CTC Chest

Question 1

How are lateral CXRs taken?

Answer 1

Left lateral position - left side against film.

Left ribs will not be magnified.
Right ribs will be magnified and be more posterior

Question 2

What is the normal hilum on a lateral CXR?

Answer 2

Put your finger in the “dark hole” - the LUL bronchus.

Front will be the R PA and overtop will be the L PA.

Posterior wall of the bronchus intermedius runs through the black hole and can be thickened by edema.

Question 3

What is Raider Triangle?

What variant runs through it?

Answer 3

Sits on the aortic arch posterior to the trachea and anterior to the vertebral bodies.

Aberrant right subclavian artery will obliterate this.

Question 4

How are the heart valves drawn on CXR?

Answer 4

Frontal:
Cross down center: Aortic over X. Pulmonic = upper right. Mitral = lower left. Mitral = lower right.

Lateral:
Aortic = upper anterior
Pulmonic = upper posterior
Tricuspid = lower anterior
Mitral = lower posterior

Pulomonic valve is most superior in location.

Question 5

If you see two metallic heart valves on a CXR, which is bigger?

Answer 5

Mitral and aortic - Mitral is bigger.

Pacer wire going through a valve makes it the tricuspid valve.

Question 6

How is the R major fissure oriented with the left on the lateral CXR?

Answer 6

Right is anterior to the left.

Question 7

How many pulmonary segments are there in the R and L lungs?

Answer 7

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

L = 8 (4 upper/lingula and 4 lower)

Question 8

What is in the posterior mediastinum?

Answer 8

Esophagus, thoracic duct, and descending aorta.

Trachea is in middle.

Question 9

What is the MC pulmonary venous variation?

Answer 9

Separate vein draining the RML

Usually have upper and lower on each side.

Question 10

What is Proximal Interruption of the PA?

Answer 10

Congential abscence of the R or L PA with the more distal PA vasculature present

Shown with volume loss of one hemi-thorax (CXR or CT), then contrast shot through the heart with only 1 PA.
Volume loss + 1 PA

Seen on the opposite side of the aortic arch - Absent R PA with left arch and absent L PA with right arch

Associated witih PDA
Interrupted L PA is associated with TOF and Truncus

Question 11

What is interrupted L PA associated with?

Answer 11

TOF and Truncus

Question 12

What does infection with Anthrax look like?

Answer 12

Hemorrhagic lymphadenitis, mediastinitis, and hemothrax.

Classic look: Mediastinal widening with pleural effusion in the setting of bio-terrorism.

Question 13

What does Klebsiella pneumonia look like?

Answer 13

Buzzword: Bulging fissure from exuberant inflammation. More likely to have pleural effusions, empyema, and cavity than conventional pneumonia,

Alcoholic and nursing home patient. Currant jelly sputum.

Question 14

What does H. flu pneumonia look like?

Answer 14

Usually bronchitis, sometimes bilateral lower lobe bronchopneumonia.

COPDers and ppl w/o a spleen

Question 15

Post Bone Marrow Transplant lung findings

Answer 15

Early Neutropenic (0-30): Pulmonary edema, hemorrhage, drug induced lung injury. Fungal pneumonia (invasive aspergillosis)

Early (30-90): PCP and CMV

Late (>90): Bronchiolitis obliterans, cryptogenic organizing pneumonia

Question 16

What does post bone marrow transplant GVH pulmonary disease look like?

Answer 16

Acute (20-100 days): Favors extrapulmonary symptoms (skin, liver, GI tract)

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

Question 17

Infections in AIDS by CD4

Answer 17

> 200: Bacterial infections, TB

<200: PCP; Atypical mycobacterial

<100: CMV, disseminated fungal, mycobacterial

Question 18

CT patterns with pulmonary infection with AIDS

Answer 18

Focal airspace opacity: Bacterial infection (Strep pneumonia) is MC. DDx should include TB if CD4 is low. If it’s chronic think lymphoma or Kaposi.

Multi-focal Airspace Opacity: Bacterial or fungal

Ground Glass: PCP (if not a choice, could be CMV if CD4 <100).

Question 19

AIDS trivia and buzzwords

Answer 19

MC airspace opacity = S pneumonia
CT with ground glass = PCP
“Flame shaped” perihilar opacity = Kaposi Sarcoma
Persistent opacities = Lymphoma
Lung cysts = LIP
Lung cysts + Ground Glass + Pneumothorax = PCP
Hypervascular LN = Castlemans or Kaposi

Question 20

What are the stages of TB?

Answer 20

Primary - Inhaled and causes necrosis - body forms granuloma (Ghon Focus). Nodal expansion which calcifies (Ranke complex). If node ruptures get endobronchial spread or hematogenous spread. Cavitation is NOT common.

Primary Progressive - Local progression of parenchymal disease with development of cavitation (at the initial site of infection/or hematogenous spread) - uncommon, primary risk is AIDS, immunosuppressed, transplant patients, people on steroids.

Post Primary - Reactivation - 5% - Apical and posterior upper lobe and superior lower lobe (more oxygen, less lymphatics) - progression. Development of a cavity. Can get pseudoaneurysms - Rasmussen.

Question 21

What is pleural involvement with TB?

Answer 21

Can occur at any time at infection. In primary, can be seen 3-6 months after as a hypersensitivity response. Usually culture negative. Have to biopsy pleura. Don’t see effusions as much with post primary disease, but when you do, the fluid is usually culture positive.

Question 22

Facts about TB

Answer 22

Primary = no cavity, post primary/primary progressive = cavity
Ghon Lesion = Calcified TB granuloma; sequela of primary TB
Ranke Compes = Calcified TB granuloma + calcified hilar node; healed primary TB.
Bulky hilar and paratracheal LAD = kids
Location for reactivation TB = posterior/apical upper lobes, superior lower lobes.
Miliary spread when? - Hematogenous dissemination (usually in setting of reactivation), but can be in primary progressive as well
Reactive TB pattern (cavitation) seen in HIV patient when 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.

Question 23

What are the patterns of Non-Tuberculous Mycobacteria?

Answer 23

MAC and Mycobacterium Kanasii.

Cavitary (Classic)- Usually MAC - Old white man with COPD (or other chronic lung disease), look like reactivation TB. Upper lobe cavitary lesion with adjacent nodules (suggesting endobronchial spread).

Bronchiectatic (“Non-Classic”) - Lady Windermere Disease - Do not cough and are asymptomatic. Favors old white lady. Tree-in-bud opacities with cylindric bronchiectasis in the RML and lingula

HIV - Low CD4 (<100). GI infection disseminated in the blood. Get a big spleen and liver. Mixed with other pulmonary infections (PCP, etc) given the low CD4 - so lungs can look like anything. Mediasinal LAD is MC.

Hypersensitivity Pneumonitis - Hot tub lung. Aerosolized bugs. Ill-defined, ground glass centrilobular nodules.

Question 24

What does Aspergillus look like with normal immune, immune depressed, or hyperimmune?

Answer 24

Normal Immune = makes a fungus ball “aspergilloma” in an existing cavity. Show a fungus ball = don’t call it invasive. Cavity from prior trauma or infection.

Immune Suppressed (AIDS or Transplant)- Invasive Aspergillus. Halo sign consolidative nodule/mass with a ground glass halo. Air Crescent Sign - thin crescent of air w/in the consolidative mass. Healing as the necrotic lung separates from the parenchyma. Usually 2-3 weeks after treatment.

Hyper-immune- ABPA. Long-standing asthma

Question 25

What does Mucomycosis of the lungs look like?

Answer 25

Aggressive fungal infection in impaired patients (AIDS, steroids, Bad diabetes, etc..). Usually in the sinuses, but can get invasion of the mediastinum, pleura, and chest wall.

Question 26

What is Lemierre Syndrome?

Answer 26

Jugular vein thrombosis with septic emboli - usually seen after oropharyngeal infection or recent ENT surgery. Fusobacterium Necrophorum

Question 27

What causes Lemierre Syndrome?

Answer 27

Fusobacterium Necrophorum Jugular vein thrombosis with septic emboli - usually seen after oropharyngeal infection or recent ENT surgery.

Question 28

What are the guidelines for lung cancer screening?

Answer 28

Low dose CT for asymptomatic - 55-80 with 30 pack-year history and currently smoke (or have quit w/in the past 15 years)

Question 29

What are the four "benign" calcification patterns with pulmonary nodules?

Answer 29

Solid/diffuse Laminated Central Popcorn

Question 30

Qualities of nodules that make you thing benign vs cancer?

Answer 30

Benign: Presence of fat Rapid doubling time - less than 1 month Slow doubling time - longer than 16 months - stable at two years = benign. Cancer: Spiculated margins - "Corona Radiata Sign" Air bronchogram through the nodules (usually adeno in situ) Partially solid lesions with GG component

Question 31

What findings of a GG nodule on PET make you think cancer vs infection?

Answer 31

``` HOT = infection COLD = cancer ```

Question 32

Paraneoplastic syndromes with squamous and small cell lung cancers?

Answer 32

Squamous = PTH Small Cell = SIADH Lambert Eaton: Paraneoplastic syndrome with small cell - proximal weakness from abnormal release of ACh at the NM junction. Usually comes before cancer diagnosis

Question 33

What is Lambert Eaton Syndrome?

Answer 33

Paraneoplastic syndrome with small cell - proximal weakness from abnormal release of ACh at the NM junction. Usually comes before cancer diagnosis

Question 34

What are the precursor lesions of lung cancer?

Answer 34

Atypical Adenomatous Hyperplasia of Lung (AAH): Precursor of adeno Adenocarcinoma in situ (ACIS): <3 cm. Multiple subtypes - MC is non-mucinous. Minimally Invasive Adeno (MIA): <3 cm. The distinction is that there is <5mm of stromal invasion (>5 mm will be called lepidic predominant adenocarcinoma).

Question 35

What stage of lung cancer is unresectable?

Answer 35

3B Supraclavicular, scalene, or contralateral mediastinal or hilar LAD. Tumor in the same lung but different lobes from the primary mass. Malignant pleural effusion Two lesions in same lobe is T3 Two lesions in different lobes is T4 Two lesions in different lungs is M1a.

Question 36

MC extrathoracic causes of lymphatic carcinomatosis?

Answer 36

Breast, stomach, pancreas, and prostate.

Question 37

How is carcinoid classified?

Answer 37

Peripheral pulmonary or bronchial Typical or atypical - typical grow slower and locally invasive. No association with smoking. Central bronchus, can cause obstructive symptoms. Can cause hemoptysis b/c highly vascular. Octreotide scan can be used to localize. Can cause carcinoid syndrome with flushing, etc... Valvular regurgitation on left side as opposed to GI which affects the right side. Atypical are rare, seen in older patients, more likely to be a mass.

Question 38

What is Adenoid Cystic Carcinoma?

Answer 38

MC bronchial gland tumor. NOT associated with smoking. Usually in the main or lobar bronchus. More common than carcinoid in the trachea.

Question 39

Differences between primary, secondary, PTLD, and AIDS related pulmonary lymphoma?

Answer 39

Primary: Rare, usually NHL subtype. Lack of extrathoracic involvement for 3 months. Low grade MALToma. Secondary: Pulmonary involvement of systemic lymphoma. Much more likely. NHL is much more common, but if you have HL it is more likely to involve the lungs. With HL you get nodes and parenchyma, in NHL you might just get parenchyma. PTLD- seen after organ or stem cell transplant. Usually w/in a year of transplant (late presentation >1 yr have more aggressive course). B-cell lymphoma with relationship to the EB virus. Nodal or extranodal disease. Well-defined pulmonary nodules/mass, patchy airspace consolidation, halo sign, and interlobular septal thickening. AIDS-related: 2nd MC lung tumor in AIDS (Kaposi's is first). Almost exclusively a high grade NHL. Relationship with EBV - CD4 <100. Variable presentation with multiple peripheral nodules ranging from 1-5 cm. Extranodal locations (CNS, bone marrow, lung, liver, and bowel) is common. AIDS patient with lung nodule, pleural effusion, and LAD = lymphoma

Question 40

Differences between Secondary NHL and HL

Answer 40

Secondary NHL: 80-90% of lyphoma cases 45% have intrathoracic disease at presentation 25% have pulmonary parenchymal disease Pulmonary involvement frequently occurs in the absence of mediastinal disease. Secondary HL: 10-20% of lymphoma cases 85% have intrathoracic disease at presentation 40% have pulmonary parenchymal disease Lung involvement almost always associated with intrathoracic LN involvement.

Question 41

AIDS patient with lung nodules, pleural effusion, and LAD =

Answer 41

Lymphoma

Question 42

Things to know about Kaposi Sarcoma?

Answer 42

MC lung tumor in AIDS (requires CD4 <200) MC hepatic neoplasm in AIDS Buzzword = Flame shaped opacities - tracheobronchial mucosa and perihilar lung. Slow growth, and asymptomatic patients (despite terrible looking lungs) Thallium positive and Gallium negative.

Question 43

Difference between Kaposi and Lymphoma on Gallium and Thallium

Answer 43

Kaposi: Thallium positive and Gallium Negative Lymphoma: Thallium positive and Gallium positive

Question 44

What can pulmonary hamartomas look like on PET?

Answer 44

Can be hot.

Question 45

What is Swyer-James?

Answer 45

Unilateral lucent lung. After viral infection in childhood resulting in post infectious obliterative bronchiolitis - from constrictive bronchiolitis. SMALLER lung - not hyperexpanded.

Question 46

What is Pulmonary Langerhans Cell Histiocytosis (LCH)?

Answer 46

Cystic lung disease - smokers who are young (20s-30s). Starts out with centrilobular nodules with an upper lobe predominance. Eventually cavitate into cysts which are thin walled to start, then some become more thick walled. Buzzword = bizarre shaped- which two or more cysts mrege together. Can spontaneously resolve if you quit smoking. Spares the costophrenic angles

Question 47

What diseases spare the costophrenic angles?

Answer 47

LCH | HSP

Question 48

Differences between LCH and LAM?

Answer 48

LCH: Cysts and nodules; Smoker; Upper and mid lungs; Thicker cysts (bizarre) LAM: Cysts (no nodules); Women, patients with TS; Difuse; Thin round cysts

Question 49

Differences in cysts with LCH, LAM and Birt Hogg Dube?

Answer 49

LCH: Bizarre shape, thick walled LAM: Round, thin walled BHD: Oval, thin wall

Question 50

What is Birt Hogg Dube?

Answer 50

Cystic lung disease with thin walled "oval" shaped cysts. Association with renal findings (bilateral oncocytomas and chromophobe RCCs) Also have skin stuff.

Question 51

What is Lymphocytic Interstitial Pneumonia (LIP)?

Answer 51

Benign lymphoproliferative disorder with infiltration of the lungs. Association with autoimmune diseases (SLE, RA, and Sjogrens - Sjogrens is MC). Other one to know is HIV in younger patients. Also association with Castlemans. Appearance varies depending on the underlying cause. Cystic lung disease usually thin walled, "deep w/in the lung parenchyma," seen predominantly with Sjogrens.

Question 52

LIP =

Answer 52

Sjogrens and HIV

Question 53

LIP in a kid =

Answer 53

HIV

Question 54

What is Pneumocystis Pneumonia (PCP)?

Answer 54

MC opportunistic infection in AIDS. GG predominantly in the hilar and mid lung zones. Pneumatoceles in 30% of cases. In patients receiving aerosolized prophylaxis, a cystic form is more common and may have bilateral thin walled upper lung predominant cysts. Gallium will show diffuse uptake (Thallium will be negative)

Question 55

Emphysema with central dot sign?

Answer 55

Centri-lobular emphysema. Central dot represents central bronchovascular bundle.

Question 56

What is Pan-lobular emphysema?

Answer 56

Favor the lower lobes. More uniform distribution. Coronal CT with lower lobe predominance Association with alpha-1-antitrypsin deficiency. "Ritalin Lung" from IV Ritalin use can also cause pan-lobular appearance.

Question 57

What is Vanishing Lung Syndrome?

Answer 57

Idiopathic cause of giant bullous emphysema resulting from avascular necrosis of the lung parenchyma and hyperinflation. Favors the bilateral upper lobes and is defined as bullous disease occupying at least 1/3 of a hemithorax. Young man - about 20% have alpha-1-antitrypsin deficiency.

Question 58

Things to know about Asbestos?

Answer 58

"Asbestosis" = lung fibrosis associated with exposure, NOT actual exposure Interstitial pattern looksk like UIP + parietal pleural thickening 20 year latency between initial exposure and development of lung cancer or pleural mesothelioma. Association with extrapleural cancer - peritoneal mesothelioma, GI cancer, renal cancer, laryngeal cancer, and leukemia. Benign pleural effusions are the "earliest pleural based phenomenon" associated with exposure - still with lag time of around 5 years.

Question 59

What are Benign Asbestos Related Changes?

Answer 59

Pleural effusion is earliest and MC. Pleural plaques may develop 20-30 years, with calcs occuring around 40 years. Tend to spare the costophrenic angles. Round atelectasis - is sometimes called the "asbestos pseudotumor"

Question 60

What is Malignant Mesothelioma?

Answer 60

MC cancer of the pleura. 80% have asbestos exposure and development is NOT dose dependent. Lag time around 30-40 years from exposure. Buzzword = pleural rind. Extension into the fissure is highly suggestive.

Question 61

What is Silicosis?

Answer 61

Miners and quarry workers. Simple silicosis = multiple nodular opacities favoring the upper lobes with egg shell calcs of the hilar nodes. Can get perilymphatic nodules. Can get Progressive Massive Fibrosis - formation of large masses in the upper lobes with radiating strands. Can get with Silicosis and coal workers (something similar can occur with Talcosis). Can sometimes cavitate, but should always raise suspicion of TB when see this (especially in the setting of silicosis).

Question 62

What is Progressive Massive Fibrosis?

Answer 62

Complicated Silicosis. Can get with coal workers or Talcosis. Formation of large masses in the upper lobes with radiating strands. Can sometimes cavitate, but should always raise suspicion of TB when see this (especially in the setting of silicosis.

Question 63

What is Silicotuberculosis?

Answer 63

Silicosis raises your risk of TB by 3 fold. If see cavitation in the setting of silicosis, think about TB. Also get increased risk with coal workers.

Question 64

Look of cancer vs progressive massive fibrosis on MRI?

Answer 64

Cancer = T2 bright PMF = T2 dark.

Question 65

What is Berryliosis?

Answer 65

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

Question 66

What is Silo Filler's Disease?

Answer 66

Nitrogen Dioxide Pulmonary edema pattern. Recovery is typically w/in 5 weeks.

Question 67

What is Talcosis?

Answer 67

Filler in tablets, sometimes injected (along with drugs) in IVDU. Hyperdense micronodules with conglomerate masses (similar to PMF). GGO.

Question 68

DDx of Perilymphatic Nodules?

Answer 68

Sarcoid - 90% Lymphangitic spread of CA Silicosis

Question 69

DDx of Random Nodules?

Answer 69

Miliary TB Mets Fungal

Question 70

DDx of Centrilobular Nodules?

Answer 70

Infection RB-ILD HSP (if ground glass)

Question 71

What are Idiopathic Interstitial Pneumonas?

Answer 71

NOT diseases, but lung reactions to lung injury. Variety of patterns and variable degrees of inflammation and fibrosis. Causes: Idiopathic, collagen vascular disease, medications, and inhalation.

Question 72

What is UIP?

Answer 72

Usual Interstitial Pneumonia - MC interstitial lung disease. When idiopathic = IPF. CXR volumes are reduced. Reticular pattern in the posterior costophrenic angles first finding on CXR. ``` Buzzwords: Apical to basal gradient: worse in lower lobes Traction bronchiectasis and honeycombing Honeycombing -70%. Histology = Heterogeneous ```

Question 73

What is NSIP?

Answer 73

Nonspecific Interstitial Pneumonia - less common than UIP. Homogeneous inflammation or fibrosis (UIP is heterogeneous). Common pattern in collagen vascular disease and drug reactions. GG alone = cellular GG + reticulation = cellular or fibrotic Reticulation + Traction bronchiectasis = fibrotic NSIP Honeycombing - uncommon and usually minimal in extent. Lower lobe, posterior, peripheral predominance with sparing of the immediate subpleural lung seen in up to 50% of cases. Immediate subpleural sparing is said to be highly suggestive. GG is the NSIP equivalent of honeycombing.

Question 74

Differences between UIP and NSIP?

Answer 74

``` UIP: Apical to basal gradient Heterogeneous histology Honeycombing Traction bronchiectasis ``` ``` NSIP: Gradient is less obvious (but still more in lower lobes) Homogeneous histology Ground glass Micronodules ```

Question 75

Prognosis of interstial lung disease

Answer 75

``` Best = cellular NSIP OK = fibrotic NSIP Terrible = UIP/IPF ```

Question 76

What are RB-ILD and DIP?

Answer 76

Spectrum of smoking-related diseases ``` RB-ILD = apical centrilobular GG nodules DIP = More diffuse GGO with patchy or subpleural distribution. ``` RB-ILD = respiratory bronchiolitis + symptoms. Tends to be more upper lobe predominant (DIP is more lower lobe predominant). Localized centrilobular GG nodules. Pathology tends to involve the entire cross section of the lung. DIP: End spectrum of RB-ILD. Peripheral lower lobe predominant GG, with small cystic spaces.

Question 77

What is Sarcoid?

Answer 77

Multi-system disease that creates "non-caseating granulomas" 20-40 African American female. Lungs are most common organ affected. Angiotensin-converting enzyme is elevated Hypercalcemia 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 of nodules) with satellite nodules

Question 78

CXR stages of sarcoid

Answer 78

``` 0 = normal 1 = HIlar/Mediastinal Nodes Only 2 = Nodes + Parenchyma Disease 3 = Parenchymal Disease 4 = End stage fibrosis ```

Question 79

What are the stages of CHF?

Answer 79

1 = Redistribution - Wedge pressure 13-18 Cephalization of vessels. Big heart, big vascular pedicle 2 = Interstitial Edema - Wedge pressure 18-25 Kerley lines, peribronchial cuffing, less distinct contour of central vessels 3 = Alveolar Edema - Wedge pressure >25 Airspace "fluffy" opacity, pleural effusion

Question 80

What are the immediate complications of lung transplant (<24 hrs)?

Answer 80

Donor-recipient size mismatch - Mismatch up to 25% is okay. Can have a compressed lung (by hyperexpanded emphysematous lung). Imaging is usually atelectasis. Hyperacute Rejection- Secondary to HLA and ABO antigens. Rapid and often fatal. Imaging shows homogeneous infiltration.

Question 81

What are the early complications of lung transplant (24 hours - 1 week)?

Answer 81

Reperfusion injury - Peaks at day 4 as a non-cardiogenic edema related to ischemiai-reprofusion. Typically improves by day 7. Air Leak/Persistent Pneumothorax - Defined as a continuous leak for more than 7 days.

Question 82

What are the Intermediate Complications of lung transplant (8 days - 2 months)?

Answer 82

Acute Rejection - Ground glass opacities and intralobular septal thickening. (No GG - no rejection). Improves with steroids. Bronchial Anastomotic Complications - Leaks can occur in the first month, sternosis can develop later (2-4 months)

Question 83

What are the Late Complications of lung transplant (2-4 months)?

Answer 83

CMV Infection - The MC opportunistic infection. GG, TIB. Rare before 2 weeks.

Question 84

What are the Later Complications of lung transplant (>4 months)?

Answer 84

Chronic Rejection - Bronchiolitis Oblierans. Affects 50% at 5 years. Bronchiectasis, bronchial wall thickening, air trapping. Cryptogenic Organizing Pneumonia - Occurs with chronic rejection (but more commonly with acute rejection). Responds to steroids. PTLD - Typically seen w/in the first year. EBV in 90% Upper lobe fibrosis - Associated with chronic rejection.

Question 85

What is Chronic Rejection/Bronchiolitis Obliterans Syndrome?

Answer 85

Major late complication- affects at least half of the transplants at 5 years (MC at 6 months). Term bronchiolitis obliterans is often used interchangeably with chronic rejection = bronchiectasis, bronchial wall thickening, air trapping, and interlobular septal thickening. Just think air trapping on expiration seen at or after 6 months = chronic rejection.

Question 86

What is the MC recurrence of primary disease after transplant?

Answer 86

Sarcoidosis - ~35%.

Question 87

What is Pulmonary Alveolar Proteinosis (PAP)?

Answer 87

Show crazy paving lung (interlobular septal thickening, with GG). Can be primary or secondary - Secondary can be cancer or inhalation (silico-proteinosis) Increased risk of Nocardia infections and can be nocardia brain abscess. Smoking is strongly associated When seen in children (before age 1) a known association with alymphoplasia. Can progress to pulmonary fibrosis.

Question 88

What does Pulmonary Alveolar Proteinosis (PAP) assocaited with?

Answer 88

Nocardia infections - can get Nocardia brain abscesses. Smoking strongly associated When seen in children (<1) - known association with alymphoplasia Can progress to pulmonary fibrosis.

Question 89

What Endogenous Lipoid Pneumonia?

Answer 89

More common than exogenous type - results from post-obstructive process (cancer) causing building up of lipid laden macrophages.

Question 90

What is the Atoll Sign and DDx?

Answer 90

Reverse Halo - Consolidation around a GG center ``` Cryptogenic Organizing Pneumonia - classic Fugal pneumonia TB Wegeners Pulmonary Infarct ```

Question 91

What is Chronic Eosinophilic Pneumonia?

Answer 91

Idiopathic or associated with known antigen. Peripheral eosinophilia is usually present. Asthma history about 50%. Looks exactly like COP. CT: Peripheral GGO or consolidation. Upper lobes tend to be favored.

Question 92

What is Hypersensitivity Pneumonitis?

Answer 92

Inhaled organic antigens. Subacute: Patchy GGO. Ill-defined centrilobular GG nodules. Often has mosaid perfusion, and air trapping. Chronic: Looks like UIP + air trapping. Traction bronchiectasis and air trapping. Buzzword is "headcheese" b/c it's a mix of everything (GG, Consolidation, Air-trapping, and normal lung).

Question 93

What does chronic HSP look like?

Answer 93

"Head cheese" - Looks like UIP + air trapping. Traction bronchiectasis and air trapping. Buzzword is "headcheese" b/c it's a mix of everything (GG, Consolidation, Air-trapping, and normal lung).

Question 94

What is the Halo sign and DDx?

Answer 94

Nodule with GG around it Represents hemorrhage/invasion into surrounding tissues ``` DDx: Invasive Aspergillosis - classic Other fungus Hemorrhagic Mets Wegeners ```

Question 95

What is Relapsing Polychondritis?

Answer 95

Spares the posterior membrane. Diffuse thickening of the trachea. NO CALCIFICATIONS Characterized by recurrent episodes of cartilage inflammation, and recurrent pneumonia.

Question 96

What is Tracheobronchoplathia Osteochondroplastica (TBO)?

Answer 96

Spares the posterior membrane. | Cartilaginous and osseous nodules within the submucosa of the tracheal and bronchial walls.

Question 97

What does Amyloidosis of the trachea look like?

Answer 97

Irregular focal or short segment thickening, which can involve the posterior membrane. Calcifications are common.

Question 98

Tracheal pathologies that involve and spare the posterior membrane

Answer 98

Spares the Posterior Membrane: Relapsing Polychondritis - Recurrent episodes of cartilage inflammation (ears, nose, joints, laryngeal and thyroid cartilage). Recurrent pneumonia is the MC cause of death. Tracheobronchopathia Osteochondroplastica (TBO)- Development of cartilaginous and osseous nodules. Typically occurs in men older than 50. Does NOT spare the posterior membrane: Amyloid: Often confined to the trachea and main bronchi. Calcs are common. Wegeners: C-ANCA +, sub-glottic trachea is MC location.

Question 99

What Saber Sheath Trachea?

Answer 99

Coronal diameter is less than 2/3 the sagittal diameter. Older men w/ COPD. Main bronchi will be normal in size. Tracheal wall will be normal in thickness.

Question 100

What are the tracheal tumors?

Answer 100

SCC - MC. Associated with smoking. Often multifocal (10%), favors the lower trachea/proximal bronchus. Adenoid Cystic- 2nd MC. Favors the upper trachea and prefers the posterior lateral trachea. Varible look - can be thickening, a mass, or a nodule. Mets- Usually via direct extension (lung, thyroid, esophagus) Squamous Cell Papilloma- MC benign tumor. When it's a single papilloma think smoking. When it's multiple think HPV.

Question 101

What percentage of primary ciliary dyskinesia patients have Kargagener's Syndrome?

Answer 101

50%. Kartagener Syndrome: Primary Ciliary Dyskinesia + Situs Inversus

Question 102

Difference between CF and Primary Ciliary Dyskinesia?

Answer 102

CF: Abnormal mucus, cilia cannot move it; Normal sperm, absent vas deferens; Upper lobe bronchiectasis Primary Ciliary Dyskinesia: Normal mucus, cilia don't work; Abnormal sperm (they can't swim), normal vas deferens; Lower lobe bronchiectasis.

Question 103

What is Williams Campbell Syndrome?

Answer 103

Congenital cystic bronchiectasis from the deficiency of cartilage in the 4th-6th order bronchi.

Question 104

What is Follicular Bronchitis?

Answer 104

Inflammatory process seen in RA or Sjogrens. Not well understood and related to some lymphoid hyperplasia. Looks like centrilobular GGN with scattered areas of bronchial dilation.

Question 105

Pulmonary manifestations of Lupus?

Answer 105

More pleural effusions and pericardiac effusions than with other connective tissue disease. Fibrosis is uncommon. Can get "shrinking lung."

Question 106

Pulmonary manifestations of RA?

Answer 106

Looks like UIP and COP. Lower lobes are favored. Reticulations with or w/o honeycombing, and consolidative opacities which are organizing pneumonia.

Question 107

Pulmonary manifestations of Scleroderma?

Answer 107

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

Question 108

Pulmonary manifestations of Sjogrens?

Answer 108

LIP Extensive GG attenuation with scattered thin walled cysts

Question 109

Pulmonary manifestations of Ankylosing Spondylitis?

Answer 109

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

Question 110

What is Caplan Syndrome?

Answer 110

RA + Upper lobe predominant lung nodules. Can cavitate and there may also be a pleural effusion

Question 111

What is "Shrinking Lung"?

Answer 111

Progressive loss of lung volume in both lungs seen in patients with Lupus. ("S"hrinking "L"ung for "SLe") Etiology is either diaphragm dysfunction of pleuritic chest pain.

Question 112

What is Hepatopulmonary Syndrome?

Answer 112

"Shortness of breath when sitting up" - Opposite of CHF. Develop distal vascular dilation in the lung bases (subpleural telangectasia), with dilated subpleural vessels that don't taper and instead extend to the pleural surface. Sits up and they engorge and shunt blood = SOB. Tc MAA scan will show shunting with tracer in the brain (outside the lungs). Will have to tell you cirrhosis, show you a cirrhotic liver or give you classic history.

Question 113

DDx of pleural plaques other than asbestos

Answer 113

Old Hemothorax Old infection TB Extraskeletal osteosarcoma

Question 114

What is Fibrous Tumor of the Pleura?

Answer 114

Solitary tumor arising from the visceral pleura. Not associated with asbestosis, smoking, or other environmental pollutants. Can get very large and be a source of chest pain - 50% incidental. Hypoglycemia and hypertrophic osteoarthropathy.

Question 115

Mets to pleura

Answer 115

Lung cancer Breast Lymphoma Pleural effusion is MC manifestation

Question 116

What is Empyema Necessitans?

Answer 116

Empyema that eats through the chest wall and into the soft tissues. Classically - TB, second is Actinomyces.

Question 117

When is a Superior Sulcus (Pancoast) tumor unresectable?

Answer 117

Brachial Plexus involvement above T1 (C8 or higher) Diaphragm Paralysis (infers involvement of C3-4-5) Greater than 50% vertebral body Distal Nodes or mets

Question 118

How to tell thymic rebound vs residual lymphoma?

Answer 118

PET may help - both are hot, but lymphoma is hotter MRI- Thymic rebound should drop out on in-out phase imaging (has fat in it). Lymphoma will not drop out.

Question 119

Associations with Thymoma

Answer 119

Myasthenia Gravis Pure Red Cell Aplasia Hypogammaglobulinemia

Question 120

Thymic lesion that is fatty mass with interspersed soft tissue?

Answer 120

Thymolipoma

Question 121

What are mediastinal teratomas associated with?

Answer 121

Klinefelter Syndrome

Question 122

Causes of Pulmonary Artery Aneurysm/Pseudoaneurysm

Answer 122

Iatrogenic from Swan Ganz Catheter - MC - ICU PATIENT Behcets - TURKISH DECENT, MOUTH AND GENITAL ULCERS Chronic PE

Question 123

What is Hughes-Stovin Syndrome?

Answer 123

PA aneruysm that is similar to Behcets. Recurrent thrombophlebitis and PA aneurysm formation and rupture.

Question 124

What is Rasmussen Aneurysm?

Answer 124

PA pseudoaneurysm 2/2 pulmonary TB. Upper lobes in the setting of reactivation TB.

Question 125

What is Pulmonary HTN?

Answer 125

PA pressure >25 mmHg Primary: Idiopathic Secondary: Chronic PE, RHF, Lung parenchyma problems

Question 126

What is Pulmonary Veno-Occlusive Disease?

Answer 126

Cause of pulm HTN that affects the post capillary pulmonary vasculature. PAH + normal wedge - differentiates it from LH issues.

Question 127

What is the Macklin Effect?

Answer 127

MC cause of pneumediastinum in trauma. Alveolar rupture from blunt trauma and air dissects along bronchovascular sheaths into the mediastinum

Question 128

What is an Extrapleural Hematoma?

Answer 128

Injury to chest wall that damages the pariental pleura then get a hemothorax Have injury to the chest wall but parietal pleura is still intact get extrapleural hematoma. "Persistent fluid collection after pleural drain/tube placement" Displaced extrapleural fat.

Question 129

What is Fat Embolization Syndrome?

Answer 129

Long bone fracture or intramedullary rod placement. Fat embolized to lungs, brain, and skin (clinical: rash, AMS, and SOB). 1-2 days after femur fracture. GG makes you think pulmonary edema. Will not see filling defect.

Question 130

ACR appropriateness first line for suspected metastatic disease?

Answer 130

CXR

Question 131

ACR appropriateness recommendation for patients on mechanical ventilation?

Answer 131

Daily CXR

Question 132

ACR appropriateness first line for chest pain and high suspicion for aortic dissection?

Answer 132

CXR