1. Centriacinar (cenrolobular) emphysema. The distinctive feature of this type is the pattern of involvement of the lobules; the central or proximal parts of the acini, formed by respiratory bronchioles, are affected, whereas distal alveoli are spared. The walls of the emphysematous spaces often contain large amount of black pigment. Inflammation around bronchi and bronchioles and in the septa is common. Moderate-to-severe degrees of emphysema occur predominantly in heavy smokers, often in association with chronic bronchitis. In addition, some lesions of so-called coal workers’ pneumoconiosis bear a striking resemblance to centriacinar emphysema.
2. Panacinar (panlobular) emphysema. In this type the acini are uniformly enlarged from the level at the respiratory bronchiole to the terminal blind alveoli. This type of emphysema is associated with alpha-1-antitrypsin deficiency.
3. Paraseptal (distal acinar) emphysema. In this type the proximal portion of the acinus is normal, but the distal part is dominantly involved. The emphysema is more striking adjacent to the pleura, along the lobular connective tissue septa, and at the margins of the lobules. This type of emphysema probably underlies many of the cases of spontaneous pneumothorax in young adults.
4. Irregular emphysema, so named because the acinus is the irregularly involved, is almost invariably associated with scarring. Thus, it may be the most common form of emphysema, as careful search of most lungs at autopsy shows one or more scars from a healed inflammatory process. In most instances, these foci of irregular emphysema are asymptomatic.
Types of emphysema according to cause
1. Compensatory E. This term is sometimes used to designate dilation of alveoli but not destruction of septal walls in response to loss of lung substance elsewhere. It is best exemplified by the hyperexpansion of the residual lung parenchyma that follows surgical removal of a diseased lung or lobe.
2. Obstructive overinflation refers to the condition in which the lung expands because air is trapped within it.
3. Senile E. refers to the overdistended, sometimes voluminous lungs found in the aged.
Bullous E. refers merely to at any form of E. that produces large subpleural blebs or bullae (spaces more than 1 cm in diameter in the distended state).
4. Interstitial E. The entrance of air into the connective tissue stroma of the lung, mediastinum, or subcutaneous tissue is designated interstitial emphysema.
Morphology
The diagnosis and classification of the emphysemas are based on naked eye (or hand lens) examination of lungs fixed in a state of inflation.
Panacinar emphysema, when well developed, produces voluminous lungs, often overlapping the heart and hiding it when the anterior chest wall is removed.
The macroscopic signs of centriacinar emphysema are less impressive. The lungs may not appear particularly pale or voluminous unless the disease is well advanced.
Generally, the upper two-thirds of the lungs are more severely affected.
Large apical blebs or bulla are more characteristic of irregular emphysema secondary to scarring.
Microscopical examination is accessory to visualize the abnormal fenestrations in the walls of the alveoli, the complete destruction of septal walls, and the distribution of damage within the pulmonary lobule. With advance of the disease, adjacent alveoli fuse, producing even larger abnormal airspaces and possibly blebs or bulla. Often the respiratory bronchioles and vasculature of the lung are deformed and compressed by the emphysematous distortion of the airspaces, and, as mentioned, there may or may not be evidence of bronchitis or bronchiolitis.
Bronchial Asthma (BA)
Bronchial asthma is a disease characterized by hyper-reactive airways, leading to episodic, reversible bronchoconstriction, owing to increased responsiveness of the tracheobronchial tree to various stimuli. A severe and unremitting type of the disease termed status asthmaticus may prove fatal.
Pathogenesis
Chronic airway inflammation involving many cell types and inflammatory mediators accompanies the bronchial hyper-responsiveness of asthma.
Nevertheless, the relationship of the inflammatory cells and their mediators to airway hyper-reactivity is not fully understood.
Classification
1. Extrinsic BA is initiated by a type 1 hypersensitivity reaction induced by exposure to an extrinsic antigen. Subtypes include atopic (allergic), BA, occupational BA (many forms), and allergic bronchopulmonary aspergillosis (bronchial colonization with aspergillus organisms followed by development of IgE antibodies).
2. In contrast, intrinsic BA is initiated by diverse, nonimmune mechanisms, including aspirin, pulmonary infections; especially those caused by viruses, cold, inhaled irrigants (pollutants such as sulfur dioxide), stress, and exercise.
Morphology
The morphologic changes in asthma have been described principally in patients dying of status asthmaticus, but it appears that the pathology in nonfatal cases is similar.
Grossly, the lungs are overdistended because of overinflation, and there may be small areas of atelectasis.
The most striking macroscopic finding is occlusion of bronchi and bronchioles by thick, tenacious mucous plaques.
Histologically, the mucous plaques whorls of shed epithelium, which give, rise to the well-known Curschmann’s spirals.
Numerous eosinophils and Charcot-Leyden crystals are present.
The other characteristic histologic findings of BA include:
- Thickening of the basement membrane of the bronchial epithelium.
- Edema and inflammatory infiltrate in the bronchial walls, with a prominence of eosinophils, which form 5 to50% of the cellular infiltrate.
- An increase in size of the submucosal glands.
- Hypertrophy of the bronchial wall muscle, a reflection of prolonged bronchoconstriction.
- Emphysematous changes sometimes occur, and if chronic bacterial infection has supervened, bronchitis may occur.
The classic asthmatic attack lasts up to several hours and is followed by prolonged coughing; the raising of copious mucous secretions provides considerable relief of the respiratory difficulty. In some patients, these symptoms persist at a low level all the time. In its most severe form, status asthmaticus, the severe acute paroxysm persists for days and even weeks, and, under these circumstances, ventilatory function may be so impaired as to cause severe cyanosis and even death.
Chronic Lung Abscess (LA)
The term “LA” describes a local suppurative process within the lung characterized by necrosis of lung tissue.
Oropharyngeal surgical procedures, bronchial infections, dental sepsis, and bronchiectases play important roles in their development.
The causative organisms are introduced by the following mechanisms:
- Aspiration of infective material.
- Antecedent primary bacterial infection.
- Septic embolism.
- Obstructive tumors.
- Direct traumatic punctures.
- Miscellaneous.
When all these causes are excluded, there are still cases in which no reasonable basis for the LA formation can be identified. These are referred to as “primary cryptogenic” LA.
Morphology
Abscesses vary in diameter from lesions of a few millimeters to large cavities of 5 to 6 cm.
They may affect any part of the lung and may be single or multiple.
The cavity may or may not be filled with suppurative debris, depending on the presence or absence of a communication with one of the air passages.
When such communications exist, the contained exudate may be partially drained to create an air-containing cavity.
Superimposed saprophytic infections are prone to flourishing within the already necrotic debris of the abscess cavity.
Continued infection leads to large, fetid, green-black, multilocular cavities with poor demarcation of their margins, designated gangrene of the lung.
The cardinal histologic change in all abscesses is suppurative destruction of the lung parenchyma within the central area of cavitation.
A reactive fibrous wall often surrounds chronic abscesses.
Complications include extension of the infection into the pleural cavity, hemorrhage, the development of brain abscesses or meningitis from septic emboli, and rarely reactive secondary amyloidosis.
Idiopathic Pulmonary Fibrosis
Diffuse interstitial fibrosis occurs as a result of different pulmonary diseases. It is so called “idiopathic pulmonary fibrosis” or “cryptogenic fibrosing alveolitis” or “chronic interstitial pneumonitis”
Morphology
Pathological changes are bilateral and widespread.
Macroscopically the lungs are dense, reduced volume.
Honey-combing (i.e. enlarged, thick-walled air spaces) develops in parts of lung. Microscopically, changes vary according to the stage of the disease with formation of hyaline membranes.
There is edema and cellular infiltrate in the alveolar septa in early stage.
There is organization of the alveolar exudate and replacement fibrosis in the alveoli and in the interstitial septal wall with variable amount of inflammation in advanced stage.
DISEASES OF ALIMENTARY SYSTEMS
Tonsillitis
Tonsillitis is infectious disease and is characterized by inflammatory changes in the crypts of the adenoids and the tonsils on the anterior wall of the pharynx.
Tonsillitis can be acute and chronic.
Etiophathogenesis
Infectious agents are staphylococcus, streptococcus, adenovirus and bacterium’s assotiations.
Transephithelial, hematogenic pathways are responsible for the transmission. Autoinfection is most often cause of tonsillitis against a background the cooling and trauma
Acute edema and erythema, and sometimes purulent exudates and abscesses, may develop in the crypts of the adenoids and the tonsils on the anterior wall of the pharynx.
Lymphoid tissue is distributed on the posterior pharyngeal wall and under the tongue, but not as masses of nodes with crypts such as composes the palatine adenoids and facial tonsils.
Tonsils and adenoids are usually unapparent in early infancy, but gradually undergo hypertrophy and hyperplasia to rich their relatively greatest mass between 2 and 5 years of age.
Their location is such that they are exposed to inspired air and food and whatever antigens may be carried in either one. These tissues are part of the bursal system of immunity and consist mostly of B cells.
Classification
Acute tonsillitis:
Cattharal tonsillitis is characterized by hyperemia and serous or mucous leucocytic infiltration.
Fibrinous tonsillitis the deposition of whitish-yellowish fibrinous films (in diphtheria) occurs.
Purulent tonsillitis is characterized by phlegmonous inflammation or the formation of abscesses. Tonsils are enlarged due to edema and leucocytic infiltration.
Follicular tonsillitis is characterized by hyperplasia of tonsils. Leucocytic infiltration and necrosis of follicles take place. Tonsils are enlarged and hyperemic.
Cryptous tonsillitis is characterized by the deposition of the serous, mucous or purulent exudates, which are located in crypts.
Necrotic tonsillitis the ulceration occurs and can be in leukemia and scarlet fever.
Gangrenous tonsillitis the ulceration and hemorrhages occurs also.
Chronic tonsillitis
Chronic tonsillitis is characterized by the persistence of infection or due to relapse of acute tonsillitis.
Hyperplasia and sclerosis of lymphoid tissue, sclerosis of tonsil’s capsule, increasing of crypts, ulceration of the epithelium are morphological features of chronic tonsillitis.
Chronic infection can present as anorexia, failure to gain weight, low-grade fever, or recurrent sore throats with high fever. Hypertrophy can be considerable and lead to mouth breathing, or even upper airway obstruction, retention, sleep apnea, and, rarely, cor pulmonale.
Persistent anterior and posterior cervical adenopathy in the absence of generalized lymphadenopathy is evidence of chronic or recurrent infection. Inspection of the tonsils is of limited help during acute episode.
Complication of tonsillitis
Extension of tonsillar infection can take place in the surrounding tissues and is called peritonsillar abscess or quinsy. The retropharyngeal nodes drain both the adenoids and the nasopharynx and can become chronically infected. This is known as retropharyngeal abscess.
These complications of tonsillitis are usually caused by B-hemolytic streptococci, which are almost sensitive to penicillin. Consequently, the widespread use of antibiotics to treat streptococcal pharingitis has been associated with less suppuration in the peritonsillar of retropharyngeal spaces.
Peritonsillar cellulitis and abscess are characterized by an extremely sore throat and often high fever. If the condition is untreated, it may lead to significant swelling and even occlusion of the oral pharynx.
Retropharyngeal abscess is virtually limited to infants in the first 2 years of life. The characteristic findings and fever, hyperextension of the neck, dysphagia, and noisy respirations. There is prominence of the infected pharyngeal wall but swelling is almost always unilateral.
The importance of this disease is that it is commonly a precursor of rheumatic fever or one form of glomerulonephritis.
Gastritis
Gastritis is an inflammation of gastric mucosa and can be acute and chronic.
Acute gastritis
Acute inflammation develops due to injury of the mucosa by the alimentary, drugs, toxic and bacterial agents.
Morphologic classification of acute gastritis:
Catarrhal gastritis.
Fibrinous gastritis.
Phlegmonous gastritis.
Necrotic (or Corrosive).
Hemorrhagic gastritis.
Pseudomembranous.
Chronic gastritis
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.
Collectively constitute a morphologic continuum of increasingly intense inflammation of mucosa accompanied by progressively more marked atrophy of the mucosa glands.
Glandular atrophy is often accompanied by metaplasia, dysplasia and atypia of the surface epithelium.
Our understanding of the etiology and mechanism of gastritis and gastroduodenal ulceration has been radically altered by the discovery of specific infective agent Helicobacter pylori.
The Sidney System is a new classification based on this recent new knowledge. It incorporates two separate divisions: histological and endoscopic.
Clasification
The histological classification incorporates three main positions:
1. Etiology.
2. Topography (i.e.-site affected: antrum, body or both).
3. Morphology (including information about activity, intestinal metaplasia - graded as mild, moderate or severe).
The three main types of chronic gastritis are examples of this classification according to topography use:
I. Autoimmune associated chronic pangaslritis with severe atrophy (Type A fundal gastritis)
Associated with circulating antibodies to parietal cells and intrinsic factor and complete loss of parietal cells.
Loss of parietal cells leads to hypo- or achlorhydria, hypergastrinemia, inadequate synthesis of intrinsic factor and vitamin B12 absorption.
Overt pernicious anemia develops in 10%.
Associated with Hashimoto’s thyroiditis and Addison’s disease, hence the term autoimmune gastritis.
Intestinal metaplasia and dysplasia may occur and possibly resulting in gastric carcinoma.
II. Helicobacter pylori associated chronic gastritis of the antrum with moderate activity (Type B gastritis)
The most common form of gastritis in all age groups.
Background factors are environmental such as intoxication, abnormal dietary, and alcohol.
Associated with gastric atrophy, intestinal metaplasia, gastric polyps, and gastric cancer.
Initially superficial, gradually becomes deeper to affect the entire mucosa with glandular atrophy, leading to “chronic atrophic gastritis”.
Colonization of mucous layer and surface of mucosal cells with curved organisms, with little to no tissue invasion, confined to areas of gastric mucosa.
Small foci of neutrophils, some passing to surface or into superficial crypt lumen occur, superimposed on a variable background of chronic gastritis (active chronic gastritis with abundant neutrophils).
III. Reflux-gastritis (formerly known as Type C gastritis)
Associated with reflux of duodenal contents in stomach.
May occur after gastric surgery, or with weakened pyloric sphincter tone.
Localization is antrum.
Achlorhydria and hypergastrinemia is absent.
According to topography
1. Antral gastritis.
2. Fundal gastritis.
3. Pangastritis.
According to morphology
Chronic superficial gastritis (early stage): lymphocytes and plasma cells in the upper third of the lamina propria, some mucosal flattening.
Chronic atrophic gastritis (later stage): flattening of rugal folds, mucosa thinned and flattened, chronic inflammation of full thickness of the mucosa, loss of glands, metaplasia of mucosa to the intestinal type.
Peptic Ulcer Disease
Ulcerative disease is chronic disease with development chronic recurrent peptic ulcer.
Background factors:
Age. Often diagnosed in middle-aged to elder adults, but may appear in young adult life.
Common in industrialized nations.
Sex. Mail-female ratio 3:1.
Familial tendency and genetic factors for duodenal ulcer.
Environmental and geographical factors.
Dietary habits.
The ingestion of drugs (especially aspirin, corticosteroids).
Stresses may be important.
Cigarette smoking and alcohol.
Pathogenesis
Hypersecretion of gastric juice and emotional factors have been considered to be important in the pathogenesis of peptic ulcers. The gastroduodenal mucous membrane is protected against digestion of normal gastric secretions not only by its mucus coating but also by dilution and neutralization with swallowed food, saliva, and regurgitated duodenal fluids. This is considered to be the result of vagal stimulation and can be abolished by section of the vagus nerve. The spiral bacterium Helicobacter (campylobacter pylori) has been frequently isolated from patients with gastritis or peptic ulcer disease, but its pathogenic role remains to be determined. Prostaglandin deficiency has also been implicated as a possible cause of peptic ulcer disease.
For duodenal ulcers, the most important cause is excess exposure to acid and pepsin. Major influences for duodenal ulcers:
Hypertone of vagus with increasing of acid-peptic factors.
Abnormally rapid gastric emptying, exposing the duodenum to a greater acid load.
Increasing of the level of ACTG and glucocorticoids.
Duodenal ulcer has been associated with tension, stress, and anxiety but this is by no means always the case and there is no agreement on the importance of stress in its pathogenesis.
For gastric ulcers, breakdown in mucosal defenses appears to be most important. Major influences for gastric ulcers:
Suppression of hypothalamic and hypophysic functions.
Hypotone of vagus and decreasing of gastric secretion.
May involve decreased pyloric sphincter tone, and reflux of bile acids.
Weakening of protective factors of gastric mucosa.
Exogenous agents that damage the mucosa are more likely to cause gastric ulcers than duodenal ulcers (alcohol, drugs, chemical substance).
Possible defect in gastric mucus with the presence of Helicobacter.
Morphogenesis and morphology
I. Erosion is superficial necrosis of mucosal epithelial elements.
These are tiny ulcers, a few millimeters in diameter, which are formed by the digestion of the mucosal membrane overlying small hemorrhage.
They are usually multiple and affect all parts of the stomach.
They occur mostly on the apex of mucosal folds and involve only the mucosa.
Note that the changes are superficial so that restoration to normal can very quickly occur.
II. Acute ulcer
Loss of tissue penetrating into the submucosa.
Location: single or multiple lesions throughout the stomach and duodenum.
Circular and small, less than 1 cm in diameter.
Inflammatory reaction absent initially, develops secondarily.
Massive hemorrhage may be fatal.
Perforation can lead to peritonitis.
This type of ulcer usually heals without a visible scar.
III. Chronic peptic ulcer
The term “chronic” is applied when the pathological changes have penetrated and destroyed the muscle coat; they are also, of course, of much longer duration than acute ulcers.
Gastric ulcers are located along the distal lesser curvature, usually within about 5 cm of the pylorus.
Duodenal ulcers usually occur in the first centimeter or two distal to the pylorus on the anterior or posterior wall rather that laterally (kissing ulcers).
Classic peptic ulcer is small (about 1 cm in the duodenum; 1 to 2,5 cm in the stomach), round-to-oval. It is characteristically “punched out”, with sharply defined margins, and has overhanging mucosa producing a flashlike appearance. Its edges are not raised, and the mucosal folds covering on the ulcer are distinct to its edge. Frequently it has a terraced structure.
Malignant gastric ulcers are generally bowel shaped, with margins that are usually sloped and generally without overhanging mucosa. The edges are raised and indurated, and nodular mucosal or submucosal thickening interrupts the mucosal folds toward the crater.
Microscopically:
The bed of the ulcer is covered by fibrinous exudate containing fragmented leukocytes.
Fibrinoid necrosis.
Granulation tissue with plasma cell and lymphocytic infiltration.
Fibrous tissue.
The principal complications of peptic ulcer
I. Ulcerative-destructive:
Perforation. Anterior duodenal ulcers may perforate into the free peritoneal cavity, with resultant peritonitis. The peritonitis from perforated peptic ulcer is initially a chemical inflammation, but bacterial contamination soon follows. 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 that may later infect the pleura.
Penetration. Extension of the inflammation to the serous coat may result in adhesion to the adjacent organs. Perforating posterior ulcers more often penetrate the pancreas, producing intractable pain. Posterior perforation also may occur into the lesser peritoneal sac, leading to localized peritonitis. The omentum or adhesions to adjacent organs may also serve to localize peritoneal inflammation.
Hemorrhage. Both gastric and duodenal ulcers are subject to massive hemorrhage. Duodenal ulcers are especially prone to perforation. Any ulcer, but especially those located posterior, may bleed in smaller amounts, producing melena or evidence of occult blood in the stool. It may be abundant and give rise to “coffee-grounds” vomit. Sometimes a major artery may be eroded and a large, even fatal, hemorrhage takes place.
II. Ulcerative- cicatricial (obstruction or healing and scarring).
Pyloric obstruction may be a complication of an ulcer, gastric or duodenal, situated near the pylorus. It usually results from a combination of cicatricial narrowing and spasm.
Scarring in the duodenum may lead to serious stricture (pyloric stenosis). The stomach becomes greatly dilated and hypertrophied and lead to chronic vomiting with alkalosis and malnutration.
III. Malignization.
The development of carcinoma has been reffered to as one of the complications of peptic ulcer. It seems probable that carcinoma can develop in a preexisting ulcer, but it is equally probable that it is a rare event. It is extremely difficult to establish the occurrence of such a sequence of events in any particular case.
IV. Inflammatory (gastritis, perigastritis, duodenitis, periduodenitis).
V. Mixed.
Appendicitis
Appendicitis results in severe acute or chronic inflammation of the vermiform appendix.
Acute appendicitis
Acute appendicitis is the most common acute abdominal condition requiring surgery.
Acute appendicitis is uncommon at the extremes of age and it is most frequently seen in elder children and young adults.
The most important factor in its pathogenesis is obstruction of the lumen, with the most frequent cause being a fecalith, a molded mass of inspissated fecal material that may develop rock-hard consistency.
Other causes of obstruction are scars representing a residuum of previous attacks of appendicitis, tumors, external bands, and adhesions, rarely masses of parasites, foreign bodies, and possibly spasm of the muscle at the base of the appendix.
The immediate cause of acute appendicitis is bacterial infection from the intestinal lumen, though bacterial invasion from the bloodstream in systemic disease is possible.
The appendix may be involved in diseases primarily affecting other portions of the gastrointestinal tract, such as Crohn’s disease, typhoid fever, and amebiasis, and in certain systemic diseases (such as measles).
Clinical-morphological classification of acute appendicitis
Simple appendicitis is characterized by hyperemia; small hemorrhages and primary affect including small foci leucocytes.
Superficial appendicitis is characterized by focus of suppurative inflammation in mucosa and edema. Serous membrane is dim.
Destructive forms:
Flegmonous appendicitis occurs the diffuse infiltration of leucocytes in wall of appendix. Gross appearance: appendix is increased, swollen; tense and markedly congested and covered by fibrinous exudate.
Flegmonous-ulcerative appendicitis is characterized by flegmonous inflammation with necrosis and ulceration in mucosa.
Apostematous appendicitis the formation of small abscesses occurs. The primary inflammatory lesion may increase in intensity and lead to a small abscess in the wall, and this may perforate.
Gangrenous appendicitis occurs large areas of necrosis, the immediate antecedent of rupture and may has two causes:
Thrombosis and thromboembolism of mesentery artery (primary gangrene of appendix) due to obstraction of the lumen by fecoliths.
Thrombosis due to development of periappendicitis (secondary gangrenous appendicitis).
The complications of acute appendicitis
Necrosis of appendix wall (gangrenous appendicitis), leading to perforation, with subsequent generalized peritonitis.
Involvement of adjacent bowel loops, causing perforation of small bowel.
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.
Empyema of appendix due to obstruction of proximal parts.
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.
Chronic appendicitis
Chronic appendicitis is characterized by sclerosis and atrophy, lipomatosis and diffuse infiltration by lymphocytes and hystiocytes.
Obliteration of part or all of the appendiceal lumen by a mixture of fibrous tissue, lymphocytes, lymphoid follicles, and nerve bundles is common.
In the fibrosis causes complete of the lumen, continued mucous secretion might result in cystic dilatation – mucocele.
Such a cyst may rupture, giving rise to myxoma peritonei: the mucus-secreting epithelium is spilled into the peritoneal cavity and loculations of mucin and adhesions result.
Surgically removed appendix may be histologically normal (false-positive clinical diagnosis). If the appendix is normal, but clinical cymptomes took place is called “false appendicitis”. It may be due to mimicking acute appendicitis some diseases: salpingitis, ectopic pregnancy, Meckel’s diverticulitis, peptic ulcer, and pain cause by trivial pelvic bleeding at the time ovulation.
DISEASES OF THE LIVER
There are various diseases of the liver.
In some instances, the disease is primary to the liver, as in viral hepatitis and hepatocellular carcinoma.
More often the hepatic involvement is secondary, often to some of the most often diseases in humans, such as cardiac decompensation, disseminated cancer, alcoholism, and extrahepatic infections.
Some general aspects of liver disease are reviewed.
Morphologic patterns of hepatic injury
The liver is an inherently simple organ, with a limited repertoire of responses to injurious events. Regardless of cause, five general reactions may occur.
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