In the gastric mucosa, the defects of various sizes are visible, the bottom of which are painted with hydrochloric hematine in black and brown color.
Macrofreate chronic gastritis.
The smoothing of the stomach mucosa forces is detected, the wall is hyperemic, thinned, is flattened. Multiple point erosion are noted.
Micropreparation NO 422. Helicobacter pylori. In the trim mucus in gastric pits (gastrobyopotate, painting by gymzema).
Spiral-like bacteria are visible, located near the surface epithelium with a superliste of a bar. Surface cells are damaged, infiltration of the stomach mucosa by polymorphic nuclear leukocytes.
MicroPreparation N 423 Chronic Active Gastritis Antrum with atrophy of the glands and full intestinal metaplasia (gastrobyopotate, painting by alzian-blue and hematoxylin).
In its own plate of the mucous membrane between the glands, a large number of lymphocytes with the formation of lymphoid follicles is revealed. There is a destruction of glands and a decrease in their number, the atrophy of the mucous membrane.
Macropreach chronic stomach ulcer (CALE).
At the low curvature of the stomach, a deep defect of the stomach wall is visible, penetrating to the serous shell, oval shape, with raised edges. The edge addressed to the gatekeeper is gentle, has the form of a terrace formed by mucous membranes, submucosal and muscle shells. The edge addressed to the esophagus is bent. In the bottom of the ulcers necrotic dedrita brown brown. The folds of the stomach mucosa are smoothed, rays converge to the ulcene defect (convergence of folds).
(E) MicroPreparation N 106 Chronic stomach ulcer (with exacerbation) (hematoxylin and eosin painting.
Defect of the wall of the stomach, which captures the mucous membrane, sublitty and muscle shell. Around the defect one edge of the mucous membrane is bred, the other is gentle. At the bottom of the defect of the wound 4 layers - from the lumen to the serous shell: fibrin-purulent exudate (fibrin, neutrophils, admixture of necrotic tissue), fibrinade necrosis, granulation fabric, scar cloth. The muscular sheath at the bottom is not determined, it is visible to open on the border of the ulcer defect. In the mucous membrane near ulcers - a picture of chronic atrophic gastritis.
View a set of macropreats illustrating complications of chronic ulcers: penetrating stomach penetrating ulcer, arriney vessel in the day of ulcers, ulcer-cancer stomach, scar deformation of the stomach
Six stomach cancer -at the low curvature of the stomach, the formation on a wide base with raised dense roluned edges and a sealing bottom is located over the surface of the mucous membrane. The bottom is covered with gray-brown disintegrating masses.
Macrofrets of different forms of gastric cancer.
Diffuse gastric cancer -the wall of the stomach (especially the mucous and submucoscent shell) is diffusefully thickened in all departments. On the cut it can be seen that gray-pink dense tissue sprout through it. The mucous membrane is uneven, its folds of various thickness, the serous sheath is thickened, dense, litter. The lumen of the stomach is narrowed.
MicroPreparation N 424 is highly differentiated with an adenocarcinoma of the stomach (intestinal type) (hematoxylin and eosin color).
In the wall of the growth of atypical ferrous structures of various sizes and shapes built from atypical polymorphic cells. The kernels are large, hyperchromic.
MicroPreparation N 225 Untifferentiated Cancer - Pisnevelo cell cell (painting by hematoxylin and eosin and alzian blue).
In the cytoplasm of Muzin tumor cells (mucus) painted in blue color. Tumor cells in the form of pistevoid, the core is pushed back to the periphery, the cytoplasm is filled with mucus.
Intestinal diseases
Macrobreparation FLEGMONOSNY Appendicitis.
Cell-shaped process is increased, thickened. Serous shell hyperemic, dim, with fibrin overlay. When cutting a process, a greenish-gray thick content is distinguished from its lumen.
(Э) MicroPreparation N 107 FLEGMONOSNY Apandicitis (gematoxylin and eosin color). The mucous membrane of the appendix is \u200b\u200bfocal destroyed, in the lumen of the appendix of the mass of pus, the layers of the wall diffusely infiltrated with leukocytes.
Macrobreparation Chronic Apandicitis.
The clearance is filled with mucus. Obliteration cavity. The mucus turns into globules. Muscular layer atrophy and sclerosis.
MicroPreparation N 133 Chronic appendicitis (gematoxylin and eosin color).
Fibrous tightness is formed. The proper plate of the mucous membrane is subjected to lipomatosis, muscle layer atrophy, sclerosis. Inflammatory infiltration is observed, characteristic of chronic inflammation.
Macrobreparation Abshasa liver (Pylephlegitic), as complication of appendicitis
In the area of \u200b\u200bthe gate of the liver - cavity with thick grayish-white walls filled with greenish-gray dense content. On the context of the liver cloth yellowish.
View set of intestinal tumors macroprets.
Circular stenosis cancer of the sigmoid gut -in a sigmoid intestine - a ring-shaped formation with raised edges and an ulcerated bottom. On the cut, grayish-white fabric with hemorrhages, germinating in the layers of the intestine.
Diseases of the liver
Macrobreparatic liver dystrophy (fatty hepatosis). The liver is increased in sizes, diryabe consistency, yellow-white (clay species), on the cut has a greasy shine ("goose liver")
Micropreparation N 4 Massive liver necrosis is a subacted form (hematoxylin and eosin color). In the central departments of fractions, necrotic deriters in the peripheral departments in the cytoplasm of hepatocytes are large vacuoles.
MicroPreparation N 5 Chronic hepatitis of weak activity, stage I (hematoxylin and eosin color). Mark the signs of hepatitis activity: intrapulous lobular lymphoid infiltrates, "spreading" lymphocytes in sinusoids, dystrophic changes hepatocytes, lymphogistocitary infiltration of portal paths. Mark the signs of chronicness of inflammation (hepatitis stage): fibroids of portal portal paths, fibrous septa, growing into slices. Pay attention to cholestases: the expansion of bile capillaries, the immigination of hepatocytes with bile pigments.
The lolly structure of the liver is broken. In portal paths - sclerosis, pronounced lymphoid infiltrate with the formation of lymphoid follicles. In places, infiltrate penetrates her slices through the border plate and surrounds the hepatocyte groups. Proliferation in the portal tractors of bile ducts and periportal sclerosis are visible. Hepatocytes in the course of infiltration in the state of necrosis, in other areas the signs of hydropic and fatty dystrophy.
Electron diffraction method of hepatocyte hydropic dystrophy during viral hepatitis(Atlas, Fig. 14.5). Pay attention to the expansion of the hepatocyte endoplasmic network and the sharp swelling of mitochondria.
When electronically microscopic examination, the EPS tank is sharply expanded, the mitochondria of swelling.
Macrofrants of cirrhosis of the liver. Note the size, color, consistency, view of the liver from the surface and on the context. Assess the size of regenerate nodes and determine the macroscopic form of the cirrhosis on this basis.
Alcohol Melkozlova portal cirrhosis liver - The liver is deformed, yellow, fine surface.
(E) MicroPreparation N 48 Chronic hepatitis of moderate activity with the transition to cirrhosis of the liver (painting by hematoxylin and eosin and picrophoxin). The presence of moderately pronounced signs of inflammation activity (lymphoid infiltration of stroma, applies to the parenchyma, hepatocyte fatty dystrophy), the dominance of fibrosis (portal portal, port-central septa with the formation of false poles) and the regeneration of hepatocytes (the loss of the beam building, the presence of cells with large cores .
Macrofrets: Primary liver cancer, metastases in the liver of tumors of another primary localization.
Morphological equivalents glomerulonephritis
Micropreparation N 112 Intrakapillar proliferative glomerulonephritis (hematoxylin and eosin color).
There is an increased multicellular tank. Hyperclelligence is associated with proliferation and swelling of endothelial and mesangial cells. There is a narrowing of the lumen of capillary loops that perform the cavity of the capsule, as well as their massive neutrophilic infiltration.
MicroPreparation fixation of deposits of imune complexes in the renal glomerulum in acute glomerulonephritis(Atlas, Fig.15.2).
In the course of the basal membrane, a granular glow can be seen (deposits in the form of boulders)
Macrobreparation of subacute glomerulonephritis("big motley kidney").
The kidneys is increased in size, flaky, pale with phetechial hemorrhages on the surface.
MicroPreparation N 113 subighteous mainly extracapillary glomerulonephritis (hematoxylin and eosin color).
Semi-lunishes are visible, formed by proliferation of the epithelium of the external leaflet of Capsules of the Callean-Bowman and migration of monocytes and macrophages into the space between the capsule and the capillary glomer. Between the layers of cells in the lunaries - the accumulation of fibrin. Clubs are siled - they have focal necrosis, diffuse and focal proliferation of endothelium, the proliferation of Mesangia. Part of the tubules are atrophic, in the epithelium of some convinced tubules - hydropic or hyalin-drip dystrophy. In the stroma kidney - sclerosis, lymphomacrophaphagal infiltration.
Morphological options for chronic glomerulonephritis
Electron diffraction pattern membrane nephropathy (Atlas, Fig.15.6).
With an electron microscopic examination, subepithelial deposits are visible in the glomerular basement membrane, the accumulation of the substance of the basal membrane between the legs of the poverty, the loss of the processpocytes and their melting on the thickened and deformed basal membrane.
Electronogram membrancial glomerulonephritis (Atlas, Fig.15.9).
With an electron microscopic examination, sub-replica electron-dense deposits are noted.
Electron diffraction pattern Mesangioproliferative glomerulonephritis (Atlas, Fig.15.10).
With an electron microscopic examination, deposits in Mesangia are visible.
Macrobreparation Secondary shredded kidney (chronic glomerulonephritis, with an outcome in nephrosclerosis).
The kidneys are symmetrically shorn and have a fine-grained surface.
(E) MicroPreparation N 114 Fibroplastic glomerulonephritis (terminal) (hematoxylin and eosin color).
Sclerosis and hyalos of most of the glomers, in the preserved hypertrophic gloms, the proliferation of mesangium cells, scleroso vascular loops. Notes sclerosis and hyaline arterioles. Hyalin cellets in the enlightenment of the tubules.
Secondary damage to kidneys
Macrobreparate amyloid nephrris("big white", "big greasy kidney").
Mark the increase in the size of the kidney, dense consistency, the coole of the surface.
The kidneys are increased in sizes, dense consistency, a smooth surface. On the cut with greedy glitter. The border between Cork and brainstan erase
(E) MicroPreparation N 16 amyloid nephrosis (color of the Congo Roth). Note the deposition of the amyloid in the capillary loops of the glorula, in the course of the tube's own membrane, in the walls of the vessels, as well as in the stroma kidney in the course of reticular fibers.
Mark the color of amyloid.
Under the basal membrane of the tubuline, in the glomers, in the course of the reticular fibers of the stroma in the intima vessels - painted in the red color of the sediment of the amyloid.
Acute renal failure (OPON)
(E) MicroPreparation N 6 Non-necrotic nephrosis (hematoxylin and eosin painting). Clubs and epithelium of straight tubules are saved. The cells contain the kernel. The epithelium of the convulsion canal does not contain nuclei (Caryolysis).
Organopathology of chronic renal failure
View a set of macropreats reflecting the morphological manifestations of Uremia: fibrinous pericarditis ("hairy heart"), a bruboral tracheitis, diphtheric colitis.
Domor monomic diseases of the genitals
Macrobre Polyp uterus. Note the localization of the polyp, its shape, dimensions, surface nature, connection with the subject to the cloth.
Endometrial grows gray-red, with an uneven surface.
(Э) MicroPreparation N 142 Irony Endometrial hyperplasia (hematoxylin and eosin color).
The endometrium glands are built from the proliferating type epithelium, have different magnitudes and shape, have a convulsion and cystic extension, very closely arranged, the branching and binding of the glands.
MicroPreparation N 57 Pseudo-erosion cervix (gematoxylin and eosin color).
In the uterus cervical erosion zone, two epithelium views: a multi-layered flat epithelium, non-refined and prismatic. There is an ectopia of the cylindrical epithelium in Exoceservix.
Pathology of pregnancy
Macrobreparation postpartum endometritis.
The casing of the vagina and cervix is \u200b\u200bhyperemic, edema, sometimes with hemorrhages. In the lumen of the vagina, especially in the cervix, is exudate, released from the uterus. The cervical channel is ajar.
Macrobreparat Liver with eclampsia.
Single or drain white and yellow foci of necrosis and multiple hemorrhages appear in the liver different sizes - Landscooting liver.
Chapter 17. Gastrointestinal Diseases
Chapter 17. Gastrointestinal Diseases
Power and pharynx diseases. Diseases of the stomach. Eidiopathic bowel diseases (Crohn's disease and ulcerative colitis) Diseases of the draft
Procession blind intestine
Angina (tonsillitis)- an infectious disease characterized by inflammatory changes in the lymphoid tissue of the pharynx and chicken almonds (rings of Pirogov). Forms of tonsillitis: acute, chronic (recurrent).Shaped sharp tonsillitis:exudative - catarrhal, fibrinous, purulent; Non-necrotic - necrotic, gangrenous, ulcer-film (special shape - simanovsky-plat-Wensen's angina); Localization is lacuniary, follicular.Complications of tonsillitis:local - paratronzillar abscess, phlegmon fiber, thrombophlebitis; General - sepsis, rheumatism, glomerulonephritis.
Gastritis- Inflammation of the mucous membrane of the stomach.Types of gastritis:acute and chronic;on topography- diffuse and focal (anthral, \u200b\u200bfoundal, pyloroantral, pylorododenal).
Shaped sharp gastritis:catarial, fibrinous, purulent (phlegmonous), necrotic. With any form - erosion and sharp ulcers.Erosion- Surface defect of the mucous membrane is not deeper than its muscle plate.Ulcer- A deep defect, the bottom of which is muscular or even a serous layer of the organ wall.
Chronic gastritis- This is a group of diseases of the stomach of different etiologies, characterized by a combination of chronic inflammation and disorders of regeneration with the structural restructuring of the stomach mucosa.Classification of chronic
nicke Gastritis:on etiology and pathogenesis- Helicobacter (type B), autoimmune (type A), reflux gastritis (type C);on topography; According to morphological type- surface and atrophic;according to activity.Consider the availability, nature and degree of severityintestinal metaplasia and dysplasia (intraepithelial neoplasia).Chronic atrophic pantastrite is an optional preference.
Ulcerative disease- chronic, cyclically current disease, the main clinical and morphological manifestation of which is chronic recurrent gastric ulcer or duodenum.Complications peptic disease: destructive- bleeding, perforation (running with the development of peritonitis), penetration (in the liver, gallbladder, gland, pancreas);scar- deformation and stenosis of the entrance and weekend sections of the stomach and the bulbs of the duodenum;malignization- Largeness (extremely rare).
Stomach tumors:epithelial(adenoma and cancer) and neepithelial(mesenchymal, lymphoma). Macroscopically exofic stomach formations (hyperplastic growth, adenoma) is customary calledpolypami.Stomach Cancer Classification:on macroscopic growth- Exofite (polypose, mushroom, saucer), endophytic (blade-shaped), ulcerative-infiltrative, plastic linite;by
histological title- intestinal type (intestinal - types of adenocarcin et al.) and diffuse (SCIRR, solid, cerebral cell, etc.);in the depth of invasion and the stage of generalization of the tumor process(TNM system). Diagnostically significant lymphogenic metastases:in the left pressed lymphatic node(Metastasis Virchova),retrograde - in ovaries(Crokenberg Cancer),in paragrevy fiber(Schnitzler metastasis).
Idiopathic bowel diseases: Crohn's disease(granulomatous inflammation of any digestive tract) andulcerative colitis.Ulcerative colitis is an optional precancerous disease.
Appendicitis- inflammation draw-shaped process blind intestine. In surgical practice, a group of diseases denoted as acute abdomen (ulcerative disease with perforation, ulcerative disease with bleeding, acute intestinal obstruction, strangulated hernia, acute cholecystitis, acute appendicitis).Appandcite forms:acute - simple, surface, phlegmonous (options - apostleatous, phlegmosno-ulcerative), gangrenous (primary and secondary); chronic.Complications of acute appendicitis:peritonitis, mesenteriolite, pylephlebit, pylephlegitic liver abscesses.
Fig. 17-1.MicroPreparation. Chronic tonsillitis in the aggravation stage: surface epithelium is damaged (dystrophic and necrotic changes, areas of ulcerations), infiltrated by neutrophilic leukocytes (1). Lymphoid follicles are atrophied, in stroma sclerosis (2). In extended lacunas, neutrophilic leukocytes and bacteria colonies (3) are determined.
Hematoxylin and eosin painting: x160
Fig. 17-2.Macrobreparations (A, B). Chronic multifocal atrophic gastritis: stomach mucosa with smoothed folds, thinned, pale, grayish color, with fine-point hemorrhages, erosions (b - preparation I.N. Shestakova)
Fig. 17-3.Micropreparations (AA). Chronic atrophic gastritis: the mucous membrane of the feet of the stomach is sharply elapsed, 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, secrete mucus. There are focus of intestinal metaplasia with glassoid cells (1). In its own plate of mucous membrane, diffuse lymphoplasmocyte infiltrate, lymphoid follicles (2), expressed sclerosis; in, g - Helicobacter Pilori.in the lumen of the glands.
a, B - painting with hematoxylin and eosin, in - Coloring on Vartin-Stari, G - immunohistochemical method: a - x 100, b - x200, in, g - x400
Fig. 17-4.Macrobreparations (AA). Gastric erosion and ulcers: in the gastric mucosa multiple small surface (erosion) and deeper, exciting submucoscent and muscle strata stars of the stomach (sharp ulcers), rounded shape defects with soft smooth edges and a bottom of a brown-black or gray-black color ( due to salt-painted hematine, which is formed from the hemoglobin of erythrocytes under the action of hydrochloric acid and gastric juice enzymes); (See also Fig. 3-4, 4-10) (A, B - Preparations I.N. Shestakova, G, D - drugs N.O. Kryukova)
Fig. 17-4.Continued
Fig. 17-4.The ending
Fig. 17-5.Micropreparations (A, B). The erosion of the gastric mucosa: the surface (within the mucous membrane) is determined in the mucous membrane of the stomach (within the mucous membrane) the focus of necrosis with the formation of a shallow defect - erosion with perifocal leukocyte inflammatory infiltration. At the bottom of the erosion of the deposition of salty hematine (1). Coloring hematoxylin and eosin: x 100 (b - drug N.O. Kryukova)
Fig. 17-6.Macrobreparations (AN). Chronic ulcer of the stomach (A, B D, ZH) and duodenal estate (B, E): Chronic bleeding ulcers - Arrochaled and thrombic vessels in the bottom of the ulcer (in, e, l, n), perforation (d, to - view from the outside, from the abdominal cavity - K) and penetration (b, g, zh,, n). The round shape of the defects of the mucous membrane and the walls of the stomach (or duodenum) with rolic-shaped compacted edges. The cardiac edge of ulcers bezed, hangs, and the edge, addressed to the pylorical stomach, is gentle, has the form of a terrace, the steps of which are formed by the mucous membrane, submucms and muscle layers. This configuration is due to the constant displacement of the edges of the ulcers during the peristaltic. The mucous membrane around the ulcers is changed, the folds can be located radially towards the ulcerative defect (the convergence of folds -
a, f, and, m); (A-B, E - drugs I.N. Shestakova,
b, G, I, - Preparations N.O. Kryukov)
R iP. 17-6.Continued
Fig. 17-6.Continued
Fig. 17-6.Continued
Fig. 17-6.Continued
Fig. 17-6.The ending
Fig. 17-7.Micropreparations (A, B). Chronic ulcer of the stomach (a) and duodenum (b): defect of the wall of the stomach or duodenum, breathtaking mucous membrane, subliminate and muscle shell. In the bottom of the defect 4 layers: 1 - fibrinous-purulent exudate; 2 - fibrinoid necrosis; 3 - granulation tissue; 4 - curtain fabric with sclerized and hyalinized vessels. In the edges of the chronic ulcer of the stomach, the processes of the epithelium (cable epithelium hyperplasia, atrophy glands, intestinal metaplasia, weak or moderate dysplasia). Coloring hematoxylin and eosin: a - x 120, b - x60 (b - drug N.O. Kryukova)
Fig. 17-8.Macrobreparations (A, B). Polyp of the stomach: a small exofite formation on a wide base, covered with mucous membrane (histologically: A - adenoma, b - leuomioma); (A - drug N.O. Kryukov, b - preparation I.N. Shestakova)
Fig. 17-9.Macrobreparations (AA-D). Stomach cancer (noded or diffuse forms): a - fungosic, b - cross-shaped, in, r - endophytic diffuse cancer (r - view from the outside of the stomach, from the side of the serous shell); A noded shape - on a small crumism of the stomach, a large node of a mushroom-shaped or sword-shaped shape with raised uneven edges and lowered by an ulcerated bottom is determined. The tissue of the whores-colored knot, dense consistency, grows all the layers of the stomach wall, does not have clear boundaries. Diffuse shape: the wall of the stomach at a considerable distance is sharply thickened due to the growing of a dense whiskered tissue that does not have clear boundaries. Mucous membrane with smoothed folds, rigidna (see also Fig. 9-5, 10-7); (A - drug N.O. Kryukov, b - preparation I.N. Shestakova)
Fig. 17-9.The ending
Fig. 17-10.Micropreparations (A, B). Stomach adenocarcinoma: In the thickness of the mucous membrane and the muscular layer of the stomach, atypical, different sizes and shapes are glazed complexes (tissue atypia). Tumor cells and their kernels are polymorphic, different sizes and shapes, hyperchromic kernels (cell atiphy). Mitoses (typical and atypical) are few, the level of proliferative activity of the tumor is moderate. Tumor complexes penetrate their own plate and muscular layer - invasive growth (see also Fig. 9-6). Hematoxylin and eosin coloring: x 160
Fig. 17-11.Macropreach. Phlegmosic appendicitis: Cell-shaped exhaust increased in size, the walls are thickened, diffusely impregnated with pus (with pressure from the lumen, the grina is also released), the surface is dim, reddish-blue, with full-blood vessels; The mesenter of the process is also full, with foci of suppuration, hemorrhages (see also Fig. 6-6); (Preparation I.N. Shestakova)
Fig. 17-12.Micropreparations (A, B). FLEGMONOZA-Yazznogenic appendicitis: pronounced leukocyte infiltration of all layers of the wall of appendix, edema, inflammatory hyperemia, necrosis and ulceration of the mucous membrane, lymphoid tissue atrophy.
Coloring hematoxylin and eosin: a - x 60, b - x 200
Fig. 17-13.Macropreach. Chronic appendicitis: a worm-shaped outflow of ordinary sizes (but can be increased or reduced), a serous shell is smooth, brilliant, whisen, whisker, with fragments. The wall of the process is thickened, compacted (sclerosis). The mucous membrane of pale pink colors (atrophy). Gloss the process in some places
Fig. 17-14.Micropreparations (A, B). Crohn's disease: deep sloppy ulcers of the mucous membrane, lymphomacrophagoal, with admixture of plasmacites Infiltration and sclerosis of all intestinal wall layers (A), granuloma with giant multi-core cells in the layer subliminate (b). Painting hematoxylin and eosin: a - x 100, b - x 200
Fig. 17-15.Micropreps (a, b). Ulcerative colitis: pronounced diffuse lymphomacrofagal with admixture of leukocytes Inflammatory infiltrate, swelling, microcirculatory disorders of the gauge of the colon, crypt-abscess (1).
Painting hematoxylin and eosin: a - x 100, b - x 200
Fig. 17-16.Macrobreparations (A, B). Gangrene guts: Ischemic necrosis of a piece of fine or colon in the obstruction of mesenterical arteries with blood closures, thromboembols, atherosclerotic plaques (acute ischemic intestinal disease); (A - drug A.N. Kuzina and B.A. Primaris)
Fig. 17-17.Macrobreparations (A, B). Colon's diverticulosis: multiple finger-shaped digs in the wall of the colon, on the side of the mucous membrane The inputs in the diverticulus have a kind of dark spots (arrows); (drugs I.N. Shestakova)
Fig. 17-18.Macropreach. Mekkel's diverticulus (drug I.N. Shestakova)
Figure 7-1 of the esophagus and stomach in the norm, macropreparation
B norm The color of the mucous membrane of the esophagus (left) varies from white to yellowish brown.
In the area of \u200b\u200bthe gastroofic compound (in the center and left) there is a lower sphincter of the esophagus (NSP), whose function is to maintain muscle tone. The stomach is opened in great curvature (at the top and right). B The bottom of the bottom is visible by a small curvature of the stomach. An Arm is a gatekeeper, which goes into the initial duodenal department (incomparable). A chipping seal is a thick ring-shaped layer of a smooth muscles. B norms of the stomach mucous membrane is clearly pronounced.
Figure 7-2 Esophagus Norma, Endoscopy
Endoscopic painting of gastroofic and esophageal compound (A). The color of the mucous membrane of the esophagus, lined with a multilayer flat non-coronting epithelium, has shades from pale pink to yellowish-brownish color. The mucous membrane of the stomach lined with glazed epithelium is dark pink. NSP supports smooth muscle. The lower part of the esophagus during the passage is expanding due to the relaxation of NSP and the recipe relaxation of the proximal stomach unit under the influence of a vasoactive intestinal peptide produced by postganglyonary peptide -urgic vagus nerve fibers. When the tone of the NSP decreases, the reflux of acidic gastric content in the lower diver of the esophagus occurs, which is accompanied by burning painful sensations (heartburn) behind the sternum and under it. Disorders of the functioning of esophagus sphincters can also cause difficulty swallowing (dysfagia). Damage to the mucous membrane of the esophagus is accompanied by pain when swallowing (identifiable). Congenital or acquired disorders of the innervation of the esophagus lead to difficulties of relaxation of NSPs, Ahalasia, progressive dysfagia and the expansion of the esophagus above NSP.
Figure 7-3 esophagus normally, micro
The mucous membrane (left) is enjoyed by a multilayer flat non-reflective epithelium, there are small mucous glands and an output duct, surrounded by a lymphoid fabric. The right is the muscular shell. In the upper esophageal department where the process of swallowing food begins, arbitrary transverse muscles prevail. They are located together with smooth muscle cells, whose share in the underlying sites gradually increases, and skeletal muscle tissue is supplanted. In the lower part of the esophagus, the muscular shell is represented by an involuntary smooth muscle tissue, which provides peristaltic advancement of food and liquid in the stomach. Here is the smooth muscles of NSP, the muscular tone of which is an effective barrier against regurgitation of gastric content. B areas of gastroofic compound Multilayer flat epithelium alternates with glands of stomach epithelium.
Figure 74 Trachecopic fistula, Macrove Repair
K congenital esophageal anomalies include its atresia and tracheopic fistula. B embryogenesis The development of the esophagus and light as the derivatives of the endoderma is interconnected with the subsequent buds of them from each other. HA with the right figure is the atresia of the esophagus (a) in the middle third. HA left figure below Kiel trachea is located tracheopic fistula (♦). B depending on the localization of atresia or a fistula in a newborn can develop vomiting or aspiration. Often simultaneously develop other congenital anomalies. Agnesia (complete absence) of the esophagus is very rare.
Figures 7-5, 745 Stricks of the esophagus and Ring of Shatzki (SCHATZKI), radiographs with bary
HA two pictures on the left are shown strictures (♦) (scar stenosis) of the lower third of the esophagus. The stricture of the esophagus occurs during reflux-esophagite, sclerodermia, radial lesions, chemical burns. On the right side of the side image in the lower esophageal department, the so-called Shattsky ring (A) is seen directly above the diaphragm. This place has muscle shell folds. In such a state, progressive dysfaia is observed, more pronounced when todded food compared to liquid.
Figure 7-7 Hatal hernia (hernia of the esophageal hole of the diaphragm), KT
HA KT chest is visible to chital hernia (*). The area of \u200b\u200bthe gastric bottom dilated and moved to the chest cavity through an extended esophageal hole of the diaphragm. This kind of movement or slipping of the part of the stomach is observed in about 95% of the hiatal hernia. Approximately 9% of patients with diaphragmal hernias have symptoms of gastroesophageal reflux disease (GERD). On the other hand, some cases of GERD development are associated with a diaphragmal hernia. The expansion of the esophageal hole of the diaphragm prevents the normal functioning of the NSP. Due to the reflux of the gastric content in the bottom of the esophagus, the patient develops symptoms of heartburn, cardialgia with burning pain behind the sternum, especially pronounced after eating and amplifying in the position of lying.
Figure 7-8 Equaline hernia, KT
HA KT without contrasting strengthening in the left half of the chest next to the heart is visible by the Bblestous part of the stomach (*). Such a movement of the stomach occurred due to the complication of the accumulative ("rolling") hiatal hernia - a rare, but serious form of diaphragmal hernia. Bo Time to move the stomach into the chest cavity through a small hole may violated the blood supply to the stomach with the development of ischemia and heart attack.
Figure 7-9 Food Diverticulus, Radiographs
HA two serial radiographs in the top of the esophagus can be seen from the veil, or the diverticulus (♦). The contrast agent fills the pricing cavity. The diverticulus is a plot of expansion and protrude the wall of the esophagus through weak points in the muscle shell. As a rule, the diverticulus sput between compressive muscles in the upper esophagus or through the muscular shell of the lower esophagus directly above the diaphragm. This pathology Known as a coder diverticulus (Zenker). When the food is passed through the esophagus, it can accumulate in the diverticulus and decompose, which leads to the appearance of a silent smell of the patient's mouth.
4 Figure 7-10 Mallori Weiss Syndrome (Mallory-Weiss), KT
In severe and long-term vomiting, longitudinal dumping walls of the esophagus and subsequent bleeding can occur. HA This KT with a contrasting amplification is visible signs of Bourgeave syndrome (BOERHAAVE). This syndrome, in turn, is a variety of Mallory Weiss syndrome. The mediance is visible to the enlightenment area (♦), indicating the presence of air that penetrated through the spontaneous tearing of the esophagus. The gap is localized at the bottom of the esophagus, above the gastrointestinal compound. The ingress of the contents of the esophagus to the mediastum leads to inflammation, which quickly applies to other chest departments.
Figure 7-11 Varicose veins of the esophagus, macro-treatment
Varicose-expanded veins that were the source of bleeding and hemattemesis (bloody vomiting) are located in the region of the gastroofic compound. Varicosis of the submucosal base of the esophagus is developing with portal hypertension, usually complicating the course of alcoholic alcoholic liver cirrhosis. Esophaid venous plexus is one of the main collateral routes for venous blood outflow. Despite the fact that blood from the upper stations of the stomach also comes into the esophageal venous plexus, it is called esophageal plexus, and the bleeding of this localization is also called esophageal bleeding.
Figure 7-12 Varicose veins of the esophagus, endoscopy
Expanded veins of esophageal plexus, located in the submucosal basis, will sput in the lumen of the lower duty station. Such extensions are most often complicated by portal hypertension during liver cirrhosis. It has been established that the varicose veins of the esophagus develops approximately 60-70% of patients with liver cirrhosis. Erosions and breaks of thinned venous walls lead to suddenly emerging and extremely dangerous to life massive bloody vomit. For the treatment and prevention of bleeding, such methods are used as a bandaging of varicose veins, injection of sclerosing substances (sclerotherapy) and a balloon tamponade of the esophagus.
Figure 7-13 Ezophagitis, micro
Reflux-esophagitis with GERB arises due to the deficiency of the NPC, leading to the regurgitation of the acidic content of the stomach into the lower diver of the esophagus. With moderately pronounced reflux-esophagitis, microscopic signs are revealed in the wall of the esophagus: the epithelial hyperplasia with the predominant hyperplasia of the basal layer and the formation of elongated epithelial papillas (acanthosis), inflammatory infiltration neutrophilic and eosinophilic granulocytes and lymphocytes. The presence of eosinophils (in the figure they are painted by gymze pink color) It is a specific and sensitive sign of reflux-esophagitis, especially in children. The causes of reflux-esophagitis are the diaphragmal hernia, neurological disorders, sclerodermia, disorders of the clearance of the esophagus and the evacuation function of the stomach. The difficult course of reflux-esophagitis may be complicated by the cure and the subsequent formation of scar stricture of the esophagus.
Figure 7-14 Barrett Food (Barrett), Macropreparation
The damage to the mucous membrane of the esophagus in chronic GERD can lead to a metaplasia of a multilayer flat epithelium of the esophagus into a cylindrical gastric epithelium with the presence of intestinal heap-shaped cells, which got the name of the esophagus of Barrett. It occurs about 10% of patients with chronic reflux gastritis. The lower separation of the esophagus above the gastroof compound on the background of the preserved multilayer flat epithelium of whitish color is visible reddish sections of the mucous membrane metaplasia. The ulceration of the mucous membrane is accompanied by bleeding and pain. Due to inflammation, the stricture of the esophagus arise. Endoscopy with biopsy is required for diagnosis.
Figure 7-15 Food Barrett (Barrett), Endoscopy
HA endoscopic images of the lower part of the esophagus are reddish areas of the mucous membrane of the esophagus, characteristic of the esophagus of Barrett, are located against the background of the pale whimsal islands of a multi-layer flat epithelium of the unchanged mucous membrane. If the length of the lesion at the Barrett esophagus is not higher than 2 cm from the place of contact of the ferrous and multilayer flat epithelium, similar pathology is called a short segment of Barrett's esophagus.
Figure 7-16 Food Barrett (Barrett), MicroPreparation
On the left there is a ferrous epithelium, and on the right - a multi-layered flat epithelium. On the left is presented a "typical" mucosa Barrett mucosa, since there are also signs of intestinal metaplasia (glasslike cells are visible among cylindrical cells of the glazed epithelium). The predisposing factor for the development of metaplasia is chronic gastric content reflux to the lower part of the esophagus. In most observations, Barrett's esophagus is diagnosed in patients aged 40 to 60 years. The risk of esophageal adenocarcinoma increases 30-40 times, if the length of the bareretta esophagus exceeds 3 cm.
Figure 7-1 7 Food Barrett (Barrett) with dysplasia, micro
K Preserved multi-layered flat epithelium of the esophela (right), the metaplastic ironic epithelium is inserted, in which the lesions of heavy dysplasia are determined. Attention should be paid to the densely located hyperchromic cores of ferrous epithelium, a small number of preserved glass-shaped cells on the surface of the mucous membrane (at the top of the left) and tissue amateur tissue. The basal orientation of the core cells is a sign of weak dysplasia, apical orientation - heavy dysplasia and the high probability of developing adenocarcinoma. In the absence of treatment, dysplasia can develop a few years after the occurrence of Barrett's esophagus.
Figure 7-18 Herpety esophagitis, macro production
B of the bottom of the esophagus against the background of a conventional whitish multilayer flat epithelium is visible clearly delimited oblong ulceration of browned color. The cause of such ulcers with the appearance of "probins" is the defeat of a simple herpes virus (HSV). Opportunist infections caused by HSV, Candida and Cytomegalovirus are most often observed in immunosuppressive states. A typical symptom is the same phage. Herpetic esophagitis, as a rule, has a local character and is rarely complicated by bleeding or esophageal obstruction. The dissemination of the process is not characteristic.
Figure 7-19 Candidial esophagitis, macropreparation
HA background of the hyperemia of the mucous membrane in the lower third of the esophagus is visible brownish-yellow plaques. The same lesions are available in the area upper departments The bottom of the stomach (at the top on the right). Candidoid infection with the defeat of the oral cavity ("Mouth Milkin") and upper departments gastrointestinal tract It is usually superficial, however, in conditions of immunosuppression, invasion and dissemination of the process are possible. Some representatives of the genus Candida are part of the normal microflora of the oral cavity. Focal damasses at the candidical are rarely the cause of bleeding or obstruction of the esophagus, but their merger is possible with each other with the formation of pseudomambranous lesions.
Figure 7-20 Flusted Esophageal Cancer (Epidermal), Macrous
HA mucous membrane in the middle part of the esophagus is an ulcerated exofite tumor of reddish color. Effectiveness of the esophagus reduces and makes imperceptible early manifestations of the effect of mass. K Moment of diagnosis, as a rule, there are already signs of cancer germination in the mediastinum, and the disease may be inoperable. This explains the unfavorable prediction for the patient with esophageal cancer. K Risk factors for the development of esophageal cancer in the United States include smoking and alcohol abuse. B other countries indicate such risk factors as the high content of nitrates and nitrosamines in food, zinc deficiency or molybdenum in food products, as well as infection with the human papilloma virus.
Figure 7-21 PlateLock Cancer Cancer, Endoscopy
In the middle part of the esophagus there is an ulced flat-cell cancer, which caused the cause of the lumen stenosis. Characteristic symptoms representing serious problem For patients, there are pains and dysphagia. Disruption of food leads to weight loss and cachexia.
Figure 7-22 PlateLock Cancer Cancer, Micro
Only below the right there is a small portion of the remains of a normal multi-layer flat epithelium, which is replaced by a thick layer of flat-belling cancer structures. Solid nests of tumor cells infiltrate the subliminate base and the walls are subject to layers (left). The tumor often sprouts into the surrounding tissues, which makes it difficult to surgically removal. Tumor cells with flat-milk cancer have pink cytoplasm and clear boundaries. B Tumor cells with a frequency of 50% marked the Mutation of the P53 tumor suppressor. B some observations there is a mutation of the PL6 / CDKN2A suppressor gene, in others - amplification of the Cyclin DL gene. Such mutations may arise in the process of chronic inflammation, in which the proliferation of epithelium cells is enhanced.
Figure 7-23 Adenokarcinoma, Macropreparation
Left is visible to the normal mucous membrane of the yellowish-brown color of the top of the esophagus. B distal esophagus The appearance of the mucous membrane with dark erythematous sections is characteristic of the esophagus of Barrett. In the distal part of the esophagus near the gastroofic and esophageal compound is a major creened adenocarcinoma node, which germinates in the wall of the stomach in the area of \u200b\u200bits upper departments. The most often adenocarcinoma is developing at the Barrett esophagus with the mutation of the P53 tumor-suppressor, the nuclear translocation p ^ cannin and the amplification of C-ERB B2. HA early stages of adenocarcinoma, as with a flat-stitch carcinoma, there are often no clinical manifestations of the disease, which necessitates a bad forecast.
Figure 7-24 Adenokarcinoma, KT
HA KT abdominal cavity with a contrast gain in the lower esophageal department is visible tumor (♦), which extends to the adjacent stomach departments and the ring-shaped escalaza lumen. In this observation of the adenocarcinoma arose in the esophagus of Barrett, which, in turn, was formed against the background of chronic GERD. The presence of epithelium dysplasia at the Barrett esophagus increases the risk of developing adenocarcinoma. The adenocarcinoma of the esophagus is developing in patients over the age of 40, which suffered from GERD, as a rule, for many years. Strengthening the processes of cellular update and raising the proliferative activity of the epithelium in the mucous membrane at the Barrett esophagus is a background for mutations leading to the loss of cell cycle control.
Figure 7-25 Adenokarcinoma, Endoscopy
B by the lower part of the esophagus are visible dark-red loose areas of the mucous membrane, relating to the esophage of Barrett. The polypovoid tumor, with a biopsy of which was supplied by a PATO histological diagnosis of moderately differentiated adenocarcinoma, grows into the lumen of the esophagus. Patient for 30 years suffered from GERD and received inadequate treatment. Clinical manifestations of the adenocarcinoma of the esophagus include hemamples, dysfagium, chest pain, body weight loss.
Figure 7-26 The mucous membrane of the stomach is normal, micro
The gastric mucous membrane in the bottom area there are shallow gastric pits (♦), under which are located in the depth of the gland (■). Oblast, or parietal, cells (a) gastric bottom seals secrete hydrochloric acid and internal factor. The secretion of hydrochloric acid by parietal glands is carried out using H * / K * - ATP-AZ (proton pump) under the influence of acetylcholine produced by vagous nerve fibers and affecting muscarinic receptors, as well as histamine of fat cells acting on H 2 -Repceptors, and gastrin . In glands of the bottom of the stomach, there are also main cells secreting the proteolytic enzyme pepsinogen. In the neck of the neck of the glaze are cubic mucous cells, or mucocytes, which produce a mucus protecting the gastric mucosa from the action of acid and pepsin.
Figure 7-27 The mucous membrane of the stomach is normal, micro
The mucous membrane of the anthral stomach (♦) stomach (♦) is deeper, and the glands (■) are shorter than in the wall of the dna stomach. Bosses and glands of the anthral and pylorial sections of the stomach are located mucous cells (mucocytes) of the cylindrical shape. The mucous cells secrete the procentle, which contribute to the production of mucins and bicarbonate and strengthen the blood flow in the mucous membrane. These factors play a protective role, protecting the mucous membrane from the action of acidic content of the stomach. Thanks to the peristaltic movements of the stomach, mixing the chimus. The rate of emptying of the stomach depends on the concentration of hydrogen ions and the amount of fat arrived in the duodenum. Under the influence of fat in the duodenum intestine, the secretion of cholecystokinin, which hold the emptying of the stomach.
Figures 7-28, 7-29 Top departments of the gastrointestinal tract Normally, Endoscopy
HA left figure shows an endoscopic pattern of the bottom of the stomach normal, on the right - the initial department of the duodenum.
Figure 7-30 Congenital diaphragmal hernia, appearance, section
The left dome of the diaphragm is absent, as a result, the contents of the abdominal cavity of the fetus are located in the chest. The metallic probe is inserted behind the left lung, which is located in the right half of the chest, as its left half is occupied by the stomach moving here. Below the stomach is visible to a dark color spleen, lying above the left lodge of the liver, shifted up. The fetus moves the contents of the abdominal cavity b to the chest leads to the lung hypoplasia. The diaphragmal hernia as a single congenital anomaly can be potentially curable. However, it is more commonly combined with multiple defects, as well as with chromosomal disorders, such as caracomomy 18.
Figure 7-31 Stenosis of the gatekeeper, macro-treatment
B Wall of the outlet of the stomach There is a pronounced muscle shell hypertrophy (a). Stenosis of the gatekeeper is rare, however, it is the cause of the fountaining vomiting among babies aged from 3 to b weeks. Muscle hypertrophy can be expressed to such an extent that can be determined during palpation. Stenosis of the gatekeeper as a multifactorial disease is a manifestation of the genetic phenomenon of the "Poslizability", which, with an increase in genetic risks, symptoms of the disease appear. Stenosis has been observed 8 1 case at 300-900 newborns, more often in boys, since girls have a smaller level of risk factors.
Figure 7-32 Gastropathy, Macrobreparation
In the mucous membrane of the stomach, hemorrhage of various sizes and shapes are visible. These areas have surface damage to the mucous membrane, called erosions. The erosive lesions of the gastric mucosa are a morphological substrate of the collective concept of "gastropathy". For gastropathies, focal lesions of the gastric mucosa and hemorrhage, developed due to damage to epithelocytes or endotheliocytes, but without signs of pronounced inflammation. The reasons for the development of gastrophotas are similar to the reasons for the development of acute gastritis and include the reception of medicines of the type of anti-inflammatory non-steroidal drugs, alcohol, stress, yellow reflux, uremia, portal hypertension, ionizing radiation and chemotherapy. The changes presented in the figure correspond to the picture of an acute erosive gastropathy.
The mucous membrane of the bottom of the stomach diffusely hyper-mounted, with multiple petechias, but erosion and creeps are missing. Acute gastritis (Hemorrhagic gastritis, acute erosive gastritis) can develop as a result of ischemia (shock, burns, injury) or under the influence of toxic substances such as alcohol, salicylate, non-steroidal anti-inflammatory drugs. Damage to the mucous barrier contributes to the inverse diffusion into the acid of the acid of the gastric juice. The course of acute gastritis can be both asymptomatic and complicated massive bleeding. The progression of damage leads to erosions and sharp ulcers. In stress, hypersecretion of hydrochloric acid occurs, which leads to the formation of sharp lesions of the gastric mucosa: Curling ulcers (Curiing) during burning injury and Cushing ulcers (Cushing) during the injury of the central nervous system.
Figure 7-34 Acute gastritis, micro
Microscopic signs of acute gastritis include hemorrhage, edema, neutrophilic infiltration of varying degrees as an indicator of acute inflammation. HA Figure - Infiltration of neutrophilic granulocytes of glazes and its own plates of the gastric mucosa. Characteristic clinical symptoms Are moderate or severe pain in the epigastria, nausea, vomiting. Blood cases of acute hemorrhagic gastritis can develop a bloody vomiting. Especially often this is observed in patients longly abusing alcohol. The effect of gastric juice is preceded by ulceration, but its quantity is not a determining factor for the development of most stomach ulcers.
Figure 7-35 Chronic gastritis, micro
Chronic nonspecific (antral) gastritis usually develops as a result of the infection of Helicobacter Pylori. Other reasons are reflux boots and reception medicinal preparations (Salicylate) and alcohol. Inflammatory infiltrate consists mainly of lymphocytes, plasma cells; Sometimes a small amount of neutrophilic granulocytes is revealed. B Subsequently develops atrophy of the mucous membrane and intestinal metaplasia, which can be the "first step" on the path to the occurrence of the stomach adenocarcinoma. Autoimmune gastritis develops under the influence of autoantaitol to parietal gastric hectares and the inner stomach factor, which leads to atrophic gastritis and pernicious anemia. The level of gastrine in blood serum is inversely proportional to the products of gastric juice acid, so high concentration Gastrin contributes to the development of atrophic gastritis.
Figure 7-36 Helicobaaer Pylori, MicroPreparation
Helicobacter pylori - chopped gram-negative bacterium not large sizeshaving an S-shaped shape and leaving in microaerobic conditions in a neutral medium under mucus on the surface of the stomach mucosa, next to cylindrical mucous cells (mucocots). When painting with hematoxylin and eosin bacteria, there are a view of pale pink sticks (a). Conditionally pathogenic strains Helicobacter pylori potentially can cause more pronounced lesions in gastritis, increase the risk of developing ulcer and stomach cancer. These microorganisms are not implemented and do not directly damage the mucous membrane, but rather change the microenvironment in the stomach, which contributes to the damage to the mucous membrane. Helicobacter pylori contain uraase and produce ammonia, the cloud-shaped clusters of which surround microorganisms and protect them from the actions of the gastric juice. The clinic for identifying Helieobacter pylori use breathing sample with urea.
Figure 7-37 Helicobacter Pylori, MicroPreparation
Helicobaeter pylori (▲) stimulate the production of epithelial cells of cytokines, which activate immune and inflammatory cells in the subject to their own plate. It is believed that infection occurs in childhood, and inflammatory changes Progress with age. USA 20% of residents are infected with Helicobacter pylori, and only a small part of patients develop such complications as chronic gastritis, stomach and duodenal ulcers, lymphoid fabric lymphoma, associated with the gastric mucosa (Maltoma), and adenocarcinoma. Most patients with active gastritis Helieobacter pylori detect the mucus on the surface of the epithelium. HA This Helicobacter Pylori preparation is revealed with a solution of methylene blue solution.
Figure 7-38 Acute stomach ulcer, macropreparation
The ulcer is a defect of the mucous membrane for the whole thickness, while erosion is a surface, or partial, defect mucous membrane. Ulcers can be complicated by bleeding, penetration into the neighboring organ, perforating into the cavity of the peritoneum, scar strictures. B The area of \u200b\u200bthe stomach bottom is visible a shabby declaration of 1 cm in size, surrounded by zone of hyperemia. It can be assumed that this ulcer is benign. However, all the stomach ulcers must be subjected to biopsy to eliminate malignancy. Insulated stomach ulcers are observed with chronic atrophic gastritis. They are usually localized in the anthral departments in a small curvature or in the transition of the body of the stomach in Antrum. HelicobaeterPylori is the most frequent reason, the second place is occupied by nonsteroidal anti-inflammatory drugs. The level of acidity of gastric content in patients is usually normal or reduced.
Figures 7-39, 7 ^ 0 Sharp ulcers Stomach, Endoscopy.
HA left drawing shows a small ulcer in a prebillard department, on the right - a large ulcer in the antrheral department. BCE stomach ulcers subjected biopsy, since the visual inspection does not allow to establish malignation. Little stomach ulcers that have clear outlines are most likely benign.
Figure 7-41 Acute stomach ulcer, micro
B The site of the ulceration of the epithelium is destroyed, the wall defect covers the mucous membrane and applies to muscular layers. The ulcer is sharply deliberate from the normal mucous membrane (left), which is fused to the bottom of the ulcers represented by inflammatory and necrotic detritus. Small arterial branches in the bottom of the ulcers are damaged, which leads to bleeding. The penetration of ulcers in the deeper layers occurs in the absence of healing and preserving the activity of the process, which is accompanied by pain. The destruction of the ulcer of muscle and serous shells leads to peritonitis with a clinical picture of an acute abdomen. This type of ulcers is called perforative ulcer. When perforations on radiographs, signs of free gas in the peritonean cavity can be determined.
Figure 7 ^ 2 Perforative gastric ulcer, radiograph
HA anti-radiograph of the chest obtained on a portable installation at vertical position The body of the patient, under the right dome of the diaphragm in the abdominal cavity is visible free gas (A). The patient revealed the peptic duodenal ulcer with perforation. When perforation of the hollow organ, the gases contained in it go into the abdominal cavity and are detected mainly under the diaphragm at the vertical radiographic research. Patients develop a picture of an acute abdomen with pain syndrome and sepsis. In the pathogenesis of peptic ulcers of the duodenum, an important role belongs to the increased acidity of the gastric juice. They arise in the proximal duodenal department against the background of peopenite. Almost always, with a duodenal ulcer diagnose the infection of the stomach Helicobacter pylori.
Figure 7 ^ 3 adenocarcinoma, macropreparation
B The stomach wall is a small gastric ulcer with a size of 2 to 4 cm. In a biopsy study, it was found that this ulcer is a malignant neoplasm, therefore the stomach was resteed. B. USA Most observations of stomach cancer are diagnosed in later stages when there are already signs of invasion or metastase. BCE ulcers of the stomach and all the neoplasms in it necessarily must be subjected to biopsy, since with a visual macroscopic study, it is impossible to establish a malignant nature of the defeat. B The opposition of the stomach ulcer is almost all the peptic ulcers of the duodenum are benign. Stomach cancer is the second in the frequency of distribution in the world. B For the last decades, the incidence rackening rack in the United States decreased somewhat.
Figure 7 ^ 4 Adenokarcinoma, KT
HA KT abdominal cavity with a contrast enhanced tumor has the form of an exofic formation (a), which deforms the cavity of the stomach. In pathogistological examination, the tumor is diagnosed by adenocarcinoma. B for many years patient suffered chronic gastritis With infection with Helicobacter Pylori. However, it is known that the cancer of the stomach develops in a minor number of patients with infection with Helicobacter Pylori. Eating marinated, smoked and salty products, as well as education in the stomach of nitrosamines from food nitrites is the risk of developing an intestinal type cancer. The normalization of the diet leads to a significant reduction in the frequency of this form of cancer. Less than definite are risk factors for the development of diffuse type cancer. The clinical manifestations of the stomach adenocarcinoma include nausea, vomiting, abdominal pain, gem-tempois, body weight loss, intestinal discomfort, dysfagium. Early cancer The stomach, limited by the lesion of the mucous membrane, proceeds, as a rule, asymptomatic; It is detected during an endoscopic study.
Figure 7 ^ 5 Adenocarcinoma, MicroPreparation
An intestinal type adenocarcinoma is constructed from newly formed glands that infiltrate the subliminate base. B some tumor cells are visible mitoses (a). Tumor cells are characterized by an increased nuclear-cytoplasmic ratio and nuclei hyperchromatosis. B stroma develops a desmoplastic reaction associated with germination of cancer glasses. Genetic disorders in the intestinal type of the stomach cancer include the mutation of the P53 gene, the atypical expression of E-cadhelerin and the instability of TGFFI and Wah genes.
Figure 7-46 adenocarcinoma, macro
With a diffuse infiltrating growth of adenocarcinoma, a special form of stomach cancer is developing - plastic linite (Linitis Plastica). The appearance of the stomach resembles a wrinkled leather bag or a burdyuk. The wall of the stomach is considerable thicken, multiple erosion and creek are defined in the mucous membrane. The forecast with such a variety of stomach cancer is extremely unfavorable. Ha Low Curvatina Stomach There are more limited shapes of cylinder gastric cancer. For an intestinal type of stomach cancer, its occurrence is more typical against the background of preceding changes associated with the infection of Helicobacter Pylori. The decrease in the share of the intestinal type of stomach cancer in the United States, apparently due to a decrease in the infection rate of Helicobacter Pylori. B The same time remains the constant frequency of the incidence of diffuse stomach cancer, the sample of which is presented in this picture.
Figure 7 ^ 7 Adenokarcinoma, Endoscopy
With an endoscopic study of the stomach of the diffuse type adenocarcinoma, has a form of plastic line (Linitis Plastica) with pronounced erosions of the mucous membrane.
Figure 7 ^ 8 Adenokarcinoma, MicroPreparation
The diffuse type of the stomach adenocarcinoma is characterized by so low differentiation that it is not possible to identify the gland structures. Instead of glands, chains of tumor cells are formed with severe polymorphism and infiltrating growth. B The cytoplasm of many tumor cells there are light vacuoles (a) containing mucus and push the core to the cell periphery. Such cells are called robust cells. They are a typical sign of diffuse type adenocarcinoma, which is characterized by rapid infiltrating growth and an extremely unfavorable forecast.
Figure 7 ~ 49 Gastrointestinal Stromal Tumor, KT
Gastrointestinal Stromal Tumor (CIST) is represented by a large neoplasm (♦), which is localized at the bottom of the esophagus and the upper sections of the don of the stomach. Education is characterized by a smaller signal intensity, as well as its variability in connection with the presence of necrosis and cyst foci. Discrete tumor boundaries. Previously, such tumors were classified as smooth muscle neoplasms. However, 8 is currently believed that they occur from the interstitial cells of Kakhal, which are an integral part of the nerve weaving of the muscle shell of the intestines, which regulate the peristaltics in the gastrointestinal tract.
Figure 7-50 Gastrointestinal Stromal Tumor, Macrobreparation
The gastrointestinal stromal tumor has its source a muscular sheath of the stomach, growing an extractite into the lumen, is covered with a mucous membrane, with the exception of the expression section in the center of the tumor. Gastrointestinal stromal tumor can be solitary or multiple.
Figure 7-51 Gastrointestinal Stromal Tumor, Micro
The gastrointestinal stromal tumor is divided into spindle cell, epithelioid and mixed types. This tumor is built of characteristic beams of spindle-shaped cells. The immunohistochemical reaction to C-Kit (CDI 17) is positive in 95% of observations, on CD34 - in 70%. In addition to C-Kit mutations, in 35% of observations, mutations of the receptors of the a-chains of the thrombocyte growth factor (PDCFA) are revealed. The assessment of the biological potential of these tumors is certain difficulties. The most important indicators are the mitotic index, the size of the tumor and its cellularity. For the treatment of these tumors, a newly created tyrosine kinase inhibitor preparation (STI57I) is used with a good effect.
Figure 7-52 Thin intestine and mesenter Norma, appearance
Loop guts with adjacent mesenter. Attention should be paid to the pronounced venous drainage, thanks to which the blood through the rowing vein system takes towards the liver. Here, in the mesentery, arcades of arteries supplying the gut segments are located. The blood supply to the intestine is carried out by the main and collateral branches of the ventricular barrel, the upper and lower mesenteric arteries. The presence of a pronounced collateral network protects the pile of heart attack. Pushun, covering the intestine, is smooth and brilliant.
Figure 7-53 Thin intestine in normal, macro products
The terminal department of the iliac with an ileocecal (Bauginiyevaya) flap (upper drawing on the right). B mucous membrane shows a somewhat darker peer plaques of oval shape. Ha Lower Pictures Also visible Peyerova Plaska, which is a compact lymphoid fabric. B duodenal intestine in the fine-like mucous membrane and submucosal plate there is a larger amount of lymphoid tissue compared to other gastrointestinal tract departments. B iliac intestine - a more pronounced submembrance lymphoid fabric, which is represented in the form of small single nodules or elongated peer plaques of the ovoid shape. The lymphoid fabric associated with the gastrointestinal tract (Calt) is detected throughout the root of the language to the rectum; Overall, it is the largest lymphoid man.
Figure 7-54 Thin intestine normal, micro
HA surfaces of the mucous membrane of the small intestine there are patches lined with prismatic cells (♦), among which beam-like cells (A) are scattered. B area of \u200b\u200btheir own plate mucous membrane is complete, intestinal glands are formed here, known as Crypt Liborkyunov (■). Thanks to the vile, the surface area of \u200b\u200bsuction is significantly increased. In addition, there are more pronounced mucous membrane folds, which also increase the suction surface. B each intestinal plate there is a blindly ending lymphatic capillary, known as a Milky vessel. Immunoglobulin A, the so-called secretory LGA, is the main immunoglobulin produced by plasma cells Gastrointestinal tract (and respiratory tract). It connects the protein on the glycicalce covering the microwaves, which contributes to neutralization of pathogens, including microorganisms.
Figure 7-55 transverse colon in normal, endoscopy
For colon, the gastral folds of the mucous membrane are characteristic. The colon function is primarily in the absorption of water and electrolyte remnants received from the small intestine. Intestinal content is concentrated, so the person per day with the feces loses only about 100 ml of water. Approximately 7-10 liters of gases passes daily through the colon. They are formed mainly as a result of the growth of normal bacterial flora. B lumen accumulates only about 0.5 liters of gases. The contents of the gases are air, which fell under swallowing (nitrogen and oxygen), methane and hydrogen, resulting from the processes of digestion and bacterial growth. Syndrome of irritable colon does not have any specific macroscopic or microscopic signs. It develops under stress as a result of a pathological increase in the sensitivity of the intestine wall on physiological gas incentives in the lumen. The use of anticholinergic drugs can lead to a temporary improvement.
Figure 7-56 Thick intestine normal, microlrea
The mucous membrane of the colon is represented by long tubular intestinal glands (librice crypts) lined with prismatic mucous cells. A large number of glazing cells provide lubrication of the wheel masses. Lymphatic nodules are localized in the own plate of the mucous membrane and in the submucosal basis. The outer longitudinal muscular layer is assembled in three long ribbons, known as Taenia Coli. In the anorectal junction area there is a transition of ferrous epithelium into a multilayer flat. Above and below this compound b, the lumen is the submissible base (internal and external rectal veins). When they are expanded hemorrhoidal nodeswhich may be accompanied by itching and bleeding. Control of the volume of the intestine carries out the sphincter in the anus area, formed by a layer of skeletal muscle.
Figure 7-57 Endocrine cells of the small intestine normally, micro
B Crypts of the mucous membrane of the small intestine there are point-colored entero-finnish, or neuroendocrine, cells (cages of Kulchitsky). These cells are scattered in the glands, the number of them increases in the distal divisions of the small intestine. In the intestinal mucosa detect various types of enteroendocrine cells depending on the products secreted by them. Under the passage of the contents of the stomach in the small intestine, individual enteroendocrine cells produce cholecystokinin (HCC), slowing the emptying of the stomach, causing a reduction in the horizontal bubble and the highlighting of yellow, which contributes to the digestion of fats. HCC also contributes to the release of various enthimens from the acinar cells of the pancreas.
Figure 7-58 Ommopholezel, appearance
A newborn girl in the middle departments of the abdominal wall has a defect that captures the area of \u200b\u200bthe umbilical cord; This defect is called the ommopalcela (embryonic umbilical hernia, or embryonic eumentration). The contents of the abdominal cavity, including the intestinal loops and the liver, are covered with thin film. Since in the embryonic period of the intestinal loop, they were mainly developing outside the abdominal cavity, their mal-rotation occurred, or an unfinished turn, and the abdominal cavity was not formed properly and remained too small. Obviously it is necessary operational treatment Similar defect. Perhaps the sporadic appearance of the Ommopalcela. However, there are usually an association with other defects of development, and the ommophalcela can be the result of genetic anomalies by type of trisomy 18.
Figure 7-59 Gastroshisis, Appearance
A large defect of the side wall of the abdominal cavity, not affecting the umbilical cord and no membrane. Bblestous part of the intestines, stomach and liver developed outside the abdominal cavity. For this embodiment, the gastrossisis was formed a single complex of limbs and torso, which is sometimes binding to amniotic chickery syndrome, however, this kind of fibrous fragmentation of amnion is observed only in 50% of observations. Early damage to amnion occurs sporadically in the embryonic period and is not a manifestation of genetic disorders. B This observation, along with a single complex of limbs and the body, there is a decrease in the size of the limbs, especially the left upper limb, and scoliosis. B The same time there are no cheap-facial clefts and defects that are with such malformation.
Figure 7 ^\u003e 0 Atresia guts, appearance
The intestine is filled with Mekonia and ends with a blind bag (a). Such changes are the manifestation of complete obstruction or atresia of the intestine. Partial or incomplete blockage of the intestinal lumen is called stenosis. Atresia of the intestines like many anomalies is often combined with other defects of development. In Utero Atresia intestines develops against the background of a multi-way (polyhydramnion), since the fetus is violated the processes of swallowing and absorption of amniotic fluid. Atresia is rare, but attention should be paid to one localization: the atresia of the duodenum, 50% of the observations of which falls on Down syndrome (DOWN), but only in several observations of Down syndrome, the duodenal atresia is detected. With ultrasound examination in an extended duodenalist above the place of atresia and a nearby stomach is determined by the sign "Double gas or liquid" (Double-Bubble).
Figure 74\u003e 1 Meckel diverticulum (Meckel), macro
Congenital intestinal anomalies are presented mainly by diverticulas and atresses, which are often combined with others. congenital defects development. The diverticulus of meckel (*) is the most frequent spanking of the gastrointestinal tract. Approximately 2% of people reveal meckkel diverticulus, which is usually located 60 cm from the ileocecal damper. B The wall of the meckel diverticulus there are all three wall shells of the intestine, so it is believed to true diverticulus, which in adults are usually identified by chance. Exceptions are the promptly remote meckel diverticulus, complicated by bleeding or ulceration. B The diverticular wall can be observed heterotopy of the stomach mucosa, exposed to ulceration with subsequent pain in the abdomen and possible development of iron deficiency anemia. The heterotopia of the pancreas fabric in the wall of the diverticulus have, as a rule, minor consequences.
At large heterotopy sizes are predisposed to invagination.
Figure 7-62 Girshprung disease (Hirschsprung), macro
Congenital expansion of the colon (megacoon) caused by a violation of the migration of neuroblasts involved in the formation of neuromuscular plexuses in the wall of the distal departments of the intestine. The expanded thick intestine (*) is localized proximally towards the affected, aganglionic segment of the sigmoid intestine (g). In newborns, due to the absence of peristaltics in the aganglionary zone, the passage of feces is slowed down, intestinal obstruction develops and significantly expands the clearance of the proximal part of the intestine. The frequency of occurrence of the disease is 1 case per 5,000 newborn children; The disease amazes predominantly boys. Different genetic defects can serve as a disease of Giršsprung, but approximately 50% of family and 1,5-20% of sporadic observations were revealed by the Mutation of the RET gene. Complications are damage to the mucous membrane and secondary infection.
Figure 7-63 Maconial intestinal obstruction (Mekonia Ileus), MicroPreparation
This form of obstruction of the intestine is most often observed in newborns with cystic fibrosis, but it is very rarely found in normal babies. In cystic fibrosis, the violation of pancreatic secretion leads to condescension of semination and intestinal obstruction. HA Figure shows an extended ileum filled with Mekonia (*). Macroscopically Mekonia has a green color and a tar-shaped or sandy consistency. Bo time of generics of Mekonia is either at all passes through the rectum, or it is distinguished from it in minor quantities. Possible complication is the Mekonia peritonitis due to the gap. With a radiographic study in Mekonia traffic jams there may be areas of petrification. Another complication of Mekonia Ileus is the vicen of the intestine.
The surface of the hyperemic mucous membrane of the colon is partially covered with yellowish-green exudate, with surface damage, Ho without formation of erosions. Such changes may be the cause of acute or chronic diarrhea, which can develop with long-term treatment of a wide range of action (such as clindamy) or immunosuppressive preparations. This is due to the prevailing and excessively fast growth Intestinal bacterial and fungal flora (Oostridium Difficile, Staphylococcus aureus or mushrooms type Candida), usually suppressed under normal conditions. Exotocins of microorganisms damage the mucous membrane, induction of cytokines causing apoptosis of cells.
Figure 7-65 Pseudommbranous colitis, KT
HA KT abdominal cavity is visible transverse colon and spray bend of the colon (A) with a pseudo-membrane colitis associated with antibiotic therapy. The intestinal lumen is narrowed, the wall is thickened, edema. Such changes can also be observed with ischemic colitis and neutropenic colitis (tiflite). The tiplit is affected by the blind intestine, in the wall of which the blood supply in patients with weakened immunity and neutropenia is most reduced.
Figure 7-66 PseudoMembranous colitis, endoscopy
HA surfaces of the tumper mucous membrane have an exudable and brown and greenish color. Such changes may be observed with ischemia or severe acute infectious colitis. Patients have abdominal pain, expressed diarrhea develops. The progression of the disease can lead to sepsis and shock. There may be indications for resection of the affected intestine.
Figure 7-67 giardia (hyardiosis), smear
Figure 7-68 Ambiaz, MicroPreparation
Figure 7-69 cryptosporidia, micro
Perforation of the wall of the blind intestine (left *) was the complication of the tiflite. Due to the rupture of the wifth of the intestine and the exit of the cavalous content in the peritoneal cavity, the peritonitis developed. HA serous shell (right *) is visible greenish-brown exudate. Tiflite is rare, but it can develop in patients with weakened immunity, including for malignant neutropenia and leukemia. The term "neutropenic enterocolit" is used in cases of extensive intestinal lesion. The emergence of the inflammatory process contributes to the combination of the weakening of cellular immune reactions and blood supply disorders in the intestinal mucosa.
Figure 7-71 Tuberculosis enteritis, macro
Circular ulcers (one - small, other - big) are characteristic of the infection of Mycobacterium bovis. B. Currently, they are rarely found in connection with the use of pasteurized milk. K Similar changes can sometimes be swallowing with patients with a moal tuberculosis of a sputum infected with M. tuberculosis. B The outcome of the healing of tuberculosis ulcers can be formed by strictures, resulting in obstruction of the intestinal lumen.
Figure 7-72 \u200b\u200bColecia (SPRU), MicroPreparations
HA left drawing is the normal structure of the mucous membrane of the small intestine. HA with the right figure is shown pronounced changes in celiac disease (SPRU). B The process of the disease first comes thickening and shortening the villi, and then their complete disappearance. The inner surface of the mucous membrane, devoid of villi, smoothes. Gradually disappears the brush curios of enterocytes, the mitotic activity increases, the crypts first are perplaced and deepen, and then gradually disappear. The own plate infiltrated with C04 cells and plasma cells sensitive to glyadin. B population of white race celiac disease occurs with a frequency of 1: 2000. Very rarely, this disease amazes representatives of other races. More than 95% of patients identify leukocyte antigens (HLA DQ2 or DQ8), which confirms the role of genetic disorders in the pathogenesis of the disease. There is an abnormal sensitivity to gluten, which is contained in wheat, oats, barley and rye. The elimination of these cereals from food leads to an improvement in the state of patients.
Figure 7-73 Crown disease (Crohn), macro
The bridge of the terminal department is thickened (mid-drawing), the folding of the mucous membrane is absent, there are deep cracks or longitudinal ulcers. HA serous shell has a compacted fatty flavored tissue, "grimaceous" on the surface. Inflammation in the form of limited sites amazes various intestinal deposits (the so-called "jumping" damage, spaced apart at a high distance). In case of Crohn's disease, any department of the gastrointestinal tract can be amazed, but the small intestine is stronger, especially the terminal department of the ileum. The disease is most common in the United States and Western Europe, and women are sick more often. There is a genetic predisposition for the occurrence of a disease that may be related to the presence of certain types of HLA and the mutations of the NOD2 gene. Running the products of the transcription factor NF-κβ leads to the release of pro-inflammatory cytokines.
Figure 7-74 Crohn Disease (Crohn), MicroPreparation
In case of crown disease, transmural inflammation develops in the sister wall. Inflammatory infiltrates (in the figure they have the form of bluish clusters) diffusely propagate from the isyazened mucosa of the sheath, is affixed by the submembratus base, the muscular shell and switch to the serous shell, on the surface of which novel clusters in the form of granuloma form. Due to the transmural inflammation with the damage of the serous shell, there are prerequisites for the formation of adhesions and fistulas with adjacent abdominal organs. Interchepted and paragreught fistula are characteristic complications of Crohn's disease. Damage to the mucous membrane of the terminal department of the underground intestine leads to a violation of suction processes, including vitamin B 12. In addition, violation of the recycling of gilt acids leads to a steamer.
Figure 7-75 Crohn disease (Crohn), MicroPreparation
In case of Crohn's disease, the granular character of inflammation is characterized by nodular clusters of epithelioid cells, giant cells and a large amount of lymphocytes. Microorganisms with special coloring do not detect. In most patients, recurrences of the disease occur in decades after primary lesion, while other disease for a long time It may have either asymptomatic flow or a continuous active course from the very beginning of the disease. Antibodies to Saccharomyces Cerevisiae (ASCA) are highly specific and sensitive to crown disease and are not found with non-specific ulcerative colitis. Antine-hydrophilic cytoplasmic autoantilers with perinuclear staining (PANCA) can be detected in 75% of patients with Crohn's disease and only at 11% - with a nym.
Figures 7-76, 7-77 Crohn disease (Crohn), radiograph and KT
HA left drawing of the upper departments of the gastrointestinal tract with a bright barium contrast, filling the intestinal lumen, visible the extended area of \u200b\u200bnarrowing (a), exciting almost the entire terminal department of the iliac - "favorite" place of lesion during the Crohni disease. The skinny intestine and the colon is not changed, although they can also be amazed during Crohn's disease. The stomach is rarely involved. HA with the right figure with a kt of the abdominal cavity with contrast is visible by the intercircuit fistula. In the result of the adhesive process due to transmural inflammation, there was a convergence (▲) loop of the small intestine.
Figures 7-78, 7-79 Nonspecific ulcerative colitis, radiographs
HA left figure (after the introduction of the barium suspension using the enema) is a small granularity (♦) of the mucous membrane, which starts from the rectum and continues to the transverse colon, which is typical for early changes in non-specific ulcerative colitis. Like the Crohn's disease, the nap belongs to idiopathic inflammatory diseases of the intestine. HA with the right figure (after the barium enema), the large-rod granularity (♦) of the mucous membrane is shown in a close-up heavy flow Nym For the notch, the diffuse damage of the gum mucosa is characterized throughout, which starts from the rectum and extends to a different length in the proximal direction.
Figures 7-80, 7-81 Non-specific ulcerative colitis, macro production
HA left figure is presented with a lessed gauge with a pronounced lesion at a hann, beginning in the rectum and completely affecting all the departments up to the ileocecal damper. There is a diffuse inflammation of the mucous membrane, the areas of ulceration, pronounced full-blooded and large grain of the surface. In progression of the disease of the erosion of the mucous membraid, they merge into linear shapes and penetrate under the saved areas. The islands of the preserved mucous membrane are called pseudopolypace. HA with the right figure is pseudopolypes with a heavy nap. The preserved mucous membrane is not ulcerated, there is only hyperemia of the submissible base and muscle shell.
Figures 7-82, 7-83 Nonspecific ulcerative colitis, endoscopy
With colonoscopy (left figure), a loose erythematous mucous membrane and the reduction of the gustral folds was revealed, which indicates the absence of a pronounced nap. HA with the right figure - a picture of an active branch, but without pronounced ulcerations and pseudopolypes. The idiopathic disease is found most often in the United States and Europe compared to other regions. The course of the disease is usually chronic, with the development of the majority of recurrence patients, which may be single or repeated continuously. The first signs of the disease are the bloody diarrhea of \u200b\u200ba small volume with mucus, grabs-like pain in the abdomen, tenesms and an increase in temperature. The extraordinary manifestations of the nym are developing as inflammation progress in the colon and include sclerosing cholangitis, migrating polyarthritis, sacroileit, will, and acanthosis nigricans. In addition, there is a risk of developing adenocarcinoma of colon. In case of Croh's disease, extorticed manifestations are also found, but the risk of developing adenocarcinoma is not as big as at the nym.
The inflammation at the nym is localized mainly in the mystery of the colon. HA Figure shows the ulceration of the mucous membrane, resembling the neck of the bottle. Inflammation applies under the adjacent mucous membrane, the edges of which become "beacons", which causes the peculiar form of the ulcerative defect. B Squake and on the surface there is exudate. The cell composition of infiltrates is represented by cells of acute and chronic inflammation. Chair is usually a small volume with blood and mucus. The most typical (in 60% of observations) is the moderate course of the disease with the development of relapses and remissions. However, in some patients, the disease can manifest itself a single episode or, on the contrary, to have a continuous current. Some patients (30%) due to a complicated number of colitis that cannot be treated for 3 years from the beginning of the disease is carried out by a kolactomium. The formidable complication is toxic megalolon, in which the gut is sharply expanding, the wall is thinned and the threat of its rupture occurs.
Figure 7-85 Non-specific ulcerative colitis, micro
With an active branch, crypt-abscesses, or accumulation of neutrophilic granulocytes (*), in the lumens of the inflamed crypt or Liborkyanic glasses are obversed. The submissive basis reveals pronounced inflammation. Involvement in the inflammatory process of intestinal glands leads to a violation of their architectonics, loss of glassoid cells, nuclear hydrochromatosis, inflammatory atipients of cells. The identification of crypt-abscess with histological examination is more typically for the nym than for Crohn's disease. However, partial coincidences of morphological paintings can occur with these two forms of idiopathic intestinal inflammation, which does not allow to classify such observations in full volume.
Figure 7 86 Non-specific ulcerative colitis, micro
HA drawing on the left of the bridge of colon has a common structure, contain glassoid cells, right - the crippes of the wrong shape, with signs of dysplasia, which is the first indicator of the development of neoplasia during chronic nic. During dysplasia, DNA damage with microsatellite instability is observed. The risk of developing adenocarcinomas with the duration of Pankolitis for 10-20 years is so large that total kingctomy can be shown. To identify signs of development of dysplasia, the sick nap conduct screening colonis.
Figure 7-87 Ischemic intestinal disease, macropreparation
Early changes in ischemic enteritis are characterized by pronounced hyperemia of the tops of the mucous membrane of the small intestine. The intestinal ischemia is most often evolving in arterial hypotension (shock) due to heart failure, massive blood loss, as well as due to a blood supply to be bleeding during mechanical obstruction (grinding the intestine in the hernial opening, breaking of intestines, invagination). Less often K. acute ischemia The intestine cites thrombosis or embolism of one or more branches of the mesenteric arteries. Sometimes the reason can be venous thrombosis In the syndrome of increased blood intake. If the blood supply is not quickly restored, the intestine can develop.
Figure 7-88 Ischemic enteritis, appearance
Infarction of the small intestine. The plot of infarction from the gross color to gray contrasts with a normal bowl of pale pink colors (lower part of the figure) · Some organs (for example, an intestine with developed collaterals, or a liver having a double blood supply) is more resistant to the occurrence of heart attack. The affected intestine was localized in the jewelry bag formed due to adhesive disease after the previous operation. Such changes could also develop due to the infringement of the intestine at groin hernia. The mesenteric blood supply in this observation was violated due to infringement in a narrow junk gate, in which Kelly surgical clamp introduced. Come Ischemia due to its stretching is often accompanied by acute abdominal pain. The absence of intestinal peristaltics, determined by the absence of intestinal noise, testifies to the development of Ileus.
Figure 7-89 Ischemic enteritis, micro
The intestine mucosa is necrotic. The full-blooded vessels of the mucous membrane applies to the submissive basis and the muscle shell, which remain relatively intact. More pronounced ischemia and necrosis of the mucous membrane are accompanied by hemorrhages and acute inflammation. The progression of ischemia can lead to transmural nurses of the intestine. Patients arise abdominal pain, vomiting, bloody chair or melen. With ischemic necrosis of the intestinal microflora penetrates blood vesselsWhat leads to the development of septicemia, or in the cavity of the peritoneum, which leads to peritonitis and septic shock.
When endoscopy of the upper departments of the gastrointestinal tract, an anchodisplasision area (a) was revealed. More often, it is detected in adults in the clarification of the cause of gastrointestinal bleeding, which occurs periodically and is rarely massive. The lesions are usually localized in the colon, but can be in other places. In the mucous membrane and the submucosal base, one or more foci are located, in which unevenly extended, winding, thin-walled veins or capillary vessels are determined. The lesion foci is usually small - less than 0.5 cm, which makes it difficult to search. For diagnostics, a colonoscopy and mesenteric angiography are used, and the affected sections of the intestine can be restessing. Sometimes an anchodisplicity of the intestines is associated with a rare systemic disease, known as hereditary hemorrhagic teneangectasia, or Osler-Weber-Rendu Osler-Weber-Rendu. The so-called Dielafoy lesions (dielafoy) have a similar picture, which are most often localized in the stomach wall and lead to the development of bleeding. They are focal arterial or arteriovenous malformations of the submissible base of the stomach or intestine, resulting in the damage in this place of the mucous membrane.
Figure 7-91 Hemorrhoids, Appearance
B area of \u200b\u200bthe anus and perianally disposed of true (internal) hemorrhoidal nodes represented by advanced veins (cavernous calves) of the submucosal bases that dropped from the distal repayment of the ampoule of the rectum. Hemorrhoidal nodes are predisposed to thrombosis and breaking the wall with the formation of hematoma and the development of bleeding. External hemorrhoidal nodes are formed above the cross-fifth groove, as a result, acute hemorrhoids occurs with localization along the edge of the anal ring. A long-term increase in venous pressure leads to the expansion of the veins. With hemorrhoids are characterized by anal itching and bleeding during a defecation or immediately after it. Blood in feces is usually bright red, scarlet. Another complication is the loss of the rectum. Hemorrhoidal nodes can be expanded. In the result of healing processes, the organization of thrombied hemorrhoidal nodes occurs and a fibrous polyp can be formed in the field of anal opening.
Figure 7-92 Hemorrhoids, Endoscopy
B areas of anorectal compound are hemorrhoidal nodes having a type of polyp (a). The vessels are wrung and have signs of thrombosis, at least partial. The outer surface of the walls of the vessels, which are included in the nodes, whorescent shade. The prerequisites for the development of hemorrhoid are chronic constipation, low fiber diet, chronic diarrhea, pregnancy and portal hypertension. Hemorrhoids are relatively rare in persons younger than 30 years.
Figure 7-93 Diverticular disease, appearance, section
B The wall of the sigmoid intestine (right part of the figure) is visible to be whoresal tapes of longitudinal muscles (♦), so it looks brighter compared to a nearby small intestine. Multiple rounded bluetic diverting (a), or diverticulous walls of the sigmoid intestine. The dimensions of the diverticulus are from 0.5 to I cm and are most common in the colon compared to the small intestine, striking its left left departments. The diverticulus is more often diagnosed in residents of developed countries, which is due to a diet with a low content of fibers leading to a decrease in peristaltic and increased intranacious pressure. The frequency of the disease is growing with age.
Figure 7-94 Diverticular disease, macropreparation
The thick intestine is opened longitudinally. The diverticulus have narrow stakes, open in the intestinal lumen. The dimensions of the diverticulus of the colon rarely exceed i cm in diameter. They are not true diverticulus, since their wall consists of only the mucous membrane and the submucosal base. Diverticulus have the kind of hernia-like protrusion, which are formed in the places of the acquired weakening of the muscular sheath of the intestine. Bo Time Peristaltics Diverticulus is not exempt from the carte masses that fill their lumen. The pronounced failure of the intestinal wall structures and increased pressure in the intestinal lumet contribute to the formation of multiple diverticulus, or diverticulose. The diverticulas of the colon rarely develop in persons younger than 30 years.
Figure 7-95 Diverticular disease, KT
With Abdominal KT at the level of the pelvis with a contrast gain, diverticulosis (♦) was revealed, the most pronounced in the sigmoid intestine. Small rounded digs have a dark color, since they are filled with wheel masses and air, not a contrasting agent. Most diverticulus are asymptomatic. Complications are developing at about 20% of the observations of the diverticulosis and are manifested by pain in the abdomen, constipation, periodic bleeding, inflammation (diverticulitis) with possible perforation and peritonitis.
When colonoscopy in a sigmoid intestine, two diverticulus are visible, which revealed by chance. The complication of the diverticulus is inflammation, which usually begins in the narrow region of the cable of the diverticula, leading to erosion of the mucous membrane and the appearance of painful sensations. Further development of inflammation leads to a diverticulite. Possible manifestations of diverticular disease are grabs-like pain in the lower abdomen, constipation (less often - diarrhea), rare periodic bleeding. Di-vertical and diverticulitis can cause iron deficiency anemia. Sometimes pronounced inflammation can develop, exciting the wall of the diverticulus and leading to perforation and peritonitis.
Figure 7-97 hernia, appearance, section
Outdoor hernias are made of peritoneum through defects or weak sections of the abdominal wall. Most often it happens in pakhova region. Similarly, the umbilical hernia can also develop, presented in this picture. The inner hernia in the abdominal cavity is formed during adhesive disease as a result of the formation of anomalous holes between spikes. Such holes can be so big that they pass the seaflings and hinges of the intestine. When opening the anterior abdominal wall, a small hernia bag (*) was revealed, which contains the adipose tissue of the large gland. The intestinal loop in the pure hernia can be moving, passing through the hernia, both inside the hernial bag and outward. In case of a non-commissioned or progressive hernia, the ranks of the intestine may occur with the subsequent decrease in the blood supply and development of the ischemia of the intestine.
Figure 7-98 Spikes, Appearance, Section
Between the loops of the small intestine, spikes were formed having a type of fibrous seewer. Most often, the spikes are formed after operations on the abdominal organs. Multiple spikes also occur after peritonitis. Spikes can lead to obstruction of the intestine loops during localization of them in the inspection bags, which are formed due to the adhesive process. In patients who have had an operation on the abdominal cavity about acute appendicitis, spikes in the peritonean cavity are the most common cause of intestinal obstruction. The presence of scars on the abdominal wall in patients with sharp bellyThe symptoms of expanding the lumen of the intestine and intestinal obstruction make it possible to assume adhesive disease.
Figure 7-99 Invagination, macrolections
Invagination is a rare form of intestinal obstruction, at which the proximal segment of the intestine in the lumen of the distal one occurs. Breasting violation in this sector of the intestine leads to a heart attack. HA left drawing is an open leased section of a dark red intestine, inside of which an invalid integration segment is located. HA with the right figure is a cross-section of invaginate, having a peculiar type of intestine in the intestine. In children, such a condition is, as a rule, idiopathic. In adult patients, peristaltics during polyps or diverticulas can lead to invagination.
Figure 7-100 Invagination, KT
HA KT abdominal cavity is visible to the thickened part of the small intestine, having a type of target (▲), due to invagination, when one sector is located in the opening of the other. With the radiography of the abdominal cavity, extended loops of the small intestine, air-liquid bowls, which are signs of intestinal obstruction are revealed. Patients have abdominal pains, the voltage of the anterior silent wall, constipation, as well as the weakening or anomaly of intestinal noise in physical examination.
Figure 7-101 Coloring of the intestine, appearance, section
When the intestine is breaking, the blood supply to the intestine leading to its ischemia and heart attack. Violation of venous outflow leads to stagnation of blood. B Case early diagnosis The intestine can be promoted with blood supply to normalization, but it happens infrequently. HA Figure is visible to break (*) mesenter of the small intestine, as a result, the latter on the site from the skinny intestine to the ileum underwent ischemia and is dark red due to the developed infarction. The breakthrough is a rare disease, more often occurs in adult patients and with the same frequency affects the small intestine (around the axis of the mesentery), and the colon (sigmoid or blind intestines that are more mobile). The small children have almost always amazed at the breakthrough, the small intestine is almost always amazed.
A slightly size adenomatous polyp is visible in the left colon department. The polyp is an education that performs above the surrounding mucous membrane. It can be on a leg or located on a wide base. The polyp has the structure of the tubular adenoma and is built from rounded newly formed gloys. The outer surface of the polyps is smooth, the boundaries of the neoplasm are clear. Usually polyps are found in adult patients. Adenoma is a benign precursor of adenocarcinoma. Adenomas of small sizes are almost always benign, with more than 2 cm, the risk of maligination increases significantly. B such adenomas reveal Mutations of APC 1 SMAD4, K-RAS 1 P53 genes and age disorders of DNA genes accumulated over the years.
Figure 7-103 Adenoma, Endoscopy
At colonoscopy, the rectal polyps were revealed, which have the structure of tubular adenomes. HA Left Figure Polyp has a view of a rounded formation on a small leg with a smooth outer surface. HA with the right drawing of the adenoma has a bble sizes, the abundance of vessels is determined on the surface, which explains the presence of hidden blood in the feces of patient.
Figure 7-104 adenoma, micro
The colon adenoma is a benign tumor, built of newly formed glands and villings lined and covered with dyslastic epithelium. This small polyp on a short leg is a tubular version of the adenoma. It is characterized by the accumulation of disorganized rounded ferrous structures, differing from glands in the surrounding unchanged mucous membrane of the colon in shape and at a smaller number of glass-shaped cells. Cells, lining glands are tightly located, their kernels are hyperchromic. B The same time, this small benign neoplasm is highly differentiated and limited, there is no invasion of the tumor into the polypa leg. The accumulation of additional mutations during the continuing growth of the polyp increases the risk of malignancy.
Figure 7-105 Hyperplastic Polyp, Colonoscopy
HA both drawings are visible small, not more than 0.5 cm in diameter, flat polyps of the mucous membrane. They are tumor-like formations constructed from the enlarged crypt of the mucous membrane. Most often they are observed in the rectum. The amount of polyps increases by age, while more than 50% of people have, at least, at least one such polyp. Hyperplastic polyps are not true neoplasias, there is no risk of malignization. It is unlikely that they can cause the appearance of hidden blood in feces. However, the most often polyps develop in patients with tubular adenomas and can gradually increase in size. Hyperplastic polyps are usually random finds when conducting colonoscopy.
Figure 7-106 Polyp Petez-Jershs (Peutz-Jeghers), Endoscopy
Peteza-Jersey syndrome includes a combination of focal hyperpigmentation of the skin and mucous membranes with gamarten polyps in the gastrointestinal tract. Polyps may occur in all departments of the gastrointestinal tract, but mainly in the small intestine. HA Figure shows the small duodenal polites identified during endoscopy, which during biopsy was diagnosed as a gamartomic. This rare auto-dominant disease may be associated with polyps in any other gastrointestinal tract departments. Patients with this syndrome have an increased risk of developing malignant neoplasms in various organs, in particular in the mammary gland, ovaries. The testicles, concubine gland, but the polyps themselves are not mistaken. Lentginal pigmentation type of freckles is observed mainly on the mucous membrane of the mouth and cheeks, in the field of genital organs, brushes and stop. Polyps can achieve sufficiently large sizes and cause the intestine or invagination obstruction.
Figure 7-107 Village (Willeznaya) Adenoma, MacrousPares
HA left drawing shows a puffed adenoma, having a view of cauliflower, on the right figure - the type of tumor on the cross section of the intestine. The puffed adenoma has a wide base of attachments, not a leg, and large dimensions compared to a tubular adenoma (adenomatous polyp). The average diameter of the vintage adenomes is several centimeters, but can reach and 10 cm. Village adenoma of large sizes have an increased risk of developing adenocarcinoma. Polyps constructed from tubular and porcered structures are called tubulum-free (tubullastic) adenomas.
Figure 7-108 Village (WILLOM) adenoma, micro
HA left drawing shows the edge of the vile adenoma, on the right - a plot over the basal membrane. Appearance color cabbageis due to the presence of elongated ferrous structures covered with dysplastic epithelium. Village adenomas are less common than adenomatous polyps, in them with the greatest probability (about 40%) can "hide" invasive carcinoma.
Figure 7-109 hereditary non-polisher carcinoma colon, macro production
The hereditary non-polisher carcinoma of the colon (NSPTK), or Lynch syndrome (Lynch) 1 has a genetic nature and develops in the right sections of the colon in young patients. NNPCTK is combined with extraordinary malignant neoplasms (endometrial, urinary tract) and is associated with gene mutations, leading to an abnormal level of expression of HMLHL and HMSH2 proteins. B tumors combined with NSPTK, reveal microsatellite instability (with sporadic cases it is 10-15%). These ony are characterized by a much smaller amount of polyps compared to family adenomatous polyposis associated with APC mutations, but the polyps have a more aggressive flow. HA Figure shows multiple polyps of a blind intestine (right is the terminal department of the ileum).
Figures 7-110, 7-111 Family adenomatous polyposis, macro production
With family adenomatous polypose, the Mutation of the APC genes leads to the accumulation of β-catenin with its translocation into the kernel and activation of the transcription of MYC and Cyclin DL genes. This is an autosomal dominant pathology, leading to the development of more than 100 polyps on the gum mucosa in adolescence (right drawing). Almost all patients develop adenocarcinoma, if not to take into account the observations of total kingctomy. A more gently underlying form (left drawing) is less common, characterized by a greater variability of the number of polyps and the development of colon cancer at older age. In the Gardner syndrome (Gardner), there is also a mutation of the APC gene, but at the same time, the polypose syndrome is accompanied by osteomes, periampular adenocarcinoma, cancer thyroid gland, Fibromatosis, teeth anomalies and epidermal cysts.
HA drawing on the right is represented by adenocarcinoma, which has developed from the vilitary (villezny) adenoma. The surface of the tumor is polypovoid, reddish-pink color. Bleeding from the surface vessels of the tumor is detected using a positive guveau sample for hidden in feces. This tumor is usually localized in a sigmoid intestine, which does not allow it to reveal it with a finger study. However, it is relatively easy to recognize during sigmoscopy. Roeteitmgo Narcipte Pliste Khimym is preceded by the RVLiOobroeees to the Toptemekma Mutation, including ARS / $ - Catenin Carcercine, Loss SMAD and P53, activation of telomerase, microsatellite instability.
Figure 7-113 adenocarcinoma, macro-treatment
Due to the exofite growth of the tumor, obstruction (usually partial) lumen of the colon, which is one of the complications of adenocarcinoma may occur. Violations of the chair and digestion can also be due to the tumor.
Figures 7-114, 7-115 Adenokarcinoma, Endoscopy
Detected in colonoscopy adenocarcinoma colon. HA left drawing in the educational center there are ulceration and hemorrhage. The presence of these changes explains the need to study the feces on the hidden blood under this pathology. HA with the right drawing, the tumor-like formation of large sizes led to partial obstruction of the intestinal lumen.
Figures 7-116, 7-117 adenocarcinoma, enema with barium and kt
The equipment of the belly with Barium is to be introduced by drops of X-ray-contrast barium suspension into the colon, as a result, the intestine wall is determined and its neoplasms. HA left drawing in the transverse and downstream colon is presented two ring-shaped formations (*) having the morphological structure of adenocarcinoma and led to narrowing the intestinal lumen. HA with the right figure in a stretched blind intestine at KT abdominal cavity with contrasting revealed, large neoplasm (♦) was revealed, which is adenocarcinoma. Cancer blind intestine often reaches large sizes. Its first manifestation may be iron deficiency anemia due to blood loss.
Figures 7-118, 7-119 adenocarcinoma, micro
HA left drawing - adenocarcinoma. Tumor glands of an elongated branching form resemble the leaves of the fern and are similar to the structures of the vile (willest) adenoma, but significantly more disorganized. The nature of growth is predominantly exofic (in the intestinal lumen), invasion in the picture is not visible. The determination of the degree of malignancy and the tumor stage occurs in the study of a plurality of histological sections. With a large increase (right figure), the kernel of tumor cells is hyperchromic and polymorphic. Normal glazing cells are absent. A number of genetic mutations can be preceded by the development of colon cancer. The mutation of the APC gene can be noted, as well as K-RAS, SMAD4 and P53 mutations. It has been established that with various solid malignant neoplasms, including the adenocarcinoma of the colon, the receptor of the epidermal growth factor (EGFR) can be detected. For the treatment of an adenocarcine of colon expressing EGFR, monoclonal antibodies against EGFR can be used.
Figures 7-120, 7-121 Carcinoid, macro-preparation and microprelarate
Tumors of the small intestine - rare neoplasms. K benign tumors of the small intestine include leomiomes, fibromes, neurofibromes and lipomas. HA left drawing in the region of the ileocecal damper is a carcinoid tumor of light yellow color. Most benign tumors are submissible formations that are randomly identified, although sometimes they can be quite large and lead to obstruction of the intestinal lumen. HA with a right figure with a large magnification, a microscopic pattern of carcinoid is presented, which is constructed from nest clusters of rounded endocrine cells of small size having small rounded kernels and pink or pale blue cytoplasm. Sometimes malignant carcinoid has large sizes. With carcinoid with metastases in the liver, the so-called carcinoid syndrome may occur.
Figures 7-122, 7-123 Lipoma and Non-Hodgkinskaya Lymphoma, Macrous
HA left drawing There is a small yellowish subserosaceous formation - a lipom of a small intestine, identified by chance during an autopsy. It is built of cells of mature adipose tissue. Benign neoplasms are constructed from cells close to the structure of the cells of the maternal tissue, are characterized by clear boundaries and slow growth. HA with the right figure in the mucous membrane of the small intestine is visible multiple uneven formations of reddish and brown and brown - non-Hodgkinskaya lymphoma, developed in a patient AIDS. AIDS lymphoma are highly differentiated. On the other hand, the pathology of the lymphoid fabric associated with the mucous membrane is sporadic, in the stomach, it can be associated with chronic infection with Helicobacter pylori. More than 95% of the lemph of the gastrointestinal tract occur from B cells. The wall of the affected intestine thickens, the peristalistic is broken. Limphomes of large sizes can be expanded or cause obstruction of the gut.
Figure 7-124 Acute appendicitis, KT
The increased worm-shaped exhaust (A) is visible with a hiding stone having increased brightness due to partial calcinosis. The blind intestine (left) is partially filled with bright contrast. A worm-shaped process located distal than calm stone has a dark clearance due to air availability. There are more striking areas corresponding to the inflammation sites, exciting the surrounding fat tissue. In patients with acute appendicitis, characteristic symptoms are a sudden beginning with acute pain, which is localized in the right lower abdominal quadrant, and sharp pain in palpation of the anterior abdominal wall. Blood is often marked leukocytosis. W. this patient There is an increased operational risk due to obesity (pay attention to the thickened subcutaneous fatty fiber of dark color).
Figure 7-125 Acute appendicitis, macropreparation
Presented a lessed worm-shaped process after a laparoscopic operation. HA serous shell is a brownish yellow exudate, but the first major signs of acute appendicitis are edema and hyperemia. In this patient, there was an increase in temperature and an increase in the number of leukocytes in the blood with a shift of the formula to the left (an increase in the number of segmented neutrophils). In addition, the patient had weak abdominal pain and severe pain in the side due to the retrocecal arrangement of the process.
Figure 7-126 Acute appendicitis, micro
Acute appendicitis is characterized by pronounced inflammation and necrosis of the mucous membrane. HA Figure shows an abundance of neutrophil granulocytes, which infiltrate the entire thickness of the appendix wall. In peripheral blood, it often marks an increase in the number of neutrophils with the shift of the formula to the left. Surgical removal of the inflamed duct-like process must be carried out before the development of potential complications in the form of perforation of the process and sepsis. With the localization of inflammation only in the serous shell (periappendiscitis), the primary focus of inflammation is apparently located in another department of the abdominal cavity, and the progestion in this case is not involved in inflammation.
Figure 7-127 Mukocele Appendix, Macrobreparation
The lumen of a worm-like process is sharply expanded and filled with a transparent viscous mucus. A persistent Mukocele is perhaps a true tumor, most often a mochinous cystademic, and not just obstruction of the process. When the wall is broken, the mucus falls into the cavity of the peritoneum, which is accompanied by the symptoms of the tension of the abdominal wall. Similar changes in the name of the pseudomyxomy of the peritoneum may also occur with the Music Cystaudicarcinoma of Apandix, colon or ovaries, but they are distinguished by the presence of cancer cells in mucus.
Figure 7-128 Perforation with free air, KT
The abdominal cavity is visible freely located gas bubble (♦) as a result of perforation of the hollow organ. Inflammation with the ulceration of the intestine, the stomach or gallbladder may complicate perforation. The presence of free air is a sign of a rupture of a hollow organ or perforation. HA Figure is also visible ascitic fluid to the right of the liver forming an air-liquid level (A). The perng may develop and OCA execution (spontaneous bacterial peritonitis). It is usually developing against the background of ascites, which is more likely to be at nephrotic syndrome in children or in chronic liver disease in adults.
Figure 7-129 Peritonitis, Appearance, Section
Perforation in any departments of the gastrointestinal tract (from the bottom of the esophagus to the colon inclusive) can lead to peritonitis. HA autopsy has been detected exudate in the form of thick yellowish purulent overlaps on the surface of the peritoneum. The contamination of the abdominal cavity can cause various microorganisms, including enterobacteria, streptococci, clostridium. Ovarian cancer caused the obstruction of the sigmoid gut and its perforation. Sigmoid colon The gray-black color is noticeably expanded and localized in the pelvis cavity. Peritonitte can cause the development of functional intestinal obstruction due to paralytic IleusIt is revealed in a radiographic study in the form of extended intestinal loops with air-liquid levels.
Topic 4. Diseases of the esophagus, stomach and intestines.Relevance of the topic. The knowledge of the theme is necessary for the study of gastritis, ulcerative diseases of the stomach and 12-rosewood, appendicitis on clinical departments and in the practical work of the doctor for clinical and anatomical analysis of the data of the pathoanatomic opening and studying the biopsies of the patient.
The purpose of the lesson. Disassemble pathogenesis, morphological manifestations and main complications, and the outcomes of the above pathological processes. To understand the principles of classifying these diseases, learn to differentiate them when studying macro and microscopic drugs.
№ 23. Chronic fibroplastic (slotting) glomerulonephritis with an outcome in nephrosclerosis. Describe the size of the glomers, the condition of the capsules. Describe the condition of the tubules and the stroma of the kidneys.
№ 29. Non-necrotic nephrosis. Describe changes in the epitheliums of the proximal tubules: a) in the cytoplasm, b) in the nuclei.
№ 53. Proliferative intracapillary glomerulonephritis. The size of the glomers is increased due to the proliferation of endothelial and merzangial cells. The lumen of the Bowman capsule is narrowed. The epithelium of the proximal tubules edema, extremal capillaries - with pronounced hyperemia.
III. Explore the electronogram:
No. 13. Immunomorphology Glomerulonephritis. Pay attention to the deposition of immune complexes under the basal membrane capillaries of the glomeruli.
Situational tasks
Task 1. At the opening of a woman with age of 56 years, which died from renal failure, the kidneys are unevenly reduced in size, the surface is large-born; At the autopsy - plots of scar tissue alternate with the unchanged parenchyma, the lochanks are expanded, the walls are thickened. Microscopically in the walls of lochanks, cups and in the interstation - phenomena of sclerosis and lymphoplasmocyte infiltration.
What is the diagnosis of most likely?
Task 2. In a child of 15 years, after 14 days after the suffered angina, edema appeared in the morning, an increase in blood pressure, urine in the form of "meat oots". The immunohistochemical study of the kidney bioption showed the deposition of immune complexes in the basal membranes of capillaries and in Mesangia of the glomeruli.
What disease developed in a patient?
Task 3. Have a man of 42 years old who sick heavy form abdominal typhoidA sharp renal failure has developed from which he died. With autopsy: the kidneys are increased in size, swelling, the fibrous capsule is easily removed; At the autopsy - a pale gray bark, the pyramids are dark red. With histological examination - in most tubules, the lumen is narrowed, epithelial cells are increased in size, do not contain cores; Clubs are collaborated; in stroma - swelling, small leukocyte infiltration, small hemorrhages.
Indicate the kidney pathology, which is a morphological substrate of acute renal failure in this case.
Task 4. On autopsy deceased from renal failure, it is noted that the kidneys are increased, dense, the bark is wide yellow-gray with a red grip. With a microscopic study, the epithelium of the glomerulum capsules proliferates with the formation of "lunk", capillary loops with necrosis foci and fibrin thrombami in the lumen.
What disease led to the patient's death?
Task 5. On autopsy men 62 years old, gray-earth leather with fine-point hemorrhages, face - as if powdered with a whitish powder, fibrinous hemorrhagic laryngitis, tracheitis, fibrinous pericarditis, gastritis, enterocolit.
For which pathology is characterized by this complex of morphological changes?
Description of macropreparats
Figures of micro-preparations
386. Chronic stomach ulcer.
On the small curvature of the stomach, the ulcerative defect is visible to 1 cm in diameter, bottom and edges dense, rolic-shaped.
108. Chronic stomach and 12-rosisse ulcers.
On the mucous membrane of the stomach and the 12-repulitory intestine, 3 ulcerative defects in the stomach of the ulveneous shape with imputed dense edges and a dense bottom are visible. In a 12-risen intestine of 2 ulcers of a rounded form, located against each other ("kissing ulcers"), in one of them perforated hole
128. Melena (bleeding in the gastrointestinal clearance).
Black gloss mucosa (pigment salty hemathine, methemoglobin, sulfur iron)
149. Swifts of stomach cancer. 184. SKIRR stomach.
Stomach cancer.
Ex-and endophyte growth.
146. Non-specific ulcerative colitis.
On the mucous membrane of the colon multiple ulcerative defects
various shapes and sizes.
A. Polypoid cancer.
75b. Myoma stomach.
Examine microspections:
62a. Chronic stomach ulcer (aggravation stage).
In the bottom of chronic ulcers, 4 layers are distinguished:
1) On the surface of the ulcerative defect there is a necrosis area with leukocytes, 2) under it - fibrinoid necrosis, 3) below the zone of granulation tissue is visible, followed by 4) the sclerosis zone with lymphoid infiltrates and sclerized vessels.
90. Acute purulent appendicitis (phlegmozno-ulceal).
(see simultaneously drug 151. Normal appendix)
All layers of the process infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosal shell, full-blooded vessels and hemorrhage
177. Chronic appendicitis with the regeneration of the mucous membrane.
The wall of the process is thickened due to the growth in all layers of fibrous connective tissue, the newly formed low cubic cells of the epithelium are enclosed on the ulcerative defect
140. Cholecystitis.
The wall of the gallbladder is thickened due to the sprouting of the connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophic
74. Solid stomach cancer.
Parenchima and stromium in tumors are uniformly developed. Parenchima is represented by atypical cells forming cells. Anaplazated epithelium proliferates, it germs outside the mucous membrane - infiltrating growth
And t (drawings):
T e s t s: Select the right answers.
433. The causes of acute gastritis are:
1- alcoholism
2 - infection
3- Swallowing of traumatic substances
434. The following changes are characteristic of atrophic gastritis:
1- mucous pink, with well-pronounced folds
2- mucous pale
3- in the stomach a lot of mucus
4- focal regeneration of the epithelium
435. The main heavy complication of the stomach ulcers is:
1- lymphadenitis of regional nodes
2- perforation
3-perigastrites
4- "inflammatory" polyps around ulcers
436. The most characteristic changes in vessels in the bottom of chronic ulcers are:
1- Inflammation and sclerosis of the wall
2- full-range
3- Malokrovia
4- large thin-walled sinusoidal vessels
437. To the local factor having a value in the pathogenesis of ulcerative disease of the stomach and duodenum, refers:
1- infectious
2- trophic violation
3- toxic
4- Reducing the secretion of gastrin and histamine
5-exogenous
438. Layers of the bottom of chronic stomach ulcers are:
1- Exusudate
3- granulation fabric
4- sclerosis
439. Many stomach erosions from the burn coated with salty hematine detected at the opening of the deceased. Erosion formed:
1- to burn
2- During burn
440. On the gastric mucosa, the liquid of the coffee form. When cleaning from it, dotted hemorrhages and defects with a magnitude with a pin head are visible. Specify the name of the process:
1 - Petechia
3-sharp ulcers
441. At opening in the stomach, two round ulcers were found, located on a small curvature, the edges are smooth, the bottom is thin. Ulcers are:
1-sharp
2-chronic
442. Signs of chronic ulcers are:
1- Repeated bleeding
2- dense sclerosed bottom
3- multiplicity of ulcers
4- one, two ulcers
443. The most frequent localization of the stomach cancer is:
2- big curvature
3- small curvature
444. The cancer tumor sprouts diffuse all the layers of the stomach wall, dense, the cavity of the stomach is reduced. Cancer refers to:
1- Differentiated adenocarcinoma
445. Women clinically defines dense ovarian tumors from two sides. It is necessary to investigate the presence of a tumor first:
1- in the lungs
2- in the stomach
446. Acute gastritis is usually manifested in shape:
1- Atrophic
2- Hypertrophic
3-purulent
4- surface
5- with restructuring epithelium
447. For chronic atrophic gastritis, it is characteristic:
1- ulceration
2 - hemorrhage
3- fibrinous inflammation
4- enterization of the mucous membrane
5- Full-wheel and diffuse infiltration by leukocytes of the eaves of the mucous membrane
448. To exacerbate the stomach ulcers are characteristic:
1- hyaliosis
2 ENVERYSION
3- Regeneration
4- lymphoplasmocyte infiltrate
5- necrotic changes
449. The characteristic feature of Menetry disease is:
1- enterization of the mucous membrane of the stomach
2- chlorohydreenic uremia (gastric tetania)
3- Virkhov metastases
4- Giant hypertrophic folds of the gastric mucosa
5- Non-specific granulomatosis of the intestine
450. Ischemic colitis can be detected:
1 - at atherosclerosis
2- with sclerodermia
3- with diabetes
4- with rheumatic arthritis
451. Rectal changes are characteristic:
1- for ulcerative colitis
2- for Crohn's Disease
3- for Girshprung Disease
452. When maligning ulcerative colitis, the intestinal mucosa happens:
1- smooth
2- polypovoid (grainy)
3- atrophic
453. Malignation of adenomatous polyps is often found:
1- in basal departments
2- in surface departments
3- in the middle departments
454. Family multiple colon polyposis is detected more often:
1-9 from birth
4- at the end of the first year of life
5- after 3 years
455. The characteristic histological signs of Wipple disease are detected:
1- in the lungs
2- in myocardium
3- in the liver
4- in kidneys
456. The most characteristic histological sign of Wipple disease:
1- hemorrhage
3- macrophageal infiltrate
4 leukocytosis
457. A depleted patient is suspected of cancer. Above the left brace is tested by an enlarged, compacted lymphatic node. Must be examined primarily:
2- stomach
3 - esophagus
458. Appendix is \u200b\u200bthickened in the distal department, serous cover is dim, hyperemic, in the lumen of the carte masses and purulent exudate. Microscopically - diffuse infiltration of the wall by neutrophils, there is no ulcers. Appendicitis refers:
1- To the simple
2- to destructivative
459. Appendix is \u200b\u200bthickened in the middle segment, serous cover is covered with fibrinous films. Histologically against the background of diffuse infiltration of the entire thickness of the wall of the ulcer.
Appendicitis refers:
1- to phlegmosno-ulcene
2- to gangrenoz
3- to the simple
460. Appendix is \u200b\u200bthickened, serous cover is covered with fibrin, wall all over black, dim. Appendicitis refers:
1- to catroll
2- to gangrenoz
3- to phlegmonous
461. For abortive appendicitis, it is characteristic:
1- Inflammation is weakly expressed
2- Primary changes were sissing
3- inflammation plot is extremely small
462. The thickening of the mucus in the scorerized appendix is \u200b\u200bcalled:
1 - Mukobovacednium
2- Moobcele
3- Melanosis
463. The characteristic signs of acute appendicitis are:
2 - serous exudate in mucosa and muscle shell
3- hyperemia
4- sclerosis wall process
5- Destruction of muscle fibers
464. Characteristic features chronic appendicitis are:
1- sclerosis of the walls of the vessels
2- sclerosis wall process
3-purulent Tales
4- lymphoplasmocyte infiltration
5-granulomas
465. The morphological forms of appendicitis are.
Cystitis during pregnancy: to cure and prevent repeated development can be pregnant during cystitis
Is it possible to make a pregnant cherry?
Cesarean without indications possible operation?
Cesarean section: from preparation for surgery before extracting from the maternity hospital What you need to make caesarean section
Menstrual-like bleeding in the middle of the cycle