This document provides an overview of chronic liver disease (CLD) including:
- CLD results from long-term inflammation and damage to the liver that can progress to cirrhosis over 6 months. Common causes include alcohol, viral hepatitis, fatty liver disease, and genetic/autoimmune conditions.
- Clinical manifestations range from asymptomatic to jaundice, abdominal pain/swelling, bleeding, confusion and liver failure. Complications include portal hypertension, ascites, hepatic encephalopathy and liver cancer.
- Investigations include blood tests of liver function and damage, imaging like ultrasound/CT, and biopsy. Prognosis is assessed using Child-Pugh or MELD scores. Management focuses on treating the underlying
1) Acute pancreatitis is defined as an acute inflammatory process of the pancreas with variable involvement of other tissues. It is diagnosed when a patient presents with abdominal pain consistent with the disease as well as serum amylase or lipase levels over three times the upper limit of normal.
2) Common causes of acute pancreatitis include gallstones, alcohol use, hypertriglyceridemia, endoscopic retrograde cholangiopancreatography (ERCP), trauma, postoperative complications, and certain drugs.
3) Management involves adequate hydration, analgesia, monitoring for organ failure, cautious administration of fluids and insulin, and consideration of endoscopic procedures or surgery in severe cases with complications like necrosis
This document discusses alcoholic liver disease (ALD). It notes that ALD ranges in severity from fatty liver to alcoholic hepatitis to cirrhosis. Risk factors include the amount of alcohol consumed daily and genetically. Diagnosis involves blood tests like GGT and liver biopsy. Severe alcoholic hepatitis has high short-term mortality and is treated with corticosteroids or pentoxifylline to reduce inflammation. Prognosis can be predicted using scores like Maddrey DF and management involves lifestyle changes like abstaining from alcohol and adequate nutrition.
Diabetic nephropathy is a chronic kidney disease characterized by gradually increasing urinary albumin excretion, high blood pressure, declining kidney function, and presence of diabetic retinopathy. It develops in 20-40% of people with diabetes and is the leading cause of end-stage renal disease. The pathophysiology involves metabolic and hemodynamic pathways as well as genetic factors. Hyperglycemia causes kidney damage through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and other mechanisms. Hemodynamic changes from hypertension increase glomerular pressure and permeability. Genetic factors like ACE polymorphisms also influence risk. Progression is associated with proteinuria, anemia
This document discusses chronic kidney disease (CKD), including its definition, stages, pathophysiology, clinical manifestations, and relationship to kidney failure, end-stage renal disease, and uremia. CKD is defined as glomerular filtration rate below 60 mL/min/1.73m2 or kidney damage for over 3 months. As CKD progresses, compensatory mechanisms disrupt homeostasis, leading to accumulation of waste and abnormalities. Later stages involve loss of over 90% of nephrons and inability to maintain fluid, electrolyte and hormone balance without dialysis or transplant.
This document summarizes acute and chronic pancreatitis. It covers the anatomy and physiology of the pancreas, pathophysiology, causes, symptoms, signs, diagnostic testing including labs and imaging, medical and surgical treatment options, and prognosis. The main causes of acute pancreatitis are biliary disease and alcohol use, while chronic pancreatitis is primarily caused by alcohol use long-term. Complications can include pseudocysts, abscesses, pancreatic necrosis, and pancreatic duct disruption. Treatment depends on the severity and includes pain control, antibiotics, nutritional support, enzyme replacement, and possible surgery.
This document defines cirrhosis as a condition where the liver slowly deteriorates and malfunctions due to chronic injury, with scar tissue replacing healthy liver tissue and partially blocking blood flow. It discusses the anatomy, physiology, causes including hepatitis and alcohol abuse, pathophysiology, clinical manifestations such as jaundice and ascites, diagnostic studies, collaborative care including management of ascites and esophageal varices, drug therapy, surgical management, nutritional management focusing on low protein and sodium diets, nursing management, and patient education on continuing healthcare and avoiding alcohol and aspirin.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
1) Acute pancreatitis is defined as an acute inflammatory process of the pancreas with variable involvement of other tissues. It is diagnosed when a patient presents with abdominal pain consistent with the disease as well as serum amylase or lipase levels over three times the upper limit of normal.
2) Common causes of acute pancreatitis include gallstones, alcohol use, hypertriglyceridemia, endoscopic retrograde cholangiopancreatography (ERCP), trauma, postoperative complications, and certain drugs.
3) Management involves adequate hydration, analgesia, monitoring for organ failure, cautious administration of fluids and insulin, and consideration of endoscopic procedures or surgery in severe cases with complications like necrosis
This document discusses alcoholic liver disease (ALD). It notes that ALD ranges in severity from fatty liver to alcoholic hepatitis to cirrhosis. Risk factors include the amount of alcohol consumed daily and genetically. Diagnosis involves blood tests like GGT and liver biopsy. Severe alcoholic hepatitis has high short-term mortality and is treated with corticosteroids or pentoxifylline to reduce inflammation. Prognosis can be predicted using scores like Maddrey DF and management involves lifestyle changes like abstaining from alcohol and adequate nutrition.
Diabetic nephropathy is a chronic kidney disease characterized by gradually increasing urinary albumin excretion, high blood pressure, declining kidney function, and presence of diabetic retinopathy. It develops in 20-40% of people with diabetes and is the leading cause of end-stage renal disease. The pathophysiology involves metabolic and hemodynamic pathways as well as genetic factors. Hyperglycemia causes kidney damage through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and other mechanisms. Hemodynamic changes from hypertension increase glomerular pressure and permeability. Genetic factors like ACE polymorphisms also influence risk. Progression is associated with proteinuria, anemia
This document discusses chronic kidney disease (CKD), including its definition, stages, pathophysiology, clinical manifestations, and relationship to kidney failure, end-stage renal disease, and uremia. CKD is defined as glomerular filtration rate below 60 mL/min/1.73m2 or kidney damage for over 3 months. As CKD progresses, compensatory mechanisms disrupt homeostasis, leading to accumulation of waste and abnormalities. Later stages involve loss of over 90% of nephrons and inability to maintain fluid, electrolyte and hormone balance without dialysis or transplant.
This document summarizes acute and chronic pancreatitis. It covers the anatomy and physiology of the pancreas, pathophysiology, causes, symptoms, signs, diagnostic testing including labs and imaging, medical and surgical treatment options, and prognosis. The main causes of acute pancreatitis are biliary disease and alcohol use, while chronic pancreatitis is primarily caused by alcohol use long-term. Complications can include pseudocysts, abscesses, pancreatic necrosis, and pancreatic duct disruption. Treatment depends on the severity and includes pain control, antibiotics, nutritional support, enzyme replacement, and possible surgery.
This document defines cirrhosis as a condition where the liver slowly deteriorates and malfunctions due to chronic injury, with scar tissue replacing healthy liver tissue and partially blocking blood flow. It discusses the anatomy, physiology, causes including hepatitis and alcohol abuse, pathophysiology, clinical manifestations such as jaundice and ascites, diagnostic studies, collaborative care including management of ascites and esophageal varices, drug therapy, surgical management, nutritional management focusing on low protein and sodium diets, nursing management, and patient education on continuing healthcare and avoiding alcohol and aspirin.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
Peptic ulcers are lesions that occur in areas of the gastrointestinal tract exposed to stomach acid. Risk factors include H. pylori infection and NSAID use. Clinical features include recurrent abdominal pain related to food. Diagnosis involves endoscopy with biopsy or breath/stool tests for H. pylori. Management involves eradicating H. pylori with triple therapy antibiotics and PPIs. Surgery is rarely needed and reserved for complications like perforation or bleeding.
Hepatic encephalopathy occurs when the liver fails to detoxify toxic substances, such as ammonia, which are then able to pass into the brain. This causes neurological symptoms ranging from mild confusion to coma. Precipitating factors include gastrointestinal bleeding, infections, and certain drugs. Treatment focuses on reducing ammonia production in the gut through lactulose, antibiotics, and low-protein diets. Correcting electrolyte imbalances and removing precipitating medications or infections are also important for management of hepatic encephalopathy.
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.
This document provides an outline and details regarding chronic liver disease. It begins with an introduction defining chronic liver disease and its causes. Key points include that chronic liver disease lasts over 6 months and can result from viral infections, autoimmune conditions, inherited diseases, cancer or toxin consumption. The document then covers the epidemiology, etiology, pathophysiology, risk factors, complications, signs and symptoms, investigations and treatments of chronic liver disease in greater detail over multiple pages.
This document provides an overview of chronic pancreatitis, including its definition, epidemiology, pathology, classification, clinical features, diagnosis and treatment. Chronic pancreatitis is defined as permanent and irreversible damage to the pancreas resulting in inflammation, fibrosis and destruction of pancreatic tissue. It has an annual incidence of 3-9 cases per 100,000 people. Alcohol is a major risk factor. Diagnosis involves evaluating pancreatic function and structure through imaging, endoscopy and genetic/serological testing. Treatment focuses on pain management, pancreatic enzyme supplementation and surgery for severe cases.
This document discusses dyspepsia, defined as epigastric pain, burning, postprandial fullness, or early satiety. Dyspepsia can be caused by organic diseases like peptic ulcers, GERD, or malignancies. It can also be functional in nature. The evaluation of dyspepsia involves history, physical exam, and testing for H. pylori infection or structural abnormalities. Treatment depends on identified causes, but may include H. pylori eradication therapy, PPIs, or endoscopy.
Inflammatory bowel disease (IBD) includes two major types: Crohn's disease and ulcerative colitis. Crohn's disease can affect any part of the gastrointestinal tract and often involves the full thickness of the intestinal wall. Ulcerative colitis only involves the innermost layers of the colon and rectum. Both conditions result from an interaction between genetic, immune, environmental, and bacterial factors. Symptoms include diarrhea, abdominal pain, and weight loss. Treatment focuses on inducing remission through medications like aminosalicylates or surgery to remove the colon. Crohn's disease is characterized by "skip lesions" and strictures while ulcerative colitis causes inflammation and ulcers confined to the colon.
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.
An introduction to alcoholic liver disease part1Pratap Tiwari
This document provides an overview of alcoholic liver disease (ALD). It begins with an introduction to ALD and outlines the spectrum of conditions it can cause, from fatty liver to alcoholic hepatitis to cirrhosis. Key points covered include:
- ALD is caused by chronic, excessive alcohol consumption and results in liver dysfunction.
- The amount and duration of alcohol intake are major risk factors, and women are more susceptible than men.
- Chronic hepatitis C infection can also contribute to progression to cirrhosis in heavy drinkers.
- Clinical manifestations of ALD include jaundice, coagulopathy, and hepatic encephalopathy as liver functions like detoxification and protein synthesis are affected.
Cirrhosis is a diffuse process characterized by liver necrosis and fibrosis that converts the normal liver architecture into abnormal nodules lacking a normal lobular organization. It has many causes including viral hepatitis infections, alcohol toxicity, autoimmune diseases, and genetic disorders. Pathologically, cirrhosis involves nodularity, fibrosis from collagen deposition, and abnormal hepatocyte changes. Portal hypertension develops due to increased resistance to blood flow from architectural disruption of the cirrhotic liver, leading to formation of portosystemic collaterals that bypass the liver. The severity of cirrhosis is classified using the Child-Pugh or MELD scoring systems to determine prognosis and need for transplantation.
This document provides an overview of pancreatitis, including:
- It describes acute and chronic pancreatitis, with acute pancreatitis presenting with abdominal pain and elevated enzymes.
- The mechanism involves premature enzyme activation leading to autodigestion and inflammation of the pancreas.
- Signs, symptoms, and imaging findings are discussed for assessing severity and managing acute pancreatitis. Complications like fluid collections, necrosis, and abscesses are also covered.
- Treatment involves conservative management for mild cases and intensive care, monitoring, antibiotics and drainage procedures for more severe cases.
This document discusses the pathophysiology of portal hypertension. Portal hypertension occurs when there is an elevation in portal venous pressure above 10 mmHg. It can be caused by pre-hepatic issues like portal vein thrombosis, or intrahepatic issues like cirrhosis. The pathophysiology involves increased resistance to portal blood flow from vasoconstriction and fibrosis, as well as increased blood flow from splanchnic vasodilation. This leads to the formation of portosystemic shunts and complications like variceal bleeding, ascites, and hepatic encephalopathy. Management involves general measures during bleeding, pharmacological agents, endoscopic therapy of varices, and procedures like TIPS or transplantation.
Tubulointerstitial nephritis involves inflammatory reactions in the renal tubules and interstitium. It can be primary, secondary to other renal diseases, idiopathic, reactive to infections, or infectious itself. Acute tubular necrosis is characterized by tubular epithelial cell death due to ischemia or toxins and can cause acute kidney injury. Chronic tubulointerstitial nephritis develops over months or years and is associated with progressive loss of kidney function. It has many etiologies including drugs, infections, obstructive nephropathy, and autoimmune diseases.
Chronic pancreatitis is a progressive inflammatory condition of the pancreas characterized by irreversible morphological changes and loss of function. It is most commonly caused by long term heavy alcohol use. Symptoms include recurrent abdominal pain, steatorrhea due to exocrine insufficiency, and diabetes mellitus due to endocrine insufficiency. Diagnosis involves functional tests like fecal elastase and imaging modalities like CT, MRI, ERCP and EUS which demonstrate findings of pancreatic duct abnormalities, parenchymal changes and calcifications.
Cirrhosis is a chronic, progressive disease of the liver caused by extensive liver cell damage and regeneration. It results in the formation of fibrous scar tissue and loss of normal liver architecture. Common causes include alcohol abuse and viral hepatitis. Complications arise due to liver dysfunction and portal hypertension, such as jaundice, ascites, variceal bleeding, and hepatic encephalopathy. Treatment focuses on managing complications, dietary changes, and medication to reduce ammonia levels and symptoms.
This document summarizes key information about pancreatitis. It discusses the definition, incidence, etiology, pathogenesis, symptoms, investigations and management of both acute and chronic pancreatitis. For acute pancreatitis, it covers risk stratification, treatment including fluid resuscitation and antibiotics, and complications. For chronic pancreatitis, it discusses etiology, consequences, diagnosis using imaging and functional tests, and the spectrum of disease damage.
This document summarizes cirrhosis of the liver. It defines cirrhosis as irreversible liver damage characterized by abnormal liver structure and function. The main causes listed are chronic alcohol abuse, hepatitis B and C, non-alcoholic steatohepatitis (NASH), and genetic disorders. Complications include hepatic failure, portal hypertension, ascites, variceal bleeding, and hepatocellular carcinoma. Tests used to diagnose and monitor cirrhosis are also outlined. Management focuses on treating the underlying cause, nutrition, screening for complications, and liver transplantation in severe cases.
1. Chronic hepatitis represents liver inflammation that lasts at least 6 months and can range from mild and nonprogressive to severe, leading to cirrhosis.
2. Chronic hepatitis is classified by cause, grade or stage of liver damage, and different types include hepatitis B, C, NAFLD, alcoholic hepatitis, and autoimmune hepatitis.
3. Hepatitis B is further classified into phases including immune tolerant, immune clearance, and inactive or reactivation phases based on viral markers and liver damage.
Chronic Kidney Disease (CKD) is characterized by a progressive decline in kidney function over time and is classified into 5 stages based on glomerular filtration rate. CKD has many potential causes including diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. As kidney function declines, patients experience complications such as anemia, bone disease, electrolyte imbalances, cardiovascular disease, and other systemic effects. Treatment focuses on slowing progression, managing complications, and renal replacement therapy for stage 5 CKD.
Etiology, Pathology and presentation of Cirrhosis of live. signs and symptoms and complication of the disease. Its a basic level Presentation on this given topic to have an idea about the Cirrhosis of Liver.
This document provides information on liver cirrhosis, including its definition, causes, epidemiology, pathophysiology, diagnosis, and management. Key points include:
- Liver cirrhosis is defined histopathologically by liver fibrosis and architectural distortion leading to regenerative nodules and loss of liver function.
- Major causes include alcohol consumption, viral hepatitis, NAFLD/NASH, and genetic diseases.
- Complications arise due to portal hypertension and include ascites, variceal bleeding, and hepatic encephalopathy.
- Diagnosis involves clinical features, labs, imaging, and sometimes biopsy. Non-invasive methods can assess liver fibrosis.
- Management focuses on treating the underlying cause, complications
1. The document discusses factors to consider when prescribing psychiatric medications in patients with liver disease. Liver disease can impact the pharmacokinetics of drugs by altering absorption, metabolism, protein binding, and excretion.
2. Drugs are categorized based on their hepatic extraction ratio and metabolism. High extraction drugs are more susceptible to fluctuations. Interactions with liver enzyme inducers/inhibitors and alcohol are also discussed.
3. When prescribing for patients with liver disease, the degree of impairment, drug metabolism pathway, interactions, and narrow therapeutic index drugs should be considered. Dose adjustments and monitoring are often needed.
Peptic ulcers are lesions that occur in areas of the gastrointestinal tract exposed to stomach acid. Risk factors include H. pylori infection and NSAID use. Clinical features include recurrent abdominal pain related to food. Diagnosis involves endoscopy with biopsy or breath/stool tests for H. pylori. Management involves eradicating H. pylori with triple therapy antibiotics and PPIs. Surgery is rarely needed and reserved for complications like perforation or bleeding.
Hepatic encephalopathy occurs when the liver fails to detoxify toxic substances, such as ammonia, which are then able to pass into the brain. This causes neurological symptoms ranging from mild confusion to coma. Precipitating factors include gastrointestinal bleeding, infections, and certain drugs. Treatment focuses on reducing ammonia production in the gut through lactulose, antibiotics, and low-protein diets. Correcting electrolyte imbalances and removing precipitating medications or infections are also important for management of hepatic encephalopathy.
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.
This document provides an outline and details regarding chronic liver disease. It begins with an introduction defining chronic liver disease and its causes. Key points include that chronic liver disease lasts over 6 months and can result from viral infections, autoimmune conditions, inherited diseases, cancer or toxin consumption. The document then covers the epidemiology, etiology, pathophysiology, risk factors, complications, signs and symptoms, investigations and treatments of chronic liver disease in greater detail over multiple pages.
This document provides an overview of chronic pancreatitis, including its definition, epidemiology, pathology, classification, clinical features, diagnosis and treatment. Chronic pancreatitis is defined as permanent and irreversible damage to the pancreas resulting in inflammation, fibrosis and destruction of pancreatic tissue. It has an annual incidence of 3-9 cases per 100,000 people. Alcohol is a major risk factor. Diagnosis involves evaluating pancreatic function and structure through imaging, endoscopy and genetic/serological testing. Treatment focuses on pain management, pancreatic enzyme supplementation and surgery for severe cases.
This document discusses dyspepsia, defined as epigastric pain, burning, postprandial fullness, or early satiety. Dyspepsia can be caused by organic diseases like peptic ulcers, GERD, or malignancies. It can also be functional in nature. The evaluation of dyspepsia involves history, physical exam, and testing for H. pylori infection or structural abnormalities. Treatment depends on identified causes, but may include H. pylori eradication therapy, PPIs, or endoscopy.
Inflammatory bowel disease (IBD) includes two major types: Crohn's disease and ulcerative colitis. Crohn's disease can affect any part of the gastrointestinal tract and often involves the full thickness of the intestinal wall. Ulcerative colitis only involves the innermost layers of the colon and rectum. Both conditions result from an interaction between genetic, immune, environmental, and bacterial factors. Symptoms include diarrhea, abdominal pain, and weight loss. Treatment focuses on inducing remission through medications like aminosalicylates or surgery to remove the colon. Crohn's disease is characterized by "skip lesions" and strictures while ulcerative colitis causes inflammation and ulcers confined to the colon.
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.
An introduction to alcoholic liver disease part1Pratap Tiwari
This document provides an overview of alcoholic liver disease (ALD). It begins with an introduction to ALD and outlines the spectrum of conditions it can cause, from fatty liver to alcoholic hepatitis to cirrhosis. Key points covered include:
- ALD is caused by chronic, excessive alcohol consumption and results in liver dysfunction.
- The amount and duration of alcohol intake are major risk factors, and women are more susceptible than men.
- Chronic hepatitis C infection can also contribute to progression to cirrhosis in heavy drinkers.
- Clinical manifestations of ALD include jaundice, coagulopathy, and hepatic encephalopathy as liver functions like detoxification and protein synthesis are affected.
Cirrhosis is a diffuse process characterized by liver necrosis and fibrosis that converts the normal liver architecture into abnormal nodules lacking a normal lobular organization. It has many causes including viral hepatitis infections, alcohol toxicity, autoimmune diseases, and genetic disorders. Pathologically, cirrhosis involves nodularity, fibrosis from collagen deposition, and abnormal hepatocyte changes. Portal hypertension develops due to increased resistance to blood flow from architectural disruption of the cirrhotic liver, leading to formation of portosystemic collaterals that bypass the liver. The severity of cirrhosis is classified using the Child-Pugh or MELD scoring systems to determine prognosis and need for transplantation.
This document provides an overview of pancreatitis, including:
- It describes acute and chronic pancreatitis, with acute pancreatitis presenting with abdominal pain and elevated enzymes.
- The mechanism involves premature enzyme activation leading to autodigestion and inflammation of the pancreas.
- Signs, symptoms, and imaging findings are discussed for assessing severity and managing acute pancreatitis. Complications like fluid collections, necrosis, and abscesses are also covered.
- Treatment involves conservative management for mild cases and intensive care, monitoring, antibiotics and drainage procedures for more severe cases.
This document discusses the pathophysiology of portal hypertension. Portal hypertension occurs when there is an elevation in portal venous pressure above 10 mmHg. It can be caused by pre-hepatic issues like portal vein thrombosis, or intrahepatic issues like cirrhosis. The pathophysiology involves increased resistance to portal blood flow from vasoconstriction and fibrosis, as well as increased blood flow from splanchnic vasodilation. This leads to the formation of portosystemic shunts and complications like variceal bleeding, ascites, and hepatic encephalopathy. Management involves general measures during bleeding, pharmacological agents, endoscopic therapy of varices, and procedures like TIPS or transplantation.
Tubulointerstitial nephritis involves inflammatory reactions in the renal tubules and interstitium. It can be primary, secondary to other renal diseases, idiopathic, reactive to infections, or infectious itself. Acute tubular necrosis is characterized by tubular epithelial cell death due to ischemia or toxins and can cause acute kidney injury. Chronic tubulointerstitial nephritis develops over months or years and is associated with progressive loss of kidney function. It has many etiologies including drugs, infections, obstructive nephropathy, and autoimmune diseases.
Chronic pancreatitis is a progressive inflammatory condition of the pancreas characterized by irreversible morphological changes and loss of function. It is most commonly caused by long term heavy alcohol use. Symptoms include recurrent abdominal pain, steatorrhea due to exocrine insufficiency, and diabetes mellitus due to endocrine insufficiency. Diagnosis involves functional tests like fecal elastase and imaging modalities like CT, MRI, ERCP and EUS which demonstrate findings of pancreatic duct abnormalities, parenchymal changes and calcifications.
Cirrhosis is a chronic, progressive disease of the liver caused by extensive liver cell damage and regeneration. It results in the formation of fibrous scar tissue and loss of normal liver architecture. Common causes include alcohol abuse and viral hepatitis. Complications arise due to liver dysfunction and portal hypertension, such as jaundice, ascites, variceal bleeding, and hepatic encephalopathy. Treatment focuses on managing complications, dietary changes, and medication to reduce ammonia levels and symptoms.
This document summarizes key information about pancreatitis. It discusses the definition, incidence, etiology, pathogenesis, symptoms, investigations and management of both acute and chronic pancreatitis. For acute pancreatitis, it covers risk stratification, treatment including fluid resuscitation and antibiotics, and complications. For chronic pancreatitis, it discusses etiology, consequences, diagnosis using imaging and functional tests, and the spectrum of disease damage.
This document summarizes cirrhosis of the liver. It defines cirrhosis as irreversible liver damage characterized by abnormal liver structure and function. The main causes listed are chronic alcohol abuse, hepatitis B and C, non-alcoholic steatohepatitis (NASH), and genetic disorders. Complications include hepatic failure, portal hypertension, ascites, variceal bleeding, and hepatocellular carcinoma. Tests used to diagnose and monitor cirrhosis are also outlined. Management focuses on treating the underlying cause, nutrition, screening for complications, and liver transplantation in severe cases.
1. Chronic hepatitis represents liver inflammation that lasts at least 6 months and can range from mild and nonprogressive to severe, leading to cirrhosis.
2. Chronic hepatitis is classified by cause, grade or stage of liver damage, and different types include hepatitis B, C, NAFLD, alcoholic hepatitis, and autoimmune hepatitis.
3. Hepatitis B is further classified into phases including immune tolerant, immune clearance, and inactive or reactivation phases based on viral markers and liver damage.
Chronic Kidney Disease (CKD) is characterized by a progressive decline in kidney function over time and is classified into 5 stages based on glomerular filtration rate. CKD has many potential causes including diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. As kidney function declines, patients experience complications such as anemia, bone disease, electrolyte imbalances, cardiovascular disease, and other systemic effects. Treatment focuses on slowing progression, managing complications, and renal replacement therapy for stage 5 CKD.
Etiology, Pathology and presentation of Cirrhosis of live. signs and symptoms and complication of the disease. Its a basic level Presentation on this given topic to have an idea about the Cirrhosis of Liver.
This document provides information on liver cirrhosis, including its definition, causes, epidemiology, pathophysiology, diagnosis, and management. Key points include:
- Liver cirrhosis is defined histopathologically by liver fibrosis and architectural distortion leading to regenerative nodules and loss of liver function.
- Major causes include alcohol consumption, viral hepatitis, NAFLD/NASH, and genetic diseases.
- Complications arise due to portal hypertension and include ascites, variceal bleeding, and hepatic encephalopathy.
- Diagnosis involves clinical features, labs, imaging, and sometimes biopsy. Non-invasive methods can assess liver fibrosis.
- Management focuses on treating the underlying cause, complications
1. The document discusses factors to consider when prescribing psychiatric medications in patients with liver disease. Liver disease can impact the pharmacokinetics of drugs by altering absorption, metabolism, protein binding, and excretion.
2. Drugs are categorized based on their hepatic extraction ratio and metabolism. High extraction drugs are more susceptible to fluctuations. Interactions with liver enzyme inducers/inhibitors and alcohol are also discussed.
3. When prescribing for patients with liver disease, the degree of impairment, drug metabolism pathway, interactions, and narrow therapeutic index drugs should be considered. Dose adjustments and monitoring are often needed.
The document summarizes renal support in patients with hepatic disease. It defines hepatorenal syndrome as renal failure that develops in patients with advanced liver disease due to alterations in renal physiology. HRS is diagnosed when renal dysfunction occurs in the absence of other identifiable kidney problems. The document outlines risk factors, types, diagnostic criteria, and management approaches for HRS, including prevention through infection control and treatment with vasoconstrictors, renal support, and liver transplantation.
Chronic kidney disease (CKD) consists of a spectrum of different pathophysiologic processes associated with abnormal kidney function, and a progressive decline in glomerular filtration rate (GFR).
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. It is most often caused by gallstones or heavy alcohol use. A patient presents with acute upper abdominal pain that may radiate to the back. Laboratory tests show elevated pancreatic enzymes and imaging can identify gallstones or complications. Severity is assessed by the presence of organ failure or local complications like necrosis. Treatment involves fluid resuscitation and management of complications. The Ranson criteria uses factors at admission and within 48 hours to predict severe acute pancreatitis.
This document discusses renal function tests and their importance in assessing kidney function and detecting impairment. It describes various tests including urine analysis, blood tests of creatinine and urea, and glomerular function tests. Common indications for evaluating renal function are listed, such as older age, diabetes, and hypertension. The document also outlines approaches to interpreting test results and diagnosing different kidney conditions like acute injury, nephritic syndrome, and nephrotic syndrome.
This document provides information on obstructive jaundice, including:
- Causes of obstructive jaundice include gallstones, tumors, strictures.
- Clinical features include jaundice, itching, steatorrhea.
- Investigations include liver function tests, ultrasound, CT, MRCP, ERCP.
- ERCP allows both diagnosis and treatment by sphincterotomy and stone extraction.
- Surgical management of stones includes open exploration or laparoscopic removal.
- Benign strictures are often post-surgical and may require stenting or reconstruction.
The document discusses pancreatitis, including defining acute pancreatitis as an inflammation of the pancreas that can range from mild edema to severe hemorrhagic necrosis. It outlines causes such as gallstones and alcohol, pathophysiology, clinical manifestations like abdominal pain and vomiting, potential complications, diagnostic tests, treatment including pain management and nutritional support, and discusses chronic pancreatitis.
Chronic excessive alcohol consumption can lead to a spectrum of alcoholic liver disease including fatty liver, alcoholic hepatitis, and cirrhosis. Fatty liver is most common, while only 10-20% of alcoholics develop hepatitis. Hepatitis is characterized by hepatocyte injury, ballooning, and inflammation. Cirrhosis results in fibrosis and nodular regeneration of liver architecture. Complications include ascites, variceal bleeding, and hepatic encephalopathy. Treatment of alcoholic liver disease involves abstaining from alcohol and managing complications. Corticosteroids may benefit severe hepatitis. Liver transplantation is an option for end-stage disease if abstinence is maintained.
Medical Surgical Nursing - I
UNIT: IV -Nursing Management of Patients With Disorder of Digestive System "Cirrhosis of liver"
the topic covers
- the stages, Pathophysiology and clinical manifestation of Cirrhosis of liver
- diagnostic evaluation and complication of Cirrhosis of liver
- medical, surgical and nursing management of patient with Cirrhosis of liver
This document discusses chronic kidney disease (CKD) in pediatrics. It defines CKD as kidney damage lasting at least 3 months as determined by structural abnormalities and/or a glomerular filtration rate below 60 mL/min/1.73m2. The stages of CKD are described based on GFR. Common causes in children include congenital abnormalities and glomerulonephritis. The pathogenesis involves hyperfiltration injury and other factors like proteinuria that accelerate kidney damage. Management aims to address complications through careful monitoring, nutrition, treatment of mineral bone disorders, and controlling blood pressure and electrolyte abnormalities.
Pancreatitis - etiology, pathophysiology and nutritionmunniradhika
The document summarizes acute and chronic pancreatitis. It describes the pancreas and defines pancreatitis as inflammation of the pancreas that can cause organ damage. It discusses the differences between acute and chronic pancreatitis, including presentation and development of fibrosis over time for chronic cases. For acute pancreatitis, it outlines signs and symptoms, causes, investigations, severity assessments, medical nutrition therapy including the use of enteral feeding, and appropriate formulas. For chronic pancreatitis it discusses classification, etiology, pathophysiology, symptoms, and nutritional management focusing on fat intake and supplementation.
Controverse in terapia cu statine in hepatopatiile cronice difuzeALEXANDRU ANDRITOIU
sunt prezentate rezultate din studii si cazuri clinice particulare, exemplificand-se dislipidemia din diverse afectiuni hepatice difuze si rolul terapiei cu statine, intre riscuri si beneficii la acesti pacienti
This document provides an overview of pancreatitis and pancreatic pseudocysts. It defines acute and chronic pancreatitis, describes the pathogenesis involving premature activation of pancreatic enzymes, and lists common causes like gallstones. Signs and symptoms include abdominal pain while complications involve local issues like pseudocysts or systemic problems. Diagnosis involves blood tests, imaging, and assessing severity with tools like BISAP score. Management focuses on supportive care, treating underlying causes, and draining complications surgically or minimally invasively. Pseudocysts are pancreatic fluid collections that often resolve on their own but sometimes require intervention.
This document discusses various types of cirrhosis including alcoholic cirrhosis, cirrhosis due to viral hepatitis, autoimmune hepatitis, nonalcoholic fatty liver disease, biliary cirrhosis, and cardiac cirrhosis. It provides details on the pathogenesis, clinical features, diagnosis, and treatment of alcoholic cirrhosis. It also discusses cirrhosis due to hepatitis C and B viruses, noting the progression of liver disease and treatments including antiviral therapy. Finally, it covers cirrhosis due to autoimmune hepatitis, nonalcoholic steatohepatitis, and biliary cirrhosis.
The document discusses chronic kidney disease (CKD) in children. It defines CKD, describes the stages and progression of disease. Common causes in children include congenital abnormalities and inherited disorders. Clinical features range from asymptomatic to growth retardation, hypertension, anemia and bone disease. Investigations include blood and urine tests to assess kidney function and damage. Management involves fluid, electrolyte, nutritional, anemic and bone disease management tailored to the stage of CKD.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
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4. 1. INTRODUCTION
Chronic liver disease (CLD) is a progressive deterioration of liver functions for more
than 6 months, which includes synthesis of clotting factors other proteins,
detoxification of harmful products of metabolism, and excretion of bile.
CLD is a continuous process of inflammation, destruction, and regeneration of liver
parenchyma, → fibrosis and cirrhosis.
Cirrhosis is a final stage of chronic liver disease that results in disruption of liver architecture,
the formation of widespread nodules, vascular reorganization, neo-angiogenesis, and
deposition of an extracellular matrix.
6. 2. AETIOLOGY (1)
1 Alcoholic Liver
Disease
➔ A spectrum of disease which includes alcoholic fatty liver with/ without hepatitis, alcohol
hepatitis → cirrhosis.
➔ Alcohol use disorder is the most frequent cause of CLD
2 Non-alcoholic Fatty
Liver Disease
(NAFLD/NASH)
➔ NAFLD has an association with metabolic syndrome (obesity, hyperlipidemia, DM)
➔ Some of these patients develop non-alcoholic steatohepatitis → liver fibrosis
3 Chronic Viral
Hepatitis
➔ Chronic hepatitis B,C and D infections are the most common causes of chronic liver
disease in East Asia and Sub-Saharan Africa
4 Genetic causes Alpha-1 antitrypsin
deficiency
➔ The most common genetic cause of CLD among children
Hereditary
hemochromatosis
➔ Autosomal recessive disorder of iron absorption
➔ Mutation involving HFE gene that regulates the iron absorption
from the intestine → excessive iron is absorbed from the GI
tract → pathological increase in ferritin and hemosiderin →
generation of hydroxyl free radicals → organ fibrosis
Wilson disease ➔ Autosomal recessive disorder leading to copper accumulation
7. 2. AETIOLOGY (2)
5 Autoimmune
Causes
Primary biliary
cirrhosis (PBC)
➔ An autoimmune and progressive disease of liver
➔ There is a destruction of intrahepatic biliary channel and portal
inflammation and scarring → cholestatic jaundice and fibrosis
of liver parenchyma
➔ Common in middle aged women
Primary sclerosing
cholangitis (PSC)
➔ Commonly associated with ulcerative colitis
➔ Characterized by a decrease in the size of intrahepatic and
extrahepatic bile ducts due to inflammation and fibrosis
Autoimmune
hepatitis (AIH)
➔ A form of chronic inflammatory hepatitis
➔ Women > men
➔ Characterized by elevated autoantibodies such as antinuclear
antibodies, anti - smooth muscle antibodies and
hypergammaglobulinemia
6 Other Causes Of
CLD
➔ Drugs: amiodarone, isoniazid, methotrexate, phenytoin, nitrofurantoin
➔ Vascular: Budd-Chiari syndrome
➔ Idiopathic/ cryptogenic around 15%
9. Kumar and Clark Clinical Medicine 8th ed.
LET’S GET TO KNOW..
10. Hepatotoxicity Cholestatic injury
Chronic injury to hepatocytes
Released of cytokines and RO
intermediates
INFLAMMATION
Stellate cells activated
Upregulation of receptors
E.g. PDGF
, TGF-B
Hepatocyte death
Myofibroblast
Normal matrix is replaced by
collagen
Increase resistance to portal flow
PORTAL HYPERTENSION
Endothelial barrier disruption
LIVER FUNCTION IMPAIRED
Kumar and Clark Clinical Medicine 8th ed.
11. Pellicoro, A., Ramachandran, P., Iredale, J. et al. Liver fibrosis and repair: immune regulation of
wound healing in a solid organ. Nat Rev Immunol 14, 181–194 (2014).
https://doi.org/10.1038/nri3623
13. History taking
SPECIFIC SYMPTOMS
● Right hypochondrial pain: liver distension
● Abdominal distension: ascites
● Ankle swelling: fluid retention
● Haematemesis and melaena: GI hemorrhage
● Pruritus: cholestasis
● Gynaecomastia, loss of libido, amenorrhea:
endocrine dysfunction
● Confusion and drowsiness: portosystemic
encephalopathy
May be asymptomatic
Non-specific : Fatigue
17. Portal hypertension ● Elevated pressure in the portal venous system
● Increased resistance of blood flow
● Gastrointestinal bleeding, splenomegaly and
ascites. Often asymptomatic
Variceal bleed ● dilated veins in distal esophagus or proximal
stomach cause by elevated pressure in the
portal venous system.
● Sudden, painless, upper GI bleeding,
Hematemesis,melena, or hematochezia.
18. Ascites ● Cause: portal hypertension
● Clinical features: abdominal distension, loss of appetite,
shortness of breath and weight gain
● Examination: shifting dullness and fluid thrills can be elicited
Spontaneous bacterial
peritonitis
● Infection of abdominal fluid
● Clinical features: fever, malaise, and symptoms of ascites and
worsening hepatic failure. Present of peritoneal sign (eg.
abdominal tenderness and rebound tenderness).
● Diagnose by: diagnostic paracentesis
19. Hepatic encephalopathy ● Reversible brain dysfunction caused by liver
insufficiency and portosystemic shunts.
● Clinical features: wide spectrum of neurological
and psychiatric abnormalities.
● Precipitants: gastrointestinal bleeding,
constipation, infection, dehydration and
portosystemic shunts
Hepatorenal syndrome ● Occurs in advanced liver disease and is a
diagnosis of exclusion
● Pathophysiology: vasoconstriction of a renal
vessels from RAAS activation leading to renal
hypoperfusion
20. Hepatocellular carcinoma ● The risk is higher in chronic liver disease
such as cirrhosis caused by hepatitis B or C
infection
● Clinical features: abdominal pain, weight
loss, early satiety, right upper quadrant mass
and jaundice
● Diagnosis: alpha-fetoprotein measurement
or imaging (CT or MRI)
21. Overall, the 5-year survival rate is approximately 50%.
This is variable and depends on the aetiology and presence of complications.
The severity and prognosis of liver disease can be graded according to the
- modified Child–Pugh classification
Or
- MELD score (modification of end-stage liver disease)
PROGNOSIS
23. MELD SCORE (MODIFICATION OF
END STAGE LIVER DISEASE)
To convert:
• bilirubin from umol/L to mg/dL divide by 17
• creatinine from umol/L to mg/dL divide by 88.4
[ 3.8 x LN (bilirubin in mg/dL)] + [ 9.6 x LN
(creatinine in mg/dL) ] + [ 11.2 x LN (INR) ] + 6.4
25. LAB FINDINGS
1.FULL BLOOD COUNT
● Anaemia
● Leukopenia
● Thrombocytopenia
● Prolonged prothrombin
time (PT) and partial
thromboplastin time
(aPTT)
● Elevated internalized
normalized ratio (INR)
● Liver enzymes elevated
(AST, ALT, ALP, GGT)
● Hyperbilirubinemia
● Hypoalbuminemia
● Hyponatremia (Na+)
● Elevated Urea
● Elevated creatinine
2. LIVER FUNCTION
TEST
3. COAGULATION
PROFILE
4. RENAL PROFILE
5. BIOMARKERS
● Serum
alpha-fetoprotein
> 200mg/ml
● Enhanced liver
fibrosis test
- < 7.7: None to mild
- 7.7 - 9.8: Moderate
- > 9.8: Severe
26. 6. LIVER BIOPSY
Performed percutaneously with a Trucut or Menghini needle, usually through an
intercostal space under local anaesthesia or radiologically using a transjugular
approach. Wisely not done if coagulation profile is deranged due to risk of
bleeding.
28. RADIOLOGICAL FINDINGS
8. ABDOMINAL
ULTRASOUND
● Non-invasive, safe and
widely available
● Routinely used to
evaluate liver cirrhosis.
● To detect size and
echogenicity nodularity
of the liver cirrhosis.
● Used to measure the
diameter of portal vein.
● Assess the clot in
hepatic vein
29. RADIOLOGICAL FINDINGS
9. CT SCAN
● Not routinely used to
evaluate liver cirrhosis
● CT findings shows
hepatic nodularity,
atrophy of the right
lobe, hypertrophy of
caudate/left lobe,
ascites or varices.
● CT portal phase
imaging can
demonstrate the
patency of portal vein
and assess the
obstruction of biliary
channel.
31. Major goals of managing patients with CLD
31
● Prevent superimposed insults
to the liver
- Vaccinations
● To slow progression of
liver disease
● Avoid any complications
- Antiviral treatments for
hep C
- Alcohol abstinence
32. GENERAL MANAGEMENT
● Diet control
- reduce intake of red meat, eggs, cheese
- Sodium restriction
● Weight loss, control metabolic risk factors
- Glucose
- Blood pressure
- Cholesterol
● Avoid hepatotoxins
- Alcohol
- Hepatotoxic meds eg acetaminophen, azathioprine
- Herbal remedies
● Vaccinations
- Hep A & B vaccines
- Pneumococcal vaccines
- Influenza vaccines
33. SPECIFIC MANAGEMENT
Alcoholic liver disease
● Cessation of alcohol
consumption
● Alcohol abstinence (most
effective in preventing
progression of liver
disease)
● Alcohol rehabilitation
program
Non - alcoholic fatty liver disease (NAFLD)
Treatment of metabolic syndrome
● Metformin 1st line treatment in T2DM patient with NAFLD
● Thiazolidinediones such as pioglitazone could improve
inflammation and fibrosis in T2DM patient
● Weight loss
Viral hepatitis
● Continuous viral
suppression with
nucleoside and
nucleotide analogs
● Direct- acting antivirals
achieving hep C virus
eradication
● Interferon alpha
34. MANAGEMENT OF CIRRHOSIS COMPLICATIONS
Portal hypertension leads to :
1. Ascites
● Sodium & fluid retention
● Diuretics
- Spironolactone (mainstay)
- Frusemide
● Chart daily weight
● Large volume paracentesis (in massive ascites)
● Transjugular intrahepatic portosystemic shunts
(TIPS)
2. Variceal bleeding
● Resuscitate, stabilize patient
● Fluid, blood infusion
● IV somatostatin
● Antibiotic prophylaxis
● Acid suppression
- omeprazole, pantoprazole
● Emergency endoscopy
- diagnostic and therapeutic
- Esophageal varices : variceal ligation
- Gastric varices : injection with cyanoacrylate
glue
● Transjugular intrahepatic portosystemic shunts
(TIPS)
Spontaneous bacterial peritonitis
● Empirical antibiotics
- immediately after diagnosis
● 3rd gen cephalosporin (IV
cefotaxime)
- for 5 days or until
sensitivities is known
Hepatic encephalopathy
● Stop all meds that depress
CNS functions
- such as sedatives and
benzodiazepine
● Eliminate precipitating factors
- such as hypovolaemia,
hypokalemia, GI bleed,
constipation
● Lactulose
Hepatorenal syndrome
● Type 1 HRS
- Terlipressin + albumin
● Type 2 HRS
- TIPS
● Liver transplant is the treatment
of choice
Hepatocellular carcinoma
● Initial stage (single HCC lesion )
- resection and ablation
● Intermediate stage
- transarterial
chemoembolization and
radio-embolization
● Metastatic disease
- sorafenib