Asthma Flashcards
asthma
chronic disease w/ acute, reversible episodes of air way obstruction
reversible episodes of airway obstruction d/t what
- muscle hyperactivity (bronchospasm)
- inflm (exudate + swelling)
chronic inflm of the a/w (URT) d/t what
- hyper-responsive a/w
- “known” trigger
hyper responsive a/w
structures are easily irritated
“known” trigger
recognizable trigger that would cause an episode of a/w obstr –> bronchospasm, inflm & hyper-responsive to unknown triggers
bronchospasm
reversible + recurrent spasm where a/w locks in constricted state
extrinsic (atopic) form
- genetic tendency to develop allergic diseases (ex. allergic rhinitis, asthma, dermatitis)
- commonly assoc w/ heightened IR to common allergies, esp inhaled + food allergens
intrinsic (non-atopic) form
responses to triggers that are not genetically based
etiology
- complex trait –> genetic factors + enviro factors
- hypersensitivity to triggers (hyper-responsiveness)
trigger examples
allergen, strong odor, a/w irritant, exercise
patho
a/w become more hyper-responsive to other allergens/triggers + leads to bronchospasm & airflow limitation
early phase of asthma
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
late phase of asthma
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
acute phase response
- 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
acute phase response sequence
- prior sensitization to allergen (T1 HS)
- subsequent exposure = IgE Abs bind to sensitized mast cells
- mast cells on mucosa (surface of a/w) release inflm mediators
- intercellular junctions open –> allergens enter submucosa
- inc cap permb (d/t inflm) and inc mucus secretion (exudate & edema in a/w)
- bronchospasm reflex (via PNS)
- bronchoconstriction to compensate but not beneficial
late phase response
- 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
influx of inflm cells causes what
- 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
binding to beta and alpha-adrenergic receptors mediated by what
cAMP
mnfts
- 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)
Dx
- Hx, Px (resp & cardiac)
- pulmonary Fx tests
- labs (CBC, ABGs)
- CXR (exlude COPD)
- distinguish asthma vs COPD
how to distinguish asthma from COPD diagnostic test
inhalation challenge tests to assess a/w responsiveness to different substances
inhalation challenge test
pt exposed to specific agent to see what reaction occurs (gold standard in asthma Dx)
Tx
- control w/ minimal amount of meds possible
- prophylactic management
- pharmacologic agents (stage-based)
what does prophylactic management include
- cessation of smoking
- avoid triggers
pharmacologic agents and stages
- short-acting beta-agonist inhaled prn (bronchodilators)
- add inhaled steroid (dec inflm –> local
- add long-acting bronchodilator (inhaled)
- short course of steroids
when is leukotriene receptor antagonist or theophylline added
during fourth phase with short course of steroids
leukotrienes action
inhibits inflm mediators involved in allergic response
theophylline is added to which drugs
to the inhaled long-acting bronchodilators and the PO steroids
