Med Respi

30 06 Medicine
----- Active space ----- RESPIRATORY SYSTEM REVISION 1
Weibel’s generation of airways :

• Total 23 generations of airway.
• First 16 generations → Conducting zone (Upto terminal bronchioles).
• Last 7 generations → Respiratory zone
(Respiratory bronchioles + alveolar ducts + alveoli = Acinus).
Classification of Lung Diseases 00:02:47
Lung diseases
Obstructive lung diseases Vascular Restrictive lung disease

• COPD : • Pulmonary hypertension.
Chronic bronchitis. • Pulmonary thromboembolism.
Emphysema.
Small airway disease (<2mm). Intraparenchymal Extraparenchymal
• Bronchial asthma (BA). Interstitial lung • Neuromuscular (NM) disorders :
• Bronchiectasis except disease (ILD) Myasthenia, ALS, GBS.
tractional bronchiectasis. ALS : Amyotrophic Lateral Sclerosis.
• Bronchiolitis. GBS : Guillain Barre Syndrome.
• Cystic fibrosis (CF). • Chest wall issues :
Kyphoscoliosis, obesity.
• Filling disorders + Parenchymal destruction : Lung abscess (Necrotizing pneumonia).

• Pleural disease : Pleural effusion
Note : Lung parenchyma is Alveoli + alveolar interstitium + vascular interstitium.
Interstitial Lung Disease (ILD) :
• Diffuse lung parenchymal fibrosis.
• Early stage :
Hypoxia Type 1 respiratory failure (RF).
(↓PaO2) Pulmonary vasoconstriction → Pulmonary hypertension.
• Late stage : More lung parenchyma is involved → Hypoxia + Hypercarbia →
Type 3 RF.
COPD (Chronic Obstructive Pulmonary Disease) :

Larger airway + Smaller airway + Parenchymal + Vascular involvement.
Chronic bronchitis : Type 2 RF.
Pulmonary hypertension.
Lung parenchyma involved
Right ventricular failure (Cor pulmonale).
Emphysema : Alveolocapillary membrane involved → Type 1 RF.
Medicine Revision • v1.0 • Marrow 6.5 • 2023
RS Revision 1 06 31
Respiratory failure 00:18:32 ----- Active space -----
Types Physiology PaO2 PaCO2 P(A-a)O2 Examples

Type 1 Diffusion failure Normal • Alveolar filling disorders :
Pneumonia.
Diffuse Alveolar Hemorrhage.
ARDS.
• ILD.
• Vascular disorders.
• Emphysema.
Type 2 Ventilatory failure Normal Pump :
Neuromuscular disorders.
Chest wall issues.
Effector organ : Chronic bronchitis.
Generator : Brainstem disorders.
Type 3 Combined ILD (Type 1 → Type 3).
diffusion & Type 2 → Type 3 RF is rare.
ventilatory failure
Spirometry 00:21:17
FEV1 /Forced Expirato-

ry Volume in 1 second :
Amount of FVC exhaled in
1st second.
FVC = 5L
Volume (l)
FEV1 = 4L
FEV1 /FVC > 80%.
Time (sec)
Lung volumes in obstructive and restrictive lung disease :
Obstructive lung disease Restrictive Lung disease
Elastic recoil pressure (ERP) is low There is ventilation issue.
d/t loss of alveolar attachments ERP is high d/t fibrosis → Difficult to
→ Hyperinflation→ Dynamic inflate alveoli.
compression of airways.

32 06 Medicine
----- Active space ----- Obstructive lung diseases Restrictive lung diseases
Vascular
Hyperinflation Air trapping Intra Extra parenchymal lung
phase phase parenchymal diseases
1 FEV 1 ↓↓ ↓↓ Normal to ↑ Normal
FVC
2 FEV 1 ↓↓ ↓↓ Normal Normal
3 FVC Normal ↓↓ ↓↓ Normal
4 DLCO Emphysema = ↓↓ ↓ Normal Very low
NM Chest
issues wall
5 RV ↑↑ ↑↑ ↓ Normal Normal Normal
6 TLC ↑↑ Normal ↓↓ ↓↓ Normal Normal
7 RV/ TLC - - - ↑↑ Normal -
Lung volumes in smaller airway disease :

• FEV 1 /FVC : Normal
• Forced expiratory flow 25-75% (FEF 25-75) /
Volume (l)
Maximal Mid Expiratory Flow Rate (MMEFR) is
used to identify small airway disease.
Time (sec)
DLCO 00:45:30
Measurement of lung’s ability to transfer gas (O2) across alveolocapillary

membrane.
• Normal Value of DLCO : 20-30 ml/min/mm Hg.
• Normal Value of DLCO : 70 to 140 %.
Carbon monoxide/CO used for measuring DLCO because :
• CO affinity to hemoglobin is very high.
• CO is diffusion limited gas.
• There is negligible amount of CO in the blood.
Alveolocapillary membrane : Diffusion takes place across

1. Alveolar epithelium + Basement membrane.
2. Interstitium.
3. Capillary endothelium + Basement membrane.
Surface area of alveolocapillary membrane : 70 m2
Thickness of alveolocapillary membrane : 0.2 - 0.5 micrometre.
RS Revision 1 06 33
Factors affecting DLCO : ----- Active space -----
Factors that increase DLCO Factors that decrease DLCO

• ↑ Blood volume : Supine position, ↑cardiac output, • Valsalva maneuver.
congestive cardiac failure, polycythemia. • Smoking (↑ CO Hb).
• ↓ PaO2 : High altitude. • High flow O2 therapy (↑ OxyHb).
• Exercise and Obesity. • Anemia.
• Left to right cardiac shunts.
Clinical application of DLCO :

Diseases with ↑ DLCO Diseases with↓ DLCO
Diffuse alveolar hemorrhage: Helps in early diagnosis of ILD in
Sensitive indicator for early rheumatological disorders:
bleeding into alveoli. Eg: • Rheumatoid arthritis (RA)
• Goodpasteur disease • Scleroderma
• Wegener granulomatosis • Mixed connective tissue disease
• Microscopic Poly Angiitis • Polymyositis
• Dermatomyositis
In asymptomatic patients → DLCO falls >15%
within 6 months. → marker of progression of ILD
Bronchial asthma Pulmonary vascular diseases
Bronchitis Bleomycin toxicity
Emphysema
Pleura 01:00:42
Fluid in pleural cavity Detected

10 -30 mL Normal fluid in pleural cavity.
50 mL USG.
60- 80 mL Chest X-ray Lateral view.
200 mL Chest X-ray PA view.
300 mL Clinically.
Pleural effusion :
Light’s criteria distinguish transudates from exudates :
• The fluid is considered as exudative pleural effusion if any one of the
following are found :
1. Ratio of pleural fluid to serum protein ≥0.5.
2. Ratio of pleural fluid to serum LDH ≥0.6.
3. Pleural fluid LDH ≥2/3rd of the upper limits of normal serum LDH.
• The fluid is considered a transudate if all the above are absent.
34 06 Medicine
----- Active space -----

Causes of transudative pleural effusion :
• Congestive heart failure. • Hypoalbuminemia.
• Cirrhosis. • Budd Chiari Syndrome.
• Nephrotic syndrome. • Urinothorax.
• Superior vena cava obstruction. • Peritoneal dialysis.
• Hypothyroidism.
Can cause Transudative/Exudative effusion :
• Chronic constrictive pericarditis. • Pulmonary infarction.
• Pulmonary embolism. • Acute pancreatitis.
Note : Methotrexate causes HSP.
Pleural fluid analysis :
• Cells : 1700 cells/μl (75% macrophages, 25% lymphocytes, < 1% mesothelial cells).
• LDH : <50 % of Serum LDH.
• Protein : 1 to 1.5 g/dL.
• Glucose : Same as Serum glucose.
Causes of eosinophilc effusion ( >10 % eosinophils in pleural fluid) :
• Hemothorax /Pneumothorax. • Drugs.
• Parasitic : Paragonimus westermani. • Eosinophilic Granulomatosis with
• Histoplasmosis/Coccidioidomycosis. Polyangiitis (EGPA).
• Asbestosis. • Pulmonary infarction.
Pleural fluid abnormalities and associated diseases :
1. Empyema : 2. RA :
• LDH >1000 U/L • pH <7.2
• Neutrophils in pleural fluid • Glucose <30 mg/dL
• pH < 7.2 • Macrophages and multinucleate
• Glucose 30 -60 g/dl giant cells (tadpole cells)
3. Malignancy :
• Glucose 30-60 mg/dL
Community acquired pneumonia associated pleural effusion :
Effusion Pathology Investigations
LDH
Simple parapneumonic Culture
Inflammation → ↑ vascular permeability. Normal
effusion Glucose
pH
Complicated Simple parapneumonic effusion + bacterial LDH increased.
parapneumonic effusion invasion ( fibrin deposition & septation). Culture +.
Complicated parapneumonic effusion + Glucose reduced.
Empyema pH < 7.2.
Macroscopic pus in pleural cavity.
Empyema : Any pneumonia not responding to antibiotics within 72 hours

Clinical features : Fever not responding to antibiotics, Pleuritic pain,
Pleuritic tenderness, tachycardia, clubbing.
RS Revision 1 06 35
Investigations : Chest x-ray → D sign/pregnant belly sign. ----- Active space -----
IOC : CECT → Split Pleura Sign (Differentiates empyema from
necrotising lung abscess).
Treatment : Intercostal drainage (ICD). No role for intrapleural antibiotics.
D Sign/Pregnant belly sign USG : Septations in empyema Split pleura sign
Indications of ICD :
• Empyema (Absolute indication).
• Pleural fluid pH < 7.2.
• Organism in culture.
• Loculated pleural effusion.
• Massive effusion.
Massive pleural effusion
Pleural TB :
• If left untreated → pulmonary TB/extrapulmonary TB within 5 years.
• Gene Xpert/CBNAAT/Pleural fluid ADA/ pleural fluid culture → Inconclusive in
pleural TB.
• Pleural biopsy (Medical thoracoscopy/wax guided) is conclusive
ADA (Adenosine DeAminase) :

Pleural fluid ADA Interpretation
< 40 U/L Not suggestive of TB.
>70 U/L + lymphocytes + exudative effusion Highly suggestive of TB.
40 to 70 U/L Lymphoma, empyema, malignancy, brucellosis, TB.
Note : Mesothelial cells→< 5% in TB. (Normal <1%).

Connective tissue disorder related to pleural effusion :
• Most important lung manifestation of SLE and RA : Pleuritis ± effusion.
Chylous vs. pseudochylous pleural effusion :
Chylous pleural effusion Pseudochylous pleural effusion
Usually after trauma or tumor Usually after RA/TB.
• Triglycerides : High.
• Chylomicrons present.
• Milky lymphocytic exudative effusion. • Contains cholesterol crystals
• Normal glucose.
• Low LDH.

36 07 Medicine
----- Active space ----- RESPIRATORY SYSTEM REVISION 2
Pulmonary thromboembolism 00:00:22
Causes of pulmonary thromboembolism :

• Venous thromboembolism (VTE) from suprapopliteal veins → femoral vein
(Pelvic veins in pregnancy).
• Inherited cause : Factor V Leiden mutation (M/c).
• Acquired causes : Antiphospholipid antibody syndrome (M/c), nephrotic syn-
drome, post orthopedic surgery, malignancy (Adenocarcinoma), COPD.
Note : M/c site of DVT : Deep veins of calf.
Types of pulmonary thromboembolism :

1. Massive, 2. Submassive & 3. Non-massive.
Massive Submassive Non-massive
Hypotension. No hypotension. No hypotension.
D/t RV dilatation → RV dilatation + markers of RV No RV dilatation or
septum pushed to ischemia ↑ (NT proBNP, trop I). biomarker rise.
left → small LV → If both markers are ↑ : High risk. Presents with
↓ CO (Cardiac out- If any one ↑ : Low risk. recurrent pneu-
put). monia.
Evaluation of pulmonary embolism :

Clinical :
Symptoms Signs
• Unexplained dyspnea with clear lung fields. • Tachycardia, tachypnea.
• Syncope. • S3, ↑ JVP : Acute right
• Chest pain (Pleuritic). heart failure.
• Cough with hemoptysis (Non-massive). • Clear lung fields.
• Sudden cardiac death. • ↓ breath sounds, rales
Investigations :
ABG : Hypoxemia, respiratory alkalosis, widening of (A-a) O2 gradient.
ECG : T inversion in V1 to V4 correlates with severity.
S1Q3T3.
RS Revision 2 07 37
Echo : ----- Active space -----

Findings seen in echo :
• RA & RV dilatation, septal push, small LV.
• Cardiac tamponade.
• Mc Connell’s sign : Hypocontractile RV free wall
+ hypercontractile apex. CTPA : Saddle thrombus.
Imaging : IOC -CTPA (CT pulmonary angiography).

• Clot.
• Pulmonary artery dilatation.
• RV dilatation.
• Polo mint sign : Thin rim of contrast persists
around a central filling defect d/t thrombus.
CTPA : Saddle thrombus.
Well’s score :
Parameter Score
Clinical signs of DVT. 3
Alternate diagnosis less likely than 3
pulmonary embolism. After interpretation of
Well’s score :
Heart rate >100/min 1.5
High risk → CTPA.
Recent surgery or immobilisation. 1.5
Low risk → D-dimer.
Previous pulmonary embolism or DVT. 1.5
Score ≤4 : PE unlikely.
Hemoptysis. 1
Malignancy. 1
Management :
Start anticoagulation : Unfractionated heparin (80 U/kg) or low molecular
weight heparin (1 mg/kg s/c) followed by warfarin to maintain INR of 2-3.
If massive (or) submassive high risk :
• Thrombolysis (Alteplase 100 mg i/v over 2 hours x 14 days).
• If thrombolysis is C/I : Embolectomy.
After thrombolysis → Anticoagulation : Newer oral anticoagulants (NOAC) better
than warfarin.
If submassive low risk (or) non-massive : Continue anticoagulation.
If patient is not a candidate for NOAC : IVC filter.

38 07 Medicine

Pulmonary hypertension 00:19:29
Pulmonary hypertension : Resting mean pulmonary artery pressure ≥20 mmHg

with right sided heart catheterisation.
Types :
A. Due to ↑ pulmonary vascular resistance (PVR) B. Due to ↑Left atrial

Type 1 Pulmonary artery hypertension (PAH). pressure (LAP)
Plexiform arteriopathy d/t remodelling/ Type 2 D/t cardiac
vasoconstriction/thrombosis. causes.
Type 3 Lung related causes : ILD, c/c bronchitis.
Type 4 C/c thromboembolic pulmonary hyper-
tension.
Pulmonary vascular resistance (PVR)
Note : PVR <3 Wood units in type 2.
PVR >3 Wood units in other types. = Change in pressure/ flow
Rt. heart pressure - Lt. heart pressure
=
Cardiac output
Type 1 : PAH
Idiopathic : Should be termed idiopathic after ruling out
• Limited systemic sclerosis.
• Toxins : Rapeseed oil.
• Serotonergic substances : Fenfluramine. Molecular pathogenesis :
• BMPR-2 mutation. • Endothelin ↑.
• Infections : HIV, Schistosomiasis. • Nitric oxide ↓.
• Portal hypertension. • Prostacyclin ↓.
O/E : Clinical presentation of PAH :
• Loud, palpable P2. Fatigue (M/c symptom).
• Parasternal heave. Breathlessness.
• Epigastric pulsations. Chest pain (RV ischemia).
• 2 ICS pulsations.
nd
• High pitched pansystolic murmur along left sternal border which ↑ on

inspiration 20 to PAH : Hypertensive tricuspid regurgitation.
• High pitched early diastolic murmur d/t pulmonary regurgitation or
pulmonary artery dilatation : Graham steel murmur.

RS Revision 2 07 39
Evaluation : ----- Active space -----

Echo : Pulmonary artery dilatation, RV function, TR.
PFT : FEV1/FVC normal, FVC normal, DLCO ↓.
Polysomnography & HRCT : To rule out obstructive sleep apnea syndrome & ILD.
V/Q scan : To rule out c/c thromboembolic PAH (Rx : Pulmonary
endarterectomy).
6 minute walk test : Predictor of survival.
Management :
Supportive care :
• Avoid pregnancy.
• Oral anticoagulants.
• Long term oxygen therapy.
• Diuretics for RHF.
Specific therapy :
• CCB.
• Endothelin receptor antagonists (ERA).
• PDE 5 inhibitors.
• Prostanoids.
• Guanylyl cyclase stimulants.
Vasoreactivity test
Positive Negative
CCB No role for CCB
(Nifedipine 240 mg)
Class 1 to 3 symptoms Class 4 symptoms
Ambrisentan (ERA) + Prostanoids (Epoprostenol,

Tadalafil (PDE 5 inhibitor) Troprostinil)
Note : If prostanoids fail in class 4 symptoms → Atrial septostomy (or) lung

transplantation.
Interstitial lung diseases (ILD) 00:36:38
Parenchyma : Alveoli + alveolar interstitium + vascular interstitium.

ILD : Diffuse parenchymal lung fibrosis.
Mediator : TGFβ, PDGF.
40 07 Medicine
Idiopathic interstitial pneumonia :

Forms of idiopathic interstitial pneumonia :
1. Idiopathic pulmonary fibrosis (IPF) :
• M/c.
• Histological counterpart : Usual interstitial pneumonia (UIP).
2. Non specific interstitial pneumonia (NSIP).
3. Cryptogenic organising pneumonia (COP).
4. Respiratory bronchiolitis associated ILD (RB-ILD).
5. Desquamative interstitial pneumonia (DIP). ILD a/w smoking
6. Diffuse alveolar damage : • RB-ILD.
• Acute interstitial pneumonia. • DIP.
• Poor prognosis. • LCH.
• Eg : COVID pneumonia. • Rheumatoid arthritis
7. Lymphocytic interstitial pneumonia (LIP). associated ILD (RA-ILD).
Patterns of ILD :
Pattern Seen in Onset Treatment
UIP RA (Majority : Idiopathic) Chronic. Anti PDGF : Nintedanib.
NSIP Connective tissue diseases, Subacute. Steroid + MMF
drugs. (Mycophenolate mofetil)
COP Polymyositis, dermatomyositis, Subacute. Steroid + MMF.
anti synthetase syndrome.
LIP Sjogren’s syndrome, HIV.
Clinical features : CTD a/w ILD

Symptoms : • Diffuse systemic sclerosis.
• Dyspnea on exertion. • MCTD.
• Dry, non productive cough. • Sjogren’s syndrome.
• Compliance/hypoventilation • Polymyositis, dermatomyositis.
(Type 3 respiratory failure). • IgG4 related disease.
Signs : • Ankylosing spondylitis.
• Clubbing.
• Velcro crackles : B/L, bibasal, end
inspiratory to early expiratory, fine
crackles, not varying with cough.

RS Revision 2 07 41
Investigations : ----- Active space -----

PFT :
• FEV1/FVC : ↑ (FVC ↓ & FEV1 normal).
• DLCO : ↓.
IOC : HRCT.
HRCT findings :
CXR : Shows B/L, bibasal,
Non specific : Reticular & linear shadows.
subpleural reticulonodular infiltrates.
Pattern HRCT findings
UIP Honeycombing, cystic spaces, loss of lung architecture, traction
bronchiectasis.
NSIP Ground glass opacities (GGO).
COP Consolidation.
Reverse halo sign : GGO surrounded by consolidation.
Reverse halo sign

LIP NSIP + nodules + cysts.

42 07 Medicine
Conditions causing cysts in lungs :

• LCH : Langerhans cell histiocytosis.
• LAM : Lymphangioleiomyomatosis.
• LIP.
LCH
Young male smoker.
LAM
Upper lobe ILD (Nodules + cysts).
Young females with tuberous
Associated with diabetes insipidus.
sclerosis.
CD1a cells ≥5% : Birbeck granules,
Cysts in lungs.
tennis racquet shaped.
Pneumothorax.
LCH LAM
Drug induced ILD : Causes of upper lobe ILD :
1. Amiodarone. • Ankylosing spondylitis.
2. Bleomycin. • Sarcoidosis.
3. Busulfan. • Silicosis.
4. Cyclophosphamide. • Coal worker’s pneumoconiosis.
5. Mitomycin. • ABPA : Allergic bronchopulmonary
6. Methotrexate. aspergillosis.
Rare causes. • Hypersensitivity pneumonitis.
7. Anti TNFα drugs.
• Berylliosis.
• TB.
• LCH.
Occupational lung diseases 01:11:26
Pneumoconiosis :
1. Silicosis.
2. CWP. Complicated
3. Asbestosis.
4. Berylliosis. → Uncomplicated

RS Revision 2 07 43
Silicosis : Caused by exposure to SiO2 (Quartz) in rock cutting, slate cutting, sand ----- Active space -----
blasting & mining industries.
1. Acute silicosis :
Seen when there is large exposure to SiO2 (crystalline silica) within 2 years.
Symptom : Dyspnea on exertion.
Findings : Crazy pavement
• PAS +ve macrophages. pattern
• Milky white bronchoalveolar lavage. • Acute silicosis.
• CT : Crazy pavement pattern (GGO + nodules + • Diffuse alveolar
cysts). hemorrhage.
Poor prognosis. • Pulmonary alveolar
proteinosis.
2. Chronic silicosis :
M/c pneumoconiosis.
10-30 years of exposure.
Cell affected : Pulmonary alveolar macrophage (PAM) → Reactivation of TB.
A/w autoimmune conditions (Scleroderma).
Pleural involvement : Nil.
Parenchymal involvement :
• Upper lobe ILD.
• B/L upper lobe nodules : Nodules
join together → conglomerate
nodules (Angel wing sign). Egg shell calcification
• Hilar adenopathy with peripheral
calcification (Egg shell calcification).
• Cavitation ±.
• Lung signs in 25%.
• Dyspnea & cough.
• Mixed pattern on spirometry.
Coal worker’s pneumoconiosis (CWP) :

Cell affected : PAM → But, no risk of TB reactivation.
A/w autoimmune conditions : Caplan’s syndrome (RA + active synovitis + nodules
+ IgA rheumatoid factor +ve).
• No hilar lymphadenopathy.
• No egg shell calcification.
• Nodules.
• Upper lobe fibrosis.
• Cavitation ±.

44 07 Medicine

Berylliosis :
Ceramic industry.
• Upper lobe infiltrates.
• Non caseating granulomas.
• Thickening of bronchovascular bundles.
• Hilar adenopathy.
• NSIP pattern.
Note : Smoking is a risk factor in silicosis, CWP & berylliosis.
Asbestosis :
Serpentine (90%)
2 types of fibres Crocidolite
Chrysotile (10%)
• Around 10 years of exposure. Amosite (Most dangerous)
Pleural involvement :
• Pleural manifestations are not related to smoking.
• Parietal pleural thickening (M/c) : Pleural plaques with
calcification → Seen as Holly leaf sign/table mountain
sign/candle drip sign in CXR.
• Earliest : Benign asbestos related pleural effusion (BAPE)
→ exudative, eosinophilic with mesothelial cells.
Pleural plaques
• Lower lobe ILD : Diffuse massive fibrosis.
• Infiltrates result in dyspnea.
• No lung signs.
• Restrictive pattern in spirometry.
Malignancy Holly leaf sign

Pleural mesothelioma Ca lung

• Unrelated to smoking. • Related to smoking.
• Occurs after 30 years of exposure. • Occurs 10-30 years after exposure.
• Epithelioid type is m/c. • Adenocarcinoma.
• Markers : Pan cytokeratin, calreticulin. • Symptoms : Cough with hemoptysis.
• Symptoms : Chest pain (or) mass.

RS Revision 3 08 45
RESPIRATORY SYSTEM REVISION 3 ----- Active space -----
Airway diseases :
• No parenchymal involvement.
• Type 1 respiratory failure (Normal PaCO2).
Eosinophilic lung disease 00:02:05
Defined by :
a. BAL eosinophilia >25% (or)
b. Lung tissue eosinophilia (or)
c. Peripheral eosinophilia + Lung infiltrates.
Causes :
Known causes Unknown causes
1. Parasite 1. Eosinophilic granulomatous polyangiitis
a. Loeffler’s syndrome : Hypersensitivity to (EGPA).
ascaris. 2. Acute eosinophilic pneumonia (ARDS like
b. Lung fluke invasion. presentation).
2. Drugs : Nitrofurantoin. 3. Chronic eosinophilic pneumonia/CEP
3. Tropical pulmonary eosinophilia (d/t (Reverse batwing : Photographic negative
microfilaria). of pulmonary edema on radiology).
4. Allergic bronchopulmonary aspergillosis (ABPA) 4. Idiopathic hyper eosinophilic syndrome.
Note :
HSP (Hypersensitivity pneumonitis).
Bronchial asthma (A/w eosinophilia). Not eosinophilic lung diseases.
Pulmonary eosinophilic granuloma diseases.
BAL eosinophilia with > 40% : CEP & Tropical Pulmonary eosinophilia.
Aspergillus in lung 00:06:56
Organism : Aspergillus fumigatus with septate hyphae (Forms mucus plug).

Not a highly contagious disease.
Presentations of aspergillus infection :
1. ABPA : Eosinophilic lung disease.
2. Aspergilloma : Seen in old tuberculosis cavity.
3. CCPA (Chronic cavitary pulmonary aspergillosis) : Thick walled cavities +
bronchial wall invasion in COPD patients.
46 08 Respiratory System

4. Invasive aspergillosis :
• Neutropenic patients.
• CT : Halo sign (consolidation surrounded by ground glass opacities).
ABPA :
A. fumigatus colonizes airways in bronchial asthma or cystic fibrosis patients
(Acute/remission/exacerbations/steroid dependent asthma/fibrosis).
Type 1 + Type 3 hypersensitivity (type 1 > 3).
Lung findings seen in 20% patients.
Pathology :
Bronchiectasis : Proximal bilateral cylindrical symmetrical central type.
C/F of ABPA :
• Fever and cough with brownish thick mucosal plugs.
• Rarely gets converted to ILD (Involves upper lobe).
Investigation :
• IgE >1000 (Part of obligatory criteria + used for Tram track lines in CXR
follow up).
• Precipitin +ve.
• Imaging :
a. Chest Xray :
- Transient irregular parenchymal infiltrates.
- Atelectasis.
Finger in glove appearance
- Tram track appearance. (d/t mucoid impaction
- Finger in glove appearance. in distal bronchi)
b. CT : Tree in bud appearance.
Treatment :
a. Steroids for 12 weeks (DOC).
b. Steroid non responders : Itraconazole for 16 weeks.
c. Omalizumab (Monoclonal antibody against IgE). HRCT showing
central bronchiectasis
(tree in bud pattern)
Hypersensitivity pneumonitis (Extrinsic allergic alveolitis) :

Inflammatory disorder of the lung involving the alveolar wall & terminal airways.
Repeated exposure to organic dust Type 4 + Type 3 HS Involves
airway > Parenchyma.

RS Revision 3 08 47
Characterised by : ----- Active space -----

• IgE/eosinophil absent + Precipitin +ve + Non caseating granuloma & infiltrates.
• If parenchyma is involved : Non fleeting Interstitial infiltrates.
• Subacute form (M/c) : A/w response to steroids.
• No systemic symptoms.
HRCT : Mosaic/Head cheese pattern

(Different kind of densities seen).
Rx : Steroids . Mosaic attenuation/

Head cheese pattern
Organic dust :
Microorganisms serve as antigen in dust/animal proteins/chemicals :
Disease Exposure Antigen
Farmers lung Moldy hay Thermophilic actinomycete
Bagassosis Moldy sugarcane (M/C antigen) :
Mushroom worker’s lung Moldy compost/mushroom Thermoactinomycetes vulgaris
Malt workers lung Barley
Aspergillus clavatus
Tobacco workers lung Mold on tobacco
(2nd m/c)
Compost lung Compost
Wood workers lung Wood pulp
Bird fancier’s lung (Obstructive/ Avian droppings
emphysematous pattern) (Pigeon, parrot, chicken)
Chemical workers lung Polyurethane foams
(Isocyanates)
Note :
Disease Antigen
Hot tub lung, or humidifier or
Cladosporium, MAC
air conditioner lung
Wood trimmers lung Rhizopus
Familial HP/wood workers Bacillus subtilis

----- Active space ----- Hypersensitive reactions to Aspergillus

Extrinsic allergic
Asthma ABPA
alveolitis/HSP
Colonization of airways, Lymphocytic infiltration of
Hypertrophied
Pathology viscid mucoid impaction, interstitium, noncaseating
mucus gland
tissue eosinophilia granuloma
Radiographic features
Migratory peripheral
Normal Diffuse alveolar
Early infiltrates, atelectasis,
hyperinflation interstitial infiltrates
bronchiectasis
Normal Reticulonodular
Late Fibrosis
hyperinflation interstitial opacities
Skin test reactions to Aspergillus antigens
Immediate Positive Positive Positive
Delayed Negative Positive Positive
Other findings
Peripheral
Negative Positive Negative
eosinophilia
IgG aspergillus
Positive Positive Positive
precipitins
Normal or
Serum IgE levels Marked elevation Normal
mildly elevated
BAL lymphocytosis :
CD4/CD8 (>2 : 1) : Sarcoidosis.
CD8/CD4 (>2 : 1) : HSP.
Bronchiectasis 00:23:50
Obstructive type of airway disease.

Abnormal irreversible dilatation of bronchi + obliterative fibrosis of bronchioles.
D/t destruction of smooth muscles and elastic tissue of lung.
Types of dilatation : Tubular, cylindrical (M/C), varicose & cystic dilatation.
Cystic dilatation : Seen in children & a/w clubbing.
Traction bronchiectasis (Part of ILD) : Restrictive type.
Causes for loss of smooth muscles & elastic tissue :

1. Idiopathic (30%).
2. Tuberculosis (40-50%).
3. Genetic causes : Alpha-1 antitrypsin deficiency.
4. Childhood infections : Measles & pertussis.
5. Genetic syndromes : Yellow nail syndrome, William Campbell syndrome.
RS Revision 3 08 49
Pathophysiology : ----- Active space -----
• Lt lobe > Rt; F > M; 50-70 yrs.

• Dry bronchiectasis (Sicca) : Tuberculosis .
• Right middle lobe bronchiectasis :
K/a Brocks syndrome (d/t lymph node in TB).
• Middle lobe bronchiectasis : D/t MAC.
C/F :
• Chronic cough.
• Foul smelling sputum.
• Hemoptysis.
• Early & mid inspiratory coarse crackles.
• Diffuse rhonchi.
Imaging :
1. Volumetric multidetector helical CT scan (Best) : Absence of bronchial
tapering.
2. Airway dilatation (Parallel lines or ring shadows) : 1-1.5 times adjacent vessel
diameter : Signet ring sign.
3. Tram track sign.
4. Tree in bud pattern.
5. Central distribution, upper lobe
& fibrotic band : ABPA.
Bronchiectasis : Signet ring in CT s/o cylindrical bronchiectasis

Rx :
1. Airway clearance with physiotherapy and postural drainage (Cornerstone of
therapy).
2. Nebulized 7% hypertonic saline or steam inhalation to clear secretions .
3. Recombinant DNase for cystic fibrosis associated bronchiectasis .
4. Resection : If localized bronchiectasis with recurrent infection unresponsive
to drugs .
5. Prophylaxis : Macrolides (Azithromycin) for 6-9 months.
M/c organism causing infection : Pseudomonas .


Chronic obstructive pulmonary disease (COPD) 00:36:00
Acinus (Respiratory unit) : Respiratory bronchiole + Alveolar ducts + Alveoli .

COPD has 2 diseases :
1. Chronic bronchitis (clinical) : Cough with sputum for 3 months for 2 consecutive
years.
2. Emphysema (Pathological) : Dilatation of airspace distal to terminal bronchiole
followed by destruction of walls of airspaces .
Types of emphysema :
Centriacinar Panacinar Paraseptal

• Most common. • Complete involvement. • Young, male, smokers.
• Respiratory • Young, non smoker, α-1 • Associated with
bronchiole involved. antitrypsin deficiency & pneumothorax.
• Smoker & males . liver disease.
• Upper lobe • Lower lobe
predominant. predominant.
α-1 antitrypsin Phenotypes :
1. Pimm : Normal phenotype.
2. Pizz : Severe deficiency.

RS Revision 3 08 51
Chronic bronchitis Emphysema ----- Active space -----
Structure involved Parenchymal +++ Airway +++

Gaseous changes PaO2 PaO2
PaCO2 Normal PaCO2
Type of Respiratory failure Type 2 Type 1
Hypoxia More Less severe
Pulmonary HTN/ More common Less common
RV failure/ Infection
Prognosis More mortality Better outcomes
Complications :
V/P mismatch (Characteristic of COPD)
Severe chronic hypoxia

Muscularization
Intimal hyperplasia
Pulmonary hypertension Fibrosis
Obliteration
Cor pulmonale Edema
Death
Rx : Based on categories.
mMRC 0-1, CAT< 10 mMRC ≥2, CAT ≥10
0 to 1 moderate Group A Group B
exacerbations A bronchodilator A long acting
(Not leading to (Short acting bronchodilator
hospital admission) bronchodilator) Dyspnea (LABA or LAMA)
Exacerbation
≥2 moderate Group D
exacerbations Group C LAMA or
or LAMA LAMA + LABA
≥ 1 leading to (Long acting ± ICS
hospitalization anti-muscarinic drugs) (If eosinophils ≥ 300).
mMRC : modified medical research council dyspnea questionnaire ;
CAT : COPD assessment test.
For exacerbations : SABA + Short oral steroid therapy for 5-10 days.

----- Active space ----- LTOT (Long term oxygen therapy) :

• Given for 14-18 hrs/day.
• After exacerbation is over.
• Indications :
a. PaO2 <55 mmHg.
b. PaO2 of 55-60 mmHg if patient has pulmonary HTN/ RV failure.
Lung transplant : Last option.
Localised emphysema : Lobe resection (If not much cardiac problem & FEV1 >20%)
Pneumonia Management 00:53:34
CURB score :
Score of 1 to each point. Score 0, 1 : Outpatient management.
C : Confusion. Score 2 : Inpatient management.
U : Urea > 42 mg/dl. Score 3 : ICU management.
� : Respiratory rate >30/min.
B : <90/60 mm of Hg.
Age : ≥ 65 years.
Outpatient Mx :
Amoxicillin 1 gm TDS/Amoxiclav 625 mg BD (If risk factors like DM is present)
+ Azithromycin 500mg OD /Doxycycline 100mg BD.
Inpatient Mx :
a. Severe (ICU) : Beta-lactam + Macrolide (or) Beta lactam + Levofloxacin.
b. Non severe :
• Beta-lactam (Ampicillin-sulbactum 1.5-3gm Q6h).
+ Macrolide (Azithromycin 500mg OD) (or)
• Levofloxacin 750 mg OD alone.

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30 06 Medicine

----- Active space ----- RESPIRATORY SYSTEM REVISION 1

Weibel’s generation of airways :

Classification of Lung Diseases 00:02:47

Obstructive lung diseases Vascular Restrictive lung disease

• Filling disorders + Parenchymal destruction : Lung abscess (Necrotizing pneumonia).

COPD (Chronic Obstructive Pulmonary Disease) :

Respiratory failure 00:18:32 ----- Active space -----

Types Physiology PaO2 PaCO2 P(A-a)O2 Examples

FEV1 /Forced Expirato-

Medicine Revision • v1.0 • Marrow 6.5 • 2023

Lung volumes in smaller airway disease :

Measurement of lung’s ability to transfer gas (O2) across alveolocapillary

Alveolocapillary membrane : Diffusion takes place across

Factors affecting DLCO : ----- Active space -----

Factors that increase DLCO Factors that decrease DLCO

Clinical application of DLCO :

Fluid in pleural cavity Detected

----- Active space -----

Empyema : Any pneumonia not responding to antibiotics within 72 hours

D Sign/Pregnant belly sign USG : Septations in empyema Split pleura sign

ADA (Adenosine DeAminase) :

Note : Mesothelial cells→< 5% in TB. (Normal <1%).

Medicine Revision • v1.0 • Marrow 6.5 • 2023

----- Active space ----- RESPIRATORY SYSTEM REVISION 2

Pulmonary thromboembolism 00:00:22

Causes of pulmonary thromboembolism :

Note : M/c site of DVT : Deep veins of calf.

Types of pulmonary thromboembolism :

Evaluation of pulmonary embolism :

Echo : ----- Active space -----

Imaging : IOC -CTPA (CT pulmonary angiography).

Medicine Revision • v1.0 • Marrow 6.5 • 2023

----- Active space -----

Pulmonary hypertension : Resting mean pulmonary artery pressure ≥20 mmHg

A. Due to ↑ pulmonary vascular resistance (PVR) B. Due to ↑Left atrial

• High pitched pansystolic murmur along left sternal border which ↑ on

Medicine Revision • v1.0 • Marrow 6.5 • 2023

Evaluation : ----- Active space -----

Class 1 to 3 symptoms Class 4 symptoms

Ambrisentan (ERA) + Prostanoids (Epoprostenol,

Note : If prostanoids fail in class 4 symptoms → Atrial septostomy (or) lung

Interstitial lung diseases (ILD) 00:36:38

Parenchyma : Alveoli + alveolar interstitium + vascular interstitium.

Idiopathic interstitial pneumonia :

Clinical features : CTD a/w ILD

Medicine Revision • v1.0 • Marrow 6.5 • 2023

Investigations : ----- Active space -----

NSIP Ground glass opacities (GGO).

Reverse halo sign

Medicine Revision • v1.0 • Marrow 6.5 • 2023

Conditions causing cysts in lungs :

Occupational lung diseases 01:11:26

Medicine Revision • v1.0 • Marrow 6.5 • 2023

Coal worker’s pneumoconiosis (CWP) :

Medicine Revision • v1.0 • Marrow 6.5 • 2023

----- Active space -----

Malignancy Holly leaf sign

Pleural mesothelioma Ca lung

Medicine Revision • v1.0 • Marrow 6.5 • 2023

RESPIRATORY SYSTEM REVISION 3 ----- Active space -----

Eosinophilic lung disease 00:02:05