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.
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.
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).
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
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).
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.
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.
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.
•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 %