The treatment of stage 1 Hodgkin's disease is:

Correct Answer: A

Rationale: Stage I Hodgkin's single node region treats with intensive irradiation (A e.g., 36 Gy), curing 90% by targeting lymphoma (e.g., mantle field). Surgery (B) is diagnostic. Chemo (C) is for advanced stages. None' (D), transfusion unfit. Radiation's efficacy is key, guiding nursing for planning and skin care.

Correct Answer: B

Rationale: Infant respiratory distress syndrome (IRDS), or hyaline membrane disease, occurs in premature infants due to insufficient surfactant production by immature type II alveolar cells. Surfactant lowers alveolar surface tension (T), facilitating lung expansion. In IRDS, reduced surfactant leads to increased surface tension, causing alveoli to collapse (atelectasis) after each breath. This high tension decreases lung compliance (C), as the lungs become stiffer and harder to inflate, requiring greater pressure for ventilation. Consequently, collapsed alveoli impair gas exchange, reducing arterial oxygen partial pressure (PaO2) below normal (hypoxemia), often to levels like 50-60 mmHg instead of the typical 75-100 mmHg. The correct combination increased T, decreased C, decreased PaO2 reflects the pathophysiology of IRDS, where surfactant deficiency drives a cascade of respiratory challenges. Other combinations, like increased compliance or unchanged PaO2, contradict the condition's mechanics, where stiff lungs and poor oxygenation are hallmark features.

Correct Answer: A

Rationale: The volume of air entering the lung during inspiration is driven by Boyle's law: lung volume increases as intrapulmonary pressure decreases relative to atmospheric pressure. This pressure gradient is created by the diaphragm and intercostal muscles contracting, expanding the thoracic cavity, and dropping intrapulmonary pressure (e.g., from 760 mmHg to 758 mmHg), allowing air to flow in. Increasing this gradient via greater muscle contraction or thoracic expansion directly increases inspired volume, making it the primary factor. Increase in action potential' is vague but likely refers to neural impulses to respiratory muscles; while more frequent or intense action potentials could enhance muscle effort, this is secondary to the mechanical pressure gradient they produce. Combining both doesn't elevate action potentials to equal status, as pressure is the direct mechanism. Decreasing the gradient reduces airflow, opposing the goal. Thus, the pressure gradient is the most critical factor, as it's the physical driver of ventilation, rooted in respiratory mechanics.

Correct Answer: D

Rationale: Respiratory minute ventilation (VE) is tidal volume (VT) × respiratory rate (RR), fixed here at 6 L/min (6000 ml/min). Alveolar ventilation (VA) is the air reaching alveoli for gas exchange: VA = (VT - VD) × RR, where anatomic dead space (VD) is 150 ml. For 200 ml at 30/min: VE = 200 × 30 = 6000 ml/min, VA = (200 - 150) × 30 = 50 × 30 = 1500 ml/min. For 300 ml at 20/min: VE = 300 × 20 = 6000 ml/min, VA = (300 - 150) × 20 = 150 × 20 = 3000 ml/min. For 400 ml at 15/min: VE = 400 × 15 = 6000 ml/min, VA = (400 - 150) × 15 = 250 × 15 = 3750 ml/min. For 600 ml at 10/min: VE = 600 × 10 = 6000 ml/min, VA = (600 - 150) × 10 = 450 × 10 = 4500 ml/min. The 600 ml at 10/min yields the highest VA (4.5 L/min), as larger VT maximizes air past the fixed VD, despite lower RR. Higher rates with smaller VT waste more ventilation in dead space, reducing VA efficiency, making the deeper, slower pattern optimal.

Correct Answer: D

Rationale: Pneumothorax occurs when air enters the pleural space, disrupting negative intrapleural pressure (~-4 mmHg), causing lung collapse and chest wall expansion. The thorax's diameter increases as the chest wall springs outward due to its elastic recoil. Venous return decreases because positive pleural pressure compresses the vena cava, reducing preload, especially in tension pneumothorax. Vital capacity (VC) drops as the collapsed lung reduces expirable volume (e.g., from 4-5 L to much less). However, lung compliance (C = ΔV / ΔP) doesn't increase it's a lung property (stiffness), not directly altered by pneumothorax. The collapsed lung's volume change per pressure is irrelevant, as it's deflated; compliance may appear effectively zero, but the lung tissue itself isn't more compliant. Increased compliance misrepresents pneumothorax's mechanics, where the issue is pressure loss, not lung elasticity, making this the untrue statement.