BSN4A (GROUP 2) 31

X. Pathophysiology Predisposing Factors Age: 59 years old Gender: Male Biological: History of PTB infection Ethnicity: Asian Precipitating Factors >Alcohol drinking >Cigarette smoking >Poor socioeconomic factor >Poor hygiene >Poor access to health care >Poor nutrition >Poor family support >Contact of person with PTB >Lack of information regarding PTB

Inhalation of droplet infected with Mycobacterium Tuberculosis

It is trapped first in the upper airways, where the primary defenses is activated referring to the mucus secreting 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 and the alveoli Mycobacterium tuberculosis multiply in the alveoli Bronchopneumonia develops in the lung tissue 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 lymph nodes Resulted to the Ghon Complex As macrophages (epithelial cells) engulf the bacteria, these cells join and form into giant cells that encircle the foreign cell As a result of hypersensitivity to the organism, inside the giant cells caseous necrosis/necrotic degeneration occurs Production of cavities filled with cheese-like mass of tubercle bacilli, dead WBCs, necrotic lung tissue Proliferation of T-lymphocytes in the surrounding of the central core of the caseous necrosis

Infection of airways Results to brochial edema, increased mucus secretion, bronchoconstriction, and bronchial spasm Worsening of obstructions Oversecretion of fluids and mucus Accumulation of fluids Multiplication of the bacteria Inflammation in the epithelial wall Rupture of inflamed endothelial cells Increased capillary permeability Increased production of fluid in the alveoli and the lung compartment

Atherosclerotic aorta Hardening & narrowing of blood vessels Increase vascular resistance

Backflow of blood to from the heart to the pulmonary circulation Increase pressure in the pulmonary artery Increase in capillary hydrostatic pressure in the pleural cavity

Decrease blood flow of blood from the lungs to systemic circulation

Decrease in oncotic pressure

Decrease lymphatic flow of fluid out of the pleural cavity Excess fluid accumulation in the pleural space

Pleural effusion

BSN4A (GROUP 2) 32
Lesions occurs 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. Primary Tuberculosis chest pain chest tightness or felt heavier dyspnea fever anorexia weakness fatigue tachycardia distressed upon exertion hurried respiration cyanosis with clubbing of fingers restricted movement on the affected side shift of mediastinum on the opposite side diminished expansion on the affected side cardiac apex is moved away from the fluid stony dullness over the effusion above the fluid level a high-pitched note may be elicited absent or diminished breath sound increase fremitus

dyspnea non-productive or productive cough* hemoptysis* dull or pleuritic chest pain chest tightness shortness of breath crackles upon auscultation fatigue anorexia weight loss persistent, long term low grade fever* chills and night sweats* anemia in some non-resolving bronchopneumonia

(Note: All highlighted words are the signs and symptoms that R.C. manifested as claimed; All signs and symptoms that has an asterisk (*) symbol was manifested by R.C. before and not already manifested during admission)