Chapter 12 - Lung Flashcards
What are the different types of Atelectasis?
1) Resorption: airway obstruction, O2 is absorbed into circulation collapsing alveoli
2) Compression: accumulation of blood, air, fluid in pleural cavity
3) Contraction, scarring in lung parenchyma or pleura
Acute Respiratory Distress Syndrome (ARDS)
Noncardiogenic pulmonary edema, manifests as rapidly progressive dyspnea, tachypnea, and hypoxemia
Pathophysiology: occurs when a pulmonary or extrapulmonary insult causes the release of inflammatory mediators
Inflammatory cells damage the vascular endothelium and alveolar epithelium -> pulmonary edema, hyaline membrane formation, decreased lung compliance, decreased gas exchange
Most cases are associated with pneumonia or sepsis
Treatment is supportive (mechanical ventilation, prophylaxis for stress ulcers and venous thromboembolism, nutritional support, treatment of underlying injury)
What are key points of obstructive lung diseases
Reduced FEV1, normal or nearly normal forced vital capacity, FEV1:FVC is reduced, lung volume may be inc, outflow is obstructed
Forced exp. volume in 1 second (FEV1) is the volume of air that can forcibly be blown out the first 1 second, after full inspiration
Forced vital capacity (FVC) is the amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible
Asthma
Most common chronic disease in childhood (7 million children)
Inflammatory disorder of airways, episodic, reversible, bronchospasm
Symptoms: dyspnea, cough, wheezing, excessive mucus production
Eosinophils are important in both immune & non-immune types (amplify and sustain inflammatory response, can result in sustained symptoms)
Occlusion of bronchi & bronchioles by thick, tenacious, mucus plugs
Patchy necrosis & shedding of bronchial epithelial cells
Hypertrophy & hyperplasia of bronchial smooth muscle
Asthma "attack" during procedure Oral Candidiasis ( from steroid inhalers)
Immune Type (Type 1 Hypersensitivity)
Atopic - Allergic Onset 0-20 yrs Elevated blood IgE & eosinophils Th2 CD4+ T-cell driven Most common type
Nonimmune (Nonatopic) Type
Normal IgE levels
- Viral infections (Rhinovirus, influenza, RSV)
- Inhaled air pollutants (sulfur dioxide, ozone, nitrogen dioxide
- NSAID sensitivity
- Exercise-induced asthma
Mediators of Asthma: Early and Late Phase
Early: Leukotrienes C4, D4, & E4 (bronchoconstriction, inc vascular permeability, increased mucin, nasal polyps)
Prostaglandins D2, E2, F2 (Bronchoconstriction, Vasodilation)
Histamine (Bronchospasm, inc vascular permeability)
Platelet activating factor (release of more histamine from platelets, vasodilation)
Late: Inflammatory cells recruited by mast cell factors (eosinophils**, neutrophils, basophils)
Augment the TH2 CD4+ response
Chronic Obstructive Pulmonary Disease
Emphysema and chronic bronchitis
usually emphysema exists along w/ chronic bronchitis since both are related to cigarette smoking
Emphysema
Permanent (non-reversible) enlargement of airspaces distal to terminal bronchioles due to destruction of their walls
First symptom is dyspnea
Centriacinar (associated w/ cigarette smoking, involves respiratory bronchiole first)
Clinical Features: Dyspnea (shortness of breath)
Cough & wheezing (present if chronic bronchitis coexists, often the case)
Weight loss common
Barrel-chested, prolonged expiration
Gas exchange & blood gas values are normal until very late
Alpha-1-antitrypsin
Emphysema unrelated to smoking - inherited, caused by mutation in the SERPINA1 gene
Protein produced mostly in the liver
Main purpose is to destroy an enzyme called neutrophil elastase in the lungs
Distal Acinar Emphysema
emphysema unrelated to smoking
Alveolar ducts and sacs are particularly involved, related to scarring, just under pleura, may rupture into pleural space, Spontaneous pneumothorax of young adults
Chronic Bronchitis
Persistent productive cough for 3 consecutive months in at least 2 consecutive years
Causes: cigarette smoking and severe air pollution
Prominent cough and sputum production
Hypercapnia (CO2 retention) hypoxemia (low blood O2)
May terminate w/ pulmonary hypertension and cor pulmonale w/ congestive heart failure
Chronic Bronchitis vs Emphysema
Emphysema: dyspnea, no cough, no wheezing, weight loss, barrel chested, good gas exchange until late, not hypoxic until advanced
Bronchitis: cough, wheezing, much sputum constant inflammation of airways w/ scarring as disease progresses, poor gas exchange, hypoxic
Bronchiectasis
Permanent dilation of bronchi & bronchioles
Caused by destruction of the muscular and elastic supporting tissue
Affects lower lobes, bilaterally
Airways dilated to as much as 4X normal diameter
Localized: Bronchial obstruction by tumors, foreign bodies or mucus plugs
Widespread: Cystic fibrosis, necrotizing pneumonias, immunoglobulin deficiency states, Kartagener syndrome
Cystic Fibrosis
Most common lethal AR disorder to affect caucasians, uncommon in asians and blacks, severity of clinical disease may depend upon which mutation is present
Pathogenesis: primary defect is the transport of chloride ions across epithelia
Defective cAMP-dependent Cl- channels, called cystic fibrosis transmembrane conductance regulators (CFTRs)
Mutation in the CFTR gene renders epithelial cells impermeable to Cl
Respiratory tract: absorption of Na+ and water from airspace to blood resulting in thick, viscid mucus
Pseudomonas aeruginosa resistant to neutrophilic phagocytosis. Neutrophils damage normal tissue while bacteria go home free (S. aureus & H. influenzae)
Genetics: CFTR gene on chromosome 7, 1300 mutations
Features: widespread defect in secretory function of exocrine glands, chronic pulmonary infections, pancreatic insufficiency
Consequences:
Pancreas-85% are affected, Atrophy of exocrine glands: pancreatic insufficiency
Pulmonary-Retention of viscid secretions leads to dilation of bronchioles and bronchi w/ infection: bronchiectasis
Course of Disease:
pulmonary infections main problem, median life expectancy is 30 yrs, pancreatic insufficiency, sweat chloride
Dental Implications:
no definitive alterations, incidence of caries actually less presumably, mild enamel defects
Restrictive Lung Disease
Characterized by reduced lung compliance, reduced FVC & FEV1, FEV1:FVC is normal