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GI > Liver Pathology > Flashcards

Liver Pathology Flashcards

1
Q

What shape are the lobules of the liver? Which cells in these lobules are most vulnerable to injury?

A
  • hexagonal lobules
  • portal triad at each corner (artery, vein and bile duct)
  • central draining vein
  • cell types - periportal (most peripheral), mid acinar, pericentral
  • pericentral cells most likely to be affected by pathology
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2
Q

Describe the 4 pathological stages of liver disease

A
  • Insult to hepatocytes (e.g. virus, drug, toxin, antibody)
  • inflammation
  • fibrosis
  • Cirrhosis
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3
Q

What symptom is commonly associated with acute liver failure?

A
  • acute onset of jaundice
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4
Q

What can cause acute liver failure?

A
  • viruses
  • alcohol
  • drugs
  • bile duct obstruction
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5
Q

Describe how a paracetamol overdose causes acute liver failure

A
  • Confluent necrosis (necrosis and assoc. inflammation)

- This produces massive acute necrosis and liver failure

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6
Q

What are the 3 potential outcomes of acute liver failure?

A
  • complete recovery
  • chronic liver disease
  • death from liver failure
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7
Q

How can jaundice be classified?

A

By site:

  • Pre-hepatic
  • Hepatic
  • Post-hepatic

By Type:

  • Conjugated
  • Unconjugated
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8
Q

What causes jaundice to be PRE-HEPATIC?

A

Too much haem to break down
=> Haemolytic conditions e.g. anaemias can cause this
=> Unconjugated bilirubin

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9
Q

What can cause HEPATIC jaundice?

A
  • the Liver cells are injured/ dead

=> Causes:

  • Acute liver failure (virus,drugs,alcohol)
  • Alcoholic hepatitis
  • Cirrhosis
  • Bile duct loss (atresia, PBC, PSC)
  • Pregnancy
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10
Q

What causes POST HEPATIC jaundice?

A
  • Bile cannot escape into the bowel
    => bilirubin is CONJUGATED as liver is working

=> Causes:

  • Congenital biliary atresia
  • Gallstones blocking Duct
  • Strictures of Common bile Duct
  • Tumours (Ca head of pancreas)
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11
Q

Cirrhosis is irreversible. TRUE/FALSE?

A

TRUE

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12
Q

How does cirrhosis appear on histology?

A
  • Bands of fibrosis separating regenerative nodules of hepatocytes
  • Can be Macronodular or micronodular (alcoholic)
  • Changes hepatic microvasculature
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13
Q

What can cause cirrhosis of the liver?

A
  • Alcohol
  • Hep B/C infection
  • Iron overload (Fe3+)
  • Gallstones
  • autoimmune liver disease
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14
Q

What complications can arise elsewhere in the body, after a patient develops cirrhosis of the liver?

A
  • Portal hypertension
    => oesophageal varices
    => caput medusa
    => haemorrhoids
  • Ascites
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15
Q

Why may patients with cirrhosis/liver failure have bruising or excessive bleeding?

A

May struggle to make clotting factors in the liver

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16
Q

How does alcohol cause direct damage to the cells of the liver?

A
  • Acetaldeyhde (a product of alcohol metabolism) causes injury to the cells
  • neutrophils then are attracted to the inflammation and cause necrosis
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17
Q

If a patient has been drinking alcohol excessively, how long does it take for the damage to their liver to become irreversible?

A

Drinking for 2-3 days = Fatty liver => Reversible
Drinking for 4-6 weeks = Hepatitis => Reversible

Drinking for Months-Years = Fibrosis => Irreversible
Drinking for Years = Cirrhosis => Irreversible

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18
Q

What medical term describes “fatty liver” disease?

A

Steatohepatitis

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19
Q

How do fat molecules appear on liver histology?

A
  • Fat vacuoles appear clear in hepatocytes
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20
Q

Other than alcohol excess, what can cause steatohepatitis in liver?

A
  • Non-Alcoholic Liver disease
  • Pregnancy
  • Drugs
  • Nutritional
  • Diabetes
  • Hep C virus (type 3)
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21
Q

Describe how the histological appearance of alcoholic hepatitis is different from just steatohepatitis?

A
  • Hepatocyte necrosis
  • Neutrophils
  • Mallory Bodies
  • Pericellular fibrosis
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22
Q

Describe how collagen appears on histology if a patient has liver fibrosis?

A
  • it is laid down around cells

- appears blue due to the stain

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23
Q

Describe how cirrhosis appears on liver histology and how this is different from fibrosis.

A
  • Bands of collagen laid down during fibrosis are larger

- They now separate regenerative nodules

24
Q

What groups of patients usually get non-alcoholic steatohepatitis?

A
  • diabetes
  • obesity
  • hyperlipidaemia
25
Q

What viruses commonly cause hepatitis?

A

Hep A, B, C, D (less common), E

26
Q

What viruses can rarely cause hepatitis?

A
  • Epstein Barr (EBV)
  • Yellow Fever
  • Herpes Simplex (HSV)
  • Cytomegalovirus (CMV)
27
Q

How is Hep A spread and how long does it normally last?

A
  • Faecal-oral spread
  • Short incubation period
  • acute illness, no carrier/ chronic state
  • Mild illness, usually full recovery
28
Q

How is Hep B transmitted and how long does infection last?

A
  • Spread by blood products, sexually, vertically (in utero)
  • Long incubation period
  • Carriers exist
  • Liver damage from antiviral immune response
29
Q

How is Hep C transmitted and how long does infection persist?

A
  • Spread by blood products, sexually
  • Has short incubation period, but can become chronic
  • Often asymptomatic
30
Q

How does chronic viral hepatitis appear on histology?

A
  • Portal inflammation (lots of lymphocytes)
  • Interface Hepatitis (piecemeal necrosis)
  • Lobular inflammation
  • Fibrosis (collagen)
31
Q

What autoimmune causes are there for chronic hepatitis?

A
  • Autoimmune hepatitis
  • Primary Biliary Cirrhosis
  • Primary Sclerosing Cholangitis
32
Q

Primary Biliary Cirrhosis is caused by autoantibodies to what?

A
  • mitochondria
33
Q

Is it mainly males or females who get PBC?

A

Females (90%)

34
Q

What can be seen on histology of PBC if a biopsy is taken?

A

Granulomas and bile duct loss

- portal inflammation and bile duct inflammation common

35
Q

If PBC is left untreated, what can occur as a result?

A
  • bile duct loss leads to cholestasis
    => liver injury
    => inflammation, fibrosis and cirrhosis
36
Q

Are males or females more likely to get autoimmune hepatitis?

A

Commoner in females

37
Q

What causes autoimmune hepatitis?

A
  • Numerous plasma cells
  • Autoantibodies to smooth muscle, raised IgG
  • May have triggers, including some drugs
38
Q

What problems occur if patients develop Primary Sclerosing Cholangitis?

A
  • Chronic inflammatory process affects intra- and extra-hepatic bile ducts

=> Periductal fibrosis, duct destruction, jaundice and fibrosis

39
Q

Are males or females more likely to develop PSC?

A
  • Males
40
Q

PSC is associated to which autoimmune disease of the bowel?

A
  • Associated with Ulcerative Colitis
41
Q

PSC causes an increased cancer risk. TRUE/FALSE?

A

TRUE

  • Increased risk of malignancy in bile ducts
  • AND COLON (due to UC link)
42
Q

What histological feature is typical of PSC?

A
  • Periductal onion-skinning fibrosis
43
Q

What is Haemochromatosis and what is the difference between Primary and Secondary types of this disease?

A

Iron overload

Primary = Genetic => increased absorption of iron

Secondary = Iron overload from diet, transfusions, iron therapy

44
Q

How is haemochromatosis inherited?

A

Autosomal recessive

- Worse in male homozygotes

45
Q

What problems can haemochromatosis eventually cause?

A
  • Asymptomatic for years
  • deposits in portal connective tissue and stimulates fibrosis
  • Cirrhosis if not treated
  • Predisposes to carcinoma
  • Causes diabetes, cardiac failure and impotence
46
Q

HOw is haemochromatosis confirmed on histology?

A

Using Perl’s stain highlights the iron in blue

47
Q

How can Haemochromatosis be treated in early stages in an attempt to prevent liver damage?

A
  • regular venesection
48
Q

What is Wilson’s disease?

A
  • Autosomal recessive disorder of copper metabolism

- Copper accumulates in liver and brain (basal ganglia)

49
Q

How do patient’s present with Wilson’s disease?

A
  • Kayser-Fleischer rings in eye at corneal limbus
  • Low serum caeruloplasmin
  • Chronic hepatitis and neurological deterioration
50
Q

What is Alpha-1-Antitrypsin deficiency and what does it cause?

A
  • Autosomal Recessive disorder
  • Patients don;t produce enough Alpha-1-antitrypsin
  • A1AT normally protects the lungs against neutrophil elastase (which disrupts connective tissue)
  • if deficient, the A1AT that is produced stays in the liver and clogs it up causing cirrhosis
51
Q

What primary tumours can occur in the liver?

A
  • Hepatocellular adenoma (BENIGN)

- Hepatocellular carcinoma (Hepatoma)

52
Q

What secondary tumours commonly occur in the liver

A
  • metastases are usually multiple

- From colon, pancreas, stomach, breast, lung etc

53
Q

Hepatocellular adenomas are more common in females. TRUE/FALSE?

A

TRUE

54
Q

What symptoms can benign hepatocellular adenomas cause?

A
  • become large and can rupture or bleed

- Most remain asymptomatic

55
Q

HCC is associated with which other conditions?

A
  • Hep B and C

- Cirrhosis

56
Q

HOw does HCC normally present?

A
  • Usually presents as a mass, pain, obstruction
  • Presents advanced unless discovered incidentally
    => Poor prognosis
57
Q

When are liver metastases potentially curable?

A

If it is a single solid metastases, then it may be able to be operated on

GI (33 decks)

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