أسئلة المحاضرة الرابعة باثولوجي RESP (قبل التعديل)

A respiratory condition characterized by increased airway responsiveness, leading to bronchospasm and inflammation. This causes recurrent episodes of wheezing, breathlessness, and cough.

Sudden tightening and narrowing of the bronchial tubes.

A predisposition to developing allergic diseases like asthma, with a family history of similar conditions.

Asthma triggered by an allergic reaction to specific allergens, involving type I hypersensitivity.

Asthma with no clear identified trigger or allergic link.

An exaggerated response of the airways to various stimuli.

An antibody that plays a key role in allergic reactions.

Substances or factors that can initiate an asthma attack.

IL-4, IL-5, and IL-13 stimulate IgE production and mast cell growth, playing a key role in the allergic response in asthma.

The initial response to an allergen, occurring 30-60 minutes after exposure, involving the release of mediators like leukotrienes, histamine, and platelet-activating factor, leading to bronchoconstriction and inflammation.

The later inflammatory response to an allergen, occurring 4-8 hours after exposure, involving the release of secondary mediators and intensified inflammatory response from eosinophils and neutrophils, further damaging the airway.

Asthma driven by an allergic response and mediated by type I hypersensitivity to environmental antigens, often in childhood and with family history of allergy.

Asthma not associated with a clear allergic response, often in adults, triggered by factors like respiratory infections, irritants or aspirin.

Asthma causes over-inflation of the lungs, mucus buildup in the airways, and narrowed airways due to bronchospasm.

Asthma symptoms can be triggered by various factors like aspirin, infections, cold exposure, stress, exercise, and inhaled irritants.

Asthma leads to inflamed and swollen bronchial and bronchiole airways, which are often narrowed and plugged with mucus.

Asthma microscopic examination shows glandular hyperplasia, mucous plug in the lumen, and inflammation.

Asthma involves chronic inflammation with an influx of inflammatory cells like eosinophils.

Whorled mucous plugs found in asthma.

Eosinophil debris found in asthma.

Allergens binding to IgE on mast cells trigger degranulation in asthma.

Whorled mucous plugs found in the airways of asthmatic patients, caused by the accumulation of thick mucus and cellular debris.

Crystals formed from the breakdown of eosinophil granules, commonly found in the sputum of asthmatic patients.

Allergens bind to IgE antibodies on mast cells, triggering the release of inflammatory mediators like histamine, leading to bronchospasm and airway inflammation.

An allergic reaction where allergens bind to IgE on mast cells, leading to degranulation and the release of histamine and other inflammatory mediators.

Eosinophils, a type of white blood cell, play a significant role in asthma inflammation. They release inflammatory mediators and contribute to airway remodeling.

These interleukins play a key role in the allergic response in asthma by stimulating the production of IgE antibodies and the growth of mast cells.

These factors include dust, pollen, and food. They trigger an allergic response in individuals with atopic asthma.

These factors involve triggers that are not related to allergies, including respiratory infections, aspirin, cold exposure, stress, exercise, and inhaled irritants.

Asthma causes inflammation and swelling of the bronchial and bronchiole airways. These airways are often narrowed and plugged with mucus.

Microscopic examination of the airways of an asthma patient reveals glandular hyperplasia, mucous plugs in the lumen, and inflammation.

Substances or factors that can initiate an asthma attack, such as dust mites, pollen, air pollution, tobacco smoke, and respiratory infections.

Atopic asthma has a family history of allergies and is triggered by allergens, while non-atopic asthma doesn't have a clear allergic link.

In atopic asthma, IgE antibodies bind to mast cells, and when exposed to allergens, they release inflammatory chemicals that trigger bronchospasm.

The immediate response to an allergen, occurring within 30-60 minutes, causing bronchospasm and inflammation.

The delayed inflammatory response to an allergen, occurring 4-8 hours after exposure, intensifying inflammation and airway damage.

The sudden tightening and narrowing of the bronchial tubes caused by muscle contractions, making it difficult to breathe.

Under the microscope, asthma lungs show glandular hyperplasia, mucus plugs in the airways, and chronic inflammation.

Crystallized eosinophil debris found in asthma, indicating the presence of these inflammatory cells.