- 1Causes of pain
- 2 Gastritis
- 3 peptic ulcer
- 5 food poisoning
- 6 Duodenitis and pancreatitis
- 7 Diagnosis and treatment
1Causes of pain
If you feel severe discomfort, you should consult a specialist. An important aspect of diagnosis is to clarify the nature of the pathology. Stomach pains are most often concentrated in the area of the organ's projection onto the abdominal wall. This area is called epigastric. Pain in the stomach can be localized, diffuse, radiating, acute, dull, paroxysmal, burning and cutting.
To establish the cause of its appearance, the intensity of the syndrome should be identified. In this case, the main characteristics of pain are determined:
- character;
- time of appearance;
- duration;
- localization;
- connection with food intake;
- weakening or strengthening with movement, after a bowel movement, or with a change in posture;
- combination with other symptoms (nausea, loss of appetite, vomiting, bloating).
The feeling of pain in the stomach in most cases is associated with organ damage. The most common causes are:
- acute and chronic gastritis;
- stomach ulcer;
- the presence of polyps;
- damage to the mucous organ in case of food poisoning (intoxication or toxic infection);
- damage due to abdominal trauma;
- severe stress;
- intolerance to certain products;
- injury to the mucous membrane by accidentally swallowed objects.
Stomach pain may be due to other causes. These include pancreatitis, peptic ulcer of the 12th intestine, colitis, enterocolitis, cholecystitis, biliary dyskinesia, irritable bowel syndrome, appendicitis, heart disease.
2 Gastritis
The most common causes of stomach pain are acute or chronic gastritis. These forms of the disease are characterized by inflammation of the mucous layer of the organ against the background of exposure to irritating factors. Quite often, gastritis is of an infectious nature. In this case, Helicobacter pylori bacteria act as a starting point. The disease occurs in children, young people and the elderly. When it hurts in the stomach, in this case there is acute gastritis, which is divided into simple, catarrhal, erosive, fibrinous and phlegmonous. If the disease becomes chronic, organ atrophy often develops. The main provoking factors for the onset of gastritis are:
- abuse of spicy, fried, hot or cold foods;
- alcohol consumption;
- smoking;
- infection with Helicobacter bacteria;
- accidental or deliberate use of acids or alkalis;
- uncontrolled intake of medications (drugs of the NSAID group).
The symptoms of gastritis are varied. In children and adults, stomach discomfort is the main symptom of the disease. Most often worried about Blunt pain... Sharp manifestations are typical of acute mucosal inflammation. With gastritis, the pain syndrome can be paroxysmal or constant. There is a clear connection with food intake (spasm appears after eating and when a person is hungry). Additional symptoms of the disease may include belching, nausea, disturbed stools, bloating, and acidic sensation in the mouth. Not pronounced aching pain is characteristic of chronic gastritis with normal acidity.
3 peptic ulcer
Acute stomach pain associated with eating may indicate the presence of peptic ulcer... It is chronic. Pain syndrome is most pronounced during an exacerbation. Ulcers form against the background of stress, gastritis, the use of certain medications, endocrine diseases... The pathogenesis of the formation of this defect is associated with suppression defense mechanisms(a violation of the synthesis of mucus covering the stomach), as well as an increase in the acidity of gastric juice. The symptoms of stomach ulcers are similar to those of gastritis. The main signs of the disease include:
- severe pain in the epigastric region;
- nausea and vomiting after eating;
- weight loss;
- violation of appetite.
With ulcerative lesions, the stomach hurts after eating. This is the main difference from the pathology of the 12 intestine. Pain syndrome occurs almost immediately after eating (within an hour and a half). There is a definite connection between the exacerbation and the season. Most often, a person suffers from bouts of pain in the fall and spring. In the event of complications (perforation, bleeding), the symptoms can increase dramatically. This state requires emergency care... The processes occurring in the stomach, the causes of which can be different, are often reversible.
4 Cancer
If the stomach hurts, the reason may lie in oncology. This is one of the most common malignant pathologies. Nearly a million people worldwide die from stomach cancer each year. For a long time, the disease may not manifest itself in any way. Quite often, cancer is detected already at 3 or 4 stages, when treatment is ineffective. Men suffer from this disease more often than women. Cancer is dangerous because the tumor in its later stages is capable of metastasizing to other organs, which is why patients die. Exact reason the disease is still unknown. Possible etiological factors are: the presence of atrophic gastritis, organ infection with Helicobacter bacteria, exposure to toxic and carcinogenic substances, inappropriate nutrition, drug intake, alcoholism, burdened heredity, Menetrie's disease.
Early cancer symptoms are represented by decreased appetite, aversion to meat, nausea, bloating, weight loss, malaise, weakness, and swallowing problems. In the later stages, patients may experience aching pain. In most cases, it is caused by the growth of the tumor into neighboring organs. Constant pain of a girdle character appears when a neoplasm is introduced into the pancreas. Operative treatment should be started as soon as possible. Acute pains, reminiscent of an attack of angina pectoris, are characteristic of a tumor that has grown into the diaphragm. If the pain syndrome is combined with a transfusion in the abdomen, a stool disorder of the constipation type, this may indicate the involvement of the transverse colon in the process.
5 food poisoning
Sharp stomach pain may be a sign food poisoning... This is a disease that develops when eating poor-quality food containing pathogenic microorganisms, their decay products or various toxic compounds. All food poisoning is divided into the following forms:
- microbial;
- non-microbial etiology;
- mixed.
The first group includes foodborne diseases and intoxication. In this situation, the causative agents are bacteria (clostridia, colibacillus, proteus, streptococci), mushrooms, toxins. Poisoning is also possible with poisonous plants, mushrooms, berries, fish roe, seafood, heavy metal salts, pesticides, pesticides. Symptoms in this pathology are caused by inflammation of the stomach against the background of exposure to toxins.
In most cases, there are signs of gastroenteritis. These include constant pain in the muscles, head, nausea, vomiting, fever, weakness, and increased stool frequency. Symptoms of dehydration are common. Diagnostic signs food poisoning are:
- acute, sudden onset;
- the connection of pain with food intake;
- the simultaneous appearance of symptoms in a group of individuals;
- the transience of the disease.
6 Duodenitis and pancreatitis
Pain in the epigastric region can be a symptom of duodenitis (inflammation of the mucous membrane of the 12th intestine). It can be acute or chronic. This is the most common pathology of this organ. Quite often, this disease is combined with enteritis and gastritis. The main causes of inflammation of the 12th intestine are:
- inaccuracies in nutrition;
- drinking alcoholic beverages;
- bacterial infection;
- the presence of an ulcer or gastritis;
- violation of blood supply;
- chronic pathology of the liver and pancreas.
The main symptoms of the disease depend on its form. Duodenitis, which has arisen against the background of an ulcer or infectious gastritis, is characterized by pain on an empty stomach, at night and a few hours after eating. Strong manifestations are characteristic of the acute type of pathology. When combined with inflammation of other departments small intestine symptoms may include malabsorption syndrome, dyspeptic disorders. In case of stagnation of the secretion of the 12th intestine, paroxysmal pains, belching, nausea, vomiting, bloating, rumbling occur. With duodenitis, the outflow of bile may be impaired. In this situation, pain appears in the epigastric region. Clinical picture resembles biliary dyskinesia.
If something hurts in the stomach, the reason may be pancreatitis, the symptoms of which are usually quite pronounced. Pain syndrome is most pronounced in acute inflammation of the pancreas. The latter is located next to the stomach. This pathology is characterized by the appearance of pain in the upper abdomen. It can last from several minutes to several days. The pain is intense, constant and distressing to the patient. It can give to the left or right half of the body, depending on which part of the organ is affected (head, body or tail). The pain syndrome increases with food intake and treatment is required. It often takes on a shingles character. Additional signs of the disease include nausea, vomiting, bloating, tenderness to palpation, and an increase in overall body temperature.
7 Diagnosis and treatment
If your stomach is sick, then you should not postpone the visit to the doctor indefinitely, because the consequences can be dangerous. Treatment is carried out only after establishing the cause of the pain syndrome. Diagnostics includes:
- detailed survey of the patient;
- physical examination (palpation of the abdomen, listening to the lungs and heart);
- general and biochemical analysis blood;
- carrying out FGDS;
- determination of gastric acidity;
- a blood test for the presence of Helicobacter pylori;
- Ultrasound of the abdominal organs;
- laparoscopy;
- fecal examination;
- contrast radiography;
- CT or MRI;
- duodenal intubation;
- Analysis of urine.
Colonoscopy may be done if colitis is suspected. A biopsy is done to rule out stomach cancer. How to get rid of stomach pain? Therapy should be directed at the underlying cause. If the stomach is inflamed, what to do in this situation? Treatment of gastritis involves adherence to a strict diet, the use of drugs (antacids, proton pump blockers, gastroprotectors). The use of Almagel, Fosfalugel and Omez is indicated in the form of the disease with high acidity. If the bacterium Helicobacter is detected, antibiotics and Metronidazole are used.
Therapy acute pancreatitis includes temporary fasting, applying cold to the stomach, the use of antispasmodics, Omeprazole, diuretics, infusion therapy.
With purulent pancreatitis, treatment necessarily includes antibiotics. If vomiting is present, use antiemetic drugs (metoclopramide). With the development of peritonitis and organ necrosis, an operation is indicated. Chronic form pancreatitis involves adherence to a diet, taking enzyme preparations (Panzinorm, Pancreatin, Mezima). In case of stomach cancer, surgical treatment (organ resection or removal). Thus, the causes of abdominal pain can be very different. If any, you should consult your doctor.
What to do in case of exacerbation of gastric ulcer?
If the patient has an acute critical situation associated with perforation of the gastric ulcer, it is necessary emergency treatment, since peritonitis in this case progresses rapidly. Symptoms of perforation in this case are:
- the appearance of a sharp pain that quickly spreads throughout the abdomen;
- muscle tension of the walls of the peritoneum;
- phenomena preceding fainting (dizziness, ringing in the ears, weakness);
- chills;
- nausea;
- dry mouth.
Traditional therapies
Therapeutic assistance in the phase of exacerbation of gastric ulcer is determined based on the patient's condition, age, and the nature of clinical symptoms. However, the treatment of uncomplicated forms is almost always based on the use of bactericidal agents, for example, Amoxicillin, Metranidazole, Clarithromycin. Due to these drugs and some others, also belonging to the group of antibiotics, it becomes possible to cure the pathology of the gastric mucosa, since they eliminate the main reason- pathogenic microorganism Helicobacter pylori.
In addition to antibacterial drugs in the treatment of acute ulcers, the following can be used:
1. means that normalize the level of acidity of the digestive juice (Omeprazole, Ranitidine);
2. drugs with gastroprotective (protective) properties (De-nol and other bismuth-containing medicines);
3. blockers of dopamine central receptors (Primperan, Raglan, Cerucal);
4. drugs with a psychotropic effect, if the patient suffers from irritability, insomnia, a feeling of constant anxiety (Tazepam, Elenium);
5. adrenergic drugs that have an anti-secretory and suppressive gastrin release effect (Obzidan, Inderal).
In the treatment of exacerbation of gastric ulcer, certain physiotherapeutic methods have also proven themselves well: ozokerite and paraffin applications, magneto- and hydrotherapy, sessions of modulated sinusoidal currents.
Carrying out all activities in combination with a diet in 80-90% of cases allows you to achieve a stable remission of the pathology. but conservative treatment does not always help, and then the patient is shown surgical intervention in different ways from the circumstances (by the method of selective proximal vagotomy, resection, endoscopy).
Indications for stomach surgery:
- perforation of ulceration;
- an ulcer complicated by profuse bleeding (bleeding leading to hypovolemia);
- pyloric stenosis;
- defect penetration.
Traditional recipes for treatment
Apply folk ways to cure the ulcer, experts do not recommend due to the risk of aggravating the situation. Such treatment is especially prohibited in complicated acute forms. But in order to prevent exacerbation, use some unconventional recipes doctors admit, for example, a remedy:
1.from birch leaves (1 teaspoon of chopped fresh leaves of this tree is poured with a glass of boiling water, infused for 1-2 hours);
2. from mother-and-stepmother (the infusion is prepared similarly to the previous method with one difference that not only the leaves of the plant, but also the flowers themselves can be used); in addition, this folk recipe helps to heal both the stomach and bronchi;
3. from medicinal marshmallow (1 large spoonful of its crushed rhizome is poured with 250 ml of boiling water, for 30 seconds everything is simmering over low heat, and then infused for about half an hour).
All listed funds traditional medicine you need to drink before meals 3 times a day.
Diet for ulcers
Compliance with dietary nutrition is equally important during an exacerbation of the inflammatory process, and in the stage of its remission, and in case of complications with stenosis, bleeding and other life-threatening factors. Therefore, the doctor prescribes a personal diet for the patient based on:
- sparing the gastroduodenal mucosa with the elimination of all chemical, thermal and mechanical irritants;
- fractional nutrition (the patient is recommended to eat and drink in small portions, but every 3-4 hours);
- correction of fat in the direction of increase;
- increasing the protein quota;
- lowering the proportion of carbohydrates in the daily diet.
The diet for the treatment of stomach ulcers should be followed for at least 6-9 months. When the disease recedes, going into a phase of remission, and food will not cause discomfort to the stomach, you can gradually return to the usual type of dishes (not mashed and not very boiled), but you still have to completely abandon rough and harmful industrial products.
In addition to diet, an important role in the prevention and treatment of acute ulcers is played by the exclusion of alcohol and energy drinks due to their causing bleeding and the growth of erosive inflammations.
Duodenal bulb ulcer
One of the most common types of erosive formations of the gastrointestinal tract is a bulb ulcer. duodenum... The disease is common. According to official data, up to 10% of the world's population are sick. Deformation develops due to a failure in the chemical processing of food. The anatomy of erosive formations is different, but more often they form on a bulb shaped like a ball. The duodenal bulb is located at the very beginning of the intestine, when it leaves the stomach. The treatment is long and difficult.
It can be deformed on the front and back walls (kissing ulcers). The ulcer of the duodenal bulb also has a special location - at the end or at the beginning (mirrored). Mirror erosion is treated like other forms. Negative factors that affect the work of the stomach and intestines, provoke the appearance of ulcers of various shapes. The risk group includes middle-aged people and those who are forced to work the night shift.
If there is a failure in the processing of food by the stomach, an ulcer of the duodenal bulb may occur.
Causes of ulcers of the duodenal bulb
Most often, inflammation of the duodenum occurs due to the aggressive action of acid. In the absence of therapy, perforated ulcers and bleeding may develop. There can be a number of reasons:
- disturbed diet (a lot of fatty, spicy, diet abuse, carbonated drinks);
- Helicobacter bacteria is the cause of ulcerative formations in most cases;
- smoking, alcohol;
- severe stress or systematic stay in a state of emotional stress;
- hereditary predisposition;
- long-term use of certain anti-inflammatory drugs;
- incorrectly prescribed treatment for initial stage illness.
Kissing ulcers in the intestines may appear due to concomitant causes: HIV infection, liver cancer, hypercalcemia, renal failure, Crohn's disease, etc.
Symptoms
Symptoms of duodenal ulcer are characteristic of other types of gastrointestinal ulcers, and they appear depending on the stage of the disease:
- heartburn;
- nausea in the morning or after eating;
- pain in the epigastric region;
- pain in the stomach at night;
- flatulence;
- the appearance of a feeling of hunger after a short period of time after eating;
- if the disease is in neglected form bleeding may open;
- vomit;
- pain localized in the lumbar region, or the chest part.
The inflammatory lymphofollicular form of the duodenum has a different nature of pain: stabbing pain, sharp or aching. Sometimes it passes after a person has eaten. Hunger pains usually occur at night, and to eliminate unpleasant sensations it is recommended to drink a glass of milk or eat a little. Nocturnal pain is caused by a sharp rise in acid levels.
Stages
The intestinal healing process is divided into 4 main stages:
- Stage 1 - initial healing, characteristic is the creeping of the layers of the epithelium;
- Stage 2 - proliferative healing, in which protrusions in the form of papillomas appear on the surface; these formations are covered with regenerating epithelium;
- Stage 3 - the appearance of a polysadny scar - an ulcer on the mucous membrane is no longer visible; a more detailed study shows many new capillaries;
- Stage 4 - scar formation - the bottom of the ulcer is completely covered with new epithelium.
Erosive kissing formations on the duodenum are healed after the application of therapy. Multiple ulcers in a small area of the intestine result in multiple scars. The result of such healing is cicatricial and ulcerative deformity of the duodenal bulb. The appearance of fresh scars leads to a narrowing of the lumen of the bulbous sector. Inflammatory cicatricial deformity duodenal bulb has Negative consequences, for example, food stagnation and malfunctioning of the entire gastrointestinal tract.
There is also a distribution at the stage: exacerbation, scarring, remission.
One of the forms of intestinal ulcers is lymphoid hyperplasia of the duodenal bulb, which is characterized by inflammation due to a disturbance in the outflow of lymph. The causes are exactly the same as for duodenal ulcers. There is also similar symptoms... Lympofollicular dysplasia is a pathology in the mucous membrane of the intestine or stomach. It is characterized by the appearance of formations of a rounded shape on a broad base. Lymphofollicular dysplasia is deformed and has a dense consistency and point size. The lymphofollicular mucosa is infiltrated. Development stages:
- sharp;
- chronic.
Diagnosis of the disease
Accurately diagnose the presence of a duodenal ulcer will help FGDS method(fibrogastroduodenoscopy). Using a special probe with a camera, the intestinal surface is examined. It is this diagnostic method that will make it possible to establish the location of the ulcer, its size and the stage of the disease. Usually there is inflammation, or the surface is hyperemic, covered with punctate erosions of a dark red color. The area of the intestine is inflamed in the area of the mouth, and the mucous membrane is hyperemic.
Tests are required to determine the Helicobacter bacteria. As a material for testing, not only blood and feces are used, but also vomit, material after biopsy. Ancillary diagnostic methods include x-rays, palpation in the stomach, and a complete blood count.
Treatment
After the diagnosis of "inflammation of the duodenal bulb" is made, treatment should be started immediately, since serious complications may develop. Kissing ulcers are treated mainly with medications. During an exacerbation, hospitalization is necessary.
The doctor selects drugs and physiotherapy individually for each patient, taking into account the characteristics of the body and stage. For example, the chronic or lymphofollicular stage is treated differently than during an exacerbation. This scheme usually includes the following medications:
- bismuth-based medicines, in case of detection of the Helicobacter bacteria; such drugs have a depressing effect on pathogenic microflora;
- drugs that reduce the amount of gastric juice produced: blockers, inhibitors, anticholinergics;
- prokinetics - improve intestinal motility;
- unpleasant pain sensations are eliminated with the help of antacids;
- antibiotics are prescribed to combat the bacterial cause of the appearance of a lymphofollicular ulcer;
- gastroprotectors will help prevent the negative effects of hydrochloric acid on the affected area;
- inflammation is relieved by analgesics and antispasmodics.
The combination of medication and physical therapy contributes to a faster recovery of the body. These techniques include: electrophoresis, ultrasound exposure, the use of microwaves, therapy with modulated currents to relieve pain. Special physiotherapy exercises will help to normalize gastric motility. Gymnastics is good prophylactic agent from stagnation in the intestines and stomach.
In addition to the generally accepted methods of healing intestinal ulcers, traditional medicine has long been proven to be effective. In first place with ulcerative lesions there is freshly squeezed potato juice. It must be drunk three times a day, and only freshly squeezed. The potatoes are pre-peeled, grated, and squeezed through cheesecloth. The first few days, the dosage is one tablespoon. Gradually, it can be increased to half a glass. You must drink before eating.
To others, no less effective means, include honey, healing herbs(calendula, St. John's wort, plantain), olive and sea buckthorn oils.
During the period acute form be sure to comply with bed rest. After the exacerbation has passed, you can take short walks. Heavy physical activity and exercise are prohibited. The army is contraindicated for those who have an ulcer. In order not to provoke new attacks, it is important to avoid stress and protect the nervous system.
Dieting is one of the important factors on the path to recovery and reduction of inflammation. General dietary guidelines are as follows:
- small portions;
- chew each piece thoroughly;
- temporarily exclude foods that provoke the active production of gastric juice (vegetable soups, fish and meat broths);
- in order not to irritate the mucous membrane additionally, the food should be grated;
- fruit juices must be diluted with water;
- drink milk more often;
- do not use spices in dishes;
- cook grated porridge;
- eat food at the optimal temperature, not too hot or too cold;
- fractional meals, up to 5 times a day.
Food should be steamed or in the oven. The diet must include non-acidic fruits, kefir, milk, cottage cheese, boiled or steamed vegetables. It is necessary to stop drinking alcohol and smoking, as this can lead to the development of serious complications.
Forecast
A favorable prognosis for recovery can be if the treatment was carried out on time and the correct diet was followed. With an untimely visit to a doctor or improperly prescribed drugs, serious complications can develop: lymphatic follicular ulcer, bleeding (vomiting of blood), perforation of the ulcer (acute pain under the sternum) and penetration (due to adhesions, the contents of the intestine enter neighboring organs). In each of these cases, the only option is surgery.
Duodenal stenosis is a complication. After healing, there are cicatricial changes that can subsequently cause swelling and spasm. Stenosis usually manifests itself during the acute form or after therapy. Stenosis occurs in those patients in whom the ulcer does not heal for a long time. Stenosis is accompanied by impaired intestinal and gastric motility.
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This macro-preparation is the stomach. The masses and sizes of the organ are normal, the shape is preserved. The organ is light gray in color, the relief is strongly developed. On the lesser curvature of the stomach in the pyloric section, there is a significant depression in the stomach wall 2x3.5 cm. Its limiting surface of the organ is devoid of characteristic folding. The folds converge to the boundaries of the formation. In the area of the pathological process, there are no mucous, submucous and muscular layers of the stomach wall. The bottom is smooth, filled with a serous membrane. The edges are ridge-like raised, dense, have a different configuration: the edge facing the gatekeeper is shallow (due to gastric motility).
Description of pathological changes:
These pathological changes could develop as a result of general and local factors (general: stressful situations, hormonal disorders; medicinal; bad habits that lead to local disorders: hyperplasia of the glandular apparatus, increased activity of the acid-peptic factor, increased motility, an increase in the number of gastrin-producing cells; and general violation: excitation of the subcortical centers and hypothalamic-pituitary region, increased tone vagus nerve, increase and subsequent depletion of the production of ACTH and glucocarticoids). Acting on the gastric mucosa, these violations lead to the formation of a defect in the mucous membrane - erosion. Against the background of non-healing erosion, an acute peptic ulcer develops, which, with continued pathogenic effects, turns into a chronic ulcer, which goes through periods of exacerbation and remission. During the period of remission, the bottom of the ulcer can be covered with a thin layer of epithelium, layering on the scar tissue. But during the period of exacerbation, "healing" is leveled as a result of fibrinoid necrosis (which leads to damage not only directly, but also by fibrinoid changes in the walls of blood vessels and disruption of the trophism of the ulcer tissues).
1) favorable: remission, healing of the ulcer by scarring, followed by epithelialization.
2) unfavorable:
a) bleeding;
b) perforation;
c) penetration;
d) malignancy;
e) inflammation and ulcerative cicatricial processes.
Conclusion: these morphological changes indicate a destructive process in the stomach wall, which leads to the formation of a defect in the mucosa, submucosa and muscular membrane - ulcers.
Diagnosis: Chronic gastric ulcer.
Description of drugs by Pathological Anatomy in Lesson number 26
(This is an indicative description, not a cathedral, some drugs may be missing, since the description of past years)
LESSON number 26stomach diseases: gastritis, peptic ulcer, stomach tumors
Micropreparation № 37 "Acute catarrhal gastritis" - description .
The mucous membrane of the stomach is covered with purulent exudate, which penetrates into all layers of the stomach wall. The openings of the glands are widened. The cytoplasm of the epithelium is vacuumed. Own layer of the mucous membrane with congested vessels, in places with diapedesic hemorrhages, polymorphonuclear leukocytes (PMN).
Micropreparation № 112 "Chronic superficial gastritis" - demo .
Micropreparation № 229 "Chronic atrophic gastritis" - description .
The mucous membrane of the stomach is sharply thinned, the number of glands is reduced, in place of the glands, fields of growing connective tissue... The fossa epithelium with symptoms of hyperplasia. Epithelium of the glands with signs of intestinal metaplasia. The entire wall of the stomach is diffusely infiltrated by histolymphocytic elements with an admixture of polymorphonuclear leukocytes.
Macrodrug "Acute erosions and stomach ulcers" - description .
The mucous membrane of the stomach with smooth folds and numerous defects of the mucous membrane of a round and oval shape, the bottom of which is painted black.
Macrodrug "Chronic stomach ulcer" - description .
On the lesser curvature of the stomach, a deep defect of the mucous membrane is determined, affecting muscle layer, rounded with dense, raised, amoosolized edges. The edge of the defect facing the esophagus is undermined, to the gatekeeper it is shallow.
Micropreparation № 121 "Chronic stomach ulcer in the acute stage" - description .
A defect in the wall of the stomach is determined, capturing the mucous and muscular layer, with an undermined edge facing the esophagus, and shallow, facing the gatekeeper. At the bottom of the defect, 4 layers are determined. The first is external - fibrinous-purulent exudate. The second is fibrinoid necrosis. The third is granulation tissue. The fourth is scar tissue. At the edges of the defect, strips of muscle fibers, amputation neuroma are visible. Vessels of the cicatricial zone with sclerosed thickened walls. The mucous membrane at the edges of the defect with symptoms of hyperplasia.
Macrodrug "Polyp of the stomach" - description .
On the gastric mucosa, a tumor formation on a broad base (pedicle) is determined.
Macrodrug "Saucer-shaped stomach cancer" - description .
The tumor looks like a rounded flat formation on a wide base. The central part of the tumor sinks, the edges are somewhat raised.
Macrodrug "Diffuse stomach cancer" - description .
The wall of the stomach (mucous and submucous layers) is sharply thickened, represented by a uniform grayish-white dense tissue. The mucous membrane over the tumor with symptoms of atrophy with smoothed folding.
Micropreparation № 77 "Adenocarcinoma of the stomach" - description .
Micropreparation № 79 Cricoid cell carcinoma - demo .
The tumor is built of atypical glandular complexes formed by cells with pronounced cellular polymorphism. The stroma is not developed.
Micropreparation № 70 "Metastasis of adenocarcinoma in the lymph node" - description .
The pattern of the lymph node is erased, the growth of tumor tissue is represented by atypical glandular cosplexes.
9. What is, on average, the total duration of the first three stages of development of lobar pneumonia?
10. Specify the ways of spreading inflammation in lobar pneumonia.
11. List the pulmonary complications of lobar pneumonia caused by Streptococcus pneumoniae.
12. Describe the composition of the exudate in case of lobar pneumonia in the tidal stage.
13. Describe the composition of the exudate in case of lobar pneumonia in the stage of red hepatization.
14. Describe the composition of the exudate in lobar pneumonia in the stage of gray hepatization.
15. Specify the extrapulmonary complications of lobar pneumonia caused by Streptococcus pneumoniae.
16. Give the macroscopic characteristics of changes in the lungs with bronchopneumonia.
17. Give a microscopic characterization of changes in the lungs with focal pneumonia.
18. Name the features of the causative agents of nosocomial pneumonia.
19. Name the complication of lobar pneumonia that develops with excessive activity of neutrophils with massive destruction lung tissue.
20. Specify the complication of lobar pneumonia that develops with insufficient activity of neutrophils and the development of the organization of fibrinous exudate.
21. Name the reasons for the formation of a lung abscess.
22. List the reasons for the formation of a lung abscess.
23. Give a definition of the term atelectasis.
24. What develops when the airway is completely closed?
25. What develops with partial filling pleural cavity liquid exudate?
26. What develops when respiratory distress syndrome, due to the destruction of the surfactant?
27. Specify the cause of hemodynamic pulmonary edema.
28. A 25-year-old patient fell ill suddenly after hypothermia while intoxicated. Complains of a rise in body temperature to 390C, chills, dagger pain in the right side and severe weakness for 7 days. Objectively: a dull sound is heard above the lower lobe of the right lung during percussion, during auscultation, breathing is not performed, a pleural friction noise is heard. Radiographically - darkening of the lower lobe of the right lung, in the region of the 8th segment there is a cavity, thickening of the pleura. Your conclusion.
29. In a patient with a stroke and left-sided hemiparesis on the 14th day, the body temperature increased to 380C, which was accompanied by the appearance of cough and small bubbling rales in the lower parts of the left lung. Your conclusion.
30. A 67-year-old man who is on inpatient treatment about phlegmon of the scalp, shortness of breath, cough appeared, body temperature rose to 38.50C. 4 weeks after the massive antibiotic therapy, the body temperature dropped, dyspnea decreased, and moderate leukocytosis persisted. During an X-ray examination, an annular shadow with a fluid level appeared in the second segment of the right lung. Your diagnosis.
II lesson
CHRONIC NON-SPECIFIC LUNG DISEASES. INTERSTITIAL LUNG DISEASES. PNEUMOCONIOSIS. LUNG CANCER.
1. Diffuse chronic lung lesions: definition of the concept and classification. Chronic obstructive pulmonary disease. General characteristics.
2. Chronic obstructive pulmonary emphysema- definition, classification, epidemiology, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes, causes of death. Other types of emphysema (compensatory, senile, vicarious, interstitial): clinical and morphological characteristics.
3. Chronic obstructive bronchitis: definition, classification, etiology, epidemiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes.
4. Bronchiectasis and bronchiectasis. Concept, classification, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes, causes of death. Kartagener's syndrome. Clinical and morphological characteristics.
5. Diffuse interstitial lung disease. Classification, clinical and morphological characteristics, pathogenesis. Alveolitis. Morphological characteristics, pathogenesis. Pneumoconiosis (anthracosis, silicosis, asbestosis, beryllium). Pathogenesis and morphogenesis, clinical manifestations, complications, causes of death. Sarcoidosis Clinical and morphological characteristics, morphology of extrapulmonary lesions.
6. Idiopathic pulmonary fibrosis. Classification, etiology, pathogenesis and morphogenesis, stages and variants, clinical and morphological characteristics, prognosis.
7. Pneumonitis(desquamative interstitial pneumonitis, hypersensitivity pneumonitis): patho - and morphogenesis, clinical and morphological characteristics, causes of death. Eosinophilic lung infiltrate. Classification, causes, clinical and morphological characteristics.
8. Tumors of the bronchi and lungs. Epidemiology, principles of classification. Benign tumors. Malignant tumors... Lung cancer. Bronchogenic cancer. Epidemiology, etiology. Biomolecular markers of lung cancer. Precancerous changes in the bronchi and lung. The concept of "cancer in the rumen". Clinical manifestations. Diagnostic methods, morphological characteristics, macroscopic variants, histological types (squamous cell, adenocarcinoma, small cell, large cell). Bronchioloalveolar cancer: clinical and morphological characteristics.
1. Lecture material.
vol. 2, part I: p. 415-433, 446-480.
vol. 2, part I: pp. 293-307, 317-344.
4. Guide to practical training in pathological anatomy (2002) p. 547-567.
5. Atlas on pathological anatomy (2003) p. 213-217.
LEARNING CARD
PURPOSE INSTALLATION OF THE LESSON: to study the morphology of the main forms by macrospecimens, microspecimens and electronograms chronic diseases lungs and conduct clinical and anatomical comparisons.
CHRONIC NON-SPECIFIC
LUNG DISEASES
View macropreparations, the main clinical and anatomical forms of chronic nonspecific lung diseases. Describe CHRONIC LUNG ABSCESS, CHRONIC BRONCHITIS WITH BRONCHEECTASES, PULMONARY EMFYZEMA.
Micropreparation No. 12 CHRONIC DEFORMAL BRONCHITIS (staining with hematoxylin and eosin). To note the components of chronic inflammation of the bronchi: peribronchial sclerosis, vascular pericalibration, inflammatory infiltration in the wall of the bronchi and peribronchial tissue, metaplasia of the bronchial epithelium.
Electronogram Intracapillary sclerosis in pulmonary emphysema (atlas, fig. 11.13). Note the formation of a capillary with a sclerosed wall and the destruction of the air-blood barrier.
PNEUMOCONIOSIS
Macrodrug ANTHRAKO-LUNG SILICOSIS. Pay attention to the change in volume and decrease in the airiness of the lung tissue. To characterize the sclerotic areas in the lung: their shape, size, color, prevalence.
Micropreparation No. 000 LUNG ANTHRAKO-SILICOSIS (staining with hematoxylin and eosin). Outline the structure of the silicotic nodule, concentrically located collagen fibers around the sclerosed vessels. Pay attention to the significant amount of coal dust contained both in the cytoplasm of macrophages (coniophages) and freely lying in the interalveolar septa.
LUNG CANCER
By a set of macro-preparations to determine the forms of growth and localization of cancerous tumors in the lungs.
Micropreparation No. 33 SQUAT CELL LUNG CANCER (staining with hematoxylin and eosin). Pay attention to the degree of atypia of tumor cells, signs of infiltrating growth.
Micropreparation No. 34 UNDIFFERENTIATED (anaplastic) LUNG CANCER (stained with hematoxylin and eosin). Assess the degree of anaplasia of cancer cells (shape, size, layout). Pay attention to the invasive nature of tumor growth.
BASIC Vocabulary for Lesson
Bronchiectasis- chronic pathological expansion of the bronchi.
Obstructive pulmonary disease- a group of diseases characterized by obstruction of the airways.
Restrictive lung diseases- a group of diseases characterized by the predominance of restrictive (restrictive) changes, usually in the intermediate tissue.
Pneumoconiosis- the general name for occupational lung diseases caused by exposure to industrial dust.
Epidermoid cancer- squamous cell carcinoma.
Hammen-Rich syndrome- idiopathic pulmonary fibrosis, diffuse fibrosing alveolitis, chronic interstitial pneumonitis.
Emphysema- excessive and stable expansion of the airways and respiratory structures located distal to the terminal bronchioles.
Bullous emphysema- emphysema, characterized by the formation of large subpleural bubbles (bullae).
Emphysema vicar (compensatory)- emphysema, which develops with the loss of a significant part of the lung (for example, with pulmonectomy, lobectomy).
Interstitial emphysema (interstitial)- emphysema, localized in the interstitium (stroma) of the lung.
Irregular emphysema- emphysema affecting the acini unevenly, which is almost always associated with scarring changes in the lung tissue.
Obstructive emphysema- emphysema caused by incomplete blockage (obstruction) of the airways with the formation of a valve mechanism.
Panacinar emphysema (panlobular)- emphysema, capturing acini from respiratory bronchioles to terminal alveoli.
Emphysema paraseptal- emphysema, characterized by changes in the distal part of the acin, while the proximal part remains normal.
Emphysema centriacinar (centrilobular)- emphysema, affecting the central or proximal part of the acinus, leaving the distal alveoli intact.
The list of questions for the lesson,
1. Specify the change in the myocardium underlying the development of cor pulmonale in COPD.
2. Select obstructive pulmonary disease.
3. What is the name of the excessive and persistent expansion of the airways and respiratory structures (or spaces) located distal to the respiratory bronchioles, with the destruction of the walls of these structures without subsequent fibrosis?
4. Name the types of pulmonary emphysema.
5. What causes the predisposition to chronic obstructive pulmonary emphysema?
6. Select the most important factors in the development of chronic bronchitis.
7. Name the pathogenetic variants of chronic bronchitis.
8. Name possible complications chronic obstructive bronchitis.
9. In what disease does the increased reactivity of the mucous membrane of the airways occur?
10. Specify the pathogenetic variant of bronchial asthma.
11. Specify a molecule that fixes on mast cells in atopic bronchial asthma.
12. Name the changes in the bronchial wall during bronchiectasis.
13. Name the macroscopic types of bronchiectasis.
14. Name the complications of bronchiectasis.
15. What is the name of an occupational disease associated with exposure to industrial dust and characterized by a gradual development sclerotic changes pulmonary parenchyma?
16. Name the etiological factors in the development of silicosis.
17. Name the etiological factors in the development of asbestosis.
18. Name the etiological factors in the development of anthracosis.
19. Select the components of the sarcoid granuloma.
20. In what disease are asteroid inclusions found in the cytoplasm of multinucleated cells?
21. Name the types of lung cancer classified by location.
22. Name the most common histological type of central lung cancer.
23. Name the most common histological type of peripheral lung cancer.
24. What is the name of lung cancer that develops from the epithelial lining of the distal third of the segmental bronchi, bronchioles or alveolar epithelium?
25. What is the name of lung cancer that develops from the epithelial lining of the main, lobar and proximal third of the segmental bronchi?
26. Indicate precancerous conditions in the lungs.
27. What are the complications of bronchial cancer?
28. A 53-year-old patient has been smoking 2 packs of cigarettes a day for 30 years. I went to the clinic with complaints of persistent productive cough, worsening in the morning after waking up, and progressive shortness of breath. On X-ray images, an increase in the airiness of the lung tissue and an increase in the pulmonary pattern are determined. Your conclusion.
29. A 30-year-old patient was admitted to the clinic with complaints of shortness of breath, general cyanosis, weakness. It is known from the anamnesis that the woman has been working on a poultry farm for a long time. In the study: the level of immunoglobulins in the blood is increased, immune complexes are determined. At X-ray examination- a picture of a "cell lung". Indicate the most likely diagnosis.
30. A 67-year-old patient, suffering from chronic diffuse bronchitis for a long time, died with increasing symptoms of pulmonary heart disease. At postmortem examination of the lungs of increased airiness, in the peripheral regions there are many different-sized bubbles. Indicate changes internal organs found at the autopsy.
DISEASES OF THE DIGESTIVE ORGANS
(the section is studied in two laboratory sessions)
Learning objectives
The student must know :
1. The cause and the main nosological forms of diseases of the digestive system.
2. Classification, morphological manifestations of diseases of the digestive system, their complications and causes of death.
The student must be able to :
1. Describe the morphological changes of the studied macro-preparations and micro-preparations.
2. Based on the descriptions, compare the structural manifestations of diseases of the heart and blood vessels at various levels of the structure of organs, tissues and cells.
The student must understand :
Mechanisms of the formation of structural changes that occur in organs in diseases of the digestive system.
Iclass
DISEASES OF THE STOMACH AND INTESTINAL
1. Gastritis. Definition. Acute gastritis: etiology, pathogenesis, clinical and morphological characteristics. Chronic gastritis, concept, etiology, pathogenesis, classification principles. Forms identified on the basis of the study of gastrobiopsies, and their morphological characteristics. Complications, outcomes, prognosis. Chronic gastritis as a precancerous condition.
2. Peptic ulcer disease. Definition. General characteristics of peptic (chronic) ulcers of different localizations. Epidemiology, etiology, patho - and morphogenesis, its features in pyloric-duodenal and medio-gastric ulcers. Morphological characteristics of chronic ulcers during exacerbation and remission. Complications, outcomes. Acute stomach ulcers: etiology, pathogenesis, morphological characteristics, outcomes.
3. Tumors of the stomach. Classification. Hyperplastic polyps. Adenoma of the stomach. Morphological characteristics. Malignant tumors of the stomach. Stomach cancer. Epidemiology, etiology, classification principles. Features of metastasis. Macroscopic and histological forms.
4. Idiopathic inflammatory bowel disease. Nonspecific ulcerative colitis. Crohn's disease. Epidemiology, etiology, pathogenesis and morphogenesis, clinical manifestations, complications, outcomes, prognosis. Criteria for the differential diagnosis of chronic colitis.
5. Intestinal epithelial tumors. Benign tumors. Adenomas: epidemiology, classification, clinical and morphological characteristics, prognosis. Familial adenomatous polyposis. Adenoma and cancer: a concept of multistage colon carcinogenesis. Colon cancer. Epidemiology, etiology, classification, macro- and microscopic morphological characteristics, clinical manifestations, prognosis.
6. Diseases of the appendix of the cecum. Appendicitis. Classification, epidemiology, etiology, pathogenesis. Morphological characteristics and clinical manifestations of acute and chronic appendicitis. Complications.
1. Lecture material.
2. Textbook on pathological anatomy (, Anichkov N. M, 2000) vol. 2, part I: pp. 537-562, 586-593, 597-618.
3. Textbook on pathological anatomy (, Anichkov N. M, 2005) vol. 2, part I: p. 384-405, 416-422, 425-441.
4. Guide to practical training in pathological anatomy (, 2002) p.580-585, 601-612.
5. Atlas on pathological anatomy (2003) p. 256-265.
LEARNING CARD
PURPOSE INSTALLATION OF THE LESSON: to study the morphology of certain nosological forms of organ diseases using macropreparations and micropreparations gastrointestinal tract and conduct clinical and anatomical comparisons.
DISEASES OF THE STOMACH
Macrodrug MULTIPLE STOMACH EROSION. Pay attention to the gastric mucosa with multiple superficial defects, note the color of the bottom of the erosion.
Macrodrug CHRONIC GASTRITIS. Pay attention to the relief of the mucous membrane in various parts (body, pyloric canal), the presence of erosion.
Micropreparation No. 000 Helicobacter pylori in parietal mucus in gastric fossa (gastrobiopsy, Giemsa stain). View, note the ability of bacteria to adhere to the epithelial cell.
Micropreparation No. 000 CHRONIC ACTIVE GASTRITIS OF ANTHRUM WITH IRON ATROPHIA AND COMPLETE INTESTINAL METAPLASIA (gastrobiopsy, staining with alcian blue and hematoxylin). To describe and evaluate semi-quantitatively morphological signs of chronic gastritis: activity (presence of neutrophilic leukocytes) and severity of inflammation (density of mononuclear infiltrate), degree of atrophy of the lamina propria glands, prevalence of intestinal metaplasia of the integumentary epithelium.
Macrodrug CHRONIC STOMACH Ulcer (kalezny). Pay attention to the localization of the ulcer, its shape, edges, depth, the nature of the bottom. Determine which edge is facing the esophagus and which is the gatekeeper.
Micropreparation No. 000 CHRONIC STOMACH Ulcer (with exacerbation) (staining with hematoxylin and eosin). Mark the layers in the bottom of the ulcer that characterize chronic course illness. Mark fibrinoid necrosis and leukocyte infiltration, indicating an exacerbation of the process.
View a set of macro-preparations, illustrating the complications of chronic ulcers: PASSING STOMACH ULTRA, PENETRATING STOMACH ULTRA, ARROSION OF THE VASCULAR IN THE BOTTOM OF THE ULTRA, ULTRA-CANCER OF THE STOMACH, CURRIC DEFORMATION OF THE STOMACH. Pay attention to the localization of ulcers, the shape, nature of the edges, changes in the bottom and edges of the ulcer.
Macro preparations different forms of STOMACH CANCER. Determine the macroscopic forms of the tumor. Describe one of the forms.
Micropreparation No. 000 HIGHLY DIFFERENTIATED GASTRIC ADENOCARCINOMA (intestinal type) (stained with hematoxylin and eosin). Identify the signs of tissue and cellular atypism, the invasive nature of tumor growth.
Micropreparation No. 000 UNDIFFERENTIATED CANCER - signet ring (staining with hematoxylin and eosin and alcian blue). Pay attention to tumor cells with alcyanophilic cytoplasm, located in the "pools" of mucus. Mark the shape of the cell - cricoid, the nucleus is pushed back to the periphery, the cytoplasm is filled with mucus.
INTESTINAL DISEASES
Macrodrug Phlegmonous appendicitis. Pay attention to the size of the appendix, the state of the serous membrane ( appearance, degree of blood filling), wall thickness, nature of the contents in the lumen.
Micropreparation No. 000 PHLEGMONOUS APPENDI-CITY (staining with hematoxylin and eosin). Describe. To note the degree of preservation of the mucous membrane, the nature of the exudate, its distribution in the layers of the wall and the mesentery (mesenteriolitis).
Macrodrug CHRONIC APPENDICITIS. Pay attention to the size of the appendix, the state of the serous membrane, the thickness and the appearance of its wall in section.
Micropreparation No. 000 CHRONIC APPENDICITIS (staining with hematoxylin and eosin). Describe. Mark sclerotic changes in the wall and obliteration of the lumen of the appendix. Pay attention to lipomatosis and diffuse chronic inflammatory infiltration.
Macrodrug Liver abscesses (pylephlebitic), as a complication of appendicitis. View.
View set of macro-preparations intestinal tumors.
BASIC Vocabulary for Lesson
Acute gastritis- diseases manifested by inflammation of the gastric mucosa.
Chronic gastritis- Dative inflammation-dysregenerative diseases of the gastric mucosa.
Hematomesis- bloody vomiting.
Colitis- a group of inflammatory diseases of the colon.
Crohn's disease- terminal ileitis, regional ileitis.
Mallory-Weiss syndrome- longitudinal ruptures of the mucous membrane in the region of the esophageal-gastric junction.
Penetration- penetration of the defect into adjacent organs ("covered" perforation).
Perforation- perforation.
Pylorospasm- a steady contraction of the pyloric sphincter of the stomach, leading to a violation of the evacuation function.
Polyp- any exophytic node that rises above the surface of the mucous membrane.
Enteritis- a group of inflammatory diseases of the small intestine.
Erosion- a defect that does not go beyond the mucous membrane.
Ulcer- a defect extending beyond the mucous membrane.
Stricture- stenosis, narrowing.
The list of questions for the lesson,
which are the basis of the control test
1. Give the definition of Barrett's esophagus.
2. Specify the features of Zenker's diverticulum.
3. Indicate the positions characteristic of Mallory-Weiss syndrome.
4. Indicate the factors providing the cytoprotective function of the gastric mucosa.
5. Indicate the most common cause (etiological factor) of chronic gastritis.
6. Specify the methods for detecting H. pylori in biopsy.
7. Indicate the positions typical for chronic stomach ulcers.
8. List the factors that significantly reduce the synthesis of prostaglandins and have an ulcerogenic effect.
9. Specify the microscopic features of an acute stomach ulcer.
10. Describe the perforation of the gastric ulcer.
11. Note statements specific to Zollinger-Ellisson syndrome.
12. Specify the preferred localization of stomach ulcers.
13. Select the positions characteristic of the cambial cells of the intestinal epithelium.
15. The predisposing factors for the development of hemorrhoids are.
16. Select the extraintestinal manifestations of Crohn's disease.
17. Specify the complications of Crohn's disease.
18. Specify a disease characterized by a combination of the following microscopic characteristics - crypt-abscesses, granulomas with the presence of giant cells of Pirogov-Langhans.
19. Specify microscopic signs of exacerbation of Crohn's disease.
20. Select statements specific to volvulus.
21. Specify the pathogenetic factors of colon diverticulosis.
22. Describe the pseudopolyps in ulcerative colitis.
23. What disease is characterized by a macroscopic appearance of the mucous membrane of the large intestine of the "cobblestone" type?
24. What disease can be suspected in the presence of the following signs: hyperpigmentation of the skin, lymphadenopathy and the presence of a large number macrophages with swollen cytoplasm and PAS-positive granules in intestinal biopsy?
25. Indicate the characteristic features of celiac disease.
26. In what conditions does malabsorption syndrome occur?
27. A 64-year-old patient with diabetes mellitus developed sharp pains in the epigastric region, which after a few hours moved to the right iliac region, fever up to 39 ° C, single vomiting. The patient was hospitalized 12 hours after the onset of the disease. On examination by the doctor of the emergency room, confusion, fever of 39.6 ° C, symptoms of peritoneal irritation are positive. Indicate the presumptive diagnosis.
28. A 28-year-old patient has been losing weight, pain in the epigastric region for several years, in the last month, pallor of the skin, black feces, girdle pain at the epigastric level, yellowness of the skin and visible mucous membranes have appeared. With FGDS, a callous ulcer of the posterior wall of the stomach with undermined edges was found, the bottom is deep, filled with dirty gray contents. What complication of the ulcer are we talking about in this case?
29. In the gastrobiopsy of a 43-year-old patient, the presence of a lymphoplasmacytic infiltrate in the lamina propria of the mucous membrane is determined, there are accumulations of lymphocytes with light centers. Histobacterioscopically, when staining according to Giemsa, S-shaped sticks are determined in the layer of superficial mucus. What is the presumptive diagnosis?
IIclass
DISEASES OF THE LIVER, GALL BLADDER
AND PANCREAS
1. Hepatitis: definition, classification. Acute viral hepatitis. Epidemiology, etiology, transmission routes, patho - and morphogenesis, clinical and morphological forms, viral markers, outcomes. Chronic hepatitis: concept, etiology, clinical and morphological characteristics and classification, signs of activity, outcomes, prognosis.
2. Alcoholic liver damage. Alcoholic obesity of the liver. Alcoholic hepatitis. Alcoholic cirrhosis of the liver. Epidemiology, pathogenesis and morphogenesis, clinical manifestations, complications and causes of death, outcomes, prognosis.
3. Cirrhosis of the liver. Concept. Pathomorphological signs and classification of cirrhosis by etiology, pathogenesis, macro-, microscopic changes, etc. Clinical and morphological characteristics of the most important types of cirrhosis. Alcoholic cirrhosis. Cirrhosis after viral hepatitis. Biliary cirrhosis (primary, secondary). Liver changes in hemochromatosis, Wilson-Konovalov disease, alpha-1-antitrypsin deficiency. Pathogenesis, clinical and morphological characteristics.
4. Liver tumors. Classification, epidemiology. Benign neoplasms... Hepatocellular adenoma. Intrahepatic bile duct adenoma. Malignant neoplasms. Classification. Hepatocellular adenocarcinoma. Epidemiology, etiology. Classification according to macro - and microscopic features. Complications. Regularities of metastasis. Levels of spread of hepatocellular adenocarcinoma according to the TNM system. Cholangiocellular carcinoma.
5. Diseases of the gallbladder and bile ducts. Cholelithiasis (cholelithiasis). Etiology, pathogenesis, types of stones. Cholecystitis, definition. Sharp and chronic cholecystitis: etiology, pathogenesis, clinical and morphological characteristics, complications, causes of death.
6. Diseases of the exocrine pancreas. Acute pancreatitis (pancreatic necrosis) and chronic. Epidemiology, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications and causes of death. Tumors of the exocrine pancreas. Cystadenoma. Pancreas cancer. Epidemiology, classification, morphological characteristics, prognosis.
1. Lecture material.
2. Textbook on pathological anatomy (, Anichkov N. M, 2000) vol. 2, part I: pp. 637-669, 672-682, 687-709.
3. Textbook on pathological anatomy (, Anichkov N. M, 2005) vol. 2, part I: pp. 452-477, 479-487, 489-501.
4. Guide to practical training in pathological anatomy (, 2002) p.634-654, 585-589.
5. Atlas on pathological anatomy (2003) p. 282-288.
LEARNING CARD
PURPOSE INSTALLATION OF THE LESSON: to study the morphology of individual nosological forms of liver diseases using macropreparations, microspecimens and electron diffraction patterns and conduct clinical and anatomical comparisons.
LIVER DISEASES
Macrodrug TOXIC LIVER DYSTROPHY (fatty hepatosis). Pay attention to the size of the liver, its color, consistency, the state of the capsule.
Micropreparation No. 4 MASSIVE LIVER NECROSIS - subacute form (staining with hematoxylin and eosin). To note the discomplexation of the beams, signs of fatty degeneration and necrosis of hepatic cells. Compare the state of hepatocytes in the center and periphery of the lobules. Pay attention to the incipient stromal fibrosis and infiltration of the portal tracts with lymphoid-macrophage elements.
Micropreparation No. 5 CHRONIC HEPATITIS OF WEAK ACTIVITY, STAGE I (staining with hematoxylin and eosin). To note signs of hepatitis activity: intralobular lobular lymphoid infiltrates, "spreading" of lymphocytes along sinusoids, dystrophic changes in hepatocytes, lymphohistiocytic infiltration of portal tracts. Note the signs of chronic inflammation (stage of hepatitis): fibrosis of the portal portal tracts, fibrous septa growing into the lobules. Pay attention to cholestasis: expansion of bile capillaries, imbibition of hepatocytes with bile pigments.
Electronogram HYDROPIC HEPATOCYTE DYSTROPHY IN VIRAL HEPATITIS (atlas, Fig. 14.5). Pay attention to the expansion of the endoplasmic reticulum of the hepatocyte and the sharp swelling of mitochondria.
Macro preparations LIVER CIRROSIS. Mark the size, color, consistency, surface and section view of the liver. Estimate the size of the regenerated nodes and determine the macroscopic form of cirrhosis based on this feature.
Micropreparation No. 48 CHRONIC HEPATITIS OF MODERATE ACTIVITY WITH TRANSITION TO LIVER CIRROSIS (staining with hematoxylin and eosin and picrofuchsin). Pay attention to the presence of moderately pronounced signs of inflammation activity (lymphoid infiltration of the stroma, extending to the parenchyma, fatty degeneration of hepatocytes), dominance of fibrosis (port-portal, port-central septa, formation of false lobules) and regeneration of hepatocytes (loss of the beam structure, presence of cells with large nuclei).
Macro preparations: PRIMARY LIVER CANCER, LIVER METASTASES, TUMORS OF ANOTHER PRIMARY LOCALIZATION.
BASIC Vocabulary for Lesson
Budd-Chiari syndrome- obstruction of the main hepatic veins as a result of thrombosis.
Hepatitis- any diffuse inflammatory liver disease.
Hepatosis- a group of liver diseases characterized by the dominance of degenerative changes and necrosis of hepatocytes.
Jellyfish head- expansion of the veins of the anterior abdominal wall with portal hypertension.
Portal hypertension- increased hydrodynamic pressure in the portal vein system.
Kaiser-Fleischer rings- greenish-brown or yellowish-green pigment rings in the cornea of the eyes in Wilson's disease.
Kaunsilmana Taurus- eosinophilic rounded formations in the perisinusoidal space.
Mallory Taurus- alcoholic hyaline, homogeneous eosinophilic inclusions in the cytoplasm of hepatocytes.
Massive liver necrosis (confluent)- extensive widespread necrosis of most of the hepatic parenchyma.
Liver necrosis bridged (bridge necrosis)- confluent necrosis of a large number of hepatocytes with the formation of "bridges" between adjacent lobules.
Graded liver necrosis (periportal)- destruction of hepatocytes along the border of the parenchyma and stroma, i.e. in the peripheral parts of the lobule.
Focal liver necrosis (macular)- death of individual small groups of hepatocytes in different parts of the acinus.
Pancreatitis- an inflammatory disease of the pancreas, often accompanied by its necrosis.
Goose liver- a macroscopic view of an organ with fatty degeneration.
Hepatolienal syndrome- enlargement of the spleen in liver diseases, accompanied by hypersplenism.
Wilson's disease (Wilson-Konovalov's disease)- hepatolenticular degeneration, hepatocerebral dystrophy.
Cholangitis- inflammatory disease of the bile ducts.
Cholelithiasis- cholelithiasis.
Cholestasis- insufficiency of bile flow.
Cholecystitis- inflammatory disease of the gallbladder.
Cirrhosis- Excessive proliferation of connective tissue in the organ against the background of degenerative and regenerative processes, accompanied by a change in the shape of the organ.
The list of questions for the lesson,
which are the basis of the control test
1. Specify the options for the structure of the liver.
2. List the variants of liver parenchyma necrosis.
3. What results in the formation of Kaunsilman's little bodies?
4. List the forms of acute hepatitis.
5. Specify the route of transmission of the virus when acute hepatitis A.
6. Specify the routes of transmission of the virus in acute hepatitis B.
7. What are the indirect markers of viral damage to hepatocytes.
8. Specify the predominant localization of HBcAg in hepatocytes.
9. What kind does the accumulation of HBsAg in the hepatocyte impart to the cytoplasm?
10. List the etiological options chronic hepatitis.
11. Specify the microscopic signs of chronic hepatitis.
12. List the morphological forms of chronic hepatitis.
13. Specify the characteristic signs of alcoholic liver damage.
14. List the options for alcoholic liver damage.
15. Name the cells responsible for collagen formation in alcoholic liver damage.
16. Describe the macroscopic changes in the liver in alcoholic steatosis.
17. List the microscopic signs of a false lobule in liver cirrhosis.
18. Name the morphological forms of liver cirrhosis.
19. List the acquired forms of liver cirrhosis.
20. List the hereditary forms of liver cirrhosis.
21. Indicate the signs of portal hypertension.
22. List the causes of death of patients with liver cirrhosis.
23. Give the characteristics of primary sclerosing cholangitis.
24. Give a characteristic of primary biliary cirrhosis of the liver.
25. Give a characteristic of Wilson-Konovalov's disease.
26. Changes in the wall of the gallbladder in acute cholecystitis.
27. Changes in the wall of the gallbladder in chronic cholecystitis.
28. A 60-year-old patient has suffered from chronic alcoholism for 30 years. On examination, the liver is dense, the surface is bumpy. On the anterior abdominal wall, the veins are dilated, the spleen is palpable. Indicate the possible histological manifestations in the biopsy material.
29. A 50-year-old woman has been worried about fast fatigue and itchy skin... In a laboratory study, a minimal increase in the level of transaminases, a significant increase in the level of alkaline phosphatase, and high titers of antimitochondrial antibodies were found. A biopsy study revealed a granulomatous nature of inflammation in the cholangioli and a decrease in the number of bile ducts with pronounced lymphoma-macrophage infiltration along the portal tracts with symptoms of sclerosis. Your conclusion.
30. A 63-year-old male patient, who had suffered from chronic viral hepatitis B for a long time, was admitted to the clinic with complaints of heaviness in the right hypochondrium, yellowness of the skin. On examination, the liver is dense, its edge is bumpy, there is an increase in the spleen and expansion of the veins of the anterior abdominal wall. Note possible histological manifestations in the biopsy material.
Toxic liver dystrophy
Toxic liver dystrophy or progressive massive liver necrosis is acute or chronic illness characterized by massive tissue necrosis and the development of liver failure. Toxic dystrophy develops as a result of the action of exogenous (fungi, foodstuffs with toxins, etc.) and endogenous (pregnancy toxicosis, thyrotoxicosis) toxins. These substances have a hepatotoxic effect and damage hepatocytes.
Pathological anatomy. Toxic liver dystrophy has various manifestations that depend on the duration of the damage to the liver cells. In the first few days, the organ grows, it becomes dense, yellow in color. Further, there is a progressive decrease in liver tissue and shrinkage of the capsule. On the cut, the liver is clay-colored or gray. Under a microscope, at first, fatty degeneration of hepatocytes is found in the center of the lobules, these changes are quickly replaced by necrosis and autolysis of the hepatic tissue. The progression of necrosis leads to the end of the second week to complete necrosis of the lobule, and only along the periphery there is a narrow strip of fatty degeneration. All this is a stage of yellow dystrophy. At the 3rd week, the liver decreases further and it turns red. These are manifestations of phagacytosis and resorption of necrotic detritus. At the same time, the stroma of an organ with dilated blood vessels is exposed. Changes at the 3rd week are a manifestation of the stage of red liver dystrophy.
With progressive necrosis, patients die from acute hepatic renal failure. Survivors have liver changes characteristic of postnecrotic cirrhosis.
24. Toxic liver dystrophy.
The liver is enlarged, flabby, with a wrinkled capsule. On the cut, the structure is erased, variegated
305. Portal cirrhosis of the liver.
The liver is deformed, compacted, reduced in size, the surface is granular. The section shows large and small nodules of liver tissue of various sizes, surrounded by a ring of connective tissue - the so-called “false lobules”.
553. Cirrhosis of the liver.
The liver is dense, tuberous, with yellow lesions and false lobules on a cut.
325. Fatty degeneration of the liver of the "goose" type. Chronic fatty hepatosis.
The liver is enlarged, yellow.
279. Liver cancer on the background of cirrhosis.
Against the background of cirrhosis of the liver, a focus of tumor tissue of a variegated appearance is visible.
198. Hepatic vein thrombosis.
A part of the liver with a hepatic vein, in the lumen of which a thrombus is visible.
127. Icteric necrotizing nephrosis.
The kidney in the section is yellow-green, the border of the cortex and medulla of the sperm cortex is dull and wide.
462. Splenomegaly. Hyalinosis capsules.
The spleen is enlarged, on the capsule there are opaque translucent lesions
37. Hemorrhoids. In the distal colon, varicose veins are brown.
Fake 35. Varicose veins of the esophagus in liver cirrhosis.
Sharp plethora and enlargement of the veins of the esophagus with arrosia of the vessel wall.
Examine micropreparations:
38. Acute viral hepatitis.
Hepatocytes in a state of hydropic (balloon) dystrophy and coagulation necrosis. Hyaline-like Kaunsilman's little bodies are found in the perisinusoidal lumens Cholestasis and lymphohistiocytic infiltration of the portal tracts are expressed
Indicate in the picture:
1 - balloon dystrophy of hepatocytes.
2 - Kounsilman's little body.
3 - cholestasis
4 - histiolymphocytic infiltration of the portal tracts
171. Subacute toxic liver dystrophy(acute hepatosis, stage of red dystrophy).
The structure of the hepatic lobules is broken. Hepatocytes in a state of necrosis cells are homogeneous, eosinophilic, without nuclei. Many necrotic hepatocytes have undergone phagocytosis and resorption.In these areas, bare (free) reticular stroma with dilated sinusoids and bile capillaries.
Indicate in the picture:
1 - necrotic hepatocytes.
2 - free stroma.
3 - dilated sinusoids and bile capillaries.
99. Portal cirrhosis.
The proliferation of connective weavers along the portal tracts in the form of rings with the formation of the so-called "false lobules" in which the architectonics of the vessels is disturbed. hepatocytes in a state of fatty degeneration (cells in the form of vacuoles) and regeneration (large nets with large or double nuclei)
Indicate in the picture:
1 - connective tissue
2 - false lobules
3 - hepatocytes in a state of fatty degeneration
4 - young liver cells
44. Biliary cirrhosis.
The proliferation of connective tissue along the periphery of the lobules Expressed cholestasis bile ducts dilated, filled with yellow or dark green bile.
76. Postnecrotic cirrhosis (Masson's stain).
The structure of the liver is sharply disturbed by extensive areas of connective tissue blue in place of necrotic liver tissue. The preserved liver cells in a state of necrosis are homogeneous, pink-violet, without nuclei. Regeneration is not pronounced.
397. Toxic liver dystrophy is based on:
fatty degeneration
inflammation
protein dystrophy
398. The outcomes of toxic dystrophy are:
hepatic renal failure
cirrhosis of the liver
399. The cause of toxic liver dystrophy is:
infection
alcohol poisoning
poisoning with mushrooms and poisons
toxicosis of pregnancy
400. "Goose" liver develops when:
acute hepatosis
chronic hepatosis
401. The mechanism of hepatocyte alteration in serum hepatitis is:
direct action of viruses
immune cytolysis
402. AIDS is accompanied by hepatitis:
whey
epidemic
403. Dystrophy of hepatocytes in serum hepatitis:
grainy
vacuolar
404. K etiological factors hepatitis include:
medications
allergy
dystrophy
405. The morphological form of chronic hepatitis is:
phlegmonous
persistent
fibrinous
fatty hepatosis
406. Hepatitis is considered chronic:
after 1 month
after 3 months
after 6 months
after 1 year
407. Indications for biopsy for the clinical diagnosis of hepatitis are:
verification of the diagnosis
establishing the form and severity of hepatitis
evaluation of treatment results
408. The safest type of biopsy for diffuse liver damage is:
puncture
transvenous
marginal liver resection
pinched at laparoscopy
409. The main histological signs of chronic active hepatitis are:
stepwise necrosis
empiopolesis
bridge necrosis
410. The main histological sign of persistent hepatitis is:
1- clear border of the boundary plate
2- sclerosis of the periportal tracts
3- granulomatous inflammation in the centrilobular zones
4- pericellular fibrosis
411. One of the main histological signs of viral hepatitis is:
1- Kounsilman's little body
2- giant mitochondria
3- granulomatous inflammation
4- pericellular fibrosis
5- sclerosis
412. The histological signs of liver tissue regeneration include:
1- binucleated hepatocytes
2- giant multinucleated hepatocytes, such as symplasts
3- "rosette-like" structures
413. Most common reason toxic liver dystrophy is:
414. The following stages of toxic liver dystrophy are distinguished:
1- active
2- red dystrophy
3- moderate
4- persistent
415. Signs of stage 1 of toxic liver dystrophy include:
bright yellow liver
the liver is reduced in size
the liver is dense, sclerosed
diffuse hemorrhages in liver tissue
416. The histological signs of the II stage of toxic liver dystrophy include:
necrosis of hepatocytes in the centrilobular regions
carbohydrate dystrophy
large focal sclerosis
Mallory's little body
417. The macroscopic sign of the liver in cirrhosis is:
liver of soft-elastic consistency
the liver is enlarged
dense liver
liver of "nutmeg" type
418. Acute viral hepatitis is characterized by:
extralobular cholestasis
bilious lakes
fatty degeneration of hepatocytes
Kounsilman's little body
419. Kaunsilman's bodies refer to hepatitis:
serum
alcoholic
to none of the above
420. What changes do hepatocytes undergo during the formation of Kaunsilman's bodies:
hyalinosis
colliquation necrosis
coagulation necrosis
421. Necrosis spreading between the center of the liver lobules and the branches of the black vein are called:
massive
stepped
bridged
422. Inflammatory infiltrates in acute serum hepatitis are dominated by:
neutrophils
macrophages
lymphocytes
423. Inflammatory infiltrates in alcoholic hepatitis must contain:
lymphocytes
neutrophils
macrophages
424. Reddish (light) color of the liver in cirrhosis depends on:
dystrophies
obstruction of blood flow through the inferior vena cava
obstruction of blood flow through the portal vein
425. "Lobular liver" refers to cirrhosis:
1- circulatory
3- infectious
4- exchange.
Topic VI. Diseases of the gastrointestinal tract.
Gastritis is an inflammatory disease of the stomach lining. Distinguish between acute and chronic gastritis.
Acute gastritis is characterized by:
Macroscopically - thickening of the mucous membrane due to edema, redness, erosion.
FORMS OF ACUTE GASTRITIS:
1. Catarrhal (simple)
2. Fibrinous
3. Purulent
4. Necrotic
Chronic gastritis is a chronic inflammation of the gastric mucosa, accompanied by disorders of the carotid epithelial renewal.
Morphologically forms of chronic gastritis:
surface
atrophic
hypertrophic
combined atrophic-hyperplastic.
Modern international classification chronic gastritis:
autoimmune (type A)
bacterial (type B)
mixed (type A and B)
chemically-toxic (type C)
lymphocytic
special forms (Menetrie's disease)
acute ulcer- an ulcer that covers the thickness of the mucous membrane, which does not have sclerotic changes in the bottom and at the edges; is usually secondary.
symptomatic ulcers are observed when:
stressful conditions
endocrine diseases
acute and chronic circulatory disorders
after taking medications
chronic ulcer - an ulcer that penetrates beyond the mucous membrane into the thickness of the stomach wall, has gross fibrous changes in the bottom and roller-like raised edges; the proximal edge of the ulcer is undermined.
LAYERS OF CHRONIC GASTRIC ULTRA:
1.zone of exudation or necrosis
2.zone of fibrinoid swelling
3.zone of granulation tissue
4. zone of sclerosis.
THE MAIN COMPLICATIONS OF THE PURPOSE DISEASE:
penetration
perforation
malignancy
pyloric stenosis
bleeding
perigastrid, periduodenitis
diverticulum - protrusion of the wall of the gastrointestinal tract.
Appendicitis is an inflammation of the appendix of the cecum, which gives a characteristic clinical syndrome.
Acute appendicitis happens:
1.simple
2.surface
3.destructive (phlegmanous, phlegmanous-ulcerative, apostematous, gangrenous)
chronic appendicitis develops after acute appendicitis and is characterized by sclerotic and atrophic processes, against the background of which inflammatory and destructive changes may appear.
forms of CHOLECYSTITIS:
1. Catarrhal
2. Purulent (phlegmonous)
3. Diphtheritic
4. Chronic
Crohn's disease is a chronic recurrent disease of the gastrointestinal tract, characterized by nonspecific granulomatosis, necrosis, scarring of the intestinal wall.
Examine macro-preparations:
79. Phlegmanous appendicitis.
The appendix is thickened, the serous membrane is dull, with fibrinous overlays, the vessels are full-blooded. The enlarged lumen is filled with pus (appendix epiema),
570. Normal gallbladder.
The wall of the gallbladder is thin, velvety mucous.
49. Calculous cholecystitis.
The wall of the gallbladder is thickened, sclerosed, there are many stones in the lumen of the gallbladder.
50, 180. Cholecystitis.
The wall of the gallbladder is unevenly thickened, the mucous membrane is swollen, dark red
348. Erosion of the gastric mucosa.
On the gastric mucosa, there are multiple superficial defects of the mucous membrane with smooth edges, the bottom is black (hematin hydrochloric acid pigment).
376. Acute stomach ulcers.
On the gastric mucosa, surface defects with smooth dark red edges from 1.5 to 3 cm in diameter are visible
183. Acute duodenal ulcer with perforation.
386. Chronic stomach ulcer.
On the lesser curvature of the stomach, a steep ulcerative defect is visible up to 1 cm in diameter, the bottom and edges are dense, ridge-like.
108. Chronic stomach and duodenal ulcers.
On the mucous membrane of the stomach and duodenum, 3 ulcerative defects are visible. In the stomach, an elongated ulcer with undermined dense edges and a dense bottom. In the duodenum 2 ulcers of a rounded shape, located opposite each other ("kissing ulcers"), in one of them there is a perforated hole
128. Melena (bleeding into the lumen of the gastrointestinal tract).
The intestinal mucosa is black (pigment hematin hydrochloric acid, methemoglobin, iron sulfide)
149, 184. Saucer-shaped stomach cancer. Skirr of the stomach.
178. Stomach cancer.
Exo- and endophytic growth.
146. Ulcerative colitis.
On the mucous membrane of the colon, multiple ulcerative defects
of various shapes and sizes.
75. Polypoid cancer.
Myoma of the stomach.
Examine micropreparations:
62a. Chronic stomach ulcer ..
At the bottom of a chronic ulcer, 4 layers are distinguished:
1) on the surface ulcerative defect there is a zone of necrosis with leukocytes, 2) under it - fibrinous exudate, 3) below is a zone of granulation tissue, followed by 4) a zone of deep sclerosis with lymphoid infiltrates and sclerosed vessels.
Indicate in the picture:
1 - I zone - necrosis.
2 - II zone - fibrinoid
3 - III zone - granulation tissue.
4 - IV zone - sclerosis.
90. Acute suppurative appendicitis (phlegmanous-ulcerative).
(see at the same time the drug 151. The appendix is normal)
All layers of the appendix are infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosa, congested vessels and hemorrhages
Indicate in the picture:
1 - mucous membrane with ulceration
2 - submucosa
3 - muscular layer.
4 - serous membrane
5 - leukocyte infiltration of all layers of the wall of the appendix.
177. Chronic appendicitis with regeneration of the mucous membrane.
The wall of the appendix is thickened due to the proliferation of fibrous connective tissue in all layers of the newly formed low cubic epithelial cells creep onto the ulcer
140. Cholecystitis.
The wall of the gallbladder is thickened due to the proliferation of connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophied
74. Solid stomach cancer.
The parenchyma and stroma in the tumor are evenly developed. The parenchyma is represented by atypical cells that form cells. Anaplastic epithelium proliferates, in places it grows outside the mucous membrane - infiltrating growth
Tests: choose the right answers.
426. The causes of acute gastritis are:
1- alcoholism
2- infection
3- ingestion of traumatic substances
427. The following changes are characteristic of atrophic gastritis:
1- pink mucosa, with well-defined folds
2- mucous membrane pale
3- there is a lot of mucus in the stomach
4- focal regeneration of the epithelium
428. Main severe complication stomach ulcers are:
1- lymphadenitis of regional nodes
2- perforation
3- perigastritis
4- "inflammatory" polyps around the ulcer
429. The most characteristic changes in blood vessels in the bottom of a chronic ulcer are:
1- inflammation and sclerosis of the wall
2- plethora
3- anemia
4- large thin-walled sinusoidal vessels
430. The local factor of importance in the pathogenesis of gastric ulcer and duodenal ulcer includes:
1- infectious
2- violation of trophism
3- toxic
4- decrease in the secretion of gastrin and histamine
5- exogenous
431. The layers of the bottom of a chronic gastric ulcer are:
1- exudate
3- granulation tissue
4- sclerosis
432. An autopsy of the deceased revealed a lot of stomach erosions from burns, covered with hydrochloric acid hematin. Erosion formed:
1- before the burn
2- during a burn
433. On the mucous membrane of the stomach, there is a liquid of a coffee type. When cleansing from it, punctate hemorrhages and defects the size of a pinhead are visible. Specify the name of the process:
1- petechiae
3- acute ulcers
434. An autopsy in the stomach found two round ulcers located on the lesser curvature, the edges are even, the bottom is thin. The ulcers are:
1- sharp
2- chronic
435. The signs of a chronic ulcer are:
1- recurrent bleeding
2- dense sclerosed bottom
3- multiple ulcers
4 - one, two ulcers
436. The most common localization of stomach cancer is:
2- large curvature
3- small curvature
437. Cancer grows diffusely all layers of the stomach wall, dense, stomach cavity is reduced. Cancer refers to:
1- differentiated adenocarcinoma
2- mucous cancer
438. A woman has clinically determined solid tumors of the ovary on both sides. It is necessary to investigate the presence of metastases, first of all:
1- in the lungs
2- in the stomach
439. Acute gastritis usually manifests itself in the form of:
1- atrophic
2- hypertrophic
3- purulent
4- superficial
5- with restructuring of the epithelium
440. Chronic atrophic gastritis is characterized by:
1- ulceration
2- hemorrhages
3- fibrinous inflammation
4- enterolization of the mucous membrane
5- plethora and diffuse leukocyte infiltration of its own layer of the mucous membrane
441. Exacerbation of stomach ulcers is characterized by:
1- hyalinosis
2- enterolization
3- regeneration
4- lymphoplasmacytic infiltrate
5- necrotic changes
442. The characteristic symptom of Menetrie's disease is:
1- enterolization of the gastric mucosa
2- hydrohydrolenic uremia (gastric tetany)
3- Virchow metastases
4- giant hypertrophic folds of the gastric mucosa
5- nonspecific intestinal granulomatosis
443. Ischemic colitis can be detected:
1- with atherosclerosis
2- with scleroderma
3- with diabetes
4- with rheumatoid arthritis
444. Rectal changes are characteristic:
1- for ulcerative colitis
2- for Crohn's disease
3- for Hirschsprung's disease
445. When ulcerative colitis is malignant, the intestinal mucosa is:
1- smooth
2- polypoid (granular)
3- atrophic
446. Malignancy of adenomatous polyps is more often found:
1- in the basal departments
2- in the superficial departments
3- in the middle departments
447. Familial multiple colon polyposis is found more often:
1- from birth
4- at the end of the first year of life
5- after 3 years
448. The characteristic histological signs of Whipple's disease are revealed:
1- in the lungs
2- in the myocardium
3- in the liver
4- in the kidneys
449. The most characteristic histological sign of Whipple's disease:
1- hemorrhage
3- macrophage infiltrate
4- leukocytosis
450. Cancer is suspected in an emaciated patient. Above the left clavicle, an enlarged, compacted lymph node... It is necessary to examine first of all:
2- stomach
3- esophagus
451. The appendix is thickened in the distal part, the serous cover is dull, hyperemic, in the lumen there is fecal masses and purulent exudate. Microscopically - diffuse infiltration of the appendix wall with neutrophils, no ulcers. Appendicitis refers to:
1- to simple
2- to destructive
452. The appendix is thickened in the middle segment, the serous membrane is covered with fibrinous films. Histologically, against the background of diffuse infiltration of the entire thickness of the ulcer wall.
Appendicitis refers to:
1- to phlegmonous-ulcerative
2- to gangrenous
3- to simple
453. The appendix is thickened, the serous cut is covered with fibrin, the wall is black throughout, dull. Appendicitis refers to:
1- to catarrhal
2- to gangrenous
3- to phlegmonous
454. Abortive appendicitis is characterized by:
1- inflammation is mild
2- primary changes have resolved
3- the site of inflammation is extremely small
455. Thickening of mucus in the lumen of the sclerosed appendix is called:
1- cystic fibrosis
2- mucocele
3- melanosis
456. The characteristic features acute appendicitis are:
2- serous exudate in the mucous and muscular membranes
3- hyperemia
4- sclerosis of the wall of the appendix
5- destruction of muscle fibers
457. The characteristic signs of chronic appendicitis are:
1- sclerosis of the vessel walls
2- sclerosis of the wall of the appendix
3- purulent bodies
4- lymphoplasmacytic infiltration
5- granulomas
458. The morphological forms of appendicitis are:
1- acute purulent
2- acute superficial
3- acute destructive
4- chronic
5- croupous
459. The complications of appendicitis are:
1- perforation
2- peritonitis
3- liver abscesses
460. Most often cause subhepatic jaundice:
1- cancer of the Vater's nipple
2- cancer of the head of the pancreas
3- liver cancer
461. Cancer of the head of the pancreas causes jaundice:
1- parenchymal
2- hemolytic
3- mechanical
462. Crohn's disease in the destructive phase is characterized by:
1- mucous membrane in the form of "cobblestone pavement"
2- deep slit longitudinal ulceration of the mucosa
3- superficial ulceration
4- granulomas in the intestinal wall
463. The mucous membrane of the ileum is divided by deep ulcers in the form of slits and resembles a cobblestone pavement. Name the disease:
3- typhoid fever
464. For ulcerative colitis allergic origin are characteristic:
1- fibrinous inflammation
2- multiple ulcers
3- polypoid protrusions of excessively regenerating epithelium
4- fibrinous necrosis of individual sections of the intestine.
Topic VII. An introduction to infections. Typhus: abdominal, typhus, recurrent.
Infectious - diseases caused by infectious agents are called: viruses, bacteria, fungi.
Invasive - diseases are called when protozoa and helminths are introduced into the body.
Typhoid fever - acute and long-lasting infection caused by salmonella (Salmonella typhi), in the first week of the disease is characterized by symptoms of general intoxication (fever, chills) associated with bacteremia; wide involvement of the reticuloendothelial system, accompanied by a rash, abdominal pain and severe weakness in the second week of the disease; ulceration in Peyer's patches with bleeding from the small intestine and the development of shock in the third week of the disease.
stages of CHANGE OF GROUP LYMPHATIC FOLLICLES OF THE SMALL INTESTINE IN ABDOMINAL TYPHUS:
1. Brain swelling
4. Clean ulcers
5. Regeneration
the cellular composition of typhoid granuloma - macrophages, the so-called typhoid and lymphoid cells.
Atypical forms of abdominal typhoid:
1. Kolotif
2. Laryngotif
3. Pneumotif
4. Cholecystotyphoid
THE MOST COMMON AND DANGEROUS COMPLICATIONS OF ABDOMINAL FEVER:
1. Intra-intestinal bleeding
2. Perforation of ulcers followed by peritonitis
Epitemic typhus. European typhus (lousy fever) -
an acute infectious disease caused by rickettsia is characterized by a lesion nervous system and blood vessels... It is manifested by general toxic phenomena, fever, roseolo-petechial rash and disruption of the activity of internal organs, especially the circulatory system.
Macroscopic characteristics are often poorly expressed - skin rash in the form of red or brown roseola, petechiae, small-point hemorrhages of the conjunctiva of the eyeball (Chiari symptom). In advanced cases, foci of skin necrosis with areas of gangrene are possible.
Microscopic changes in the capillaries develop - destructive-proliferative-endo-thrombotic-vyskulitis.
Types of granules for typhus:
1.mesenchymal - Davydovsky
microglial - Popova.
Recurrent disease is very rare - this is Brill-Zinser disease. (Repeated sporadic typhus).
Examine macro-preparations:
Description of drugs in Pathological Anatomy in Lesson No. 28
LESSON number 28diseases of the liver and biliary system.
Macrodrug "Massive progressive necrosis liver - stage yellow dystrophy " .
The liver is sharply reduced in size, its capsule is wrinkled, the consistency is flabby, the liver tissue is clay-like in the cut.
Micropreparation № "Massive progressive necrosis liver - stage yellow dystrophy ".
V central departments lobules of hepatocytes in a state of necrosis. Some PMNs are found among the necrotic masses. In the peripheral sections of the lobules, hepatocytes are in a state of fatty degeneration: when staining Sudan III, in the center of the lobules, fatty detritus is visible in the hepatocytes of the peripheral sections of the lobules - a drop of fat.
Macrodrug "Fatty dystrophy liver ( fatty hepatosis ) »
The liver is enlarged, the surface is smooth, the edge is rounded, the consistency is flabby, ocher-yellow on the cut.
Micropreparation № "Spicy viral hepatitis ».
Hepatocytes in a state of hydropic and balloon dystrophy, which is an expression of focal colliquation necrosis. Some hepatocytes in a state of apoptosis: reduced in size, with eosinophilic cytoplasm and pycnotic nucleus, or have the appearance of a hyaline-like body, which is pushed into the lumen of the sinusoid (Kaunsilman's body). Bile capillaries are dilated, filled with bile. The portal tracts are dilated, infiltrated with lymphohistiocytic elements, the accumulations of which are visible inside the lobules in the sinusoids, as well as in areas where groups of hepatocytes are in a state of necrosis. In the peripheral parts of the lobules, binucleated and large hepatocytes (regenerative forms) are often found.
Electronogram "Balloon dystrophy hepatocyte at acute viral hepatitis " - demonstration .
Micropreparation № "Chronic viral hepatitis V moderate activity " .
The portal tracts are thickened, sclerosed, abundantly infiltrated with lymphocytes, macrophages (histiocytes), plasma cells with an admixture of PMNs. The infiltrate exits through the border plate into the parenchyma and destroys hepatocytes. The foci of necrotic hepatocytes are surrounded by lymphocytes and macrophages (stepwise necrosis). Infiltration foci are visible inside the lobules. Outside of areas of necrosis, hepatic cells are in a state of hydropic dystrophy.
Electronogram "Destruction of the hepatocyte by the killer lymphocyte in chronic active hepatitis."
In the place of contact of the lymphocyte with the hepatocyte, destruction of its cytoplasmic membrane is visible.
Macrodrug "Viral large-node ( postnecrotic ) cirrhosis liver "
The liver is reduced in size, dense, the surface is large-nodular: nodes of uneven size, more than 1 cm, separated by wide fields of connective tissue.
Micropreparation № "Viral multilobular ( postnecrotic ) cirrhosis liver " - drawing . The liver parenchyma is represented by false lobules (regenerated nodes) of various sizes. In each node, fragments of several lobules can be seen (multilobular cirrhosis), the hepatic tracts are indistinguishable, the central vein is absent or displaced to the periphery. Protein dystrophy and necrosis of hepatocytes. There are large hepatocytes with two or more nuclei. Areas of the parenchyma are separated by wide fields of connective tissue stained red with picrofuchsin. In the connective tissue fields, contiguous triads, sinusoidal vessels, proliferating cholangioli, and lymphohistiocytic infiltrates are seen.
Macrodrug "Alcoholic fine-knot ( portal ) cirrhosis liver "
The liver is enlarged (in the final - reduced) in size, yellow, dense, with a uniform small-knotted (small-knot) surface; nodes no more than 1 cm in diameter, separated by uniform narrow layers of connective tissue.
Micropreparation № "Alcoholic monolobular ( portal ) cirrhosis liver " - drawing . The parenchyma is represented by false lobules, uniform in size, built on fragments of one lobule (monolobular cirrhosis). The nodes are separated by narrow bands of connective tissue (septa), hepatocytes with signs of fatty degeneration. In connective tissue septa, lymphohistiocytic infiltration with an admixture of PMNs and proliferation of bile ducts is visible.
Macrodrug "Liver at mechanical jaundice " - demonstration .
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