386. chronic ulcer stomach.
On the lesser curvature of the stomach is visible ulcer defect steep shape up to 1 cm in diameter, the bottom and edges are dense, roll-like.
108. Chronic ulcers of the stomach and duodenum.
3 ulcerative defects are visible on the mucous membrane of the stomach and duodenum. In the stomach, an elongated ulcer with undermined dense edges and a dense bottom. In the duodenum 12 rounded ulcers located opposite each other ("kissing ulcers"), one of them has a perforated hole
128. Melena (bleeding into the lumen of the gastrointestinal tract).
The mucous membrane of the intestine is black (pigment hematin hydrochloride, methemoglobin, iron sulfide)
149. Saucer-shaped cancer of the stomach. 184. Scirrhus of the stomach.
Stomach cancer.
Exo- and endophytic growth.
146. Nonspecific ulcerative colitis.
On the mucous membrane of the large intestine, multiple ulcerative defects
various shapes and sizes.
A. Polypoid cancer.
75b. Myoma of the stomach.
EXPLORE MICROSPREGATIONS:
62a. Chronic stomach ulcer (stage of exacerbation).
In the bottom of a chronic ulcer, 4 layers are distinguished:
1) on the surface of the ulcerative defect there is a zone of necrosis with leukocytes, 2) under it - fibrinoid necrosis, 3) a zone is visible below granulation tissue followed by 4) area of sclerosis with lymphoid infiltrates and sclerotic vessels.
90. Acute purulent appendicitis (phlegmanous-ulcerative).
(see preparation 151 at the same time. Normal appendix)
All layers of the process are infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosa, plethoric vessels and hemorrhages
177. Chronic appendicitis with regeneration mucous membrane.
The wall of the process is thickened due to the growth of fibrous connective tissue in all layers. Newly formed low cubic epithelial cells creep onto the ulcerative defect.
140. Cholecystitis.
The wall of the gallbladder is thickened due to the growth of connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophied
74. Solid cancer of the stomach.
The parenchyma and stroma in the tumor are evenly developed. The parenchyma is represented by atypical cells forming cells. The anaplastic epithelium proliferates, in some places it grows beyond the mucosa - infiltrating growth
A t l a s (drawings):
Tests: choose the correct answers.
433. The causes of acute gastritis are:
1- alcoholism
2- infection
3- ingestion of traumatic substances
434. Atrophic gastritis is characterized by following changes:
1 - mucous pink, with well-defined folds
2- pale mucous
3- there is a lot of mucus in the stomach
4- focal regeneration of the epithelium
435. Basic serious complication 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. To a local factor important in pathogenesis peptic ulcer stomach and duodenum, refers to:
1- infectious
2- violation of trophism
3- toxic
4- decrease in the secretion of gastrin and histamine
5- exogenous
438. 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 erosions of the stomach from a burn, covered with hematin hydrochloric acid. Erosion formed:
1- before the burn
2- during a burn
440. Coffee-like liquid on the gastric mucosa. When cleared of it, pinpoint hemorrhages and defects the size of a pinhead are visible. Specify the name of the process:
1- petechiae
3- acute ulcers
441. An autopsy revealed two round ulcers in the stomach, located on the lesser curvature, the edges are even, the bottom is thin. Ulcers are:
1- sharp
2- chronic
442. Signs of a chronic ulcer are:
1 - recurrent bleeding
2- dense sclerosed bottom
3- multiplicity of ulcers
4- one, two ulcers
443. The most common localization of stomach cancer is:
2- big curvature
3- lesser curvature
444. Cancer tumor diffusely sprouts all layers of the stomach wall, dense, the 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- surface
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 infiltration by leukocytes of the own layer of the mucous membrane
448. Exacerbation of gastric ulcer is characterized by:
1- hyalinosis
2- enterolization
3- regeneration
4- lymphoplasmacytic infiltrate
5- necrotic changes
449. A characteristic symptom of Menetrier's disease is:
1- enterolization of the gastric mucosa
2- chlorhydrolenic 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- in diabetes
4- for rheumatoid arthritis
451. Rectal changes are characteristic:
1- for ulcerative colitis
2- for Crohn's disease
3- for Hirschsprung 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 detected:
1- in the basal sections
2- in 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. 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 palpated above the left clavicle. It is necessary to examine first of all:
2- stomach
3- esophagus
458. The appendix is thickened in the distal section, the serous cover is dull, hyperemic, there are feces and purulent exudate in the lumen. Microscopically - diffuse infiltration of the process 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 cover 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 cover 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 have dissipated
3- area of inflammation is extremely small
462. Thickening of mucus in the lumen of a sclerosed appendix is called:
1- cystic fibrosis
2- mucocele
3- melanosis
463. Characteristic signs of acute appendicitis are:
2- serous exudate in the mucosa and muscle membrane
3- hyperemia
4- sclerosis of the process wall
5- destruction of muscle fibers
464. Characteristic signs of chronic appendicitis are:
1- sclerosis of the walls of blood vessels
2- sclerosis of the process wall
3- purulent bodies
4- lymphoplasmacytic infiltration
5- granulomas
465. Morphological forms appendicitis are.
In the gastric mucosa, defects of various sizes are visible, the bottom of which is stained with hydrochloric acid hematin in a black-brown color.
Macrodrug CHRONIC GASTRITIS.
Smoothing of the folds of the gastric mucosa is found, the wall is hyperemic, thinned, flattened. Multiple point erosions are noted.
Micropreparation No 422 Helicobacter pylori in the parietal mucus in the gastric pits (gastrobiopsy, Giemsa stain).
Spiral-shaped bacteria are visible, located near the surface epithelium of the supramucosal barrier. Surface cells are damaged, infiltration of the gastric mucosa with polymorphonuclear leukocytes.
Micropreparation N 423 CHRONIC ACTIVE ANTRUMA GASTRITIS WITH GLANDS ATROPHY AND COMPLETE INTESTINAL METAPLASIA (gastrobiopsy, stained with alcian blue and hematoxylin).
In the own plate of the mucous membrane between the glands, a large number of lymphocytes are detected with the formation of lymphoid follicles. There is a destruction of the glands and a decrease in their number, atrophy of the mucous membrane.
Macropreparation CHRONIC GASTRIC ULCER(kaleznaya).
On the lesser curvature of the stomach, a deep defect in the wall of the stomach is visible, penetrating up to serous membrane, oval shape, with raised edges. The edge facing the pylorus is flat, has the appearance of a terrace, formed by the mucous, submucosal and muscular membranes. The edge facing the esophagus is undermined. At the bottom of the ulcer, necrotic brown-brown detritus. The folds of the gastric mucosa are smoothed, the rays converge to the ulcerative defect (convergence of the folds).
(E) Micropreparation N 106 CHRONIC GASTRIC ULCER (with exacerbation) (staining with hematoxylin and eosin.
Defect in the wall of the stomach, which captures the mucous, submucosal and muscular membranes. Near the defect, one edge of the mucous membrane is undermined, the other is flat. There are 4 layers at the bottom of the wound defect - from the lumen to the serous membrane: fibrinous-purulent exudate (fibrin, neutrophils, an admixture of necrotic tissue), fibrinoid necrosis, granulation tissue, scar tissue. The muscular membrane at the bottom is not determined, its breakage is visible at the border of the ulcerative defect. In the mucous membrane near the ulcer - a picture of chronic atrophic gastritis.
View a set of macroscopic slides illustrating the complications of a chronic ulcer: PUNCHED GASTRIC ULCER, PENETRATING GASTRIC ULCER, ARROSION OF THE VESSEL IN THE BOTTOM OF THE ULCER, GASTRIC ULCER-CANCER, GASTRIC DEFORMATION
Saucer-shaped stomach cancer on the lesser curvature of the stomach, there is a formation protruding above the surface of the mucous membrane on a wide base with raised dense roller-like edges and a sinking bottom. The bottom is covered with gray-brown decaying masses.
Gross preparations of different forms of GASTRIC CANCER.
Diffuse stomach cancer the wall of the stomach (especially the mucous and submucosal membranes) is diffusely thickened in all departments. The section shows that a gray-pink dense tissue grows through it. The mucous membrane is uneven, its folds are of different thickness, the serous membrane is thickened, dense, bumpy. The lumen of the stomach is narrowed.
Micropreparation N 424 HIGHLY DIFFERENTIATED GASTRIC ADENOCARCINOMA (intestinal type) (staining with hematoxylin and eosin).
In the wall of the growth of atypical glandular structures of various sizes and shapes, built from atypical polymorphic cells. The nuclei are large, hyperchromic.
Micropreparation N 225 UNDIFFERENTIATED CANCER - cricoid (stained with hematoxylin and eosin and alcian blue).
In the cytoplasm of tumor cells, mucin (mucus), stained blue. Tumor cells are cricoid in shape, the nucleus is pushed to the periphery, the cytoplasm is filled with mucus.
DISEASES OF THE INTESTINE
Macropreparation PHEGMONOUS APPENDICITIS.
The appendix is enlarged, thickened. The serous membrane is hyperemic, dull, with fibrin overlays. When the process is cut, greenish-gray thick contents are released from its lumen.
(E) Micropreparation N 107 PHEGMONOUS APPENDICITIS (stained with hematoxylin and eosin). The mucous membrane of the appendix is focally destroyed, in the lumen of the appendix there is a mass of pus, the layers of the wall are diffusely infiltrated with leukocytes.
Macropreparation CHRONIC APPENDICITIS.
The lumen is filled with mucus. Cavity obliteration. Mucus turns into globules. Muscular atrophy and sclerosis.
Micropreparation N 133 CHRONIC APPENDICITIS (staining with hematoxylin and eosin).
Fibrous obliteration is formed. The lamina propria undergoes lipomatosis, muscle layer atrophy, and sclerosis. There is an inflammatory infiltration characteristic of chronic inflammation.
Macropreparation of LIVER ABSCESSES(pylephlebitic), as a complication of appendicitis
In the region of the gate of the liver there are cavities with thick grayish-white walls filled with greenish-gray dense contents. On section, the liver tissue is yellowish.
View a set of gross specimens of intestinal tumors.
Circular stenosing cancer of the sigmoid colon - in the sigmoid colon - an annular formation with raised edges and an ulcerated bottom. On section, grayish-white tissue with hemorrhages growing into the layers of the intestinal wall.
LIVER DISEASES
Macropreparation TOXIC LIVER DYSTROPHY (fatty hepatosis). The liver is enlarged in size, flabby, yellow-white in color (clay type), on the cut has a greasy sheen ("goose liver")
Micropreparation N 4 MASSIVE LIVER NECROSIS - subacute form (staining with hematoxylin and eosin). In the central sections of the lobules, necrotic detritus in the peripheral sections in the cytoplasm of hepatocytes, large vacuoles.
Micropreparation N 5 CHRONIC HEPATITIS OF WEAK ACTIVITY, STAGE I (staining with hematoxylin and eosin). Note the signs of hepatitis activity: intralobular lobular lymphoid infiltrates, "spreading" of lymphocytes along the sinusoids, degenerative changes in hepatocytes, lymphohistiocytic infiltration of the portal tracts. Note the signs of chronic inflammation (hepatitis stage): fibrosis of the portal portal tracts, fibrous septa growing into the lobules. Pay attention to cholestasis: expansion of bile capillaries, imbibition of hepatocytes by bile pigments.
The lobular structure of the liver is broken. In the portal tracts - sclerosis, a pronounced lymphoid infiltrate with the formation of lymphoid follicles. In some places, the infiltrate penetrates into the lobules through the border plate and surrounds groups of hepatocytes. Visible proliferation in the portal tracts bile ducts and periportal sclerosis. Hepatocytes along the course of infiltration are in a state of necrosis, in other areas there are signs of hydropic and fatty degeneration.
Electronogram HYDROPIC DYSTROPHY OF HEPATOCYTE IN VIRAL HEPATITIS(atlas, fig. 14.5). Pay attention to the expansion of the endoplasmic reticulum of the hepatocyte and the sharp swelling of mitochondria.
An electron microscopic examination of the EPS cistern was sharply expanded, the mitochondria were swollen.
Gross preparations of liver cirrhosis. Mark the size, color, consistency, appearance of the liver from the surface and in section. Assess the size of regenerated nodes and determine the macroscopic form of cirrhosis by this feature.
Alcoholic small nodular portal cirrhosis- the liver is deformed, yellow in color, the surface is small-hilly.
(E) Micropreparation N 48 CHRONIC MODERATE HEPATITIS WITH TRANSITION TO LIVER CIRRHOSIS (staining with hematoxylin and eosin and picrofuchsin). The presence of moderately pronounced signs of inflammation activity (lymphoid infiltration of the stroma, extending to the parenchyma, fatty degeneration of hepatocytes), fibrosis dominance (porto-portal, porto-central septa with the formation of false lobules) and regeneration of hepatocytes (loss of the beam structure, the presence of cells with large nuclei .
Gross preparations: PRIMARY LIVER CANCER, LIVER METASTASES OF TUMORS OF ANOTHER PRIMARY LOCATION.
MORPHOLOGICAL EQUIVALENTS OF GLOMERULONEFRITIS
Micropreparation N 112 INTRACAPILLARY PROLIFERATIVE GLOMERULONEFRITIS (staining with hematoxylin and eosin).
An enlarged multicellular glomerulus is noted. Hypercellularity is associated with proliferation and swelling of endothelial and mesangial cells. There is a narrowing of the lumen of the capillary loops that fill the cavity of the capsule, as well as their massive neutrophilic infiltration.
Micropreparation FIXATION OF DEPOSITS OF IMMUNE COMPLEXES IN THE RENAL GLUMER IN ACUTE GLOMERULONEPHRITIS(atlas, fig. 15.2).
A granular glow is visible along the basement membrane (deposits in the form of lumps glow)
Macropreparation SUBACCUTE GLOMERULONEPHRITIS("large motley kidney").
The kidney is enlarged, flabby, pale with petechial hemorrhages on the surface.
Micropreparation N 113 SUBACUTE PREFERREDLY EXTRACAPILLARY GLOMERULONEPHRITIS (staining with hematoxylin and eosin).
The crescents are visible, formed due to the proliferation of the epithelium of the outer leaf of the Shumlyansky-Bowman capsule and the migration of monocytes and macrophages into the space between the capsule and the capillary glomerulus. Between the layers of cells in the crescents is an accumulation of fibrin. The glomeruli are compressed - they show focal necrosis, diffuse and focal proliferation of the endothelium, and mesangial proliferation. Part of the tubules is atrophic, in the epithelium of some convoluted tubules - hydropic or hyaline-drop dystrophy. In the stroma of the kidney - sclerosis, lymphomacrophage infiltration.
MORPHOLOGICAL VARIANTS OF CHRONIC GLOMERULONEPHRITIS
Electronogram MEMBRANOUS NEPHROPATHY(atlas, fig. 15.6).
Electron microscopic examination shows subepithelial deposits in the glomerular basement membrane, accumulation of the basement membrane substance between the peduncles of podocytes, loss of processes by podocytes and their spreading on the thickened and deformed basement membrane.
Electronogram MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS(atlas, fig. 15.9).
Electron microscopic examination reveals subepithelial electron-dense deposits.
Electron diffraction pattern(atlas, fig. 15.10).
Electron microscopic examination shows deposits in the mesangium.
Macropreparation SECONDARY SHRINKLED KIDNEY (CHRONIC GLOMERULONEPHRITIS WITH OUTCOME IN NEPHROSCLEROSIS).
The kidneys are symmetrically wrinkled and have a fine-grained surface.
(E) Micropreparation N 114 FIBROPLASTIC GLOMERULONEPHRITIS (terminal) (staining with hematoxylin and eosin).
Sclerosis and hyalinosis of most glomeruli, proliferation of mesangial cells, sclerovascular loops in the remaining hypertrophied glomeruli. Sclerosis and hyalinosis of arterioles are noted. Hyaline cylinders in the lumen of the tubules.
SECONDARY KIDNEY DAMAGE
Macropreparation AMYLOID NEPHROSIS("big white", "big greasy kidney").
Note an increase in the size of the kidney, a dense texture, a greasy appearance of the surface.
The kidneys are enlarged in size, dense texture, smooth surface. On the cut with a greasy sheen. The boundary between the cortex and medulla erased
(E) Micropreparation N 16 AMYLOID NEPHROSIS (congo-mouth stain). Designate amyloid deposits in the capillary loops of the glomerulus, along the proper membrane of the tubules, in the walls of blood vessels, and also in the stroma of the kidney along the reticular fibers.
Note the color of the amyloid.
Under the basement membrane of the tubules, in the glomeruli, along the reticular fibers of the stroma in the intima of the vessels, there are red-colored amyloid deposits.
ACUTE RENAL FAILURE (ARF)
(E) Slide No. 6 NECROTIC NEPHROSIS (staining with hematoxylin and eosin). The glomeruli and epithelium of the direct tubules are preserved. Their cells contain nuclei. The epithelium of the convoluted tubules does not contain nuclei (karyolysis).
ORGANOPATOLOGY OF CHRONIC RENAL INSUFFICIENCY
View a set of macropreparations reflecting the morphological manifestations of uremia: FIBRINOSIS PERICARDITIS ("hairy heart"), croupous tracheitis, diphtheritic colitis.
DISHORMONAL DISEASES OF THE GENITAL ORGANS
Macropreparation UTERINE POLYP. Note the localization of the polyp, its shape, size, nature of the surface, connection with the underlying tissue.
The outgrowth of the endometrium is gray-red in color, with an uneven surface.
(E) Micropreparation N 142 Glandular endometrial hyperplasia (staining with hematoxylin and eosin).
The endometrial glands are built from proliferating type epithelium, have different sizes and shapes, have a tortuous course and cystic expansion, are very closely located, branching and budding of the glands are noted.
Micropreparation N 57 PSEUDOEROSION OF THE CERVICE (staining with hematoxylin and eosin).
In the area of erosion of the cervix, there are two types of epithelium: stratified squamous non-keratinized and prismatic epithelium. There is an ectopic columnar epithelium in the exocervix.
PATHOLOGY OF PREGNANCY
Macropreparation POSTPARTUM ENDOMETRITIS.
The membrane of the vagina and cervix is hyperemic, edematous, sometimes with hemorrhages. In the lumen of the vagina, especially in the cervix, there is exudate released from the uterus. The cervical canal is ajar.
Macropreparation LIVER IN ECLAMPSIA.
Single or confluent white-yellow foci of necrosis and multiple hemorrhages appear in the liver. different sizes- landcart liver.
CHAPTER 17. DISEASES OF THE GASTROINTESTINAL TRACT
CHAPTER 17. DISEASES OF THE GASTROINTESTINAL TRACT
DISEASES OF THE pharynx and throat. DISEASES OF THE STOMACH. IDIOPATHIC DISEASES OF THE INTESTINE (CROHRON'S DISEASE AND ULCERATIVE COLITIS)
PROCESS OF THE CECAQUS
Angina (tonsillitis)- an infectious disease characterized by inflammatory changes in the lymphoid tissue of the pharynx and palatine tonsils (Pirogov rings). Forms of tonsillitis: acute, chronic (recurrent).Forms of acute tonsillitis:exudative - catarrhal, fibrinous, purulent; necrotic - necrotic, gangrenous, ulcerative-membranous (a special form is Simanovsky-Plaut-Vincent's angina); by localization - lacunar, follicular.Complications of tonsillitis:local - paratonsillar abscess, cellular phlegmon, thrombophlebitis; common - sepsis, rheumatism, glomerulonephritis.
Gastritis- inflammation of the gastric mucosa.Types of gastritis:acute and chronic;by topography- diffuse and focal (antral, fundal, pyloroanthral, pyloroduodenal).
Forms of acute gastritis:catarrhal, fibrinous, purulent (phlegmonous), necrotic. In any form - erosion and acute ulcers.Erosion- a superficial defect of the mucous membrane is not deeper than its muscular plate.Ulcer- a deep defect, the bottom of which is the muscular or even serous layer of the organ wall.
Chronic gastritis- this is a group of diseases of the stomach of different etiologies, characterized by a combination of chronic inflammation and impaired regeneration with a structural reorganization of the gastric mucosa.Chro-classification
nic gastritis:by etiology and pathogenesis- Helicobacter pylori (type B), autoimmune (type A), reflux gastritis (type C);by topography; by morphological type- superficial and atrophic;by activity.Take into account the presence, nature and severityintestinal metaplasia and dysplasia (intraepithelial neoplasia).Chronic atrophic pangastritis is an optional precancer.
peptic ulcer- a chronic, cyclically current disease, the main clinical and morphological manifestation of which is a chronic recurrent gastric or duodenal ulcer.Complications of peptic ulcer:destructive- bleeding, perforation (perforation with the development of peritonitis), penetration (into the liver, gallbladder, omentum, pancreas);cicatricial- deformation and stenosis of the inlet and outlet sections of the stomach and duodenal bulb;malignancy- malignancy (very rare).
Tumors of the stomach:epithelial(adenoma and cancer) and non-epithelial(mesenchymal, lymphomas). Macroscopically, exophytic formations of the stomach (hyperplastic growths, adenomas) are calledpolyps.Classification of stomach cancer:macroscopic form of growth- exophytic (polypous, mushroom-shaped, saucer-shaped), endophytic (plaque-like), ulcerative-infiltrative, plastic linitis;on
histological type- intestinal type(intestinal - types of adenocarcinomas, etc.) and diffuse (skirr, solid, cricoid, etc.);according to the depth of invasion and the stage of generalization of the tumor process(TNM system). Diagnostically significant lymphogenous metastases:to the left supraclavicular lymph node(Virchow's metastasis),retrograde - to the ovaries(cancer of Krukenberg)into the pararectal tissue(Schnitzler metastases).
Idiopathic bowel disease: Crohn's disease(granulomatous inflammation of any department digestive tract) Andulcerative colitis.Ulcerative colitis- facultative precancerous disease.
Appendicitis- inflammation of the appendix of the caecum. In surgical practice, it belongs to the group of diseases referred to as acute abdomen (peptic ulcer with perforation, peptic ulcer with bleeding, acute intestinal obstruction, strangulated hernia, acute cholecystitis, acute appendicitis).Forms of appendicitis:acute - simple, superficial, phlegmonous (options - apostematous, phlegmonous-ulcerative), gangrenous (primary and secondary); chronic.Complications of acute appendicitis:peritonitis, mezenteriolit, pylephlebitis, pylephlebitic liver abscesses.
Rice. 17-1. Micropreparation. Chronic tonsillitis in the acute stage: the surface epithelium is damaged (dystrophic and necrotic changes, areas of ulceration), infiltrated by neutrophilic leukocytes (1). Lymphoid follicles are atrophied, there is sclerosis in the stroma (2). In dilated lacunae, neutrophilic leukocytes and bacterial colonies are determined (3).
Staining with hematoxylin and eosin: x160
Rice. 17-2. Macropreparations (a, b). Chronic multifocal atrophic gastritis: gastric mucosa with smoothed folds, thinned, pale, grayish in color, with small punctate hemorrhages, erosions (b - preparation by I.N. Shestakova)
Rice. 17-3. Micropreparations (а-d). Chronic atrophic gastritis: the mucous membrane of the fundus of the stomach is sharply thinned, the glands are reduced in size, the distance between them is increased, the epithelium of the glands acquires more primitive features, loses the ability to produce gastric juice and hydrochloric acid, and secretes mucus. There are foci of intestinal metaplasia with goblet cells (1). In the lamina propria of the mucous membrane diffuse lymphoplasmacytic infiltrate, lymphoid follicles (2), severe sclerosis; c, g - Helicobacter pylori in the lumen of the glands.
a, b - hematoxylin and eosin staining, c - Vartin-Stari staining, d - immunohistochemical method: a - x 100, b - x200, c, d - x400
Rice. 17-4. Macropreparations (a-e). Acute erosions and ulcers of the stomach: in the gastric mucosa, there are multiple small superficial (erosions) and deeper, capturing submucosal and muscular layers of the stomach wall (acute ulcers), rounded defects with soft, even edges and a brownish-black or gray-black bottom ( due to hematin hydrochloride, which is formed from erythrocyte hemoglobin under the action of of hydrochloric acid and enzymes of gastric juice); (see also Fig. 3-4, 4-10) (a, c - preparations by I.N. Shestakova, d, e - preparations by N.O. Kryukov)
Rice. 17-4. Continuation
Rice. 17-4. Ending
Rice. 17-5. Micropreparations (a, b). Erosion of the gastric mucosa: in the gastric mucosa, a superficial (within the mucous membrane) focus of necrosis is determined with the formation of a shallow defect - erosion with perifocal leukocyte inflammatory infiltration. At the bottom of the erosion there are deposits of hematin hydrochloric acid (1). Staining with hematoxylin and eosin: x 100 (b - preparation by N.O. Kryukov)
Rice. 17-6. Macropreparations (a-n). Chronic ulcer of the stomach (a, c-d, g-n) and duodenal ulcer (b, f): chronic ulcers with bleeding - arrosed and thrombosed vessels in the bottom of the ulcers (c, f, l, n), perforation (e, k - view from the outside, from the side of the abdominal cavity - j) and penetration (b, d, g-i, n). Round-shaped defects of the mucous membrane and the wall of the stomach (or duodenum) with roller-shaped compacted edges. The cardial edge of the ulcer is undermined, overhangs, and the edge facing the pyloric section of the stomach is flat, has the form of a terrace, the steps of which are formed by the mucous membrane, submucosal and muscle layers. This configuration is due to the constant displacement of the edges of the ulcer during peristalsis. The mucous membrane around the ulcer is changed, its folds can be located radially in relation to the ulcer defect (fold convergence -
a, g, i, m); (а-c, f - preparations of I.N. Shestakova,
b, d, i-n, - preparations of N.O. Kryukov)
R is. 17-6. Continuation
Rice. 17-6. Continuation
Rice. 17-6. Continuation
Rice. 17-6. Continuation
Rice. 17-6. Ending
Rice. 17-7. Micropreparations (a, b). Chronic gastric ulcer (a) and duodenal ulcer (b): a defect in the wall of the stomach or duodenum, involving the mucosa, submucosa and muscle membrane. There are 4 layers in the bottom of the defect: 1 - fibrinous-purulent exudate; 2 - fibrinoid necrosis; 3 - granulation tissue; 4 - scar tissue with sclerosed and hyalinized vessels. At the edges of a chronic gastric ulcer, the processes of restructuring of the epithelium (hyperplasia of the cervical epithelium, atrophy of the glands, intestinal metaplasia, mild or moderate dysplasia). Staining with hematoxylin and eosin: a - x 120, b - x60 (b - preparation by N.O. Kryukov)
Rice. 17-8. Macropreparations (a, b). Polyp of the stomach: a small exophytic formation protruding into the lumen of the stomach on a wide base, covered with a mucous membrane (histologically: a - adenoma, b - leiomyoma); (a - preparation by N.O. Kryukov, b - preparation by I.N. Shestakova)
Rice. 17-9. Macropreparations (а-d). Gastric cancer (nodular or diffuse forms): a - fungous, b - saucer-shaped, c, d - endophytic diffuse cancer (d - view from the outside of the stomach, from the side of the serous membrane); nodular form - on the lesser curvature of the stomach, a large mushroom-shaped or saucer-shaped node with raised jagged edges and a lowered ulcerated bottom is determined. The tissue of the node is whitish in color, dense in consistency, grows through all layers of the stomach wall, has no clear boundaries. Diffuse form: the wall of the stomach is sharply thickened over a considerable extent due to the growth of a dense whitish tissue that does not have clear boundaries. The mucous membrane with smoothed folds, rigid (see also Fig. 9-5, 10-7); (a - preparation by N.O. Kryukov, b - preparation by I.N. Shestakova)
Rice. 17-9. Ending
Rice. 17-10. Micropreparations (a, b). Adenocarcinoma of the stomach: in the thickness of the mucous membrane and muscular layer of the stomach there are atypical glandular complexes of different sizes and shapes (tissue atypia). Tumor cells and their nuclei are polymorphic, of different sizes and shapes, the nuclei are hyperchromic (cellular atypia). Mitoses (typical and atypical) are not numerous, the level of tumor proliferative activity is moderate. Tumor complexes penetrate into the lamina propria and muscle layer - invasive growth (see also Fig. 9-6). Staining with hematoxylin and eosin: x 160
Rice. 17-11. macropreparation. Phlegmonous appendicitis: the appendix is enlarged, the walls are thickened, diffusely saturated with pus (pus is also released from the lumen of the appendix when pressed), the surface is dull, reddish-bluish, with full-blooded vessels; the mesentery of the process is also full-blooded, with foci of suppuration, hemorrhages (see also Fig. 6-6); (preparation by I.N. Shestakova)
Rice. 17-12. Micropreparations (a, b). Phlegmonous-ulcerative appendicitis: pronounced leukocyte infiltration of all layers of the appendix wall, edema, inflammatory hyperemia, necrosis and ulceration of the mucous membrane, atrophy of the lymphoid tissue.
Staining with hematoxylin and eosin: a - x 60, b - x 200
Rice. 17-13. macropreparation. Chronic appendicitis: appendix of normal size (but can be enlarged or reduced), the serous membrane is smooth, shiny, whitish, with scraps of adhesions. The wall of the process is thickened, compacted (sclerosis). The mucous membrane is pale pink (atrophy). The lumen of the process is obliterated in places
Rice. 17-14. Micropreparations (a, b). Crohn's disease: deep slit-like ulcerative defect of the mucous membrane, lymphomacrophage, with an admixture of plasmocytes, infiltration and sclerosis of all layers of the intestinal wall (a), granuloma with giant multinucleated cells in the submucosal layer (b). Staining with hematoxylin and eosin: a - x 100, b - x 200
Rice. 17-15. Micropreparations (a, b). Ulcerative colitis: pronounced diffuse lymphomacrophage with an admixture of leukocytes, inflammatory infiltrate, edema, microcirculatory disorders of the colon mucosa, crypt abscess (1).
Staining with hematoxylin and eosin: a - x 100, b - x 200
Rice. 17-16. Macropreparations (a, b). Gangrene of the intestine: ischemic necrosis of a part of the small or large intestine with obstruction of the mesenteric arteries by blood clots, thromboembolism, atherosclerotic plaques (acute ischemic bowel disease); (a - preparation by A.N. Kuzin and B.A. Kolontarev)
Rice. 17-17. Macropreparations (a, b). Diverticulosis of the colon: multiple finger-like protrusions in the wall of the colon, from the side of the mucous membrane, the entrances to the diverticula look like dark spots (arrows); (preparations by I.N. Shestakova)
Rice. 17-18. macropreparation. Meckel's diverticulum (preparation by I.N. Shestakova)
Stained with hematoxylin and eosin. There is fibrinous-purulent exudate in the area of the defect in the stomach wall (a), with underlying vast area fibrinoid necrosis (b), the presence of granulation tissue (c) and the growth of coarse fibrous connective tissue penetrating to different depths of the muscle layer (d). The serous membrane of the stomach wall is preserved (e).
2. Chronic atrophic gastritis. Heme coloring
toxin and eosin. In the gastric mucosa, atrophy of the integumentary epithelium (a) and epithelium of the glands with restructuring
which glands according to the intestinal type - "intestinal metaplasia" (b), in the lamina propria of the mucous membrane of the field of sclerosis
(c) and lymphoplasmacytic infiltration with the formation of lymphoid follicles (d).
3. Adenocarcinoma. Stained with hematoxylin and eosin. All layers of the stomach wall are infiltrated with tumor tissue with signs of cellular atypism (a). Multiple pathological mitoses are seen in hyperchromic (b) and polymorphic tumor cells (c).
4. Mucous cancer stomach. Stained with hematoxylin and
eosin. The tumor tissue is represented by an abundance of large atypical "cricoid" cells (a) with the formation of a large amount of mucus (b). The infiltrative character of tumor growth is visible (c). Demonstration.
5. Scirrhus of the stomach. Stained with hematoxylin and eosin. In the wall of the stomach, a group of atypical cells with large hyperchromic nuclei (a), in the stroma of the tumor there is an overgrowth of fibrous connective tissue (b). Demonstration.
MACRO PREPARATIONS.
1. Sharp catarrhal gastritis: in stomach preparation, the mucous membrane is thickened, with high hyperemic folds, covered with thick viscous mucus, with petechial hemorrhages. Causes: poor-quality food, the use of alcohol surrogates, antitumor chemotherapy drugs, burns with acids and alkalis, uremia, salmonellosis, shock, severe stress.
Complications: acute ulcers, transition to chronic gastritis. Exodus: mucosal restoration.
2. Erosions and acute stomach ulcers: in the preparation of the stomach,
the mucous membrane is edematous, on the surface there are multiple petechial hemorrhages and conical defects of various sizes, their bottom and edges are black. Erosions are localized within the mucosa, and ulcers penetrate
cabins at different depths of the mucous membrane, some reach the muscular membrane.
Causes: endocrine diseases (Zolinger-Ellison syndrome, hyperparathyroidism), acute and chronic circulatory disorders, intoxication, allergies, chronic infections (tuberculosis, syphilis), postoperative, steroid and stress ulcers.
Complications: perforation, peritonitis.
Exodus: erosions are epithelialized, the ulcerative defect is replaced by scar tissue.
3. Chronic stomach ulcer in remission: in the stomach preparation, on the lesser curvature, there is a pathological focus in the form of a deepening of the mucous membrane, rounded in shape, 3 cm in diameter. The folds of the mucous membrane radially converge to the defect, the edges of which are dense, raised in a roller-like manner, and calloused (calculous ulcer). On the cut, the inlet is a crater, smaller than the inner part of the ulcer. The edge facing the cardia is undermined, the mucous membrane hangs over it. The edge facing the gatekeeper is flat - terraced. The thickness of the ulcer is represented by connective tissue, gray-white, 2.5 cm. At the bottom of the ulcer, the vessels are sclerotic, their lumen is gaping.
Causes: genetic predisposition, Helicobacter pylori, inflammatory and dysregenerative changes in the mucous membrane, leading to exposure to peptic aggression factors (hydrochloric acid and pepsinogen).
Complications: perigastritis, bleeding, perforation, penetration, cicatricial deformity stomach with the development of stenosis behind the inlet or outlet. Against the background of a chronic ulcer, a second disease can develop - stomach cancer.
4. Polyps of the stomach (adenomas): in the antrum
In the stomach there are two tumor-like formations the size of pigeon eggs, on thin legs, irregular oval shape with a villous surface, soft consistency.
In the section, pathological neoplasms are abundantly vascularized and localized exclusively on the surface of the mucous membrane, without sprouting the underlying tissues.
Complications: bleeding, torsion of the leg, obturation of the exit or inlet.
Exodus: malignancy.
5. Various forms stomach cancer.a) Fungal cancer:
on the surface of the mucous membrane there is a tumor-like formation growing into the lumen of the stomach, of an irregular round shape, 5 cm in diameter, on a wide base in the form of a mushroom cap, with a retraction in the center. The cut shows that the tumor sprouts the entire wall of the stomach.
b) Diffuse gastric cancer: the organ is reduced in size, the wall is thickened up to 1 cm along its entire length, it has a dense “woody” consistency, it is represented by a gray-pinkish tissue on the section. The mucous membrane is uneven, its folds of various thicknesses, the serous membrane is thickened, dense, tuberous. The lumen of the stomach is narrowed.
c) Saucer-shaped stomach cancer: on the lesser curvature there is a pathological focus in the form of a formation rising above the surface of the mucous membrane with dense roller-like edges and a sinking bottom, measuring 3.5 cm by 2.0 cm. The bottom is covered with gray-brown decaying masses. On section, the tumor tissue infiltrates the entire thickness of the organ wall.
Causes: nutrition (smoked meats, canned food, pickled vegetables, peppers), biliary reflux (after stomach operations, especially according to Billroth II), Helicobacter pylori (contributes to the development of mucosal atrophy, intestinal metaplasia, epithelial dysplasia). Metastasis: 1. Orthograde lymphogenous metastases to regional nodes on the lesser and greater curvature, retrograde lymphogenic metastases in the left supraclavicular lymph node - Virchow's metastasis, in the ovaries - Krukenbergovsky
cancer, pararectal tissue - Schnitzler metastases, 3. Hematogenous metastases to the liver, lungs, brain, bones, kidneys, less often to the adrenal glands and pancreas. 4. Implantation- carcinomatosis of the pleura, pericardium, diaphragm, peritoneum, omentum.
TEST CONTROL
Choose one or more correct answers
1. SIGNS OF ACUTE CATHARAL GASTRITIS
1) thickening of the mucosa
2) glandular atrophy
3) multiple erosions
4) mucosal sclerosis
5) neutrophilic infiltration of the mucosa
6) lymphoid infiltration of the mucosa
2. MORPHOLOGICAL FORMS OF ACUTE GASTRITIS
1) fibrinous
2) atrophic
3) hypertrophic
4) catarrhal
5) corrosive (necrotic)
3. CHANGES IN THE EPITHELIUM IN CHRONIC GASTRITIS
1) atrophy
2) intestinal metaplasia
3) hyperplasia
4) dysplasia
5) the appearance of Mallory bodies in the cytoplasm
4. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS A
2) autoantibodies in the blood
to parietal cells
3) Helicobacter pylori -
5. PATHOGENESIS OF PERNICIOUS ANEMIA IN AUTOIMMUNE GASTRITIS
1) cessation of HCl production
2) production of antibodies to Helicobacter pylori
3) production of antibodies to parental cells
4) production of antibodies to intrinsic factor
5) destruction of the glands and atrophy of the mucous membrane
6. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS IN
1) predominant localization - antrum
2) autoantibodies in the blood
to parietal cells
3) Helicobacter pylori -
main etiological factor
4) accompanied by G-cell hyperplasia, gastrinemia
5) often associated with pernicious anemia
6) is localized in the fundus
7) reflux of duodenal contents into the stomach - the basis of pathogenesis
ACUTE EROSION OF THE STOMACH IS
mucosal inflammation
mucosal necrosis,
nonmuscular
3) atrophy of the mucous membrane
4) mucosal sclerosis
5) necrosis involving the muscle layer
8. CLINICAL AND MORPHOLOGICAL SIGNS OF CHRONIC ATROPHIC GASTRITIS
IN THE STAGE OF EXAMINATION
1) often occurs in patients with alcoholism
2) the mucous membrane is not changed
3) diffuse lymphoid-plasmacytic infiltration with a significant admixture of PMN
4) foci of pyloric and intestinal metaplasia
5) increased acidity of gastric juice
9. MORPHOLOGICAL SUBSTRATE OF ULCER
1) inflammation of the gastric mucosa
2) erosion of the gastric mucosa
and 12 duodenal ulcer
3) acute stomach ulcer
and duodenum
4) chronic recurrent gastric and duodenal ulcer
5) inflammation of the mucous membrane of the duodenum
10. Sclerotic deformity of the stomach IS THE OUTCOME
1) catarrhal gastritis
2) diphtheritic gastritis
3) corrosive gastritis
4) phlegmonous gastritis
11. SIGNS of chronic atrophic gastritis as a precancerous disease
1) lymphoplasmacytic infiltration
2) sclerotic processes
3) structural restructuring of the epithelium
(intestinal metaplasia)
4) all answers are correct
5) all answers are wrong
12. ULCEROGENIC PROMOTORS
1) corticosteroids
3) aspirin
4) smoking
5) increased tone of the vagus nerve
13. Stomach ulcers include
1) endocrine ulcers of the stomach
2) allergic ulcers
4) postoperative ulcers
5) tuberculous ulcers
14. LOCAL FACTORS IN THE DEVELOPMENT OF Peptic Ulcer
1) increased aggressiveness of gastric juice
2) campillobacteria
3) the presence of chronic gastritis
4) circulatory disorders
5) all answers are correct
6) all answers are wrong
15. REASONS FOR THE DEVELOPMENT OF ACUTE GASTRIC ULCER
1) corticosteroids
3) aspirin
4) smoking
5) increase in tone
vagus nerve
16. MORPHOLOGICAL SIGNS OF ACUTE gastric ulcer
1) funnel shape
2) the shape of a truncated pyramid
in cross section
3) soft jagged edges
4) dense callused edges
7) multiple ulcers
17. MORPHOLOGICAL SIGNS of chronic gastric ulcer
1) funnel shape
2) the shape of a truncated pyramid
in cross section
3) soft jagged edges
4) dense callused edges
5) the bottom of the ulcer, as it is cleansed, is stained black with hematin hydrochloride
6) the edge of the ulcer, facing the pylorus, looks like a terrace, the cardial edge is undermined
18. SIGNS OF CHRONIC GASTRIC ULCER
DURING REMISSION
1) the presence of exudate on the surface
2) scar tissue interrupts the muscle membrane to different depths
3) endovasculitis
4) fibrinoid changes in the bottom and vessels
5) surface epithelialization
19. SIGNS OF CHRONIC GASTRIC ULCER
IN THE PERIOD OF EXAGENCE
1) the presence of fibrinous-purulent exudate
on the surface 2) scar tissue interrupts muscle
shell at different depths
3) endovasculitis
4) fibrinoid changes in the walls of blood vessels and in the bottom of the ulcer
12. Bleeding mechanism in peptic ulcer
arrosive
diapedetic
due to rupture of a blood vessel
as a result of purulent fusion
21. Chlorhydropenic uremia - the result
1) bleeding from an ulcer
2) chronic nephritis
3) ulcer penetration
4) cicatricial pyloric stenosis
5) all answers are correct
6) all answers are wrong
22. Peritonitis complicating a chronic ulcer is the result of
1) penetration
2) perforations
3) gastritis
4) duodenitis
5) cicatricial stenosis of the pylorus
23. COMPLICATIONS OF CHRONIC ULCER
1) penetration
2) perforations
3) empyema
4) hypercalcemia
5) cicatricial stenosis
and wall deformation
6) bleeding
24. TYPES OF GASTROPATHIES
1) Meniere's disease
2) Menetrier's disease
3) Wernicke's syndrome
4) Zollinger-Ellison syndrome
5) hypertrophic hypersecretory gastropathy
25. HISTOLOGICAL SIGNS OF GASTROPATHIES
1) hypertrophy of the gastric mucosa
2) atrophy of the gastric mucosa
3) hyperplasia of the integumentary pit epithelium
4) hyperplasia of the glandular epithelium
5) severe sclerosis
26. MORPHOLOGICAL SIGNS OF THE INFLAMMATORY POLYP
1) inflammatory infiltrate in the stroma
2) atypical cells
3) without a clear differentiation into the leg and body
4) dysplasia of the glandular epithelium
5) surface erosion
27. BENIGN TUMORS OF THE STOMACH
1) angiosarcoma
2) adenoma
3) leiomyoma
4) adenocarcinoma
5) hyperplasiogenic polyp
28. BACKGROUND FOR THE DEVELOPMENT OF GASTRIC ADENOMA
1) chronic superficial gastritis
2) acute erosive-hemorrhagic gastritis
3) acute fibrinous gastritis
4) chronic gastritis with enterolization
29. ADENOMA IS THIS
1) benign tumor
from glandular epithelium
2) a malignant tumor of the glandular epithelium
3) epidermal cancer
4) malignant tumor from transitional cell epithelium 5) benign tumor from squamous epithelium
30. DISEASES WITH A RISK OF CANCER
1) superficial gastritis
2) chronic stomach ulcer
3) acute erosive gastritis
4) chronic atrophic gastritis
5) adenomatous polyps
31. HISTOLOGICAL VARIANTS OF GASTRIC CANCER
1) adenocarcinoma
2) sarcoma
3) cricoid
4) undifferentiated
32. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF INTESTINAL TYPE GASTRIC CANCER
1) occurs more often before the age of 30 years
2) has a high degree of differentiation
3) develops against the background of chronic gastritis
4) 2 times more likely to affect men
5) develops from metaplastic epitheliocytes
33. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF DIFFUSE TYPE GASTRIC CANCER
1) develops from epitheliocytes
2) occurs in relatively young age
3) histologically cricoid-cell
4) occurs against the background of chronic gastritis
5) has a low degree of differentiation
34. PROGNOSTIC SIGN IN GASTRIC CANCER
1) histological variant
2) macroscopic form
3) depth of invasion
4) mucus formation
5) secondary changes
35. HISTOLOGICAL SIGNS OF POLYPOID STOMACH CANCER
1) atypical glandular structures of a bizarre shape
2) cricoid cells
3) an abundance of mucus in the lumen of the glands
4) atypical polymorphic cells with large hyperchromic nuclei
5) atypical cells characterized by monomorphism
36. HISTOLOGICAL SIGNS OF CRIC CELL GASTRIC CANCER
1) extensive hemorrhages are characteristic
2) the nuclei of atypical cells are displaced
to the cell membrane
3) poorly differentiated cells with very large hyperchromic nuclei irregular shape
4) atypical glandular structures
5) massive sclerosis and hyalinosis in the wall
37. MICROSCOPIC CHARACTERISTICS OF SCIRRHOUS GASTRIC CANCER
1) atypical cells with large
nuclei are arranged in groups
2) atypical cells form glands
3) massive growths of connective tissue
4) an abundance of mucus in the lumen of the glands
5) atypical cells do not form glands
38. KRUKENBERG AND SCHNITZLER METASTASES OF GASTRIC CANCER
1) hematogenous
2) implantation
3) lymphogenous orthograde
4) lymphogenous retrograde
39. COMPLICATIONS OF GASTRIC CANCER
1) hemoptysis
2) dilatation of the pylorus
3) perforation
4) exhaustion
5) stomach bleeding
40. SIGNS OF VIRCHOV METASTASIS
1) hematogenous metastasis
2) retrograde lymphogenous metastasis
3) peritoneal carcinomatosis
4) defeat of the left supraclavicular lymph node
5) ovarian damage
Sample answers To test tasks
Description of drugs Pathological Anatomy in Lesson No. 26
(This is an indicative description, not a cathedral one, some preparations may be missing, as a description of past years)
LESSON No. 26 stomach diseases: gastritis, peptic ulcer, stomach tumors
Micropreparation No. 37 "acute catarrhal gastritis" - description.
The mucous membrane of the stomach is covered with purulent exudate, penetrating into all layers of the stomach wall. The lumen of the glands is dilated. The cytoplasm of the epithelium is vacuolated. Own layer of the mucous membrane with full-blooded vessels, in places with diapedetic hemorrhages, polymorphonuclear leukocytes (PMNs).
Micropreparation No. 112 "chronic superficial gastritis" - demo.
Micropreparation No. 229 "chronic atrophic gastritis" - description.
The mucous membrane of the stomach is sharply thinned, the number of glands is reduced, in place of the glands, fields of expanding connective tissue are visible. Integumentary pit epithelium with hyperplasia. Epithelium of glands with signs of intestinal metaplasia. The entire wall of the stomach is diffusely infiltrated with histolymphocytic elements with an admixture of polymorphonuclear leukocytes.
Macropreparation "acute erosions and stomach ulcers" - description.
The mucous membrane of the stomach with smoothed folding and numerous defects of the mucous membrane of a rounded and oval shape, the bottom of which is colored black.
Macropreparation "chronic stomach ulcer" - description.
On the lesser curvature of the stomach, a deep defect of the mucous membrane is determined, affecting the muscle layer, rounded in shape with dense, raised, callused edges. The edge of the defect, facing the esophagus, is undermined, towards the pylorus - gently sloping.
Micropreparation No. 121 "chronic gastric ulcer in the acute stage" - description.
A defect in the wall of the stomach is determined, capturing the mucous and muscle layer, with an undermined edge facing the esophagus, and a flat one facing the pylorus. At the bottom of the defect, 4 layers are determined. The first external - fibrinous-purulent exudate. The second is fibrinoid necrosis. The third is granulation tissue. The fourth is scar tissue. At the edges of the defect, fragments of muscle fibers, an amputation neuroma, are visible. Vessels of the cicatricial zone with sclerosed thickened walls. The mucous membrane at the edges of the defect with hyperplasia.
Macropreparation "polyp of the stomach" - description.
On the gastric mucosa, a tumor formation is determined on a wide base (pedicle).
Macropreparation "saucer-shaped stomach cancer" - description.
The tumor has the appearance of a rounded flat formation on a wide base. The central part of the tumor sinks, the edges are somewhat raised.
Macropreparation "diffuse gastric cancer" - description.
The wall of the stomach (mucosal and submucosal layers) is sharply thickened, represented by a homogeneous grayish-white dense tissue. The mucous membrane over the tumor with symptoms of atrophy with smoothed folding.
Micropreparation No. 77 "Adenocarcinoma of the stomach" - description.
Micropreparation No. 79 "cricoid cell cancer» - demo.
The tumor is built from atypical glandular complexes formed by cells with pronounced cellular polymorphism. The stroma is not developed.
Micropreparation No. 70 "Metastasis of adenocarcinoma in the lymph node" - description.
The drawing of the lymph node is erased, the growth of the tumor tissue is represented by atypical glandular cosplexes.
studfiles.net
Types of chronic gastritis
| Etiology | Pathogenetic mechanism | Histological changes | |
| autoimmune | pernicious anemia |
||
| Peptic ulcers Stomach cancer |
|||
| Peptic ulcers Stomach cancer |
Other forms of gastritis
lymphocytic;
eosinophilic;
granulomatous.
Acute ulcers
chronic ulcers
Helicobacter pylori infection.
Chronic distress syndrome.
fibrinoid necrosis;
granulation tissue;
fibrous tissue.
Pathomorphosis of peptic ulcer.
studfiles.net
Educational lesson card (for independent work)
1. Diagnose catarrhal serous gastritis by macroscopic picture. To study and write down the name of the macropreparation "Catarrhal serous gastritis". Pay attention to the thickening of the folds of the mucous membrane, its hyperemia, a large amount of cloudy viscous exudate on its surface (see "Textbook", p. 344).
2. Diagnose acute catarrhal gastritis by microscopic picture. To study the micropreparation "Acute catarrhal gastritis" (staining with hematoxylin and eosin). Write down the name of the drug. The mucous membrane of the stomach is covered with serous-mucous exudate with an admixture of polymorphonuclear leukocytes. Desquamation of the integumentary epithelium is observed. The cytoplasm of the epithelium of the glands is vacuolated. The own layer of the mucous membrane is plethoric with focal accumulations of predominantly neutrophilic leukocytes (see "Textbook" p. 344; "Atlas", p. 100, Fig. 101). Solve a problem similar to problem number 1.
3. Diagnose chronic superficial gastritis by microscopic picture. Examine the micropreparation "Chronic superficial gastritis" (staining with hematoxylin and eosin). Write down the name of the drug. The surface epithelium is flattened in places, desquamated, the glands are not changed. The own layer of the mucous membrane is edematous, infiltrated by lymphoid, plasma cells, polymorphonuclear leukocytes (see "Textbook", p. 346, Fig. 267, a).
4. Diagnose chronic atrophic gastritis with restructuring according to the microscopic picture. To study and describe the micropreparation "Chronic atrophic gastritis with restructuring" (staining with hematoxylin and eosin). With a small magnification of the microscope, note the thickness of the gastric mucosa, a decrease in the number of glands. At high magnification, pay attention to the nature of changes in the glands: the absence of the main, additional, parietal (parietal) cells, the appearance of light cubic cells characteristic of the pyloric glands, and intestinal-type epithelium, goblet cells (see "Textbook", p. 346-347; "Atlas", p. 278, Fig. 290).
5. Diagnose erosion and acute gastric ulcers by macroscopic picture. To study the macropreparation "Multiple erosions and acute stomach ulcers". Write down the name of the drug. The mucous membrane of the stomach with multiple superficial defects mainly on the lesser curvature, in the antrum and pyloric regions. In the same departments there are deeper wall defects - acute ulcers. They have a round or oval shape, their bottom is formed muscle layer. The bottom of erosions and ulcers is colored dirty gray or black due to the formation of hydrochloric acid hematin (see "Textbook", p. 349).
6. Diagnose chronic gastric ulcer by macroscopic picture. To study and describe the macropreparation "Chronic gastric ulcer". Pay attention to the localization of the ulcer, its shape, edges, depth, density of the walls, the nature of the bottom. Determine and describe which edge faces the esophagus, which one - to the pylorus (see "Textbook", p. 350-351, Fig. 268; "Atlas", p. 281, Fig. 293).
7. Diagnose chronic gastric ulcer by microscopic picture. Examine the micropreparation "Chronic gastric ulcer with exacerbation" (staining with hematoxylin and eosin) and sketch it. With a low magnification of the microscope, find the cardiac and pyloric edges and the bottom of the ulcer. Determine the depth of the defect. At high magnification, note layer-by-layer changes in the bottom of the ulcer, characterizing chronic course and aggravation of the process (see "Textbook", p. 351; "Atlas", p. 282, fig. 294). Solve a problem similar to problem number 2.
8. Diagnose an ulcer, stomach cancer by a macroscopic picture. To study and write down the name of the macropreparation "Stomach ulcer-cancer". Pay attention to the growth of dense whitish-gray tumor tissue at the edges of the ulcer (see "Textbook", p. 356, Fig. 271).
9. Diagnose phlegmonous appendicitis by macroscopic picture. To study and describe the macropreparation "Phlegmonous appendicitis". Pay attention to the size of the process, the state of the serous membrane ( appearance, the degree of blood filling), the thickness and type of its wall in the section, the nature of the contents in the lumen (“see the “Textbook”, p. 372).
10. Diagnose phlegmonous-ulcerative appendicitis by microscopic picture. To study and describe the micropreparation "Phlegmonous-ulcerative appendicitis" (staining with hematoxylin and eosin). Pay attention to the degree of preservation of the mucous membrane, the nature of the exudate, its distribution in the layers of the wall (see "Textbook", p. 372, Fig. 281; "Atlas", p. 289, Fig. 300). Solve a problem similar to problem number 3.
www.studfiles.ru
Types of chronic gastritis
| Etiology | Pathogenetic mechanism | Histological changes | Associated clinical changes |
| autoimmune | Antibodies against parietal cells and receptors for external factor Castle. Sensitized T-lymphocytes. | Atrophy of the glands in the body of the stomach. Intestinal metaplasia. | pernicious anemia |
| bacterial infection(H. pylori) | Cytotoxins. mucolytic enzymes. Synthesis of ammonium ions by bacterial urease. Tissue damage in an immune response. | Active chronic inflammation. Multifocal atrophy, more in the antrum. Intestinal metaplasia. | Peptic ulcers Stomach cancer |
| Chemical damage Non-steroidal anti-inflammatory drugs Bile reflux Alcohol | Direct damage. Damage to the mucous layer. Degranulation of mast cells. | Hyperplasia of the pit epithelium. Edema. Vasodilation. A small number of inflammatory cells. | Peptic ulcers Stomach cancer |
Other forms of gastritis
Separately, the following types of chronic gastritis are distinguished:
lymphocytic;
eosinophilic;
granulomatous.
In lymphocytic gastritis, the main histological manifestation is the presence of numerous mature lymphocytes in the superficial layers of the epithelium. This form is sometimes found in patients with specific erosions along the enlarged mucosal folds. The etiology and relationship with Helicobacter-associated gastritis has not been established.
Eosinophilic gastritis is characterized by mucosal edema and the presence of numerous eosinophils in the inflammatory infiltrate. It is assumed that eosinophilic gastritis is an allergic response to a food antigen to which the patient is sensitized.
Granulomatous gastritis is rare form gastritis, in which epithelioid cell granulomas are formed. These granulomas can be a manifestation of Crohn's disease or sarcoidosis, but in rare cases it can be cryptogenic.
Micropreparation "Chronic atrophic gastritis with restructuring of the epithelium" (staining with hematoxylin and eosin). The mucous membrane of the stomach is thinned, lined in some places with integumentary epithelium, in some places with border and goblet cells. The main, parietal and mucous cells in the fundic glands are replaced by large cells with 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.
Peptic ulcer of the stomach and duodenum
Peptic ulceration is a violation of the integrity of the epithelial cover and underlying tissues of the digestive tract as a result of damage to them by acid and pepsin. According to the clinical course, ulcers are divided into acute and chronic.
Acute ulcers
The cause of the development of acute ulcers can be:
Severe course of acute gastritis. Deep spread of erosion acute gastritis usually occurs with the use of non-steroidal anti-inflammatory drugs or alcohol, during treatment with corticosteroids, which leads to the appearance of deep ulcers.
Strong stress. Acute ulcers can occur as a result of various factors that lead to stress, for example, with extensive burns, brain injuries. In this case, ulcers are formed as a result of mucosal ischemia, which leads to a decrease in its resistance to acid.
Pronounced increase in acidity. Increased acidity, for example, in patients with gastrin-secreting tumors (Zollinger-Ellison syndrome), leads to the formation of multiple ulcers in the antrum, duodenum, and even jejunum.
chronic ulcers
The cause of the development of chronic ulcers can be:
Helicobacter pylori infection.
Chemical exposures, including steroid drugs and non-steroidal anti-inflammatory drugs.
Chronic distress syndrome.
Chronic peptic ulcers most often form at the junction of different types of mucous membranes. So, for example, in the stomach, ulcers are observed at the point of transition of the body to the antrum, in the duodenum 12 - in the proximal area on the border with the pylorus, in the esophagus - in stratified epithelium before the esophageal-gastric junction, postoperative ulcers are localized in the stoma (in the anastomosis). That is, ulcers appear in those places where acid and pepsin come into contact with an unprotected mucosa.
Pathogenesis. For many years it was thought that the cause of peptic ulcers was hyperacidity. However, in many cases, patients observed normal and even reduced acidity of gastric juice. Conversely, ulceration was rarely observed in patients with hyperacidity. In addition, during treatment with antacids (drugs that reduce acidity), relapses were observed in many cases. This led to the idea that it is not acidity that plays the main role in the development of ulcers, but the ratio of aggression factors and mucosal defense factors. It is believed that in the genesis of duodenal ulcer, the main role is played by the increase in aggression factors, and in the development of gastric ulcer, the decrease in protection factors comes first. With a decrease in the latter, it is possible to develop ulcers even with low acidity.
Gastric ulcer. Gastric juice is strongly acidic (pH
The surface epithelium forms the second line of defense; to ensure this function, the correct functioning of both the apical membrane, which prevents the transport of ions, and the synthetic apparatus that produces bicarbonates, are necessary. Both of these functions depend on the blood supply to the mucosa.
Ulceration occurs as a result of either violation and destruction of the mucous barrier, or violation of the integrity of the epithelium. As a result of bile reflux, the mucous barrier is easily destroyed by its components. Acid and bile together destroy the surface epithelium, increasing the permeability and vulnerability of the mucous membrane. This leads to congestion and swelling in the lamina propria, which is seen in reflux gastritis.
The epithelial barrier may also be disrupted by the use of NSAIDs, as they disrupt the synthesis of prostaglandins, which normally protect the epithelium. Helicobacter pylori infection also plays a significant role in the destruction of the epithelium, in which both cytotoxins and ammonium ions and an inflammatory reaction have a destructive effect.
Ulcer of the 12 duodenal ulcer. Increased acidity plays a major role in the development of duodenal ulcers. In half of the patients hypersecretion of acid is observed, however, even with normal stomach acidity, the daily secretion cycle can be disturbed: there is no decrease in secretion at night. It is also known that during stimulation with gastrin in patients infected with Helicobacter pylori, acid synthesis is 2-6 times higher than in non-infected patients.
Factors damaging the anti-acid protection in the stomach usually do not affect the duodenum: Helicobacter pylori does not colonize the duodenal mucosa, the mucosa is resistant to the action of bile and alkaline ions of pancreatic juice, medications significantly diluted and absorbed before entering the intestine. However, Helicobacter pylori affects ulcer formation, because infection promotes gastric hypersecretion, which leads to the development of gastric metaplasia in the duodenum, and then colonization of the metaplastic epithelium of Helicobacter pylori occurs, which leads to the development of chronic inflammation, which also provokes ulceration.
Morphological changes. Macroscopically, chronic ulcers usually have a round or oval shape. Their sizes, as a rule, do not exceed 2 cm in diameter, however, cases are described when ulcers reached 10 cm in diameter or more. The depth of the ulcer is different, sometimes it reaches the serous membrane. The edges of the ulcer are clear, dense and rise above the normal surface.
In the stage of exacerbation in the bottom of the ulcer, 4 layers are clearly distinguishable:
Fibrinous-purulent exudate;
fibrinoid necrosis;
granulation tissue;
fibrous tissue.
Vascular sclerosis is noted, in the walls of some of them - fibrinoid necrosis.
Macropreparation "Chronic gastric ulcer". On the lesser curvature, a deep defect in the wall of the stomach is visible, capturing the mucous and muscular membranes, oval-rounded in shape with very dense, callused, ridge-like raised edges. The edge facing the esophagus is undermined; the edge facing the pylorus is gently sloping and looks like a terrace formed by the mucous membrane, submucosa and muscular membrane of the stomach wall. The bottom of the ulcer is represented by a dense whitish tissue.
Micropreparation "Chronic gastric ulcer in the period of exacerbation" (staining with hematoxylin and eosin). A defect in the wall of the stomach captures the mucous and muscular membranes, while the muscle fibers in the bottom of the ulcer are not determined, their breakage is visible at the edges of the ulcer. One edge of the ulcer is undermined, the other is flat. In 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 sclerotic walls and fibrinoid necrosis are visible.
During the period of remission, scar tissue is found at the edges of the ulcer. The mucosa is thickened at the edges, hyperplastic.
Complications. Ulcer healing occurs by regeneration of the epithelium and fibrosis of the underlying tissues. At the same time, as a result of contraction and compaction of scars, a narrowing of the lumen of the organ may develop: pyloric stenosis or central narrowing of the stomach (stomach in the form of an hourglass). Perforation of the wall of the stomach or duodenum is also possible, while the contents of the digestive tract are poured into the abdominal cavity, which leads to the development of peritonitis. During penetration, the ulcer perforates into a nearby organ, such as the pancreas or liver. With erosion blood vessels bleeding may occur, which can be fatal. With prolonged existence, gastric ulcers can become malignant, duodenal ulcers are very rarely malignant.
Pathomorphosis of peptic ulcer.
1. Rejuvenation of peptic ulcer.
2. An increase in the number of combined ulcers of the stomach and duodenum.
3. Reducing the number of malignant ulcers.
4. Increase in the number of acute ulcers.
5. Increase in the number of ulcers of medicinal origin.
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