Pathology Liver Flashcards

1
Q

How does oxygen tension change across the hexagonal structures in the liver?

A

Oxygen tension is greater at the peripheries near the mini portal triad and this decreases as you move across the mid acinar zone towards the central vein.
=> Periportal an pericentral hepatocytes have slightly different functions

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2
Q

Which cells of the liver are most vunrable to injury?

A

Pericentral cells

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3
Q

The liver has a large functional reserve- how much can be removed and the liver heal entirely be restitution?

A

Approximately half of the liver

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4
Q

How long does it take for a liver to cirrhose?

A

At least 20 years

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5
Q

What is cirrhosis?

A

Terminal fibrosis of the liver

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6
Q

What are the causes of acute liver failure (jaundice)?

A

Acute onset Hep A/B
Alcohol
Drugs
Bile duct obstruction

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7
Q

What is Acetoaminophen toxicity?

A

Paracetamol overdose producing confluent necrosis

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8
Q

What are the consequences of acute liver failure?

A

1) Complete resolution
2) Chronic liver disease (alcoholics or chronic hepatitis B/C)
3) Death from liver failure

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9
Q

Do all patients with severe liver disease have jaundice?

A

No

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10
Q

What does the liver do to bilirubin?

A

Conjugates it

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11
Q

What is pre hepatic jaundice?

A

Where there is too much haem to break down

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12
Q

What causes prehepatic jaundice?

A

Haemolytic anaemias (sickle cell)

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13
Q

Prehepatic jaundice: Conjugated or unconjugated bilirubin?

A

Unconjugated

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14
Q

What is hepatic jaundice?

A

Liver cells injured or dead

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15
Q

What are the causes of hepatic jaundice?

A
Acute liver failure
Alcoholic hepatitis
Cirrhosis (decompensated)
Pregnancy
Autoimmune (Primary biliary cirrhosis, Primary sclerosing cholangitis)
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16
Q

What is post hepatic jaundice?

A

Where bile cannot escape into the bowel

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17
Q

Post hepatic jaundice: conjugated or unconjugated bilirubin?

A

Conjugated bilirubin

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18
Q

What are the causes of post hepatic jaundice?

A

Congenital biliary atresia
Gallstones blocking CBD
Strictures in CBD
Tumours (head of pancreas or cholangiocarcinoma

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19
Q

Is cirrhosis reversible?

A

No- its the primary end point for all liver disease.

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20
Q

What does cirrhosis look like?

A

Bands of fibrosis separating regenerative nodules of hepatocytes. The blood which enters the liver cannot be filtered and the proteins produced by the liver cannot be secreted due to the alteration of hepatic microvasculature.

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21
Q

Common causes of cirrhosis?

A
Haemochromatosis (iron overload)
Autoimmune (PSC, PBC)
Alcohol
Hepatitis
Gall stones
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22
Q

What are the complications of cirrhosis?

A

1) Portal hypertension
2) Ascites
3) Liver failure- not carrying out its functions, detoxifying, producing proteins
4) HHC

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23
Q

Why is ascites a complication of cirrhosis?

A

Liver is not producing enough albumin which lowers the osmotic pressure in the circulation so much of the plasma water can enter the peritoneal cavity

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24
Q

What are the consequences of portal hypertension?

A

Portocaval anastamosis issues:

1) Oesophageal varacies
2) Caput medusa
3) Haemorrhoids (rectal varacies)

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25
Q

What are the causes of portal hypertension other than cirrhosis?

A

Portal fibrosis

Portal vein thrombosis

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26
Q

What are the features of cirrhosis and what are the causes of these features?

A

Oedema: Hypoalbuminaemia
Ascites: Portal hypertension and hypoalbuminaemia
Haematemisis: Oesophageal varacies (portal hypertension)
Spender navi (Hypoeostrogenism)
Bleeding and bruising (reduced clotting factor synthesis)
Coma- inability to eliminate toxic bacteria
Infection: reduced Kupffer cell number and function

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27
Q

What is the pathophysiology of alcoholic liver disease?

A

Alcohol causes increased peripheral release of fatty acids and increased synthesis of fatty acids and triglycerides within the liver.
Acetylaldehyde, a product of alcohol metabolism is toxic to liver cells

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28
Q

Alcoholic fatty liver is reversible and forms over what time scale?

A

A few days- liver turns pale fatty lump. Steatosis

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29
Q

Alcoholic hepatitis is reversible and forms over what time scale?

A

4-6 weeks

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30
Q

What is the differential diagnosis for steatosis?

A
Alcoholic hepatisis
NASH,
Diebetes type 2
Drugs
Pregnancy
Nutritional (TPN)
Hepatitis C
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31
Q

What are Mallory bodies?

A

Damaged intermediate filaments in hepatocytes, typical of alcoholic hepatisis.

32
Q

What are the histopathological features of alcoholic hepatitis?

A

Hepatocyte necrosis
Neutrophils
Mallory bodies
Pericellular fibrosis

33
Q

What are the features of Alcoholic fibrosis?

A

Collagen laid down between single hepatocytes

34
Q

What is NASH?

A

Non alcoholic steatohepatitis.

Non drinkers with pathology identical to alcoholis hepatitis.

35
Q

Which patients get NASH?

A

Diabetes, obesity, hyperlipidaemia. Due to insulin resistance
On the increase and can lead to fibrosis

36
Q

What is the most common cause of HCC?

A

NASH

37
Q

What are the common causes of viral hepatitis?

A

Hep A, B, C and E.

38
Q

What are the rare causes of viral hepatitis?

A
Hep D (Delta agent
Ebstein-Barr virus 
Yellow fever virus 
Herpes Simplex virus 
Cytomegalovirus
39
Q

What is the incubation for hep A and the transmission?

A
Incubation= 2-6 weeks (short)
Transmission = foecal oral
40
Q

Explain sporadic Hep A?

A

Like the UK. Low incidence in geographical population. Adults get it later in life due to travel or contaminated food. Symptomatic infection

41
Q

Explain endemic Hep A?

A

Developing world. High incidence due to poor sanitation and environmental issues. Children infected early. Silent and assymptomatic and immunity is developed.

42
Q

Can you have Hep A carriers?

A

No. Usually full recovery to resolution or occasionally acute liver failure and death

43
Q

What are the features of acute liver inflammation?

A
Ballooning degeneration (Hepatocyte damage/swelling/clear cytoplasm)
Diffuse damage 
Dead hepatocytes (dense ed blobs)
44
Q

What is the incubation and transmission of Hep B?

A

Incubation is long

Transmission = blood born or mother to foetus

45
Q

What causes liver damage in Hep B?

A

Normally the antiviral immune response (interferons) rather than the virus its-self

46
Q

Are there hep B carriers?

A

Yes

47
Q

What are the five outcomes of Hep B infection?

A

1) Acute hepatitis and resolution
2) Acute hepatitis and acute liver failure and death
3) Silient acute infection leading to non progressive chronic hepatitis
4) Silient acute infection leading to progressive chronic hepatitis (cirrhosis)
5) Develop HCC

48
Q

What is the incubation and transmission for HepC?

A

Transmission, Blood borne

Incubation is short

49
Q

Why is there no Hep C vaccine and why is often chronic?

A

There are multiple sub and sero types which means there is not one single vaccine target. This also makes it harder for the body to eliminate and there fore it tends to become chronic

50
Q

What are the features of chronic inflammation of the liver?

A

Portal inflammation of lymphocytes.
WHen the inflammation spreads outwards from the portal triad to the parenchyma. it becomes interface hepatitis (piecemeal necrosis)
When inflammation is in the parenchyma it is lobular inflamation.
NB: Less ballooning degeneration

51
Q

What is a dead hepatocyte referred to as?

A

Councilman body

52
Q

What is bridging fibrosis?

A

Fibrosis which bridges 2 potral triads.

53
Q

WHat are the features of cirrhosis?

A

Contraction and shrinking of liver.
Disorganised parenchyma
Nodular appearence

54
Q

What is macronodular and micronodular?

A
Macro = >3mm diameter
Micro = <3mm diameter
55
Q

When do you get assymptomatic carriers of Hep B?

A

Mother to child transmission

56
Q

Features of Primary Biliary Cholangitis?

A

Autoimmune
Antimitochondrial antibodies
Small bile ducts
More common in females.

57
Q

When would you use a biopsy in Primary Billary cholangitis and what would you see?

A

Stage the disease.

See: granulomas and bile duct loss (bile ducts are not normally effected in chronic hepatitis.

58
Q

What is the macroscopic features of PBC?

A

Green liver with fibrosis and cirrhosis if not treated. The bile cannot leave the liver

59
Q

What are the features of autoimmune hepatitis?

A
Females.
Associated with other AI diseases
Autoantibodies to smooth muscle or nucleus and a raised IgG.
Numerous plasma cells .
May have a drug trigger
60
Q

What are the features of drug included hepatitis and what are some of the common drug causes?

A
Similar to all chronic hepatitis.
may trigger AI hepatitis.
Can be dose related or not dose related.
Can mimic any liver disease.
Common causes: Fluclox, co-amoxiclav.
61
Q

What are the features of Primary sclerosisng cholangitis?

A

Effects mediuma dn large bile ducts both intra and extra hepatic.
Effects more men than women.
Associated with UC
Greater risk of colangiocarcinoma and colorectal carcinoma.

62
Q

What are the histological features of PSC?

A

Periductal onion skinning fibrosis, duct destruction and fibrosis

63
Q

Which Autoimmune liver disease puts you at greater risk of Cholangiocarcinoma?

A

PSC

64
Q

Which autoimmune liver disease is associated with UC?

A

PSC

65
Q

Haemachromatosis is excess iron within the liver. What is the primary and secondary causes?

A

Primary is inherited autosomal recessive condition leading to increased absorption of iron
Secondary is iron overload from diet, multiple transfusions or iron therapy

66
Q

Can the body produce iron?

A

No- it must be obtained in the diet

67
Q

When is haemachromatosis worse?

A

Men and homozygotes

68
Q

What is the outcome of primary haemochromotosis?

A

Assymptomatic fr years but iron deposited in liver => fibrosis and cirrhosis. Predisposes to HHC.

69
Q

What other diseases outside of the liver can be as a result of primary haemochromatosis?

A

Diabetes,
Cardiac failure,
Impotence

70
Q

What is the stain used to confirm haemochromatosis?

A

Perls stain- iron is stained dark blue

71
Q

What is Wilson’s disease?

A

Autosomal recessive disorder of copper metabolism. Copper accumulates in liver and brain but serum blood levels (caeruloplasmin) will be low.

72
Q

What is the clinical sign in the eye used for wilsons disease?

A

Kayser-Fleischer rings around cornea

73
Q

What are the outcomes of Wilson’s disease?

A

Chronic hepatitis and neurological deterioration

74
Q

What is Alpha 1 anti trypsin deficiency and what are the consequences?

A
Inherited autosomal recessive disorder where you produce a faulty antitrypsin.
Causes emphysema (excess trypsin digestes lung protein) and cirrhosis (Faulty antitrypsisn accumulates in the liver.
75
Q

What are the 2 histopathological types of HCC?

A

Hepatocytic and cholangio (associated with PSC)