Respiratory Pathology Flashcards
what is atelectasis
refers to an area of airless pulmonary parenchyma due to collapse or incomplete expansion
what is resorption atelectasis
- complete obstruction of an airway
- air within the dependent lung is resorbed -> collapse
- mediastinum shifts toward the affected lung
what is compression atelectasis
- fluid, tumor, or air accumulate within the pleural space, preventing normal expansion
- mediastinum shifts away from the affected lung
what is contraction atelectasis
- pulmonary or pleural fibrosis preventing normal expansion
- not reversible
what is hemodynamic pulmonary edema
- intra alveolar fluid accumulation due to increased hydrostatic pressure in the pulmonary circulation
- hemosiderin-laden macrophages may be seen within alveoli with chronic pulmonary edema
- decreased oxygenation, increased chance of infection
what is edema secondary to microvascular (alveolar) injury
- injury to and inflammation of alveolar vascular endothelium and/or respiratory epithelium
- infectious or toxic insults
- may be localized or diffuse
what is obstructive lung disease chracterized by
an increase in resistance to airflow due to partial or complete obstruction at any level from the trachea and larger bronchi to the terminal and respiratory bronchioles
what will pulmonary function tests show in obstructive lung diseases
decreased maximal flow rates during forced expiration
what are the diseases in obstructive lung diseases
- emphysema
- chronic bronchitis
- asthma
- bronchiesctasis
which groups are more susceptible to COPD
women and african americans
what is the association of COPD and smoking
- strong
- approximately 35-50% of heavy smokers develop COPD
- 80% of COPD is due to smoking
what is emphysema
destruction of airway walls and irreversible enlargement of the airways distal to the terminal bronchiole
what are the classifications of emphysema
- centriacinar
- panacinar
- distal acinar
- irregular
describe centriacinar emphysema
- occurs predominantly in heavy smokers, often along with chronic bronchitis (COPD)
- the respiratory bronchioles are involved, sparing the distal alveoli
- more lesions are seen in the upper lobes/ apical segments
describe panacinar emphysema
- associated with alpha1 antitrypsin deficiency
- alveoli distal to the respiratory bronchioles are involved
- occurs more frequently in the lower and anterior aspects of the lungs - lung bases are most severely involved
what is the pathogenesis of emphysema
- exposure to injurious particles in tobacco smoke stimulates inflammation
- imbalance of proteases and antiproteases
- oxidative stress
how does exposure to injurious particles in tobacco smoke stimulate inflammation
- lung epithelial cells and macrophages release chemotactic factors to recruit inflammatory cells from circulation
what releass destructive proteases
inflammatory cells
what causes oxidative stress
smoke, inflammatory cell products containing oxidants, continuing the cycle of tissue damage and inflammation
what is alpha-1 antitrypsin deficiency
- alpha 1 antitrypsin is a potent antiprotease, encoded by the Pi locus on chromosome 14
- homozygotes for the Z allele (0.012% of US population) have a significant decrease in alpha 1 antitrypsin
- 80% of homozygotes will develop symptomatic panacinar emphysema, accelerated and more severe if the patient smokes
how is emphysema an obstructive lung disease
- small airways are normally held open by the elastic recoil of lung parenchyma
- destruction of elastic alveolar walls surrounding respiratory bronchioles leads to the collapse of those bronchioles during expiration
describe the clinical course of emphysema
- no symptoms until one third of lung tissue is affected
- initial symptoms include dyspnea, cough and wheezing
- with severe emphysema: weight loss, barrel chest, prolonged expiration
what might emphysema progress to
pulmonary hypertension and right sided heart failure
what is death from emphysema usually due to
- respiratory failure
- RHF
- pneumothorax -> lung collapse
what is chronic bronchitis and what population is common
- a chronic, persistent productive cough without any other identifiable cause
- common in smokers and inhabitatns of polluted environments
what is the pathogenesis of chronic bronchitis
- initiating factor is exposure of the bronchi to inhaled irritants
- mucus hypersecretion
- chronic inflammation -> damage and fibrosis of small airways
- diminished ciliary action of respiratory epithelium, leading to stasis of mucus
what are the morphologic changes with chronic bronchitis
- edema and swelling of the respiratory mucosa, often with squamous metaplasia
- hyperplasia of submucosal mucous glands of the trachea and larger bronchi (thickness of the mucus gland layer increases)
- increased goblet cells in small bronchi and bronchioles and extensive small airway mucous plugging
what is the clinical course of chronic bronchitis
- persistent productive cough
- dypsnea on exertion
- classically: hypercapnia, hypoxia, mild cyanosis
what is asthma
- chronic disorder of the conducting airways characterized by:
- recurrent bronchoconstriction associated with a variety of stimuli
- inflammation of bronchial walls
- increased mucus secretion
what are the symptoms of asthma
- recurent wheezing, shortness of breath/chest tightness, cough
- more frequently at night/early morning
describe atopic asthma
- type I (IgE mediated) hypersensitivity reaction
- usually onset in childhood
- triggered by a variety of allergens: dust, animal dander, dust, foods
- patients may have high serum IgE, a positive skin test for the inciting allergen or may demonstrate IgE antibodies to specific allergens and often have a family history of asthma
what is atopic asthma pathogenesis
- sensitization occurs when Th2 cell in response to antigen presentation stimulate producion of IgE (IL4, IL13) recruits eospinophils (IL5) and stimulates mucus production (IL13)
- IgE binds to Fc receptors on mast cells
describe the reaction upon re exposure to antigen in atopic asthma pathogenesis
cross linking of IgE molecules on mast cells, triggering degranulation and inducing the immediate hypersensitivity reaction
the immediate phase of atopic asthma pathogenesis is characterized by:
- bronchoconstriction
- mucus secretion
- increased vascular permeability
the late phase (hours) of atopic asthma is characterized by
- recruitment of more inflammatory cells ( neutrophils, eosinophils, lymphocytes)
- results in damage to the mucosal tissue
in non atopic asthma bronchoconstriction is triggered by:
- respiratory viruses
- inhalation of irritants
- cold air
- exercise
what are the morphologic changes in asthma
- repeated allergen exposure and reaction induced airway remodeling which includes:
- bronchial wall smooth muscle hypertrophy and hyperplasia
- subepithelial fibrosis
- submucosal gland hyperplasia; increased goblet cells
- increased airway vascularity
- increased thickness of the airway wall
what are the morphologic changes in severe cases of asthma
bronchi and bronchioles become occluded by thick mucus plugs, which may be expelled in sputum or BAL specimens (Curschmann spirals)
- sputum and BAL specimens may also contain numerous eosinophils and charcot- leyden crystals
what is the clinical course of asthma
- attacks may last hours, but some patients may experience symptoms at a lower baseline level constantly
- in severe acute asthma the attack may last for days and result in obstruction sufficient to cause death
what is bronchiectasis
- chronic recurrent necrotizing infections eventually destroy smooth muscle and elastic tissue, leadig to permanent dilation of bronchi and bronchioles
- the infection with associated inflammation and destruction may follow obstruction and impedance of normal drainage; of severe bronchial infections may cause enough inflammatory damage and necrosis to bring about the bronchiectatic changes
what are the predisposing conditions for bronchiectasis
- conditions affecting mucus clearing (primary ciliary dyskinesia, cystic fibrosis, other bronchial obstruction)
- immunodeficiency conditions
repeated attempts to resolve the inflammatory process in bronchiectasis may result in______
peribronchial fibrosis
what are pneumoconioses
- nontumor lung diseases in the setting of exposure to mineral dusts, inorganic and organic particles and chemical fumes
what is particle pathogenicity influenced by
- particle size (1-5um are most pathogenic)
- particle solubility
- level and duration of exposure. effectiveness of clearance
- intensity of immune response