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-idiopathic interstitial pneumonias
-environmental/occupational exposures
-systemic ddiseases (sarcoidosis
name the different diffuse parenchymal lung diseases
shipyard, construction
typical exam setting for abestos exposure
mining, sandblasting
typical exam setting for silica exposure
hypersensitivity pneumonitis
birds/mold exposure in the setting of interstitial lung disease indicates
amiodarone, bleomycin, methotrexate, nitrofurantoin
medications causing interstitial lung disease
interstitial ffibrosis
fine "velco" inspiratory crackles is a exam finding of
idiopathic pulmonary ffibrosis, abestosis
digital clubbing indicates these interstitial lungg diseases
Diffuse reticular or ground-glass opacities, honeycombing in fibrosis
imaging findings indicating interstitial lung disease
loud P2, RV heave, JVDD, peripheral edema, tricuspird regurg
physical exam findings indicative of pulmonary vascular disease
ILD: Progressive dyspnea on exertion, chronic nonproductive cough, fatigue
PVD: Dyspnea, fatigue, syncope, chest pain, edema
symptoms of interstitial lung disease vs pulmonary vascular diseases
idiopathic pulmonary fibrosis
Gradual progressive dyspnea, dry cough, age >50, clubbing, Velcro crackles
Poor prognosis, responds poorly to steroids
prognosis associated with idiopathic pulmonary fibrosis
sarcoidosis
Nonproductive cough, dyspnea, systemic symptoms, young adults, African Americans; extrapulmonary: skin, eye
-Noncaseating granulomas; ↑ ACE, hypercalcemia
hypersensitivity pneumonitis
Acute/subacute dyspnea, cough, fever, occurs after antigen exposure (birds, mold, hot tub)
Ground-glass opacities, centrilobular nodules, air-trapping
imaging findings off hypersensitivity pneumonitis
RA, SLE, systemic sclerosis
connective tissue disease-associated interstitial lung diseases
asbestosis
exposure: Shipbuilding, construction, insulation, brake pads
bronchogenic carcinoma, mesothelioma
abestosis increases risk of
sillicosis
exposure: Mining, quarrying, sandblasting, foundry
Silicosis
-Upper lobe nodules, "eggshell" calcification of hilar nodes
-increases risk of TB, lung cancer
coal miner's pneumoconiosis
"black lung"
may cause cor pulmonale
Beryllliosis
exposure: Aerospace, electronics, ceramics
Berylliosis
-Dyspnea, cough, systemic features (like sarcoid)
-Noncaseating granulomas, hilar adenopathy
-↑ Risk of lung cancer; resembles sarcoidosis
Farmer's lung (hypersensitivity pneumonitis subtype)
exposure: moldy hay
Bimodal — 20-40 yrs (most common), smaller peak in >60 yrs
age distribution associated with sarcoidosis
Respiratory: Dyspnea, nonproductive cough, chest pain
Constitutional: Fatigue, fever, weight loss, night sweats
primary clinical presentation of sarcoidosis
-erythema nodosum
-uveitis, conjunctivity
-arthralgias
-CN VII palsy
-caridomyopathy
extrapulmonary manifestations of sarcoidosis
bilateral hilar lymphadenopathy
classic physical exam finding associated with sarcoidosis
Chest X-ray: Bilateral hilar adenopathy (stage I); interstitial infiltrates (stage II/III)
High-resolution CT: Nodules along lymphatic distribution, adenopathy
imaging findings associated with sarcoidosis
↑ ACE levels, hypercalcemia/hypercalciuria (macrophage 1α-hydroxylase ↑ vitamin D activation)
lab findings associated with sarcoidosis
non-caseating granulomas
diagnostic gold standard of sarcoidosis
sarcoidosis
autoimmune disease with fibrous lesions forming in lymph nodes, liver, skin, lungs, spleen, eyes, and small bones of hands and feet
Antifibrotics: pirfenidone, nintedanib; lung transplant if advanced; avoid chronic steroids (harmful in IPF)
standard therapies for idiopathic pulmonary fibrosis
corticosteroids
stanard therapy for sarcoidosis
Supportive (O₂, pulmonary rehab, vaccination); no role for steroids; monitor for malignancy
standard treatment for asbestosis
Stop exposure; supportive; TB surveillance (↑ risk of TB); O₂, lung transplant if advanced
standard treatment for silicosis
Remove exposure; corticosteroids if granulomatous inflammation is symptomatic
standard treatment of berylliosis
Group 1: PAH (idiopathic)
Group 2: PH due to left heart disease
Group 3: PH due to lung disease/hypoxia (COPDD, OSA)
Group 4: chronic thromboembolic PH (chronic PE)
Group 5: PH with unclear/multifactorial mechanisms (sarcoid)
define the different classes of pulmonary hypertension
Progressive exertional dyspnea
Fatigue, syncope, chest pain (angina)
Peripheral edema, ascites (if RV failure develops)
primary symptoms of pulmonary HTN
pulmonary hypertension
exam findings:
Loud P2 (accentuated pulmonic component of S2)
Right ventricular heave
Tricuspid regurgitation murmur
Jugular venous distension, hepatomegaly, edema (late RV failure signs)
right ventricular heave
seen in pulmonary hypertension
right axis deviation, RBBB
ECG findings associated with pulmonary HTN
right heart cath
PCWP >15 mmHg
gold standard diagnostic test for pulmonary HTN
Endothelin receptor antagonists
-PDE 5 inhibitors
-prostacyclin analogs
treatment for group 1 PAH (idiopathic)
Treat underlying HF/valvular disease; PAH drugs not effective
treatment for group 2 PAH (left heart disease)
Treat lung disease, give O₂; avoid routine PAH drugs
treatment for group 3 PAH (COPD/hypoxia)
Lifelong anticoagulation; surgical pulmonary thromboendarterectomy (potentially curative); riociguat if inoperable
treatment for group 4 PAH (thrombotic dx)
bilateral opacities on CXR/CT not fully explained by effusions, collapse, or nodules
imaging indicative of diagnosis off ARDS
TV 6 mL/kg IBW, aim plateau ≤30 cm H₂O, driving pressure as low as possible
PEEP per ARDSNet tables; avoid derecruitment
lung-protective ventilation of ARDS
Tall, thin young men, smoking/vaping, family history
Marfan, Ehlers-Danlos, Birt–Hogg–Dubé
etiologies of primary pneumothorax (no known lung disease)
COPD/emphysema, severe asthma, CF, interstitial lung disease, PJP pneumonia (esp. HIV), TB, necrotizing pneumonia, LAM
etiologies of secondary pneumothorax (underlying lung disease)
Central line, thoracentesis, transbronchial/pleural biopsy, mechanical ventilation (high pressures), CPR, rib fractures, penetrating/blast injury
iatrogenic/trauma etiologies of pneumothorax
-Sudden pleuritic chest pain, acute dyspnea; risk factors above; tension → hemodynamic collapse
-↓/absent breath sounds, hyperresonance, ↓ fremitus; tracheal deviation away if tension
history and exam findings associated with pneumothorax
barcode/stratosphere sign
POCUS finding associated with pneumothorax
tension pneumothorax
a type of pneumothorax in which air that enters the chest cavity is prevented from escaping
Small primary & stable → O₂ + observe/needle aspiration; large/symptomatic or any secondary → chest tube. Tension: immediate needle decompression then tube. Recurrent/air leak → pleurodesis/VATS blebectomy.
first line treatment of pneumothorax
-Progressive dyspnea, orthopnea, pleuritic pain
-↓ breath sounds, dullness to percussion, ↓ fremitus; egophony just above fluid line
history and exam findings associatedd with pleural effusion
pleural effusion on CXR
Blunted costophrenic angle, meniscus sign; large → mediastinal shift
meniscus sign
Curvilinear line seen at the upper end of a pleural effusion
thoracentesis
confirmatory test for pleural effusion
therapeutic thoracentesis if symptomatic. Transudate (CHF, cirrhosis) → diuretics/salt restriction. Exudate → treat underlying (PNA → abx; empyema or pH <7.20 → tube drainage ± tPA/DNase; malignancy → indwelling catheter/pleurodesis).
first line therapy of pleural effusion
platypnea-orthodeoxia
syndrome of dyspnea (and oxygen desaturation) that worsens with sitting upright.
-associated with pulmonary AV fistula
Solitary or multiple round, well-circumscribed nodules with feeding/draining vessels (sometimes subtle)
pulmonary AV fistula CXR
pulmonary AV fistula
an abnormal connection between a pulmonary artery (carrying oxygen-rich blood from the heart to the lungs) and a pulmonary vein (carrying oxygen-poor blood back to the heart)
cirrhosis, malignancy, pneumonia, PE, pancreatitis
Dyspnea, hypoxemia, platypnea–orthodeoxia; HHT (epistaxis, telangiectasias) → paradoxical emboli, stroke/brain abscess
presentation of pulmonary AV fistula
ARDS
acute, bilateral opacities, non-cardiogenic, PaO₂/FiO₂ ≤300 with PEEP ≥5 → low-tidal-volume, high-PEEP, prone.