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174 Cards in this Set
- Front
- Back
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Where does oxygen exchange occur?
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from the alveoli and the pumonary capillaries
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Where does exchange of carbon dioxide and other metabolites occur?
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from the pulmonary capillaries to the alveoli
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Conducting System
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except for the vocal cords which are covered by stratifited squamous epi, the entire resp. tract is lined by pseudostratified, tall, columnar, ciliatd epi cells, heavily admixed with mucus secreting goblet cells
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Type I Alveoli
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-95% of surface
-thin and flat -participate in gas exchange |
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Type II Alveoli
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-5% of surface
-produce surfactant -multiply and differentiate into Type I if lung is injured |
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What is the function of the nose and trachea?
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-warm and humidify air
-trap particles >10um |
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What is the function of the mucociliary blanket?
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-dispse of particles 2-10um
-swallow and cough |
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What is the function of the alveolar macrophages?
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-engulf particles <2um
-smaller particles are exhaled |
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Atelectasis (collapse)
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-los of lung volume due to inadequate expansion of airspaces resulting in shunting of sub-optimally oxygenated blood from pulm. arterial system to veins
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What are the signs and symptoms of atelectasis?
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-surgery- postoperative pain
-preexisting lung diseases- asthma, pneumonia, etc. |
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What causes resorption atelectasis?
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obstruction that prevents air from reaching distal airways and residual air is resorbed and lung tissue collapses
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What are the causes of obstruction in the lung? (6)
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1. mucous plug
2. foreign bodies 3. blood clot post operatively 4. tumor 5. enlarged lymph nodes 6. vascular aneurysms |
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What causes a mucous plug? (4)
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1. post-op
2. bronchial asthma 3. bronchiectasis 4. chronic bronchitis |
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What are the 4 types of atelectasis based on underlying mechanism?
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1. resorption
2. compression 3. microatelectasis 4. contraction |
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Compression Atelectasis
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assoc. with accumulations of blook, fluid, or air within pleural space
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How does fluid usually get into the lung?
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secondary to pleural effusion secondary to CHF
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How does air usually get into the lung?
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pneumothorax
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Basal atelectasis
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elevated diaphragm seen in patient who are bedridden, have ascites, before and after surgery
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Contraction Atelectasis
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localized/generalized fibrosis hampers expansion
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Microatelectasis
(non-obstructive atelectasis) |
loss of lung expansion caused by complex events most result in loss of surfactant
-neonatal and adult RDS -interstitial inflamm. -post-surgical |
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Is atelectasis treatable?
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most are treatable EXCEPT contraction atelectasis
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What does treatment of atelectasis prevent?
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-hypoxemia
-superimposed infection |
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Obstructive Lung Disease
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Limitation of airflow due to partial or complete obstruction at any level
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What are the forms of obstructive lung disease? (5)
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1. asthma
2. emphysema 3. bronchitis 4. bronchiectasis 5. foreign body |
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What are the common causes of pulmonary congestion and edema? (3)
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1. left-sided heart failure
2. decreased oncotic pressure 3. microvasuclar disease |
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What are the clinical symptoms for pulmonary congestion and edema?
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SOB, dyspnea, wet rales
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What is the pathology of pulmonary congestion and edema?
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-capillary engorgement
-intra-alveolar precipitate -hemosiderin-laden macrophages -pneumonia complication |
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How is obstructive lung disease measured clinically?
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pulmonary function tests
-FEV decreased -FVC normal -ratio FEV/FVC <0.7 |
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Asthma
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episodic, reversible bronchospasm resulting from an exaggerated response to various stimuli
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What are the symptoms of asthma and who has it?
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-acute episodic dyspnea, cough and wheezing
-5% adults -7-10% children |
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Intrinsic Asthma
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normal IgE levels
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What are the nonimmune triggers for intrinsic asthma? (6)
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1. aspirin
2. pulmonary infections 3. cold 4. exercise 5. psychological stressors 6. chemical stressors |
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Extrinsic Asthma
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-elevated IgE levels buy may be other immunoglobulins
-hypersensitivity of the airways to a variety of inciting agents |
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What are the three types of extrinsic asthma?
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1. atopic asthma- IgE related asthma to foreign Ag
2. occupational asthma- immune reaction related to pneumoconiosis Ags (organic and inorganic dusts in the environment) 3. bronchopulmonary aspergilosis- IgE mediated asthma to fungal elements |
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What is the pathogenesis of extrinsic asthma?
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-inc. sensitivity to histamine and methacholine
-inflamm. in airways -inc. Th2 cells and get eosinophils and mast cells through production of IL-4,5,13 -divided into early and late phases |
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Early Phase Asthma
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mast cells release histamine which triggers increased inflammation through mucosal intercellular junctions
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Leukotrienes C4, D4 and E4
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increase mucin secretion
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Prostaglandins D2, E2 and F2a
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bronchoconstriciton and increased vascular permeability
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Histamine
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bronchospasm and inc. vascular permeability
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Platelet activating factor
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aggregation of platelets
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Mast cell tryptase
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inhibits normal bronchodilatory peptide
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What are the most important late phase cells?
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eosinophils
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What do eosinophils do?
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-release MBP and ECP which are directly toxic to lung epi cells
-relase peroxidase which causes tissue destruction -damage through oxidative stress -cycle of amplified and sustained inflammatory stress w/o additional exposure to triggering Ag |
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Late phase asthma
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cellular phase with recruitment of neutrophils, eosinophils, and basophils followed by lymphocytes
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Leukotriene B4
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chemotactic factors
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IL-4,5
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augment Th2 response
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What is chemotactic for eosinophils?
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platelet activation factor
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Tumor necrosis factor (TNFa)
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upregulates adhesion molecules on vascular endo
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What is the pathogenesis of intrinsic asthma?
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mediated through nonspecific inflamm. triggered in response to viral infections and noxious pollutants
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Respiratory Synctial Virus
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promotes secretion of Th2 cells which promote eosinophil chemotaxis in infants around 1st year of life
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What dominates asthma?
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mucus plugging
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What are the two histological finding of mucus?
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1. curschman spirals- mucus and shed epi
2. charcot-leyden crystals- crystallized eosinophil proteins |
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What is the treatment for asthma
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bronchdilators and corticosteroids- inhaled and systemic
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Status Asthmaticus
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severe asthma resistant to therapy
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What does long term asthma cause?
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hyperinflation of the affected lung with air trapping distal to the obstruction
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Chronic Obstructive Pulmonary Disease
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-affects 10% of US population and 4th leading cause of death
-defines both emphysema with chronic bronchitis -chronic irreversible lung injury -most common cause is smoking injury |
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Emphysema
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permanent enlargement of airspaces distal to the terminal bronchioles with destrcution of the alveolar walls
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Where is emphysema restricted to?
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lung acinus (the terminal bronchioles icluding resp. bronchiole, alveolar duct and alveolus)
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What are the three types of emphysema?
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1. centriacinar
2. panacinar 3. distal acinar |
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Centriacinar Emphysema
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central or proximal parts affected commonly cigarette smoking with apical lung portions more involved
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Panacinar Emphysema
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al parts of the acinus are affected commonly a1 antitrypsin deficiency with lower lungs more involved
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What typically results from a1 antitrypsin deficiency?
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panacinar emphysema
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Distal Acinar Emphysema
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distal parts affected commonly producing bullae distally in the subpleural lungs with spontaneous pneumothorax
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What is the pathogenesis of emphysema?
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current theory includes an imbalance between protease-antiprotease activity (a1 antitrypsin deficiency and smoking) and oxidant antioxidant activity (smoking)
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What genotype gives the deficiency of the enzyme a1 antitrypsin?
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PiZZ genotype
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TNFa and IL-8 attracts _______
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neutrophils
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What do neutrophils express?
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cellular elastic proteases normally sequestered with elastic tissue destruction
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What is the clinical course of emphysema?
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1. dyspnea with hyperventilation
2. weight loss 3. reduced FEV and normal FVC and reduced FEV1/FVC- prolonged expiration with less retention of CO2 4. barrel chest |
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What is the treatment for emphysema?
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bronchodilators, steroids, and oxygen
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How does death occur with emphysema?
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pulmonary failure with respiratory acidosis, recurrent infection, hypoxia, coma, and right sided heart failure (cor pulmonale) due to pulm. HTN
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Bronchitis is more common in _________ and ________
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male smokers
city dwellers |
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Bronchitis
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-cough >3 months in at least 2 conseecutive years
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What is the defining feature of bronchitis?
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-mucus hypersecretion with large bronchial involvement
-also inflamm, fibrosis, and resultant narrowing of the bronchioles |
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Compensatory emphysema
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compensatory dilatation of the alveoli in response to loss of lung (post surgery)
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Senile emphysema
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overdistended lung form age related alterations with no tissue destruction
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Obstructive overinflation
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air trapped within the lung by subtotal occlusion by tumor or foreign body
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Mediastinal emphysema
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entrance of air into connective tissue from violent coughing or emesis; whooping cough, respiratory injury
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What is chronic bronchitis almost always associated with?
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emphysema
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What do irritants produce in bronchitis?
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1. hypersecretion of mucus
2. hypertrophy of mucus glands 3. metaplastic formation of mucin secreting goblet cells in the bronchiole surface epi 4. inflamm. with CD8 cells, macrophages, and neutrophils |
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What is the histopathology of bronchitis? (5)
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1. Reid index
2. goblet cells 3. inflamm. infiltrate 4. squamous metaplasia 5. dysplasia of epi cells that may lead to bronchogenic carcinoma |
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Reid Index
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ratio of the thickness of submucosal gland layer to that of the bronchial wall
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What are the symptoms of bronchitis?
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chronic cough with productive sputum, hypercapnia (retention of CO2) with cyanosis, hypoxemia
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How do we treat bronchitis?
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bronchodilators and steroids
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How does death occur with bronchitis?
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respiratory acidosis, hypoxemia, coma recurrent infection, and pulmonary hypertension leading to right sided heart failure (cor pulmonale)
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Bronchiolitis
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small airway disease characterized by:
-goblet cell metaplasia -inflamm. -fibrosis -SM hypertrophy |
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Bronchiectasis
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permanent dilation of bronchi and bronchioles caused by destruciton of muscle and elastic supporting tissue from chronic infections
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What is bronchiectasis a secondary disease from?
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persistent infection due to obstruction by tumor, foreign bodies, or mucus plugging
-cough with copious sputus |
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Bronchiectasis may be caused by ______ and _______ diseases.
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congenital
hereditary |
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Cystic Fibrosis
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widespread bronchiectasis with resultant viscous mucus plugging obstruction, superimposed infection, and dilatation of the bronchi
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Immunoglobuling deficiency
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states with chronic infections
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Kartagener Syndrome
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recessive disorder frequently assoc. with bronchiectasis and sterility in males
-cilia abnormal -organs may be reverse |
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What is the pathogensis of bronchiectasis?
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-obstruction, chronic persistent infection
-normal clearance of mucus is hindered -chronic infection destroys elastic tissue and fibrosis leads to dilatation of the bronchial walls |
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Necrotizing pneumonias associated with _______ or ______ may predispose to bronchiectasis.
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S. aureus
Klebsiella sp. |
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What may lead to end stage bronchiectasis?
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tuberculosis
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What are the symptoms of bronchiectasis?
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-chronic cough with mucopurulent, fetid sputum
-hemoptysis in some cases -clubbing of the fingers |
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What is the treatment for bronchiectasis?
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-antibiotics for infection and treat underlying disease process
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How does death occur from bronchiectasis?
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hypoxemia, resp. acidosis, coma, pulm. HTN leading to rt. sided heart failure, embolic abscesses to the systemic circulation
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Restrictive Lung Disease
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characterized by reduced compliance (more pressure equired to expand the lung)
-changes affect alveoli and capillaries -fibrosis producing stiff lungs -can be acute or chronic |
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How are restrictive lung diseases diagnosed?
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by decreased FVC, CT scan of thorax and open lung biopsy
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What is the only acute restrictive lung disease?
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ARDS
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What are the five chronic restrictive lung disease?
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1. idiopathic pulmonary fibrosis (intersitial pneumonia or desquamative interstitial pnemonia)
2. sarcoidosis 3. hypersensitivity pneumonitis 4. asbestosis and silicosis 5. difuse alveolar hemorrhage syndromes |
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What is the pathogenesis of ARDS?
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-direct injury to the lung alvioli or indirect injury in the setting of a systemic process
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What is ARDS direct lung injury?
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-pneumonia
-aspiration of gastric contents |
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What is ARDS indirect lung injury?
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-sepsis
-severe shock due to trauma (blood loss) |
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ARDS
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acute lung injury that represents a continuum of progressive resp. failure
-acute dyspnea -dec. arterial oxygen -develop bilateral pulm. infiltrates -absence of lt. sided heart failure = non-cardiogenic pulm. edema |
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What is the histopatholgy of ARDS?
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-inc. permeability into the alveolus
-widespread surfactant loss -oxidation-antioxidation imbalance -activated neutrophils -hyaline membrane formation lining distended alveolar ducts |
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What intrinsic repair takes place with ARDS?
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-pulm. macrophages phagocytize hyaline membranes
-type II pneumocytes differentiate into type I pneumocytes |
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What is the outcome of intrinsic ARDS repair?
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results in marked distrotion of lung parenchyma leading to diffuse interstitial fibrosis with distorted airways (honeycomb lung)
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__% develop ARDS after acute insult within __hours.
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85
72 |
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What is the mortality rate of ARDS?
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30-40%
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What is associated with poor outcome in ARDS?
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high levels of IL1 and procollagen peptide III in BALs
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What is the treatment for ARDS?
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pressor support, ventilation, steroids, and treatment of underlying cause
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Chronic Interstitial Lung Disease
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progressive fibrosis of pulm. parenchyma (honeycomb lung)
-15% non-infectious lung processes |
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How do we diagnos chronic interstitial lung disease?
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dec. FVC with dec. FEV and ratio unchanged
-need to rule out occupational exposure |
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Idiopathic Pulmonary Fibrosis
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unknown etiology with resultant hypoxia and cyanosis
-male predominance -diagnosis of exclusion -soluble mediators attract inflammatory cells and produce fibrosis |
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What is the sequence of events for idiopathic pulmonary fibrosis?
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interstitial edema and accumulation of inflammatory cells leading to fibrosis and inflammation
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Usual Interstitial Pneumonia
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heterogenous appearance of normal lung admixed with fibrosed lung
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Desquamative Interstitial Pneumonia
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assoc. w/ smoking and hypersensitivity with resultant pulmonary fibrosis
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What is the clincical course and survival for idiopathic pulmonary fibrosis?
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-insidiousl, chronic onset of nonproducting cough, cyanosis, cor pulmonale, and peripheral edema
-mean survival 2-4yrs |
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What is the treatment for idiopathic pulmonary fibrosis?
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UIP- non-responsive to steroids
DIP- usually responds to steroids |
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Sarcoidosis
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multisystemic disease primarily affecting the lungs characterized by noncaseating, tight granulomas histologically
-must rule out TB and occupational lung disease |
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What is the pathogenesis of sarcoidosis?
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-immune regulated, genetically predisposed
-Th1 driven process to inc. T cells and monocytes w/in granuloma -anergy to candida and polyclonal hypergammaglobulinema -driven by unknown Ag |
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How do we diagnose sarcoidosis?
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-chest x-ray
-eye and sken involvement -black pop. and females more -higher prevalence in non-smokers -histology diagnosed |
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What is the histopathology of sarcoidosis?
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-noncaseating granulomas with central monocytes and rim of T cells, giant cells, asteroid bodies, schaumann bodies
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Asteroid Bodies
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stellate inclusions within giant cells, not specific for sarcoid
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Schaumann bodies
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laminated concretions of calcium and proteins
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Where and the granulomas found in sarcoidosis?
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-bronchiole connective tessue
-pulmonary venules -pleura |
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In sarcoidosis, granulomas can be found in the ______ 75% of the time and in the ______ 40% of the time.
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spleen
bone marrow |
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What is increased in a patient with sarcoidosis? (3)
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1. vitamin D
2. calcium 3. angiotensin converting enzyme |
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Mikulicz Syndrome
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combined eye and parotid involvement in sarcoidosis
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What is the treatment for sarcoidosis?
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steroids
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What is the mortality rate from progressive pulmonary fibrosis?
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10-15%
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What is the pathogenesis in hypersensitivity pneumonitis?
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bronchoalveolar lavage and blood specimens show:
-inc. inflamm. chemokines -inc. CD4 and CD8 -precipitating Ab. w/ complement activation -noncaseating granulomas |
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Hypersensitivity Pneumonitis
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-immunologically mediated inflammatory lung disease primarily affecting the alveoli (extrinsic allergic alveolitis)
-presents as restrictive process -occupational exposure |
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Pneumoconioses
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organic and inorganic dust syndromes
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What is the histopathology of hypersensitivity pneumonitis?
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-predominance of lymphocytes with plasma cells and epitheloid histiocytes
-interstitial noncaseating granulomas in 2/3 of specimens |
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What is a necessity when diagnosing hypersensitivity pneumonitis?
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clinical correlation with occupational exposure
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What does a diagnosis of hypersensitivity pneumonitis depend on?
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specific precipitating antibodies to environmental dust
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Asbestosis
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-a type of pneumoconiosis where exposure occurs in shipyards and industrial areas where asbestos was used
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What asbestos fibers cause disease?
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blue, brown and white
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Lung reacts to asbestos when the fibers reach the ______ and ______ and cause fibrous thickening in the lower lung.
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bronchioles
air sacs |
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What is the clinical course for asbestos exposure?
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dyspnea following exposure to inciting Ag dependent on temporal exposure to Ag w/ fever, cough and constitutional complaints
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What are the symptoms for asbestos?
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1. breathlessness w/ loss of elasticity
2. NO cough or chest pain 3. progressive dyspnea w/ weight loss 4. asbestosis predisposes to bronchogenic carcinomas and mesthelioma, a risk inc. by cigarette smoking |
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What are the most common forms of chrystalline silica?
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1. quartz
2. tridymite 3. cristobalite |
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Where does silica exposure occur?
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mining, quarrying, stone cutting, sand blasting, some foundries
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What happens when silica is inhaled?
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it enters the lungs and there become engulfed by macrophages in which are destroyed and liberate a fluid causing a localized fibrous nodule which will obliterate the air sacs
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What are the symptoms of silicosis?
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dry morning cough (initially), dyspnea with exercise, fever, weight loss, and bloody sputum
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What is the one form of pneumoconiosis that predisposes TB?
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silicosis
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Diffuse Alveolar Hemorrhage Syndrome
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primary disease not related to pneumonia, coagulation problems, or venous congestion
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What is the triad for diffuse alveolar hemorrhage syndrome?
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1. hemoptysis
2. anemia 3. diffuse pulm. infiltrates |
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What are the five types of diffuse alveolar hemorrhage syndrome?
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1. Goodpasture syndrome
2. idiopathic pulm. hemosiderosis 3. Wegner's granulomatosis 4. collagen vascular disorders 5. severe lung transplantation rejection |
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Idiopathic Pulm. Hemosiderosis
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-pulm. manifestatins similar to Good pasture syndrome in the lung
-no circulating anti-BM Ab in serum -usually milder presentation than Goodpasture syndrome with most spontaneously recovering |
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Goodpasture Syndrome
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-rapid concentric glomerulonephritis
-hemorrhagic interstitial pneumonitis -caused by Ab to the BM found in kidneys and lungs -progressive with most dying from disease |
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What does Goodpasture syndrom immunofluorescence detect?
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linear deposition of IgG, sometimes IgA and IgM in renal biopsy
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Wegener's Granulomatosis
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necrotizing granulomas attacking both pulm. arteries, bronchi, and rapid crescenteric glomeruonephritis
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What is the triad seen with Wegener's Granulomatosis?
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1. chronic sinusitis
2. pulm. symptoms 3. renal disease |
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What are the four collagen vascular disorders?
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1. SLE
2. rheumatoid arthritis 3. scleroderma 4. dermatomyositis-polymositis |
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Caplan syndrome
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accelerated rheumatoid arthritis and coal miner's lung pneumoconiosis
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What are the two vascular disorders of the lung?
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1. pulm. thromboembolism
2. pulm. HTN |
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Pulmonary Thromboembolism
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causes 50,000 deaths/yr from hemorrhage or infarction
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What is the transplant pathogenesis?
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1. lung susceptible to rejection and inflamm. destruction
2. chronicfejection targets airways and vessels leading to bronchiolitis obliterans 3. immunosuppression has decreased this disease in modern transplants |
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Bronchiolitis Obliterans
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progressive obliteration of bronchiolar lumina by fibrosis
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Pulmonary Thromboembolism
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more than 95% from deep leg veins of lower legs, especially popliteal veins
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What are the risk factors for pulm. thromboembolism? (6)
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1. prolonged bed rest
2. surgery on legs 3. severe trauma/burns 4. birth control pill and peripartum 5. factor V leiden hyperhomocysteinemia 6. disseminated cancer (Trousseau syndrome) |
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How does death occur from pulm. thromboembolism?
|
hypoxemia
-perfusion of lung zones that are atelectatic -dec. in CO causes differenc ein arterial-venous oxygen saturation -rt. to lt. shunting of blood through a patent foramen ovale |
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Saddle embolus
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large emboli that impact the bifurcation of large pulm. arteries causing rt. sided heart failure (cor pulmonale)
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What happens to the remainder of lung after thromboembolism?
|
infarction
-wedge shaped w/ base at pleural surface producing coagulative necrosis of the lung parenchyma and hemorrhage |
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Patients who have one pulm. embolus have a __% chance of having another.
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30
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What is the treatment for a pulm. thromboembolism?
|
anticoagulation w/ heparin and warfarin, Greenfield filter placement in the IVC
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What is the pathogenesis of pulmonary hypertension?
|
Unknown mechanism
1. vasospasm theory- Raynaud's phenomenon 2. inimal and medial thickening theory |
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What are the primary forms of pulmonary hypertension? (3)
|
1. plexiform pulmonary arteriopathy
2. thrombotic pulm. arteriopathy 3. pulm. venoocclusive disease |
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What are the secondary forms of pulmonary hypertension? (3)
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1. Cardiac- septal defects, lt. to rt. shunts, atrial myxoma, mitral stenosis
2. inflamm.- scleroderma, etc. 3. lung parenchymal disease- COPD, interstitial lung disease |
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What is the clinical course of pulmonary hypertension?
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progesses to hypoxemia, cor pulmonale, and sudden death
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What is the treatment for pulmonary hypertension?
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treat underlying disease if secondary, use oxygen and calcium channel blockers
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