Disorders Associated With Airway Obstruction

Front 1

Name the three components of asthma that differentiate it from COPD:

Back 1

1. Recurrent episodes of REVERSIBLE airway obstruction
2. Airway hyperresponsiveness
3. Inflammation of airways

Front 2

What percentage of the population is affected w/ asthma?

Back 2

5%, develops before age of 25

Front 3

Increase of prevalence of asthma in what group?

Back 3

low socioeconomic groups due to exposure to indoor allergens

Front 4

Asthma is bronchitis w/ ____ infiltration compared to bronchitis due to smoking which has ______ infiltration.

Back 4

eosinophil, neutrophil

Front 5

Give 6 components of the pathology of asthma.

Back 5

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

Front 6

Compare the airway epithelium in asthma and bronchitis from smoking.

Back 6

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

Front 7

In any obstructive lung disease which PFT decreases?

Back 7

FEV1 and peak flow

Front 8

Eosinophils ____ steroids. Neutrophils ____ steroids.

Back 8

hate, like

Front 9

Which cytokines attract eosinophils?

Back 9

IL-5, IL-4, Leukotriene B4

Front 10

What PFT increases in obstructive disease?

Back 10

residual volume

Front 11

Low O2 in an asthma patient suggests?

Back 11

respiratory failure

Front 12

What is the most common cause of asthma?

Back 12

allergen-induced

Front 13

How does aspirin precipitate asthma?

Back 13

blocks the cyclooxygenase pathway, thus arachidonic acid precursors are shunted to the leukotriene pathway, causing the symptoms of asthma

Front 14

How do beta blockers induce asthma?

Back 14

make beta receptors less sensitive to endogenous/exogenous beta agonists

Front 15

What are 6 factors that can induce asthma?

Back 15

1) allergen
2) excercise
3) medication
4) occupation
5) GERD
6) unknown

Front 16

What are some common physical findings in an asthmatic patient?

Back 16

increased RR, increased pulsus paradoxus, wheezing during expiration, ronchi

Front 17

What is pulsus paradoxus?

Back 17

normally, there is a difference in BP in inspiration and expiration, however in asthma, you get more than a 10 mmHg difference in SBP

Front 18

What happens to the ABG early on in an asthma attack?

Back 18

respiratory alkalosis with normal or high pO2 b/c they're hyperventilating and blowing out all CO2

Front 19

What happens to the ABG later on in an asthma attack?

Back 19

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

Front 20

Two findings in the sputum of an asthma patient:

Back 20

Charcot-Leyden crystals and Creola bodies

Front 21

Found in the sputum of asthma patients, made of eosinophil lysophospholipase from degradation of eosinophils.

Back 21

Charcot-Leyden crystals

Front 22

Clusters of epithelial cells in the sputum of asthma patients.

Back 22

Creola bodies

Front 23

Classification: Don't have many symptoms or only symptoms when excercising.

Back 23

Mild intermittent

Front 24

Treatment for mild intermittent asthma?

Back 24

steroids not necessary, Beta agonists

Front 25

Classification: Patient still having symptoms. Wake up wheezing. May be due to reduction in endogenous corticosteroids or cholinergic tone.

Back 25

Mild persistent or moderate/severe

Front 26

Treatment for mild persistent or moderate/severe.

Back 26

Relieve medications used intermittently - Beta agonists, anticholinergics

Front 27

Who do Beta agonists work?

Back 27

through beta 2 receptors to relax airway smooth muscles and decrease mucus secretion

Front 28

What are some side effects from a non-selective Beta agonists (albuterol, terbutaline)?

Back 28

tachycardia and tremor

Front 29

What are the main treatment for controlling inflammation in asthma?

Back 29

inhaled corticosteroids

Front 30

How do steroids work in asthma patients?

Back 30

decrease mediator release

Front 31

What is the benefit of newer preparations of inhaled corticosteroids?

Back 31

more affinity for steroid receptors and less absorption, so fewer side effects

Front 32

Side effects of corticosteroids?

Back 32

initial growth retardation, bone loss, cataracts, glaucoma, and oral candidiasis

Front 33

How do anti-leukotriene receptor antagonists work?

Back 33

Block leukotrienes C, D, & E which are important for eosinophil recruitment and mucus hypersecretion

Front 34

How does a lipoxygenase inihibitor work?

Back 34

blocks production of all leukotrienes

Front 35

T/F: Anti-leukotrienes are effective monotherapy for asthma.

Back 35

False, no studies to show that these drugs reduce mortality of asthma

Front 36

How does theophylline work?

Back 36

inhibits phosphodiesterase, w/ antiinflammatory effect

Front 37

What is the problem with theophylline?

Back 37

significant GI, cardiac, and CNS toxicity, serum levels must be monitored

Front 38

What are two ways that theophylline levels may be increased?

Back 38

use of certain drugs (Cipro, Biaxin, clarithromycin) and CHF

Front 39

What are two long acting beta agonists?

Back 39

salmeterol (slow onset) and formoterol (fast onset)

Front 40

Dr. Deldar prescribes Jordan a long acting beta agonist for his asthma. What else should be prescribed?

Back 40

an inhaled steroid

Front 41

What is a difference in the inflammation in COPD compared to asthma?

Back 41

inflammation from neutrophils and macrophages instead of eosinophils.... neutrophil specific cytokines (IL-8).... toxic neutrophil products such as reactive oxygen species and proteases

Front 42

Structural changes in COPD.

Back 42

destruction of alveoli due to proteases followed by collage deposition (fibrosis)

Front 43

Centrilobular emphysema is associated w/? Predominant alveolar damage occurs in?

Back 43

smoking, respiratory bronchiole

Front 44

Panlobular emphysema is associated w/ ?

Back 44

alpha 1 antitrypsin deficiency, whole alveolar lobule affected

Front 45

Total lung capacity in emphysema ?

Back 45

increased due to hyperinflation

Front 46

Diffusion capacity in emphysema?

Back 46

diminished due to destruction of alveolar capillary membrane

Front 47

What are two things that have been shown to improve survival in patients w/ COPD?

Back 47

smoking cessation and oxygen therapy

Front 48

Exacerbations in COPD are defined by having at least 2 of the following?

Back 48

increased sputum, increased purulence of sputum, and increased dyspnea