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Flashcards

Liver Disease

sophietevans English 185 cards

Cards in this deck (185)

  1. 1List some sample types that can be tested to investigate possible liver disease.Venous blood (glucose), serum and plasma (leukocyte count/infection), arterial blood, capillary blood, cerebrospinal fluid (markers for multiple sclerosis), urine (though hygiene, volume and the time collected can affect the result), faeces, sputum, saliva, aspirates (e.g. plural fluid), synovial fluid, tissues and cells (biopsies, carcinogenesis).
  2. 2Why are samples often asked for at particular times of day?The markers you are looking for are often released at particular times of day, so it is important to collect the sample at this time to get an accurate result.
  3. 3List 3 clinical signs of potential liver disease.Yellow tinge to sclera of the eyes (possible jaundice), frequent urination, and thirst.
  4. 4What substances should not be present in urine, but might be as a result of liver disease, and can be tested for using a dipstick?Glucose, proteins, blood, ketone bodies.
  5. 5What is cholestasis?Cholestasis refers to a blockage within the bile duct system, be it from the smaller tubules (the bile canaliculi) which collect bile secreted by the hepatocytes, or from the bile ductulse that eventually merge to form the common hepatic duct. This results in an accumulation in the blood of bile materials including bilirubin, cholesterol, bile salts and alkaline phosphatase.
  6. 6List some pathological situations in which enzyme levels would be elevated from an individual's basal level.When there is extensive cell damage (e.g. in myocardial infarction), when there is cell proliferation (e.g. normally in bone metabolism/growth but pathologically in cancer), when there is enzyme induction (the body is stimulated to produce enzyme e.g. in alcoholic liver disease), or when there is duct obstruction.
  7. 7In measurements of enzyme activity in biological fluid, activity is related to concentration. What concentrations might be measured?The concentration of a product formed, the concentration of substrate disappearance (as a rate), or the increase/decrease in cofactor absorbance.
  8. 8What are the units of measurement of enzyme activity?International units (IU).
  9. 9What is IU defined as?The amount of enzyme that will catalyse the reaction of 1 µmol of substrate per minute under specified conditions.
  10. 10What are the conventional units for enzyme concentration?IU/L
  11. 11What is a normal concentration of bilirubin in the blood?1.0 mg/dL
  12. 12In what range of very high bilirubin concentrations does jaundice tend to occur?2.0 - 2.5mg/dL
  13. 13Is there always jaundice in liver disease?No, it is not a guarantee. In some individuals it occurs at relatively low bilirubin concentrations (though raised from normal) whereas others can have very high bilirubin concentrations and severe liver disease and still not present with jaundice.
  14. 14Describe where pain would be located in liver disease.In the upper right quadrant of the abdomen, or the right hypochondriac region (going in to the epigastric, right flank and right umbilical regions).
  15. 15In which two organs can cholestasis occur to produce a partial or full bilirubin build up?The liver or the gallbladder.
  16. 16What is the correct term for increased concentration of bilirubin in the blood?Hyperbilirubinaemia.
  17. 17What type of bilirubin cannot be present in the urine?Unconjugated bilirubin, because it is insoluble.
  18. 18What can cause unconjugated hyperbilirubinaemia?Haemolytic disease (in which there is increased bilirubin synthesis as erythrocyte destruction is increased), decreased liver uptake of unconjugated bilirubin, or decreased conjugation of bilirubin (as in Gilbert's disease).
  19. 19What is the correct term for ineffective erythropoiesis?Dyserythropoiesis.
  20. 20Which cells carry out the majority of erythrocyte senescence?Macrophages.
  21. 21During erythrocyte senescence, what is haemoglobin broken down into before being broken down further in to bilirubin?Haem.
  22. 22Once released from phagocytes, what does bilirubin form a complex with in order to travel through the circulation?Albumin.
  23. 23At which membrane of a hepatocyte does the bilirubin-albumin complex dissociate so that bilirubin can be transported across the plasma membrane by a carrier?The sinusoidal membrane.
  24. 24Once across the hepatocyte plasma membrane, what is the purpose of bilirubin binding to ligandin?It prevents the reflux of bilirubin into the circulation and the non-specific diffusion of bilirubin into inappropriate parts of the hepatocyte.
  25. 25In which organelle is bilirubin conjugated?The endoplasmic reticulum.
  26. 26What is bilirubin conjugated with, what is the complex formed called, and which enzyme carries out the conjugation?Bilirubin is conjugated with glucuronic acid to form bilirubin diglucuronide by the enzyme UDP-glucuronyltransferase.
  27. 27What property of bilirubin diglucuronide allows it to diffuse through the cytosol to the bile canaliculus?It is water soluble.
  28. 28What is the rate-limiting step of the transhepatic transport of bilirubin?The excretion of bilirubin from the bile canaliculi into the bile by a carrier mediated process.
  29. 29After excretion into the small bowel, where does the conjugated bilirubin travel to, unabsorbed, to become unconjugated again?The distal small bowel and colon, as the unconjugation is carried out by bacteria that are part of the microbiome of this area.
  30. 30Once the conjugated bilirubin is hydrolysed to unconjugated, free bilirubin again, what is it then reduced to?A mixture of heterocyclic aromatic organic compounds (pyrroles), collectively called urobilinogen.
  31. 31What happens to urobilinogen once it is formed?Most urobilinogen is excreted in the faeces, but a small proportion is absorbed in the terminal ileum and colon, returned to the liver and re-excreted into the bile. Some of the reabsorbed urobilinogen is transported by the blood to the kidneys where it is excreted as a normal component of urine.
  32. 32What three things can elevated unconjugated bilirubin be a result of?Haemolytic disease (the levels are already high in the circulation due to increased senescence), decreased uptake of the unconjugated bilirubin by the liver, or decreased conjugation of bilirubin (as in Gilbert's disease).
  33. 33What is Gilbert's disease?A deficiency of UDP-glucuronyl transferase that occurs in inborn errors, starvation and neonatal jaundice.
  34. 34What three things can result in elevated conjugated bilirubin in the blood?Hepatocellular disease, cholestatic disease, or genetic conditions.
  35. 35Name five causes of haemolytic disease that can result in elevated unconjugated bilirubin concentrations in the blood.Intrinsic erythrocyte defects, erythrocyte membrane defects, hereditary spherocytosis, extrinsic erythrocyte defects, or nutritional aspects.
  36. 36Give examples of intrinsic erythrocyte defects that could cause haemolytic disease.Alterations in haemoglobin structure leading to instability of the molecule (e.g. thalassaemias), or deficiencies of enzymes such as pyruvate kinase which restrict erythrocyte metabolism and energy generation.
  37. 37In what way might erythrocyte membrane defects result in elevated concentrations of unconjugated bilirubin in the blood?Erythrocyte membrane defects affect the biconcave discoid shape and erythrocyte deformability (so that they can fit through tiny capillaries), so erythrocytes are trapped in splenic sinusoids and removed from the circulation prematurely. They are broken down by macrophages and unconjugated bilirubin is released in to the circulation.
  38. 38In what way might extrinsic erythrocyte defects result in haemolytic disease?Defects such as infection with malarial parasites or acquisition of autoantibodies to erythrocyte antigens 'targets' the erythrocytes for premature removal from the circulation, resulting in a higher proportion of erythrocytes being destroyed at a faster rate than normal, and high concentrations of unconjugated bilirubin being released into the circulation.
  39. 39How might nutritional deficiencies result in high concentrations of unconjugated bilirubin in the blood?Erythropoiesis increases in anaemia to try to compensate for it, and this can deplete folate and other mineral stores and actually proliferate the anaemia. Iron deficiency anaemia results in microcytes whereas vitamin B12 anaemia results in macrocytes, both of which are incorrect shapes and can be prematurely removed from the circulation, resulting in higher than normal concentrations of unconjugated bilirubin in the blood.
  40. 40The raised bilirubin in haemolytic disease is not caused by liver complications, but it ? the liver?Overwhelms.
  41. 41Name two situations in which hepatocyte uptake of unconjugated bilirubin is decreased/impaired and the result is accumulation of unconjugated bilirubin in the blood?In liver cell injury, such as viral hepatitis, or when taking some drugs such as Rifampin, which are metabolised by the liver and either their products are directly hepatotoxic or they induce an immunological reaction which causes the hepatocytes to be destroyed by the immune system.
  42. 42What is rifampin used for?It is an antimycobacterial used in the treatment of tuberculosis, leprosy and other meningococcal conditions.
  43. 43Name two pathologies that cause decreased bilirubin conjugation, resulting in elevated unconjugated bilirubin levels?Crigler-Najjar disease, and Gilbert syndrome.
  44. 44Describe type 1 Crigler-Najjar disease.This is a recessively inherited condition in which little or no bilirubin is conjugated in the liver due to the complete absence of UDP-glucuronyltransferase. This leads to unconjugated hyperbilirubinaemia, and is usually fatal by bilirubin encephalopathy.
  45. 45Describe type two Crigler-Najjar disease.This is a familial partial decrease in UDP-glucuronyltransferase resulting in decreased bilirubin conjugated and unconjugated hyperbilirubinaemia. Unlike type 1, type 2 can be treated with phenobarbitol (a sedative barbiturate) which decreases the unconjugated hyperbilirubinaemia.
  46. 46What is Gilbert syndrome?Gilbert syndrome is an inherited autosomal dominant condition which affects 5-10% of the population. It is relatively mild but is a chronic condition in which a decrease in UDP-glucuronyltransferase activity results in unconjugated hyperbilirubinaemia of around <6 mg/dL blood.
  47. 47How does Gilbert syndrome differ from Crigler-Najjar disease?Gilbert syndrome is a dominantly inherited condition, whereas Crigler-Najjar disease is recessively inherited, and Gilbert syndrome is less severe, more common and virtually asymptomatic, whereas Crigler-Najjar disease is rare but either fatal (type 1) or symptomatic and requires treatment (type 2).
  48. 48Define anicteric.'Without jaundice'
  49. 49What is hepatitis?A viral infection of hepatocytes that produces necrosis and swelling of the liver.
  50. 50What type of infection does hepatitis A cause?An acute infection of between 4 to 6 weeks.
  51. 51What type of virus is hepatitis A and what does it use hepatocytes for?It is a small RNA-containing enterovirus that only uses hepatocytes for replication.
  52. 52How is hepatitis A hepatotoxic?Hepatitis A may be directly cytopathic or may cause liver damage by initiating a response from natural killer cells.
  53. 53What are typical symptoms of hepatitis A?Jaundice, though the infection is usually anicteric, and non-specific symptoms such as fever, malaise, and anorexia.
  54. 54Is there a carrier state for hepatitis A?No.
  55. 55Does hepatitis A infection provide lifelong immunity?Yes.
  56. 56How is hepatitis A spread?Via the faecal-oral route, often in contaminated water but frequently in oral-anal contact of homosexual males.
  57. 57Why can the hepatitis A virus be detected in faeces 3 weeks after infection?Because viral progeny shed into the bile and are carried through the intestines and excreted in the faeces.
  58. 58Which virus-antibody complexes exist for 3-5 months after infection and for life?IgM-anti-HAV (Hepatitis A Virus) exists for 3-5 months after infection as IgM is a relatively non-specific antibody that can capture foreign antigens readily due to its pentameric structure, whereas IgG-anti-HAV exists for life.
  59. 59Is there a vaccine for hepatitis A virus?Yes!
  60. 60What type of virus is hepatitis B?A hepatotrophic double-stranded DNA virus.
  61. 61What is the cytopathic mechanism for hepatitis B virus that results in liver damage?As with hepatitis A, it appears to be related to immunity and destruction of hepatocytes by killer T cells.
  62. 62The surface coat of hepatitis B contains lipid, protein and carbohydrate and expresses which surface antigen that is produced in the infected hepatocyte, separately from the viral core, and secreted into the blood in vast amounts?Hepatitis B surface antigen (HBsAg).
  63. 63Which bodily secretions is the hepatitis B surface antigen found in?It is found in most bodily secretions, including blood, saliva, semen and tears.
  64. 64How is hepatitis B transmitted?Through blood, saliva and semen in blood transfusions, and breaks in the skin/mucous membranes/intimate contact.
  65. 65What are the four clinical courses of hepatitis B?Acute self-limited hepatitis B; fulminant hepatitis B; chronic carrier state hepatitis B; and chronic, asymptomatic carrier state hepatitis B.
  66. 66Describe the course of acute, self-limited hepatitis B.This is similar to hepatitis A, except that it tends to be more severe and have a longer incubation period of 2-3 months.
  67. 67What are the two serum markers that can be tested for, that are released at different times, in cases of acute self-limited hepatitis B?HBsAg is is the first serum marker to appear (1 week to 2 months before symptoms) and HBeAg (e antigen) is found after HBsAg.
  68. 68Which extrahepatic ailments can circulating complexes of HBsAg-anti-HBsAg cause?Arthritis, polyarteritis, glomerulonephritis, pancreatitis, and a rash (all caused by deposition).
  69. 69Which two words best describe fulminant hepatitis B?Sudden and severe.
  70. 70What is fulminant hepatitis B characterised by?Massive liver cell necrosis, hepatic failure and high mortality.
  71. 71What has been suggested for the cause of fulminant hepatitis B being so severe?A possible mutant strain of hepatitis B.
  72. 72In what proportion of hepatitis B cases does the chronic carrier state occur?5-10% of hep B cases.
  73. 73What happens in the chronic carrier state of hepatitis B?Patients do not develop antibodies and consequently do not resolve their antigenaemia, and the infection persists.
  74. 74What are the two main outcomes for patients that develop the chronic carrier state of hepatitis B?Patients either develop antibodies and clear the infection after many years, or they never develop antibodies and suffer from relentless chronic hepatitis B and sometimes cirrhosis.
  75. 75What does the chronic, asymptomatic carrier state of hepatitis B tend to follow?An inapparent, or mild, transient episode of acute hepatitis B.
  76. 76What state are the blood and hepatocytes in, in chronic asymptomatic carrier state hepatitis B?They remain infected and infective.
  77. 77What is there a high risk of developing, in chronic hepatitis B?Hepatocellular carcinoma.
  78. 78What does the hepatitis B vaccine consist of?Synthesised HBsAg.
  79. 79What type of virus is hepatitis D?A single stranded RNA virus.
  80. 80What is the hepatitis D virus coated in, in the blood?HBsAg (the hepatitis B surface antigen).
  81. 81Which type of people is hepatitis D infection limited to, and why?Hepatitis D infection is limited to those already infected with hepatitis B as the HBsAg is required to stabilise and protect the genome of hepatitis D.
  82. 82Where does hepatitis D/HBsAg assembly occur?In the hepatocytes.
  83. 83Why might infection with both hepatitis B and hepatitis D lead to the clearance of both infections?Because clearing hepatitis B with the immune system would leave hepatitis D without HBsAg to protect it, so it would either be unstable or would instantly be detected and destroyed by the immune system too.
  84. 84What is the general outcome of co-infection/superinfection of hepatitis B and then D?Severe, fulminant and often fatal hepatitis, as superinfection typically increases the severity of existing chronic hepatitis.
  85. 85What type of virus is hepatitis C?A single-stranded RNA virus.
  86. 86How is hepatitis C transmitted?Similarly to hepatitis B, through the bodily fluids (typically blood, saliva and/or semen) of an infected person through breaks in the skin or mucous membranes of an uninfected person.
  87. 87Which two types of people is hepatitis C commonly seen in?Post-blood transfusion patients and intravenous drug users.
  88. 88What proportion of sporadic, acute viral hepatitis cases is hepatitis C generally responsible for?~50%
  89. 89Is the acute illness of hepatitis C more or less severe than that of hepatitis B?Less.
  90. 90What complication occurs more frequently with hepatitis C than hepatitis B?Chronic liver disease.
  91. 91What type of liver disease is hepatitis C frequently associated with?Alcoholic liver disease.
  92. 92What two complications do a small number of people develop following hepatitis C?Cirrhosis and hepatocellular carcinoma.
  93. 93What type of virus is hepatitis E?A single stranded RNA virus.
  94. 94How is hepatitis E transmitted?Through the faecal-oral route, like hepatitis A.
  95. 95What type of infection does hepatitis E cause?An acute infection.
  96. 96What does 'chronic hepatitis' refer to?The presence of inflammation and necrosis in the liver for more than 6 months.
  97. 97Which two hepatitis viruses, when they cause chronic disease, have a high risk of leading to cancer?Hepatitis B and C.
  98. 98Why might unconjugated hyperbilirubinaemia be caused by any of the hepatitis viruses?The hepatitis viruses cause inflammation and necrosis of the hepatocytes and result in cell-mediated immunity destroying them, so given that there are fewer hepatocytes and many are having all their energy used in viral replication, it is easy to see that taking up unconjugated bilirubin would be decreased, and unconjugated hyperbilirubinaemia and jaundice may result.
  99. 99As well as the hepatitis viruses, what may also cause hepatitis?Toxins, paracetamol overdose, Epstein-Barr virus, the Rubella virus and more.
  100. 100How much bile is produced per day?500 - 1000ml.
  101. 101Blockage in the canaliculi or the bile duct leads to the obstruction of bile flow into the duodenum. What results from this?There is evidence of regurgitation and bile is absorbed into the blood, and an excess of bile pigments (yellow) is deposited in the tissues from the blood, which can lead to jaundice.
  102. 102What can result in impairment of the canalicular bile flow?Impairment of the structural and functional characteristics of the canalicular microvilli; impairment of the permeability of the canalicular plasma membrane (e.g. some drugs alter this and alter bile flow); impairment of the intracellular contractile system surrounding the canaliculi (e.g. similar drugs inhibit peristalsis-like contractile activity of the hepatocytes); and the interaction of bile acids with secretory apparatus.
  103. 103What are intrahepatic causes of cholestasis often secondary features of?Hepatitis.
  104. 104What is a common cause of impairment of bile flow through the hepatic/common bile duct?Gallstones!
  105. 105Which system can gallstones move throughout?The biliary system.
  106. 106What is the correct term for gallstones?Cholelithiasis.
  107. 107What proportion of gallstones are composed mostly of cholesterol?~75%
  108. 108Other than cholesterol, what else might gallstones be composed of?Calcium bilirubinate and other calcium salts (pigment gallstones, which are often black).
  109. 109How do gallstones result in conjugated hyperbilirubinaemia?They provide an obstruction to prevent the secretion of bile into the duodenum, and this can result in regurgitation into the blood and accumulation of bile pigments in the tissues (conjugated hyperbilirubinaemia).
  110. 110List three extrahepatic causes of cholestasis.Gallstones in the common bile duct, malignancy, or pancreatitis.
  111. 111What are the three distinct stages of alcoholic liver disease?Fatty liver disease, alcoholic hepatitis and cirrhosis.
  112. 112Do the three stages of alcoholic liver disease occur separately and in order?Not always, they may coexist or exist independently.
  113. 113What term describes an accumulation of fat in a cell?Steatosis.
  114. 114What is fatty liver disease?Fatty liver disease is a reversible lesion in which steatosis occurs in hepatocytes and can lead to cholestasis.
  115. 115Macroscopically, what do livers of individuals with alcoholic liver disease look like?They are two to three times their normal size, and appear yellow, soft and greasy.
  116. 116What are the intracellular changes in hepatocytes of an individual with fatty liver disease?Initially, cytoplasmic fat deposits are small and are found near the endoplasmic reticulum. Later, as steatosis increases, fat 'vacuoles' take up the majority of the cell and force the nucleus to the margin.
  117. 117How does ethanol cause hepatocytes to accumulate fat?By increasing fatty acid synthesis (hydrolysing dietary/endogenous fat depots to make it available), decreasing mitochondrial oxidation of fatty acids, decreasing the production of triglycerides so that the fat is left in the cell, and impairing the release of lipoproteins.
  118. 118Other than chronic alcohol consumption, what else can fatty liver disease be caused by?Obesity, uncontrolled diabetes, and kwashiorkor (malnutrition including protein deficiency).
  119. 119How can fatty liver disease be tested for?The are no clinical markers, identification is by biopsy only.
  120. 120What is alcoholic hepatitis?It is an acute necrotising lesion, characterised by necrosis of hepatocytes, cytoplasmic hyaline aggregations of eosinophilic materials within hepatocytes, a neutrophilic inflammatory response, and perivenular fibrosis.
  121. 121When does alcoholic hepatitis develop?Alcoholic hepatitis is usually superimposed on an existing fatty liver, although there is no evidence of predisposition to hepatitis.
  122. 122Roughly what proportion of alcoholic hepatitis cases does cholestasis occur in?~1/3
  123. 123Why does perivenular fibrosis occur in alcoholic hepatitis, and what can it cause?Perivenular fibrosis is a result of collagen deposition, which can result in portal hypertension, in which the portal veins protrude from the abdomen.
  124. 124What symptoms do patients with alcoholic hepatitis typically present with?Malaise, anorexia, fever, right upper quadrant abdominal pain, and jaundice.
  125. 125The activity of which serum enzyme is usually increased in alcoholic hepatitis?Serum alkaline phosphatase.
  126. 126What is the prognosis for a person with alcoholic hepatitis?This depends on the severity of the hepatocyte injury, it can lead to chronic alcoholic hepatitis, or even to hepatic failure and death.
  127. 127What does 'cirrhosis' refer to?The widespread replacement of normal liver architecture by fibrous tissue and regenerating nodules of hepatocytes, resulting from persistent liver cell necrosis.
  128. 128List three types of cirrhosis.Micronodular cirrhosis, macronodular cirrhosis, and biliary cirrhosis.
  129. 129Is liver cirrhosis reversible?Nope.
  130. 130What is the appearance of the liver in micronodular cirrhosis?Small (~3mm), uniform nodules are separated by thin fibrous septa giving a granulated appearance.
  131. 131What is the appearance of the liver in macronodular cirrhosis?Large (>3mm), irregular nodules are separated by broad septa of inflammatory cells and proliferated bile ducts etc. The surface is irregular.
  132. 132Which cirrhosis morphology is most often found with alcoholic cirrhosis?Micronodular cirrhosis.
  133. 133Which cirrhotic morphology is most often found with chronic activate hepatitis?Macronodular cirrhosis.
  134. 134What does biliary cirrhosis result from?Longstanding obstruction of hepatic biliary ducts.
  135. 135In what situation might biliary cirrhosis be secondary to obstruction?In a person with gallstones.
  136. 136In what situation might biliary cirrhosis be primary to obstruction? What evidence is there for this?In an immunological reaction, evidenced by its frequent association with other immunological disorders, and by the presence of antimitochrondrial/antinuclear antibodies - typical of women in their mid-40s.
  137. 137What happens to the bile ductules in primary biliary cirrhosis?There is destruction and inflammation.
  138. 138What happens to bile ductules in secondary biliary cirrhosis?Ducts proximal to obstructions dilate and dark green 'bile lakes' are formed.
  139. 139In both primary and secondary biliary cirrhosis, what is the morphology of the liver?The liver is finely granulated, with delicate fibrous scars, and stained a dark green (from bile).
  140. 140How might cirrhosis predispose to primary liver cancer?Liver cell dysplasia (the enlargement of the tissue by proliferation of abnormal cells) resulting from regenerating nodules may predispose to primary liver cancer.
  141. 141What is another term for hepatocellular carcinoma?Hepatoma.
  142. 142Which are the most common malignant tumours in humans?Hepatomas.
  143. 143In Japan, what proportion of people suffering from hepatitis B virus and hepatitis C virus develop hepatomas?A quarter and a third, respectively.
  144. 144What does the correlation between people suffering from viral hepatitis and those that develop hepatic carcinomas suggest?That persistent cell injury, caused by the virus or by cell-mediated immunity, may be crucial in the pathogenesis of hepatic carcinoma.
  145. 145How would it look if hepatocellular carcinoma occupied a 'trabecular' pattern?One large solitary tumour would occupy the liver and resemble the normal liver 'plate'.
  146. 146Where might hepatocellular carcinomas metastasise?Intrahepatically, to the lungs, and portal lymph nodes, also to the portal veins through which it can metastasise to the vena cava and even the right atrium. Hepatocellular carcinomas tend to reach large sizes before metastasising extrahepatically.
  147. 147How do patients with hepatocellular carcinomas typically present?They present with a painful and enlarging mass in the upper right abdominal quadrant, ascites (fluid accumulation in the peritoneal cavity), portal vein thrombosis, occlusion of hepatic veins (sometimes resulting in prominence from the abdomen), and haemorrhage from oesophageal varices.
  148. 148What kind of prognosis do patients with hepatocellular carcinoma have, and what do they typically die of?These patients have a dismal prognosis, and typically die either from rupture of the tumour with catastrophic bleeding into the peritoneal cavity, or of hepatic failure.
  149. 149What circulating marker is produced by hepatocellular carcinomas, as well as benign tumours and extrahepatic disorders? What concentration will it be compared to normal?α-fetoprotein is produced at over 400ng/mL, as opposed to the normal 10ng/mL which makes it a useful tool for exluding these disorders.
  150. 150What is the correct term for bile duct carcinoma?Cholangiocarcinoma.
  151. 151What is a bile duct carcinoma defined as?A malignant hepatic tumour of the biliary epithelium.
  152. 152Where can bile duct carcinomas arise?Anywhere from the large intrahepatic bile ducts to the small bile ductules.
  153. 153How do peripheral cholangiocarcinomas look microscopically and morphologically, and why might this make them different to distinguish from cirrhosis?Peripheral cholangiocarcinomas are composed of small cuboidal cells in glandular formations, and they characteristically show significant fibrosis, which makes the tumour difficult to separate from the nodules if it occurs in a cirrhotic liver.
  154. 154What might result if cholangiocarcinoma occurs in the bile canaliculae?Regurgitation of conjugated bilirubin into the blood, and then into the urine.
  155. 155What colour is urine if bilirubin is present in it?Dark yellow/orange.
  156. 156What three bodily samples might bilirubins be tested for in?Blood, urine and faeces.
  157. 157If conjugated bilirubin is present in the blood, what colours with the urine and faeces be?Dark yellow/orange, and pale respectively.
  158. 158What is alkaline phosphatase?An enzyme which catalyses the hydrolysis of phosphate monoesters (dephosphorylation).
  159. 159Where do the two isoenzymes of alkaline phosphatase originate?One in the bone marrow and one in the liver.
  160. 160What normal physiological process might an increase in serum alkaline phosphatase represent?Bone growth.
  161. 161What pathologies might increased serum alkaline phosphatase represent?Bone disease, or cholestasis caused by tumour, gallstones, or functional impairment of the bile canaliculae.
  162. 162What is gamma-glutamyl transferase (GGT) and why might it strengthen the evidence towards a diagnosis of liver or bile duct disease?GGT is an enzyme that is not elevated in bone growth or disorders, so if it is elevated alongside alkaline phosphatase, it distinguishes between skeletal and liver disease.
  163. 163Which type of liver disease is gamma-glutamyl transferase typically raised in?In biliary outflow obstruction, rather than hepatocellular damage.
  164. 164What other conditions has raised gamma-glutamyl transferase been a feature in?Pancreatic disease, renal failure, and diabetes.
  165. 165What are transaminases and which two are tested for in liver function tests?Transaminases are enzymes involved in amino acid metabolism, and aspartate aminotransferase and alanine aminotransferase are tested for in liver function tests.
  166. 166How do aspartate aminotransferase (AST) and alanine aminotransferase (ALT) differ in their distribution within cells?AST is present in both mitochrondria and the cytoplasm, whereas ALT is only cytoplasmic.
  167. 167How might the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) differ in liver diseases?AST and ALT are necessary for energy production, so their concentrations may be reduced in fatty liver disease due to mitochrondrial dysfunction, and increased if hepatocytes are damaged or destroyed as they would be released from cells.
  168. 168Which liver disease do aspartate aminotransferase (AST) and alanine aminotransferase (ALT) tend to be raised in?AST and ALT levels are higher when hepatocytes are damaged, as in viral hepatitis or that caused by toxic substances, as opposed to biliary obstruction.
  169. 169What is prothrombin time?The rate at which prothrombin is converted to thrombin in citrated blood with added calcium.
  170. 170What is the international normalised ratio reference range for prothrombin time?0.9-1.2
  171. 171What two things commonly cause a prolongation of prothrombin time?Liver disease and use of anticoagulants.
  172. 172Why might liver disease result in an elevated prothrombin time?Prothrombin is a thrombotic protein produced in the liver, so when hepatocytes are damaged and destroyed and not functional to their maximum potential, less prothrombin or less functional prothrombin is produced, and then time taken for it to be converted to thrombin will be increased.
  173. 173What type of liver lesion does a high prothrombin time usually correspond with?Cirrhosis.
  174. 174What is albumin and why is it significant?Albumin is a protein produced by the liver, which maintains the amount of blood in arteries and veins by maintaining the osmotic pressure. Low levels result in fluid leaking out from vessels into nearby tissues and causing swelling of the feet and ankles (peripheral oedema).
  175. 175Why might chronic liver disease result in low serum albumin?Because hepatocyte damage and death reduces albumin production.
  176. 176In advanced liver disease, how low might serum albumin be?<3.5mg/dL
  177. 177What is globulin?A class of proteins containing enzymes and antibodies, as well as others.
  178. 178What does total protein measure?The concentration of both albumin and globulin, which produces a ratio as well as a combined amount.
  179. 179What are the optimal concentrations of albumin and globulin, and what is the optimal ratio?Albumin: 4.1 g/dL, globulin: 3.2 g/dL, A/G ratio: 1.9.
  180. 180Total protein is not a specific test for liver disease. Although both high and low total protein may be seen in liver disease, what is the most common?High albumin is rare, and as it is the more frequently occurring of the serum proteins (>50%), it follows that both values are usually low in liver disease, probably as a result of reduced function of hepatocytes due to damage and destruction.
  181. 181Why are ammonia levels usually very low in the blood?Because ammonia is converted to urea in the liver.
  182. 182In severe liver disease there is failure of the urea cycle. How will this present in tests?As high blood ammonia (and therefore a high blood pH), and a low concentration of urea in the urine.
  183. 183Increasing blood ammonia signals end-stage liver disease and a high risk of hepatic coma. What causes hepatic coma?Hepatic encephalopathy, accumulation of toxins resulting from liver disease/failure.
  184. 184What are ketone bodies?Compounds produced as by-products when fatty acids are broken down for energy in the liver.
  185. 185Why might liver disease result in lower ketone concentrations in the blood?Because hepatocyte damage and dysfunction leads to impaired lipid metabolism which leads to lower concentrations of ketones and steatosis in hepatocytes.

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(Biology of Disease) Flashcards on Liver Disease, created by sophietevans on 11/08/2013.
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