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Liver injury Flashcards

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1
Q

What are some causes of acute hepatitis?

A 
Viral (HepA/B/E)
Drug induced liver injury
Natural remedies
Autoimmune hepatitis
Idiopathic (seronegative, acute non A non B hep)
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2
Q

When are liver biopsies taken?

A

Biopsies are not usually done unless the disease is severe, the cause is uncertain, or there is concern for chronic liver disease

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3
Q

What is the clinical definition of acute hepatitis?

A

Elevation of serum transaminase enzymes for a period of less than 6 months duration, in a patient with no history of chronic liver disease

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4
Q

What do pathologist mean by acute hepatitis?

A

A process with the same pathological changes in the liver as acute viral hepatitis.
Acute hepatitis is a non-specific pattern of liver injury shared by many different causes.

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5
Q

What are the hallmark features of acute hepatitis histologically?

A

Death of hepatocytes
Regeneration of hepatocytes to repopulate the areas of death
ABSENCE of fibrosis

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6
Q

What is the acinar model of the liver?

A

based on terminal portal tract with blood passing through successively less oxygenated zones to reach efferent venule -> useful concept for understanding tissue injury

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7
Q

Which is the vulnerable zone of the acinar?

A

Zone 3 around the central vein = less oxygenated than hepatocytes in zone 1; therefore more vulnerable to liver injury (toxic or metabolic or ischaemic)
Liver injury therefore most severe in this region

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8
Q

What is cholestasis?

A

Any condition in which the flow of bile from the liver is blocked

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9
Q

What are the catabolic functions of the liver?

A

Removal of harmful compound (particularly toxins absorbed in the gut); major contributors to hepatic encephalopathy)

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10
Q

What is synthesised in the liver?

A

Serum proteins (albumin, clotting factors)

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11
Q

What happens if the synthetic function of the liver ceases?

A

Hypoalbuminaemia (oedema, ascites = accumulation of fluid in peritoneal cavity)
Coagulopathy (bleeding)

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12
Q

What is the difference between necrosis and apoptosis of liver cells?

A

Single cell death is by apoptosis (look for the apoptotic bodies).

Death of groups of adjacent hepatocytes is by necrosis

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13
Q

What are 4 types of regional necrosis in the liver?

A

Single cell
Zonal necrosis
Bridging necrosis
Multi-acinar necrosis

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14
Q

What is zonal necrosis?

A

Necrosis which is observed in the area surrounding a single central vein

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15
Q

What is bridging necrosis?

A

Cell death from central veins to portal tracts

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16
Q

What is multi-acinar necrosis?

A

Cell death involving multiple lobules/acinars etc it is very severe

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17
Q

What is generally seen if the hepatocytes undergo necrosis?

A

In most cases of necrosis in the liver, the hepatocytes undergo severe osmotic failure and burst (lysis); you will not see the necrotic cells themselves, but the aftermath (collapse of liver reticulin framework and the presence of scavenger macrophages in the liver tissue)

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18
Q

When looking a gross specimen of a liver what do reddish brown areas represent?

A

Necrosis

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19
Q

When looking a gross specimen of a liver what do yellow nodules represent?

A

Regenerating group of hepatocytes

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20
Q

What are is seen in acute viral hepatitis?

A 
Pan-lobular disarray
Swollen liver cells, 
Apoptosis. 
Necrosis of variable extent depending on severity. 
Aggregates of enlarged macrophages. 
Cholestasis.
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21
Q

What are the sequelae of acute hepatitis?

A

Resolution with restoration of normal structure and function.

Massive hepatic necrosis – death or liver transplantation.

Chronic hepatitis – HBV, autoimmune hepatitis and some drugs

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22
Q

What happens in paracetamol induces liver necrosis?

A

Intrinsic liver toxin (causes hepatocellular injury in a predictable and dose dependent fashion)
Liver injury caused by a toxic metabolite (NAPQ1) which
→ Injures hepatocytes
→ Causes depletion of glutathione ( a natural anti-oxidant)
→ Coagulative necrosis

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23
Q

Where does necrosis typically occur in paracetamol induced liver necrosis?

A

Necrosis occurs preferentially in zone 3 (this is where the enzyme CPY2E1 is located) but can be pan-acinar, multiacinar, or massive

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24
Q

Is inflammation present in acute hepatitis?

A

Inflammation present, variable severity, portal and lobular, mixed composition (lymphocytes, plasma cells, macrophages > neutrophils and eosinophils)

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25
Q

Is inflammation present in Paracetemol induced liver necrosis?

A

Inflammation minimla

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26
Q

What type of necrosis occurs in acute hepatitis?

A

Necrosis is “lytic” i.e. hepatocytes rupture

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27
Q

Is lobular disarray seen in Paracetemol induced liver necrosis?

A

Necrosis of hepatocytes involving zone 3; lobular disarray not seen.

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28
Q

What can be said about the livers reserve?

A

The liver has a high functional reserve, but when necrosis is extensive acute liver failure may develo

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29
Q

Are alcoholic liver disease, NASH, chronic inflammatory liver disease, classified as “chronic hepatitis”?

A

No

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30
Q

What is the clinical definition of chronic hepatitis?

A

Raised serum for more than 6 months

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31
Q

What are the most common causes of chronic hepatitis?

A

HBV and HCV

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32
Q

Aside from HBV and HCV what are some common causes of chronic liver disease?

A

Autoimmune hepatitis, drugs also ideopathic hepatitis (very rare)

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33
Q

What are some cases in which patients may have chronically raised liver enzymes and not have chronic hepatitis?

A

Alcohol
NASH
(Just a definition thing really)

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34
Q

What percentage of HCV infected individuals will develop chronic disease?

A

80%

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35
Q

What percentage of patients will chronic HCV will develop cirrhosis?

A

20%

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36
Q

What are some commonalities between chronic and acute hepatitis?

A

Inflammatory infiltrate is mainly T lymphocytes

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37
Q

What is the difference between chronic and acute hepatitis?

A

Pattern of injury:
Acute hepatitis: Predominantly pan-lobular hepatocellular injury
Chronic hepatitis: Inflammation of the portal tracts and the periportal liver tissue associated with injury of the periportal hepatocytes

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38
Q

What does periportal mean?

A

Situated around the portal vein of the liver

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39
Q

What is interface hepatitis?

A

Death of hepatocytes at the interface between portal tracts and lobular parenchyma
+
Lymphoplasmacytic inflammation

40
Q

What is the result of lymphoplasmacytic inflammation?

A

Periportal ‘spill’ of chronic inflammation into periportal parenchyma

Results in irregular portal tract border

41
Q

Is interface hepatitis specific to chronic hepatitis?

A

No

42
Q

How is interface hepatitis measured?

A

Grade

Determinant of the rate at which fibrosis develops

43
Q

Are lobular changes seen in chronic hepatitis?

A

They are commonly present, bnut usually mild

44
Q

How is the type of hepatitis determined with severe lobular activity?

A

Pathologist find it difficult to distinguish between acute and chronic.
Clinicians need assist with information about the patient often

45
Q

When does fibrosis of the liver occur?

A

Can occur and progress in chronic hepatitis (resulting in cirrhosis)
It is ascent in acute hepatitis

46
Q

What happens in the earliest form of fibrosis?

A

Earliest form recognized = portal tract has smooth outline BUT it is bigger than it should be as there is more portal fibrous tissue than there is normally

47
Q

What happens in the later form of fibrosis?

A

Later form = progression leads to growth of fibrous septa out from the edge of the portal tract, called septal fibrosis -> characteristic of chronic liver disease
a. Portal tract is irregular with speculated boundary

48
Q

What happens in the advanced form of fibrosis?

A

Advanced = lots of fibrous septa surrounding the portal tract extending out into the lobule which end up linking up to form bridging fibrous tissue -> on the way to developing cirrhosis

49
Q

What cells are responsible for producing the fibrosis of the liver?

A 
Portal fibroblast (only a little bit)
Hepatic stellate cell (mostly)
50
Q

Where is the hepatic stellate cell found?

A

In the space of disse

51
Q

What activates the hepatic stellate cell?

A

Cytokines

52
Q

What type of cells are hepatic stellate cells?

A

Myofibroblasts

53
Q

Where is the fibrosis laid down?

A

In the space of disse

54
Q

How is stage of fibrosis defined?

A

Degree of fibrosis (how far is the liver towards cirrhosis) (0-4)

55
Q

What is stage 1 fibrosis?

A

Enlarged portal tracts, no septa

56
Q

What is stage 2 fibrosis?

A

Septa but not much linking between portal tracts

57
Q

What is stage 3 fibrosis?

A

Portal to portal bridging

58
Q

What is stage 4 fibrosis?

A

Cirrhosis

59
Q

What is alcoholic liver disease?

A

Very common cause of liver disease induced by overconsumption of alcohol
It may present acutely

60
Q

What is the pathogenesis of ALD?

A
  • Hepatocellular damage from acetaldehyde
  • Oxidative stress
  • Impaired carbohydrate and fat metabolism
  • Stimulation of collagen synthesis by alcohol
  • Genetic susceptibility
61
Q

What is a fatty change (steatosis)?

A

Abnormal accumulation of lipid in hepatocytes (reversible and does not cause hepatocellular death or fibrosis)

Occurs after consumption of alcohol

62
Q

What is alcoholic steatohepatitis ?

A

A process which leads to heaptocellular death and fibrosis.

Progressive fibrosis eventually leads to cirrhosis

63
Q

What differentiates steatohepatitis from steatosis?

A

Steatohepatitis is defined by the presence of fat + hepatocellular injury

Steatosis = just fat

64
Q

What are the characteristics of hepatocellular injury a seen in Steatohepatitis?

A

Ballooning (swelling) and formation of Mallory-Denk bodies

65
Q

What are Mallory-Denk bodies?

A
  • Collapse of the hepatic cytoskeleton.
  • Intermediate filaments (cytokeratin 8 and 18) and other proteins including ubiquitin.
  • Attract neutrophils (not seen in this image)
66
Q

What happens in severe Alcoholic steatohepatitis?

A

If severe can cause “acute alcoholic hepatitis” which is a syndrome with features of jaundice, fever, hepatomegaly, markedly impaired liver function, and leucocytosis. This disease carries a 50% 30 day mortality.

67
Q

What is seen histologically in steatohepatitis?

A

Inflammatory cells (mainly neutraphils)
Densely stained Mallory bodies
Large fat vacuoles
Blue stained collagen surrounds individual hepatocytes: “chicken wire fibrosis”

68
Q

What are the associations with Non-alcoholic fatty liver disease?

A

Obesity
Metabolic syndrome
Diabetes

69
Q

What is seen histologically in NAFLD?

A

Histological spectrum the same as for alcoholic, although severe steatohepatitis with numerous Mallory bodies is much less common.

70
Q

How does one distinguish between NAFLD and ALD?

A

Clinical rather than histological

71
Q

What is NASH?

A

Non-alcoholic steatohepatitis

72
Q

What are the two catagories of NAFLD?

A

Isolated fatty liver >80%
(Minimal chance of progression to cirrhosis, no increased risk of death as compared to general pop)

NASH
Nash cirrhois
↓
Decompensation 
Noncirrhotic Hepatocellular Carcinoma (can also result directly from NASH without cirrhosis)
73
Q

How rapid is the onset with autoimmune hepatitis?

A

It is an aggressive from of chronic hepatitis

74
Q

How long does autoimmune hepatitis take to progress to cirrhosis if untreated?

A

85% progress to cirrhosis within 5 years

75
Q

Who is mostly affected by autoimmune hepatitis?

A

Women

Those with a genetic predisposition

76
Q

How is autoimmune hep detected?

A

Presence of serum auto-antibodies

77
Q

How is autoimmune hep treated?

A

Therapeutic response to immune suppression

78
Q

What are the 2 types of autoimmune hep?

A

Type 1

Type 2

79
Q

What is type 1 autoimmune hep?

A

Occurs in adults women - associated with anti-smooth muscle antibodies

80
Q

What is type 2 autoimmune hep?

A

Occurs in children and teenagers, associated with anti-liver kidney microsome

81
Q

What is a microsome?

A

Microsomes are vesicle-like artifacts re-formed from pieces of the endoplasmic reticulum (ER) when eukaryotic cells are broken-up in the laboratory; by definition, microsomes are not ordinarily present in living cells

82
Q

How does autoimmune hep present?

A

acute hep (both clinically and pathologically)

83
Q

Define cirrhosis

A

Describes the anatomical end stage common to many chronic liver diseases

84
Q

What happens to the liver during cirrhosis

A

Conversion of the liver into nodules of regenerating hapatocytes surrounded by bands of fibrous scar tissue
This is a diffuse process

85
Q

What is used to score the Child-Pugh?

A 
Total bilirubin
Serum albumin
PT INR
Ascites
Hepatic encephalopathy
86
Q

What are the classes of Child-Pugh and what is the one year survival?

A

A 100%
B 81%
C 45%

87
Q

What does the external surface of the liver look like in cirrhosis?

A

It has green/black nodes = bile

88
Q

What do white nodes on the liver mean?

A

Heptocellular carcinoa

89
Q

What are the common causes of cirrhosis?

A 
ALD
NASH
Chronic Viral Hep B/C
Autoimmune Hep
Chronic biliary disease 
Wilson's disease
Drugs
90
Q

What is the current thinking with regard to cirrhosis?

A

It may be regressive

91
Q

Is it possible to determine the cause of cirrhosis just by looking at the path report?

A

No - it is a non specific endpoint

92
Q

What is the new model of cirrhotic development?

A

Portal vein is occluded leading to an area of hepatocellular extinction (driven perhaps by vascular occlusion)
Scar tissue contracts
Fibrous septa form
Fibrous septa are deformed
Fibrous septa perforate - portal veins have dropped out entirely

93
Q

What is the definition of portal hypertension?

A

> 8mm Hg
or
Increase in the pressure gradient between the portal vein and hepatic vein of 5mmHg

94
Q

What causes portal hypertension?

A

Obstruction to flow

95
Q

What are the three causes of portal hypertension

A

Post
Intra
Pre
(sinusoidal)

96
Q

What is the post common cause of portal hypertension?

A

Cirrhosis

97
Q

What are the clinical signs of portal hypertension?

A

Ascites
Porto-systemic anastomoses
Congestive splenomegaly
Hepatic encephalopathy

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