Disease of the Hepatobiliary system

Question 1

Describe the anatomy of the hepatobiliary system (liver)

Answer 1

• The liver, which weighs 1200-1500 g in the average adult, is divided into 2 main lobes, the right and the left lobes. Has 2 other lobes as well - caudate and quadrate. Mahogany brown appearance.
• The liver is found in the right upper quadrant just below the diaphragm.
• Gall bladder is tucked underneath the liver
• The liver has a dual blood supply (rare), deriving blood from the hepatic artery- oxygenated (ex the celiac artery) and from the portal vein (deoxygenated).
  -> Blood moves in between hepatocyte plates - towards the centre. While bile moves the opposite way, outwards towards the portal tracts - drains into biliary system.
• Bile leaves the liver via the right and left hepatic ducts which join to form the common hepatic duct; this then becomes known as the common bile duct (CBD) after it is joined by the cystic duct, which drains the gallbladder. The CBD is joined by the pancreatic duct just before it enters the duodenum at the ampulla of Vater; the ampulla is guarded by the sphincter of Oddi. (biliary system)
  -> If the cystic duct is blocked though (gallstones e.g.) - bile can still enter into the gallbladder along the length of the gallbladder in little ducts (much slower way - trickle through small ducts)
  -> A common place for gallstones is in the common bile duct - may move up and down - intermittent obstruction

Question 2

Describe the histology of the liver

Answer 2

• The liver is divided into hexagonal lobules - hepatic lobules. At the centre of each lobule is the central vein which joins the hepatic veins. At the periphery of the lobules are the portal tracts, each of which contains a branch of the hepatic artery, portal vein and bile duct.
• The lobules are stacked together to comprise the parenchyma of the liver and consist of anastomosis sheets or cords of liver cells (hepatocytes). Between these cords are vascular sinusoids.
  -> Hepatocytes have pale pink cytoplasm and darker pink nucleus.
• Arterial and venous blood enters the liver via the hepatic artery and portal veins, flows through the sinusoids during which it washes over the hepatocytes, and then exits through the central veins into the hepatic veins and vena cava.

Question 3

What are the functions of the liver? describe

Answer 3

The liver has a variety of functions, which can be categorised as follows:

1. Metabolic: the liver plays a role in both glucose and lipid physiology. Excess blood glucose is stored in the liver as glycogen. Glucose is released into the blood through glycogenolysis; through gluconeogenesis, the liver produces glucose from amino acids. During fasting, the liver converts free fatty acids to triglycerides which are secreted in the form of lipoproteins.
2. Synthetic: with the exception of immunoglobulins (made in plasma cells in the blood), most serum proteins (such as albumin, clotting factors, complement, iron and copper binding proteins) are synthesized in the liver.
3. Storage: the liver is an important storage site for glycogen, triglycerides, iron, copper and lipid soluble vitamins.
4. Catabolic: endogenous substances such as hormones and serum proteins are catabolized by the liver to maintain a balance in their levels. Exogenous substances such as drugs are also catabolized by the liver.
5. Excretory: the main excretory product is bile which is important for fat absorption in the small intestine.

Question 4

Describe how liver diseases are diagnosed?

Answer 4

1. liver function tests - blood tests for bilirubin, albumin, INR (blood clotting test) - ensure the liver is clearing toxins and producing proteins and clotting factors. If not excreting enough bilirubin, this will build up in blood. If not producing enough albumin, will not have enough in the blood. Without proper blood clotting factors, the INR test will become abnormal (elevated in this case)
2. liver enzyme tests - ALT, AST, GGT, and LDH (cheap and easy to do). This tells us whether the liver cells are inflamed. When liver cells are inflamed they secrete more enzymes into the blood, so the levels will increase.
3. liver ultrasound - tells us whether there is a lesion in the liver - screening for cancer typically. A bit more difficult as it requires a radiologist.
4. liver biopsy - most invasive. What is the microscopic appearance of the liver/ lesion? Targeted after ultrasound. A biopsy helps to tell us whether there is chronic hepatitis - liver disease. And what is the degree of inflammation (grade). How advanced is the disease, ie. How much fibrosis is there? (stage)
   -> In hepatitis see dense aggregates of inflammatory cells - may look darker/ purple after stain. -in normal liver - see very few purple cells present.
   -> To see fibrosis - use stains which show blue. Stage 4 fibrosis = cirrhosis

Question 5

Describe viral hepatitis - what are the different types?

Answer 5

Viral hepatitis is inflammation of the liver caused by viruses; these viruses can be those that exert their sole effect on the liver (the “hepatitis viruses”), or by viruses that produce liver damage as part of systemic infection, in which the liver is only one of several organs/ systems affected e.g. cytomegalovirus or Epstein Barr virus
1. Hepatitis A
2. Hepatitis B
3. Hepatitis C
4. Hepatitis D

Question 6

Describe Hepatitis A

Answer 6

• Hepatitis A typically causes mild or asymptomatic hepatitis.
• The virus is spread by the fecal-oral route (person-person or via contaminated food or water). Only one spread this way.
• Epidemics are quite common, and there is a high rate of infection with oro-anal sexual practices.
• Serology is used in diagnosis - anti-HAV IgM is indicative of current infection, while anti-HAV IgG is indicative of past infection.
• In those with symptoms, the illness is usually mild and self-limited, although protracted or relapsing hepatitis can occur on occasion.
• Very few patients develop fulminant hepatitis (liver begins to fail very quickly), and chronic hepatitis does not occur (or is extremely rare).
• There is no carrier state (a carrier is an asymptomatic individual who harbours- and can therefore transmit- a virus but may not have clinical disease; a carrier may also have asymptomatic chronic hepatitis.

Question 7

Describe Hepatitis B

Answer 7

• A blood and body fluid borne disease
• Hepatitis B infection is a major world-wide problem; an estimated 2 billion people have been infected and 400 million people have chronic hepatitis B infection worldwide. 75% of these live in south east asia.
• The carrier rate is particularly high (~20%) in SouthEast Asia. It is estimated that there are 300,000 new cases/year in the U.S. and 3000/year in Canada.
• In infected persons, HBV is present in all body fluids except feces; spread occurs by parenteral, intravenous, routes and close contact, including sexual activity.
  -> Highest concentration in blood, serum and wound exudates
  -> Moderate concentrations in semen, vaginal fluid and saliva
  -> Lowest concentration in urine, sweat, tears and breastmilk.
• Transplacental (vertical) spread also occurs - mother to baby.
• At risk are recipients of blood transfusions and blood products, IV drug abusers, health care workers (including dentists), and those on hemodialysis or who practice oro-anal sex - or high risk sex.
• Outcome of infection with HBV:
  -> Subclinical disease with clearing of the virus and complete recovery (most individuals, approx. 65%)
  -> Acute hepatitis (approx. 25%) - 99% recover, 1% develop fulminant hepatitis resulting in death or transplant
  -> Chronic hepatitis (5-10%)- Approx. 1% of these recover, Approx. 20% develop cirrhosis, 2-3% develop hepatocellular carcinoma
  -> Asymptomatic carrier state (5-10%)
  -> Hepatocellular carcinoma (HCC) (risk is increased 200X over the general population)

Question 8

Describe the role of serum antigens and antibodies in Hepatitis B

Answer 8

• A variety of serum antigens and antibodies occur in hepatitis B infection making serology useful in diagnosis. - HBsAg (surface antigen) - first marker to appear.
• The various antigens and antibodies appear in the serum in a specific order, and therefore can be useful to assess a patient’s stage of disease as well as prognosis. For example, HBsAg (surface antigen) is the first marker to appear in the blood, followed by HBeAg (E antigen), HBCab (core antibody), HBEAb (E antibody) and HBSAb (surface antibody).
• Presence and timing provide clinical information
• HBsAg (or HBeAg) for >4-6 months = chronic disease
• HBsAb “normally” persists for life and confers protection (basis for vaccination).
  -> If this antibody tests shows - then means someone has had hepatitis B and is now immune, or successfully has had the vaccination.
• The presence and timing of serum markers may provide important clinical information, e.g. persistence in the blood of HBsAg or HBeAg for longer than 6 months or 4 months respectively implies that the disease has become chronic. HBSAb is an antibody that “normally” persists for life and confers protection to HBV for life; it is the basis for the vaccine.

Question 9

Describe Hepatitis C

Answer 9

• The virus accounts for the majority (80-90%) of parenterally transmitted, post-transfusion and sporadic hepatitis in the general population. It is a major problem in Canada with about 5,000 new cases reported per year and a total of approximately 240,000 infected persons.
• Transmission is similar to hepatitis B.
• Off all patients with hepatitis C, approximately 5-10% have a history of blood transfusion; most of the remainder will have acquired the virus from some form of parenteral transmission. The commonest source of hepatitis C is in populations engaged in IV drug abuse and related practices. Needle stick transmission is less “efficient” than HBV.
• As with hepatitis B, most patients have subclinical disease and a small number have an acute, self-limiting disease.
• Fulminant hepatitis is rare. Of those infected, the majority (80%) will develop chronic hepatitis; progression usually takes many years, measured in decades.
• The carrier state is also more common than with hepatitis B (80%).
• Cirrhosis occurs in approx. 20% of patients with chronic hepatitis. There is an increased risk of HCC (200X) - hepatocellular carcinoma.
• Serological diagnosis is made via the presence of anti-HCV antibodies or using PCR to detect viral RNA.
• Treatment options include the use of interferon and related drugs, antivirals - treatment changing rapidly (used to be incurable - not the case anymore). There is no vaccine.

Question 10

Describe Hepatitis D

Answer 10

• HDV is a defective virus that can only replicate in the presence of HBV - cannot only be infected by hepatitis D - must be both B and D.
• The virus is transmitted parenterally or intravenously
  -> parenterally = administered or occurring elsewhere in the body than the mouth and alimentary canal.
• This virus is an important modifier of both acute and chronic hepatitis B.
• The clinical presentation depends on whether the virus was acquired concurrently with hepatitis B (co-infection) or after (superinfection - tends to have a worse prognosis), and can take the form of acute or chronic hepatitis.

Question 11

What is cirrhosis?

Answer 11

Cirrhosis is an end stage in the evolution of many chronic liver diseases including viral hepatitis. It is a diffuse process in which there is deposition of fibrous tissue (fibrosis) and conversion of the normal architecture into regenerative nodules.

Question 12

Describe the etiology/ causes of cirrhosis

Answer 12

• Infections - HBV, HCV, schistosomiasis - hepatitis B and C
• Drugs & toxins - alcohol, methotrexate, amiodorone, etc.
• Metabolic diseases - NAFLD (non-alcoholic fatty liver disease)/NASH, hemochromatosis (iron storage disorder), Wilson’s disease, alpha-1-antitrypsin deficiency, etc.
• Cardiovascular disease - right heart failure (“cardiac cirrhosis”)
• Autoimmune disease- primary biliary cirrhosis etc. Biliary obstruction - calculi, sclerosing, cholangitis, etc. - autoimmune hepatitis
• Vascular - veno-occlusive disease, Budd-Chiari syndrome, etc.
• Miscellaneous- neonatal hepatitis syndrome, etc.
• Cryptogenic: of obscure or uncertain origin`

Question 13

What is the pathogenesis of cirrhosis?

Answer 13

Three major mechanisms common to all the above etiological causes combine to create cirrhosis- cell death, fibrosis and regeneration.
1. Cell death is usually the initiating factor and has to occur continuously over a long period of time to induce cirrhosis. There are many causes of cell death including, amongst other factors, alcohol and drugs.- has to be sustained, if short the liver can recover.
2. Fibrosis is a repair mechanism that follows cell death, although fibrogenesis can probably be initiated directly without the intervention of cell death and inflammation. -layed down to provide structure - often when cell cannot divide or regenerate fast enough.
3. Regeneration completes the reparative process. Regeneration is influenced by a variety of hormones, including insulin and glucagon, by cytokines and by polypeptide growth factors. -because fibrosis has already occurred, we get regenerative nodules.
-> colour changes to more greenish (bile trapped in hepatocytes), multi-nodular appearance, with yellow bands of fibrosis.

Question 14

What are the complications of cirrhosis?

Answer 14

There are several adverse consequences of cirrhosis; these include mechanical effects with abnormal shunting of blood, and functional effects, with failure to perform normal physiological functions of the liver.
1. Abnormal blood flow: this leads to portal hypertension with secondary dilation of veins at the base of the esophagus (esophageal varices); these varices can rupture leading to hematemesis (vomiting blood - can be fatal). Portal hypertension also causes splenomegaly (enlargement of the spleen) and ascites (build-up of fluid within the abdominal cavity - leaked out of the vascular system).
2. Parenchymal insufficiency: this manifests with impaired protein synthesis (decreased albumin - important to keep blood plasma within vascular system - also decreased clotting factors), inadequate deactivation of drugs and hormones, jaundice (failure to excrete bile), clotting abnormalities and hepatic encephalopathy (poorly understood - results in altered mental state - uncommon).
3. Hepatocellular carcinoma: can occur as a late complication. Very unusual to see in someone who is not cirrhotic.

Question 15

What is alcoholic liver disease? What are the 3 major forms? describe

Answer 15

Alcohol is one of many toxins that can adversely affect the liver. There are 3 major forms of alcoholic liver disease:
1. Steatosis (fatty change) - the earliest manifestation of alcoholic liver injury, usually disappears 2-4 weeks after abstinence. It is typically macro-vesicular. Few symptoms or signs. Due to deranged lipid metabolism.
-> See fat droplets histologically. May damage hepatocytes.
2. Alcoholic hepatitis (steatohepatitis)- a form of hepatitis with a triad of steatosis, inflammation and liver cell damage - result of inflammation (the presence of Mallory bodies in liver cells). Elevated liver enzymes.
-> Fat droplets and inflammatory cells histologically. Mallory bodies are markers of hepatocyte damage usual caused by fat.
3. Cirrhosis - most often due to alcohol in the Western world and caused by persistent hepatitis. HCC (hepatocellular carcinoma) develops in 5-15%.
-> Usually see pattern of fibrosis known as pericellular fibrosis - forms fine fibrous strands around individual hepatocytes.
-> alcohol may act as a promoter or co-carcinogen related to induction of microsomal enzymes.

Question 16

How much alcohol causes liver disease?

Answer 16

• Short term ingestion of 80 g alcohol (8 beers) leads to mild, reversible changes e.g. steatosis - binge
• Chronic ingestion of 80-160 g/day produces borderline risk for severe injury - 8-16 drinks per day (somewhat surprising that this is borderline).
• Chronic daily ingestion of 160 g/day x 10-20 years has a more consistent association with severe injury - more than 16 drinks daily
  10-15% of alcoholics develop cirrhosis

Question 17

What is fatty liver disease? What are the 2 morphological types? describe difference between grade and stage

Answer 17

• Fatty liver is the most common liver abnormality in North America and up to 25% of the population are affected. Its increase in prevalence has occurred in association with increasing obesity rates.
• Non alcoholic fatty liver disease is considered to be hepatic expression of the metabolic syndrome (syndrome X).
• Non alcoholic fatty liver disease can be broken down into 2 main morphological types:
  1. NAFL (non-alcoholic fatty liver - sometimes interchangeable with NAFLD): Steatosis without hepatocellular injury
• Usually macrovesicular (but may be admixed microvesicular)
• Zone 3 or diffuse
• Quantified as 66%

2. NASH (non-alcoholic steatohepatitis): Steatosis with inflammation and hepatocellular injury +/- fibrosis = Steatohepatitis
   - Steatosis
   - Hepatocyte ballooning
   - Inflammation (lobular +/- portal)
   - +/- Mallory Denk bodies (Mallory bodies, Mallory’s hyaline)
   - +/- fibrosis
   - NASH grading: how much inflammation and cellular damage is there?
   - NASH staging: how much fibrosis is there?
   - Not all patients with NAFL progress to NASH and cirrhosis (estimated 10-20% will progress). But 15-25% of patients with NASH will progress to cirrhosis. The risk of cirrhosis is increased if other liver disease is also present (e.g. HCV)

• Microscopically look the same as the alcoholic versions
• NAFL and NASH are now the number 1 cause of liver disease in Western countries.
• Most common cause of elevated liver enzymes and possibly the most common reason for liver transplant

Question 18

What are the metabolic disorders of the liver?

Answer 18

There are a number of metabolic disorders that affect the liver. These include hemochromatosis, alpha-1-antitrypsin (AAT) deficiency and Wilson’s disease (also includes NAFLD).

Question 19

Describe hemochromatosis. what is it? genetic cause? diagnosis? treatment?

Answer 19

• One of the most common inherited/ genetic diseases in the west - autosomal recessive
• A condition of iron overload caused by inherited disorders of iron metabolism. This is associated with mutations in several genes, the most well-characterized of which is that caused by a point mutation at position 282 of the HFE gene.
• Individuals homozygous for the C282Y mutation of the HFE gene have:
  -> life-long excessive iron absorption (at duodenum) which results in a massive increase in body iron.
  -> deposition of iron in cells and tissues throughout the body - eventually results in multi-organ failure, leading to cirrhosis (in liver), cardiac failure (heart), diabetes mellitus (pancreas), arthropathy (joint tissue iron deposition), and skin discolouration occurs- so-called bronze diabetics (bronze skin).
  -> Homozygous patients have an increased incidence of HCC, possibly higher than with other types of cirrhosis.
• The diagnosis is made by evaluating serum iron and transferrin saturation levels and by estimation of tissue iron stores. PCR is used to detect HFE gene in blood.
• Treatment involves removal of iron by phlebotomy (remove blood and excess iron along with it).

Question 20

What are non-inherited iron overload disorders?

Answer 20

Iron overload can occur secondary to parenteral administration, as occurs when patients with certain haematological disorders (e.g. chronic aplastic or hypoplastic anemias) receive repeated blood transfusions. Dietary iron excess can also lead to iron overload.

Question 21

Describe Alpha-1-Antitrypsin deficiency. what is it? consequences? treatment?

Answer 21

• Alpha1-AT is a protein involved in inhibiting proteinase digestion and is synthesized in the liver.
• In alpha-1-AT “deficiency”- inherited as an autosomal recessive trait- an abnormal or mutant protein is produced and accumulates in the liver.
• The main consequences are seen in the liver and lungs. Chronic hepatitis and cirrhosis develops - usually in childhood. Adults are predisposed toward the development of emphysema - alveolar membranes get broken down by proteinases - not inhibited anymore.
• Treatment = augmentation therapy - providing proper Alpha-1-Antitrypsin protein. Or liver transplant. If lung disease is severe - lung transplant.

Question 22

Describe Wilson’s disease. what is it? effects? treatment?

Answer 22

• Copper storage disorder
• Wilson’s disease is an autosomal recessive disorder of copper metabolism in which copper accumulates in the liver and multiple other organs.
• Patients develop hepatitis and cirrhosis along with manifestations related to copper deposition in other organs
• degenerative neurological disease from brain involvement is most prominent other organ manifestation
• The precise pathogenetic mechanism is unknown.
• Treatment = copper chelating agents - to bind excess copper in the blood

Question 23

What is Cholestasis? What are the two types?

Answer 23

Refers to the impaired excretion of bile, from hepatocytes into bile canaliculi.
Cholestasis can be classified, according to etiology, into:
1. intrahepatic and
2. extrahepatic causes.
Cholestasis leads to hyperbilirubinemia. Hyperbilirubinemia (increased levels of bilirubin in the blood) manifests clinically as jaundice (yellow discoloration of the sclera) or as pruritus (itching) due to deposition of bile salts in the skin.

Question 24

Describe extrahepatic cholestasis. etiology? complications?

Answer 24

Typically implies obstruction to large bile ducts outside the liver or within the porta hepatis.
Etiology:
1. Gallstones in the common bile duct (3 types: cholesterol (80% in western countries), black pigment, and brown pigment) - mostly asymptomatic
-> Cholethiasis = gallbladder stones
-> Complications - swelling, acute inflammation (acute cholecystitis), if persists for long time - fibrosis (chronic cholecystitis) - complications depend on where gallstone is
-> Choledocholithiasis = bile duct stones
-> Ball-valve obstruction (can move up and down) - fibrotic stricture (constant moving may cause this - rubbing against)
-> Rather than bile flushing out the stones, bacteria from GI tract can actually climb up from the other side - this is called ascending bacterial cholangitis - inflammation of the biliary tree
-> If stone blocks the common outlet (from bile duct + pancreatic duct) - pancreatic enzymes leak out into the pancreatic tissue -> acute pancreatitis (severe, sometimes fatal)
->Eventually prolonged obstruction -> secondary biliary cirrhosis
2. Tumours - primary neoplasms anywhere within the duct system down to the ampulla, or metastases in lymph nodes at the hilum - anywhere within or around the ducts
3. Congenital abnormalities - atresia, choledochal cyst - failure to develop
4. Strictures - following biliary tract surgery, sclerosing cholangitis
5. Rarer causes - parasites, heterotopic pancreatic/gastric mucosa, annular pancreas

Question 25

Describe intrahepatic cholestasis. etiology? what is PBC?

Answer 25

due to failure of bile secretion within the liver or obstruction of intrahepatic biliary passages. Etiology:
1. Congenital/ familial e.g. newborn jaundice, AAT deficiency, Crigler-Najjar, Dubin-Johnson Acquired e.g. viral hepatitis, drugs and toxins, sepsis, passive venous congestion, primary biliary cirrhosis, primary sclerosing cholangitis, liver tumours.
2. Acquired: viral hepatitis, drugs and toxins, sepsis, liver tumours
-> Primary biliary cholangitis (PBC)
-> Primary sclerosing cholangitis (PSC)

Question 26

What is PBC?

Answer 26

PBC (primary biliary cholangitis) is an autoimmune disorder in which cytotoxic T-cells play a role in bile duct destruction. This ultimately leads to cirrhosis. Autoimmune disorder which leads to the inflammation of intrahepatic ducts
-> The peak incidence is in the 40-60 age group, and it is 9X more common in females than males.
-> Almost all patients have antimitochondrial antibodies in their serum diagnosed through blood test, >95%.
-> Treatment is with immunosuppressive agents; transplantation may be performed. (damp down autoimmune response)
-> “Florid duct lesion” - inflammation + damage of bile duct
-> “Granulomatous portal / bile duct inflammation” - granulomas

Question 27

What is PSC?

Answer 27

PSC in contrast with PBC, occurs more commonly in men in the 30-40 age groups, and is an inflammatory and fibrosing process that causes narrowing and obstruction of both intra and extrahepatic ducts.
-> Chronic obstruction eventually leads to cirrhosis.
-> Two-thirds of patients have ulcerative colitis.
-> There is an increased incidence of cholangiocarcinoma.
-> “Stricturing and beading” - areas of narrowing and widening
-> “Onion skinning fibrosis” - bile duct surrounded by rings of fibrosis
-> Treatment = transplantation (liver)

Question 28

What is Cholecystitis? Describe the two types

Answer 28

Cholecystitis: inflammation of the gallbladder. May be:
1. Calculous - with stones (most common)
- 90% of acute cholecystitis
- Cystic duct obstruction
- Chemical irritation and inflammation
- Increased pressure leads to decreased blood flow to mucosa (ischemia)
- Infection
- Complications: perforation (bile leaks out into the abdomen), gangrenous cholecystitis, and gallstones ileus (rare - gallbladder wall becomes so inflamed that it sticks to duodenum - fistulous tract develops between them - gallstone can pass directly, and may cause dilation of the small bowel.
2. Acalculous - without stones (most dangerous)
- 10% of acute cholecystitis
- Usually results in patients who are critically ill, or who have undergone major surgery
- Multifactorial: bile stasis (in immobile, dehydrated person), increased bile viscosity, decreased blood flow
- Increased gangrene, perforation rates
- Increased morbidity, mortality

*Both may be acute or chronic

Question 29

Describe secondary neoplasms of the liver (secondary liver tumours)

Answer 29

Secondary liver tumours: non-cirrhotic liver. Tumours that have come from somewhere else - very common in the liver due to the fact that it gets a very large blood supply, that passes through the GI tract
-> Often come from the colon, pancreas, lung, breast, and melanoma, etc.

Question 30

Describe the types of primary neoplasms of the liver (primary liver tumours)

Answer 30

1. Epithelial (hepatocytes and bile ducts)
   - benign: liver cell adenoma (hepatocytes), and bile duct adenoma
   - malignant: hepatocellular carcinoma (hepatocytes - cirrhotic), and cholangiocarcinoma (bile ducts), hepatoblastoma
2. Non-epithelial
   - Benign: Hemangioma* (benign tumour of blood vessels)
   - Malignant: Angiosarcoma (benign tumour of blood vessels), and Rhabdomyosarcomas (malignant tumour of a type of muscle cell)

*Note: both lesions arising from hepatocytes and from bile duct cells are considered in the classification of “liver” tumours.

Question 31

What is hemangioma?

Answer 31

the most common benign tumour of the liver, and is composed of proliferating vascular spaces - benign tumour of blood vessels (non-epithelial)

Question 32

What is liver cell adenomas?

Answer 32

occur predominantly in women and are related to the use of oral contraceptive steroids
benign epithelial liver tumour

Question 33

What is hepatocellular carcinoma (HCC)

Answer 33

the most common primary malignant tumour of the liver, and probably the most common malignant tumour world-wide - malignant, epithelial hepatocytes
- Most patients die within weeks or months of diagnosis.
- There is considerable geographic variation, with countries in South-East Asia and tropical Africa having the highest incidences. In such countries HCC is typically the most common or second most common tumour overall.
- The lowest incidence is in Western countries.
- Hepatitis B & C and a variety of forms of cirrhosis are important predisposing factors.
- Rarely occurs in a non-cirrhotic liver

Question 34

What is cholangiocarcinoma?

Answer 34

malignant, epithelial cell tumour of the liver
arises from bile duct epithelium