Liver, biliary tract and pancreatic disease

7 Liver, biliary tract and pancreatic disease



Questions




Question 1


Please could you tell me the normal range of values for the liver function test serum alkaline phosphatase. The only mention of the parameters is that a reading of > 1000 = serious liver condition.



Question 2


What is the best single test of liver function to exclude liver cell failure in the routine work-up of a patient with early dementia?



Question 3


How valuable is the measurement of the liver span in a physical examination?



Question 4


Why has the term ‘chronic liver disease’ replaced terms such as ‘chronic hepatitis’? What exactly does this new term mean and what conditions does it cover?



Question 5


Can jaundice occur early in schistosomal hepatic fibrosis and, if so, how?



Question 6


My patient has been found to have a serum bilirubin of 34μmol/L (2mg/dL) on three occasions. The other liver tests are normal. He tells me he has Gilbert’s disease; how can I prove this?



Question 7


Why is urinary urobilinogen increased in haemolytic jaundice? If the bilirubin in this condition is unconjugated, how does it reach the terminal ileum to be converted into urobilinogen?



Question 8


How does cholestatic jaundice affect the kidney?



Question 9


What is the mechanism by which cholestatic jaundice causes bradycardia?



Question 10


Are ‘jaundice’ and ‘icterus’ one and the same? I was taught that icterus is yellowing of the sclera, while jaundice is yellowing of the skin and the mucous membranes. As a result, carotenaemia can produce jaundice but not icterus: is this so? I would be grateful if you would clarify this for me.



Question 11


I am a third-year student nurse and am currently researching a case study based on the biopsychosocial history of a patient who suffers from chronic hepatitis C, which initially occurred as a result of injecting drugs. I am confused about the biological effect of hepatitis: how exactly does it affect the liver?



Question 12


What are the admission criteria for a case of acute viral hepatitis?



Question 13


I would like to know where I can find details on hepatitis B virus (HBV) infection: chronic carrier, asymptomatic [normal liver function tests, HBV DNA/real-time polymerase chain reaction (PCR) = 240 copies/mL, core less than 0.1]. Does a patient with such a profile need therapy or fine needle aspiration (FNA) biopsy? What is the possibility of hepatocellular carcinoma (HCC) in such a patient?



Question 14


In chronic hepatitis B virus (HBV) infection, when anti-hepatitis B e antibody (anti-HBe) develops (seroconversion), the antigen disappears and there is a rise in alanine transferase (ALT). However, the graph in your book (K&C 7e, p. 337, Fig. 7.16) seems to show a fall in ALT at this point. Which is correct?



Question 15


Interferon can be used in prophylaxis from hepatitis C after exposure. Could you explain how this can be used, and what degree of success can be expected as a result?



Question 16


What is the latest recommended drug treatment for hepatitis C?



Question 17


Can hepatitis C disease be treated in a carrier state completely by giving interferon?



Question 18


I am a carrier of hepatitis C (HCV) and am going to have antiviral treatment soon. Are the side-effects of antiviral treatment for HCV bound to occur? I am very worried.



Question 19


Besides needle-pricks, how else is it possible to contract hepatitis C from a hepatitis C (HCV)-positive patient? Are the patient’s skin/sweat (or other bodily secretions) infectious?



Question 20


What is the risk of infection with hepatitis C from blood splashed into the eyes?



Question 21


Hepatitis C (HCV): if results from the polymerase chain reaction (PCR) examination are inconclusive, what does this mean? Should further investigations be undertaken and, if so, will there be a risk of chronicity?



Question 22


In a patient with hepatitis C and autoimmune hepatitis, can corticosteroids be prescribed for the autoimmune hepatitis?



Question 23


We were told that the more vascular a structure is, the more antigen (HLA/blood groups) matching is needed for transplantation, e.g. cornea transplant needs no matching. However, the liver is a very vascular organ; I don’t know why liver transplantation needs blood group matching only but renal transplantation needs much more HLA matching.



Question 24


About steatohepatitis: please give me more information about the occurrence of cirrhosis in such patients (non-alcoholic) and is there any role and indication for lipotropic agents and hypocholesterolaemic drugs?



Question 25


I am working on non-alcoholic fatty liver disease (NAFLD) but I did not find anything regarding it. Can you tell me about its relationship with lipids?



Question 26


Is NASH a valid term or not and what manifestation has it?



Question 27


Is terlipressin better in controlling variceal bleeding than somatostatin?



Question 28


Why is there a hyperdynamic circulation in cirrhosis?



Question 29


Why is there an increased level of immunoglobulin G (IgG) in patients with cirrhosis?



Question 30


Cirrhosis of liver is reversible according to your book. What is the progress and when will we be able to counteract the ‘tissue inhibitors of metalloproteinases’ (TIMPs) and thus save the lives of our patients?



Question 31


What are the criteria for knowing the prognosis of cirrhosis (Child’s criteria)?



Question 32


What is the recommended treatment for cirrhosis of the liver?



Question 33


Is there any role for liver dialysis in hepatic encephalopathy?



Question 34


I have been asked to write an essay on ‘caring’ for a client who has been an alcohol abuser for more than 10 years and is in the ‘recovery’ stage. I am aware there are many different factors, such as length of abuse, amount consumed, age, gender etc.… My question is: how long will it take the liver to ‘recover’ or to return to normal after stopping drinking? I am especially interested in blood tests, fatty deposits and gamma-glutamyl transpeptidases (γ-GTs).



Question 35


Can patients with liver cell failure suffer from myocardial infarction?



Question 36


What is the definition of liver cell failure (decompensated liver disease)?



Question 37


Flapping tremors: why do we get flapping tremors and no other types of tremor in liver failure? What is their mechanism and in which other conditions do they occur?



Question 38


In a patient with liver cell failure, can there be resting and action tremors or parkinsonian features if it is confirmed that the patient does not have Wilson’s disease?



Question 39


Does the absence of any cirrhosis of the liver, together with normal liver enzymes, in a 9-year-old boy complaining of chorea of a 5-year duration, exclude Wilson’s disease?



Question 40


Can Wilson’s disease be excluded in a patient complaining of movement disorder for over 2 years, when there is an absence of cirrhotic liver change?



Question 41


What drugs cause Budd-Chiari syndrome?



Question 42


I recently saw a patient with pyrexia of unknown origin (PUO). He was not particularly unwell and not jaundiced. But 1 week later he was found to have a liver abscess on ultrasound. How can one make the diagnosis earlier?



Question 43


What is the most recent management of HCC (hepatocellular carcinoma)? What is radiofrequency ablation? What is its role in the management of HCC and its prognosis?



Question 44


How do you differentiate haemorrhagic ascitic fluid due to malignancy and accidental rupture of blood vessel while withdrawing the fluid?



Question 45


Is there any place for the medical treatment of gallstones with ursodeoxycholic acid?



Question 46


In a case of common bile duct stones, where it is acknowledged that spontaneous passage within 24 hours is observed in approximately 50% of patients provided the stone is small, and that in these cases there is no need for a sphincterotomy, is the use of antispasmodics, e.g. Buscopan (active ingredient hyoscine-N-butylbromide), recommended? Surely these will reduce the pain and improve the chance of a spontaneous release of obstruction without surgical procedure?



Question 47


What is sphincter of Oddi dysfunction?



Question 48


I would like to know: what is the role of lysosomal hydrolases (cathepsin B) in the pathogenesis of acute pancreatitis?



Question 49


What is the role of octreotide in management of acute pancreatitis?



Question 50


Why does paralytic ileus occur in pancreatitis?



Question 51


How sensitive is the increase in serum lipase levels in the case of acute pancreatitis?



Question 52


What is the association between chronic pancreatitis and peripheral vascular disease (PVD)?



Question 53


Please, can you explain to us the mechanism of pancreatitis in hypertriglyceridaemias?



Question 54


Is there any role for chemotherapy in carcinoma of the pancreas?



Question 55



1. How should portal hypertension be managed in patients with bronchial asthma, where beta-blockers are contraindicated?

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Dec 3, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Liver, biliary tract and pancreatic disease

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