Respiratory Pathology I: Bronchial Asthma & ARDS

Flashcards covering the definitions, pathogenesis, morphology, and clinical features of Bronchial Asthma and Acute Respiratory Distress Syndrome (ARDS).

Bronchial Asthma

A chronic inflammatory disorder of the airways characterized by increased responsiveness of the tracheobronchial tree, resulting in widespread but variable bronchoconstriction and airflow limitation.

Atopic Asthma

The most common type of asthma, characterized as an $IgE$-mediated hypersensitivity reaction that typically begins in childhood and is triggered by environmental allergens.

Non-Atopic Asthma

A form of asthma with no evidence of allergen sensitization, often triggered by respiratory viral infections or inhaled air pollutants, most frequently affecting adults.

$TH2$ cells

Type 2 helper $CD4$ T cells that secrete interleukins like $IL-3$, $IL-4$, and $IL-5$, stimulating B cells to produce $IgE$ and recruiting eosinophils.

$$IL-13$$

A cytokine that stimulates mucus secretion from bronchial submucosal glands and promotes $IgE$ production by B cells.

Curschmann spirals

Microscopic findings in the sputum of asthma patients resulting from the extrusion of mucus plugs from subepithelial mucous gland ducts or bronchioles.

Charcot-Leyden crystals

Crystals found in asthma patients composed of the eosinophil-derived protein galectin-10.

Airway remodeling

Collective structural changes in the bronchial wall due to repeated allergen exposure, including sub-basement membrane fibrosis, increased vascularity, and muscle hypertrophy.

Status asthmaticus

A state of acute severe asthma where symptoms persist for days or weeks, causing extreme airflow obstruction that may result in cyanosis or death.

Hygiene Hypothesis

The theory that limiting exposure of very young children to certain antigens, particularly microbial antigens, may lead to an increase in asthma and atopy in industrialized societies.

Leukotrienes $C_4$, $D_4$, and $E_4$

Mediators that cause prolonged bronchoconstriction and increased vascular permeability in asthma.

Acute Lung Injury (ALI)

The abrupt onset of hypoxemia and bilateral pulmonary edema in the absence of cardiac failure, characterized by increased pulmonary vascular permeability.

Acute Respiratory Distress Syndrome (ARDS)

A severe manifestation of ALI characterized by diffuse alveolar damage, inflammation-associated edema, and epithelial cell death.

Diffuse Alveolar Damage (DAD)

The histologic manifestation of ALI and ARDS.

Hyaline membranes

Waxy membranes lining alveolar walls in ARDS, composed of fibrin-rich edema fluid mixed with remnants of necrotic epithelial cells.

Acute Interstitial Pneumonia

A condition where ALI appears acutely in the absence of known triggers and follows a rapidly progressive clinical course.

Phase 2 (Latent Period) of ARDS

A stage lasting approximately $6-48$ hours after injury where the patient remains clinically stable despite persistent hyperventilation and hypocapnia.

Phase 3 (Acute Respiratory Failure) of ARDS

A stage characterized by decreased lung compliance, marked tachypnea, dyspnea, and diffuse infiltrates on chest radiographs.