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E. Morning headaches
Which of the following is the most likely cause of this patient’s abdominal pain?
A. Exacerbation of chronic intestinal pseudo-obstruction
B. Irritable bowel syndrome
C. Diverticulitis
D. Distal intestinal obstruction syndrome
E. Exacerbation of chronic pancreatitis
D. A new-generation macrolide
Which of the following is the most likely cause of the patients dyspnea?
A. Bronchiolitis obliterans
B. Interstitial lung disease
C. Congestive heart failure
D. Obesity
Chest radiograph shows prominent central pulmonary arteries; the lung fields are
clear.
Echocardiogram shows concentric left ventricular hypertrophy with normal left
ventricular systolic function (ejection fraction 55%) and a mildly dilated right
ventricle with normal function. The aortic, mitral, and tricuspid valves are normal in
structure. The estimated pulmonary artery systolic pressure measured at rest is 59
mm Hg (assuming an estimated right atrial pressure of 10 mm Hg).
Spirometry and lung volumes are normal. Diffusing lung capacity for carbon
monoxide (DLCO) is 40% of predicted. Ventilation/perfusion scan shows normal
ventilation and mild heterogeneity of perfusion but no segmental or larger defects.
Right heart catheterization shows right atrial pressure 10 mm Hg, right ventricular
pressure 50/10 mm Hg, pulmonary artery pressure 50/20 mm Hg, pulmonary
capillary wedge pressure 26, cardiac output 3.1 L/min, cardiac index 2.0 L/min/m2.
Which one of the following is the most likely cause of this patients pulmonary
hypertension?
A. Left ventricular diastolic dysfunction
B. Chronic pulmonary embolism
C. Primary pulmonary hypertension
D. Pulmonary veno-occlusive disease
E. Constrictive pericarditis
D. Radiation therapy
E. Palliative care
C. Measure the D-dimer level in the serum and re-initiate anticoagulation therapy if it
is elevated.
D. Measure the D-dimer level in the serum and perform Doppler ultrasound imaging
of the lower
extremities if it is elevated.
pressure is 130/75 mm Hg. Her breathing is unlabored, and she has inspiratory and
expiratory wheezes but is otherwise normal.
What is the most likely explanation for this patients lack of response to corticosteroid
therapy?
A. The patient has chronic obstructive pulmonary disease.
B. The patient has vocal cord dysfunction.
C. The patient has corticosteroid-resistant asthma.
D. The patient has asthma with allergic bronchopulmonary aspergillosis.
Which of the following findings would warrant a trial of oral corticosteroid therapy?
A. Bilateral anterior uveitis
B. Hypercalcemia
C. Fever and tender red nodules over the anterior shins
D. Persistent cough
dyspnea, minimally productive cough, and limited exercise tolerance. He thinks his
dyspnea on exertion has worsened. He stopped smoking cigarettes 8 years ago and
is currently using an ipratropium inhaler four times per day and salmeterol discus
twice per day. His body mass index, which 6 months ago was 21, is now 19.
On physical examination, he is afebrile, his pulse rate is 94/min and regular, and
respiration rate is 20/min. His breathing is unlabored at rest. He has signs of chest
hyperinflation and decreased breath sounds without wheezing. He has no peripheral
edema. The remainder of his examination is normal; results of a fecal occult blood
test are negative.
Baseline spirometry is unchanged.
Forced expiratory volume in 1 sec (FEV1) 35% of predicted
Forced vital capacity (FVC) 85% of predicted
FEV1/FVC ratio50%
PO2 62 mm Hg
PCO2 45 mm Hg
pH 7.38 (with the patient breathing room air)
Chest radiograph reveals only hyperinflation.
What is the best way to manage this patient’s weight loss?
A. Provide dietary instructions to increase his caloric intake.
B. Treat him with anabolic steroids.
C. Refer him for pulmonary rehabilitation with exercise and nutritional counseling.
D. Prescribe oxygen supplementation to improve his oxygen consumption.
E. Add inhaled corticosteroids to his medical regimen.
B. Haloperidol
C. Lorazepam
D. Phenytoin
E. Acetaminophen
cough.
On physical examination, there is no peripheral edema or abnormal jugular venous
distention. There are no crackles or rub on lung auscultation. Chest radiograph is
normal except for low lung volumes and bibasilar platelike atelectasis. Pulmonary
function testing shows:
Forced expiratory volume in 1 sec (FEV1) 75% of predicted
Forced vital capacity (FVC)73% of predicted
FEV1/FVC 90%
Total lung capacity 72%
Residual volume 95%
Diffusing lung capacity for carbon monoxide (DLco) 80%
CT scan of the chest reveals symmetrical lower lobe volume loss without pulmonary
infiltrates or fibrosis.
Which of the following best characterizes this patients restrictive lung disease?
A. Diffuse alveolar hemorrhage
B. Small airways disease secondary to systemic lupus erythematosus
C. Interstitial pneumonitis
D. Respiratory muscle weakness
mm Hg. Measurement of arterial blood gases with the patient breathing room air
shows PO2 of 55 mm Hg, PCO2 of 30 mm Hg, pH of 7.41. Chest radiograph reveals
bilateral alveolar infiltrates with no effusions. Gram stain of the sputum reveals
gram-positive diplococci.
Which of the following is the most appropriate for this patient?
A. Treat him as an outpatient with oral therapy.
B. Treat him as an outpatient with intravenous therapy.
C. Hospitalize him.
D. Hospitalize the patient in the intensive care unit.
without angina. For several years, he has had fatigue, dysphagia with symptomatic
gastroesophageal reflux, and pain with blanching in his fingers while shoveling snow.
He takes a β-blocker for mild hypertension.
On physical examination, he has perioral skin tightening, numerous telangiectasias
on both sun-exposed and protected surfaces, and ‘sausage shaped” fingers without
digital ulcerations. His lungs are clear. On cardiac examination, he has a right
parasternal lift with a loud pulmonic valve component. The S2 does not split on
inspiration. He has pitting edema to the mid-shin bilaterally and 8 cm of jugular
venous distention while seated at 45 degrees from horizontal. Left ventricular
systolic and diastolic functions are normal on transthoracic echocardiogram. Both the
right atrium and right ventricle are dilated with moderate tricuspid regurgitation.
Pulmonary artery pressure is estimated to be 52 mm Hg by echocardiography.
Which of the following statements is true about patients with these symptoms?
A. Pulmonary hypertension is a frequent cause of death.
B. Pulmonary hypertension indicates an overlap syndrome.
C. Pulmonary hypertension occurs only in the setting of an associated interstitial lung
disease.
D. Recurrent venous thromboembolism due to an associated hypercoagulable state is
the usual cause of pulmonary hypertension.
Which of the following medications is most effective for the treatment of this
patient’s sleep disorder?
A. Clonazepam
B. Pramipexole
C. Oxycodone
D. Gabapentin
E. Ketorolac
intravenously every 6 hours; and oxygen by nasal cannula. During the first 2 hospital
days, her condition remains unchanged. On hospital day 3, she develops increased
dyspnea and a cough productive of sputum.
On physical examination, she is awake and alert and in moderate respiratory
distress. Her temperature is 36.7 C (98 F), pulse rate is 110/min, respiration rate is
20/min, and blood pressure is 150/90 mm Hg. Her lungs are hyperresonant to
percussion, with accessory muscle use, poor air movement, mild wheezing, and no
crackles. Chest radiograph demonstrates hyperinflation, with no other abnormalities.
Leukocyte count is 16,000/μL. Arterial blood gas measurements, with the patient
breathing 1.5 L oxygen, show PO2 of 55 mm Hg, PaCO2 of 55 mm Hg, and pH of
7.32. She is transferred to the intensive care unit for close observation and possible
assisted ventilation.
Which of the following is most appropriate additional management for this patient?
A. Discontinue azithromycin and begin levofloxacin.
B. Begin intravenous aminophylline.
C. Increase methylprednisolone to 250 mg every 6 hours.
D. Add albuterol to ipratropium bromide by nebulizer every 4 hours.
E. Increase oxygen by nasal cannula to 3 L/min.
generalized pruritic rash and difficulty breathing, both of which developed minutes
after she ate at a nearby restaurant. The patient developed a rash some years ago
after eating in a restaurant, but she is unsure whether she has food allergy.
On physical examination, the patient is very anxious and in significant respiratory
distress. Her temperature is 36.7 C (98 F), pulse rate is 120/min and regular,
respiration rate is 30/min, and blood pressure is 85/50 mm Hg. Periorbital edema is
present. Diffuse wheezing and prolonged expiratory phase are noted on auscultation.
There is diffuse erythema over the trunk and extremities.
The patient is promptly treated with subcutaneous epinephrine, intravenous fluids,
inhaled β-agonist
s, corticosteroids, and antihistamines. After 2 hours she feels better, her vital signs
have returned to normal, and there is no wheezing on minimal prolongation of
expiratory phase.
Which of the following is the most appropriate next step in this patient’s
management?
A. Observe her in the emergency room for another hour, and discharge her if she
remains stable.
B. Discharge her and prescribe a tapering dose of corticosteroids for 1 week.
C. Hospitalize her for further observation.
D. Discharge her with an epinephrine and instructions to consult an allergist.
night sweats.
On physical examination, his body mass index is 42. His heart and lungs are normal.
Laboratory studies yield normal results except hemoglobin of 16.8 g/dL. Trace
edema of the lower extremities is noted. Chest radiograph shows that his heart is of
normal size and that his lung fields are clear.
Which of the following is most likely to show the cause of the fatigue and headaches?
A. Echocardiogram
B. Spirometry
C. Beck Depression Inventory
D. CT scan of the brain
E. Overnight polysomnography
intravenously daily.
Which of the following is the most appropriate additional management?
A. Intubate and begin mechanical ventilation.
B. Initiate mucloytic therapy, chest physiotherapy, and oral-tracheal suctioning.
C. Administer a helium-oxygen mixture of 70%:30%, delivered by face mask.
D. Initiate bilevel noninvasive positive-pressure ventilation by face mask
E. Administer 40% oxygen by Venturi mask
green sputum. She reports a long-standing history of loose bowel movements and
intermittent abdominal bloating. Physical examination is notable for bilateral nasal
polyps, crackles in the upper lung zones bilaterally, and early digital clubbing.
Which of the following is the best initial test to evaluate this patient for cystic
fibrosis?
A. Gene mutation test (buccal swab or blood test)
B. Quantitative pilocarpine iontophoresis sweat chloride test
C. 72-hour fecal fat test
D. Measurement of nasal potential difference
E. Sputum culture
concentration with normal urine output. His hemodynamic status has remained
stable. Prothrombin time and partial thromboplastin time are mildly elevated. Platelet
count is mildly depressed, and his leukocyte count is elevated. His blood pressure is
normal.
In addition to the proper antibiotics, which of the following is likely to benefit this
patient?
A. Antithrombin III
B. A single large dose of methylprednisolone
C. Low-dose (stress dose) corticosteroids
D. Drotrecogin alfa (activated)
E. Low-dose dopamine (2 μg/kg of body weight/mm)
E. Malignant effusion
B. Seizures
C. Gastric aspiration
D. Systemic hypertension
E. Anxiety disorder
ANSWERS
cm (17 in) or more is strongly associated with OSA. In patients who seek evaluation
at a sleep center, habitual snoring, choking arousals, and hypertension are also
predictive of the disorder.
Although excessive daytime sleepiness is common in OSA, it is not very predictive of
the disease because there are other common causes. Moreover, the presence and
severity of daytime sleepiness correlates poorly with the severity of OSA as
measured by the apnea-hypopnea index. Although ethanol ingestion has been shown
to reduce upper airway dilator function and increase the severity of OSA, ethanol use
has a poor predictive value for OSA. Nocturnal sexual dysfunction is common in OSA,
but it is not predictive of the disorder. Morning headaches are thought to occur
secondary to recurrent hypercapnia/hypoxemia with apnea and hypopnea throughout
the night, but the presence of morning headaches is not a sensitive test for OSA.
Two nonpharmacologic interventions have also been shown to prolong life for
patients with chronic airflow obstruction: smoking cessation and lung-volume-
reduction surgery in carefully selected patients.
will first need better anatomic information about possible tumor invasion.
CT scan of the brain should be limited to such patients who have neurologic signs or
symptoms. Bone scan will not help define the anatomic issues raised in this case and
is unlikely to be helpful in the absence of symptoms or laboratory abnormalities
suggesting bone involvement.
of elevated levels of carbon dioxide or the presence of anemia would not affect
oximetry readings. Smoke inhalation is responsible for most accidental cases of
carbon monoxide poisoning. Carbon monoxide diffuses rapidly across the pulmonary
capillary membrane and is able to bind the iron moiety of heme (and other
porphyrins) with approximately 240 times the affinity of oxygen. The result is
deformation and leftward shift of the oxyhemoglobin dissociation curve and
impairment of tissue oxygen delivery.
Mild or moderate carbon monoxide intoxication can cause constitutional symptoms
including headache (the most common presenting symptom), malaise, nausea, and
dizziness. Severe toxicity can produce seizures, syncope, or coma, accompanied by
myocardial ischemia, ventricular arrhythmias, pulmonary edema, and profound lactic
acidosis.
greater than that of doubling the dosage of inhaled corticosteroids. Antibiotics have
not been shown to improve asthma control. Nebulizers can increase the dose of β-
agonist, usually equivalent to four to six puffs of a metered-dose inhaler, but
nebulizers do not lead to increased asthma control. Adding ipratropium bromide is
recommended in an acute exacerbation in an emergency situation but has not been
shown to add to the long-term control of asthma. Adding a leukotriene receptor
antagonist is an alternative approach but not the preferred approach in this setting.
Educational Objectives
Treat cough that is due to gastroesophageal reflux disease.
Critique
The patient has cough secondary to gastroesophageal reflux disease (GERD), which
is among the three most common causes of chronic cough in all age groups. A
diagnosis of GERD should be considered when patients experience heartburn, a sour
taste, regurgitation, or globus hystericus (frequent throat clearing secondary to a
sensation that something is stuck in the back of the throat). The most sensitive and
specific test for GERD is 24-hour esophageal pH monitoring. The objective of therapy
is to decrease the frequency and duration of reflux events and decrease the irritative
nature of gastric secretions. Therapy includes conservative dietary and lifestyle
measures, prokinetic agents, and acid-suppressing drugs. It may take as long as 3
months for symptoms to resolve.
Because cough may be simultaneously caused by more than one condition as much
as 93% of the time, therapy should not be stopped if partially successful; instead,
other therapies should be added sequentially. Patients who do not respond to
medical therapy may benefit from antireflux surgery including fundoplication, but it is
too early to consider surgery for this patient.
predictive value of 100%, in the context of cough, this test is extremely useful in
ruling out asthma.
Most patients with postnasal drip syndrome will have symptoms or evidence of one
or more of the following: postnasal drainage, throat clearing, nasal discharge,
cobblestone appearance of the oropharyngeal mucosa, or mucus in the oropharynx.
The patient had none of these symptoms or findings and empiric therapy for
postnasal drip syndrome failed to alleviate his symptoms.
There is nothing about the character and timing of chronic cough due to GERD that
distinguishes it from other conditions; in addition, it can be “silent” from a
gastrointestinal standpoint up to 75% of the time. However, the patient failed 3
months of empiric therapy for GERD. It is logical to rule out cough-variant asthma,
especially with symptoms coinciding with the addition of a β-blocker, before pursuing
24-hour esophageal pH testing.
Some data suggest that anabolic steroids may be beneficial, but the absence of
comprehensive and long-term studies as well as the toxicity of these drugs make
such an approach investigational at this time. The patient does not meet the criteria
for oxygen supplementation, and there are no data to suggest that either oxygen or
inhaled corticosteroids would help reverse his weight loss.
The signs and symptoms of Legionella pneumonia are nonspecific and can range in
severity from mild illness (walking pneumonia) to fatal multilobar pneumonia.
Patients may have high, unremitting fever and cough with little sputum production;
the time between exposure and onset of illness is approximately 2 to 10 days.
Extrapulmonary symptoms include gastrointestinal disturbances and involvement of
the central nervous system, liver, and kidney; pericarditis and endocarditis are rare.
The presence of such abnormalities as diarrhea and elevated serum creatine kinase
levels has a sensitivity of about 30%.
compliance. Whatever the cause, the syndrome is associated with low lung volumes
in the absence of parenchymal or pleural fibrotic disease. Although the disorder has
been found to respond to corticosteroid therapy, it may relentlessly progress to
hypercapnic respiratory failure.
Alveolar hemorrhage is unlikely because there is no history of hemoptysis or cough,
the DLCO is normal, and there are no infiltrates on imaging. Acute lupus pneumonitis
is a fulminant disorder presenting with fever, hypoxemia, and pulmonary infiltrates
and is not associated with small-airways disease. Chronic interstitial lung disease is
uncommon in SLE and may develop independently of acute pneumonitis or as its
sequela. It is more common in patients with SLE whose symptoms overlap those of
systemic sclerosis. As in any form of fibrosing lung disease, CT scan would likely
show reticular infiltrates. A reduction in both total lung capacity and residual volume
due to increased elastic recoil of the scarred pulmonary parenchyma would also be
likely.
is now acidemic. Furthermore, the patient is showing new signs of cor pulmonale.
These symptoms are all indications for hospitalization. It would not be appropriate to
discharge him.
tuberculous antigens, which rupture into the pleural space from a peripheral focus of
active disease. These effusions may develop 3 to 6 months following the primary
infection or may reactivate anytime thereafter, usually caused by an impairment in
the immune system. The typical clinical presentation includes cough, chest pain, and
fever. Radiography shows a unilateral, small-to-moderate effusion; only one third of
patients have an associated infiltrate. On CT scan of the chest, however, a lesion is
found 75% of the time.
It is rare for a patient younger than 40 years and with a <20-pack-year history of
smoking to develop lung cancer. In patients with a malignant pleural effusion, the
percentage of lymphocytes in the pleural fluid is usually 50% to 70% and is rarely
higher than 80%. Furthermore, patients with lung cancer typically have ipsilateral
shift or an absence of contralateral mediastinal shift with a moderate pleural
effusion.
Patients with pneumonia develop parapneumonic effusions several days after the
onset of symptoms of pneumonia. The effusions are classically neutrophil-
predominant exudates, which become lymphocyte-predominant only in the resolution
phase after treatment with appropriate antibiotics. Patients with pulmonary
embolism typically have obvious risk factors for the development of deep venous
thrombosis (although some patients have hereditary thrombophilia that is unknown
at the time of presentation). The typical presentation is ipsilateral chest pain and a
small (less than one third of the hemithorax) exudative pleural effusion, which does
not have a high lymphocyte count. If the patient is treated with anticoagulation
therapy and does not have a pulmonary infarction, the effusion should peak by 72
hours and resolve in 7 to 10 days. If there is evidence of a radiographic infarction,
resolution time may be as long as 2 to 3 weeks.
Patients with benign asbestos pleural effusions have a known history of heavy
asbestos exposure and a latency period that averages 20 to 30 years from time of
initial asbestos exposure. In the acute phase, the effusion is neutrophil-predominant
and, in a later stage, may be lymphocyte-predominant, with percentages <80%.
There is a 30% incidence of pleural fluid eosinophilia.
The finding of a precipitin band in a life-long farmer does not of itself imply a
diagnosis of HP. The disease represents a specific immunologic response in
susceptible persons to repeated antigen exposure, which distinguishes it from the
nonspecific lower respiratory tract inflammation seen after a high-level organic dust
exposure (as occurs in mycotoxicosis, endotoxin inhalation, and organic toxic dust
syndrome). Thus, simultaneous disease in similarly exposed persons argues against
a diagnosis of HP. HP is not associated with immediate skin test reactivity because it
is not mediated by IgE. The demonstration of reversible airflow obstruction is a
nonspecific finding and can occur with asthma, postinfectious bronchial
hyperreactivity, endotoxin inhalation, or HP.
By contrast, eosinophils move rapidly into pleural tissue and pleural fluid following a
pneumothorax. Approximately 30% of patients with benign asbestos pleural effusion,
who are typically asymptomatic, may develop pleural fluid eosinophilia. Benign
asbestos pleural effusion is usually associated with heavy asbestos exposure. Other
causes of pleural fluid eosinophilia (>10% of total nucleated cells) include pulmonary
infarction, parasitic disease, fungal disease (coccidioidomycosis and histoplasmosis),
drug-induced pleural effusion (dantrolene and nitrofurantoin), Hodgkin’s lymphoma,
carcinoma, and Churg-Strauss syndrome. Pleural fluid eosinophilia is exceedingly
rare in tuberculous pleurisy. The prevalence of malignancy has been shown to be
similar in eosinophilic and noneosinophilic pleural effusions.
Although the patient was a smoker and at increased risk for lung cancer, malignant
effusions do not resolve spontaneously. The patient has no medical risk factors for
deep venous thrombosis. He did not have spontaneous chest pain, and he has a
large pleural effusion (the effusion with pulmonary embolism is virtually always less
than a third of the hemithorax).
Although paragonimiasis is considered a tropical disease, it has been diagnosed in
North Americans. Worms migrate through and sometimes remain in the pleura.
Affected patients may have gastrointestinal and constitutional symptoms several
weeks before they develop pleurisy; most patients with paragonimiasis, however, are
not systemically ill. Patients who have predominantly pleural paragonimosis are not
likely to have ova in the sputum and are often misdiagnosed as having tuberculosis,
as the majority will have concomitant pulmonary abnormalities. The definitive
diagnostic test is demonstration of the ova in sputum or stool.
pulmonary disease, and neuromuscular disease have been excluded. A body mass
index of 42 is diagnostic of morbid obesity.
An echocardiogram might show pulmonary artery hypertension but is not likely to
lead to the diagnosis. Headaches in this patient are due to carbon dioxide retention;
a CT scan of the brain will likely be unrevealing. The Beck Depression Inventory, a
measure of depression symptoms, might be abnormal in this patient but would not
diagnose the underlying cause of the symptoms.
multiple sleep latency test (MSLT) and early onset of REM sleep on MSLT or
polysomnography.
Temporal lobe epilepsy sometimes occurs predominantly at night but is not
associated with cataplexy. Panic disorder can also occur predominantly during sleep
but does not cause cataplexy. The parasomnias are motor disorders of sleep,
including sleep walking. They do not cause persistent daytime hypersomnolence or
cataplexy.
Educational Objectives
Recognize potential complications of continuous high-dose sedation with
benzodiazepines.
Critique
The best approach is continued observation. The patient has received large
quantities of lorazepam for more than a week, which have undoubtedly accumulated
in fat stores. It may take several days more before drug levels decrease, allowing
her to wake up.
There is no indication to resume plasmapheresis unless there are signs of recurrent
thrombotic thrombocytopenic purpura. Although a tracheostomy and percutaneous
gastrostomy tube may be necessary at some point, it is reasonable to expect that
her mental status will improve in a timely manner, making these interventions
unnecessary.
Metabolic acidosis due to propylene glycol toxicity has been described in patients
receiving high-dose lorazepam, but this is an unlikely explanation for the depressed
mental status and there is no clinical indication to measure propylene glycol levels.
Clinical sedation guidelines emphasize avoiding oversedation and drug accumulation
by providing the smallest amount of drug necessary to achieve clinical end points.
Daily interruption of sedation and avoiding continuous infusions have also been
advocated to avoid excessive sedation.
Although reactive airways dysfunction syndrome does cause acute airway symptoms
within 24 hours of toxic inhalation, this patient’s known exposure to nitrogen dioxide,
as well as the bimodal distribution of symptoms, is most compatible with bronchiolitis
obliterans. Acute respiratory distress syndrome is an acute rather than late
complication of nitrogen dioxide inhalation.
(1) Adrenal shock may present in a similar fashion as septic shock and have a similar
clinical profile including fever—unlikely in this case because the chest radiograph
supports a diagnosis of pneumonia. (2) Steroid release is the primary way that the
body handles the pro-inflammation response of severe sepsis. In patients previously
taking corticosteroids, there may be adrenal gland suppression that prevents
adequate adrenal response—the primary concern in this case. (3) Recently described
is a relative adrenal insufficiency that may occur in septic shock, which is thought to
occur when the pro-inflammatory response overwhelms the ameliorating effect of
adrenal release of corticosteroids. It is characterized by inability to raise cortisol level
in response to ACTH stimulation test in patients with septic shock.
Patients with relative adrenal insufficiency are at increased risk for mortality and
survival may be improved by administration of stress-dose steroids (hydrocortisone
50 mg intravenously every 6 hours and fludrocortisone 50 μgld administered orally,
both for 7 days).
Obstructive sleep apnea (OSA) has been strongly associated with systemic
hypertension. The degree of hypertension correlates closely with the severity of OSA
as measured by the apnea-hypopnea index. OSA is not associated with worsening
renal function, although long-standing untreated hypertension can bring about renal
dysfunction indirectly. Gastric aspiration, seizures, and anxiety are not known to
occur more commonly in patients with OSA.