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Y5 Pathology > HistoPath - Liver Pathology > Flashcards

HistoPath - Liver Pathology Flashcards

1
Q

What is the blood supply of the liver

A

Dual: portal vein and hepatic artery

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2
Q

What cells are found in the liver (+ function of hepatocytes and bile ducts)

A
  1. Hepatocytes (Carries out the metabolic activity, have microvilli)
  2. Bile ducts (cholangiocytes) - Carries bile from hepatocytes to the duodenum
  3. Blood vessels (Portal vein, hepatic artery)
  4. Endothelial cells
  5. Kupffer cells
  6. Stellate cells
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3
Q

what is normal weight of the liver

A

1500g

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4
Q

Describe the structure of the liver and how blood flows through it

A

Portal vein → portal tract → central vein
Blood enters the portal tract, and the blood from the hepatic artery and portal vein mix, then diffuse down the sinusoids (Spaces between hepatocytes)
The blood will flow from the portal tract to the central vein

There are 3 zones with each having different functions

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5
Q

What makes up the portal tract

A

Hepatic artery (branch)
Portal vein (branch)
Bile duct

There is usually a ring of collagen around the portal triad - this is called the limiting plate

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6
Q

What does the ‘streaming river’ of the liver describe

A

They begin life in zone 1, grow up in zone 2 and retire in zone 3’
Therefore, cells in zone 3 have more metabolically active enzymes
Most alcoholic liver damage will be in zone 3
Most chronic hepatitis will occur in zone 1 (near portal vein)

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7
Q

What is the cellular mechanism during liver injury

A
  1. Hepatocytes lose microvilli
  2. Stellate cells are activated → myofibroblasts
  3. Endothelial cells become continuous/join together
  4. Collagen production into the space of Disse (where stellate cells sit)

This all means that blood does not interact with hepatocytes well

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8
Q

Define cirrhosis of the liver

A

The WHOLE liver is involved, where there is fibrosis, distortion of liver vascular architecture (intra- and extra-hepatic, e.g. gastro-oesophageal, shunting of blood), and nodules of regenerating hepatocytes

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9
Q

what types of shunts can be found in a cirrhotic liver

A

Extrahepatic shunt
Blood is bypassing the portal vein, liver and hepatic veins
E.g. oesophageal varices (blood is not coming back from the portal circulation into the systemic)

Intrahepatic shunt
Blood passes through the live, but straight from the portal vein to the hepatic vein (Bypassing hepatocytes) -> unfiltered blood

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10
Q

How is cirrhosis in the liver classified

A

a) according to nodule size: micronodular or macronodular
b) according to aetiology:
1) alcohol / insulin resistance (usually micronodular)
2) viral hepatitis etc. (usually macronodular, may be reversible)

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11
Q

What are the complications of liver cirrhosis

A

Portal hypertension
Hepatic encephalopathy
Liver cell cancer (Cirrhosis is the most important risk factor)

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12
Q

What is acute hepatitis and what are the causes

A

hepatitis <6 months

Viruses (hep A and E)
Drugs

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13
Q

What are the histological features of acute hepatitis

A

Spotty Necrosis (common in all types of acute hepatitis)
Lots of apoptosis
Lymphocyte and macrophages damage hepatocytes

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14
Q

What is chronic hepatitis and what are the causes

A

Hepatitis > 6 months

Viral hepatitis (Hep B,C,D)
Drugs
Auto-immune

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15
Q

What does grade and stage refer to in the context of chronic hepatitis

A

Grade = severity of inflammation
Stage = severity of fibrosis

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16
Q

What is the difference between portal inflammation, interface hepatitis, and lobular inflammation

A

Portal inflammation: inflammation limited to the portal tract, hepatocytes can be distinguished

Interface hepatitis: T cell mediated destruction of hepatocytes via apoptosis, inflammation crosses the limiting plate

Lobular inflammation: similar to acute hepatitis, spotty necrosis seen

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17
Q

What are the stages of liver disease

A

At the onset of a new disease, patients begin to develop fibrosis (F0-F3)
At F2-F3, there is shunting of blood
At F4, patients have developed compensated cirrhosis which can become:
Decompensated if the liver loses its mass → liver transplant needed
Hepatocellular carcinoma (HCC)

18
Q

What are the 3 patterns of alcoholic liver disease

A

Fatty liver
Alcoholic (fatty liver) hepatitis
Cirrhosis

These patterns often co-exist

19
Q

Describe fatty liver

A

Macroscopically: liver is pale and yellow (fat)
Microscopically: hepatocytes full of fat droplets

Can be reversible in alcoholics - when drinking cessation occurs, the fatty change reverses (but hepatitis will not)

20
Q

What are the histological features of alcoholic hepatitis

A

Ballooning/swelling of cells
Mallory Denk/Mallory-Hyaline bodies - pink material that represents the collapsed cytoskeleton of hepatocytes
Hepatocyte apoptosis
Pericellular fibrosis (individual/groups of cells are marked by collagen)
Neutrophil polymorphs

The cells containing the most acetaldehyde dehydrogenase lie in Zone 3 - breakdown of acetaldehyde (toxic metabolite of alcohol) → hypoxic cells due to metabolic effort required

21
Q

Describe the microscopic and macroscopic appearance of the liver in alcoholic cirrhosis

A

Micronodular cirrhosis - small uniform nodules seen
Pale with fatty change

22
Q

What are the histological features of cirrhosis

A

Nodular regenerating hepatocytes surrounded by fibrosis
Fat droplets observable

23
Q

Describe Non-Alcoholic Fatty Liver Disease (NAFLD) and its histological appearance

A

includes non-alcoholic steatohepatitis (NASH)
Due to insulin resistance (associated with BMI and DM)

Histology: looks like alcoholic liver disease

24
Q

Describe primary biliary cholangitis (PBC) and its histological features (+marker)

A

Bile duct loss secondary to chronic inflammation (often with granulomatous inflammation from granuloma formation)

Granulomatous structure of bile ducts which are surrounded by epithelioid macrophages (↓)

Anti-mitochondrial antibodies (AMA)

25
Q

What is primary sclerosing cholangitis, describe its histological features, and how is it diagnosed

A

Periductal bile duct fibrosis → loss of bile ducts

Associated with ulcerative colitis and Crohn’s disease
Increased risk of cholangiocarcinoma

Diagnosis is via bile duct radiological imaging (ERCP or MRCP) → onion skin fibrosis

26
Q

What is haemochromatosis

A

Haemochromatosis is a genetic condition leading to ↑intestinal Fe2+ absorption
Driven by a HFe gene on Chr6
80% will carry a single mutation in this gene
Men tend to present earlier than women

27
Q

What is the pathophysiology behind haemochromatosis

A

Parenchymal damage to organs arises secondary to Fe2+ deposition → bronzed diabetes
Iron accumulates in the liver hepatocytes → damage → loss, cirrhosis and cancer
Iron also accumulates in the pancreas → disruption of normal function

28
Q

What are the microscopic and macroscopic features of haemochromatosis

A

Microscopically: liver full of brown pigment - accentuated with Perl stain

Macroscopically: brown liver due to iron deposition; bronzed heart and bronzed adrenal gland

29
Q

What is haemosiderosis and its histological features

A

Iron overload due to blood transfusion, but the iron accumulates in the macrophages/Kupffer cells

Perl stain shows iron lying within macrophages

30
Q

What is Wilson’s disease and what are its histological features

A

The accumulation of copper, due to failure of excretion by hepatocytes into the bile

Defective genes on Chr 13

Rhodanine stain for copper demonstrates accumulation in hepatocytes

31
Q

What symptoms arise for Wilson’s disease

A

Copper accumulates in the liver and lentiform nucleus in the CNS → hepato-lenticular degeneration
* BG affected → Parkinsonian-like features
* It also accumulates in the iris → Kayser-Fleischer rings

32
Q

Describe autoimmune hepatitis and its histological features

A

Very active form of chronic hepatitis

Plasma cells produce anti-smooth muscle actin antibodies

Histology: portal tract flooded with inflammatory cells | Interface hepatitis (difficult to see where the portal tract ends and hepatocytes begin)

33
Q

What is α-1 anti-trypsin (A1AT) Deficiency

A

Liver + lung disease
Gross excess of A1AT as the protein sequences are misfolded → cannot be excreted → forms globules → damage → hepatitis + cirrhosis

↑risk of emphysema

34
Q

What does liver biopsy show for drug-related liver injury

A

Pale areas, usually in zone 3
Surviving hepatocytes in zone 1 around the portal tract are darker pink

35
Q

What are the causes of granulomas of the liver

A

Specific causes:
Primary Biliary Cholangitis
Drugs
General causes:
TB
Sarcoid

36
Q

What are the types of benign liver tumours

A

Liver cell adenoma
Bile duct adenoma (bile duct cells)
Haemangioma (endothelial cells)

37
Q

What are the most common type of hepatocyte cancer

A

Secondary (due to drainage blood into this side)
Source: oesophagus, stomach, SI, pancreas

38
Q

What are the types of primary liver cancer

A

Hepatocellular carcinoma liver/cell
Hepatoblastoma (primitive hepatocytes)
Cholangiocarcinoma: asssociated with PSC, worms and infection
Haemangiosarcoma: endothelial cells of blood vessels

39
Q

What are the specific features of endothelial cells of the liver

A

In the liver, the endothelial cells do NOT sit on a basement membrane

The endothelium is discontinuous - there are no tight junctions and spaces between them

40
Q

What is the function of the stellate cells

A

Store vitamin A
When activated they become myofibroblasts and lay down collagen
They are responsible for most of the scarring in liver disease

41
Q

What are kupffer cells

A

Resident macrophages of the liver, found in the sinusoids

Y5 Pathology (71 decks)

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