Obstructive Airway Diseases (Asthma) Flashcards

1
Q

Complications of Chronic Obstructive Pulmonary Diseases

A
  • Permanent remodeling of the airway

- Chronic, persistent airflow limitation

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2
Q

Pulmonary Remodeling

A
  • Increased collagen in the basement membrane causing thickening of the airway wall
  • Increased smooth muscle mass
  • Inflammatory cell infiltration
  • Mucous gland hyperplasia
  • Results in an airway that is chronically narrowed & thus, more susceptible to enhanced narrowing during smooth muscle constriction
  • Clinically this causes decreased forced expiratory volume in 1 second (FEV1) & persistent airflow limitation
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3
Q

Atopy

A

Genetic predisposition to hypersensitivity reaction due to production of specific IgE antibody

  • Asthmatics often suffer from allergic rhinitis or atopic dermatitis
  • *Not all atopic pt’s develop asthma (combination of genetic and environmental factors)

MC allergens leading to sensitization: (1) house dust mites (2) pet fur (3) cockroaches (4) grass (5) pollen (6) rodents

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4
Q

Intrinsic (non-atopic) Asthmatics

A

Negative skin tests to inhalant allergens, normal serum IgE, usually later onset of the disease, commonly have nasal polyps, & may be sensitive to ASA

  • Usually more severe, persistent asthma
  • Unknown pathophysiology, but related to the increase in local IgE in airways
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5
Q

Infection & Asthma

A
  • Viral infections may trigger exacerbations (unknown etiology)
  • Some associations between RSV virus, mycoplasma and chlamydophila pneumonia bacteria and the development of asthma
  • Specific pathophysiology is unknown
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6
Q

Diet & Asthma

A

Controversial role

  • Diets low in antioxidants and vitamin D may trigger asthma
  • Obesity is a risk for asthma, especially in women
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7
Q

Environmental Exposures & Asthma

A
  • “Hygiene hypothesis”
  • Air pollution: sulfur dioxide, ozone, diesel particulates, cigarette smoking (esp. during pregnancy)
  • Occupation exposures: chemicals, fungus, animals (~10% of young adults)
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8
Q

Asthma Triggers

A
  • Allergens –> activate mast cells with bound IgE, causing bronchoconstriction (MC = dust mites)
  • Viral infections –> URI causes airway inflammation, eosinophils, neutorphils
  • Drugs –> B-blockers (increased cholinergic bronchoconstriction) & ASA
  • Exercise –> hyperventilation triggers mast cell release & bronchoconstriction (usu. lasts 30 min, worse in cold/dry climates)–B-agonists/steroids usually used as prevention
  • Food –> salicylate
  • Air pollution
  • Occupational factors
  • Hormonal factors –> premenstrual period
  • GERD
  • Stress
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9
Q

Pulmonary Function Tests

A
  • Measure: airflow rates, lung volumes, ability of the lung to transfer gas across the alveolar-capillary membrane
  • Help asses type and extent of lung dysfunction, causes of dyspnea and cough, detection of early lung dysfunction, & follow-up in response to therapy

Disadvantages: Effort-dependent, measured against predicted values derived from large studies of healthy patients, vary with age, gender, height, weight, and ethnicity

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10
Q

Spirometry

A

Measurement of how much air can be inhaled/exhaled

- Allows assessment of the presence and severity of obstructive and restrictive pulmonary dysfunction

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11
Q

Obstructive Dysfunction

A

A reduction in airflow rates (FEV1/FVC ration)

  • FEV1 = forced expiratory volume in the first second
  • FVC = forced vital capacity–the largest amount of air that can be forcefully exhaled after a deep breath
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12
Q

Restrictive Dysfunction

A

Marked by a reduction in lung volumes with a normal to increased FEV1/FVC ration

  • Severity graded by a reduction in total lung capacity
  • EX. Pulmonary fibrosis
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13
Q

Peak Expiratory Flow Meters

A

Handheld devices used by patients to monitor severity of their asthma exacerbation

  • Helps set parameters for treatment measures
  • Predicted values vary with age, height, and gender
  • PEFs vary throughout the day–usually lowest on first awakening & highest several hours before the midpoint of the waking day
  • PEF should be measured in the AM before bronchodilator administration & in the afternoon after administration
    • 20% + change from AM to PM = poorly controlled asthma
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14
Q

Mild Intermittent Asthma

A
  • Sxs of cough, wheeze, chest tightness, or difficulty breathing less than 2x/week
  • Flare-ups brief with varying intensity
  • Nighttime sxs 2+ times/month
  • No sxs between flare-ups
  • Lung function test FEV1 equal to or above 80% of normal values
  • Peak flow less than 20% variability AM-to-AM or AM-to-PM, day to day
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15
Q

Mild Persistent Asthma

A
  • Sxs of cough, wheeze, chest tightness or difficulty breathing 3-6x/week
  • Flare-ups may affect activity level
  • Nighttime sxs 3-4x/month
  • Lung function test FEV1 equal to or above 80% of normal values
  • Peak flow less than 20-30% variability
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16
Q

Moderate Persistent Asthma

A
  • Sxs of cough, wheeze, chest tightness or difficulty breathing daily
  • Flare-ups may affect activity level
  • Nighttime sxs 5+ times/month
  • Lung function test FEV1 between 60-80% of normal values
  • Peak flow greater than 30% variability
17
Q

Severe Persistent Asthma

A
  • Sxs of cough, wheeze, chest tightness, or difficulty breathing continually
  • Nighttime sxs frequently
  • Lung function test FEV1 less than or equal to 60% of normal values
  • Peak flow greater than 30% variability
18
Q

Goals of Asthma Therapy

A
  • Reduce/eliminate chronic sxs
  • Eliminate exacerbations/ED visits
  • Reduce need for B-agonists
  • Reduce side effects of medications
  • Eliminate activity restrictions
  • Children follow a step-wise approach to therapy starting with B2-agonists then adding additional agents as needed
19
Q

Airway Hyper-Responsiveness

A
  • Exaggerated bronchoconstrictor response to stimuli
  • Related to inflammation and structural changes
  • Reduced when inflammatory inflammation is treated
20
Q

Airway Obstruction

A

Symptoms: Chest tightness, cough, wheezing

Causes:

  1. Airway smooth muscle constriction
  2. Airway edema
  3. Mucus hyper-secretion
  4. Airway remodeling
21
Q

Disposition

A

Discharge vs. Admission, consider

  • Social situation (i.e., homelessness, access to medications)
  • Prior hospitalizations
  • Compliance history
  • History of intubation

Discharge:

  • Resolution of symptoms (improved PEF or FEV to > 70% predicted value)
  • Pulse oximetry of at least 92%
  • Pt can speak, eat, and drink with ease

Admit:
- Poor/slow response to treatment (PEF or FEV < 40% predicted value)

22
Q

B1-Receptors

A
  • Adrenergic*
  • Widely expressed in the airways
  • Relax smooth muscle
  • Inhibit inflammatory cells
  • -> B2-agonists facilitate this (prevent smooth muscle contraction) (e.g. Albuterol, Salmeterol)
  • Usually given via inhalation
23
Q

Leukotrienes

A
  • Inflammatory mediators produced by mast cells that cause bronchoconstriction
  • -> Antileukotrienes block receptors
  • Less effective than ICS (used in conjunction in pts not controlled w/ ICS)
24
Q

Asthma & Poverty

A

Asthma in poor pts causes more…

  • Frequent asthma symptoms (every day or every week)
  • School absenteeism
  • Poor health status
  • ED visits (2x higher)

Causes:

  • Lack of health insurance, regular primary care, and/or asthma management plans
  • Increased exposure to second-hand smoke, cockroaches, air pollution, and allergens
25
Q

Pathology of Cigarette Smoke

A

Affects large airways, small airways (< or equal to 2mm diameter), & alveoli

Large airways:
Goblet cell increase in #, bronchi undergo squamous metaplasia, smooth muscle hypertrophy & bronchial hyperactivity, neutrophil influx, neutrophil elastase (proteolytic)