1) A 35-year old female presented with hematemesis and was found to have signs of portal hypertension including splenomegaly and visible veins on her abdominal wall.
2) Portal hypertension is increased blood pressure in the portal vein, usually caused by cirrhosis of the liver. It can lead to dangerous variceal bleeding from enlarged veins in the esophagus or stomach.
3) Diagnosis involves ultrasound, endoscopy, and liver tests. Treatment focuses on stabilizing any bleeding, identifying its cause via endoscopy, and managing the underlying cause of portal hypertension like cirrhosis.
portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, IndiaDivya Khanna
This document provides information on portal hypertension, including its definition, anatomy, pathophysiology, etiology, clinical features, investigations, treatment of variceal bleeding, ascites, encephalopathy, Budd-Chiari syndrome, and various surgical procedures. Portal hypertension is defined as a portal venous pressure greater than 12 mmHg and is characterized by the development of portosystemic collaterals. Common causes include liver cirrhosis, portal vein thrombosis, and Budd-Chiari syndrome. Treatment involves reducing portal pressure, treating complications, and addressing the underlying liver disease.
Cirrhosis is the end stage of many chronic liver diseases where the liver architecture is completely disrupted by extensive fibrosis and the formation of regenerating nodules. It results from chronic liver injury and inflammation that causes hepatocyte necrosis initially and progresses to bridging fibrosis that destroys the liver structure. Common causes include alcohol, viral hepatitis, and primary biliary cirrhosis. Cirrhosis leads to liver failure and complications of portal hypertension like ascites, variceal bleeding, and hepatic encephalopathy.
This document discusses complications that can arise in patients with cirrhosis, including portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. It provides details on the pathophysiology, clinical presentation, diagnosis, and treatment of these complications. Specifically, it focuses on portal hypertension and the development of varices, describing the risks of variceal bleeding and approaches to prevention and management. It also covers ascites extensively, explaining how and why it develops in cirrhosis and its treatment with diuretics and sodium restriction.
Portal hypertension, liver cirrhosis and liver transplantAnshu Yadav
Portal hypertension occurs when blood pressure within the portal venous system increases. It is commonly caused by liver cirrhosis and affects 5-10% of patients in developed countries. Cirrhosis results from chronic liver damage and scarring of the liver tissue. It can be caused by alcoholism, viral hepatitis, NASH, or genetic diseases. Common signs include fatigue, abdominal pain, and jaundice. Treatment focuses on managing complications through medications, procedures like TIPS or banding of varices, and potentially liver transplantation.
This document provides information on cirrhosis including its causes, types, pathophysiology, clinical features, diagnosis, management, and treatment according to Ayurveda. Some key points:
- Cirrhosis is a diffuse process of fibrosis that converts the liver architecture into structurally abnormal nodules. It is caused by chronic liver injury and can result from conditions like alcohol abuse, viral hepatitis, and non-alcoholic fatty liver disease.
- Clinical features may include hepatomegaly, jaundice, ascites, and hepatic encephalopathy. Diagnosis involves blood tests and imaging scans. Management focuses on treating the underlying cause and complications.
- In Ayurveda, cir
This document discusses portal hypertension and variceal bleeding. It begins by describing portal hemodynamics and defining clinically significant portal hypertension as a hepatic venous pressure gradient (HVPG) greater than 10-12 mm Hg.
The etiology of portal hypertension is categorized as prehepatic, hepatic, or posthepatic. Prehepatic causes include portal/splenic vein thrombosis. Hepatic causes include cirrhosis, which leads to fibrosis and increased production of vasoconstrictors. Posthepatic causes include Budd-Chiari syndrome.
Complications of portal hypertension include variceal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome. Investigations for diagnosis include ultrasound Doppler,
This document provides information on ascites including its definition, causes, diagnosis, and management. Ascites is defined as the accumulation of free fluid in the peritoneal cavity, most often caused by liver cirrhosis (75% of cases), malignancy, or heart failure. Diagnosis involves history, physical exam finding shifting dullness or fluid wave, and abdominal ultrasound or paracentesis. Initial ascites management consists of sodium restriction, diuretics, and large volume paracentesis for refractory ascites.
1) A 35-year old female presented with hematemesis and was found to have signs of portal hypertension including splenomegaly and visible veins on her abdominal wall.
2) Portal hypertension is increased blood pressure in the portal vein, usually caused by cirrhosis of the liver. It can lead to dangerous variceal bleeding from enlarged veins in the esophagus or stomach.
3) Diagnosis involves ultrasound, endoscopy, and liver tests. Treatment focuses on stabilizing any bleeding, identifying its cause via endoscopy, and managing the underlying cause of portal hypertension like cirrhosis.
portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, IndiaDivya Khanna
This document provides information on portal hypertension, including its definition, anatomy, pathophysiology, etiology, clinical features, investigations, treatment of variceal bleeding, ascites, encephalopathy, Budd-Chiari syndrome, and various surgical procedures. Portal hypertension is defined as a portal venous pressure greater than 12 mmHg and is characterized by the development of portosystemic collaterals. Common causes include liver cirrhosis, portal vein thrombosis, and Budd-Chiari syndrome. Treatment involves reducing portal pressure, treating complications, and addressing the underlying liver disease.
Cirrhosis is the end stage of many chronic liver diseases where the liver architecture is completely disrupted by extensive fibrosis and the formation of regenerating nodules. It results from chronic liver injury and inflammation that causes hepatocyte necrosis initially and progresses to bridging fibrosis that destroys the liver structure. Common causes include alcohol, viral hepatitis, and primary biliary cirrhosis. Cirrhosis leads to liver failure and complications of portal hypertension like ascites, variceal bleeding, and hepatic encephalopathy.
This document discusses complications that can arise in patients with cirrhosis, including portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. It provides details on the pathophysiology, clinical presentation, diagnosis, and treatment of these complications. Specifically, it focuses on portal hypertension and the development of varices, describing the risks of variceal bleeding and approaches to prevention and management. It also covers ascites extensively, explaining how and why it develops in cirrhosis and its treatment with diuretics and sodium restriction.
Portal hypertension, liver cirrhosis and liver transplantAnshu Yadav
Portal hypertension occurs when blood pressure within the portal venous system increases. It is commonly caused by liver cirrhosis and affects 5-10% of patients in developed countries. Cirrhosis results from chronic liver damage and scarring of the liver tissue. It can be caused by alcoholism, viral hepatitis, NASH, or genetic diseases. Common signs include fatigue, abdominal pain, and jaundice. Treatment focuses on managing complications through medications, procedures like TIPS or banding of varices, and potentially liver transplantation.
This document provides information on cirrhosis including its causes, types, pathophysiology, clinical features, diagnosis, management, and treatment according to Ayurveda. Some key points:
- Cirrhosis is a diffuse process of fibrosis that converts the liver architecture into structurally abnormal nodules. It is caused by chronic liver injury and can result from conditions like alcohol abuse, viral hepatitis, and non-alcoholic fatty liver disease.
- Clinical features may include hepatomegaly, jaundice, ascites, and hepatic encephalopathy. Diagnosis involves blood tests and imaging scans. Management focuses on treating the underlying cause and complications.
- In Ayurveda, cir
This document discusses portal hypertension and variceal bleeding. It begins by describing portal hemodynamics and defining clinically significant portal hypertension as a hepatic venous pressure gradient (HVPG) greater than 10-12 mm Hg.
The etiology of portal hypertension is categorized as prehepatic, hepatic, or posthepatic. Prehepatic causes include portal/splenic vein thrombosis. Hepatic causes include cirrhosis, which leads to fibrosis and increased production of vasoconstrictors. Posthepatic causes include Budd-Chiari syndrome.
Complications of portal hypertension include variceal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome. Investigations for diagnosis include ultrasound Doppler,
This document provides information on ascites including its definition, causes, diagnosis, and management. Ascites is defined as the accumulation of free fluid in the peritoneal cavity, most often caused by liver cirrhosis (75% of cases), malignancy, or heart failure. Diagnosis involves history, physical exam finding shifting dullness or fluid wave, and abdominal ultrasound or paracentesis. Initial ascites management consists of sodium restriction, diuretics, and large volume paracentesis for refractory ascites.
Portal hypertension:A disease better controlled than cured.KETAN VAGHOLKAR
Portal hypertension is one of the common causes of upper gastrointestinal bleeding. It is a very lethal condition. Prompt diagnosis and commencement of early medical treatment can help keeping the disease under control. Surgery is a very useful adjunct in uncontrollable bleeding and in long term prevention in certain selected cases.
1. The pancreas is an elongated organ located in the abdominal cavity behind the stomach. It has three parts - head, body, and tail.
2. The pancreas has both exocrine and endocrine functions. Exocrine functions include producing pancreatic juice containing enzymes that digest carbohydrates, proteins, and fats. Endocrine functions include production of insulin, glucagon, and somatostatin by islets of Langerhans cells.
3. Pancreatitis is inflammation of the pancreas that can be acute or chronic. Acute pancreatitis symptoms include severe abdominal pain and its causes include gallstones and alcohol use. Chronic pancreatitis involves long-term inflammation that destroys the pancreas over
G I bleeding with radiological interventions(ACR Appropriateness Criteria).Tc-99m RBC scintigraphy,Catheter-directed Angiography,Pharmacological control,Embolization,Arterial interventions,Endoscopy,CT Angiography
Ascites is an accumulation of fluid in the peritoneal cavity that is clinically detectable when fluid volume exceeds 500 ml. It is caused by portal hypertension (PH) in conditions like cirrhosis and liver disease. There are two types - high serum-ascites albumin gradient (SAAG) ascites caused by PH and low SAAG ascites caused by things like cancer. Treatment involves sodium and fluid restriction with diuretics like frusemide and spironolacton. Refractory ascites does not respond to diuretics and requires procedures like large volume paracentesis or TIPS. New aquaretic diuretics that work by blocking vasopressin receptors are a promising treatment for ascites
This document provides information on gastrointestinal bleeding, including its anatomy, definition, epidemiology, clinical features, etiology, history and examination, investigation, and management. It discusses the major sites of upper and lower GI bleeding. For upper GI bleeding it covers topics such as esophageal varices, Mallory-Weiss tears, esophageal cancer, peptic ulcer disease, erosive gastritis, gastric cancer, and Dieulafoy's disease. For lower GI bleeding it briefly mentions duodenitis. It provides details on the pathogenesis, clinical presentation, investigations and treatment of many of these conditions.
this ppt presents pancreatitis and tumors of the pancreas
The fourth leading cause of cancer-related death in the United States and has a mean age of 55 at diagnosis.
I GET SMASHED
This document provides information about a case of upper gastrointestinal bleeding. It begins with definitions of gastrointestinal bleeding and descriptions of upper and lower GI bleeding. Symptoms of GI bleeding are then outlined. The learning objectives, anatomy and physiology of the digestive system, and pathophysiology of upper GI bleeding are reviewed. Patient assessment data including health history, physical exam findings, and initial lab/diagnostic results are presented. Finally, the patient's medications and proposed nursing care plan are detailed.
This document provides an overview of approaches to gastrointestinal bleeding. It discusses the common clinical presentations including hematemesis, melena, hematochezia, and occult bleeding. For hematemesis, the most common causes are discussed such as stress ulcers, Mallory-Weiss tears, peptic ulcer disease, gastroesophageal varices, and Dieulafoy's lesion. For hematochezia, common causes include colonic diverticula, internal hemorrhoids, colon cancer, and inflammatory bowel disease. The document provides details on evaluating each potential cause and characteristics to consider in the clinical history and examination.
Approach to a child with hematemesis or melenaAvijeet Mishra
1. A 32 month old male presented with a 2 day history of abdominal pain, black stools, and fresh blood in stool. Physical exam showed pallor and splenomegaly.
2. Initial workup revealed anemia and thrombocytopenia. Further imaging found portal cavernoma and esophageal varices, indicating extrahepatic portal vein obstruction.
3. The patient was stabilized and treated for upper gastrointestinal bleeding from esophageal varices caused by extrahepatic portal vein obstruction, the most common cause of variceal bleeding in older children in India. Endoscopy is the gold standard for diagnosis and management of upper GI bleeding.
1. The document discusses gastrointestinal bleeding, describing different types including hematemesis, melena, hematochezia, occult blood, and chronic blood loss.
2. It examines causes of upper and lower GI bleeding such as peptic ulcers, varices, hemorrhoids, and tumors.
3. Evaluation and management are outlined, including resuscitation of hypovolemic shock, determining bleeding location, and considering high risk patients.
1. The document discusses gastrointestinal bleeding, describing its various presentations including hematemesis, melena, hematochezia, occult blood in stools, and chronic blood loss/anemia.
2. Upper GI bleeding occurs above the ligament of Treitz and can cause hematemesis or melena, while lower GI bleeding occurs below and causes melena and hematochezia but no hematemesis.
3. Common causes of upper GI bleeding include peptic ulcer disease, gastritis, and esophageal varices, while common causes of lower GI bleeding include hemorrhoids, diverticulosis, and polyps.
1. Ascites is an accumulation of fluid in the peritoneal cavity, most commonly caused by cirrhosis of the liver.
2. Diagnosis involves physical exam findings, ultrasound imaging, and analysis of ascitic fluid. A serum ascites albumin gradient (SAAG) can help determine if ascites is caused by portal hypertension.
3. Initial treatment involves sodium restriction, diuretics like spironolactone and furosemide, and therapeutic paracentesis if needed. Refractory ascites may require transjugular intrahepatic portosystemic shunt or liver transplantation.
This document discusses gastrointestinal (GI) bleeding in infants and children. It covers:
1. Definitions of different types of GI bleeding like melena, hematochezia, and hematemesis.
2. Pathophysiology of GI bleeding including consequences of blood loss, higher risk in children, and compensatory mechanisms.
3. Causes of GI bleeding in different age groups ranging from neonates to adolescents. Common causes include esophagitis, gastritis, ulcers, varices, and infections.
4. Evaluation involves a thorough history, physical exam, lab tests like CBC and coagulation studies, and endoscopic procedures to identify the source of bleeding. Management is then
Portal hypertension is high blood pressure in the portal vein system that supplies blood to the liver. It has various clinical manifestations that may require surgical management. The surgical approach depends on factors like the underlying liver disease severity and venous anatomy. The main goals of surgery are to decrease portal pressure and prevent complications by bypassing resistance sites or directly treating complications. Procedures include devascularization to reduce variceal blood flow or decompression procedures to reduce portal pressure while maintaining hepatic blood flow. Selective shunts only decompress the variceal compartment while non-selective or partial shunts provide complete or incomplete decompression of the entire portal system. The distal splenorenal shunt is a commonly used selective shunt that
This document discusses gastrointestinal bleeding, including defining acute upper and lower GI bleeding, assessing the severity of bleeding, determining the location of bleeding, differential diagnoses, and management approaches. It provides details on the signs and symptoms of upper and lower GI bleeding, common causes, and first aid measures. The management of GI bleeding involves assessing the patient's hemodynamic status, localizing the bleeding source, checking blood work, addressing risk factors, and stopping active bleeding while preventing recurrence.
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
This document discusses the pathophysiology of upper GI bleeding. It describes how portal hypertension can lead to esophageal varices and the development of portosystemic collaterals. It also discusses how peptic ulcer disease associated with H. pylori infection can cause ulcers that weaken blood vessels and rupture. Acute stress gastritis is described as resulting from conditions that alter mucosal barriers like decreased blood flow or ischemia from shock/trauma. Mallory-Weiss tears occur when forceful vomiting causes tears in the gastric mucosa at the gastroesophageal junction.
The document discusses liver regeneration and function. It states that individual liver cells can regenerate destroyed liver tissue, while larger destroyed sections will cause surrounding tissue to expand. Complete liver function relies on unimpeded blood flow, as cirrhosis can only generate poorly perfused nodules. The document also outlines the liver's role in bile production, blood filtration, nutrient breakdown, and more. It describes various tests of liver function including bilirubin levels, clotting factors, and enzymes that indicate tissue damage.
The liver has several important metabolic functions including producing bile, metabolizing hormones and drugs, synthesizing proteins and clotting factors, storing vitamins and minerals, and maintaining glucose homeostasis. The liver also plays a key role in metabolizing fats and carbohydrates. Jaundice occurs when there is an abnormally high accumulation of bilirubin in the blood, and can be caused by excessive red blood cell destruction, impaired bilirubin uptake or conjugation by the liver, or obstruction of bile flow. Tests of liver function include serum enzyme levels, protein and clotting factor synthesis rates, and measures of bilirubin and biliary excretion.
Portal hypertension:A disease better controlled than cured.KETAN VAGHOLKAR
Portal hypertension is one of the common causes of upper gastrointestinal bleeding. It is a very lethal condition. Prompt diagnosis and commencement of early medical treatment can help keeping the disease under control. Surgery is a very useful adjunct in uncontrollable bleeding and in long term prevention in certain selected cases.
1. The pancreas is an elongated organ located in the abdominal cavity behind the stomach. It has three parts - head, body, and tail.
2. The pancreas has both exocrine and endocrine functions. Exocrine functions include producing pancreatic juice containing enzymes that digest carbohydrates, proteins, and fats. Endocrine functions include production of insulin, glucagon, and somatostatin by islets of Langerhans cells.
3. Pancreatitis is inflammation of the pancreas that can be acute or chronic. Acute pancreatitis symptoms include severe abdominal pain and its causes include gallstones and alcohol use. Chronic pancreatitis involves long-term inflammation that destroys the pancreas over
G I bleeding with radiological interventions(ACR Appropriateness Criteria).Tc-99m RBC scintigraphy,Catheter-directed Angiography,Pharmacological control,Embolization,Arterial interventions,Endoscopy,CT Angiography
Ascites is an accumulation of fluid in the peritoneal cavity that is clinically detectable when fluid volume exceeds 500 ml. It is caused by portal hypertension (PH) in conditions like cirrhosis and liver disease. There are two types - high serum-ascites albumin gradient (SAAG) ascites caused by PH and low SAAG ascites caused by things like cancer. Treatment involves sodium and fluid restriction with diuretics like frusemide and spironolacton. Refractory ascites does not respond to diuretics and requires procedures like large volume paracentesis or TIPS. New aquaretic diuretics that work by blocking vasopressin receptors are a promising treatment for ascites
This document provides information on gastrointestinal bleeding, including its anatomy, definition, epidemiology, clinical features, etiology, history and examination, investigation, and management. It discusses the major sites of upper and lower GI bleeding. For upper GI bleeding it covers topics such as esophageal varices, Mallory-Weiss tears, esophageal cancer, peptic ulcer disease, erosive gastritis, gastric cancer, and Dieulafoy's disease. For lower GI bleeding it briefly mentions duodenitis. It provides details on the pathogenesis, clinical presentation, investigations and treatment of many of these conditions.
this ppt presents pancreatitis and tumors of the pancreas
The fourth leading cause of cancer-related death in the United States and has a mean age of 55 at diagnosis.
I GET SMASHED
This document provides information about a case of upper gastrointestinal bleeding. It begins with definitions of gastrointestinal bleeding and descriptions of upper and lower GI bleeding. Symptoms of GI bleeding are then outlined. The learning objectives, anatomy and physiology of the digestive system, and pathophysiology of upper GI bleeding are reviewed. Patient assessment data including health history, physical exam findings, and initial lab/diagnostic results are presented. Finally, the patient's medications and proposed nursing care plan are detailed.
This document provides an overview of approaches to gastrointestinal bleeding. It discusses the common clinical presentations including hematemesis, melena, hematochezia, and occult bleeding. For hematemesis, the most common causes are discussed such as stress ulcers, Mallory-Weiss tears, peptic ulcer disease, gastroesophageal varices, and Dieulafoy's lesion. For hematochezia, common causes include colonic diverticula, internal hemorrhoids, colon cancer, and inflammatory bowel disease. The document provides details on evaluating each potential cause and characteristics to consider in the clinical history and examination.
Approach to a child with hematemesis or melenaAvijeet Mishra
1. A 32 month old male presented with a 2 day history of abdominal pain, black stools, and fresh blood in stool. Physical exam showed pallor and splenomegaly.
2. Initial workup revealed anemia and thrombocytopenia. Further imaging found portal cavernoma and esophageal varices, indicating extrahepatic portal vein obstruction.
3. The patient was stabilized and treated for upper gastrointestinal bleeding from esophageal varices caused by extrahepatic portal vein obstruction, the most common cause of variceal bleeding in older children in India. Endoscopy is the gold standard for diagnosis and management of upper GI bleeding.
1. The document discusses gastrointestinal bleeding, describing different types including hematemesis, melena, hematochezia, occult blood, and chronic blood loss.
2. It examines causes of upper and lower GI bleeding such as peptic ulcers, varices, hemorrhoids, and tumors.
3. Evaluation and management are outlined, including resuscitation of hypovolemic shock, determining bleeding location, and considering high risk patients.
1. The document discusses gastrointestinal bleeding, describing its various presentations including hematemesis, melena, hematochezia, occult blood in stools, and chronic blood loss/anemia.
2. Upper GI bleeding occurs above the ligament of Treitz and can cause hematemesis or melena, while lower GI bleeding occurs below and causes melena and hematochezia but no hematemesis.
3. Common causes of upper GI bleeding include peptic ulcer disease, gastritis, and esophageal varices, while common causes of lower GI bleeding include hemorrhoids, diverticulosis, and polyps.
1. Ascites is an accumulation of fluid in the peritoneal cavity, most commonly caused by cirrhosis of the liver.
2. Diagnosis involves physical exam findings, ultrasound imaging, and analysis of ascitic fluid. A serum ascites albumin gradient (SAAG) can help determine if ascites is caused by portal hypertension.
3. Initial treatment involves sodium restriction, diuretics like spironolactone and furosemide, and therapeutic paracentesis if needed. Refractory ascites may require transjugular intrahepatic portosystemic shunt or liver transplantation.
This document discusses gastrointestinal (GI) bleeding in infants and children. It covers:
1. Definitions of different types of GI bleeding like melena, hematochezia, and hematemesis.
2. Pathophysiology of GI bleeding including consequences of blood loss, higher risk in children, and compensatory mechanisms.
3. Causes of GI bleeding in different age groups ranging from neonates to adolescents. Common causes include esophagitis, gastritis, ulcers, varices, and infections.
4. Evaluation involves a thorough history, physical exam, lab tests like CBC and coagulation studies, and endoscopic procedures to identify the source of bleeding. Management is then
Portal hypertension is high blood pressure in the portal vein system that supplies blood to the liver. It has various clinical manifestations that may require surgical management. The surgical approach depends on factors like the underlying liver disease severity and venous anatomy. The main goals of surgery are to decrease portal pressure and prevent complications by bypassing resistance sites or directly treating complications. Procedures include devascularization to reduce variceal blood flow or decompression procedures to reduce portal pressure while maintaining hepatic blood flow. Selective shunts only decompress the variceal compartment while non-selective or partial shunts provide complete or incomplete decompression of the entire portal system. The distal splenorenal shunt is a commonly used selective shunt that
This document discusses gastrointestinal bleeding, including defining acute upper and lower GI bleeding, assessing the severity of bleeding, determining the location of bleeding, differential diagnoses, and management approaches. It provides details on the signs and symptoms of upper and lower GI bleeding, common causes, and first aid measures. The management of GI bleeding involves assessing the patient's hemodynamic status, localizing the bleeding source, checking blood work, addressing risk factors, and stopping active bleeding while preventing recurrence.
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
This document discusses the pathophysiology of upper GI bleeding. It describes how portal hypertension can lead to esophageal varices and the development of portosystemic collaterals. It also discusses how peptic ulcer disease associated with H. pylori infection can cause ulcers that weaken blood vessels and rupture. Acute stress gastritis is described as resulting from conditions that alter mucosal barriers like decreased blood flow or ischemia from shock/trauma. Mallory-Weiss tears occur when forceful vomiting causes tears in the gastric mucosa at the gastroesophageal junction.
The document discusses liver regeneration and function. It states that individual liver cells can regenerate destroyed liver tissue, while larger destroyed sections will cause surrounding tissue to expand. Complete liver function relies on unimpeded blood flow, as cirrhosis can only generate poorly perfused nodules. The document also outlines the liver's role in bile production, blood filtration, nutrient breakdown, and more. It describes various tests of liver function including bilirubin levels, clotting factors, and enzymes that indicate tissue damage.
The liver has several important metabolic functions including producing bile, metabolizing hormones and drugs, synthesizing proteins and clotting factors, storing vitamins and minerals, and maintaining glucose homeostasis. The liver also plays a key role in metabolizing fats and carbohydrates. Jaundice occurs when there is an abnormally high accumulation of bilirubin in the blood, and can be caused by excessive red blood cell destruction, impaired bilirubin uptake or conjugation by the liver, or obstruction of bile flow. Tests of liver function include serum enzyme levels, protein and clotting factor synthesis rates, and measures of bilirubin and biliary excretion.
The document summarizes the functions and structure of the liver. It notes that the liver is the largest internal organ, located on the right side below the diaphragm. The liver has important metabolic, storage, excretory, protective, circulatory and coagulation functions, including breaking down toxins, producing bile and proteins, and regulating blood flow. The liver is made up of lobules containing hepatocytes and sinusoids that receive blood flow and allow for nutrient exchange. Damage to the liver can cause jaundice and diseases like hepatitis, cirrhosis, and cancer.
This document discusses the anatomy, functions, and disorders of the liver and biliary system. It provides details on:
- The liver's role in producing bile to aid digestion, regulating blood clotting factors, filtering toxins, and storing vitamins and minerals.
- The structure of the liver including lobules, hepatocytes, blood supply from the hepatic artery and portal vein, and bile duct network.
- Common liver disorders like hepatitis, cirrhosis, cancer, and how they impact liver function and cause symptoms like jaundice, abdominal pain, and fatigue.
- Tests used to evaluate liver function such as albumin, prothrombin time, and transaminase levels.
Hepatic physiology & liver function testsImran Sheikh
The liver is the largest organ in the body, weighing between 1500-1600 grams. It has a dual blood supply of 80% from the portal vein and 20% from the hepatic artery. The liver has important vascular, metabolic and excretory functions. It plays a key role in carbohydrate, protein and fat metabolism. The liver also performs the vital functions of drug metabolism, hormone production, and coagulation factor synthesis.
CHEMICAL PATHOLOGY OF LIVER DISEASE.pptxJasperOmingo
The document summarizes the microscopic structure and functions of the liver. It discusses that the liver is made up of lobules containing hepatocytes and sinusoids which receive blood. The blood flows through sinusoids and drains into central veins. Bile produced by hepatocytes drains into bile ducts. The liver's blood supply comes from the hepatic artery and portal vein. The liver performs important metabolic functions like carbohydrate, lipid, and protein metabolism. It also breaks down bilirubin from broken down red blood cells and conjugates it for excretion in bile. Bile acids are also conjugated and undergo enterohepatic circulation between the liver and intestines.
The liver is the largest organ in the abdominal cavity and performs many metabolic functions. It is composed of hepatocytes arranged in lobules around a central vein. Blood flows from the hepatic portal vein and hepatic artery into sinusoids between hepatocytes. Bile is secreted into bile canaliculi and flows through bile ducts. The liver regulates nutrients, metabolizes drugs and toxins, and synthesizes proteins. It is innervated by the hepatic plexus and refers pain to the epigastrium.
The document discusses the liver and its metabolic, excretory, and synthetic functions. It covers the liver's role in carbohydrate, lipid, and protein metabolism as well as bile production. Pathologies of the liver discussed include jaundice, hepatitis (viral and alcoholic), and cirrhosis. Viral hepatitis can be acute and resolve or become chronic, possibly resulting in a carrier state. Jaundice has prehepatic, intrahepatic, and posthepatic causes. Tests of liver function evaluate enzymes, bilirubin, proteins, and imaging.
This document provides information on the anatomy, physiology, and functions of the liver. It discusses that the liver has a dual blood supply from the portal vein (80%) and hepatic artery (20%). It is divided into lobes and lobules and carries out important metabolic functions like carbohydrate, protein, and fat metabolism as well as drug biotransformation. The liver plays a key role in maintaining blood glucose levels and produces many plasma proteins and coagulation factors.
The document provides information about the anatomy, blood supply, microcirculation, functions, and clinical assessment of the liver. It discusses that the liver is located in the upper right abdomen and has two lobes. It receives dual blood supply from the portal vein and hepatic artery. The functional unit of the liver is the lobule, which contains hepatocytes arranged in plates around a central vein. The liver performs many metabolic functions and can regenerate after injury. Clinical assessment of liver disease involves history, examination, and blood tests of liver enzymes and function.
INTERGRATED RESPONSE TO A MEAL V. INTESTINAL PHASE (ii)SAMOEINESH
The document summarizes the anatomy and physiology of the liver and biliary system. It describes:
1. The liver's dual secretory and excretory functions, and its location in the abdomen.
2. The hepatic lobes, lobules, hepatocytes, and bile canaliculi that make up the liver's structure.
3. How bile is secreted by hepatocytes and stored/concentrated in the gallbladder before release into the small intestine.
LIVER FUNCTION TESTS from Millers Anesthesia CharanKamal11
The document discusses liver function tests and what they indicate about liver health. It covers tests that detect hepatocellular injury like ALT and AST, tests that detect cholestatic disorders like alkaline phosphatase, and tests that assess hepatic protein synthesis like albumin. Elevations in ALT and AST generally indicate liver cell damage, while increases in alkaline phosphatase and GGT suggest problems with bile flow in the liver or bile ducts. Albumin levels reflect protein production by the liver, though other factors can also influence albumin levels. Together these tests provide insight into liver health and the type of underlying liver condition.
The document discusses the functions of the liver, including its structure and role in metabolic, storage, excretory, protective, circulatory, and coagulation functions. It notes that the liver is the largest internal organ, located on the right side of the abdominal cavity. It has a double blood supply and is divided into four lobes. The liver plays a vital role in metabolizing nutrients, storing vitamins and minerals, filtering toxins from the blood, and producing bile and blood proteins. Common diseases that can damage the liver include hepatitis, cirrhosis, cancer, and genetic disorders.
The liver is the largest gland in the human body, located in the upper right abdominal cavity beneath the diaphragm. It has four lobes and is made up of lobules that contain hepatocytes arranged in plates with blood sinusoids between them. The liver receives blood from the hepatic portal vein and hepatic artery, and filters toxins and produces bile, which is stored in the gallbladder and released into the small intestine after meals to aid in fat digestion. The liver performs many essential metabolic functions including carbohydrate, protein, and fat metabolism, hormone inactivation, and production of bile and proteins.
The liver plays a key role in metabolism and homeostasis. It receives a dual blood supply and filters waste from the blood to produce urea, which is excreted. Excess alcohol is broken down but can overload the liver, causing fatty deposits. The kidneys filter blood to produce urine via nephrons and selective reabsorption maintains electrolyte balance. Kidney failure requires dialysis or transplant. Pregnancy and drug tests analyze samples for target hormones or compounds.
The liver performs many vital functions: (1) It filters blood from the digestive system and removes toxins. (2) It regulates carbohydrate and fat metabolism, storing glucose and producing cholesterol. (3) It synthesizes proteins and aids in protein metabolism, forming urea to remove ammonia from the body. The liver's high blood flow and unique lobule structure enable these diverse metabolic roles.
Lect. 14 digestive system - associated glandsHara O.
This document provides information about the accessory organs of the digestive system, including the salivary glands, liver, and pancreas. It describes the structure and function of the parotid, submandibular, and sublingual salivary glands. It also discusses the role of the liver in vascular functions, metabolism, secretion, and excretion. Additionally, it outlines the structure of liver lobules and hepatocytes. The document concludes by examining the exocrine and endocrine functions of the pancreas.
Enterohepatic circulation and Hepatic Portal circulationjohnedward869
This document discusses enterohepatic circulation and hepatic portal circulation. Enterohepatic circulation refers to the recycling of bile acids, bilirubin, drugs, and other substances from the liver to the bile and back to the liver via the small intestine. The hepatic portal vein collects blood from the gastrointestinal tract and transports it to the liver before entering systemic circulation. When portal vein pressure is elevated in conditions like liver cirrhosis, portosystemic anastomoses allow blood to bypass the liver and enter systemic veins.
The liver performs numerous vital metabolic functions:
- It regulates blood glucose levels through glycogenesis, glycogenolysis, and gluconeogenesis.
- It breaks down amino acids from proteins and converts excess amounts into glucose, fatty acids, and urea.
- It synthesizes, modifies, and excretes lipids like cholesterol, triglycerides, and phospholipids.
The liver receives a dual blood supply and is composed of lobules containing hepatocytes and sinusoids that facilitate exchange of materials. It plays a key role in carbohydrate, protein, and lipid metabolism, as well as other processes like detoxification.
Similar to Upper GI Bleeding (Liver and Spleen) Bambury (20)
The document discusses benzodiazepines, including their uses, effects, risks of dependence and withdrawal, assessment and treatment of withdrawal, and overdose management. Benzodiazepines are widely used to treat anxiety, insomnia, and other conditions but can cause dependence, and withdrawal symptoms may include rebound anxiety, insomnia, tremors, and potentially seizures. Detoxification and tapering regimens aim to safely reduce the dose over time to minimize withdrawal symptoms.
Opioids are a class of drugs that have morphine-like effects on the central nervous system. They are commonly used analgesics but prolonged use can lead to tolerance and dependence. Opioid withdrawal can be managed in the hospital setting using buprenorphine or methadone to relieve symptoms, along with supportive medications for nausea, muscle aches, diarrhea and sleeplessness. It is important for hospital staff to continue patients' opioid maintenance treatment and provide adequate pain relief while avoiding precipitated withdrawal.
This document provides information on alcohol, its effects on the body, alcohol dependence and withdrawal, and treatment approaches. It discusses how alcohol acts in the brain to produce both pleasurable and reinforcing effects. It outlines recommended daily and weekly drinking limits, signs and symptoms of alcohol intoxication at different blood alcohol levels. It also summarizes common presentations to the emergency department related to alcohol, approaches to assessing and managing alcohol withdrawal, risks of Wernicke's encephalopathy from thiamine deficiency, and options for ongoing treatment and support.
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From: UCD PAEDS <ucdpaeds@gmail.com>
Date: 2009/2/12
Subject: Fwd: Bambury Tutorial on Head and Neck
To: ucdgrad09@gmail.com
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From: Henning L. Stokmo <helangen@gmail.com>
Date: Wed, Feb 11, 2009 at 7:07 PM
Subject: Bambury Tutorial on Head and Neck
To: ucdpaeds@gmail.com
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From: cormac joyce <cjoyce78@hotmail.com>
Date: 2009/2/28
Subject: lecture
To: ucdgrad09@gmail.com
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Join the all-new Windows Live Messenger family Click here!<http://get.live.com/>
Head injuries most commonly occur in individuals aged 15-24 from vehicular accidents or falls in those over 75. The brain is surrounded by meninges including the dura, arachnoid and pia mater. Increased intracranial pressure can decrease cerebral perfusion and cause neurological deterioration, so monitoring and medical or surgical interventions aim to reduce pressure and maintain blood flow to the brain.
Fwd: Bambury lecture on venous and lymphatic disorders of the limbJeku Jacob
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From: Henning L. Stokmo <helangen@gmail.com>
Date: 2009/2/12
Subject: Bambury lecture on venous and lymphatic disorders of the limb
To: ucdgrad09@gmail.com
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From: UCD Graduate '09 None <ucdgrad09@gmail.com>
Date: 2009/2/12
Subject: Bambury tutorial Upper GI Surgery
To: ucdgrad09@gmail.com
She does not know that we have this so please don't print it and bring it to
the lecture
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.