Lung

• Alveoli – Exchange of gases occur
• Type I pneumocytes - covering 95% of the alveolar surface. Plate like-cells
• Type II cells synthesize surfactant - involved in the repair of alveolar damage through their ability to proliferate and give rise to type I cells.
• ATELECTASIS:

  Incomplete expansion of the lungs (neonatal atelectasis)

  • Collapse of previously inflated lung, and results in areas of poorly aerated pulmonary parenchyma.
• Resorption atelectasis - obstruction of an airway.
• Compression atelectasis - results whenever significant volumes of fluid (transudate, exudate, or blood), tumor, or air (pneumothorax) accumulate within the pleural cavity.
• Contraction atelectasis - occurs when focal or generalized pulmonary or pleural fibrosis prevents full lung expansion.
• Emphysema

  Centriacinar – most common, the central or proximal parts of the acini
• Emphysema

  Panacinar — α1-antitrypsin deficiency. acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli.
• Paraseptal - spontaneous pneumothorax. The proximal portion of the acinus is normal, and the distal part is predominantly involved.
• Irregular — The acinus is irregularly involved, is almost invariably associated with scarring.
• 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.
• The primary or initiating factor in the genesis of chronic bronchitis is exposure to noxious or irritating inhaled substances such as tobacco smoke
• ASTHMA

  Chronic airway inflammation and variable expiratory airflow obstruction that produces symptoms such as :

  • Wheezing

  • Shortness of breath • Chest tightness

  • Cough
• Atopic Asthma:

  • Begins in childhood and is triggered by environmental allergens.
  • IgE-mediated (type I) hypersensitivity reaction.
• Non-Atopic Asthma:

  • Individuals with non-atopic asthma do not have evidence of allergen sensitization.
  • Respiratory infections due to viruses (e.g., rhinovirus, parainfluenza virus, and respiratory syncytial virus) are common triggers
• Drug-Induced Asthma:

  • pharmacologic agents provoke asthma.
• BRONCHIECTASIS

  • Destruction of smooth muscle and elastic tissue by inflammation stemming from persistent or severe infections leads to permanent dilation of bronchi and bronchioles.
• Lobar pneumonia - Consolidation of a large portion of a lobe or of an entire lobe
• Bronchopneumonia - Patchy consolidation of the lung
• Congestion - the lung is heavy, boggy, and red.
• Red Hepatization – the lobe is red, firm, and airless, with a liver-like consistency, hence the name hepatization.
• Gray hepatization - Color change to grayish-brown
• Resolution - Exudate within the alveolar spaces is broken down by enzymatic digestion to produce granular, semifluid debris.
• Tuberculosis

  • Chronic pulmonary and systemic disease caused most often by M. tuberculosis.

  • Leading infectious cause of death worldwide.
• Ghon focus — Parenchymal lesion only
• Adenocarcinoma –

  invasive malignant epithelial tumor with glandular differentiation or mucin production by the tumor cells. Grow in various patterns, including acinar, lepidic, papillary, micropapillary, and solid
• Squamous cell carcinoma –

  more common in men and is strongly associated with smoking.

  Presence of keratinization and/or intercellular bridges. Keratinization may take the form of squamous pearls or individual cells with markedly eosinophilic cytoplasm.
• Small cell carcinoma –

  highly malignant tumor with a strong relationship to cigarette smoking.

  comprised of relatively small cells with scant cytoplasm, ill- defined cell borders.
• Large cell carcinoma -

  Undifferentiated malignant epithelial tumor that lacks the cytologic features of other forms of lung cancer.

  The cells typically have large nuclei, prominent nucleoli, and a moderate amount of cytoplasm