Liver CPC

Question 1

2. What are the three components of a portal triad?

Answer 1

Portal vein
Hepatic artery
Bile duct

Question 2

3. Describe the arrangement of endothelial cells within the hepatic sinusoids.

Answer 2

The endothelial cells are discontinuous
There are spaces between the hepatocytes and the endothelium of the sinusoids called the space of Disse
This space allows blood to come into contact with liver enzymes

Question 3

4. Describe the differences between zone 1 and zone 3.

Answer 3

Zone 1 – receives the highest oxygen concentration
Zone 3 – receives the lowest oxygen concentration, therefore it is most vulnerable to hypoxia. It is the most metabolically active zone

Question 4

5. Which investigations are performed if a pre-hepatic cause of jaundice is suspected?

Answer 4

FBC
Blood film
HAEMOLYTIC ANAEMIA

Question 5

6. What reaction is used to measure fractions of bilirubin? Describe how this works.

Answer 5

Van den Bergh reaction
The direct reaction measures conjugated bilirubin
Methanol is added which completes the reaction and gives you a value for total bilirubin
The difference between these two values is used to measure the unconjugated bilirubin (indirect reaction)

Question 6

7. What is the most common cause of paediatric jaundice?

Answer 6

Neonates have immature livers that cannot conjugate bilirubin fast enough resulting in a UNconjugated hyperbilirubinaemia

Question 7

8. Describe how phototherapy for jaundice works.

Answer 7

Phototherapy converts unconjugated bilirubin into lumirubin and photobilirubin which are soluble and do not require conjugation for excretion

Question 8

10. Which drug can reduce bilirubin levels in Gilbert’s syndrome?

Answer 8

Phenobarbital

Question 9

9. What is the inheritance pattern of Gilbert’s syndrome?

Answer 9

Autosomal recessive

Question 10

11. Outline the pathophysiology of Gilbert’s syndrome.

Answer 10

UDP glucuronyl transferase activity is reduced to 30% of normal
Unconjugated bilirubin is tightly albumin bound and does not enter the urine

Question 11

13. Describe how urobilinogen is formed. What is the significance of absent urobilinogen in the urine?

Answer 11

Bilirubin released into the bowels will be converted by bacteria in the colon, into urobilinogen and stercobilinogen
Some urobilinogen will be absorbed and transported via the enterohepatic circulation to the liver
Some of this urobilinogen will then be excreted in the urine
The presence of urobilinogen in the urine is NORMAL
The absence of urobilinogen in the urine is suggestive of biliary obstruction

Question 12

16. Outline how hepatitis A serology changes over time.

Answer 12

As viral titres start to drop following initial infection, there will be a rise in IgM antibodies (during this time you will be unwell with jaundice)
After a few weeks, you will start to produce IgG antibodies (leading to cure and ongoing protection from Hep A)
NOTE: hepatitis A does NOT recur

Question 13

18. Outline the features of hepatitis B serology in acute infection.

Answer 13

Initial rise in HBeAg and HBsAg
Eventually you will develop HBeAb and HBsAb resulting in a decline in HBeAg and HBsAg
You will also develop HBcAb which suggests previous infection

Question 14

19. Outline the features of hepatitis B serology in someone who has been vaccinated.

Answer 14

They will have HBsAb but no other antibodies

This is because the vaccine consists of administering HBsAg only

Question 15

20. Outline the features of hepatitis B serology in a chronic carrier.

Answer 15

The patient will mount an immune response but will never clear the virus
HBeAg will decline but HBsAg will persist

Question 16

21. Describe the histology of hepatitis.

Answer 16

Hepatocytes will become fatty and swell (balloon cells), containing a lot of Mallory hyaline
There will also be a lot of neutrophil polymorphs

Question 17

22. What are the defining and associated histological features of alcoholic hepatitis?

Answer 17

Defining: liver cell damage, inflammation, fibrosis
Associated: fatty change, megamitochondria

Question 18

24. Outline the treatment of alcoholic hepatitis.

Answer 18

Supportive
Stop alcohol
Nutrition (vitamins especially thiamine)
Occasionally steroids (controversial but may have useful anti-inflammatory effects)

Question 19

25. What is the issue with regeneration of hepatocytes following alcohol-related damage?

Answer 19

They regenerate in a disorganised manner and produce lots of nodules
The disorganised growth interferes with blood flowing through the liver leading to a rise in portal pressure

Question 20

26. Why is Pabrinex yellow?

Answer 20

Presence of riboflavin (B2)

Question 21

27. What conditions are caused by the following vitamin deficiencies:
    a. B1
    b. B3

Answer 21

a. B1
Beri Beri
b. B3
Pellagra

Question 22

30. What is flapping tremor caused by?

Answer 22

Hepatic encephalopathy

Question 23

31. What is liver failure defined by?

Answer 23

Failed synthetic function
Failed clotting factor and albumin production
Failed clearance of bilirubin
Failed clearance of ammonia

Question 24

33. What is intrahepatic shunting?

Answer 24

The bridge of fibrosis between portal tracts and central veins means that blood does not come into close contact with hepatocytes and get filtered

Question 25

34. Which type of jaundice is associated with itching? What causes the itching?

Answer 25

Obstructive jaundice

This is because the itching is caused by bile salts and bile acids

Question 26

35. State Courvoisier’s law.

Answer 26

If the gallbladder is palpable in a jaundiced patient, the cause is unlikely to be gallstones (i.e. more likely to be pancreatic cancer)