EXAM #1: OBSTRUCTIVE DISEASE Flashcards
What is atelectasis?
Incomplete expansion of the lung
What are the four types of atelectasis?
1) Resorption= airway obstruction leading to incomplete expansion
2) Compression= excess matter in lung space preventing expansion
3) Patchy=microatelectasis/ loss of surfactant (post-op)
4) Contraction= fibrosis around the lung preventing full expansion
What is the difference between the direction of medisatinum shift in resorption and compression atelectasis?
Resorption= mediastinal shift TOWARD affected lung
Compression= mediastinal shift AWAY from affected lung
What are the two major types of pulmonary edema?
1) Hemodynamic distrubance
2) Microvascular injury
What is the most common cause of hemodyamic pulmonary edema?
Increased hydrostatic pressure e.g. left-sided CHF
What are heart failure cells?
Hemosiderin-laden macrophages
What is the mechanism of edema caused by microvascular injury?
1) Injury to capillaries in alveolar septa
2) Leakage of fluid and proteins
What is the major difference between restrictive and obstructive lung disease?
Obstructive= can’t get air OUT
Restrictive= can’t get air IN
What are the major obstructive lung diseases?
1) COPD
2) Asthma
3) Bronchiectasis
What happens to FEV1 and FVC in obstructive disease?
- FEV1= decreased b/c difficulty getting air OUT
- FVC= normal or slightly decreased
FEV1/FVC is LOW
What happens to FEV1 and FVC in restrictive disease?
Can’t get air IN, but what you do get in can go OUT
Thus, FVC is low and TLC are low–BUT, FEV1/FVC is normal
When does one see the sx. of emphysema i.e. how bad does the disease have to be for there to be clinical significance?
1/3 of pulmonary capacity impaired
What airways are affected in emphysema?
Airways DISTAL to the terminal bronchiole
Destruction of the airway WITHOUT obvious fibrosis
Describe the pathogenesis of emphysema.
1) Smoking is proinflammatory increase neutrophil recruitment and alveolar macrophage activity
2) Neutrophils/ alveolar macrophages increase elastase/protease secretion that induces tissue damage
3) Furthermore, smoking inhibits antielastase
What cytokines are induced by smoking to attract neutrophils to the lungs?
1) IL-8
2) LTB4
3) TNF
What is the normal alpha-1 antitrypsin phenotype?
PiMM
What is the phenotype associated with severe alpha-1 antitrypsin disease?
PiZZ
What are the different types of emphysema?
1) Centriacinar= center of the acinus
2) Panacinar= entire acinus
3) Paraseptal
4) Irregular
What type of emphysema is most associated with smoking?
Centriacinar
*Inhalation of smoke affects the center of the acinus the most
Where is centriacinar emphysema most severe in the lung?
Apex
*Remember that smoke rises–mnemonic to remember the apex is most affected
What type of emphysema is most assocaited with alpha-1 antitrypsin deficiency?
Panacinar
*Lack of anti-protease causes damage to the entire acinus vs. just the central portion that is most exposed to smoke
What part of the lung is most affected by panacinar emphysema?
Base
What kind of emphysema is associated with bullae and pneumothorax?
Paraseptal/ distal acinar emphysema
What is the surgical procedure that can aid patients with very severe emphysema?
Volume reduction surgery
Anatomically, where is the inflammation of chronic bronchitis seen?
Larger airways
What are the morphologic changes that are seen in chronic bronchitis?
1) Goblet cell metaplasia
2) Mucus hypersecretion with plugging
What is the Reid index?
Gland/airway wall ratio
*Greater than 0.4= bronchitis, there has been hyperplasia of the mucous glands that cause the ratio to increase
What are the most common pathogens to cause acute exacerbations of chronic bronchitis?
Bacterial= H. influenza and S. pneummoniae
Viral= Adenovirus and RSV
What is cor pulmonale?
Lung disease leading to right-heart failure
*Increased PVR from lung disease causes RVH. When the right heart FAILS, this is cor pulmonale
Outline the pathogenesis of allergic asthma.
1) Sensitization to inhaled allergen causes induction of TH2 CD4+ cells
2) TH2 releases cytokines i.e. IL-4, IL-5, and IL-10
What is the role of IL-4 in allergic asthma?
Class switching to IgE
What is the role of IL-5 in allergic asthma?
Attraction of eosinophils
What is the role of IL-10 in allergic asthma?
1) Inhibition of TH1
2) Stimulation of TH2 (perpetuates TH2 response)
When is a patient is re-exposed to their allergen/trigger, what happens?
1) IgE cross-links mast cells
2) Mast cell degranulation
Outline the sequence of events that occurs following mast cell degranulation in the pathogenesis of allergic asthma.
1) Preformed histamine granules are released
2) Leukotrienes C4, D4, and E4 are generated
3) Major basic protein is released from eosinophils
What is the “early phase reaction” in asthma? Late-phase?
Early=
- Histamine
- Leukotrienes C4, D4, and E4
Late=
- MBP
Classically, what can be seen on histology of the sputum from an asthmatic patient?
1) Curshmann spirals
2) Charcot-Leyden crystals
What are Cruschmann spirals?
Spiral-shaped mucus plugs
What are Charcot-Leyden crystals?
Eosinophil derived crystals
What is classically associated with aspirin-intolerant asthma in adults?
Nasal polyps
What condition should a child with nasal polyps be worked up for?
Cystic Fibrosis
How does one develop bronchiectasis?
1) Obstruction
2) Persistent infection–gets fibrosed OPEN
What can cause obstructive bronchiectasis?
1) Tumor
2) FB
3) Secretions
What are the genetic diseases that can cause bronchiectasis?
1) CF
2) Kartanganer Syndrome
What infectious diseases cause bronchiectasis?
Necrotizing pneumonia
- S. aureus
- Klebsiella
What is Kartagener Syndrome?
AR defect in dynein in cilia
What are the classic features of Kartagener Syndrome?
1) Sinusitis
2) Bronchiectasis
3) Situs inversus
4) Infertility
What are the symptoms of bronchiectasis?
- Chronic productive cough
- Dyspnea
- Foul-smelling sputum
What is one of the major complications of bronchiectasis?
Amyloidosis (AA) from chronic inflammation
