Pulmonology — MCQs

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?

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What is a universal finding in asthma?

Pulmonology Indian Medical PG Practice Questions and MCQs

Question 491: Which of the following correlates well with the severe type of bronchial asthma exacerbation?

A. Bradycardia with HR less than 100/min
B. Pulsus paradoxus less than 10/min
C. Tachypnea with RR less than 30/min
D. Usual use of accessory muscles of respiration (Correct Answer)

Explanation: 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].

Question 492: Which of the following statements is true regarding interstitial lung disease?

A. Decreased FVC
B. Decreased FEV1
C. Presence of end-inspiratory crackles
D. All of the above (Correct Answer)

Explanation: 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].

Question 493: What is the current terminology for status asthmaticus?

A. Episodic asthma
B. Chronic asthma
C. Acute asthma
D. Severe acute asthma (Correct Answer)

Explanation: **Explanation:** **Status asthmaticus** is a historical term used to describe an extreme form of asthma exacerbation that is unresponsive to standard initial bronchodilator therapy. In modern clinical practice and international guidelines (such as GINA), this is now formally termed **Severe Acute Asthma** [1]. **Why "Severe Acute Asthma" is correct:** The shift in terminology emphasizes the clinical urgency and the severity of the airway obstruction. It is characterized by a patient who is breathless at rest, has a respiratory rate >30/min, heart rate >120/min, and a Peak Expiratory Flow (PEF) ≤ 50% of their predicted or best value [1]. If the condition progresses to "Life-threatening asthma," the PEF drops below 33% with associated signs like silent chest, cyanosis, or exhaustion. **Why other options are incorrect:** * **A. Episodic asthma:** Refers to asthma symptoms that occur intermittently with periods of normal lung function in between, usually triggered by specific allergens or exercise. * **B. Chronic asthma:** Refers to the long-term, persistent nature of the underlying airway inflammation rather than a sudden, life-threatening crisis. * **C. Acute asthma:** This is a broad term for any exacerbation [1]. While status asthmaticus is acute, the specific terminology requires the qualifier "Severe" to indicate the failure of initial therapy and the need for intensive management. **High-Yield Clinical Pearls for NEET-PG:** * **Silent Chest:** A grave sign in severe acute asthma indicating insufficient airflow to even produce a wheeze. * **Pulsus Paradoxus:** Often present in severe cases (fall in systolic BP >10 mmHg during inspiration). * **ABG Findings:** A "normal" $PaCO_2$ (35-45 mmHg) in a patient with severe acute asthma is an ominous sign of impending respiratory failure, as it suggests the patient is tiring and can no longer hyperventilate. * **First-line treatment:** Oxygen, high-dose inhaled SABA (Salbutamol), and systemic corticosteroids [1].

Question 494: Egg-shell calcification in hilar lymph nodes is seen in:

A. Sarcoidosis
B. Histoplasmosis (Correct Answer)
C. Tuberculosis
D. Carcinoma lung

Explanation: **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].

Question 495: What is the most common cause of pulmonary thromboembolism?

A. Disseminated intravascular coagulation
B. Coagulation disorder
C. Deep vein thrombosis (Correct Answer)
D. Venous hypertension

Explanation: **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.

Question 496: In left-sided massive pneumothorax, ECG shows all of the following findings EXCEPT:

A. Left axis deviation (Correct Answer)
B. Absent R wave
C. Peaked P wave
D. Precordial T wave inversion

Explanation: 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].

Question 497: Acute Lung Injury (ALI) is characterized by all of the following features except:

A. PaO2 / FiO2 < 200 mm Hg (Correct Answer)
B. Bilateral interstitial infiltrates
C. Pulmonary capillary wedge pressure (PCWP) < 18 mm Hg
D. Normal left atrial pressure

Explanation: **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.

Question 498: What is platypnea?

A. Dyspnea in the supine position and relief in the upright position
B. Dyspnea in the upright position with relief in the supine position (Correct Answer)
C. Dyspnea on exertion
D. Dyspnea waking the patient during deep sleep

Explanation: **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)**.

Question 499: 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?

A. Systemic anticoagulation with heparin infusion (Correct Answer)
B. Systemic anticoagulation with warfarin
C. Placement of an inferior vena cava filter
D. Thrombolytic therapy

Explanation: ### Explanation **1. Why Option A is Correct:** The patient presents with an acute pulmonary embolism (PE) confirmed by CT angiogram [1]. In a **hemodynamically stable** patient (normotensive), the standard of care is immediate **systemic anticoagulation** [2]. Unfractionated heparin (UFH) or Low Molecular Weight Heparin (LMWH) is preferred in the acute setting because they prevent further clot propagation and allow the body’s endogenous fibrinolytic system to dissolve the existing thrombus [2]. UFH is often favored post-surgery due to its short half-life and easy reversibility if bleeding occurs. **2. Why the Other Options are Incorrect:** * **Option B (Warfarin):** Warfarin has a delayed onset of action (3–5 days) and initially induces a pro-thrombotic state by inhibiting Proteins C and S. It must always be "bridged" with a parenteral anticoagulant and is never used as monotherapy for acute PE [2]. * **Option C (IVC Filter):** This is indicated only if there is an **absolute contraindication** to anticoagulation (e.g., active major bleeding) or if a patient has recurrent PE despite adequate anticoagulation [2]. This patient has no documented contraindication. * **Option D (Thrombolytic Therapy):** Thrombolysis (e.g., Alteplase) is reserved for **Massive PE**, defined by hemodynamic instability (systolic BP <90 mmHg or obstructive shock) [1]. Since this patient is hemodynamically stable (Submassive or Low-risk PE), the risk of major hemorrhage from thrombolysis outweighs the benefits. **3. NEET-PG High-Yield Pearls:** * **Gold Standard Investigation:** CT Pulmonary Angiogram (CTPA) [1]. * **Most Common ECG Finding:** Sinus tachycardia [1]. * **Treatment Strategy:** * Stable + No contraindications $\rightarrow$ Anticoagulation (Heparin) [2]. * Unstable (Shock/Hypotension) $\rightarrow$ Thrombolysis [1]. * Stable + Contraindication to Anticoagulation $\rightarrow$ IVC Filter [2]. * **Wells’ Score:** Used to determine the pre-test probability of PE before ordering investigations [2].

Question 500: What is a universal finding in asthma?

A. Hypoxia (Correct Answer)
B. Hypercarbia
C. Respiratory acidosis
D. Metabolic acidosis

Explanation: 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.

Practice by Chapter

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