OBSTRUCTIVE PULMONARY DISEASE
Chronic obstructive pulmonary disease (COPD) is a general term used to indicatechronic decreased respiratory function due to chronic bronchitis or emphysema. Both diseases are associated with smoking.
Chronic bronchitis is a clinical diagnosis made when a patient has a persistent coughand copious sputum production for at least 3 months in 2 consecutive years. It is highly associated with smoking (90%). Clinical findings include cough, sputum production, dyspnea, frequent infections, hypoxia, cyanosis, and weight gain.
Microscopic examination demonstrates hypertrophy and hyperplasia of bronchial mucous glands (Reid index equals the submucosal gland thickness divided by the bronchial wall thickness between the pseudostratified columnar epithelium and the perichondrium; normal ratio is ≤0.4).
Complications include increased risk for recurrent infections; secondary pulmonary hypertension leading to right heart failure (cor pulmonale) and lung cancer.
Emphysema is the term used when destruction of alveolar septa results in enlargedair spaces and a loss of elastic recoil. The 4 types of emphysema are named for the anatomical distribution of the septal damage.
· In centrilobular emphysema, the damage is in the proximal portion of the acinus and the cause is cigarette smoking.
· In panacinar emphysema, the damage affects the entire acinus and the com-mon cause is alpha-1 antitrypsin deficiency.
· In distal acinar emphysema (unknown cause), extension to the pleura causes pneumothorax.
· In irregular emphysema, post-inflammatory scarring involves the acinus in an irregular distribution.
The etiology of emphysema involves a protease/antiprotease imbalance. On gross examination, the lungs are overinflated and enlarged, and have enlarged, grossly visible air spaces. Clinical findings include progressive dyspnea, pursing of lips and use of accessory respiratory muscles to breathe, barrel chest (increased anterior-posterior diameter), and weight loss.
Asthma is due to hyperreactive airways, which undergo episodic bronchospasmwhen triggered by certain stimuli.
· Atopic (type I IgE-mediated hypersensitivity reaction) asthma (most com-mon form) usually affects children and young adults. There is often a positive family history.
· Nonatopic asthma is triggered by processes including respiratory infections(usually viral), stress, exercise, or cold temperatures.
· Drug-induced asthma affects about 10% of adults with a diagnosis of asthma.Aspirin is a key example of a precipitating drug.
· Occupational asthma is caused by workplace triggers including fumes anddusts.
An asthma attack is characterized by wheezing, severe dyspnea, and coughing. Prob-lems with expiration cause lung overinflation. Status asthmaticus is a potentially fatal unrelenting attack of asthma.
Microscopic examination of sputum cytology may show Curschmann spirals (twisted mucus plugs admixed with sloughed epithelium), eosinophils, or Charcot-Leyden crystals (protein crystalloids from broken down eosinophils).
In patients dying from disease, autopsy findings include mucus plugs, increased mucous glands with goblet cell hyperplasia, inflammation (especially with eosino-phils), edema; hypertrophy and hyperplasia of bronchial wall smooth muscle, and thickened basement membranes.
Bronchiectasis is an abnormal permanent airway dilatation due to chronic necro-tizing inflammation. Clinical findings include cough, fever, malodorous purulent sputum, and dyspnea. Causes are diverse, and include bronchial obstruction by for-eign body, mucus, or tumor, necrotizing pneumonias, cystic fibrosis, and Kartagener syndrome.
· Kartagener syndrome is an autosomal recessive condition caused by immotilecilia due to a defect of dynein arms (primary ciliary dyskinesia). It is character-ized clinically by bronchiectasis, chronic sinusitis, and situs inversus (a con-genital condition where the major visceral organs are anatomically reversed compared with their normal anatomical positions).
On gross examination, bronchiectasis shows dilated bronchi and bronchioles extend-ing out to the pleura. These changes may also be appreciated on chest x-ray. Compli-cations include abscess, septic emboli, cor pulmonale, and secondary amyloidosis.
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