Obstructive Pulomary Disorders
- Obstruction of airflow
- Manifested by increased resistance to airflow
Classifications of OPD
1. Obstruction from conditions in the wall of the lumen
2. Obstruction resulting from increasing pressure around the outside of the airway lumen
3. Obstruction of the airway lumen
Asthma Etiology
1. Airway obstruction is is reversible (not in all pt)
2. Airway inflammation
3. Increased airway responsiveness to a variety of stimuli
4. Occurs in 7-14% of US population
5. Common chronic disease of children
Two types of Asthma
1. Intrinsic
2. Extrinsic
Intrinsic Asthma
- Non-allergic; adult onset
- Develops in middle age; less favorable prognosis
- No history of allergies
- Respiratory infections or psych factors (contributory)
- Allergen specific immunotherapy and environmental control not helpful
Extrinsic Ashtma
- Allergic; pediatric onset
- 1/3 to 1/2 of asthma cases
- IgE mediated response is common
- Treatment: pharmacologic therapy, allergen specific immunotherapy (injection), environmental control
Exercise Induced Asthma
- common in children an adolescents
- bronchospasm occurs within 3 min after end of exercise; resolves in 60 min
- heat loss, water loss, increased osmolarity of lower respiratory mucosa stimulant mediator, release from basophils, and tissue mast cells ca
Occupational Asthma
- Often have positive skin test reactions to protein allergens in work environment
- May need to conduct challenge tests (illicit reactions)
Tends to have progressively more severed attacks with subsequent exposures
- Sensitization is ineffective
Drug- Induced Asthma
- Can produce symptoms ranging from mild rhinorrhea to respiratory arrest
- Aspiring, NSAIDs can trigger attack
Food additivies
- Trigger asthma attacks
- Tartrazine (yellow dye 5), MSG, Sodium or potassium metabisulfite, hops in beer
Pathogenesis of Asthma
-immunohistopathologic features include edema, mast cell activation, inflammatory cell infiltration by neutrophils, eosinophils, lymphocytes
- Inflammation of airway
- Acute brochospasms
- Mucosa edema, mucous plug formation
- Airway wall remodeling thick
Allergic Asthma Pathogenesis
- IgE mediated response is common
- Manifested by elevated IgE levels, allergic rhinitis, eczema, and possible family history of allergy attacks associated with seasonal, environmental, or occupational exposure
Allergic Asthma mechanism of action
- Exposure to a specific antigen that has previously sensitized mast cells in airway mucosa; antigen reacts with the antibody releasing chemical mediator substances.
- Cytokines: most important inflammatory mediators
Normal respiratory epithelium replaced by goblet cells results in
-Mucosal edema, inflammatory exudates, and hyperresponsiveness of the airway (bronchoconstriction and leakage from increased microvascular permeability).
- Secondary mediator response occurs 6 to 12 hours later; more refractory to treatment; neutrophil ch
Clinical Manifestations of Asthma
- Wheezing
- Feeling of tightness of chest
- Dyspnea
- Cough (dry or productive)
- Increased sputum production (thick, tenacious, scant, and viscid)
- Hyperinflated chest
- Decreased breath sounds
Clinical Manifestations of Severe Asthma Attack
- Use of accessory muscles of respiration
- Intercostal refractions
- Distant breath sounds with inspiratory wheezing
- Orthopnea
- Agitation
Signs/Symptoms of Severe Asthma Attack
- Tachypnea >30 breath/min
- Tachycardia >120 beats/min
- Wheezing is not a good indicator of air flow
- PERF: <80 L/min
PERF
Peak expiratory flow rate
Determines index of airway function
Ratio of FEV1/FVC before and after administration of short-acting bronchodilator
Obstruction indicated by FEV1/FVC < 75%
Diagnosis of Asthma
Radiographic Finding
Physical Findings
Sputum exam (culture)
Pulmonary function test
PERF
Skin testing
ABG
Bronchial provocation testing
CBC
Sputum Exam (culture)
Charcot-Leyden Crystals (crystallized eosinophil)
Eosinophil
Curschmann Spitals (dry mucous)
Asthma treatment
- Avoid triggers
- Environmental controls
- Preventative therapy
- Desensitization (allergen specific immunotherapy)
Asthma Treatment Medications
- O2 therapy, small-volume nebulizers, B2 agonists, corticosteroids, leukotriene modifiers, mast cell inhibitors
- For status asthmaticus (severe attack unresponsive to routine therapy): epinephrine, subcutaneous terbutaline, aminophylline, intravenous co
B2 agonists
bronchodilators
Corticosteroids
Relax airway muscles
Acute Bronchitis
Acute inflammation of trachea and bronchi
Acute Bronchitis Etiology
- Viral or nonviral
- Heat
- Smoke inhalation
- Inhalation of irritant chemicals
- Allergic reactions
Asthmatic bronchitis
- Swelling of bronchial mucosa in children, associated with obstruction, respiratory distress, and wheezing
Acute Bronchitis Pathogenesis
- Airways become inflamed and narrowed from capillary dilation
- Swelling from fluid exudation
- Infiltration with inflammatory cells
- Increased mucus production
- Loss of ciliary function
- Loss of portions of the ciliated epithelium
Acute Bronchitis Clinical Manifestations
- Usually mild and self limiting
- Cough (productive or nonproductive)
- Low-grade fever
- Substernal chest discomfort
- Sore throat
- Postnasal drip
- Fatigue
Acute Bronchitis Diagnosis
1. Clinical presentations
2. Distinct hallmark of disease: recent onset of cough
3. Chest X-ray to distinguish acute bronchitis from pneumonia
Acute Bronchitis Treatment
- Usually no treatment needed for viral
- Antibiotic therapy (bacterial)
- Codeine- containing medications (for cough)
- Increase fluid intake
- Avoid smoke
- Use a vaporizer in room
Chronic Bronchitis Causes
- Cigarette smoking (90%)
- Repeated airway infections
- Genetic predisposition
- Inhalation of physical or chemical irritants
Chronic Bronchitis Etiology
- Type B COPD, "blue bloater"
- Hypersecretion of bronchial mucus
- Chronic or recurrent productive cough >3 months >2+ successive years
- Persistent, irreversible when paired with emphysema
- 1:2 male to female ratio
- >30 to 40 years
Chronic Bronchitis Pathogenesis
- Chronic inflammation and swelling of the bronchial mucosa resulting in scarring
- Hypertrophy of bronchial mucous gland/goblet cells
- Increased bronchial wall thickness
- Pulmonary hypertension
- Destruction of bronchial walls
Chronic Bronchitis Clinical Manifestations
- Typical patient is overweight.
- Commonly associated with emphysema
- SOB on exertion
- Excessive sputum
- Chronic cough (more severe in mornings)
- Evidence of excess body fluids (edema, hypervolemia)
- Cyanosis (late sign)
Chronic Bronchitis Diagnosis
- Chest X-ray
- Pulmonary function test
- ABG
- ECG
- Secondary polycythemia
Chronic Bronchitis Treatment Goals
- Block the progression of the disease
- Return to optimal respiratory function
- Return to usual activities of daily living
Chronic Bronchitis Treatment Meds
- Inhaled short-acting B2 agonists
- Inhaled anticholinergic bronchodilators
- Cough suppressants
- Antimicrobial agents (bacterial infections)
- Inhaled/oral corticosteroids
- Theophylline products
Chronic Bronchitis Treatment and Management
Treatment
1. low dose O2 therapy
2. Mechanical ventilation may be necessary
Management
1. Smoke cessation
2. Bronchodilator therapy
3. Reduction of exposure to irritants
Chronic Bronchitis Management
- Adequate rest
- Proper hydration
- Physical reconditioning
- Treadmill/stationary bike
- Alternating rest and exercise
- Walking best exercise
- Influenza and pneumococcal vaccines
Emphysema
lung condition that involves the permanent destruction of very fine airways and alveoli, thus decreasing respiratory function
Emphysema Etiology
- Type A COPD : "Pink puffer"
- Destructive changes of the alveolar walls without fibrosis
- Abnormal enlargement of the distal air sacs
- Damage is irreversible.
- Associated with chronic bronchitis
Emphysema Causes
- Smoking >70 packs/year
- Air pollution
- Certain occupations (mining, welding, working with or near asbestos)
- ?1-Antitrypsin deficiency (agent that makes surfactant) (genetic)
Emphysema Pathogenesis
- Groups of genes
- Release of proteolytic enzymes from neutrophils and macrophages leading to alveolar damage
- Smoking causes alveolar damage
- Reduction in pulmonary capillary bed
- Loss of elastic tissue in lung
- Air becomes trapped in distal alveoli
Emphysema Classifications
1. Centriacinar
2. Panacinar
3. Paraseptal
Centriacinar
- Associated with smoking and chronic bronchitis
- Destroys respiratory bronchitis
Panacinar
Destroys the alveoli
Paraseptal
Affects peripheral lobules
Emphysema Clinical Manifestations
- Progressive, exertional dyspnea
- Thin
- Use of accessory muscles
- Pursed-lip breathing
- Cough (minimal or absent)
- Digital clubbing
- Barrel chest
- Leaning forward to breath
Emphysema Diagnosis
- Pulmonary function tests (PFT)
- Chest X-ray
- ECG
- ABG
- Patient history
- Physical findings
Emphysema Treatment
- O2 therapy
- Smoking cessation
Medications:
- Inhaled short-acting B2 agonists
- Inhaled anticholinergic bronchodilators
- Cough suppressants
- Antimicrobial agents (infections)
- Inhaled/oral corticosteroids
- Theophylline products
Bronchiolitis
- Widespread inflammation of the bronchioles as a result of infectious agents
- Occasionally relate to allergic rxns
- RSV is most common (winter/spring; children<2)
- Adults- smoking, toxic fumes, immunosuppressants
Bronchiolitis Pathogenesis
- Proliferation and necrosis of bronchiolar epithelium
- Production of thick, tenacious mucus
- Airway obstruction
- Atelectasis (collapse of lung tissue)
- Hyperinflation
Possible mechanisms of airway obstruction (bronchiolitis)
- Development of inflammatory exudate: displaces surfactant
- Release of chemical mediators: produces bronchiolar constriction
- Inflammation: induces fibrosis and airway narrowing
- Goblet cell metaplasia
- Increased bronchial muscle mass
Bronchiolitis Clinical Manifestations
- Severity and course range from mild to fatal
- Wheezing r/t bronchospasm
- Crackles
- Decreased breath sounds
- Retractions
- Increased sputum
- Dyspnea
- Tachypnea
- Low-grade fever
Bronchiolitis Diagnosis
- Elevated WBC
- Chest x-ray: enlarged air sacs, interstitial infiltrates, atelectasis, severe hyperinflation
- PFT: severe obstruction to airflow
- Nasal swab: determine RSV
Bronchiolitis Treatment
- Adequate humidified oxygenation
- Bronchodilator agents
- Corticosteroids
- Sedation (for anxiety)
- Hydration
- Antiviral/antibiotics
- Smoking cessation and avoidance of second-hand smoke
- For RSV�health care workers wear eye and nose goggles.
Cystic Fibrosis (CF) Etiology
- Autosomal recessive disorder of exocrine glands
- Most common genetic lung disease in the United States
- Classified as airflow or suppurative (pus-forming)
- Hypersecretion of abnormal, thick mucus that obstructs exocrine glands and ducts
- Median surv
CF Pathogenesis
- Dysfunction of CFTR gene
- Primarily affects the pancreas, intestinal tract, sweat glands, and lungs, and in males causes infertility
- High concentrations of sodium and chloride in sweat, salivary, and lacrimal secretions
- Mucous-producing glands in t
CF Clinical Manifestations
- History of cough in young adult or child
- Thick, tenacious sputum
- Recurrent pulmonary infections and bronchitis
- Dyspnea, tachypnea
- Sternal retractions
- Unequal breath sounds
- Moist basilar crackles and rhonchi
- Barrel chest hyperresonant to pe
CF Diagnosis
- ABG
- PFT
- Chest Xray
- Sputum C&S
- 72-hour stool collection
- Sweat test (pilocarpine iontophoresis)
- Genetic testing (AF-508)
CF Treatment
- Aggressive treatment of respiratory infections
- Postural drainage and chest physiotherapy (priority)
- Forced expiratory technique
- Nutritional Therapy
- Heart-lung or lung transplant
CF Treatment Medications
- Bronchodilators
- Recombinant human deoxyribonuclease I (Dornase alfa): digest extracellular DNA present in the viscid sputum
- High dose antibiotics (bacterial infections)
- Influenza vaccine