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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
.pdf
USMLE Step 2 CK
l Internal Medicine
Note
The answers can be found at
the end of this chapter.
Respiratory acidosis or ‘normalization’ of pH in patients with acute asthma exacerbation may
be an indication for intubation.
Three days after hospitalization the patient is improving, and you decide to send her home.
What is her drug regimen likely to be at this time?
She comes to you 3 months later for follow-up. She needs documentation of asthma for her
work. What will you do now? What medications is she likely to be taking now?
For testing purposes, we will simplify the guidelines into the following classifications.
• Mild Intermittent Asthma
– Symptoms of cough, wheeze, chest tightness, or difficulty breathing ˂2x/week
– Flare-ups-brief, but intensity may vary
– Nighttime symptoms <2x/month
– No symptoms between flare-ups
– Lung function test FEV1 that is ≥80 percent of normal values
– Treatment: inhaled short-acting bronchodilators as needed
• Mild Persistent Asthma
– Symptoms of cough, wheeze, chest tightness or difficulty breathing 3−6x/week
– Flare-ups-may affect activity level
– Nighttime symptoms 3−4x/month
– Lung function test FEV1 that is ≥80 percent of normal values
– Treatment: start with inhaled corticosteroid and SABA; if not enough improve-
ment, add leukotriene inhibitor and possible LABA
• Moderate Persistent Asthma
– Symptoms of cough, wheeze, chest tightness, or difficulty breathing daily
– Flare-ups-may affect activity level
– Nighttime symptoms ≥5x/month
– Lung function test FEV1 that is >60 percent but <80 percent of normal values
– Treatment: start with inhaled corticosteroid and SABA; leukotriene inhibitor and
LABA will likely be needed to improve nighttime symptoms
• Severe Persistent Asthma
– Symptoms of cough, wheeze, chest tightness or difficulty breathing continual
– Nighttime symptoms frequently
– Lung function test FEV1 that is ≤60 percent of normal values
– Treatment: inhaled corticosteroid, SABA (as needed), leukotriene inhibitor, and
LABA will likely be needed, as well as oral steroids (prednisone) at lowest possible
dose
– Do not stop leukotriene inhibitors and LABA once oral corticosteroids have been
started
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Allergic Bronchopulmonary Aspergillosis
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Allergic bronchopulmonary aspergillosis (ABPA) is an allergic lung reaction to a fungus (most
commonly Aspergillus fumigatus) seen in some patients with asthma or cystic fibrosis. Other
fungi, including Penicillium and Candida, can cause an identical illness. In some people, the
effects of the allergic reaction combine with the effects of the fungus to damage the airways
and lungs further.
• The fungus does not actually invade the lung tissue and directly destroy it; rather, it
colonizes the mucus in the airways of patients with asthma or cystic fibrosis (both of
whom have increased amounts of mucus) and causes recurrent allergic inflammation
in the lung.
• The alveoli become packed primarily with eosinophils.
• If the disease has caused extensive damage, bronchiectasis and scarring occur.
The first indications of allergic bronchopulmonary aspergillosis are usually progressive symptoms of asthma, such as wheezing and shortness of breath, and mild fever. The person usually
does not feel well. Appetite may decrease. Brownish flecks or plugs may appear in coughedup sputum. Repeated chest x-rays show areas that look like pneumonia, but they appear to
persist or migrate to new areas of the lung (most often the upper parts). In people with longstanding disease, chest x-ray or CT may show bronchiectasis.
Chapter 9
l Pulmonology
The fungus itself, along with excess eosinophils, may be seen when a sputum sample is examined
under a microscope. Blood test reveal high levels of eosinophils and antibodies to Aspergillus.
The level of immunoglobulin E in the blood is also elevated. Skin testing can determine if the
person is allergic to Aspergillus, though it does not distinguish between allergic bronchopulmonary aspergillosis and a simple allergy to Aspergillus. Treatment is with corticosteroids.
Chronic Obstructive Pulmonary Disease (COPD)
A 67-year-old woman with COPD is evaluated for dyspnea that occurred the prior
day. She denies fever and chills but has noted productive cough. Her medications
include ipratropium MDI. Her respiratory rate is 32/min and pulse 106/min;
she is afebrile. She looks cachectic and is breathing fast. You note an increased
anteroposterior diameter, distant heart sounds, and expiratory wheezing.
Definition. COPD includes patients with emphysema and chronic bronchitis. Emphysema and
bronchitis must be identified as separate entities, but most patients with COPD have characteristics of both conditions. Patients with chronic bronchitis have productive cough for most days of
a 3-month period for at least 2 consecutive years. In emphysema patients have abnormal permanent dilation of air spaces distal to the terminal bronchioles with destruction of air space walls.
Both of these processes are defined by nonreversible obstruction of the airways. This is the
pathognomonic differentiating finding on PFTs when compared with asthma.
Cigarette smoking is a cause of COPD, with 10–15% of smokers developing COPD (80–90%
of COPD patients are cigarette smokers). COPD symptoms usually begin after at least
20 pack-years of tobacco exposure. The number of pack-years of smoking correlates to the
reduction of FEV1. The fact that a small percentage (10–15%) of smokers develops COPD
suggests that other factors may be involved in the pathogenesis. Air pollution, airway infections, and allergies can lead to bronchitis.
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a1-antitrypsin deficiency is a rare hereditary autosomal recessive disease that can cause
emphysema and liver abnormalities.
Pathogenesis. After long-term exposure to cigarette smoke, inflammatory cells are recruited
in the lung. These inflammatory cells in turn secrete proteinases, which may lead to air
space destruction and permanent enlargement. Eventually, decreased elastic recoil (mainly in
emphysema) and increased airway resistance (mainly with chronic bronchitis) occur.
Physical Examination. In emphysema, distant breath sounds will be heard on auscultation. In
chronic bronchitis, there may be evidence of rhonchi and wheezes to auscultation. Signs and
symptoms of right heart failure (cor pulmonale) and clubbing can also be seen on physical
examination in COPD.
Note
The answer to this
question can be
found at the end
of this chapter.
wikipedia.com
Figure 9-9. Clubbing of the Fingers Seen with Chronic Hypoxemia
In chronic bronchitis, increased pulmonary markings can be seen on chest x-ray; in emphysema, hyperinflation of bilateral lung fields with diaphragm flattening, small heart size, and
increase in retrosternal space can be seen.
Cor pulmonale in COPD is associated with chronic pulmonary hypertension.
Diagnosis. PFTs are the diagnostic test of choice. On PFT, a reduction in FEV1/FVC ratio and
FEF
occurs. RV and TLC are usually increased in COPD. Emphysema will have a decreased
25–75
DLco, whereas chronic bronchitis will generally have a normal DLco.
After a bronchodilator is given, you would expect the FEV1/FVC to __________.
Complications. Hypoxemia with nocturnal desaturation is sometimes seen. Secondary eryth-
rocytosis can result from chronically low Po2. Pulmonary hypertension is a complication that
can lead to cor pulmonale and subsequent right heart failure. Chronic ventilatory failure and
CO2 retention are seen in chronic bronchitis early and at the end stages of emphysema.
Management of Stable Phase COPD. The goal in treatment is to treat airway inflammation and bronchospasm, reduce airway resistance and work of breathing, and improve gas
exchange and ventilation-perfusion (V •/Q) mismatching.
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Anticholinergic agents (ipratropium bromide [Atrovent®] and tiotropium) are the first-line drugs
in COPD. These agents are given via MDI and control airway caliber and tone. Anticholinergic
agents can be used synergistically with b2-adrenergic agonists in patients with COPD.
b2-adrenergic agonists (albuterol) are used after anticholinergic agents. The inhaled route is
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the preferred administration.
Beta agonists are not first-line agents in the management of COPD because many of the
patients have underlying heart disease and the tachycardia commonly associated with these
agents may precipitate heart failure.
Chronic inhaled corticosteroids are reserved for severe cases of COPD.
Theophylline, a xanthine derivative, may be added to the regimen if beta-2 agonists and anticholinergics are not effective in managing the symptoms of chronic obstructive lung disease.
Remember that theophylline has significant toxicity. Symptoms include nausea and vomiting, palpitations, and tremulousness. Death can occur from theophylline toxicity from cardiac
arrhythmias.
The list of drug interactions with theophylline is significant. Theophylline levels increase with
fluoroquinolones, clarithromycin, H2-blockers (cimetidine, ranitidine), certain beta blockers
and calcium channel blockers. Theophylline levels decrease (due to increased clearance) with
rifampin, dilantin, phenobarbital, and smoking.
Despite the above treatments, the only interventions which have been shown to decrease mortality in patients with COPD are home oxygen and smoking cessation.
Chapter 9
l Pulmonology
Home oxygen therapy is given to patients with hypoxemia (Pao2 <55 mm Hg or saturation
<88%), and the goal is to try to keep the O2 saturation >90% as much as possible, especially at
night when patients generally desaturate. Patients with cor pulmonale will benefit from home
oxygen when Pao2 <59 mm Hg. A special category is the patient who desaturates with exercise;
she or he will benefit from intermittent oxygen.
All patients with COPD must have the pneumococcal vaccine (Pneumovax®) every 5 years and
the influenza vaccine yearly. They should also receive the H. influenzae vaccine if they were not
previously immunized.
Several trials have failed to find a beneficial effect for the regular chronic use of inhaled corticosteroids in patients with COPD.
Management and Treatment of COPD Exacerbation (Acute Setting Treatment). Acute
exacerbation of COPD is considered acute worsening of the patient’s respiratory symptoms
(increased dyspnea, increased sputum volume, production of purulent sputum) that necessitates a change in medications.
The most common causes of COPD exacerbation are viral lung infections. Other precipitating
causes that should be sought out are bacterial infections, heart failure, myocardial ischemia, pulmonary embolism, lung cancer, esophageal reflux disease, and medications (e.g., beta-blockers).
Initial Management
Measure O2 saturation via pulse oximetry (on the spot) to determine oxygen saturation.
1.
2. ABG determination is very useful to identify the level of hypercapnia and thus the
severity of exacerbation.
3. Chest x-ray is expected in all patients with COPD exacerbation to identify pulmonary
infiltrates consistent with pneumonia. It may also show evidence of pulmonary edema,
indicating possible heart failure as the cause of the exacerbation.
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4. Spirometry (and other PFT evaluation) is not helpful in COPD exacerbation because
measurements (FEV1, etc.) have not been shown to correlate well with the severity of
the exacerbation.
5. In the acute setting, check levels in patients on chronic treatment with theophylline.
Drugs like erythromycin, cimetidine, and ciprofloxacin may decrease theophylline
clearance and cause theophylline toxicity.
6. Other tests as part of the initial evaluation of COPD exacerbation might include CBC
(looking for elevated WBCs and polycythemia); ECG (looking for new arrhythmias, e.g.,
atrial fibrillation that may precipitate heart failure and exacerbate COPD).
7. Any significant changes of hypercapnia or hypoxemia from baseline should prompt
consideration for admission to the hospital. Also, patients on home O2 who have exacerbation, and those with severe symptoms, should be hospitalized.
8. Consider intubation and mechanical ventilation in patients with decreased levels of
consciousness, cyanosis, or hemodynamic instability and in those with persistent
hypoxemia despite adequate oxygen supplementation.
Specific Therapy
1. Oxygen supplementation should be titrated to ~90% saturation on the pulse oximeter.
The first and foremost concern is to deliver adequate oxygenation. In COPD exacerbation, we should be concerned about CO2 retention as a secondary issue.
2. Inhaled bronchodilators are the most effective medications to improve airway
diameter (the drugs of choice). In acute COPD exacerbations, use both beta-agonists
(albuterol) and anticholinergics (ipratropium) simultaneously. Trials have shown
that administration of these drugs by a nebulizer or metered dose inhaler (MDI) with
a spacer is equally efficacious. Patients with severe exacerbations are unable to hold
their breath for more than a few seconds and are thus initially treated with nebulizers
and then switched to the MDIs.
3. Systemic corticosteroids have now been shown in multiple trials to shorten the
recovery time of lung function and decrease the length of stay in patients with COPD
exacerbation. Corticosteroids may be given intravenously or orally because the effi-
cacy is similar in both modes of administration. The equivalent of 60 mg prednisone appears to be the sufficient starting dose and is usually continued for 2 weeks.
It makes sense clinically to start patients who have a severe exacerbation with IV
methylprednisolone (it is difficult for these patients to take oral meds), then change
to oral prednisone as they improve. Inhaled corticosteroids have not been shown to
improve outcomes in patients with COPD exacerbation and cannot be substituted for
systemic corticosteroids.
4. Antibiotics seem to be beneficial in COPD exacerbations despite “normal” chest
radiograms. Patients with productive, purulent cough benefit the most because they
are more likely to have an underlying bacterial infection. Antibiotics commonly used
are second-generation macrolides (clarithromycin, azithromycin), extended-spectrum
fluoroquinolones (levofloxacin, moxifloxacin), cephalosporins (second- and thirdgeneration), and amoxicillin clavulanate.
5. There is no real benefit to using IV aminophylline. However, if the patient is using
theophylline on a chronic basis (in outpatient setting), it should be continued during
the exacerbation because abrupt discontinuation may worsen symptoms.
6. Always avoid opiates and sedatives because they may suppress the respiratory system.
7. Although specific chest physiotherapy (postural drainage, etc.) has not been shown to
benefit patients with exacerbation, they should be encouraged to increase activities as
tolerated to prevent deconditioning.
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8. Counseling the patient on smoking cessation in the hospital setting is the single most
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important intervention.
9. Teaching the patient optimal use of MDIs has been shown to reduce readmission rates.
Prognosis. FEV1 is the best predictor of survival (the higher the FEV1, the better the survival
and the less symptomatic the patients). The rate of FEV1 decline may also predict survival
because patients with a faster decline will have increased morbidity. Patients that have a FEV1
≤25% will usually complain of dyspnea at rest.
Tobacco cessation is the only means of slowing progression of COPD and the decrease in FEV1.
It is very important that patients with COPD have vaccinations against Pneumococcus with a
booster at 5 years and yearly for influenza. Some experts consider the H. influenzae vaccine
mandatory.
Chapter 9
l Pulmonology
Let’s go back to our patient.
What are you likely to find on her PFTs? How will you treat this patient in the acute exacerbation? What are your treatment options after she goes home?
She asks you to inform her about “how bad her disease is.” What will you do next to assess the
severity of her disease?
Bronchiectasis
A 17-year-old girl is admitted to the hospital with a right lower lobe pneumonia.
She gives you a history of recurrent pneumonias, some of which have kept her
in the hospital for weeks, and of chronic productive cough that occurs every day.
Her parents inform you that she has had “loose stools” since childhood. On the
examination she is thin and in distress. There are diminished breath sounds on
the right lower lobe with rhonchi.
Definition and Etiology. Bronchiectasis is the permanent dilation of small- and medium-sized
bronchi that results from destruction of bronchial elastic and muscular elements. Eventually the
bronchi become fibrotic. Bronchiectasis can occur secondary to repeated pneumonic processes
such as tuberculosis (TB), fungal infections, lung abscess, and pneumonia (focal bronchiectasis)
or when the defense mechanisms of the lung are compromised as in cystic fibrosis and immotile
cilia syndrome (diffuse bronchiectasis).
About 50% of patients with primary ciliary dyskinesia will have situs inversus and sinusitis—
Kartagener syndrome.
Bronchiectasis should be suspected in any patient with chronic cough, hemoptysis, foul-smelling
sputum production, and recurrent pulmonary infections, sinusitis, and immune deficiencies.
Signs and Symptoms. Patients will have persistent cough with purulent copious sputum
production, wheezes, or crackles. There is a significant history of recurrent pneumonias that
commonly involve gram-negative bacteria, especially Pseudomonas species.
Hypoxemia may occur causing secondary polycythemia.
Note
The answers to these
questions can be found at the
end of this chapter.
Clinical Pearl
• 5–7% of patients with cystic
fibrosis initially present in
early adulthood.
• Consider cystic fibrosis
in adult patients with
chronic productive
cough (symptoms of
bronchiectasis), especially
if they have history of
recurrent sinusitis, nasal
polyps, and weight loss.
Most males are infertile.
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Diagnosis. Early chest x-ray findings may be normal. Chest x-ray in advanced cases may show 1to 2-cm cysts and crowding of the bronchi (tram-tracking). High-resolution CT scan of the chest
is the best noninvasive test to detect bronchiectasis.
Treatment. Bronchodilators, chest physical therapy, and postural drainage are used to control
and improve drainage of bronchial secretions. Patients should be treated with antibiotics such
as trimethoprim sulfamethoxazole, amoxicillin, and amoxicillin/clavulanic acid (Augmentin®)
when sputum production increases or they have mild symptoms. This is referred to as “rotating antibiotics” because a different antibiotic is chosen each time to diminish resistance of
microorganisms. Chronic prophylaxis with antibiotics is not recommended.
If the patient exhibits significant symptoms or pneumonia, treat with IV antibiotics that cover
gram-negative bacteria, e.g., quinolones, ceftazidime, or aminoglycosides. Consider surgical
therapy for patients with localized bronchiectasis who have adequate pulmonary function or
in massive hemoptysis.
All patients with bronchiectasis require yearly vaccination for influenza and vaccination for
pneumoccocal infection with a single booster at 5 years.
Specific considerations for the treatment of CF include:
• Aggressive percussion and lung exercises
• Pancreatic enzymes
• Supplemental vitamins
• Recombinant human DNAse
• Inhaled hypertonic saline
Note
The answers to these
questions can be found at the
end of this chapter.
Complications include massive hemoptysis, amyloidosis, cor pulmonale, and visceral abscesses.
Let’s go back to our patient.
How would you treat this patient?
What investigations will you consider based on her history?
INTERSTITIAL LUNG DISEASE
Interstitial lung disease (ILD) is a group of heterogeneous diseases and includes >100 disorders. ILD is characterized by chronic inflammation and fibrosis of the interstitium and lung
parenchyma. The worst prognosis is with idiopathic pulmonary fibrosis and usual interstitial
pneumonitis.
The interstitium of the lung (supporting structure) is the area in and around the small
blood vessels and alveoli where the exchange of oxygen and carbon dioxide takes place.
Inflammation and scarring of the interstitium (and eventually extension into the alveoli) will
disrupt normal gas exchange. Although the progression of ILD may be variable from one disease to another, they have common clinical, radiographic, and spirometric findings.
All patients with ILD develop exertional dyspnea (the most common complaint that brings
them to the physician) and nonproductive cough. The examination shows the typical coarse
crackles, evidence of pulmonary hypertension (increased pulmonic sound, right heart failure),
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and clubbing (not always). The chest x-ray is consistent with reticular or reticulonodular pat-
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tern (“ground-glass” appearance). PFTs show evidence of intrapulmonary restrictive pattern.
Causes include:
• Idiopathic pulmonary fibrosis
• Sarcoidosis
• Pneumoconiosis and occupational lung disease
• Connective tissue or autoimmune disease–related pulmonary fibrosis
• Hypersensitivity pneumonitis
• Eosinophilic granuloma (a.k.a. Langerhan cell histiocytosis)
• Chronic eosinophilic pneumonia
• Wegener granulomatosis
• Idiopathic pulmonary hemosiderosis
• Bronchiolitis obliterans
• Lymphangioleiomyomatosis
Diagnostic evaluation should include high-resolution CT scan and, eventually, biopsy via
bronchoscopy or open lung biopsy.
Chapter 9
l Pulmonology
Idiopathic Pulmonary Fibrosis (IPF)
A 55-year-old man comes for evaluation of exercise intolerance over the past 6
months. He has no significant past medical history. He informs you that over the
past week he cannot walk across the room without getting “short of breath.” He
takes no medications and has never smoked. The physical exam is significant for
a respiratory rate of 24/min, jugular venous distention ~8 cm, coarse crackles
on auscultation, clubbing, and trace pedal edema on both legs. The chest x-ray
reveals diffuse reticular disease.
Definition. IPF is an inflammatory lung disease of unknown origin that causes lung fibrosis
and restrictive lung disease. This disease characteristically involves only the lung and has no
extrapulmonary manifestations except clubbing.
Prevalence. IPF occurs in patients in the fifth decade of life, with an equal distribution
between men and women.
Clinical Manifestations. Progressive exercise intolerance and dyspnea are seen most commonly. There are coarse dry crackles on auscultation.
The chest x-ray reveals reticular or reticulonodular disease. High-resolution CT scan may
show ground-glass appearance. As IPF progresses, there is evidence on imaging of extensive
fibrosis with honeycomb pattern. A restrictive intrapulmonary process is evident on PFTs.
Bronchoalveolar lavage will show nonspecific findings, specifically increased macrophages.
A lung biopsy is done to exclude other causes that may have similar findings, e.g., vasculitis,
infections, cancer.
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Treatment.
Pharmacologic treatment includes pirfenidone, a new small-molecule compound that
has antifibrotic effects. A recent trial showed that pirfenidone significantly reduced decline
in lung function and IPF disease progression.
Drugs no longer used in the treatment of IPF include corticosteroids, anticoagulants,
interferon, and bosentan.
Non-pharmocologic treatment includes lung transplantation and is suitable for those
patients physically eligible to undergo a major transplant operation. In IPF patients, lung
transplant has been shown to reduce the risk of death by 75% as compared with those
who remain on the waiting list.
Sarcoidosis
A 27-year-old woman comes to your office with painful erythematous papules
that occurred yesterday. She has no other complaints except joint swelling and
pain that occurred 3 days ago. Physical examination discloses low-grade fever,
symmetric swelling of the knees, PIP (proximal interphalangeal) and MCP
(metacarpophalangeal) joints, and well demarcated, 3- to 4-cm papules over the
anterior aspect of her legs. What is the next step in confirming the likely diagnosis?
Definition. Sarcoidosis is a systemic disease of unknown cause, characterized histologically by
the presence of nonspecific noncaseating granulomas in the lung and other organs.
Prevalence. There is an increased incidence of sarcoidosis among blacks and patients age
20–40 years.
Clinical Manifestations. Sarcoidosis can involve almost any organ system, but pulmonary
involvement is most common. Ocular, cutaneous, myocardial, rheumatologic, GI, and neurologic
manifestations can also occur. The dermatologic manifestations occur in 25% of patients with
sarcoidosis; they include lupus pernio, erythema nodosum, non-scarring alopecia, and papules.
Commonly, sarcoidosis is discovered in a completely asymptomatic patient, usually in the
form of hilar adenopathy on a chest x-ray.
There are 2 distinct sarcoid syndromes with acute presentation:
• Löfgren syndrome includes erythema nodosum, arthritis, and hilar adenopathy.
• Heerfordt-Waldenstrom syndrome describes fever, parotid enlargement, uveitis, and
facial palsy.
Lung involvement in sarcoidosis occurs in 90% of patients at some time in their course. Hilar
and left paratracheal adenopathy is the most common presentation. Interstitial lung disease
with or without hilar adenopathy can also be a presentation of sarcoidosis.
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Dermatoweb.net
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Figure 9-10. Lupus Pernio Sometimes Seen with Sarcoidosis
Chest X-Ray. Chest x-ray findings can show 4 stages of disease (the stages are not progressive),
which include bilateral hilar adenopathy, hilar adenopathy with reticulonodular parenchyma,
reticulonodular parenchyma alone, or honeycombing of bilateral lung fields with fibrosis.
Chapter 9
l Pulmonology
Laboratory Findings. Hypercalcemia or hypercalciuria caused by increased circulation of
vitamin D produced by macrophages.
Elevation in angiotensin-converting enzyme (ACE) can be seen in 60% of patients with sarcoidosis. ACE levels are nonspecific but can be used to follow the course of the disease.
Abnormalities in liver function tests are seen in 30% of patients with liver involvement, with
90% of patients being symptomatic.
Other findings on diagnosis of sarcoidosis include skin anergy, and PFTs may be normal or
show a restrictive pattern. All patients with suspected sarcoidosis should have an ophthalmologic examination because uveitis and conjunctivitis are found in >25% of the cases.
Diagnosis. The definitive diagnosis of sarcoidosis rests on biopsy of suspected tissues, which
show noncaseating granulomas.
Prognosis. Eighty percent of patients with lung involvement from sarcoidosis remain stable,
or the sarcoidosis spontaneously resolves. Twenty percent of patients develop progressive disease with evidence of end-organ compromise.
Treatment. There is no evidence that any therapy alters the course of disease. Generally in
the setting of organ impairment, a trial of steroids may be used, giving a high dose for 2
months followed by tapering the dose over 3 months. There are certain scenarios in which
steroids are mandatory: uveitis, sarcoidosis involving the CNS, and heart, and in those who
develop hypercalcemia.
Clinical Pearl
Don’t use serum ACE levels to
diagnose sarcoidosis.
Clinical Pearl
If a patient is asymptomatic
and has bilateral hilar
adenopathy on a routine
chest x-ray, assume this is
sarcoidosis and follow with
imaging.
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