Upper GI bleed is a common, scary and life threatening medical condition usually caused by peptic ulcer disease or oesophageal varices. Uncommon causes include neoplasms, aortoenteric fistulas, vascular lesions, Dieulafoy's lesion etc. Patients usually present with hematemesis or melena. GIST is the third most common tumor of stomach and also the most common mesenchymal tumor. GIST may be asymptomatic and discovered incidentally or they may cause nonspecific symptoms like early satiety and fullness. Although major presentation of GIST is upper GI bleed, GIST as a cause of upper GI bleed is very rare. We here present a patient admitted to us with massive upper GI bleed due to gastrointestinal stromal tumor.
The document discusses management of gastrointestinal bleeds in the emergency department, noting that identifying the bleed source is important but often challenging without endoscopy. While medications like H2 blockers, PPIs, and octreotide are commonly used, the evidence for their effectiveness is mixed and in some cases they may even increase mortality risk, so the priority should be stabilizing unstable patients and arranging prompt endoscopy.
- This document describes the case of a 62-year-old male (Mr. JR) presenting for follow up of chronic liver disease and a recent episode of hematemesis.
- His past medical history included esophageal variceal bleeding managed with band ligation four years prior. Current evaluation showed features of cirrhosis on ultrasound and severe diffuse gastric antral varices (GAVE) on endoscopy.
- He was managed conservatively with blood transfusion, medications, and three sessions of endoscopic band ligation of the GAVE over three weeks. No further bleeding episodes occurred on eight months of follow up.
This 55-year-old Hispanic woman with a history of Wegener's granulomatosis presented with a nosebleed. She had bruising on her arms and legs over the past 1.5 months and bleeding gums. Lab work showed thrombocytopenia. A bone marrow biopsy showed orderly trilineage maturation with adequate megakaryocytes. She was diagnosed with idiopathic thrombocytopenic purpura (ITP) rather than thrombocytopenia related to her Wegener's. Treatment options for ITP include corticosteroids, IVIG, anti-D immunoglobulin, and splenectomy.
This document summarizes several gastrointestinal emergencies, including upper GI bleeding, variceal bleeding, paracetamol overdose, severe ulcerative colitis, Crohn's colitis, and liver failure. For upper GI bleeding, it discusses causes, risk factors, management including resuscitation and endoscopy, and factors affecting prognosis. For variceal bleeding, it outlines treatment including banding, medical therapy, tamponade, TIPSS, and prevention. It also summarizes management of paracetamol overdose, criteria for severe colitis, and approaches to investigating and treating liver failure and associated complications like hepatorenal syndrome.
Monday, February 17,
2014
side effects
1) A 50-year-old male presented with swelling of the legs, abdominal distension, and constipation for 1 month and was diagnosed with liver cirrhosis with decompensation and portal hypertension based on his history of alcohol use for 15 years.
2) Laboratory tests showed anemia, elevated bilirubin and decreased albumin consistent with liver disease.
3) He was treated with paracentesis, diuretics, and discharged after 8 days of inpatient management with improvement of symptoms.
Upper GI bleed is a common, scary and life threatening medical condition usually caused by peptic ulcer disease or oesophageal varices. Uncommon causes include neoplasms, aortoenteric fistulas, vascular lesions, Dieulafoy's lesion etc. Patients usually present with hematemesis or melena. GIST is the third most common tumor of stomach and also the most common mesenchymal tumor. GIST may be asymptomatic and discovered incidentally or they may cause nonspecific symptoms like early satiety and fullness. Although major presentation of GIST is upper GI bleed, GIST as a cause of upper GI bleed is very rare. We here present a patient admitted to us with massive upper GI bleed due to gastrointestinal stromal tumor.
The document discusses management of gastrointestinal bleeds in the emergency department, noting that identifying the bleed source is important but often challenging without endoscopy. While medications like H2 blockers, PPIs, and octreotide are commonly used, the evidence for their effectiveness is mixed and in some cases they may even increase mortality risk, so the priority should be stabilizing unstable patients and arranging prompt endoscopy.
- This document describes the case of a 62-year-old male (Mr. JR) presenting for follow up of chronic liver disease and a recent episode of hematemesis.
- His past medical history included esophageal variceal bleeding managed with band ligation four years prior. Current evaluation showed features of cirrhosis on ultrasound and severe diffuse gastric antral varices (GAVE) on endoscopy.
- He was managed conservatively with blood transfusion, medications, and three sessions of endoscopic band ligation of the GAVE over three weeks. No further bleeding episodes occurred on eight months of follow up.
This 55-year-old Hispanic woman with a history of Wegener's granulomatosis presented with a nosebleed. She had bruising on her arms and legs over the past 1.5 months and bleeding gums. Lab work showed thrombocytopenia. A bone marrow biopsy showed orderly trilineage maturation with adequate megakaryocytes. She was diagnosed with idiopathic thrombocytopenic purpura (ITP) rather than thrombocytopenia related to her Wegener's. Treatment options for ITP include corticosteroids, IVIG, anti-D immunoglobulin, and splenectomy.
This document summarizes several gastrointestinal emergencies, including upper GI bleeding, variceal bleeding, paracetamol overdose, severe ulcerative colitis, Crohn's colitis, and liver failure. For upper GI bleeding, it discusses causes, risk factors, management including resuscitation and endoscopy, and factors affecting prognosis. For variceal bleeding, it outlines treatment including banding, medical therapy, tamponade, TIPSS, and prevention. It also summarizes management of paracetamol overdose, criteria for severe colitis, and approaches to investigating and treating liver failure and associated complications like hepatorenal syndrome.
Monday, February 17,
2014
side effects
1) A 50-year-old male presented with swelling of the legs, abdominal distension, and constipation for 1 month and was diagnosed with liver cirrhosis with decompensation and portal hypertension based on his history of alcohol use for 15 years.
2) Laboratory tests showed anemia, elevated bilirubin and decreased albumin consistent with liver disease.
3) He was treated with paracentesis, diuretics, and discharged after 8 days of inpatient management with improvement of symptoms.
Wilson disease with acute liver failure case presentationSanjeev Kumar
The document describes a case of a 30-year-old woman presenting with jaundice and altered mental status who was diagnosed with acute liver failure of unknown etiology. On examination, she had signs of hepatic encephalopathy and lab work showed elevated liver enzymes and coagulopathy. Further testing ruled out common causes of viral hepatitis and Wilson's disease, and the patient's condition deteriorated requiring ventilator support and consideration for liver transplant.
A good PG case presentation on abdominal case, liverKurian Joseph
This document discusses the case of a 43-year-old male agriculturalist presenting with jaundice, leg swelling, and occasional dark stools over the past few months. On examination, he is found to have pallor, jaundice, leg swelling, hepatomegaly, and signs of chronic alcohol use. The doctor diagnoses the patient with compensated liver disease in the form of early cirrhosis likely related to alcohol, with no current signs of portal hypertension or encephalopathy.
A 45-year-old male presented with hematemesis after vomiting blood the previous night. When confronted with a patient with hematemesis, the doctor should determine if it is truly hematemesis, assess the stability and estimated blood loss of the patient, consider possible lesions and their locations and blood supplies. A thorough history and examination is needed to correctly diagnose the source of bleeding. Initial management includes resuscitation with fluids and blood products as needed, passing a nasogastric tube, and arranging for urgent endoscopy within 18 hours. Long-term management depends on the findings and may include treatments like antibiotics, pharmacotherapy, endoscopic therapy, TIPS, or surgery.
Case presentation on alcoholic liver diseaseRavali Naidu
A 41-year-old male was admitted to the hospital with fever and chills for two days. His medical history revealed jaundice three times previously and a family history of diabetes and hypertension. Laboratory tests showed elevated liver enzymes and bilirubin, indicating alcoholic liver disease. He was prescribed medications to treat his condition, manage symptoms, and prevent drug interactions. The patient was counseled on lifestyle changes including abstaining from alcohol to prevent further liver damage.
Rifaximin treatment in hepatic encephalopathyPratap Tiwari
Rifaximin treatment significantly reduced the risk of hepatic encephalopathy episodes and hospitalizations over a 6-month period compared to placebo. In the study, 22.1% of patients taking rifaximin experienced a breakthrough hepatic encephalopathy episode, compared to 45.9% of patients taking placebo. The incidence of adverse events was similar between the two groups. The study demonstrates that rifaximin is effective for maintaining remission from hepatic encephalopathy in patients with cirrhosis.
Abdomen and liver case presentation by PGKurian Joseph
Abdomen and liver case presentation by PG
Chronic decompensated parenchymal liver disease - cirrhosis with portal hypertension probably of alcoholic etiology with no ascites with no features of hepatic encephalopathy and coagulopathy
To rule out malignancy
A 51-year-old man who had undergone surgery for stage II colon cancer two years prior presented with an elevated CEA level. Differential diagnoses included recurrent colorectal cancer or other cancers. Additional tests such as a CT scan, PET scan, and liver function tests were recommended to identify any masses in the abdomen or liver. Possible scenarios included a solitary 2 cm liver mass that could be surgically resected, with a 20-30% 5-year survival rate for patients with resectable liver metastases from colorectal cancer.
This document discusses hepatomegaly (enlarged liver). It describes the location and extent of the liver, clinical presentations of hepatomegaly including pain and jaundice, and examination techniques like inspection, palpation, percussion, and auscultation to evaluate the liver. Some causes of hepatomegaly mentioned are congestive heart failure, hepatic vein outflow obstruction, amoebic hepatitis, liver abscess, carcinoma, and hydatid cysts.
This document presents a case of traumatic liver injury in a 17-year old male patient who was in a motorcycle accident. He presented with abdominal pain and vomiting. Imaging showed a liver laceration and bleeding in the abdomen. He underwent an exploratory laparotomy where a left lobe liver laceration and diaphragm perforation were found and repaired. He recovered well after surgery with drain removal after one week and was discharged. Traumatic liver injuries can range from minor injuries treated non-operatively to severe injuries requiring surgery like lobectomy or packing to control bleeding. Both non-operative and surgical management were discussed.
The document discusses hepatic encephalopathy, a neurological syndrome caused by liver dysfunction. It covers the pathogenesis, which involves neurotoxins like ammonia crossing the blood brain barrier and disrupting neurotransmitter levels. Symptoms range from mild confusion to coma and can be precipitated by factors that increase ammonia production or permeability of the blood brain barrier. Treatment focuses on managing precipitating factors and restricting protein intake to control ammonia levels.
1. An 18-year-old female student presented with progressive lethargy, fever, and body aches for one month. She had a history of similar symptoms since age 12.
2. Initial examinations found splenomegaly but no clear diagnosis. Imaging showed a liver mass. Biopsies and further testing were needed to determine the cause.
3. The patient ultimately underwent laparotomy and biopsy of the liver mass. Post-operative histopathological examination revealed the diagnosis and further testing was done.
A 42-year-old male farmer presented with abdominal distension, pain, decreased urine output, and weight loss over the past two weeks. His history revealed chronic alcohol use over 30 years consuming 4.5-5.6 units daily. Examination found ascites and coagulopathy. Tests showed renal failure, cirrhosis, and transudative ascites. He was diagnosed with alcoholic liver disease complicated by ascites and hepatorenal syndrome due to chronic alcohol-induced cirrhosis. Management involved lifestyle changes including abstaining from alcohol and nutritional support.
Hepatic encephalopathy, short review & updateRushdanZakariah
This document provides an overview of hepatic encephalopathy. It describes hepatic encephalopathy as a complex neuropsychiatric syndrome characterized by disturbances in consciousness and personality changes. Acute episodes can be reversible while chronic cases may progress to coma or death. Precipitating factors include constipation, surgery, and progressive liver disease. Ammonia plays a central role in pathogenesis, as the liver is unable to metabolize and excrete nitrogenous waste products, leading to accumulation of ammonia in the blood and brain. Treatment aims to remove precipitating factors, reduce nitrogenous load from the gut, and manage symptoms. Options include nutritional management, laxatives, antibiotics like rifaximin, and lactulose to produce
A 59-year-old Chinese man was admitted to the hospital for vomiting blood. He has a history of hepatitis C and is a smoker, drinker, and former drug user. Physical examination found abdominal distension with fluid thrill and shifting dullness. Testing showed signs of liver dysfunction. The provisional diagnosis is esophageal varices secondary to liver disease, likely cirrhosis. Esophageal varices form as a result of portal hypertension in liver disease and can bleed, potentially severely. Treatment focuses on stopping the bleeding and lowering portal pressure through various medical and procedural options.
This document provides an overview of the approach to upper GI bleeding. It begins with definitions of terms like hematemesis, melena, and hematochezia. It then discusses the causes of upper GI bleeding, which can be variceal or non-variceal. For patients presenting with upper GI bleeding, the summary provides that history, physical exam, and investigations like endoscopy are important to determine the cause and guide management. Management may involve treating any active bleeding, administering PPIs for non-variceal bleeding, or using vasoactive agents, balloon tamponade, or endoscopic therapies for variceal bleeding.
Primary biliary cirrhosis and autoimmune hepatitis 20120902 Chien-Wei Su
This document summarizes a case of primary biliary cirrhosis (PBC) in a 66-year-old man who presented with intermittent pruritus for 8 years. Laboratory tests showed elevated liver enzymes and positive anti-mitochondrial antibodies, confirming the diagnosis of PBC. Liver biopsy showed features characteristic of PBC including destruction of bile duct epithelium and lymphocyte infiltration. The document then provides information on the epidemiology, risk factors, pathogenesis, natural history, diagnosis, treatment and prognosis of PBC.
This case report describes a 38-year-old man admitted to the hospital with black stools for 20 days and shortness of breath for 5 days. Examination found pallor and bruises. Tests showed severe anemia, elevated coagulation times, and a positive HCV antibody test. Upper endoscopy revealed stomach and duodenal erosions with oozing blood. The patient was diagnosed with type 1 von Willebrand disease based on a low von Willebrand factor level. He received transfusions, cryoprecipitates, factor replacement therapy, and endoscopic coagulation to treat his gastrointestinal bleeding.
This document presents a case study of a 63-year-old male who developed fatal cholestatic liver failure. He had undergone surgery for bladder cancer and cholecystectomy. His liver function tests continued rising after surgery. Extensive testing found no clear cause of cholestasis. Liver biopsies showed features of obstruction or drug effect. He was exposed to imipramine and amoxicillin-clavulanic acid, both known to cause cholestasis. Literature review found rare cases of progressive cholestasis and liver failure from these drugs. The patient's declining condition was treated supportively but he ultimately died of sepsis.
This presentation provides an overview of UGI Corporation, which distributes energy products including natural gas, propane, butane, and electricity. It operates in the United States and Europe through various business segments. The presentation discusses UGI's business model, growth strategy, and financial performance. It also highlights recent acquisitions, expansion projects, and growth opportunities across its utility, energy services, and propane distribution businesses.
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver failure that results in a reversible decrease in brain function. It is most common in patients with cirrhosis. Symptoms include disturbances in consciousness, personality changes, neurological signs like tremors, and confusion. It is caused by factors that increase the level of toxins in the blood that are normally processed by the liver, such as infections, bleeding, or kidney failure. Diagnosis is clinical but may include blood tests showing elevated ammonia levels or EEG changes. Treatment focuses on removing the precipitating cause and aiding liver function.
This document summarizes toxicant-associated fatty liver disease (TAFLD) and its causes. TAFLD ranges from simple steatosis to more severe nonalcoholic steatohepatitis (NASH) which can lead to cirrhosis or liver cancer. The main cause of TAFLD is food pollution by heavy metals like lead and mercury, and persistent organic pollutants. These toxic chemicals accumulate in foods like meat, dairy and certain fruits and vegetables due to environmental pollution and agricultural practices. When the liver is overloaded with these toxins, it can cause fatty deposits to form and liver cell damage or death.
This document discusses toxicant-associated fatty liver disease (TAFLD) and toxicant-associated steatohepatitis (TASH). It defines these conditions as forms of hepatic disease caused by food pollution from heavy metals and persistent organic pollutants. The main causes of TAFLD/TASH are identified as food pollution from heavy metals like lead and mercury, as well as pollutants like PCBs. Several studies have found associations between these toxicants and non-alcoholic fatty liver disease. The document discusses the pathogenesis and progression of TAFLD/TASH, as well as symptoms, diagnosis, and the role of endocrine disrupting chemicals in relation to these conditions.
Wilson disease with acute liver failure case presentationSanjeev Kumar
The document describes a case of a 30-year-old woman presenting with jaundice and altered mental status who was diagnosed with acute liver failure of unknown etiology. On examination, she had signs of hepatic encephalopathy and lab work showed elevated liver enzymes and coagulopathy. Further testing ruled out common causes of viral hepatitis and Wilson's disease, and the patient's condition deteriorated requiring ventilator support and consideration for liver transplant.
A good PG case presentation on abdominal case, liverKurian Joseph
This document discusses the case of a 43-year-old male agriculturalist presenting with jaundice, leg swelling, and occasional dark stools over the past few months. On examination, he is found to have pallor, jaundice, leg swelling, hepatomegaly, and signs of chronic alcohol use. The doctor diagnoses the patient with compensated liver disease in the form of early cirrhosis likely related to alcohol, with no current signs of portal hypertension or encephalopathy.
A 45-year-old male presented with hematemesis after vomiting blood the previous night. When confronted with a patient with hematemesis, the doctor should determine if it is truly hematemesis, assess the stability and estimated blood loss of the patient, consider possible lesions and their locations and blood supplies. A thorough history and examination is needed to correctly diagnose the source of bleeding. Initial management includes resuscitation with fluids and blood products as needed, passing a nasogastric tube, and arranging for urgent endoscopy within 18 hours. Long-term management depends on the findings and may include treatments like antibiotics, pharmacotherapy, endoscopic therapy, TIPS, or surgery.
Case presentation on alcoholic liver diseaseRavali Naidu
A 41-year-old male was admitted to the hospital with fever and chills for two days. His medical history revealed jaundice three times previously and a family history of diabetes and hypertension. Laboratory tests showed elevated liver enzymes and bilirubin, indicating alcoholic liver disease. He was prescribed medications to treat his condition, manage symptoms, and prevent drug interactions. The patient was counseled on lifestyle changes including abstaining from alcohol to prevent further liver damage.
Rifaximin treatment in hepatic encephalopathyPratap Tiwari
Rifaximin treatment significantly reduced the risk of hepatic encephalopathy episodes and hospitalizations over a 6-month period compared to placebo. In the study, 22.1% of patients taking rifaximin experienced a breakthrough hepatic encephalopathy episode, compared to 45.9% of patients taking placebo. The incidence of adverse events was similar between the two groups. The study demonstrates that rifaximin is effective for maintaining remission from hepatic encephalopathy in patients with cirrhosis.
Abdomen and liver case presentation by PGKurian Joseph
Abdomen and liver case presentation by PG
Chronic decompensated parenchymal liver disease - cirrhosis with portal hypertension probably of alcoholic etiology with no ascites with no features of hepatic encephalopathy and coagulopathy
To rule out malignancy
A 51-year-old man who had undergone surgery for stage II colon cancer two years prior presented with an elevated CEA level. Differential diagnoses included recurrent colorectal cancer or other cancers. Additional tests such as a CT scan, PET scan, and liver function tests were recommended to identify any masses in the abdomen or liver. Possible scenarios included a solitary 2 cm liver mass that could be surgically resected, with a 20-30% 5-year survival rate for patients with resectable liver metastases from colorectal cancer.
This document discusses hepatomegaly (enlarged liver). It describes the location and extent of the liver, clinical presentations of hepatomegaly including pain and jaundice, and examination techniques like inspection, palpation, percussion, and auscultation to evaluate the liver. Some causes of hepatomegaly mentioned are congestive heart failure, hepatic vein outflow obstruction, amoebic hepatitis, liver abscess, carcinoma, and hydatid cysts.
This document presents a case of traumatic liver injury in a 17-year old male patient who was in a motorcycle accident. He presented with abdominal pain and vomiting. Imaging showed a liver laceration and bleeding in the abdomen. He underwent an exploratory laparotomy where a left lobe liver laceration and diaphragm perforation were found and repaired. He recovered well after surgery with drain removal after one week and was discharged. Traumatic liver injuries can range from minor injuries treated non-operatively to severe injuries requiring surgery like lobectomy or packing to control bleeding. Both non-operative and surgical management were discussed.
The document discusses hepatic encephalopathy, a neurological syndrome caused by liver dysfunction. It covers the pathogenesis, which involves neurotoxins like ammonia crossing the blood brain barrier and disrupting neurotransmitter levels. Symptoms range from mild confusion to coma and can be precipitated by factors that increase ammonia production or permeability of the blood brain barrier. Treatment focuses on managing precipitating factors and restricting protein intake to control ammonia levels.
1. An 18-year-old female student presented with progressive lethargy, fever, and body aches for one month. She had a history of similar symptoms since age 12.
2. Initial examinations found splenomegaly but no clear diagnosis. Imaging showed a liver mass. Biopsies and further testing were needed to determine the cause.
3. The patient ultimately underwent laparotomy and biopsy of the liver mass. Post-operative histopathological examination revealed the diagnosis and further testing was done.
A 42-year-old male farmer presented with abdominal distension, pain, decreased urine output, and weight loss over the past two weeks. His history revealed chronic alcohol use over 30 years consuming 4.5-5.6 units daily. Examination found ascites and coagulopathy. Tests showed renal failure, cirrhosis, and transudative ascites. He was diagnosed with alcoholic liver disease complicated by ascites and hepatorenal syndrome due to chronic alcohol-induced cirrhosis. Management involved lifestyle changes including abstaining from alcohol and nutritional support.
Hepatic encephalopathy, short review & updateRushdanZakariah
This document provides an overview of hepatic encephalopathy. It describes hepatic encephalopathy as a complex neuropsychiatric syndrome characterized by disturbances in consciousness and personality changes. Acute episodes can be reversible while chronic cases may progress to coma or death. Precipitating factors include constipation, surgery, and progressive liver disease. Ammonia plays a central role in pathogenesis, as the liver is unable to metabolize and excrete nitrogenous waste products, leading to accumulation of ammonia in the blood and brain. Treatment aims to remove precipitating factors, reduce nitrogenous load from the gut, and manage symptoms. Options include nutritional management, laxatives, antibiotics like rifaximin, and lactulose to produce
A 59-year-old Chinese man was admitted to the hospital for vomiting blood. He has a history of hepatitis C and is a smoker, drinker, and former drug user. Physical examination found abdominal distension with fluid thrill and shifting dullness. Testing showed signs of liver dysfunction. The provisional diagnosis is esophageal varices secondary to liver disease, likely cirrhosis. Esophageal varices form as a result of portal hypertension in liver disease and can bleed, potentially severely. Treatment focuses on stopping the bleeding and lowering portal pressure through various medical and procedural options.
This document provides an overview of the approach to upper GI bleeding. It begins with definitions of terms like hematemesis, melena, and hematochezia. It then discusses the causes of upper GI bleeding, which can be variceal or non-variceal. For patients presenting with upper GI bleeding, the summary provides that history, physical exam, and investigations like endoscopy are important to determine the cause and guide management. Management may involve treating any active bleeding, administering PPIs for non-variceal bleeding, or using vasoactive agents, balloon tamponade, or endoscopic therapies for variceal bleeding.
Primary biliary cirrhosis and autoimmune hepatitis 20120902 Chien-Wei Su
This document summarizes a case of primary biliary cirrhosis (PBC) in a 66-year-old man who presented with intermittent pruritus for 8 years. Laboratory tests showed elevated liver enzymes and positive anti-mitochondrial antibodies, confirming the diagnosis of PBC. Liver biopsy showed features characteristic of PBC including destruction of bile duct epithelium and lymphocyte infiltration. The document then provides information on the epidemiology, risk factors, pathogenesis, natural history, diagnosis, treatment and prognosis of PBC.
This case report describes a 38-year-old man admitted to the hospital with black stools for 20 days and shortness of breath for 5 days. Examination found pallor and bruises. Tests showed severe anemia, elevated coagulation times, and a positive HCV antibody test. Upper endoscopy revealed stomach and duodenal erosions with oozing blood. The patient was diagnosed with type 1 von Willebrand disease based on a low von Willebrand factor level. He received transfusions, cryoprecipitates, factor replacement therapy, and endoscopic coagulation to treat his gastrointestinal bleeding.
This document presents a case study of a 63-year-old male who developed fatal cholestatic liver failure. He had undergone surgery for bladder cancer and cholecystectomy. His liver function tests continued rising after surgery. Extensive testing found no clear cause of cholestasis. Liver biopsies showed features of obstruction or drug effect. He was exposed to imipramine and amoxicillin-clavulanic acid, both known to cause cholestasis. Literature review found rare cases of progressive cholestasis and liver failure from these drugs. The patient's declining condition was treated supportively but he ultimately died of sepsis.
This presentation provides an overview of UGI Corporation, which distributes energy products including natural gas, propane, butane, and electricity. It operates in the United States and Europe through various business segments. The presentation discusses UGI's business model, growth strategy, and financial performance. It also highlights recent acquisitions, expansion projects, and growth opportunities across its utility, energy services, and propane distribution businesses.
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver failure that results in a reversible decrease in brain function. It is most common in patients with cirrhosis. Symptoms include disturbances in consciousness, personality changes, neurological signs like tremors, and confusion. It is caused by factors that increase the level of toxins in the blood that are normally processed by the liver, such as infections, bleeding, or kidney failure. Diagnosis is clinical but may include blood tests showing elevated ammonia levels or EEG changes. Treatment focuses on removing the precipitating cause and aiding liver function.
This document summarizes toxicant-associated fatty liver disease (TAFLD) and its causes. TAFLD ranges from simple steatosis to more severe nonalcoholic steatohepatitis (NASH) which can lead to cirrhosis or liver cancer. The main cause of TAFLD is food pollution by heavy metals like lead and mercury, and persistent organic pollutants. These toxic chemicals accumulate in foods like meat, dairy and certain fruits and vegetables due to environmental pollution and agricultural practices. When the liver is overloaded with these toxins, it can cause fatty deposits to form and liver cell damage or death.
This document discusses toxicant-associated fatty liver disease (TAFLD) and toxicant-associated steatohepatitis (TASH). It defines these conditions as forms of hepatic disease caused by food pollution from heavy metals and persistent organic pollutants. The main causes of TAFLD/TASH are identified as food pollution from heavy metals like lead and mercury, as well as pollutants like PCBs. Several studies have found associations between these toxicants and non-alcoholic fatty liver disease. The document discusses the pathogenesis and progression of TAFLD/TASH, as well as symptoms, diagnosis, and the role of endocrine disrupting chemicals in relation to these conditions.
1) The study develops a new parameter called the ALT-LDH index to predict prognosis in patients with acute liver injury using serum levels of alanine aminotransferase (ALT) and lactate dehydrogenase (LDH).
2) The ALT-LDH index was calculated as serum ALT divided by serum LDH minus the median normal LDH range.
3) The study found that the ALT-LDH index increased rapidly in patients who were conservative survivors but remained low in patients with progressive fatal liver failure, suggesting persistent hepatic hypoxia in fatal cases.
This document summarizes various types and causes of food pollution. It discusses how toxic chemicals and biological contaminants can contaminate food at various stages of production and processing. Specific causes of food pollution discussed include heavy metals from the environment entering the food supply, persistent organic pollutants such as PCBs and dioxins, and certain food additives like MSG, BHA/BHT, and sodium nitrate/nitrite which have been linked to health issues. The document also examines how food can become contaminated by bacteria, viruses, or parasites leading to food poisoning if improperly handled or cooked.
Hematologic Disorders Related to HCV Infection and their management
1) HCV can cause various extrahepatic manifestations including blood disorders, autoimmune disorders, skin conditions, and kidney disease. Common blood disorders include anemia, thrombocytopenia, and cryoglobulinemia.
2) Cryoglobulinemia is the precipitation of immune complexes containing rheumatoid factor and cryoproteins in the blood vessels. This can lead to vasculitis and is associated with HCV infection in 50-100% of cases.
3) Treatment of HCV-related conditions may involve antiviral therapy with interferon or pegylated interferon, which can help reduce HCV RNA levels and cryoglobulin levels
This document summarizes the causes and health effects of food pollution. It discusses various types of contaminants including agrochemicals, heavy metals, persistent organic pollutants, and microorganisms that can cause food poisoning. Major sources of contamination are discussed such as environmental pollution from air, water and soil; packaging materials; food processing equipment; and cross-contamination. Specific heavy metals like lead, mercury, arsenic and cadmium are examined in depth regarding their sources and impacts on health. Common persistent organic pollutants known as the "dirty dozen" are also outlined.
1. A 62-year-old patient presented with fever and abdominal pain in the right
upper quadrant. He had an 18-month history of adenocarcinoma of the colon
(T3N1M1) with liver metastases, for which he underwent a right hemicolectomy
and received chemotherapy with irinotecan and cetuximab; in addition he
underwent chemoembolization of the liver lesion. His past medical history was
significant for diverticulosis, atrial fibrillation, hypertension (amlodipine 5 mg
every 12 hours per os and atenolol 25 mg once a day) and appendectom