This macro-preparation is a liver. The shape is preserved, the weight and dimensions are reduced. Liver yellow color.
These pathological changes could develop as a result of intoxication, allergic or viral damage liver. In the organ, fatty (yellow) dystrophy develops, the morphogenetic mechanism of which is decompensation. Dystrophy spreads from the center to the periphery of the lobules. It is replaced by necrosis and autolytic decay of central hepatocytes. The fatty protein detritus is phagocytosed, while the reticular stroma with dilated vessels is exposed (red dystrophy). Due to necrosis of hepatocytes, the liver shrinks and shrinks in size.
1) favorable: transition to a chronic form.
2) unfavorable:
a) death from hepatic or renal failure;
b) post-necrotizing cirrhosis of the liver;
c) damage to other organs (kidney, pancreas, myocardium, central nervous system) as a result of intoxication.
Conclusion: these morphological changes indicate fatty degeneration of hepatocytes and their progressive necrosis.
Diagnosis: Toxic liver dystrophy. Stage of yellow dystrophy.
^ 10. Stomach cancer.
This macro-preparation is the stomach. The shape and size of the organ are changed due to the proliferation of whitish-yellow tissue, which has sprouted the stomach wall and significantly thickens it (up to 10 cm or more). The relief of the mucosa is not pronounced. In the central part of the growth, depressions, loosening and hanging areas - ulceration are visible.
Description of pathological changes:
These pathological changes could develop as a result of precancerous conditions and precancerous changes (intestinal metaplasia and severe dysplasia).
In the foci of changes in the epithelium, cells malignancy and the development of tumors (or cancer develops de novo). Guided by the macroscopic picture, we can say that this is a cancer with predominantly endophytic infiltrating growth - infiltrative-ulcerative cancer (as evidenced by the ulceration of the tumor). Histologically, it can be both adenocarcinoma and undifferentiated cancer. Progression, the tumor invades the wall of the stomach and significantly thickens it.
1) favorable:
a) slow growth of cancer;
b) highly differentiated adenocarcenoma;
c) late metastasis;
2) unfavorable: death from exhaustion, intoxication, matastases; spread of cancer outside the stomach and germination into other organs and tissues, secondary necrotic changes and decay of carcinoma; dysfunction of the stomach.
Conclusion: these morphological changes indicate mutational transformation of epithelial cells with their malignancy and subsequent tumor progression, which, with infiltrating growth, led to the invasion of the stomach wall with ulcerations, which may represent secondary necrotic changes and tumor decay.
Diagnosis: Infiltrative ulcerative gastric cancer.
^ 11. Erosions and acute stomach ulcers.
This macro-preparation is the stomach. The shape and size of the organ have been preserved, the mass has not been changed. The organ is whitish in color. The mucous membrane is strewn with black formations of a dense consistency. Among the numerous small ones, the diameter is 1-5 mm. there are also larger ones with a diameter of 7 mm, as well as conglomerates of 8x1 cm, 3x0.5 cm, consisting of merged formations with a diameter of 5 mm. Near one of them we see the formation of a triangular shape, the boundaries of which have pronounced differences from the gastric mucosa, since they are formed by connective tissue.
These morphological changes could develop as a result of exogenous and endogenous influences: malnutrition, bad habits and harmful agents, as well as autoinfection, chronic autointoxication, reflux, neuro-endocrine, vascular allergic lesions... Since the lesions are localized in the fundus, we can talk about an autoimmune process with damage to the parietal cells, which led to dystrophic and necrobiotic changes in the epithelium, a violation of its regeneration and atrophy. Probably in this case, chronic atrophic gastritis developed with atrophy of the mucous membrane and its glands. Defects in the mucosa lead to erosion, which is formed after hemorrhage and rejection of dead tissue. The black pigment at the bottom of the erosion is hydrochloric acid hematin. These changes are joined by the restructuring of the epithelium. Education, the border of which is formed by the mucous membrane and represents the healing of acute gastric ulcer by scarring and epithelialization.
1) favorable:
a) healing of acute ulcers by scarring or epithelialization;
b) inactive chronic gastritis(remission);
c) mild or moderate changes;
d) epithelialization of erosion;
2) unfavorable:
a) the development of chronic peptic ulcer disease;
b) malignancy of epithelial cells;
c) pronounced changes;
d) active pronounced gastritis.
Conclusion: these morphological changes indicate long-term dystrophic and necrobiotic changes in the epithelium of the mucous membrane with impaired regeneration and structural rearrangement of the mucous membrane.
Diagnosis: chronic atrophic gastritis, erosion and acute gastric ulcer.
^ 12. Chronic ulcer stomach.
This macro-preparation is the stomach. The masses and sizes of the organ are normal, the shape is preserved. The organ is light gray in color, the relief is strongly developed. On the lesser curvature of the stomach in the pyloric section, there is a significant depression in the stomach wall 2x3.5 cm. Its limiting surface of the organ is devoid of characteristic folding. The folds converge to the boundaries of the formation. In the area of the pathological process, there are no mucous, submucous and muscular layers of the stomach wall. The bottom is smooth, made serous membrane... The edges are ridge-like raised, dense, have a different configuration: the edge facing the gatekeeper is shallow (due to gastric motility).
Description of pathological changes:
These pathological changes could develop as a result of general and local factors (general: stressful situations, hormonal disorders; medicinal; bad habits that lead to local disorders: hyperplasia of the glandular apparatus, increased activity of the acid-peptic factor, increased motility, increased number of gastrin-producing cells; and a general disorder: excitation of the subcortical centers and the hypothalamic-pituitary region, increased tone vagus nerve, increase and subsequent depletion of the production of ACTH and glucocarticoids). Acting on the gastric mucosa, these violations lead to the formation of a defect in the mucous membrane - erosion. Against the background of non-healing erosion, an acute peptic ulcer develops, which, with continued pathogenic effects, turns into a chronic ulcer, which goes through periods of exacerbation and remission. During the period of remission, the bottom of the ulcer can be covered with a thin layer of epithelium, layering on the scar tissue. But during the period of exacerbation, "healing" is leveled as a result of fibrinoid necrosis (which leads to damage not only directly, but also by fibrinoid changes in the walls of blood vessels and disruption of the trophism of the ulcer tissues).
1) favorable: remission, healing of the ulcer by scarring, followed by epithelialization.
2) unfavorable:
a) bleeding;
b) perforation;
c) penetration;
d) malignancy;
e) inflammation and ulcerative cicatricial processes.
Conclusion: these morphological changes indicate a destructive process in the stomach wall, which leads to the formation of a defect in the mucosa, submucosa and muscular membrane - ulcers.
Diagnosis: Chronic peptic ulcer stomach.
^ 13. Hyalinosis of the spleen capsule. Glaze spleen.
This macro-preparation is the spleen. The masses and sizes of the organ are not increased, the shape is preserved. The color of the capsule is white, it is coarse, and the tuberosity is more pronounced in the front. The depressions are more and less large. An area with a diameter of 0.5 cm is noticeable on the anterior surface of the organ of yellow color. Behind and from the side of the capsule, areas of yellowish tissue are soldered.
Descriptions of pathological changes.
These pathological changes could develop as a result of the destruction of fibrous structures and an increase in tissue-vascular permeability (plasmorrhage) in connection with angioneurotic metabolic and immuno-pathological processes. Plasmorrhage - tissue impregnation with plasma proteins, their absorption on fibrous structures, precipitation and formation of hyaline. Hyalinosis can develop as a result of plasma impregnation, fibronoid swelling, inflammation, necrosis, sclerosis. In the spleen capsule, hyalinosis develops as an outcome of sclerosis. The connective tissue swells, loses fibrillarity, its bundles merge into a homogeneous dense, cartilaginous mass, the cells are compressed, atrophy. The tissue becomes dense, whitish, translucent. Along with hyalinosis connective tissue in the spleen, local hyalinosis of arterioles may be present as a physiological phenomenon. In this case, simple hyaline is formed (due to sweating of unchanged or slightly changed components of blood plasma).
1) favorable:
a) was possible only as a stage in the process during its stabilization and resorption of hyaline masses;
b) unfavorable - the most frequent: violation of the function of an organ, limitation of its functionality.
Conclusion: the data of morphological changes indicate dystrophic processes in the spleen capsule, which led to its hyalinosis.
Diagnosis: Hyalinosis of the spleen capsule.
^ 14. Dysentery colitis.
This macro-preparation is the large intestine. The shape of the organ is preserved, the mass and dimensions are increased due to the thickening of the wall. The mucous membrane is of a dirty gray color, at the apex of the folds and between them, the film overlays of a brown-green color covering the mucous mass are necrotic, ulcerated, in many places freely hanging down into the intestinal lumen (which is narrowed).
Description of pathological changes:
These pathological changes could develop as a result of acute intestinal disease with a predominant lesion of the large intestine, the cause of which was the penetration, development and reproduction in the epithelium of the mucous membrane of Shigella bacteria and their species. This group of bacteria has a cytoplasmic effect on these cells, which is accompanied by the destruction and desquamation of the latter, the development of desquamative catarrh. Enterotoxin of bacteria carries out vaseoneuroparalytic action, with which paralysis is associated blood vessels> increased exudation and damage to the intramural nerve ganglia, which leads to the progression of processes and the development of fibrinoid inflammation (as a result of increased sweating of fibrinogen from the dilated vessels). If in the first stage we find only superficial necrosis and hemorrhage, then in the second stage a fibrinoid film appears at the apex and between the folds. The necrotic masses of the mucosa are permeated with fibrin. Dystrophic and necrotic changes nerve plexuses combined with leukocyte infiltration of the mucosa and submucosa, its edema, hemorrhages. With the further development of the disease in connection with the rejection of fibrin films and necrotic masses, ulcers are formed, which at 3-4 weeks of the disease are filled with granulation tissue, which matures and leads to the regeneration of ulcers.
1) favorable:
a) complete regeneration with minor defects;
b) abortive form;
2) unfavorable:
a) incomplete regeneration with scar formation> narrowing of the intestinal lumen;
b) chronic dysentery;
c) lymphadenitis;
d) follicular, polycular-ulcerative colitis;
e) severe general changes (necrosis of the epitaleal tubules of the kidneys, fatty degeneration of the heart and liver, impairment mineral metabolism). Complications:
a) perforation of the ulcer: peritonitis; paraproctitis;
b) phlegmon;
c) intraintestinal bleeding.
Extraintestinal complications - bronchopneumonia, pilonephritis, serous arthritis, liver abscesses, ameloidosis, intoxication, exhaustion.
Conclusion: these morphological changes indicate colon diphtheria colitis associated with toxic effects shigella.
Diagnosis: Dysentery and colitis. Stage of diphtheria colitis.
^ 15. Typhoid fever.
This macro-preparation is the ileum. The shape of the organ is preserved, the weight and dimensions are normal. The intestine is whitish in color, the mucous membrane is folded, on which formations 4x2.5 cm and 1x1.5 cm are noticeable, which protrude above the surface of the mucous membrane. Grooves and convolutions are noticeable on them, the surface itself is uneven, loosened. These formations are dirty gray in color. A formation with a diameter of 0.5 cm is noticeable, with a loss of characteristic folding, whitish color, slightly deepened and compacted.
Description of pathological changes:
These pathological changes could develop as a result of infection (parenteral) with typhoid bacillus and their multiplication in the lower part of the small intestine (with the release of endotoxin). By lymphatic tract -> to Peyer's patches -> salitaric follicles -> regional lymph nodes -> blood -> bacteremia and bacteriocholia
-> into the lumen of the intestine -> hyperergic reaction in the follicles, which leads to an increase and swelling of follicles, tortuosity of their surface. This occurs as a result of the proliferation of monocytes, histiocytes, reticulocytes, which extend beyond the follicles into the underlying layers. Monocytes turn into macrophages (typhoid cells) and form clusters - typhoid granulomas. Catarrhal enteritis joins these changes. With the further progression of the process, typhoid granulomas necrotize and are surrounded by a zone of demarcation inflammation, sequestration and rejection of necrotic masses leads to the formation of "dirty ulcers" (as a result of soaking with bile), which eventually change their appearance: they are cleared of necrotic masses, the edges are rounded. The proliferation of granulation tissue and its maturation leads to the formation of delicate scars in their place. Lymphoid tissue is restored. Exodus:
1.favorable:
Complete regeneration of lymphoid tissue and healing of ulcers;
2.adverse:
Death as a result of intestinal (bleeding, perforation of ulcers, peritonitis) and extraintestinal complications (pneumonia, osteomyelitis, intramuscular abscesses, sepsis, waxy necrosis of the rectus abdominis muscles);
dystrophic changes in the parenchymal organs, the formation of typhoid granulomas in them.
Conclusion: these morphological changes indicate an acute infectious disease with local changes in the small intestine - ileolitis.
Diagnosis: Ileolith.
^ 16. Gangrene of the small intestine.
This macro-preparation is a section of the small intestine. Its dimensions and weight have not been changed. The bowel loops are enlarged, the consistency of one part is loose, the second is not changed. The surface is smooth. The serous membrane is dull and dull. Between the loops, a sticky, viscous, stretching liquid in the form of threads. On the section of the intestine, the walls are enlarged, the lumen is narrowed.
Possible causes: impaired blood supply as a result of strongometic necrochodemonia of the mesenteric arteries.
Morphogenesis: ischemia, dystrophy, atrophy, necrosis of an organ in contact with the external environment - gangrene.
1) unfavorable - putrefactive fusion, will distill.
Conclusion: indirect vascular necrosis.
Diagnosis: Wet gangrene of the small intestine.
Toxic liver dystrophy
Toxic liver dystrophy or progressive massive liver necrosis is acute or chronic illness characterized by massive tissue necrosis and the development of liver failure. Toxic dystrophy develops as a result of the action of exogenous (fungi, foodstuffs with toxins, etc.) and endogenous (pregnancy toxicosis, thyrotoxicosis) toxins. These substances have a hepatotoxic effect and damage hepatocytes.
Pathological anatomy. Toxic liver dystrophy It has various manifestations which depend on the duration of the damage to the liver cells. In the first few days, the organ grows, it becomes dense, yellow in color. Further, there is a progressive decrease in liver tissue and shrinkage of the capsule. On the cut, the liver is clay-colored or gray. Under a microscope, at first, fatty degeneration of hepatocytes is found in the center of the lobules, these changes are quickly replaced by necrosis and autolysis of the hepatic tissue. The progression of necrosis leads to the end of the second week to complete necrosis of the lobule, and only along the periphery there is a narrow strip of fatty degeneration. All this is a stage of yellow dystrophy. At the 3rd week, the liver decreases further and it turns red. These are manifestations of phagacytosis and resorption of necrotic detritus. At the same time, the stroma of an organ with dilated blood vessels is exposed. Changes at the 3rd week are a manifestation of the stage of red liver dystrophy.
With progressive necrosis, patients die from acute hepatic renal failure. Survivors have liver changes characteristic of postnecrotic cirrhosis.
24. Toxic liver dystrophy.
The liver is enlarged, flabby, with a wrinkled capsule. On the cut, the structure is erased, variegated
305. Portal cirrhosis of the liver.
The liver is deformed, compacted, reduced in size, the surface is granular. The section shows large and small nodules of liver tissue of various sizes, surrounded by a ring of connective tissue - the so-called “false lobules”.
553. Cirrhosis of the liver.
The liver is dense, tuberous, with yellow lesions and false lobules on a cut.
325. Fatty degeneration of the liver of the "goose" type. Chronic fatty hepatosis.
The liver is enlarged, yellow.
279. Liver cancer on the background of cirrhosis.
Against the background of cirrhosis of the liver, a focus of tumor tissue of a variegated appearance is visible.
198. Hepatic vein thrombosis.
A part of the liver with a hepatic vein, in the lumen of which a thrombus is visible.
127. Icteric necrotizing nephrosis.
The kidney on the cut is yellow-green, the border of the cortical and medulla stale bark is dull, wide.
462. Splenomegaly. Hyalinosis capsules.
The spleen is enlarged, on the capsule there are opaque translucent lesions
37. Hemorrhoids. In the distal colon, varicose veins are brown.
Dummy 35. Varicose veins veins of the esophagus with cirrhosis of the liver.
Sharp plethora and enlargement of the veins of the esophagus with arrosia of the vessel wall.
Examine micropreparations:
38. Acute viral hepatitis.
Hepatocytes in a state of hydropic (balloon) dystrophy and coagulation necrosis. Hyaline-like Kaunsilman's little bodies are found in the perisinusoidal lumens Cholestasis and lymphohistiocytic infiltration of the portal tracts are expressed
Indicate in the picture:
1 - balloon dystrophy of hepatocytes.
2 - Kounsilman's little body.
3 - cholestasis
4 - histiolymphocytic infiltration of the portal tracts
171. Subacute toxic liver dystrophy(acute hepatosis, stage of red dystrophy).
The structure of the hepatic lobules is broken. Hepatocytes in a state of necrosis cells are homogeneous, eosinophilic, without nuclei. Many necrotic hepatocytes have undergone phagocytosis and resorption. In these areas, a bare (free) reticular stroma with dilated sinusoids and bile capillaries is visible.
Indicate in the picture:
1 - necrotic hepatocytes.
2 - free stroma.
3 - dilated sinusoids and bile capillaries.
99. Portal cirrhosis.
The proliferation of connective weavers along the portal tracts in the form of rings with the formation of the so-called "false lobules" in which the architectonics of the vessels is disturbed. hepatocytes in a state of fatty degeneration (cells in the form of vacuoles) and regeneration (large nets with large or double nuclei)
Indicate in the picture:
1 - connective tissue
2 - false lobules
3 - hepatocytes in a state of fatty degeneration
4 - young liver cells
44. Biliary cirrhosis.
The proliferation of connective tissue along the periphery of the lobules. Cholestasis is expressed. The bile ducts are dilated, filled with yellow or dark green bile.
76. Postnecrotic cirrhosis (Masson's stain).
The structure of the liver is sharply disturbed by extensive areas of blue connective tissue in place of necrotic liver tissue. The preserved liver cells in a state of necrosis are homogeneous, pink-violet, without nuclei. Regeneration is not pronounced.
397. Toxic liver dystrophy is based on:
fatty degeneration
inflammation
protein dystrophy
398. The outcomes of toxic dystrophy are:
hepatic renal failure
cirrhosis of the liver
399. The cause of toxic liver dystrophy is:
infection
alcohol poisoning
poisoning with mushrooms and poisons
toxicosis of pregnancy
400. "Goose" liver develops when:
acute hepatosis
chronic hepatosis
401. The mechanism of hepatocyte alteration in serum hepatitis is:
direct action of viruses
immune cytolysis
402. AIDS is accompanied by hepatitis:
whey
epidemic
403. Dystrophy of hepatocytes in serum hepatitis:
grainy
vacuolar
404. K etiological factors hepatitis include:
medications
allergy
dystrophy
405. Morphological form chronic hepatitis is an:
phlegmonous
persistent
fibrinous
fatty hepatosis
406. Hepatitis is considered chronic:
after 1 month
after 3 months
after 6 months
after 1 year
407. Indications for biopsy in clinical diagnosis"Hepatitis" are:
verification of the diagnosis
establishing the form and severity of hepatitis
evaluation of treatment results
408. The safest type of biopsy for diffuse liver damage is:
puncture
transvenous
marginal liver resection
pinched at laparoscopy
409. The main histological signs of chronic active hepatitis are:
stepwise necrosis
empiopolesis
bridge necrosis
410. The main histological sign of persistent hepatitis is:
1- clear border of the boundary plate
2- sclerosis of the periportal tracts
3- granulomatous inflammation in the centrilobular zones
4- pericellular fibrosis
411. One of the main histological signs of viral hepatitis is:
1- Kounsilman's little body
2- giant mitochondria
3- granulomatous inflammation
4- pericellular fibrosis
5- sclerosis
412. The histological signs of liver tissue regeneration include:
1- binucleated hepatocytes
2- giant multinucleated hepatocytes, such as symplasts
3- "rosette-like" structures
413. Most common reason toxic liver dystrophy is:
414. The following stages of toxic liver dystrophy are distinguished:
1- active
2- red dystrophy
3- moderate
4- persistent
415. Signs of stage 1 of toxic liver dystrophy include:
bright yellow liver
the liver is reduced in size
the liver is dense, sclerosed
diffuse hemorrhages in liver tissue
416. The histological signs of the II stage of toxic liver dystrophy include:
necrosis of hepatocytes in the centrilobular regions
carbohydrate dystrophy
large focal sclerosis
Mallory's little body
417. The macroscopic sign of the liver in cirrhosis is:
liver of soft-elastic consistency
the liver is enlarged
dense liver
liver of "nutmeg" type
418. Acute viral hepatitis is characterized by:
extralobular cholestasis
bilious lakes
fatty degeneration of hepatocytes
Kounsilman's little body
419. Kaunsilman's bodies refer to hepatitis:
serum
alcoholic
to none of the above
420. What changes do hepatocytes undergo during the formation of Kaunsilman's bodies:
hyalinosis
colliquation necrosis
coagulation necrosis
421. Necrosis spreading between the center of the liver lobules and the branches of the black vein are called:
massive
stepped
bridged
422. Inflammatory infiltrates in acute serum hepatitis are dominated by:
neutrophils
macrophages
lymphocytes
423. Inflammatory infiltrates in alcoholic hepatitis must contain:
lymphocytes
neutrophils
macrophages
424. Reddish (light) color of the liver in cirrhosis depends on:
dystrophies
obstruction of blood flow through the inferior vena cava
obstruction of blood flow through the portal vein
425. "Lobular liver" refers to cirrhosis:
1- circulatory
3- infectious
4- exchange.
Topic VI. Diseases gastrointestinal tract.
Gastritis - inflammatory disease gastric mucosa. Distinguish between acute and chronic gastritis.
Acute gastritis is characterized by:
Macroscopically - thickening of the mucous membrane due to edema, redness, erosion.
FORMS OF ACUTE GASTRITIS:
1. Catarrhal (simple)
2. Fibrinous
3. Purulent
4. Necrotic
Chronic gastritis is a chronic inflammation of the gastric mucosa, accompanied by disorders of the carotid epithelial renewal.
Morphologically forms of chronic gastritis:
surface
atrophic
hypertrophic
combined atrophic-hyperplastic.
Modern international classification of chronic gastritis:
autoimmune (type A)
bacterial (type B)
mixed (type A and B)
chemically-toxic (type C)
lymphocytic
special forms (Menetrie's disease)
acute ulcer - an ulcer that covers the thickness of the mucous membrane, which does not have sclerotic changes in the bottom and at the edges; is usually secondary.
symptomatic ulcers are observed when:
stressful conditions
endocrine diseases
acute and chronic circulatory disorders
after taking medications
chronic ulcer - an ulcer that penetrates beyond the mucous membrane into the thickness of the stomach wall, has gross fibrous changes in the bottom and roller-like raised edges; the proximal edge of the ulcer is undermined.
LAYERS OF CHRONIC GASTRIC ULTRA:
1.zone of exudation or necrosis
2.zone of fibrinoid swelling
3.zone of granulation tissue
4. zone of sclerosis.
THE MAIN COMPLICATIONS OF THE PURPOSE DISEASE:
penetration
perforation
malignancy
pyloric stenosis
bleeding
perigastrid, periduodenitis
diverticulum - protrusion of the wall of the gastrointestinal tract.
Appendicitis is an inflammation of the appendix of the cecum, which gives a characteristic clinical syndrome.
Acute appendicitis happens:
1.simple
2.surface
3.destructive (phlegmanous, phlegmanous-ulcerative, apostematous, gangrenous)
chronic appendicitis develops after acute appendicitis and is characterized by sclerotic and atrophic processes, against the background of which inflammatory and destructive changes may appear.
forms of CHOLECYSTITIS:
1. Catarrhal
2. Purulent (phlegmonous)
3. Diphtheritic
4. Chronic
Crohn's disease is a chronic recurrent disease of the gastrointestinal tract, characterized by nonspecific granulomatosis, necrosis, scarring of the intestinal wall.
Examine macro-preparations:
79. Phlegmanous appendicitis.
The appendix is thickened, the serous membrane is dull, with fibrinous overlays, the vessels are full-blooded. The enlarged lumen is filled with pus (appendix epiema),
570. Normal gallbladder.
The wall of the gallbladder is thin, velvety mucous.
49. Calculous cholecystitis.
The wall of the gallbladder is thickened, sclerosed, there are many stones in the lumen of the gallbladder.
50, 180. Cholecystitis.
The wall of the gallbladder is unevenly thickened, the mucous membrane is swollen, dark red
348. Erosion of the gastric mucosa.
On the gastric mucosa, there are multiple superficial defects of the mucous membrane with smooth edges, the bottom is black (hematin hydrochloric acid pigment).
376. Acute stomach ulcers.
On the gastric mucosa, surface defects with smooth dark red edges from 1.5 to 3 cm in diameter are visible
183. Acute ulcer duodenum with perforation.
386. Chronic stomach ulcer.
On the lesser curvature of the stomach is visible ulcerative defect steep, up to 1 cm in diameter, the bottom and edges are dense, ridge-like.
108. Chronic stomach and duodenal ulcers.
On the mucous membrane of the stomach and duodenum, 3 ulcerative defects are visible. In the stomach, an elongated ulcer with undermined dense edges and a dense bottom. In the duodenum 2 ulcers of a rounded shape, located opposite each other ("kissing ulcers"), in one of them there is a perforated hole
128. Melena (bleeding into the lumen of the gastrointestinal tract).
The intestinal mucosa is black (pigment hematin hydrochloric acid, methemoglobin, iron sulfide)
149, 184. Saucer-shaped stomach cancer. Skirr of the stomach.
178. Stomach cancer.
Exo- and endophytic growth.
146. Ulcerative colitis.
On the mucous membrane of the colon, multiple ulcerative defects
of various shapes and sizes.
75. Polypoid cancer.
Myoma of the stomach.
Examine micropreparations:
62a. Chronic stomach ulcer ..
At the bottom of a chronic ulcer, 4 layers are distinguished:
1) on the surface of the ulcer defect there is a zone of necrosis with leukocytes, 2) underneath is fibrinous exudate, 3) a zone of granulation tissue is visible below, followed by 4) a zone of deep sclerosis with lymphoid infiltrates and sclerosed vessels.
Indicate in the picture:
1 - I zone - necrosis.
2 - II zone - fibrinoid
3 - III zone - granulation tissue.
4 - IV zone - sclerosis.
90. Acute suppurative appendicitis (phlegmanous-ulcerative).
(see at the same time the drug 151. The appendix is normal)
All layers of the appendix are infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosa, congested vessels and hemorrhages
Indicate in the picture:
1 - mucous membrane with ulceration
2 - submucosa
3 - muscular layer.
4 - serous membrane
5 - leukocyte infiltration of all layers of the wall of the appendix.
177. Chronic appendicitis with regeneration of the mucous membrane.
The wall of the appendix is thickened due to the proliferation of fibrous connective tissue in all layers of the newly formed low cubic epithelial cells creep onto the ulcer
140. Cholecystitis.
The wall of the gallbladder is thickened due to the proliferation of connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophied
74. Solid stomach cancer.
The parenchyma and stroma in the tumor are evenly developed. The parenchyma is represented by atypical cells that form cells. Anaplastic epithelium proliferates, in places it grows outside the mucous membrane - infiltrating growth
Tests: choose the right answers.
426. The causes of acute gastritis are:
1- alcoholism
2- infection
3- ingestion of traumatic substances
427. The following changes are characteristic of atrophic gastritis:
1- pink mucosa, with well-defined folds
2- mucous membrane pale
3- there is a lot of mucus in the stomach
4- focal regeneration of the epithelium
428. Main severe complication stomach ulcers are:
1- lymphadenitis of regional nodes
2- perforation
3- perigastritis
4- "inflammatory" polyps around the ulcer
429. The most characteristic changes in blood vessels in the bottom of a chronic ulcer are:
1- inflammation and sclerosis of the wall
2- plethora
3- anemia
4- large thin-walled sinusoidal vessels
430. The local factor of importance in the pathogenesis of gastric ulcer and duodenal ulcer includes:
1- infectious
2- violation of trophism
3- toxic
4- decrease in the secretion of gastrin and histamine
5- exogenous
431. The layers of the bottom of a chronic gastric ulcer are:
1- exudate
3- granulation tissue
4- sclerosis
432. An autopsy of the deceased revealed a lot of stomach erosions from burns, covered with hydrochloric acid hematin. Erosion formed:
1- before the burn
2- during a burn
433. On the mucous membrane of the stomach, there is a liquid of a coffee type. When cleansing from it, punctate hemorrhages and defects the size of a pinhead are visible. Specify the name of the process:
1- petechiae
3- acute ulcers
434. An autopsy in the stomach found two round ulcers located on the lesser curvature, the edges are even, the bottom is thin. The ulcers are:
1- sharp
2- chronic
435. The signs of a chronic ulcer are:
1- recurrent bleeding
2- dense sclerosed bottom
3- multiple ulcers
4 - one, two ulcers
436. The most common localization of stomach cancer is:
2- large curvature
3- small curvature
437. Cancer tumor diffusely germinates all layers of the stomach wall, dense, the stomach cavity is reduced. Cancer refers to:
1- differentiated adenocarcinoma
438. A woman has clinically determined solid tumors of the ovary on both sides. It is necessary to investigate the presence of metastases, first of all:
1- in the lungs
2- in the stomach
439. Acute gastritis usually manifests itself in the form:
1- atrophic
2- hypertrophic
3- purulent
4- superficial
5- with restructuring of the epithelium
440. Chronic atrophic gastritis is characterized by:
1- ulceration
2- hemorrhages
3- fibrinous inflammation
4- enterolization of the mucous membrane
5- plethora and diffuse leukocyte infiltration of its own layer of the mucous membrane
441. Exacerbation of stomach ulcers is characterized by:
1- hyalinosis
2- enterolization
3- regeneration
4- lymphoplasmacytic infiltrate
5- necrotic changes
442. The characteristic symptom of Menetrie's disease is:
1- enterolization of the gastric mucosa
2- hydrohydrolenic uremia (gastric tetany)
3- Virchow metastases
4- giant hypertrophic folds of the gastric mucosa
5- nonspecific intestinal granulomatosis
443. Ischemic colitis can be detected:
1- with atherosclerosis
2- with scleroderma
3- with diabetes
4- with rheumatoid arthritis
444. Rectal changes are characteristic:
1- for ulcerative colitis
2- for Crohn's disease
3- for Hirschsprung's disease
445. When ulcerative colitis is malignant, the intestinal mucosa is:
1- smooth
2- polypoid (granular)
3- atrophic
446. Malignancy of adenomatous polyps is more often found:
1- in the basal departments
2- in the superficial departments
3- in the middle departments
447. Familial multiple colon polyposis is found more often:
1- from birth
4- at the end of the first year of life
5- after 3 years
448. The characteristic histological signs of Whipple's disease are revealed:
1- in the lungs
2- in the myocardium
3- in the liver
4- in the kidneys
449. The most characteristic histological sign of Whipple's disease:
1- hemorrhage
3- macrophage infiltrate
4- leukocytosis
450. Cancer is suspected in an emaciated patient. An enlarged, indurated lymph node is felt over the left clavicle. It is necessary to examine first of all:
2- stomach
3- esophagus
451. The appendix is thickened in the distal part, the serous cover is dull, hyperemic, in the lumen there is fecal masses and purulent exudate. Microscopically - diffuse infiltration of the appendix wall with neutrophils, no ulcers. Appendicitis refers to:
1- to simple
2- to destructive
452. The appendix is thickened in the middle segment, the serous membrane is covered with fibrinous films. Histologically, against the background of diffuse infiltration of the entire thickness of the ulcer wall.
Appendicitis refers to:
1- to phlegmonous-ulcerative
2- to gangrenous
3- to simple
453. The appendix is thickened, the serous cut is covered with fibrin, the wall is black throughout, dull. Appendicitis refers to:
1- to catarrhal
2- to gangrenous
3- to phlegmonous
454. Abortive appendicitis is characterized by:
1- inflammation is mild
2- primary changes have resolved
3- the site of inflammation is extremely small
455. Thickening of mucus in the lumen of the sclerosed appendix is called:
1- cystic fibrosis
2- mucocele
3- melanosis
456. The characteristic signs of acute appendicitis are:
2- serous exudate in the mucous and muscular membranes
3- hyperemia
4- sclerosis of the wall of the appendix
5- destruction of muscle fibers
457. Characteristic features chronic appendicitis are:
1- sclerosis of the vessel walls
2- sclerosis of the wall of the appendix
3- purulent bodies
4- lymphoplasmacytic infiltration
5- granulomas
458. Morphological forms appendicitis are:
1- acute purulent
2- acute superficial
3- acute destructive
4- chronic
5- croupous
459. The complications of appendicitis are:
1- perforation
2- peritonitis
3- liver abscesses
460. Most often cause subhepatic jaundice:
1- cancer of the Vater's nipple
2- cancer of the head of the pancreas
3- liver cancer
461. Cancer of the head of the pancreas causes jaundice:
1- parenchymal
2- hemolytic
3- mechanical
462. Crohn's disease in the destructive phase is characterized by:
1- mucous membrane in the form of "cobblestone pavement"
2- deep slit longitudinal ulceration of the mucosa
3- superficial ulceration
4- granulomas in the intestinal wall
463. The mucous membrane of the ileum is divided by deep ulcers in the form of slits and resembles a cobblestone pavement. Name the disease:
3- typhoid fever
464. For ulcerative colitis allergic origin are characteristic:
1- fibrinous inflammation
2- multiple ulcers
3- polypoid protrusions of excessively regenerating epithelium
4- fibrinous necrosis of individual sections of the intestine.
Topic VII. An introduction to infections. Typhus: abdominal, typhus, recurrent.
Infectious - diseases caused by infectious agents are called: viruses, bacteria, fungi.
Invasive - diseases are called when protozoa and helminths are introduced into the body.
Typhoid fever - acute and long-lasting infection caused by salmonella (Salmonella typhi), in the first week of the disease is characterized by symptoms of general intoxication (fever, chills) associated with bacteremia; wide involvement of the reticuloendothelial system, accompanied by a rash, abdominal pain and severe weakness in the second week of the disease; ulceration in Peyer's patches with bleeding from small intestine and the development of shock in the third week of illness.
stages of CHANGE OF GROUP LYMPHATIC FOLLICLES OF THE SMALL INTESTINE IN ABDOMINAL TYPHUS:
1. Brain swelling
4. Clean ulcers
5. Regeneration
the cellular composition of typhoid granuloma - macrophages, the so-called typhoid and lymphoid cells.
Atypical forms of abdominal typhoid:
1. Kolotif
2. Laryngotif
3. Pneumotif
4. Cholecystotyphoid
THE MOST COMMON AND DANGEROUS COMPLICATIONS OF ABDOMINAL FEVER:
1. Intra-intestinal bleeding
2. Perforation of ulcers followed by peritonitis
Epitemic typhus. European typhus (lousy fever) -
An acute infectious disease caused by rickettsia is characterized by damage to the nervous system and blood vessels. It is manifested by general toxic phenomena, fever, roseolo-petechial rash and disruption of the activity of internal organs, especially the circulatory system.
Macroscopic characteristics are most often mild - skin rash in the form of red roseola or Brown color, petechiae, punctate conjunctival hemorrhages eyeball(Chiari symptom). In advanced cases, foci of skin necrosis with areas of gangrene are possible.
Microscopic changes in the capillaries develop - destructive-proliferative-endo-thrombotic-vyskulitis.
Types of granules for typhus:
1.mesenchymal - Davydovsky
microglial - Popova.
Recurrent disease is very rare - this is Brill-Zinser disease. (Repeated sporadic typhus).
Examine macro-preparations:
Description of drugs in Pathological Anatomy in Lesson number 28
LESSON number 28diseases of the liver and biliary system.
Macrodrug "Massive progressive necrosis liver - stage yellow dystrophy " .
The liver is sharply reduced in size, its capsule is wrinkled, the consistency is flabby, the liver tissue is clay-like in the cut.
Micropreparation № "Massive progressive necrosis liver - stage yellow dystrophy ".
V central departments lobules of hepatocytes in a state of necrosis. Some PMNs are found among the necrotic masses. In the peripheral sections of the lobules, hepatocytes are in a state of fatty degeneration: when staining Sudan III, in the center of the lobules, fatty detritus is visible in the hepatocytes of the peripheral sections of the lobules - a drop of fat.
Macrodrug "Fatty dystrophy liver ( fatty hepatosis ) »
The liver is enlarged, the surface is smooth, the edge is rounded, the consistency is flabby, ocher-yellow on the cut.
Micropreparation № "Spicy viral hepatitis ».
Hepatocytes in a state of hydropic and balloon dystrophy, which is an expression of focal colliquation necrosis. Some hepatocytes in a state of apoptosis: reduced in size, with eosinophilic cytoplasm and pycnotic nucleus, or have the appearance of a hyaline-like body, which is pushed into the lumen of the sinusoid (Kaunsilman's body). Bile capillaries are dilated, filled with bile. The portal tracts are dilated, infiltrated with lymphohistiocytic elements, the accumulations of which are visible inside the lobules in the sinusoids, as well as in areas where groups of hepatocytes are in a state of necrosis. In the peripheral parts of the lobules, binucleated and large hepatocytes (regenerative forms) are often found.
Electronogram "Balloon dystrophy hepatocyte at acute viral hepatitis " - demonstration .
Micropreparation № "Chronic viral hepatitis V moderate activity " .
Portal tracts are thickened, sclerosed, abundantly infiltrated with lymphocytes, macrophages (histiocytes), plasma cells with an admixture of PML. The infiltrate exits through the border plate into the parenchyma and destroys hepatocytes. The foci of necrotic hepatocytes are surrounded by lymphocytes and macrophages (stepwise necrosis). Infiltration foci are visible inside the lobules. Outside of areas of necrosis, hepatic cells are in a state of hydropic dystrophy.
Electronogram "Destruction of the hepatocyte by the killer lymphocyte in chronic active hepatitis."
In the place of contact of the lymphocyte with the hepatocyte, destruction of its cytoplasmic membrane is visible.
Macrodrug "Viral large-node ( postnecrotic ) cirrhosis liver "
The liver is reduced in size, dense, the surface is large-nodular: nodes of uneven size, more than 1 cm, separated by wide fields of connective tissue.
Micropreparation № "Viral multilobular ( postnecrotic ) cirrhosis liver " - drawing . The liver parenchyma is represented by false lobules (regenerated nodes) of various sizes. In each node, fragments of several lobules can be seen (multilobular cirrhosis), the hepatic tracts are indistinguishable, the central vein is absent or displaced to the periphery. Protein dystrophy and necrosis of hepatocytes. There are large hepatocytes with two or more nuclei. Areas of the parenchyma are separated by wide fields of connective tissue stained red with picrofuchsin. In the connective tissue fields, contiguous triads, sinusoidal vessels, proliferating cholangioli, and lymphohistiocytic infiltrates are seen.
Macrodrug "Alcoholic fine-knot ( portal ) cirrhosis liver "
The liver is enlarged (in the final - reduced) in size, yellow, dense, with a uniform small-knotted (small-knot) surface; nodes no more than 1 cm in diameter, separated by uniform narrow layers of connective tissue.
Micropreparation № "Alcoholic monolobular ( portal ) cirrhosis liver " - drawing . The parenchyma is represented by false lobules, uniform in size, built on fragments of one lobule (monolobular cirrhosis). The nodes are separated by narrow bands of connective tissue (septa), hepatocytes with signs of fatty degeneration. In connective tissue septa, lymphohistiocytic infiltration with an admixture of PMNs and proliferation of bile ducts is visible.
Macrodrug "Liver at mechanical jaundice " - demonstration .
Time: 2 hours.
Motivational characteristics of the topic: knowledge of the topic is necessary for further study of stomach diseases, stomach cancer at clinical departments of general and private courses of pathological anatomy, in practical work a doctor it is necessary for the clinical and anatomical analysis of sectional observations and the comparison of clinical data with the results of a biopsy study.
General learning objective: to study the etiology, pathogenesis and pathological anatomy esophagitis, gastric ulcer and duodenal ulcer, stomach cancer; be able to distinguish between them, guided by morphological characteristics.
Specific objectives of the lesson:
1. To be able to define gastritis, explain its classification, characterize the morphology of various forms of gastritis;
2. To be able to give a definition of peptic ulcer disease, explain its classification;
3. To be able to characterize the morphology of gastric ulcer and duodenal ulcer, depending on the stage of the course, to be able to name its complications;
4. To be able to name the macroscopic forms and histological types of stomach cancer, to explain the features of their growth and metastasis;
5. To be able to name the complications and causes of death in stomach cancer. Required initial level of knowledge: the student must remember the anatomical and histological structure of the esophagus, stomach, intestines, the physiology of their activity, the types and morphology of inflammation and regeneration.
Questions for self-study (initial level of knowledge):
1. Etiology, pathogenesis, morphological characteristics of acute and chronic esophagitis and gastritis;
2. Etiology, pathogenesis, morphological characteristics of peptic ulcer disease, its complications and outcomes;
3. Risk factors for developing stomach cancer. Classification of stomach cancer. Morphological characteristics, features of metastasis.
Terminology
Callous (callus - corn) - callous, dense.
Penetration - (penetratio - penetration) - the penetration of an ulcer through the wall of the stomach or duodenum 12 into a neighboring organ (for example, into the pancreas), fused with it due to the organization of fibrinous overlays during perigastritis (periduodenitis). Perforation (perforatio - perforation) - through perforation of the wall of a hollow organ.
Ulceration (ulcus - ulcer) - ulceration.
1. To study gastritis using the example of macro-preparations "Chronic hypertrophic gastritis", "Chronic atrophic gastritis" and micro-preparations "Chronic superficial gastritis"," Chronic atrophic gastritis with restructuring of the epithelium. "
2. To study the morphology of the stages and complications of gastric ulcer and duodenal ulcer on the example of macro-preparations " Multiple erosion and acute stomach ulcers "," Chronic stomach ulcer "," Ulcer-stomach cancer "and micropreparations" Chronic stomach ulcer during an exacerbation. "
3. To study precancerous processes in the stomach, macroscopic forms and histological types of cancer of the stomach and esophagus using the example of macro-preparations "Polyposis of the stomach", "Squamous cell carcinoma of the esophagus", "Fungal cancer of the stomach", "Saucer-shaped cancer of the stomach", "Ulcer-stomach cancer", "Diffuse gastric cancer" and micropreparation "Adenocarcinoma of the stomach".
Equipment of the lesson, characteristics of the studied drugs Micropreparations
1. Chronic superficial gastritis (staining with hematoxylin and eosin) - mucous membrane of normal thickness, integumentary fossa epithelium with moderate dystrophic changes. In the lamina propria of the mucous membrane at the level of the ridges, there is moderate lymphoplasmacytic infiltration with an admixture of a small amount of polymorphonuclear leukocytes. The fundic glands are not changed.
2. Chronic atrophic gastritis with restructuring of the epithelium (staining with hematoxylin and eosin) - the gastric mucosa is thinned, lined in places with integumentary epithelium, in places with limp and goblet cells. The main parietal and mucous cells in the fundic glands are displaced by large cells with a foamy cytoplasm characteristic of the pyloric glands. The number of glands is small, they are replaced by growths of connective tissue. In the lamina propria of the mucous membrane, lymphohistiocytic infiltration is noted.
3. Chronic stomach ulcer (staining according to Van Gieson) - in the wall of the stomach, the defect captures the mucous and muscular membranes, while the muscle fibers in the bottom of the ulcer are not detected, their break is visible at the edges of the ulcer. One edge of the ulcer is undermined, the other is shallow. At the bottom of the ulcer, 4 layers are distinguishable: fibrinous-purulent exudate, fibrinoid necrosis, granulation tissue and scar tissue. In the last zone, vessels with thickened sclerosed walls (endovasculitis) and destroyed nerve trunks are visible, which have grown like amputation neuromas.
4. Squamous cell carcinoma of the esophagus (stained with hematoxylin and eosin) - in the wall of the esophagus, cords and complexes of atypical squamous epithelium cells are visible. In the center of the complexes, there is an excessive formation of the horny substance in the form of layered structures called "cancer pearls". The tumor stroma is well expressed, represented by coarse fibrous connective tissue infiltrated with lymphocytes.
5. Adenocarcinoma of the stomach (staining with hematoxylin and eosin) - growths of bizarre, atypical glands are visible in all layers of the stomach wall. The cells that form these glands are of various sizes and shapes, with hyperchromic nuclei and figures of pathological mitoses
Macro preparations
1. Erosions and acute stomach ulcers. In the gastric mucosa, numerous small (0.2-0.5 cm) conical defects are visible, the bottom and edges of which are dark brown colored with hematin hydrochloric acid. Several deeper rounded defects with soft edges are visible.
2. Chronic stomach ulcer. On the lesser curvature, a deep defect of the stomach wall is visible, capturing the mucous and muscular membranes, oval-round in shape with very dense, callous, roller-like raised edges. The edge facing the esophagus is undermined, the edge facing the pyloric section is flat, looks like a terrace formed by the mucosa, submucosa and muscle layer of the stomach. The bottom of the ulcer is represented by a dense whitish tissue.
3. Chronic hypertrophic gastritis. The mucous membrane of the stomach is thickened, edematous, with high hypertrophied folds covered with thick viscous mucus, few small punctate hemorrhages are visible.
4. Chronic atrophic gastritis. The gastric mucosa is sharply thinned, in fact smooth, with single atrophied folds, numerous small punctate hemorrhages and erosions are visible.
5. Polyposis of the stomach. On the gastric mucosa, many rounded outgrowths on the pedicle are visible, grayish in color, with an uneven surface. Histologically, a polyp of the stomach often has an adenomatous structure.
6. Fungal stomach cancer. On the lesser curvature of the stomach, a nodular, broad-based formation resembling a fungus is visible. It is grayish red in color. On the periphery of the tumor, the mucous membrane is thinned, its folds are smoothed (signs of atrophic gastritis). Ulceration of mushroom stomach cancer leads to its transition to a saucer shape.
7. Saucer-shaped stomach cancer. The tumor has the appearance of a rounded formation on a broad base with raised roller-like edges, which gives the tumor some resemblance to a saucer. The bottom of the ulcer is covered with dirty gray decaying masses.
8. Ulcer-stomach cancer. It occurs with the malignancy of a chronic stomach ulcer. In the wall of the stomach (more often on the lesser curvature) - a deep round defect. At the bottom of the ulcer there is a dense grayish tissue. One of the edges of the ulcer is raised in a roller-like manner, represented by gray-pink tissue, which invades the surrounding mucous membrane. There are histological differences between saucer carcinoma and ulcer-carcinoma. With ulcerated stomach cancer, complications such as bleeding, perforation are frequent; development of stomach phlegmon is possible.
9. Diffuse stomach cancer. The wall of the stomach (especially the mucous membrane and submucosal layer) is sharply thickened throughout, whitish on the cut. The mucous membrane is uneven, folds of varying thickness; the serous membrane is thickened, dense, tuberous. The lumen of the stomach is narrowed (stomach of the "pistol holster" type). With diffuse cancer, complications are frequent due to germination in the surrounding organs (intestinal obstruction, jaundice, ascites, etc.).
Gastritis is an inflammatory disease of the stomach lining. Acute and chronic gastritis are distinguished along the course.
Acute gastritis develops as a result of irritation of the gastric mucosa by alimentary, toxic and microbial agents. Morphologically acute gastritis is characterized by a combination of alterative, exudative and proliferative processes.
Depending on the features of morphological changes in the mucous membrane, the following forms of acute gastritis are distinguished: catarrhal (simple), fibrinous, purulent (phlegmonous), necrotic (corrosive).
Chronic gastritis can develop in connection with relapses of acute gastritis or not associated with it. Chronic gastritis is characterized by long-term dystrophic and necrobiotic changes in the epithelium, as a result of which there is a violation of its regeneration and restructuring. Changes in the mucous membrane in chronic gastritis go through certain stages (phases), well studied with the help of repeated gastrobiopsies.
The appearance of epithelium in the stomach intestinal type is called enterolization, or intestinal metaplasia, and the presence of pyloric glands in the body of the stomach, called pseudopyloric, is called pyloric restructuring. Both of these processes reflect the perverse regeneration of the epithelium.
Peptic ulcer is a chronic, cyclically current disease, the main clinical and morphological expression of which is a recurrent ulcer of the stomach or duodenum. Depending on the localization of the ulcer and the characteristics of the pathogenesis of the disease, peptic ulcer disease is distinguished with the localization of the ulcer in the pyloroduodenal zone and in the body of the stomach. Among the pathogenetic factors of peptic ulcer disease, there are general (violations of the nervous and hormonal regulation of the stomach and duodenum) and local factors (violations of the acid-septic factor, mucous barrier, motility and morphological changes in the gastroduodenal mucosa). The significance of these factors in the pathogenesis of pyloroduodenal and fundic ulcers is not the same.
The morphological substrate of peptic ulcer disease is a chronic recurrent ulcer, which initially goes through the stages of erosion and acute ulcer. Erosion is a defect in the stomach lining. An acute ulcer is a defect not only of the mucous membrane, but also of other membranes of the stomach wall. The presence of necrosis in the bottom of the ulcer and fibrinoid changes in the vessel walls indicates an exacerbation of the pathological process. In the period of remission, the bottom of the ulcer is usually scar tissue, sometimes epithelialization of the ulcer is noted.
The period of exacerbation of the ulcer is dangerous with complications of an ulcerative-destructive nature: perforation, bleeding and penetration of the ulcer. In addition, complications of an ulcerative-cicatricial nature are distinguished: deformity, stenosis of the inlet and outlet of the stomach and an inflammatory nature: gastritis, perigastritis, duodenitis, periduodenitis. Malignancy of a chronic ulcer is possible.
Precancerous processes in the stomach include chronic gastritis, chronic ulcers, and gastric polyposis. The clinical and anatomical classification of stomach cancer takes into account the localization of the tumor, the nature of growth, macroscopic forms, histological types, the presence and nature of metastases, complications. Most often, stomach cancer is localized in the pyloric region (up to 50%) and on the lesser curvature (up to 27%), most rarely in the fundic region (2%). Depending on the nature of growth, the following clinical and anatomical forms are distinguished:
I. Cancer with predominantly exophytic expansive growth: plaque-like; polypous; fungal (mushroom); ulcerated cancer (primary ulcerative, saucer-shaped, cancer from a chronic ulcer, or ulcer-cancer);
II. Cancer with predominantly endophytic infiltrative growth: infiltrative-ulcerative, diffuse (limited and total);
III. Cancer with exoendophytic, mixed growth.
These types of gastric cancer can be phases of the development of carcinoma at the same time.
The following histological types of stomach cancer are distinguished: adenocarcinoma, solid cancer, undifferentiated cancer (mucous, fibrous, small cell), squamous cell carcinoma. Adenocarcinoma, as a more differentiated form of cancer, occurs more often in forms with predominantly exophytic expansive growth. Fibrous cancer (skyr), as a type of undifferentiated, occurs very often in forms with predominantly endophytic infiltrating growth. The first metastases of gastric cancer are found in the regional lymph nodes. The liver is the main target organ for hematogenous metastasis.
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This macro-preparation is the stomach. The masses and sizes of the organ are normal, the shape is preserved. The organ is light gray in color, the relief is strongly developed. On the lesser curvature of the stomach in the pyloric section, there is a significant depression in the stomach wall 2x3.5 cm. Its limiting surface of the organ is devoid of characteristic folding. The folds converge to the boundaries of the formation. In the area of the pathological process, there are no mucous, submucous and muscular layers of the stomach wall. The bottom is smooth, filled with a serous membrane. The edges are ridge-like raised, dense, have a different configuration: the edge facing the gatekeeper is shallow (due to gastric motility).
Description of pathological changes:
These pathological changes could develop as a result of general and local factors (general: stressful situations, hormonal disorders; medicinal; bad habits that lead to local disorders: hyperplasia of the glandular apparatus, increased activity of the acid-peptic factor, increased motility, an increase in the number of gastrin-producing cells; and a general disorder: excitation of the subcortical centers and the hypothalamic-pituitary region, an increase in the tone of the vagus nerve, an increase and subsequent depletion of the production of ACTH and glucocarticoids). Acting on the gastric mucosa, these violations lead to the formation of a defect in the mucous membrane - erosion. Against the background of non-healing erosion, an acute peptic ulcer develops, which, with continued pathogenic effects, turns into a chronic ulcer, which goes through periods of exacerbation and remission. During the period of remission, the bottom of the ulcer can be covered with a thin layer of epithelium, layering on the scar tissue. But during the period of exacerbation, "healing" is leveled as a result of fibrinoid necrosis (which leads to damage not only directly, but also by fibrinoid changes in the walls of blood vessels and disruption of the trophism of the ulcer tissues).
1) favorable: remission, healing of the ulcer by scarring, followed by epithelialization.
2) unfavorable:
a) bleeding;
b) perforation;
c) penetration;
d) malignancy;
e) inflammation and ulcerative cicatricial processes.
Conclusion: these morphological changes indicate a destructive process in the stomach wall, which leads to the formation of a defect in the mucosa, submucosa and muscular membrane - ulcers.
Diagnosis: Chronic gastric ulcer.
386. Chronic stomach ulcer.
On the lesser curvature of the stomach, a steep ulcerative defect is visible up to 1 cm in diameter, the bottom and edges are dense, ridge-like.
108. Chronic stomach and duodenal ulcers.
On the mucous membrane of the stomach and duodenum, 3 ulcerative defects are visible. In the stomach, an elongated ulcer with undermined dense edges and a dense bottom. In the duodenum 2 ulcers of a round shape, located opposite each other ("kissing ulcers"), in one of them a perforated hole
128. Melena (bleeding into the lumen of the gastrointestinal tract).
The intestinal mucosa is black (pigment hematin hydrochloric acid, methemoglobin, iron sulfide)
149. Saucer-shaped stomach cancer. 184. Skirr of the stomach.
Stomach cancer.
Exo- and endophytic growth.
146. Ulcerative colitis.
On the mucous membrane of the colon, multiple ulcerative defects
of various shapes and sizes.
A. Polypoid cancer.
75b. Myoma of the stomach.
EXPLORE MICROPREPARATIONS:
62a. Chronic stomach ulcer (exacerbation stage).
At the bottom of a chronic ulcer, 4 layers are distinguished:
1) on the surface of the ulcer defect there is a zone of necrosis with leukocytes, 2) beneath it, fibrinoid necrosis, 3) a zone of granulation tissue is visible below, followed by 4) a zone of sclerosis with lymphoid infiltrates and sclerosed vessels.
90. Acute suppurative appendicitis (phlegmanous-ulcerative).
(see at the same time the drug 151. The appendix is normal)
All layers of the appendix are infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosa, congested vessels and hemorrhages
177. Chronic appendicitis with regeneration of the mucous membrane.
The wall of the appendix is thickened due to the proliferation of fibrous connective tissue in all layers of the newly formed low cubic epithelial cells creep onto the ulcer
140. Cholecystitis.
The wall of the gallbladder is thickened due to the proliferation of connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophied
74. Solid stomach cancer.
The parenchyma and stroma in the tumor are evenly developed. The parenchyma is represented by atypical cells that form cells. Anaplastic epithelium proliferates, in places it grows outside the mucous membrane - infiltrating growth
At l and with (pictures):
Testes: choose the correct answers.
433. The causes of acute gastritis are:
1- alcoholism
2- infection
3- ingestion of traumatic substances
434. The following changes are characteristic of atrophic gastritis:
1- pink mucosa, with well-defined folds
2- mucous membrane pale
3- there is a lot of mucus in the stomach
4- focal regeneration of the epithelium
435. The main severe complication of gastric ulcer is:
1- lymphadenitis of regional nodes
2- perforation
3- perigastritis
4- "inflammatory" polyps around the ulcer
436. The most characteristic changes in blood vessels in the bottom of a chronic ulcer are:
1- inflammation and sclerosis of the wall
2- plethora
3- anemia
4- large thin-walled sinusoidal vessels
437. The local factor of importance in the pathogenesis of gastric ulcer and duodenal ulcer includes:
1- infectious
2- violation of trophism
3- toxic
4- decrease in the secretion of gastrin and histamine
5- exogenous
438. The layers of the bottom of a chronic stomach ulcer are:
1- exudate
3- granulation tissue
4- sclerosis
439. An autopsy of the deceased revealed a lot of stomach erosions from burns, covered with hydrochloric acid hematin. Erosion formed:
1- before the burn
2- during a burn
440. On the mucous membrane of the stomach there is a liquid of coffee appearance. When cleansing from it, punctate hemorrhages and defects the size of a pinhead are visible. Specify the name of the process:
1- petechiae
3- acute ulcers
441. An autopsy in the stomach found two round ulcers located on the lesser curvature, the edges are even, the bottom is thin. The ulcers are:
1- sharp
2- chronic
442. The signs of a chronic ulcer are:
1- recurrent bleeding
2- dense sclerosed bottom
3- multiple ulcers
4 - one, two ulcers
443. The most common localization of stomach cancer is:
2- large curvature
3- small curvature
444. Cancer grows diffusely all layers of the stomach wall, dense, stomach cavity is reduced. Cancer refers to:
1- differentiated adenocarcinoma
2- mucous cancer
445. A woman has clinically determined solid tumors of the ovary on both sides. It is necessary to investigate the presence of a tumor first of all:
1- in the lungs
2- in the stomach
446. Acute gastritis usually manifests itself in the form of:
1- atrophic
2- hypertrophic
3- purulent
4- superficial
5- with restructuring of the epithelium
447. Chronic atrophic gastritis is characterized by:
1- ulceration
2- hemorrhages
3- fibrinous inflammation
4- enterolization of the mucous membrane
5- plethora and diffuse leukocyte infiltration of its own layer of the mucous membrane
448. Exacerbation of stomach ulcers is characterized by:
1- hyalinosis
2- enterolization
3- regeneration
4- lymphoplasmacytic infiltrate
5- necrotic changes
449. The characteristic symptom of Menetrie's disease is:
1- enterolization of the gastric mucosa
2- chlorohydrolenic uremia (gastric tetany)
3- Virchow metastases
4- giant hypertrophic folds of the gastric mucosa
5- nonspecific intestinal granulomatosis
450. Ischemic colitis can be detected:
1- with atherosclerosis
2- with scleroderma
3- with diabetes
4- with rheumatoid arthritis
451. Rectal changes are characteristic:
1- for ulcerative colitis
2- for Crohn's disease
3- for Hirschsprung's disease
452. When ulcerative colitis is malignant, the intestinal mucosa is:
1- smooth
2- polypoid (granular)
3- atrophic
453. Malignancy of adenomatous polyps is more often found:
1- in the basal departments
2- in the superficial departments
3- in the middle departments
454. Familial multiple colon polyposis is found more often:
1- from birth
4- at the end of the first year of life
5- after 3 years
455. The characteristic histological signs of Whipple's disease are revealed:
1- in the lungs
2- in the myocardium
3- in the liver
4- in the kidneys
456. The most characteristic histological sign of Whipple's disease:
1- hemorrhage
3- macrophage infiltrate
4- leukocytosis
457. Cancer is suspected in an emaciated patient. An enlarged, indurated lymph node is felt over the left clavicle. It is necessary to examine first of all:
2- stomach
3- esophagus
458. The appendix is thickened in the distal part, the serous cover is dull, hyperemic, in the lumen there is fecal masses and purulent exudate. Microscopically - diffuse infiltration of the appendix wall with neutrophils, no ulcers. Appendicitis refers to:
1- to simple
2- to destructive
459. The appendix is thickened in the middle segment, the serous membrane is covered with fibrinous films. Histologically, against the background of diffuse infiltration of the entire thickness of the ulcer wall.
Appendicitis refers to:
1- to phlegmonous-ulcerative
2- to gangrenous
3- to simple
460. The appendix is thickened, the serous integument is covered with fibrin, the wall is black throughout, dull. Appendicitis refers to:
1- to catarrhal
2- to gangrenous
3- to phlegmonous
461. Abortive appendicitis is characterized by:
1- inflammation is mild
2- primary changes resolved
3- the site of inflammation is extremely small
462. Thickening of mucus in the lumen of the sclerosed appendix is called:
1- cystic fibrosis
2- mucocele
3- melanosis
463. The characteristic signs of acute appendicitis are:
2- serous exudate in the mucous and muscular membranes
3- hyperemia
4- sclerosis of the wall of the appendix
5- destruction of muscle fibers
464. The characteristic signs of chronic appendicitis are:
1- sclerosis of the vessel walls
2- sclerosis of the wall of the appendix
3- purulent bodies
4- lymphoplasmacytic infiltration
5- granulomas
465. The morphological forms of appendicitis are.
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