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Respiratory Medicine - Symptomatology: A Complete Student Guide
How to Use This Guide
Think of each respiratory symptom as a story. The symptom is just the last chapter - to understand it, you need to know what happened earlier (the cause), how the body reacted (the mechanism), and what clues the history and examination give you (the diagnostic workup).
1. COUGH
What Is a Cough, Really?
A cough is not just "making a sound." It is the body's security guard for the airways - when something irritates or blocks the airway (mucus, a foreign body, bacteria, smoke), the body triggers a cough to clear it out.
The Mechanism (Step by Step)
Think of it like a 3-step fire alarm:
-
Trigger (Sensor): An irritant (mucus, dust, acid from stomach, a tumor) touches sensitive nerve endings (called cough receptors) lining the throat, larynx, trachea, and bronchi. These nerve endings also exist in the ear canal (Arnold's nerve) and esophagus - which explains why ear wax or acid reflux can make you cough without any lung problem!
-
Signal (Alarm): The signal travels via the vagus nerve to the brainstem, which processes it as "urge to cough."
-
Response (Action): The vocal cords snap shut, the breathing muscles build up enormous pressure (up to 300 mmHg - like squeezing a bottle), and then the vocal cords suddenly open - the air shoots out at explosive speed, dragging mucus or particles with it. This is what clears the airway.
Types of Cough by Duration
| Type | Duration | Most Common Causes |
|---|
| Acute | < 3 weeks | Viral URTI (common cold), bronchitis, pneumonia |
| Subacute | 3-8 weeks | Post-infectious (after a cold), pertussis |
| Chronic | > 8 weeks | Asthma, GERD, post-nasal drip, ACE inhibitors, TB, lung cancer |
Causes and How They Produce Cough
A. Respiratory Tract Infections (e.g., common cold, bronchitis, pneumonia)
- Viruses/bacteria infect the airway lining → the lining becomes inflamed and produces excess mucus
- The mucus sits in the airway → the cough receptors sense it → cough reflex fires repeatedly to clear it
- Example: The wet, productive cough with green/yellow sputum in pneumonia
B. Asthma
- Airways are hyperreactive (over-sensitive) - dust, cold air, exercise, allergens trigger inflammation
- The bronchial muscles go into spasm, the lining swells, mucus is produced → narrowed airways
- Narrowed airways stimulate cough receptors AND the body tries to cough to re-open them
- Clue: Cough worse at night, with exercise, after cold air. Usually accompanied by wheeze.
C. GERD (Acid Reflux)
- Stomach acid travels up the esophagus and either directly irritates the larynx/upper airway OR the acid touches the esophageal cough receptors (the vagus nerve innervates the esophagus too)
- Either way, cough is triggered without any actual lung disease
- Clue: Cough worse after meals, when lying down, or with spicy food. Often associated with heartburn/sour taste.
D. Post-Nasal Drip (Upper Airway Cough Syndrome)
- Sinusitis, allergic rhinitis, or a common cold produces excess mucus in the nose
- This mucus drips down the back of the throat (nasopharynx) → irritates cough receptors there
- Clue: Patient says "something keeps dripping down my throat," frequent throat-clearing, sneezing. Cough worse at night when lying flat.
E. ACE Inhibitor Drugs (e.g., Enalapril, Ramipril)
- These BP medications block an enzyme that normally breaks down bradykinin
- Bradykinin accumulates and sensitizes the cough nerve endings → chronic dry cough
- Affects 5-30% of patients taking these drugs
- Clue: Dry, tickly cough starting after BP medication was started. No sputum. Stops when medication is changed.
F. TB (Tuberculosis)
- Mycobacterium tuberculosis infects the lung tissue → causes cavitation (holes in the lung)
- Necrotic (dead) tissue and pus in the cavities acts as a continuous irritant → persistent cough
- Clue: Chronic cough >3 weeks + weight loss + night sweats + evening fever = TB until proven otherwise.
G. Lung Cancer
- A tumor growing inside a bronchus (airway) is a physical mass sitting in the airway
- It blocks normal secretion drainage and directly irritates cough receptors
- Clue: Chronic cough in a smoker, change in character of cough, blood in sputum, weight loss.
H. Cough Hypersensitivity Syndrome (Chronic Unexplained Cough)
- The cough nerve pathways become over-sensitized - like a fire alarm that goes off even from a gentle breeze
- No identifiable cause found. More common in women.
- Worsened by talking, laughing, cold air, strong smells.
History Questions to Ask (Cough)
- How long has the cough been there?
- Is it dry or productive (producing sputum)?
- When is it worst? Morning (chronic bronchitis/COPD), night (asthma, GERD, post-nasal drip), all day?
- What triggers it? Allergens, cold air, exercise, food?
- Is there blood in the sputum?
- Are you on ACE inhibitors?
- Do you smoke? (how many cigarettes/day for how many years - "pack years")
- Any fever, weight loss, night sweats? (points to TB or malignancy)
- Any heartburn or sour taste in mouth? (GERD)
- Does it feel like something is dripping down the back of your throat?
2. EXPECTORATION (Sputum)
What Is Expectoration?
Expectoration is the production and coughing up of sputum (mucus from the lower airways). Normally, the airways produce mucus that is moved up silently by tiny hairs (cilia) and swallowed without notice. When disease strikes, mucus production increases or its character changes - and it gets coughed up.
The Appearance of Sputum Tells You a Lot
| Sputum Type | Appearance | What It Suggests |
|---|
| Mucoid | Clear/white, sticky | Chronic bronchitis, asthma (no infection yet) |
| Purulent | Yellow or green | Bacterial infection (neutrophils turning green from their enzyme myeloperoxidase) |
| Rusty/brown | Rust-colored | Lobar pneumonia (Streptococcus pneumoniae) - blood + mucus mixed |
| "Currant jelly" | Dark red, thick, gelatinous | Klebsiella pneumonia (blood mixed with necrotic tissue) |
| Frothy pink | Pink, bubbly, watery | Pulmonary edema (heart failure - plasma fluid with a little blood enters the airways) |
| Anchovy paste" | Dark brown, thick | Amoebic liver abscess rupturing into the lung |
| Black | Black/dark grey | Coal miners (pneumoconiosis), heavy smokers |
Causes and Mechanisms
A. Chronic Bronchitis (COPD)
- Repeated smoke/irritant exposure → chronic inflammation → goblet cells (mucus-producing cells) multiply abnormally
- The airway becomes a "factory" for excess mucus
- Clinically defined: productive cough for at least 3 months in a year, for 2 consecutive years
- Clue: The "Blue Bloater" - overweight, cyanosed, edematous patient with productive morning cough
B. Bronchiectasis
- Repeated infections damage and permanently dilate the bronchi (like a weakened, bulging pipe)
- Secretions pool in these dilated pouches → bacteria colonize → chronic purulent sputum
- Sputum is copious (large amounts, up to 200-300 mL/day), often positional (more when lying on one side)
- Clue: Patient says "I cough up cupfuls every morning when I wake up"
C. Lung Abscess
- A walled-off pocket of pus forms in the lung (often after aspiration of oral bacteria)
- When the abscess ruptures into a bronchus → suddenly coughs up large volumes of foul-smelling, purulent sputum
- Clue: Sudden large amount of foul-smelling sputum, especially in alcoholics or after unconsciousness/aspiration
D. Cystic Fibrosis
- A genetic defect causes the mucus to be abnormally thick and sticky (like glue instead of oil)
- Normal ciliary clearance fails, bacteria colonize → chronic purulent expectoration from childhood
History Questions (Expectoration)
- How much sputum per day? (a teaspoon vs. a cupful)
- Color and consistency?
- Smell? (foul-smelling = anaerobic infection, abscess)
- Does position change the amount? (bronchiectasis)
- Morning heaviness? (chronic bronchitis)
- Any blood mixed in? (moves into hemoptysis workup)
3. HEMOPTYSIS (Coughing Up Blood)
What Is Hemoptysis?
Hemoptysis = coughing up blood from the respiratory tract (below the larynx). Must be distinguished from:
- Hematemesis - vomiting blood (from stomach - darker, mixed with food, acidic, preceded by nausea)
- Epistaxis - nosebleed dripping into the throat and being "coughed up"
Blood from the lungs is typically bright red, frothy, alkaline, and mixed with sputum.
Blood Supply to the Lungs (Key Concept)
The lung has two blood supplies:
- Pulmonary arteries - low pressure, carry deoxygenated blood for gas exchange
- Bronchial arteries - high pressure, from the aorta, supply nutrition to the airway walls
Most hemoptysis comes from bronchial arteries (high pressure) - which is why some cases can be life-threatening.
Causes and Their Mechanisms
A. Tuberculosis (most common globally)
- TB bacteria create cavities in the lung with local tissue destruction
- Rasmussen's aneurysm: a blood vessel wall weakened by the surrounding inflammation can rupture into the cavity
- OR: simple erosion of a vessel by the necrotizing granuloma
- Clue: Young patient, contact history, fever/night sweats/weight loss, upper lobe cavity on X-ray
B. Bronchiectasis
- The dilated, inflamed bronchial walls have abnormally enlarged, fragile bronchial arteries running through them
- Chronic inflammation + pressure → these vessels rupture → blood mixed with copious sputum
- Clue: Known bronchiectasis patient, productive cough + blood
C. Lung Cancer (Bronchogenic Carcinoma)
- A tumor grows inside or invades a bronchial wall
- It has its own chaotic blood supply (neovascularization) - abnormal vessels that bleed easily
- As the tumor ulcerates → blood enters the airway
- Clue: Smoker >40 yrs, change in cough pattern, weight loss, blood-streaked sputum
D. Pulmonary Embolism (PE)
- A blood clot blocks a pulmonary artery → the lung tissue supplied by it gets no blood → infarcts (dies)
- Dead lung tissue breaks down → bleeds into the alveoli → hemoptysis
- BUT: Hemoptysis occurs only in minority of PE (those with actual pulmonary infarction)
- Clue: Sudden breathlessness + pleuritic chest pain + hemoptysis after long immobility/surgery/DVT
E. Mitral Stenosis (Cardiac Cause)
- The narrowed mitral valve blocks blood flow → pressure backs up into pulmonary veins → pulmonary venous hypertension
- Increased pressure in the pulmonary capillaries → they leak/rupture → blood into alveoli
- Clue: Middle-aged woman with rheumatic heart disease history, pink frothy sputum, exertional dyspnea
F. Congestive Heart Failure
- Similar mechanism to above - raised pulmonary venous pressure
- Classically produces pink, frothy sputum (not pure blood - fluid + small amounts of blood)
- Clue: Bilateral ankle swelling, orthopnea, raised JVP, S3 gallop
G. Vasculitis (e.g., Wegener's/GPA, Goodpasture's)
- The immune system attacks the small vessels (capillaries) in the lung
- Pulmonary capillaritis → diffuse alveolar hemorrhage → hemoptysis
- Clue: Young patient, bilateral lung infiltrates, often with kidney involvement (hematuria)
H. Bronchitis (most common cause of mild hemoptysis in developed countries)
- Acute bronchitis causes mucosal inflammation → small surface vessels bleed → blood-streaked sputum
- Usually self-limiting and minor
Grading Hemoptysis
| Grade | Volume | Action |
|---|
| Mild | Blood-streaked sputum | Investigate electively |
| Moderate | < 200 mL/24 hrs | Urgent investigation |
| Massive | > 200-600 mL/24 hrs | Life-threatening emergency |
In massive hemoptysis, the danger is drowning in your own blood (flooding of normal alveoli), not blood loss. Airway protection is the priority.
History Questions (Hemoptysis)
- Is it truly from the lungs? (exclude nose and stomach as source)
- How much? Streaks vs. cups of blood?
- Onset? Sudden (embolism, rupture) vs. gradual (cancer, TB)
- Associated symptoms? Chest pain (PE, pneumonia), weight loss (TB, cancer), leg swelling (PE), fever (infection)
- Smoking history?
- Travel? (TB endemic areas)
- Medications? Anticoagulants increase risk of bleeding
- Any heart disease? (Mitral stenosis)
4. DYSPNEA (Breathlessness)
What Is Dyspnea?
Dyspnea is the subjective, uncomfortable sensation of difficult or labored breathing. The patient may describe it as "I can't get enough air," "My breathing is hard work," or "I feel like I'm suffocating."
It is not the same as rapid breathing (tachypnea) - a patient can breathe fast without feeling breathless, and can feel breathless while breathing normally.
The Mechanism (Why Does It Happen?)
The brain gets two sets of signals:
-
Afferent signals (sensory inputs to brain):
- Chemoreceptors (in carotid body and medulla): detect low oxygen (hypoxia), high CO2 (hypercapnia), or acidosis → signal brain "we need more air"
- Mechanoreceptors (in lungs, airways, chest wall): detect stretch, pressure, airway resistance → signal brain "breathing is harder than normal"
- Metaboreceptors (in muscles): sense lactic acid buildup during exercise
-
Efferent signals (brain commands to breathing muscles): Brain tells muscles to breathe harder
Dyspnea occurs when there is a MISMATCH - the brain is commanding more breathing effort than the body can deliver. Imagine asking a car engine to go 100 km/h but the gear is stuck in second - the effort is high, the result is poor. That frustrating mismatch = dyspnea.
Causes and Mechanisms
A. Obstructive Lung Disease (Asthma, COPD)
- Airways are narrowed → increased airway resistance → breathing requires more muscular effort
- Mechanoreceptors in the airways sense the increased resistance → "chest tightness" sensation
- In COPD: air trapping causes hyperinflation → the breathing muscles are in a mechanically disadvantaged position → feel like they are "working against a wall"
- Clue: Asthma - episodic, reversible, wheeze. COPD - smoker, progressive, irreversible, barrel chest
B. Pneumonia/Pulmonary Fibrosis (Restrictive Disease)
- The lungs become "stiff" (reduced compliance) - like trying to inflate a stiff balloon
- More muscular effort needed to take each breath → effort-related dyspnea
- Fibrosis also reduces gas exchange surface → hypoxia → chemoreceptors activated
- Clue: Fine crackles at bases, clubbing, restrictive pattern on spirometry
C. Pulmonary Embolism
- Clot blocks a pulmonary artery → that part of the lung is ventilated but not perfused (dead space)
- CO2 accumulates locally, blood oxygen drops → chemoreceptors fire → intense air hunger (most dramatic dyspnea)
- Also: right heart strain → reduced cardiac output → less oxygen to tissues
- Clue: Sudden onset dyspnea, pleuritic chest pain, tachycardia, risk factors for clot (immobility, surgery, cancer)
D. Heart Failure (Cardiac Dyspnea)
- Failing left ventricle cannot pump blood forward → blood backs up into pulmonary veins → pulmonary edema
- Fluid floods the alveolar spaces → J-receptors in the alveolar walls are stimulated → signals "danger" to the brain → intense dyspnea
- Classic clue: Orthopnea (worse lying flat - more blood shifts to the lungs), Paroxysmal Nocturnal Dyspnea (wakes at night gasping)
E. Pleural Effusion
- Fluid accumulates in the pleural space → compresses the underlying lung → less expandable lung tissue
- Mechanoreceptors sense the reduced lung expansion → dyspnea
- Clue: Stony dull percussion, reduced breath sounds at base
F. Pneumothorax
- Air enters the pleural space → lung collapses → sudden dramatic loss of lung volume
- Clue: Sudden sharp chest pain + dyspnea in a tall, thin young man (spontaneous) or after trauma
G. Anemia
- Reduced hemoglobin → less oxygen carried in blood → muscles and brain get less O2
- Metaboreceptors and chemoreceptors sense the deficiency → signal brain to breathe more
- Clue: Pallor, dyspnea on exertion, palpitations. No wheeze or crackles on examination.
Clinically Important Patterns of Dyspnea
| Pattern | What It Suggests |
|---|
| Orthopnea (worse lying flat) | Heart failure, bilateral diaphragm palsy |
| Paroxysmal Nocturnal Dyspnea (wakes from sleep gasping) | Heart failure |
| Episodic/variable | Asthma |
| Progressive with exercise | COPD, heart failure, interstitial lung disease, anemia |
| Sudden onset at rest | PE, pneumothorax, acute asthma attack |
| Positional (only when lying on one side) | Unilateral pleural effusion |
| Platypnea (worse sitting up, better lying down) | Hepatopulmonary syndrome (rare) |
History Questions (Dyspnea)
- Onset: Sudden or gradual?
- Duration: Months (COPD, fibrosis) or minutes/hours (PE, pneumothorax)?
- Triggers: Exercise? Cold air? Allergens? Lying flat?
- Grading: Use MRC scale - "Can you walk on level ground? Upstairs? At your own pace? Even while dressing?"
- Orthopnea: "How many pillows do you sleep on?" (more pillows = compensating for heart failure)
- Associated symptoms: Wheeze (asthma/COPD), ankle swelling (heart failure), chest pain, fever
- Smoking history, occupational history (dust, asbestos)
5. CHEST PAIN (Respiratory Causes)
Important First Point: Lung Parenchyma Has NO Pain Fibers
The lung tissue itself cannot feel pain - so you won't feel pain from a small pneumonia deep in the lung. Pain comes from the pleura (the lining around the lung), the chest wall, or the large central airways.
Types of Respiratory Chest Pain
A. Pleuritic Chest Pain
- Mechanism: The parietal pleura (outer layer) is richly innervated with pain fibers. When it becomes inflamed (pleuritis), the two pleural surfaces rub against each other during breathing → sharp, stabbing pain
- Key characteristic: Pain is worse on deep breathing and coughing (the two surfaces rub more when the lung expands), relieved by shallow breathing or lying on the affected side (pressure limits movement)
- Causes:
- Pneumonia extending to the pleural surface (parapneumonic pleuritis)
- Pulmonary embolism with infarction
- Viral pleuritis (Bornholm disease/epidemic pleurodynia)
- Pneumothorax
- Pleural mesothelioma
- SLE and rheumatoid arthritis (autoimmune pleuritis)
B. Pneumothorax Pain
- Sudden, sharp, unilateral chest pain + breathlessness
- Occurs when air enters the pleural space (spontaneous or from trauma)
- Mechanism: The parietal pleura is stretched by the air, and the sudden lung collapse stimulates pleural pain receptors
C. Tracheobronchitis Pain
- A raw, burning, central chest pain (retrosternal) that worsens with coughing
- Mechanism: Inflamed tracheal/bronchial mucosa → direct irritation of submucosal pain receptors
- Clue: Burning in the middle of the chest that is worse with every cough. Common in flu and bronchitis.
D. Malignant Infiltration of the Chest Wall
- Lung cancer invading the parietal pleura or rib cage causes constant, dull aching pain
- Unlike pleuritic pain, this is NOT made worse specifically by breathing
- Pancoast tumor (lung apex) invades the brachial plexus → pain radiating down the arm
E. Mediastinal Pain (from central mass/lymphadenopathy)
- Deep, pressure-like, central chest discomfort from enlarged mediastinal lymph nodes (lymphoma, sarcoidosis, metastatic cancer)
- May be associated with SVC obstruction (face/arm swelling)
Always remember: You must rule out cardiac, aortic, and esophageal causes before attributing chest pain to the respiratory system. Use ECG, troponin, history carefully.
History Questions (Chest Pain - Respiratory)
- Character: Sharp and stabbing (pleuritic) or dull aching (malignancy) or burning (tracheitis)?
- Is it worse with breathing/coughing? (pleuritic - this is the key question)
- Localization: Unilateral (pleuritis, pneumothorax) or central (tracheitis, mediastinal)?
- Onset: Sudden (pneumothorax, PE) or gradual (malignancy)?
- Associated features: Fever (infection), breathlessness (PE, pneumothorax), leg swelling (PE), weight loss (malignancy)
6. OTHER IMPORTANT RESPIRATORY SYMPTOMS
A. Wheeze
- A high-pitched musical sound heard on breathing out (expiration), due to turbulent flow through narrowed airways
- The patient may describe it as "whistling in the chest"
- Causes: Asthma (reversible, episodic), COPD (fixed), cardiac asthma (heart failure)
- Remember: "All that wheezes is not asthma" - a foreign body, anaphylaxis, or tumor can also cause wheeze
B. Stridor
- A harsh, high-pitched sound on INSPIRATION (or both inspiration and expiration)
- Indicates upper airway obstruction (above the carina)
- Causes: Foreign body, epiglottitis, croup (in children), tracheal tumor, anaphylaxis, vocal cord paralysis
- Stridor is an emergency - the airway may close completely
C. Hoarseness (Dysphonia)
- Respiratory cause: Lung cancer invading the left recurrent laryngeal nerve (which loops around the aortic arch) → vocal cord palsy → hoarse voice
- Clue: A smoker with chronic cough + new hoarseness = lung cancer until proven otherwise
D. Clubbing
- Bulbous swelling of the fingertips (watch-glass nails, Hippocratic fingers)
- Respiratory causes: Bronchiectasis, lung cancer (especially squamous cell), pulmonary fibrosis, empyema
- Mechanism not fully understood - possibly related to megakaryocytes/VEGF bypassing pulmonary circulation
E. Night Sweats
- Drenching sweats that wake the patient at night, requiring change of clothes/bedsheets
- Respiratory causes: TB (classic), lung cancer, lymphoma involving mediastinum
F. Weight Loss
- Any chronic respiratory infection (TB, bronchiectasis), malignancy, or severe COPD can cause involuntary weight loss
- In combination with cough + hemoptysis + hoarseness = high suspicion for lung cancer
7. TAKING A RESPIRATORY HISTORY: THE FRAMEWORK
Step 1 - Presenting Complaint
Write down exactly what the patient says in their own words. ("I've been coughing blood for 2 days.")
Step 2 - History of Presenting Complaint (SOCRATES for each symptom)
- Site / Character
- Onset (sudden or gradual?)
- Character (dry, wet, blood-streaked?)
- Radiation / Associated symptoms
- Alleviating factors
- Time course / Duration
- Exacerbating factors
- Severity (grading of breathlessness, amount of blood, etc.)
Step 3 - Specific Respiratory History
Always ask about:
- Smoking: Pack years = cigarettes per day ÷ 20 × years smoked
- Occupation: Asbestos (mesothelioma, asbestosis), coal/silica dust (pneumoconiosis), poultry farmers (hypersensitivity pneumonitis), chemical workers
- Pets at home: Birds → psittacosis or bird fancier's lung
- Travel history: TB endemic area? Southeast Asia → melioidosis? Southwest US → coccidioidomycosis?
- Drug history: ACE inhibitors (cough), amiodarone (pulmonary toxicity), methotrexate (pneumonitis), bleomycin (fibrosis)
- Family history: Cystic fibrosis, alpha-1 antitrypsin deficiency, asthma
- Immunization status: BCG for TB
- HIV/Immunosuppression status: Increases risk of TB, PCP (Pneumocystis) pneumonia, fungal infections
Step 4 - Review of Other Systems
- Cardiac symptoms (orthopnea, ankle swelling = heart failure causing respiratory symptoms)
- Skin (sarcoidosis - erythema nodosum, SLE - malar rash)
- Joints (rheumatoid - pulmonary fibrosis, ankylosing spondylitis - apical fibrosis)
- Eyes (sarcoidosis - uveitis)
8. ARRIVING AT A DIAGNOSIS: THE CLINICAL REASONING PROCESS
Step 1: Narrow the differential by symptom pattern
| Symptom Pattern | Think of |
|---|
| Chronic productive cough + smoker + morning | COPD/Chronic Bronchitis |
| Dry cough + wheeze + episodic + young | Asthma |
| Cough + fever + pleuritic pain + breathlessness | Pneumonia |
| Cough + weight loss + night sweats + hemoptysis | TB or Lung Cancer |
| Sudden breathlessness + pleuritic pain + leg swelling | PE |
| Orthopnea + PND + frothy sputum | Heart Failure |
| Cough on ACE inhibitor | Drug-induced cough |
Step 2: Physical Examination - What to Look For
| Finding | Suggests |
|---|
| Wheeze on expiration | Asthma/COPD |
| Coarse crackles | Bronchiectasis, pulmonary edema |
| Fine crackles (Velcro sound) | Interstitial fibrosis |
| Dull to percussion | Pleural effusion, consolidation |
| Hyperresonant | Pneumothorax, emphysema |
| Absent breath sounds | Effusion/pneumothorax |
| Bronchial breathing | Consolidation (pneumonia) |
| Clubbing | Fibrosis, cancer, bronchiectasis |
| Raised JVP + edema | Heart failure |
Step 3: Investigations - Guided by History
First Line:
- Chest X-Ray - ALWAYS the first investigation. Looks for consolidation, effusion, masses, hyperinflation, cavities
- Sputum examination - Culture, sensitivity, AFB (for TB), cytology (for cancer)
- Spirometry - FEV1/FVC ratio - obstructive (asthma/COPD) vs. restrictive (fibrosis)
- CBC - Eosinophilia (asthma, parasites), anemia (chronic disease), raised WBC (infection)
- ESR/CRP - Raised in infection and malignancy
Second Line (based on findings):
- CT Chest (HRCT): Better than X-ray for interstitial disease, small nodules, PE (CTPA)
- Bronchoscopy: To visualize airways, take biopsies (suspected cancer/TB)
- CBNAAT/Gene Xpert: For rapid TB diagnosis
- D-Dimer + CTPA: For PE
- Echocardiogram: Cardiac causes of dyspnea
- Mantoux/IGRA: TB exposure testing
- ABG (Arterial Blood Gas): Assesses oxygenation and CO2 retention
A Simple Clinical Reasoning Example
Scenario: A 55-year-old male smoker (30 pack years) comes with 3 months of cough, 1 week of blood-streaked sputum, and 5 kg weight loss.
Step 1 - Red flags: Smoker + chronic cough + hemoptysis + weight loss = LUNG CANCER UNTIL PROVEN OTHERWISE
Step 2 - Differential: Also consider TB (check for night sweats, fever, travel), bronchiectasis
Step 3 - Examination: Look for clubbing, lymphadenopathy (neck, axilla), signs of consolidation, Horner's syndrome (ptosis + miosis + anhidrosis if Pancoast tumor)
Step 4 - Investigations:
- Chest X-ray → if mass or opacity seen
- CT Chest → better characterize the lesion
- Sputum for AFB (TB) and cytology (malignant cells)
- Bronchoscopy + biopsy → tissue diagnosis (histology for cancer type)
- CBNAAT for TB
Step 5 - Diagnosis: Based on CT + histology, arrive at lung cancer (type, stage) or TB (sensitivity pattern).
Sources: Harrison's Principles of Internal Medicine 22E (2025) - Chapters 39 (Dyspnea), 40 (Cough), 41 (Hemoptysis); Murray & Nadel's Textbook of Respiratory Medicine; Frameworks for Internal Medicine.
This guide covers the full arc from symptom → mechanism → cause → history → diagnosis for the major respiratory symptoms. The key principle throughout is: symptoms don't arise randomly - there is always a biological reason, and understanding that reason tells you what to look for in the history and what tests to order.