أسئلة الرابعة باثولوجي RESP (قبل التعديل)

A respiratory condition where the bronchial tubes become overly sensitive to stimuli, leading to bronchospasm (tightening of the airways).

A sudden tightening of the bronchial tubes, making breathing difficult.

A tendency to develop allergic reactions.

Allergic asthma triggered by an external allergen.

Asthma caused by non-allergic factors.

An exaggerated response of the airways to certain stimuli.

An allergic reaction involving IgE antibodies.

A substance that causes an allergic reaction.

The lungs become overinflated due to airway obstruction caused by bronchospasm and mucous plugs. This trapping of air reduces lung elasticity and makes breathing difficult.

In asthma, the bronchi become thickened due to inflammation and are often blocked by thick mucus plugs, further obstructing airflow.

These are tightly coiled, spiral-shaped mucous plugs found in the bronchi of asthmatic patients. They consist of mucus, epithelial cells, and inflammatory cells.

These needle-shaped crystals are found in the sputum of asthmatic patients. They are formed from the breakdown of eosinophils, a type of white blood cell.

Eosinophils are a type of white blood cell that are abundant in the airways of asthmatic patients. They release chemicals that contribute to inflammation and airway narrowing.

Stimulate IgE production and mast cell growth.

Starts 30-60 minutes after allergen exposure, involves mediator release.

Develops 4-8 hours after allergen exposure, involves secondary mediator release.

Histamine, leukotrienes, platelet-activating factor; causing bronchoconstriction, inflammation.

Eosinophil and neutrophil chemotactic factors, IL-4 & 5; increase mast cell activation and epithelial damage.

Overinflation, mucus plugging, and bronchospasm; leading to airway narrowing.

Substances or situations that can trigger an asthma attack, such as dust mites, pollen, air pollution, and emotional stress.

Atopic asthma is linked to allergies and family history, while non-atopic asthma is not, but both types involve airway hyper-responsiveness.

Allergens stimulate the production of IgE antibodies, which bind to mast cells and trigger the release of inflammatory mediators.

Asthma can be classified based on the cause, including extrinsic (allergic) asthma and intrinsic (non-allergic) asthma.

The initial reaction to an allergen, occurring 30-60 minutes after exposure. It involves the release of primary mediators like histamine, leukotrienes, and platelet-activating factor.

Develops 4-8 hours after allergen exposure. Secondary mediators, such as eosinophil and neutrophil chemotactic factors, are released. This phase intensifies the initial response and causes damage to the airway.

These interleukins stimulate the production of IgE, a key antibody in allergic reactions, and promote the growth of mast cells, the cells responsible for releasing inflammatory mediators.

They cause bronchoconstriction (airway narrowing), vasodilatation (blood vessel widening), increased vascular permeability (leaky blood vessels) and mucus secretion.

They bring in more inflammatory cells (eosinophils and neutrophils) and cause cell damage. These cells amplify the initial response, making asthma symptoms worse.

The lungs become overinflated, airways are blocked with thick mucus plugs, and bronchospasm occurs, all leading to airway narrowing.

The lining of the airways (mucosa) becomes inflamed and swollen, and the airway walls thicken. Thick mucus plugs obstruct the airway lumen.

Eosinophils are the predominant inflammatory cell type in the airways of asthma patients. They contribute to the inflammation and airway narrowing characteristic of the disease.

Curschmann's spirals are tightly coiled, spiral-shaped mucous plugs found in the bronchi of asthmatic patients. They are composed of mucus, epithelial cells, and inflammatory cells.

Charcot-Leyden crystals are needle-shaped crystals found in the sputum of asthmatic patients. They are formed from the breakdown of eosinophils.

Interleukins (IL-4, 5, and 13) play a role in asthma by stimulating IgE production and mast cell growth, contributing to the inflammatory response and allergy development.

The lungs in asthma undergo hyperinflation, mucus plugging, and bronchospasm. These changes, caused by airway obstruction, lead to impaired airflow and difficulty breathing.