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Flashcards in Asthma Deck (11):
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1. Describe the epidemiology of asthma.

asthma affects 5% of general population, onset is most frequent at age 5-25 (1-12 males are most common)

prevalence has increased in the 80's and 90's mostly in industrialized countries, allergies and family history are common amount patients

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2. Define asthma and its key characteristics.

reversible airway obstruction (12% increase in FEV considered significant reversibility), hyper responsiveness, (more sever air flow limitation in response to given stimulus) and inflammation (manifest by infiltrate of leukocytes)

airway remodeling including sub-basement membrane fibrosis, submucosal edema and increased mucous gland number, size and smooth muscle hypertrophy

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4. Identify gross and microscopic pathologic changes seen in a patient with asthma.

Gross: mucus thick plugs occluding small bronchi and bronchioles associated with inflammation
Histologic: mucus infiltrate with eosinophils, Charcot-Leyden crystals; bronchial epithelium desquamates, goblet cell and squamous cell metaplasia may be prominent, airway appears thickened due to edema, increase in smooth muscle and increased size of mucous glands, basement membrane may appear thickened

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3. Define the factors that promote asthma and understand how they contribute to symptom onset.

1. allergies- can cause obstruction and inflammation
2. infections: stimulate IgE, damage airway epithelium, enhance allergic reaction can promote inflammation or bronchospasm
3. exercise: likely related to airway heat or water loss due to hyperventilation
4. occupational, esp in plastic industry or with lab animal allergy
5. nocturnal, frequently around 4 am
6. medications: B-adrenergic blockade, or aspirin/NSAID

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5. Understand how airway obstruction contributes to change in lung volumes.

during attacks, both residual volume and functional residual capacity increase secondary to premature closure of the airway during expiration and air trapping

during attack, TLC can increase due to decreased lung elastic recoil and more negative pleural pressure during expiration (due to continued activity of muscles and hyperinflation)

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6. Describe the evolution of arterial blood gases during an attack of asthma as it progresses from mild to moderate to severe airways obstruction .

narrowed airways during asthma attack can lead to low V/Q and cause hypoxemia, corresponding hyperventilation can cause respiratory alkalosis; in severe attacks hypoxemia worsens and PaCO2 normalizes ending in metabolic and respiratory acidosis

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7. Define pulses paradoxus and explain the mechanisms of its occurrence in asthma.

exaggerated (greater than 10mmHg) variation in systolic blood pressure during the respiratory cycle and is a marker of clinically sever acute asthma attack

the cause in asthma is thought to be the more negative intrathoracic pressure during inspiration which increases lung volume and pulmonary vascular resistance, this increases RV after load or boosting return of extra thoracic blood to the RV resulting exaggerated LV stroke during inspiration

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8. Be able to work up a patient who is being evaluated for asthma including understanding the pertinent history and physical exam findings.

symptoms: cough, wheeze, SOB (due symptoms occur after exercise, cold days, at night or due to exposure of allergens, does it respond to inhaled beta agonists

FH: history of allergic disease (rhinitis, atopic dermatitis, or asthma)

associated conditions (hay fever, atopic dermatitis and sinusitis)

polyphonic wheezing, prolonged expiration and tachypnea

acute asthma attacks: tachypnea, tachycardia, pulses paradoxes, intercostal retraction, use of accessory muscles, cyanosis, silent breath sounds in very severe disease due to hyperinflation

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9. Interpret pulmonary function test results and laboratory results of a patent with asthma.

airflow reduction via reduced FEV1, FEV1/FVC, PEFR and increased airway resistance

in extreme cases hyperinflation increased TLC is also demonstrated

eosinophillia in blood and sputum are seen in allergic asthma (modest elevation) and evidence of IgE sensitivity demonstrated by skin test or by measurement of circulatory IgE levels

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10. Understand the goals of asthma therapy and describe the different treatment options available.

prevent attacks, control attacks, normalize pulmonary functions

Bronchodilators: beta-agonsits, theophylline, anticholinergics
Anti-inflammatory: corticosteriods, cromolynn sodium (mast cell stabilization)
anti-leukotrienes: receptor blockers, synthesis inhib
anti-IgE monoclonal antibody
environmental control
tx. of associated conditions
patient education

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11. Define occupational asthma and understand how air pollution and occupational exposures can contribute to asthma.

airflow obstruction, hyper responsiveness, inflammation resulting from workplace stimulus (plant or animal antigens, pesticides, formaldehyde, di-isocyanates, epoxy resins, wood dust, exhaust; work place can also aggregate asthma

specifically particulate matter
air pollution can exacerbate heart and lung problems