Questions to control the knowledge
1. What common diseases of the respiratory system do you know?
2. Croupous pneumonia: etiology and pathogenesis, stages of development; complications (pulmonary, non-pulmonary, atypical forms).
3. Name acute destructive processes in the lungs. What is abscess, gangrene of the lung?
4. What pathological processes are called chronic nonspecific lung diseases?
5. What changes develop in the lungs in bronchiectasias?
6. Concept of «bronchoectatic disease». What are as complications?
7. Are pneumosclerosis andpneumocirrhosis independent diseases or unfavorable outcome of other diseases of the lungs?
8. Concept of emphysema of the lungs. What are the forms of emphysema?
9. Precancerous conditions of the lungs?
10. Name clinico-anatomical classification of lung cancer: a) according to the localization, b) according to the character of growth, c) according to the microscopic picture, d) according to the character of complications.
Croupous pneumonia, abscess, gangrene, pneumonitis, pleuritis, bronchiectasias, pneumofibrosis, emphysema, fibrous alveolitis, spontaneous pheumothorax, bullous emphysema, intracapillary sclerosis, pneumocirrhosis, chronic bronchitis, chronic pneumonia, bronchopneumonia, stage of inflow, stage of red hepatization, stage of grey hepatization.
DISEASES OF ALIMENTARY SYSTEM
DISEASES OF THE ESOPHAGUS
From its origin at the cricoid cartilage to its termination at the esophagogastric junction, the esophagus is normally lined by stratified non-keratinising 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 neutrophils, 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. Intraepithelial 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 epithelium, 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 clinical intervention.
Esophageal varices are an important cause of vomiting blood. At the lower end of the esophagus the submucosal venous plexus drains into both the
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.
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.
Pseudomembranous 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.
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 an 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 pylori, by Australian workers Marshall et al. The Sidney System is a new classification based on this recent new knowledge. 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. pylori 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 fundal 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 of
the mucosal glands to resemble closely those of the intestine.
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.
Focal chronic gastritis
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 epithelium 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.
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» may be 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.
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. 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
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.
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 ulcersmay be single or multiple. They tend to be encountered in what might be regarded as «stressful» situations. They are seen, for example, in patients with extensive burns, especially infants, and as complication of lesions of the CNS or chronic debilitating disease both in adults and children. Chronic ulcersmay 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. 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.
Results and complications of peptic ulceration
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 «hour-glass» 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, or to «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.
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.
Gastric carcinoma (See Epithelial tumors).
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. 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. In most 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.
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 fulminant 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 local 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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