Liver, Gall Bladder and Pancreas

Chapter 10 Liver, Gall Bladder and Pancreas



Liver – Anatomy 338

Anatomy – Hepatic Lesions 339

Jaundice 340

Viral Hepatitis 341–343

Hepatitis B Infection 344

Viral Hepatitis 345

Chronic Hepatitis 346

Alcoholic Liver Disease 347

Alcoholic Hepatitis 348

Cirrhosis 349–350

Biliary Disease 351

Hepatocellular Failure 352–354

Portal Hypertension 355

Metabolic Disorders of the Liver 356

Infections 357–360

Tumours of the Liver 361

Primary Carcinoma of Liver 362

Primary Liver Cell Tumours 363

Gallbladder and Bile Duct – Anatomy 364

Gallstones 365, 366

Gallstones – Aetiology 367

Pancreas 368

Acute Pancreatitis 369–370

Chronic Pancreatitis 371, 372

Cystic Fibrosis (Mucoviscidosis) 373

Tumours of Pancreas 374


Liver – Anatomy


Conventionally the liver was considered to be composed of regular lobules, each arranged around a ‘central vein’ with portal tracts at the periphery.


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The acinar concept is now used.


The smallest unit is the simple acinus.


The portal venule and hepatic arteriole both send terminal branches into the acinus (2/3 of the blood supply is portal and 1/3 arterial). They join to form a common trunk which will then contain partially oxygenated blood, and this percolates through the sinusoids to several ‘terminal hepatic venules’ (as in diagram).


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In terms of oxygen supply and other nutrients, 3 zones exist.


Zone 1, with the best supply;

Zone 2, with a reasonable supply;

Zone 3, with the poorest supply which makes it most vulnerable to hypoxia.

In Zone 1, glycogen synthesis and glycogenolysis take place. It is also the main area of protein metabolism and formation of plasma proteins. Conjugation of certain drugs takes place.


Zone 3 is associated with glycogen storage, lipid and pigment formation and metabolism of certain drugs and chemicals. Zone 2 shares functions with the other zones.



Anatomy – Hepatic Lesions


Adjacent liver acini form a complex architecture best appreciated when diseases affect the varying zones. Factors involved in this include the pO2 of blood and enzyme function of the zones.



Liver Necrosis



Perivenular Necrosis


This form is a feature of many apparently unrelated conditions. It is brought about by damage in zone 3 (A in diagram). Thus it is a feature of shock due to circulatory collapse reducing the oxygen supply to zone 3. It also occurs in poisoning with chlorinated hydrocarbons (e.g. chloroform) and drugs, e.g. paracetamol, metabolised in zone 3.


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It is important to realise that zone 3, particularly, is continuous from one acinus to another, and in severe cases the hepatic venules are linked together by necrotic tissues.


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Mid-Zonal Necrosis


This is uncommon. It is seen in yellow fever and injury affecting zones 2 and 1 (B in diagram).


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Periportal Necrosis


Rarely necrosis in zone 1 is due to its metabolism of drugs and chemicals; e.g. phosphorus poisoning causes marked fatty change in the periportal parenchyma, followed by necrosis.



Massive Necrosis


This is an unusual lesion which can follow poisoning due to drugs, industrial chemicals or mushrooms. Rarely it is a complication of viral hepatitis.



Jaundice


If the serum bilirubin level exceeds 50 μmol/l, the patient becomes jaundiced.


Bilirubin is derived from the breakdown of aged red cells by the macrophage system, mainly in the spleen. It is conjugated to glucuronic acid in the liver and secreted in the bile.


Study of haemoglobin catabolism shows 3 main forms of jaundice:


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Viral Hepatitis



Acute Viral Hepatitis


Viral hepatitis is the most important form of hepatitis. It is seen worldwide. Viral hepatitis may be sporadic or epidemic and, depending on the responsible virus, transmitted by the faeco-oral or parenteral route.



Clinical Features


Many episodes of viral hepatitis are subclinical; mild symptomatic cases are characterised by nausea, fever and anorexia. Severe attacks are characterised by jaundice and hepatic failure, and may be fatal.



Pathological Features


EARLY stage


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Liver cell necrosis is always present. It is most marked in Zone 3 (p.338).


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Necrosis may be:


(a) focal (spotty) – scattered as single cells or

(b) more severe – forming areas of bridging between vessels (portal to hepatic venule) or

(c) panacinar – necrosis of complete acini up to massive necrosis of a large part of the liver occasionally occurs. When it does, it is most marked in the left lobe.

LATER stage


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Liver is smaller, yellow or greenish



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There is evidence of healing with mitotic activity in the hepatocytes.



Biochemical Changes



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Clinical Progress



1. In most cases, the disease is self-limiting and complete recovery occurs within 4–6 weeks.

2. Rarely death may occur due to massive (panacinar) liver necrosis.
(a) In the early pre-icteric stage within 10 days – fulminant hepatic failure.

(b) In 2–3 weeks. The liver is reduced in size.
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Loss of substance


Remaining liver tissue opaque, yellowish, without markings and is largely necrotic


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This condition was often termed ‘acute yellow atrophy’.


(c) Several weeks later. At this stage, regeneration is well advanced in places but function is inadequate and progressive failure occurs.
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Some types of hepatitis may progress to


3. Chronic hepatitis (p.346),

4. Cirrhosis,

5. Hepatocellular carcinoma.

At least 5 viruses cause liver damage without significantly damaging other tissues (hepatitis A,B,C,D and E). The features are summarised and then discussed individually.



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Other viruses which can affect the liver, but also affect other tissues include:


Yellow fever

Herpes viruses – Epstein-Barr, Cytomegalovirus, Herpes simplex

Coxsackie A and B

Lassa fever.


Hepatitis B Infection


The hepatitis B virus is a member of the HEPA DNA virus group. Infection is by the parenteral route – mainly IV drug abuse, blood products and sexual transmission, and in high prevalence areas in childbirth.


The virus has several components:


A core containing


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The complete virion is known as the Dane particle. Spherical and tubular structures derived from the surface coat can also be found in the peripheral blood.


These antigens and antibodies to them are the basis for diagnosis of hepatitis B infection.


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In histological preparations


HBsAg accumulates in the cytoplasm of cells – giving a ‘ground glass’ appearance.


HBcAg is found in the nuclei


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or can be stained by immunocytochemistry.


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Serology: Antibodies to the various antigens appear in the blood.


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Six weeks after infection the surface antigen (HBsAg) appears in the blood, followed two weeks later by the e antigen (HBeAg), at the time of maximal viral replication.



Viral Hepatitis




Outcome of Hepatitis B Infection


In >90% of cases there is a vigorous immune reaction (cell mediated and humoral) to the virus resulting in its elimination. In the remaining patients, the illness pursues one of several courses:


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Hepatitis D


This is a defective RNA virus which requires HB virus for its release and infectivity. There are 2 patterns of infection:


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Hepatitis C


This small RNA virus is transmitted parenterally and is seen in IV drug users or following infected blood transfusion. Acute hepatitis is mild and patients are rarely jaundiced. It is important because of the high risk of chronicity.


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Hepatitis A


This picornavirus is transmitted by the faeco-oral route, especially where hygiene is poor. Hepatitis is usually mild in children, but more severe in adults. IgM antibodies appear in the blood in the acute phase, and IgG during convalescence, thus conferring life long immunity. Chronic liver disease does not occur.



Hepatitis E


This is most commonly seen in Africa and Asia. Although usually mild, it is particularly severe in pregnant women with a mortality of approximately 20%.



Chronic Hepatitis


Inflammation of the liver which lasts for more than 6 months is regarded as chronic. (This definition excludes disorders such as alcoholic hepatitis.)


There are 4 main causes:


1. Persistent viral infection – hepatitis B, D and C.

2. Autoimmune hepatitis. This occurs especially in young women. In classic (type I) disease antinuclear and anti-smooth muscle antibodies are present in the serum. Liver specific autoantibodies e.g. to a sialoglycoprotein receptor (ASGP-R) on periportal hepatocyte cell surfaces can also be found. These patients often have other autoimmune diseases e.g. thyroiditis. A smaller subgroup, type II is defined by anti-Liver Kidney Microsomal antibodies (anti-LKM-1) and has a more aggressive disease.

3. Drugs – e.g. methyldopa, nitrofurantoin.

4. In metabolic disorders – e.g. α1-antitrypsin deficiency, Wilson’s disease (p. 356).

Histologically, three areas of inflammation are seen to varying degrees.


• Portal tract.

• Parenchymal (within the acinus).

• At the interface (limiting plate).
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Alcoholic Liver Disease


Excess consumption of alcohol is associated with liver disease in three main forms.


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The progression from left to right does not occur in all patients: genetic predisposition, coexistant nutritional deficiencies, amount and duration of drinking and other factors determine the risk.



Fatty Liver


This occurs in most heavy drinkers, even after a single episode of heavy intake. Fat accumulates in the hepatocytes due to abnormalities in the intermediate metabolism of lipids and carbohydrates.


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Note: Fatty liver usually resolves within 2–4 weeks of abstinence.



Alcohol Metabolism



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Alcoholic Hepatitis


In 20–40% of heavy drinkers, alcoholic hepatitis is superimposed on fatty change. This varies from asymptomatic hepatitis to a life threatening condition with nausea, vomiting, abdominal pain and jaundice. Signs of liver failure and portal hypertension may be found.


Histologically, the main features are seen around hepatic venules:


1. Liver cell swelling – ballooning.

2. Accumulation of Mallory’s hyaline – protein derived from intermediate filaments (mainly cytokeratin).

3. Liver cell necrosis.

4. Neutrophil polymorph reaction.

5. Pericellular fibrosis.



Acute Phase



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Progressing to Pericellular Fibrosis



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Alcoholic hepatitis is important as a cause of liver damage, especially because of the high risk of progression to cirrhosis.


The term ‘nonalcoholic fatty liver disease’ covers a range of fatty disorders of the liver in non-drinkers. This includes simple fatty change and a histologically similar form of hepatitis to alcoholic hepatitis. Diabetes mellitus, severe obesity, jejuno-ileal bypass for obesity and certain drugs (e.g. amiodarone) appear to be responsible.



Cirrhosis


Cirrhosis is the end stage of many liver diseases. It is defined as:


A diffuse process (i.e. the whole liver is affected) characterised by fibrosis and conversion of the liver architecture into abnormal NODULES.




Aetiology


There are many causes including:


(i) Drugs and toxins, e.g. alcohol, methotrexate, methyldopa.

(ii) Infections, e.g. Hepatitis B and C.

(iii) Autoimmune diseases – chronic active hepatitis; primary biliary cirrhosis.
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Related posts:

  1. Healing
  2. Cell and Tissue Damage
  3. Musculo-skeletal System
  4. Neoplasia

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Jul 23, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Liver, Gall Bladder and Pancreas

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