A42-year-old man without prior significant medical history comes to your office for evaluation of chronic diarrhea of 12 months duration, although the patient states he has had loose stools for many years. During this time he has lost 25 lbs. The diarrhea is large volume, occasionally greasy, and nonbloody. In addition, the patient has mild abdominal pain for much of the day. He has been smoking a pack of cigarettes a day for 20 years and drinks approximately five beers per day. His physical examination reveals a thin male with temporal wasting and generalized muscle loss. He has glossitis and angular cheilosis. He has excoriations on his elbows and knees and scattered papulovesicular lesions in these regions as well. Which of the following is the most likely diagnosis for this patient?
A. chronic pancreatitis
B. Crohn's disease
C. celiac sprue
D. Whipple disease
E. ulcerative colitis
Correct Answer: C Section: (none)
Explanation:
The patient has chronic diarrhea superimposed on a long history of loose stools, steatorrhea, and significant weight loss. While these features could be seen in several diseases, the presence of the pruritic vesiculopapular lesions on his extensor surfaces makes the diagnosis highly likely to be celiac sprue, with its frequently accompanying skin manifestation dermatitis herpetiformis. Crohn's disease is not usually associated with steatorrhea, and ulcerative colitis is often associated with bloody stools. Chronic pancreatitis and Whipple disease could cause a similar clinical picture but would not have the associated skin findings. A small bowel biopsy would confirm histopathologic features consistent with celiac sprue, such as villous atrophy and crypt hyperplasia. A small bowel biopsy could also diagnose or rule out Whipple disease by looking for the pathognomonic PAS (periodic acid-Schiff) positive organism Tropheryma whippelii. Colonic biopsies would be unhelpful in celiac sprue. A fecal fat quantification would likely confirm and assess the degree of steatorrhea, but would offer little other diagnostic information. A small bowel x-ray is too nonspecific to confirm the diagnosis and an abdominal CT scan would likely be normal unless the patient had developed a complication of advanced sprue, such as intestinal lymphoma. Patients with celiac sprue are at increased risk for malignancies of the small bowel with adenocarcinoma and lymphoma being the two most commonly encountered. Patients with celiac sprue are not at greatly increased risk of the other malignancies listed. Limited data suggest that strict adherence to a glutenfree diet may decrease the incidence of malignancy in these patients.
Question 22:
A 72-year-old male with type II diabetes, hypertension, and a history of recurrent pneumonia is admitted to
the Medical intensive care unit (ICU) with a diagnosis of septic shock. His vital signs are:
BP 80/60 mmHg, RR 24 breaths per minute, pulse 120 beats per minute (bpm), temp. 102.4°F, O2
saturation 99% on room air. Of the choices listed below, what would be your initial management?
A. start IV dopamine
B. start empiric IV broad-spectrum antibiotics
C. bolus IV fluids
D. intubate and start ventilator support
E. start IV norepinephrine
Correct Answer: C Section: (none)
Explanation:
Septic shock results from inflammatory effects secondary to infection that ultimately leads to hemodynamic decompensation. The treatment encompasses three primary goals. The initial priority is to maintain a reasonable mean arterial pressure and cardiac output to keep the patient alive. Then the nidus of infection must be treated and the pathogenic sequence leading to septic shock should be interrupted. While these latter goals are being pursued, adequate organ system perfusion and function must be maintained, guided by cardiovascular monitoring. Large fluid deficits exist in patients with septic shock. Up to 610 L of crystalloid solutions or 24 L of colloid solutions may be required for initial resuscitation in the first 24 hours. Volume repletion in patients with septic shock produces significant improvement in cardiac function and systemic oxygen delivery, thereby enhancing tissue perfusion and reversing anaerobic metabolism. Cardiac index will usually improve by 2540% during fluid resuscitation. In approximately 50% of septic patients who initially present with hypotension, fluids alone will reverse hypotension and restore hemodynamic stability. Fluid resuscitation with isotonic crystalloids, such as normal saline or lactated Ringers solution, should be the initial therapy in shock. When fluid resuscitation fails to maintain adequate arterial pressure and organ perfusion, vasopressor therapy should be initiated. In this patient, the initial therapy should be fluid resuscitation. If fluid resuscitation fails, then vasopressor therapy should be initiated with dopamine. If this alone fails, then adding another vasopressor/inotropic agent, such as norepinephrine, may be warranted.
Although patients with septic shock should receive broad antibiotic coverage after being pan-cultured, this should not precede fluid resuscitation. As this patient is able to breathe independently while maintaining good O2 saturation, intubation may be held off for now. If the patient starts to deteriorate (increased respiratory rate, low O2 saturation, poor excursion, hypercapnia, hypoxia), intubation could be considered.
Question 23:
A 35-year-old woman with a history of major depressive disorder is brought into the ED by her boyfriend. He believes she may have overdosed on pain medication in an effort to hurt herself. He gives you three medication bottles which he discovered empty and states that they were nearly full before leaving for work earlier that morning. However, the timing of the ingestion is unclear. All three of the bottles apparently held acetaminophen-containing medications. Examination of the patient reveals a tired-appearing woman complaining of nausea and right upper quadrant abdominal pain. Which of the following is the worst prognostic indicator if present in this patient?
A. arterial pH greater than 7.3
B. arterial lactate greater than 3.5 mmol/L
C. initiation of therapy 8 hours after acetaminophen ingestion
D. "probable-risk" of hepatotoxicity by the Rumack-Matthew nomogram
E. a history of chronic acetaminophen abuse
Correct Answer: B Section: (none)
Explanation:
When acetaminophen is taken in normal doses, it is conjugated in the liver to harmless glucuronide and
sulfate metabolites. These metabolic pathways become easily overwhelmed in the setting of a large
overdose, however. If this occurs, the cytochrome P450 system directs conversion of the excess
acetaminophen to a compound called NAPQI, which is conjugated with glutathione to form a nontoxic
mercapturate metabolite. Once glutathione stores are exhausted in the liver, however, the excess NAPQI
combines with proteins within hepatic cells causing hepatic cell death. Taurine is a mercaptan-containing
amino acid involved in bile acid biochemistry. Citrulline aids in the detoxification and elimination of
ammonia. Ornithine plays an important role in the urea cycle.
N-acetylcysteine should be administered as promptly as possible for treatment of acetaminophen
overdose. It works by helping restore hepatic glutathione stores and by providing sulfhydryl groups that bind
toxic metabolites. N-acetylcysteine is administered orally in the form of an initial loading dose (140 mg/kg)
followed by 17 doses (70 mg/kg each) given every 4 hours. In addition to this oral therapy, the Food and
Drug Administration (FDA) approved 21-hour and 48-hour long intravenous treatment regimens in 2004.
Left untreated, acetaminophen overdose carries a significant risk for hepatic failure and subsequent death
depending on the amount of acetaminophen ingested, the presence of any preexisting liver disease, and
interactions with any other medications that induce cytochrome P450 enzyme activity. Naloxone,
flumazenil, and physostigmine are given as antidotes for toxicity related to opioid analgesics,
benzodiazepines, and muscarinic receptor blockers, respectively.
Poor prognosis is associated with elevated serum lactate levels (above 3.5 mmol/L), acidemia (arterial pH
less than 7.3), renal failure, and coagulopathy. The Rumack-Matthew nomogram provides a means of
determining whether an individual falls into the possible-, probable-, or high-risk categories for developing
hepatotoxicity based on serum acetaminophen levels and the number of hours since ingestion. Therapy
with N-acetylcysteine is most effective if begun within 8 hours of the toxic ingestion but still has proven
benefit if started within 24 hours
Question 24:
A 35-year-old woman with a history of major depressive disorder is brought into the ED by her boyfriend. He believes she may have overdosed on pain medication in an effort to hurt herself. He gives you three medication bottles which he discovered empty and states that they were nearly full before leaving for work earlier that morning. However, the timing of the ingestion is unclear. All three of the bottles apparently held acetaminophen-containing medications. Examination of the patient reveals a tired-appearing woman complaining of nausea and right upper quadrant abdominal pain. Which of the following pharmacologic treatments is most appropriate at this time?
A. no pharmacologic treatment is necessary
B. naloxone
C. flumazenil
D. physostigmine
E. N-acetylcysteine
Correct Answer: E Section: (none)
Explanation:
When acetaminophen is taken in normal doses, it is conjugated in the liver to harmless glucuronide and sulfate metabolites. These metabolic pathways become easily overwhelmed in the setting of a large overdose, however. If this occurs, the cytochrome P450 system directs conversion of the excess acetaminophen to a compound called NAPQI, which is conjugated with glutathione to form a nontoxic mercapturate metabolite. Once glutathione stores are exhausted in the liver, however, the excess NAPQI combines with proteins within hepatic cells causing hepatic cell death. Taurine is a mercaptan-containing amino acid involved in bile acid biochemistry. Citrulline aids in the detoxification and elimination of ammonia. Ornithine plays an important role in the urea cycle.
N-acetylcysteine should be administered as promptly as possible for treatment of acetaminophen overdose. It works by helping restore hepatic glutathione stores and by providing sulfhydryl groups that bind toxic metabolites. N-acetylcysteine is administered orally in the form of an initial loading dose (140 mg/kg) followed by 17 doses (70 mg/kg each) given every 4 hours. In addition to this oral therapy, the Food and Drug Administration (FDA) approved 21-hour and 48-hour long intravenous treatment regimens in 2004. Left untreated, acetaminophen overdose carries a significant risk for hepatic failure and subsequent death depending on the amount of acetaminophen ingested, the presence of any preexisting liver disease, and interactions with any other medications that induce cytochrome P450 enzyme activity. Naloxone, flumazenil, and physostigmine are given as antidotes for toxicity related to opioid analgesics, benzodiazepines, and muscarinic receptor blockers, respectively.
Poor prognosis is associated with elevated serum lactate levels (above 3.5 mmol/L), acidemia (arterial pH less than 7.3), renal failure, and coagulopathy. The Rumack-Matthew nomogram provides a means of determining whether an individual falls into the possible-, probable-, or high-risk categories for developing hepatotoxicity based on serum acetaminophen levels and the number of hours since ingestion. Therapy with N-acetylcysteine is most effective if begun within 8 hours of the toxic ingestion but still has proven benefit if started within 24 hours
Question 25:
A 35-year-old woman with a history of major depressive disorder is brought into the ED by her boyfriend. He believes she may have overdosed on pain medication in an effort to hurt herself. He gives you three medication bottles which he discovered empty and states that they were nearly full before leaving for work earlier that morning. However, the timing of the ingestion is unclear. All three of the bottles apparently held acetaminophen-containing medications. Examination of the patient reveals a tired-appearing woman complaining of nausea and right upper quadrant abdominal pain. Depletion of which of the following is primarily responsible for the hepatotoxicity being experienced by the patient?
A. N-acetyl-p-benzoquinone-imine (NAPQI)
B. taurine
C. citrulline
D. glutathione
E. ornithine
Correct Answer: D Section: (none)
Explanation:
When acetaminophen is taken in normal doses, it is conjugated in the liver to harmless glucuronide and
sulfate metabolites. These metabolic pathways become easily overwhelmed in the setting of a large
overdose, however. If this occurs, the cytochrome P450 system directs conversion of the excess
acetaminophen to a compound called NAPQI, which is conjugated with glutathione to form a nontoxic
mercapturate metabolite. Once glutathione stores are exhausted in the liver, however, the excess NAPQI
combines with proteins within hepatic cells causing hepatic cell death. Taurine is a mercaptan-containing
amino acid involved in bile acid biochemistry. Citrulline aids in the detoxification and elimination of
ammonia. Ornithine plays an important role in the urea cycle.
N-acetylcysteine should be administered as promptly as possible for treatment of acetaminophen
overdose. It works by helping restore hepatic glutathione stores and by providing sulfhydryl groups that bind
toxic metabolites. N-acetylcysteine is administered orally in the form of an initial loading dose (140 mg/kg)
followed by 17 doses (70 mg/kg each) given every 4 hours. In addition to this oral therapy, the Food and
Drug Administration (FDA) approved 21-hour and 48-hour long intravenous treatment regimens in 2004.
Left untreated, acetaminophen overdose carries a significant risk for hepatic failure and subsequent death
depending on the amount of acetaminophen ingested, the presence of any preexisting liver disease, and
interactions with any other medications that induce cytochrome P450 enzyme activity. Naloxone,
flumazenil, and physostigmine are given as antidotes for toxicity related to opioid analgesics,
benzodiazepines, and muscarinic receptor blockers, respectively.
Poor prognosis is associated with elevated serum lactate levels (above 3.5 mmol/L), acidemia (arterial pH
less than 7.3), renal failure, and coagulopathy. The Rumack-Matthew nomogram provides a means of
determining whether an individual falls into the possible-, probable-, or high-risk categories for developing
hepatotoxicity based on serum acetaminophen levels and the number of hours since ingestion. Therapy
with N-acetylcysteine is most effective if begun within 8 hours of the toxic ingestion but still has proven
benefit if started within 24 hours.
Question 26:
Your patient who was recently prescribed an antibiotic returns to your clinic for a follow-up visit. Although she was feeling better, the instructions on the bottle were to take the medication for total of 10 days. She wants to know if she still has to take the medication three times daily as she has improved. You explain to her that the dosing regimen is based on the biological half-life of a drug, which is generally related to which of the following?
A. the time for a drug to be absorbed into the blood
B. the time for a drug to take effect following administration
C. the time for the body burden of a drug to be reduced by 50%
D. the serum concentration of a drug that is 50% of the toxic level
E. a value that is half the duration of action of a drug
Correct Answer: C Section: (none)
Explanation:
The biological half-life of a drug is the time required for 50% of the dose to be eliminated. This value is useful in determining the duration of a drug's effect and therefore proper drug dose regimes.
Question 27:
A 48-year-old female with a history of mild congestive heart failure (CHF) treated with furosemide presents to the emergency room (ER) for evaluation of 24 hours of epigastric pain, nausea, and vomiting after eating a large meal in a restaurant. Previously, the patient had experienced intermittent right upper quadrant pain after eating. On examination, the patient has a temperature of 98.5°F and a pulse of 100. Her examinat ion is remarkable for epigastric tenderness to palpation, normal bowel sounds, and no rebound tenderness or guarding. Laboratory studies are as follows:
The patient is made NPO (nothing by mouth) and vigorously hydrated. After 3 days, the amylase and lipase normalize, but the bilirubin rises to 4.2 mg/dL. An endoscopic retrograde cholangiopancreatography (ERCP) is performed, and the following cholangiogram is obtained. What is the best treatment option at this time?
A. papillary dilation and stone extraction
B. papillotomy (aka sphincterotomy) and stone extraction
C. placement of a transpapillary stent in the biliary tree
D. placement of a transpapillary stent in the pancreatic duct
E. no further manipulations are required
Correct Answer: B Section: (none)
Explanation:
The patient has clinical and biochemical evidence of gallstone pancreatitis including epigastric pain, a history suggestive of prior biliary colic, elevated transaminases and bilirubin (suggestive of an obstructing common bile duct stone), and an elevated amylase and lipase. Gastroenteritis would not be expected to alter liver chemistries. Drug-induced pancreatitis is possible as furosemide has been shown to cause pancreatitis, but would not result in the abnormal liver chemistries. Acute cholecystitis and cholangitis would likely be associated with an elevated leukocyte count, right upper quadrant abdominal pain, and fever. An abdominal ultrasound could assess the gallbladder for the presence of stones and signs of cholecystitis, such as gallbladder wall thickening or pericholecystic fluid. It could also look for a dilated biliary tree or an obstructing stone in the common bile duct. An abdominal x-ray could reveal a localized ileus ("sentinel loop") or calcifications suggestive of chronic pancreatitis, but would be of significantly lesser yield. A CT or MRI of the abdomen would provide images of the pancreas and liver, but are often clinically unhelpful early in the course of acute pancreatitis. An ERCP is not indicated at this point, as only one set of liver chemistries is available. Should the bilirubin rise or fail to fall, an ERCP might be warranted to decompress the biliary tree. The patient has a common bile duct stone causing biliary obstruction. This stone likely caused the patient's acute pancreatitis as well. Papillotomy (also known as sphincterotomy) will allow endoscopic removal of the stone. The stone cannot be removed through the native papilla, as the sphincter of Oddi musculature would not allow such a large stone to pass. Thus, sphincterotomy must be performed to disrupt the sphincter musculature. Papillary balloon dilation is possible but is associated with an increased risk of pancreatitis. Abiliary stent is a viable option to provide drainage, but is inferior to sphincterotomy and stone extraction. No manipulation of the pancreatic duct is warranted. The stone should not be left in place as it could lead to recurrent pancreatitis or cholangitis.
Question 28:
A 48-year-old female with a history of mild congestive heart failure (CHF) treated with furosemide presents to the emergency room (ER) for evaluation of 24 hours of epigastric pain, nausea, and vomiting after eating a large meal in a restaurant. Previously, the patient had experienced intermittent right upper quadrant pain after eating. On examination, the patient has a temperature of 98.5°F and a pulse of 100. Her examinat ion is remarkable for epigastric tenderness to palpation, normal bowel sounds, and no rebound tenderness or guarding. Laboratory studies are as follows:
What would the most appropriate next test to order be?
A. abdominal x-ray
B. abdominal computed tomographic (CT) scan
C. abdominal ultrasound
D. magnetic resonance imaging (MRI) of the abdomen
E. stool cultures and assessment for ova and parasites
Correct Answer: C Section: (none)
Explanation:
The patient has clinical and biochemical evidence of gallstone pancreatitis including epigastric pain, a history suggestive of prior biliary colic, elevated transaminases and bilirubin (suggestive of an obstructing common bile duct stone), and an elevated amylase and lipase. Gastroenteritis would not be expected to alter liver chemistries. Drug-induced pancreatitis is possible as furosemide has been shown to cause pancreatitis, but would not result in the abnormal liver chemistries. Acute cholecystitis and cholangitis would likely be associated with an elevated leukocyte count, right upper quadrant abdominal pain, and fever. An abdominal ultrasound could assess the gallbladder for the presence of stones and signs of cholecystitis, such as gallbladder wall thickening or pericholecystic fluid. It could also look for a dilated biliary tree or an obstructing stone in the common bile duct. An abdominal x-ray could reveal a localized ileus ("sentinel loop") or calcifications suggestive of chronic pancreatitis, but would be of significantly lesser yield. A CT or MRI of the abdomen would provide images of the pancreas and liver, but are often clinically unhelpful early in the course of acute pancreatitis. An ERCP is not indicated at this point, as only one set of liver chemistries is available. Should the bilirubin rise or fail to fall, an ERCP might be warranted to decompress the biliary tree. The patient has a common bile duct stone causing biliary obstruction. This stone likely caused the patient's acute pancreatitis as well. Papillotomy (also known as sphincterotomy) will allow endoscopic removal of the stone. The stone cannot be removed through the native papilla, as the sphincter of Oddi musculature would not allow such a large stone to pass.
Thus, sphincterotomy must be performed to disrupt the sphincter musculature. Papillary balloon dilation is possible but is associated with an increased risk of pancreatitis. Abiliary stent is a viable option to provide drainage, but is inferior to sphincterotomy and stone extraction. No manipulation of the pancreatic duct is warranted. The stone should not be left in place as it could lead to recurrent pancreatitis or cholangitis.
Question 29:
A 48-year-old female with a history of mild congestive heart failure (CHF) treated with furosemide presents to the emergency room (ER) for evaluation of 24 hours of epigastric pain, nausea, and vomiting after eating a large meal in a restaurant. Previously, the patient had experienced intermittent right upper quadrant pain after eating. On examination, the patient has a temperature of 98.5°F and a pulse of 100. Her examinat ion is remarkable for epigastric tenderness to palpation, normal bowel sounds, and no rebound tenderness or guarding. Laboratory studies are as follows:
Which of the following is the most likely diagnosis?
A. acute gastroenteritis
B. acute gallstone pancreatitis
C. drug-induced pancreatitis
D. acute cholecystitis
E. acute cholangitis
Correct Answer: B Section: (none)
Explanation: The patient has clinical and biochemical evidence of gallstone pancreatitis including epigastric pain, a history suggestive of prior biliary colic, elevated transaminases and bilirubin (suggestive of an obstructing common bile duct stone), and an elevated amylase and lipase. Gastroenteritis would not be expected to alter liver chemistries. Drug-induced pancreatitis is possible as furosemide has been shown to cause pancreatitis, but would not result in the abnormal liver chemistries. Acute cholecystitis and cholangitis would likely be associated with an elevated leukocyte count, right upper quadrant abdominal pain, and fever. An abdominal ultrasound could assess the gallbladder for the presence of stones and signs of cholecystitis, such as gallbladder wall thickening or pericholecystic fluid. It could also look for a dilated biliary tree or an obstructing stone in the common bile duct. An abdominal x-ray could reveal a localized ileus ("sentinel loop") or calcifications suggestive of chronic pancreatitis, but would be of significantly lesser yield. A CT or MRI of the abdomen would provide images of the pancreas and liver, but are often clinically unhelpful early in the course of acute pancreatitis. An ERCP is not indicated at this point, as only one set of liver chemistries is available. Should the bilirubin rise or fail to fall, an ERCP might be warranted to decompress the biliary tree. The patient has a common bile duct stone causing biliary obstruction. This stone likely caused the patient's acute pancreatitis as well. Papillotomy (also known as sphincterotomy) will allow endoscopic removal of the stone. The stone cannot be removed through the native papilla, as the sphincter of Oddi musculature would not allow such a large stone to pass. Thus, sphincterotomy must be performed to disrupt the sphincter musculature. Papillary balloon dilation is possible but is associated with an increased risk of pancreatitis. Abiliary stent is a viable option to provide drainage, but is inferior to sphincterotomy and stone extraction. No manipulation of the pancreatic duct is warranted. The stone should not be left in place as it could lead to recurrent pancreatitis or cholangitis.
Question 30:
A 67-year-old male with a history of type II diabetes and hypertension is hospitalized with complaints of retrosternal chest pain that radiates to the left arm and jaw. In the ED, an electrocardiogram (ECG) showed S-T segment depressions in the inferior and lateral leads. He has been given the diagnosis of acute coronary syndrome and admitted to the coronary care unit for further evaluation and treatment. Admission laboratory values reveal a total cholesterol of 270, a lowdensity lipoprotein (LDL) of 190, and a high-density lipoprotein (HDL) of 28. He is currently smoking a pack of cigarettes per day and lives a sedentary life. He is clearly overweight and his blood pressure, despite medication, remains elevated at 150/88. His last HgbA1C less than a month ago was 9.8%.
In addition to diet, exercise, and smoking cessation, which of the following would have the largest impact in reducing his cholesterol?
A. controlling his blood pressure
B. increasing his consumption of alcoholic beverages to three to four glasses of wine per day
C. improving his sleeping habits
D. adding thyroid hormone to his medications
E. controlling his diabetes
Correct Answer: E Section: (none)
Explanation:
The history of acute coronary syndrome and diabetes places this patient at high risk for cardiovascular complications (MI or stroke). His diabetes, as well as all other risk factors, must be better controlled in order to decrease this risk. Statins (HMG-CoA reductase inhibitors) have been shown to lower cardiovascular morbidity and mortality in the primary and secondary prevention of cardiovascular complications. While niacin would indeed likely raise his HDL, data are still insufficient to recommend this as the main goal in reduction of cardiovascular events in patients with known CAD. The main goal at this point should be to lower LDL levels and total cholesterol to at least the recommended levels for patients at the highest risk for cardiovascular complication, with an emphasis on lowering the LDL to <100 mg/dL and total cholesterol to <200 mg/dL. Although both hypothyroidism and diabetes are well-known causes of secondary hyperlipidemia, the case makes no mention of depressed thyroid function in this patient. It would be unreasonable to start hormone supplementation without evidence of hypothyroid state. Although beneficial in cardiovascular disease and stroke, controlling blood pressure has no known direct effect on lipid profile. Controlling diabetes would therefore be the only choice that would directly contribute to positively affecting his lipid profile, by lowering LDL and TG levels and, therefore, decreasing total cholesterol. Sleeping, although healthy and beneficial to general well being, has no direct effect on lipid metabolism.
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