Asthma

chronic inflammatory disease of the respiratory system characterized by

mucosal inflammation, bronchial musculature constriction, and
excessive secretion of viscous mucus-causing mucous plugs will
produce episodic exacerbation (asthma attacks), and reversible airflow
obstruction.
A. Intrinsic or idiosyncratic asthma: a bronchial reaction occurs secondary to
nonimmunologic stimuli, such as infection, irritating inhalant, cold air, exercise,
and emotional upset. associated with a poor response to standard treatment.

B. Extrinsic (allergic, atopic) asthma: Specific immunoglobulins (IgE class [type 1])
are produced, and total serum IgE concentration is elevated. There is a positive
family history of allergic disease. associated with, eczema, rhinitis and a good
response to treatment.
 epidemiology
• More common in black than white patients.
• Sex: differs depending on age of onset
♂ > ♀ in patients < 18 years
♀ > ♂ in patients > 18 years
• Age of onset:
Allergic asthma: typically, in childhood.
Nonallergic asthma: typically, > 40 years.
Causes of acute exacerbations of
symptoms include:
• Infection and cold air: Respiratory infections are the most common stimuli to
cause asthma exacerbation; viruses (respiratory syncytial virus in young
children, rhinoviruses in adults) are the major causes.
• Allergens: pollen, dust mites, cockroaches, and cat dander, cleaning agent,
tobacco .
• Emotional stress or exercise.
• Aspirin, NSAIDs, beta blockers, histamine, any nebulized medication,
tobacco smoke.
• Gastroesophageal reflux disease (GERD).
 Exercise induces bronchoconstriction

High volume of Triger mast cell bronchoconstrictio

dry cold air degranulation n

 Beta agonists and mast cell stabilizers(anti leukotriene) are important in the
management of EIB
 Aspirin-exacerbated respiratory
disease (AERD) is a pseudoallergic
reaction; not IgE-mediated but
typically occur in patients with
asthma, chronic rhinosinusitis with
nasal polyposis.

 The use of leukotriene inhibitors

(zileuton) and leukotriene receptor
antagonists (montelukast) can also
improve respiratory and nasal
symptoms.
 microaspiration increase in bronchoconstrictio
of gastric contents vagal tone n

 Proton-pump inhibitor (PPI) therapy has been shown to improve both asthma
symptoms
presentation
• In a mild attack:

1. slight tachypnea
2. prolonged expirations
3. mild, diffuse wheezing
4. Asthma can present exclusively as a cough
• In a severe attack:

1. use of accessory muscles of respiration

2. diminished breath sounds
3. loud wheezing
4. hyper-resonance (increased vocal fremitus)
5. unable to speak in full sentences
6. intercostal retraction

- Poor prognostic factors include fatigue, diaphoresis, inaudible breath sounds,

decreased wheezing, cyanosis, and bradycardia
Diagnostic Tests:
• The best initial test in an acute exacerbation: peak expiratory flow (PEF) or
arterial blood gas (ABG).
• The most accurate diagnostic test is pulmonary function testing (PFTs).
• CBC may show an increased eosinophil count.
• Skin testing is used to identify specific allergens that provoke
bronchoconstriction.
• Increased IgE levels suggest an allergic etiology
 Acute Asthma
Exacerbation:
1. Decreased peak expiratory flow (PEF).

2. hyperventilation, leading to decreased partial pressure of carbon dioxide

(PaCO2).

3. primary respiratory alkalosis

• Decreased FEV1 and decreased FVC with a decreased ratio of
FEV1/FVC.

• Increase in FEV1 of more than 12% with the use of albuterol.

• Decrease in FEV1 of more than 20% with the use of methacholine or histamine.

• Increase in the diffusion capacity of the lung for carbon monoxide (DLCO).

• PFTs are normal in between exacerbations.

- When the patient is asymptomatic, the most accurate test of reactive airway
disease is a 20% decrease in FEV1 with the use of methacholine (provocative
challenge test).
Indicated Nighttime awakenings Symptom frequency Asthma
therapy severity

Step 1 ≤2 times a month ≤2 days a week Intermittent

Step 2 3-4 times a month >2 days a week but not Mild persistent
daily

Step 3 >1 time a week but not Daily Moderate

nightly persistent

Step 4 or 5 4-7 times a week Throughout the day Severe

persistent
Step
1:
Always start the treatment of asthma with an inhaled short-acting beta agonist
(SABA) as needed.
 Albuterol, Pirbuterol, Levalbuterol.

Step
2: a long-term control agent(Low-dose inhaled corticosteroids) to a SABA.
Add
• Beclomethasone, budesonide, flunisolide, fluticasone, mometasone, triamcinolone.

Alternate long-term control agents include:

• Cromolyn or nedocromil , Theophylline, montelukast or zafirlukast, zileuton.
Step
3:
Add a long-acting beta agonist (salmeterol or formoterol) to a SABA and ICS
or increase the dose of the ICS (medium dose).
- Never use LABA first or alone!

Step
4:
Increase the dose of the ICS (medium dose) in addition to the LABA and SABA
 Step
5:
Increase the dose of the ICS to maximum.
- Omalizumab may be added in those who have an increased IgE level

Step
6:
Oral corticosteroids such as prednisone are added when all the other therapies
are not sufficient to control symptoms.

▪ Influenza and pneumococcal vaccine are given in

all asthma patients
 When use
Anticholinergics ?
▪ Anticholinergic drugs (ipratropium bromide and tiotropium) have
particular benefit in patients with heart disease, in whom the use of β-
adrenergic agonists and theophylline may be dangerous.

▪ Their major disadvantages are that they take significant time to achieve maximal
bronchodilation (~90 min) and they are only of medium potency.

▪ Anticholinergic agents will dilate bronchi and decrease secretions.

▪ They are very effective in COPD.

Treatment
1. Oxygen.
2. Albuterol.
3. Steroids.
4. Ipratropium.

The best initial therapy is oxygen combined with inhaled short-acting beta
agonists such as albuterol and a bolus of steroids. Corticosteroids need 4 to 6
hours to begin to work.
The following are not effective in acute exacerbations:

o Theophylline.
o Cromolyn and nedocromil
o Leukotriene modifiers.
o Omalizumab.
o LABAs

If the patient does not respond to oxygen, albuterol, and steroids

or develops respiratory acidosis (increased pCO2), the patient
may have to undergo endotracheal intubation for mechanical
ventilation. These patients should be placed in the intensive care
unit.