DONE BY: KURBENOVA N.N. KOZHABAYEVA N. CHECKED BY: OMAROV T.M. Presentation «Astana Medical Universityі» JSC Department of pathological anatomy Theme : Esophageal and gastric diseases Astana 2017

Contents: Esophageal disease Diverticula Inflammation Cancer Gastric disease Gastritis Ulcers Cancer

Diseases of the esophagus Diverticula Inflammation (esophagitis) Tumors (cancer).

Diverticulum of the esophagus The diverticulum of the esophagus is a limited blind protrusion of its wall: Тrue diverticulum - can consist of all layers of the esophagus Consist the mucous and submucosal layer Muscular diverticulum – consist only muscular layer

Diverticulum of the esophagus Classification Depending on the localization and topography Pharyngo-esophagealBifurcationEpinephalic Multiple diverticula The causes of the formation of a diverticulum Congenital Inferiority of connective and muscular tissues of the esophagus wall, pharynx Acquired Iinflammation, sclerosis, scar scarring, increased pressure inside the esophagus

Diverticulum of the esophagus Classification From the features of origin Adhesive diverticula Arising from inflammatory processes in the mediastinum Relaxation diverticula Based on local relaxation of the esophageal wall. * Diverticulum of the esophagus can be complicated by inflammation of its mucous membrane - diverticulitis.

Esophagitis Esophagitis - inflammation of the mucosa of the esophagus - usually develops after many diseases, rarely - primarily. It can be acute or chronic.

Acute esophagitis Etiologycal factors: influence of chemical, thermal and mechanical factors, infectious diseases (diphtheria, scarlet fever, typhus), allergic reactions. Acute esophagitis can be catarrhal, fibrinous, phlegmonous, ulcerative, gangrenous. A special form of acute esophagitis is membranous, when the impression of the mucosa of the esophagus occurs. After deep membranous esophagitis, which develops during chemical burns, cicatricle stenosis of the esophagus is formed.

Chronic esophagitis With chronic esophagitis, the development of which is associated with chronic irritation of the esophagus (the effect of alcohol, smoking, hot food) or blood circulation in its wall (venous congestion with cardiac decompensation, portal hypertension), the mucosa is hyperemic and swollen, with sites of epithelial destruction, leukoplakia and sclerosis. For a specific chronic esophagitis, which occurs in tuberculosis and syphilis, the morphological pattern of the corresponding inflammation is characteristic.

Special form of esophagitis – Reflux esophagitis Regurgitation esophagitis Regurgitation of gastric contents into esophagus Gastric contents damage mucous layer of esophagus Peptic esophagitis Inflammation, erosion and ulcers are occur Erosive, ulcerative esophagitis

Esophageal cancer Esophageal cancer most often occurs at the border of the middle and lower third of it, which corresponds to the level of bifurcation of the trachea. It is much less common in the initial part of the esophagus and at the entrance to the stomach. Esophageal cancer accounts for 2-5% of all malignant tumors.

Etiology of esophageal cancer Chronic irritation of its mucous membrane (hot rough food, alcohol, smoking), Cicatricial changes after a burn, Chronic gastrointestinal infections, anatomical disorders (diverticula, ectopia of cylindrical epithelium and gastric glands, etc.). Among the precancerous changes, leukoplakia and severe dysplasia of the epithelium of the mucous membrane are of the greatest importance.

Macroscopic forms Ring-shaped dense cancer is a tumor which circularly covers the esophagus wall at a certain site. The lumen of the esophagus is narrowed. During the decay and ulceration of the tumor, the permeability of the esophagus is restored. Papillary cancer of the esophagus is similar to mushroom-like stomach cancer. It easily disintegrates, resulting in the formation of ulcers that penetrate into neighboring organs and tissues. Ulcerous cancer is an oval shaped and is stretched along the esophagus.

Microscopic forms Among the microscopic forms of esophageal cancer are squamous cell carcinoma, adenocarcinoma, glandular-squamous, glandular-cystic, mucoepidermal and undifferentiated cancer

Complications Metastasis of esophageal cancer is mainly lymphogenous. Complications are associated with germination in neighboring organs - trachea, stomach, mediastinum, pleura. Oesophageal and tracheal fistulas are formed, aspiration pneumonia, abscess and gangrene of the lung, pleural empyema, purulent mediastinitis develop. In cancer of the esophagus, cachexia appears early.

Acute gastritis Etiology: Exogenous gastritis - In some cases, for example, alcohol poisoning, poor quality food, pathogenic factors directly affect the gastric mucosa Endogenous gastrits - in others - this effect is mediated and carried out with the help of vascular, nervous, humoral and immune mechanisms,

Pathological anatomy Acute gastritis Diffuse gastritis Focal gastritis FoundationAntralPyloroanthral Pyloroduodenal gastritis.

Morphological characteristics Acute gastritis are distinguished: 1) catarrhal (simple); 2) fibrinous; 3) purulent (phlegmous); 4) necrotic (corrosive). Catarrhal (simple) gastritis, the mucous membrane of the stomach is thickened, edematous, hyperemic, its surface is abundantly covered with mucous masses, numerous small hemorrhages, erosion are seen. At a microscopic examination, dystrophy, necrobiosis and sloughing of the superficial epithelium are revealed, cells of which are characterized by increased mucus formation. Cellular debriding leads to erosion. In cases where there are multiple erosions, they speak of an erosive gastritis. The gland changes slightly, but their secretory activity is suppressed. Its own layer is full-blooded and edematous, infiltrated with neutrophils, diapedemic hemorrhages occur.

Fibrinous gastritis Fibrinous gastritis - a fibrinous peel of gray or yellow-brown color forms on the surface of a thickened mucous membrane. The depth of necrosis of the mucous membrane can be different: croupous (surface necrosis) diphtherian (deep necrosis)

Phlegmonous gastritis Phlegmonous gastritis, the stomach wall becomes sharply thickened, especially due to the mucous membrane and the submucosal layer. The folds of the mucous membrane are coarse, with hemorrhages, fibrinous-purulent overlays. Yellow-green purulent fluid drains from the surface of the incision. Leukocyte infiltrate containing a large number of microbes diffusely covers the mucosa, submucosal and muscle layers of the stomach and covers its peritoneum. Therefore, often with phlegmonous gastritis, perigastritis and peritonitis develop. The phlegmon of the stomach sometimes complicates his trauma, develops also in chronic ulcers and ulcerated stomach cancer.

Necrotic gastritis Necrotic gastritis usually occurs when chemicals (alkali, acid, etc.) enter the stomach, cauterize and destroy the mucous membrane (corrosive gastritis). Necrosis can cover the superficial or deep sections of the mucosa, be coagulated or colliquated. Necrotic changes usually result in the formation of erosions and acute ulcers, which can lead to the development of phlegmon and perforation of the stomach.

Outcome of acute gastritis The outcome of acute gastritis depends on the depth of the mucous membrane (wall) of the stomach. Catarrhal gastritis can result in complete restoration of the mucosa. With frequent relapses, it can lead to the development of chronic gastritis. After significant destructive changes, characteristic for phlegmonous and necrotic gastritis, mucosal atrophy and sclerotic deformation of the stomach wall develops-cirrhosis of the stomach.

Chronic gastritis Etiology. Exogenous factors: a disturbance in the diet and rhythm of nutrition, alcohol abuse, the effects of chemical, thermal and mechanical agents, the effect of occupational hazards, etc. Endogenous factors - autoinfection (Campylobacter piloridis), chronic auto-toxication, neuroendocrine disorders, chronic cardiovascular insufficiency, allergic reactions, regurgitation of duodenal contents into the stomach (reflux) is also important. An important condition for the development of chronic gastritis is a long-term exposure of exogenous or endogenous pathogenic factors that can "break" the habitual regenerative mechanisms of the constant renewal of the epithelium of the gastric mucosa. It is often possible to prove the long-term effect of not one, but several pathogenic factors.

Pathogenesis. Chronic gastritis Chronic gastritis can be autoimmune (gastritis type A) and non-immune (gastritis type B). Autoimmune gastritis is characterized by the presence of antibodies to parietal cells, and therefore the damage to the fundus of the stomach, where the lining cells are many (base gastritis). There is a high level of gastrin in blood. In connection with the damage to the lining cells, the secretion of hydrochloric (hydrochloric) acid is reduced.

Non-immune gastritis, antibodies to parietal cells are not detected, so the fundus of the stomach is relatively preserved. The main changes are localized in the antral department (antral gastritis). Gastrinemia is absent, the secretion of hydrochloric acid is only moderately reduced.

By the topography chronic gastritis are divided: AntralPangastritisBase

Morphological types There are two morphological types of chronic gastritis - superficial and atrophic. Chronic surface gastritis is characterized by dystrophic changes in the surface (pit) epithelium. In some areas, it flattenes, approaches the cubic and is characterized by a decreased secretion, in others - high prismatic with increased secretion. There is a translocation of additional cells from the isthmus to the middle third of the glands, histamine-stimulated secretion of hydrochloric acid by parietal cells decreases and pepsinogen - the main cells. The own layer (plate) of the mucous membrane is swollen, infiltrated by lymphocytes, plasma cells, and single neutrophils

Chronic surface gastritis

Chronic atrophic gastritis At a chronic atrophic gastritis there is a new and basic quality - an atrophy of a mucosa, its glands which defines development of a sclerosis. The mucous membrane is thinned, the number of glands decreases. On the site of atrophied glands, connective tissue grows. The remaining glands are located in groups, the ducts of the glands are enlarged, some types of cells in the glands are poorly differentiated. In connection with the mucoidal glands, the secretion of pepsin and hydrochloric acid is disrupted. The mucous membrane is infiltrated by lymphocytes, plasma cells, single neutrophils. These changes are accompanied by a restructuring of the epithelium, with both superficial and glandular epithelium undergoing metaplasia

Micro preparations (a-г). Chronic atrophic gastritis: the mucous membrane of the fundus of the stomach is sharply thinned, the glands are reduced in size, the distance between them is increased, the epithelium of the glands acquires more primitive features, loses the ability to produce gastric juice and hydrochloric acid, secrete mucus. There are foci of intestinal metaplasia with goblet cells (1). In its own plate of the mucous membrane diffuse lymphoplasmocytic infiltrate, lymphoid follicles (2), severe sclerosis; в, г - Helicobacter pilori in the lumen of the glands.

Macro-preparations (b). Chronic multifocal atrophic gastritis: mucous membrane of the stomach with smoothed folds, thinned, pale, grayish color, with small-dot hemorrhages, erosions

Ulcer Ulcer is a chronic disease, the main clinical and morphological expression of which is a recurrent ulcer of the stomach or duodenum. Etiology: - psychoemotional overstrain -alimentary factors (violation of the regime and the nature of nutrition), -bad habits (smoking, and alcohol abuse), -the effects of a number of drugs (acetylsalicylic acid, indomethacin, corticosteroids, etc.) - hereditary constitutional factors - Campylobacter piloridis

Acute gastric ulcers Acute gastric ulcers usually appear on a small curvature, in the antral and pyloric sections, which is explained by the structural-functional features of these departments. It is known that small curvature is a "food path" and therefore easily traumatized

Macro-preparations (a-б). Acute erosion and stomach ulcers: in the gastric mucosa, multiple small surface (erosions) and deeper, capturing submucosal and muscular layers of the stomach wall (acute ulcers), round-shaped defects with soft even margins and a brownish-black or gray- black bottom ( due to hydrochloric acid hematin, which is formed from hemoglobin erythrocytes under the influence of hydrochloric acid and gastric juice enzymes);

Micro preparations (a, b). Acute erosion of the gastric mucosa: in the gastric mucosa, a superficial (within the mucous membrane) foci of necrosis is formed with the formation of a shallow defect-erosion with perifocal leukocyte inflammatory infiltration. In the day of erosion deposits of hydrochloric acid hematin (1). Staining with hematoxylin and eosin: x 100 (b - preparation of NO Kryukov)

Chronic stomach ulcer Chronic stomach ulcer is usually single, multiple ulcers are rare. The ulcer has an oval or round shape (ulcus rotundum) and sizes from a few millimeters to 5-6 cm. It penetrates into the wall of the stomach at various depths, sometimes reaching the serous layer. The bottom of the ulcer is smooth, sometimes rough

Хроническая язва желудка (а,) и двенадцатиперстной кишки (б)

Сhronic ulcers with bleeding - arrozired and thrombosed vessels in the bottom of ulcers ( в, н)

Micro preparations (a, b). Chronic ulcer of stomach (a) and duodenum (b): defect of the wall of the stomach or duodenum, which seizes the mucosa, submucosal and muscular membrane. In the bottom of the defect 4 layers: 1 - fibrinous-purulent exudate; 2 - fibrinoid necrosis; 3 - granulation tissue; 4 - scar tissue with sclerotized and hyalineized vessels. In the margins of chronic gastric ulcer processes of epithelial restructuring (cervical epithelial hyperplasia, gland atrophy, intestinal metaplasia, mild or moderate dysplasia). Staining with hematoxylin and eosin: a - x 120, b - x60 (b - preparation of NO Kryukov)

Chronic ulcer Chronic ulcer of the duodenum is overwhelmingly formed on the anterior or posterior wall of the bulb (bulbar ulcer); Only in 10% of cases it is located below the bulb (postbulbarnaya ulcer). Quite often there are multiple ulcers duodenum, they are located opposite each other along the anterior and posterior walls of the bulb (kissing ulcers).

Complications Among the complications of chronic ulcer in peptic ulcer disease (Samsonov VA, 1975): 1) ulcerative-destructive (bleeding, perforation, penetration); 2) inflammatory (gastritis, duodenitis, perigastritis, periduodenitis); 3) ulcerative cicatricial (narrowing of the entrance and exit sections of the stomach, deformation of the stomach, narrowing of the lumen of the duodenum, deformation of its bulb); 4) malignant ulcers (development of cancer from ulcers); 5) combined complications.

Etiology of gastric cancer Intestinal" type of gastric cancer - exogenous carcinogens Diffuse" type of gastric cancer is largely associated with the individual genetic characteristics of the organism.

Pathological anatomy Plaque carcinoma (flattened, superficial, stalking) occurs in 1-5% of cases of stomach cancer and is the rarest form. The tumor is found more often in the pyloric department, on a small or large curvature in the form of a small 2-3 cm long, plaque-like thickening of the mucosa (Figure 199). Mobility of the folds of the mucosa in this place is somewhat limited, although the tumor rarely sprouts the submucosa. Histologically, a plaque-like cancer usually has the structure of adenocarcinoma, less often undifferentiated cancer. Polypase cancer accounts for 5% of cases of carcinoma of the stomach. It has the form of a node with a villous surface 2-3 cm in diameter, which is located on the stem (see Figure 199). Tissue tumor is gray-pink or gray-red, rich in blood vessels. Sometimes polypous cancer develops from the adenomatous polyp of the stomach, but more often it represents the next phase of exophytic growth of plaque-like cancer. At a microscopic examination, adenocarcinoma is often found, sometimes - undifferentiated cancer.

Pathological anatomy Fungal (mushroom) cancer occurs in 10% of cases. Like polypous cancer, it has the appearance of a knobby, tuberous (less often smooth surface) formation, sitting on a short wide base (see Figure 199). On the surface of the tumor node, erosions, hemorrhages, or fibrinous-purulent overlays are often encountered. Tumor soft, gray-pink or gray-red, well- delimited. Fungal cancer can be considered as a phase of exophytic growth of polyposis cancer, therefore, when histologically examined, it is represented by the same types of carcinoma as polyposis. Ulcerated cancer is very common (more than 50% of cases of stomach cancer). It combines various genetically malignant gastric ulcers, which include primary-ulcerous cancer, saucer- like cancer (cancer-ulcer) and cancer from a chronic ulcer (ulcer-cancer).

Pathological anatomy Primary ulcer cancer of the stomach (Figure 200) has been little studied. It is rarely found. This form includes exophytic cancer with ulceration in the very beginning of its development (plaque-like cancer), the formation of an acute and then chronic cancer ulcer, which is difficult to distinguish from a cancer ulcer. With microscopic examination, undifferentiated cancer is more often found. Saucer-like cancer (cancer-ulcer) is one of the most common forms of stomach cancer (see Figure 200). Occurs when the exophytally growing tumor is ulcerated (polypous or fungal cancer) and represents a rounded formation, sometimes reaching a large size, with roll-like whitish edges and ulceration in the center. The bottom of the ulcer can be adjacent organs, in which the tumor grows. Histologically, it is often represented by adenocarcinoma, less often by undifferentiated cancer.

Infiltrative-ulcerous cancer occurs in the stomach quite often. This form is characterized by severe cankerous wall infiltration and tumor ulceration, which in a time sequence can compete: in some cases it is later ulceration of massive endophytic carcinomas, in others - endophytic tumor growth from the margins of a malignant ulcer. Diffuse cancer (see Figure 199) is observed in 20-25% of cases. The tumor grows endophytic in the mucous, submucosal and muscle layers along the connective tissue layers. The wall of the stomach becomes thickened, dense, whitish and immobile at the same time. Mucous membrane loses its usual relief: its surface is uneven, folds of uneven thickness, often with small erosions.

Complications. There are two groups of complications of stomach cancer: the first are associated with secondary necrotic and inflammatory changes tumors, the latter - with the germination of gastric cancer in neighboring organs and tissues and metastases. As a result of secondary necrotic changes and decay of the carcinoma, there are perforation of the wall, bleeding, peritumorous (periulcerous) inflammation, up to the development of phlegmon of the stomach.

Macro-preparations (a, b). Polyp of the stomach: a small exophytic formation protruding into the lumen of the stomach on a broad base, covered with a mucous membrane (histologically: a - adenoma, b - leiomyoma); (a - preparation of NO Kryukov, b - preparation of IN Shestakova)

Cancer of the stomach (nodular or diffuse forms): a - fungous, b - saucer-like,

Микропрепараты (а, б). Аденокарцинома желудка: в толще слизистой оболочки и мышечного слоя желудка располагаются атипичные, разных размеров и формы железистые комплексы (тканевая атипия). Опухолевые клетки и их ядра полиморфны, разных размеров и формы, ядра гиперхромны (клеточная атипия). Митозы (типичные и атипичные) немногочисленны, уровень пролиферативной активности опухоли умеренный. Опухолевые комплексы проникают в собственную пластинку и мышечный слой - инвазивный рост

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