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Thoracic Imaging
CORE Radiology
| Question | Answer |
|---|---|
| What are the two direct signs of atelectasis? | 1) Displacement of the lung fissures and 2) vascular crowding |
| What are the 5 indirect signs of atelectasis? | 1) Elevation of the diaphragm, 2) Rib crowding on the side with volume loss, 3) Mediastinal shift to the side with volume loss, 4) Overinflation of adjacent or contralateral lobes and 5) Hilar displacement |
| When does obstructive atelectasis occur? | Obstructive atelectasis occurs when alveolar gas in absorbed by blood circulating through alveolar capillaries but is not replaced by inspried air due to bronchial obstruction |
| When does relaxation atelectasis occur? | When adjacent lung to an intrathoracic lesion causing mass effect, such as a pleural effusion, pneumothorax or pulmonary mass |
| Deficiency of what substance causes adhesive atelectasis? | Surfactant |
| What is cicatricial atelectasis? | Volume loss due to architectural distortion of lung parenchyma secondary to fibrosis |
| What is lobar atelectasis typically caused by? | Central bronchial obstruction by mucus plug (acute) or neoplasm (occurs over a longer period of time, often as an outpatient) |
| Describe the "luftsichel sign." | Luftsichel means air-sickle in German. It is a sign of left upper lobe collapse. It describes a crescent of air seen on frontal radiograph which represents the interface between the aorta and the hyperexpanded superior segment of the left lower lobe. |
| Describe the "Reverse S Sign of Golden." | Reverse S sign of golden is a sign which is seen in right upper lobe collapse caused by an obstructing mass. The central convex margins of the mass form a reverse S. |
| Describe the "Flat waist sign." | The Flat waist sign described the flattening of the left cardiac border as a result of downward shift of hilar structures and resultant cardiac rotation. It is seen in left lower lobe collapse. |
| Round atelectasis is a focal atelectasis with a round morphology that is always associated with what type of abnormality? | Round atelectasis is always associated with an adjacent pleural abnormality such as pleural effusion, thickening, plaque or pleural neoplasm. |
| What is the elemental unit of lung function? | The secondary pulmonary lobule |
| Describe an air bronchogram. | An air bronchogram represents a lucent air-filled bronchus (or bronchiole) seen within a consolidation |
| What are the 4 differential diagnoses for acute consolidation? | 1) Pneumonia (by far the most common cause), 2) Pulmonary hemorrhage, 3) ARDS and 4) Pulmonary edema (though this is an uncommon manifestation) |
| What are the 3 differential diagnoses for chronic consolidation? | 1) Bronchioalveolar carcinoma (mucinous type), 2) Organizing pneumonia and 3) Chronic eosinophilic pneumonia |
| What is "consolidation", histologically speaking? | Histologically, consolidation is opacification due to complete filling of the alveoli with a liquid-like substance (blood, pus, water or cells) |
| What is "ground glass", histologically speaking? | Histologically, consolidation is opacification due to either partial filling of the alveoli (water, blood, pus or cells), alveolar wall thickening or reduced aeration of the alveoli (atelectasis) |
| What are the 4 differential diagnoses for acute ground glass consolidation? | 1) Pulmonary edema, 2) Pneumonia (more commonly seen in atypical pneumonia such as those caused by viral entities or pneumocystis jiroveci), 3) pulmonary hemorrhage and 4) ARDS |
| What are the 6 differential diagnoses for chronic ground glass consolidation? | 1) Bronchioalveolar carcinoma, 2) Organizing pneumonia, 3) Chronic eosinophilic pneumonia, 4) Idiopathic pneumonia, 5) Hypersensitivity pneumonitis and 6) Alveolar proteinosis |
| What are the 4 differential diagnoses for ground glass consolidation in a central distribution? | 1) Pulmonary edema, 2) Alveolar hemorrhage, 3) Pneumocystis jiroveci pneumonia and 4) Alveolar proteinosis |
| What are the 4 differential diagnoses for ground glass consolidation in a peripheral distribution? | 1) Organizing pneumonia, 2) Chronic eosinophilic pneumonia, 3) Atypical pneumonia and 4) pulmonary edema (peripheral pulmonary edema tends to be non-cardiogenic in etiology) |
| Describe the pathophysiology that results in smooth interlobular septal thickening? | Any condition that dilates the pulmonary veins will result in smooth interlobular septal thickening |
| What are the 4 differential diagnoses for smooth interlobular septal thickening? | 1) Pulmonary edema (by far the most common cause), 2) alveolar proteinosis, 3) pulmonary hemorrhage and 4) atypical pneumonia (often Pneumocystis jiroveci) |
| What is alveolar proteinosis? | An idiopathic disease characterized by filling of the alveoli with proteinaceous material. |
| What type of hypersensitivity reaction is Hypersensitivity Pneumonitis? | Type III - it is hypersensitivity to inhaled organic antigens (immune complex reaction) |
| Describe the pathophysiology that results in nodular/irregular/asymmetric septal thickening. | Nodular/Irregular/asymmetric septal thickening tends to be caused by processes that infiltrate peripheral lymphatics. |
| What are the 2 differential diagnoses for nodular/irregular.asymmetric septal thickening? | 1) Sarcoidosis and 2) Lymphangitic carcinomatosis |
| Describe the cause and appearance of "Crazy Paving". | Crazy paving describes interlobular septal thickening with superimposed ground glass consolidation which resembles the appearance of broken pieces of stone |
| What are the 7 differential diagnoses for crazy paving? | 1) Alveolar proteinosis, 2) Pneumocystis jiroveci pneumonia, 3) Organizing pneumonia, 4) Bronchioalveolar carcinoma, 5) Lipoid pneumonia, 6) Acute respiratory distress syndrome and 7) pulmonary hemorrhage |
| Describe the CT appearance of centrilobular nodules. | Nodules seen in the center of a secondary pulmonary lobule which never extend to the pleural surface. They represent opacification of the centrilobular bronchiole (or less commonly, the centrilobular artery) |
| What are the 3 *infectious* differential diagnoses for centrilobular nodules? | 1) Endobronchial spread of tuberculosis or atypical bacteria such as MAI, 2) Bronchopneumonia, 3) Atypical pneumonia (such as Mycoplasma) |
| What are the 5 *inflammatory* differential diagnoses for centrilobular nodules? | 1) Hypersensitivity pneumonitis, 2) Respiratory bronchiolitis interstitial lung disease (RB-ILD, caused by inhaled cigarette smoke), 3) Hot tub lung (caused by inhaled atypical mycobacteria, 4) Diffuse panbronchiolitis (Asians) and 5) Silicosis |
| What are the three locations within the lung where lymphatic vessels can be seen? | 1) Subpleural, 2) Peribronchovascular and 3) Septal |
| What are perilympahtic nodules? | Nodules found along the anatomic distribution of lymphatic vessels within the lung |
| What are the 3 differential diagnoses for perilympathic nodules? | 1)Sarcoidosis (by far the most common cause, typically in upper lobe distribution), 2) Pneumoconioses (silicosis and coal workers pneumoconiosis which are reactions to inorganic dust inhalation) and 3) Lymphangitic carcinomatosis |
| What are the 3 differential diagnoses for randomly distributed nodules and how are these type of nodules spread? | 1) Hematogenous metastasis, 2) septic emboli, 3) Pulmonary Langerhan's Cell Histiocytosis - random pulmonary nodules are spread via hematogenous dissemination and are thus, angiocentric in location |
| What is a "military" pattern? What are the 3 differential diagnoses of military nodules? | Miliarity describes innumerable tiny random nodules disseminated in a hematogenous manner. Ddx includes 1) Disseminated TB, 2) Disseminated fungal infection and 3) disseminated hematogenous metastasis |
| Describe "tree-in-bud" nodules. | Tree-in-bud nodules are multiple small nodules connected to linear branching structures, they give the appearance of a budding tree branch in spring time. They are due to mucus, pus, or fluid impacting terminal bronchioles. |
| What are the 4 differential diagnoses for tree-in-bud nodularity? | 1) TB and other atypical mycobacteria, 2) bacterial pneumonia, aspiration pneumonia and 4) airway invasive aspergillus |
| What are the 2 differential diagnoses for a solitary cavitary lesion? | 1) Primary bronchogenic carcinoma (both squamous cell and adenocarcinoma cavitate but squamous cell does it more frequently) and 2) TB (upper lobe predominance) |
| What are the 3 differential diagnoses for multiple cavitary lesions? | 1) Septic emboli, 2) Vasculitis (including Wegener's Granulomatosis and 3) Metastases (squamous cell carcinoma and uterine carcinosarcoma) |
| What are the 6 differential diagnoses for multiple lung cysts? | 1) Lymphangioleiomyomatosis (LAM), 2) Emphysema (upper lobe), 3) Pulmonary Langerhan's Cell Histiocytosis (upper lobe), 4) Diffuse cystic bronchiectasis (CF), 5) Pneumocystis jiroveci infection and 6) Lymphoid interstitial pneumonia (LIP) |
| With which autoimmune disease is Lymphoid interstitial pneumonia always associated? | Sjogren's syndrome |
| What are the 3 differential diagnoses for a single pulmonary cyst? | 1) Bulla (>1cm), 2) Bleb (<1cm) and 3) Pneumatocele |
| What are the 3 differential diagnoses for basal-predominant fibrosis? | 1) Idiopathic pulmonary fibrosis (honeycombing), 2) End-stage asbestosis (often in association with pleural plaques) and 3) Nonspecific interstitial pneumonia-fibrotic form (associated with collagen vascular disease and drug reactions, no honeycombing) |
| What are the 3 differential diagnoses for apical-predominant fibrosis? | 1) End stage sarcoidosis, 2) Chronic hypersensitivity pneumonitis and 3) End stage silicosis |
| Which bug is the most common cause of community acquired pneumonia? | Strep pneumoniae |
| Which bugs are the most common cause of hospital acquired pneumonia? | MRSA and Pseudomonas |
| Which bugs are the most common cause of ventilator acquired pneumonia? | Pseudomonas and Acinetobacter |
| What are the 3 stages of empyema and how is each treated? | 1) Free flowing exudative effusion (tap and drain), 2) development of fibrous strands (large bore chest tube and fibrinolytics) and 3) Thickening/solidification of fluid (surgery) |
| Are pneumomatoceles permanent or do they resolve? | They resolve with time, not permanent. Often result from trauma. |
| What is empyema necessitans? | Extension of an empyema into the adjacent chest wall (often due to TB, nocardia or actinomyces) |
| Describe the two potential outcomes of TB exposure. | 1) Contained disease (90% of cases, caseating granulomas eventually calcified granulomas +/- calcified hilar lymph nodes) or 2) Primary tuberculosis (consolidation, pleural effusion, lymphadenopathy or military disease) |
| What is a "Ghon focus"? | Initial focus of TB parenchymal infection in primary TB, usually mid-lung in location |
| What is a "Ranke complex"? | A Ghon focus plus lymphadenopathy |
| In what stage of disease do TB-related pulmonary lesions cavitate? | Reactivated TB (NOT primary TB) |
| What is another name for reactivated TB? | Post-primary TB |
| In what stage of disease is TB-related adenopathy seen? | Primary TB (NOT reactivated TB) |
| If tree-in-bud nodules are seen in the setting of TB infection, what do they signify? | TB-related tree in bud nodules indicate endobronchial spread of disease |
| What is a tuberculoma and in which stage of disease does it occur? | Well-defined opacity in the lung apices, usually seen in reactivation stage |
| How do locations within the lungs vary depending on stage of TB infection (Primary vs. Reactivation) | Primary infection = upper portion of lower lobes and lower portion of upper lobes (mid lung) while reactivation = apices |
| In which stage of disease does "miliary" TB occur? | Miliary TB can occur in both primary TB and during reactivation |
| Describe "Lady Windermere" syndrome. Which type of bacteria is it associated with? | An elderly woman presents with cough, low-grade fever and weight loss = infection with atypical mycobacteria like M. avium intracellulare and M. kansasii. Classic findings are tree-in-bud nodules and bronchiectasis of the right middle lobe or lingula. |
| Describe "Hot Tub Lung". Which type of bacteria is it associated with? | Hypersensitivity pneumonitis in response to inhaled atypical mycobacteria which are often found in hot tubs. There's no activity infection and the patient is otherwise fine. Features centrilobular nodules. |
| Where in the USA is Histoplasma typically found? | Ohio and Mississippi river valleys. |
| What is the most common sequela of Histoplasma infection? | Calcified granulomas |
| What are some defining radiological findings of Histoplasma infection? | It can mimic reactivation TB with fibrocavitary lesions in the upper lobes and calcified lymph nodes. Fibrosing mediastinitis is a rare complication. |
| Where in the USA is Coccidioides typically found? | The Southwestern US. |
| Where in the USA is Blastomyces typically found? | The Southeast and central US. |
| At what CD4 count are AIDS patients at risk for Pneumocystis jiroveci? | CD4 < 200 cells/cc |
| What is the classic chest x-ray appearance of an AIDS patient with Pneumocystis? | Bialteral perihilar (central) airspace opacities with peripheral sparing |
| What is the classic CT appearance of an AIDS patient with Pneumocystis? | Bilateral perihilar ground glass opacification+/- crazy paving |
| Which infectious entity has a propensity to cause upper lobe pneumatoceles (thus predisposing the patient to pneumothorax and pneumomediastinum) | Pneumocystis |
| Most common fungal infection in AIDS patients? | Cryptococcus |
| At what CD4 count are AIDS patients at risk for Cryptococcus? | CD4 < 100 cells/cc |
| True or False: Cryptococcal pulmonary infection usually coexists with cryptococcal meningitis? | True, concomitant pulmonary and CNS infections are typical |
| What are the 5 types of pulmonary Aspergillosis? | 1) Allergic bronchopulmonary aspergillosis, 2) Saprophytic aspergilloma/mycetoma, 3) Semi-invasive/chronic necrotizing, 4) Airway invasive and 5) Angioinvasive |
| Which type of Aspergillus infection is associated with the "Finger in glove" sign? What does this sign represent? | Allergic bronchopulmonary aspergillosis. Finger in glove sign represents mucoid impaction of bronchiectasis. |
| Which type of Aspergillus infection is associated with the "Monod" sign? What does this sign represent? | Saprophytic aspergilloma/Mycetoma. It represents the sliver of air surrounding the fungal ball in the cavity. |
| Which type of Aspergillus infection is associated with the "Halo" sign? What does this sign represent? | Angioinvasive aspergillosis. The halo sign is seen in acute infection; ground glass halo around a consolidation. It is thought to represent surrounding hemorrhagic infarction. |
| Which type of Aspergillus infection is associated with the "Air Crescent" sign? What does this sign represent? | Angioinvasive aspergillosis. The air crescent sign is seen in chronic; crescent of air from retraction of infarcted lung. Considered a good prognostic indicator, patient in recovery phase. |
| In which patient population is allergic bronchopulmonary aspergillosis most often seen? | Chronic asthmatics |
| What are the clinical signs/symptoms of allergic bronchopulmonary aspergillosis? | Wheezing, low grade fever, cough and sputum production. Sputum will contain fungal hyphae. The key CT finding is upper lobe bronchiectasis with mucoid impaction (finger in glove sign). |
| What is an "aspergilloma"? | A conglomeration of intertwined aspergillus fungal hyphae and cellular debris ("fungal ball") in a pre-existing pulmonary cavity. It will be mobile when patient changes position. |
| What are the most causes of a pre-existing cavity in a patient with saprophytic aspergilloma/mycetoma? | Prior TB or sarcoidosis |
| What is the most common symptom of aspergilloma/mycetoma (if symptomatic)? | Hemoptysis |
| In which patient population is semi-invasive/chronic necrotizing aspergillosis most often seen? | Debilitated patients (Diabetics, alcoholics, COPD pts) |
| In which patient populations are airway invasive and angioinvasive aspergillosis most often seen? | Immunocompromised patients (AIDS, chemotherapy, solid organ transplant) |
| List the 3 stages of pulmonary edema. | Vascular redistribution (increased pulmonary venous pressure) >> Interstitial edema >> Alveolar edema |
| Pulmonary edema is usually symmetric in distribution and dependent in location, what is a classic cause of asymmetric/non-dependent pulmonary edema? | Acute mitral regurgitation 2/2 myocardial infarction with papillary muscle rupture (Right upper lobe pulmonary edema) |
| Describe the pulmonary edema which is associated with aggressive thoracentesis? | Re-expansion pulmonary edema. Caused by rapid re-expansion of a lung which has been collapsed due to a large effusion for more than 3 days. |
| What is the single greatest modifiable risk factor for lung cancer? | Tobacco smoking |
| Occupational exposures like Radon, Beryllium, arsenic etc. increase the risk of lung cancer by what factor? | By a factor of 5 |
| Pulmonary fibrosis increases the risk of lung cancer by what factor? | By a factor of 10 |
| Which is more likely to be malignant: A solid pulmonary nodule or a ground glass nodule? | Ground glass nodule (or mixed solid/ground glass) are more likely to be malignant |
| Does calcification of a pulmonary lesion (nodule, etc) make it more likely to be malignant or benign? | Calcification generally confers benignity |
| Does intralesional fat make a lesion more likely to be benign or malignant? | Fat confers benignity |
| Which shape of pulmonary nodule confers malignancy? | Round shape is more likely to be malignant than any other shape (oval, oblong, polygonal, etc) |
| Which location(s) of pulmonary nodules generally confer benignity? | Subpleural location = generally benign |
| What is the single most important risk factor for malignancy of a pulmonary lesion, regardless of morphology? | Size. The bigger the lesion is, the more likely it is to be malignant. |
| What is the most common subtype of lung cancer? | Adenocarcinoma |
| Which tumor marker is useful for diagnosing primary lung adenocarcinoma? | TTF-1 (Thyroid Transcription Factor 1) - it will be positive in primary lung adenocarcinoma but negative in extra-pulmonary primary adenocarcinomas that have metastasized to the lung |
| Where in the lung, centrally or peripherally, is pulmonary adenocarcinoma typically found? | Peripherally |
| Where in the lung, centrally or peripherally, is pulmonary squamous cell carcinoma typically found? | Centrally/Hilar region |
| Which type of lung cancer has the greatest propensity to cavitate? | Squamous cell carcinoma |
| Does the growth pattern of Bronchoalveolar carcinoma. | "Lepidic" growth along the alveolar walls without invasion of the lung parenchyma. As such, it is generally indolent. |
| How does Small Cell lung cancer generally present? | As extensive disseminated disease (not a few nodules) along the hilum which is generally not amenable to surgery because of how widespread it is |
| How does Large Cell lung cancer generally present? | A very large solitary mass in the peripheral lung |
| How does pulmonary Carcinoid tumor present? | Endobronchial mass distal to the carina which caused obstructive atelectasis. |
| What is the size cut off for nodule vs. mass? | Nodule <3cm while Mass >3cm |
| A tapered bronchus is highly specific for which pulmonary pathology? | Lung cancer |
| Where is a "superior sulcus tumor" found? | Apex of the lung |
| Describe a "Pancoast" tumor. | Superior sulcus tumor with involvement of the sympathetic ganglia causing Horner Syndrome (ipsilateral ptosis, miosis and anhidrosis) |
| Describe lymphangitic carcinomatosis in the setting of lung cancer spread. | Diffuse spread of neoplasm through pulmonary lymphatics, typically seen late in the disease process. Appears as nodular interlobular septal thickening. |
| Why is the presence of malignant cells in a pleural effusion of importance? | A malignant effusion is an "M1a" lesion on the TNM staging scale which means it precludes curative resection if present. |
| At what level are (arterial and venous) pulmonary pressures considered to be elevated? | Arterial = pulmonary arterial systolic pressure >25mmHg (rest) or >30mmHg (exercising). Venous = capillary wedge pressure > 18mmHg. |
| What is the difference between precapillary and postcapillary caused of pulmonary hypertension? | Pre-capillary = abnormality in the pulmonary parenchyma and/or pulmonary arteries or the blood flow within them (before or within the lungs). Post-capillary: abnormality in the pulmonary veins (after the lungs). |
| Describe the 5 WHO groups for classification of pulmonary hypertension | 1) PAH (congenital or due to ASD/VSD), 2) Pulmonary venous HTN (left heart dz), 3) Pulmonary HTN 2/2 chronic hypoxic lung dz (COPD, apnea, fibrosis), 4) Pulmonary HTN 2/2 chronic thromboembolic dz, 5) Misc (Sarcoidosis, neoplasm, fibrosing mediastinitis) |
| At what diameter is the main pulmonary artery considered enlarged? | >3cm |
| What are pulmonary artery calcification pathognomonic for? | Pulmonary artery hypertension |
| What is the "Hilum convergence" sign. | Describes the appearance of hilar pulmonary arteries converging into an enlarged pulmonary artery |
| What is the "Hilum overlay" sign? | Describes the visualization of hilar vessels through a mass. It indicates that 1) a mediastinal mass is present and 2) the mass cannot be in the middle mediastinum (usually anterior) |
| What is the significance of a negative vs. positive D-dimer? | Negative D-dimer has a high negative predictive value. Positive D-dimer means nothing; it's not sensitive or specific. |
| Which findings suggestion a pulmonary embolus is chronic in nature? | Eccentric location, circumferential shape |
| What is Fleishner's sign? | Widening of the pulmonary arteries on x-ray, due to the presence of a pulmonary embolus |
| What is the "Hampton's Hump" sign? | Peripheral wedge shaped opacity on x-ray which represents pulmonary infarct (typically due to a pulmonary embolus) |
| What is the "Westermark" sign? | Regional oligemia in the lung distal to the pulmonary artery containing an embolus on x-ray |
| How is the right ventricle used to clue an observer in the presence of pulmonary embolus? | Acute right ventricular dilation with bowing of the intraventricular septum to the left is a result of backup of blood due to blockage of flow through the pulmonary arteries due to embolus. |
| How many "Interstitial Idiopathic Pneumonias" exist? How are they described? | 7different idiopathic interstitial pneumonias: 1)IPF/UIP, 2) NSIP, 3) COP/BOOP/OP, 4) RB-ILD, 5) DIP, 6) LIP, 7) AIP. Each of these has a corresponding clinical scenario and a corresponding biopsy/pathology finding |
| Idiopathic pulmonary fibrosis is one of the idiopathic interstitial pneumonias. Which pathology finding and which clinical scenario are associated with IPF? | Entity/Clinical Scenario: Idiopathic pulmonary fibrosis Pathology: Usual Interstitial Pneumonia (interstitial fibroblastic foci and chronic alveolar inflammation) IPF = UIP |
| Non-specific interstitial pneumonitis is one of the idiopathic interstitial pneumonias. Which pathology finding and which clinical scenario are associated with NSIP? | Non-specific interstitial pneumonitis is both the entity/clinical scenario and the pathology diagnosis(thickened alveolar septa from chronic inflammation +/- minimal fibrosis). |
| Does idiopathic pulmonary fibrosis respond to steroids? | Yes |
| What is the major clinical/radiological difference between IPF/UIP and NSIP? | NSIP does not respond to steroids while IPF/UIP does. NSIP also features ground glass which IPF/UIP does not. There is little to no fibrosis seen in NSIP. |
| Which diseases are associated with/known to cause NSIP? | Collagen vascular disease, drug reaction, dermatomyositis |
| What are the two forms of NSIP? | 1) Fibrotic NSIP (ground glass + small amount of fibrosis) and 2) Cellular NSIP (ground glass + no fibrosis). Both feature sparing in the immediate subpleural region. |
| Cryptogenic organizing pneumonia (COP) is one of the idiopathic interstitial pneumonias. Which pathology finding and which clinical scenario are associated with COP? | Entity/Clinical syndrome: Cryptogenic organizing pneumonia (aka BOOP, bronchiolitis obliterans organizing pneumonia) Pathology: Organizing pneumonia (myxoid fibroblastic material fills alveoli, thick alveolar septa 2/2 chronic lymphocytic inflammation) |
| Does NSIP respond to steroids? | No |
| Does COP/BOOP/OP respond to steroids? | Yes |
| What is known to cause COP/BOOP/OP? | infections, drug reactions, inhalation (nothing super specific) |
| What is the "Reverse Halo" or "Atoll" sign and which Idiopathic Interstitial Pneumonia is it associated with? | Central lucency surrounded by a ground glass halo (fairly specific for COP/BOOP/OP) |
| What's the difference between the "Halo" sign and the "Reverse Halo" sign? | Halo sign: central opacity with surrounding ground glass (Invasive aspergillus) Reverse Halo sign: central lucency with surrounding ground glass (COP/BOOP/OP) |
| Respiratory Bronchiolitis - Interstitial Lung Disease is one of the idiopathic interstitial pneumonias. Which pathology finding and which clinical scenario are associated with RB-ILD? | Both the clinical syndrome and pathology are referred to as RB-ILD. RB-ILD is seen in smokers and features pigmented macrophages filling the terminal airways while sparing the alveoli. "RB only" if asymptomatic. "RB-ILD" if symptomatic (cough, sob). |
| What are the classic imaging findings seen in RB-ILD? | Random (neither central nor peripheral) centrilobular nodules and patchy ground glass opacities. |
| Desquamative Interstitial Pneumonia is one of the idiopathic interstitial pneumonias. Which pathology finding and which clinical scenario are associated with DIP? | DIP is both the clinical syndrome and pathology. Pigmented macrophages fill the terminal bronchioles and alveoli. |
| How are RB, RB-ILD and DIP related? | They are a continuous spectrum of smoking-related lung disease. RB/RB-ILD feature pigmented macrophages in the terminal bronchioles with sparing of the alveoli. DIP features pigmented macrophages in both the terminal bronchioles and the alveoli. |
| How does the imaging findings of RB/RB-ILD and DIP vary? | Both feature ground glass opacities but this finding is more extensive in DIP. DIP may also feature a few cysts. |
| Lymphoid Interstitial Pneumonia is one of the idiopathic interstitial pneumonias. Which pathology finding and which clinical scenario are associated with LIP? | LIP is both the clinical syndrome and the pathology. It is commonly associated with Sjogren syndrome and HIV. Features diffuse infiltration/expansion of the interstitium by lymphocytes/immune cells with compression/distortion of the adjacent alveoli. |
| What are the classic imaging findings of DIP? | Diffuse or lower lobe ground glass opacities . Scattered, thing-walled perivascular cysts. Complicated by pneumothorax in advanced disease. |
| Acute Interstitial Pneumonia is one of the idiopathic interstitial pneumonias. Which pathology finding and which clinical scenario are associated with AIP? | AIP is the clinical scenario. Diffuse alveolar damage (DAD) is the pathology. IT is associated with ARDS. |
| What sets AIP apart from the other interstitial lung diseases? | It is the only interstitial lung disease with an acute onset. It also has the worst prognosis of all interstitial lung diseases. It results from surfactant destruction. |
| Describe the two phases of AIP. | Early/exudative phase: hyaline membranes, diffuse alveolar infiltration by lymphocytes/immune cells and non-cardiogenic pulmonary edema. Chronic/organizing: alveolar wall thickening due to granulation tissue. begins >1 week after the initial injury. |
| What are the classic imaging findings in AIP. | There are no classic findings, only diffuse ground glass opacities which are a very non-specific finding. |
| What are the causes of Hypersensitivity pneumonitis? | Common lung disease caused by a hypersensitivity reaction to inhaled organic antigens such as bird proteins or thermophilic actinomycetes. It features 3 phases: acute, subacute and chronic. |
| Describe the 3 phases of HSP. | Acute: inflammatory exudates fill the alveoli, appears as nonspecific ground glass opacities. Subacute: centrilobular ground glass nodules +/- mosaic attenuation (air trapping). Chronic (long term exposure to the inciting antigen): upper lobe fibrosis. |
| What is the "Head Cheese" sign? Which stage of HSP is it associated with? | Patchy ground glass + Mosaic attenuation (air trapping). Associated with subacute phase of HSP. |
| What is the difference in cause between HSP and Pneumoconioses? | HSP = reaction to organic antigens. Pneumoconioses = reaction to inorganic antigens. |
| What are the three main causes/types of pneumoconiosis? | 1) Silica = silicosis, 2) Coal = coal workers pneumoconiosis, 3) Asbestos = asbestosis. These three entities appear indistinguishable on imaging but have different histological findings. |
| Which pneumoconiosis features lymph nodes with eggshell calcification? | Silicosis |
| What is Caplan syndrome? | Rheumatoid arthritis + coal worker's pneumoconiosis (more common) or silicosis. It features necrobiotic rheumatoid nodules superimposed on the smaller centrilobular and subpleural nodules of the pneumoconiosis. |
| Where are inhalational lung disease (HSP, Penumoconioses) predominantly seen within the lungs? Which disease is the exception? | Inhalational disease are predominantly an upper lobe finding because the lower lobes have more blood flow and lymphatic drainage, clearing offending antigens more efficiently. Asbestosis is the exception = lower lobes (particles too big to be cleared). |
| How does one distinguish between Asbestosis and IPF on imaging? | They appear identical, both involving the lower lobes. However, with asbestosis you will see additional signs of asbestos exposure such as pleural thickening and pleural plaques. |
| What are the two eosinophilic lung diseases? | 1) Simple pulmonary eosinophilia/Loffler's pneumonitis and 2) Chronic eosinophilic pneumonia |
| Describe the imaging findings seen in Simple pulmonary eosinophilia/Loffler syndrome. | Transient and *migratory* areas of focal consolidation with an elevated eosinophil count in peripheral blood smear. Parasitic lung infection appears identically but "SPE/Loffler" is the name reserved for idiopathic cases. |
| Describe the imaging findings seen in Chronic eosinophilic pneumonia. | Chronic (unchanged for months) patchy peripheral consolidation with upper lobe predominance due to extensive alveolar filling and interstitial infiltration by eosinophils. IT responds rapidly to steroids. |
| What are the 3 main types of pulmonary vasculitis? | 1) Churg-Strauss, 2) Microscopic polyangiitis and 3) Wegener's granulomatosis |
| What is the alternative name for Churg-Strauss vasculitis? What clinical entity is it associated with? | Allergic angiitis with granulomatosis. Churg Strauss is strongly associated with asthma/eosinophilia. |
| Which antibody is positive in Churg-Strauss? | P-ANCA |
| What are the classic imaging findings in Churg-Strauss? | There are no classic/specific findings. One may see ground glass opacities which are very non-specific. |
| Which antibody is positive in Microscopic Polyangiitis? | P-ANCA |
| Which pulmonary vasculitis is the most common cause of pulmonary hemorrhage *with concomitant renal failure*? | Microscopic polyangiitis |
| What are the classic imaging findings in Microscopic Polyangiitis? | There are no classic/specific findings. One may see central-predominant ground glass opacities representing hemorrhage. |
| What is the classic clinical triad for Wegener's Granulomatosis? | 1) Sinusitis, 2) Pulmonary involvement and 3) Renal insufficiency |
| Which antibody is positive in Wegener's Granulomatosis? | C-ANCA |
| Involvement of which bodily areas differentiates Wegener's Granulomatosis from the other pulmonary vasculitides? | Upper airways (nasopharynx, larynx and large bronchi) and eustachian tubes. The other vasculitides only effect the smaller/lower airways. |
| What are the classic imaging findings in Wegener's Granulomatosis? | Multiple cavitary pulmonary nodules (that do not respond to antibiotic therapy). Intracavitary air-fluid levels suggest superimposed infection. |
| What are the two stages of radiation-induced lung injury? | 1) Radiation pneumonitis (early) and 2) Radiation Fibrosis (later) |
| Describe Radiation pneumonitis (what are the findings, how long after treatment does it occur, etc.) | Onset within 1 month of treatment, with most severe response at approximately 3-4 months. Ground glass will be seen along the radiation port. |
| Describe Radiation Fibrosis (what are the findings, how long after treatment does it occur, etc.) | Occurs approximately 6-12 months after initial treatment. Localized fibrosis and traction bronchiectasis along the radiation port. |
| Describe the progression of pulmonary sarcoidosis. | formation on non-caseating granulomas which coalesce to form nodules which coalesce to form masses. Eventual progression to fibrosis/honeycombing. |
| How does the fibrosis seen in end stage pulmonary sarcoidosis vary from that of idiopathic pulmonary fibrosis? | IPF is lower lobe predominance. Fibrosis is sarcoidosis is mid to upper lung predominance, similar to that seen in Hypersensitivity pneumonitis. |
| List and describe the 5 stages of Pulmonary Sarcoidosis. | Staging is based on x-ray (not CT) findings! Stage 0: Normal radiograph, Stage 1: Hilar or mediastinal lymphadenopathy without lung changes, Stage 2: Adenopathy with lung changes, Stage 3: Diffuse lung disease without adenopathy, Stage 4) Fibrosis |
| What is the most common radiographic finding in sarcoidosis? | Hilar lymphadenopathy with stippled/eggshell calcification. |
| What is the most common cross-sectional finding in sarcoidosis? | Hilar/mediastinal lymphadenopathy +/- eggshell calficiation plus upper lobe perilymphatic nodules of variable size |
| What is the most common presentation in a patient with pulmonary Langerhan cell histiocytosis? | Spontaneous pneumothorax |
| Is pulmonary Langerhan's cell histiocytosis associated with smoking? Treatment? | Yes - nearly 100% of cases are related to smoking. Steroids and smoking cessation is a big component of treatment. |
| What are the extra-pulmonary manifestations of Langerhan's cell histiocytosis? | Lucent bone lesions, diabetes insipidus 2/2 hypophysitis and skin lesions |
| What is the differential for diseases involving both bone and lung? | 1) Malignancy, 2) tuberculosis, 3) Fungal disease (blasto, histo and coccidio), 4) sarcoidosis and 5) Gaucher's disease (lysosomal storage disorders) |
| Describe the progressive imaging findings in pulmonary Langerhan's cell histiocytosis. | airway-adjacent nodules which cavitate and result in irregular cysts. Upper lobe predominance. |
| What is the pathological process that occurs in Primary Alveolar Proteinosis? | Idiopathic filling of the alveoli with proteinaceous lipid-rich material. |
| What is the hallmark CT finding in Primary Alveolar Proteinosis? | Crazy paving |
| Describe the cause of lymphangioleiomyomatosis (LAM) and the disorder it is associated with. | LAM is a diffuse cystic lung disease caused by bronchiolar obstruction and lung destruction due to proliferation of immature smooth muscle cells in small vessels, lymphatics, and bronchioles. It is associated with Tuberous sclerosis. |
| Who does lymphangioleiomyomatosis affect more often, men or women? | Nearly 100% of cases of LAM (both Tuberous sclerosis related and idiopathic) are found in women. |
| In addition to diffuse cysts and pneumothorax, what other clinical finding is associated with lympangioleiomyomatosis (LAM)? | Chylous pleural effusion |
| How do the imaging findings in lymphangioleiomyomatosis (LAM) vary from Langerhan's cell histiocytosis (LCH). | Both are diseases which feature cysts. The cysts in LAM are thin walled, round/regular and found throughout all 5 lobes. LCH cysts feature thickened walls, irrgeular configuration and are located only in the mid to upper lobes. |
| What are the "4 T" lesions of the anterior mediastinum? | 1) Thymus lesion (Thymoma, Thymic carcinoma, Thymic carcinoid, Thymic cyst or Thymolipoma), 2) Teratoma (or other germ cell tumor like seminoma)), 3) Thyroid lesion (goiter, neoplasm, enlarged gland 2/2 thyroiditis) and 4) Terrible Lymphoma |
| Describe Castleman's Disease. | Angiofollicular lymph node hyperplasia. When it is seen in young people, it is localized to one area of the body, and is cured by resection. When in older people, it is multifocal and associated with AIDS, treated by chemotherapy. |
| What is the key imaging finding in Castleman's disease. | Avidly enhancing lymphadenopathy (though this is non-specific). |
| Which additional lesions, besides the 4T's, can be seen in the anterior mediastinum? | Adenopathy (unrelated to lymphoma), epicardial fat pad, pericardial cyst and Morgagni hernia |
| What disorders/disease are associated with thymoma? | Myasthenia gravis, red cell aplasia, hypogammaglobulinemia, paraneoplastic syndromes and malignancies such as lymphoma and thyroid cancer |
| Which hormone (and the syndrome an excess of that hormone can cause) are associated with Thymic Carcinoid? | Thymic carcinoids are known to secrete ACTH and cause Cushing's Syndrome. |
| Which disorder is associated with Thymic Carcinoid? | MEN (Multiple Endocrine Neoplasia) Type I and II |
| Which test can be performed if the diagnosis of Thymic Carcinoid is suspected? | Indium-111 Octreotide nuclear medicine scan |
| What the potential causes of a thymic cyst? | 1) radiation therapy, 2) AIDS or 3) congenital |
| From which embryological structure do thymic cysts arise? | Thymopharyngeal duct |
| What is the most common malignant anterior mediastinal germ cell tumor? | Seminoma |
| Where, specifically, are pericardial cysts seen? | Right cardiophrenic angle |
| What are the 4 differential diagnoses for middle mediastinal mass? | 1) Lymphadenopathy, 2) Ascending aortic or aortic arch aneurysm, 3) Enlarged pulmonary artery or 4) Foregut duplication cyst |
| Foregut duplication cysts include which 3 types of cysts? | 1) Bronchogenic cysts, 2) Esophageal duplication cysts and 3) neurenteric cysts |
| What are the 8 differential diagnoses for posterior mediastinal mass? | 1) Neurogenic tumors, 2) hiatal hernia, 3) descending thoracic aortic aneurysm, 4) extramedullary hematopoiesis, 5) lateral meningocele, 6) esophageal malignancy, 7) Foregut duplication cysts and 8) paraspinal abscess |
| Which specific tumors fall under the diagnosis of "neurogenic tumors" as they relate to Posterior Mediastinal Masses | 1) Peripheral nerve sheath tumors/adults (Schwannoma, neurofibroma, malignant peripheral nerve sheath tumor and 2) Sympathetic ganglion tumors/kids (ganglioneuroma, neuroblastoma, and ganglioneuroblastoma), |
| Patients with which disorders may have paraspinal masses caused by extramedullary hematopoiesis? | Thalassemia and Sickle Cell Anemia |
| Patients with which disorder may have lateral meningoceles in the posterior mediastinum? | Neurofibromatosis |
| What are the 6 differential diagnoses for diffuse or multifocal non-neoplastic stenosis/wall thickening? | 1) Relapsing polychondritis, 2) Tracheobornchopathia osteochrondroplastica, 3) Tuberculosis, 4) Amyloidosis, 5) Wegener's granulomatosis and 6) Sarcoidosis |
| Describe Relapsing Polychondritis and it's effect on airways. | Relapsing poltchondritis is recurrent inflammation of cartilaginous structures like the nose, ears, joints, larynx, trachea and bronchi. Occurs in middle age women. |
| What are the imaging findings seen in Relapsing Polychondritis of the airways. | Smooth tracheal/bronchial wall thickening with sparing of the posterior membrane |
| Describe Tracheobronchopathia osteochondroplastica and it's imaging findings in the airways. | Benign condition of multiple submucosal calcified osteocartilaginous nodules along the trachel walls with sparing of the posterior membranous trachea. |
| Describe the appearance of Tuberculosis in the airways. | TB usually causes a smooth, concentric narrowing of a relatively long segment (>3cm) of airway following endobronchial spread of disease from the lungs. Usually distal trachea/proximal bronchi. |
| Describe the appearance of Amyloidosis in the airways. | Irregular narrowing of the airways due to submucosal deposition of amyloid, which may or may not calcify. |
| Describe the appearance of Wegener's granulomatosis in the airways. | Subglottic tracheal stenosis with circumferental mucosal thickening. Does NOT spare the posterior aspect of the trachea. |
| Describe the appearance of Sarcoidosis in the airways. | Smooth or nodular/mass like stenosis. Does NOT spare the posterior aspect of the trachea. |
| What are the 3 differential diagnoses for focal non-neoplastic tracheal stenosis/wall thickening? | 1) Intubation/tracheostomy, 2) Behcet disease, 3) Crohn's disease |
| What are the 3 structural changes that can lead to bronchiectasis? | 1) Bronchial wall injury from infection or inflammation, 2) bronchial lumen obstruction and 3) traction from adjacent fibrosis |
| What is the mnemonic to remember the common causes of bronchiectasis? | CAPTAIn Kangaroo has Mounier Kuhn. C (cystic fibrosis), A (allergic bronchopulmonary aspergillosis), P (post-infectious), T (tuberculosis/atypical mycobacteria), A (agammaglobulinemia), I (immunodeficiency), K (Kartagener), Mounier Kohn |
| Describe Mounier Kuhn disease and it's effect on airways. | Mounier Kuhn is a congenital connective tissue disorder causing tracheobronchomegaly which leads to recurrent pneumonia. Recurrent pneumonia eventually leads to bronchiectasis. |
| How does the bronchiectasis of cystic fibrosis vary from that of post-infectious bronchiectasis? | CF bronchiectasis = upper lobes. Post-infectious bronchiectasis = lower lobes. |
| What are the 3 morphological variants of bronchiectasis? | 1) Cylindrical (mild bronchial dilation), 2) Varicose (moderate, beaded/irregular bronchi) and 3) Cystic (severe, markedly enlarged airways with multiple cysts that may or may not connect with the airways). |
| What imaging findings are considered a precursor to bronchiectasis? | "Tram tracks" which represent thickened bronchial walls and "Signet ring sign" which describes a dilated bronchus adjacent to a normal pulmonary artery branch |
| Describe the rare condition known as Broncholithiasis. | Calcified/ossified material within the bronchial lumen most commonly caused by erosion of an adjacent calcified granulomatous lymph nodes. Presents with non-productive caough, hemoptysis and air trapping. |
| What does the pathophysiology of emphysema entail? | Destruction of alveolar walls resulting in irreversible enlargement of the distal airspaces. Although it does involve fibrosis initially, end stage emphysema may lead to a reparative response that may ultimately lead to fibrosis. |
| What is the role of the enzyme "Elastase" in the pathophysiology of Emphysema. | Elastase is released by alveolar macrophages and neutrophils, which are increased in number in emphysema. Elastase destroys alveolar walls but is neutralized by Alpha-1-antitrypsin. Surplus elastase or deficient A1A can result in lung destruction. |
| What are the three varieties of Emphysema? | Centrilobular, Paraseptal and Panacinar Emphysema |
| Where, within the lung, does Centrilobular Emphysema occur. | Upper lobes. |
| Which of the three varieties of Emphysema are smoking related? | Centrilobular and Paraseptal. |
| Which of the three varieties of Emphysema are Alpha-1-Antitrypsin deficiency related? | Panacinar |
| Where within the lungs does Paraseptal Emphysema occur? | Subpleural throughout all lobes. Can pre-dispose to pneumothroax. |
| Where within the lungs does Panacinar Emphysema occur? | Throughout the lungs but most severe at the bases |
| What are the most common airway tumor in adults? | Squamous cell carcinoma. It is related to smoking. |
| What are the typical imaging findings in tracheal squamous cell carcinoma? | Polypoid intraluminal mass which can invade the adjacent esophagus and cause tracheoesophageal fistula and bronchoesophagus fistula |
| Is Adenoid cystic carcinoma associated with smoking? | No |
| What is the primary way in which adenoid cystic carcinoma spreads? | Perineural (along the nerves) spread. It may also spread submucosally as well. |
| What are the typical imaging findings in adenoid cystic carcinoma? | Infiltrative, submucosal mass that may or may not present as circumferential bronchial wall thickening which causes airway stenosis |
| List the 15 differential diagnoses for airway tumors. | SCC, Adenoid cystic carcinoma, Carcinoid, Mucoepidermoid carcinoma, Tracheal lymphoma, Endobronchial metastasis, invasion by airway-adjacent malignancy, Papilloma, Chondroma, Schwannoma, Adenoma, Hamartoma, hemangioma, lipoma, leiomyoma |
| Where within the airways does pulmonary carcinoid occur? | Distal to the carina |
| What are the 4 differential diagnoses for an avidly (arterial) enhancing endobronchial mass? | 1) Carcinoid, 2) Mucoepidermoid carcinoma, 3) Hemangioma, and 4) Glomus tumor |
| Describe Laryngotracheal papillomatosis. | Multiple papillomas in the airway caused by HPV. Rarely, they can spread to the lung and cavitate, forming multiple cavities. |
| What are the 4 differential diagnoses for pleural tumors? | 1) Mesothelioma, 2) Metastasis, 3) Multiple myeloma/plasmacytoma and 4) Fibrous tumor of the pleura |
| What are most cases of mesothelioma due to? | Asbestos exposure, >20 years prior to disease development |
| What are the three subtypes of Mesothelioma and which carry a better prognosis? | 1) Epithelial subtype (best prognosis), 2) sarcomatoid and mixed subtypes which carry worse prognoses |
| What is the surgical treatment of locally invasive mesothelioma? | Extrapleural pneumonectomy |
| What is the surgical treatment for less invasive instances of mesothelioma where the fissures are spared? | Pleurectomy and decortication |
| Describe "Fibrous tumor of the pleura". | Non-mesothelial fibrous lesion that is not related to mesothelioma or asbestosis. They may be associated with hypoglycemia and hypertrophic pulmonary osteoarthropathy. IT can be pedunculaed and change position on imaging. |
| What are the 3 causes of transudative pleural effusion? | Heart failure, low-protein states and nephrotic syndrome |
| What are the 7 causes of exudative pleural effusion? | Pneumonia, empyema, tuberculosis, mesothelioma, pleural metastasis, rheumatoid arthritis or other collagen vascular diseases |
| What is Light's criteria? | Criteria for determining if a pleural effusion is transudative vs. exudative. Pleural fluid protein to serum protein >0.5 Pleural fluid LDH: serum LDH >0.6 Pleural fluid LDH > 2/3 upper limit of normal for serum (Any one of these = exudative) |
| Describe Chylothorax. | Pleural effusion consisting of intestinal lymph, most commonly caused by neoplastic obstruction of the thoracic duct. |
| Which disorder/disease is chylothorax associated with? | Lymphangioleiomyomatosis (LAM). |
| Where does the thoracic duct originate and terminate? | Thoracic duct originates at the cisterna chylli in the upper abdomen. It terminates in the left brachiocephalic or subclavian vein. |
Created by:
stephanie.prater
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