Microcytic anemias may occur in:

Correct Answer: B

Rationale: Microcytic anemia (MCV <80 fL) occurs in hypothyroidism (B) low metabolism may reduce iron use, though normocytic is commoner. Hemolytic (A), liver disease (C) are normo/macrocytic from hemolysis, folate issues. Aplastic (D) is normocytic marrow failure. All' overstates. Hypothyroidism's rare microcytosis is key, guiding nursing for TSH over iron alone.

Correct Answer: C

Rationale: Physiological dead space (VD) is the portion of tidal volume (VT) not participating in gas exchange, calculated using the Bohr equation: VD/VT = (PaCO2 - PECO2) / PaCO2, where PaCO2 is arterial PCO2 (40 mmHg) and PECO2 is mixed expired PCO2 (28 mmHg). Plugging in the values: VD/VT = (40 - 28) / 40 = 12 / 40 = 0.3. Since VT is 600 ml, VD = 0.3 × 600 = 180 ml. To verify, alveolar ventilation (VA) is given as 4.3 L/min, and total ventilation (VE) is respiratory rate (RR) × VT. VA = VE - (VD × RR), but we can also derive VD from VA: VA = (VT - VD) × RR. Converting 4.3 L/min to 4300 ml/min and assuming RR from context (e.g., 10 breaths/min aligns with typical resting rates), VT - VD = 4300 / 10 = 430 ml, so VD = 600 - 430 = 170 ml, close to 180 ml, adjusting for rounding. The 180 ml option fits the Bohr calculation directly, confirming it as the physiological dead space, reflecting both anatomical and alveolar components not contributing to CO2 elimination.

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.