Pulmonary embolism — MCQs

10 questions

A 56-year-old man presents with progressive dyspnea and chest tightness. He works in coal mining. Chest X-ray shows bilateral upper lobe nodules. What is the most likely diagnosis?

A 56-year-old man presents with progressive dyspnea and dry cough. HRCT shows bilateral lower lobe fibrosis with honeycombing. He has clubbing and restrictive spirometry. What medication may slow disease progression?

A 54-year-old man presents with progressive dyspnea and chest tightness. Spirometry shows FEV1 1.8L (60% predicted), FEV1/FVC 0.55. He has a 40 pack-year smoking history. What is the most important intervention?

A 58-year-old man presents with progressive dyspnea and fatigue. Chest X-ray shows bilateral lower lobe shadowing. HRCT shows honeycombing and traction bronchiectasis. He has finger clubbing. What is the prognosis?

A 55-year-old man presents with progressive dyspnea and dry cough over 6 months. He has finger clubbing. HRCT shows honeycombing and reticular opacities in lower lobes. What is the most likely diagnosis?

A 48-year-old man presents with progressive breathlessness and fatigue. Chest X-ray showed bilateral hilar lymphadenopathy. Serum ACE is elevated. Transbronchial biopsy shows no caseating granulomas. What is the most likely diagnosis?

A 54-year-old man presents with progressive dyspnea and bilateral lower lobe crackles. Chest X-ray shows bilateral infiltrates. He works in shipbuilding. What is the most likely diagnosis?

A 56-year-old man presents with progressive dyspnea and dry cough. HRCT shows honeycombing and traction bronchiectasis in lower lobes. He has clubbing. What is the most likely diagnosis?

A 42-year-old man presents with progressive dyspnea and chest tightness. Spirometry shows FEV1 45% predicted, FEV1/FVC 0.85. HRCT shows lower lobe fibrosis. What is the most likely diagnosis?

Q10

A 45-year-old man presents with progressive shortness of breath and fatigue. Chest X-ray shows bilateral hilar lymphadenopathy and pulmonary infiltrates. Serum ACE is elevated. Bronchoscopy with biopsy shows non-caseating granulomas. What is the most likely diagnosis?

Pulmonary embolism UK Medical PG Practice Questions and MCQs

Question 1: A 56-year-old man presents with progressive dyspnea and chest tightness. He works in coal mining. Chest X-ray shows bilateral upper lobe nodules. What is the most likely diagnosis?

A. Lung cancer
B. Silicosis
C. Coal worker's pneumoconiosis (Correct Answer)
D. Tuberculosis
E. Sarcoidosis

Explanation: ***Coal worker's pneumoconiosis***- This diagnosis is strongly supported by the patient's occupational exposure to **coal dust** and the progressive respiratory symptoms like **dyspnea** and **chest tightness**.- The characteristic Chest X-ray finding of bilateral, often small, **pulmonary nodules** predominantly located in the **upper lung zones** is classic for this condition.*Lung cancer*- Although coal miners have an increased risk of lung cancer, the presentation of diffuse **bilateral small nodules** is more typical of a pneumoconiosis than primary malignancy.- Lung cancer usually manifests as a single, dominant mass, or less commonly as reticulonodular interstitial disease, not typically as diffuse, symmetrical small nodules.*Silicosis*- Silicosis is caused by the inhalation of **crystalline silica** dust, prevalent in occupations like sandblasting or quarrying, which differs from pure coal mining exposure.- While silicosis also causes upper lobe nodules, it often presents radiologically with **"eggshell" calcification** of the hilar lymph nodes, a finding not specified in this case.*Tuberculosis*- Although **post-primary TB** targets the upper lobes, generalized diffuse nodularity suggests pneumoconiosis rather than a primary mycobacterial infection.- TB typically presents with systemic symptoms like **fever**, **night sweats**, and **weight loss**, which are not mentioned in this patient's presentation.*Sarcoidosis*- Sarcoidosis is a systemic disease of unknown etiology characterized by **non-caseating granulomas** and classically presents with **bilateral hilar lymphadenopathy (BHL)** on chest imaging.- The strong history of **coal mining** is the key factor favoring an occupational lung disease over sarcoidosis, as BHL is also absent.

Question 2: A 56-year-old man presents with progressive dyspnea and dry cough. HRCT shows bilateral lower lobe fibrosis with honeycombing. He has clubbing and restrictive spirometry. What medication may slow disease progression?

A. Prednisolone
B. Azathioprine
C. Pirfenidone (Correct Answer)
D. Cyclophosphamide
E. N-acetylcysteine

Explanation: ***Pirfenidone***- The clinical presentation with progressive dyspnea, dry cough, clubbing, restrictive spirometry, and HRCT showing bilateral lower lobe fibrosis with **honeycombing** is highly characteristic of **Idiopathic Pulmonary Fibrosis (IPF)**.- **Pirfenidone** is an **anti-fibrotic** agent, along with nintedanib, approved for the treatment of mild to moderate IPF to slow disease progression by reducing the decline in **Forced Vital Capacity (FVC)**.*Prednisolone*- Systemic corticosteroids like **Prednisolone** are not recommended as monotherapy for **Idiopathic Pulmonary Fibrosis (IPF)** due to lack of proven long-term efficacy and potential harm.- They are primarily indicated for inflammatory interstitial lung diseases, such as those associated with **connective tissue diseases**, or for **acute exacerbations** of IPF.*Azathioprine*- **Azathioprine** is an immunosuppressant that was shown to be ineffective and potentially harmful in a triple-drug regimen for IPF in the **PANTHER-IPF trial**.- Immunosuppression is generally avoided in **Idiopathic Pulmonary Fibrosis** unless there is a strong suspicion of an alternative, inflammatory interstitial lung disease.*Cyclophosphamide*- **Cyclophosphamide** is a potent cytotoxic immunosuppressant typically reserved for severe, rapidly progressive forms of **connective tissue disease-associated ILD** (e.g., scleroderma-associated ILD or vasculitis).- It is not indicated for the primary management of **Idiopathic Pulmonary Fibrosis**, which is characterized by relentless fibrosis rather than a primary inflammatory process responsive to this therapy.*N-acetylcysteine*- Although previously studied for its antioxidant properties, the **PANTHER-IPF trial** demonstrated that **N-acetylcysteine** offered no benefit in slowing the progression of IPF and is no longer recommended.- Its primary clinical uses are as a mucolytic agent and as an antidote for **acetaminophen overdose**.

Question 3: A 54-year-old man presents with progressive dyspnea and chest tightness. Spirometry shows FEV1 1.8L (60% predicted), FEV1/FVC 0.55. He has a 40 pack-year smoking history. What is the most important intervention?

A. Bronchodilators
B. Inhaled corticosteroids
C. Smoking cessation (Correct Answer)
D. Pulmonary rehabilitation
E. Long-term oxygen therapy

Explanation: ***Smoking cessation***- This is the **single most important intervention** for patients with **COPD** who smoke, as it is the only measure proven to slow the rate of **FEV1 decline** and disease progression.- Quitting smoking significantly reduces symptoms, exacerbations, and mortality, directly addressing the primary etiological factor in this patient's 40 pack-year history.*Bronchodilators*- **Bronchodilators** (e.g., beta-agonists, anticholinergics) provide crucial **symptomatic relief** by improving airflow and reducing dyspnea, but they do not alter the natural history of COPD or stop the underlying disease progression.- They are essential for managing symptoms but are not the **most important intervention** to halt the destruction caused by smoking.*Inhaled corticosteroids*- **Inhaled corticosteroids (ICS)** are typically indicated for patients with more severe COPD (e.g., FEV1 < 50% predicted) and a history of **frequent exacerbations**, often in combination with long-acting bronchodilators.- While they can reduce inflammation and exacerbation rates, ICS do not reverse or prevent the progressive lung damage caused by smoking.*Pulmonary rehabilitation*- **Pulmonary rehabilitation** is a highly effective intervention that improves **exercise capacity**, reduces dyspnea, and enhances quality of life in patients with COPD.- However, it does not modify the underlying **disease progression** or stop the decline in lung function, which is the primary benefit of smoking cessation.*Long-term oxygen therapy*- **Long-term oxygen therapy (LTOT)** is indicated for patients with **severe chronic hypoxemia** (PaO2 < 55 mmHg or SaO2 < 88%) to improve survival and quality of life.- This intervention addresses a consequence of advanced COPD but does not directly prevent or slow the progression of the disease itself, which is the focus of the question.

Question 4: A 58-year-old man presents with progressive dyspnea and fatigue. Chest X-ray shows bilateral lower lobe shadowing. HRCT shows honeycombing and traction bronchiectasis. He has finger clubbing. What is the prognosis?

A. Excellent with treatment
B. Good with early intervention
C. Variable depending on cause
D. Poor with median survival 2-5 years (Correct Answer)
E. Benign condition

Explanation: ***Poor with median survival 2-5 years***- The progressive dyspnea, fatigue, finger clubbing, and HRCT findings of **honeycombing** and **traction bronchiectasis** are classic features of **Idiopathic Pulmonary Fibrosis (IPF)**.- IPF is a relentlessly progressive lung disease with a **poor prognosis**, typically having a median survival of **2 to 5 years** from diagnosis without lung transplantation.*Excellent with treatment*- IPF is an **irreversible, progressive fibrotic lung disease** for which there is currently no curative medical treatment, precluding an excellent prognosis.- Although anti-fibrotic medications can slow the rate of decline, they do not halt or reverse the underlying **pulmonary fibrosis**.*Good with early intervention*- Despite early diagnosis and intervention with anti-fibrotic drugs, the established **Usual Interstitial Pneumonia (UIP)** pattern of IPF implies a rapid and unfavorable progression.- Patients with IPF remain at high risk of **acute exacerbations** and progressive **respiratory failure**, even with timely management.*Variable depending on cause*- The classic presentation of progressive dyspnea, clubbing, and a definable **UIP pattern** on HRCT points strongly to **Idiopathic Pulmonary Fibrosis**, which has a consistently unfavorable prognosis.- Prognostic variability is more often associated with other Interstitial Lung Diseases (ILDs) like non-specific interstitial pneumonia (**NSIP**), not IPF.*Benign condition*- IPF is far from benign; it is a serious, ultimately **fatal condition** characterized by continuous and irreversible destruction of lung architecture.- The presence of **traction bronchiectasis** and **honeycombing** signifies advanced, non-reversible scarring and distortion of lung tissue, indicating a severe disease.

Question 5: A 55-year-old man presents with progressive dyspnea and dry cough over 6 months. He has finger clubbing. HRCT shows honeycombing and reticular opacities in lower lobes. What is the most likely diagnosis?

A. COPD
B. Asthma
C. Idiopathic pulmonary fibrosis (Correct Answer)
D. Hypersensitivity pneumonitis
E. Sarcoidosis

Explanation: ***Idiopathic pulmonary fibrosis*** - The combination of progressive dyspnea, dry cough, and **finger clubbing** in an older patient strongly suggests a chronic fibrotic lung process. - HRCT findings of **honeycombing** and **reticular opacities** primarily in the lower lobes are pathognomonic for the Usual Interstitial Pneumonia (**UIP**) pattern, which defines Idiopathic Pulmonary Fibrosis (IPF). *COPD* - COPD is an **obstructive lung disease** and typically presents with chronic productive cough and sputum, often related to smoking. - HRCT features usually involve **emphysema** (air space enlargement) or bronchial wall thickening, not severe lower lobe fibrosis with honeycombing. *Asthma* - Asthma is characterized by **reversible airway obstruction** and episodic wheezing, often triggered by specific exposures. - HRCT is usually normal or shows mild signs of **air trapping**, and **clubbing** is not a feature of asthma. *Hypersensitivity pneumonitis* - Acute or subacute forms often show **centrilobular nodules** or ground-glass opacities, often with a documented environmental exposure history. - While chronic HP can cause fibrosis, the pattern is often different from UIP, frequently involving the **upper or mid-lung zones** and sparing the bases. *Sarcoidosis* - Sarcoidosis is classically associated with **hilar lymphadenopathy** and primarily affects the **upper and mid-lung zones**, showing peribronchovascular nodularity. - **Clubbing** is very rare, and the typical HRCT pattern is **perilymphatic**, unlike the peripheral subpleural pattern seen here.

Question 6: A 48-year-old man presents with progressive breathlessness and fatigue. Chest X-ray showed bilateral hilar lymphadenopathy. Serum ACE is elevated. Transbronchial biopsy shows no caseating granulomas. What is the most likely diagnosis?

A. Tuberculosis
B. Sarcoidosis (Correct Answer)
C. Lung cancer
D. Histoplasmosis
E. Silicosis

Explanation: ***Sarcoidosis*** - The presentation of progressive breathlessness and fatigue, coupled with **bilateral hilar lymphadenopathy (BHL)** on Chest X-ray and an **elevated serum ACE**, strongly indicates sarcoidosis. - The transbronchial biopsy showing **no caseating granulomas** is consistent with sarcoidosis, a disease characterized by **non-caseating granulomas**. *Tuberculosis* - Typically presents with **caseating granulomas** on biopsy, and hilar lymphadenopathy is often unilateral, unlike the patient's bilateral presentation. - Other common features include fever, night sweats, and weight loss, and **serum ACE** is not typically elevated. *Lung cancer* - While it can cause lymphadenopathy, it would typically show **malignant cells** on biopsy, not granulomas, and **elevated serum ACE** is not a diagnostic marker for lung cancer. - Clinical presentation often includes hemoptysis, unexplained weight loss, or persistent cough, which are not highlighted here. *Histoplasmosis* - This fungal infection can cause hilar lymphadenopathy and granulomas (often with subsequent calcification), but it is geographically endemic and **does not typically elevate serum ACE**. - Biopsy would reveal fungal organisms, which is not described in the patient's findings. *Silicosis* - An occupational lung disease due to **silica dust** exposure, which is not mentioned in the patient's history. - It typically causes upper lobe nodules and characteristic **eggshell calcification** of hilar lymph nodes, and **serum ACE** levels are usually normal.

Question 7: A 54-year-old man presents with progressive dyspnea and bilateral lower lobe crackles. Chest X-ray shows bilateral infiltrates. He works in shipbuilding. What is the most likely diagnosis?

A. COPD
B. Asbestosis (Correct Answer)
C. Silicosis
D. Coal worker's pneumoconiosis
E. Hypersensitivity pneumonitis

Explanation: ***Asbestosis***- The patient's history of working in **shipbuilding** is a classic exposure for **asbestos** fibers.- Asbestosis typically causes **interstitial pulmonary fibrosis**, preferentially affecting the **lower lobes**, leading to progressive dyspnea and **bibasilar crackles**. *COPD*- This involves **obstructive lung disease** (e.g., chronic bronchitis or emphysema) characterized by airflow limitation, not the restrictive pattern suggested by crackles and infiltrates.- CXR typically shows signs of **hyperinflation** or large bullae, rather than diffuse bilateral interstitial infiltrates.*Silicosis*- Silicosis is caused by inhaling **free crystalline silica** (e.g., mining, quarrying, sandblasting), an exposure typically unrelated to shipbuilding.- Radiographically, silicosis usually presents with **nodular opacities**, classically affecting the **upper lobes**.*Coal worker's pneumoconiosis*- This condition is due to the inhalation of **coal dust**, almost exclusively seen in **coal miners**.- Simple CWP generally causes small **nodular opacities**, also predominantly in the **upper lung fields**.*Hypersensitivity pneumonitis*- Caused by immunologic reactions to inhaled **organic antigens** (e.g., bird droppings, mold from farmers' lung), not asbestos exposure.- HP often presents with systemic symptoms, and the pathology involves the **alveolar walls** and terminal bronchioles, lacking the specific pleural/parenchymal changes linked to asbestos.

Question 8: A 56-year-old man presents with progressive dyspnea and dry cough. HRCT shows honeycombing and traction bronchiectasis in lower lobes. He has clubbing. What is the most likely diagnosis?

A. COPD
B. Asthma
C. Idiopathic pulmonary fibrosis (Correct Answer)
D. Sarcoidosis
E. Hypersensitivity pneumonitis

Explanation: ***Idiopathic pulmonary fibrosis***- The clinical presentation of **progressive dyspnea**, **dry cough**, and **clubbing** in an older patient, coupled with HRCT findings of **honeycombing** and **traction bronchiectasis** predominantly in the **lower lobes**, are classic features of **Usual Interstitial Pneumonia (UIP)** pattern, diagnostic of IPF.- **UIP** pattern on HRCT signifies extensive subpleural and basilar fibrosis with architectural distortion, where **honeycombing** represents clustered cystic airspaces and **traction bronchiectasis** indicates bronchial dilation due to surrounding fibrotic retraction.*COPD*- **COPD** is characterized by persistent **airflow limitation**, often with a history of smoking and a productive cough, contrasting with the dry cough and restrictive pattern of fibrosis seen here.- HRCT in COPD typically shows **emphysema** (centrilobular or panlobular) or **airway wall thickening**, but not the **honeycombing** and **traction bronchiectasis** indicative of severe pulmonary fibrosis.*Asthma*- **Asthma** is an inflammatory airway disease marked by **reversible airflow obstruction** and bronchial hyperresponsiveness, presenting with episodic wheezing, chest tightness, and dyspnea, which usually respond to bronchodilators.- HRCT in asthma may show **bronchial wall thickening** or **air trapping**, but it does not exhibit the progressive fibrotic changes like **honeycombing** or **traction bronchiectasis** seen in this patient.*Sarcoidosis*- **Sarcoidosis** is a multisystem granulomatous disease, often involving the lungs with **bilateral hilar lymphadenopathy** and a **perilymphatic distribution** of nodules, typically in the upper and mid lung zones.- While sarcoidosis can cause fibrosis (Stage 4), it typically manifests as **upper lobe predominant fibrosis** with conglomerate masses and volume loss, rather than the lower lobe predilection and characteristic UIP pattern.*Hypersensitivity pneumonitis*- Chronic **hypersensitivity pneumonitis (HP)** can lead to fibrosis, but HRCT often reveals a mosaic attenuation pattern, **centrilobular nodules**, and **air trapping**, with fibrosis potentially sparing the subpleural regions.- Although HP can mimic a UIP pattern in some cases, the classic presentation of progressive dyspnea, dry cough, clubbing, and strict lower lobe **honeycombing** and **traction bronchiectasis** points more strongly to IPF.

Question 9: A 42-year-old man presents with progressive dyspnea and chest tightness. Spirometry shows FEV1 45% predicted, FEV1/FVC 0.85. HRCT shows lower lobe fibrosis. What is the most likely diagnosis?

A. COPD
B. Asthma
C. Interstitial lung disease (Correct Answer)
D. Bronchiectasis
E. Pneumothorax

Explanation: ***Interstitial lung disease***- This pattern—low FEV1 (45% predicted) with a preserved FEV1/FVC ratio (0.85)—is characteristic of a **restrictive ventilatory defect**, where **lung volumes** are reduced due to stiff lungs.- The HRCT finding of **lower lobe fibrosis** directly confirms a restrictive pathology and is a hallmark of many Interstitial Lung Diseases (ILDs), such as **Idiopathic Pulmonary Fibrosis (IPF)**.*COPD*- COPD is an **obstructive lung disease** characterized by a **reduced FEV1/FVC ratio**, typically less than 0.70, which contradicts the given ratio of 0.85.- While it causes dyspnea, the primary HRCT findings are **emphysema** (centrilobular or panlobular) or **airway wall thickening**, not primarily lower lobe fibrosis.*Asthma*- Asthma is also an **obstructive lung disease** with variable and reversible airflow limitation, meaning the FEV1/FVC ratio would be **reduced**, often improving with bronchodilators.- HRCT findings in asthma might show **airway wall thickening** or **hyperinflation**, but it does not cause **pulmonary fibrosis**.*Bronchiectasis*- Bronchiectasis is characterized by permanent **dilation of the bronchi** and often presents with a chronic cough and sputum production.- Spirometry typically shows an **obstructive or mixed ventilatory defect**, not a purely restrictive pattern with a preserved FEV1/FVC ratio. HRCT shows **dilated airways** ("tram tracks" or "signet ring sign").*Pneumothorax*- A pneumothorax is the presence of **air in the pleural space**, causing acute dyspnea and chest pain, and resulting in a **collapsed lung** on imaging.- Spirometry would show severely reduced lung volumes, but the HRCT finding of **lower lobe fibrosis** is inconsistent with a pneumothorax, which is an acute air leak.

Question 10: A 45-year-old man presents with progressive shortness of breath and fatigue. Chest X-ray shows bilateral hilar lymphadenopathy and pulmonary infiltrates. Serum ACE is elevated. Bronchoscopy with biopsy shows non-caseating granulomas. What is the most likely diagnosis?

A. Tuberculosis
B. Sarcoidosis (Correct Answer)
C. Lung cancer
D. Histoplasmosis
E. Hypersensitivity pneumonitis

Explanation: ***Sarcoidosis***- The combination of **progressive shortness of breath** and **fatigue**, along with classic radiographic findings of **bilateral hilar lymphadenopathy** and pulmonary infiltrates, strongly suggests sarcoidosis.- The diagnosis is confirmed by the presence of **non-caseating granulomas** on biopsy and supported by an elevated **Angiotensin-Converting Enzyme (ACE)** level, which reflects granuloma burden.*Tuberculosis*- Tuberculosis typically presents with **caseating granulomas** (with central necrosis) on biopsy, not the non-caseating type seen in the patient.- Hilar adenopathy is often **unilateral** or accompanied by other findings like **apical infiltrates** or cavitations, rather than prominent bilateral hilar lymphadenopathy alone.*Lung cancer*- Lung cancer causes malignancy, and biopsy would reveal **atypical cells** and tumor architecture, not **non-caseating granulomas**.- While it can cause lymphadenopathy, **elevated ACE** is not a characteristic diagnostic feature.*Histoplasmosis*- This fungal infection can cause granulomas and hilar adenopathy, but the granulomas are often **caseating** or show evidence of fungal organisms upon special staining.- Diagnosis typically requires positive **fungal cultures** or serology, which are not described.*Hypersensitivity pneumonitis*- Although it can occasionally cause **non-caseating granulomas**, prominent **bilateral hilar lymphadenopathy** and **elevated serum ACE** are not typical primary features.- This condition is primarily an interstitial lung disease usually related to known environmental **antigen exposure**, which is not mentioned in the presentation.

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