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Pathology - Wilson Disease
This is a rare autosomal recessive condition caused by a mutation in the copper-transporting protein (P-type ATPase), resulting in impaired copper conjugation to ceruloplasmin.
The condition typically begins between the ages of 10 and 30.
Pathophysiology: Enhanced copper uptake in the intestines and reduced elimination through bile results in copper buildup in several tissues, particularly in the parenchymal cells of the liver, kidney, brain, and cornea.
The liver can exhibit a range of conditions from acute and chronic hepatitis to micronodular or macronodular cirrhosis, with Mallory bodies being seen on biopsy.
Brain: Degeneration and formation of empty spaces in basal ganglia
Hepatitis, hypersplenism, hemolytic anemia, portal hypertension, psychosis, or dementia: Kayser-Fleischer rings are thin brown rings observed around the corneas during eye examinations. Choreiform movements refer to extrapyramidal motor symptoms that resemble those seen in Parkinson's disease.
Complications involve a higher likelihood of developing hepatocellular carcinoma.
Laboratory results include reduced serum ceruloplasmin, increased copper in urine, amino acids in urine, glucose in urine, and potentially very low alkaline phosphatase levels.
Penicillamine is used for copper chelation in treatment. Liver transplant for severe instances. diet low in copper
This is a rare autosomal recessive condition caused by a mutation in the copper-transporting protein (P-type ATPase), resulting in impaired copper conjugation to ceruloplasmin.
The condition typically begins between the ages of 10 and 30.
Pathophysiology: Enhanced copper uptake in the intestines and reduced elimination through bile results in copper buildup in several tissues, particularly in the parenchymal cells of the liver, kidney, brain, and cornea.
The liver can exhibit a range of conditions from acute and chronic hepatitis to micronodular or macronodular cirrhosis, with Mallory bodies being seen on biopsy.
Brain: Degeneration and formation of empty spaces in basal ganglia
Hepatitis, hypersplenism, hemolytic anemia, portal hypertension, psychosis, or dementia: Kayser-Fleischer rings are thin brown rings observed around the corneas during eye examinations. Choreiform movements refer to extrapyramidal motor symptoms that resemble those seen in Parkinson's disease.
Complications involve a higher likelihood of developing hepatocellular carcinoma.
Laboratory results include reduced serum ceruloplasmin, increased copper in urine, amino acids in urine, glucose in urine, and potentially very low alkaline phosphatase levels.
Penicillamine is used for copper chelation in treatment. Liver transplant for severe instances. diet low in copper
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Pathology - Portal Hypertension
Prehepatic portal venous blockage is caused by either portal vein thrombosis or splenic intrahepatic portal venous obstruction. Resulting from cirrhosis, metastatic tumor, or schistosomiasis
Posthepatic portal venous blockage can be caused by constrictive pericarditis, tricuspid insufficiency, congestive heart failure, or Budd-Chiari syndrome.
Portal venous blockage causes an increased utilization of venous collaterals in the portal systemic anastomoses, resulting in varices in the submucosal veins of the esophagus, rectal veins, and paraumbilical-inferior epigastric veins. Moreover. Elevated portal vein pressure causes reduced capillary fluid reabsorption, resulting in the accumulation of fluid in the peritoneal cavity known as ascites.
Clinical Symptoms
Enlarged spleen; swollen veins in the esophagus; swollen veins in the rectum; swollen veins around the belly button; vomiting blood; little dilated blood vessels on the skin. Hypotension and pallor are symptoms of ascites.
Therapy
Splenectomy cures portal hypertension resulting from splenic vein thrombosis.
Treatment options for variceal hemorrhage include band ligation or sclerotherapy. Anticoagulation for portal vein thrombosis Cirrhosis treatment notes
Prehepatic portal venous blockage is caused by either portal vein thrombosis or splenic intrahepatic portal venous obstruction. Resulting from cirrhosis, metastatic tumor, or schistosomiasis
Posthepatic portal venous blockage can be caused by constrictive pericarditis, tricuspid insufficiency, congestive heart failure, or Budd-Chiari syndrome.
Portal venous blockage causes an increased utilization of venous collaterals in the portal systemic anastomoses, resulting in varices in the submucosal veins of the esophagus, rectal veins, and paraumbilical-inferior epigastric veins. Moreover. Elevated portal vein pressure causes reduced capillary fluid reabsorption, resulting in the accumulation of fluid in the peritoneal cavity known as ascites.
Clinical Symptoms
Enlarged spleen; swollen veins in the esophagus; swollen veins in the rectum; swollen veins around the belly button; vomiting blood; little dilated blood vessels on the skin. Hypotension and pallor are symptoms of ascites.
Therapy
Splenectomy cures portal hypertension resulting from splenic vein thrombosis.
Treatment options for variceal hemorrhage include band ligation or sclerotherapy. Anticoagulation for portal vein thrombosis Cirrhosis treatment notes
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Pathology - Budd-Chiari Syndrome
Resulting from the blockage of the hepatic veins by a blood clot
Linked to polycythemia vera, pregnancy, hepatocellular carcinoma, traumatic abdominal trauma, malignancy, oral contraceptive use, and paroxysmal nocturnal hemoglobinuria
More frequently observed in women
The liver shows centrilobular congestion and necrosis, along with sinusoidal dilatation leading to centrilobular fibrosis. Thrombi are present in main veins.
Symptoms include tender and painful liver enlargement, jaundice, yellowing of the eyes, enlarged spleen, vomiting, accumulation of fluid in the abdomen, visible veins in the abdomen and back while standing, swelling in the legs, and no jugular venous distention. These symptoms may indicate potential liver failure.
Imaging: Identification of hepatic venous or IVC thrombosis using Doppler ultrasonography or CT imaging.
Laboratory results indicate elevated liver function tests.
Anticoagulation for hypercoagulable state, thrombolytic treatment for acute hepatic vein presentation, surgical bypass for severe patients, diuretics and salt restriction for ascites.
Resulting from the blockage of the hepatic veins by a blood clot
Linked to polycythemia vera, pregnancy, hepatocellular carcinoma, traumatic abdominal trauma, malignancy, oral contraceptive use, and paroxysmal nocturnal hemoglobinuria
More frequently observed in women
The liver shows centrilobular congestion and necrosis, along with sinusoidal dilatation leading to centrilobular fibrosis. Thrombi are present in main veins.
Symptoms include tender and painful liver enlargement, jaundice, yellowing of the eyes, enlarged spleen, vomiting, accumulation of fluid in the abdomen, visible veins in the abdomen and back while standing, swelling in the legs, and no jugular venous distention. These symptoms may indicate potential liver failure.
Imaging: Identification of hepatic venous or IVC thrombosis using Doppler ultrasonography or CT imaging.
Laboratory results indicate elevated liver function tests.
Anticoagulation for hypercoagulable state, thrombolytic treatment for acute hepatic vein presentation, surgical bypass for severe patients, diuretics and salt restriction for ascites.
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Pathology - Jaundice
Resulting from hepatic illness, biliary blockage, hemolytic anemia, and congenital hyperbilirubinemias.
Bilirubin is produced by the breakdown of heme. After heme is broken down outside the liver, unconjugated bilirubin binds to albumin and is carried to the liver for further processing. Hepatocytes typically convert bilirubin into conjugated bilirubin and release it into bile. Bile is transformed into urobilinogen by intestinal bacteria in the gastrointestinal system, then reabsorbed and eliminated through urine. Conjugated bilirubin is the only form that is soluble and can be reabsorbed from the intestine.
Pathological mechanisms lead to elevated bilirubin synthesis, reduced hepatic uptake or outflow of bilirubin, inadequate conjugation, or hindered bile flow, resulting in bilirubin buildup. All of these factors result in jaundice.
Jaundice is characterized by yellowing of the skin, sclera, and tissues, as well as black urine.
Laboratory results: It depends on the cause of jaundice. (1) Hepatocellular disease jaundice presents with both conjugated and unconjugated hyperbilirubinemia, elevated urine bilirubin, normal or reduced urine urobilinogen, increased levels of ALT and AST, and elevated ALP. (2) Biliary obstructive jaundice is characterized by conjugated hyperbilirubinemia, increased urine bilirubin, decreased urine urobilinogen, elevated ALP, and hypercholesterolemia. (3) Hemolytic anemia jaundice is identified by unconjugated hyperbilirubinemia and the absence of urine bilirubin (acholuria). elevated urinary urobilinogen levels.
Treat the underlying cause.
Resulting from hepatic illness, biliary blockage, hemolytic anemia, and congenital hyperbilirubinemias.
Bilirubin is produced by the breakdown of heme. After heme is broken down outside the liver, unconjugated bilirubin binds to albumin and is carried to the liver for further processing. Hepatocytes typically convert bilirubin into conjugated bilirubin and release it into bile. Bile is transformed into urobilinogen by intestinal bacteria in the gastrointestinal system, then reabsorbed and eliminated through urine. Conjugated bilirubin is the only form that is soluble and can be reabsorbed from the intestine.
Pathological mechanisms lead to elevated bilirubin synthesis, reduced hepatic uptake or outflow of bilirubin, inadequate conjugation, or hindered bile flow, resulting in bilirubin buildup. All of these factors result in jaundice.
Jaundice is characterized by yellowing of the skin, sclera, and tissues, as well as black urine.
Laboratory results: It depends on the cause of jaundice. (1) Hepatocellular disease jaundice presents with both conjugated and unconjugated hyperbilirubinemia, elevated urine bilirubin, normal or reduced urine urobilinogen, increased levels of ALT and AST, and elevated ALP. (2) Biliary obstructive jaundice is characterized by conjugated hyperbilirubinemia, increased urine bilirubin, decreased urine urobilinogen, elevated ALP, and hypercholesterolemia. (3) Hemolytic anemia jaundice is identified by unconjugated hyperbilirubinemia and the absence of urine bilirubin (acholuria). elevated urinary urobilinogen levels.
Treat the underlying cause.
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Pathology - Congenital Hyperbilirubinemias
Cause of Gilbert Syndrome: Autosomal dominant disease causing reduced UDP-glucuronyl transferase activity and diminished bilirubin absorption by the liver.
Symptoms and signs. Typically without symptoms, with just some yellowing of the white part of the eyes, possibly brought on by stress. Unconjugated hyperbilirubinemia
Treatment: Reassurance: typically follows a harmless path
Crigler-Najjar Syndrome Type I and Type II
Cause: Conditions can be either autosomal recessive (type I) or autosomal dominant with variable penetrance (type II), leading to a lack of UDP-glucuronyl transferase activity.
Clinical features: Type I is more severe than type II, typically appears in early childhood with jaundice, kernicterus, CNS degeneration, and unconjugated hyperbilirubinemia.
Treatment: Plasmapheresis and phototherapy for type I, phenobarbital for type II.
Dubin-Johnson (D-J) Syndrome and Rotor Syndrome
Cause: Autosomal recessive disorders caused by impaired bilirubin transport from the liver. Symptoms: Periodic yellowing of the skin; Pain in the upper right abdomen and upper middle abdomen; increased levels of conjugated bilirubin in the blood; slightly higher liver function tests; liver seeming black (Dubin-Johnson syndrome); Rotor syndrome is milder in comparison.
Treatment: Providing reassurance; both D-J syndrome and Rotor syndrome have a mild course.
Distinguish between hereditary hyperbilirubinemias and benign physiologic jaundice of the newborn (neonatal hyperbilirubinemia), which occurs in the first week of life due to elevated bilirubin production and a relative lack of UDP-glucuronyl transferase in the developing liver.
Cause of Gilbert Syndrome: Autosomal dominant disease causing reduced UDP-glucuronyl transferase activity and diminished bilirubin absorption by the liver.
Symptoms and signs. Typically without symptoms, with just some yellowing of the white part of the eyes, possibly brought on by stress. Unconjugated hyperbilirubinemia
Treatment: Reassurance: typically follows a harmless path
Crigler-Najjar Syndrome Type I and Type II
Cause: Conditions can be either autosomal recessive (type I) or autosomal dominant with variable penetrance (type II), leading to a lack of UDP-glucuronyl transferase activity.
Clinical features: Type I is more severe than type II, typically appears in early childhood with jaundice, kernicterus, CNS degeneration, and unconjugated hyperbilirubinemia.
Treatment: Plasmapheresis and phototherapy for type I, phenobarbital for type II.
Dubin-Johnson (D-J) Syndrome and Rotor Syndrome
Cause: Autosomal recessive disorders caused by impaired bilirubin transport from the liver. Symptoms: Periodic yellowing of the skin; Pain in the upper right abdomen and upper middle abdomen; increased levels of conjugated bilirubin in the blood; slightly higher liver function tests; liver seeming black (Dubin-Johnson syndrome); Rotor syndrome is milder in comparison.
Treatment: Providing reassurance; both D-J syndrome and Rotor syndrome have a mild course.
Distinguish between hereditary hyperbilirubinemias and benign physiologic jaundice of the newborn (neonatal hyperbilirubinemia), which occurs in the first week of life due to elevated bilirubin production and a relative lack of UDP-glucuronyl transferase in the developing liver.
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Pathology - Viral Hepatitis
Hepatitis A virus (HAV) and Hepatitis E virus (HEV) are transmitted by the fecal-oral route. Hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis D virus (HDV) are transmitted by blood.
Pathology
Acute hepatitis (all types): Gross: liver is enlarged and crimson, appearing green if cholestatic. Microscopic findings include hepatocyte enlargement, ground-glass appearance in hepatocytes (HBV), cholestasis, macrophage aggregation, bridging necrosis, portal tract inflammation, and hyperplasia of Kupffer cells.
Chronic hepatitis caused by hepatitis B virus (HBV), hepatitis C virus (HCV), or hepatitis D virus (HDV): Pathological findings: cirrhotic liver with fibrous septa and irregular lesions. Minuscule. Bridging fibrosis in the portal and periportal areas is associated with lymphoid aggregates.
Symptoms include abdominal pain, black urine, enlarged liver, yellowing of the skin, and exhaustion.
HBV and HCV are closely linked to chronic active hepatitis, cirrhosis, and hepatocellular cancer.
Laboratory results: Increased ALT and AST levels
Serologic indicators: HAV: IgM antibodies to HAV indicates current HAV infection.
An IgG antibody to HAV signifies a past HAV infection and provides immunity. HBV: The presence of HBsAg indicates infection, which can persist in a carrier form. Antibodies against hepatitis B surface antigen confer immunity against hepatitis B virus. Detecting IgM antibodies to HBcAg is crucial for diagnosing acute illness in the window period.An antibody against HBeAg suggests minimal transmissibility. HCV Antibody signifies past infection, but HCV RNA levels suggest current infection.
Therapy includes vaccinations for Hepatitis A Virus (HAV) and Hepatitis B Virus (HBV). Hepatitis B virus is managed with antiviral medication, such as entecavir. Hepatitis C virus is treated with PEG-interferon and ribavirin. Screening for hepatocellular carcinoma is recommended for people with chronic hepatitis B or C virus.
HCV is a prevalent cause of hepatitis among intravenous drug users.
HEV leads to higher death rates in pregnant women.
Hepatitis A virus (HAV) and Hepatitis E virus (HEV) are transmitted by the fecal-oral route. Hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis D virus (HDV) are transmitted by blood.
Pathology
Acute hepatitis (all types): Gross: liver is enlarged and crimson, appearing green if cholestatic. Microscopic findings include hepatocyte enlargement, ground-glass appearance in hepatocytes (HBV), cholestasis, macrophage aggregation, bridging necrosis, portal tract inflammation, and hyperplasia of Kupffer cells.
Chronic hepatitis caused by hepatitis B virus (HBV), hepatitis C virus (HCV), or hepatitis D virus (HDV): Pathological findings: cirrhotic liver with fibrous septa and irregular lesions. Minuscule. Bridging fibrosis in the portal and periportal areas is associated with lymphoid aggregates.
Symptoms include abdominal pain, black urine, enlarged liver, yellowing of the skin, and exhaustion.
HBV and HCV are closely linked to chronic active hepatitis, cirrhosis, and hepatocellular cancer.
Laboratory results: Increased ALT and AST levels
Serologic indicators: HAV: IgM antibodies to HAV indicates current HAV infection.
An IgG antibody to HAV signifies a past HAV infection and provides immunity. HBV: The presence of HBsAg indicates infection, which can persist in a carrier form. Antibodies against hepatitis B surface antigen confer immunity against hepatitis B virus. Detecting IgM antibodies to HBcAg is crucial for diagnosing acute illness in the window period.An antibody against HBeAg suggests minimal transmissibility. HCV Antibody signifies past infection, but HCV RNA levels suggest current infection.
Therapy includes vaccinations for Hepatitis A Virus (HAV) and Hepatitis B Virus (HBV). Hepatitis B virus is managed with antiviral medication, such as entecavir. Hepatitis C virus is treated with PEG-interferon and ribavirin. Screening for hepatocellular carcinoma is recommended for people with chronic hepatitis B or C virus.
HCV is a prevalent cause of hepatitis among intravenous drug users.
HEV leads to higher death rates in pregnant women.
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Pathology - Autoimmune Hepatitis
Autoimmune disease frequently co-occurs with other autoimmune disorders.
Sjogren's syndrome, thyroiditis, ulcerative colitis, and arthritis.
Most prevalent in young ladies but can impact individuals of various ages.
Pathology
Pathological findings: Liver showing cirrhosis with fibrous septa and nodular structure
Microscopic findings include bridging fibrosis in the portal and periportal areas, as well as hepatocyte necrosis.
May have no symptoms at first or may show signs of acute hepatitis, jaundice, enlarged liver, spider nevi, and absence of menstruation Laboratory results: Increased -globulin levels, raised bilirubins and transaminases, positive antinuclear antibody (ANA), positive anti-smooth muscle antibody (ASMA) type 1, positive anti-liver kidney microsomal antibody (anti-LKM-1) type 2.
Treatment: Prednisone with or without azathioprine may be used. Liver transplant should be considered for patients with severe cirrhosis.
Autoimmune disease frequently co-occurs with other autoimmune disorders.
Sjogren's syndrome, thyroiditis, ulcerative colitis, and arthritis.
Most prevalent in young ladies but can impact individuals of various ages.
Pathology
Pathological findings: Liver showing cirrhosis with fibrous septa and nodular structure
Microscopic findings include bridging fibrosis in the portal and periportal areas, as well as hepatocyte necrosis.
May have no symptoms at first or may show signs of acute hepatitis, jaundice, enlarged liver, spider nevi, and absence of menstruation Laboratory results: Increased -globulin levels, raised bilirubins and transaminases, positive antinuclear antibody (ANA), positive anti-smooth muscle antibody (ASMA) type 1, positive anti-liver kidney microsomal antibody (anti-LKM-1) type 2.
Treatment: Prednisone with or without azathioprine may be used. Liver transplant should be considered for patients with severe cirrhosis.
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Pathology - Liver Cirrhosis
Micronodular cirrhosis can be caused by alcoholism, hemochromatosis, or Wilson disease.
Macronodular liver cirrhosis can be caused by hepatitis B virus (HBV), hepatitis C virus (HCV), drug-induced hepatitis, or biliary cirrhosis. Wilson's disease: lack of alpha-1-antitrypsin; advanced cirrhosis caused by alcohol consumption.
Pathology
In micronodular cirrhosis, nodules are homogenous and smaller than 3 mm. In macronodular cirrhosis, fibrous bands divide the liver into irregular nodules larger than 3 mm.
Microscopic findings show widespread liver fibrosis followed by nodular regeneration without typical hepatic structure, along with reconfiguration of vascular patterns.
Pathophysiology: Liver damage causes elevated portal venous pressures, leading to redirected blood flow to portosystemic anastomoses such as gastroesophageal collaterals, resulting in esophageal varices. Reduced plasma oncotic pressure caused by decreased albumin production in the failing liver, along with impaired breakdown of aldosterone, leads to peripheral edema and ascites.
Encephalopathy occurs due to the liver's inability to metabolize ammonia, which is a neurotoxic.
Weakness: weight loss; ascites; jaundice; spider nevi; gynecomastia; testicular atrophy; asterixis; coarse hand tremor; ankle edema.
Complications may involve gastrointestinal hemorrhage from esophageal or gastric varices. Hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis, and heightened susceptibility to hepatocellular cancer.
Laboratory results include macrocytic anemia, thrombocytopenia, delayed prothrombin time due to coagulation-factor insufficiency, hypoalbuminemia, hyperbilirubinemia, elevated ALT, AST, and ALP values, and high blood ammonia levels.
Treatment includes alcohol abstinence, low-salt diet, diuretic therapy, lactulose for encephalopathy, and liver transplant.
Micronodular cirrhosis can be caused by alcoholism, hemochromatosis, or Wilson disease.
Macronodular liver cirrhosis can be caused by hepatitis B virus (HBV), hepatitis C virus (HCV), drug-induced hepatitis, or biliary cirrhosis. Wilson's disease: lack of alpha-1-antitrypsin; advanced cirrhosis caused by alcohol consumption.
Pathology
In micronodular cirrhosis, nodules are homogenous and smaller than 3 mm. In macronodular cirrhosis, fibrous bands divide the liver into irregular nodules larger than 3 mm.
Microscopic findings show widespread liver fibrosis followed by nodular regeneration without typical hepatic structure, along with reconfiguration of vascular patterns.
Pathophysiology: Liver damage causes elevated portal venous pressures, leading to redirected blood flow to portosystemic anastomoses such as gastroesophageal collaterals, resulting in esophageal varices. Reduced plasma oncotic pressure caused by decreased albumin production in the failing liver, along with impaired breakdown of aldosterone, leads to peripheral edema and ascites.
Encephalopathy occurs due to the liver's inability to metabolize ammonia, which is a neurotoxic.
Weakness: weight loss; ascites; jaundice; spider nevi; gynecomastia; testicular atrophy; asterixis; coarse hand tremor; ankle edema.
Complications may involve gastrointestinal hemorrhage from esophageal or gastric varices. Hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis, and heightened susceptibility to hepatocellular cancer.
Laboratory results include macrocytic anemia, thrombocytopenia, delayed prothrombin time due to coagulation-factor insufficiency, hypoalbuminemia, hyperbilirubinemia, elevated ALT, AST, and ALP values, and high blood ammonia levels.
Treatment includes alcohol abstinence, low-salt diet, diuretic therapy, lactulose for encephalopathy, and liver transplant.
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Pathology - Alcohol Liver Disease
Cause:
Drinking ethanol.
More prevalent among women.
Study of diseases
Hepatic steatosis, often known as fatty liver, is an early and reversible condition characterized by the accumulation of lipid droplets in centrilobular hepatocytes, resulting in a yellow greasy appearance of the liver.
Alcoholic hepatitis is characterized by hepatocyte enlargement and necrosis, along with the presence of Mallory bodies, which are intracytoplasmic eosinophilic hyaline structures. Neutrophils have infiltrated the hepatocytes, leading to fibrosis in the sinusoidal and perivenular areas.
Alcoholic cirrhosis is characterized by a fatty enlarged liver that can become brown and shrink, along with uneven nodularity giving a hobnail appearance and fibrosis causing loss of hepatic architecture.
Hepatic steatosis with mild elevation in bilirubin levels and elevated alkaline phosphatase.
Clinical Symptoms
Alcoholic hepatitis is a condition that develops following a period of excessive alcohol consumption and is characterized by symptoms such as loss of appetite, abdominal pain, and enlargement of the liver. The AST to ALT ratio is greater than 1.5, and there is an elevated white blood cell count.
Symptoms of alcoholic cirrhosis may include portal hypertension, jaundice, ascites, and increased liver function tests (LFTs).
Therapy
Refraining from drinking; taking vitamins, particularly folate and thiamine; using methylprednisolone or pentoxifylline for severe instances of alcoholic hepatitis
Fatty liver can also be observed in cases of Reye syndrome viral infection, salicylate use in children, tetracycline toxicity, diabetes, malabsorption disorders, kwashiorkor, and hepatic failure during pregnancy.
Cause:
Drinking ethanol.
More prevalent among women.
Study of diseases
Hepatic steatosis, often known as fatty liver, is an early and reversible condition characterized by the accumulation of lipid droplets in centrilobular hepatocytes, resulting in a yellow greasy appearance of the liver.
Alcoholic hepatitis is characterized by hepatocyte enlargement and necrosis, along with the presence of Mallory bodies, which are intracytoplasmic eosinophilic hyaline structures. Neutrophils have infiltrated the hepatocytes, leading to fibrosis in the sinusoidal and perivenular areas.
Alcoholic cirrhosis is characterized by a fatty enlarged liver that can become brown and shrink, along with uneven nodularity giving a hobnail appearance and fibrosis causing loss of hepatic architecture.
Hepatic steatosis with mild elevation in bilirubin levels and elevated alkaline phosphatase.
Clinical Symptoms
Alcoholic hepatitis is a condition that develops following a period of excessive alcohol consumption and is characterized by symptoms such as loss of appetite, abdominal pain, and enlargement of the liver. The AST to ALT ratio is greater than 1.5, and there is an elevated white blood cell count.
Symptoms of alcoholic cirrhosis may include portal hypertension, jaundice, ascites, and increased liver function tests (LFTs).
Therapy
Refraining from drinking; taking vitamins, particularly folate and thiamine; using methylprednisolone or pentoxifylline for severe instances of alcoholic hepatitis
Fatty liver can also be observed in cases of Reye syndrome viral infection, salicylate use in children, tetracycline toxicity, diabetes, malabsorption disorders, kwashiorkor, and hepatic failure during pregnancy.
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Pathology - Biliary Cirrhosis
Primary biliary cirrhosis (PBC) is an autoimmune illness that typically affects women between the ages of 40 and 60. It can coexist with other autoimmune disorders such as Sjogren syndrome, thyroiditis, and rheumatoid arthritis.
SBC, or secondary biliary cirrhosis: caused by biliary blockage outside of the liver
Pathology
PBC: Gross: liver begins to turn green gradually. Microscopic factors include lymphocyte infiltration in the portal system, periportal granuloma development that destroys bile ducts, and the final destruction of hepatic parenchyma that results in hepatic cirrhosis.
SBC: Vellow-green liver, disgusting. Microscopic features include bile stasis, bile lakes (an buildup of bile in the hepatic parenchyma), fibrous septa, and variations in bile duct size.
Pathophysiology: a bacterial infection of the intrahepatic ducts known as ascending cholangitis can exacerbate extrahepatic biliary blockage by raising intrahepatic duct pressure, which in turn causes ductal damage and ultimately fibrosis.
Clinical Signs and Symptoms
severe obstructive jaundice, xanthomas, pruritus, weariness, hepatosplenomegaly, and ultimately portal hypertension-associated liver failure.
Results from the lab: elevated bilirubin levels, elevated ALP, hypercholesterolemia, and antimitochondrial antibodies (PBC).
Treatment
Vitamin supplements, cholestyramine for itching, ursodeoxycholic acid, and live transplants in cases of severe illness.
Primary biliary cirrhosis (PBC) is an autoimmune illness that typically affects women between the ages of 40 and 60. It can coexist with other autoimmune disorders such as Sjogren syndrome, thyroiditis, and rheumatoid arthritis.
SBC, or secondary biliary cirrhosis: caused by biliary blockage outside of the liver
Pathology
PBC: Gross: liver begins to turn green gradually. Microscopic factors include lymphocyte infiltration in the portal system, periportal granuloma development that destroys bile ducts, and the final destruction of hepatic parenchyma that results in hepatic cirrhosis.
SBC: Vellow-green liver, disgusting. Microscopic features include bile stasis, bile lakes (an buildup of bile in the hepatic parenchyma), fibrous septa, and variations in bile duct size.
Pathophysiology: a bacterial infection of the intrahepatic ducts known as ascending cholangitis can exacerbate extrahepatic biliary blockage by raising intrahepatic duct pressure, which in turn causes ductal damage and ultimately fibrosis.
Clinical Signs and Symptoms
severe obstructive jaundice, xanthomas, pruritus, weariness, hepatosplenomegaly, and ultimately portal hypertension-associated liver failure.
Results from the lab: elevated bilirubin levels, elevated ALP, hypercholesterolemia, and antimitochondrial antibodies (PBC).
Treatment
Vitamin supplements, cholestyramine for itching, ursodeoxycholic acid, and live transplants in cases of severe illness.
