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24 Cards in this Set

  • Front
  • Back
What is asthma?
Airway obstruction that is REVERSIBLE, either spontaneously or with tx

Airway inflammation

Inc'd airways responsiveness to variety of stimuli
What are possible causes of asthma?
Atopy (allergies): eczema, hay fever, high IgE levels
Allergens
Tobacco
Infectious agents: RSV (respiratory syncytial virus), Rhinovirus, chlamydia, mycoplasm

GERD
Sinusitis
Nasal Polyps
Obesity

**asthma is not likely one disease, and likely does not have a single cause.

Smaller causes:
Exercise, occupational, reactive airway dysfn syndrome (RADS), ASA, cough variant
Intrinsic vs Extrinsic Asthma
Intrinisic:
Often no clear precipitating factor (viral)
Attacks often longer and stronger and lifelong
Chronic inflammation

Extrinsic:
Clear precipitating environmental factors (dust, allergens, chemicals)
Short lived once exposure removed
Behaves like allergy (histmaine/bradykinin)

Most peopl ehave features of both
Which interleukins are secreted by T cells to recruit B cells in asthma?
IL-4, IL-5 are most important
What are the "big three" effects (anatomical problems) of asthma?
Bronchospasm
Airway edema
Mucous production

Which can lead to V/Q mismatch from plugging and air trapping (dynamic hyperinflation)
Events of early and late phases of asthma.

Which phase is more reversible?
Early phase:
Bronchoconstriction, mucous production, more reversibility

Late phase:
Airway edema
Inflammatory cells
Hyperresponsiveness
Less reversibility
Asthma results in the narrowing of airways. Which in particular? Effect on resistance? Consequences of this?
Dec'd radius = Inc'd resistance (to the 4th power)

Asthma narrows small, floppy airways and creates one way valves-->obstruction-->air-trapping (lung over-inflation)

Thus: air goes in, but not out. leads to ASYMMETRIC resistance (worse when breathe out--prolonged expiratory breathing).

Note:
Resistance is asymmetrical (normally) bc in inhalation low intrathoracic pressures outside bronchi open the airways; and in exhalation, positive intrathoracic pressure outside bronchi collapse them (milk out the air)
What is dynamic hyperinflation and how does it come about?
Asthmatics facing inc'd expiratory resistance. Normal response to hypoxia/hypercarbia/dyspnea is to breath faster.

This amplifies the problem because more air is going in, and less of it is coming out, thus increasing dead space and compressing lung.

Don't breathe rapidly in asthma attack. Need more time to exhale!
Slide 34, 1:22:14
xxx
Diagnosing asthma

PFTs?
Confirm wheezing (by healthcare professional)
Confirm normalcy between attacks
Establish precipitating factors

Obstruciton with change from bronchodilators >12%
Low FEV1 (less force of expiration during first second)

+methacholine provocation suggestive but NOT diagnostic; best for r/o asthma

Peak flow variability between
AM and PM of >20%
Asthma treatment:
Non-pharmacalogic
-Allergen avoidance: remove rugs, encase pillows/mattresses, HEPA filters
-Avoid irritants
-Avoid beta-blockers (may change) and ASA!
Heliox therapy:
Benefits
Use
Use as a 2nd line tx in severe asthma

Mix of O2 and He allows O2 to penetrate smaller airways and get trapped air out--also allows O2 into lung
Mild Intermittent Asthma:
Criteria
Treatment
Syx < 2x/week
Asyx between episodes
Nocturnal syx <2x/month
FEV1 >80%
PEFR variability <20%

Tx: as needed short acting beta agonist (albuterol)
Mild Persistent Asthma:
Criteria
Treatment
Syx > 2x/week, but <daily
Nighttime syx >2x month
Normal PFTs
PEFR variability 20-30%

Rx: SABA + anti-inflammatory (inhaled steroid)
Moderate Persistent:
Criteria
Daily syx
Daily use of rescue inhaler
Exacerbations affect activity
Nocturnal Syx >1/week
Mild obstruction on PFTs
Severe Persistent:
Criteria
Continual syx
Limited physical activity
Frequent exacerbations
Long Acting Beta Agonists:
Controversy
-Asthma-related death rate is higher in long-acting beta agonists!

-Only get it if not taking it with an inhaled corticosteroid
Disadvantages of chronic beta-agonist use.
-Tachyreflexia
-Promotes inflammn
What viruses can trigger asthma in children under 2 years of age? Over 2 years?
Under 2 years and WHEEZING:
Respiratory viruses, mostly RSV

Over 2 years and WHEEZING:
Rhinovirus predominant (common cold)
How do viruses act as an asthma trigger?
Viruses enter cells and reproduce (auto-infect)

Asthma attacks due to viruses can last a long time!
What conclusions have been made about the role that childhood viral infections play in asthma?
Childhood viral infections may play a role in asthma, but it's very complex and involves many host and viral factors.
Genetic associations of asthma.
Glucocorticoid receptor SNP

beta-adrenergic receptor mutation: Gly 16 mutation in steroid dependent asthmatics (down-regulates a lot faster)
Hygiene theory of asthma.
Asthmatics tend to have a larger TH2 response than TH1 response (no longer balanced)
Airway remodeling in asthma
SM hypertrophy, loss of columnar epithelium, goblet cell hyperplasia, thickened BM

Much more poised to cause inflammatory response