45. Liver Disorders

Question 1

What 2 things supply blood to the liver (give %)?

List 7 functions of the liver.

Where is 95% of bile salts reabsorbed?

Answer 1

Hepatic artery (25% or total blood flow), portal vein (75% - drains GI tract and spleen)

1. Protein metabolism (synthesis/degradation)
2. Coagulation factors
3. Carb metabolism (glycogen)
4. Lipid metabolism (lipoproteins/chol)
5. Bile formation
6. Hormone and drug inactivation
7. Immunological function (a sieve)

Ileum

Question 2

Describe 3 liver-related lab investigations.

What would lab tests would you order to investigate:

a) liver biochemistry
b) liver function

List some causes of jaundice:

a) prehepatic
b) intrahepatic
c) extrahepatic

Answer 2

Bilirubin (tells you you’re yellow), ALT and AST (liver cells are in trouble - hepatocellular), Alkaline phosphatase (bile ducts in trouble - cholestatic)

a) ALT, AST, alkaline phosphatase
b) albumin, prothrombin time (INR), bilirubin
a) haemolysis (due to bilirubin)
b) viral hepatitis, drugs, alcoholic hepatitis, cirrhosis,pregnancy, infections
c) common duct stones, carcinoma (bile duct, head of pancreas, ampulla), biliary structure

Question 3

What do levels of bilirubin need to be for jaundice to be detected?

What causes haemolytic jaundice? What lab results would you see? What are possible clinical features?

What is Gilbert’s syndrome?

Answer 3

Bilirubin > 50mcgmol/L

Increased RBC breakdown (e.g. Haemolytic anaemia), unconjugated bilirubin. AST, ALT, albumin, Alk P all normal. Serum hepatoglobulins low. Clinical features: (depend on cause) anaemia, jaundice, splenomegaly

Question 4

What are some symptoms and signs of viral hepatitis?

Which types of hepatitis do not cause chronic liver disease?

What other type of hepatitis is D usually found with?

Is hep C chronic?

Are hep F and G hepatic viruses?

Answer 4

Symptoms: unwell, nausea, anorexia, +/- jaundice, pale stool/dark urine

Signs: enlarged liver, +/- splenomegaly/lymphadenopathy, extra hepatic - arthritis, vasculitis

A and E, usually can get better, but can kill you

B (not oral - always blood products) -> chronic. Vaccination for B

Yes. No vaccination, mostly spread by IV drug use, treatment depends on genotype

No but can cause liver disease

Question 5

What would you see in a histology investigation of liver cirrhosis?

What are some physical signs?

What conditions may a liver transplant be used for?

What are some complications?

Answer 5

Nodules of various size surrounded by fibrosis

General: jaundice, fever, loss of body hair. Compensated: xanthelasmas, spider naevi, splenomegaly, clubbing, scratch marks, pigmented ulcers. Decompensated: neurological, drowsy, hepatic flap, ascites, oedema

Alcoholic liver disease, hep C and B, primary biliary cholangitis, autoimmune hep

Primary non-function, organ rejection, infections, hepatic artery/portal vein thrombosis

Question 6

What are the main causes of liver cirrhosis?

What are the consequences?

How is it managed?

Answer 6

Alcohol, NASH, chronic viral hepatitis (HCV, HBV), autoimmune hep, haemochromatosis

Decline in liver function (decreased serum albumin, coagulopathies, jaundice). Portal hypertension (ascites, oedema, splenomegaly etc.). Increased risk of hepatocellular carcinoma.

Question 7

What might gallstones be composed of?

Where do gallstones get stuck, and what does it cause?

Answer 7

Chol (75%), pigment (<10%), mixed (20%)

1. In gallbladder (cystic duct): biliary colic, epigastric pain, Kehr’s sign (migrates to R shoulder). No fever/rebound/tenderness
2. In gallbladder: acute cholecystitis, fever, guarding, rebound tenderness
3. In common bile duct: ascending cholangitis, fever, jaundice, epigastric pain (Charcot s triad). Can resolve if gallstone passes on its own
4. In sphincter of Oddi: acute pancreatitis - epigastric or mid-abdo main

Question 8

How is hep B transmitted?

Describe the pathogenesis of hepatitis.

How does chronic hepatitis present?

How is it investigated and treated?

Answer 8

Via blood e.g. Blood products, IVD users, direct contact, vertical (birth). (8 genotypes of hep, partially ds)

Enters hepatocyte via blood stream, hepatocyte receptor, conversion to fully dsDNA, translation to viral processes in ER. Not cytopathic (hepatocyte damage due to host immunity). Infected hepatocytes present viral antigen via cells surface proteins. CDB and HBV specific T-cells recognise and kill via cell apoptosis

Asymptomatic, fatigue, nausea, upper quadrant pain/discomfort. 5-10% of acute hep B pts. Chronic liver inflammation and disease: heptomegaly, splenomegaly, ascites etc.

Investigations: moderate rise in aminotransferases, normal serum bilirubin, histological changes, HBsAg and HBV DNA on serum. Treatment: prevent disease progression, eliminate HBsAg, interferons, oral nucleotides

Question 9

What is hep C?

How is it diagnosed?

How is it treated?

Answer 9

Disease mainly affecting the liver, caused by hep C virus, acute or chronic, no symptoms until liver severely damaged, spread mainly by blood, diff genotypes/subtypes in diff areas

ELISA, liver biochem and function tests, HCV RNA test, HCV genotypic testing, liver biopsy

Tailored (dependant on genotype, liver damage, treatment history). Oral protease inhibitors, direct acting antivirals e.g. Sofosbuvir