A 69-year-old woman presents to her physician complaining of a hoarse voice for the past 3 weeks. She has never had these symptoms before, and cannot identify any alleviating or aggravating factors. She denies any recent respiratory tract infections, difficulty swallowing, or difficulty breathing. Her past medical history is significant for hypertension and diabetes. She has never had any surgeries. She has smoked 2 packs of cigarettes a day for the past 23 years, and does not use any drugs or alcohol. Other than voice hoarseness, her physical examination is unremarkable, including a full neurologic examination. She is referred to an otolaryngologist, who finds that she has left-sided vocal cord paralysis.
Which of the following should be part of the workup of this patient’s complaint?
CT scan of the chest. This is an older patient with a significant smoking history, raising the suspicion for lung cancer. One of the potential manifestations of lung cancer is a hoarse voice, which occurs due to damage of the ipsilateral recurrent laryngeal nerve. This is a branch of the vagus nerve that innervates all of the intrinsic muscles of the larynx except the cricothyroid muscle. Because lung cancer is suspected, a CT scan of the chest would be more appropriate than a chest x-ray (since there is a higher pretest probability of lung cancer in this patient and a higher rate of false negatives with chest x-rays). (A) Hoarseness can be associated with GERD when it causes irritation of the vocal cords; however, this diagnosis does not fit the patient’s history and unilateral nature of the vocal cord paralysis. (B) Bronchoscopy would be useful to biopsy the lung cancer if it is present, but it must be localized first with a CT scan. (D) The neurologic examination was normal, suggesting that her hoarseness is not related to a cranial nerve palsy. The diagnosis of lung cancer must be made first with a CT before a metastatic workup for staging is completed (which includes an MRI of the brain).
A 32-year-old woman with a history of moderate persistent asthma complains of “white stuff ” on her tongue and a feeling of “cotton mouth.” Her asthma is well controlled without any recent exacerbations. Examination shows white plaques adherent to the tongue and buccal mucosa that are removed with scraping.
Which of the following is most likely responsible?
Fluticasone. Inhaled corticosteroids cause local immunosuppression and increase the risk of oral candidiasis. Local treatment is preferable to systemic treatment, and a good option is nystatin swish and swallow. (A, C, D, E) Prednisone is the only other medication on this list that would also increase the risk of oral candidiasis; however, this patient has no reason for taking oral steroids (they are given during exacerbations and for severe persistent asthma). Albuterol and salmeterol are short- and long-acting β2 agonists, respectively, and would not cause oral candidiasis. Montelukast is a leukotriene inhibitor with adverse effects of drowsiness, GI complaints, and hypersensitivity reactions. Epstein–Barr virus causes oral hairy leukoplakia, which manifests with white plaques that cannot be removed with scraping (differentiates it from candidiasis). Unlike oral leukoplakia, which is a precancerous lesion, oral hairy leukoplakia is not precancerous and is fairly specific for HIV infection.
A 56-year-old man with a history of hypertension presents for follow-up after recently increasing his dose of hydrochlorothiazide. He takes no other medications and has no other medical history. There is no family history of hypertension or coronary artery disease, and he does not smoke or drink alcohol. On review of systems, he reports some mild weight gain and daytime fatigue. On examination, he is afebrile with a blood pressure of 154/96 mmHg, which is similar to his blood pressure at his last visit. His BMI is 36 kg/m2 .
Which of the following is the most appropriate next step in management?
Polysomnography. Although the vast majority of patients with hypertension have an unknown cause (essential hypertension), there are some secondary causes that are important to remember. Patients with obstructive sleep apnea (OSA) will often complain of loud snoring, daytime sleepiness, and gasping for air or choking during the night. Risk factors for OSA include obesity, male gender, alcohol and tobacco use, and increasing age. It is diagnosed with a sleep study (polysomnography) and treated with continuous positive airway pressure (CPAP) during sleep. Treatment of OSA in this patient will help to reduce his blood pressure.
Other important causes of secondary hypertension include renal artery stenosis (from atherosclerosis or fibromuscular dysplasia), advanced renal disease, hyperaldosteronism, hypercortisolism (Cushing syndrome), pheochromocytoma, and coarctation of the aorta (hypertension in the upper extremities and normo- or hypotension in the lower extremities). It is also important that patients do not take medications that can exacerbate hypertension, such as NSAIDs, OCPs, and steroids. Licorice can also exacerbate hypertension by inhibiting 11β-hydroxysteroid dehydrogenase, which normally degrades cortisol so that it cannot act on mineralocorticoid receptors and increase sodium reabsorption in the distal nephron.
(A) The dose of hydrochlorothiazide has already been increased without any effect. (B) Adding an additional agent such as an ACE inhibitor is a good idea for essential hypertension; however, this patient likely has a secondary cause of hypertension that needs to be addressed first. (C) Though weight gain and fatigue are some of the symptoms of hypothyroidism, it would be inappropriate to start treatment with thyroid hormone replacement before the diagnosis is confirmed with thyroid function tests.
A 23-year-old woman is brought into the Emergency Department by her mother for sudden onset of shortness of breath. Her medical history is significant for mental retardation and a DVT of the left lower extremity. She is currently normotensive but tachycardic and tachypneic, and appears very tall with an arm span longer than her body. Examination of the eyes is significant for bilateral lens subluxation inferonasally. The cardiac and pulmonary examinations are normal. There is swelling of her right lower extremity with pain on dorsiflexion of her right foot.
Which of the following is the best next step in management?
Start IV heparin. The patient in this vignette has a history of DVT and clinical signs of a current DVT in her right lower extremity. (Note that Homans sign, which is calf pain with dorsiflexion, is not specific at all.) She is now presenting with shortness of breath, tachypnea, and tachycardia, which is concerning for a pulmonary embolism. Her risk factor for developing clots likely stems from her undiagnosed homocystinuria, which is a genetic disease due to a deficiency in cystathionine β synthase. These patients present with a Marfanoid body habitus, but unlike Marfan syndrome they have mental retardation and a propensity to form clots. Ectopia lentis is seen in both Marfan syndrome and homocystinuria; however, the lens will sublux superotemporally in Marfan syndrome and inferonasally in homocystinuria. Diagnosis of homocystinuria can be made by measuring elevated levels of the amino acid homocysteine in the blood and urine.
When there is a high probability that the diagnosis is pulmonary embolism, then IV anticoagulation may be started during the diagnostic workup. (A) Checking D-dimers is reserved for patients with a low pretest probability of pulmonary embolism, since it is a sensitive but not specific test (and therefore good at ruling out disease but not ruling in disease). The next diagnostic step should be a CT angiogram. (B) IV alteplase is a recombinant tissue plasminogen activator (tPA) and may be used as a fibrinolytic in hemodynamically unstable patients. This patient is currently stable. (D) IV anticoagulation is preferred to oral anticoagulation, and warfarin is a poor choice since it takes days to weeks to achieve a therapeutic effect. Oral warfarin will likely be started during this patient’s hospitalization and taken indefinitely (since she has had multiple DVTs now), but the time to reach its therapeutic effect will need to be bridged with an IV anticoagulant like heparin.
A 65-year-old man comes to the Emergency Department with several days of difficulty breathing. His medical history is significant for hypertension, for which he takes propranolol. He has not been to the doctor in years, and reports that he has decreased his level of exercise over the past few years. The patient works in a casino and drinks alcohol moderately. He is afebrile with a respiratory rate of 32 breaths per minute and oxygen saturation of 86% on room air. He has a large chest wall with a decreased diaphragmatic excursion, and there are wheezes and rhonchi heard over both lung fields. An initial arterial blood gas shows a pH of 7.30 and PaCO2 of 65 mmHg. He is given supplemental oxygen and some additional laboratory values are drawn, including another arterial blood gas.
Arterial blood gas
Which of the following is NOT a mechanism responsible for this finding?
Accumulation of lactate. An acute worsening of hypercapnia and respiratory acidosis can be seen when oxygen is administered to patients with COPD who are chronic CO2-retainers. For this reason, when oxygen is administered to these patients the goal is an SaO2 of 90% to 94% or a PaO2 of 60 to 70 mmHg. (B, C, D) There are three reasons why COPD patients can become hypercapnic when excessive oxygen is administered. The primary reason is an increase in V/Q mismatch. Arterioles in the lung are unique compared to the rest of the body in that they vasoconstrict in the presence of hypoxia; with excessive oxygen administration, arterioles in poorly ventilated regions lose this mechanism and vasodilate, leading to increased dead space ventilation and worsened V/Q mismatch. The second mechanism is the Haldane effect, in which an increase in the proportion of oxyhemoglobin decreases the availability of binding sites for CO2. This causes dissociation of CO2 from hemoglobin, increasing the concentration of CO2 in the plasma. The last mechanism is a decrease in minute ventilation that results from loss of the hypoxemic respiratory drive signaled by peripheral chemoreceptors. This plays a minor role in the development of hypercapnia in these patients. (A) Lactic acidosis causes an anion gap metabolic acidosis (anion gap >12 mEq/L), which is not the acid–base abnormality in this patient. This patient’s acid–base status represents a chronic respiratory acidosis (from chronic COPD) with a superimposed acute respiratory acidosis due to both the COPD exacerbation and the worsening hypercapnia following oxygen administration. He likely has COPD as a result of his chronic secondhand smoke exposure (casino worker). The patient should also switch antihypertensive medications since nonselective β-blockers cause bronchoconstriction through inhibition of β2 receptors.
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