TUBERCULOSIS.  Definition: chronic infective granuloma affecting nearly all body systems but mainly the lungs.  Predisposing factors: A) Environmental.

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Presentation transcript:

TUBERCULOSIS

 Definition: chronic infective granuloma affecting nearly all body systems but mainly the lungs.  Predisposing factors: A) Environmental b) Personal factors  Causative Agents: T.B. bacilli

 Structure o f T.B. bacilli: Carbohydrate, lipid and protein (tuberculoprotein)  Types of TB Bacilli: Human type Human type Bovine type Bovine type

Primary tuberculosis (childhood type)  Methods of infections: 1- Inhalation. 2- Ingestion 3- Direct contact.  Sites of primary complex: 1- lung. 2- Intestine 3- Tonsils 4- Skin 5- Nose (rare site).

Reaction of the body against bacilli Proliferative reaction (tubercle formation)

 N/E of tubercle: Small, 1-3 mm, with central yellow caseation and grey periphery.  M/E of tubercle: Central caseating material (structureless eosinophilic material, epithelioid cells, macrophages, Langhan ’ s giant cells, lymphocytes and peripheral fibroblastic reaction.

 The constituents of primary complex: 1. Parenchymatous lesion 2. Tuberculous lymphangitis 3. Tuberculous lymphadenitis

 Fate of primary complex: 1- Good fate: Healing 2- Bad fate: spread: 1.Local. 2.Lymphatic. 3.Hematogenous 4.Natural passage.

Secondary tuberculosis Adult hood type  Methods of infection: 1. Endogenous by reactivation of dormant focus. 2. Exogenous by inhalation or ingestion.  Sites: Any site, mainly the lung & intestine are affected.

 Reaction of the body against bacilli in secondary infection. 1.Proliferative reaction in solid organs. 2.Exudative reaction in serous sacs and sometimes in soft parenchymatous organs.

 Fate of secondary T.B: 1. Good fate: Healing. 2. Bad fate: Extension and spread: 1.Local. 2.Natural passages. 3.Blood (rare) 4.Lymphatic.

Tuberculoma  Definition: Tumor-like tuberculous lesion formed of inspissated caseating material surrounded by fibrous capsule  Sites: Lung, brain, kidney, and spinal cord.

Miliary Tuberculosis  Definition: acute hematogenous dissemination of large dose of T.B bacilli with wide spread involvement of multiple organs.  NAKED EYE EXAMINATION: Multiple, scattered, uniform, small size (3mm) tubercles separated from each other by normal tissue and not surrounded by area of congestion and present on outer and cut surface of organs.

 MICROSCOPIC EXAMINATION: They are related to blood vessels are poorly developed tubercle with central necrosis and absent giant cells.

Miliary T.B of the lung

Pulmonary T.B

Lung is a favorable site for T.B. (easy inhalation and aeration). Lung is a favorable site for T.B. (easy inhalation and aeration).  Predisposing Factors: Decrease immunity Decrease immunity contact with patients contact with patients Silicosis Silicosis congenital heart diseases. congenital heart diseases.

Primary Pulmonary Tuberculosis  Primary pulmonary complex: Consists of 3 parts: 1. Parenchymatous lesion (Ghon ’ s focus). 2. Tuberculous lymphangitis. 3. Tuberculous lymphadenitis.

Ghon ’ s focus

Ghon ’ s triad

 Fate: 1. Good fate: Healing. 2. Bad fate: Spread.

SECONDARY PULMONARY T.B  Sources of Infection: 1. Reactivation of dormant focus. 2. Exogenous by inhalation.  Site: Apical or subapical Apical or subapical More in Rt. Lung than left lung. More in Rt. Lung than left lung.

The Morphological Feature: Simon ’ s focus (Assman- Simon ’ s focus) Chronic apical lesion formed by fusion of many tubercles. Not associated with lymphangitis or lymphadenitis. Chronic apical lesion formed by fusion of many tubercles. Not associated with lymphangitis or lymphadenitis.

M/P of pulmonary T.B

T.B bacilli detected by bacteriologic examination

 The Fate: A. Regression (good fate) B. progressive lesion (Bad Fate) 1. Cavitary Tuberculosis 2. Chronic fibrocaseous pulmonary tuberculosis 3. Acute tuberculous bronchopneumonia & acute caseous pneumonia.

Chronic fibrocaseous pulmonary tuberculosis  Naked Eye and Pathogenesis: 1. Mother cavity. 2. Daughter cavities (acinar lesions). 3. Insignificant hilar lymphadenopathy.  Microscopic examination: Extensive caseation necrosis form multiple Caseating tubercles healing by fibrosis, epithelialization of cavities, calcification.

 Complications: 1- Local tissue destruction: Hemoptysis. Hemoptysis. Spontaneous pneumothorax. Spontaneous pneumothorax. Pyopneumothorax. Pyopneumothorax. 2ry Amyloidosis. 2ry Amyloidosis.

2- Peptic ulcer: 20% of cases; related to stress. 3- Fibrosis: of the lung, bronchus & pleura leads to bronchiectasis and pulmonary hypertension and cor- pulmonale. 4- Spread.

Caseating lung T.B