Coloring hematoxylin and eosin. In the area of \u200b\u200bthe defect wall of the stomach, there is a fibrinous-purulent exudate (A), with a sub-lying extensive zone of fibrinoid necrosis (b), on the rubbing tissue (B) and the growth of rude-lines connective tissuepenetrating the different depth of the muscular layer (g). The serous sheath of the stomach wall is preserved (e).
2. Chronic atrophic gastritis.The color of the hem
toxyl and eosin. In the mucous membrane of the stomach of the citric epithelium (a) and the epithelium glands with reorganization
schai glands on intestinal type - "intestinal metaplasia" (b), in its own plate mucosa of the sclerosis field
(c) and lymphoplasmocyte infiltration with formation of lymphoid follicles (g).
3. Adenokarcinoma.Coloring hematoxylin and eosin. All layers of the stomach wall infiltrated tumor tumor-New with signs of cellular atypism (a). Multiple pathological mitoses are visible in hyperchromic (b) and lurry-free tumor cells (B).
4. Gastric mucous cancer.Coloring hematoxylin I.
eosin. Tumor tissue is represented by an abundance of large atypical "pisteless" cells (a) with the formation of a large amount of mucus (b). The infiltrative ha-racter of tumor growth (B) is visible. Demonstration.
5. SKIRR stomach.Coloring hematoxylin and eosin. Companion of the stomach of the group of atypical cells with large hy-dust nuclei (a), in the stroma tumor, the growth of the locomotive connective tissue (b). Demonstration.
Macrobrerats.
1. Acute catarrhal gastritis:in the preparation of the stomach, the mucous membrane is thickened, with high hyperemic folds, covered with thick viscous mucus, with pete-chailed hemorrhages. The reasons: Effective food, use of alcohol surrogates, anti-opening chill chemotherapy, burns with acids and alkalis, uremia, salmonellosis, shock, severe stress.
Complications:acute ulcers, transition to chronic gastritis. Exodus:restoration of the mucous membrane.
2. Erosions and sharp stomach ulcers:in the preparation of the stomach
the mucous membrane of the female, on the surface there are many-sided dotting hemorrhages and defects of the conical shape of various sizes, their bottom and edges of black. Erosion is localized within the mucous membrane, and the ulcers penetrate
kyut on various depth of the mucous membrane, some reach the muscular shell.
The reasons:endocrine diseases (Solinger-Ellison syndrome, hyperparathyroidism), acute and chronic circulatory disorders, intoxication, allergies, chronic infections (tuberculosis, syphilis), postoperative, stey-ration and stressful ulcers.
Complications:perforation, peritonitis.
Exodus:erosion epithelizes, the ulcerative defect is replaced by a scar cloth.
3. Chronic ulcer Stomach during remission:in the pre-parat of the stomach, on a small curvature there is a pathological center in the form of deepening the mucous membrane, a rounded fortune, 3 cm in diameter. The folds of the mucous membrane radiosta converge to the defect, the edges of which are dense, rolic-shaped raised, cooked (caloric ulcer). On the cutting the inlet - the crater, less than the inner part of the ulcer. The edge, addressed towards the cardia, bezed, mucus-flock shell hangs over it. The region, facing a hundred-rone gatekeeper, gentle - terrace. The thickness of the ulcers is represented by the connective tissue, gray-white color, 2.5 cm. At the bottom of the ulcers, the vessels are scruised, the lumen is gaping.
The reasons:genetic predisposition, Helicobac-ter pylori, inflammatory and disperserateration changes in the mucous membrane, leading to the effects of peptic aggression factors (hydrochloric acid and pepsinogen).
Complications:perigastrate, bleeding, perforation, ne-non-prison, scar deformation of the stomach with the development of a wall behind the input or outlet. Against the background of chronic ulcers, the second disease can develop - the stomach cancer.
4. Polyps of the stomach (adenoma):in the antrotence department
the lodge has two tumor formations with sizes with pigeons, on thin legs, an incorrect oval shape with a porcedal surface, a soft consistency.
On the section, pathological neoplasms are abundantly vascularized and localized exclusively on the surface of the mucous membrane, not sprinkled to be fabric.
Complications:bleeding, twist legs, obturation, or inlet.
Exodus:malignation.
5. Various forms of stomach cancer.a) mushroom cancer:
on the surface of the mucous membrane, there is a tumor-like formation that is growing in the lumen of the stomach, the incorrect rounded shape with a size of 5 cm in diameter, on a wide base in the form of a mushroom cap, with an increase in the center. On the cut it can be seen that the tumor germinates the entire wall of the stomach.
b) Diffuse gastric cancer:the organ is reduced in size, the wall all over is thickened to 1 cm, a dense "de-ricycled" consistency, a gray-pink tissue is represented on the section. The mucous membrane is uneven, its folds of various thickness, serous shell Thickened, dense, buggy. The lumen of the stomach is narrowed.
c) Six stomach cancer:in a small curvature, there is a pathological center in the form of a towering over the surface of the mucous membrane of the formation with dense cuitive edges and a sealing bottom, sizes of 3.5 cm by 2.0 cm. The bottom is covered with gray-brown disintegrating masses. On the section, the tumor tissue infiltrates the entire body of the organ.
The reasons:meals (smoked meals, canned, pickled vegetables, pepper), biliary reflux (after the stomach operations, especially by Bilrot II), Helicobacter pylori. (contributes to the development of atrophy of the mucous membrane, ki-none metaplasia, epithelium dysplasia). Metastasiro: 1. Orthodox lymphogenicmetastasis in regional nodes in small and large curvature, retrograde Lim-Foenmetastases in the left inspection lymphhatic node - Metastasis Virchova, in ovaries - Krokenberg
cancer, paragrevy fiber - Schnitzer metastases, 3. Hematogenicmetastases in the liver, light, brain, bones, kidneys, less often in adrenal glands and pancreatic jelly. 4. Implantation - carcinomatosis of pleura, pericardium, diaphragms, peritoneum, glax.
Test control
Select one or more correct answers.
1. Signs of acute catarrhal gastritis
1) thickening of the mucous
2) Atrophy glands
4) mucosa sclerosis
5) neutrophilic infiltration mucous
6) Lymphoid infiltration of the mucous
2. Morphological forms of acute gastritis
1) fibrinous
2) Atrophic
3) Hypertrophic
4) Catarval
5) corrosive (necrotic)
3. Changes in the epithelium in chronic gastritis
1) Atrophy
2) intestinal metaplasia
3) hyperplasia
4) Dysplasia
5) The appearance in the cytoplasm Taurus Mallory
4. Characteristic features of chronic gastritis A
2) in the blood of autoantibody
to parietal cells
3) Helicobacter pylori -
5. Pathogenesis of pernicious anemia with autoimmune gastritis
1) termination of HCL generation
2) antibody products to Helicobacter pylori
3) antibody products to parity cells
4) antibody products to the internal factor
5) Destruction of glazed glaas and atrophy
6. The characteristic features of chronic gastritis in
1) Preferential Localization - Anthral Division
2) in the blood of autoantibody
to parietal cells
3) Helicobacter pylori -
the main etiological factor
4) accompanied by G-cell hyperplasia, gastrine
5) often combined with pernicious anemia
6) Localizes in the Foundal Department
7) reflux duodenal content in the stomach - the basis of pathogenesis
Sharp erosion of the stomach - this
inflammation of the mucous membrane
necrosis mucous membranes
muscular plate
3) Atrophy of the mucous membrane
4) sclerosis mucous membrane
5) necrosis capturing muscular layer
8. Clinical and morphological signs of chronic atrophic gastritis
In the stages of exacerbation
1) often occurs in patients with alcoholism
2) the mucous membrane is not changed
3) diffuse lymphoid-plasmocyte infiltration with significant admixture of Pyat
4) focuses of the pyloric and intestinal metaplasia
5) Increased acidity of gastric juice
9. Morphological substrate of ulcerative disease
1) Inflammation of the gastric mucosa
2) erosion of the gastric mucosa
and 12 pans
3) acute ulcer Stomach
and duodenal gut
4) Chronic recurrent gastric and duodenal ulcer
5) inflammation of the mucous membrane of the duodenum
10. Sclerotic stomach deformation is the outcome
2) diphtheritic gastritis
3) corrosion gastritis
4) phlegmonous gastritis
11. Signs of chronic atrophic gastritis as a precancerous disease
1) lymphoplasmocyte infiltration
2) sclerotic processes
3) Structural Perestroika Epithelia
(intestinal metaplasia)
4) all answers are true
5) all answers are incorrect
12. Ulzerogenic promoters
1) Corticosteroids
3) Aspirin
4) Smoking
5) Increased tone wandering nerve
13. The stomach ulcer disease belongs
1) Endocrine stomach ulcers
2) allergic ulcers
3) peptic ulcers
4) postoperative ulcers
5) tuberculosis ulcers
14. Local factors in the development of gastric ulcer disease
1) increase the aggressiveness of the gastric juice
2) Campillobacteria
3) the presence of chronic gastritis
4) circulatory disorder
5) all answers are true
6) all answers are incorrect
15. Causes of the development of acute stomach ulcers
1) Corticosteroids
3) Aspirin
4) Smoking
5) Increased tone
wandering nerve
16. Morphological signs of acute stomach ulcers
1) funnel form
2) Form of a truncated pyramid
on cross-cut
3) Soft uneven edges
4) dense carotine edges
7) multiple ulcers
17. Morphological signs of chronic stomach ulcers
1) funnel form
2) Form of a truncated pyramid
on cross-cut
3) Soft uneven edges
4) dense carotine edges
5) bottom of ulcers as it purified painted with salt-sized hematine black
6) The edge of ulcers addressed to the gatekeeper has the look of the terrace, the cardiac edge bends
18. Signs of chronic stomach ulcers
During the remission
1) the presence of exudate on the surface
2) scar cloth interrupts muscle shell at different depths
3) endovasculit
4) fibrinoid changes in the day and vessels
5) Surface epithelization
19. Signs of chronic stomach ulcers
In the period of exacerbation
1) The presence of fibrin-purulent exudate
on the surface 2) scar cloth interrupts muscle
shell at different depths
3) endovasculit
4) fibrinoid changes in the walls of blood vessels and in the bottom of the ulcers
12. Bleeding mechanism for ulcerative disease
arrosive
diapened
as a result of breaking the vessel
as a result of purulent melting
21. Chlorohydropenic Uremia - Result
1) bleeding from ulcers
2) chronic nephritis
3) penetration of ulcers
4) scar stenosis gatekeeper
5) all answers are true
6) all answers are incorrect
22. Peritonitis complicating chronic ulcer - result
1) Penetration
2) Perforation
3) Gastritis
4) Duodenita
5) scar stenosis gatekeeper
23. Complications of chronic ulcers
1) Penetration
2) Perforation
3) Empirea
4) Hypercallesemia
5) scar stenosis
and wall deformation
6) Bleeding
24. Types of gastropathy
1) Menieret's disease
2) Menelry's disease
3) Wandering Syndrome
4) Zollinger Ellison syndrome
5) hypertrophic hypersecreator gastropathy
25. Histological signs of gastropathy
1) Hypertrophy of the gastric mucosa
2) Atrophy of the gastric mucosa
3) Hyperplasia of the Pokrovnel Epithelium
4) Gyperplasia of ferrous epithelium
5) pronounced sclerosis
26. Morphological signs of inflammatory polypa
1) Inflammatory infiltration in stroma
2) atypical cells
3) without a clear differentiation of the leg and body
4) Irony epithelium dysplasia
5) erosion on the surface
27. Benign stomach tumors
1) Angiosarcoma
2) Adenoma
3) Leiomiomoma
4) adenocarcinoma
5) hyperplaziogenic polyp
28. Background for the development of the stomach adenoma
1) Chronic surface gastritis
2) acute erosive hemorrhagic gastritis
3) acute fibrinous gastritis
4) chronic gastritis with enterolyization
29. Adenoma is
1) benign tumor
from ferrous epithelium
2) malignant tumor from ferrous epithelium
3) epidermal cancer
4) malignant tumor of transit-cell epithelium 5) benign tumor from flat epithelium
30. Diseases with risk of cancer
1) Surface gastritis
2) chronic gastric ulcer
3) sharp erosive gastritis
4) chronic atrophic gastritis
5) adenomatous polyps
31. Histological options for gastric cancer
1) adenocarcinoma
2) Sarcoma
3) Pisnevenoid cells
4) undifferentiated
32. Clinical and morphological characteristics of an intestinal type stomach cancer
1) occurs more often under the age of 30
2) has a high degree of differentiation
3) develops against chronic gastritis
4) 2 times more often struck men
5) develops from metaplazed epitheliocytes
33. Clinical and morphological characteristics of diffuse type stomach cancer
1) develops from epitheliocytes
2) arises in a relatively young age
3) Histologically Pisnoid Cellular
4) arises against the background of chronic gastritis
5) has a low degree of differentiation
34. Prognostic feature for gastric cancer
1) Histological option
2) macroscopic form
3) depth of invasion
4) mucus formation
5) Secondary Changes
35.Gistological signs of polypovoid gastric cancer
1) atypical ferrous structures of bizarre
2) Pisnoid cells
3) abundance of mucus in the lumen of glands
4) Atypical polymorphic cells with large hyperchromic cores
5) Atypic cells that differ in monomorphism
36. Histological signs of pistened-shaped gastric cancer
1) are characterized by extensive hemorrhages
2) the nuclei of atypical cells are shifted
to cell membrane
3) low-differentiated cells with very large hyperchromic nuclei incorrect form
4) atypical ferrous structures
5) in the wall massive sclerosis and hyaline
37. Microscopic Characteristics of Squirry Cancer Stomach
1) atypical cells with large
nuclei are located groups
2) atypical cells form glands
3) massive sprouting of connective tissue
4) abundance of mucus in the lumen of glands
5) Atypic cells do not form glands
38. Krokenberg and Schnitzer stomach cancer metastasis
1) Hematogenic
2) implantation
3) lymphogenic orthograd
4) lymphogenic retrograde
39. Complications of gastric cancer
1) hemochkalny
2) dilatation of gatekeeper
3) Perforation
4) Exhaustion
40. Signs that are characterized by Wirch metastasis
1) Hematogenic metastasis
2) retrograde lymphogenic metastasis
3) peritonean carcroids
4) lesion of the left pressed lymphatic node
5) ovarian lesions
Standards Responses to Test Questions
Catad_TEMA Ulcerative Disease - Articles
Catad_TEMA Anesthesiology Resuscitation - Articles
Prevention of stressful erosive-ulcerative lesions of the gastroduodenal zone in patients in critical states
D.M. MA Evseev
MMA named I.M. Sechenov
The occurrence of acute erosive-ulcer damage to the mucous membrane of the gastroduodenal zone in patients in critical states, including in postoperative periodIt is, on the one hand, an extremely unfavorable, but natural consequence of available multisystem disorders and, on the other hand, a factor fundamentally worsening the patient's life forecast. According to M. Fennerty (2002), B. Raynard (1999), sharp erosion and ulcers in the gastroduodenal zone are revealed already in the first hours of patient's stay in the separation of intensive therapy in 75% of cases. According to V.A. Kubyushkin and K.V. Shishishin (2005), in the postoperative period, sharp ulceration of gastroduodenal mucous membrane, having clinical manifestations of no more than 1% of patients, are detected at openings in 24% observations, and with non-recreational esophagastrodenoscopy - in 50-100% operated on. 75% of acute ulcers are complicated by bleeding, while on esophagogastroscopy, signs of continuing bleeding are noted in 20-25% of patients. Acute ulceration of the mucous membrane of the stomach and duodenum develops over the next 3-5 days under the influence of provoking factors (operation, shock, sepsis, extensive burns, etc.). General mortality in the operated patients with the development of acute erosive-yazine damage to the stomach, complicated by bleeding, reaches 80%. The same authors are the main cause of the relevance of the problem discussed in the almost complete absence of clinical symptoms of erosive-ulcerative lesion and manifestation of the latter only by their complications, in the overwhelming majority of cases - gastroduodenal bleeding. At the same time, ulcerative bleeding even low intensity deteriorate sharply general state patients, which is manifested primarily by the disorders of central hemodynamics. Significantly later, local symptoms appear in the form of vomiting with blood or melan, which is observed only in 36-37% of patients.
A.A. Kurygin, O.N. Scriabin, Yu.M. Stall (2004) reported that with the help of systematic fibrogastroduodenoscopy, acute ulcenes were discovered in 64% of the operated patients who had increased risk of ulcerative formation. Even 6% of patients, this complication either appeared to an unexpected find in autopsy, or was detected by clinical signs. Gastrointestinal bleeding served as the main manifestation of sharp ulcers in the postoperative period in 60% of patients, of which in 33% it was massive, and at the same time only 13% of patients presented complaints about increased pain in the opposite region, nausea, sharp weakness, dizziness. In four cases, a faint condition is noted. More than half of all sharp ulcers (56%) is formed in the first three days and the more often the harder preceding surgical intervention and concomitant diseases. Acute ulceration of the gastric mucosa in more late time It is usually associated with complications of operation in the form of cardiovascular, renal and respiratory failure, as well as with purulent processes.
For the first time, the occurrence of acute erosive-ulcer lesion in the postoperative period was described by TH. BILLROTH in 1867, suggesting the existence of a causal relationship between operating injury and damage to the gastroduodenal zone. In 1936, G. Selye proposed the term "stress-ulcer" to designate the relationship between psychosomatic disease and a gastroduodenal ulcer. Currently near the authors (B.R. Gel Fand, A.N. Martynov, V.A. Guryanov et al., 2004) proposed the term "syndrome of acute damage to the stomach", which implies damage to the mucous membrane of the stomach and duodenal intestine Violation of the mechanisms of its protection in patients in critical states, and includes swelling and disruption of the integrity of the mucous membrane, as well as a violation of the engine-evacuator function of the stomach.
It should be borne in mind that the morphology and pathogenesis of acute erosive-ulcer damage to the stomach and duodenum differ in many ways from chronic gastroduodenal erosions and ulcers (L.I. Aruin, V.A. Isakov, 1998) (Fig. 1). Erosions Called defects of the mucous membrane, which do not penetrate the muscle plate of the mucous membrane. The most often erosion arising under the influence of stress factors is localized in the Foundal Stomach Department. Acute erosion can be superficial and deep. Surface erosions are characterized by necrosis and rejection of the epithelium, localized on the vertices of gastric rollers and are usually multiple. Deep erosion destroy their own plate mucous membrane, not capturing the muscular plate. The microscopic pattern of sharp erosions is not characteristic of damage to the mucosa with an acidic peptic factor of the gastric juice, but is a consequence of trophic disorders. It has been established that the development of erosions is preceded by significant disturbances of microcirculation, which gives the basis to most morphologists to consider sharp erosion as ischemic infarction of the mucous membrane.
. A) Macropreparation: multiple acute stomach ulcers with bleeding; B) Microdrug of acute stomach ulcers, complicated by bleeding: necrotic masses of the bottom of the ulcer, unchanged muscular sheath, salt-oxidic hemathine
Acute ulcers Called defects (necrosis) of the mucous-submembered layer, propagating deep into the wall of the organ on the muscular shell and associated with the influence of a pronounced stress factor. You are dividing "postoperative" acute ulcers, "Yazv Kushing", "Jazv Koronga" has extremely historical interest, since morphological differences do not have these ulcers, and their treatment and prevention are universal. The sharp ulcers are usually multiple, localized predominantly in a small crision stomach, the diameter of the sharp ulcers usually does not exceed 1 cm. Microscopically, areas of granulation tissue in the depth of the gastric or duodenal wall, full-blooded, stakes, edema, thrombosis, hemorrhage, are detected. What testifies to vascular or, rather, the ischemic genesis of acute ulcerations.
Currently, most authors are supported by the concept of ischemic damage in the occurrence of stressful ulcerations in the gastroduodenal zone, arguing that the main cause of stress-ulcers is the inadequate blood supply to the wall of the stomach and duodenum. Improving the acidity of gastric juice becomes important only when the protective barrier is damaged earlier than local ischemia occurs. A.L. Kostyuchenko et al. (2000), N.A. Maystrenko et al. (1998) indicate that the result of the assisted effects of the resistant spasm of the vascular zone with a violation of both arterial perfusion and venous outflows is indicated. At the same time, the latter leads to stagnation of blood in the mucous-subliftedness of the layer of the stomach and duodenum, an increase in capillary pressure, intragrogenous loss of plasma, local hemokoncentration, followed by the appearance of microtrombosis. Synchronically discloses the preterminal arterio-venous shunts, which further aggravates the ischemia of the mucous membrane.
B.R. Gelfand et al. (2004) It is believed that the most pronounced microcirculation disorders in patients in critical states occur precisely in the proximal sections of the digestive tube due to the greatest content in their arteries of α-adrenoreceptors. In this connection, the main causes of the occurrence of gastroduodenal stress-ulcers are local ischemia, activation of free-radical oxidation in the insufficiency of antioxidant protection systems, reducing the content of prostaglandin E1, which are implemented by the occurrence of foci of typical ischemic necrosis. The restoration of the regional blood circulation after long-term hypoperfusion leads to a non-pilus impaired of the splashing blood flow, which, leading to the reperfusion syndrome, further aggravates damage to the gastroduodenal zone.
On the other hand, a number of authors adhere to a somewhat different point of view on the pathogenesis of stressful erosions and an ulcers of the gastroduodenal zone. So, V.A. Cuba Kin and K.V. Shishin (2005) It is believed that the main pathogenetic mechanism for the formation of erosive-ulcer damage is to strengthen the factors of intragastric aggression in relation to protection factors. The complex assessment of the acid-forming function of the stomach with the help of several methods (titration, intragastric and aiming ph-metry) showed that in the first 10 days after the operation, the maximum stimulation of the acid-forming function of the stomach occurs, and its "peak" falls on 3-5 days, that is, For the period of the most likely ulcerative formation. At the same time, the greatest increase in proteolytic activity is recorded in the field of the bottom - the places most frequently susceptible to the erosive-ulcer process. The study of night secretion, which is a particular case of basal secretion and reflecting, mainly the vagus phase, made it possible to establish the maximum increase in the acidity of the gastric juice in the first 4 h. It is interesting that the increase in free hydrochloric acid products is observed even in cases where akhlorhydria is registered on the eve of the operation. The authors argue that the specified reaction of the digestive system on surgical stress underlies the formation of early true stress YazvThe share of which accounts for about 80% of all ulcerations of the mucous membrane of the upper sections of the tract, resulting in the postoperative period. In the remaining 20% \u200b\u200bof cases of ulcers occur in the phase of dystrophy of the mucous membrane in a more long time after surgery, with a complicated monthly period of the postoperative period in the form of cardiovascular, renal and respiratory failure, as well as purulent and septic complications, leading to the development of polyorgan deficiency, one of the manifestations Which are just ulcers. The occurrence of sharp ulcerations of the mucous membrane of the stomach on a background no longer depends on the acid-peptic aggression.
It would be quite logical to doubt in the possibility of gastric hypersecretion in the conditions of stress activation of the sympathy-adrenal system in the oppression of vagal influences. But, as often happens, the pathogenesis mechanisms turn out to be at first not so obvious to us, and the evidence subsequently increases directly proportional to our awareness of the subject. Thus, in the context of this report, it should be noted that an indirect morphological confirmation of the eligibility of the point of view on the determining role of the acid-peptic factor is the fact of the presence in the bottom of the sharp ulcers (not always) areas of fibrinoid necrosis, which indicates the participation in ulcergenesis of acute oral-peptic ulcers factor a. Back in 1957, N. nechels and M. Kirsten in the experiment showed that acid production is in direct connection with the level of hypercapinia and the severity of metabolic acidosis, that is, it is compensatory in relation to disorders of acid-alkaline equilibrium by the mechanism.
It should be noted that the concept of the priority of the ischemic or acid-peptic factor in the pathogenesis of stress-ulcers are not mutually exclusive (Fig. 2). A provision seems to be quite logical according to which the ischemic damage to the mucous membrane of the gastroduodenal zone is a predisposing factor, and hydrochloric acid and pepsin - a factor producing. As indicated by A.L. Kostyuchenko et al. (2000), under the conditions of ischemia of the mucous membrane, the natural neutralization of hydrochloric acid becomes insufficient, and even at the usual level of acidic products, acidosis of the mucous membrane develops, which is easily subjected to a digestive action of pepsin. These changes are exacerbated under the influence of bile acid salts (duodenogastral reflux during violations of the stomach motility), to which the urban mucosa is particularly sensitive in the 4dal stomach department. Ischemia joins the activation of intraprometal and intricumenate proteolysis, which limits the possibility of forming full-fledged thrombus in arrine vessels of the bottom of the ulcer.
. Pathogenesis of gastroduodenal stress-ulcers
Thus, a number of circumstances become obvious. First, given the high frequency of erosive-ulcerative lesion of the gastroduodenal zone in patients in critical condition, the fatal effects of bleeding from stress-ulcers and almost complete absence of clinical symptoms of sharp ulcers, the only method of solving the problem is the prevention of erosive-ulcer lesion. Every surgeon and resuscitator is known not one sad clinical caseWhen on the background of the background with such labor to stabilization of the patient's condition, which suffered not one relaparotomy, "suddenly" is developing difficult to actually corrected hypotension, a "coffee thick" begins to receive a "coffee thick" with unchanged blood, the endoscopists are bred by their hands ("crying" the whole mucous Reliable endohemostasis is unlikely), and it is impossible to operate the patient due to the severity of the state. Secondly, taking into account the significance of the acid-panic factor for the occurrence of acute erosive-ulcerative damage to the gastroduodenal mucosa, pathogenetically reasonable will be preventive use in patients in the critical states of antisecretory drugs. Third, the pathogenetically reasonable method of preventing stressful damage to gastroduodenal mucosa will be applied medicinal preparations, improving hemoperfusion, contributing to an increase in the delivery of oxygen, as well as the activation of free radical oxidation in the mucosa of the digestive tube.
The question is natural from the point of view of a practical doctor: to whom and when preventive use of antisecretory preparations is shown? That is what is the objective criteria for the risk of stress-ulcers in the postoperative period and in patients in critical condition? Agree that retrospective data that "acute ulceration of mucosa is detected in 20-50% of those who died after various abdominal operations," are small help in solving daily clinical issues.
To date, the following risk factors for the occurrence of acute erosive-ulcer damage to gastroduodenal mucosa in patients in critical states are proven. artificial ventilation Lungs, long hypotension various origin, sepsis, hemokoagulation disorders (hypercoagulant and waf syndromes), liver and renal failure, as well as elderly and old age, malignant tumors, acute pancreatitis, hypovolemia, peritonitis, cardiovascular failure, exhaustion. The frequency of the occurrence of bleeding from sharp ulcers increases many times during extensive traumatic interventions, reaching, according to some authors, 60%. MB Yarustovsky et al. (2004) Indicates that the use of artificial blood circulation during operational interventions on the heart and mainstream vessels increases the frequency of bleeding from acute stress-ulcers in the postoperative period by more than 6 times compared with operations performed without artificial blood circulation. Nevertheless, the overwhelming majority of postoperative bleeding from the top departments digestive tract It develops in patients who have overwhelmed extensive surgical interventions over severe diseases of the hepatopancreatoobiliary zone (tumors and scar strictures bile ducts, primary and metastatic liver tumors, pancreatic tumors, pseudotumorous pancreatitis, gall-eyed disease complicated by jaundice, cholanthitis and choledocholiticiasis, pancreaticosis, etc.). Yu.I. Pathetko and A.G. Kotelnikov (2007) indicate that bleeding from sharp erosions and ulcers complicate the flow rate of the postoperative period in each tenth patient who has undergone gastropancratopodogenic resection. In this regard, the appropriateness is apparent to the allocation of specific risk factors for the development of acute gastroduodenal stress-ulcers. For this purpose, N. Stollman, D. Metz (2004) conducted a meta-analysis of several prospective studies: D. Cook et al. (1994) - 2200 patients in the postoperative period; P. Hastings et al. (1998) and R. Fiddian-Green (1993) - 100 and 564 patients in the separation of intensive therapy, respectively. Based on the analysis carried out by the authors, the following risk factors for the development of erosive-ulcer affects of the stomach in critical states are presented in descending order of importance:
- Respiratory failure C IVL lasting more than 48 hours
- Coagulopathy
- Long hypotension or shock
- Sepsis
- Liver failure
- Renal failure
- Operational interventions
- Burn disease
- Heavy injuries
- Acute coronary syndrome
- CNS damage
- Polyorgan deficiency.
B.R. Gelfand, A.N. Martynov, V.A. Guryanov, A.S. Bazarov (2004) cause more specific criteria for the occurrence of erosive-ulcerative stress-lesion of the stomach:
- IVL more than 48 hours
- Coagulopathy
- Acute hepatic insufficiency
- Pronounced arterial hypotension and shock
- Sepsis
- Chronic renal failure
- Alcoholism
- Treatment of glucocorticoids
- Long nasogastric intubation
- Heavy brain injury
- Burns are more than 30% of the body area.
It is obvious that the patient corresponding to one or more risk criteria for the occurrence of a gastroduodenal zone stress-ulcer needs a complex of preventive measures. At the same time, it is quite difficult to distinguish between these events for "specific" and "non-specific". Patients in critical condition are shown:
- correction of hypoperfusion and local ischemia of the gastroduodenal zone;
- an increase in the protective properties of the gastroduodenal zone mucosa and stimulation of its reparative potential;
- inhibition of gastric secretion.
Correction of hypoperfusion and local ischemia of the gastroduodenal zone are carried out using infusions of rheological solutions (solutions of hydroxyethyl stroke, refooliglucin, gelatinoly, emulsion of perfluorocarbons), oxygen-visiting media (perfluorocarbon emulsion, erythrocyte mass - in the presence of a proven hemic component of hypoxia), drugs, increasing mining, preparations, drugs, providing a compensatory effect on oxidative stress (calcium oxibutic, mafusol, ascorbic acid, tocopherol, piracetam).
Speaking about increasing the protective properties of the mucous membrane of the gastroduodenal zone, first of all, they mean the use of drugs with antacid and gastroprotective effects. Antacid preparations (magnesium hydroxide, aluminum hydroxide, calcium carbonate, magnesium trisilicate, sodium bicarbonate) implement its effect by neutralizing already available hydrochloric acid. However, the practical application of these drugs in patients in critical states revealed a number of significant drawbacks. First of all, the oral use of drugs in the patient in a critical condition (artificial ventilation of the lungs, the state after operations in the gastroduodenal zone, the paresis of the gastrointestinal tract) is technically very problematic, since it is necessary for an hourly administration of drugs. In addition, the separation of carbon dioxide in the process of the interaction of hydrochloric acid and carbonates can lead to stretching the stomach and regurgitation of gastric content in the trachea and bronchi (Mendelssohn syndrome, aspiration pneumonia). With systematic use of antacids, systemic alkalosis is possible.
The sukralfat gastroprotector does not have an acid-meal effect and has its own protective effect by forming a film on the gastric mucosa and duodenum. It should be noted that the formation of a polymer film from sublofate occurs only at pH below 4, which far from always occurs, and, in addition, the frequency of bleeding from stress-ulcers with the prophylactic use of sublofate, according to D. Cook (1998), was Twice above compared to that when using antisecretory preparations. However, Sukral Fat is still better than nothing.
Today, generally accepted the fact that the leading component of the prevention and pharmacotherapy of acute erosive-ulcerative lesions of the stomach is modern antisecretory drugs.
In the 70-90s of the twentieth century, H 2-blocks were quite widely used for the prevention of stress damage to the gastroduodenal zone. Based on the analysis of a large sample of patients in critical states in 1992, D. Cook concluded that the preventive use of H 2-blocks prevents sharp erosive-ulcerative lesions of the gastroduodenal zone much more efficiently of antacids and sucralfat. However, many authors indicate that achieving reliable control over the state of the gastroduodenal mucosa during prophylactic use of H 2-blocks is sufficiently problematic. So, B. Erstadt et al. (1999), M. Feldman (1990) lead data on a short antisecretoric effect of H 2-blocks, due to a short period of semi-liquefaction of these drugs. The same authors noted the instability of the antisecretory effect, manifested by a decrease in intragastric pH less than 3.5-4, both in the Bolus and with continuous mode of administration of drugs, including when a dose increases. P. Netzer (1999) explains this fact that the effect of "fatigue H 2 -receptors" is already on the first day of the start of therapy.
We want to draw the attention of readers for another feature of pharmacodynamics H 2-blocks, which is questionable by the expediency of their use for the prevention of stress-ulcers, namely, exacerbation of the ischemia of the gastric or duodenal wall due to the blocking of H 2 receptors of the arteries of the submembratus and muscular layers and, as Corollary, vasoconstrictions with a decrease in the volumetric rate of blood flow. Thus, n 2-blocks in patients in critical states, on the one hand, reduce the intensity of acid-peptic aggression, but on the other, the local ischemia is enhanced, which is the main pathogenetic factor in stressful ultercerenesis.
In addition, the use of H 2-blocks, especially in large doses, is extremely negatively affected by the disinfectivation function of the liver (the inhibition of the cytochrome R450 system), leads to the aggravation of already existing encephalopathy, which can be concerned, disorientation, delirium and hallucinoses. It should be remembered for the possibility of negative chron and inotropic effects, extrasystoles and an atrio-ventricular blockade due to the action of H 2-blocks.
It is obvious that the appearance in the wide clinical practice of proton pump inhibitors (IPP), which are the most powerful antisecretory drugs and possessing a favorable security profile, immediately attracted the attention of researchers the possibility of prophylactic use of these drugs in patients in critical states. Initially, an IPP was tested in the clinic with an oral administration - the suspension of the drug was injected with patients through a nasogastric probe. However, due to the small number of observations, the effectiveness of oral ipp for the prevention of stress-ulcers was not formally proven. In turn, I want to emphasize once again that attempts to oral administration of antisecretory drugs, including through a nasogastric probe in the form of suspensions, in patients in critical states (acute blood loss, sepsis, sharp heart or respiratory failure), in our opinion, initially Lained any meaning. It is connected with a number of circumstances. First, the proton pump inhibitors are acid-resistant compounds inactivating in contact with hydrochloric acid, which determines the need to conclude an active substance of oral molds of the IPP in a capsule or gelatin shell. The introduction of unprotected active form The IPP in the form of a suspension into the lumen of the stomach naturally leads to its inactivation. Secondly, since the absorption of IPP occurs in a small intestine, reduced due to blood loss, peritonitis or polyorganic insufficiency The motor activity of the digestive tube determines the pronounced decrease in the bioavailability of IPS. A. Dunn et al. (1999), D. Heyland et al. (1995) indicate that the IPP injected in the form of suspension may have unstable bioavailability and require patient adequate absorbative activity, which changes in critical states. Thirdly, to ensure the informativeness of dynamic endoscopic control, it is necessary to maintain the lumen of the stomach and duodenum "clean". In this regard, it should be recognized that only the parenteral administration of proton pump inhibitors is considered the only acceptable embodiment of antisecretory prevention of stressful erosive-ulcerative damage to the gastroduodenal zone.
The real possibility of the prophylactic use of IPPs in patients in critical states has appeared with the introduction into the clinical practice of omeprazole parenteral administration. Currently, another representative of IPP with the possibility of parenteral administration is available for clinical use - Pantoprazole (controls).
Pantoprazole is a highly efficient inhibitor H + / K + -ATF-Ase. The drug reduces the level of basal and stimulated (regardless of the type of irritant) secretion of hydrochloric acid in the stomach. As is known, the duration of the validity of the IPP depends on the rate of regeneration of new proton pumps, and not on the duration of finding the drug in the body. The average half-life of pantoprazole after its single intravenous administration at a dose of 40 mg is about one hour. Nevertheless, the suppression of the secretion of hydrochloric acid is preserved for about three days. This is due to the achievement of a certain balance between the number of newly synthesized proton pump molecules and the number of already inhibited molecules. The unit / in Pantoprazole dose provides fast (for 1 hour) dose-dependent inhibition of acidic products: with the introduction of 40 mg - acidic products decreases by 86%, 60 mg - by 98%, 80 mg - by 99%, and not only acidic acid decreases Products, but also the volume of gastric secretion. After intravenous administration of a standard dose of pantoprazole in 80 mg after 12 hours, the degree of acidity decrease is 95%, and after 24 hours - 79%. In a person, a half-period of the oppression of the secretion of acid after taking Lansoprazole is ~ 13 hours, omeprazole - ~ 28 hours and pantoprazole - ~ 46 hours. Consequently, Pantoprazole is caused by the longest oppression of the secretion of acid compared to the listed IPSs. This is due to the specific binding of it with a cysteine \u200b\u200blocated in 822, which is immersed in the transport domain of the gastric acid pump. Binding precisely with this amino acid determines the longest effect of pantoprazole compared to other IPPs (Fig. 3). This is an important factor, since the restoration of acid products is completely dependent on self-renewal of proteins of the proton pump.
. Advantages of controllers in patients with gastrointestinal bleeding (HCR)
Controls has a permanent linear predictable pharmacokinetic. Just doubling the dose of IPPs having nonlinear pharmacokinetics, their serum concentration will be either lower or higher than expected, i.e. She is unpredictable. This can lead to inadequate monitoring of acid secretion or affect the safety of the use of the drug.
A distinctive feature of the controller is its lowest potential. medicinal interaction. Pantoprazole's ability to interact with other simultaneously injected drugs is very small due to its low affinity to the metabolizing isoenzyme of cytochrome P-450 and passing in the II phase of the conjugation reaction. Pantoprazole is not included in the well-known metabolic pathways of interaction with other drugsIt is of fundamental importance for patients of intensive therapy offices receiving a large amount of drugs at the same time.
Metz D. et al. (2001) A study was conducted in the effectiveness of the use of pantoprazole for the prevention of repeated bleeding from peptic Yazv. Used two doses of pantoprazole - 40 mg 1 / day. For 3 days (low dose) and 40 mg, followed by continuous administration (8 mg / h) for 3 days (large dose). 168 patients with bleeding ulcers (forrest IA, IB and IIA) after endoscopic hemostasis by the introduction of adrenaline on a randomized principle was administered a large or low dose of pantoprazole. The frequency of recycling of bleeding for 72 hours in both groups was the same - 12% in the group that received a small dose, and 13% is a large dose. The need for blood transfusions was also the same with both types of treatment. The authors concluded that "both continuous B / in pouring pantoprazole after the injection of the initiating dose and the repeated introduction is equally effective for the prevention of re-ulcer bleeding." For the prevention of re-IDC after its primary stop, it is necessary to maintain ahhorhydria, which requires repeated injections or constant slow pantoprazole infusion. To this end, it is recommended to be permanent in / under the main dose of 8 mg / h.
The positive role of intravenously administered pantoprazole for the prevention of stress-ulcers in the departments of intensive therapy was also demonstrated in the study of ARIS R. et al. (2001), which is a retrospective analysis of the clinical use of an intravenous IPN form for a six-month period. Of 97% of patients who had a high risk of developing stressful ulcers, preventive effect Against the background of intravenous administration of 40 mg pantoprazole, once a day was achieved in almost 90% of cases. Only in 7% of cases it took treatment for ulcerative bleeding. A very important result of this study was the lack of indications of adverse effects and significant interactions of intravenously administered pantoprazole with drugs traditionally used with intensive care departments in urgent situations.
A number of researchers (based on more of theoretical conclusions) is a fear that increasing the intragastric pH can enhance the bacterial colonization in the rotoglot and appear by the risk factor for the development of nosocomial pneumonia. However, the works of W. Geus (2000), D. Cook and SowA. (1991, 1996, 1998) and M. Tryba et al. (1991) It is proved that the colonization of bacteria in the stomach rarely leads to the pathological colonization of bacteria in the rotoglot, and the risk of developing nosocomial pneumonia when using proton pump inhibitors does not increase.
To determine the prophylactic administration of proton pump inhibitors, it is advisable to use prognostic risk criteria for the development of gastroduodenal stress-ulcers proposed by D. Cook back in 1994 (Table 1).
Table 1. Significance of risk factors for the development of gastroduodenal stress-ulcers in patients in critical states
At the same time, if the sum of RR in a particular patient is equal to or exceeds the value 2, then the use of IPP V / V according to the scheme is shown: 40 mg twice a day Bolus or continuous infusion of the drug at a rate of 4 mg / h. If the sum of RR in a particular patient is less than the value 2, the use of IPP V / V according to the scheme: 40 mg once a day Bolus or continuous infusion of the drug at a speed of 2 mg / h.
In conclusion, we will focus on another aspect of the prevention of stress damage to gastroduodenalzones, namely, on the pharmacoeconomic significance of prevention. Domestic studies on this issue has not been conducted to date. On the contrary, foreign colleagues, for whom, the concept of adequacy of treatment is invariably included its value, demonstrated that in the absence of full-fledged prevention in patients with risk groups under stress ulcers, "the miser is forced to pay twice." So, S. CONRAD ET AL. (2002) indicate that when bleeding from stress-ulcer, the patient in the separation of intensive therapy is required, additional 7 hematological studies are required, 11 units of erythrocyte mass, at least two endoscopic studies. D. Heyland et al. (1995) under similar circumstances noted an increase in the period of finding a patient in the separation of intensive therapy to 11.4 days, and the required period of use of anti-rich agents - up to 23.6 days. B. ERSTAD (1997) noted that the average cost of treating one patient from the risk group on the occurrence of stress-ulcers without preventing stressful damage is $ 19850, and using antisecretory prophylaxis - $ 15812. Moreover, if the cost of prophylactic parenteral use H 2-blocks amounted to $ 2275, then the cost of using proton pump inhibitors is only $ 1417.
Thus, the high frequency of stressful erosive-ulcerative lesions of the gastroduodenal zone and the enormous figures of mortality during bleeding from stressful ulcers require bonded adequate prophylactic measures in patients in critical states. The main component of this prevention is preventive administration of risk group patients on the occurrence of stress-ulcers of parenteral forms of proton pump inhibitors.
Literature
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. For atrophic gastritis characteristic the following changes:
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. Characteristic features acute appendicitis are:
2 - serous exudate in mucosa and muscle shell
3- hyperemia
4- sclerosis wall process
5- Destruction of muscle fibers
464. Characteristic signs of 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.
- 1 The occurrence of pain
- 2Gastritis
- Suman disease
- 5pish and poisoning
- 6Odenitis and pancreatitis
- 7 Diagnostics and treatment
1 The occurrence of pain
With a sense of strong discomfort, consult with a specialist. An important aspect of diagnosis is to clarify the nature of pathology. Pain in the stomach is most often concentrated in the area of \u200b\u200bthe projection of the organ on the abdominal wall. This site is called epigastric. The pain in the area of \u200b\u200bthe stomach can be localized, spilled, irradiating, sharp, stupid, parotid, burning and cutting.
To establish the cause of its appearance, the intensity of the syndrome should be identified. In this case, the main characteristics of pain are determined:
- character;
- time of appearance;
- duration;
- localization;
- communication with meals;
- attenuation or gain when moving, after defecation or when the poses change;
- a combination with other symptoms (nausea, decreased appetite, vomiting, bloating).
The feeling of pain in the stomach in most cases is associated with the injury of the body. The most frequent reasons are:
- acute and chronic gastritis;
- stomach ulcer;
- the presence of polyps;
- damage to the mucous membrane in food poisoning (intoxication or toxicinfection);
- damage due to abdomen injuries;
- strong stress;
- intolerance to individual products;
- inhibit the mucosa by randomly swallowed objects.
Pain in the area of \u200b\u200bthe stomach may be due to other reasons. These include pancreatitis, ulcerative disease 12th intestine, colitis, enterocolitis, cholecystitis, dyskinesia bile paths, irritable bowel syndrome, appendicitis, heart disease.
2Gastritis
Self frequent reasons Pain in the stomach is a sharp or chronic gastritis. These forms of the disease are characterized by inflammation of the organ of the organ against the background of the effects of irritating factors. Quite often gastritis has an infectious nature. At the same time, the bacteria of Helicobacter pylori appear as a starting point. The disease occurs in children, young and older people. When the stomach hurts, in this case there is a place acute gastritiswhich is divided into simple, catarrhal, erosive, fibrinous and phlegmonous. If the disease becomes chronic, the atrophy of the organ is often developing. The main provoking factors of the occurrence of gastritis are:
- abuse of acute, fried, hot or cold food;
- alcohol consumption;
- smoking;
- infection with bacteria Helicobacter;
- random or intentional acid use or alkalis;
- uncontrolled medication (NSAIDs group drugs).
Gastritis symptoms are diverse. Children and adult discomfort in the area of \u200b\u200bthe stomach is the main sign of the disease. Most often disturbing stupid pain. Slow manifestations are typical for acute mucosa inflammation. When gastritis, pain syndrome may be parotid or constant. There is a clear connection with meals (spasm appears after meals and when a man is hungry). Additional symptoms Diseases may include belching, nausea, stool impairment, bloating, the feeling of acid in the mouth. Not sharply pronounced pain is characteristic of chronic gastritis with normal acidity.
Suman disease
Acute pain in the stomach associated with meals may indicate the presence of ulcerative disease. It proceeds in chronic form. Pain syndrome is most pronounced during the period of exacerbation. Ulcers are formed against the background of stress, gastritis, the use of certain drugs, endocrine diseases. The pathogenesis of the formation of this defect is associated with suppression protective mechanisms (Violation of the synthesis of mucus covering the stomach), as well as with an increase in the acidity of the gastric juice. The symptoms of the stomach ulcers remind those with gastritis. The main signs of the disease include:
- severe pain in the epigastric area;
- nausea and vomiting after meals;
- reducing body weight;
- disruption of appetite.
With ulcerative damage, the stomach hurts after eating. This is the main difference from the pathology of the 12th day. Pain syndrome occurs almost immediately after meals (within one and a half hours). A certain connection between exacerbations over time of the year is traced. Most often, the attacks of pain people suffer in autumn and spring. In the case of the development of complications (perforation, bleeding), symptoms can sharply increase. Such a condition requires emergency care. The processes occurring in the stomach, the reasons for which can be different are often reversible.
4rak
If the stomach hurts, the reason may wage in oncology. This is one of the most common malignant pathologies. Every year, almost a million people all over the world die from the stomach cancer. For a long time, the disease may not appear in any way. Quite often, cancer is already detected by 3 or 4 stages, when treatment is ineffective. Men suffer from this ailment more than women. Cancer is dangerous in that the tumor in the later stages is able to give metastases to other organs, which is killed and patients die. Accurate reason Diseases are still unknown. Possible etiological factors These are: the presence of atrophic gastritis, the infection of organ with bacteriums Helicobacter, the impact of toxic and carcinogenic substances, irrational nutrition, reception of drugs, alcoholism, burdened heredity, Mealry's disease.
The symptoms of cancer in the early stages are represented by a decrease in appetite, disgusting to meat, nausea, bloating, decrease in body weight, malaise, weakness, violation of swallowing. In the later stages of patients can disturb the best pain. In most cases, it is due to the germination of the tumor into neighboring organs. Permanent hair pains appear in the introduction of a neoplasm in the pancreas. Operational treatment Must be started as soon as possible. Acute pains resembling angina attack are characteristic of a tumor that sprout into a diaphragm. If the painful syndrome is combined with a transfusion in the abdomen, a violation of the stool by the type of constipation, this may indicate the involvement of the transverse colon.
5pish and poisoning
A sharp pain in the stomach can be a sign of food poisoning. This is a disease that develops with poor-quality food containing pathogenic microorganisms, their decay products or various toxic compounds. All food poisoning is divided into the following forms:
- microbial;
- non-library etiology;
- mixed.
The first group includes food toxicoin intakes and intoxication. In this situation, the pathogens are bacteria (Klostridia, intestinal wand, protea, streptococci), mushrooms, toxins. Poisoning is also possible to poisonous plants, mushrooms, berries, fish caviar, seafood, salts of heavy metals, pesticides, pesticides. Symptoms with such pathology are due to inflammation of the stomach against the background of the effects of toxins.
In most cases, signs of gastroenteritis appear. These include constant pain in the muscles, head, nausea, vomiting, fever, weakness, rigging chair. Often there are symptoms of dehydration. Diagnostic signs Food poisoning are:
- acute, sudden start;
- communication of pain with meals;
- the simultaneous appearance of symptoms in a group of persons;
- disease vehicles.
6Odenitis and pancreatitis
The pain in the epigastric region may be a symptom of duodenitis (inflammation of the mucous membrane of the 12th intestine). It can leak in acute and chronic form. This is the most common pathology of this organ. Quite often, such a disease is combined with enteriti and gastritis. The main causes of inflammation of the 12th intestine are:
- error in nutrition;
- drinking alcohol;
- infection with bacteria;
- the presence of ulcers or gastritis;
- infringement of blood supply;
- chronic liver and pancreas pathology.
The main symptoms of the disease depends on its shape. Duodenitis, arising against the background of ulcers or infectious gastritis, is characterized by pain on an empty stomach, at night and a few hours after eating. Strong manifestations are characteristic of the acute type of pathology. When it combines with inflammation of other departments fine intestine Symptoms may include mallabsorption syndrome, dyspeptic disorders. In the case of stagnation of the 12th intestine, parole pains, belching, nausea, vomiting, bloating, rumbling. When duodenitis, bile outflow may be impaired. In this situation, soreness appears in the epigastric area. The clinical picture resembles the dyskinesia of the biliary tract.
If something hurts in the stomach, the reason for this may be pancreatitis, the symptoms of which are usually quite pronounced. Pain syndrome is most pronounced when acute inflammation pancreas. The latter is located near the stomach. Such pathology is characterized by the appearance of pain in the top of the abdomen. She can last from a few minutes to several days. The pain is intense, constant and worried about the patient. It can give to the left or right half of the body, depending on which organ department is amazed (head, body or tail). Pain syndrome is enhanced during food intake and treatment is required. Often he takes a sinking character. Additional signs of the disease include nausea, vomiting, bloating, pain in palpation, increasing the total body temperature.
7 Diagnostics and treatment
If the stomach fell ill, then you should not postpone the visit to the doctor in a long box, for the consequences can be dangerous. Treatment is carried out only after establishing the cause owl syndrome. Diagnosis includes:
- detailed patient survey;
- physical research (abdomen palpation, listeners of lungs and hearts);
- general and biochemical blood test;
- conducting FGDS;
- determination of gastric juice acidity;
- blood test for the presence of Helicobacter pylori;
- Ultrasound of the abdominal organs;
- laparoscopy;
- cala's study;
- contrast radiography;
- CT or MRI;
- duodenal probing;
- analysis of urine.
With suspicion of colitis, a colonoscopy can be conducted. To exclude a stomach cancer, biopsy is made. How to get rid of pain in the stomach? Therapy should be aimed at eliminating the main reason. If the stomach inflamed, what to do in this situation? Treatment of gastritis involves compliance with a strict diet, the use of drugs (antacid agents, proton pump blockers, gastroprotectors). The use of Almagel, phosphhalugel and ohmosis is shown in the form of a disease with increased acidity. If the bacterium Helicobacter is revealed and antibiotics and metronidazole are used.
Therapy of acute pancreatitis includes temporary fasting, applying cold on the stomach, the use of antispasmodics, omeprazole, diuretics, infusion therapy.
With purulent pancreatitis, treatment necessarily includes antibiotics. If vomiting is present, antiwheat preparations are used (metoclopramide). When developing peritonitis and necrosis, the organ is shown. Chronic form Pancreatitis involves compliance with the diet, the reception of enzyme preparations (panzinorma, pancreatin, mesima). When grazing the stomach treatment surgical treatment (organ resection or removal). Thus, the causes of abdominal pain can be the most different. If any, you should consult with your doctor.
What to do with the exacerbation of the stomach ulcer?
If the patient has an acute critical condition associated with the perforation of the stomach ulcers, then emergency treatment is necessary, since peritonitis in this case is rapidly progressing. The symptoms of the velocity are:
- the appearance of a sharp pain quickly propagating throughout the abdomen;
- muscular stress of peritonean walls;
- phenomena preceding fainting (dizziness, ringing in ears, weakness);
- chills;
- subtaching;
- dry mouth.
Traditional ways of therapy
Therapeutic assistance in the aggravation phase of the stomach ulcer disease is determined on the basis of the state of the patient, its age, the nature of clinical symptoms. However, the treatment of non-comprehensible forms is almost always a reception of bactericidal agents, for example, amoxicillin, metranucleazole, clarithromycin. Due to these drugs and some others, also related to the antibiotic group, it becomes possible to cure the pathology of the gastric mucosa, as they eliminate the main reason - pathogen Helicobacter Pilori.
In addition to drugs of antibacterial action in therapy, acutely occurring ulcers can be used:
1. Means normalizing the acidity level of the digestive juice (omeprazole, ranitidine);
2. Preparations with gastroprotective (protective) property (de nol and other bismuth-containing medicines);
3. Blockers of dopamine central receptors (Primperan, Raglan, Cerukal);
4. Medicines with a psychotropic effect, if the patient suffers from irritability, insomnia, a sense of constant anxiety (pyazepam, elenium);
5. Adrenergic agents that have anti-cosinery and overwhelming release of gastrene Action (Obizant, Inderal).
In the treatment of exacerbation of ulcerative ulcer of the stomach, certain physiotherapeutic methods were also proven: ozkhelorite and paraffin applications, magneto and hydrotherapy, sessions of modulated sinusoidal currents.
All activities in combination with a diet in 80-90% of cases make it possible to achieve a resistant remission of pathology. However, conservative treatment does not always help, and then the patient shows surgical interference with various circumstances in ways (using the method of selective proximal vagotomy, resection, endoscopy).
Indications for the operation on the stomach:
- perforation of ulceration;
- an ulcer complicated by bleeding of a profuse nature (bleeding leading to hypovolemia);
- pylorostenosis;
- penetration of defect.
Folk recipes treatments
Use folk waysTo cure an ulcer, specialists are not recommended due to the risk of exacerbation of the situation. Especially prohibited by such treatment with complicated sharp forms. But with the aim of preventing exacerbation to use some non-traditional recipes Doctors admit, for example, tool:
1. From birch leaves (1 teaspoon of crushed fresh leaflets of this tree poured with a glass of boiling water, it insists 1-2 hours);
2. From coltsfoot (infusion is prepared similar to the previous method with one difference, which can be used not only the leaves of the plant, but also the flowers themselves); In addition, this folk recipe helps to treat both the stomach and bronchi;
3. Of the medicinal altea (1 large spoon of a grinding rhizoma is flooded with 250 ml. Boiling water, for 30 seconds everything will be all tummet on slow heat, and then it is about half an hour).
All the listed funds of traditional medicine need to drink before meals 3 times a day.
Diet with ulcers
Compliance with dietary nutrition is equally important and in the exacerbation of the inflammatory process, and in the stage of its remission, and in the case of complication by stenosis, bleeding and other life-threatening lifests. Therefore, the patient is prescribed a personal diet based on:
- gastroduodenal mucosagliness with elimination of all chemical, thermal and mechanical stimuli;
- fractional diet (the patient is recommended to eat and drink small portions, but every 3-4 hours);
- correction of fats in the direction of increasing;
- increase the quota of protein;
- reducing the share of carbohydrates in a daily diet.
Diet in the treatment of stomach ulcers should be respected at least 6-9 months. When the disease is retreating, turning to the phase of remission, and the food of the stomach will not deliver discomfort, gradually can be returned to the usual view of the dishes (not witching and not strong), but from coarse and harmful industrial products will still have to be abandoned at all.
In addition to the diet, the prevention and treatment of acute ulcers plays the exclusion of alcohol and energy drinks due to the cause of the bleeding and growing erosion inflammation.
Duodenal bulbs ulcer
One of the most common types of erosive formations of the gastrointestinal tract is the duodenal bulbs ulcer. Disease common. According to official data, up to 10% of the world's population is sick. Deformation is developing due to failure in chemical processing of food. Anatomy of erosive formations is different, but more often they are formed on a bulb having a shape of a ball. There is a bulb of the duodenum at the very beginning of the intestine, when leaving the stomach. Treatment is long and complex.
It can be deformed on the front and rear wall (kissing ulcers). The bulbs of the 12-rosewoman also has a special location - at the end or at the beginning (mirror). Mirror erosions are treated, like other forms. Negative factors affecting the work of the stomach and intestines provoke the appearance of an ulcer of various shapes. The risk group includes middle-aged people, and those who are forced to work in the night shift.
In case of failure in the processing of stomach, the duodenal bulbs may occur.
Causes of ulcers of the bulbs of the 12thist
Most often, the inflammation of the 12-pans arises due to an aggressive acid action. In the absence of therapy, the development of probulous ulcers and bleeding is possible. The reasons can be a number of:
- broken power mode (a lot of fat, acute, abuse of diets, carbonated drinks);
- bacterium Helicobacter - the cause of peptic formations in most cases;
- smoking, alcohol;
- severe stress or systematic stay in the state of emotional voltage;
- hereditary predisposition;
- long reception of certain anti-inflammatory drugs;
- incorrect treatment at the initial stage of the disease.
Kissing ulcers in the intestine may appear due to concomitant reasons: HIV infection, liver cancer, hypercallesemia, renal failure, Crohn's disease, etc.
Symptoms
The symptoms of the bulbs of the bulbs of the 12-rosewood are characteristic of other types of gastrointestinal ulcers, and they are manifested depending on the stage of the disease:
- heartburn;
- nausea in the morning or after meals;
- pain in the opposite region;
- pain in the area of \u200b\u200bthe stomach at night;
- flatulence;
- the appearance of a feeling of hunger after a short time after meals;
- if the disease is in a launched form, bleeding can be opened;
- vomiting;
- pain, localized in the area of \u200b\u200bthe belt, or the overseas part.
The inflammatory lymphocular shape of the 12-pans has a different character of pain: stitching pain, acute or new. Sometimes it passes after a person has attempted. Hunger pains usually arise at night, and to eliminate unpleasant sensations It is recommended to drink a glass of milk or eat a little. Night pain is caused by a sharp increase in the level of acidity.
Stages
The intestinal healing process is divided into 4 main stages:
- 1 stage - initial healing, characteristic of the epithelial layers;
- 2 stage - proliferative healing, in which protrusions appear in the form of papilloma appear on the surface; covered with these formations regenerating epithelium;
- 3 Stage - the appearance of a polisada - an ulcer on the mucosa is no longer visible; With a more detailed study, many new capillaries are visible;
- 4 Stage - the formation of a scar - the bottom of the ulcers is completely covered with a new epithelium.
Erosive kissing formations on a 12-risen intestine are frozen after the use of therapy. Many ulcers in a small sector of the intestine leads to the formation of several scars. The result of such healing becomes a bunching and ulcerative deformation of the bulb of a 12-rosewoman. The emergence of fresh scars leads to the alignment of the lunar of the bulb. Inflammatory scar deformations of the bulb of the 12-rosewood has negative consequences, such as stagnation and malfunction in the work of the whole gastrointestinal tract.
There is also a distribution in the stage: exacerbation, scarring, remission.
One of the forms of the intestinal ulcers is the lyonic fluid hyperplasia of a 12-rig, which is characterized by inflammation due to violations in the outflow of lymph. The causes of the occurrence are exactly the same as in the ulcers of the 12th-rosewoman. There are also similar symptoms. Lymphocolicular dysplasia - pathology in the mucous membrane of the intestine or stomach. It is characterized by the emergence of the formations of a rounded form on a wide basis. Lymphocular dysplasia is deformed and has a dense consistency and point dimensions. Lymphoclicular mucosa infiltrated. Stages of development:
- acute;
- chronic.
Diagnosis of disease
The FGDS method will help to accurately diagnose the presence of a 12-rosen ulcers (fibrogastroduodenoscopy). With the help of a special probe with the camera, a study of the intestinal surface is carried out. It is this method of diagnosis that will allow you to establish the location of the ulcers, its size and stage of the disease. Typically, inflammation is observed, or the surface is hyperemic, covered with dotted erosions of dark red. The intestinal section is inflamed in the field of mouth, and the mucosa is hyperemic.
Must be assigned analyzes to determine the bacteria Helicobacter. As a material for testing, not only blood and feces are used, but also vomit masses, material after biopsy. The auxiliary diagnostic methods include x-ray, palpation in the area of \u200b\u200bthe stomach, the overall blood test.
Treatment
After the diagnosis of the "inflammation of the bulb of a 12-rosewoman", treatment must be started at once, as it is possible to develop serious complications. Kissing ulcers are treated mainly by medicines. During the exacerbation, hospitalization is necessary.
The doctor selects drugs and physiotics individually for each patient, taking into account the characteristics of the body and stage. For example, a chronic or lymphocular stage is treated not as during exacerbation. This scheme usually includes such medicines:
- bismuth-based drugs, in case of detection of bacteria, Helicobacter; Such drugs oppressively affect the pathogenic microflora;
- preparations that reduce the amount of gastric juice produced: blockers, inhibitors, cholinolics;
- prokinetics - improve the intestine motorcy;
- unpleasant pain eliminate with the help of antacids;
- antibiotics are prescribed antibiotics to combat the bacterial cause of the appearance of lymphocular ulcers;
- prevent the negative impact of hydrochloric acid to the affected area will help gastroprotstectors;
- inflammation remove analgesics and antispasmodics.
The combination of medication and physiotherapy contributes to a faster recovery of the body. Such methods include: electrophoresis, ultrasound exposure, the use of microwaves, therapy by modulated currents to remove pain. Normalize the stomach motor will help special medical physical education. Gymnastics is good preventive tool From stagnation in the intestines and stomach.
In addition to the generally accepted methods of healing the intestinal ulcers, the funds of traditional medicine have long been their effectiveness. In the first place with ulcerative lesions, freshly squeezed potatoes juice. It must be drunk three times a day, and only freshly squeezed. Pre-potatoes are clean, the rubber is on the grater, and pressed through the gauze. The first few days the dosage is on one tablespoon. Gradually, it can be increased to half a cup. You need to drink before meals.
To other no less effective means include honey healing herbs (Calendula, St. John's wort, plantain), olive and sea buckthorn oil.
In the period of acute form, constantly observance of the bed regime. After the aggravation passes, you can make short walks. Heavy physical exercise and exercises are prohibited. The army is contraindicated to those who have an ulcer. In order not to provoke new attacks, it is important to avoid stress and take care of the nervous system.
Compliance with diet - one of the important factors on the way to recovery and decrease inflammatory processes. General recommendations for dietary nutrition are as follows:
- small portions;
- thoroughly chew each piece;
- to eliminate products provoking the active production of gastric juice (soups from vegetables, fish and meat broths);
- in order not to irritate additionally the mucous membrane, the food must be reversed;
- fruit juices should be diluted with water;
- more often use milk;
- do not use in spice dishes;
- cook overhead porridge;
- eating the optimal temperature, not too hot and not too cold;
- food fractional, up to 5 times a day.
Food should be prepared for a couple or in the oven. In the ration necessarily include non-acidic fruits, kefir, milk, cottage cheese, boiled vegetables or a couple. It is necessary to abandon the use of alcohol and smoking, as this can lead to the development of serious complications.
Forecast
A favorable preparation for recovery can be in the event that the treatment was carried out on time and the correct power regimen was observed. In case of untimely appeal to the doctor or incorrectly designated drugs, serious complications may develop: lymphocolicular ulcer, bleeding (vomiting with blood), punching ulcers ( acute pain Under the sneaker) and penetration (due to adhesions, the contents of the intestine fall into neighboring organs). In each of these cases, the only option is surgical intervention.
Stenosis of the 12-rosician refers to complications. After healing, there are scarmers that later can cause swelling and spasm. Stenosis is usually manifested in the period of acute form or after the therapy. Stenosis occurs in those patients who have ulcers for a long time Does not heal. Accompanied by stenosis disruption of intestinal motorcycle and stomach.
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)- infectious disease characterized by inflammatory changes lymphoid tissue of pharynx and chicken almonds (Pirogov rings). 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 of peptic ulcer: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, pistened-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 of the worm-shaped process of a blind intestine. In surgical practice, a group of diseases denoted as a sharp belly (ulcerative disease with perforation, peptic disease with bleeding, sharpness 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 stomach of the stomach is sharply thinned, the glands are reduced in size, the distance between them is increased, the epithelium glands acquires more primitive features, loses the ability to produce gastric juice and hydrochloric acid, secrete a 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 are atypical, different sizes and forms of ferrous 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)
Cystitis during pregnancy: to cure and prevent repeated development can be pregnant during cystitis
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