Physician Assistant National Certifying Examination (PANCE) Pulmonary System Flashcards

24 sample cards from the Pulmonary System deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. How does the Wells criteria score guide PE workup with regard to D-dimer and CT angiography?

   Low/unlikely pretest probability → obtain a D-dimer; if negative, PE is excluded. High/likely probability → proceed directly to CT pulmonary angiography (the diagnostic gold standard). A normal D-dimer has a high negative predictive value only in low-probability patients.

2. What is the first-line treatment of acute PE in a hemodynamically stable patient versus an unstable (massive) PE?

   Stable: anticoagulation (e.g., DOAC such as rivaroxaban/apixaban, or heparin bridging to warfarin). Unstable/massive (hypotension, shock): systemic thrombolysis (e.g., alteplase tPA), or embolectomy if thrombolysis contraindicated.

3. What hemodynamic value defines pulmonary hypertension?

   A resting mean pulmonary arterial pressure $> 20\,\text{mmHg}$ measured by right heart catheterization (the prior threshold was $\geq 25\,\text{mmHg}$).

4. List the 5 WHO clinical groups of pulmonary hypertension.

   Group 1: pulmonary arterial hypertension (PAH). Group 2: left heart disease. Group 3: chronic lung disease/hypoxia. Group 4: chronic thromboembolic (CTEPH). Group 5: multifactorial/unclear mechanisms.

5. What is the gold standard diagnostic test for pulmonary hypertension and what does it directly measure?

   Right heart (Swan-Ganz) catheterization, which directly measures mean pulmonary arterial pressure, pulmonary capillary wedge pressure, and cardiac output to confirm and classify PH.

6. How is acute respiratory distress syndrome (ARDS) defined by the Berlin criteria?

   Acute onset within 1 week; bilateral pulmonary infiltrates on imaging not fully explained by effusions/atelectasis; respiratory failure not fully explained by cardiac failure/fluid overload; and hypoxemia graded by $\frac{PaO_{2}}{FiO_{2}}$ ratio with PEEP $\geq 5\,\text{cmH}_2\text{O}$.

7. What $\frac{PaO_{2}}{FiO_{2}}$ ratios define mild, moderate, and severe ARDS?

   Mild: $200 < \frac{PaO_{2}}{FiO_{2}} \leq 300$; Moderate: $100 < \frac{PaO_{2}}{FiO_{2}} \leq 200$; Severe: $\frac{PaO_{2}}{FiO_{2}} \leq 100$ (all with PEEP $\geq 5\,\text{cmH}_2\text{O}$).

8. What is the cornerstone ventilator strategy that reduces mortality in ARDS?

   Lung-protective (low tidal volume) ventilation: tidal volume of $6\,\text{mL/kg}$ of ideal body weight, with plateau pressure kept $< 30\,\text{cmH}_2\text{O}$ and appropriate PEEP (permissive hypercapnia is accepted).

9. What are the ABG criteria distinguishing type 1 from type 2 respiratory failure?

   Type 1 (hypoxemic): $PaO_{2} < 60\,\text{mmHg}$ with normal or low $PaCO_{2}$ (oxygenation failure). Type 2 (hypercapnic): $PaCO_{2} > 50\,\text{mmHg}$, often with hypoxemia (ventilation failure).

10. Write the alveolar gas equation and the formula for the A-a oxygen gradient.

    Alveolar oxygen: $P_{A}O_{2} = FiO_{2}(P_{atm} - P_{H_2O}) - \frac{PaCO_{2}}{R}$, commonly $P_{A}O_{2} = 150 - \frac{PaCO_{2}}{0.8}$ on room air at sea level. A-a gradient $= P_{A}O_{2} - PaO_{2}$; a normal estimate is $\frac{\text{age}}{4} + 4$.

11. In mechanical ventilation, what do PEEP and $FiO_{2}$ each primarily control, versus respiratory rate and tidal volume?

    PEEP and $FiO_{2}$ primarily control oxygenation ($PaO_{2}$). Respiratory rate and tidal volume (i.e., minute ventilation) primarily control $CO_{2}$ elimination/ventilation ($PaCO_{2}$).

12. What is the most common type of lung cancer overall, and which type is most strongly linked to smoking and central location?

    Adenocarcinoma is the most common overall (and most common in non-smokers, typically peripheral). Small cell lung cancer and squamous cell carcinoma are the most strongly smoking-associated and are typically central.

13. Which lung cancers are most associated with these paraneoplastic syndromes: SIADH, ectopic ACTH, Lambert-Eaton, hypercalcemia (PTHrP)?

    Small cell lung cancer → SIADH, ectopic ACTH (Cushing), and Lambert-Eaton myasthenic syndrome. Squamous cell carcinoma → hypercalcemia from PTHrP.

14. What is the key treatment distinction between small cell and non-small cell lung cancer?

    Small cell lung cancer is usually disseminated at diagnosis and treated primarily with chemotherapy $\pm$ radiation (rarely surgical). Non-small cell lung cancer, if localized (early stage), is treated with surgical resection $\pm$ adjuvant therapy.

15. What pulmonary function pattern (spirometry and DLCO) characterizes interstitial lung disease / pulmonary fibrosis?

    A restrictive pattern: reduced FVC and reduced total lung capacity, with a normal or increased $\frac{FEV_{1}}{FVC}$ ratio, and a decreased diffusing capacity (DLCO).

16. What are the classic high-resolution CT findings of idiopathic pulmonary fibrosis (usual interstitial pneumonia pattern)?

    Subpleural, basal-predominant reticular opacities with honeycombing and traction bronchiectasis; ground-glass is minimal. Antifibrotics (pirfenidone, nintedanib) slow progression.

17. What are the characteristic chest X-ray and laboratory findings of sarcoidosis?

    Bilateral hilar lymphadenopathy on chest X-ray, with noncaseating granulomas on biopsy. Labs often show elevated ACE level and hypercalcemia/hypercalciuria (from $1\alpha$-hydroxylase activity in granulomas).

18. What is Lofgren syndrome and what is its prognostic significance in sarcoidosis?

    Lofgren syndrome is the acute triad of erythema nodosum, bilateral hilar lymphadenopathy, and arthralgias (often with fever). It carries a good prognosis with frequent spontaneous remission.

19. Match the pneumoconiosis to its exposure: silicosis, asbestosis, coal worker's lung, berylliosis.

    Silicosis → mining, sandblasting, quarrying (eggshell-calcified hilar nodes; upper lobes; increased TB risk). Asbestosis → shipbuilding, insulation, brake linings (lower lobes, pleural plaques, mesothelioma/bronchogenic cancer). Coal worker's pneumoconiosis → coal dust. Berylliosis → aerospace/electronics (granulomas mimicking sarcoidosis).

20. How does asbestos exposure interact with smoking to affect lung cancer risk?

    Asbestos and smoking are synergistic (multiplicative): together they raise bronchogenic carcinoma risk far more than either alone. Asbestos alone is most specifically linked to malignant pleural mesothelioma, which is not strongly smoking-related.

21. State Light's criteria for an exudative pleural effusion.

    An effusion is exudative if ANY one is met: (1) $\frac{\text{pleural protein}}{\text{serum protein}} > 0.5$; (2) $\frac{\text{pleural LDH}}{\text{serum LDH}} > 0.6$; (3) pleural LDH $> \frac{2}{3}$ of the upper limit of normal serum LDH. If none are met, the effusion is a transudate.

22. Give two common causes each of transudative and exudative pleural effusions.

    Transudate (imbalance of hydrostatic/oncotic pressure): congestive heart failure, cirrhosis, nephrotic syndrome. Exudate (increased capillary permeability/inflammation): pneumonia (parapneumonic), malignancy, pulmonary embolism, tuberculosis.

23. What is the difference between a primary spontaneous and a tension pneumothorax in presentation?

    Primary spontaneous pneumothorax: occurs in tall, thin young men from ruptured apical blebs; presents with sudden pleuritic pain and dyspnea, decreased breath sounds, hyperresonance. Tension pneumothorax: life-threatening with tracheal deviation AWAY from the affected side, hypotension, distended neck veins, and hemodynamic collapse.

24. What is the immediate treatment of a tension pneumothorax?

    Emergent needle decompression (large-bore needle in the 2nd intercostal space at the midclavicular line, or the 4th/5th intercostal space at the anterior axillary line), followed by chest tube (tube thoracostomy) placement. Do NOT wait for imaging.

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