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276 Cards in this Set
- Front
- Back
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What accompanies the branching airways of the lungs?
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The pulmonary and bronchial arteries
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Bronchioles differ from bronchi with what?
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Bronchioles are:
1. of smaller caliber 2. lack cartilage. |
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The larynx, trachea, and bronchioles are lined by what?
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Pseudostratified, tell, columnar, ciliated epithelial cells
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The true vocal cords are covered by what?
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Stratified squamous epithelium
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Bronchial mucosa neuroendocrine cells release what?
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Neurosecretory-type granules that contain serotonin, calcitonin, and gastrin-releasing peptide (bombesin)
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Causes of neonatal pulmonary hypoplasia
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1. space occupying lesion in the uterus
2. oligohydramnios 3. impaired fetal respiratory movements |
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Congestion, interstitial edema, inflammation, fibrin deposition, and alveolar walls lined by hyaline membranes; type II pneumocytes may later proliferate
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ARDS w/ DAD
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Fibrin-rich edema fluid mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells
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Alveolar hyaline membrane
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What cell plays an important role in the pathogenisis of acute lung injury and ARDS?
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Neutrophils
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Oxidants, proteases, platelet-activating factor, and leukotrienes are released by what cell?
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Neutrophils
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Profound dyspnea and tachypnea; increasing cyanosis, hypoxemia, respiratory failure, diffuse bilateral infiltrates, unresponsive to oxygen therapy and respiratory acidosis are all typical of what condition?
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ARDS
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ARDS is classified as what kind of pulmonary disease?
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Acute restrictive disease
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Pneumoconioses, interstitial fibrosis, and most infiltrative conditions are what kind of pulmonary diseases?
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Chronic restrictive diseases
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Poliomyelitis, severe obesity, pleural disease, and kyphoscoliosis are considered what kind of pulmonary disease?
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Restrictive disease
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What percent of COPD patients are smokers?
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90%
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The main cell types associated with COPD
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Macrophages, CD8+ T lymphocytes, and neutrophils
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In the protease-antiprotease theory of alveolar wall destruction, what is the primary protease associated with this destruction?
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Elastase, secreted from neutrophils
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Alpha1-Antitrypsin is synthesized in what organ? And where is it usually present?
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Liver; usually present in serum, tissue fluids, and macrophages
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What is the most important therapeutic intervention in A1AT deficiency?
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Cessation of smoking
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Besides A1AT, what are other proteins with antielastase activity?
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1. secretory leuoprotease inhibitor in bronchial mucus
2. serum alpha1-macroglobulin |
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Besides neutrophils, what else releases elastases?
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macrophages, mast cells, pancreas, and bacteria
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What do neutrophils release that lead to elastolytic activity?
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Elastase and oxygen free radicals (which inhibit A1AT)
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Smoking acts as what in contributing to lung destruction in emphysema?
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1. nicotine as a chemoattractant for neutrophils and macrophages
2. smoke has reactive oxygen species |
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Normal defense to free radicals in the lungs?
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SOD, glutathione --> tobacco smoke depletes these
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What pattern of emphysema occurs in smokers?
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Centriacinar since smoke particles accumulate at the bifurcations of the respiratory bronchioles
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"Cough is often slight, overdistension is severe, diffusion capacity is low, and blood gas values are relatively normal at rest" exemplifies what condition?
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Severe emphysema
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Barrel-chested and dyspneic, prolonged expiration, sits forward in hunche-over position, breathes through pursed lips
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Emphysema
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Hx of recurrent infection, abundant purulent sputum, hypercapnea, and severe hypoxemia
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Chronic bronchitis
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Death in most patients with COPD
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1. respiratory acidosis and coma
2. right-sided heart failure 3. massive collpase of the lungs secondary to pneumothorax |
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Treatment options for COPD
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Bronchodilators, sterpoids, bullectomy, lung volume reduction surgery
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Clinical definition of COPD
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Persistent cough with sputum production for at least 3 months in at least 2 consecutive years
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Patients with a productive cough but no physiologic evidence of airflow obstruction
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Simple chronic emphysema
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Hyperreactive airways with intermittent bronchospasm and wheezing
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Chronic asthmatic bronchitis
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Earliest features of chronic bronchitis
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1. hypersecretion of mucus in large airways
2. hypertrophy of the submucosal glands in the trache and bronchi |
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Mucus hypersecretion in chronic bronchitis is stimulated by...
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...protease released from neutrophils, such as neutrophil elastase and cathepsin, and matrix metalloproteases.
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As chronic bronchitis persists, there is a marked increase in what kind of cells in which airways?
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Goblet cells in small bronchi and bronchioles
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Protective metaplastic reactions against tobacco smoke?
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increase in goblet cells and submucosal gland hypertrophy
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How does cigarette smoke predispose patients to infection?
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1. interferes wiuth ciliary action of the respiratory epithelium
2. cause direct damage to airway epithelium 3. inhibits the ability of bronchial and alveolar leukocytes to clear bacteria |
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Severe chronic bronchitis may present with obliteration of the airway lumen due to fibrosis. What is this called?
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Bronchiolitis obliterans
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Recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and/or in the early morning.
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Asthma
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Cells associated with asthma
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Eosinophils, mast cells, macrophages, T lymphocytes, neutrophils, and epithelial cells
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Type I hypersensitivity reaction induced by exposure to an extrinsic antigen (in the airways)
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Extrinsic asthma
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Non-immune mechanisms of asthma
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Intrinsic asthma:
1. ASA 2. pulmonary infections, esp. viral 3. cold 4. inhaled irritants 5. stress 6. exercise |
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What Ig often is at elevated levels in asthmatics?
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IgE
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High serum IgE levels, eosinophilia, and serum antibodies to Aspergillus
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Allergic bronchopulmonary aspergillosis where the fungus colonizes the bronchial mucosa
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What kind of CD4+ helper T cells are prominent in asthma?
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Th2 --> so that B lymphocytes produce IgE
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"Airway remodeling" in asthma
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1. hypertrophy of bronchial smooth muscle
2. deposition of subepithelial collagen = thickening of the basement memebrane 3. increase in submucosal glands 4. edema and an inflammatory infiltrate in the bronchial walls with mast cells and eosinophils |
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Mast cells release what?
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1. vasoactive mediators
2. cytokines 3. PDGF 4. proteases --> trigger smooth muscle proliferation |
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Common environmental antigens for atopic asthma
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Dusts, pollens, animal dander, and foods
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Th2 CD4+ helper T cells release what cytokines?
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IL-4 IgE, IL-5 eosinophils
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Acute asthma presents with...
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...bronchoconstriction, edema, mucus secretion, and, in extreme instances, hypotension
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Late-phase asthma presents with...
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...swarm of leukocytes (recruited from cytokines from mast cells), sp. eosinophils that cause epithelial damage and airway constriction via major basic protein.
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Bronchospasm of asthma occurs through...
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1. leukotriene C4, D4, and E4 --> causes prolonged bronchoconstriction and increased vascular permeability and increased mucus secretion
2. Acetylcholine, stimulate muscarinic receptors to vasoconstrict |
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1. leukotrienes
2. Ach 3. histamine (bronchoconstriction) 4. PGD2 (bronchoconstriction and vasodilation) 5. PAF (aggr. platelets, release histamine and 5-HT) |
Associated with asthma
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Rhinovirus and parainfluenza virus may trigger what?
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Nonatopic asthma where serum IgE's may be normal
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What histological features may appear in the mucus of an asthmatic?
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1. eosinophils
2. whorls of shed epithelium called Curschmann spirals 3. Chacot-Leyden crystals of eosinophil membrane protein |
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Airflow obstruction in asthma is due to...
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...muscular bronchoconstriction.
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Dyspnea, tachypnea, end-inspiratory crackles, and eventual cyanosis, without wheezing or other evidence of airway obstruction describes...
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...diffuse interstitial diseases.
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Reductions in CO diffusing capacity, lung volume, and compliance are classic physiologic features of...
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...diffuse interstitial diseases.
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End-stage interstitial lung diseases present with what gross finding?
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Honeycombing
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The most common infiltrative diseases are...
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1. environmental 25%
2. sarcoidosis 20% 3. idiopathic pulmonary fibrosis 15% 4. collagen vascular disease 10% 5. other random dz's 10% |
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The earliest manifestation of infiltrative interstitial disease is...
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...alveolitis, an accumulation of inflamatory and immune effector cells within the alveolar walls and spaces.
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What are the two consequences of alveolitis?
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1. accumulation of leukocytes distorts the normal alveolar structures
2. leukocytes release mediators that can injure parenchymal cells and stimulate fibrosis |
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Categories of chronic interstitial lung disease?
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1. fibrosing
2. granulomatous 3. eosinophilic 4. smoking-related 5. other |
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Name 4 fibrosing chronic interstitial lung diseases
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1. UIP/IPF
2. NSIP 3. COP 4. associated with collagen vascular diseases 5. pneumoconiosis 5. drug reactions 7. radiation pneumonitis |
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Name 2 granulomatous chronic interstitial lung diseases
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1. sarcoidosis
2. hypersensitivity pneumonitis |
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Name 2 smoking-related chronic insterstitial lung diseases
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1. DIP
2. respiratory bronchiolitis-associated interstitial lung disease |
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Beyond direct toxicity, what is the critical event in diffuse interstitial diseases?
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recruitment and activation of inflammatory and immune effector cells:
1. neutrophils caused by complement activation 2. alveolar macrophages that release IL-8 and leukotriene B4 to attract neutrophils |
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What histological pattern of fibrosis is required for the diagnosis of IPF?
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Usual interstitial pneumonia, which can also be seen in collagen vascular disease and asbestosis
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A rapidly progressuve type of IPF that is now considered a form of acute lung injury?
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Hamman-Rich syndrome = acute interstitial pneumonia
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Why is IPF no longer considered fibrosis as a result of chronic inflammation?
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Anti-inflammatory therapy has failed to provide much benefit
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What is IPF caused by?
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"Repeated cycles" of acute lung injury (alevolitis) by some unidentified agent
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What histological feature is characteristic of IPF?
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"Fibroblastic foci", which is would healing mediated by TGF-beta
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The inflammatory response of IPF is characterized by what kind of helper T response?
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Th2, which typically has eosinophils, mast cells, and FIBROSIS! as well as IL-4 and IL-13
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Hallmark of UIP?
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Patchy interstitial fibrosis with early lesions presenting with fibroblastic foci, later lesions being more collagenous
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Clinical course of IPF?
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Begins insidiously, gradually increasing dyspmea on exertion and dry cough, age 40-70, hypoxemia, cyanosis, and clubbing occur late in the course; gradual deterioration despite medical treatment (steroids, cyclophosphamide, or azathioprine). Mean survival = 3 years.
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Nonspecific Interstitial Pneumonia differs from IPF in what sense?
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It is also a diffure interstitial lung disease of unknown etiology with a biopsy that fails to be diagnostic of other interstitial diseases. Maybe of fibrosing pattern (diffuse, patchy, no fibroblastic foci) OR cellular pattern (better outcomes).
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Unknown etiology, cough, dyspnea, subpleural or peribronchial patchy areas of airspace consolidation, consisting of polypoid plugs of loose organizing connective tissue within alveolar ducts, alveoli, and bronchioles, no honeycombing, no interstitial fibrosis
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COP a.k.a. BOOP; treat with oral steroids for 6 months for complete recovery (but may recover spontaneously)
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Name 3 collagen vascular diseases
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1. SLE
2. rheumatoid arthritis 3. scleroderma (systemic sclerosis) 4. dermatomyositis-polymyositis 5. mixed connective tissue disease |
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In what patterns can collagen vascular diseases present in the lungs?
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1. NSIP (more common than UIP)
2. UIP-pattern 3. vascular sclerosis 4. organizing pneumonia 5. bronchiolitis (most common) |
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Pulmonary involvement in rheumatoid arthritis occurs in what possible four forms?
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1. chronic pleuritis
2. diffuse interstitial pneumonitis and fibrosis 3. intrapulmonary rheumatoid nodules 4. pulmonary hypertension |
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What is a pneumoconiosis?
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Non-neoplastic ling reaction to inhalation of mineral dusts encountered in the workplace
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The development of pneumoconiosis depends on what?
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1. amount of dust retained in lungs and airways
2. size, shape, and bouyancy of particles 3. particle solubility and physiochemical reactivity 4. additional effects of other irritants (concomitant tobacco exposure) |
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What may predispose one to the accumulation of dust?
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Any influence that affects the integrity of mucociliary apparatus like tobacco smoke or Kartegner's syndrome
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What's the difference between small dust particles and larger ones?
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Smaller particles are more likely to appear in pulmonary fluids and reach toxic levels (depending on solubility) while larger particles resist dissolution and remain in the lung parenchyma for years.
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Which pneumoconiosis is more likely to be fibrotic?
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Silicosis, where macrophages are triggered to release mediators to promote fibroblast proliferation and collagen deposition. Also asbestosis!
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Tobacco worsens the effects of all inhaled mineral dusts, especially...
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...asbestos.
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What are the three ways that Coal Workers' Pneumoconiosis may present?
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1. asymptomatic anthracosis
2. simple coal workers' pneumoconiosis with little to no pulmonary dysfunction 3. complicated CWP or progressive massive fibrosis |
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What contaminating dust in coal can favor progressive massive fibrosis?
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Silica dust, which tends to be more effective in recruiting macrophages than just coal dust
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Simple CWP is characterized by what gross findings?
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Coal macules (carbon laden macrophages) and larger coal nodules (with a network of collagen fibers)
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Which lobes of the lungs are most affected by CWP?
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Upper lobes and upper zones of the lower lobes, adjacent to respiratory bronchioles
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What kind of emphysema can CWP progress to?
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Centrilobular emphysema (smoking is centriacinar; A1AT def is panacinar)
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What is the most prevalent chronic occupational disease in the world?
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Silicosis
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How does silicosis usually present?
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Decades after exposure, as a slowly progressing nodular, fibrosing pneumoconiosis
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Silica comes in two forms. Name them and indicate which is more pathogenic.
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1. amorphous
2. crystalline (like quartz), which is more fibrogenic |
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Is silica toxic?
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Yes, it is toxic to macrophages. But before they succumb to the toxic effects, silica causes activation and release of mediators by viable macrophages such as IL-1, TNF, fibronection, lipid mediators, oxygen-derived free radicals, and fibrogenic cytokines (IL-13?)
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Silicosis presents where and like what in the lungs?
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Upper zones of lungs, hard, collagenous scars/nodules, eggshell calcification; sometimes there may also be TB
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When is silicosis often detected?
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With routine chest radiography of an asymptomatic worker with fine nodularity in the upper zones of the lungs with normal pulmonary function
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What bacterial infection is silicosis associated with?
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TB, due to a depression in cell-mediated immunity, which would present nodules of silicotuberculosis often displaying a central zone of caseation
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Name occupational asbestos related diseases in order of prevalence
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1. localized fibrous plaques or diffuse pleural fibrosis
2. pleural effusions 3. parenchymal interstitial fibrosis (asbestosis) 4. lung carcinoma (10 yrs to develop) 5. mesothelioma (25 yrs to develop) 6. laryngeal and other extrapulmonary neoplasms |
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What are the two geometric forms of asbestos?
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1. serpetine chrysotile
2. amphibole, which are more pathogenic based on aerodynamics and solubility with the longer, thinner fibers being more pathogenic, esp. with MESOTHELIOMA Both amphiboles and serpentines are fibrogenic and increasing dose is associated with increaced incidence of disease. |
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How does asbestos increase risks of cancer?
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Asbestos acts as a tumor initiator and tumor promoter
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What is the risk of lung cancer with asbestos exposure?
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Five fold increase risk of lung cancer with asbestos exposure; 55-fold increase in risk of lung cancer with asbestos and tobacco synergy
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Explain the morphology of asbestosis.
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Diffuse pulmonary interstitial fibrosis with the presence of asbestos bodies, coated with iron-containing proteinaceous material from macrophages = ferruginous bodies
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Where does asbestosis occur?
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Fibrosis occurs around respiratory bronchioles and alveolar ducts and adjacent alveoli in the lower lobes and subpleurally (vs. other silicosis and CWP which occur in upper lobes)
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What is the most common manifestation of asbestos exposure?
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Pleural plaques = well-circumscribed plaques of dense collagen, often calcified on parietal pleura, do not contain asbestos bodies
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With asbestos exposure, what is the risk of mesothelioma compared to the unexposed?
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1000-fold greater risk with asbestos exposure (normal risk is 2-17 per 1 million persons)
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What are the first manifestations of asbestos related disease?
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Dyspnea, especially with exertion, later cough with sputum, usually 10-20 years after initial exposure
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What are drugs that may cause lung disease?
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Bleomycin (pulmonary damage and fibrosis)
Amiodarone (5% of patients with ARDS, interstitial pneumonitis) Methotrexate (hypersensitivity pneumonitis) Aspirin (bronchospasm) Nitrofurantoin (hypersensitivity pneumonitis) |
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How does radiation-induced ling disease present?
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Acute radiation pneumonitis = fever, dyspnea, pleural effusion, and radiologic infiltrates; chronic radiation pneumonitis = leads to pulmonary fibrosis, appears like DAD
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Noncaseating granulomas in many tissues, bilateral hilar lymphadenopathy, eye and skin lesions, AA women
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Sarcoidosis
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What kind of immunological response is produced by sarcoidosis? What cytokines are produced?
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Cell mediated Th1 CD4+ helper T, with IL-2 and IFN-gamma; as well as, IL-8, TNF, macrophage inflammatory protein 1alpha --> form granduloma
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Anergy to Candida and PPD skin tests, hypergammaglobulinemia
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Sarcoidosis
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Schaumann bodies (laminated concentrations of Ca2+ and proteins), asteroid bodies (stellate inclusions within giant cells)
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Sarcoidosis
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Respiratory sx's of sarcoidosis
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Insidious onset of SOB, cough, chest pain, hemoptysis, fever, fatigue, wt loss, night sweats; CXR shows bilateral hilar lymphadenopathy
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What is the treatment for sarcoidosis?
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Steroids
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What is another name for hypersensitivity pneumonitis?
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Allergic alveolitis
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How does hypersensitivity pneumonitis differ from asthma?
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Asthma involves the bronchi and bronchioles while hypersensitivity pneumonitis involves the ALVEOLI
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Untreated hypersensitivity pneumonitis may progress to what?
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Chronic fibrotic lung dz
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Most common cause of hypersensitivity pneumonitis?
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Inhalation of organic dust containing antigens of spores of thermophilic bacteria (acintomyces), true fungi, animal proteins, or bacterial products
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Farmer's lung, pdgeon breeder's lung, and air-conditioner lung are all examples of what?
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Hypersensitivity pneumonitis
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Bronchoalveolar lavage specimens of a patient with hypersensitivity pneumonitis would produce what cells and what cytokines in the acute phase?
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MIP-1alpha, IL-8, both CD4+ and CD8+ lymphocytes
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What would suggest that hypersensitivity pneumonitis is a type II hypersensitivity?
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Immune complex hypersensitivities present with increased specific antibodies in serum
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Noncaseating granulomas found in what disease would indicate it is a type IV hypersensitivity (in addition to another hypersensitivity)?
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In hypersensitivity pneumonitis, which is a type III (immune complex) and type IV (delayed type) hypersensitivity
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What are three histological morphologies present in hypersensitivity pneumonitis?
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1. interstitial pneumonitis with lymphocytes, plasma cells, and macrophages
2. noncaseating granulomas 3. interstitial fibrosis and obliterative bronchiolitis in late stages |
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Acute hypersensitivity presents as what kind of disease according to PFTs?
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An acute restrictive disorder with diffuse infiltrates, dyspnea, cough, and leukocytosis
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Chronic hypersensitivity pneumonitis may produce what findings in PFTs?
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Decrease TLC and decreased compliance, similar to a restrictive chronic interstitial disease
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BAL more than 25% eosinophils, IL-5, fever, dypsnea, hypoxemic respiratory failure, diffuse infiltrates, responds to corticosteroids
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Eosinophilic pneumonia
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Desquamative intersitial pneumonia and respiratory bronchiolitis-associated interstitial lung disease are associated with what?
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Tobacco smoking
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DIP is characterized by large collections of what cells in the airspaces?
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Macrophages
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In the majority of cases, is DIP progressive and fibrosing?
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No, DIP is nonprogressive with minimal fibrosis
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What are the clinical features of a patient with DIP?
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Male smokers, insidious onset of dyspnea and dry cough for weeks or months, often clubbing, mild restrictive disorder on PFTs, good prognosis with response with steroid treatment and cessation of smoking; 100% survival!
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Respiratory bronchiolitis is associated with what histological finding?
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Pigmented intraluminal macrophages within the first- and second-order respiratory bronchioles
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Is RB-ILD a disease like DIP in being insidious onset?
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No, RB-ILD has a mild, gradual onset cough in male smokers with a 30 pack-years cigarette smoking hx
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Accumulation of acellular surfactant in the intra-alveolar and bronchiolar spoaces
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Pulmonary alveolar proteinosis
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Virchow's triad for thrombosis?
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1. hypercoaguability
2. endothelial injury 3. altered flow |
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Patients at risk of PE?
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1. hospitalized patients of trauma, burns, fractures
2. patients recovering from surgery 3. primary hypercoaguable states (factor V Leiden, prothrombin 20210, hyperhomocysteinemia, antiphospholipid syndrome) 4. secondary hypercoaguable states (obesity, recent surgery, cancer, oral contraceptive use, pregnancy) |
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What are the two pathophysiologic consequences of pulmonary embolus?
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1. respiratory compromise where V/Q approaches infinity
2. hemodynamic compromise where there is increased resistance to blood flow due to the obstruction |
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Large emboli at the bifurcation of the main pulmonary artery
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Saddle embolus
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Acute failure of the right side of the heart as a result of a large pulmonary embolus
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acute cor pulmonale
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What percent of emboli actual cause infarction and why?
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10% of emboli cause infarction since the lungs are supplied by two blood sources and only patients with underlying heart or lung disease tend to inadequately perfuse their lungs by the bronchial arterial source.
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Which lobes are most often affected by PE?
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3/4 of all infarcts occur in the lower lobes, and in more than half, there are multiple lesions; often wedge shaped infarct
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Septic infarcts differ from other infarcts in what sense?
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Normal infarcts will cause ischemic coagulative necrosis of lung substance while septic infarcts have a more intense neutrophilic embolus and have a more intense inflammatory reaction; septic infarcts may also produce abscess
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May mimic MI, sudden sever chest pain, dyspnea, shock, elevation of temperature, increase serum lactaic dehydrogenase
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Massive PE
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A pleural friction rub and fibrinous pleuritis is often found in what acute event?
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PE
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What are diagnostic tests for PE?
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Spiral CT angiography and D-dimer testing; chest radiograph may show a wedge-shaped infiltrate 12-36 hours after it occured
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In young patients, how may a PE resolve?
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After the initial insult, contraction and fibrinolysis may happen by itself, without intervention. However, unresolved PE over tme may lead to pulmonary hypertension, pulmonary vascular sclerosis, and chronic cor pulmonale.
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How to prevent PE?
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1. early ambulation post-op and postpartum patients
2. elastic stockings 3. graduated compression stockings 4. anti-coagulation in high risk patients 5. filter in IVC |
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Nonthrombotic forms of PE?
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1. air
2. bone marrow 3. fat 4. amniotic fluid 5. foreign bodies |
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Causes of pulmonary hypertension
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1. chronic obstructive or interstitial lung disease (COPD msot common)
2. congenital or acquired heart disease 3. recurrent thromboemboli 4. autoimmune disorders 5. idiopathic |
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Vasoconstriction in pulmonary hypertension may be mediated by what mediators?
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1. decreased prostacyclin
2. decreased NO 3. increased endothelin |
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Fenfluramine, phentermine (anti-obesity drugs), crotalaria spectabilis, and adulterated olive oil can all cause what disorder?
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Pulmonary hypertension
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Pulmonary hypertension presents with what histological features?
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Affects arterioles and small arteries; medial hypertrophy, intimal fibrosis, sometimes narrowing of lumina to pinpoint channels
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Primary pulmonary HTN or congenital heart disease may present with what feature in pulmonary HTN?
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Plexogenic pulmonary arteriopathy where a tuft of capillary formations span the lumens of dilated thin-walled, small, arteries
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Who is at greatest risk of pulmonary hypertension?
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Women between ages 20 to 40 years
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Severe respiratory distress, cyanosis, RV hypertrophy, and death from decompensated cor pulmonale
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Late stage pulmonary hypertension
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Treatment for pulmonary hypertension?
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With response to prostacyclin, CCBs have good prognosis; Other meds include inhaled NO, prostacyclin, endothelin receptor antagonist
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Causes of diffuse pulmonary hemorrhage?
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1. Goodpasture syndrome
2. idiopathic pulmonary hemosiderosis 3. vasculitis-associated hemorrhage, such as hypersensitivity angiitis, Wegner granulomatosis, lupus erythematosus |
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Autoantibodies targeting noncollagenous domain of the alpha-3 chain of collagen IV, which initiates an inflammatory destrxn of basement membrane in kidney glomeruli and lung alveoli
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Goodpasture syndrome
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Progressive glomerulonephritis and necrotizing hemorrhagic intersitial pneumonitis; death by uremia
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Goodpasture syndrome
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Goodpasture is more prevalent in men or women?
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Men in their teens or twenties
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Treatment for Goodpasture syndrome?
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Invasive plasma exchange and immunosuppression
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What general category of infections cause the majority of upper respiratory tract infections?
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Viruses
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Define pneumonia.
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Any infection of the lung parenchyma
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Name 3 mechanisms by which normal respiratory "clearing mechanisms" are compromised.
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1. loss or suppression of cough reflex, as a result of coma, anesthesia, neuromuscular disorders, drugs, or chest pain
2. injury of mucociliary apparatus, via cigarette smoke, inhalation of hot or corrosive gases, viral disease, Kartegener's 3. interference with phagocytic or bactericidal action of alveolar macrophages by alcohol, tobacco smoke, anoxia, or O2 tox 4. pulmonary congestion and edema 5. accumulation of secretions in conditions such as cystic fibrosis and bronchial obstruction |
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What defects can lead to increased incidence of infection with pyogenic bacteria?
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Defects in innate immunity (including neutrophil and complement defects) and humoral immunodeficiency
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Defects in cell-mediated immunity may lead to increases in what kinds of infections?
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Intracellular microbes, like mycobacteria and herpesvirus, as well as low virulence microorganisms, such as Pneumocystis jiroveci
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Viral influenza may predispose one to...
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...bacterial pneumonia.
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what are possible ways one may acquire pneumonias? (Portal of entry)
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1. respiratory tract
2. hematogenous spread from one organ to other organs |
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Top 3 CA acute pneumonias
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1. Strep pnemoniae
2. H flu 3. Moraxella catarrhalis 4. Staph aureus 5. Legionella pneumophila 6. Enterobacteriaeceae (Klebsiella) and Pseudomonas spp. |
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Top 3 CA atypical pneumonias
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1. Mycoplasma pneumoniae
2. Chlamydia spp. 3. Coxiella burnetti (Q fever) 4. Viruses: RSV, parainfluenza (children), influenza A and B (adults), adenovirus (military recruits), SARS virus |
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Top 3 nosocomial pneumonias
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1. Klebsiella
2. Serratia 3. E. coli 4. Pseudomonas 5. MRSA (Lots of gram-negatives) |
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Top 3 aspiration pneumonias
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There is really no top 3. Anaerobic oral flora + maybe some aerobic bacteria
Anaerobic bacteria = Bacteroides, Prevotella, Fusobacterium, Peptostrptococcus Aerobic bacteria = Strep pneumoniae, Staph aureus, H flu, and Pseudomonas |
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Top 3 chronic pneumonias
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1. Nocardia
2. Acintomyces 3. granulomatous pneumonias like TB, atypical mycobacteria, Histoplasma, Coccidioides immitis, Blastomyces dermatitidis |
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Top 3 necrotizing pneumonias/lung abscess bugs
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1. Anaerobic bacteria (extremely common)
2. Staph aureus 3. Klebsiella 4. Strep pyogenes 5. type 3 pneumococcus |
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Top 3 pneumonias in the immunocompromised
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1. Strep pneumoniae and the usual organisms
2. CMV 3. Pneumocystis jiroveci 4. MAC 5. Inv aspergillosis 6. Inv candidiasis |
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In CA pneumonias, bacterial infection of lung parenchyma causes what?
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Alveoli to be filled with an inflammatory exudate, causing consolidation of the pulmonary tissue = increased fremitus, dullness on percussion
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Extremes of age, chronic dz (COPD, CHF, and diabetes), congenital or acquired immune deficiencies, and decreased or absent splenic fxn (sickle cell or post splenectomy) increases risk of what?
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CA pneumonia (post-splenectomy puts pt at risk with encapsulated bacteria like pneumococcus)
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Most common CA acute pneumonia; sputum contains neutrophils, with Gram-positive, lancet-shaped diplococci
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Streptococcus pneumoniae, which is normal flora in 20% of adults, so false positives are very possible; blood culture is more specific and less sensitive than sputum
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Tx of pneumococcal pneumonias?
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Penicillin ro for resistant strains, ampicillin + beta-lactamase inhibitor (clavulanic acid, sulbactam, or tazobactam)
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Haemophilus influenzae is associated with what chronic respiratory disease?
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COPD
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Life-threatening acute lower respiratory tract infection and miningitis in young children?
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H. flu
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Where is H. flu found?
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It's a ubiquitous colonizer of the pharynx, existing 95% in its unencapsulated form (the encapsulated form can acutally secrete haemocin to kill the unencapsulated form)
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What kind of H. flu can be prevented via vaccine?
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The encapsulated b serotype via conjugated vaccines. The nonencapsulated forms are nontypable and can produce otitis media, sinusitis, and bronchopneumonia
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How does H. flu adhere to the respiratory epithelium? What other virulence factors does it have?
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Pili; IgA protease, capsule prevents opsonization by complement
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What is pneumonia from H. flu like?
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Usually lobular and patchy with airway obstruction of smaller bronchi (with dense, fibrin-rich exudate of neutrophils), consolidation; also may cause meningitis up to age 5; acute purulent conjunctivitis; septicemia in older patients
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CA bacterial pneumonia in the elderly, second most common bacterial cause fo acute exacerbation of COPD; in addition to Strep pneumonia, H flu, also causes otitis media in children
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Moraxella Catarrhalis
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Bacterial pneumonia following viral respiratory illness; complications such as lung abscess and empyema, IV drug abusers are at high risk of endocarditis
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Staphylococcus Aureus
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Most frequent Gram-neg bacterial pneumonia; debilitated and malnourished people, particularly chronic alcoholics; thick gelatinous sputum of the viscid capsular polysaccharide
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Klebsiella Pneumoniae
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Cystic fibrosis patients, patients who are neutropenic are predisposed to this CA bacterial pneumonia
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Pseudomonas Aeruginosa
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Epidemic, sporadic form of pneumonia; associated with Pontiac fever (self-limited upper respiratory tract infxn); floursishes in artificial aquatic environments, such as water cooling towers, humidifiers; transmission through inhalation of aerosolized organisms
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Legionella Pneumophila
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Patients with predisposing conditions such as cardiac, renal, immunologic, or hematologic; organ tranplant recipients; dx via antigens in urine or positive fluorescent antibody test on sputum samples
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Legionella Pneumophila
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Four stages of lobar pneumonia
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1. congestion
2. red hepatization 3. gray hepatisation 4. resolution |
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Lung is heavy, boggy, and red; vascular engorgement, intra-alveolar fluid with few neutrophils, presence of numerous bacteria
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Congestion
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Massive confluent exudation of red cells, neutrophils, fibrin filling the alveolar spacesl on gross exam, the love appears red, firm, and airless, with liver-like consistency
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Red hepatization
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Progressive disintegration of red cells and persistence of a fibrinosuppurative exudate, giving the fross appearance of a grayish brown, dry surface
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Gray hepatization
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Consolidated exudate within the alveolar spaces undergoes progressive enzymatic digestion to produce a granular, semifluid. debris that is resorbed, ingested by macrophages, coughed up, or organized by fibroblasts
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Resolution
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What are the two categories of pneumonia and how do they differ?
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1. lobar pneumonia, often with Strep pneumonia, where an entire lobe appears affected
2. lobular pneumonia, which can also be Strep pneumonia but there are many other etiologies; diffuse and patchy |
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What are 3 complications of pneumonia
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1. abscess formation with tissue destruction and ecrosis (often with type 2 pneumococci, Staph aureus, or Klebsiella infxn)
2. spread of the infxn to the pleural cavity, causing a intrapleural fibrinosuppurative reaction known as empyema 3. organziation of the exudate into solid tissue 4. dissemination |
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Abrupt onset of high fever, chills, cough of mucopurulent sputum, occasionally hemoptysis, with pleuritis - pleuritic pain and pleural friction rub
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Acute CA pneumonia
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After initiation of antibiotics, how quickly may symptoms disappear?
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Fever may decrease rapidly with few clinical signals after 48 to 72 hours
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Inflammatory changes in the lungs, largely confined to the alveolar septa and pulmonary interstitium; moderate amounts of sputum; no consolidation; moderate elevation of white cell count; lack of alveolar exudate
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CA atypical pneumonia (viral and mycoplasmal)
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Most common cause of atypical pneumonia?
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Mycoplasma
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Where do atypical pneumonias cause pathology? In the alveoler spaces or where?
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Predominatly in the interstitial walls of alveoli; the alveolar septa are widened and edematous; neutrophils in acute cases, macrophages in lymphocytes otherwise; diffuse alveolar damage like ARDS maay occur; superimposing bacterial infections may make dx more difficult
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Clearance of pneumonia by influenza virus is mainly via what kind of cells?
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CD8+ cytotoxic T cells
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In 60% of lung abscesses, what anaerobic organisms of the oral cavity may be found?
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Bacteroides, Fusobacterium, and Peptococcus
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Methods of introducing organisms to lungs to cause abscesses
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1. Aspiration of infective material
2. antecedent primary bacterial infection (post-pneumonic abcess via S. aureus, Klebsiella, or type 3 pneumococcus) 3. septic embolism 4. neoplasia with post-obstructive pneumonia 5. misc. such as traume, hematogenous seeding, cryptogenic |
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Copious amounts of fetid, green-black, death smelling vomit from a patient with chest pain on their right side
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Abscess?
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1. granulomatous disease of the lungs that may resemble TB
2. caused by fungi that are thermally dimorphic 3. geographic |
Histoplasmosis, blastomycosis, and coccidioidomycosis
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Cave dweller, soil contaminated with bird or bat droppings, intracellular parasite of macrophages, small spores, lung apices, extrapulmonary sites (mediastinum, lover, adrenals, or meninges), disseminated in immunosuppressed
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Histoplasma capsulatum = Ohio and Mississippi River Valleys
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The fungus expresses HSP60 and bings to beta-2 integrins on macrophages. Secretes IFN-gamma to activate macrophages and induces macrophages to secrete TNF to recruit more macrophages.
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Histoplasmosis
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Concentric calcifications around granulomas; intracellular yeast stained with methenamine silver; may persist in tissues for years; apices of lungs
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Histoplasmosis
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Soil inhabiting; dimorphic fungus; central and south eastern US; pulmonary form is an abrupt illness with productive cough, headache, wt loss, fever, abdominal pain, nt sweats, chills, and anorexia; lobar consolidation, multilobular infiltrate, perihilar infiltrates, multiple nodules, or miliary infiltrates; suppuratuve granulomas; broad-based budding
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Blastomycosis
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Soutwestern US; primary infections are asymptomatic; within macropahges, non-budding spherules 20-60 microns in diameter, often filled with small endospores
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Coccidioidomycosis
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<200 cells/mm3 in AIDS
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Pneumocystis jiroveci
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<50 cells/mm3 in AIDS
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CMV and MAC
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>200 cells/mm3 in AIDS
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Any bacterial and tubercular infection
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Most common pneumonia in AIDS pt?
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The usual, Strep pneumoniae
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How do you treat PCP (Pneumocystis jiroveci pneumonia)?
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Bactrim (TMP-SMZ)
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5-year survival rate for all lung cancers is...
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...15%.
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87% of lung carcinomas occur in...
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...active smokers.
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The frequency of lung cancer is associated with
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1. amount of daily smoking
2. tendency to inhale 3. duration of the smoking habit |
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What effect does cessation of smoking have on lung cancer risk?
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Cessation fo smoking for 10 years reduces risk but never to control evels.
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Do cigar smoking, pipe smoking, and cigarette smoking all carry the same risk?
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No, cigarette smoking carries a greater risk of lung cancer.
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What is the normal progression to invasive carcinoma?
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1. squamous metaplasia
2. squamous dysplasia 3. carcinoma in situ 4. invasive carcinoma |
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What roles do substance in tobacco cigarettes play in the development of cancer?
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1. initiators like polycyclic aromatic hydrocarbons
2. promoters like phenol derivatives |
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What industrial hazards are associated with an increased risk of lung cancer?
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1. high-dosing ionization radiation, such as with uranium miners who have a 4 times increased risk of lung cancer compared to the general population
2. Exposure to asbestos increases of risks of lung cancer (synergistic with smoking) and mesothelioma |
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What indoor air pollutant is associated with increased risk of lung cancer?
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Radon
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What is a common genetic mutation that occurs in small cell and non-small cell carcinomas?
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p53 mutation
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What are the most common bronchogenic cancers?
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1. adenocarcinoma
2. squamous cell carcinoma 3. small cell carcinoma 4. large cell carcinoma |
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What is the most common form of lung cancer in women?
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Adenocarcinoma, which has increased in incidence in the last two decades
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What lung cancer is most often metastatic and has high initial response to chemotherapy?
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Small cell carcinomas
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What group of lung cancer is less often metastatic and less responsive to chemotherapy?
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Non-small cell carcinoma
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What are the most common locations outside the lungs for lung cancer to metastasize to?
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1. adrenals
2. liver 3. brain 4. bone |
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What lung cancer is more commonly found in men, closely correlated with a hx of smoking, and is characterized by "keratin pearls", "intracellular bridges", p53 mutations, and overexpression of EGFR?
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Squamous cell carcinoma
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What lung cancer is a malignant epithelial tumor with glandular differentiation or mucin production? Most common lung cancer in women and nonsmokers; peripherally located and smaller; grow slower than squamous cell carcinoma; less frequently associated with a hx of smoking.
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Adenocarcinoma
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Lung cancer occuring in the pulmonary parenchyma in the terminal bronchioloaveolar regions, in the periphery, and may present with multiple diffuse nodules. Mucinous, lepidic.
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Bronchioloalveolar carcinoma as a sub-category of adenocarcinomas
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Highly malignant; small epithelial cells with scant cytoplasm, ill-defined cell borders, finely granular nuclear chromatin (salt and pepper pattern), and absent or inconspicuous nucleolus; cells grow in clusters; necrosis is common and extensive; high grade; dense-core neurosecretory granules in neuroendocrin argentaffin/Kulchitsky cells; associated with inappropriate ADH and ACTH secretion; strong relationship to cigarette smoking; metastasize widely
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Small cell carcinoma
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Malignant epithelial carcinoma, undifferentiated; large cell neuroendocrine carcinoma
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Large cell carcinoma
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Superior vena cava syndrome
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When a lung tumor causes compression of the SVC and cause venous congestion, dusky head and arm edema, and circulatory compromise.
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What lung cancer is associated with cavitation/abscess?
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Squamous cell carcinoma
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Common presentation of pt's with lung cancer
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1. cough 75%
2. weight loss 40% 3. chest pain 40% 4. dyspnea 20% |
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Are bronchioalveolar carcinomas invasive?
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No, they are by definition noninvasive and do not metstasize. However, they do kill by suffocation.
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Which two lung cancers tend to remain localized longer and have a better prognosis than undifferentiated ones?
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Squamous cell carcinoma and adenocarcinoma
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For which lung cancer is resection not an option? What is survival estimates like for this cancer?
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Small cell carcinoma, which untreated, has a survival time of 6 to 17 weeks. With radiation and chemotherapy, suvival after diagnosis is about 1 year.
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What paraneoplastic syndrome is associated with squamous cell carcinoma?
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Inappropriate production of PTH, which causes hypercalcemia
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What paraneoplastic syndromes are associated with small cell carcinoma?
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1. Inappropriate ADH syndrome,
2. A Cushing-oid syndrome with inappropriate ACTH secretion 3. Lambert-Eaton syndrome |
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A single tumor found of less than 3 cm without metastasis to nodes or other sites would be what stage?
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Stage I
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Any tumor with distant metastasis would be of what stage?
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Stage IV
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Horner's syndrome and pain in the ulnar distribution due to an apical cancer is called what?
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Pancoast syndrome
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Neuoendocrine tumor; central tumors with a finger-like or polypoid appearance projecting into the lumen of the bronchus; releases vasoactive amines; diarrhea, flushing, and cyanosis
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Carcinoid tumor
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What paraneoplastic syndromes are associated with small cell carcinoma?
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1. Inappropriate ADH syndrome,
2. A Cushing-oid syndrome with inappropriate ACTH secretion 3. Lambert-Eaton syndrome |
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A single tumor found of less than 3 cm without metastasis to nodes or other sites would be what stage?
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Stage I
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Any tumor with distant metastasis would be of what stage?
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Stage IV
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Horner's syndrome and pain in the ulnar distribution due to an apical cancer is called what?
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Pancoast syndrome
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Neuoendocrine tumor; central tumors with a finger-like or polypoid appearance projecting into the lumen of the bronchus; releases vasoactive amines; diarrhea, flushing, and cyanosis
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Carcinoid tumor
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Incidental, rounded focus of radio-opacity (coin lesion); peripheral, soliatry, less than 4 cm in diameterl benign
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Hamartoma
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Multiple discrete nodules (cannonball lesions) scattered throughout all lobes; growths everywhere
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Metastatic cancer to the lungs
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What is the most common manifestation of both primary and secondary pleural disease?
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Pleural effusion
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Increased pleural fluid can be due to...
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1. increased hydrostatic pressure (CHF)
2. increased vascular permeability (pneumonia, sepsis) 3. decreased osmotic pressure (nephrotic syndrome, liver disease, malnutrition) 4. increased intrapleural negative pressure (atelectasis) 5. decreased lymphatic drainage (mediastinal carcinomatosis) |
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Inflammatory disease within the lungs such as TB, pneumonia, ling infarcts, lung abscess, and bronchiectasis can all cause what?
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Yes, dyspnea, but also pleuritis
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What is empyema?
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A purulent pleural exudate, usually resulting from bacterial or mycotic seeding of the pleural space. Empyema is usually a loculated, yellow-green, creamy pus composed of masses of neutrophils admixed with other leukocytes.
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Hemorrhagic diatheses, rickettsial diseases and neoplastic involvement of the pleural cavity can produce what bloody mess?
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Hemmorrhagic pleuritis with a sanguineous inflammatory exudate
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What is the most common cause of hydrothorax, which is a noninflammatory collection of serous fluid within the serous cavity?
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Cardiac failure, which usually presents with bilateral hydrothorax (essentiall a transudate, I think)
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What may cause hemothorax?
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Aortic aneurysm or vascular trauma
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What is chylothorax and where is it most commonly found?
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An accumulation of milky fluid, usually of lymphatic origin, of finely emulsified fats. Chylothorax is most often ont he left side from thoracic duct trauma or obstruction
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Air or gas in the pleural cavity is called what?
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Pneumothorax
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Pneumothorax is most commonly associated with...
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...emphysema, asthma, and TB.
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Tension pneumothorax refers to what?
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Pneumothorax with some one way valve mechanism to cause increased pressure in the collapsed lung and dangerous compression of mediastinal structures and the contralateral lung.
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Mesothelioma is associated with what what potential causes?
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Shipyards, asbestos, old bioldings
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What is the latent period before mesothelioma presents after exposure?
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25-45 years
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Is there a link between smoking and mesothelioma?
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No, only asbestos increases risk of mesothelioma.
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What can you expect to find in the lungs of a patient with mesothelioma?
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Asbestos/ferruginous bodies, asbestos plaques
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These features favor what dx?
1. positive staining for acid mucopolysaccharide 2. lack of staining for carcinoemryonic antigen 3. strong staining for keratin proteins 4. positive staining for calretinin, Wilms timor 1 product, cytokeratin, mesothelin 5. EM showing presence of long microvilli and abundant tonofilaments but absent microvillous rootlets and lamellar bodies |
Mesothelioma
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What is the gold standard in dx of mesothelioma?
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Long, slender microvilli (numerous) via electron microscopy
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What is the clinical course of a patient dx'ed with mesothelioma?
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Chest pain, dyspnea, recurrent pleural effusions, hx of pulmonary asbestosis, metastatic spread to hilar lymph nodes and liver; death within 12 mo's (50% of pt's)
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