Lung cancer and pneumonia
Lung cancer, pneumonia, tuberculosis, fungal infection and pulmonary embolism
Lung cancer, pneumonia, TB, aspergillosis, oedema, pulmonary embolism and pulmonary hypertension for FCPS Part 1. Each is linked to its host, mechanism and chest imaging.
Lung cancer
| Type | Site and behaviour | Key associations |
|---|---|---|
| Adenocarcinoma | Peripheral; commonest overall and in non-smokers and women | EGFR mutation in never-smokers (ALK rearrangement too); lepidic growth gives ground-glass nodules |
| Squamous cell carcinoma | Central; often cavitates | Smoking; keratin pearls, intercellular bridges; PTHrP hypercalcaemia |
| Small cell carcinoma | Central, early spread | Neuroendocrine (Kulchitsky) cells; SIADH, ectopic ACTH, Lambert–Eaton |
| Large cell carcinoma | Peripheral, undifferentiated | Poor prognosis |
| Carcinoid | Endobronchial, enhancing | Collapse or recurrent infection beyond it |
- TP53 is the most commonly mutated gene in lung (and many other) cancers. Risk factors: smoking, asbestos (multiplies smoking risk), radon, silica.
- Spread: hilar and mediastinal nodes, then adrenal (the endocrine gland most often involved), brain (grey–white junction), bone and liver. A lung deposit of clear cells suggests a renal primary.
- Pancoast tumour: brachial plexus (T1 wasting) and sympathetic chain (Horner syndrome). Central tumours compress the SVC. Left hilar tumours can trap the left recurrent laryngeal nerve under the arch (hoarseness).
- Right middle lobe has two segments, medial and lateral; lobectomy removes both.
- Pulmonary hamartoma: fat and popcorn calcification, stable for years. Bronchogenic cyst lies in the middle mediastinum near the carina.
- Metastases to the lung: multiple round "cannonball" nodules (choriocarcinoma, renal, sarcoma).
Pneumonia: patterns and organisms
- Lobar pneumonia (pneumococcus): congestion, red hepatisation, grey hepatisation, resolution. Air bronchograms show airless alveoli around patent bronchi.
| Organism | Host and features |
|---|---|
| Streptococcus pneumoniae | Commonest community-acquired cause; rusty sputum; first-line treatment amoxicillin (penicillin) |
| Klebsiella | Alcoholics and diabetics; upper lobe, red currant jelly (red-brown) sputum, bulging fissure, cavity with fluid level |
| Staphylococcus aureus | After influenza; cavities and pneumatoceles; septic emboli from tricuspid endocarditis; abscesses anywhere (lung, brain) |
| Oral anaerobes | Lung abscess after aspiration (alcohol, poor teeth): putrid sputum, thick-walled cavity with air-fluid level in dependent segments (superior segment of right lower lobe when supine, posterior upper lobe) |
| Pseudomonas, Gram-negatives, S. aureus | Hospital-acquired and ventilator pneumonia; Pseudomonas is the commonest cause of death in cystic fibrosis |
| Legionella | Air-conditioning water; hyponatraemia, diarrhoea |
| Chlamydia psittaci | Bird handlers |
| Burkholderia pseudomallei | Melioidosis: diabetic rice farmers; lung, liver and spleen abscesses |
| SARS-CoV-2 | ACE2 on type II pneumocytes; bilateral peripheral ground glass |
- Inhalational anthrax (raw wool sorters): spores carried by macrophages to mediastinal nodes, where toxin causes haemorrhagic mediastinitis: flu-like illness, then shock, widened mediastinum with high-density (haemorrhagic) nodes and effusions, but little consolidation. It is a mediastinitis, not a pneumonia.
- A thick-walled cavity in a smoker may be cavitating carcinoma; follow it to resolution.
Tuberculosis in the lung
- Primary: Ghon focus plus hilar nodes (Ghon complex), common in children.
- Post-primary: apical and posterior segments, because M. tuberculosis is an obligate aerobe and the apex has the highest alveolar PO₂ (high V/Q). Caseation, cavitation, tree-in-bud spread. Rasmussen aneurysm in a cavity wall causes massive haemoptysis.
- Miliary: innumerable 1–2 mm nodules from haematogenous spread.
- Spread elsewhere: genital TB reaches the tubes by blood, often years after lung disease, giving infertility, amenorrhoea (destroyed endometrium) and beaded, rigid tubes on HSG (tobacco-pouch ends); intestinal TB favours the ileocaecal region, with transverse ulcers following lymphatics around the bowel.
- Drugs: ethambutol causes optic neuritis with red–green colour blindness; isoniazid peripheral neuropathy (pyridoxine); rifampicin orange secretions and enzyme induction; pyrazinamide gout.
Fungal and eosinophilic disease
| Form | Host | Imaging and diagnosis |
|---|---|---|
| Aspergilloma | Old TB cavity | Mobile ball with an air crescent; non-invasive |
| ABPA | Asthma, cystic fibrosis | Central bronchiectasis; very high IgE, Aspergillus precipitins |
| Invasive aspergillosis | Neutropenia (leukaemia on chemotherapy) | Nodule with a halo (haemorrhage around angioinvasion); septate hyphae branching at acute angles; serum galactomannan antigen supports it |
| Mucormycosis | Diabetic ketoacidosis | Broad non-septate hyphae at right angles |
- Tropical pulmonary eosinophilia: immune hyper-response to filarial antigens (Wuchereria) trapped in the lungs: nocturnal cough and wheeze, eosinophils over 3 × 10⁹/L, very high IgE, strongly positive filarial antibodies but no microfilariae in blood; diffuse reticulonodular shadowing. Treat with diethylcarbamazine; untreated it leads to fibrosis.
- Löffler syndrome: transient migrating infiltrates with eosinophilia as Ascaris larvae pass through the lungs.
Pulmonary oedema and effusion
| Type | Mechanism | Example |
|---|---|---|
| Cardiogenic | Raised capillary hydrostatic pressure | Left ventricular failure: upper lobe diversion, Kerley B lines, bat-wing shadowing |
| ARDS | Increased permeability; hyaline membranes | Sepsis, pancreatitis |
| Negative pressure | Inspiration against a closed glottis | Laryngospasm at extubation |
| Re-expansion | Rapid drainage of a large effusion | Unilateral oedema after a chest drain |
- Pleural transudate causes: heart failure (over 90%), cirrhosis, nephrotic syndrome, peritoneal dialysis. Exudates: pneumonia, TB, malignancy, pulmonary embolism (can be either).
Pulmonary vascular disease
- Pulmonary embolism: most arise from deep veins of the leg (femoral and iliac veins) and pelvis. Virchow triad: stasis, hypercoagulability, endothelial injury.
- Effect of complete occlusion: the occluded lung is ventilated but not perfused: dead space (V/Q infinite). Its alveolar PO₂ rises towards inspired air and alveolar PCO₂ falls towards zero. Arterial PO₂ falls (blood diverted to the other lung with V/Q mismatch) and arterial PCO₂ usually falls because the patient hyperventilates. Regional hypocapnia constricts the airways of the affected lung, and surfactant falls over hours, causing patchy atelectasis.
- Infarction is uncommon because bronchial arteries also supply the lung; when present it is a peripheral wedge (Hampton hump).
- Pulmonary arterial hypertension: BMPR2 mutations in familial forms; pulmonary trunk wider than aorta, pruned peripheral vessels. The most specific sign is a loud pulmonary component of the second heart sound (P2), with right ventricular heave. A left-to-right shunt that reverses when pulmonary pressure exceeds systemic gives cyanosis (Eisenmenger syndrome).
- Pulmonary AVM (HHT): paradoxical embolism and brain abscess.
- Fat embolism: after long bone fractures (petechiae, confusion, hypoxia) and in sickle cell acute chest syndrome.
Remember Squamous and small cell carcinomas are central; adenocarcinoma is peripheral and is the type seen in non-smokers.
Exam trap Most pulmonary emboli do not cause infarction, because the bronchial circulation keeps lung tissue alive.
Exam trap A halo around a nodule in a neutropenic patient means invasive aspergillosis; an air crescent around a mobile ball in an old cavity means aspergilloma.
How FCPS asks about this
- Commonest lung cancer in non-smokers: adenocarcinoma, peripheral.
- Red currant jelly sputum, upper lobe cavity: Klebsiella pneumoniae.
- Putrid sputum, cavity in superior segment of right lower lobe: oral anaerobes after aspiration.
- Neutropenic patient, halo sign, acute-angle septate hyphae: Aspergillus fumigatus; galactomannan supports it.
- Wool sorter, widened mediastinum, shock: inhalational anthrax.
- Eosinophilia, high IgE, filarial antibodies, no microfilariae: tropical pulmonary eosinophilia.
- Red–green colour loss on TB treatment: ethambutol.
Test yourself on this topic
5 of the 63 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 50-year-old man with heavy alcohol use and very poor dental hygiene has 3 weeks of fever and cough with foul-smelling, putrid sputum. He has a thick-walled abscess in the superior segment of the right lower lobe. Which organisms are most likely responsible?
Answer: Oral anaerobic bacteria
Lung abscesses usually follow aspiration of oropharyngeal contents when consciousness or the cough reflex is impaired, as with heavy drinking, seizures or anaesthesia. Gum disease raises the load of anaerobes such as Prevotella, Fusobacterium, Peptostreptococcus and Bacteroides, which cause necrosis and cavitation with putrid sputum. Aspiration while lying on the back goes to the superior segments of the lower lobes and the posterior segments of the upper lobes. The abscess often shows an air-fluid level on imaging.
Aspiration lung abscess
- Reduced consciousness, poor teeth
- Oral anaerobes
- Putrid sputum
- Superior segment RLL, air-fluid level
Remember Foul sputum + cavity in a dependent segment = anaerobic abscess.
Exam trap A thick-walled cavity in a smoker can also be a cavitating carcinoma; follow it to resolution.
Why the other options are wrong
- Mycobacterium tuberculosis TB cavities are usually apical and the sputum is not putrid.
- Streptococcus pneumoniae alone Pneumococcus rarely causes abscesses.
- Pseudomonas aeruginosa Pseudomonas affects ventilated or immunocompromised patients and those with CF.
- Pneumocystis jirovecii Pneumocystis causes ground glass in immunosuppressed patients.
A 40-year-old man who sorts imported raw wool in a factory has 3 days of fever and muscle aches, then sudden severe breathlessness and shock. His chest radiograph shows a widened mediastinum and bilateral pleural effusions, with little lung consolidation. What is the diagnosis?
Answer: Inhalational anthrax
Inhaled spores of Bacillus anthracis are carried by alveolar macrophages to the mediastinal lymph nodes, where they germinate. The bacteria release lethal toxin and oedema toxin, causing haemorrhagic necrosis of the nodes and mediastinitis, with haemorrhagic pleural effusions, rather than pneumonia. This gives a widened mediastinum after a flu-like prodrome. Wool and hide workers are at risk.
Inhalational anthrax
- Wool and hide workers
- Spores carried to mediastinal nodes
- Haemorrhagic lymphadenitis
- Wide mediastinum, effusions
Remember Wool worker + widened mediastinum + shock = inhalational anthrax.
Exam trap Inhalational anthrax is a mediastinitis, not a primary pneumonia.
Why the other options are wrong
- Aortic dissection No tearing pain, and fever with a prodrome points to infection.
- Mediastinal lymphoma Lymphoma does not cause sudden shock after a short febrile illness.
- Tuberculous lymphadenitis TB lymphadenitis has a slower course.
- Oesophageal perforation No vomiting or instrumentation is described.
A 25-year-old man from coastal Sindh has had 2 months of cough and wheeze that are much worse at night. His eosinophil count is 9 × 10⁹/L, IgE is very high and filarial antibodies are strongly positive, but no microfilariae are seen in night blood films. What is the diagnosis?
Answer: Tropical pulmonary eosinophilia
Tropical pulmonary eosinophilia is an exaggerated immune response to microfilariae of Wuchereria bancrofti or Brugia malayi, which are trapped and destroyed in the lung capillaries. The intense eosinophil- and IgE-driven reaction causes nocturnal cough and wheeze, very high eosinophil counts and diffuse small nodular shadows. Microfilariae are cleared from the blood, so night films are negative. It responds to diethylcarbamazine; untreated, it can progress to fibrosis.
Tropical pulmonary eosinophilia
- Immune reaction to microfilariae
- Nocturnal cough and wheeze
- Eosinophils very high, IgE high
- Night films negative; treat with DEC
Remember Night-time wheeze + huge eosinophil count in an endemic area = TPE.
Exam trap Do not label it asthma; untreated TPE can lead to fibrosis.
Why the other options are wrong
- Allergic bronchopulmonary aspergillosis Occurs in asthmatics with central bronchiectasis and Aspergillus sensitisation.
- Löffler syndrome from Ascaris Transient, mild and lasts a week or two, not months.
- Chronic eosinophilic pneumonia Peripheral consolidation, not filarial antibodies.
- Miliary tuberculosis Fever and wasting with negative filarial tests; eosinophilia is not typical.
A thin 68-year-old woman who does not smoke has had a chronic cough for 2 years from bronchiectasis confined mainly to the right middle lobe and lingula. Sputum is smear positive for acid-fast bacilli, but the cultures grow slowly and the organism is not M. tuberculosis. Which organism is most likely?
Answer: Mycobacterium avium complex
Mycobacterium avium complex is an environmental non-tuberculous mycobacterium found in water and soil. In older, slender women without obvious lung disease it causes a slowly progressive nodular bronchiectasis affecting the middle lobe and lingula (the 'Lady Windermere' pattern), possibly because poor clearance of these narrow, horizontally draining airways allows infection to persist. It is acid-fast but grows differently from M. tuberculosis in culture, and it is not spread from person to person.
MAC lung disease
- Environmental mycobacterium
- Older, slender women
- Middle lobe and lingula bronchiectasis
- Not spread person to person
Remember Middle lobe and lingula bronchiectasis in an older woman: MAC.
Exam trap A positive AFB smear is not always TB; culture and speciation guide treatment.
Why the other options are wrong
- Mycobacterium leprae Cannot be grown in culture and does not cause this lung disease.
- Nocardia asteroides Weakly acid-fast branching rods, mainly in immunosuppressed patients.
- Actinomyces israelii Not acid-fast; causes abscesses crossing tissue planes.
- Mycobacterium bovis (BCG) Belongs to the M. tuberculosis complex, usually from unpasteurised milk.
A 35-year-old man with active cavitating tuberculosis coughs up a cupful of bright red blood. The bleeding comes from a pseudoaneurysm of a pulmonary artery branch bulging into the wall of an upper lobe cavity. What is this lesion called?
Answer: Rasmussen aneurysm
A Rasmussen aneurysm is a pseudoaneurysm of a pulmonary artery branch next to or within the wall of a tuberculous cavity. Granulation tissue and caseous necrosis weaken the arterial wall, which is replaced by fibrin, and it bulges into the cavity and may rupture, causing massive haemoptysis. Most TB haemoptysis comes from hypertrophied bronchial arteries, but a Rasmussen aneurysm arises from the pulmonary artery, so bronchial artery embolisation alone may not stop it.
Rasmussen aneurysm
- Pseudoaneurysm of pulmonary artery branch
- In the wall of a TB cavity
- Wall weakened by granulation tissue
- Massive haemoptysis
Remember Pulmonary artery pseudoaneurysm in a TB cavity wall = Rasmussen aneurysm.
Exam trap If bronchial artery embolisation fails, look for a pulmonary artery source.
Why the other options are wrong
- Aspergilloma in the cavity A fungal ball is a mass of hyphae in an old cavity, not a vessel.
- Bronchial artery hypertrophy Bronchial arteries arise from the aorta, not the pulmonary artery.
- Pulmonary arteriovenous malformation An AVM has feeding and draining vessels and is not in a TB cavity.
- Bronchogenic carcinoma A tumour is not a pseudoaneurysm.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Lungs, heart and vessels, Lung tumours, infections and pulmonary vascular disease
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