Gastrointestinal pathology

Associate professor Bagriy M.M.

 The plan
• Tonsillitis
• Gastritis
• Peptic Ulcer Disease
• Gastric Carcinoma
• Appendicitis
• Regional Enteritis (Crohn’s Disease)
 Tonsillitis

Tonsillitis or angina is an infectious disease with evident

inflammatory changes of the lymphoid tissue of the
pharynx and tonsils.

•Tonsillitis can be acute and chronic.

•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 tonsillitis is divided according to the character of inflammation
•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 the enlargement of the tonsils due
to their swelling and neutrophil infiltration. According to the character of the
suppurative inflammation, this type is subdivided into quinsy (angina) and
abscess tonsillitis.
•Follicular tonsillitis - is characterized by hyperplasia of tonsils. Leucocytic
infiltration and necrosis of follicles take place. Tonsils are enlarged and
hyperemic.
•Lacunar tonsillitis - is characterized by the accumulation of serous, mucous
or suppurative exudation in the depth of lacunas. It can be seen on the
surface of the swollen tonsils in the form of yellow coats which are easy to
remove.
•Necrotic tonsillitis - one observes superficial or deep necrosis of the
mucous tunic of tonsils with haemorrhage. It can be in leukemia and scarlet
fever.
•Gangrenous tonsillitis – is characterized by tissue destruction. It can be in
leukemia and scarlet fever as well.
Fibrinous tonsillitis
Purulent tonsillitis
Follicular tonsillitis

Lacunar tonsillitis
Necrotic tonsillitis
 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.
 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.
•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 importance of this disease is that it is commonly a
precursor of rheumatic fever or one form of
glomerulonephritis.
 Tonsillitis forms and complications

Acute Chronic

catarrhal
Complications
fibrinous
Rheumatism
lacunar
Glomerulonephritis
follicular
Complications
suppurative
Retropharyngeal
abscess
necrotic
Ludwig's angina
gangrenous
Thrombophlebitis

Sepsis
 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.

According to affected area there are distinguished:

•Acute diffuse gastritis;
•Acute focal gastritis (fundal part, antral, piloroantral and
pyloroduodenal).
 Morphologic classification of acute gastritis:
• Catarrhal gastritis.
• Fibrinous gastritis.
• Phlegmonous gastritis.
• Necrotic (or Corrosive).
• Hemorrhagic gastritis.
• Pseudomembranous.
•Catarrhal (simple) gastritis (gastritis cataralis s. simplex) - the
mucous tunic is thickened, swollen and hyperaemic, its surface is
covered with a lot of mucus. Histologically one finds dystrophy and
desquamation of the superficial epithelium, with the formation of
erosions. When they are numerous, it is called erosive gastritis.

Endoscope research
•Fibrinous gastritis (gastritis fibrinosa) - can be manifested in
the form of catarrhal or diphtheritic inflammation. In this case
the mucous tunic is covered with a fibrinous coat of grey or
yellow-brown colour.
•Suppurative (phlegmonous) gastritis (gastritis phlegmonosa) -
is a serious disease occurring due to stomach trauma,
stomach ulcer and ulcerative gastric carcinoma. The mucous
tunic is drastically thickened, folds are thick with
haemorrhages and fibrinous-suppurative deposition.
Leucocytic infiltration penetrates all stomach layers and the
surrounding peritoneum, leading to the development of
perigastritis and peritonitis.
•Necrotic (corrosive) gastritis (gastritis necrotica s. corrosiva) -
is the result of acid and alkali influence on the mucous tunic of
stomach, when they coagulate and destroy it. The necrotic
process may lead to the development of phlegmon and even
perforation.
Suicidal ingestion of potassium permanganate crystals
 Outcomes
•Catarrhal gastritis treated in time ends with
recovery but it may sometimes be recurrent and
develop into the chronic form.
•Necrotic and phlegmonous gastritis end with
sclerotic deformation of the organ – gastric
cirrhosis.
 Chronic gastritis
•Chronic gastritis (gastritis chronica) is a different disease with its own etiology
and pathogenesis, rarely connected with acute gastritis.
•Chronic gastritis is characterized by chronic dystrophic and necrobiotic
changes of the mucous tunic epithelium in combination with regeneration
disorder and structural change of the mucous tunic. The process ends with
atrophy and sclerosis. 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.
•The factors that can disturb the regenerative process are important for the
etiology of chronic gastritis.
•First and foremost, these are exogenous factors – eating pattern disorder,
alcohol abuse, the effect of thermal, chemical and mechanical stimuli.
•Among the endogenous factors the greatest attention is paid to autoinfection,
in particular Helicobacter pylori, to chronic autointoxication, endocrine and
cardiovascular diseases, allergic reactions and duodenogastric reflux.
•Regeneration disorders mainly influence the slowing-down of differentiation
of the parietal cells. Immature cells that perish early before the differentiation
is completed appear.
 Classification of gastritis

The histological classification incorporates three

main positions:
1. Etiology.
2. Topography (antrum, body or both).
3. Morphology (including information about activity,
intestinal metaplasia - graded as mild, moderate or
severe).
 There are three main types of chronic gastritis
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 Helicobacter pylori
and environmental such as intoxication,
abnormal dietary, alcohol. Helicobacter
pilori is found out in 100% of patients;
•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”.
•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).
Gastritis is often accompanied by infection with Helicobacter
pylori. This small curved to spiral rod-shaped bacterium is found in
the surface epithelial mucus of most patients with active gastritis.
The rods are seen here with a methylene blue stain.
 III. Reflux-gastritis
(formerly known as Type C gastritis, chemical
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 morphology
• Chronic superficial gastritis (early stage, nonatrophic gastritis ) -
lymphocytes and plasma cells in the upper third of the lamina
propria, some mucosal flattening.
• Chronic atrophic gastritis (later stage) – glands atrophy that
precedes the development of sclerosis; mucosa thinned and
flattened, chronic inflammation of full thickness of the mucosa, loss
of glands, metaplasia of mucosa to the intestinal type.

The exacerbation of chronic gastritis manifests itself in stromaedema,

hyperaemia, considerable cellular infiltration with the increase of
neutrophile level, occasionally microabscesses and erosions may
occur. At remissions there are no such manifestations.

With the most evident processes of disturbed regeneration and

structural formation which lead to cellular atypism (dysplasia), chronic
gastritis is often the basis for the development of gastric carcinoma.
 Gastritis

Acute
Chronic
catarrhal
Nonatrophic (type B)
fibrinous
Atrophic (type A)
suppurative
Specific forms
necrotic
chemical

fundic lymphocytic

noninfectious
antral
granulomatous
diffuse eosinophilic

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

Ulcerative disease is chronic disease with development

chronic recurrent peptic ulcer in the the stomach or
duodenum.
The ulcer has a polycyclic progression and is characterized by
seasonal exacerbations.
 Etiology and background factors:
• According to contemporary view, the main role in the
disease’s etiology is played by psycho-emotional and
physical overstress. Under stress conditions the system’s
„hypothalamus – adenohypophysis – adrenal gland cortex”
gets activated and glucocorticoid production eventually
increases. This hormone stimulates gastric secretion and
increases the acidity of gastric contents. At the same time it
decreases mucus secretion, hinders protein synthesis and
cell reproduction in the mucous tunic of the stomach. The
ulcerogenic action of glucocorticoids also reveals itself
when they are introduced for medical purposes.
• Direct damaging influences on the stomach are also
important – constant eating of too hot, too coarse or too
spicy food, eating pattern disorder, alcohol abuse and
smoking, the ingestion of drugs (especially aspirin,
corticosteroids).
 Etiology and background factors:
• In recent years a significant role has been allotted to
Helicobacter pylori that destroys the mucous barrier of the
stomach and makes its mucous tunic vulnerable to the
digestive action of gastric juices.
• The etiologic role of hereditary factor has also been proved.
Peptic ulcer is associated with blood group 0 (I) and the
presence of Rh-antigen. The prevailing tonus of the
parasympathetic part of the vegetative nervous system over
the sympathetic part lies in the basis of the hereditary
susceptibility. The vagotonia stimulates gastric secretion and
creates favourable conditions for the development of ulcer.
• 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.
 Pathogenesis

• The pathogenesis of peptic ulcer may be imagined as an

imbalance between the factors that damage and protect the
mucous tunic.
• Among the damaging factors are acidic gastric juices and
various physical and chemical stimulations; among the
protective ones – the mucous barrier, adequate blood
supply, high regenerative capacity of the mucous tunic,
alkalinity of saliva and pancreatic juice.
• All influences that cause the predominance of the damaging
factors over the protective ones play a certain role in the
etiology and pathogenesis of ulcer.
 Morphogenesis and morphology

The morphogenesis of chronic recurrent gastric or

duodenal ulcer includes the following stages:
erosion, acute ulcer and chronic ulcer.

I. Erosion (erosio) - is a superficial defect of mucous tunic

that does not go deeper than its muscular laminar.
• These are tiny defects, 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.
Here are some larger areas of gastric hemorrhage that could best be termed
"erosions" because the superficial mucosa is eroded away. Such erosions are
typical for the pathologic process termed gastropathy, which describes gastric
mucosal injury without significant inflammation. The findings here fit with
acute erosive gastropathy, but there are other patterns. Etiologies for the
various gastropathies can include: alcohol, drugs such as NSAIDS, stress,
uremia, bile reflux, portal hypertension, radiation, and chemotherapy.
 II. Acute ulcer
Under the influence of gastric juices, the layers of the stomach wall
necrotize deeper and deeper and the erosion develops into an acute
peptic ulcer .
Location: single or multiple lesions throughout the stomach and
duodenum, especially in the area of lesser curvature of the stomach.
The lesser curvature is known to be a ‘food pathway’, so it is easily
traumatized. Its glands secrete very active digestive juice. The lesser
curvature is rich in receptors and extremely reactive but its folds are rigid,
and at the contraction of the muscular layer they cannot cover the defect.
This causes improper closing up of lesser curvature injuries and the
development of the acute ulcer into a chronic one. That’s why chronic
ulcers are usually located on the lesser curvature, in the antral and pyloric
part. Ulcers in the cardial part and on the greater curvature of stomach are
rare.
•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.
A 1 cm acute gastric ulcer is shown here in the upper fundus. The ulcer is
shallow and sharply demarcated, with surrounding hyperemia. It is probably
benign. However, all gastric ulcers should be biopsied to rule out a
malignancy. The endoscopic appearance of a similar acute peptic ulcer in the
prepyloric region is seen below.
III. Chronic peptic ulcer
•The term “chronic” is applied
when the pathological changes
have penetrated and destroyed
the muscle layer; 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).
 Chronic peptic ulcer
•Classic peptic ulcer is small (about 1 cm in the duodenum; 1 to 2,5 cm in
the stomach), round-to-oval. Its edges look like cushions, they are dense,
sometimes callous (callous ulcer) and its bottom is smooth or rough. The
edge of ulcer, extends towards the esophagus, is undermined and the
mucous tunic hangs over the defect. This results in the formation of a
pocket in which gastric contents accumulate. The edge of the ulcer, turned
towards the hilus, is sloppy.
•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.
 Chronic peptic ulcer
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.

Microscopically, the
ulcer here is sharply
demarcated, with
normal gastric mucosa
on the left falling away
into a deep ulcer whose
base contains infamed,
necrotic debris. An
arterial branch at the
ulcer base is eroded
and bleeding.
 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.
 The principal complications of peptic ulcer
I. Ulcerative-destructive:
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
malnutrition.
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.
 Stomach Cancer (Gastric Carcinoma)
•More often it occurs in men older than 50.
•Among the etiologic factors are endogenous
nitrosoamines, exogenous nitrates and Helicobacter pylori.
•The precancerous conditions are adenomatous polyp,
chronic atrophic gastritis, chronic stomach ulcer, gastric
stump, pernicious anaemia, high epithelial dysplasia of the
mucous tunic of the stomach.
According to localization:

 1. Pyloric (50%) gastric

carcinoma.
 2. Lesser curvature of the
stomach (27%) with the
transition on back and front
walls
 3. Cardial gastric carcinoma
(15%).
 4. Greater curvature of the
stomach (3%).
 5. Fundal gastric carcinoma
(2%).
 6. Total gastric carcinoma (3%).
According to the character of growth, the following clinicoanatomic
(macroscopic) forms of gastric carcinoma can be distinguished:
• exophytic expansive growth (plaque-forming, polypous, fungous,
ulcerative);
• endophytic infiltrating growth;
• exoendophyticgrowth.
According to the histologic structure:
•Adenocarcinoma: tubular, papillary, mucoid, trabecular
(well-differentiated).
•Squamous-cell carcinoma.
•Adenosquamous carcinoma.
•Solid carcinoma (poorly-differentiated).
•Undifferentiated carcinoma (medullar, fibrotic cancer –
scirrhous (characterized by endophytic diffuse growth
forms).
The first metastases arise up in regional lymphatic ways
along large and lesser curvature of stomach.
Haematogenic metastases arise up in a liver and in lungs.

Retrograde metastases have

the role as the diagnostic
moment among distant
lymphogenic metastases:
- In both ovaries (Krukenberg
tumor);
- In a pararectal tissue (Shnitsler
metastases);
- In the left supraclavicular
lymphnode (Virchow's gland).
 Implant
metastases

Implant metastases result to

canceromatosis of peritoneum,
pleura, pericardium, diaphragm.

Metastatic carcinoma (paraaortic)

 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).
 Appendicitis

Acute Chronic

Simple Atrophic catarrh

Superficial Obliterating

Destructive Hydrocele

phlegmonous Mucocele

ulcerophlegmonous Myxoglobulosis

apostematous

gangrenous
 Clinical-morphological classification of acute
appendicitis

• Simple appendicitis is characterized by blood and lymph

circulation disorders, namely – stasis, edema,
haemorrhages, marginal elevation of leucocytes and
leucodiapedesis.

• Superficial appendicitis manifests itself morphologically

in the primary site of inflammation. This term denotes a focus
of suppurative inflammation with mucous tunic erosion on the
basis of circulation disorders. The appendix grows thick and
the serous tunic becomes plethoric and of dirty-grey colour.
Acute appendicitis with yellow to tan exudate and hyperemia,
including the periappendiceal fat superiorly, rather than a
smooth, glistening pale tan serosal surface.
This is the tip of the appendix from a patient with acute
appendicitis. The appendix has been sectioned in half. The
serosal surface at the left shows a tan-yellow exudate. The cut
surface at the right demonstrates yellowish-tan mucosal
exudation with a hyperemic border.
 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).
Microscopically, acute appendicitis is marked by mucosal
inflammation and necrosis.
Neutrophils extend into and through the wall of the appendix in
a case of acute appendicitis. Clinically, the patient often
presents with right lower quadrant abdominal pain. Rebound
tenderness is noted on physical examination. An elevated
WBC count is usually present.
 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.
• If 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
adhesions result.
• Surgically removed appendix may be histologically normal (false-
positive clinical diagnosis). If the appendix is normal, but clinical
symptomes 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.
 Regional Enteritis (Crohn’s Disease)
• Regional enteritis is a chronic inflammatory lesion of the
intestinal wall, usually of the terminal part of the ileum,
though it may affect all parts of the digestive tract.
• There develops a nonspecific granulomatous inflammation
without necrosis (it looks like sarcoidosis) and with
submucous tunic fibrosis and narrowing of the intestinal
lumen.
• Typical of the disease is the alternation of the affected and
unaffected areas. In the mucous tunic one finds deep
transverse and longitudinal ulcers, edema of the submucous
tunic. Macroscopically the mucous tunic resembles a
cobblestone pavement.
• Among the complications are diarrhoea, malabsorption
syndrome, intestinal obstruction, fistulas and degeneration
into cancer.
This is another example of Crohn's disease involving the small
intestine. Here, the mucosal surface demonstrates an irregular nodular
appearance with hyperemia and focal superficial ulceration.
At higher magnification, the pseudopolyps can be seen clearly as
raised red islands of inflamed mucosa. Between the pseudopolyps is
only remaining muscularis.
Microscopically, Crohn's disease is characterized by transmural
inflammation. Here, inflammatory cells (the bluish infiltrates) extend
from mucosa through submucosa and muscularis and appear as
nodular infiltrates on the serosal surface with pale granulomatous
centers.