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48 Cards in this Set

  • Front
  • Back
Name the three components of asthma that differentiate it from COPD:
1. Recurrent episodes of REVERSIBLE airway obstruction
2. Airway hyperresponsiveness
3. Inflammation of airways
What percentage of the population is affected w/ asthma?
5%, develops before age of 25
Increase of prevalence of asthma in what group?
low socioeconomic groups due to exposure to indoor allergens
Asthma is bronchitis w/ ____ infiltration compared to bronchitis due to smoking which has ______ infiltration.
eosinophil, neutrophil
Give 6 components of the pathology of asthma.
1. edema and hyperemia of mucosa
2. infiltration w/ lymphocytes, mast cells, and eosinophils
3. increased mucus secretion
4. constriction of airway smooth muscle
5. airway remodeling - fibrosis
6. shedding of airway epithelium
Compare the airway epithelium in asthma and bronchitis from smoking.
more inflammatory cells and epithelium is lost in asthma
in smoking airway epithelium is relatively intact and there is an increase in mucus secreting cells
In any obstructive lung disease which PFT decreases?
FEV1 and peak flow
Eosinophils ____ steroids. Neutrophils ____ steroids.
hate, like
Which cytokines attract eosinophils?
IL-5, IL-4, Leukotriene B4
What PFT increases in obstructive disease?
residual volume
Low O2 in an asthma patient suggests?
respiratory failure
What is the most common cause of asthma?
How does aspirin precipitate asthma?
blocks the cyclooxygenase pathway, thus arachidonic acid precursors are shunted to the leukotriene pathway, causing the symptoms of asthma
How do beta blockers induce asthma?
make beta receptors less sensitive to endogenous/exogenous beta agonists
What are 6 factors that can induce asthma?
1) allergen
2) excercise
3) medication
4) occupation
6) unknown
What are some common physical findings in an asthmatic patient?
increased RR, increased pulsus paradoxus, wheezing during expiration, ronchi
What is pulsus paradoxus?
normally, there is a difference in BP in inspiration and expiration, however in asthma, you get more than a 10 mmHg difference in SBP
What happens to the ABG early on in an asthma attack?
respiratory alkalosis with normal or high pO2 b/c they're hyperventilating and blowing out all CO2
What happens to the ABG later on in an asthma attack?
patient will tire and get a metabolic acidosis b/c of increased lactic acid, CO2 goes up b/c they're tired...
low pH, high pCO2, low pO2
Two findings in the sputum of an asthma patient:
Charcot-Leyden crystals and Creola bodies
Found in the sputum of asthma patients, made of eosinophil lysophospholipase from degradation of eosinophils.
Charcot-Leyden crystals
Clusters of epithelial cells in the sputum of asthma patients.
Creola bodies
Classification: Don't have many symptoms or only symptoms when excercising.
Mild intermittent
Treatment for mild intermittent asthma?
steroids not necessary, Beta agonists
Classification: Patient still having symptoms. Wake up wheezing. May be due to reduction in endogenous corticosteroids or cholinergic tone.
Mild persistent or moderate/severe
Treatment for mild persistent or moderate/severe.
Relieve medications used intermittently - Beta agonists, anticholinergics
Who do Beta agonists work?
through beta 2 receptors to relax airway smooth muscles and decrease mucus secretion
What are some side effects from a non-selective Beta agonists (albuterol, terbutaline)?
tachycardia and tremor
What are the main treatment for controlling inflammation in asthma?
inhaled corticosteroids
How do steroids work in asthma patients?
decrease mediator release
What is the benefit of newer preparations of inhaled corticosteroids?
more affinity for steroid receptors and less absorption, so fewer side effects
Side effects of corticosteroids?
initial growth retardation, bone loss, cataracts, glaucoma, and oral candidiasis
How do anti-leukotriene receptor antagonists work?
Block leukotrienes C, D, & E which are important for eosinophil recruitment and mucus hypersecretion
How does a lipoxygenase inihibitor work?
blocks production of all leukotrienes
T/F: Anti-leukotrienes are effective monotherapy for asthma.
False, no studies to show that these drugs reduce mortality of asthma
How does theophylline work?
inhibits phosphodiesterase, w/ antiinflammatory effect
What is the problem with theophylline?
significant GI, cardiac, and CNS toxicity, serum levels must be monitored
What are two ways that theophylline levels may be increased?
use of certain drugs (Cipro, Biaxin, clarithromycin) and CHF
What are two long acting beta agonists?
salmeterol (slow onset) and formoterol (fast onset)
Dr. Deldar prescribes Jordan a long acting beta agonist for his asthma. What else should be prescribed?
an inhaled steroid
What is a difference in the inflammation in COPD compared to asthma?
inflammation from neutrophils and macrophages instead of eosinophils.... neutrophil specific cytokines (IL-8).... toxic neutrophil products such as reactive oxygen species and proteases
Structural changes in COPD.
destruction of alveoli due to proteases followed by collage deposition (fibrosis)
Centrilobular emphysema is associated w/? Predominant alveolar damage occurs in?
smoking, respiratory bronchiole
Panlobular emphysema is associated w/ ?
alpha 1 antitrypsin deficiency, whole alveolar lobule affected
Total lung capacity in emphysema ?
increased due to hyperinflation
Diffusion capacity in emphysema?
diminished due to destruction of alveolar capillary membrane
What are two things that have been shown to improve survival in patients w/ COPD?
smoking cessation and oxygen therapy
Exacerbations in COPD are defined by having at least 2 of the following?
increased sputum, increased purulence of sputum, and increased dyspnea