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Questions and Answers
Which of the following is NOT a systemic feature of chronic inflammation?
What is a characteristic morphological feature of chronic inflammation?
Which type of chronic inflammation is primarily characterized by the formation of granulation tissue?
Which cell type is dominant in chronic inflammation and plays key roles in the immune response?
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Chronic granulomatous inflammation is associated with which of the following infections?
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Which of the following responses is a function of macrophages in chronic inflammation?
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The presence of which type of cells is indicative of chronic granulomatous inflammation?
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What is one potential long-term complication of chronic suppurative inflammation?
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What role does Interferon-γ play in the immune response?
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Which transmission mode of tuberculosis is considered the least common?
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What is a characteristic feature of secondary tuberculosis infection?
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Which cytokine is primarily involved in stimulating the proliferation of T cells?
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What characterizes chronic granulomatous inflammation?
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What is a common feature of granuloma formation in chronic inflammation?
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Which type of cell is predominantly found in granulomas?
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In what way does TNF-α contribute to the inflammatory response?
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What best describes the formation of Langhans’ giant cells?
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What is the primary method used in the Mantoux test for tuberculosis screening?
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What role do macrophages play in granuloma formation?
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What complication can occur from haematogenous spread of tuberculosis?
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Which feature is indicative of caseous necrosis in granulomas?
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Which component of granulomas indicates accelerated humoral immune response?
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In chronic suppurative inflammation, what is typically observed?
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The primary immune response in granuloma formation is associated with which type of hypersensitivity reaction?
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Study Notes
Cytokines
- Interleukin-1 (IL-1) and Interleukin-2 (IL-2) stimulate the proliferation of T cells
- Interferon-gamma (IFN-γ) activates macrophages
- Tumor necrosis factor-alpha (TNF-α) promotes fibroblast proliferation. It also activates the endothelium to secrete prostaglandins, which are involved in the vascular response to inflammation.
- Transforming growth factor-beta (TGF-β) and platelet-derived growth factor (PDGF) are growth factors that stimulate fibroblast growth. These factors are released by activated macrophages.
Tuberculosis
- Etiology: Mycobacterium tuberculosis
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Mode of Transmission
- Inhalation (most common)
- Ingestion
- Inoculation of the organisms into skin
- Transplacental route (rare) results in congenital tuberculosis in the fetus from an infected mother
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Spread of Tuberculosis
- Local spread: by macrophages carrying the bacilli into surrounding tissues.
- Lymphatic spread: lymphoid follicles of pharynx, bronchi, intestines, or regional lymph nodes resulting in regional tuberculous lymphadenitis. This is typical of childhood infections.
- Haematogenous spread: tuberculous bacillaemia produces millet seed-sized lesions in different organs of the body, such as lungs, liver, kidneys, bones, and other tissues. This is known as miliary tuberculosis.
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By the natural passages:
- Lung lesions into the pleura (tuberculous pleurisy)
- Transbronchial spread into adjacent lung segments
- Infected sputum into the larynx (tuberculous laryngitis)
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Lesions in Tuberculosis
- Primary Infection: Tissue reaction to tubercle bacilli in a healthy individual not previously infected, resulting in a small consolidation in the lung (primary focus) with prominent lymphadenopathy. This is common in children.
- Secondary infection (Post-primary infection): Tissue reaction to tubercle bacilli in an individual who is previously infected or vaccinated. The granulomatous inflammation is much more intense and widespread with caseation/cavitation being more common.
- Immunisation against tuberculosis: Bacille Calmette-Guérin (BCG)
- Tuberculin (Mantoux) skin test: Testing is done by injecting intradermally (0.1 ml of tuberculoprotein, purified protein derivative (PPD)) on the forearm.
Chronic Ulcer
- A chronic suppurative inflammation, where infiltration by polymorphs and abscess formation are additional features. An example is actinomycosis.
Chronic Granulomatous Inflammation
- In chronic granulomatous inflammation, the injurious agent causes a characteristic histologic tissue response by formation of granulomas. Examples include tuberculosis, leprosy, syphilis, actinomycosis, sarcoidosis, etc.
- Granuloma: a circumscribed, tiny lesion, about 1 mm in diameter, composed predominantly of a collection of modified macrophages called epithelioid cells, and rimmed at the periphery by lymphoid cells.
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Composition of Granuloma
- Epithelioid cells: Modified macrophages/histiocytes with epithelial cell-like appearance, and are weakly phagocytic.
- Multinucleate giant cells: Formed by fusion of epithelioid cells and with 20 or more nuclei. Examples include Langhans’ giant cells in tuberculosis (with nuclei arranged at the periphery like a horseshoe or ring) and foreign body giant cells, which are common in foreign body tissue reactions (nuclei are clustered at the two poles, or present centrally).
- Lymphoid cells: lymphocytes are an integral part of granulomas, as the granuloma is a cell-mediated immune response to an antigen. Plasma cells, indicative of an accelerated humoral immune response, are also present in some types of granulomas.
- Necrosis: A feature of some granulomatous conditions, e.g., central caseous necrosis of tuberculosis (so-called because of the cheese-like appearance and consistency of the necrosis).
- Fibrosis: A feature of healing, with proliferating fibroblasts present at the periphery of the granuloma.
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Pathogenesis of Granuloma:
- Formation of granulomas is a type IV granulomatous hypersensitivity reaction.
- It is a defense reaction by the host, but eventually causes tissue destruction due to the persistence of poorly digestible antigens (e.g., M. tuberculosis, M. leprae, suture material, etc).
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Sequence of events:
- Engulfment of poorly degradable antigen by macrophages: the cells fail to digest and degrade the antigen, and instead undergo morphologic changes to epithelioid cells.
- Activation of CD4+ T cells: Macrophages, being antigen-presenting cells, having failed to deal with the antigen, present it to CD4+ T lymphocytes, which become activated and release lymphokines.
Chronic Inflammation
- Prolonged process in which tissue destruction and inflammation occur simultaneously.
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Causes:
- Chronic inflammation following acute inflammation: when tissue destruction is extensive, or bacteria survive and persist in small numbers at the site of acute inflammation, for example, in osteomyelitis or pneumonia that terminates in lung abscess.
- Recurrent attacks of acute inflammation: Repeated bouts of acute inflammation can lead to chronicity, for example, recurrent urinary tract infections can lead to chronic pyelonephritis.
- Chronic inflammation starting de novo: Infection with organisms of low pathogenicity can be chronic from the beginning, for example, infection with Mycobacterium tuberculosis.
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Systemic Effects of Chronic Inflammation:
- Fever
- Anemia
- Leucocytosis-lymphocytosis
- Elevated Erythrocyte Sedimentation Rate (ESR)
- Amyloidosis: Long-term cases of chronic suppurative inflammation may develop secondary systemic (AA) amyloidosis.
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General (morphological) characteristics of chronic inflammation
- Mononuclear cell infiltration (macrophages, T and B lymphocytes, plasma cells)
- Tissue destruction (induced by injurious agents or by inflammatory cells themselves)
- Healing
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Phagocytes in chronic inflammation
- Tissue macrophages
- Epithelioid cells (transformed macrophages)
- Multinucleated giant cells (formed by fusion of macrophages/epithelioid cells, e.g. Langhan's giant cells).
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Macrophages are the dominant cells in chronic inflammation. Their functions include:
- Phagocytosis
- Initiating tissue repair
- Secreting inflammatory mediators like TNF, IL1, chemokines, etc.
- Displaying antigens to lymphocytes.
Types of Chronic Inflammation
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Chronic non-specific inflammation: reaction leads to the formation of granulation tissue and healing by fibrosis, e.g.
- Fibrosis in chronic hepatitis
- Chronic inflammation in the lungs, following repeated episodes of pneumonia, leading to fibrosis
- Chronic inflammation in the kidney due to long-standing glomerulonephritis, leading to fibrosis.
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Chronic granulomatous inflammation:
- Reaction leads to the formation of granulomas (tuberculosis, leprosy, etc.)
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Description
This quiz covers key aspects of cytokines, including their roles in stimulating T cell proliferation and activating macrophages. It also explores the etiology, transmission modes, and spread of tuberculosis caused by Mycobacterium tuberculosis. Test your knowledge on these crucial immunological processes and disease mechanisms.
