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Thoracic 1 Flashcards

1
Q

How can you differentiate the L and R ribs on a lateral chest X-ray?

A

Left ribs are smaller with sharper edges

Note: Lateral CXRs are taken in the left lateral position, meaning the left ribs are against the detector.

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2
Q

How can you differentiate L and R diaphragms on a lateral CXR?

A
  • Left has stomach bubble under
  • Left is not seen anteriorly (due to heart)
  • Left is lower
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3
Q

What structure appears as “the dark hole” on a lateral CXR?

A

The left upper lobe bronchus (en face)

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4
Q

How can you differentiate the L and R main pulmonary arteries on a lateral CXR?

A

L pulmonary artery is posterior to “the dark hole” (en face bronchus)

R pa is anterior (and also more inferior)

Note: “L”osers to the back.

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5
Q

Retrotracheal triangle

A

Dark triangle behind the trachea on the lateral CXR (above the aortic arch and anterior to the spine)

Note: This should always be black.

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6
Q

Common reason for an opacified retrotracheal triangle

A

Aberrant right subclavian artery

Note: The retrotracheal triangle is the (usually) dark triangle behind the trachea on the lateral CXR (above the aortic arch and anterior to the spine).

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7
Q

Which “hilar point” should be superior?

A

The left hilar point should be ~1 cm above the right hilarity point on CXR

Note: The hilar point is the medially oriented “V” at the hill: > <

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8
Q

On lateral CXR, which major fissure is anterior?

A

The right major fissure is anterior to the left

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9
Q

How many layers of pleura make up an azygos lobe fissure?

A

4 (2 visceral and 2 parietal)

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10
Q

How many bronchopulmonary segments are there on the right?

A

10 (3 upper, 2 middle, and 5 lower)

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11
Q

How many bronchopulmonary segments are there on the left?

A

8 (4 upper and 4 lower)

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12
Q

What are the bronchopulmonary segments on the right?

A
  • R upper (apical, posterior, anterior)
  • R middle (medial and lateral)
  • R lower (superior, anterior, posterior, medial, and lateral)
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13
Q

What are the bronchopulmonary segments on the left?

A
  • L upper (apicoposterior, anterior, superior singular, and inferior lingular)
  • L lower (superior, anteromedial, lateral, posterior)
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14
Q

Pig bronchus

A

AKA tracheal bronchus, a normal variant where the right upper lobe bronchus originates directly from the trachea

Note: May cause recurrent RUL pneumonia.

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15
Q

Cardiac bronchus

A

An accessory bronchus that originates from the right bronchus intermedius

Note: It is usually blind ending, but may cause recurrent infections.

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16
Q

What separates the superior mediastinum from the rest of the mediastinum?

A

A plane at the level of the sternomanubrial junction (also at the level of T4)

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17
Q

What is the posterior border of the anterior mediastinal space?

A

Pericardium

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18
Q

What is in the middle mediastinum?

A
  • The heart
  • Roots of central vessels (e.g. aorta)
  • Tracheal bifurcation
  • Phrenic nerves
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19
Q

What are the borders of the posterior mediastinum?

A
  • Posterior pericardium
  • Spine (anterior longitudinal ligament)

Note: Contains the esophagus, lower thoracic duct, and descending aorta.

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20
Q

What is the most anterior structure in the superior mediastinum?

A

The thymus

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21
Q

What is the normal number of pulmonary veins?

A

4

  • R superior
  • R inferior
  • L superior
  • L inferior

Note: This is highly variable.

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22
Q

Supernumerary pulmonary veins predispose to…

A

Atrial fibrillation

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23
Q

What is the most common supernumerary vein?

A

Right middle

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24
Q

What is the most common vein sleeve to cause atrial fibrillation?

A

Left superior pulmonary vein

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25
Q

What is a common ostium (in the context of pulmonary veins)?

A

A common origin of the left superior and inferior pulmonary veins (can also occur on the right)

Note: This is important to identify preop so that the common ostium isn’t ligated if you only want to remove the left upper lobe.

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26
Q

What are the 4 major etiologies of atelectasis?

A
  • Obstructive (AKA absorptive)
  • Compressive (AKA relaxation/passive)
  • Fibrotic (AKA cicatrization)
  • Adhesive
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27
Q

Common causes of obstructive atelectasis

A
  • Obstructing neoplasm
  • Mucous plugging
  • Foreign body aspiration
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28
Q

Common causes of compressive atelectasis

A
  • Pleural effusion
  • Mass
  • Hiatal hernia
  • Large pulmonary bleb
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29
Q

Common causes of cicatrization atelectasis

A

Anything that causes fibrosis (e.g. tuberculosis and other infections, radiation scarring, etc.)

Note: Cicatrization occurs when fibrosis doesn’t allow the lung to fully expand.

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30
Q

Common causes of adhesive atelectasis

A

Insufficient surfactant:

  • Respiratory distress syndrome (in preterm infants)
  • ARDS
  • Pulmonary embolism (loss of blood flow and lack of CO2 prevents surfactant from working)
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31
Q

What are the direct signs of atelectasis?

A
  • Displacement of the fissures
  • Crowding of vessels/bronchi in the atelectatic area
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32
Q

What are indirect signs of atelectasis?

A
  • Opacified collapsed lung with a typical appearance
  • Negative mass effect (e.g. shifting hilarity points up/down, tenting of the diaphragm, mediastinal shifting, rib space narrowing, etc.)
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33
Q

How can you differentiate acute vs chronic atelectasis?

A

Acute atelectasis tends to cause diaphragmatic/mediastinal/hilar displacement

Chronic atelectasis has less negative mass effect due to hyper expansion of the remaining lung (which appears as oligemia)

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34
Q
A

RUL collapse

Look for: RUL opacity, upward bowing of minor fissure, elevated right hilum

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35
Q
A

RUL collapse

Look for: RUL opacity, upward bowing of minor fissure, elevated right hilum, anterior bowing of superior oblique fissure

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36
Q
A

RML collapse

Look for: loss of the right heart border, downward bowing of the minor fissure

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37
Q
A

RML collapse

Look for: Anterior linear density over the heart

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38
Q
A

RLL collapse

Look for: Density at the right heart border, but right heart border is NOT silhouetted out, mediastinal vessels pulled to the right so far there is a triangle of black between them and the mediastinum (superior triangle sign)

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39
Q
A

RLL collapse

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40
Q
A

LUL collapse

Look for: Luftsichel sign, non visualization of the aortic knob, peaking of left diaphragm

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41
Q
A

LLL collapse

Look for: Opacity hidden behind heart, “flat waist sign” (linear appearance of the left heart border)

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42
Q

S sign of golden

A

A reverse S-shaped appearance of the minor fissure due to a centrally obstructing mass causing RUL collapse

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43
Q

Chronic right middle lobe collapse, think…

A

Lady Windermere syndrome (chronic MAI infection in an elderly woman who is too proper to cough)

Note: Look for small nodules and bronchiectasis with additional involvement of the lingual.

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44
Q

CXR showing loss of the right diaphragm and loss of the right heart border…

A

Think RLL and RML collapse

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45
Q

Luftsichel sign

A

A crescent of air surrounding the aortic knob (a sign of left upper lobe collapse)

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46
Q
A

Luftsichel sign (LUL collapse)

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47
Q

Hilum overlay sign

A

If you can see the hilar vessels through an overlying mass on CXR, then the mass is not in the hilum (it is anterior or posterior to the hilum)

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48
Q

Cervicothoracic sign

A

Any mass that extends above the clavicles is not in the anterior mediastinum (which ends at the clavicles)

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49
Q

What produces the posterior junction line on CXR?

A

Airspaces of the left and right lungs touching posterior to the trachea

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50
Q

Incomplete border sign on CXR

A

A peripheral mass with an incomplete border may be pleural or chest wall based (pulmonary masses should have a crisp border around the entire mass)

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51
Q

Classic presentation of Strep pneumo pulmonary infection?

A

Lobar consolidation

Note: Can be severe in sickle cell pts post splenectomy.

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52
Q

Classic presentation of Staph aureus pulmonary infection?

A

Bronchopneumonia (patchy opacities), often bilateral and may produce an abscess

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53
Q

Classic presentation of anthrax pulmonary infection?

A

Mediastinal widening and a pleural effusion in the setting of bio-terrorism

Note: This is due to hemorrhagic lymphadenitis, mediastinitis, and hemothorax.

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54
Q

Classic presentation of Klebsiella pulmonary infection?

A

“bulging fissure” due to exuberant inflammation (and more likely to have pleural effusions, empyemas, and cavitations) in an alcoholic or nursing home pt (aspiration risk)

Note: “currant jelly sputum”

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55
Q

Classic presentation of H influenza pulmonary infection?

A

Bronchitis in COPD pts and people without a spleen, but can also present as bilateral lower lobe bronchopneumonia (patchy opacities)

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56
Q

Classic presentation of pseudomonas pulmonary infection?

A

Patchy opacities with abscess formation in high risk pts (ventilated ICU pts, cystic fibrosis, or primary ciliary dyskinesia)

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57
Q

Classic presentation of Legionella pulmonary infection?

A

Peripheral and sublobar airspace opacity often in COPD pts or epidemic from water towers/air conditioners

Note: Only cavities in immunosuppressed pts.

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58
Q

Classic presentation of aspiration pneumonia?

A

Airspace opacities (cavitation and abscess are common) in the dependent portions of the lung

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59
Q

Which portions of the lung are most likely to develop aspiration pneumonia?

A

Posterior upper lobes and superior lower lobes (if pt supine during aspiration)

Basal lower lobes, lingual, and middle lobe (if pt upright during aspiration)

Note: More likely on the right than left.

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60
Q

Classic presentation of Actinomyces pulmonary infection?

A

Airspace opacities in the peripheral lower lobes +/- rib osteomyelitis/invasion of chest wall

Note: Classic story is a dental procedure gone bad, leading to mandibular osteomyelitis and aspiration.

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61
Q

Classic presentation of Mycoplasma pulmonary infection?

A

Fine reticular pattern on CXR and patchy airspace opacities with tree-in-bud nodules

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62
Q

Most common community-acquired pneumonia in 5-20 y/o?

A

Mycoplasma

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63
Q

Mycoplasma pneumonia is associated with what syndrome?

A

Sayer-James syndrome (classically appearing as a unilateral Lucent lung due to hyperinflation)

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64
Q

To exclude an underlying mass, a follow up CXR is recommended following pneumonia to confirm resolution when?

A

6 weeks later (young pt)

3 months later (elderly pt)

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65
Q

Classic appearance of graft vs host disease in the lungs s/p bone marrow transplant?

A

Bronchiolitis obliterates (seen as air trapping: mosaic attenuation on expiratory imaging)

Note: This usually occurs in the chronic (>100 days) phase of graft vs host disease.

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66
Q

Pulmonary findings s/p bone marrow transplant are divided into what three timeframes?

A
  • Early neutropenic (0-30 days)
  • Early (30-90 days)
  • Late (>90 days)
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67
Q

What pulmonary findings are common in pts in the early neutropenic phase (0-30 days) s/p bone marrow transplant?

A
  • Pulmonary edema
  • Pulmonary hemorrhage
  • Drug induced lung injury
  • Fungal pneumonia (invasive aspergillosis)
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68
Q

What pulmonary findings are common in pts in the early phase (30-90 days) s/p bone marrow transplant?

A
  • PCP
  • CMV
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69
Q

What pulmonary findings are common in pts in the late phase (>90 days) s/p bone marrow transplant?

A
  • Bronchiolitis obliterans
  • Cryptogenic organizing pneumonia
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70
Q

Bilateral perihilar ground glass opacities in a pt with AIDS…

A

Think PCP

Note: There may also be cysts.

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71
Q

Most common cause of an airspace opacity in pts with AIDS…

A

Strep pneumoniae

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72
Q

“flame-shaped” perihilar opacities in a pt with AIDS…

A

Think Kaposi sarcoma

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73
Q

Persistent pulmonary opacities in a pt with AIDS…

A

Think lymphoma

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74
Q

Many pulmonary cysts in a pt with AIDS…

A

Think lipoid pneumonia

Note: PCP can have cysts in 30% of cases.

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75
Q

Lung cysts, ground glass opacities, and pneumothorax in a pt with AIDS…

A

Think PCP

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76
Q

Hypervascular lymph nodes in a pt with AIDS…

A

Think Castleman or Kaposi sarcoma

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77
Q

Pulmonary infection in a pt with CD4 > 200

A
  • Bacterial infections
  • Tuberculosis
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78
Q

Pulmonary infection in a pt with CD4 < 200

A
  • PCP
  • Atypical mycobacteria
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79
Q

Pulmonary infection in a pt with CD4 < 100

A
  • CMV
  • Disseminated fungal infection
  • Mycobacterial infection
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80
Q

Acute focal airspace opacity in a pt with AIDS…

A
  • Think bacterial infection (most commonly strep pneumonia)
  • Think TB (if CD4 is on the lower end)
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81
Q

Chronic focal airspace opacity in a pt with AIDS…

A

Think lymphoma or Kaposi sarcoma

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82
Q

Ground glass opacities in a pt with AIDS…

A

Think PCP

Note: If not a choice and CD4 < 100, think CMV.

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83
Q

What are the different phases of pulmonary tuberculosis?

A
  • Primary
  • Primary progressive
  • Latent
  • Post primary (reactivation)
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84
Q

Common sequela of primary pulmonary TB

A
  • Ghon focus (focal calcified granuloma formation)
  • Ranke complex (Ghon focus + calcified hilar lymph nodes, more common in kids)
  • Lobar atelectasis (if bulky lymphadenopathy cause compression)

Note: Cavitation is not common in primary TB.

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85
Q

What happens if a primary TB granuloma ruptures?

A
  • Endobronchial spread
  • Hematogenous spread, which can cause miliary TB if progression/reactivation
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86
Q

Primary progressive pulmonary TB

A

Local progression of TB infection with the development of cavitation (either at primary site or site of hematogenous spread)

Note: This is uncommon, but may occur in pts with immunosuppression (e.g. HIV).

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87
Q

Risk factors for primary progressive pulmonary TB

A

Immunosuppression:
- HIV
- Organ transplant
- Steroids
- Jejunoileal bypass
- Subtotal gastrectomy
- Silicosis

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88
Q

Latent pulmonary TB

A

When you have a positive PPD, but a negative CXR and no symptoms

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89
Q

Pt has a positive PPD with negative CXR in the setting of prior TB vaccination…

A

The US considers these pts to have latent TB (even though PPD positivity is likely due to vaccination) and pts are treated with 9 months of isoniazid

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90
Q

What percentage of latent TB will reactivate?

A

Approximately 5%

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91
Q

Where is reactivation TB most likely to occur?

A

Apical and posterior upper lobe and superior lower lobe

Note: These areas get more oxygen and less lymphatics.

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92
Q

When would you consider a TB pulmonary infection more likely to be latent?

A

When there is cavitation

Note: Also classic locations in the pulmonary apex/superior lower lobe.

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93
Q

Rasmussen aneurysm

A

An arterial pseudoaneurysm that develops due to pulmonary cavitation in tuberculosis

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94
Q

Pt with active tuberculosis develops sudden worsening after being started on HAART for HIV…

A

Immune reconstitution syndrome

Note: Treatment is with steroids.

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95
Q

Is pleural involvement common in TB?

A

Pleural effusions can occur any time after the primary infection, but is usually seen around 3-6 months after primary TB

Note: This is due to a hypersensitivity reaction (pleural fluid sampling is usually culture negative, you need to actually do a pleural biopsy to make the culture more sensitive).

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96
Q

Why is identifying cavitation important when diagnosing pulmonary TB?

A

Cavitation is rare in primary TB, so is suggestive of post primary (reactivation) or, less likely, primary progressive TB

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97
Q

When is miliary TB seen?

A

Hematogenous spread during post primary (reactivation) or primary progressive TB

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98
Q

When can a latent TB infection reactivate in pts with HIV?

A

Anytime, even if CD4 > 200

Note: Primary progressive TB usually only occurs if CD4 < 200.

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99
Q

What are the two most significant nontuberculous mycobacteria that cause pulmonary infections?

A
  • Mycobacterial avium-intracellulare complex (MAC)
  • Mycobacterium Kansasii
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100
Q

Upper lobe cavitary lesion with adjacent nodules suggesting end-bronchial spread in an older male with COPD…

A

Think nontuberculous mycobacterial infection (e.g. MAC or M. kansasii)

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101
Q

Elderly lady with tree-in-bud opacities and cylindrical bronchiectasis in the right middle lobe and lingula…

A

Think Lady Windermere syndrome (mycobacterium avium complex infection in the setting of an old lady too polite to cough)

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102
Q

HIV pt (CD4 < 100) with hepatosplenomegaly, MEDIASTINAL LYMPHADENOPTHY, and mixed pulmonary opacities…

A

Think nontuberculous mycobacterial infection

Note: This is a GI infection with hematogenous spread.

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103
Q

Ill defined ground glass centrilobular nodules in a pt with recent history of hot tub use…

A

Think nontuberculous mycobacterial infection (hot tub lung)

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104
Q

What are the three categories of pulmonary aspergillus infections?

A
  • Normal immunity (e.g. aspergilloma)
  • Immunosupressed (e.g. invasive aspergillosis)
  • Hyper-immune (e.g. allergic bronchopulmonary aspergillosis)
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105
Q

Otherwise healthy pt with a solid mass sitting dependently in a pulmonary bleb or cavity…

A

Think aspergilloma in a pre-existing cavity

Note: Confirm that the fungus ball moves dependently with different positions.

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106
Q

When should you be concerned about invasive pulmonary aspergillosis?

A
  • Immunocompromised pt (e.g. AIDS, organ transplant)
  • Halo sign (consolidate nodule/mass with a ground glass “invasive” halo)
  • Air crescent sign (a thin crescent of air within a consolidative mass)
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107
Q

Upper lobe central saccular bronchiectasis with mucoid impaction (finger-in-glove opacities) in a pt with long standing asthma…

A

ABPA (allergic bronchopulmonary aspergillosis)

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108
Q

Agressive pulmonary infection with invasion of the mediastinum, pleura, and chest wall in a pt with AIDS and uncontrolled diabetes…

A

Think mucormycosis (aggressive fungal infection in high risk pts)

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109
Q

Multiple groundglass and/or consolidate nodules in a pt who had a bone marrow transplant 45 days prior…

A

Think cytomegalovirus infection

Note: Classic scenarios for CMV pulmonary infection is reactivation after prolonged immunosuppression (e.g. AIDS, organ transplant) or a bone marrow transplant with CMV positive marrow.

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110
Q

Classic appearance of CMV pulmonary infection?

A

Multiple groundglass or consolidate nodules in immunocompromised pt

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111
Q

Classic appearance of measles pulmonary infection?

A

Multifocal ground glass opacities with small nodular opacities

Note: Pneumonia can occur before or after measles skin lesions.

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112
Q

Classic appearance of influenza pulmonary infection?

A

Coalescent lower lobe opacity

Note: Pleural effusions are rare.

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113
Q

Classic appearance of varicella pulmonary infection?

A

Multiple peripheral nodular opacities that become calcified after healing in an immunocompromised adult (e.g. AIDS, lymphoma)

114
Q

Classic appearance of Epstein Barr virus pulmonary infection?

A

Lymph node enlargement and splenomegaly

Note: lung opacities are rare.

115
Q

What is the radiographic definition of severe COVID19?

A

> 50% pulmonary involvement on imaging within 24-48 hours

116
Q

Classic appearance of COVID19?

A

Bilateral peripherally-based ground glass opacities with or without “reversed halos” (ground glass opacity surrounded by consolidation)

Note: Pleural effusions are uncommon.

117
Q

CT findings in the late/absorption state of COVID19

A

“fibrous stripes” (e.g. sub pleural bands) in the regions of previous disease

118
Q

Common sources of septic emboli to the lungs

A
  • Infected tricuspid valve
  • Systemic infection
  • Infected catheters
  • Dental infections
119
Q

Classic appearance of septic emboli to the lungs

A

Peripheral round caveating nodules (some may show a large feeding vessel suggestive of hematogenous spread) with a lower lobe predominance (due to increased dependent blood flow)

120
Q

Lemierre syndrome

A

Jugular vein thrombosis in the setting of oropharyngeal infection with septic pulmonary emboli

Note: Commonly there is a recent ENT surgery.

121
Q

What is the bacterial agent responsible for the majority of septic pulmonary emboli?

A

Fusobacterium necrophorum

122
Q

Common causes of pulmonary cavitating disease

A

CAVITY:

  • Cancer (usually squamous cell)
  • Autoimmune (Wegners, Rheumatoid, Caplan syndrome)
  • Vascular (septic emboli, bland emboli)
  • Infection (TB)
  • Trauma (pneumatoceles)
  • Young (congenital: CCAMs, sequestrations)
123
Q

What is the cutoff between a pulmonary nodule and a pulmonary mass?

A

3 cm

124
Q

What are the 4 major “benign calcification” patterns for a pulmonary nodule?

A
  • Solid/diffuse
  • Laminated (concentric)
  • Central
  • Popcorn

Note: Any other types of calcifications are considered suspicious.

125
Q

What are some common suspicious calcifications patterns for pulmonary nodules?

A
  • Eccentric
  • Stippled (many small flecks)
126
Q

What medical histories should make you suspicious of what would otherwise be considered benign appearing calcifications in a pulmonary nodule?

A
  • GI cancer (can have pulmonary mets with popcorn or central calcifications)
  • Osteosarcoma (can have pulmonary mets with solid calcifications)
127
Q

What findings suggest that a pulmonary nodule is benign?

A
  • Macroscopic fat
  • Slow doubling time (longer than 16 months)
  • Rapid doubling time (shorter than 1 month)
128
Q

What pulmonary nodule findings are suspicious for cancer?

A
  • Spiculated margins (corona radiata)
  • Air bronchograms running through the nodule (suggestive of adenocarcinoma)
  • Partially solid lesions with a ground glass component
  • Moderate doubling time (>1 month, but less than 16 months)
129
Q

Are solid or ground glass pulmonary nodules more concerning?

A
  • Part solid part ground glass (most concerning)
  • Entirely ground glass (concerning)
  • Entirely solid (least concerning)
130
Q

Should solitary pulmonary nodules that are malignant be hot on PET/CT?

A

If the nodule is solid, FDG uptake is suspicious for cancer

If the nodule is groundglass, FDG uptake is more suggestive of infection/inflammation (cold ground glass nodules are suspicious for cancer)

Note: The nodule must be 1 cm or more to be within the resolution of PET/CT.

131
Q

Can perifissural nodules be spherical?

A

No, this suggests a pulmonary nodule that is growing through the fissure rather than along it (more concerning for cancer, less likely to be an intro pulmonary lymph node)

132
Q

Lung cancer is more commonly found in which lung?

A

The right lung (1.5x)

133
Q

Where in the lung is lung cancer most likely to be found?

A

Upper lobes (70%)

Note: In pulmonary fibrosis, lung cancer is more commonly found in the lower lobes.

134
Q

A ground glass pulmonary nodule gets smaller and more dense on follow up imaging…

A

Suspicious for neoplasia

Note: Just because a pulmonary nodule get smaller doesn’t mean its benign, especially if it gets more dense.

135
Q

A new solitary pulmonary nodule in a pt with known head and neck cancer…

A

More likely to be a primary bronchogenic carcinoma rather than a metastases (these types of cancers have similar risk factors)

136
Q

Do air bronchograms make a solitary pulmonary nodule more or less likely to be neoplastic?

A

Air bronchograms are 5x more common in malignant solitary pulmonary nodules

137
Q

Who qualifies for lung cancer screening?

A

Adults age 50-80 years with a 20 pack year history of smoking (and are currently smoking or have quit within the past 15 years)

138
Q

What is the radiation dose for lung cancer screening chest CTs?

A

Low dose: recommended to be less than CTDI(vol) 3 mGy

139
Q

What is the maximum slice thickness for a low dose chest CT for lung cancer screening?

A

2.5 mm (though most recommend 1.5 mm or thinner)

140
Q

What is considered “growth” on lung cancer screening chest CTs?

A

Increase of 1.5 mm or more in one year

141
Q

How are end-bronchial lesions treated during lung cancer screening?

A

Category 4a (suspicious), with recommendation for a 3 month follow up scan

Note: Many of these will end up just being mucous.

142
Q

Can people with a history of prior lung cancer be enrolled in a lung cancer screening program?

A

Yes, but the lung cancer must be treated and remote (> 5 years)

143
Q

How should lung nodule sizes be reported on lung cancer screening chest CTs?

A

To the 0.1 mm (e.g. 7.9 mm)

144
Q

Which lung rads categories require shorter term follow-up than the standard annual chest CT?

A

Categories 3 and 4

Note: Category 0 (incomplete) requires a repeat scan or comparison with priors.

145
Q

Lung-RADS category 0

A

Incomplete exam

Note: Needs repeat scan or comparison with priors that aren’t available.

146
Q

Lung-RADS category 1

A

Negative (no nodules or only granulomas)

Note: Continue annual chest CT.

147
Q

Lung-RADS category 2

A

Benign

Baseline: No nodules 6 mm or more

Subsequent: No new nodules 4 mm or more, ground glass nodules 30 mm or more, or perifissural nodules 10 mm or more.

Note: Continue annual chest CT.

148
Q

Lung-RADS category 3

A

Probably benign

Baseline: Nodules 6-8 mm

Subsequent: New nodule 4 mm or more. Ground glass nodule 30 mm or more.

Note: Recommend 6 month follow up chest CT.

149
Q

Lung-RADS category 4a

A

Suspicious (5-15% chance of cancer)

Baseline: Nodules 8-15 mm

Subsequent: New nodule 6-8 mm

Note: Recommend 3 month follow up chest CT or PET/CT.

150
Q

Lung-RADS category 4b

A

Suspicious (>15% chance of cancer)

Baseline: Nodules 15 mm or more

Subsequent: New nodule 6 mm or more

Note: Recommend PET/CT or tissue sampling.

151
Q

Lung-RADS category 4x

A

Suspicious (>15% chance of cancer)

Baseline: N/a
Subsequent: worsening of category 3 or 4 nodules (growth or new spiculation)

Note: Recommend PET/CT or tissue sampling.

152
Q

What are the Lung-RADS categories and recommendations

A
  • 0 (incomplete, repeat scan or get priors)
  • 1 (negative, continue annual)
  • 2 (benign, continue annual)
  • 3 (probably benign, repeat chest CT in 6 months)
  • 4a (suspicious, repeat chest CT in 3 months or PET)
  • 4b (suspicious, PET or tissue sampling)
  • 4x (suspicious, PET or tissue sampling)
153
Q

When do you use Lung-RADS vs Fleischner guidelines?

A

Lung-RADS is only used for low-dose CTs for lung cancer screening

Fleischer guidelines are used for nodules incidentally discovered on non-screening chest CTs (with some exceptions)

154
Q

When should Fleischner guidelines NOT be used?

A
  • Pts under age 35
  • Pts with known or suspected cancer
  • Immunocompromised pts
155
Q

How should solid pulmonary nodules be measured according to the Fleischner Society?

A

Average of longest diameter and perpendicular diameter measured in the same plane (usually axial)

156
Q

Why is it recommended to evaluate pulmonary nodules using slice thickness of 1.5 mm or less?

A

To look for a small solid component within a ground glass nodule (which might not be seen on thicker slices due to volume averaging)

157
Q

Follow up recommendations for a low-risk solitary solid pulmonary nodule according to Fleiscner guidelines

A
  • <6 mm (no follow up)
  • 6-8 mm (6-12 month repeat chest CT)
  • > 8 mm (PET or biopsy)
158
Q

Follow up recommendations for a high-risk solitary solid pulmonary nodule according to Fleiscner guidelines

A
  • <6 mm (12 month repeat chest CT)
  • 6-8 mm (6-12 month repeat chest CT)
  • > 8 mm (PET or biopsy)
159
Q

Follow up recommendations for low-risk multiple solid pulmonary nodules according to Fleiscner guidelines

A
  • <6 mm (no follow up)
  • 6-8 mm (3-6 month repeat chest CT)
  • > 8 mm (3-6 month repeat chest CT)

Note: Recommendation according to largest nodule.

160
Q

Follow up recommendations for high-risk multiple solid pulmonary nodules according to Fleiscner guidelines

A
  • <6 mm (12 month repeat chest CT)
  • 6-8 mm (3-6 month repeat chest CT)
  • > 8 mm (3-6 month repeat chest CT)

Note: Recommendation according to largest nodule.

161
Q

Recommendation for solitary incidental solid pulmonary nodule <6 mm

A
  • No follow up (low risk)
  • 12 month repeat chest CT (high risk)
162
Q

Recommendation for solitary incidental solid pulmonary nodule 6-8 mm

A

6-12 month repeat chest CT (low and high risk)

163
Q

Recommendation for solitary incidental solid pulmonary nodule >8 mm

A

PET or biopsy (low and high risk)

164
Q

Recommendation for multiple incidental solid pulmonary nodules measuring up to <6 mm

A
  • No follow up (low risk)
  • 12 month repeat chest CT (high risk)
165
Q

Recommendation for multiple incidental solid pulmonary nodules measuring up to 6-8 mm

A

3-6 month repeat chest CT (low and high risk)

166
Q

Recommendation for multiple incidental solid pulmonary nodules measuring up to >8 mm

A

3-6 month repeat chest CT

Note: This recommendation is less stringent than for solitary pulmonary nodules, which have a higher chance of malignancy.

167
Q

Follow up recommendations for incidental solitary ground glass pulmonary nodules

A
  • <6 mm (no follow up)
  • 6 mm or more (6-12 month repeat chest CT, then every 2 years until resolution up to a total of 5 years)

Note: Follow-up is extended to 5 years if 6 mm or more due to the potential for slow growing adenocarcinoma in situ.

168
Q

Follow up recommendations for incidental multiple ground glass pulmonary noduels

A

3-6 month repeat chest CT

169
Q

When can a solitary solid pulmonary nodule stop being followed?

A

If it is stable for 2 years or more

170
Q

Follow up recommendations for an incidental part solid pulmonary nodule

A
  • <6 mm (no follow up)
  • 6 mm or more (3 month repeat chest CT, then repeated at widening intervals for a total of 5 years if persistent)
171
Q

What are the main histologic subtypes of bronchogenic carcinoma?

A
  • Non small cell (adenocarcinoma, squamous, and large cell)
  • Small cell
172
Q

Which bronchogenic carcinoma subtypes are more likely to be found peripherally?

A
  • Large cell
  • Adenocarcinoma

Note: “LA” is on the coast. squamous and small cell carcinomas are mote likely to be central.

173
Q

What bronchogenic carcinoma subtype is most common in non-smokers?

A

Adenocarcinoma

Note: This subtype is also common in smokers.

174
Q

Which bronchogenic carcinoma subtype is most likely to cavitate?

A

Squamous cell carcinoma

175
Q

Which bronchogenic carcinoma subtype is associated with ectopic parathyroid hormone production?

A

Squamous cell carcinoma

176
Q

Which bronchogenic carcinoma subtype is most common?

A

Adenocarcinoma

177
Q

What is the most common bronchogenic carcinoma subtype to present as a solitary pulmonary nodule?

A

Adenocarcinoma

178
Q

What is the most common bronchogenic carcinoma subtype to cause SVC obstruction and paraneoplastic syndromes?

A

Small cell carcinoma

179
Q

Which bronchogenic carcinoma subtype has the strongest association with smoking?

A

Small cell carcinoma (nonsmokers virtually never get small cell carcinoma)

180
Q

Which bronchogenic carcinoma subtype may present with only central lymphadenopathy?

A

Small cell carcinoma

Note: Small cell carcinoma tends to metastasize early.

181
Q

What paraneoplastic syndromes are associated with small cell lung cancer?

A
  • SIADH
  • Ectopic ACTH production
  • Lambert-Eaton syndrome
182
Q

68 y/o smoker who presents with proximal muscle weakness with chest CT demonstrating mediastinal/hilar lymphadenopathy…

A

Think small cell carcinoma with the Lambert-Eaton syndrome (paraneoplastic syndrome)

183
Q

Which bronchogenic carcinoma subtype is associated with the Lambert-Eaton paraneoplastic syndrome?

A

Small cell carcinoma

184
Q

Which bronchogenic carcinoma subtype has the worst prognosis?

A

Small cell carcinoma (metastasizes early)

185
Q

What are presenting symptoms that can help predict whether a lung cancer is peripheral or central?

A
  • Hemoptysis (central lung cancer)
  • Pleuritic chest pain (peripheral lung cancer)
186
Q

Which bronchogenic carcinoma subtype has an association with pulmonary fibrosis?

A

adenocarcinoma

187
Q

What is adenocarcinoma in situ?

A

A localized adenocarcinoma that is <3 cm and exhibits a lepidocrocite growth pattern with neoplastic cells along the alveolar structures (but no stroll/vascular/pleural invasion)

188
Q

What is the spectrum of adenocarcinoma?

A

Pre-invasive lesions:
- Atypical adenomatous hyperplasia of lung (usually a small <5 mm ground glass nodule)
- Adenocarcinoma in situ (usually 5-30 mm part solid nodule)

Invasive lesions:
- Minimally invasive adenocarcinoma (<5 mm of stromal invasion)
- Invasive mutinous adenocarcinoma (used to be called bronchoalveolar carcinoma)

Note: These tend to progress from groundlass to part solid to solid/invasive.

189
Q

Which lung cancer subtype is classically cold on PET/CT?

A

Adenocarcinoma in situ spectrum (lepidic growth appearing as a ground glass nodule getting progressively more dense)

190
Q

What are the symptoms associated with a pancoast tumor?

A
  • Shoulder pain
  • C8-T12 radiculopathy
  • Horner syndrome (ptosis/droopy eyelid and miosis/small pupil)
191
Q

What is the best way to stage pancoast tumors?

A

MRI (to evaluate the brachial plexus)

192
Q

What are general contraindications to surgical resection of a pancoast tumor?

A
  • Vertebral body invasion >50%
  • Spinal canal invasion
  • Involvement of the upper brachial plexus (C8 or higher)
  • Diaphragm paralysis (due to C3-C5 involvement)
  • Distal metastases
193
Q

What is a pancoast tumor?

A

An apical pulmonary tumor with associated symptoms (shoulder pain, Horner syndrome, etc.)

194
Q

T classification of lung cancer staging by size

A
  • T1 (<3 cm)
  • T2 (3-5 cm)
  • T3 (5-7 cm)
  • T4 (>7 cm)
195
Q

What characteristics make a lung cancer T2 even if smaller than 3 cm?

A
  • Invasion of visceral pleura
  • Invasion of a main bronchus (without involvement of the carina, which would make it T4)
  • Causes obstruction (atelectasis or pneumonia) that extends to the hilum
196
Q

What characteristics make a lung cancer T3 even if smaller than 5 cm?

A
  • Invasion of the chest wall
  • Invasion of the pericardium
  • Invasion of the phrenic nerve (diaphragmatic paralysis)
  • One or more satellite nodules in the same lung lobe
  • Pancoast tumor involving the T1/T2 nerve roots
197
Q

What characteristics make a lung cancer T4 even if smaller than 7 cm?

A
  • Invasion of mediastinal fat or great vessels
  • Invasion of the diaphragm
  • Involvement of the carina
  • One or more satellite nodules in the same lung, but a different lobe
  • Pancoast tumor involving the C8 nerve roots or higher
198
Q

T classification of a lung cancer that involves the intrapericardial portion of the pulmonary veins

A

T4

199
Q

N staging of lung cancer

A
  • N0 (no nodal involvement)
  • N1 (Ipsilateral nodal involvement up to the hilar nodes)
  • N2 (ipsilateral mediastinal or subcarinal nodes), often not resectable
  • N3 (contralateral mediastinal/hilar nodes OR scalene/supraclavicular nodes), rarely resectable

Note: PET/CT is the preferred method for N staging.

200
Q

What is an important anatomical boundary when evaluating N stage in lung cancer?

A

Level 1 lymph nodes (above the upper border of the manubrium/lower border of the clavicles), indicates N3 stage

Note: Level 2 lymph node involvement (below manubrium/clavicles) indicates N2 stage.

201
Q

What are typical contraindications to lobectomy of lung cancer?

A
  • Growth of tumor through a fissure
  • Invasion of pulmonary vasculature
  • Invasion of main bronchus
  • Invasion of both upper and lower lobe bronchi
202
Q

What are typical contraindications to resection of lung cancer?

A
  • N3 nodal disease (contralateral mediastinal/hilar nodes OR scalene/supraclavicular nodes)
  • Tumor >5 cm AND N2 disease (ipsilateral mediastinal/subcarinal nodes)
  • Multi-lobar disease
  • Malignant pleural effusion
203
Q

Which mediastinal nodes are not easily reached by mediastinoscopy and therefore important for the radiologist to identify prior to mediastinoscopy?

A

Prevascular lymph nodes

204
Q

Treatment of a stage 1A or 1B lung cancer that is peripheral and <2 cm…

A

Wedge resection (to preserve more pulmonary reserve than a lobectomy)

Note: In general, if the tumor is >3 cm, lobectomy is usually a better option.

205
Q

Following a pneumonectomy for lung cancer, there is progressively increasing air in the pneumonectomy cavity over the following 3 days…

A

Bronchopleural fistula

206
Q

What are the risk factors for a bronchopleural fistula following a pneumnectomy?

A
  • Ischemia of the bronchi (due to disrupted blood supply from aggressive lymph node dissection)
  • Using a long bronchial stump
207
Q

Postpneumonectomy syndrome

A

A compensatory emphysema following pneumonectomy, where the contralateral lung hyperexpands to compensate for the absent contralateral lung

208
Q

How do radiation changes appear in the lung following radiotherapyfor lung cancer?

A
  • Homogenous or patchy ground glass opacities (early: 1-3 months)
  • Dense consolidation, traction bronchiectasis, and volume loss (late)
209
Q

Is it common to develop rib fractures within the radiation field s/p treatment for lung cancer?

A

Yes, ribs within the radiation field are susceptible to degradation and fracture

210
Q

Bubbles found within a pulmonary lesion immediately following radio frequency/microwave ablation…

A

Bubbles are a normal finding post RFA/MWA

211
Q

What is the best way to evaluate for recurrent lung cancer s/p treatment?

A

Look for enhancing areas with a round morphology (radiation changes should not have a round morphology and should not increase in size over time)

Note: Focus on the periphery of the radiation bed, regional lymph nodes, and the bronchial stump.

212
Q

New pleural effusion s/p treatment for lung cancer that persists on follow up imaging…

A

Suspicious for recurrent lung cancer

213
Q

Pulmonary lesion with macroscopic fat and popcorn calcifications…

A

Pulmonary hamartoma

214
Q

What is the most common benign lung mass?

A

Pulmonary hamartoma

215
Q

Are pulmonary hamartomas symptomatic

A

Usually not, but they can be if they are end-bronchial (2% of cases)

216
Q

Pulmonary lesion with macroscopic fat that is FDG avid on PET…

A

Pulmonary hamartoma (benign lesion, but can still be hot on PET)

217
Q

What is the most common lung tumor in AIDS pts?

A

Kaposi sarcoma (followed by lymphoma)

218
Q

Flame shaped consolidation along the perihilar pulmonary parenchyma in an AIDS pt (CD4 < 200)…

A

Think Kaposi sarcoma

219
Q

What is the most common hepatic neoplasm in AIDS pts…

A

Kaposi sarcoma

220
Q

Common findings of pulmonary kaposi sarcoma in an AIDS pt

A
  • Flame shaped central opacities
  • Slow growth without symptoms
  • Bloody pleural effusion
  • Thallium positive and gallium negative
221
Q

What are the 3 categories of metastatic disease to the lungs?

A
  • Direct invasion
  • Hematogenous metastases
  • Lymphangitic carcinomatosis
222
Q

What tumors most commonly cause direct invasion of the pulmonary parenchyma?

A
  • Esophageal carcinoma
  • Lymphoma
  • Malignant germ cell tumor
  • Pleural metastases
  • Malignant mesothelioma

Note: Cancers of the mediastinum, pleura, or chest wall are most likely to directly invade the lungs.

223
Q

How do hematogenous metastases to the lungs appear?

A

Diffuse pulmonary nodules with a random distribution and a lower lobe predominance (due to greater blood volume)

224
Q

Which primaries are most likely to produce “cannonball” pulmonary metastases?

A
  • Renal cell carcinoma
  • Testicular choriocarcinoma
225
Q

Pulmonary hematogenous metastases are most likely from which primary tumors?

A
  • Breast
  • Kidney
  • Thyroid
  • Colon
  • Head and neck squamous cell carcinoma (often cavitating)
226
Q

Prominent pulmonary vessels leading to pulmonary nodules…

A

Think hematongeous metastases or septic emboli

227
Q

What is the most common primary in lymphangitis carcinomatosis?

A

Bronchogenic carcinoma invading the lymphatics

Note: The most common extra thoracic primaries are breast, stomach, pancreas, and prostate cancers.

228
Q

What are the 4 main categories of pulmonary lymphoma?

A
  • Primary lymphoma
  • Secondary lymphoma
  • AIDS-related lymphoma
  • Post-transplant lymphoproliferative disorders (PTLDs)
229
Q

What is the most common subtype of primary pulmonary lymphoma?

A

Non-Hodgkin, low grade MALToma (80% of primary pulmonary lymphoma cases)

230
Q

Primary pulmonary lymphoma

A

Pulmonary lymphoma without extrathoracic involvement for 3 months

Note: This is much more rare than secondary pulmonary lymphoma.

231
Q

Secondary pulmonary lymphoma

A

Pulmonary involvement of a systemic lymphoma

232
Q

If there is secondary pulmonary lymphoma, is this more likely to be Hodgkin or non-Hodgkin?

A

non-Hodgkin

Note: Although Hodgkin lymphoma is more likely to involve the lungs, non-Hodgkin lymphoma is much more common in general.

233
Q

Pulmonary parenchymal involvement in seconday lymphoma without mediastinal involvement is likely to be what type of lymphoma?

A

non-Hodgkin

Note: If there is pulmonary involvement in Hodgkin lymphoma, there is almost always also mediastinal lymph node involvement as well.

234
Q

Post transplant lymphoproliferative disorders

A

B-Cell lymphoma secondary to Epstein Barr virus infection following a solid organ or stem cell transplant

Note: This usually occurs within 1 year of the transplant, but can happen later (later ones are usually more aggressive).

235
Q

AIDS pt with CD4 < 100 and pulmonary nodules, pleural effusions, and lymphadenopathy…

A

AIDS-related pulmonary lymphoma

236
Q

AIDS-related pulmonary lymphoma

A

A high grade non-Hodgkin lymphoma that occurs in AIDS pts with CD4 < 100 secondary to epstein barr virus infection

Note: Extranodal involvement is common (CNS, bone marrow, lung, liver, bowel).

237
Q

What nuclear medicine tests can help distinguish pulmonary Kaposi sarcoma from pulmonary lymphoma?

A

Thallium-201 and Gallium-67 scans

Note: Both will be positive on Thallium scans (live tissue), but only lymphoma will be gallium positive (inflammatory).

238
Q

What tissues light up on thallium scans?

A

Anything that is alive (i.e. has a functional Na/K ATPase pump

Note: Thallium is a potassium analog.

239
Q

What tissues light up on a gallium scan?

A

Inflamed tissues (infection, sarcoid, most cancers)

Note: Gallium is an iron analog (acute phase reactant analog). Things that are “smoldering” tend to be gallium-negative.

240
Q

Which lymphomas are Gallium-positive

A

Most lymphomas are gallium positive, especially Hodgkin lymphoma. Some Non-Hodgkin subtypes can be gallium-negative, which is why PET/CT is used for staging and not gallium.

241
Q

Poland syndrome

A

Congenital unilateral absence of a pectoral muscle, which can appear as a unilateral hyper lucent chest on radiographs

Note: Often associated with ipsilateral limb abnormalities (small/abnormal arms/hands).

242
Q

Bronchial atresia

A

Congenital obliteration of a shirt segment of a lobar/segmental/subsegmental bronchus near its origin (most often affecting the apical-posterior segment of the left upper lobe)

243
Q

Next step if you see hyperlucency and oligemia of the left upper lobe apical-posterior segment with a perihilar nodule demonstrating finger-in-glove morphology…

A

Bronchoscopy

Note: This is most likely bronchial atresia with mucoid impaction of the blind-ending bronchus, but could also be an obstructing endobronchial tumor.

244
Q

Why does bronchial atresia lead to hyperlucency of the obliterated pulmonary segments?

A

Collateral air flow through the various pores of Kohn and canals of Lambert

245
Q

When can you be confident that a perihilar nodule is due to mucoid impaction from bronchial atresia rather than an obstructing endobronchial tumor?

A

If you can measure a low density focus (<25 HU), you can safely call it mucoid impaction.

Note: If you cannot measure this low density focus, then you should get bronchoscopy to rule out an endobronchial tumor.

246
Q

What symptoms are associated with bronchial atresia?

A

Usually asymptomatic, but can be associated with recurrent pneumonias

247
Q

When should a pulmonary AVM be treated?

A

If the afferent vessel measures 3 mm or more

248
Q

Pulmonary AVMs are associated with…

A
  • Hereditary hemorrhagic telangiectasia
  • Osler Weber Rendu
249
Q

Where are pulmonary AVMs most likely to be found?

A

Lower lobes (due to increased blood flow)

250
Q

What are possible significant complications of a pulmonary AVM?

A

Strokes and brain abscesses (due to right to left shunting)

251
Q

Homogenous, well-circumscribed pulmonary nodule with intense enhancement and a feeding artery and draining vein…

A

Pulmonary AVM

252
Q

What is the most common congenital venous anomaly of the chest?

A

Persistent left SVC

253
Q

Where does a persistent left SVC usually drain to?

A

The coronary sinus, though in 5% of cases can drain directly to the left atrium causing a mild right to left shunt

254
Q

Central line appears in a left paramedial location and terminates in the left atrium…

A

Think about persistent left SVC draining into the left atrium

255
Q

Swyer-James syndrome

A

Unilateral hyperlucent lung secondary to post infectious obliterative bronchiolitis

Note: The size of the affected lobe is smaller than the normal lobe (not hyperexpanded, as in bronchial atresia).

256
Q

Horseshoe lung

A

A rare congenital anomaly where there is fusion of the posterior basilar segments of the bilateral lower lobes

Note: This is associated with Scimitar syndrome.

257
Q

Horseshoe lung is associated with…

A

Scimitar syndrome

Note: Horseshoe lung is fusion of the posterior basilar segments of the bilateral lower lobes.

258
Q

Upper-mid lung zone predominant cysts with bizarre shapes in a smoker sparing the costophrenic angles…

A

Pulmonary Langerhans cell histiocytosis

259
Q

Which cystic lung disease is associated with chylothorax development?

A

LAM (lymphangiomyomatosis)

260
Q

Pulmonary langerhans cell histiocytosis has what pulmonary distribution?

A

Upper/midzone predominant cysts sparing the costophrenic angles

Note: LCH starts out with centrilobular nodules that then cavitate into cysts which coalesce into bizarre, thick-walled cystic cavities.

261
Q

Treatment for pulmonary langerhans cell histiocytosis

A

Stop smoking (50% of cases spontaneous resolve)

262
Q

Epidemiology of lymphangiomyomatosis (LAM)

A

Young women of child bearing age (LAM is estrogen-dependent)

263
Q

Lymphangiomyomatosis (LAM) is associated with…

A

Tuberous sclerosis

Note: Look for TS triad (seizures, mental retardation, facial angiofibromas) or multiple renal angiomyolipomas in addition to diffuse pulmonary cysts.

264
Q

Lymphangiomyomatosis has what pulmonary distribution?

A

Diffuse thin-walled cysts with uniform distribution

265
Q

Treatment for lymphangiomyomatosis

A

Hormonal therapy (tamoxifen)

Note: Cysts usually progress despite treatment.

266
Q

Diffuse pulmonary cysts in a pt with multiple renal angiomyolipomas…

A

Lymphangiomyomatosis (LAM) in a pt with tuberous sclerosis

267
Q

Diffuse pulmonary cysts in a pt with seizures, intellectual disability, and facial angiofibromas…

A

Lymphangiomyomatosis (LAM) in a pt with tuberous sclerosis

268
Q

What are the renal findings associated with Birt-Hogg-Dube syndrome?

A
  • Bilateral oncocytomas
  • Chromophobe renal cell carcinomas
269
Q

Birt-Hogg-Dube syndrome

A

Multi-system disease characterized by:

  • Cutaneous manifestations (typically fibrofolliculomas)
  • Multiple lung cysts predisposing to spontaneous pneumothoraces
  • Renal tumors (oncocytomas, chromophobe renal cell carcinomas)
270
Q

Thin-walled, oval, “floppy” pulmonary cysts with lower lobe predominance in a pt with innumerable skin lesions…

A

Birt-Hogg-Dube syndrome

Note: Predisposed to cutaneous fibrofolliculomas and renal tumors (oncocytomas and chromophobe RCC)

271
Q

Pulmonary cysts in Birt-Hogg-Dube syndrome have what distribution>

A

Lower zone predominance, favoring the paramediastinal regions, with thin-walled oval/floppy morphology

272
Q

Lymphocytic interstitial pneumonitis (LIP)

A

A benign lymphoproliferative disorder associated with autoimmune diseases (SLE, PA, Sjogrens) resulting in cystic lung disease

273
Q

Lymphocytic interstitial pneumonitis (LIP) is associated with…

A
  • Autoimmune diseases in adults (mostly Sjogrens, also SLE and RA)
  • HIV in kids
  • Castleman disease
274
Q

Thin-walled cysts in the deep pulmonary parenchyma in a pt with sicca syndrome…

A

Lymphocytic interstitial pneumonitis (LIP) in a pt with Sjogrens (presenting with sicca syndrome)

275
Q

Perivascular pulmonary cysts…

A

Think lymphocytic interstitial pneumonitis (LIP)

276
Q

What is the most common opportunistic pulmonary infection in AIDS pts?

A

Pneumocystis pneumonia (PCP)

277
Q

AIDS pt with ground glass opacities predominantly in the hilar and mid lung zones…

A

Think pneumocystic pneumonia (PCP)

278
Q

Apical pulmonary cysts in an AIDS pt with hilar/mid lung zone ground glass opacities…

A

Cystic form of pneumocystis pneumonia (PCP)

Note: The cystic form most often occurs in AIDS pts receiving aerosolized prophylaxis and predisposes to pneumothorax development.

279
Q

AIDS pt with a new pneumothorax…

A

Think pneumocystis pneumonia (PCP)

Note: The cystic form that is common in pts receiving aerosolized prophylaxis is associated with pneumothorax development.

280
Q

Vanishing lung syndrome

A

Defined as bullous disease occupying at least one-third of a hemithorax

Note: This is due to avascular necrosis of the lung parenchyma and hyperinflation, leading to giant bullous emphysema favoring the bilateral upper lobes.

281
Q

Epidemiology of vanishing lung syndrome

A

Young males

Note: 20% of cases have alpha-1 antitrypsin deficiency.

282
Q

Major complication of vanishing lung syndrome

A

Tension pneumothorax

Core (98 decks)

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