Obstructive Pulmonary Disorders – Chapt 22

Overview – Obstructive Pulmonary Disorders (OPD)

• Cardinal feature:

  • resistance to expiratory airflow

  • ↓ expiratory flow rates

  • ↑ RV.

• Three anatomic classes of obstruction

  1. Conditions within the airway wall (e.g., asthma, bronchitis)

  2. ↑ external pressure on airway wall (e.g., loss of radial traction in emphysema)

  3. Material inside airway lumen (e.g., mucus, foreign body)

Conditions in the Wall of the Lumen

Asthma

• Etiology & Types

  • Reversible airway obstruction, chronic inflammation, airway hyperreactivity.

  • Intrinsic (non-allergic, adult-onset) vs. Extrinsic (IgE-mediated, pediatric-onset).

  • Phenotypes: early-onset, late-onset eosinophilic, exercise-induced, obesity-related, neutrophilic.

• Immunopathogenesis

  • Allergen → IgE production by B-cells → IgE binds mast cells → repeat exposure → mast-cell degranulation (histamine, leukotrienes, cytokines).

  • Histologic features: epithelial denudation, sub-basement collagen, edema, mast-cell activation, eosinophil/lymphocyte/neutrophil infiltration.

  • Results: acute bronchospasm, mucosal edema, mucus plugs, airway remodeling (wall thickening, ↑ mucus glands).

• Clinical Manifestations

  • Classic triad: wheeze, dyspnea, chest tightness; + cough & sputum.

  • Severe: accessory-muscle use, intercostal retractions, silent chest, PEFR < 80\;\text{L·min}^{-1}, tachycardia, orthopnea.

  • Status Asthmaticus: life-threatening attack non-responsive to bronchodilators.

• Diagnosis: H&P, spirometry (↓FEV_1), sputum eosinophils/Charcot-Leyden crystals, ABGs, CXR.

• Treatment

  • Prevention: trigger avoidance, desensitization.

  • Controller drugs: inhaled corticosteroids, leukotriene modifiers.

  • Relievers (acute): short-acting β2-agonists, systemic steroids, O2 .

  • Education on airway remodeling & medication adherence (patient‐question answer page 44).

Acute Bronchitis

• Etiology: Acute inflammation of trachea & bronchi, usually viral; “asthmatic bronchitis” seen in children.

• Pathogenesis: mucosal edema, capillary dilation, ↑ mucus, ciliary loss, viral/bacterial inhibition of macrophages.

• Clinical: recent cough (hallmark), mild wheeze; self-limited.

• Dx: clinical.

• Tx: supportive; antibiotics if bacterial; symptom management.

Chronic Bronchitis (Type B COPD – “Blue Bloater”)

• Etiology: >90\% linked to cigarette smoke; also repeated infections, irritants, genetics.

• Pathogenesis

  • Chronic mucosal inflammation → scarring/fibrosis.

  • Goblet-cell hyperplasia & gland hypertrophy → thick mucus.

  • ↑ bronchial wall thickness, smooth-muscle hypertrophy.

  • Mucus stasis fosters bacterial infection.

• Clinical

  • Overweight, 30−40 yrs+, dyspnea on exertion, chronic productive cough ≥3 mo/yr × 2 yrs, excess body fluids (edema), coarse lung sounds.

  • Air trapping → ↑RV → “barrel chest”.

  • Complication: cor pulmonale (↑ pulmonary vascular resistance → RV failure); polycythemia.

• Dx: symptom criteria above, CXR, PFTs, ABGs, ECG.

• Tx Goals: halt progression, optimize respiration, maintain ADLs.

  • Smoking cessation, bronchodilators, inhaled steroids, O_2 , vaccines, rehab.

Chronic Obstructive Pulmonary Disease (COPD)

• Umbrella term: emphysema (Type A), chronic bronchitis (Type B), chronic asthma not fully reversible; may coexist.

Loss of Lung Parenchyma

Emphysema (Type A COPD – “Pink Puffer”)

• Etiology: Destructive enlargement of distal airspaces & alveolar walls; often accompanies chronic bronchitis; can follow bacterial infections.

• Pathogenesis

  • Inflammatory cells (neutrophils, macrophages) release proteases → destroy elastin.

  • Deficiency of \alpha_1-antitrypsin → unchecked elastase activity.

  • Smoking inactivates \alpha_1-antitrypsin.

  • ↓ surface area for gas exchange; loss of radial traction → airway collapse on expiration → air trapping & hyperinflation.

  • Subtypes: centriacinar, panacinar, paraseptal.

• Clinical: thin, ~55 yrs, progressive exertional dyspnea, minimal cough, barrel chest, clubbing.

• Dx: PFT (↑TLC, ↑RV, ↓DLCO), CXR (hyperlucent), ABGs (near-normal early), ECG.

• Tx: smoking cessation, nutrition, bronchodilators, steroids, O_2 , rehab; severe → lung reduction/transplant.

Obstruction of the Airway Lumen

Bronchiectasis

• Etiology: congenital or acquired; obstructive & suppurative; shapes: saccular, cylindrical, fusiform.

• Pathogenesis: recurrent infection → permanent dilation & destruction of bronchi/bronchioles.

• Clinical: chronic productive cough with copious foul purulent sputum (layers in cup), hemoptysis, night sweats, halitosis, crackles, clubbing (if chronic). Not contagious.

• Dx: H&P, high-resolution CT (gold standard), PFT, ABG.

• Tx: antibiotics, bronchodilators, chest physiotherapy/postural drainage; severe → bronchoscopy lavage or resection.

Bronchiolitis (often infants/children)

• Etiology: diffuse bronchiolar inflammation from viruses, smoke, toxins, immunosuppression.

• Pathogenesis: epithelial necrosis, mucus plugging, obstruction.

• Clinical: wheeze, crackles, ↓ breath sounds, retractions, sputum, dyspnea, tachypnea, low-grade fever.

• Dx: ↑WBC, CXR hyperinflation, PFT, cultures.

• Tx: O_2 , bronchodilators, steroids, hydration, antivirals/antibiotics, quit smoking.

Cystic Fibrosis

• Etiology: autosomal-recessive CFTR mutation; median survival ≈31 yrs; accounts for 50\% of bronchiectasis.

• Pathogenesis: defective Cl^-/H_2O transport → thick secretions; affects lung, pancreas, GI, sweat glands, male infertility.

• Clinical: chronic cough with thick sputum, recurrent infections/bronchitis → pneumonia, bronchiectasis; barrel chest, clubbing, RHF.

• Dx: sweat test (pilocarpine iontophoresis), genetic test, stool fat, PFT, CXR, ABG.

• Tx: bronchodilators, chest PT, postural drainage, dornase alfa, aggressive antibiotics, nutrition, lung/heart-lung transplant.

Acute Tracheobronchial Obstruction

• Etiology: foreign body aspiration, malpositioned ETT, laryngospasm, epiglottitis, smoke injury, clot, external compression by tumors/adenopathy.

• Clinical: silent chest, inability to speak, tachycardia, cyanosis → rapid LOC.

• Dx: clinical, ABG, CXR.

• Tx: airway opening (Heimlich/back blows), suction, tracheostomy.

Epiglottitis

• Etiology: rapidly progressive bacterial cellulitis of epiglottis (H. influenzae type b historically).

• Pathogenesis: supraglottic infection → massive edema → airway obstruction (fatal if untreated).

• Clinical: sudden fever, dysphagia, drooling, muffled voice, inspiratory stridor/retractions, “sniffing-dog” posture; cherry-red epiglottis.

• Dx: fiberoptic visualization (caution), lateral neck X-ray (“thumb sign”), CBC.

• Tx: IV antibiotics, airway protection (intubation), Hib vaccination prevention.

Croup Syndrome (Laryngotracheobronchitis)

• Etiology: group of viral/inflammatory laryngeal diseases (parainfluenza etc.).

• Pathogenesis: diffuse airway inflammation → subglottic edema.

• Clinical: child with URI → barking cough, stridor.

• Dx: clinical; neck films exclude epiglottitis.

• Tx

  • Outpatient: cool mist, hydration, rest.

  • Inpatient/severe: O_2 , nebulized epinephrine, possible intubation.

Case Study – 50-Year-Old With Chronic Bronchitis Exacerbation

Potential In-Hospital Risks (marked X in exercise)

• Cough with purulent sputum, exertion-induced dyspnea, polycythemia, muscle aches, insomnia, edema.

• Weight loss NOT typical of chronic bronchitis.

  Rationale highlights: diagnostic criteria (>3 mo cough ×2 yrs), typical overweight phenotype, excess fluids, RBC ↑ to compensate hypoxemia.

Patient Education Q&A (Common Queries)

1. Importance of taking asthma drugs: prevents attacks & airway remodeling; uncontrolled attacks → irreversible structural changes.

2. Definition of airway remodeling: permanent thickening of airway walls, ↑ mucus-gland numbers; unlike house remodeling—no demolition but pathologic buildup; worsens symptoms/control.

3. Explanation of airway hyperresponsiveness: asthmatic airways over-react to small irritant doses → inflammation & constriction more readily than normal.

Cross-Links & Practical / Ethical Points

• Smoking cessation is the single most effective intervention across COPD, chronic bronchitis, emphysema; ethical duty to counsel.

• Vaccinations (influenza, pneumococcal, Hib) are preventive ethics to reduce morbidity.

• Airway management (Heimlich, intubation) involves rapid decision-making to prevent hypoxic injury—high-stakes clinical ethic of beneficence.

Numerical / Statistical References & Equations

• VC = IRV + TV + ERV

• FEV_1

  • 
    \ge 0.75\; (75\%) \; \text{of VC in healthy adults}
    

• PEFR < 80\;\text{L·min}^{-1} signals severe asthma attack.

• Median survival age in cystic fibrosis ≈ 31\;\text{yrs}.

• Diagnostic cough criterion for chronic bronchitis:
  \ge 3\;\text{mo·yr}^{-1}\; \text{for}\; 2\;\text{consecutive yrs}
  

Study Tips

• Memorize the hallmark features that distinguish Type A (emphysema) vs. Type B (chronic bronchitis).

• Practice interpreting spirometry: ↓FEV_1/FVC ratio & ↑RV/TLC hallmark obstructive pattern.

• Link pathogenesis (e.g., \alpha_1-antitrypsin deficiency) to clinical picture & therapy.

• Use patient scenarios (case study) to apply cue analysis & prioritize interventions.