Respiratory

A chronic inflammatory airway disease causing reversible bronchospasm and mucosal swelling that narrows the airways episodically, so triggers, variability and reversibility (not fixed obstruction) define both the symptoms and the treatment ladder.

Chronic infection and inflammation destroy the structural components of the bronchial wall, causing permanent, irreversible dilatation that pools mucus and perpetuates further infection, so the disease becomes a self-sustaining cycle of damage and re-infection rather than a single resolving illness.

A progressive, largely irreversible airflow limitation from smoking-driven small-airway inflammation and alveolar destruction; because the damage is structural, treatment focuses on slowing decline, relieving symptoms and preventing exacerbations.

Infection filling the alveoli with inflammatory exudate outside a hospital setting, so the alveolar space (not the airway) is consolidated, producing focal signs of consolidation, hypoxia and a systemic inflammatory response whose severity must be scored to guide urgent treatment.

Inflammation and progressive fibrosis thicken and stiffen the interstitium between the alveolus and its capillary, so the lung becomes small and stiff rather than obstructed, impairing oxygen diffusion out of proportion to airflow and producing the restrictive, breathless, dry-cough picture that distinguishes it from obstructive airway disease.

Malignant transformation of bronchial or alveolar epithelial cells, overwhelmingly driven by cumulative carcinogen exposure (chiefly smoking), produces a locally growing mass that can obstruct airways, invade neighbouring structures or spread distantly, so the clinical picture is dictated by exactly where the tumour sits and what it presses on.

Loss of upper airway muscle tone during sleep allows soft tissue (worsened by obesity and anatomical crowding) to collapse the pharynx, causing repeated episodes of partial or complete airway obstruction that fragment sleep and cause intermittent hypoxia, so the daytime and cardiovascular consequences all trace back to sleep that is never allowed to become restorative.

Fluid accumulates in the pleural space when the normal balance between fluid formation and pleural lymphatic drainage is disrupted, and whether that imbalance is from raised hydrostatic/low oncotic pressure (transudate) or local pleural or lung pathology (exudate) determines both the underlying cause and the diagnostic pathway.

Air enters the pleural space and abolishes the negative pressure that normally holds the lung expanded against the chest wall, so the lung collapses inward under its own elastic recoil, and if the air entry becomes one-way the resulting pressure buildup can compress the heart and great vessels, a time-critical emergency.

A venous clot, usually from the deep leg veins, lodges in the pulmonary arterial tree and abruptly creates ventilated-but-unperfused lung and a sudden rise in right ventricular afterload, so the clinical picture is driven by gas-exchange mismatch and acute right heart strain rather than by the lung itself being diseased.