Which of the following is caused by arsenic poisoning
Extrahepatic poal vein obstruction is a vascular disorder of liver, which results in obstruction and cavernomatous transformation of poal vein with or without the involvement of intrahepatic poal vein, splenic vein, or superior mesenteric vein. of 10 mg daily for up to 60 days, followed by different dosing in consolidation and maintenance regimens. Hepatotoxicity Acute poisoning with arsenic is marked by severe abdominal pain, nausea and vomiting, diarrhea, muscle cramps, metallic taste and extreme thirst, followed by stupor, coma, cardiovascular collapse and death. Death can occur within 24 hours of exposure, but with sublethal doses, survival is possible and liver injury may arise 24 to 48 hours after the acute ingestion. Other symptoms include conjunctival and respiratory tract inflammation, epistaxis, rash, renal insufficiency and painful neuropathy. The characteristics of the liver injury have not been well defined, but are likely similar to those with acute iron poisoning, with a clinical phenotype of acute hepatic necrosis, marked elevations in serum aminotransferase levels, early onset of hepatic failure and rapid recovery in cases without early fatality. Chronic, lower dose exposure to arsenic can be toxic and result in arsenosis, a syndrome marked by fatigue, nausea and vomiting, abdominal crampy pain, weakness, stupor, seizures and neuropathy. Skin manifestations are frequent and characteristic with chronic excessive exposure marked by hyper- and hypo-pigmentation, a "rain-drop" pattern of skin discoloration, skin dryness and exfoliation, keratosis of the palms and soles, and skin cancers. Arsenic is also deposited in the hair and nails, where it can be detected even after it is no longer measureable in urine. Liver injury can also occur with chronic arsenic exposure, typically with appearance of signs and symptoms of poal hypeension, without obvious cirrhosis (idiopathic or noncirrhotic poal hypeension). The clinical onset of noncirrhotic poal hypeension is often insidious with weight loss, fatigue and abdominal swelling and minor, nonspecific elevations in serum enzymes, followed by appearance of variceal hemorrhage or ascites. Features of poal hypeension (ascites, variceal hemorrhage) rather than hepatic failure (jaundice, encephalopathy or coagulopathy) predominate. Ref Harrison 20th edition pg 789
Extra hepatic poal vein obstruction
Hepatic carcinoma
Poal hypeension
Cirrhosis
Toxicology