http://allnurses.com/nursing-student-assistance/pulmonary-tuberculosis-pneumonia273191.

html Tuberculosis: From Nurse's 5-Minute Clinical Consult: Diseases by Lippincott Williams & Wilkins, page 824, on the pathophysiology of tuberculosis:

"Multiplication of the bacillus mycobacterium tuberculosis causes an inflammatory process where deposited. A cell-mediated immune response follows, usually containing the infection within 4 to 6 weeks. The T-cell response results in the formation of granulomas around the bacilli, making them dormant. This confers immunity to subsequent infection. Bacilli within granulomas may remain viable for many years, resulting in a positive purified protein derivative or other skin test for TB. Active disease develops in 5% to 15% of those infected. Transmission occurs when an infected person coughs or sneezes."

From Pathophysiology: The Biologic Basis for Disease in Adults and Children, third edition, by Kathryn L. McCance and Sue E. Heuther, page 1185, on the pathophysiology of tuberculosis: "Like some types of pneumonia, tuberculosis is transmitted from person to person in airborne droplets. Microorganisms lodge in the lung periphery, usually in the upper lobe. Once the bacilli are inspired into the lung, they multiply and cause nonspecific pneumonitis (lung inflammation). Some bacilli migrate through the lumphatics and become lodged in the lymph nodes, where they encounter lymphocytes and initiate the immune response. Inflammation in the lung causes neutrophils and then alveolar macrophages to migrate to the area. These cells are phagocytes that engulf the bacilli and begin the process by which the body's defense mechanisms isolate the bacilli, preventing their spread. The neutrophils and macrophages seal off the colonies of bacilli, forming a granulomatous lesion called a tubercle. Infected tissues within the tubercle die, forming cheeselike material called caseation necrosis. Collagenous scar tissue then grows around the tubercle, completing isolation of the bacilli. The immune response is complete after 10 days or so, preventing further multiplication of the bacilli. Once the bacilli are isolated in tubercles and immunity develops, tuberculosis may remain dormant for life. If the immune system is impaired, however, or if live bacilli escape into the bronchi, active disease occurs and may spread through the blood and lymphatics to other organs. Endogenous reactivation

of dormant bacilli in elderly persons may be caused by poor nutritional status, insulin-dependent diabetes, long-term corticosteroid therapy and other debilitating diseases." Pneumonia: From Nurse's 5-Minute Clinical Consult: Diseases by Lippincott Williams & Wilkins, page 614, on the pathophysiology of pneumonia:
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"A gel-like substance forms as micoorganisms and phagocytic cells break down. This substance consolidates within the lower airway structure. Inflammation involves the alveoli, alveolar ducts, and interstitial spaces surrounding the alveolar walls. In lobar pneumonia, inflammation starts in one area and may extend to the entire lobe. In bronchopneumonia, it starts simultaneously in several areas, producing patchy, diffuse consolidation. In atypical pneumonia, inflammation is confined to the alveolar ducts and interstitial spaces."

From Pathophysiology: The Biologic Basis for Disease in Adults and Children, third edition, by Kathryn L. McCance and Sue E. Heuther, page 1183 on the pathophysiology of pneumonia: "Pathogenic organisms can reach the lung by the following routes:

when an infected individual coughs, sneezes, or talks, microorganisms are released into the air to be inhaled by other people. Microorganisms can be inspired with aerosols (nebulized gas) from contaminated respiratory therapy equipment. In illness or poor dental hygiene, normal flora of the oropharynx can become pathogenic. Staphylococcus and gram-negative bacteria can be spread by the circulation from a systemic infection, sepsis, or contaminated needles of intravenous (IV) drug abusers.

In healthy individuals pathogens that reach the lungs are expelled or held in check by mechanisms of self-defense. The lungs' defense mechanisms--the cough reflex, mucociliary clearance, and phagocytosis by alveolar macrophages--are backed up by the body's immune system and various components of the inflammatory response, including the release of biochemical mediators by alveolar mast cells. In susceptible individuals the invading pathogen is not held in check but multiplies, releasing damaging toxins and stimulating full-scale inflammatory and immune responses, both of which have damaging side effects. The immune response (antigenantibody reaction) and the endotoxins released by some microorganisms damage bronchial mucous membranes and alveolocapillary membranes. Inflammation and edema cause the acini and terminal bronchioles to fill with

infectious debris and exudate, leading to ventilation-perfusion abnormalities. If the pneumonia is caused by Staphylococcus or gram-negative bacteria, necrosis of lung parenchyma also may occur."