Macro preparations. Acute duodenal ulcer with perforation Chronic gastric ulcer in the acute phase micropreparation

  • Date: 19.07.2019

In the gastric mucosa, defects of various sizes are visible, the bottom of which is colored black-brown with hydrochloric acid hematin.

Macrodrug CHRONIC gastritis.

Smoothing of the folds of the gastric mucosa is found, the wall is hyperemic, thinned, flattened. There are multiple point erosion.

Micropreparation No 422 Helicobacter pylori in parietal mucus in the gastric fossa (gastrobiopsy, Giemsa stain).

Coiled bacteria are visible, located near the superficial epithelium of the supra-mucous barrier. Superficial cells are damaged, infiltration of the gastric mucosa with polymorphonuclear leukocytes.

Micropreparation N 423 CHRONIC ACTIVE GASTRITIS OF ANTHRUM WITH IRON ATROPHY AND COMPLETE INTESTINAL METAPLASIA (gastrobiopsy specimen, stained with alcian blue and hematoxylin).

In the lamina propria 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.

Macrodrug CHRONIC STOMACH Ulcer(kaleznaya).

On the lesser curvature of the stomach, a deep defect of the stomach wall is visible, penetrating to the serous membrane, oval in shape, with raised edges. The edge facing the gatekeeper is gently sloping, it looks like a terrace, formed by mucous, submucous and muscular membranes. The edge facing the esophagus is undermined. At the bottom of the ulcer there is necrotic brownish detritus. The folds of the gastric mucosa are smoothed, the rays converge to an ulcerative defect (convergence of folds).

(E) Micropreparation N 106 CHRONIC STOMACH Ulcer (with exacerbation) (staining with hematoxylin and eosin.

A defect in the stomach wall that invades the mucous membranes, submucosa and muscular membranes. Near the defect, one edge of the mucous membrane is undermined, the other is shallow. At the bottom of the wound defect there are 4 layers - 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 break is visible at the border of the ulcer defect. In the mucous membrane near the ulcer - a picture of chronic atrophic gastritis.

View a set of macro-preparations illustrating the complications of chronic ulcers: PASSING GASTRIC ULTRA, PENETRATING GASTRIC ULTRA, ARROSION OF THE VASCULAR IN THE BOTTOM OF THE ULTRA, ULTRA-STOMACH CANCER, CURRIC DEFORMATION OF THE STOMACH

Saucer-shaped stomach cancer - on the lesser curvature of the stomach, there is a formation on a broad base protruding above the surface of the mucous membrane with raised dense roller-like edges and a sunken bottom. The bottom is covered with gray-brown decaying masses.

Macro preparations of different forms of STOMACH CANCER.

Diffuse stomach cancer - the wall of the stomach (especially the mucous and submucous membranes) are diffusely thickened in all parts. The section shows that a gray-pink dense tissue grows through it. The mucous membrane is uneven, its folds are of varying thickness, serous membrane thickened, dense, bumpy. The lumen of the stomach is narrowed.

Micropreparation N 424 HIGHLY DIFFERENTIATED GASTRIC ADENOCARCINOMA (intestinal type) (stained with hematoxylin and eosin).

In the wall of 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 - signet ring (staining with hematoxylin and eosin and alcian blue).

In the cytoplasm of tumor cells, mucin (mucus) is colored blue. Tumor cells are cricoid in shape, the nucleus is pushed to the periphery, the cytoplasm is filled with mucus.

INTESTINAL DISEASES

Macrodrug PHLEGMONOUS APPENDICITIS.

The appendix is ​​enlarged, thickened. The serous membrane is hyperemic, dull, with fibrin overlays. When the appendix is ​​cut, a greenish-gray thick content is released from its lumen.

(E) Micropreparation N 107 PHLEGMONOUS APPENDICITIS (staining 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 by leukocytes.

Macrodrug CHRONIC APPENDICITIS.

The lumen is filled with mucus. Obliteration of the cavity. The mucus turns into globules. Atrophy of the muscle layer and sclerosis.

Micropreparation N 133 CHRONIC APPENDICITIS (staining with hematoxylin and eosin).

Fibrous obliteration is formed. The proper lamina of the mucous membrane undergoes lipomatosis, atrophy of the muscle layer, and sclerosis. There is an inflammatory infiltration characteristic of chronic inflammation.

Macro-preparation of the Liver abscess(pylephlebitic), as a complication of appendicitis

In the area of ​​the gate of the liver - cavities with thick grayish-white walls, filled with greenish-gray dense contents. On the cut, the liver tissue is yellowish.

View a set of intestinal tumors macro-preparations.

Circular stenosing cancer of the sigmoid colon - v sigmoid colon- an annular formation with raised edges and an ulcerated bottom. The section shows a grayish-white tissue with hemorrhages, growing into the layers of the intestinal wall.

LIVER DISEASES

Macrodrug TOXIC LIVER DYSTROPHY (fatty hepatosis). The liver is enlarged, flabby consistency, yellow-white (clay-like), has a greasy sheen in the cut ("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 are large vacuoles.

Micropreparation N 5 CHRONIC HEPATITIS OF WEAK ACTIVITY, STAGE I (staining with hematoxylin and eosin). To note signs of hepatitis activity: intralobular lobular lymphoid infiltrates, "spreading" of lymphocytes along sinusoids, dystrophic changes in hepatocytes, lymphohistiocytic infiltration of portal tracts. Note the signs of chronic inflammation (stage of hepatitis): fibrosis of the portal portal tracts, fibrous septa growing into the lobules. Pay attention to cholestasis: expansion of bile capillaries, imbibition of hepatocytes with bile pigments.

The lobular structure of the liver is disturbed. In the portal tracts - sclerosis, pronounced lymphoid infiltrate with the formation of lymphoid follicles. In some places, the infiltrate penetrates into the lobules through the boundary plate and surrounds groups of hepatocytes. Proliferation in the portal tracts is visible bile ducts and periportal sclerosis. Hepatocytes in the course of infiltration in a state of necrosis, in other areas signs of hydropic and fatty degeneration.

Electronogram HYDROPIC HEPATOCYTE DYSTROPHY 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.

During electron microscopic examination, the EPS cisterns are sharply expanded, the mitochondria are swollen.

Macro-preparations of LIVER CIRROSIS... Mark the size, color, consistency, surface and section view of the liver. Estimate the size of the regenerated nodes and determine the macroscopic form of cirrhosis based on this feature.

Alcoholic small-node portal cirrhosis of the liver- the liver is deformed, yellow, the surface is small-knobby.

(E) Micropreparation N 48 CHRONIC HEPATITIS OF MODERATE ACTIVITY WITH TRANSITION TO LIVER CIRROSIS (staining with hematoxylin and eosin and picrofuchsin). The presence of moderately pronounced signs of inflammation activity (lymphoid infiltration of the stroma, extends to the parenchyma, fatty degeneration of hepatocytes), the dominance of fibrosis (port-portal, port-central septa with the formation of false lobules) and regeneration of hepatocytes (loss of the beam structure, the presence of cells with large nuclei ...

Macro-preparations: PRIMARY LIVER CANCER, LIVER METASTASES OF TUMORS OF ANOTHER PRIMARY LOCALIZATION.

MORPHOLOGICAL EQUIVALENTS OF GLOMERULONEPHRITIS

Micropreparation N 112 INTRACAPILLARY PROLIFERATIVE GLOMERULONEPHRITIS (stained 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 IMUNE COMPLEXES IN THE RENAL BLOOD IN ACUTE GLOMERULONEFRITIS(atlas, fig. 15.2).

Along the course of the basement membrane, a granular glow is visible (deposits in the form of lumps glow)

Macro-preparation SUBCUTE GLOMERULONEPHRITIS("large variegated kidney").

The kidney is enlarged, flabby, pale with petechial hemorrhages on the surface.

Micropreparation N 113 SUBCUTE, MOSTLY EXTRACAPILLARY GLOMERULONEPHRITIS (stained with hematoxylin and eosin).

Semi-moon formed due to the proliferation of the epithelium of the outer layer of the Shumlyansky-Bowman capsule and the migration of monocytes and macrophages into the space between the capsule and the capillary glomerulus are visible. Between the layers of cells in the crescent moon there is an accumulation of fibrin. The glomeruli are compressed - they show focal necrosis, diffuse and focal proliferation of the endothelium, proliferation of the mesangium. Part of the tubules is atrophic, in the epithelium of some convoluted tubules - hydropic or hyaline droplet dystrophy. In the stroma of the kidney - sclerosis, lymphomacrophage infiltration.

MORPHOLOGICAL OPTIONS OF CHRONIC GLOMERULONEPHRITIS

Electron diffraction pattern MEMBRANOSE NEPHROPATHY(atlas, fig. 15.6).

Electron microscopic examination shows subepithelial deposits in the glomerular basement membrane, accumulation of the basement membrane substance between the legs of podocytes, loss of processes by podocytes and their spreading on a thickened and deformed basement membrane.

Electron diffraction pattern MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS(atlas, fig. 15.9).

Electron microscopic examination reveals subepithelial electron-dense deposits.

Electronogram MESANGIOPROLIFERATIVE GLOMERULONEPHRITIS(atlas, fig. 15.10).

Electron microscopic examination shows deposits in the mesangium.

Macrodrug SECONDARY SHRINKED KIDNEY (CHRONIC GLOMERULONEPHRITIS WITH OUTCOME TO NEPHROSCLEROSIS).

The buds 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, in the preserved hypertrophied glomeruli proliferation of mesangial cells, sclero-vascular loops. There are sclerosis and hyalinosis of arterioles. Hyaline cells in the lumen of the tubules.

SECONDARY KIDNEY DAMAGE

Macrodrug AMYLOID NEPHROSIS("large white", "large sebaceous kidney").
Note the increase in the size of the kidney, dense consistency, greasy appearance of the surface.

The kidneys are enlarged in size, dense texture, smooth surface. On the cut with a greasy sheen. The border between cortical and medulla is erased

(E) Micropreparation N 16 AMYLOID NEPHROSIS (coloration of Congo-mouth). Designate deposits of amyloid in the capillary loops of the glomerulus, along the tubular membrane of its own, in the walls of blood vessels, as well as in the stroma of the kidney along the reticular fibers.
Mark 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 deposits of amyloid.

ACUTE RENAL FAILURE (ARF)

(E) Micropreparation N 6 NECROTIC NEPHROSIS (staining with hematoxylin and eosin). The glomeruli and epithelium of the rectus tubules are preserved. Their cells contain nuclei. The epithelium of the convoluted tubules does not contain nuclei (karyolysis).

ORGANOPATHOLOGY OF CHRONIC RENAL FAILURE

View a set of macro-preparations reflecting the morphological manifestations of uremia: fibrinous pericarditis ("hairy heart"), gross tracheitis, diphtheritic colitis.

DISHORMONAL DISEASES OF THE GENITAL ORGANS

Macro-preparation POLYP UTERUS. Mark the localization of the polyp, its shape, size, surface nature, connection with the underlying tissue.

The outgrowth of the endometrium is gray-red, with an uneven surface.

(E) Micropreparation N 142 IRON HYPERPLASIA ENDOMETRY (staining with hematoxylin and eosin).

The endometrial glands are built from the epithelium of the proliferating type, have a different size and shape, have a convoluted course and cystic expansion, are very closely located, branching and budding of the glands is noted.

Micropreparation N 57 PSEUDOEROSIS OF THE CERVIC (staining with hematoxylin and eosin).

In the area of ​​cervical erosion, there are two types of epithelium: the epithelium is stratified squamous non-keratinizing and prismatic. Ectopia of the columnar epithelium in the exocervix is ​​noted.

PATHOLOGY OF PREGNANCY

Macro-preparation POSITIVE ENDOMETRITIS.

The lining 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 slightly open.

Macrodrug LIVER IN ECLAMPSION.

In the liver, single or confluent white-yellow foci of necrosis and multiple hemorrhages of various sizes appear - a landcartoid liver.

MACROPREPARATION No. 1 FATTY LIVER DYSTROPHY

Liver incisions are visible in the specimen.

The liver is small, as it is the liver of a child. But nevertheless, the size of the liver is increased, since its capsule is tense, and the corners are rounded.

The color of the liver is yellow on the cut.

The consistency of the liver is flabby.

When such a liver is cut with a knife, droplets of fat remain on its blade.

This is parenchymal fatty degeneration of the liver, or "goose" liver.

It can develop in people suffering from chronic cardiovascular diseases, chronic lung diseases, diseases of the blood system, chronic alcoholism.

As a result of parenchymal fatty degeneration, portal, small-nodular cirrhosis of the liver may develop over time.

MACROPREPARATION No. 2 BLEEDING IN THE BRAIN

A horizontal section of the brain tissue is visible in the specimen. The cerebellum is visible below and behind the brain.

In the right hemisphere of the brain, in the region of the subcortical nuclei, there is a focus of dark brown color due to the fact that in the focus of hemorrhage we see caked blood. This is a focus of hemorrhage in the necrotic tissue of the brain, with fairly clear boundaries - a hematoma. In the center of the hematoma under anaerobic conditions, the pigment hematoidin is formed, and along the periphery, on the border with healthy tissues, hemosiderin. Blood from the focus of hemorrhage broke into the anterior horn of the right lateral ventricle, into the third ventricle of the diencephalon, the Silvian aqueduct of the midbrain and into the fourth ventricle of the rhomboid brain.

Hematoma is a type of hemorrhagic stroke.

Clinically it was accompanied by the development of focal symptoms on the opposite side of the body - left-sided paresthesia, hemiplegia, hemiparesis, paralysis.

If the patient had not died, then a cyst with walls rusty from hemosiderin would have formed at the site of the hemorrhage.

MACROPREPARATION No. 3 KEPHALOGEMATOMA

The preparation contains the integumentary bone of the newborn's skull. On the upper - lateral surface of the bone, under its periosteum there is caked blood of a dark brown, almost black color - this is a subperiosteal hemorrhage. This is a birth injury to the skull related to external cephalohematoma.



MACROPREPARATION No. 4"TAMPONADA" OF THE HEART

The preparation presents a longitudinal section of the heart from the side of the left ventricle, since the thickness of the ventricular myocardium is more than 1 cm. It is noteworthy that the cavity of the left ventricle is slit-like, that is, the heart is compressed by something from the outside. The subepicardial fat layer, epicardium, pericardium are determined. In the pericardial cavity, gray-brown blood clots are visible. It is due to their presence in the pericardial cavity that the heart was compressed from all sides, and the cavity of the left ventricle became slit-like. This is bleeding into the pericardial cavity - hemopericardium, for example internal bleeding, figuratively - "tamponade" of the heart. Attention is also drawn to the fact that in the region of the posterior - lower wall of the heart, the myocardial tissue is stained with hemosiderin in a brown color, due to the rupture of the heart wall in this place and hemorrhage from the damaged vessel. The rupture of the heart wall occurred due to myomalacia in the area of ​​transmural myocardial infarction.

Thus, the hemorrhage in the cardiac shirt was a consequence of myomalacia and rupture of the heart wall in the area of ​​transmural myocardial infarction.

MACROPREPARATION No. 5 Purulent Meningitis

In the preparation, the brain is visible from the side of its upper - lateral surfaces. Under the pia mater, an accumulation of exudate of white-yellow color, the consistency of thick sour cream, is determined. This is a purulent exudate. The exudate lies on the surface of the convolutions, enters the grooves, smoothing the relief of the surface of the brain.

Inflammation of the pia mater is meningitis.

Primarily purulent meningitis can occur with meningococcal infection, and secondarily can complicate infectious diseases with generalization of infection (with sepsis).

MACROPREPARAI No. 6 A BRAIN TUMOR

The preparation shows a horizontal section of the brain. In one of the hemispheres (in the left), in the white matter, there is a focus of pathological proliferation of brain tissue with indistinct contours, indistinct growth boundaries. The consistency of the node of pathological growth of brain tissue approaches the consistency of the brain itself. The color is variegated, since there are hemorrhages and necrosis in the focus. This is a brain tumor. Since the boundaries of tumor growth are indistinct, there is malignant tumor... It can be assumed that this is glioblastoma, the most common malignant tumor in adults.

MACROPREPARATION No. 7 Tibial sarcoma

The preparation contains bones that form knee-joint... In the area of ​​the upper part of the diaphysis of the tibia, there is a pathological proliferation of tissue that destroys the posterior surface of the bone, which has indistinct growth boundaries. This is a tumor. It is white, layered, reminiscent of fish meat. The indistinctness of the growth boundaries indicates the malignant nature of the tumor. Malignant tumor from bone tissue - osteosarcoma. Since the process of bone destruction prevails over the process of bone formation, this is osteolytic osteosarcoma.

MACROPREPARATE No. 8 BRAIN ABSCESSES IN SEPTICOPYEMIA

The preparation contains sections of the brain. In each section, there are multiple foci of irregular rounded shape, clearly delimited from the brain tissue by a thick wall. Filled with contents of white - yellowish or white - greenish color, consistency of thick sour cream. This is a purulent exudate.

Focal accumulations of pus, separated from the brain tissue by a wall, are abscesses.

The wall of an acute abscess consists of two layers: 1) the inner layer - the pyogenic membrane and 2) the outer layer - nonspecific granulation tissue.

In the wall of a chronic abscess, three layers are distinguished: 1) inner - pyogenic membrane, 2) middle - nonspecific granulation tissue and 3) outer - coarse fibrous connective tissue.

Brain abscesses develop with the generalization of purulent inflammation in the lungs, intestines and other organs, that is, with sepsis, septicopyemia.

MACROPREPARATE No. 9 Stenosis of the mitral orifice (rheumatic heart disease)

The specimen presents a cross-section of the heart, produced above the level of the atrio-ventricular foramen, so that the cusps of the bicuspid, mitral and tricuspid valves are clearly visible.

The leaflets of the mitral valve are deformed. They are sharply thickened, with a bumpy surface, opaque, rigid due to the growth in them connective tissue... There is a gap between the closed valve leaflets, that is, mitral valve insufficiency has developed.

In addition, there is a narrowing of the left atrio-ventricular opening.

Thus, in the area of ​​the mitral valve there is a combined heart defect - insufficiency and stenosis of the mitral valve.

Such acquired heart defects most often form in the course of rheumatic valvular endocarditis.

The described changes in the mitral valve correspond to the stage of fibroplastic endocarditis.

It can be assumed that the patient died of progressive chronic cardiovascular failure due to decompensated rheumatic heart disease.

MACROPREPARATE No. 10 UTERINE CHORIONEPITELIOMA

The preparation contains a longitudinal section of the uterus with appendages.

The size of the uterus is increased (normally the height of the poppy is 6 - 8 cm, the width is 3 - 4 cm and the thickness is 2 - 3 cm). In the uterine cavity, the growth of tumor tissue is visualized, which grows into the myometrium, that is, invasive tumor growth takes place.

The consistency of the tumor is soft, porous, since the tumor contains absolutely no connective tissue.

The color of the tumor tissue in the preparation is gray with dark brown blotches. In a fresh preparation, it is dark red, variegated, since the tumor has cavities, lacunae filled with blood.

Based on the nature of the growth, the tumor is malignant. It develops from the epithelium of the chorionic villi (placenta). This is chorionepithelioma.

It is an organ-specific tumor. It is built of two types of cells - large mononuclear cells with light cytoplasm, or Langhans cells, derived from cytotrophoblast, and large ugly multinucleated cells, derived from synticyotrophoblast. The tumor is hormonally active. Tumor cells secrete the hormone gonadotropin found in a woman's urine; thanks to the hormone, the uterus is enlarged.

The tumor developed in connection with pregnancy. This is a differentiated tumor.

Metastasizes mainly by hematogenous route to the liver, lungs, vagina.

In the present preparation, in the area of ​​the vaginal portion of the cervix and in the wall of the vagina, rounded foci similar in appearance to the primary tumor are visible. These are tumor metastases.

MACROPREPARATE No. 11 CHRONIC STOMACH ULTRA WITH PENETRATION INTO THE PANCREAS

The preparation shows a fragment of the stomach wall from the side of the mucous membrane and the pancreas located behind the stomach.

In the wall of the stomach there is an ulcerative defect with raised dense, callous, callous edges and a shallow bottom. One edge of the defect facing the esophagus, the proximal one is subdued, with an overhanging mucous membrane. The other edge, opposite, distal, is gently sloping or terraced. The difference in edges is due to the presence of a peristaltic wave.

A defect in the wall of the stomach is a chronic ulcer, since at the edges of it there was an overgrowth of connective tissue, which caused a change in the edges of the defect.

At the bottom of the ulcer, it is not the tissue of the stomach wall that is determined, but the lobular, white tissue of the pancreas.

Thus, there is an ulcerative - destructive complication of chronic gastric ulcer - penetration into the pancreas.

It can be assumed that the patient died from a spilled den.

MACROPREPARATE No. 12 MUSKATIC LIVER

A frontal section of the liver is visible in the specimen.

The liver is enlarged.

The color of the liver tissue on the cut is variegated: areas of gray - black color (these are areas with clotted blood) interspersed with areas of gray - brown color (color of hepatocytes).

Areas of gray-black color, and in a fresh preparation - red, are caused by plethora and expansion of the central veins and the central 2/3 of the sinusoids of the liver lobules flowing into them.

Due to the similarity of the surface of the liver incision to the surface of the cross section of nutmeg, the drug got its name.

It takes place during the development of chronic venous plethora in the body, which occurs in conditions of chronic cardiovascular insufficiency, which is a complication of chronic diseases of the heart, such as mitral valve disease, myocarditis with an outcome in cardiosclerosis, chronic ischemic disease hearts.

MACROPREPARATION No. 13 Adenoma of the prostate gland with ureterohydronephrosis

The preparation contains an organocomplex consisting of a longitudinal section of the kidney with the ureter, longitudinal sections of the bladder and prostate gland.

Changes in the structure of the prostate gland entailed compensatory - adaptive changes in the structure of the overlying organs.

The prostate gland is enlarged, due to the proliferation of a tumor node in one of its lobes, rounded, with clear boundaries of growth, delimited from the prostate tissue by a connective tissue capsule. it benign tumor- prostate adenoma.

Due to the presence of an adenoma, the prostatic part urethra narrowed sharply, which led to a violation of the outflow of urine.

Working hypertrophy developed in the bladder wall. Along with wall hypertrophy, the bladder cavity expanded, that is, eccentric decompensated bladder hypertrophy developed.

The ureter, pelvis and cups of the kidney have dilated due to impaired outflow of urine - hydroureteronephrosis.

In the parenchyma of the kidney, a type of local pathological atrophy has developed - atrophy from pressure.

MACROPREPARATE No. 14 CENTRAL LUNG CANCER

The trachea with cartilaginous half-rings located on its front surface, the main bronchi, a part of the left lung adjacent to the left main bronchus are visible in the preparation.

The lumen of the left main bronchus is sharply narrowed due to the fact that around the bronchus in the lung tissue there is a pathological proliferation of gray - beige tissue, dense consistency, in the form of a node with indistinct growth boundaries. This is a malignant tumor growing from the epithelium of the main bronchus - lung cancer. Outside the main node of the tumor, there are multiple foci, irregularly rounded, - cancer metastases to the lungs.

Since cancer grows from the main bronchus, it is central in localization.

Since tumor growth is represented by a nodule, the macroscopic form of cancer is nodular.

Most often, the histological form of central lung cancer is squamous, the development of which is preceded by metaplasia of the glandular epithelium of the bronchi into stratified squamous non-keratinizing epithelium in the course of chronic bronchitis.

In relation to the surrounding tissues, cancer grows infiltratively.

In relation to the lumen of the main bronchus - into its wall, that is, endophytic, compressing the lumen of the bronchus.

Due to a violation of the patency of the bronchus due to its compression by a tumor in the lung tissue adjacent to the bronchus, such diseases as atelectasis, abscess, pneumonia, bronchiectasis can develop.

Lung cancer is an organ-specific epithelial tumor.

Metastasizes mainly by the lymphogenous pathway. The first lymphogenous metastases are found in the regional lymph nodes - peribronchial, paratracheal, bifurcation.

MACROPREPARATION No. 15 POLIPOSO - ULCER AORTIC VALVE ENDOCARDITIS

We see the heart preparation in a longitudinal section from the side of the left ventricle, since its myocardium has a thickness of more than 1 cm. The cavity of the left ventricle is expanded. There is eccentric decompensated working hypertrophy of the left ventricular myocardium and tonogenic dilation.

The crescent moon of the aortic valve is changed, they are thickened, tuberous, rigid, opaque. On two of the three half-moon, an ulcerative defect is clearly visible, on the surface of which thrombotic overlays in the form of polyps have formed. Such changes I in the aortic valve crescent are called polypoid - ulcerative endocarditis, which is one of the clinical and morphological forms of sepsis.

Microscopically, microbial colonies and lime scale deposits can be detected in the thickness of these thrombotic deposits.

Complications of this process can be thrombobacterial embolism and the formation of aortic heart disease.

Since polyposis - ulcerative endocarditis has developed on the already altered aortic valve crescents, this is secondary endocarditis.

MACROPREPARATE No. 16 STOMACH CANCER (Saucer-shaped)

The preparation contains a fragment of the stomach from the side of the mucous membrane. The stomach is cut along the greater curvature.

In the area of ​​the lesser curvature of the body of the stomach, there is a pathological proliferation of tumor tissue into the lumen of the stomach with loose raised edges and a shallow bottom. The boundaries of tumor growth are indistinct in places. At the bottom of the tumor growth, there are foci of white necrosis.

The indistinct boundaries of tumor growth and the presence of secondary changes in it in the form of foci of necrosis indicate the malignancy of the tumor.

A malignant tumor growing from the epithelium of the stomach is stomach cancer.

By localization, it is a cancer of the body of the stomach.

By the nature of its growth, it is an ecophytic - expansive cancer.

On a macroscopic basis, it is a saucer-shaped cancer.

Microscopically, it will most often be represented by a differentiated form of cancer - adenocarcinoma.

Since stomach cancer is international classification tumors belong to the group of organ-specific epithelial tumors, then the predominant way of its metastasis will be lymphogenous. The first lymphogenous metastases can appear in the regional lymph nodes - four collectors of lymph nodes located along the lesser and greater curvatures of the stomach.

Since the stomach is an unpaired abdominal organ, the first hematogenous metastases are found in the liver.

MACROPREPARATION No. 17 ABSCEDING PNEUMONIA IN SEPTICOPYEMIA

We see a cross section of the right lung, as it contains three lobes.

In each lobe, against the background of an airy tissue of a light beige color, there are multiple foci of a round and irregular shape, the size of a match head, in places merging with each other, dense consistency, airless or low-air, with a smooth cut surface, white-gray. These are foci of inflammation in the lung tissue - foci of pneumonia.

A white wall is formed around some foci, and the contents of the foci become the consistency of thick sour cream. A complication of pneumonia, abscess formation, develops.

Absolute pneumonia can develop with septicopyemia, one of the clinico-morphological forms of sepsis.

MACROPREPARATE No. 18 LARGE PNEUMONIA (WITH ABSCEDING)

The preparation shows a longitudinal section of the right lung, as three lobes are visible.

The lower lobe is entirely gray, airless. The surface of its section is fine-grained.

The consistency of the lung lobe corresponds to the hepatic density.

The interlobar pleura is thickened with gray-beige filmy overlays.

This is croupous pneumonia, hepatization stage, a variant of gray hepatization.

In the lower segments of the lobe, cavities are determined, delimited from the lung tissue by the wall. These are abscess cavities.

There is one of the pulmonary complications of pneumonia - abscess formation. Its cause is the addition of a secondary purulent infection due to decreased immunity and increased fibrinolytic activity of neutrophilic leukocytes.

MACROPREPARATE No. 19 SMALL-NODED LIVER CIRROSIS

A section of the liver is presented in the preparation.

The liver is reduced in size, since its corners are pointed, and the capsule is wrinkled.

On the outer surface of the liver, multiple nodes of regenerates are determined, up to 1 cm in size, making the surface of the liver non-smooth.

On the surface of the incision, the boundaries of the false lobules are clearly visible (whereas in the norm the boundaries of the hepatic lobules are not visualized) due to the proliferation of fibrous tissue in the area of ​​the portal tracts.

This is cirrhosis of the liver.

In macroscopic form, it is small-knot. In microscopic form, it is monolobular, since the size of the false lobules corresponds to the size of the nodes - regenerates.

By pathogenesis, it is portal cirrhosis of the liver, in which the primary develops portal hypertension, and secondarily - hepatic - cellular insufficiency.

Such cirrhosis can develop as a result of fatty hepatosis, chronic viral hepatitis B and chronic course of alcoholic hepatitis.

MACROPREPARATE No. 20 UTERINE BODY CANCER

A longitudinal section of the uterus is shown.

The uterus is enlarged. It can be seen that in the uterine cavity there is a pathological proliferation of tissue with a non-smooth, papillary surface, in places with ulceration, with indistinct growth boundaries. This is a tumor growth.

The tumor develops from the endometrium, it can be seen that it grows into the wall of the uterus. This is a malignant tumor from the epithelium - cancer of the body of the uterus.

Histologically, it is represented by a differentiated form of cancer - adenocarcinoma.

The nature of tumor growth in relation to the lumen of the uterus is exophytic, in relation to the surrounding tissues - infiltrating.

It can develop as a result of atypical glandular hyperplasia of the endometrium.

It is an organ-specific epithelial tumor. Metastasizes mainly by the lymphogenous pathway. The first lymphogenous metastases are found in the regional lymph nodes.

MACROPREPARATION No. 21 PURULENT - FIBRINOUS ENDOMYOMETRITIS

A longitudinal section of the uterus with appendages is visible.

The uterus is sharply increased in size, its cavity is sharply expanded, the wall is thickened.

The endometrium is dirty gray in color, dull, covered with filmy beige overlays, hanging in places into the uterine cavity. In the endometrium there is an inflammatory process - purulent - fibrinous endometritis.

In addition, the inflammation has spread to the muscular membrane of the uterus, since the myometrium is dull, dirty gray in color.

Thus, in the presented preparation there is purulent - fibrinous endomyometritis, which could arise as a result of a criminal abortion and cause uterine sepsis.

MACROPREPARATE No. 22 MULTIPLE UTERINE FIBROMIOMAS

A cross section of the uterus is shown.

In the wall of the uterus, the growth of tumor tissue in the form of nodes, of different sizes, round and oval, with clear boundaries of growth, surrounded by a thick-walled capsule, is visible, which is a reflection of the expansive growth of the tumor.

The nodes located inside the wall of the uterus - intramural, lying under the endometrium - submucous, lying under the serous membrane - subserous.

The nodes are built of two types of fibrous structures - some beige fibers are smooth muscle fibers, the other gray-white fibers are connective tissue fibers. Fibrous structures have different thicknesses and go in different directions, which are manifestations of tissue atypism.

Since the tumor nodes contain a large number of connective tissue fibers, their consistency is dense.

Due to the fact that the tumor grows expansively and has only signs of tissue atypism, it is benign. A benign tumor of smooth muscle with an admixture of fibrous tissue is called fibroids.

Based on the international classification of tumors, it belongs to mesenchymal tumors.

MACROPREPARATE No. 23 BUBBLE FAN

The drug is represented by an uviform cluster of thin-walled vesicles adhered to each other and filled with a transparent liquid. This is a cystic mole, a benign organ-specific tumor that develops during and after pregnancy from the epithelium of the chorionic villi.

The development of cystic drift is based on hydropic degeneration of epithelial cells.

A vesicular mole is benign until it begins to grow into the wall of the uterus, into the veins. After that, it becomes malignant, or destructive. Against the background of a malignant cystic drift, a malignant organ-specific tumor of chorionepithelioma may develop.

MACROPREPARATE No. 24 THROMBOEMBOLIA OF THE PULMONARY ARTERY

The drug is represented by an organocomplex: the heart and fragments of both lungs.

The heart is clipped from the side of the right ventricle, since the thickness of its myocardium is approximately 0.2 cm. The pulmonary trunk emerges from the right ventricle, which is divided into two pulmonary arteries, respectively, to the right and left lungs.

In the lumen of the pulmonary trunk and its bifurcation there are massive, heavy, dense, crumbling masses with a corrugated surface that are not attached to the walls of blood vessels. These are thromboemboli. The source of such massive thromboemboli could most likely be the veins of the lower extremities.

The thromboembolus located in the lumen of the pulmonary artery trunk and its bifurcation irritates the reflexogenic zone receptors located in the intima of the above vessels and causes the development of the pulmo - coronary reflex, which consists in an instant spasm of small bronchi and bronchioles and coronary arteries heart, with the development of acute cardiovascular failure and the onset of instant death.

MACROPREPARATION No. 25 AORTIC ATHEROSCLEROSIS WITH ATHEROMATOSIS AND PARALLEL THROMBOSIS

The abdominal aorta in a longitudinal section and the area of ​​bifurcation of the aorta to the common iliac arteries are presented.

The intima of the aorta is changed. It defines multiple round-longitudinal spots of white-yellow color, which are lipid deposits and proliferation of fibrous tissue. These are atherosclerotic plaques. They bulge into the lumen of the aorta, making it narrower. Below the opening of the inferior mesenteric artery, the plaques are ulcerated, atheromatous (necrotic) masses have formed on their surface, and hemorrhages have occurred.

The appearance of atherosclerotic plaques in the intima of the aorta indicates the presence of a disease of atherosclerosis, a clinical and morphological form of atherosclerosis of the aorta.

The described plaque changes correspond to the macroscopic stage of complicated lesions.

Damage to the aortic intima was one of the local prerequisites for thrombus formation. In the lumen of the abdominal aorta and in the lumen of the iliac arteries, parietal and even obstructing blood clots formed, disrupting the passage of blood through the aorta to the lower extremities.

MACROPREPARATE No. 26 Lesion of the small intestine with abdominal typhus

The specimen presents the small intestine in a longitudinal section from the side of the mucous membrane.

On the mucous membrane, longitudinal oval-shaped formations are visible, protruding above the surface of the mucous membrane and having on their surface a kind of grooves and convolutions, as in the brain. These formations are pathognomonic for typhoid fever. They arose as a result of acute productive inflammation in the area of ​​lymphatic follicles located in the submucosa of the intestine. Due to the proliferation of macrophage and histiocytic elements, the follicles increased in volume, size and began to rise above the mucosal surface.

Due to the presence of grooves and convolutions on the surface of the follicles, the first stage of typhoid fever is called cerebral swelling.

MACROPREPARATE No. 27 FIBROZOUS - CAvernous pulmonary tuberculosis

The specimen is represented by a longitudinal section of the right lung, since it has 3 lobes. Each of the lobes has cavities, large cavities with thick, non-collapsing walls. Since the walls of the cavities do not collapse, these are old, chronic cavities inherent in fibrous-cavernous pulmonary tuberculosis, one of the phases of forms of secondary pulmonary tuberculosis.

The wall of the old cavity consists of 3 layers: 1) internal - caseous necrosis; 2) medium - specific granulation tissue; 3) external - fibrous tissue.

The patient develops cor pulmonale, chronic pulmonary heart failure, tuberculous intoxication and cachexia, from which he dies.

MACROPREPARATE No. 28 PARA-AORTIC LYMPHONULOMATOSIS

The specimen shows the aorta in longitudinal section.

In the intima of the aorta, atherosclerotic plaques are determined.

On both sides of the abdominal aorta, above the bifurcation, sharply enlarged and because of this lymph nodes welded to each other are determined, forming "packets" of lymph nodes.

The consistency of the lymph nodes is densely elastic, the surface is smooth, the color on the cut is gray-pink.

The lymph nodes that lie on the sides of the aorta are called paraaortic.

Enlargement of the paraaortic lymph nodes and their fusion into packets occurs in lymphogranulomatosis, malignant Hodgkin's lymphoma.

MACROPREPARATE No. 29 ARTERIOLOSCLEROTIC NEPHROSCLEROSIS

Two whole kidneys are visible in the preparation.

Their size and weight are sharply reduced (both kidneys in humans weigh 300 - 350 g). The surface of the kidneys is wrinkled, fine-grained. The consistency of the kidneys is very dense.

This is primarily a wrinkled kidney due to the benign course of the primary arterial hypertension... At the heart of wrinkling is hyalinosis and sclerosis of the capillaries of the renal glomeruli - arteriolosclerotic nephrosclerosis.

The same appearance is secondary - a wrinkled kidney, which develops as a result of chronic glomerulonephritis.

Clinically, against the background of primary and secondary shrunken kidneys, chronic renal failure, accompanied by the development of azotemic uremia, which can be treated with chronic hemodialysis or kidney transplantation.

MACROPREPARATE No. 30 MILIARY TUBERCULOSIS OF PULMONARY

An enlarged longitudinal section of the lung is presented.

It is clearly seen that the entire surface of the lung tissue is diffusely dotted with small, millet-sized grain, dense tubercles, light yellow in color.

The lung has this type in miliary tuberculosis, which develops in hematogenous generalized and hematogenous tuberculosis with a predominant lesion of the lungs.

Each tubercle has the following structure: in the center there is a focus of caseous necrosis, the severity of which depends on the state of the patient's immunity; it is surrounded by a cell wall of epithelioid cells, lymphocytes, plasma cells and single multinucleated cells of Pirogov-Langhans.

According to the classification of granulomas, tuberculous granulomas are infectious, specific. Specific cells of a tuberculous granuloma are epithelioid cells of hematogenous, monocytic origin, which are the most in the granuloma.

MACROPREPARATION No. 31 NODULAR GOITER

The preparation contains thyroid on the cut.

Its dimensions are dramatically increased (normally weighs 25 g).

Outside surface bumpy.

On the surface of the incision, the lobular structure of the gland is distinguished, and in the lobules there are follicles of different sizes filled with a brown colloid.

A persistent increase in the size of the thyroid gland that is not associated with inflammation, swelling, or poor circulation in it is called a goiter.

In appearance, it is a nodular goiter.

Internal structure - colloid goiter.

Most often occurs with endemic goiter, the occurrence of which is associated with a deficiency of exogenous iodine.

Despite the compensatory increase in the size of the gland, its function is reduced.

MACROPREPARATE No. 32 TUBULAR PREGNANCY

The fallopian tube is visible in cross section.

The pipe is sharply expanded. Its wall is thinned in places, thickened in places. In places of thickening of the wall of the tube, the tissues have a dark brown color due to hemorrhage. In the center of the tube is a human embryo, in which the head, torso, hands and fingers are clearly distinguishable. The embryo is surrounded by membranes.

This is an ectopic, tubal pregnancy, complicated by an incomplete tubal abortion.

The ovum separated from the walls of the fallopian tube, as evidenced by hemorrhage, but remained in the tube.

MACROPREPARATE No. 33 RENAL - CELLULAR CANCER

It is represented by a section of the kidney, in the upper pole of which tumor tissue grows in the form of a node with clear growth boundaries, forming a pseudocapsule around itself, which indicates the expansive growth of the tumor.

The tumor node is light yellow in color, since the tumor cells contain a large amount of lipids; motley, since the tumor is characterized by the development of necrosis and hemorrhage; soft consistency, since the tumor contains little fibrous tissue.

Despite the nature of growth, the tumor is malignant, differentiated, organ-specific epithelial, developing from the epithelium of the kidney tubules.

It occurs in adults.

MACROPREPARATE No. 34 DRY GANGRENA FOOT

The foot of the right lower limb is visible in the specimen.

In the area of back surface the metatarsus, at the base of the toes, the skin is absent, and the soft tissues are dry, mummified, gray-black.

This is dry gangrene of the foot, one of the clinical and morphological forms of necrosis.

Gangrene is called necrosis of tissues in contact with the external environment.

With gangrene, soft tissues are stained in a gray-black color with a pigment pseudomelanin, or iron sulfide.

Gangrene of the foot can develop as a result of atherosclerotic damage to the vessels of the lower extremities, which occurs primarily or as a result diabetes mellitus due to the development of macroangiopathy.

MACROPREPARATION No. 35 EMBRYONIC KIDNEY CANCER

It is represented by a kidney in longitudinal section.

In the upper pole of the kidney there is an overgrowth of tumor tissue, large in size, with clear boundaries of growth, forming a pseudocapsule around itself. In the center of the tumor node there is a large cavity due to necrosis of the tumor tissue.

The lower pole of the kidney is small, which indicates that the kidney belongs to a small child.

Despite the nature of tumor growth - expansive and given the presence of secondary changes in the tumor - this is a malignant, undifferentiated tumor that develops from metanephrogenic tissue and affects children from two to six years old.

Expansive growth gives way to invasive growth over time.

The tumor is organ-specific epithelial.

Metastasizes mainly by hematogenous route to the opposite kidney, lungs, bones, brain.

MACROPREPARATE No. 36 MAMMARY CANCER

The drug is represented by the mammary gland.

In one of the quadrants of the mammary gland, a pathological proliferation of tumor tissue occurred, emanating from the epithelium of the mammary gland ducts, and grown to the surface of the skin, which indicates an invasive tumor growth.

This is a malignant, epithelial organ-specific tumor - breast cancer.

Description of drugs in Pathological Anatomy in Lesson No. 26

(This is an indicative description, not a cathedral, some drugs may be missing, since the 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, which penetrates into all layers of the stomach wall. The openings of the glands are widened. The cytoplasm of the epithelium is vacuumed. Own layer of the mucous membrane with congested vessels, in places with diapedesic hemorrhages, polymorphonuclear leukocytes (PMN).

Micropreparation № 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 growing connective tissue are visible. The fossa epithelium with symptoms of hyperplasia. Epithelium of the glands with signs of intestinal metaplasia. The entire wall of the stomach is diffusely infiltrated by histolymphocytic elements with an admixture of polymorphonuclear leukocytes.

Macrodrug "acute erosions and stomach ulcers" - description.

The mucous membrane of the stomach with smooth folds and numerous defects of the mucous membrane of a round and oval shape, the bottom of which is painted black.

Macrodrug "chronic stomach ulcer" - description.

On the lesser curvature of the stomach, a deep defect of the mucous membrane is determined, affecting the muscular layer, of a rounded shape with dense, raised, amosolized edges. The edge of the defect facing the esophagus is undermined, to the gatekeeper it is shallow.

Micropreparation № 121 "chronic stomach ulcer in the acute stage" - description.

A defect in the wall of the stomach is determined, capturing the mucous and muscular layer, with an undermined edge facing the esophagus and shallow, facing the gatekeeper. At the bottom of the defect, 4 layers are determined. The first is 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, strips of muscle fibers, amputation neuroma are visible. Vessels of the cicatricial zone with sclerosed thickened walls. The mucous membrane at the edges of the defect with symptoms of hyperplasia.

Macrodrug "stomach polyp" - description.

On the gastric mucosa, a tumor formation on a broad base (pedicle) is determined.

Macrodrug "saucer-shaped stomach cancer" - description.

The tumor looks like a rounded flat formation on a wide base. The central part of the tumor sinks, the edges are somewhat raised.

Macrodrug "diffuse stomach cancer" - description.

The wall of the stomach (mucous and submucous layers) is sharply thickened, represented by a uniform 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 № 79 "cricoid cell carcinoma" - demo.

The tumor is built of atypical glandular complexes formed by cells with pronounced cellular polymorphism. The stroma is not developed.

Micropreparation № 70 "metastasis of adenocarcinoma in the lymph node" - description.

Drawing lymph node is erased, the growth of tumor tissue is represented by atypical glandular cosplexes.

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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.

Peptic ulcer pathomorphosis.

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Training card of the lesson (for independent work)

1. To diagnose catarrhal serous gastritis according to the macroscopic picture. Study and write down the name of the macro-preparation "Catarrhal serous gastritis". Pay attention to the thickening of the folds of the mucous membrane, its hyperemia, a large amount of turbid viscous exudate on its surface (see "Textbook", p. 344).

2. To diagnose acute catarrhal gastritis by a 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 mixed with polymorphonuclear leukocytes. Desquamation of the integumentary epithelium is observed. The cytoplasm of the epithelium of the glands is vacuolated. The proper layer of the mucous membrane is full-blooded with focal accumulations of predominantly neutrophilic leukocytes (see "Textbook" p. 344; "Atlas", p. 100, Fig. 101). Solve a problem similar to problem No. 1.

3. To diagnose chronic superficial gastritis by a microscopic picture. To study the micropreparation "Chronic superficial gastritis" (staining with hematoxylin and eosin). Write down the name of the drug. The superficial epithelium is flattened in places, desquamated, the glands are not changed. The own layer of the mucous membrane is swollen, infiltrated with lymphoid, plasma cells, polymorphonuclear leukocytes (see "Textbook", p. 346, Fig. 267, a).

4. To 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). At low 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 the changes in the glands: the absence of the main, accessory, parietal (parietal) cells, the appearance of light cubic cells characteristic of the pyloric glands, and intestinal epithelium, goblet cells (see "Textbook", pp. 346-347; "Atlas", p. 278, fig. 290).

5. To diagnose erosion and acute gastric ulcers according to the macroscopic picture. To study the macro-preparation "Multiple erosions and acute gastric 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 sections, there are deeper wall defects - acute ulcers. They have a round or oval shape, their bottom is formed by the 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. To diagnose chronic gastric ulcer according to the macroscopic picture. To study and describe the macro-preparation "Chronic gastric ulcer". Pay attention to the localization of the ulcer, its shape, edges, depth, wall density, the nature of the bottom. Determine and describe which edge faces the esophagus, which one - to the gatekeeper (see "Textbook", pp. 350-351, Fig. 268; "Atlas", p. 281, Fig. 293).

7. Diagnose chronic gastric ulcer by microscopic picture. To study the micropreparation "Chronic gastric ulcer with exacerbation" (staining with hematoxylin and eosin) and sketch it. Find the cardiac and pyloric edges and the bottom of the ulcer at low magnification of the microscope. Determine the depth of the defect. At high magnification, note the layer-by-layer changes in the bottom of the ulcer, characterizing chronic course and exacerbation of the process (see "Textbook", p. 351; "Atlas", p. 282, fig. 294). Solve a problem similar to problem number 2.

8. To diagnose an ulcer, stomach cancer according to the macroscopic picture. To study and write down the name of the macro-preparation "Ulcer-stomach cancer". Pay attention to the proliferation of dense whitish-gray tumor tissue at the edges of the ulcer (see "Textbook", p. 356, Fig. 271).

9.To diagnose phlegmonous appendicitis according to the macroscopic picture. To study and describe the macropreparation "Phlegmonous appendicitis". Pay attention to the size of the appendix, the state of the serous membrane (appearance, degree of blood filling), the thickness and appearance of its wall in section, the nature of the contents in the lumen (see "Textbook", p. 372).

10. To diagnose phlegmonous-ulcerative appendicitis by a 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 No. 3.

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Types of chronic gastritis

Etiology

Pathogenetic mechanism

Histological changes

Associated clinical changes

Autoimmune

Antibodies against parietal cells and receptors for external factor Kastl. Sensitized T-lymphocytes.

Atrophy of the glands in the body of the stomach. Intestinal metaplasia.

Pernicious anemia

Bacterial infection(H. pilori)

Cytotoxins. Mucolytic enzymes. Synthesis of ammonium ions by bacterial urease. Tissue damage during immune response.

Active chronic inflammation. Multifocal atrophy, more in the antrum. Intestinal metaplasia.

Peptic Ulcers Stomach Cancer

Chemical damage Nonsteroidal anti-inflammatory drugs Bile reflux Alcohol

Direct damage. Damage to the mucous layer. Mast cell degranulation.

Hyperplasia of the pit epithelium. Edema. Vasodilation. A small number of inflammatory cells.

Peptic Ulcers Stomach Cancer

Other forms of gastritis

The following types are distinguished separately. chronic gastritis:

lymphocytic;

eosinophilic;

granulomatous.

With lymphocytic gastritis, the main histological manifestation is the presence of numerous mature lymphocytes in the surface layers of the epithelium. This form is sometimes found in patients with specific erosions along the enlarged folds of the mucous membrane. 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 form. These granulomas can be a manifestation of Crohn's disease or sarcoidosis, but in rare cases it is cryptogenic.

Microdrug "Chronic atrophic gastritis with epithelial restructuring" (staining with hematoxylin and eosin). The mucous membrane of the stomach is thinned, lined in places with integumentary epithelium, in places with limb 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.

Peptic ulcer and duodenal ulcer

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. Ulcers by clinical course divided into acute and chronic.

Acute ulcers

Acute ulcers can be caused by:

    Severe acute gastritis. The deep spread of erosions in acute gastritis usually occurs with the use of non-steroidal anti-inflammatory drugs or alcohol, with corticosteroid treatment, which leads to the appearance of deep ulcers.

    Severe stress. Acute ulcers can result from a variety of stressful factors, such as extensive burns or trauma to the brain. In this case, ulcers form as a result of ischemia of the mucous membrane, which leads to a decrease in its resistance to acid.

    A 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 the jejunum.

Chronic ulcers

Chronic ulcers can be caused by:

    Helicobacter pylori infection.

    Chemical influences, including steroid drugs and non-steroidal anti-inflammatory drugs.

    Chronic distress syndrome.

Chronic peptic ulcers most often formed at the junction of various types of mucous membranes. So, for example, in the stomach, ulcers are observed at the place of transition of the body to the antrum, in the duodenum - in the proximal area on the border with the pylorus, in the esophagus - in the stratified epithelium in front of the esophageal-gastric junction, postoperative ulcers are localized in the stoma (in the anastomosis ). That is, ulcers appear in places where acid and pepsin come into contact with the unprotected mucous membrane.

Pathogenesis. For many years, it was believed that the cause of peptic ulcer disease is hyperacidity. However, in many cases, patients were observed to have normal and even reduced acidity of gastric juice. Conversely, ulcers were rarely observed in patients with high acidity. In addition, during treatment with antacids (drugs that reduce acidity), relapses were observed in many cases. This prompted the idea that the main role in the development of ulcers is played not by acidity, but by the ratio of factors of aggression and factors of mucous protection. It is believed that in the genesis of duodenal ulcer the main role an increase in factors of aggression plays, and in the development of gastric ulcer, a decrease in defense factors is in the first place. With a decrease in the latter, ulcers may develop even with low acidity.

Stomach ulcer. Gastric juice is a highly acidic medium (pH

The superficial epithelium forms the second line of defense; To ensure this function, proper functioning of both the apical membrane, which prevents the transport of ions, and the synthetic apparatus, which produces bicarbonates, is necessary. Both of these functions depend on the blood supply to the mucous membrane.

Ulceration occurs as a result of either a violation and destruction of the mucous barrier, or a 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 can also be disrupted by the use of NSAIDs. they disrupt the synthesis of prostaglandins, which normally protect the epithelium. Also, in the destruction of the epithelium, an infection with Helicobacter pylori plays a significant role, in which both cytotoxins and ammonium ions and an inflammatory reaction have a destructive effect.

Duodenal ulcer. High acidity plays a major role in the development of duodenal ulcers. In half of the patients, acid hypersecretion is observed, however, even with normal stomach acidity, the daily cycle of secretion may be disrupted: there is no decrease in secretion at night. It is also known that when stimulated with gastrin in patients infected with Helicobacter pylori, acid synthesis is 2-6 times higher than in uninfected ones.

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, drugs are significantly diluted and absorbed before entering the intestine. However, Helicobacter pylori affects ulceration, because the infection promotes gastric hypersecretion, which causes 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 are usually round or oval in shape. Their sizes, as a rule, do not exceed 2 cm in diameter, however, cases have been 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.

Macrodrug "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, calcified, roller-like raised edges. The edge facing the esophagus is undermined; the edge facing the pylorus is flat and looks like a terrace formed by the mucous membrane, the submucosa and the muscular membrane of the stomach wall. The bottom of the ulcer is represented by a dense whitish tissue.

Microdrug "Chronic gastric ulcer during an 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 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 and manifestations of fibrinoid necrosis are visible.

During the period of remission, scar tissue is found at the edges of the ulcer. The mucous membrane is thickened at the edges, hyperplastic.

Complications. Ulcer healing occurs by regeneration of the epithelium and fibrosis of the underlying tissues. In this case, as a result of the reduction and compaction of scars, a narrowing of the lumen of the organ can develop: stenosis of the pylorus 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 is perforated into the closer lying organs, for example, the pancreas or liver. With erosion blood vessels bleeding can occur, which can be fatal. With prolonged existence, stomach ulcers can become malignant, duodenal ulcers are very rarely malignant.

Peptic ulcer pathomorphosis.

1. Rejuvenation of peptic ulcer disease.

2. An increase in the number of combined ulcers of the stomach and duodenum.

3. Reducing the number of ulcers malignancy.

4. Increase in the number of acute ulcers.

5. An increase in the number of ulcers of medicinal origin.

Staining with hematoxylin and eosin. In the area of ​​the defect of the stomach wall, there is a fibrinous-purulent exudate (a), with an underlying extensive zone of fibrinoid necrosis (b), the presence of granulation tissue (c) and the growth of coarse-lined connective tissue penetrating to different depths muscle layer (d). The serous membrane of the stomach wall is preserved (e).

2. Chronic atrophic gastritis. Heme staining

toxylin and eosin. In the gastric mucosa, atrophy of the integumentary epithelium (a) and epithelium of the glands with restructuring

coy glands of 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. Staining with hematoxylin and eosin. All layers of the stomach wall are infiltrated by tumor tissue with signs of cellular atypism (a). Multiple pathological mitoses are seen in hyperchromic (b) and polymorphic tumor cells (c).

4. Mucous stomach cancer. Hematoxylin staining and

eosin. 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 nature of tumor growth is visible (c). Demonstration.

5. Skirr of the stomach. Staining with hematoxylin and eosin. The lining of the stomach is a group of atypical cells with large hyperchromic nuclei (a), in the stroma of the tumor is the growth of fibrous connective tissue (b). Demonstration.

MACROPREPARATIONS.

1. Acute catarrhal gastritis: in the preparation the stomach, 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 substitutes, anticancer chemotherapy drugs, burns with acids and alkalis, uremia, salmonellosis, shock, severe stress.

Complications: acute ulcers, transition to chronic gastritis. Exodus: restoration of the mucous membrane.

2. Erosions and acute stomach ulcers: in the preparation stomach,

the mucous membrane is edematous, on the surface there are multiple punctate hemorrhages and conical defects of various sizes, their bottom and edges are black. Erosions are localized within the mucous membrane, and ulcers penetrate

cabins to 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: erosion is epithelized, the ulcerative defect is replaced by scar tissue.

3. Chronic stomach ulcer in remission: in the preparation the stomach, on the lesser curvature, there is a pathological focus in the form of a deepening of the mucous membrane, rounded, 3 cm in diameter. The folds of the mucous membrane converge radially to the defect, the edges of which are dense, roller-like raised, callous (callosal ulcer). In the section, the inlet is a crater, smaller than the inner part of the ulcer. The edge facing the cardia is undermined, a 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 sclerosed, their lumen gapes.

Causes: genetic predisposition, Helicobacter pylori, inflammatory and dysregenerative changes in the mucous membrane, leading to the effects of peptic aggression factors (hydrochloric acid and pepsinogen).

Complications: perigastritis, bleeding, perforation, penetration, cicatricial deformity stomach with the development of steno-for the inlet or outlet. Against the background of a chronic ulcer, a second disease, stomach cancer, can develop.

4. Polyps of the stomach (adenomas): in the antrum

There are two tumor-like formations the size of pigeon eggs, on thin legs, irregular oval shape with a villous surface, soft consistency.

On the cut, pathological neoplasms are abundantly vascularized and localized exclusively on the surface of the mucous membrane, without invading the underlying tissues.

Complications: bleeding, torsion of the leg, obstruction of the outlet or inlet.

Exodus: malignancy.

5. Various forms of 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, irregularly rounded, 5 cm in diameter, on a broad base in the form of a mushroom cap, with a retraction in the center. The section shows that the tumor invades the entire wall of the stomach.

b) Diffuse gastric cancer: the organ is reduced in size, the wall is thickened throughout its length to 1 cm, with a dense “woody” consistency, and on the cut it is represented by a gray-pinkish tissue. The mucous membrane is uneven, its folds are of varying thickness, the serous membrane is thickened, dense, and bumpy. 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 towering above the surface of the mucous membrane with dense cushion-shaped edges and a sinking bottom, measuring 3.5 cm by 2.0 cm. The bottom is covered with gray-brown decaying masses. On the cut, the tumor tissue infiltrates the entire thickness of the organ wall.

Causes: food (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 lymphogenous metastases in the left supraclavicular lymph node - Virchow's metastasis, in the ovaries - Krukenberg's

cancer, perrectal tissue - Schnitzler metastases, 3. Hematogenous metastases to the liver, lungs, brain, bones, kidneys, less often to the adrenal glands and pancreas. 4. Implant- carcinomatosis of the pleura, pericardium, diaphragm, peritoneum, omentum.

TEST CONTROL

Choose one or more correct answers

1. SIGNS OF Acute catarrhal gastritis

1) thickening of the mucosa

2) atrophy of the glands

3) multiple erosion

4) mucosal sclerosis

5) neutrophilic mucosal infiltration

6) lymphoid mucosal infiltration

2. MORPHOLOGICAL FORMS OF ACUTE GASTRITIS

1) fibrinous

2) atrophic

3) hypertrophic

4) catarrhal

5) corrosive (necrotic)

3. CHANGES IN EPITHELIUM IN CHRONIC GASTRITIS

1) atrophy

2) intestinal metaplasia

3) hyperplasia

4) dysplasia

5) the appearance in the cytoplasm of Mallory's bodies

4. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS A

2) autoantibodies in the blood

to parietal cells

3) Helicobacter pylori -

5. PATHOGENESIS OF PERNICIAL ANEMIA IN AUTOIMMUNE GASTRITIS

1) stopping the production of HCl

2) production of antibodies to Helicobacter pylori

3) production of antibodies to parient cells

4) production of antibodies to intrinsic factor

5) destruction of glands and mucosal atrophy

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) is accompanied by G-cell hyperplasia, gastrinemia

5) often combined with pernicious anemia

6) localized in the fundus

7) reflux of duodenal contents into the stomach - the basis of pathogenesis

ACUTE EROSION OF THE STOMACH IS

inflammation of the mucous membrane

necrosis of the mucous membrane,

not affecting the muscle plate

3) mucosal atrophy

4) sclerosis of the mucous membrane

5) necrosis involving the muscle layer

8. CLINICAL AND MORPHOLOGICAL SIGNS OF CHRONIC ATROPHIC GASTRITIS

IN THE STAGE OF EXCERVATION

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 DISEASE

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 ulcers

5) inflammation of the duodenal mucosa

10. Sclerotic deformity of the stomach IS an outcome

1) catarrhal gastritis

2) diphtheria 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 reconstruction of the epithelium

(intestinal metaplasia)

4) all answers are correct

5) all answers are wrong

12. ULTSIROGENIC PROMOTORS

1) corticosteroids

3) aspirin

4) smoking

5) increased tone vagus nerve

13. Stomach ulcers include

1) endocrine stomach ulcers

2) allergic ulcers

3) peptic ulcers

4) postoperative ulcers

5) tuberculous ulcers

14.Local factors in the development of gastric ulcer

1) increasing the aggressiveness of gastric juice

2) campylobacter

3) the presence of chronic gastritis

4) circulatory disorders

5) all answers are correct

6) all answers are wrong

15. REASONS OF DEVELOPMENT OF ACUTE STOMACH ULTRA

1) corticosteroids

3) aspirin

4) smoking

5) increased tone

vagus nerve

16. MORPHOLOGICAL SIGNS OF Acute gastric ulcer

1) funnel-shaped

2) the shape of the truncated pyramid

cross-section

3) soft jagged edges

4) dense calcified edges

7) multiple ulcers

17. MORPHOLOGICAL SIGNS of chronic gastric ulcer

1) funnel-shaped

2) the shape of the truncated pyramid

cross-section

3) soft jagged edges

4) dense calcified edges

5) the bottom of the ulcer is colored black with hydrochloric acid hematin

6) the edge of the ulcer, facing the gatekeeper, looks like a terrace, the cardiac edge is undermined

18. SIGNS OF CHRONIC STOMACH ULTRA

IN THE PERIOD OF REMISSION

1) the presence of exudate on the surface

2) scar tissue interrupts the muscular layer to different depths

3) endovasculitis

4) fibrinoid changes in the bottom and blood vessels

5) epithelialization of the surface

19. SIGNS OF CHRONIC STOMACH ULTRA

IN THE PERIOD OF EXCERVATION

1) the presence of fibrinous-purulent exudate

on the surface 2), the scar tissue interrupts the muscle

shell at different depths

3) endovasculitis

4) fibrinoid changes in the walls of blood vessels and in the bottom of the ulcer

12. MECHANISM of bleeding in peptic ulcer disease

arrosive

diapedetic

as a result of vessel rupture

as a result of purulent fusion

21. Chlorohydropenic 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 - the result

1) penetration

2) perforation

3) gastritis

4) duodenitis

5) cicatricial pyloric stenosis

23. COMPLICATIONS OF CHRONIC Ulcer

1) penetration

2) perforation

3) empyema

4) hypercalcemia

5) cicatricial stenosis

and wall deformation

6) bleeding

24. TYPES OF GASTROPATHIES

1) Meniere's disease

2) Menetrie'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 fossa epithelium

4) hyperplasia of the glandular epithelium

5) severe sclerosis

26. MORPHOLOGICAL SIGNS OF INFLAMMATORY POLYPS

1) inflammatory infiltrate in the stroma

2) atypical cells

3) without clear differentiation on the leg and body

4) dysplasia of the glandular epithelium

5) surface erosion

27. BENEFITS 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

1) benign tumor

from glandular epithelium

2) a malignant tumor from the glandular epithelium

3) epidermal cancer

4) malignant tumor from transitional cell epithelium 5) benign tumor from squamous epithelium

30. DISEASES WITH RISK OF CANCER

1) superficial gastritis

2) chronic stomach ulcer

3) sharp erosive gastritis

4) chronic atrophic gastritis

5) adenomatous polyps

31. HISTOLOGICAL OPTIONS OF STOMACH CANCER

1) adenocarcinoma

2) sarcoma

3) cricoid

4) undifferentiated

32. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF INTESTINAL STOMACH CANCER

1) occurs more often before the age of 30

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 epithelial cells

33. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF DIFFUS TYPE STOMACH CANCER

1) develops from epithelial cells

2) arises in a relatively young age

3) histologically cricoid-cellular

4) occurs against the background of chronic gastritis

5) has a low degree of differentiation

34. PREDICTIVE SIGN IN STOMACH CANCER

1) histological variant

2) macroscopic shape

3) depth of invasion

4) mucus formation

5) secondary changes

35. HISTOLOGICAL SIGNS OF POLYPOSE 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 PERSONOID CELL GASTRIC CANCER

1) are characterized by extensive hemorrhages

2) the nuclei of atypical cells are displaced

to the cell membrane

3) poorly differentiated cells with very large hyperchromic nuclei of irregular shape

4) atypical glandular structures

5) massive sclerosis and hyalinosis in the wall

37. MICROSCOPIC CHARACTERISTICS OF 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 METASTASIS OF GASTRIC CANCER

1) hematogenous

2) implantation

3) lymphogenous orthograde

4) lymphogenous retrograde

39. COMPLICATIONS OF GASTRIC CANCER

1) hemoptysis

2) dilatation of the gatekeeper

3) perforation

4) exhaustion

5) stomach bleeding

40. SIGNS WHICH VIRKHOVSKY METASTASIS IS CHARACTERIZED

1) hematogenous metastasis

2) retrograde lymphogenous metastasis

3) peritoneal carcinomatosis

4) defeat of the left supraclavicular lymph node

5) ovarian damage

Standards of answers To test tasks

  • 1Causes of pain
  • 2 Gastritis
  • 3 peptic ulcer
  • 5 food poisoning
  • 6 Duodenitis and pancreatitis
  • 7 Diagnosis and treatment

1Causes of pain

If you feel severe discomfort, you should consult a specialist. An important aspect of diagnosis is to clarify the nature of the pathology. Stomach pains are most often concentrated in the area of ​​the organ's projection onto the abdominal wall. This area is called epigastric. Pain in the stomach can be localized, diffuse, radiating, acute, dull, paroxysmal, burning and cutting.

To establish the cause of its appearance, the intensity of the syndrome should be identified. In this case, the main characteristics of pain are determined:

  • character;
  • time of appearance;
  • duration;
  • localization;
  • connection with food intake;
  • weakening or strengthening with movement, after a bowel movement, or with a change in posture;
  • combination with other symptoms (nausea, loss of appetite, vomiting, bloating).

The feeling of pain in the stomach in most cases is associated with organ damage. The most common causes are:

  • acute and chronic gastritis;
  • stomach ulcer;
  • the presence of polyps;
  • damage to the mucous organ in case of food poisoning (intoxication or toxic infection);
  • damage due to abdominal trauma;
  • severe stress;
  • intolerance to certain products;
  • injury to the mucous membrane by accidentally swallowed objects.

Stomach pain may be due to other causes. These include pancreatitis, peptic ulcer of the 12th intestine, colitis, enterocolitis, cholecystitis, biliary dyskinesia, irritable bowel syndrome, appendicitis, heart disease.

2 Gastritis

The most common reasons stomach pains are acute or chronic gastritis. These forms of the disease are characterized by inflammation of the mucous layer of the organ against the background of exposure to irritating factors. Quite often, gastritis is of an infectious nature. In this case, Helicobacter pylori bacteria act as a starting point. The disease occurs in children, young people and the elderly. When it hurts in the stomach area, in this case it takes place acute gastritis, which is divided into simple, catarrhal, erosive, fibrinous and phlegmonous. If the disease becomes chronic, organ atrophy often develops. The main provoking factors for the onset of gastritis are:

  • abuse of spicy, fried, hot or cold foods;
  • alcohol consumption;
  • smoking;
  • infection with Helicobacter bacteria;
  • accidental or deliberate use of acids or alkalis;
  • uncontrolled intake of medications (drugs of the NSAID group).

The symptoms of gastritis are varied. In children and adults, stomach discomfort is the main symptom of the disease. Most often worried about Blunt pain... Sharp manifestations are typical for acute mucosal inflammation. With gastritis, the pain syndrome can be paroxysmal or constant. There is a clear connection with food intake (spasm appears after eating and when a person is hungry). Additional symptoms of the disease may include belching, nausea, disturbed stools, bloating, and acidic sensation in the mouth. Not pronounced It's a dull pain characteristic of chronic gastritis with normal acidity.

3 peptic ulcer

Acute stomach pain associated with food intake may indicate the presence of a peptic ulcer. It is chronic. Pain syndrome is most pronounced during an exacerbation. Ulcers form against the background of stress, gastritis, the use of certain medications, endocrine diseases... The pathogenesis of the formation of this defect is associated with the suppression of defense mechanisms (a violation of the synthesis of mucus covering the stomach), as well as an increase in the acidity of gastric juice. The symptoms of stomach ulcers are similar to those of gastritis. The main signs of the disease include:

  • severe pain in the epigastric region;
  • nausea and vomiting after eating;
  • weight loss;
  • violation of appetite.

With ulcerative lesions, the stomach hurts after eating. This is the main difference from the pathology of the 12 intestine. Pain syndrome occurs almost immediately after eating (within an hour and a half). There is a definite connection between the exacerbation and the season. Most often, a person suffers from bouts of pain in the fall and spring. In the event of complications (perforation, bleeding), the symptoms can increase dramatically. This condition requires urgent care. The processes occurring in the stomach, the causes of which can be different, are often reversible.

4 Cancer

If the stomach hurts, the reason may lie in oncology. This is one of the most common malignant pathologies. Nearly a million people worldwide die from stomach cancer each year. For a long time, the disease may not manifest itself in any way. Quite often, cancer is detected already at 3 or 4 stages, when treatment is ineffective. Men suffer from this disease more often than women. Cancer is dangerous because the tumor in its later stages is capable of metastasizing to other organs, which is why patients die. The exact cause of the disease is still unknown. Possible etiological factors are: the presence of atrophic gastritis, organ infection with Helicobacter bacteria, exposure to toxic and carcinogenic substances, inappropriate nutrition, drug intake, alcoholism, burdened heredity, Menetrie's disease.

Cancer symptoms on early stages represented by a decrease in appetite, aversion to meat, nausea, bloating, weight loss, malaise, weakness, swallowing disorder. In the later stages, patients may experience aching pain. In most cases, it is caused by the growth of the tumor into neighboring organs. Constant pain of a girdle character appears when a neoplasm is introduced into the pancreas. Surgical treatment should be started as soon as possible. Acute pains, reminiscent of an attack of angina pectoris, are characteristic of a tumor that has grown into the diaphragm. If the pain syndrome is combined with a transfusion in the abdomen, a stool disorder of the constipation type, this may indicate the involvement of the transverse colon in the process.

5 food poisoning

A sharp pain in the stomach can be a sign of food poisoning. This is a disease that develops when eating poor-quality food containing pathogenic microorganisms, their decay products or various toxic compounds. All food poisoning is divided into the following forms:

  • microbial;
  • non-microbial etiology;
  • mixed.

The first group includes foodborne diseases and intoxication. In this situation, the causative agents are bacteria (clostridia, colibacillus, proteus, streptococci), mushrooms, toxins. Poisoning is also possible with poisonous plants, mushrooms, berries, fish roe, seafood, heavy metal salts, pesticides, pesticides. Symptoms in this pathology are caused by inflammation of the stomach against the background of exposure to toxins.

In most cases, there are signs of gastroenteritis. These include constant pain in the muscles, head, nausea, vomiting, fever, weakness, and increased stool frequency. Symptoms of dehydration are common. Diagnostic signs of food poisoning are:

  • acute, sudden onset;
  • the connection of pain with food intake;
  • the simultaneous appearance of symptoms in a group of individuals;
  • the transience of the disease.

6 Duodenitis and pancreatitis

Pain in the epigastric region can be a symptom of duodenitis (inflammation of the mucous membrane of the 12th intestine). It can be acute or chronic. This is the most common pathology of this organ. Quite often, this disease is combined with enteritis and gastritis. The main causes of inflammation of the 12th intestine are:

  • inaccuracies in nutrition;
  • drinking alcoholic beverages;
  • bacterial infection;
  • the presence of an ulcer or gastritis;
  • violation of blood supply;
  • chronic pathology of the liver and pancreas.

The main symptoms of the disease depend on its form. Duodenitis, which has arisen against the background of an ulcer or infectious gastritis, is characterized by pain on an empty stomach, at night and a few hours after eating. Strong manifestations are characteristic of the acute type of pathology. When combined with inflammation of other departments small intestine symptoms may include malabsorption syndrome, dyspeptic disorders... In case of stagnation of the secretion of the 12th intestine, paroxysmal pains, belching, nausea, vomiting, bloating, rumbling occur. With duodenitis, the outflow of bile may be impaired. In this situation, soreness appears in the epigastric region. Clinical picture resembles biliary dyskinesia.

If something hurts in the stomach, the reason may be pancreatitis, the symptoms of which are usually quite pronounced. Pain syndrome is most pronounced in acute inflammation of the pancreas. The latter is located next to the stomach. This pathology is characterized by the appearance of pain in the upper abdomen. It can last from several minutes to several days. The pain is intense, constant and distressing to the patient. It can give to the left or right half of the body, depending on which part of the organ is affected (head, body or tail). The pain syndrome increases with food intake and treatment is required. It often takes on a shingles character. Additional signs of the disease include nausea, vomiting, bloating, tenderness to palpation, and an increase in overall body temperature.

7 Diagnosis and treatment

If your stomach is sick, then you should not postpone the visit to the doctor indefinitely, because the consequences can be dangerous. Treatment is carried out only after establishing the cause. pain syndrome... Diagnostics includes:

  • detailed survey of the patient;
  • physical examination (palpation of the abdomen, listening to the lungs and heart);
  • general and biochemical blood test;
  • carrying out FGDS;
  • determination of gastric acidity;
  • a blood test for the presence of Helicobacter pylori;
  • Ultrasound of the abdominal organs;
  • laparoscopy;
  • fecal examination;
  • contrast radiography;
  • CT or MRI;
  • duodenal intubation;
  • Analysis of urine.

Colonoscopy may be done if colitis is suspected. A biopsy is done to rule out stomach cancer. How to get rid of stomach pain? Therapy should be directed at the underlying cause. If the stomach is inflamed, what to do in this situation? Treatment of gastritis involves adherence to a strict diet, the use of drugs (antacids, proton pump blockers, gastroprotectors). The use of Almagel, Fosfalugel and Omez is indicated in the form of the disease with high acidity. If the bacterium Helicobacter is detected, antibiotics and Metronidazole are used.

Therapy for acute pancreatitis includes temporary fasting, applying cold to the stomach, using antispasmodics, Omeprazole, diuretics, and infusion therapy.

With purulent pancreatitis, treatment necessarily includes antibiotics. If vomiting is present, use antiemetic drugs (metoclopramide). With the development of peritonitis and organ necrosis, an operation is indicated. The chronic form of pancreatitis involves adherence to a diet, taking enzyme preparations (Panzinorma, Pancreatina, Mezima). In case of stomach cancer, surgical treatment (organ resection or removal). Thus, the causes of abdominal pain can be very different. If any, you should consult your doctor.

What to do in case of exacerbation of gastric ulcer?

If the patient has an acute critical situation associated with perforation of the gastric ulcer, it is necessary emergency treatment, since peritonitis in this case progresses rapidly. Symptoms of perforation in this case are:

  • the appearance of a sharp pain that quickly spreads throughout the abdomen;
  • muscle tension of the walls of the peritoneum;
  • phenomena preceding fainting (dizziness, ringing in the ears, weakness);
  • chills;
  • nausea;
  • dry mouth.

Traditional therapies

Therapeutic assistance in the phase of exacerbation of gastric ulcer is determined based on the patient's condition, age, and the nature of clinical symptoms. However, the treatment of uncomplicated forms is almost always based on the use of bactericidal agents, for example, Amoxicillin, Metranidazole, Clarithromycin. Due to these drugs and some others, also belonging to the group of antibiotics, it becomes possible to cure the pathology of the gastric mucosa, since they eliminate the main cause - the pathogenic microorganism Helicobacter pylori.

In addition to antibacterial drugs in the treatment of acute ulcers, the following can be used:

1. means that normalize the level of acidity of the digestive juice (Omeprazole, Ranitidine);

2. drugs with gastroprotective (protective) properties (De-nol and other bismuth-containing medicines);

3. blockers of dopamine central receptors (Primperan, Raglan, Cerucal);

4. drugs with a psychotropic effect, if the patient suffers from irritability, insomnia, a feeling of constant anxiety (Tazepam, Elenium);

5. adrenergic drugs that have an anti-secretory and suppressive gastrin release effect (Obzidan, Inderal).

In the treatment of exacerbation of gastric ulcer, certain physiotherapeutic methods have also proven themselves well: ozokerite and paraffin applications, magneto- and hydrotherapy, sessions of modulated sinusoidal currents.

Carrying out all activities in combination with a diet in 80-90% of cases allows you to achieve a stable remission of the pathology. However, conservative treatment does not always help, and then the patient is shown surgical intervention in different ways from the circumstances (by the method of selective proximal vagotomy, resection, endoscopy).

Indications for stomach surgery:

  • perforation of ulceration;
  • an ulcer complicated by profuse bleeding (bleeding leading to hypovolemia);
  • pyloric stenosis;
  • defect penetration.

Traditional recipes for treatment

Experts do not recommend using folk methods to cure an ulcer due to the risk of aggravating the situation. Such treatment is especially prohibited in complicated acute forms. But in order to prevent exacerbation, doctors use some unconventional recipes, for example, a remedy:

1.from birch leaves (1 teaspoon of chopped fresh leaves of this tree is poured with a glass of boiling water, infused for 1-2 hours);

2. from mother-and-stepmother (the infusion is prepared similarly to the previous method with one difference that not only the leaves of the plant, but also the flowers themselves can be used); besides this folk recipe helps to heal both the stomach and bronchi;

3.from medicinal marshmallow(1 large spoonful of ground rhizome is poured into 250 ml. Boiling water, for 30 seconds everything is simmering over low heat, and then infused for about half an hour).

All of the listed traditional medicine should be drunk before meals 3 times a day.

Diet for ulcers

Compliance with dietary nutrition is equally important during an exacerbation of the inflammatory process, and in the stage of its remission, and in case of complications with stenosis, bleeding and other life-threatening factors. Therefore, the doctor prescribes a personal diet for the patient based on:

  • sparing the gastroduodenal mucosa with the elimination of all chemical, thermal and mechanical irritants;
  • fractional nutrition (the patient is recommended to eat and drink in small portions, but every 3-4 hours);
  • correction of fat in the direction of increase;
  • increasing the protein quota;
  • lowering the proportion of carbohydrates in the daily diet.

The diet for the treatment of stomach ulcers should be followed for at least 6-9 months. When the disease recedes, going into a phase of remission, and food will not cause discomfort to the stomach, you can gradually return to the usual type of dishes (not mashed and not very boiled), but you still have to completely abandon rough and harmful industrial products.

In addition to diet, an important role in the prevention and treatment of acute ulcers is played by the exclusion of alcohol and energy drinks due to their causing bleeding and the growth of erosive inflammations.

Duodenal bulb ulcer

One of the most common types of erosive formations of the gastrointestinal tract is an ulcer of the duodenal bulb. The disease is common. According to official data, up to 10% of the world's population are sick. Deformation develops due to a failure in the chemical processing of food. The anatomy of erosive formations is different, but more often they form on a bulb shaped like a ball. The duodenal bulb is located at the very beginning of the intestine, when it leaves the stomach. The treatment is long and difficult.

It can be deformed on the front and back walls (kissing ulcers). The ulcer of the duodenal bulb also has a special location - at the end or at the beginning (mirrored). Mirror erosion is treated like other forms. Negative factors affecting the work of the stomach and intestines provoke the appearance of ulcers of various shapes. The risk group includes middle-aged people and those who are forced to work the night shift.

If there is a failure in the processing of food by the stomach, an ulcer of the duodenal bulb may occur.

Causes of ulcers of the duodenal bulb

Most often, inflammation of the duodenum occurs due to the aggressive action of acid. In the absence of therapy, perforated ulcers and bleeding may develop. There can be a number of reasons:

  • disturbed diet (a lot of fatty, spicy, diet abuse, carbonated drinks);
  • Helicobacter bacteria is the cause of ulcerative formations in most cases;
  • smoking, alcohol;
  • severe stress or systematic stay in a state of emotional stress;
  • hereditary predisposition;
  • long-term use of certain anti-inflammatory drugs;
  • incorrectly prescribed treatment at the initial stage of the disease.

Kissing ulcers in the intestines can appear due to concomitant causes: HIV infection, liver cancer, hypercalcemia, renal failure, Crohn's disease, etc.

Symptoms

Symptoms of duodenal ulcer are characteristic of other types of gastrointestinal ulcers, and they appear depending on the stage of the disease:

  • heartburn;
  • nausea in the morning or after eating;
  • pain in the epigastric region;
  • pain in the stomach at night;
  • flatulence;
  • the appearance of a feeling of hunger after a short period of time after eating;
  • if the disease is in neglected form bleeding may open;
  • vomit;
  • pain localized in the lumbar region, or the chest part.

The inflammatory lymphofollicular form of the duodenum has a different nature of pain: stabbing pain, sharp or aching. Sometimes it passes after a person has eaten. Hunger pains usually occur at night, and to eliminate the discomfort, it is recommended to drink a glass of milk or eat a little. Nocturnal pain is caused by a sharp rise in acid levels.

Stages

The intestinal healing process is divided into 4 main stages:

  • Stage 1 - initial healing, characteristic is the creeping of the layers of the epithelium;
  • Stage 2 - proliferative healing, in which protrusions in the form of papillomas appear on the surface; these formations are covered with regenerating epithelium;
  • Stage 3 - the appearance of a polysadny scar - an ulcer on the mucous membrane is no longer visible; a more detailed study shows many new capillaries;
  • Stage 4 - scar formation - the bottom of the ulcer is completely covered with new epithelium.

Erosive kissing formations on the duodenum are healed after the application of therapy. Multiple ulcers in a small area of ​​the intestine result in multiple scars. The result of such healing is cicatricial and ulcerative deformity of the duodenal bulb. The appearance of fresh scars leads to a narrowing of the lumen of the bulbous sector. Inflammatory cicatricial deformation of the duodenal bulb has negative consequences, for example, food stagnation and malfunctioning of the entire gastrointestinal tract.

There is also a distribution at the stage: exacerbation, scarring, remission.

One of the forms of intestinal ulcers is lymphoid hyperplasia of the duodenal bulb, which is characterized by inflammation due to a disturbance in the outflow of lymph. The causes are exactly the same as for duodenal ulcers. There are also similar symptoms. Lympofollicular dysplasia is a pathology in the mucous membrane of the intestine or stomach. It is characterized by the appearance of formations of a rounded shape on a broad base. Lymphofollicular dysplasia is deformed and has a dense consistency and point size. The lymphofollicular mucosa is infiltrated. Development stages:

  1. sharp;
  2. chronic.

Diagnosis of the disease

The FGDS method (fibrogastroduodenoscopy) will help to accurately diagnose the presence of a duodenal ulcer. Using a special probe with a camera, the intestinal surface is examined. It is this diagnostic method that will make it possible to establish the location of the ulcer, its size and the stage of the disease. Usually there is inflammation, or the surface is hyperemic, covered with punctate erosions of a dark red color. The area of ​​the intestine is inflamed in the area of ​​the mouth, and the mucous membrane is hyperemic.

Tests are required to determine the Helicobacter bacteria. As a material for testing, not only blood and feces are used, but also vomit, material after biopsy. Ancillary diagnostic methods include x-rays, palpation in the stomach, general analysis blood.

Treatment

After the diagnosis of "inflammation of the duodenal bulb" is made, treatment should be started immediately, since serious complications may develop. Kissing ulcers are treated mainly with medications. During an exacerbation, hospitalization is necessary.

The doctor selects drugs and physiotherapy individually for each patient, taking into account the characteristics of the body and stage. For example, the chronic or lymphofollicular stage is treated differently than during an exacerbation. This scheme usually includes the following medications:

  • bismuth-based medicines, in case of detection of the Helicobacter bacteria; such drugs have a depressing effect on pathogenic microflora;
  • drugs that reduce the amount of gastric juice produced: blockers, inhibitors, anticholinergics;
  • prokinetics - improve intestinal motility;
  • unpleasant pain sensations are eliminated with the help of antacids;
  • antibiotics are prescribed to combat the bacterial cause of the appearance of a lymphofollicular ulcer;
  • gastroprotectors will help prevent the negative effects of hydrochloric acid on the affected area;
  • inflammation is relieved by analgesics and antispasmodics.

The combination of medication and physical therapy contributes to a faster recovery of the body. These techniques include: electrophoresis, ultrasound exposure, the use of microwaves, therapy with modulated currents to relieve pain. Special physiotherapy exercises will help to normalize gastric motility. Gymnastics is good prophylactic agent from stagnation in the intestines and stomach.

In addition to the generally accepted methods of healing intestinal ulcers, traditional medicine has long been proven to be effective. In first place with ulcerative lesions there is freshly squeezed potato juice. It must be drunk three times a day, and only freshly squeezed. The potatoes are pre-peeled, grated, and squeezed through cheesecloth. The first few days, the dosage is one tablespoon. Gradually, it can be increased to half a glass. You must drink before eating.

To others, no less effective means, include honey, medicinal herbs (calendula, St. John's wort, plantain), olive and sea buckthorn oils.

During the period acute form be sure to comply with bed rest. After the exacerbation has passed, you can take short walks. Heavy physical exercise and exercise is prohibited. The army is contraindicated for those who have an ulcer. In order not to provoke new attacks, it is important to avoid stress and protect the nervous system.

Dieting is one of the important factors on the path to recovery and decrease inflammatory processes... General recommendations for dietary nutrition the following:

  • small portions;
  • chew each piece thoroughly;
  • temporarily exclude foods that provoke the active production of gastric juice (vegetable soups, fish and meat broths);
  • in order not to irritate the mucous membrane additionally, the food should be grated;
  • fruit juices must be diluted with water;
  • drink milk more often;
  • do not use spices in dishes;
  • cook grated porridge;
  • eat food at the optimal temperature, not too hot or too cold;
  • fractional meals, up to 5 times a day.

Food should be steamed or in the oven. The diet must include non-acidic fruits, kefir, milk, cottage cheese, boiled or steamed vegetables. It is necessary to stop drinking alcohol and smoking, as this can lead to the development of serious complications.

Forecast

A favorable prognosis for recovery can be if the treatment was carried out on time and the correct diet was followed. With an untimely visit to a doctor or improperly prescribed drugs, serious complications can develop: lymphatic follicular ulcer, bleeding (vomiting of blood), perforation of the ulcer (acute pain under the sternum) and penetration (due to adhesions, the contents of the intestine enter neighboring organs). In each of these cases, the only option is surgery.

Duodenal stenosis is a complication. After healing, there are cicatricial changes that can subsequently cause swelling and spasm. Stenosis usually manifests itself during the acute form or after therapy. Stenosis occurs in those patients who have an ulcer long time does not heal. Stenosis is accompanied by impaired intestinal and gastric motility.