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a path 3 > HISTO: Liver CPC > Flashcards

HISTO: Liver CPC Flashcards

1
Q

Why is the endothelium in the liver special compared to the rest of the body?

A

The cells are discontinuous in the liver, spaces in between so that blood can come in between. This space where the blood comes in is called Space of Disse.

The blood can come into contact with the endothelial cells this way and all the liver enzymes.

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2
Q

Which zone of the hepatocytes is the blood least oxygenated in? Where are the most metabolically active cells located?

A

Both in Zone 3

  • Zone 1 damage (periportal) – damage for substances that are directly damaging…
    • Directly hepatoxic substances
    • N.B. damage to zone 1 makes ALP rise more due to close proximity to the bile ducts
  • Zone 3 damage (centrilobular) – damage for substances that require bioactivation…
    • Hypoxic damage (blood lost quite a lot of oxygen by the time it passes through zones 1 and 2)
    • Metabolised hepatotoxic substances
    • Zone 1 and 2 cells look similar at first but zone 3 are the most metabolically active cells in the liver
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3
Q

What does the portal triad consist of?

A
  1. Artery
  2. Vein
  3. Duct

They are hexagonal with trabecula with sinusoids between them

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4
Q

What substances can damage each of the zones of hepatocytes?

A
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5
Q

How do you categorise and investigate the causes of a high bilirubin?

A
  1. Pre-hepatic (unconjugated) BR conjugates once it has passed through the liver
    1. Haemolysis (Ix: FBC and blood film)
  2. Hepatic (Ix: repeat LFTs)
  3. Post-Hepatic (i.e. obstructive jaundice)
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6
Q

How do you assess fractions of bilirubin/measure the split bilirubin?

A
  • This is done using the van den Bergh reaction
  • A DIRECT reaction measures conjugated bilirubin
  • Add methanol which –> complete reaction to allow you to measure total bilirubin –> difference between two values gives the unconjugated bilirubin (i.e. an INDIRECT reaction)
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7
Q

In a prehepatic cause would you have more unconjugated or conjugated bilirubin?

A

More conjugated bilirubin because the liver is fine to conjugate it.

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8
Q

In children, what forms should most of the bilirubin be in and why?

A

This is usually NORMAL –> usually caused by liver immaturity and it should be an UNCONJUGATED hyperbilirubinaemia (because the liver cannot conjugate the bilirubin fast enough)

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9
Q

How do you manage high bilirubin in a child first line?

A
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10
Q

How does phototherapy work? What should you do if it doesn’t help?

A
  • Converts bilirubin into lumirubin + photo-bilirubin
  • These are isomers that do NOT need conjugation for excretion

If the bilirubin does NOT resolve, other causes should be considered such as hypothyroidism and other causes of haemolysis (perform a Coombs’ test and measure unconjugated bilirubin levels)

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11
Q

How common is Gilberts and how is it inherited?

A

Gilbert’s syndrome is autosomal recessive

50% carry the gene –> 6% (1 in 20) have Gilbert’s

(25% risk of child having it if two carriers)

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12
Q

How do you know it is Gilberts syndrome using investigations?

A
  • This is an entirely benign condition (no need for a liver biopsy – identify from history)
  • If all the other enzymes are normal on LFTs, it tells you that there aren’t any other problems in the liver
  • It’s probably Gilbert’s
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13
Q

What exacerbates Gilberts syndrome? What can reduce bilirubin levels (not done anymore)?

A

The bilirubin in Gilbert’s is worsened by fasting

Phenobarbital can reduce bilirubin levels in Gilbert’s syndrome

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14
Q

What is the pathophysiology of Glberts? Is unconjugated bilirubin found in urine and if so why? Is urobilinogen present in urine?

A
  • UDP glucuronyl transferase activity is reduced to 30%​

Unconjugated bilirubin is tightly albumin bound and does NOT enter the urine

  • So, NO bilirubinuria
  • Urobilinogen is ALWAYS present in the urine of normal people – this comes from the enterohepatic circulation
  • The bilirubin that you make will go through the biliary tree/gall bladder and into the bowel, where bacteria will convert bilirubin to stercobilinogen and urobilinogen – this is then reabsorbed into the circulation and you excrete it
  • So, the presence of urobilinogen in the urine tells you that the enterohepatic circulation is intact
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15
Q

What does absence of urobilinogen in the urine indicate?

A

Negative urobilinogen is suggestive of biliary obstruction

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16
Q

What does ALT, ALP and AST stand for?

A

Alanine aminotrasferase - ALT

Alkaline phosphatase - ALP

Aspartate aminotransferase - AST

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17
Q

Which investigation is the most representative of liver function?

A
  • Prothrombin time is the most representative marker of liver function
  • This is telling you that the liver is failing to make clotting factors (hence, it is not functioning well)
  • Albumin is also a good marker (because it is representative of the liver’s synthetic function) but PT is better
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18
Q

What is the normal PT? How is this important in liver failure?

A

Normal PT is about 12-14 seconds

General rule: if the PT (s) is higher than the number of hours since the overdose, the patient should be transferred to a liver unit for a transplant

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19
Q

Which investigations are best at indicating that there is liver damage?

A
  • ALT and AST are enzymes that tell you that there is damage rather than telling you how your liver is actually functioning
  • Function of the liver is measured by:
    • Albumin
    • Clotting factors (PT, PTTK)
    • Bilirubin
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20
Q

What are 6 causes of abnormal LFTs?

A
  • Pre-hepatic – Gilberts, haemolysis
  • Hepatic – viral hepatitis, alcoholic hepatitis, cirrhosis
  • Post-hepatic – gallstones, pancreatic
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21
Q

When is AST>ALT? What are the other general rules for liver enzymes?

A
  • ALT > AST = other forms of hepatitis
  • AST > ALT = alcoholic hepatitis
  • S = Stella
  • High ALP = obstructive jaundice e.g. jaundice or cancer or head of the pancreas
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22
Q

Name 3 causes of hepatitis.

A
  • Viral causes – check viral titres
  • Autoimmune
  • Alcoholic
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23
Q

What are the 3 features of hepatitis clinically?

A

Fever

Janudice

Raised ALT/AST

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24
Q

What is the route of transmission of Hep A? What are the most common sources?

A
  • fAEco-oral transmission route – food or men-on-men sex
  • Contaminated water is often the major source
    • E.G. Recent shellfish consumption (improper washing)
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25
Q

What are the symptoms of hepatitis A and when are carriers infectious? How long is the course of infection?

A

Acute – asymptomatic, or – nausea, D+V, fever, jaundice, RUQ pain

Onset = 2-6 weeks;

Symptoms last = ~8 weeks

Often infectious whilst asymptomatic

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26
Q

What is the antibody response pattern to hepatitis A?

A

After viral titres start to drop, you get a rise in IgM antibodies and you become unwell with jaundice

If you survive the initial few weeks, you will produce IgG antibodies and from that point onwards you are cured, and you are immune - KILL OR CURE.

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27
Q

How is hepatitis A managed? What is the vaccine against it called?

A

Treatment supportive (alcohol avoided) – vaccine called Havrix exists that contains some antigens of hepatitis A

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28
Q

What percentage of hepatitis B becomes chronic?

A

5-10%

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29
Q

What are the two antigens which can be detected in Hep B infection?​

A

HBe and HBs (surface) antigens. HBe antigen is highly infectious. Cannot measure core Ag.

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30
Q

What are the routes of infection for Hep B?

A
  • Sex (more commonly through unprotected sex than HCV)
  • Vertically (mother –> child)
  • Blood products
31
Q

What is the most common presentation of patients with Hep B?

A

Normally acute presentation (can be acute ± chronic) - lasts 2-6 months

Hepatitis symptoms – fever, jaundice, N+V, RUQ pain)

But a chronic infection follows in ~10% of people

32
Q

How do the antigen titres change during the disease course? Which antibodies are left at the end?

A

Once antibodies start to appear there are no antigens left

You end with 3 antibodies and no antigens

Anti-HBc tells you that they have been exposed to hepatitis B in the past, but we don’t have the capability to measure HBc antigen

33
Q

What does the Hep B vaccine consist of?

A

The vaccine contains HBsAg (so, if you have been vaccinated you will have anti-HBs)

However, you will NOT have HBeAg or anti-HBe

34
Q

How do chronic carriers immune profiles to Hep B differ from the acute one?

A

Chronic carriers (bottom image) never clear the HBsAg however infectivity decreases with time

They can remain for 10 years time; some remain asymptomatic

They are highly infectious and cannot e.g. be surgeons

35
Q

How is hepatitis B managed?

A

Treatment:

  • Acute – supportive
  • Chronic – anti-viral therapy
36
Q

What type of viruses are HepA/B/C?

A

Hep A - RNA virus

Hep B - DNA virus

Hep C - RNA virus

37
Q

What percentage of Hep C becomes chronic?

A

60-80%

38
Q

What hepatitis viruses are associated with hepatocellular carcinoma?

A

Hep B and C

In SBAs: “Hx of jaundice, hepatomegaly, weight loss”, “raised aFP”

39
Q

Why might thalassaemia patients get hep C?

A

Frequent blood transfusions

NB:

Blood transfusions are a major risk factor for HCV (90%) and a minor risk factor for HBV (10%).

40
Q

What is the time of onset of hepatitis C after infection?

A

6-8 weeks (unsure if this is what notes mean)

41
Q

Which hepatitis infection can be treated and eradicated with antivirals?

A

Hepatitis C

42
Q

How is hepatitis D contracted?

A

Only when there is co-infection with hepatitis B (HDV needs HBV surface antigen to invade liver cells)

43
Q

What is the transmission route for hepatitis E?

A

fAEco-oral transmission - foor or MSM

44
Q

Which food can contain hepatitis E?

A

Shellfish and uncooked pork

45
Q

Who is at increased risk of hepatitis E?

A
  • Expectant mothers
  • E-mmunocompromised patients
46
Q

What is the time of onset and duration of illness of hepatitis E?

A

Onset - 2-6 weeks

Duration of symptoms - about 8 weeks

47
Q

What does this liver biopsy show?

A

Cells full of fat

Swollen cells with pink material inside (arrows) = Mallory’s hyaline, also known as “alcoholic” hyaline because it is most often seen in conjunction with chronic alcoholism

  • Too much alcohol –> fat deposits in their liver, however, these will go away if they stop drinking alcohol
  • If alcohol abuse persists, you may develop alcoholic hepatitis (neutrophils will infiltrate the liver)
  • When hepatocytes get damaged by alcohol hepatitis, you see balloon cells containing mallory hyaline
  • This may NOT be reversible
48
Q

What are the forms of alcoholic liver damage?

A
  1. Fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis

OR stages:

  1. Alcoholic hepatitis
  2. Chronic stable liver disease
  3. Resultant portal hypertension
  4. Liver failure (asterixis)
49
Q

What does this liver biopsy show?

A

Bile accumulation in the liver because the hepatic cells are swollen and they have Mallory hyaline in them. This will cause high bilirubin in the blood.

50
Q

What does this biopsy with staining show?

A
  1. This is a histochemical stain that stains collagen blue.
  2. This collagen around individual cells is characteristic of alcohol abuse.
  3. Some cells also have Mallory hyaline and swelling.
  4. This patient is likely to go on to end stage liver disease with cirrhosis.
51
Q

What are the 3 DEFINING histological features of alcoholic hepatitis?

A
  1. Liver cell damage (ballooning ± Mallory-Denk bodies)
  2. Inflammation
  3. Fibrosis

May also see: megamitochondria (alcohol damages mitochondria) and fatty change from the previous stages

52
Q

What are the differential diagnoses for Fatty Liver Disease?

A
  1. Non-alcoholic steatohepatitis (NASH)
    • This looks exactly like alcoholic hepatitis (therefore pathologists need a good history to differentiate)
    • It is the most common cause of liver disease in the Western world
  2. Alcoholic hepatitis
  3. Malnourishment (Kwashiorkor)
53
Q

What is the management of alcoholic liver disease?

A
  • Treatment required:
    • Supportive
    • Stop alcohol
    • Nutrition
    • Vitamins (esp. Pabrinex containing B1 and thiamine)
    • Occasionally steroids (anti-inflammatory)
54
Q

Name the deficiencies from:

  • B1
  • B3
  • B12
A
  • B1 (thiamine) = Beri-Beri;
  • B3 (niacin)= pellagra;
  • B12 (cobalamin) = B12 deficiency / SCDC

NB: rickets = vitamin D deficiency; scurvy = vitamin C deficiency; pernicious anaemia = IF deficiency treated by B12 deficiency; neural tube defects = folic acid deficiency

55
Q

What is the remaining complication even when you stop chronic alcohol abuse?

A

If alcohol is stopped, the liver can regenerate.

However, it will heal in a disorganised fashion which makes it difficult for the blood to flow through it leading to increased blood pressure (portal HTN)

56
Q

What are 4 features of chronic STABLE liver disease?

A
  • Palmar erythema
  • Spider naevi (>5)
  • Gynaecomastia (failure of liver to break oestradiol down)
  • Dupuytren’s contracture
57
Q

Name the 3 features of portal HTN (usually caused by cirrhosis).

A
  • Visible veins
  • Ascites
  • Splenomegaly
  • NB: Not hepatomegaly because the liver will be small and cirrhosed by this stage.
58
Q

What 4 features is liver failure is defined by?

A
  1. Failed synthetic function
  2. Failed clotting factor and albumin production
  3. Failed clearance of bilirubin
  4. Failed clearance of ammonia (leads to encephalopathy)
    • Flapping tremor (asterixis) = manifestation of hepatic encephalopathy
59
Q

What does the liver flap signify?

A
  • Failed clearance of ammonia (leads to encephalopathy)
    • Flapping tremor (asterixis) = manifestation of hepatic encephalopathy
60
Q

What does this pale fatty liver show? What does it signify

A
  • Lots of nodules (= regenerating hepatocytes) AND + can identify nodules very clearly (= they have a cuff of fibrous tissue)
  • Alcoholic livers tend to have small nodules (micronodular cirrhosis)
61
Q

Name two causes of micronodular and macronodular hepatitis.

A
  • Micronodular = alcoholic hepatitis, biliary tract disease
  • Macronodular = viral hepatitis, Wilson’s disease, A1AT
62
Q

Describe what happens in alcoholic intrahepatic shunting.

A
  • There is scarring between the portal tracts and the central veins
  • This bridge of fibrosis, means that the blood does NOT get in close contact with the hepatocytes and hence the blood does not get filtered
  • It only goes straight in with no benefit to the blood or the liver and out via the central veins
63
Q

What are the 4 sites of portosystemic anastomoses?

A
  • Oesophageal varices
  • Rectal varices
  • Umbilical vein recanalizing
  • Spleno-renal shunt
64
Q

Case:

  • Severely jaundiced
  • Cachectic
  • Palpable gall bladder
  • Multiple scratch marks – what do these suggest?
A
  • Suggest obstructive jaundice
    • ONLY post-hepatic causes of jaundice make you itchy (gallstones, pancreatic cancer)
    • That is because of the bile salts and bile acids
    • They only appear in the blood stream when the bile duct is physically blocked
65
Q

What causes of post-hepatic/obstructive jaundice will cause itching?

A

gallstones and pancreatic cancer

66
Q

How are the two causes of obstructive jaundice clinically distinguished?

A
  • They can be distinguished clinically (i.e. gallstones are painful)
  • Courvoisier’s law
67
Q

Define Courvoisier’s Law.

A

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

If you have gallstones, it will make your gallbladder be small and fibrotic (i.e. non-palpable)

68
Q

What type of cancer is commonly pancreatic cancer?

A

Ductal adenocarcinoma

69
Q

What is the specific cause of itching in obstructive jaundice? (bilirubin/ bile salts/ bile acids/ urobilinogen/ stercobilinogen)

A

Bile salts and bile acids.

70
Q

What does this blood test suggest? (pre-hepatic/hepatic/post-hepatic causes?):

BR = 340; ALP = 1750; AST = 50; ALT = 45

A

High ALP –> suggests obstruction

71
Q

Where does pancreatic cancer typically metastasise to?

A

Pancreatic cancer typically metastasises to the liver because the portal vein transports blood from the cancer to the liver

72
Q

Name 6 categorical causes of chronic hepatitis.

A
  1. Alcoholic liver disease
  2. Non-alcoholic fatty liver disease (most common cause of chronic liver disease in the west):
    1. Simple steatosis
    2. NASH (Non-alcoholic steatohepatitis) – steatosis + hepatitis
  3. Chronic viral hepatitis (HCV > HBV)
  4. Autoimmune hepatitis (HLA-DR3):
    • Type 1 = ANA, anti-SMA, anti-actin Ig, anti-soluble liver antigen Ig
    • Type 2 = anti-LKM Ig
  5. Biliary (PBC, PSC):
    • PBC = AMA, no duct dilatation, bile duct loss
    • PSC = p-ANCA, bile duct dilatation, beading bile ducts, onion skinning fibrosis, cholangiocarcinoma, UC
  6. Genetic (Haemachromatosis, Wilson’s disease, A1AT, Galactosaemia, glycogen storage disease)
  7. Drugs (methotrexate)
73
Q

Which scoring system is used to predict prognosis in liver cirrhosis?

A

Modified Child-Pugh score

74
Q

Why does fasting increase bilirubin in Gilbert’s?

A

Enzymes become saturated more because of increased cell turnover

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