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Chest Study Index and Classifications

Written by Betra Youhanna, a medical student and not a doctor — check every detail against your own teaching.

ICC-1 finals revision · 25 diseases + 39 criteria · Compiled from TheStudyFix deck

C/P
Inves
Mng
Special — pathognomonic

Obstructive airway

4 entries
1

Bronchial Asthma

C/P
  • Variable cough, SOB, wheeze, chest tightness
  • Worse at night and on waking
  • Triggered by viral infection, exercise, cold air, allergens, NSAIDs
  • Childhood onset, family history of atopy
  • Examination often normal between attacks; nasal polyps if Samter's
  • Acute severe: silent chest, RR >30, SpO₂ <90%, confusion, hypotension
  • Personal atopy — eczema, allergic rhinitis / sinusitis (supportive history)
Inves
  • Spirometry: pre-BD FEV1/FVC <80%, FEV1 <80% predicted
  • Reversibility: FEV1 ↑ ≥200 mL AND ≥12% post-salbutamol 200–400 mcg
  • PEF diurnal variability >10%
  • Bronchial challenge (histamine / methacholine): fall in FEV1 ≥20%
  • ↑ FeNO, ↑ blood / sputum eosinophils
  • Th2-high phenotyping (biologic eligibility): sputum eosinophils ≥2%, FeNO ≥20 ppb, blood eosinophils ≥150/µL
Mng
  • ICS controller (Budesonide, Fluticasone) ± LABA (Formoterol, Salmeterol)
  • LAMA add-on (Tiotropium bromide); LTRA Montelukast 10 mg/d
  • Reliever: as-needed ICS-Formoterol (GINA 2025 MART)
  • Exacerbation: OCS Prednisolone 40 mg/d × 5–7 d; SABA + SAMA + ICS nebs; IV MgSO₄ 2 g over 20 min if FEV1 <25–30%
  • Severe: Omalizumab (anti-IgE), Reslizumab (anti-IL5), Dupilumab (anti-IL4); Azithromycin; bronchial thermoplasty
  • Discharge: SpO₂ >94% RA, PFT >60–80% predicted, step-up + review 1–2 wk
  • Severe biologics also include Benralizumab (anti-IL5R)
  • Severe: Azithromycin 250 mg every other day × 6 months
  • Montelukast — caution in patients with neuropsychiatric problems
  • All asthma treatment must contain ICS — GINA no longer recommends SABA-only reliever monotherapy; every patient needs an ICS-containing controller (reliever = as-needed ICS-formoterol) to cut severe-exacerbation risk
  • GINA 2025 step ladder (1–5): Steps 1–2 (symptoms <3–5 days/wk, normal/mildly-reduced lung function) → as-needed low-dose ICS-formoterol only; Step 3 (symptoms most days, night waking ≥1×/wk, low lung function) → low-dose MART; Step 4 (daily symptoms, night waking ≥1×/wk, recent exacerbation) → medium-dose MART; Step 5 → refer for expert phenotyping + add-on severe-asthma therapy; reliever across ALL steps = as-needed low-dose ICS-formoterol (AIR = anti-inflammatory reliever)
Special
  • Variability defines asthma (vs persistent COPD)
  • Samter's triad: asthma + rhinitis / nasal polyps + NSAID sensitivity
  • Late-onset = neutrophilic, ICS-unresponsive → LTRA / macrolide
  • Exercise-induced: ICS-Formoterol prophylaxis before exercise
  • Occupational: PEF ↓ on workdays, ↑ on holidays → change job
  • ACOS: persistent limitation, ICS mandatory ± LABA/LAMA
  • LABA monotherapy contraindicated
  • Features making asthma less likely: isolated cough, chronic sputum production, chest pain, dyspnoea with dizziness / paraesthesia, stridor
  • Risk factors for severe / fatal exacerbation: prior ICU or mechanical ventilation, frequent SABA use, inadequate ICS adherence, high Th2 inflammation
  • Diagnostic histology (mucous plugs): Curschmann spirals (whorls of shed epithelium) + Charcot-Leyden crystals (crystalloids from degenerating eosinophil proteins) + eosinophilic infiltrate + sub-basement membrane fibrosis
physiology · background · low-yield
Epidemiology/Risk
  • Burden: ~300 million worldwide, more in developing countries; causes productivity loss, family disruption, healthcare-system burden
  • Host risk factors: FH atopy (×6 risk), obesity (BMI >30 → more symptoms, harder to control), gender (childhood ×2 boys → adulthood more women)
  • Environmental development factors: diet (soy milk, processed food), infection (RSV), allergens (pets, mites), pollution (indoor/outdoor), occupation (bakers, poultry, farmers, HCWs), smoking (active/passive)
  • Climate change worsens control — wildfire pollution, prolonged viral survival, ↑ mould/pollen → ↑ exacerbations, ER visits, mortality
Mechanism
  • Chronic inflammation / remodelling: ↑ smooth muscle (number + contractility), ↑ mucus glands, ↑ airway vascularity, ↑ sensory-nerve sensitivity → airway hyper-responsiveness (key feature)
  • Acute-attack triad: smooth-muscle contraction + microvascular leak (mucosal oedema) + mucus hypersecretion → bronchospasm
  • Bronchodilator mechanisms: β2-agonist → adenylyl cyclase → ↑cAMP → smooth-muscle relaxation + mast-cell stabilization + ↑mucociliary clearance; antimuscarinics block M1/M2/M3 → ↓Ca influx; methylxanthines inhibit PDE (preserve cAMP) + antagonize adenosine A1 receptors + ↑diaphragmatic contraction
  • Airway remodeling (5 changes): airway-wall thickening; sub-basement membrane fibrosis; increased submucosal vascularity; increased submucosal glands / goblet-cell metaplasia; bronchial smooth-muscle hypertrophy/hyperplasia — makes obstruction progressively less reversible
Background
  • ICS side effects: oral candidiasis, hoarseness, pneumonia risk with prolonged high dose (rinse mouth after use)
  • ICS stepwise dosing (low/med/high): Budesonide 200–400 / >400–800 / >800 mcg; Fluticasone 100–250 / >250–500 / >500 mcg
  • OCS (Prednisolone) systemic SE: immunosuppression, myopathy, gastritis / PUD, mineralocorticoid (HTN, hyperglycaemia, oedema), osteoporosis, adrenal suppression
  • β2-agonist SE: tachycardia, hypokalaemia, tremor, anxiety (less with inhaled / low dose)
  • Antimuscarinic SE: dry mouth, bitter/metallic taste; poor systemic absorption (generally safe)
  • Methylxanthines (aminophylline / theophylline) — should NOT be used in asthma; SE gastritis, arrhythmia, convulsions
  • Corticosteroid forms & uses beyond asthma: injectable hydrocortisone/dexamethasone for COPD & ILD exacerbation; steroids also used in autoimmune vasculitis and tuberculous pleural/pericardial effusion
Exam technique
  • Bronchodilator side effects: β2-agonists → tachycardia, tremor, nervousness, hypokalemia, tolerance (β-receptor downregulation); antimuscarinics → dry mouth, bitter/metallic taste; xanthines → arrhythmia, seizures, gastritis
  • Inhaler devices: MDI (Ventolin, needs press-breathe coordination), SMI (Spiriva), DPI (Miflonide, needs forceful deep inhalation), nebulizer (no effort, emergency use); ~60% of patients use inhalers incorrectly
Other
  • ICS local side effects: oral candidiasis (thrush) and hoarseness of voice; ↑pneumonia risk with high dose / prolonged use (months–years) — rinse mouth after use
  • Systemic corticosteroid side effects: immunosuppression (pneumonia), muscle weakness, gastritis/peptic ulcer, mineralocorticoid effects (hypertension, hyperglycemia, edema), osteoporosis, adrenal suppression (loss of endogenous cortisol → Addisonian crisis on abrupt withdrawal)
  • Leukotriene antagonists: Montelukast / Zafirlukast / Pranlukast (adult 10 mg/day, pediatric 5 mg/day) — for aspirin-induced & exercise-induced asthma and allergic rhinitis; SE neuropsychiatric problems, reversible ↑liver enzymes
2

COPD (Emphysema + Chronic Bronchitis)

C/P
  • Onset middle age (40s), persistent + progressive dyspnoea
  • Cough + sputum in ~30%, "winter colds"
  • Hyperresonance, flat diaphragm, prolonged expiration, wheezes
  • Clubbing absent → if present, think bronchiectasis or cancer
  • Pink Puffer: cachectic, barrel chest, pursed-lip, pink, no oedema (emphysema)
  • Blue Bloater: obese, cyanosis, cor pulmonale + oedema (chronic bronchitis)
  • Acute exacerbation: worsening over <14 d, usually infection
  • AATD: early-onset COPD, panacinar emphysema
  • Chronic bronchitis definition: productive cough for ≥3 consecutive months in ≥2 consecutive years
Inves
  • Spirometry mandatory: post-BD FEV1/FVC <70% (not fully reversible)
  • GOLD 1 ≥80% / GOLD 2 50–80% / GOLD 3 30–50% / GOLD 4 <30%
  • Plethysmography: ↑ RV, ↑ TLC, ↑ RV/TLC; ↓ DLCO in emphysema
  • CXR: hypertranslucency, flat diaphragm, ribbon heart, rapid tapering vessels
  • CT: dilated air spaces / bullae
  • ABG: ↓ PaO₂ ± ↑ PaCO₂ (Type II)
  • Secondary polycythaemia; eosinophils >300 predicts ICS benefit
  • WHO: screen all COPD patients once for AATD
  • GOLD ABE groups (symptoms mMRC/CAT + exacerbation history): A = 0–1 exac (no hospitalisation) + mMRC 0–1 or CAT <10; B = 0–1 exac + mMRC ≥2 or CAT ≥10; E = ≥2 moderate exac or ≥1 leading to hospitalisation
Mng
  • Smoking cessation, vaccinations (influenza, pneumococcal, COVID-19, pertussis), rehabilitation
  • Bronchodilators are cornerstone — SABA Salbutamol, LABA Formoterol/Salmeterol, Ultra-LABA Indacaterol
  • SAMA Ipratropium, LAMA Tiotropium (LAMA > LABA for exacerbation prevention)
  • Group A: single BD; B/E: LABA + LAMA; add ICS if eosinophils ≥300
  • ICS: Beclomethasone, Budesonide, Fluticasone — limited as monotherapy
  • Roflumilast (PDE4i) if FEV1 <50% and frequent exacerbations
  • Azithromycin 250 mg/d × 1 yr for frequent exacerbators
  • Dupilumab (anti-IL4/IL13) SC q2wk
  • Methylxanthines (Aminophylline / Theophylline): avoid — narrow therapeutic index
  • Ensifentrine (dual PDE3/4 inhibitor, nebulized q12h)
  • Exacerbation: Prednisolone 40 mg/d × 5–7 d
  • Surgical: lung volume reduction, transplantation, bullectomy
  • N-acetyl cysteine; Alpha-1 antitrypsin supplementation in AATD
  • ICS contraindicated if blood eosinophils <100 cells/µL, recurrent pneumonia, or history of TB infection
  • Acute exacerbation: rule out DDx (PE, pneumothorax, ACS); antibiotics cover H. influenzae, S. pneumoniae, M. catarrhalis; ventilation = BIPAP (CPAP only for sleep apnoea)
Special
  • Cor pulmonale = right HF from chronic lung disease via hypoxic pulmonary vasoconstriction
  • AATD: elastase uninhibited → early panacinar emphysema
  • GETomics paradigm: Genetics + Environment + Time
  • Post-BD FEV1/FVC <70% differentiates COPD from asthma
  • Arrhythmia + COPD → use LAMA/SAMA (avoid SABA, Aminophylline)
  • Complications: Type II resp failure, cor pulmonale, pneumothorax (bulla rupture), bronchiectasis
  • Emphysema anatomic types: Centriacinar (smokers, upper lobes, commonest symptomatic, 20:1 vs panacinar); Panacinar (α1-antitrypsin deficiency, lower lobes); Paraseptal/distal (subpleural upper lobes → young spontaneous pneumothorax); Irregular (commonest overall, around scars, asymptomatic)
  • Complications list also includes depression and recurrent exacerbations (alongside Type II resp failure, cor pulmonale, pneumothorax, bronchiectasis)
physiology · background · low-yield
Epidemiology/Risk
  • Global burden: one of top 3 causes of death worldwide; ~3 million deaths/yr; 90% of deaths in low/middle-income countries; ~50% of smokers develop COPD
  • Non-smoking risk factors: impaired lung development (pre-term birth, maternal smoking in pregnancy), severe childhood infection (measles), accelerated lung aging, long-standing bronchial asthma (12-fold ↑ COPD risk); climate-change extreme weather (heatwaves, dust storms) ↑ exacerbations
Mechanism
  • Emphysema histology: destruction of alveolar walls, loss of elastic tissue without fibrosis, diminished alveolar capillaries; fragmented "free-floating" septa
  • Chronic bronchitis dual pathogenesis: main bronchi mucous-gland hypertrophy + goblet-cell hyperplasia → hypersecretion/productive cough; peripheral small airways mucous plugging + inflammation (CD8, macrophages, PNLs) + bronchiolar wall fibrosis → airflow obstruction; histology = squamous metaplasia + mucous-gland hyperplasia
  • Hypoxemia in COPD is mixed: both poor ventilation (chronic bronchitis, Type II) and V/Q mismatch (emphysematous capillary-bed destruction, Type I) lower oxygen saturation
  • Emphysema → secondary pulmonary hypertension via hypoxia-induced vascular spasm + loss of pulmonary capillary surface area → cor pulmonale; death from pulmonary failure + right heart failure
  • Emphysema anatomic types: Centriacinar (respiratory bronchiole, distal alveoli spared; smoking; upper lobes; most common type causing symptoms); Panacinar (entire acinus; AATD; voluminous lower lobes; most common form overall, ~20:1 centriacinar:panacinar); Distal/Paraseptal (distal acinus, subpleural spaces → spontaneous pneumothorax); Irregular (around scarring foci)
Other
  • Roflumilast (PDE4 inhibitor) side effects: GI upset and psychological problems; once-daily oral dose
Background
  • Chronic bronchitis histology: submucosal mucous gland hypertrophy/hyperplasia (Reid index ↑) + goblet cell hyperplasia in smaller bronchi/bronchioles + squamous metaplasia + bronchiolar wall fibrosis
3

Bronchiectasis

C/P
  • Irreversible abnormal dilatation of medium-sized airways
  • Persistent productive cough, voluminous purulent sputum (bronchorrhoea)
  • Recurrent LRTIs; sometimes massive haemoptysis
  • Clubbing; coarse early/mid-inspiratory + expiratory crackles that shift with cough
  • Six aetiology categories: primary infective insult (bronchitis, pneumonia, TB; adenovirus, measles); abnormal immune (HIV, ABPA, SLE, RA); developmental (bronchomalacia); abnormal cilia (immotile cilia); viscid mucus (CF); bronchial obstruction
  • Distribution: typically bilateral, lower-lobe predominant, more severe in distal bronchi/bronchioles
  • Also malaise/weight loss (constitutional) and asthma exacerbations (seen in ABPA) round out the 6-symptom picture
Inves
  • CXR not sensitive: ring shadows, tramline shadows
  • HRCT = gold standard: tubular bronchiectasis, signet ring sign (airway > artery)
  • Spirometry: obstructive pattern
  • Sputum culture; TB sputum testing
  • Reid classification: cylindrical, varicose, cystic
  • Microbiology: H. influenzae (most common), Strep pneumoniae, Klebsiella, Pseudomonas aeruginosa
Mng
  • Six lines: antibiotics, mucolytics (N-acetyl cysteine), ICS (only if COPD/asthma overlap), bronchodilators, surgery (lobectomy in localized only), chest physiotherapy
  • Pseudomonas 1st isolation: Ciprofloxacin 750 mg q12h × 2 wk → inhaled Colistin ≥3 mo
  • Non-Pseudomonas + ≥3 exacerbations/yr: culture-based abx + Azithromycin ≥3 mo
  • Inhaled antibiotics via nebulizer: Colistin, Garamycin
Special
  • Cole's vicious cycle: insult → stagnation → colonization → inflammation → wall damage → dilatation
  • 3 pathogenesis theories: atelectasis (negative pressure), pressure of secretions, traction fibrosis
  • Pseudomonas isolation = aggressive eradication needed
  • Surgery never in generalized disease
  • Complications: respiratory insufficiency, cor pulmonale, brain abscess (septic emboli), secondary amyloidosis
physiology · background · low-yield
Mechanism
  • Dilation reflects destruction of the muscle and supporting elastic tissue of the bronchial wall
Other
  • Alternate causes classification — obstructive (foreign bodies, tumours, mucous plugs) vs non-obstructive (congenital/hereditary, suppurative necrotizing pneumonia)
  • Bronchodilator indications: significant dyspnoea, coexisting COPD or asthma
  • Antibiotic routes of administration: oral, injection, inhaled
Background
  • Pathology: airways dilated up to 4× normal diameter; histological spectrum of inflammation, ulceration, necrosis, fibrosis with squamous metaplasia and peribronchiolar fibrosis
Exam technique
  • Rhonchi/wheeze may also be present on auscultation (alongside coarse crackles)
4

Lung Abscess

C/P
  • Circumscribed pus / necrotic debris in lung parenchyma with cavity + air-fluid level (broncho-pulmonary fistula)
  • Early pneumonia-like: fever, sweating, cough, dyspnoea
  • Sputum: dry then productive, large volume (bronchorrhoea), foul-smelling = anaerobic
  • Chronic: weight loss, clubbing
  • Local: dullness, ↓ breath sounds ± bronchial breathing if large + superficial + bronchus-connected, crackles
  • Aspiration predisposers: dental/peridental infection, stroke, alcohol, frequent vomiting (bulimia, seizures)
  • Pathogenesis beyond aspiration: colonization of pre-existing lung disease (bronchiectasis, cystic fibrosis, bullous emphysema, infected pulmonary infarcts) and blood spread (IV drug use, IV cannula, haemodialysis, abdominal sepsis, UTI) — blood-borne seeding gives multiple bilateral abscesses
Inves
  • CXR: cavity with air-fluid level
  • Bronchoscopy: visualize abscess, exclude foreign body / endobronchial mass, BAL, transbronchial biopsy
  • Sputum + blood culture; CBC (anaemia of chronic disease, leukocytosis)
  • 90% polymicrobial; anaerobes (Bacteroides fragilis) most common
  • Inhalation aerobes → necrotizing pneumonia: S. aureus / MRSA, Strep milleri, Klebsiella, Pseudomonas
Mng
  • Two branches: medical (antibiotics) + drainage (closed intercostal tube / open surgery)
  • Clindamycin (anti-anaerobe) + Meropenem (adjunct) × 4–6 wk
  • Percutaneous drainage (sonar/CT-guided, LA) if antibiotics fail; complications: bleeding, empyema, broncho-pulmonary fistula
  • Lobectomy if size >6 cm, symptoms >12 wk, failed medical Rx, suspect malignancy
Special
  • DDx cavitary lesion: excavating bronchial carcinoma, localized pleural empyema, cavitary pneumoconiosis, hydatid cyst
  • Acute (<6 wk) = poorly defined wall; Chronic (>6 wk) = pyogenic membrane (fibrosis)
  • Aspiration → superior segment of right lower lobe (dependent)
physiology · background · low-yield
Mechanism
  • Inhalation route: entry via small-particle aerosols → necrotizing pneumonia
Background
  • Histology: acute (<6 wk) = central necrotic tissue + bacteria, surrounded by dilated vessels + inflammatory exudate; chronic (>6 wk) = central pus ± bacteria, walled by pyogenic membrane (fibrosis)
Microbiology
  • Less common organisms: TB, fungi, parasites (vs the usual anaerobic/polymicrobial picture)

Interstitial / Occupational

5 entries
5

Interstitial Lung Disease (general)

C/P
  • >150 disorders with inflammation + fibrosis of interstitium
  • Dyspnoea hallmark; cough common but non-specific
  • Acute (days–wk): SLE pneumonitis, acute HP, drugs, acute eosinophilic pneumonia, diffuse alveolar haemorrhage, acute interstitial pneumonia (Hamman-Rich syndrome) when rapidly progressive
  • Chronic (mo–yr): CTD-ILD, chronic HP, occupational, chronic eosinophilic pneumonia, IPF
  • Bilateral end-inspiratory Velcro rales (basal → apical progression)
  • Mid-inspiratory squeaks suggest HP (airway-centred)
  • Cyanosis + clubbing; signs of CTD (Raynaud, proximal weakness, joint pain)
  • Smoking-related: IPF, PLCH; smoking-protected: sarcoidosis, HP
Inves
  • HRCT = gold standard (CXR can be falsely negative)
  • IPF: bilateral basal honeycombing + traction bronchiectasis, BAL neutrophil-predominant
  • Sarcoidosis HRCT: septal beading, nodules abutting bronchovascular bundles, hilar lymphadenopathy
  • HP HRCT: headcheese sign
  • LAM: diffuse bilateral thin-walled cysts, normal intervening lung
  • PLCH: bizarre-shaped cysts, abnormal intervening lung
  • PAP: crazy paving; milky BAL with foamy macrophages
  • BAL CD4/CD8: HP <1, Sarcoidosis ≥2.5; Eosinophilic pneumonia: BAL eos >50%; PLCH: Langerhans cells >3%, CD1a + S100 positive
  • Surgical lung biopsy preferred over transbronchial (except sarcoidosis, up to 90% sensitive)
  • PFTs: restrictive (↓ TLC, RV, VC), ↑ FEV1/FVC, ↓ DLCO; 6-min walk test if normal rest
  • Anti-Scl-70 (scleroderma); ssDNA + complement (SLE)
  • Drug causes: Amiodarone (fibrosis), Nitrofurantoin (alveolar haemorrhage), Methotrexate
  • Diffuse alveolar haemorrhage BAL: increasing red-cell count on sequential lavages (>20%) + haemosiderin-laden macrophages
Mng
  • Remove offending agent (smoking IPF/PLCH, antigen HP, drug DI-ILD)
  • O₂ if hypoxic, pulmonary rehab, pneumococcal + influenza vaccines
  • Immunosuppressants: Cyclophosphamide, Azathioprine, Methotrexate
  • Pirfenidone → IPF; Sirolimus → LAM (avoid pregnancy); Cladribine → PLCH
  • GM-CSF + whole lung lavage → PAP
  • Plasmapheresis → diffuse alveolar haemorrhage
  • Lung transplantation = definitive for end-stage
Special
  • Restrictive pattern with preserved/↑ FEV1/FVC ratio
  • IPF >50 yr, worst prognosis among IIPs
  • Exposure clues: bird breeders/farmers (HP); pipefitters/shipyard (asbestosis); miners/ceramic (silicosis); coal miners (CWP)
  • BAL neutrophilia → worse prognosis
physiology · background · low-yield
Background
  • Interstitium composition: cells — fibroblasts, myofibroblasts, macrophages; matrix — collagens, elastin, proteoglycans
  • IIP subtypes: major — IPF (only important one), NSIP, cryptogenic organising pneumonia, respiratory bronchiolitis-ILD, desquamative interstitial pneumonia, acute interstitial pneumonia; rare — lymphocytic interstitial pneumonia, idiopathic pleuro-parenchymal fibroelastosis; plus an unclassifiable subset
  • CTD associated with ILD: SLE, polymyositis-dermatomyositis, mixed CTD, systemic sclerosis, rheumatoid arthritis
  • BAL performed to exclude infection and malignancy (cytology + bacterial/fungal/mycobacterial and viral cultures)
  • Family-history clues: sarcoidosis, LAM
  • Cough is common, non-specific and can be disabling; routine bloods neither sensitive nor specific
Epidemiology/Risk
  • Pneumoconioses (exposure-related ILD): asbestosis, silicosis, coal workers' lung, berylliosis
  • Age clue: post-adolescence–40 → CTD-ILD, sarcoidosis, LAM, PLCH; after 50 → IPF; pneumoconiosis male-predominant, CTD-ILD & LAM female-predominant
Exam technique
  • Systemic signs of underlying CTD: proximal muscle weakness, muscle tenderness, dermatological sign (dermatomyositis)
  • Surgical biopsy: sample multiple lobes, avoid areas of severe honeycombing (larger tissue improves pattern visualisation)
Physiology
  • Respiratory muscle weakness → low maximal voluntary ventilation (suggests CTD); resting hypoxaemia from V/Q inequality (unmasked by 6-min walk test)
Mechanism
  • PAP: whole lung lavage physically clears accumulated surfactant from defective surfactant clearance
Other
  • Diffuse alveolar haemorrhage: most common cause = vasculitis
  • Radiation pneumonitis/fibrosis: unilateral dense consolidation/fibrosis strictly conforming to a radiation port
6

Sarcoidosis

C/P
  • Idiopathic systemic granulomatous disease, non-caseating granulomas
  • Young adults 20–40, female > male, 10–12× more in blacks
  • Pulmonary involvement >90% — dyspnoea, cough, chest pain, pulmonary HTN
  • Löfgren's: fever + arthralgia + erythema nodosum + bilateral hilar adenopathy — excellent prognosis, NSAIDs + bed rest
  • Heerfordt-Waldenström: anterior uveitis + fever + parotid enlargement + facial palsy
  • Skin (25%): erythema nodosum (lower legs/ankles), lupus pernio (face)
  • Eyes (20–25%): uveitis, lacrimal gland enlargement, sicca, optic neuropathy
  • Cardiac (10–20%): heart block, arrhythmias, sudden death
  • CNS (10–25%): cranial neuropathy, aseptic meningitis
  • Renal (5–10%): hypercalcaemia, hypercalciuria, nephrocalcinosis, stones
  • Hematologic >50%: peripheral lymphopenia, hypergammaglobulinaemia
  • Musculoskeletal: chronic arthritis, dactylitis, lytic bone lesions, myopathy
Inves
  • CXR Scadding staging (NOT progressive): I bilateral hilar adenopathy; II hilar + infiltrates; III infiltrates only; IV honeycombing/fibrosis
  • HRCT: septal beading, perilymphatic nodules along bronchovascular bundles
  • D'Espine sign on chest (resonance of hilar lymph nodes)
  • ↑ ESR, mild normochromic anaemia, hypercalcaemia 10–20% (macrophage 1α-hydroxylase → active vit D), hypercalciuria 30–50%
  • Serum ACE elevated >75% — screening + monitor disease activity, non-specific
  • PFTs: restrictive, ↓ gas transfer
  • BAL: lymphocytosis, CD4/CD8 ≥2.5
  • Transbronchial biopsy positive up to 90% (tissue is the issue)
  • Definitive: non-caseating granulomas on biopsy
  • PFTs may show mixed abnormalities — obstruction, restriction and diffusion deficits (not purely restrictive)
Mng
  • Prednisolone 0.5 mg/kg × 4–6 wk → taper to maintenance ≥12 mo
  • Steroid-sparing: Methotrexate, Azathioprine, Hydroxychloroquine
  • Löfgren's needs no investigation — clinical diagnosis, symptomatic Rx only
Special
  • Lupus pernio = pathognomonic facial lesion
  • Hypercalcaemia mechanism = macrophage-produced active vit D
  • High CD4/CD8 BAL distinguishes from HP (low CD4/CD8)
  • Acute syndromes (Löfgren, Heerfordt) carry very good prognosis
physiology · background · low-yield
Other
  • Ocular symptoms: burning, itching, tearing, pain
  • Löfgren's symptomatic treatment also includes antipyretics (with bed rest + NSAIDs)
  • Erythema nodosum = itchy, painful rashes on lower legs/ankles
  • Lupus pernio = painful skin sores on the face
  • Skin lesions also distributed on back, arms, neck, face, scalp
Background
  • Symptomatic disease presents with symptoms of the affected organ (asymptomatic = incidental hilar adenopathy only on imaging)
  • GI & reproductive involvement: gastric nodules, ovarian or testicular masses
Mechanism
  • Erythema nodosum is histologically a nongranulomatous panniculitis (contains no sarcoid granulomas itself)
  • Serum ACE is released from the granulomas (reflects total granuloma burden)
7

Asbestos-related pleural disease + Asbestosis

C/P
  • Exposure: mining/milling, insulation, brake linings, ship construction (WWII), pipefitting
  • Long latency: 20–30 yr (rarely <10 yr if massive exposure)
  • Pleural disease: pleural plaques (most common, asymptomatic, diaphragm-level, calcified), diffuse pleural thickening, pleural effusion, rounded atelectasis, mesothelioma
  • Asbestosis (lower-lobe fibrosis): dyspnoea, dry cough, clubbing, cor pulmonale, bilateral inspiratory rales
Inves
  • CXR asbestosis: bilateral diffuse reticulonodular opacities, honeycombing
  • PFTs: restrictive, ↓ DLCO, normal FEV1/FVC
  • ABG: hypoxaemia + ↑ A-a gradient
  • Pleural plaques: localized thickening + calcifications at diaphragm
  • Rounded atelectasis: round opacity with irregular outlines, comet tail sign → biopsy / PET-CT to exclude cancer
  • Biopsy: barbell-shaped golden-brown fusiform rods = ferruginous bodies; Prussian blue stain on sputum
  • Diffuse pleural thickening: obliteration of the costophrenic angle on CXR → assess with CT / chest US
Mng
  • No specific Rx, symptomatic
  • Smoking cessation critical (lung cancer risk 75× higher with smoking)
  • Avoid further exposure
Special
  • Ferruginous bodies = pathognomonic asbestos fibres coated with iron-protein
  • Asbestos + smoking = synergistic bronchogenic carcinoma risk
  • Rounded atelectasis: pleural scarring fuses + traps lung — comet tail sign
  • Pleural plaques most common manifestation
physiology · background · low-yield
Background
  • Asbestos = crystalline hydrated silicates; acts as both a cellular/fibrotic agent and a tumour initiator + promoter
  • Fibrosis begins in lower lobes/subpleural → progresses to middle & upper lobes → contraction distorts architecture (enlarged air spaces within thick fibrous walls)
Mechanism
  • Oncogenesis mediated by reactive free radicals generated by fibres localizing in distal lung close to the mesothelial layer
Other
  • Honeycomb changes: cysts up to ~15 mm + diffuse visceral pleural fibrosis with blunting of the costophrenic angle
Epidemiology/Risk
  • Tobacco smoking worsens the effect of all inhaled mineral dusts, especially asbestos
8

Silicosis

C/P
  • Silica dust (Earth's crust major component)
  • Exposures: mining, quarrying, drilling, tunneling, sandblasting, cement/concrete, glass/pottery
  • Chronic: >15 yr latency, dyspnoea, dry cough
  • Acute: massive inhalation → onset within months → rapid hypoxaemic ventilatory failure → death
  • Agent = crystalline silica (mainly quartz)
Inves
  • Chronic CXR: nodules 1–10 mm upper lobes, coalesce >10 mm = PMF, eggshell calcification of hilar lymph nodes (characteristic), lower lobe scarring
  • Acute CXR: diffuse alveolar filling, lower-zone predominant
  • Diagnosis: exposure history + lung biopsy (silicotic nodule = concentrically arranged hyalinized collagen fibres)
Mng
  • No effective therapy → symptomatic
  • Smoking cessation, supplemental O₂
  • Influenza + pneumococcal vaccines
Special
  • Eggshell calcification of hilar nodes = pathognomonic
  • Silica impairs macrophages → TB risk ↑ → annual tuberculin skin test mandatory
  • Chronic = upper lobes; Acute = lower zones (rapid, fatal)
physiology · background · low-yield
Epidemiology/Risk
  • Most prevalent chronic occupational disease worldwide
Mechanism
  • Inhaled silica engulfed by alveolar macrophages → release IL-1 / TNF / fibronectin, oxygen free radicals and fibrogenic cytokines → inflammation + fibrosis
  • TB susceptibility mechanism: silica depresses cell-mediated immunity and inhibits macrophage killing of phagocytosed mycobacteria
  • Particle-size fate (all pneumoconioses): 1–5 μm lodge at distal-airway bifurcations (most harmful); >5–10 μm do not reach distal airways; <0.5 μm move freely without deposition
  • Pathogenesis: inhaled crystalline silica (quartz) engulfed by macrophages → oxygen free radicals + fibrogenic cytokines (IL-1, TNF, fibronectin) → inflammation & nodular fibrosis; also depresses cell-mediated immunity (→ TB risk)
9

Coal Worker's Pneumoconiosis (CWP) + Caplan syndrome

C/P
  • Coal mine dust → "Coal miner's lung" / "Black lung disease"
  • Progressive dyspnoea
  • Clubbing + crackles characteristically ABSENT → if present, look for another cause
  • ↑ COPD risk (focal emphysema)
  • Caplan syndrome: nodular opacities + Rheumatoid Arthritis in coal/silica-exposed workers
Inves
  • Simple CWP: small rounded opacities <1 cm in upper zones
  • Complicated CWP / PMF: large opacities >1 cm, upper-lobe; massive lesions = "angel wings"
  • Biopsy: coal macule → coal nodule (palpable, fibrotic) → PMF
  • Focal emphysema adjacent to dust macule
  • Caplan: circulating Rheumatoid Factor in miners with PMF
Mng
  • No cure, symptomatic
  • Avoid further dust exposure
  • Caplan: treat as PMF + RA rheumatologic protocol
Special
  • Clubbing + crackles ABSENT (vs asbestosis where present) — exam pearl
  • Caplan = CWP/silica + RA = necrobiotic lung nodules
  • Coal macule (microscopic) → coal nodule (palpable) → PMF (radiological)
  • "Angel wings" = massive upper-lobe PMF
physiology · background · low-yield
Background
  • Pulmonary anthracosis = benign first stage of the CWP spectrum (Anthracosis → Simple CWP → Complicated CWP): pigment accumulation without cellular reaction in connective tissue, along lymphatics or in lymph nodes; often clinically insignificant
  • Complicated CWP: coalescence of coal nodules → black scars 2–10 cm of dense collagen + pigment
Mechanism
  • Coal dust is relatively inert (needs large deposition to cause disease); silica & asbestos are more reactive → fibrosis at lower concentrations

Infection

6 entries
10

Community-Acquired Pneumonia (CAP)

C/P
  • Acute infection + signs of consolidation
  • Respiratory: dyspnoea, cough, fever, sputum, chills, pleuritic chest pain
  • Haemodynamic: hypotension, shock, tachycardia
  • Extrathoracic: otitis/pharyngitis, skin alteration, haemolytic anaemia (Mycoplasma), headache, GIT symptoms, confusion, hyponatraemia
  • Elderly: vague — GIT upset, confusion, absent fever, no chest symptoms
  • Chest: cyanosis, accessory muscles, dullness, ↓ breath sounds, bronchial breathing, crackles
  • Transmission: inhalation, aspiration (anaerobes), colonization (smoking), blood spread
  • Increased vocal resonance — bronchophony and whispering pectoriloquy (confirms consolidation, accompanies bronchial breathing)
Inves
  • CXR consolidation; lung US, CT chest if needed; CBC, ABG, BUN
  • IDSA/ATS severe criteria (1 major or 3 minor)
  • Normal PaO₂ ≈ 100 − (1/3 age); FiO₂ on 2 L = 0.29
  • Hospitalized + severe OR resistant-bacteria risk: sputum Gram + culture, blood culture
  • Microbiology: S. pneumoniae 35% (most common), atypicals 22%, H. influenzae 12%, others 31%
  • Urinary antigen test (Legionella + Pneumococcus) — indicated in Legionella outbreak/recent travel OR severe pneumonia
  • Procalcitonin: >0.25 mg/L favours bacterial (75–80% accurate; unreliable in atypical or viral/bacterial co-infection) — but start empiric antibiotics regardless of initial level
Mng
  • CURB-65: 0–1 home, 2 ward, 3–5 ICU
  • Outpatient 0–1 no comorbidity: Amoxicillin / doxycycline / macrolide
  • Outpatient + comorbidity: Amoxicillin/clavulanate or Ceftriaxone + macrolide/doxycycline, OR fluoroquinolone
  • Inpatient non-severe: β-lactam + macrolide OR fluoroquinolone monotherapy
  • Inpatient severe: β-lactam + macrolide OR β-lactam + fluoroquinolone (no monotherapy)
  • MRSA: Vancomycin (red-person syndrome) / Linezolid
  • Pseudomonal cover: MAFIA PCC mnemonic
  • Aspiration: Clindamycin only if abscess or empyema suspected
  • Antiviral: molecular flu test → Oseltamivir (Tamiflu) / Favipiravir
  • Corticosteroid in severe CAP + (shock OR P:F <300 OR rapid progression ≤3 d)
  • Duration: 3–4 d non-severe; ≥5 d severe; 7+ d Egypt
  • Vaccination: influenza annual; pneumococcal ≥65 or high-risk
  • Suspect + empirically cover MRSA / Pseudomonas if: recent hospitalization + IV antibiotics within 90 days, OR previous isolation of that organism
  • Non-responding pneumonia = inadequate response despite antibiotics — persistent fever, haemodynamic instability, respiratory failure, need for mechanical ventilation, radiological worsening
  • Non-response causes: organism (virulent/resistant/unusual e.g. TB), patient (comorbidity, abscess, non-adherence), doctor (wrong antibiotic/diagnosis); if misdiagnosed, DDx = heart failure, PE, cancer, vasculitis, ILD
Special
  • MAFIA PCC anti-Pseudomonal (Moxifloxacin EXCLUDED, Aminoglycosides nephrotoxic)
  • Legionella: atypical, aerosolized water, hemoptysis 1/3, confusion + diarrhoea + bradycardia + hyponatraemia
  • Klebsiella (Friedlander's): rare, DM + alcoholics, RUL, bulging fissure sign
  • Aspiration → superior segment RLL, foul sputum, anaerobes
  • Complications: para-pneumonic effusion (aseptic), empyema, lobar collapse, Type 1 resp failure, lung abscess, AF, septicaemia, pericarditis/myocarditis, ARDS
  • Pathology: lobar (4-stage) vs bronchopneumonia vs atypical (no consolidation)
  • Also complicated by thromboembolic disease and pneumothorax
physiology · background · low-yield
Epidemiology/Risk
  • Kills ~3 million/year worldwide; UK incidence 79.9/10,000 person-years; poor outcomes relate to CAP severity, patient characteristics, comorbidities
Background
  • Pneumonia = parenchymal vs acute bronchitis = airway; acute tracheobronchitis (winter, viral — rhinovirus/coronavirus/influenza/adenovirus)
  • Classification by site: CAP (community); HAP ≥48h after admission; VAP ≥48h on ventilator (timeframe = colonization time) → different organisms & treatment
  • Influenza vaccine for all ≥6 months by end of October; types IIV/RIV/LAIV — LAIV contraindicated in vaccine/egg allergy, age >65, immunosuppression, pregnancy (give IIV/RIV); pneumococcal for ≥65 or 2–64 with splenectomy/leukaemia/lymphoma/renal failure
Mechanism
  • Risk factors act via ↓ lung immunity: suppressed cough (stroke), inhibited cilia (smoking, immotile-cilia syndrome), defective macrophages/neutrophils (old age, HIV, steroids, chemo), impaired IgA
  • Colonization: pre-existing lung disease (bronchiectasis, chronic bronchitis, CF) → exacerbation → pneumonia; CF thick mucus → stasis; organisms Pseudomonas + S. pneumoniae
  • Lobar pneumonia histology: congestion (hyperaemia + oedema) → red hepatization (neutrophils, fibrin) → grey hepatization (RBC breakdown, fibrinosuppurative exudate); ~7–10 days; permanent scarring if incomplete resolution
  • Atypical pneumonia pathology: interstitial + alveolar-wall (less alveolar space), less exudate/consolidation, hyaline membrane → poor diffusion → hypoxia; extra-thoracic affection (Legionella, Mycoplasma)
  • Lung defence mechanisms: mucociliary entrapment; secretory IgA (upper tract) blocks epithelial attachment; serum IgG/IgM → complement → C3b opsonization; alveolar macrophage phagocytosis (primary alveolar defence)
Microbiology
  • Blood spread (bacteraemia — IV drug use, cannula, haemodialysis) → Staph aureus + Gram-negatives → multiple lung cavities on imaging
  • Bacterial–viral co-infection in ~30% of influenza pneumonia (virus disrupts alveolar epithelium, dysregulates immunity, enriches nutrients → bacterial overgrowth)
  • Respiratory pathogen PCR panel: simultaneously detects wide range of viral + bacterial pathogens; fast/accurate but costly/limited; samples = sputum, nasopharyngeal swab, BAL; out- and inpatients
Other
  • Clinical/lab resolution timeline: fever 2–4 d, leukocytosis 3–4 d, crackles 3–6 d, cough 4–9 d
11

Pulmonary Tuberculosis

C/P
  • Mycobacterium tuberculosis; acid-fast bacillus
  • 4 diagnostic pillars: Clinical, Radiological, Bacteriological, Pathological
  • Chronic cough, sputum, haemoptysis (cavitary), fever, night sweats, weight loss
  • HIV: atypical, lower zone infiltrates, false-negative sputum
  • Latent TB: persistent immune response without active disease
  • Primary TB (previously unsensitised host) → Ghon (primary) complex = subpleural mid-zone Ghon focus (~1–1.5 cm, caseous) + lymphangitis + caseous hilar lymphadenitis
  • Secondary (post-primary) TB = reactivation of dormant lesion / reinfection in sensitised host; localises to apices of upper lobes (high O₂ tension) with vigorous hypersensitivity → high risk of cavitation
  • Miliary TB (historically “galloping consumption”) = haematogenous dissemination → scattered <2 mm foci of consolidation throughout lungs & multiple organs
Inves
  • "TB can mimic any chest disease"
  • CXR/CT: apical infiltrates/cavitation, mediastinal LN, pleural effusion, miliary shadows; Ghon's focus, RUL consolidation
  • Sputum (3 consecutive morning): Ziehl-Neelsen (cheap, threshold-limited), fluorescent (faster, more sensitive)
  • Culture: Lowenstein-Jensen (egg, most common), Middlebrook media; 6–8 wk
  • BACTEC 460 (¹⁴C-palmitic acid, 10–12 d, GI ≥10 = positive); MGIT
  • PCR drug resistance: katG (high-level INH), inhA promoter (low-level INH), rpoB (Rifampicin)
  • ADA: pleural >70 IU/L suggestive, <40 excludes; CSF >8; ascitic >36
  • IGRA (QFT-G, ELISPOT): ESAT-6 + CFP-10 (NOT in BCG); one visit, 24h, processed within 12h
  • TST (Koch's phenomenon, Type IV): 5 TU PPD intradermal, read 48–72 h, measure induration
Mng
  • First-line: HRZES — Streptomycin only injectable, rest oral
  • Mechanisms: H mycolic acid, E arabinogalactan, Z plasma membrane, R RNA polymerase, S protein synthesis
  • Standard new: 2 mo HRZE → 4 mo HR
  • Daily/daily optimal; intermittent (3×/wk) only with DOT and NOT HIV
  • Monitor: clinical, sputum 2 mo + completion, AST/ALT/bilirubin/CBC
  • Major SE: rash (any); deafness/vertigo (S); ↓ urine (S/E); jaundice (H/R/Z); red-green vision (E — avoid kids + psychiatric)
  • Minor SE: GIT (H/R/Z); gouty arthritis (Z); peripheral neuropathy (H — give B6 50–75 mg/d); orange urine (R); flu-like (intermittent R → daily)
  • MDR-TB = resistance to R + H → DOT, admission if non-compliant
  • Pregnancy: HRZE safe, S contraindicated (fetal ototoxicity)
  • Renal: R/H/Z safe; aminoglycosides reduce if CrCl <50; avoid cycloserine/PAS/E; if E used → daily serum <5 µg/mL, dose interval 48h
  • HIV: ART 2–8 wk after TB Rx (CD4 <200); IRIS risk
Special
  • Koch's phenomenon = Type IV delayed hypersensitivity basis of TST
  • BCG vaccine prevents miliary TB + TB meningitis
  • ESAT-6 + CFP-10 absent in BCG → IGRA specificity
  • Rifampicin (1969) shortened therapy 12–24 mo → 6–8 mo by killing dormant bacilli
  • Thiacetazone implicated in cutaneous reactions in HIV
  • Tubercle = caseating granuloma: central caseous necrosis (pale-yellow, cheese-like) surrounded by epithelioid cells + Langhans giant cells (nuclei in peripheral horse-shoe pattern), rimmed by lymphocytes + fibrosis
physiology · background · low-yield
Microbiology
  • Virulence factors: mycolic acids (60–90 C long-chain FA → acid-fastness, impermeable to stains), cord factor (cytotoxin), sulfolipids (inhibit phagolysosome fusion → intracellular survival in macrophages)
  • Bovine type (M. bovis) acquired from milk of infected cows → intestinal & tonsillar TB, mainly in children
  • Classical TB principles: “no TB without the TB bacillus”, “no healthy carriers of tubercle bacilli”, and all bacillus-containing material is pathologic
Mechanism
  • Fate of primary TB: healing by fibrosis/encapsulation (most common, good resistance) vs haematogenous spread — few bacilli destroyed, moderate load → single-organ TB, heavy load → disseminated/miliary; encapsulated focus can reactivate if resistance falls
  • Secondary-TB lesion spectrum by host resistance: healed fibrotic (good) → chronic fibro-caseous (partial) → acute caseating pneumonia or miliary spread (very low resistance)
  • Secondary-TB complications: haemoptysis (erosion of vessels crossing the cavity), intestinal TB (swallowed infected sputum), cor pulmonale/heart failure (extensive lung fibrosis)
  • Pathogenesis cascade: inhaled droplet nuclei → alveolar macrophage phagocytosis → bacillus blocks phagolysosome fusion (sulfolipids/cord factor) → intracellular replication → macrophage rupture & spread → CD4 T-cells + IFN-γ/IL-12 → epithelioid + Langhans giant-cell granuloma with central caseous necrosis
Background
  • Plombage — historical collapse therapy packing inert material (Lucite/acrylic balls, paraffin wax, rubber sheets) under the upper ribs to collapse the diseased lung
12

Extrapulmonary Tuberculosis

C/P
  • Spread routes: haematogenous, lymphatic, contiguous
  • Miliary TB: children, immunocompromised; fever, weight loss, hepatosplenomegaly, miliary CXR
  • TB meningitis: insidious headache, altered mental status, cranial nerve palsies
  • Genitourinary TB: sterile pyuria, haematuria, infertility
  • TB peritonitis: ascites, abdominal pain
  • TB pericarditis: pericardial effusion → constrictive pericarditis
  • TB lymphadenitis: scrofula
  • Cutaneous: lupus vulgaris
  • Pott's disease (spinal TB): cold abscess → spinal cord compression, kyphosis
  • GI TB: malabsorption, obstruction
  • Hepatic TB: hepatomegaly + granulomas
  • TB pericarditis: fever, pleuritic + positional chest pain, pericardial friction rub; progresses to cardiac tamponade (dyspnoea, distended neck veins, pulsus paradoxus, muffled heart sounds, hypotension); withholding steroids → adhesions → constrictive pericarditis → cardiac arrest
  • Adrenal TB → Addison disease (adrenal insufficiency)
  • Miliary TB = classic cause of prolonged fever of unknown origin (FUO); progressive dyspnoea; bone-marrow involvement → anaemia, thrombocytopenia, leukemoid reaction
  • TB lymphadenitis (scrofula): posterior cervical / supraclavicular nodes → progressive swelling → inflamed, tender → overlying skin breaks down → draining fistula
  • GI TB (M. bovis from contaminated dairy): ileocaecal disease mimicking IBD — diarrhoea, obstruction, ulceration, fistulae
  • Skeletal TB: favours weight-bearing joints (spine, hips, knees) but also wrist/hand/elbow (esp. post-injury); chronic/subacute arthritis, usually monoarticular, constant bony pain
  • TB meningitis: focal neuro signs suggest a tuberculoma (intracranial mass); stroke from thrombosis of a major cerebral vessel
  • Genitourinary TB spreads to bladder and the male genital tract — epididymis, prostate, seminal vesicles (beyond sterile pyuria / haematuria / infertility)
Inves
  • Same TB labs (ZN, culture, PCR, ADA)
  • MRI spine (Pott's), CT abdomen (peritoneal/lymphadenitis)
  • Biopsy: lymph node, pleural, peritoneal — definitive
  • Treatment trial sometimes diagnostic
  • Psoas abscess in genitourinary TB
  • ADA elevated in fluids
  • TB serous fluid / CSF: glucose <50% of serum, elevated protein, ADA >8 U/L; ADA differentiates TB meningitis from other lymphocytic meningitis
Mng
  • Same anti-TB regimen, often longer for CNS/bone (9–12 mo)
  • Corticosteroids in: TB meningitis, TB pericarditis (prevent constriction)
  • Surgical: drainage of abscess, fixation for spinal instability (Pott's), pericardiectomy if constrictive
  • Corticosteroids for TB serositis — pericarditis, peritonitis, pleuritis, meningitis — to prevent fibrosis; avoid if drug resistance suspected
  • TB in renal impairment: rifampicin (excreted in bile), isoniazid, pyrazinamide safe at standard dose; reduce aminoglycosides if CrCl <50 mL/min; avoid cycloserine, PAS, ethambutol
  • TB meningitis: ethambutol replaced by streptomycin; treat 9–12 months (bone/joint 9 months)
  • Surgery: drain empyema / cardiac tamponade / CNS abscess, close bronchopleural fistulae, resect infected bowel; Pott's — correct deformity, relieve cord compression, bone-graft fixation
Special
  • Pott's disease = spinal TB → cold abscess + cord compression
  • Constrictive pericarditis from chronic TB pericarditis
  • Miliary TB ↑ in children, immunocompromised; prevented by BCG
  • Scrofula = classic cervical lymphadenitis
physiology · background · low-yield
Other
  • Ethambutol in renal failure/dialysis: monitor serum levels daily (not to exceed 5 µg/mL), lengthen dosing interval to 48 h or reduce to 8–10 mg/kg/day; give dose 4–6 h before dialysis
  • TST may be initially negative but positive on repeat weeks later; if still negative, question diagnosis and seek causes of anergy; blood culture positive in ~50% (disseminated / HIV)
  • Drug-resistant TB caused by poor adherence, use of too few drugs, and inadequate treatment duration or doses
Mechanism
  • Miliary spread: a TB lesion erodes into a blood vessel → lymphatics → venous system → right heart → pulmonary arteries, seeding numerous <2 mm foci ('millet seed')
  • Pott's mechanism: haematogenous seeding of anterior vertebral body → osteomyelitis/caseous necrosis → vertebral collapse (wedge fracture) → deformity + inflammatory mass compress cord → paraplegia
  • From the primary complex TB may spread via lymph nodes, collapse/bronchiectasis, pleural effusion, pneumonic spread, or blood-borne spread; the primary complex mostly heals asymptomatically in 4–8 weeks
Background
  • Prognosis: systemic miliary TB is poor despite treatment; isolated single-organ TB is good
  • Rare sites: tuberculous tenosynovitis (from adjacent bone or haematogenous spread); vascular erosion has even ruptured the aorta
  • Miliary pulmonary TB historically 'galloping consumption' — especially virulent, progressive, almost always fatal
Epidemiology/Risk
  • GI TB needs prolonged exposure + huge bacillary inoculum (mucosal resistance); very unusual in developed countries now that bovine TB is rare
  • Miliary TB demographics: children <4 yr, elderly, immunocompromised; commonest sites lungs and bone marrow; occurs during primary infection or after reactivation of a latent focus
13

Non-Tuberculous Mycobacteria (NTM / MAC)

C/P
  • >190 species, most non-pathogenic
  • Transmission: inhalation, ingestion, percutaneous; reservoirs = tap water, cockroaches
  • Indolent / subacute course; fever most common
  • Pulmonary (85%): chronic cough, sputum, haemoptysis, fatigue, weight loss — non-specific
  • Lymphadenitis: immunocompetent children 1–5 yr, female predominance, isolated cervical/submandibular; benign self-limiting
  • Disseminated: immunocompromised (HIV, transplant, steroids, TNF-α inhibitors), 90% MAC; cutaneous lesions
  • SSTI: linear nodules along lymphatics; fish tank granuloma (M. marinum), Buruli ulcer (M. ulcerans)
  • Predominant species: MAC (most common slow), M. kansasii, M. abscessus (rapid)
  • Host risk: pre-existing lung disease, immunodeficiency (IFNγ-IL12, HIV, biologics)
Inves
  • Runyon classification (Groups 1–4 by growth + pigment)
  • Imaging: fibro-cavitary (upper-lobe, mimics TB) vs nodular bronchiectatic (RML + lingula = Lady Windermere)
  • Diagnosis pulmonary: ALL radiological + ONE microbiological (two positive sputum cultures OR one bronchial wash OR biopsy + histology)
  • Smear: cannot distinguish TB from NTM
  • PCR = only rapid method to differentiate NTM from TB DNA
  • Children lymphadenitis: 80% MAC, 2nd M. scrofulaceum
Mng
  • MAC lung disease (ATS/IDSA): macrolide (azithromycin / clarithromycin) + ethambutol + rifampin — continue 12 months after culture conversion (culture turns pos → neg)
  • M. kansasii: rifampin + ethambutol + isoniazid + pyridoxine — also 12 months after culture conversion (conversion takes ~1 yr)
  • Lymphadenitis: surgical excision (do not I&D — avoids fistula formation)
  • Disseminated MAC in HIV: macrolide-based regimen + ART
  • Localized disease surgery: surgical drainage, debridement, excision + prolonged (>3 months) combined antimicrobials; cervical lymphadenectomy in children → quick resolution
Special
  • Lady Windermere syndrome: nodular bronchiectatic NTM in elderly women, RML/lingula
  • Fish tank granuloma = M. marinum; Buruli ulcer = M. ulcerans
  • "Diagnosis is a challenge" — colonization vs disease
  • IGRA may cross-react with M. marinum, M. szulgai, M. kansasii
physiology · background · low-yield
Microbiology
  • NTM synonyms: atypical mycobacteria / environmental mycobacteria / nontuberculous mycobacteria — species outside M. tuberculosis complex & M. leprae
  • Runyon classification based on growth rate + pigment production + colony morphology
  • Disseminated disease without HIV also in leukaemia; organisms commonly isolated = M. kansasii & M. haemophilum
  • Smear acid-fast staining via fluorochrome technique (or Ziehl-Neelsen) for preliminary result; culture of tissue (skin/LN/blood) = optimal method
Epidemiology/Risk
  • Risk: trauma/surgery (e.g. breast prostheses) — consider NTM if not responding to standard antibiotic regimens
  • Immunodeficiency risk: inherited IFNγ–IL12 pathway / cytokine-signalling / macrophage–dendritic-cell defects; acquired — immunosuppressants (TNF-α inhibitors, azathioprine, mycophenolate mofetil, cyclosporine)
  • More common in men and older patients (decline in health + other predisposing conditions)
Background
  • Lymphadenitis node progression: enlarge → ulcerate → drainage → fistula formation (excise, do not I&D)
  • SSTI nonspecific lesions: papules, plaques, abscesses, cellulitis, folliculitis, subcutaneous nodules, ulcerations, panniculitis, draining sinus tracts
14

Pulmonary Aspergillosis

C/P
  • Three subtypes (Simple / Chronic / Invasive)
  • Simple (Aspergilloma): fungus ball in pre-existing cavity (often post-TB), often asymptomatic, may cause haemoptysis
  • Chronic: chronic cough, sputum, weight loss, mild haemoptysis in structural lung disease
  • Invasive: immunocompromised (neutropenia, transplant); fever, dyspnoea, pleuritic pain, haemoptysis; angioinvasion → infarction → necrosis
  • ABPA: asthma exacerbations, bronchiectasis
Inves
  • Simple: CXR/CT shows fungus ball within cavity
  • Chronic: cavitary disease, cavity wall thickening, fibrosis
  • Invasive: angioinvasion on histology
  • Biopsy
  • Bronchoscopy + BAL or image-guided biopsy for histological + microbiological confirmation
  • GMS special stain on biopsy demonstrates branching septate Aspergillus hyphae → confirms causative organism (definitive)
Mng
  • Simple aspergilloma: usually conservative; surgery if massive haemoptysis
  • Chronic: long-term antifungal
  • Invasive: urgent antifungal
Special
  • 3-subtype master concept (Simple = aspergilloma in cavity / Chronic = structural / Invasive = immunocompromised)
  • Aspergilloma classically in old TB cavity
  • Chronic = transitional/semi-invasive stage between simple aspergilloma and invasive disease: cavity wall eroded and invaded by elongated hyphae once host defences are lowered
  • Post-TB cavity mass differential: aspergilloma vs TB reactivation vs lung abscess vs bronchogenic carcinoma in a healed cavity
  • Severity tracks directly with degree of immunosuppression — invasive form = highest mortality
physiology · background · low-yield
Microbiology
  • Four species virulent against humans: A. fumigatus, A. niger, A. terreus, A. flavus (branching septate hyphae)
  • Species & morphology: A. fumigatus (most common), niger, terreus, flavus; branching septate hyphae. Spectrum: noninvasive (fungal ball in cavity) → transitional (host defences lowered) → invasive/angioinvasive (radial hyphae, coagulative necrosis with peripheral haemorrhage)
Epidemiology/Risk
  • Ubiquitous environmental mould — found in ground, air and plants worldwide; occupational spore exposure (e.g. farmer) is a risk
Background
  • Simple aspergilloma histology: well-circumscribed round mass of compacted hyphae with concentric laminated structure sitting in a cystic cavity, no wall invasion
  • Invasive disease has two histopathological patterns: Pattern 1 (discrete coagulation-necrosis nodule, radial hyphae, circumferential haemorrhage, few inflammatory cells) and Pattern 2 (lobular consolidation/bronchopneumonia, liquefactive necrosis, neutrophil-filled alveoli)
Mechanism
  • Angioinvasion: hyphae invade the vessel wall and lumen with surrounding necrotic tissue → widespread/haematogenous infection
15

Pneumocystis jiroveci pneumonia (PCP)

C/P
  • Opportunistic infection in immunocompromised host (HIV/AIDS, transplant, chemotherapy)
  • Listed under opportunistic pneumonia / immunocompromised host pathogens
  • Most common opportunistic infection in HIV/AIDS
  • PCP is an opportunistic fungal infection (a fungus)
Inves
  • Sputum / BAL for cysts
Mng
  • Standard therapy (covered in opportunistic pneumonia context)
Special
  • Opportunistic pathogen in immunocompromised alongside CMV, MAC, invasive aspergillosis, invasive candidiasis
  • Foamy alveolar exudate with proliferating fungi/cysts — characteristic histology
physiology · background · low-yield
Epidemiology/Risk
  • Ubiquitous exposure — all children develop antibodies to it by age 2
Microbiology
  • Other opportunistic-pneumonia pathogen groups: viruses (CMV, measles), Aspergillus & Candida, bacterial pneumonia & TB (all commoner in the immunosuppressed)

Tumour

3 entries
16

Bronchogenic Carcinoma (NSCLC + SCLC)

C/P
  • 95% of primary lung tumours; males > females; smoking dominant; peak 50–70 yr
  • Red flag: "Old man, smoker, new chest symptoms = bronchogenic carcinoma until proven otherwise"
  • Types: NSCLC 85% (squamous 30%; non-squamous 70% → adeno 90%, large-cell 10%); SCLC 15%
  • Risk: smoking (60× heavy, 80% cases), asbestos (synergistic), pollution, scarring, genetic
  • Intra-thoracic: bronchial irritation (cough), erosion (haemoptysis, dull aching pain), obstruction (wheeze, atelectasis, post-obstructive pneumonia)
  • Pleural: transudate (SVC compression), exudate, haemorrhagic (invasion), chylothorax (thoracic duct), pyothorax; pleuritic pain
  • Pancoast / thoracic inlet: apical mass invading 1st/2nd ribs, subclavian vessels, brachial plexus → shoulder pain to axilla/scapula, dullness at Kronig's/clavicle, unequal pulse + BP, unilateral clubbing, upper limb oedema, wasting of small hand muscles; Horner's (ptosis + myosis + anhidrosis + enophthalmos + unilateral nasal obstruction + loss of spino-ciliary reflex)
  • Mediastinal: trachea (brassy cough, stridor), oesophagus (dysphagia); vagus (brady → tachy, bronchospasm), phrenic (shoulder pain + hiccups → paralysis), left recurrent laryngeal (hoarseness); D'Espine sign = LN enlargement
  • SVC syndrome (often SCLC): facial plethora, distended JVP, lip cyanosis, arm swelling, chest collateral circulation
  • Metastatic: liver, brain, bone, adrenal
  • Paraneoplastic (mostly SCLC): hypercalcaemia (SqCC — PTHrP), hypoglycaemia (SqCC — insulin-like), SIADH (SCLC), ectopic ACTH (SCLC), somatostatinoma (SCLC), gynaecomastia (large-cell + adeno), carcinoid
  • Paraneoplastic — neuromuscular: Lambert–Eaton myasthenic syndrome (SCLC; weakness improves with use), peripheral & autonomic neuropathy (postural hypotension, colic), cerebellar ataxia, transverse myelitis, PML, polymyositis/dermatomyositis
  • Paraneoplastic — vascular/haematogenous: migrating thrombophlebitis (Trousseau) → pulmonary embolism; fibrinogen deficiency, anaemia (iron-deficiency / aplastic / megaloblastic), eosinophilia
  • Paraneoplastic — skeletal: finger clubbing + hypertrophic osteoarthropathy (HOA — subperiosteal new bone, painful periostitis)
  • Paraneoplastic — skin / renal: acanthosis nigricans, dermatomyositis, scleroderma; nephrotic syndrome (immune-complex glomerulonephritis)
Inves
  • CXR, CT chest, PET-CT for staging
  • Tissue biopsy (bronchoscopic, transthoracic, surgical)
  • TNM staging (NSCLC); SCLC limited vs extensive (single radiation port)
  • IHC: TTF-1 + Napsin-A positive in primary lung adeno; TTF-1 negative in metastatic adeno (except thyroid)
  • Histology: SCC central / smoking; Adeno peripheral / lepidic; Large-cell peripheral / poorly differentiated; SCLC central / neuroendocrine
  • IHC for subtyping: CK5/6 + p63/p40 positive → squamous cell; chromogranin + synaptophysin positive → neuroendocrine (SCLC/carcinoid) — complements TTF-1/Napsin-A for adenocarcinoma
  • Paraneoplastic screen: serum calcium, glucose, ACTH, sodium (endocrine markers); markedly ↑ ESR
  • Metastatic workup: abdominal US/CT (liver, adrenal), CT brain, bone scan, PET-CT
Mng
  • NSCLC: surgery if early-stage, chemotherapy ± radiotherapy, targeted therapy
  • SCLC: chemotherapy + radiotherapy; rarely surgical
  • Paraneoplastic: address tumour ± symptomatic management
  • NSCLC (stage-based): surgery if resectable & no metastasis → chemoradiation → Stage IV platinum-based chemo + targeted therapy (EGFR / ALK / ROS1 in adeno) + immune checkpoint inhibitors
  • SCLC: platinum–etoposide chemotherapy (highly chemosensitive); limited stage adds concurrent chemoradiation + prophylactic cranial irradiation; radiotherapy for SVC obstruction; surgery contraindicated (disseminated at presentation)
Special
  • Pancoast tumour → Horner's syndrome
  • SVC syndrome dominantly SCLC
  • Paraneoplastic syndromes mostly SCLC; SqCC owns hypercalcaemia + hypoglycaemia
  • Pulmonary neuroendocrine spectrum: carcinoid → SCLC
  • Pleural metastases more common than primary pleural tumours; cytology = dual cell population
  • Unilateral clubbing in Pancoast (subclavian artery compression)
  • Thick-walled cavity on CT → suggests malignancy (vs thin wall = benign)
  • Localized / monophonic wheeze = fixed obstruction red flag → bronchogenic carcinoma (vs diffuse polyphonic wheeze of asthma/COPD)
  • Histology hallmarks: SqCC = keratin pearls + intercellular bridges (desmosomes); SCLC = small blue cells with scant cytoplasm, salt-and-pepper chromatin, nuclear molding, absent nucleoli, high mitotic rate; Adeno = glandular/acinar formation + mucin (TTF-1+); Large-cell = no differentiation (diagnosis of exclusion)
physiology · background · low-yield
Other
  • TNM cutoffs (8th ed): T1 ≤3 cm (T1a ≤1, T1b >1–2, T1c >2–3), T2 >3–5 cm, T3 >5–7 cm, T4 >7 cm; N1 ipsilateral hilar/peribronchial, N2 ipsilateral mediastinal/subcarinal, N3 contralateral/supraclavicular/scalene; M1a contralateral nodule/pleural effusion, M1b single extra-thoracic, M1c multiple
  • Histology hallmarks: SCC = keratin pearls + intercellular bridges + central cavitation; adeno = glandular/mucin + lepidic growth; SCLC = small “oat” cells, scant cytoplasm, nuclear moulding, salt-and-pepper chromatin, high mitoses; large-cell = pleomorphic, no differentiation (diagnosis of exclusion)
  • Prognosis: NSCLC 5-yr survival ~15–20% overall (stage-dependent range 3–60%); SCLC ~10–20 months treated, 2–4 months untreated (limited disease 1–2 yr, extensive 6–12 months)
  • Bronchial carcinoid (low-grade neuroendocrine, central mass, typical vs atypical): carcinoid syndrome = flushing, nausea/vomiting, abdominal pain, cough/wheeze + carcinoid heart disease (endocardial + tricuspid + pulmonary valve scarring; rarely aortic/mitral). Syndrome is RARE in lung carcinoid (more common with hepatic mets of GI carcinoid)
Mechanism
  • Carcinogenesis sequence: normal epithelium → hyperplasia → squamous metaplasia → dysplasia → carcinoma in situ → invasive carcinoma (reversibility decreases); adeno pathway: atypical adenomatous hyperplasia → adenocarcinoma in situ → invasive
  • Precancer sequence (SqCC): normal epithelium → hyperplasia → squamous metaplasia → dysplasia → carcinoma in situ (atypia without breach of basement membrane) → invasive carcinoma, with accumulating mutations
Background
  • Carcinoid: low-grade neuroendocrine tumour, younger / non-smoker patients, central polypoid endobronchial mass; excellent prognosis (typical ~90% 5-yr)
  • Respiratory epithelium cell types: ciliated columnar, goblet (mucin), Kulchitsky (neuroendocrine — origin of carcinoid/SCLC), reserve (stem cells)
Epidemiology/Risk
  • Full risk-factor list also names effect of gender and nutritional factors (alongside smoking, pollution, occupational/asbestos, previous lung disease/scarring, genetic predisposition); 95% of smokers show atypical cells in bronchial mucosa
17

Malignant Mesothelioma

C/P
  • Primary pleural tumour from mesothelial cells
  • Extensive bilateral pleural spread, aggressive local invasion, metastasis less common
  • 50% asbestos exposure; latency up to 40 yr; lifetime risk does not diminish
  • Smoking does NOT increase mesothelioma risk
  • Sources: mining, fabrication, insulation, pipefitting
  • Progressive dyspnoea, unilateral chest pain, cough, systemic (fever, malaise, myalgia, weight loss)
  • 10% lifetime risk of mesothelioma with heavy asbestos exposure
Inves
  • CT: encapsulation of lung by malignant fibrous rind
  • Pleural effusion: very cellular, large clusters with scalloped contours
  • Cytology cannot assess invasion → biopsy
  • Gross: pleural plaques first → diffuse thickening encasing lung in yellow-white firm rind
  • Histology: epithelial (cuboidal, tubular/microcystic, favourable, mimics adeno) / sarcomatous (spindled, unfavourable) / biphasic (both, unfavourable)
  • IHC: Calretinin POSITIVE / TTF-1 NEGATIVE (vs adenocarcinoma)
  • Pathogenesis: fibres → mesothelial layer → ROS → DNA damage → mutations (p16, NF2)
  • Cytological malignancy criteria in pleural effusion: profusion of mesothelial proliferation, cytological atypia, macro-nucleoli, frequent cytoplasmic vacuoles
Mng
  • Limited — surgical, chemo, radiotherapy
  • Poor prognosis: surgery rarely possible, poor response to radio/chemotherapy — 50% dead within 1 year, most dead within 2 years
  • Fatal cases with unconfirmed diagnosis require referral to Coroner / inquest (industrial asbestos disease)
Special
  • Pleural rind encasing lung = mesothelioma gross hallmark
  • Calretinin+/TTF-1− distinguishes from adenocarcinoma
  • p16 and NF2 tumour suppressor mutations
  • Asbestos fibres not removed/metabolized → lifetime risk
  • Smoking does NOT add to mesothelioma risk (unlike bronchogenic carcinoma)
physiology · background · low-yield
Background
  • Experimental strategies under study: chemotherapy, photodynamic therapy, targeted therapy (anti-mesothelin), immune therapy, gene therapy, vaccine therapy
Other
  • Effusion cytology hard to distinguish from reactive mesothelial cells (variable atypia) — biopsy needed as cytology cannot assess invasion
  • Effusion cytology: PAS stain shows abundant cytoplasmic glycogen granules
Mechanism
  • Fibre carcinogenesis: asbestos fibres localize in distal lung near mesothelial layer → generate reactive oxygen species → DNA damage; fibres act as tumour initiator AND promoter
18

Lung Metastases

C/P
  • Common in both carcinoma and sarcoma
  • Most common primary origins: breast, GI tract, kidney
  • Most common histological type: adenocarcinoma
  • Can't usually distinguish histologically from primary
Inves
  • IHC to clue primary origin (TTF-1 negative; lung primary positive)
  • Gross: multiple well-circumscribed round nodules — "cannonball" pattern
  • Lepidic growth pattern favours primary lung adenocarcinoma over metastasis
  • Napsin-A positive in primary lung adenocarcinoma — used alongside TTF-1 to confirm primary lung origin vs a metastasis
  • TTF-1 negative in metastatic adenocarcinoma except thyroid primary (thyroid metastases are TTF-1 positive)
  • Malignant (metastatic) pleural effusion cytology shows a dual cell population — clustered malignant carcinoma cells alongside benign reactive mesothelial cells (distinguishes from mesothelioma)
Mng
  • Address underlying primary
Special
  • Cannonball pattern = pathognomonic metastatic gross morphology
  • Bilateral multiple peripheral nodules + extra-pulmonary primary history → secondary
physiology · background · low-yield
Epidemiology/Risk
  • Secondary (metastatic) pleural tumours are more common than primary mesothelioma
Background
  • Pleural metastases: common primaries = lung, breast, GIT, ovary; spread via lymphatics; usually adenocarcinoma; produce fibrous adhesions + malignant exudative effusion

Pleural

4 entries
19

Pleural Effusion

C/P
  • Pleural space normally has thin film for lubrication
  • Progressive dyspnoea, dull side-pain, dry cough
  • Reduced expansion, stony dullness, ↓ breath sounds, ↓ vocal resonance, tracheal/mediastinal shift away (massive)
  • Pleuritic chest pain → PE or inflammatory pleural process; constant dull-aching pain → chest-wall invasion by bronchogenic carcinoma / malignant mesothelioma
  • Clinical signs need >300 mL fluid; mediastinal shift needs >1000 mL
Inves
  • CXR: meniscus sign (concave upper border), mediastinal pulling/shifting away, costophrenic angle obliteration
  • Lateral decubitus: 1 cm layering = significant
  • US: highly sensitive
  • Light's criteria for exudate (any one): protein ratio >0.5; LDH ratio >0.6; LDH >2/3 ULN serum
  • Transudate: heart failure, cirrhosis, hypoalbuminaemia, nephrotic syndrome
  • Exudate: infection, malignancy, TB (high ADA), PE, autoimmune
  • Pleural fluid analysis: gross, chemistry (Light's, glucose, pH, ADA), differential cell count
  • ADA >70 IU/L highly suggestive TB; <40 excludes
  • Encysted (loculated); hydropneumothorax (air-fluid level)
  • Minimal detectable volume: upright PA ≈200–300 mL vs lateral decubitus ≈75–100 mL (far more sensitive; 1 cm layering ≈ >200 mL)
  • Transudate causes also include constrictive pericarditis and SVC syndrome (alongside heart failure, cirrhosis, hypoalbuminaemia, nephrotic syndrome)
  • Exudate causes also include pancreatitis, trauma, oesophageal perforation, asbestos exposure, radiation pleuritis, drugs
  • Pleural fluid protein >2.9 g/dL = exudate; triglyceride >110 mg/dL = chylothorax
  • Pleural biopsy techniques: closed-needle biopsy, medical thoracoscopy, open biopsy (thoracotomy)
  • Differential count: lymphocytes >85% → TB / lymphoma; eosinophils >10% → air or blood in space, PE with infarction, parasites (paragonimiasis), drugs; WBC <1000 transudate vs >1000 exudate
Mng
  • Thoracentesis (contraindications + complications: bleeding, pneumothorax, infection)
  • Treat underlying cause
  • Drainage for symptomatic / large effusion
  • Pleurodesis for recurrent malignant effusion
  • Thoracentesis: remove max 1–1.5 L per session to avoid re-expansion pulmonary oedema; enter above the upper border of the lower rib (spares the neurovascular bundle)
  • Indwelling tunnelled (pig-tail) catheter into a negative-pressure one-way-valve bottle for recurrent effusion
Special
  • Light's criteria = exudate gate
  • Pleural fluid ADA + lymphocyte/neutrophil >0.75 → TB highly suggestive
  • Meniscus sign on CXR
  • Malignant pleural effusion = exudate, often haemorrhagic
  • Pleural transudate from SVC compression by lung tumour
  • Mediastinal shift toward the effusion = obstructive lobar collapse from an endobronchial lesion (malignancy / foreign body) pulling the mediastinum — vs shift away when fluid pushes it
  • Malignant pleural effusion: massive, rapidly accumulating, haemorrhagic, and shifts the mediastinum to the same side (associated collapse)
physiology · background · low-yield
Physiology
  • Normal pleural fluid 1–15 mL (~0.2 mL/kg), maintained by balance of hydrostatic/oncotic forces (visceral + parietal pleural vessels) and lymphatic drainage; effusion = disruption of this balance
Microbiology
  • Bacterial culture & sensitivity positive in only ~60% of infected pleural fluid
Exam technique
  • Thoracentesis absolute contraindications: bleeding disorder / anticoagulation, mechanical ventilation, cutaneous disease over the puncture site; also avoid if <1 cm on lateral decubitus film; stop immediately if the patient coughs
  • Thoracentesis technique: patient sits upright, puncture 2 interspaces below the level of dullness (US/CT-guided), betadine + 1% lidocaine to skin→periosteum→parietal pleura, confirm with a 25-G needle, post-procedure expiratory CXR to exclude pneumothorax
20

Empyema

C/P
  • Infected pleural fluid (gross D-shape on test tubes)
  • Fever, pleuritic chest pain, systemic toxicity, productive cough
  • Often complicates parapneumonic effusion
Inves
  • Pleural fluid: pus, low pH, low glucose, high LDH
  • Loculations on imaging
  • Fluid thresholds: pH <7.2, glucose <30 mg/dL, LDH >1000 IU/L
Mng
  • Drainage (intercostal tube) + targeted antibiotics
  • Decortication if chronic
  • Add Clindamycin if aspiration / lung abscess context
  • Drain with a large-bore intercostal tube (20 French) — pus is too thick for a small drain
  • Always drain the pus regardless of contraindications
Special
  • D-shaped gross appearance
  • Parapneumonic effusion → empyema when fluid infected
  • Pleural fluid analysis confirms (gross pus)
  • Pyothorax = synonym for empyema
physiology · background · low-yield
Mechanism
  • Chronic empyema treated by decortication (removing thickened pleura so the lung can re-expand)
21

Haemothorax

C/P
  • Blood in pleural space
  • Dyspnoea, chest pain, haemodynamic instability if massive
  • Reduced breath sounds, dullness on affected side
  • Trauma + iatrogenic + malignancy + ruptured vessel
  • Causes: chest trauma (usually blunt), iatrogenic (cardiac surgery, chest-drain or central venous catheter insertion — commonest iatrogenic cause), spontaneous (rare, even in clotting disorders)
Inves
  • Erect CXR: blunted costophrenic angle, opacity with fluid level
  • US sensitive
  • Pleural fluid aspirate confirms blood
  • Defining criterion: pleural fluid haematocrit >50% of peripheral haematocrit (needle aspiration confirms blood)
  • Serial erect CXR every ~20 min to detect an enlarging haemothorax
Mng
  • Intercostal drain
  • Massive haemothorax → urgent thoracotomy
  • Treat haemodynamic compromise
  • Resuscitate concurrently: cross-match blood for urgent transfusion + correct coagulopathy (FFP / platelets)
  • Insert a large-bore chest drain (large bore avoids the tube clotting)
  • Refer to thoracic surgery if drainage >1000 mL immediately or >200 mL/h for 3 h
Special
  • Erect CXR is the classic image
  • Surgical drainage threshold based on initial volume + rate
22

Pneumothorax (spontaneous + tension)

C/P
  • Air in pleural space
  • Sudden chest pain, dyspnoea, hyperresonance, ↓ breath sounds, ↓ tactile fremitus
  • Tension pneumothorax: hypotension, tachycardia, tracheal deviation AWAY, distended neck veins, severe distress — emergency
  • Classification: spontaneous (primary tall young men, secondary underlying lung disease — COPD bulla rupture) vs traumatic vs iatrogenic
  • Secondary spontaneous PTX underlying lung disease also includes asthma and cystic fibrosis (not only COPD)
Inves
  • Erect CXR: visceral pleural line, absent lung markings beyond
  • Tension: contralateral mediastinal shift, diaphragm depression
  • ABG: hypoxia
  • Don't delay imaging if tension is clinically obvious
  • CT chest = most sensitive modality; thoracic ultrasound also used (operator-dependent)
  • Tension CXR also: hyperlucent hemithorax devoid of lung markings, widened intercostal spaces
Mng
  • Spontaneous primary: small + asymptomatic → observe; symptomatic → aspiration or intercostal tube
  • Spontaneous secondary: admit + intercostal tube (low threshold)
  • Tension: emergency needle decompression (2nd intercostal space, midclavicular line) → intercostal tube
  • Persistent air leak → surgery (pleurodesis, bullectomy)
  • Primary spontaneous: size >2cm and/or breathless → aspirate (16-18G cannula, <2.5L); if <2cm + not breathless → discharge + OPD review 2-4 weeks; aspiration fails → chest drain (8-14Fr) + admit
  • Secondary spontaneous: >2cm or breathless → chest drain + admit; 1-2cm → aspirate (16-18G, fails → chest drain); <1cm → admit, high-flow O₂, observe 24h
Special
  • Tension pneumothorax = clinical diagnosis, treat before CXR
  • Trachea deviation AWAY (vs collapse where it deviates TOWARD)
  • Pneumothorax = complication of COPD (bulla rupture)
  • Secondary spontaneous PTX also in connective-tissue disease — Marfan & Ehlers-Danlos syndrome
physiology · background · low-yield
Mechanism
  • Closed (pleural pressure < atmospheric; air from lung, intact skin), open (= atmospheric; air from chest-wall wound e.g. bone fragment), tension (> atmospheric) — pathophysiological classification
  • Tension = one-way valve: air enters on inspiration (valve open) but cannot escape on expiration (valve closed)
  • Tension physiology: compression of venae cavae (↓ venous return → obstructive shock), aorta, heart and contralateral lung; diaphragm pushed down
  • Needle decompression causes an immediate rush of air converting tension pneumothorax into a simple pneumothorax
Other
  • In ventilated patients, tension shows increasing airway pressures and difficulty to ventilate
Background
  • Primary-vs-secondary triage questions: age >50, smoking history, evidence of underlying lung disease on exam/CXR

Vascular / Emergency

3 entries
23

Pulmonary Embolism

C/P
  • Virchow's triad: stasis + endothelial injury + hypercoagulability
  • Risk factors: surgery, immobility, malignancy, OCP/HRT, pregnancy, thrombophilia, prior VTE
  • Non-thrombotic: fat embolism, amniotic fluid
  • Sudden dyspnoea, pleuritic chest pain, haemoptysis, syncope
  • Tachypnoea, tachycardia, hypoxia; signs of DVT
  • Massive PE: shock, hypotension, RV strain, cardiac arrest
  • Life-threatening distress signs in respiratory emergencies
  • Non-thrombotic emboli (6): fat (fracture), amniotic fluid (pregnancy), tumour, septic (right-sided endocarditis), particulate (IV injection), gas/air (central venous cannulation, surgery)
  • Medium-to-large PE also shows: pyrexia, raised JVP, pleural effusion (often blood-stained)
Inves
  • ABG: hypoxia + hypocapnia (respiratory alkalosis)
  • ECG: sinus tachycardia most common; S1Q3T3, RV strain
  • CXR: often normal; 4 eponymous signs — Hampton's hump (peripheral wedge opacity = infarct), Westermark's (regional oligaemia), Fleischner sign (enlarged pulmonary artery), Palla's sign (enlarged right descending pulmonary artery)
  • CTPA = imaging gold standard: filling defect, infarction
  • Revised Geneva score for clinical probability
  • Simplified PESI for risk stratification of early death
  • V/Q scan if CTPA contraindicated
  • ECG also: P pulmonale, RBBB (rSR' in V1–V3, wide slurred S in lateral leads), right axis deviation
  • Revised Geneva criteria (8; stable patients, 6 history + 2 exam, OSPE): previous PE/DVT, HR 75–94 (1pt) / ≥95 (2pt), surgery or fracture within 1 month, haemoptysis, active cancer, unilateral lower-limb pain, pain on deep venous palpation + unilateral oedema, age >65 — score 0–2 = PE-unlikely, ≥3 = PE-likely
  • D-dimer: good negative test — normal excludes PE when clinical probability low/intermediate; not diagnostic if raised (also ↑ in cancer, hospitalised, severe infection, inflammatory disease, pregnancy). High probability → straight to CTPA
  • Compression ultrasound for suspected DVT — incomplete compressibility of the vein is the only validated diagnostic criterion
  • Cardiac biomarkers: elevated troponin (+ BNP / pro-BNP) mark RV strain and drive early-death risk stratification
Mng
  • Haemodynamic instability: hemodynamic support + reperfusion (systemic thrombolysis)
  • Without instability: initial anticoagulation (LMWH, fondaparinux) → Apixaban / Rivaroxaban / Edoxaban / Dabigatran / Warfarin
  • Vena cava filter if anticoagulation contraindicated
  • Discharge algorithm based on PESI
  • Risk-stratify by PESI + RV dysfunction
  • Haemodynamic instability = too unstable for CT → bedside TTE for RV strain; if RV dysfunction + CTPA feasible → CTPA, otherwise treat high-risk PE directly
  • Haemodynamic support: cautious fluid loading (saline ≤500 ml) — avoid over-filling the failing RV; vasopressor norepinephrine + inotrope dobutamine; ECMO if refractory
  • Reperfusion: systemic fibrinolysis (rtPA, streptokinase, urokinase); if contraindicated → catheter-directed therapy (femoral: fragmentation, aspiration, pharmacomechanical) or surgical embolectomy
  • Absolute contraindications to thrombolysis: stroke, CNS tumour, major trauma/surgery/head injury within 3 weeks, bleeding diathesis, active bleeding
  • Anticoagulation (all PE patients): parenteral = LMWH / fondaparinux / IV UFH; warfarin must be bridged with parenteral A/C ≥5 days until INR 2–3; NOACs — dabigatran (thrombin inhibitor) vs apixaban / edoxaban / rivaroxaban (factor Xa); rivaroxaban needs no heparin bridging
  • IVC filter also indicated for recurrent PE despite adequate anticoagulation and primary prophylaxis in very high VTE risk
Special
  • Hampton's hump = peripheral wedge-shaped infarct
  • Westermark sign = oligaemia distal to occlusion
  • Revised Geneva score (deck uses Geneva, not Wells)
  • PESI for mortality prediction
  • Sinus tachycardia most common ECG (S1Q3T3 classic but less common)
physiology · background · low-yield
Epidemiology/Risk
  • Strong risk factors specifically: recent hospitalisation (within 3 months) for HF/AF/MI, previous VTE, major trauma, spinal cord injury, lower-limb fracture, hip/knee replacement
Other
  • Non-eponymous CXR findings: pulmonary opacities (any size/shape, can cavitate), horizontal linear opacities (bilateral, lower zones), pleural effusion (blood-stained), elevated hemidiaphragm — last two clinically observable at bedside
  • Imaging-modality choice: CTPA for segmental/sub-segmental emboli, V/Q scan for smaller (sub-subsegmental); V/Q preferred in low probability + normal CXR, young/pregnant women, contrast anaphylaxis, severe renal failure
  • sPESI applied post-CTPA in haemodynamically stable patients (unstable = automatically high risk); 30-day mortality: 0 points ≈ 1.0%, ≥1 point ≈ 10.9%
  • ESC 4-tier early-death risk: High (haemodynamic instability), Intermediate-high (RV dysfunction + positive troponin), Intermediate-low (RV dysfunction with negative troponin), Low
  • Early discharge / home treatment requires: low risk + no other reason for hospitalisation + family/social support + easy access to medical care
  • O2 therapy FiO2 0.6–1.0 (target SaO2 93–98%); after giving a thrombolytic in cardiac arrest continue CPR 60–90 min before stopping
Background
  • Pulmonary angiography = historical gold standard; now rarely used (invasive, highest radiation, not widely available)
24

ARDS

C/P
  • Acute hypoxaemic respiratory failure with bilateral infiltrates not explained by cardiac cause
  • Sudden severe dyspnoea, hypoxia refractory to O₂
  • Causes: pulmonary (pneumonia, aspiration, inhalation, contusion) + extrapulmonary (sepsis, trauma, transfusion, pancreatitis, burns)
  • Phases: exudative → proliferative → fibrotic
  • Pathophysiology: alveolar-capillary membrane damage → protein-rich exudate → hyaline membranes → impaired gas exchange
  • Sepsis = most common cause overall; core mechanism = exaggerated inflammatory response (diffuse alveolar damage) after a major insult
Inves
  • Berlin definition: acute onset, bilateral opacities, not cardiogenic, P:F with PEEP ≥5
  • Severity by P:F: mild >200, moderate 100–200, severe ≤100
  • CXR + CT: bilateral infiltrates, ground-glass, consolidation
  • ABG: severe hypoxia
  • PCWP <18 mmHg (objective assessment via echo) — excludes cardiogenic / left-heart-failure oedema; PCWP represents left atrial pressure
  • Distinguished from cardiogenic oedema on imaging: no cardiomegaly and no prominent upper-lobe vessel engorgement
Mng
  • Mechanical ventilation (low tidal volume, PEEP)
  • Treat underlying cause
  • ECMO in severe refractory cases
  • Lung-protective ventilation: tidal volume 6 mL/kg predicted body weight, plateau pressure ≤30 cmH₂O, permissive hypercapnia (pH ≥7.25)
  • Refractory hypoxaemia (P:F ≤150): sedate and prone, neuromuscular blockade (paralysis when fighting the ventilator), lung recruitment manoeuvres
  • High-dose steroids (early)
  • Inhaled pulmonary vasodilators (nitric oxide, epoprostenol); neutral/conservative fluid balance
Special
  • Berlin definition distinguishes ARDS (non-cardiogenic pulmonary oedema) from heart failure
  • P:F ratio defines severity
  • Hyaline membranes histological hallmark
  • Phases: exudative → proliferative → fibrotic
  • Bat-wing (perihilar bilateral) opacities = raised left-atrial-pressure cardiogenic oedema pattern — the cardiogenic contrast to ARDS's more peripheral infiltrates
physiology · background · low-yield
Mechanism
  • Exudative phase (first 7 days): neutrophil aggregation & activation, injury to type I pneumocytes + capillary endothelium → increased permeability → interstitial oedema; most patients recover here
  • Proliferative phase (after 7 days): type II pneumocytes proliferate and differentiate into type I cells; oedema fluid resorbed via lymphatics; ventilation may no longer be needed
  • Fibrotic phase (very few patients): fibroblast proliferation → intra-alveolar, interstitial, capillary and lymphatic fibrosis → pulmonary hypertension, poor prognosis, ventilator dependence
  • Both direct and indirect injuries converge via a cytokine storm that damages the alveolar-capillary membrane
Epidemiology/Risk
  • Mortality rises with severity: mild 27%, moderate 32%, severe 45% (all grades require PEEP ≥5 cmH₂O)
Other
  • Oxygenation targets: PaO₂ 55–80 mmHg or SpO₂ 88–95%; if stable and tolerating with P:F >200, continue noninvasive (NIPPV / HFNC)
25

Atelectasis

C/P
  • Collapse of lung tissue
  • Macro vs micro
  • Massive postoperative collapse — postop complication
  • Dyspnoea, ↓ breath sounds, dullness, tracheal/mediastinal shift TOWARD affected side
  • Clinical picture varies with extent and rate of collapse
  • 5 types by mechanism: obstructive/absorption (FB, tumour, blood clot, mucous plug, misplaced ET tube), compressive (intrapulmonary lesion compresses lung), relaxation (extrapulmonary — loss of Pp–Vp contact: pleural effusion, pneumothorax), cicatricial (severe scarring/fibrosis — post-TB, asbestosis; irreversible), adhesive (lack of surfactant — ARDS)
  • Massive postop collapse — presentation: acute chest pain, severe dyspnoea & cyanosis, acute RVF, shock — mimics massive MI, massive PE, tension pneumothorax
  • Complications: prone to infection, abscess formation, bronchiectasis, failure of re-expansion after treatment, respiratory failure in massive collapse
Inves
  • CXR: opacity + volume loss (mediastinal shift toward, elevated hemidiaphragm, crowded ribs)
  • Lobar-collapse eponymous signs — Sail sign (LLL collapse: triangular retrocardiac opacity, apex to hilum, base on diaphragm); Luftsichel sign (LUL collapse: crescent of air / "air crescent" from the hyperinflated LLL superior segment interposing between mediastinum & collapsed LUL)
Mng
  • Chest physiotherapy, deep breathing, mobilization
  • Treat obstruction (bronchoscopy if foreign body / mucus plug)
  • Address postop pain to enable deep breathing
  • Treat the cause; O2 therapy, bronchodilators, antibiotics for infection
Special
  • Mediastinal shift TOWARD side = atelectasis (vs away = pneumothorax/effusion)
  • Postop hypoxia + ↓ breath sounds at base → atelectasis until proven otherwise
  • Round atelectasis = pseudotumour in asbestos-related disease
  • Patent-bronchus exception: if the collapsed lobe stays connected to a patent bronchus → BRONCHIAL breathing + INCREASED VR (opposite of the usual diminished VR / absent breath sounds)
physiology · background · low-yield
Physiology
  • Pathophysiological cascade: ↓ lung compliance → ↑ airway pressures → ↑ work of breathing → ↓ tidal volume → poor gas exchange (shunt) → ↓ PaO2; if severe, circulatory collapse
Background
  • Macroatelectasis: evident volume loss on CXR. Microatelectasis: CXR may be normal, due to inadequate depth of respiration
  • Obstructive causes of massive postop collapse: aspiration of vomitus (full stomach), lack of preanaesthetic medication, anaesthetic irritation (esp. chronic bronchitis), neglected postop aspiration of secretions, inability to cough (chest pain), inadequate chest expansion (pain / restrictive bands)
  • Lobar collapse patterns: RUL, RLL, LLL, LUL collapse
Exam technique
  • Syndrome of multiple negatives (all give ↓ VR / ↓ breath sounds / dullness): pleural effusion, lung fibrosis, lung collapse
Other
  • Handwritten margin — conditions causing sudden dyspnoea: massive PE, tension pneumothorax, lung collapse, MI

Approach · PFT · Pharmacology

3 entries
26

Respiratory Symptoms & Examination (approach)

C/P
  • Cough by duration: acute <3 wk (acute bronchitis, pneumonia, PE) · subacute 3–8 wk (post-infectious, asthma exacerbation) · chronic >8 wk (ILD, COPD)
  • Cough by nature: dry (pleurisy, laryngeal cancer, early URI) vs productive (lung abscess, COPD exacerbation, pulmonary oedema)
  • Dyspnoea by onset: sudden/minutes → PE, pneumothorax, inhaled foreign body, MI · hours–days → pneumonia, asthma/COPD exacerbation, CHF · weeks–months → ILD
  • Orthopnoea (relieved by sitting up) most often LVF; PND ~2 h after sleep = cardiac; early-morning waking/wheeze = asthma; waking + clearing sputum = COPD
  • Haemoptysis — Big 4 in practice: malignancy, TB, PE, bronchiectasis
  • Chest pain: pleuritic = sharp/stabbing, worse on inspiration/cough, localized; cardiac = retrosternal crushing radiating to neck/left arm, relieved by rest/GTN
  • Wheeze aetiology: upper airway (post-nasal drip, vocal-cord dysfunction, angioedema, foreign body, tracheal tumour) vs lower airway (asthma, COPD, bronchiectasis, aspiration, heart failure = "cardiac asthma", bronchogenic carcinoma)
  • General exam: central cyanosis (tongue + lips) when SaO₂ <85% (PaO₂ ~60 mmHg / 8 kPa); asterixis = Type II respiratory failure (CO₂ retention); clubbing stages 1 loss of nail-bed angle → 2 parrot-beak → 3 drumstick → 4 hypertrophic osteoarthropathy
Inves
  • True vs false haemoptysis: haemoptysis = blood from below vocal cords; hematemesis = blood mixed with food particles + melena; exclude nose/mouth/pharynx/larynx bleeding (above cords)
  • Percussion notes: hyperresonance = pneumothorax · impaired = fibrosis · dull = consolidation/mass/collapse · stony dull = effusion
  • Auscultation localizers: bronchial breathing (3 C's) = consolidation / collapse with patent bronchus / cavity; increased vocal resonance confirms these; decreased VR = pneumothorax / emphysema / effusion
  • Crackles: coarse early/mid-inspiratory = pulmonary oedema, bronchiectasis, lung abscess; fine late-inspiratory (Velcro) = ILD, LVF, pneumonia
Mng
  • Massive haemoptysis = >150 mL/attack; kills by suffocation (blood floods bronchial tree), not exsanguination. Mng: IV fluids/blood, cough suppressants, bronchoscopy — blood aspiration, balloon tamponade, bronchial artery embolization
Special
  • Chest pain "big 6" emergencies (sudden + severe): MI, aortic dissection, PE, tension pneumothorax, acute mediastinitis, perforated viscus
  • Stridor = high-pitched, mainly inspiratory, extra-thoracic obstruction (supraglottis/glottis/trachea), audible without stethoscope; rhonchi = low-pitched snoring, large-airway secretions → COPD / bronchiectasis
  • Rule: all wheeze = obstruction but not all wheeze = asthma; intra-thoracic obstruction limits expiration, extra-thoracic obstruction limits inspiration
  • Tracheal deviation: AWAY = tension pneumothorax / massive effusion; TOWARD = upper-lobe collapse or fibrosis, lobectomy
  • Named signs: Litten's (inspiratory indrawing of lower intercostal spaces, diaphragm descent) · Trail's (unilateral sternomastoid bulge from tracheal shift) · D'Espine (bronchial breath sounds over spine at T2 = mediastinal mass)
physiology · background · low-yield
Physiology
  • Cough = protective reflex; intrathoracic receptors (sinuses, nose, larynx/pharynx, trachea, bronchial tree, bronchioles/alveoli, pleura/diaphragm/mediastinum) + extrathoracic (brain/meninges, ear, mouth, stomach)
  • Visceral pleura & lung parenchyma are insensitive to pain — chest pain arises only when parietal pleura, chest wall, or mediastinum is involved
Background
  • GERD — very common cause of chronic cough that mimics asthma; worse supine / after meals, with heartburn, bitter taste, dysphonia
  • Psychogenic cough — young female, barking, triggered in front of an audience; diagnosis of exclusion (rule out all organic causes)
Mechanism
  • ACE-inhibitor cough — dry, ~10% of users, onset 3–6 months, commoner in women (bradykinin accumulation)
  • Cough complications from high intrathoracic pressure — cough syncope, rib fracture, pneumothorax, subconjunctival/retinal haemorrhage, stress incontinence
Exam technique
  • Kronig's isthmus = lung apices; dullness → apical TB/fibrosis, Pancoast tumour, apical abscess/effusion
  • Traub's area (gastric fundus / left pleura) — dullness = splenomegaly, left pleural effusion, full stomach, left hepatic-lobe enlargement
  • Raised JVP causes — cor pulmonale, SVC compression (lung cancer / lymphoma / thymoma), tension pneumothorax, massive PE
  • Vesicular breathing (soft rustling, I:E 3:1, no pause) vs bronchial breathing (hollow, I = E, pause between phases)
  • Tar staining (from tar, not nicotine) on fingers/nails = marker of cigarette smoking
Other
  • Drugs with respiratory side-effects — β-blockers → bronchospasm; ACE inhibitors → cough; amiodarone / methotrexate → lung fibrosis; oestrogen (OCP/HRT) → PE risk
27

Spirometry & PFT interpretation

Inves
  • Step 1 — FEV1/FVC ratio: if < lower limit of normal (or <0.7) = obstructive; if normal but FVC < lower limit = restrictive
  • Quantify obstruction by FEV1 %predicted; quantify restriction by FVC %predicted (or TLC if known)
  • Bronchodilator reversibility positive if FEV1 ↑ >12% AND >200 mL
  • DLCO subtyping — obstruction: low DLCO = emphysema, normal/high DLCO = asthma; restriction: low DLCO = ILD, normal DLCO = neuromuscular / chest-wall disease
  • Normal ranges: FEV1 80–120%, FVC 80–120%, TLC 80–120%, RV 75–120%, DLCO >60–<120%
  • Obstructive vs restrictive: obstructive = ↓FEV1/FVC, ↓FEV1, ↓FEF25–75, FVC normal/↓, TLC normal/↑; restrictive = normal FEV1/FVC, FEV1 normal/↓, ↓FVC, ↓TLC
  • TLC measured in a PFT lab = gold standard to confirm restriction; spirometry cannot measure RV, FRC or TLC (needs helium dilution or body plethysmography)
Special
  • Reduced DLCO (5): ILD, pneumonectomy, emphysema, anaemia, V/Q mismatch. Increased DLCO (2): pulmonary haemorrhage (Goodpasture's), polycythaemia
  • Flow-volume loops: obstruction (COPD) = scooped-out expiratory limb; restriction (fibrosis) = tall, narrow, short expiratory phase; variable extra-thoracic upper-airway obstruction (goitre / tracheal compression) = limited/flattened inspiratory loop
  • Air-trapping = ↑ RV; hyperinflation defined as TLC >120% predicted
  • Volume–time curve: obstructive = slow rise, no early plateau; restrictive = fast rise, early plateau at a lower volume
  • Asthma trap: spirometry & lung volumes often entirely normal between episodes — diagnosis rests on episodic history + reversibility
physiology · background · low-yield
Physiology
  • Lung volumes/capacities: TV, IRV, ERV, RV; VC = IRV+ERV+VT, FRC = ERV+RV, IC = VT+IRV, TLC = VC+RV; expressed in litres at BTPS
  • Efficiency of gas exchange (in alveolar air sacs) depends on ventilation, perfusion and diffusion
  • DLCO/TLCO test: single-breath-hold technique; CO used (same diffusion as O₂ but higher Hb affinity); He measures alveolar volume (VA) available; gas mix 0.3% CO, 14% He, 18% O₂, balance N₂; KCO = TLCO/AV
Background
  • Spirometer types: volume-displacing (large, bulky) vs flow-sensing (smaller, portable — integrates flow to volume)
  • Static lung volumes: helium dilution measures only ventilated lung (FRC); body plethysmography measures total thoracic gas incl. non-ventilated areas (TGV)
  • Spirometry uses: dyspnoea work-up, pre-op assessment, monitoring over time, occupational/environmental exposure, disability evaluation, therapeutic response
Exam technique
  • Pre-test rules: no bronchodilator, no smoking ≥1 h, no heavy exercise ≤30 min, no heavy meals ≤2 h, avoid tight clothing
  • Predictive equations need gender, height, weight, age (±race); predicted range = the values within which 90% of the population falls
  • Technique/acceptability: effort-dependent; min 3–max 8 efforts, take best FVC/FEV1/PEF; min exhalation 6 s; reproducible within 5% / 100 mL (FVC & FEV1 within 0.150 L)
28

Respiratory Pharmacology — Antibiotic Classes

Mng
  • Penicillins (4 groups by PK/activity): Natural (Pen G IV/IM, Pen V) — Strep pneumoniae, Enterococci, syphilis (Pen G for neurosyphilis), Bacteroides; Anti-staphylococcal (Nafcillin, Oxacillin, Dicloxacillin) — MSSA (endocarditis, skin/soft-tissue), NO GNR/anaerobe/MRSA; Anti-pseudomonal (Piperacillin, Ticarcillin) — Pseudomonas, E. coli, Klebsiella; Amino-penicillins (Amoxicillin, Ampicillin) — Strep/Enterococci + URTIs (strep pharyngitis, otitis media)
  • β-lactamase inhibitor combos: Sulbactam+Ampicillin, Clavulanate+Amoxicillin/Ticarcillin, Tazobactam+Piperacillin — cover MSSA, anaerobes, enteric GNR; do NOT cover MRSA or ESBL producers
  • Cephalosporins (5 generations): 1st Cefazolin (GP/MSSA, no BBB), 2nd Cefuroxime (extended GN, no BBB), 3rd Ceftriaxone/Ceftazidime (cross BBB; Ceftazidime = only 3rd-gen covering Pseudomonas), 4th Cefepime (Pseudomonas, crosses BBB), 5th Ceftaroline = only β-lactam covering MRSA
  • Carbapenems (Imipenem/cilastatin 500 mg/6h, Meropenem 1 g/8h, Ertapenem 1 g/24h; oral Tebipenem): broadest spectrum — ESBL GNR, anaerobes, Pseudomonas; do NOT cover MRSA
  • Monobactam — Aztreonam: Gram-negative only (Pseudomonas, Acinetobacter); IV/IM/inhaled (inhaled for cystic bronchiectasis); not oral (acid-labile); safe in penicillin allergy
  • Aminoglycosides (Amikacin/Streptomycin/Kanamycin 15 mg/kg/day; Tobramycin inhaled only): Gram-negatives + Pseudomonas + MDR-TB; no GP/anaerobe/atypical/MRSA cover
  • Macrolides (Azithromycin 250–500 mg/day, Clarithromycin 500 mg q12h, Erythromycin): atypicals + NTM (M. avium complex); URTIs + pneumonia
  • Fluoroquinolones: Ciprofloxacin (2nd gen, best anti-Pseudomonal), Levofloxacin 500–750 mg/day (3rd, “respiratory FQ” — Strep pneumoniae), Moxifloxacin 400 mg/day (4th — adds anaerobes + TB)
  • Glycopeptide — Vancomycin: covers MRSA + MSSA; NO Gram-negative/anaerobe/Pseudomonas activity
Special
  • Only 2 agents cover MRSA: Vancomycin (glycopeptide) + Ceftaroline (5th-gen cephalosporin)
  • Anti-Pseudomonal agents: Piperacillin/Ticarcillin (± tazobactam/clavulanate), carbapenems, Aztreonam, Ceftazidime (3rd), Cefepime (4th), Levofloxacin, Amikacin
  • Vancomycin Red Man Syndrome: flushing of face/neck, pruritus, hypotension on FIRST dose or too-fast infusion (histamine-mediated, not allergy) — prevent by infusing over ≥1 h, treat with Benadryl. Toxicity mnemonic “A TON” = Thrombophlebitis, Ototoxicity, Nephrotoxicity
  • Aminoglycoside toxicity: ototoxicity (vestibular + cochlear), nephrotoxicity, neuromuscular blockade — monitor with audiometry
  • Fluoroquinolones: QT prolongation + growing-cartilage damage → contraindicated in patients <18 years (and pregnancy)
  • Macrolides: QT prolongation / arrhythmia + GI upset
  • Imipenem uniquely causes nephrotoxicity + seizures
  • Giving two β-lactams together is NOT useful (compete for the same penicillin-binding proteins)
physiology · background · low-yield
Microbiology
  • Gram classification: GP cocci (S. aureus/MSSA, S. pneumoniae, Enterococci); GP rods (Clostridia, Bacillus anthracis, Corynebacterium diphtheriae); GN cocci (Moraxella, N. meningitidis, N. gonorrhoeae); GN rods (E. coli, Legionella, Pseudomonas, Klebsiella, Acinetobacter, Haemophilus); anaerobes (Bacteroides); atypicals (Mycoplasma, Chlamydia, Legionella)
  • ESBL = extended-spectrum β-lactamases conferring resistance to most penicillins, cephalosporins and the monobactam; produced by Klebsiella & E. coli (covered by carbapenems, not by β-lactam/inhibitor combos)
Mechanism
  • Antimicrobial targets: cell wall (β-lactams, Vancomycin, Bacitracin); 30S ribosome (tetracyclines, aminoglycosides); 50S ribosome (macrolides, clindamycin, linezolid, chloramphenicol, streptogramins); DNA gyrase (quinolones); RNA polymerase (rifampin); folate synthesis (sulfonamides, trimethoprim); cell membrane (polymyxins)
Background
  • Antibiotics covering MSSA: anti-staphylococcal penicillins, β-lactam/β-lactamase inhibitor combos, 1st-generation and 5th-generation cephalosporins

Asthma

4 entries
1

GINA 2025 — Asthma definition

  • Chronic airway inflammation
  • Variable chest symptoms (cough, SOB, wheeze, chest tightness)
  • Variable expiratory airflow limitation
  • Asthma = variable; COPD = persistent
2

Asthma diagnostic criteria

Required: clinical variable symptoms + physiological test of variable airway obstruction.

TestThreshold
Pre-BD FEV1/FVC<80%
Pre-BD FEV1 % predicted<80%
Reversibility post Salbutamol 200–400 mcg (wait 10–15 min)FEV1 ↑ ≥200 mL AND ≥12%
PEF diurnal variability>10%
Bronchial challenge (histamine / methacholine)Fall in FEV1 ≥20%
FeNOIncreased
Blood / sputum eosinophilsIncreased

PEF formula: ((highest PEF − lowest PEF) / mean) × 100

3

Acute exacerbation — life-threatening signs

  • Confusion
  • Hypotension
  • RR >30
  • SpO₂ <90%
  • Silent chest
4

GINA discharge criteria

  • SpO₂ >94% on room air
  • PFT >60–80% predicted
  • Step-up drugs + follow-up 1–2 wk

COPD

6 entries
5

COPD definition (GOLD 2025)

Heterogeneous lung condition + chronic respiratory symptoms (dyspnoea, cough, sputum) + airway and/or alveolar abnormalities → persistent often progressive airflow obstruction.

Diagnosis = clinical presentation + spirometry showing post-BD FEV1/FVC <70%.

6

GOLD severity grades (1–4)

Based on post-BD FEV1 % predicted:

GradeFEV1 % predicted
GOLD 1 (Mild)≥80%
GOLD 2 (Moderate)50 ≤ FEV1 < 80%
GOLD 3 (Severe)30 ≤ FEV1 < 50%
GOLD 4 (Very Severe)<30%

FEV1 <50% = threshold to start Roflumilast.

7

GOLD groups (A / B / E)

GroupExacerbations / hospSymptoms
A0–1 moderate (no hosp)mMRC 0–1 OR CAT <10
B0–1 moderate (no hosp)mMRC ≥2 OR CAT ≥10
E≥2 moderate OR ≥1 hospAny

Initial therapy

  • A → single bronchodilator
  • B → LABA + LAMA
  • E → LABA + LAMA; consider triple if blood eosinophils ≥300

Single inhaler preferred.

8

mMRC dyspnoea scale

GradeDescription
0Dyspnoea only with strenuous exercise
1Dyspnoea when hurrying or walking up a slight hill
2Walks slower than peers / stops for breath on level ground
3Stops for breath after ~100 yards or a few minutes on level
4Too breathless to leave the house, breathless when dressing

mMRC ≥2 = highly symptomatic threshold (Group B or E).

9

CAT score grouping cut-off

  • <10 = less symptomatic (Group A)
  • ≥10 = more symptomatic (Group B)
10

COPD acute exacerbation definition

  • Acute worsening of symptoms over <14 days
  • Most common cause: infection

CAP

7 entries
11

IDSA/ATS severe pneumonia criteria

Severe CAP = 1 major OR 3 minor criteria

Major (need 1)

  • Septic shock requiring vasopressors
  • Respiratory failure requiring mechanical ventilation

Minor (need 3)

  • RR ≥30 b/min
  • Hypotension corrected by IV fluid
  • Hypothermia
  • Confusion / disorientation
  • Leukopenia <4,000 cells/μL
  • Thrombocytopenia <100,000/μL
  • Uremia (BUN) ≥20 mg/dL (indicates sepsis)
  • PaO₂/FiO₂ ratio ≤250
  • Multilobar infiltrates

Calculations

  • Normal PaO₂ ≈ 100 − (1/3 × age)
  • FiO₂ room air = 0.21; on 2 L O₂ = 0.29
  • Neutrophil shift LEFT = infection; RIGHT = steroids
12

CURB-65 (site of care)

ComponentThreshold
C ConfusionNew
U Urea>7 mmol/L (20 mg/dL)
R Respiratory rate>30 breaths/min
B Blood pressureSBP <90 OR DBP <60 mmHg
65 Age>65 years

Site of care

ScoreSetting
0–1Home (outpatient)
2Ward
3–5 (or Severe by IDSA/ATS)ICU

Inpatient treatment

  • Non-severe: β-lactam (+ β-lactamase inhibitor) + macrolide OR fluoroquinolone monotherapy
  • Severe: β-lactam + macrolide OR β-lactam + fluoroquinolone (NO monotherapy)
13

MAFIA PCC (anti-Pseudomonal coverage)

LetterDrugClass
MMeropenemCarbapenem
AAminoglycosides(nephrotoxic — kidneys!)
FFluoroquinolonesCiprofloxacin / Levofloxacin (NOT Moxifloxacin)
IImipenemCarbapenem
AAztreonamMonobactam
PPiperacillin-tazobactamPenicillin
CCeftazidimeCephalosporin
CCefepimeCephalosporin

Anti-MRSA: Vancomycin (red-person syndrome) / Linezolid.

14

Responsive pneumonia at 72h

All seven required:

  • Temperature ≤37.8°C
  • Heart rate ≤100 b/min
  • Respiratory rate ≤24 b/min
  • SBP ≥90 mmHg
  • SpO₂ ≥90% on room air
  • Normal mental status
  • Normal oral intake
15

Treatment duration

  • Non-severe + clinically stable: 3–4 days
  • Severe CAP OR non-severe + deteriorating: ≥5 days
  • Egypt-specific: 7 days or more

Radiological resolution lags clinical → don't reorder before 3 weeks.

OrganismRadiological resolution
Mycoplasma2–4 wk
Legionella2–6 mo
Staph3–5 mo
S. pneumoniae + shock3–5 mo
16

Corticosteroid indication

Severe CAP + at least ONE of:

  • Septic shock
  • Respiratory failure (P:F <300)
  • Rapid progression: ≤3 d between symptom onset and severe CAP presentation
17

Lobar pneumonia stages (timeline)

StageDuration
1. CongestionEarly, 1–2 days
2. Red hepatization3–4 days
3. Grey hepatization1 week
4. Resolution1–2 weeks

Tuberculosis

7 entries
18

TST positivity criteria (5 / 10 / 15 mm)

Measure induration (not erythema), perpendicular to forearm long axis, 48–72 h after intradermal 5 TU PPD.

ThresholdPatient groups
≥5 mmHIV+; recent TB contact; old healed TB on CXR; immunosuppressed (transplant, etc.)
≥10 mmRecent arrival (<5 yr) from high-prevalence; IVDU; residents/staff of high-risk settings (prisons, nursing homes, hospitals, homeless shelters); mycobacteriology lab; high-risk conditions: DM, silicosis, CKD, prolonged corticosteroids, malignancy
≥15 mmNo known risk factor

Immunocompromised TST-negative → check IGRA (anergy can mask). BCG-vaccinated TST-positive → check IGRA (false positive).

19

ADA cut-offs by fluid

FluidCut-off
CSF8 U/L → distinguishes TB meningitis from other lymphocytic causes
Ascitic>36 U/L → suggests TB
Pleural>70 IU/L → highly suggestive TB
Pleural<40 IU/L → excludes
Pleural>40 U/L + fluid/serum ratio ≥2 → TB effusion / empyema
Pleural lymphocyte/neutrophil>0.75 ↑ specificity
20

QFT-G (IGRA) vs TST

FeatureQFT-GTST
SettingIn-vitroIn-vivo
AntigensESAT-6 + CFP-10 (multiple)PPD (single)
BCG cross-reactNoYes (false positive)
SpecificityHigherLower
Visits12
Reader biasMinimalSignificant
Result time24 h48–72 h
BoostingNoneYes (2-step in immunocompromised)
ConstraintBlood processed within 12 h of drawPatient must return
21

Pulmonary TB regimen — new patient

  • Intensive (2 mo): HRZE (Isoniazid + Rifampicin + Ethambutol + Pyrazinamide)
  • Continuation (4 mo): HR (Isoniazid + Rifampicin)

Daily/daily optimal. Intermittent (3×/wk) only if DOT + NOT HIV.

22

HRZES doses (daily + 3×/wk)

DrugDaily mg/kgDaily max3×/wk mg/kg3×/wk max
Isoniazid (H)5 (4–6)300 mg10 (8–12)900 mg
Rifampicin (R)10 (8–12)600 mg10 (8–12)600 mg
Pyrazinamide (Z)25 (20–30)—35 (30–40)—
Ethambutol (E)15 (15–20)—30 (25–35)—
Streptomycin (S)15 (12–18)—15 (12–18)1000 mg

Streptomycin = only injectable first-line; rest oral.

23

TB monitoring schedule

  • Clinical: general condition, fever, appetite, side effects
  • Sputum (culture + PCR): at 2 mo + completion of therapy
  • Labs (AST, ALT, bilirubin, CBC):
    • First 2 weeks: twice weekly
    • At 1 month then monthly
24

MDR-TB definition

Resistance to both Isoniazid + Rifampicin. Non-compliant → DOT → hospital admission if DOT fails.

Pleural

1 entry
25

Light's criteria (exudate)

Exudate if any one met:

  • Pleural fluid protein / serum protein >0.5
  • Pleural fluid LDH / serum LDH >0.6
  • Pleural fluid LDH >2/3 upper limit normal serum LDH

Sarcoidosis

2 entries
26

Scadding CXR staging (I–IV)

Stages NOT progressive — they describe pattern, not time course.

StageFinding
IBilateral hilar lymphadenopathy
IIBilateral hilar adenopathy + pulmonary infiltrates
IIIPulmonary disease only (infiltrates / reticulonodular)
IVIrreversible fibrosis + honeycombing
27

BAL CD4/CD8 ratio

DiseaseCD4/CD8
Sarcoidosis≥2.5
Hypersensitivity pneumonitis<1

BAL neutrophilia → worse prognosis (sarcoid, HP, IPF).

Bronchiectasis

1 entry
28

Reid morphological classification

Three patterns of bronchiectasis (mildest → most severe):

  • Cylindrical — tubular dilation
  • Varicose — alternating dilation + constriction
  • Cystic (saccular) — balloon-like cavities

NTM

2 entries
29

Runyon classification (4 groups)

GroupGrowthPigmentSpecies
1SlowPhotochromogen (in light)M. kansasii, M. marinum, M. simiae
2SlowScotochromogen (without light)M. scrofulaceum, M. szulgai, M. gordonae
3SlowNon-photochromogenM. avium, M. intracellulare, M. ulcerans, M. haemophilum
4Fast (<7 d)—M. fortuitum, M. chelonae, M. abscessus, M. smegmatis
30

NTM pulmonary disease diagnostic criteria

ALL radiological + ONE microbiological

Radiological (all required)

  • Pulmonary symptoms
  • Cavitary or nodular lesion on CXR / HRCT
  • Exclusion of other diagnosis

Microbiological (one required)

  • Two positive sputum cultures
  • One positive bronchial wash / lavage culture
  • Lung biopsy positive for NTM with consistent histology

NTM lymphadenitis in children 1–5 yr: 80% MAC, 2nd M. scrofulaceum.

Lung Cancer

3 entries
31

Lung cancer classification (% breakdown)

Category%
All primary lung tumours95% of lung tumours overall
NSCLC85% of lung cancers
└ Squamous30% of NSCLC
└ Non-squamous70% of NSCLC
└ Adenocarcinoma90% of non-squamous
└ Large-cell10% of non-squamous
SCLC15% of lung cancers

Smoking: 80% of cases; 60× ↑ in heavy smokers; 95% of smokers have atypical bronchial mucosa cells.

32

NSCLC TNM staging

  • T (primary tumour): T1–T4 by size + local invasion
  • N (regional lymph node): N0–N3 by node location/extent
  • M (distant metastasis): M0 / M1
  • Common metastasis sites: liver, brain, bone, adrenal
33

SCLC staging (limited vs extensive)

  • Limited: confined to one hemithorax, treatable with single radiation port
  • Extensive: outside that field

Vascular / Emergency

4 entries
34

Berlin definition — ARDS

Distinguishes ARDS (non-cardiogenic pulmonary oedema) from heart failure.

ElementCriterion
TimingAcute onset within 1 week of known insult
Chest imagingBilateral opacities not fully explained by effusion / collapse / nodules
OriginNot fully explained by cardiac failure / fluid overload
OxygenationPaO₂/FiO₂ with PEEP ≥5 cmH₂O

Severity

SeverityPaO₂/FiO₂
Mild>200
Moderate100–200
Severe≤100
35

Revised Geneva score (PE)

Used for clinical probability of PE. Guides next step:

  • PE-unlikely → D-dimer
  • PE-likely → imaging (CTPA)
36

Simplified PESI (sPESI)

Predicts 30-day mortality risk in PE. sPESI ≥1 = higher risk.

Components (each = 1 point):

  • Age >80 years
  • Chronic cardiopulmonary disease (chronic heart / lung disease)
  • Cancer history
  • Heart rate ≥110 b/min
  • SBP <100 mmHg
  • Arterial oxyhaemoglobin saturation <90%
37

PE risk stratification

  • Low risk: sPESI = 0, no RV strain
  • Intermediate: sPESI ≥1 (PESI class III–V) OR RV strain
  • High: haemodynamic instability → systemic thrombolysis + hemodynamic support

Pneumoconiosis

2 entries
38

Pneumoconiosis CXR signatures

DiseaseCXR finding
AsbestosisBilateral diffuse reticulonodular + honeycombing (lower lobes)
Asbestos pleural plaquesLocalized thickening + calcifications at diaphragm
Rounded atelectasisRound opacity, irregular outlines, comet tail sign
Silicosis (chronic)Upper-lobe nodules 1–10 mm → coalesce >10 mm (PMF) + eggshell calcification of hilar LN
Silicosis (acute)Diffuse alveolar filling, lower-zone predominant
Simple CWPSmall rounded opacities <1 cm in upper zones
Complicated CWP / PMFLarge opacities >1 cm; "angel wings"
39

Latency periods

DiseaseLatency
Asbestosis (standard)20–30 yr
Asbestosis (very heavy exposure)<10 yr
MesotheliomaUp to 40 yr
Chronic silicosis>15 yr
Acute silicosisWithin months