Thoracic Flashcards
What are the two types of pulmonary sequestration and how are they different?
Both are a “bronchopulmonary foregut malformation.” Abnormal lung tissue with no connection to the bronchial tree and systemic arterial supply.
Intralobar- more common (75%). Venous drainage through the pulmonary veins.
Extralobar- more common in the left lower lobe, rarely can be seen below the diaphragm. Has its own pleura. Systemic venous drainage. Usually presents earlier. Associated with other anomalies (diaphragmatic hernia, congenital heart disease, CCAM), and may be connected to the GI tract.
Patient with recurrent epistaxis. Diagnosis?
Genetics?
Multiple (coiled) AVMs in hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu). Telangiectasia, recurrent epistaxis, and multiple-organ AV malformations.
Autosomal-dominant disorder of variable penetrance, chromosomes 9 and 12.
Diagnosis?
Other imaging findings?
Associations?
Proximal interruption of the (right) pulmonary artery. Can occur on either side, typically on the side opposite the aortic arch. The distal pulmonary vasculature receives blood from systemic collaterals.
Volume loss of the affected hemithorax and deviation of the mediastinum to the affected side.
Interruption of the left PA is associated with congenital heart disease, including tetralogy of Fallot and truncus arteriorus.
Genetics of alpha1-antitrypsin deficiency?
Complications?
Inherit 2 protease inhibitor deficiency alleles of the AAT gene on chromosome 14. Leads to absent or reduced serum levels of AAT (a protein that prevents enzymes such as elastase from digesting normal tissue).
Panlobular emphysema, greatest in the lower lungs. Can also develop liver disease (cholestasis and cirrhosis), have an increased risk of HCC.
What is a Pancoast tumor?
What stage?
Symptoms of Pancoast syndrome?
A primary lung cancer in the apex that invades the chest wall and thoracic inlet. Usually a non-small cell cancer: 40% SCC, 20% adenocarcinoma, 25% anaplastic or poorly differnetiated.
T3 due to chest wall invasion. T4 if invasion extends to mediastinum or vertebral body.
Shoulder and arm pain (usually along C8-T2 distributions), Horner syndrome (ptosis, ipsilateral myosis, anhidrosis), weakness and atrophy of the muscles of the hand.
Most common imaging appearance of small cell lung cancer?
Demographic?
Staging?
Large, bulky mediastinal or hilar mass causing bronchial narrowing or obstruction.
Almost exclusively in smokers. More common in men. Presents younger than non-small-cell, worse prognosis. Arises from the epithelium of the proximal airways (neuroendocrine cells), and is considered a type of neuroendocrine carcinoma- some secrete metabolically active substances).
Pre-2013, was classified as limited (tumor confined to one hemithorax, the mediastinum, and one ipsilateral supraclavicular node) or extensive (metastatic to the contralateral hemithorax or beyond, or if can’t be encompassed by one radiation port). Now uses same TMN system as non-small cell.
What are some things on the differential diagnosis for ground glass opacities?
Low grade adenocarcinoma (BAC), pneumonia (viral, PCP, or atypical- legionella, mycoplasma, chlamydia), DIP, NSIP, pulmonary edema, drug toxicity, alveolar hemorrhage.
This patient has chronic TB. Diagnosis?
Rasmussen aneurysm- a rare complication of pulmonary TB that can cause massive hemoptysis.
It is a pulmonary artery pseudoaneurysm which develops as a result of direct continuity with the fibrocaseous TB infection, get direct invasion of the artery wall (versus typical mycotic aneurysm caused by septic emboli).
What is this pattern?
What is the etiology?
What disease processes can cause it?
Tree in bud pattern.
Caused by bronchiolar impaction and dilation by pus/mucus/fluid/inflammatory exudate.
Nonspecific- mostly caused by infections/inflammatory conditions. Possibilities include: active TB, MAI, viral pneumonia, fungal pneumonia, obliterative bronchiolitis, cystic fibrosis, immotile cilia syndrome, RA, and neoplastic.
25 year old with asthma and chronic cough. Diagnosis?
Cause?
Allergic bronchopulmonary aspergillosis (ABPA). Imaging findings: upper lobe predominant central bronchiectasis, mucus plugging (may be high density due to presence of fungus), and pulmonary consolidation (may represent eosinophilic pneumonia).
A rare complication of persistent asthma and cystic fibrosis. A hypersensitivity reaction to Aspergilus organisms, which colonize and multiply in mucus. The fungus does not invade tissue. Marked local and systemic eosinophilia.
What are 2 possible appearances of Klebsiella pneumonia?
One of the Gram-negative bacilli that is commonly seen in hospital acquired pneumonias. Very commonly cavitates. Can also cause lobar consolidation with lobar expansion and bulging of the interlobar fissures (bulging fissure sign, below).
What are some of the typical imaging features of viral pneumonia?
Common causative organisms in immunocompetent / immunocompromised hosts?
Reflects the combination of interstitial and air-space disease. May see: multifocal, poorly defined areas of patchy consolidation, ground-glass opacities, centrilobular nodules, reticular opacities (resulting from interlobular septal thickening), consolidation, bronchial wall thickening, atelectasis.
Immunocompetent: Influenza A and B, adenovirus, Epstein-Barr virus, hantavirus.
Immunocompromised: CMV, herpes simplex, varicella-zoster, measles, adenovirus.
AIDS patient. Diagnosis?
Other imaging appearances?
Pneumocystis pneumonia. An opportunistic infection caused by Pneumocystis jiroveci. Most common in AIDS patients with profound T-cell immunosuppression, less commonly seen in patients with other forms of immunosuppression.
Imaging appearance: Ground-glass opacities in the parahilar regions and upper lobes. Severe cases may present with dense air-space consolidation. If there is interlobular septal thickening, can have crazy-paving pattern. May develop pulmonary cysts (risk of spontaneous pneumothorax). Chest x-ray can be normal. Pleural effusion and LAD uncommon.
What causes tracheobronchial papillomatosis?
Imaging appearance?
Human papillomavirus infection (types 6 and 11), usually acquired at birth from a mother with genital papillomas. The virus induces a papillary proliferation of epithelial cells, which projects into the lumen of affected airways.
The most common site of involvement is the larynx > trachea > lung parenchyma. If in the lungs, see multiple small pulmonary nodules that may cavitate. Risk of malignant transformation to SCC or adenocarcinoma.
In an immunosuppressed patient (especially neutropenic), what should a dense nodule with surrounding ground glass halo make you think of?
Angioinvasive aspergillosis. The ground-glass represents alveolar hemorrhage and the consolidation corresponds to a focus of infarction.
Could also be other fungal infection (esp mucormycosis, less likely candidiasis or coccidiomycosis). About half of these nodules evolve to cavitation.
Patient with right lung transplant 3 days ago. Diagnosis? Appearance on CT?
Differential?
Reperfusion pulmonary edema. Noncardiogenic pulmonary edema commonly seen in the first 2-3 days after lung transplant.
On CT, see ground-glass opacities that may progress to consolidation. Start in the perihilar regions. May also see interlobular septal thickening.
If the opacities last beyond 10 days, think of other causes such as rejection or pneumonia.
HIV positive patient. Diagnosis?
What is this condition?
Multicentric Castleman disease (multicentric because of simultaneous involvement of different anatomic sites).
Castleman disease (aka angiofollicular lymph node hyperplasia) - is an uncommon benign lymphoproliferative condition. Most commonly described as a solitary mediastinal mass. In the HIV population, mediated by HHV type 8.
45 year old woman with an autoimmune disease. Diagnosis? What underlying disease is she most likely to have?
What about if she was a child?
Cause of this diagnosis?
Lymphocytic interstitial pneumonia. Imaging findings consist of ground-glass opacities, centrilobular nodules, bronchovascular bundle thickening, and pulmonary cysts. The lower lobes are most involved.
Most common in middle aged women with some sort of immune dysfunction, most commonly Sjögren syndrome. Other conditions include autoimmune thyroiditis and lupus.
In children, LIP is considered to be an AIDS-defining illness.
This is a lymphoproliferative condition in which the lungs are diffusely infiltrated with benign lymphoid elements, especially in the interlobular and alveolar septa.
What is re-expansion pulmonary edema?
Pulmonary edema developing following rapid re-expansion of a lung collapsed by pneumothorax or large effusion (especially if it was collapsed > 72 hours). Edema can rarely be bilateral.
A patient comes in with heroin overdose, shortness of breath, and bilateral alveolar opacities. Diagnosis?
Heroin-induced pulmonary edema. A rare but serious complication of heroin overdose. Caused by increased capillary permeability, not heart failure. Can also see patchy atelectasis and nodular opacities.
Note- cocaine is known to produce both cardiogenic and noncardiogenic pulmonary edema.
What are the manifestations of asbestos-related pleural disease?
Earliest manifestation- pleural effusion. Typically hemorrhagic, occurs ~10 years after exposure, then should resolve.
Most common manifestation- pleural plaques. Occur 20-30 years after exposure. Commonly bilateral, involve mid and lower pleural surfaces, calcified in ~15%. Composed mainly of acellular collagen.
Malignant mesothelioma- 20+ years post exposure; recurrence of effusion, nodular and enhancing pleural thickening, invasion of adjacent structures.
60 year old miner. Diagnosis?
Early appearance?
Complicated silicosis (progressive massive fibrosis). This is the most prevalent pneumoconiosis, a result of silicone dioxide depositing in the respiratory bronchioles. Seen in mining, tunneling, quarrying, sandblasting, polishing, and stonecutting.
Simple silicosis- multiple small (1-10 mm) uniform pulmonary nodules, often in a centrilobular distribution. Greatest in the upper lobes, peripherally. Can progress to complicated silicosis (PMF) as in this case- confluent nodules and fibrosis. May see eggshell calcifications in hilar and mediastinal lymph nodes.
What is Caplan syndrome?
Rheumatoid pneumoconiosis. A rare variant of pneumoconioses, seen in patients with rheumatoid disease and lung involvement. Large necrobiotic nodules superimposed on a background of multiple pulmonary nodules.
Woodworker. Diagnosis?
Cause?
Imaging findings?
Hypersensitivity pneumonitis (acute-subacute). A result of inhalation of airborne particles, which cause an immune mediated reaction. Causative particles include bacteria, fungi, avian proteins, wood dusts, and chemical compounds.
Acute/subacute- centrilobular ground glass nodules and patchy ground glass opacities, air trapping (due to respiratory bronchiolitis). Usually greatest in the mid lungs.
Chronic- air trapping, interstitial fibrosis with traction bronchiectasis, may develop some honeycoming, tends to be worst in the upper lungs. Poor prognosis if fibrosis develops.
What is the cause of pulmonary alveolar proteinosis?
Types?
Abnormal intra-alveolar accumulation of surfactant-like lipoproteinaceous material due to reduced clearance. Bilateral air-space disease on CXR, greatest in the parahilar regions and mid lungs. Typically spares apices and lateral costophrenic angles. Crazy paving on CT.
3 forms:
- Congenital- rare, seen in neonates, poor prognosis.
- Secondary- likely autoimmune, associated with cancer, HIV, some chemicals.
- Idiopathic (acquired)- most common, often men around age 40 with a history of smoking.
Common presentation- cough, dyspnea, fever, hemoptysis, chest pain.
75 year old male with chronic constipation. Diagnosis?
Cause?
Exogenous lipoid pneumonia.
Aspiration of oily substances such as mineral oil induces a foreign body inflammatory reaction. See pulmonary opacity (which often has low density areas within it), lipid-laden macrophages on BAL.
Can also get endogenous lipoid pneumonia: a result of the degeneration of alveolar cell walls distal to an airway obstruction, usually from a lung cancer.
Diagnosis?
Other imaging findings?
Cause?
Differential for these findings?
Relapsing polychondritis.
Smooth anterior and lateral tracheal wall thickening (can calcify), spares the membranous posterior portion. Concentric bronchial wall thickening.
Multisystem autoimmune inflammatory disorder- recurrent episodes of inflammation and destruction of cartilaginous tissue. All types of cartilage may be involved. Other sites of involvement - nose (saddle nose deformity), ear, larynx, eyes, large joints, heart.
Differential for the airway involvement - amyloidosis, sarcoidosis, tracheopathia osteochondroplastica (nodular tracheal wall thickening, usually with calcifications, also spares posterior wall).
Diagnosis?
Cause?
Tracheomalacia (tracheobronchomalacia if affects bronchi as well). >50% tracheal narrowing during expiration.
Can be congenital (most common in premature infants) or acquired (secondary). Causes of secondary tracheomalacia include prolonged intubation, trauma, surgery, vascular rings, mediastinal tumors, and inflammation.
What is this sign and what is the diagnosis?
What other sign may be seen?
Dependent viscera sign of diaphragmatic rupture- abdominal viscus lying immediately on top of the posterior ribs due to the lack of diaphragmatic support.
May also see waistlike constriction of the herniated viscus (collar sign), direct visualization of the diaphragmatic defect, thickened diaphragmatic crus.
40 year old man with chest pain following upper GI endoscopy. Diagnosis?
Possible complication?
Boerhaave syndrome- esophageal perforation following instrumentation or trauma (vomiting, weightlifting, coughing, childbirth, etc). Also see pneumomediastinum, pneumothorax, pneumopericardium, and pleural effusions.
Can lead to polymicrobial mediastinitis and sepsis.
HIV postive patient. Skin thickening on soft tissue windows. Diagnosis?
Imaging findings?
How can nuclear medicine scans help differentiate this from other things on the differential?
Kaposi sarcoma. HIV-related Kaposi sarcoma in patients infected with HHV8. A multicentric disease that may involve the lymph nodes, lung parenchyma, GI tract, and skin.
Bilateral pulmonary nodules in a peribronchovascular distribution, may become coalescent and “flame shaped” (like this case), pleural effusions common. Enhancing lymphadenopathy.
Nuc med can help if unclear diagnosis. Thallium scan: postive in lymphoma and KS. Gallium scan: positive in lymphoma and infection, negative in KS.
In this patient with sickle cell disease, what might be causing the paraspinal masses?
What are some of the common causes of acute chest syndrome?
Extramedullary hematopoiesis. Can confirm with sulfur colloid scan.
Both infectious and noninfectious conditions can lead to ACS: infection (esp chlamydia, mycoplasma), fat embolism, and rib infarction are most common.
Diagnosis?
Rounded atalectasis.
Atalectasis associated with pleural thickening or effusion. Comet tail sign- swirling bronchovascular bundle. The atalectatic lung parenchyma may show homogeneous contrast enhancement. Air bronchograms common.
Diagnosis?
Hamartoma. The most common benign tumor of the lung.
Popcorn calcifications virtually diagnostic. Commonly contain fat. ~20% can be endobronchial- cause symptoms of airway obstruction.
50 year old female with uveitis. Diagnosis?
Other imaging findings in the chest?
Sarcoidosis. An immuneologically mediated granulomatous disase, can affect any organ.
Symmetric hilar and right paratracheal lymphadenopathy; nodes may calcify in an amorphous or eggshell pattern. Small peribronchovascular nodules, typically upper-lobe predominant. End-stage disease can cause upper lobe predominant architectural distortion, traction bronchiectasis, honeycombing, and cysts. Activity on gallium scan results in the “lambda sign” with paratracheal and hilar uptake, and the “panda” sign with lacrimal and parotid uptake.
Diagnosis?
Associated conditions?
Thymoma. Well-defined, homogeneous, smooth anterior mediastinal mass.
Associated with myasthenia gravis, pure red cell aplasia, and hypogammaglobulinemia.
Watch out for invasive thymoma (growth outside the capsule, can cause pleural thickening) and thymic carcinoma (heterogeneous, local invasion, paraneoplastic syndromes uncommon).
45 year old female with sinusitis. Diagnosis?
Other imaging findings?
Granulomatosis with polyangiitis (formerly Wegener).
Multiple pulmonary nodules that may be poorly defined (ground glass halo) due to surrounding hemorrhage. 50% cavitate. Can see diffuse air-space opacitiy as a result of hemorrhage. Airway involvement- focal or elongated segments of stenosis or thickening.
Most likely diagnosis?
Typical imaging findings?
Associated conditions?
Nonspecific interstitial pneumonia (NSIP).
Patchy subpleural ground glass and reticular opacities. Typically immediate subpleural sparing. Lower lobes more frequently involved. May be fibrosis, traction bronchiectasis, subpleural cysts (“microcystic honeycombing”) in advanced disease.
May be idiopathic or secondary to: connective tissue diseases (SLE, scleroderma, Sjogrens, polymyositis, dermatomyositis), other autoimmune diseases (RA, PBC, Hashimoto), drug induced (chemo).
Diagnosis?
Usual interstitial pneumonia (UIP).
Honeycombing, traction bronchiectasis, and architectural distortion. Subpleural distribution with apicobasal gradient. The clinical syndrome is called idiopathic pulmonary fibrosis.
Heavy smoker with a cough. Diagnosis?
Respiratory bronchiolitis-interstitial lung disease (RB-ILD).
Diagnosis?
Complications?
Extra-throacic findings?
Lymphangioleiomyomatosis (LAM). Proliferation of smooth muscle in the pulmonary lymphatics, vessels, and airways. Women of childbearing age. Round, thin-walled, uniformly distributed cysts. Parenchyma between the cysts is normal.
Chylothorax (low density on CT) and pneumothorax.
Renal angiomyolipomas, retroperitoneal cystic masses (lymphangioleiomyomas), lymphadenopathy, and chylous ascites. Can be seen with tuberous sclerosis.
Young adult smoker. Diagnosis?
Imaging features?
Pulmonary Langerhans cell histiocytosis. Peribronchiolar proliferation of Langerhans cells results in granulomatous infiltration. May be an allergic reaction to cigarette smoke.
Irregularly-shaped, upper lobe predominant cysts with variable wall thickness. The costophrenic angles are spared. Scattered small centrilobular nodules. Pneumothorax may occur.
Diagnosis?
Primary ciliary dyskinesia (Kartagener syndrome- a subtype with PCD, situs inversus, and sinusitis). Lower lobe-predominant bronchiectasis. 50% have situs inversus. Also associated with congenital cardiac abnormalities such as transposition, pyloric stenosis, and epispadias. Autosomal recessive.
