Pulmonology Practice Questions

Q: Which of the following correlates well with the severe type of bronchial asthma exacerbation?

Usual use of accessory muscles of respiration. The severity of an acute asthma exacerbation is categorized into mild, moderate, severe, and life-threatening based on clinical and physiological parameters. **1. Why Option D is Correct:** The **use of accessory muscles** (sternocleidomastoid, scalene) and **suprasternal retractions** are hallmark clinical signs of a **severe asthma exacerbation**. These signs indicate that the work of breathing has significantly increased to overcome high airway resistance and lung hyperinflation [1]. In severe cases, the patient often speaks in single words rather than sentences and prefers sitting upright (orthopnea). **2. Why the Other Options are Incorrect:** * **Option A (Bradycardia):** In severe asthma, the heart rate is typically **tachycardic (>120 bpm)** due to stress and sympathetic overactivity [1]. Bradycardia is a "near-fatal" or **life-threatening** sign, indicating impending respiratory arrest and exhaustion. * **Option B (Pulsus Paradoxus):** Pulsus paradoxus (an exaggerated drop in systolic BP during inspiration) is a feature of severe asthma, but the value must be **greater than 25 mmHg**. A value less than 10 mmHg is considered normal. * **Option C (Tachypnea):** While tachypnea is present, a respiratory rate **less than 30/min** usually points toward a mild-to-moderate exacerbation. In **severe asthma**, the RR is typically **>30/min**. **Clinical Pearls for NEET-PG:** * **Silent Chest:** The most ominous sign in asthma; it indicates such severe airflow limitation that no wheeze is heard. * **ABG in Asthma:** Initially, patients show Respiratory Alkalosis (low $PaCO_2$) due to hyperventilation. A **"Normal" $PaCO_2$** in a distressed patient is a danger sign, indicating muscle fatigue and transition to respiratory failure [2]. * **PEFR:** A Peak Expiratory Flow Rate **<50%** of the predicted/personal best defines a severe attack [1].

Q: Which of the following statements is true regarding interstitial lung disease?

All of the above. Interstitial Lung Disease (ILD) is a group of disorders characterized by inflammation and progressive fibrosis of the pulmonary interstitium, leading to a **Restrictive Lung Disease** pattern [1]. 1. **Decreased FVC (Option A):** In ILD, the lung parenchyma becomes stiff and non-compliant ("stiff lungs"). This restriction limits the total volume of air the lungs can hold, leading to a significant reduction in Forced Vital Capacity (FVC) and Total Lung Capacity (TLC) [1]. 2. **Decreased FEV1 (Option B):** While the primary defect is restrictive, the Forced Expiratory Volume in 1 second (FEV1) also decreases because the total volume available to be exhaled is reduced [3]. However, the hallmark of restriction is that the **FEV1/FVC ratio remains normal or is increased** (unlike obstructive diseases where it is decreased) [3]. 3. **End-inspiratory Crackles (Option C):** On auscultation, "Velcro-like" fine end-inspiratory crepitations are a classic clinical sign [1]. These occur due to the sudden opening of small airways that were collapsed by the surrounding fibrotic tissue. **Conclusion:** Since all three features—reduced FVC, reduced FEV1, and characteristic crackles—are hallmark findings of ILD, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **PFT Pattern:** ↓ TLC, ↓ FVC, ↓ FEV1, but **Normal/↑ FEV1/FVC ratio** [1], [3]. * **DLCO:** Characteristically **decreased** due to the thickening of the alveolar-capillary membrane [1]. * **Radiology:** HRCT is the gold standard; look for "honeycombing" and reticular opacities (especially in IPF) [1]. * **6-Minute Walk Test:** Used to assess exertional desaturation, a common feature of ILD [2].

Q: Egg-shell calcification in hilar lymph nodes is seen in:

Histoplasmosis. **Explanation:** **Egg-shell calcification** refers to a distinctive radiological pattern where calcium deposits occur in the periphery of a lymph node, creating a thin, radiopaque rim. **Why Histoplasmosis is correct:** While **Silicosis** [1] is the most classic association for egg-shell calcification, among the provided options, **Histoplasmosis** is a well-documented cause. In Histoplasmosis, healed granulomatous inflammation in the hilar and mediastinal lymph nodes can undergo peripheral calcification over time. It is a common fungal cause of this radiological sign, particularly in endemic regions. **Analysis of Incorrect Options:** * **Sarcoidosis:** Although Sarcoidosis causes bilateral hilar lymphadenopathy [1], the calcification pattern is typically "popcorn" or amorphous/chunky rather than egg-shell. * **Tuberculosis:** TB usually results in dense, solid, or stippled calcification of the lymph nodes (Ghon’s complex/Ranke complex). Egg-shell calcification is extremely rare in TB. * **Carcinoma Lung:** Malignancy typically presents with lymph node enlargement or necrosis; calcification is rare unless the patient has received prior radiation therapy. **High-Yield NEET-PG Pearls:** 1. **Most Common Cause:** Silicosis [1] (Classic "Must-know" for exams). 2. **Differential Diagnosis for Egg-shell Calcification:** * Silicosis & Coal Worker’s Pneumoconiosis (CWP) [1] * Histoplasmosis * Sarcoidosis [1] (Rarely) * Post-irradiation (e.g., Hodgkin Lymphoma) * Blastomycosis 3. **Radiological Tip:** If the question asks for "Bilateral hilar lymphadenopathy with egg-shell calcification" and Silicosis is not an option, look for Histoplasmosis or Sarcoidosis [1].

Q: What is the most common cause of pulmonary thromboembolism?

Deep vein thrombosis. **Explanation:** **Deep Vein Thrombosis (DVT)** is the most common cause of pulmonary thromboembolism (PTE). [1] Approximately 90% of all pulmonary embolic events originate from thrombi in the deep veins of the lower extremities, particularly the proximal-level veins like the popliteal, femoral, and iliac veins. These thrombi dislodge, travel through the right heart, and lodge in the pulmonary arterial circulation. **Analysis of Options:** * **Disseminated Intravascular Coagulation (DIC):** While DIC involves widespread microvascular thrombosis and subsequent hemorrhage, it is not a primary cause of large pulmonary emboli. It is a systemic complication of underlying conditions like sepsis or malignancy. * **Coagulation Disorders:** Conditions like Factor V Leiden or Protein C/S deficiency are *predisposing risk factors* (thrombophilias) that lead to DVT, but they are not the immediate anatomical source of the embolus itself. * **Venous Hypertension:** This is a clinical manifestation of chronic venous insufficiency or heart failure. While it may lead to stasis, it is a hemodynamic state rather than the direct source of an embolus. **High-Yield Clinical Pearls for NEET-PG:** * **Virchow’s Triad:** The three factors contributing to venous thrombosis are stasis, endothelial injury, and hypercoagulability. * **Most Common Source:** Proximal leg veins (above the knee) are more likely to embolize than calf veins. * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA) is the investigation of choice for diagnosing PTE. * **ECG Finding:** The most common ECG finding is sinus tachycardia; the "classic" S1Q3T3 pattern is specific but seen in less than 20% of cases.

Q: In left-sided massive pneumothorax, ECG shows all of the following findings EXCEPT:

Left axis deviation. In a **left-sided massive (tension) pneumothorax**, the accumulation of air in the pleural space causes a significant mediastinal shift toward the right. This anatomical displacement, combined with the insulating effect of the air, leads to characteristic ECG changes that can mimic an acute myocardial infarction. ### Why "Left Axis Deviation" is the Correct Answer: In a left-sided pneumothorax, the heart is pushed toward the right side of the chest. This physical displacement causes a **Right Axis Deviation (RAD)**, not a left axis deviation [4]. Therefore, Option A is the incorrect finding and the correct answer to the question. ### Explanation of Other Options (Expected Findings): * **Absent R wave (Option B):** The air trapped between the heart and the chest wall acts as an insulator, leading to a loss of R-wave voltage in the precordial leads (V1–V6). This can sometimes be mistaken for an anterior wall MI (pseudoinfarction pattern) [3]. * **Peaked P wave (Option C):** Increased intrathoracic pressure and right heart strain can lead to prominent, peaked P waves (P-pulmonale), especially in the inferior leads [1]. * **Precordial T wave inversion (Option D):** Massive pneumothorax causes acute right ventricular strain and cardiac rotation, frequently resulting in T-wave inversions in the precordial leads [1]. ### High-Yield Clinical Pearls for NEET-PG: * **Phasic Voltage Variation:** Similar to electrical alternans in pericardial effusion, pneumothorax can cause beat-to-beat voltage changes due to the heart's movement within the shifted mediastinum. * **QRS Voltage:** A sudden decrease in QRS voltage in a patient with acute respiratory distress should raise suspicion for either pericardial effusion or tension pneumothorax. * **Diagnosis:** While ECG changes are helpful, the gold standard for diagnosis in an emergency is clinical examination (absent breath sounds, hyper-resonance) followed by a Chest X-ray [2].

Q: Acute Lung Injury (ALI) is characterized by all of the following features except:

PaO2 / FiO2 < 200 mm Hg. **Explanation:** The diagnosis of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS) was traditionally based on the **American-European Consensus Conference (AECC) definitions**. According to these criteria, both ALI and ARDS share the same clinical features, differing only in the severity of hypoxemia [1]. 1. **Why Option A is the correct answer:** In the AECC definition, **ALI** is defined by a $PaO_2/FiO_2$ ratio of **$\leq$ 300 mm Hg**. A ratio of **$<$ 200 mm Hg** specifically defines **ARDS**. Therefore, stating that ALI is characterized by a ratio $< 200$ is incorrect as it describes the more severe form (ARDS). 2. **Analysis of Incorrect Options:** * **Option B:** Bilateral infiltrates on chest X-ray (interstitial or alveolar) are a hallmark of both ALI and ARDS, representing non-cardiogenic pulmonary edema [1]. * **Options C & D:** These options refer to the same physiological state. To diagnose ALI/ARDS, one must exclude hydrostatic (cardiogenic) pulmonary edema. This is confirmed by a **PCWP < 18 mm Hg** or the absence of clinical evidence of increased **Left Atrial Pressure** [1]. **Clinical Pearls for NEET-PG:** * **Berlin Definition (2012):** The term "ALI" has been largely replaced. ARDS is now categorized into [1]: * **Mild:** $PaO_2/FiO_2$ 201–300 mm Hg * **Moderate:** $PaO_2/FiO_2$ 101–200 mm Hg * **Severe:** $PaO_2/FiO_2 \leq$ 100 mm Hg * **Key Histopathology:** The pathological hallmark of ALI/ARDS is **Diffuse Alveolar Damage (DAD)**. * **Management:** The mainstay of treatment is **low tidal volume ventilation** (6 mL/kg) to prevent ventilator-associated lung injury.

Q: What is platypnea?

Dyspnea in the upright position with relief in the supine position. **Explanation:** **Platypnea** is a rare clinical symptom defined as shortness of breath (dyspnea) that is induced by the **upright position** (sitting or standing) and is relieved by lying flat (**supine position**). **Pathophysiology:** It is most commonly associated with **Orthodeoxia** (a drop in arterial oxygen saturation upon standing), forming the **Platypnea-Orthodeoxia Syndrome (POS)**. This occurs due to a functional right-to-left shunt. In the upright position, gravity redirects blood flow to the lung bases. If there is a structural defect (like a Patent Foramen Ovale or Atrial Septal Defect) combined with a positional change in the heart's anatomy or basal pulmonary arteriovenous malformations (AVMs), deoxygenated blood bypasses the lungs, leading to hypoxemia and dyspnea. **Analysis of Incorrect Options:** * **Option A (Orthopnea):** This is the opposite of platypnea. It is common in Congestive Heart Failure (CHF) where the supine position increases venous return, overloading a failing left ventricle [1], [2]. * **Option C (Exertional Dyspnea):** This is the most common form of dyspnea, seen in chronic stable angina, COPD, and interstitial lung disease [1], [2]. * **Option D (Paroxysmal Nocturnal Dyspnea - PND):** This is a classic sign of left-sided heart failure where the patient wakes up gasping for air after a few hours of sleep [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Association:** **Hepatopulmonary Syndrome** (in patients with Cirrhosis) due to intrapulmonary vascular dilatations at the lung bases. * **Cardiac Causes:** Patent Foramen Ovale (PFO) or Atrial Septal Defect (ASD), especially after pneumonectomy or with aortic aneurysms. * **Pulmonary Causes:** Pulmonary Arteriovenous Malformations (AVMs), often seen in **Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu syndrome)**.

Q: What is a universal finding in asthma?

Hypoxia. In bronchial asthma, the primary pathophysiological mechanism is airway inflammation and bronchoconstriction, leading to **Ventilation-Perfusion (V/Q) mismatch**. This mismatch is the most common cause of arterial hypoxemia in asthmatic patients [1]. Even in mild exacerbations, some degree of **hypoxia** is almost universally present due to the uneven distribution of airflow across different lung segments [1]. **Analysis of Options:** * **A. Hypoxia (Correct):** As discussed, V/Q mismatching occurs early and consistently during an attack. While the body initially compensates by increasing the respiratory rate, the underlying oxygenation deficit remains a hallmark. * **B. Hypercarbia:** This is a **late and ominous sign** [2]. Most patients with asthma are tachypneic and "blow off" $CO_2$, leading to *hypocarbia*. A "normal" or rising $PCO_2$ in a severe attack indicates respiratory muscle fatigue and impending respiratory failure [2]. * **C. Respiratory Acidosis:** This occurs only when hypercarbia develops (late stage). The typical early finding in asthma is **Respiratory Alkalosis** due to hyperventilation. * **D. Metabolic Acidosis:** This is not a standard finding in asthma. It may occasionally occur in very severe, prolonged cases due to increased work of breathing and lactic acid accumulation, but it is far from universal. **Clinical Pearls for NEET-PG:** * **The "Silent Chest":** A dangerous sign where bronchoconstriction is so severe that there is insufficient airflow to produce a wheeze. * **Pulsus Paradoxus:** A drop in systolic BP >10 mmHg during inspiration; indicates severe airway obstruction. * **ABG Trend:** The progression in worsening asthma is: Respiratory Alkalosis $\rightarrow$ Normalization of $pH/PCO_2$ (Warning!) $\rightarrow$ Respiratory Acidosis.

Question 1

Which of the following correlates well with the severe type of bronchial asthma exacerbation?

Accepted Answer

Usual use of accessory muscles of respiration

Answer

Bradycardia with HR less than 100/min

Answer

Pulsus paradoxus less than 10/min

Answer

Tachypnea with RR less than 30/min

Question 2

Which of the following statements is true regarding interstitial lung disease?

Accepted Answer

All of the above

Answer

Decreased FVC

Answer

Decreased FEV1

Answer

Presence of end-inspiratory crackles

Question 3

What is the current terminology for status asthmaticus?

Accepted Answer

Severe acute asthma

Answer

Episodic asthma

Answer

Chronic asthma

Answer

Acute asthma

Question 4

Egg-shell calcification in hilar lymph nodes is seen in:

Accepted Answer

Histoplasmosis

Answer

Sarcoidosis

Answer

Tuberculosis

Answer

Carcinoma lung

Question 5

What is the most common cause of pulmonary thromboembolism?

Accepted Answer

Deep vein thrombosis

Answer

Disseminated intravascular coagulation

Answer

Coagulation disorder

Answer

Venous hypertension

Question 6

In left-sided massive pneumothorax, ECG shows all of the following findings EXCEPT:

Accepted Answer

Left axis deviation

Answer

Absent R wave

Answer

Peaked P wave

Answer

Precordial T wave inversion

Question 7

Acute Lung Injury (ALI) is characterized by all of the following features except:

Accepted Answer

PaO2 / FiO2 < 200 mm Hg

Answer

Bilateral interstitial infiltrates

Answer

Pulmonary capillary wedge pressure (PCWP) < 18 mm Hg

Answer

Normal left atrial pressure

Question 8

What is platypnea?

Accepted Answer

Dyspnea in the upright position with relief in the supine position

Answer

Dyspnea in the supine position and relief in the upright position

Answer

Dyspnea on exertion

Answer

Dyspnea waking the patient during deep sleep

Question 9

Following pelvic gynecologic surgery, a 34-year-old woman becomes dyspneic, her peripheral arterial O2 saturation falls from 94% to 81%, and her measured PaO2 is 52 on a 100% non-rebreather mask. She is hemodynamically stable. A CT angiogram is consistent with a right lower lobe pulmonary embolus. Which of the following is the next step in her management?

Accepted Answer

Systemic anticoagulation with heparin infusion

Answer

Systemic anticoagulation with warfarin

Answer

Placement of an inferior vena cava filter

Answer

Thrombolytic therapy

Question 10

What is a universal finding in asthma?

Accepted Answer

Hypoxia

Answer

Hypercarbia

Answer

Respiratory acidosis

Answer

Metabolic acidosis

Pulmonology — MCQs

Pulmonology — MCQs

On this page

Practice by Chapter

Want unlimited practice?