Tonsillitis (as a side effect causes digestive function disorder) or angina is an infectious disease with evident inflammatory changes of the lymphoid tissue of the pharynx and tonsils. Tonsillitis is caused by streptococci, staphylococci, adenoviruses, etc. The inflammation is usually caused by general or local hypothermia. Important to the disease etiology is the sensitization of the body. More often, the disease occurs in teenagers and adults up to 40 years of age, rarely – in babies and elderly people. It can be explained by age-related peculiarities of pharyngeal lymphoid apparatus development and the body’s reactivity.

Tonsillitis progression may be acute or chronic. Acute tonsillitis is divided according to the character of inflammation, into catarrhal, fibrinous, suppurative, lacunar, follicular, necrotic tonsillitis and angina gangrenosa.

In catarrhal tonsillitis the mucous tunic of the tonsils and palatal arches is drastically plethoric, cyanotic, swollen and covered with serous-mucous (catarrhal) exudation.

Fibrinous tonsillitis usually occurs in diphtheria and is present in diphtheritic inflammation. The mucous tunic of the tonsils is covered with white-yellow coat which is difficult to remove.

Suppurative tonsillitis is characterized by the enlargement of the tonsils due to their swelling and neutrophil infiltration. According to the character of the suppurative inflammation, this type is subdivided into quinsy (angina) and abscess tonsillitis.

Lacunar tonsillitis is characterized by the accumulation of serous, mucous or suppurative exudation in the depth of lacunas. It can be seen on the surface of  the swollen tonsils in the form of yellow coats which are easy to remove.

In follicular tonsillitis tonsils are large and hyperaemic, follicles are considerably bigger in size, with central suppurative fluidizing.

Necrotic tonsillitis and angina gangrenosa occurs in people affected with scarlet fever and leukemia. In necrotic tonsillitis one observes superficial or deep necrosis of the mucous tunic of tonsils with haemorrhage. It may develop into angina gangrenosa characterized by tissue destruction.

Chronic tonsillitis develops as a result of numerous recurrences of the acute form. It is characterized by hyperplasia and sclerosis of the lymphoid tissue of the tonsils and their capsules, dilation of lacunas, occasionally by superficial ulcers.

Local complications of tonsillitis are connected with the inflammation spreading to the surrounding tissues and the development of paratonsillar or retropharyngeal abscess, Ludwig's angina and thrombophlebitis. Generalization may lead to sepsis. Tonsillitis recurrences facilitate the development of rheumatism, glomerulonephritis and other infectious-allergic diseases.

From its origin at the cricoid cartilage to its termination at the esophagogastric junction, the esophagus is normally lined by stratified nonkeratinising squamous epithelium.

The esophageal wall contains both striated muscle (in its upper portion) and smooth muscle (in the lower portion). A competent lower esophageal sphincter is essential to prevent the reflux of gastric contents back into the esophagus.


Predisposing factors to acid reflux include those that increase intra-abdominal pressure, e.g. overeating, pregnancy, and poor posture; and those that render the lower esophageal sphincter lax or incompetent, e.g. hiatus hernia, smoking, and alcohol ingestion. Reflux of gastric acid into the lower esophagus produces a burning pain in the center of the lower chest or hypochondrium, commonly known as heartburn.

The normal squamous epithelium of the lower esophagus is sensitive to the effects of the acid and is frequently damaged.

Several complications may arise:

1. Reflux esophagitis.

2. Peptic ulceration of lower esophagus (small ulcers usually develop, which become chronic, with fibrosis).

3. Lower esophageal stricture (chronic peptic ulceration causes progressive fibrous thickening of the lower oesophagus wall; the resultant narrowing causes difficulty in swallowing).

4. Barrett’s esophagus. Persistent esophageal reflux causes metaplasia of the lower esophageal mucosa, the squamous epithelium being replaced by glandular epithelium composed of tall columnar cells.

Reflux esophagitis. Pathogenesis. Among these conditions, reflux of gastric contents (reflux esophagitis) is the first and foremost cause of esophagitis. Many causative factors are implicated, less well characterized than the name implies:

• decreased efficacy of esophageal antireflux mechanisms;

• inadequate or slowed esophageal clearance of refluxed material;

• the presence of a sliding hiatal hernia;

• increased gastric volume, contributing to the volume of refluxed material;

• reduction in the reparative capacity of the esophageal mucosa by protracted exposure to gastric juices.

Any one of these influences may assume primacy in an individual case, but more than one is likely to be involved in most instances.

Morphology. The anatomic changes depend on the causative agent and on the duration and severity of the exposure. Simple hyperemia may be the only alteration. In uncomplicated reflux esophagitis, three features are characteristic eosinophils, with or without ieutrophils, in the epithelial layer; basal zone hyperplasia; and elongation of lamina propria papillae. infiltrates of intraepithelial eosinophils are believed to be the earliest histologic abnormality because they occur even in the absence of basal zone hyperplasia. lntraepithelial neutrophils are markers of more severe injury, such as ulceration, rather than reflux esophagitis per SE. The many other causes of esophagitis exhibit their own characteristic features; the final common pathway for all is severe acute inflammation, superficial necrosis and ulceration with the formation of granulation tissue, accumulation of adherent purulent debris, and eventual fibrosis.


Barrett’s esophagus predisposes to the development of adenocarcinoma.

Barrett’s esophagus can progress from metaplastic glandular epithelium to epithelial dysplasia (with nuclear plemorphism and hyperchromicity), and then to frank adenocarcinoma. Patients with Barrett’s esophagus are kept under surveillance through repeated endoscopy and biopsy to detect early neoplastic changes.

Morphology. Barrett’s esophagus is apparent as a red, velvety mucosa located between the smooth, pale pink esophageal squamous mucosa and the more lush, light brown gastric mucosa. It may exist as tongues extending up from the gastroesophageal junction, as an irregular circumferential band displacing the squamocolumnar junction cephalad, or as isolated patches (islands) in the distal esophagus. Microscopically, the esophageal squamous epithelium is replaced by metaplastic columnar epithelium. Barrett’s mucosa may be quite focal and variable from one site to the next.

Critical to the pathologic evaluation of patients with Barrett’s mucosa is the recognition of associated dysplasia, the presumed precursor of malignancy. Dysplasia is recognized by the presence of cytologic and architectural abnormalities in glandular epithehum, consisting of enlarged, crowded, and stratified hyperchromatic nuclei and loss of intervening stroma between adjacent glandular structures. Dysplasia is classified as low grade or high grade, with the predominant distinction being a basal orientation of all nuclei in low-grade dysplasia versus nuclei reaching the apex of epithelial cells in high-grade dysplasia. Persistent high-grade dysplasia demands clinica intervention.

Esophageal varices are an important cause of vomiting blood. At the lower end of the esophagi the submucosal venous plexus drains into stomach.



Gastritis is the inflammation of the mucous tunic of the stomach – the prevailing pathology of the digestive tract. The progression of the disease may be acute or chronic. It should be noted that acute and chronic gastritis are caused by different factors.

ACUTE GASTRITIS systemic venous system and the portal venous system. When the pressure in the portal venous system is high, e.g. as a result of severe diffuse long-standing liver disease, the esophageal submucosal venous channels become enormously dilated to form esophageal varices, which may protrude slightly into the lumen. Rupture of the varices, or ulceration of the overlying mucosa, can produce torrential hemorrhage into the esophagus and stomach, often precipitating vomiting of blood (hematemesis). The most common cause of esophageal varices is portal hypertension associated with cirrhosis of the liver.

Acute inflammation may be produced by the swallowing of irritants such as aspirin and other analgetics, hot fluids or strong alcohol. Acute fevers in children, viral infections and bacterial food poisoning may also be responsible, the latter usually taking the form of acute gastroenteritis. The most severe variety, known as acute hemorrhagic gastritis produces extensive edema and focal erosion of the mucosa, commonly associated with mucosal or submucosal hemorrhage. This has been observed especially following aspirin ingestion and in severely shocked patients; the mechanism is thought to be similar in both instances, the back diffusion of hydrogen ions into the mucosa. In aspirin poisoning, acute ulceration may lead to hematemesis and even perforation.

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Multi erosion of stomach

Acute gastritis (gastritis acuta) is caused by physical and chemical stimuli (overeating, too cold or too hot food, alkalis, acids), medicines (salicylates, sulfanilamides, corticosteroids), microorganisms, mushrooms, exo- and endotoxins, for example in uraemia. The inflammation of the mucous tunic of the stomach may be diffuse or focal (focal gastritis). The latter is divided into fundic, antral, pyloroantral and pyloroduodenal. According to the exudation character, catarrhal (simple), fibrinous, suppurative (phlegmonous) and necrotic (corrosive) gastritis are distinguished.

In catarrhal (simple) gastritis (gastritis cataralis s. simplex) the mucous tunic is thickened, swollen and hyperaemic, its surface is covered with a lot of mucus. Histologically one finds dystrophy and desquamation of the superficial epithelium, with the formation of erosions. When they are numerous, it is called erosive gastritis.

Fibrinous gastritis (gastritis fibrinosa) can be manifested in the form of catarrhal or diphtheritic inflammation. In this case the mucous tunic is covered with a fibrinous coat of grey or yellow-brown colour.

Phlegmonous gastritis, with extensive necrosis and suppuration in the wall of the stomach, occurs very rarely when bacteria, usually streptococci, penetrate into the submucosa through some local lesion, e.g. an injury caused by an ingested sharp foreign body. Suppurative (phlegmonous) gastritis (gastritis phlegmonosa) is a serious disease occurring due to stomach trauma, stomach ulcer and ulcerative gastric carcinoma. The mucous tunic is drastically thickened, folds are thick with haemorrhages and fibrinous-suppurative deposition. Leucocytic infiltration penetrates all stomach layers and the surrounding peritoneum, leading to the development of perigastritis and peritonitis.

Pseudometnbranous gastritis can result from ingestion of irritant chemicals. It is rarely due to bacterial infection, but may occur in typhoid fever and septicemia.

Corrosive poisons. Strong acids and alkalis cause extensive necrosis of the gastric wall, often with hemorrhage and changes in appearance of the necrotic tissue and blood which depend on the particular chemical swallowed. Chemicals which fix proteins, e.g. carbolic acid or mercuric chloride, may result in good preservation of the stomach at autopsy.

Necrotic (corrosive) gastritis (gastritis necrotica s. corrosiva) is the result of acid and alkali influence on the mucous tunic of stomach, when they coagulate and destroy it. The necrotic process may lead to the development of phlegmon and even perforation.

Catarrhal gastritis treated in time ends with recovery but it may sometimes be recurrent and develop into the chronic form. Necrotic and phlegmonous gastritis end with sclerotic deformation of the organ – gastric cirrhosis.


Chronic inflammatory changes in the mucosa of the stomach, with various degrees of loss of the specialized glandular tissue, are extremely common, although often clinically silent. There is also any association between chronic gastritis and gastric ulcer, and an increased incidence of gastric carcinoma. Our understanding of the etiology and mechanism of gastritis and gastroduodenal ulceration has been radically altered by the discovery of a specific infective agent Helicobacter pylory, by Australian workers Marshall et al. The Sidney System is a new classification based on this recent new knowledge.

Chronic gastritis (gastritis chronica) is a different disease with its own etiology and pathogenesis, rarely connected with acute gastritis. Chronic gastritis is characterized by chronic dystrophic and necrobiotic changes of the mucous tunic epithelium in combination with regeneration disorder and structural change of the mucous tunic. The process ends with atrophy and sclerosis. The factors that can disturb the regenerative process are important for the etiology of chronic gastritis. First and foremost, these are exogenous factors – eating pattern disorder, alcohol abuse, the effect of thermal, chemical and mechanical stimuli. Among the endogenous factors the greatest attention is paid to autoinfection, in particular Helicobacter pylori, to chronic autointoxication, endocrine and cardiovascular diseases, allergic reactions and duodenogastric reflux. Regeneration disorders mainly influence the slowing-down of differentiation of the parietal cells. Immature cells that perish early before the differentiation is completed appear. So, chronic gastritis is not an inflammatory process but a manifestation of regeneration disorder and dystrophy.

According to topography, chronic gastritis is divided into fundic, antral and pangastritis. According to etiology and pathogenesis, gastritis A, B and C are distinguished. The prevailing one is gastritis B – nonimmune gastritis. It is caused by Helicobacter pylori, intoxications, alcohol abuse and malnutrition. According to Houston classification there are 3 types of chronic gastritis: nonatrophic, atrophic and specific forms. Gastritis A is an autoimmune gastritis caused by the appearance of antibodies to parietal cells and is characterized by the lesion of the fundic part. It often occurs with other autoimmune diseases and is accompanied by the decrease of hydrochloric acid secretion and the development of pernicious anaemia. Gastritis C is reflux gastritis caused by duodenogastric reflux and characterized by lesion of the antral part. It often occurs after stomach resection.

Chronic atrophic gastritis is characterized by a qualitatively new peculiarity – glands atrophy that precedes the development of sclerosis. From the endoscopic point of view, stomach mucosa is either smoothed or looks like villi and resembles polyps. They are covered with epitheliocytes with mucus and goblet cells (intestinal metaplasia of epithelium). Glands atrophy and mucoid degeneration of the epithelium cause the disorder of pepsin and hydrochloric acid secretion. It manifests itself clinically with the increased gastrin level in blood and decreased acidity of gastric juice. This gastritis is connected with autoimmune processes, pernicious anaemia and gastric carcinoma. It occurs in patients’ close relatives, in combination with thyroiditis and diffuse toxic goiter.

In nonatrophic chronic gastritis there is no gastrinaemia, the hydrochloric acid secretion is in the normal range, slightly decreased or increased. This gastritis is connected with Helicobacter pylori and the development of peptic ulcer.

Among specific gastritis forms, reflux gastritis is the most frequent.

Morphologically, one distinguishes between superficial and atrophic gastritis. Superficial gastritis is characterized by disturbed regeneration and dystrophy of the superficial epithelium. Some areas of mucous tunic become similar to the cuboidal tunic and is characterized by hyposecretion. In other areas the epithelium resembles high prismatic form and hypersecretion. Later the dystrophic changes affect the glands. The mucous tunic layer proper gets densely infiltrated with lymphocytes, plasmocytes and solitary neutrophils.

It incorporates two separate divisions: histological and endoscopic.

The histological classification incorporates three main element: 1. Etiology. 2. Topography (i.e. site affected: antrum, body or both). 3. Morphology (including information activity, intestinal metaplasia — graded as mild, moderate or severe).


The two main types of chronic gastritis are examples of this classification use:

1. Autoimmune associated chronic pangastritis with severe atrophy (formerly known as Type A gastritis).

2. H. pylon associated chronic gastritis of the antrum with moderate activity (formerly known as Type B gastritis).

The endoscopic classification uses the same topography and categorizes gastritis in terms of the endoscopic appearances.

Diffuse Chronic Gastritis

In this form of gastritis, the changes may initially be focal, but in many cases they are progressive, and as the condition becomes more advanced, it extends to involve the whole of the acid-secreting mucosa. The mucosa of the antrum may show similar changes, but the occurrence of lesions in the two areas may be coincidental.

Pathological changes. Macroscopic examination of the gastric mucosa in vivo is of little value in diagnosing chronic gastritis.

Microscopically, the condition may be divided into superficial chronic gastritis, atrophic gastritis of various degrees and gastric atrophy.

In chronic superficial gastritis, the necks of the gastric glands are increased in length, and the superficial lamina propria is infiltrated with lymphocytes and plasma cells, together with a few neutrophils and eosinophils polymorphs: the mucosa is of approximately normal thickness and the inflammatory changes are confined to its superficial part.

In atrophic gastritis, the inflammatory changes are similar to those of superficial chronic gastritis, but extend more deeply into the mucosa and are accompanied by various degrees of loss of the specialized (i.e. parietal and chief) cells of the mucosal glands. In its extreme degree, the changes affect the flindal mucosa diffusely and there is virtually complete loss of the specialized glandular cells. In gastric atrophy the fundal mucosa is diffusely atrophic, with virtually complete replacement of parietal and chief cells by mucus-secreting glandular epithelium, and increase of loose vascular connective tissue in the lamina propria. The appearances resemble closely those of severe atrophic gastritis except for the much smaller numbers of lymphocytes and plasma cells in gastric atrophy. A very common feature in both atrophic gastritis and gastric atrophy is metaplasia the mucosal glands to resemble closely those of the intestine.

Atrophy gastritis

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Physiological disturbances. The degree to which the specialized gastric glands are lost or replaced in chronic gastritis correlates relatively well with the functional results observed clinically. Thus, in superficial gastritis there is little functional upset; with progressing glandular atrophy varying degrees of hypochlorhydria develop, culminating eventually in complete achlorhydria as seen in severe atrophic gastritis. Even at this latter stage, some intrinsic factor is still secreted, and megaloblastic anemia is not common. In the extreme gastric atrophy of pernicious anemia, there is, however, absence of hydrochloric acid and pepsin, and near or complete absence of intrinsic factor, from the gastric juice.



Chronic gastritis with the general features described above may occur focally in the fundal and antral mucosa, but often affecting especially the junctional zone between the two types of mucosa. While the etiology is obscure, it seems likely that prolonged injury to the mucosa, e.g. by aspirin, alcohol, smoking and reflux of bile, results in increased desquamation of the surface epitheliam and allows back diffusion of acid into the mucosa. Dyspeptic symptoms are common and acid secretion variable: the condition appears to predispose to gastric ulcer and possibly also to gastric carcinoma.

Ménétrier's disease (giant hypertrophic gastritis) is a specific form of chronic gastritis in which the mucous tunic is greatly thickened and looks like convolutions of the brain. The morphologic basis of the disease is the proliferation of glandular epithelium cells, hyperplasia of glands, infiltration of mucous tunic with lymphocytes, plasmocytes, epithelioid and giant cells, and the formation of cysts.

The exacerbation of chronic gastritis manifests itself in stroma edema, hyperaemia, considerable cellular infiltration with the increase of neutrophile level, occasionally microabscesses and erosions may occur. At remissions there are no such manifestations.

With the most evident processes of disturbed regeneration and structural formation which lead to cellular atypism (dysplasia), chronic gastritis is often the basis for the development of gastric carcinoma.



Incidence. The incidence of the different types of peptic ulcer has changed considerably since the beginning of the century. Before that time the prevalent type was acute perforating ulcer which was usually found in the anterior wall of the pylorus or duodenum and predominantly affected young women; it was frequently associated with a disease called "chlorosis", a form of anemia which has long since disappeared. After the World War I gastric ulcer became much commoner in men and to a lesser extent in older women. At present, gastric ulcer is more common in men than in women at all ages up to 65, but thereafter the sex difference becomes less marked: on the other hand duodenal ulceration, which became more frequent at about the same time, is much commoner in men in all age groups and is between 4 and 10 times as common as gastric ulcer in the general population.

Etiology of peptic ulcers. Although it is convenient to discuss the causes of peptic ulceration in general, chronic gastric and duodenal ulcers differ in many respects, including age and sex distribution, occupational incidence and familial tendency, genetic factors, environmental and geographical factors, their causes may therefore differ. Peptic ulcer is essentially a disease of developed, industrialized communities. Factors such as dietary habits, the ingestion of drugs (especially aspirin) and occupational or social "stresses" maybe important. Cigarette smoking is also a contributory factor, especially in gastric ulcer, and may account for the association between peptic ulcer and chronic bronchitis. In any case, no single factor is clearly responsible and causation is complex.

Erosion (erosio) is a superficial defect of mucous tunic that does not go deeper than its muscular laminar. Such defects are usually acute and rarely chronic. They occur as a result of necrosis of an area of mucous tunic with subsequent haemorrhage and rejection of the dead tissue. In the depths of such defects one finds muriatic haematin of black colour and at its edges – a leucocytic infiltration.


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In the course of ulcer development, erosions, especially on the lesser curvature of stomach, do not close up. Under the influence of gastric juices, the layers of the stomach wall necrotize deeper and deeper and the erosion develops into an acute peptic ulcer (ulcus acutum pepticum) of round or oval form. The lesser curvature is known to be a ‘food pathway’, so it is easily traumatized. Its glands secrete very active digestive juice. The lesser curvature is rich in receptors and extremely reactive but its folds are rigid, and at the contraction of the muscular layer they cannot cover the defect. This causes improper closing up of lesser curvature injuries and the development of the acute ulcer into a chronic one (ulcus chronicum). That’s why chronic ulcers are usually located on the lesser curvature, in the antral and pyloric part. Ulcers in the cardial part and on the greater curvature of stomach are rare.


Morphology. Macroscopically three main types of peptic ulcer are recognized, namely acute, subacute and chronic.

Acute peptic ulcer. This type involves only the mucosa and submucosa in the ulcerative process; it is usually small, but may occasionally reach 1—2 cm diameter. The ulcers may be single, or may occur in large numbers and, unlike chronic ulcers, have a wide distribution. They rarely produce symptoms other than hemorrhage, which on occasion may be severe when a mucosal artery in the base of an acute ulcer is eroded. This type of ulcer usually heals without a visible scar. Subacute peptic ulcers are usually fewer in number than the acute type, and not infrequently single. They extend down to the muscular coat, the superficial part of which may be involved; like chronic ulcers, they tend to be found on the lesser curvature of the stomach and they may represent a transition from the acute to the chronic type.


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Acute peptic ulcer.

Chronic peptic ulcer. Complete penetration of the muscular coat is regarded as the most important criterion of chronicity in a peptic ulcer. This type of ulcer is usually solitary; two appeased peptic ulcers are found Duodenal ulcers in a small proportion of cases and there are practically never more than two in the stomach although there may be a duodenal ulcer as well. The commonest site in the stomach is the lesser curvature between 5 and 10 cm from the pylorus; the pyloric canal is the next most frequent site. Their occurrence in other sites is rare, and should make one look for some unusual cause. Chronic ulcers are usually ovoid and larger than subacute or acute ones, ranging from a few mm to several cm in diameter. The base of the ulcer may be formed by the outer part of the stomach wall, the floor being usually smooth and fibrous with induration of the surrounding tissues. More frequently, however, fibrous adhesions have developed over the ulcer and the base is firmly fixed to adjacent tissues; large ulcers often penetrate the gastric wall and erode into adjacent structures, usually the pancreas or liver. When this advanced stage has been reached, the ulcer margin is smooth with overhanging edges, the crater is deep and the floor is firm and nodular, being formed by a fibrosed layer of the eroded organ. Occasionally an ulcer may burrow into the large intestine, a gastro-colic fistula resulting. Perforation in the chronic type may be prevented by fibrous thickening and adhesions but, in. about a third of cases, occurs obliquely through one margin of the ulcer beneath the overhanging edge and beyond the adhesions. Erosion of a large artery in the floor of a chronic ulcer not uncommon and may lead to fatal haemorrhage.

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Peptic ulcer of stomach.

Peptic ulcers in the duodenum are similar to those in the stomach. The area affected by peptic ulceration is, however, remarkably restricted; over 99% of chronic ulcers arise within the first centimeter of the duodenum. Acute ulcers may be single or multiple. They tend to be encountered in what might be regarded as "stress" situations. They are seen, for example, in patients with extensive bums, especially infants, and as complication of lesions of the CNS or chronic debilitating disease both in adults and children. Chronic ulcers may be as large as in the stomach, especially those arising in the posterior wall of the duodenum. As a rule there is a single ulcer on the anterior or posterior wall, but in about 15% of cases two ulcers are present, and they may appose one another at a corresponding level "kissing ulcers". Severe hemorrhage usually occurs from ulcers on the posterior wall, which tend to erode the gastroduodenal artery.

The indications of the exacerbation of peptic ulcer are the appearance of fibrinoid necrosis isolated with a leucocytic layer and granulation tissue, and fibrinoid changes of vessel walls in the depth of the ulcer. Upon healing,, one can observe  connective tissue with obliterated vessels, the epithelization of the mucous tunic defect in the depth of ulcer.

The morphogenesis of duodenal ulcer is identical. According to the localization, one distinguishes between bulbar ulcer (on the front or the back wall of the bulb), postbulbar (below the bulb) and “kissing” ulcers (located opposite each other on the front and the back wall of the bulb).

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  All complications of peptic ulcer are divided, according to V.Samsonov, into the following groups: ulcerative-destructive – haemorrhage, perforation, penetration (into pancreas, large intestine wall, liver, etc.); inflammatory – gastritis, duodenitis, perigastritis, periduodenitis; ulcerocicatricial – narrowing of the upper and the lower (outlet) part of stomach, deformation of stomach, narrowing of the duodenal lumen, deformation of the duodenal bulb; ulcer malignization – the development of cancer; combined complications.

Microscopic appearances. The base of a peptic ulcer of the stomach or duodenum has a clean macroscopic appearance, presumably because of the digestive action of the gastric juice. Microscopically, the ulcer crater is lined by a thin layer of tissue showing the changes of fibrinoid necrosis, beneath which is a layer of granulation tissue showing some leucocytic infiltration. In chronic ulcers the muscle coat is interrupted and at either side of the ulcer merges into the fibrous tissue which forms the outer layer of ulcer lining and may extend for some distance beyond it. The muscle coat thus ends high up in the lateral walls of the crater. In the floor, obliterate changes are frequently seen in the arteries. At the margin of the ulcer, the mucosal epithelium may show active regenerative changes; fragments of mucosa may also be "buried" in fibrous tissue.



1. Healing and scarring. Acute peptic ulcers usually undergo healing and leave no visible scar. Healing is the rule also in the subacute type and it is common too in chronic ulcers, even when large, as is shown by the common necropsy finding of contracted scars in the ulcer-prone sites. If the ulcer has been superficial, the scar may be merely a small depression with a smooth whitish surface; if, however, it has penetrated more deeply, there is often a radiating indrawing of the surrounding mucous membrane, so that a stellate appearance results. Scarring of an ulcer at or near the pylorus commonly results in pyloric stenosis, and the stomach may gradually become enlarged due to repeated retention of food and secretion. The muscle of the pylorus is apt to be thickened and edematous, and the appearance may suggest scirrhous carcinoma; only microscopic examination can rule this out. Stenosis of the adjacent duodenum or pyloric antrum by the scarring of chronic ulcers has similar effects, and ulcers higher up on the lesser curvature of the stomach may, by scarring and contraction, produce the deformity of structure of stomach. Since active peptic ulcers often cause spasm of the muscle coat, caution is necessary in the radiological diagnosis of fibrous stricture.

2. Perforation. Perforation may occur, and, if rapid, it allows the stomach contents to escape into the general peritoneal cavity or, posteriorly, into the lesser sac. The pain, abdominal rigidity and symptoms of collapse which follow are caused by the acid gastric contents; these are virtually sterile at first, but without prompt surgical treatment, organisms soon flourish and acute peritonitis results. After successful surgical treatment of the perforation, there is a risk that infected material lodged between the liver and diaphragm may become sealed off by fibrinous exudate and cause an abscess which may later infect the pleura.

3. Hemorrhage. This is common and varies greatly in degree. Often there is oozing of blood from an acute or a chronic ulcer. The blood may be scanty and detectable in the stools only by chemical examination, or it may be abundant and give rise to <<coffee-grounds>> vomit, otto <<tarry>> stools. Sometimes a major artery may be eroded and a large, even fatal, hemorrhage takes place.

4. Development of carcinoma: ulcer-cancer. Although it cannot be doubted that carcinoma may arise in a chronic gastric ulcer, the frequency of this event has probably been overestimated in the past. One reason for this lies in the difficulty in distinguishing between a chronic peptic ulcer, which has undergone malignant change, and a carcinoma, which has ulcerated. In the former case, it is necessary to demonstrate clear evidence of pre-existing chronic peptic ulceration, i.e. complete inter ruption of the muscular coat.

Benign tumours

Epithelial benign tumors are rare. Mucosal polyps occur, but are usually chronic inflammatory lesions, not true neoplasms. The commonest benign tumour is the leiomyoma, which is sometimes multiple: it arises from the muscular layer and projects into the lumen. Although usually small, it may show a characteristic type of clean punched-out ulceration and can produce very brisk bleeding. Some well-differentiated <<leiomyoma>> invade locally and even produce metastasis: it is therefore important to ensure that excision is complete. Lipoma, fibroma and neurofibroma associated with generalised neurofibromatosis, and a glomus tumour may also occur.

Stomach Cancer (Gastric Carcinoma)

More often it occurs in men older than 50.

Among the etiologic factors are endogenous nitrosoamines, exogenous nitrates and Helicobacter pylori. The precancerous conditions are adenomatous polyp, chronic atrophic gastritis, chronic stomach ulcer, gastric stump, pernicious anaemia, high epithelial dysplasia of the mucous tunic of the stomach.

According to the localization, gastric carcinoma usually occurs in the pyloric part and on the lesser curvature.

According to the character of growth, the following clinicoanatomic (macroscopic) forms of gastric carcinoma can be distinguished: exophytic expansive growth (plaque-forming, polypous, fungous, ulcerative); endophytic infiltrating growth; exoendophytic growth. One can distinguish early gastric carcinoma that grows not deeper than the submucous layer.

According to the histologic structure, one distinguishes between adenocarcinoma, undifferentiated carcinoma, squamous cell carcinoma, squamous cell adenocarcinoma, unclassified carcinoma.

Metastasis of gastric carcinoma: lymphogenic (lymph nodes along the greater and the lesser curvature of stomach, Virchow’s metastasis – left supraclavicular lymph nodes, Krukenberg’s tumour – both ovaries, Schnitzler’s metastasis – pelvic (perirectal) fat tissue), hematogenic and implantation metastasis.

Acute appendicitis

Acute appendicitis results in severe acute inflammation of the vermiform appendix. This lesion is of the highest importance on account of its frequency and the serious results which often follow. Individuals of either sex and of virtually any age may be affected but the disease is commonest in children and young adults.

Macroscopical appearances. The condition occurs in three forms: simple acute appendicitis, supurative or phlegmonous and gangrenous appendicitis.

The first two of these types may be regarded as different degrees of severity of the same condition; the third has special features of its own. Perforation may occur in both suppurative and gangrenous types. In all cases, the whole thickness of the wall is involved. In the earlier stages of acute appendicitis, the appendix is swollen, tense and markedly congested, and there may be a little fibrin on the surface. When the appendix is cut into, the mucosa bulges owing to the swelling, and purulent looking material may exude from the lumen. In other cases, the changes are of greater severity. The primary inflammatory lesion may increase in intensity and lead to a small abscess in the wall, and this may perforate. There may occur also more general suppuration and necrosis with multiple abscesses and perforations. The presence of a concretion in the lumen may predispose to perforation because, in acute appendicitis, the swollen wall becomes stretched over the concretion with consequent ischemia and gangrene.

Gangrenous appendicitis.

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In the course of acute appendicitis, gangrene may affect the distal portion, sometimes in relation to a concretion in the lumen, or it may occur in patches. In some cases it appears to be due to thrombosis of the veins in the meso-appendix, which, aided by the inflammatory condition, leads to hemorrhage and arrests the circulation. But in other cases gangrene develops early and rapidly and affects the whole appendix apart from any vascular lesion.


Microscopic appearances. Inmost cases of acute appendicitis, there is an acute inflammatory reaction involving the entire thickness of the appendicular wall, with a fibrinopurulent exudate on the peritoneal surface. It seems likely that this inflammatory reaction originates from a focus of mucosal ulceration, possibly in the deeper parts of the epithelial crypts with subsequent extension into the lamina propria. Several foci of inflammation are sometimes observed, but the changes are usually most marked in the distal part (i.e. the blind end) of the appendix. Sometimes the inflammation is localized and can easily be missed on cursory examination. In some patients with an appendicitis-like syndrome the only changes seen are pus cells in the appendicular lumen, associated with some foci of polymorph infiltration in the superficial parts of the mucosa, or the occasional crypt abscess.


The complications of acute appendicitis are:

1. Necrosis of appendix wall (gangrenous appendicitis), leading to perforation, with subsequent generalized peritonitis.

2. Involvement of adjacent bowel loops, causing perforation of small bowel.

3. The omentum may become adherent, localizing the peritonitis to the right iliac fossa. Fibrosis and continued inflammation cause development of a mass in the right iliac fossa. This may resolve with scarring, may form an abscess that drains to the surface, or may rupture, with development of generalized peritonitis.

4. Spread of infection by portal vein branches may propagate to the liver; this was formerly an important cause of portal pyemic abscesses in the liver.


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Chronic obliterated appendicitis.



Ulcerative colitis affects the rectum and variable amounts of colon. Ulcerative colitis starts at the rectum (proctitis) and may extend for a variable distance around the colon. In the most extensive disease the whole colonic mucosa is affected. Patients typically develop diarrhea, the feces being mixed with blood, mucus and pus.

There are three clinical patterns of the disease:

1. In active acute disease the mucosa in the rectum and affected colon shows areas of shallow ulceration, which become confluent. In contrast with Crohn’s disease, ulceration does not extend through the muscular mucosa, and inflammation is limited to the mucosa and lamina propria.

2. In chronic quiescent or treated disease — ulceration is not prominent and the mucosa appears red, granular and thinned. Biopsy reveals chronic inflammation.

3. In flilminant active disease — the colon shows extensive confluent mucosal ulceration. Edema and inflammation extend into the muscle layer of the colon, which progressively dilates (toxic dilatation <<acute toxic megacolon>>).

Ulcerative colitis has local as well as systemic effects. The direct oca1 complications of ulcerative colitis include blood and fluid loss from extensive ulceration, both of which may be severe. Acute disease may progress rapidly to toxic dilatation and perforation and, in long-standing disease, dysplasia and neoplastic change may occur.

Morphology. In active disease — the ulcerated areas are hemorrhagic, leading to bloody diarrhea. Intact mucosa remains as islands sitting above areas of ulceration (pseudopolyps). Histology of the intact mucosa shows edema and an increase in numbers of lymphoid cells and plasma cells in lamina propria. Neutrophils are seen in lamina propria as well as in gland epithelium. Neutrophils migrate through the walls of glands to form collections, termed crypt abscesses, in the gland lumen. There is depletion of goblet cells and mucin from gland epithelium.


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Pseudomembranous colitis.

Regional Enteritis (Crohn’s Disease)

Regional enteritis is a chronic inflammatory lesion of the intestinal wall, usually of the terminal part of  the ileum, though it may affect all parts of the digestive tract. There develops a nonspecific granulomatous inflammation without necrosis (it looks like sarcoidosis) and with submucous tunic fibrosis and narrowing of the intestinal lumen. Typical of the disease is the alternation of the affected and unaffected areas. In the mucous tunic one finds deep transverse and longitudinal ulcers, edema of the submucous tunic. Macroscopically the mucous tunic resembles a cobblestone pavement. Among the complications are diarrhoea, malabsorption syndrome, intestinal obstruction, fistulas and degeneration into cancer.




Peritonitis (inflammation of the peritoneal cavity) maybe acute or chronic.

Acute peritonitis is most commonly caused by extension of inflammatory processes in the abdominal cavity particularly after perforation of the gut. Less commonly, peritonitis may be a primary infection, seen in patients with nephrotic syndrome and cirrhosis. Peritonitis maybe localized by adherent loops of bowel and adherence of the omentum. Organization of fibrinous adhesion by granulation tissue leads to by fibrous tissue. Localization of infection in the peritoneal cavity may form local abscesses, particularly in the paracolic gutters and beneath the diaphragm (subphrenic abscesses).

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Fibrinous-suppurative of peritoneum.


Chronic peritonitis may be caused by infection with tuberculosis. Granulomatous inflammation leads to organization and fibrosis, with adhesions between bowel ioops (plastic peritonitis). In patients treated by ambulatory peritoneal dialysis, there may be a chronic, low-grade peritonitis caused by a mixed flora of organisms.

Peritoneal tumors are most commonly the result of metastatic spread. The peritoneal cavity is most commonly affected by metastatic tumors that have spread from one of the abdominal organs, the main primary sites being stomach, ovary, uterus and colon. Deposits of metastatic tumour are seen as small nodules seeding the peritoneum, which often cause thickening of the omentum. In disseminated mucinsecreting carcinomas the peritoneal cavity may be filled with mucinous material (pseudomyxoma peritonea).

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Intestinal adenocarcinoma.

Tumour may grow as larger nodules and cause adhesions between bowel ioops, resulting in bowel obstruction. Infiltration of tumour in the peritoneum may also cause accumulation of fluid in the peritoneal cavity in the form of ascites. Malignant mesotheliomas may develop as primary malignant tumors of the peritoneum. As with the pleural tumors, these are also predisposed by exposure to asbestos.



The anal canal, lined by squamous mucosa, is prone to several groups of diseases, many of which are extensions of diseases in the rectum.

Anal fissures (splitting of the mucosa with chronic inflammation) and fistulae (a sinus extending from the anus or the rectum) are commonly seen in association with Crohn’s disease, but may also occur spontaneously.

Infections of the anal canal may be the result of sexually transmitted diseases, particularly chancres of syphilis, gonorrhea and amebic infections in homosexuals. Infection with human papillomavirus may cause condylomas in the perianal skin.

Tumors of the anal canal are most commonly squamous cell carcinomas. Less commonly, adenocarcinomas, and small-cell carcinomas resembling oat-cell carcinomas occur.


Massive hepatic necrosis (acute hepatic injury) is characterized by the progressive necrosis of the liver parenchyma. It is usually caused by exogenous (mushroom poison, chemical compounds) and endogenous (pregnancy, thyrotoxicosis) factors. In the progression of massive hepatic necrosis the stages of yellow atrophy, red atrophy and recovery are distinguished. The duration of the disease is about three weeks.

During the first days one can observe fatty degeneration of hepatocytes in the centre of the heptic lobule. It is quite soon followed by necrosis and autolytic destruction. The liver becomes smaller, flaccid and turns yellow. That’s why it is called yellow atrophy.

The detritus yields to resorption by macrophages. The stroma becomes “uncovered” and sinusoids, finding no resistance of hepatocytes, become overfilled with blood. The liver turns yellow with red spots (the stage of red atrophy). At this stage hepatic failure often develops.

Hepatic failure has general clinical representations of tissue turgor decline, xeroderma, icteric skin and sclera, vessel “stars” and skin haemorrhages, enlargement or reduction of liver, and there often occurs splenomegaly, ascites and edemas. The pathologic process progression provokes a complex of hepatic, mental and neurologic disorders. The affected person has fetor hepaticus, the liver aches at palpation and he/she suffers from fever and leucocytosis.

The gravity of hepatic failure is usually estimated according to how deep the nervous and mental disorders develop. Three stages of hepatic failure are singled out. The stage of psycho-emotional disorders is characterized by emotional instability: swift change of humour, depression or euphoria, insomnia at night and sleepiness in daytime, headache, overexcitement and memory weakening. The stage of neurologic disorders and impairment of consciousness manifests itself in sudden excitation which is followed by inhibition, tremor of hands, lips and eyelids. Progressive hepatic failure ends with coma (the third stage).

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There are various diseases of the liver.

According to the origin they are classified into inherited and acquired, primary or secondary (as a result other diseases).

According to the morphological changes there are several groups of these diseases: hepatosis (when degeneration and necrosis in the hepatocytes prevail), hepatitis (when inflammation in the liver prevail), cirrhosis (when disregeneration is observed) and hepatic tumors.


The term hepatosis is used to describe degeneration and necrosis in the liver caused by microbiologic, toxic, circulatory or traumatic agents.

Hepatosis may be inherited and acquired. Inherited hepatosis develops in accumulation diseases or enzymopathy. Acquired hepatosis may be acute and chronic.

The massive necrosis is the most common acute hepatosis. The steatosis (fat hepatosis) is the most common chronic one. Massive necrosis (toxic degeneration of the liver) is acute (rarely chronic) diseases characterized by massive necrosis of the hepatocytes with development of the hepatic failure.

Etiology. It is most commonly caused by viral hepatitis, drug or mushroom toxicity.


There are 2 stages in this hepatosis.

1. Stage of yellow degeneration, when liver becomes enlarged, dense and yellow. Then it size increases, it consistency becomes flabby, capsule is shrunken. The cut surface is grey. Microscopically fat degeneration, necrosis and autolysis of hepatocytes are observed.

2. Stage of red degeneration is characterized by progressive reduction of liver size and mass. MacroL scopically the liver is red due to necrosis and autolysis of hepatocytes with appearance of plethoric blood vessels. Jaundice, hyperplasia of lymph nodes and spleen, numerous hemorrhages in the skin and mucous, necrosis of the renal epithelium, degenerative and necrotic changes in pancreas, myocardial, CNS are observed in the patients with massive necrosis of the liver.


STEATOEIS is a chronic disease which characterized by increase of fat amount in the cytoplasm of the hepatocytes.

Etiology of steatosis is similar to massive necrosis of the liver. But in this case pathologic agent has less. toxicity and as a rule human compensatory and adaptive processes are higher.

Macroscopically the liver is enlarged, flabby. Fat drops are seen on the incision. The colour is yellow. This is called <(gooses’s>> liver.

Microscopically—dust-like, small and large drop in the liver cells are observed.



Viral hepatitis is infection of the liver caused by hepatotropic viruses. There are 6 varieties of these viruses. Four of them are main ones causing distinct types of viral hepatitis:

1. Hepatitis A virus (HAV), causing a fecallyspread self-limiting disease.

2. Hepatitis B virus (HBV), causing a parenterally transmitted disease that may become chronic.

3. Hepatitis C virus (HCV), also termed non-A, non-B (NANB) hepatitis virus involved chiefly in transfusion-related hepatitis.

4. Hepatitis delta virus (HDV), which is sometimes associated as superinfection with hepatitis B infection.

Hepatitis A is responsible for 20-—25% of clinical hepatitis in the developing countries of the world. The disease occurs in epidemic form as well as sporadically. The spread is related to close personal contact such as in overcrowding, poor hygiene and sanitation. An incubation period carries on 15-45 days. Hepatitis B has a longer incubation period (30— 180 days) and is transmitted parenterally such as in recipients of blood and blood products, intravenous drugs, etc.

Pathology. The typical pathologic changes of hepatitis A, B and C are similar. The various clinical patterns and pathologic consequences of different hepatotropic viruses can be considered under the following headings:

1. Carrier state.

2. Acute hepatitis.

3. Chronic hepatitis.

4. Fulminant hepatitis (Submassive to massive necrosis).


Acute hepatitis clinically is divided into 4 phases: incubation period, pre-icteric phase, icteric phase and post-icteric phase. Macroscopically the liver is slightly enlarged, soft and greenish.


Microscopically the changes are follows:

1. Hepatocellular injury: a) ballooning degeneration, b) appearance of the necrotic acidophilic mass, d) bridging necrosis is characterized by bands necrosis linking portal tracts to central hepatic veins, one central hepatic vein to another, or a portal tract to another tract.

2. Inflammatory infiltration by mononuclear cells in the portal tracts.

3. Kupifer cell hyperplasia.

4. Cholestasis biliary stasis.

5. Regeneration — as a result of necrosis of hepatocytes, there is lobular disarray.


Hepatitis is an acute or chronic liver disease characterized by dystrophic and necrobiotic changes of the parenchyma combined with the inflammatory stroma infiltration. Hepatitis may be a separate nosologic unit (primary) or a manifestation of other diseases (secondary).

Primary hepatitis develops under the influence of hepatotropic viruses (viral hepatitis), alcohol (alcoholic hepatitis), medicines (medicamentous hepatitis), cholestasis (cholestatic hepatitis). Viral and alcoholic hepatitis are the most common forms of hepatitis.

Secondary hepatitis accompanies a wide range of diseases. They are infectious diseases (typhoid fever, dysentery, cytomegaly, yellow fever, malaria, tuberculosis and sepsis), thyrotoxicosis, rheumatic diseases, digestive tract pathology and intoxications.


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Acute hepatitis can be exudative or productive. Exudative hepatitis is in turn divided into serous and suppurative.

Chronic hepatitis is characterized by parenchyma destruction, cellular infiltration of stroma, sclerosis and changed regeneration. Three types are distinguished – aggressive, where hepatocytes dystrophy and necrosis prevails; persistent, where cellular infiltration of portal areas and intraparticular stroma prevails; and cholestatic characterized by cholestasis, cholangitis and cholangiolitis.

Light cases of hepatitis end with full recovery but massive liver lesion may lead to the development of cirrhosis.

Viral hepatitis is caused by hepatotropic viruses. Liver cells are damaged either by the allergic reaction of cytolytic type or by the hypersensibility of delayed type. Autoimmunisation is connected with a specific liver lipoprotein that forms as a result of virus replication in hepatocytes and acts as an auto-antigen. After the recovery the disease leaves type-specific immunity that’s why the person may be affected by a different type of viral hepatitis.

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The following clinicopathologic forms of viral hepatitis are distinguished: acute cyclic (icteric), anicteric, necrotic (malignant), cholestatic and chronic.

At its peak the cyclic (icteric) form is characterized by the ballooning degeneration(diffuse swelling), focal and coagulation necrosis of hepatocytes. Groups of hepatocytes that have undergone coagulation necrosis form round homogenous eosinophilic structures which are forced out into perisinusoid spaces – Councilman’s corpuscles (body). Cholestasis and necrosis of hepatocytes results in hepatocellular jaundice. At the same time there occurs lympho- and macrophage infiltration of portal tracts and sinusoids. Macroscopically, the liver is larger in size, the capsule is tense, dense and red (large red liver).

In the course of recovery the liver returns to normal size and hyperaemia decreases.     The capsule is somewhat thickened and dingy; adhesions appear between the capsule and the peritoneum. Reparative processes prevail over the destructive ones, lympho- and macrophage infiltration becomes focal. The process ends with liver sclerosis that may develop into cirrhosis.

The anicteric form of viral hepatitis, compared to the icteric one, is characterized by less evident morphologic changes although at laparoscopy one finds the picture of large red liver. Ballooning degeneration and Councilman’s corpuscles are rarely found in this form. But one can clearly observe proliferation of reticuloendotheliocytes. Lympho- and macrophage infiltrations do not destroy the terminal plate and there is no cholestasis.

The necrotic form is first and foremost marked by the progressive necrosis of parenchyma. The liver rapidly reduces in volume and becomes contracted and grey-brown in section. Microscopically one can observe necroses of hepatocytes, accumulation of reticuloendotheliocytes, Councilman’s corpuscles, “uncovered” stroma as a result of resorption of necrotic masses, haemorrhages and cholestasis in capillaries. If the affected person does not die of hepatic coma, postnecrotic liver cirrhosis develops.

The cholestatic form is manifested with prevailing cholestasis with the development of cholangitis and cholangiolitis on the basis of hepatocytes destruction, and lympho-, macrophage and neutrophil infiltration of stroma. One often finds Councilman’s corpuscles.

The chronic form of viral hepatitis is represented by active or persistent hepatitis. Active hepatitis develops on the basis of sclerotic liver changes. It is characterized by ballooning degeneration, necrosis of hepatocytes and inflammatory stroma infiltration. Liver regeneration is incomplete which leads to the development of cirrhosis. The persistent form is characterized by prevailing infiltration of sclerosed portal areas with lymphocytes, histiocytes and plasmatic cells. Dystrophic hepatocyte changes are low-grade. Chronic persistent hepatitis rarely develops into cirrhosis.

In viral hepatitis death occurs due to acute or chronic hepatic failure.



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Alcoholic hepatitis exhibits the following. Liver cell necrosis, single or scattered foci of cells undergo swelling (ballooning) and necrosis, more frequently in the centrolobular regions of the lobule. Mallory bodies, scattered hepatocytes accumulate tangled skeins of cytokeratin intennediate filaments and other proteins, visible as eosinophilic cytoplasmic inclusions. These may also be seen in primary biliary cirrhosis, Wilson’s disease, chronic cholestatic syndromes, focal nodular hyperplasia, and hepatocellular carcinoma. Neutrophilic reaction, neutrophils permeate the lobule and accumulate around degenerating liver cells, particularly those having Mallory bodies.

Lymphocytes and: macrophages also enter portal tracts and spill into the lobule. Fibrosis-alcoholic hepatitis is almost always accompanied by a brisk sinusoidal and perivenular fibrosis; occasionally periportal fibrosis may predominate, particularly with repeated bouts of heavy alcohol intake. Fat may be present or entirely absent.

Alcoholic hepatitis is an acute or chronic liver disease caused by alcoholic intoxication. Ethanol and acetaldehyde are hepatotropic poisons. Ethanol is neutralized by liver enzyme - alcohol dehydrogenase. Its synthesis in the liver is genetically predetermined and quantitatively specific for each individual. After a long period of alcohol abuse the alcohol dehydrogenase’s protective effect is not sufficient to safeguard the liver from destruction and at a certain alcohol concentration there occurs hepatocyte necrosis. The cytotoxic effect of alcohol, even in small doses, occurs in the liver which has been previously affected by such diseases as chronic hepatitis, fatty liver and cirrhosis. Cessation of alcohol consumption leads the process into a benign course. But if alcohol consumption continues chronic hepatitis progresses and ends with liver cirrhosis as ethanol drastically suppresses the regenerative potential of the organ.

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In acute alcoholic hepatitis the liver is larger in volume and density and light brown areas alternate with brown-red ones. Microscopically one can observe necrosis of centrolobular hepatocytes. The so called alcoholic hyaline (Mellori’s corpuscles) can be found in their cytoplasm which is an important diagnostic sign. Peripheral hepatocytes are in the state of fatty degeneration. Necrotic areas and portal tracts are infiltrated with neutrophils. Occasionally, especially in a previously affected liver, massive hepatic necrosis occurs. In most cases after the cessation of alcohol consumption the liver structure regenerates.

Chronic alcoholic hepatitis does not differ morphologically from active and persistent viral hepatitis. It is identified by the presence of Mellori’s corpuscles in the cytoplasm of hepatocytes and beyond the cells.

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Alcoholic hyaline is a fibrillar protein which is synthesized by hepatocytes under the influence of ethanol and causes their destruction. Chronic alcoholic hepatitis ends with the development of cirrhosis.


Chronic hepatitis is a chronic inflammatory hepatic disease continuing for more than six months. It is divided into 2 types:persistent hepatitis and active (aggressive) hepatitis.

Two important factors which determine the vulnerability of a patient of viral hepatitis to develop chronicity are: the impaired immunity, and the extremes of age at which the infection is contracted.

Chronic persistent hepatitis is a benign, seiflimiting condition in which recovery from an attack of acute viral hepatitis is delayed beyond six months.

Pathology. The diagnosis of chronic persistent hepatitis is confirmed by needle biopsy of the liver which is invaluable in distinguishing it from more serious form of chronic active hepatitis.

Microscopically: 1) there is portal triaditis characterized by expansion of the portal tract by mononuclear inflammatory cells, 2) the lobular architecture of hepatic parenchyma is usually preserved, 3) there is absence of piecemeal necrosis.

Chronic active (aggressive) hepatitis is defined as a progressive form of chronic necrotising and fibrosing disease involving portal tracts as well as hepatic parenchyma. Microscopically: 1) there is abundant mononuclear inflammatory cell infiltrate that is not confined to portal tracts, but the infiltrate spills out into the periportal hepatic parenchyma after eroding the limiting plate. There may be formation of lymphoid follicles, 2) two types of necrosis develop. They are piecemeal and bridging, 3) the collapsed reticulin framework left at the areas of bridging necrosis undergoes fibrous scarring, eventually progressing to cirrhosis.

The major cases of death are liver failure with hepatic encephalopathy, cirrhosis with hematemesis, and hepatocellular carcinoma.


Morphologic symptoms of cirrhosis are dilatation and rupture of bile capillaries, which causes peripheral hepatocytes necrosis. Connective tissue expands according to the morphogenesis of portal cirrhosis. In secondary biliary cirrhosis the liver is enlarged, dense and green due to bile impregnation, in section one can see dilated ducts filled with bile.

Mixed cirrhosis appears as a result of portal cirrhosis supplemented at a certain stage by necrotic liver changes.

Liver cirrhosis causes typical extrahepatic disorders: jaundice and haemorrhagic syndrome as a sign of hepatocellular deficiency, cholestasis and cholemia; exhaustion as a result of digestion disorders caused by stasis and atrophy of gastrointestinal tract in portal hypertension, splenomegaly as a result of reticuloendothelium hyperplasia and sclerosis. This leads to the development of extrahepatic porta-caval shunts due to which some blood bypasses the liver and discharges the portal vein. Affected people have dilated veins in the esophagus, hemorrhoidal plexus and dilated hypodermic veins in the thorax and the abdominal wall. The latter are called “Medusa heads”. The varicosity of the above mentioned veins goes together with the thinning of their walls which is often the cause of profuse esophageal, gastric or hemorrhoidal haemorrhage. As a result of portal hypertension and the lesion of liver parenchyma where the degradation of antidiuretic hormone occurs, the transudate infiltrates into the abdominal cavity, sometimes up to a volume of 10 litres. This phenomenon is called ascites. The ascitic fluid, accumulated in the abdominal cavity, compresses blood vessels and internal organs distorting the blood flow. In the kidneys, one finds signs of acute renal insufficiency (tubular epithelium necrosis) and, occasionally, hepatic immune complex glomerulonephritis, which cause the development of hepatorenal syndrome. In most cases people affected by cirrhosis die of chronic hepatic failure. Besides, cirrhosis may be the basis for the development of liver cancer.

Cirrhosis of the liver is a diffuse disease having the following 4 features:

1. It involves the entire liver.

2. The normal lobular architecture of hepatic parenchyma is disorganized.

3. There is formation of nodules separated from one another by irregular bands of connective tissue.

4. It occurs following hepatocellular necrosis of varying etiology so that there are alternate areas of necrosis and regenerative nodules.


The fibrosis once developed is irreversible.

Morphological classification

There are 3 morphological types of cirrhosis micronodular (the nodules are usually regular and small, less than 3 mm in diameter), macronodular (the nodules are of variable size and are generally large than 3 mm in diameter) and mixed (some part of the liver show micronodular appearance while other parts show macronodular pattern). Each of these forms may have an active and inactive form. An active form is characterized by hepatocellular necrosis and inflammatory reaction, a process that closely resembles chronic active hepatosis. An inactive form, vise verse, has no evidence of continuing hepatocellular necrosis and has sharply-defined nodules of surviving hepatic parenchyma without any significant inflammation.

Etiologic classification

1. Alcoholic cirrhosis (the most common, 60—70%).

2. Post-necrotic cirrhosis (10%).

3. Biliary cirrhosis (5—10%).

4. Pigment cirrhosis in hemochromatosis (5%).

5. Cirrhosis in Wilson’s disease.

6. Cirrhosis in u-I antitrypsin deficiency.

7. Cardiac cirrhosis.

8. Indian childhood cirrhosis.

9. Miscellaneous forms of cirrhosis.

10. Cryptogenic cirrhosis (10—15%).


According to etiology

According to morphology

According to morphogenesis

According to clinicofunctional criteria

Infectious (viral hepatitis, parasitic liver diseases)



Toxic and toxicoallergic (alcohol, hepatotropic poisons, medicines, allergens)









According to the extent of hepatocellular deficiency (cholemia, hypoalbuminemia, hypothrombinemia, hypoonchia, haemorrhages, coma)


According to the extent of portal hypertension (ascites, oesophagogastric haemorrhage)

Biliary (cholangitis, cholestasis)




According to the process activity (active, moderately active, inactive)

Metabolic-alimentary (insufficiency of proteins, vitamins and lipotropic factors, accumulation diseases)





Circulatory (chronic venous stasis)




According to progression (progressive, stable, regressive)

Cryptogenic (of unidentified etiology)





Pathology. Irrespective of type of cirrhosis morphological changes are similar. Macroscopically the liver is small, having distorted shape with irregular and coarse scars and nodules of varying size. The cut surface shows scars and nodules varying in diameter from 3 mm to a few centimeters.


Microscopically, the features are following:

1. Abnormal lobular architecture can be identified and central veins are hard to find.

2. The fibrous septa dividing the variable-sized nodules are generally thick.

3. Active liver cell necrosis is observed. Fibrous septa contain prominent mononuclear inflammatory cell infiltrate even with follicles. Often there is extensive proliferation of bile ductules derived from collapsed liver lobules.

4. Liver cells vary considerably in size and multiple large nuclei are common in regenerative nodules. Fatty degeneration may be present.


Specific types of cirrhosis

Post-necrotic cirrhosis is characterized by large and irregular nodules with broad bands of connective tissue and occurring most commonly after viral hepatitis.

Biliary cirrhosis is defined as a chronic disorder characterized by clinical, biochemical and morphological features of long-continued cholestasis of extrahepatic or intrahepatic origin. There are primary and secondary biliary cirrhosis. In primary one the destructive process of unknown etiology affects intrahepatic bile ducts. Secondary cirrhosis resulting from prolonged mechanical obstruction of the extrahepatic biliary passages.

Indian childhood cirrhosis is an unusual form of cirrhosis seen in children at the age of 6 months and 3 years. The disease has some familial incidence suggesting a possible genetic or common environmental origin. Death occurs due to hepatic failure within a year of diagnosis. There are 5 histologic types of ICC. The type 2 is the most common. It is characterized by ballooning degeneration of hepatocytes, with some liver cells showing Mallory bodies and surrounded by neutrophilic exudate. As a rule micronodular cirrhosis develops.

Cardiac cirrhosis is uncommon complication of severe right-sided congestive heart failure of longstanding duration. The common causes culminating in cardiac cirrhosis are cor pulmonale, tricuspid insufficiency or constrictive pericarditis. Microscopically, the hepatic sinusoids are dilated and congested with hemorrhagic necrosis of centrolobular hepatocytes. Then fibrous strands radiating from the central veins are observed.

Alcoholic cirrhosis. The final and irreversible form of alcoholic liver disease usually evolves slowly and sidiously. At first the cirrhotic liver is yellow-fatty, and enlarged, usually weighing more than 2 kg. Over the span of years, it is transformed into a brown, shrunken, nonfatty organ, sometimes less than 1 kg in weight. Cirrhosis may develop within 1 to 2 years in the setting of alcoholic hepatitis. Initially the developing fibrous septae delicate and extend from central vei& to portal regions as well as from portal tract to portal tract. Regenerative activity of the entrapped parenchymal acini generates fairly uniformly sized <<micronodules>>. With time, the nodularity becomes more prominent; scattered nodules may become large, and occasionally nodules more than 2 cm diameter may develop. As fibrous septae dissect and surround nodules, the liver becomes more fibrotic, loses fat, and shrinks progressively in size. Parenchymal islands are engulfed by ever wider bands of fibrous tissue, and the liver is converted into a mixed micronodular and macronodular pattern. Further ischemic necrosis and fibrous obliteration of nodules eventually create broad expanses of tough, pale scar tissue, leaving residual parenchymal nodules that protrude like <<hobnails>> from the surface of the liver. By microscopy, the septae contains variable amounts of scattered lymphocytes and some reactive bile duct proliferation.


Complications are subdivided into 2 groups:

Hepatic and Non-hepatic.

Hepatic complication:

1. Progressive hepatic failure.

2. Development of hepatocellular carcinoma.

3. Steatorrhea due to reduced hepatic bile secretion.

4. Gall stones usually of pigment type, are seen twice more frequently in patients with cirrhosis than in general population.

Non-hepatic complication:

1. Portal hypertension and its effects such as ascites, splenomegaly and development collaterals (e.g. esophageal varices, spider nevi etc.).

2. Chronic relapsing pancreatitis, especially in alcoholic liver disease.

3. Infections are more frequent in patients with cirrhosis due to impaired phagocytic activity of reticuloendothelial system.

4. Hematologic derangements such as bleeding disorders and anemia due to impaired hepatic synthesis of coagulation factors and hypoalbuminemia are present.

5. Cardiovascular complications such as atherosclerosis of coronaries and aorta and myocardial infarction are more frequent in these patients.

6. Musculoskeletal abnormalities like digital clubbing, hypertrophic osteoarthropathy.

7. Endocrine disorders such as gynecomastia, testicular atrophy and impotence, whereas in cirrhotic women amenorrhea is a frequent abnormality.

8. Hepatorenal syndrome leading to renal failure may occur in late stages of cirrhosis.

Causes of death are hepatic coma, massive gastrointestinal hemorrhage from esophageal varices, intercurrent infections, hepatorenal syndrome and development of hepatocellular carcinoma.


There are benign tumors, primary and metastatic malignant tumors in the liver. Metastatic malignant tumors are much more common than priniary ones. Primary tumors may arise from hepatic cells (hepatocellular tumor), bile duct epithelium (biliary tumor) and mesodermal structures.

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Liver cell adenomas are pale, yellow-tan, and frequently bile-stained nodules, found anywhere in the hepatic substance but often beneath the capsule. They may reach 30 cm in diameter. Although they are usually well demarcated, encapsulation may not be macroscopically evident. Microscopically, liver cell adenomas are composed of sheets and cords of cells that may resemble normal hepatocytes or have some variation in cell and nuclear size. Portal tracts are absent; instead prominent arterial vessels and draining veins are distributed through the substance of the tumor. A capsule that ranges from delicate collapsed reticulin to well-defined connective tissue usually separates the lesion from the surrounding parenchyma, but it may be deficient in places or entirely absent.

Bile duct adenomas are firm, pale, and usually single discrete nodules rarely more than 1 cm in diameter, frequently found in a subcapsular location. In contrast to the liver cell adenoma, they are almost never bile stained. Microscopically they are composed of uniformly sized, epithelium-lined channels or ducts separated by a scant-to-abundant connective tissue stroma and sharply demarcated from the surrounding liver.

Hepatocellular carcinoma, cholangiocarcinoma  may appear macroscopically as a unifocal (usually large) mass; multifocal, widely distributed nodules of variable size; or a diffusely infiltrative cancer, permeating widely and sometimes involving the entire liver. All three patterns may cause liver enlargement (2000 to 3000 gm), particularly the unifocal massive and multinodular patterns. The diffusely infiltrative tumor may blend imperceptibly into a cirrhotic liver background. When discrete masses can be seen, they are basically yellow-white, punctuated sometimes by areas of hemorrhage or necrosis. Hepatocellular carcinoma sometimes take on a green hue when composed of well-differentiated hepatocytes capable of secreting bile.

Cholangiocarcinomasare rarely bilestained because differentiated bile duct epithelium does not synthesize pigmented bile. All patterns of hepatocellular carcinoma have a strong propensity for invasion vascular channels.

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Hepatocellular carcinoma range from well- differentiated to highly anaplastic undifferentiated lesions. In well-differentiated and moderately well- differentiated tumors, cells recognizable as hepatocytic in origin are disposed either in a trabecular pattern or in an acinar, pseudoglandular pattern. Supporting connective tissue is minimal to absent, explaining the soft consistency of most hepatocellular carcinoma. Bile may occasionally be seen in canalicular spaces or lumens between tumor cells, and bile canaliculi may be present ultrastructurally.

A distinctive variant of hepatocellular carcinoma is the fibrolamellar carcinoma. This tumor occurs in young men and women (20 to 40 years of age) with equal incidence, has no association with HBV or cirrhosis factors, and has a distinctly better prognosis. It usually constitutes a single large, hard <<scirrhous’ tumor with fibrous bands coursing through it. Histologically it is composed of well-differentiated polygonal cells growing in nests or cords and separated by parallel lamellae of dense collar bundles, hence the name <<fibrolamellar>>.

Cholangiocarcinomas resemble adenocarcinomas arising in other parts of the body. Most are well-differentiated sclerosing adenocarcinomas with clearly defined glandular and tubular structures lined by somewhat anaplastic cuboidal to low columnar epithelial cells. These neoplasms are often markedly desmoplastic, so dense collagenous stroma separates the glandular elements. Mucus is frequently present within cells and the lumina but not bile.

Metastatic tumors in the liver develop resulting metastasis to the liver from the cancer of stomach, breast, lungs, colon, esophagus, pancreas, malignant melanoma. Sarcomas rarely produce metastases to the liver.


Hepatocellular Carcinoma

Hepatocellular carcinoma, which occurs in adults with cirrhotic livers (in children it is seen without cirrhosis), is associated with persistent infection by HBV and HCV, including asymptomatic carriers (i.e., patients with occult liver cirrhosis). Other patients with liver cirrhosis who are at risk for developing HCC are those with hemochromatosis and al-antitrypsin deficiency. Most patients with alcoholic cirrhosis and HCC are also infected with HCV or HBV. The gross picture of HCC is that of one or several irregular soft yellowish-green nodules in a cirrhotic liver with intrahepatic (parenchymatous, intravascular) spread. The histologic appearance varies from a trabecular and acinar pattern of well-differentiated hepatocytes to a poorly differentiated fibrolamellar tumor or a tumor with cholangiocellular features. The ascites color may change to bloody. Serum levels of a-fetoprotein increase dramatically (400-4000 ng/mL).



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Intrahepatic Cholangiocarcinoma

Although more rare than HCC, intrahepatic (peripheral) CAC also is associated with cirrhosis. It is derived from small intrahepatic bile canaliculi with lymphatic spread to portal lymph nodes (less frequently than HCC via hepatic vessels). The tumor is usually well differentiated with clearly defined tubular structures and pronounced desmoplasia (tumor fibrosis). Bile pigment is absent.


Gallstones are formed from constituents of the bile (viz, cholesterol, bile pigments and calcium salts) along with other organic components. Accordingly, the gallstones commonly contain cholesterol, bile pigment and calcium salts in varying proportions. They are usually formed in the gall bladder, but sometimes may develop within extrahepatic biliary passages, and rarely in the larger intrahepatic bile duct.

The incidence of gallstones varies markedly in different geographic areas, age, sex, diet and various other risk factors.

The mechanism of cholesterol gallstone formation or lithogenesis is determined by 3 major factors, namely supersaturation of bile with cholesterol, cholesterol nucleation, and the hyperfunction of gallbladder.

Types of gallstones. As stated before, gallstones contain cholesterol, bile pigment and calcium carbonate, either in pure form or in various combinations. Accordingly, gallstones are of 3 major types — pure gallstones, mixed gallstones and combined gallstones. Mixed gallstones are the most common while pure and combined gallstones comprise 10% each. In general, gallstones are formed most frequently in the gallbladder but may occur in extrahepatic as well as intrahepatic biliary passages.

Numerous complications develop in cholelithiasis. They are cholecystitis, choledocholithiasis, mucocele or hydrops of the gallbladder, biliary fistula, gallstone ileus, gallbladder cancer.


Cholecyscitis or inflammation of the gallbladder may be acute, chronic, or acute superimposed on chronic. Though chronic cholecyscitis is more common.

Acute Cholecystitis

In many ways, acute cholecystitis is similar to acute appendicitis. The condition usually begins with obstruction, followed by infection later.

Based on the initiating mechanisms, acute cholecystitis occurs in two types of situations — acute calculous and acute acalculous cholecystitis. In majority of cases, acute cholecystitis is caused by obstruction in the neck of the gallbladder or in the cystic duct by a gallstone. The commonest location of impaction of a gallstone is in Hartman’s pouch. After that secondary bacterial infection, for instance E. coli and Streptococcus faecalis, supervenes.

Acute acalculous cholecystitis. The remaining 10% cases of acute cholecystitis do not contain gallstones. In such cases, a variety of causes have been assigned such as previous non-biliary surgery, multiple injuries, bums, severe sepsis, diabetes mellitus, etc.



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Morphology. Except for the presence or absence of calculi, the two forms of acute cholecystitis are morphologically similar. Macroscopically, the gallbladder is distended and tense. The serosal surface is coated with fibrinous exudate with congestion and hemorrhages. The mucosa is red. The lumen is filled with pus mixed with green. bile. In calculous cholecystitis, a stone is generally impacted in the neck or in the cystic duct. When obstruction of the cystic duct is complete, the lumen is filled with purulent exudate and the condition is known as empyema of the gall bladder. Microscopically, wall of the gall bladder shows marked inflammatory edema, congestion and neutrophilic exudate. There may be frank abscesses in the wall and gangrenous necrosis with rupture into the peritoneal cavity (gangrenous cholecystitis).

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Chronic Cholecystitis

Chronic cholecystitis is the commonest type of clinical gall bladder disease. The association of chronic cholecystitis with mixed and combined goll-stones is virtually always present.

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Morphology. Macroscopically, the gall bladder is generally contracted but may be normal or enlarged. The wall of the gall bladder is thickened which on cut section is grey-white due to dense fibrosis or may be even calcified. The mucosal folds may be intact, thickened, or flattened and atrophied. The lumen commonly contains multiple mixed stones or a combined stone. Microscopically, the following signs may be observed: thickened and congested mucosa but occasionally mucosa may be totally destroyed; penetration of the mucosa deep into the wall of the gall bladder up to muscular layer to form RokitanskyAschoff sinuses; variable degree of chronic inflammatory reaction, consisting of lymphocytes, plasma cells and macrophages, present in the lamina propria and subserosal layer; variable degree of fibrosis in the subserosal and subepithelial layers.

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Pancreas diseases

Pancreatitis. One distinguishes acute and chronic pancreatitis.

Acute pancreatitis is connected to 80 % of cases with cholelithiasis or with alcoholism. Important to the pathogenesis of the disease development is the ischemic lesion of the organ’s parenchyma due to arterial thrombosis; medication damage, etc.  With the disease progression there appear white or yellow-white areas of fat necrosis in the surrounding tissues (steatonecrosis). The gland is swollen, sometimes one can observe haemorrhagic imbibition of parenchyma. In such cases the tissue turns black-brown with the areas of necrosis.

Chronic pancreatitis often occurs after a long period of alcohol consumption. Fibrosis, cicatricial narrowing of ducts, acinar tissue atrophy develops in the tissue. The gland is dense and grey; in some places cysts with calcareous content can be seen.

Pancreas tumours are divided into benign (adenoma) and malignant (carcinoma). The head of pancreas is affected in 60% of cases, the body – in 20%, the tail – in 5%. Head carcinomas obstruct the outlet of general bile duct and cause obstructive jaundice.


Diarrheal diseases of the bowel make up a veritable Augean stable of entities (a messy situation cleaned by the fifth task of Hercules). Many are caused by microbiologic agents; others arise in the setting of malabsorptive disorders and idiopathic inflammatory bowel disease. Consideration should first be given to the conditions known as diarrhea and dysentery.



Pancreatitis is inflammation of the pancreas with acinic cell injury. It is classified into acute and chronic forms both of which are two distinct entities.

Acute Pancreatitis

Acute pancreatitis is an acute inflammation of the pancreas. The severe form of the disease associated with macroscopic hemorrhages and fat necrosis in and around the pancreas is termed acute hemorrhage pancreatitis or acute pancreatic necrosis. The condition occurs in adults between the age of 40 and 70 years and is commoner in females than in males.

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The onset of acute pancreatitis is sudden, occurring after about of alcohol or a heavy meal. The patient presents with abdominal pain, vomiting and collapse and the condition must be differentiated from other diseases producing acute abdomen such as acute appendicitis, perforated peptic ulcer, acute cholecystitis.

Etiology. The two leading causes associated with acute pancreatitis are alcoholism and cholelithiasis, both of which are implicated in more than 80% of cases. Less common causes of acute pancreatitis include trauma, ischemia, shock, extension of inflammation from the adjacent tissues, blood-borne bacterial infection, viral infections, certain drugs, etc.

Morphology. The morphology of acute pancreatic necrosis stems directly from the action of activated pancreatic enzymes that are released into the pancreatic substance. The basic alterations are proteolytic destruction of pancreatic substance, necrosis of blood vessels with subsequent hemorrhage, necrosis of fat, and an accompanring inflammatory reaction. The extent and predominance of each of these features depend on the duration and severity of the process, in the very early stages, only interstitial edema is present. Soon after, focal and confluent areas of frank necrosis of endocrine and exocrine tissue are found. Neutrophilic infiltration and interstitial hemorrhage eventually ensue. The most characteristic histologic lesions of acute pancreatic necrosis are the focal areas of fat necrosis that occur in the pancreatic and peripancreatic fat. Following enzymatic destruction, adipocytes are transformed into shadowy outlines of cell membranes filled with pink, granular, opaque precipitates.                         Amorphous basophilic calcium precipitates may be visible within the necrotic focus.

With severe pancreatic necrosis, a variegated pattern of blue-black hemorrhages and gray-white necrotic softening alternates with sprinkled foci of yellow-white, chalky fat necrosis.

Complications. A patient of acute pancreatitis who survives may develop a variety of systemic and local complications. Systemic complications are chemical and bacterial peritonitis, endotoxic shock, acute renal failure. Local complications are pancreatic abscess, pancreatic pseudocyst, duodenal obstruction.


Chronic Pancreatitis

Chronic pancreatitis is the progressive destruction of the pancreas due to repeated mild and subclinical attacks of acute pancreatitis. Most patients present with recurrent attacks of severe abdominal pain at intervals of months to years. Weight loss and jaundice are often associated. Later manifestations include associated diabetes mellitus and steatorrhea.

Etiology. Most cases of chronic pancreatitis are caused by the same factors as for acute pancreatitis.

Morphology. Chronic pancreatitis is distinguished by irregularly distributed fibrosis, reduced number and size of acini with relative sparing of the islets of Langerhans, and variable obstruction of pancreatic ducts of all sizes. The lesions have a macroscopic lobular distribution and may involve portions or all of the pancreas. A chronic inflammatory infiltrate around lobules and ducts is usually present. The interlobular and intralobular ducts are dilated and contain protein plugs in their lumina.

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The ductal epithelium may be atrophied or hyperplastic or may show squamous metaplasia. Macroscopically, the gland is hard and exhibits foci of calcification and fully developed pancreatic calculi. These concretions vary from calculi invisible to the naked eye, to stones 1 cm to several centimeters in diameter, giving rise to the term <<chronic calcifying pancreatitis’. With chronic ductal obstruction, the distribution of lesions is irregular, and the ductal epithelium generally is less severely damaged. Protein plugs and calcified stones are rare.

Complications. Last stage of chronic pancreatitis may be complicated by diabetes mellitus, pancreatic insufficiency with steatorrhea and malabsorption and formation of pancreatic pseudocysts.

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Cystic Fibrosis

More than 80% of patients with CF (mucoviscidosis) have visible secretory abnormalities of the pancreas, which cause mucus inspis-sation in major ducts and secondary atrophy of exocrine glands. Dilated and plugged ducts may cause multiple cysts, and degrading (sometimes superinfected) mucus leads to chronic resorptive in-

flammation with lymphoplasmacytic and phagocytic infiltration and progressive collagenous fibrosis. Ductal epithelia may undergo squamous metaplasia (supported by deficient vitamin A resorption). Clinical features are those of malabsorption with abdominal distention, bulky foul stools, and a failure to thrive

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Pancreatic Cancer

Carcinoma of the pancreas develops from ductal epithelial cells. Approximately 60% of pancreatic cancers are located in the head of the organ, 10% are located in the body, and 5% are located in the tail. The residual tumors show diffuse organ involvement without indication of their initial site. Usually, the tumor has already metastasized at the time of diagnosis. On gross inspection, the carcinoma of pancreas appears as poorly demarcated, white scarred or nodular areas with or without involvement of the common duct, the papilla, or the duodenum. Obstruction of the common bile du< t may cause a characteristic dilatation of the gallbladder with jaundice (Courvoisier sign). An important complication of pancreatic cancer is a variable and migrating thrombosis (migratory thrombophlebitis), which may bring patients to clinical attention for multiple pulmonary thromboses and infarcts of unknown origin.

Wilson Disease

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Wilson disease (WD; hepatolenticular degeneration) is an autosomal recessive disorder of hepatobiliary copper excretion with progressive accumulation of the toxic metal in the liver, the brain, the eyes, and many other organs. The genetic disturbance is located on chromosome 13. The incidence of WD is 1:30,000. First symptoms are usually noted during the second decade of life. Liver pathology shows acute (necrotizing) hepatitis, chronic active hepatitis with cholestasis, or cirrhosis with or without copper deposition (copper

usually in excess of 250 u.g/g dry weight). Hepatic changes without excess copper are indistinguishable from viral hepatitis and cirrhosis. Of diagnostic value are copper deposits in the corneal limbus, which impress on inspection as brown-greenish rings (Kaiser-Fleischer rings). WD runs a progressive downhill course until copper is reduced by chelating agents, except for rare cases of fulminant hepatitis, which have an unfavorable prognosis.

Amyloidosis of the Liver

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Amyloidosis of the liver occurs in 2 forms: diffuse perisinusoidal amyloidosis (secondary amyloidosis) after chronic infections, and focal vascular (portal) amyloidosis (primary amyloidosis). Secondary amyloidosis causes enlargement of the liver with efface-ment of the gross lobular structure. The cut surface is smooth and rubbery and of yellowish-brown color. Primary amyloidosis, which is not associated with inflammatory diseases of other organs, frequently follows abnormal protein production by plasma cells (plasma cell dyscrasia). Therefore, it is frequently accompanied by diffuse plasmacytosis or malignant plasmacytoma. Vascular (primary) amyloidosis typically involves mesenchymal tissues of other organs such as the myocardium, skeletal muscle, the tongue, the skin, the kidneys, and the spleen. Both forms of liver amyloidosis are part of a systemic process, and involvement of other organs may determine the outcome

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