Unit 10 Obstructive Disorders

Obstructive Airway Disorders→ getting air OOOut

  • Definition: Obstructive airway disorders are conditions that limit expiratory airflow.

    • Characteristics:

    • The airway obstruction primarily causes difficulties during expiration, with a requirement for increased force or time to expel air.

    • Dyspnea & Wheezing → universal to all OAD

    • Affected individuals experience increased work of breathing, ventilation-perfusion mismatching, and reduced forced expiratory volume in one second (FEV1).


  • Common Disorders:

    • Asthma

    • Chronic Bronchitis

    • Emphysema

    • Coexisting conditions of chronic bronchitis and emphysema are categorized as Chronic Obstructive Pulmonary Disease (COPD).

Physiology of Airway Disease

  • Airway Anatomy: Air travels from upper airways (trachea and major bronchi) to lower airways (bronchi and alveoli).

  • Airway Structure:

    • In pulmonary airways, cartilage transitions into smooth muscle strips the closer you get the to alveoli

    • Smooth Muscle Control:

    • Controlled by the autonomic nervous system (ANS).

    • Parasympathetic stimulation (via the vagus nerve) causes bronchoconstriction.

    • Sympathetic stimulation (via beta-2 adrenergic receptors) promotes dilation

Asthma

Definition and Risk Factors

  • Asthma: A chronic obstructive airway disorder characterized by episodes of airway obstruction, bronchial hyper-responsiveness, airway inflammation, and occasionally airway remodeling.

  • Major Risk Factor: Genetic predisposition identified (over 100 genes linked to asthma susceptibility and IgE-mediated responses to allergens).

  • Onset: Can occur at any age; predominantly in childhood or early adulthood.

    • Approximately 50% of asthma cases begin in childhood; 30% before age 40.

  • Childhood Risk Factors: Family history, allergies, and prenatal exposure to tobacco smoke and pollution.

Classification

  • Types of Asthma:

    • Acute (single episode) vs. Chronic (long-term condition).

    • Extrinsic: Triggered by Type I hypersensitivity (allergens).

    • Intrinsic: Adult-onset asthma.

    • Exacerbations: Recurrent episodes

  • Severity Factors: Genetics, allergens, pollution exposure, and environmental triggers (e.g., tobacco smoke).

    • Increased risks associated with viral infections (trigger exacerbations) and obesity.

    • Emotional factors and hormonal changes may exacerbate symptoms.

    • Current trends show decreased mortality rates but increased morbidity, particularly among Blacks and older adults (>85 years).

Etiology and Pathogenesis

  • Underpinning Factor: Exaggerated IgE mediated hyper-responsiveness to stimuli, leading to:

    • Inflammation with eosinophils, lymphocytes, mast cells.

    • Damage to bronchial epithelium.

  • Chronic Inflammation:

    • Causes bronchial hyper-responsiveness, mucosal edema, and airflow obstruction, often reversible.

    • Episodes include bronchospasm, inflammation, edema, and increased mucus production.

  • Cytokine Role: Involved in inflammatory responses and asthma complications.

  • Exacerbation:

    • 1)Inflammation of the mucosa with noted edema;

      2)↑ contraction of respiratory-associated smooth muscles (bronchoconstriction); and

      3)Secretions of thick mucus in the respiratory passages

  • vInflammatory process → recurrent episodes (i.e., exacerbations) of airway obstruction and episodic bronchospasms

    §Characterized by:

    oInspiratory and expiratory wheezing, breathlessness or dyspnea, tachypnea, chest tightness, and a non-productive cough that is often worse at night and in the early morning

Clinical Manifestations

  • Asthma Attacks: Can occur spontaneously or due to triggers (e.g., infections, emotional stress).

    • Nocturnal asthma is common due to circadian variations and hormone changes.

    • Symptoms:

    • Episodic bronchospasms, expiratory and inspiratory wheezing.

    • Dyspnea, nonproductive cough, tachypnea.

    • Asymptomatic between exacerbations with normal pulmonary function tests.

  • Additional Symptoms:

    • Tightness in the chest, agitation, inability to talk, accessory muscle use, potential hypoxia.

    • Initial respiratory alkalosis leads to respiratory acidosis over time due to air trapping.

Diagnosis and Treatment Goals

  • Diagnosis: Based on history, physical exams, lab findings, and pulmonary function studies.

  • Treatment Goals:

    • Minimize frequency and severity of acute attacks to avoid lung damage.

    • Reduce risks for chronic obstructive lung disease.

    • Most effective strategy: Avoidance of triggers

Severe or Refractory Asthma

  • Definition: Refers to asthma individuals requiring high medication dosages for symptom control or who experience persistent symptoms despite treatment.

  • Risks: Increased likelihood of fatal asthma outcomes.

  • Etiologies: Include genetic factors, infections, continued allergen exposure, and comorbidities such as gastroesophageal reflux.

  • Acute Attack Risk Factors: Cardiac arrhythmia and asphyxia may cause death during attacks.

Asthma in Older Adults

  • Immunologic Considerations: Decreased immunity with age heightens asthma control difficulties.

  • Comorbidities: Older adults are more likely to have conditions affecting asthma management.

  • Management Challenges: Complexity of treatment regimens and potential physical or cognitive impairments impede control.

Asthma in Children

  • Prevalence: Leading cause of chronic illness in children; more frequent admissions in Black children.

  • Pathogenesis: IgE-mediated responses to respiratory viruses often precede asthma onset.

  • Contributing Factors: Environmental allergens and tobacco smoke increase risk.

  • Clinical Manifestations: Include symptoms of prolonged cough without cold symptoms in infants.

    • Potential rapid progression with irritability, cough, tachypnea, and severe respiratory distress indicated by cyanosis and tachycardia.

Chronic Obstructive Pulmonary Disease (COPD)

Definition and Epidemiology

  • Definition: Chronic obstructive pulmonary disease is marked by persistent and progressive airflow obstruction due to inflammatory responses to harmful particles and gases.

  • Epidemiology: Fourth leading cause of mortality in the US; disproportionately affects assigned-at-birth females (56%) compared to males (44%).

    • §COPD is a leading etiology of worldwide morbidity and mortality

  • Leading Etiology: Smoking (80% of COPD deaths attributed to smoking); hereditary deficiency of alpha-1 antitrypsin is rarer.

Risk Factors and Diagnosis

  • At-Risk Populations: Older adults with recurrent respiratory infections, asthma, and those with chronic productive cough are at higher risk.

  • Recognition: Symptoms are often advanced by the time they are noted, with many smokers being undiagnosed.

  • Potential Indicators: Chronic cough, sputum production, and dyspnea should prompt suspicion of COPD.

Etiology and Pathogenesis

  • Mechanisms: COPD involves inflammation and fibrosis of bronchial walls, mucus hypersecretion, and loss of lung elasticity.

  • Consequences:

    • Inflammation obstructs airflow, leads to mismatching ventilation/perfusion, and reduces gas exchange surface area.

    • Loss of elastic recoil exacerbates airflow limitation and increases air trapping, resulting in airway collapse.

Emphysema

Definition and Pathology

  • Definition: Emphysema is characterized by loss of lung elasticity and abnormal enlargement of airspaces distal to terminal bronchioles and alveolar wall destruction.

  • Mechanism: Caused by protease activity that breaks down elastin and alveolar structures.

  • Physiological Changes: Results in hyperinflation of the lungs and increased total lung capacity.

  • Clinical Manifestations:

    • Presents with barrel chest (increased anterior-posterior diameter), circumoral cyanosis, and pursed-lip breathing during prolonged expiration.

Types of Emphysema

  1. Centriacinar (Centrilobular):

    • Most common form, predominantly in smoking males, affecting bronchioles while preserving alveolar ducts initially.

  2. Panacinar:

    • Involves alveoli and typically occurs in alpha-1 antitrypsin deficiency cases; can occur with centriacinar features in smoking.

Chronic Bronchitis

Pathogenesis and Definition

  • Definition: Chronic bronchitis is marked by inflammation leading to airway obstruction, characterized by hypersecretion of mucus and chronic productive cough.

  • Pathological Changes:

    • Initiated by inhaled irritants that induce neutrophilic infiltration, bronchial edema, and thick mucus production due to increased mucous gland size.

    • This compromises lung defense mechanisms, enhancing susceptibility to infections.

Diagnosis

  • Clinical Criteria: Diagnosis requires a chronic productive cough lasting at least three consecutive months for two consecutive years, with typical findings of purulent sputum during exacerbations.

  • Clinical Findings: Most common in middle-aged individuals with chronic irritative smoke exposure and recurrent infections.

  • Irreversibility: Unlike acute bronchitis, chronic bronchitis leads to irreversible airway changes.

COPD Clinical Manifestations

Symptoms and Progression

  • Symptom Onset: Progressive and insidious; typically features morning productive cough with worsening dyspnea.

  • Exacerbation: Frequent respiratory infections and failure are common in advanced COPD.

  • Presentation: Clinical attention is usually sought in the fifth or sixth decade of life due to symptoms such as fatigue, intolerance, and cough.

  • Mortality: Often occurs during infectious exacerbations leading to respiratory failure.

Emphysema vs. Chronic Bronchitis Differences

  • Emphysema:

    • Presentation: “Pink puffers”, accessory muscle use, breathlessness, barrel chest due to air trapping.

  • Chronic Bronchitis:

    • Presentation: “Blue bloaters”, cyanosis indicating hypoxia, potential heart failure.

  • Despite differences, patients often exhibit symptoms of both conditions.

Diagnosis and Management of COPD

  • Diagnosis: Based on history, physical examination, pulmonary function testing, imaging, and lab tests.

  • Management: No cure exists; however, treatment can modify disease progression with smoking cessation being crucial in managing COPD and emphysema.

Bronchiectasis

Definition and Pathophysiology

  • Definition: Bronchiectasis is an uncommon type of COPD characterized by permanent dilation of bronchi and bronchioles due to elastic tissue destruction.

  • Etiology: Not a primary disease; often occurs secondary to frequent pulmonary infections.

  • Associated Conditions: Seen in individuals with cystic fibrosis, tuberculosis, and previously after bacterial pneumonia.

Etiology and Pathogenesis

  • Mechanism: Mucus obstruction and persistent infection weaken and dilate bronchial walls.

  • Forms:

    1. Localized: Affects specific lung segments, usually due to obstruction of airways.

    2. Generalized: Bilateral and mainly affects lower lobes, associated with hereditary or acquired disorders.

Clinical Manifestations and Diagnosis

  • Symptoms: Include recurrent infections, copious purulent sputum, and hemoptysis. Weight loss and anemia are potential complications.

  • Additional Signs: May show signs of chronic bronchitis and emphysema leading to significant dyspnea and cyanosis, with digital clubbing commonly seen.

  • Diagnosis: Based on history, imaging studies, and high-resolution CT scans.

Cystic Fibrosis (CF)

Definition and Pathogenesis

  • Definition: Cystic fibrosis is an autosomal recessive disorder with defective chloride ion transport, causing thick mucus that obstructs airways and various ducts.

  • Pathophysiology: Abnormal protein production leads to respiratory, digestive, and reproductive system complications.

  • Common Manifestations:§Respiratory manifestations: persistent cough or wheeze, sputum production (most often characterized as “sticky”—difficult for infants and young children to expectorate), and recurrent or severe pneumonia

    §Gastrointestinal manifestations: meconium ileus, constipation, gastroparesis, biliary cirrhosis, cholangiectasis, pancreatic insufficiency, distal intestinal obstruction syndrome (DIOS)

  • CF children get these infections→ Pseudomonas aeruginosa; Staphylococcus aureus; Haemophilus influenza; Burkholderia cepacia→ KNOW THIS

Diagnosis and Treatment

  • Diagnosis: Now involves universal newborn metabolic screening; the sweat test (sweat chloride concentration > 60 mEq/L) remains the gold standard.

  • Treatment Goals: Focus on limiting symptoms and managing complications; mortality is mainly due to respiratory disease.