Quiz 3

(Ref: Harrison 20th edition, p 579; Harrison 19th edition p 544-545)
Integration of HBV DNA is seen in > 90% of Hepatitis B related HCC. This can lead to truncation of HBx gene which happens to be a potent tumor activator. This explains the difficulty in achieving a cure as the viral inserts itself into host DNA and allows it to persist in the face of drugs that impair its replication.
Harrison has used the term insertional mutagenesis.

(Ref: Pediatric Transfusion medicine volume 1 p 94)
Choice C & D are ruled out as current screening tests are sensitive for detecting surface antigen and HCV testing is routinely done.
Possible reasons for post transfusion hepatitis in spite of screening:
1. CMV can cause asymptomatic infection
2. Transfusion transmitted CMV can cause problems in premature neonates, allograft recipients, splenectomized patients.
3. Leukocytes depleted blood use of frozen deglycerolized RBCs and screening of donors for the absence of antibody to CMV.
4. Inactive hepatitis B carrier does not mean patient is HBsAg negative. It means persistent HBV infection of liver with low or undetectable serum HBV DNA/levels with normal serum aminotransferase.

(Ref: CMDT 2019 edition, p 692)
 The patient's initial symptoms during the prodromal period include low-grade fever, nausea, vomiting, decreased appetite, and abdominal pain. Older children and adults are more likely to report pain in the right upper quadrant.
 Diarrhea may occur in young children, whereas constipation is more common in adults. If present, jaundice, dark urine, and light-colored stool develop several days to a week after the onset of systemic symptoms. Anicteric infections are common in young children

(Ref: Harrison 20th edition, p 2340; Harrison 19th edition p 284, 2029, 2078)
 The presence of pruritus with jaundice points to presence of cholestatic component.
 The presence of SAP increasing the credibility of diagnosis of obstetric cholestatis
 HELLP syndrome is ruled out as coagulation profile is normal
 Hepato-renal syndrome is ruled out as RFT is normal.
 The closest choice is viral hepatitis which presents with jaundice with marked elevation of AST, ALT and SAP being mostly normal.

(Ref: Nelson 19th p 1385-1387)
 The best test for diagnosis of biliary atresia is percutaneous liver biopsy procedure and provides the most reliable discriminatory evidence.
 Since it is not in the choices Hepatobiliary scintigraphy is the best answer. It is a sensitive test but not specific
 Hepatobiliary scintigraphy with technetium-labeledimino-diacetic acid derivatives is used to differentiate biliary atresia from non-obstructive causes of cholestasis.
 Although the uptake may be impaired in neonatal hepatitis, excretion into the bowel will eventually occur.
 USG shows small or absent gall bladder with non-visualization of the common duct and presence of triangular cord sign.

(Ref: Nelson 20th edition, p 1960)
The sign and symptoms of Reye syndrome include protracted vomiting, with or without clinically significant dehydration; hepatomegaly in 50%; minimal or absent jaundice; and lethargy progressing to encephalopathy, obtundation, coma, seizures, and paralysis. Notably, patients are afebrile.
The CDC developed the following diagnostic criteria for Reye syndrome:
 Acute noninflammatory encephalopathy with an altered level of consciousness
 Hepatic dysfunction with a liver biopsy showing fatty metamorphosis without inflammation or necrosis or a greater than 3-fold increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), or ammonia levels
 No other explanation for cerebral edema or hepatic abnormality
 Cerebrospinal fluid with a white blood cell count of 8 cells/μL
 Brain biopsy with findings of cerebral edema without inflammation or necrosis

(Ref: Harrison 20th edition, p 2413; Harrison 19th p 739)
Upper GI bleeding will provide the bacteria in the gut with lots of nutrition to multiply and this will lead to increase in production of ammonia.

(Ref: Harrison 20th edition, p 2402; Harrison 19th p 2057)
 NAFLD is most commonly associated with metabolic syndrome. This includes carrying the diagnosis of type II diabetes, obesity, or hypertriglyceridemia.
 Other factors, such as drugs (eg, amiodarone, tamoxifen, methotrexate), alcohol, metabolic abnormalities (e.g., galactosemia, glycogen storage diseases, homocystinuria, and tyrosinemia), nutritional status (e.g., overnutrition, severe malnutrition, total parenteral nutrition [TPN], or starvation diet), or other health problems (e.g., celiac sprue and Wilson disease) may contribute to fatty liver disease.