Overview Of Respiratory Pathology

Respiratory System Overview

• Conducting Airways and Respiratory Bronchioles

  • Respiratory bronchioles branch from terminal bronchioles.

  • Each respiratory bronchiole branches into 2 to 11 alveolar ducts, retaining cuboidal epithelium.

  • Alveolar ducts lead to single alveoli and numerous alveolar sacs.

  • Alveolar duct entrance = atrium.

• Histology of Respiratory Bronchioles

  • Cells include simple squamous epithelium.

  • Nasal hair plays a role in respiratory defense.

  • IgA secretion influenced by turbinates.

  • Respiratory Defense Mechanisms

    • Mucociliary apparatus helps clear pathways.

    • Nasopharynx interfered by resident flora, saliva, sloughing, and epithelial cells.

    • Oropharynx aids in local complement production, with cough and epiglottic reflexes.

    • Immunoglobulins (IgG, IgM, IgA) contribute to defense in sharp-angled airways.

• Conducting Airways

  • Include Trachea and bronchi, with contributions from the mucociliary apparatus and alveolar lining fluid (surfactant).

  • Involvement of neutrophils, cytokines, and cell-mediated immunity in respiratory processes.

• Lower Respiratory Tract

  • Comprises terminal airways and alveoli, where alveolar macrophages are present.

Respiratory Disorders

Obstructive Disease

• Definition

  • Characterized by limitation of airflow due to obstruction and increased airway resistance.

• Causes

  • Airway narrowing (asthma), loss of elasticity (emphysema), or increase in secretions (bronchitis).

Restrictive Disease

• Definition

  • Restricts normal lung movement during respiration; involves reduced expansion of lung parenchyma leading to decreased total lung capacity.

Specific Disorders of the Respiratory System

Chronic Obstructive Lung Disease (COPD)

• Components

  • Includes chronic bronchitis and emphysema; chronic inflammatory lung disease with obstruction in distal respiratory tree.

  • Primarily caused by smoking; irreversible disease.

• Chronic Bronchitis

  • Mucous hyper-secretion in large/small airways.

  • Diagnosed clinically by persistent cough for three months.

  • Pathogenesis:

    • Hypertrophy and hyperplasia of mucous glands.

    • Inflammation involves increased T-cells, neutrophils, and macrophages (absence of eosinophils).

    • Pathology characterized by small airway disease, goblet cell metaplasia, fibrosis without autonomic control.

• Emphysema

  • Destruction of alveoli leading to permanent dilation of respiratory pathways without fibrosis.

  • Clinical picture varies with/without bronchitis:

    • Dyspnea, barrel chest, and hypoxemia observed.

    • Types: Centriacinar, Panacinar, and Para-septal emphysema; centriacinar is most common.

Asthma

• Characteristics

  • Chronic inflammation of airways, leading to hyper-responsiveness; marked by intermittent and reversible airway obstruction.

  • Key features include eosinophilic inflammation, bronchial smooth muscle hypertrophy.

• Triggers

  • Atopic (extrinsic) triggers include seasonal allergies. Non-atopic (intrinsic) triggers include injections, exercise, and drugs.

• Clinical Manifestations

  • Shortness of breath, chest tightness, wheezing, cough due to reversible airway narrowing.

• Reaction Mechanisms

  • Early reactions: hypersecretion of mucus leading to airway plugging.

  • Late reactions: mucosal edema, muscle hypertrophy causing lumen narrowing.

• Morphological Changes

  • Excess mucus production from goblet cells.

Bronchiectasis

• Description

  • Permanent dilation of main bronchi and bronchioles; caused by pulmonary inflammation, scarring, infection, or lung fibrosis.

  • Symptoms include chronic cough and the production of copious amounts of sputum.

Restrictive Disease

Acute Respiratory Distress Syndrome (ARDS)

• Causes

  • Direct: pneumonia/aspiration of gastric contents.

  • Indirect: sepsis, severe trauma.

• Mechanism

  • Acute inflammation in alveoli damages capillaries and endothelium.

  • Leads to an imbalance between pro-inflammatory and anti-inflammatory mediators, causing uncontrolled inflammation.

  • Symptoms include acute dyspnea and hypoxemia due to vascular leakiness and loss of surfactant.

Idiopathic Pulmonary Fibrosis (IPF)

• Pathogenesis

  • Persistent alveolitis leads to inflammation in alveolar walls/spaces; abnormal repair mechanism results in excessive collagen deposition.

• Morphology

  • Patchy interstitial fibrosis leads to honeycomb formation with elastic tissue collapse.

Pneumoconiosis

• Definition

  • Results from exposure to toxic inhaled particulates (e.g., asbestos, silica).

• Mechanism

  • Particle size influences deposition and macrophage phagocytosis leading to fibroblast proliferation.

  • Lesions consist of pigmented nodules populated by macrophages and dense collagen; associated with increased cancer risk.