Pulmonology Practice Questions

Q: Pulmonary embolism is most commonly caused by:

Deep vein thrombosis (DVT) of the leg. ***Deep vein thrombosis (DVT) of the leg*** - **Deep vein thrombosis (DVT)** in the leg is the most common source of emboli that travel to the lungs, leading to pulmonary embolism [1]. - The thrombus breaks off from the deep veins, typically in the **lower extremities**, and propagates through the venous system to the pulmonary arteries [1]. *Increased pulmonary pressure (a consequence of PE)* - **Increased pulmonary pressure** is a physiological consequence of a significant pulmonary embolism, as blood flow is obstructed, but it is not the cause of the embolism itself. - This option describes a **downstream effect**, rather than the origin of the embolus. *Fat embolism from pelvic fracture* - **Fat embolisms** can occur after long bone fractures (especially pelvic or femur fractures) and surgeries, but they are a less common cause of PE compared to DVT. - While they can lead to pulmonary symptoms, the mechanism involves **fat globules** entering the circulation, distinct from a thrombus. *Cardiac emboli from heart disease* - **Cardiac emboli** typically originate from the heart (e.g., from atrial fibrillation, mural thrombi after myocardial infarction, or valvular disease) and usually cause **systemic emboli** leading to strokes or limb ischemia. - While rare, paradoxal emboli can occur via a patent foramen ovale but are not the leading cause of "pulmonary" embolism.

Q: Which of the following is NOT a contributing factor to pulmonary hypertension in COPD?

Bronchoconstriction. ***Bronchoconstriction*** - While common in COPD, **bronchoconstriction primarily increases airway resistance** and affects airflow, not directly pulmonary vascular pressure. - It does not directly cause the **remodeling** or **vasoconstriction** of pulmonary arteries that leads to sustained pulmonary hypertension. *Hypoxia* - **Chronic alveolar hypoxia** in COPD is a major driver of pulmonary hypertension by causing **pulmonary vasoconstriction**. - It also contributes to vascular remodeling, leading to sustained increases in pulmonary vascular resistance. *Pulmonary vasoconstriction* - **Hypoxia-induced pulmonary vasoconstriction** [1] is a primary and immediate response in the lungs that leads to increased pulmonary arterial pressure. - Over time, chronic vasoconstriction contributes to **vascular remodeling**, further exacerbating pulmonary hypertension. *High lung volume* - The **hyperinflation** characteristic of COPD can compress pulmonary capillaries and small vessels [2], leading to increased pulmonary vascular resistance. - This extrinsic compression contributes mechanically to the elevated pulmonary pressures seen in these patients.

Q: Which of the following statements about pulmonary embolism is false?

Most commonly presents within 2 weeks. Most commonly presents within 2 weeks - This statement is **false** because while pulmonary embolism can occur at any time, its onset is not restricted to or "most commonly presents" within a two-week period. - The timing of presentation can vary widely depending on the predisposing factors and the specific event leading to the embolus formation and migration. *Dyspnea is the most common symptom* - **Dyspnea** (shortness of breath) is indeed the **most frequent symptom** reported by patients experiencing pulmonary embolism. - This symptom often occurs acutely and can range from mild to severe, correlating with the size and location of the embolism. *Pulmonary embolism often arises from deep vein thrombosis in the legs.* - The vast majority of **pulmonary emboli (PEs)** originate from **deep vein thromboses (DVTs)**, particularly those located in the large veins of the legs and pelvis [1, 2]. - These clots can detach and travel through the venous system to the heart and then into the pulmonary arteries [2]. *Longer survival time generally indicates a better chance of recovery.* - Patients who survive longer after a pulmonary embolism are more likely to have received timely treatment and may have experienced a less severe embolic event or have better underlying health. - Prolonged survival after the initial acute phase suggests the patient has overcome the immediate life-threatening aspects and is on the path to recovery, potentially with less long-term sequelae.

Q: Hamman's sign is seen in:

Pneumomediastinum. ***Pneumomediastinum*** - **Hamman's sign** is a classic auscultatory finding in pneumomediastinum, characterized by **crunching, bubbling, or clicking sounds synchronized with the heartbeat**. - These sounds are heard due to the presence of **air in the mediastinum** being displaced by the contracting heart. *Pericardial effusion* - **Pericardial effusion** involves fluid accumulation around the heart, which typically causes muffled heart sounds and, in severe cases, signs of **cardiac tamponade**. - It does not produce the characteristic **crunching sound** associated with Hamman's sign. *Superior vena cava obstruction* - **Superior vena cava obstruction** is characterized by symptoms like **facial swelling**, **distended neck veins**, and dyspnea due to impaired venous return. - It does not lead to the presence of air in the mediastinum or the specific auscultatory findings of Hamman's sign. *Thyrotoxicosis* - **Thyrotoxicosis** is a hypermetabolic state with symptoms such as **tachycardia**, palpitations, and heat intolerance. - While it affects the cardiovascular system, it does not involve the presence of air in the mediastinum or the development of Hamman's sign.

Q: Hemoptysis is said to be massive when it exceeds what amount in 24 hours?

600mL. 600mL - Hemoptysis is considered **massive** when the volume of blood expectorated exceeds **600 mL within a 24-hour period**, or **100 mL per hour**, indicating a life-threatening emergency. - This threshold is crucial because it significantly increases the risk of **airway obstruction** and **hypovolemic shock**, which requires immediate medical intervention. *400mL* - While 400 mL in 24 hours is a significant amount of bleeding, it is generally not classified as **massive hemoptysis** according to most clinical definitions. - Significant hemoptysis can still be dangerous and require investigation, but it does not meet the criteria for immediately life-threatening massive hemoptysis. *500mL* - This volume is close to the threshold for massive hemoptysis but is still typically not the **definitive cutoff** used in clinical practice. - It would still warrant aggressive management and consideration for interventions like bronchoscopy or embolization. *800mL* - While certainly a severe amount, 800 mL in 24 hours **exceeds** the generally accepted definition of massive hemoptysis. - The 600 mL threshold is based on the point at which there is a critical risk of **asphyxiation** or **hemodynamic instability** [1].

Q: Which of the following is the least likely cause of bronchiectasis?

Primary TB. Primary TB - While post-primary (reactivation) tuberculosis can lead to **bronchiectasis**, primary tuberculosis is less commonly a direct cause of established, widespread bronchiectasis in the acute phase. - Primary TB more often causes **lymphadenopathy** and localized parenchymal disease, with bronchiectasis being a rarer, late complication if airway obstruction or severe destruction occurs. *Pneumonia* - Severe or recurrent bacterial pneumonias can cause **irreversible damage** to the bronchial walls, leading to dilation and fibrosis, which is characteristic of bronchiectasis [1]. - The inflammatory process and **mucociliary dysfunction** during pneumonia contribute to ongoing infection and structural changes [1]. *Inhaled foreign body* - A persistent **foreign body** in the airway can cause localized obstruction, leading to chronic inflammation, infection, and subsequent dilation of the bronchi distal to the obstruction [1]. - This recurrent infection and inflammation weaken the bronchial walls over time, defining localized bronchiectasis. *Chronic aspiration* - **Recurrent aspiration** of gastric contents or oral secretions causes repeated injury and inflammation to the bronchial epithelium. - This chronic irritation and potential for bacterial colonization damage the airway walls, predisposing to **bronchial dilation** and infection, characteristic of bronchiectasis.

Q: Most common clinical presentation of sarcoidosis is?

Hilar lymphadenopathy. ***Hilar lymphadenopathy*** - The most common clinical presentation of **sarcoidosis** is **hilar lymphadenopathy**, often discovered incidentally on chest X-ray [1]. - It is associated with **granulomatous inflammation** within the lymph nodes, which is a hallmark of sarcoidosis [1]. *Pleural plaque* - Typically associated with **asbestosis**, not sarcoidosis; involves localized fibrous thickening of the pleura. - Rarely presents as a predominant feature in sarcoidosis cases. *Interstitial calcification* - While calcification can occur in sarcoidosis, it is not a primary or common presentation; it pertains more to chronic cases. - It may result from granulomatosis, but the initial clinical manifestation is usually hilar lymphadenopathy. *Pulmonary fibrosis* - Pulmonary fibrosis can develop in advanced sarcoidosis but is not the most common initial presentation. - The early stage is characterized more by **inflammation and lymphadenopathy**, rather than fibrosis.

Q: A 45-year-old man presents with a dry cough, fatigue, and bilateral hilar lymphadenopathy on chest X-ray. What is the most likely diagnosis?

Sarcoidosis. ***Silicosis*** - The patient's **occupation in a mine** suggests exposure to **silica dust**, leading to lung diseases including silicosis [1]. - **Bilateral hilar lymphadenopathy** and dry cough are common findings, aligning well with the symptoms presented. *Tuberculosis* - Typically presents with **cough**, but more often with **hemoptysis** and systemic symptoms like **weight loss** and **night sweats**. - **Hilar lymphadenopathy** may be present, but not as clearly related to mining exposure as in silicosis. Notably, silicosis is associated with increased susceptibility to tuberculosis [1]. *Sarcoidosis* - Can cause **bilateral hilar lymphadenopathy** [2], but often presents with additional systemic symptoms and is less directly connected to occupational exposure to dust. - Frequently associated with **skin lesions** and **uveitis**, which are not mentioned in this case. *Asbestosis* - Primarily associated with **exposure to asbestos**, typically causing symptoms like **dyspnea** and **pulmonary fibrosis**, rather than hilar lymphadenopathy. - The occupational history does not support asbestosis, as mining exposure is more indicative of silicosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 697-698. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701.

Question 1

Pulmonary embolism is most commonly caused by:

Accepted Answer

Deep vein thrombosis (DVT) of the leg

Answer

Fat embolism from pelvic fracture

Answer

Cardiac emboli from heart disease

Answer

Increased pulmonary pressure (a consequence of PE)

Question 2

Which of the following is NOT a contributing factor to pulmonary hypertension in COPD?

Accepted Answer

Bronchoconstriction

Answer

High lung volume

Answer

Hypoxia

Answer

Pulmonary vasoconstriction

Question 3

Which of the following statements about pulmonary embolism is false?

Accepted Answer

Most commonly presents within 2 weeks

Answer

Pulmonary embolism often arises from deep vein thrombosis in the legs.

Answer

Dyspnea is the most common symptom

Answer

Longer survival time generally indicates a better chance of recovery.

Question 4

What is the most likely cause of the pleural effusion in a previously healthy 63-year-old man with pneumonia, as indicated by a chest x-ray showing consolidation and pleural fluid analysis revealing a cell count of 1110/mm3, glucose of 75 mg/dL, protein of 4.0 g/dL, LDH of 400 U/L, and pH of 7.35?

Accepted Answer

Increased permeability of pleural membranes due to pneumonia

Answer

Increased hydrostatic pressure

Answer

Decreased oncotic pressure

Answer

Parapneumonic effusion without infection

Question 5

Hamman's sign is seen in:

Accepted Answer

Pneumomediastinum

Answer

Pericardial effusion

Answer

Superior vena cava obstruction

Answer

Thyrotoxicosis

Question 6

Hemoptysis is said to be massive when it exceeds what amount in 24 hours?

Accepted Answer

600mL

Answer

400mL

Answer

500mL

Answer

800mL

Question 7

Which of the following is the least likely cause of bronchiectasis?

Accepted Answer

Primary TB

Answer

Pneumonia

Answer

Inhaled foreign body

Answer

Chronic aspiration

Question 8

Patient with pulmonary parenchymal fibrosis (PPF) who complains of breathing difficulty, is tachycardic, and tachypneic, and has a Batwing sign present on X-ray. What is the possible reason?

Accepted Answer

Due to fluid overload in a patient with pulmonary parenchymal fibrosis

Answer

Transfusion-related lung injury

Answer

Acute renal failure due to tubular acidosis

Answer

Hemolysis leading to hemoglobinuria

Question 9

Most common clinical presentation of sarcoidosis is?

Accepted Answer

Hilar lymphadenopathy

Answer

Pleural plaque

Answer

Pulmonary fibrosis

Answer

Interstitial calcification

Question 10

A 45-year-old man presents with a dry cough, fatigue, and bilateral hilar lymphadenopathy on chest X-ray. What is the most likely diagnosis?

Accepted Answer

Sarcoidosis

Answer

Silicosis

Answer

Tuberculosis

Answer

Asbestosis

Pulmonology — MCQs

Pulmonology — MCQs

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