Flashcards in The Lungs 1 Deck (73):
What three things do primary lung diseases effect?
1. The airways
2. The interstitium
3. The pulmonary vascular system
What is atelectasis aka pulmonary collapse?
Loss of lung volume caused by inadequate expansion of airspaces
Is atelectasis reversible? What does treatment aim to do?
Yes (except for contraction atelectasis). Tx helps to prevent hypoxemia and infection of the collapsed lung.
What is resorption atelectasis?
When alveoli distal to an obstruction collapse because the air that was present prior to the obstruction event was eventually absorbed.
What is compression aka passive aka relaxation atelectasis? Name five causes.
Alveolar collapse due to external pressure such as from: 1) pleural effusion (from CHF), 2) hemothorax, 3) pneumothorax, 4) neoplasm, or 5) from being bedridden (diaphragm moves superiorly when lying flat)
What is contraction aka cicatrization atelectasis? Is it reversible?
Fibrotic changes that increase the elastic recoil, causing decreased lung compliance and an inability to fill. Not reversible.
What are the four clinical indicators of an acute lung injury?
1. Acute onset of dyspnea
2. Decreased O2 sats
3. Bilateral pulmonary infiltrates on CXR
4. No evidence of left heart failure
What can untreated acute lung injury potentially progress to?
Acute respiratory distress syndrome (ARDS)
Acute respiratory distress syndrome (ARDS) is caused by diffuse _______ damage involving the pulmonary capillaries and endothelium.
Name five common causes of ARDS.
2. Pneumonia with sepsis
5. Aspiration of gastric contents
Name five less common causes of ARDS.
1. Inhalation of toxic gas or very hot air.
3. Near drowning.
4. Metabolic disorders.
How serious is ARDS aka "shock lung" and what are some clinical manifestations?
Respiratory failure is rapid and life threatening. Patients are cyanotic with severe arterial hypoxemia. O2 treatment doesn't work. Can progress to organ failure.
Describe the pathogenesis of acute respiratory distress syndrome (7 steps).
1. Alveolar damage (epithelial, endothelial, or commonly both).
2. Pro-inflammatory imbalance caused by nuclear factor kB.
3. Cytokine release within 30 minutes: IL-8, IL-1, TNF.
4. The cytokines activate endothelial cells and NEUTROPHILS.
5. Neutrophils release factors that maintain the inflammatory cascade.
6. Endothelial and epithelial injury leads to loss of surfactant.
7. Alveolar collapse.
What is nuclear factor kB?
Pro-inflammatory thing that plays a role in ARDS!
Name three anti-inflammatory factors that play a role in ARDS.
1. Endogenous anti-proteases
3. Anti-inflammatory cytokines
What is the #1 factor that determines the degree of tissue injury in ARDS?
The balance between pro and anti-inflammatory factors in the lungs.
What are the two phases of ARDS?
1. Initial (acute) exudative phase
2. Organizing phase
Name five morphological features of the acute exudative phase of ARDS.
1. Lungs are dark red, firm, airless, and heavy.
2. Alveolar edema.
3. Epithelial necrosis.
4. Accumulation of neutrophils.
5. HYALINE MEMBRANES lining the alveolar ducts.
When does the organizing phase of ARDS begin?
A week after the initial injury.
Describe five morphological changes of the organizing phase of ARDS.
1. Fibroblast proliferation.
2. Type II pneumocyte proliferation.
3. Alveolar macrophages trying to digest the hyaline crap.
4. Fibrin organization --> intra-alveolar fibrosis and thickening of the septa.
5. Unusual resolution.
Within 72 hours of the initiating insult, _____% of patients develop the clinical signs of ARDS; the mortality rate is _____%.
85% develop clinical signs. 40% mortality rate
For those who have an uncomplicated outcome following ARDS, normal respiratory function returns within ____ to ____ months.
6 to 12 months
What does the term "wet lung" refer to?
Obstructive pulmonary disease is a disease of the airways characterized by a ________ of airflow resulting from a ________ in resistance of the lung tissue.
limitation of airflow due to an increase of resistance.
Name two examples of obstructive pulmonary diseases.
1. Chronic bronchitis
What are the differences between pure chronic bronchitis and pure emphysema?
Pure chronic bronchitis includes hypersecretion of mucus and inflammation of the upper large airways, peribronchiolar fibrosis and obstruction of the small airways (bonchioles).
Pure emphysema is loss of elastic recoil and overinflation of the ACINI (respiratory bronchiole, alveolar ducts, and alveoli).
COPD is characterized by ________ airflow obstruction, whereas asthma is characterized by _______ airflow obstruction.
asthma is reversible
Is fibrosis present in the acini of a emphysematous lung? What is the major cause of emphysema?
There is NOT obvious fibrosis. Major cause is cigarette smoking.
Centriacinar emphysema is characterized by loss of elasticity and overinflation of the ________ ________, whereas panacinar emphysema is characterized by loss of elasticity and overinflation of the ________ ________, and ________.
Centriacinar: overinflation of the respiratory bronchioles (just proximal to the alveolar ducts).
Panacinar is overinflation of the alveolar ducts and alveoli.
With centriacinar aka centrilobular emphysema, are both normal and emphysematous airspaces present in the same acini and lobules? How does this differ from panacinar emphysema?
Yeah. Different than panacinar emphysema, in which there is UNIFORM enlargement of the structures distal to the respiratory bronchiole.
In which lobes are more common and severe lesions seen in a lung with centriacinar emphysema?
In the apical segments of the upper lobes
Which type of emphysema is more common: Panacinar or centriacinar?
Centriacinar by 20X
What endogenous molecules are responsible for destruction of of alveolar ducts and alveoli in panacinar emphysema? In which parts of the lungs is this most commonly seen?
Proteases and elastase destroy the alveolar ducts and alveoli. Seen more commonly in lower lung zones.
More than ___% of people with alpha-1-antitrypsin deficiency can develop symptomatic _________ emphysema.
Exposure to toxic substances such as tobacco smoke and inhaled pollutants induces ongoing inflammation with accumulation of ________, _________, and ________ in the lungs.
neutrophils, macrophages, and lymphocytes
Do cytokines like IL-8, MMPs, and oxidants play a role in the pathogenesis of emphysema?
Name three endogenous molecules that normally inhibit lung destruction.
3. Anti-inflammatory cytokines
TGF-beta1 polymorphisms may play a role in _________ pathogenesis.
What is the main cause of chronic airflow obstruction in severe emphysema?
Collapse of the alveoli during expiration.
Morphological features of emphysema include _______ of the airspaces and _______ of the alveolar walls.
dilation of the airspaces and thinning of the alveolar walls
Is air flow obstruction from emphysema reversible?
The clinical manifestations of emphysema appear after _____% of the functioning pulmonary parenchyma is damaged.
What is the first symptom of emphysema? Name three other symptoms.
3. Weight loss
What is the "classical presentation" of emphysema?
Barrel-chest, dyspneic, prolonged expiration, sits in a forward and hunched-over position, breathes through pursed lips.
What is key to diagnosing emphysema?
Poor expiration measured by spirometry.
What is a "pink puffer?"
A patient with emphysema that ventilates well and remains well oxygenated.
What three things may cause death from emphysema?
1. Respiratory acidosis
2. Right heart failure
3. Collapse of lungs secondary to pneumothorax
What are the treatments for emphysema (5)?
Bronchodilators, steroids, bullectomy, lung volume reduction surgery, lung transplant
What is the definition of chronic bronchitis?
Persistent, productive cough that lasts for at least three months and occurs in two or more consecutive years in the absence of another identifiable cause
What are the three types of chronic bronchitis? Describe each.
1. Simple chronic bronchitis: Most common. Productive cough that raises mucoid sputum. Airflow is NOT obstructed.
2. Chronic asthmatic bronchitis: Hyper-responsive airways; intermittent bronchospasm and wheezing.
3. Chronic obstructive bronchitis: Chronic outflow obstruction, often in association with emphysema, mainly in heavy smokers.
Chronic bronchitis is characterized by increase in the size of the ________ __________ apparatus, causing ___________ of mucus in the large airways.
increase in size of the bronchial mucus-secreting apparatus causing hypersecretion of mucus in the large airways
What is seen regarding goblet cells and serous cells in chronic bronchitis?
Hyperplasia and hypertrophy of the goblet cells leads to an increased ratio of the goblet to serous cells
What does "small airway disease" refer to?
Chronic bronchitis: Goblet cells proliferate and plug the bronchial lumen with mucus. There is also inflammation and bronchiolar wall fibrosis.
Describe the morphology of chronic bronchitis (6).
1. Increased blood flow (hyperemia) and swollen mucosal lining in the large airways.
2. Large airways covered by mucus secretions (can also be seen in smaller airways).
3. Enlargement of mucus-secreting glands.
4. Increased Reid index.
5. Inflammatory infiltrate in the bronchial mucosa (monocytes and neutrophils)
6. Peribronchiolar fibrosis and luminal narrowing.
Are eosinophils seen in chronic bronchitis?
Only in asthmatic bronchitis.
Is chronic bronchitis often accompanied by emphysema?
Asthma is characterized by ________ bronchoconstriction caused by airway ____________ to a variety of stimuli.
reversible bronchoconstriction caused by hyper-responsiveness
Name four symptoms of asthma.
3. Chest tightness
Particularly at night and in the early morning
What type of hypersensitivity reaction is atopic/extrinsic asthma? What cellular mechanisms are responsible?
Type 1 - acute and late phase. Caused by TH2 which release IL-4, IL-5, and IL-13, causing B cells to differentiate into plasma cells that make IgE --> allergic reactions.
What are the three main features of asthma?
1. Intermittent and reversible airway obstruction.
2. Chronic bronchial inflammation with lots of EOSINOPHILS.
3. Bronchial smooth muscle cell hypertrophy and hyper-reactivity.
What causes non-atopic/intrinsic asthma (6)?
Non-immune stimuli like aspirin, cold, psychological stress, exercise, viral infection and inhaled air pollutants.
Does airway remodeling add to the element of the obstructive disease in asthmatic patients?
In what disease does one see "mucus plugs" in bronchi and bronchioles?
Describe the morphology of asthma (9).
1. Mucus plugs that contain Curschmann spirals (whorls of shed epithelium).
3. Charcot-Leyden crystals made up of eosinophil proteins.
4. Airway remodeling, causing:
5. Thickening of the BM
7. Inflammatory infiltrate including eosinophils and mast cells.
8. Increase in submucosal gland size.
9. Hypertrophy of the bronchial muscle walls.
The chief difficulty in asthmatics is _______ (inspiration or expiration).
What is "status asthmaticus?"
Severe asthma attack that doesn't respond to therapy and can last for days to weeks.
What are three major complications from asthma?
2. Hypercapnia (increased CO2)
3. Severe hypoxia
What is bronchiectasis?
Permanent dilation of the bronchi and bronchioles secondary to obstruction or persistent infection --> destruction of smooth muscle and supporting elastic tissue in the airway walls.
What is the major symptom of bronchiectasis?
Coughing up lots of purulent sputum
What are the three overarching causes of bronchiectasis?
1. Bronchial obstruction.
2. Congenital or hereditary conditions, including CF, immunodeficiency status, primary ciliary dyskinesia.
3. Necrotizing of suppurative pneumonia from virulent organisms like Staph aureus.
Describe the morphology of bronchiectasis (8).
1. Lower lung involvement
2. Vertical airway involvement
3. Dilation of airways
4. Intense acute and chronic inflammation within walls of lungs (during an active case).
5. After healing some abnormal dilation and scarring is present.
6. Fibrosis of the walls.
7. Peribronchiolar fibrosis develops in chronic cases.
8. Lung abscesses in some cases.
What are the clinical manifestations of bronchiectasis (4)?
1. Severe, persistent cough with mucopurulent sputum and possibly hemoptysis.
2. Upper resp. infections.
3. Clubbing of fingers.
4. Severe cases: hypercapnia, pulmonary hypertension, hypoxemia, and rarely cor pulmonale.