Ascites
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1) Ascites refers to the accumulation of fluid in the peritoneal cavity, most commonly caused by cirrhosis of the liver. 2) Cirrhosis leads to portal hypertension and sodium retention, causing excess fluid to accumulate in the peritoneal space. 3) Clinical features include abdominal distention and shortness of breath. Diagnostic paracentesis helps determine the cause by examining fluid characteristics and serum-ascites albumin gradient.
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Portal hypertension by kiran maindale
Portal hypertension occurs when blood pressure in the portal vein system, which drains blood from the gastrointestinal tract to the liver, increases above normal levels. It is defined as a hepatic venous pressure gradient greater than 15 mmHg. Two key factors that contribute to portal hypertension are increased vascular resistance and increased blood flow. Investigation may include blood tests and imaging of the liver, portal system, and varices. Complications include variceal bleeding, ascites, and hepatic encephalopathy. Treatment depends on severity but may involve medication, endoscopic procedures, transjugular intrahepatic portosystemic shunt placement, or surgical shunting of blood flow to reduce portal pressure.
Portal hypertension
Portal hypertension occurs when hepatic venous pressure gradient exceeds 10 mm Hg and risk of variceal bleeding increases above 12 mm Hg. It can be caused by prehepatic issues like portal vein thrombosis, intrahepatic issues like cirrhosis, or post-hepatic issues like Budd-Chiari syndrome. Clinical signs include splenomegaly, ascites, collateral veins, and risk of gastrointestinal bleeding from esophageal varices. Management involves beta-blocker therapy to reduce pressure, antibiotics and endoscopic therapy for acute bleeding, and TIPSS or shunting for refractory cases. Complications include variceal bleeding, ascites, and hypersplenism.
1. portal hypertension converted
Here are the revisions to the document:
1. Normal portal venous pressure is less than 5 mm Hg.
2. Oesophageal balloon used to achieve temporary haemostasis is Sengstaken-Blakemore tube.
3. TIPSS stands for transjugular intrahepatic portosystemic shunt.
4. Median GCS score in hepatic coma is below 8.
5. Diet recommended for hepatic coma is low in protein and sodium.
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This document defines and describes hydronephrosis, which is the chronic dilatation of the pelvi-calyceal system due to partial or complete intermittent obstruction of urine flow. It discusses the etiology, pathophysiology, clinical presentation, investigations, and treatment of hydronephrosis. Treatment involves treating the underlying cause if kidney function is good or performing nephrostomy or nephrectomy if function is impaired. The role of the urologist is to rule out correctable obstructions and perform surgery for obstructive causes of chronic renal failure.
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Dr. Roshan Kumar Shah's document discusses portal hypertension, which is an increase in blood pressure within the portal vein system. It defines portal hypertension as a portal vein pressure above 40 mm Hg and describes its causes such as liver cirrhosis. It then covers the anatomy of the portal vein system, pathophysiology of increased resistance to blood flow, clinical signs including gastrointestinal bleeding, and approaches to diagnosis and management including medications, endoscopic therapy, surgery, and liver transplantation.
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Portal hypertension syndrome is characterized by increased pressure in the portal vein system due to obstructed blood flow out of the liver. The causes of obstructed blood flow can be divided into intrahepatic, subhepatic, and prehepatic blocks. Clinical features include collateral vein circulation around the liver, ascites, and splenomegaly. Ascites and hepatic encephalopathy are also signs of hepatocellular failure, where all liver functions are disrupted. Cholestasis syndrome results from obstructed bile flow and causes jaundice, itching, and fat malabsorption.
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Ascites is an abnormal collection of fluid in the peritoneal cavity, commonly caused by portal hypertension due to cirrhosis. It results from sodium and water retention triggered by vasodilation and activation of the renin-angiotensin system, as well as increased hydrostatic pressure and transudation of fluid from the liver and spleen into the peritoneal cavity. Hypoalbuminemia due to decreased liver function also contributes by reducing plasma oncotic pressure. Spironolactone is used as treatment as it is an aldosterone antagonist. Management involves dietary sodium restriction, diuretics, stopping alcohol, monitoring for complications, and procedures such as paracentesis or shunts.
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Portal hypertension by kiran maindale
Portal hypertension occurs when blood pressure in the portal vein system, which drains blood from the gastrointestinal tract to the liver, increases above normal levels. It is defined as a hepatic venous pressure gradient greater than 15 mmHg. Two key factors that contribute to portal hypertension are increased vascular resistance and increased blood flow. Investigation may include blood tests and imaging of the liver, portal system, and varices. Complications include variceal bleeding, ascites, and hepatic encephalopathy. Treatment depends on severity but may involve medication, endoscopic procedures, transjugular intrahepatic portosystemic shunt placement, or surgical shunting of blood flow to reduce portal pressure.
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Portal hypertension occurs when hepatic venous pressure gradient exceeds 10 mm Hg and risk of variceal bleeding increases above 12 mm Hg. It can be caused by prehepatic issues like portal vein thrombosis, intrahepatic issues like cirrhosis, or post-hepatic issues like Budd-Chiari syndrome. Clinical signs include splenomegaly, ascites, collateral veins, and risk of gastrointestinal bleeding from esophageal varices. Management involves beta-blocker therapy to reduce pressure, antibiotics and endoscopic therapy for acute bleeding, and TIPSS or shunting for refractory cases. Complications include variceal bleeding, ascites, and hypersplenism.
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1. Normal portal venous pressure is less than 5 mm Hg.
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Portal hypertension syndrome is characterized by increased pressure in the portal vein system due to obstructed blood flow out of the liver. The causes of obstructed blood flow can be divided into intrahepatic, subhepatic, and prehepatic blocks. Clinical features include collateral vein circulation around the liver, ascites, and splenomegaly. Ascites and hepatic encephalopathy are also signs of hepatocellular failure, where all liver functions are disrupted. Cholestasis syndrome results from obstructed bile flow and causes jaundice, itching, and fat malabsorption.
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Ascites is an abnormal collection of fluid in the peritoneal cavity, commonly caused by portal hypertension due to cirrhosis. It results from sodium and water retention triggered by vasodilation and activation of the renin-angiotensin system, as well as increased hydrostatic pressure and transudation of fluid from the liver and spleen into the peritoneal cavity. Hypoalbuminemia due to decreased liver function also contributes by reducing plasma oncotic pressure. Spironolactone is used as treatment as it is an aldosterone antagonist. Management involves dietary sodium restriction, diuretics, stopping alcohol, monitoring for complications, and procedures such as paracentesis or shunts.
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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.
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Portal hypertension is caused by increased vascular resistance and blood flow and can result from cirrhosis, vascular diseases, or other conditions. It leads to complications like ascites, variceal bleeding, and hepatic encephalopathy. Treatment involves general measures, variceal treatment including banding, TIPS procedure, and in some cases transplantation. Ascites is treated with paracentesis and diuretics along with albumin to prevent renal failure.
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This document discusses portal hypertension, including its definition, causes, clinical presentations, investigations, and management.
Portal hypertension is defined as elevated hepatic venous pressure gradient above 5 mmHg. It is clinically significant when the HVPG exceeds 10-12 mmHg. Common causes include cirrhosis, schistosomiasis, and portal or hepatic vein thrombosis.
The clinical triad of portal hypertension includes esophageal varices, splenomegaly, and ascites. Investigations include liver function tests, ultrasound, and endoscopy. Management involves general measures, treatment of varices with medications or endoscopic therapy, management of ascites and encephalopathy, and procedures to lower portal pressure such as T
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This document provides information on portal hypertension, including its definition, causes, presentations, investigations, and management. Some key points:
- Portal hypertension is defined as a sustained elevation of portal pressure above 12 mm Hg. It can be caused by conditions affecting blood flow pre-sinusoidally (e.g. portal vein thrombosis), sinusoidally (e.g. cirrhosis), or post-sinusoidally (e.g. Budd-Chiari syndrome).
- Common presentations include esophageal varices, splenomegaly, ascites, and features of hepatic encephalopathy. Investigations include liver function tests, ultrasound, and endoscopy to identify varices.
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Portal Hypertension
Portal hypertension occurs when scar tissue from liver injuries disrupts blood flow, increasing pressure in the main and portal veins and diverting blood away from the liver. The most common cause is cirrhosis, but it can also be caused by blood clots, fatty liver disease, hepatitis, or schistosomiasis. Symptoms include gastrointestinal bleeding, abdominal fluid buildup, and varicose veins. Diagnosis involves medical history, lab tests, and imaging exams. Treatment focuses on medications and procedures to reduce blood pressure such as sclerotherapy and TIPS or DSRS shunt surgery in severe cases. Lifestyle changes like quitting drinking and smoking can help prevent portal hypertension.
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- Normal portal venous pressure is generally considered to be between 5-10 mm Hg. Once it rises to 12 mm Hg or greater, complications can arise such as varices and ascites.
- Portal hypertension is defined as an elevation of the hepatic venous pressure gradient to over 5 mmHg. This gradient is the difference between the wedged hepatic venous pressure (sinusoidal pressure) and the free hepatic venous pressure.
- The two main types of portal hypertension are sinusoidal, where the sinusoidal pressure is elevated, and presinusoidal, where the portal venous pressure is increased but the sinusoidal pressure is normal. Sinusoidal hypertension commonly results in ascites due to increased transudation of fluid from the sin
Portal hypertension
Portal hypertension is defined as an elevation of pressure greater than 6mmHg in the portal venous system. It occurs when there is increased resistance to blood flow into the liver, which can be prehepatic, hepatic, or posthepatic in nature. Common causes include cirrhosis and thrombosis of the portal vein. Portal hypertension presents with ascites and variceal bleeding. Treatment options include medical management with diuretics and paracentesis, peritoneo-venous shunting, transjugular intrahepatic portosystemic shunt (TIPS), and liver transplantation.
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Cirrhosis is a chronic disease characterized by the replacement of normal liver tissue with scar tissue. This disrupts liver function and structure. Major complications of cirrhosis include ascites, portal hypertension, hepatic encephalopathy, and esophageal varices. Ascites is the accumulation of fluid in the abdominal cavity caused by portal hypertension and sodium retention. It is managed medically through dietary changes, diuretics, and paracentesis. Hepatic encephalopathy occurs when toxic metabolites accumulate in the bloodstream due to liver damage. Esophageal varices develop due to portal hypertension and can rupture, causing life-threatening bleeding.
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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.
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The clinical triad of portal hypertension includes esophageal varices, splenomegaly, and ascites. Investigations include liver function tests, ultrasound, and endoscopy. Management involves general measures, treatment of varices with medications or endoscopic therapy, management of ascites and encephalopathy, and procedures to lower portal pressure such as T
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- Common presentations include esophageal varices, splenomegaly, ascites, and features of hepatic encephalopathy. Investigations include liver function tests, ultrasound, and endoscopy to identify varices.
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Portal hypertension occurs when scar tissue from liver injuries disrupts blood flow, increasing pressure in the main and portal veins and diverting blood away from the liver. The most common cause is cirrhosis, but it can also be caused by blood clots, fatty liver disease, hepatitis, or schistosomiasis. Symptoms include gastrointestinal bleeding, abdominal fluid buildup, and varicose veins. Diagnosis involves medical history, lab tests, and imaging exams. Treatment focuses on medications and procedures to reduce blood pressure such as sclerotherapy and TIPS or DSRS shunt surgery in severe cases. Lifestyle changes like quitting drinking and smoking can help prevent portal hypertension.
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- Normal portal venous pressure is generally considered to be between 5-10 mm Hg. Once it rises to 12 mm Hg or greater, complications can arise such as varices and ascites.
- Portal hypertension is defined as an elevation of the hepatic venous pressure gradient to over 5 mmHg. This gradient is the difference between the wedged hepatic venous pressure (sinusoidal pressure) and the free hepatic venous pressure.
- The two main types of portal hypertension are sinusoidal, where the sinusoidal pressure is elevated, and presinusoidal, where the portal venous pressure is increased but the sinusoidal pressure is normal. Sinusoidal hypertension commonly results in ascites due to increased transudation of fluid from the sin
Portal hypertension
Portal hypertension is defined as an elevation of pressure greater than 6mmHg in the portal venous system. It occurs when there is increased resistance to blood flow into the liver, which can be prehepatic, hepatic, or posthepatic in nature. Common causes include cirrhosis and thrombosis of the portal vein. Portal hypertension presents with ascites and variceal bleeding. Treatment options include medical management with diuretics and paracentesis, peritoneo-venous shunting, transjugular intrahepatic portosystemic shunt (TIPS), and liver transplantation.
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This document discusses portal hypertension and its management. It defines portal hypertension as increased portal pressure and describes how hepatic venous pressure gradient (HVPG) is used to measure it noninvasively. The main causes of portal hypertension are discussed as pre-hepatic, intra-hepatic, and post-hepatic. Clinical features include gastroesophageal varices, ascites, and splenomegaly. Management involves screening and treatment of varices, diuretics for ascites, and splenectomy in rare cases. Transjugular intrahepatic portosystemic shunt (TIPS) or surgical shunts are considered if medication fails or is not available.
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ascites.pptx
1. The document outlines an approach to evaluating and diagnosing a patient presenting with ascites. It discusses taking a thorough history, performing a physical exam, considering differential diagnoses, and ordering appropriate investigations.
2. Key physical exam findings for ascites include shifting dullness on percussion and a fluid thrill. Complications can include spontaneous bacterial peritonitis.
3. Causes of ascites are categorized as transudative or exudative based on serum-ascites albumin gradient. The most common cause is cirrhosis, while other potential etiologies include heart failure, infections, cancers, and pancreatic disorders.
Hyponatremiappt 170315180214
Hyponatremia
Presented by- Dr. Mohammad Rehan
DNB Medicine
SDMH Jaipur
Moderator- Dr. Madhulika Sharma
HOD (General Medicine)
Ascitis
This document discusses ascites, which is an accumulation of fluid in the peritoneal cavity. It defines ascites and lists its main causes as increased hydrostatic pressure, decreased colloid osmotic pressure, increased permeability of capillaries, and leakage of fluid. The document describes the pathophysiology and classification of ascites as transudative or exudative. It outlines the clinical signs and diagnostic workup of ascites including abdominal examination, imaging, and analysis of ascitic fluid. Treatment approaches include dietary changes, diuretics, therapeutic paracentesis, TIPS procedure, and liver transplantation.
Dyselectrolytemias
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CRF update medical surgical nursing. .pdf
Chronic renal failure, also known as end-stage renal disease (ESRD), is an irreversible deterioration of kidney function that results in a buildup of waste products in the blood. The leading causes of ESRD are diabetes and hypertension. As kidney function declines, symptoms develop affecting every system and include fluid overload, electrolyte imbalances, anemia, and neurological changes. Treatment options include medications to manage complications, dietary modifications, and renal replacement therapies like hemodialysis. Nursing care focuses on monitoring the patient's fluid status, nutrition, and factors contributing to fatigue.
ACUTE RENAL FAILURE
This document summarizes the pathogenesis and management of acute renal failure. It discusses the causes and stages of pre-renal, intrinsic renal, and post-renal acute kidney injury. Key factors in preventing acute renal failure in surgical patients include adequate hydration, maintaining renal perfusion pressure, avoiding nephrotoxins, and aggressive treatment of complications such as hyperkalemia. Treatment may involve renal replacement therapies like hemodialysis when criteria for initiation are met.
Shock
Shock is characterized by impaired cellular metabolism and decreased tissue perfusion. There are four main types of shock: hypovolemic, vasogenic, cardiogenic, and neurogenic. The stages of shock progression include initial, compensatory, progressive, and irreversible. Management aims to restore fluid volume, increase cardiac output, and remove the precipitating cause. Nursing care focuses on monitoring vital signs, administering IV fluids and oxygen, maintaining perfusion, preventing complications, and supporting organ function.
Liver cirrhosis (Causes, clinical manifestation, complications, diagnosis, tr...
Cirrhosis is a diffuse process characterized by liver necrosis and fibrosis that converts the normal liver architecture into abnormal nodules lacking lobular organization. It has many causes including alcohol, viral hepatitis, fatty liver disease, and genetic disorders. Clinically, it manifests as asymptomatic or symptoms like vomiting and weight loss. Complications arise from portal hypertension and include ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome. Diagnosis involves liver function tests, imaging, and biopsy. Treatment focuses on managing complications and the underlying cause. For end-stage disease, liver transplantation may be required.
ABG ^0 CVP Monitoring.ppt
ABG and CVP monitoring are important procedures to assess acid-base balance, oxygenation status, and circulatory function. An ABG analyzes gases and electrolytes in arterial blood to evaluate ventilation and oxygenation, while CVP monitoring uses a catheter in the central veins to measure right atrial pressure and circulating blood volume. Nurses must carefully manage lines to prevent complications like infection and monitor for imbalances that require treatment through medication, fluids, or ventilation changes.
ARF- acute renal failure
The document discusses the anatomy and physiology of the nephron, the functional unit of the kidney. It describes how nephrons filter blood to form urine via glomerular filtration. Damage to nephrons or decreased blood flow can cause acute kidney injury (AKI), also called acute renal failure (ARF). The causes, types (prerenal, intrinsic renal, postrenal), diagnosis and treatment of ARF are explained in detail. Early dialysis is important for managing complications of severe ARF like fluid overload, electrolyte abnormalities and uremia.
Fluid & electrolyte balance and nutrition in OMFS- prashanth panicker.pdf
This document discusses fluid and electrolyte balance in oral and maxillofacial surgery (OMFS). It begins with an introduction on the importance of fluid and electrolyte regulation for homeostasis. It then covers topics like the fluid compartments in the body, exchange of fluids between compartments, fluid gain and loss, regulation of balance, and causes of imbalance in surgical patients. The document discusses intravenous fluids, routes of fluid/electrolyte correction, and fluid therapy. It also covers electrolyte imbalances and their management. The document provides an overview of important concepts regarding fluid and electrolyte balance for optimal patient care in OMFS.
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Liver cirrhosis (Causes, clinical manifestation, complications, diagnosis, tr...
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Ascites
- 1. ASCITES DR. YAGNIK CHHOTALA ASSISTANT PROFESSOR, MEDICINE
- 2. DEFINITION • Pathologic accumulation of fluid within the peritoneal cavity. • It is the most common complication of cirrhosis. • Most common cause of ascites: Cirrhosis
- 3. PATHOPHYSIOLOGY IN CIRRHOSIS 1. Portal hypertension with portal pressure >12 mmHg translation of fluid into the peritoneal space in excess capacity of the lymphatic system to remove fluid. 2. Progressive peripheral vasodilationreduction in pressure measured at carotid and renal baroreceptorsactivation of sodium retaining neurohormonal mechanisms (Renin Angiotensin Aldosterone System, Sympathetic Nervous System, ADH)sodium and water retention
- 4. CLINICAL FEATURES • Symptoms: abdominal distention, shortness of breath • Signs: shifting dullness, fluid thrill
- 5. DIAGNOSIS: DIAGNOSTIC PARACENTESIS 1. Cell count in ascitic fluid: In uncomplicated (uninfected) cirrhotic ascites, WBC count <500 mm3 and Polymorphonuclear neutrophil (PMN) count <250 mm3. PMN >= 250 mm3 suggests a bacterial infection. 2. SAAG (Serum-Ascites Albumin Gradient): • >=1.1gm%: cirrhosis, alcoholic, Budd-Chiari syndrome, portal vein thrombosis • >=1.1gm% with ascitic total protein level >2.5 gm%: cardiac ascites • <1.1gm%: peritoneal carcinomatosis, biliary or pancreatic leaks, nephrotic syndrome, tuberculosis peritonitis. All hospitalized patients with cirrhosis and ascites should under go a diagnostic paracentesis.
- 6. TREATMENT 1. Dietary Sodium restriction: <2gm per day 2. Spironolactone + Furosemide (100:40 ratio once daily): maximum 400:160. Diuretics should be discontinued in patients who develop hepatic encephalopathy, S.Na <120mEq/l, AKI. 3. Large volume paracentesis: performed in tense ascites or in patients refractory to diuretics. IV albumin 6-8g per litre of fluid removed should be administered to prevent circulatory failure. 4. TIPS Placement and Liver transplantation in refractory ascites