Chest Flashcards
3 causes of chronic consolidation?
Adenocarcinoma in situ/minimally invasive adenocarcinoma/invasive adenocarcinoma
Organizing pneumonia
Chronic eosinophilic pneumonia
4 causes of central ground glass opacities?
Pulmonary oedema
Alveolar haemorrhage
Pneumocystis jiroveci pneumonia (PCP) - cancer, HIV, transplant
Alveolar proteinosis
Fibrosing mediastinitis
- Causes?
- Pathologic mechanism?
- Imaging appearance?
- Idiopathic (?IgG4), TB, histoplasmosis, radiation, sarcoid, drugs
- Causes compression of mediastinal structures
- Increased mediastinal soft tissue/mass, obliteration of mediastinal fat, calcification within mass or calcified nodes, may be focal lung abnormalities - opacities, septal thickening
8 causes of pulmonary hypertension?
- Primary (idiopathic) arterial hypertension
- Chronic thromboembolic pulmonary HTN
- Pulmonary veno-occlusive disease
- Chronic hypoxia - COPD, interstitial fibrosis, sleep apnoea
- Pulmonary venous HTN secondary to left-sided heart disease incl. aortic/mitral pathology
- Left-to-right sided shunt (ASD, VSD)
- Sarcoid
- Fibrosing mediastinitis
A few key points about staging of lung cancer:
- General cut off point for surgical resection?
- stage IV can be resected when?
- Tends to be stage IIB/IIIA - when there is contralateral nodal involvement or tumour >7cm
- solitary adrenal or brain metastasis
Solid pulmonary nodules
- at what size do they not need follow up?
- when to do a Brock score?
- what is a raised Brock score and what to do next?
- when can you discharge a solid nodule from follow up?
- <5 mm
- solid nodule >8 mm
- > 10% - do a PET-CT
- if the nodule is stable (<25% increase on volumetry, VDT >600 days)
Aspergillus - categories of pulmonary disease?
- Allergic bronchopulmonary aspergillosis (asthmatics, CF)
- Aspergilloma - in a pre-existing lung cavity (Monod sign)
- Subacute invasive pulmonary aspergillosis. Affects the debilitated, diabetic, etoh, COPD. Upper lobe consolidation → cavitation, pleural thickening
- Airway-invasive. Severely immunocompromised patients. Centrilobular and tree-in-bud nodularity.
- Angio-invasive. Severely immunocompromised. Halo sign (haemorrhagic infarction of surrounding lung), air crescent sign (air from retraction of infarcted lung - a good sign!)
Lady Windermere syndrome
Right middle lobe or lingula lobe bronchiectasis and tree-in-bud change in an older female, non-smoker, with cough, weight-loss, low-grade fever. Secondary to atypical Mycobacteria (avium intracellulare, kansasii).
Imaging manifestations of primary TB?
Nothing
Ill-defined consolidation
Adenopathy (peripheral enhancement, central low attenuation)
Pleural effusion
Miliary disease
Aspergillosis imaging findings?
Fleeting pulmonary opacities
Mucoid impaction - “finger in glove”
Bronchiectasis
Centrilobular nodules
Causes of lymphangitis carcinomatosis?
Certain Cancers Spread By Plugging The Lymphatics
Cervix
Colon
Stomach
Breast
Pancreas
Thyroid
Lung
Chest x-ray signs of PE
Westermark sign - regional oligaemia
Hampton’s hump - wedge shaped peripheral opacity
Fleischner sign - enlargement of the pulmonary arteries
4 causes of UIP pattern?
Trio of signs for UIP?
Idiopathic pulmonary fibrosis
Collagen vascular disease - rheumatoid arthritis, scleroderma
Drug injury
Asbestosis
Subpleural reticulation
Honeycombing with traction bronchiectasis
Apicobasal gradient
NSIP
- 2 forms of NSIP?
- Imaging findings?
- Most commonly seen in which patients?
- Steroid responsive?
- Fibrotic and cellular - cellular has better prognosis
- Bilateral symmetrical ground glass opacities, less prominent fibrotic changes, immediate subpleural sparing (this is v. specific), homogenous lung involvement in a subpleural pattern, microcysts and micronodules
- Those with collagen vascular diseases (SLE, scleroderma, RA, polymyositis)
- Yes - important to make the diagnosis as better prognosis than UIP/IPF
COP aka BOOP
1. Associations?
2. Steroid-responsive?
3. Imaging findings?
- Idiopathic, post-infectious, rheumatological conditions, CF, post-transplant, medications (bleomycin, nitrofurantoin)
- Very - but frequent relapse on cessation
- Peripheral patchy lung consolidation/GGO Atoll sign/reverse halo sign
Nodules - small centrilobular mimicking HSP
Larger nodules which cavitate
Or may be a single mass that mimics lung cancer
Perilobular fibrosis “arcade sign”
May be bronchial dilatation within consolidation
May be subpleural sparing
RB-ILD - respiratory bronchiolitis-interstitial lung disease
Demographics?
Imaging?
Young smokers
Centrilobular nodules and patchy GGO, upper lobes
Continuum with DIP
DIP - desquamative interstitial pneumonia
Imaging?
Patchy or subpleural GGO - more extensive that RB-ILD, peripheral predominance
LIP - lymphoid interstitial pneumonia
Causes?
In a child?
Imaging?
Idiopathic, HIV, Sjogren’s, autoimmune, infection (HBV, PCP, EBV), Castleman’s
Think HIV
Diffuse (or lower lobe) GGO
Thin-walled perivascular cysts
Pneumothorax
AIP
- Clinical features?
- Imaging?
- Bad prognosis, acute onset, Previously fit and well require ventilation in 1-4 weeks.
- Bilateral, symmetrical, lower lobe GGO and alveolar consolidation from oedema/haemorrhage, then later fibrotic changes in non-dependent lung
Classically spares the costophrenic angles
Pleural fibroma
- associations?
- imaging findings?
- management?
Hypoglycaemia, HPOA, not asbestosis
Smooth with contrast enhancement
Surgical resection - 1/3 undergo malignant transformation
Hypersensitivity pneumonitis (HSP) - organic!
Imaging findings?
Acute - GGO or consolidation
Subacute - ground glass centrilobular nodules, mid to lower zones, mosaicism
Chronic - fibrosis affecting the upper lobes
Coal worker’s pneumoconiosis
- classification?
- CWP imaging findings?
- PMF imaging findings?
Simple or complicated - complicated has PMF pulmonary massive fibrosis
Multiple small upper and mid zone opacities +/- calcification; enlarged hilar LNs, which are often calcified
Peripheral upper/mid zone mass >1cm, may be bilateral, may become necrotic + cavitate