Pulmonology Syllabus

Define functional residual capacity (FRC) and vital capacity (VC) as sums of lung volumes.

$$FRC = ERV + RV$$ (air remaining after normal expiration, ~2400 mL). $$VC = TV + IRV + ERV$$ (max air expelled after max inspiration, ~4800 mL).

What does the diffusing capacity of the lung for carbon monoxide (DLCO) measure?

DLCO measures the ability of gas to transfer from alveoli across the alveolar-capillary membrane into the blood. CO is used because it binds hemoglobin avidly, making transfer limited by the membrane rather than blood flow.

Give examples of conditions that decrease DLCO and one that increases it.

Decreased DLCO: emphysema (loss of surface area), pulmonary fibrosis (thickened membrane), pulmonary embolism, anemia, pulmonary hypertension. Increased DLCO: alveolar hemorrhage, polycythemia, and left-to-right shunts / early asthma.

State Fick's law of diffusion as it applies to the alveolar membrane.

$$\dot{V}_{gas} \propto \frac{A \cdot D \cdot (P_1 - P_2)}{T}$$ Gas transfer is proportional to surface area $A$, the diffusion constant $D$, and the partial-pressure gradient $(P_1 - P_2)$, and inversely proportional to membrane thickness $T$.

How do you distinguish emphysema from chronic bronchitis (the two main COPD phenotypes)?

Emphysema ("pink puffer"): destruction of alveolar walls, decreased DLCO, hyperinflation, less hypoxemia. Chronic bronchitis ("blue bloater"): productive cough for at least 3 months in 2 consecutive years, mucus hypersecretion, more hypoxemia/cyanosis and cor pulmonale; DLCO often normal.

What is the pathophysiologic hallmark of asthma, and what reversibility criterion supports the diagnosis on spirometry?

Asthma is characterized by reversible bronchial hyperresponsiveness and airway inflammation. Diagnosis is supported by a post-bronchodilator increase in $FEV_1$ of $\geq 12\%$ and $\geq 200$ mL.

Which deficiency causes early-onset panacinar emphysema, especially in non-smokers or the lung bases?

Alpha-1 antitrypsin ($\alpha_1$-antitrypsin) deficiency. Loss of this protease inhibitor allows unopposed elastase to destroy alveolar walls, causing panacinar (panlobular) emphysema.

Classify restrictive lung diseases into intrinsic (parenchymal) and extrinsic causes with examples.

Intrinsic/parenchymal: idiopathic pulmonary fibrosis, sarcoidosis, pneumoconioses, hypersensitivity pneumonitis. Extrinsic: neuromuscular disease (ALS, myasthenia), chest wall disorders (kyphoscoliosis, obesity), and pleural disease.

What is the characteristic HRCT pattern of idiopathic pulmonary fibrosis (IPF)?

Usual interstitial pneumonia (UIP) pattern: subpleural, basal-predominant reticular opacities with honeycombing and traction bronchiectasis, typically without significant ground-glass.

Match the pneumoconioses to their exposures and typical lung zone: silicosis, asbestosis, coal worker's lung.

Silicosis — silica/mining, upper lobes, eggshell-calcified hilar nodes. Asbestosis — asbestos/insulation, lower lobes, pleural plaques, increased mesothelioma/bronchogenic carcinoma risk. Coal worker's pneumoconiosis — coal dust, upper lobes.

What triad defines a pulmonary embolism risk (Virchow's triad)?

Virchow's triad: (1) venous stasis, (2) endothelial injury, and (3) hypercoagulability. These predispose to deep vein thrombosis and subsequent pulmonary embolism.

What is the classic arterial blood gas finding in acute pulmonary embolism, and the most common ECG finding?

ABG typically shows hypoxemia with respiratory alkalosis (low $PaO_2$, low $PaCO_2$) and an increased A-a gradient. The most common ECG finding is sinus tachycardia; the classic (but uncommon) pattern is $S_1Q_3T_3$.

Define pulmonary hypertension by mean pulmonary arterial pressure and name its 5 WHO groups conceptually.

Pulmonary hypertension = mean pulmonary artery pressure $> 20$ mmHg at rest. WHO groups: (1) pulmonary arterial hypertension, (2) left heart disease, (3) lung disease/hypoxia, (4) chronic thromboembolic, (5) multifactorial/unclear.

What is cor pulmonale?

Right ventricular hypertrophy and/or failure resulting from pulmonary hypertension caused by a primary lung or pulmonary vascular disorder (not from left heart disease).

List the most common typical bacterial cause of community-acquired pneumonia and the classic "atypical" pathogens.

Most common typical: Streptococcus pneumoniae. Atypical pathogens: Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila (the last associated with hyponatremia and GI symptoms).

Which organism causes tuberculosis, and what is the characteristic histologic lesion?

Mycobacterium tuberculosis, an acid-fast bacillus. The characteristic lesion is a caseating (necrotizing) granuloma; the Ghon complex refers to a parenchymal focus plus hilar lymph node involvement.

What clinical setting and radiographic finding suggest Pneumocystis jirovecii pneumonia (PJP)?

Occurs in immunocompromised patients (especially HIV with CD4 count $< 200/\mu L$). Chest imaging shows bilateral diffuse perihilar/interstitial (ground-glass) infiltrates; treatment is trimethoprim-sulfamethoxazole.

Divide lung cancers into their two main histologic categories and state which is more strongly linked to smoking.

Small cell lung cancer (SCLC, ~15%) and non-small cell lung cancer (NSCLC, ~85%: adenocarcinoma, squamous cell, large cell). SCLC and squamous cell carcinoma are most strongly linked to smoking; adenocarcinoma is the most common type overall and in non-smokers.

Match these paraneoplastic syndromes to their lung cancer types: SIADH, hypercalcemia, Lambert-Eaton.

SIADH (and ectopic ACGH) — small cell carcinoma. Hypercalcemia (PTHrP secretion) — squamous cell carcinoma. Lambert-Eaton myasthenic syndrome — small cell carcinoma.

What is a Pancoast tumor and what syndrome can it produce?

A tumor at the lung apex (superior sulcus) that can invade the brachial plexus and cervical sympathetic chain, causing Horner syndrome (ptosis, miosis, anhidrosis) and shoulder/arm pain.

On a chest X-ray, what does silhouette sign loss of the right heart border versus the left hemidiaphragm localize?

Loss of the right heart border indicates right middle lobe pathology; loss of the left hemidiaphragm border indicates left lower lobe pathology. Adjacent structures of equal density obscure the normal silhouette.

When is a CT pulmonary angiogram versus a V/Q scan preferred for suspected pulmonary embolism?

CT pulmonary angiography (CTPA) is the first-line imaging test for PE. A ventilation-perfusion (V/Q) scan is preferred when CT contrast is contraindicated (e.g., renal failure, contrast allergy, pregnancy).

What is the role of low-dose CT in lung cancer, and who is screened?

Annual low-dose CT screening reduces lung cancer mortality in high-risk patients: typically adults ~50-80 years with a $\geq 20$ pack-year smoking history who currently smoke or quit within the last 15 years.

What is flexible bronchoscopy and list two diagnostic and two therapeutic uses.

Flexible bronchoscopy passes a fiberoptic scope into the airways. Diagnostic: visualize airways, obtain bronchoalveolar lavage (BAL), biopsies, and brushings. Therapeutic: remove foreign bodies/mucus plugs, control bleeding, and place stents.

What is endobronchial ultrasound (EBUS) primarily used for?

EBUS combines bronchoscopy with ultrasound to visualize and perform transbronchial needle aspiration (TBNA) of mediastinal and hilar lymph nodes — key for lung cancer staging and evaluating mediastinal lymphadenopathy (e.g., sarcoidosis).

Compare transbronchial biopsy, CT-guided percutaneous needle biopsy, and surgical (VATS) biopsy.

Transbronchial biopsy (via bronchoscope): for central lesions/diffuse disease, low bleeding risk. CT-guided percutaneous needle biopsy: for peripheral nodules, higher pneumothorax risk. Surgical/VATS or open lung biopsy: largest, most definitive sample for diffuse interstitial disease when others are non-diagnostic.

Interpret a pleural effusion using Light's criteria — what makes an effusion an exudate?

An effusion is an exudate if ANY of: (1) pleural/serum protein ratio $> 0.5$; (2) pleural/serum LDH ratio $> 0.6$; (3) pleural LDH $>$ two-thirds the upper limit of normal serum LDH. Otherwise it is a transudate.

How do the mechanism of action of $\beta_2$-agonists and muscarinic antagonists differ in bronchodilation?

$\beta_2$-agonists (e.g., salbutamol/albuterol, salmeterol) stimulate $\beta_2$ receptors, raising cAMP to relax airway smooth muscle. Muscarinic antagonists (e.g., ipratropium, tiotropium) block M3 receptors, preventing acetylcholine-mediated bronchoconstriction.

What is the role of inhaled corticosteroids (ICS) in asthma, and name a leukotriene modifier.

ICS (e.g., budesonide, fluticasone) are the cornerstone anti-inflammatory controller therapy in asthma, reducing airway inflammation and exacerbations. Montelukast is a leukotriene receptor antagonist used as add-on/alternative controller therapy.

What non-pharmacological therapy improves survival in chronic hypoxemic COPD, and at what threshold is it indicated?

Long-term oxygen therapy (LTOT), indicated when resting $PaO_2 \leq 55$ mmHg (or $SpO_2 \leq 88\%$), or $PaO_2$ 56-59 mmHg with evidence of cor pulmonale/polycythemia. Used $\geq 15$ hours/day, it is one of few interventions proven to improve COPD survival.

List key non-pharmacological interventions for chronic respiratory disease besides oxygen.

Smoking cessation (most important, slows COPD decline), pulmonary rehabilitation (exercise + education), vaccination (influenza, pneumococcal, COVID-19), non-invasive ventilation (CPAP/BiPAP) for OSA or chronic hypercapnia, and nutritional support.