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MSK CORE > CHEST CORE 500 > Flashcards

CHEST CORE 500 Flashcards

1
Q

Solitary Pulmonary Nodule

A
  • Granuloma
  • Neoplasm (bronchogenic carcinoima, solitary met)
  • Hamartoma = Round pneumonia (under 8yo) = AVM
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2
Q

Multiple Pulmonary Nodules

A
  • Mets
  • Granulomas (TB or fungal)
  • Septic emboli
    = Wegener’s
    = Rheumatoid
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3
Q

Cavitary Pulmonary Nodule

A
  • TB
  • Fungal disease
  • Sqaumous cell carcinoma
    = Pyogenic infection (abscess or septic emboli)
    = Wegener’s
    = Rheumatoid arthritis
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4
Q

Milary Pulmonary Nodule

A
  • TB
  • Fungal disease
  • Mets
    = Pneumoconioses
    = Healed Varcicella
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5
Q

Centrilobular Pulmonary Nodules

A
  • Infectious bronchiolitis (MAC, TB) - Hypersensitivity pneumonitits - Endobronchial spread of tumor = RB-ILD = Pneumoconioses
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6
Q

Cystic Lung Disease

A
  • Emphysema - LAM - LCH/EG = Pneumocystis pneumonia = LIP
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7
Q

Lower Lobe Interstitial Disease

A
  • Idiopathic pulmonary fibrosis/UIP
  • Collagen vascular dz (scleroderma)
  • Asbestos-related lung dz
    = drug toxicity
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8
Q

Upper Lobe Interstitial Disease

A
  • TB - Sarcoidosis - Cystic Fibrosis = Pneumoconioses = LCH
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9
Q

Hyperlucent Lung

A
  • Chest wall abnormality (Polan, mastectomy) - Swyer-James - Acute asthma = Airway obstruction = PE = Pneumothorax
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10
Q

Anterior Mediastinal Mass

A
  • Lymphoma - Thymic lesion - Thyroid lesion = Germ cell neoplasm (teratoma)
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11
Q

Middle Medistinal Mass

A
  • Lymphadenopathy - Vascular abnormality (aneurysm) - Congenital cyst / bronchogenic cyst = hiatal hernia
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12
Q

Posterior Mediastinal Mass

A
  • Neurogenic tumor - Lymphoma - Developmental cyst (neuroenteric cyst) = extramedullary hematopoiesis = mediastinal hematoma
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13
Q

Chronic Airspace Disease

A
  • Cryptogenic Organizing Pneumonia - Pulmonary Alveolar Proteinosis - Bronchioloalveolar Cell Carcinoma [BAC] = Chronic Eosinophilic Pneumonia = Lipoid Pneumonia
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14
Q

Peripheral Airspace Disease

A
  • Cryptogenic Organizing Pneumonia - Eosinophilic Pneumonia - Pulmonary Infarction = Pulmonary Contusion = Alveolar Sarcoidosis
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15
Q

Ground Glass Opacification

A
  • Pulmonary edema - Atypical infection - Pulmonary hemorrhage = ARDS = Alveolar proteinosis = Vasculitis
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16
Q

Mediastinal/Hilar lymphadenopathy

A
  • Infection - Lymphoma - Sarcoidosis = Mets = Pneumoconioses
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17
Q

Calcified Pleural Disease

A
  • Asbestos related pleural disease - Fibrothorax (prior infex or hemorrhage) - Iatrogenic (pleurodesis)
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18
Q

Bronchiectasis

A
  • Postinfectious (bacterial, TB, MAC) - Cystic Fibrosis - ABPA = Obstructive lesion/mass = Ciliary dyskinesia
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19
Q

Perilymphatic Pulmonary Nodules

A
  • Sarcoidosis - Lymphangitic spread of tumor - Pneumoconioses = Lymphoproliferative disorder
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20
Q

Pleural Based Mass

A
  • Pleural mets - Empyema - Mesothelioma = Fibrous tumor of the pleura = Fibrothorax
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21
Q

Parenchymal Disease in an HIV patient

A
  • PCP - TB - Fungal infection = Invasive aspergillosis = Kaposi Sarcoma = Pulmonary lymphoma
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22
Q

Abnormal left ventricular contour

A
  • True LV aneurysm - False LV aneurysm - Pericardial cyst/ mass = Calcified pericarditis
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23
Q

Cardiac mass

A
  • Thrombus
  • Mets
  • Benign Neoplasm (myxoma, rhabdomyoma)

= Malignant neoplasm (sarcoma, lymphoma)

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24
Q

Delayed myocardial enhancement

A
  • Infarction/scar - Myocarditis - Cardiac mass = Infiltrative disease (amyloid, granulomatous)
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25
Q

Cardiac wall fatty deposit

A
  • Lipoma - Lipomatous hypertrophy of the interatrial septum - Arrhythmogenic RV dysplasia
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26
Q

Unilateral interstitial lung disease

A
  • Lymphangitic carcinomatosis - lymphoma - sarcoid - pulmonary edema
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27
Q

Multiple diffuse calcified nodules

A
  • Histo - Healed varicella - silicosis
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28
Q

Honeycombing

A
  • Sarcoid (upper lobe) - EG (upper lobe) - UIP (lower lobe, idiopathic) - Asbestosis (lower lobe) - Pneumoconiosis (upper lobes) - Scleroderma (lower lobe)
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29
Q

4 types of Asprergillus

A
  • ABPA (asthmatics) - Noninvasive (normal people, fungus ball) - Semi invasive (mild immunosuppressed) - Invasive (very compromised, ill defined pulm nodules)
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30
Q

Crazy Paving

A
  • PAP
  • BAC
  • lipoid pneumonia
  • Drug induced pneumonitis
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31
Q

Peripheral ground glass opacification

A
  • COP - sarcoid - BAC - Eosinophilic pneumonia
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32
Q

Anterior Mediastinal Mass

A
  1. Thymus (thymoma, carcinoma, thymolipoma) 2. Germ cell neoplasm (teratoma) 3. Lymphoma 4. Throid (goiter, cancer) 5. Vascular abnormality (aneurysm)
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33
Q

Multiple cavitary lesions

A
  1. Infection (fungal, bacterial) 2. Wegener’s ganulomatosis 3. Septic emboli 4. Cavitary Mets 5. Rheumatoid Nodules 6. Pulmonary lacerations
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34
Q

Ground Glass Opacities - Acute

A
  1. Edema 2. Hemorrhage 3. Infection (PCP) 4. Hypersensitivity Pneumonitis 5. Drug Toxcicity/Inhalation
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35
Q

Ground Glass Opacities - Chronic

A
  1. BAC 2. NSIP 3. LIP
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36
Q

Endotracheal mass

A
  1. Neoplasm (squamous, adenoid cystic, mucoepidermoid)
  2. Papillomatosis
  3. Tracheopathica Osteoplastica
  4. Saroidosis, Amyloidosis, Relapsing Polychondritis
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37
Q

Pleural Mass

A
  1. Mesothelioma
  2. Pleural Mets
  3. Fibrous tumor of pleura
  4. Lipoma
  5. Empyema/loculated effusion
  6. Infection / empyema necessitans
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38
Q

Pneumomediastinum causes

A
  1. Esophageal injury/rupture 2. Pulmonary/tracheal trauma 3. Rupture of bleb, asthma, severe coughing 4. Barotrauma 5. Surgery 6. Retropharyngeal infection
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39
Q

Basilar Fibrosis

A
  1. UIP / IPF 2. CVD (scleroderma, rheumatoid) 3. Aspiration 4. Asbestosis 5. Durg toxicity (methotrexate, chemo, busulfan)
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40
Q

Bilateral hilar adenonopathy

A
  1. Sarcoidosis 2. Lymphoma 3. Mets 4. Small cell lung cancer 5. Infections (TB) 6. Castleman’s Dz
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41
Q

Small nodules, random distribution

A
  1. Miliary TB / Histo
  2. Hematogenous mets (thyroid, renal)
  3. Silicosis
  4. EG
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42
Q

Posterior Mediastial Mass

A
  1. Neruogenic tumor (schwannoma, neurofibroma, paraganglioma, ganglioneuroma)
  2. Hematoma
  3. Abscess (Pott’s dz)
  4. Vascular (aortic aneurysm)
  5. Extramedullary hematopoesis
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43
Q

Bronchiectasis

A
  1. Cystic Fibrosis
  2. Kartagener’s / Ciliary Dyskinesia
  3. Chronic aspiration
  4. Chronic infection
  5. Inhalation injury
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44
Q

Solitary Lung Mass

A
  1. Maligancy (primary and mets) 2. Hamartoma 3. AVM 4. Infection 5. Fluid/effusion 6. Round atelectasis (a/w asbestos exposure)
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45
Q

Middle Mediastinal Mass

A
  1. Esophagus (mass, tic, hiatal hernia) 2. Varicies 3. Foregut cyst 4. Lymphadenopathy 5. Pericardial mass/ cyst 6. LV pseudoanerysm 7. Aortic or PA aneurysm
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46
Q

Bilateral Patchy Opacities - Acute

A
  1. Edema 2. Hemorrhage / Contusion 3. Infection 4. Drug toxicity 5. Hypersensitivity Pneumontis
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47
Q

Bilateral Patchy Opacities - Non-Acute

A
  1. BAC 2. Sarcoidosis 3. COP / BOOP 4. Eosinophilic Pneumonia 5. PAP 6. NSIP
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48
Q

Causes of azygous vein enlargement

A
  • Azygous continuation of IVC - Obstruction of vena cava - Tricuspid insufficiency - Rt sided heart failure
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49
Q

Causes of unilateral absent perfusion on VQ scan

A
  • Pulmonary embolism - Extrinsic compression of PA (mass, aortic aneurysm [Ehlor-Danlos, Marfan’s, syphilis]) - Aortic dissection
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50
Q

Upper Lung Chronic Infiltrative Disease

A
  • silicosis - sarcoidosis - Coal worker’s pneumoconisosis - ankylosing spondylitis - EG - cystic fibrosis
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51
Q

Causes of ascending aortic aneurysms [>4cm]

A
  • Cystic medial necrosis (marfan’s, Ehlers-Danlos) - atherosclerosis - syphilis
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52
Q

Common extrathoracic sites with endobronchial mets

A
  • kidney - melanoma - thyroid - breast - colon
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53
Q

Bilaterally enlarged apical caps

A
  • radiation fibrosis - mediastinal lipomatosis - vascular abnormalites (coarc)
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54
Q

Unilateral apical cap

A
  • Bronchogenic carcinoma - lymphoma - extrapleural hematoma - abscess - radiation fibrosis
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55
Q

In an HIV + patient, what fungal infection presents with pulmonary nodules, pleural effusion, and lymph node enlargement?

A

Cryptococcus

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56
Q

Disorders that are associated with Hypertrophic Pulmonary Osteoarthropathy

A
  • maligancy - cystic fibrosis - IPF - localized fibrous lesions of the pleura
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57
Q

Three types of bronchiectasis (Reid classification)

A

Cylindrical Varicoid Cystic/Saccular

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58
Q

Congenital disorders associated with bronchiectasis

A

Cystic Fibrosis Williams-Campbell Immotile cilia syndrome Mounier-Kuhn Primary hypogammaglobulinemia

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59
Q

Peripheral distribution of consolidation

A
  • Loffler’s syndrome
  • Chronic eosinophilic pneumonia
  • BOOP
  • pulmonary infarcts
  • vasculitides
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60
Q

4 types of emphysema

A
  1. centrilobular 2. paraseptal 3. panlobular 4. paracicatricial
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61
Q

Panlobular emphysema with basilar predominance

A

Alpha-1-antitrypsin
Ritalin lung
IV methylphenidate

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62
Q

CT findings of bronchiolitis obliterans

A
  • mosaic perfusion - bronchial dilation - air trapping
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63
Q

Conditions associated with bronchilitis obliterans

A
  • bone marrow txplant - viral infections - toxic inhalation - rheumatoid arthritis - lung txplant - IBD
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64
Q

5 CT findings of asbestosis

A
  1. curvilinear subpleural lines 2. thickened septal lines 3. subpleural dependent density 4. parenchymal bands 5. honeycombing
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65
Q

Define crazy paving

A

ground glass opacification with smooth septal thickening in a geographic distribution

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66
Q

Peripheral pattern of consilidation

A
  • BOOP
  • Loffler’s syndrome
  • chronic eosinophilic pneumonia
  • pulmonary infarcts
  • vasculitidies
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67
Q

CHF in a newborn

A
  • Left to right shunt (Vein of Galen, hemangioendothelioma) - Coarctation - Hypoplastic left heart - narrow proximal Aorta, MV, and LV - Arrhythmia - Cardiomyopathy
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68
Q

Head Cheese (air trapping, normal lung, GGO)

A
  • Hypersensitivity pneumonitis
  • Sarcoid
  • Acute on chronic PE
  • GVHD/CVD (BO and OP)
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69
Q

Mosaic Attenuation with air traping

A

Think small airways disease - BO - Asthma

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70
Q

Mosaic attenuation with no air trapping

A
  • Chronic PE (pulmonary HTN and enlarged RVH) - Vasculitis - Fibrosing mediastinitis (ST around aorta, RVH, RVE)
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71
Q

Neonate with CHD with decreased pulmonary vascularity

A
  • TOF - Ebsteins - Severe pulmonary stenosis - Tricuspid atresia
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72
Q

Neonate with CHD and increased pulmonary vascularity

A
  • D-transposition
  • Truncus arteriosis
  • TAPVR
  • VSD
  • ASD
  • PDA
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73
Q

Neonate with CHD and pulmonary venous HTN

A
  • hypoplastic L heart - coarcation - ?TAPVR
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74
Q

Noncardiogenic edema

A
  • Neurogenic - ARDS - Near drowning - Re-expansion pulmonary edema - Acute inhalational injury
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75
Q

Acyanotic, no shunt vascularity, big heart, +/- edema

A
  • Pericardial effusion - oreo cookie sign - Bicuspid aortic valve, aortic stenosis - Coarctation - figure of 3 sign, rib notching (ddx NF) - Extrathoracic shunt - Vein of galen, hemangioendothelioma - Cardiomyopathy - infiltrating (sarcoid,amyloid,HOCM) - Cardiomyopathy - ischemic/infarction - Kawasaki - coronary artery aneurysms - Cor tritriatrium
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76
Q

Types of Atelectasis

A

Obstructive, Relaxation, Adhesive, Cicatricial

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77
Q

Luftsichel sign

A

Crescent of air on frontal CXR, interface between aorta and hyperexpanded superior segment of LLL

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78
Q

Lymphangiomyomatosis findings and association

A

Diffuse cysts , round in shape, thin walled, diffuse, female childbearing age, assoc with tuberous sclerosis 1%

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79
Q

Golden’s S sign

A

RUL atelectasis, usually due to obstructing mass

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80
Q

Flat waist sign

A

LLL atelectasis with downward shift of hilar structures causing flattening of left heart border and cardiac rotation

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81
Q

Signs of round atelectasis

A

1) abnormal adjacent pleura (effusion or pleural thickening/plaque); 2) peripheral, touching pleura; 3) round or elliptical; 4) volume loss in lobe; 5) comet tail sign (pulmonary vessels and bronchi leading to opacity)

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82
Q

Ddx of acute consolidation/GGO

A

Pneumonia (atypical in GGO such as viral or PJP) Pulmonary hemorrhage/edema ARDS

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83
Q

Ddx of chronic consolidation/GGO

A

-Mucinous adenocarcinoma -Organizing pneumonia -Chronic eosinophilic pneumonia GGO add Idiopathic pneumonia Hypersensitivity pneumonitis Alveolar proteinosis

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84
Q

Ddx of GGO in central distribution

A

Pulmonary hemorrhage
Pulmonary edema - cardiogenic
PJP
Alveolar proteinosis

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85
Q

DDx for peripheral consolidation/GGO

A

Organizing pneumonia Chronic eosinophilic pneumonia Atypical pneumonia Pulmonary edema - noncardiogenic

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86
Q

Interlobular septal thickening types and ddx

A

Smooth - pulmonary edema/hemorrhage, Alveolar proteinosis, Atypical pneumonia Nodular - Sarcoid, lymphangitic carcinomatosis

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87
Q

Ddx for crazy paving

A

Alveolar proteinosis PJP Organizing pneumonia Mucinous adenocarcinoma Lipoid pneumonia ARDS Pulmonary hemorrhage

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88
Q

Ddx of Centrilobular pulmonary nodules

A

Subpleural sparing –Infectious - endobronchial TB or MAI, bronchopneumonia, atypical PNA –Inflammatory - HSP, RB-ILD, diffuse panbronchiolitis, silicosis, hot tub lung (rxn to atypical mycobacterium like HSP)

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89
Q

Ddx of perilymphatic nodules

A

Sarcoid Pneumoconiosis Lymphangitic carcinomatosis

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90
Q

Interstitial lung disease, nodules, acute

A

Fungal Miliary TB

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91
Q

Interstitial lung disease, nodular, chronic

A

Silicosis Sarcoidosis LCH Lymphangitic carcinomatosis

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92
Q

Eggshell calcifications in lungs

A

Silicosis Sarcoid Treated lymphoma

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93
Q

Interstitial,lung disease, reticular, acute

A

Interstitial edema Atypical pneumonia (viral, PJP)

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94
Q

Interstitial lung disease, reticular, chronic

A

Fibrosis Emphysema Cystic lung dz Bronchiectasis

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95
Q

Fibrosis, upper lobe distribution

A

Sarcoid Chronic HSP Cystic fibrosis Prior TB Ankylosing spondylitis XRT Silicosis

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96
Q

Fibrosis, lower lobe distribution

A

UIP, NSIP Connective tissue disorders with UIP-like findings Chronic aspiration End stage asbestosis

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97
Q

Interstitial lung disease, septal lines, chronic

A

Lymphangitic carcinomatosis
Lymphoma
Kaposi’s sarcoma
Amyloid - rare

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98
Q

Interstitial lung disease, septal lines, acute (Kerley B lines)

A

Pulmonary edema Atypical infections

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99
Q

Tree in bud nodules

A

Mycobacterium TB or atypical mycobacterium, bacterial or aspiration pneumonia, airway invasive aspergillus

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100
Q

Random nodules

A

Hematogenous metasteses, septic emboli, pulmonary LCH

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101
Q

Miliary nodules

A

Disseminated TB, fungal or hematogenous mets

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102
Q

Cavitary lesion, solitary and multiple

A

Solitary - primary bronchogenic carcinoma (cavitary adenocarcinoma or squamous cell), TB (upper lobe) Multiple - septic emboli, vasculitis, mets (squamous cell or uterine)

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103
Q

Lung cysts , solitary and multiple

A

Solitary - bulla, bleb, pneumatocoele Multiple - lymphangiomyomatosis, emphysema, pulmonary LCH, diffuse cystic Bronchiectasis, PJP pneumonia, lymphoid interstitial pneumonia

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104
Q

Halo sign in pulmonary

A

Ground glass attenuation surrounding consolidation. Ddx angioinvasive aspegillosis, hemorrhage met, Wegeners granulomatosis, Kaposi’s sarcoma, viral infection

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105
Q

Tracheal thickening, diffuse, sparing of posterior trachea

A

Relapsing polychondritis - usu involves ears and nose in middle age female Tracheobrochopathi osteochondroplastica - nodular with calcifications

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106
Q

Tracheal thickening, diffuse, circumferential

A

TB

  • smooth long segment Amyloid
  • nodular +/- calcifications Wegeners granulomatosis
  • subglottic stenosis Sarcoid
  • hilar LAD, differing presentations
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107
Q

RUL segments?

A

Apical, posterior, anterior

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108
Q

RML segments?

A

Lateral and medial

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109
Q

RLL and LLL segments?

A

Superior, Lateral, Anterior, Posterior, Medial

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110
Q

LUL segments.

A

Apical posterior. Anterior. Superior lingula. Inferior lingula.

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111
Q

**In lower lobes, medial and anterior are anterior, posterior and lateral are posterior

A
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112
Q

Minor fissure?

A

RUL from RML. Fine horizontal line.

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113
Q

Azygos lobe?

A

1%. RUL apical or posterior segments are encased in their own parietal and visceral pleura

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114
Q

In which type of atelectasis would you expect to see air bronchograms?

A

Subsegmental atelectasis. Dont see them in obstructive atelectasis because airways are obstructed of course.

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115
Q

Subsegmental atelectasis?

A

Obstruction of small peripheral bronchi usually due to secretions

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116
Q

**Obstructive atelectasis happens more quickly in patients breathing supplemental oxygen because its absorbed from the alveoli quicker than nitrogen. Obstructive atelectasis happens when oxygen from air is absorbed by blood and not replaced.

A
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117
Q

**In general obstructive atelectasis is associated with volume loss, but in critically ill ICU patients, there may be rapid transudation of fluid into obstructed alveoli, causing superimposed consolidation

A
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118
Q

Relaxation atlectasis?

A

This is what is seen adjacent to a mass or pleural effusion causing mass effect

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119
Q

Adhesive atelectasis?

A

Lack of surfactant. RDS. ARDS.

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120
Q

Cicatrical atelectasis?

A

Volume loss from architectural distortion of lung parenchyma by fibrosis

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121
Q

Acute lobar atelectasis?

A

Mucus plugging

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122
Q

Lobar atelectasis in an outpatient?

A

Obstructing central tumor must be ruled out

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123
Q

What sign in LUL atelectasis?

A

Luftsichel sign. Crescent of air on the frontal radiograph representing the interface between the aorta and the hyperexpanded superior segment of LLL

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124
Q

Sign in RUL collapse?

A

Reverse S sign of Golden.

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125
Q

Juxtraphrenic peak sign?

A

Peridiaphragmatic triangular opacity caused by diaphragmatic traction from an inferior accessory fissure or an inferior pulmonary ligament

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126
Q

What do you see in LLL collapse?

A

Heart rotates and the L hilum is pulled down.

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127
Q

What sign in LLL collapse?

A

Flat waist sign describes flattening of the L heart border as a result of downward shift of hilar structures

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128
Q

**RLL collapse is a mirror image of LLL collapse

A
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129
Q

RML atelectasis?

A

You may only seen loss of R heart border.

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130
Q

Round atelectasis?

A

Focal atelectasis with a round morphology, always associated with an adjacent pleural abnormality

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131
Q

Diagnostic criteria for round atelectasis?

A

All five have to met. Adjacent pleura has to be abnormal. Opacity must be peripheral and in contact with pleura. Must be round or elliptical. Volume loss in affected lobe. Pulmonary vessels and bronchi leading into the opacity must be curved causing comet tail

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132
Q

Center of each secondary pulmonary lobule?

A

Centrilobular artery and central bronchus.

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133
Q

Periphery of each pulmonary lobule?

A

Pulmonary veins and lymphatics

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134
Q

Size of SPL?

A

Between 1-2.5 cm

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135
Q

**Only call ground glass on CT

A
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136
Q

Histology of consolidation?

A

Complete filling of the affected alveoli with a liquidlike substance- Blood, pus, water, or cells

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137
Q

**Can’t see pulmonary vessels through the consolidatoin on unenhnaced CT, but you can with ground glass opacification (GGO)

A
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138
Q

Differenential of acute consolidation?

A

Pneumonia.
Pulmonary Hemorrhage.
ARDS.
Pulmonary edema.

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139
Q

Differential of chronic consolidation?

A

BAC. Organizing pneumonia. Chronic eosinophilic pneumonia.

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140
Q

Distribution of chronic eosinophilic pneumonia?

A

Upper lobes

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141
Q

Histology of ground glass opacification?

A

Incomplete filling of alveoli (blood, pus, water, or cells). Alveolar wall thickneing, or reduced aeration.

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142
Q

Differential of acute GGO?

A

Edema. Pna (Atypical more common). Pulm hemorrhage. ARDS.

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143
Q

Chronic GGO differential?

A

BAC. Organizing pneumonia. Chronic eosinophilic pneumonia. Idiopathic pneumonias. HP (subacute phase). Alveolar proteinosis.

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144
Q

Central distribution of GGO?

A

Edema. Alveolar hemorrhage. Pneumocystis Jiroveci. Alveolar proteinosis.

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145
Q

Peripheral consolidation or GGO?

A

Organizing pna. Chronic eosinophilic (upper lobes). Atypical or viral pna. Edema (noncardiac, cardiac will be central)

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146
Q

By far, most common cause of smooth interlobular septal thickening?

A

Edema

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147
Q

Diff for smooth interlobular septal thickening?

A

Edema. PAP. Pulm hemorrhage. Atypical pna. (Same diff as central GGO)

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148
Q

Nodular, irregular, or assymetric septal thickening?

A

Lymphangitic carcinomatosis. Sarcoidosis.

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149
Q

Crazy paving?

A

Interlobular septal thickening with superimposed GGO

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150
Q

Why does PAP cause crazy paving?

A

Filling of alveoli with proeinaceous material and septal thickening caused by lymphatics taking up the same material

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151
Q

Differential for crazy paving? (7)

A 
PAP. 
Pneumocystic Jiroveci. 
Organizing pna. 
BAC (mucinous). 
Lipoid pneumonia. 
ARDS. 
Pulm Hemorrhage.
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152
Q

**Centrilobular nodules never extend to the pleural surface

A
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153
Q

Infectious causes of centrilobular nodules?

A

Endobronchial spread of TB or atypical mycobacteria. Bronchonpneumonia. Atypical pneumonia (esp. mycoplasma)

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154
Q

Inflammatory causes of centrilobular nodules?

A

HSP and RB ILD are most common. Otehrwise Hot tub lung, diffuse panbronchiolitis, and silicosis.

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155
Q

Diffuse panbronchiolitis?

A

Chronic inflammatory disorder characterized by lymphoid hyperplasia of the walls of respiratory bronchioles, usually patients are Asian.

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156
Q

What type of hypersensitivity reaction is HSP?

A

Type III

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157
Q

Three locations of perilymphatic nodules?

A

Subpleural. Peribronchovascular. Septal.

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158
Q

Most common cause of perilymphatic nodules?

A

Sarcoid.

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159
Q

Galaxy sign?

A

Sarcoid. Confluent perilymphatic nodules.

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160
Q

Other causes of perilymphatic nodules?

A

Pneumoconioses and lymphangitic carcinomatosis.

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161
Q

Random nodule distribution?

A

Mets. Septic emboli. Pulmonary LCH.

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162
Q

Miliary pattern of nodules?

A

Diseminated TB. Diseminated fungal infection. Diseminated mets.

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163
Q

**Most effusions associated with pneumonia are not empyemas but instead are a sterile effusion caused by increaed capillary permeability

A
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164
Q

**Treatment of BPF is very contraversial and individualized

A
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165
Q

**Miliary TB can be primary or reactivation TB

A
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166
Q

**Normal CT rules out P Jiroveci but it can hide in a normal chest radiograph

A
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167
Q

What are the linear branching structures in the tree in bud pattern? The nodules?

A

Impacted bronchioles, nodules are the impacted terminal bronchioles.

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168
Q

Tree in bud are almost always associated with what?

A

Small airways infection

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169
Q

Diff for tree in bud nodules?

A

Mycobacteria.
Bacterial pna.
Aspiration pna.
Airway invasive aspergillosis

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170
Q

Wall thickness for definite benign or malignant cavitary lesions?

A

Under 4 mm will be benign and over 15 mm will be malignant

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171
Q

Solitary cavitary lesion is almost always what?

A

Cancer or infection

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172
Q

Diff for cavitary lesions?

A

Carcinoma (SCC or adno, usually SCC). TB (Upper lobe cavitation). Septic emboli. Vasculitis (Wegeners). Metastases.

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173
Q

Diff for multiple lung cysts?

A

LAM. Emphysema (upper lobe in a smoker). Pulmonary LCH (cysts and nodules in upper lungs). Diffuse cystic bronchiectasis. Pneumocystis jiroveci. LIP

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174
Q

Bulla vs bleb?

A

Bulla is big, larger than 1 cm, occupies at least 30% of volume of the thorax. Bleb is an air filled structure contiguous with pleura less than 1 cm

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175
Q

Diff for lower lobe fibrotic changes?

A

IPF. End stage asbestosis. NSIP.

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176
Q

NSIP usually associated with what?

A

Collagen vascular disease or drug reaction.

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177
Q

Two types of NSIP?

A

Cellular and fibrotic.

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178
Q

Honeycombing in NSIP?

A

NO

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179
Q

Which type of NSIP causes basilar fibrosis?

A

Fibrotic

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180
Q

Upper lobe firbosis differential?

A

End stage sarcoidosis. Chronic hypersensitivity pneumonitis. End stage silicosis.

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181
Q

Types of pneumonia which affect young otherwise healthy patients?

A

Mycoplasma. Viral. Chlamydia.

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182
Q

Who gets legionella?

A

Elderly smokers. Severe infections

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183
Q

Who gets klebsiella?

A

Alcoholics and aspirators

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184
Q

Klebsiella leads to what?

A

Voluminous inflammatory exudates causing the bulging fissure sign.

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185
Q

Most important pathogens in HAP?

A

MRSA and resistent gram negatives including pseudomonas

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186
Q

Pathogens in VAP?

A

Usually polymicrobial but pseudomonas and acinetobacter are useful

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187
Q

What is bronchopneumonia?

A

Patchy consolidation with poorly defined airspace opacities usually involving several lobes. Usually S Aureus.

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188
Q

Interstitial pneumonia?

A

Inflammatory cells in the interstitial tissues of the alveolar septa. Atypical agents.

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189
Q

What causes round pneumonia?

A

Children. Incomplete pohrs of Kohn. S. Pneumonia.

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190
Q

Pulmonary gangrene?

A

Necrosis or sloughing of a pulmonary segment or lobe, severe manifestation of pulmonary abscess.

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191
Q

3 Stages of Empyema?

A

1- Free flowing exudative effusion- treat with needle aspiration or simple drain. 2- Development of fibrous strands- Large bore chest tube and fibrinolytic therapy. 3- Fluid becomes solid and jelly like- Requires surgery.

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192
Q

**Most effusions associated with pneumonia are not empyemas but instead are a sterile effusion caused by increaed capillary permeability

A
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193
Q

Most common cause of bronchopleural fistula?

A

Surgery. More rare causes are lung abscess, empyemia, trauma.

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194
Q

Imaging of BPF?

A

New or increasing gas in a pleural effusion.

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195
Q

**Treatment of BPF is very contraversial and individualized

A
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196
Q

Empyema necessitans?

A

Extension of empyema to chest wall, usually due to TB. Can also be caused by Nocardia and Actinomyces

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197
Q

Initial exposure to TB can lead to what two clinical outcomes?

A

Contained disease. Primary TB.

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198
Q

Describe contained TB?

A

90%. Results in calcified granulomas and/or calcified hilar lymph nodes. Normal immune patients will sequester the bacilli with a caseating granuloma.

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199
Q

Describe primary TB?

A

Host cannot contain the organism- Seen in immunocompromised and children

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200
Q

What percentage of primary TB have normal radiographs?

A

15%

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201
Q

4 Imaging features of pulmonary primary TB?

A

Ill defined consolidation.
Pleural effusion.
Lymphadenopathy.
Miliary disease.

202
Q

Most common lobes for primary TB?

A

Lower lobes and RML.

203
Q

Ghon Focus?

A

Initial focus of parenchymal infection.

204
Q

Ranke complex?

A

Ghon focus and lymphadenopathy

205
Q

Which TB gets cavitation?

A

Rare in primary TB. Common in reactivation TB.

206
Q

Adeonpathy in TB?

A

Low attenuation centrally and peripheral enhancement.

207
Q

Which TB gets adenopathy?

A

Primary. Rare in post primary.

208
Q

Where does reactivation TB usually occur?

A

Upper lobe apical and posterior segments.

209
Q

Reactivation TB in an immunocompetent patient?

A

Cavitation and lack of adenopathy. Focal upper lobe consolidation and endobronchial spread (Tree in bud) is common.

210
Q

Reactivation TB in an immunocompromised patient?

A

Low attenuation adenopathy. May mimic immune reconstitution syndrome seen in HIV patients.

211
Q

Tuberculoma?

A

Well defined rounded opacity in the upper lobes

212
Q

Healed TB?

A

Apical scarring with upper lobe volume loss and superior hilar retraction.

213
Q

Calcified granulomas signify what?

A

Containment of initial infection by a delayed hypersensitivity response.

214
Q

**Miliary TB can be primary or reactivation TB

A
215
Q

Classic radiographic findings of Lady Windermere syndrome?

A

Bronchiectasis and tree in bud nodules in the RML or lingula.

216
Q

Clinical presentation of Lady Windermere syndrome?

A

Elderly woman with cough, low grade fever and weight loss

217
Q

Organisms in Lady Windermere syndrome?

A

MAI. M. Kansasii

218
Q

What is hot tub lung?

A

Hypersensitivity pneumonitis in response to atypical mycobacteria which are often found in hot tubs. Patient is otherwise healthy, no active infection. Imaging is similar to other causes of HP with centrilobular nodules.

219
Q

Rare complication of histoplasmosis?

A

Fibrosing mediastinitis, infection of lymph nodes leading to pulmonary venous obstruction, bronchial stenosis, and pulmonary artery stenosis.

220
Q

Chronic histoplasmosis can mimic what?

A

TB- Upper lobe fibrocavitary consolidation

221
Q

Focal airspace opacity in an immunocompromised patient?

A

Bacterial pna. Consider TB if CD4 count is low.

222
Q

Who gets pneumocystic jiroveci?

A

CD4 less than 200

223
Q

Classic radiographic findings of P Jiroveci?

A

Bilateral perihilar airspace opacities with peripheral sparing.

224
Q

Classic CT of P Jiroveci?

A

Perihilar GGO sometimes with crazy paving.

225
Q

**Normal CT rules out P Jiroveci but it can hide in a normal chest radiograph

A
226
Q

P Jiroveci has a propensity to lead to what?

A

Upper lobe pneumotoceles which may predispose to pneumothorax or pneumomediastinum.

227
Q

Most common fungal infection in AIDS patients?

A

Cryptococcus

228
Q

Pulmonary infection with cryptococcus usually coexists with what?

A

Cryptococcus meningitis

229
Q

CD4 in cryptococcus?

A

Less than 100

230
Q

Imaging of cryptococcus?

A 
Wide range: 
GGO,
 Focal consolidation, 
cavitating nodules, 
miliary diseaes, lymphadenopathy, 
effusions
231
Q

Aspergillus only affects who?

A

Individuals with abnormal immunity or pre-existing pulmonary disease

232
Q

Types of aspergillus infection?

A

ABPA, Aspergilloma (Saprophytic), Semi invasive. Airway invasive. Angioinvasive.

233
Q

What is allergic bronchopulmonary aspergillosis and who gets it?

A

Hypersensitivity reaction to aspergillus in patients with long standing asthma

234
Q

Presentation of ABPA?

A

Recurrent wheezing, low grade fever, cough, sputum production. Sputum contains fragments of aspergillus hyphae.

235
Q

Key finding on CT of ABPA?

A

Upper lobe bronchiectasis and mucoid impaction which can be high attenuation or even calcified

236
Q

Combination of mucoid impaction within bronchiectatic airways represents what sign?

A

Finger in glove

237
Q

What is saprophytic aspergillosis?

A

An aspergilloma develops in a pre-existing cavity.

238
Q

**Imaging of patient in different positions causes the aspergilloma to move

A
239
Q

Most common causes of a pre-existing cavity?

A

TB and sarcoid.

240
Q

Most common symptom of aspergilloma?

A

Hemoptysis

241
Q

Monod sign?

A

Crescent of air outlines the mycetoma against the wall of the cavity.

242
Q

What is semi-invasive aspergillosis?

A

Necrotizing granulomatous inflammation (analogous in pathology to reactivation tb) in response to chronic aspergillus infection.

243
Q

Who gets semi-invasive aspergillosis?

A

Debilated, diabetic, alcoholic, and COPD patients

244
Q

CT of semi-invasive aspergillosis?

A

Segmental areas of consolidation, often with cavitatoin and pleural thickening, which progress slowly over months or years

245
Q

What is airway invasive aspergillosis?

A

Infection deep to the airway epithelial cells

246
Q

Who gets airway invasive aspergillosis?

A

Only the immunocompromised, including neutropenic and AIDS patients

247
Q

Spectrum of clinical disease in airway invasive aspergillosis?

A

From bronchiolitis to bronchopneumonia

248
Q

CT findings of airway invasive aspergillosis?

A

Centrilobular and tree in bud nodules. Also bronchopneumonia which is indistinguishable from other causes of bronchopneumonia

249
Q

What is angioinvasive aspergillosis?

A

Aggressive infection characterized by invasion and occlusion of arterioles and smaller pulmonary arteries by fungal hyphae.

250
Q

Who gets angioinvasive aspergillosis?

A

Severely immunocompromised patients, including patients on chemotherapy, stem cell or solid organ trasplant recipients, and in AIDS

251
Q

Air cresent sign in angioinvasive aspergillosis?

A

Represents a crescent of air from retraction of infarcted lung. Good prognostic sign indicating patient is in recovery phase.

252
Q

What do Kerley A lines represent?

A

Dilated lymphatic channels radiating from hila, clinically insignificant

253
Q

Kerley B lines?

A

Radiate from periphery- Thickened interlobular septa

254
Q

3 stages of pulmonary edema radiographically?

A

Vascular redistribution (increased caliber of the upper lobe vessels compared to lower lobe vessels). Interstitial edema. Alveolar edema (Pleural effusions and cardimegaly are usually present)

255
Q

GGO in intrathoracic causes of edema vs non thoracic causes?

A

Intrathoracic- Patchy. Nonthoracic- Diffuse.

256
Q

When does reexpasion pulmonary edema occur?

A

Aggressive thoracentesis- reexpansion of lung in a state of collapse for more than 3 days

257
Q

Vascular pedicle?

A

Transverse width of the upper mediastinum

258
Q

Right border of vascular pedicle?

A

Interface of the SVC and R mainstem bronchus.

259
Q

L border of the vascular pedicle?

A

Lateral border of the takeoff of the subclavian from the aorta

260
Q

Normal vascular pedicle width?

A

Less than 58 mm

261
Q

**Vascular pedicle widths of 63 and 70 have been proposed as cutoffs for increased pulmonary capillary wedge pressure

A
262
Q

**ET Tube can be slightly lower in situations with low pulmonary compliance like ARDS to reduce barotrauma

A
263
Q

Look at pics of azygous malposition of catheter, what risks? What percentage of patients have azygous malposition.

A

1% of patients. Increased risk of venous perforation and thrombosis

264
Q

Risks of Swan Ganz distal to proximal interlobar pulmonary artery? General risks of Swan Ganz.

A

Rupture or pseudoanerysm.

Also intracardiac catheter knot and arrythmias are other complications of swan ganz catheters

265
Q

Tobacco is thought to cause what percentage of lung cancers?

A

80-90%

266
Q

**Asbestos increases lung ca risk by 5 and is synergistic with smoking

A
267
Q

**Pulmonary fibrosis increases lung ca risk by 10

A
268
Q

**Scarring also increases risk

A
269
Q

More likely malignant, solid or gg nodule?

A

GG nodule

270
Q

What types of calcification are benign?

A

Central. Laminar. Diffuse.

271
Q

What nodules have popcorn calcification?

A

Hamartoma

272
Q

Shape of pulmonary nodule and correlation with ca?

A

Non round is usually benign

273
Q

Clustering of nodules suggests?

A

Infection

274
Q

Nodule .8-3cm?

A

18% of malignancy.

275
Q

Nodules over 3 cm?

A

Very high chance of malignancy

276
Q

Margins which are concerning?

A

Irregular edge or spiculated margin

277
Q

Doubling in volume corresponds to what increase in diameter?

A

26%

278
Q

**Decrease in size of a suspicious nodule isn’t sufficient to diagnose benignity, can occur with collpase of aerated alveoli or necrosis

A
279
Q

Histology of lung ca with the worst prognosis?

A

Small cell

280
Q

Most common histological subtype of lung ca?

A

Adneocarcinoma

281
Q

Adenocarcinoma, central or peripheral?

A

Peripheral

282
Q

Pathologic marker of adenocarcinoma of the lung?

A

TTF-1 (Thyroid transcription factor). Positive in adenocarcinoma and negative in pulmonary mets

283
Q

Majority of SCC arise from where?

A

Main lobar or segmental bronchi. Causes symptoms early due to bronchial obstruction.

284
Q

Lepidic growth?

A

BAC. Spreading of malignant cells using the alveolar walls as a scaffold

285
Q

Hilic growth?

A

Most other types of lung cancer. Cancer growth by invasion and destruction of lung parenchyma.

286
Q

BAC on PET?

A

Negative

287
Q

**New classification of BAC- Going to ignore this

A
288
Q

Better prognosis, nonmucinous or mucinous BAC?

A

Nonmucinous

289
Q

Imaging of nonmucinous BAC?

A

Solid or gg nodule with air bronchograms

290
Q

Imaging of mucinous BAC?

A

Chronic consolidation.

291
Q

CT angiogram sign?

A

Describes prominent appearance of enhancing pulmonary vessels seen in low attenuation mucin rich consolidation of mucinous BAC

292
Q

Third most common histologic subypte of lung cancer?

A

Small cell (after adeno and scc)

293
Q

In small cells, neoplastic cells are of what origin?

A

Neuroendocrine

294
Q

Small cell associated with what?

A

Smoking

295
Q

Where dose small cell tend to occur?

A

Central bronchi with invasion through the bronchial wall, typically presenting as a large hilar or perihilar mass.

296
Q

**Small cell is considered disemminated disease, rarely amenable to surgery

A
297
Q

**Large cell is a wastebasket diagnosis for tumors which aren’t squamous, adenocarcinoma, or small cell

A
298
Q

Large cell associated with what?

A

Smoking

299
Q

Where do large cell carcinomas usually occur?

A

Periphery as a large mass

300
Q

Common presentation of carcnoid?

A

Endobronchial mass distal to the carina which may cause obstructive atelectasis. Up to 20% of cases present as a pulmonary nodule

301
Q

Describe two subtypes of carcinoid?

A

Typical- without mets has an excellent prognosis (92% survival over 5 years). Atypical has a worse prognosis and arises in periphery.

302
Q

What is diffuse idiopathic pulmonary neuroendocrine cell hyperplasia?

A

DIPNECH- Extremely uncommon precursor lesion to typical carcinoid tumor, characterized by mutiple foci of neurondocrine hyperplasia or tumorlets (Carcinoid foci less than 5 mm) and bronchiolitis obliterans

303
Q

50% of cancrs presenting as a solitary pulmonary nodule is what?

A

Adenocarcinoma, including BAC

304
Q

Hilar mass is a common presentation of which lung cancers?

A

SCC and Small cell

305
Q

**Tapered bronchus is highly specific for lung cancer

A
306
Q

What is a superior sulcus tumor?

A

Lung ca occuring in the lung apex

307
Q

What is a pancoast tumor?

A

Type of superior sulcus tumor with involvement of the sympathetic ganglia causing Horner syndrome

308
Q

Horner syndrome?

A

Ipsilateral ptosis, miosis, anhidrosis

309
Q

What stage is a superior sulcus tumor?

A

T3

310
Q

What is lymphangitic carcinomatosis?

A

Diffuse spread of neoplasm through the pulmonary lymphatics, typically seen in late stage disease. Nodular interlobular septal thickening, usually asymmetric

311
Q

What stage is a malignant effusion?

A

M1a- meaning it precludes curative resection. Have to do cytologic evaluation to be sure.

312
Q

Surgery is performed for what stages of lung cancer?

A

Early stages up to IIB and sometimes IIIA. Can do neoadjuvant or adjuvant chemo and radiotherapy also.

313
Q

What makes a tumor IIIb or unresectable?

A

Contralteral or supraclavicular lymph nodes.

314
Q

**Skipped lung cancer staging. Probably need to review later?

A
315
Q

When can you use pulmonary arterial hypertension instead of pulmonary hypertension?

A

WHO Class 1 entities

316
Q

Definition of pulmonary arterial hypertension?

A

Pulmonary arterial systolic pressure greater than 25 at rest or 30 during exercise.

317
Q

When are elevated pulmonary venous pressures present?

A

When pulmonary capillary wedge pressure is greater than 18

318
Q

Causes of pulmonary hypertension?

A

Chronic thromboembolic disease, chronic respiratory disease, chronic heart disease, idipathic causes

319
Q

Most common classification of pulmonary hypertension?

A

Pre-capillary and Post-capillary.

320
Q

Precapillary is what?

A

Causes clear up to the pulmonary parenchyma.

321
Q

Postcapillary is what?

A

Problems with pulmonary veins or pulmonary venous pressure.

322
Q

5 classes of pulmonary hypertension according to WHO?

A

Pulmonary arterial hypertension. Pulmonary venous hypertension. Pulmonary hypertension associated with chronic hypoxemia. Pulmonary hypertension due to thromboembolic disease. Pulmonary hypertension due to miscellaneous disorders.

323
Q

Causes of grade 1 pulmonary hypertension?

A

Primary (Idiopathic or familial). Congenital L to R shunts. Pulmonary venous or capillary involvement such as pulmonary venoocclusive disease and pulmonary capillary hemangiomatosis

324
Q

Causes of grade 2 pulmonary hypertension?

A

L sided heart disease.

325
Q

Causes of grade 5 pulmonary hypertension?

A

Sarcoid, compression of vessels, etc.

326
Q

Pathognominic for pulmonary artery hypertension?

A

Pulmonary artery calcifications

327
Q

Lungs in pulmonary hypertension?

A

Mosaic attenuation due to perfusion abnormalities

328
Q

Hilum convergence sign?

A

Confirms that a hilar mass is in fact a pulmonary artery. There is a convergence of hilar pulmonary artery branches into an enlarged pulmonary artery

329
Q

Hilum overlay sign?

A

Visualization of hilar vessels thorugh a mass- indicates that a mass is actually present.

330
Q

Where is mass in hilum overlay sign?

A

Anterior mediastinum, never middle.

331
Q

Imaging of pulmonary arteries in pulmonary hypertension?

A

Enlarged centrally. Taper distally.

332
Q

Plexiform lesion?

A

In wall of muscular arteries in pulmonary hypertension- Focal disruption of the elastic lamina by an obstructing plexus of endothelial channels. Relative paucity of prostacyclins and nitric oxide expressed by endothelial cells

333
Q

Pulmonary veno-occlusive disease?

A

Fibrotic obliteration of the pulmonary veins and venules.

334
Q

Associations of pulmonary veno-occlusive disease?

A

May be idiopathic but is associated with pregnancy, drugs, and bone marrow transplant

335
Q

Imaging of pulmonary veno-occlusive disease?

A

Pulmonary arterial enlargement. Pulmonary edema and gg centrilobular nodules are often present

336
Q

Treatment of chronic thromboembolic pulmonary hypertension?

A

Surgical thromboendartectomy (similar to carotid endarterectomy)

337
Q

Most common cause of fibrosing mediastinitis?

A

Histoplasmosis and TB

338
Q

Imaging of fibrosing mediastinitis?

A

Increased mediastinal soft tissue

often with calcified lymph nodes due to prior granulomatous infection

339
Q

Fleishner sign?

A

Widening of pulmonary arteries due to clot

340
Q

Hamptoms hump?

A

Peripheral wedge shaped opacity representing pulmonary infarct.

341
Q

Westermark sign?

A

Regional oligemia in lung distal to pulmonary artery thrombus

342
Q

Type 1 pneumocytes?

A

Form alveolar wall and participate in gas exchange

343
Q

Type 2 pneumocytes?

A

Produce surfactant, which prevents atelectasis

344
Q

Mean survival of interstitial pulmonary fibrosis

A

2-4 years

345
Q

Only interstitial pneumonia with a worse prognosis than pulmonary fibrosis?

A

AIP

346
Q

Clinical syndrome of UIP?

A

IPF

347
Q

Other triggers of lung injury that may result in a UIP pattern?

A

Collagen vascular disease (RA more than scleroderma). Drug injury. Asbestosis.

348
Q

NSIP vs UIP histology

A

Less fibrotic change in NSIP

349
Q

Treatment difference between NSIP and UIP?

A

NSIP responds to steroids

350
Q

Most common pulmonary manifestation in patients with collagen vascular disase?

A

NSIP

351
Q

Important imaging feature of NSIP?

A

Ground glass opacities, nearly always bilateral

352
Q

Fibrotic NSIP appearance?

A

Features GGO with fine reticulation and traction bronchiectasis

353
Q

Which NSIP has worse prognosis?

A

Fibrotic

354
Q

Cellular NSIP appearance?

A

GGO without much fibrotic changes

355
Q

Which NSIP is more common?

A

Fibrotic

356
Q

Very specific but uncommon finding in NSIP?

A

Sparing of immediate subpleural lung

357
Q

What is COP?

A

Cryptogenic organizing pneumonia- Clinical syndrome of organizing pneumonia without known cause

358
Q

**COP used to be called BOOP

A
359
Q

Treatment and prognosis of COP?

A

Responds to steroids with a good prognosis, may resolve completely, although recurrences are common

360
Q

Pathologic pattern of OP?

A

Granulation tissue polyps that fill the distal airway and alveoli

361
Q

CT of OP?

A

Mixed consolidation and ground glass opacities in a peripheral and peribronchovascular distribution

362
Q

What sign is specific for COP?

A

Reverse halo or Atoll sign- Central lucency surrounded by a GG halo

363
Q

Central opacity with peripheral GG?

A

Halo sign- Invasive aspergillus

364
Q

RB-ILD associated with what?

A

Smoking

365
Q

Pathological finding in RB-ILD?

A

Pigmented macrophages are found in respiratory bronchioles

366
Q

Key imaging findings of RB-ILD?

A

Centrilobular nodules and patchy GGO.

367
Q

Distribution of GGO in RB-ILD vs NSIP?

A

More random in RB-ILD where it is more peripheral in NSIP

368
Q

**RB-ILD and DIP represent a continous spectrum of smoking related lung disease

A
369
Q

Pathology of RB-ILD vs DIP?

A

In DIP, the brown pigmented macrophages also extend into the alveoli

370
Q

Imaging of DIP?

A

Diffuse basal predominant patchy or subpleural GGO, more extensive than RB-ILD. A few cysts may also be present although predominant abnormality is GGO

371
Q

LIP is very rare, associated with what?

A

Sjogrens, HIV

372
Q

Histology of LIP?

A

DIffuse infiltration of the interstitium by lymphocytes and other immune cells, with resultant distortion of the avleoli.

373
Q

Imaging of LIP?

A

Diffuse or lower lobe predominant GGO with scattered thin walled perivascular cysts, thought to be due to air trapping from peribronchiolar cellular debris

374
Q

LIP may be complicated by what in advanced disease?

A

PTX

375
Q

AIP is synonomous with what?

A

DAD- Diffuse alveolar damage.

376
Q

What is AIP?

A

Clinical syndrome of ARDS

377
Q

Primary cause of AIP?

A

Surfactant destruction

378
Q

Two phases of AIP?

A

Early (Exudative) and chronic (Organizing)

379
Q

Phases of HP?

A

Acute, subacute, chronic

380
Q

Acute HP?

A

Inflammatory exudate filling the alveoli, manifests on imaging as groundglass or consolidation. Small, ill defined centrilobular nodules.

381
Q

Subacute HP?

A

Centrilobular GG nodules. Mosaic attenuation

382
Q

Head cheese sign?

A

Describes combination of patchy GG and areas of lucency due to mosaic perfusion or air trapping

383
Q

**Abnormalities of HP involve entire axial cross section of lung

A
384
Q

Chronic HP?

A

Upper lobe predominant pulmonary fibrosis superimposed on findings of subacute and acute HP

385
Q

Honeycombing in HP?

A

Can be seen in upper lobes but is uncommon.

386
Q

Pneumoconioses vs HP?

A

Pneumoconiosis is due to inorganic dust inhalation where HP is organic dust inhalation

387
Q

Two most common pneumoconioses?

A

Silicosis and coal workers pneumoconiosis

388
Q

**Findings of CWP and Silicosis are indistinguishable

A
389
Q

Who gets silicosis?

A

Miners, from inhalation of silica dust

390
Q

CWP is due to what?

A

Inhalation of coal dust

391
Q

Most characteristic finding of uncomplicated disease in silicosis and CWP?

A

Upper lobe predominant centilobular and subpleural nodules

392
Q

Eggshell lymph node calcifications?

A

Silicosis. Less commonly CWP

393
Q

Complications of silicosis or CWP?

A

Large conglomerate masses (Progressive massive fibrosis)

394
Q

Both silicosis and CWP have increased risk of?

A

TB

395
Q

Caplan syndrome?

A

RA and either CWP (more common) or silicosis- represents necrobiotic rheumatoid nodules superimposed on the smaller centrilobualr and subleural nodules of the pneumoconiosis.

396
Q

End stage asbestosis?

A

Pulmonary fibrosis with a UIP pathology

397
Q

Upper or lower lobes for asbestosis? Why?

A

Lower lobes, the asbestos fibers are too large to be removed by the alveolar macrophages and lymphatic system

398
Q

Clue to asbestos exposure?

A

Pleural thickening and plaques (May or may not be calcified).

399
Q

**Even though pleural plaques are due to asbestos exposure, they are not a component of asbestosis, do not lead to fibrosis, and are usually asymptomatic

A
400
Q

**Eosinophilic lung disease is a spectrum of diseases that feature accumulation of eosinophils in the pulmonary airspaces and interstitium

A
401
Q

Simple pulmonary eosinophilia?

A

Also called Loeffler syndrome- Transient and migratory areas of focal consolidation, with an elevated eosinophilic count in the peripheral smear

402
Q

**Identical appearance to eosinophilia can be seen with parasites and drugs but simple pulmonary eosinophilia is reserved for idiopathic causes

A
403
Q

Consolidation in chronic eosinophlic pneumonia?

A

Peripheral with upper lobe predominance- pattern can remain unchanged for months.

404
Q

Treatment of chronic eosinophilic pneumonia?

A

Steroids- Responds rapidly

405
Q

Churg Strauss?

A

Systemic small vessel disease associated with asthma and peripheral eosinophilia

406
Q

What is positive in Churg Strauss?

A

p ANCA

407
Q

Imaging findings of Churg Strauss?

A

Varied, most common appearance is peripheral consolidation or GG

408
Q

Microscopic polyangiitis is most common cause of what? What is positive?

A

p ANCA. Most common cuase of pulmonary hemorrhage with renal failure

409
Q

Imaging of microscopic polyangiitis?

A

Central predominant GG representing hemorrhage

410
Q

Triad of Wegeners?

A

Sinusitis, lung involvement, and renal insufficiency

411
Q

Lab tests specific for Wegeners?

A

c ANCA

412
Q

Upper airways in Wegeners?

A

Nasopharyngeal and eustachian tube obstruction. Involvement of trachea and bronchi is common, leading to airway stenosis

413
Q

Lungs in Wegeners? Superimposed infection?

A

Multiple cavitary nodules which don’t respond to abx. Intra-cavitary fluid level suggests superimposed infection

414
Q

**Drugs can elicit numerous pulmonary responses

A
415
Q

What percentage of patients develop radiographic abnormalities after external radiotherapy?

A

40%

416
Q

Radiation pneumonitis?

A

Early stage of radiation injury, can occur within one month of radiotherapy, most severe 3-4 months after treatment. GG centered on radiation port, but can extend out of radiation port

417
Q

Radiation fibrosis?

A

Late stage of radiation injury. Fibrosis becomes apparent 6-12 months after therapy. Key imaging finding is distribution of fibrosis and traction bronchiectasis within the radiation port, but may extend out of the port

418
Q

Pulmonary sarcoidosis may progress to what in lungs?

A

Pulmonary fibrosis with honeycombing, slight upper lobe predominance

419
Q

Staging of sarcoid?

A

Radiographs only- 0 Normal radiograph. 1- Hilar or mediastinal adenopathy only. 2- Adenopathy with lung changes 3- Lung w/o adenopathy. 4- Endstage fibrosis

420
Q

Most common radiographic finding in sarcoid?

A

Symmetric addenopathy with stippled or egg shell calcification in up to 50%

421
Q

Where is adenopathy in sarcoid?

A

Right paratracheal, R hilar, L hilar- Completely encircles trachea on lateral- donut sign

422
Q

In addition to lymphadenopathy, most common ct finding in sarcoid?

A

Upper lobe predominant perilymphatic nodules of variable sizes representing sarcoid granulomas

423
Q

May see superimposed GGO in sarcoid

A
424
Q

Bronchial involvement of sarcoid?

A

Mosaic perfusion due to air trapping

425
Q

Pulmonary LCH associated with?

A

Smoking- Nearly 100% association

426
Q

How may pumonary LCH present?

A

PTX

427
Q

What other associated findings may be seen with pulmonary LCH?

A

Diabetes insipidus from inflammation of pituitary stalk (hypophysitis), lucent bone lesions, skin involvement.

428
Q

Differential for dz affecting bone and lung?

A

LCH. Malignancy. TB. Fungal. Sarcoid. Gaucher.

429
Q

Gaucher in lungs?

A

Rare, but may resemple DIP

430
Q

First detectable abnormality and progression in LCH?

A

Nodules associated with airways, as they progress they will cavitate and resultant irregular cysts predominate

431
Q

Treatment of pulmonary LCH?

A

Smoking cessation is critical.

Responds to steroids.

432
Q

So overall findings in LCH?

A

Upper lobe predominant cysts and irregular peribronchovascular nodules both sparing the costophrenic sulci

433
Q

PAP vs pulmonary edema?

A

In PAP, there are no effusions and the heart is normal in size

434
Q

Patients with PAP are susceptible to what?

A

Superimposed infection, especially with nocardia

435
Q

Treatment of PAP?

A

Bronchialveolar lavage

436
Q

What percentage of TS patients have LAM?

A

1%

437
Q

Almost all cases of sporadic LAM are in what patients?

A

Women of child-bearing age

438
Q

Some cases of LAM respond to what?

A

Estrogen

439
Q

LAM is associated with what two things?

A

PTX, Chylous effusion

440
Q

Cysts in LAM vs LCH?

A

Cysts are round and regular and affect all five lobes where LCH is just upper lobe

441
Q

Two compartments in anterior mediastinum?

A

Prevascular superiorly and precardiac inferiorly (Precardiac is only a potential space)

442
Q

**Bascially all of the mediastinal structures are in the middle mediastinum including the phrenic, vagus, and recurrent laryngeal nerve

A
443
Q

Anterior border of the posterior mediastinum?

A

Posterior trachea and posterior pericardium

444
Q

Anterior junction line?

A

Formed by four laters of pleura at the anterior junction of the R and L lungs. Projections over the superior 2/3 of the sternum.

445
Q

Abnormal convexity or displacement of the anterior junction line?

A

Anterior mediastinal mass

446
Q

Posterior junction line?

A

Four layers of pleura, seen projection through the trachea on frontal view, more superior than the anterior junction line.

447
Q

Which extend more superiorly, posterior or anterior lungs?

A

Posterior

448
Q

Abnormal convexity or displacement of the posterior junction line?

A

Posterior mediastinal mass

449
Q

Right and Left paratracheal stripes?

A

Formed by two layers of pleura where the medial aspect of each lung abuts the lateral wall of the trachea and intervening mediastinal fat

450
Q

Thickening of the R paratracheal stripe?

A

Usually pleural thickening, although a paratracheal or tracheal mass can be the cause

451
Q

Thickening of the L paratracheal stripe?

A

Same diff as on the R except add mediastinal hematoma in setting of trauma

452
Q

Posterior tracheal stripe?

A

Only interface seen on lateral view, representing interface of posterior wall of trachea with two pleural layers of the medial right lung

453
Q

Why do we see R and L paraspinal lines?

A

Mach effect

454
Q

What forms the paraspinal lines?

A

2 layers of pleura abutting the posterior mediastinum

455
Q

Paraspinal line abnormality?

A

Posterior mediastinal mass

456
Q

Azygoesophageal recess?

A

Interface formed by contact of the posteromedial RLL and retrocardiac mediastinum. Extends from the subcarinal region to the diaphragm inferiorly

457
Q

Distortion of the azygoesophageal recess?

A

Esophageal mass, hiatal hernia, L atrial enlargement and adenopathy

458
Q

What lives in the AP window?

A

Lymph nodes (most common cause of AP abnormality). L Phrenic nerve. Recurrent laryngeal nerve. L vagus nerve. Ligamentum arteriosum. L bronchial arteries

459
Q

Obliteration of the retrosternal clear space?

A

Anterior mediastinal mass, RV dilatation, Pulmonary artery enlargement

460
Q

Increase in retrosternal clear space?

A

Emphysema

461
Q

Aortic nipple?

A

From the L superior intercostal vein, not usually seen on radiography. It may be dilated in SVC obstruction as a collateral.

462
Q

Easiest way to infer an anterior mediastinal mass on cxr?

A

Normal posterior junction line because ant junction line isn’t always seen

463
Q

Anterior mediastinal mass diff dx?

A

Thymic epithelial neoplasm. Germ cell tumor. Thyroid lesion if it extends above thoracic inlet. Lymphoma.

464
Q

Most common primary tumor of the anterior mediastinum? Who gets it?

A

Thymoma. Middle aged to older individuals, 45-60.

465
Q

What percentage of thymoma patients have MG? Other way around.

A

33%. 10%

466
Q

Thymomas are associated with what other diseases?

A 
MG. 
Red cell aplasia. 
Hypogammaglobulinemia. 
Paraneoplastic syndromes. 
Malignancies such as lymphoma and thyroid cancer.
467
Q

Invasive and non invasive thymoma?

A

Whether capsule is intact

468
Q

What percentage of thymomas are invasive?

A

30%. May invade adjacent structures.

469
Q

Thymoma with L hemidiaphragm elevation?

A

Phrenic nerve invasion

470
Q

Where does invasive thymoma spread?

A

Drop mets along pleural and pericardial surfaces. Hematogenous mets are very rare.

471
Q

**Thymomas are classfied into A, AB, B1, B2, B3, C, with C being the worst

A
472
Q

Other less common thymic lesions?

A

Thymic carcinoma. Thymic carcinoid. Thymic cyst. Thymolipoma.

473
Q

Thymic carcinoma characteristics?

A

Histologically malignant. Aggressive. Hematogenous mets. Poor prognosis.

474
Q

Distinguishing between thymic carcinoma and thymoma on CT?

A

Metastatic pattern.

475
Q

50% of thymic carcinoids secrete and cause what?

A

ACTH, causing Cushing syndrome

476
Q

Thymic carcinoid is associated with what?

A

MEN 1 and 2

477
Q

Imaging of thymic carcinoid?

A

Indistinguishable from thymoma and thymic carcinoma.

478
Q

If carcinoid is suspected, what imaging?

A

Preoperative Indium 111 Octreotide.

479
Q

Thymic cyst often caused by what?

A

Radiation therapy, AIDS, Congenital

480
Q

When thymic cysts are congenital they arise from what?

A

Remnants of the thymopharyngeal duct

481
Q

Congenital thymic cyst may occur anywhere along the descent of the course of the thymus from neck but usually occur where?

A

Anterior mediastinum

482
Q

Characteristics of a thymolipoma?

A

Benign fat containing lesion with interspersed soft tissue. Can become really large and drape over the mediastinum.

483
Q

Malignant germ cell tumor- which gender?

A

Males

484
Q

What is specific for a teratoma?

A

Fat fluid level. Not commonly seen.

485
Q

Most common anterior mediastinal germ cell tumor?

A

Teratoma

486
Q

**Aorta is in posterior mediastinum, posterior mediastinal mass would silhouette the aorta

A
487
Q

What is most common malignant mediastinal germ cell tumor?

A

Seminoma

488
Q

Cervicothoracic sign?

A

Obscuration of the superior border of the mass implying mass is in continuity with the soft tissues of the neck

489
Q

Key to diagnosing a thyroid lesion as an anterior mediastinal mass?

A

Continuity with the superior thyroid obviously

490
Q

**Calcification is rare in untreated lymphoma.

A
491
Q

Lymphoma most commonly in thorax?

A

Hodgkins

492
Q

Egg shell calcification?

A

Usually happens in CWP and silicosis. Less commonly in sarcoid, but sarcoid is more common.

493
Q

Low attenuation lymph nodes should raise concern for what?

A

TB.

Mets

sometimes TB or Lymphoma

494
Q

Avid lymph node enhancement?

A

Castleman disease. Sarcoid. TB. Vascular mets.

495
Q

What is castleman disease?

A

Angiofollicular lymph node hyperplasia- cause of highly vascular thoracic lymph node enlargement, uncertain etiology.

496
Q

Who gets localized Castlemen and what is cure?

A

Children. Surgical resection.

497
Q

Who gets multicentric Castleman disease?

A

Older patients or AIDS patients.

498
Q

Symptoms of multicentric Castlemans? Treatment?

A

Systemic illness including fever, anemia, lymphoma. Treat with chemo.

499
Q

Key imaging feature of Castemans?

A

Avidly enhancing lymphadenopathy

500
Q

Most common location of pericardial cyst? Appearnce.

A

R cardiophrenic angle. Cystic lesion abuts pericardium, can change shape.

MSK CORE (5 decks)

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