Lower Airway Diseases

Question 1

Prevalence of asthma:

Answer 1

• continues to increase in the US
  
  • 8% in 2019
• Adults: 20 million (8%)
• Children: 5.1 (7%)
  
  • leading chronic disease in children
• Sex:
  
  • Female>Males
• Race:
  
  • Black>White>Mexican
    
    • Peurto Rican highest among hispanics
• Income:
  
  • lower income families
• Geographic and Urban/rural-no significant difference

Question 2

Asthma: Morbidity & Mortality

Answer 2

• Mortality is low (3500), but morbidity is HIGH
• Morbidity: HIGH
  
  • Hospitlizations
  • ED visit
  • Physician office visits
• COST:
  
  • 82 billion in total costs (3,300/ person)

Question 3

Asthma: Risk factors:

Answer 3

• Intrinsic Factors
  
  • Sex and Age
    
    • Boys>girls-age: 0-5
      
      • 5-24; no difference
    • Women>men
      
      • 25+
  • Family history
    
    • genetics
  • Atopy
    
    • IgE to allergens
  • Airway hyperreactivity:
    
    • all asthmatics have AHR, but not everyone with AHR has asthma
  • Obesity
• Extrinsic/Enviromental factors
  
  • Allergen exposure
  • Tobacco smoke
  • Air pollution (NO2)
  • occupational exposures
  • Respiratory infections
    
    • (RSV, HRV in infants/small children)
  • Acetominophen use
    
    • depletes lung glutathione
  • diet

Question 4

Asthma: Signs and Symptoms:

Answer 4

• recurrent
  
  • airway obstruction
  • cough
  • wheezing
  • difficulty breathing
  • chest tightness
• Symptoms occur or get wosre:
  
  • at night
  • excerise
  • viral infection
  • exposure to allergens and irritants
  • changes in weather
  • hard laughing or crying
  • stress

Question 5

Asthma Classification:

Answer 5

• types of triggers
  
  • Allergy induced asthma
  • Exercise induced asthma
    
    • worse when air is cold and dry
  • Occupational asthma
    
    • workplace irritaants
• Types of airway inflammation:
  
  • Eosinophilic astham=Allergic asthma
    
    • most prevalent type
    • respond to corticosteroids
  • Neutrophilic Asthma=intrinsic asthma (non-allergic)
  • Mixed inflammation=refractory asthma
    
    • unresponsive to all treatments
  • Paucigranulocytic asthma=non-inflammatory asthma
    
    • least prevalent

Question 6

Goals of Asthma Management

Answer 6

• Reduce impairment
  
  • prevent chronic symptoms
  • require infrequent use of short-acting beta-2 agonists (SABA)
  • maintain (near) normal lung fxn and normal activity levels
• Reduce risk
  
  • prevent exacerbations
  • minimize need for emergency care, hospitalization
  • prevent loss of lung function
  • minimize adverse effects of therapy

Question 7

Astham Pathophysiology: 3 airway responses

Answer 7

• Bronchoconstriction
  
  • Smooth muscle contracts in response to Histamine binds H1 receptors
  • and Ach from parasympathetic binding M3
• Mucus hypersecretions
  
  • induced by:
    
    • Th2 cytokines (IL-13)
    • cholinergic stimulation
    • LTCs
    • histamine
• Airway wall swelling
  
  • edema
  • influx of eosinophils

Question 8

Allergic Asthma: Early vs Late reaction

Answer 8

• Early Reaction (Type 1)
  
  • allergin binds IgE on mast cells
  • Mast cells degranulate
  • release preformed mediators
  • cause:
    
    • airway smooth muscle contraction
    • activate nerves
    • cause mucus secretion
• Late reaction (Type II)
  
  • take longer to cause an effect
  • recruit inflammatory cells (eosinophils) which release more mediators

Question 9

COPD

Answer 9

• Chronic Obstructive Pulmonary Disease
• umbrella term for progressive obstructive lung diseases:
  
  • emphysema
  • chronic bronchitis
• Common, preventable and treatable disease
• persistent respiratory systems and airflow limitation
• Airflow obstruction not as reversible as in asthma
• most people with COPD have both emphysema and chronic bronchitis
• 4th leaidng cause of death in the US

Question 10

COPD is the result of:

Answer 10

• long term exposure to noxious gases and parties combined with
• host factors:
  
  • genetics
  • airway hyperresponsiveness
  • poor lung growth during childhood

Question 11

COPD prevalence:

Answer 11

• 13 million diagnosed in US
  
  • many more undiagnosed
  • continues to rise
• Sex:
  
  • Women>Men
• Increases with age
• Higher in whites, lowest income and in South (vs NE, West and Midwest)

Question 12

COPD morbidity in the us:

Answer 12

• Costs:
  
  • 32.1 billion in 201-
  • 49 billion in 2020
• Loss of production
  
  • 16.4 million days of work lost costing 3.9 billion

Question 13

Who pays for COPD direct costs

Answer 13

• 51% medicare
• 25% medicaid
• 18% private insurance

Question 15

COPD Risk factors:

Answer 15

• Smoking or exposure to enviromental tobacco
• Asthma and smoke
• occupation exposure to dusts and chemicals
• Fumes from buring fuels for heating and cooking
  
  • developing countries
• Age
• Genetics
  
  • alpha-1-antitrypsin deficiency

Question 16

Chronic Bronchitis vs Emphysema

Answer 16

• Chronic Bronchitis:
  
  • chronic airway inflammation
  • daily cough and mucus production for at least 3 months a year over 2 years
• Emphysema:
  
  • alveolar wall destruction

Question 17

COPD symptoms:

Answer 17

• do not become known until significant lung damage
• susceptible to exacerbations

Question 18

Chronic Bronchitis

Answer 18

• Aka Blue Bloaters
• inflammation of airways and bronchoconstriction leads to expiratory wheezing and dyspnea
• Mucus production and hyper secretion=Productive cough

Question 19

Chronic Bronchitis: Physiological effects

Answer 19

• Airway obstruction causes alveolar hypoxia–>hypoxic vasoconstriction
  
  • may lead to pulmonary HTN and cor pulmonale, edema, and renal effects in late disease)
• Hypoxemia leads to:
  
  • cyanosis
  • polycythemia
  • V/Q mismatch also causes CO2 retention leading to respiratory acidosis

Question 20

Empysema

Answer 20

• aka pink puffers
• Neutrophilic inflammation in alveoli breaks down elastin fibers
  
  • neutrophil elastase
    
    • loss of elastic recoild and enlarged airspaces
    • Airways collapse & gas trapped
  • Have High lung volumes:
    
    • increased RV and FRC
  • Barrel Chests
  • WOB=increase
  • skinny
• Macrophages release proteases which destroy alveolar walls
  
  • reduced perfusion and ventilation
  • V/Q is matched but reduced
  • hypoxemia and hypercapnia occur later in the disease (vs chronic bronchitis)

Question 21

Emphysema Gross Pathology

Answer 21

• Bullae
  
  • large dilated airspaces that bulge out
• Large damged alveoli means there is:
  
  • less surface area for gas exchange
  • less elastic recoil

Question 22

Centrilobular vs Panloblular Emphysema

Answer 22

• Centrilobular
  
  • primarily upper lobes
  • loss of respiratory bronchioles in proximal portion of acinus
  • spare distal alveoli
  • smokers
• Panlobular
  
  • all lung fields, mainly base of lungs
  • lose prtions of acinus from respiratory bronchiole to alveoli
  • alpha-1-antitrypsin deficiency

Question 23

If emphysema breaks down alveolar walls, why is it an obstructive disease?

Answer 23

loss of elastic recoil so airways more susceptible to dynamic compression and collapse during forced expiraiton