Hello Everyone, here is a respiratory lecture on Tuberculosis made easy to understand to help aide in your study sessions. I have gathered all of the important information from my Med- Surg Book (Brunners and Suddarth 12th edition) and NCLEX review (Saunders 6th edition) that will prepare you for your nursing test whether it is for school or NCLEX.
Here are some Extra information that may help and guide you...
Preventing TB transmission:
1. Early identification and treatment of persons with active TB:
a. Maintain a high index of suspicion for TB to identify cases rapidly.
b. Promptly initiate effective multidrug anti-TB therapy based on clinical and drug-resistance surveillance data.
2. Prevention of spread of infectious droplet nuclei by source control methods and by reduction of microbial contamination of indoor air
a. Initiate acid-fast bacilli (AFB) isolation precautions immediately for all patients who are suspected or confirmed to have active TB and who may be infectious. AFB isolation precautions include use of a private room with negative pressure in relation to surrounding areas and a minimum of six air exchanges per hour. Air from the room should be exhausted directly to the outside. Use of ultraviolet lamps and/or high efficiency particulate air filters to supplement ventilation may be considered.
b. Persons entering the AFB isolation room should use disposable particulate respirators that fit snugly around the face.
c. Continue AFB isolation precautions until there is clinical evidence of reduced infectiousness (ie, cough has substantially decreased, and the number of organisms on sequential sputum smears is decreasing). If drug resistance is suspected or confirmed, continue AFB precautions until the sputum smear is negative for AFB.
d. Use special precautions during cough-inducing procedures.
3. Surveillance for TB transmission
a. Maintain surveillance for TB infection among health care workers (HCWs) by routine, periodic tuberculin skin testing. Recommend appropriate preventive therapy for HCWs when indicated.
b. Maintain surveillance for TB cases among patients and HCWs.
c. Promptly initiate contact investigation procedures among HCWs, patients, and visitors exposed to an untreated, or ineffectively treated, patient with infectious TB for whom appropriate AFB procedures are not in place. Recommend appropriate therapy or preventive therapy for contacts with disease or TB infection without current disease. Therapeutic regimens should be chosen based on the clinical history and local drug resistance surveillance data.
Risk Factors of TB:
• Preexisting medical conditions or special treatment (eg, diabetes, chronic renal failure, malnourishment, selected malignancies, hemodialysis, transplanted organ, gastrectomy, jejunoileal bypass)
• Immigration from countries with a high prevalence of TB (southeastern Asia, Africa, Latin America, Caribbean)
• Institutionalization (eg, long-term care facilities, psychiatric institutions, prisons)
Patho:
TB begins when a susceptible person inhales mycobacteria and becomes infected. The bacteria are transmitted through the airways to the alveoli, where they are deposited and begin to multiply. The bacilli also are transported via the lymph system and bloodstream to other parts of the body (kidneys, bones, cerebral cortex) and other areas of the lungs (upper lobes). The body’s immune system responds by initiating an inflammatory reaction. Phagocytes (neutrophils and macrophages) engulf many of the bacteria, and TB-specific lymphocytes lyse (destroy) the bacilli and normal tissue. This tissue reaction results in the accumulation of exudate in the alveoli, causing bronchopneumonia. The initial infection usually occurs 2 to 10 weeks after exposure. Granulomas, new tissue masses of live and dead bacilli, are surrounded by macrophages, which form a protective wall. They are then transformed to a fibrous tissue mass, the central portion of which is called a Ghon tubercle. The material (bacteria and macrophages) becomes necrotic, forming a cheesy mass. This mass may become calcified and form a collagenous scar. At this point, the bacteria become dormant, and there is no further progression of active disease. After initial exposure and infection, active disease may develop because of a compromised or inadequate immune system response. Active disease also may occur with reinfection and activation of dormant bacteria. In this case, the Ghon tubercle ulcerates, releasing the cheesy material into the bronchi. The bacteria then become airborne, resulting in further spread of the disease. Then the ulcerated tubercle heals and forms scar tissue. This causes the infected lung to become more inflamed, resulting in further development of bronchopneumonia and tubercle formation. Unless this process is arrested, it spreads slowly downward to the hilum of the lungs and later extends to adjacent lobes.
