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RS Pathology
Respiratory System Pathology - Chronic Bronchitis, Asthma, and Bronchiectasis
| Question | Answer |
|---|---|
| Chronic Bronchitis is most common in what patients? | Cigarette smokers and urban dwellers in cities with excessive pollution |
| How is chronic bronchitis diagnosed? | On Clinical grounds Presence of a persistent productive cough for at least 3 consecutive months, in at least 2 consecutive years |
| In the early stages of the disease is airflow obstructed? | No |
| What purpose does the productive cough serve? | To raise the mucoid sputum |
| Patients with chronic bronchitis show what symptoms? | Hyper responsive airways, intermittent bronchospasm, and wheezing |
| Heavy smokers with bronchitis and associated emphysema develop chronic: | Outflow obstruction |
| What is the distinctive feature of chronic bronchitis? | Hypersecretion of mucous |
| Where does this symptom begin? | In the large airways |
| Is smoking the only cause of chronic bronchitis? | No, sulfur dioxide and nitrogen dioxide may contribute |
| What is the effect of these environmental irritants (smoking, NO2, SO2)? | 1) Hypertrophy of mucous glands in the trachea and main bronchi 2) Marked increase in goblet cells in small bronchi and bronchioles 3) Infiltration of CD8+ lymphocytes and neutrophils -- No eosinophils unless there's Asthma |
| The effects of environmental irritants on the respiratory epithelium are mediated by? | Local release of T-cell cytokines (IL-13) |
| Which gene is transcripted as a consequence of exposure to tobacco smoke? | MUC5AC |
| What is the main defining feature of chronic bronchitis? | Large bronchial involvement |
| Airflow obstruction in chronic bronchitis is characteristic in: | More peripheral airways |
| Airflow obstruction is due to: | 1) Chronic Bronchiolitis 2) Coexistent emphysema |
| What is chronic bronchiolitis induced by? | 1) Goblet cell metaplasia --> plugging of the bronchiolar lumen 2) Inflammation 3) Bronchiolar wall fibrosis |
| What is the most important component of early and mild airflow obstruction? | Chronic bronchiolitis |
| What is the most important component of significant airflow obstruction? | Coexisting emphysema |
| What is the general morphology in chronic bronchitis? | 1) Hypermia and swelling of the mucosal lining of the large airways 2) Mucosa of the bronchi are covered by mucinous or mucopurulent secretions |
| On histologic examination what do we see? | 1) Enlargement of mucous secreting glands in the trachea and large bronchi 2) Magnitude of increase is assessed by the Reid index (should be higher than 4/10 or 0.4 relative to the thickness of the wall) In the bronchitic patient --> 0.6/0.7 |
| What is the main cause of the luminal narrowing airway obstruction? | Submucosal fibrosis |
| What are the clinical features of symptoms with chronic bronchitis? | 1) Prominent cough with sputum production (without ventilatory dysfunction) 2) Significant COPD with outflow obstruction 3) COPD accompanied with hypercapnia, hypoxemia, and cyanosis ( blue bloaters with obesity) 4) Cardiac and respiratory failure |
| What is asthma? | chronic inflammation of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and/or early in the morning. |
| Why are the symptoms particularly significant at night or early in the morning? | The most significant allergy is to pollen This allergy is a type 1 hypersensitivity reaction This reaction takes time to develop so is most significant hours after exposure |
| What are the hallmarks of asthma? | 1) Reversible airway obstruction 2) Chronic bronchial inflammation with eosinophils 3) Bronchial smooth muscle hypertrophy and hyperreactivity 4) Increased mucous secretion |
| What is the most common type of asthma? | Atopic asthma |
| When does atopic asthma usually begin? | Childhood |
| Atopic asthma is an example of which type of hypersensitivity reaction? | Type 1 IgE mediated |
| A positive family history is common is which type of asthma? | Atopic |
| In atopic asthma, asthmatic attacks are preceded by: | Rhinitis, urticaria, or eczema |
| Atopic asthma is triggered by: | Environmental antigens, dusts, pollen, and foods |
| A skin test with the offending antigens results in an immediate: | Wheal and flare reaction |
| Atopic asthma can also be diagnosed based on | Serum radioallergosorbent tests (RASTs) *Identify the presence of IgE for a specific panel of allergens |
| In which type of asthma is there no evidence of allergen sensitization? | Non atopic asthma |
| In atopic asthma, skin test results are usually: | Negative |
| A family history of asthma is less common in: | Non-Atopic asthma |
| What are common triggers of non atopic asthma? | Respiratory infections due to viruses (e.g.rhinovirus, parainfluenza virus) and inhaled air pollutants (e.g., sulfur dioxide) |
| What effect does virus induced inflammation of the respiratory mucosa have? | It lowers the threshold of the subepithelial vagal receptors to irritants |
| The ultimate humoral and cellular mediators of airway obstruction (e.g. eosinophils) are common to which type of asthma? | Atopic and nonatopic |
| Which pharmacologic agent is the most likely to cause drug induced asthma? | Aspirin |
| Patients with aspirin sensitivity present with which symptoms? | Recurrent rhinitis and nasal polyps, urticaria, and bronchospasm. |
| Why is aspirin presumably the most common cause? | Aspirin inhibits the cyclooxygenase pathway of arachidonic acid metabolism without affecting the lipoxygenase route, thereby shifting the balance of production toward leukotrienes that cause bronchial spasm. |
| The major etiologic factors of asthma are: | 1) Genetic predisposition to type I hypersensitivity (atopy) 2) Acute and chronic airway inflammation 3) Bronchial hyper responsiveness to a variety of stimuli |
| How is the role of type 2 helper T (TH2) cells critical to the pathogenesis of asthma? | TH2 cells produce cytokines, like: 1) IL-4 stimulating IgE production (which coats mast cells releasing granule contents with allergen contact) 2) IL-5 activates eosinophils 3) IL-13 stimulates mucus production and promoting IgE production by B cells |
| There are two waves of reaction induced by inflammation, which are: | Early and late reactions |
| The early reaction is dominated by: | 1) Bronchoconstriction 2) Increased mucus production 3) Vasodilation |
| The late phase reaction consists of: | 1) Activation of eosinophils, neutrophils, and T-cells 2) Epithelial cells are activated to produce chemokines that promote recruitment of more TH2 cells and eosinophils (including eotaxin, a potent chemoattractan and activator of eosinophils) |
| Airway remodeling is: | 1) Hypertrophy of bronchial smooth muscle and mucus glands, 2) Deposition of subepithelial collagen, which may occur as early as several years before initiation of symptoms. |
| Gross morphology of asthma: (described in persons who die of prolonged severe attacks (status asthamticus)) | The most striking macroscopic finding is occlusion of bronchi and bronchioles by thick, mucous plugs |
| Describe the histologic appearance: | 1) The mucous plugs contain whorls of shed epithelium (Curschmann spirals). 2) Numerous eosinophils 3) Charcot-Leyden crystals (collections of crystalloids made up of eosinophil proteins) in the mucus. |
| Airway remodeling includes: | 1) Thickening of airway wall 2) Increased vascularity in submucosa 3) An increase in size of the submucosal glands and goblet cell metaplasia 4) Hypertrophy/hyperplasia of the bronchial muscle- this is the basis for the novel therapy |
| Susceptibility genes affected in asthma: | 1) Chromosome 5q (IL-12, CD14, IL4) 2) Chromosome 20q (ADAM-33) |
| Chromosome 5q abnormalities: | 1) IL13 (genetic polymorphisms linked with susceptibility to the development of atopic asthma) 2) CD14 3) IL-4 receptor gene (atopy, total serum IgE level, and asthma). |
| ADAM-33 regulates: | Proliferation of bronchial smooth muscle and fibroblasts is located; this controls airway remodeling |
| Clinical features of asthma: | 1) Severe dyspnea with wheezing (difficulty in expiration) 2) Progressive hyperinflation |
| Other characteristics of asthma: | 1) Intervals between attacks free from overt respiratory difficulties persistent, subtle deficits can be detected by spirometry 2) Severe paroxysm may occur (status asthmaticus) 3) Hypercapnia, acidosis, and severe hypoxia more disabling than lethal |
| What is bronchiectasis? | Permanent dilation of bronchi and bronchioles caused by destruction of muscle and the elastic tissue Secondary to persisting infection or obstruction |
| What are some characteristic symptoms? | 1) Cough 2) Expectoration of copious amount of purulent sputum |
| How is bronchiectasis diagnosed? | History along with radiographic demonstration of bronchial dilation |
| The Predisposing conditions include: | 1) Bronchial obstruction 2) Congenital or hereditary conditions 3) Kartagener syndrome 4) Necrotizing or suppurative pneumonia |
| The common causes of bronchial obstruction: | 1) Tumors, foreign bodies, and impaction of mucus *With these conditions, the bronchiectasis is localized to the obstructed lung segment 2) Bronchiectasis can also complicate atopic asthma and chronic bronchitis |
| Congenital and hereditary conditions include: | 1) Cystic fibrosis, widespread severe bronchiectasis from obstruction secretion of abnormally viscous mucus 2) Immunodeficiency states- immunoglobulin deficiencies, localized or diffuse bronchiectasis--> increased susceptibility to bacterial infections |
| Kartagener syndrome is: | An autosomal recessive disorder associated with bronchiectasis due to structural abnormalities of the cilia that impair mucociliary clearance in the airways *Persistent infections and reduce mobility of sperms |
| Necrotizing or suppurative pneumonia is particulary associated with: | Staphylococcus aureus or Klebsiella spp. and may predispose affected patients to development of bronchiectasis. |
| Another significant cause of microbiologic bronchiectasis that is a significant cause of morbidity is: | Posttuberculosis bronchiectasis in endemic areas |
| What two processes are crucial in pathogenesis: | 1) Obstruction 2) Chronic infection *Either may come first |
| How can these two processes be connected? | Normal clearance mechanisms are hampered by obstruction, so secondary infection soon follows conversely Chronic infection over time causes damage to bronchial walls, leading to weakening and dilation. |
| What is one example of pathogeneses which cause bronchietasis? | Obstruction caused by a primary lung cancer or a foreign body impairs clearance of secretions--> superimposed infection --> inflammatory damage to the bronchial wall--> further distension of airways --> irreversible dilation. |
| What is another example of pathogeneses which cause bronchietasis? | Persistent necrotizing inflammation in the bronchi or bronchioles may cause obstructive secretions, inflammation in the wall (with peribronchial fibrosis and traction on the walls) |
| Morphology of bronchietasis: | *The lower lobes *Involvement may be localized to single segment and most sever involvement in more distal bronchi and bronchioles *Dilated 4x the usual diameter and bronchioles can be followed to the pleural surfaces |
| Histologic findings in full blown acute cases: | 1)Intense acute and chronic inflammatory exudate within the walls of the bronchi and bronchioles 2) Desquamation and ulceration of lining epithelium. 3) Mixed flora can be cultured |
| Histologic findings in healing: | 1)The lining epithelium may regenerate completely, however, usually abnormal dilation and scarring persist 2) Fibrosis of the bronchial and bronchiolar walls develop in more chronic cases 3) Necrosis may results in the formation of an abcess cavity |
| Clinical features of bronchietasis: | 1) Severe, persistent cough with expectoration of mucopurulent sputum 2) Sputum may contain blood, hemoptysis can occur 3) Symptoms are episodic and precipitated by URT infections 4) Clubbing of the fingers my develop |
| Complications of bronchiectasis: | 1) In cases of severe, widespread bronchiectasis, significant obstructive ventilatory defects are usual, with hypoxemia, hypercapnia, pulmonary hypertension, and (rarely) cor pulmonale. 2) Metastatic brain abscesses 3) Reactive amyloidosis |
Created by:
Ulaisl
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