Bronchial Asthma Clinical Notes

• Asthma is s syndrome characterized by airflow obstruction.

• There is airway narrowing with consequent reduced airflow and symptomatic wheezing and dyspnea.

• Most of the patient are atopic, with allergic sensitization to the house dust mite Dermatophagoides pteronyssinus.

• ASTHMA CAN PRESENT AT ANY AGE, with a peak age of 3 years

Ø RISK FACTORS AND TRIGGERS:

Asthma is a heterogeneous disease that has genetic as well as environmental factors.

-       Atopy: Patient with Asthma commonly suffer from other Atopic disease like allergic rhinitis and atopic dermatitis (eczema).

-       Genetic Predisposition: Asthma is Polygenic. Most consistent findings have been associations with polymorphisms of genes on chromosome 5q.

Novel gene associated with asthma: ADAM-33, DPP-10 and ORMDL3.

-       Infections: Commonly Rhinovirus, atypical bacteria like Mycoplasma and Chlamydophilia.

“Hygiene Hypothesis”: Lack of infections in early childhood preserves the Th2 cell bias at birth. Exposure to infections and endotoxin results in a shift towards a predominant protective Th1 immune response. So, children brought up on farms who are exposed to a high level of endotoxin are less likely to develop allergic sensitization than children raised on dairy farms.

-       Diet, Air Pollution, Occupational exposures, Obesity (BMI>30 kg/m²).

-       Intrinsic Asthma: Patients with intrinsic asthma have negative skin tests to common inhaled allergens and normal concentrations of IgE. Commonly associated with nasal polyps, and maybe Aspirin sensitive.

-       Pharmacologic agents: All beta-blockers (even selective or topical Beta Blockers). Aspirin may worsen asthma in some patients.

-       Exercise-induced asthma: Typically begins after exercise and recovers within 30 minutes.

Ø DIAGNOSIS:

•         Lung Function Tests:
  
  

Spirometry: Reduced FEV1, FEV1/FVC ratio and PEF.

     Reversibility: >12% and 200mL increase in FEV1 15 minutes after an inhaled short-acting Beta2 agonist (SABA).

-         Total serum IgE and specific IgE to inhaled allergens.

•          Chest Xray: Usually normal or hyperinflated lungs. In exacerbations, there may be evidence of pneumothorax.

•          Skin tests: It is positive in allergic asthma and negative intrinsic asthma.

•          Exhaled Nitrous Oxide: Elevated levels are reduced by Inhalational Corticosteroid therapy, May be useful to test compliance with therapy.

•          ABG analysis: Hypoxaemia and Hypocarbia during acute attack. In severe acute asthma,  hypercarbia develops.

Ø TREATMENT:

I.                  Bronchodilator therapies.

II.               Controller therapies.

III.            Management of Chronic Asthma.

   
     I. Bronchonchodilator therapies:

a.   Beta2 agonists:

§  Primary action: relaxes smooth muscle cells of all airways.

§ Has additional non-bronchodilator effects, including mast cell inhibition, reduction in plasma exudation, etc.

§ Used as Inhalers – because of its rapid actions used for acute exacerbations (relievers).

§ Increased use of SABA (e.g.: albuterol and terbutaline) indicates poorly controlled asthma.

§ LABA (Long acting B2 agonists) e.g. Salmeterol and formeterol, can be given twice daily.

§ LABA should NOT be given in absence of Inhalational Corticosteroid (ICS) therapy as they do not control underlying inflammation.

§ Side effect: Tremors and palpitations.

b.   Anticholinergics:

§  Long-acting Muscarinic agonists (LAMA) like tiotropium bromide may be used as an additional bronchodilator when controlled is not achieved by ICS-LABA combination.

§  These are less effective than Beta-agonists.

§  Side effects: Dry mouth, urinary retention, and glaucoma.

c.    Theophylline:

§  Inhibits Phosphodiesterases in airway smooth muscle cells, which increases cAMP.

§  It activates histone deacetylase-2 (HDAC2) – Switches off activated inflammatory genes.

§  Can be given orally or IV route.

§  Required plasma therapeutic concentration: 10-20 mg/L.

§  Side effects: Nausea, Vomiting headaches, palpitations, diuresis and at high concentrations can cause arrhythmias and seizures.

                                      II.   Controller therapies:

a.   Inhaled corticosteroids:

§  Most effective controllers.

§  They are NOT bronchodilators but they relieve or prevent airflow obstruction by their anti-inflammatory effect and decrease bronchial hyperresponsiveness.

§  Usually given twice daily.

§  Now given as first-line therapy for patients with persistent asthma.

b.   Systemic corticosteroids:

§  IV route (like hydrocortisone or methylprednisolone) is used for acute severe asthma.

§  Oral steroids (Prednisolone 30-45 mg once daily for 5-10 days) to treat acute exacerbation can be used; no tapering is needed.

§  Intramuscular Triamcinolone acetonide can be used occasionally in non-compliant patients.

c.    Antileukotrienes:

§  E.g.: Montelukast, Zafirlukast.

§  Used in patient who require high dose of steroid therapy.

d.   Cromones:

§  E.g. Sodium Chromoglycate.

§  It inhibits degranulation of mast cells.

§  Only used as prophylactic treatment of Asthma.

e.   Steroid sparing therapies:

§  Can be used in patients who have serious side effects from steroid therapy.

§  E.g.: Methotrexate, cyclosporine A, Azathioprine, etc.

f.      Anti-IgE:

§  Omalizumab.

§  Route: Subcutaneous, every 2-4 weeks.

            III.   Management of Chronic Asthma:

§  Stepwise therapy:

• Step 1: Prefer SABA as required for symptom relief.
• Step 2: Prefer low dose ICS to be given twice daily.
• Step 3: If not controlled, add LABA (use of combination inhaler).
• Step 4: If not controlled, use High dose ICS with LABA.
• Step 5: I not controlled, add OCS therapy along with LABA + ICS.