PATHOPHYSIOLOGY

Etiologic agents: Predisposing factors:

• Elderly
• streptococci • Hospitalization
• Immobilization
• pneumococci • Immune deficiency
• bacterium • Long term illness
• mycoplasma pneumonia • Secondhand smoke
• Exposure to
microorganism

Microorganism enter alveolar spaces

by droplet inhalation/aspiration

Inflammation occurs
(mucus,crackles)

Red hepatization and consolidation of Gray hepatization and

lung parenchyma deposition of fibrin on pleural
surfaces
Leukocyte infiltration

Alveolar sacs filled with

exudates

There is loss of air spaces and

replacement with fuid (consolidation)

bronchopneumonia

Complications: Signs and symptoms:

1.emphysema 1.cough with greenish or
Collection of pus and yellowish sputum
liquid from infected tissue) 2.fever
2.pleurisy 3.rapid,shallow breathing
(inflammation of membrance) 4.shortness of breath
3.lung abscess 5.loss of appetite(unable
(collection of pus, inflammation to breastfeed)
and desctruction of tissue)
Cancer of lungs
Narrative Pathophysiology:

Aspiration of orophayrngeal secretions is the most common route of lower respiratory

tract infection, thus nasopharynx and oropharynx constitute the first line of defense for
most infectious agents. Another route of infection is through the inhalation of
microorganisms that have been released into the air when an infected infected individual
coughs, sneezes or talks, or from aerololized water such as that from contaminated
respiratory equipment.

Inoculation of the respiratory tract by infectious organisms leads to acute inflammatory

response in the host that is typically 1-2 weeks in duration.This inflammatory response
differs according to the type of infectious agent present.

The alveoli fill with proteinaceous fluid, which triggers a brisk influx of red blood cells
and polymorphonuclear cells(red hepatization).

It will be followed b the deposition of fibrin and the degradation of inflammatory

cells( gray hepatization). During resolution,intra-alveolar debris is ingested and removed
by the alveolar macrophages. This consolidation leads to decreased air entry and dullness
to percussion. Inflammation in the small airways leads to crackles.

Inflammation and pulmonary edema resulting from these infections causes the lungs to
become stiff and less distensible, thereby decreasing tidal volume.

The patient must increase his respiratory rate to maintain adequate ventilation. Poorly
ventilated areas of the lung may remain well perfused,resulting in ventilation.perfusion
(v/q) mismatch and hypoxemia. Tachypnea and hypoxia are common.

Ventilation: is the amount of air in the alveoli.

Perfusion: is the amount of air in the pulmonary capillaries.
 The ratio between the ventilation and perfusion is called v/q ratio.
 Ventilation and perfusion must match closely as possible
 Normal v/q ratio is 4:5