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Nonspecific ulcerative colitis
Nonspecific ulcerative colitis (UC) is a chronic recurrent bowel disease of unknown etiology, characterized by diffuse inflammation of the mucous membrane of the rectum and colon.
In the early stage of NUC, there is a violation of the integrity of the epithelium and vascular reaction; later, ulcerations of the mucous membrane, which do not spread deep into the intestinal wall, join. In the severe stage, the mucous membrane is swollen, with numerous small or extensive ulcers of irregular shape. Pseudopolyps develop in the mucosa, which is associated with epithelial regeneration. When the process of reparative-sclerotic changes is chronized, the predominant changes begin to occur, scarring occurs, extensive areas of scar tissue are formed, leading to a sharp deformation and shortening of the intestine, and its lumen is narrowed.
NYA ill people of all age groups (most often between the ages of 20-40 and 60-70 years), men and women suffer equally often.
Etiology. Accurate information about the cause of the disease is currently not available. Hereditary predisposition (connection of the disease with the carrier of antigens HLA-DR27 and B27) is assumed, in which infectious factors (including dysbacteriosis) and immune reactions trigger the inflammatory process.
Pathogenesis. The main pathogenetic mechanisms are changes in the immunological reactivity, dysbacteriosis and the peculiarity of the neuro-vegetative reactions of the body (Scheme 16).
Dysbacteriosis and, in particular, an increase in the number of Escherichia coli and Yersinia have a local toxic and allergenic effect. Peculiarities of neuro-vegetative reactions cause dysfunction of vegetative and hormonal regulation, as well as changes in the permeability of the colon mucosa. As a result, the penetration of substances with antigenic properties is facilitated. It is known that the antigens of some Escherichia coli strains induce the synthesis of antibodies to the intestinal tissue. The cytopathogenic effect of anti-tumor antibodies is combined with the action of proteolytic and other metabolic products of the intestinal microflora and causes immune and non-immune inflammation of the intestinal wall.
Immune mechanisms determine the involvement in the pathological process of other organs and systems (extraintestinal lesions), which include lesions of the skin, organ of vision, oral cavity, musculoskeletal system, blood system.
Classification. At present, there is no generally accepted classification of NLK. For practical purposes, there are three main forms: acute, chronic and recurrent. Within each clinical form, there are mild, moderate and severe variants of the disease.
Acute, or fulminant, form is rare, it is characterized by the severity of general and local manifestations, early development of complications. The process develops rapidly, as a rule, captures the entire colon.
The chronic form is characterized by a continuous, long-lasting, debilitating course, with a gradual increase in symptoms.
Recurrent form occurs most frequently. It is characterized by remission lasting from 3-6 months or more, alternating with exacerbations of varying severity. One clinical form can move to another.
In NUC, the severity of the disease is due to the degree of involvement of the colon in the pathological process. Proctosigmoiditis is most often observed (67%), total colitis occurs in 16% of patients, isolated proctitis - in 5%.
Clinical picture. Manifestations of the disease are due to the extensiveness and severity of colon lesions and extraintestinal manifestations, but the “intestinal” symptoms are in the first place.
At the first stage of the diagnostic search, there are complaints about diarrhea, liquid or pasty stools, the presence of blood, mucus and pus in it.
There are several options for the onset of the disease.
• Gradual diarrhea; After a few days, mucus and blood are found in the liquid smears.
The disease makes its debut with rectal bleeding with a decorated or pasty stool. Blood loss during bowel movements in the first days is usually insignificant.
• The appearance of diarrhea with blood and mucus, pain, intoxication.
When the picture of the disease is unfolded, the dyskinetic and ulcerative-hemorrhagic syndromes manifest themselves in the form of frequent liquid stools with an admixture of Blood and pus, sometimes mucus, which is the main symptom. The chair is up to 20 times a day, and in severe cases the number of bowel movements reaches 40 or more, mostly at night and in the morning. Patients with severe NUC often suffer from fecal incontinence, which is associated with lesions of the external
sphincter of the anus and general weakness. The admixture of blood in the stool is significant, sometimes the discharge from the colon consists of one blood. During an exacerbation, patients lose 100–300 ml of blood per day.
The amount of mucus in the stool depends on the safety of the intestinal mucosa. With a total deep lesion of the mucous membrane mucus in the stool is absent.
In the period of exacerbation, feces are a fetid purulent-mucous fluid mixed with blood. During remission, diarrhea may stop completely, but more often the stool is mushy, 3-4 times a day, with a slight inclusion of mucus and blood.
Mandatory symptom of total NUC - cramping pain. Patients are not always able to accurately determine the localization of pain, only approximately indicating the zone of the main lesion. Most often this is the region of the sigmoid colon and rectum, less often - the area of the navel and the caecum. Typical is increased pain before stool and weakening after emptying the bowel. Meal also increases pain and diarrhea, so that sometimes patients refuse to eat.
The defeat of the rectum and sigmoid colon leads to themes. The urge to defecate are dramatically imperative. Patients often note a feeling of incomplete emptying of the rectum.
With nonspecific ulcerative proctitis and proctosigmoiditis, some patients notice constipation for 2–3 days, alternating diarrhea with constipation, which are spastic in nature.
Almost all patients complain of weakness, weight loss. During remission, the condition improves, body weight increases. With each relapse, weakness and weight loss progress. With proctitis and proctosigmoiditis, body weight is usually not reduced, appetite is preserved, moderate weakness.
In the case of the lightning form, the effects of intoxication are growing rapidly: nausea, vomiting, high body temperature, weakness or adynamia. Slimming quickly reaches the degree of cachexia. The syndrome of organ lesions and asthenoneurotic syndrome develops in the form of a sharp change in the psyche (patients become touchy, tearful, lose their sense of humor).
The ineffectiveness of dysmodic therapy in the opening, the further progression of the disease, the involvement of other organs and systems make it possible to suspect a severe bowel injury, including UC, tumor, tuberculosis, etc.
At stage II of the diagnostic search, clinical signs of dystrophic-anemic and dyskinetic syndromes, local and systemic complications are revealed.
In acute and total intestinal lesions, patients fall into prostration, exhausted, dehydrated. Dryness of the skin and mucous membranes is observed, turgor is sharply reduced. Pale skin, body temperature 39-40 C and above. Marked tachycardia, arterial hy-potency, decreased diuresis. The liver and spleen are often enlarged. A painful rumbling large intestine with packed walls is palpable. The skin around the anus is macerated, the mucous membrane of the rectum prolabiruet.
The acute form is often accompanied by complications. Perforation poses the greatest danger; multiple perforations are possible. Perforations arising on the background of severe intoxication, sharp pain in the abdomen, often occur atypically, without a violent onset, without acute pain.
jje immediately arises muscle protection. In this regard, the presence of perforation can be assumed on the basis of only the general deterioration of the patient's condition in combination with an increase in pulse rate, a fall in blood pressure.
For acute toxic dilatation of the colon is characterized by a sharp expansion and swelling of individual segments, often the transverse colon. The area of the intestine dramatically stretched fluid and gases, which may result in perforation and peritonitis. With this complication, the frequency of bowel movements decreases, the stool loses fecal character, the excretion of blood, pus and mucus increases. High fever, significant tachycardia, collapse are determined. The stomach is swollen, palpation along the swollen areas of the large intestine is sharply painful. Peristalsis sluggish or absent.
In the chronic form of NUC, manifestations of hypovitaminosis, anemia, and endocrine disorders (dystrophic-anemic syndrome) predominate in the clinical picture.
At stage II, a number of pathological changes in other organs and systems (organ lesion syndrome) are also detected. A typical manifestation of skin changes in UC is erythema nodosum: single or multiple nodes appear, often on the extensor surface of the legs. In severe forms of the disease, pyoderma gangrenosum and massive ulceration of the skin of the lower extremities are found.
Severe forms of NUC are also characterized by lesions of the oral mucosa, aphthous stomatitis, glossitis and gingivitis. Usually marked ulceration of the edge or lower surface of the tongue, less gums. The pain of eating is so severe that the sick refuse to eat. Possible ulcerative esophagitis.
In UCs, iritis, conjunctivitis, and blepharitis may occur. There is a clear dependence of the severity of eye symptoms on the form and
phases of the disease.
UC can be complicated by polyarthritis. Ankle and knee joints are usually affected with a slight restriction of movement and mild pain. Arthritis occurs simultaneously with NUC and disappears during remission, leaving no deformity. Some patients develop
Relatively often, NUC is complicated by a narrowing of the intestinal lumen, which is manifested by a pattern of intestinal obstruction.
At the digital examination of the rectum, it is possible to identify complications that occur frequently in UCN (perianal abscesses, anal fissures, paraproctitis, cellulitis of the paralectal rectal space, rectal and rectovaginal fistulas).
At stage III, the identification of characteristic changes in the mucous membrane of the colon allows you to make a final diagnosis.
For the diagnosis of NUC (taking into account the permanent lesion of the rectum) is enough rectoromanoscopy. At the onset of the disease, edema and contact hypersensitivity of the mucous membrane are observed. The slightest mechanical irritation leads to bleeding (contact bleeding). The mucous membrane is hyperemic, edematous, covered with mucus, under which is marked "granularity" with punctate and small ulcerations. Later, under the mucous membrane, characteristic prosophageal abscesses are formed; after opening them, small ulcers remain, which later merge.
In severe acute form, complete destruction of the mucous membrane and deep-lying layers is possible; the inner surface becomes smoother, the wall is fragile, it is easily torn.
The endoscopic picture in the form of partial epithelization, reduction of the size of ulcers, and the appearance of pseudopolyps corresponds to the abating of clinical manifestations. During remission, complete epithelization occurs, the mucous membrane is smooth, with a blurred vascular pattern, small pseudopolyps can be detected.
To determine the extent and nature of the lesion of the colon, identifying a number of complications should be carried out irrigoscopy.
The X-ray picture in the early stages of NUC with shallow morphological changes is scarce and nonspecific.
After long-term treatment, an X-ray examination reveals the absence of haust rapia, rigidity, uniform atrophy and narrowing of the intestine, and its shortening. The gut has the appearance of a "water pipe". In the aggravation phase, a relief change can be detected: wide transverse ridges with edge teeth, pseudopolyposes. This method allows to detect intestinal stricture and possible malignancy.
In case of toxic dilatation of the colon due to the danger of ir-rigoscopy (provocation of perforation), radiographic radiography acquires diagnostic value: the images show stretched (10 cm and more) segments of the intestine. If you suspect perforation should often resort to review fluoroscopy of the abdominal cavity to detect "free" gas.
Fibrocolonoscopy allows you to accurately determine the nature of changes throughout the colon, as well as to identify the lesion of the ileocecal valve (Bauhinia valve) and the terminal part of the small intestine.
In the chronic course of NUC and in the remission phase, endomicroscopic examination and biopsy of the mucous membrane help in the diagnosis.
Laboratory blood tests can determine the degree and nature of anemia. In case of massive intestinal bleeding, acute post-hemorrhagic anemia occurs. Constant daily, even “hidden” blood loss, also leads to iron deficiency in the body and the development of anemia.
Acute autoimmune hemolytic anemia develops in some patients (with a positive Coombs reaction, reticulocytosis and unconjugated hyperbilirubinemia). With total NUC with involvement of the small intestine there is a deficiency of folic acid and vitamin B, 2, in the genesis of which dysbacteriosis plays a certain role.
Acute NUC and relapses are characterized by increased ESR and small leukocytosis with a shift of the leukocyte formula to the left. It is important to determine the ESR in dynamics, since the number of leukocytes often remains normal even in severe cases, which is associated with hypocorticism and sulfonamide intake. Infrequently occurring high leukocytosis is almost always a signal of a severe complication.
Biochemical analysis of blood helps to establish the degree of violation of protein and electrolyte metabolism, as well as to identify damage to the liver and kidneys.
Coprological examination reflects the degree of the inflammatory-destructive process. Microscopically detect clusters of leukocytes, red blood cells, large clusters of intestinal epithelial cells. A sharply positive reaction to the soluble protein in the feces (Triboule's test) also indicates inflammation of the intestinal wall.
Bacteriological examination of feces in the NUC debut helps to eliminate acute dysentery. Determination of the nature and extent of dysbacterium
Riosa is necessary for antibiotic therapy. Indicative of the disturbed intestinal biocenosis are the quantitative shifts of obligate microflora: the lack of growth of bifidobacteria at a dilution of 10 ~ 7 and a sharp change in the number of E. coli. Dysbacteriosis is also manifested by a high representation of Escherichia coli with mild enzymatic properties (more than 10%), lactose-negative enterobacteria (more than 5%), the appearance of microorganisms of the genus Proteus, fungi of the genus Candida, hemolyzing Escherichia,
Diagnostics. The recognition of ulcerative colitis is based on the identification of the following symptoms:
1) “characteristic” changes in the stool: frequent, unformed stools with blood and pus;
2) pathological changes in scatological research: poor unformed feces, blood, mucus, pus in feces, stools like raspberry jelly. Sharply positive reaction to soluble
3) “specific” changes of the mucous membrane: contact bleeding, absence of vascular pattern, prostate abscesses, ulcers of various sizes and shapes, pseudopolyps;
4) “typical” changes of the intestine during irrigoscopy: shortening, contraction, absence of haustration, intestine in the form of a “water pipe”.
On the basis of data obtained at all three stages of the diagnostic search, criteria for severity of NK (Table 18) were developed. Differential diagnosis. Due to the fact that the clinical picture of NUC is similar to the manifestations of other intestinal lesions, neo-dima has a thorough differential diagnosis.
First of all, NUC is differentiated from acute diarrhea. UC is harder, complications quickly arise, the administration of antibiotics does not improve the condition, as in bacterial dysentery, and aggravates it. in bacterial dysentery, in contrast to NUC, rectoromanoscopy does not reveal extensive ulcer fields, diffuse bleeding, pseudo-polyporoscopy
UCI should also be differentiated from Crohn's disease (terminal ileitis), which causes pain in the ileocecal region, diarrhea,
alternating with constipation (without blood), fever, anemia. The transverse and descending colon is intact, therefore diarrhea and pronounced bleeding are not observed. In some cases, the sigmoid, colon and rectum are involved in the pathological process, and then NUC can be differentiated only according to endoscopic data, as well as microscopy of mucosal biopsy material.
In chronic forms of NUC, when the main symptoms are pasty stools and discharge of blood from the rectum, differential diagnosis is carried out with a colon and colon neoplasm, chronic colitis. The final diagnosis is made taking into account the results of endoscopy.
The wording of the expanded clinical diagnosis is based on the following scheme: 1) the clinical form; 2) the degree of involvement of the colon; 3) severity; 4) the phase of the disease; 5) complications.
Treatment. The volume of therapeutic measures depends on the severity of the disease, the phase (exacerbation or remission) and the presence or absence of complications. Комплексное лечение предусматривает борьбу с воспалительным процессом, воздействие на моторику и микрофлору кишечника, коррекцию обменных нарушений, создание психического и физического покоя.
Общие мероприятия включают диету и психотерапию. Пища должна быть достаточно калорийной и включать 110—120 г/сут белка, в период обострения больного переводят на диету № 4, при стихании обострения пиша может быть непротертой.
Больной не требует каких-либо особых ограничений в питании. Однако некоторые больные не переносят определенные продукты, которые следует исключить из рациона.
Психотерапия чрезвычайно важна. Большая роль принадлежит доверительным взаимоотношениям врача и больного. При необходимости назначают седативные препараты или психотропные средства (в основном антидепрессанты).
Больные с тяжелым течением болезни нуждаются в неотложной госпитализации и строгом постельном режиме. Назначают парентеральное питание (путем катетеризации подключичной вены вводят различные растворы — аминопептид, альвезин, липофундин или интралипид, глюкозу вместе с электролитами и витаминами комплекса В).
Из противовоспалительных препаратов (если нет показаний к хирургическому лечению) назначают глюкокортикстероиды (ГКС), в особенности если одновременно имеются внекишечные проявления болезни. Преднизо-лон вначале вводят внутривенно (в дозе, эквивалентной 40 мг преднизоло-на), при недостаточном эффекте добавляют цитостатики (азатиоприн внутрь по 2,5 мг/(кгсут). Затем переходят на прием преднизолона внутрь (1 мг/кг массы тела); при достижении эффекта дозу постепенно снижают. При лихорадке, клинических симптомах септического состояния назначают антибактериальную терапию — ципрофлоксацин внутривенно по 500 мг каждые 8 ч до стихания симптомов.
При НЯК легкой и средней тяжести в периоде обострения больные также госпитализируются. Назначают преднизолон по 40—60 мг/сут (снижая дозу в зависимости от клинической картины на 5—10 мг/нед) или ме-салазин внутрь по 4 мг/сут, снижая дозу при достижении ремиссии приблизительно на 1 мг/нед.
Исчезновение симптомов, нормализация эндоскопической картины и лабораторных показателей свидетельствуют об эффективности лечения.
Эффективность сульфасалазина и месалазина оценивают на 14—21-й день •терапии, ГКС — на 7—21-й день, азатиоприна — через 2—3 мес.
В фазе ремиссии, для которой характерно отсутствие жалоб, лихорадки, анемии и других патологических показателей, обычно назначают на длительное время прием сульфасалазина по 2 г/сут без существенных ограничений в диете или месалазин по 1,5—3 г/сут. Если рентгенологические, эндоскопические данные нормальны в течение длительного времени (не менее 2 лет), то можно на несколько месяцев полностью отменить прием
В периоды обострения или же при сохранении ряда симптомов в периоде улучшения состояния при частом стуле используют антидиарейные препараты — реасек (ломотил) по 20—30 мг в день, желательно сочетание его с м-холинолитиками и спазмолитиками; следует применять также вяжущие средства (отвар коры дуба, плодов черники, черемухи).
Лицам с длительностью НЯК более 10 лет 1—2 раза в год следует проводить колоноскопию (опасность малигнизации).
Борьба с осложнениями включает в себя консервативное лечение острой токсической дилатации толстой кишки. Для этого необходимо ограничить прием пищи и полностью отменить холинолитики и опиаты. Требуется полноценная коррекция электролитного обмена, особенно калиевого, а также восполнение потери жидкости и белка. Проводят гемотрансфузии, как правило, прямое переливание крови. Назначают антибиотики широкого спектра действия. Осторожно проводится декомпрессия желудка с помощью зонда. Клизмы противопоказаны. Необходимо соблюдать осторожность с газоотводной трубкой (опасность перфорации сигмовидной и ободочной кишки).
При неэффективности консервативных мероприятий проводится тотальная колэктомия с наложением илеостомы (одномоментно).
В случае перфорации толстой кишки ушивание не производится. Показана геми- или тотальная колэктомия с наложением илеостомы. Показаниями к оперативному лечению являются:
• обоснованное подозрение на перфорацию;
• острая токсическая дилатация толстой кишки, не поддающаяся терапии в течение 6—24 ч;
• профузное кишечное кровотечение;
• неэффективность комплексной интенсивной терапии при острой тяжелой форме в течение 7—10 дней;
• неэффективность комплексной терапии рецидивирующего НЯК;
• развитие стриктур с явлениями частичной кишечной непроходимости;
У больных с илеостомой в дальнейшем необходимо стремиться к осуществлению реконструктивных и восстановительных операций (илеорек-тальный анастомоз, создание искусственной ампулы и т.д.).
Forecast. Прогноз при НЯК зависит от клинической формы заболевания, распространенности процесса и тяжести его течения. При тяжелом течении НЯК прогноз неблагоприятный вследствие развития различных осложнений. Комплексная терапия может смягчить проявления болезни, °Днако полной и длительной ремиссии обычно не наступает.
Prevention. Специфические профилактические меры неизвестны. Профилактика сводится к предупреждению обострений, что достигается Упорным лечением. Больных ставят на диспансерный учет, чтобы своевременно выявить начинающееся обострение или осложнение
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Неспецифический язвенный колит
- Nonspecific ulcerative colitis
Nonspecific ulcerative colitis (UC) is a chronic disease of unknown etiology characterized by a continuous or undulating course, which is based on a diffuse inflammatory process of the mucous membrane of the colon, starting in the rectum and extending in the proximal direction. The first report on NLK belongs to K. Rokityansky, described in 1842.
- NONSPECIFIC ULCERATIVE COLITIS
- A disease with a primary lesion of the colon, with ulceration of the mucous membrane. Classification (according to Yu. V. Baltaitis et al., 1986) 1. Flow pattern: acute, chronic, recurrent, continuous. 2. The development of the disease: intermittent, remittent. 3. The severity of the disease: mild, moderate, severe. 4. The prevalence of lesions:
- NONSPECIFIC ULCERATIVE COLITIS
Nonspecific ulcerative colitis is a chronic disease with a progressive course, which is based on the inflammatory process in the large intestine with pronounced necrotic changes of the mucous membranes and submucous membranes, up to their ulceration with bleeding and perforations, severe immunological reactions, and manifested in persistent and growing disorders of the fat intestines
- Nonspecific ulcerative colitis.
The pathological process in ulcerative colitis always begins in the rectum and in rare cases is limited only by this section (proctitis). Inflammation gradually spreads in the proximal direction, capturing the adjacent parts of the sigmoid (proctosigmoiditis), then the descending colon (left-sided colitis) and from a relatively isolated collar to total colitis. Sometimes in
- NON-SPECIFIC ULCEROUS COLITIS (code K 51)
Ulcerative colitis is a chronic necrotizing lesion of the mucous and sub mucous layers of the colon. The nature of the disease is unknown. More often men of young and mature age are ill. The lesion of the rectum (in 100% of cases) and the distal colon is characteristic. Pancolitis occurs in 25% of cases. Clinic. Stool with blood, mucus, more often at night and in the morning. Moderate pain in the left
- 5.9. NONSPECIFIC ULCERATIVE COLITIS
The purpose of pharmacotherapy: to conduct course therapy, providing symptomatic remission of the disease (normal weight, passage of excreted feces, absence of fever, anemia, erosions and ulcerations of the rectal mucosa (rectoromanoscopy is carried out in the course of treatment and always in clinical remission). Therapeutic measures in the active phase (during exacerbation): Distal proctitis:
- Inflammatory bowel disease (ulcerative colitis, Crohn's disease)
Inflammatory bowel disease (ulcerative colitis, disease
- Bowel disease. Infectious enterocolitis (dysentery, typhoid fever, cholera). Nonspecific ulcerative colitis. Crohn's disease. Ischemic bowel disease. Appendicitis. Colon cancer.
1. Macroscopic characteristics of the small intestine with cholera enteritis 1. gray-yellow film tightly soldered to the wall 2. ulceration of the mucous membrane 3. multiple hemorrhages 4. wall sclerosis 2. Elements of the pathogenesis of typhoid fever 1. bacteremia 2. bacteriochemia 3. cerebral swelling 4. exudative inflammation 5. hypersensitivity reaction in the lymphoid apparatus 3. Modern
- ULCERATIVE COLITIS
Inflammatory disease of the colon, affecting, as a rule, the mucous membrane of the rectum and other parts of the colon, having a relapsing or continuous chronic course. The etiological factor of ulcerative colitis is not exactly established. Attempts are being made periodically to associate this disease with any infectious agent, in recent years, for example, with the measles virus or the bacillus.
- Chronic chronicle
Chronic colitis is a disease characterized by an inflammatory lesion of the colon mucosa. Many authors use the definition of “irritable bowel syndrome” - a functional disease characterized by impaired intestinal motility. This does not exclude catarrhal inflammation of the mucous membrane of the colon. The pathological process may be involved as
- Large intestine inflammation (colitis)
Colitis is a disease resulting from inflammatory and dystrophic changes in the colon. The inflammatory process may be limited or common to several segments. The most commonly affected is the distal colon (proctitis) or the rectum and sigmoid colon (proctosigmonditis). There are acute and chronic colitis. The most common non-infectious colitis occurs.
Colitis is an inflammation of the mucous membrane of the colon, the longest and most important part of the colon. Colitis is accompanied by severe abdominal pain, diarrhea, alternating with constipation, severe general fatigue, and sometimes intermittent fever. See the articles PONOS, DOSE, and INTESTINE (PROBLEMS), with the addition that the person is experiencing or has experienced intense anger. See also page.
1. What are the epidemiological features of acute colitis? • German shepherds and golden retrievers are the most common illnesses. • Dogs from 1 to 4 years of age are sick more often. • Males are sick more often than females (3: 2). 2. What are the main clinical symptoms of acute colitis? • Diarrhea or mushy stools (watery, slimy, mixed with fresh blood, frequent in small quantities). • Tenesmus. •
- Chronic colitis
Chronic colitis is a disease characterized by inflammatory lesions of the mucous membrane of the colon, the clinical picture of which is dominated by pain and dyspeptic syndromes, and the morphological basis is a combination of inflammatory elements with signs of epithelial dystrophy, a decrease in the depth of crypts and the development of varying degrees of lymphoplasmacytic infiltration. In those
- Pseudomembranous colitis associated with antibiotics
Pathophysiology Pseudomembranous colitis is caused by a toxin produced by Clostridium difficile. This toxin directly affects the colon cells, causing damage to the mucosal areas that form the characteristic "pseudomembrane". Although classically this syndrome is described after intravenous therapy with clindamycin, Clostridium difficile can suppress the normal flora.
- 67. Chronic enteritis and colitis
Enteritis Etiology and pathogenesis 1) infections - typhoid fever, dysentery, salmonellosis, etc .; 2) transferred acute enteritis; 3) dysbacteriosis - microbial imbalance in the intestine; 4) nutritional factor - irregular food, dry meal, chronic intestinal overload of digestible food; 5) radiation exposure; 6) alcohol abuse; 7) allergic effects; eight)
- Nonspecific immunity
Nonspecific immunity is a system of immune defense that is not associated with antigens and antibodies, which includes phagocytosis and general non-specific resistance. Phagocytosis is the active capture, absorption and digestion of living cells and non-living particles by special cells of the body - phagocytes. These are the largest cells of the human body, they perform an important nonspecific defense function.
- Peptic ulcer
Epidemiology Accurate epidemiological data on the frequency and prevalence of peptic ulcer are not available. According to various studies, in the United States every 10th man and every 20th woman has a peptic ulcer. Most likely, the prevalence and frequency of the disease tend to decrease. Previously, peptic ulcer disease was more common in men than in women (4: 1).
- Peptic ulcer
Peptic ulcer is a chronic recurrent disease, characterized by a defect in the mucous membrane area and ulceration in the stomach and / or duodenum. Along with peptic ulcer as an independent nosological form, it is now customary to distinguish secondary, symptomatic ulcers and gastroduodenal ulcers that occur when exposed to a known etiological
- Peptic ulcer
Peptic ulcer is a group of heterogeneous diseases, a common manifestation of which is a local defect or erosion in the mucous membrane of the stomach and / or duodenum. This is a very common pathology, which, for example, in the United States for life endure about 10% of men and 5% of women. It should be noted that the prevalence of gastrointestinal