Focuses on the management of airway inflammation
Prevent exacerbations (asthma attack)
Minimize symptoms
Maintain near normal lung function

Strategies
Educate patient and family about asthma and participating in the management
Allergen and irritant avoidance strategies avoidance of identified causes where possible
Use of the lowest effective does of convenient medications to minimized short-term and long term side effects

Control of Extrinsic Factors
Avoid causative allergens such as house-dust mite, pets, moulds, certain food stuff, smokes and etc..
Skin Scratch testing to identify causative allergens

Drug treatment
Short acting bronchodilators such as Beta 2-2 agonist and anti-muscarinic on acute management of exacerbations
Long acting anti-inflammatory such as corticosteroids to prevent chronic inflammation of the airways

Beta 2 Adrenergic Agonist
Reverse smooth muscle bronchospasm regardless of the stimulus, inhibit histamine and other mediator release from inflammatory cells, inhibit cholinergic neurotransmitter, inhibit airway vascular leakage and increase mucocilliary clearance.

Effective in relieving symptoms of acute asthma attack not preventing asthma occurrence
Can be use as a marker of disease control base on the frequency of usage.
Eg.--> R-albuterol, Salbutamol (100 micro g) and terbutaline (250) Short actingDelivered through Metered Dose Inhaler with a spacer or wet nebuliser if air flow is severely restricted.
Long Acting Beta-2 agonist—Salmeterol and formoterol used in conjunction with inhaled steroids.Effective by inhalation for up to 12 hours reducing the need for administration to once or twice daily.Improve symptoms, lung function and reduce exacerbations in patients who are poorly controlled on standard doses of inhaled steroids.

Steroids
Preferably inhaled than oral.
Inhibitors of Inflammatory mediator production to control chronic asthma.
Side Effects oral candidiasis (5%of patients) and hoarseness due to effect if corticosteroids on the laryngeal muscles. Abnormal bone metabolism if on high doses of beclometasone or budesonide >800.In children doses greater than 400 can retart short-term growth.

Oral CorticosteroidsNecessary for individual whos asthma are not controlled well by inhaled steroids.Eg Prednisolone 30mg daily, or methotrexate 15mg weekly

Leukotriene Modifiers
Inhibiting the cysteinyl LT1 receptor, inflammation cascade.
Acceptable second choice to treat chronic asthma synergistically with steroids.
Improves lung function and decreases beta agonist rescue and inhaled corticosteroids use.

Ipratropium Bromide
anti muscarinic bronchodilator but less potent than beta agonist.
Indications- patient on beta blockers and children and severe adult exacerbations when routine agents fail.

Inhaler Devices
Pressurised aerosol inhaler aka. Metered Dose Inhaler
MDI and spacer
Dry powder Inhaler
Breath activated inhaler
Nebuliser

Definition

• variable airflow obstruction and airway hyper responsiveness
• variable means that the airflow obstruction is temporary and reversible
• inflammation causes hyper responsiveness and this further cause more inflammation leading into a viscous cycle.

Cause

• inflammation of the airways due to hypersensitivity reaction which further obstruct the airways during expiration.

Epidemiology

• 4^th May = World Asthma Day
• 300 million people (2004)
• the prevalence of asthma is increasing throughout the world, and the rate appears to increase as communities adopt western lifestyles and become urbanized

General Risk Factors

• parents with asthma
• respiratory infection during childhood
• low birth weight (due to smaller airway)
• obesity (fat under diaphragm which limits diaphragm contraction)

Explaination for exercise (Exercise Induce Asthma)

1. Exercise induce asthma; the cause is unclear
1. Exercise increases oxygen demand. Usually a person will breathe through their mouth at a higher rate (normally, nasal breathing will humidify and heat the air as alveoli needs to be protected from cold, dry air). Mouth breathing will then lead to lost of heat and water from the tracheobranchial tree. Rapid breathing during exercise also reduces the humidity of the airways. Cold, dry air has high tonicity. This will cause fluid movements from the surrounding capillary (which is hypotonic) to diffuse into the airways. This causes the airway to narrow.

· Under normal condition, parasympathetic (vagal) innervations will cause bronchoconstriction. On the other hand, sympathetic (B₂ adrenergic receptor) increase bronchodilation. During exercise, the increase of air-flow is required thus inhibiting the bronchoconstriction and promotes bronchodilation. This is why asthmatic patient do not get breathlessness during exercise but complains of shortness of breath hours later (due to the gradual build up of fluid)

Explanation for cold air

Besides increasing tonicity, cold air also causes bronchospasm.

GERD

The explanation is unclear. Unable to link between GERD and asthma. Some possible theories;

1. asthma triggers GERD
1. bronchodilators can relax the LES (lower esophageal sphincter)
2. small amount of the medication is swallowed when patient inhale the bronchodilators.
2. GERD triggers asthma. There are two possible mechanism
1. Acid reflux will cause injury to the lining of the throat, airways and lungs, making inhalation difficult and often causing a persistent cough. It may also cause the formation of a fistula.
2. Acid reflux into the esophagus will stimulate a nerve reflex somehow which cause the the airway to constrict in order to prevent the acid from entering. This leads to shortness of breath.

Occupational asthma

• A lung condition caused by inhaling workplace fumes, gases or dust
• Can develop if you never had asthma before or had childhood asthma that later cleared. It can also worsen any pre-existing asthma

Cause

1. Direct irritation of the allergens which induces pre-existing asthma.
2. Allergic sensitization which arise from the same concept of pathophysiology of asthma.

Risk factors

EARLY ONSET/ CHILDHOOD ASTHMA

- Childhood asthma and adult asthma have the same underlying cause — continuous inflammation of the airways leading to the lungs – which makes the airways overly sensitive and prone to tightening and constricting when irritated

- Treatable- with right meds and action plan

Signs and Symptoms

- coughing

- wheezing- not all children with asthma wheeze; not all children who have wheezing episodes have asthma

- s.o.b

- chest congestion

- chest tightness

Additional signs and symptoms of asthma in infants include:

- Rattly cough

- Recurrent bronchitis with croup, bronchiolitis or pneumonia

Causes

Most common triggers

Irritants

- tobacco smoke

- exercise

- weather changes or cold air

- environmental pollutants

Allergens

- dust mites

- pet dander

- pollen

- mold

Other factors

- Upper resp infections

- Rhinitis/ sinusitis

- GORD

Risk factors

- family history of asthma, allergic rhinitis (hay fever), hives or eczema

- env. factors:

o prev. allergic reactions (stuffy nose/ skin rash) to env. allergens

o exposure to tobacco smoke

o living in large urban area with ↑ exposure to env. air pollutants

o low birth weight- ↓ pulmonary function and consequently develop asthma

o obesity - ↑ abdominal and chest wall mass in obese people causes ↓ functional residual capacity. And since lung volume is a major determinant of airway diameter, it is possible that these changes in residual capacity allow smooth airway muscles to shorten excessively when activated.

Adult onset asthma

- onset of asthma for the first time in someone of middle age or older

- usual symptoms of asthma are generally present: varying degrees of breathlessness, wheeze and productive cough..

- develops after age 20; possible to first develop asthma at age 50, 60 or even later in life

- less common than asthma in children

- affects more women than men

- many develop asthma in childhood but symptoms can appear at any time in life

-

Causes

- symptoms are less likely to be triggered by allergies eg house-dust mites, animals and pollens

- symptoms are more likely to be triggered by:

o flu, clods or other viral infections

o exercise

o laughing or getting excited

o depression/anxiety

o meds inc aspirin and other NSAIDS, oral beta-blockers for HPT and HD and beta-blocker eyedrops for glaucoma

o irritants eg cigarette smoke, cold air, perfumes and chemical fumes.

- Indiv who had allergies as children/ young adults with no asthma symptoms could develop asthma as older adults

Pathophysiology

Airway Inflammation
Infectious agents constantly enter the body via the respiratory system. The bronchi have several protective methods against these invaders. These include:

The following figure depicts some of the histologic features of airway inflammation. Plasma leakage from blood vessels contributes to bronchial wall edema, which results in thickening of the bronchial wall. Eosinophils migrate from the bloodstream into the bronchial wall and the airway lumen and can release eosinophil cationic protein and leukotrienes. Enlarged mucus glands secrete excess mucus that can plug the airway lumen.

In about 50% of patients, there can be a spontaneous return of bronchoconstriction that occurs several hours after the allergen challenge (and after the EAR has resolved). This late phase response usually occurs 6-24 hours after exposure to the allergen and is termed the late asthmatic response (LAR). This late decline in FEV1 may be less severe than during the EAR but is generally more prolonged, lasting several hours.
The EAR results from binding of inhaled allergen to mast cell membrane-bound IgE with subsequent release of mediators (e.g., histamine, leukotrienes, and prostaglandins). Among these mediators, the cysteinyl leukotrienes appear to account for a significant part of the early bronchoconstrictor response.

The LAR to an allergen is typified not only by a decline in FEV1 but also by the influx of inflammatory cells, most notably eosinophils, and airway edema. The intensity of LAR inflammation correlates with the degree of airflow obstruction that occurs during the LAR. Note that the airflow obstruction of the LAR usually lasts longer, as much as several hours or more.

Inflammatory and Bronchoconstriction Events of the Late Phase of an Acute Asthmatic

The LAR often resembles asthma, which is a chronic inflammatory disease. It is possible that repeated or prolonged episodes of LAR may approximate the events in the airways in both chronic allergic and nonallergic asthma.

"Airway remodeling"
The term airway remodeling is widely used to refer to the development of specific structural changes in the airway wall in asthma accompanying long-standing and severe airway inflammation. Airway remodeling and fibrosis may be the cause of "fixed" airflow obstruction in asthma that is not reversible with steroids, bronchodilators, or both. Interest has especially been focused on subepithelial collagen deposition, myofibroblast accumulation, airway smooth muscle hyperplasia and hypertrophy, mucous gland and goblet cell hyperplasia, and epithelial disruption.

Leader- Maz
Scribe- Saree

Tasks:

1) Aetiology + Risk Factors –occupational causes of asthma (soldering)+ triggers for asthma (exercise-+ve and –ve) + air-cond ----- Yazid

2) Pathophysiology of asthma, signs and symptoms -----Chris

3) Investigations- spirometry + interpretation of findings + conditions that are irreversible/x + diurnal variability with peak flow----Saree

4) Management- pharmaco + non-pharm, nebulizers vs. inhalers------Alvin

5) Complications of asthma + relationship with polypectomy, chronic persistent nasal obstruction, heartburn + relationship with naproxen/ hypersensitivity-----Christine

6) Asthma- early + late onset------Maz

p/s: i really don't know how to rearrange all the posts..somebody else has to do it..(Chris?)=D