Asthma Flashcards

1
Q

Where are the highest rates of asthma

A

Ontario and Nova Scotia

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2
Q

Prevalence of Asthma

A
  • asthma is increasing (major cause of hospitalization in children)
  • prevalence increased as more people are living with asthma due to decreased mortality of disease
  • incidence decline
  • Higher prevalence in boys and women
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3
Q

Where are the lowest rates of asthma

A

Northwest Territories, Yukon, Nunavut

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4
Q

Annual Canadian asthma trends

A
  • 20-25% of asthma exacerbation occur in September (back to school)
  • Adults tend to experience more exacerbations in winter (flu season)
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5
Q

Causes of Childhood Asthma

A
  • susceptible in first 3-5 years of life
  • family hx of allergy and allergic disorders
  • high exposure to airborne allergens
  • exposure to tobacco smoke
  • low birth weight and respiratory distress syndrome
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6
Q

What is Asthma?

A

An inflammatory disorder of the airways characterized by paroxysmal or persistent symptoms

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7
Q

Characterizing symptoms of Asthma

A

dyspnea, chest tightness, wheezing, sputum production and cough

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8
Q

Main mechanism causing development and persistence of asthma

A

Inflammation of the airways and consequential damage

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9
Q

What are the main effects of asthma on the airways?

A

Inflammation, bronchospasm, increased mucus production, airway remodelling, extrinsic and intrinsic factors, early and late phase response

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10
Q

What are the extrinsic triggers for asthma?

A

Type I IgE mediated hypersensitivity reaction

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11
Q

What are intrinsic triggers for asthma

A

respiratory tract infections, exercise, hyperventilation, cold air / weather, drugs (NSAIDs & chemicals), irritants, hormonal changes, emotional upset, airborne pollutants, GERD

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12
Q

Early Phase Response

A

Occurs within 10-20 minutes to 2 hours
- Allergen binds to performed IgE on sensitized mast cells on mucosal surface of airways
Mast cell activation releasing inflammatory mediators
- Pre-formed granules —> Histamine, chemotactic chemokine (mast cell degranulation)
Leukotrienes, prostaglandin D2, cytokines
- Cause infiltration of inflammatory cells, opening intracellular cell junctions allowing access to submucosal mast cells = further inflammation, Increase mucus secretion, increased vascular permeability and bronchoconstriction

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13
Q

Late Phase Response

A

Occurs 4-8 hours to days after trigger
- Release of inflammatory mediators causing recruitment of neutrophils, eosinophils, basophils, T lymphocytes (TH2)
- Inflammatory cells cause epithelial injury and edema, increased mucus, change in mucociliary functions —> accumulation go mucus and increased airway responsiveness and bronchospasm
- Change in mucociliary function due to toxic effects of cells (eosinophils) causing local autonomic parasympathetic nerves to be stimulated = further inflammation

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14
Q

What causes bronchospasm

A

due to parasympathetic stimulation through vagal pathways
- Histamine (early phase)
- Leukotrines (late phase)
- PAF (platelet activating factor)
- Prostaglandins
- Autonomic nervous system dysregulation (PNS)
Increase Cholinergic mediator responsiveness —> due to alteration of muscarinic receptor function = increase in acetylcholine = bronchial smooth muscle constriction & more mucus secretion

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15
Q

What causes mucus hyper-secretion?

A

goblet cell hyperplasia and submucosal gland atrophy

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16
Q

When does airway remodelling occur?

A

appear parallel with inflammation (i.e as inflammation increases, airway remodelling increases)

17
Q

Physical Assessment findings during an asthma exacerbation

A

Inspection: increase work of breathing, use of accessory muscles, prolonged extirpation, wheezing, cough, inability to maintain a conversation

Auscultation: wheezing, distant breath sounds, other adventitious breath sounds (crackles, infection)

Vital Signs: tachypnea, tachycardia, decreased oxygen saturations (hypoxemia)

18
Q

Arterial Blood Gas findings during an asthma exacerbation

A

Initially see respiratory alkalosis, hyperventilation, hypoxemia

Progress to respiratory acidosis due to hypercapnia and hypoxemia

19
Q

Normal ABG Values (pH, pCO2, HCO3, PO2)

A

pH: 7.35-7.45
pCO2: 35 - 45
hCO3-: 22-26
pO2: 80 - 100

20
Q

Chest x-ray findings of asthma exacerbation

A

hyperinflation and flattening on the hemidiaphragm, possible infection

21
Q

Long term controls for asthma

A

Inhaled corticosteroids, long-acting beta-2 agents, leukotriene modifiers, systemic corticosteroids, mast cell stabilizers, monoclonal antibody

22
Q

Quick relief medication

A

beta-2 agonists, anticholinergics

23
Q

What does the lipooxygenase pathway produce?

A

Leukotrienes - induce smooth muscle contraction, constrict pulmonary airways, increase microvascular permeability

24
Q

What does the cyclooxygenase pathway produce?

A

Prostaglandins - induces vasodilation and bronchoconstriction, inhibits inflammatory cell function

Thromboxane - vasoconstriction, bronchoconstriction, promotes platelet function