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WHAT IS ASTHMA?

A reversible, obstructive lung disease caused by an excessive reaction of the airways to certain stimuli or triggers Asthma is a disease of airways that is characterized by increased responsiveness of the tracheobronchial tree to various stimuli; resulting in spasmodic narrowing of the air passages

Asthma is a chronic inflammatory disorder of the


airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils,

T-lymphocytes, macrophages, neutrophils, and epithelial cells.

Asthma Types

1. Extrinsic (atopic, allergic) asthma

2. Intrinsic (non-atopic, idiosyncratic) asthma

Extrinsic (atopic, allergic) asthma


Most common type Begins in childhood or in early adult life Patients have family history/personal preceding of allergic diseases like rhinitis, urticaria, eczema

Hypersensitivity to allergens is usually present IgE in serum (initiating acute immediate response and a late
phase reaction )

Acute Immediate Response

Initiated by IgE-sensitised mast cells on the mucosal surface Mast cells on degranulation release Histamine, LTs, PGs, PAF, chemotactic factors for eosinophils and neutrophils Net effects are bronchoconstriction, oedema, mucus hypersecretion, accumulation of eosinophils and neutrophils

Allergen

IgE

sensitise

Mast cells (on the mucosal surface)


Degranulate and Release

Histamine, LTs, PGs, PAF, chemotactic factors for eosinophils and neutrophils

bronchoconstriction

oedema Mucus hypersecretion


Accumulation of eosinophils and neutrophils

Disease pattern

Episodic --- acute exacerbations interspersed with


symptom-free periods

Chronic --- daily AW obstruction which may be mild,


moderate or severe superimposed acute exacerbations

Life-threatening--- slow-onset or fast-onset (fatal within 2


hours)

Pathogenesis:
Airway Hyperresponsiveness Genetic*

INDUCERS Allergens,Chemical sensitisers, Air pollutants, Virus infections

INFLAMMATION
Airflow Limitation

TRIGGERS Allergens, Exercise, Cold Air, SO2 Particulates

SYMPTOMS Cough, Wheeze Dyspnoea

3 Components of an Asthma Attack


1. Bronchospasm The smooth muscles that wrap around the windpipe (bronchi) tighten, reducing the size of the airway.
normal

Asthma attack

Components of an Asthma Attack


2. Inflammation The mucosal lining of the windpipe becomes inflamed and swells, thereby reducing the size of the airway even further. 3. Mucus Increased mucus production takes up more space; causing airway constriction.

Pathophysiology

Airway inflammation Intermittent airflow obstruction Bronchial hyper responsiveness

Hypersecretion of mucous

Mucous gland hypertrophy Mucous is thick Airways can be blocked by mucous plugs

Inflamatory cell infiltration

Eosinophils, mast cells, neutrophils, macrophages,


basophils all implicated Lymphocytes, including T-cells Inflamatory mediators including cytokines Abnormal antibodies including IgE

Other constituent airway cells:

Fibroblasts Endothelial cells Epithelial cells

Contribute to the chronicity of the disease.

Airway inflammation

Principal cells in airway inflammation include mast cells, eosinophils, epithelial cells, macrophages and activated T lymphocytes. T lymphocytes release numerous cytokines. fibroblasts, endothelial cells, and epithelial cells, contribute to the chronicity of the disease. Adhesion molecules (eg. selectins, integrins) are critical in directing the inflammatory changes in the airway.

Finally, cell-derived mediators influence smooth muscle tone and produce structural changes and remodeling of the airway.

Airway hyperresponsiveness

Airway hyperresponsiveness or bronchial hyperreactivity is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by cells like mast cells or non-myelinated sensory neurons. The degree of airway hyperresponsiveness correlates with the severity of asthma.

Airflow obstruction

Can be caused by acute bronchoconstriction, airway edema, chronic mucous plug formation and airway remodeling. Acute bronchoconstriction results from IgEdependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. Airway edema occurs 6-24 hours following an allergen challenge and is referred to as the late asthmatic response. Chronic mucous plug formation consists of an exudate of serum proteins and cell debris Airway remodeling is associated with structural changes due to long-standing inflammation and may profoundly affect the extent of reversibility of airway obstruction.

During acute attack


Antigen antibody interaction Stimulation/degranulation of mast cells with release of:

Histamine Leukotriens Chemotactic factors Bradykinin

Resulting in:

Smooth muscle contraction (decreased camp) Increased capillary permeability, causing edema

SIGNS AND SYMPTOMS OF AN ASTHMA ATTACK


Wheezing, coughing Shortness of breath Chest tightness Dry mouth Fatigue Itchy chin or clipped speech Headache

ASTHMA ATTACK TRIGGERS!


Pets Weather Pollens Exercise Indoor pollution

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