Which of the following is true of idiopathic thrombocytopenic purpura:

Correct Answer: A

Rationale: Idiopathic thrombocytopenic purpura (ITP) true: prolonged bleeding time (A low platelets, e.g., <50,000/μL, delay clot formation). Prothrombin (B) is normal coagulation intact. Retraction (C) slows with low platelets. Not always viral (D idiopathic common). Rumpel-Leede is positive petechiae form. Bleeding time's prolongation is key, guiding nursing for steroids and hemorrhage watch.

Correct Answer: D

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

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.