أسئلة الثالثة باثولوجي RESP (قبل التعديل)

A chronic infectious disease caused by a bacterium called Mycobacterium tuberculosis, mainly affecting the lungs and sometimes other body systems.

Factors that increase the risk of developing tuberculosis, including low socioeconomic status, poor hygiene, contact with TB patients, overcrowding, environmental pollution, malnutrition, and debilitating diseases like diabetes.

TB bacteria are aerobic, acid-fast, non-motile, and do not produce exotoxins. They are often carried within macrophages (immune cells).

TB is usually spread through the air via inhalation of TB bacteria.

The initial infection site in the lungs or other locations where TB first establishes.

TB bacteria are structured with carbohydrates, lipids, and proteins (including tuberculoprotein, or PPD).

Human type (inhaled) and bovine type (ingested) infections exist, with inhalation being the most common.

Macrophages initially take up TB bacteria, but are unable to destroy them. They then present parts of the bacteria to T cells.

A caseous lesion, about 1-2 cm in diameter, found beneath the pleura in the lower part of the upper lobe or upper part of the middle lobe of the lung. It's a grayish-yellow, parenchymal lesion.

Inflammation of the lymphatic vessels.

Inflammation of the lymph nodes.

Good fate: Healing, Bad fate: Spreading. Spreading can be local (to the pleura causing TB Pleurisy), lymphatic (to peri and paratracheal lymph nodes and mediastinal structures) or hematogenous (causing miliary tuberculosis).

Multiple small (3mm) tubercles scattered throughout the body, separated by normal tissue. They are poorly developed with central necrosis and no giant cells.

Macrophages engulf bacilli, releasing IL-12 to activate helper T cells, triggering an immune response, and converting to epithelioid cells.

IL-12 activates helper T cells to produce INF-γ, crucial for immunity and granuloma formation in Tuberculosis.

INF-γ activates immune cells, promotes granuloma formation, and enhances the ability of macrophages to fight TB bacilli.

TNF-α increases blood flow to inflamed areas, attracting immune cells to fight infection.

Macrophages transform into epithelioid cells, which are larger, and have a distinctive appearance due to the engulfed bacilli in Tuberculosis.

Fusion of multiple epithelioid cells forms these cells, with a distinctive horseshoe or central arrangement of nuclei, in response to TB infection.

Fibroblasts create a structure around the infection, resulting in a visible tubercle in TB progression, that encloses the infection.

Central softening (caseation) of a tubercle develops in Tuberculosis after several weeks, causing a yellowish appearance.

Tuberculosis can spread within the respiratory system, leading to TB pneumonia and bronchopneumonia.

TB can travel through the bloodstream, resulting in isolated organ TB or widespread miliary TB.

A dormant form of TB where bacteria are contained but not active, often due to a strong immune system.

The body often forms a hard, calcium-filled capsule around the dormant TB bacteria.

Primary TB involves a slow, well-formed reaction, while Secondary TB is rapid, softer, more liquefying, and spreads more easily.

Multiple small, rounded abscesses caused by septic emboli impacting small blood vessels. They are often found on the outer surface of organs and are surrounded by a zone of hyperemia.

Miliary tuberculosis lesions exhibit poorly formed tubercles with little caseation (cheese-like necrosis) and no giant cells.

An apical lesion in the lung, starting as a small caseating tuberculous granuloma, and often develops into a cavitation.

Destruction of lung tissue leads to cavities, which are hollow spaces within the lung.

TB can spread from the bronchi to the pleura, leading to pneumothorax (air in the pleural space) and pyopneumothorax (pus and air in the pleural space).

Pulmonary fibrosis and hypertension caused by TB can lead to right-sided heart failure (cor pulmonale).

A Ghon's focus can either heal, or it can spread locally to the pleura causing pleurisy, lymphatically to lymph nodes, or hematogenously causing miliary TB.

A form of tuberculosis characterized by many small, scattered tubercles throughout the body, typically seen in the spleen.

Miliary TB lesions are poorly developed, with central necrosis and no giant cells.

Inflammation of the lymph nodes due to tuberculosis infection.

TB bacteria are aerobic, acid-fast, non-motile, and don't produce exotoxins. They are often carried by immune cells called macrophages.

IL-12 is released by macrophages in response to TB bacteria. It activates helper T cells to produce interferon-gamma (INF-γ), which is crucial for controlling the infection by stimulating the immune response.

INF-γ is a key cytokine released by helper T cells. It activates macrophages to kill TB bacilli, promotes granuloma formation, and enhances the ability of immune cells to fight the infection.

TNF-α is a cytokine that increases blood flow to the infected area. This attracts immune cells to the site and helps them fight the infection.

An epithelioid cell is a modified macrophage. It has a larger size, a distinctive appearance, and is formed when macrophages engulf TB bacilli.

A Langhan's Giant cell is a large cell formed by the fusion of multiple epithelioid cells. It contains many nuclei arranged in a horseshoe or central pattern.

A tubercle is a structure formed by fibroblasts that encircle the area where TB bacteria are located. It helps to contain the infection and prevent it from spreading.

Caseation is the central softening and necrosis (cell death) that occurs in a tubercle. This forms a soft, cheesy-like material in the center.

Tubercles are visible under a microscope. They show central caseous material, a surrounding layer of epithelioid cells, Langhan's giant cells, lymphocytes, and peripheral fibrosis.

Pyemia, a condition where bacteria enter the bloodstream and form emboli (blood clots) that lodge in small blood vessels.

Pyemic abscesses are larger and surrounded by a zone of hyperemia, while Miliary TB tubercles are smaller, uniform, and not surrounded by hyperemia.

It starts as a small caseating tuberculous granuloma in the lung apex and often develops into a cavitation.

A characteristic structure formed in TB infection, consisting of a central area of caseation surrounded by a granulomatous inflammatory reaction.

It can either regress (heal) or progress (get worse). Progressive lesions can lead to lung damage, blood vessel problems, and spread to other organs.

It can lead to pneumothorax (air in the pleural space) or pyopneumothorax (pus and air in the pleural space).

TB can involve complications that are localized to the pleura (pleurisy), spread through the bronchial system (TB pneumonia and bronchopneumonia), or through the bloodstream (isolated organ TB or miliary TB).

Primary TB is characterized by a slow, firm, well-formed reaction, while Secondary TB is rapid, softer, and more prone to liquefaction, cavitation, and spread through natural passages.

Conditions that increase the risk of developing tuberculosis. Examples include poverty, overcrowding, malnutrition, weak immune system, and contact with infected individuals.

A characteristic grayish-yellow lesion in the lung, usually in the upper lobe, formed during the initial stage of TB infection.

TB infection can either be controlled (latent TB) or progress to active disease. Progression can affect different organs, leading to varying complications.

TB Lymphangitis is the inflammation of lymphatic vessels caused by TB bacteria. It happens when the bacteria spread to nearby lymphatic vessels, leading to inflammation.

Miliary TB in the spleen appears as multiple, tiny, scattered tubercles, each about 3mm in size. These tubercles are separated by normal tissue, with poorly developed structure and no giant cells.

A Ghon's focus can either heal completely, leaving a scar, or it can spread locally to the pleura (causing pleurisy), lymphatically to lymph nodes, or hematogenously causing miliary TB.

Primary TB is slow and well-formed, while Secondary TB is rapid and prone to liquefaction, cavitation, and spread through natural passages.

An apical lesion in the lung, starting as a small caseating tuberculous granuloma. It often develops into a cavitation.

TB can spread from the bronchi to the pleura, leading to pneumothorax (air in the pleural space) and pyopneumothorax (pus and air in the pleural space).

A TB lesion that worsens and can lead to lung damage, blood vessel problems, and spread to other organs.

IL-12 is released by macrophages in response to TB bacteria. It activates helper T cells to produce interferon-gamma (INF-γ), which is crucial for controlling the infection by stimulating the immune response.

INF-γ is a key cytokine released by helper T cells. It activates macrophages to kill TB bacilli, promotes granuloma formation, and enhances the ability of immune cells to fight the infection.

TNF-α is a cytokine that increases blood flow to the infected area. This attracts immune cells to the site and helps them fight the infection.

A tubercle is a structure formed by fibroblasts that encircle the area where TB bacteria are located. It helps to contain the infection and prevent it from spreading.

Caseation is the central softening and necrosis (cell death) that occurs in a tubercle. This forms a soft, cheesy-like material in the center.