Internal Med Case Questions

Your new admission is a 60-year-old male with a massive retroperitoneal hemorrhage which required embolization in interventional radiology. His only past medical history is atrial fibrillation, for which he takes rivaroxaban. His blood pressure was 70/30 mmHg upon arrival in the emergency department (ED) and has since stabilized. His admission labs show his blood urea nitrogen (BUN) is 45 mg/dL and creatinine (Cr) is 3.2 mg/dL. His urine microscopy shows muddy brown casts (see pic image). What is the most-likely diagnosis? A. Acute glomerulonephritis (Acute GN) B. Acute interstitial nephritis (AIN) C. Acute pyelonephritis D. Acute tubular necrosis (ATN) E. Chronic kidney disease (CKD)

D. Acute tubular necrosis (ATN) Acute tubular necrosis (ATN) is the most-common cause of intrinsic renal injury, and results from ischemic or toxic insult to the tubules. For this patient, it was his hypovolemia from massive acute blood loss that led to tubular ischemia. Muddy brown casts, as depicted in the image, can be seen in ATN, but are absent in 20-30% of cases. Management of ATN includes correcting the underlying condition (i.e. improving renal perfusion, stopping offending medication) and close monitoring and management of fluid and electrolytes. Acute GN results from an autoimmune response that leads to inflammation and damage to the glomeruli. The urinalysis (UA) in Acute GN shows hematuria, proteinuria, and red blood cell (RBC) casts AIN is most-commonly caused by infections and medications (i.e. antibiotics, proton pump inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), etc.) and the UA often shows sterile pyuria. Urine eosinophils can be seen, but this test lacks both sensitivity and specificity. Acute pyelonephritis is an infection of the kidney, and patients generally present with signs and symptoms of an active infection. In addition, the UA should support the diagnosis of an active urinary tract infection (UTI), such as the presence of white blood cells (WBCs) CKD is defined as either kidney damage or a decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for at least three months. This patient's kidney damage is likely acute.

A 72-year-old male with a history of hypertension, tobacco use, and hyperlipidemia and family history of coronary artery disease presents with one hour of chest pain. The pain is vague, difficult to localize, gives a "squeezing" sensation, and is associated with dyspnea and nausea. On examination, his pulse is 110 beats/minute and regular, respiratory rate is 22 breaths/minute, blood pressure is 160/95 mmHg, and oxygen saturation is 92% on ambient air. He appears to be in moderate distress from pain. The rest of the exam is normal. What is the most likely diagnosis? A. Acute coronary syndrome B. Aortic dissection C. Pericarditis D. Pneumothorax E. Pulmonary embolism

A. Acute coronary syndrome Ischemic chest pain is often described as squeezing, tightness, pressure, or a crushing sensation. It's classically substernal and difficult to localize to a specific spot. Often there is radiation to the shoulders or lower jaw. Common associated symptoms include dyspnea, diaphoresis, and nausea. Aortic dissection typically presents with sudden onset of severe pain. The location of pain can depend on the location of dissection—tearing or ripping back pain is characteristic of a descending aorta dissection, whereas pain radiating to the jaw or neck is more typical of an aortic arch dissection, and severe anterior chest pain is common with aortic root or ascending aorta dissection. Acute pericarditis typically presents with sudden onset of sharp, stabbing pain localized over the center or left side of the chest. Pain is worse with deep breathing and laying down, but improved with sitting up or leaning forward. A pneumothorax typically presents with sudden onset of sharp unilateral pain associated with dyspnea. A pulmonary embolism characteristically presents with sudden onset of unilateral pleuritic chest pain. It is often associated with dyspnea, and cough with hemoptysis may also be present. A central pulmonary embolism can present without much chest pain, but with predominant signs and symptoms of dyspnea, tachycardia, and lightheadedness.

A 68-year-old male with hypertension and non-ischemic cardiomyopathy is admitted to the hospital with an acute exacerbation of his congestive heart failure (CHF) with preserved ejection fraction. An echocardiogram (ECG) one month ago showed left-ventricular hypertrophy and a left-ventricular ejection fraction (LVEF) of 60%. He takes ramipril and chlorthalidone at home, and these are continued. His pulse is 85 beats/minute, blood pressure is 134/88 mmHg, and oxygen saturation is 95% on two liters of oxygen by nasal cannula. His exam is notable for jugular venous pulse and pressure (JVP) of 12, bilateral leg edema, and crackles at his lung bases. What will be the next step in management of this man? A. Add furosemide intravenously B. Add metoprolol orally C. Add valsartan D. Increase dose of chlorthalidone E. Increase dose of ramipril

A. Add furosemide intravenously The acute management of a congestive heart failure (CHF) exacerbation severe enough to require hospitalization includes loop diuretics such as furosemide. Because a CHF exacerbation can cause splanchnic edema, oral diuretics may be poorly absorbed, so the initial doses should be administered intravenously. Adding an angiotensin receptor blocker (ARB) such as valsartan is not indicated, as he is already taking an angiotensin-converting-enzyme (ACE) inhibitor. An increased dose of chlorthalidone would be insufficient to diurese a patient in the setting of an acute CHF exacerbation. A beta-blocker or increased dose of ramipril will not help his symptoms acutely, though they should be considered after he is euvolemic.

In the emergency department, you are evaluating a 64 year old previously healthy male presenting with fever, altered mental status and shortness of breath. At admission, his temperature is 103 degrees Fahrenheit, pulse is 128 beats per minute, respiratory rate is 27 breaths per minute, oxygen saturation 94% on 15L non-rebreather. On exam, he is hypotensive and appears acutely ill, with somnolence and respiratory distress with diffuse crackles. While your attending prepares to intubate the patient, bloodwork is collected. Labs show the following: Na 134 mEq/L Cl 100 mmol/L HCO3 14 mmol/L Lactic acid 4.9 mmol/L ABG: pH 7.33 / PaO2 61 mm Hg / PaCO2 31 mm Hg How do you interpret his acid/base status? A. Anion gap metabolic acidosis B. Anion gap metabolic alkalosis C. Anion gap respiratory alkalosis D. Non-anion gap metabolic acidosis E. Non-anion gap metabolic alkalosis

A. Anion gap metabolic acidosis The patient's bicarbonate is low, which indicates a likely primary metabolic acidosis, which is more common than metabolic compensation for a respiratory alkalosis. In addition, based on the ABG collected, the patient does not have a respiratory alkalosis. Once a metabolic acidosis has been determined, the next step is to calculate the anion gap (Na - [Cl + HCO3]); for this patient it is 20 mEq/L, which is above the normal range of 8-16, indicating an anion gap metabolic acidosis. A couple of helpful mnemonics for etiologies of anion gap metabolic acidosis are MUDPILES or GOLD MARK (see case for description). For this patient, his acidosis is likely due to severe sepsis from his acute illness with an elevated lactic acid.

A 70-year-old female is seen in the emergency department for palpitations. She states that over the last day she felt her heart beating "funny". She denies any chest pain, shortness of breath, cough, or fever. The paramedics obtained the electrocardiogram (ECG) prior to arrival. What is the diagnosis based on the ECG (see txts)? A. Atrial fibrillation B. Atrial flutter with variable block C. Sinus arrhythmia D. Sinus rhythm with frequent premature atrial contractions E. Wandering atrial pacemaker

A. Atrial fibrillation The answer is atrial fibrillation. The ECG shows a narrow, complex, irregularly irregular rhythm and there are no discernible p waves. Atrial flutter with variable block should have p waves in a saw-tooth fashion (usually running 280-300 beats/minute) with variable conduction resulting in QRS complexes after some of the p waves. Sinus arrhythmia varies in rate, but it has normal p waves before every QRS. Sinus rhythm with frequent premature atrial contractions would have sinus beats and frequent premature beats with a different p wave morphology. With a wandering atrial pacemaker, the ECG must show three different morphologies of p waves, which come from random ectopic atrial foci.

A female with human immunodeficiency virus (HIV) and a CD4 count of 24 cells/mm3 presents with fever and diarrhea for two months. She states no blood or mucus in her stool. She has not had any problems with diarrhea in the past. She reports no change in her diet. She does not take any medications. Which of the following would be the most likely diagnosis in this patient? A. Cytomegalovirus (CMV)-associated colitis B. E. coli O157:H7 infection C. Gluten intolerance D. Lymphocytic colitis E. Ulcerative colitis

A. Cytomegalovirus (CMV)-associated colitis The patient's CD4 count is below 100 cells/mm3, which increases her risk for CMV colitis. Gluten intolerance and lymphocytic colitis are usually not associated with fever. The diarrhea in an E. coli O157:H7 infection and ulcerative colitis is most often bloody.

A 23-year-old female with diabetes mellitus type 1, hypertension, and hypothyroidism is admitted to the intensive care unit (ICU) with lethargy, nausea, and diarrhea. She is somnolent on admission, but her boyfriend provides some history. She has not taken her insulin for the past three days due to nausea and vomiting, she has had a poor appetite and diarrhea. She is difficult to arouse. On exam, she is afebrile. She has no other neurologic deficits. Her admission labs are shown: Sodium: 123 mEq/ Potassium: 4.8 mEq/L Chloride: 91 mEq/L Bicarbonate (HCO3): 10 mEq/L Blood urea nitrogen (BUN): 48 mg/dL Creatinine (Cr): 1.5 mg/dL Serum glucose: 540 mg/dL White blood cell (WBC): 8 cells x 103/μL Serum osmolality: 285 mosm/kg Urinalysis is pending. What is the most likely cause of her clinical presentation? A. Diabetic ketoacidosis B. Diarrhea C. Pseudohyponatremia D. Sepsis with lactic acidosis E. Surreptitious consumption of isopropanolol SUBMIT

A. Diabetic ketoacidosis The patient's anion gap and serum osmolol gap must be calculated: Anion gap = [Na - (Cl + bicarb)]. Values over 12 are considered elevated. Calculated osmolality = (2 x Na) + (glucose/18) +(BUN/2.8). This patient has an anion gap of 22, a calculated osmolality of 293, and an osmolol gap of 8.1 (both values elevated). Causes of an elevated anion gap and elevated osmolality gap include diabetic ketoacidosis, lactic acidosis, paraldehyde ingestion, and uremia. While the patient does have diarrhea which can cause a low serum bicarbonate, her other lab abnormalities and lethargy are explained by her diabetic ketoacidosis. Her low sodium is explained by her hyperglycemia, which causes osmotic shifts and a dilution hyponatremia. Pseudohyponatremia, on the other hand, is due to elevated serum lipids or proteins, which interfere with the sodium assay. She has no signs, symptoms, or clinical history to suggest lactic acidosis, uremia, or toxic ingestions.

An 85-year-old male undergoes evaluation for syncope that occurred while climbing up a flight of stairs. He has a history of hypertension and takes hydrochlorothiazide. He has been feeling lightheaded with exertion for about six months, but has never had a syncopal event until today. He denies any chest pain. On examination, his vital signs reveal his temperature is 36.6C (98F), pulse is 85 beats/minute, respiratory rate is 14 breaths/minute, supine blood pressure is 125/79 mmHg, and standing blood pressure is 119/74 mmHg. His neurologic exam is normal. Lungs reveal normal breath sounds bilaterally. A cardiovascular exam reveals diminished carotid pulse upstroke and a grade II/VI systolic murmur heard best at the right-upper sternal border. His abdomen is soft, and the extremities reveal trace edema bilaterally. His electrocardiogram (ECG) is shown below (see txts). What should you do next? A. Echocardiogram B. Exercise stress testing C. Serial troponin testing D. Stop the hydrochlorothiazide and bolus 500 ml normal saline E. Tilt-table testing

A. Echocardiogram This male is older with exertional syncope and an exam consistent with aortic stenosis, so the next-appropriate step is to obtain an echocardiogram. Exercise stress testing is not indicated yet, and if the aortic stenosis is severe it could be dangerous. Serial troponin testing is indicated if ongoing ischemia or infarction is suspected, but the ECG shows only left ventricular hypertrophy (LVH), and the echo would be more important at this time. The patient is not orthostatic (defined as a systolic decrease of 20 mmHg or diastolic decrease of 10 mmHg with positional change), so it is less likely he has volume depletion as his cause of syncope. Tilt-table testing can sometimes help diagnose a patient with neurocardiogenic causes of syncope, but this patient is more likely to have aortic stenosis.

You are working at a skilled nursing facility, rounding on your patients. The nurse tells you that Mrs. Viera, an 83-year-old resident with a history of heart failure, has been having vomiting, diarrhea, and fever since the previous afternoon. The nurse also reports a decrease in urine output since early that morning. On your assessment, you notice that Mrs. Viera is slightly more confused than baseline, with dry mucous membranes. On chart review, you see that her baseline creatinine is 1.6 mg/dL, and that her medication list includes furosemide. You order stat labs which return with the following results: Serum sodium: 134 mEq/L Serum blood urea nitrogen (BUN): 17 mg/dL Serum creatinine: 2.1 mg/dL Urinary sodium: 200 mEq/L Urinary blood urea nitrogen (BUN): 385 mg/dL Urinary creatinine: 220 mg/dL How does the fractional excretion of sodium (FENa) help you identify the etiology of the patient's acute kidney injury (AKI)? A. FENa cannot be reliably interpreted in this patient B. FENa is < 1%, indicating a prerenal etiology C. FENa is < 1%, indicating likely acute tubular necrosis (ATN) D. FENa is > 1%, indicating a prerenal etiology E. FENa is > 1%, indicating likely acute tubular necrosis (ATN)

A. FENa cannot be reliably interpreted in this patient This patient's calculated FENa is 1.4%. FENa < 1 has a 96% sensitivity and 95% specificity for distinguishing prerenal causes from acute tubular necrosis (ATN). However, since the equation uses the urinary sodium, this calculation cannot be reliably interpreted in patients taking loop diuretics, which cause an increase in urinary sodium excretion. Therefore, in patients taking loop diuretics presenting with AKI, the fractional excretion of urea (FEUrea) is the preferred equation: FEUrea ≤ 35% indicates prerenal etiology with 78% sensitivity and 88% specificity, whereas FEUrea > 50% indicates a diagnosis of ATN. This patient's calculated FEUrea is 21.6%, which supports the presumptive diagnosis of prerenal AKI based on the patient's history and exam.

While on call in the hospital, you are called to the bedside of a female who was admitted four hours ago with severe pneumonia. Her breathing has become more shallow, she is increasingly lethargic and her oxygen saturation has dropped to 85% despite high-flow oxygen. You request an arterial blood gas (ABG) to help determine your next steps. Which of the following ABG results is most consistent with this patient's clinical presentation? A. pH: 7.15 pCO2: 70 mmHg pO2: 60 mmHg HCO3: 28 mEq/L B. pH: 7.30 pCO2: 30 mmHg pO2: 90 mmHg HCO3: 12 mEq/L C. pH: 7.37 pCO2: 40 mmHg pO2: 90 mmHg HCO3: 22 mEq/L D. pH: 7.50 pCO2: 60 mmHg pO2: 90 mmHg HCO3: 44 mEq/L E. pH: 7.65 pCO2: 20 mmHg pO2: 70 mmHg HCO3: 16 mEq/L

A. pH: 7.15 pCO2: 70 mmHg pO2: 60 mmHg HCO3: 28 mEq/L Option A reflects an acute respiratory acidosis which is the acid-base disorder that best supports an acute respiratory decompensation. Note that the pCO2 is elevated. However, pCO2 cannot be the only variable to be relied on as elevations of pCO2 could be expected in someone with a chronic respiratory condition such as interstitial lung disease, or chronic obstructive pulmonary disease (COPD). We can infer that there has been a rapid decompensation if the bicarbonate is not significantly elevated in efforts to correct the pH. The hypoxia in this example also matches the clinical scenario. In addition, metabolic alkalosis (option D) would also typically lead to elevations in pCO2 as lungs retain CO2 to help correct the bicarbonate elevation that is acting to raise pH. Option B reflects a metabolic acidosis with low pH and bicarbonate, and a correspondingly low pCO2 due to respiratory compensation for the acidosis. Option C reflects the normal state. Option D represents a metabolic alkalosis. Option E reflects an acute respiratory alkalosis that can arise with hyperventilation due to drugs, anxiety, pulmonary embolism, acute asthma, pneumonia, etc. The hypoxia drives an increased respiratory rate, but because CO2 diffuses across the alveoli faster than oxygen (O2), the pCO2 decreases, and the pH subsequently increases.

A 28-year-old Caucasian female presents to the clinic for her annual exam. She has no complaints. On exam, her pulse is 84 beats/minute, her blood pressure is 116/70 mmHg, and her body mass index (BMI) is 28 kg/m2. Which of the following would prompt screening for diabetes? A. A hemoglobin A1c (HbA1c) of 5 at last year's exam B. A history of gestational diabetes with her last pregnancy, seven years ago C. A mother recently diagnosed with hypothyroidism D. A paternal aunt with diabetes E. Frequent consumption of refined carbohydrates

B. A history of gestational diabetes with her last pregnancy, seven years ago According to the American Diabetes Association, all individuals should be screened for diabetes by age 45. In addition, screening should be pursued in any adult who is overweight (BMI > 25) with at least one of the following risk factors: Physical inactivity First-degree relative with diabetes High-risk race/ethnicity (ex, African American, Latin, Native American, Asian American, Pacific Islander) Females who delivered a baby weighing more than nine pounds or who was diagnosed with gestational diabetes Blood pressure greater than or equal to 140/90 mmHg or on therapy for hypertension Females with polycystic ovary syndrome HbA1c greater than or equal to 5.7% Other clinical conditions associated with insulin resistance History of cardiovascular disease Diet is not included as a risk factor for diabetes screening. First-degree relatives with medical conditions other than diabetes are also not considered a risk factor.

A 35-year-old female with no significant past medical history presents with two days of constant, sharp, left-sided chest pain. There was no clear precipitant for her pain, and she does not identify any alleviating or aggravating factors. On physical exam, she appears comfortable and has normal vital signs. Cardiac exam demonstrates regular rate and rhythm, normal S1 and S2, and no murmurs. She has point tenderness over the left-upper-sternal border. Electrocardiogram (ECG) showed normal sinus rhythm with no ST or T wave changes. What is the most likely diagnosis? A. Acute coronary syndrome B. Costochondritis C. Panic disorder D. Pneumothorax E. Pulmonary embolism

B. Costochondritis Focal chest wall tenderness increases the likelihood of the etiology of a musculoskeletal etiology, such as trauma, muscular strain, rib fracture, or costochondritis. Although acute coronary syndrome (ACS) can occasionally cause reproducible chest tenderness, the long duration of constant chest pain without any findings of infarction or ischemia on ECG makes ACS very unlikely. A negative troponin would rule out ACS completely. Chest pain can be associated with anxiety or panic disorder, but the patient is not presenting with panic symptoms, and other life-threatening etiologies should be ruled out first. A pneumothorax significant enough to cause pain for two days is typically associated with tachycardia and respiratory symptoms, including tachypnea, hypoxia, or both. Chest pain due to pulmonary embolism can cause reproducible tenderness with palpation, but it is typically worsened with deep breathing and is often associated with dyspnea and tachycardia.

A 26-year-old male with human immunodeficiency virus (HIV) presents to the clinic with one week of blurry vision and floaters in his right eye. He has not had any exposure to bacterial conjunctivitis at his work in an elementary school. He does not wear corrective lenses. He had a fever this morning to 38.2 C (100.8 F) with associated malaise and mild abdominal pain and one watery stool. He admits to nonadherence with his HIV medication regimen. A funduscopic exam was performed, which showed the following. What is the most-likely organism responsible for these findings? (see txts for pic) A. Chlamydia trachomatis B. Cytomegalovirus C. Herpes zoster D. Retinitis pigmentosa E. Toxoplasmosis

B. Cytomegalovirus Acute cytomegalovirus (CMV) infection often presents with visual symptoms due to retinitis, and colitis. Usually the CD4+ count will be less than 100 cells/mcl. This patient has been non-adherent with his medication, increasing the risk that his HIV will progress to AIDS. CMV infection involving the eye is an AIDS-defining opportunistic infection. Chlamydia and zoster do not affect the retina. Retinitis pigmentosa is a genetic disease. Toxoplasmosis is also an opportunistic infection, but the retina findings demonstrate necrotizing retinochoroiditis and are usually bilateral.

A 52-year-old bisexual male presents with difficulty swallowing solid foods for two weeks. He has also experienced low-grade fevers, weight loss, and anorexia. He admits to not consistently using condoms. He reports no vomiting, melena, or hematochezia. He takes no medications and does not smoke or drink alcohol. On exam, his oropharynx is normal. He has mild epigastric tenderness and appears cachectic. Laboratory evaluation reveals the following: White blood cell count (WBC): 3.5K (4.5-11); Hemoglobin: 10.2 gm/dl (12-15 gm/dl); Platelet count: 136K (150-420); Human immunodeficiency virus (HIV): PositiveCD4+ T-cell count: 188 cells/ml. An esophagogastroduodenoscopy (EGD) is ordered. What is the most likely finding on the EGD? A. Barrett's esophagus B. Esophageal candidiasis C. Gastritis D. Non-bleeding duodenal ulcer E. Normal

B. Esophageal candidiasis This is a male with newly diagnosed HIV and a CD4 count less than 200 cells/mm3 presenting with dysphagia to solid foods. Candidal esophagitis is the most likely diagnosis considering his HIV status, low CD4 count, and presenting symptoms. Candida esophagitis is considered an acquired immune deficiency syndrome (AIDS)-defining illness. It will be unlikely for him to have a normal EGD. The acuity of his presentation, lack of risk factors, and lack of associated symptoms, such as gastrointestinal (GI) bleeding or epigastric pain, make gastritis, Barrett's esophagus, or a duodenal ulcer much less likely.

A 50-year-old male with history of alcohol use disorder, type 2 diabetes mellitus, and cirrhosis presents to the emergency department with hematochezia and lightheadedness. He reports a large amount of painless bright-red rectal bleeding for the past one hour. He has not experienced this before. He denies vomiting. His home medications include metformin and propranolol. He drinks half a pint of vodka daily. On physical exam, his temperature is 37.3C (99.2F), pulse is 120 beats/minute, and blood pressure is 82/60 mmHg. His abdomen is soft and non-tender. He is jaundiced and has distended veins on his anterior abdominal wall. Laboratory testing reveals a hemoglobin of 8.8 mg/dL and platelet count of 69,000/µL. Two large-bore peripheral IVs are placed, a fluid bolus is started, and a blood type and crossmatch is ordered. What diagnosis is the most likely cause of this patient's hematochezia? A. Alcoholic gastritis B. Esophageal varices C. Internal hemorrhoids D. Mallory-Weiss tear E. Meckel diverticulum

B. Esophageal varices The most likely cause of bleeding in this patient with cirrhosis and hematochezia, is esophageal varices. In order to produce bright-red blood from an upper gastrointestinal (GI) source, the hemorrhage must be brisk enough for blood to pass through the intestines without oxidating. Because varices bleed at arterial pressure, they often (but not always) produce brisk hemorrhages and hemodynamic instability, as with this man. His medication list includes a non-selective beta-blocker, which may indicate a known diagnosis of varices. Gastritis does not typically cause large-volume bleeding. Internal hemorrhoids and Meckel diverticulum both could present with painless hematochezia, but hemorrhoidal bleeding is typically mild, and Meckel diverticula present more commonly in younger patients. Mallory-Weiss tears typically cause hematemesis after vomiting.

Two victims of a multiple-vehicle car accident are being treated in the emergency department trauma bay. Both have severe injuries resulting in blood loss, and four units of packed red blood cells (PRBCs) are ordered from the blood bank for each patient. The stickers to label each patient's blood samples were mixed up, so these two patients each mistakenly receive the blood intended for the other. The patient with type O+ blood ends up receiving a transfusion of B+ blood, and you are concerned that she will develop an acute hemolytic transfusion reaction. What findings would be most consistent with this type of transfusion reaction? A. Fever and nausea within hours of the transfusion, with normal urine output B. Fever, dyspnea, hypotension, and dark urine within minutes of starting the transfusion C. Fever, spherocytosis, and hyperbilirubinemia 2 to 10 days after the transfusion D. Hypotension and angioedema within minutes of starting transfusion E. Pulmonary edema within hours of transfusion

B. Fever, dyspnea, hypotension, and dark urine within minutes of starting the transfusion Acute hemolytic transfusion reaction can occur due to mis-labeling of specimens and ABO incompatibility. Classic findings include fever, dyspnea, hypotension, and dark urine within minutes of starting the transfusion. A febrile non-hemolytic transfusion reaction can cause fever and nausea within hours of a transfusion, but the urine is unaffected. A delayed hemolytic transfusion reaction can cause fever, spherocytosis, and hyperbilirubinemia 2 to 10 days after transfusion. Hypotension and angioedema within minutes of starting the transfusion may be due to anaphylaxis. Transfusion-related acute lung injury (TRALI) can present with pulmonary edema within hours of a transfusion.

You are working in the emergency department, and your attending asks you to see a 65-year-old male presenting with abdominal pain. In gathering the history, the patient tells you that he has had two to three days of progressive generalized "achy" abdominal pain, along with decreased appetite and decreased urine output. On further clarification, he reports not urinating in the past two days. On examination, vital signs are normal. He is alert, oriented, and in no acute distress. His exam is benign with the exception of mild abdominal distention, a palpable bladder, and an enlarged prostate on digital rectal exam. Which of the following is the next best step? A. Computed tomography (CT) of his abdomen and pelvis B. Foley catheter placement C. Intravenous (IV) diuretics D. IV fluids E. Renal ultrasound

B. Foley catheter placement This patient is presenting with symptoms of postrenal obstruction. The urgent next step is foley catheter placement to relieve the obstruction, which can be both diagnostic and therapeutic. Alternatively, a bedside bladder scan can be performed to confirm the enlarged bladder (many bedside nurses can do this technique), prior to catheter placement. The patient's enlarged prostate increases the likelihood of bladder outlet obstruction. Post-obstructive renal failure is a "can't miss" diagnosis, as longer obstruction time leads to an increased incidence of acute kidney injury, infection, and urosepsis. Prompt relief of the obstruction is important. A urologic CT scan (without contrast) can be utilized to evaluate patients with presumed obstruction. Additionally, magnetic resonance imaging (MRI) has very high sensitivity and specificity for identifying the obstruction and may also be able to differentiate acute versus chronic renal failure. Its main limitations are cost and accessibility. However, these modalities would be reserved for cases in which the cause of obstruction may be unclear, which is not the case in this patient. This patient is presenting with signs and symptoms of a urinary obstruction. IV fluids are indicated in prerenal acute kidney injury, but would not treat this patient's most-likely underlying pathology. In addition, diuretics (to promote urine output) would be contraindicated in a complete obstruction, and would not be recommended in this setting without any additional information about the underlying etiology of his symptoms. Renal ultrasound is a quick, safe, and relatively inexpensive way to evaluate for hydronephrosis; however, in this patient with a palpable bladder and high degree of suspicion of obstruction below the bladder outlet, the first step should be Foley insertion.

Mary is an 18-year-old female with a past medical history significant for type 1 diabetes mellitus who was admitted to the intensive care unit (ICU) yesterday with nausea, vomiting, and a decreased level of consciousness. Her labs were consistent with diabetic ketoacidosis, and she was started on an insulin drip and intravenous fluids. Today, she is more alert and has no further nausea or vomiting. Her anion gap has closed. Prior to stopping the insulin drip, which type of insulin is most likely to prevent a recurrence of ketoacidosis? A. Intermediate-acting insulin B. Long-acting insulin C. Premixed insulin (combination of short- and long-acting insulin) D. Rapid-acting insulin E. Short-acting insulin

B. Long-acting insulin During diabetic ketoacidosis, an insulin drip using rapid- or short-acting insulin is necessary to close the anion gap. Once the anion gap has normalized, and if the patient is alert and able to eat, subcutaneous insulin may be started. A long-acting insulin is the preferred subcutaneous insulin because it has no peak and covers basal insulin needs for a full day. Because long-acting insulin does not start working for one to one-and-a-half hours, the insulin drip should continue for one to two hours after the subcutaneous insulin has been administered.

Six weeks ago, a 67-year-old female presented to her primary care physician with dyspepsia and epigastric pain. She did not drink alcohol and took no medications. Testing revealed a positive stool-occult blood test and mild microcytic anemia. She underwent upper and lower endoscopy and was found to have a duodenal ulcer. Biopsy was positive for Helicobacter pylori (H. pylori), and she completed the prescribed course of proton-pump inhibitor and antibiotics. Now she is returning to the clinic and reports that her symptoms have not resolved. What is the best next step in diagnosis and management for this patient? A. Perform computed tomography (CT) of the abdomen B. Perform H. pylori stool antigen test C. Repeat upper endoscopy with biopsy D. Resume proton-pump inhibitor indefinitely E. Test serum gastrin level SUBMIT

B. Perform H. pylori stool antigen test H. pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) cause the vast majority of peptic ulcer disease. In this patient's case, it would be appropriate to do testing for eradication of H. pylori since her symptoms did not respond to appropriate treatment. This could be done with the H. pylori stool antigen test or urease breath test - invasive testing with repeat endoscopy is not necessary. It would be best to confirm eradication of the underlying cause of the ulcer before committing her to lifelong acid suppressant therapy. If testing confirms H. pylori eradication, then it would be appropriate to consider investigating for less-common causes of peptic ulcer disease, such as gastrinoma with a gastrin level. A CT scan of the abdomen is unlikely to help you currently. Resuming the proton pump inhibitor may be reasonable but only after checking for H. pylori eradication.

You are seeing a delightful 62-year-old female in the primary care clinic for follow-up of pulmonary function tests (PFTs). She has long been your patient, although you have never been able to get her to quit smoking. She has had no hospitalizations since her children were born. Over the past three months she has felt dyspneic with exertion. Her complete blood count (CBC), basic metabolic panel, and stress echo were normal. Her PFTs showed a post-bronchodilator FEV1/FVC of 65% and FEV1 of 41% predicted. Based on this data, what additional information do you need to guide pharmacologic therapy? A. Computed tomography (CT) of her chest B. Folate level C. History of breathlessness with getting dressed D. History of headaches E. Troponin T measurement

C. History of breathlessness with getting dressed The post-bronchodilator FEV1/FVC of 65% confirms the diagnosis of chronic obstructive pulmonary disease (COPD) by PFTs, and her FEV1 of 41% predicted places her in the GOLD 3 class of 'severe' airflow limitation. This continues to have a certain prognostic significance, but as of the latest iteration of the Global Initiative for Obstructive Lung Disease (GOLD) guidelines, spirometry is no longer used to guide therapy. Instead, functional assessment is used, the Modified MRC (mMRC) dyspnea scale, the COPD Assessment Test (CAT), together with history of previous COPD exacerbations and hospitalizations to guide therapy. Breathlessness with dressing (C) or undressing or with leaving the house is considered grade 4 on the mMRC. Although a low-dose chest CT (A) may be warranted to screen for lung cancer, it is not necessary to guide therapy of her COPD. A history of headaches (D) is not part of either standardized functional assessment tool for COPD. A troponin T (E) measurement is not useful in the absence of symptoms of acute coronary syndrome, and she recently had a negative stress test. She is not anemic; a folate level (B) is not indicated.

An 82-year-old female with diabetes, hypertension, hyperlipidemia, and a stroke three years ago with residual dysarthria, is admitted to the intensive care unit (ICU) after her daughter was unable to wake her up this morning. On exam, she is afebrile, and her neurological exam is not focal. A head computed tomography (CT) scan did not reveal any acute pathology. Labs are as follows: white blood count (WBC) 12.4 cells x 10 3 /μL sodium 123mEq/L, potassium 5.3 mEq/L, chloride 107 mEq/L, bicarbonate 22 mEq/L, blood urea nitrogen (BUN) 42 mg/dL, creatinine (Cr) 2.3 mg/dL, glucose 840 mg/dL. A serum osmolality is 410 mosm/kg. In addition to insulin, which of the following interventions is most likely to improve her outcome? A. Antibiotics B. Dialysis C. Intravenous (IV) fluids D. Potassium supplementation E. Sodium bicarbonate

C. Intravenous (IV) fluids This patient has hyperosmolar hyperglycemic state. Her glucose is significantly elevated in the absence of ketoacidosis; her anion gap is only 12 (141-107-22). Her serum osmolality is increased, and she has mental status changes. Due to osmotic diuresis in the setting of hyperglycemia, patients are profoundly volume depleted and may develop acute kidney injury. Treatment includes IV insulin and aggressive hydration with IV normal saline fluid. Her sodium, corrected for hyperglycemia, is 141 mg/dL (using a correction factor of 2.4mEq/L for every 100 mg/dL increase in serum glucose above 100 mg/dL). The patient does not have any localizing signs or symptoms of infection, so antibiotics are not indicated. Her potassium is slightly low, but she is not acidemic; therefore potassium and bicarbonate are not indicated. While her creatinine is 2.3 mg/dL and she is older, she is significantly volume depleted with her hyperosmolar state, and her creatinine and urine output should be monitored for improvement with fluid administration.

A 65-year-old female is brought to the emergency department by the paramedics after a syncopal event. She reports a prodrome of lightheadedness and diaphoresis while straining to have a bowel movement. Her husband says that she lost consciousness for fewer than five minutes in the bathroom. Her medical history is significant for diabetes mellitus type 2 for the past 10 years. She takes metformin, aspirin, and furosemide daily. She is currently awake and oriented to person, place, and time. Her vital signs are normal, including orthostatic vitals, and she was able to stand for the orthostatic vitals without symptoms. Physical examination and routine blood tests are normal. Her electrocardiogram (ECG) is normal. Which of the following is the most likely etiology of syncope in this patient? A. Hypoglycemia B. Medication-induced bradycardia C. Neurocardiogenic syncope D. Orthostatic syncope E. Tachyarrhythmia

C. Neurocardiogenic syncope Neurocardiogenic (often called vasovagal) syncope is commonly associated with prodrome of lightheadedness, diaphoresis, dizziness, vertigo, etc., and is often situational. Triggers can include coughing, sneezing, gastrointestinal (GI) stimulation, or micturition, especially straining to urinate with an enlarged prostate (in men) or constipation. This patient had both a prodrome and was straining for a bowel movement. Hypoglycemia can cause loss of consciousness, however, this would not result in spontaneous reversal. In addition, her blood tests were normal. The patient's medications are not commonly associated with bradycardia. Positional change is consistent with an orthostatic cause of syncope, however, the patient's orthostatic vital signs were negative (importantly, including her absence of symptoms) and there was not a history of standing prior to loss of consciousness, making this less likely. Women (and men) with a tachyarrhythmia often do not have a prodrome prior to loss of consciousness. In addition, her lab tests (electrolytes) and ECG were normal, making this less likely. Please note, however, that a paroxysmal tachyarrhythmia cannot be completely ruled out at this time.

A 66-year-old male is admitted to the hospital for treatment of new-onset atrial fibrillation with a rapid ventricular rate. The troponin, complete blood count (CBC), and basic metabolic profile are within normal limits. Which additional laboratory test is indicated as part of the initial workup for new-onset atrial fibrillation? A. Creatine kinase-MB (CK-MB) B. Prothrombin time and international normalized ratio (ProTime INR) C. Thyroid stimulating hormone (TSH) D. Urinalysis E. Vitamin B12

C. Thyroid stimulating hormone (TSH) Initial laboratory evaluation of new-onset atrial fibrillation should focus on identifying the underlying etiology. Laboratory evaluation includes: thyroid function test to evaluate for thyrotoxicosis troponin to evaluate for inciting ischemic event basic metabolic profile to evaluate for electrolyte abnormality (particularly K and Mg) CBC to evaluate for infection and/or anemia Although CK-MB was used in the past to diagnose acute myocardial infarction, it is not necessary if a troponin is available and negative. A ProTime may be obtained as a baseline if anticoagulation will be initiated, but it is not helpful in diagnosing the underlying etiology of new atrial fibrillation. If recreation stimulant use is suspected (e.g. cocaine), then a drug screen would also be indicated. However, a urinalysis alone would not provide useful information. Vitamin B12 is not known to directly contribute to atrial fibrillation.

A 56-year-old male presents to the emergency department with shortness of breath with minimal activity for two days. He endorses orthopnea and paroxysmal nocturnal dyspnea. Past medical history is significant for hypertension, hyperlipidemia, and peripheral vascular disease for which he takes aspirin, amlodipine, and atorvastatin. He has a 20-pack-per-year history of smoking. Vital signs are as follows: temperature is 37.1 C (98.7 F), pulse is 102 beats/minute, blood pressure is 180/100 mmHg, body mass index (BMI) is 36 kg/m2 and oxygen saturation is 94% on two liters of air via nasal cannula. Physical exam is significant for crackles at both lung bases, jugular venous pressure of 9 cm of water, S3 gallop at cardiac apex, and bilateral pitting edema to mid-calves. A complete blood count, basic metabolic panel, troponin T assay, and b-type natriuretic peptide level return within normal limits. An electrocardiogram (ECG) shows sinus tachycardia. His chest radiograph is shown. Which of the following is the most likely cause of this patient's symptoms? (see pic) A. Acute coronary syndrome B. Acute exacerbation of asthma C. Acute exacerbation of chronic obstructive pulmonary disease D. Acute exacerbation of congestive heart failure E. Pulmonary embolism

D. Acute exacerbation of congestive heart failure This patient's symptoms of shortness of breath with orthopnea and paroxysmal nocturnal dyspnea, and his exam findings of bibasilar crackles, elevated jugular venous pressure, S3 gallop, and bilateral pitting edema are consistent with acute exacerbation of congestive heart failure (CHF). Chest radiograph shows cardiomegaly, alveolar edema, and haziness of vascular margins. Of note, B-type natriuretic peptide level can be falsely normal in obese patients with CHF exacerbation. Asthma exacerbation is unlikely in this patient without a prior history of asthma and absence of wheezing on physical exam. While he has a history of smoking, lack of productive cough and absence of wheezing on exam makes a diagnosis of chronic obstructive pulmonary disease (COPD) exacerbation less likely. Acute coronary syndrome (ACS) can present with shortness of breath as an anginal equivalent, but this is more common in female and older adult patients. Lack of ST-T changes on an ECG and a normal troponin T level make ACS much less likely in this patient. Patients with pulmonary embolism typically present with pleuritic chest pain. Leg swelling may be present, but it is usually unilateral, and not bilateral as in this patient.

A 70-year-old female presents to the emergency department with moderately severe chest pain. She describes the pain as a vague, deep discomfort and notes associated nausea, diaphoresis, and dyspnea. The pain has no clear aggravating or alleviating factors. Her pain began early on the morning of presentation, waking her from sleep, and has persisted for two hours. Her exam, including vital signs, is normal. What is the most important initial diagnostic test? A. Chest x-ray B. Complete blood count C. Computed tomography (CT) angiography of the chest D. Electrocardiogram (ECG) E. Troponin

D. Electrocardiogram (ECG) The first step in evaluating this patient with severe chest pain is an ECG. An ECG can differentiate an ST-segment elevation myocardial infarction from the other acute coronary syndromes. It can also provide other evidence of coronary ischemia, including T-wave inversion and ST-segment depression. Since the outcome of a myocardial infarction depends on timely intervention, rapid identification is essential and an ECG is the most efficient diagnostic test. A chest X-ray may be reasonable for evaluating the source of the chest pain, but with normal vital signs and lung exam, and a primary complaint of anginal chest pain, an ECG should be performed first. A complete blood count would be helpful in evaluating for infection or an acute anemia which could be contributing to the patient's presenting symptoms, but it is a nonspecific test that would not be useful in the timely evaluation for acute coronary syndrome. A CT angiogram of the chest would be obtained to evaluate for pulmonary embolism. This may be appropriate if acute coronary syndrome is ruled out, and suspicion for pulmonary embolism increases. However, the lack of pleuritic chest pain, tachycardia, and hypoxia makes this diagnosis less likely. A troponin test may also be helpful in identifying an acute coronary syndrome in this patient, but the process of drawing blood and lab analysis will take time, during which she could already be receiving appropriate treatment. Additionally, since her pain began only two hours earlier, it is possible that the troponin measurement may be negative. In some instances, depending on the troponin assay used, serum troponin elevations may not be detectable for four to eight hours after onset of anginal symptoms.

A 52-year-old male with hypertension and hyperlipidemia comes to the clinic for a routine follow-up. He has no symptoms. His mother was recently diagnosed with diabetes, and he wants to know if he is also diabetic. He quit smoking two years ago after being admitted to the hospital with chest pain. He has gained 30 pounds since that time, and his body mass index (BMI) is currently 30 kg/m2. His last meal was breakfast two hours ago, which consisted of a bagel and orange juice. Which of the following studies is most likely to support a diagnosis of diabetes? A. Blood glucose level in the clinic of 160 mg/dL B. Blood glucose level of 190 mg/dL two hours after a 75 g glucose load C. Decreased sensation in feet by monofilament test D. Hemoglobin A1c (HbA1c) of 6.8% E. Urinalysis with glucosuria

D. Hemoglobin A1c (HbA1c) of 6.8% There are four ways to diagnose diabetes: 1) HbA1c > 6.5% 2) Blood sugar > 200 mg/dL, accompanied by polyuria, polydipsia, and unexplained weight loss 3) Fasting blood sugar > 126 mg/dL on two separate occasions 4) Blood sugar > 200 mg/dL two hours after 75 g glucose load, confirmed on a second occasion. Decreased sensation in feet by monofilament and a urinalysis with glucosuria are compatible with diabetes, however, neither is diagnostic.

A 68-year-old female is admitted to the hospital because of increasing dyspnea and orthopnea over the past two weeks. Her medical history is significant for ischemic cardiomyopathy with an ejection fraction of 40% and low back pain for one month. She reports no chest pain, palpitations, fever, or cough. She has been adherent to a low-sodium diet. She does not use alcohol or tobacco. Daily medications are carvedilol, lisinopril, amlodipine, atorvastatin, aspirin, and ibuprofen. Which medication would most likely cause her worsening symptoms? A. Amlodipine B. Atorvastatin C. Carvedilol D. Ibuprofen E. Lisinopril

D. Ibuprofen (dec PG synthesis, no VD of afferent arteriole, may precipitate fluid retention in patients with HF) When evaluating a patient with a congestive heart failure (CHF) exacerbation, it is important to identify the trigger. Medications which can trigger CHF exacerbation include NSAIDs (e.g. ibuprofen), non-dihydropyridine calcium channel blockers (verapamil and diltiazem), and thiazolidinediones (pioglitazone). Other common triggers include non-adherence with diet or medications (e.g. diuretics), ischemia, thyroid disorders, uncontrolled hypertension, arrhythmia, and anemia. Angiotensin-converting-enzyme (ACE) inhibitors (e.g. lisionpril) and long-acting beta-blockers (e.g. carvedilol) decrease mortality in CHF. Dihydropyridine calcium channel blockers (e.g. amlodipine) can cause leg edema, but do not trigger CHF. Statins do not trigger CHF.

You are evaluating a 53-year-old male in the emergency department who is presenting with a chief concern of shortness of breath. He reports a one-day history of progressively worsening dyspnea on exertion, productive cough, and subjective fever. His past medical history includes chronic obstructive pulmonary disease (COPD) and ischemic cardiomyopathy with a stable ejection fraction (EF) of 40%. Which of the following physical exam findings is most supportive of an infectious etiology of his shortness of breath? A. Absent breath sounds on one side B. Bibasilar crackles and mild wheezes C. Diminished inspiratory effort D. Increased fremitus and egophony over part of the lung E. Tachycardia with normal breath sounds on exam

D. Increased fremitus and egophony over part of the lung Physical exam findings most consistent with infectious etiology include rhonchi, crackles, egophony ("E" to "A" changes with auscultation due to consolidated tissue not transmitting the "E" pitch) and increased fremitus (on chest examination can palpate the vibration when patient says ninety-nine, indicates denser, more inflamed tissue) over a localized lung area (D). Absent breath sounds (A), along with a deviated trachea, should raise concern for a possible pneumothorax. BIbasilar crackles and wheezing (B) may be consistent with congestive heart failure (CHF). Wheezing can also be heard in COPD and asthma, however the edema associated with CHF can also cause airway narrowing leading to wheezing. A diminished respiratory effort (C) in a patient with shortness of breath would prompt an evaluation for a neuromuscular etiology of their dyspnea. Tachycardia with normal breath sounds on exam (E) in a patient presenting with dyspnea may be concerning for pulmonary embolism (PE).

A 51-year-old female with a history of rheumatoid arthritis and coronary artery disease is admitted to the hospital with acute liver failure. During the admission process, the team calls her pharmacy and primary care physician and confirms the doses and route of administration and her adherence to her prescription medications. What additional information should be obtained in the medication reconciliation process? A. Allergies to medications B. Cost of prescriptions C. List of all medications taken in the last five years D. List of over-the-counter medications taken E. Number of refills remaining on prescriptions

D. List of over-the-counter medications taken Medication reconciliation is the process of obtaining an accurate list of medications, both prescription and over-the-counter, along with dosages, route of administration, and an assessment of adherence to the medications. Obtaining an accurate medication list on admission increases the likelihood of an accurate medication list on discharge. Over-the-counter medications and traditional remedies are easily overlooked, but should be considered when new findings, such as liver toxicity, are diagnosed. While medication allergies should be assessed with every admission, this is not considered part of medication reconciliation. Cost of medications should be considered, especially if there is an issue with adherence, but this is not part of reconciliation. Prior history of medications and number of refills are also not part of reconciliation.

A 50-year-old male is brought to the hospital by paramedics after a witnessed syncopal event. The event occurred at a local baseball game where he was a spectator. He was evaluated by paramedics at the scene within three minutes of the event and arrived at your hospital within 15 minutes. An intravenous (IV) line was started, but no fluid was given. The patient states that he stood up to get some lunch and suddenly became very lightheaded. He collapsed and does not recall anything until he awoke with many bystanders attending to him. He was aware of his surroundings immediately upon regaining consciousness and was not confused. Bystanders state he had a 30-second period of loss of consciousness and did not hit his head when he collapsed. His vital signs are as follows: temperature is 36.7 C (98 F), pulse is 90 beats/minute, respiratory rate is 12 breaths/minute, and blood pressure is 110/65 mmHg. What is the next best step to determine the cause of the patient's syncopal episode? A. Assessment for pain with passive ankle dorsiflexion (Homan's sign) B. Auscultation of the carotid arteries C. Cranial nerve exam D. Orthostatic blood pressure measurement E. Pulmonary exam

D. Orthostatic blood pressure measurement Syncope is caused by decreased perfusion to the brain. This patient collapsed after a sudden positional change, therefore orthostatic hypotension should be high in the differential diagnosis and should be assessed with orthostatic blood pressure measurement before fluids are given. Homan's sign is a poor test for deep-vein thrombosis (David L. Simel, Drummond Rennie. The Rational Clinical Examination: Evidence-Based Clinical Diagnosis. New York, NY: McGraw-Hill Education, 2016.) and a pulmonary embolism should give the patient more symptoms if it was large enough to result in syncope. Auscultation of the carotids is not necessary in syncope evaluation, because carotid artery stenosis alone does not result in syncope (due to effective collateral supply). A cranial nerve exam should be performed to assess for neurologic damage from a traumatic fall, but the results will not determine a cause of sudden drop in perfusion. A pulmonary exam is unlikely to help you determine a cause of syncope.

A 45-year-old human immunodeficiency virus (HIV)-infected male presents to the emergency department with nonproductive cough, fever, and progressive exertional dyspnea for one week. His CD4 count was 150/microliter one month ago. He has not been adherent to his antiretroviral regimen. On arrival, his temperature is 38.3 C (100.9 F), heart rate is 98 beats/minute, blood pressure is 110/70 mmHg, and oxygen saturation is 89% on room air. Physical exam is unremarkable except for oral thrush. Chest x-ray shows diffuse bilateral infiltrates with early cystic changes. Which organism is most likely causing this patient's acute symptoms? A. Aspergillus fumigatus B. Candida albicans C. Mycobacterium tuberculosis D. Pneumocystis jirovecii E. Streptococcus pneumoniae

D. Pneumocystis jirovecii Pneumocystis jirovecii is the most likely cause of pneumonia in this patient with a CD4 count of less than 200/microliter and characteristic chest x-ray findings. While Streptococcus pneumoniae remains the most common cause of community-acquired bacterial pneumonia in HIV patients, it typically presents with lobar or focal consolidation. Invasive aspergillus infections usually present with solitary or multiple nodules that may be cavitary, or areas of patchy consolidation or infiltrates. Candida albicans is a rare cause of primary pulmonary infections, even in immunocompromised patients. Mycobacterium tuberculosis causes a more-indolent infection than Pneumocystis jirovecii, and is less likely to present with diffuse, bilateral infiltrates on chest radiography.

A 78-year-old male has been admitted to the hospital after a severe stroke. Past medical history is significant for congestive heart failure, hypertension, and chronic obstructive pulmonary disease (COPD). On day five of his hospitalization, he develops a fever, productive cough, pleuritic chest pain, and shortness of breath. Pulmonary exam reveals bronchial breath sounds, dullness to percussion, increased tactile vocal fremitus, and whispered pectoriloquy in the right-lower lung fields. There are no adventitious sounds. What is the most likely diagnosis? A. Chronic obstructive pulmonary disease exacerbation B. Congestive heart failure exacerbation C. Pleural effusion D. Pneumonia E. Pulmonary embolism

D. Pneumonia Cerebrovascular accidents frequently lead to dysphagia and predispose patients to aspiration. This patient's pulmonary exam findings are consistent with a right-lower lobe consolidation from an aspiration pneumonia. Lung exam findings that should raise the suspicion for chronic obstructive pulmonary disease exacerbation include wheezing and coarse crackles. Congestive heart failure exacerbations are typically associated with fine bibasilar crackles. Lung exam is usually unremarkable in pulmonary embolism. Presence of fluid in the pleural space is associated with dullness to percussion. However, breath sounds and tactile vocal fremitus are typically decreased in patients with a pleural effusion.

You are seeing a frail 85-year-old female who was admitted to your service three months ago with a chronic obstructive pulmonary disease (COPD) exacerbation. Despite your tobacco cessation counseling, she continued to smoke after discharge. She returns with shortness of breath. Six days ago, she had sudden worsening of her shortness of breath, and has since felt progressively more breathless, and is now unable to walk more than 30 feet. She can also no longer climb the stairs to her bedroom, so she is sleeping on the living room sofa. She has no cough, fever, or new orthopnea. In addition to a COPD exacerbation, what other illness most likely explains her acute presentation? A. Acute myocardial infarction B. Idiopathic pulmonary fibrosis C. Lung cancer D. Pulmonary embolism E. Tension pneumothorax

D. Pulmonary embolism Pulmonary embolism (PE) (D) can often coexist with COPD, and smoking is a strong risk factor for venous thromboembolism (VTE). Most of the time, PE presents with acute onset of dyspnea and/or chest pain. However, small PEs can occasionally present more subacutely. An acute myocardial infarction (A) could be a consideration, but would also be expected to present in a matter of minutes to hours. A fairly recent MI causing new onset heart failure may be a possibility, but not an acute infarction alone. In heart failure, we would more likely see orthopnea besides dyspnea in most cases. Idiopathic pulmonary fibrosis (IPF) (B) has more insidious onset with usually dry cough accompanying dyspnea. Lung cancer (C) would also have a more insidious onset with dyspnea, cough, hemoptysis, weight loss, and other constitutional symptoms. Tension pneumothorax (E) would likely have a more-acute presentation (minutes to hours instead of days), and is often accompanied by ipsilateral chest pain and hypotension. In addition, patients with poor underlying pulmonary reserve are generally severely symptomatic and unstable.

A 67-year-old male is admitted to the hospital with a non-ST elevation myocardial infarction. He took no medications prior to admission. During his hospital stay, he is noted to have hypertension. Echocardiogram shows left ventricular hypertrophy, an ejection fraction of 60%, and normal wall motion and valvular function. Which of the following is the best antihypertensive agent to start in this patient? A. Hydralazine B. Isosorbide mononitrate C. Lisinopril D. Metoprolol E. Spironolactone

D. metoprolol. Beta-blockers, like metoprolol, are first-line agents for hypertension in the setting of coronary artery disease. Angiotensin-converting enzyme (ACE) inhibitors are recommended in the setting of new left-ventricular systolic dysfunction. Spironolactone can be used for hypertension, but is typically not a first-line agent; it has been shown to reduce mortality in patients with reduced ejection fraction. Similarly, hydralazine and nitrates may be added to a multidrug, antihypertensive regimen. The combination of both has been shown to decrease morbidity and mortality in select patients with heart failure with reduced ejection fraction.

It is the Monday after a major national holiday, and you are seeing a 58-year-old male in the emergency department with progressive shortness of breath and generalized weakness over the previous two days. He has a history of end-stage renal disease (ESRD) due to diabetes and hypertension. He is chronically anuric and undergoes hemodialysis (HD) every Tuesday, Thursday, and Saturday. He says, "You know, Doc, I definitely indulged a bit too much at the holiday dinner." On exam, he appears short of breath, sitting upright on the gurney and speaking in 2- to 3-word sentences. His temperature is 36.1 C (97 F), pulse is 75 beats/minute, respiratory rate is 20 breaths/minute, blood pressure is 180/60 mmHg, and oxygen saturation is 94% on 10 liters/minute face mask. His exam is notable for diffuse crackles bilaterally, jugular venous pulse and pressure (JVP) of 12 cm while upright, lower extremity pitting edema to above his knees bilaterally, and a left arteriovenous (AV) fistula with a strong thrill. His labs are notable for the following: Sodium (Na): 132 mEq/L Potassium (K): 5.5 mEq/L Chloride (Cl): 111 mEq/L Bicarbonate (HCO3): 19 mEq/L Blood urea nitrogen (BUN): 48 mg/dL Creatinine (Cr): 5.9 mg/dL Phosphorus: 5.1 mg/dL Albumin: 3.4 g/dL Troponin: 0.04 ng/mL pH: 7.35 Chest x-ray shows pulmonary vascular congestion and pulmonary edema. Electrocardiogram (ECG) is normal. What is the next-best step in evaluation and/or management of this patient? A. Blood cultures and intravenous (IV) antibiotics B. Calcium gluconate IV C. Computed tomography angiography (CTA) of the chest D. Furosemide 40 mg IV push and reevaluation in four hours E. Nephrology consult for urgent hemodialysis

E. Nephrology consult for urgent hemodialysis This patient has ESRD and volume overload with pulmonary edema due to dietary indiscretion, which is an indication for urgent hemodialysis. While he has ESRD rather than AKI, the indications for urgent dialysis apply to both ESRD and AKI patients. A helpful mnemonic for remembering indications for urgent hemodialysis is "AEIOU" (see case): Acidosis - mild acidosis can sometimes be managed with bicarbonate replacement, but more severe or refractory acidosis requires hemodialysis for correction. Electrolytes - particularly hyperkalemia refractory to conservative measures. Ingestion - of toxins or medications that can be removed with hemodialysis. This includes toxic alcohols, salicylates, phenobarbital, and lithium. Overload - volume overload that is either refractory or cannot be managed with conservative measures. This patient is significantly volume overloaded, manifested by respiratory distress from acute hypoxia, crackles on lung exam, elevated JVP, and leg edema. Uremia - based on clinical assessment. Findings of symptomatic uremia include altered mental status, nausea, generalized pruritus, asterixis, and uremic pericardial friction rub. Calcium gluconate can be given acutely in hyperkalemia to stabilize the cardiac membrane, but does not lower the total body potassium level and is therefore a temporizing measure. This patient's potassium was within the upper limit of normal with a normal ECG. Additionally, his hypoxia should be addressed more urgently. The history, exam, and imaging are all supportive of pulmonary edema from volume overload; this is much more likely than a pulmonary embolism (PE), and therefore delaying treatment for a CTA would not be appropriate. The patient is anuric (does not make urine), so treatment with furosemide and re-evaluating four hours later is not correct and would result in a delay of more-appropriate treatment. There is no evidence of an active infection currently that would prompt the need for blood cultures and antibiotics.

A 56-year-old female with non-ischemic cardiomyopathy and hypertension presents to the office for a routine followup. Her last hospitalization for a congestive heart failure (CHF) with reduced ejection fraction exacerbation was two years ago. Currently, she has no shortness of breath, orthopnea, leg edema, or chest pain. She has been following a low-salt diet and does not drink alcohol. Her medications are carvedilol and a baby aspirin. Her home blood pressure measurements have ranged from 140-150/80-90 mmHg. Her exam is notable for a blood pressure of 150/90 mmHg. Her pulse is 60 beats/minute with normal S1 and S2 with no murmurs or gallops, and she has a normal respiratory rate. Her jugular venous pulse and pressure (JVP) is normal and her lungs are clear. Her point of maximal impulse (PMI) is laterally displaced. What medication should you add that can also improve her mortality from heart failure? A. Amlodipine B. Digoxin C. Furosemide D. Hydrochlorothiazide E. Ramipril

E. Ramipril Angiotensin-converting-enzyme (ACE) inhibitors, such as ramipril, angiotensin receptor blockers (ARBs), and long-acting cardio-selective beta-blockers improve survival in heart failure patients. In advanced cases (New York Heart Association (NYHA) class II - IV and with left-ventricular ejection fracture (LVEF) of 35% or less), aldosterone antagonists improve survival as well.

A 38-year-old female with human immunodeficiency virus (HIV) infection presents to her primary care doctor with concern for daily intermittent fevers to 38.6 C (101.5 F) for four weeks. She also has night sweats and some dyspnea, especially when hiking near her home in Louisville, Kentucky. She doesn't have any additional symptoms. She reports no recent dental work or travel. She has no pets. Her physical exam is unremarkable. Laboratory testing reveals a CD4 count of 220 cells/mcl, normal basic metabolic panel, and a complete blood count (CBC) remarkable for stable mild thrombocytopenia (125,000 mm3). Bacterial blood cultures demonstrate no growth after five days. Chest x-ray shows diffuse pulmonary infiltrates. Which of the following would be the most appropriate test to order for this patient? A. Echocardiogram B. Funduscopic examination C. Lymph node biopsy D. Serum cryptococcal antigen E. Serum histoplasma antigen

E. Serum histoplasma antigen The correct answer is E. This patient's fever and pulmonary infiltrates are due to histoplasmosis. Her CD4 count is above 100 cells, and her physical exam is unremarkable. She lives in the Ohio River Valley, where histoplasmosis is endemic. She has no risk factors or physical findings consistent with endocarditis, so doing an echocardiogram would not be appropriate at this time. Performing a lymph node biopsy without presence of lymphadenopathy, or before any imaging or less invasive testing, would not be appropriate at this point in the evaluation of fever. With a CD4 count > 100, she is less likely to have cryptococcus, particularly with normal mentation and lack of a headache. Cytomegalovirus (CMV) will often manifest with CMV retinitis, but with a CD4 count > 100, it is less likely.

A 55-year-old male presents with acute, severe, substernal chest pressure. He has a history of peptic ulcer disease. He drinks two beers daily and smokes a half-a-pack of cigarettes daily. He has multiple family members with inflammatory bowel disease. He works long hours outdoors in construction. Electrocardiogram (ECG) confirms an ST-elevation myocardial infarction (STEMI). Which of the following is a cardiac risk factor in this patient? A. Construction work B. Drinking two beers a day C. Having a family history of inflammatory bowel disease D. Having peptic ulcer disease E. Smoking half-a-pack of cigarettes a day

E. Smoking half-a-pack of cigarettes a day Chest pain history includes assessing for cardiac risk factors. Cardiac risk factors include smoking, hypertension, dyslipidemia, diabetes, other cerebrovascular disease, or family history of coronary artery disease (CAD). The patient's active job in construction could increase his risk for musculoskeletal cause of chest pain related to overuse or injury but would not be a cardiac risk factor. While excessive alcohol intake has been associated with an increased risk of cardiovascular disease, the majority of studies on low to moderate alcohol consumption (up to two alcohol-containing beverages per day for males) suggest that this may be beneficial or at least not harmful to the cardiovascular system. The patient's family history of inflammatory bowel disease and personal history of peptic ulcer disease may increase his risk for upper abdominal pain or chest pain from a gastrointestinal source, but these are not cardiac risk factors.

A 33-year-old previously healthy female is admitted to the hospital with pneumonia. Two weeks prior to admission, she developed fever and myalgias. She was diagnosed with influenza at an urgent care clinic. Five days ago, she developed a productive cough, fever, and chills. Today, her temperature is 38.9 C (102 F), pulse is 110 beats/minute, respiration rate is 22 breaths/minute, blood pressure is 90/68 mmHg, and pulse oximetry is 89% on room air. Respiratory exam reveals crackles at the lung bases bilaterally. White blood cell count is 3,400/mm3. The chest x-ray shows multilobular cavitating alveolar infiltrates. Which of the following organisms is the most likely cause of pneumonia in this patient? A. Adenovirus B. Legionella pneumophila C. Mycoplasma pneumoniae D. Pseudomonas aeruginosa E. Staphylococcus aureus

E. Staphylococcus aureus The most likely etiology would be Staphylococcus aureus, which can present in young, previously healthy patients as severe pneumonia after an influenza-like illness, and is characterized by severe respiratory symptoms, high fever, leukopenia, and hypotension, as in this patient. The chest x-ray often shows multilobular cavitating alveolar infiltrates. Adenovirus pneumonia would be less likely, as it is more commonly seen in infants and immunosuppressed patients. The patient does not have any risk factors for Legionella pneumonia such as diabetes mellitus, smoking, chronic obstructive pulmonary disease (COPD), or immunosuppression. Mycoplasma pneumonia usually presents with a more gradual, subacute course. Pseudomonas aeruginosa is an uncommon cause of pneumonia and is most often seen in immunosuppressed patients, ventilated patients, or patients with chronic lung disease.

A 33-year-old male with a history of human immunodeficiency virus (HIV) from sexual contact presents with one day of fever, cough productive of green sputum, and a left-lower-lobe infiltrate on chest radiograph. His CD4 count is 440 cells/mm3. What is the most-likely cause of his pneumonia? A. Adenovirus B. Methicillin-resistant Staphylococcus aureus C. Mycobacterium avium complex D. Pneumocystis jiroveci E. Streptococcus pneumoniae

E. Streptococcus pneumoniae The respiratory tract is the most-common site of invasive pneumococcal infection in HIV-infected persons. In a prospective multicenter study, bacterial pneumonia was more common than Pneumocystis pneumonia in HIV-infected persons. S. pneumoniae was the most-common pathogen isolated. Pneumococcal disease can occur at any time during the course of HIV-1 infection. (Ref: Wallace JM et al. PubMed ID: 8256894) Pneumocystis pneumonia is more common when the CD4 count drops below 200 cells/mm3, and Mycobacterium avium complex pneumonia when CD4 is <50 cells/mm3. Methicillin-resistant Staphylococcus aureus (MRSA) and adenovirus pneumonias can occur in HIV-infected persons, but are not the most common.

A 66-year-old female is evaluated in the emergency department with a two-day history of right-sided pleuritic chest pain and intermittent shortness of breath. Past medical history is significant for hypertension, chronic kidney disease, and depression. Medications include lisinopril, baby aspirin, and oral hormone replacement therapy. Physical examination shows her temperature is 37.8 C (100.1 F), pulse is 112 beats/minute, respiratory rate is 22 breaths/minute, blood pressure is 158/76 mmHg, body mass index (BMI) is 32 kg/m2 and oxygen saturation is 89% on room air. Her lungs are clear and heart sounds are normal. Her left leg is edematous and tender to palpation. An electrocardiogram (ECG) shows no ST or T wave changes. Chest x-ray is normal. Laboratory studies are unremarkable except for a creatinine of 2.1 mg/dL. Which of the following is the most appropriate diagnostic test at this time? A. Computed tomography (CT) of the chest B. D-dimer test C. Troponin T test D. Venous ultrasonography of left leg E. Ventilation perfusion (V/Q) scan

E. Ventilation perfusion (V/Q) scan This patient's symptoms of acute pleuritic chest pain and dyspnea, and her physical exam findings of tachycardia, low-grade fever, hypoxia, and left leg swelling are all consistent with the diagnosis of pulmonary embolism (PE). Obesity and hormone replacement therapy are additional risk factors for PE. A ventilation-perfusion scan can confirm the diagnosis of PE by showing an area of the lung that is normally ventilated but poorly perfused. Chest CT is an excellent test for diagnosis of PE. However, intravenous contrast administered during the test can worsen renal function and would be contraindicated in this patient with a creatinine of 2.1 mg/dL. D-dimer is a sensitive, but non-specific, test for PE. It is helpful in ruling out PE in a patient with low pretest probability of PE. This patient has a high pretest probability for PE with a simplified Wells score of 3 (1 point each for tachycardia; signs and symptoms of deep vein thrombosis; and alternative diagnosis being less likely than PE). A definitive diagnostic test such as a CT scan or a V/Q lung scan is recommended as the next-best step in patients with a high pretest probability of a PE (simplified Wells score >1). A troponin T level is helpful in detection of myocardial injury. If the patient has a PE on V/Q, then a troponin T would be helpful in determining if it is a submassive PE, which might benefit from thrombolytics. However, this patient is unlikely to be suffering from an acute coronary syndrome, based on the duration of symptoms, pleuritic nature of her chest pain, and lack of ECG changes, so it is not necessary as a first test to diagnose PE. Venous ultrasonography of the left leg could confirm the diagnosis of deep-vein thrombosis and could be considered if results of the V/Q scan return indeterminate or if V/Q scan is not available. However, a V/Q scan is a better test to make a diagnosis of PE in this patient with chest pain and shortness of breath.

You admit a 65-year-old male with a severe chronic obstructive pulmonary disease (COPD) exacerbation. He has a 40-pack-per-year smoking history, and quit five years ago. He has not followed up with primary care appointments in the past, so you take the opportunity to ensure he is up-to-date with preventive measures. Which of the following preventive measures should be addressed at this time? A. Dual energy x-ray absorptiometry (DEXA) scan B. Haemophilus influenzae type b (Hib) vaccination C. Hepatitis A vaccination D. Sputum cytology E. Streptococcus pneumoniae vaccination

The U.S. Centers for Disease Control and Prevention (CDC) guidelines for adults with lung disease including chronic obstructive pulmonary disease (COPD) and asthma recommend vaccinations for Streptococcus pneumoniae. Hib and hepatitis A vaccines are not recommended in this population. In addition, an abdominal ultrasound should be performed to screen for aortic aneurysm in men aged 65 to 75 years old who have ever smoked. Screening DEXA scans are recommended for women aged 65 years old or older, but not men. Sputum cytology is used to diagnose malignancy when cancer is suspected, but is not a useful preventive measure. However, given his >30 pack-per-year smoking history, with <15 years since quitting, and age within the 55-year-old to 80-year-old range, he would be a candidate for low-dose chest CT screening for lung cancer.