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Flashcards in Chest Deck (55):

A solitary pulmonary nodule

1. Granuloma
2. Neoplasm (bronchogenic carcinoma or solitary metastasis)
3. Hamartoma

Additional diagnostic considerations:
1. Round pneumonia
2. Arteriovenous malformation


Multiple pulmonary nodules

1. Metastatic disease
2. Granulomatous disease (TB or fungal)
3. Septic emboli
Additional diagnostic considerations:
1. Granulomatosis with polyangiitis (GPA), formerly Wegener granulomatosis
2. Rheumatoid arthritis


A cavitary pulmonary nodule

Most likely cancer or infection:
1. Tuberculosis (usually upper lobe)
2. Fungal disease
3. Squamous cell carcinoma (primary or metastatic - note adenocarcinoma can cavitate, small cell never cavitates)
Additional diagnostic considerations:
1. Pyogenic infection (pulmonary abscess and septic emboli)
2. Granulomatosis with polyangiitis (GPA), formerly Wegener granulomatosis
3. Rheumatoid arthritis


Miliary pulmonary nodules

1. Disseminated tuberculosis
2. Disseminated fungal infection
3. Disseminated haematogenous metastases
Additional diagnostic considerations:
1. Pnemoconioses
2. Healed varicella


Centrilobular pulmonary nodules

1. Infectious bronchiolitis (MAC and TB)
2. Hypersensitivity pneumonitis
3. Endobronchial spread of tumour
Additional diagnostic considerations:
1. Respiratory bronchiolitis associated interstitial lung disease
2. Pneumoconioses


Multiple lung cysts

1. Emphysema (upper lobe predominant in a smoker)
2. Lymphangioleiomyomatosis, a diffuse cystic lung disease caused by smooth muscle proliferation of the distal airways. LAM causes uniformly distributed, thin-walled cysts in a diffuse distribution. It is classically associated with chylous effusion.
3. Langerhans cell histiocytosis, which features irregular cysts and nodules predominantly in the upper lungs.
Additional diagnostic considerations:
1. Diffuse cystic bronchiectasis. Bronchiectasis is dilation of the bronchioles. Although cystic fibrosis is the most common cause of bronchiectasis and has an upper-lobe predominance, congenital or post-infectious causes can have a diffuse or lower-lobe distribution.
2. Pneumocystis pneumonia, which features cysts in late-stage disease.
3. Lymphoid interstitial pneumonia (LIP), an exceptionally rare disease usually associated with Sjögren syndrome and characterized by alveolar distortion from lymphocytic infiltrate and multiple cysts.


Lower lobe interstitial disease

1. Usual interstitial pneumonia
2. Collagen vascular disease (scleroderma)
3. Asbestos-related lung disease
Additional diagnostic considerations:
1. Drug toxicity


Upper lobe interstitial disease

1. Tuberculosis
2. Sarcoidosis
3. Cystic fibrosis
Additional diagnostic considerations:
1. Pneumoconioses
2.Langerhans cell histiocytosis


A hyperlucent lung

1. Chest wall abnormality (mastectomy or Poland syndrome)
2. Swyer-James syndrome
3. Acute asthmatic attack
Additional diagnostic considerations:
1. Airway obstruction
2. Pulmonary embolism
3. Pneumothorax


An anterior mediastinal mass

The 5 T's:
1. Terrible lymphoma (Hodgkin lymphoma; non-Hodgkin lymphoma)
2. Thymus lesion (thymoma: most common primary neoplasm of the anterosuperior mediastinum; invasive thymoma; thymic carcinoma; thymolipoma/thymoliposarcoma; thymic cyst; thymic hyperplasia; thymic carcinoid)
3. Thyroid lesion (thyroid neoplasms; thyroid goitre; parathyroid neoplasms)
4. Teratoma and germ cell neoplasm (teratoma - 75% are mature, immature, teratocarcinoma is a malignant teratoma; seminoma; embryonal cell carcinoma; yolk sac tumour; choriocarcinoma; mediastinal mixed cell type germ cell tumour)
5. Thoracic aortic aneurysm


A middle mediastinal mass

1. Lymphadenopathy
2. Vascular abnormality (aortic or pulmonary artery aneurysm)
3. Congenital cyst (bronchogenic cyst)
Additional diagnostic considerations:
1. Hiatal hernia


A posterior mediastinal mass

1. Neurogenic tumour
2. Lymphoma
3. Developmental cyst (neuroenteric cyst)
Additional diagnostic considerations:
1. Extramedullary haematopoiesis
2. Mediastinal haematoma


Chronic air space disease

1. Cryptogenic organising pneumoniae
2. Pulmonary alveolar proteinosis
3. Bronchioloalveolar carcinoma
Additional diagnostic considerations:
1. Chronic eosinophilic pneumonia
2. Lipoid pneumonia


Peripheral air space disease

1. Cryptogenic organising pneumoniae
2. Eosinophilic pneumonia
3. Pulmonary infarct
Additional diagnostic considerations:
1. Pulmonary contusion
2. Alveolar sarcoidosis


Ground glass opacification

1. Pulmonary oedema
2. Atypical infection
3. Pulmonary haemorrhage
Additional diagnostic considerations:
1. Acute respiratory distress syndrome
2. Alveolar proteinosis
3. Vasculitis


Mediastinal/hilar lymphadenopathy

1. Infection
2. Lymphoma
3. Sarcoidosis
Additional diagnostic considerations:
1. Metastatic disease
2. Pneumoconioses


Calcified pleural disease

1. Asbestos related pleural disease
2. Fibrothorax (prior infection or haemorrhage)
3.Iatrogenic (pleurodesis)
Additional diagnostic considerations:



1. Post-infectious (bacterial, TB and mycobacterium avium complex)
2. Cystic fibrosis
3. Allergic bronchopulmonary aspergillosis
Additional diagnostic considerations:
1. Obstructive lesion/mass
2. Ciliary dyskinesia


Perilymphatic pulmonary nodules

1. Sarcoidosis
2. Lymphangitic spread of tumour
3. Pneumoconioses
Additional diagnostic considerations:
1. Lymphoproliferative disorder


A pleural-based mass

1. Pleural-based metastatic disease
2. Empyema
3. Mesothelioma
Additional diagnostic considerations:
1. Fibrous tumour of the pleura
2. Fibrothorax


Parenchymal disease in an HIV patient

1. Pneumocystis pneumonia (PCP), caused by the yeast-like fungus Pneumocystis jirovecii
2. Tuberculosis
3. Fungal infection
Additional diagnostic considerations:
1. Invasive aspergillosis
2. Kaposi sarcoma
3. Pulmonary lymphoma


An abnormal left ventricular contour

1. True left ventricular aneurysm
2. False left ventricular aneurysm
3. Pericardial cyst/mass
Additional diagnostic considerations:
1. Calcific pericarditis


A cardiac mass

1. Thrombus
2. Metastatic disease
3. Benign cardiac neoplasm (atrial myxoma and rhabdomyoma)
Additional diagnostic considerations:
1. Malignant cardiac neoplasm (sarcoma and lymphoma)


Delayed myocardial enhancement

1. Infarction/scar
2. Myocarditis
3. Cardiac mass
Additional diagnostic considerations:
1. Infiltrative disease (granulomatous and amyloidosis)


Cardiac wall fatty deposition

1. Lipoma
2. Lipomatous hypertrophy of the interatrial septum
3. Arrhythmogenic right ventricular dysplasia
Additional diagnostic considerations:


What are the mechanisms of atelectasis?

1. Obstructive (alveolar oxygen absorbed by circulating blood and not replaced)
2. Relaxation (caused by an adjacent intrathoracic lesion such as mass, effusion or pneumothorax
3. Adhesive (surfactant deficiency, seen in neonatal respiratory distress syndrome and ARDS
4. Cicatrical (volume loss from architectural distortion of lung parenchyma by fibrosis)


What is the juntaphrenic peak sign?

A peridiaphragmatic triangular opacity caused by diaphragmatic traction from an inferior accessory fissure or an inferior pulmonary ligament.


What is the flat waist sign?

Flattening of the left heart border as a result of downward shift of hilar structures and resultant cardiac rotation in left lower lobe collapse.


What findings are required to diagnose round atelectasis?

1) Adjacent pleura must be abnormal.
2) Opacity must be peripheral and in contact with the pleura.
3) Opacity must be round or elliptical.
4) Volume loss must be present in the affected lobe.
5) Pulmonary vessels and bronchi leading into the opacity must be curved — this is the comet tail sign.


What is the (Core) differential diagnosis for acute consolidation?

1. Pneumonia (by far the most common cause of acute consolidation).
2. Pulmonary hemorrhage (primary pulmonary hemorrhage or aspiration of hemorrhage).
3. Acute respiratory distress syndrome (ARDS), which is noncardiogenic pulmonary edema seen in critically ill patients and thought to be due to increased capillary permeability.
4. Pulmonary edema may cause consolidation, although this is an uncommon manifestation.


What is the (Core) differential for chronic consolidation?

1. Bronchioloalveolar carcinoma mucinous subtype, a form of adenocarcinoma.
2. Organizing pneumonia, which is a nonspecific response to injury characterized by granulation polyps which fill the distal airways, producing peripheral rounded and nodular consolidation.
3. Chronic eosinophilic pneumonia, an inflammatory process characterized by eosinophils causing alveolar filling in an upper-lobe distribution.


What causes ground glass opacification?

1. Partial filling of the alveoli (by blood, pus, water, or cells).
2. Alveolar wall thickening.
3. Reduced aeration of alveoli (atelectasis).


What is the (Core) differential diagnosis for acute ground glass opacity?

1. Pulmonary edema, which is usually dependent.
2. Pneumonia. Unlike consolidation, ground glass is more commonly seen in atypical pneumonia such as viral or Pneumocystis jiroveci pneumonia.
3. Pulmonary hemorrhage.
4. Acute respiratory distress syndrome (ARDS).


What is the (Core) differential diagnosis for chronic ground glass opacity?

1. Bronchioloalveolar carcinoma, which tends to be focal or multifocal.
2. Organizing pneumonia, typically presenting as rounded, peripheral chronic consolidation.
3. Chronic eosinophilic pneumonia, usually with an upper-lobe predominance.
Idiopathic pneumonias, which are a diverse group of inflammatory responses to pulmonary injury.
4. Hypersensitivity pneumonitis (HSP), especially the subacute phase. HSP is a type III hypersensitivity reaction to inhaled organic antigens. In the subacute phase there is ground glass, centrilobular nodules, and mosaic attenuation.
5. Alveolar proteinosis, an idiopathic disease characterized by alveolar filling by a proteinaceous substance. The distribution is typically central, with sparing of the periphery.


What is the (Core) differential diagnosis for glass opacity in a central distribution?

1. Pulmonary edema.
2. Alveolar hemorrhage.
3. Pneumocystititis jiroveci pneumonia.
4. Alveolar proteinosis.


What is the (Core) differential diagnosis for peripheral consolidation or glass opacity?

1. Organizing pneumonia.
2. Chronic eosinophilic pneumonia, typically with an upper lobe predominance.
3. Atypical or viral pneumonia.
4. Pulmonary edema. Peripheral pulmonary edema tends to be noncardiogenic in etiology, such as edema triggered by drug reaction. Peripheral consolidation/ground glass is unusual for cardiogenic pulmonary edema.


What is the (Core) differential for smooth interlobular septal thickening?

Identical to the differential for central ground glass:
1. Pulmonary edema (by far the most common cause of smooth interlobular septal thickening).
2. Pulmonary alveolar proteinosis.
3. Pulmonary hemorrhage.
4. Atypical pneumonia, especially Pneumocystis jiroveci pneumonia.


What is the (Core) differential for nodular, irregular, or asymmetric septal thickening?

1. Lymphangitic carcinomatosis is tumor spread through the lymphatics.
2. Sarcoidosis is an idiopathic, multi-organ disease characterized by non-caseating granulomas, which form nodules and masses primarily in a lymphatic distribution.


What is the (Core) differential for crazy paving?

1. Alveolar proteinosis, where the ground glass opacification is caused by filling of alveoli by proteinaceous material and the interlobular septal thickening is caused by lymphatics taking up the same material.
2. Pneumocystis jiroveci pneumonia.
3. Organizing pneumonia.
4. Bronchioloalveolar carcinoma, mucinous subtype.
5. Lipoid pneumonia, an inflammatory pneumonia caused by a reaction to aspirated lipids.
6. Acute respiratory distress syndrome.
7. Pulmonary hemorrhage.


What is the (Core) differential for centrilobular nodules?

1. Endobronchial spread of tuberculosis or atypical mycobacteria. Atypical mycobacteria are a diverse spectrum of acid-fast mycobacteria that do not cause tuberculosis. The typical pulmonary manifestation of atypical mycobacteria is a low-grade infection typically seen in elderly women, most commonly caused by Mycobacterium avium-intracellulare.
2. Bronchopneumonia, which is spread of infectious pneumonia via the airways.
3. Atypical pneumonia, especially mycoplasma pneumonia.

Inflammatory (HSP & RB-ILD most common):
1. HSP is a type III hypersensitivity reaction to an inhaled organic antigen. The subacute phase of HSP is primarily characterized by centrilobular nodules. Generally more prominent nodules than RB-ILD.
2. Respiratory Bronchilitis-ILD (RB-ILD) is an inflammatory reaction to inhaled cigarette smoke mediated by pigmented macrophages.
3. Hot tub lung is a hypersensitivity reaction to inhaled atypical mycobacteria, with similar imaging to HSP.
4. Diffuse panbronchiolitis is a chronic inflammatory disorder characterized by lymphoid hyperplasia in the walls of the respiratory bronchioles resulting in bronchiolectasis. It typically affects patients of Asian descent.
5. Silicosis, an inhalation lung disease that develops in response to inhaled silica particles, is characterized by upper lobe predominant centrilobular and perilymphatic nodules.


What is the (Core) differential for peri-lymphatic nodules?

1. Sarcoidosis.
2. Pneumoconioses (silicosis and coal workers pneumoconiosis) are reactions to inorganic dust inhalation. The imaging may look identical to sarcoidosis with perilymphatic nodules, but there is usually a history of exposure (e.g. a sandblaster who develops silicosis).
3. Lymphangitic carcinomatosis.


What is the (Core) differential for randomly distributed nodules?

Usually occur via hematogenous spread and have an angiocentric distribution.
1. Hematogenous metastases.
2. Septic emboli. Embolic infection has a propensity to cavitate but early emboli may be irregular or solid.
3. Pulmonary Langerhans's cell histiocytosis (PLCH), a smoking-related lung disease that progresses from airway-associated and random nodules to irregular cysts. PLCH is usually distinguishable from other causes of random nodules due to the presence of cysts and non-angiocentric distribution.


What is the (Core) differential for tree-in-bud nodules?

Linear branching structures represent the impacted bronchioles (normally invisible) and the nodules represent impacted bronchioles/terminal bronchioles due to mucus, pus, or fluid.
1. Mycobacteria tuberculosis and atypical mycobacteria.
2. Bacterial pneumonia.
3. Aspiration pneumonia.
4. Airway-invasive aspergillus. Aspergillus is an opportunistic fungus with several patterns of disease. The airway-invasive pattern is seen in immunocompromised patients and may present either as bronchopneumonia or small airways infection.


What is the (Core) differential for multiple cavity lesions?

1. Septic emboli.
2. Vasculitis, including Wegener granulomatosis, which is especially prone to cavitate.
3. Metastases, of which squamous cell carcinoma and uterine carcinosarcoma are known to cavitate.


What is the (Core) differential for a single cyst?

1. Bulla. A bulla is an air-filled cyst measuring >1 cm. A giant bulla occupies at least 30% of the volume of the thorax.
2. Bleb. A bleb is a air-filled cystic structure contiguous with the pleura measuring <1 cm. Rupture of a bleb is the most common cause of spontaneous pneumothorax.
3. Pneumatocele, which is an air-filled space caused by prior lung trauma or infection.


What is the (Core) differential for basal-predominant fibrotic change?

1. Idiopathic pulmonary fibrosis (IPF), which is a clinical syndrome of progressive pulmonary fibrosis of unknown etiology and is most common cause of basilar fibrosis. It almost always features basilar honeycombing.
2. End-stage asbestosis. Asbestosis is an asbestos-induced inflammatory process ultimately producing pulmonary fibrosis. Usually other signs of asbestos exposure are present, such as pleural plaques.
3. Nonspecific interstitial pneumonia (NSIP), fibrotic form. NSIP is an idiopathic pneumonia. It is a lung response to injury commonly associated with collagen vascular disease and drug reaction. The two histologic subtypes are cellular and fibrotic forms, of which the latter may produce basal- predominant fibrosis. In contrast to IPF, honeycombing is usually absent.


What is the (Core) differential for upper lobe predominant fibrotic change?

1. End-stage sarcoidosis. Sarcoidosis is a disease that primarily affects the upper lobes. The late stage of sarcoidosis leads to upper-lobe predominant fibrosis.
2. Chronic hypersensitivity pneumonitis may cause upper-lobe fibrosis in long-standing disease.
3. End-stage silicosis. The late stage of silicosis may lead to fibrosis with an upper lobe predominance.


Why are round pneumonia's only found in children?

As children have incompletely formed pores of Kohn (connections between alveoli) and canals of Lambert (connections between diesel bronchiolar tree and adjacent alveoli) the infection remains somewhat confined..


What is Lady Windermere syndrome and what organisms are common?

A pattern of atypical mycobacterium infection typically seen in an elderly woman who chronically suppresses the normal cough reflex, low-grade fever and weight loss. Mycobacterium avium intracellulare and M. kansasii are the two most common organisms.
Classic radiographic findings are bronchiectasis and tree-in-bud nodules, most common in the right middle lobe or lingula.


What are the causes of finger in glove sign?

In bronchial obstruction, the portion of the bronchus distal to the obstruction is dilated with the presence of mucous secretions (mucus plugging).

1. Bronchial hamartoma
2. Bronchial lipoma
3. Bronchial carcinoid
4. Bronchogenic carcinoma
5. Congenital bronchial atresia (rarely)

Non-obstructive causes include:
1. Asthma
2. Allergic bronchopulmonary aspergillosis (ABPA)
3. Cystic fibrosis


What are the most common causes of a pre-existing cavity that an aspergilloma can form in?

1. TB
2. Sarcoid

Additional causes:
1. Congenital abnormalities such as bronchogenic cyst or sequestration
2. Post infectious pneumatocele
3. Post traumatic pneumatocele


What is the Monod sign?

When a crescent of air is seen outlining the aspergilloma against the wall of the cavity. The air crescent sign is reserved for angioinvasive aspergillus!


What is the differential for a halo sign?

1. Angioinvasive aspergillosis
2. Viral infection
3. GPA
4. Kaposi sarcoma
5. Hemorrhagic metastasis


What is the air crescent sign?

The air crescent sign, visually similar to the Monod sign surrounding an aspergilloma, represents a crescent of air from retraction of infarcted lung. It a good prognostic sign as it indicates that the patient is in the recovery phase.


What is a classic cause of isolated right upper lobe pulmonary oedema?

Acute mitral regurgitation secondary to myocardial infarction and papillary muscle rupture.