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Secondary tuberculosis



SECONDARY TUBERCULOSIS (Fig. 110-183) - (reinfectional, post-primary) develops in the lungs of an adult who has previously had a primary infection. The main pathway of progression is intracanalicular (bronchi, intestine), less commonly contact and hematogenous. In the pathogenesis of pulmonary foci of secondary T, preference is given to the endogenous theory of their origin: reactivation of foci for eliminating the period of primary infection during the reversal of attenuated persistent MW in pathogenic forms

FOCUS tuberculosis (Fig. 111-120) of the lungs is characterized by the presence of single or multiple foci in the cortical regions of the lungs, with a diameter of 1 cm and a total length of pulmonary changes of up to 2 segments, depending on the process phase, soft-focal T is released - the focus of caseous pneumonia (the Abrikosov infection center ) and fibrous focal T (Aschoff focus - Bullet). Focal T may be an independent form of the disease or a healing option for infiltrative fibrous-cavernous and hematogenous pulmonary tuberculosis.

INFILTRATIVE tuberculosis (Fig. 121) is a focus of tuberculous pneumonia with caseification in the center, the so-called early subclavian Assman-Redeker infiltration. Focus caseification is limited to a wide area of ​​perifocal serous exudative inflammation. Infiltrative T occurs as a result of the progression of an early focal process or reactivation of old tuberculous changes. Clinical and radiological variants of infiltrative T: cloud-like, round, lobit, pericyssuritis, lobular variant.

Flow:

• progressive, undulating, with destruction and transition to caseous pneumonia or cavernous tuberculosis and

• involutive, with the resorption of inflammatory foci, their encapsulation, the formation of a tubouclema, the fibrotization of the cirrhosis of a segment or lung lobe.

TUBERKULEMA (fig. 122-137) - a foci of encapsulated caseosis, more than 1 cm in size, the result of involution of infiltrative tuberculosis or filling, "blocking" a cavity. Types of tuberculosis:

• by structure - homogeneous (caseoma), layered, conglomerate;

• by quantity - solitary, multiple;

• in size - small, medium, large, giant (1-2 cm, 2-4 cm, 4-6 cm, more than 6 cm in diameter, respectively).

Differential diagnosis with tumors, especially lung cancer, malformations, mycetoma.

TUBERCULOSIS (CASEOUS) PNEUMONIA (Fig. 138-141) - pathogenetically most often associated with the progression of infiltrative T, characterized by case-finding perifocal inflammation.

In the development of caseous pneumonia, primary or repeated infection with drug-resistant MBT with increased virulence, as well as stressful situations, starvation, and immunosuppressive therapy are of particular importance. Caseous pneumonia can also be associated with the progression of primary pulmonary affect and large-focal dissemination in hematogenous T.

As a complication, caseous pneumonia develops during aspiration of blood, caseous masses, which is observed in cavernous and primary T, as well as in the pericavernous zone during the progression of cavernous T. The lesion in caseous pneumonia from pulmonary acini to the lung lobe.

CAVIARY TUBERCULOSIS (fig. 142-179) is formed from progressive forms of T of the lungs with disintegration - infiltrative, caseous pneumonia, hematogenous, focal, primary (primary pulmonary consumption).

By the nature of the clinical course and the structure of the cavern wall, acute cavernous and chronic, or fibrous-cavernous T are distinguished. The most severe variant of fibrous-cavernous T with extensive cirrhotic deformity is often defined as cirrhotic T.

The wall of the chronic cavity has a three-layer structure: a caseous layer, a layer of specific and nonspecific granulations and fibrous tissue. The wall contains draining and obliterated bronchi, as well as vessels, which macroscopically creates the impression of balsam.

In the pericavernous zone, there is perifocal inflammation, foci of bronchogenic dissemination. Chronic cavern has an irregular shape. A cavity system may form in the lungs. The severity of the process is exacerbated by the development of bronchiectasis, pneumosclerosis and cirrhotic changes. The progression of the process in fibrous-cavernous T occurs due to perifocal inflammation and bronchogenic dissemination with the development of acinous and lobular foci of specific pneumonia and cavities in the lower sections of the lungs. The bacterial population in the wall of the cavern reaches 1010-1012MBTvmkm3.

Complications of Fibrous-Cavernous Tuberculosis:

• specific - caseous pneumonia, bronchial and intestinal tuberculosis, bronchial and thoracic fistula, empyema tuberculosis and

• non-specific - pulmonary hemorrhage, spontaneous pneumothorax, pulmonary heart, amyloidosis, a range of severe structural and functional disorders of a number of organs and systems.

Cirrhotic pulmonary tuberculosis (fig. 155-160) develops on the basis fibrocavernous, chronic hematogenous, less infiltrative pleura and T, characterized by the powerful development of connective tissue, the presence of slot-like cavities, caseation foci, bronchiectasis, emphysema, pleural adhesions, preserving activity tuberculous process.
A cirrhotic T can be one- and two-sided, segmental, lobar, total. The most severe form of cirrhotic T is “destroyed lung” of cavernous-cirrhotic, polycavernous-cirrhotic, or apneumatic-cirrhotic types.

Cirrhotic T should not be confused with cirrhosis of the lungs in the outcome of the clinical cure of T with the loss of manifestations of specific inflammation activity.

Major complications: pulmonary heart failure, amyloidosis.

CHANGES IN RESPIRATORY TRACT IN TUBERCULOSIS (Fig. 161-170). The defeat of the respiratory tract in T lung has a specific (productive, ulcerative T) and non-specific expression (chronic bronchitis, bronchiectasis, post-tuberculosis stenosis). Specific changes are "contact" in nature, with the greatest constancy and severity develop during the destructive pulmonary process. In the pathogenesis of nonspecific changes, a significant role belongs to the "secondary" infection. The spread of pathogenic material through the bronchi is one of the most significant pathways for the progression of tuberculous inflammation in secondary T of the lungs.

The peculiarities of the healing of cavernous forms of tuberculosis (Fig. 171-179) are determined by the initial form of the disease, its prevalence, the nature of the course, and the therapy used. Reparation changes begin with resorption and rejection of necrotic masses of the inner layer of the cavity wall. The granulation layer of the wall gradually loses the signs of specificity, multinucleated giant cells like foreign bodies appear on its surface, a network of capillaries is found in the thickness of the layer, fibrosisation processes are enhanced. As a result, the cavernous cavity is scarring, transforming into a lesion or a post-tuberculous cyst-like cavity with fibrous walls capable of epithelialization from the draining bronchi. Patients with "abacillary, sanitized" cavities belong to a high risk group with respect to the possibility of recurrence of the disease. However, in itself, the closure of the cavity is not equivalent to the concept of clinical cure: in the lung there are long-lasting screenings of varying degrees of activity, inclusions of caseous are found in the folds of the cyst-like cavity. The healing of T is adversely affected by the presence of nonspecific changes of different volume and severity - pneumosclerosis, cirrhotic deformity, emphysema, chronic bronchitis and bronchiectasis.

Tuberculosis pleurisy (Fig. 180-183) is most often combined with a primary tuberculosis complex, bronchoadenitis, hematogenous, infiltrative, cavernous forms of tuberculosis. As a manifestation of primary tuberculosis infection may be accompanied by the development of conflict, erythema nodosum, polyarthritis. Exudate in nature can be serous, serous-fibrinous, hemorrhagic, serous-hemorrhagic, purulent, purulent-caseous, rarely so-called. "Cholesterol pleurisy". Along with the exudate in the pleura, dissemination of different types of tuberculous foci is possible. T pleura with purulent exudate (empyema) is caused by pneumothorax, a breakthrough into the pleural cavity of a cavity or the presence of a bronchopleural fistula after surgery. A prolonged course of T pleura is accompanied by the development of pneumocirrhosis, fibrothorax, and chest deformity.

CONIOTUBERCULOSIS (fig. 184-195)

Pneumoconioses - occupational dust diseases of the lungs are characterized by irreversibility of the course and the absence of specific therapies. The most severe form of the left pathology is silicosis. In the series of fibrogenic dust diseases, silicosis is most often combined with T.

Silicotuberculosis usually develops in an endogenous way based on the interaction of silicon dioxide and mycobacterium tuberculosis. Pathological anatomy: The basis of the lesion is fibrin-malignant nodules and silicotuberculosis necrotic foci with peripheral connective tissue shaft of varying degree of maturity and with hyalinosis. Necrotic foci merge, accompanied by bronchogenic spread, the formation of cavities. In silicotuberculosis foci, destructive changes can be combined with calcification. The decrease in the concentration of industrial dust was reflected in the severity of clinical and anatomical forms: the appearance of “isolated” forms of silicotuberculosis was noted.

Clinical and anatomical forms of silicotuberculosis:

• isolated silicotuberculous lymphadenitis,

• disseminated silicotuberculosis,

• caseous pneumonia,

• focal silicotuberculosis,

• silicotuberculoma,

• conglomerate silicotuberculosis,

• destructive (cavernous) silicotuberculosis.

Complications: pneumosclerosis, emphysema, pulmonary heart.

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