GI & Surgery 6

oelomar's version from 2016-05-13 19:48


Question Answer
What is haemolytic jaundice?Jaundice caused by haemolytic anaemia. Haemolytic anaemia is a form of anaemia due to haemolysis. The increased breakdown of erythrocytes leads to an increase in the production of bilirubin.
What would investigations show in someone with haemolytic jaundice?Investigations show features of haemolysis. The level of unconjugated bilirubin is raised but the serum ALP, transferases and albumin are normal. Serum hepatoglobins are low.
What is Gilbert’s syndrome?A common genetic liver disorder found in 3-12% of the population. This is the most common familial hyperbilirubinaemia but this normally has no serious consequences. The raised unconjugated bilirubin is diagnostic and rises on fasting and during a mild illness. Most patients have reduced levels of UGT-1 activity, the enzyme that conjugates bilirubin.
What is Crigler-Najjar syndrome (types I & II) and how can it be treated?A rare autosomal recessive condition. Type II is a decrease while type I (incompatible with life) is absence of UGT-1 (the enzyme that conjugates bilirubin). Liver histology is normal. Transplantation is the only effective treatment.
What are Dubin-Johnson syndrome (black liver) and Rotor syndrome?The conditions are similar to one another. Both are autosomal-recessive disorders that are due to defects in bilirubin handling in the liver, and both therefore cause an increase in conjugated bilirubin.
What is the difference between intrahepatic and obstructive (extrahepatic) cholestasis?Cholestasis is a condition in which bile cannot flow from the liver to the duodenum. Obstructive cholestasis is due to large duct obstruction of bile flow at any point in the biliary tract distal to the bile canaliculi. Intrahepatic cholestasis occurs owing to failure of bile secretion.
What are the signs/symptoms or cholestasis?(Dependant on cause) + pruritus, jaundice (uncommon in intrahepatic cholestasis), dark urine, and pale stools (implies obstructive cholestasis). Serum bilirubin is conjugated.
Out of the hepatitis viruses, which ones are RNA viruses?All of them apart from hepatitis B (DNA virus).
What is the mean incubation period of hepatitis A?2-4 weeks.
What is the mean incubation period of hepatitis B?1-4 months.
What is the mean incubation period of hepatitis C?7-8 weeks.
What is the mean incubation period of hepatitis E?4-5 weeks.


Question Answer
If levels of ALT>AST, what does that indicate?Viral hepatitis.
If levels of AST>ALT, what does that indicate?Alcoholic hepatitis (ratio usually>1.5).
If levels of GGT are high, what does that indicate?Various liver disease. It also increases with heavy alcohol consumption.
If levels of ALP are high, what does that indicate?Obstructive liver disease (hepatocellular carcinoma), bone disease, bile duct disease.
If levels of amylase are high, what does that indicate?Acute pancreatitis, mumps.
If levels of lipase are high, what does that indicate?Acute pancreatitis.
If levels of ceruloplasmin are low, what does that indicate?Wilson’s disease (accumulation of copper in the liver). (Ceruloplasmin is the major copper-carrying protein in the blood).
What is suggested by high levels of ALP without raised GGT?It is very suggestive of bone pathology e.g. fracture, Paget’s disease.


Question Answer
How is the hepatitis A virus spread?Faecal-oral route or by consumption of shellfish.
What are the symptoms in someone infected with hepatitis A?Clinical disease tends to be mild or asymptomatic. Affected individuals have nonspecific symptoms such as fatigue and loss of appetite, and often develop jaundice.
Which serum antibodies are detected in someone infected with hepatitis A?Specific IgM antibody against HAV appears in the blood at the onset of symptoms. The IgM response declines in a few months and is followed by the appearance of IgG anti-HAV. The IgG confers lifelong immunity.
What are the symptoms in someone infected with hepatitis B?Approximately 70% have mild or no symptoms and do not develop jaundice. The remaining 30% have nonspecific constitutional symptoms such as anorexia, fever, jaundice, and upper right quadrant pain.
When does HBsAg appear in hepatitis B?HBsAg appears before the onset of symptoms, peaks during overt disease, and then declines to undetectable levels (in acute infection).
When does HBeAg appear in hepatitis B?HBeAg rises early and usually declines rapidly (in acute infection).
What does the presence of anti-HBs indicate?Immunity to hepatitis B.
What does the presence of anti-HBc indicate?IgM anti-HBc suggest an acute and continuing viral replication. It persists for many months. Over a period of months the IgM anti-HBc antibody is replaced by IgG anti-HBc.
What does the presence of anti-HBe indicate?Anti-HBe appears after the anti-HBc and its appearance relates to a decreased infectivity.
What does the presence of HBV DNA suggest?Continual viral replication.
Which antiviral drugs can be used in the treatment of chronic hepatitis B?Pegylated α-2a, lamivudine, adefovir, entecavir, and tenofovir.
Name a side-effect of the interferons used for chronic HBV treatment.Neutropenia (leading to increased susceptibility to infection).
If someone were to have a needle-stick injury and hepatitis B infection was suspected, what should be done?Give an accelerated course of the hepatitis B vaccine + hepatitis B immunoglobulin; screen for hepatitis B HBsAg.


Question Answer
What is the most common cause of chronic liver disease and the most common indication for liver transplantation in the west?Hepatitis C.
How is hepatitis C spread?Primarily by blood-to-blood contact associated with IV drug use, poorly sterilised medical equipment, and transfusions.
Is someone infected with hepatitis C likely to become chronically infected?Yes. 80-85 become chronically infected. Only 15-20% of patients will clear the virus after an acute infection.
How is hepatitis C infection diagnosed?In chronic HCV infection, circulating HCV RNA persists. Therefore, PCR for HCV RNA must be performed to assess viral replication and to confirm the diagnosis of HCV infection. A clinical feature that is quite characteristic of chronic HCV infection is episodic elevations in serum aminotransferases, with intervening normal or near-normal periods.
How is hepatitis C infection treated?In mild chronic disease the decision between immediate treatment and “watchful waiting” until the disease has reached a moderate stage should be made on an individual basis. Otherwise, current treatment is combination therapy with pegylated α-2a (or 2b) and ribavirin.
What are the side-effects of ribavirin?Haemolytic anaemia. It is also a severe teratogen.
Hepatitis D infection can only occur when which other hepatitis infection is present?Hepatitis B.
How is hepatitis D infection diagnosed?Detection of serum IgM anti-HDV and IgG anti-HBc, or by finding HDV RNA.
How is chronic hepatitis D infection treated?Pegylated α-2a (but response is poor).
What is the link between hepatitis E and pregnant women?There is a high mortality rate.
How is hepatitis E infection diagnosed?HEV Ag can be identified in the cytoplasm of hepatocytes during active infection, and virions are shed in stool during the acute illness.
Which of the hepatitis viruses are not associated with chronic hepatitis or hepatocellular carcinoma?A & E.
Hepatitis G is the most severe of the viral hepatitis’. True or false?False. Hepatitis G is not known to cause human disease.


Question Answer
Hepatitis G commonly co-infects individuals with which other medical condition?HIV. Curiously this dual infection is somewhat protective against HIV disease.
50% of cases of hepatic failure in the UK are due to what?Paracetamol overdose.
Most cases of hepatic failure are due to what?Viral hepatitis.
What are the clinical features of hepatic failure?Examination shows a jaundiced patient with a small liver and signs of hepatic encephalopathy (altered level of consciousness). Fever, vomiting, hypotension and hypoglycaemia occur. Neurological examination shows spasticity and hyperreflexia. A condition known as foetor hepaticus can also occur. Cerebral oedema develops in 80% of patients, and its consequences of intracranial hypertension and brain herniation are the most common causes of death.
What is foetor hepaticus?A condition seen in portal hypertension where thiols (an organic compound containing the –SH group) pass directly into the lungs. It is a late sign of liver failure and is one of the clinical features of hepatic encephalopathy. The breath has a sweet, faecal smell to it.
What investigations can be done for a patient with hepatic failure?There is hyperbilirubinaemia, high serum aminotransferases and low levels of coagulation factors. An EEG is sometimes helpful in grading the encephalopathy. Ultrasound will define liver size and may indicate underlying liver pathology.
How is the cerebral oedema that might occur in hepatic failure treated?20% mannitol is given.
How is the hypoglycaemia, hypokalaemia, hypomagnesaemia, hypophosphataemia, and hypocalceamia that might occur in hepatic failure treated?10% dextrose infusion, potassium, magnesium, phosphate, and calcium.
What is hepatopulmonary syndrome?Hepatopulmonary syndrome is a syndrome of shortness of breath and hypoxemia (low oxygen levels in the blood of the arteries) caused by vasodilation in the lungs of patients with advanced liver disease.
What is hepatorenal syndrome?A life-threatening condition in which patients with cirrhosis or fulminant liver failure have rapid deterioration in kidney function.
What may precipitate hepatorenal syndrome?Overvigorous diuretic therapy, NSAIDs, diarrhoea, and infection (particularly spontaneous bacterial peritonitis).
How is hepatorenal syndrome treated?IV albumin with terlipressin, but liver transplantation is the best option.
What would investigations find in a patient with autoimmune hepatitis?Absence of serologic markers of viral infection, elevated serum IgG and γ-globulin levels, and high serum titres of autoantibodies.
How is autoimmune hepatitis treated?Prednisone is the mainstay of therapy. Azathioprine can also be used as a steroid sparing drug. Liver transplantation is indicated for patients failing to respond to medical treatment.


Question Answer
Which drugs can lead to chronic histological changes in the liver (i.e. drug-induced hepatitis)?Isoniazid, amiodarone, and methotrexate.
What is steatohepatitis and what is it associated with?Also known as fatty liver disease, this is a type of liver disease characterised by inflammation with concurrent fat accumulation. Progressive disease may cause fibrosis and liver cirrhosis. It is classically seen in alcoholics as part of alcoholic liver disease. When not associated with alcohol, it is referred to as non-alcoholic steatohepatitis.
What is the most common liver disorder in developed countries?Non-alcoholic steatohepatitis.
What is non-alcoholic steatohepatitis caused by?Insulin resistance and metabolic syndrome (particularly obesity).
How is steatohepatitis managed?The mainstay of treatment is lifestyle changes (particularly weight loss) and monitoring (fatty liver on its own does not progress).
What are the features of non-alcoholic steatohepatitis?It is usually asymptomatic. Otherwise, hepatomegaly can occur. ALT is typically greater than AST. On ultrasound, there is increased echogenicity (ability to bounce an echo).
How is non-alcoholic steatohepatitis diagnosed?Diagnosis is by demonstration of a fatty liver on ultrasound, with the exclusion of other causes of liver injury, e.g. alcohol. Liver biopsy allows staging of the disease.
What is the most common cause of liver cirrhosis in the west? What about the most common cause worldwide?In the west: Alcohol. Worldwide: viral infection.
What are the two types of cirrhosis and what are the differences between them?Micronodular and macronodular. Micronodular cirrhosis: nodules are less than 3 mm in size and the liver is involved uniformly. It is often caused by ongoing alcohol damage or biliary tract disease. Macronodular cirrhosis: nodules are of variable size and normal acini may be seen within the larger nodules. Often seen following chronic viral hepatitis. (Note that a mixed picture is sometimes seen).
Name some of the complications of cirrhosis.Portal hypertension, GI haemorrhage, renal failure, hepatic encephalopathy, hepatocellular carcinoma, infections.
What is decompensated cirrhosis?Decompensated cirrhosis is defined by the development of jaundice, ascites, variceal haemorrhage, or hepatic encephalopathy.


Question Answer
What is the Child-Pugh score?A score out of 15 used to assess the prognosis of chronic liver disease, mainly cirrhosis. It is also used to determine the required strength of treatment and the necessity of liver transplantation.
Which variables are measured in the Child-Pugh score and what scores are they out of?There are 5 variables all of which can be scored from 1-3, which are: total bilirubin, serum albumin, prothrombin time, ascites, and hepatic encephalopathy. The scores are added up to give a total.
How is the Child-Pugh score interpreted/classified?<7 classifies one as Child’s A. One year survival=100%; two year=85%. 7-9=Child’s B. One year survival=81%; two year=57%. 10-15=Child’s C. One year survival=45%; two year=35%.
What is the MELD score?Model for End-Stage Liver Disease, or MELD, is a scoring system for assessing the severity of chronic liver disease, and for prioritising allocation of liver transplants (instead of the older Child-Pugh score).
Which variables are measured in the MELD score?Serum bilirubin, serum creatinine, and INR.
How is the MELD score interpreted?In interpreting the MELD score for hospitalised patients, the 3 month mortality is: 40 or more=71.3% mortality; 30-39=52.6% mortality; 20-29=19.6% mortality; 10-19=6.0% mortality; <9=1.9% mortality.
What is the normal blood pressure in the hepatic portal vein?5-10mmHg.