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Module 10 - Pulmonary Disorders > Asthma > Flashcards

Asthma Flashcards

1
Q

What are obstructive lung diseases?

A

Lung disorders characterized by impaired airflow caused by an airway obstruction (partial or complete) at any level from the trachea to the bronchioles.

Includes:
1. asthma
2. COPD (emphysema and/or chronic bronchitis)
3. cystic fibrosis (also restrictive)

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2
Q

What are the 4 mechanisms of airway obstruction?

A
  1. increased thickness of airway walls.
  2. Airway occlusion
  3. Loss of elastic fibres
  4. bronchoconstriction
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3
Q

What are the effects of airway obstructive lung disease on ventilation?

A

During inhalation the airways are pulled open and air rushes past the obstruction.

During exhalation obstructed airways collapse before exhalation is complete (can’t get the air out).
- trapped air makes it difficult to take another breath
- increased work of breathing = accessory muscles are required
- air trapping causes lung hyperinflation

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4
Q

What is FVC (forced vital capacity)?

A

Part of a pulmonary function test that measures the volume forcibly exhaled after a full inhalation.

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5
Q

What is FEV1 (forced expiratory volume in 1 second)?

A

Part of a pulmonary function test that measures volume forcibly exhaled within 1 second.

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6
Q

How is spirometry measured?

A

Expressed as a ratio (FEV1/FVC) or FEV1 as a percentage of a predicted value.

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7
Q

What is asthma?

A

Chronic inflammatory disease of airways characterized by airway hyperresponsiveness (exaggerated tendancy to narrow in response to various triggers) resulting in airflow limitation.

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8
Q

Asthma mainly affects which part of the lungs?

A

Bronchioles and small bronchi. The more airway inflammation present the more hyperresponsive the airways.

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9
Q

What is the clinical presentation of asthma?

A
  • variability of frequency, severity and triggers
  • recurrent episodes of wheezing, chest tightness, cough an dyspnea
  • airflow limitation is at least partially reversible (spontaneously or with treatment)
  • treatment goals involve reducing the frequency of asthma episodes and severity of symptoms.
  • poorly managed asthma results in airway remodeling (= permanent thickening of airway walls) and chronic obstruction
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10
Q

Describe the etiology of asthma.

A

Genetic and environmental factors are proposed to play a role in the underlying airway inflammation and hyperresponsiveness.

  1. genetic predispostion (> 100 genes identified in genome-wide studies associated with asthma)
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11
Q

What are some proposed environmental factors across the lifespan that cause asthma?

A
  • prenatal/perinatal: exposure to maternal smoking, maternal vitD deficiency, prematurity, c-section delivery
  • childhood: exposure to allergens, microbiome dysbiosis (early abx exposure), childhood respiratory infections (RSV), exposure to air pollution and tobacco smoke
  • adolescence/adult: exposure to chlorinated pools, active smoking, occupational exposures.
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12
Q

What is the difference between allergic and non-allergic asthma?

A
  1. Allergic (atopic) = initiated by exposure to an allergen.
  2. non-allergic (non-atopic) = initiated by exposure to an airway irritant

Many asthmatics have a combination of both.

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13
Q

Which kind of asthma accounts for most cases of childhood onset asthma?

A

Allergic asthma.

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14
Q

Describe the genetic component to allergic asthma.

A

Individuals with allergic (atopic) asthma have a genetic predisposition to develop IgE in response to allergens (=atopy)

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15
Q

What other atopic disorders are often present with allergic asthma?

A
  • eczema, food allergies, allergic rhinitis
  • tend to present with eczema from birth, food allergies around 1-2 years, rhinitis around 3 years and asthma around 7 years
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16
Q

Describe the bodies initial immune response in allergic asthma.

A

With initial exposure to allergen:

  • an abnormal immune response = large amounts of allergen specific-IgE in those genetically predisposed
  • response involves an imbalance between Th1 and Th2 production (favouring Th2 cells and activation of B cells)
  • IgE that isn’t exposed to the allergen, binds to airway mast cells = airway sensitization
17
Q

Describe the bodies subsequent response to an allergen in allergic asthma.

A
  • The allergen cross-links IgE molecules bound to mast cells of sensitized airways
  • Mast cell activation & degranulation cause the early phase of an acute asthma attack.
18
Q

What are triggers for non-allergic asthma?

A

Viral respiratory infections and exposure to bronchial irritants

19
Q

What percentage of asthmatics does non-allergic asthma account for?

A

30%

20
Q

When in the lifetime does non-allergic asthma typically evolve?

A

Adulthood

21
Q

How do respiratory infections lead to non-allergic asthma?

A
  • viral infections harm the epithelium, causing airway inflammation
  • increases airway sensitivity, including to other triggers
22
Q

What is exercise-induced bronchoconstriction?

A

Loss of heat and water from airways causes irritation and inflammation (worse in cool, dry weather)

Attacks often occur when exercise stops and airways are less dilated (within 3 mins)

Tend to resolve within 60 mins

23
Q

How do aspirin, NSAIDs cause to non-allergic asthma?

A
  • block the COX enzyme and PG synthesis and a relative increase in leukotrines = bronchoconstriction
  • attacks occur within minutes to hours (up to 12 hours) of ingestion
24
Q

How do inhaled irritants cause non-allergic asthma?

A
  • cigarette smoke, air pollutants, strong odours = stimulate irritant receptors in airway walls causing reflex bronchoconstriction
25
Q

What happens in the acute asthmatic response phase?

A
  • allergens activate mast cells and Th2 cells within airway walls
  • mast cell activation = release of preformed inflammatory mediators such as histamine and chemotactic factors
  • Th2 cells produce cytokines that contribute to B cell activation and IgE synthesis

Airway changes:
- bronchoconstriction
- airway swelling (edema)
- mucous production

26
Q

How does a bronchodilater work?

A

relaxes bronchial smooth muscle and typically increases airflow within 5 mins

27
Q

What happens in the late asthmatic response?

A
  1. the effects of slower acting cytokines, prostaglandins, and leukotrines
  2. epithelial injury by recruited eosinophils
  3. the activation of parasympathetic reflexes
28
Q

What the slower acting prostaglandins and leukotrines do in asthma?

A

Contribute to inflammation, bronchoconstriction, and mucus production.

29
Q

What role to eosinophils play in asthma?

A

Eosinophils are recruited by chemotactic factors released by Th2 cells (IL-5) and mast cells.

They release damaging proteins (e.g. major basic protein)
- normally toxic to parasites
- cause airway epithelial damage (along with tryptase from mast cells) and inflammation

30
Q

What are creola bodies?

A

Shed epithelial cells found in the sputum of symptomatic asthmatics.

31
Q

Describe the activation of parasympathetic reflexes in late asthmatic response?

A

Epithelial damage exposes subendothelial sensory nerve endings.

  • activates the parasympathetic (vagal) reflexes causing further bronchoconstriction and mucus secretion
32
Q

What are the effects of partial obstruction on lung function?

A
  • air trapping and hyperinflation
  • increased work of breathing
33
Q

What are the effects of total obstruction of airways?

A
  • obstructive atelectasis = collapse of alveoli
34
Q

What is airway remodelling?

A

Occurs with frequent asthma attacks and persistent inflammation and is irreversible.

  1. epithelial cell damage stimulates collagen deposition and subepithelial fibrosis
  2. airway smooth muscle layer thickens
35
Q

Why do attacks occur at night or upon waking?

A
  • muscle relax during sleep and tend to narrow
  • reclining position causes secretions to accumulate
  • low epinephrine (especially at 4am) which normally causes bronchodilation
36
Q

Describe 6 steps in diagnosing asthma.

A
  1. patient history
  2. physical exam
  3. spirometry (pre and post bronchodilator), peak flow monitoring (PFM), methacholine challenge
  4. lab tests (CBC (elevated eosinophils, serum IgE)
  5. chest x-ray (r/o other causes, may show lung hyperinflation during an attack)
  6. allergy testing
36
Q

What do FEV1 and FVC stand for in spirometry?

A

FEV1 = forced expiratory volume in 1 second, or the amount of air you can exhale in the first second after a deep breath.

FVC = Forced vital capacity, or the total amount of air you can exhale forcefully in one breath

37
Q

Describe 4 steps to manage asthma.

A
  1. Prevention:
    - removal of triggers (#1 preventative measure)
    - vaccinations
  2. Develop an asthma action plan/ regular follow up care
    - educate patient on how to self-manage worsening symptoms and when to seek medical help
  3. Quick relief of acute attacks e.g. short-acting beta-2 agonist (SABAs) or budesonide/formeterol (symbicort)
    - goal is to minimize use (>2 uses/week is a sign of poorly controlled asthma)
  4. Long-term management (controller meds)
    - used on a regular basis
    - treat underlying inflammation, maintain asthma control, and prevent attacks
    - e.g. inhaled corticosteroids, long-acting beta-2 agonists (LABAs), leukotrine receptor antagonists.
38
Q

What is ‘good control’ of asthma defined as?

A
  • daytime asthma symptoms < or equal to 2 days/week and no nighttime symptoms
  • little to no need for reliever meds (< or equal to 2 days/week)
  • no limitations to physical activity or absence from school/work
  • normal or near normal lung function

Module 10 - Pulmonary Disorders (4 decks)

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