Chest Flashcards

Question

Anterior mediastinal border

Answer 1

The posterior border is the pericardium

Answer 2

The heart, pericardium, and bifurcation o f the trachea are all included. On lateral CXR, people sometimes say posterior to the trachea, and anterior to the vertebral bodies (or 1cm posterior to the vertebral bodies).

Answer 3

From the back o f the heart to the spine. Contains the esophagus, thoracic duct, and descending aorta.

Answer 4

Pulmonary vein anatomy is highly variable. You typically have 4 total (2 right - upper and lower, 2 left - upper and lower). The most common anatomic variation is a separate vein draining the right middle lobe (seen 30% o f the time). Who cares??? Two people (1) People who write multiple choice tests, (2) Electrophysiologists prior to ablations.

Answer 5

Basically you have congenital absence o f the right (or left) PA with the more distal pulmonary vasculature present. It’s also called unilateral absence o f the PA, but that is confusing because the distal pulmonary vasculature is present.

Answer 6

Classically with volume loss o f one hemi-thorax (could be on CXR or CT), then a contrast CT shot through the heart with only one PA. Normally, you might think one PA is just volume averaging - but once you’ve been shown volume loss on one side your suspicion for this should be raised.

Answer 7

* It’s seen on the opposite side o f the aortic arch (Absent right PA with left-sided aortic arch, Absent left PA with right-sided aortic arch). * Associated with PDA * Interrupted left PA is associated with TOF and Truncus

Answer 8

tiny horizontal “plate-like” / “discoid” subsegmental to complete collapse of the lung (lobar). the degree of collapse depends on the location of obstuction (peripheral vs central)

Answer 9

* Result o f complete obstruction o f an airway * No new air can enter and any air that is already there is eventually absorbed leaving a collapsed section o f lung * Causes: Obstructing neoplasms, mucous plugging in asthmatics or critically ill patients, and foreign body aspiration.

Answer 10

* Results from direct mass • effect on the lung * Causes: Most classically seen adjacent to a pleural effusion. Could also be seen from adjacent compression o f lung from a mass, hiatal hernia, or a large bleb - anything directly pushing on the lung.

Answer 11

Results from scarring / fibrosis which fails to allow the lung to collapse completely. Causes: Most classic is TB , but scarring from radiation, other infections, or really any other cause o f fibrosis can do this.

Answer 12

* Results from loss o f surface tension / inadequate pleural adherence o f the alveolar walls - from a surfactant deficiency. * Alveoli become unstable and collapse. * Causes: RDS (premature infants), ARDS (more diffuse pattern), and in the setting o f pulmonary embolism (loss o f blood flow / lack o f CO2 disrupts integrity o f surfactant).

Answer 13

Another easily testable topic related to atelectasis are the primary and secondary signs. The big 3 ones being shadow, silhouette, and shift. Just like any normal person would, when I think of the word “shadow,” I immediately think of either Lamont Cranston (hypnotist and master detective), or Carl Jung’s “Phenomenology of the Self.” I’m sure you do too. However, in the case of atelectasis “shadow” refers to the shadow made by the opacified (collapsed lung). This is the direct sign, The silhouette refers to the loss of interface between this opacity and the adjacent normal structures. This is useful in localization. The shift refers to the movement of structures as they are “pulled” towards the site of volume loss. Remember, space occupying things (tumors, pneumonia, pleural effusion, cavitary lesions, etc...) push things away. Atelectasis is a volume losing process - so it pulls (examples - pulling the right hilar point above the left, pulling the left hilar point below the right, shifting the mediastinum, etc...).

Answer 14

- Classic look is increased density at the right heart border with loss of that border (shadow and silhouette) - The lateral will show anterior density over the heart (as the RML is anterior)

Answer 15

Chronic collapse of the RML is classically described with MAI infection in an elderly women who is too proper too cough (Lady Windermere syndrome). On CT you’d see additional findings of small nodules and bronchiectasis - with additional involvement of the Lingula.

Answer 16

- Classic look is increased density at the right heart border similar to collapse of the RML. - The critical distinction is the right heart border. You should NOT lose the border of the right heart with RLL collapse. In fact it should be easier to see from compensatory hyper-expansion of the RML.

Answer 17

In some cases, the mediastinal vessels are pulled to the right creating a triangle of opacity to the right of the trachea (Superior Triangle Sign)

Answer 18

- Uncommon Combination and a Sneaky Move | - The trick is a loss of visualization of the right hemidiaphragm and right heart border

Answer 19

- Closes like a fan attached at the Hilum - Horizontal Fissure may bow upward - Hilum may elevate - The lateral will again show this hilar attachment with the lobe collapsing from both the anterior and posterior directions. - The top half of the oblique fissure will be pulled anterior.

Answer 20

Refers to a reverse "S" shape that the minor fissure in cases of RUL collapse resulting from a central obstructing mass.

Answer 21

- This is different than the right upper lobe (which collapsed like a fan making a dense wedge shaped opacity. - The LUL tends to be more subtle with a subtle increased density medially. There won’t be any well defined borders - A hint may be non-visualization of the aortic knob. - Sometimes (if you are lucky) you can get some nonspecific peaking of the diaphragm from upward traction

Answer 22

“Air Sickle” - appearance from the lucent stripe appearance of the hyper inflated superior (apical) segment of the lower lobe pinned between the medial edge of the collapsed segment and the aortic arch

Answer 23

- Can Be sneaky on a frontal only (opacity is hidden behind the heart) - The lateral makes it more obvious with a posteriorly directed triangular opacity

Answer 24

``` The Flat Waist Sign - has been used as a description of the flattened appearance of the contours of the hilum and heart border. ```

Answer 25

above the clavicles

Answer 26

This takes advantage of the posterior junction line, which demonstrates that things above the clavicles are in the posterior mediastinum.

Answer 27

Mass at the level o f the hilum arising from the hilum will obliterate the silhouette o f the pulmonary vessels. If you can see the edge o f the vessels through the mass, then the mass is not in the hilum (so it is either anterior or posterior).

Answer 28

``` The easiest trick is if they show you air bronchograms. Only a pulmonary mass will have air bronchograms. The harder trick is the angle with the lung. The mass will make an acute angle with the lung if it’s within the lung. The mass will make an obtuse margin with the lung if it’s in the mediastinum. ```

Answer 29

-makes an acute angle with the lung

Answer 30

-makes an obtuse angle with the lung

Answer 31

Lobar Consolidation Favors lower lobes. Can be severe in sickle cell patients post splenectomy. The most common cause of pneumonia in AIDS patient.

Answer 32

Bronchopneumonia - patchy opacities Often bilateral, and can make abscess. Can be spread via the blood in endocarditis patients

Answer 33

Hemorrhagic lymphadenitis, mediastinitis, and hemothorax Classic Look: Mediastinal widening with pleural effusion in the setting of bio-terrorism

Answer 34

``` Buzzword: “Bulging Fissure” from exuberant inflammation. More likely to have pleural effusions, empyema, and cavity than conventional pneumonia. ``` Alcoholic and Nursing Home Patients. Step 1 Buzzword was “currant jelly sputum”

Answer 35

Usually bronchitis, sometimes bilateral lower lobe bronchopneumonia Seen in COPDers, and people without a spleen

Answer 36

Patchy opacities, with abscess formation ICUers on a ventilator (also CF and Primary Ciliary Dyskinesia). Pleural effusions are common, but usually small

Answer 37

Peripheral and sublobar airspace opacity Seen in COPDers, and around crappy air conditioners. Only cavitates in immunosuppressed patients. X-ray tends to lag behind resolution of symptoms.

Answer 38

Anaerobes, with airspace opacities. They can cavitate, and abscess is not uncommon Posterior lobes if supine when aspirating, Basal Lower lobes in upright aspiration May favor the right side, just like an ET tube. The most common complication is empyema (which can get a bronchopleural fistula).

Answer 39

Airspace in peripheral lower lobes. Can be aggressive and cause rib osteomyelitis/ invade adjacent chest wall. Classic story is dental procedure gone bad, leading to mandible osteo, leading to aspiration.

Answer 40

Fine reticular pattern on CXR, Patchy airspace opacity with tree-in-bud

Answer 41

You see pulmonary infections in nearly 50% of people after bone marrow transplant, and this is often listed as the most common cause of death in this population. Findings are segregated into: early neutropenic, early, and late - and often tested as such.

Answer 42

Acute (20-100 Days) Favors extrapulmonary systems (skin, liver, GI tract)

Answer 43

Chronic (> 100 days) Lymphocytic Infiltration of the airways and obliterative bronchiolitis.

Answer 44

(0-30 days Pulmonary Edema, Flemorrhage, Drug Induced Lung Injury ``` Fungal Pneumonia (invasive aspergillosis) ```

Answer 45

Early (30-90) PCP, CMV

Answer 46

Late > 90 Bronchiolitis Obliterans, Cryptogenic Organizing Pneumonia

Answer 47

Questions related to AIDS and pulmonary infection are typically written in one of two ways (1) with regard to the CD4 count, and (2) by showing you a very characteristic infection.

Answer 48

This is the most classic AIDS infection. This is the one they are most likely to show you. Ground glass opacity is the dominant finding, and is seen bilaterally in the perihilar regions with sparing of the lung periphery. Cysts, which are usually thin-walled, can occur in the ground glass opacities about 30% of the time.

Answer 49

*Most common airspace opacity = Strep Pneumonia *If they show you a CT with ground glass = PCP •“Flame-Shaped” Perihilar opacity = Kaposi Sarcoma ’Persistent Opacities = Lymphoma ’Lung Cysts = LIP ‘Lungs Cysts + Ground Glass + Pneumothorax = PCP ‘Hypervascular Lymph Nodes = Castleman or Kaposi

Answer 50

Bacterial, TB

Answer 51

PCP, Atypical Mycobacterial

Answer 52

CMV, Disseminated Fungal, Mycobacterial

Answer 53

Bacterial Infection (Strep Pneumonia) is the most common. DDx should include TB if low CD4. If it’s a chronic opacity think Lymphoma or Kaposi.

Answer 54

Bacterial, or Fungal

Answer 55

PCP (if that’s not a choice it could be | CMV if CD4 is < 100).

Answer 56

(a) Primary, (b) Primary Progressive, (c) Latent or (d) Post Primary / Reactivation.

Answer 57

Essentially you inhaled the bug, and it causes necrosis. Your body attacks and forms a granuloma (Ghon Focus). You can end up with nodal expansion (which is bulky in kids, and less common in adults), this can calcify and you get a “Ranke Complex. ” The bulky nodes can actually cause compression leading to atelectasis (which is often lobar). If the node ruptures you can end up with either (a) endobronchial spread or (b) hematogenous spread - depending on if the rupture is into the bronchus or a vessel. This hematogenous spread manifests as a miliary pattern. Cavitation in the primary setting is NOT common. Effusions can be seen but are more common in adults (uncommon in kids).

Answer 58

This term refers to local progression of parenchymal disease with the development of cavitation (at the initial site of infection / or hematogenous spread). This primary progression is uncommon - with the main risk factor being HIV. Other risk factors are all the things that make you immunosuppressed - transplant patients, people on steroids. The ones you might not think about is jejunoileal bypass, subtotal gastrectomy, and silicosis. This form is similar in course to post primary disease.

Answer 59

This is a positive PPD, with a negative CXR, and no symptoms. If you got the TB vaccine, you are considered latent by the US health care system/industry if your PPD converts. This scenario buys you 9 months of INH and maybe some nice drug induced hepatitis.

Answer 60

This happens about 5% of the time, and describes an endogenous reactivation of a latent infection. The classic location is in the apical and posterior upper lobe and superior lower lobe (more oxygen, less lymphatics). In primary infection you tend to have healing. In post primary infection you tend to have progression. The development of a cavity is the thing to look for when you want to call this. Arteries near the cavity can get all pseudoaneursym’d up - “Rasmussen Aneurysm” they call it - in the setting of a TB cavity.

Answer 61

``` The story will be a patient with TB and AIDS started on highly active anti-retroviral therapy (HAART) and now doing worse. The therapy is steroids. ```

Answer 62

This can occur at any time after initial infection. In primary TB development of a pleural effusion can be seen around 3-6 months after infection - hypersensitivity response. This pleural fluid is usually culture negative (usually in this case is like 60%). You have to actually biopsy the pleura to increase your diagnostic yield. You don’t see pleural effusions as much with post primary disease, but when you do, the fluid is usually culture positive.

Answer 63

This is a positive PPD, with a negative CXR, and no symptoms. If you got the TB vaccine, you are considered latent by the US health care system/industry if your PPD converts. This scenario buys you 9 months of INH and maybe some nice drug induced hepatitis.

Answer 64

High Yield Factoids Regarding TB: * Primary = No Cavity, Post Primary / Primary Progressive = Cavity * Ghon Lesion = Calcified TB Granuloma ; sequela of primary TB * Ranke Complex = Calcified TB Granuloma + Calcified Hilar Node ; Healed primary TB * Bulky Hilar and Paratracheal Adenopathy = Kids * Location for Reactivation TB = Posterior / Apical upper lobes, Superior Lower Lobes * Miliary Spread when? - Hematogenous dissemination (usually in the setting of reactivation), but can be in primary progressive TB as well * Reactive TB Pattern (Cavitation) seen in HIV patient when the CD4 is > 200 * Primary Progressive Pattern (Adenopathy, Consolidation, Miliary Spread) in HIV is CD4 < 200 * TB does NOT usually cause a lobar pattern in HIV

Answer 65

(“Classic”) - This one is usually caused by MAC. It favors an old white man with COPD (or other chronic lung disease), and it looks like reactivation TB. So you have an upper lobe cavitary lesion with adjacent nodules (suggesting endobronchial spread).

Answer 66

(“Non-Classic”) - This is the so-called “Lady Windermere” disease (everyone knows it’s just not lady-like to cough). They often do not cough, and are asymptomatic. This favors an old white lady. You see tree-in-bud opacities and cylindric bronchiectasis in the right middle lobe and lingula.

Answer 67

You see this with low CD4s (< 100). The idea is that it’s a GI infection disseminated in the blood. You get a big spleen and liver. It frequently is mixed with other pulmonary infections (PCP, e tc ...) given the low CD4 - so the lungs can look like anything. Mediastinal lymphadenopathy is the most common manifestation.

Answer 68

This is the so-called “hot-tub lung.” Where you get aerosolized bugs (which exist in natural sea water and in fresh water). The lungs look like ill-defined, ground glass centrilobular nodules.

Answer 69

O ld W h ite M a le Sm o k e r L o o k s lik e re a c tiv a tio n TB

Answer 70

O ld L ady M id d le Lobe an d L in g u la , b ro n c h ie c ta s is a n d tre e in bud.

Answer 71

Low CD 4 (< 100) M e d ia s tin a l L ym p h a d en o p a th y

Answer 72

H isto ry o f h o t tub use G ro u n d g la ss c e n trilo b u la r n o d u le s

Answer 73

H isto ry o f h o t tub use G ro u n d g la ss c e n trilo b u la r n o d u le s

Answer 74

(1) Normal Immune, (2) Suppressed Immune, or (3) Hyper-Immune.

Answer 75

Aspergillus makes a fungus ball “Aspergilloma” in a pre-existing cavity. The fungus didn't make the cavity - it found the cavity. It is squatting in an abandoned cavity - Fungus balls can occur normal people who have a cavity from trauma, or prior infection ec t... like a hobo.

Answer 76

You could be shown a fungus ball, and they want you to call it invasive. Don’t fall for that. This is not invasive.

Answer 77

Aspergillus is NOT getting held in check by a normal immune system, invasive Aspergillus” they call it. You are gonna see this in your AIDS, or Transplant Patients.

Answer 78

(1) Halo Sign - consolidative nodule/mass with a ground glass halo. The halo o f ground glass is actually the invasive component.

Answer 79

``` a thin crescent o f air within the consolidative mass. This actually represents healing, as the necrotic lung separates from the parenchyma. The timing is usually about 2-3 weeks after treatment. Lastly, they could show you some peripheral wedge shaped infarcts in the setting o f some halo signs. ```

Answer 80

``` Aspergillus behaves differently in the setting o f a hyper-acute immune system. Allergic Broncho- Eulmonary Aspergillosis (A BPA I they call it. ```

Answer 81

``` This is “Always” seen in patients with long standing Asthma (sometimes CF). You classically have upper lobe central saccular bronchiectasis with mucoid impaction (finger-in-glove). Central Bronchiectasis + Asthma (or CF) = ABPA ```

Answer 82

``` • Elevated Serum Immunoglobulin E levels OR a positive skin hypersensitive test against the asshole fungus • Elevated Total IgE levels > 1000 ```

Answer 83

■ Normal immune system **That ball will move with positional change

Answer 84

• Air Crescent Sign | ~ Dude has AIDS

Answer 85

- Finger in Glove; think asthma

Answer 86

h is can be seen in two classic scenarios: (1) Reactivation o f the latent virus after prolonged immunosuppression (post bone marrow transplant), and (2) Infusing o f CMV positive marrow or in other blood products. The timing for bone marrow patients is “early” between 30-90 days. The radiographic appearance is multiple nodules, ground glass or consolidative.

Answer 87

Multifocal ground glass opacities with small nodular opacities ``` Pneumonia can be before or after the skin lesions. Complications higher in pregnant and immunocompromised ```

Answer 88

Coalescent lower lobe opacity. Pleural effusion is rare.

Answer 89

Lower lobe predominant | ground glass opacities

Answer 90

Multiple peripheral nodular opacities. They form small round calcific lung nodules in the healed version. ``` Most commonly causes Chickenpox in kids. The pneumonia more commonly occurs in immunocompromised adults (with AIDS or lymphoma). ```

Answer 91

Uncommonly affects the lung. Can cause lymph node enlargement Most common radiographic abnormality is a big spleen

Answer 92

* It’s lower lobe predominant (more blood flow) * You get peripheral nodular densities and wedge shaped densities (can infarct). * They can cavitate, and likely will be cavitated if they show you a CT image. * The feeding vessel sign - nodule with a big vessel going into it can be shown (also seen with hematogenous mets). * Empyema and pneumothorax are both known complications.

Answer 93

This is an eponym referring to jugular vein thrombosis with septic emboli classically seen after an oropharyngeal infection or recent ENT surgery.

Answer 94

Q: What is the bacterial agent responsible in the majority o f cases? ACFusobacterium Necrophorum.”

Answer 95

Cancer (usually squamous cell) Auto-immune (Wegeners, Rheumatoid / Caplan Syndrome) Vascular - Septic Emboli / Bland Emboli Infection - TB Trauma - Pneumatoceles Young - “Congenital” - CCAMs, Sequestrations

Answer 96

being over 30 (under 30 is super rare), exposures to bad stuff (arsenic, nickel, uranium, asbestos, chromium, beryllium, radon), having lung fibrosis, COPD (even if you didn’t smoke), and family history. Diffuse fibrosis supposedly gives you 1 Ox the risk. Having said all o f that, smoking is still the big one - supposedly a factor in 90% o f cases.

Answer 97

Recently, the US preventive services task force has approved lung cancer screening with low dose CT for asymptomatic adults aged 55-80 who have a 30 packyear history and currently smoke (or have quit within the past 15 years).

Answer 98

``` Number of packs of cigarettes smoked per day multiplied by number of years the person has smoked = “Pack Years” 30 pack years will qualify you for screening ```

Answer 99

• Shockingly, it is backed up by evidence (which is extremely rare in medical screening programs), and legit improves outcomes (also rare in medicine). • The follow up recommendations are NOT the same as the Fleischner Society Recommendations. So nodules found on a CT done for any reason other than official lung cancer screening will follow Fleischner and not the LUNG RADS recommendations used with the screening program. • Dose on the screening CTs is supposed to be low - recommended below CTDIvoi 3 mGy • “Growth” is considered 1,5mm or more in one year • LUNG RADS scoring is based off the most suspicious nodule. You don’t give multiple ratings for multiple nodules. • Endobronchial “lesions” (mucus) are treated as 4a - and given a 3 month follow up. • A treated remote (> 5 years) lung cancer patient must still meet the normal screening criteria toenrolled in the lung cancer screening program

Answer 100

Scan is a piece of shit and you can’t read, or you need priors Repeat or get priors

Answer 101

Negative, < 1 % chance of cancer. Either no nodules or granulomas. 1 year follow up

Answer 102

Benign < 1 % chance of cancer. Baseline exam - nodules smaller than 6mm. Subsequent exam - no new nodules larger than 4mm. Ground glass nodule smaller than 20mm. 1 year follow up

Answer 103

Probably Benign, 1-2% chance of cancer. Baseline nodule 6-8mm. Subsequent exam new nodule > 4mm. Ground glass > 20mm. 6 month follow up

Answer 104

Suspicious, 5-15% chance of cancer, Baseline 8-15mm. New nodule 6-8mm 3 month follow up vs PET

Answer 105

Suspicious, > 15% chance of cancer, > 15mm at baseline New nodule > 8mm PET vs Tissue Sampling

Answer 106

> 1 5% chance of cancer Worsening of category 3 or 4 nodules (growth or new spiculation) PET vs Tissue Sampling

Answer 107

As discussed on the prior page, nodules discovered incidentally on non-screening scans are treated different for followup. These nodules are the captives of the dreaded Fleischner Society recommendations.

Answer 108

* Fleischner guidelines only apply for patients older than 35 * They do NOT apply to patients with known or suspected cancer * They do NOT apply to patients who are immunocompromised * Measurements are reported as the average diameter (short + long / 2) obtained in the same plane. * Risk stratification for followup (low, intermediate, high) is based on multiple risk factors (smoking, cancer history, family history, age, uranium / random / asbestos exposure and nodules characteristics / size). * Follow up is based off the arbitrary guess of a cancer risk > 1% * Perifissural nodules (discussed later) - do not need a follow up, even if they are > 6mm in size. * Nodule characterization should be performed on thin-slice CT images <1.5 mm. This is done to look for a small solid component hiding behind partial volume effect in a ground glass nodule. * Multiple nodules (> 5) makes malignancy statistically less likely.

Answer 109

no follow up

Answer 110

12 month repeat

Answer 111

no follow up

Answer 112

12 month repeat

Answer 113

6-12 month follow up

Answer 114

6-12 month follow up

Answer 115

3-6 month rollow up

Answer 116

3-6 month follow up

Answer 117

PET or biopsy

Answer 118

3-6 month followup

Answer 119

follow up recommendations are variable. Most people will not follow up nodules smaller than 6mm. If they are greater than 6mm people will either do 6 month or 1 year (depends on who you ask). Follow up is persistent for 5 years, because of the slow growth of the potential adenocarcinoma in situ.

Answer 120

maller than 6mm still gets ignored. However, the ones larger than 6mm get a 3 month follow up - with interval widening but persisting up to 5 years. Regular solid nodules typically get set free after 2 years of stability.

Answer 121

A SPN is defined as a round or oval lesion measuring less than 3cm in diameter (more than 3cm = mass). Technically to be “solitary” it needs to be surrounded by lung parenchyma, with no associated adenopathy, or pleural effusion. So, you can have numerous “solitary” nodules in the lungs.

Answer 122

``` solid/diffuse laminated central popcorn ?eccentric (suspicious) ```

Answer 123

Presence of Fat Rapid Doubling Time (less than 1 month) Slow Doubling Time (longer than 16 months) *Stable at two years = B9

Answer 124

Spiculated Margins “Corona Radiata Sign” Air Bronchogram through the nodules (usually Adenocarcinoma in situ) Partially solid lesions with ground glass component

Answer 125

A part solid lesion with a ground glass component is the most suspicious morphology you can have. Non-solids (only ground glass) is intermediate. Totally solid is actually the least likely morphology to be cancer.

Answer 126

You can use PET for SPNs larger than 1 cm. Lung Cancer is supposed to be HOT (SUV > 2.5). Having said that, infectious and granulomatous nodules can also be hot.

Answer 127

HOT = Cancer, COLD = Not Cancer

Answer 128

HOT = Infection , COLD = Cancer

Answer 129

• Lung Cancer is 1.5 x more likely in the Right Lung • 70% of Lung Cancer is in the Upper Lobes • Exception to the rule is pulmonary fibrosis - where peripheral basilar cancer is more common. • SPN in the setting of head and neck CA is more likely to be a primary bronchogenic carcinoma rather than a metastasis (they have similar risk factors). • Lung Cancer is very rare under 40 (unless the patient has AIDS) • Air Bronchograms are 5x more common in malignant SPN • Air Bronchograms are found in 50% of BACs • Just because a nodule gets smaller doesn’t mean it is benign. Especially if the nodule increases

Answer 130

Most people will call nodule “growth” at 1.5 mm per year. Anything smaller than that can easily be attributed to technical factors. Anyone who describes 0.1mm differences in stuff sucks at Radiology. This growth, in particular the concept of “doubling time ” makes up the basis of differentiated benign vs malignant. With out this concept you would be forced into follow nodules forever. The trivia worth knowing is that lung cancers doubling times range from 20 days to 400 days. Any nodule that doubles in size in less than 20 days is almost certainly benign (statistically infectious or inflammatory). The same is true with doubling times greater than 400 days. The notable difference is the ground glass or part solid nodule vs the solid nodule. Ground glass and part solid nodules are more characteristic of the adenocarcinoma in situ (formerly BAC) and they tend to grow slower. This is why the follow up term for GGN and part solid nodules in 5 years, vs 2 years for a pure solid nodule.

Answer 131

Typical morphological features would include well circumscribed, smoothly marginated, triangular, oval, or polygonal nodules which either contact the fissure or pleural surface directly. ``` They technically don’t have to contact a pleural surface, as long as they are within 15 mm (some people say 20mm). ``` ``` Spiculated or Round nodules are not typical for PFNs. These two guys should be treated like “regular” nodules. ```

Answer 132

PFNs are probably lymph nodes • They are almost certainly benign and treated as such by the Fleischner society • LUNG-RADS v l.l says mean diameter less than 10mm = category 2 (benign), larger than 10mm means you treat than like any other nodule • Interval growth does NOT mean they are full of cancer - lymph nodes normally fluctuate in size. • Size greater than 6mm still doesn’t justify follow up per Fleischner.

Answer 133

Strong Association with Smoking Cavitation is Classic Does NOT express the tissue maker thyroid transcription factor 1 “TTF-1” (other subtypes can).

Answer 134

``` Paraneoplastic Syndromes can be associated with ectopic Parathyroid Hormone ```

Answer 135

Peripheral

Answer 136

Least common subtype (15%) Usually large (> 4cm) Prognosis Suck — this is the subtype of Cancer that killed comedy legend Andy Kaufman in his 30s.

Answer 137

peripheral

Answer 138

Most Common subtype (35%) Favors the upper lobe Most Common subtype to present as a solitary pulmonary nodule Most Common subtype in a non smoker (although also common in smokers) Known association with pulmonary fibrosis

Answer 139

Strong Association with Smoking (nearly every case is a smoker)

Answer 140

May only present with central lymphadenopathy Most Common primary lung CA to cause SVC obstruction and paraneoplastic syndromes Terrible Horrible Incredibly Shitty Prognosis (metastasizes early) Paraneoplastic Syndromes can be associated with SIADH and ACTH

Answer 141

``` Lambert Eaton. They get proximal weakness from abnormal release of acetylcholine at the neuromuscular junction. The clinical presentation often comes before the cancer diagnosis. ```

Answer 142

Large and Adeno favor peripheral locations

Answer 143

Location o f the tumor can sometimes be predicted based on symptoms. Central tumors = hemoptysis. Peripheral tumors = pleuritic chest pain.

Answer 144

Atypical Adenomatous Hyperplasia of Lung (AAH): The smaller (< 5mm) and more mild pre invasive subtype. Usually a pure ground glass nodule.

Answer 145

Adenocarcinoma in situ (ACIS): Typically larger than AAH but < 3 cm. Although features overlap with AAH, they tend to be more part-solid (rather than pure ground glass)

Answer 146

These are also < 3 cm. The distinction is that there is < 5 mm of stromal invasion ( > 5 mm will be called a lepidic predominant adenocarcinoma).

Answer 147

This is what most people used to call BAC | bronchoalveolar carcinoma

Answer 148

The larger the solid component of the “part solid” nodule gets the more likely it is to be malignant. Partially solid nodules are more likely to be cancer than ground glass nodules.

Answer 149

Some people make a big deal about only using the word “pancoast” when the tumor causes the associated syndrome (shoulder pain, C8-T2 radiculopathy, and Homer Syndrome). In my experience most everyone just calls apical tumors “pancoast” with no regard to symptoms. Having said that, I would remember “shoulder pain” as a possible hint in the question header. These things are typically non-small cell cancers.

Answer 150

MRI is the tool of choice (you need to look at that brachial plexus).

Answer 151

invasion of the vertebral body (> 50%), invasion of the spinal canal, involvement in the upper brachial plexus (C8 or higher), diaphragm paralysis (infers phrenic nerve C3-5 involvement), distal mets.

Answer 152

Lung cancer staging used to be different for small cell vs non-small cell (NSCLC). In 2013 the 7thedition of the TNM made them the same. Below is a chart describing the staging based on tumor size. For a solid lesion, the size is defined as maximum diameter in any of the three orthogonal planes - measured on lung window. If the lesion is subsolid, then you define the T classification by the diameter of the solid component only (NOT the ground glass part).

Answer 153

Tumor is < 3cm

Answer 154

Tumor is 3-5 cm Irregardless of size the tumor • Invades the visceral pleura • Invades the main bronchus • Causes obstruction (atelectasis or pneumonia) that extends to the hilum

Answer 155

Tumor is 5-7 cm Irregardless of size the tumor • Invades the chest wall • Invades the pericardium • Invades the phrenic nerve (diaphragm paralysis) • Has one or more satellite nodule in the same lung lobe Pancoast (Superior Sulcus) Tumor that is limited to involvement o f Tl and T2 nerve roots

Answer 156

Tumor > 7cm Irregardless of size the tumor • Invades the mediastinal fat or great vessels • Invades the diaphragm • Involves the carina • Has one or more satellite nodule in another lobe in the same long Pancoast (Superior Sulcus) Tumor that involves level C8 or higher

Answer 157

The handling of multiple lung lesion is complicated. Deciding if lesions are going to be treated as synchronous primaries or a single lung cancer with metastatic disease often requires a discussion at tumor board (after imaging, and path results). If the lesions are decided to be separate primaries each cancer will be staged separately within the TNM system and given an overall stage. If the lesions arc decided to be metastatic their distribution will alter the stage.

Answer 158

Two or more primary carcinomas which coexist at the time of diagnosis.

Answer 159

A cancer that develops consequently (some time interval) after the first primary.

Answer 160

Ipsilateral within the lung up to the hilar nodes. Nl is a worse prognosis than NO (no nodes) but the management is not changed.

Answer 161

Ipsilateral mediastinal or subcarinal nodes In many cases NOT Resectable Only those with microscopic disease (negative mediastinoscopy) will benefit from resection

Answer 162

Contralateral mediastinal or contralateral hilum. or scalene or supraclavicular nodes not resectable (probablyl)

Answer 163

First it is important to point out that CT is unreliable for nodal staging. PET-CT is far superior, regardless of the size threshold that is chosen. This is why PET is pretty much always done on lung cancer patients prior to surgical evaluation. For the purpose o f multiple choice (and real life) the most important anatomy boundary to consider is the distinction between level l nodes (which at N3) and level 2 nodes (which are N2). In some cases, this can literally make the difference between resectable disease or not. The border is the lower level of the clavicles / upper border of the manubrium (above this is level I).

Answer 164

* G row th o f the tum o r th ro u g h a fissure * In v asio n o f the P u lm o n a ry V asculature * In v a sio n o f the m a in b ro n ch u s * In v a sio n o f bo th th e u p p e r an d low e r lobe bro n ch i. * N 2 * (if th e tum o r is > 5cm ) o r N3 N o d a l D ise a se — co rre sp o n d in g to a Sti * M u lti-lo b a r Disease * M a lig n an t P leu ral Effusion

Answer 165

N3 o r T 4 d ise a se

Answer 166

3b is surgically unresectable (technically this varies widely by institution and depends on lots o f factors).

Answer 167

This is on the fringe of what should be considered fair game, and I’m certain the decision varies by institution and the size and composition (percentage of brass) of the surgeon’s testicles. In general, if a stage 1A or IB cancer is peripheral and less than 2cm they can consider a wedge resection. The advantage to doing this over a lobectomy is preserving pulmonary reserve. If the tumor is larger than 3cm then lobectomy seems to (in general) be a better option.

Answer 168

This is an uncommon complication of pneumonectomy, that has a characteristic look and therefore easy to test. So normally after a pneumonectomy the space will fill with fluid. If you see it filling with air than this is the dead give away. If you are a weirdo, you could confirm the diagnosis with a xenon nuclear medicine ventilation study, which will show xenon in the pneumonectomy space. The major risk factor is ischemia to the bronchi (disrupted blood supply from aggressive lymph node dissection, or using a long bronchial stump).

Answer 169

become more fluid filled

Answer 170

become more air filled

Answer 171

The appearance of radiation pneumonitis is variable and based on the volume of lung involved, how much/long radiation was given, and if chemotherapy was administered as well.

Answer 172

Ribs within the treatment field are | susceptible to degradation and fracture.

Answer 173

It is normal to see bubbles in the | lesion immediately after treatment.

Answer 174

Homogenous or patchy ground glass opacities.

Answer 175

``` Dense consolidation, traction bronchiectasis, and volume loss. ```

Answer 176

Recurrence rates are relatively high (especially in the first 2 years). From a practical stand point, I always focus my attention towards the periphery of the radiation bed, regional nodes, and/or the bronchial stump. A useful concept is to focus on morphology - radiation scarring is usually not round. If you see something with a round morphology - especially if it is growing over time, that is highly suspicious.

Answer 177

* Enhancing solid tissue along the resection line (or bronchial stump) which is enlarging over time. * New enlarged mediastinal nodes with a short axis greater than 1 cm * New pleural effusion (that persists on follow ups)

Answer 178

This is not a cancer, but to the uninitiated can look scary. It is usually described as is an Aunt Minnie because it will have macroscopic fat and “■popcorn” calcifications. It is the most common benign lung mass. It’s usually incidental, but can cause symptoms if it’s endobronchial (rare - like 2%). Technically the fat is only seen in 60%, but for sure if the exam shows it, it will have fat. These can be hot on PET, they are still benign.

Answer 179

popcorn calcs | fat density

Answer 180

Metastatic disease to the lungs can be thought of in 3 categories; direct invasion, hematogenous, lymphangitic:

Answer 181

This is seen with cancer of the mediastinum, pleura, or chest wall. The most common situation is an esophageal carcinoma, lymphoma, or malignant germ cell tumor. More rarely you are going to have mets to the pleura then invading the lung. Even more rarely you can have malignant mesothelioma, which can invade the lung. It should be obvious.

Answer 182

The most common manifestation of hematogenous mets to the lung is the pulmonary nodule (usually multiple, in a random distribution, and favoring the lower lobes which have greater blood volume). The nodules tend to be smoother than the primary neoplasm. The main culprits are breast, kidney, thyroid, colon, and head & neck squamous cells. Obviously the squamous mets can cavitate. “Cannonball Mets” are classically from renal cell or choriocarcinoma (testicle).

Answer 183

The most common cause of unilateral LC is actually bronchogenic carcinoma lung cancer invading the lymphatics. The most common extrathoracic culprits are breast, stomach, pancreas, and prostate. The finding is nodular thickening of the interlobular septa and subpleural interstitium. Unlike interstitial fibrosis, this thickening classically does NOT distort the pulmonary lobule.

Answer 184

``` A prominent pulmonary vessel heading into a nodule. This supposedly means it’s from a hematogenous origin. It’s nonspecific - but if you see it the answer is (1) mets , or (2) septic emboli. ```

Answer 185

’ Most common lung tumor in AIDS (requires CD4 < 200) ‘Most common hepatic neoplasm in AIDS ‘Buzzword = Flame Shaped Opacities ‘Slow Growth, with asymptomatic patients (despite lungs looking terrible) ‘Thallium Positive, Gallium Negative

Answer 186

This is the most common lung tumor is AIDS patients (Lymphoma is number two). The tracheobronchial mucosa and perihilar lung are favored. The buzzword is “flame shaped.” A bloody pleural effusion is common (50%).

Answer 187

There are basically 4 flavors of pulmonary lymphoma; primary, secondary, AIDS related, or PTLD. Radiographic patterns are variable and can be lymphangitic spread (uncommon), parahilar airspace opacities, and/or mediastinal adenopathy.

Answer 188

``` This is rare, and usually non- Hodgkin in subtype. You define it as the lack of extrathoracic involvement for 3 months. Almost always (80%) we are talking about a low grade MALToma. ```

Answer 189

``` Here we are talking about pulmonary involvement of a systemic lymphoma. This is much much much more common than primary lung lymphoma. The thing to see is that NHL is much more common, but if you have HL it is more likely to involve the lungs. With HL you gets nodes and parenchyma, in NHL you might just get parenchyma. ```

Answer 190

This is seen after solid organ or stem cell transplant. This usually occurs within a year of transplant (late presentations > 1 year have a more aggressive course). This is a B-Cell lymphoma, with a relationship with EB Virus. You can have both nodal and extra nodal disease. The typical look is well-defined pulmonary nodules / mass, patchy airspace consolidation, halo sign, and interlobular septal thickening.

Answer 191

This is the second most common lung tumor in AIDS patients (Kaposi’s is first). Almost exclusively a high grade NHL. There is a relationship with EBV. It is seen in patients with a CD4 < 100. The presentation is still variable with multiple peripheral nodules ranging from 1 cm-5 cm being considered the most common manifestation. Extranodal locations (CNS, bone marrow, lung, liver, bowel) is common. AIDS patient with lung nodules, pleural effusion, and lymphadenopathy = Lymphoma.

Answer 192

80-90% of lymphoma cases 45% have intrathoracic disease at presentation 25% have pulmonary parenchymal disease Pulmonary involvement frequently occurs in the absence of mediastinal disease

Answer 193

10-20% of lymphoma cases 85% have intrathoracic disease at presentation 40% have pulmonary parenchymal disease Lung involvement almost always associated with intrathoracic lymph node enlargement

Answer 194

Things with afunctional Na/K/ATP pump tend to be alive, Hence anything htat is alive will be positive.

Answer 195

Iron is an inflammatory marker (acute phase reactant) hence things that are “smoldering” tend to be gallium negative, and things that are inflamed - infection, active sarcoid, most cancers - tend to be Gallium hot.

Answer 196

HOT on Gallium.” Where things can get sneaky is the subtype. Hodgkin is nearly always Gallium Avid. Certain Non-Hodgkin subtypes can be Gallium cold. As such (and because it’s not 1970) PET is usually used for staging and not Gallium.

Answer 197

Thallium 201 Positive Gallium67 Negative

Answer 198

Thallium 201 Positive Gallium67 Positive

Answer 199

Unilateral absence of a pectoral | muscle (white arrow). Can cause a unilateral hyper-lucent chest. Can have limb issues (small weird arms / hands).

Answer 200

This is a congenital obliteration of a short segment of a lobar, segmental, or subsegmental bronchus near its origin (most commonly involves the apical-posterior segment of the left upper lobe). Like many atresias a vascular insult in utero is the probable etiology.

Answer 201

On CT, you will see a hyper lucent region with decreased vascularity. It is somewhat counterintuitive that loss of the bronchus would make the lung trap air (hyper lucent). The explanation is collateral flow through the varies pores of Kohn and canals of Lambert. You will often see a large “nodule” (sometimes with a branching or “finger in the glove” morphology) nearby in the hilum — which represents mucoid impaction in the blind ended bronchus.

Answer 202

The primary differential would be an endobronchial tumor. If you can measure (or they show you) a low density focus (< 25 HU) in the mucus plug then you are safe to call it mucoid impaction. If you can’t make the distinction the next step should be bronchoscopy to be certain.

Answer 203

Bronchial atresia is usually asymptomatic, although they can presentation

Answer 204

Hyperinflated lobe is the most common radiographic appearance (sometimes with a hilar nodule visible). CT will show a blind ending bronchus, filled with mucus and the distal lung Hvper-lnflated (lucent).

Answer 205

They can occur sporadically. For the putpose of multiple choice when you see them think about HHT (Hereditary Hemorrhagic Telangiectasia / Osier Weber Rendu). Pulmonary AVMs are most commonly found in the lower lobes (more blood flow), and can be a source of right to left shunt (worry about stroke and brain abscess). The rule of treating once the afferent vessel is 3 mm is based on some tiny little abstract and not powered at all. Having said that, it’s quoted all the time, and a frequent source of trivia that is easily tested.

Answer 206

This is the most common congenital venous anomaly of the chest. It usually only matters when the medicine guys drop a line in it on the floor and it causes a confusing post CXR (line is in a left paramedian location). It usually drains into the coronary sinus. In a minority of cases (like 5%) it will drain into the left atrium, and cause right to left shunt physiology (very mild though). This is typically shown on an axial CT at the level of the AP window, or with a pacemaker (or line) going into the right heart from the left.

Answer 207

This is the classic unilateral lucent lung. It typically occurs after a viral lung infection in childhood resulting in post infectious obliterative bronchiolitis (from constrictive bronchiolitis). The size o f the affected lobe is smaller than a normal lobe (it’s not hyper-expanded).

Answer 208

Defined by fusion of the posterior basilar segments of the lower lobes behind the heart. The most likely testable points are: (1) What is it ? and (2) What is the association ? Scimitar syndrome

Answer 209

``` lch lam birt hogg dube LIP PCP ```

Answer 210

``` This is a total zebra. This cystic lung disease has thin walled “oval” shaped cysts. There is an association with renal findings (bilateral oncocytomas, and chromophobe RCCs). They also have a bunch of gross skin stuff. ```

Answer 211

This cystic lung disease can occur in child bearing aged women or in association with Tuberous Sclerosis (a trick is to show the kidneys with multiple AMLs first). The cysts are thin walled with a uniform distribution. There is an association with chylothorax (which is HIGH YIELD Trivia). The pathophysiology is that it is estrogen dependent (why it strongly favors women). This is usually progressive despite attempts at hormonal therapy (tamoxifen).

Answer 212

``` ould be the step 1 “clinical triad” — even though < 50% o f TS patients have the complete triad. 1 - Seizures, 2- Mental Retardation, 3 - Adenoma Sebaceum SSS: Seizures, Sebaceum, & Stupid ```

Answer 213

This cystic lung disease classically effects smokers, who are young (20s-30s). The disease starts out with centrilobular nodules with an upper lobe predominance. These nodules eventually cavitate into cysts which are thin walled to start, and then some become more thick walled. Late in the disease you are primarily seeing cysts. The buzzword is bizarre shaped, which occurs when 2 or more cysts merge together. In about half the cases this spontaneously resolves (especially if you stop smoking). Another piece of trivia is that LCH spares the costophrenic angles.

Answer 214

(1) LCH and (2) Hypersensitivity Pneumonitis

Answer 215

Cysts and Nodules Cysts (no nodules) Smoker Women, Pts with Tuberous Sclerosis Upper and Mid Lungs Diffuse Thicker Cysts (Bizarre) Thin Round Cysts

Answer 216

Bizarre Shape, ThickWall Round, thin wall oval, thin wall

Answer 217

This is a benign lymphoproliferative disorder, with infiltration of the lungs. It has an association with autoimmune diseases (SLE, RA, Sjogrens). The big one to know is Sjogrens which is concomitant in 25% of LIP cases. The other one to know is HIV - which is the LIP in a younger patient (children, - LIP in HIV positive adults is rare). There is also an association with Castlemans. The appearance of LIP varies depending on the underlying cause. The cystic lung disease is usually thin walled, “deep within the lung parenchyma,” and seen predominantly with Sjogrens. The dominant feature described as ground glass or nodules is seen more in the other causes and is far beyond the scope o f the exam.

Answer 218

you say sjogrrens and HIV

Answer 219

you say HIV

Answer 220

This is the most common opportunistic infection in AIDS. The typical buzzword is ground glass appearance, predominantly in the hilar and mid lung zones. Pneumatoceles are present in 30% of cases. In patients receiving aerosolized prophylaxis, a cystic form is more common, which may have bilateral thin walled upper lung predominant cysts. Gallium 67 scan will show diffuse uptake (Thallium will be negative).

Answer 221

The textbook definition is "permanent enlargement o f the airspaces distal to the terminal bronchioles accompanied by destruction o f the alveolar wall without clear fibrosis.” What you need to know are (1) the CXR findings and (2) the different types.

Answer 222

Until it’s really really bad, CXR doesn’t have direct signs, but instead has indirect signs. Flattening of the hemidiaphrams is regarded as the most reliable sign. The AP diameter increases. The retrosternal clear space becomes larger. There is a paucity of, or pruning o f the blood vessels.

Answer 223

By far the most common type. Common in asymptomatic elderly patients. It has an apical to basal gradient - favoring the upper zones of each lobe. It appears as focal lucencies, located centrally within the secondary pulmonary lobule, often with a central dot representing the central bronchovascular bundle. This central dot sign is a buzzword. This is the type of emphysema dominant in smokers.

Answer 224

In contradistinction to centrilobular this one favors the lower lobes. It also has a more uniform distribution across parts o f the secondary pulmonary lobule. The association is with alpha 1 antitrypsin. A piece o f trivia is the “'Ritalin Lung” from IV Ritalin use can also cause a pan-lobular appearance (“Ritalin keeps you from ‘trypsn’ out”). I f they show this it will be in the coronal view on CT to demonstrate the lower lobe predominance. Patient’s will present in their 60s and 70s (unless they smoke - then they present in their 30s). Smoking accelerates the process.

Answer 225

This one is found adjacent to the pleura and septal lines with a peripheral distribution within the secondary pulmonary lobule. The affected lung is almost always sub-pleural, and demonstrates small focal lucencies up to 10 mm in size. This looks like honeycombing but is less than 3 bubbles thick.

Answer 226

• Saber Sheath Trachea - Diffuse coronal narrowing o f the trachea, sparing the extrathroacic portion. This is said to be pathognomonic for COPD. • If the Main PA is larger than the Aorta COPD patients have a worse outcome (pulmonary HTN can be caused by emphysema). • Surgery to remove bad lung “volume reduction” is sometimes done

Answer 227

This is an idiopathic cause of giant bullous emphysema, resulting from avascular necrosis of the lung parenchyma and hyperinflation. It favors the bilateral upper lobes, and is defined as bullous disease occupying at least one-third of a hemithorax. The most common demographic is a young man. About 20% of these guys have alpha-1 antitrypsin deficiency. Tension pneumothorax is a described complication.

Answer 228

``` • Smoking (tobacco) • Alpha-1 antitrypsin deficiency • Male • Smoking Marijuana is also a described risk factor (although it is probably bullshit propaganda from the pharmaceutical industry) ```

Answer 229

There is no obstructive process here. Instead you have hyper-expansion of one lung to compensate for the absence o f the other one.

Answer 230

When I say honeycombing you should say UIP. However, this is seen with a variety of causes o f end stage fibrotic lung processes. The cysts are tightly clustered (2-3 rows thick) and subpleural. The walls are often thick.

Answer 231

As a general rule, these are inhaled so they tend to be upper lobe predominant. You can have centrilobular nodules (which makes sense for inhalation), or often perilymphatic nodules - which makes a little less sense, but is critical to remember * especially with silicosis and CWP.

Answer 232

``` asbestosis silicosis silicotuberculosis coal workers lung talcosis silo fillers dz berylliosis ```

Answer 233

The term “Asbestosis” refers to the changes o f pulmonary fibrosis - NOT actual exposure to the disease. The look is very similar to UIP, with the presence of parietal pleural thickening being the “most important feature” to distinguish between IPF and Asbestosis. Obviously, the history o f working in a ship yard or finding asbestos bodies in a bronchoalveolar lavage is helpful.

Answer 234

“Asbestosis” = the lung fibrosis associated with exposure, NOT actual exposure • Interstitial pattern looks like UIP + parietal pleural thickening * There is a 20 year latency between initial exposure and development of lung cancer or pleural mesothelioma * There is an association with extrapulmonary cancer including: Peritoneal mesothelioma, GI cancer, Renal Cancer, Laryngeal Cancer, and Leukemia # Benign pleural effusions are the “earliest pleural-based phenomenon” associated with exposure - still with a lag time of around 5 years

Answer 235

Pleural effusion is the earliest and most common. Pleural plaques may develop around 20-30 years, with calcifications occurring around 40 years. These plaques tend to spare the apices and Costophrcnic angles. Round atelectasis - which is associated with pleural findings is sometimes called the “asbestos pseudotumor. "

Answer 236

The most common cancer of the pleura. About 80% of them have had asbestos exposure, and development is NOT dose-dependent. The lag time is around 30-40 years from exposure.

Answer 237

• Circumferential Pleural Thickening extending to the medial surface of the pleura (near the heart) • Pleural Thickness > 1 cm • Extension into the fissure = highly suggestive

Answer 238

Mesothelioma believes in nothing Lebowski with a known tendency for direct invasion. MRI with Contrast = For evaluating local chest wall, diaphragm and pericardial invasion PET CT = Good for mets. Useful for evaluating treatment response.

Answer 239

pleural rind

Answer 240

Common | **think old rib fx

Answer 241

NOT Common | **think mesothelioma.

Answer 242

``` This is seen in miners, and quarry workers. You can have simple silicosis, which is going to be multiple nodular opacities favoring the upper lobes, with egg shell calcifications o f the hilar nodes. You also get perilymphatic nodules. The complicated type is called progressive massive fibrosis (PMF). This is the formation of large masses in the upper lobes with radiating strands. You can see this with both silicosis and coal workers pneumoconiosis (something similar also can happen with Talcosis). These masses can sometimes cavitate - but you should always raise the suspicion o f TB when you see this (especially in the setting o f silicosis). ```

Answer 243

lare paical masses with radiating strands silicosis

Answer 244

Silicosis actually raises your risk of TB by about 3 fold. If you see cavitation in the setting o f silicosis you have to think about TB.

Answer 245

``` Cancer = T2 Bright PMF = T2 Dark ```

Answer 246

This is the result o f exposure to “washed coal.” Just like silicosis there are simple and complicated forms. There is also an increased risk of TB (just like silicosis). The simple form was multiple nodular opacities, with calcifications showing a central nodular dot. The small nodule pattern tends to have a perilymphatic distribution. The complicated form gives you a progressive massive fibrosis that is similar to that seen in silicosis.

Answer 247

Metal used in aircraft and space industries Generalized granulomatous disease with hilar adenopathy and upper lobe predominant reticular opacities.

Answer 248

Nitrogen Dioxide Pulmonary Edema Pattern. Recovery is typically within 5 weeks.

Answer 249

Filler in tablets, sometimes injected (along with drugs) in IV drug users. Hyperdense micronodules, with conglomerate masses (similar to PMF). Ground glass opacities

Answer 250

Density that obscures underlying vessels

Answer 251

Density that does NOT obscure underlying vessels

Answer 252

The basic unit o f pulmonary structure and function. It is the smallest part of the lung that is surrounded by connective tissue. In the middle runs a terminal bronchial with an accompanying artery. Around the periphery runs the vein and lymphatics

Answer 253

centrilobular

Answer 254

yes then perilymphatic no then random

Answer 255

* S a rco id (9 0% ), * L ym p h an g itic S p re ad o f CA * S ilico sis

Answer 256

* M ilia ry TB * M e ts * Funga l

Answer 257

* In fec tio n * R B -ILD * H y p e rs en s itiv ity P n eum o n itis ( i f g rou n d g la ss )

Answer 258

Reticular abnormality, that outlines the lobules’ characteristic shape and size (about 2 cm). It’s usually from pulmonary edema (usually symmetric and smooth), or lymphangitic spread of neoplasm (often asymmetric and nodular). Kerley B Lines are the plain film equivalent.

Answer 259

Cystic areas of lung destruction in a subpleural location. This is a hallmark o f U1R Paraseptal emphysema is a mimic, but the distinction is made by how many rows o f bubbles.

Answer 260

paraseptal emphysema

Answer 261

honeycombing

Answer 262

These are NOT diseases, but instead lung reactions to lung injury. They occur in a variety o f patterns and variable degrees o f inflammation and fibrosis. The causes include: idiopathic, collage vascular disease, medications, and inhalation. For practical purposes the answer is either (a) UIP or (b) Not U1P. Not U1P will get better with steroids. UIP will not. UIP has a dismal prognosis (similar to lung cancer). Not UIP often does ok. The exam will likely not make it this simple, and will instead focus on buzzwords, patterns, and associations (which I will now discuss).

Answer 263

The most common ILD. When the cause is idiopathic it is called 1PF. On CXR the lung volume is reduced (duh, it’s fibrosis). Reticular pattern in the posterior costophrenic angle is supposedly the first finding on CXR.

Answer 264

Apical to basal gradient (it’s worse in the lower lobes) Traction bronchiectasis, and honeycombing Honeycombing is found 70% of the time, and people expect you to knee jerk UIP when that term is uttered Histologic Buzzword = Heterogeneous. “Histology was heterogeneous” = UIP

Answer 265

It’s important to know that basically any end stage lung disease (be it from sarcoid, RA, Scleroderma, or other collagen vascular disease) has a similar look once the disease has ruined the lungs. *Technically honeycombing is uncommon in end stage sarcoid - but the rest o f the lung looks jacked up. The prognosis is terrible (similar to lung cancer).

Answer 266

Features that favor Chronic HP over UIP: • Air Trapping involving 3 more lobes • Mid-Upper lobe predominant fibrosis

Answer 267

• Honeycombing (must be present) • +/- traction bronchiectasis • Reticular abnormalities • Subpleural basal predominant distribution • Absence o f inconsistent features: upper lobe predominance, ground glass > reticulations, air trapping involving 3 or more lobes Definite UIP Pattern = Don’t Need to Biopsy to Prove Diagnosis

Answer 268

Pulmonary fibrosis is a risk factor for lung cancer | especially if these patients are dumb enough to also smoke

Answer 269

Cancer in the Fibrotic Lung Trivia: • Favors the lower lobes • Favors the interface between the fibrotic cvsts and normal lung • Progressive wall thickening or a developing nodule within a cyst is suspicious for cancer (enlarging pericystic nodules are dodgy as fuck - hide your kids / hide your wife) • NELSON Lung Cancer Screening Trial showed cancers associated with cystic lesions were commonly missed (people thought they were just areas of focal thickening within a bulla). — Then I said “Come on Judge... let him go, h e ’s doing his best. ’’

Answer 270

Less Common than UIP. Even though the name infers that its non-specific, it’s actually is a specific entity. Histologically it is homogenous inflammation or fibrosis (UIP was heterogeneous). It is a common pattern in collagen vascular disease, and drug reactions.

Answer 271

It comes in 2 flavors (cellular or fibrotic): ■ Ground Glass Alone = Cellular ■ Ground Glass + Reticulation = Cellular or Fibrotic ■ Reticulation + Traction Bronchiectasis = Fibrotic NSIP ■ Honeycombing - uncommon and usually minimal in extent

Answer 272

NSIP is the most common Interstitial Lung Disease in Scleroderma

Answer 273

The disease has a lower lobe, posterior, peripheral predominance with sparing of the immediate subpleural lung seen in up to 50% o f cases. This finding of immediate subpleural sparing is said to be highly suggestive. Ground glass is the NSIP equivalent o f honeycombing.

Answer 274

P e rip h e ra l G ro un d Glass with S u b p le u ra l Sparing

Answer 275

Apical to Basal Gradient Heterogeneous Histology Honeycombing Ground Glass Traction Bronchiectasis .

Answer 276

Gradient is less obvious (but still more in lower lobes) Homogenous Histology Ground Glass Micronodules .

Answer 277

I’m going to discuss these two together because some people feel they are a spectrum. For sure they are both smoking related diseases. • RB-ILD - Apical Centrilobular ground glass nodules • DIP - More diffuse GGO, with patchy or subpleural distribution

Answer 278

``` This tends to be more upper lobe predominant (note that DIP tends to be more lower lobe predominant). Localized centrilobular ground glass nodules. The pathology tends to involve the entire cross section of lung. ```

Answer 279

Apical Centrilobular ground glass nodules + Smoking History

Answer 280

Desquamative interstitial pneumonia is thought o f as the end spectrum of RB-ILD, and generally seen in 50 year old heavy smokers. Extras from 1984 comedy classic “Revenge o f the Nerds” seem to enjoy going to radiology conferences to voice their disapproval o f the term “DIP” because the pathology is not desquamation of alveolar epithelium but instead represents a filling of alveolar spaces with macrophages. Could these same weirdos be writing the questions ? The dark side clouds everything. Impossible to see the future is.

Answer 281

peripheral lower lobe predominant ground glass, with small cystic spaces You can see consolidations - but they are usually associated with cryptogenic pneumonia. You can see fibrosis - but it is rare (like 5-10%) - I would not expect that on the exam.

Answer 282

B ila te ra l F airly S ym m e tric B a sila r | P re d om in a n t G ro u n d G lass

Answer 283

``` This is a multi-system disease that creates “non-caseating granulomas.” The classic age is between 20-40. Along those lines, if the header to the question describes an African American female in her 20s-30s the answer is probably sarcoid. The lungs are by far the most common organ affected (90%). ```

Answer 284

Elevated angiotensin-converting enzyme (ACE) | Hypercalcemia

Answer 285

Mediastinal lymph nodes are seen in 60-90% o f patients (classically in a 1-2-3 pattern of bilateral hila and right paratracheal). They have perilymphatic nodules, with an upper lobe predominance. Late changes include, upper lobe fibrosis, and traction bronchiectasis (honeycombing is rare). Aspergillomas are common in the cavities o f patients with end stage sarcoid.

Answer 286

``` Stage 0 = Normal Stage 1 = Hilar / Mediastinal Nodes Only Stage 2 = Nodes + Parenchyma Disease Stage 3 = Parenchymal Disease Stage 4 = End Stage (Fibrosis) ```

Answer 287

* 1-2-3 Sign - bilateral hila and right paratracheal * Lambda Sign - same as 1-2-3, but on Gallium Scan * CT Galaxy Sign - upper lobe masses (conglomerate o f nodules) with satellite nodules

Answer 288

CHF is obviously not an ILD. However, it can sorta look like one on Chest X-Ray so I opted to lump it in here. Congestive heart failure occurs because of cardiac failure, fluid overload, high resistance in the circulation, or some combination o f the three. There are three phases o f CHF, and these lend themselves to testable trivia.

Answer 289

Stage 1 “ Redistribution” Wedge Pressure 13-18 Cephalization o f vessels, Big heart, Big Vascular Pedicle

Answer 290

Stage 2 “ Interstitial Edema” Wedge Pressure 18-25 Kerley Lines, Peribronchial Cuffing, Less distinct contour of Central Vessels

Answer 291

Stage 3 “Alveolar Edema” Wedge Pressure > 2 5 Airspace “fluffy” opacity, Pleural effusion

Answer 292

Swan Ganz Pulmonary Wedge Pressures are an indirect measurement o f left atrial pressure. They can help prove a cardiogenic etiology> to pulmonary edema.

Answer 293

This is less common than left heart failure, which ironically is the most common cause. Left heart failure causes pulmonary venous HTN which causes pulmonary arterial HTN, which causes right heart failure. Some other less common causes o f right heart failure include chronic PE and right-sided valve issues (tricuspid regurg). The imaging features of right heart failure include dilation of the azygos vein, dilation o f the right atrium, dilation of the SVC, ascites, big liver, and contrast reflux into the hepatic veins on CTPA.

Answer 294

Mismatch up to 25% is ok. You can have a compressed lung (by the hyperexpanded emphysematous lung). Imaging is usually atelectasis.

Answer 295

Secondary to HLA and ABO antigens. It’s rapid and often fatal. Imaging shows massive homogenous infiltration

Answer 296

Peaks at day 4 as a non-cardiogenic edema related to ischemia-reperfusion. Typically improves by day 7.

Answer 297

Defined as a continuous leak for more than 7 | days.

Answer 298

Ground Glass opacities and intralobular septal thickening. (No ground glass = no rejection). Improves with steroids.

Answer 299

``` Leaks occur in the first month, stenosis can develop later (2-4 months). ```

Answer 300

The most common opportunistic infection. | Ground glass, tree-in-bud. Rare before 2 weeks.

Answer 301

Bronchiolitis Obliterans; Affects 50% at 5 years. Brochiectasis, bronchial wall thickening, air trapping.

Answer 302

Occurs with chronic rejection (but more | commonly with acute rejection). Responds to steroids.

Answer 303

Typically seen within the first year. EBV in 90%.

Answer 304

Associated with chronic rejection

Answer 305

This is the major late complication, that affects at least half o f the transplants at 5 years (most commonly at 6 months). The term bronchiolitis obliterans is often used interchangeably with chronic rejection. The findings on CT include bronchiectasis, bronchial wall thickening, air trapping, and interlobular septal thickening. Just think air trapping on expiration seen at or after 6 months = chronic rejection.

Answer 306

For the purpose of multiple choice tests know that sarcoidosis is the most common recurrent primary disease (around 35%). Lots o f other things can recur.

Answer 307

Just remember that the native lung is still diseased, and can get cancer. The highest rate is with pulmonary fibrosis, and the most common risk factor is heavy tobacco use.

Answer 308

For the purpose o f multiple choice, this is an Aunt Minnie - always shown as crazy paving lung (interlobular septal thickening with ground glass). This can be primary (90%), or secondary (10%). The secondary causes worth knowing are cancer or inhalation (silico-proteinosis).

Answer 309

• They are at increased risk o f Nocardia infections, and can have nocardia brain abscesses. • Smoking is strongly associated with the disease. • When seen in children (presenting before age 1) there is a known association with alymphoplasia. • Can progress to pulmonary fibrosis (30%). • Treatment is bronchoalveolar lavage

Answer 310

``` Interlobular septal thickening and ground glass. This isn’t always PAP, in fact in real life that it is usually NOT PAP. There is a differential that includes common things like edema, hemorrhage, BAC, Acute Interstitial Pneumonia. ``` always pap on test

Answer 311

There are actually two types; endogenous and exogenous.

Answer 312

A certain percentage o f elderly people become absolutely obsessed with their bowel movements. If you did Family Medicine addressing this psychopathology would steal a certain amount of hours out o f your life per week. Lipoid pneumonia is seen in old people who like to drink/aspirate mineral oil (as a laxative). It can also be seen with the aspiration o f vegetable oil or other animal oils. The look on plain film is an area o f lung opacification that is chronic or slowly increases with time. The look on CT is a dead give away and the most likely way this will be shown is with low attenuation / fat density in the consolidation. Having said that this is also in the crazy paving differential.

Answer 313

This is seen in children who accidentally poison | themselves with hydrocarbons, or idiots trying to perform fire-eating or flame blowing

Answer 314

This is actually more common than the exogenous type, and results from post obstructive processes (cancer) causing build up o f lipid laden macrophages

Answer 315

Fat Density in the Consolidation

Answer 316

“Why a re you showing me th e lung on that window?” O b v io u sly p u lm o n a ry p a th o lo g y is b e s t sh ow n on a lu n g window. So an y tim e the te s t w rite r is sh ow in g y o u a p u lm o n a ry p a th o lo g y on a n o n -lu n g window, that ™ y sh o u ld cu e you to th in k ab o u t som e d iffe ren t things. (1): Is th e fin d in g in the m e d ia s tin um or ribs? (2): I f it’s c le a rly a lung fin d in g then w h a t w in d ow are th ey u sin g ? • S o ft tis su e w in d ow is c la s s ic a lly u se d to sh ow fa t in a le sio n - th in k h am a rtom a o r lip o id p n eum o n ia. • B o n e w in d ow might be u sed to sh ow a d iffu s e p ro c e s s su ch a s p u lm o n a ry m ic ro lith ia sis.

Answer 317

``` This used to be called BOOP, which was a lot more fun to say. It’s not an active infection (as the name would suggest) but instead granulation tissue deposition within the alveolar spaces secondary to fibroblast proliferation. Because it is not an active infection antibiotics won’t help. However, it does respond well to steroids, and has an excellent prognosis. ```

Answer 318

``` There are lots o f different causes; idiopathic, prior infection, drugs (amiodarone), collagen vascular disease, fumes, etc... You will see the word “cryptogenic” used when there is no specific cause known. Then it is COP instead of OP. ```

Answer 319

Patchy air space consolidation or GGO (90%), in a peripheral or peri-bronchial distribution. Opacities tend to be irregular in shape. Both OP and Chronic Eosinophilic Pneumonia can present as peripheral consolidations. Findings of fibrosis are typically absent.

Answer 320

The history o f “persistent symptoms following treatment for pneumonia” could be a clue to think OP. The most common “persistent symptoms” are a cough lasting several months, low grade fever, SOB, and just generally feeling like shit.

Answer 321

COP the classic sign - seen in around 30% of cases: Consolidation around a ground glass center.

Answer 322

Can be idiopathic or associated with a known antigen. Peripheral eosinophilia (blood test) is usually present. An asthma history is found in about 50% o f cases. It looks exactly look COP (both can present as peripheral consolidations). When you say COP you should say this one too (some people think it’s the same disease as COP).

Answer 323

Peripheral GGO or consolidation. Upper lobes tend to be favored.

Answer 324

- Nodule with ground glass around it - Represents hemorrhage / invasion into surrounding tissues - Invasive Aspergillosis (Classic) - Other Fungus - Hemorrhagic Mets - Adenocarcinoma in Situ (BAC) - Wegeners

Answer 325

``` Central ground glass with rim of consolidation - COP (Classic) - TB - Pulmonary Infarct - Invasive Fungal and Wegeners ** these can also be seen with regular Halo ```

Answer 326

This is actually common. It’s caused by inhaled organic antigens. It has acute, subacute, and chronic stages. Most of the time it’s imaged in the subacute stage.

Answer 327

Patchy ground glass opacities. Ill-defined Centrilobular ground glass nodules (80%). Often has mosaic perfusion, and air trapping.

Answer 328

Looks like UIP + Air trapping. You are gonna have traction bronchiectasis and air trapping.

Answer 329

“headcheese” because it’s a mix o f everything (Ground Glass, Consolidation, Air-Trapping, and Normal Lung)

Answer 330

Features that favor Chronic HP over UIP: • Air Trapping involving 3 more lobes • Mid-Upper lobe predominant fibrosis

Answer 331

The basic anatomy of the trachea is a bunch of anterior horseshoes of cartilage, with a posterior floppy membrane. This membrane can bow inward on expiratory CT (and this is normal). The transverse diameter should be no more than 2.5 cm (same as the transverse diameter of an adjacent vertebral body).

Answer 332

Three big questions to ask yourself. | (1) Does it involve the posterior membrane ? (2) is it focal or diffuse ? and (3) is there calcification ?

Answer 333

Spares the posterior membrane. Diffuse thickening o f the trachea. No calcifications. Characterized by recurrent episodes of cartilage inflammation, and recurrent pneumonia. ``` Recurrent episodes of cartilage inflammation (ears, nose, joints, laryngeal and thyroid cartilage). Recurrent pneumonia is the most common cause of death. ```

Answer 334

Focal Subglottic circumferential stenosis, with an hourglass configuration. Focal Subglottic

Answer 335

Circumferential thickening, which can be focal or long segment. No calcifications. Subglottic involvement is common. C-ANCA+, Sub-glottic trachea is the most common location.

Answer 336

Spares the posterior membrane. You have development of cartilaginous and osseous nodules within the submucosa of the tracheal and bronchial walls. ``` Development of cartilaginous and osseous nodules. Typically occurs in men older than 50. ```

Answer 337

``` Irregular focal or short segment thickening, which can involve the posterior membrane. Calcifications are common. ``` Often confined to the trachea and main bronchi. Calcifications are common.

Answer 338

Relapsing Polychondritis Tracheobronchopathia Osteochondroplastica (TBO):

Answer 339

amyloid post intubation wegeners

Answer 340

Coronal diameter of less than two thirds the sagittal diameter. I say “saber-sheath trachea,” you say COPD. Trivia: The main bronchi will be normal in size. The tracheal wall will be normal in thickness.

Answer 341

Typical Carcinoid -Low-Grade Malignant- < 3cm More Likely to Be Central (tracheal bifurcation) More likely to appear to be within the lumen o f the airway. More likely to be calcified (-30%). Age - 50s

Answer 342

Atypical Carcinoid -Intermediate Malignant- > 3cm More Likely to Be Peripheral (distal to the segmental bronchi). May not show a bronchial relationship - or be partially endobronchial. Age - 6 0 s Association with Smoking

Answer 343

Large Cell (LCNEC) and Small Cell (SCLC) -High Grade Malignant- LCNEC: Peripheral pulmonary mass - around 3.5 cm SCLC: Large central / mediastinal mass involving the hilum

Answer 344

``` Bronchial Carcinoid is more likely to Met inside the eyeball (uveal tract). Where as a GI carcinoid is most likely to met to the extra ocular muscles ```

Answer 345

• Extremely rare in the trachea (< 1%). • More typically seen Endobronchial • Carcinoids usually have a central endobronchial location (although they can rarely be found in the pulmonary parenchymapresented as a nodule or mass in an older patient). • Pulmonary carcinoid tends to be slow growing and locally invasive (only met to nodes about 10% o f the time). • No surprise they can cause obstructive symptoms. They can also cause hemoptysis because they are highly vascular. • For the purpose of multiple choice = No association with smoking (**there maybe an association with the atypical sub-type) • An octreotide scan can be used to localize a carcinoid tumor. • PET can be falselv negative in ~ 25% o f cases (thev can be cold on PETV • Rarely they can cause a carcinoid syndrome with flushing etc... The valvular degradation that occurs tends to be on the left side (mitral and aortic), as opposed to the GI carcinoid syndrome which targets the right side (tricuspid and pulmonic).

Answer 346

* 2nd Most common tracheal malignancy * Favors the upper trachea, and prefers the posterior lateral trachea * 20x more likely to be in the trachea (relative to carcinoid). * Has a variable look - can be thickening, a mass, or a nodule. * It is NOT associated with smoking. * They are usually in the main or lobar bronchus.

Answer 347

• Most Common tracheal malignancy. • Associated with smoking, • Often multifocal (10%), favors the lower trachea / proximal bronchus

Answer 348

Usually via direct extension (lung, thyroid, esophagus)

Answer 349

* Most common benign tumor o f the trachea * When it’s a single papilloma think smoking. * When it’s multiple papillomas think HPV.

Answer 350

Bronchiectasis (begins as cylindrical and progresses to varicoid) It has an apical predominance (lower lobes are less affected) Hyperinflation Pulmonary Arterial Hypertension- Mucus plugging (finger in glove)

Answer 351

Those little hairs in your lungs that clear secretions don’t work. You end up with bilateral lower lobe bronchiectasis (remember that CF is mainly upper lobe). Other things these kids get is chronic sinusitis (prominent from an early age), and impaired fertility (sperm can’t swim, girls get ectopics). They have chronic mastoid effusions, and conductive hearing loss is common (those little ear nerve hair things are fucked up too). An important testable fact is that only 50% of the primary ciliary dyskinesia patients have Kartagener’s Syndrome.

Answer 352

Abnormal Mucus, Cilia cannot move it Normal Sperm, Absent Vas Deferens Upper lobe bronchiectasis

Answer 353

Normal Mucus, Cilia don’t work ``` Abnormal Sperm (they can’t swim), Normal Vas Deferens ``` Lower lobe bronchiectasis

Answer 354

Huge zebra that manifests as | congenital cystic bronchiectasis from a deficiency of cartilage in the 4,h-6" order bronchi

Answer 355

There is a massive dilatation o f the trachea (> 3cm). It’s not well understood, and really the only thing that does this.

Answer 356

Big Fucking Trachea

Answer 357

This is an inflammation o f the small airways. It can be infectious (like the viral patterns you see in kids) or inflammatory like RB-ILD in smokers, or asthma in kids.

Answer 358

When you see areas o f lung that are more lucent than others - you are likely dealing with air trapping. Technically, air trapping can only be called on an expiratory study as hypoperfusion in the setting of pulmonary arterial hypertension can look similar. Having said that, for the purpose of multiple choice test taking, I want you to think (1) bronchiolitis obliterans in the setting o f a lung transplant, or (2) small airway disease - asthma / bronchiolitis.

Answer 359

This is a nonspecific finding that can make you think small airway disease. It’s caused by dilation and impaction o f the centrilobular airways. Because the centrilobular airways are centered 5-10 mm from the pleural surface, that’s where they will be. It’s usually associated with centrilobular nodules.

Answer 360

This is an inflammatory process seen in rheumatoid arthritis or Sjogrens. It's not well understood and is related to lymphoid hyperplasia. It looks like centrilobular ground glass nodules with scattered areas o f bronchial dilation.

Answer 361

This is an inflammatory process seen in rheumatoid arthritis or Sjogrens. It's not well understood and is related to lymphoid hyperplasia. It looks like centrilobular ground glass nodules with scattered areas o f bronchial dilation.

Answer 362

This is another inflammatory process that can be seen in viral illness, transplant patients, drug reactions, or inhalation injury. It is also often identified in patients with DIPNECH. It occurs secondary to mononuclear cells which form granulation tissue and plug the airway. You see air trapping on expiratory imaging. This is supposedly the cause o f Swyer-James hyperlucent lung.

Answer 363

tree in bud

Answer 364

Smokers. Centrilobular ground glass nodules | upper lobe predominant

Answer 365

Inhaling dust / other misc garbage. | Centrilobular Ground glass nodules

Answer 366

RA and Sjogrens. Centrilobular ground glass nodules

Answer 367

Viral, Drugs, Transplant, Inhalation. | Air-Trapping. DIPNECH

Answer 368

Stroked-out old people and drunks love to aspirate. The testable trivia is to know the typical location o f aspiration; posterior segment o f upper lobes and superior segment o f lower lobes if supine when aspirating, bilateral basal lower lobes in upright aspiration. May favor the right side, just like an ET tube. The most common complication is infection which can manifest as an empyema (which can then get a broncho-pleural fistula).

Answer 369

Gives you an airspace opacity, if massive | can look like pulmonary edema

Answer 370

“Fleeting Opacity” that resolves in hours

Answer 371

Gives you a real pneumonia, can get parapneumonic effusion, empyema, or even broncho-pleural fistula.

Answer 372

Lipoid Pneumonia. Will be low density

Answer 373

Interstitial lung diseases are common in patients with collagen vascular diseases. The association are easily tested, so I made you this chart. I tried to hit the high points of testable trivia.

Answer 374

More pleural effusions and pericardial effusions than with other connective tissue disease Fibrosis is uncommon. Can get a “shrinking lung.”

Answer 375

Looks like UIP and COP. Lower lobes are favored. Reticulations with or without honeycombing, and consolidative opacities which are organizing pneumonia

Answer 376

NSIP> UIP; lower lobe predominant findings. Look for the dilated fluid filled esophagus.

Answer 377

LIP Extensive ground glass attenuation with scattered thin walled cysts.

Answer 378

Unoer lobe fibrobullous disease Usually unilateral first, then progresses to bilateral.

Answer 379

Rheumatoid Arthritis + Upper Lobe Predominant Lung Nodules. | These nodules can cavitate, and there may also be a pleural effusion.

Answer 380

This is a progressive loss of lung volume in both lungs seen in patients with Lupus ( “S” hrinking “L” ung for “SLe”). The etiology is either diaphragm dysfunction or pleuritic chest pain.

Answer 381

Most common manifestation of SLE in Chest = Pleuritis with/without pleural effusion.

Answer 382

This is seen in liver patients with the classic history of “shortness o f breath when sitting up." The opposite of what you think about with a CHF patient. The reason it happens is that they develop distal vascular dilation in the lung bases (subpleural telangiectasia), with dilated subpleural vessels that don’t taper and instead extend to the pleural surface. When the dude sits up, these things engorge and shunt blood - making him/her short of breath. A Tc MAA scan will show shunting with tracer in the brain (outside the lungs). They have to either tell you the patient is cirrhotic, show you a cirrhotic liver, or give you that classic history if they want you to get this.

Answer 383

The classic triad is upper tract, lung, and kidneys (although this triad is actually rare). The lungs are actually the most common organ involved (95%). There is a highly variable look.

Answer 384

The most common presentation is also probably the most likely to be tested; nodules with cavitation. The nodules tend to be random in distribution with about half o f them cavitating. They can also show you ground glass changes which may represent hemorrhage.

Answer 385

``` “Granulomatosis with Polyangiitis ” because Wegener was a member of the Nazi party. It is also possible that he worked with the deep science unit Hydra which plagued the world with schemes of global domination and genocide. Seriously, I’ve heard the guy was a real asshole. Not just a Nazi, but a bad tipper, and a habitual line stepper (deliberately didn’t wash his hands after he took a shit). ```

Answer 386

Another autoimmune pulmonary renal syndrome. It favors young men. It’s a super nonspecific look with bilateral coalescent airspace opacities that look a lot like edema (but are hemorrhage). They resolve quickly (within 2 weeks). If they are having recurrent bleeding episodes then they can get fibrosis. Pulmonary hemosiderosis can occur from recurrent episodes o f bleeding as well, with iron deposition manifesting as small, ill-defined nodules.

Answer 387

If they show you a pleural plaque they probably want you to say asbestos-related disease. Remember the plaque doesn’t show up for like 20-30 years after exposure. Remember that the pleural plaque of asbestosis typically spares the Costophrenic angles.

Answer 388

* Old Hemothorax * Old Infection * TB * Extraskeletal Osteosarcoma

Answer 389

• Most common cancer of the pleura. • About 80% of them have had asbestos exposure (NOT dose-dependent). • Lag time is around 30-40 years from exposure. • “Pleural rind” - thickening that wraps all the way around the lung - including the medial surface of the pleura (near the heart) • Extension into the fissure is highly suggestive.

Answer 390

This is a solitary (usually) tumor arising from the visceral pleura. The key is to know that they are NOT associated with asbestos, smoking, or other environmental pollutants. They can get very large, and be a source of chest pain (although 50% are incidentally found).

Answer 391

- Not associated with asbestos, smoking, or other environmental pollutants - Even when they are big, they are usually benign - Doege-Potter syndrome occurs in like 5% of cases. This is an episodic hypoglycemia (tumor can secrete an insulin like growth factor) - Hypertrophic osteoarthropathy occurs in like 30% of the cases.

Answer 392

Here is the high yield trivia on this. As a general rule the subtype of adenocarcinoma is the most likely to met to the pleura. Lung cancer is the most common primary, with breast and lymphoma at 2nd and 3rd. Remember that a pleural effusion is the most common manifestation of mets to the pleura

Answer 393

This is the most common benign soft tissue tumor of the pleura. The patients sometimes feel the “urge to cough.” They will not cause rib erosion. They “never” turn into a sarcoma. The differential consideration is extra-pleural fat, but it is usually bilateral and symmetric.

Answer 394

Some random factoids on pleural effusions that could be potentially testable. There has to be around 175 cc of fluid to be seen on the frontal view (around 75cc can be seen on the lateral). Remember that medicine docs group these into transudative and exudative based on protein

Answer 395

A pleural effusion can accumulate between the lung base and the diaphragm. These are more common on the right, with “ski-slopping” or lateralization of the diaphragmatic peak. A lateral decubitus will sort it out in the real world.

Answer 396

Notice the high point o f the diaphragm is shifted laterally

Answer 397

``` The key here is the increased space between the stomach bubble and lung base. ```

Answer 398

It is possible to have pleural fluid collect between the layers o f the pleura creating a oval / round appearance mimicking a Cancer.

Answer 399

Basically this is an infected pleural effusion. It can occur with a simple pneumonia but is seen more in people with AIDS. Usually these are more asymmetric than a normal pleural effusion. Other features include enhancement of the pleura, obvious septations, or gas

Answer 400

This is the fancy Latin word for when the empyema eats through the chest wall and into the soft tissues. It’s classically seen with TB (70%), with the second most common cause being actinomyces.

Answer 401

lentiform ``` Split Pleural Sign (thickening and separation o f the visceral and parietal pleura) ``` Treated with chest tube

Answer 402

round claw sign (acute angle with pleura NOT treated with chest tube (risk o f bronchopleural fistula).

Answer 403

These can be acquired via trauma, or congenital. The congenital ones are most common in the back left (Bochdalek), with anterior small and right being less common (Morgagni). The traumatic ones are also more common on the left (liver is a buffer).

Answer 404

This is a high yield topic because you can use fluoro to help make the diagnosis. Obviously the dinosaurs that write these tests love to ask about fluoro (since that was the only thing they did in residency). Diaphragmatic paralysis is actually idiopathic 70% of the time, although when you see it on multiple choice tests they want you to think about phrenic nerve compression from a lung cancer. Normally the right diaphragm is higher, so if you see an elevated left diaphragm this should be a consideration.

Answer 405

On a fluoroscopic sniff test you are looking for paradoxical movement (going up on inspiration - instead of down).

Answer 406

``` thymus thyroid thoracic aorta teratoma (germ cell tumors) terrible lymphoma ```

Answer 407

The thymus can do a bunch of sneaky things. It can rebound from stress or chemotherapy and look huge. It can get cysts, cancer, carcinoid, etc...

Answer 408

Discussed in detail in the Peds chapter. After stress or chemotherapy the thing can blow up 1.5 times the normal size and simulate a mass. Can be hot on PET.

Answer 409

Can be congenital or acquired. Acquired is classic after thoracotomy, chemotherapy, or HIV. They can be unilocular or multilocular. T2 bright is gonna seal the deal for you.

Answer 410

So this is kind of a spectrum ranging from non-invasive thymoma, to invasive thymoma, to thymic carcinoma. Calcification makes you think it’s more aggressive. The thymic carcinomas tend to eat up the mediastinal fat and adjacent structures. The average age is around 50, and they are rare under 20. These guys can “drop met” into the pleural and retroperitoneum, so you have to image the abdomen.

Answer 411

Myasthenia Gravis, Pure Red Cell Aplasia, Hypogammaglobinemia.

Answer 412

1 only mention this zebra because it has a characteristic look. It’s got a bunch of fat in it. Think “fatty mass with interspersed soft tissue.”

Answer 413

``` • PET might help - both arc hot, but lymphoma is hotter. • MRI - Thymic Rebound should drop out on in-out of phase imaging (it has fat in it). Lymphoma will not drop out. ```

Answer 414

Almost always Teratoma (75%). Mediastinal Teratoma - This is the most common extragonadal germ cell tumor. They occur in kids (below age 1) and adults (20s-30s). They are benign, but carry a small malignant transformation risk. Mature subtypes arc equal in Men and Women, but immature subtypes are exclusively seen in men (which should be easy to remember). There is an association with mature teratomas and Klinefelter Syndrome. The imaging features include a cystic appearance (90%), and fat. They can have calcifications including teeth - which is a dead give away

Answer 415

This is uncommon and benign. The classic location is the right anterior cardiophrenic angle. This classic location is the most likely question.

Answer 416

This is a proliferation o f fibrous tissue that occurs within the mediastinum.

Answer 417

(the one everyone thinks about) classically caused by histoplasmosis). Other causes include TB, and Sarcoid. This will look like a soft tissue mass with calcifications that infiltrates the normal fat planes of the mediastinum.

Answer 418

is the more rare subtype that people read about once and then forget. Some people will call this form “idiopathic” although the subtype is better thought o f as a response to an autoimmune disease (SLE, RA, Behcet, etc...) or a complication to radiation therapy. There is also a testable association with the headache medication methysergide. It’s associated with retroperitoneal fibrosis when idiopathic. This subtype also looks like a soft tissue mass but tends to be more infiltrative, lack calcifications, and can enhance post contrast.

Answer 419

superior vena cava syndrome.

Answer 420

These congenital lesions are usually within the mediastinum (most commonly found in the subcarinal space) or less commonly intraparenchymal. For the purpose of the exam, they are going to be in the subcarinal region, causing obliteration of the azygoesophageal line on a CXR, and being waterish density on CT.

Answer 421

Could be mets, could be infection, could be reactive. It is | generally abnormal to be larger than 2cm in short axis (makes you suspect cancer).

Answer 422

Excess unencapsulated fat seen in patients with iatrogenic | steroid use, Cushings, and just plain old obesity.

Answer 423

The most common posterior mediastinal mass is one of neurogenic origin. This includes schwannomas, neurofibromas, and malignant peripheral nerve sheath tumors.

Answer 424

Extramedullary hematopoiesis (EMH) is a response to failure of the bone marrow to respond to EPO. Classic conditions include CML, Polycythemia vera, myelofibrosis, sickle cell, and thalassemia.

Answer 425

This is a significant cause of mortality in hospitalized patients. The gold standard is catheter angiography, although this is invasive and carries risks. As a result tests like the D-Dimer (which has an almost 100% negative predictive value), and the DVT lower extremity ultrasound were developed. Now, the CTPA is the primary tool.

Answer 426

Westermark Sign Regional Oligemia Fleischner Sign Enlarged Pulmonary Artery Hampton's Hump Peripheral Wedge Shaped opacity Pleural Effusion Obviously not specific, but seen in 30% of PEs.

Answer 427

Clot is Central Venous Dilation Perivenous soft tissue edema Pleural Effusion is common Acute PE can cause sudden death from arrhythmia or acute right heart failure CTPA is the exam of choice.

Answer 428

Clot (if seen) is more Peripheral. May be “web like” Shrunken Veins with collateral vessels Calcifications within the thrombi and within the venous walls Lungs may show a mosaic attenuation pattern Chronic PE is a well described cause of pulmonary hypertension (obstruction in the vascular bed causes an increase in vascular resistance) VQ Scan (believe it or not) is probably superior to CT.

Answer 429

Hypotension (SBP < 90)

Answer 430

Stable BP, but RV dysfunction or positive cardiac enzymes (myocardial necrosis).

Answer 431

RV Dilated Larger Than LV - Probably the best sign - Leftward bowing of the ventricular septum is also helpful Contrast Reflux into the Hepatic Veins -Less Reliable.

Answer 432

A pulmonary infarct is a wedge-shaped opacity that is going to “melt” (resolve slowly), and sometimes can cavitate. Obviously a cavitary lesion throws up lots of flags and makes people say TB, or cancer. When it’s an opacity in the lung and the patient doesn’t have a fever, sometimes people think cancer - plenty of pulmonary infarcts have been biopsied

Answer 433

Uncommon variant of primary pulmonary hypertension, that affects the post capillary pulmonary vasculature. For gamesmanship: PAH + Normal Wedge, you should think this. The normal wedge pressure differentiates it from other post capillary causes; such as left atrial myxoma, mitral stenosis, and pulmonary vein stenosis.

Answer 434

Think about three things for multiple choice; (1) Iatrogenic from swan ganz catheter *most common (2) Behcets, (3) Chronic PE. When they want to lead towards swan ganz they may say something like “patient in the ICU.” The buzzwords for Behcets are: “Turkish descent” and “mouth and genital ulcers.”

Answer 435

This has a cool name, which instantly makes it high yield for testing. This is a pulmonary artery pseudoaneurysm secondary to pulmonary TB. It usually involves the upper lobes in the setting of reactivation TB.

Answer 436

This is a zebra cause of pulmonary artery aneurysm that is similar (and maybe the same thing) as Behcets. It is characterized by recurrent thrombophlebitis and pulmonary artery aneurysm formation and rupture

Answer 437

So another possible testable scenario is the patch | aneurysm, from the RVOT repair.

Answer 438

Pulmonary arterial pressures over 25 are going to make the | diagnosis. I prefer to use the “outdated” primary and secondary way of thinking about this

Answer 439

Idiopathic type is very uncommon, seen in a small group of young women in their 20s.

Answer 440

This is by far the majority, and there are a few causes you need to know: Chronic PE , Right Heart Failure/ Strain, Lung Parenchymal Problems- (This would include emphysema, and various causes of fibrosis). COPDers with a pulmonary artery bigger than the aorta (A/PA ratio) have increased mortality (says the NEJM).

Answer 441

The numbers people use for what is abnonnal are all over the place - if forced I'd pick 29 mm. A superior strategy is to compare the size of the aorta and pulmonary artery (a normal PA should not be bigger than the aorta). You can also compare the segmental artery-to adjacent bronchus (>1:1 is abnonnal). Mural calcifications of central pulmonary arteries (seen in Eisenmenger phenomenon) have been described. Additional nonspecific signs include right ventricular dilation / hypertrophy, and centrilobular ground-glass nodules.

Answer 442

visualization of th main pulmonary artery (egg) at the level of the aortic arch (banana)

Answer 443

right pa crosses the carina midline anteriorly. it normally crosses more caudally

Answer 444

* Left side is involved 3 times more than the right (liver is a buffer) * Most ruptures are “radial”, longer than 10 cm, and occur in the posterior lateral portion * Collar Sign - This is sometimes called the hour glass sign, is a waist-like appearance o f the herniated organ through the injured diaphragm * Dependent Viscera Sign - This is an absence o f interposition of the lungs between the chest wall and upper abdominal organs (liver on right, stomach on left).

Answer 445

Airway injury is actually pretty uncommon. When it does occur it’s usually within 2 cm o f the carina. Injury close to the carina is going to cause a pneumomediastinum rather than a pneumothorax - that is a testable fact. When you get a tracheal laceration, it most commonly occurs at the junction o f the cartilaginous and membranous portions o f the trachea.

Answer 446

This is probably the most common cause o f pneumomediastinum in trauma patients (and most people haven’t heard of it). The idea is that you get alveolar rupture from blunt trauma, and the air dissects along bronchovascular sheaths into the mediastinum.

Answer 447

You probably remember this from step 1. The physical exam buzzword was “Hammonds Crunch.” Basically you have a ruptured esophageal wall from vomiting, resulting in pneumomediastinum / mediastinitis

Answer 448

This is 3 or more segmental (more than one fracture in a rib) fractures, or more than 5 adjacent rib fractures. The physical exam buzzword is “paradoxical motion with breathing.”

Answer 449

Obviously you don’t want to miss the tension pneumothorax. The thing they could ask is “inversion or flattening o f the ipsilateral diaphragm.”

Answer 450

Sometimes the ED will ram them into the parenchyma. This is more likely to occur in the setting o f background lung disease or pleural adhesions. You’ll see blood around the tube. Bronchopleural fistula may occur as a sequela. The placement o f a tube in a fissure is sorta controversially bad (might be ok).

Answer 451

If you see pleural fluid in the setting o f trauma, it’s probably blood. The only way 1 can see them asking this is a density question; a good density would be 35-70 H.U.

Answer 452

This is a little tricky, and they could show you a picture o f it. If you have an injury to the chest wall that damages the parietal pleura then you get a hemothorax. If you have an injury to the chest wall, but your parietal pleural is still intact, you get an extrapleural hematoma. The classic history is “persistent fluid collection after pleural drain/tube placement.” The buzzword / sign is displaced extrapleural fat. There is a paper out there that suggests a biconvex appearance is more likely arterial and should be watched for rapid expansion. This may be practically useful, but is unlikely to be asked. Just know the classic history, and displaced extrapleural fat sign.

Answer 453

This is the most common lung injury from blunt trauma. Basically you are dealing with alveolar hemorrhage without alveolar disruption. The typical look is non-segmental ill-defined areas of consolidation with sub pleural sparing. Contusion should appear within 6 hours, and disappear within 72 hours (if it lasts longer it’s probably aspiration, pneumonia, or a laceration).

Answer 454

So a tear in the lung will end up looking like a pneumatocele. If they show you one it will probably have a gas -fluid (blood) level in it. These things can be masked by surrounding hemorrhage early on. The major difference between contusion and laceration is that a laceration resolves much more slowly and can even produce a nodule or a mass that persists for months.

Answer 455

The aorta is injured most commonly at the aortic isthmus (some sources say 90%). The second and third most common locations are the root and at the diaphragm. Some people say the root is actually the most common, but most o f these people die prior to making it to the hospital. This is a minority opinion. If asked what is the most common site o f traumatic aortic injury, the answer is isthmus. It’s usually obvious on a candy cane CTA. The main mimic would be a “ductus bump,” which is a normal variant. The way to tell (if it isn’t obvious) is the presence of secondary signs o f trauma (mediastinal hematoma).

Answer 456

If you have hemopericardium in the setting o f trauma, you | can suggest this and have the ED correlate with cardiac enzymes and EKG findings.

Answer 457

This is seen in the setting of a long bone fracture or Intramedullary rod placement. You get fat embolized to the lungs, brain, and skin (clinical triad of rash, altered mental status, and shortness o f breath). The timing is 1-2 days after the femur fracture. The lungs will have a ground glass appearance that makes you think pulmonary edema. You will not see a filling defect - like a conventional PE. If they don’t die, it gets better in 1-3 weeks.

Answer 458

Positive pressure ventilation can cause alveolar injury, with air dissecting into the mediastinum (causing pneumomediastinum and pneumothorax). Patients with acute lung injury or COPD have a high risk o f barotrauma from positive pressure ventilation. Lungs with pulmonary fibrosis are actually protected because they don’t stretch.

Answer 459

The main way to ask questions about central lines is to show them being malpositioned and asking you where they are. An abrupt bend at the tip of the catheter near the cavo-atrial junction should make you think azygos. If it’s on the left side of the heart, it’s either (1) arterial or (b) in a duplicated SVC. This is a sneaky trick, related to Central Lines. They can show you the pseudo lesion / hot quadrate sign (seen with SVC syndrome), and then show you a CXR with a central venous catheter. The idea is that central lines are a risk factor for SVC occlusion.

Answer 460

The tip o f the ETT should be about 5 cm from the carina (halfway between the clavicles and the carina). The tip will go down with the chin tucked, and up with the chin up (“the hose goes, where the nose goes”). Intubation o f the right main stem is the most common goof (because of the more shallow angle) - this can lead to left lung collapse. You can sometimes purposefully intubate one lung if you have massive pulmonary hemorrhage (lung biopsy gone bad), to protect the good lung.

Answer 461

This is used in cardiogenic shock to help with “diastolic augmentation,” - essentially providing some back pressure so the vessels of the great arch (including the coronaries) enjoy improved perfusion.

Answer 462

decrease LV afterload and increase myocardial perfusion,

Answer 463

``` the balloon should be located in the proximal descending aorta, just below the origin of the left subclavian artery (balloon terminates just above the splanchnic vessels) ``` ideal position is in the region of the left main stem

Answer 464

dissection during insertion, obstruction of the left subclavian from malpositioning

Answer 465

• Pacemakers • Implantable Cardiac Defibrillators (ICDs) - the one with “shock coils” - i.e. the thick bands. • Mixed (Pacemaker + ICD)

Answer 466

• Leads are placed in the RV, RA, and LV. The LV leads get there via the coronary sinus to the posterior / lateral cardiac vein. • "Cardiac resynchronization therapy device” is the vocab word the bi-ventricular pacemaker (RV + LV and usually RA). Remember vocab words are easily testable. • Pearls on locations: (1) The RV lead should cross the midline on a frontal view, (2) The RA and RV leads are anterior on the lateral view, (3) The LV lead should be posterior on the lateral, (4) the idea location for the RA lead is actually the RA appendage - so it should course down then back up/anterior.

Answer 467

• Myocardial Perforation - The number is 3 mm. If the lead is 3 mm within the epidcardial fat you should suspect penetration. • Rib Clavicle Crush - The leads are mostly commonly fractured in the region o f the clavicle, and first rib. • Twiddler Syndrome - The generator pack gets flipped and twisted in the pocket, leading to lead displacement. This happens because Grandpa just can’t leave the thing alone (gotta put those dementia mittens on him). Can’t have him dying on us... we need those social security checks. • Acute - All the stuff you get with central line placement: pneumothorax, hemothorax, etc... Generator Related - Terminal connector pin displacement. This is actually common.

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