. For dilated cardiomyopathy, it describes the etiologies, clinical features, investigations, and treatments. It notes dilated cardiomyopathy is the most common cardiomyopathic phenotype and often a final common pathway of cardiac injuries. For hypertrophic cardiomyopathy, it discusses the pathophysiology, clinical manifestations, investigations, and treatments including the use of beta-blockers and surgical procedures. For restrictive cardiomyopathy, it lists possible causes and notes the hallmark is abnormal diastolic function with excessive ventricular wall rig
This document provides an overview of drugs for congestive heart failure. It defines heart failure as the heart's inability to pump sufficient blood to meet the body's needs. Causes include diseases like atherosclerosis, heart attacks, and hypertension. Signs and symptoms include dyspnea, fatigue, edema, and confusion. Angiotensin receptor blockers work by competitively blocking angiotensin II receptors, reducing blood pressure, afterload, and remodeling of the left ventricle. Common drug classes discussed are ACE inhibitors, ARBs, diuretics, beta-blockers, and aldosterone antagonists. Stages of heart failure and appropriate therapies are also covered.
AKI is characterized by a sudden impairment of kidney function resulting in the retention of waste products normally cleared by the kidneys. It is diagnosed by an increase in BUN/creatinine and/or decrease in urine output. AKI can range from asymptomatic lab abnormalities to life-threatening complications. Common causes include ischemia, nephrotoxins, sepsis, surgery, and obstruction of urine flow. A careful history, physical exam, urine analysis, and consideration of potential causes are used to diagnose the type and severity of AKI.
Journal of Gastroenterology, Liver & Pancreatic diseases is an open access, peer reviewed, scholarly journal dedicated to publish articles covering all areas of Gastroenterology, Liver & Pancreas.
The journal aims to promote latest information and provide a forum for doctors, researchers, physicians, and healthcare professionals to find most recent advances in the areas of Gastroenterology, Liver & Pancreas. Journal of Gastroenterology, Liver & Pancreatic diseases accepts research articles, reviews, mini reviews, case reports and rapid communication covering all aspects of Gastroenterology, Liver & Pancreas.
Journal of Gastroenterology, Liver & Pancreatic diseases strongly supports the scientific up gradation and fortification in related scientific research community by enhancing access to peer reviewed scientific literary works. Austin Publishing Group also brings universally peer reviewed journals under one roof thereby promoting knowledge sharing, mutual promotion of multidisciplinary science.
This document provides an overview of hypersensitivity and its classification. It discusses the four main types of hypersensitivity: Type I is anaphylactic and mediated by IgE antibodies, examples include anaphylaxis and atopy. Type II involves IgG antibodies causing blood transfusion reactions, hemolytic disease of newborn, and drug-induced hemolysis. Type III hypersensitivity involves immune complex deposition that can cause localized or generalized tissue damage. Type IV is cell-mediated and causes delayed reactions like tuberculin reactions and contact dermatitis. It provides details on the mechanisms, features, and examples of each type of hypersensitivity reaction.
Este documento trata sobre la geografía y el medio ambiente. Explica que la geografía describe y representa gráficamente la Tierra, mientras que el medio ambiente se refiere a las relaciones entre los humanos y la Tierra. También define el medio ambiente como todo aquello que nos influye y sobre lo que podemos actuar. Finalmente, señala que la ecología estudia a los seres vivos, su ambiente y cómo las interacciones entre organismos y ambiente afectan sus propiedades.
El documento presenta una serie de ejercicios fotográficos en los que se varían los parámetros de contraste, saturación y nitidez para diferentes motivos como una persona, un paisaje y un objeto. Se definen primero los conceptos de contraste, saturación y nitidez y luego se muestran 12 variaciones para cada motivo, modificando uno de los parámetros en cada toma mientras se mantienen los otros constantes. El objetivo es observar el efecto producido en la imagen al variar estos elementos.
This coupon is for $8 off a cocktail at a popular East County cocktail bar that features a signature "Golden State" Moscow Mule made with Brentwood sweet corn vodka and topped with locally grown fruit, putting a new twist on the typical U-pick experience by enjoying a locally flavored, refreshing drink.
Este documento resume los criterios para sustentar declaraciones de propiedades saludables generalmente aceptadas en alimentos funcionales. Explica que existen regulaciones como la japonesa FOSHU de 1991 y la europea de 2006 que establecen evidencias científicas como criterio. También describe los pasos de investigación necesarios para desarrollar un alimento funcional, incluyendo obtención de ingredientes, caracterización, estudios in vitro e in vivo, y clínicos.
The document provides an overview of the Intercultural Management Institute (IMI) at American University. IMI consults with organizations and trains personnel to manage cultural differences and leverage diversity for competitive advantage. They offer customized training in areas like cross-cultural communication, negotiation, and leadership. Trainers include intercultural experts and American University faculty. Training methods are grounded in research and tailored to each client's needs. Services aim to develop global leaders and support international growth. IMI is located at American University in Washington, D.C. and can deliver programs onsite or at the client's location.
Dokumen tersebut memberikan panduan lengkap tentang pemeriksaan fisik ibu hamil, meliputi prosedur, alat, dan prinsip pelaksanaannya. Pemeriksaan fisik ibu hamil mencakup pemeriksaan umum, inspeksi, palpasi, auskultasi, dan pemeriksaan khusus seperti payudara, abdomen, dan panggul untuk menilai keadaan ibu dan janin. Pemeriksaan dilakukan dengan memperhatikan privasi pasien dan men
Troy Buckner, a private art dealer from Southampton, NY, is the former owner of Clark Fine Art. Troy Buckner has showcased the work of many artists, including Larry Rivers at the Southampton gallery.
CPSP is a new emerging disease but can be a silent epidemic.
Optimal perioperative management may reduce the incidence of CPSP.
Minimal invasive surgical techniques
Agressive perioperative multimodal analgesia, inluding epidural or nerve blocks.
Appropriate management of acute pain is therefore not only a humane obligation, but also may prevent of chronic pain!
The document discusses medulloblastoma (MB), the most common malignant brain tumor in children. MB originates in the cerebellum and projects into the fourth ventricle. It is thought to arise from primitive neuroepithelial cells. On imaging, MB typically appears as a large lobulated mass in the posterior fossa that compresses the fourth ventricle and causes hydrocephalus. Molecular analysis has classified MB into four subgroups: SHH, WNT, Group III, and Group IV, which have different characteristics and prognoses. Prognostic factors include age at diagnosis, extent of disease, extent of resection, histology, and biological markers.
Moyamoya disease and syndrome an unusal cause of strokeSurendra Godara
This document provides information on moyamoya disease, including:
1. Moyamoya disease is a cerebrovascular disease characterized by progressive stenosis of the carotid arteries and the formation of abnormal blood vessels at the base of the brain.
2. The cause is unknown but genetics are believed to play a role, as the disease has a higher incidence in Asia and some familial patterns.
3. Clinical presentations in children include transient ischemic attacks, ischemic strokes, headaches and seizures. The disease is most common in the first decade of life.
This document provides an overview of meningitis and encephalitis. It discusses the different types of bacterial, viral and fungal meningitis including their causes, symptoms, diagnosis and treatment. Key points include that bacterial meningitis can be caused by organisms like pneumococcus, meningococcus and haemophilus influenza. Viral meningitis causes aseptic meningitis while encephalitis involves brain inflammation. Diagnosis involves lumbar puncture and CSF analysis. Treatment depends on the identified organism and may involve antibiotics, antivirals or antifungals.
The document is a lesson by Lauren Williams for her 6-3 technology class that teaches the alphabet by listing an object that begins with each letter from A to Z, such as A is for apple, B is for bunny, and C is for Christmas. It concludes by celebrating learning the ABCs.
Decompressive craniectomy is a surgical procedure where part of the skull is removed to relieve pressure on the brain from swelling after severe traumatic brain injury. There are various techniques for decompressive craniectomy including size and location of bone flap removed and methods for opening and repairing the dura mater. Key goals are to provide space for brain swelling, improve blood flow, and reduce pressure while preventing complications like brain herniation. The author discusses their experience with standard large frontotemporoparietal decompressive craniectomy and considerations for optimal decompression balancing risks.
This document discusses the pathogenesis and diagnosis of acute decompensated heart failure (ADHF). It defines ADHF and describes its epidemiology, including the high rates of hospitalization. Common comorbidities are hypertension, coronary artery disease, diabetes, and COPD. ADHF can be classified based on history, blood pressure, signs/symptoms, and ejection fraction. Causes include nonadherence, infection, ischemia, and arrhythmias. Pathophysiology involves impaired function, renal dysfunction, neurohormonal activation, and fluid overload leading to congestion. Evaluation includes symptoms, vital signs, jugular vein pressure, lung sounds, and edema. Labs include BNP/NT-proBNP, troponin,
This document discusses several vascular disorders of the hepatobiliary system, including hepatic infarction, peliosis hepatis, veno-occlusive disease, portal hypertension, Budd-Chiari syndrome, ischemic hepatitis, and ischemic cholangiopathy. Hepatic infarction is a rare condition caused by compromise of both the hepatic artery and portal vein blood flows. Ischemic hepatitis results from impaired hepatic perfusion due to conditions like heart failure or sepsis. Ischemic cholangiopathy involves damage to the bile ducts from disruption of hepatic artery blood flow, such as after liver transplantation or tumors.
This document summarizes complications that can arise from cirrhosis and portal hypertension. It discusses hepatorenal syndrome, where renal failure develops due to renal vasoconstriction from advanced cirrhosis. It also covers hepatic encephalopathy, where confusion and other neurological signs appear due to liver disease. Finally, it examines portal hypertension complications like variceal bleeding, ascites, and hepatopulmonary syndrome where blood vessels in the lungs become enlarged due to high portal pressure.
This document provides an overview of heart failure, including its epidemiology, causes, pathophysiology, clinical presentation, diagnosis, and management. Heart failure is defined as the inability of the heart to pump sufficient blood to meet the body's needs. It can be caused by any condition that impairs the heart's ability to contract or relax. Management involves identifying and treating underlying causes, restricting sodium and fluid intake, using diuretics, and administering medications like ACE inhibitors, ARBs, and beta blockers to improve symptoms and outcomes.
This document provides an overview of congestive cardiac failure, including its pathophysiology, causes, clinical presentation, and treatment. It discusses how chronic heart failure results from the heart's inability to adequately pump blood to meet the needs of tissues. Common symptoms include shortness of breath, fatigue, and ankle swelling. Treatment aims to improve heart function, control secondary symptoms, and delay disease progression through drug therapy and management of underlying causes and risk factors.
Congestive heart failure is a condition where the heart is unable to pump enough blood to meet the body's needs. It affects over 20 million people worldwide and prevalence increases significantly with age. There are two main types - heart failure with reduced ejection fraction and heart failure with preserved ejection fraction. Common causes include heart attack, hypertension, and cardiomyopathies. Treatment aims to relieve symptoms, slow progression, and prevent hospitalizations through lifestyle changes, medications to reduce preload and afterload, and device-based therapies in severe cases.
Is life worth living? It depends on the liver by Dr Stephen WarrillowSMACC Conference
The document discusses critical care hepatology and management of acute and chronic liver conditions in the intensive care unit. It covers topics such as acute liver failure, decompensated chronic liver disease, abnormal liver function tests, and liver injury in multi-organ failure syndromes. Management of specific conditions is discussed, including cerebral edema in acute liver failure, variceal hemorrhage, spontaneous bacterial peritonitis, and hepatic encephalopathy. The "4H therapy" approach to preventing neurological deaths in acute liver failure using hyperventilation, hypernatremia, hemodiafiltration, and mild hypothermia is also summarized.
Heart failure is a clinical syndrome where the heart is unable to pump enough blood to meet the body's needs. It can be caused by conditions that reduce the heart's ability to contract or fill properly and common symptoms include dyspnea, fatigue, and edema. Upon presentation, patients exhibiting signs of congestion such as elevated jugular pressure, rales, and edema are treated with diuretics, while those with low blood pressure or organ dysfunction may require inotropic support or mechanical circulatory support.
Heart failure with preserved ejection fractionRajat Jain
This document provides an overview of heart failure with preserved ejection fraction (HFpEF). It defines HFpEF as heart failure with an ejection fraction above 40-50%. The document discusses the epidemiology, etiology, pathophysiology, diagnosis and treatment of HFpEF. Key points include that HFpEF is more common in older women and is associated with hypertension, obesity and diabetes. The main mechanism is diastolic dysfunction leading to impaired relaxation and increased stiffness of the left ventricle.
Cardiorenal syndromes describe disorders where dysfunction in the heart and kidneys negatively impact one another. There are 5 subtypes based on etiology and chronicity. Type 1 involves acute kidney injury secondary to heart failure. Type 2 is chronic cardiac dysfunction causing chronic kidney disease. Type 3 is acute worsening of kidney function inducing heart issues. Type 4 is primary chronic kidney disease contributing to cardiac complications. Type 5 involves systemic conditions affecting both organs. Managing cardiorenal syndromes focuses on decongestion through diuresis while preventing worsening of renal function with neurohormonal blockade.
This document provides information on heart failure, including:
1) It defines heart failure and discusses its epidemiology, types, prognosis, and basic mechanisms including systolic and diastolic dysfunction.
2) It covers left ventricular remodeling, diagnosis including biomarkers and imaging, and management of acute heart failure syndromes.
3) It discusses pharmacological treatments for chronic heart failure including vasodilators, inotropic agents, vasopressin antagonists, and diuretics.
This document discusses heart failure, providing definitions, epidemiology, classifications, etiologies, pathophysiology, clinical manifestations, diagnosis, differential diagnosis, and treatment. Heart failure is defined as a clinical syndrome resulting from structural or functional impairment of ventricular filling or ejection of blood. Approximately 2% of developed countries have heart failure, with risk increasing with age. Coronary artery disease is the leading cause. Heart failure can be classified as systolic or diastolic, high-output or low-output, acute or chronic, and right-sided or left-sided. Common causes include coronary artery disease, hypertension, cardiomyopathy, and valvular disease. Treatment involves removing precipitating causes, correcting underlying causes, preventing cardiac
Atrial fibrillation is the most common arrhythmia and becomes more prevalent with age. It is associated with increased risks of mortality, stroke, and heart failure. The estimated global prevalence is over 30 million people and is expected to rise significantly by 2030. Treatment involves rate or rhythm control, with rhythm control indicated to improve symptoms in those remaining symptomatic on rate control. Anticoagulation therapy is crucial to prevent stroke in high risk patients based on risk scores like CHA2DS2-VASc. Non-vitamin K antagonist oral anticoagulants are suitable alternatives to warfarin for stroke prevention.
This document discusses heart failure with preserved ejection fraction (HFpEF). It defines HFpEF and describes the pathophysiology as being related to diastolic dysfunction from impaired relaxation and stiffness of the left ventricle. Common causes include hypertension, coronary artery disease, and obesity. Patients typically present with signs and symptoms of congestion. Echocardiography is used to diagnose HFpEF by showing preserved ejection fraction and evidence of diastolic dysfunction. Treatment focuses on controlling hypertension, congestion with diuretics, and some evidence that ARBs and spironolactone may reduce hospitalizations for HFpEF patients.
1) Portal hypertension results from increased resistance to blood flow through the portal vein, most commonly due to cirrhosis.
2) Management of acute variceal bleeding from portal hypertension involves airway protection, volume resuscitation, antibiotics, pharmacotherapy with octreotide or vasopressin, and endoscopic ligation or sclerotherapy of the varices.
3) The mortality of variceal hemorrhage depends on the severity of liver disease and ranges from 5% for mild cirrhosis to over 50% for decompensated cirrhosis.
The document defines heart failure as a clinical syndrome characterized by typical symptoms such as breathlessness and swelling caused by structural or functional abnormalities of the heart. This results in reduced cardiac output and elevated pressures in the heart at rest or during stress. Heart failure is classified based on ejection fraction and other factors, and can involve either the left or right side of the heart. Long term, heart failure leads to neurohormonal activation and pathological remodeling of the heart muscle over time.
Anaesthesia for patients_with_liver_disease_ceaccp_2010simegnewyismaw
Patients with end-stage liver disease face high risks from anaesthesia and surgery. Their livers are impaired in processing drugs and coagulation factors, and they may have complications like ascites, gastrointestinal bleeding, and hepatic encephalopathy. Careful preoperative evaluation of liver function and other organ systems is important. During surgery, anaesthetic drug doses must be reduced and extrahepatic complications addressed. Close monitoring of liver and kidney function, fluid balance, and other vital signs is also needed.
Cardiorenal syndrome (CRS) refers to conditions where acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. CRS is classified into 5 subtypes based on pathophysiology. Type 1 involves acute cardiac failure leading to kidney injury. Type 2 involves chronic cardiac abnormalities causing progressive kidney disease. Type 3 involves primary worsening of kidney function leading to cardiac issues. Type 4 involves primary chronic kidney disease contributing to cardiac dysfunction. Type 5 involves combined cardiac and kidney dysfunction due to systemic conditions like diabetes or sepsis. Early diagnosis and treatment tailored to the CRS subtype is important for improving survival.
Dietary fiber from whole foods like grains, legumes, vegetables, and fruits has demonstrated benefits for gastrointestinal (GIT) health. Isolated and extracted fibers also show promising regulatory effects on the gut and microbiome. However, fibers have varying physicochemical properties depending on their origin and processing that influence their functional characteristics and clinical applications. More research is needed, including well-designed randomized controlled trials, to determine which fiber sources, characteristics, doses and durations optimize GIT health benefits and manage gastrointestinal disorders. Combining fibers with different physiological effects may be a promising therapeutic strategy.
- Coronaviruses typically cause common colds but SARS-CoV and MERS-CoV can cause pneumonia, respiratory failure, and death. A novel coronavirus, SARS-CoV-2, emerged in Wuhan, China in late 2019 and caused a global pandemic.
- SARS-CoV-2 spreads mainly through respiratory droplets when people cough, sneeze or talk within 6 feet of each other. Asymptomatic and pre-symptomatic people are highly infectious.
- COVID-19 symptoms range from mild to critical illness. The elderly and those with pre-existing conditions are at higher risk for severe disease. Diagnosis involves PCR testing of respiratory samples.
- Sexual dysfunction and infertility are more prevalent in men with IBD compared to the general population.
- Depression is the most consistent negative predictive factor of sexual function among men with IBD.
- Sulfasalazine can reversibly reduce male fertility, so it is recommended to discontinue 3-4 months prior to conception. Most other IBD medications do not significantly impact fertility.
- Men with IBD have an increased risk of prostate cancer and prostate cancer screening guidelines for higher risk patients should be followed.
The document summarizes a consensus clinical care pathway for women with inflammatory bowel disease (IBD) who are considering pregnancy or are pregnant. The pathway was created by an expert multidisciplinary team representing multiple societies to provide standardized, evidence-based recommendations for gastroenterology and obstetric providers to ensure healthy pregnancies for women with IBD. It addresses the lack of consistent advice available previously by compiling available data on therapeutic options for IBD that have increased over the last 15 years and putting them into an easily accessible format for clinical practice.
This document provides an overview of geriatrics and common issues in caring for elderly patients. It discusses how biological age is more important than chronological age in clinical decision making. Frailty and disability are also addressed. Common geriatric problems like falls, delirium, incontinence and adverse drug reactions are examined in terms of presentation, evaluation, and management strategies. The importance of a comprehensive assessment, considering multiple comorbidities and functional status, is emphasized in developing treatment plans for elderly patients.
Upper and lower GI endoscopies have diagnostic, therapeutic, and screening indications. For upper endoscopy, common diagnostic indications include dyspepsia in patients over age 60 or with red flags, upper GI bleeding, and dysphagia. Therapeutic uses include treatment of bleeding, removal of foreign bodies, dilation of strictures, and stenting. Screening is done for portal hypertension, Barrett's esophagus, eosinophilic esophagitis, and cancers. Lower endoscopy indications involve diagnostic evaluation of bleeding, abdominal pain, diarrhea, and screening of average-risk adults over 50 and high-risk groups. Therapeutic colonoscopy is used for polypectomy, bleeding treatment, and stricture dilation
Dr. Hiwa Abubakir and Dr. Mohamed Alshekhani discuss the management of nonvariceal gastrointestinal bleeding. They recommend endoscopy within 24 hours, or earlier for high-risk patients, to identify and treat the bleeding source. A variety of endoscopic tools can be used for hemostasis, including injection of adrenaline combined with clips, bands, electrocautery, or laser coagulation. Newer tools like over-the-scope clips are best for high-risk or recurrent bleeders. Doppler probes help ensure complete vessel occlusion. Additional prothrombotic agents or interventions may be needed in some cases.
The document discusses antithrombotic strategies for patients with diabetes who are at risk of cardiovascular events. It proposes strategies for primary prevention, stable coronary artery disease, acute coronary syndromes, ischemic stroke, peripheral artery disease, atrial fibrillation, and venous thromboembolism. More aggressive antithrombotic therapies are associated with greater reduction in recurrent cardiovascular events for patients with diabetes. However, these strategies must be weighed against the risk of bleeding. Further clinical trials are still needed to better understand optimal antithrombotic treatment for cardiovascular patients with diabetes.
1) Gastric carcinoma is the third leading cause of cancer death worldwide, with highest incidence in East Asia and parts of South America.
2) Risk factors include H. pylori infection, smoking, diet high in salted/preserved foods, and family history of gastric cancer.
3) Early detection through endoscopy in dyspeptic patients over 50 years old or with red flags can improve outcomes, as resection allows for potential cure in early gastric cancer confined to mucosa or submucosa.
This document summarizes guidelines for the diagnosis and management of irritable bowel syndrome (IBS). It defines IBS and its subtypes based on the Rome IV criteria. It recommends diagnosing IBS based on symptoms in the absence of alarm features or abnormal test results. Limited testing like fecal calprotectin can help distinguish IBS from inflammatory bowel disease. Treatment involves dietary changes, probiotics, antispasmodics, antidepressants, and targeted therapies depending on IBS subtype and predominant symptoms. For refractory cases, a multidisciplinary approach including psychological support may help manage persistent symptoms.
GIT 4th indication for upper GI endoscopy.Shaikhani.
Upper gastrointestinal endoscopy has diagnostic, therapeutic, and screening indications. Diagnostically, it is used to detect diseases causing dyspepsia like gastric cancer, investigate upper GI bleeding, diagnose dysphagia, remove foreign bodies, assess GERD, detect esophageal varices, and diagnose celiac disease. Therapeutically, it treats upper GI bleeding, removes foreign bodies, dilates strictures, treats achalasia, places stents, treats GERD, eradicates Barrett's esophagus, inserts feeding tubes, and performs bariatric procedures. Screening indications include detecting Barrett's esophagus, portal hypertension, and cancers of the esophagus and stomach in high-risk patients
The document discusses various autoimmune and cholestatic liver diseases including primary biliary cholangitis, primary sclerosing cholangitis, and intrahepatic cholestasis of pregnancy. It provides details on the epidemiology, clinical features, diagnosis, and management of these conditions. It also includes several multiple choice questions to test understanding of topics covered in the document.
1. The document outlines 19 potential mistakes that can occur during colonoscopy procedures. These include doing colonoscopies without proper indications or patient evaluation, failing to adequately prepare the colon, misdiagnosing conditions like ulcerative colitis or hemorrhoids, not performing important parts of the exam like ileal intubation or biopsies, and not adhering to quality standards. Addressing these issues can help improve safety, accuracy of diagnoses, and overall quality of colonoscopy.
This document provides an overview of inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease. It discusses risk factors, clinical manifestations, diagnostic testing, and treatment approaches. The main points are:
- IBD is characterized by idiopathic inflammation of the gastrointestinal tract. The two main types are ulcerative colitis and Crohn's disease.
- Genetic and environmental factors contribute to risk. Smoking increases risk for Crohn's but decreases risk for ulcerative colitis.
- Symptoms vary based on disease location but may include abdominal pain, diarrhea, bleeding, weight loss, and nutritional deficiencies. Extraintestinal manifestations are more common with Crohn's.
This document provides information on irritable bowel syndrome (IBS), including its definition, diagnostic criteria, subtypes, differential diagnosis, evaluation, and management approaches. Some key points:
- IBS is a common functional gastrointestinal disorder characterized by abdominal pain and altered bowel habits. It affects 10-15% of the population.
- Diagnosis is based on fulfilling the Rome symptom criteria, with subtyping based on predominant stool pattern. Additional testing is usually not needed in absence of alarm features.
- Treatment involves reassurance, dietary modifications, antispasmodics, laxatives/antidiarrheals based on subtype, and tricyclic antidepressants/SSRIs for refractory cases.
This document discusses the classical and long-term indications for PPI use, including GERD, Barrett's esophagus, use with NSAIDs, use with anti-platelets, and non-ulcer dyspepsia. For GERD, guidelines recommend daily PPI for erosive esophagitis but intermittent PPI courses may be sufficient for many patients. For Barrett's esophagus, the absolute cancer risk reduction with daily PPI is low. For NSAID and anti-platelet users at high risk of bleeding, the benefits of daily PPI are well documented. Intermittent PPI courses are often sufficient for non-ulcer dyspepsia, though some patients may require long-
This document discusses potential long-term side effects of PPI use including increased risk of dementia, chronic kidney disease, and fractures. It notes that the evidence for associations between PPI use and these conditions is not conclusive. The document advises using the lowest effective dose of PPIs for indicated conditions and avoiding long-term daily use when possible. It also stresses the importance of only prescribing PPIs for appropriate indications and discontinuing them when no clear benefit exists.
The document summarizes short-term side effects of PPIs (proton pump inhibitors), which are generally well tolerated. The most common side effects are headache, diarrhea, abdominal pain and nausea. Diarrhea appears to be related to acid suppression and the overall incidence is less than 5%, though it may be dosage and age related. PPIs are considered safe for short-term use and have similar safety profiles to H2 blockers. PPIs should be used cautiously in patients with liver disease.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
2. Overview:
• Cardiac hepatopathy: any liver damage caused by cardiac disorders
in the absence of other possible causes of liver damage.
• Cardiac hepatopathy includes congestive hepatopathy (CH) & acute
cardiogenic liver injury (ACLI).
• CH is caused by passive venous congestion of the liver that
generally occurs in the setting of chronic cardiac conditions such as
chronic HF, constrictive pericarditis, tricuspid regurgitation, or right-
sided heart failure (HF) of any cause,
• ACLI is most commonly associated with acute cardiocirculatory
failure resulting from acute myocardial infarction, acute
decompensated HF, or myocarditis.
• Acute & chronic HF may be complicated with liver damage, which
has significant implications on the patient management&underlying
heart disease outcomes.
2
3. Overview:
• Histologically:
• CH is characterized by sinusoidal dilation, replacement of
hepatocytes with red blood cells extravasating from the sinusoids,
& necrosis/apoptosis of zone 3 of the Rappaport acinus& it could
progress to cirrhosis in advanced cases.
• In ACLI, massive necrosis of zone 3 is the main histological finding.
3
4. Overview:
• Primary lab findings of:
• CH: elevated serum cholestasis markers including bilirubin, alkaline
phosphatase, γ-glutamyl-transpeptidase.
• ACLI: striking elevation in transaminase & lactate dehydrogenase.
• Both CH &ACLI have a prognostic value for identifying CV events &
mortality& have some special implications in the management of
patients undergoing ventricular assist device implantation or
cardiac transplantation.
• There is no specific treatment for CH or ACLI other than treatment
of the underlying cardiac disorder.
4
5. INTRODUCTION:
• HF, a systemic clinical syndrome with typical symptoms/signs
(dyspnea, leg swelling, PND&orthopnea) result from any structural
or functional impairment of ventricular filling or ejection
• . HF is a major health problem with significant personal&public
implications.
• 5.1 million people have HF, 50% die within 5 years of diagnosis,
despite improved survival during the recent years with some
advances in medical / device therapies.
• HF may result from congenital or acquired disorders of the
pericardium, myocardium, endocardium,heart valves, great vessels,
heart rhythm, or conduction or from certain metabolic
abnormalities.
• Disorders of the left ventricular myocardium impairing the ability of
the left ventricle (LV) to fill with or eject blood is the underlying
cause in the most. 5
6. INTRODUCTION:
• HFpEF>50% is predominantly a disease affecting older women with
hypertension with prevalence of 50% with morbidity&mortality
rates comparable with those of HFrEF<50%.
• In HF, the heart cannot deliver oxygen at a rate proportionate to
the demands of the metabolizing tissues that may result in damage
to other organ systems such as kidney, BM, or liver.
• A spectrum of liver damages from mild (LFT) abnormalities to
cardiac cirrhosis has been reported in both chronic & acute HF.
6
7. Pathophysio of liver damage in HF:
• In primary pathophysio is either:
• Chronic passive venous congestion causing congestive hepatopathy
• Or low CO & arterial hypoperfusion results in “ (ACLI)” ,Synonomes;
Ischemic hepatitis, shock liver, or hypoxic hepatopathy.
• CH generally occurs in chronic cardiac conditions increasing systemic
venous pressure as chronic HF, constrictive pericarditis, MS, TR, cor
pulmonale, severe PAHT, long-standing Fontan procedure, or right-
sided HF of any cause.
• Acute cardiogenic liver injury, is most commonly associated with
acute cardiocirculatory failure from AMI, ADHF, myocarditis, or
massive PE.
• Passive congestion secondary to right-sided HF& reduced arterial
perfusion&oxygenation due to left-sided HF often coexist&
potentiate the deleterious effects of each other on the liver.
7
8. Pathophysio of liver damage in HF:
• The liver is enlarged, tender, firm in CH.
• The main histological finding in a congestive liver is hemorrhage /
necrosis of zone 3 of the Rappaport acinus with normal or mildly
steatotic areas in zones 1 & 2.
• Because obesity, hyperlipidemia,diabetes are common risk factors
for both HF&hepatosteatosis, non-alcoholic hepatosteatosis is
frequently observed in CH patients.
• The changes in zone 3,largely depend on the transmission of
elevated systemic venous pressure to hepatic sinusoids through
hepatic vessels that result in sinusoidal dilation, replacement of
hepatocytes with red blood cells extravasating from the sinusoids,
& centrilobular tissue destruction.
• Apoptosis is the major process of cell death in chronic HF, whereas
necrotic cell death is prominent in acute HF.
8
9. Pathophysio of liver damage in HF:
• In CH, increased venous pressure also promotes ascites formation,
which is present in up to 60% of cardiac hepatopathy patients, bile
duct damage & thrombi formation in sinusoids, hepatic venules,
portal tracts.
• If congestion remains for a longer duration, these changes are
followed by the deposition of collagen to forming fibrous septa and
bridges between adjacent central veins ultimately cardiac cirrhosis.
• To date, cardiac cirrhosis, in general, is rare, but it is still important
in special patient groups such as Fontan survivors, overlooked
constrictive pericarditis&untreated severe TR.
• In contrast to primary liver disease-related cirrhosis, cardiac
cirrhosis shows a reverse lobulated pattern, in which damage is
more prominent in zone 3 than in zone 1.
9
10. Pathophysio of liver damage in HF:
• Another distinct feature of cardiac cirrhosis is the presence of a
matched distribution pattern between liver fibrosis& fibrous
obliteration of hepatic& portal veins caused by organized thrombi.
Through fibroblast activating effect of focal thrombi.
• Vascular congestion caused by HF can induce a transient increase in
liver stiffness assessed by elastography, which can mislead the
diagnosis of liver cirrhosis.
• In HF patients, the diagnosis of cardiac cirrhosis should be based on
clinical, biochemical&radiographic findings.
10
11. Pathophysio of liver damage in HF:
• Because the liver has a high metabolic activity / perfusion rate,
acute circulatory changes such as cardiogenic shock or ADHF may
result in ACLI when the liver’s compensatory mechanism of
increasing oxygen extraction from the blood (up to 95%) is being
insufficient in the setting of persistent circulatory failure.
• Hepatic blood flow declines by 10% for every 10 mmHg drop in
arterial pressure; but with this excellent compensatory mechanism,
previously healthy individuals with shock do not appear to
frequently develop liver damage frequently &all ischemic hepatitis
patients had a severe underlying cardiac disorder with passive
congestion of the liver,suggesing that a baseline hepatic congestion
is required to predispose the liver to damage induced by a
hypotensive event.
• Histologically, ACLI is characterized by necrosis of pericentral zone 3
hepatocytes, which receive poorly oxygenated blood compared to
periportal zone 1 & 2. 11
12. Clinical implications:
• Congestive hepatopathy is generally asymptomatic, but a mild
discomfort in RUQ caused by liver capsule stretching, early satiety,
nausea& anorexia is reported by some.
• Jaundice (1.2% of jaundice due to HF ), tender hepatomegaly, HJ
reflux, ascites, pulsatile liver are the main findings on PE.
• HJR: sustained rise of >3 cm in the jugular venous pressure
elucidated by the application of firm consistent pressure to the right
upper quadrant,a very useful maneuver for predicting HF.
• Pulsatile liver is generally caused by TR, TS, constrictive pericarditis,
restrictive cardiomyopathy, or pulmonary hypertension.
• Splenomegaly is present in a minority of chronic HF, but esophageal
varices are rare because of a normal hepatic venous pressure
gradient in majority.
12
13. Clinical implications:
• Acute cardiogenic liver injury is generally asymptomatic, but
nausea, vomiting, weakness, right upper quadrant pain,apathy may
be present after a latent period of 2–24 h after the acute event.
• In minority of cases, mental confusion,jaundice, flapping tremor, or
hepatic coma might develop;but mental confusion/coma generally
represent cerebral hypoxia rather than hepatic encephalopathy.
• Fulminant hepatic failure reported in rare cases of HF ,4.4% had
ischemic hepatitis.
• Only 31% had knowledge regarding their cardiac disease before
presentation,but a cardiopulmonary precipitant of hepatic ischemia
was identified in 69%&hepatic encephalopathy was found to be
associated with short-term mortality, but long-term prognosis was
largely determined by the underlying cardiac disorder.
• In another study of ALF, cardiogenic shock found in 13 with
mortality of 54% &only cardiac index was different between
survivors &non-survivors. 13
14. Clinical implications:
• In some patients with ALF, underlying cardiogenic cause may not be
so obvious at first.
• An abnormal ECG associated with cardiac murmurs should warrant
an Echo for diagnosis in patients with acute liver failure of unknown
etiology.
14
15. Acute Ischemic Hepatitis:
• Recently, the prodrome of acute ischemic hepatitis (shock liver) has
been reported in patients with cardiogenic shock ,who have acute
DIC along with symmetric peripheral gangrene or purpura
fulminans.
• Combined acral & nonacral skin necrosis (i.e.purpura fulminans)
developes.
• Before the onset of ischemic limb necrosis, acute ischemic hepatitis
(peak ALT´, severe thrombocytopenia.
• DIC shown by an elevated INR, hypofibrinogenemia (fibrinogen
nadir,, elevated APTT& greatly elevated fibrin- specific markers.
• At the onset of necrosis, the protein C activity markedly reduced.
15
16. Acute Ischemic Hepatitis:
• Protein C severely reduced& irreversible tissue necrosis evident.
• Marked thrombin generation &fibrin formation continued, as
shown by greatly elevated thrombin–antithrombin complexes /
fibrin d-dimer levels, respectively .
• Treatment with unfractionated heparin to a therapeutic level
(according to anti–factor Xa levels) was accompanied by APTT levels
of >150 seconds
• Preceding shock liver is a common finding that is observed in 90% of
critically ill patients with DIC in whom acral ischemic necrosis
develops.
16
17. Acute Ischemic Hepatitis:
• The onset of ischemic limb necrosis usually begins 2 -5 days after
the initial elevation in liver enzymes, a similar time for skin necrosis
after the initiation of warfarin therapy,presumably reflects the time
required for the development of critically low levels of protein C
when its synthesis is impaired by acute liver dysfunction or
warfarin.
• Some implicate hypotension requiring vasopressors (e.g. dopamine,
noradrenaline,or phenylephrine5) in the pathogenesis of symmetric
peripheral gangrene.
• In parallel with the role of DVT in predisposing the patient to
warfarin-associated microthrombosis in the same limb with large-
DVT, it seems plausible that hypotension& vasopressors, by
reducing blood flow into the distal extremities, could predispose
the patient with DIC to acral microthrombosis.
17
21. Lab implications:
• In CH, primary laboratory findings are elevated serum cholestasis
markers including bilirubin,SAP),GGT.
• ALT&AST generally show mild elevations up to 2-3 times the normal
• A mild decrease in albumin (in 25%) &a slight increase in
prothrombin time are also frequent in CH.
• Increase in liver function tests are more strongly correlated with
decreased cardiac index, increased filling pressures& severe TR.
• Elevated GGT 43% in men,48% in women ,total bilirubin 17% in men
, 8% in women.
• Both GGT & TSB found to be associated with disease severity, but
only GGT is independently associated with adverse outcomes.
• TSB is above the upper limit of normal in 13%.
• After adjustment for other variables, only TSB was independently
associated with morbidity & mortality.
• 21
22. Lab implications:
• Abnormal LFTs are markedly associated with mortality, but AST/ TSB
show the highest association.
• AP &GGT are independent predictors of death from any cause.
• TSB, AP,GGT independently correlate with functional class and
clinical signs of HF including jugular venous distention, TR,
peripheral edema.
• TSB was independent marker for right ventricular failure & LVAD
implantation&it is a component of risk models for adverse
outcomes after LVAD implantation or cardiac transplantation
• Hypoalbuminemia, mainly caused by HF-associated systemic
inflammation, is another prognostic marker in acute & chronic HF
• Hypoalbuminemia has a prognostic value in LVAD& is a component
of risk models.
22
23. Lab implications:
• The ascites associated with chronic HF also has distinct features that
may aid in making the differential diagnosis.
• Cardiac ascites has high protein content (usually≥2.5g/dL) and high
serum ascites albumin gradient (>1.1g/dL) due to preserved
synthetic function of the liver.
• Red blood cell counts &LDH are also higher in cardiac ascites than in
cirrhotic ascites of other causes due to the extravasation of red
blood cells into the ascites with resultant lysis.
• In the differential diagnosis, another useful marker is serum or
ascites NT-proBNP&both serum &ascites NT-proBNP have high
sensitivity / specificity in predicting HF as the cause of ascites.
• Both ACC &ESC HFGuidelines recommend the inclusion of LFTs in
the diagnostic workup of all patients presenting with HF.
•
23
24. Lab implications:
• The typical laboratory finding of ACLI is the presence of a striking
elevation in transaminase &LDH (generally to 10-20 times the
normal values, even up to 2000-fold).
• Transaminases&LDH reach their peak 1-3 days after the acute event
&return to normal limits within 7-10 days if the patient’s
hemodynamics recover.
• In ACLI, an early& rapid increase of LDH in parallel with
transaminases, a ratio of ALT to LDH <1.5&decrease in ALT by > 50%
within 72 h are characteristic findings that can be useful in the
differential diagnosis of acute viral, alcoholic, or drug-induced
hepatitis .
• Other lab findings are mild elevations of TSB, AP &PT.
• Aabnormal transaminases, low albumin& elevated TSB have a
prognostic value for mortality.
24
25. Management:
• There is no specific treatment of CH other than the treatment of the
underlying cardiac disease.
• In symptomatic HFrEF patients, diuretics are recommended to
reduce fluid retention&improve symptoms.
• Advanced liver dysfunction may have a negative impact on renal
function (hepato-renal syndrome) by way of splanchnic
vasodilatation resulting in arterial underfilling&renal
vasoconstriction
• In chronic HF, liver congestion may directly contribute to impaired
natriuresis.
• Liver congestion, ascites,jaundice may improve with diuretics
therapy, but in refractory cases, combination therapy with diuretics
paracentesis, ultrafiltration, or peritoneal dialysis may be needed.
• Paracentesis results in a reduction of elevated intraabdominal
pressure with corresponding improvement in renal function. 25
26. Management:
• ACEI or ARBs in ACE inhibitor intolerant & beta blockers are
recommended in all symptomatic HFrEF, unless contraindicated to
reduce morbidity and mortality
• Low-dose mineralocorticoid receptor antagonists (MRAs) are also
recommended in symptomatic HFrEF patients with an estimated
glomerular filtration rate>30 mL/min/1.73 m2&potassium<5.0
mEq/L to reduce morbidity / mortality.
• In HF patients, MRAs are used in low doses (spironolactone up to 50
mg/day); however, in cirrhosis, natriuretic doses of MRAs
(spironolactone up to 400 mg) are recommended as the main
therapy to produce a negative sodium balance.
• In suitable refractory HF patients’ cardiac resynchronization
therapy, LVAD, or cardiac transplantation are recommended.
26
27. Management:
• Cardiac transplantation/ LVAD implantation can improve abnormal
LFTs, but if there is a strong suspicion of advanced liver disease,
cirrhosis must be ruled out before the cardiac transplantation or
combined liver-heart transplantation is performed in suitable cases.
• In HFpEF, no treatment has shown reduction in morbidity/mortality
• Diuretics; controlling systolic/diastolic HT, particularly with ACEI or
ARBs; coronary revascularization; & AF management are
recommended in suitable HFpEF patients to relieve symptoms.
• In ACLI, restoration of CO&hemodynamics is the primary goal.
• Ventilator support, inotropes/vasopressors, cor recanalization,
mechanical circulatory support should be used in suitable patients.
• LFTs should be monitored for recovery.
• Seralaxin (recombinant human relaxin-2)improved LFTs in acute HF,
which is consistent with more effective prevention of organ
damage 27
28. Cardiac hepatopathy&cardiovascular drugs:
• The liver, metabolizes many cardiovascular drugs in contrast to the
kidney
• Although there are no rules for the modification of drug dosage in
the cases of liver dysfunction,because none of the LFT
abnormalities sufficiently correlate with the degree of alterations in
hepatic drug metabolism ,but it is suggested that individual
pharmacokinetic profile of the drug should be considered for the
modification of drug dosage.
28