Liver Flashcards

1
Q

What is the space between the hepatocytes and the endothelium

A

The ‘Space of Disse’ – the spaces between the hepatocytes and the endothelium (discontinuous organisation) of the sinusoids meaning that the blood comes into contact with the all the liver enzymes

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2
Q

What is the arrangement of hepatocytes and sinusoids

A

Hepatic artery, portal vein and bile duct sit on outside with sinusoid bringing these past the hepatocytes to the central vein

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3
Q

Difference between zone 1 and 3 damage

A

Zone 1 is directly hepatoxic substances

Zone 3 is hypoxic or metabolised damage due to it being closer to the central vein and further from the artery

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4
Q

How is paediatric jaundice treated

A

o Phototherapy

Converts bilirubin into lumirubin + photo-bilirubin

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5
Q

What inheritance is Gilberts syndrome

A

Autosomal Recessive

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6
Q

What happens in Gilberts syndrome

A

UDP glucuronyl transferase activity is reduced to 30%

The bilirubin in Gilbert’s is worsened by fasting

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7
Q

What is the main marker of liver function

A

Pro-thrombin time

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8
Q

Causes of pre hepatic jaundice

A

Haemolysis

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9
Q

Cause of hepatic jaundice

A

Gilberts
Infective Hepatitis
Alcoholic Hepatitis
PBC

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10
Q

Cause of post hepatic jaundice

A

Obstructive- stones

Pancreatic cancer

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11
Q

What can the ratio of ALT to AST inform you

A

ALT > AST = other forms of hepatitis

AST > ALT = alcoholic hepatitis

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12
Q

Hepatitis A- transmission and disease course

A

ofAEco-oral transmission route – food or men-on-men sex
o Contaminated water is often the major source E.G. Recent shellfish consumption

o Acute – asymptomatic, or – nausea, D+V, fever, jaundice, RUQ pain
 Onset = 2-6 weeks; symptoms last = ~8 weeks
 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

Treatment- supportive, avoid alcohol

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13
Q

Hepatitis B- transmission and disease course

A

Only 5-10% go chronic

Routes of infection:
 Sex (more commonly through unprotected sex than HCV)
 Vertically (mother - child)
 Blood products

o Normally acute presentation (can be acute ± chronic)
 Hepatitis symptoms – fever, jaundice, N+V, RUQ pain)

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

Acute- supportive, Chronic- anti-viral

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14
Q

Hepatitis C- transmission and disease course

A

60-80% go chronic

o Features of HCV:
 Blood-product spread
 Normally results in an asymptomatic presentation leading to a chronic infection (60-80%)
 Can be treated and eradicated with anti-virals (~100% clearance rates)

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15
Q

What conditions are HBV and HCV associated with

A

o HBC and HCV may be associated with:
 HCC (Hepatocellular carcinoma) – seen in SBAs with:
• “Hx of jaundice, hepatomegaly, weight loss”, “raised aFP”

 History of thalassaemia (hints at recurrent blood transfusions) – leading to chronic infection:
• Blood transfusions are a major risk factor for HCV (90%) and a minor risk factor for HBV (10%)
o HCV is much more likely to become chronic than HBV

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16
Q

Disease course of HDV

A

Requires HBV infection

17
Q

Hepatitis E- transmission and disease course

A

o fAEco-oral transmission route – food or men-on-men sex- uncooked pork/shellfish

o Acute – asymptomatic, or – nausea, D+V, fever, jaundice, RUQ pain
 Onset = 2-6 weeks; symptoms last = ~8 weeks

18
Q

Histology of an alcohol damaged liver

A

Liver cell damage (ballooning ± Mallory-Denk bodies)
Inflammation
Fibrosis

19
Q

What does a nutmeg liver mean

A

Venous congestion (Budd-Chiari, congestive HF, etc.)

20
Q

Features of chronic STABLE (alcoholic) liver disease:

A

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

21
Q

Features of portal HTN

A

o Visible veins- varices and caput medusa
o Ascites
o Splenomegaly

22
Q

Signs and symptoms of post hepatic jaundice

A

o Severely jaundiced
o Cachectic
o Palpable gall bladder
o Multiple scratch marks – suggest obstructive jaundice
 It is ONLY post-hepatic causes of jaundice that make you itchy
 They only appear in the blood stream when the bile duct is physically blocked

23
Q

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

24
Q

Where does pancreatic cancer usually metastasise to

A

Liver- do to hepatic portal vein

25
Q

Acute vs chronic hepatitis histology

A
  • Acute hepatitis - spotty necrosis
  • Chronic hepatitis - piecemeal necrosis, hepatocyte necrosis, fibrosis, nodules of regenerating hepatocytes, Bridging from the portal vein to central vein
26
Q

Micro-nodular vs. macronodular hepatitis causes

A

o Micronodular = alcoholic hepatitis, biliary tract disease

o Macronodular = viral hepatitis, Wilson’s disease, A1AT

27
Q

Stages of alcoholic liver disease and their histology

A
  1. Hepatic steatosis – fat droplets in hepatocytes
  2. Alcoholic hepatitis – ballooning ± Mallory Denk bodies
  3. Alcoholic cirrhosis – micronodular fibrosis (small nodules + bands of fibrous tissue)
28
Q

Most common cause of chronic hepatitis

A

o Non-alcoholic fatty liver disease

 Simple steatosis
 NASH (Non-alcoholic steatohepatitis) – steatosis + hepatitis