NURS 503 – Respiratory Pharmacology
Comprehensive Management of Asthma & COPD
Pathophysiology · Diagnosis · Evidence-Based Treatment
Carson-Newman University | NP Program | Study Guide
,SECTION 1: Overview of Lung Disease Types
1.1 Restrictive Lung Disease
• Definition: Conditions that make it hard for the patient to inhale
• Caused by stiffening of tissue in the chest wall, weakened muscles, or damaged nerves
• Key symptom: Shortness of breath
• Examples of causes:
○ Lupus (connective tissue disorder)
○ Kyphosis (forward rounding of the back)
○ Drug-induced: e.g., macrobid – 1 in 5,000 patients have a hypersensitivity reaction causing
pulmonary symptoms (rare but testable)
1.2 Interstitial Lung Disease
• Umbrella term for conditions that cause permanent scarring of the lungs
• Involves inflammatory processes
1.3 Obstructive Lung Disease
• Main diseases: Asthma and COPD – very common
• Signs & symptoms: Coughing (may be nocturnal, seasonal, or exposure-specific), wheezing,
dyspnea
• Precipitating factors: Cold air, exercise, hot/cold weather, chemical exposures (e.g., cleaning
products), allergens
,SECTION 2: Asthma – Pathophysiology
2.1 Risk Factors
• Obesity: Adipose tissue releases pro-inflammatory mediators
• Allergen exposure (cat hair, dust, pollution, pollen, etc.)
2.2 Asthma as an Allergic/Immune Response
• Airway biopsies show same inflammatory markers as nasal rhinitis, hives, and eczema →
asthma is essentially an allergic response in the bronchioles
• The body mounts an inflammatory response to inhaled allergens
The Immune Cascade
• Step 1: Macrophages ingest foreign material (allergens) and display antigen fragments on their
cell surface – this happens in ALL people
• Step 2 (Normal): T cells ignore the presented antigen
• Step 2 (Asthma): T cells mount an immune response to the antigen – exact reason unknown;
theories include the Hygiene Hypothesis
• Step 3: Subsequent exposure to the same allergen triggers a full allergic/asthmatic response
Inflammatory Mediators Recruited
• Eosinophils and mast cells are recruited to the airway
• Release of histamine and IgE
• All are pro-inflammatory
Acute Result: Bronchoconstriction
• Smooth muscle contraction in small and large airways
Chronic Result: Airway Remodeling (IRREVERSIBLE)
• Thickening of the reticular basement membrane (attaches epithelium to underlying tissue)
• Hypertrophy of large and small smooth muscle
• Airway fibrosis – scarring that is irreversible
• Asthma does NOT directly affect alveoli; increased mucus and inflammation causes indirect air
trapping
⚠️ KEY EXAM POINT – Why Albuterol Alone is Inadequate
• Beta agonists (SABAs and LABAs) provide only bronchodilation – they do NOTHING to
prevent airway remodeling
• Only inhaled corticosteroids slow/prevent the irreversible structural damage
• Overuse of albuterol → tolerance via downregulation of beta-2 receptors on cell
surfaces
,
Comprehensive Management of Asthma & COPD
Pathophysiology · Diagnosis · Evidence-Based Treatment
Carson-Newman University | NP Program | Study Guide
,SECTION 1: Overview of Lung Disease Types
1.1 Restrictive Lung Disease
• Definition: Conditions that make it hard for the patient to inhale
• Caused by stiffening of tissue in the chest wall, weakened muscles, or damaged nerves
• Key symptom: Shortness of breath
• Examples of causes:
○ Lupus (connective tissue disorder)
○ Kyphosis (forward rounding of the back)
○ Drug-induced: e.g., macrobid – 1 in 5,000 patients have a hypersensitivity reaction causing
pulmonary symptoms (rare but testable)
1.2 Interstitial Lung Disease
• Umbrella term for conditions that cause permanent scarring of the lungs
• Involves inflammatory processes
1.3 Obstructive Lung Disease
• Main diseases: Asthma and COPD – very common
• Signs & symptoms: Coughing (may be nocturnal, seasonal, or exposure-specific), wheezing,
dyspnea
• Precipitating factors: Cold air, exercise, hot/cold weather, chemical exposures (e.g., cleaning
products), allergens
,SECTION 2: Asthma – Pathophysiology
2.1 Risk Factors
• Obesity: Adipose tissue releases pro-inflammatory mediators
• Allergen exposure (cat hair, dust, pollution, pollen, etc.)
2.2 Asthma as an Allergic/Immune Response
• Airway biopsies show same inflammatory markers as nasal rhinitis, hives, and eczema →
asthma is essentially an allergic response in the bronchioles
• The body mounts an inflammatory response to inhaled allergens
The Immune Cascade
• Step 1: Macrophages ingest foreign material (allergens) and display antigen fragments on their
cell surface – this happens in ALL people
• Step 2 (Normal): T cells ignore the presented antigen
• Step 2 (Asthma): T cells mount an immune response to the antigen – exact reason unknown;
theories include the Hygiene Hypothesis
• Step 3: Subsequent exposure to the same allergen triggers a full allergic/asthmatic response
Inflammatory Mediators Recruited
• Eosinophils and mast cells are recruited to the airway
• Release of histamine and IgE
• All are pro-inflammatory
Acute Result: Bronchoconstriction
• Smooth muscle contraction in small and large airways
Chronic Result: Airway Remodeling (IRREVERSIBLE)
• Thickening of the reticular basement membrane (attaches epithelium to underlying tissue)
• Hypertrophy of large and small smooth muscle
• Airway fibrosis – scarring that is irreversible
• Asthma does NOT directly affect alveoli; increased mucus and inflammation causes indirect air
trapping
⚠️ KEY EXAM POINT – Why Albuterol Alone is Inadequate
• Beta agonists (SABAs and LABAs) provide only bronchodilation – they do NOTHING to
prevent airway remodeling
• Only inhaled corticosteroids slow/prevent the irreversible structural damage
• Overuse of albuterol → tolerance via downregulation of beta-2 receptors on cell
surfaces
,
