system Pathology Respiratory

PATHOLOGY OF DISEASES OF THE RESPIRATORY SYSTEM

Atelectasis collapse of lung tissue ? an airless lung parenchyma. Inherited or acquired. ? Acquired atelectasis can be subdivided into: 1. Resorption (obstructive) atelectasis: consequence of complete obstruction of an airway ?resorption of the oxygen trapped in alveoli, without impairment of blood flow. (reversible) 2. Compression atelectasis: pleural cavity (partially or completely) filled by fluid exudates (pleural effusion), tumor, blood (h?mothorax), or air (pneumothorax). (reversible) 3. Contraction atelectasis: local or generalized fibrotic changes in the lung or pleura prevent full expansion. (irreversible)
Causes: 1. Hemodynamic: - ? hydrostatic pressure (? pulmonary venous pressure) •Left-sided heart failure (common) •Volume overload •Pulmonary vein obstruction - ? oncotic pressure (less common) •Hypoalbuminemia
Pulmonary Oedema
accumulation of excess fluid in the interstitial (extracellular) spaces of lung tissue (alveolar lumen) as transudate or noninflammatory fluid, Alveolar walls are thickened due to acute distention of capillaries and interstitial edema
- Shock, trauma - Radiation - Transfusion 3. Unknown: - High altitude - Neurogenic (CNS trauma)
2. Microvascular injury (alveolar injury): - Infections: pneumonia, septicemia - Inhaled gases: oxygen, smoke - Liquid aspiration: gastric contents - Drugs and chemicals (bleomycin, amphotericin B, heroin)
•Nephrotic syndrome •Liver disease •Protein-losing enteropathies - Lymphatic obstruction (rare)
Acute Respiratory Distress Syndrome (ARDS) and Diffuse Alveolar Damage (DAD) Clinical syndrome caused by diffuse alveolar capillary damage, with rapid onset of severe lifethreatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia refractory to oxygen therapy that may progress to extrapulmonary multisystem organ failure.

Causes: 1. Infection Viral, Mycoplasma, and Pneumocystis pneumonia; miliary tuberculosis , Gastric aspiration 2. Physical/Injury Mechanical trauma, Fractures with fat embolism, Burns, Ionizing radiation 3. Inhaled Irritants Oxygen toxicity, Smoke 4. Chemical Injury Heroin overdose, Acetylsalicylic acid, Barbiturate overdose 5. Hematologic Conditions Multiple transfusions, Disseminated intravascular coagulation



6. Pancreatitis 7. Uremia 8. Cardiopulmonary Bypass 9. Hypersensitivity Reactions Organic solvents, Drugs
Obstructive Pulmonary Diseases Include emphysema, chronic bronchitis, asthma, and bronchiectasis. Both emphysema and chronic bronchitis are often grouped together under the term "chronic obstructive pulmonary disease-COPD".
Clinical Term Anatomic Site
Major Pathologic Changes Etiology Signs/Symptoms
Chronic bronchitis
Bronchus Mucous gland hyperplasia, hypersecretion
Tobacco smoke, air pollutants
Cough, sputum production
Bronchiectasis Bronchus Airway dilation and scarring
Persistent or severe infections
Cough, purulent sputum, fever
Asthma Bronchus Smooth muscle hyperplasia, excess mucus, inflammation
Immunologic or undefined causes
Episodic wheezing, cough, dyspnœa
Emphysema Acinus (alveoli) Airspace enlargement; wall destruction
Tobacco smoke Dyspnœa
Condition of the lung characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis.
Emphysema
Four pathologic variants are recognized: centriacinar, panacinar (panlobular), distal acinar (paraseptal) and irregular. Death in most patients with is due to (1) respiratory acidosis and coma, (2) right-sided heart failure, and (3) massive collapse of the lungs secondary to pneumothorax. Treatment options include bronchodilators, steroids, bullectomy, and in selected patients, lung volume reduction surgery and lung transplantation. Chronic bronchitis persistent cough with sputum production for at least 3 months in at least 2 consecutive years, in the absence of any other identifiable cause. It is so common among habitual smokers and inhabitants of smog-laden cities.
When persistent for years, it may (1) progress to chronic obstructive airway disease, (2) lead to cor pulmonale and CHF (3) cause atypical metaplasia and dysplasia of the respiratory epithelium, with malignant transformation. The key pathological change is mucus hypersecretion caused by hyperplasia of submucous glands and goblet cells. Histologically: 1. Goblet cell metaplasia with mucus plugging of the lumen. 2. Clustering of alveolar macrophages. 3. Inflammatory infiltration. 4. Fibrosis of the bronchiolar wall. Asthma chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and/or in the early morning, usually associated with reversible bronchoconstriction and airflow limitation.