Floral Effusion Patho 1z4j2v

I.

PATHOPHYSIOLOGY Microorganisms that produce pneumonia can end up in air sacs in several ways.

In some cases, people inhale microorganisms (which are present in tiny droplets) when they are near someone already infected. Spread in hospitals and nursing homes often occurs this way. More common among older people, however, is the presence of bacteria in their throat (colonization). These bacteria may remain there harmlessly or suddenly cause pneumonia if mucus or food is inhaled into the airway (aspiration) instead of ed into the esophagus. When aspiration occurs, the food or mucus can make its way into the lungs, carrying the bacteria from the throat along for the ride. Rarely, microorganisms from elsewhere in the body reach the lungs by traveling through the bloodstream. These are usually blood borne microorganisms that enter the pulmonary circulation and are trapped in the capillary bed, becoming a potential source of pneumonia. Pneumonia often affects both ventilation and diffusion. An inflammatory reaction can occur in the alveoli, producing an exudate that interferes with the diffusion of oxygen and carbon dioxide. White blood cells, mostly neutrophils, also migrate into the alveoli and fill the normally air-containing spaces. Areas of the lung are not adequately ventilated because of secretions and mucosal edema that cause partial occlusion of the bronchi or alveoli, with a resultant decrease in the alveolar oxygen tension. Because of hypoventilation, a ventilation-perfusion mismatch occurs in the affected area of the lung. Venous blood entering the pulmonary circulation es through the underventilated area and exits to the left side of the heart poorly oxygenated. The mixture of oxygenated and unoxygenated blood eventually results in arterial hypoxemia. Pleural effusion is an indicator of an underlying disease process that may be pulmonary or nonpulmonary in origin, acute or chronic. 

Normal pleural fluid has the following characteristics: o

Clear ultrafiltrate of plasma that originates from the parietal pleura

o

pH 7.60-7.64

o

Protein content less than 2% (1-2 g/dL)

o

Fewer than 1000 WBCs per cubic millimeter

o

Glucose content similar to that of plasma

o

Lactate dehydrogenase (LDH) less than 50% of plasma

o

Sodium, potassium, and calcium concentration similar to that of the interstitial fluid



The following mechanisms play a role in the formation of pleural effusion: o

Altered permeability of the pleural membranes (eg, inflammation, malignancy, pulmonary embolus)

o

Reduction in intravascular oncotic pressure (e.g., hypoalbuminemia, cirrhosis)

o

Increased capillary permeability or vascular disruption (e.g., trauma, malignancy,

inflammation,

infection,

pulmonary

infarction,

drug

hypersensitivity, uremia, pancreatitis) o

Increased capillary hydrostatic pressure in the systemic and/or pulmonary circulation (eg, congestive heart failure, superior vena cava syndrome)

o

Reduction of pressure in the pleural space, preventing full lung expansion (eg, extensive atelectasis, mesothelioma)

o

Decreased lymphatic drainage or complete blockage, including thoracic duct obstruction or rupture (eg, malignancy, trauma)

o

Increased peritoneal fluid, with migration across the diaphragm via the lymphatics or structural defect (eg, cirrhosis, peritoneal dialysis)

o

Movement of fluid from pulmonary edema across the visceral pleura

o

Persistent increase in pleural fluid oncotic pressure from an existing pleural effusion, causing further fluid accumulation

The net result of effusion formation is a flattening or inversion of the diaphragm, mechanical dissociation of the visceral and parietal pleura, and a restrictive ventilatory defect.

A. SCHEMATIC DIAGRAM Predisposing factor: >stress >exposure to polluted air >depressed cough reflex

Precipitating factor: >prolonged back rest >aspiration >inhaled microorganism (Bacteria) Inhalation of causative agents (CA): Streptococcus pneumoniae

Inhaled in the alveolus

Reproduction of CA in the lungs Activation of first line of defense S/sx: cough, mucus production

Partial occlusion of bronchus alveoli

Inflammation

Increased capillary permeability or vascular disruption

Exudates SIGNS AND SYMPTOMS:  Dyspnea  chest pain  decreased tactile fremitus  diminished or absent breath sounds  pleural friction rub during both inspiration and expiration  dry nonproductive cough  shortness of breath

Complication:  Atelectasis  Infection  hypoxemia

Pleural Effusion

Treated

Not treated

Prevents serious Complications

Metastasis of Complications

Recovery

Danger to health (serious)