THEME OF THE LECTURE

Diseases of the
gastrointestinal tract
 Diseases of the stomach
Among diseases of the stomach the most
important are:
•Gastritis

•Stomach
ulcer

•Stomach
cancer
 Gastritis
- inflammatory disease of the gastric mucosa.
 Along the course: acute and chronic gastritis.
 On topography:
- diffuse gastritis (inflammation covers the entire
stomach)
- focal gastritis (fundal, antral, piloranthral and
pyloroduodenal gastritis)
 Acute gastritis
• It develops due to irritation of the mucous
membrane with alimentary, toxic, microbial
factors

• Depending on the features of morphological

changes, the following forms are distinguished:

 Catarrhal (simple)
 Fibrinous
 Purulent (phlegmonous)
 Necrotic (corrosive)
With catarrhal (simple) gastritis, the
mucous membrane of the stomach is
thickened, edematous, hyperemic, its surface
is abundantly covered with mucous masses,
numerous small hemorrhages, erosion are
seen.

With fibrinous gastritis, a fibrinous film of

gray or yellow-brown color forms on the
surface of a thickened mucous membrane.
Isolate croupous (superficial necrosis) and
diphtheria (deep necrosis) variants.
With purulent gastritis, a leukocyte infiltrate
containing a large number of microbes
diffusely covers the mucosa, submucosal and
muscle layers of the stomach and peritoneum.
There is a purulent meltdown of the stomach
wall.

Necrotic gastritis usually occurs when

chemicals (alkali, acid, etc.) enter the
stomach, cauterizing and destroying the
mucous membrane (corrosive gastritis). It
ends with the formation of erosions and acute
ulcers.
A typical picture of acute gastritis.
Mucous membrane diffusely hyperemic, swollen
Acute gastritis. The gastric mucosa is
infiltrated by neutrophils
 Chronic gastritis
• disease characterized by inflammatory,
dystrophic and disregenerative changes in the
gastric mucosa.
 In the morphogenesis of chronic gastritis, an
important role is played by disruption of
regeneration and structural reconstruction of the
mucosa of the mucous membrane.
• Etiological and pathogenetic classification:
 autoimmune (type A)
 Helicobacter pylori (type B)
 reflux gastritis (type C)
Gastritis A is an autoimmune gastritis.
 the appearance of autoantibodies to the lipoprotein
of parietal cells and the internal factor blocking its
binding to vitamin B12
 It is often combined with other autoimmune
diseases (thyroiditis, Addison's disease)
 It appears mainly in children and the elderly
 It is localized in the fundus of the stomach
 Characterized by a sharp decrease in the secretion
of HCl (achlorhydria), G-cell hyperplasia and
gastrinemia
 It is accompanied by the development of pernicious
anemia
 Autoimmune gastritis

Atrophy of the gastric mucosa Intestinal mucosal metaplasia

with intestinal metaplasia stomach, hyperplasia of endocrine
G-cells
 Gastritis B - non-immune gastritis
 Etiology: Helicobacter pylori
 Contributing factors: intoxication, disturbed
eating rhythm, alcohol abuse
 It is localized in the antrum, it can spread to the
entire stomach
 Symptoms:
 cytotoxic damage to the epithelium, active
chronic inflammation. Multifocal atrophy,
intestinal metaplasia.
 acidity of gastric juice increases, which
increases the risk of ulcers.
Chronic gastritis B, associated with Helicobacter pylori
Helicobacter pylori in the stomach of a patient with
chronic gastritis B.
Gastritis C - reflux gastritis
 Associated with the transfer of the contents of the
duodenum to the stomach
 It often occurs in people who have undergone
gastrectomy
 It is localized in the antrum part of the stomach
 HCl secretion is not compromised and the amount of
gastrin is not changed
 Morphology:
- Hyperplasia of the pit epithelium.
- Edema. Vasodilation.
- A small number of cells of inflammation.
 Adverse outcomes: Peptic ulcers. Stomach
Depending on the morphological
pattern:
1- normal gastric mucosa
 
 2-- atrophic gastritis.
non-atrophic gastritis- decrease in the
amount of spices. Cells

3-atrophic gastritis - qualitative changes in the

composition of the epithelium:
fibrosis, lymphocytes (3a). Intestinal
metaplasia(3b)
2
3a 3b

1
Superficial gastritis
Lymphocytoplasmocyte infiltrate
is located in the superficial parts
of the gastric mucosa
The prognosis of the disease is
usually favorable.
ATROPHIC GASTRITIS
 Mucous is thin, the
number of glands is
reduced.
 In its own plate, a
diffuse lymphoid-
plasmocyte infiltrate,
multiple sclerosis
 Characteristic
structural restructuring
with the appearance of
focal points of
intestinal and pyloric
metaplasia
 Often there are focal
points of dysplasia,
which can lead to
stomach cancer.
Chronic atrophic gastritis: gastric mucosa with
smoothed folds, thinned, pale, grayish color, with
small-to-large hemorrhages
Ulcer disease is a chronic disease whose
morphological substrate is a chronic recurrent
ulcer of the stomach or duodenum

Main causes of development:
• infection with Helicobacter pylori
• neuropsychic overstrain (prolonged stress)
• excess production of hydrochloric acid
• the violation of gastroduodenal motility
• a violation of diet and its nature
• taking medications that have ulcerogenic
effects (aspirin, corticosteroids, non-steroidal
anti-inflammatory drugs)
• bad habits (smoking, alcohol)
The main link of pathogenesis is an imbalance
between the factors of aggression and defense
 erosion ulcer

mucous
submucos
a
muscular
layer
Erosion is a superficial defect resulting from
necrosis of the mucous membrane.

Acute ulcer is a profound defect in the mucosa,

submucosal and muscular layers. The most
frequent localization is a small curvature. Has an
irregular round-oval shape and soft edges. The
bottom of acute erosions and ulcers is colored black
due to the accumulation of hydrochloric acid
hematin.

Chronic ulcer is characterized by processes of

epithelization, regeneration and scarring.
3 zones - 1 \ internal - necrosis and inflammation
2 \ medium - granulation tissue 3 \ external-fibrosis.
Acute erosion and
stomach ulcers:
in the gastric mucosa,
multiple small surface
defects (erosions) and
deeper defects (acute
ulcers) of rounded
shape with soft even
edges and a
brownish-black bottom
(due to hydrochloric
acid hematin, which is
formed from
hemoglobin of
erythrocytes under the
action of hydrochloric
acid and gastric juice
enzymes)
Chronic
Stomach
Ulcer:

defect of the
mucous
membrane
and the walls
of the
stomach of a
rounded
shape with
roller-shaped
compressed
edges. The
bottom is
sclerotized.
 Complications of peptic ulcer
1. Evidently destructive:

PERFORATION OF THE ULCER (this is the

destruction of the entire wall of the stomach
with the formation of a perforation through
which the gastric contents enter the abdominal
cavity and develops peritonitis)

PENETRATION (penetration of an ulcer beyond

the walls of the stomach or duodenum into
neighboring organs - into the pancreas, the wall
of the colon, the liver, etc.)
BLEEDING (according to morphogenesis is
arrosive - occurs in connection with the erosion of
the walls of the vessels (inflammation, fibrinoid
necrosis) during periods of exacerbation

2. Inflammatory
•gastritis, perigastritis
•duodenitis, periduodenitis

3. Ulcerative - scarring :
•Stenosis of the inlet and outlet of the stomach
•stenosis and deformation of the duodenal bulb
4. Malignancy of the stomach ulcer
(transition to cancer)

5. Combined complications
(combination of different types of complications)
 Stomach Tumors
Benign Malignant
• Polyps of the stomach • Cancer
• Adenoma (adenocarcinoma) of the
• Leiomyoma stomach
• Fibroma • Leiomyosarcoma
• Fibromyoma • Gastric carcinoid
• lipoma

Precancerous processes:
 chronic atrophic gastritis
 chronic gastric ulcer
 adenomatous polyps
 intestinal metaplasia of the gastric mucosa
 severe dysplasia of the gastric mucosa
Polyp of the
stomach:
protruding into the
lumen of the
stomach a small
exophytic
formation on a
wide base, covered
with a mucous
membrane.

Hyperplastic
polyps constitute
80-90% of all
benign neoplastic
processes of the
stomach.
Cancer of the stomach is a malignant tumor
from the epithelium of the gastric mucosa.

Etiopathogenetic factors:
• precancerous processes
• long-term use of carcinogens in food
MORPHOGENESIS OF STOMACH CANCER
(successive stages of development)

precancerous conditions (atrophic gastritis,

intestinal metaplasia)
↓
precancerous changes (epithelial dysplasia)
↓
non-invasive carcinoma (carcinoma in situ)
↓
invasive cancer
Severe dysplasia of the epithelium of the stomach is a
violation of the structure of the mucosa with
pronounced cellular and nuclear atypia. Dysplasia
often undergoes metaplastic epithelium (ie,
reconstructed by intestinal type)
 Classification of stomach cancer
Depending on the location of the cancer:

 pyloric stomach
 small curvature with transition to the posterior and
anterior walls of the stomach
 cardiac part of the stomach
 great curvature
 the bottom of the stomach

In the pyloric department and small curvature, 3/4

of all carcinomas of the stomach are localized.
Gastric cancer can be subtotal and total
Depending on the nature of growth, the following
macroscopic forms of gastric cancer are
distinguished:

I. Cancer with predominant exophytic growth:

• Plaque-like
• polypous
• mushroom
• ulcerated (primary-ulcerative, saucer-like, cancer from a
chronic ulcer = ulcer-cancer)

II. Cancer with predominant endophytic growth:

• infiltrative-ulcerative
• diffuse

III. Cancer with exo-endophytic, mixed growth:

• Transitional forms
I. Polyposis - well-delimited,
looks like a knot on the leg

II. Ulcerous - with saucer-like

raised edges

III. Infiltrativno-ulcerative -
with the germination of deep
layers of the wall without a
clear distinction from healthy
tissues

IV. diffuse-infiltrative type

(scirrhous) (grows in the
submucosa base)
Fungal
(mushroom)
cancer

has the
appearance of a
knobby, tuberous
formation, sitting
on a short, broad
base. On the
surface of the
tumor node,
erosion,
hemorrhage, or
fibrinous-purulent
imposition is
determined.
Saucer-like cancer is one of the most common forms of stomach cancer. Occurs
when the tumor is ulcerated.

It is a rounded formation with raised uneven edges and a lowered ulcerated bottom.
Diffusive form:

the wall of the

stomach over a
considerable
length is sharply
thickened by the
growth of dense
whitish tissue,
which does not
have clear
boundaries.
HISTOLOGICAL TYPES OF STOMACH
CANCER (MICROSCOPIC STRUCTURE):

1.adenocarcinoma
(tubular, papillary, mucinous)

2. undifferentiated (solid, scirrhous, cricoid-

cell)
3. squamous cell

4. glandular squamous cell

5. unclassified cancer.
 Adenocarcinoma
of the stomach:

in the thickness of
the mucous
membrane and the
muscle layer of the
stomach are
located atypical, of
different sizes and
forms of glandular
complexes (tissue
atypia).

Tumor cells and their nuclei are polymorphic, of different

sizes and forms, the nuclei are hyperchromic (cellular atypia).
Skirr of the
stomach- among
the coarse-fiber
connective tissue in
the mucosa and
submucosal layer:
1- groups of small
hyperchromic
undifferentiated
cancer cells
infiltrating the
gastric wall.
 Metastasis of stomach cancer
1. Lymphogenous path of metastasis:
•   in the regional lymph nodes located on the small and
large curvature of the stomach.
•   in both ovaries
• in the pararectal tissue
• in the left supraclavicular lymph node

2. Implantation metastases:
in the form of pleural carcinomatosis, pericardium,
diaphragm, peritoneum, omentum.

3. Hematogenous metastases:
in the liver, lungs, brain, bones, kidneys.
metastases of different locations
Diseases of the
intestine
 Pathology of the intestine:
malformations
(megacolon, megasigma, diverticula, stenosis
and atresia)

inflammatory diseases
(enteritis, appendicitis, colitis)

Idiopathic bowel disease (Crohn's disease

and ulcerative colitis)

tumors
(polyps, carcinoid, intestinal cancer).
Megacolon -
pathological
expansion and
hypertrophy of
the walls of the
colon.

megasigma -
a significant
expansion of the
sigmoid colon
(b)
Diverticulosis of
the large
intestine:

multiple fingerlike
protrusions in the
wall of the colon,
from the side of
the mucous
membrane, the
entrances to the
diverticula have
the appearance
of dark spots
(arrows)
 CLASSIFICATION OF INFLAMMATORY
BOWEL DISEASES
By topography:
colitis (inflammation of the
enteritis large intestine):
(inflammation of
the small • tiflitis (inflammation of the
intestine): caecum)
• transversitis
• sigmoiditis
• duodenitis • proctitis (inflammation of the
• jejnite rectum)
• ileitis • Pancolitis (Inflammation of the
entire colon)
In the course of the disease: acute and chronic

By morphology:
acute enteritis: acute colitis:
- catarrhal - catarrhal
- fibrinous - fibrinous
- purulent - purulent
- necrotic ulcerative - hemorrhagic
- necrotic (gangrenous)
- ulcerative
Chronic enteritis / colitis:
- without mucosal atrophy
- atrophic
 Chronic enteritis
On the etiology:
primary chronic enteritis:
a) infectious / postinfectious;
b) toxic;
c) medicamentous;
d) allergic

secondary:
a) with diseases of the digestive system (stomach,
pancreas, hepatobiliary system, large intestine);
b) with congenital enzymopathies;
c) with immunodeficiency states;
d) after operations on the small intestine.
inflammation of the appendix cecum
Etiopathogenesis:

- activation of nonspecific infection (E. coli,

enterococcus)
- spasm, thrombosis, embolism of the
appendicular artery
- violation of general and local reactivity
- ischemia and trophic disorders of the
appendix
- stagnation in the lumen of the process of
intestinal contents (associated with
impairment of peristalsis, atony,
infringements of the appendix)
1. Simple appendicitis:
• It is accompanied by circulatory disorders,
small hemorrhages, small accumulations of
leukocytes.

2. Superficial.
• There is a focus
of purulent
inflammation in
the mucosa
3. Destructive appendicitis

Phlegmonous:

• The appendix is ​enlarged, the serous

membrane is dull, full-blooded, covered with
fibrinous coating; walls are thickened, purulent
contents are released from the lumen.

• diffuse infiltration by polymorphonuclear

leukocytes of all layers of the appendix is ​
microscopically detected.  
the appendix is enlarged in size, the walls are thickened, diffusely
impregnated with pus, the surface is dull, reddish-cyanotic, with full blood
vessels
Phlegmonous-ulcerative:
° diffuse purulent inflammation with necrosis
and ulceration mucous membrane.
Apostematous:
° on a background of diffuse purulent
inflammation are determined abscesses.
Gangrenous:
° occurs with thrombosis or thromboembolism
of the artery appendix:
the walls acquire a gray-black color,
on the serous membrane fibrinous-purulent
overlap.
marked leukocyte infiltration of all layers of the
appendix wall, edema, inflammatory hyperemia,
necrosis and ulceration of the mucosa, atrophy of
lymphoid tissue.
gangrenous appendicitis
 Complications of acute appendicitis
Occur with destructive forms of appendicitis.
•perforation:
•with development of diffuse purulent peritonitis
•with the development of periapendicular abscess
•empyema of the appendix
• Intra-abdominal abscesses (pelvic, intercellular,
sub-diaphragmatic)
•Pylephlebitis (septic thrombophlebitis of the
portal vein and its tributaries)
•Abscess of the liver
•Sepsis.
Among the diseases of the large intestine
the most important:

•  for young
people:
-nonspecific
ulcerative colitis
-Crohn's disease

•  for the elderly

ischemic colitis
 DISTINCTIVE FEATURES OF KOLITS
(ON ZONES OF LOSS)
1. Nonspecific ulcerative colitis
2. Crohn's disease
3. Ischemic colitis

1.progressive 2.segmental 3.the main

ulceration of lesion of the changes in
the mucosa gastrointestinal splenic flexure
from top to tract (narrowing of
bottom (adhesions) the luminal gut)
CROWN DISEASE is a chronic recurrent disease of the
gastrointestinal tract of unclear etiology, characterized by
transmural segmental granulomatous inflammatory
disease with the development of local and systemic
complications.

Probable etiological factors:

a) infectious (mycobacterium tuberculosis, measles virus);
b) allergic (food allergy to milk protein, hydrated fats,
flavors, disaccharides);
c) smoking (increases the likelihood of the disease by 4
times);
d) genetic (defect in the 16th chromosome).

  Pathogenesis realizes an autoimmune mechanism

 Morphological characteristics
•In the wall of the intestine develops chronic
inflammation, which engulfs all layers of the
wall.
•  characterized by the formation of
nonspecific granulomas without necrosis,
fibrosis of the submucosa

•Typically a spasmodic bowel lesion: the

affected areas of the intestine alternate with
normal.
•It is characteristic thickening of the wall of
the affected segment of the intestine with a
narrowing of the lumen.

•Deep slit-shaped transverse and

longitudinal ulcers;

•swelling of the submucosal layer of intact

intestinal areas with the swelling of the
mucous membrane covering them, which
gives it the appearance of a "cobblestone
pavement"
Small intestine with Crohn's disease. The surface
of the mucosa is nodular, with hyperemia, focal
superficial ulceration.
Microscopically, Crohn's disease is characterized by
transmural inflammation. Cells of inflammation pass
through submucosal and muscular membranes and
manifest on the serous surface in the form of nodal
infiltrates with pale granulomatous centers
With a large increase in granulomatous nature
of Crohn's disease confirms the presence of
epithelioid cells, giant cells, many
lymphocytes.
 Complications of Crohn's disease

 Diarrhea, malabsorption syndrome

 Intestinal obstruction
(due to cicatricial narrowing)
 Fistulas - intestinal, intestinal-vesical, intestinal-
vaginal, external, etc.
 Approximately 3% of patients develop colon
cancer
 Nonspecific ulcerative colitis
Morphological characteristics
 Changes are limited to the colon
 Inflammation and ulceration are confined to
the mucosa and submucosa;
 Ulceration can be extensive with the
preservation of only small areas of the
mucosa, which form "pseudopolips"
 Macroscopically, the intestinal mucosa is
usually red with a granular surface
Nonspecific ulcerative colitis. There are
pseudopolypes in the form of raised red islets of the
inflamed mucosa
Microscopically inflammation with ulcerative
colitis is limited by the mucous membrane. Here
the mucous membrane is destroyed by the
inflammatory process with ulceration
With a large increase in markedly intense
inflammation of the mucosa, loss of goblet cells in
the epithelium, exudate on the surface, cells of
acute and chronic inflammation
 Complications

 Toxic megacolon is a condition in which

there is a significant expansion of the gut
 Perforation of the intestine
 5-10% of patients develop colon cancer
 Ischemic colitis

 It develops mainly in the elderly

 It is associated with sclerosis of the vessels of
the intestinal wall, arising from
atherosclerosis, diabetes mellitus and other
diseases accompanied by arteriosclerosis.
 Microscopically expressed fibrosis, deposits
of hemosiderin.
 Complications: bleeding, perforation,
peritonitis