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What cells produce surfactant?
Type 2 pneumocytes.
What distinguishes bronchioles from bronchi?
Lack of cartilage and submucosal glands.
The bronchioles branch into?
Terminal bronchioles -> acini (respiratory bronchioles) -> alveolar ducts -> alveolar sacs.
Which type of cell covers 95% of alveolar surface?
Type 1 pneumocyte (flattened, platelike).
What are pores of Kohn?
Perforations through alveolar walls allowing for pasage of bacteria and exudates between alveoli.
What is atelectasis?
- Loss of lung volume caused by inadequate expansion of airspaces.
What are the three types of atelectasis?
- Resorption: airflow obstruction into lung
- Compression: accumulation of fluid, blood, air in pleural cavity
- Contraction: (cicatrization) fibrotic changes in lung or pleura (not reversible).
How does acute lung injury manifest?
- Acute onset of dyspnea
- Decreased arterial oxygen pressure (hypoxemia)
- Bilateral pulmonary infiltrates on cxr
- Absence of primary left heart failure.
What is ARDS?
Progressive respiratory insufficiency.
What causes Acute Respiratory Distress Syndrome (ARDS)?
Diffuse alveolar capillary and epithelial damage.
What (macroscopically) causes ARDS?
- Severe trauma
- Diffuse pulmonary infections.
What is the name for the histologic manifestation of ARDS?
Diffuse alveolar damage.
What two barriers form the alveolar capillary membrane?
- Microvascular endothelium
- Alveolar epithelium.
What is thought of as the molecular basis of lung injury in ARDS?
Imbalance of pro and anti-inflammatory mediators.
What is the likely candidate shifting the lung to an pro-inflammatory state?
NF-kB: Nuclear Factor kB, transcription factor usually tightly regulated.
What are other chemotactic agents leading to lung injury in ARDS?
What is the most characteristic (histologic) finding in the acute phase of ARDS?
Hyaline membranes lining distended alveolar ducts.
What are the two types of diffuse pulmonary diseases?
- Obstructive: limitation of air flow from and increase in resistance
- Restrictive: reduced expansion of lung parenchyma.
What TLC, FVC, FEV1, and FEV1/FVC do you expect in obstructive diseases?
- TLC: normal or increased
- FVC: normal or increased
- FEV1: Decreased
- FEV1/FVC: Decreased.
What TLC, FVC, FEV1, and FEV1/FVC do you expect in restrictive diseases?
- TLC: Decreased
- FVC: Decreased
- FEV1: normal or decreased proportionally
- FEV1/FVC: normal or near normal.
Emphysema affects what part of the lungs?
The acini (respiratory bronchioles, alveolar ducts, alveoli).
What characterizes emphysema?
- Abnormal permanent enlargement of airspaces
- destruction of walls without obvious fibrosis.
What are the four types of emphysema?
- Centriacinar: most common clinically significant, near apex
- Panacinar: a1at deficiency, lower lung zones
- Distal acinar: adjacent to pleura, fibrosis, scarring, atelectasis
- Irregular: associated with scarring, most common, though not clinically significant.
What are the two imbalances implicated in the pathogenesis of emphysema?
- Protease-anti-protease imbalance: a1at
- Oxidant-antioxidant imbalance: ROS in cigarette smoke.
What is usually the first symptom of emphysema?
What is compensatory emphysema?
compensatory dilation of alveoli in response to loss of lung substance elsewhere (i.e. lung resection).
What is mediastinal emphysema?
Entrance of air into mediastinum, interstitium, or subcutaneous tissue.
What is the definition of chronic bronchitis?
A persistent productive cough for at least three consecutive months in at least two consecutive years.
What are the three types of chronic bronchitis?
- Simple chronic bronchitis: productive cough with mucoid sputum but no obstruction of airflow
- Chronic asthmatic bronchitis: hyper-responsive airways with intermittent bronchospasm and wheezing
- Chronic obstructive bronchitis: chronic outflow obstruction with evidence of emphysema.
What is the distinctive feature of chronic bronchitis?
What causes "small airway disease"?
- Goblet cell metaplasia -> mucus plugging of lumen, with inflammation and bronchiolar wall fibrosis
- Chronic bronchiolitis.
What is the triad seen in asthma?
- intermittent and reversible airway obstruction
- chronic bronchial inflammation with eosinophils
- Smooth muscle hypertrophy and hyperreactivity.
What is "airway remodelling"?
Changes in bronchial wall including hypertrophy of bronchial smooth muscle and depostion of subepithelial collagen.
What is the most common type of asthma?
What does the acute response in asthma consist of?
- Mucus secretion.
what are some inflammatory mediators involved in the acute phase response?
- Leukotrienes C4, D4, E4: Bronchoconstriction, increased vascular permeability, mucin production
- Acetylcholine: smooth muscle constriction
- Histamine: bronchospasm
- Prostoglandin D2: bronchoconstriction and vasodilation
- Platelet activating factor: aggregation of platelets.
When does the late-phase reaction begin, how long does it last?
4-8 hours after initial insult, 12-24 or more hours.
What cells are specifically important in the late-phase reaction?
Eosiniphils: amplify and sustain inflammatory response without additional exposure to antigen.
What is bronchiectasis?
Permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic supporting tissue.
Bronchiectasis is secondary to what?
Obstruction or chronic necrotizing infection.
What is the hallmark of chronic restrictive diseases?
What is the usual endpoint of chronic restricitive diseases?
Diffuse interstitial pulmonary fibrosis, with or without honeycombing.