Thoracic 2 Flashcards

1
Q

Emphysema

A

Permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of the alveolar wall without clear fibrosis

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2
Q

Chest radiograph findings of emphysema

A
  • Flattening of the diaphragm due to hyperinflation
  • Increased AP diameter due to hyperinflation
  • Large retrosternal clear space
  • Paucity/pruning of vessels
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3
Q

Definition of flattening of the diaphragm

A

Diaphragmatic dome less than 1.5 cm above a ling drawn between the costophrenic and cardiophrenic sulci

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4
Q

Saber sheath trachea

A

Diffuse narrowing of the trachea from O -> I on axial slices and chest radiograph

Note: This is fairly specific for COPD.

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5
Q

What are the main types of pulmonary emphysema?

A
  • Centrilobular
  • Panlobular
  • Paraseptal
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6
Q

How does centrilobular emphysema appear?

A

Upper zone predominant centrilobular lucencies with a central dot (representing the bronchovascular bundle within the secondary pulmonary lobule)

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7
Q

Lower lobe predominant emphysema…

A

Think pan lobular emphysema in pts with alpha-1 antitrypsin deficiency or prior IV Ritalin use

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8
Q

Subpleural lucencies that look like honeycombing, but is less than 3 bubbles thick…

A

Think paraseptal emphysema

Note: This can be smoking-related or idiopathic.

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9
Q

Which trip of emphysema is most associated with smoking?

A

Centrilobular emphysema

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10
Q

What is asbestosis?

A

A form of pulmonary fibrosis secondary to exposure to asbestos

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11
Q

How can you distinguish asbestosis from usual interstitial pneumonia?

A

Look for parietal pleural thickening, which suggests asbestosis

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12
Q

How long does it usually take between initial exposure to asbestos and development of lung cancer or pleural mesothelioma?

A

20 years

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13
Q

Absestos exposure increases the risk of which extra pulmonary cancers?

A
  • Peritoneal mesothelioma
  • GI cancer
  • Renal cancer
  • Laryngeal cancer
  • Leukemia
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14
Q

What is the earliest pleural-based finding secondary to asbestos exposure?

A

Benign pleural effusions

Note: Even these take about 5 years to develop after exposure.

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15
Q

Chest radiograph demonstrating “holly-leaf” scattered pleural thickening bilaterally sparing the apices and costophrenic angles…

A

Think pleural plaques in the setting of asbestosis

Note: Plaques develop about 20-30 years after exposure and may calcify after about 40 years.

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16
Q

Rounded consolidation with “comet tail” in an adult adjacent to some pleural thickening…

A

Think round atelectasis

Note: If there is not adjacent pleural thickening, this is suspicious for cancer and should get a PET/CT and/or biopsy.

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17
Q

What is the typical distribution of pneumoconiosis?

A

Upper lobe predominant and centrilobular (due to pathogenic particles being inhaled)

Note: Perilymphatic nodules are also common, especially in silicosis and coal workers pneumoconiosis.

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18
Q

Risk factors for silicosis

A
  • Mining
  • Quarry workers
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19
Q

Multiple nodular opacities with upper lobe predominance and hilar nodes with eggshell calcifications in a pt who used to be a miner…

A

Silicosis

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20
Q

Large masses in the bilateral upper lobes with radiating strands in a pt who used to be a miner…

A

Progressive massive fibrosis (complicated form of silicosis/coal workers pneumoconiosis)

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21
Q

Cavitation in the setting of silicosis…

A

Think tuberculosis

Note: Silicosis triples your risk of TB.

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22
Q

How can you differentiate cancer from progressive massive fibrosis

A

Get an MRI. Progressive massive fibrosis should be T2 dark, whereas cancer would be T2 bright

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23
Q

Progressive massive fibrosis

A

A complicated form of silicosis or coal workers pneumoconiosis resulting in large masses in the upper lobes with radiating strands

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24
Q

Multiple nodular opacities with calcifications showing a central nodular dot in a perilymphatic distribution in a pt who used to be a miner…

A

Think coal workers pneumoconiosis

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25
Q

Generalized granulomatous disease with hilar adenopathy and upper lobe predominant reticular opacities in a pt who used to work in aircraft/space manufacturing…

A

Think berylliosis

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26
Q

Risk factors for berylliosis

A

Exposure to metals used in aircraft and space industries

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27
Q

Silo filler’s disease

A

Pulmonary edema and/or ARDS due to exposure to nitrogen dioxide from silage on farms

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28
Q

Acute respiratory distress in a farm worker with extensive pulmonary edema on CT…

A

Think silo fillers disease (pulmonary edema secondary to nitrogen dioxide exposure from farm silage)

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29
Q

Hyperdense pulmonary micronodules with coalescent masses and ground glass opacities in a pt with history of IV drug use…

A

Think talcosis secondary to IV administration of ground tablets

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30
Q

What is at the center of the secondary pulmonary lobule?

A

Terminal bronchiole and accompanying pulmonary artery

Note: The pulmonary veins and lymphatics are located in the periphery of the secondary lobule.

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31
Q

What distribution pattern is most likely if you see many pulmonary nodules without any abutting the pleural surfaces?

A

Centrilobular

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32
Q

Best way to determine the distribution pattern of pulmonary nodules

A

Look for nodules abutting pleural surfaces (if there aren’t any, the pattern is likely centrilobular)

If there are pleural-based nodules, look for a subpleural/peribronchovascular predominance (perilymphatic distribution) or no clear distribution (random)

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33
Q

What is the major differential for perilymphatic pulmonary nodules?

A
  • Sarcoidosis (90% of cases)
  • Lymphangitic carcinomatosis
  • Silicosis
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34
Q

What is the major differential for randomly distributed pulmonary nodules?

A
  • Miliary TB
  • Hematogenous spread of metastases
  • Fungal infection
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35
Q

What is the major differential for centrilobular pulmonary nodules?

A
  • Infection
  • Respiratory bronchiolitis- ILD
  • Hypersensitivity pneumonitis (if nodules are ground glass)
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36
Q

What is the major differential for interlobular septal thickening?

A
  • Pulmonary edema (smooth and symmetric)
  • Lymphangitic carcinomatosis (nodular and asymmetric)
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37
Q

Honeycombing

A

Multiple layers of cysts in a subpleural location, a hallmark of UIP

Note: If there is only one row of cysts, its more likely parasepmtal emphysema.

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38
Q

What is the first finding of UIP on chest radiographs?

A

Reticular opacities in the posterior costophrenic angle

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39
Q

Basilar predominant opacities with traction bronchiectasis and honeycombing…

A

Definite UIP

Note: Do not biopsy if it’s definite UIP.

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40
Q

Criteria for “definite” UIP

A
  • Honeycombing
  • Reticular opacities
  • Subpleural and basal predominant
  • Absence of inconsistent features (ground glass opacities more pronounced than reticular opacities, air trapping involving 3 or more lobes)
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41
Q

Pulmonary fibrosis with biopsy demonstrating “heterogeneous” histology…

A

UIP

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42
Q

What are common causes of UIP

A
  • Idiopathic (idiopathic pulmonary fibrosis)
  • Collagen-vascular diseases (e.g. Rheumatoid arthritis, scleroderma)
  • Sarcoidosis
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43
Q

How can you differentiate UIP from chronic hypersensitivity pneumonitis?

A

Chronic HP should be mid-upper lobe predominant

Air trapping involving 3 or more lobes also favors chronic HP

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44
Q

Pulmonary fibrosis greatly increases the risk of lung cancer. Where does lung cancer most often arise in these pts?

A
  • Lower lobes
  • The interface between the fibrotic cysts and normal lung
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45
Q

In a pt with pulmonary fibrosis, you identify progressive wall thickening of a pulmonary cyst…

A

Suspicious for cancer

Note: Enlarging pericystic nodules are likewise very suspicious for cancer.

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46
Q

What are the two types of NSIP?

A

Cellular (ground glass alone) and fibrotic (reticulations and traction bronchiectasis)

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47
Q

What is the most common interstitial lung disease in scleroderma?

A

NSIP

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48
Q

Pulmonary fibrosis with a lower lobe and peripheral predominance that demonstrates subpleural sparing…

A

NSIP

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49
Q

Respiratory bronchiolitis-ILD

A

A smoking-related pulmonary disease that appears as apical centrilobular ground glass nodules

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50
Q

Desquamative interstitial pneumonia

A

A severe form of smoking-related respiratory bronchiolitis where there are diffuse ground glass opacities with a patchy/subpleural distribution

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51
Q

Peripheral, lower-lobe predominant ground glass opacities with small cystic spaces in a pt with a long extensive history of smoking…

A

Think desquamative interstitial pneumonia (severe form of respiratory bronchiolitis-ILD)

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52
Q

Why are the ground glass nodules of respiratory bronchiolitis in a centrilobular distribution?

A

The ground glass nodules are due to macrophages filling up the terminal bronchioles

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53
Q

African American female in her 30s…

A

Think sarcoidosis

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54
Q

Epidemiology of sarcoidosis

A
  • Usually presents in 20s or 30s
  • More common in black females
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55
Q

What laboratory abnormalities are associated with sarcoidosis?

A
  • Elevated angiotensin-converting enzyme (ACE)
  • Hypercalcemia
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56
Q

Bilateral hila and right paratracheal lymphadenopathy where the lymph nodes do not abut the cardiac border…

A

Think sarcoidosis (1-2-3 sign, Garland triad)

Note: This is equivalent to the lambda sign on Gallium scans. If the lymph nodes abut the cardiac border, consider lymphoma.

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57
Q

Bilateral hilar lymph node enlargement, arthritis, and erythema nodosum…

A

Acute sarcoidosis (AKA Lofgren syndrome)

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58
Q

Perilymphatic nodules with an upper lobe predominance and associated lymphadenopathy…

A

Think sarcoidosis

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59
Q

Upper lobe conglomerate masses with satellite nodules…

A

Think sarcoidosis (CT galaxy sign)

Note: Can also be seen with tuberculosis.

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60
Q

What are the stages of sarcoidosis?

A
  • 0 (normal CXR)
  • 1 (hilar/mediastinal lymph nodes)
  • 2 (nodal and pulmonary parenchymal disease)
  • 3 (parenchymal disease only)
  • 4 (end stage fibrosis)
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61
Q

What are the two classic signs of sarcoidosis on Gallium scans?

A
  • Lambda sign (gallium uptake resembling lambda symbol due to bilateral hilar and right paratracheal lymphadenopathy)
  • Panda sign (gallium uptake in the lacrimal glands, nasopharynx, and parotid glands giving the appearance of a panda face)
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62
Q

Immediate complications of lung transplant (<24 hours)

A
  • Donor-recipient size mismatch
  • Hyperacute rejection
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63
Q

Donor-recipient size mismatch complication following lung transplant

A

When there is a mismatch between the size of the donor lung and the recipients thoracic cavity (a mismatch of up to 25% is considered fine)

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64
Q

Pathophysiology of hyper acute rejection following lung transplant

A

HLA or ABO antigen incompatibility

Note: This is rapid and often fatal.

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65
Q

Pt dies within hours of receiving a lung transplant and imaging showed massive homogenous pulmonary infiltration…

A

Hyperacute rejection secondary to HLA/ABO antigen incompatability

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66
Q

What are the early complications status post lung transplant (24 hours to 1 week)

A
  • Repercussion injury
  • Air leak/persistent pneumothorax
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67
Q

Pulmonary edema on POD 4 s/p lung transplant that improves by POD 7…

A

Reperfusion injury (noncardiogenic pulmonary edema secondary to reperfusion ischemia)

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68
Q

Postoperative pneumothorax s/p lung transplant that persists for > 7 days…

A

Air leak

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69
Q

What are the intermediate (8 days - 2 months) complications s/p lung transplant?

A
  • Acute rejection (+/- cryptogenic organizing pneumonia)
  • Bronchial anastomotic complications (leaks in first month, stenoses later in months 2-4)
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70
Q

Ground glass opacities and interlobular septal thickening on POD 14 s/p lung transplant…

A

Acute rejection

Note: Should improve with steroids.

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71
Q

What bronchial anastomotic complications should you look for and when s/p lung transplant?

A
  • Bronchial anastomotic leak (usually occurs in the first month)
  • Bronchial anastomotic stenosis (usually develops 2-4 months s/p transplant)
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72
Q

Ground glass and tree-in-bud opacities 3 months following a lung transplant…

A

Think cytomegalovirus infection

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73
Q

What is the most common opportunistic infection following lung transplant?

A

Cytomegalovirus infection

Note: This is rare in the first 2 weeks s/p transplant.

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74
Q

Late complications of lung transplant (>4 months)

A
  • Chronic rejection
  • Cryptogenic organizing pneumonia
  • Post-transplant lymphoproliferative disorder (PTLD)
  • Upper lobe fibrosis
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75
Q

Bronchiectasis, bronchial wall thickening, and air trapping with remote history of lung transplant…

A

Chronic rejection (bronchiolitis obliterans)

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76
Q

Post transplant lymphoproliferative disorder is associated with…

A

Epstein Barr virus infection (90% of cases)

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77
Q

What percentage of lung transplant pts develop chronic rejection?

A

50% at 5 years s/p transplant

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78
Q

Air trapping on expiratory imaging 6 months following lung transplant…

A

Think chronic rejection/bronchiolitis obliterans

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79
Q

What is the most common recurrent primary disease following lung transplant for that disease?

A

Sarcoidosis (approximately 35% of cases recur following transplant)

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80
Q

Pulmonary alveolar proteinosis

A

Pulmonary disease caused by surfactant accumulation in the alveoli and terminal bronchioles leading to a crazy paving appearance

Note: Associated with smoking.

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81
Q

Crazy paving

A

Interlobular septal thickening with ground glass opacities, classically seen with pulmonary alveolar proteinosis on multiple choice tests

Note: In real life, crazy paving is also seen with pulmonary edema/hemorrhage, bronchoalveolar carcinoma, acute interstitial pneumonia, and COVID.

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82
Q

Pts with pulmonary alveolar proteinosis are at an increased risk for…

A

Nocardia infections (including Nocardia brain abscesses)

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83
Q

Pulmonary alveolar proteinosis presenting in a child <1 y/o is associated with…

A

Alymphoplasia

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84
Q

Pulmonary alveolar proteinosis can progress to…

A

Pulmonary fibrosis

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85
Q

Treatment for pulmonary alveolar proteinosis

A

Bronchoalveolar lavage

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86
Q

What is the classic appearance of pulmonary alveolar proteinosis?

A

Central, symmetric crazy paving that spares the apices and costophrenic angles

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87
Q

What are the two types of lipoid pneumonia?

A
  • Endogenous (due to a post obstructive process leading to a buildup of lipid-laden macrophages)
  • Exogenous (aspiration of oils/hydrocarbons)
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88
Q

Common causes of exogenous lipoid pneumonia

A

Aspiration of oils/hydrocarbons:

  • Mineral oil laxative use
  • Vegetable/animal oil aspirations
  • Hydrocarbon exposure
  • Fire eating/blowing oils
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89
Q

Pulmonary consolidation with low attenuation/fat density in the consolidation in an elderly pt taking laxatives…

A

Think lipoid pneumonia due to mineral oil (laxative) aspiration

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90
Q

Pulmonary opacity being shown on a soft tissue window…

A

Soft tissue windows are usually used to demonstrate fat within a pulmonary opacity, so think hamartoma or lipoid pneumonia

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91
Q

Pathophysiology of organizing pneumonia

A

Fibroblast proliferation leading to deposition of granulation tissue within the alveolar spaces

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92
Q

Treatment for organizing pneumonia

A

Steroids

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93
Q

Etiologies of organizing pneumonia

A
  • Idiopathic (cryptogenic OP)
  • Post-infectious
  • Certain drugs (e.g. Amiodarone)
  • Collagen vascular diseases
  • Fumes
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94
Q

Persistent cough and low-grade fever lasting several months after being treated for pneumonia with associated patchy consolidate and ground glass opacities…

A

Think post-infectious organizing pneumonia

Note: Treatment is with steroids.

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95
Q

Reverse halo (atoll) sign

A

A crescent of consolidation surrounding a ground glass opacity, classically seen in organizing pneumonia

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96
Q

Peripheral patchy consolidations in a pt with a history of asthma

A

Think chronic eosinophilic pneumonia

Note: Organizing pneumonia looks the same, but labwork should show eosinophilia.

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97
Q

Chronic eosinophilic pneumonia is associated with…

A

Asthma (50% of cases)

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98
Q

Differential for reverse halo (atoll) sign

A
  • Organizing pneumonia (classic)
  • Tuberculosis
  • Pulmonary infarction
  • Invasive fungal disease
  • Granulomatosis with polyangiitis
  • COVID
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99
Q

Differential for halo sign (nodule with ground glass surrounding it)

A
  • Invasive aspergillosis (classic)
  • Other invasive fungal infections
  • Hemorrhagic metastases
  • Adenocarcinoma in situ (bronchoalveolar carcinoma)
  • Granulomatosis with polyangiitis
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100
Q

Classic appearance of subacute hypersensitivity pneumonitis

A

Ill-defined centrilobular ground glass opacities with mosaic perfusion and air trapping

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101
Q

Headcheese sign

A

Ground glass opacities, air trapping, and normal lung parenchyma mixed together, classically seen in chronic hypersensitivity pneumonitis

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102
Q

Pulmonary fibrosis and air trapping…

A

Think chronic hypersensitivity pneumonitis

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103
Q

Classic appearance of chronic hypersensitivity pneumonitis

A
  • UIP with air trapping
  • Headcheese sign (ground glass, air trapping, and normal lung)
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104
Q

Saber sheath trachea

A

Narrowed trachea (TV diameter < 2/3 the AP diameter), seen in COPD

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105
Q

What is the upper limit of normal for tracheal width?

A

2.5 cm (no more than the transverse diameter of an adjacent vertebral body)

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106
Q

Thickening of the anterior and lateral tracheal cartilage, sparing the posterior membrane, without associated calcifications in a pt with recurrent pneumonia…

A

Relapsing polychondritis

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107
Q

Circumferential thickening of the trachea (focal or long segment) with subglottic involvement without associated calcifications…

A

Granulomatosis with polyangiitis

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108
Q

Cartilaginous and osseous nodules within the submucosa of the tracheal and bronchial walls, sparing the posterior membrane…

A

Tracheobronchopathia osteochondroplastica (TBO)

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109
Q

Irregular focal or short segment thickening of the trachea with calcifications (+/- posterior membrane involvement)…

A

Amyloidosis

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110
Q

Differential for tracheal thickening that spares the posterior membrane

A
  • Relapsing polychondritis (diffuse tracheal thickening)
  • Tracheobronchopathia osteochondroplastica (nodular thickening)
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111
Q

Differential for tracheal thickening that does not spare the posterior membrane

A
  • Amyloidosis (calcifications common)
  • Post intubation (focal in the subglottic region)
  • Granulomatosis with polyangiitis (sub glottic location is the most commonly involved)
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112
Q

Pt is C-ANCA positive

A

Granulomatosis with polyangiitis

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113
Q

Do bronchal carcinoid and GI carcinoid metastasize to the orbit?

A

Yes, bronchial carcinoid tumors tend to metastasize to the uveal tract (inside eyeball) and GI carcinoid tumors tend to metastasize to the extraoccular muscles (outside eyeball)

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114
Q

Pulmonary nodule that lights up on an octreotide scan and is associated with mitral valve degradation…

A

Think bronchial carcinoid tumor with carcinoid syndrome leading to left-sided valve degradation

Note: In GI carcinoid, valvular degradation tends to be right-sided (tricuspid, pulmonic valves)

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115
Q

Classic appearance of a typical bronchial carcinoid tumor

A

Soft tissue nodule (<3 cm) located centrally (e.g. tracheal bifurcation) within the airway lumen +/- calcifications

Note: These are low-grade malignant and NOT associated with smoking.

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116
Q

Classic appearance of an atypical bronchial carcinoid tumor

A

Soft tissue mass (>3 cm) in a peripheral pulmonary location that may be partially endobronchial or not appear to be associated with a bronchiole at all without calcifications

Note: These are intermediate-grade malignant.

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117
Q

What is the most common tracheal malignancy?

A

Squamous cell carcinoma (followed by adenoid cystic carcinoma)

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118
Q

Are pulmonary carcinoids fast or slow growing?

A

Slow growing and locally invasive (only 10% of cases have nodal metastases)

119
Q

Are pulmonary carcinoid tumors associated with smoking?

A

No

Note: There may be an association between smoking and atypical pulmonary carcinoid.

120
Q

What imaging follow up should you recommend if you are suspecting a pulmonary carcinoid?

A

Octreotide scan (neuroendocrine tumor)

Note: 25% of carcinoid tumors will be PET negative, so octreotide is better.

121
Q

Which valves are susceptible to degradation in the setting of carcinoid syndrome secondary to pulmonary carcinoid?

A

Left-sided valves (mitral and aortic)

Note: GI carcinoid tumors are more likely to result in right-sided valve degradation (tricuspid and pulmonic).

122
Q

Most common location for a tracheal adenoid cystic carcinoma

A

Submucosa of the upper trachea

123
Q

Most common location for a tracheal squamous cell carcinoma

A

Lower trachea/proximal main bronchus

124
Q

Which tracheal malignancy is associated with smoking

A

Squamous cell carcinoma

125
Q

What are the most common tracheal/bronchial tumors?

A
  • Carcinoid
  • Squamous cell carcinoma
  • Adenoid cystic carcinoma
  • Metastases
  • Squamous cell papilloma
126
Q

What is the most common benign tumor of the trachea?

A

Squamous cell papilloma

127
Q

Common causes of tracheal squamous cell papillomas

A
  • Smoking (usually single papilloma)
  • HPV infection (usually multiple papillomas)
128
Q

What is the most common cause of subglottic tracheal stenosis in an adult?

A

Post intubation stenosis

129
Q

Focal subglottic circumferential stenosis with an hourglass configuration…

A
  • Post intubation stenosis (adult)
  • Croup/acute laryngotracheobronchitis (child)

Note: If you see this in an adult, but the pt has never been intubated before it could be a rare case of adult croup.

130
Q

Pathophysiology of cystic fibrosis

A

Genetic mutation resulting in poorly functioning chloride ion transporters, resulting in too little chloride ions (and subsequently water) in the airway lumen and thick secretions which predispose to recurrent pulmonary infections

131
Q

Pulmonary findings of cystic fibrosis

A
  • Bronchiectasis with an apical predominance (cylindrical progressing to varicoid)
  • Hyperinflation
  • Pulmonary arterial hypertension
  • Mucous plugging (finger-in-glove opacities)
132
Q

Apical-predominant bronchiectasis in a pt with an abnormal looking/absent pancreas…

A

Think cystic fibrosis

133
Q

Bilateral lower-lobe predominant bronchiectasis in a pt with a history of chronic sinusitis as a child…

A

Think primary ciliary dyskinesia

134
Q

Clinical manifestations of primary ciliary dyskinesia

A
  • Bilateral lower lobe bronchiectasis (due to recurrent pulmonary infections)
  • Chronic sinusitis from an early age
  • Impaired fertility/ectopic pregnancies
  • Chronic mastoid effusions
  • Conductive hearing loss
135
Q

Kartageners syndrome

A
  • Situs inversus
  • Chronic sinusitis
  • Bronchiectasis
136
Q

Primary ciliary dyskinesia is associated with what syndrome?

A

Kartageners syndrome (situs inversus, chronic sinusitis, and bronchiectasis)

Note: Only 50% of people with PCD actually have Kartageners.

137
Q

How can you differentiate cystic fibrosis from primary ciliary dyskinesia based on pulmonary findings?

A

Bronchiectasis is upper lobe predominant in CF and lower lobe predominant in PCD

138
Q

Williams campbell syndrome

A

Congenital deficiency of cartilage in the 4th-6th order bronchi resulting in congenital cystic bronchiectasis

139
Q

“That’s one big fucking trachea”

A

Tracheobronchomegaly (Mounier-Kuhn syndrome), defined by massive dilatation of the tarchea (>3 cm)

140
Q

Major differential for air trapping

A
  • Small airway disease
  • Bronchiolitis obliterans (if prior lung transplant)
141
Q

Tree-in-bud nodules

A

Small branching nodules typically 5-10 mm from the pleural surface, representing dilated and impacted centrilobular airways

Note: This is suggestive of small airways disease, specifically infectious bronchiolitis.

142
Q

Follicular bronchitis

A

A small airway inflammatory disease that can occur in rheumatoid arthritis and Sjogrens related to lymphoid hyperplasia and appearing as centrilobular ground glass nodules with scattered areas of bronchial dilatation

143
Q

Lower lobe predominant centrilobular ground glass nodules and scattered bronchiectasis in a pt with Sjogrens…

A

Follicular bronchiolitis

144
Q

Follicular bronchitis is associated with…

A
  • Rheumatoid arthritis
  • Sjogrens
145
Q

Constrictive bronchiolitis

A

A small airway inflammatory disease leading to air trapping that can occur following viral infection, lung transplant, drug reactions, or inhalational injury

146
Q

DIPNECH

A

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia, a pulmonary disorder caused by hyperplastic neuroendocrine cells lining the peripheral airways that can lead to constrictive bronchiolitis

147
Q

What is the cause of the hyperlucent lung in Swyer-James syndrome?

A

Constrictive bronchiolitis leading to air trapping

148
Q

What is the typical location of aspiration pneumonitis?

A
  • Posterior segment of upper lobes and superior segment of lower lobes (if supine aspiration)
  • Bilateral basal lower lobes (if upright aspiration)

Note: Right side more common than left.

149
Q

What is the most common complication of aspiration pneumonitis?

A

Pneumonia, which can lead to an empyema, which can lead to a bronchopleural fistula

150
Q

How can you tell the difference between gastric acid aspiration and aspiration of neutralized gastric contents?

A

Gastric acid aspiration usually results in a persistent airspace opacity and can look like pulmonary edema

Neutralized gastric content aspiration should cause a “fleeting opacity” that resolved in hours

151
Q

Which collagen vascular diseases are commonly associated with interstitial lung diseases?

A
  • Systemic lupus erythematosus
  • Rheumatoid arthritis
  • Scleroderma
  • Sjogrens
  • Ankylosing spondylitis
152
Q

What pulmonary findings are more common in systemic lupus erythematosus than other collagen vascular diseases?

A
  • Pleural effusions
  • Pericardial effusions

Note: Pulmonary fibrosis is uncommon in SLE.

153
Q

Which interstitial lung diseases are common in pts with rheumatoid arthritis?

A
  • UIP
  • Organizing pneumonia
154
Q

Which interstitial lung diseases are common in pts with scleroderma?

A

NSIP

Note: UIP can also occur.

155
Q

NSIP with a dilated, fluid-filled esophagus

A

Think scleroderma

156
Q

Which interstitial lung diseases are common in pts with Sjogrens disease?

A

Lymphoid interstitial pneumonia (LIP)

Note: Look for extensive ground glass attenuation with scattered thin-walled cysts.

157
Q

Which interstitial lung diseases are common in pts with ankylosing spondylitis?

A

Upper lobe fibrobullous disease (initially unilateral, then progressing to bilateral)

158
Q

Rheumatoid arthritis and upper lobe predominant lung nodules +/- cavitation +/- pleural effusion…

A

Caplan syndrome (AKA rheumatoid pneumoconiosis)

159
Q

Progressive loss in lung volume bilaterally in pts with systemic lupus erythematosus…

A

“shrinking lung”, which is caused by either diaphragmatic dysfunction or pleuritis chest pain

Note: “S”hrinking “L”ung for SLe.

160
Q

What is the most common manifestation of systemic lupus erythematosus in the chest?

A

Pleuritis +/- pleural effusion

161
Q

Cirrhotic liver and shortness of breath while sitting up…

A

Hepatopulmonary syndrome

Note: The SOB while sitting up is due to vascular dilatation at the pulmonary bases. While sitting up, these dilated vessels engorge and shunt blood away from the lungs.

162
Q

Diagnostic test for hepatopulmonary syndrome

A

Tc MAA scan demonstrating vascular shunting (radiotracer uptake outside the lungs in the brain)

163
Q

What is the most commonly involved organ in granulomatosis with polyangiitis?

A

The lungs (95% of cases)

Note: Pulmonary findings have a variable appearance, but pulmonary nodules with cavitation are the most common.

164
Q

Diffuse pulmonary nodules (some cavitating) in a pt with nasal septal perforation…

A

Think granulomatosis with polyangiitis

165
Q

Young male with recurrent bilateral coalescent airspace opacities that resolve within a few weeks and may lead to fibrosis over time with persistent small ill-defined pulmonary nodules…

A

Think Goodpasture syndrome (an autoimmune pulmonary-renal syndrome)

166
Q

What are the major autoimmune pulmonary-renal syndromes?

A
  • Granulomatosis with polyangiitis
  • Goodpasture syndrome
167
Q

What is the classic appearance of Goodpasture syndrome?

A
  • Bilateral coalescent airspace opacities that resolve within weeks (looks like pulmonary edema, but is actually hemorrhage)
  • Recurrent episodes can lead to fibrosis and pulmonary hemosiderosis (small ill-defined nodules due to iron deposition from recurrent bleeding)
168
Q

Pleural plaque…

A

Think asbestos-related disease

169
Q

Differential for pleural calcifications

A
  • Asbestos-related disease
  • Old hemothorax/infection
  • Tuberculosis
  • Extraskeletal osteosarcoma
170
Q

What is the most common cancer of the pleura?

A

Mesothelioma (80% are associated with asbestos exposure)

171
Q

Risk factors for malignant mesothelioma

A

Asbestos exposure

Note: This is not dose dependent.

172
Q

What is the lag time between asbestos exposure and mesothelioma development?

A

30-40 years

173
Q

Circumferential pleural thickening with extension to pleural fissure thickening…

A

Highly suggestive of mesothelioma

174
Q

Focal lateral pleural thickening…

A

Think post-traumatic pleural thickening and look for prior rib fractures

175
Q

Focal thickening of the medial pleura…

A

Think mesothelioma

Note: Traumatic pleural thickening is usually lateral.

176
Q

What should you recommend if you are suspicious for mesothelioma on a chest CT?

A
  • Chest MRI with contrast (to evaluate chest wall, diaphragm, and pericardial invasion)
  • PET/CT (to evaluate for metastases)
177
Q

Solitary fibrous tumor of the pleura

A

SFTP is a usually benign solitary tumor arising from the visceral pleura that is NOT associated with asbestos exposure or smoking. They can get very large and cause chest pain, but are usually benign.

178
Q

Focal pleural thickening in a pt without asbestos exposure and episodic hypoglycemia…

A

Doege-Potter syndrome (episodic hypoglycemia due to secretion of insulin-like growth factor from a solitary fibrous tumor of the pleura)

179
Q

What musculoskeletal disorder is associated with solitary fibrous tumor of the pleura?

A

Hypertrophic osteoarthropathy (30% of cases)

180
Q

What metabolic disorder is associated with solitary fibrous tumor of the pleura?

A

Episodic hypoglycemia due to tumor secretion of insulin-like growth factor

181
Q

What is the most common benign soft tissue tumor of the pleura?

A

Lipoma

182
Q

Asymmetric fat-containing pleural lesion in a pt complaining of the “urge to cough”

A

Lipoma

183
Q

Which lung cancer subtype is most likely to metastasize to the pleura?

A

Adenocarcinoma

184
Q

If you find pleural metastases, what are the most likely primaries?

A
  • Lung cancer (#1)
  • Breast cancer (#2)
  • Lymphoma (#3)
185
Q

What is the most common manifestation of metastatic pleural disease?

A

Pleural effusion

186
Q

How much fluid is needed for a pleural effusion to be visible on chest radiograph?

A
  • 175 cc (frontal view)
  • 75 cc (lateral view)
187
Q

Subpulmonic effusion

A

When a pleural effusion accumulates between the lung and the diaphragm (more common on the right)

188
Q

On short interval follow up chest radiograph, you notice that the right diaphragmatic peak has shifted laterally…

A

Think subpulmonic effusion

Note: Lateralization of the diaphragmatic peak is sometimes called “ski-slipping”. You can get a lateral decubitus radiograph to confirm.

189
Q

Chest radiograph showing increased space between the stomach bubble and the left lung base…

A

Think subpulmonic effusion

Note: Get a lateral decubitus to confirm.

190
Q

Encysted pleural effusion

A

When a pleural effusion collects between the pleural layers of a fissure, appearing as an oval/round mass

191
Q

What characteristics are more common in empyemas than regular pleural effusions?

A
  • Pleural enhancement (split-pleura sign)
  • Gas
  • Septations
  • More asymmetric, loculated appearance
192
Q

Empyema necessitans

A

When an empyema eats through the chest wall into the soft tissues, most commonly seen in TB

193
Q

Empyema eating through the chest wall and into the soft tissues…

A

Empyema necessitans

Note: Most often seen with tuberculosis, but can also be seen in actinomyces infections.

194
Q

Congenital diaphragmatic hernia in the back left…

A

Bochdalek hernia

195
Q

Congenital diaphragmatic hernia in the anterior right…

A

Morgagni hernia

196
Q

Traumatic diaphragmatic hernias are more likely to occur on the…

A

Left (the liver is protective on the right)

197
Q

Why should pulmonary abscesses not be treated with a chest tube?

A

Risk of bronchopleural fistula

198
Q

How can you distinguish an empyema from a pulmonary abscess?

A

Split pleura sign and lentiform shaped empyemas

Claw sign (acute angle with the pleura) and round shaped pulmonary abscesses

199
Q

Most common cause of diaphragmatic paralysis

A

Idiopathic, but think about phrenic nerve compression from a lung cancer

200
Q

Paradoxical movement on a fluoroscopic sniff test…

A

Diaphragmatic paralysis

201
Q

Left hemidiaphragm is higher than the right…

A

Think about left diaphragmatic paralysis

202
Q

How can you discern between a mediastinal mass and a large pulmonary artery?

A

Hilum overlay sign (if you can see the bifurcation of the pulmonary vessels through the hilar opacity, then there is a hilar mass separate from the vessels)

203
Q

Thymic rebound

A

Reactive enlargement of the thyroid gland following stress or chemotherapy

Note: It can be FDG avid on PET.

204
Q

T2 bright anterior mediastinal mass in a pt s/p thoracotomy…

A

Thymic cyst

205
Q

What are common causes of an acquired thymic cyst?

A
  • Thoracotomy
  • Chemotherapy
  • HIV
206
Q

What is the spectrum of thymoma?

A
  • Thymoma
  • Invasive thymoma
  • Thymic carcinoma
207
Q

What features make you suspicious a thymoma may be invasive or malignant?

A
  • Infiltrating appearance
  • Calcifications suggest more aggressive lesion
208
Q

Thymomas are associated with…

A
  • Myasthenia gravis
  • Pure red cell aplasia
  • Hypogammaglobulinemia
209
Q

Fatty mass with interspersed soft tissue in the anterior mediastinum…

A

Think thymolipoma

210
Q

What is the most common mediastinal germ cell tumor?

A

Teratoma (75% of cases)

Note: Mediastinal teratoma is the most common extragonadal germ cell tumor.

211
Q

Epidemiology of mediastinal teratoma

A
  • Kids (<1 y/o)
  • Adults (20s-30s)

Note: Immature teratomas occur exclusively in men, but M = F for mature teratomas.

212
Q

Mature mediastinal teratomas are associated with…

A

Klinefelter syndrome

213
Q

Cystic appearing mass containing fat in the anterior mediastinum…

A

Think teratoma

Note: If there is also calcification/teeth, this is pretty specific.

214
Q

Round cyst in the right anterior cardiophrenic angle…

A

Pericardial cyst

215
Q

What are the two subtypes of fibrosing mediastinitis?

A
  • Granulomatous (superior mediastinal soft tissue mass with calcifications)
  • Non-granulomatous (superior mediastinal infiltrating soft tissue mass without calcifications)
216
Q

What are the common causes of granulomatous fibrosing mediastinitis?

A
  • Histoplasmosis (classic)
  • Tuberculosis
  • Sarcoidosis
217
Q

Superior mediastinal soft tissue mass in a pt with sarcoidosis…

A

Think fibrosing mediastinitis

218
Q

What are the common causes of non-granulomatous fibrosing mediastinitis?

A
  • Autoimmune diseases (SLE, RA, Behcet, etc.)
  • Radiation therapy
  • Headache medication methysergide use
  • Idiopathic (associated with retroperitoneal fibrosis)
219
Q

Complications of fibrosing mediastinitis

A

Superior vena cava syndrome

220
Q

Infiltrating enhancing superior mediastinal soft tissue mass without calcifications in a pt taking methysergide for headaches…

A

Non-granulomatous fibrosing mediastinitis

221
Q

Cystic lesion in the subcarinal region with obliteration of the azygoesophageal line on chest radiograph…

A

Think bronchogenic cyst

222
Q

Excessive unencapsulated fat in the anterior mediastinum…

A

Mediastinal lipomatosis

223
Q

Common causes of mediastinal lipomatosis

A
  • Iatrogenic steroid use
  • Cushings syndrome
  • Obesity
224
Q

What is the most common posterior mediastinal mass?

A

Neurogenic tumors (schwannomas, neurofibromas, malignant peripheral nerve sheath tumors)

Note: Extramedullary hematopoiesis can also present as a posterior mediastinal mass.

225
Q

What are common causes of posterior mediastinal extramedullary hematopoiesis?

A
  • Chronic myelogenous leukemia
  • Polycythemia vera
  • Myelofibrosis
  • Sickle cell disease
  • Thalassemia
226
Q

Partial anomalous pulmonary venous return

A

When one or more of the 4 pulmonary veins drains into the right atrium or SVC rather than the left atrium (a left to right shunt)

227
Q

Total anomalous pulmonary venous return

A

When all 4 pulmonary veins drain into the right atrium or SVC rather than the left atrium (a complete left to right shunt that results in cyanotic heart disease)

228
Q

Partial anomalous pulmonary venous return is associated with…

A

Atrial septal defects (most commonly the sinus venosus type)

229
Q

Partial anomalous pulmonary venous return and pulmonary hypoplasia…

A

Think Scimitar syndrome

230
Q

Complications of partial anomalous pulmonary venous return

A

Pulmonary hypertension and right sided heart failure (due to the left to right shunting)

231
Q

Vertically oriented pulmonary vein draining into the left brachiocephalic vein…

A

Partial anomalous pulmonary veinous return

Note: This “vertical vein: is classic for left-sided PAPVR (less common than right-sided).

232
Q

Scimitar sign

A

A dilated curvilinear right inferior pulmonary vein draining into the IVC (with associated pulmonary hypoplasia), indicating partial anomalous pulmonary veinous return in Scimitar syndrome

233
Q

Meandering pulmonary vein

A

Term given to a pulmonary vein that takes a long, meandering course to the left atrium, but does drain correctly into the left atrium (unlike in anomalous pulmonary veinous return)

Note: There is no left to right shunt here.

234
Q

Pulmonary vein varix

A

Pulmonary vein aneurysm/varix refer to any dilated pulmonary veins, often due to mitral regurgitation

235
Q

Asymmetric pulmonary edema affecting the right upper lobe…

A

Look for a lower right pulmonary vein varix/aneurysm secondary to mitral regurgitation

236
Q

Right hemithorax volume loss with absence of the ipsilateral main pulmonary artery…

A

Proximal interruption of the pulmonary artery

Note: The distal pulmonary arterial tree is still perfused through collateral vessels.

237
Q

On which side is it more common to have proximal interruption of the pulmonary artery?

A

The right

Note: Proximal interruption of the pulmonary artery always occurs on the opposite side of the aortic arch (and left-sided arches are far more common).

238
Q

Proximal interruption of the pulmonary artery is associated with…

A

Patent ductus arteriosus

239
Q

New peripheral wedge-shaped opacity on chest radiograph of an inpatient…

A

Think pulmonary embolism (Hamptons hump)

240
Q

Massive vs submassive pulmonary embolism

A

Massive PE is associated with hypotension (SBP<90)

Submassive PE is associated with right heart dysfunction or positive cardiac enzymes

241
Q

Acute vs chronic PE

A

Acute PEs tend to be central within the vessel and associated with vascular dilatation

Chronic PEs tend to be more peripheral with shrunken vessels and collateral flow and may have calcifications

242
Q

What is the best test to evaluate for chronic PE burden?

A

V/Q scan

243
Q

Imaging findings of right heart strain

A
  • Right ventricle dilatation (larger than left ventricle)
  • Leftward bowing of the interventricular septum
  • Contrast reflux into the hepatic veins
244
Q

Differential for a peripheral wedge-shaped pulmonary opacity that cavitates

A
  • Pulmonary infarction
  • Tuberculosis
  • Lung cancer
245
Q

Pulmonary arterial hypertension with a normal wedge pressure…q

A

Think pulmonary veno-occlusive disease

246
Q

Pulmonary veno-occlusive disease

A

An uncommon variant of primary pulmonary hypertension that affects the post capillary pulmonary vasculature leading to pulmonary hypertension with a normal wedge pressure

247
Q

Common causes of pulmonary artery aneurysms

A
  • Iatrogenic from a swan ganz catheter (most common)
  • Behcet disease
  • Chronic PEs
248
Q

Pulmonary artery aneurysm in a pt of Turkish descent with a histoy of mouth and genital ulcers…

A

Behcet disease

249
Q

Recurrent thrombophlebitis and pulmonary artery aneurysm formation and repair…

A

Hughes-Stovin syndrome

250
Q

Upper lobe pulmonary artery pseudoaneurysm in the setting of reactivation tuberculosis…

A

Rasmussen aneurysm

251
Q

Diagnosis of pulmonary artery hypertension

A

Pulmonary arterial pressures > 25

252
Q

Common causes of pulmonary arterial hypertension

A
  • Chronic PEs
  • Right heart failure/strain
  • Pulmonary parenchymal disease (e.g. emphysema, fibrosis, COPD)
  • Idiopathic (rare, affecting young females)
253
Q

Imaging signs of pulmonary arterial hypertension

A
  • Enlarged pulmonary trunk (larger than aorta)
  • Enlarged segmental pulmonary arteries (larger than adjacent bronchi)
  • Mural calcifications of central pulmonary arteries
  • Visualization of the main pulmonary trunk at the level of the aortic arch (“banana and egg”
  • Right pulmonary artery crossing over the airways at the level of the carina, rather than more inferiorly (“carina crossover”)
254
Q

Imaging signs of traumatic diaphragmatic herniation

A
  • Collar sign (waist-like hourglass appearance of herniated organs with the waist being the injured diaphragm)
  • Dependent viscera sign (herniated organs lying directly against the chest wall without the usual interposition of lung parenchyma on CT)
255
Q

What is the most common location of a blunt tracheo-bronchial injury?

A

Within 2 cm of the carina, usually at the junction of the cartilaginous and membranous trachea

Note: This will cause pneumomediastinum (not a pneumothorax).

256
Q

Macklin effect

A

Pneumomediatinum from blunt trauma due to alveolar rupture and air dissecting along bronchovascular sheaths into the mediastinum

Note: This is probably the most common cause of pneumomediastinum in trauma pts.

257
Q

Chest pain in a pt with persistent vomiting…

A

Get chest X-ray and esophagram with water soluble contrast to evaluate for esophageal rupture (Boerhaave syndrome)

258
Q

Common causes of pneumopericardiu

A
  • Mechanical ventilation (high PEEP)
  • Thoracic surgery
  • Penetrating trauma
  • Infectious pericarditis
259
Q

How can you differentiate pneumomediastinum from pneumopericardium?

A

In pneumopericardium, the air should not extend above the origins of the great vessels

260
Q

Definition of flail chest

A

3 or more segmental fractures (more than 1 fracture per rib)

OR

More than 5 adjacent rib fractures

261
Q

Paradoxical motion while breathing on exam s/p MVC…

A

Think flail chest, look for multiple rib fractures

262
Q

High density pleural effusion s/p trauma…

A

Hemothorax

263
Q

Deep sulcus sign

A

Unusually deep costophrenic angle due to excess air in a pneumothorax

264
Q

Signs of a tension pneumothorax?

A
  • Deviation of the trachea/mediastinum
  • Flattening/inversion of the ipsilateral diaphragm
265
Q

Treatment for tension pneumothorax

A

Needle thoracotomy (4G needle inserted at the 2nd intercostal space in the midclavicular line)

266
Q

Extrapleural hematoma

A

A hematoma in the chest wall with an intact parietal pleura (i.e. not a hemothorax)

Note: Look for displaced extra pleural fat or a persistent fluid collection following pleural drain placement.

267
Q

You see what looks like a hemothorax s/p trauma, but the fluid collection persists after pleural drain placement and there is displacement of the extrapleural fat…

A

Extrapleural hematoma

268
Q

What is the most common pulmonary injury s/p blunt trauma?

A

Pulmonary contusion

269
Q

Non-segmental, ill-defined areas of consolidation with sub pleural sparing s/p blunt trauma…

A

Pulmonary contusion

Note: If consolidative opacities persist >72 hours, think aspiration, pneumonia, or laceration.

270
Q

Pneumatocele with an air-fluid level s/p trauma that persists for more than a week…

A

Pulmonary laceration

271
Q

SOB, AMS, and rash with ground glass opacities bilaterally 2 days after a displaced femoral fracture…

A

Fat embolization syndrome (fat emboli to the lungs, brain, and skin following a long bone fracture or intramedullary rod placement)

272
Q

Which pts are at high risk for barotrauma (pneumomediastinum/pneumothorax secondary to positive pressure ventilation)?

A

Pts with acute lung injury or COPD

Note: Pts with pulmonary fibrosis are actually protected against barotrauma due to lower pulmonary flexibility.

273
Q

Proper chest tube placement on radiographs…

A

All chest tube side holes should be within the pleural space (if you see a side hole that is not overlying pulmonary parenchyma, then it needs to be repositioned)

274
Q

Hemopericardium in the setting of trauma…

A

Suggest blunt cardiac injury and recommend correlation with cardiac enzymes and ECG

275
Q

Central line malposition with an abrupt bend in the tip of the catheter near the cavoatrial junction…

A

Tip likely in the azygos vein

276
Q

Central line malposition with line appearing on the left side of the heart…

A

Either arterial placement or duplicated SVC

277
Q

Chest radiograph shows a central line with good positioning and imaging of the liver shows a hyper dense quadrate lobe…

A

Think SVC occlusion

Note: Hot quadrate sign is suggestive of SVC occlusion in the setting of a central line (risk factor for SVC occlusion).

278
Q

What is the optimal position of a Swan Ganz catheter?

A

Between the main pulmonary artery and the interlobular arteries (tip should be no more than 2 cm lateral to the mediastinal shadow)

279
Q

What is the purpose of an intra-aortic balloon pump?

A

Decrease left ventricular afterload and increase myocardial perfusion

280
Q

What is the correct position of an intra-aortic balloon pump?

A

Tip in the proximal descending aorta (just below the origin of the left subclavian artery)

281
Q

Common complications of intra-aortic balloon pump placement?

A
  • Aortic dissection during placement
  • Obstruction of the left subclavian artery from malpositioning
282
Q

What are the stages of pulmonary edema?

A
  • Redistribution (cephalization of vessels, big vascular pedicle)
  • Interstitial edema (Kerley B lines, peribronchial cuffing, less distinct central vessels)
  • Alveolar edema (airspace fluffy opacities, pleural effusion)
283
Q

What are the stages of pulmonary edema?

A
  • Redistribution (cephalization of vessels, big vascular pedicle)
  • Interstitial edema (Kerley B lines, peribronchial cuffing, less distinct central vessels)
  • Alveolar edema (airspace fluffy opacities, pleural effusion)
284
Q

Most common cause of right heart failure

A

Left heart failure

Note: Chronic PEs and tricuspid regurgitation are also causes of right heart failure.

285
Q

Imaging features of right heart failure

A
  • Dilatation of azygos vein
  • Dilatation of right atrium
  • Dilatation of SVC
  • Ascites
  • Hepatomegaly
  • Contrast reflux into the hepatic veins on CTPA
286
Q

Proper positioning of en endotracheal tube

A

5 cm above the carina (halfway between the clavicles and the carina)

287
Q

How does endotracheal tube positioning change with chin movement?

A

ET tube will move up when the chin is up and will move down when the chin is down (“the hose goes where the node goes”)

288
Q

When might a bronchial intubation be a good idea?

A

Massive pulmonary hemorrhage with unilateral ventilation to protect the good lung

289
Q

Where are cardiac pacing leads usually placed?

A
  • Right atrial appendage
  • Right ventricular apex
  • Left ventricle (via coronary sinus)
290
Q

What is the most common location of a cardiac lead fracture?

A

At the level of the clavicle and first rib (rib clavicle crushing)

291
Q

If a lead is more than ____ within epicardial fat, you should suspect myocardial perforation

A

3 mm

292
Q

Twisting of the cardiac pacing leads near the generator with shortening of the leads…

A

Twiddler syndrome due to the pt twisting the generator in its pocket

293
Q

How can you tell the difference between cardiac conduction devices?

A
  • Pacemaker (thin wires only)
  • ICDs (shock coils present)
  • Cardiac resynchronization device (both LV and RV leads present)