Asthma

Question 1

asthma

Answer 1

chronic disease w/ acute, reversible episodes of air way obstruction

Question 2

reversible episodes of airway obstruction d/t what

Answer 2

• muscle hyperactivity (bronchospasm)

- inflm (exudate + swelling)

Question 3

chronic inflm of the a/w (URT) d/t what

Answer 3

• hyper-responsive a/w

- “known” trigger

Question 4

hyper responsive a/w

Answer 4

structures are easily irritated

Question 5

“known” trigger

Answer 5

recognizable trigger that would cause an episode of a/w obstr –> bronchospasm, inflm & hyper-responsive to unknown triggers

Question 6

bronchospasm

Answer 6

reversible + recurrent spasm where a/w locks in constricted state

Question 7

extrinsic (atopic) form

Answer 7

• genetic tendency to develop allergic diseases (ex. allergic rhinitis, asthma, dermatitis)
• commonly assoc w/ heightened IR to common allergies, esp inhaled + food allergens

Question 8

intrinsic (non-atopic) form

Answer 8

responses to triggers that are not genetically based

Question 9

etiology

Answer 9

• complex trait –> genetic factors + enviro factors

- hypersensitivity to triggers (hyper-responsiveness)

Question 10

trigger examples

Answer 10

allergen, strong odor, a/w irritant, exercise

Question 11

patho

Answer 11

a/w become more hyper-responsive to other allergens/triggers + leads to bronchospasm & airflow limitation

Question 12

early phase of asthma

Answer 12

release of chemical mediators –> inc mucus prod from goblet cells –> creates mucosal intercellular junctions (gaps b/w epith cells) once allergen is exposed to mast cell –> bronchospasm

Question 13

late phase of asthma

Answer 13

allergen moves in –> influx of inflm cells into submucosa that release more inflm mediators, epith cell injury w/ dec mucociliary Fx & accum of mucus, inc vascular permb & edema; results in dec a/w patency d/t bronchospasm

Question 14

acute phase response

Answer 14

• can last upto 1h
• inhaled allergen –> prev sensitized mast cells degranulate & IgE mediated release inflm mediators –> irritation of inflm cells & bronchospasm (limiting airflow) but the inflm cells do not move into the submucosa

Question 15

acute phase response sequence

Answer 15

1. prior sensitization to allergen (T1 HS)
2. subsequent exposure = IgE Abs bind to sensitized mast cells
3. mast cells on mucosa (surface of a/w) release inflm mediators
4. intercellular junctions open –> allergens enter submucosa
5. inc cap permb (d/t inflm) and inc mucus secretion (exudate & edema in a/w)
6. bronchospasm reflex (via PNS)
7. bronchoconstriction to compensate but not beneficial

Question 16

late phase response

Answer 16

• can last hrs-wks
• a/w is inflamed further –> edema, inflm damage & hypersecretion of mucus –> dec mucociliary Fx –> further limits airflow (peaks 4-8h post-exposure)
• pt becomes hyperresponsive to new triggers
• causes influx of inflm cells
• beta-adrenergic receptors cause bronchodilation (inc breathing)
• alpha-adrenergic receptors cause bronchoconstriction

Question 17

influx of inflm cells causes what

Answer 17

• inflm damage to epith cells (difficult to regen new epith cells)
• compromises mucociliary blanket (dec defences –> inc susceptibility to infect)
• hyperresponsive a/w to new triggers
• every response inc chance of responding again, every subsequent rxn gets more severe

Question 18

binding to beta and alpha-adrenergic receptors mediated by what

Answer 18

cAMP

Question 19

mnfts

Answer 19

• dyspnea w/ wheezing & coughing
• hunched over during attack
• inc ventilatory effort (accessory muscle use)
• pursed-lip breathing
• nasal flaring (to inc air flow)
• barrel chest (develops over time)
• altered resp status & ABGs during attack (hypoxemia & hypercapnia)

Question 20

Dx

Answer 20

• Hx, Px (resp & cardiac)
• pulmonary Fx tests
• labs (CBC, ABGs)
• CXR (exlude COPD)
• distinguish asthma vs COPD

Question 21

how to distinguish asthma from COPD diagnostic test

Answer 21

inhalation challenge tests to assess a/w responsiveness to different substances

Question 22

inhalation challenge test

Answer 22

pt exposed to specific agent to see what reaction occurs (gold standard in asthma Dx)

Question 23

Tx

Answer 23

• control w/ minimal amount of meds possible
• prophylactic management
• pharmacologic agents (stage-based)

Question 24

what does prophylactic management include

Answer 24

• cessation of smoking

- avoid triggers

Question 25

pharmacologic agents and stages

Answer 25

1. short-acting beta-agonist inhaled prn (bronchodilators) 2. add inhaled steroid (dec inflm --> local 3. add long-acting bronchodilator (inhaled) 4. short course of steroids

Question 26

when is leukotriene receptor antagonist or theophylline added

Answer 26

during fourth phase with short course of steroids

Question 27

leukotrienes action

Answer 27

inhibits inflm mediators involved in allergic response

Question 28

theophylline is added to which drugs

Answer 28

to the inhaled long-acting bronchodilators and the PO steroids