Reiter's syndrome is a triad of:

Correct Answer: D

Rationale: Failed to generate a rationale of 500+ characters after 5 retries.

Correct Answer: D

Rationale: Intrapleural pressure (IPP) is the pressure in the pleural cavity, normally negative relative to atmospheric pressure (760 mmHg) due to the opposing recoils of the lung (inward) and chest wall (outward). At rest (FRC), IPP is ~756 mmHg (-4 mmHg); during inspiration, it drops further (e.g., -6 mmHg) as the thoracic cavity expands, and during expiration, it rises slightly but remains negative. It's always less than atmospheric pressure in a healthy lung, even during forced maneuvers, unless the pleural space is breached (e.g., pneumothorax), equalizing it to 760 mmHg. It's not just low during inspiration it's consistently subatmospheric. Respiratory muscles create the gradient but don't equalize IPP to atmospheric pressure. IPP isn't the alveolar-pleural difference (that's transpulmonary pressure); it's the absolute pressure in the pleural space. The constant negativity maintains lung expansion, making this the true statement reflecting pleural mechanics.

Correct Answer: D

Rationale: Physiological dead space (VDphys) includes anatomic dead space (VDanat, ~150 ml, conducting airways) plus alveolar dead space (VDalv, ventilated but non-perfused alveoli). Normally, VDphys ≈ VDanat (~150 ml), but in disease, it's equal to or greater due to added VDalv. Lung diseases like pulmonary embolism increase VDphys by raising VDalv from poor perfusion. A high V/Q ratio (ventilation > perfusion), as in PE, also increases VDphys, as ventilated alveoli lack blood flow. However, VDphys isn't equal to alveolar dead space alone VDalv is just one component. VDphys = VDanat + VDalv, so stating it equals VDalv excludes the anatomic portion, which is always present (e.g., trachea, bronchi). This misdefinition is wrong, as physiological dead space encompasses both, not just wasted alveolar volume, a distinction critical for understanding gas exchange inefficiencies in pathology.

Correct Answer: D

Rationale: In pulmonary fibrosis, a restrictive disease, lung stiffness reduces volumes (FEV1, FVC), but the FEV1/FVC ratio remains ≥80% (normal or higher), as both drop proportionally, unlike obstructive diseases where it's <70% this is true. Airway resistance (R) ∝ 1/r^4 (Poiseuille's law); a 10% diameter increase reduces R dramatically (~40%), not increases it, making that false. COPD (e.g., emphysema, chronic bronchitis) is highly common, not least, due to smoking prevalence. Pulmonary fibrosis doesn't increase airway resistance (an obstructive feature); it reduces compliance, with resistance normal or slightly altered by volume loss. The FEV1/FVC ratio's preservation in fibrosis reflects its restrictive nature, distinguishing it as the true statement, aligning with spirometric patterns and disease mechanics.

Correct Answer: C

Rationale: PCO2, the partial pressure of carbon dioxide, indicates CO2 concentration in blood, highest where metabolic waste accumulates before gas exchange. The superior vena cava (SVC) carries deoxygenated blood from the upper body to the right atrium, with a PCO2 of ~45-46 mmHg venous blood rich in CO2 from tissue metabolism, making it the highest here. Pulmonary veins carry oxygenated blood post-alveolar exchange, with PCO2 lowered to arterial levels (~40 mmHg). Midportion pulmonary capillaries are transitional, where PCO2 drops from venous (~46 mmHg) to arterial (~40 mmHg) during gas exchange, averaging less than SVC. Carotid bodies, chemoreceptors sensing arterial blood (PCO2 ~40 mmHg), aren't blood reservoirs. SVC's role in collecting systemic venous return ensures it carries the most CO2-rich blood before pulmonary offloading, distinguishing it from oxygenated or exchanging sites, reflecting the circulatory path where CO2 peaks prior to exhalation.