lung tissue
lobar pneumonia
hematoxylin and eosin staining
stomach wall
chronic stomach ulcer
hematoxylin and eosin staining
metastasis of mucous cancer in lymph nodes
with tumor progression
coloring Sudan Sh
Congo red coloring
kidney tissue
kidney amyloidosis
hematoxylin and eosin staining
LN tissue section
tuberculosis
hematoxylin and eosin staining
septic myocarditis
causes – sepsis
hematoxylin and eosin staining
cause - damage
brain tissue
local hemosiderosis
hematoxylin and eosin staining
skin section
the reasons are polyetiological
hematoxylin and eosin staining
gastric mucosa
gastric adenocarcinoma
the reasons are polyetiological
hematoxylin and eosin staining
aortic section
the wall of the aorta, in its middle shell, where the vasavasorum are located, there is an inflammatory infiltrate consisting of lymphocytes, plasma cells, fibroblasts and single giant cells of the Pirogov-Langhans type. There are also small foci of necrosis.
syphilitic mesaortitis
hematoxylin and eosin staining
myocardial hypertrophy
hematoxylin and eosin staining
brain tissue
purulent leptomeningitis
meningococcal infection
picrofuchsin staining according to Van Gieson
fibroids
the reasons are polyetiological
MICROPREPARATION No. 58. Fibromyoma ()
hematoxylin and eosin staining
kidney tissue
ischemic renal infarction
hematoxylin and eosin staining
lung tissue
hemorrhagic pulmonary infarction
thrombosis, embolism
MICROPREPARATION No. 62.
hematoxylin and eosin staining
brain tissue
cerebral hemorrhage
coloring Sudan Sh
lung tissue
pulmonary fat embolism
Glandular hyperplasia of the endometrium
MICROPREPARATION No. 80.
hematoxylin and eosin staining
LU for lymphogranulomatosis
the reasons are polyetiological
hematoxylin and eosin staining
papillary thyroid cancer
the reasons are polyetiological
MICROPREPARATION No. 87.
hematoxylin and eosin staining
ovary slice
actinomycosis
picrofuchsin staining according to Van Gieson
cardiosclerosis
hematoxylin and eosin staining
kidney tissue
the reasons are polyetiological
hematoxylin and eosin staining
acute myocardial infarction
Perls reaction
lung tissue
brown induration of the lung
picrofuchsin staining according to Van Gieson
liver tissue
hematoxylin and eosin staining
liver tissue section
nutmeg liver
hematoxylin and eosin staining
lung tissue
focal influenza pneumonia
hematoxylin and eosin staining
cross section of a vessel
hematoxylin and eosin staining
lung tissue
miliary pulmonary tuberculosis
hematoxylin and eosin staining
thyroid tissue
hematoxylin and eosin staining
section of tumor tissue (skin)
skin melanoma
hematoxylin and eosin staining
lung tissue
bronchopneumonia
hematoxylin and eosin staining
lung tissue
emphysema
hematoxylin and eosin staining
lung tissue, pleura
pleural hyalinosis
hematoxylin and eosin staining
lung tissue
healed tubercular affect
hematoxylin and eosin staining
leather tissue
skin papilloma
the reasons are polyetiological
hematoxylin and eosin staining
uterine tissue
hydatidiform mole
the reasons are polyetiological
coloring Sudan Sh
cross section of an artery
artery atherosclerosis
hematoxylin and eosin staining
fallopian tube section
tubal pregnancy
hematoxylin and eosin staining
breast tissue
the reasons are polyetiological
hematoxylin and eosin staining
liver tissue
cavernous hemangioma of the liver
the reasons are polyetiological
hematoxylin and eosin staining
small intestine section
reasons - salmonellosis
hematoxylin and eosin staining
uterine tumor tissue
chorionepithelioma
the reasons are polyetiological
hematoxylin and eosin staining
subarachnoid hemorrhage
MICROPREPARATION No. 185.
hematoxylin and eosin staining
pancreatic tissue
pancreatic atrophy in diabetes
reasons – diabetes
hematoxylin and eosin staining
tracheal tissue
MICROPREPARATION No. 187.
hematoxylin and eosin staining
cross section of the appendix
hematoxylin and eosin staining
kidney tissue
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MICROPREPARATIONS (treat)
MICROPREPARATION No. 2. Croupous pneumonia
hematoxylin and eosin staining
lung tissue
Almost all alveoli are filled with fibrinous exudate, the septa are thickened, and the vessels are full of blood. In the lumen of the alveoli there is pink exudate. It contains fibrin filaments (homogeneous in the form of a network or grains) and polymorphonuclear leukocytes. A characteristic pathognomonic symptom is the presence of Kohn bridges (fibrin threads from one alveoli pass to another). The capillaries of the interalveolar septa are empty, different from the
lobar pneumonia
infectious agents - pneumococci, streptococci, staphylococci
MICROPREPARATION No. 8. Chronic gastric ulcer
hematoxylin and eosin staining
stomach wall
There is an ulcerative defect in the wall of the stomach. The bottom of the ulcer is filled with necrotic masses. The defect extends to the mucous and muscular membranes. Muscle fibers in the bottom of the ulcer are not identified. In the bottom, 4 layers can be distinguished: fibrinous-purulent exudate, fibrinoid necrosis, granulation and scar tissue
chronic stomach ulcer
The reasons are polyetiological: stress, nutritional factors, bad habits, helicobacter pylori
MICROPREPARATION No. 9. Metastasis of mucous cancer in lymph nodes
hematoxylin and eosin staining
on the preparation, the pattern of the lymph nodes is erased due to the proliferation of atypical cells containing a large amount of mucus. Among the tumor cells there are signet ring-shaped (the nucleus is pushed to the periphery by the mucous mass)
metastasis of mucous cancer in lymph nodes
with tumor progression
MICROPREPARATION No. 14. Fatty liver (Sudan III stain)
coloring Sudan Sh
liver tissue (peripheral cells)
on the preparation in the cytoplasm of hepatocytes there are accumulations of large droplets of fat, colored yellow-orange. Larger fat droplets are contained in the cytoplasm of hepatocytes of the peripheral (periportal) sections of the hepatic lobules, smaller ones - in the cells of the central zone of the lobule
large fatty liver degeneration
causes – chronic alcoholism, intoxication, protein starvation, vitamin deficiencies, anemia, transfusion of incompatible blood
MICROPREPARATION No. 15. Kidney amyloidosis (Congo red staining)
Congo red coloring
kidney tissue
in the capillary loops of the renal glomeruli, in the walls of the arterioles and under the basement membrane of the renal tubules there are red deposits of amyloid. Amyloid deposited along the reticular fibers
kidney amyloidosis
causes - chronic infections (tuberculosis), purulent-destructive processes, malignant neoplasms, rheumatoid diseases
MICROPREPARATION No. 16. Caseous necrosis of lymph nodes in tuberculosis
hematoxylin and eosin staining
LN tissue section
focus - homogeneous substance, in healthy tissue - lymphocytes, at the border - macrophage productive reaction
caseous necrosis of lymph nodes in tuberculosis
tuberculosis
MICROPREPARATION No. 18. Septic myocarditis
hematoxylin and eosin staining
in the myocardium there are foci of purulent melting of tissue, in the center of which bacterial emboli are visible among polymorphonuclear leukocytes
septic myocarditis
causes – sepsis
MICROPREPARATION No. 20. Granulation tissue
hematoxylin and eosin staining
section of skin (granulation tissue)
superficial leukocyte-necrotic layer; superficial layer of vascular loops; layer of vertical vessels; maturing layer (collagen fibers, fewer vessels); horizontal layer of fibroblasts (black elongated cells); fibrous layer
regeneration through the formation of granulation tissue (the outcome is scar formation)
cause - damage
MICROPREPARATION No. 23. Hemosiderin at the site of hemorrhage (Perls reaction)
Perls reaction (Prussian blue)
brain tissue
in the macrophages located in the cyst wall, bluish-green granules of the Prussian blue dye are visible, deposited in places where hemosiderin granules accumulate. The formation of Prussian blue is due to the presence of iron cation in hemosiderin. There is a focus of hemorrhage in the brain tissue: hematoidin (light brown) is formed in the center under anaerobic conditions, hemosiderin (turquoise) is formed at the periphery
local hemosiderosis
atherosclerosis, cerebral form of hypertension, cerebral aneurysm, stroke, trauma
MICROPREPARATION No. 25. Squamous cell keratinizing carcinoma
hematoxylin and eosin staining
skin section
the tumor consists of strands and layers of atypical squamous epithelium that grow into the underlying dermis. At high magnification, signs of polymorphic cells with hyperchromic nuclei of different sizes, containing 2 or more nucleoli, are visible. Figures of pathological mitoses are detected. In the center of the tumor cells, formed bulbous structures of keratinized cells are visible - cancer pearls
squamous cell keratinizing skin cancer
the reasons are polyetiological
MICROPREPARATION No. 27. Adenocarcinoma of the stomach
hematoxylin and eosin staining
gastric mucosa
growths of atypical glands are visible in all layers of the stomach wall. Cells forming glands of various sizes and shapes with hyperchromic nuclei, with figures of pathological mitoses
gastric adenocarcinoma
the reasons are polyetiological
MICROPREPARATION No. 36. Syphilitic mesaortitis
hematoxylin and eosin staining
aortic section
the wall of the aorta, in its middle shell, where the vasa vasorum is located, there is an inflammatory infiltrate consisting of lymphocytes, plasma cells, fibroblasts and single giant cells of the Pirogov-Langhans type. There are also small foci of necrosis.
syphilitic mesaortitis
Causes: syphilis (pale spirochete)
MICROPREPARATION No. 38. Myocardial hypertrophy
hematoxylin and eosin staining
muscle cells are thickened and increased in size. The nuclei are large, hyperchromatic. There are many blood vessels in the enlarged myocardial stroma
myocardial hypertrophy
MICROPREPARATION No. 39. Purulent leptomeningitis
hematoxylin and eosin staining
brain tissue
the pia mater is sharply thickened and diffusely infiltrated with polymorphonuclear leukocytes. The vessels of the membranes are dilated and full of blood. Perivascular and pericellular edema is expressed in the brain substance
purulent leptomeningitis
meningococcal infection
picrofuchsin staining according to Van Gieson
muscle and connective tissue
smooth muscle fibers alternate with bundles of collagen fibers of varying thickness. Muscle and collagen fibers are arranged randomly (tissue atypia). Muscle fibers are colored yellow-green, connective tissue is pink. The nuclei are black, randomly arranged
fibroids
the reasons are polyetiological
MICROPREPARATION No. 61. Ischemic renal infarction
hematoxylin and eosin staining
kidney tissue
against the background of unchanged components of the kidney, a triangular-shaped lesion is visible, in which only the contours of the glomeruli and tubules are preserved. In the cells of these structures there are no nuclei (karyolysis), in some places the cytoplasm is in a state of lysis, and there are pink areas lacking organization (necrotic detritus). This is the zone of necrosis. It is separated from the unchanged tissue by a demarcation zone 9 in which there are full-blooded vessels and an accumulation of leukocytes)
ischemic renal infarction
thrombosis, embolism, prolonged spasm, atherosclerosis of the renal arteries
hematoxylin and eosin staining
lung tissue
the focus of necrosis is red. The septal cells and alveolar epithelium lack nuclei. Some alveolar septa are torn. The area of necrosis is infiltrated with red blood cells. Around the necrosis there is congestion of blood vessels, an accumulation of leukocytes, and in the lumen of the alveoli there is protein fluid. Many branches of the pulmonary artery are thrombosed.
hemorrhagic pulmonary infarction
thrombosis, embolism
MICROPREPARATION No. 71. Hemorrhage in the brain
hematoxylin and eosin staining
brain tissue
brain tissue is swollen. The focus of hemorrhage is represented by an accumulation of red blood cells in the brain tissue, located in the form of a lake around anatomically intact vessels (diapedetic hemorrhage). In the area of the hemorrhage, arterioles with thickened walls and signs of plasmorrhagia are visible
cerebral hemorrhage
atherosclerosis, cerebral aneurysm, trauma, hypertension
MICROPREPARATION No. 75. Fat embolism of the lung (Sudan Sh staining)
coloring Sudan Sh
lung tissue
interalveolar septa are practically invisible. The lumen of the vessel is obstructed by bright orange fat emboli
pulmonary fat embolism
fractures of tubular bones, crushing of subcutaneous fat, use of oil preparations in the form of intravenous injections
Hematoxylin and eosin staining
section of uterine tissue (endometrial scraping)
The endometrium is thickened, has many elongated glands with a convoluted course. In some places, the lumen of the glands is expanded and looks like cysts. The epithelium of the glands proliferates, the endometrial stroma is rich in cellular elements.
Glandular hyperplasia of the endometrium
Causes: ovarian dysfunction, ovarian cyst
MICROPREPARATION No. 81. Lymphogranulomatosis
hematoxylin and eosin staining
in the lymph nodes there are conglomerates of remaining cells (lymphatic), some of the tissue is necrotic (a focus without cellular infiltrates), areas of fibrosis (bundles of collagen fibers with fibroblasts). In the lymph node there are cells that are not typical for it: reticular (irregularly shaped, large, purple cells with one nucleus), plasmacytes (oval cells with a rounded nucleus, displaced to the periphery), eosinophils (the nucleus is pushed to the periphery, the cytoplasm is orange). Uncharacteristic cells - Berezovsky-Stenberg-Reed cells (large, similar to a reticulocyte, but multinucleated - 2 large nuclei next to each other owl's eye syndrome)
LU for lymphogranulomatosis
the reasons are polyetiological
hematoxylin and eosin staining
section of a thyroid tumor
the tumor consists of cavities of varying sizes, filled with villi - papillary papillae, emanating from the walls of the cavities, covered with atypical epithelium. In some places, the tumor papillae grow into the wall of the cavities and the tumor capsule. There are practically no follicles.
papillary thyroid cancer
the reasons are polyetiological
MICROPREPARATION No. 88. Actinomycosis
hematoxylin and eosin staining
ovary slice
Irregularly shaped fungal drusen are observed in the ovarian tissue. The surrounding tissue is infiltrated with polymorphonuclear leukocytes. Around the growth of connective tissue - capsule
actinomycosis
radiant fungus (actinomycetes)
MICROPREPARATION No. 89. Cardiosclerosis (picrofuchsin staining according to Van Gieson)
picrofuchsin staining according to Van Gieson
among the normal myocardium, extensive fields of scar tissue are visible (colorless with dots - fibroblast cells), surrounded by hypertrophied cardiomyocytes (green with nuclei)
cardiosclerosis
productive inflammation, myocardial infarction, ischemic heart disease
MICROPREPARATION No. 90. Kidney for myeloblastic leukemia
hematoxylin and eosin staining
kidney tissue
the tissue is diffusely infiltrated with tumor cells such as myeloblasts. Areas of hemorrhage and necrosis are noted. In the lumens of blood vessels there are leukemic thrombi
kidney in myeloblastic leukemia
the reasons are polyetiological
MICROPREPARATION No. 94. Myocardial infarction
hematoxylin and eosin staining
3 zones are visible on the preparation: 1) a zone of necrosis with characteristic changes in cardiomyocytes, lysis of nuclei, coagulation and clumpy disintegration of myoplasm, disappearance of transverse striations and cell boundaries; 2) demarcation zone - dilation and congestion of blood vessels, hemorrhages and infiltration of polymorphonuclear leukocytes; 3) zone of healthy myocardium along the periphery
acute myocardial infarction
spasm of the coronary arteries, thrombosis, embolism, atherosclerosis of the coronary arteries, functional overstrain of the myocardium with insufficient blood supply
MICROPREPARATION No. 97. Brown induration of the lung (Perls reaction)
Perls reaction
lung tissue
the interalveolar septa are thickened due to the expansion and overflow of blood vessels. Some of the alveoli are filled with edematous fluid, in others there are accumulations of siderophages with hemosiderin - a bluish-green color. Part of the interalveolar septa is thickened and sclerotic. Overgrowth of connective tissue around the bronchi
brown induration of the lung
general and chronic venous congestion, heart defects, vascular atherosclerosis, congestion and hypertension in the ICC
MICROPREPARATION No. 100. Liver cirrhosis (picrofuchsin staining according to Van Gieson)
picrofuchsin staining according to Van Gieson
liver tissue
The liver parenchyma is represented by false lobules of various sizes. In each pseudolobule, fragments of several pre-existing normal liver lobules can be seen (multiglobular cirrhosis). The hepatic beams are indistinguishable. The central lobular vein is absent or displaced to the periphery of the false lobule. Hepatocytes of false lobules are in a state of protein degeneration and necrosis. There are large hepatocytes with 2 or more nuclei. Areas of hepatic parenchyma are separated by wide fields of connective tissue stained magenta pink. Among the fields of connective tissue, close hepatic triads are visible, which are infiltrated with lymphocytes and histiocytes
multiglobular cirrhosis of the liver
hepatitis, hepatosis of various etiologies
MICROPREPARATION No. 103. Nutmeg liver
hematoxylin and eosin staining
liver tissue section
in the liver, the veins and sinusoids in the central zone of the lobules are dilated and full of blood. Foci of diapedetic hemorrhages in the form of “lakes”, discomplexation of the hepatic beams, necrosis and atrophy of hepatocytes are also visible. In the peripheral, periportal zone of the lobules, the blood supply to the capillaries and venules is normal, the structure of the hepatic beams is preserved. Hepatocytes are in a state of fatty degeneration (variegation of color)
nutmeg liver
chronic cardiovascular failure, heart defects, hepatic vein thrombosis
MICROPREPARATION No. 109. Focal influenza pneumonia
hematoxylin and eosin staining
lung tissue
against the background of airy lung tissue, airless areas are visible. The alveoli are filled with serous-hemorrhagic exudate. In places, accumulations of polymorphonuclear leukocytes forming microabscesses are visible. The bronchial epithelium is desquamated and rejected; there is exudate in the bronchial lumen
focal influenza pneumonia
influenza virus, bacterial infection
MICROPREPARATION No. 110. Mixed thrombus
hematoxylin and eosin staining
cross section of a vessel
the lumen of the vessel is completely obstructed by a thrombus, which consists of platelets, fibrin threads, hemolyzed erythrocytes and leukocytes. In a mixed thrombus, the quantitative composition of formed elements is proportional to their number in the blood. A significant part of the thrombotic masses has grown with connective tissue, which grows from the intimal side of the vessel. Thrombotic masses have gaps lined with endothelium
damage to the vessel wall, disruption of the interaction between the coagulation and anticoagulation systems of the blood, increased blood viscosity, slowing of blood flow as a result of cardiovascular failure, decreased muscle tone of the veins
MICROPREPARATION No. 113. Miliary pulmonary tuberculosis
hematoxylin and eosin staining
lung tissue
Numerous tuberculous granulomas are visible in the preparation. In the center of the granulomas there is caseous necrosis, around it there are epithelioid, individual multinucleated giant Pirogov-Langhans macrophages, lymphocytes and individual plasmacytes. There are no vessels in the granuloma
miliary pulmonary tuberculosis
Mycobacterium tuberculosis, hematogenous generalization of primary tuberculosis
MICROPREPARATION No. 117. Colloid goiter
hematoxylin and eosin staining
thyroid tissue
The follicles of the thyroid gland are round in shape and dilated. Their wall is thinned, its ruptures and fusion of fluids with each other are visible with the formation of cysts of various sizes. The epithelium lining the follicles is flattened. The lumen of follicles and cysts is filled with a thick mucus-like mass (colloid). Full-blooded vessels and hemorrhages are visible (brownish contents in the follicles)
mucous (colloid) dystrophy (colloid goiter)
iodine deficiency, impaired thyroid hormone synthesis, goitrogens, immunopathology
MICROPREPARATION No. 126. Skin melanoma
hematoxylin and eosin staining
section of tumor tissue (skin)
a tumor node is located in the skin - it has an intense brown color due to accumulations of mealnin in tumor cells located along the periphery of the tumor node. Tumor cells vary in size and shape.
skin melanoma
reasons are polyetiological (with tumor progression)
MICROPREPARATION No. 127. Bronchopneumonia
hematoxylin and eosin staining
lung tissue
the wall of the bronchus is diffusely infiltrated with polymorphonuclear leukocytes (panbronchitis), in the lumen of the bronchi there is serous-leukocyte exudate with an admixture of desquamated epithelial cells. Perifocally, sharply dilated, air-filled alveoli are visible (perifocal emphysema)
bronchopneumonia
The reasons are polyetiological: inflammation in the respiratory tract, pneumococci, viruses
MICROPREPARATION No. 133. Emphysema of the lung
hematoxylin and eosin staining
lung tissue
in dilated acini - complete smoothing of the walls, the walls of the alveoli become thinner and straighten. The capillaries of the interalveolar septa become empty. The alveoli are increased in volume. Black inclusion – tobacco
emphysema
chronic bronchitis, age-related changes in lung tissue, vicarious in pathology of another lung
MICROPREPARATION No. 135. Hyalinosis of the pleura
hematoxylin and eosin staining
lung tissue, pleura
the visceral pleura is thickened, its fibrous structures are difficult to distinguish. The mesothelium covering the pleura is atrophic. The thickening of the pleura occurred due to the coarsening of bundles of collagen fibers, which turned into translucent glassy formations. Around the pleural vessels there is a pronounced proliferation of connective tissue
pleural hyalinosis
Causes: metabolic disorders in connective tissue, formation of hyaline. The result of progression of fibrinoid swelling, inflammation, necrosis, sclerosis
MICROPREPARATION No. 136. Healed tuberculous affect in the lung
hematoxylin and eosin staining
lung tissue
purple areas are visible in the lung tissue, representing lime deposits. They are surrounded by a connective tissue capsule - this is a healed tuberculous affect. In the field of view, a focus of necrosis surrounded by connective tissue, as well as an island of nascent bone tissue (pseudobone). Along the periphery in the zone of necrosis - deposition of calcium salts
healed tubercular affect
causes – primary tuberculosis
MICROPREPARATION No. 141. Skin papilloma
hematoxylin and eosin staining
leather tissue
numerous outgrowths of stratified squamous keratinizing epithelium that make up the tumor parenchyma. The tumor has a well-defined stroma, represented by outgrowths of the dermis, which, like the fingers of a glove, are covered with multilayered squamous epithelium. Tissue atypia is characteristic (increase in epithelial layers, hyperkeratosis). This is a papillary formation covered with stratified squamous epithelium with underlying stroma and blood vessels
skin papilloma
the reasons are polyetiological
MICROPREPARATION No. 150. Hydatidiform mole
hematoxylin and eosin staining
uterine tissue
the chorionic villi are cystically changed, their stroma is swollen, the central vessel is absent, the trophoblast has a two-row structure, and is atrophic in places
hydatidiform mole
the reasons are polyetiological
MICROPREPARATION No. 153. Atherosclerosis of the artery (Sudan III staining)
coloring Sudan Sh
cross section of an artery
yellow spots, stripes (lipid deposits) and whitish-gray plaques protruding into the lumen are visible on the intima. Some of the plaques are ulcerated. Around the growth of connective tissue
artery atherosclerosis
unbalanced diet, physical inactivity, genetic defect of cholesterol receptors (hypercholesterolemia)
MICROPREPARATION No. 159. Tubal pregnancy
hematoxylin and eosin staining
fallopian tube section
a decidual reaction is observed in the CO of the pipe. In the lumen of the tube, chorionic villi are visible, penetrating into the thickness of the muscular membrane
tubal pregnancy
reasons – disruption of the passage of the fetus through the tube (inflammation, tumor, defective tube development, etc.)
MICROPREPARATION No. 163. Fibroadenoma of the mammary gland
hematoxylin and eosin staining
breast tissue
The ducts are visible in the form of oddly shaped slits. Connective tissue grows into them. The color is yellow. Pink connective tissue visible
intracanalicular fibroadenoma
the reasons are polyetiological
MICROPREPARATION No. 178. Cavernous hemangioma of the liver
hematoxylin and eosin staining
liver tissue
the tumor is well demarcated from the surrounding liver tissue by a pronounced fibrous capsule. The tumor consists of large cavernous vascular thin-walled cavities (cavities), lined with endothelium and filled with liquid or clotted blood
cavernous hemangioma of the liver
the reasons are polyetiological
MICROPREPARATION No. 182. Ulcerative enteritis due to salmonellosis
hematoxylin and eosin staining
small intestine section
There is an ulcerative defect in the wall of the small intestine. The bottom of the ulcer is filled with necrotic masses. The mucous and submucous membranes around the ulcer are infiltrated with polymorphonuclear leukocytes
ulcerative enteritis due to salmonellosis
reasons - salmonellosis
MICROPREPARATION No. 183. Chorionepithelioma
hematoxylin and eosin staining
uterine tumor tissue
the tumor is composed of two types of tumor cells: monomorphic light epithelial cells (Langhans cells) and giant dividing cells with hyperchromic polymorphic nuclei (syncytiotrophoblasts). There is no stroma in the tumor. Instead of vessels, cavities filled with red blood cells are visible. The walls of the cavities are lined with tumor cells instead of endothelium
chorionepithelioma
the reasons are polyetiological
hematoxylin and eosin staining
brain tissue, subarachnoid space
the artery wall is thickened, erythrocyte diapedesis, signs of plasmorrhagia
subarachnoid hemorrhage
closed craniocerebral injury, cerebral atherosclerosis
hematoxylin and eosin staining
pancreatic tissue
some lobules are atrophied, others are compensatory hypertrophied. Atrophy of the islets of Langerhans. They are reduced in size. The specimen shows the proliferation of connective tissue (sclerosis), fat deposition (lipomatosis - transparent cells). Hyalinosis, fibrosis and lymphoid infiltration of microvessels are observed. Sclerosis and lipomatosis, both intralobular and interlobular
pancreatic atrophy in diabetes
reasons – diabetes
MICROPREPARATION No. 196. Croupous tracheitis
hematoxylin and eosin staining
tracheal tissue
on the surface of the tracheal mucosa there is fibrinous exudate infiltrated with polymorphonuclear leukocytes. In the underlying tissues, capillaries and venules are sharply expanded and full of blood
purulent-nercotic tracheitis with influenza
Causes: influenza virus and bacterial infection
MICROPREPARATION No. 198. Phlegmonous-ulcerative appendicitis
hematoxylin and eosin staining
cross section of the appendix
the wall of the process is thickened, all its layers are diffusely infiltrated with polymorphonuclear leukocytes. On the serous surface there are deposits of fibrinous exudate, intensely stained with eosin. Lymphatic follicles are enlarged.
phlegmonous-ulcerative appendicitis
reasons are polyetiological, autoinfection
MICROPREPARATION No. 203. Serous extracapillary glomerulonephritis
hematoxylin and eosin staining
kidney tissue
there is a sharp congestion of the capillaries, the lumen of the Shumlyansky-Bowman capsule is enlarged and filled with serous exudate. As a result of proliferation of the capsule epithelium, podocytes and macrophages, crescent formations (crescents) appear. The capillary loops undergo necrosis, and there are fibrin thrombi in their lumen
serous (productive) extracapillary glomerulonephritis
causes - infectious and allergic diseases
MICROPREPARATION No. 205. Septic warty endocarditis
hematoxylin and eosin staining
in the area of necrosis of the valve leaflet, massive thrombotic deposits and colonies of bacteria appear. Growing granulation tissue, when mature, deforms the valve leaflets. Histiolymphocytic infiltrates and granulomas are found in the interstitial myocardial tissue
septic verrucous endocarditis
causes: rheumatism, sepsis
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Methodological developments
practical classes for students
Diseases of the digestive organs and liver
Peptic ulcer of the stomach and duodenum
| Study macroscopic specimens: stomach ulcer, ulcer duodenum, hemorrhagic erosions of the stomach. |
|
| Acute stomach ulcers | |
| Describe the macroscopic specimen Hemorrhagic erosions of the stomach
№88 Hemorrhagic gastric erosion
| Pay attention to the extent of the lesion; determine the shape, color of defects, as well as the type and consistency of the edges of defects. Note the superficial nature of the defect in the stomach wall and find brownish-brown masses of hydrochloric acid hematin. |
| Describe the macroscopic specimen Chronic stomach ulcer
| Pay attention to the extent of the lesion, determine the shape, type and consistency of the edges of the defects, the condition and surface of their bottom. |
| Sketch and describe microscopic specimen Stomach ulcer Helicobacter pylori (1) in the lumen of the glands (Romanovsky Giemsa stain)
Overhanging edge of a stomach ulcer Undermined edge of a stomach ulcer
The bottom of a stomach ulcer during an exacerbation
| Find a defect in the stomach wall and determine its depth. Characterize changes in the area of the bottom of the ulcer and the edges of the defect. Describe changes in the deeper layers of the stomach wall and determine the nature of the ulcerative process. |
Appendicitis. Peritonitis.
| Study macroscopic specimens: phlegmonous appendicitis, gangrenous appendicitis, appendicular empyema, chronic appendicitis. Describe one of the macroscopic preparations. |
|
| Describe the macroscopic specimen Phlegmonous appendicitis
Gangrenous appendicitis
| Pay attention to the size, wall thickness, and condition of the serous membrane of the appendix. |
| Draw and describe the microslide No. 90 Phlegmonous appendicitis
| Characterize the condition of the mucous membrane of the appendix and its lumen. Determine the nature and prevalence of exudate, the degree of blood filling of the vessels. |
| Sketch and describe microscopic specimen Obliteration of the appendix
| Determine the topography of the growth of connective tissue, note the presence of islands of adipose tissue, atrophy of the layers of the appendage wall. |
| Examine a microscopic specimen Fibrinous purulent peritonitis | Characterize the state of the peritoneal mesothelium, blood vessels, and exudate. Note changes in the underlying fiber and muscle tissue. |
Hepatitis. Toxic liver dystrophy. Cirrhosis of the liver.
| 1. Study macroscopic preparations: toxic liver dystrophy, cirrhosis of the liver, varicose veins of the esophagus. 2. Describe one of the macroscopic preparations. |
|
| Describe the macroscopic specimen Toxic liver dystrophy
| Pay attention to size, consistency; mark the color on the cut surface; determine the stage of the disease. |
| Examine a microscopic specimen No. 93a Toxic liver dystrophy. (Sudan III staining) | Note the violation of the liver structure, obesity and necrobiosis of liver cells in the center of the lobule. |
| Sketch and describe microscopic specimen No. 93 Toxic liver dystrophy
| Note the violation of liver architecture, find foci of necrosis. Describe changes in the stroma of the organ. Determine the stage of the process. |
| Describe the macroscopic specimen Postnecrotic cirrhosis of the liver
Portal cirrhosis of the liver
| Pay attention to the configuration, size, consistency, color of the organ; note the sizes of the nodes. Pay attention to the size, consistency, color of the organ; note the sizes of the nodes. |
| Sketch and describe microscopic specimen No. 94 Portal cirrhosis of the liver (picrofuchsin staining)
| Determine the topography of the newly formed connective tissue, the degree of its maturity, and identify the morphological features of the “false lobules”. Note changes in liver cells (phenomena of fatty degeneration and perverted regeneration), bile ducts. Pay attention to the distinctive features of various forms of cirrhosis. |
Adjacent files in item [UNSORT]
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Pathological anatomy of peptic ulcer
Pathological anatomy. Initial ulcers do not penetrate deeper than the mucous membrane. A chronic ulcer can spread to the muscular and serous membranes. An ulcer with hard, raised edges is called a callous ulcer. An ulcer that involves all layers of the gastric wall can cause perforation. An ulcer that penetrates into neighboring organs, most often the pancreas, is called penetrating. After the ulcer heals, scars appear, sometimes deforming the stomach (“hourglass”, snail-shaped stomach) or causing narrowing (stenosis) of the pylorus of the stomach. Inflammation of the serous membrane at the location of the ulcer leads to perigastritis or periduodenitis and the formation of adhesions with nearby organs.
Acute ulcers are usually round or oval in shape. The edges of the ulcers are clear, the bottom is usually clean, without overlaps. Acute ulcers can cause perforation of the stomach wall and fatal gastric bleeding.
A chronic ulcer, according to most researchers, is the outcome of an acute one and differs from it by the significant development of fibrous tissue in the bottom and edges. A chronic ulcer is usually round or oval in shape, less often it has an irregular outline. The cardial edge of the ulcer seems to be undermined, the pyloric edge is flat. The bottom is covered with dirty gray deposits; the organ into which penetration occurred is visible in the bottom of the penetrating ulcers. A stomach ulcer is usually larger than a duodenal ulcer. The size of the niche determined by x-ray examination does not always correspond to the size of the ulcer. Due to swelling of the edges, filling of the ulcer crater with mucus, exudate or food masses, the ulcerative defect may not be completely filled with barium. Most gastric ulcers are located on the lesser curvature and in the pylorus. Duodenal ulcers are usually localized 1-2 cm from the pylorus, equally often on the anterior and posterior walls of the intestine. Postbulbar ulcers are less common. Chronic ulcers are usually single, but multiple lesions also occur. During gastroscopy, near a large ulcer, several small ones are sometimes found that are not detectable x-ray. In patients with gastric ulcers, duodenal ulcers are sometimes simultaneously detected. Multiple duodenal ulcers are often located on opposite walls of the intestine (“kissing” ulcers). The most rare locations of ulcers in the stomach are the cardia, fundus and greater curvature.
Upon microscopic examination, four layers are distinguished at the bottom of the ulcer. On the inside, fibrinous-necrotic deposits, desquamated epithelium, leukocytes, erythrocytes and hydrochloric acid hematin are visible, coloring the bottom of the ulcer gray or dark brown. Under this layer is a layer of fibrinoid necrosis, formed by disorganized and necrotic collagen fibers. In rapidly and rapidly progressing ulcers, this layer can reach several millimeters in width. The granulation tissue lies deeper. Often it is not detected, since it is completely involved in the destructive process. Granulation tissue passes into the next, most developed layer - scar tissue, which is formed by loose and dense fibrous connective tissue. There are small lymphoid follicles with pronounced reactive centers. When the ulcer recurs, many mast cells with signs of increased secretory activity can be seen in the scars. Scar tissue grows into the muscle layers, submucosal layer, its volume significantly exceeds the size of the ulcer itself.
With an exacerbation of peptic ulcer disease, necrosis of granulation tissue and collagen fibers, an inflammatory reaction in the surrounding tissues, rejection of areas of necrosis and, as a result, an increase in the ulcerative defect usually occur. Yu. M. Lazovsky believes that the progressive proliferation of fibrous tissue at the bottom of the ulcer is not associated with the transformation of granulation tissue into a scar, but with the direct formation of collagen fibers from the ground substance.
In the area of the ulcer, changes in the blood vessels are usually observed with the development of inflammatory-necrotic processes in them, areas of fibrinoid necrosis of the arterial walls, thrombosis of the arteries and veins and their subsequent recalibration. These secondary vascular lesions disrupt tissue trophism and serve as one of the reasons preventing the healing of chronic ulcers. At the bottom of the ulcer there are nerve trunks immured in scar tissue and growths of nerve fibers such as amputation neuromas. In the ganglion cells of the intramural nerve nodes, dystrophic changes and irritation phenomena are observed (S. S. Weil, P. V. Sipovsky).
With a peptic ulcer, changes occur in the entire mucous membrane of the stomach and duodenum. At the edges of a gastric ulcer, proliferation of epithelium is observed, which can grow deep into the mucosa and along its surface, taking the form of polyps. The pyloric glands undergo hynerplasia and show signs of increased mucoid secretion. Acid mucopolysaccharides, which are normally absent, appear in the secretion. With the long-term existence of an ulcer, atrophic changes in the glands occur, and their secretion weakens. In the fundic glands, patterns of atrophy and intestinal metaplasia are observed; the so-called pseudopyloric glands of Stern, containing mucoid secretion, are formed. In the stroma one can see diffuse lymphoplasmacytic infiltrates, large lymphoid follicles, and growths of smooth muscle fibers. With a duodenal ulcer, the number of parietal cells increases significantly, which are found even in the pyloric region.
Healing of chronic ulcers occurs through the formation of a scar. Before healing begins, swelling and inflammatory infiltration of the edges of the ulcer occur. The edges smooth out, approach the bottom, and the necrotic masses covering the bottom are torn away. Granulations appear in the bottom and edges, which gradually fill the ulcer crater. The surface epithelium, saturated with RNA, grows onto the granulation tissue and lines it. The muscular layer of the mucous membrane, gastric and duodenal glands do not regenerate. The accumulation of acidic mucopolysaccharides is of great importance in the healing of ulcers. It takes about 5-7 weeks for an ulcer with mild fibrosis of the bottom and edges to heal. Sometimes complete healing occurs within 10 days, sometimes it takes several months. As a result of healing of deep, especially penetrating ulcers, gastric deformities may occur. Scar healing of pyloric ulcers can lead to pyloric stenosis. Diverticula (ulcus diverticulum) may develop between a healed duodenal ulcer and the pylorus.
Complications. V. M. Samsonov identifies five groups of complications of peptic ulcer disease. 1. Complications of ulcerative-destructive origin: perforation, arrosive bleeding and penetration. Perforation of an ulcer is one of the most dangerous complications. Most often, perforation occurs in the second half of the day. The diameter of the perforation hole is about 0.5 cm. Histological examination reveals a picture of exacerbation of peptic ulcer disease, necrosis and leukocyte infiltration of the edges and bottom of the ulcer, and fibrin overlay on the serous surface.
Arrosive bleeding occurs from large vessels at the bottom of the ulcer. M.K. Dahl et al. found that vessel arrosion may be preceded by limited necrosis of the wall with the formation of an aneurysm and its subsequent rupture. Bleeding from chronic ulcers, the vessels of which are fixed by scar tissue that prevents the contraction of the arteries, is especially dangerous. Ulcers of the lesser curvature of the stomach usually penetrate into the lesser omentum, and duodenal ulcers into the pancreas.
When ulcers penetrate into hollow organs, gastric fistulas occur (gastrocolic, gastrointestinal, gastrointestinal). Ulcers of the cardial and subcardial sections can penetrate into the diaphragm. In the future, such an ulcer may break through into the pleural cavity, into the pericardial cavity. 2. Complications of an inflammatory nature: gastritis, duodenitis, perigastritis, periduodenitis, gastric phlegmon, hepatocholangitis. 3. Complications of ulcerative-scar origin: stenosis of the cardiac part of the stomach, pylorus, duodenum, shortening of the lesser curvature, hourglass deformation of the stomach, diverticula of the stomach and duodenum. 4. Malignancy of a stomach ulcer, according to A.I. Abrikosov, occurs in 8-10% of cases. The lack of consensus on the frequency of ulcer malignancy is associated with the difficulties of differential diagnosis of malignant ulcers and primary ulcerative cancer. Malignancy of duodenal ulcers is extremely rare.
Toxic liver dystrophy
Toxic liver dystrophy or progressive massive liver necrosis is an acute or chronic disease characterized by massive tissue necrosis and the development of liver failure. Toxic dystrophy develops as a result of the action of exogenous (mushrooms, foods with toxins, etc.) and endogenous (toxicosis of pregnancy, thyrotoxicosis) toxins. These substances have a hepatotoxic effect and damage hepatocytes.
Pathological anatomy. Toxic liver dystrophy has various manifestations that depend on the duration of the damage to liver cells. In the first few days, the organ enlarges and becomes dense and yellow in color. Next, there is a progressive decrease in liver tissue and wrinkling of the capsule. On section, the liver is clay-colored or gray. Under a microscope, fatty degeneration of hepatocytes is first found in the center of the lobules; these changes are quickly replaced by necrosis and autolysis of the liver tissue. The progression of necrosis leads by the end of the second week to complete necrosis of the lobule and only a narrow strip of fatty degeneration remains along the periphery. All this is the stage of yellow dystrophy. At week 3, the liver shrinks further and becomes red. These are manifestations of phagacytosis and resorption of necrotic detritus. This exposes the stroma of the organ with dilated blood vessels. Changes in the 3rd week are a manifestation of the stage of red liver degeneration.
With progressive necrosis, patients die from acute hepatic-renal failure. Survivors have liver changes characteristic of postnecrotic cirrhosis.
24. Toxic liver dystrophy.
The liver is enlarged in size, flabby in consistency, with a wrinkled capsule. In the section the structure is erased, variegated in color
305. Portal cirrhosis of the liver.
The liver is deformed, compacted, reduced in size, the surface is granular. The section shows large and small nodules of liver tissue of various sizes, surrounded by a ring of connective tissue - the so-called “false lobules”.
553. Cirrhosis of the liver.
The liver has a dense consistency, lumpy, with yellow foci and false lobules when cut.
325. Fatty liver degeneration of the “goose liver” type. Chronic fatty hepatosis.
The liver is enlarged and yellow in color.
279. Liver cancer due to cirrhosis.
Against the background of liver cirrhosis, a mottled focus of tumor tissue is visible.
198. Thrombosis of the hepatic vein.
Part of the liver with the hepatic vein, in the lumen of which a thrombus is visible.
127. Icteric necrotic nephrosis.
The kidney on a section is yellow-green in color, the border of the cortex and medulla is dense, the cortex is dull and wide.
462. Splenomegaly. Hyalinosis of the capsule.
The spleen is enlarged, there are dull translucent lesions on the capsule
37. Hemorrhoids. In the distal part of the colon, varicose veins are brown in color.
Dummy 35. Varicose veins of the esophagus in liver cirrhosis.
Sudden congestion and dilation of the veins of the esophagus with arrosion of the vessel wall.
Study micropreparations:
38. Acute viral hepatitis.
Hepatocytes are in a state of hydropic (balloon) degeneration and coagulative necrosis. Hyaline-like Councilman bodies are found in the perisinusoidal lumens. Cholestasis and lymphohistiocytic infiltration of the portal tracts are pronounced.
Indicate in the picture:
1 - balloon degeneration of hepatocytes.
2 - Councilmen's bodies.
3 - cholestasis
4 - histiolymphocytic infiltration of the portal tracts
171. Subacute toxic liver dystrophy(acute hepatosis, stage of red dystrophy).
The structure of the liver lobules is disrupted. Hepatocytes in a state of necrosis are homogeneous, eosinophilic, and without nuclei. Many necrotic hepatocytes have undergone phagocytosis and resorption. In these areas, exposed (free) reticular stroma with dilated sinusoids and bile capillaries is visible.
Indicate in the picture:
1 - necrotic hepatocytes.
2 - free stroma.
3 - dilated sinusoids and bile capillaries.
99. Portal cirrhosis.
The growth of connective tissue along the portal tracts in the form of rings with the formation of so-called “false lobules”, in which the architectonics of the vessels is disrupted. hepatocytes in a state of fatty degeneration (cells in the form of vacuoles) and regeneration (large cells with large or double nuclei)
Indicate in the picture:
1 - connective tissue
2 - false lobes
3 - hepatocytes in a state of fatty degeneration
4 - young liver cells
44. Billiary cirrhosis.
Proliferation of connective tissue along the periphery of the lobules. Cholestasis is pronounced; bile ducts are dilated and filled with yellow or dark green bile.
76. Postnecrotic cirrhosis (Masson stain).
The structure of the liver is sharply disturbed; large areas of blue connective tissue replace necrotic liver tissue. The surviving liver cells in a state of necrosis are homogeneous, pink-violet, without nuclei. Regeneration is not expressed.
397. The basis of toxic liver dystrophy is:
fatty degeneration
inflammation
protein dystrophy
398. The outcomes of toxic dystrophy are:
hepatic-renal failure
cirrhosis of the liver
399. The cause of toxic liver dystrophy is:
infection
alcohol poisoning
poisoning with mushrooms and poisons
toxicosis of pregnancy
400. Goose liver develops when:
acute hepatosis
chronic hepatosis
401. The mechanism of alteration of hepatocytes in serum hepatitis is:
direct effect of viruses
immune cytolysis
402. AIDS is accompanied by hepatitis:
whey
epidemic
403. Dystrophy of hepatocytes in serum hepatitis:
grainy
vacuolar
404. Etiological factors of hepatitis include:
medicines
allergy
dystrophy
405. The morphological form of chronic hepatitis is:
phlegmonous
persistent
fibrinous
fatty liver disease
406. Hepatitis is considered chronic:
after 1 month
after 3 months
after 6 months
after 1 year
407. Indications for a biopsy for a clinical diagnosis of hepatitis are:
diagnosis verification
establishing the form and severity of hepatitis
evaluation of treatment results
408. The safest type of biopsy for diffuse liver damage is:
puncture
transvenous
marginal liver resection
pinch during laparoscopy
409. The main histological signs of chronic active hepatitis are:
stepwise necrosis
emperiopolosis
bridging necrosis
410. The main histological sign of persistent hepatitis is:
1- clear border of the marginal plate
2- sclerosis of periportal tracts
3- granulomatous inflammation in the centrilobular zones
4- pericellular fibrosis
411. One of the main histological signs of viral hepatitis is:
1- Councilmen's corpuscles
2- giant mitochondria
3- granulomatous inflammation
4- pericellular fibrosis
5- sclerosis
412. Histological signs of liver tissue regeneration include:
1- binucleate hepatocytes
2- giant multinucleated hepatocytes, symplast type
3- “rosette-like” structures
413. The most common cause of toxic liver dystrophy is:
414. The following stages of toxic liver dystrophy are distinguished:
1- active
2- red dystrophy
3- moderate severity
4- persistent
415. Signs of stage 1 toxic liver dystrophy include:
bright yellow liver
the liver is reduced in size
liver is dense, sclerotic
diffuse hemorrhages in the liver tissue
416. Histological signs of stage II toxic liver dystrophy include:
necrosis of hepatocytes in the centrilobular regions
carbohydrate dystrophy
macrofocal sclerosis
Mallory bodies
417. A macroscopic sign of the liver with cirrhosis is:
liver of soft-elastic consistency
liver is enlarged
liver of dense consistency
nutmeg liver
418. Acute viral hepatitis is characterized by:
extralobular cholestasis
gall lakes
fatty degeneration of hepatocytes
Councilman's corpuscles
419. Councilman's bodies belong to hepatitis:
whey
alcoholic
none of the above
420. What changes do hepatocytes undergo during the formation of Councilman’s bodies:
hyalinosis
liquefaction necrosis
coagulative necrosis
421. Necrosis spreading between the center of the liver lobules and the branches of the crow vein is called:
massive
stepped
bridge-like
422. Inflammatory infiltrates in acute serum hepatitis are dominated by:
neutrophils
macrophages
lymphocytes
423. Inflammatory infiltrates in alcoholic hepatitis necessarily contain:
lymphocytes
neutrophils
macrophages
424. The reddish (light) color of the liver in cirrhosis depends on:
dystrophy
obstruction of blood flow through the inferior vena cava
obstruction of blood flow through the portal vein
425. “Lobulated liver” refers to cirrhosis:
1- circulatory
3- infectious
4- exchange.
Topic VI. Diseases of the gastrointestinal tract.
Gastritis is an inflammatory disease of the gastric mucosa. There are acute and chronic gastritis.
Acute gastritis is characterized by:
Macroscopically – thickening of the mucous membrane due to edema, redness, and formation of erosions.
FORMS OF ACUTE GASTRITIS:
1. Catarrhal (simple)
2. Fibrinous
3. Purulent
4. Necrotic
Chronic gastritis is a chronic inflammation of the gastric mucosa, accompanied by impaired cell renewal of the epithelium.
Morphological forms of chronic gastritis:
surface
atrophic
hypertrophic
combined atrophic-hyperplastic.
Modern international classification of chronic gastritis:
autoimmune (type A)
bacterial (type B)
mixed (type A and B)
chemically toxic (type C)
lymphocytic
special forms (Menetrier's disease)
acute ulcer - an ulcer that involves the thickness of the mucous membrane, without sclerotic changes in the bottom and at the edges; is usually of a secondary nature.
symptomatic ulcers are observed with:
stressful conditions
endocrine diseases
acute and chronic circulatory disorders
after taking medications
chronic ulcer - an ulcer that penetrates beyond the mucous membrane into the thickness of the stomach wall, has rough fibrous changes in the bottom and raised ridge-like edges; the proximal edge of the ulcer is undermined.
LAYERS OF CHRONIC STOMACH ULCERS:
1. zone of exudation or necrosis
2. zone of fibrinoid swelling
3. granulation tissue zone
4. sclerosis zone.
MAIN COMPLICATIONS OF Peptic Ulcer:
penetration
perforation
malignancy
pyloric stenosis
bleeding
perigastrid, periduodenitis
diverticulum is a protrusion of the wall of the gastrointestinal tract.
Appendicitis is an inflammation of the appendix of the cecum, giving a characteristic clinical syndrome.
Acute appendicitis occurs:
1. simple
2. superficial
3. destructive (phlegmanous, phlegmanous-ulcerative, apostematous, gangrenous)
chronic appendicitis develops after acute appendicitis and is characterized by sclerotic and atrophic processes, against the background of which inflammatory and destructive changes may appear.
forms of CHOLECYSTITIS:
1. Catarrhal
2. Purulent (phlegmonic)
3. Diphtheritic
4. Chronic
Crohn's disease is a chronic relapsing disease of the gastrointestinal tract, characterized by nonspecific granulomatosis, necrosis, and scarring of the intestinal wall.
Study macropreparations:
79. Phlegmanous appendicitis.
The vermiform appendix is thickened, the serous membrane is dull, with fibrinous overlays, the vessels are full of blood. The enlarged lumen is filled with pus (epyema of the appendix),
570. Normal gallbladder.
The wall of the gallbladder is thin, the mucosa is velvety.
49. Calculous cholecystitis.
The wall of the gallbladder is thickened, sclerotic, and there are many stones in its lumen.
50, 180. Cholecystitis.
The wall of the gallbladder is unevenly thickened, the mucous membrane is swollen, dark red in color.
348. Erosion of the gastric mucosa.
On the gastric mucosa there are multiple surface mucosal defects with smooth edges, the bottom is black (hematin hydrochloride pigment).
376. Acute stomach ulcers.
On the mucous membrane of the stomach, surface defects with smooth edges of a dark red color from 1.5 to 3 cm in diameter are visible
183. Acute duodenal ulcer with perforation.
386. Chronic gastric ulcer.
On the lesser curvature of the stomach, a steep ulcerative defect up to 1 cm in diameter is visible, the bottom and edges are dense, roll-shaped.
108. Chronic ulcers of the stomach and duodenum.
On the mucous membrane of the stomach and duodenum, 3 ulcerative defects are visible. In the stomach, an ulcer of an elongated shape with undermined dense edges and a dense bottom. In the duodenum there are 2 round ulcers located opposite each other (“kissing ulcers”), in one of them there is a perforated hole
128. Melena (bleeding into the lumen of the gastrointestinal tract).
The intestinal mucosa is black (pigment hydrochloric acid hematin, methemoglobin, iron sulfide)
149, 184. Saucer-shaped gastric cancer. Skirrus of the stomach.
178. Stomach cancer.
Exo- and endophytic growth.
146. Nonspecific ulcerative colitis.
There are multiple ulcerative defects on the colon mucosa
various shapes and sizes.
75. Polypoid cancer.
Gastric fibroids.
Study micropreparations:
62a. Chronic stomach ulcer..
At the bottom of a chronic ulcer there are 4 layers:
1) on the surface of the ulcerative defect there is a zone of necrosis with leukocytes, 2) underneath there is fibrinous exudate, 3) below there is a zone of granulation tissue, followed by 4) a zone of deep sclerosis with lymphoid infiltrates and sclerotic vessels.
Indicate in the picture:
1 - I zone – necrosis.
2 - II zone – fibrinoid
3 - III zone – granulation tissue.
4 - IV zone – sclerosis.
90. Acute purulent appendicitis (phlegmanous-ulcerative).
(see at the same time drug 151. Appendix is normal)
All layers of the appendix are infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosa there are full-blooded vessels and hemorrhages
Indicate in the picture:
1 - mucous membrane with ulcerations
2 - submucosa
3 - muscular layer.
4 - serous membrane
5 - infiltration of all layers of the process wall by leukocytes.
177. Chronic appendicitis with regeneration of the mucous membrane.
The wall of the process is thickened due to proliferation in all layers of fibrous connective tissue. Newly formed low cubic epithelial cells creep onto the ulcerative defect
140. Cholecystitis.
The wall of the gallbladder is thickened due to the proliferation of connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophied
74. Solid gastric cancer.
The parenchyma and stroma in the tumor are developed evenly. The parenchyma is represented by atypical cells forming cells. Anaplastic epithelium proliferates, in some places it grows beyond the mucous membrane - infiltrating growth
Tests: choose the correct answers.
426. The causes of acute gastritis are:
1- alcoholism
2- infection
3- ingestion of traumatic substances
427. The following changes are characteristic of atrophic gastritis:
1- pink mucosa, with well-defined folds
2- mucous membrane pale
3- there is a lot of mucus in the stomach
4- focal epithelial regeneration
428. The main severe complication of a stomach ulcer is:
1- lymphadenitis of regional nodes
2-perforation
3-perigastritis
4- “inflammatory” polyps around the ulcer
429. The most characteristic changes in blood vessels at the bottom of a chronic ulcer are:
1- inflammation and sclerosis of the wall
2- plethora
3- anemia
4- large thin-walled sinusoidal vessels
430. A local factor that is important in the pathogenesis of gastric and duodenal ulcers includes:
1- infectious
2- trophic disturbance
3- toxic
4- decreased secretion of gastrin and histamine
5- exogenous
431. The layers of the bottom of a chronic gastric ulcer are:
1- exudate
3-granulation tissue
4- sclerosis
432. The autopsy of the deceased revealed many erosions of the stomach from a burn, covered with hydrochloric acid hematin. Erosion was formed:
1- before burn
2- during a burn
433. There is a coffee-like liquid on the gastric mucosa. When cleansed, pinpoint hemorrhages and defects the size of a pinhead are visible. Specify the name of the process:
1- petechiae
3- acute ulcers
434. At autopsy, two round ulcers were found in the stomach, located on the lesser curvature, the edges were smooth, the bottom was thin. Ulcers are:
1- spicy
2- chronic
435. Signs of a chronic ulcer are:
1- recurring bleeding
2- dense sclerotic bottom
3- multiplicity of ulcers
4- one, two ulcers
436. The most common location of stomach cancer is:
2- greater curvature
3- small curvature
437. A cancerous tumor grows diffusely through all layers of the stomach wall, it is dense, the stomach cavity is reduced. Cancer refers to:
1- differentiated adenocarcinoma
2- mucous cancer
438. A woman is clinically diagnosed with dense ovarian tumors on both sides. It is necessary to investigate the presence of metastases first of all:
1- in the lungs
2- in the stomach
439. Acute gastritis usually manifests itself in the form of:
1- atrophic
2- hypertrophic
3-purulent
4- superficial
5- with epithelial restructuring
440. Chronic atrophic gastritis is characterized by:
1- ulcerations
2- hemorrhages
3- fibrinous inflammation
4- enterolization of the mucous membrane
5- plethora and diffuse infiltration of the own layer of the mucous membrane by leukocytes
441. Exacerbation of a stomach ulcer is characterized by:
1- hyalinosis
2- enterolization
3- regeneration
4- lymphoplasmacytic infiltrate
5- necrotic changes
442. A characteristic sign of Ménétrier’s disease is:
1- enterolization of the gastric mucosa
2-chlorohydrolenic uremia (gastric tetany)
3- Virchow metastases
4- giant hypertrophic folds of the gastric mucosa
5- nonspecific intestinal granulomatosis
443. Ischemic colitis can be detected:
1- for atherosclerosis
2- for scleroderma
3- for diabetes
4- for rheumatoid arthritis
444. Rectal changes are typical:
1- for ulcerative colitis
2- for Crohn's disease
3- for Hirschsprung's disease
445. With malignancy of ulcerative colitis, the intestinal mucosa is:
1- smooth
2- polypoid (granular)
3- atrophic
446. Malignancy of adenomatous polyps is more often detected:
1- in the basal sections
2- in superficial sections
3- in the middle sections
447. Familial multiple polyposis of the colon is detected more often:
1- from birth
4- at the end of the first year of life
5- after 3 years
448. Characteristic histological signs of Whipple's disease are revealed:
1- in the lungs
2- in the myocardium
3- in the liver
4- in the kidneys
449. The most characteristic histological sign of Whipple’s disease is:
1- hemorrhage
3- macrophage infiltrate
4- leukocytosis
450. Cancer is suspected in an exhausted patient. An enlarged, hardened lymph node is palpable above the left collarbone. It is necessary to examine first of all:
2- stomach
3- esophagus
451. The appendix is thickened in the distal section, the serous cover is dull, hyperemic, there is feces and purulent exudate in the lumen. Microscopically - diffuse infiltration of the wall of the appendix with neutrophils, no ulcers. Appendicitis refers to:
1- to simple
2- to destructive
452. The appendix is thickened in the middle segment, the serous cover is covered with fibrinous films. Histologically, against the background of diffuse infiltration of the entire thickness of the ulcer wall.
Appendicitis refers to:
1- to phlegmonous-ulcerative
2- to gangrenous
3- to simple
453. The appendix is thickened, the serous part is covered with fibrin, the wall is black and dull throughout. Appendicitis refers to:
1- to catarrhal
2- to gangrenous
3- to phlegmonous
454. Abortive appendicitis is characterized by:
1- inflammation is mild
2- primary changes have resolved
3- the area of inflammation is extremely small
455. Thickening of mucus in the lumen of the sclerotic appendix is called:
1- cystic fibrosis
2- mucocele
3- melanosis
456. Characteristic signs of acute appendicitis are:
2- serous exudate in the mucous and muscular membranes
3- hyperemia
4- sclerosis of the process wall
5- destruction of muscle fibers
457. Characteristic signs of chronic appendicitis are:
1- sclerosis of vessel walls
2- sclerosis of the process wall
3- purulent bodies
4- lymphoplasmacytic infiltration
5- granulomas
458. Morphological forms of appendicitis are:
1- acute purulent
2- sharp superficial
3- acute destructive
4- chronic
5-lobar
459. Complications of appendicitis are:
1- perforation
2- peritonitis
3- liver abscesses
460. Subhepatic jaundice is most often caused by:
1- Cancer of Vater's nipple
2- cancer of the head of the pancreas
3- liver cancer
461. Cancer of the head of the pancreas causes jaundice:
1- parenchymal
2- hemolytic
3- mechanical
462. Crohn's disease in the destructive phase is characterized by:
1- mucous membrane in the form of a “cobblestone street”
2- deep slit-like longitudinal ulcerations of the mucosa
3- superficial ulcerations
4- granulomas in the intestinal wall
463. The ileal mucosa is divided by deep ulcers in the form of slits and resembles a cobblestone street. Name the disease:
3- typhoid fever
464. Nonspecific ulcerative colitis of allergic origin is characterized by:
1- fibrinous inflammation
2- multiple ulcers
3- polyp-like projections of excessively regenerating epithelium
4- fibrinous necrosis of individual sections of the intestine.
Topic VII. Introduction to infections. Typhus: abdominal, typhus, relapsing.
Infectious diseases are diseases caused by infectious agents: viruses, bacteria, fungi.
Invasive is a disease caused by the introduction of protozoa and helminths into the body.
Typhoid fever is an acute and long-term infectious disease caused by salmonella (Salmonella typhi), in the first week of illness it is characterized by symptoms of general intoxication (fever, chills) associated with bacteremia; widespread involvement of the reticuloendothelial system, accompanied by rash, abdominal pain and severe weakness in the second week of the disease; ulceration in Peyer's patches with bleeding from the small intestine and the development of shock in the third week of the disease.
stages of CHANGES IN GROUP LYMPHATIC FOLLICLES OF THE SMALL INTESTINE IN TYPHUS:
1. Brain swelling
4. Clean ulcers
5. Regeneration
the cellular composition of typhoid granuloma is macrophages, the so-called typhoid and lymphoid cells.
ATYPICAL FORMS OF TYPHUS:
1. Colotif
2. Laryngotiphos
3. Pneumotyphoid
4. Cholecystotyphoid
THE MOST COMMON AND DANGEROUS COMPLICATIONS OF TYPHUS:
1. Intestinal bleeding
2. Perforation of ulcers followed by peritonitis
Epithemic typhus. European typhus (louse typhus) -
an acute infectious disease caused by rickettsiae, characterized by damage to the nervous system and blood vessels. It manifests itself as general toxic phenomena, fever, roseola-petechial rash and disruption of the functioning of internal organs, especially the circulatory system.
Macroscopic characteristics are most often poorly expressed - skin rash in the form of red or brown roseola, petechiae, pinpoint hemorrhages of the conjunctiva of the eyeball (Chiari symptom). In advanced cases, areas of skin necrosis with areas of gangrene are possible.
Microscopic changes in the capillaries develop - destructive-proliferative-endo-thrombotic-vyskulitis.
TYPES OF GRANULOMAS IN TYPHUS:
1. mesenchymal - Davydovsky
microglial – Popova.
Recurrent disease is very rare - this is Brill-Zinser disease. (Repeated sporadic typhus).
Study macropreparations:
Description of drugs in Pathological Anatomy in Lesson No. 28
LESSON No. 28diseases of the liver and biliary system.
Macropreparation "Massive progressive necrosis liver - stage yellow dystrophy" .
The liver is sharply reduced in size, its capsule is wrinkled, the consistency is flabby, and when cut, the liver tissue has a clayey appearance.
Microslide № "Massive progressive necrosis liver - stage yellow dystrophy."
In the central sections of the lobules, hepatocytes are in a state of necrosis. Individual PMNs are found among the necrotic masses. In the peripheral sections of the lobules, hepatocytes are in a state of fatty degeneration: when stained with Sudan III, in the center of the lobules fatty detritus is visible in the hepatocytes of the peripheral sections of the lobules - drops of fat.
Macropreparation "Fat dystrophy liver ( fatty hepatosis ) »
The liver is enlarged in size, the surface is smooth, the edge is rounded, the consistency is flabby, and when cut it is ocher-yellow in color.
Microslide № "Spicy viral hepatitis ».
Hepatocytes are in a state of hydropic and balloon degeneration, which is an expression of focal liquefaction necrosis. Some hepatocytes in a state of apoptosis: reduced in size, with eosinophilic cytoplasm and pyknotic nucleus, or have the appearance of a hyaline-like body that is pushed into the lumen of the sinusoid (Councilman's body). The bile capillaries are dilated and filled with bile. The portal tracts are dilated, infiltrated with lymphohistiocytic elements, accumulations of which are visible inside the lobules in the sinusoids, as well as in areas where groups of hepatocytes are in a state of necrosis. In the peripheral parts of the lobules, binuclear and large hepatocytes (regenerative forms) are often found.
Electron diffraction pattern "Balloon dystrophy hepatocyte at acute viral hepatitis" - demonstration .
Microslide № "Chronic viral hepatitis IN moderate activity" .
The portal tracts are thickened, sclerotic, abundantly infiltrated with lymphocytes, macrophages (histiocytes), plasma cells with an admixture of PMNs. The infiltrate exits through the border plate into the parenchyma and destroys hepatocytes. Foci of necrotic hepatocytes are surrounded by lymphocytes and macrophages (stepwise necrosis). Foci of infiltration are visible inside the lobules. Outside areas of necrosis, liver cells are in a state of hydropic degeneration.
Electron diffraction pattern "Destruction of a hepatocyte by a killer lymphocyte in chronic active hepatitis."
At the site of contact of the lymphocyte with the hepatocyte, destruction of its cytoplasmic membrane is visible.
Macropreparation "Viral large-knot ( post-necrotic ) cirrhosis liver"
The liver is reduced in size, dense, the surface is large-nodular: nodes of uneven size, more than 1 cm, separated by wide fields of connective tissue.
Microslide № "Viral multilobular ( post-necrotic ) cirrhosis liver" - drawing . The liver parenchyma is represented by false lobules (regenerated nodes) of various sizes. In each node one can see fragments of several lobules (multilobular cirrhosis), the hepatic beams are not distinguishable, the central vein is absent or displaced to the periphery. Protein dystrophy and necrosis of hepatocytes. Hepatocytes are large in size, with two or more nuclei. Areas of parenchyma are separated by wide fields of connective tissue stained red with picrofuchsin. In the connective tissue fields, close triads, sinusoidal vessels, proliferating cholangioles, and lymphohistiocytic infiltrates are visible.
Macropreparation "Alcoholic fine-knotted ( portal ) cirrhosis liver"
The liver is enlarged (finally reduced) in size, yellow in color, dense, with a uniform finely tuberous (finely nodular) surface; nodes no more than 1 cm in diameter, separated by uniform narrow layers of connective tissue.
Microslide № "Alcoholic monolobular ( portal ) cirrhosis liver" - drawing . The parenchyma is represented by false lobules, uniform in size, built on fragments of one lobule (monolobular cirrhosis). The nodes are separated by narrow strands of connective tissue (septa), hepatocytes with symptoms of fatty degeneration. In the connective tissue septa, lymphohistiocytic infiltration with an admixture of PMNs and proliferation of the bile ducts is visible.
Macropreparation "Liver at mechanical jaundice" - demonstration .
Defects of various sizes are visible in the gastric mucosa, the bottom of which is painted black-brown with hydrochloric acid hematin.
Macrodrug CHRONIC GASTRITIS.
Smoothing of the folds of the gastric mucosa is detected, the wall is hyperemic, thinned, and flattened. Multiple point erosions are noted.
Microspecimen No. 422 Helicobacter pylori in parietal mucus in the gastric pits (gastrobiopsy, Giemsa stain).
Spiral-shaped bacteria are visible located near the surface epithelium of the supramucosal barrier. Surface cells are damaged, infiltration of the gastric mucosa with polymorphonuclear leukocytes.
Microslide N 423 CHRONIC ACTIVE GASTRITIS OF THE ANTRUM WITH GLAND ATROPHY AND COMPLETE INTESTINAL METAPLASY (gastrobioptat, 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 destruction of the glands and a decrease in their number, atrophy of the mucous membrane.
Macrodrug CHRONIC STOMACH ULCER(kalezny).
On the lesser curvature of the stomach, a deep defect in the stomach wall is visible, penetrating to the serous membrane, oval in shape, with raised edges. The edge facing the pylorus is gentle, looks like a terrace, formed by the mucous, submucosal and muscular membranes. The edge facing the esophagus is undermined. At the bottom of the ulcer, necrotic detritus is brown-brown in color. The folds of the gastric mucosa are smoothed, the rays converge towards the ulcerative defect (convergence of folds).
(E) Microslide N 106 CHRONIC STOMACH ULCER (with exacerbation) (staining with hematoxylin and eosin.
A defect in the stomach wall that involves the mucous, submucosal and muscular membranes. Near the defect, one edge of the mucous membrane is undermined, the other is flat. 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 identified; its break is visible at the border of the ulcerative defect. In the mucous membrane near the ulcer there is a picture of chronic atrophic gastritis.
View a set of macroscopic specimens illustrating the complications of a chronic ulcer: PERFORMED STOMACH ULCER, PENETRATING STOMACH ULCER, ARROSION OF A VESSEL IN THE BOTTOM OF AN ULCER, ULCER-CANCER OF THE STOMACH, SCAR DEFORMITY OF THE STOMACH
Saucer-shaped stomach cancer - on the lesser curvature of the stomach there is a formation protruding above the surface of the mucous membrane on a wide base with raised dense roll-like edges and a sinking bottom. The bottom is covered with gray-brown decaying masses.
Macropreparations of different forms of STOMACH CANCER.
Diffuse gastric cancer – the wall of the stomach (especially the mucous and submucosal membranes) is diffusely thickened in all parts. The section shows that gray-pink dense tissue grows through it. The mucous membrane is uneven, its folds are of varying thickness, the serous membrane is thickened, dense, and lumpy. The lumen of the stomach is narrowed.
Microslide N 424 HIGHLY DIFFERENTIATED STOMACH ADENOCARCINOMA (intestinal type) (hematoxylin and eosin staining).
In the wall there is a proliferation of atypical glandular structures of various sizes and shapes, built from atypical polymorphic cells. The nuclei are large, hyperchromatic.
Microslide N 225 UNDIFFERENTIATED CANCER - signet ring cell (stained with hematoxylin and eosin and alcian blue).
In the cytoplasm of tumor cells there is mucin (mucus), colored blue. Tumor cells are ring-shaped in shape, the nucleus is pushed to the periphery, the cytoplasm is filled with mucus.
GUT DISEASES
Macro specimen PHLEGMONIC APPENDICITIS.
The vermiform appendix is enlarged and thickened. The serous membrane is hyperemic, dull, with fibrin deposits. When the appendix is cut, a greenish-gray thick content is released from its lumen.
(E) Microslide N 107 PHLEGMONIC APPENDICITIS (hematoxylin and eosin staining). The mucous membrane of the appendix is focally destroyed, there is a mass of pus in the lumen of the appendix, the layers of the wall are diffusely infiltrated with 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.
Microslide N 133 CHRONIC APPENDICITIS (hematoxylin and eosin staining).
Fibrous obliteration forms. The lamina propria of the mucous membrane is subject to lipomatosis, atrophy of the muscular layer, and sclerosis. Inflammatory infiltration, characteristic of chronic inflammation, is observed.
Macro specimen of LIVER ABSCESSES(pylephlebitic), as a complication of appendicitis
In the area of the liver gate there are cavities with thick grayish-white walls, filled with greenish-gray thick contents. On the section, the liver tissue is yellowish.
View a set of macroscopic specimens of intestinal tumors.
Circular stenotic cancer of the sigmoid colon - in the sigmoid colon there is a ring-shaped formation with raised edges and an ulcerated bottom. The section shows grayish-white tissue with hemorrhages, growing into the layers of the intestinal wall.
LIVER DISEASES
Macropreparation TOXIC LIVER DYSTROPHY (fatty hepatosis). The liver is enlarged in size, flabby in consistency, yellow-white in color (clayey appearance), and has a greasy sheen when cut (“goose liver”)
Microslide No. 4 MASSIVE LIVER NECROSIS - subacute form (stained with hematoxylin and eosin). In the central sections of the lobules there is necrotic detritus in the peripheral sections in the cytoplasm of hepatocytes there are large vacuoles.
Microslide No. 5 CHRONIC HEPATITIS OF WEAK ACTIVITY, STAGE I (staining with hematoxylin and eosin). Note the signs of hepatitis activity: intralobular lobular lymphoid infiltrates, “spreading” of lymphocytes along the sinusoids, dystrophic changes in hepatocytes, lymphohistiocytic infiltration of the portal tracts. Note the signs of chronic inflammation (hepatitis stage): fibrosis of the portal tracts, fibrous septa growing into lobules. Pay attention to cholestasis: dilation of bile capillaries, imbibition of hepatocytes by bile pigments.
The lobular structure of the liver is disturbed. In the portal tracts there is sclerosis, a pronounced lymphoid infiltrate with the formation of lymphoid follicles. In some places, the infiltrate penetrates the lobules through the border plate and surrounds groups of hepatocytes. Proliferation in the portal tracts of the bile ducts and periportal sclerosis are visible. Hepatocytes along the course of infiltration are in a state of necrosis, in other areas there are signs of hydropic and fatty degeneration.
Electron diffraction pattern HYDROPIC DYSTROPHY OF HEPATOCYTE IN VIRAL HEPATITIS(atlas, Fig. 14.5). Pay attention to the expansion of the endoplasmic reticulum of the hepatocyte and the sharp swelling of mitochondria.
Electron microscopic examination showed that the ER cisterns were sharply expanded and the mitochondria were swollen.
Macropreparations CIRRHOSIS OF THE LIVER. Note the size, color, consistency, appearance of the liver from the surface and in the section. Assess the size of regenerated nodes and determine the macroscopic form of cirrhosis based on this feature.
Alcoholic small-nodular portal cirrhosis of the liver– the liver is deformed, yellow in color, the surface is finely lumpy.
(E) Microslide No. 48 CHRONIC HEPATITIS OF MODERATE ACTIVITY WITH TRANSITION TO LIVER CIRRHOSIS (staining with hematoxylin and eosin and picrofuchsin).
The presence of moderately pronounced signs of inflammatory activity (lymphoid infiltration of the stroma, spreading to the parenchyma, fatty degeneration of hepatocytes), dominance of fibrosis (porto-portal, porto-central septa with the formation of false lobules) and regeneration of hepatocytes (loss of the beam structure, presence of cells with large nuclei .
Macro specimens: PRIMARY LIVER CANCER, LIVER METASTASES OF TUMORS OF ANOTHER PRIMARY LOCALIZATION.
MORPHOLOGICAL EQUIVALENTS OF GLOMERULONEPHRITIS
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 capsule cavity, as well as their massive neutrophil infiltration.
Microspecimen FIXATION OF IMMUNE COMPLEX DEPOSITS IN THE RENAL glomerulus IN ACUTE GLOMERULONEPHRITIS(atlas, Fig. 15.2).
Along the basement membrane, a granular glow is visible (deposits in the form of lumps glow)
Macro specimen SUBACUTE GLOMERULONEPHRITIS("big mottled bud").
The kidney is enlarged, flabby, pale with petechial hemorrhages on the surface.
Microslide N 113 SUBACUTE PRIMARILY EXTRACAPILLARY GLOMERULONEPHRITIS (hematoxylin and eosin staining).
Crescents are visible, 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. Between the layers of cells in the crescents there is an accumulation of fibrin. The glomeruli are compressed - they show focal necrosis, diffuse and focal endothelial proliferation, and mesangial proliferation. Some tubules are atrophic; in the epithelium of some convoluted tubules there is hydropic or hyaline-droplet degeneration. In the stroma of the kidney there is sclerosis, lymphomacrophage infiltration.
MORPHOLOGICAL VARIANTS OF CHRONIC GLOMERULONEPHRITIS
Electron diffraction pattern MEMBRANOSAL NEPHROPATHY(atlas, Fig. 15.6).
Electron microscopic examination reveals subepithelial deposits in the glomerular basement membrane, accumulation of basement membrane substance between the podocyte stalks, 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.
Electron diffraction pattern MESANGIOPROLIFERATIVE GLOMERULONEPHRITIS(atlas, Fig. 15.10).
Electron microscopic examination reveals deposits in the mesangium.
Macroscopic specimen of SECONDARY WRINKLED KIDNEY (CHRONIC GLOMERULONEPHRITIS WITH OUTCOME IN NEPHROSCLEROSIS).
The buds are symmetrically wrinkled and have a fine-grained surface.
(E) Microslide N 114 FIBROPLASTIC GLOMERULONEPHRITIS (terminal) (hematoxylin and eosin staining).
Sclerosis and hyalinosis of most glomeruli; in the remaining hypertrophied glomeruli, proliferation of mesangial cells and sclerovascular loops. Sclerosis and hyalinosis of arterioles are noted. Hyaline cylinders in the lumen of the tubules.
SECONDARY KIDNEY DAMAGE
Macro specimen AMYLOID NEPHROSIS(“big white”, “big greasy kidney”).
Note the increase in the size of the kidney, dense consistency, greasy appearance of the surface.
The buds are enlarged in size, dense in consistency, and have a smooth surface. On the cut with a greasy sheen. The boundary between the cortex and medulla is erased
(E) Microslide No. 16 AMYLOID NEPHROSIS (Congo stain). Indicate amyloid deposits in the capillary loops of the glomerulus, along the intrinsic membrane of the tubules, in the walls of blood vessels, as well as in the stroma of the kidney along the reticular fibers.
Note the color of the amyloid.
Under the basement membrane of the tubules, in the glomeruli, along the reticular fibers of the stroma in the intima of the vessels, there are red-colored amyloid deposits.
ACUTE RENAL FAILURE (AKI)
(E) Microslide No. 6 NECROTIC NEPHROSIS (hematoxylin and eosin staining). The glomeruli and epithelium of the straight tubules are preserved. Their cells contain nuclei. The convoluted tubule epithelium does not contain nuclei (karyolysis).
ORGANOPATHOLOGY OF CHRONIC RENAL FAILURE
View a set of macropreparations reflecting the morphological manifestations of uremia: FIBRINOUS PERICARDITIS (“hairy heart”), LOUS TRACHEITIS, DIPTHERITIC COLITIS.
DISHORMONAL DISEASES OF THE GENITAL ORGANS
Macro specimen of UTERINE POLYP. Note the location of the polyp, its shape, size, nature of the surface, connection with the underlying tissue.
The growth of the endometrium is gray-red in color, with an uneven surface.
(E) Microslide No. 142 GLANTIC ENDOMETRIAL HYPERPLASIA (hematoxylin and eosin staining).
The endometrial glands are built from proliferating epithelium, have different sizes and shapes, have a tortuous course and cystic expansion, are very closely located, branching and budding of the glands are noted.
Microslide N 57 PSEUDOEROSION OF THE CERVIX (stained with hematoxylin and eosin).
In the zone of erosion of the cervix, there are two types of epithelium: non-keratinized stratified squamous epithelium and prismatic epithelium. There is ectopia of columnar epithelium in the exocervix.
PATHOLOGY OF PREGNANCY
Macrodrug POSTPARTUM ENDOMETRITIS.
The membrane of the vagina and cervix is hyperemic, edematous, sometimes with hemorrhages. In the lumen of the vagina, especially in the cervix, there is exudate released from the uterus. The cervical canal is slightly open.
Macropreparation LIVER FOR ECLAMPSIA.
In the liver, single or confluent white-yellow foci of necrosis and multiple hemorrhages of different sizes appear - a landcart-shaped liver.
CHAPTER 17. DISEASES OF THE GASTROINTESTINAL TRACT
CHAPTER 17. DISEASES OF THE GASTROINTESTINAL TRACT
DISEASES OF THE Pharynx and pharynx. DISEASES OF THE STOMACH. IDIOPATHIC INTESTINAL DISEASES (CROHN'S DISEASE AND ULCERATIVE COLITIS) VOREMICAL DISEASES
PROCESS OF THE CAECAL
Sore throat (tonsillitis)- an infectious disease characterized by inflammatory changes in the lymphoid tissue of the pharynx and palatine tonsils (Pirogov’s rings). Forms of tonsillitis: acute, chronic (recurrent).Forms of acute tonsillitis:exudative - catarrhal, fibrinous, purulent; necrotic - necrotic, gangrenous, ulcerative-membranous (a special form is Simanovsky-Plaut-Vincent angina); by localization - lacunar, follicular.Complications of tonsillitis:local - peritonsillar abscess, cellulitis, thrombophlebitis; general - sepsis, rheumatism, glomerulonephritis.
Gastritis- inflammation of the gastric mucosa.Types of gastritis:acute and chronic;by topography- diffuse and focal (antral, fundal, pyloroantral, pyloroduodenal).
Forms of acute gastritis:catarrhal, fibrinous, purulent (phlegmonous), necrotic. In any form - erosion and acute ulcers.Erosion- a superficial defect of the mucous membrane is not deeper than its muscular plate.Ulcer- a deep defect, the bottom of which is the muscular or even serous layer of the organ wall.
Chronic gastritisis a group of stomach diseases of different etiologies, characterized by a combination of chronic inflammation and impaired regeneration with structural changes in the gastric mucosa.Classification of chro-
nic gastritis:on etiology and pathogenesis- Helicobacter (type B), autoimmune (type A), reflux gastritis (type C);by topography; by morphological type- superficial and atrophic;by activity.Take into account the presence, nature and severity ofintestinal metaplasia and dysplasia (intraepithelial neoplasia).Chronic atrophic pangastritis is an optional precancer.
Peptic ulcer- a chronic, cyclical disease, the main clinical and morphological manifestation of which is a chronic recurrent ulcer of the stomach or duodenum.Complications of peptic ulcer:destructive- bleeding, perforation (perforation with the development of peritonitis), penetration (into the liver, gall bladder, omentum, pancreas);cicatricial- deformation and stenosis of the inlet and outlet sections of the stomach and duodenal bulb;malignancy- malignancy (extremely rare).
Stomach tumors:epithelial(adenoma and cancer) and non-epithelial(mesenchymal, lymphomas). Macroscopically exophytic formations of the stomach (hyperplastic growths, adenomas) are usually calledpolyps.Classification of stomach cancer:according to macroscopic growth form- exophytic (polypous, mushroom-shaped, saucer-shaped), endophytic (plaque-shaped), ulcerative-infiltrative, plastic linitis;By
histological type- intestinal type (intestinal - types of adenocarcinomas, etc.) and diffuse (scirrhus, solid, signet ring cell, etc.);by depth of invasion and stage of generalization of the tumor process(TNM system). Diagnostically significant lymphogenous metastases:to the left supraclavicular lymph node(Virchow's metastasis),retrograde - to the ovaries(Krukenberg's cancer),into pararectal tissue(Schnitzler metastases).
Idiopathic bowel diseases: Crohn's disease(granulomatous inflammation of any part of the digestive tract) andulcerative colitis.Ulcerative colitis is an optional precancerous disease.
Appendicitis- inflammation of the vermiform appendix of the cecum. In surgical practice, it is included in the group of diseases designated as acute abdomen (peptic ulcer with perforation, peptic ulcer with bleeding, acute intestinal obstruction, strangulated hernia, acute cholecystitis, acute appendicitis).Forms of appendicitis:acute - simple, superficial, phlegmonous (variants - apostematous, phlegmonous-ulcerative), gangrenous (primary and secondary); chronic.Complications of acute appendicitis:peritonitis, mesenteriolitis, pylephlebitis, pylephlebitic liver abscesses.
Rice. 17-1. Microslide.
Chronic tonsillitis in the acute stage: the surface epithelium is damaged (dystrophic and necrotic changes, areas of ulceration), infiltrated with neutrophilic leukocytes (1). Lymphoid follicles are atrophied, there is sclerosis in the stroma (2). In the enlarged lacunae, neutrophilic leukocytes and bacterial colonies are detected (3).
Hematoxylin and eosin staining: x160 Rice. 17-2.
Macropreparations (a, b). Chronic multifocal atrophic gastritis: the gastric mucosa with smoothed folds, thinned, pale, grayish in color, with pinpoint hemorrhages, erosions (b - preparation by I.N. Shestakova) Rice. 17-3. Microslides (a-d). Chronic atrophic gastritis: the mucous membrane of the fundus of the stomach is sharply thinned, the glands are reduced in size, the distance between them is increased, the epithelium of the glands acquires more primitive features, loses the ability to produce gastric juice and hydrochloric acid, and secretes mucus. There are foci of intestinal metaplasia with goblet cells (1). In the lamina propria of the mucous membrane there is a diffuse lymphoplasmacytic infiltrate, lymphoid follicles (2), severe sclerosis; c, d - Helicobacter pylori
in the lumen of the glands.
a, b - hematoxylin and eosin staining, c - Warthin-Stary staining, d - immunohistochemical method: a - x100, b - x200, c, d - x400 Rice. 17-4.
a, b - hematoxylin and eosin staining, c - Warthin-Stary staining, d - immunohistochemical method: a - x100, b - x200, c, d - x400 Macropreparations (a-d). Acute erosions and gastric ulcers: in the gastric mucosa there are multiple small superficial (erosions) and deeper, involving the submucosal and muscular layers of the stomach wall (acute ulcers), round defects with soft, even edges and a brownish-black or gray-black bottom ( due to hydrochloric acid hematin, which is formed from hemoglobin of erythrocytes under the influence of hydrochloric acid and gastric juice enzymes); (see also Fig. 3-4, 4-10) (a, c - preparations by I.N. Shestakova, d, e - preparations by N.O. Kryukov)
a, b - hematoxylin and eosin staining, c - Warthin-Stary staining, d - immunohistochemical method: a - x100, b - x200, c, d - x400 Continuation
Ending Rice. 17-5.
Microslides (a, b). Erosion of the gastric mucosa: in the gastric mucosa, a superficial (within the mucous membrane) focus of necrosis is determined with the formation of a shallow defect - erosion with perifocal leukocyte inflammatory infiltration. At the bottom of the erosion there are deposits of hydrochloric acid hematin (1). Staining with hematoxylin and eosin: x 100 (b - preparation by N.O. Kryukov) Macropreparations (a-n). Chronic ulcer of the stomach (a, c-e, g-n) and duodenum (b, f): chronic ulcers with bleeding - arrozed and thrombosed vessels in the bottom of the ulcers (c, f, l, n), perforation (d, j - external view, from the abdominal cavity - j) and penetration (b, d, g-i, n). Round-shaped defects of the mucous membrane and wall of the stomach (or duodenum) with roller-like compacted edges. The cardial edge of the ulcer is undermined, overhangs, and the edge facing the pyloric part of the stomach is gentle, looks like a terrace, the steps of which are formed by the mucous membrane, submucosal and muscular layers. This configuration is due to the constant displacement of the edges of the ulcer during peristalsis. The mucous membrane around the ulcer is changed, its folds can be located radially in relation to the ulcerative defect (convergence of folds -
a, g, i, m); (a-c, e - preparations by I.N. Shestakova,
b, d, i-n, - preparations N.O. Kryukov)
R is. 17-6. Macropreparations (a-d). Acute erosions and gastric ulcers: in the gastric mucosa there are multiple small superficial (erosions) and deeper, involving the submucosal and muscular layers of the stomach wall (acute ulcers), round defects with soft, even edges and a brownish-black or gray-black bottom ( due to hydrochloric acid hematin, which is formed from hemoglobin of erythrocytes under the influence of hydrochloric acid and gastric juice enzymes); (see also Fig. 3-4, 4-10) (a, c - preparations by I.N. Shestakova, d, e - preparations by N.O. Kryukov)
Microslides (a, b). Erosion of the gastric mucosa: in the gastric mucosa, a superficial (within the mucous membrane) focus of necrosis is determined with the formation of a shallow defect - erosion with perifocal leukocyte inflammatory infiltration. At the bottom of the erosion there are deposits of hydrochloric acid hematin (1). Staining with hematoxylin and eosin: x 100 (b - preparation by N.O. Kryukov) Macropreparations (a-d). Acute erosions and gastric ulcers: in the gastric mucosa there are multiple small superficial (erosions) and deeper, involving the submucosal and muscular layers of the stomach wall (acute ulcers), round defects with soft, even edges and a brownish-black or gray-black bottom ( due to hydrochloric acid hematin, which is formed from hemoglobin of erythrocytes under the influence of hydrochloric acid and gastric juice enzymes); (see also Fig. 3-4, 4-10) (a, c - preparations by I.N. Shestakova, d, e - preparations by N.O. Kryukov)
Microslides (a, b). Erosion of the gastric mucosa: in the gastric mucosa, a superficial (within the mucous membrane) focus of necrosis is determined with the formation of a shallow defect - erosion with perifocal leukocyte inflammatory infiltration. At the bottom of the erosion there are deposits of hydrochloric acid hematin (1). Staining with hematoxylin and eosin: x 100 (b - preparation by N.O. Kryukov) Macropreparations (a-d). Acute erosions and gastric ulcers: in the gastric mucosa there are multiple small superficial (erosions) and deeper, involving the submucosal and muscular layers of the stomach wall (acute ulcers), round defects with soft, even edges and a brownish-black or gray-black bottom ( due to hydrochloric acid hematin, which is formed from hemoglobin of erythrocytes under the influence of hydrochloric acid and gastric juice enzymes); (see also Fig. 3-4, 4-10) (a, c - preparations by I.N. Shestakova, d, e - preparations by N.O. Kryukov)
Microslides (a, b). Erosion of the gastric mucosa: in the gastric mucosa, a superficial (within the mucous membrane) focus of necrosis is determined with the formation of a shallow defect - erosion with perifocal leukocyte inflammatory infiltration. At the bottom of the erosion there are deposits of hydrochloric acid hematin (1). Staining with hematoxylin and eosin: x 100 (b - preparation by N.O. Kryukov) Macropreparations (a-d). Acute erosions and gastric ulcers: in the gastric mucosa there are multiple small superficial (erosions) and deeper, involving the submucosal and muscular layers of the stomach wall (acute ulcers), round defects with soft, even edges and a brownish-black or gray-black bottom ( due to hydrochloric acid hematin, which is formed from hemoglobin of erythrocytes under the influence of hydrochloric acid and gastric juice enzymes); (see also Fig. 3-4, 4-10) (a, c - preparations by I.N. Shestakova, d, e - preparations by N.O. Kryukov)
Microslides (a, b). Erosion of the gastric mucosa: in the gastric mucosa, a superficial (within the mucous membrane) focus of necrosis is determined with the formation of a shallow defect - erosion with perifocal leukocyte inflammatory infiltration. At the bottom of the erosion there are deposits of hydrochloric acid hematin (1). Staining with hematoxylin and eosin: x 100 (b - preparation by N.O. Kryukov) Continuation
Rice. 17-7. Microslides (a, b). Chronic ulcer of the stomach (a) and duodenum (b): a defect in the wall of the stomach or duodenum, involving the mucous, submucous and muscular membrane. There are 4 layers at the bottom of the defect: 1 - fibrinous-purulent exudate; 2 - fibrinoid necrosis; 3 - granulation tissue; 4 - scar tissue with sclerotic and hyalinized vessels. At the edges of a chronic gastric ulcer, epithelial restructuring processes occur (hyperplasia of the cervical epithelium, glandular atrophy, intestinal metaplasia, mild or moderate dysplasia). Staining with hematoxylin and eosin: a - x 120, b - x60 (b - preparation by N.O. Kryukov)
Rice. 17-8. Macropreparations (a, b). Gastric polyp: a small exophytic formation protruding into the lumen of the stomach on a wide base, covered with a mucous membrane (histologically: a - adenoma, b - leiomyoma); (a - preparation by N.O. Kryukova, b - preparation by I.N. Shestakova)
Rice. 17-9. Macropreparations (a-d). Stomach cancer (nodular or diffuse forms): a - fungoous, b - saucer-shaped, c, d - endophytic diffuse cancer (d - view from the outside of the stomach, from the side of the serous membrane); nodular form - on the lesser curvature of the stomach a large mushroom-shaped or saucer-shaped node with raised uneven edges and a drooping ulcerated bottom is determined. The tissue of the nodule is whitish in color, dense in consistency, grows through all layers of the stomach wall, and has no clear boundaries. Diffuse form: the wall of the stomach is sharply thickened over a significant extent due to the proliferation of dense whitish tissue that does not have clear boundaries. The mucous membrane has smoothed folds and is rigid (see also Fig. 9-5, 10-7); (a - preparation by N.O. Kryukova, b - preparation by I.N. Shestakova)
Rice. 17-9. Continuation
Rice. 17-10. Microslides (a, b). Adenocarcinoma of the stomach: in the thickness of the mucous membrane and muscular layer of the stomach there are atypical glandular complexes of different sizes and shapes (tissue atypia). Tumor cells and their nuclei are polymorphic, of different sizes and shapes, the nuclei are hyperchromic (cellular atypia). Mitoses (typical and atypical) are few, the level of proliferative activity of the tumor is moderate. Tumor complexes penetrate the lamina propria and muscle layer - invasive growth (see also Fig. 9-6). Hematoxylin and eosin staining: x 160
Rice. 17-11. Macropreparation.
Phlegmonous appendicitis: the appendix is enlarged in size, the walls are thickened, diffusely saturated with pus (when pressure is applied, pus is also released from the lumen of the appendix), the surface is dull, reddish-bluish, with full-blooded vessels; the mesentery of the appendix is also full-blooded, with foci of suppuration and hemorrhages (see also Fig. 6-6); (preparation by I.N. Shestakova) Rice. 17-12.
Microslides (a, b). Phlegmonous-ulcerative appendicitis: pronounced leukocyte infiltration of all layers of the appendix wall, edema, inflammatory hyperemia, necrosis and ulceration of the mucous membrane, atrophy of lymphoid tissue.
Staining with hematoxylin and eosin: a - x 60, b - x 200 Rice. 17-13.
Macropreparation. Microslides (a, b). Crohn's disease: deep slit-like ulcerative defect of the mucous membrane, lymphomacrophagic, with an admixture of plasma cells, infiltration and sclerosis of all layers of the intestinal wall (a), granuloma with giant multinucleated cells in the submucosal layer (b). Staining with hematoxylin and eosin: a - x 100, b - x 200
Rice. 17-15. Microslides (a, b). Ulcerative colitis: pronounced diffuse lymphomacrophagic inflammatory infiltrate with an admixture of leukocytes, edema, microcirculatory disorders of the colon mucosa, crypt abscess (1).
Staining with hematoxylin and eosin: a - x 100, b - x 200
Rice. 17-16. Macropreparations (a, b). Intestinal gangrene: ischemic necrosis of part of the small or large intestine due to obstruction of the mesenteric arteries by blood clots, thromboembolism, atherosclerotic plaques (acute ischemic intestinal disease); (a - drug by A.N. Kuzin and B.A. Kolontarev)
Rice. 17-17. Macropreparations (a, b). Diverticulosis of the colon: multiple finger-like protrusions in the wall of the colon; from the side of the mucous membrane, the entrances to the diverticula look like dark spots (arrows); (preparations by I.N. Shestakova)
Rice. 17-18. Macropreparation. Meckel's diverticulum (preparation by I.N. Shestakova)
Hematoxylin and eosin staining. In the area of the gastric wall defect there is fibrinous-purulent exudate (a), with an underlying large area of fibrinoid necrosis (b), the presence of granulation tissue (c) and the proliferation of coarse fibrous connective tissue penetrating to varying depths muscle layer (d). The serous membrane of the stomach wall is preserved (e).
2. Chronic atrophic gastritis. Heme staining
toxilin and eosin. In the gastric mucosa there is atrophy of the integumentary epithelium (a) and the epithelium of the glands with restructuring
which glands are of intestinal type - “intestinal metaplasia” (b), in the lamina propria of the mucous membrane of the sclerosis field
(c) and lymphoplasmacytic infiltration with the formation of lymphoid follicles (d).
3. Adenocarcinoma. Hematoxylin and eosin staining. All layers of the stomach wall are infiltrated with tumor tissue with signs of cellular atypia (a). Multiple pathological mitoses are visible in hyperchromic (b) and polymorphic tumor cells (c).
4. Mucosal cancer of the stomach. Hematoxylin staining and
eosin. The tumor tissue is represented by an abundance of large atypical “ring-shaped” cells (a) with the formation of a large amount of mucus (b). The infiltrative nature of tumor growth is visible (c). Demonstration.
5. Scirrhus of the stomach. Hematoxylin and eosin staining. In the wall of the stomach there are groups of atypical cells with large hyperchromatic nuclei (a), in the stroma of the tumor there is a proliferation of fibrous connective tissue (b). Demonstration.
MACRO-PREPARATIONS.
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, consumption of alcohol substitutes, anti-tumor 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. Erosion and acute gastric ulcers: in the preparation the stomach,
the mucous membrane is swollen, on the surface there are multiple pinpoint hemorrhages and conical defects of various sizes, their bottom and edges are black. Erosions are localized within the mucous membrane, and ulcers penetrate
They reach different depths of the mucous membrane, some reach the muscular layer.
Causes: endocrine diseases (Solinger-Ellison syndrome, hyperparathyroidism), acute and chronic circulatory disorders, intoxication, allergies, chronic infections (tuberculosis, syphilis), postoperative, steroid and stress ulcers.
Complications: perforation, peritonitis.
Exodus: erosions are epithelialized, the ulcerative defect is replaced by scar tissue.
3. Chronic gastric ulcer during remission: in the preparation of the stomach, on the lesser curvature there is a pathological focus in the form of a depression in the mucous membrane, round in shape, measuring 3 cm in diameter. The folds of the mucous membrane converge radially towards the defect, the edges of which are dense, raised in a roller-like manner, and calloused (calecal ulcer). On the cut, the entrance hole is a crater, smaller than the inside of the ulcer. The edge facing the cardia is undermined, the mucous membrane hangs over it. The edge facing the gatekeeper is gentle - terrace-like. The thickness of the ulcer is represented by connective tissue, gray-white, 2.5 cm. At the bottom of the ulcer, the vessels are sclerotic, their lumen gapes.
Causes: genetic predisposition, Helicobacter pylori, inflammatory and dysregenerative changes in the mucous membrane, leading to exposure to factors of peptic aggression (hydrochloric acid and pepsinogen).
Complications: perigastritis, bleeding, perforation, penetration, cicatricial deformation of the stomach with the development of stenosis of the inlet or outlet. Against the background of a chronic ulcer, a second disease can develop - stomach cancer.
4. Stomach polyps (adenomas): in the antrum
stomach there are two tumor-like formations the size of pigeon eggs, on thin stalks, irregular oval shape with a villous surface, soft consistency.
On the section, pathological neoplasms are abundantly vascularized and localized exclusively on the surface of the mucous membrane, without growing into the underlying tissue.
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, of an irregular round shape measuring 5 cm in diameter, on a wide base in the form of a mushroom cap, with a retraction in the center. The section shows that the tumor grows throughout the entire wall of the stomach.
b) Diffuse gastric cancer: the organ is reduced in size, the wall is thickened throughout its entire length to 1 cm, has a dense “woody” consistency, and is represented by gray-pinkish tissue in the section. The mucous membrane is uneven, its folds are of varying thickness, the serous membrane is thickened, dense, and lumpy. The lumen of the stomach is narrowed.
c) Saucer-shaped stomach cancer: on the lesser curvature there is a pathological focus in the form of a formation rising above the surface of the mucous membrane with dense roll-like edges and a sinking bottom, measuring 3.5 cm by 2.0 cm. The bottom is covered with gray-brown disintegrating masses. On the section, the tumor tissue infiltrates the entire thickness of the organ wall.
Causes: nutrition (smoked meats, canned food, pickled vegetables, peppers), biliary reflux (after gastric surgery, especially Billroth II), Helicobacter pylori (promotes the development of mucosal atrophy, intestinal metaplasia, epithelial dysplasia). Metastasis: 1. Orthograde lymphogenous metastases to regional nodes on the lesser and greater curvature, retrograde lymphogenic metastases to the left supraclavicular lymph node - Virchow's metastasis, to the ovaries - Krukenberg's
cancer, perirectal tissue - Schnitzler metastases, 3. Hematogenous metastases to the liver, lungs, brain, bones, kidneys, and less often to the adrenal glands and pancreas. 4. Implantation- carcinomatosis of the pleura, pericardium, diaphragm, peritoneum, omentum.
TEST CONTROL
Select one or more correct answers
1. SIGNS OF ACUTE CATARHAL GASTRITIS
1) thickening of the mucosa
2) atrophy of the glands
3) multiple erosions
4) sclerosis of the mucosa
5) neutrophilic infiltration of the mucosa
6) lymphoid infiltration of the mucosa
2. MORPHOLOGICAL FORMS OF ACUTE GASTRITIS
1) fibrinous
2) atrophic
3) hypertrophic
4) catarrhal
5) corrosive (necrotic)
3. CHANGES IN THE EPITHELIUM IN CHRONIC GASTRITIS
1) atrophy
2) intestinal metaplasia
3) hyperplasia
4) dysplasia
5) appearance of Mallory bodies in the cytoplasm
4. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS A
2) autoantibodies in the blood
to parietal cells
3) Helicobacter pylori -
5. PATHOGENESIS OF PERNICIOUS ANEMIA IN AUTOIMMUNE GASTRITIS
1) stopping the production of HCl
2) production of antibodies to Helicobacter pylori
3) production of antibodies to parental cells
4) production of antibodies to intrinsic factor
5) destruction of glands and atrophy of the mucous membrane
6. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS
1) predominant localization - antrum
2) autoantibodies in the blood
to parietal cells
3) Helicobacter pylori -
main etiological factor
4) accompanied by G-cell hyperplasia, gastrinemia
5) often 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,
does not affect the muscle plate
3) atrophy of the mucous membrane
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 ACHIEVEMENT
1) often occurs in patients with alcoholism
2) the mucous membrane is not changed
3) diffuse lymphoid-plasmacytic infiltration with a significant admixture of PMNs
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 duodenum
3) acute stomach ulcer
and duodenum
4) chronic recurrent ulcer of the stomach and duodenum
5) inflammation of the duodenal mucosa
10. Sclerotic deformation of the stomach IS an outcome
1) catarrhal gastritis
2) diphtheritic gastritis
3) corrosive gastritis
4) phlegmonous gastritis
11. SIGNS of chronic atrophic gastritis, as a precancerous disease
1) lymphoplasmacytic infiltration
2) sclerotic processes
3) structural restructuring of the epithelium
(intestinal metaplasia)
4) all answers are correct
5) all answers are incorrect
12. ULCEROGENIC PROMOTERS
1) corticosteroids
3) aspirin
4) smoking
5) increased tone of the vagus nerve
13. Gastric ulcers include
1) endocrine gastric ulcers
2) allergic ulcers
3) peptic ulcers
4) postoperative ulcers
5) tuberculous ulcers
14. local factors in the development of gastric ulcer
1) increased aggressiveness of gastric juice
2) campillobacteria
3) presence of chronic gastritis
4) circulatory disorders
5) all answers are correct
6) all answers are incorrect
15. REASONS FOR THE DEVELOPMENT OF ACUTE STOMACH ULCER
1) corticosteroids
3) aspirin
4) smoking
5) increased tone
vagus nerve
16. MORPHOLOGICAL SIGNS of acute gastric ulcer
1) funnel shape
2) the shape of a truncated pyramid
on a cross section
3) soft jagged edges
4) dense calloused edges
7) multiple ulcers
17. MORPHOLOGICAL SIGNS of chronic gastric ulcer
1) funnel shape
2) the shape of a truncated pyramid
on a cross section
3) soft jagged edges
4) dense calloused edges
5) the bottom of the ulcer is painted black with hydrochloric acid hematin as it is cleansed
6) the edge of the ulcer, facing the pylorus, has the appearance of a terrace, the cardiac edge is undermined
18. SIGNS OF CHRONIC STOMACH ULCER
DURING REMISSION
1) the presence of exudate on the surface
2) scar tissue interrupts the muscle sheath to varying depths
3) endovasculitis
4) fibrinoid changes in the fundus and vessels
5) epithelization of the surface
19. SIGNS OF CHRONIC STOMACH ULCER
DURING THE PERIOD OF EXCERNSATION
1) the presence of fibrinous-purulent exudate
on the surface 2) scar tissue interrupts muscle
shell at different depths
3) endovasculitis
4) fibrinoid changes in the walls of blood vessels and in the bottom of the ulcer
12. MECHANISM OF Bleeding in peptic ulcer disease
arrosive
diapedetic
as a result of a ruptured vessel
as a result of purulent melting
21. Chlorohydropenic uremia – result
1) bleeding from an ulcer
2) chronic nephritis
3) penetration of ulcers
4) cicatricial pyloric stenosis
5) all answers are correct
6) all answers are incorrect
22. Peritonitis complicating a chronic ulcer is the result
1) penetration
2) perforation
3) gastritis
4) duodenitis
5) cicatricial pyloric stenosis
23. COMPLICATIONS OF CHRONIC ULCERS
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) Ménétrier's disease
3) Wernicke's syndrome
4) Zollinger-Ellison syndrome
5) hypertrophic hypersecretory gastropathy
25. HISTOLOGICAL SIGNS OF GASTROPATHIES
1) hypertrophy of the gastric mucosa
2) atrophy of the gastric mucosa
3) hyperplasia of the integumentary pit epithelium
4) hyperplasia of the glandular epithelium
5) severe sclerosis
26. MORPHOLOGICAL SIGNS OF INFLAMMATORY POLYP
1) inflammatory infiltrate in the stroma
2) atypical cells
3) without clear differentiation into pedicle and body
4) dysplasia of the glandular epithelium
5) erosion on the surface
27. BENIGN TUMORS OF THE STOMACH
1) angiosarcoma
2) adenoma
3) leiomyoma
4) adenocarcinoma
5) hyperplasiogenic polyp
28. BACKGROUND FOR THE DEVELOPMENT OF GASTRIC ADENOMA
1) chronic superficial gastritis
2) acute erosive-hemorrhagic gastritis
3) acute fibrinous gastritis
4) chronic gastritis with enterolization
29. ADENOMA IS
1) benign tumor
from glandular epithelium
2) malignant tumor of the glandular epithelium
3) epidermal cancer
4) malignant tumor from transitional cell epithelium 5) benign tumor from squamous epithelium
30. DISEASES WITH A RISK OF CANCER
1) superficial gastritis
2) chronic gastric ulcer
3) acute erosive gastritis
4) chronic atrophic gastritis
5) adenomatous polyps
31. HISTOLOGICAL VARIANTS OF STOMACH CANCER
1) adenocarcinoma
2) sarcoma
3) signet ring cell
4) undifferentiated
32. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF INTESTINAL TYPE 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) affects men 2 times more often
5) develops from metaplastic epithelial cells
33. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF DIFFUSE TYPE STOMACH CANCER
1) develops from epithelial cells
2) occurs at a relatively young age
3) histologically signet ring cell
4) occurs against the background of chronic gastritis
5) has a low degree of differentiation
34. PROGNOSTIC SIGN FOR STOMACH CANCER
1) histological variant
2) macroscopic shape
3) depth of invasion
4) mucus formation
5) secondary changes
35. HISTOLOGICAL SIGNS OF POLYPOID STOMACH CANCER
1) atypical glandular structures of bizarre shape
2) signet ring cells
3) an abundance of mucus in the lumen of the glands
4) atypical polymorphic cells with large hyperchromatic nuclei
5) atypical cells, characterized by monomorphism
36. HISTOLOGICAL FEATURES OF SIGNET CELL CANCER OF THE STOMACH
1) characterized by extensive hemorrhages
2) the nuclei of atypical cells are displaced
to the cell membrane
3) poorly differentiated cells with very large hyperchromatic nuclei of irregular shape
4) atypical glandular structures
5) massive sclerosis and hyalinosis in the wall
37. MICROSCOPIC CHARACTERISTICS OF SCIRROUS GASTROCANCER
1) atypical cells with large
the 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. KRUCKENBERG AND SCHNITZLER METASTASES OF STOMACH CANCER
1) hematogenous
2) implantation
3) lymphogenous orthograde
4) lymphogenous retrograde
39. COMPLICATIONS OF STOMACH CANCER
1) hemoptysis
2) pyloric dilatation
3) perforation
4) exhaustion
5) stomach bleeding
40. SIGNS THAT CHARACTERIZE VIRCHOWSKI METASTASIS
1) hematogenous metastasis
2) retrograde lymphogenous metastasis
3) peritoneal carcinomatosis
4) damage to the left supraclavicular lymph node
5) ovarian damage
Standard answers for test tasks
