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73 Cards in this Set

  • Front
  • Back
Lining of a normal bronchus
Pseudostratified columnar epithelium
Abnormalities of alveoli
1. Visible endothelial cells
2. More than one layer of RBCs
3. Expansion of walls
4. Loss of room architecture
5. Visible alveolar cells
6. Anything in the lumens
Defense mechanisms of the lung
1. Brain
2. Free flowing body fluids
3. Mucociliary elevator
4. Phagocytosis (activation of neutrophils and macrophages, is of course, by itself a problem)
5. Immune system
6. Neurologic
Effect of a tracheoesophageal fistula and esophageal origin of bronchus
Cyanosis when feeding
Bronchopulmonary sequestration
Lobes/segments lacking normal communication with bronchial tree (abnormal vasculature is common).
2 types - extralobar and intralobar.
Extralobar bronchopulmonary sequestration (has its own pleura because it is external to the lung)
Congenital anomaly-diaphragmatic defect, pectus excavatum, and vascular malformations. Presents at less than 6 mos, M:F is 4:1.
Intralobar bronchopulmonary sequestration)
Acquired by repeated pneumonias, anyone can get it, 50% are over the ag of 20. Usually fed by systemic arterial system but dump into the pulmonary veins. 10% can have associated anomalies.
Problems with bronchopulmonary sequestration
1. Pneumonia/cough
2. Hypoplasia of other lung
3. Compression of normal lung
4. Abnormal x-ray
5. Cyanosis, feeding difficulty.
Bronchogenic cysts
Extra buds of the foregut during development.
Problem with bronchogenic cysts
1. Infxn
2. Rupture
3. Compression of normal lung
Bronchial atresia
Abnormal closure or absence of a bronchus. Causes overinflation of adjacent area. Can cause recurrent pneumonia, common in left upper lobe.
Effects of vascular pulmonary malformations
Dilated blood vessels due to abnormal communication. Causes cyanosis, dyspnea, failure of normal lung development, hemoptysis, hemothorax.
Osler-Weber-Rendu syndrome
Hereditary hemorrhagic telangiectasia. AD, many mucosal abnormal vascular connections
Septal deviation
Nasal blockage that can lead to infection. Congenital or acquired.
Uncomplicated obstructive lung disease: definition
Lung is enlarged and rate of airflow is reduced.
Histology of emphysema
Expanded alveoli, loss of rooms, thickened pink (hyaline) walls, and decreased vasculature.
2 patterns of obstructive disease
1. Hyperinflation
2. Focal alectasis with adjacent compensatory hyperinflation.
Abnormal, permanent enlargement of airspaces (alveoli) where the alveolar walls are destroyed but not fibrotic.
Normal behavior of alveoli and bronchioles in relation to air flow
1. Elastic network and chest pressure collapse alveoli uniformly on beginning of exhalation.
2. Due to shared walls the collapse opens bronchioles, allowing all air to escape.
Abnormal (emphysema) behavior of alveoli and bronchioles in relation to air flow
1. Lack of alveolar elasticity means they do not close uniformly.
2. Open alveoli crush the bronchioles closed as the chest compresses
3. Air does not escape from either the damaged portion or adjacent normal alveoli
Is the amount of air in the lungs after expiration increased or decreased in uncomplicated emphysema?
Five types of emphysema
1. Centracinar: upper lobes, heavy smokers, chronic bronchitis
2. Panacinar: alpha-1-antitrypsin deficiency
3. Paraseptal (bullous): near pleura, causing fibrosis and pneumothorax
4. Irregular: caused by scarring
5. Interstitial: trauma, obstruction, ventilation
How does smoking contribute to emphysema?
1. Tobacco promotes formation of reactive oxygen species, which themselves damage tissue and recruit neutrophils via IL-8, LTB4, and TNF
2. The radicals inactivate alpha-1-antitrypsin, such that neutrophilic products are not broken down
3. The high levels of neutrophilic elastase damage tissue
4. Alveolar macrophages attempting to clear damaged tissue and foreign objects will make more elastase and metalloproteinases (remodeling proteins) that contribute to alveolar disfunction.
What is the key ratio to consider when talking about emphysemal damage?
The protease (elastase)-antiprotease (alpha-1-antitrypsin) ratio. Not enough antiproteases allow inflammatory proteases to continually damage tissue.
What will the alveoli look like on gross examination of emphysema?
Dilated. The larger the dilation, the greater the loss of surface area for gas exchange (think of how many folds there are in a deflated balloon, and then the tension in an inflated one)
Microscopic hallmark of emphysema
Enlarged alveolar spaces lined by slightly thickened alveolar walls with thin fibrosis and relative avascularity. INFOLDING WILL BE LOST, AND SO WILL SURFACE AREA.
Dilated alveoli with thin walls and NO FIBROSIS due to loss of intrinsic elasticity.
Compensatory hyperinflation
Caused by focal atelectasis (collapse) so that other portions must hyperinflate to compensate.
Obstructive hyperinflation
When the gas cannot leave. It can be congenital, there can be a blockage in the lumen, etc.
How can you tell the difference between emphysema and hyperinflation?
Hyperinflation does not involve an inflammatory, fibrotic process. The walls just lose their stretch, not their basic structure.
Is there a pathologic definition for chronic bronchitis?
No, it is clinical.
Clinical definition of chronic bronchitis
Persistent productive cough for at least three months in at least two years.
How is chronic bronchitis different from emphysema?
For one, the lung involvement is widespread and almost immediate. Chronic bronchitis is also the compensatory response against irritation, IT IS NOT A CAUSE.
What is the disease process in chronic bronchitis?
Resistance to airflow due to clogged bronchial tree either by inflammatory corrosion or by mechanical obstruction. Work of breathing must increase to maintain normal rate.
Gross appearances of bronchitis
1. Change in mucosal color
2. Mucus plugs, mucus!!
3. Thickened, narrowed lumens.
Microscopic appearance of bronchitis
1. Curschmann spiral: mucus shape cast in the shape of lumen .
2. Increase in size and number of mucous glands.
3. Increased goblet cells.
4. Decreased serous glands
Etiology of bronchitis
1. Chronic irritation
2. Infection: does NOT CAUSE, but can aggravate.
Sequelae of chronic bronchitis
1. COPD (when you add emphysema to the mix)
2. Cor pulmonale/cyanosis
3. Carcinoma (if smoking is a cause)
4. Bronchiectasis
5. COP
6. Fistulas
7. Chronic infection
Bronchiestasis: definition
Permanent abnormal dilatation of the bronchial tree. You should not be able to see bronchi close to the pleural surface. If you can, then you have this condition.
3 types of bronchiectasis
1. Saccular
2. Varicose
3. Cylindrical
Clinical appearance of bronchiectasis
Paroxysms of coughing, copious nasty pus-y sputum, hemoptysis, dyspnea.
Etiology of bronchiectasis
Bottom line: obstruction and infection.
Sequelae of bronchiectasis
1. Obstruction (bronchi are too wide!)
2. Fistulas/pleurisy
3. Cor pulmonale
4. Metastases
5. Amyloidosis
7. Chronic infection
Types of asthma
1. Atopic: don't forget aspergillus
2. Nonatopic (asthmatic bronchitis)
3. Drug-induced
4. Occupational
Pulmonary hypoplasia
defective development of both lungs (one may be more affected than the other) resulting in decreased weight, volume, and acini
Foregut cysts
abnormal detachment of primitive foregut and are most often located in the hilum or middle mediastinum
How do you repair foregut cysts?
Surgical resection is curative.
Pulmonary sequestration
a discrete mass of lung tissue without any normal connection to the airway system
incomplete expansion of the lungs (neonatal atelectasis) or to the collapse of previously inflated lung
3 types: resorption (or obstruction), compression, and contraction atelectasis
Resorption atelectasis
1. consequence of complete obstruction of an airway,
2. mediastinum shifts toward the atelectatic lung
3. caused principally by excessive secretions
Compression atelectasis
1. Something in the pleural cavity compresses the lung
2. Can be due to pneumothorax
3.most commonly encountered in patients with cardiac failure
4. Mediastinum shifts away from atelectic lung
Contraction atelectasis
local or generalized fibrotic changes prevent full expansion of the lung
Is atelectasis reversible?
Yes. Bronchiectasis is not.
Cytokine mediators of acute lung injury
tumor necrosis factor (TNF), interleukin (IL)-1, IL-6, IL-10, and transforming growth factor (TGF)-β
Progression of acute lung injury
acute respiratory distress syndrome or acute interstitial pneumonia
Examples of hemodynamic edema
Left-sided heart failure, increased hydrostatic pressure, pulmonary vein obstruction
The major diffuse obstructive disorders
emphysema, chronic bronchitis, hyperinflation, bronchiectasis, and asthma
Two major causes of obstructive lung disorders and their related diseases
1. Narrowing of the airway (asthma)
2. Loss of alveolar elasticity (emphysema)
Emphysema w/chronic bronchitis
Major difference between centroacinar and panacinar emphysemal changes.
Associated causes of panacinar emphysema
Alpha-1-antitrypsin deficiency
Pathogenesis of emphysema (image)
Classic presentation of emphysema
Classically, the patient is barrel-chested and dyspneic, with obviously prolonged expiration, sits forward in a hunched-over position, and breathes through pursed lips
How do you diagnose emphysema?
Expiratory airflow limitation, best measured through spirometry, is the key to diagnosis.
Blue bloaters vs. pink puffers
Chronic bronchitis vs. emphysema
Histologic study of the airways in chronic bronchitis reveals
(1) goblet cell metaplasia with mucus plugging of the lumen, (2) clustering of pigmented alveolar macrophages, (3) inflammatory infiltration, and (4) fibrosis of the bronchiolar wall
the ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage
The Reid Index, increased in chronic bronchitis.
Proposed mechanistic malfunction in asthma
The inhibitory interferon-gamma from TH1 cells fails to stop overproduction of TH2, which in turn continue the asthmatic formation of reactive memory cells.
A busy pictorial representation of atopic asthma
Major chemokines implicated in causality of asthma
(1) leukotrienes C4, D4, and E4
(2) acetylcholine
(1) histamine
(2) prostaglandin D2
primary ciliary dyskinesia
poorly functioning cilia contribute to the retention of secretions and recurrent infections that in turn lead to bronchiectasis
Kartagener syndrome
bronchiectasis, sinusitis, and situs inversus or partial lateralizing abnormality
Usual flora cultured from bronchiectasis
Haemophilus influenzae and Pseudomonas aeruginosa specifically, and then a whole mix of everyone else.