Long-standing chronic obstructive pulmonary disease

Correct answer: B. Stratified squamous epithelium

• A. Simple squamous epithelium is the single flat layer of alveoli, endothelium and mesothelium — built for exchange, not protection, and the opposite of what a chronically injured airway needs.
• B. CORRECT. METAPLASIA is the reversible replacement of one differentiated cell type by another better able to withstand a chronic stress. In the airway, the normal PSEUDOSTRATIFIED CILIATED COLUMNAR epithelium with goblet cells is replaced by STRATIFIED SQUAMOUS epithelium, which is tougher but has NO CILIA and NO mucus clearance. That loss of the mucociliary escalator is why secretions accumulate and why these patients get recurrent infections. Persistent injury on a metaplastic field is the substrate on which DYSPLASIA and ultimately carcinoma develop.
• C. Simple cuboidal epithelium lines ducts and renal tubules and provides no protective advantage against inhaled irritants.
• D. Transitional (urothelial) epithelium is confined to the urinary tract, where it accommodates distension.

Note: Two other metaplasias worth carrying: BARRETT oesophagus, where squamous becomes columnar intestinal-type under acid reflux — the mirror image of this one — and squamous metaplasia of salivary ducts after obstruction or irradiation, which can be mistaken for carcinoma histologically.

Correct answer: C. It decreases — breathing becomes slower and shallower

• A. Increased ventilation is the response to a RISE in CO₂ (hypercapnia), not a fall.
• B. Oxygen is the SECONDARY drive, mediated by the peripheral chemoreceptors in the carotid and aortic bodies, and it only becomes significant when PaO₂ falls below about 60 mmHg.
• C. CORRECT. CO₂ is the PRIMARY drive to respiration in health. Central chemoreceptors in the medulla sense hydrogen ion concentration in the cerebrospinal fluid, which tracks arterial CO₂ because CO₂ crosses the blood-brain barrier freely and forms carbonic acid. A FALL in CO₂ means fewer hydrogen ions, less chemoreceptor stimulation, and therefore REDUCED rate and depth of breathing — the negative feedback that corrects the hypocapnia. This is precisely what happens after hyperventilation, and why the appropriate response to a hyperventilating anxious patient is to have them rebreathe into cupped hands rather than give oxygen.
• D. That describes Cheyne-Stokes respiration, seen in heart failure and central neurological disease, not the normal response to hypocapnia.

Note: The relevance to this patient is the HYPOXIC DRIVE question. In severe long-standing COPD with chronic CO₂ retention, the central chemoreceptors adapt and hypoxaemia becomes the more important stimulus — so uncontrolled high-flow oxygen can theoretically blunt respiratory drive. In practice, never withhold oxygen from a patient in genuine distress; titrate it to a target saturation of 88–92% rather than the usual 94–98%.