Medical tb,kaposis sarcoma,ascitis;causes of,fluid thrill,succusion splash,check them..mechanism of oedema...heart failure-ever heard of framingham criteria for dx of heart failure?it is easy...i tackled tb in long case and heart failure..grading of heart failure Pathophysiology Once inhaled, the infectious droplets settle throughout the airways. The majority of the bacilli are trapped in the upper parts of the airways where the mucus-secreting goblet cells exist. The mucus produced catches foreign substances, and the cilia on the surface of the cells constantly beat the mucus and its entrapped particles upward for removal. 8This system provides the body with an initial physical defense that prevents infection in most persons exposed to tuberculosis. 9 Bacteria in droplets that bypass the mucociliary system and reach the alveoli are quickly surrounded and engulfed by alveolar macrophages, 7, 8the most abundant immune effector cells present in alveolar spaces. 10These macrophages, the next line of host defense, are part of the innate immune system and provide an opportunity for the body to destroy the invading mycobacteria and prevent infection. 11Macrophages are readily available phagocytic cells that combat many pathogens without requiring previous exposure to the pathogens. Several mechanisms and macrophage receptors are involved in uptakeof the mycobacteria. 11The mycobacterial lipoarabinomannan is a key ligand for a macrophage receptor. 12The complement system also plays a role in the phagocytosis of the bacteria. 13The complement protein C3 binds to the cell wall and enhances recognition of the mycobacteria by macrophages. Opsonization by C3 is rapid, even in the air spaces of a host with no previous exposure toM tuberculosis. 14The subsequent phagocytosis by macrophages initiates a cascade of events that results in either successful control of the infection, followed by latent tuberculosis, or progression to active disease, called primary progressive tuberculosis. 8The outcome is essentially determined by the quality of the host defenses and the balance that occurs between host defenses and the invading mycobacteria. 11, 15 After being ingested by macrophages, the mycobacteria continue to multiply slowly, 8with bacterial cell division occurring every 25 to 32 hours. 4, 7Regardless of whether the infection becomes controlled or progresses, initial development involves production of proteolytic enzymes and cytokines by macrophages in an attempt to degrade the bacteria. 11, 12Released cytokines attract T lymphocytes to the site, the cells that constitute cell-mediated immunity. Macrophages then present mycobacterial antigens on their surface to the T cells. 11This initial immune process continues for 2 to 12 weeks; the microorganisms continue togrow until they reach sufficient numbers to fully elicit the cell-mediated immune response, which can be detected by a skin test. 4, 8, 11 For persons with intact cell-mediated immunity, the next defensive step is formation of granulomas around theM tuberculosisorganisms 16(Figure 1 ⇓). Thesenodular-type lesions form from an accumulation of activated T lymphocytes and macrophages, which creates a micro-environment that limits replication and the spread of the mycobacteria. 8, 12This environment destroys macrophages and produces early solid necrosis at the center of the lesion; however, the bacilli are able to adapt to survive. 18In fact,M tuberculosisorganisms can change their phenotypic expression, such as protein regulation, to enhance survival. 13By 2 or 3 weeks, the necrotic environment resembles soft cheese, often referred to caseous necrosis, and is characterized by low oxygen levels, low pH, and limited nutrients. This condition restricts further growth and establishes latency. Lesions in persons with an adequate immunesystem generally undergo fibrosis and calcification, successfully controlling the infection so that the bacilli are contained in the dormant, healed lesions. 18Lesions in persons with less effective immune systems progress to primary progressive tuberculosis. Summary:- Pathophysiology of tuberculosis: inhalation of bacilli (A), containment in a granuloma (B),and breakdown of the granuloma in less immunocompetent individuals (C). For less immunocompetent persons, granuloma formation is initiated yet ultimately is unsuccessful in containing the bacilli. The necrotic tissue undergoes liquefaction, and the fibrous wall loses structural integrity. The semiliquid necrotic material can then drain into a bronchus or nearby blood vessel, leaving an air-filled cavityat the original site. In patients infected withMtuberculosis,droplets can be coughed up from the bronchus and infect other persons. If discharge into a vessel occurs, occurrence of extrapulmonary tuberculosis is likely. Bacillican also drain into the lymphatic system and collect in the tracheobronchial lymph nodes of the affected lung, where the organisms can form new caseous granulomas. 18
Posted on: Sun, 23 Jun 2013 20:09:35 +0000
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