Asthma

Question 1

asthma

Answer 1

• quite prevalent
• can be associated with COPD
• reversible recurrent episodes of a/w obstr d/t:
  
  1. muscle hyperactivity -> bronchospasm to decrease inhalation of the trigger
  2. inflmtn -> exudate + swelling = compromised lumen of a/w

Question 2

what type of inflammation do you have with asthma?

Answer 2

chronic infltm of the a/w

• known trigger, if encountered will cause bronchospasm and inflammation, but the pt will be hyperresponsive to other unknown triggers
• reversible, recurrent bronchospasm (a/w locks in a constricted state)

Question 3

forms of asthma?

Answer 3

1. Atopic (Extrinsic) Form
   - atopy = genetic tendency to develop allergic diseases (ie. allergic asthma)
   - typically associated with heightened IR to common allergens, esp inhaled and food allergens
2. Non-Atopic (Intrinsic) Form
   - responses to triggers that are not genetically based

Question 4

etiology

Answer 4

• complex trait, but has triggers that induce episodes; genetic and environmental factors
• hypersensitivity to certain stimuli = hyperresponsiveness
  –> exercise, allergens, strong odours, a/w irritants
  –> 2 categories of stimuli are inflmtry and
  bronchospastic
• T2H differentiation
  • -> T2H responds to inhalation of allergens

Question 5

patho

Answer 5

• you have chronic inflmtn so there’s always some WBCs present, but its not until the late phase that the WBCs enter the submucosa
• a/w becomes more hyperresponsive to other allergens/triggers = more bronchospasm and airflow limitation
• have either early or late phase, one doesn’t lead into the other

Question 6

acute phase response

Answer 6

• can last up to 1 hr
  i. inhaled allergen -> previously sensitized mast cell degranulates -> IgE mediated release of inflm mediators -> causes infiltration of inflm cells and bronchospasm (limits airflow) but inflm cells do not move into the submucosa
  ii. prior sensitization to allergen (T1 HS)
  iii. subsequent exposure -> IgE binds to sensitized mast cells -> mast cells on surface of submucosa release inflm mediators -> inflmtn
  iv. intercellular junctions open -> allergens enter submucosa
  v. increased capillary permb and mucous hypersecretion -> edema of the a/w d/t exudate from inflmtn
  vi. bronchospasm (via PNS) = reflex resulting in dyspnea and wheezing; person will have a response to irritants but compromise their breathing
  vii. bronchoconstriction = attempt at compensation, but is not beneficial

Question 7

late phase response

Answer 7

• can last up to days, self-sustaining cycle
• 1/2 of people with asthma will experience this

i. infmtn of a/w is worsened -> edema, inflm damage, and hypersecrection of mucous resulting in decreased mucociliary fx -> limits airflow even further
ii. T1H, but response is delayed post-exposure (peaks 4-8 hours)
iii. pt. becomes hyperresponsive to new triggers

iv. causes an influx of inflm cells
- inflm damage to epithelial cells
- compromises mucociliary blanket (decreased
defense = increased susceptibility to infection)
- frequent, severe triggers

v. beta adrenergic receptors = bronchodilation to increase breathing for fight or flight response
- asthmatics lack B-receptor stimulation
(bronchodilation doesn’t occur when its required)

vi. alpha adrenergic receptors = bronchoconstriction
- binding to both of these receptors is mediated by cAMP

Question 8

manifestations

Answer 8

• wide range of intensity (ie. immobilization)
• dyspnea, wheezing, cough
• increased resp effort and compromised breathing
• abnormal ABG profile (increased PaCO2)

Question 9

diagnosis

Answer 9

• Hx, Px
• labs (CBC, ABGs)
• pulmonary fx tests
• inhalation challenge tests

Question 10

inhalation challenge tests

Answer 10

assess a/w responsiveness to different substances; gold standard for dx asthma

Question 11

treatment

Answer 11

• shift from episodic to chronic management
• prophylactic management (smoking cessation, avoid allergens and irritants)
• drugs

Question 12

explain what drugs you would use for treatment of asthma

Answer 12

i. short acting b-agonist (bronchodilator) inhaled prn
ii. add inhaled steroid (decrease inflmtn) -> local not systemic
iii. add long-acting bronchodilator (inhaled) to steroid
iv. short course of PO steroids to deal with acute flare-ups + add a 3rd drug (leukotriene receptor antagonist or theophylline)

Question 13

leukotriene receptor antagonist

Answer 13

inflm mediator and involved in allergic response, so drug inhibits both of these actions