Medicine Practical Examination Questions: Respiratory System

Complete Question Bank - Basics to Higher Level

SECTION A: GENERAL RESPIRATORY EXAMINATION

Basic / Foundational Questions

1. What are the normal respiratory rate values for adults, children, and neonates?
2. Describe how you would perform a systematic respiratory examination (inspection, palpation, percussion, auscultation).
3. What is the normal tracheal position? When does it shift toward the lesion and when away from it?
4. What is tactile vocal fremitus? How do you elicit it and what does it signify?
5. What are the different types of breath sounds? Describe vesicular, bronchial, and bronchovesicular sounds.
6. What is the difference between crackles (crepitations) and wheeze?
7. What is vocal resonance? How is it tested? What is whispering pectoriloquy and aegophony?
8. Define chest expansion. How do you measure it? What is normal?
9. What is the significance of clubbing in respiratory disease? Name 4 causes.
10. What is pursed-lip breathing and why do patients do it?

Intermediate - Examination Technique

1. What signs on inspection suggest chronic respiratory disease?
2. How do you differentiate consolidation from pleural effusion on clinical examination?
3. How do you differentiate pleural effusion from pneumothorax?
4. What is Hoover's sign? What disease is it seen in?
5. What does hyperresonance on percussion indicate?
6. Describe the signs of respiratory failure - type 1 vs type 2.
7. What is paradoxical breathing and when does it occur?
8. What is the clinical significance of accessory muscle use?
9. What is the difference between dull and stony dull percussion notes?
10. What are the signs of tracheal shift - name 3 conditions that cause shift toward the lesion and 3 that cause shift away?

SECTION B: PNEUMONIA

Basic Questions

1. Define pneumonia. What is the difference between lobar pneumonia, bronchopneumonia, and atypical pneumonia?
2. What is the most common causative organism of community-acquired pneumonia (CAP)?
3. What are the classic symptoms of lobar pneumonia?
4. What is the typical sputum in pneumococcal pneumonia? (Rusty sputum - due to RBC breakdown in alveoli)
5. What are the 4 pathological stages of lobar pneumonia? (Congestion, red hepatization, grey hepatization, resolution)
6. What is "herald stage" in pneumonia?
7. What are the auscultatory findings in early pneumonia vs. established consolidation?
8. What is the CXR finding in lobar pneumonia?

Moderate Questions

1. What are the clinical signs of consolidation?
   • Inspection: reduced chest movement on affected side
   • Palpation: increased tactile vocal fremitus, trachea central or shifted slightly toward lesion
   • Percussion: dull note over consolidated area
   • Auscultation: bronchial breathing, increased vocal resonance, whispering pectoriloquy, crackles (crepitations), aegophony
2. What is the CURB-65 score? What does each letter stand for? How do you use it to decide admission?
   • C: Confusion; U: Urea >7 mmol/L; R: Respiratory rate ≥30/min; B: Blood pressure systolic <90 or diastolic ≤60; 65: Age ≥65. Score 0-1: treat at home; 2: consider hospital; 3+: hospitalize/ICU
3. What organisms cause atypical pneumonia? How does it differ clinically from typical pneumonia?
   • Mycoplasma, Chlamydia, Legionella, Coxiella - dry cough, minimal signs on examination despite significant CXR changes ("walking pneumonia")
4. What is Legionnaire's disease? What is its distinguishing feature?
5. What investigations do you order for a patient with suspected pneumonia? (CBC, CRP, blood cultures x2, sputum culture + sensitivity, ABG, CXR PA view, urine Legionella/pneumococcal antigen)
6. What are the complications of pneumonia?
   • Parapneumonic effusion, empyema, lung abscess, septicaemia, respiratory failure, ARDS, pericarditis, metastatic abscess
7. What is the mechanism of hypoxemia in pneumonia?
   • Increased shunt (blood perfusing consolidated, non-ventilated alveoli) + low V/Q units. In mild pneumonia: shunt ~7.5%, low V/Q ~4.2%. In severe pneumonia: shunt up to 22% (Murray & Nadel's)
8. What is the difference between community-acquired (CAP), hospital-acquired (HAP), and ventilator-associated pneumonia (VAP)?
9. What is aspiration pneumonia? Who is at risk?
10. What is the empirical antibiotic treatment of mild, moderate, and severe CAP?

Hard / Higher Order Questions

1. A patient with pneumonia fails to improve after 72 hours of antibiotics. What do you do? (Consider resistant organism, wrong diagnosis - TB/malignancy, empyema, lung abscess, obstruction, immunocompromised)
2. What is the difference between a parapneumonic effusion and empyema? How do you manage each?
3. Explain the pathophysiology of type 1 respiratory failure in pneumonia using V/Q concepts.
4. Why does bronchial breathing occur over consolidation? (Consolidated lung transmits sounds better - solid medium conducts sound; the lung acts like solid tissue)
5. What is "round pneumonia"? In which age group is it more common?
6. What are the indications for ICU admission in pneumonia? (PSI class V, CURB-65 ≥3, need for mechanical ventilation or vasopressors)
7. What is the role of corticosteroids in severe CAP?
8. Compare the CXR findings of Klebsiella pneumonia vs. Pneumococcal pneumonia.
9. What organisms are responsible for pneumonia in an immunocompromised patient (HIV with CD4 <200)?

SECTION C: COPD (Chronic Obstructive Pulmonary Disease)

Basic Questions

1. Define COPD. What two conditions commonly coexist in it?
2. What is the definition of chronic bronchitis? (Productive cough for ≥3 consecutive months in ≥2 consecutive years)
3. What is emphysema pathologically? (Enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls by proteases - Robbins Pathology)
4. What is the single most important risk factor for COPD?
5. What spirometric pattern is seen in COPD? (Obstructive: reduced FEV1, reduced FEV1/FVC ratio <0.70, normal or near-normal FVC)
6. What is the "Blue Bloater" vs. "Pink Puffer" distinction?
7. What is the barrel chest? How does it develop in COPD? (Air trapping → hyperinflation → increased AP diameter = AP diameter equals transverse diameter)

Moderate Questions

1. Describe the full clinical examination findings in a patient with COPD/emphysema:
   • Inspection: barrel chest, pursed-lip breathing, use of accessory muscles, tachypnea, cyanosis (in advanced), reduced chest expansion, hunched-forward posture
   • Palpation: reduced chest expansion bilaterally, reduced tactile vocal fremitus, trachea may be central
   • Percussion: hyperresonance, loss of cardiac and hepatic dullness, low-lying flattened diaphragms
   • Auscultation: reduced breath sounds, prolonged expiration, wheeze (polyphonic), distant heart sounds
2. What is Hoover's sign and how is it specific to COPD? (Inward movement of lower costal margins during inspiration due to flat diaphragm pulling inward)
3. What are the two emphysema subtypes and how do they differ?
   • Centriacinar (centrilobular): affects respiratory bronchioles first; strongly linked to smoking; upper lobe predominance
   • Panacinar (panlobular): affects the entire acinus; seen in alpha-1-antitrypsin deficiency; lower lobe predominance
4. What is alpha-1-antitrypsin deficiency? How does it cause COPD? (Loss of protease inhibitor → unopposed neutrophil elastase → alveolar wall destruction)
5. What are the GOLD stages of COPD (GOLD 1-4 based on FEV1 % predicted)?
6. What is the ABG pattern in a "Blue Bloater" (type 2 respiratory failure)? (Low PaO2, raised PaCO2, respiratory acidosis + metabolic compensation)
7. What is cor pulmonale? How does COPD lead to it? (Hypoxic pulmonary vasoconstriction → pulmonary hypertension → right ventricular hypertrophy and failure)
8. What is the ECG finding in cor pulmonale? (Right axis deviation, P pulmonale, right ventricular hypertrophy, right bundle branch block)
9. What investigations do you order for COPD? (Spirometry, CXR, ABG, CBC for polycythemia, ECG, echo)
10. What is the CXR appearance in COPD/emphysema? (Hyperinflated lungs, low flat diaphragms, increased retrosternal airspace, bullae, narrow mediastinum)

Hard / Higher Order Questions

1. Why is high-flow oxygen dangerous in type 2 respiratory failure in COPD? (Hypoxic drive is the main respiratory stimulus when CO2 drive is blunted. Giving high O2 removes hypoxic drive → hypoventilation → CO2 narcosis → respiratory arrest. Target SpO2: 88-92%)
2. What is the Hering-Breuer reflex? Is it relevant in COPD?
3. Explain the mechanism of pursed-lip breathing. (Creates back-pressure that splints airways open during expiration, preventing dynamic airway collapse and improving gas exchange)
4. What is the MRC dyspnea scale?
5. What is a COPD exacerbation? What are the common precipitants? (Infection - bacterial or viral - air pollution, non-compliance with medication)
6. What is the Reid Index? What is abnormal? (Ratio of mucous gland thickness to bronchial wall thickness. Normal <0.4; in chronic bronchitis >0.5)
7. What are the pharmacological and non-pharmacological management options for stable COPD?
   • Short-acting bronchodilators (SABA, SAMA), long-acting bronchodilators (LABA, LAMA), ICS in selected patients, theophylline, pulmonary rehabilitation, smoking cessation, oxygen therapy (LTOT), influenza and pneumococcal vaccines
8. What is the OVERLAP SYNDROME (ACOS - Asthma-COPD Overlap Syndrome)?
9. When is long-term oxygen therapy (LTOT) indicated in COPD? (PaO2 ≤55 mmHg at rest on room air, or ≤59 mmHg with cor pulmonale/polycythemia; must use >15 h/day)
10. Explain why patients with COPD-OSA overlap syndrome have worse outcomes than either condition alone.

SECTION D: TUBERCULOSIS (TB)

Basic Questions

1. What is the causative organism of TB? What is its staining characteristic? (Mycobacterium tuberculosis; acid-fast bacillus - Ziehl-Neelsen/ZN stain)
2. What type of hypersensitivity reaction forms the TB granuloma? (Type IV - cell-mediated, delayed hypersensitivity)
3. What is a Ghon focus? What is the Ghon complex (primary complex)? (Ghon focus = primary lung lesion + hilar lymphadenopathy = Ghon/Ranke complex)
4. Define primary TB vs. post-primary (reactivation) TB.
5. What are the classical symptoms of pulmonary TB? (Chronic cough >2-3 weeks, hemoptysis, fever, night sweats, weight loss/anorexia, fatigue)
6. What is the CXR appearance of active pulmonary TB? (Upper lobe infiltrates, patchy shadows, cavitation, hilar lymphadenopathy)
7. What is the difference between sputum smear and sputum culture for TB?

Moderate Questions

1. What are the 4 first-line anti-TB drugs (HRZE)? What is each drug's mechanism?
   • H (Isoniazid): inhibits mycolic acid synthesis
   • R (Rifampicin): inhibits DNA-dependent RNA polymerase
   • Z (Pyrazinamide): disrupts membrane energy metabolism, active in acidic pH
   • E (Ethambutol): inhibits arabinosyl transferase (arabinogalactan synthesis)
2. What is the standard treatment regimen for new pulmonary TB? (2HRZE + 4HR: 2 months intensive + 4 months continuation phase)
3. What are the side effects of each first-line drug?
   • H: peripheral neuropathy (prevented by pyridoxine), hepatotoxicity, lupus-like syndrome
   • R: hepatotoxicity, orange discoloration of urine/secretions, drug interactions (enzyme inducer), flu-like syndrome
   • Z: hepatotoxicity, hyperuricemia/gout, arthralgia
   • E: optic neuritis (red-green color blindness), retrobulbar neuritis
4. What is the Mantoux test? How is it performed? How is it interpreted? (0.1 mL PPD intradermally, read at 48-72 hours. ≥5 mm in HIV/contacts; ≥10 mm in high-risk groups; ≥15 mm in general population = positive)
5. What is BCG vaccine? When is it given? What protection does it offer?
6. What is MDR-TB? What is XDR-TB?
   • MDR: resistant to at least H and R
   • XDR: MDR + resistant to any fluoroquinolone + at least one of the injectable second-line drugs (amikacin, kanamycin, capreomycin)
7. What are the extrapulmonary manifestations of TB? (Lymphadenitis most common extrapulmonary; also pleural, pericardial, CNS/meningitis, bone - Pott's disease, intestinal, renal, disseminated/miliary)
8. What is miliary TB? What are the CXR findings? (Hematogenous dissemination; CXR: 1-2 mm nodules uniformly distributed throughout both lung fields resembling millet seeds)
9. What is the most common location for post-primary TB on CXR and why? (Apical and posterior segments of upper lobes + superior segments of lower lobes - high O2 tension, less lymphatic flow)
10. What are the clinical features of TB pleuritis/pleural effusion due to TB?

Hard / Higher Order Questions

1. What is the pathogenesis of cavitation in TB? (Caseating granuloma liquefies → caseous material drains into bronchus → cavity forms → aerobic environment favors rapid bacterial multiplication)
2. Explain the immunology of TB granuloma formation. (CD4+ T helper cells activated by APC presenting TB antigens → IL-2, IFN-γ production → macrophage activation → giant cell formation → granuloma with central caseation)
3. What is a tuberculoma? How does it appear on CT?
4. What is the paradoxical reaction in TB? How do you manage it?
5. What is Addison's disease in the context of TB? (Adrenal TB → bilateral adrenal destruction → primary adrenal insufficiency)
6. Why does TB reactivate in the apical segments? Explain the physiological basis.
7. What is drug-induced hepatitis in TB management? At what ALT level do you stop drugs?
8. What is the difference between IGRA (interferon-gamma release assay) and Mantoux in diagnosing latent TB? Which is more specific and why?
9. What is the role of steroids in TB? (Indicated in: TB meningitis - reduces ICP and sequelae; TB pericarditis - reduces constrictive pericarditis risk; also TB adrenal insufficiency)
10. A patient on TB treatment develops jaundice. What is your approach? (Stop all drugs. Check LFTs. If AST/ALT >5x normal = drug-induced hepatitis. Restart sequentially after normalization: R first, then H, then others)

SECTION E: PLEURAL EFFUSION

Basic Questions

1. What is a pleural effusion? How much fluid must accumulate before it is visible on a standard PA CXR? (>200 mL; lateral decubitus CXR can detect as little as 50 mL)
2. What is the difference between a transudate and an exudate?
3. Name 3 causes of transudative effusion. (CCF, liver cirrhosis/hypoalbuminemia, nephrotic syndrome, hypothyroidism)
4. Name 3 causes of exudative effusion. (TB, malignancy, pneumonia/parapneumonic, pulmonary embolism, autoimmune)
5. What are the symptoms of pleural effusion? (Dyspnea, pleuritic chest pain, dry cough)
6. What is the most common cause of pleural effusion overall? (Congestive heart failure)

Moderate Questions

1. Describe the clinical signs of pleural effusion:
   • Inspection: reduced chest movement on affected side, fullness of intercostal spaces
   • Palpation: reduced/absent tactile vocal fremitus, trachea shifted AWAY from effusion (if large), absent apex beat on ipsilateral side
   • Percussion: STONY DULL note (dull to percussion - important: stony dull distinguishes effusion from consolidation which is merely dull)
   • Auscultation: absent/reduced breath sounds, reduced/absent vocal resonance; at the upper border of effusion: bronchial breathing + aegophony (E to A change) - known as Skodaic resonance
2. What are Light's Criteria for exudate? Name all three:
   • Pleural fluid protein / serum protein > 0.5
   • Pleural fluid LDH / serum LDH > 0.6
   • Pleural fluid LDH > 2/3 of upper limit of normal serum LDH (Any ONE criterion met = exudate)
3. What is the Ellis-Damoiseau line (S-shaped curve)? When does it appear?
4. What is thoracentesis? What are its indications? What are the complications? (Pneumothorax, hemothorax, infection, re-expansion pulmonary edema if >1.5 L removed at once)
5. What is a parapneumonic effusion? What are the criteria that determine if it needs drainage (empyema/complicated parapneumonic effusion)?
6. What is the significance of a unilateral right-sided pleural effusion in CHF? (CHF effusions are usually bilateral; a unilateral right-sided effusion in CHF is most common side due to larger surface area of right lung; if unilateral only - consider alternative diagnosis)
7. What laboratory tests do you order on pleural fluid? (Protein, LDH, glucose, pH, cell count and differential, culture + sensitivity, cytology, ADA for TB, amylase)
8. What is adenosine deaminase (ADA) in pleural fluid? What level suggests TB? (ADA >40 U/L is highly suggestive of TB pleuritis)
9. What is the effect of pleural effusion on gas exchange? (Mild hypoxemia; increased shunt ~7%. After thoracentesis of ~700 mL, PaO2 does not significantly improve and low V/Q regions may even slightly increase - Murray & Nadel's)
10. What are the CXR findings of pleural effusion at different volumes?
    • Obliteration of costophrenic angle: 200-300 mL
    • Meniscus sign (concave upper border): 500+ mL
    • Opacification of hemithorax with mediastinal shift: massive effusion

Hard / Higher Order Questions

1. What is hepatic hydrothorax? How does it develop? (Small diaphragmatic defects allow ascitic fluid to pass from peritoneum to pleural space in patients with cirrhosis; affects ~5-10% of cirrhotics; 85% are right-sided - Murray & Nadel's)
2. A patient's pleural fluid just meets Light's Criteria but clinically looks like CHF. What is the next step? (Calculate serum-pleural fluid protein gradient: if >31 g/L, reclassify as transudate. Also check NT-proBNP)
3. What is Meigs syndrome? (Ovarian fibroma/thecoma + ascites + pleural effusion, which resolves after tumor removal)
4. What is chylothorax? What does the pleural fluid look like? What are the causes? (Milky white fluid; high triglycerides >1.24 mmol/L; causes: lymphoma, thoracic duct trauma, malignancy)
5. What is the difference between empyema necessitans and simple empyema?
6. What is pleurodesis? When is it indicated? What agents are used? (Talc most effective; doxycycline, bleomycin alternatives; indicated for recurrent malignant effusions)
7. What is the significance of a pH <7.2 and glucose <3.3 mmol/L in pleural fluid? (Indicates complicated parapneumonic effusion or empyema requiring drainage; also seen in TB, malignancy, esophageal rupture)
8. Why does thoracentesis sometimes DECREASE PaO2? (Removal of fluid re-expands collapsed lung → relative reperfusion of previously atelectatic segments → transient increase in low V/Q perfusion)
9. What is pseudochylothorax (cholesterol effusion)? How do you differentiate from chylothorax? (Cholesterol crystals, triglycerides are LOW, cholesterol is HIGH; long-standing effusions in TB/rheumatoid arthritis)

QUICK-REFERENCE: DISTINGUISHING SIGNS AT BEDSIDE

HIGHER-LEVEL INTEGRATIVE QUESTIONS

1. A patient has a right-sided pleural effusion, hemoptysis, weight loss, and night sweats. What is your differential diagnosis and how do you approach it?
2. Explain the pathophysiology of cor pulmonale in a patient with advanced COPD step by step.
3. A patient with known COPD presents with acute deterioration. How do you differentiate between an acute exacerbation of COPD vs. pneumonia vs. pulmonary embolism?
4. A patient with treated TB comes back 3 months later with a pleural effusion. Is this treatment failure, drug resistance, or paradoxical reaction? What investigations do you do?
5. Explain why a patient with a large pleural effusion can have NO dyspnea and another patient with a small effusion can be severely dyspneic. What physiological factors determine symptom severity?
6. What is the Ghon complex and how does it relate to post-primary TB reactivation decades later?
7. A patient with COPD suddenly deteriorates with worsening dyspnea and tracheal shift. What is your immediate diagnosis and management?
8. A patient with CAP is given high-flow oxygen but develops worsening hypercapnia. Explain the mechanism.
9. What is the commonest cause of bloody pleural effusion in a patient above 50 years? How do you investigate?
10. Explain why TB preferentially causes upper lobe disease while pneumonia tends to involve the lower lobes.