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What cells produce surfactant?
Type 2 pneumocytes.
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What distinguishes bronchioles from bronchi?
Lack of cartilage and submucosal glands.
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The bronchioles branch into?
Terminal bronchioles -> acini (respiratory bronchioles) -> alveolar ducts -> alveolar sacs.
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Which type of cell covers 95% of alveolar surface?
Type 1 pneumocyte (flattened, platelike).
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What are pores of Kohn?
Perforations through alveolar walls allowing for pasage of bacteria and exudates between alveoli.
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What is atelectasis?
- Collapse
- Loss of lung volume caused by inadequate expansion of airspaces.
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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).
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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.
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What is ARDS?
Progressive respiratory insufficiency.
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What causes Acute Respiratory Distress Syndrome (ARDS)?
Diffuse alveolar capillary and epithelial damage.
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What (macroscopically) causes ARDS?
- Sepsis
- Severe trauma
- Diffuse pulmonary infections.
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What is the name for the histologic manifestation of ARDS?
Diffuse alveolar damage.
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What two barriers form the alveolar capillary membrane?
- Microvascular endothelium
- Alveolar epithelium.
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What is thought of as the molecular basis of lung injury in ARDS?
Imbalance of pro and anti-inflammatory mediators.
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What is the likely candidate shifting the lung to an pro-inflammatory state?
NF-kB: Nuclear Factor kB, transcription factor usually tightly regulated.
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What are other chemotactic agents leading to lung injury in ARDS?
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What is the most characteristic (histologic) finding in the acute phase of ARDS?
Hyaline membranes lining distended alveolar ducts.
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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.
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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.
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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.
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Emphysema affects what part of the lungs?
The acini (respiratory bronchioles, alveolar ducts, alveoli).
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What characterizes emphysema?
- Abnormal permanent enlargement of airspaces
- destruction of walls without obvious fibrosis.
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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.
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What are the two imbalances implicated in the pathogenesis of emphysema?
- Protease-anti-protease imbalance: a1at
- Oxidant-antioxidant imbalance: ROS in cigarette smoke.
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What is usually the first symptom of emphysema?
Dyspnea.
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What is compensatory emphysema?
compensatory dilation of alveoli in response to loss of lung substance elsewhere (i.e. lung resection).
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What is mediastinal emphysema?
Entrance of air into mediastinum, interstitium, or subcutaneous tissue.
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What is the definition of chronic bronchitis?
A persistent productive cough for at least three consecutive months in at least two consecutive years.
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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.
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What is the distinctive feature of chronic bronchitis?
Mucus hypersecretion.
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What causes "small airway disease"?
- Goblet cell metaplasia -> mucus plugging of lumen, with inflammation and bronchiolar wall fibrosis
- Chronic bronchiolitis.
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What is the triad seen in asthma?
- intermittent and reversible airway obstruction
- chronic bronchial inflammation with eosinophils
- Smooth muscle hypertrophy and hyperreactivity.
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What is "airway remodelling"?
Changes in bronchial wall including hypertrophy of bronchial smooth muscle and depostion of subepithelial collagen.
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What is the most common type of asthma?
Atopic asthma.
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What does the acute response in asthma consist of?
- Bronchoconstriction
- Edema
- Mucus secretion.
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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.
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When does the late-phase reaction begin, how long does it last?
4-8 hours after initial insult, 12-24 or more hours.
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What cells are specifically important in the late-phase reaction?
Eosiniphils: amplify and sustain inflammatory response without additional exposure to antigen.
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What is bronchiectasis?
Permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic supporting tissue.
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Bronchiectasis is secondary to what?
Obstruction or chronic necrotizing infection.
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What is the hallmark of chronic restrictive diseases?
Decreased compliance.
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What is the usual endpoint of chronic restricitive diseases?
Diffuse interstitial pulmonary fibrosis, with or without honeycombing.
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