Asthma

Question 1

Where are the highest rates of asthma

Answer 1

Ontario and Nova Scotia

Question 2

Prevalence of Asthma

Answer 2

• 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

Question 3

Where are the lowest rates of asthma

Answer 3

Northwest Territories, Yukon, Nunavut

Question 4

Annual Canadian asthma trends

Answer 4

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

Question 5

Causes of Childhood Asthma

Answer 5

• 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

Question 6

What is Asthma?

Answer 6

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

Question 7

Characterizing symptoms of Asthma

Answer 7

dyspnea, chest tightness, wheezing, sputum production and cough

Question 8

Main mechanism causing development and persistence of asthma

Answer 8

Inflammation of the airways and consequential damage

Question 9

What are the main effects of asthma on the airways?

Answer 9

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

Question 10

What are the extrinsic triggers for asthma?

Answer 10

Type I IgE mediated hypersensitivity reaction

Question 11

What are intrinsic triggers for asthma

Answer 11

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

Question 12

Early Phase Response

Answer 12

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

Question 13

Late Phase Response

Answer 13

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

Question 14

What causes bronchospasm

Answer 14

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

Question 15

What causes mucus hyper-secretion?

Answer 15

goblet cell hyperplasia and submucosal gland atrophy

Question 16

When does airway remodelling occur?

Answer 16

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

Question 17

Physical Assessment findings during an asthma exacerbation

Answer 17

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)

Question 18

Arterial Blood Gas findings during an asthma exacerbation

Answer 18

Initially see respiratory alkalosis, hyperventilation, hypoxemia

Progress to respiratory acidosis due to hypercapnia and hypoxemia

Question 19

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

Answer 19

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

Question 20

Chest x-ray findings of asthma exacerbation

Answer 20

hyperinflation and flattening on the hemidiaphragm, possible infection

Question 21

Long term controls for asthma

Answer 21

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

Question 22

Quick relief medication

Answer 22

beta-2 agonists, anticholinergics

Question 23

What does the lipooxygenase pathway produce?

Answer 23

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

Question 24

What does the cyclooxygenase pathway produce?

Answer 24

Prostaglandins - induces vasodilation and bronchoconstriction, inhibits inflammatory cell function

Thromboxane - vasoconstriction, bronchoconstriction, promotes platelet function