CTC Chest Flashcards
How are lateral CXRs taken?
Left lateral position - left side against film.
Left ribs will not be magnified.
Right ribs will be magnified and be more posterior
What is the normal hilum on a lateral CXR?
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.
What is Raider Triangle?
What variant runs through it?
Sits on the aortic arch posterior to the trachea and anterior to the vertebral bodies.
Aberrant right subclavian artery will obliterate this.
How are the heart valves drawn on CXR?
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.
If you see two metallic heart valves on a CXR, which is bigger?
Mitral and aortic - Mitral is bigger.
Pacer wire going through a valve makes it the tricuspid valve.
How is the R major fissure oriented with the left on the lateral CXR?
Right is anterior to the left.
How many pulmonary segments are there in the R and L lungs?
R = 10 (3 upper, 2 middle, and 5 lower)
L = 8 (4 upper/lingula and 4 lower)
What is in the posterior mediastinum?
Esophagus, thoracic duct, and descending aorta.
Trachea is in middle.
What is the MC pulmonary venous variation?
Separate vein draining the RML
Usually have upper and lower on each side.
What is Proximal Interruption of the PA?
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
What is interrupted L PA associated with?
TOF and Truncus
What does infection with Anthrax look like?
Hemorrhagic lymphadenitis, mediastinitis, and hemothrax.
Classic look: Mediastinal widening with pleural effusion in the setting of bio-terrorism.
What does Klebsiella pneumonia look like?
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.
What does H. flu pneumonia look like?
Usually bronchitis, sometimes bilateral lower lobe bronchopneumonia.
COPDers and ppl w/o a spleen
Post Bone Marrow Transplant lung findings
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
What does post bone marrow transplant GVH pulmonary disease look like?
Acute (20-100 days): Favors extrapulmonary symptoms (skin, liver, GI tract)
Chronic (>100 days): Lymphocytic infiltration of the airways and obliterative bronchiolitis.
Infections in AIDS by CD4
> 200: Bacterial infections, TB
<200: PCP; Atypical mycobacterial
<100: CMV, disseminated fungal, mycobacterial
CT patterns with pulmonary infection with AIDS
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).
AIDS trivia and buzzwords
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
What are the stages of TB?
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.
What is pleural involvement with TB?
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.
Facts about TB
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.
What are the patterns of Non-Tuberculous Mycobacteria?
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.
What does Aspergillus look like with normal immune, immune depressed, or hyperimmune?
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
What does Mucomycosis of the lungs look like?
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.
What is Lemierre Syndrome?
Jugular vein thrombosis with septic emboli - usually seen after oropharyngeal infection or recent ENT surgery.
Fusobacterium Necrophorum
What causes Lemierre Syndrome?
Fusobacterium Necrophorum
Jugular vein thrombosis with septic emboli - usually seen after oropharyngeal infection or recent ENT surgery.
What are the guidelines for lung cancer screening?
Low dose CT for asymptomatic - 55-80 with 30 pack-year history and currently smoke (or have quit w/in the past 15 years)
What are the four “benign” calcification patterns with pulmonary nodules?
Solid/diffuse
Laminated
Central
Popcorn
Qualities of nodules that make you thing benign vs cancer?
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
What findings of a GG nodule on PET make you think cancer vs infection?
HOT = infection COLD = cancer
Paraneoplastic syndromes with squamous and small cell lung cancers?
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
What is Lambert Eaton Syndrome?
Paraneoplastic syndrome with small cell - proximal weakness from abnormal release of ACh at the NM junction. Usually comes before cancer diagnosis
What are the precursor lesions of lung cancer?
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).
What stage of lung cancer is unresectable?
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.
MC extrathoracic causes of lymphatic carcinomatosis?
Breast, stomach, pancreas, and prostate.
How is carcinoid classified?
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.
What is Adenoid Cystic Carcinoma?
MC bronchial gland tumor. NOT associated with smoking. Usually in the main or lobar bronchus.
More common than carcinoid in the trachea.
Differences between primary, secondary, PTLD, and AIDS related pulmonary lymphoma?
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
Differences between Secondary NHL and HL
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.
AIDS patient with lung nodules, pleural effusion, and LAD =
Lymphoma
Things to know about Kaposi Sarcoma?
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.
Difference between Kaposi and Lymphoma on Gallium and Thallium
Kaposi: Thallium positive and Gallium Negative
Lymphoma: Thallium positive and Gallium positive
What can pulmonary hamartomas look like on PET?
Can be hot.
What is Swyer-James?
Unilateral lucent lung.
After viral infection in childhood resulting in post infectious obliterative bronchiolitis - from constrictive bronchiolitis. SMALLER lung - not hyperexpanded.
What is Pulmonary Langerhans Cell Histiocytosis (LCH)?
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
What diseases spare the costophrenic angles?
LCH
HSP
Differences between LCH and LAM?
LCH:
Cysts and nodules; Smoker; Upper and mid lungs; Thicker cysts (bizarre)
LAM:
Cysts (no nodules); Women, patients with TS; Difuse; Thin round cysts
Differences in cysts with LCH, LAM and Birt Hogg Dube?
LCH: Bizarre shape, thick walled
LAM: Round, thin walled
BHD: Oval, thin wall
What is Birt Hogg Dube?
Cystic lung disease with thin walled “oval” shaped cysts.
Association with renal findings (bilateral oncocytomas and chromophobe RCCs)
Also have skin stuff.
What is Lymphocytic Interstitial Pneumonia (LIP)?
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.
LIP =
Sjogrens and HIV
LIP in a kid =
HIV
What is Pneumocystis Pneumonia (PCP)?
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)
Emphysema with central dot sign?
Centri-lobular emphysema.
Central dot represents central bronchovascular bundle.
What is Pan-lobular emphysema?
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.
What is Vanishing Lung Syndrome?
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.
Things to know about Asbestos?
“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.
What are Benign Asbestos Related Changes?
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”
What is Malignant Mesothelioma?
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.
What is Silicosis?
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).
What is Progressive Massive Fibrosis?
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.
What is Silicotuberculosis?
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.
Look of cancer vs progressive massive fibrosis on MRI?
Cancer = T2 bright
PMF = T2 dark.
What is Berryliosis?
Metal used in aircraft and space industries.
Generalized granulomatous disease with hilar adenopathy and upper lobe predominant reticular opacities.
What is Silo Filler’s Disease?
Nitrogen Dioxide
Pulmonary edema pattern. Recovery is typically w/in 5 weeks.
What is Talcosis?
Filler in tablets, sometimes injected (along with drugs) in IVDU.
Hyperdense micronodules with conglomerate masses (similar to PMF). GGO.
DDx of Perilymphatic Nodules?
Sarcoid - 90%
Lymphangitic spread of CA
Silicosis
DDx of Random Nodules?
Miliary TB
Mets
Fungal
DDx of Centrilobular Nodules?
Infection
RB-ILD
HSP (if ground glass)
What are Idiopathic Interstitial Pneumonas?
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.
What is UIP?
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
What is NSIP?
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.
Differences between UIP and NSIP?
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
Prognosis of interstial lung disease
Best = cellular NSIP OK = fibrotic NSIP Terrible = UIP/IPF
What are RB-ILD and DIP?
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.
What is Sarcoid?
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
CXR stages of sarcoid
0 = normal 1 = HIlar/Mediastinal Nodes Only 2 = Nodes + Parenchyma Disease 3 = Parenchymal Disease 4 = End stage fibrosis
What are the stages of CHF?
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
What are the immediate complications of lung transplant (<24 hrs)?
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.
What are the early complications of lung transplant (24 hours - 1 week)?
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.
What are the Intermediate Complications of lung transplant (8 days - 2 months)?
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)
What are the Late Complications of lung transplant (2-4 months)?
CMV Infection - The MC opportunistic infection. GG, TIB. Rare before 2 weeks.
What are the Later Complications of lung transplant (>4 months)?
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.
What is Chronic Rejection/Bronchiolitis Obliterans Syndrome?
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.
What is the MC recurrence of primary disease after transplant?
Sarcoidosis - ~35%.
What is Pulmonary Alveolar Proteinosis (PAP)?
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.
What does Pulmonary Alveolar Proteinosis (PAP) assocaited with?
Nocardia infections - can get Nocardia brain abscesses.
Smoking strongly associated
When seen in children (<1) - known association with alymphoplasia
Can progress to pulmonary fibrosis.
What Endogenous Lipoid Pneumonia?
More common than exogenous type - results from post-obstructive process (cancer) causing building up of lipid laden macrophages.
What is the Atoll Sign and DDx?
Reverse Halo - Consolidation around a GG center
Cryptogenic Organizing Pneumonia - classic Fugal pneumonia TB Wegeners Pulmonary Infarct
What is Chronic Eosinophilic Pneumonia?
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.
What is Hypersensitivity Pneumonitis?
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).
What does chronic HSP look like?
“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).
What is the Halo sign and DDx?
Nodule with GG around it
Represents hemorrhage/invasion into surrounding tissues
DDx: Invasive Aspergillosis - classic Other fungus Hemorrhagic Mets Wegeners
What is Relapsing Polychondritis?
Spares the posterior membrane.
Diffuse thickening of the trachea.
NO CALCIFICATIONS
Characterized by recurrent episodes of cartilage inflammation, and recurrent pneumonia.
What is Tracheobronchoplathia Osteochondroplastica (TBO)?
Spares the posterior membrane.
Cartilaginous and osseous nodules within the submucosa of the tracheal and bronchial walls.
What does Amyloidosis of the trachea look like?
Irregular focal or short segment thickening, which can involve the posterior membrane.
Calcifications are common.
Tracheal pathologies that involve and spare the posterior membrane
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.
What Saber Sheath Trachea?
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.
What are the tracheal tumors?
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.
What percentage of primary ciliary dyskinesia patients have Kargagener’s Syndrome?
50%.
Kartagener Syndrome: Primary Ciliary Dyskinesia + Situs Inversus
Difference between CF and Primary Ciliary Dyskinesia?
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.
What is Williams Campbell Syndrome?
Congenital cystic bronchiectasis from the deficiency of cartilage in the 4th-6th order bronchi.
What is Follicular Bronchitis?
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.
Pulmonary manifestations of Lupus?
More pleural effusions and pericardiac effusions than with other connective tissue disease.
Fibrosis is uncommon. Can get “shrinking lung.”
Pulmonary manifestations of RA?
Looks like UIP and COP. Lower lobes are favored.
Reticulations with or w/o honeycombing, and consolidative opacities which are organizing pneumonia.
Pulmonary manifestations of Scleroderma?
NSIP > UIP; lower lobe predominant findings.
Look for dilated fluid filled esophagus.
Pulmonary manifestations of Sjogrens?
LIP
Extensive GG attenuation with scattered thin walled cysts
Pulmonary manifestations of Ankylosing Spondylitis?
Upper lobe fibrobullous disease
Usually unilateral first, then progresses to bilateral.
What is Caplan Syndrome?
RA + Upper lobe predominant lung nodules.
Can cavitate and there may also be a pleural effusion
What is “Shrinking Lung”?
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.
What is Hepatopulmonary Syndrome?
“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.
DDx of pleural plaques other than asbestos
Old Hemothorax
Old infection
TB
Extraskeletal osteosarcoma
What is Fibrous Tumor of the Pleura?
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.
Mets to pleura
Lung cancer
Breast
Lymphoma
Pleural effusion is MC manifestation
What is Empyema Necessitans?
Empyema that eats through the chest wall and into the soft tissues.
Classically - TB, second is Actinomyces.
When is a Superior Sulcus (Pancoast) tumor unresectable?
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
How to tell thymic rebound vs residual lymphoma?
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.
Associations with Thymoma
Myasthenia Gravis
Pure Red Cell Aplasia
Hypogammaglobulinemia
Thymic lesion that is fatty mass with interspersed soft tissue?
Thymolipoma
What are mediastinal teratomas associated with?
Klinefelter Syndrome
Causes of Pulmonary Artery Aneurysm/Pseudoaneurysm
Iatrogenic from Swan Ganz Catheter - MC - ICU PATIENT
Behcets - TURKISH DECENT, MOUTH AND GENITAL ULCERS
Chronic PE
What is Hughes-Stovin Syndrome?
PA aneruysm that is similar to Behcets.
Recurrent thrombophlebitis and PA aneurysm formation and rupture.
What is Rasmussen Aneurysm?
PA pseudoaneurysm 2/2 pulmonary TB.
Upper lobes in the setting of reactivation TB.
What is Pulmonary HTN?
PA pressure >25 mmHg
Primary: Idiopathic
Secondary: Chronic PE, RHF, Lung parenchyma problems
What is Pulmonary Veno-Occlusive Disease?
Cause of pulm HTN that affects the post capillary pulmonary vasculature.
PAH + normal wedge - differentiates it from LH issues.
What is the Macklin Effect?
MC cause of pneumediastinum in trauma.
Alveolar rupture from blunt trauma and air dissects along bronchovascular sheaths into the mediastinum
What is an Extrapleural Hematoma?
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.
What is Fat Embolization Syndrome?
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.
ACR appropriateness first line for suspected metastatic disease?
CXR
ACR appropriateness recommendation for patients on mechanical ventilation?
Daily CXR
ACR appropriateness first line for chest pain and high suspicion for aortic dissection?
CXR
