The nurse caring for a patient recently diagnosed with lung disease encourages the patient not to smoke. What is the primary rationale behind this nursing action?

Correct Answer: D

Rationale: Smoking cessation is a cornerstone of lung disease management because it directly damages the ciliary cleansing mechanism, a critical defense of the respiratory tract. Cilia, hair-like structures lining the airways, sweep mucus and trapped particles upward for clearance, but smoking paralyzes and destroys them, leading to mucus accumulation, chronic irritation, and increased infection risk. Contrary to decreasing mucus, smoking stimulates goblet cells to overproduce mucus, exacerbating airway obstruction. Smoke does reduce oxygen-carrying capacity by forming carboxyhemoglobin, but this is secondary to ciliary damage in most lung diseases like COPD. Alveolar distention, not atrophy, occurs in emphysema due to air trapping, and while smoking contributes, the primary harm is ciliary dysfunction. By stopping smoking, the patient can slow disease progression, reduce inflammation, and preserve remaining lung function, making this the nurse's primary rationale.

Correct Answer: C

Rationale: In ARDS, hypotension often results from hypovolemia due to capillary leakage, where fluid shifts into interstitial spaces and alveoli, reducing circulating volume. Toxic fume inhalation damages alveolar-capillary membranes, increasing permeability (non-cardiogenic pulmonary edema), a hallmark of ARDS pathophysiology. This fluid loss, compounded by potential positive end-expiratory pressure (PEEP) reducing venous return, lowers blood pressure. Pulmonary hypotension isn't a recognized term; pulmonary hypertension may occur in ARDS from hypoxic vasoconstriction but doesn't directly cause systemic hypotension. High PEEP can decrease cardiac output by compressing thoracic vessels, but increased cardiac output isn't typical. The nurse's understanding of hypovolemia guides fluid resuscitation and vasopressor use, balancing oxygenation (via PEEP) and perfusion, critical in managing ARDS's systemic effects.

Correct Answer: C

Rationale: During an asthma attack, the preferred intervention is an inhaled beta-adrenergic agonist (e.g., albuterol), which rapidly relaxes bronchial smooth muscle, reversing airflow obstruction from bronchospasm, mucus, and inflammation. This short-acting bronchodilator acts within minutes, opening airways and relieving acute dyspnea, aligning with asthma guidelines (e.g., GINA) for exacerbations. Corticosteroids reduce inflammation but take hours, unsuitable for immediate relief. Anticholinergics (e.g., ipratropium) complement beta-agonists in severe cases but aren't first-line alone. Peak flow monitoring assesses obstruction severity, not treating it. The nurse's swift administration via inhaler ensuring proper technique (e.g., spacer use) restores ventilation, critical for this child's acute respiratory crisis, preventing escalation to status asthmaticus.

Correct Answer: C

Rationale: For a COPD client, diaphragmatic breathing is a key exercise to include in discharge teaching, retraining the patient to use the diaphragm over accessory muscles. This technique inhaling to expand the abdomen, exhaling to contract it reduces respiratory rate, enhances alveolar ventilation, and eases dyspnea by countering the shallow, rapid breathing typical in COPD's hyperinflated state. Lying supine restricts diaphragm movement, worsening air trapping. Pursed-lip breathing, far from avoided, slows expiration, preventing airway collapse a complementary skill. Chest breathing relies on upper thorax muscles, inefficient in COPD. The nurse's teaching on diaphragmatic breathing demonstrated with hand placement (e.g., on abdomen) improves oxygenation and energy efficiency, vital for home management, per respiratory therapy evidence.

Correct Answer: D

Rationale: Prednisone, an oral corticosteroid, is prescribed for asthma to gain prompt control of inadequately controlled, persistent symptoms, typically as a short-term burst (3-10 days). It rapidly reduces severe inflammation driving exacerbations swelling, mucus, and bronchospasm when inhaled therapies fail, restoring airway patency fast. Long-term prevention relies on inhaled corticosteroids, not oral prednisone, due to systemic side effects (e.g., osteoporosis). Asthma isn't infection-driven; prednisone doesn't cure systemic infections, nor is it for pulmonary infection prevention antibiotics serve that role if needed. The nurse's explanation clarifies prednisone's acute role highlighting duration and monitoring (e.g., glucose spikes) ensuring the patient understands its temporary, potent purpose in asthma crisis management, per clinical guidelines.