METHODICAL INSTRUCTION for STUDENTS of the THIRD COURSE
Medical Faculty
LESSON № 10 (PRACTICAL – 6 hours)
Theme: 1) Disease of oesophagus, stomach.
2) Disease of intestine (duodenum and appendix).
3) Disease of liver, biliary system and exocrine pancreas.
The place of class – the department of pathoanatomy.
Actuality of theme: due to the prevalence of digestive tract diseases and the development of methods of research and treatment, the profession of gastroenterology was singled out as a separate medical speciality. Due to access to the mucous tunics, gastroenterologists constantly use the morphologic method – biopsy examination in their practice. Yet, the problems of gastroenterology are of great interest not only for particular specialists but for a wide range of medical workers of other specialities. The knowledge of the structural bases of gastrointestinal tract pathology ensures the understanding and proper treatment of certain stages of disease progression, enables the prediction and avertion of possible complications.
Aim: to study the etiology, pathogenesis, pathologic anatomy and complications of esophagus, stomach and duodenum diseases, appendicitis and peritonitis, liver and gall bladder.
Task: 1. To know the etiology, pathogenesis and classification of the pharynx and esophagus diseases, gastritis, stomach ulcer, appendicitis and peritonitis, hepatitis and hepatosis, gall bladder diseases.
2. To learn to identify the morphologic signs of gastrointestinal tract diseases and illness of liver and gall bladder.
3. To be able to explain the possible complications and consequences of gastrointestinal system diseases.
4. To learn morphology of ulcerative diseases of stomach and duodenum, cancer of stomach and their complications.
5. To be able to determine macro- and microscopic signs of the cirrhosis of liver, explain causes and morphogenesis, evaluate organism s meaning of possible complications.
6. Answer the questions of the theoretical part, which are offered in the album for class-room and extra-class-room work of students
Professional orientation of students: The knowledge of theme is necessary for future studying of ulcerative disease on clinical department. In doctors practical work the deep investigation of pathogenesis is important for diagnosis and providing of prophylaxis and treatment; for doctors-pathologists it is important for diagnosis. The illness of liver is studing well-founded during the last 30-35 years, that is conditioned by introduction of morphological research methods into clinic practice. Morphological hepar stading in vivo provocate new direction in medicine – clinical hepatology. Liver diseases are typical for people of different ages, that is why students must have good knowlege in clinical and morphological signs and illness consequences for the adequacy and pathogenically graunded therapy, helding prophylactic measures between people.
Initial level of knowledge and skills:
1. To know the normal anatomy of stomach (department of normal human anatomy).
2. To know the physiology and functions of stomach (department of normal physiology).
3. To be able to distinguish micro- and macroscopic structure of stomach (department of histology, cytology and embryology).
4. To know the normal anatomy and hepatic blood stream. (department of normal anatomy).
5. To be able to distinguish micro- and ultrastructure of hepatic parenchyma. (department of histology, cytology and embryology).
6. To know the function of the hepar. Exchange of bile pigments. (department of medical chemistry).
7. To know the auto- and heteroimmunologic processes. (department of pathologic physiology).
8. To know the general pathological processes: dystrophia, necrosis and regeneration. (department of pathologic anatomy).
Methodology of Practical Class.
Individual Students Program.
I. Practical work – 9.00 – 12.00
Work 1.
Practical work with album & micropreparations
– Students must answer the questions, draw the micropreparations or microslides in album and describe the micropreparates with pathology, designate the main signs of pathologic process.
Class equipment by Illustrative material:
Micropreparations or microslides:
1. Necrotic tonsillitis. The specimen is stained with hematoxylin and eosin. In the specimen one can observe the mucous tunic necrosis spreading to the underlying tissues. There is an inflammatory leucocytic infiltration around it. The picture of the characteristic organ structure is effaced; only in some areas lymphoid tissue beds are preserved. Designate: 1 – lymphoid follicle, 2 – necrosis focus, 3 – leucocytic infiltration.
2. Erosive gastritis. The specimen is stained with hematoxylin and eosin. The mucous tunic is swollen, hyperaemic and the epithelium is desquamated. Numerous haemorrhages, red colour and inflammation focuses, beds of densely located neutrophils, inflammatory infiltration. Dystrophic and necrotic changes in the muscular layer can be seen. Vascular hyperaemia, slight haemorrhages in the underlying layers can also be observed. Erosive gastritis develops after intoxication with alkalis, acids, etc. Designate: 1 – epithelium desquamation, 2 – inflammatory exudation.
3. Chronic stomach ulcer. The specimen is stained with hematoxylin and eosin. With the naked eye one can see a mucous tunic defect (niche). Microscopically one can see that the mucous tunic is destroyed. The ulcer edges are represented by necrotizing tissue delimited by a scarcely evident demarcation zone and granulation tissue, and at the periphery there is connective tissue. In the muscular layer one can observe excessive excrescence of fat tissue which is a variety of connective tissue. On the basis of histologic examination one can diagnose exacerbation of chronic stomach ulcer. Designate: 1 – epithelium necrosis, 2 – granulation tissue, 3 – connective tissue, 4 – muscular layer.
4. Phlegmonous appendicitis. The specimen is stained with hematoxylin and eosin. All appendix layers are infiltrated with inflammatory exudation – one can see accumulations of neutrophil leucocytes. The mucous tunic is to a large extent destroyed, in the appendix lumen, there are fecal masses (a homogenous, pink-blue mass without nuclei) and inflammatory exudation – accumulations of neutrophil and leucocytes. The vessel lumens are drastically widened and plethoric. On the serous tunic there is a fibrinous-suppurative deposition – peritonitis. Designate: 1 – neutrophil infiltration of the wall, 2 – vessels plethora, 3 – fibrinous-suppurative exudation on the serous tunic.
5. Stomach ulcer penetration into pancreas. The specimen is stained with hematoxylin and eosin. With the naked eye one can see a blue tissue (pancreas) with a defect filled with light pink tissue (connective tissue). Microscopically one finds in the connective tissue many vessels with thick walls, haemorrhages, fat tissue (areas with densely located nuclei – many cells). So, the bottom of the chronic ulcer is in the pancreas tissue. Designate: 1 – stomach wall, 2 – pancreas.
6. Adenocarcinoma (ulcer – cancer). Microscopically one can see a mucous tunic defect. The bottom of the ulcer is represented by connective tissue of pink colour. In the underlying tissues, one can observe deranged glandular structures and infiltration growth. In the deranged glands nuclei are located not basally but chaotically. The nuclei are of different form, size and colour intensity and there are numerous mitoses. Designate: 1 – the bottom of the ulcer, 2 – excrescence of atypical cells.
7. Obliterating appendicitis. The specimen is stained according to van Gison’s method. The appendix is thinned. The wall layers are moderately infiltrated with leucocytes. Sclerotic changes prevail in the wall – the excrescence of fibrous connective tissue. One can find inflammatory infiltrations with prevailing lymphocytes. The appendix lumen is obliterated due to excrescence of granulation tissue (there are a lot of black nuclei) that differentiates to a mature fibrous connective structure. There is no mucous tunic. Designate: 1 – lymphocytic infiltration, 2 – excrescence of connective tissue.
8. Massive hepatic necrosis, the stage of red atrophy. The specimen is stained with hematoxylin and eosin. Only solitary hepatocyte areas are preserved. They are a little more intensely coloured and have preserved nucleuses and radial orientation of trabecules. Around the intact liver tissue one can observe a homogenous anhistous mass – detritus (parenchyma destruction products) – and massive haemorrhages. Designate: 1 – preserved hepatocytes, 2 – detritus, 3 – haemorrhage.
9. Fatty liver. The specimen is stained with hematoxylin and eosin. The liver’s structure is preserved. In centrolobular hepatocytes one can find light-coloured vesicles – drops of fat that have been eluated at the preparation of histologic sections with alcohol. At the particles’ periphery some hepatocytes have big hyperchromic nuclei, some of them contain three nucleuses, which is the sign of regeneration. In some areas of the stroma there are small clusters of cells: lymphocytes, fibroblasts and histiocytes, which indicate productive inflammation that precedes sclerosis. Designate: 1 – centrolobular hepatocytes, 2 – multinuclear hepatocytes, 3 – cellular infiltration.
10. Portal liver cirrhosis. The specimen is stained according to van Gison’s method. The liver’s structure is deranged – one can see false particles which are the areas of liver parenchyma fragmented with connective tissue after bridging necroses. Thus one can observe several central veins located eccentrically. The false particles are confined by thick layers of connective tissue. The sclerotic process progresses, which is indicated by the presence of granulation tissue in the stroma. Besides, one can see regeneratioodes – small areas of liver parenchyma in which the hepatocyte trabecules have no radial orientation and central veins are missing. So in this case we have progressive portal liver cirrhosis. Designate: 1 – false particle, 2 – connective tissue layers, 3 – eccentrically located central veins.
11.Biliary liver cirrhosis. The specimen is stained using van Gison’s method. One can see dark brown granules in the lumen of dilated bile capillaries – cholestasis. The stroma is thickened due to connective tissue. Basically the liver’s structure is preserved, but one can observe fatty degeneration of hepatocytes – light-coloured vesicles – which is neutral fat in hepatocytes which has been eluated at the preparation of sections with alcohol. One finds false particles and regeneratioodes. Designate: 1 – bile capillaries, 2 – connective tissue layers, 3 – fatty degeneration of hepatocytes.
12. Acute viral hepatitis. The specimen is stained with hematoxylin and eosin. In the parenchyma one can observe inflammatory infiltrations of various sizes with lymphocytes prevailing in their cellular composition. The liver preserves the particular structure, in the particles hepatocytes are located radially, the spaces between trabecules are widened. In centrolobular hepatocytes the cytoplasm and nuclei are of lighter colour (dystrophic effect) in comparison with the periphery. Designate: 1 – trabecules, 2 – cellular lymphocytic infiltration.
Additionally:
Erosive gastritis. № 234. Preparation is colored by hematoxylin and eosin. Mucous membrane is destructed. Glandular structures are absent. Cells of mucous membrane are necrosed (nucleus is absent). Mucous membrane has different thickness and places of partial desquamation. In mucous membrane one can see number of hemorrhages (red color) and places of inflammation (places of compressed nucleuses). Dystrophic and necrotic changes are present in muscular layer (nucleuses are absent). Vessels are full of blood. One can see small hemorrhages in other layers. Erosive gastritis develops after poisoning by acids and alkalis.
Stomach ulcer. № 177. The preparation is colored by hemotoxylin and eosin. Without microscope one can see the defect of mucous membrane. With microscope one can see destructed mucous membrane. Glandular structures and nucleuses are absent. The borders of ulcer are presented by necrotic tissue. Necrotic tissue is limited with badly developed zone of demarcation. In the preparation one can see nearly situated nucleuses of blue color (granular tissue). Peripherally connective tissue is situated. In the muscular layer highly developed adipose tissue (kind of connective tissue). Due to histological research we may put diagnosis: worsening of chronic ulcer of stomach.
Ulcer of duodenum. № 293. The preparation is colored with hematoxylin and eosin. Without microscope one can see defect of mucous membrane. With microscope one can see borders and base of ulcer. They are presented with such layers:
Exudative layer is consists of mucous, gastric juice (it is colored pink) and small quantity of cells (bluish nucleus) Layer of fibrinoid necrosis. It looks like narrow strip of necrotic tissue (nucleuses are absent) having pink color.Layer of granulocytes. One can see nearly situated bluish nucleuses. Tissue has well-developed vessels.Connective tissue. One can see fibrous structures of pink color. And some extended nucleuses.Intestinal wall’s tissue. On the borders mucous membrane is present. On the base of ulcer one can see muscular layer. Due to histological research we may put diagnosis: worsening of ulcer of duodenum.
Penetration of stomach ulcer in pancreas. № 317. The preparation is colored with hematoxylin and eosin. Without microscope one can see blue color tissue (pancreas) with defect. This defect is full of light – pink tissue (connective tissue). With microscope one can see connective tissue with numerous vessels. Like this one can see hemorrhages, adipose tissue and granulocytic tissue (places with numerous nucleuses). So base of chronic ulcer is situated in tissue of pancreas.
Ulcer – cancer (adenocarcinoma) № 81. The preparation is colored by method of van Hizon. One can see defect of mucous membrane of stomach. Base of ulcer is presented with connective tissue, which is colored pink. In the tissues, which are situated near the ulcer one can see changed glandular structures (infiltrative growth). In these glands nucleuses are not situated in the basal part of cells but in different places. Nucleuses have different forms, sizes and with intensified colorization. There are many mitosis.
Diphtheritic-necrotic colitis with dysentery №111, №273. On the mucosal membrane of the intestine the fibrinous panniculus places; it penetrates through whole thickness of the mucosal and submucous layers. The mucosal membrane here and there is completely injured and necrotized with formation of the rather shallow ulcerous defects, which penetrates into submucous layer. Almost along whole mucosal and submucous layers one can see hyperemia, edema and infiltration by leukocytes and lymphocytes.
Typhoid fever ulcer №100, №
Lymph node with typhoid fever № 149. The structure of the lymph node is effaced. If increasing is big, one can see that lymph cells are ejected by reticular “typhoid” cells, which actively multiply. In the cytoplasm of these cells we can meet the leavings of the phagocytosed nuclei. The general hyperplasia and hyperemia of the parenchyma of the lymph node are marked. At the same time the inflammatory prolipheration of the reticular cells exposes, they form “typhoid cells” and “typhoid granulomas”.
Spleen with typhoid fever №
Waxy cenker necrosis of the muscle № 194. The coloration of the preparation is by hematoxylin and eosin. The muscular fibrae here and there are necrotized and looked on the preparation as dark-blue macules and looked as waxy candle, that is the striates and nuclei are absent; the sarcoplasm is homogeneous as wax, pink. Around such necrotized fibrae the inflammatory cell infiltration and hemorrhages are revealed.
Work 2.
Practical work with macropreparations near stands.
– Students must recognize the pathology of organs which are presented on the stand.
Macropreparations:
1. Acute ulcer of stomach is presented by two macro preparations:
Mucous membrane is hypertrophied, folds are well developed. In the upper part of preparation one can see round shape defect in mucous membrane (diameter
One can see well developed folds of mucous membrane of stomach. One can see oval shaped defect of mucous membrane. The size of defect is approximately 1 x
2. Chronic ulcer of stomach is presented by three macro preparations:
Mucous membrane of stomach is atrophied. Folds are absent. One can see deep defect of mucous membrane (size 4 x
3. Acute ulcer of stomach:
Mucous membrane of stomach is atrophied. Folds are absent. One can see deep oval shape defect of mucous membrane (3 x
Mucous membrane of the stomach is atrophied. Approximately folds are absent. On the lower border of preparation one can see three oval or round shape ulcers (Diameter of them is near
4. Perforative ulcer of stomach is presented by three preparations: Stomach is opened (dissected on the great curvature). In the center one can see small curvature with less folds. On the other places folds are well developed. In small curvature near to the pylorus one can see perforative defect. Upper part of that is hanging and lower is inclined. Borders of ulcer are little bit thickened. Explain which ulcer is presented in macro preparation (acute or chronic) and morphogenesis of perforation?
Mucous membrane of stomach is atrophied. Folds are absent. Mucous membrane is covered by dark brown coating. In the upper part of preparation one can see ulcer that is passing through all the wall of stomach. Borders of ulcer are little bit thickened and have dark brown color.
Mucous membrane is smooth and without folds. In the mucous membrane present some ulcers with different sizes and forms. One of these is perforated. Borders of ulcers are not thickened. Tell which ulcer is presented in the preparation (acute or chronic)?
5. Penetrative ulcer of stomach. Mucous membrane has well developed folds. One can see perforative defect of not big size. Borders of ulcer are not thickened and drugged. In which organs penetration may occur?
6. Acute ulcer of duodenum. Under the pyloric fold one can see oval form defect on mucous membrane. Upper border is hanging. Lower border is inclined. Borders of ulcer are not thickened. Base is smooth with dark brown spots.
7. Chronic ulcer of duodenum. Wall of intestine is deformed due to big thickened border of ulcer. Ulcer is deep with white color walls.
8. Atrophic gastritis. Mucous membrane is atrophied without folds (“bald mucous membrane”).
9. Hypertrophic gastritis is presented by two macropreparations with similar changes. Mucous membrane is hypertrophied with well-developed folds. Between the folds one can see deep furrow.
10. Cancer of stomach is presented by three preparations:
One can see tumor of big size. It is developed in the cavity of stomach. In the center of tumor one can see necrotic area. Tumor has indistinct borders.
On the lower part of preparation one can see well-developed folds of mucous membrane. On the upper part folds are not present. Wall of stomach is thickened due to infiltrative growth of tumor. One can see necrosis of mucous membrane within with growing tumor.
Mucous membrane is without folds. It is thickened due to infiltrative growth of tumor. One can see necrosis of mucous membrane and hemorrhages.
11. Cancer of stomach with necrosis. Wall of stomach is very thickened due to infiltrative growth of tumor. Tumor is growing in serous layer. One can see necrosis of mucous membrane.
12. Fungating carcinoma of stomach. One can see big tumor. It is connected with small curvature with help of wide foot. Surface of tumor is succulent with ulceration.
13. Cancer of stomach. One can see cylindrical thickness of mucous membrane, which is formed by closed ring. Mucous membrane’s folds in the ring are absent. One can see necrosis of tissue. On the transverses dissection one can see saucer shape tumor.
14. Scirrhous carcinoma. Wall of stomach is thickened and deformed due to infiltrative growth of tumor. The folds are absent.
15. Diffuse cancer of stomach. Wall of stomach is thickened due to infiltrative growth of tumor. On the place of infiltration the folds are absent.
16. Cancer of esophagus is presented by three preparations with similar changes. In the lumen of esophagus one can see tumor’s polyps of different sizes and localizations. On some places one can see ulceration of tumors. Tell the histogenesis of tumors and complications.
Additionally:
Diphtheritic colitis. On the mucosal membrane of the intestine one can see tighly fastened grey-yellow coloured fibrinous panniculus, which are covered all surface. The wall of the intestine is thickened on account of the seropurulent and hemorrhagic percolation. The serous cover is plethoric. Here and there we can meet ulserous defects of the mucosal membrane. Such changes are peculiar to dysentery.
Ulserous colitis with dysentery. On the mucosal membrane on can see numerous ulcers of the irregular forms, which here and there merge. Here and there the ulcers have a character of the superficial defects only on the apex of the folds. At most the deep ulcers are founded. They reach muscular layer of the intestine and have undermined edges. One can meet the places with unbroken big sites of the ulcerity of the mucosal membrane. Against a background of the enormous ulcers there are small islands of the preserved mucosal membrane.
Stenosis of the intestine. On the mucosal membrane one can see cicatricial growing on the place on the deep ulcers. On the periphery of the such cicatricial ulcers the regererative growing of the mucosal membrane takes place, in some cases it is atypical with formation of the polyps. The cicatricial growing led to narrowing of the clear space of the intestine. It is a complication of the dysentery.
The stage of the clear ulcers in the intestine. On the mucosal membrane of the intestine one can see numerous ulcers, which are free from necrotic massae. The edges of the ulcer are smoothed out. The ulcers on the places of the Peyer’s patches look as oval, stretched along the long axis of the intestine defects with straight, as if cut off not undermined edges and with smooth bottom in which one can see diametrical striatality, that belongs to the circular layer of the musculation of the intestine wall. The ulcers on the places of the folliculi have round forms.
Hyperplasia of the spleen. When typhoid fever takes place, the spleen increases in 3-4 times at the expence of plethora the hyperplasia of the red pulp; the hyperplasia of the reticular cells with formation the typhoid granulomas. The organ is flabby, the pulp is dark-red and gives big seraper.
Toxic dystrophy of the liver. The liver is increased, evenly yellow on account of the diffusive dystrophy of the hepatocytes, very flabby (extends on the table surface), here and there is looked argillaceous. The fat dystrophy of the liver develops with typhoid fever, dysentery on account of the intoxication.
Pylephlebitic abscess of the liver. On the sagittal section one can see the abscess that has big sizes. Abscess is represented by grey mass with cracks. Only in the bottom part of the macropreparation one can see narrow stria of the preserved liver tissue what looks argillaceous. In the upper part of the macropreparation glisonic capsule of the liver is at the same time the capsule of the abscess. Pylephlebitic abscess of the liver can develop as complication of the dysentery. With dysentery the development of the periproctitis, pelvioperitonitis or general peritonitis in possible. The rami of the portal vein participate in the inflammatory process, phlebitis and phlebothrombosis develop. The septic embolus by system of the portal vein pool fetches up at liver, where abscess forms.
Work 3.
Analytical work.
– Students must analyze the pathology of organs of gross preparations and micropreparations and explain the possible reasons of their beginning (etiology), basics of morphological change and mechanism of their development (pathomorphosis& pathogenesis).
Brake time: 12.00 – 12.30
I. Seminar discussion of practical work – 12.30 – 14.00
Main questions for self work:
Esophagus diseases: congenital diseases, anatomic anomalies (atresia, fistulas, stenosis, congenital webs and rings).
Stomach diseases: protective barriers of the mucous tunic of the stomach, congenital stomach anomalies.
Gastritis: its definition. Acute gastritis: etiology, pathogenesis, morphologic forms and clinicopathologic description. Chronic gastritis: the essence of the process, etiology, pathogenesis principles of classification, forms defined on the basis of gastrobiopsies studies, morphologic description, complications and consequences; chronic gastritis as a precancerous condition. Hypertrophic gastropathy:
Ulcer diseases: definition, general description, patho– and morphogenesis, morphologic description of chronic ulcer in the periods of exacerbation and remission, complications and consequences.
Stomach tumours: classification- hyperplastic polyps, stomach adenoma, malignant stomach tumours. Stomach cancer: morphologic description, epidemiology, etiology, classification principles, peculiarities of its metastasis, macroscopic and histologic forms.
Tumours of large and small intestine: Epidemiology and nomenclature.
Appendix diseases. Normal appendix: anatomic and histologic peculiarities. Appendicitis: classification, epidemiology, etiology, pathogenesis, morphologic description and clinical signs of acute and chronic appendicitis and their complications.
The causes and mechanisms of the development of liver diseases. General symptoms of necrosis, apoptosis and regeneration of hepatocytes; etiology, classification, patho– and morphogenesis, morphologic description and consequences. Hyperplasia and hypertrophy of hepatocytes.
The influence of metabolic disorders on liver: fatty liver: etiology, clinicopathologic description and prognosis; lipid accumulation diseases and glycogen accumulation diseases.
Massive hepatic necrosis: definition, etiology, pathogenesis, pathologic anatomy; hepatorenal syndrome.
Hepatitis: definition, classification. Acute viral hepatitis: epidemiology, aetiology, ways of infection transmission, patho– and morphogenesis, clinicopathologic forms, morphologic description, viral markers, consequences; clinical and biochemical signs of acute hepatitis. Chronic hepatitis: etiology, morphologic description and classification, activity signs, consequences and prognosis.
Alcoholic lesions of the liver: Alcoholic fatty liver: complications and causes of death, consequences and prognosis.
Liver cirrhosis: pathomorphologic signs and morphologic classification of cirrhosis, etiologic classification of cirrhosis,.
Gallbladder and bile duct: morpho-functional description and composition of bile. Cholecystitis: definition. Acute and chronic cholecystitis: etiology, pathogenesis, clinicopathologic description, complications and causes of death.
The diseases of the exocrine part of pancreas: acute (pancreatonecrosis) and chronic pancreatitis.
List of theoretical questions for the discussion:
1. Patological anatomy of reflux esophagitis.
2. Patological anatomy of chemical esophagitis.
3. Patological anatomy of carcinoma of the esophagus.
4. Pathogenic classification of gastritis.
5. Pathogenic classification of gastritis.
6. Morphogenesis of erosive gastritis (acute gastritis).
7. Morphology of chronic idiopathic gastritis.
8. Pathogenesis and morphology infectious gastritis.
9. Morphology hyperplastic gastropathy (Menetrier disease).
10. Stages of development of the stomach ulcer.
11. Morphology peptic ulcer disease.
12. Wall layers of acute and chronic stomach ulcerю
13. Complications of chronic stomach ulcer by V. A. Samsonov.
14. Morphology epithelial polyps in stomach.
15. Pathogenesis of carcinoma of the stomach.
16. Distant haematogenic and lymphogenic metastases of stomach cancer.
17. Tumors complications of stomach.
18. Epidemiology of typhoid fever.
19. Pathogenesis of typhoid fever.
20. Morphology of the typhoid fever.
21. Clinical features of typhoid fever.
22. Epidemiology of bacterial dysentery.
23. Pathogenesis of bacterial dysentery.
24. Morphology of shigellosis.
25. Clinical features of bacterial dysentery.
26. Construction of classic lobule as structure-functional unit of the liver and it blood stream.
27. Morphogenetic classification of the liver diseases.
28. Outcomes and causes of death because of progressive massive necrosis.
29. Etiologic and morphologic classification of hepatocirrhosis.
30. Pathological changes in the liver because of cirrhosis.
31. Nodes morphogenesis of regeneration and hepatic sinusoids capillarization.
32. Main point of hepatic structure reconstruction in case of cirrhosis.
33. Morphogenesis of postnecrotic hepatocirrhosis.
34. Morphogenesis of portal hepatocirrhosis.
35. Morphogenesis of biliar hepatocirrhosis.
36. Morphogenesis of alcocholic hepatocirrhosis.
37. Morphogenesis of primary and secondary biliar hepatocirrhosis.
38. Morphology of portal hypertension.
39. Clinic-functional characteristics of hepatocirrhosis.
40. Macro- and microscopic forms of hepatic cancer.
41. Pathogenesis of the hepatocellular carcinoma.
Practical skills and abilities of students
Student should know: the classification, etiology, pathogenesis, pathologic anatomy and complications of esophagus, stomach and duodenum diseases;
– the classification, etiology, pathogenesis, pathologic anatomy and complications of appendicitis and peritonitis;
– the classification, etiology, pathogenesis, pathologic anatomy and complications of liver and pancreas diseases.
Students should be able:
– to distinguish the pathomorphological manifestations different forms of gastritis and hepatitis;
– to identify the morphologic signs of gastrointestinal tract diseases;
– to explain the possible complications and consequences of gastrointestinal tract diseases;
– to explain the possible complications of fatty liver, hepatitis, liver cirrhosis, cholecystitis, pancreatitis and cholelithiasis.
III. INDEPENDENT WORK OF STUDENT – 14.15 – 15.00
TEST EVALUATION AND SITUATIONAL TASKS
Situation Tasks:
1. An X-ray examination has revealed a filling defect in the antral part of the stomach. At the examination of post-operational material one has established that the defect is of oval form, its edges are dense and the bottom is black. Identify the pathologic process, describe the possible microscopic changes of the defect’s bottom and name the possible complications.
2. The patient came to the doctor complaining of pain in the right hypochondrium which has lasted for two days. At operation was found a thickened appendix and hyperaemic serous tunic covered with fibrinous-suppurative exudation. Identify the disease, describe the microscopic changes and name the possible complications.
4. Two months after blood transfusion, jaundice was found in the patient’s body, with liver enlargement, increased level of transaminases and sedimentary test derangement. What is the presumable disease, its etiology and the type of jaundice?
5. The jaundice developed suddenly in the body of a person who had suffered for a long time from calculous cholecystitis. Identify the presumable cause and type of jaundice.
Answers to the Situation Tasks:
1. Stomach ulcer; muriatic haematin, fibrinoid necrosis, granulation tissue, demarcation border , scar tissue, vasculitis; ulcerative-destructive, inflammatory, ulcerocicatricial, malignization, combined complications.
2. Phlegmonous appendicitis; diffuse leucocytic infiltration; perforation, peritonitis, pylephlebitic abscesses, development into secondary gangrenous one.
3. Alcoholic cirrhosis (portal); the haemorrhage comes from varicose veins of the stomach and esophagus.
4. Viral hepatitis; hepatitis virus B; hepatic jaundice.
5. Bile duct occlusion; obstructive.
Tests
1. The cell types in the corpus gastric glands are all of the following, EXCEPT:
A. Mucous cells.
B. Parietal cells.
C. Chief cells.
D. * Hurtle cells.
E. Endocrine cells.
2. The gastric mucosal protection from autodigestion is possible due to all of the following factors, EXCEPT:
A. Mucus secretion.
B. Bicarbonate secretion.
C. *Gastrin receptor activation.
D. Epithelial barrier .
E. Mucosal blood flow.
3. Chronic infection of the gastric mucosa is associated with which of the following bactertia:
A. Escherichia coli.
B. *Helicobacter pylori.
C. Campilobacter jejuni.
D. Enterococcus falcium.
E. Escherichia chaffeensis.
4. Chronic gastritis may be characterized by all of the following features, EXCEPT:
A. *Suppurative inflammation.
B. Lymphocyte infiltration.
C. Plasma cell infiltration.
D. Intestinal metaplasia.
E. Atrophy.
5. Acute gastritis is commonly caused by all of the following factors, EXCEPT:
A. Excessive use of aspirin.
B. Heavy smoking.
C. Excessive alcohol consumption.
D. Treatment
E. starvation
Answers for the tests
1) D; 2) C; 3) B, 4) A, 5) E.
References:
А – Basic:
1. Ya. Bodnar, A. Romanyuk, R. Bodnar, K. Romanyuk, V. Voloshyn. Short cours of patomorphology: Textbook. – Ternopil: TSMU,2011. – 544 p.
2. Practical classes materials.
3. Anderson’s Pathology //Edited by Jonh M. Kissane. The C.V. Mosby Company. – Toronto – Philadelphia, 1990. – 2196 p.
4. Emanuel Rubin, John L. Farber. Pathology. – Philadelphia, 1994. –1200 p.
5. Harsh Mohan. Textbook of Pathology. — Jaypee Brothers, Medical publishers (P) LTD., New Delhi, 1995. — 980 p.
6. Ramzi S. Kotran, Vinay Kumar, Stanley S. Robbins. Robbins Pathologic Basis of Disease, W.B. Saunders Company, USA, 1994. – 1400 p.
7. Robbins and Contran Kumar. Pathologic Basis of Disease /Eighth edition. – Saunders, Elsevier, 2010. – 1450 p.
8. Thomas C. Histopathology. – B.C. Decker Inc. – Toronto – Philadelphia, 1989. – 386 p.
9. Thomas C. Macropathology. – B.C. Decker Inc. – Toronto – Philadelphia, 1990. – 355 p.
10. Zagoruyko A.K. Short lectures on pathology (pathological anatomy). – Simferopol: 2 ed. CSMU, 2002 – 196 p.
11. Lectury presentation. http://intranet.tdmu.edu.ua/data/kafedra/internal/index.php?&path=patologanatom/presentations/en/med/lik/ptn/Pathomorphology/3/ ….
B – Additional :
1.Sorokina I. Pathological anatomy. Kharkov: Fact, 2005, P. 564
2.Струков А.И., Серов В.В. Патологическая анатомия. – М.: Медицина, 1993. – C. 47-59.
3.Серов В.В., Ярыгин Н.Е., Пауков В.С. Патологическая анатомия. Атлас. – М., 1986. – C. 5-25.
4.Ramzi S. Kotran, Vinay Kumar, Stanley S. Robbins. Robbins Pathologic Basis of Disease, W.B. Saunders Company, USA, 1994 – P. 24-28.
Methodical instruction has been worked out by: as.-prof. Volodymyr Voloshyn
Methodical instruction was discussed and adopted at the Department sitting
August, 26, 2010. Minute № 1
Methodical instruction was discussed and adopted at the Department meeting
27.08.2013. Minute № 1
