UVA FM quiz

A four week old male infant is brought by his mother to the physician following one week of emesis. The patient's mother states that the patient has been vomiting non-bilious material immediately after each feeding, but then becomes fussy and demands to be fed again. She denies ever seeing any blood in the emesis. Over the past two or three days, the infant's vomiting has become increasingly sudden and forceful. The child is irritable, with few tears. The oropharynx is dry, the infant's fontanelles appear sunken, and moderate skin tenting is noted. Capillary refill is approximately 2 seconds. On abdominal exam, visible peristaltic waves are observed, and a 1cm firm mass is palpated in the right upper quadrant. What is the most likely laboratory finding? A. Na+ 130, K+ 2.9, Cl- 89, HCO3- 35 B. Na+ 138, K+ 3.8, Cl- 100, HCO3- 26 C. Na+ 150, K+ 4.0, Cl- 100, HCO3- 24 D. Na+ 140, K+ 3.8, Cl- 100, HCO3- 15 E. Na+ 130, K+ 5.8, Cl- 110, HCO3- 20

A. Na+ 130, K+ 2.9, Cl- 89, HCO3- 35 Key teaching point #1: When you see a 3-6 week old infant with projectile vomiting, and an olive-like mass on physical exam, think pyloric stenosis! Key teaching point #2: Losing HCl in emesis leads to a hypochloremic, hypokalemic metabolic alkalosis. This vignette describes a classic presentation of pyloric stenosis, a commonly-tested disorder for which the associated electrolyte abnormality is a hypochloremic, hypokalemic metabolic alkalosis (answer A). Even without recognizing that this is a case of pyloric stenosis, you should be able to think through the question and arrive at the correct answer. Think about what is going on with this patient. Repetitive vomiting of acidic gastric juices causes the loss of HCl - thus, the patient's Cl- should be low. Since you're losing H+, there will also be a metabolic alkalosis, so the HCO3- will be elevated as well. Finally, in order to maintain pH balance, the kidneys avidly reabsorb H+, but they can only do this at the expense of K+, resulting in hypokalemia. (Review Dr. Barrett's diagrams of the principal and intercalated cells of the cortical collecting duct from her second year "Diuretics" lecture to remind yourself of how this happens physiologically. http://www.med-ed.virginia.edu/courseSites/subjects.cfm?CID=1) Thinking about things this way, you're looking for the answer that shows a decrease in Cl- and K+, and an increase in HCO3- (answer A). As previously mentioned, the question stem describes a truly classic case of pyloric stenosis, which is important to recognize. Key features include: 1) palpable abdominal mass - often described as an "olive" (Sometimes, the olive is only palpable after feedings, so doing a test feeding in clinic can confirm the diagnosis.); 2) projectile vomiting; 3) vomiting immediately after feeding, then demanding to be refed - "hungry vomiters"; 4) presentation at age 3-6 weeks. The initial test of choice when the diagnosis is unclear is abdominal ultrasound, which will reveal the hypertrophied pylorus. (Barium studies may also be used, but these have the undesirable side effect of exposing an infant to radiation.) The treatment of pyloric stenosis is, of course, surgical - the patient needs a pyloromyotomy. Answer B represents essentially normal lab values, which this child would not be expected to demonstrate given his dehydration and one week history of vomiting. The primary abnormality in answer C is hypernatremia. This situation results when a patient has hypotonic fluid loss, or loses more water than they do sodium - as can happen in patients with dehydration with inadequate free water intake. It is important to realize that this patient is not losing hypotonic fluids, however - he is losing large amounts of electrolytes with each episode of vomiting. The primary abnormality in Answer D is a low bicarbonate - which, in this situation, represents an anion gap metabolic acidosis. Remember that Anion gap = sodium - chloride - bicarbonate = 12 +/- 4 The anion gap in this question stem would be 140 - 100 - 16 = 24, which is elevated. Possible etiologies of an anion gap metabolic acidosis include the things on the MUDPILES mnemonic - none of which would apply to this patient. For an eMedicine article on metabolic acidosis (including the MUDPILES mnemonic) check out: http://www.emedicine.com/ped/topic15.htm Answer E represents a patient with hyponatremia and hyperkalemia. This situation could arise in adrenal insufficiency due to insufficient aldosterone.

A 74 year old man presents with double vision. He first noticed this several months ago, and although his symptoms wax and wane, he now experiences daily episodes of "seeing double," most frequently in the evenings. He also reports increased generalized fatigue and notes that he sometimes gets so tired at dinner that he "can hardly chew" his food. Past medical history includes osteoarthritis, hypertension, and abdominal aortic aneurysm repair. Physical examination reveals a comfortable, age-appropriate elderly gentleman with mild dysarthria. Cardiac auscultation reveals both an S4 and a 2/6 holosystolic murmur heard best at the left upper sternal border with radiation to the carotids. On neurologic exam, the patient has 5/5 strength proximally and distally. Sensation is intact and reflexes are 2+ throughout. Ocular movements are sluggish but intact in all directions. The patient has mild bilateral ptosis, which is noted to increase with sustained upward gaze. Stroking the bottom of the foot results in downward deflection of the great toe bilaterally. Which of the following is the most appropriate next step in diagnosis? A. Administer i.v. edrophonium B. CT of chest C. MRI/MRA of brain and cerebral vessels D. Temporal artery biopsy E. CSF examination for oligoclonal bands

A. Administer i.v. edrophonium This is a presentation of oculobulbar myasthenia gravis. The easiest way to confirm the diagnosis in a patient such as this one with overt ptosis is to administer i.v. edrophonium (answer A). Edrophonium is an acetylcholinesterase inhibitor with a short onset of action and half life. If you give the medication and the patient's symptoms immediately improve, you have essentially confirmed the diagnosis. Edrophonium's trade name is Tensilon, so you may hear neurologists talk about giving a patient the "Tensilon Test" to confirm MG. Alternately, EMG can diagnose MG if you see a decremental response to repetitive nerve stimulation. Here are some additional teaching points about myasthenia gravis: 1) The key feature of MG is fatigable muscle weakness. Patients will typically report that their symptoms worsen throughout the day. Oculobulbar myasthenia gravis is the most common type, resulting in the signs and symptoms presented in the question stem: double vision, ptosis, dysarthria, and difficulty chewing. 2) Myasthenia gravis has a bimodal age distribution, so there are two classic groups of patients who get MG: young women in their 20s or 30s with autoimmune disorders (RA, SLE, hyperthyroidism, etc.), and men in their 70s or 80s. 3) MG is caused by autoantibodies that bind to postsynaptic ACh receptors. A commonly tested point is distinguishing myasthenia gravis from Lambert-Eaton syndrome, which is a paraneoplastic disorder (usually associated with small cell lung cancer) in which antibodies are produced against the pre-synaptic Ca2+ channels. 4) The treatment of myasthenia gravis begins with anticholinesterase drugs like neostigmine or pyridostigmine, which increase the amount of ACh in the synapse, overcoming the antibody blockade. Prednisone or other immunosuppressive drugs are also used, and i.v. Ig or plasmaphresis are used for refractory cases to more directly target the responsible autoantibodies. 5) Myasthenia gravis almost always have some abnormality of the thymus: 75% will have thymic hyperplasia, and 15% will have an overt thymoma. Since the disease is mediated by T cells, removal of the thymus can be curative in patients who fail medical therapy. Regardless, once the diagnosis of MG has been established, it is reasonable to rule out thymoma via CT scan. If you answered B, a chest CT, you either recognized that this was a case of myasthenia gravis and were pursuing a thymoma, or you thought that this was a case of Lambert-Eaton myasthenic syndrome and were looking for a small cell lung cancer. A chest CT will provide useful - and potentially even necessary - diagnostic and prognostic information, but first you should confirm the initial diagnosis of myasthenia gravis with the edrophonium test or EMG. MRI/MRA of the brain and cerebral vessels (answer C) would be useful if you suspected a stroke or brain mass. This patient's symptoms are confined to the neuromuscular junction, however, so there is no reason to initially search out an upper motor neuron cause. A temporal artery biopsy (answer D) is useful if you are pursuing a diagnosis of temporal arteritis, which is more likely to present with jaw claudication, vision loss, and an elevated ESR. A lumbar puncture (answer E) with a CSF finding of oligoclonal bands would be consistent with a diagnosis of multiple sclerosis. To have MS, though, you must have multiple neurological complaints that are separated in time and space and cannot be explained by a single lesion.

A 30 year old female comes to her physician's office for a routine health examination. She has been in good health recently and is up to date with her gynecological examinations. Her only medication is loratadine for seasonal allergies and ibuprofen for occasional headaches. Physical examination shows temperature 37.1 C (98.8 F), pulse 80, BP 170/92, RR 14, oxygen saturation of 99% on room air. A 3/6 mid-systolic ejection murmur is present. Abdomen is nontender with a soft systolic-diastolic bruit that lateralizes to the left side. The patient is grossly intact neurologically, and fundoscopic examination shows sharp optic disc margins. Laboratory evaluation shows Na+ 141, K+ 3.9, Cl- 106, HCO3- 27, BUN 18, Cr 1.0, glucose 98. Urinalysis shows trace proteinuria and no casts. What is the most likely pathological mechanism causing this patient's hypertension? A. Fibromuscular dysplasia B. Oversecretion of aldosterone C. Exogenous administration of corticosteroids D. Atherosclerotic disease E. Catecholamine-producing tumor

A. Fibromuscular dysplasia This is a case of secondary hypertension caused by renal artery stenosis. They key clues are the markedly elevated blood pressure in an otherwise healthy young person and the presence of an abdominal bruit. In a patient without vascular risk factors, the stenosis is likely to be caused by fibromuscular dysplasia of the vessel wall (answer A) instead of atherosclerotic disease. Two quick teaching points: 1) This patient is a textbook example of fibromuscular dysplasia, which typically occurs in females under 50 years old. To confirm the diagnosis requires imaging - typically renal ultrasound with Doppler or CT or MR angiography. 2) Although the vast majority of patients with hypertension have essential hypertension, elevated blood pressure can be a sign of a more serious underlying disorder. You should always consider the diagnosis of secondary hypertension in patients who have a known onset of hypertension before age 30, patients whose blood pressure remains elevated despite multiple medications, patients who have severe (>160/100 mm Hg) hypertension above age 55, or patients with a sudden increase in their blood pressure from a stable baseline. The remaining answer choices all are pathological mechanisms for other causes of secondary hypertension. Oversecretion of aldosterone (answer B) describes primary hyperaldosteronism or Conn's syndrome. Patients with Conn's syndrome should present with hypokalemia and hypertension. Exogenous administration of corticosteroids (answer C) is the most common cause of Cushing's syndrome, which is another cause of secondary hypertension. You should know the key features of Cushing's, which include obesity, bone loss, glucose intolerance, moon facies, a "buffalo hump," purple striae, and hypertension. Atherosclerotic disease (answer D) is certainly a cause of renal artery stenosis, and would explain her abdominal bruit. The tip off in this question was that the patient was a young, previously-healthy woman - just the kind of patient who gets fibromuscular dysplasia. Atherosclerotic plaques are more likely to cause stenosis in older patients with vascular risk factors such as smoking, diabetes, or hyperlipidemia. A pheochromocytoma is a catecholamine-producing tumor (answer E). The classic triad of symptoms includes episodic headache, sweating, and tachycardia.

A 23 year old male presents with syncope. He reports that while walking briskly to his car, he felt his heart "racing" in his chest, and shortly thereafter passed out. The patient denies any prior syncopal episodes, but does note occasional episodes of palpitations that occur after moderate activity or during periods of increased stress. There is no family history of neurological disease, cardiac disease, or sudden cardiac death. On physical examination, pulse is 85 and regular, BP is 124/74, respiratory rate is 16, and oxygen saturation is 98% on room air. Cardiac examination reveals pulsation at the fifth intercostal space at the left parasternal area in the midclavicular line. S1 is within normal limits, and S2 is heard to split on inspiration. The remainder of the physical exam is unremarkable. EKG taken in the office shows the following tracing in lead II. Which of the following would be the most appropriate treatment for this patient's disorder? A. Radiofrequency ablation of pre-excitation pathway B. Urgent DC cardioversion C. Heart transplant D. Biventricular pacemaker placement E. Coronary angioplasty

A. Radiofrequency ablation of pre-excitation pathway This question describes a classic presentation of Wolff-Parkinson-White (WPW) syndrome, a rare disease that is frequently tested on the USMLE. This disorder is caused by the presence of an "accessory pathway," an abnormal conduction pathway that allows electrical impulses from the SA node to reach the ventricle without having to conduct through the AV node. Normal conduction through the AV node is slower than conduction through this accessory or "pre-excitation" pathway, so the ventricle gets activated at different times by the two different pathways. At rest, this produces the pathognomonic EKG finding of a delta wave, seen above. However, this pre-excitation pathway can lead to a number of cardiac arrhythmias, ranging from atrial fibrillation or flutter with a rapid ventricular response to ventricular tachycardia or fibrillation. Patients may experience a range of symptoms, from mild palpitations, to syncope, to sudden cardiac death. Although you may attempt to control the arrhythmias pharmacologically, the ultimate treatment for Wolff-Parkinson-White is radiofrequency ablation of the abnormal accessory conduction pathway (answer A). To answer this question correctly, you had to diagnose WPW from the EKG. If you'd like a more comprehensive tutorial on EKG, check out these websites from the University of Wisconsin or McGill University: http://www.fammed.wisc.edu/pcc/ecg/ecg.html http://sprojects.mmi.mcgill.ca/cardiophysio/ Briefly, to interpret the strip presented, first note the short PR interval - the P wave almost runs into the following QRS complex! In WPW, the PR interval is typically <.12s (three small boxes). The QRS is wide (>.12s) thanks to the fusion of the accessory pathway and the normal conduction pathway through the normal pathway through the AV node-His-Purjinje system. Thus, instead of a brisk, nearly vertical upstroke, you see a "slurred upstroke" - this is the delta wave that is pathognomonic for Wolff-Parkinson-White. This question also raises an important general teaching point about the causes of syncope in a young person. Far and away the most common cause of syncope in a young person is vasovagal, but you should always be aware of the more serious cardiac causes, which include Wolff-Parkinson-White, hypertrophic cardiomyopathy, congenital long QT or short QT syndromes, or valvular heart disease. Patients with Wolff-Parkinson-White typically have few or no findings on physical examination, and this patient's cardiac exam is indeed normal. The descriptions of the patient's PMI and heart sounds are those of a normal patient's. This is a common trick on the USMLE - just because a physical finding is described in detail doesn't mean that it is abnormal. (Occasionally, patients with WPW will have conduction abnormalities that result in paradoxical splitting of S2 or other abnormalities, but these are likely beyond the scope of the USMLE Step 2.)

An otherwise healthy 8 year old girl presents with two weeks of perianal pruritis. She has two younger brothers, one of whom has had similar complaints for the past few days. Physical exam reveals perianal erythema with mild excoriations. The "scotch tape test" reveals several bean-shaped white eggs. What is the most likely diagnosis in this patient? A. Trichuriasis B. Enterobiasis C. Child abuse D. Fecal soilage E. Atopic dermatitis

B. Enterobiasis This is a classic case of enterobiasis (answer B) or "pinworm." The most common presenting symptom is intense anal itching or pruritus ani. Other symptoms (such as abdominal pain/fullness or nausea and vomiting) may occur if the worm burden is high. Girls may also present with a vulvovaginitis or urinary tract infection if the worms migrate. Eosinophilic enterocolitis and appendicitis are rarer complications. Some teaching points: 1) The first line treatment of enterobiasis is either mebendazole or albendazole - one dose is usually sufficient, but a second dose 1-2 weeks later can help prevent reinfection. Pyrantel pamoate is second line because of its side effects (nausea, vomiting, abdominal cramping, neurotoxicity, and elevated LFTs). However, pyrantel pamoate is first line if the patient is pregnant, since mebendazole and albendazole are teratogenic. 2) Enterobiasis is spready by a fecal-oral route and usually presents in kids ages 5-10 years old. It is very uncommon in children less than 2 years old. 3) The "scotch tape" test is the best way to confirm the diagnosis. It involves covering a wooden stick with scotch tape with the sticky side facing outward, and then pressing the tape against the perianal skin. Bean-shaped eggs stick to the tape which can then be visualized under a microscope. Sometimes whole adult worms can be found perianally - they are white, pin-shaped and can be up to 13 mm long. 4) Treatment should include simultaneous treatment of all household members to prevent reinfection. Bedding and clothing should be washed, fingernails should be clipped (since this is the most common place for eggs to hide out), and hygienic measures increased (handwashing and bathing). Whipworm or trichuriasis (choice A) is a common intestinal helminthic infection worldwide, with the highest prevalence in tropical regions. Hosts are usually asymptomatic, though the disease can cause loose stools that contain mucus or blood, resulting in a secondary anemia. Trichuriasis is also classically associated with rectal prolapse in a patient with a heavy parasite load. Heavy loads can affect a child's growth and cognition. Diagnosis is made by stool examination for eggs, which are barrel shaped with a hyaline plug at each end. Child abuse (choice C) is not the best answer, though it isn't unreasonable to have this on your differential when children present with genital or anal complaints. In this case, we have a clear, identifiable cause of the perianal itching. Fecal soilage (choice D) is part of the differential of anal pruritis and can be due to any cause of diarrhea or loose stools. Some patients have an abnormality with internal anal sphincter relaxation. When anal itching is otherwise unexplained, this diagnosis should be entertained. Eczema or atopic dermatitis (choice E) is certainly part of the differential diagnosis of anal pruritis, though just the history does suggest an infectious cause. This familial allergic reaction is often associated with asthma and allergic rhinitis. The rash of eczema is intensely pruritic, and usually appears as erythematous patches with scaling. In children, eczema usually occurs on the face, scalp, extremities, diaper area and trunk, and usually presents by age 7.

A 55 year old female comes to the emergency department complaining of a headache for the past six hours. Her headache began abruptly after she finished eating breakfast, and quickly increased to 8/10 throbbing pain located mainly over her right temple. The pain has been associated with mild nausea but no vomiting. She denies chronic or recurrent headaches, but did have one headache similar to this one two weeks ago, which resolved after taking ibuprofen and lying in a quiet, dark room. She has smoked one pack of cigarettes daily for 38 years. On physical exam, the patient has temperature of 37.0 C (98.6 F), pulse of 99, and BP 147/95. Neurological examination is nonfocal, but mild photophobia and nuchal rigidity are noted. Fundoscopic examination reveals no papilledema. Skin exam shows no lesions. CT of the head, obtained without contrast, reveals no abnormalities. What is the most appropriate next step in the management of this patient? A. Obtain head CT with contrast B. Lumbar puncture C. Administer i.m. sumatriptan D. Administer oral ibuprofen E. Administer i.v. ceftriaxone

B. Lumbar puncture

A 66 year old male presents to the emergency department with chest pain. The pain began two hours ago as the patient was watching television. The pain is described as "squeezing" and is located primarily substernally with radiation to the jaw. Past medical history includes diabetes mellitus, hypertension, hyperlipidemia, and a 50 pack/year smoking habit. On physical exam, the patient appears anxious and diaphoretic. The patient is given supplemental oxygen by nasal cannula, and aspirin, morphine, and nitroglycerin are administered. EKG obtained on presentation to the ED is shown. Of the following, which is the most appropriate study to obtain next? A. Aortogram B. Troponin I C. Stress echo D. Exercise stress test E. CT angiogram of chest

B. Troponin I Key teaching point: To evaluate acute coronary syndrome, you need both an EKG and serial troponins. The patient presents with symptoms highly suggestive of acute coronary syndrome (ACS). Collectively, ACS consists of three ischemic cardiac disorders: ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina. Distinguishing between these entities is important, as both the therapy and the prognosis depends on the diagnosis. The first thing to do when sorting out ACS is to check an EKG - the presence of ST segment elevation (>1 mm in two or more anatomically contiguous leads) confirms the diagnosis of a STEMI. STEMI carries the worst prognosis of any of any of the acute coronary syndromes, so finding "tombstones" of ST elevation on EKG is a clear indication for immediate reperfusion therapy, either with thrombolytics or percutaneous interventions in the cath lab. This patient's EKG shows little more than normal sinus rhythm. The lack of ST elevation means that the diagnosis of STEMI is ruled out. (As a sidenote: If you answered this question incorrectly because you thought that there was miniscule ST elevation on this EKG, here is the teaching point for you. When you are looking at an image on the USMLE or shelf exam, whether that image is a CT scan, a radiograph, or an EKG, expect any abnormalities to be STRIKING. The testmakers do not expect you to be a radiologist or to hold your EKG calipers up to the computer monitor. You need to use the information from the question stem to know whether you're looking for a fracture, a head bleed, atrial fibrillation, etc., but so long as you know what to look for, the finding in the image will either be obvious - or it will be absent.) So now that the patient has a relatively normal EKG, how do we distinguish between the other acute coronary syndromes - NSTEMI and unstable angina? You need a biomarker to tell you if the patient's cardiac tissue has infarcted, and although you could use CK-MB or LDH, the most sensitive and specific test is cardiac troponins (answer B). If this patient's troponin I were elevated, it would indicate ischemic necrosis of the myocardium - therefore, the patient is having an MI, even if we don't see it on EKG. The appropriate diagnosis would thus be NSTEMI. (Pathologically, to have ST segment elevation on EKG requires a full-thickness infarction of the myocardium. If an infarction does not penetrate the entire thickness of the heart wall, the heart's electrical conduction is relatively undisturbed and there will not be diagnostic findings on EKG.) The management of NSTEMI is still evolving and remains somewhat controversial. Reperfusion with primary percutaneous interventions in the cath lab is beneficial for high-risk patients, but thrombolytic therapy carries greater risks and is reserved for those patients with persisting ST elevations. Many patients with NSTEMI can also be managed medically with antiplatelet therapy and beta blockers. If the patient's troponin I were not elevated, then the patient has not yet infarcted his myocardium. The diagnosis would therefore be unstable angina, which requires intensive medical management to prevent MI. The patient should be started on some regimen of heparin, beta blockers, and antiplatelet therapy. The patient should also receive EKG monitoring and serial troponins to ensure that his unstable angina does not eventually cause infarction. An aortogram (answer A) used to be the gold standard for the diagnosis of an aortic aneurysm. Now, less-invasive imaging modalities such as CT, MRI, and echo have largely supplanted aortograms for the diagnosis of aortic dissection. In any case, while aortic dissection ought to be considered in patients with chest pain, this patient's history is strongly suggestive of ACS, and this should be investigated first. A stress echocardiogram (answer C) or exercise stress test (answer D) might be good tests to risk stratify a medically stable, low-risk patient with suspected coronary artery disease. This patient, however, requires further evaluation to rule out MI, and stressing the heart is a bad idea in a patient with probable ongoing ischemic pain. Obtaining a CT pulmonary angiogram (answer E) would be a great test to rule out pulmonary embolism, which can be a cause of chest pain. Here, though, the patient's history and cardiac risk factors strongly suggest a cardiac etiology for his pain, so until that is ruled out, searching for a PE is inappropriate.

A 20 year old healthy female presents to her family physician for routine annual gynecological exam. She is sexually active with her monogamous male partner and currently uses the withdrawal method for contraception. Although this is her first sexual partner, she thinks her boyfriend has probably had intercourse with other women prior to their relationship. Her LMP was 2 days ago. She agrees to routine gonorrhea and Chlamydia testing. On speculum exam after swabbing for the test, some bleeding from the cervical mucosa is noted. Bimanual exam is normal. The test returns positive for N. gonorrheae. What is the best initial step in the management of this patient? A. Reassurance and encourage condom use B. Start and oral contraceptive pill (OCP) C. Ceftriaxone and azithromycin D. Doxycycline E. Ciprofloxacin

C. Ceftriaxone and azithromycin This question addresses the appropriate management of a patient who has just tested positive for gonorrhea. Gonorrhea is much less prevalent than chlamydia, and patients with gonorrhea tend to be co-infected with Chlamydia. (The reverse is much less often true since chlamydia is easier to acquire statistically.) In a patient with a positive test for gonorrhea, you should therefore treat for both gonorrhea and chlamydia to avoid complications such as PID (which can lead to infertility). The combination of a one time injection of ceftriaxone and a one-time dose of azithromycin is the most appropriate choice to address the positive gonorrhea test. Some additional teaching points... 1) Gonorrhea infection is more likely to be asymptomatic in females than it is in males. Because gonorrhea can lead to PID and infertility, screening is important for women and recommended for all sexually active females <25 years old. 2) Remember that if a patient tests positive for chlamydia or gonorrhea, her partner MUST be treated or she will likely be reinfected. Health departments in some states employ a system of anonymous sexual partner notification, but patients should be urged to notify their partners as well to seek treatment. 3) Treating gonorrhea with a one-time ceftriaxone injection in the office ensures compliance. Several of the fluoroquinolones (like ciprofloxacin, ofloxacin, and levofloxacin) are acceptable alternatives and are orally dosed. (Remember, though - no fluoroquinolones for pregnant women (fetal toxicity) or the pediatric population (possible link with arthrotoxicity).) 4) The two most frequently used treatments for chlamydia include either a one time dose of azithromycin or one week of doxycycline. 5) A friable cervix is a sign of a possible cervicitis, which explains why this patient bled so easily when her cervix was swabbed. The other answer choices are incorrect drug regimens to address the positive gonorrhea test. Reassurance (answer A) is unacceptable - gonorrhea must be treated to prevent spread and avoid complications like PID and infertility. Encouraging condom use, however, would certainly be an appropriate discussion to have with this patient to prevent future STIs. Starting an oral contraceptive (answer B), though not the best next step, would probably eventually be a good idea. The withdrawal method is an inadequate form of birth control (up to 20% failure rate) so a discussion about her interest in preventing pregnancy would be a good idea. Remember, however, that OCPs don't prevent STIs. Doxycycline (answer C) is an acceptable treatment for chlamydia, but not for gonorrhea. Ciprofloxacin (answer D) would only address the gonorrhea infection and would go against the recommendation to also treat the likely chlamydia infection that so frequently accompanies a positive gonorrhea test result.

A 71 year old male comes to his physicians office complaining of muscle weakness. The weakness began insidiously several weeks ago, and has now progressed to the point where he has difficulty with normal activities such as brushing his hair or sitting unsupported. Past medical history is significant for hyperlipidemia, chronic renal insufficiency, coronary artery disease, and coronary artery bypass and grafting. Current medications include atorvastatin, fosinopril, metoprolol, aspirin, and spironolactone. Physical examination reveals diminished deep tendon reflexes and decreased motor strength. Laboratory evaluation shows Na+ 143, K+ 7.4, Cl- 101, HCO3- 28, BUN 30, and creatinine 1.8. EKG is obtained on presentation and is seen here. What is the most appropriate initial step in the management of this patient? A. Administer i.v. insulin and glucose B. Administer p.o. sodium polystyrene sulfate C. Administer i.v. sodium bicarbonate D. Administer i.v. calcium gluconate E. Urgent hemodialysis

D. Administer i.v. calcium gluconate Key teaching point: Hyperkalemia with EKG changes needs immediate treatment with i.v. calcium to protect the heart. Although this patient presents with a nonspecific complaint - weakness - evaluation reveals a serious underlying cause: hyperkalemia. Hyperkalemia causing EKG changes (such as the "peaked T" waves seen here) is a legitimate medical emergency, as the patient can progress to heart block or ventricular fibrillation very quickly. Thus, the most appropriate first step in management of this patient is the administration of calcium gluconate (answer D). Although this does not affect the serum K+ concentration, calcium does decrease cardiac membrane excitability and provide short-term cardioprotection from the membrane depolarizing effects of hyperkalemia. This buys you some time to work on correcting the underlying abnormality of high potassium. There are some other teaching points to be learned from this question stem as well. First, why is this patient hyperkalemic? First, he has some baseline kidney disease, which is exacerbated by the fact that his heart is likely not perfusing his kidneys as well as it might if he had no history of coronary artery disease. Remember that for a person eating a normal diet, the kidneys must excrete a certain amount of potassium each day to maintain homeostasis. Secondly, this patient's doctors likely also set him up to become hyperkalemic - he unfortunately had been taking two medications which can cause hyperkalemia: fosinopril, an ACE inhibitor, and spironolactone, a "potassium sparing" diuretic. Second, while this patient presented with weakness related to his hyperkalemia, most patients are not so "fortunate." Although muscle weakness progressing to flaccid paralysis can and does occur, most patients are asymptomatic, at least until their K+ levels get very high (above 7.0 or so). Third, it is important to recognize the classic EKG finding of hyperkalemia: the "peaked T wave." True EKG findings of hyperkalemia are not subtle. As one UVA attending says, a peaked T wave should be sharp enough to really hurt if you sat down on it. (Would you like to sit on the T wave in lead V4?) If you'd like a comprehensive online tutorial on EKG interpretation, try this one from the University of Wisconsin: http://www.fammed.wisc.edu/pcc/ecg/ecg.html Answers A, B, C, and E all are treatments for hyperkalemia - but none will provide immediate benefit for this patient, whose heart could slip into a terminal rhythm while you're working on correcting their electrolytes. The USMLE loves questions like this one that distinguish between the immediate treatment and the ultimate treatment for a condition. If you find yourself thinking that there is more than one correct response to a question, ask yourself which alternative provides the most immediate benefit. While insulin and glucose (answer A) or sodium bicarbonate (answer C) lower the serum potassium, they do so by causing a shift of potassium from the serum into cells, not by causing a net loss of total potassium. Sodium polystyrene sulfonate or Kayexelate (answer B) is a cation exchange resin that removes potassium from the gut. Its effects are not immediate. Hemodialysis (answer E) is an excellent treatment for hyperkalemia, but it is typically reserved for cases in which other methods have failed, or when there is ongoing release of potassium from injured cells (such as in a patient with severe myonecrosis).

On routine examination, a five year old child is noted to have a loud S1 with a fixed and widely split S2 that does not vary with respiration. A soft, mid-systolic ejection murmur is heard best on the left in the second intercostal space. Remainder of physical exam is otherwise unremarkable. There is no nail clubbing, hepatomegaly, or jugular venous distension. The child is healthy and active and her mother has no health concerns. Which of the following is the most likely diagnosis in this patient? A. Mitral valve prolapse B. Pulmonic regurgitation C. Tetralogy of Fallot D. Atrial septal defect E. Ventricular septal defect

D. Atrial septal defect This is an atrial septal defect, or ASD (answer D). There are certain "buzzwords" that you'll come across on the USMLE that almost always indicate a particular diagnosis, and this question stem has one of them. When you see fixed splitting of S2, the first thing you should think of for your shelf exam is an ASD. (As a reminder, S2 normally splits only on inspiration.) Here are some additional teaching points about ASDs... 1) ASDs, can remain asymptomatic for a long time - they are frequently picked up on routine exam. Because the pressure in the left atrium is slightly higher than the pressure in the right atrium, there is a net movement of blood from left-to-right. Over time, this overloads the pulmonary circulation and leads to pulmonary hypertension. Eventually, the pressure in the pulmonary vascular bed gets so high that the shunt reverses, causing a right-to-left shunt. This is the dreaded Eisenmenger syndrome, in which a left-to-right shunt reverses flow and turns into right-to-left shunt. 2) ASDs are silent! The murmur that is heard in this case is NOT blood flow through the ASD. Remember that to hear a murmur, you have to have turbulent blood flow. The difference in pressures between the right and left atria is so small that the blood flows easily, without turbulence. However, since there is a net left-to-right movement of blood, there is an increased volume of blood coursing across the pulmonary valve. This leads to a flow or ejection murmur heard best in the listening area for the pulmonic valve. Although mitral valve prolapse (answer A) is often found incidentally in asymptomatic patients, the classic murmur is not present in this case. The auscultory finding of a midsystolic click (another one of those USMLE buzzwords) followed by a late systolic murmur heard best at the apex of the heart is characteristic. Isolated pulmonic regurgitation (answer B) is rare, and would cause a diastolic murmur. The Tetralogy of Fallot (answer C) is a combination of four off-setting cardiac defects. Because the net result is a right-to-left shunting of blood, patients should have some degree of cyanosis and symptomatology. (A useful mnemonic for remembering all of the defects in Tetralogy of Fallot is "PROVE": pulmonary stenosis, right ventricular hypertrophy, overriding aorta, ventricular septal defect, and early cyanosis.) Ventricular septal defects (answer E) are another cause of left-to-right shunting, but the classic finding on physical exam is a low-pitched, harsh holosystolic murmur heard best at the left lower sternal border.

A 73 year old male presents to his physician complaining of cough and fatigue. His cough began 6 months ago and has steadily worsened, and is now associated with occasional expectoration of mucus streaked with bright red blood. Patient has also noted worsening dyspnea on exertion and a weight loss of 15 lbs. The patient has smoked a pack and a half of cigarettes every day for the past 60 years. Past medical history is significant for bipolar disorder treated with lithium. Physical exam shows unilateral localized wheezing on the left chest and clubbing of the distal extremities. Capillary refill is brisk. No skin tenting is observed. Chest X-ray is obtained, which shows a large mass at the left hilum. Labs show: Glucose 130, Na+ 125, K+ 4.0, Cl- 91, HCO3- 25, BUN 15, Creatinine 1.0; Plasma osmolality 270 (Normal: 282-295 mOsm/kg); Urine osmolality 650 mOsm/kg (Normal: 50 - 1400 mOsm/kg). Which of the following is the most likely mechanism for this patient's hyponatremia? A. Increased oral intake of hypotonic fluids B. Decreased oral intake of solutes C. Impaired secretion of ADH in the posterior pituitary D. Ectopic overproduction of vasopressin E. Resistance to ADH action on the cortical and medullary collecting tubules

D. Ectopic overproduction of vasopressin Key teaching point: When you see euvolemic hyponatremia (especially on the USMLE), think SIADH! The constellation of findings in this patient, including euvolemic hyponatremia, hypotonicity (plasma osmolality <280 mOsms), inappropriately concentrated urine, and normal renal function are diagnostic for the syndrome of inappropriate ADH secretion (SIADH). SIADH has a number of causes. The most common include: 1) Cancer - ectopic production of ADH by small cell lung cancers or pancreatic malignancies; 2) CNS disturbances - traumatic injuries, strokes, infections, and hemorrhages can all cause increased ADH production; 3) Drugs - most commonly caused by antipsychotic medications or chemotherapeutics, but the old (and seldom used) insulin secretagogue chlorpropamide is a commonly-tested causative agent. This question stem is loaded with findings consistent with primary lung carcinoma in general and small cell carcinoma in particular: a older patient with an extensive smoking history; insidious onset of cough, fatigue, and weight loss; localized wheezing and clubbing of the nails; and a chest x-ray showing a central mass. Therefore, it is overwhelmingly likely that overproduction of ADH - also known as vasopressin - by the patient's lung tumor is causing his hyponatremia (answer D). Both answers A and B are plausible explanations for hyponatremia in general. However, as mentioned above, this patient's history and physical exam strongly suggest lung cancer, which is associated with SIADH. Additionally, either of these situations would be associated with a maximally diluted urine osmolality, while the patient in the question stem has inappropriately concentrated urine. Increased free water intake (answer A) describes the situation seen in psychogenic polydipsia, a disorder in which patients - most commonly schizophrenics receiving antipsychotics - drink excessive amounts of free water. The kidneys have an incredible capacity for regulating fluids and solutes. Normal patients can excrete more than 10-15 L of urine per day, so for a patient with a dietary solute intake to become hyponatremic, they would have to have a very impressive water intake! Decreased solute intake (answer B) is the mechanism for "beer potomania," in which patients drink excessive amounts of beer without taking in enough food to provide adequate solutes. The minimum urine osmolality is 60mOsm/kg, so there is a certain amount of obligatory solute lost in the urine every day. If a patient is only drinking beer (and massive quantities of it) and not taking in any solutes, he can deplete his solute reserves over time just through this obligatory solute loss. Answers C and E describe the abnormalities present in diabetes insipidus (DI). DI is a frequently-tested topic on the USMLE, but it is most likely to present with HYPERnatremia, not HYPOnatremia. There are two types of DI: central and nephrogenic. In central DI (answer C), there is not enough ADH produced by the pituitary, while in nephrogenic DI (answer E), there is end-organ resistance to ADH action. In either case, the kidney is no longer able to reabsorb H2O from the urine, leading to free water losses and copious polyuria. Since the body is losing more free water than solute, patients typically become hypernatremic. In children, nephrogenic DI is almost always inherited, while in adults it is commonly caused by drugs - most notably lithium. Central DI is most commonly caused by surgical trauma to the hypothalamus or pituitary, such as might occur with a trans-sphenoidal removal of a pituitary adenoma.

A seven year old female is brought to the physician by her mother because of facial swelling and dark, cola-colored urine. These symptoms began abruptly two days ago and have been associated with anorexia and malaise. There have been no known sick contacts. Her mother states that the child is up to date with her immunizations and has been in good health except for a runny nose and sore throat around two weeks ago, which resolved after a few days without treatment. Vital signs are temperature 37.2 C (98.9 F), heart rate 95, and blood pressure of 148/86. There is diffuse edema of the lower extremities, face, and eyelids. Lungs and heart are clear to auscultation. Urinalysis shows moderate hematuria and proteinuria, and dysmorphic RBCs and occasional RBC casts are noted on microscopic examination. Based on these findings, what is the most likely diagnosis? A. IgA nephropathy B. Alport syndrome C. Thin basement membrane nephropathy D. Postinfectious glomerulonephritis E. Henoch-Schonlein purpura

D. Postinfectious glomerulonephritis This is a very typical presentation of postinfectious (or poststreptococcal) glomerulonephritis (answer D). Even if you recognized this diagnosis immediately based on the history, there may be some more subtle teaching points regarding the presentation of this disease or the interpretation microscopic urinalysis. First, the key features of post-streptococcal GN were all there. These include the patient's age (<7 years old), dark brown colored urine (representing hematuria), and periorbital and peripheral edema. There is also a latent period of around 10 days following pharyngitis before symptoms of glomerulonephritis occur, although for glomerulonephritis following streptococcal impetigo, the latent period can be as long as 3-4 weeks. One diagnostic finding not mentioned was the anti-streptolysin O titer, which you would expect to be positive (indicating recent exposure to Group A strep). Finally, the finding of RBC casts is an important one. When you see casts in the urine sediment - whether WBC, RBC, or granular - you have glomerular disease. This is a useful pearl to remember - it's only when cells get squeezed through the glomerulus that they will form casts. Dysmorphic RBCs (especially acanthocytes) are also highly suggestive of glomerular disease. Patients with bleeding from sources other than the glomerulus - such as a patient with renal stones, bladder cancer, or a urinary tract infection - should have RBCs with normal morphology, since those cells are not being squeezed from the glomerulus into the collecting tubule. IgA nephropathy (answer A) is the most common cause of primary glomerulonephritis. The most common presentation is recurrent episodes of gross hematuria that occur around 5 days after an upper respiratory infection. To truly confirm the diagnosis requires a renal biopsy. Although the disease is generally benign, some patients will progress to end-stage renal disease, and treatment with ACE inhibitors or ARBs may minimize glomerular injury and disease progression. Alport syndrome (answer B) is yet another example of a disease that is rare in real life but common on examinations. The key features are glomerular hematuria along sensorineural deafness and ocular abnormalities. Since this is an inherited disease, there should also be a family history of renal failure and deafness. The primary defect is a genetic mutation in collagen type IV. Thin basement membrane nephropathy (answer C) is a benign and usually hereditary disorder that is associated with glomerular hematuria. Although minimal to moderate proteinuria may be seen on occasion, having the degree of proteinuria described in the question stem would be distinctly unusual. Most often, these patients are completely asymptomatic, and their hematuria is only picked up on routine urinalysis. Henoch-Schonlein purpura (answer E) is a systemic vasculitis that commonly affects children. The classic triad of HSP is abdominal pain; a vasculitic, raised skin rash; and renal involvement. Questions that describe "palpable purpura" usually give away the diagnosis. The renal findings are variable, but include hematuria, proteinuria, and rising creatinine.

A 50 year old female with a ten year history of type II diabetes presents for regularly-scheduled follow up. She has no complaints, and just visited her ophthalmologist last week. Current medications include glyburide, metformin, and simvastatin. On physical exam, vital signs are virtually unchanged from previous visits, with temperature 37.1 C (99 F), HR 80, BP 140/83, RR 15, and O2 Sat 98% on room air. Neurological examination reveals diminished sensation to light touch and pinprick in a stocking distribution on the lower extremities bilaterally. Remainder of physical exam is benign. Laboratory evaluation reveals: Na+ 136, K+ 3.9 Cl- 104, HCO3- 25, BUN 15, Cr 1.0, Glucose 150; hemoglobin A1c: 7.1%; Urinalysis: negative for ketones, glucose, bilirubin, leukocyte esterase, or blood; moderate protein; Lipid profile: Total cholesterol 146, HDL 46, LDL 100. At this time, which of the following would be the most appropriate intervention? A. Increase simvastatin B. Increase glyburide C. Increase metformin D. Add hydrochlorothiazide E. Add lisinopril

E. Add lisinopril Key teaching point: All diabetics should be on an ACE inhibitor or ARB for cardiovascular and renal protection. This is a dense question stem, but the important things to note are that this is a patient with type II diabetes who also has proteinuria and elevated blood pressure. Since her medication list does not include any mention of an ACE inhibitor or ARB, beginning one at this time would be the appropriate next step in management (answer E). As it turns out, microalbuminuria is a risk factor for both cardiovascular disease and progression of renal disease to ESRD and dialysis - and this patient already has macroalbuminuria, since dipsticks are not sensitive enough to pick up small amounts of protein! ACE inhibitors and ARBs have been shown to reduce these outcomes - even in normotensive diabetics. All diabetics, therefore, should be on an ACE inhibitor or ARB. Since this patient is hypertensive as well, she has all the more reason to begin a medication such as lisinopril. (It is, however, also important to note that the diagnosis of hypertension should not be made on the basis of a single blood pressure measurement in a physician's office. In this case, the question stem mentions that her vital signs have been similar to those recorded in the past, so making a diagnosis of hypertension is more acceptable. Additionally, diabetics have a target blood pressure of systolic less than 130 mm Hg, a more stringent guideline than for non-diabetic patients.) As an additional teaching point, every health maintenance visit with a diabetic patient should focus on the "Diabetic Five" - these five things, in this order: 1) Smoking cessation 2) Blood pressure control 3) Lipid control 4) Aspirin/metformin 5) Glucose control Adding hydrochlorothiazide (answer D) could improve her hypertension, and would be a reasonable first-line antihypertensive in a patient without diabetes. It is worth noting that this patient IS hypertensive - all diabetics should have a systolic blood pressure of less than 130. Still, diabetic patients have a compelling reason to begin antihypertensive therapy with ACE inhibitors or ARBs, however, due to the reno-protective effects of these drugs mentioned above. Either increasing glyburide (answer B) or increasing metformin (answer C) would be helpful for reducing the patient's blood sugar and better controlling her diabetes. However, her most recent Hgb A1c was not that bad - remember that the goal for diabetic patients is less than 7.0%. For more on Hgb A1c, including how to correlate the test result with the patient's average blood glucose, check out Diabetes Care 2002;25:275-8 or http://www.metrika.com/3medical/hemoglobin-m.html. Similarly, the patient's lipid profile is at her target LDL - thus, she does not need an increase in her statin (answer A). Under the ATP III guidelines, patients with diabetes are considered to have known coronary heart disease, and therefore have a target LDL of less than 100.

A 30 year old female presents to her physician with a breast mass. She first noted a small "lump" in her left breast while showering about six weeks ago. She has noted no change in the size of the mass since that time, and she denies pain or nipple discharge. Family history is significant for a paternal grandmother who had breast cancer at age 79. Physical examination reveals a soft, round, mobile 1cm mass in the lower outer quadrant of the left breast. No skin changes are noted. What is the most appropriate next step in the management of this patient? A. Mammography B. Refer the patient for radical mastectomy C. Begin levonorgestrel/etinyl estradiol D. Genetic testing for BRCA1 and BRCA2 E. Ultrasound of breast mass

E. Ultrasound of breast mass Key teaching point: Mammogram is the preferred imaging study for women over 35, while women younger than 35 should get ultrasound to evaluate a breast mass. In women younger than 35, the breast tissue is often too dense to evaluate mammographically, and the incidence of breast cancer younger women is still very low. Studies have shown that routine mammography is not cost-effective nor clinically beneficial for younger women unless there is a high suspicion of cancer by clinical examination. The clinical characteristics of this mass are non-suspicious for malignancy, though. Features commonly associated with malignancy include hard, irregularly-shaped, immobile masses >2cm in size. Since this patient's mass is soft, small, rounded, and mobile, it is likely to be a benign fibroadenoma. Thus, the patient should receive ultrasound, and the correct answer is E. If the patient were over 35, she should get a diagnostic mammogram (answer A). Questions about the workup of a breast mass are common on the USMLE, so it is worth thinking about how the workup would proceed in this patient. If ultrasound were obtained and the mass is found to be cystic in nature, it is very unlikely to be malignant, and no further evaluation is necessary (although the cyst may be aspirated if it is causing the patient pain). If it is solid, however, tissue will be required to make a definitive diagnosis, and the patient should receive a biopsy. Since breast tissue may undergo changes related to the menstrual cycle, many clinicians will simply ask a young patient with a breast mass to return 3-10 days following her next menstrual cycle to re-evaluate the lump. Answer B might be an appropriate treatment for some breast cancers. But to make a diagnosis of cancer requires tissue, so referral for mastectomy would certainly not be appropriate at this time. Many oral contraceptive pills (OCPs) contain combinations of levonorgestrel and ethinyl estradiol (answer C). There are some non-contraceptive indications for prescribing OCPs, such as dysmenorrhea or endometriosis, and some practicioners do prescribe OCPs to help reduce the pain caused by hormonal fluctuations of benign breast cysts. This patient does not complain of pain, however, and more importantly, you do not yet know what her breast mass is. While not all breast masses are pathological, they all demand an explanation. Since this patient is less than 35, she needs ultrasound. Genetic testing for BRCA1 and BRCA2 (answer D) might be an appropriate step for an asymptomatic woman with a strong family history of breast cancer, or to evaluate ovarian cancer risk in a patient with proven breast cancer. There are two reasons why this response is incorrect for this question, however. First, this patient's family history of breast cancer is not terribly impressive. Breast cancer is so common that 12% of all women will have a positive family history. To identify patients at risk for BRCA1 and BRCA2 mutations, look for patients with multiple first-degree relatives (mothers, daughters, or sisters) who had breast or ovarian cancer at young ages (less than 40-50). In general, the USMLE tests the most classic presentation of any disease - for the correct answer to be BRCA1/BRCA2 testing, the question stem would have to give you more than just one relative who had breast cancer at age 79. Second, and more important, even if this patient had a family history that was suggestive for a BRCA1 or BRCA2 mutation, her problem right now is a breast mass that needs to be evaluated with imaging and potentially a biopsy. Genetic testing might help you assess the patient's lifetime breast cancer risk, but it will not help you determine if this particular breast mass is something bad or not.

A 25 year old student presents with three days of vulvar pruritis. She has had a total of six lifetime partners, and is currently sexually active with one partner and states that they "occasionally" use condoms. One year ago, she was successfully treated for a Chlamydia infection. The patient denies vaginal odor or increased vaginal discharge. Physical exam reveals slight vulvar erythema, and speculum exam shows moderate clumpy white discharge. Vaginal discharge pH is 4.0. Whiff test is negative. Wet mount results: KOH prep shows occasional budding yeast and hyphae. Saline prep shows 3 WBCs, occasional squamous cells, and no bacteria. What is the next best step in the management of this patient? A. Clotrimazole vaginal cream B. Azithromycin and recommend that her partner see a physician for Chlamydia screening and treatment C. Metronidazole D. Ceftriaxone E. Reassurance and follow up in two weeks

This is a classic case of vulvovaginal candidiasis, which is usually treated with a single dose of oral fluconazole or several days of miconazole or clotrimazole vaginal creams (answer A). A handful of additional teaching points... 1) A key clue to the diagnosis is the vulvar pruiritis, which is often the dominant feature of a yeast infection (and may be the only complaint from the patient). Other symptoms could include dysuria, vulvovaginal irritation, or dyspareunia. Classically, the discharge of a yeast infection is described as white with a curd-like consistency (often described as "cottage cheese" like), but many real-life patients will not complain of increased discharge. 2) The low pH (<4.5) of the vaginal discharge points to yeast; the other two main causes of vaginitis (trichomoniasis and bacterial vaginosis) create more alkaline conditions with pH > 4.5. The diagnosis of candidiasis should be confirmed by finding budding yeast and hyphae on the 10% KOH wet mount. 3) This patient's yeast infection was uncomplicated, but it is important to recognize the difference between a complicated and an uncomplicated infection. Infections are uncomplicated when the patient experiences mild to moderate symptoms, the infections are sporadic, the suspected organism is Candida albicans, and the host is otherwise healthy. Complicated yeast infections are those with any of the following features: infection occurring in a host with pre-existing conditions (uncontrolled diabetes, immunosuppression, pregnancy), severe symptoms, infection with non-albicans species, or recurrent infections (>4 per year). Questions on the USMLE seldom give you all of the characteristic features of a particular type of vaginitis, so if you're interested in reading more, here's a succinct review of the diagnosis of vaginitis from the American Family Physician: http://www.aafp.org/afp/20000901/1095.html Re-infection with Chlamydia (choice B) is not the most likely diagnosis. Chlamydia causes cervicitis, but most women are asymptomatic: possible Chlamydia symptoms include vaginal discharge and poorly described lower abdominal pain. Metronidazole (choice C) is the treatment for the other forms of vaginitis - both bacterial vaginosis (BV) or trichomoniasis. BV and trichomoniasis can present with similar symptoms, though classically BV discharge is usually described as malodorous, thin, and grey-white, while trichomoniasis is described as purulent, green-grey, or frothy. The vaginal pH for both of BV and trichomoniasis is >4.5 and the whiff test is often positive in both. The saline wet mount for BV often shows increased numbers of cocobacilli and the classic "clue cells," which are vaginal epithelial cells studded by adherent coccobacilli around the cell's edges. A saline wet mount for trichomoniasis will show motile trichomonads. Administering a ceftriaxone injection (choice D) is a treatment for acute gonorrhea, whose prevalence is much lower than chlamydia. Gonorrhea can infect any portion of the female genital tract, but most often presents as a cervicitis, urethritis or proctitis. Female patients may complain of increased discharge, vaginal pruritis or symptoms of upper tract infection such as lower abdominal pain, and dyspareunia. On speculum exam, the cervix is often friable and cervical discharge may be seen. The gold standard for diagnosis is culture on Thayer-Martin medium. While the patient's symptoms point to a yeast vaginitis, STI testing in this patient is also prudent. Reassurance with follow-up (choice E) isn't the best answer. Treatment is indicated for the relief of symptoms. Up to 20% of sexually active women of reproductive age asymptomatically harbor candida; these patients do not require treatment.

A 62 year old woman with COPD presents to her physician complaining of two days of increasing dyspnea and cough. She uses supplemental oxygen at home and has had to increase her oxygen flow to relieve her shortness of breath. Recently, her cough has been productive of copious amounts of thick, dark yellow sputum. Although she never checked her temperature at home, she thinks she might have had a fever last night. Past medical history includes hypertension and peripheral arterial disease. She has smoked 1 ½ -2 packs of cigarettes per day for the last 45 years and continues to smoke. Current medications include nebulized albuterol, tiotropium, inhaled fluticasone/salmeterol, lisinopril, and pentoxyfylline. Physical examination reveals an uncomfortable, thin female appearing older than her stated age. Vital signs are: temperature 37.2 C (99.0 F), pulse 80, blood pressure 136/70, respirations 20/min, oxygen saturation 88% on 2 L O2 by nasal cannula. The patient is using accessory muscles to breathe, and prolonged expirations and faint expiratory wheezes throughout the lung fields. Coarse crackles are heard at the lung bases. The patient's chest X-ray is shown. Which of the following is the most appropriate treatment for this patient? A. Methylprednisolone B. Prednisone and amoxicillin C. Guaifenasin D. Trimethoprim/sulfamethoxazole E. Aminophylline

This is a patient with COPD who is experiencing an acute exacerbation of her disease. COPD is a slowly progressive disease, so sudden worsening is usually set off by a particular trigger such as an environmental irritant or an infection by bacteria or viruses. Studies have shown that corticosteroids, antibiotics, and inhaled bronchodilators all are beneficial in acute COPD exacerbations, and since this patient is already taking bronchodilators, the best answer is prednisone and amoxicillin (answer B). A few brief teaching points: 1) Although it may not make intuitive sense to treat a patient with antibiotics when it is not clear what exactly you are treating, the evidence in COPD clearly supports empiric antibiotic therapy. The antibiotics most commonly used for COPD exacerbations include amoxicillin, trimethoprim/sulfamethoxazole, and doxycycline. 2) The chest x-ray here shows the classic findings of COPD - hyperexpanded lungs, flattened diaphragms, and a narrow cardiac silhouette. This x-ray does not change your management of the patient in any way, since there are no findings to suggest an alternate diagnosis, such as consolidation suggesting a pneumonia or pneumothorax suggesting a ruptured emphysematous bulla. 3) For stable COPD, the cornerstones of treatment are inhaled beta agonists like albuterol and anticholinergic bronchodilators like tiotropium or ipratropium. Oral steroids may be need for patients with more severe disease. Supplemental oxygen has clearly been shown to prolong life in COPD patients - the only other intervention that does so is smoking cessation! Both methylprednisolone (answer A) and trimethoprim/sulfamethoxazole (answer D) are helpful for COPD exacerbations. However, the patient needs both antibiotics and corticosteroids, so neither one is the best answer to this question. Repeated studies of the mucolytic guaifenasin (answer C) have shown no benefit for either stable COPD patients or COPD exacerbations. Similarly, methylxanthines like aminophylline (answer E) or theophylline have shown no benefit for acute COPD exacerbations beyond the benefit of inhaled bronchodilators and corticosteroids.