Adult Chest Flashcards
1
Q
Mnemonic for DDx of a lung cavitation
A
CAVITY
- Cancer: usually squamous
- Autoimmune: Wegeners, rheumatoid/Caplan syndrome
- Vascular: septic/bland emboli (Lemierre)
- Infection: TB (primary progressive or reactivation), mycobacterial
- Trauma: pneumatoceles
- Young/congenital: CPAMs, sequestrations
2
Q
Which structure is responsible for a juxtaphrenic peak?
A
The inferior pulmonary ligament.
- The juxtaphrenic peak is assoc w/upper lung volume loss of any cause.
3
Q
What forms the medial border of the R paratracheal stripe?
A
R tracheal wall.
- The medial pleura forms its lateral border.
- If it’s widened (>4mm) then it’s often due to lymphadenopathy.
- Other causes: mediastinal hemorrhage, mediastinal mass, vessel enlargement.
4
Q
What’s the name of the fissure that separates the medial basal segments from the other basilar segments (in both lungs)?
A
Inferior accessory fissure.
- It’s typically vertical & complete.
- More commonly seen on the R.
- The superior accessory fissure separates the lower lobe superior segment from the basilar segments.
5
Q
Which LN station is this?
A
- R lower paratracheal (4R).
6
Q
Which airway level is the first to lack cartilage in its wall?
A
Terminal bronchiole.
- Respiratory bronchioles branch off these & so are the 2nd airway to lack cartilage.
- These are the first airways to contain alveoli.
- They terminate as alveolar ducts.
7
Q
In the intercostal spaces, what is the cranial to caudal order of the neurovascular bundle?
A
VAN: vein, artery, nerve.
8
Q
Into what structure does the thoracic duct typically drain?
A
L subclavian vein + IJV confluence.
9
Q
What parts of the body does the thoracic duct not drain directly or indirectly?
A
- R upper extremity & chest.
10
Q
In which decade of life should there be complete fatty replacement of the thymus?
A
Eighth! So it’s entirely fatty by age 80.
- Don’t mistake a normal thymus for a thymolipoma, as the latter will have a discrete mass, containing fat (see below).
- A normal thymus will appear strandy.
11
Q
Name the muscle.
A
Supraspinatus
- The scapula creates a “T” shape dividing the muscles into subscapularis deep (or anterior) to the scapula, infraspinatus lateral and inferior to the spine of the scapula, and supraspinatus medial and superior to the spine of the scapula. Teres minor courses along the lateral aspect of infraspinatus.
12
Q
Which connective tissue disease is most highly associated w/obliterative bronchiolitis?
A
Rheumatoid arthritis.
- Obliterative bronchiolitis = air trapping.
13
Q
Pulmonary infarction typically involves which vessels?
A
- Pulmonary arteries.
- You know this b/c of PEs, which travel to the lungs via PAs.
- PEs & pulmonary involvement of vasculitis are the most frequent causes.
14
Q
DDx for tree-in-bud opacities & why?
A
DDx: endobronchial spread of infection (TB) & aspiration.
- It represents filling of the branching distal airways, and the centrilobular nodule/airway.
15
Q
What is the Monod sign?
A
- Fungal ball within a pre-existing cavity = aspergilloma.
- Frequently the mass is gravity dependent & can move.
16
Q
Name of this sign in the setting of PE?
A
Hampton hump
- Peripheral consolidation of a pulmonary infarct.
17
Q
With what exposure is pulmonary alveolar proteinosis associated?
A
- Silica.
- It can also be idiopathic.
18
Q
What is the name of this sign and what disorder is most closely related?
A
- Galaxy sign
- Sarcoid
19
Q
What is the max size limit of a pulmonary bleb?
A
- 1cm.
- Bulla >1cm
20
Q
At what CD4 count does PJP begin to occur in HIV pts?
A
<200
- CMV appears in sicker pts, CD4<100.
- So does aspergillus & nontuberculous mycobacterial, as well as cryptococcus, disseminated histoplasmosis.
- Ix findings of PJP & CMV are similar.
21
Q
MRSA infection:
- What is a risk factor for community-acquired infection?
- What abx are used to treat it?
A
- Incarceration.
- Ceftazidime & vancomycin: broad-spectrum.
22
Q
What is the most common infectious agent to cause pulmonary septic emboli?
A
- S. aureus
- May see the “feeding vessel” sign, which is a vessel supplying the infarcted parenchyma. This can also be seen in cancer.
23
Q
What is the next step in mgt for an immunocompromised patient with an acute respiratory illness and an abnormal chest radiograph with multiple, diffuse, or confluent opacities?
A
- CT chest w/o IV contrast.
- According to ACR Appropriateness Criteria.
24
Q
Dx? Pt who underwent heart xsplant 3 months prior.
A
Dx: aspergillis, “halo sign”.
- In the setting of heart transplant, new pulmonary parenchymal nodules are more likely infectious than neoplastic, though both should be considered depending on the clinical context. In this case, there is a solid nodule with surrounding ground-glass opacity, known as the halo sign. This sign is associated with invasive fungal infection, especially angioinvasive aspergillosis, which is a common opportunistic infection following transplant. CMV pneumonia much more commonly presents with diffuse ground-glass opacities than an isolated discrete nodule. There are no features to suggest rounded atelectasis in this case.
Posttransplant lymphoproliferative disease (PTLD) should be considered for nodules/masses in a posttransplant patient; however, it typically occurs at least 1 year after transplantation. Nodular disease prior to that time frame is much more likely to be infectious. PTLD is also commonly accompanied by intrathoracic lymphadenopathy.
25
What does this sign mean in a pt w/AML diagnosed w/invasive aspergillus?
* Healing infection.
* Angioinvasive aspergillosis occurs in severely immunosuppressed patients and is particularly common in leukemic patients with neutropenia. Early in the disease course, invasion of the pulmonary vasculature by the fungal hyphae results in vascular thrombosis, pulmonary infarction, and hemorrhage. The hemorrhage creates ground-glass opacity surrounding the nodule on CT, known as the halo sign. After recovery of a neutropenic patient’s granulocyte count—typically 2 weeks after disease onset—the devitalized necrotic center separates from the surrounding rim of hemorrhagic tissue. On CT, this appears as a peripheral crescentic collection of air surrounding the nodule, known as the “air crescent sign.” The presence of the air crescent sign portends a favorable prognosis, as it is associated with relatively improved survival.
26
What lobes are commonly affected in MAC infection?
RML/lingula
27
Which radiologic study is used to stage sarcoid?
CXR
* Named the "Scadding" classification system.
28
29
Dx?
**Dx: Langerhans cell histiocytosis**
Upper and mid lung–predominant centrilobular micronodules and thin-walled, bizarre-shaped cavitary lesions sparing the costophrenic angles are hallmarks of smoking-related PLCH. Upper and mid lung–predominant micronodules could be seen in upper respiratory viral infection or respiratory bronchiolitis related to smoking but have no association with cystic lesions. Vegetations on cardiac valves (usually tricuspid) with history of illicit drug use could lead to septic emboli but show a predilection to the lower lungs, migratory character, and foci of peripheral consolidation with frequent cavitation. Hypersensitivity pneumonitis (HP) caused by exposure to inhaled antigens presents with centrilobular micronodules and ground-glass opacities, but cysts seen in HP are distinct from the thin-walled cavitary lesions of PLCH.
PLCH lesions evolve from early bronchiolocentric multicellular dense infiltrates with Langerhans cells (with characteristic Birbeck granules) into a predominantly fibroblast-containing lesion with bronchiole dilatation (mid to late phase) followed by end-stage fibrotic stellate scars with paracicatricial airspace enlargement.
30
DDx thin-walled cystic lung:
* PLCH: bizarre-shaped, smoking, upper lung
* LAM: chylothorax, TS (AMLs)
* BHD: renal lesions
* LIP: Sjogrens
31
Difference b/w simple and chronic eosinophilic pneumonia?
Initial time course of disease in this patient, spontaneously resolving after 1 month, is consistent with simple eosinophilic pneumonia, also known as **Loeffler syndrome**, and helps differentiate from chronic eosinophilic pneumonia, which generally requires steroid treatment and/or identification of an underlying process.
Simple eosinophilic pneumonia also typically causes “shifting consolidations,” where chronic eosinophilic pneumonia will produce more static homogenous consolidations. Otherwise, both of these types of eosinophilic lung disease may produce similar peripheral consolidations, symptoms, and blood eosinophilia.
32
**Pulmonary alveolar proteinosis:**
1. What is the etiology of the majority of cases of PAP?
2. Which occupational exposure is associated?
3. Which medication types?
1. The majority of pulmonary alveolar proteinosis cases are primary/idiopathic and present in mid to late adulthood with progressive dyspnea or cough.
2. Silica.
3. Immunosuppressive therapies, such as sirolimus, are the primary mediations associated with secondary PAP.
33
With what disease is the following sign most highly associated?
**Hypersensitivity pneumonitis**
The head cheese sign reflects adjacent low, normal, and high attenuation in adjacent secondary pulmonary lobules. It reflects a combination of airspace disease (high attenuation) and obstructive disease (low attenuation). The low-attenuation small airway disease component reflects mosaic attenuation, and the high-attenuation component reflects ground-glass opacity.
The disease is most highly associated with subacute hypersensitivity pneumonitis and was initially considered pathognomonic. However, other diseases including sarcoidosis, atypical infections (such as Mycoplasma), respiratory bronchiolitis, and DIP have demonstrated this feature. Additionally, this sign can manifest in patients with multiple pathologic processes, such as constrictive bronchiolitis and pulmonary hemorrhage.
34
Dx? This previously healthy 36-year-old male experienced acute-onset worsening shortness of breath after traveling to the mountains for a hiking trip. No fever or chills are present.
**Dx: non-cardiogenic pulmonary edema/high-altitude pulmonary edema**
The radiograph demonstrates asymmetric, right greater than left airspace disease in an alveolar pattern. The airspace disease is greatest in the central lungs, and there are no identifiable effusions. Also, the heart is not enlarged. Given patient age and the lack of cardiac findings and effusions, cardiogenic edema is less likely. The other three considerations are possible; however, the history of recent high-altitude travel should make one strongly suspicious of high-altitude pulmonary edema (HAPE), a noncardiogenic pulmonary edema.
HAPE is a potentially fatal condition that occurs after traveling to a low-oxygen and low–atmospheric pressure environment (generally found at high altitudes). Most frequently, it occurs in young male patients 1 to 2 days after rapid ascent to elevations above 3,000 m. The mechanism is not well understood but likely is related to vasoconstriction and acute-onset pulmonary hypertension with resulting capillary leak. Treatment is supportive with return to normal altitude being critical.
35
What % of pts w/primary ciliary dyskinesia have Kartagener's?
50%!
here is significant lower lung predominant bronchial wall thickening and varicoid bronchiectasis with areas of consolidation and tree-in-bud opacity. Considerations for only those findings would include immunodeficiency (such as CVID), ciliary dyskinesia, or diffuse panbronchiolitis. However, this patient also has situs inversus totalis (note the right aortic arch and dextrocardia). This combination is characteristic of Kartagener syndrome, a subtype of primary ciliary dyskinesia, which also features infertility and chronic sinus disease. Fifty percent of patients with immotile cilia syndrome will have situs inversus totalis as the determination of situs during embryologic development requires normal ciliary beating. Nonfunctioning cilia result in situ being determined randomly with half being normal and half inverted.
Other common associations for the other answer choices include splenomegaly with CVID and East Asian heritage with diffuse panbronchiolitis. Sarcoid can present with central bronchiectasis related to fibrosis, but the distribution is typically upper lobe predominant.
36
Dx?
Dx: relapsing polychondritis.
* Posterior membrane spared.
* Thickening & increased attenuation, but no calcs.
37
To where are most FBs aspirated?
Right mainstem bronchus.
38
Which common connective tissue disease will present as bronchiolitis obliterans?
RA
* Will typically show air trapping (hallmark of small vessel disease).
39
1. What is the cause of these findings in a pt w/chronic renal failure?
2. What % on dialysis will get this?
1. Chronic dialysis causing metastatic calcs.
2. 60-75%.
40
What is the most common CT pattern found in pts w/rheumatoid arthritis?
UIP
41
1. Which autoimmune disorder has the highest risk of PE?
SLE, Lupus
42
What is the most common thoracic complication of lupus (SLE)?
* Pleural effusion.
* ~1/3 of SLE pts have antiphospholipid Ab syndrome, which increases their risk for PE.
43
What percentage of Wegener's (granulomatosis w/polyangitis) pts have cavitations of pulmonary nodules?
50%
44
What systemic disease causes this finding?
SLE (lupus), causes shrinking lungs syndrome.
* It causes progressive diaphragm weakening and restricted chest wall expansion.
45
