Coloring according to van Gieson. In the lung, the focus of caseous necrosis is surrounded by a thick capsule of a fibrous structure, painted brick-red.
Caseous necrosis is a type of coagulative necrosis. Tissue affected by this type of necrosis is transformed into a soft, white, proteinaceous, cottage cheese-like mass (casein). The causes of cheesy necrosis can be tuberculosis, syphilis and a special type of fungus.
Often such a pathology is observed with deep, systemic mycosis, an infectious disease caused by yeast fungi, and with damage to dangerous dimorphic fungi. With caseous necrosis, the histological structure is completely destroyed; under a microscope you can see pink zones, devoid of cells, surrounded by a granulomatous inflammatory process.
Caseous necrosis of the lung is characterized by a yellowish-brown tint of the surface. In case of severe destruction, cystic spaces appear. Cheesy necrosis develops in a granuloma in the event of a change in the reactivity of the body, as evidenced by fibrous transformations. In some cases, a strong increase in the tuberculosis focus is possible, and subsequently its tendency to cheesy necrosis and destruction.
Cheesy necrosis of the lung develops after caseous necrosis. Approaching any surface and touching an organ or tissue, the lesion opens, allowing the curdled mass to be emptied. In this case, cavities (extensive defects) are formed. The rapid liquefaction of the curdled masses contributes to the formation of a huge cavity. Clinical symptoms are expressed by dysfunction of the bronchopulmonary system, respiratory failure, and serious changes in the functional systems of homeostasis.
The disease progresses very quickly and can be fatal. The disease occurs with manifestations of intoxication syndrome, body temperature rises and remains constant to 39-40 °C. There is a lack of appetite, refusal to eat, sudden and significant weight loss, and weakness.
In patients, pain is localized in the chest area, shortness of breath appears, wet with copious sputum, often rusty in color. With extensive damage to the lung, necrosis is found in both the visceral and parietal pleura. If the disease is detected too early, there is every chance of a quick recovery. At a later date, surgery is scheduled.
Caseous necrosis of the lymph node
Lymph nodes are defense organs that produce lymphocytes that prevent harmful microbes from entering the body. In a healthy state, they have a round, bean-shaped, less often spindle-shaped, slightly flattened shape. The length can be from a few millimeters to 2-3 cm. Near large blood vessels, the lymph nodes form “clusters”.
Any lymph node has afferent and efferent lymphatic vessels through which lymph flows. Foreign beneficial, including harmful, substances usually accumulate in the nodes. This is the body's filter. Lymphatic fluid passes through the lymph node, then enters the blood, and from there to the liver and kidneys.
Enlarged lymph nodes are an important symptom indicating some pathological process in the body. When affected, at the stage when it is replaced by tuberculous granuloma, the formation of caseous necrosis is a dangerous moment. In this case, the help of a surgeon is required, because the curd masses do not dissolve, but rather become increasingly denser due to the deposition of calcium salts in them. Also, another unfavorable fact is not compaction, but purulent melting of the caseous-transformed lymph node with pus.
If it breaks through, a tuberculous fistula is formed, and a closed tuberculosis process turns into an open one. If we examine caseous necrosis of a lymph node under a microscope, then in the cortical layer there is an accumulation of lymphocytes tightly adjacent to each other. Their nuclei are dark blue, surrounded by rims of cytoplasm.
In some areas of the node, a pink mass with a large number of blue lumps of different shapes and sizes is formed. The lymph node usually increases in volume.
The boundaries between the cortical and medulla layers are erased, small lesions appear, consisting of a dry crumbling mass of gray-white color similar to dry cottage cheese, around which connective tissue is formed.
The changing structure of caseous necrosis of the lymph node leads to a chronic course. The disease becomes practically incurable with the help of drugs, because the blood vessels are preserved only in the capsule of the node and therefore the penetration of fluid is excluded.
New diagnostic capabilities in the field of immunology and biochemistry make it possible to accurately determine the nature of pathological changes in the lymph node, which indicates the choice of treatment tactics.
Expert editor: Mochalov Pavel Alexandrovich| Doctor of Medical Sciences general practitioner
Education: Moscow Medical Institute named after. I. M. Sechenov, specialty - "General Medicine" in 1991, in 1993 "Occupational diseases", in 1996 "Therapy".
- Definition of secondary tuberculosis.
- Characteristics of secondary tuberculosis
- Pathological anatomy. Complications
(reinfected) develops in the body of an adult who has previously suffered a primary infection, which provided him with relative immunity, but did not protect him from the possibility of re-illness - after primary tuberculosis, which is characterized by:
- selective pulmonary localization of the process;
- contact and intracanalicular (bronchial tree, gastrointestinal tract) distribution;
- change of clinical and morphological forms.
Pathological anatomy. Highlight eight shapes secondary tuberculosis, each of which represents a further development of the previous form. Among the form-phases there are:
- acute focal;
- fibrous-focal;
- infiltrative;
- tuberculosis;
- caseous pneumonia;
- acute cavernous;
- fibrous-cavernous;
- cirrhotic.
Acute focal tuberculosis morphologically characterized by the presence in segments I and II, most often of the right lung, of one or two foci (foci of Abrikosov’s reinfection), which consist of specific endobronchitis, mesobronchitis and ossobronchitis of the extrasybridal bronchus. The process through the bronchioles spreads to the pulmonary parenchyma, as a result of which acinous or lobular cheesy bronchopneumonia develops. In the lymph nodes of the root lung, a reactive nonspecific process develops. With timely treatment, and mostly spontaneously, the process subsides, foci of caseous necrosis are encapsulated and untrified, and foci of reinfection appear.
Fibrous focal tuberculosis - the phase of the course of acute focal tuberculosis, when after a period of subsidence of the disease the process flares up again. During the healing of Abrikosov's lesions, large encapsulated and partially non-periformed lesions appear, which are given importance in the exacerbation of the process, which is characterized by the appearance of acinous, lobular foci of caseous pneumonia, which are again encapsulated, untrified. But the tendency to exacerbation remains. The process does not go beyond I and II segments, and in them, among the encysted and calcified foci of tuberculosis, there are not only foci of reinfection, but also those that represent the outcome of hematogenous cultures during the period of primary infection (Simonov foci).
Infiltrative tuberculosis- the next phase of the process, in which exudative changes around caseous foci extend beyond the boundaries of the lobule and even the segment. Perifocal inflammation prevails over caseous changes. This lesion is called Assmann-Redeker infiltrate. Perifocal inflammation can resolve, and during the healing period one or two unresolved small caseous foci remain, which are encapsulated, and the disease again takes on the character of fibrous-focal tuberculosis.
Tuberculoma arises as a unique phase in the evolution of infiltrative tuberculosis, when perifocal inflammation resolves and a focus of cheesy necrosis remains, surrounded by a capsule. Tuberculoma reaches 2-5 cm in diameter, located in segments I and II, most often on the right. Caseous pneumonia is observed with the progression of infiltrative tuberculosis, as a result of which caseous changes begin to predominate over perifocal ones. Acinous, lobular, segmental caseous-pneumonic foci are formed, which can merge into large areas of the lungs. Has a lobar character
caseous pneumonia that developed against the background of lobitis. In case of caseous pneumonia, the lung is enlarged, dense, yellow in color on the section, fibrinous deposits on the pleura.
Acute cavernous tuberculosis characterized by the rapid formation of a decay cavity, and then a cavity at the site of the outbreak - infiltration or tuberculoma. The decay cavity occurs as a result of purulent melting and liquefaction of caseous masses, which are secreted along with mycobacteria along with sputum. This creates a great danger of bronchogenic contamination of the lungs, as well as the release of mycobacteria into the environment. The cavern communicates with the lumen of the segmental bronchus.
Fibrous-cavernous tuberculosis arises from acute cavernous tuberculosis, when the process takes a chronic course. The inner layer of the cavity is pyogenic (necrotic), rich in decaying leukocytes, the middle layer is a layer of tuberculous granulation tissue; external - connective tissue. The cavity occupies one or both segments. Various foci and bronchiectasis are identified around it. The process gradually spreads in the anicocaudal direction, descending from the upper segments to the lower ones both by contact and through the bronchi.
Cirrhotic tuberculosis - a variant of the development of fibrous-cavernous tuberculosis, when in the affected lungs around the cavities there is a powerful development of connective tissue, a linear scar is formed at the site of healing of the cavity, pleural adhesions appear, the lungs are deformed, become dense and inactive, numerous broncho-ecstasies appear.
Complications. In secondary tuberculosis, the greatest number of complications is associated with the cavity: bleeding, breakthrough of the contents of the cavity into the pleural cavity, which leads to pneumothorax and purulent pleurisy (pleural empyema).
In sarcoidosis, the lungs, as a rule, are involved in the pathological process in the form of mild alveolitis, granulomatosis and fibrosis of lung tissue. With sarcoidosis, mosaic bronchial stenoses may occur (in cases where granulomas are located in the walls of the bronchi), focal atelectasis, areas of irregular emphysema, foci of calcification in granulomas, areas of pneumosclerosis and fibrinous pleurisy. Sometimes fibrinoid swelling and coagulation, but not caseous necrosis, can be detected in the center of granulomas.
Tuberculosis. Signs of pulmonary tuberculosis.
Tuberculosis- a chronic infectious disease that can affect all organs and tissues, but most often the lungs are involved.
If disease occurs during the period of infection, i.e. at the first meeting of the macroorganism and Mycobacterium tuberculosis, then this is primary tuberculosis. If the disease develops some time after the primary one, but is “genetically” associated with it, then such tuberculosis is called post-primary hematogenous. When reinfection occurs after primary tuberculosis, secondary tuberculosis occurs.
When diagnosing tuberculosis Cytological examination of sputum or bronchial secretions is important, in which acid-fast mycobacteria can be detected cytobacterioscopically.
Morphological basis of tuberculosis is a tuberculous granuloma (nodule, tubercle), in the center of which there is a focus of caseous necrosis, surrounded by epithelioid cells, giant multinucleated Pirogov-Langhans cells, lymphocytes, plasma cells, and macrophages.
For primary tuberculosis the morphological substrate is the primary tuberculosis complex: the lesion in the organ (primary focus or affect), lymphangitis and inflammation in the regional lymph nodes (lymphadenitis). The primary affect in the lungs during aerogenic infection occurs, as a rule, subpleurally in the 3rd, 8th, 9th, 10th segments of the right lung. The focus of exudative inflammation quickly undergoes necrosis with the formation of caseous pneumonia with perifocal inflammation, involving lung tissue from the alveoli to an entire segment, in rare cases - an entire lobe, almost always with an area of fibrinous or serous-fibrinous pleurisy. There are three variants of the course: 1) attenuation of primary tuberculosis and healing of the primary affect; 2) progression of primary tuberculosis with generalization of the process; 3) chronic course (chronically current primary tuberculosis).
When primary tuberculosis subsides at the site of the primary focus, a petrified, and subsequently ossified, Gon focus appears.
Generalization of the process can occur by hematogenous or lymphogenous route, due to the growth of the primary focus with the appearance of lobar caseous pneumonia and/or primary pulmonary cavity; taking a chronic course, primary pulmonary consumption develops with the presence of caseous bronchadenitis, which distinguishes it from secondary fibrous-cavernous tuberculosis.
In weakened patients A mixed form of progression may occur - simultaneous growth of the primary lesion, caseous bronchadenitis and numerous tuberculous screenings in other organs. With long-term steroid therapy, drug-induced tuberculosis occurs as a manifestation of endogenous infection. The chronic course of primary tuberculosis is characterized by alternating outbreaks and subsidence with damage to the lymph nodes (adenogenic form). In hematogenous (post-primary) tuberculosis, three types are distinguished: generalized hematogenous; hematogenous tuberculosis with predominant damage to the lungs; hematogenous with predominantly extrapulmonary damage. In the second form of hematogenous tuberculosis, acute or chronic miliary tuberculosis (or hematogenously disseminated pulmonary tuberculosis) develops, which occurs only in adults.
For such tuberculosis Characterized by corticopleural lesions in the lungs, productive tissue reaction, pneumosclerosis, emphysema, cor pulmonale and extrapulmonary focus of tuberculosis.
Secondary (rV infectious) tuberculosis occurs in adults who have had a primary one. This type of tuberculosis is characterized by pulmonary localization, contact and canalicular (along the bronchial tree) spread, and a change in clinical and morphological forms, which are also phases of tuberculosis. There are eight forms of secondary tuberculosis: focal, fibrous-focal, infiltrative, tuberculoma, caseous pneumonia, acute cavernous, fibrous-cavernous, and cirrhotic. In acute focal tuberculosis, in the 1st-2nd segments, as a rule, of the right lung, one or two foci of Abrikosov reinfection are found. The initial phenomena of secondary tuberculosis are represented by specific endo-, meso- and panbronchitis of the intralobular bronchus with lobular cheesy bronchopneumonia with the formation of epithelioid cell granulomas along the periphery.
With timely treatment these foci are encapsulated and petrified; ossification never occurs. Such foci of reinfection are called Aschoff-Pull foci. With a new outbreak of infection, caseous pneumonia occurs around these foci, which is subsequently encapsulated without going beyond the 1st-2nd segments. This phase is called fibrous-focal tuberculosis. Infiltrative tuberculosis develops with the progression of acute focal tuberculosis or exacerbation of fibrous-focal tuberculosis. In this case, exudation can extend beyond the lobule and even the segment. When a lobule is captured, one should speak of lobita. Perifocal inflammation prevails over caseous changes.
Tuberculoma- a peculiar form of evolution of infiltrative tuberculosis (a focus of cheesy necrosis in a capsule with a diameter of 2-5 cm) in the 1st-2nd segments, most often the right lung. Tuberculoma should first of all be differentiated from peripheral lung cancer.
Caseous pneumonia occurs with the progression of infiltrative or in the terminal period of any other form of tuberculosis, while necrosis predominates over perifocal changes. Prevalence - from acinous lesion - I hectare to the capture of the entire lobe.
Acute cavernous tuberculosis characterized by the rapid formation of a decay cavity and cavity at the site of infiltration or tuberculoma. The appearance of a cavity is fraught with bronchogenic contamination of the lungs. Cavities in the 1st and 2nd segments are usually oval or round in shape.
Fibrous-cavernous tuberculosis(chronic pulmonary consumption) occurs in cases where cavernous tuberculosis takes a chronic course. The process is more often expressed in one right lung and gradually descends to the lower sections by contact or intracanalicularly and can move to the other lung. Older changes are localized in the upper sections, and foci of caseous pneumonia are localized in the lower sections.
Cirrhotic tuberculosis- a variant of fibrous-cavernous with the growth of fibrous tissue around the caverns. In places where the cavities have healed, linear scars remain, deformation of the lung tissue occurs, pleural adhesions and a focus of hyalinosis develop. Numerous bronchiectasis appears.
Complications of tuberculosis numerous. In primary cases, meningitis, pleurisy, pericarditis, and peritonitis often develop. Secondary cases are characterized by the development of bleeding from cavities, breakthrough of their contents into the pleural cavity with the development of pneumothorax and pleural empyema.
#Question 87
Cellular composition of a specific granuloma in syphilis:
#Options for question 1
No. 1. macrophages, lymphocytes, plasma cells, Virchow cells
No. 2. lymphocytes, epithelial cells, plasma cells, Pirogov-Langhans cells
No. 3. plasma cells, lymphoid cells, Mikulicz cells
No. 4. lymphoid cells
No. 5. plasma cells
#Question 88
#Options for question 2
No. 1. pulmonary affect, lymphangitis, lymphadenitis
No. 2. focus of caseous necrosis
No. 3. miliary tubercles
No. 4. cavity
No. 5. abscess
#Question 89
Primary tuberculosis develops when:
#Options for question 3
No. 1. repeated reinfection with the pathogen
No. 2. initial contact of the body with the pathogen
No. 3. generalization of the process from existing tuberculosis foci
No. 4. healing of tuberculous lymphadenitis
No. 5. everything is true
#Question 90
The outbreak of Gon is:
#Options for question 4
No. 1. healing of the primary lesion
No. 2. fibrous scarring cavity
No. 3. infiltrate in the lung
No. 4. fibrous focal tuberculosis
No. 5. cavity
#Question 91
Paraspecific reactions in primary tuberculosis include:
#Options for question 5
No. 1. cavity in the lung
No. 2. infiltrate in the lung
No. 3. Poncet syndrome
No. 4. lymphadenitis
No. 5. lobar pneumonia
#Question 92
Hematogenous tuberculosis is:
#Options for question 6
No. 1. infection at the first meeting with the infection
No. 2. reactivation of old healed lesions in combination with superinfection
No. 3. disease after treatment of primary tuberculosis
No. 4. generalization of existing infection
No. 5. everything is true
#Question 93
The morphological substrate of primary tuberculosis is:
#Options for question 7
No. 1. Primary tuberculosis complex
No. 2. Cavity
No. 3. Miliary tubercle
No. 4. Focus of caseous necrosis
No. 5. Fibrous lymphangitis
#Question 94
The morphological manifestation of the cure of primary tuberculosis is considered to be:
#Options for question 8
No. 1. Diffuse pneumosclerosis
No. 2. Emphysema
No. 3. Presence of two petrificates in the lung and lymph node
No. 4. Miliary tubercle
No. 5. Carnification
#Question 95
One of the variants of the complicated course of primary tuberculosis is:
#Options for question 9
No. 1. The occurrence of atelectasis
No. 2. Hematogenous generalization of the process
No. 3. Presence of emphysema
No. 4. Petrification in the lungs
No. 5. Ossification
#Question 96
Hematogenous tuberculosis with predominant damage to the lungs is characterized by:
#Options for question 10
No. 1. Presence of an abscess
No. 2. Cavity formation
No. 3. The appearance of miliary tubercles in the liver and spleen
No. 4. Development of caseous pneumonia
No. 5. The appearance of miliary tubercles in the lungs
#Question 97
Characteristics of secondary tuberculosis are:
#Options for question 11
No. 1. Hematogenous generalization of the process
No. 2. Lymphogenic generalization
No. 3. Contact and intracanalicular path of propagation of the process
No. 4. Lymphoglandular pathway of generalization of the process
No. 5. Lymphohematogenous path of spread of the process
#Question 98
Focal tuberculosis is:
#Options for question 12
No. 1. Area of caseous necrosis in the lungs without clear boundaries
No. 2. Cavity
No. 3. Miliary tubercle
No. 4. Encapsulated focus of caseous necrosis less than 1 cm.
No. 5. The focus of caseous necrosis is more than 1 cm.
No. 6. Pneumocirrhosis
#Question 99
In fibrous-cavernous tuberculosis, morphological changes are characterized by:
#Options for question 13
No. 1. The presence of a cavity, the wall of which has a three-layer structure
No. 2. Presence of an abscess
No. 3. Development of diffuse fibrosis in the lung
No. 4. The presence of a cavity, the wall of which has a two-layer structure
No. 5. Development of caseous pneumonia
#Question 100
Fibrous-cavernous tuberculosis is a manifestation of tuberculosis:
#Options for question 14
No. 1. Hematogenous
No. 2. Primary
No. 3. Senile
No. 4. Secondary
No. 5. Congenital
#Question 101
Signs of secondary tuberculosis include all except:
#Options for question 15
No. 1. lesions of the apex of the lung
No. 2. bronchogenic generalization
No. 3. caseous lymphadenitis
No. 4. "spectacle" cavities in the lungs
No. 5. the presence of Abrikosov foci
#Question 102
Forms of secondary tuberculosis include:
#Options for question 16
No. 1. infiltrative
No. 2. cirrhotic
No. 3. focal
No. 4. that's right
No. 5. Everything is wrong
#Question 103
Pulmonary tuberculoma can be:
#Options for question 17
No. 1. multiple
No. 2. single.
No. 3. conglomerate.
No. 4. that's right.
No. 5. 1 and 2 are correct
#Question 104
Acute cavernous pulmonary tuberculosis can be complicated by:
#Options for question 18
No. 1. amyloidosis
No. 2. bleeding
No. 3. malignancy
No. 4. that's right
No. 5. everything is wrong
#Question 105
The cause of death in cirrhotic pulmonary tuberculosis can be:
#Options for question 19
No. 1. azotemic uremia
No. 2. tuberculous sepsis
No. 4. that's right
No. 5. 1 and 3 are correct
#Question 106
Fibrous-cavernous pulmonary tuberculosis develops as a result of:
#Options for question 20
No. 1. lung cancer
No. 2. chronic lung abscess
No. 3. tuberculoma of the lung
No. 4. miliary pulmonary tuberculosis
No. 5. everything is wrong
General issues of tumor growth
#Question 107
Cytocarcinogenesis includes:
#Options for question 1
No. 1. proto-oncogene activation
No. 2. interaction of oncogene with promoter
No. 3. emergence of new properties in daughter cells
No. 4. anti-oncogene inhibition
No. 5. all of the above
#Question 108
Histocarcinogenesis includes:
#Options for question 2
No. 1. replacement of normal tissue cells with a clone of malignant elements
No. 2. selection and proliferation of tumor cells
No. 3. infiltrative growth of tumor tissue
No. 4. that's right
No. 5. 1 and 3 are correct
#Question 109
Morphocarcinogenesis includes:
#Options for question 3
No. 1. tumor growth in an organ or system
No. 2. tumor metastasis
No. 3. tumor growth into surrounding tissues
No. 4. that's right
No. 5. 1 and 3 are correct
#Question 110
Oncogenesis includes:
#Options for question 4
No. 1. cytocarcinogenesis with the appearance of a clone of tumor cells
No. 2. histocarcinogenesis with immune reaction
No. 3. morphocarcinogenesis with clinical and laboratory manifestations
No. 4. that's right
No. 5. 2 and 3 are correct
#Question 111
Signs of expansive tumor growth include:
#Options for question 5
No. 1. the tumor grows, pushing away neighboring tissues
No. 2. A pseudocapsule forms around the tumor
No. 3. the tumor looks like a node
No. 4. that's right
No. 5. 2 and 3 are correct
#Question 112
A sign of tumor progression is:
#Options for question 6
No. 1. decrease in the degree of tumor differentiation
No. 2. increase in tumor size
No. 3. extensive metastasis
No. 4. necrosis, hemorrhages in the tumor
No. 5. severe paraneoplastic syndrome
#Question 113
The predominant route of metastasis of sarcomas:
#Options for question 7
No. 1. lymphogenous
No. 2. hematogenous
No. 3. perineural
No. 4. all of the above
No. 5. only 1 and 3
#Question 114
The most characteristic way of metastasis of malignant tumors from the epithelium:
#Options for question 8
No. 1. hematogenous
No. 2. lymphogenous
No. 3. implantation
No. 4. all of the above
No. 5. only 1 and 2
#Question 115
The etiology of tumors is explained by theories:
#Options for question 9
No. 1. viral-genetic
No. 2. physical and chemical
No. 3. dysontogenetic
No. 4. polyetiological
No. 5. molecular genetic
#Question 116
Clinical supervision is required:
#Options for question 10
No. 1. 1st degree dysplasia
No. 2. 2nd degree dysplasia
No. 3. 3rd degree dysplasia
No. 4. that's right
No. 5. only 1 and 2
#Question 117
Cellular atypia is characterized by:
#Options for question 11
No. 1. differences in cell shape and size
No. 2. nuclear hyperchromia
No. 3. increase in nuclear-cytoplasmic ratio
No. 4. that's right
No. 5. only 2 and 3
#Question 118
Tissue atypia is characterized by:
#Options for question 12
No. 1. disruption of the order of the elements that make up the fabric
No. 2. infiltration of surrounding tissue cells
No. 3. change in parenchymal-stromal ratio
No. 4. 1 and 3 are correct
No. 5. 1 and 2 are correct
#Question 119
Actually precancer is:
#Options for question 13
No. 1. metaplasia
No. 2. dysregeneration
No. 3. dysplasia
No. 4. carcinoma in situ
No. 5. dystrophy
#Question 120
Benign tumors are characterized by:
#Options for question 14
No. 1. structure of differentiated cells
No. 2. expansive growth
No. 3. no relapses after removal
No. 4. absence of metastases
No. 5. that's right
#Question 121
Malignant tumors are characterized by:
#Options for question 15
No. 1. severe cell anaplasia
No. 2. infiltrating growth
No. 3. the presence of metastases and relapses after tumor removal
No. 4. general effect on the body
No. 5. that's right
#Question 122
The main histological signs of therapeutic pathomorphosis of tumors:
#Options for question 16
No. 1. degeneration of tumor cells
No. 2. tumor cell necrosis
No. 3. fibrosis
No. 4. that's right
No. 5. 2 and 3 are correct
#Question 123
Morphological forms of tumor atypia are all except:
#Options for question 17
No. 1. cellular
No. 2. tissue
No. 3. antigenic
No. 4. pathologies of ultrastructures
No. 5. invasive growth
#Question 124
The International Classification of Neoplasms is based on the following feature:
#Options for question 18
No. 1. tumor localization
No. 2. histogenetic principle
No. 3. biological properties of the tumor
No. 4. all of the above
No. 5. only 1 and 2
#Question 125
The international TNM classification of the stage of the tumor process is based on the assessment of:
#Options for question 19
No. 1. degree of tumor invasion into surrounding tissues
No. 2. tumor size
No. 3. the presence of metastases in the lymph nodes
No. 4. presence of distant metastases
No. 5. everything is true
#Question 126
The following molecular genetic disorders lead to the formation of a tumor clone, except:
#Options for question 20
No. 1. blockade of apoptosis processes
No. 2. overexpression of wild p53
No. 3. disorders of the intracellular caspase pathway for proteolysis induction
No. 4. appearance of “mutant” p53
No. 5. overexpression of the bcl-2 gene
Lecture 24
TUBERCULOSIS
Tuberculosis- a chronic infectious disease that can affect all human organs and tissues, but most often the lungs. A number of features distinguish tuberculosis from other infections. First of all, this is the ubiquity (from the Latin ubique - everywhere) of tuberculosis in epidemiological, clinical and morphological terms. The second is the two-faced nature of tuberculosis - depending on the relationship between immunity and allergies, it
can be a manifestation of both infected ™ and disease. Therefore, it is impossible to establish an incubation period for tuberculosis. Third, there is a pronounced polymorphism of clinical and morphological manifestations of tuberculosis and its chronic wave-like course with alternating outbreaks and remissions.
Epidemiology. The incidence of tuberculosis in Russia after a sharp decline in 1950-1960. has increased, especially in the last five years: if in 1991 the incidence rate of tuberculosis was 34.0 per 100 thousand population, then in 1993 it increased to 43.0. The mortality rate from tuberculosis also increased: in 1990 it was 8.0 per 100 thousand population, in 1993 it increased to 12.6. The increase in the incidence of tuberculosis and mortality from it in Russia coincided with a similar trend in the states of the former USSR, as well as in a number of countries in Eastern and Western Europe.
The new epidemiological situation has crossed out the pathomorphosis of tuberculosis that emerged in the 60s - exudative-necrotic processes, infiltrative forms of tuberculosis with massive decay and giant cavities, caseous pneumonia, and pleurisy again began to dominate.
The reasons for the increase in morbidity and mortality from tuberculosis are considered to be a deterioration in the standard of living of the population (low-protein diet, stress, wars), a sharp increase in the migration of large groups of the population, a decrease in the level of anti-tuberculosis measures, an increase in the number of cases of tuberculosis with the development of severe exudative-necrotic forms of the disease caused by drug-resistant mycobacteria. All these reasons led to the loss of “controllability” of tuberculosis in conditions of a large reservoir of tuberculosis infection and high infection rate of the population. Therefore, there is reason to talk about an impending tuberculosis epidemic at the beginning of the new century.
Etiology. Tuberculosis is caused by the acid-fast Mycobacterium tuberculosis, discovered by Koch (1882). There are four types of mycobacteria: human, bovine, avian and cold-blooded. For humans, the first two types are pathogenic. Mycobacterium tuberculosis is characterized by optimal growth under conditions of high tissue oxygen saturation, which determines frequent lung damage. At the same time, the growth of the bacillus is possible in the absence of oxygen (facultative anaerobe), which is associated with the manifestation of the biological properties of mycobacteria in conditions of even pronounced tissue bradytrophy (for example, in fibrous tissue replacing tuberculosis foci). Mycobacterium tuberculosis is characterized by extremely pronounced variability - the existence of branched, cocci-shaped, L-forms, which under
under the influence of chemotherapy drugs they can lose their cell wall and persist in the body for a long time.
Pathogenesis. Penetration of mycobacteria into the body occurs through aerogenous or alimentary routes and leads to infection and the appearance of a latent focus of tuberculosis, which determines the formation of infectious immunity. In conditions of sensitization of the body, an outbreak of the process occurs with an exudative tissue reaction and caseous necrosis. The replacement of hyperergy by immunity leads to the appearance of a productive tissue reaction, the formation of a characteristic tuberculous granuloma, and tissue fibrosis. A constant change in immunological reactions (hyperergy-immunity-hyperergy) is a characteristic feature of the tuberculosis process, an undulating course of the disease with alternating outbreaks and remissions.
The clinical and morphological features of the disease are determined by the temporary factor of the “separation” of the disease from the period of infection. If the disease develops during the period of infection, i.e. at the first meeting of the body with an infectious agent, they speak of primary tuberculosis. In cases where the disease occurs a significant period after primary tuberculosis, but is “genetically” associated with it, tuberculosis is called post-primary hematogenous. When reinfected a considerable time after undergoing primary tuberculosis, secondary tuberculosis develops under conditions of relative immunity. However, the theory of reinfection (exogenous theory), defended by A.I. Abrikosov, is not shared by everyone. Proponents of the endogenous theory (V.G. Shtefko, A.I. Strukov) associate the development of secondary tuberculosis with hematogenous foci - screenings (Simon foci) of primary tuberculosis. Endogenists consider primary, hematogenous and secondary tuberculosis as stages in the development of a single disease, caused by a temporary change in the body’s response to an infectious agent, a change in its immunobiological status.
Classification. There are three main types of pathogenetic and clinical and morphological manifestations of tuberculosis: primary tuberculosis, hematogenous tuberculosis and secondary tuberculosis.
PRIMARY TUBERCULOSIS
Primary tuberculosis characterized by the development of the disease during the period of infection; sensitization and allergies, immediate hypersensitivity reactions; the predominance of exudative-necrotic changes; tendency to hematogenous and lymphogenous (lymphoglandular) generalization;
paraspecific reactions in the form of vasculitis, arthritis, serositis, etc.
Mostly children are affected, but nowadays primary tuberculosis has become more common in adolescents and adults.
Pathological anatomy. The morphological expression of primary tuberculosis is the primary tuberculosis complex (Scheme 47). It consists of three components: the lesion in the organ (primary focus, or afeffect), tuberculous inflammation of the draining lymphatic vessels (lymphangitis) and tuberculous inflammation in regional lymph nodes (lymphadenitis).
With aerogenic infection in the lungs, the primary affect occurs subpleurally in the most well-aerated segments, most often of the right lung - III, VIII, IX, X (especially often in III segment). The primary affect is represented by a focus of exudative inflammation, and the exudate quickly undergoes necrosis. A focus of caseous pneumonia is formed, surrounded by a zone of perifocal inflammation. The dimensions of the affect are different: from the alveolitis to the segment and, in very rare cases, to the lobe. The involvement of the pleura in the inflammatory process is constantly observed - fibrinous or serous-fibrinous pleurisy.
Tuberculous lymphangitis develops very quickly. It is represented by lymphostasis and tuberculous tubercles in the perivascular edematous tissue.
Subsequently, the inflammatory process moves to the regional bronchopulmonary, bronchial and bifurcation lymph nodes, in which a specific inflammatory process develops, and caseous necrosis quickly occurs. Total caseous tuberculous lymphadenitis occurs. Changes in regional lymph nodes are always more significant compared to the primary affect.
With alimentary infection, the primary tuberculosis complex develops in the intestine and also consists of three components: in the lymphoid tissue of the lower part of the jejunum or cecum, a primary affect in the form of an ulcer is formed, tuberculous lymphangitis is associated with caseous lymphadenitis of the lymph nodes regional to the primary affect. A primary tuberculous affect is possible in the tonsil with lymphangitis and caseous necrosis of the lymph nodes of the neck or in the skin (in the form of an ulcer with lymphangitis and regional caseous lymphadenitis).
There are three variants of the course of primary tuberculosis: 1) attenuation of primary tuberculosis and healing of foci of the primary complex; 2) progression of primary tuberculosis with generalization of the process; 3) chronic course (chronically current primary tuberculosis).
The attenuation of primary tuberculosis and the healing of foci of the primary complex begin in the primary pulmonary focus. The exudative tissue reaction is replaced by a productive one; tuberculous granulomas undergo fibrosis, and caseous masses undergo petrification, and subsequently ossification. At the site of the primary affect, a healed primary focus is formed, which, after the name of the Czech pathologist who described it, is called Ghon's focus.
At the site of tuberculous lymphangitis, as a result of fibrosis of tuberculous granulomas, a fibrous cord is formed. Healing in the lymph nodes occurs in the same way as in the pulmonary focus - foci of caseosis dehydrate, calcify and ossify. However, due to the extent of the lesion in the lymph nodes, healing is slower than in the pulmonary lesion.
During healing, a scar forms in the intestine at the site of the primary ulcer, and petrification forms in the lymph nodes; their ossification proceeds very slowly.
The progression of primary tuberculosis with generalization of the process manifests itself in four forms: hematogenous, lymphogenous, growth of primary affect and mixed.
Hematogenous form of progression(process generalization). In primary tuberculosis, it develops due to the early entry of mycobacteria into the blood (dissemination) from the primary affect or caseous lymph nodes. Mycobacteria settle in various organs and cause the formation of tubercles in them ranging in size from miliary (millet-like) - miliary tuberculosis - to large foci. In this regard, there is a distinction miliary And macrofocal form hematogenous generalization. Particularly dangerous is the eruption of miliary tuberculous tubercles in the soft meninges with the development of tuberculous leptomeningitis. With hematogenous generalization, single screenings are possible in various organs, including at the apex of the lungs (Simon's foci), which, many years after the primary infection has subsided, give rise to the tuberculosis process.
Lymphogenic form of progression(generalization of the process) in primary tuberculosis is manifested by the involvement in the process of specific inflammation of the bronchial, bifurcation, peritracheal, supra- and subclavian, cervical and other lymph nodes. Of particular importance in the clinic is tuberculous bronchoadenitis. Obstruction of the bronchus is possible when the contents of a caseous lymph node rupture into the bronchus (adenobronchial fistulas), compression of the bronchus by enlarged lymph nodes, which leads to the development of foci of atelectasis, pneumonia, and bronchiectasis.
In primary intestinal tuberculosis, lymphogenous (lymphoglandular) generalization leads to an increase in all groups of mesenteric lymph nodes. Developing tuberculousmesadenitis, which can dominate the clinical picture of the disease.
Growth of primary affect. This is the most severe form of progression of primary tuberculosis. With it, caseous necrosis of the zone of perifocal inflammation occurs. An increase in the area of caseosis can lead to lobar caseous stumpmonies. This is the most severe form of primary tuberculosis, quickly ending in the death of the patient (“fleeting consumption”). When the focus of lobular or segmental caseous pneumonia melts, primary pulmonary cavity. The process takes a chronic course and develops primarypulmonary consumption, resembling secondary fibrous-cavernous tuberculosis, but differing from it by the presence of caseous bronchoadenitis.
The primary intestinal affect grows due to the enlargement of the tuberculous ulcer, usually in the area of the cecum. Limited tuberculous peritonitis, adhesions, and packets of caseous-changed ileocecal lymph nodes appear. A dense conglomerate of tissue is formed, which is sometimes mistaken for a tumor (tumor-like primary intestinal tuberculosis). Often the process takes a chronic course.
Mixed form of progression. In primary tuberculosis, it is observed in case of weakening of the body after acute infections, such as measles, vitamin deficiencies, fasting, etc. In such cases, a large primary affect is detected, caseous bronchoadenitis, often complicated by the melting of necrotic masses and the formation of fistulas. Numerous tuberculous rashes are visible in both lungs and in all organs.
An exacerbation of tuberculosis is possible as a result of the activation of a “dormant” infection in healed petrified lymph nodes with long-term use of steroid hormones and immunosuppressants that reduce the body’s resistance. Massive tuberculous bronchoadenitis develops with lymphogenous and hematogenous generalization and a slight cellular reaction. This so called medicinevenous (steroid) tuberculosis considered as an expression of endogenous infection.
The chronic course (chronically ongoing primary tuberculosis) occurs primarily in those cases when, with a healed primary affect in the lymph glandular component of the primary complex, the process progresses, capturing more and more new groups of lymphatics.
ical nodes. The disease takes a chronic course with alternating outbreaks and subsidence. So adenogenic formstuberculosis special attention is paid because caseous lymph nodes are considered as “reservoirs of infections”, which can become a source of not only progression, but also the beginning of new forms of tuberculosis. Among them are renal tuberculosis during the transition of the process from the para-aortic and mesenteric lymph nodes, contamination of the lungs with adenobronchial fistulas, damage to the spine during the transition of the process from the paravertebral lymph nodes, etc.
In the chronic course of primary tuberculosis, sensitization of the body occurs - its sensitivity to all kinds of nonspecific influences increases. Increased reactivity of the body is clinically detected by skin tuberculin tests and the appearance in tissues and organs para-specific changes(A.I. Strukov), by which they mean various mesenchymal cellular reactions. Such reactions in the joints, occurring as immediate or delayed hypersensitivity, give chronic primary tuberculosis a great resemblance to rheumatism and are described under the name rheumatism Ponce.
Chronic primary tuberculosis is also spoken of when a primary pulmonary cavity forms and develops primary pulmonary consumption.
HEMATOGENIC TUBERCULOSIS
Hematogenous tuberculosis- this is post-primary tuberculosis. It occurs in people who have clinically recovered from primary tuberculosis, but retain increased sensitivity to tuberculin and have developed significant immunity to Mycobacterium tuberculosis.
There is an exacerbation of the screening foci of primary tuberculosis or not completely healed foci in the lymph nodes under the influence of any unfavorable factors in the presence of increased reactivity (increased sensitivity to tuberculin against the background of developed immunity to mycobacteria). Therefore, in hematogenous tuberculosis, a productive tissue reaction (granuloma) predominates, and there is a tendency to hematogenous generalization, which leads to damage to various organs and tissues.
There are three types of hematogenous tuberculosis (Scheme 48): 1) generalized hematogenous tuberculosis; 2) hematogenous tuberculosis with predominant damage to the lungs; 3) hematogenous tuberculosis with predominant extrapulmonary lesions.
Generalized hematogenous tuberculosis, which is now extremely rare, is the most severe form of the disease with a uniform eruption of tuberculous tubercles and foci in many organs. In cases where necrotic lesions are formed in all organs without a proliferative or with a mild exudative reaction, they speak of the sharpest tuberculous sepsis(in the past - Landusi typhobacillosis); if small miliary productive tubercles appear in all organs, then they talk about acute general miliary tuberculosis(in the latter case, tuberculous meningitis often develops). It is also possible acute general macrofocal tuberculosis, which usually occurs in debilitated patients and is characterized by the formation of large tuberculous foci in various organs.
Treatment of tuberculosis patients with effective chemotherapy drugs led to a sharp decrease in the number of acute forms of generalized hematogenous tuberculosis, the transfer of these forms into chronic general miliary tuberculosis, often with predominant localization in the lungs. In such cases, it differs little from chronic miliary pulmonary tuberculosis. Tuberculous meningitis has undergone the same changes and is now often a "chronic isolated disease".
Hematogenous tuberculosis with a predominant lesion of the lungs is characterized by a predominance of rashes in them, while in other organs they are absent or single. If there are many small miliary tubercles in the lungs, they speak of miliary tubercleze lungs, which can be both acute and chronic.
Acute miliary tuberculosis is rare, often ending in meningitis. At chronic miliary tuberkulese, when the miliary tubercles are scarred, emphysema of the lungs, hypertrophy of the right ventricle (cor pulmonale) develops. Chronic macrofocal, or hematogenously disseminated, pulmonary tuberculosis occurs only in adults. It is characterized by predominantly corticopleural localization of foci in both lungs and a productive tissue reaction, the development of reticular pneumosclerosis, emphysema, cor pulmonale, and the presence of an extrapulmonary tuberculosis focus.
Hematogenous tuberculosis with predominant extrapulmonary lesions arises from screening foci introduced into one or another organ by the hematogenous route during the period of primary infection. Skeletal bones are predominantly affected (osteoarticular tuberculosis) And
genitourinary system (tuberculosis of the kidneys, genitals), skin and other organs. Distinguish focal And destructive form, which may have acute or chronic flow. Tuberculosis forms become phases of its development (see Scheme 48).
SECONDARY TUBERCULOSIS
Secondary, reinfective, tuberculosis develops, as a rule, in adults who have previously had a primary infection. It is characterized by selectively pulmonary localization of the process; contact and intracanalicular (bronchial tree, gastrointestinal tract) spread; change of clinical and morphological forms, which are phases of the tuberculosis process in the lungs.
There are eight forms of secondary tuberculosis, each of which represents a further development of the previous form-phase: 1) acute focal; 2) fibrous-focal; 3) infiltrative; 4) tuberculoma; 5) caseous pneumonia; 6) acute cavernous; 7) fibrous-cavernous; 8) cirrhotic (scheme 49).
Acute focal tuberculosis is characterized by the presence of one or two foci in segments I and II of the right (less often left) lung. They got the name foci of reinfectionAbrikosova. A.I. Abrikosov (1904) was the first to show that the initial manifestations of secondary tuberculosis are represented by specific endobronchitis, mesobronchitis and panbronchitis of the intralobular bronchus. Subsequently, acinous or lobular cheesy bronchopneumonia develops, around which epithelioid cell granulomas quickly form. With timely treatment, often spontaneously, foci of caseous necrosis are encapsulated and petrified, but never undergo ossification - they are formed Ashoff-Pulevsky eyesgi reinfection(described by German scientists Aschoff and Pu-lem).
Fibrous-focal tuberculosis represents that phase of the course of acute focal tuberculosis when, after healing of the Abrikosov foci, the process flares up again. The source of exacerbation are Ashoff-Poule foci. Around them arise acinous, lobular foci of caseous stumpsmonies, which are then encapsulated and partially shrified. However, the tendency to exacerbation remains. Simonov's lesions - dropouts during the period of primary infection - can also be a source of exacerbation of the process. The process remains one-sided and does not go beyond segments I and II.
Infiltrative tuberculosis develops with the progression of acute focal or exacerbation of fibro-
Scheme49. Forms and phases of secondary pulmonary tuberculosis
rose-focal tuberculosis, and exudative changes around caseous foci extend beyond the boundaries of the lobule and even the segment. Perifocal inflammation predominates over caseous changes, which may be minor. Such a focus is called Assmann's infiltrate lesion-Redeker(named after the scientists who first described its x-ray picture). When perifocal inflammation covers the entire lobe, lobitis is said to be a special form of infiltrative tuberculosis. With the elimination of nonspecific perifocal inflammation and encapsulation of the remaining small foci of caseous necrosis, the disease again acquires the character of fibrous-focal tuberculosis.Tuberculoma is a form of secondary tuberculosis that arises as a peculiar form of the evolution of infiltrative tuberculosis, when perifocal inflammation disappears and a focus of curdled necrosis remains, surrounded by a capsule. Tuberculoma is 2-5 cm in diameter, usually located in segment I or II, usually on the right. Often, during X-ray examination, it is mistaken for peripheral lung cancer.
Caseous pneumonia develops with the progression of infiltrative tuberculosis, when caseous changes begin to predominate over perifocal ones. Acinous, lobular, segmental caseous-pneumonic foci are formed, which, when merging, can occupy the entire lobe. Caseous pneumonia, which developed against the background of lobitis, also has a lobar character. Caseous pneumonia can occur in the terminal period of any form of tuberculosis, more often in weakened patients.
Acute cavity about i and s and tuberculosis is characterized by the rapid formation of a decay cavity, and then a cavity at the site of the infiltrate focus or tuberculoma. The decay cavity arises as a result of purulent melting and liquefaction of caseous masses, which are secreted along with mycobacteria along with sputum. This creates a great danger of bronchogenic contamination of the lungs. The cavity is usually localized in segment I or II, has an oval or round shape, and communicates with the lumen of the segmental bronchus. The inner layer of the cavity is represented by caseous masses.
Fibrous-cavernous tuberculosis, or chronic pulmonary consumption, occurs in cases where acute cavernous tuberculosis takes a chronic course. The inner surface of the cavity is covered with caseous masses, uneven, with beams crossing the cavity, represented by obliterated bronchi or thrombosed vessels. The inner layer of caseous necrosis is delimited by tuberculous granulations, forming coarse fibrous connective tissue surrounding the cavity in the form of a capsule. The changes are more pronounced in one, most often in the right, lung. The process gradually spreads in the apico-caudal direction, descending from the upper segments to the lower ones both by contact and through the bronchi. Therefore, the oldest changes in fibrous-cavernous tuberculosis are observed in the upper parts of the lungs, in the form of foci of caseous pneumonia and acute cavities - in the lower parts. Over time, the process passes through the bronchi to the opposite lung, where acinar and lobular tuberculous foci appear. When they disintegrate, the formation of cavities and further bronchogenic spread of the process are possible.
Cirrhotic tuberculosis is considered as a variant of the development of fibrous-cavernous tuberculosis, when a massive proliferation of connective tissue occurs in the affected lungs around the caverns, a linear scar forms in place of the healed cavity, pleural adhesions appear, the lungs are deformed, and numerous bronchiectasis appears.
In secondary pulmonary tuberculosis, due to the fact that the infection spreads, as a rule, intracanalicular(bronchial tree, gastrointestinal tract) or contactfully, Specific damage to the bronchi, trachea, larynx, oral cavity, and intestines may develop. Hematogenous spread is rare; it is possible in the terminal period of the disease when the body's defenses decrease.
Complications tuberculosis are diverse. As already mentioned, with primary tuberculosis, tuberculous meningitis, pleurisy, pericarditis, and peritonitis can develop. With bone tuberculosis, sequestration, deformation, soft tissue damage, abscesses and fistulas are observed. In secondary tuberculosis, the greatest number of complications is caused by the cavity: bleeding, breakthrough of the contents of the cavity into the pleural cavity, which leads to pneumothorax and purulent pleurisy (pleural empyema). Due to the long course of the disease, any form of tuberculosis, especially fibrinous-cavernous, can be complicated by amyloidosis (AA amyloidosis).
Many of these complications cause death in patients with tuberculosis.
