Created by theStudyFix

Pulmonology — Disease Index + Criteria

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

C/P

Inves

Mng

Special — pathognomonic

Obstructive airway

4 entries

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

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

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

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

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

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

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

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

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

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

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)

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)

Interstitial / Occupational

5 entries

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
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

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

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

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

Mng

Prednisolone 0.5 mg/kg × 4–6 wk → taper to maintenance ≥12 mo
Steroid-sparing: Methotrexate, Azathioprine, Hydroxychloroquine

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

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

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

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

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)

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

Infection

6 entries

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

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%

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

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)

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

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

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

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

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

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

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

Pulmonary: multi-drug prolonged course (species-specific)
Lymphadenitis: surgical excision (do not I&D — avoids fistula)
Disseminated MAC in HIV: macrolide-based + ART

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

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

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

Pneumocystis jiroveci pneumonia (PCP)

C/P

Opportunistic infection in immunocompromised host (HIV/AIDS, transplant, chemotherapy)
Listed under opportunistic pneumonia / immunocompromised host pathogens

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

Tumour

3 entries

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

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

Mng

NSCLC: surgery if early-stage, chemotherapy ± radiotherapy, targeted therapy
SCLC: chemotherapy + radiotherapy; rarely surgical
Paraneoplastic: address tumour ± symptomatic management

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)

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)

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)

Mng

Limited — surgical, chemo, radiotherapy

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)

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

Mng

Address underlying primary

Special

Cannonball pattern = pathognomonic metastatic gross morphology
Bilateral multiple peripheral nodules + extra-pulmonary primary history → secondary

Pleural

4 entries

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)

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)

Mng

Thoracentesis (contraindications + complications: bleeding, pneumothorax, infection)
Treat underlying cause
Drainage for symptomatic / large effusion
Pleurodesis for recurrent malignant 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

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

Mng

Drainage (intercostal tube) + targeted antibiotics
Decortication if chronic
Add Clindamycin if aspiration / lung abscess context

Special

D-shaped gross appearance
Parapneumonic effusion → empyema when fluid infected
Pleural fluid analysis confirms (gross pus)

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

Inves

Erect CXR: blunted costophrenic angle, opacity with fluid level
US sensitive
Pleural fluid aspirate confirms blood

Mng

Intercostal drain
Massive haemothorax → urgent thoracotomy
Treat haemodynamic compromise

Special

Erect CXR is the classic image
Surgical drainage threshold based on initial volume + rate

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

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

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)

Special

Tension pneumothorax = clinical diagnosis, treat before CXR
Trachea deviation AWAY (vs collapse where it deviates TOWARD)
Pneumothorax = complication of COPD (bulla rupture)

Vascular / Emergency

3 entries

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

Inves

ABG: hypoxia + hypocapnia (respiratory alkalosis)
ECG: sinus tachycardia most common; S1Q3T3, RV strain
CXR: often normal; Hampton's hump (peripheral wedge), Westermark sign (regional oligaemia)
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

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

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)

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

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

Mng

Mechanical ventilation (low tidal volume, PEEP)
Treat underlying cause
ECMO in severe refractory cases

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

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

Inves

CXR: opacity + volume loss (mediastinal shift toward, elevated hemidiaphragm, crowded ribs)
Lobar collapse patterns with eponymous signs

Mng

Chest physiotherapy, deep breathing, mobilization
Treat obstruction (bronchoscopy if foreign body / mucus plug)
Address postop pain to enable deep breathing

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

Asthma

4 entries

GINA 2025 — Asthma definition

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

Asthma diagnostic criteria

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

Test	Threshold
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%
FeNO	Increased
Blood / sputum eosinophils	Increased

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

Acute exacerbation — life-threatening signs

Confusion
Hypotension
RR >30
SpO₂ <90%
Silent chest

GINA discharge criteria

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

COPD

6 entries

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%.

GOLD severity grades (1–4)

Based on post-BD FEV1 % predicted:

Grade	FEV1 % 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.

GOLD groups (A / B / E)

Group	Exacerbations / hosp	Symptoms
A	0–1 moderate (no hosp)	mMRC 0–1 OR CAT <10
B	0–1 moderate (no hosp)	mMRC ≥2 OR CAT ≥10
E	≥2 moderate OR ≥1 hosp	Any

Initial therapy

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

Single inhaler preferred.

mMRC dyspnoea scale

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

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

CAT score grouping cut-off

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

COPD acute exacerbation definition

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

CAP

7 entries

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

CURB-65 (site of care)

Component	Threshold
C Confusion	New
U Urea	>7 mmol/L (20 mg/dL)
R Respiratory rate	>30 breaths/min
B Blood pressure	SBP <90 OR DBP <60 mmHg
65 Age	>65 years

Site of care

Score	Setting
0–1	Home (outpatient)
2	Ward
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)

MAFIA PCC (anti-Pseudomonal coverage)

Letter	Drug	Class
M	Meropenem	Carbapenem
A	Aminoglycosides	(nephrotoxic — kidneys!)
F	Fluoroquinolones	Ciprofloxacin / Levofloxacin (NOT Moxifloxacin)
I	Imipenem	Carbapenem
A	Aztreonam	Monobactam
P	Piperacillin-tazobactam	Penicillin
C	Ceftazidime	Cephalosporin
C	Cefepime	Cephalosporin

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

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

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.

Organism	Radiological resolution
Mycoplasma	2–4 wk
Legionella	2–6 mo
Staph	3–5 mo
S. pneumoniae + shock	3–5 mo

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

Lobar pneumonia stages (timeline)

Stage	Duration
1. Congestion	Early, 1–2 days
2. Red hepatization	3–4 days
3. Grey hepatization	1 week
4. Resolution	1–2 weeks

Tuberculosis

7 entries

TST positivity criteria (5 / 10 / 15 mm)

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

Threshold	Patient groups
≥5 mm	HIV+; recent TB contact; old healed TB on CXR; immunosuppressed (transplant, etc.)
≥10 mm	Recent 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 mm	No known risk factor

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

ADA cut-offs by fluid

Fluid	Cut-off
CSF	8 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

QFT-G (IGRA) vs TST

Feature	QFT-G	TST
Setting	In-vitro	In-vivo
Antigens	ESAT-6 + CFP-10 (multiple)	PPD (single)
BCG cross-react	No	Yes (false positive)
Specificity	Higher	Lower
Visits	1	2
Reader bias	Minimal	Significant
Result time	24 h	48–72 h
Boosting	None	Yes (2-step in immunocompromised)
Constraint	Blood processed within 12 h of draw	Patient must return

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.

HRZES doses (daily + 3×/wk)

Drug	Daily mg/kg	Daily max	3×/wk mg/kg	3×/wk max
Isoniazid (H)	5 (4–6)	300 mg	10 (8–12)	900 mg
Rifampicin (R)	10 (8–12)	600 mg	10 (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.

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

MDR-TB definition

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

Pleural

1 entry

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

Scadding CXR staging (I–IV)

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

Stage	Finding
I	Bilateral hilar lymphadenopathy
II	Bilateral hilar adenopathy + pulmonary infiltrates
III	Pulmonary disease only (infiltrates / reticulonodular)
IV	Irreversible fibrosis + honeycombing

BAL CD4/CD8 ratio

Disease	CD4/CD8
Sarcoidosis	≥2.5
Hypersensitivity pneumonitis	<1

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

Bronchiectasis

1 entry

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

Runyon classification (4 groups)

Group	Growth	Pigment	Species
1	Slow	Photochromogen (in light)	M. kansasii, M. marinum, M. simiae
2	Slow	Scotochromogen (without light)	M. scrofulaceum, M. szulgai, M. gordonae
3	Slow	Non-photochromogen	M. avium, M. intracellulare, M. ulcerans, M. haemophilum
4	Fast (<7 d)	—	M. fortuitum, M. chelonae, M. abscessus, M. smegmatis

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

Lung cancer classification (% breakdown)

Category	%
All primary lung tumours	95% of lung tumours overall
NSCLC	85% of lung cancers
└ Squamous	30% of NSCLC
└ Non-squamous	70% of NSCLC
└ Adenocarcinoma	90% of non-squamous
└ Large-cell	10% of non-squamous
SCLC	15% of lung cancers

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

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

SCLC staging (limited vs extensive)

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

Vascular / Emergency

4 entries

Berlin definition — ARDS

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

Element	Criterion
Timing	Acute onset within 1 week of known insult
Chest imaging	Bilateral opacities not fully explained by effusion / collapse / nodules
Origin	Not fully explained by cardiac failure / fluid overload
Oxygenation	PaO₂/FiO₂ with PEEP ≥5 cmH₂O

Severity

Severity	PaO₂/FiO₂
Mild	>200
Moderate	100–200
Severe	≤100

Revised Geneva score (PE)

Used for clinical probability of PE. Guides next step:

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

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%

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

Pneumoconiosis CXR signatures

Disease	CXR finding
Asbestosis	Bilateral diffuse reticulonodular + honeycombing (lower lobes)
Asbestos pleural plaques	Localized thickening + calcifications at diaphragm
Rounded atelectasis	Round 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 CWP	Small rounded opacities <1 cm in upper zones
Complicated CWP / PMF	Large opacities >1 cm; "angel wings"

Latency periods

Disease	Latency
Asbestosis (standard)	20–30 yr
Asbestosis (very heavy exposure)	<10 yr
Mesothelioma	Up to 40 yr
Chronic silicosis	>15 yr
Acute silicosis	Within months