Diseases of the gastrointestinal tract
1. Diseases of the salivary glands.
2. Diseases of the esophagus. Classification.
3. Acute and chronic gastritis, classification.
4. Peptic ulcer disease, morphology of acute and chronic
ulcers.
5. Tumors of the esophagus and stomach.
6. Intestinal diseases: congenital anomalies, vascular diseases,
- non-specific ulcerative colitis
- Crohn's disease.
7. Diseases of the appendix of the cecum.
8. Intestinal tumors
Diseases of the esophagus
Esophagitis- inflammation of the esophageal mucosa.
Classification: Acute and chronic esophagitis.
•Etiology: chemical burns, thermal burns, microbial infections (diphtheria),
allergies.
Forms:
•catarrhal,
•ulcerative.
2. Esophageal diverticulum
- single blind protrusion of the wall, several
protrusions – diverticulosis.
a. True – all layers of the wall protrude.
b. False – only the mucosal and submucosal layers. In
gastroenterology, among the diverticula of the
gastrointestinal tract, they account for about 50 %.
More often, esophageal diverticula is diagnosed in
men over 50 years of age, as a rule, suffering from
other diseases of the digestive system –peptic ulcer,
cholecystitis, GI
True diverticulum
False diverticulum
Esophageal diverticulum can be manifested by a feeling of tickling, a lump in the
throat, dysphagia,putrid breath. Diverticulae are diagnosed by esophageal
radiography and esophagoscopy.
Esophageal cancer - a malignant tumor that
forms from the degenerated epithelium of the
esophageal wall. Clinically manifested by
progressive swallowing disorders, weight loss.
The tumor is detected by X-ray, endoscopic
examination, CT or ultrasound.
Stomach diseases
Gastritis - inflammation of the gastric mucosa,
accompanied by impaired secretion and motility.
There are acute and chronic gastritis.
forms of acute gastritis:
•Catarrhal (simple) gastritis - the gastric mucosa
is thickened, swollen, hyperemic, its surface is
abundantly covered with mucus.
• Fibrinous gastritis - on the surface of the mucous
membrane of the fibrinous film of yellow-brown
color.
• Phlegmonous gastritis is a pronounced thickening
of the mucous membrane and submucosal base,
diffuse impregnation with purulent exudate.
• Necrotic (corrosive) gastritis occurs when strong
acids, alkalis, cauterize and destroy the mucous
membrane. Necrosis ends with the formation of
erosions and ulcers.
Chronic atrophic gastritis.
The gastric mucosa has smoothed
folds, is thinned, pale, and grayish in
color, with pinpoint hemorrhages
and acute erosions.
Dystrophic changes in the superficial (pit)
epithelium, edema, and inflammatory infiltration by lymphocytes,
plasma cells, neutrophils, and occasional eosinophilic
leukocytes of the lamina propria of the mucous membrane
Chronic superficial antral gastritis.
Outcome of acute gastritis:
recovery, or transition to chronic. There are two forms
of chronic gastritis, which are both stages of the
disease.
• Chronic superficial gastritis is characterized by
dystrophy of the epithelium and glands without
atrophy.
•Chronic atrophic gastritis - it is expressed in
atrophy of the mucous membrane, its glands.
Connective tissue grows in place of atrophied
glands. It is important to note that chronic
atrophic gastritis is a precancerous disease of
the stomach.
Peptic ulcer disease
stomach and
duodenum
The essence of gastric ulcer and
the duodenum
These are chronic recurrent diseases that are prone to progression
and are manifested by disorders of the mucous and submucosal
layers of the stomach and duodenum.
13
Etyology
1. Genetic predisposition.
2. The presence of chronic gastritis and duodenitis.
3. Infection with Helicobacter pylori and candida.
4. Eating disorders and unbalanced nutrition.
5. Abuse of medicinal products that have the following characteristics:
ulcerogenic effects (NSAIDs, corticosteroids)
6. Smoking and drinking alcohol.
PATHOGENESIS
Theory of occurrence
Under the influence of meteorological factors, the
functional state of the cerebral cortex is disturbed, as a
result, the activity of the parasympathetic nervous
system increases, the motility of the stomach and
duodenum is disturbed, the secretion of gastric juice
increases, the formation of mucus and a protective film
on its surface is inhibited.
A dystrophic process develops in the stomach and
duodenum.
This is facilitated by Helicobocter pylori.
Pathogenesis
16
PATHOGENESIS
Helicobacter pylori in the lumen of the glands
in chronic atrophic gastritis
18
Classification by localization:
I. Peptic ulcer disease of the stomach
a) defeat of the cardial part of the stomach;
b) small curvature;
c) large curvature
d)the pyloric part of the stomach.
II. Duodenal ulcer disease
a) bulb ulcer;
b) post-pubic ulcer;
c) ulcer of unspecified localization.
Forms of peptic ulcer disease in the course of:
1. Acute
2. Chronic
Course:
1. Latent.
2. Rarely recurrent (1 time in 4-5 years).
3. Moderately recurrent (1 time in 2-3 years).
4. Often recurrent (1 time a year or more).
Acute
stomach
ulcers
21
Acute stomach ulcer
Chronic stomach ulcer
23
Chronic stomach ulcer
Chronic duodenal ulcer
Chronic stomach ulcer
Duodenal ulcer
Complications of peptic ulcer diseases:
1.Bleeding.
2.Perforation.
3.Penetration (germination).
4.Malignization.
5.Stenosis.
6.Reactive hepatitis.
7.Reactive pancreatitis.
I. Malformations
Diverticula and diverticular doubling.
Diverticulae are often multiple. Diverticular doublings of the small
and large intestines are located either in the mesentery of the intestine or have their
own mesentery. They are usually complicated by diverticulitis or bleeding without
obstruction,
Atresia and stenosis
• Accompanied by the clinic of high small bowel obstruction (more often) and low
colonic obstruction. A characteristic symptom of high atresia is vomiting with an
admixture of bile and greens, which appears shortly after the birth of the child
and then becomes repeated, occurring both after feeding and between with them.
With low atresia, vomiting and bloating appear on 2-3 days
stenosis
megacolon and megasigma
Megacolon is a pathological enlargement of the colon. It is characterized by
thickening of the walls, widening of the lumen and lengthening of the entire colon
or any part of it; subsequently, focal inflammation and atrophy of the mucous
membrane develop.
It is more common to expand the megasigma and at the same time lengthen it
(megadolichosigma).
Megacolon
II. Inflammation
Inflammation of the small intestine - enteritis, colon — colitis, and the entire
intestine-enterocolitis.
A. Depending on the localization of the pathological process, inflammation of the
duodenum is distinguished - duodenitis, jejunum - eunit, ileum - ileit.
Enteritis can be acute or chronic.
Acute enteritis can be:
- catarrhal with mucosal-serous exudate;
- fibrinous with fibrinous exudate croup or diphtheria
- purulent, when the intestinal wall is diffusely soaked with purulent exudate;
- necrotic-ulcerative.
The chronic form begins as chronic enteritis without mucosal atrophy. Gradually, it
develops into chronic atrophic enteritis, which is the next stage of chronic enteritis.
Acute enteritis manifests itself as a frequent liquid watery stool with greens, which
leads to dehydration of the body. Diarrhea is usually accompanied by loss of
appetite, nausea. Complaints of abdominal pain, bloating and rumbling.
Colitis
it is acute and chronic. Acute colitis is the result of infections (bacteria, viruses)
and intoxication.
Depending on the nature of exudate and destructive changes, the following forms
of acute colitis are distinguished::
- catarrhal.
- purulent;
- hemorrhagic;
- necrotic;
- gangrenous;
- ulcerative
Complications of acute colitis: bleeding,
perforation and peritonitis, paraproctitis with
pararectal fistulas. In some cases, acute colitis
takes a chronic course.
Chronic colitis, like chronic enteritis, initially
proceeds without mucosal atrophy, and later it
turns into chronic atrophic colitis and ends with
mucosal sclerosis.
Аcute colitis is characterized by frequent scanty stools
with an admixture of mucus and often blood (the
phenomenon of hemorrhagic colitis), tenesmus,
cramping abdominal pain. Spastic sigmoid colon is
often palpated, and in young children - compliance or
gaping of the anus.
Appendicitis
- inflammation of the appendix
of the cecum. It is a common
disease of unclear etiology. It can
be acute or chronic.
Acute appendicitis has the
following morphological forms:
- simple;
- surface;
- destructive (phlegmonous,
phlegmonous-ulcerative,
gangrenous). Complications:
perforation of the process wall
and development of peritonitis,
empyema of the process
Chronic appendicitis
occurs after acute
appendicitis and is
characterized mainly
by sclerotic and
atrophic changes in the
appendix wall.
Intestinal obstruction
It can be dynamic:
Paralytic obstruction it is observed in acute peritonitis due to poisoning and
soaking of the intestinal muscles with inflammatory exudate.
Spastic obstruction. It can be reflex, neurogenic, or toxic. This form is more rare
and is based on a spasm, most often a limited area of the intestine. Spastic
obstruction can become paralytic.
Mechanical obstruction:
Strangulation obstruction(twisting of the intestines, pinching).
Strangulation obstruction includes infringement by spikes, inversion and
invagination.
Strangulation obstruction is more common in men than in women. Children are
more likely to get invagination.
• Symptoms of obstruction include gas retention, bowel movements, flatulence,
lack of peristalsis, bloating, vomiting, and peritoneal phenomena.
Intestinal tumors
Benign and malignant diseases
There are no symptoms in the early stage of tumor
development. After some time, you may notice the
following signs of the disease::
1. Bleeding from the anus preceding the stool;
2. In the work of the intestine there are frequent
failures. Feces is ribbon-shaped feces, sometimes
involuntary self-ejaculation of feces can occur;
3. Relief after defecation does not appear, the patient
feels a foreign body;
4. Often the whole body hurts;
5. The general condition is getting worse.
Pathology of the gallbladder
• Cholecystitis - acute and chronic
1.Catarrhal
2.Phlegmonous
3.Gangrenous
- inflammatory disease of the gallbladder. Women suffer from this disease 5 times
more often than men. The average age of such women is 30 years and older.
Especially susceptible to cholecystitis are people who are overweight.
• 90% of all cases of cholecystitis are accompanied by stone formation, which
makes the disease even more dangerous. The danger lies in the accumulation of
cholesterol, calcium salts and bilirubin in the gallbladder cavity. They are
deposited on the walls of the bladder in the form of calcifications. But over time,
the deposits increase in size, interfering with the normal functioning of the organ.
It is not uncommon for stones to enter the bile ducts, where they interfere with
the outflow of bile from the bladder. All this leads first to discomfort and
heaviness in the abdominal area, and then to inflammation and peritonitis.
Prerequisites for
the development of
cholecystitis create
disorders of biliary
tract motility-
dyskinesia (hypo
and hyper)
Diseases of the pancreas
Pancreatitis – acute and chronic.
1. If the ducts are blocked by gallstones
2. Sphincter spasm, often with C2H5 poisoning OH, begins to increase the activity
of enzymes, enter the blood (amylase and elastase), lowering blood pressure, to
purulent inflammation and necrosis.
Chronic: atrophy and sclerosis predominate, with endocrine and exocrine stages.
Acute pancreatitis:
1.Serous
2.Hemorrhagic
3.Purulent
4. Necrotic
Chronic: atrophy and sclerosis
predominate, with endocrine and
exocrine stages.
• Cancer in the head causes
mechanical jaundice.
•Crohn's disease is a chronic non-
specific, granulomatous
inflammation of any parts of the
gastrointestinal tract, with a
predominant lesion of the terminal
ileum and ileocolitis in 50% of cases
(granulomatous enteritis, regional
enteritis, transmural ileitis)
Etiology
The etiology of Crohn's disease is still unknown, and the
following factors are currently being considered:
• Viral infections (measles virus)
• Bacterial infections (Chlamydia, listeria, mycobacteria)
• Environmental factors (early weaning, high socio-economic
status, steroid contraceptives, non-steroidal anti-inflammatory
drugs, titanium oxide toothpaste, tobacco smoking)
• Psychological factors
Pathogenesis
Antigen in the gut
phagocytosis by macrophages and dendrites
presentation of the antigen on its surface
activation of immune defense cells
activation of pro-inflammatory cytokines is a violation of
the balance between pro-and anti-inflammatory
cytokines
excessive activation of pro-inflammatory cytokines
destruction of the intestinal mucosa
Localization
Crohn's disease
Ulcerative colitis
 Esophagus, stomach, duodenum 3-5
%
 Small and large intestine 40-55%
 Small intestine only 25-30 %
 Colon only 20-25 %
 Rectal lesion 11-26%
 Anorectal lesions (anal fistulas, anal
fissures, abscesses resulting from
periproctitis) 30-40 %
•Total colitis 18 %
•Left-sided lesion 28 %
•Proctochygmoiditis 54 %
Crohn's disease
Transverse colon
Sigmoid colon
Rectum
Ulcerative colitis
Differential diagnosis
Ulcerative colitis Crohn's disease
Extra-intestinal manifestations
Extra-intestinal complications
Extra-intestinal manifestations and
complications of Crohn's disease

Diseases of the gastrointestinal tract (1).pptx

  • 1.
    Diseases of thegastrointestinal tract 1. Diseases of the salivary glands. 2. Diseases of the esophagus. Classification. 3. Acute and chronic gastritis, classification. 4. Peptic ulcer disease, morphology of acute and chronic ulcers. 5. Tumors of the esophagus and stomach. 6. Intestinal diseases: congenital anomalies, vascular diseases, - non-specific ulcerative colitis - Crohn's disease. 7. Diseases of the appendix of the cecum. 8. Intestinal tumors
  • 2.
    Diseases of theesophagus Esophagitis- inflammation of the esophageal mucosa. Classification: Acute and chronic esophagitis. •Etiology: chemical burns, thermal burns, microbial infections (diphtheria), allergies. Forms: •catarrhal, •ulcerative.
  • 3.
    2. Esophageal diverticulum -single blind protrusion of the wall, several protrusions – diverticulosis. a. True – all layers of the wall protrude. b. False – only the mucosal and submucosal layers. In gastroenterology, among the diverticula of the gastrointestinal tract, they account for about 50 %. More often, esophageal diverticula is diagnosed in men over 50 years of age, as a rule, suffering from other diseases of the digestive system –peptic ulcer, cholecystitis, GI
  • 4.
    True diverticulum False diverticulum Esophagealdiverticulum can be manifested by a feeling of tickling, a lump in the throat, dysphagia,putrid breath. Diverticulae are diagnosed by esophageal radiography and esophagoscopy.
  • 5.
    Esophageal cancer -a malignant tumor that forms from the degenerated epithelium of the esophageal wall. Clinically manifested by progressive swallowing disorders, weight loss. The tumor is detected by X-ray, endoscopic examination, CT or ultrasound.
  • 6.
    Stomach diseases Gastritis -inflammation of the gastric mucosa, accompanied by impaired secretion and motility. There are acute and chronic gastritis. forms of acute gastritis: •Catarrhal (simple) gastritis - the gastric mucosa is thickened, swollen, hyperemic, its surface is abundantly covered with mucus.
  • 7.
    • Fibrinous gastritis- on the surface of the mucous membrane of the fibrinous film of yellow-brown color. • Phlegmonous gastritis is a pronounced thickening of the mucous membrane and submucosal base, diffuse impregnation with purulent exudate. • Necrotic (corrosive) gastritis occurs when strong acids, alkalis, cauterize and destroy the mucous membrane. Necrosis ends with the formation of erosions and ulcers.
  • 8.
    Chronic atrophic gastritis. Thegastric mucosa has smoothed folds, is thinned, pale, and grayish in color, with pinpoint hemorrhages and acute erosions.
  • 9.
    Dystrophic changes inthe superficial (pit) epithelium, edema, and inflammatory infiltration by lymphocytes, plasma cells, neutrophils, and occasional eosinophilic leukocytes of the lamina propria of the mucous membrane Chronic superficial antral gastritis.
  • 10.
    Outcome of acutegastritis: recovery, or transition to chronic. There are two forms of chronic gastritis, which are both stages of the disease. • Chronic superficial gastritis is characterized by dystrophy of the epithelium and glands without atrophy.
  • 11.
    •Chronic atrophic gastritis- it is expressed in atrophy of the mucous membrane, its glands. Connective tissue grows in place of atrophied glands. It is important to note that chronic atrophic gastritis is a precancerous disease of the stomach.
  • 12.
  • 13.
    The essence ofgastric ulcer and the duodenum These are chronic recurrent diseases that are prone to progression and are manifested by disorders of the mucous and submucosal layers of the stomach and duodenum. 13
  • 14.
    Etyology 1. Genetic predisposition. 2.The presence of chronic gastritis and duodenitis. 3. Infection with Helicobacter pylori and candida. 4. Eating disorders and unbalanced nutrition. 5. Abuse of medicinal products that have the following characteristics: ulcerogenic effects (NSAIDs, corticosteroids) 6. Smoking and drinking alcohol.
  • 15.
    PATHOGENESIS Theory of occurrence Underthe influence of meteorological factors, the functional state of the cerebral cortex is disturbed, as a result, the activity of the parasympathetic nervous system increases, the motility of the stomach and duodenum is disturbed, the secretion of gastric juice increases, the formation of mucus and a protective film on its surface is inhibited. A dystrophic process develops in the stomach and duodenum. This is facilitated by Helicobocter pylori.
  • 16.
  • 17.
  • 18.
    Helicobacter pylori inthe lumen of the glands in chronic atrophic gastritis 18
  • 19.
    Classification by localization: I.Peptic ulcer disease of the stomach a) defeat of the cardial part of the stomach; b) small curvature; c) large curvature d)the pyloric part of the stomach. II. Duodenal ulcer disease a) bulb ulcer; b) post-pubic ulcer; c) ulcer of unspecified localization.
  • 20.
    Forms of pepticulcer disease in the course of: 1. Acute 2. Chronic Course: 1. Latent. 2. Rarely recurrent (1 time in 4-5 years). 3. Moderately recurrent (1 time in 2-3 years). 4. Often recurrent (1 time a year or more).
  • 21.
  • 22.
  • 23.
  • 24.
  • 25.
  • 26.
  • 27.
    Complications of pepticulcer diseases: 1.Bleeding. 2.Perforation. 3.Penetration (germination). 4.Malignization. 5.Stenosis. 6.Reactive hepatitis. 7.Reactive pancreatitis.
  • 31.
    I. Malformations Diverticula anddiverticular doubling. Diverticulae are often multiple. Diverticular doublings of the small and large intestines are located either in the mesentery of the intestine or have their own mesentery. They are usually complicated by diverticulitis or bleeding without obstruction,
  • 32.
    Atresia and stenosis •Accompanied by the clinic of high small bowel obstruction (more often) and low colonic obstruction. A characteristic symptom of high atresia is vomiting with an admixture of bile and greens, which appears shortly after the birth of the child and then becomes repeated, occurring both after feeding and between with them. With low atresia, vomiting and bloating appear on 2-3 days
  • 33.
  • 34.
    megacolon and megasigma Megacolonis a pathological enlargement of the colon. It is characterized by thickening of the walls, widening of the lumen and lengthening of the entire colon or any part of it; subsequently, focal inflammation and atrophy of the mucous membrane develop. It is more common to expand the megasigma and at the same time lengthen it (megadolichosigma).
  • 36.
  • 37.
    II. Inflammation Inflammation ofthe small intestine - enteritis, colon — colitis, and the entire intestine-enterocolitis. A. Depending on the localization of the pathological process, inflammation of the duodenum is distinguished - duodenitis, jejunum - eunit, ileum - ileit. Enteritis can be acute or chronic. Acute enteritis can be: - catarrhal with mucosal-serous exudate; - fibrinous with fibrinous exudate croup or diphtheria
  • 38.
    - purulent, whenthe intestinal wall is diffusely soaked with purulent exudate; - necrotic-ulcerative. The chronic form begins as chronic enteritis without mucosal atrophy. Gradually, it develops into chronic atrophic enteritis, which is the next stage of chronic enteritis. Acute enteritis manifests itself as a frequent liquid watery stool with greens, which leads to dehydration of the body. Diarrhea is usually accompanied by loss of appetite, nausea. Complaints of abdominal pain, bloating and rumbling.
  • 40.
    Colitis it is acuteand chronic. Acute colitis is the result of infections (bacteria, viruses) and intoxication. Depending on the nature of exudate and destructive changes, the following forms of acute colitis are distinguished:: - catarrhal. - purulent; - hemorrhagic; - necrotic; - gangrenous; - ulcerative
  • 41.
    Complications of acutecolitis: bleeding, perforation and peritonitis, paraproctitis with pararectal fistulas. In some cases, acute colitis takes a chronic course. Chronic colitis, like chronic enteritis, initially proceeds without mucosal atrophy, and later it turns into chronic atrophic colitis and ends with mucosal sclerosis.
  • 42.
    Аcute colitis ischaracterized by frequent scanty stools with an admixture of mucus and often blood (the phenomenon of hemorrhagic colitis), tenesmus, cramping abdominal pain. Spastic sigmoid colon is often palpated, and in young children - compliance or gaping of the anus.
  • 43.
    Appendicitis - inflammation ofthe appendix of the cecum. It is a common disease of unclear etiology. It can be acute or chronic. Acute appendicitis has the following morphological forms: - simple; - surface; - destructive (phlegmonous, phlegmonous-ulcerative, gangrenous). Complications: perforation of the process wall and development of peritonitis, empyema of the process
  • 44.
    Chronic appendicitis occurs afteracute appendicitis and is characterized mainly by sclerotic and atrophic changes in the appendix wall.
  • 45.
    Intestinal obstruction It canbe dynamic: Paralytic obstruction it is observed in acute peritonitis due to poisoning and soaking of the intestinal muscles with inflammatory exudate. Spastic obstruction. It can be reflex, neurogenic, or toxic. This form is more rare and is based on a spasm, most often a limited area of the intestine. Spastic obstruction can become paralytic.
  • 46.
    Mechanical obstruction: Strangulation obstruction(twistingof the intestines, pinching). Strangulation obstruction includes infringement by spikes, inversion and invagination. Strangulation obstruction is more common in men than in women. Children are more likely to get invagination. • Symptoms of obstruction include gas retention, bowel movements, flatulence, lack of peristalsis, bloating, vomiting, and peritoneal phenomena.
  • 47.
    Intestinal tumors Benign andmalignant diseases
  • 48.
    There are nosymptoms in the early stage of tumor development. After some time, you may notice the following signs of the disease:: 1. Bleeding from the anus preceding the stool; 2. In the work of the intestine there are frequent failures. Feces is ribbon-shaped feces, sometimes involuntary self-ejaculation of feces can occur; 3. Relief after defecation does not appear, the patient feels a foreign body; 4. Often the whole body hurts; 5. The general condition is getting worse.
  • 49.
    Pathology of thegallbladder • Cholecystitis - acute and chronic 1.Catarrhal 2.Phlegmonous 3.Gangrenous - inflammatory disease of the gallbladder. Women suffer from this disease 5 times more often than men. The average age of such women is 30 years and older. Especially susceptible to cholecystitis are people who are overweight.
  • 50.
    • 90% ofall cases of cholecystitis are accompanied by stone formation, which makes the disease even more dangerous. The danger lies in the accumulation of cholesterol, calcium salts and bilirubin in the gallbladder cavity. They are deposited on the walls of the bladder in the form of calcifications. But over time, the deposits increase in size, interfering with the normal functioning of the organ. It is not uncommon for stones to enter the bile ducts, where they interfere with the outflow of bile from the bladder. All this leads first to discomfort and heaviness in the abdominal area, and then to inflammation and peritonitis.
  • 52.
    Prerequisites for the developmentof cholecystitis create disorders of biliary tract motility- dyskinesia (hypo and hyper)
  • 53.
    Diseases of thepancreas Pancreatitis – acute and chronic. 1. If the ducts are blocked by gallstones 2. Sphincter spasm, often with C2H5 poisoning OH, begins to increase the activity of enzymes, enter the blood (amylase and elastase), lowering blood pressure, to purulent inflammation and necrosis. Chronic: atrophy and sclerosis predominate, with endocrine and exocrine stages.
  • 54.
    Acute pancreatitis: 1.Serous 2.Hemorrhagic 3.Purulent 4. Necrotic Chronic:atrophy and sclerosis predominate, with endocrine and exocrine stages. • Cancer in the head causes mechanical jaundice.
  • 55.
    •Crohn's disease isa chronic non- specific, granulomatous inflammation of any parts of the gastrointestinal tract, with a predominant lesion of the terminal ileum and ileocolitis in 50% of cases (granulomatous enteritis, regional enteritis, transmural ileitis)
  • 56.
    Etiology The etiology ofCrohn's disease is still unknown, and the following factors are currently being considered: • Viral infections (measles virus) • Bacterial infections (Chlamydia, listeria, mycobacteria) • Environmental factors (early weaning, high socio-economic status, steroid contraceptives, non-steroidal anti-inflammatory drugs, titanium oxide toothpaste, tobacco smoking) • Psychological factors
  • 57.
    Pathogenesis Antigen in thegut phagocytosis by macrophages and dendrites presentation of the antigen on its surface activation of immune defense cells activation of pro-inflammatory cytokines is a violation of the balance between pro-and anti-inflammatory cytokines excessive activation of pro-inflammatory cytokines destruction of the intestinal mucosa
  • 58.
    Localization Crohn's disease Ulcerative colitis Esophagus, stomach, duodenum 3-5 %  Small and large intestine 40-55%  Small intestine only 25-30 %  Colon only 20-25 %  Rectal lesion 11-26%  Anorectal lesions (anal fistulas, anal fissures, abscesses resulting from periproctitis) 30-40 % •Total colitis 18 % •Left-sided lesion 28 % •Proctochygmoiditis 54 %
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  • 75.