L3, Resp Pathology PDF

pathology - respiratory TUBERCULOSIS LECTURE (3) TUBERCULOSIS Dr. M. Shalaby pathology - respiratory TUBERCULOSIS  Chronic infective granuloma affecting nearly a...

pathology - respiratory TUBERCULOSIS LECTURE (3) TUBERCULOSIS Dr. M. Shalaby pathology - respiratory TUBERCULOSIS  Chronic infective granuloma affecting nearly all body systems mainly the DEFINITION lungs. ENVIRONMENTAL FACTORS PERSONAL FACTORS ① Low socioeconomic standard. ① Negroes (˃ white persons) PREDISPOSING ② Bad general hygiene. ② Malnutrition FACTORS ③ Contact with TB persons. ③ Debilitating diseases (DM) ④ Overcrowding. ④ Immune deficiency states ⑤ Environmental pollution. T.B. bacilli: ① Aerobic. ② Acid- fast. MORPHOLOGY ③ Non- motile ④ Not produce exotoxins. CAUSATIVE ⑤ Carried by macrophages. AGENTS ① Carbohydrate STRUCTURE ② Lipid ③ Protein (tuberculoprotien or PPD). ① Human type: causes infection by inhalation. TYPES ② Bovine type: causes infection by ingestion Dr. M. Shalaby pathology - respiratory TUBERCULOSIS Dr. M. Shalaby pathology - respiratory TUBERCULOSIS  Occur in young ages, non- immunized persons. INCIDENCE  Source of infection is exogenous.  About 5% of infected persons develop significant disease. ① Inhalation. METHODS OF ② Ingestion INFECTIONS: ③ Direct contact. ① Lung. SITE OF PRIMARY ④ Intestine ② Tonsils COMPLEX: ⑤ Nose (rare). ③ Skin Proliferative reaction (tubercle formation): ① At 1st: The bacilli are taken by the macrophages. The organisms multiply in macrophages, which are unable to kill the organism ② Then: The native macrophages present the (purified protein derivative PPD) on its surface to native helper T cells. Macrophages release interleukin 12 (IL-12) which activates the helper T lymphocytes to secrete the following :  Interferone gama (INFy): responsible for immunity and delayed hypersensitivity with granuloma formation. This is achieved by activation of native and blood monocytes and results in more secretion of IL- 12 with increased ability for expression of the PPD, phagocytosis and killing of bacilli. REACTION OF  Tumor necrotizing factor (TNF- α) → ↑ blood flow to the area of BODY AGAINST inflammation. Attraction of lymphocytes and blood monocytes to BACILLI: area of infection ③ Engulfed lipid part of bacilli change macrophage to epithelioid cell (larger with large vesicular nuclei and eosinophilic Cytoplasm and indistinct Cell border ④ langhans giant cells: formed by fusion of multiple epithelioid cells (Large cell with eosinophilic cytoplasm and multiple nuclei arranged in horseshoe shape(classic pattern) or in center or at periphery of cell. ⑤ Firm tubercle formation: by fibroblast that encircle the tubercle by effect of INFy ⑥ Caseation : after 2-3 weeks, central caseation start in the center of tubercle that become soft Dr. M. Shalaby pathology - respiratory TUBERCULOSIS  In 3 weeks, the tubercle is visible 1-3 mm size, with central yellow N/E caseation and its periphery is grey.  Central caseating material (sturctureless eosinophilic material with no cellular details (H &E) Ephithelioid cells, macrophages, Langhan’s giant M/E cells, lymphocytes and peripheral fibroblastic reaction surround the caseation.  The reaction ends by the formation of epithelioid granulomas with giant cells , central caseation and peripheral fibrosis. Dr. M. Shalaby  pathology - respiratory TUBERCULOSIS  SITE: Pulmonary TB Favorable site for TB (easy inhalation and aeration).  CONSISTS OF :  Is a caseous lesion 1-2cm. in diameter beneath the pleura in the lower part of upper lobe or upper part of middle lobe 1-2 cm. from pleural cavity, grayish yellow in color. PARENCHYMATOUS LESION (GHON’S FOCUS) TB LYMPHANGITIS  Inflammation of lymphatic vessels. TB LYMPHADENITIS  Inflammation of Lumph nodes.  FATE: A. Good fate → Healing B. Bad fate → Spread: LOCAL  to pleura causing TB Pleurisy LYMPHATIC  to peri and paratracheal lymph nodes & mediastinal structures. BLOOD  produce miliary tuberculosis  less common than secondary NATURAL  it leads to development of tuberculous bronchopneumonia and PASSAGES pneumonia Dr. M. Shalaby pathology - respiratory TUBERCULOSIS  The lesion appear as multiple scattered uniform small size (3mm) tubercles  Separated from each other by normal tissue  Not surrounded by area of congestion  Present on outer and cut surface of organs. N/E  They are related to blood vessels are poorly developed tubercle with central necrosis and absent giant cells. M/E MILLARY TB SPLEEN Dr. M. Shalaby pathology - respiratory TUBERCULOSIS PYEMIC ABSCESS MILIARY TB  Caused by pyemia  Spread of TB by blood  Septic emboli impacted in capillary and small  Spread by blood to different organs blood vessels  Multiple small acute abscesses, equal in  Multiple uniform size (3mm) shape, rounded, present on outer & cut  separated by normal tissue, present on outer surface, surrounded by zone of hyperaemia & cut surface , not surrounded by zone of hyperaemia  M/E: central pus, acute inflammatory cells,  Poorly formed tubercle with little caseation surrounded by zone of hemorrhage and and no giant cells congestion Fatal Fatal  May be acquired exogenously or ORGANISM  From reactivation of a healed primary complex. AGE  Occurs in adults. ① Kidney ④ Epididymis. SITE ② Suprarenal gland ⑤ Brain and meninges ③ Fallopian tube ⑥ Bone and joints.  Hypersensitivity reaction leads to excessive tissue destruction and extensive caseation.  No nodal affection as the organism is destroyed in the necrotic tissue.  An apical lesion (Assmann focus) begins as a small caseating tuberculous granuloma.  In most cases, destruction of the lung leads to cavitations. PATHOGENESIS Dr. M. Shalaby pathology - respiratory TUBERCULOSIS  Central area of caseation surrounded by granulomatous inflammatory reaction. M/E A. Regression (good fate) B. progressive lesion (Bad Fate) :  Blood vessels: hemorrhage & hemoptysis LOCAL TISSUE  Bronchi: open to the pleura leading to pneumothorax DESTRUCTION and pyopneumothorax.  Reactive systemic amyloidosis. PULMONARY  Pulmonary hypertension FATE AND FIBROSIS  Right sided heart failure (cor pulmonale). COMPLICATIONS  Local to the pleura (pleurisy) SPREAD  Bronchial: TB pneumonia and bronchopneumonia  Blood: isolated organ TB or miliary TB  With good immunity, healing of the apical lesion occurs and a dense fibrous capsule surrounds a central area of caseation  Calcification often occurs, and a (latent tuberculosis) develops which can be reactivated if the patient’s immunity is lowered. PROLIFERATIVE REACTION IN PRIMARY TB PROLIFERATIVE REACTION IN SECONDARY TB  Slow, firm, well formed  Rapid, softer, with more liquefaction cause cavitation, sinus, fistula, ulcer  Blood spread is more rapid & fatal  Blood spread is less than primary  Spread through natural passages is late and  Spread through natural passages is rapid and less easier  LN enlarged (part of complex)  No LN enlargement Dr. M. Shalaby pathology - respiratory TUBERCULOSIS  It is a localized mass of caseating tuberculous reaction surrounded by fibrous tissue.  It may reach a large size (to be mistaken for a tumor)  It can occur at any organ (lung, kidney, brain…) Dr. M. Shalaby