The document discusses liver pathology and hepatic failure. It covers the following key points:
1. The liver has many important functions including digestion, detoxification, regulation of hemostasis and metabolism.
2. Liver failure can occur due to various causes such as infections, toxins, physical impacts, nutritional factors, and blood flow disturbances.
3. Liver failure disrupts the liver's functions and can cause jaundice, coagulation problems, and accumulation of toxic substances leading to further health issues if not addressed. Timely treatment is important.
The document discusses diseases of the liver and bile excretory system. It notes that technological advances and negative environmental changes have led to an increase in the frequency and spread of liver and bile tract diseases. Urbanization, lack of exercise, and alcoholism have also contributed considerably to increased rates of hepatitis, cirrhosis of the liver, cholelithiasis, and cholecystitis. The chemicalization of industry, agriculture, and medicine has further increased the frequency of toxic and medicinal liver damage. Sharp rises in medical procedures and blood transfusions have also stimulated increased morbidity from serum hepatitis.
The document discusses the many functions of the liver, including intermediary metabolism of proteins, carbohydrates, and lipids; production of coagulation factors; bilirubin metabolism; endocrine, immune, and drug metabolism functions. It then describes evaluation of liver function through tests of hepatocellular injury like ALT and AST, hepatic protein synthesis by measuring albumin and prothrombin time, and tests for cholestatic or specific liver diseases.
Hepatic failure occurs when liver functions decrease below the level needed for homeostasis. It can be classified as absolute, relative, partial or total, and acute or chronic. Hepatic failure results from hepatocellular damage, cholestasis, or vascular issues. Signs include disturbances in carbohydrate, lipid, protein, vitamin, and toxin metabolism. Progressive hepatic failure can lead to hepatic coma, where toxic substances accumulate in the brain. Jaundice is a condition of high bilirubin in the blood and tissues, and can be hemolytic, mechanical, or hepatogenous.
Correlation liver disfunction and infection disease (dengue typhoid fever)01mataharitimoer MT
Correlation Liver Disfunction and Infection Disease (Dengue and Typhoid Fever)
Dr Erwin, SpPD, FINASIM
Disampaikan pada acara PIT VI IDI Kota Bogor | 9 Nopember 2013
The document discusses the anatomy, histology, functions and common pathologies of the liver. Key points include:
- The liver has four lobes and receives dual blood supply from the hepatic artery and portal vein. It performs many metabolic and synthetic functions.
- Common liver diseases include viral hepatitis, alcoholic liver disease and cirrhosis. Cirrhosis results from chronic liver injury and scarring that disrupts the liver architecture.
- Primary liver cancers like hepatocellular carcinoma often arise in the setting of chronic liver disease and cirrhosis. Treatment options are limited but may include transplantation or resection in early stages.
The document discusses various patterns of hepatic injury and diseases of the liver. It describes the functions of the liver and different types of necrosis, inflammation, and fibrosis that can occur from injury. Specific conditions discussed include alcoholic liver disease, cirrhosis, portal hypertension, jaundice, and several hereditary conditions involving hyperbilirubinemia.
The document discusses diseases of the liver and bile excretory system. It notes that technological advances and negative environmental changes have led to an increase in the frequency and spread of liver and bile tract diseases. Urbanization, lack of exercise, and alcoholism have also contributed considerably to increased rates of hepatitis, cirrhosis of the liver, cholelithiasis, and cholecystitis. The chemicalization of industry, agriculture, and medicine has further increased the frequency of toxic and medicinal liver damage. Sharp rises in medical procedures and blood transfusions have also stimulated increased morbidity from serum hepatitis.
The document discusses the many functions of the liver, including intermediary metabolism of proteins, carbohydrates, and lipids; production of coagulation factors; bilirubin metabolism; endocrine, immune, and drug metabolism functions. It then describes evaluation of liver function through tests of hepatocellular injury like ALT and AST, hepatic protein synthesis by measuring albumin and prothrombin time, and tests for cholestatic or specific liver diseases.
Hepatic failure occurs when liver functions decrease below the level needed for homeostasis. It can be classified as absolute, relative, partial or total, and acute or chronic. Hepatic failure results from hepatocellular damage, cholestasis, or vascular issues. Signs include disturbances in carbohydrate, lipid, protein, vitamin, and toxin metabolism. Progressive hepatic failure can lead to hepatic coma, where toxic substances accumulate in the brain. Jaundice is a condition of high bilirubin in the blood and tissues, and can be hemolytic, mechanical, or hepatogenous.
Correlation liver disfunction and infection disease (dengue typhoid fever)01mataharitimoer MT
Correlation Liver Disfunction and Infection Disease (Dengue and Typhoid Fever)
Dr Erwin, SpPD, FINASIM
Disampaikan pada acara PIT VI IDI Kota Bogor | 9 Nopember 2013
The document discusses the anatomy, histology, functions and common pathologies of the liver. Key points include:
- The liver has four lobes and receives dual blood supply from the hepatic artery and portal vein. It performs many metabolic and synthetic functions.
- Common liver diseases include viral hepatitis, alcoholic liver disease and cirrhosis. Cirrhosis results from chronic liver injury and scarring that disrupts the liver architecture.
- Primary liver cancers like hepatocellular carcinoma often arise in the setting of chronic liver disease and cirrhosis. Treatment options are limited but may include transplantation or resection in early stages.
The document discusses various patterns of hepatic injury and diseases of the liver. It describes the functions of the liver and different types of necrosis, inflammation, and fibrosis that can occur from injury. Specific conditions discussed include alcoholic liver disease, cirrhosis, portal hypertension, jaundice, and several hereditary conditions involving hyperbilirubinemia.
The document discusses patterns of hepatic injury including degeneration, intracellular accumulation, necrosis, apoptosis, inflammation, fibrosis, and failure. Specific types of liver disease are also examined such as alcoholic liver disease which can cause steatosis, hepatitis, and cirrhosis due to effects of alcohol metabolism including induction of cytochrome P450 and increased lipid biosynthesis. Chronic alcohol intake over many years can lead to severe and irreversible liver injury.
The document provides an overview of liver disease, including:
1) Jaundice and cholestasis which can occur due to increased bilirubin production, decreased uptake by hepatocytes, or impaired excretion.
2) Liver failure which can be acute or chronic, and results in hepatic encephalopathy, coagulopathy, and other systemic effects.
3) Cirrhosis, defined as diffuse liver scarring leading to regenerative nodules and altered vasculature, with complications including liver failure, portal hypertension, ascites, and hepatocellular carcinoma.
The document discusses various laboratory tests used to evaluate liver function and disease. It describes tests for hepatocellular damage like ALT and AST, tests for cholestasis like alkaline phosphatase, and tests for liver synthetic function like albumin. Common causes of abnormal liver enzymes are also summarized, along with risk factors for liver disease.
This document provides information on liver function tests. It begins with an overview of liver anatomy and functions including synthesis, metabolism, and excretion. It then discusses specific tests that evaluate these hepatic functions and their clinical implications. Details are provided on liver zonation and regeneration. Key proteins and enzymes synthesized by the liver are outlined. Metabolic functions like ammonia, carbohydrate, and xenobiotic metabolism are reviewed. Inherited disorders of bilirubin metabolism that can cause jaundice are also summarized.
1. Acute renal failure is a sudden deterioration of kidney function that results in the build up of waste products in the body. It can be caused by decreased blood flow to the kidneys, direct kidney damage, or urinary tract obstruction.
2. The kidneys normally maintain fluid and electrolyte balance and remove waste. In acute renal failure, the kidneys are unable to perform these functions. This leads to fluid, electrolyte, and acid-base imbalances.
3. Acute renal failure is classified as prerenal, intrarenal, or postrenal depending on the underlying cause. Prerenal causes decrease blood flow, intrarenal causes direct damage, and postrenal causes
This document discusses liver function and the impact of liver disease on anesthesia. It covers the key roles of the liver, signs of impaired function, and how disease affects drug metabolism, cardiovascular and pulmonary systems. Risk is assessed using Child-Pugh scoring. For patients undergoing surgery, careful fluid management, blood product administration, and hemodynamic stability are emphasized to reduce risk according to their liver disease severity.
This document provides an overview of liver anatomy and functions, as well as causes, classifications, and features of various hepatic disorders. Key points include:
- The liver's main functions are metabolism, protein synthesis, storage, detoxification, and bile production. It receives dual blood supply from the hepatic artery and portal vein.
- Liver diseases can be investigated through biochemical, hematological, immunological, and imaging tests as well as biopsy. Morphological patterns of injury include degeneration, necrosis, inflammation, regeneration, and fibrosis.
- Jaundice and cholestasis result from increased bilirubin production, decreased uptake/conjugation, or impaired excretion. They can be pre-hep
The document discusses specific types of toxicity including hematotoxicity, hepatotoxicity, and nephrotoxicity. It provides details on the targets and mechanisms of toxicity for each organ system. For example, it explains that the liver is highly susceptible to toxicants due to its rich supply of phase I and II enzymes involved in metabolizing substances. It also notes two classes of nephrotoxic chemicals - heavy metals and halogenated hydrocarbons - that are common occupational hazards. The document aims to educate students on the toxic effects of chemicals on different body systems.
The document discusses chronic liver disease and the progression from fibrosis to cirrhosis. It explains that cirrhosis is defined as the development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury. The key causes of cirrhosis mentioned include viral hepatitis, alcohol, autoimmune conditions, and genetic disorders. The role of hepatic stellate cells in the development of fibrosis through excess collagen deposition is also outlined.
The kidneys perform several important functions including regulating electrolyte, water, and acid-base balance; controlling blood pressure; and excreting waste. Glomerular damage can occur through immune complex deposition or formation of antibodies against glomerular basement membrane antigens. This elicits inflammation and injury through activation of leukocytes, complement system, and cytokines. Tubular dysfunction impairs reabsorption and can manifest as issues like aminoaciduria or proximal/distal tubular acidosis. Disorders are evidenced by changes in urine characteristics such as proteinuria, hematuria, electrolyte abnormalities, and alterations in specific gravity.
This document provides an overview of acute pancreatitis, including:
1. It discusses the pathophysiology of acute pancreatitis, including local effects within the pancreas and general systemic effects involving multiple organ systems.
2. The most common causes of acute pancreatitis are gallstones and alcohol consumption. Radiology findings and severity scores can help assess prognosis.
3. Treatment involves pain relief, fluid resuscitation for shock, and monitoring for complications like necrosis which may require drainage or necrosectomy.
Liver failure occurs when the liver rapidly loses its ability to function, resulting in mental status changes and coagulation abnormalities. It can be caused by viral hepatitis, drug toxicity, toxins, vascular issues, or metabolic diseases. Acute liver failure presents as a sudden onset of severe liver injury in someone without pre-existing liver disease. It requires emergency treatment and may necessitate a liver transplant if liver function cannot be reversed. Management involves supportive care, medications to treat complications, and sometimes a liver transplant.
Alcoholic liver disease is a spectrum of liver injury caused by alcoholism that progresses through three stages - alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Chronic excessive alcohol consumption leads to fatty liver in over 90% of alcoholics and can progress to hepatitis and cirrhosis over 10 years. Risk factors include drinking patterns, gender, malnutrition, infections, genetic factors, and hepatitis B or C coinfection. The pathogenesis involves direct hepatotoxicity of ethanol and its metabolites like acetaldehyde, oxidative stress, inflammation, and activation of hepatic stellate cells causing fibrosis. Laboratory findings include elevated liver enzymes, hyperbilirubinemia, and coagulation abnormalities.
This document provides an overview of liver anatomy, functions, and diseases. It describes the liver's structure including liver cells, bile drainage system, and blood supply. The liver's key functions are metabolism, protein synthesis, storage, detoxification, and bile production. Investigation of liver diseases includes blood tests, imaging, and biopsy. Common liver diseases discussed are jaundice, cholestasis, liver failure, and cirrhosis. Cirrhosis is the end-stage of chronic liver disease and can result from infections, toxins, autoimmune conditions, and other etiologies.
This document discusses anemic syndrome, including its causes, signs and symptoms, classifications, and complications. Key points include:
- Anemic syndrome is defined as a decrease in circulating hemoglobin below normal values and can be caused by decreased red blood cell production or increased red blood cell destruction/loss.
- Causes of decreased production include bone marrow diseases/damage, low erythropoietin from kidney/liver disease, and deficiencies in iron, B12, or folic acid.
- Increased destruction can be from bleeding, hemolytic anemias due to physical/chemical/biological factors, or corpuscular issues like enzyme deficiencies.
- Complications arise from tissue hypoxia
Este documento describe la anatomía de los vasos sanguíneos de la parte inferior de la pierna. Resume las principales arterias de la pierna, incluyendo la femoral, poplítea, tibial posterior y anterior. También describe las ramificaciones de estas arterias y las redes vasculares que forman en la rodilla, los tobillos y el pie.
NEUROLEUKEMIA
Neuroleukemia is a potentially life-threatening complication in some acute myeloid leukemia cases if the central nervous system is not protected with initial therapy. Pathological lesions include infiltration by leukemia cells, hemorrhage, and demyelination. Symptoms include intracranial hemorrhage and hyperviscosity syndrome. Treatment involves systemic chemotherapy with cytarabine and anthracyclines, and neuroprophylaxis with intrathecal methotrexate or cytarabine injections to prevent central nervous system involvement.
The document discusses patterns of hepatic injury including degeneration, intracellular accumulation, necrosis, apoptosis, inflammation, fibrosis, and failure. Specific types of liver disease are also examined such as alcoholic liver disease which can cause steatosis, hepatitis, and cirrhosis due to effects of alcohol metabolism including induction of cytochrome P450 and increased lipid biosynthesis. Chronic alcohol intake over many years can lead to severe and irreversible liver injury.
The document provides an overview of liver disease, including:
1) Jaundice and cholestasis which can occur due to increased bilirubin production, decreased uptake by hepatocytes, or impaired excretion.
2) Liver failure which can be acute or chronic, and results in hepatic encephalopathy, coagulopathy, and other systemic effects.
3) Cirrhosis, defined as diffuse liver scarring leading to regenerative nodules and altered vasculature, with complications including liver failure, portal hypertension, ascites, and hepatocellular carcinoma.
The document discusses various laboratory tests used to evaluate liver function and disease. It describes tests for hepatocellular damage like ALT and AST, tests for cholestasis like alkaline phosphatase, and tests for liver synthetic function like albumin. Common causes of abnormal liver enzymes are also summarized, along with risk factors for liver disease.
This document provides information on liver function tests. It begins with an overview of liver anatomy and functions including synthesis, metabolism, and excretion. It then discusses specific tests that evaluate these hepatic functions and their clinical implications. Details are provided on liver zonation and regeneration. Key proteins and enzymes synthesized by the liver are outlined. Metabolic functions like ammonia, carbohydrate, and xenobiotic metabolism are reviewed. Inherited disorders of bilirubin metabolism that can cause jaundice are also summarized.
1. Acute renal failure is a sudden deterioration of kidney function that results in the build up of waste products in the body. It can be caused by decreased blood flow to the kidneys, direct kidney damage, or urinary tract obstruction.
2. The kidneys normally maintain fluid and electrolyte balance and remove waste. In acute renal failure, the kidneys are unable to perform these functions. This leads to fluid, electrolyte, and acid-base imbalances.
3. Acute renal failure is classified as prerenal, intrarenal, or postrenal depending on the underlying cause. Prerenal causes decrease blood flow, intrarenal causes direct damage, and postrenal causes
This document discusses liver function and the impact of liver disease on anesthesia. It covers the key roles of the liver, signs of impaired function, and how disease affects drug metabolism, cardiovascular and pulmonary systems. Risk is assessed using Child-Pugh scoring. For patients undergoing surgery, careful fluid management, blood product administration, and hemodynamic stability are emphasized to reduce risk according to their liver disease severity.
This document provides an overview of liver anatomy and functions, as well as causes, classifications, and features of various hepatic disorders. Key points include:
- The liver's main functions are metabolism, protein synthesis, storage, detoxification, and bile production. It receives dual blood supply from the hepatic artery and portal vein.
- Liver diseases can be investigated through biochemical, hematological, immunological, and imaging tests as well as biopsy. Morphological patterns of injury include degeneration, necrosis, inflammation, regeneration, and fibrosis.
- Jaundice and cholestasis result from increased bilirubin production, decreased uptake/conjugation, or impaired excretion. They can be pre-hep
The document discusses specific types of toxicity including hematotoxicity, hepatotoxicity, and nephrotoxicity. It provides details on the targets and mechanisms of toxicity for each organ system. For example, it explains that the liver is highly susceptible to toxicants due to its rich supply of phase I and II enzymes involved in metabolizing substances. It also notes two classes of nephrotoxic chemicals - heavy metals and halogenated hydrocarbons - that are common occupational hazards. The document aims to educate students on the toxic effects of chemicals on different body systems.
The document discusses chronic liver disease and the progression from fibrosis to cirrhosis. It explains that cirrhosis is defined as the development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury. The key causes of cirrhosis mentioned include viral hepatitis, alcohol, autoimmune conditions, and genetic disorders. The role of hepatic stellate cells in the development of fibrosis through excess collagen deposition is also outlined.
The kidneys perform several important functions including regulating electrolyte, water, and acid-base balance; controlling blood pressure; and excreting waste. Glomerular damage can occur through immune complex deposition or formation of antibodies against glomerular basement membrane antigens. This elicits inflammation and injury through activation of leukocytes, complement system, and cytokines. Tubular dysfunction impairs reabsorption and can manifest as issues like aminoaciduria or proximal/distal tubular acidosis. Disorders are evidenced by changes in urine characteristics such as proteinuria, hematuria, electrolyte abnormalities, and alterations in specific gravity.
This document provides an overview of acute pancreatitis, including:
1. It discusses the pathophysiology of acute pancreatitis, including local effects within the pancreas and general systemic effects involving multiple organ systems.
2. The most common causes of acute pancreatitis are gallstones and alcohol consumption. Radiology findings and severity scores can help assess prognosis.
3. Treatment involves pain relief, fluid resuscitation for shock, and monitoring for complications like necrosis which may require drainage or necrosectomy.
Liver failure occurs when the liver rapidly loses its ability to function, resulting in mental status changes and coagulation abnormalities. It can be caused by viral hepatitis, drug toxicity, toxins, vascular issues, or metabolic diseases. Acute liver failure presents as a sudden onset of severe liver injury in someone without pre-existing liver disease. It requires emergency treatment and may necessitate a liver transplant if liver function cannot be reversed. Management involves supportive care, medications to treat complications, and sometimes a liver transplant.
Alcoholic liver disease is a spectrum of liver injury caused by alcoholism that progresses through three stages - alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Chronic excessive alcohol consumption leads to fatty liver in over 90% of alcoholics and can progress to hepatitis and cirrhosis over 10 years. Risk factors include drinking patterns, gender, malnutrition, infections, genetic factors, and hepatitis B or C coinfection. The pathogenesis involves direct hepatotoxicity of ethanol and its metabolites like acetaldehyde, oxidative stress, inflammation, and activation of hepatic stellate cells causing fibrosis. Laboratory findings include elevated liver enzymes, hyperbilirubinemia, and coagulation abnormalities.
This document provides an overview of liver anatomy, functions, and diseases. It describes the liver's structure including liver cells, bile drainage system, and blood supply. The liver's key functions are metabolism, protein synthesis, storage, detoxification, and bile production. Investigation of liver diseases includes blood tests, imaging, and biopsy. Common liver diseases discussed are jaundice, cholestasis, liver failure, and cirrhosis. Cirrhosis is the end-stage of chronic liver disease and can result from infections, toxins, autoimmune conditions, and other etiologies.
This document discusses anemic syndrome, including its causes, signs and symptoms, classifications, and complications. Key points include:
- Anemic syndrome is defined as a decrease in circulating hemoglobin below normal values and can be caused by decreased red blood cell production or increased red blood cell destruction/loss.
- Causes of decreased production include bone marrow diseases/damage, low erythropoietin from kidney/liver disease, and deficiencies in iron, B12, or folic acid.
- Increased destruction can be from bleeding, hemolytic anemias due to physical/chemical/biological factors, or corpuscular issues like enzyme deficiencies.
- Complications arise from tissue hypoxia
Este documento describe la anatomía de los vasos sanguíneos de la parte inferior de la pierna. Resume las principales arterias de la pierna, incluyendo la femoral, poplítea, tibial posterior y anterior. También describe las ramificaciones de estas arterias y las redes vasculares que forman en la rodilla, los tobillos y el pie.
NEUROLEUKEMIA
Neuroleukemia is a potentially life-threatening complication in some acute myeloid leukemia cases if the central nervous system is not protected with initial therapy. Pathological lesions include infiltration by leukemia cells, hemorrhage, and demyelination. Symptoms include intracranial hemorrhage and hyperviscosity syndrome. Treatment involves systemic chemotherapy with cytarabine and anthracyclines, and neuroprophylaxis with intrathecal methotrexate or cytarabine injections to prevent central nervous system involvement.
This document summarizes hormonal drugs and their uses. It discusses the classification of hormones, hypothalamic factors that control pituitary hormone release, and preparations of hormones from the anterior and posterior pituitary lobes. It also covers thyroid hormone preparations and their use in hypothyroidism, antithyroid drugs and their mechanisms of action, calcitonin, insulin preparations and their mechanisms of action, oral hypoglycemic drugs for diabetes, and steroid hormones from the adrenal cortex and their effects.
The document summarizes the pathophysiology of the digestive system. It discusses:
1) The regulation and components of the digestive system including afferent links, the CNS, and effectors.
2) The main functions of the digestive tract including digestion, bactericidal function, and regulation of acid-base balance.
3) Common causes of digestive disturbances including physical, biological, chemical factors as well as diseases that can affect the organs of the digestive system.
This document discusses disorders of hemostasis, including excessive bleeding disorders and hypercoagulability states. It describes tests used to evaluate hemostasis such as prothrombin time, partial thromboplastin time, and platelet counts. Vascular disorders that can cause bleeding are discussed as well as inherited and acquired bleeding disorders involving platelets or coagulation factors. Specific disorders covered include hemophilia A, hemophilia B, von Willebrand disease, disseminated intravascular coagulation, and thrombocytopenia. Causes and complications of various bleeding and thrombotic disorders are summarized.
This document discusses the pathophysiology of cardiovascular system arterial hypertension. It begins by outlining the relevance and prevalence of hypertension as a major health problem. It then describes the main mechanisms that regulate arterial pressure in the immediate, middle, and late term, including baroreceptor and chemoreceptor responses, the renin-angiotensin system, vasopressin secretion, and renal control of fluid volume. Secondary forms of hypertension are discussed which are caused by renal, endocrine, or neurogenic factors. Primary or essential hypertension is described as being caused by genetic and environmental risk factors that disrupt the balance of pressor and depressor influences on the cardiovascular system. Several theories of its pathogenesis are mentioned involving the brain, kid
1-4syndromes in Disorders of the Respiratory .pptxMeghanaPreddy
The document summarizes several basic clinical syndromes related to disorders of the respiratory organs. It describes the key symptoms, signs, and diagnostic findings for bronchial obstruction, infiltrative consolidation of the pulmonary tissue, atelectasis, pulmonary emphysema, fluid accumulation in the pleural cavity, pneumothorax, and respiratory failure syndrome. For each syndrome, it provides details on inspection, palpation, percussion, and auscultation findings, as well as results of supplementary diagnostic techniques like radiography and spirometry.
This document discusses hypoxia, or low oxygen levels. It begins by classifying hypoxia based on its causes, such as respiratory hypoxia from issues with oxygen diffusion or ventilation. It then describes the urgent reactions in response to hypoxia, including increased heart rate and blood flow. Finally, it outlines the permanent compensations that develop over time to hypoxia, such as increased capillaries and mitochondria, more efficient oxygen use, and adaptations in metabolic and cardiovascular systems to optimize function with low oxygen.
This document discusses hypoxia, or low oxygen levels. It begins by classifying hypoxia based on its causes, such as respiratory hypoxia caused by issues in oxygen diffusion or ventilation. It then describes the urgent reactions of body systems to hypoxia, such as increased heart rate and blood flow. Over time, permanent compensations develop, including growing more mitochondria and capillaries to improve oxygen use, and adaptations in metabolic and hormonal responses to be more efficient with less oxygen. The document provides detailed explanations of how cardiovascular, respiratory, blood, nervous and endocrine systems compensate for long-term hypoxic conditions.
The document discusses cancer and its causes. It defines cancer as uncontrolled cell growth that forms tumors. Some key points:
- Cancer is caused by genetic and environmental factors like tobacco use, infections, diet, obesity, and radiation.
- A healthy diet high in plants and fiber and low in red meat and processed foods can help prevent cancer. Avoiding tobacco, excessive alcohol, grilling meats, and exposure to pollutants also reduces risk.
- Early cancer often has no symptoms, so screening like mammograms and colonoscopies can find cancers early. Diagnosis involves scans, biopsies, and molecular tests to identify abnormal cells.
- Making lifestyle changes around diet, exercise,
This document discusses microbial pathogenesis and infection. It begins by defining key concepts like infection, infective process, and infection disease. It then describes the normal relationships between microorganisms and the human body, including symbiosis, commensalism, mutualism, and parasitism. The document goes on to classify microbial parasitism and characterize the spread of infection through reservoirs, transmission routes, and vectors. It also examines the infectious process, virulence factors that promote microbial growth, and the roles of exotoxins and endotoxins produced by pathogens.
This document summarizes the body's responses to hypoxia, or low oxygen levels. It describes the immediate, urgent reactions of key systems to hypoxia, including increased heart rate and blood flow. It then outlines the long-term, permanent compensations the body makes, such as growing more mitochondria and capillaries to improve oxygen use and delivery. The body also makes metabolic and hormonal adaptations to optimize energy production and use oxygen more efficiently despite low oxygen levels.
Treponema are spiral shaped bacteria that can cause diseases like syphilis. Treponema pallidum specifically causes syphilis, which has three stages - primary, secondary, and tertiary syphilis. Primary syphilis involves a sore called a chancre, secondary syphilis has rashes and skin lesions, and tertiary syphilis can involve damage to internal organs. Syphilis is diagnosed through microscopic examination of samples or serological tests that detect antibodies against Treponema, with the fluorescent treponemal antibody absorption test and Treponema pallidum haemagglutination test being specific confirmatory tests.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
How to Build a Module in Odoo 17 Using the Scaffold MethodCeline George
Odoo provides an option for creating a module by using a single line command. By using this command the user can make a whole structure of a module. It is very easy for a beginner to make a module. There is no need to make each file manually. This slide will show how to create a module using the scaffold method.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
3. The hepatic functions
. 1. A participation in the digestion – the
hepatic produces bile acids which
emulsify lipids in an intestine,
activate the enzymes of a pancreas
(a lipase), a fermentation and a
absorption of liposoluble
substances (Vit. A,D,E,K).
2. A deintoxication – in a liver we can
observe a formation of nontoxic
tandem connection with glukuronic
and sulphuric acids; an inactivation of
the ammonia, the indole, the
skatoles, the phenols and other
connection arriving from a GIT
(gastrointestinal tract) and from the
outside.
3. A regulation of a hemostasis
system maintains the equilibrium (a
contents and an activity) – the factors
by a blood coagulation and a blood
anticoagulation systems.
3
4. The hepatic functions
4
4. A metabolism regulation:
of a carbohydrates – the participation in a
glycogenesis and in a glycogenolysis, in a
gluconeogenesis.
of a lipids exchange, the oxidation of lipid
acids, a formation of ketone bodies.
a protein metabolism – the synthesis of
proteins, including a plasma, their deposition,
their transamination and their deamination, an
synthesis of an urea and a creatine.
a synthesis of the majority of the enzymes
providing a metabolism
a deposition and an exchange of many
vitamins (A, PP, D, B, K), a deposition of iron
ions, of a copper, of a zinc, of a manganese,
of a molybdenum.
5. A hemopoiesis at a fetus
6. A participation in reactions of the immune
system, because in a liver there are the
phagocytes of Kupffer.
7. The biliation.
4
5. The general etiology of hepatic diseases
Infectious hepatic damages (viruses, protozoa, bacteria, helminths, mushrooms).
Toxic hepatic damages – the effect of hepatotoxic substances (polycyclic
aromatic hydrocarbons, chlorine - and organophosphorous pesticides, the
ethanol and its substitutes, Phenolums, the bonds of phosphorus, salts of heavy
metals, CCl4, the toxins of a plant origin (a death angel), the hepatotoxic
medicines: anesthetics (Chloroformium), psychoactive (Aminazine), non-narcotic
analgesics (Indomethacinum, Paracetamolum), the antituberculous drugs.
Physical impacts (radiation, mechanical damages).
Nutritional factors (the rising of consumption of animal fats, the deficiency of the
lipotropic factors and proteins).
Disturbance of a liver blood flow: local (a clottage of a liver artery, portal vein,
cirrhosis) and systemic.
Endocrine disorders – are followed by a metabolic disorder (diabetes mellitus,
thyrotoxicosis, etc.)
Tumors (primary and metastasises).
Congenital defects – anomalies of hepatic development (cavernomatosis of a
vena portae), the disturbance of a metabolism (glycogenoses), heriditary enzyme
defect.
Autoimmune processes in a liver.
5
6. The liver failure
The liver failure is the
typical pathological
process which is
characterized by
permanent disturbance of
one, several or all
functions of a liver that is
followed by the
disturbance of vital
organism activity.
6
7. The liver failure forms are alocated
1. by origin:
hepatocellular - primary damage of hepatocytes
shunting (collateral) is the disturbance of blood current
in a liver, i.e. its dumping on the portacaval
anastomoses into the general blood circulation
2. by the quickness of its emergence and its
development:
fulminant
acute
chronic
3. by the damage scale:
partial
total
4.by the reversibility of hepatocytes damage:
reversible
irreversible 7
8. The main reasons of a liver
failure
1-hepatic: the failure caused by the
processes localized in a liver and
biliary tracts:
A) hepatitises (virus, bacterial,
toxic)
B) hepatoses (dystrophias)
C) cirrhosis
D) tumors
E) parasitogenic damages
E) genetic defects
G) stones, inflammatory processes
of the biliary tracts
2-extrahepatic pathological
processes:
A) a shock (including the
postsurgical shock)
B) a cardiac failure
C) a general hypoxia
D) a renal failure
E) a proteinic starvation
E) a hypovitaminosis E
G) a deficiency of a selenium
H) endocrinopathies: an adrenal
insufficiency, a pathology of
parathyroid glands, etc.
I) metastasises of tumors in a liver
8
15. The general pathogenesis of the liver failure
THE DAMAGING FACTOR
A partial or full
destruction of
membranes + a
rising of their
permeability
Activation of
immune and
autoimmune
reaction in a
liver
The
development
of
inflammatory
The
intensifying
of the free
radical lipid
peroxidation
An exit from
lysosomes
of their
hydrolyzing
enzyme
The massive destruction of
liver cells
LIVER INSUFFICIENSY
Each of this pathogenetic links can be dominant at the certain stage of the liver
failure development. 15
16. The hepatic cell failure -
Cytolysis and necrosis of hepatocytes →↑
in a blood of active enzymes of
alaninaminotranspherases (ALAT),
aspartate aminotransferases (ASAT),
glutaminaminotranspherases (GLAT) of the
marker of cytolytic process
The disturbances of
metabolic hepatic function:
•a protein metabolism
•a carbohydrate metabolism
•a fats metabolism
•a weakening of antitoxic function of a liver
•a weakening of barrier function
•a toxemia
•an imbalance of hormones
16
17. The disturbance of the protein metabolism
A hypoalbuminemia
and a disproteinemia
The development of
edemas and the
formation of an ascites
The augmentation in a
blood and in an urine
of amino acids
A rising of the
ammonia
concentration in a
blood and that leads
to decrease an urea
in a blood
An ammoniacal
toxicosis
The depression of
efficiency of an
amino acids
deamination
An urea
synthesis
suppression
hypocoagulation
A development of a
hemorrhagic syndrome (the
hemorrhages in a tissue, the
escapes of blood ).
It is promoted also by
decrease of an absorption in
an intestine of liposoluble
vitamin K
The inhibition
of hemostasis
system proteins
synthesis
procoagulums
(a prothrombin,
a proaccelerin,
a proconvertin)
The disturbance
of an albumins
synthesis
17
18. The disturbance
of LDL (low density lipoprotein)
metabolism
The disturbance
of HDL (high density lipoprotein)
synthesis
The rising in a blood plasma a
cholesterol level
A fatty hepatosis
And
atherosclerosis
The disturbances of a lipid metabolism
18
19. The suppression
of the glycogenesis
The depression
of the glycogenolysis
efficiency
The disturbances
of glucoses formation
A fasting
hypoglycemia
A hyperglycemia after
meal
The disturbances of the carbohydrate
metabolism
19
20. VITAMINS
Absorption A,D,E,K
↓ transformation of
provitamins in vitamins
(for example, Carotinum
in vitamin A);
Inhibitions of formation of
coenzymes from vitamins
(for example, from
pantothenic acid - acetyl A
coenzyme, from B1
vitamin - a pyruvate
cocarboxylase).
The disturbance
of the metabolism
MINERAL
SUBSTANCES
An iron
A copper
A chrome
The other disturbances of the
metabolism
20
21. The disturbance of the
antitoxic (barrier) hepatic
function
A neutralization depression by the
LIVER:
a) the intestinal poisons
b) the toxicant metabolites
c) the exogenous poisons
The autointoxication
21
23. The icterus
The JAUNDICE is the
syndrome which is
characterized by yellow
coloring of skin, mucosas
and scleras, by change of
coloring of secrets and
excretas, because there is
an augmentation in a blood
of the bilirubin which is a
sign of the pigmental
exchange disturbance
(bilirubin exchange).
23
24. The bilirubin metabolism
red blood cells
destruction
hemoglobin
a heme
biliverdin
Indirect bilirubin
Direct bilirubin
urobilinogen
stercobilinogen
blood
liver
intestine
erythrocytes
RES cells
Indirect
bilirubin
Direct bilirubin
BLOOD
Indirect
bilirubin
Urobilinogen
Urobilinoge
n
Stercobilinoge
n
Stercobilin in
FECES
Urobilin
(trases)
UREA
Absence of
bilirubin
24
27. the "leaking" through the damaged cellular membrane in a blood of
hepatic transaminases (an aspartate, alaninaminotranspherases, etc.);
a loss of ability of hepatic cells to enzymatic destruction of the
urobilinigen, arriving on a portal vein, and to development of an
urobilinogenemiya and urobilinogenuriya;
depression of quantity of a stercobilinogen in excrements.
THE MAIN LINKS OF THE PATHOGENESIS AND IMPLICATION I
STAGE of the HEPATOCELLULAR JAUNDICE
A DECREASE OF THE
ENZYMES ACTIVITY OF
THE UROBILINIGEN
DESTRUCTION
A DAMAGE OF
THE
HEPATOCYTES
MEMBRANES
THE DECREASE
OF THE ACTIVITY
OF GTF *
The
manifestation
UROBILINOGENEMIYA
Increase of
enzymes level in
blood
Increase of
potassium
level in blood
urobilinuria
27
28. A depression of formation intensity of a direct bilirubin from indirect. "The bilirubinic
conveyor": a protein of hepatocytes – a ligand – a glyukoruniltranspheraza is broken.
There are in a blood the bile acids (a cholemia). It is promoted by a compression of cholic
capillaries by edematous hepatocytes that complicates a normal evacuation from them of a
bile and creates the conditions for augmentation of its resorption in circulatory capillaries.
These disturbances are followed by a decrease of a bile entering in the intestine, and we can
observe the depression of a stercobilinogen maintenance in blood and feces (the urine
brightens, and the feces can become almost colourless).
THE MAIN LINKS OF THE PATHOGENESIS AND IMPLICATION II
STAGE of the HEPATOCELLULAR JAUNDICE
An AGGRAVATION OF
ALTERATION OF GTF
(guanosine triphosphate)*
AND OTHERS
ENZYMES
AN INCREASE OF
MEMBRANES
DAMAGE
A PRELUM OF
CHOLIC
CAPILLARIES
The manifestation
A cholehemia A bilirubinuria
Increase of
enzymes level in
blood
A DECREASE OF
UROBILINOGENEMIYA and
UROBILINOGENURIYA
DEGREE
A DEPRESSION OF THE
STERCOBILINOGEN
MAINTENANCE IN THE
BLOOD, URINE, FECES
28
29. A decrease of the activity of the hepatocytes
glukoruniltranspherase, a disturbance of transmembrane transfer
of a direct bilirubin in hepatocytes and to inhibition of a
glyukoronisation processes of a bilirubin.
In a blood: an indirect bilirubin, a direct bilirubin, a stercobilin and
an urobilin, a cholemia, an enzymes level, a potassium level, a
liver failure, a coma.
THE MAIN LINKS OF THE PATHOGENESIS AND IMPLICATION III
STAGE of the HEPATOCELLULAR JAUNDICE
The inactivation of GTF in
a progress
AN INCREASE OF hepatocytes
DAMAGE
The manifestation
An INCREASE OF LEVEL
OF THE INDIRECT
BILIRUBIN IN THE
BLOOD
A DEPRESSION OF A
DIRECT BILIRUBIN
MAINTENANCE IN THE
BLOOD
A cholemia Increase of
enzymes level in
blood
Increase of
potassium
level in blood
THE
UROBILINOGENEMIYA'S/UREMIYA's
DECREASE
A DECREASE OF THE
STERCOBILINOGEN MAINTENANCE IN
BLOOD, URINE, FECES
29
30. The enzymopathic jaundices
a Gilbert's syndrome (a benign familial icterus)
1
a Dubin– Johnson syndrome
2
a Crigler-Najjer syndrome
3
a Rotor syndrome
4
30
31. A GILBERT'S SYNDROME
1. A long rising of the
unconjugated bilirubin level.
2. A depression of the
stercobilinogen level in a
blood, an urine, feces (at
certain patients).
It is an icterus with the disturbance of active capture and transport of an indirect
bilirubin from a blood in a liver cell
31
32. A DUBIN–JOHNSON SYNDROME
1. A rising of the conjugated
bilirubin level in a blood.
2. The expressed content of
the unconjugated bilirubin in
a blood (at the expense of a
decompensation of the
hepatobiliary system).
3. The gastrointestinal
disorders.
This type of an jaundice arises owing to
defect of the enzymes participating in an
excretion of a conjugated bilirubin
through a membrane of a liver cell in
cholic capillaries.
32
33. A CRIGLER-NAJJAR DISEASE
•A rising of maintenance of the
unconjugated bilirubin in a blood
(especially at the first type).
•A depression of a stercobilinogen level in
a blood, an urine and a feces.
•The significant increase in a maintenance
of a bilirubin monoglyukoronid in bile.
•A kernicterus at children (at the first type).
This type of an enzymopathic jaundice
develops owing to deficiency of a
glyukoroniltranspherase which is a key
enzyme of transformation of a free bilirubin
in connected.
33
34. A ROTOR SYNDROME
1. A rising of a maintenance of
the conjugated bilirubin.
2. The augmentation of level
of the general
coproporphyrin in urine
A pigmental hepatosis or the Rotor syndrome is
the hereditary disease caused by a
bilirubinemia without a depression of
enzymatic activity of a liver, but with the
dysfunction of transportation of a bilirubin
from hepatocytes and not ability of its normal
capture by a sinusoidal pole of hepatic cells
34
35. A hemolytic jaundices
erythrocyte
s
RES cells
Indirect
bilirubin
Indirect
bilirubin
Direct
bilirubin
Urobili-
nogen
Urobilinogen
Stercobilinoge
n
UREA
Absence of
bilirubin
Urobilin
Stercobilin in
FECES
BLOOD
35
36. The reasons
INTERNAL AND
EXTRAVASATED
HEMOLYSIS OF
ERYTHROCYTES
HEMOLYSIS OF
ERYTHROCYTES AND
THEIR PRECURSORS IN
BONE MARROW
FORMATION OF EXCESS OF the
UNCONJUGATED BILIRUBIN AT:
• INFARCTS OF TISSUES
•HEMORRHAGES
SYNTHESIS OF the
UNCONJUGATED
BILIRUBIN FROM THE NOT
hemoglobinous HEME IN
THE LIVER AND IN THE
BONE MARROW
The manifestation
THE SIGNS OF ERYTHROCYTES
HEMOLYSIS
THE SIGNS OF THE HEPATOCYTES
DAMAGE
(AT THE CHRONIC CURRENT)
An anemia
A hemic
hypoxia
A gemoglobinuria
UROBILINOGENEMIYA,
- URIYA
A RISING IN THE BLOOD OF
THE UNCONJUGATED
BILIRUBIN LEVEL
THE AUGMENTATION OF
THE STERCOBILIN LEVEL
IN THE BLOOD, THE
URINE, THE FECES
THE SYMPTOMS OF
THE liver failure
THE SYMPTOMS OF
THE
PARENCHYMATOUS
ICTERUS
The main reasons of the hemolytic jaundice
12
36
37. The obstructive jaundice
erythrocyte
s
RES cells
Direct bilirubin
Direct bilirubin
Direct
bilirubin
Obturation
or
compressio
n of
common
bile duct
BLOOD
URINE
Urobilinogen is absent
Stercobilin in
FECES is
absent
indirect
bilirubin
37
38. The main manifestation of the obstructive
jaundice
A cholaemia
syndrome An acholia
syndrome
A high level of
conjugated bilirubin
in a blood
A hyperirritability
and an excitability
A hypercholesterolemia
A skin
itching
a brachycardia
An arterial
hypotension
Steatorhea
А DYSBACTERIOSIS.
INTESTINAL
AUTOINFECTION
AND INTOXICATION
A
polyhypovita
minosis
a light-colored feces
13
38
39. the markers А norm Hemolytic
jaundice
Obstructive
jaundice
Hepatocellular jaundice
Stage I Stage II Stage III
blood
urine
feces
blood
urine
feces
blood
urine
feces
blood
urine
feces
blood
urine
feces
blood
urine
feces
indirect bilirubin
+ - - ↑ - - N - - N - - N - - ↑ - -
direct bilirubin
+ + - N - - ↑ + - - - - ↑ + - ↓ ↓ -
Urobilinogen,
stercobilinogen
+ + + ↑ ↑ ↑ - - - N N N ↓ ↓ ↓ - - -
the bile acids
- - - - - - ↑ + - - - - + + - + + -
the hepatic
enzymes
N - - N - - ↑ + - ↑ + - ↑ + - ↑ + -
39
40. a liver cirrhosis
a classification by the morphological types :
- hepatoportal
- postnecrotic
-biliary
The etiology:
-the consequence of a viral hepatitis
-an alcoholism
-the autoimmune hepatitises
-the disturbance of a metabolism (a hemochromatosis, a failure of alfa-1-
antitrypsin, the glycogenoses)
-the diseases internal and extrahepatic cholic ways (primary and
secondary biliary cirrhosis)
This is a normal liver Тhis is a liver at the cirrhosis
40
41. The cirrhosis pathogenesis – «a chain
reaction»
the necrosis of
hepatocytes
the formation of
cicatrixes
the disturbance of a blood supply of
a liver pulp
the disturbance of a
blood outflow
a formation of a portacaval anastomoses
41
42. The role of lipocytes in development of a liver fibrosis
42
43. The manifestation of the
cirrhosis
the portal hypertension.
a hepatomegalia and splenomegalia (the dysfunction of a lien
on elimination from a blood and to destruction of old
formulated elements of a blood (an anemia, a leukopenia, a
thrombocytopenia) becomes perceptible. (The result of
difficulty of a blood outflow and regional hypoxia).
the ascites
the hepatocellular jaundice and hemorrhagic diathesis (аn
angiostaxis of the nose mucous and gums, the hypodermic
petechias and hemorrhages).
a dysproteinemia (a hypoalbuminemia, a hyper-γ-globulinemia),
a rising of activity of hepatic transaminases and concentration
of a direct bilirubin in a blood, ↑ an ESR (erythrosyte
sedimentation rate).
a pain syndrome (dyskinesia of cholic ways or necrosis of a
liver).
The liver failure (expressed in different degree) with a
hepatocerebral syndrome.
43
44. a portal hypertension
Portosystemic anasnomosis
•veins of an esophagus, of a
cardial department of a
stomach,
•veins of a forward abdominal
wall (the “Medusa head”),
• hemorrhoidal veins.
44
46. THE COMPLICATIONS OF THE
PORTAL HYPERTENSIA
- a bleeding from varicose veins of an
esophagus, of a stomach, of a rectum
- a liver encephalopathy
46
47. The liver encephalopathy
is an end-stage of a liver failure. It is characterized by the
metabolic disturbances in a brain which are shown by the
disturbance of mentality and motor and vegetative activity
(a neuro and mental syndrome).
The stages of a liver encephalopathy:
- Prodromal
- Precoma
- Stupor
- Coma
The coma is characterized by a loss of consciousness,
by a fading of reflexes, by periodic respiration that lead to death
47
48. The liver coma. Reasons
A shunting coma
An organism intoxication by
metabolism products
and the exogenous
substances, as result of
their hit in the general
blood circulation
The liver
coma
A parenchymal
coma
The intoxication of an
organism is lied with the
damage or death of
appreciable hepatic part,
and also a loss of
disintoxication function.
48
49. A pathogenesis of the hepatic
coma
Etiology
acute
hypoglycemi
a
acidosis intoxication
Ionic
imbalanse
Disorders of
microcirculation
COMA
49
50. The main factors of the neurotoxicity at the hepatic
encephalopathy
An intestinal flora
A tryptophan,
a tyrosine, a
phenylalanine
a tyramine, an
octopamine
An indole,
a skatole
bilirubin
NH3
Inhibition of
synthesis of
Dofaminum and
Noradrenalinum;
serotonin
synthesis
intensifying
a false mediator
The
toxins
A gamma-
aminobutyric
acid
50
51. The hepatic syndromes
The hepato-enteral
syndrome
The hepato-
lienal
syndrome
The disturbances of
an angiotensinogen
formation
The hypotension.
The disturbances of a
kidneys filtration.
An oliguria.
The hepato-renal
syndrome
The disturbance of a
circulation in portal
system,
the dysfunction of a lien
on elimination from a
blood and the destruction
of old formulated
elements of a blood
The disturbance of
cavitary and parietal
digestion, disturbance
of a blood outflow of a
blood from a gastro-
intestinal tract, the
emergence of erosions
of a gastro-intestinal
tract mucosa.
51
52. Thank you for your
attention!
To your success!
Send me your question
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52