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Bronchiectasis

Cystic fibrosis

ARDS/NRDS

Caused by bronchial obstruction, tumor, foreign body, mucus, chronic infections (cystic fibrosis, IgA deficiency)

Dilated airways in the lower lobes, inflammation and fibrosis of bronchial walls

Chronic cough with Purulent Sputum, hemoptysis, cyanosis, anemia Complications: lung and brain abscesses Imaging: dilated bronchioles with signet-ring appearance Decreased Hematocrit KARTAGENER SYNDROME: caused by a defect in dynein. Leading to

immotile cilia. Bronchiectasis, sterility, recurrent sinusitis, dectrocardia

Autosomal recessive disorder that is caused by a mutation Defective membrane Cl- channel Secretion of thick mucus which lodges in lungs, liver, and pancreas Mucus plugs obstruct bronchioles, hyperplasia and hypertrophy of

goblet cells occurs Productive cough, pulmonary infections, bronchiectasis, cyanosis,

meconium ileus, infertility in men High Cl- concentrations in sweat, hypoxia, increased ratio of residual

volume to TLC Lung transplant the Tx

ARDS-o Lung infections, toxin inhalation, sepsis, trauma,

pancreatitis, shocko Damage to alveolar capillary walls and alveolar walls by

cytokines o Increased vascular permeability, and decreased

surfactant leading to edema and collapseo Heavy, Red lungo Intrealveolar edema and inflammation with hyaline

membraneso Diffuse bilateral infiltrates on CXR, mismatch on

Ventilation/Perfusion scan. Hypoxia < 200 NRDS-

o Pre-me’s, maternal diabetes, c-section. Deficiency of surfactant

o Increased surface tension in the lung, leading to alveolar collapse

o Heavy, Purple lungo Eosinophilic hyaline membraneso PDA, bronchiopulmonary dysplasia

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STUBERCULOSIS

ACUTE BACTERIAL PNEUMONIA

ATYPICAL PNEUMONIA

MYCOPLASMA TB, Hypersensitivity 4 rxn Lymphocytes TH-1 Induction of T-cell response Ghon complex (primary TB) Through lymphatics -> Miliary TB Pott disease, meningitis (IFN-GAMMA)

o Primary TB - Ghon complex (upper part of the lower lobes). Caseous granuloma. Asymptomatic.

o Secondary/Miliary TB - tubercle formation (CAVITY lesion) in lung apex or hilar lymph nodes. Caseating granuloma made of Epitheloid cells (hallmark finding), and giant cells. Fatigue, weight loss, fever, productive cough with blood

Lobar pneumonia: pneumococcus pneumonia. Strep Pneumoo Intra-alveolar exudate leading to consolidationo Four stages: CONGESTION (Heavy red lung, fluid), RED

(RBCs), GRAY (Fibrin and Neutrophils), RESOLUTION (intra alveolar exudate is absorbed)

o Radio-opaque lobe Bronchiopneumonia: Staph aureus, H. influenza, klebisella, strep

pyogeneso Bilateral and multilobar, neutrophil exudate leakso Klebsiella- alcoholics, Red currant jelly sputum, fevero S. pneumo and H. influenza- In COPD patientso Patchy opacities

Complications: stony dullness on percussion, abscess

Mycoplasma pneumo, viruses (RSV, influenza, adenovirus), chlamidya pistacci, coxiella burnetii, legionella

Multilobar, patchy infiltration of mononuclear inflammatory exudate into alveolar walls

Pink hyaline membranes found Lymphocytes seen Imaging: lung not clear, interstitial infiltrates with monocytes Elevated cold agglutinin (causes anemia) seen in M. pneumo

infectionso Pneumocystis carninii pneumonia- most common

opportunistic infection seen in AIDS infections

BLACK WOMEN 20-40 Involves lung, lymph nodes, spleen, fever Noncaseating granulomas surrounded by Langhans giant cells,

asteroid bodies, and Schaumann bodies Malaise, fever, hepatosplenomegaly, dyspnea, interstitial lung

disease, erythema nodusom, polyarthritis, uveitis, and peripheral neuropathy

Bilateral hilar lymphadenopathy, and interstitial infiltrates on CXR Increased ACE, hypercalciuria, decreased TLC and DLCO

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S PNEUMOCONIOSIS

HYPERSENSITIVE PNEUMONITIS

GOODPASTURE SYNDROME

Coal worker pneumoconiosis:o Coal macules around bronchioles in the UPPER LOBESo Progressive massive fibrosis, blackened fibrotic nodules

Silicosis:o Silicotic nodules in lungs that obstruct airways and may

become scars: Honeycomb lungo Increased susceptibility to TBo UPPER LOBESo Whorled pattern, Bifringent light, Eggshell calcificationo Can lead to bronchiogenic carcinoma/mesothelioma

Asbestosis:o Inhalation of asbestoso Alveolar macrophages engulf asbestos fibers causing a

fibrostatic responseo LOWER LOBESo Diffuse interstitial fibrosiso Ferruginous bodies coated with hemosiderino Collagenous plaques on pleura and diaphragmo Dyspnea and productive cougho Clubbing of fingers and dry inspiratory crackles

Caused by sensitization to exposure of specific antigens like ACTINOMYCETES, hay, animal proteins

IgG antibodies react with antigen to form an inflammatory reaction with release of cytokines and prostaglandins

Mononuclear cell infuriation (giant cells) Noncaseating granulomas in peribronchial distribution Peripheral patchy fibrosis Acute form develops 4-12 hours after exposure- fever, malaise,

cough Chronic form presents with progressive dyspnea, insidious weight

loss, and cough Decreased DLCO Farmers lung and Bird Fancier’s lung

Antibodies against GBM (Type 2 hypersensitivity) Men aged 20-30 Intra alveolar hemorrhages, fibrosis, thickening of speta Hemosiderin-laden macrophages in alveoli Rapidly progressive crescentic glomerulonephritis Linear deposits of immunoglobulins Hemoptysis, nephritic syndrome (edema, HTN, hematuria) Anti-GBM antibodies, iron-deficiency anemia Corticosteroids, cyclophosphamides

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SPULMONARY HTN

PULMONARY FIBROSIS

PULMONARY EMBOLISM

Alveolar epithelial injury, leading to Fibroblast proliferation resulting in distortion of septa, honeycomb lung

Slow progressive dyspnea, and dry cough Physical exam: hypoxemia, inspiratory crackles, clubbing X-ray: honeycombing, reticular opacities Tx: oxygen supplementation, lung transplant

Emboli can be air, amniotic fluid, foreign bodies, or tumor cells Thromboemboli are the most common, originating from DVT in the

leg Hemorrhage or infarct of lung (lower lobes) Decreased circulation Venous thrombus (dark red wit pale-grey fibrin strands) lodged in

pulmonary vessel Mismatch ventilation perfusion scan Hypoxia, elevated d-dimer levels Virchow triad- venous stasis, hypercoaguable state, vessel wall

injury Perfusion defect

Idiopathic BMPR2 mutation – down regulates smooth muscles Young women in 20s-40s Medial hypertrophy and intimal fibrosis of the pulmonary arterioles Right ventricular hypertrophy, cor pulmonale Present with dyspnea, fatigue, chest pain, exertional syncope Complications: thrombosis, cyanosis, right ventricular hypertrophy Elevated pressures in pulmonary vasculature can be associated with

connective tissue disorders (SLE), interstitial lung dieseases (COPD, sarcoidosis)

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EMPHYSEMA

ASTHMA

CHRONIC BRONCHITIS

Extrinsic: Type 1 hypersensitivity rxn seen in children. Leukotrines in early phase, cytokines in late

Instrinsic: associated with chronic bronchitis, exercise, or cold seen in adults

Hypertrophy of bronchial smooth muscle, hyperplasia of bronchial submucosal glands containing Curshmann spirals and Charcot-Leyden crystals

Dyspnea, expiratory wheezing, cough Use of accessory muscles Complications: status asthmaticus (prolonged asthma attack),

eosinophilia Inhaled Beta-Adrenergic agonists (Albuterol)

Smoking and antitrypsin deficiency Honeycomb lung, Destruction of elastin Enlargement of air spaces, destruction of alveolar wall Centriacinar: upper lobes, seen in smokers Panacinar: associated with antitrypsin deficiency “Pink puffers” Pursed lips Use of accessory muscles Dyspnea, cyanosis, tachycardia “Barrel shaped chest” Complications: pneumothorax, cor pulmonale Imaging: Hyperinflaction and flattened diaphragm Increased residual volume, and TLC, decreased FEV1/FEVC ratio

Chronic irritation caused by smoking, air pollution, or infection Hyperplasia of submucosal glands leading to mucus plugs (increase

in goblet cells) Productive cough for at least 3 months over 2+ years “Blue bloaters” cyanosis, dyspnea Complications: cor pulmonale, polycythemia, DVT Increased residual volume, decreased FEV1/FVC ratio Reid index>50% (increased mucous gland size) Beta agonists, inhaled steroids