METHODICAL INSTRUCTION FOR STUDENTS OF THE third COURSE
Medical Faculty
Lesson 13 (PRACTICAL – 6 hours)
Theme: 1. Pathomorphology of primary and hematogenic tuberculosis.
2. Secondary (cavitary) tuberculosis.
The place of class – the department of pathoanatomy.
Actuality of theme: Tuberculosis – acute or chronic infectious disease caused by Mycobacterium tuberculosis and may wonder where all the organs of the human body, but most patients suffering from pulmonary tuberculosis. This pathology is the most frequent infectious cause of death on earth. Since the end of those 80 years of the twentieth century, an increased number of TB patients, partly due to people infected with HIV. TB is a frequent cause of disability and temporary disability. Timely diagnosis of tuberculosis is important in improving the epidemiological situation in the country and population health in general.
Aim: To be able define by macro- and microscopic picture the types of tissue reactions, responsing to invasion of tuberculosis bacillus, morphogenesis of primary and hematogenic tuberculosis, to evaluate the consequences and meaning of complications to the organism. to learn sequence of development of stages of progressed post primary tuberculosis, its consequences and complications.
Distributed throughout the world, tuberculosis is clearly one of the most important bacterial diseases in humans. Although the risk of infection has been significantly reduced in developed countries, it remains high for malnourished persons in impoverished areas.
Professional orientation of students: The knowledge of theme is necessary for future studying of tuberculosis on clinical departments. In doctor s practical work deep investigation of pathogenesis is important for diagnosis and providing of prophylaxis and treatment; for doctors-pathologists it is important for diagnosis verification.
Tuberculosis infection of the nose is almost always secondary to tuberculosis of the lungs, fromwhich the tubercule bacilli spread by dropled infection. Tuberculosis of the facial scin, called lupus vulgaris, may spread to the nasal vestibule and then to the nasal mucosa.
Initial level of knowledge and skills:
1. Normal anatomy of lungs (department of normal human anatomy).
2. Physiology of breathing process (department of normal physiology).
3. Micro- and macroscopic structure of lungs. Air-conducting and respiratory parts of lungs. Acinus and aero-hematic barrier (department of histology, cytology and embryology).
4. Microbiologic characteristics of Mycobacterium tuberculosis (department of microbiology).
5. Productive inflammation. Ways of infection spreading (department of pathological anatomy).
6. Answer the questions of the theoretical part, which are offered in the album for class-room and extra-class-room work of students
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:
Miliaric tuberculosis of lung. In pulmonary tissue there are seen dense regions with loss of lung picture. Dense regions are tuberculi, in their centers there are caseous necrosis presented by homogenous pink nucleus less mass; on the periphery one can see cell bank (nuclei are painted with blue colour). On the major enlarging there can be seen single oval nuclei with larger size and less painted – these are epithelioid cells. Small, round, intensively painted nuclei prevale – these are lymphocytes. In granular bank of some tuberculi one can see giant cells of Pirogov-Langgans (on the minor enlarging). Those cells are large and polynuclear cells; cytoplasm is intensively painted with pink; nuclei are round, hyperchromatic and situated on the periphery in a shape of moon or circle, sometimes they are gathered in the cell centre. The quantity of nuclei is from 3 to 20 and more. In tuberculosis tuberculi caseous necrosis prevales, perifocal productive reaction is shown weakly, so there is low resistance of the organism. There are a lot of tuberculi, they often connect with each other. All tuberculi are on the same stage of development, therefore it is acute miliaric tuberculosis of lungs, which belongs to hematogenic tuberculosis. Besides in lungs one can see dilated small bronchi, their lumens are full of serous exudates with desquomated mucosal epithelium. Separated bronchiolae have no mucosa, in alveolar lumen there is serous exudates (hemogenic pale-pink mass), therefore, exudative reaction takes place. Vessels are bloodful. Designate:1 – tuberculosis tuberculum in lung tissue; 1a – caseous necrosis; 1b – epithelioid cells; 1c – lymphocytes; 1d – giant cells of Pirogov-Langgans; 2 – serous exudates in alveolar lumen;
describe the microscopic structure of Pirogov-Langgans cells; note the localization of necrosis in tuberculum;
2. Tuberculosis leptomeningitis. In brain tissue there is noticeable edema, empty regions, vessels hyperemia. In pia mater there are numerous tuberculosis tuberculi with well- developed alterative reaction (caseous necrosis) and low-developed protective productive reaction – resistance of the organism is low. Pia mater is enlarged with connective tissue – it is sclerosis. Sclerosis means that inflammation of mucosa goes for a long time, the acute phase is presented by numerous new tuberculosis tuberculi. Tuberculosis leptomeningitis is mostly developed in children with hematogenic generalization of primary tuberculosis. Designate:1 –tuberculosis tuberculi; 2 – regions of sclerosis; 3 – empty parts in brain;
explain what the weak productive reaction means;
name the signs of acute phase of leptomeningitis;
3.Tuberculosis lymphadenitis. In connected tracheobronchial lymphatic nodes one can see regions of caseous necrosis; lymphoid tissue is partly uninjured; single lymphoid follicles are saved. Around the foci of caseous necrosis there is connective tissue; it means that tuberculosis was developing for a long time. Tuberculosis bronchadenitis develops as a result of lymphoglandular progressing of primary tuberculosis. Designate: 1 – caseous necrosis; 2 – single lymphoid follicles; 3 – connective tissue.
what the development of connective tissue means;
name the reason of lymphadenitis development.
Additional:
Slide №278. Local tuberculosis One can see a site of caseous necrosis- it is homogenic, pink coloured site, on the territory of which all structures are destroyed, pulmonary tissue is absent. On the territory of caseous necrosis there are nests of black points- it is dust of carbon, which is placed in lymph vessels and left on the territory of caseous necrosis. Around caseous necrosis well one can see formed connective tissue capsule- it is fibro-focal tuberculosis. Connective tissue capsule is morphologic expressing of completing of productive reaction. In next site there are numerous tuberculous colliculi that tell about progressing of tuberculous process by lymphogenous or contact ways. Productive reaction in tuberculous colliculi is expressed well. Iearly pulmonary tissue interalveolar membranes are thickened, sclerosed and here and there torn, it is emphysema. In the lumen of alveoli there is serous exudate, the vessels are dilated, plethoric – it is perifocal exudative reaction, that tells about worsening of tuberculous process.
Slide №344.Fokal tuberkulosis Coloration is by van Gison”s method. In consolidated site of pulmonary tissue of caseous necrosis with will expressed pink coloured connective tissue capsule- it is fibro – focal tuberculosis. In affected site one can see dusts of carbon. Ieared pulmonary tissue interalveolar walls are thickened, , here and there torn, it is emphysema. In the lumen of alveoli there is serous exudate, the vessels are dilated, plethoric-it is perifocal exudative reaction, that tells about worsening of tuberculosis process.
Slide № 213, № 214, № 280. Tuberculoma Preparations № 214, № 280, are coloured by hematoxylin and eozin, preparation № 213 is coloured by Veigerts Method for revealing of elastic fibrae. In all micropreparations one can see big site of caseous necrosis, fordered by connective tissue capsule. Iearly pulmonary tissue there are sites of caseous necrosis with perifocal productive reaction, numerous tuberculous colliculi, nests of swarm if lymphocytes-these are lymphomas. Also one can see well expressed pneumosclerosis. Serous exudate in the lumen of alveoli tells about worsening of process. In preparation № 280 one can see that on the territory of caseous necrosis elastic fibrae of vessels walls in interalveolar membranes were preserved, at expense of this the pulmonary picture partially is preserved.
Slide №252. The wall of cavern Coloration is hematoxylin-eosib. One can see a defect of pulmonary tissue- it is cavern (a half of cavern is represented in micropreparation ). Internal layer of cavern is by necrotizing tissue, which is not torn awey yet, it is homogenic unstructural massa, impregnated with leukocytes ( purulent melting of caseous massae). Deeper-there is a torus of granulation tissue, one can see many nuclei and connective tissue capsule, fibrillar tissue is pink. Iearly pulmonary tissue there are tuberculous colliculi, foci of caseous necrosis, here and there with destruction ( microcavern) , nests of swarm of lymphocytes (lymphomas), pneumosclerosis, thickening of interalveolar membranes, wide entire bields of connective tissue, effects of emphysema.
Slide №231. Amyloid nephrosis Coloration is by colour kongo-rot. In glomeruli of runes structural picture is alsent on the sites, glomeruli are pink coloured, it is amyloid. With post primary tuberculosis the products of destruction of the pulmonary tissue soak in the blood and taken out through renes, litter renal filter, capillaries of glomeruli. In stipulates the development of renal in-suffieciency-uremia.
Work 2.
Practical work with macropreparations near stands.
– Students must recognize the pathology of organs which are presented on the stand.
Macropreparations:
Tuberculosis lymphadenitis. Mesenterial lymphatic nodes are enlarged to
name the primary affect in alimentary tuberculosis infection;
what can the capsule destruction be complicated by?
Tuberculosis peritonitis. In peritoneum of small intestine one can see humerous white nodules – tuberculosis tuberculi. Tuberculosis peritonitis develops in hematogenic generalization of primary and secondary tuberculosis, and also as a complication of mesenterial lymph nodes tuberculosis lymphadenitis.
name the localization and size of tuberculosis tuberculi in peritonitis;
name the forms of tuberculosis where peritonitis can be possible;
Miliaric tuberculosis of lungs. On the section of lung tissue one can see numerous white points – tuberculosis tuberculi. White colour is caused by caseous necrosis. Miliaric tuberculosis of lungs belongs by classification to hematogenic acute lung tuberculosis. In such tuberculosis there must be the place left by primary tuberculosis.
explain why those tuberculi are white;
what kind of tuberculosis is miliaric one;
Tuberculosis spondylitis. It is presented by several preparates. On the sagittal backbone section one can see caseous necrosis in upper vertebra s body with the beginning of cavity formation (transformation of focal tuberculosis into caseous). Lower there are seen two vertebrae with destructed bodies. We cannot see a cavity because destructed vertebrae s bodies are pressed by body weight. During this the tuber develops, as a rule. Purulent exudate, formed as a result of caseous necrosis, sometimes goes down along interfascial spatia to lower parts of the body and forms cold abscesses in lumbal, glutal and femoral regions.
name the vertebral parts where one can see caseous masses;
name the body parts where abscesses can be present.
Tuberculosis of uteral tubes. In isthmic parts of both tubes one can see regions of caseous necrosis (diameter around
name the causes of tubal obstruction;
name the consequences of tubal tuberculosis.
Tuberculosis of adrenal gland. The gland is a lot enlarged (normally it is sickness is 2-
explain the reason of skin darkening;
name the form of adrenal gland tuberculosis.
1. Acute cavernous tuberculosis. On the section of pulmonary tissue one can see two cavities, that have diameter equal 1 and 1,5 sm. The borders of cavities are represented by pulmonary tissue with formation of connective tissue capsule. In this macropreparation also one can see white coloured sites of consolidation, that have diameter 1 sm and less; these are sites of caseous necrosis. Some foci of caseous necrosis pour together. Around sites of caseous necrosis the airiness of pulmonary tissue is lowered, the tissue is dense, it has more dark tint; it is perifocal exudative inflammation. Such foci of caseous necrosis appear on account of intracanalicular spreading of tuberculous microbacterium along lungs. With formation of cavern rarefied caseous massae through bronchi get into trachea and are ejected with sputum, near this they are got through bronchi to respiratory alveoli, where the foci of caseous necrosis are developed. So, tuberculosis is spread atmost from upper sites of lung in lower and to opposite lung. Such changes in lungs will be and with acute focal tuberculosis, that is the foci of caseous necrosis are with perifocal exudative inflammation.
2. Tuberculoma of lung. It is represented by two preparation: on the section of pulmonary tissue one can see a site of white coloured consolidation (caseous necrosis), that has diameter 3 sm and 4 sm, and is surrounded by dense connective tissue capsule. Tuberculoma is a most favourable completion of infiltrative tuberculosis. Rentgenologically it is displayed in look of round form with clear borders as with tumour, that is why name is tuberculoma.
3. Fibrocavernous pulmonary tuberculosis. On the section of pulmonary tissue one can see big cavity, walls of which are represented by thick connective tissue capsula. Around cavern the airiness of pulmonary tissue is lowed, it is pneumosclerosis at most in low parts of lungs caverns are more fresh, because tuberculous process is begun from apex and spread intracanalicular and by contact way into low parts.
4. Polycavernous tuberculosis of lungs. On the section of lung almost quite destroyed upper and middle parts are represented by big cavities. Walls of caverns are represented by connective tissue, pulmonary tissue is absent. In lower part there is pneumosclerosis. Such changes in lungs clinically are expressed by pulmonary insufficiency.
5. Acute caseous pneumonia. On the section the whole part of lung is represented by homogenic white coloured massa – it is caseous necrosis. Picture of pulmonary tissue is absent; all structures are destroyed. Caseous pneumonia is most unfavourable completion of infiltrative tuberculous – caseous is spread on whole territory of perifocal exudative inflammation. Sicks, as a rule, for this die of massive poisoning.
6. Cirrhotis pulmonary tuberculosis. On the section the lungs are completely destroyed, one can see massive growings of connective tissue course of vessels bronchi. Bronchi are deformed, the wall is thickened at expense of connective tissue; the lumen is narrowed. Big caverns are united together, their walls are represented by hyalinizated connective tissue. Pulmonary tissue is preserved only as small grey-black coloured insulae, it is cavernous pulmonary tissue with sharply lowered airiness. Cirrhosis differs from sclerosis because, with sclerosis the structure of pulmonary tissue is not broken, and connective tissue grows in places, where it is in norma – course of vessels, bronchi, interpartial, interacinous membranes. Big destructive processes – destruction of pulmonary tissue, that is finished by cicatrization, growing of connective tissue – precede cirrhosis. So, structure of lung (primary bronchus – partial- segmental- lobar-bronchiole-respiratory channel-alveoli) is broken on account of destruction of lung by tuberculous process with next cicatrization. Cirrhotic tuberculosis is a finishing stage of post primary tuberculosis. Sicks die of pulmonary-cardiac insufficiency. On thoracotomy pleural cavities are revealed obliterated by hyalinizated connective tissue, that is so dense, that it is difficult to cut its by sectional knife. Lung is removed together with periostenum of costae.
7. Pulmonary hemorrhage. It is represented by two macropreparations.
On the section of lung one can see a cavern, filled by clot of blood. Hemorrhage into cavity of cavern is stipulated by erosion of vessels in wall of cavern. From cavern blood gets into bronchi, trachea-it is pulmonary hemorrhage. Death comes from asphyxia on account of filling bronchi by blood and coming into alveoli with respiration.
On the section of lungs in left apex one can see a cavern, filling by blood. One can see blood also in the lumen of bronchi, trachea- it is pulmonary hemorrhage. Death comes from asphyxia.
8. “ Cor bovinum”. Near the heart of usual sizes the heart, increased in 4-5 time at most at expense of right heart, is represented. With pneumosclerosis and pneumocirrhosis, in theminal stage of tuberculosis the sclerosis of pulmonary vessels with obliteration is developed. Load of right ventricle of the heart is increased, its compensatory hypertrophy with next decompensatory dilatation is developed. Congestion in greater circulation comes, load of left ventricle with next hypertrophy and dilatation is increased. So, on account of sclerotic changes in lungs the sizes of heart are increased. To pulmonary insufficiency the cardiac insufficiency joins.
9. Tuberculosis of the larynx. One can see destruction of the mucous membrane of larynx- ulcering, the surface is rough, the mucous membrane is absent, the contours of pathological process are washed away. Tuberculosis of the larynx is developed, as a rule, as complication with post primary tuberculosis, if in sicks big guantity of sputum is isolated during a long time. Permanent stimulation of mucous membrane contributes to infecting with next exudative and alternative reaction. If tuberculous process affects vocal ligaments, hoarsion and speechlessness come.
Work 3.
Analyzing 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 – 13.45
List of theoretical questions for the discussion:
1. Etiology and mechanism of tuberculosis spreading.
2. Types of tissue reactions in tuberculosis inflammation.
3. Ways of primary infection (contracting) of tuberculosis
4. Pathological anatomy of tuberculosis. Primary tuberculosis complex.
5. Variants of primary tuberculosis development.
6. Healing of primary complex.
7. Ways of primary tuberculosis complex progressing.
8. Morphogenesis of hematogenic form of primary tuberculosis generalization
9. Lymphogenic (lymphoglandular) form of primary tuberculosis generalization.
10. Morphogenesis of primary affect growth as a form of primary tuberculosis progressing.
11. Morphogenesis of mixed form of primary tuberculosis progressing.
12. Morphogenesis of chronic primary tuberculosis.
13. Kinds of hematogenic tuberculosis.
14. Forms of generalized hematogenic tuberculosis.
15. Morphology of flash tuberculosis sepsis (Landusi sickness).
16. Morphology of acute disseminated miliaric tuberculosis.
17. Morphology of acute disseminated tuberculosis.
18. Forms of hematogenic tuberculosis with extrapulmonary injuries mainly.
19. Morphology of bones tuberculosis.
20. Morphology of kidney tuberculosis.
21. Pathology of the secondary (cavitary) tuberculosis.
22. Pathogenesis the secondary tuberculosis.
23. Morphology of the tuberculous spondylitis.
24. Morphology cavitary tuberculous.
25. Morphology of the tuberculoma of lung.
26. Morphology of the fibrocavernous pulmonary tuberculosis.
27. Morphology of the acute caseous pneumonia.
28. Morphology of the cirrhotis pulmonary tuberculosis.
29. Morphology of the polycavernous tuberculosis of lungs.
30. Complications of the secondary tuberculosis.
31. Complications of the secondary tuberculosis.
TEST EVALUATION AND SITUATIONAL TASKS
Situation Tasks:
1. Male, 12 years, suddenly fell ill – fever, fever. The day before, after playing soccer and bathe in a river. At examination: blood lymphocytosis, positive reaction Mantu, radiography in the lungs, numerous small shadows as “snowflakes. Your diagnosis? Pathogenesis of disease? What caused X-ray shadows in the lungs as “snowflakes“?
2. The three-year child six months ago began to refuse food, pale. A month ago, began a grueling paroxismal cough. Mantu test positive, the X-ray lung without features. Your diagnosis? What caused paroxismal cough? Pathogenesis of disease?
3. The patient died of pulmonary tuberculosis bleeding. Form of TB? The cause and mechanism of death?
4. In the long-term ill effects pulmonary tuberculosis rose heart failure. He died of pulmonary-cardiac insufficiency. Why a heart failure? Morphological changes of heart?
5. In the top of the right lung of a person who was killed in a car accident, found four calcinations diameter 0,5 – 0,7 cm other changes in the lungs were found. What evidence found calcinations? Causes and morphogenesis of their development?
6. A child is a sharp pain in swallowing, swelling of the neck, the body temperature to 39. In tonsils appeared yellow-white film, removable hard. Clean-cut signs of intoxication. What is the disease in a child? What are the possible complications?
7. Child taken to hospital in a state of asphyxia. In the larynx revealed a white and yellow, obturuyuchi clearance films, which are easily removed. A tracheotomy, but the child’s condition continued to deteriorate, there were rales in the lungs. What kind of disease in a child? What complications developed in this case?
Answers to the Situation Tasks:
1. Hematogenous tuberculosis, mycobacterium hit pockets of their eliminations, miliary foci formation of specific inflammation.
2. Primary tuberculosis, tuberculous bronhoadenit, lymphogenous generalization of primary tuberculosis.
3. Cavitary or fibro-cavernous tuberculosis. Erosion vessels. Asphyxiation and acute blood loss.
4. Pulmonary decompensation of heart. Right ventricular hypertrophy of the heart with fatty phenomena.
5. Fires of Simon. Petryfikatsiya hematogenous foci dropout in primary tuberculosis.
6. Diphtheria; asphyxia paratonzylyarni abscesses, phlegmon.
7. Diphtheria, croup, asphyxia.
Tests
1. Mycobacterium tuberculosis is characterized by all of the following features, EXCEPT:
a) Pili-forming. b) Aerobic. c) Non-spore-forming. d) Nonmotile. e) Red colored in acid-fast staining.
2. Substances that prevent complete phagocytosis of Mycobacterium tuberculosis by macrophages and induce delayed type hypersensitivity are all of the following, EXCEPT:
a) Cord factor. b) Interleukin-12. c) Lipoarabinomanan (LAM). d) Heart-shock protein. e) Activated complement.
3. A calcified focus (fibrocalcific scar) forming in the lung parenchyma and in the hilar lymph node after the primary tuberculosis infection is also referred to as:
a) Keloid. b) Granuloma. c) Ghon focus. d) Aschoff-Pule focus. e) Simon focus.
4. Favored targets for miliary extrapulmonary seeding are all of the following organs, EXCEPT:
a) Bone marrow. b) Kidneys. c) Liver. d) Uterus. e) Spleen.
5. Miliary tuberculosis is associated with which of the following pathologic conditions:
a) Reinfection. b) Localized caseation in the lungs. c) Localized caseation in the lymph node. d) Primary infection. e) Hematogenous tuberculosis.
6. All of these cells participate in immune response in primary lung tuberculosis, EXCEPT:
a) Type I pneumocytes. b) Alveolar macrophages. c) CD4+ helper T-cells. d) CD8+ suppressor T-cells. e) Double negative T-cells.
7. The most common sites of skeletal tuberculosis involvement are all of the following, EXCEPT:
a) Skull bones. b) Thoracic vertebrae. c) Lumbar vertebrae.d) Knees. e) Hips.
8. The spine tuberculosis breaking through intervertebral discs and extending into the soft tissue with cold abscess forming is also referred to as:
a) Paget’s disease. b) Pott’s disease. c) Gohn complex. d) Reinfection focus. e) Dormant disease.
9. Severe destruction of vertebrae in spine tuberculosis may result in all of the following pathologic conditions, EXCEPT:
a) Permanent compression fractures. b) Scoliotic deformities. c) Drainage tract (sequestrum) forming. d) Kyphotic deformities. e) Neurologic deficits.
10. Complications of tuberculosis osteomyelitis include all of the following, EXCEPT:
a) Tuberculosis arthritis. b) Sinus tract formation. c) Cold abscess formation. d) Caseation in the lung. e) Amyloidosis.
11. The intestine may be affected in which of the following forms of tuberculosis:
a) Secondary tuberculosis. b) Cavitary fibrocaseous tuberculosis. c) Dormant tuberculosis.d) Primary tuberculosis complex. e) Miliary tuberculosis.
12. Healed lesions in primary tuberculosis include all of the following, EXCEPT:
a) Fibrous incapsulation. b) Caseous pneumonia. c) Fibrocalcific scar.d) Foci of ossification. e) Focal pleural adhesions.
13. Primary complex in tuberculosis may directly transform in all of the following pathologic conditions, EXCEPT:
a) Fibrocalcific scars. b) Latent pulmonary lesions. c)Miliary tuberculosis. d) Latent extrapulmonary lesions. e) Progressive primary tuberculosis.
14.Tuberculous salpingitis can be found in which of the following forms of tuberculosis:
a) Secondary tuberculosis. b) Cavitary fibrocaseous tuberculosis. c) Dormant lesions. d) Miliary tuberculosis. e) Primary tuberculosis.
15. The cells playing the most important role in chronic tuberculous inflammation are which of the following:
a) Macrophages. b) Leukocytes. c) Eosinophils. d) Erythrocytes. e) Plasma cells.
16.The granuloma in tuberculosis is composed predominantly of which of the following cells:
a) Fibroblasts. b) Epithelioid cells. c) Eosinophils. d) Plasma cells. e) Neutrophils.
17. The miliary lung tuberculosis is characterized by which type of inflammation:
a) Granulomatous. b) Serous. c) Fibrinous. d) Suppurative. e) Hemorrhagic.
18. The type of necrosis that can be found in tuberculous granuloma is which of the following:
a) Coagulatioecrosis. b) Liquefactive necrosis. c) Caseous necrosis. d) Enzymatic fat necrosis. e) Fibrinoid necrosis.
19. Typical tuberculous granuloma is characterized by all of the following, EXCEPT:
a) Plasma cells. b). Area of central necrosis. c) Epithelioid cells. d) Langhans-type giant cells. e) Lymphocytes.
20. Macrophages in tuberculous granulomatous inflammation can transform into which of the following cells:
a) Monocytes. b) Epithelial cells. c) Epithelioid cells. d) Plasma cells. e) Lymphocytes.
21. A calcified focus (fibrocalcific scar) forming in the lung parenchyma and in the hilar lymph node after the primary tuberculosis infection is also referred to as:
a) Keloid. b) Granuloma. c) Ghon focus. d) Aschoff-Pule focus. e) Simon focus.
22. Favored targets for miliary extrapulmonary seeding are all of the following organs, EXCEPT:
a) Bone marrow. b) Kidneys. c) Liver. d) Uterus. e) Spleen.
23. Miliary tuberculosis is associated with which of the following pathologic conditions:
a) Reinfection. b) Localized caseation in the lungs. c) Localized caseation in the lymph node. d) Primary infection. e) Hematogenous tuberculosis.
24. Secondary tuberculosis is characterized by all of the following features, EXCEPT:
a) Caseous necrosis and cavities in the lung. b) Primary focus in the lung. c) Reinfection with Mycobacteria. d) Reactivation of dormant disease. e) Progression directly into the disseminated disease.
25. Caseous focus in tuberculosis may progress into a cavity in which of the following pathologic conditions:
a) Reactivation of dormant disease. b) Reinfection. c) Erosion into the bronchiole (drainage). d) Lobar exudate consolidation. e) Caseous pneumonia.
26. The cavity in cavitary fibrocaseous tuberculosis is characterized by all of the following features, EXCEPT:
a) Localized in the apex of the lung. b) Lined by yellow-grey caseous material. c) Walled by fibrous tissue. d) Drained by bronchus. e) Filled with suppurative exudates.
27. Severe destruction of vertebrae in spine tuberculosis may result in all of the following pathologic conditions, EXCEPT:
a) Permanent compression fractures. b) Scoliotic deformities. c) Drainage tract (sequestrum) forming. d) Kyphotic deformities. e) Neurologic deficits.
28. Complications of tuberculosis osteomyelitis include all of the following, EXCEPT:
a) Tuberculosis arthritis. b) Sinus tract formation. c) Cold abscess formation. d) Caseation in the lung.e) Amyloidosis.
29. The liver may be affected in which of the following forms of tuberculosis:
a) Secondary tuberculosis. b) Cavitary fibrocaseous tuberculosis. c) Dormant tuberculosis.. d) Primary tuberculosis complex. e) Miliary tuberculosis.
30. Caseating destructive secondary tuberculosis includes all of the following lesions, EXCEPT:
a) Caseation in the lung. b) Cavities in the lung. c) Caseation in the lung lymph nodes. d) Miliary extrapulmonary lesions. e) Extrapulmonary caseation.
31.Tuberculoma is macroscopically characterized by all of the following features, EXCEPT:
a) Intraparenchymal single mass. b) Greyish-white appearance. c) Well-circumscribed mass. d) Several centimeters in diameter. e) Several millimeters in diameter.
32.Tuberculous salpingitis can be found in which of the following forms of tuberculosis:
a) Secondary tuberculosis. b) Cavitary fibrocaseous tuberculosis. c) Dormant lesions. d) Miliary tuberculosis. e) Primary tuberculosis.
33. The cells playing the most important role in chronic tuberculous inflammation are which of the following:
a) Macrophages. b) Leukocytes. c) Eosinophils. d) Erythrocytes. e) Plasma cells.
Answers for the tests
1) a; 2) b; 3) c; 4) d; 5) e; 6) e; 7) a; 8) b; 9) c; 10) d; 11) d; 12) b; 13) c; 14) d; 15) a; 16) b; 17) a; 18) c; 19) a; 20) c; 21) c; 22) d; 23) e; 24) b; 25) c; 26) e; 27) c; 28) d; 29) e; 30) d; 31) e; 32) d; 33) a.
III. TESTING of KNOWLEDGES of STUDENTS – 14.15 – 15.00
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/stomat/ptn/Pathomorphology/2-3/ ….
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: Petro Vavrukh
Methodical instruction was discussed and adopted at the Department sitting
01 june_ 2011. Minute № _16
Methodical instruction was adopted and reviewed at the Department sitting
__07 june_2012 . Minute № _15__
