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

T-lymphocytes. eosinophils. macrophages. neutrophils. .•Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. in particular. and epithelial cells. mast cells.

Intrinsic (non-atopic. allergic) asthma 2.Asthma Types 1. 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.Extrinsic (atopic. eczema   Hypersensitivity to allergens is usually present IgE in serum (initiating acute immediate response and a late phase reaction ) . urticaria.

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

LTs.Allergen IgE sensitise Mast cells (on the mucosal surface) Degranulate and Release Histamine. chemotactic factors for eosinophils and neutrophils bronchoconstriction oedema Mucus hypersecretion Accumulation of eosinophils and neutrophils . PGs. PAF.

acute exacerbations interspersed with symptom-free periods  Chronic --.Disease pattern  Episodic --. moderate or severe ± superimposed acute exacerbations  Life-threatening--.daily AW obstruction which may be mild.slow-onset or fast-onset (fatal within 2 hours) .

Air pollutants. Exercise.Pathogenesis: Airway Hyperresponsiveness Genetic* INDUCERS Allergens. Virus infections INFLAMMATION Airflow Limitation TRIGGERS Allergens. Wheeze Dyspnoea . Cold Air. SO2 Particulates SYMPTOMS Cough.Chemical sensitisers.

3 Components of an Asthma Attack 1. Bronchospasm The smooth muscles that wrap around the windpipe (bronchi) tighten. normal Asthma attack . reducing the size of the airway.

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

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 .

basophils all implicated • Lymphocytes. macrophages. mast cells. Inflamatory cell infiltration • Eosinophils. including T-cells • Inflamatory mediators including cytokines • Abnormal antibodies including IgE . neutrophils.

. Other constituent airway cells: • Fibroblasts • Endothelial cells • Epithelial cells  Contribute to the chronicity of the disease.

fibroblasts. selectins. . contribute to the chronicity of the disease. cell-derived mediators influence smooth muscle tone and produce structural changes and remodeling of the airway. macrophages and activated T lymphocytes.Airway inflammation  Principal cells in airway inflammation include mast cells. eosinophils. and epithelial cells. T lymphocytes release numerous cytokines. Adhesion molecules (eg. integrins) are critical in directing the inflammatory changes in the airway. epithelial cells. endothelial cells.     Finally.

The degree of airway hyperresponsiveness correlates with the severity of asthma.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.

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. chronic mucous plug formation and airway remodeling. Airway edema occurs 6-24 hours following an allergen challenge and is referred to as the late asthmatic response.Airflow obstruction      Can be caused by acute bronchoconstriction. Acute bronchoconstriction results from IgE–dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. airway edema. .




causing edema .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.

coughing Shortness of breath Chest tightness Dry mouth Fatigue Itchy chin or clipped speech Headache .SIGNS AND SYMPTOMS OF AN ASTHMA ATTACK        Wheezing.

ASTHMA ATTACK TRIGGERS! Pets Weather Pollens Exercise Indoor pollution .

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