Gastritis is inflammation of the gastric mucous membrane. Acute and chronic gastritis are differentiated.

ACUTE GASTRITIS

Acute gastritis is a very common disease. Catarrhal, corrosive and acute phlegmonous gastritis are distinguished.

Aetiology and pathogenesis. The alimentary factor is the leading one among the other causes of gastritis. Ingestion of fatty, coarse, poorly assimilated or decomposed food, of very cold or hot meals or alcoholic drinks provokes gastritis. The gastric mucosa may also be ir­ritated by prolonged taking of some medicines (salicylates, sulpha preparations, steroid hor­mones, butadione, iodine preparations, etc.). An allergic reaction to some foods (fish, eggs) can sometimes also cause gastritis. Various infectious diseases, such as influenza, measles, or scarlet fever can be attended by acute gastritis. It is the leading symptom in food poisoning.

Clinical picture. Symptomatology of acute gastritis is quite varied. It may proceed asymp-tomatically or be manifested by severe local and general symptoms. Inflammation begins 2—3 hours after the irritating agent has been ingested, while the clinical picture develops in 6—8 hours. The symptoms of acute gastritis are loss of appetite, unpleasant taste in the mouth, nausea and vomiting (first with food remains and later with bile). The patient complains of pressure, bulging, and pain in the epigastrium. The rise of temperature is often preceded by chills. The patient is pale, his pulse is accelerated, the tongue coated, and breath is foul. Palpation of the epigastric region is painful and stimulates nausea. The amount of excreted urine decreases. In persistent vomiting the haemoglobin and erythrocyte counts increase while the level of chlorides decreases.

The onset of the disease is characterized by hypersecretion and hyperchlorhydria which is followed by inhibition of gastric secretion. The motor (evacuatory) function of the stomach sharply decreases, while the absorptive power of the gastric mucosa increases. Gastroscopy reveals hyperaemic mucosa coated by a thick layer of glassy mucus; haemorrhage and erosion sometimes occur. Morphological reconstruction of the gastric mucosa complete by the end of the second week. The patient recovers clinically in 3 or 4 days. X-ray examination fails to reveal any changes in the relief of the gastric mucosa.

Course. The disease ends by recovery in most cases, but acute process can convert into a chronic one in the absence of appropriate treatment and if exposure to the harmful factors (alcohol, overeating) continues.

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The special forms of acute gastritis (corrosive and phlegmonous) are called fulminant gastritis. Corrosive acute gastritis develops from irritation of the gastric mucosa by acids or alkalis, and acute phlegmonous gastritis is a rare disease characterized by purulent inflamma­tion of a part or the entire stomach wall. The clinical course of both forms is grave. Perfora­tion of the stomach is possible. Prognosis is unfavourable in most cases.

Treatment. During the first 2 or 3 days the patient is given only nutritive liquid, and the diet is then gradually enriched by the end of the second week. Bed rest is indicated during the first days of the disease; antacid and astringent preparations are given. The stomach should be lavaged as soon as possible in corrosive gastritis. Antibiotics should be given in phlegmonous gastritis.

CHRONIC GASTRITIS

Chronic gastritis is a frequently occurring disease; it affects mostly men.

Aetiology and pathogenesis. Chronic gastritis is closely connected aetiologically with acute gastritis. All exogenous aetiological factors responsible for acute gastritis are important for the development of chronic gastritis. Among important endogenous factors causing chronic gastritis are reflex effects on the stomach from pathologically changed organs (gall bladder, intestine, pancreas), upset hormone system (affection of the thyroid, pituitary, adrenal glands), chronic infections (tuberculosis, malaria, syphilis), chronic septic foci (tonsillitis, carious teeth). Chronic gastritis may develop from disordered metabolism (diabetes, obesity, gout, renal failure). Finally, chronic gastritis may be secondary to diseases ac­counting for hypoxia of tissues, the gastric mucosa included (chronic cir­culatory insufficiency, pulmonary heart, uraemia).

Chronic gastritis is a polypathogenic disease. The leading role in its development undoubtedly belongs to disorders in the nervous, humoral, and hormonal mechanisms regulating the digesting function. But the direct action of irritants on the gastric mucosa cannot be disregarded either. Autoallergic processes are important for maintaining the disease.

Pathological anatomy. Differentiated are superficial affections of the mucosa, affection of the-glands without their atrophy, atrophy of the gastric mucosa of various degree, and combination of atrophy with hyperplasia.

Classification of chronic gastritis. There is no universally accepted classification of chronic gastritis. S. Ryss proposed a classification based on four principles: aetiological (exogenous and endogenous), mor­phological, functional (chronic gastritis with preserved secretion and with secretory insufficiency of various degree, up to achlorhydria), and clinical (compensated chronic gastritis or remission phase; decompensated gastritis or exacerbation phase). Moreover, gastritis can be regarded as an indepen-

dent disease and as a disease secondary to other pathologies (peptic ulcer, chronic colitis, etc.).

Clinical picture. The signs of chronic gastritis are difficult to describe because the course and symptomatology of the disease are quite variable. Some patients do not complain of anything during remissions; the disease may also develop for a long time without any manifestations and it is therefore difficult to establish the time of its onset.

The main syndrome of chronic gastritis is gastric dyspepsia. It may combine with intestinal dyspepsia characterized by meteorism, rumbling sounds in the abdomen, constipation, and diarrhoea. The patient with chronic gastritis can also feel pressure and distention in the epigastrium, and sometimes pain. These symptoms are connected with distention of the stomach by ingested food and the attending pathological sensitivity of mucosal interoceptors. Pain is dull and boring, but sometimes becomes severe. The general condition of patients with chronic gastritis varies. Some patients do not lose weight, remain active, while others lose weight, become flaccid and slow, their appetite is poor. A pronounced decrease in gastric secretion may be attended by diarrhoea which causes even greater wasting and impairs absorption of proteins, vitamins, and iron. Anaemia develops along with signs of polyhypovitaminosis and albumin deficiency.

Examination of the abdomen sometimes reveals inflation. Palpation of the epigastrium is in most cases painless. The acid secretion may remain normal or it may decrease. Free hydrochloric acid may be absent from the gastric juice (achlorhydria). In neglected cases secretion of pepsin (achylia) is upset as well.

Roentgenography is but of little use in the diagnosis of chronic gastritis. Gastroscopy can give valuable diagnostic information, especially if it is combined with sighting biopsy. Aspiration biopsy and exfoliative cytology are also important for the study of patients with chronic gastritis.

Chronic gastritis should be differentiated from peptic ulcer and gastric neurosis (" irritated stomach") in the presence of hyperchlorhydria and functional achylia.

Course. The disease usually slowly progresses but the appropriate treat­ment improves the patient's condition. Complete anatomical restoration of the gastric mucosa and normalization of the secretory function occur rare­ly. Chronic gastritis with secretory insufficiency is considered as a precancer condition.

Treatment. Therapy of chronic gastritis should be combined, differen­tial, lengthy, and planned. Diet is especially important. When prescribing an appropriate diet, the stage of the disease, and also the secretory background of the stomach should be taken into consideration.

Substitution therapy (preparations of gastric juice) is given in anacid

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Chapter 7. Digestive System

gastritis. In spastic and pain syndromes, spasmolytics are given and ther-motherapy applied. Health-resort and sanatorium therapy are also in­dicated in combined treatment.

Prophylaxis. Rational nutrition and observation of hygienic re­quirements are requisite in prevention of chronic gastritis. Fighting against smoking and drinking alcohol, sanation of chronic inflammatory foci (carious teeth, tonsillitis) should also be included into the list of preventive measures. Patients with chronic gastritis should be regularly observed in out-patient conditions.

Peptic Ulcer Disease (Gastric and Duodenal Ulcer)

Peptic ulcer is a general chronic and relapsing disease characterized by seasonal exacerbations with ulceration of the stomach wall or the duodenum.

Aetiology and pathogenesis. The aetiology and pathogenesis of the disease is still unknown despite the intense clinical and experimental research.

The main affection, the lesion in the wall of the stomach or duodenum, is caused by the action of gastric juice. But in normal conditions the gastric or duodenal mucosa is resistant to the digestive effect of the juice due to the presence of complex protective mechanisms. Therefore, in order to cause self-digestion, certain factors should be involved which decrease resistance of the mucosa to the digestive effect of the gastric juice or in­crease its digestive properties; or both these factors should be involved. Many theories have been proposed to explain these phenomena but none of them fully explains the causes of peptic ulcer disease.

From the findings available at the present time, the following main fac­tors in the pathogenesis and aetiology of the disease have been established: (1) disordered neurohormonal mechanisms regulating digestion; (2) disorders in the local digestive mechanisms; (3) structural changes in the gastric and duodenal mucosa.

The predisposing factors are heredity and environmental factors, among which nutrition is the leading one. Irregular nutrition, with prevalence of easily assimilable carbohydrates in the diet, excess ingestion of poorly assimilated and long digested foods cause hypersecretion of the stomach. In the presence of the main factors, the predisposing factors cause ulceration with time. Alcohol and nicotine have also an adverse ef­fect on the gastric mucosa.

The central role in the aetiology and pathogenesis of peptic ulcer belongs to disorders in the nervous system which can arise in the central

and vegetative systems under the action of various effects (negative emo­tions, physical and mental overstrain, viscero-visceral reflexes, etc.).

Current research shows the important role of endocrine dysfunction in the development of peptic ulcer (dysfunction of the pituitary or the adrenal glands). Disorders in local mechanisms (the acid-peptic factor, gastric hor­mones, mucous barrier, regeneration of mucosa, blood circulation in the stomach wall and the duodenum, morphological reconstruction of the mucosa, changes in the motor function, condition of local secretory depressor mechanisms) result from disordered neurohormonal regulation of the gastroduodenal system.

It can thus be concluded that the causes of peptic ulcer are varied, while its pathogenesis is complex and uncertain. Nervous genesis may probably prevail in some cases, while humoral or neurohumoral in others; disorders in the local mechanisms of gastric digestion may also be the leading factor in the aetiology and pathogenesis of peptic ulcer.

Pathologial anatomy. Margins of a chronic ulcer are consolidated. Ulcers with especially hard elevated edges are called callous. Inflammatory infiltrations are usually formed round the ulcer. A bleeding vessel can be found on its floor. An ulcer can destroy the wall of the stomach (perforating ulcer) or it can penetrate the adjacent organs.

The ulcer is healed by epithelization or cicatrization. These processes can change the shape of the stomach and narrow its outlet. Adhesion of the stomach and duodenum to the neighbouring organs can result from the previous inflammation of the serous membrane at the site of affection.

Classification. There is no universally accepted classification of peptic ulcer disease. Location of an ulcer determines to a certain degree the clinical course of pathology. Ulcers mostly develop on the lesser curvature. The cardia is affected less frequently. The usual site of ulcer in the duodenum is the bulb. Pyloric, postbulbar, and extrabulbar ulcers are also differentiated. Age and sex are important for the clinic of the disease. Hence juvenile ulcers, ulcers of the elderly and old patients, and also peptic ulcer disease of women are differentiated.

Clinical picture. Symptoms of peptic ulcer disease vary and depend on the age, sex, the general condition of the patient, the duration of the disease, frequency of exacerbations, location, kind of lesion, and the presence of complications.

The leading symptom of peptic ulcer is pain, which may be periodic, seasonal, increasing in severity, intensifying or lessening after vomiting or taking meals, alkalis, thermal procedures, or cholinolytic preparations.

Early pain is typical of gastric ulcer; late pain, nocturnal or hunger pain are characteristic of peripyloric and duodenal ulcer. Permanent pain is atypical and is usually due to complications (perivisceritis, penetration of the ulcer). Regular connection between pain in peptic ulcer and quantity

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and quality of food is obvious. Ample, bitter, sour, salty, spicy and coarse food always cause severe pain.

The seasonal character of pain (vernal and autumnal) is very typical of peptic ulcer disease and can positively be used to differentiate it from pain in other diseases. Exacerbations of pain are alternated with remissions even in the absence of treatment. The cyclic character of peptic ulcer disease is probably due to seasonal changes in general reactivity of the human body. Upset vitamin balance in spring may play a certain role in the course of the disease as well. Periodicity of pain may be not quite obvious at the early stages of the disease. Except hunger pain, which lessens after meals, pain attains its maximum severity at the height of digestion.

Although a lesion cannot always be located by pain, it has, however, been noticed that gastric ulcer is manifested by pain in the epigastrium above the navel, while in duodenal ulcer pain is felt in the epigastrium to the right of the median line; ulcer of the cardia is characterized by pain in the vicinity of the xiphoid process. Pain may radiate into the left breast nipple, behind the sternum, the left shoulder blade, and into the thoracic part of the spine.

The pathogenesis of pain in peptic ulcer is uncertain. It has been established that common stimuli causing pain when applied to the skin are ineffective when applied to the wall of the stomach or the intestine. Ir­ritating factors for these organs are muscular strain, especially spasms, and elevation of the intravisceral pressure, which are caused by disorders of nervous regulation.

The acid factor acting on the motor function of the stomach and the duodenum, and also changes in the mucosa of these organs are very impor­tant in the aetiology of pain in peptic ulcer disease.

Vomiting occurs in 70—75 per cent of patients. It arises without preliminary nausea, at the height of pain, and relieves it. The vomitus is acid to taste and smell. Secretion of the gastric juice in a fasting stomach is often attended by vomiting as well.

Heartburn is encountered in 60—85 per cent of patients. It occurs not only during exacerbations but can also precede exacerbation for several years; it can be periodic or seasonal. The mechanism of heartburn is associated with motor dysfunction of the oesophagus (in addition to the acid factor of the gastric contents, which was formerly believed to be decisive).

Eructation, regurgitation, and salivation are frequent symptoms. Ap­petite is often increased. Regular connection between meals and develop­ment of pain is the cause of a morbid fear of eating (cibophobia).

The intestinal symptoms of peptic ulcer disease are constipations, which are closely connected with the character of nutrition and bed-rest

during exacerbations, and are mainly connected with reflex dyskinesia of the small and large intestine.

Wasting is characteristic of exacerbations. The skin and mucosa are pallid after haemorrhage. The tongue is usually clean. The configuration of the abdomen is normal. In the presence of pyloric stenosis peristaltic and antiperistaltic movements of the epigastrium can be seen. Brown pigmentation develops on the abdomen after prolonged application of warmth. During exacerbations, the epigastric region is tender to surface palpation; if the peritoneum is involved (positive Mendel's test) the muscles are strained. Late splashing sound to the right of the median line (Vasilenko's symptom) indicates gastric evacuatory dysfunction or increas­ed secretion between meals.

Gastric secretory function. If the ulcer is found in the stomach, hydrochloric acid, pepsin, mucoprotein and albumin fractions of the gastric juice vary within normal limits. In duodenal ulcer all these indices singificantly exceed normal values. Hypersecretion of the gastric juice is determined in this case by hypersensitivity of the vagus, intensified adrenal function, and increased quantity and hypersensitivity of the parietal cells. Study of the basal secretion of a fasting stomach is very important for the diagnosis of duodenal ulcer. In the presence of active basal secretion and specific complaints of the patient, he should be given the appropriate treat­ment despite negative results of X-ray examination.

The motor function of the stomach and duodenum is upset in peptic ulcer. This is the leading factor in the development of the main symptoms, e.g. pain, nausea, vomiting, and heartburn. Upset motor function in­creases the tone of the stomach and the duodenum, intensifies their peristalsis, and disturbs periodicity of their activity. The observed changes in the motor function are not specific for peptic ulcer disease and cannot therefore be regarded as its diagnostic signs. But a certain regularity of these changes can indicate the stage of the disease and be a criterion for the objective judgement about the efficacy of treatment.

Latent haemorrhage is almost always revealed on examination of faeces during exacerbation of peptic ulcer.

X-ray examination. A direct proof of peptic ulcer is a niche which is found in 75—80 per cent of patients. The ulcer is usually located on the lesser curvature (Fig. 86). It has the regular J shape, the barium depot ex­tending beyond the normal contour of the stomach. In duodenal ulcer, the niche can be found inside the bulb or outside it (extrabulbar ulcer).

In the absence of direct X-ray signs (the absence of a niche), indirect symptoms become important. These are intensified peristalsis of the stomach, and the presence of a thick layer of secretion between the air and the contrast substance.

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Fig. 86. X-ray of ulcer of the lesser curvature.

Gastroscopy. Gastroscopy is used to reveal gastric ulcer; if gastroscopy is repeated, it shows the cicatrization process. A fibroscope can be used not only to view the stomach, but the duodenum as well. Ulcers that fail to be detected by X-rays can be revealed by gastroscopy, which is also important for differentiation between benign and malignant changes (sighting biopsy).

Course. Four stages are distinguished in the clinic of peptic ulcer: stage I (" prelude to ulcer", according to M. Konchalovsky) is characterized by a marked disorder in the activity of the vegetative nervous system and gastroduodenal dysfunction; stage II is attended by development of organic changes (gastroduodenitis); stage III is formation of an ulcer; and stage IV is development of post-ulcerous processes.

This classification of ulcer stages is only conventional but still useful because it may help the physician to establish early diagnosis. Remission

periods last from several months to many years. Exacerbations continue for 4-6 weeks. Cicatrization of the ulcer is completed in 6-8 weeks. Remission may occur without treatment. Seasonal exacerbations are more characteristic of duodenal ulcer. Unless complicated by haemorrhage or perforation, peptic ulcer is never fatal.

Haemorrhage. This is the most frequent complication. It may be manifested by haematemesis (blood vomiting) and tarry faeces (melaena). Among other causes of gastric haemorrhage, peptic ulcer is accounted for 60-65 per cent. Gastric ulcers bleed more often than others. Vomiting may be absent in duodenal ulcer, and the first signs of haemorrhage are sudden weakness, giddiness and palpitation (before the appearance of tarry stools). The patient's general condition depends on the length and intensity of bleeding.

Perforation. Predisposition to open perforation depends mainly on anatomical factors: the probability of perforation is especially high in loca­tion of the ulcer on the anterior wall of the duodenum. Perforation may occur in the absence of patient's complaints (" silent ulcer") or the ap­propriate anamnesis. Signs of perforation are a sudden stabbing pain, the reflex collapse, acute abdomen, and progressive peritonitis (unless a timely surgical aid is given to the patient). The pain is felt beneath the xiphoid process or in the right hypochondrium. The abdominal wall is tense. The patient assumes a forced posture on his back; the tongue is dry and coated. The pulse is retarded, the temperature is subnormal. In most cases the diagnosis is undoubtful and a timely surgical intervention saves the patient's life.

Stenosis. Ulcers heal to leave scars. If the ulcer was in the pylorus, the cicatricial tissue may narrow the lumen and interfere with free passage of the gastric contents into the duodenum. First the narrowing is compensated for by hypertrophy of the gastric muscles, but later the stomach becomes distended, food stays inside it for a longer period, and fermentation and putrefaction occur in the stomach. Absorption of water is impaired (the impairment begins in the duodenum). This upsets the water-salt balance, causes general dehydration of the body, and decreases the chloride content in the blood and urine.

Patients complain of permanent pain (which intensifies by night), eruc­tation with rotten egg wind, and profuse morning vomiting with food that was ingested several days ago. Constipation is alternated with diarrhoea, through irritation of the small intestine by fermented food discharged into it from the pylorus which is opened by intensified peristalsis. If stenosis is pronounced, the patient is cachectic. Examination of the epigastrium reveals peristaltic and antiperistaltic contractions of the stomach. Late splashing sound can be heard.

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Treatment and prophylaxis. Anti-ulcer treatment implies combined and individual therapy. Non-complicated peptic ulcer is treated conservatively. Exacerbations should be treated in hospital where bed-rest, special diet medicinal preparations (tranquilizers, cholinolytics, antacids) and thermal procedures are given. The diet should not stimulate the secretory function of the stomach. It should decrease the motor function of the gastroduodenal system and have buffer properties. The diet should also be sparing with respect to its chemical and mechanical effect on the stomach.

Patients in remission should be regularly observed in out-patient condi­tions. Smoking and alcohol are prohibited in peptic ulcer disease. Attend­ing diseases should also be treated and sanation of the mouth carried out. Sanatorium and health-resort therapy is indicated. Employment of patients should be sparing. Persons with " irritated" stomach (functional stage of peptic ulcer) should be regularly observed in out-patient conditions.

Prophylactic measures should be aimed at prevention of the disease, its relapses or complications. Current knowledge of the developmental mechanisms of peptic ulcer suggests that population should be given infor­mation on rational nutrition, labour, and rest. The adverse effect of alcohol and smoking should be especially emphasized.