Tuberculosis_tb_ Pathophysiology _ Schematic Diagram 44ie

Clinical Manifestations of Tuberculosis  Easy fatigability  Anorexia or loss of appetite  Weight loss and body wasting  Persistent, long term low- grade fever  Chills and night sweats  Persistent, progressive cough which may be non-productive at first but may produce purulent sputum in the long term (2 weeks or more)  Non-resolving bronchopneumonia  Dull or pleuritic chest pains  Dyspnea  Hemoptysis  Anemia in some Schematic Diagram for Tuberculosis Predisposing Factors:

Precipitating Factors:

Age: Children below 14 y. o. & Adults more than 65 y. o.

Immunocompromised person

Native Americans, Eskimos, Asians and Blacks

Economically- disadvantaged or homeless/ poor housing

Malnourished individuals

Living in overcrowded areas Alcohol abuse/ dependent Poor hygiene Lack of access to health care

Inhalation of droplet infected with Mycobacterium Tuberculosis

It is trapped first in the upper airways, where the primary defenses is activated referring to the mucussecreting goblet cell and the cilia.

When the initial prevention of infection is not successful, the bacteria reaches and deposits itself in the lung periphery usually in the lower part of the upper lobe or the upper part of the lower lobe; specifically in the alveoli.

The bacteria is quickly surrounded by polymorphonuclear leukocytes and engulfed by the alveolar macrophages

Some mycobacterial organisms are carried off by the lymphatics to the hilar lymp nodes

It is now called as the Ghon Complex, but it rarely results in the spread to other body organs.

As macrophages (epithelial cells) engulf the bacteria, these cells and form into giant cells that encircle the foreign cell.

As a result of hypersensitivity to the organism, inside the giant cells caseous necrosis occurs (granular chessy appearance)

There is then the proliferation of T- lymphocytes in the surrounding of the central core of the caseous necrosis causing some lesions.

Fibrosis and calcification happens as the lesion ages resulting to granuloma formation called as tubercle.

Collagenous scar tissue encapsulates the tubercle to separate the organisms from the body.

As the process progress the bacteria may or may not be killed and it continue to grow and multiply resulting to a cell mediated immunity (which can be detected through PPD)

Pulmonary Tuberculosis

Progression of infection may lead to latent stage to active stage depending on both the virulence of the bacteria and the microbicidal ability of the alveolar macrophages

For poorly immunocompromised clients, the necrotic tissue liquefies and the fibrous walls losses its structural integrity

The semiliquid necrotic material is drained into the bronchous or in the nearby blood vessel, leaving an airfilled cavity at the original site.

If drained in the bronchous as purulent discharge, it could infect other people through droplet transmission.

If drained into a vessel, it could enter the blood stream or in the lymphatic system; where new caseous granulomas may form.

EXTRAPULMONARY TUBERCULOSIS