Chest Flashcards
Stacked cystic spaces/honeycombing, lower lobe predominant, subpleural reticulation, architectural distortion, and volume loss
UIP Pattern–
a/w connective tissue disorders (esp RA but can be seen in others//)
IF no clinical cause, then it’s IPF
Ground glass opacities + fibrosis, lower lobe predominant, peripheral, fine reticulation. NO honeycombing
usu w/subpleural sparing, more symmetric
NSIP Pattern
Fibrotic type and cellular type, fibrotic more common
a/w CTD–esp dermatomyositis/polymyositis, sjogrens, SLE
anti-synthetase, RA, etc
Drug reactions esp chemo
Castleman disease
NOT associated with smoking
Upper lobe predominant centrilobular ground glass, OR prominent mosaic pattern
Hypersensitivity Pneumonitis
(subacute)
chronic peribronchiolar inflammation w/poorly defined granulomas and giant cells in the interstitium or alveoli on pathology.
these resolved without antibiotics
Hypersensitivity pneumonitis
lobular GGO
Need constellation of findings to dx: exposure to an offending antigen, characteristic signs and symptoms, abnormal chest findings on physical examination, and abnormalities on pulmonary function tests and imaging
describe, and dx
chronic hypersensitivity pneumonitis
Mosaic pattern with areas of ground-glass atenuation and areas of low attenuation.
Fibrosis and parenchymal distortion in a mid zone distribution.
left vs right?
Left UIP w honeycombing
Right Chronic HP
Ground Glass and Fibrosis
Ddx
- NSIP
- HP in a non-smoker
- DIP in a smoker (bilateral, symmetric, peripheral, LL predominant, may be end spectrum of RB-ILD)
- RB-ILD in a smoker (may have UL predominance, or nonspecific involvement, other changes related to smoking//, patchy hypoattenuation with lower lung predominance, poorly defined CL nodules
GGO with fibrosis, and cystic changes, irregular linear opacities
DIP
classically described as triangular-shaped regions of increased density radiating from the hilar regions to the periphery; although seen in a minority
COP
Multifocal peripheral GGO and consolidations (subpleural/peribronchial)
–when there is no underlying cause identified,
otherwise it’s 2* OP
Lymphangioleiomyomatosis (LAM)
Large thin-walled cysts diffusely distributed in the lungs that will eventually replace the entire lung parenchyma.
exclusive to women of child-bearing age, except for TS associated in men
–lymphangiomas and AMLs are commonly associated.
–A/w chylothorax
Empyema necessitans
chronic empyema attempting to decompress through the chest wall.
Common organisms include Tuberculosis, Actinomycosis, Staphylococcus, Aspergillosis, Mucormycosis, and Blastomycosis.
Look for loculated pleural fluid or mass with rib destruction.
Diagnosis = fine needle aspiration biopsy and microbiology.
Treatment = surgical drainage and antibiotics.
“BATMAN”
In a patient w/remote hx of blunt chest trauma and no spleen
Splenosis
autotransplantation of splenic tissue following traumatic or surgical disruption of the spleen.
Look for multiple pleural masses in the left hemithorax in a patient with a history of remote trauma.
Tc-99m sulfur colloid is often used to diagnose (uptake in splenic tissue, specifically reticuloendothelial tissue).
63M with chronic cough
Lung Adenocarcinoma
mixed ground-glass and solid consolidation –> “cancers that look like PNA”
-> lymphoma also looks like PNA
43yo F with SLE presents with dyspnea
Pericardial Effusion
cardiac shadow is enlarged but the pulmonary vessels are not dilated –> suspect a pericardial effusion.
azygous vein and SVC may be dilated, reflecting the elevated central venous pressure necessary to maintain right ventricular filling.
mediastinal interface over the left hilum in the absence of enlargement of the pulmonary arteries should also alert you to possibility of a pericardial effusion (fluid accumulating in a pericardial recess) because an enlarged cardiac chamber, such as the left atrial appendage, will not produce an interface this high along the left cardiac border.
Asymptomatic pt with persistent opacity on CXR
Broncholith
should always be considered as a potential etiology when calcified intrapulmonary lymph nodes are present, particularly when they are located in the involved bronchopulmonary segment.
—Other things that can happen in bronchi:
—> soft tissue endobronchial lesion could be carcinoid
—> diffuse or segmental bronchial wall thickening could be seen in GPA/Wegener’s
Post-op. What are these wires?
From a sternotomy:
from a broad transverse incision across the anterior chest wall and the sternum and (typically) along the anterior 4th intercostal spaces = a redo “clamshell” sternotomy.
Elderly lady w/RUL PNA—> what is the most likely causative organism?
actinomycosis
mass-like right upper lobe consolidation with a parapneumonic pleural effusion. Bone window w/permeative destruction of adjacent skeletal structures.
49 year old woman with a rash on her face. CT chest with multiple thin walled cysts
LAM
a/w renal AMLs and LAD, seen here
Almost exclusively middle aged women although can also occur in TS
p/w exertional dyspnea, recurrent PTX is common
Newly developed
Aspiration PNA
Atalectasis in both LL but also new consolidation and fluid in the bronchi (higher up also see fluid in the esophagus)
hypoplastic right lung with ipsilateral mediastinal shift and vertical vein (PAPVR of a portion or all of the right lung)
Scimitar Syndrome
Could also px as: bilobed right lung with a hyparterial right main and upper lobe bronchus
If systemic arteries from the abdomen are found to supply a portion of the lung, the resultant “complete” entity is also known as the scimitar syndrome.
**hyparterial bronchus–bronchus is below the PA (normal on the L but not the R)
Most likely diagnosis?
Neurofibromatosis
most common thoracic manifestations include neurofibromas in the subcutaneous tissues and mediastinum. In this case, innumerable neurofibromas are present in the axillae , chest wall , and mediastinum . Although not present in this case, other regions of the chest, including the lungs and osseous structures such as the spine and ribs, may be affected.
50M w/40 year smoking hx
RB-ILD
upper lung zone predominant process that features patchy ground-glass opacities and faint centrolobular nodules, as seen in this case. On a spectrum with DIP. Can see RB-ILD within 2 years of starting smoking, and treatment is cessation.
LCH—> Langerhans cell granulomatosis is seen almost exclusively in smokers. Imaging features of Langerhans cell granulomatosis include centrilobular nodules that eventually evolve into bizarre-shaped cysts and resultant paracicatricial emphysema
Incidental finding in asx. pt
Bronchial Atresia
the combination of a blind-ending tubular opacity and a hyperinflated/hypovascular left upper lobe is typical of bronchial atresia.—> mucocele is also typical.
LUL, particularly apico-posterior segment MC location
Congenital lobar hyperinflation usu presents in neonatal period w/respiratory distress
Both AVM and intralobar sequestration would have more prominent vessels
large extrapulmonary/soft tissue mass in an adolescent or young adult, may involve ribs/chest wall
Askin tumor
form of primitive neuroectodermal tumor (PNET).
arises in the soft tissues of the thorax. Children and young adults, present with chest wall pain. Radiographs show a heterogeneous mass with or without rib destruction. Rib destruction is less common than in Ewing sarcoma. An Askin tumor may or may not have a pleural effusion. Lung and bone mets are common.
–> Ewings would be lytic lesion with cortical destruction
Pt w/prior SCC in the lungs now w/GGN opposite lung w/bx showing adeno.
Synchronous lung cancer
metachronous lung cancer
hematogenous met
Satellite nodule
Metachronous lung cancer
Metachronous lung cancers are 2 or more separate lung cancers separated by time without systemic metastases.
Satellite nodules are tumor nodules found in the same lobe as the primary tumor that also have the same histology.
Synchronous lung cancers are 2 or more separate lung cancers detected simultaneously without systemic metastases.
Smoker
DIP
60% peripheral subpleural, diffuse hyperattenuation of parenchyma 2/2 pigment laden macrophages
RB-ILD = faint centrilobular nodularity, upper lung predominant
PLCH = ?allergic or immune reaction to cigarette smoke–> diffuse centrilobular nodules that evolve into bizarre cysts.
Round or oval anterior mediastinal mass, w/calcification, drop mets may be present
Thymoma
MC anterior mediastinal mass.
Thymic carcinoma has less well defined borders and can have necrosis.
Thymic carcinoid generally has local nodal and mediastinal spread. may have paraneoplastic syndromes (usu Cushings) and 20% a/w MEN 1
GCTs have fat, cystic areas, and coarse calcs
Pt p/w acute CP and tachycardia
Westermark Sign in acute PE
decreased caliber of pulmonary vessels in affected area
Ddx for calcified parenchymal findings
Granulomas (punctate, or in nodes)
Sarcoid/other worker’s lung (eggshell calcs in silicosis, coal worker’s pneumoconiosis, histo, blasto etc
–> pulmonary sarcoid doesn’t calcify in parenchyma, while others do
pulmonary ossification (dendriform or nodular)
tumors
hamartomas
patient with Painless LAD
can also px as asx mediastinal mass(can have calcifications), periosteal reaction
+/- pleural effusion
Castleman disease (*unicentric)
aka angiofollicular lymph node hyperplasia or giant lymph node hyperplasia = uncommon benign B-cell lymphoproliferative condition.unicentric and multicentric (a/w HIV)
unicentric: more common, localized, and locally treated, associated with minimal symptoms or asymptomatic
multicentric: usually in the context of HIV infection, systemic disease characterized by diffuse lymphadenopathy, anemia, splenomegaly, and systemic inflammatory symptoms
Migratory opacities
peripheral upper lobe predominant
vs
peripheral/PBV distribution
Ddx: COP and Eosinophilic Pneumonia (CEP)
upper lobes = CEP
PBV = COP
IntRAlobular septal thickening– reticulation is more proper term
–> ‘crazy paving’
PAP is classic, although rare
can also be caused by sarcoid, asbestosis, pulmonary edema,
nodular septal thickening
think lympangitic carcinomatosis
–> in separate lobe from mass, usually asymmetric, can be isolated to one lobe
-> if more diffuse think more like sarcoid (PBV/lymphatic distribution)
perilymphatic nodules in SARCOID
Diffuse CL nodules, differential?
Atypical infection, RB-ILD, acute HP, vasculitis
if Tree in Bud–
aspiration PNA, MAI, viral/atypical infx.
PCP
Immunocompromised patients (HIV)
pneumatoceles, subpleural blebs, fine reticular (interstitial) changes, perihilar distribution
*pleural effusions not typical
LAD also rare
GG and pneumatoceles in perihilar distribution is classic on CT
*can have crazy paving, cavitary nodules,
Ddx for endobronchial mets
Kiss My RBCs
Kaposi’s sarcoma
Melanoma
RCC
Breast
Colon
Bochdalek vs Morgagni hernias?
Bochdalek: posterolateral
Morgagni: anteromedial, adjacent to lower sternum
both typically contain fat rather than hollow viscus
Esophageal hernia: sliding vs paraesophageal
Sliding: GEJ comes up into chest
Paraesophageal: GEJ stays under diaphragm and a different portion of stomach comes up
Paraneoplastic syndomes a/w Thymoma
myasthenia gravis
pure red cell aplasia
hypogammaglobulinemia
Causes of UIP Pattern?
IPF if idiopathic (exclusion)
drug toxicity
asbestosis
Collagen Vascular disease (ESP RA)
rarely, IBD
Mosaic attenuation with SMALL vessels (not absent)
Bronchiolitis obliterans
(Obstructive small vessel disease vs obstructive small airways disease)
expiratory views can confirm obstructive hyperinflation (air trapping)–> in this case, look for causes of bronchiolitis obliterans/constrictive bronchiolitis
**follicular bronchiolitis has additional findings (CL and GG nodules)
Histoplasmosis findings
uni or bilateral nodules/consolidations with reactive LAD
Tree in bud nodules: MC organisms?
viral
mycoplasma
Chlamydia pneumoniae
Causes of NSIP
collagen vascular disease, especially systemic sclerosis, mixed connective tissue disease, and polymyositis/dermatomyositis.
Other causes: drug reaction, familial fibrosis, and hypersensitivity pneumonitis.
subpleural sparing is highly specific if present **
What findings do you see with fibrosing mediastinitis?
MASS effect on mediastinal structures including compression of airway and vessels
Dystrophic calcifications often present
MCC is previous histo plasma infection(immune response to histoplasmosis antigens)—>
p/w dyspnea and can get SVC syndrome signs like facial swelling
Cavitary and solid nodules, and circumferentially thickened trachea:
Wegener’s granulomatosis
small vessel vasculitis
Mycoplasma pneumoniae infection in childhood can cause what?
swyer james mcloud syndrome–> mosaic attenuation, air trapping, and bronchiectasis.
(Mycoplasma is MC atypical organism in young adults w/atypical PNA, most in fall and winter)
sequestration: define
nonfunctioning lung that gets blood supply from systemic circulation–can see feeding artery to clinch dx. Often p/w recurrent “PNA” with left paraspinal consolidation. can have air fluid level//cycstic//solid components
MC location:
intralobar sequestration (ILS)
75-85%, present later in childhood with recurrent infections
extralobar sequestration (ELS)
less common 15-25%, usually present in the neonatal period with respiratory distress, cyanosis, or infection
M > F 4:1
~10% infradiaphragmatic
What findings to look for in airway predominant COPD/Chronic bronchitis?
Saber sheath trachea, bronchial wall thickening and mucus
Emphysematous changes can be sparse or absent
Takayasu Arteritis
Keys to Dx:
Smooth narrowing/thickening of aorta and main vessels w/predeliction for L Subclavian artery. PA involved occasionally
patchy and symmetric
Majority in <30, F>M, M/M r/t HTN and stroke
Fleischner sign for acute PE?
dilated PA
Cause of left atrial calcification?
Sequela of rheumatic heart disease
patients typically have coexisting mitral stenosis
Tracheobronchopathic osteochondroplastica
nodular excrescences of partially calcified cartilage
eldery patients, affects distal trachea and proximal bronchi
amyloid can also cause similar appearance–focal or diffuse, and MC form of pulmonary amyloid.
LIP: describe
scattered cysts in basilar predominant distribution.
scattered nodules and GG associated
pt’s commonly have Sjogren’s
Unilateral hyperlucent lung?
Swyer James syndrome
Unilateral bronchiolitis obliterans
–> regular BO ddx includes: cryptogenic, postinfectious (viral), toxic fume inhalation, bone marrow and lung transplantation rejection, rheumatoid arthritis, inflammatory bowel disease, and drug toxicity (penicillamine)
4 vessel sign: what abnormality?
Double aortic arch
get bilateral subclavian and common carotid
classic for what?
Reverse halo:
Organizing PNA, specifically COP
distribution is normally basilar predominant, peripheral
*not to be confused with halo sign of invasive fungal (although can see reverse halos in inv. fungal infx. too)
what features render a lung cancer non-resectable?
T4 tumors, N3 lymph nodes, and metastatic disease (M1a and M1b).
T4 tumors = invasion of mediastinal structures or vertebral bodies , tumor nodules in separate lobe of the same lung.
N3 lymph nodes= scalene, supraclavicular, contralateral mediastinal , and contralateral hilar
Metastatic (M1) disease= tumor nodules in contralateral lung, malignant pleural effusions, pleural metastases, metastases to distant organs
Pt px w hemoptysis
cause and differential?
(widespread GGO and consolidation)
Diffuse alveolar hemorrhage
Ddx: vasculitis: Wegener’s Granulomatosis, Microscopic polyangiitis, Churg Strauss, SLE
idiopathic pulmonary hemosiderosis
can have crazy paving as hemorrhage resolves (airspace–>interstitial progression)
diffuse pulmonary edema px within hours of toxic fume inhalation
Farmer’s lung
bronchiolitis obliterans is late manifestation
Ddx in pt with fever?
Diffuse miliary nodules and GGO
–VIral PNA
VZV esp if some are calcified
CMV, and flu also possible
pt with asthma presents with mononeuritis multiplex
Churg Strauss
small vessel vasculitis
peripheral eosinophilia, allergic hx, and systemic vasculitis
on CT –peripheral consolidation and GGO (can look like AEP- which is what pic actually w1as)
hyparterial, epiarterial bronchi?
hyparterial: bronchus below PA
Epiarterial: bronchus above PA
Osseous sclerosis, septal thickening, and perirenal encasement (‘hairy kidney’)
Erdheim Chester
non-langerhans cell Histiocytosis
–can also involve retroperitoneum and intracranial (look like meningioma)
most common tumor of cardiac valves?
papillary fibroelastoma
rounded, often <1cm, usually solitary
uncommon to embolize
Newborn. Ddx?
Ebstein anomaly
–displaced septal leaflet towards apex of heart, massively dilated RA and also RV
pulmonary atresia
tricuspid atresia
in all will get cardiomégaly and decreased pulmonary vascularity
Infective endocarditis
right sided can get associated septic emboli to the lungs (peripheral, can be cavitary
left sided can get associated septic emboli to the brain and systemic organs
here, tricuspid valve encased
Azygos vein course and pathology?
Originates from the ascending lumbar and right subcostal veins around T12-L2, and ascends through aortic hiatus or pierces right crus.
similarly on the left, hemiazygos vein which drains into azygos vein and this dumps into SVC at the arch of the right main bronchus
–dilated azygos vein can happen with aplastic or interrupted IVC
