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Terms in this set (351)

lead pipe appearance on barium enema
Lead pipe colon is the appearance on barium enema of a foreshortened, narrow colon with loss of redundancy and haustral markings. This sign is specific for ulcerative colitis (UC), an inflammatory disease of the rectum and colon. The peak incidence of UC is around 25 to 45 years. P-ANCA antibodies are associated with UC. Iron deficiency can lead to microcytic anemia. Common extra intestinal manifestations of UC are erythema nodosum (described as erythematous plaques and nodules on pretibial areas), arthritis, pyoderma gangrenosum, uveitis, episcleritis, and sclerosing cholangitis.

Toxic megacolon is a complication of UC characterized by the dilation of the colon; there is a risk of perforation. There is an increased incidence of colon cancer (10%) after 10 years of this disease. The inflammation involves the mucosal tissues only, which are friable and show ulcerations on colonoscopy. There is also a characteristic continuous involvement and pseudopolyp appearance caused by mucosal regeneration. Sulfapyridine, mesalamine, corticosteroids, 6-mercaptopurine, and azathioprine are used for treatment. Colectomy is curative and is indicated for intractable disease, or in the case of dysplasia.

An apple core appearance on barium enema is seen in patients with colon cancer. This sign refers to the shouldered margins of the stricture caused by the neoplasmic invasion.

A cobblestone appearance and string sign are characteristic for Crohn's disease, another inflammatory disease of the digestive tract. The cobblestone appearance refers to the discontinuous areas of inflammation separated by healthy bowel. String sign, seen in the small bowel series, is the appearance caused by stricture areas.

Thumb printing is a radiological sign seen in ischemic colitis, a disease most likely found in elderly patients with left lower abdominal pain and gross rectal bleeding.
lead pipe appearance on barium enema
Lead pipe colon is the appearance on barium enema of a foreshortened, narrow colon with loss of redundancy and haustral markings. This sign is specific for ulcerative colitis (UC), an inflammatory disease of the rectum and colon. The peak incidence of UC is around 25 to 45 years. P-ANCA antibodies are associated with UC. Iron deficiency can lead to microcytic anemia. Common extra intestinal manifestations of UC are erythema nodosum (described as erythematous plaques and nodules on pretibial areas), arthritis, pyoderma gangrenosum, uveitis, episcleritis, and sclerosing cholangitis.

Toxic megacolon is a complication of UC characterized by the dilation of the colon; there is a risk of perforation. There is an increased incidence of colon cancer (10%) after 10 years of this disease. The inflammation involves the mucosal tissues only, which are friable and show ulcerations on colonoscopy. There is also a characteristic continuous involvement and pseudopolyp appearance caused by mucosal regeneration. Sulfapyridine, mesalamine, corticosteroids, 6-mercaptopurine, and azathioprine are used for treatment. Colectomy is curative and is indicated for intractable disease, or in the case of dysplasia.

An apple core appearance on barium enema is seen in patients with colon cancer. This sign refers to the shouldered margins of the stricture caused by the neoplasmic invasion.

A cobblestone appearance and string sign are characteristic for Crohn's disease, another inflammatory disease of the digestive tract. The cobblestone appearance refers to the discontinuous areas of inflammation separated by healthy bowel. String sign, seen in the small bowel series, is the appearance caused by stricture areas.

Thumb printing is a radiological sign seen in ischemic colitis, a disease most likely found in elderly patients with left lower abdominal pain and gross rectal bleeding.
lead pipe appearance on barium enema
Lead pipe colon is the appearance on barium enema of a foreshortened, narrow colon with loss of redundancy and haustral markings. This sign is specific for ulcerative colitis (UC), an inflammatory disease of the rectum and colon. The peak incidence of UC is around 25 to 45 years. P-ANCA antibodies are associated with UC. Iron deficiency can lead to microcytic anemia. Common extra intestinal manifestations of UC are erythema nodosum (described as erythematous plaques and nodules on pretibial areas), arthritis, pyoderma gangrenosum, uveitis, episcleritis, and sclerosing cholangitis.

Toxic megacolon is a complication of UC characterized by the dilation of the colon; there is a risk of perforation. There is an increased incidence of colon cancer (10%) after 10 years of this disease. The inflammation involves the mucosal tissues only, which are friable and show ulcerations on colonoscopy. There is also a characteristic continuous involvement and pseudopolyp appearance caused by mucosal regeneration. Sulfapyridine, mesalamine, corticosteroids, 6-mercaptopurine, and azathioprine are used for treatment. Colectomy is curative and is indicated for intractable disease, or in the case of dysplasia.

An apple core appearance on barium enema is seen in patients with colon cancer. This sign refers to the shouldered margins of the stricture caused by the neoplasmic invasion.

A cobblestone appearance and string sign are characteristic for Crohn's disease, another inflammatory disease of the digestive tract. The cobblestone appearance refers to the discontinuous areas of inflammation separated by healthy bowel. String sign, seen in the small bowel series, is the appearance caused by stricture areas.

Thumb printing is a radiological sign seen in ischemic colitis, a disease most likely found in elderly patients with left lower abdominal pain and gross rectal bleeding.
Gilbert's disease
Your patient most probably has Gilbert's syndrome (GS), also known as Gilbert-Meulengracht syndrome. It is a relatively common genetic disease found in up to 5% - 10% of the population and generally does not need special treatment. Inherited non-haemolytic hyperbilirubinemic conditions include Dubin-Johnson, Rotor, and GB syndromes, and all are important differential diagnoses indicating benign disease that requires no immediate treatment. GB can be diagnosed by clinical presentation, biochemistry, and genotyping, and is significant because of the presence of the disposition towards drug-associated toxicity. A major characteristic is jaundice, caused by elevated levels of unconjugated bilirubin in the bloodstream. The cause of this hyperbilirubinemia is the reduced activity of the enzyme glucuronyltransferase, which conjugates both bilirubin and some lipophilic molecules, including drugs.

Intravascular hemolysis, with resulting hemoglobinemia, hemoglobinuria, and bilirubinemia, will show fragments of the red blood cells ("schistocytes") and sometimes spherocytes in peripheral blood smear, reticulocytosis, elevated unconjugated bilirubin that may lead to jaundice, elevated lactate dehydrogenase (LDH) in the blood, and decreased haptoglobin levels. If the direct Coombs test is positive, hemolysis is caused by an immune process. Hemosiderin in the urine indicates chronic intravascular hemolysis. There is also urobilinogen in the urine.

Viral hepatitis with jaundice will have elevated liver function tests (AST and ALT elevated out of proportion to alkaline phosphatase, usually with hyperbilirubinemia), and viral serologic testing will be positive.

Crigler-Najjar syndrome is a rare inherited form of non-hemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infancy.

Budd-Chiari syndrome is caused by occlusion of the hepatic veins. It presents with the classical triad of abdominal pain, ascites, and hepatomegaly. The syndrome can be fulminant, acute, chronic, or asymptomatic.
The correct response is fecal occult blood testing.

The pattern of low mean corpuscular volume and hemoglobin concentration, low ferritin, and elevated total iron-binding capacity (TIBC) is diagnostic of iron deficiency. Lack of iron inhibits hemoglobin synthesis, thereby reducing the volume and hemoglobin concentration of erythrocytes. Some patients have thrombocytosis. The mechanism is unclear, but hypotheses include stimulation by high circulating erythropoietin concentrations or circulating cytokines. Besides asthenia and pallor, other symptoms include pagophagia (craving ice or cold foods), pica (clay eating), and leg cramps; physical examination may reveal esophageal webbing, koilonychia (spoon-shaped nails), glossitis, angular stomatitis, and gastric atrophy.

New-onset anemia with hypochromia and microcytosis in an adult should be considered secondary to gastrointestinal bleeding until proved otherwise. The most common etiologies are diverticular disease, angiodysplasia, colitis (including from NSAIDs), and colon cancer, particularly left-sided colon cancer. Testing for occult blood in a stool specimen is the initial diagnostic method of choice. If the fecal occult blood test is positive, the patient should undergo upper endoscopy and colonoscopy examinations.

Colonoscopy is a useful exam for identifying sources of occult gastrointestinal bleeding. It is more sensitive than barium enema or CT scans for early lesions and permits biopsy when indicated (e.g., lesions suspicious for malignancy or colitis). However, none of these are cost-effective screening examinations.

Bone marrow biopsy can evaluate bone marrow iron stores and reveal erythroid hyperplasia. However, it has been practically abandoned in the workup of iron-deficiency anemia, as there is considerable interobserver variability and assays for iron, ferritin, and TIBC permit evaluation of the body's iron stores less invasively.

Capsule endoscopy is the most sensitive method for diagnosing small-bowel bleeding. However, small-bowel bleeding is much less common than upper (proximal to the angle of Treitz) or colonic bleeding. Therefore, it should only be undertaken after colonoscopy and upper endoscopy are negative.
The patient in this scenario is experiencing signs and symptoms from an anorectal fistula. Anorectal fistulas are commonly a chronic manifestation of an acute perirectal process that eventually comes from an anorectal abscess. Many fistulas originate from an infected anal crypt gland. Patients with anorectal fistulas usually will present with a "non-healing" area (an anorectal abscess that is draining) or may describe chronic purulent drainage and a pustule-like lesion on the perianal or buttock area. They will only have intermittent pruritus or rectal pain; pain is increased during defecation, sitting, or standing. Physical examination reveals excoriated and inflamed perianal skin. An external opening of the fistula may be visualized. If no opening is seen, palpation will reveal induration just below the skin.

Anal fissure is not the most likely diagnosis in this case scenario. Anal fissures most often affect infants as well as middle-aged individuals. The majority of fissures are considered primary and caused by local trauma such as passage of hard stool, prolonged diarrhea, vaginal delivery, or anal sex. Presentation of anal fissures is a tearing pain accompanying bowel movements as well as bright red rectal bleeding that is limited to a small amount noted on the toilet paper or surface of the stool. The patient described all of these components. Patients will also complain of perianal pruritus or irritation, which he also admits to experiencing.

Patients with Crohn's disease often have extremely variable signs and symptoms and possibly will have these for many years prior to diagnosis. Fatigue, prolonged diarrhea and abdominal pain, weight loss, and fever with or without gross bleeding are considered hallmarks of Crohn's disease.

Signs and symptoms of anal carcinoma include rectal bleeding (occurring in 45% of patients), anorectal pain or sensation of a rectal mass (30%), or even no issues (20%). Very often issues are confused with hemorrhoids and therefore patients may delay evaluation. Over 80% of patients developing anal cancer have detected human papilloma virus.

Internal hemorrhoids create principle issues of bleeding, prolapse, and mucoid discharge.Bleeding may range from bright red blood that is seen as streaks on the toilet paper to actual dripping of it into the toilet bowl after a bowel movement. Over time, hemorrhoids potentially will develop into a prolapsed state achieve a point in time when patients will note a sense of fullness or discomfort along with mucoid drainage that results in further irritation and soiling of underclothes.
PPI (proton pump inhibitor), amoxicillin, and clarithromycin twice daily for 2 weeks
There are several regimens recommended for H. pylori infection, which is an important cause of peptic ulcer disease and should be treated if found associated with symptoms. The choice of the regimen depends on considerations such as cost, side effects, and ease of administration. Allergy to one of the medications, as well as intolerance, should also be taken into account. Any proton pump inhibitor (PPI) with amoxicillin 1000 mg twice daily and clarithromycin 500 mg twice daily for 2 weeks or PPI with metronidazole 500mg twice daily and clarithromycin 500mg twice daily for 2 weeks are recommended. These are the triple drug therapies available. The other regimens suggested are bismuth, metronidazole, and tetracycline 4 times daily for 2 weeks along with PPI twice daily for 2 weeks or H2 receptor antagonist twice daily for 4 weeks (quadruple drug therapy). Dual therapy with a proton pump inhibitor and an antibiotic (amoxicillin or clarithromycin) is not recommended as primary therapy, since eradication rates are much lower than the above regimens. The most common side effect is a metallic taste in the mouth due to clarithromycin or metronidazole. Amoxicillin can cause diarrhea or a rash. Clarithromycin can also cause nausea, vomiting, abdominal pain, and (rarely) QT prolongation. Metronidazole can cause peripheral neuropathy, seizures, and a disulfiram-like reaction when taken with alcohol. Tetracycline is teratogenic and causes photosensitivity.
Prevent Constipation
Explanation This patient is already in the initial phases of hepatic encephalopathy due to alcoholic liver disease as evidenced by the disorientation and tremors, also known as asterixis. The primary cause of hepatic encephalopathy is unclear. Metabolic abnormalities due to liver dysfunction, resulting in a spectrum of neuropsychiatric signs and symptoms, are seen. High levels of ammonia are found in the blood. Constipation causes increased ammonia production and absorption due to prolonged intestinal contact and aggravates the condition. Lactulose should be administered frequently to eliminate the ammonia in the stool. It is an indigestible sugar that acts as an osmotic laxative by increasing the water content of the stool and promoting bowel movements. It is digested by the colonic bacteria, and the acidic remains convert ammonia into ammonium ions in the colon, which are then excreted in the stool. Oral antibiotics can lower blood ammonia levels by decreasing ammonia production and absorption. The commonly used ones are neomycin, metronidazole, vancomycin, and, lately, rifaximin. The last three are better tolerated than neomycin. However antibiotics have their side effects and can cause bacterial overgrowth syndromes. Their main use continues to be in patients who cannot tolerate disaccharides like lactulose. Acarbose and fermentable fiber can also cause decrease in intestinal ammonia production and absorption. Newer studies with sodium benzoate are ongoing. Benzoate and glycine react to form hippurate, and for every mole of benzoate utilized this way, one mole of nitrogen is excreted in the urine, thereby enhancing ammonia metabolism. This, however, still needs to be studied further to be used widely. Studies with ornithine-aspartate are also being done as a stimulator of ammonia metabolism. All the products mentioned are yet to replace lactulose as the first line of treatment but are potentially useful once more studies are done. Other precipitating factors for hepatic encephalopathy include azotemia, hypokalemia, gastrointestinal bleeding, high protein diet, alkalosis, infection, sedatives, and other hepatotoxic agents.
High protein diet is a contraindication in this condition, as protein catabolism causes increase in ammonia levels. Daily protein should be restricted to 40 g/day.

Sedation of the patient should also be avoided, since sedatives cause cerebral depression and worsening of encephalopathy. These drugs are also not metabolized adequately by the diseased liver.

Though infection is an important precipitating factor for hepatic encephalopathy, empiric treatment is not recommended. However, early and adequate treatment of an infection should be done, especially for spontaneous bacterial peritonitis. In fact multiple randomized control trials have been done regarding antibiotic prophylaxis for SBP, and they have shown not only a decrease in bacterial infections but also a significant reduction in mortality. Prophylaxis is recommended in cirrhotic patients with risk factors for SBP like GI bleeding, prior history of SBP, and low ascitic fluid protein.

Thiamine and folic acid should be added for nutritional support to all alcoholic patients, since they are malnourished and vitamin depleted. However, this will not change the outcome in hepatic encephalopathy as quickly or as much as avoiding constipation.
PPI (proton pump inhibitor), amoxicillin, and clarithromycin twice daily for 2 weeks
There are several regimens recommended for H. pylori infection, which is an important cause of peptic ulcer disease and should be treated if found associated with symptoms. The choice of the regimen depends on considerations such as cost, side effects, and ease of administration. Allergy to one of the medications, as well as intolerance, should also be taken into account. Any proton pump inhibitor (PPI) with amoxicillin 1000 mg twice daily and clarithromycin 500 mg twice daily for 2 weeks or PPI with metronidazole 500mg twice daily and clarithromycin 500mg twice daily for 2 weeks are recommended. These are the triple drug therapies available. The other regimens suggested are bismuth, metronidazole, and tetracycline 4 times daily for 2 weeks along with PPI twice daily for 2 weeks or H2 receptor antagonist twice daily for 4 weeks (quadruple drug therapy). Dual therapy with a proton pump inhibitor and an antibiotic (amoxicillin or clarithromycin) is not recommended as primary therapy, since eradication rates are much lower than the above regimens. The most common side effect is a metallic taste in the mouth due to clarithromycin or metronidazole. Amoxicillin can cause diarrhea or a rash. Clarithromycin can also cause nausea, vomiting, abdominal pain, and (rarely) QT prolongation. Metronidazole can cause peripheral neuropathy, seizures, and a disulfiram-like reaction when taken with alcohol. Tetracycline is teratogenic and causes photosensitivity.
Blood tests to measure level of cobalamin
Blood tests should be performed to measure the level of cobalamin. Based on the symptoms, the patient likely suffers from subacute combined degeneration of spinal cord due to degeneration of the posterior and lateral columns of the spinal cord. This is a result of a vitamin B12 (cobalamin) deficiency; a blood test to determine the level of vitamin B12 should be performed to confirm the diagnosis.

Performing blood tests to measure the level of thiamine is an incorrect response. A deficit in vitamin B1 (thiamine) causes symptoms that are characteristic of patients with Wernicke-Korsakoff syndrome. These include confusion and movement disability; however, the patients with Wernicke-Korsakoff syndrome do not generally have tingling or numbness sensations.

Performing blood tests to measure the level of glucose is an incorrect response. Symptoms such as pain, tingling, and numbness in the hands and feet, as well as depression, can be signs of developing diabetic neuropathy. This patient lacks other symptoms associated with diabetes, making this diagnosis unlikely; therefore, testing for glucose levels is not a necessary next step.

A thyroid-stimulating hormone (TSH) test is an incorrect response. Muscle weakness, numbness, pain, as well as depression, are associated with the late stages of chronic hypothyroidism; however, these symptoms are not sufficient to suspect hypothyroidism. Hypothyroidism is characterized by weight gain, loss of concentration, and hearing loss in the elderly, which are not conditions that affect this patient; therefore, a TSH test would not be useful in this case.

Neuroimaging studies are performed to provide information about brain tumors, skull fractures, and other diseases of the brain and blood vessels in the brain. Based on the symptoms seen in this patient, neuroimaging would not help in establishing a diagnosis.
A 58-year-old man presents with a 1-day history of severe abdominal pain, nausea, and vomiting. He initially thought he had some indigestion, with pain located in the epigastric region, and tried some calcium carbonate (Tums) with no relief. The pain and vomiting progressed through the night and kept him from sleeping and going to work. He feels the pain boring through to his back. He denies hematemesis, fever, diarrhea, out-of-the-country travel, and contact with sick people. Prior to onset of pain, he reports good health. He has no known medical conditions and takes no medications. He has had no surgeries. He smokes cigarettes (1ppd x 40 years), admits "moderate" alcohol use, and denies drug use. He is married and works as a welder.

Vitals are: BP: 102/56 mmHg; HR: 116bpm; RR: 15; Temp: 98.9F; O2Sat: 95% on room air.

On physical exam, the patient appears uncomfortable on the exam table and grimaces when changing position for exam. He is cooperative, alert, and oriented. Abnormal physical exam findings include: abdomen distended, decreased bowel sounds, and tender epigastric region, with guarding. He is tachycardic. No jaundice is noted. The remainder of the exam is normal.
This patient's test results are shown in the table.

Alk Phosphatase150 (50-136)
Amylase 272 (20-110)
Lipase 290 (0-160)



Question
What pharmacologic treatment is the most important intervention for this patient's likely condition?

Answer Choices
1 Ertapenem
2 Hyoscyamine
3 Lactated Ringer's
4 Pancrelipase
5 Promethazine
LR
This patient is presenting with an episode of acute pancreatitis. Pancreatitis is characterized by epigastric pain, nausea, and vomiting. Many other acute abdomen conditions may present similarly. Significant elevations of lipase and amylase, as well as CT evidence of pancreatic inflammation, fluid collections, and/or necrosis, will establish the diagnosis. Pancreatitis can be acute or chronic, and those with chronic disease may have periodic acute flares. In acute pancreatitis, early fluid resuscitation is one of the "few medical interventions that appears to affect outcome," so (of the choices listed) administering lactated Ringer's (or saline) would be the best answer for this patient. Also, ensuring the patient has "nothing by mouth" (NPO) until symptoms decrease is standard treatment.

Ertapenem is a carbapenem antibiotic, indicated for complicated intra-abdominal, skin, and urinary tract infections. Although this patient's white blood cell count (WBC) is elevated, the primary process is not infectious. The WBC increases in inflammatory states. Rarely are antibiotics needed in acute pancreatitis.

Hyoscyamine is an anticholinergic medication, with a wide range of uses, including many gastrointestinal conditions. It may be used for reducing spasm in irritable bowel syndrome and for biliary colic. Before the test results pointed to pancreatitis, as in this patient's diagnosis, biliary colic and obstruction would be on the differential. However, hyoscyamine would not be a primary treatment for pancreatitis.

Pancrelipase is a digestive enzyme, taken with meals, and indicated for pancreatic insufficiency, a common complication of many years of chronic pancreatitis. This patient may be at risk for future pancreatitic disease, but the pancrelipase would not benefit him at this time.

Promethazine is a common antiemetic with antihistamine and anticholinergic properties. Although it may be reasonable to consider antiemetic treatment for a patient with acute pancreatitis, it is an adjunct treatment and does not have a vital impact on the course of the disorder.
A 58-year-old man presents with a 1-day history of severe abdominal pain, nausea, and vomiting. He initially thought he had some indigestion, with pain located in the epigastric region, and tried some calcium carbonate (Tums) with no relief. The pain and vomiting progressed through the night and kept him from sleeping and going to work. He feels the pain boring through to his back. He denies hematemesis, fever, diarrhea, out-of-the-country travel, and contact with sick people. Prior to onset of pain, he reports good health. He has no known medical conditions and takes no medications. He has had no surgeries. He smokes cigarettes (1ppd x 40 years), admits "moderate" alcohol use, and denies drug use. He is married and works as a welder.

Vitals are: BP: 102/56 mmHg; HR: 116bpm; RR: 15; Temp: 98.9F; O2Sat: 95% on room air.

On physical exam, the patient appears uncomfortable on the exam table and grimaces when changing position for exam. He is cooperative, alert, and oriented. Abnormal physical exam findings include: abdomen distended, decreased bowel sounds, and tender epigastric region, with guarding. He is tachycardic. No jaundice is noted. The remainder of the exam is normal.
This patient's test results are shown in the table.

Alk Phosphatase150 (50-136)
Amylase 272 (20-110)
Lipase 290 (0-160)



Question
What pharmacologic treatment is the most important intervention for this patient's likely condition?

Answer Choices
1 Ertapenem
2 Hyoscyamine
3 Lactated Ringer's
4 Pancrelipase
5 Promethazine
LR
This patient is presenting with an episode of acute pancreatitis. Pancreatitis is characterized by epigastric pain, nausea, and vomiting. Many other acute abdomen conditions may present similarly. Significant elevations of lipase and amylase, as well as CT evidence of pancreatic inflammation, fluid collections, and/or necrosis, will establish the diagnosis. Pancreatitis can be acute or chronic, and those with chronic disease may have periodic acute flares. In acute pancreatitis, early fluid resuscitation is one of the "few medical interventions that appears to affect outcome," so (of the choices listed) administering lactated Ringer's (or saline) would be the best answer for this patient. Also, ensuring the patient has "nothing by mouth" (NPO) until symptoms decrease is standard treatment.

Ertapenem is a carbapenem antibiotic, indicated for complicated intra-abdominal, skin, and urinary tract infections. Although this patient's white blood cell count (WBC) is elevated, the primary process is not infectious. The WBC increases in inflammatory states. Rarely are antibiotics needed in acute pancreatitis.

Hyoscyamine is an anticholinergic medication, with a wide range of uses, including many gastrointestinal conditions. It may be used for reducing spasm in irritable bowel syndrome and for biliary colic. Before the test results pointed to pancreatitis, as in this patient's diagnosis, biliary colic and obstruction would be on the differential. However, hyoscyamine would not be a primary treatment for pancreatitis.

Pancrelipase is a digestive enzyme, taken with meals, and indicated for pancreatic insufficiency, a common complication of many years of chronic pancreatitis. This patient may be at risk for future pancreatitic disease, but the pancrelipase would not benefit him at this time.

Promethazine is a common antiemetic with antihistamine and anticholinergic properties. Although it may be reasonable to consider antiemetic treatment for a patient with acute pancreatitis, it is an adjunct treatment and does not have a vital impact on the course of the disorder.
A 58-year-old man presents with a 1-day history of severe abdominal pain, nausea, and vomiting. He initially thought he had some indigestion, with pain located in the epigastric region, and tried some calcium carbonate (Tums) with no relief. The pain and vomiting progressed through the night and kept him from sleeping and going to work. He feels the pain boring through to his back. He denies hematemesis, fever, diarrhea, out-of-the-country travel, and contact with sick people. Prior to onset of pain, he reports good health. He has no known medical conditions and takes no medications. He has had no surgeries. He smokes cigarettes (1ppd x 40 years), admits "moderate" alcohol use, and denies drug use. He is married and works as a welder.

Vitals are: BP: 102/56 mmHg; HR: 116bpm; RR: 15; Temp: 98.9F; O2Sat: 95% on room air.

On physical exam, the patient appears uncomfortable on the exam table and grimaces when changing position for exam. He is cooperative, alert, and oriented. Abnormal physical exam findings include: abdomen distended, decreased bowel sounds, and tender epigastric region, with guarding. He is tachycardic. No jaundice is noted. The remainder of the exam is normal.
This patient's test results are shown in the table.

Alk Phosphatase150 (50-136)
Amylase 272 (20-110)
Lipase 290 (0-160)



Question
What pharmacologic treatment is the most important intervention for this patient's likely condition?

Answer Choices
1 Ertapenem
2 Hyoscyamine
3 Lactated Ringer's
4 Pancrelipase
5 Promethazine
LR
This patient is presenting with an episode of acute pancreatitis. Pancreatitis is characterized by epigastric pain, nausea, and vomiting. Many other acute abdomen conditions may present similarly. Significant elevations of lipase and amylase, as well as CT evidence of pancreatic inflammation, fluid collections, and/or necrosis, will establish the diagnosis. Pancreatitis can be acute or chronic, and those with chronic disease may have periodic acute flares. In acute pancreatitis, early fluid resuscitation is one of the "few medical interventions that appears to affect outcome," so (of the choices listed) administering lactated Ringer's (or saline) would be the best answer for this patient. Also, ensuring the patient has "nothing by mouth" (NPO) until symptoms decrease is standard treatment.

Ertapenem is a carbapenem antibiotic, indicated for complicated intra-abdominal, skin, and urinary tract infections. Although this patient's white blood cell count (WBC) is elevated, the primary process is not infectious. The WBC increases in inflammatory states. Rarely are antibiotics needed in acute pancreatitis.

Hyoscyamine is an anticholinergic medication, with a wide range of uses, including many gastrointestinal conditions. It may be used for reducing spasm in irritable bowel syndrome and for biliary colic. Before the test results pointed to pancreatitis, as in this patient's diagnosis, biliary colic and obstruction would be on the differential. However, hyoscyamine would not be a primary treatment for pancreatitis.

Pancrelipase is a digestive enzyme, taken with meals, and indicated for pancreatic insufficiency, a common complication of many years of chronic pancreatitis. This patient may be at risk for future pancreatitic disease, but the pancrelipase would not benefit him at this time.

Promethazine is a common antiemetic with antihistamine and anticholinergic properties. Although it may be reasonable to consider antiemetic treatment for a patient with acute pancreatitis, it is an adjunct treatment and does not have a vital impact on the course of the disorder.
A 58-year-old man presents with a 1-day history of severe abdominal pain, nausea, and vomiting. He initially thought he had some indigestion, with pain located in the epigastric region, and tried some calcium carbonate (Tums) with no relief. The pain and vomiting progressed through the night and kept him from sleeping and going to work. He feels the pain boring through to his back. He denies hematemesis, fever, diarrhea, out-of-the-country travel, and contact with sick people. Prior to onset of pain, he reports good health. He has no known medical conditions and takes no medications. He has had no surgeries. He smokes cigarettes (1ppd x 40 years), admits "moderate" alcohol use, and denies drug use. He is married and works as a welder.

Vitals are: BP: 102/56 mmHg; HR: 116bpm; RR: 15; Temp: 98.9F; O2Sat: 95% on room air.

On physical exam, the patient appears uncomfortable on the exam table and grimaces when changing position for exam. He is cooperative, alert, and oriented. Abnormal physical exam findings include: abdomen distended, decreased bowel sounds, and tender epigastric region, with guarding. He is tachycardic. No jaundice is noted. The remainder of the exam is normal.
This patient's test results are shown in the table.

Alk Phosphatase150 (50-136)
Amylase 272 (20-110)
Lipase 290 (0-160)



Question
What pharmacologic treatment is the most important intervention for this patient's likely condition?

Answer Choices
1 Ertapenem
2 Hyoscyamine
3 Lactated Ringer's
4 Pancrelipase
5 Promethazine
Blood tests to measure level of cobalamin
Blood tests should be performed to measure the level of cobalamin. Based on the symptoms, the patient likely suffers from subacute combined degeneration of spinal cord due to degeneration of the posterior and lateral columns of the spinal cord. This is a result of a vitamin B12 (cobalamin) deficiency; a blood test to determine the level of vitamin B12 should be performed to confirm the diagnosis.

Performing blood tests to measure the level of thiamine is an incorrect response. A deficit in vitamin B1 (thiamine) causes symptoms that are characteristic of patients with Wernicke-Korsakoff syndrome. These include confusion and movement disability; however, the patients with Wernicke-Korsakoff syndrome do not generally have tingling or numbness sensations.

Performing blood tests to measure the level of glucose is an incorrect response. Symptoms such as pain, tingling, and numbness in the hands and feet, as well as depression, can be signs of developing diabetic neuropathy. This patient lacks other symptoms associated with diabetes, making this diagnosis unlikely; therefore, testing for glucose levels is not a necessary next step.

A thyroid-stimulating hormone (TSH) test is an incorrect response. Muscle weakness, numbness, pain, as well as depression, are associated with the late stages of chronic hypothyroidism; however, these symptoms are not sufficient to suspect hypothyroidism. Hypothyroidism is characterized by weight gain, loss of concentration, and hearing loss in the elderly, which are not conditions that affect this patient; therefore, a TSH test would not be useful in this case.

Neuroimaging studies are performed to provide information about brain tumors, skull fractures, and other diseases of the brain and blood vessels in the brain. Based on the symptoms seen in this patient, neuroimaging would not help in establishing a diagnosis.
Blood tests to measure level of cobalamin
Blood tests should be performed to measure the level of cobalamin. Based on the symptoms, the patient likely suffers from subacute combined degeneration of spinal cord due to degeneration of the posterior and lateral columns of the spinal cord. This is a result of a vitamin B12 (cobalamin) deficiency; a blood test to determine the level of vitamin B12 should be performed to confirm the diagnosis.

Performing blood tests to measure the level of thiamine is an incorrect response. A deficit in vitamin B1 (thiamine) causes symptoms that are characteristic of patients with Wernicke-Korsakoff syndrome. These include confusion and movement disability; however, the patients with Wernicke-Korsakoff syndrome do not generally have tingling or numbness sensations.

Performing blood tests to measure the level of glucose is an incorrect response. Symptoms such as pain, tingling, and numbness in the hands and feet, as well as depression, can be signs of developing diabetic neuropathy. This patient lacks other symptoms associated with diabetes, making this diagnosis unlikely; therefore, testing for glucose levels is not a necessary next step.

A thyroid-stimulating hormone (TSH) test is an incorrect response. Muscle weakness, numbness, pain, as well as depression, are associated with the late stages of chronic hypothyroidism; however, these symptoms are not sufficient to suspect hypothyroidism. Hypothyroidism is characterized by weight gain, loss of concentration, and hearing loss in the elderly, which are not conditions that affect this patient; therefore, a TSH test would not be useful in this case.

Neuroimaging studies are performed to provide information about brain tumors, skull fractures, and other diseases of the brain and blood vessels in the brain. Based on the symptoms seen in this patient, neuroimaging would not help in establishing a diagnosis.
PPI (proton pump inhibitor), amoxicillin, and clarithromycin twice daily for 2 weeks
There are several regimens recommended for H. pylori infection, which is an important cause of peptic ulcer disease and should be treated if found associated with symptoms. The choice of the regimen depends on considerations such as cost, side effects, and ease of administration. Allergy to one of the medications, as well as intolerance, should also be taken into account. Any proton pump inhibitor (PPI) with amoxicillin 1000 mg twice daily and clarithromycin 500 mg twice daily for 2 weeks or PPI with metronidazole 500mg twice daily and clarithromycin 500mg twice daily for 2 weeks are recommended. These are the triple drug therapies available. The other regimens suggested are bismuth, metronidazole, and tetracycline 4 times daily for 2 weeks along with PPI twice daily for 2 weeks or H2 receptor antagonist twice daily for 4 weeks (quadruple drug therapy). Dual therapy with a proton pump inhibitor and an antibiotic (amoxicillin or clarithromycin) is not recommended as primary therapy, since eradication rates are much lower than the above regimens. The most common side effect is a metallic taste in the mouth due to clarithromycin or metronidazole. Amoxicillin can cause diarrhea or a rash. Clarithromycin can also cause nausea, vomiting, abdominal pain, and (rarely) QT prolongation. Metronidazole can cause peripheral neuropathy, seizures, and a disulfiram-like reaction when taken with alcohol. Tetracycline is teratogenic and causes photosensitivity.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
Oral PPI
The correct response is oral proton pump inhibitor.

The patient in this presented scenario is showing signs and symptoms that are most consistent with esophageal dysphagia. Difficulty swallowing is the main complaint and is typically caused by 1 of 2 entities: localized neuromuscular disorders or obstructive lesions. Our patient specifically is showing issues of diffuse esophageal spasm. This is a motility disorder that is defined by simultaneous uncoordinated contraction of several esophageal segments. This can lead to potentially retrosternal pain and is worsened or precipitated by acid reflex, rapid eating, stress/anxiety, and hot/cold food. The dysphagia found in these patients is intermittent, non-progressive and does not cause weight loss. These patients have no documented abnormality in the distribution of myenteric neurons, normal lower esophageal sphincter relaxation, and no evidence of obstruction. All of these components are consistent with the patient described.

In terms of a first-line treatment, acid suppression with a proton pump inhibitor (PPI) is the first-line pharmaceutical intervention that should be initiated. Sublingual nitroglycerin and calcium channel blockers may also be considered as treatment, but they are not typically considered first-line options.

Botulinum toxin is not considered first-line treatment for diffuse esophageal spasms; it may be considered to be administered/injected in the lower esophageal sphincter and lower esophagus to reduce chest pain caused by diffuse esophageal spasm but again is not the first line treatment. Also, the patient described above is experiencing other symptoms, not just the chest pain. Prokinetic agents, such as metoclopramide, are considered treatment options for reflux esophagitis and Barrett esophagus-related causes of dysphagia. Oral corticosteroids may be considered in patients with diagnosed eosinophilic esophagitis.
Misoprostol
The correct response is misoprostol.

Besides NSAID use, this patient has several risk factors for gastric bleeding (a previous episode, advanced age, use of anticoagulants and low-dose aspirin). Therefore, prophylaxis against bleeding must be seriously considered. Prostaglandin analogues are the most effective drugs for reducing the risk of rebleeding. One study described reductions of up to fivefold in the incidence of gastric ulcers on endoscopy. However, this drug requires 2 to 4 daily doses and has several side effects. The most common are diarrhea (up to 30% of patients) and abdominal discomfort. It is also a potent abortifacient. Starting the drug at a low dose and then progressively raising it might reduce the incidence of these side effects and improve tolerance.

Proton-pump inhibitors such as omeprazole also reduce the incidence of gastrointestinal complications in chronic users of NSAIDs. They are slightly less effective than prostaglandin analogues, but their once-daily dosage is more convenient and the incidence of side effects is lower. The use of low-dose aspirin abrogates the protective effects of COX-2-selective anti-inflammatory drugs (i.e., celecoxib, rofecoxib, or valdecoxib). Therefore, switching to COX-2 inhibitors would not be advantageous for this patient.

H2-blockers such as famotidine have only marginal efficacy in reducing the incidence of NSAID-associated gastric ulcers and should not be prescribed in this case.

The medications that should be taken with at least 250 ml of water are the bisphosphonates. This precaution reduces the risk of pill esophagitis. This drug should also be taken on an empty stomach and with the patient in an upright position. If these precautions are not followed, bisphosphonates can cause severe esophagitis, which can even lead to strictures or bleeding.
Oral PPI
The correct response is oral proton pump inhibitor.

The patient in this presented scenario is showing signs and symptoms that are most consistent with esophageal dysphagia. Difficulty swallowing is the main complaint and is typically caused by 1 of 2 entities: localized neuromuscular disorders or obstructive lesions. Our patient specifically is showing issues of diffuse esophageal spasm. This is a motility disorder that is defined by simultaneous uncoordinated contraction of several esophageal segments. This can lead to potentially retrosternal pain and is worsened or precipitated by acid reflex, rapid eating, stress/anxiety, and hot/cold food. The dysphagia found in these patients is intermittent, non-progressive and does not cause weight loss. These patients have no documented abnormality in the distribution of myenteric neurons, normal lower esophageal sphincter relaxation, and no evidence of obstruction. All of these components are consistent with the patient described.

In terms of a first-line treatment, acid suppression with a proton pump inhibitor (PPI) is the first-line pharmaceutical intervention that should be initiated. Sublingual nitroglycerin and calcium channel blockers may also be considered as treatment, but they are not typically considered first-line options.

Botulinum toxin is not considered first-line treatment for diffuse esophageal spasms; it may be considered to be administered/injected in the lower esophageal sphincter and lower esophagus to reduce chest pain caused by diffuse esophageal spasm but again is not the first line treatment. Also, the patient described above is experiencing other symptoms, not just the chest pain. Prokinetic agents, such as metoclopramide, are considered treatment options for reflux esophagitis and Barrett esophagus-related causes of dysphagia. Oral corticosteroids may be considered in patients with diagnosed eosinophilic esophagitis.
Oral PPI
The correct response is oral proton pump inhibitor.

The patient in this presented scenario is showing signs and symptoms that are most consistent with esophageal dysphagia. Difficulty swallowing is the main complaint and is typically caused by 1 of 2 entities: localized neuromuscular disorders or obstructive lesions. Our patient specifically is showing issues of diffuse esophageal spasm. This is a motility disorder that is defined by simultaneous uncoordinated contraction of several esophageal segments. This can lead to potentially retrosternal pain and is worsened or precipitated by acid reflex, rapid eating, stress/anxiety, and hot/cold food. The dysphagia found in these patients is intermittent, non-progressive and does not cause weight loss. These patients have no documented abnormality in the distribution of myenteric neurons, normal lower esophageal sphincter relaxation, and no evidence of obstruction. All of these components are consistent with the patient described.

In terms of a first-line treatment, acid suppression with a proton pump inhibitor (PPI) is the first-line pharmaceutical intervention that should be initiated. Sublingual nitroglycerin and calcium channel blockers may also be considered as treatment, but they are not typically considered first-line options.

Botulinum toxin is not considered first-line treatment for diffuse esophageal spasms; it may be considered to be administered/injected in the lower esophageal sphincter and lower esophagus to reduce chest pain caused by diffuse esophageal spasm but again is not the first line treatment. Also, the patient described above is experiencing other symptoms, not just the chest pain. Prokinetic agents, such as metoclopramide, are considered treatment options for reflux esophagitis and Barrett esophagus-related causes of dysphagia. Oral corticosteroids may be considered in patients with diagnosed eosinophilic esophagitis.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
4 hrs
In an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.
Explanation Acute appendicitis is a common cause of acute abdominal pain. It can occur at any age and is caused by the obstruction of the lumen of the appendix by foreign body, inflammation, fecolith, or tumor. Increased intraluminal pressure causes necrosis and perforation with signs of localized peritonitis. Pain starting in the umbilical area and later migrating to the right lower quadrant at McBurney's point is classic. Fever, vomiting, diarrhea, and leukocytosis support the diagnosis. CT scan in adults and abdominal ultrasound in children are diagnostic, and treatment is immediate surgical removal. In a female patient, endometriosis, ovarian cyst, and ovarian torsion are the other differential diagnoses.
Acute gastroenteritis can mimic appendicitis but watery diarrhea is usually the predominant symptom with vomiting in some infections. Abdominal pain is diffuse and crampy and is not localized to McBurney's point. Fever and leukocytosis may be present. CT scan rules out localized pathology and is necessary only in limited cases. Treatment is supportive, since it is a self-limiting condition.

Acute cholecystitis is typically characterized by right upper quadrant pain with radiation to the back, nausea and vomiting, fever, and right upper quadrant tenderness, also known as Murphy's sign. Jaundice may be present occasionally, with elevated liver enzymes and leukocytosis. It is caused by inflammation of the gall bladder wall, usually with one or multiple gallstones. Infection within the biliary system also plays a role in acute cholecystitis. Ultrasound reveals gallstones in most cases. Gall bladder wall thickening more than 4-5 mm, edema (causing double wall sign), and sonographic Murphy's sign (tenderness in the right upper quadrant while palpation with the ultrasound transducer) are also seen in the ultrasound. Patients need hospitalization for proper management. Treatment is conservative with hydration, pain control, bowel rest, and correction of any electrolyte disturbances. Antibiotics are not recommended as a rule but are generally given. Cholecystectomy is recommended for empyema, gangrene, rupture of the gall bladder, recurrent disease, or gallstones. Asymptomatic gallstones, however, are not treated surgically.

Acute diverticulitis is usually left-sided and rarely right-sided. It presents with left lower quadrant pain, constipation or diarrhea, and left lower tenderness. Fever and mild leukocytosis are common but liver enzymes are normal. If right sided it is frequently mistaken for appendicitis. Diverticulitis can occur anywhere in the GI tract and may be mistaken for other common conditions. For example, diverticulitis of the transverse colon may be confused with cholecystitis, pancreatitis, and peptic ulcer disease. A tender mass may be present in a few cases. But it is very rare in less than 30 years of age and CT scan differentiates it from other conditions. Treatment is usually conservative in the first episode, with bowel rest and antibiotics. Colonic resection is advised in recurrent episode, complications like perforation, fistula or abscess, intractable symptoms, or suspicion of carcinoma.

Incarcerated hernia presents with severe pain in the groin area, with a mass that may be purplish in color due to ischemia and gangrene. It should be suspected when a reducible hernia becomes painful and non-reducible. Treatment is surgical.
Explanation Acute appendicitis is a common cause of acute abdominal pain. It can occur at any age and is caused by the obstruction of the lumen of the appendix by foreign body, inflammation, fecolith, or tumor. Increased intraluminal pressure causes necrosis and perforation with signs of localized peritonitis. Pain starting in the umbilical area and later migrating to the right lower quadrant at McBurney's point is classic. Fever, vomiting, diarrhea, and leukocytosis support the diagnosis. CT scan in adults and abdominal ultrasound in children are diagnostic, and treatment is immediate surgical removal. In a female patient, endometriosis, ovarian cyst, and ovarian torsion are the other differential diagnoses.
Acute gastroenteritis can mimic appendicitis but watery diarrhea is usually the predominant symptom with vomiting in some infections. Abdominal pain is diffuse and crampy and is not localized to McBurney's point. Fever and leukocytosis may be present. CT scan rules out localized pathology and is necessary only in limited cases. Treatment is supportive, since it is a self-limiting condition.

Acute cholecystitis is typically characterized by right upper quadrant pain with radiation to the back, nausea and vomiting, fever, and right upper quadrant tenderness, also known as Murphy's sign. Jaundice may be present occasionally, with elevated liver enzymes and leukocytosis. It is caused by inflammation of the gall bladder wall, usually with one or multiple gallstones. Infection within the biliary system also plays a role in acute cholecystitis. Ultrasound reveals gallstones in most cases. Gall bladder wall thickening more than 4-5 mm, edema (causing double wall sign), and sonographic Murphy's sign (tenderness in the right upper quadrant while palpation with the ultrasound transducer) are also seen in the ultrasound. Patients need hospitalization for proper management. Treatment is conservative with hydration, pain control, bowel rest, and correction of any electrolyte disturbances. Antibiotics are not recommended as a rule but are generally given. Cholecystectomy is recommended for empyema, gangrene, rupture of the gall bladder, recurrent disease, or gallstones. Asymptomatic gallstones, however, are not treated surgically.

Acute diverticulitis is usually left-sided and rarely right-sided. It presents with left lower quadrant pain, constipation or diarrhea, and left lower tenderness. Fever and mild leukocytosis are common but liver enzymes are normal. If right sided it is frequently mistaken for appendicitis. Diverticulitis can occur anywhere in the GI tract and may be mistaken for other common conditions. For example, diverticulitis of the transverse colon may be confused with cholecystitis, pancreatitis, and peptic ulcer disease. A tender mass may be present in a few cases. But it is very rare in less than 30 years of age and CT scan differentiates it from other conditions. Treatment is usually conservative in the first episode, with bowel rest and antibiotics. Colonic resection is advised in recurrent episode, complications like perforation, fistula or abscess, intractable symptoms, or suspicion of carcinoma.

Incarcerated hernia presents with severe pain in the groin area, with a mass that may be purplish in color due to ischemia and gangrene. It should be suspected when a reducible hernia becomes painful and non-reducible. Treatment is surgical.
Explanation Acute appendicitis is a common cause of acute abdominal pain. It can occur at any age and is caused by the obstruction of the lumen of the appendix by foreign body, inflammation, fecolith, or tumor. Increased intraluminal pressure causes necrosis and perforation with signs of localized peritonitis. Pain starting in the umbilical area and later migrating to the right lower quadrant at McBurney's point is classic. Fever, vomiting, diarrhea, and leukocytosis support the diagnosis. CT scan in adults and abdominal ultrasound in children are diagnostic, and treatment is immediate surgical removal. In a female patient, endometriosis, ovarian cyst, and ovarian torsion are the other differential diagnoses.
Acute gastroenteritis can mimic appendicitis but watery diarrhea is usually the predominant symptom with vomiting in some infections. Abdominal pain is diffuse and crampy and is not localized to McBurney's point. Fever and leukocytosis may be present. CT scan rules out localized pathology and is necessary only in limited cases. Treatment is supportive, since it is a self-limiting condition.

Acute cholecystitis is typically characterized by right upper quadrant pain with radiation to the back, nausea and vomiting, fever, and right upper quadrant tenderness, also known as Murphy's sign. Jaundice may be present occasionally, with elevated liver enzymes and leukocytosis. It is caused by inflammation of the gall bladder wall, usually with one or multiple gallstones. Infection within the biliary system also plays a role in acute cholecystitis. Ultrasound reveals gallstones in most cases. Gall bladder wall thickening more than 4-5 mm, edema (causing double wall sign), and sonographic Murphy's sign (tenderness in the right upper quadrant while palpation with the ultrasound transducer) are also seen in the ultrasound. Patients need hospitalization for proper management. Treatment is conservative with hydration, pain control, bowel rest, and correction of any electrolyte disturbances. Antibiotics are not recommended as a rule but are generally given. Cholecystectomy is recommended for empyema, gangrene, rupture of the gall bladder, recurrent disease, or gallstones. Asymptomatic gallstones, however, are not treated surgically.

Acute diverticulitis is usually left-sided and rarely right-sided. It presents with left lower quadrant pain, constipation or diarrhea, and left lower tenderness. Fever and mild leukocytosis are common but liver enzymes are normal. If right sided it is frequently mistaken for appendicitis. Diverticulitis can occur anywhere in the GI tract and may be mistaken for other common conditions. For example, diverticulitis of the transverse colon may be confused with cholecystitis, pancreatitis, and peptic ulcer disease. A tender mass may be present in a few cases. But it is very rare in less than 30 years of age and CT scan differentiates it from other conditions. Treatment is usually conservative in the first episode, with bowel rest and antibiotics. Colonic resection is advised in recurrent episode, complications like perforation, fistula or abscess, intractable symptoms, or suspicion of carcinoma.

Incarcerated hernia presents with severe pain in the groin area, with a mass that may be purplish in color due to ischemia and gangrene. It should be suspected when a reducible hernia becomes painful and non-reducible. Treatment is surgical.
Vitamin C
In cases of vitamin C (or ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions, such as pregnancy and lactation, which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, such as oranges, lemons, and tangerines, as well as tomatoes and potatoes.

Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

In cases of vitamin A deficiency, patients can present with inability to see well in dim light or night blindness. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities, and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular foamy spots on the conjunctiva. Patients may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, as well as yellow fruits and vegetables.

Niacin deficiency causes pellagra, which is characterized by:

A symmetrical dermatitis, usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations, such as memory impairment, depression, and dementia. These may appear alone or in combination. Causes include inadequate dietary intake, especially in patients with corn-based diets or alcoholism. Dietary sources include legumes, yeast, meat, and enriched cereal products.
In cases of pyridoxine or (vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory investigations reveal anemia with lymphopenia. Causes include malabsorption as well as medications, such as isoniazid and penicillamine. Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.
2 A 14% decrease of his hematocrit at 48 hours after admissionA patient who is admitted to the hospital for treatment of acute pancreatitis is assessed using the Ranson criteria to determine the severity of their disease, which in turn helps determine prognosis. About 70 - 80% of cases of acute pancreatitis are considered mild and result in virtually no morbidity or mortality. The remainder are severe attacks and have a 10 - 30% mortality rate. Fast identification of the severe cases is helpful to reduce the morbidity and mortality for each patient. There are 11 Ranson criteria, 5 of which are determined upon admission, and 6 at 48 hours after admission. Patients who have 2 or fewer of the criteria have minimal mortality. Patients with 3 - 5 of the criteria have about a 10 - 20% chance of mortality. Patients with 5 or more of the criteria have at least a 50% mortality rate. A patient with at least a 10% decrease in their hematocrit at 48 hours after admission meets one of the Ranson criteria, so the correct answer is a 14% decrease in hematocrit 48 hours after admission.

WBC count of 10,000 cells/mm3 is not one of the Ranson criteria. A WBC count of >16,000 cells/mm3 would meet one of the Ranson criteria.

Serum glucose of 130 mg/dL upon admission is also not one of the Ranson criteria. The patient's serum glucose would have to be at least 200 mg/dL to count as one of the Ranson criteria and increase the severity of their disease.

Aspartate transaminase of 240 U/dL upon admission is not one of the Ranson criteria either. The patient's aspartate transaminase would have to be at least 250 U/dL to count as a Ranson criteria and increase the severity of their disease.

A serum calcium of 10 mg/dL 48 hours after admission is not one of the Ranson criteria. If the patient's serum calcium is under 8 mg/dL 58 hours after admission, this would count as one of the Ranson criteria.
2 A 14% decrease of his hematocrit at 48 hours after admissionA patient who is admitted to the hospital for treatment of acute pancreatitis is assessed using the Ranson criteria to determine the severity of their disease, which in turn helps determine prognosis. About 70 - 80% of cases of acute pancreatitis are considered mild and result in virtually no morbidity or mortality. The remainder are severe attacks and have a 10 - 30% mortality rate. Fast identification of the severe cases is helpful to reduce the morbidity and mortality for each patient. There are 11 Ranson criteria, 5 of which are determined upon admission, and 6 at 48 hours after admission. Patients who have 2 or fewer of the criteria have minimal mortality. Patients with 3 - 5 of the criteria have about a 10 - 20% chance of mortality. Patients with 5 or more of the criteria have at least a 50% mortality rate. A patient with at least a 10% decrease in their hematocrit at 48 hours after admission meets one of the Ranson criteria, so the correct answer is a 14% decrease in hematocrit 48 hours after admission.

WBC count of 10,000 cells/mm3 is not one of the Ranson criteria. A WBC count of >16,000 cells/mm3 would meet one of the Ranson criteria.

Serum glucose of 130 mg/dL upon admission is also not one of the Ranson criteria. The patient's serum glucose would have to be at least 200 mg/dL to count as one of the Ranson criteria and increase the severity of their disease.

Aspartate transaminase of 240 U/dL upon admission is not one of the Ranson criteria either. The patient's aspartate transaminase would have to be at least 250 U/dL to count as a Ranson criteria and increase the severity of their disease.

A serum calcium of 10 mg/dL 48 hours after admission is not one of the Ranson criteria. If the patient's serum calcium is under 8 mg/dL 58 hours after admission, this would count as one of the Ranson criteria.
2 A 14% decrease of his hematocrit at 48 hours after admissionA patient who is admitted to the hospital for treatment of acute pancreatitis is assessed using the Ranson criteria to determine the severity of their disease, which in turn helps determine prognosis. About 70 - 80% of cases of acute pancreatitis are considered mild and result in virtually no morbidity or mortality. The remainder are severe attacks and have a 10 - 30% mortality rate. Fast identification of the severe cases is helpful to reduce the morbidity and mortality for each patient. There are 11 Ranson criteria, 5 of which are determined upon admission, and 6 at 48 hours after admission. Patients who have 2 or fewer of the criteria have minimal mortality. Patients with 3 - 5 of the criteria have about a 10 - 20% chance of mortality. Patients with 5 or more of the criteria have at least a 50% mortality rate. A patient with at least a 10% decrease in their hematocrit at 48 hours after admission meets one of the Ranson criteria, so the correct answer is a 14% decrease in hematocrit 48 hours after admission.

WBC count of 10,000 cells/mm3 is not one of the Ranson criteria. A WBC count of >16,000 cells/mm3 would meet one of the Ranson criteria.

Serum glucose of 130 mg/dL upon admission is also not one of the Ranson criteria. The patient's serum glucose would have to be at least 200 mg/dL to count as one of the Ranson criteria and increase the severity of their disease.

Aspartate transaminase of 240 U/dL upon admission is not one of the Ranson criteria either. The patient's aspartate transaminase would have to be at least 250 U/dL to count as a Ranson criteria and increase the severity of their disease.

A serum calcium of 10 mg/dL 48 hours after admission is not one of the Ranson criteria. If the patient's serum calcium is under 8 mg/dL 58 hours after admission, this would count as one of the Ranson criteria.
Vitamin C
In cases of vitamin C (or ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions, such as pregnancy and lactation, which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, such as oranges, lemons, and tangerines, as well as tomatoes and potatoes.

Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

In cases of vitamin A deficiency, patients can present with inability to see well in dim light or night blindness. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities, and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular foamy spots on the conjunctiva. Patients may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, as well as yellow fruits and vegetables.

Niacin deficiency causes pellagra, which is characterized by:

A symmetrical dermatitis, usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations, such as memory impairment, depression, and dementia. These may appear alone or in combination. Causes include inadequate dietary intake, especially in patients with corn-based diets or alcoholism. Dietary sources include legumes, yeast, meat, and enriched cereal products.
In cases of pyridoxine or (vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory investigations reveal anemia with lymphopenia. Causes include malabsorption as well as medications, such as isoniazid and penicillamine. Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.
Vitamin C
In cases of vitamin C (or ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions, such as pregnancy and lactation, which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, such as oranges, lemons, and tangerines, as well as tomatoes and potatoes.

Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

In cases of vitamin A deficiency, patients can present with inability to see well in dim light or night blindness. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities, and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular foamy spots on the conjunctiva. Patients may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, as well as yellow fruits and vegetables.

Niacin deficiency causes pellagra, which is characterized by:

A symmetrical dermatitis, usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations, such as memory impairment, depression, and dementia. These may appear alone or in combination. Causes include inadequate dietary intake, especially in patients with corn-based diets or alcoholism. Dietary sources include legumes, yeast, meat, and enriched cereal products.
In cases of pyridoxine or (vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory investigations reveal anemia with lymphopenia. Causes include malabsorption as well as medications, such as isoniazid and penicillamine. Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.
whipple disease
Whipple disease is a rare condition that can involve any organ of the body but principally affects the intestine, central nervous system, and joints. It is caused by gram-positive actinomycetes called Tropheryma whippelii. Histologically, the small intestinal mucosa is laden with distended macrophages in the lamina propria. These macrophages contain periodic acid-Schiff positive granules and rod-shaped bacilli by electron microscopy. These patients usually present with a form of malabsorption, including diarrhea and weight loss, and generally respond to antibiotic therapy.

Celiac sprue is a rare chronic disease in which there is a characteristic mucosal lesion of the small intestine in the form of blunting of the villi and an overall increase in plasma cells, lymphocytes, macrophages, and eosinophils in the lamina propria. Also known as the gluten-sensitive enteropathy, non-tropical sprue, and celiac disease, it is due to sensitivity to gluten, which is an alcohol soluble, water insoluble protein component called gliadin of wheat and other closely related grains. Detection of circulating anti-gliadin or anti-endomysial antibodies strongly favors the diagnosis. Both the symptoms and the mucosal histology improve on withdrawal of gluten from the diet.

Tropical sprue is a celiac-like disease occurring in people living or visiting the tropics. Bacterial overgrowth by an enterotoxigenic organism is said to be the cause for this disease. Intestinal changes are similar to celiac sprue, but injury is seen at all levels of the small intestine in contrast to celiac sprue, where it is concentrated in the proximal small intestine. It is mainly treated by broad-spectrum antibiotics.

The disaccharidases, of which the most important is lactase, are located in the apical cell membrane of the villous absorptive epithelial cells, the deficiency of which leads to the incomplete breakdown of the disaccharide lactose into its monosaccharides, glucose, and galactose, leading to diarrhea from the unabsorbed lactose. Bacterial fermentation of the unabsorbed sugars leads to increased hydrogen production, which is readily measured in the exhaled air by gas chromatography. There are both hereditary and acquired forms. Histologically in both, there is no abnormality of the mucosal cells of the bowel. Malabsorption is promptly corrected when exposure to milk and milk products is terminated.

Amebic dysentery is caused by Entamoeba histolytica, a protozoan, and generally causes diarrhea with blood and mucus. A stool examination will show the cysts and trophozoites of Entamoeba histolytica, which is diagnostic.
Niacin
This patient probably has niacin deficiency. Niacin (nicotinamide, nicotinic acid) deficiency is uncommon in the United States. It is often found in people who live on a diet that consists mainly of corn (maize). This is due to the fact that the niacin in corn cannot be absorbed unless it is chemically treated with alkali first. If a person consumes a diet rich in tryptophan, but low in niacin, they are able to compensate since tryptophan can be converted into niacin. Deficiency may also result from alcoholism, cirrhosis, or diarrhea. Men and women are affected equally. Symptoms of niacin deficiency include nausea, vomiting, diarrhea, rash, glossitis, stomatitis, depression, and psychosis. Niacin deficiency, also known as pellagra, manifests as the '3 Ds': diarrhea, dermatitis, and dementia. Treatment consists of niacin supplementation.

The causes of zinc deficiency include malnutrition, chronic debilitating diseases, chronic renal disease, alcoholism, drugs such as penicillamine and diuretic, and genetic disorders, such as sickle cell disease. Clinical manifestations in severe cases include alopecia, diarrhea, weight loss, infections, dermatitis, hypogonadism in men, and intercurrent infections. Supplementation with zinc is the treatment of choice.

Folate deficiency causes megaloblastic macrocytic anemia, as folate plays a key role in nucleic acid synthesis. The early manifestation of folate deficiency, especially in its suboptimal state, predisposes to occlusive vascular disease and thrombosis. These manifestations are linked to increased homocysteine levels found in folate deficiency. Neurological disturbances, such as mood disturbance and spinal cord syndromes, are also seen. It is also associated with predisposition to neoplasia and interferes with immunologic status. Folate replacement is the option to prevent and to treat the deficiency.

Vitamin B1 (or thiamine deficiency) causes beri beri, occurring mostly in the malnourished and alcoholics. The deficiency manifests with acute heart failure, neurologic deficits, and epilepsy. Empiric use of thiamine and prophylactic use in high-risk population is strongly recommended even before blood reports are obtained, as the treatment is inexpensive and prevents major catastrophes.

Vitamin B12 (or cobalamin deficiency) manifests as megaloblastic macrocytic anemia, pancytopenia, and a spectrum of neuropsychiatric disorders such as peripheral neuropathy, parasthesias, and demyelination of corticospinal tract. Nutritional deficiency, alcoholism, and malabsorption syndromes are some causes of B12 deficiency. It is also associated with homocysteinemia and atherosclerosis. Diagnosis is by serum estimation of B12, and oral supplementation is safe and effective. Intramuscular injections may also be used.
rectal abscess
This patient's presentation is most consistent with an anorectal abscess. Perirectal abscesses are associated with indolent, dull perirectal pain that is exacerbated by movement and increased perineal pressure from sitting or defecation. There may be associated pruritis. Those with an ischiorectal abscess often present with systemic fevers, chills, and severe perirectal pain and fullness consistent with the more advanced nature of this process. External signs are minimal and may include erythema, induration, or fluctuance. Physical examination demonstrates a small, erythematous, well-defined, fluctuant, subcutaneous mass near the anal orifice. On digital rectal examination (DRE), a fluctuant, indurated mass may be encountered.

The most common presentation of hemorrhoids is rectal bleeding, pain, pruritus, or prolapse, with rectal bleeding being the most common presenting symptom.

An anal fistula is an inflammatory tract between the anal canal and the skin. A patient with an anal fistula may complain of recurrent malodorous perianal drainage, pruritus, recurrent abscesses, fever, or perianal pain due to an occluded tract.

Inflammation of the mucosal lining of the rectum is defined as proctitis. The presentation includes persistent bright red rectal bleeding, a decrease in stool volume and an increase in mucoid consistency, tenesmus, fecal urgency or constipation, and abdominal cramping.

Necrotizing fasciitis is a rapidly progressive inflammatory infection of the fascia, with secondary necrosis of the subcutaneous tissues. It may be caused by aerobic, anaerobic, or mixed flora bacteria. Fournier gangrene is a form of necrotizing fasciitis that is localized to the scrotum and perineal area. The hallmark symptom of necrotizing fasciitis is intense pain and tenderness over the involved skin and underlying muscle. Pain usually develops prior to other symptoms, such as fever, malaise, and myalgias. Other findings include edema extending beyond the area of erythema, skin vesicles, and crepitus.
Vit E deficiency is the correct answer. Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth; this is combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

In cases of vitamin A deficiency, patients can present with night blindness or an inability to see well in dim light. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular, foamy spots on the conjunctiva. The patient may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, and yellow fruits and vegetables.

In cases of pyridoxine (vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory analysis reveals anemia with lymphopenia. Causes include malabsorption, as well as medications (e.g., isoniazid and penicillamine). Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.

In cases of vitamin C (ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to the impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions (e.g., pregnancy and lactation) which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, (e.g., oranges, lemons, and tangerines), as well as tomatoes and potatoes.

Niacin deficiency causes pellagra, which is characterized by:

A symmetrical dermatitis, usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations (e.g., memory impairment, depression, and dementia) which may appear alone or in combination
Causes of niacin deficiency include inadequate dietary intake (especially in patients with corn-based diets or alcoholism). Dietary sources include legumes, yeast, meat, and enriched cereal products.
Vitamin D deficiency
In cases of vitamin D deficiency, children can present with an inability to walk unsupported due to muscle weakness and lower limb skeletal deformities such as genu varum (bow legs) and genu valgum (knock knees). On examination, they may have prominent costochondral junctions (rachitic rosary) and indentation of the lower ribs at their diaphragmatic attachment (Harrison's groove). Causes include inadequate dietary intake and inadequate exposure to sunlight. They should be encouraged to be exposed to ultraviolet irradiation of the skin as well as increase their dietary sources of vitamin D which include fortified milk, fish liver oils, butter, egg yolk, and liver.

In cases of riboflavin (or Vitamin B2) deficiency, patients present with angular stomatitis and cheilosis. On examination, they are pale, have atrophic glossitis, and the tongue may appear magenta.

Vitamin B1 (or thiamine) deficiency results in beriberi, which is characterized by:

A bilateral symmetric peripheral neuropathy beginning in the legs.
Wernicke-Korsakoff syndrome, which is comprised of nystagmus, ophthalmoplegia, ataxia, memory loss, and confabulation.
Congestive heart failure with tachycardia, peripheral edema, and cardiomegaly.

In cases of vitamin K deficiency, patients present with bleeding tendencies, which include epistaxis, menorrhagia, and hematuria. The prothrombin time (PT) and the activated partial thromboplastin time (aPTT) are usually prolonged.

In cases of iron deficiency, patients can present with feeling weak, dizzy, and tired; they may experience syncope. On examination, they have pale conjunctivae and koilonychia.
Pyridoxine deficiency
In cases of pyridoxine or (vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory investigations reveal anemia with lymphopenia. Causes include malabsorption as well as medications, such as isoniazid and penicillamine. Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.

Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

In cases of vitamin A deficiency, patients can present with inability to see well in dim light or night blindness. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities, and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular foamy spots on the conjunctiva. Patient may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, and yellow fruits and vegetables.

Niacin deficiency causes pellagra, which is characterized by:

A symmetrical dermatitis, usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations, such as memory impairment, depression, and dementia. These may appear alone or in combination. Causes include inadequate dietary intake, especially in patients with corn-based diets or alcoholism. Dietary sources include legumes, yeast, meat, and enriched cereal products.
In cases of vitamin C (or ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions, such as pregnancy and lactation, which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, such as oranges, lemons, and tangerines, as well as tomatoes and potatoes.
Vitamin B12
The gastric bypass procedure bypasses the duodenum and much of the jejunum and can lead to malabsorption problems, particularly of vitamin B12, iron, folate, and calcium. The gastric bypass procedure done on morbidly obese patients is an operation that makes the stomach smaller and allows food to bypass part of the small intestine. This bypass of the intestine allows fewer calories to be absorbed, resulting in weight loss, but can also lead to insufficient absorption of some needed nutrients. The deficiency in vitamin B12 leads to problems associated with numbness and tingling of the hands and feet, weakness, fatigue, and anemia. Vitamin B12 is normally absorbed from the digestive system after it binds to a protein called intrinsic factor. An individual lacking intrinsic factor can also develop vitamin B12 deficiency.

Vitamin B12 is required for 2 reactions in humans: the methylation of homocysteine to form methionine and the conversion of methylmalonyl CoA to succinyl CoA. The metabolism of vitamin B12 is tied to folic acid metabolism; therefore, a deficiency in vitamin B12 can lead to a metabolic deficiency of folic acid. This lack of usable folic acid leads to deficiencies in purine and dTMP synthesis. This in turn affects nucleotide synthesis needed for DNA synthesis. Rapidly dividing cells, such as blood cells, are affected, leading to pernicious anemia in the cases of vitamin B12 deficiency. The absorption of biotin, thiamine, and vitamins K are usually less affected by the gastric bypass procedure. A deficiency in vitamin D is also possible but would not cause the numbness in her feet. Deficiencies in vitamin D would manifest themselves in bone and calcium problems.
Intussusception
Intussusception is the telescoping of a segment of intestine into the segment below due to peristalsis. The telescoped segment is called the intussusceptum and lower receiving segment is called the intussuscipiens. The condition commonly occurs in infants and young children, more often in the ileocecal region. Less commonly, ileoileal and coli-colic intussusception occurs. In children, the cause is not known, though enlargement of the lymphoid tissue in terminal ileum has been suggested. In adults, the usual causes are foreign bodies and tumors. The main complications include intestinal obstruction, infarction, gangrene, perforation, and peritonitis. The picture shows cecum, which has been cut open to show the ileum that has intussuscepted inside.

Acute appendicitis, the acute inflammation of the appendix, is the most common acute abdominal condition confronting the surgeon. The most common etiological factor is the obstruction of the lumen that leads to increased intraluminal pressure. This presses upon the blood vessels to produce ischemic injury, which in turn favors the bacterial proliferation and acute appendicitis. Grossly, the appendix is swollen and hyperemic during early stages. The serosa then is covered with fibrinopurulent exudate, called acute suppurative appendicitis. As the disease advances, there is necrosis and ulceration of the mucosa, which extends through the wall so that the appendix becomes soft and friable and the surface shows greenish black gangrenous necrosis (known as acute gangrenous appendicitis). Microscopically, the diagnostic criterion is the neutrophilic infiltration of the muscularis. Clinically, the patient presents with acute abdominal pain. If not adequately managed, complications like peritonitis, appendicular abscess, adhesions, mucocele, and portal pylephlebitis occur.

Meckel's diverticulum is the most common congenital anomaly of the gastrointestinal tract. It occurs in 2% of population, and it is more common in men. It is commonly situated on the antimesenteric border of the ileum, about 1 meter above the ileocecal valve. Meckel's diverticulum is an out pouching containing all the layers of the intestinal wall in their normal orientation. It is usually lined by small intestinal type of epithelium. At times, it may contain gastric mucosa or pancreatic tissue. Meckel's diverticulitis is the common complication of the diverticulum. If not treated, it may lead to perforation and hemorrhage.

Volvulus is the twisting of loop of intestine upon itself through 180 degrees or more. This leads to obstruction of the intestine as well as cutting of vascular supply to the affected region. It is usually due to bands, adhesions, and long mesenteric attachment. The condition affects mainly the sigmoid colon.

Ischemic bowel disease applies to the structural changes in the colon that occur due to deprivation of blood supply. The causes for deprivation of blood could be arterial occlusion, venous occlusion, and non-occlusive ischemia. The causes of non-occlusive ischemia include cardiac failure, shock, dehydration, and vasoconstrictive drugs. Depending on the severity and the presentation, it is classified into transmural, mural and mucosal infarction, and chronic ischemic colitis.

In transmural infarction, there is hemorrhagic infarction of the bowel with gangrenous changes, and a risk of perforation. In the mucosal and mural type, the mucosa is hemorrhagic and oedematous but the remaining layers will remain intact. In chronic ischemia, mucosal ulceration and inflammation develops, and sub-mucosal chronic inflammation and fibrosis may lead to stricture formation. In the setting of transmural infarction, patients generally present with acute abdominal pain, vomiting, fever, and bloody diarrhea. The patient may progress to shock and vascular collapse within hours.
Disaccharidase deficiency
The disaccharidases, of which the most important is lactase, are located in the apical cell membrane of the villous absorptive epithelial cells, the deficiency of which leads to the incomplete breakdown of the disaccharide lactose into its monosaccharides, glucose, and galactose, leading to diarrhea from the unabsorbed lactose. Bacterial fermentation of the unabsorbed sugars leads to increased hydrogen production, which is readily measured in the exhaled air by gas chromatography. There are both hereditary and acquired forms. Histologically in both, there is no abnormality of the mucosal cells of the bowel. Malabsorption is promptly corrected when exposure to milk and milk products is terminated.

Celiac sprue is a rare chronic disease in which there is a characteristic mucosal lesion of the small intestine in the form of blunting of the villi and an overall increase in plasma cells, lymphocytes, macrophages, and eosinophils in the lamina propria. Also known as the gluten-sensitive enteropathy, non-tropical sprue, and celiac disease, it is due to sensitivity to gluten, which is an alcohol soluble, water insoluble protein component called gliadin of wheat and other closely related grains. Detection of circulating anti-gliadin or anti-endomysial antibodies strongly favors the diagnosis. Both the symptoms and the mucosal histology improve on withdrawal of gluten from the diet.

Tropical sprue is a celiac-like disease occurring in people living or visiting the tropics. Bacterial overgrowth by an enterotoxigenic organism is said to be the cause for this disease. Intestinal changes are similar to celiac sprue, but injury is seen at all levels of the small intestine. This is in contrast to celiac sprue, where it is concentrated in the proximal small intestine. It is mainly treated by broad-spectrum antibiotics.

Whipple disease is a rare condition that may involve any organ of the body, but principally affects the intestine, central nervous system, and joints. It is caused by Gram-positive actinomycetes called Tropheryma whippelii. Histologically, the small intestinal mucosa is laden with distended macrophages in the lamina propria. These macrophages contain periodic acid-Schiff positive granules and rod-shaped bacilli by electron microscopy. Patients usually present with a form of malabsorption, including diarrhea and weight loss, and they generally respond to antibiotic therapy.

Amebic dysentery is caused by Entamoeba histolytica, a protozoan, and generally causes diarrhea with blood and mucus. A stool examination will show the cysts and trophozoites of Entamoeba histolytica, which is diagnostic.
Thrombotic microangiopathy
Based on the symptoms in the case, the patient is diagnosed with hemolytic uremic syndrome (HUS). E coli serotype O157:H7, which causes more than 80% of infections leading to HUS, produces shiga-like toxin. Toxin enters the circulation and causes the endothelial injury with the formation of arteriolar and capillary thrombi and red cell fragmentation. Thrombi damage glomerular filtration system in the kidneys and cause kidney failure; therefore, the progressive renal failure in HUS is the result of microangiopathic non-immune hemolytic anemia, and thrombocytopenia and the main mechanism is endothelial injury.

Consumptive coagulopathy,which is also knowndisseminated intravascular coagulation (DIC), is a result of a pathological activation of coagulation cascade that causes intravascular clot formation. Signs and symptoms depend on the organ involved, but the most common is bleeding due to the consumption of platelets and clot factors in the blood. Consumptive coagulopathy is rarely seen in HUS.

Autoimmune mechanism can also cause coagulopathy with bleeding symptoms, but the formation of autoantibodies is not the characteristic of the hemolytic uremic syndrome.

Focal segmental glomerulosclerosis is caused by a variety of factors (infections, inflammations, toxins, hemodynamic and genetics) that cause nephrotic syndrome. Proposed mechanisms are either primary alteration of epithelial cells (idiopathic, viral-associated, drug-induced, and genetic) or secondary to reduction in nephron mass or hemodynamic adaptation (obesity, a single kidney, renal dysplasia/agenesis, reflux nephropathy, sickle cell disease, hereditary nephropathies, and other primary glomerular diseases). It is not characteristic for the HUS.

In acute interstitial nephritis, renal tubular cells dysfunction is caused primarily by a hypersensitivity reaction to drugs or by infection. In hemolytic uremic syndrome, the initial damage is in the vascular endothelium.
Thrombotic microangiopathy
Based on the symptoms in the case, the patient is diagnosed with hemolytic uremic syndrome (HUS). E coli serotype O157:H7, which causes more than 80% of infections leading to HUS, produces shiga-like toxin. Toxin enters the circulation and causes the endothelial injury with the formation of arteriolar and capillary thrombi and red cell fragmentation. Thrombi damage glomerular filtration system in the kidneys and cause kidney failure; therefore, the progressive renal failure in HUS is the result of microangiopathic non-immune hemolytic anemia, and thrombocytopenia and the main mechanism is endothelial injury.

Consumptive coagulopathy,which is also knowndisseminated intravascular coagulation (DIC), is a result of a pathological activation of coagulation cascade that causes intravascular clot formation. Signs and symptoms depend on the organ involved, but the most common is bleeding due to the consumption of platelets and clot factors in the blood. Consumptive coagulopathy is rarely seen in HUS.

Autoimmune mechanism can also cause coagulopathy with bleeding symptoms, but the formation of autoantibodies is not the characteristic of the hemolytic uremic syndrome.

Focal segmental glomerulosclerosis is caused by a variety of factors (infections, inflammations, toxins, hemodynamic and genetics) that cause nephrotic syndrome. Proposed mechanisms are either primary alteration of epithelial cells (idiopathic, viral-associated, drug-induced, and genetic) or secondary to reduction in nephron mass or hemodynamic adaptation (obesity, a single kidney, renal dysplasia/agenesis, reflux nephropathy, sickle cell disease, hereditary nephropathies, and other primary glomerular diseases). It is not characteristic for the HUS.

In acute interstitial nephritis, renal tubular cells dysfunction is caused primarily by a hypersensitivity reaction to drugs or by infection. In hemolytic uremic syndrome, the initial damage is in the vascular endothelium.
99mTc scintigraphy
Lower gastrointestinal bleeding is a common complaint in infants. Diagnosis requires careful exclusion of extraintestinal bleeding sources (e.g. nasopharyngeal or maternal blood ingestion during partum) and of medications or foods that may impart a blood-like appearance to stool such as foods with red food coloring in them (e.g., red jello, etc).

The table below lists the most common etiologies of lower gastrointestinal bleeding in each age group:

Neonates
Bacterial enteritis, milk-protein allergies, anal fissures, intussusception, lymphoid nodular hyperplasia;
Infants
Intussusception, esophagitis, gastritis, duodenitis, ulcers, colonic polyps, anorectal disorders, Meckel's diverticulum, infectious diarrhea, volvulus, bowel duplication;
Children
All the above conditions; duodenal ulcer, Mallory-Weiss tears
Henoch-Schönlein purpura.
In a chronically bleeding patient without signs of anorectal disease, evaluation should start with contrasted radiography (barium swallow, upper GI series, small-bowel follow-through, or barium enema). These radiographs may reveal foreign bodies, mucosal lesions such as ulcers, esophagitis, or inflammatory bowel disease; congenital anomalies such as volvulus, duplication, and malrotation. However, colonoscopy has higher sensitivity for detecting lower gastrointestinal bleeding and enjoys an overall success rate of 80%.

The combination of a diverticulum in the distal ileum and rectal bleeding in an infant is strongly suggestive of Meckel's diverticulum. Another feature associated with this disease is passage of maroon or brick-red stools. A 99mTc scan (Meckel scan) is the examination of choice for locating this lesion.

Meckel's diverticulum is a remnant of the omphalomesenteric duct. It's present in 1-2% of the general population, and is the most common congenital anomaly of the small bowel. Most diverticula are asymptomatic, but a small percentage ulcerates because of acid-producing ectopic gastric mucosa and causes rectal bleeding. Perforation and peritonitis may also occur. Treatment is surgical.
use of ppi
This patient is presenting with Barrett's esophagus, a type of chronic esophagitis in which the normal squamous epithelium is replaced with columnar epithelium. Barrett's esophagus is a complication of chronic gastroesophageal reflux disease (GERD) and can develop into esophageal adenocarcinoma. Use of proton pump inhibitors (PPIs) reduces the risk of cancer. In order to monitor for the development of cancer, a routine endoscopy should be periodically performed in patients with known Barrett's esophagus.

While the antacids are not necessarily adequate to control the GERD and damage to this patient's esophagus, avoidance of antacids will have no role in prevent subsequent Barrett's esophagus complications, such as adenocarcinoma.

While the acid reflux appears to be a major mechanism for damage to the esophageal tissue, anti-reflux surgeries do not appear to prevent complications from Barrett's esophagus and subsequent development of adenocarcinoma. This patient does not need referral for fundoplication (surgical 'wrapping' of the stomach around the esophagus).

Regular exercise would be helpful for this patient in general terms for cardiovascular health and weight reduction. However, exercise does not play a significant role in reducing risks for Barrett's esophagus complications.

Obesity is a risk factor for development of Barrett's esophagus. (Other risk factors include male gender, smoking, and especially chronic GERD.) Once Barrett's esophagus has developed, however, weight loss does not dramatically alter the risk of complications, such as adenocarcinoma. Weight loss should be recommended for any obese patient, but the PPIs are the best approach to reduce complications from his Barrett's esophagus.
A 53-year-old man presents with a 2-day history of jaundice and malaise. His history is significant for mucosal candidiasis, for which the patient is on oral ketoconazole 200 mg daily for the past 3 weeks. He occasionally has headaches, and sometimes takes paracetamol in a daily dose of 1 gram to achieve headache relief. Two weeks before the appearance of symptoms, the patient was treated with flucloxacillin for respiratory tract infection. Except for the appearance of jaundice and malaise, the patient denies the presence of any other symptoms, and the remainder of his personal history is unremarkable.

Physical examination reveals a mildly jaundiced patient, 180 centimeters tall, 82 kilograms in weight. His blood pressure is 110/86 mmHg, and the remainder of his general physical examination revealed no abnormalities.

Laboratory analyses reveal the presence of hyperbilirubinemia and elevated serum transaminases, normal alkaline phosphatase and γ-Glutamyl transferase levels. Other routine laboratory analyses reveal no abnormalities.

Serological testing does not reveal the presence of antibodies against human immuno-deficiency, hepatitis A, C, D and E, or viruses in patient's serum. Also, HBsAg, anti-HBs or anti-HBc antibodies are not present in patient's serum. Anti-LKM-1, antinuclear, anti-thyroid, antimitochondrial, and anti-smooth muscle antibodies are absent.



Question
What is the most likely cause of liver dysfunction in this patient?

Answer Choices
1 Paracetamol-induced hepatitis
2 Primary sclerosing cholangitis
3 Ketoconazole-caused hepatitis
4 Flucloxacillin-induced hepatitis
5 Primary autoimmune hepatitis
ketoconazole induced hepatitis
Ketoconazole is an antifungal imidazole used in treating systemic mycoses. The common adverse effect of ketoconazole is hepatotoxicity. The severity of ketoconazole-induced hepatotoxicity is linked to the exposure level of the drug. Ketoconazole-induced hepatotoxicity is probably mediated through a reactive metabolite N- deacetyl ketoconazole (DAK). The latter appears to be the major metabolite, which is a hepatic cytotoxic. Ketoconazole administration results in a significantly dose-dependent increase in serum transaminase activities, as well as cloudy swelling, ballooning degeneration and centrilobular confluent necrosis of the hepatocytes. The histological feature ranges from acute hepatitis to confluent centrilobular, or massive necrosis.

Paracetamol hepatotoxicity is dose-related (i.e., signs of liver dysfunction appear only when a high dose of paracetamol, which exceeds liver metabolizing capacity for this drug, is taken). In such a case, toxic intermediary metabolites do accumulate, causing liver damage. It is considered that a daily paracetamol dose of 10 - 15 mg/kg may be considered as a safe, therapeutic dose. Therefore, liver dysfunction, in the presented case, is not the result of paracetamol-induced hepatitis.

Primary sclerosing cholangitis is frequently accompanied with elevation of serum alkaline phosphatase, and gamma-glutamyl transferase levels. Since increased serum levels of those enzymes are not noted in the presented case, it is unlikely that the patient suffers from primary sclerosing cholangitis.

Flucloxacillin administration causes cholestatic hepatitis (i.e., liver dysfunction in patients with flucloxacillin-induced hepatitis is associated with elevated alkaline phosphatase and gamma-glutamyl transferase levels, as well as with disproportionate rise of conjugated serum bilirubin level). Since hepatitis in the presented patient is not of cholestatic type, it is unlikely that he suffers from flucloxacillin-induced hepatitis.

Autoimmune hepatitis is characterized with the appearance of auto-antibodies, including liver kidney microsomal (LKM) antibodies. LKM antibodies in patients with genuine (primary) autoimmune hepatitis are of LKM1 type, not of LKM2 type.
ultrasound of the abdomen
Based on the patient's history, cholelithiasis is suspected. This condition is more common in females of Caucasian or Hispanic descent than in others. The incidence increases with age. Most (80%) of the stones in the US are the cholesterol type. Bilirubin, pigment, and calcium stones constitute the other 20%. Cholelithiasis may be asymptomatic (the presence of gallstones without symptoms), symptomatic (biliary colic), or complicated (e.g. cholecystitis, choledocholithiasis, cholangitis).

Ultrasonography is a safe, reliable, and non-invasive test that can be performed at the bedside and is also safe in pregnant women. It is quite sensitive and specific for stones larger than 2 mm.

Only about 10-30% gall stones are radio-opaque and hence abdominal X-ray may not be so useful. The oral cholecystogram is the X-ray taken after administering contrast medium to the patient. Although it can identify gall bladder pathology, it requires preparation and is not as convenient as the ultrasound. CT scan is not the first choice in suspected gallstones, although it may prove useful in intrahepatic stones. Biliary scintigraphy is of value in cystic duct obstruction. MRI is also an excellent choice but is expensive, requires sophisticated equipment, and is not used as the first choice investigation in most centers.

Symptomatic stones are treated with cholecystectomy. Asymptomatic stones may also require surgery under special circumstances such as large (>2 cm) stones, those with spinal cord injuries affecting the abdomen, and in calcified gall bladder.
ELISA for C diff
Antibiotic-associated colitis is an important complication of antibiotic use, and is estimated to occur in 1% of hospitalized patients. The etiologic agent is Clostridium difficile, a Gram-positive bacillus that colonizes the bowel of 2-3% of healthy adults.

Antibiotic use, particularly clindamycin, penicillins, and cephalosporins, can lead to proliferation of C. difficile. This organism produces 2 toxins, termed A (enterotoxic) and B (cytotoxic), which cause colitis. The most common symptoms are watery diarrhea and abdominal pain. Patients with severe disease can have intense diarrhea, with up to 30 stools per day, low-grade fever, and abdominal pain. A minority of cases progress to severe colitis and toxic megacolon.

An ELISA assay for C. difficile toxin is one of the most popular tests for diagnosing C. difficle colitis because it yields rapid results (usually within 24 hours). It is highly specific (99%), but obtaining maximum sensitivity may require repeat testing. The estimated sensitivity of ELISA testing is 60-95%. An alternative to ELISA is PCR analysis for toxic. Compared to ELISA, PCR has a relatively higher sensitivity.

Common antigen testing tests for GDH, an enzyme that is specifically produced by the C. difficle organism. This test is sometimes used to screen samples with follow-up toxin assays performed on positive samples. It is not a routine first-line test for the diagnosis of C. difficle colitis.

Anaerobic culture for C. difficile take a long time, is costly, and is primarily reserved for epidemiological purposes.

Fecal leukocytes have low sensitivity for antibiotic-associated colitis and are found in only 50% of cases.

Sigmoidoscopy or colonoscopy may be used as an adjunct to laboratory diagnosis in certain settings, such as when there is a high clinical suspicion of C. difficle colitis despite a negative toxin assay. It should be emphasized that endoscopic bowel examinations are more dangerous in patients with megacolon and should be used carefully if this complication is suspected.
Cholangitis
Cholangitis is the most common cause of pyogenic liver abscess. Biliary pathologies are the most common predisposing cause of pyogenic liver abscess and accounts for 60% of the cases.

The etiological classification of bacterial abscess of the liver (pyogenic liver abscess) is made on the basis of the route by which infection reaches the liver. There are 5 mechanisms:

Pylephlebitis is the inflammation of the portal vein or any of its branches. Portal bacteremia [via portal vein] from an intra-abdominal site, such as diverticulitis, suppurative appendicitis, and infected carcinoma of the colon, especially after resection, ulcerative colitis, inflamed hemorrhoids, typhoid, and paratyphoid fever.
Along the bile ducts, causing ascending cholangitis in a biliary tract partially or completely obstructed by stone, tumor, or stricture.
Systemic bacteremia originating in a distant location, with organisms reaching the liver via the hepatic artery; causes enumerated can be septicemia and pyemia, endocarditis, pyelonephritis, and infection of the hydatid cyst.
Direct extension from an adjacent infection outside the biliary tract, such as from a sub-diaphragmatic abscess, from an empyema thoracis, and from trauma, either penetrating (with direct implantation of bacteria into the liver) or blunt, causing a hematoma that becomes secondarily infected.
From the umbilicus along the umbilical vein of the newborn and along the paraumbilical veins.
A cause is usually obvious, but sometimes the abscess is unexplained. Although most abscesses are single, multiple (usually microscopic) abscesses are common with systemic bacteremia or complete biliary tract obstruction. Prompt antibiotic treatment, with agents such as meropenem, imipenem, and cefuroxime, followed by percutaneous drainage, form the essential components of treatment.

Biliary tract diseases account for 60% of the pyogenic liver abscess cases. Systemic bacteremia accounts for 15% of the cases. 24% of the pyogenic liver abscesses can be attributed to pylephlebitis. Direct extension from an adjacent infection like sub-phrenic abscess accounts for 4% of the cases.
hypervitaminosis A
Very large doses of the fat-soluble vitamins are definitely toxic. Acute vitamin A intoxication was first described by Arctic explorers, who developed headache, diarrhea, and dizziness after eating polar bear liver. The liver of this animal is particularly rich in vitamin A. Nausea, vomiting, papilledema, and lethargy may be seen in acute toxicity.

Chronic toxicity can occur when a person consumes 50,000 units per day for 3 months or more. Mouth sores may also be seen as an early manifestation along with those mentioned in the question. Hypercalcemia, increased intracranial pressure with papilledema, and decreased cognition may be seen in more serious cases. Hepatomegaly leading to cirrhosis may occasionally occur. Excessive vitamin A has also recently been related to increased risk of hip fracture.

Elevated vitamin A in the blood is the only clue to the diagnosis. Elimination of vitamin A from the diet usually results in rapid recovery.

Large doses of water-soluble vitamins (C and B) have been thought to be less likely to cause problems because they can be rapidly cleared from the body; however, it has been demonstrated that ingestion of large doses of vitamin B6 can produce peripheral neuropathy and large doses of niacin (B3) may cause skin flushing.

Very large doses of vitamin C can cause gastric irritation, flatulence, or diarrhea. There is a theoretical risk of oxalate stones, as oxalate is metabolized by vitamin C; however, not many such cases have been reported.

Vitamin E is the least toxic of the fat-soluble vitamins. Large doses taken over extended periods of time have not produced toxicity, except for a few GIT disturbances.
Prescribe Ursodiol
Both morbid obesity and rapid weight loss are risk factors for development of cholecystitis. Gallstones may be present within the gallbladder and remain asymptomatic, or the gallbladder walls may become inflamed, resulting in cholecystitis. Ursodiol is approved for prevention of gallstones in obesity patients with rapid weight loss. It would be the best choice in health maintenance and delaying or preventing need for surgical cholecystectomy.

Orlistat is a prescription medication approved for treatment of obesity. Its mechanism is to block fat absorption. It does not have a direct role in health maintenance or prevention of cholecystitis or cholelithiasis. In fact, it has pronounced gastrointestinal side effects.

Over-the-counter omeprazole is a commonly used proton-pump-inhibitor (PPI); it is helpful in acid lowering in the stomach and treatment of gastroesophageal reflux disease. It has not been shown to help gallbladder disease, and there is some evidence that PPIs may worsen it.

Reducing the patient's exercise may aggravate her condition and negatively impact her weight loss. Exercise has an inverse relationship with cholecystitis and rates of cholecystectomies, so this patient should be encouraged to continue frequent exercise.

This patient should not be instructed to restrict caloric consumption further. She is already losing weight quite rapidly at around 4 pounds per week. Her daily caloric intake is low; recommending further restriction will likely discourage her, and there will not be any benefit in regard to her gallbladder disease.
Zinc
This patient most probably has a zinc deficiency. The causes of zinc deficiency include malnutrition, chronic debilitating diseases, chronic renal disease, alcoholism, drugs such as penicillamine and diuretics, and genetic disorders, such as sickle cell disease. Clinical manifestations in severe cases include alopecia, diarrhea, weight loss, infections, dermatitis, hypogonadism in men, and intercurrent infections. Supplementation with zinc is the treatment of choice.

Niacin (nicotinamide, nicotinic acid) deficiency is uncommon in the United States. It is often found in people who live on a diet that consists mainly of corn. Deficiency may also result from alcoholism, cirrhosis, or diarrhea. Men and women are affected equally. Symptoms of niacin deficiency include nausea, vomiting, diarrhea, rash, glossitis, stomatitis, depression, and psychosis. Niacin deficiency, also known as pellagra, manifests as the '3 Ds': diarrhea, dermatitis, and dementia. If this diagnosis is suspected, supplemental niacin should be given immediately. Some patients deficient in niacin may also be deficient in other vitamins, such as B vitamins, so they should be given that as well.

Folate deficiency causes megaloblastic macrocytic anemia, as folate plays a key role in nucleic acid synthesis. The early manifestation of folate deficiency, especially in its suboptimal state, predisposes to occlusive vascular disease and thrombosis. These manifestations are linked to increased homocysteine levels found in folate deficiency. Neurological and immunological disturbances may also be seen. Folate replacement is the option to prevent and to treat the deficiency.

Vitamin B1 (or thiamine deficiency) causes beri beri, occurring mostly in the malnourished and alcoholics. The deficiency manifests with acute heart failure, neurologic deficits, and epilepsy. Empiric use of thiamine and prophylactic use in high-risk population is strongly recommended even before blood reports are obtained, as the treatment is inexpensive and prevents major catastrophes.

Vitamin B12 or cobalamin deficiency manifests as megaloblastic macrocytic anemia, pancytopenia, and a spectrum of neurological disorders such as peripheral neuropathy, parasthesias, and demyelination of corticospinal tract. Nutritional deficiency, alcoholism, and malabsorption syndromes are some causes of B12 deficiency. It also is associated with homocystenemia and atherosclerosis. Diagnosis is by serum estimation of B12, and oral supplementation is safe and effective, but intramuscular injections may also be used.
Chronic Pancreatitis
Pancreatitisis an inflammation or infection of the pancreas.

Chronic pancreatitis, which is the correct response, is caused by alcohol abuse, hemochromatosis (a condition of excess iron in the blood), and other unknown factors. Inflammation and fibrosis cause the destruction of functioning glandular tissue in the pancreas. This results in an inability to properly digest fat caused due to a lack of pancreatic enzymes. The production of insulin is also affected. Symptoms include abdominal pain (mainly in the upper abdomen), nausea, vomiting, weight loss, and fatty stools. Additional symptoms may include swelling (overall), stools (clay colored), and abdominal indigestion. Tests should include serum lipase (may be elevated), serum amylase (may be elevated), serum trypsinogen (may be low), and fecal fat test (shows fatty stools). Abdominal ultrasound and CT may show an enlarged pancreas. Treatment of chronic pancreatitis includes reducing pancreas stimulation, alleviating fat indigestion, reducing pain, and treating diabetes. A reduced-fat diet, vitamin supplementation, no alcohol or caffeine, and regulation of blood sugar levels are indicated in the treatment.

The chief causes of acute pancreatitis in adults are gallstones, other biliary disease, and alcohol use. Viral infection (mumps, Coxsackie B, mycoplasma pneumonia, and Campylobacter), injury, pancreatic or common bile duct surgical procedures, and certain medications (especially estrogens, corticosteroids, thiazide diuretics, acetaminophen, tetracycline) are other causes. After the triggering event, the process continues with autodigestion that causes swelling, hemorrhage, and damage to the blood vessels. An attack may last for 48 hours. Symptoms include abdominal pain (mainly located in the upper abdomen) nausea, vomiting, weakness, sweating, anxiety, fever, clammy skin, and mild jaundice. General examination may show a low blood pressure and a heart rate above 90. Most cases resolve within a week with supportive measures, such as analgesics and fluid replacement. However, some cases can be life threatening.

Pancreatic abscess occurs in 5 to 10% of people with acute pancreatitis. An abscess may be caused by inadequate drainage of a pancreatic pseudocyst, which is a complication associated with pancreatitis. Symptoms include fever, chills, abdominal pain, and abdominal mass. Physical exam will show signs of pancreatitis, and tests should include an abdominal CT and ultrasound. Treatment will include laparotomy with drainage and possible resection of dead tissue.

Pancreatic cancer is the 4th most common cancer causing death in the U.S. The disease is more common in men, especially those between 60 and 70 years. The cause is unknown; however the incidence is greater in smokers. A high fat diet and chemical exposures may increase the risk. Symptoms include weight loss, abdominal pain, loss of appetite, jaundice, nausea, weakness, fatigue, vomiting, diarrhea, indigestion, back pain, stools (clay colored), pallor, and depression. Tests should include a pancreatic biopsy, an abdominal CT scan, and abdominal ultrasound. Only 20% of the tumors are operable at the time of diagnosis. Palliation is generally the treatment, along with chemotherapy and radiation.

Insulinomas are generally benign tumors of the insulin-secreting cells of the pancreas, which secrete excess amounts of insulin. Risk factors include a prior history of multiple endocrine neoplasia Type I (MEN I). Symptoms include sweating, tremor, rapid heart rate, anxiety, hunger, dizziness, headache, clouding of vision, confusion, behavioral changes, convulsions, and loss of consciousness. Surgery is the treatment of choice to remove the tumor. If the tumor is not found during surgery, diazoxide may be given. A diuretic is always given with this medication to avoid retaining too much salt.
A 33-year-old woman presents seeking advice. She is concerned regarding the appearance of spider angiomas that are present on her trunk and face. She states that spider angiomas appeared during pregnancy and that they persist now, 9 months after delivery. Before pregnancy, she was treated with imipramine because of depression and she is currently still taking this drug. She denies alcohol intake, however she tells you that 3 years ago, she had acute infection with hepatitis C virus. She was also frequently treated with flucloxacillin during the past couple of years for recurrent respiratory tract infections. In addition, she started taking oral contraceptives after delivery. The remainder of her personal history is unremarkable.

Physical examination reveals the presence of multiple spider angiomas on the patient's face, forearms, and back. The remainder of the patient's general physical findings are unremarkable.

Routine laboratory analyses reveal normal AST (26 IU/l, reference values 8 to 27 IU/l) and ALT (22 IU/l, reference value 8 to 23 IU/l) levels. Alkaline phosphatase level is normal (43 IU/l, reference value 23-71 IU/l) and other routine laboratory analyses reveal no abnormalities. HbSAg, HbeAg, and antiHbc antibodies are not present in patient's serum. IgG antibodies to hepatitis C are present, but testing for hepatitis C virus (HCV) does not reveal the presence of HCV RNA in patient's serum.



Question
What is the most likely cause of the patient's spider angiomas?

Answer Choices
1 Flucloxacillin-induced hepatitis
2 Imipramine-induced hepatitis
3 Oral contraceptives
4 Chronic hepatitis caused by hepatitis C virus
5 Pregnancy-related appearance
OCP
The most likely cause of this patient's spider angiomas are Oral contraceptives. In conditions when estrogen hormones are present in excess such as during pregnancy, contraceptive intake, or liver disease (due to decreased degradation of estrogens), the surplus of estrogens cause the appearance of spider nevi.

In pregnant women, spider angiomas appear from the second to fifth month of pregnancy and disappear in a short period of time (within 2 months) after the delivery. Since in the presented case, spider angiomas are present for a longer period of time, it is unlikely that they are pregnancy-related.

In untreated patients with acute Hepatitis C, disease evolves towards chronicity in about 80% of patients, while only about 20% of patients recover completely. Patients who have chronic hepatitis C also have HCV RNA in their serum, but those who have recovered completely have no HCV RNA in serum and have IgG antibodies against hepatitis C virus as the marker of past hepatitis C infection. As the presented patient satisfies criteria for the patient who had hepatitis C in the past, her spider angiomas are not related to chronic hepatitis C infection.

Imipramine seldom causes liver damage. In addition, hepatitis caused by imipramine administration is of a cholestatic type, i.e. it is associated with increased serum levels of transaminases and alkaline phosphatase. Since the alkaline phosphatase level in the presented patient is normal, imipramine-induced hepatitis is not likely.

Similar to imipramine, hepatitis caused by flucloxacillin administration is also of a cholestatic type. For the reasons presented above, the possibility of flucloxacillin-induced hepatitis is also unlikely.
wireless capsule endoscopy
Wireless capsule endoscopy is performed by ingestion of a battery-powered capsule containing a camera and a transmitter. The capsule transmits images to sensors outside the patient during its transit in the gastrointestinal tract. Indications for capsule endoscopy are still evolving, but several series have shown that capsule endoscopy is more sensitive than small bowel radiography or push enteroscopy for locating the source of small-bowel bleeding. The most common etiologies of bleeding in this region are angioectasia and Crohn's disease. Several other small bowel lesions, such as tumors (leiomyoma, lymphomas, carcinoids, or carcinomas), varices, and polyps, have also been described.

An important concern is the possibility of capsule impaction and small bowel obstruction. Some centers are reluctant to perform capsule endoscopy in patients with partial or intermittent obstruction of the small bowel. However, capsule impaction may reveal the site of a lesion and allow its surgical removal, obviating the need for intraoperative enteroscopy. Other relative contraindications are incapacity of cooperating with the examination (e.g. dementia), swallowing disorders, esophageal stricture, gastroparesis, and poor surgical risk. In patients with obstruction or gastroparesis, the examiner may place the capsule endoscopically.

This patient has no signs of ulcer activity. Therefore, biopsy of the duodenal scar is not indicated.

A 99mTc scan is the test of choice for Meckel's diverticulum, a remnant of the embryonic omphalomesenteric duct found in 1.5% of the general population. Its most common location is the antimesenteric border of the mid-to-distal small bowel. Some diverticula contain ectopic, acid-producing gastric mucosa. Therefore, they can ulcerate and bleed. Rectal bleeding caused by Meckel's diverticulum is often maroon or brick-red in color, and its incidence decreases with age. Therefore, this diagnosis is unlikely in this case.

Angiography can be used if other less invasive procedures (i.e. small bowel radiography, push enteroscopy, or small bowel radiography) are non-diagnostic.

Computed tomography is not indicated in the absence of other symptoms indicating a specific etiology (e.g. a palpable mass or suspicion of pancreatic disease).

Of note, colonoscopy after rapid oral purging has emerged as the procedure of choice for the evaluation of acute lower GI bleeding, and it also provides a means for therapy. Scintigraphy and/or angiography also play important roles in diagnosis and embolization when colonoscopy reveals negative findings or when it is not feasible.
If the fluid has a protein concentration below 3 g/dL
The correct response is if the fluid protein concentration below 3/dL.

After the diagnosis of ascites is made by physical examination, all patients with new-onset ascites should undergo abdominal paracentesis and ascitic fluid analysis. The most important tests to order for fluid analysis include protein concentrationand cell count.

Fluids with protein concentration above 3 g/dL are designated as exudates. Those with values below 3 g/dL are designated as transudates. Diseases usually associated with transudates include congestive heart failure, cirrhosis, constrictive pericarditis, inferior vena cava obstruction, hypoalbuminemia, Meigs syndrome, and some cases of nephrotic syndrome.

The amount of albumin in the ascitic fluid compared to the serum albumin (the Serum Ascites Albumin Gradient, SAAG) can be indicative of the cause of ascites. Ascites related to hypertension, cirrhosis, or congestive heart failure generally shows a SAAG greater than 1.1 g/dL.

Exudates are more commonly seen with peritoneal neoplasm, pancreatic ascites, myxedema, and tuberculous peritonitis. A large number of red blood cells in the fluid or grossly bloody ascites suggests a diagnosis of neoplasm.

An acidic fluid and leukocyte count of more than 500/mm3 strongly suggests a peritoneal infection or inflammatory process. Other tests that should be ordered in the appropriate clinical setting include cytologic examination, lactic dehydrogenase (LDH), specific tumor markers, glucose, and cultures for bacteria, mycobacteria, and fungi.
copper metabolism
This young man is suffering from Wilson's disease, a genetic disorder of copper metabolism. It is inherited as an autosomal recessive mutation in the ATP7B genes located on chromosome 13. The protein of the ATP7B gene is a copper-transporting ATPase. The frequency of the heterozygous carriers is relatively high (1/90). The incidence of homozygous recessive affected individuals is about 1/30,000. It affects all ethnic groups and both sexes equally.

Neurological symptoms, hepatitis, and Kayser-Fleisher rings, greenish-brown deposits of copper in the corneal endothelial (Descemet membrane) basement membrane near the peripheral cornea where it meets the iris (limbus), are characteristic of Wilson's disease.

About 40% of the dietary copper is absorbed in the gastrointestinal tract, and makes its way to the liver bound to albumin. In the liver, it is complexed with ceruloplasmin, a blood protein that carries most of the copper. Ceruloplasmin levels are abnormally low in patients with Wilson's disease, although the disease is not, per se, a mutation in the ceruloplasmin gene. Ceruloplasmin is recycled in the liver by the usual lysosomal degradation pathway, and the unused copper is excreted in bile. When excessive copper is absorbed in the gut, it accumulates in the brain (producing neurological symptoms), the liver (producing hepatitis and hepatomegaly), and the cornea. Penicillamine can be used to treat this disease. It chelates copper and provides some symptomatic relief. Unfortunately, when used appropriately in pregnant women to treat potentially life-threatening Wilson's disease, it is harmful to the fetus and can produce cutis laxa in the newborns of penicillamine-treated patients
Hepatocellular carcinoma
This patient has signs and symptoms consistent with hemochromatosis, which is associated with hepatocellular carcinoma. Hemochromatosis is due to an increase in iron within the tissues. Hemochromatosis is a disorder of iron overload; it could be due to genetic or non-genetic causes. In hereditary hemochromatosis, there is absorption of a few milligrams of iron each day, in excess of need. As such, clinical manifestations often occur only after the age of 40 years, when body iron stores have reached 15 to 40 g. The symptoms of hemochromatosis are nonspecific and include arthralgia; abdominal pain; fatigue, weakness; impotence; weight loss; amenorrhea and early menopause; abnormal skin pigmentation; damage to the pancreas leading to diabetes; cardiomyopathy; and cirrhosis. The liver is commonly affected with hemochromatosis, and hepatosplenomegaly is commonly seen. There is an abnormal skin pigmentation that is seen with hemochromatosis. In hemochromatosis, the plasma iron will be elevated; total iron binding capacity will be normal or low; and transferrin saturation will be elevated.

Hepatocellular carcinoma is the most serious complication, and it is a major cause of death in patients with hemochromatosis. A large percentage of patients with hemochromatosis will develop problems with their pancreas; however, the pancreatic pathology commonly seen with hemochromatosis is insulin dependent diabetes, not pancreatic cancer.

Bronchogenic carcinoma, pancreatic carcinoma, lymphoma, and leukemia are not known complications of hemochromatosis.
Niacin
Niacin deficiency causes pellagra, which is characterized by:A symmetrical dermatitis, usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations, such as memory impairment, depression, and dementia. These may appear alone or in combination. Causes include inadequate dietary intake, especially in patients with corn-based diets or alcoholism. Dietary sources include legumes, yeast, meat, and enriched cereal products.
Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

In cases of vitamin A deficiency, patients can present with inability to see well in dim light or night blindness. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities, and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular foamy spots on the conjunctiva. The patient may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, as well as yellow fruits and vegetables.

In cases of vitamin C (or ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions, such as pregnancy and lactation, which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, such as oranges, lemons, and tangerines, as well as tomatoes and potatoes.

In cases of pyridoxine or (vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory investigations reveal anemia with lymphopenia. Causes include malabsorption as well as medications, such as isoniazid and penicillamine. Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.
Niacin Deficiency has been linked to pellagra. This condition, now quite rare, consists of nausea with vomiting, diarrhea, dermatitis, and cognitive decline (such as irritability and memory loss). Vitamin B6 (pyridoxine) deficiency and excess has been associated with neurological disease. Both lead to a distal symmetrical polyneuropathy. A deficiency of B6 is commonly found in patients taking INH, an anti-tuberculosis drug. INH inhibits pyridoxine phosphorylation, thereby decreasing the concentration of the active compound-pyridoxal phosphate. Excessive use of B6 leads to an excess of pyridoxine, which competes with pyridoxal phosphate for binding sites on the enzyme. Vitamin B12 deficiency causes both a peripheral neuropathy and a degeneration in the spinal cord known as subacute combined degeneration. This affects the dorsal column sensory functions (position sense and vibration) and the lateral corticospinal tract. The resulting symptoms include paresthesias of the feet and hands with subsequent weakness and stiffness of the legs and a spastic gait.

Vitamin B1 (Thiamine) deficiency has been linked to the neurological syndrome of Wernicke's encephalopathy. This condition, although often associated with alcoholism, is a true nutritional deficiency, causing neuropathological lesions in areas such as the thalamus, mammillary bodies, and the periaqueductal areas. A polyneuropathy has also been linked to Vitamin B1 deficiency, especially in alcoholism. This deficiency plays at least a role in the development of this disease, along with the possible neurotoxic role of alcohol.

Vitamin E deficiency occurs usually with malabsorption of the fat-soluble vitamins A, D, E, and K. This can occur with conditions such as cholestatic liver disease or celiac disease. Neurological symptoms include a peripheral neuropathy and spinocerebellar degeneration. The spinocerebellar degeneration can occur as a defect in abetalipoproteins, as occurs in Bassen-Kornzweig syndrome. This is also associated with acanthocytes and retinitis pigmentosa.
A 27-year-old man is seen for evaluation of a small mass in his right groin. His history reveals that this mass has been present for about 2 years, but he has suddenly been motivated to seek medical evaluation by his wife who has fears of cancer. He believes he 1st became aware of the mass when getting dressed, and notes occasional aching in the right groin. He denies trauma to the region.

His past medical history is significant for chronic low back pain, secondary to a motor vehicle accident (MVA) 9 years ago. He takes over-the-counter ibuprofen as needed, and has no known drug allergies.
He has had a tonsillectomy, appendectomy, and L4-L5 fusion, post-MVA. There is a family history of lung cancer in his paternal grandfather and diabetes in his maternal grandparents. The patient smokes, but denies alcohol and illicit drugs. He is married with 3 children, but admits to >10 sex partners previous to marriage. He works as a pipe fitter, which involves heavy lifting and frequent bending.

His physical exam is as follows: BP 115/80, pulse 72, temp 98.0 degrees, weight 190 pounds, and height 69".

Inspection of the patient in the supine position reveals no visible mass in the right inguinal region, corresponding with his description. There is no erythema or swelling in either inguinal region or abdomen. Abdominal exam reveals no tenderness, masses, hepatosplenomegaly, acites, or bruits. Inspection of the scrotum and penis shows no lesions, erythema, or tenderness. The patient is asked to stand for a testicular exam, which reveals normal-sized testes without nodules or masses. With a finger placed in the inguinal ring an impulse is felt on the right, but not on the left, when the patient is asked to cough.

Although many conditions comprise the differential for a mass in the groin, you suspect he has an inguinal hernia.



Question
What aspect of this patient's history or physical is most specific to the diagnosis of hernia?

Answer Choices
1 Absence of fever
2 Chronic nature of the mass
3 History of heavy lifting
4 History of multiple sex partners
5 Impulse felt with cough
6 Unilateral groin mass
Impulse felt with cough
The impulse the examiner felt with the cough most strongly supports the diagnosis of hernia; this is a classic finding associated with inguinal hernias. Other conditions in the differential would be much more likely to present as an inguinal mass that does not come and go with straining, coughing, or Valsava maneuvers. The individual's history and exam are most consistent with the indirect type of inguinal hernia, but distinguishing direct versus indirect does not significantly change management.

While absence of fever may help to exclude acute infectious etiology (e.g., epididymitis, orchitis, and cat-scratch disease), the differential of a groin mass in an afebrile patient still includes malignancy, hydrocele, varicocele, as well as hernia.

The chronic nature of this patient's mass helps the examiner focus away from the acute scrotal emergencies, such as testicular torsion and infectious conditions. Patients with hernias may exhibit either chronic or acute presentations. Other items on the chronic groin mass differential include malignancy, undescended testes, and dermatologic conditions; the acute versus chronic course of the complaint is not helpful in fully narrowing the differential.

While long-term heavy work seems to have an association with groin hernia, this patient's history of heavy lifting is not specific enough upon which to base the diagnosis of hernia.

The patient's history of multiple sex partners would be associated with a risk for epididymitis or orchitis. This aspect of the patient's history does not support the suspected diagnosis of inguinal hernia.

Unilateral groin mass suggests a very broad differential (e.g., lymphadenopathy, scrotal mass, vascular mass, and infectious processes). This aspect of the patient's history does not narrow the differential to hernia alone.
PPIs
The correct response is oral proton pump inhibitor.

The patient in this presented scenario is showing signs and symptoms that are most consistent with esophageal dysphagia. Difficulty swallowing is the main complaint and is typically caused by 1 of 2 entities: localized neuromuscular disorders or obstructive lesions. Our patient specifically is showing issues of diffuse esophageal spasm. This is a motility disorder that is defined by simultaneous uncoordinated contraction of several esophageal segments. This can lead to potentially retrosternal pain and is worsened or precipitated by acid reflex, rapid eating, stress/anxiety, and hot/cold food. The dysphagia found in these patients is intermittent, non-progressive and does not cause weight loss. These patients have no documented abnormality in the distribution of myenteric neurons, normal lower esophageal sphincter relaxation, and no evidence of obstruction. All of these components are consistent with the patient described.

In terms of a first-line treatment, acid suppression with a proton pump inhibitor (PPI) is the first-line pharmaceutical intervention that should be initiated. Sublingual nitroglycerin and calcium channel blockers may also be considered as treatment, but they are not typically considered first-line options.

Botulinum toxin is not considered first-line treatment for diffuse esophageal spasms; it may be considered to be administered/injected in the lower esophageal sphincter and lower esophagus to reduce chest pain caused by diffuse esophageal spasm but again is not the first line treatment. Also, the patient described above is experiencing other symptoms, not just the chest pain. Prokinetic agents, such as metoclopramide, are considered treatment options for reflux esophagitis and Barrett esophagus-related causes of dysphagia. Oral corticosteroids may be considered in patients with diagnosed eosinophilic esophagitis.
Fecal Impaction
This patient's diagnosis is a rectal impaction; the attached X-ray displays colonic distension due to fecal impaction. Risk factors include being elderly, immobile, having a spinal cord injury, chronic use of opioids, hypothyroidism and a low fiber diet. Dilated bowel as well as a large amounts of stool may be visible via radiography. Impaction may also occur due to primary colorectal disorders, such as obstruction, slow colonic motility, outlet obstruction, Hirschsprung's disease in children, and Chagas' disease.

Adenocarcinomas, the most common form of rectal cancer, most commonly present with rectal bleeding. Other signs and symptoms include a change in bowel habits, often in the form of diarrhea, occult bleeding, tenesmus, and a feeling of incomplete evacuation. Other manifestations include abdominal or back pain, urinary symptoms, malaise, pelvic pain, or (rarely) perforation.

Prostatitis is an infection or inflammation of the prostate gland that presents with fever, chills, malaise, arthralgias or myalgias, perineal/prostatic pain, dysuria, obstructive urinary tract symptoms (including frequency, urgency, dysuria, nocturia, hesitancy, weak stream, and incomplete voiding), low back or abdominal pain, urethral discharge, or may have a history of sclerotherapy for rectal prolapse. The physical exam reveals a tender, nodular, hot, boggy, or normal-feeling gland on digital rectal examination, suprapubic abdominal tenderness, or an enlarged tender bladder due to urinary retention.

Colitis is an inflammation of the colon. It may be associated with enteritis (inflammation of the intestine), proctitis (inflammation of the rectum), or both. The most common symptoms upon presentation include abdominal pain and diarrhea, with or without occult blood. The pain is frequently colicky and, in Crohn's disease, may localize to the right lower quadrant or periumbilical area. Frank rectal bleeding is more common in ulcerative colitis than Crohn's disease. On the physical, pallor, tachycardia, abdominal tenderness, blood in the stool, hyperthermia, weight loss, and signs of dehydration may be noted. Patients with pseudomembranous colitis typically present with profuse watery or mucoid diarrhea, tenesmus, fever, abdominal cramps, and tenderness, usually within 1 week of antibiotic therapy. The stools may be frankly bloody or guaiac-positive.

Perirectal abscesses are associated with indolent, dull perirectal pain exacerbated by movement and increased perineal pressure from sitting or defecation. There may be associated pruritis. Those with an ischiorectal abscess often present with systemic fevers, chills, and severe perirectal pain and fullness consistent with the more advanced nature of this process. External signs are minimal and may include erythema, induration, or fluctuance. Physical examination demonstrates a small, erythematous, well-defined, fluctuant, subcutaneous mass near the anal orifice. On digital rectal examination (DRE), a fluctuant, indurated mass may be encountered.
diffuse abdominal pain
Appendicitis is an inflammation of the appendix. Appendicitis is a common infection of the abdomen that can lead to surgical intervention. The appendix is attached to the first part of the colon, called the cecum. It is a blind pouch and is actually called the vermiform appendix (which means "worm-like appendage"). The appendix is part of the immune system and contains lymphatic tissue. The appendix produces mucus, and as objects (usually stool) enter the appendix, they can become trapped. In addition, mucus can thicken and accumulate. As a result, the appendix can become blocked by the resulting fecalith. After the appendix becomes blocked, bacteria can increase in numbers and cause infection.

The infection can spread from the appendix out into the abdomen. The appendix can rupture, and the spread of infection starts as an abscess around the appendix. Occasionally, the body can contain the infection and resolve.

Differential diagnosis includes: kidney disease, pelvic inflammatory disease, gall bladder disease, right-sided diverticulitis, and Meckel's diverticulitis.

The most common complication of appendicitis is perforation, which causes the infection to spread outside the appendix. Other complications include peritonitis, sepsis, and intestinal blockage.

Symptoms of appendicitis include abdominal pain, loss of appetite, fever, nausea, vomiting, and fever. The main symptom is abdominal pain which is poorly localized at first. The initial periumbilical pain is due to obstruction and inflammation of the appendix and is mediated through the visceral pain fibres as a mid-gut pain. When appendicitis becomes transmural, the serosa of the appendix and the parietal peritoneum are involved, causing a localised pain mediated through the somatic pain fibres in the right iliac fossa. It is usually located at McBurney's point. This is located 1/3 of the distance from the ASIS (anterior superior iliac spine) to the umbilicus.

Diagnosis is usually made by taking a thorough history and performing a physical exam. Blood and urine samples should be taken, and elevated white blood cell count can often be seen. Urinalysis may show bacteria and red and white blood cells. An abdominal radiograph may show the presence of a fecolith, but may be negative in many patients. An ultrasound should also be done. Appendicitis is usually treated by surgery.
CBC with differential
Your patient experiences recurrent respiratory infections and diarrhea; he also has skin changes and a family history highly suggestive of an immunodeficiency; most likely, it is severe combined immunodeficiency (SCID). SCID is a group of congenital diseases caused by different genetic mutations, resulting in the severe deficiency of both T- and B-lymphocytes. X-linked is the most common type. The clinical picture is, however, similar in all of them: recurrent infections caused by bacteria, viruses, fungi, and opportunistic infections. The initial step in the evaluation of immune status should be complete blood count with the differential. You should evaluate blood cell counts and cell morphology for the presence of lymphopenia, which is the classic hallmark of SCID.

KoH prep may help you to differentiate dermatophytes and Candida albicans symptoms from other skin disorders, but it will not be useful in the diagnosis of the primary condition.

You may consider genetic testing to differentiate between various forms of SCID as well as the other combined immune deficiencies, but testing should only be done after you prove the existence of immune deficiency (lymphocytes, immune globulins).

Testing stool for ova and parasites may be considered in cases of diarrhea, but the testing will not help you to establish the diagnosis of the primary condition.

The patient probably has otitis media, and he may have the mastoiditis (peak incidence for the mastoiditis is at age 6 - 13 months; it is much more common in immunocompromised patients). In the case of mastoiditis, fluid extracted from the middle ear through either perforated drums or by tympanocentesis may be sent for Gram staining, culture, and acid-fast stain; however, this procedure will not contribute to the evaluation of immune deficiency.
Screening for colon cancer in asymptomatic patients over age 85 is not recommended because the risks outweigh the benefits.

The most recent guidelines from the US Preventive Services Task Force (USPSTF) recommend against screening for colon cancer in asymptomatic persons over 85 who have had adequate screening in the past. The Task Force states that screening should increase the number of life years gained with the least amount of risk. It is felt that for persons over 85, death rates would be higher due to the likely presence of other conditions, reducing any potential benefit screening would have on mortality. In these cases, the risks of screening would outweigh the benefits.

It is estimated that 18,800 lives per year could be saved if the goals for colorectal cancer screening were met. Colorectal cancer is the 3rd most common cancer in the United States. Evidence shows that persons aged 50 - 75 gain the greatest benefit from screening for colon polyps that may grow into cancer. These guidelines refer to persons who are asymptomatic, and they do not apply to persons with inflammatory bowel disease or known inherited diseases, such as familial adenomatous polyposis. The same recommendations apply to all ethnic groups (for example, African Americans, even though they appear to have an increased mortality from colorectal cancer, and 1st-degree relatives of persons with colon cancer or adenomas. However, it may be prudent to start screening at a younger age if adenomas or cancer was found in a younger 1st-degree relative). Additionally, when cancer or large adenomas are found, persons enter a surveillance program and screening recommendations would not be applicable.

The 3 tests that are recommended for screening are colonoscopy, flexible sigmoidoscopy, and high sensitivity fecal occult blood testing. Evidence shows that any of these methods is effective in reducing mortality, but the benefits of sigmoidoscopy and fecal testing are mostly in reducing the need for colonoscopy if results are negative. Positive results would still require confirmation. Significant complications occur in about 3.4 per 10,000 sigmoidoscopies. There are not yet adequate figures to quantify harms associated with fecal testing, but the USPSTF estimates that any risk is probably no greater than small. The risk would most likely be due to colonoscopy done for a false positive test.

Potential harm from colonoscopy is significant; death can be associated with the procedure, and serious adverse effects, including major bleeding, cardiovascular events, severe pain, and perforation, are possible. These occur at a rate of about 25 per 10,000. Perforation alone occurs in 3.8 per 10,000 tests done.

While there is as yet no direct evidence as to which of the recommendations using these 3 screening methods (see table - Screening for Colorectal Cancer) is most effective, USPSTF states that any of them are an effective strategy as compared to no screening.

Screening methods that USPSTF found insufficient evidence to support include CT colonography and fecal DNA testing.

Possible benefits of CT colonography include a fewer adverse effects, and if a colonography screening test became available that did not require bowel preparation, then screening could be more acceptable and more common. CT colonography may also benefit persons who refuse colonoscopy. However, risk vs. benefit for screening could be underestimated since the studies included persons for screening and surveillance. Also, the CAT scan would include visualization of other areas in the abdomen. Finding abnormalities incidentally may be useful, but there may also be a risk for unnecessary work ups. CT colonography may also not be as good in picking up smaller adenomas. The rate of false positives (and potential for unneeded colonoscopy) is still unclear. Risks from radiation exposure may also be significant in an asymptomatic population.

According to available studies, a potential benefit for DNA stool testing may include increased specificity. However, the cost of testing would probably be high, and information and research are still very limited.

Colorectal screening for regularly followed asymptomatic persons from 76 to 85 is not recommended routinely, as researchers found little added benefit; however, USPSTF does add that there may be reasons to screen particular persons in this age group.
Open cholecystectomy
Patients withsymptomatic porcelain gallbladdersare much more commonly female than male, with the typical age range being from 38 - 70 years old. In general, patients will describe a history of biliary type pain. Diagnostically, an ultrasound or CT scan will most efficiently give the visualization of the calcification necessary to confirm a porcelain gallbladder.Those found to have complete mural calcification (complete type) generally will need to have it treated with an open cholecystectomy. This is because the mucosal calcification that creates the porcelain characteristic makes the gallbladder very thick and fibrotic, which in turn makes it potentially difficult to grab by forceps and dissect out in a laparoscopic approach. There have been recent studies suggesting a laparoscopic cholecystectomy would be acceptable in patients who have evidence of a long cystic duct and biliary anatomy that is well-defined perioperatively, as well as in those who have evidence of a less advanced form of porcelain gallbladder, although there is no confirmed change of recommended treatment plan at this time.

Anytime a porcelain gallbladder is found, there has to be a heightened alert for the suspicion of gallbladder carcinoma. The more advanced and severe the calcification is of the gallbladder, the heightened potential of it being malignant. Reassurance only and periodic ultrasounds would not be appropriate in this scenario. This approach may be followed in some part in a patient with less severe signs and symptoms. Percutaneous biliary stent placement is not the appropriate choice for this clinical scenario, as it is not treating the main pathology being presented.
Mallory weiss Syndrome
In cases of Mallory-Weiss Syndrome, patients present with hematemesis, especially after repeated severe retching and vomiting, which results in a mucosal tear at the gastroesophageal junction. They may also have retrosternal chest pain.

Tuberculous pleuritis chest pain ispleuritic and aggravated by coughing. It is described as sharp. Other symptoms (e.g., fever, dyspnea, and weight loss) may also be present. On examination, there may be dullness on percussion as well as absent breath sounds on the affected side.

In Tietze's syndrome, patients present with anterior chest pain that is aggravated by taking a deep breath, sneezing, and turning motions. On examination, the affected costochondral junctions are erythematous, warm, and tender on palpation. The most commonly affected are the 2nd or 3rd costochondral joints.

Patients with myocardial infarction usually present with a left-sided or retrosternal pain that may radiate to the jaw, neck, and shoulder. They describe it as heaviness or a squeezing sensation. It is of variable duration and often lasts for more than 30 minutes. There is a gradual intensification of the pain. The onset of the pain may be during physical exertion or at rest. It is not relieved by nitroglycerine. On examination, they may be dyspneic and diaphoretic.

Chest pain due to a panic disorder has a variable presentation. It can be retrosternal or localized, brief or over 30 minutes in duration. Numerous terms, such as aching and sharp, can be used to describe it. Other symptoms of a panic disorder include lightheadedness, shortness of breath, nausea, paresthesias, palpitations, derealization, and the fear of losing control. The history helps elicit precipitating factors and prior panic attacks.
Pyridoxine deficiency
In cases of pyridoxine or (vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory investigations reveal anemia with lymphopenia. Causes include malabsorption as well as medications, such as isoniazid and penicillamine. Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.

Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

In cases of vitamin A deficiency, patients can present with inability to see well in dim light or night blindness. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities, and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular foamy spots on the conjunctiva. Patient may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, and yellow fruits and vegetables.

Niacin deficiency causes pellagra, which is characterized by:

A symmetrical dermatitis, usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations, such as memory impairment, depression, and dementia. These may appear alone or in combination. Causes include inadequate dietary intake, especially in patients with corn-based diets or alcoholism. Dietary sources include legumes, yeast, meat, and enriched cereal products.
In cases of vitamin C (or ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions, such as pregnancy and lactation, which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, such as oranges, lemons, and tangerines, as well as tomatoes and potatoes.
Meckel Diverticulum
This patient is most likely suffering from a common congenital abnormality of the development of the ileum called a Meckel's diverticulum. In the embryo, the vitelline duct is a communication between the yolk sac and the lumen of the gastrointestinal tract at the midgut. Normally, it degenerates completely, but the persistence of a portion of the vitelline duct leads to the development of a cul-de-sac on the ileum (Meckel's diverticulum). This congenital birth defect follows a rule of 2s. It occurs in 2% of the population, but only 2% show symptoms. It is usually located about 2 feet from the ileocecal valve and is about 2 inches long. It can contain 2 types of ectopic tissue: gastric or pancreatic. It usually presents by 2 years old. The presence of ectopic gastric mucosa in the diverticulum can lead to secretion of stomach acid downstream from the duodenum, which has bicarbonate-secreting submucosal Brunner glands to neutralize gastric acid. Ectopic gastric tissue in the ileal diverticulum can lead to ulceration and bleeding of the adjacent ileal mucosa.

Vascular malformations, intussusception, and coagulation disorders are more likely to manifest themselves in the first year of life. Cow's milk colitis is a problem of the first year of life and spontaneously resolves by the end of that year for most children. NEC is a problem of the stressed, usually premature, newborn. Rectal polyps are likely to present in older children, as is HSP. Babies and older children can have gastric bleeding from gastritis or gastric ulcers. Duodenal ulcers are much more common in older children.
Toxins released by the organism are responsible for the patient's symptoms.

The symptoms of a C. difficile infection are due to the release of toxins produced by the organism into the body of humans. C. difficile produces 2 types of toxins, A and B; they enter the intestinal mucosal cells via specific receptors on their cell wall and result in inflammation of the colon, mucosal damage, and fluid and mucous secretions. These changes cause diarrhea. Toxin A has enterotoxicity and toxin B has cytotoxicity. A strain of C. difficile, NAP 1, is found to produce another type of toxin known as binary toxin. Along with toxins, colonization of the organism is also found to be an essential factor in the onset of symptoms.

The cell wall of C. difficile does not disrupt the intestinal mucosal cells. The cell wall of the organism helps in adhering to the mucosal cells at specific sites and in colonization of the organism at the site of adherence. The organisms have various proteins on their cell wall that function as adhesins and attach the organism at particular sites on the surface of mucosal cells. The proteins of the cell wall may help the organism in invading the cells. These proteins can be targeted when producing vaccines against C. difficile.

Capsules are generally not produced by Clostridium species, but a capsule-like substance has been found around C. difficile cells. The capsules were found to be composed of glycocalyx and were detected by antibody stabilization methods. These structures protect the organism from phagocytosis during infection and help in colonizing on the mucosal layer of the intestine.

A few strains of C. difficile are known to have flagella, which help the cells in motility. In this organism the flagella are also known to possess virulence factors, which result in production of antibodies against them in infected humans. The flagella are found to help the organisms in adhering to the cells of the intestinal mucosa. The flagella of C. difficile are also found to be involved in cross-reactions among serogroups.

Spores produced by Gram-positive bacteria are resistant to adverse conditions like high temperature, antibiotics, disinfectants, etc. These spores can survive in an environment for months or years without germination. C. difficile is a major source of nosocomial infections pertaining to its spores. The spores enter the human body when inhaled or through the oral route. They then geminate in the small intestine, thereby producing viable cells of C. difficile and starting the cycle of infection.
Fluticasone metered dose inhaler
The patient described in the above scenario has the diagnosis of eosinophilic esophagitis (EE). Because this is a relatively new diagnosis, the prevalence of EE is unknown, although the incidence is increasing in both children as well as adults. These patients will have symptoms typically 4 - 5 years before they have a confirmed diagnosis. EE is more commonly seen in male patients who are Caucasian, and up to 70% of patients with EE have personal history of atopy to environmental or foods.

The most common symptoms found in adults with EE are dysphasia, refractory heartburn, chest pain, and food impaction. Usually, no physical exam abnormalities will be detected. An endoscopy with esophageal biopsy is the only definitive method to diagnose EE. The presence of eosinophils of 15 or more per high power field is required for a diagnosis. Other physical findings that may be visualized during an endoscopy that are highly suggestive of EE include stacked circular rings ('feline esophagus'), proximal strictures, linear furrowing, as well as white exudates or even papules that signify eosinophilic purulent material.

Currently there are no FDA approved medications for the treatment of EE. The most efficient treatment for symptoms is topical corticosteroids, either via fluticasone metered dose inhaler or viscous budesonide. These medications are swallowed and therefore coat the esophagus; the symptoms as well as the overall eosinophilia improve fairly quickly. Patient response is usually in the first few days of treatment; however, symptoms will reoccur once the medication regimen is discontinued. Topical fluconazole is not the correct option; EE is not a fungal infection. Oral ampicillin is not correct because EE's underlying pathology is not a bacterial infection. Oral omeprazole is not specifically recommended for treatment of EE; however, it may treat the co-existent GERD. Oral cetirizine is also not an appropriate choice; if there is evidence of severe atopy, therapy should be initiated, but no evidence presents in the case scenario showing that the treatment of airborne allergic disorders improves EE.
The correct answer is a serum amylase of 310 U/L and a serum lipase of 760 U/L, as these levels are significantly elevated, which is indicative of acute pancreatitis. The normal range for serum amylase is 30-220 U/L, and the normal range for serum lipase is 0-160 U/L. Both levels being significantly elevated is typically seen in a patient with acute pancreatitis. Serum lipase is both more sensitive and more specific than serum amylase for diagnosis of acute pancreatitis, but more so when the serum lipase is at least 3 times the normal level (as is with this case). However, various other biliary and intestinal diseases can also alter these lab results.

Blood work results with a serum amylase of 250 U/L and a serum lipase of 110 U/L do not indicate acute pancreatitis. The serum amylase is slightly elevated, but the serum lipase is normal. This can occur for many gastrointestinal-related disorders and renal failure, but these lab results could also commonly be found in a patient with chronic (rather than acute) pancreatitis.

Lab results of serum aspartate aminotransferase (AST) 32 U/L and serum alanine aminotransferase (ALT) 29 U/L are actually normal results for these particular lab tests. The AST and ALT can be used to identify hepatocellular diseases of the liver. However, mildly increased levels can also be seen in patients with acute pancreatitis.

Lab results of serum aspartate aminotransferase 120 U/L and serum alanine aminotransferase 40 U/L can be seen in patients with various hepatocellular levels as both are increased from normal. These results are possible in a patient with acute pancreatitis, but are not the most indicative of the answer choices. Cirrhosis is a disease of the liver that can often occur in patients with large alcohol intake and often causes lab results such as these. Specifically, results that show an AST level that is 3 times that of the ALT level.

Lab results of serum white blood cell count 14,000/mm3 and serum total bilirubin 1.8 mg/dl could be seen with various infections separately. However, the combination of both results limits the possible disorders. The white blood cell count could be elevated in a patient with acute pancreatitis, and the serum bilirubin could also be elevated in patient with acute pancreatitis when it is associated with alcoholic hepatitis. However, these results are not the MOST indicative of acute pancreatitis when compared to the other options.
A 14% decrease of his hematocrit at 48 hours after admission is the correct response.

A patient who is admitted to the hospital for treatment of acute pancreatitis is assessed using the Ranson criteria to determine the severity of their disease, which in turn helps determine prognosis. About 70 - 80% of cases of acute pancreatitis are considered mild and result in virtually no morbidity or mortality. The remainder are severe attacks and have a 10 - 30% mortality rate. Fast identification of the severe cases is helpful to reduce the morbidity and mortality for each patient. There are 11 Ranson criteria, 5 of which are determined upon admission, and 6 at 48 hours after admission. Patients who have 2 or fewer of the criteria have minimal mortality. Patients with 3 - 5 of the criteria have about a 10 - 20% chance of mortality. Patients with 5 or more of the criteria have at least a 50% mortality rate. A patient with at least a 10% decrease in their hematocrit at 48 hours after admission meets one of the Ranson criteria, so the correct answer is a 14% decrease in hematocrit 48 hours after admission.

WBC count of 10,000 cells/mm3 is not one of the Ranson criteria. A WBC count of >16,000 cells/mm3 would meet one of the Ranson criteria.

Serum glucose of 130 mg/dL upon admission is also not one of the Ranson criteria. The patient's serum glucose would have to be at least 200 mg/dL to count as one of the Ranson criteria and increase the severity of their disease.

Aspartate transaminase of 240 U/dL upon admission is not one of the Ranson criteria either. The patient's aspartate transaminase would have to be at least 250 U/dL to count as a Ranson criteria and increase the severity of their disease.

A serum calcium of 10 mg/dL 48 hours after admission is not one of the Ranson criteria. If the patient's serum calcium is under 8 mg/dL 58 hours after admission, this would count as one of the Ranson criteria.
Gilbert's syndrome
Your patient most probably has Gilbert's syndrome (GS), also known as Gilbert-Meulengracht syndrome. It is a relatively common genetic disease found in up to 5% - 10% of the population and generally does not need special treatment. Inherited non-haemolytic hyperbilirubinemic conditions include Dubin-Johnson, Rotor, and GB syndromes, and all are important differential diagnoses indicating benign disease that requires no immediate treatment. GB can be diagnosed by clinical presentation, biochemistry, and genotyping, and is significant because of the presence of the disposition towards drug-associated toxicity. A major characteristic is jaundice, caused by elevated levels of unconjugated bilirubin in the bloodstream. The cause of this hyperbilirubinemia is the reduced activity of the enzyme glucuronyltransferase, which conjugates both bilirubin and some lipophilic molecules, including drugs.

Intravascular hemolysis, with resulting hemoglobinemia, hemoglobinuria, and bilirubinemia, will show fragments of the red blood cells ("schistocytes") and sometimes spherocytes in peripheral blood smear, reticulocytosis, elevated unconjugated bilirubin that may lead to jaundice, elevated lactate dehydrogenase (LDH) in the blood, and decreased haptoglobin levels. If the direct Coombs test is positive, hemolysis is caused by an immune process. Hemosiderin in the urine indicates chronic intravascular hemolysis. There is also urobilinogen in the urine.

Viral hepatitis with jaundice will have elevated liver function tests (AST and ALT elevated out of proportion to alkaline phosphatase, usually with hyperbilirubinemia), and viral serologic testing will be positive.

Crigler-Najjar syndrome is a rare inherited form of non-hemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infancy.

Budd-Chiari syndrome is caused by occlusion of the hepatic veins. It presents with the classical triad of abdominal pain, ascites, and hepatomegaly. The syndrome can be fulminant, acute, chronic, or asymptomatic.
In cases of vitamin A deficiency, patients can present with inability to see well in dim light or night blindness. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities, and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular foamy spots on the conjunctiva. The patient may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, yellow fruits, and vegetables.

Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

Niacin deficiency causes pellagra, which is characterized by:

A symmetrical dermatitis usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations, such as memory impairment, depression, and dementia. These may appear alone or in combination. Causes include inadequate dietary intake, especially in patients with corn-based diets and alcoholism. Dietary sources include legumes, yeast, meat, and enriched cereal products.
In cases of vitamin C (or ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions, such as pregnancy and lactation, which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, such as oranges, lemons, and tangerines, as well as tomatoes and potatoes.

In cases of pyridoxine (or vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory investigations reveal anemia with lymphopenia. Causes include malabsorption as well as medications, such as isoniazid and penicillamine. Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.
Hepatitis A
Hepatitis A is a member of the Picornaviridae family; it is a nonenveloped virus approximately 27 - 28 nm in diameter. It is spherical, with a surface structure that suggests icosahedral symmetry. It is a single-stranded RNA virus. Signs and symptoms of an infection include diarrhea, dark urine, jaundice, and flu-like symptoms. Incubation is 15 - 50 days, with an illness duration of 2 weeks - 3 months. The virus is associated with shellfish harvested from contaminated waters, raw produce, uncooked foods, and cooked foods that are not reheated after contact with an infected food handler. Confirmation is based on the presence of anti-hepatitis A antibodies, positive IgM, and increases in serum ALT and bilirubin. Treatment is supportive, and prevention is by vaccination.

Norwalk virus is a single-stranded RNA virus that is approximately 29 - 35 nm in diameter with spiky ill-defined outlines. The virus produces gastroenteritis-like symptoms that include nausea, vomiting, and watery/large volume diarrhea. Fever is usually absent. The incubation period is 24 - 48 hours, and the illness duration is 24 - 60 hours. Sources of infection include poorly cooked shellfish and ready-to-eat foods (e.g., salads and sandwiches) touched by infected food handlers. Diagnosis is based on negative stool cultures, stool that is negative for white blood cells, and serological studies for the presence of fourfold or greater increases in antibody titers of Norwalk virus antibodies. Treatment is mainly supportive; bismuth sulfate may be given.

Rotavirus is a double-stranded RNA virus belonging to the Reoviridae family. The virus is 70 nm in diameter and appears as a wheel. The virus infection has signs and symptoms that include vomiting, watery diarrhea, and low-grade fever. There may be temporary lactose intolerance. The virus is especially common in infants and children, the elderly, and the immunocompromised. The incubation period is 1 - 3 days, and the duration of illness is 4 - 8 days. The virus is associated with ready-to-eat foods touched by infected food handlers (e.g., salads and fruits) and fecally-contaminated foods. Confirmation is based on the detection of the virus antigen in stool. Stool routine cultures are negative, and stools are negative for the presence of white blood cells. Treatment is supportive in nature. Fluid electrolyte replacement may be needed in severe cases of diarrhea, especially in infants.

Adenovirus is a virus with DNA as the genetic material; it is approximately 70 nm in diameter. The virus causes gastroenteritis; symptoms include vomiting, nausea, malaise, diarrhea, headache, and fever. Incubation is 10 - 70 hours, with a duration of 2 - 9 days for symptoms. The organism is associated with ingesting food contaminated with feces and ready-to-eat foods touched by infected food workers. The virus is also found to be transmitted through the ingestion of some shellfish. The virus can be detected antigenically in acute stool samples. Stool staining for white blood cells is negative. Supportive care is the treatment of choice. The disease is usually mild and self-limiting.

Parvovirus is a single-stranded DNA virus. Infections with this virus are mostly asymptomatic, although the virus produces erythema infectiosum (fifth disease) in small children (a benign rash appears on the face, trunk, and extremities). A fever also develops. The disease can cause intrauterine infection and fetal death due to the vertical transmittance of the virus from mother to fetus. In individuals with hemoglobinopathies, there can be transient aplastic crisis. Immunodeficient patients can develop chronic anemia.
Laparoscopic fundoplication
Laparoscopic fundoplication leads to long-term relief for about 90% patients with gastroesophageal reflux disease (GERD). The most common technique is the Nissen procedure (i.e., suturing the gastric fundus to the lower esophagus throughout the full esophageal circumference). Side effects are uncommon and mostly minor: abdominal bloating, inability to belch, paraesophageal herniation, dysphagia, and diarrhea. Barrett's esophagus sometimes disappears after fundoplication, but this procedure does not eliminate the risk of dysplasia and carcinoma in all patients. Therefore, endoscopic screening after the procedure is mandatory.

The other major therapeutic option for patients with GERD is long-term proton pump inhibitors (PPIs). Patients treated with these drugs have esophageal healing and symptom relief rates comparable to those of operated patients. However, about 30-40% of patients only improve after dose escalation. Therefore, PPI users take longer on average to achieve symptom control. Esophagectomy would be an option if there were an esophageal carcinoma or high-grade dysplasia, particularly in younger patients without significant comorbidities. The decision to operate must take into account the patient's general health and comorbidities, which are common given that Barrett's esophagus often occurs in elderly patients. However, advanced age by itself does not contraindicate esophagectomy.

Several endoscopic techniques (e.g. mucosectomy, laser ablation, and photodynamic therapy) have had some success in the treatment of Barrett's esophagus. However, complication such as bleeding after extensive mucosectomies, laser perforations, and skin burns from photoporphyrin-induced photosensibility are common. Incomplete mucosectomies, after which small areas of high-grade dysplasia or even cancers remained in the esophageal wall, have also been documented.

Radiofrequency thermal coagulation of the esophageal wall (Stretta procedure) consists of using a special catheter to induce controlled heating of the esophageal wall at the level of the gastroesophageal junction. This induces fibrosis and contraction of the gastroesophageal junction, which increases sphincter pressure and improves reflux. However, recurrence is high after this procedure (about 50%), and it cannot be performed when there is a hiatal hernia, as in this case.
Vitamin C
In cases of vitamin C (or ascorbic acid) deficiency, patients can present with bleeding tendencies (as a result of weakened capillaries) and impaired wound healing due to impaired formation of connective tissue. On examination, the gums may be swollen and friable; the teeth may be loose. There may also be multiple splinter hemorrhages on the nails and ecchymoses, especially over the lower limbs. Causes include inadequate dietary intake and certain conditions, such as pregnancy and lactation, which increase vitamin C requirements. Dietary sources of vitamin C include citrus fruits, such as oranges, lemons, and tangerines, as well as tomatoes and potatoes.

Vitamin E deficiency may cause a hemolytic anemia in premature infants. Laboratory investigations reveal low plasma tocopherol levels, a low hemoglobin level, reticulocytosis, hyperbilirubinemia, and creatinuria. Causes of vitamin E deficiency in premature infants include limited placental transfer of vitamin E and the resultant low levels at birth combined with its relative deficiency in the infant diet. Dietary sources for older children and adults include wheat germ, vegetable oils, egg yolk, and leafy vegetables.

In cases of vitamin A deficiency, patients can present with inability to see well in dim light or night blindness. There may also be conjunctival and corneal xerosis, as well as pericorneal and corneal opacities, and Bitot's spots. Bitot's spots are a collection of keratin appearing as triangular foamy spots on the conjunctiva. Patients may also have xeroderma, hyperkeratotic skin lesions, and increased susceptibility to infections. Causes include inadequate dietary intake and malabsorption. Dietary sources of vitamin A include fish, liver, egg yolk, butter, cream, dark green leafy vegetables, as well as yellow fruits and vegetables.

Niacin deficiency causes pellagra, which is characterized by:

A symmetrical dermatitis, usually on parts of the body exposed to sunlight
Scarlet glossitis and stomatitis
Diarrhea
Mental aberrations, such as memory impairment, depression, and dementia. These may appear alone or in combination. Causes include inadequate dietary intake, especially in patients with corn-based diets or alcoholism. Dietary sources include legumes, yeast, meat, and enriched cereal products.
In cases of pyridoxine or (vitamin B6 deficiency), patients can present with peripheral neuropathy, seborrheic dermatosis, glossitis, and cheilosis. Laboratory investigations reveal anemia with lymphopenia. Causes include malabsorption as well as medications, such as isoniazid and penicillamine. Dietary sources of vitamin B6 include liver, legumes, whole grain cereals, and meats.
Barium Swallow
This patient has had a long standing gastrointestinal reflux disease (GERD), which is obvious based on her symptoms. She has not used H2 blockers consistently as she should have. They would have likely reduced or eliminated her symptoms. Now, due to repeated acid-induced injury to the esophageal lining, she has developed an esophageal stricture; this caused dysphagia, which usually starts with solids and progresses to both solids and liquids.

A barium swallow is indicated because it is the least invasive and will give information regarding the location, length, number of strictures, and size of the lumen. It is has a sensitivity of 100% for luminal diameter less than 9 mm and above 90% for luminal diameter greater than 10 mm. It will also impact the next step in the treatment, which includes endoscopic dilatation of the stricture, in the technique of dilatation and number of sessions needed; in addition, it impacts counseling the patient on the risks of the procedure. Dysphagia due to other pathologies, like esophageal diverticulum, extra-luminal pathology, malignancy, and perforation, can be ruled out too. Empiric treatment with proton pump inhibitors is indicated in simple GERD without symptoms of stricture. Once the patient has dysphagia, it is important to assess them for complications, like stricture, especially if they have had long standing GERD.

In the majority of patients, endoscopy is the most useful test for the work-up of dysphagia. Endoscopy can help identify structural abnormalities such as esophageal webs and strictures, as well as identify tumors and esophagitis. During endoscopy, biopsies may be performed to help confirm diagnosis and direct treatment. Therapeutic interventions may also be undertaken, such as esophageal dilatations for the treatment of strictures. In certain patients, endoscopy is not the preferred first-line test in the management of dysphagia. These include patients with a history of esophageal or laryngeal cancer and those who have been exposed to a caustic ingestion or radiation therapy. In these patients, blind insertion of the endoscope may cause esophageal damage. Therefore, barium swallow is the preferred diagnostic exam.

Swallow evaluation and video fluoroscopy permit evaluation of the cervical esophagus only. The rest of the esophagus cannot be evaluated; therefore, this option is inadequate. These tests are more important for pathology suspected in the pharynx, larynx, and upper esophageal sphincter.

Esophageal manometry is indicated in motility disorders of the esophagus. Motility disorders present with dysphagia to both liquids and solids, as in achalasia, esophageal spasms, and scleroderma. Manometry is indicated when a barium swallow has ruled out the more common causes of dysphagia.
Antacids
Mild or intermittent symptoms of gastroesophageal reflux disease (GERD) are not typically seen as adversely affecting patients' quality of life. Initially, action is taken in terms of modification of behaviors, such as eating smaller meals as well as eliminating acidic foods and foods known to precipitate the reflux (fatty foods, alcohol, chocolate, or peppermint). Weight loss has also been shown to help decrease issues, and so has advising patients to avoid lying down at least 3 hours after eating meals. Elevation of the head of the bed is also suggested to initiate relief.

From a pharmacological standpoint, antacids are considered the mainstay for rapid relief of occasional heartburn. Antacids work by neutralizing stomach acid only; alone, they will not heal any inflammation that may be caused by stomach acid. Patients should be told that the duration of action of these medications is typically less than 2 hours. Antacids are also contraindicated in any patients with renal failure. Many types of antacids are available over the counter.

The next step up in terms of treatment would be considered to be H2-receptor antagonists. These medications work by reducing stomach acid production. Again, these agents are available over the counter as 50% the prescription dose. Examples include cimetidine 200 mg, ranitidine 75 mg, and famotidine 10 mg. When these agents are taken for active reflux symptoms, they have a delay of onset of at least 30 minutes; once they do take effect, relief is supplied for up to 8 hours per dose.

Proton pump inhibitors are initial pharmacological treatment reserved for patients with moderate to severe symptoms of reflux as well as known complications from GERD. Proton pump inhibitors work by actually blocking the production of acid. Examples of these include omeprazole 20 mg or lansoprazole 30 mg. There are proton pump inhibitors available over the counter, but some are only available with a prescription. Proton pump inhibitors help patients achieve adequate control of their heartburn symptoms, and they can potentially offer resolution of these symptoms; they even aid in healing of erosive esophagitis if it is present.

Antibiotics in relation to reflux or heartburn would not be indicated directly for the symptoms of this pathology; antibiotics could potentially be used as a component of the treatment of a H. pylori infection.

Prokinetic agents are not indicated as treatment of mild, intermittent reflux symptoms.
administration of vitamin C
The patient suffers from scurvy due to a deficiency of dietary vitamin C. Absence of vitamin C leads to impaired hydroxylation of proline residues in the nascent procollagen chains leading to weakness of blood vessel walls. Clinically, the deficiency syndrome is characterized by perifollicular hemorrhages, fragmentation of hairs, purpura, ecchymoses, splinter hemorrhages, and hemorrhages into muscle. In patients with normal dentition, gum changes (e.g., swelling, bleeding, and loosening of teeth) are also noted. Without supplementation with vitamin C, death may eventually occur.

Administration of factor VIII would be indicated for factor VIII deficiency. This deficiency would lead to a prolonged PTT (partial thromboplastin time), which was not noted in this patient.

Administration of iron would be of benefit in iron-deficiency anemia, but there is no indication of a hypochromic, microcytic anemia in this patient. The anemia of scurvy is typically normochromic and normocytic due to bleeding.

Administration of vitamin B12 would be indicated for a megaloblastic anemia. Although a macrocytic anemia may be observed in scurvy (due to concomitant dietary folate deficiency or perturbations in the folate pool), this patient did not show macrocytosis.

Administration of vitamin K would be appropriate for vitamin K deficiency. This deficiency would produce prolongations of the prothrombin time (PT), followed by prolongation of the PTT as the vitamin K-dependent factors (II, VII, IX, X, protein C, and protein S) are depleted.
Upper GI endoscopy
The patient's history, clinical examination, and stool testing positive for occult blood are suggestive of peptic ulcer disease. Upper GI endoscopy is the investigation of choice in children with suspected peptic ulcer disease. Endoscopy allows direct visualization of the esophagus, stomach, and duodenum, identifies the specific lesions, and also screens for the presence of H. pylori in the biopsy specimens. H. pylori is a gram negative S-shaped rod. Biopsy should always be obtained from the antrum of the stomach regardless of endoscopic findings. Endoscopic findings may vary from grossly normal mucosa to nonspecific gastritis with prominent rugal folds to nodularity and ulcers.

Stool microscopy has no role in the diagnosis of H. pylori infection. However, stool antigen testing identifies active H. pylori infection by detecting the presence of H. pylori antigen in the stool.

Single contrast barium studies have overall sensitivity of 75%, but double contrast studies have sensitivity of 95% in detection of gastric ulcer. These results are comparable to endoscopy. However, barium studies have the disadvantage that the biopsy specimen cannot be obtained and ulcers smaller than 5mm may not be detected on barium studies.

CT san has no primary role in the detection of gastric ulcers. It is helpful in the detection of subphrenic collection that may occur after perforation of gastric ulcer.

Ultrasound abdomen has no role in the detection of gastric ulcer but is useful in the detection of other causes of upper abdominal pain like gallstones, pancreatitis, and subphrenic, as well as other collections due to perforated gastric ulcer.
Immunosuppressants (corticosteroids)
Your patient most probably has Pyoderma gangrenosum, which is a ulcerative skin lesion of an uncertain etiology; in more than 50% of cases, it is associated with systemic diseases, most commonly inflammatory bowel disease. It usually develops rapidly and can progress from a pimple to an ulcer in 1 or 2 days. In a process termed pathergy, new ulcerations may occur after trauma or injury to the skin. Pain is the predominant symptom, but symmetrical arthritis, myalgias, and malaise are also common. When the lesions heal, they usually leave the scars that are often cribriform. Immunosuppression is the mainstay of treatment; it is believed that dysregulation of the immune system (specifically, altered neutrophil chemotaxis) is involved. Most clinicians use both topical and systemic therapy. The most commonly used treatments include topical potent corticosteroids or tacrolimus to treat early lesions; systemic corticosteroids, TNF-α inhibitors, or other anti-inflammatories or immunosuppressants are used to treat more severe manifestations.

Surgery or debridement is contraindicated because of the presence of pathergy. Even if there was no pathergy, surgery is contraindicated because skin trauma can trigger the pathergy.

Acyclovir is not indicated; the clinical picture is not consistent with acute herpes infection and the patient is not immunocompromised.

Fluconazole is not indicated; the clinical picture is not consistent with tinea (or any other fungal infection).

Paracetamol alone probably will not relieve the debilitating pain. Sufficient pain medication in this case will probably include paracetamol and some other medication, sometimes opioids.
Insulinoma
Her low blood glucose levels indicate an insulinoma.

The endocrine portion of the pancreas is housed in the islets of Langerhans. Tumors that arise from this area are referred to as islet cell tumors. The specific type of tumor depends on the cell type involved. Typically, the tumor is named based on the hormone it is secreting.

An insulinoma is an islet cell tumor. Insulin is produced by the beta cells of the islets of Langerhans. Therefore, an insulinoma is a tumor of the beta cells. An insulinoma is the most frequently occurring islet cell tumor. Hypoglycemia, secondary to the insulin secretion, is a symptom.

Verner-Morrison syndrome is due to a VIPoma. This is an endocrine tumor of the pancreatic islets of Langerhans. It secretes vasoactive intestinal polypeptide. Vasoactive intestinal polypeptide is produced by the D1 cells of the islets of Langerhans. Therefore, a VIPoma is a tumor of the D1 cells. Other names for a VIPoma include pancreatic cholera and WDHA-syndrome (watery diarrhea, hypokalemia and achlorhydria).

Gastrinomas are most often due to islet cell tumors. On occasion, gastrinomas can arise outside of the pancreas. Peptic ulcers, secondary to the excessive gastrin secretion, are frequent. Gastrinomas and peptic ulcerations are referred to as the Zollinger-Ellison syndrome.

A glucagonoma is an islet cell tumor. Glucagon is produced by the alpha cells of the islets of Langerhans. Therefore, a glucagonoma is a tumor of the alpha cells. Diabetes can be seen with a glucagonoma. Other symptoms include a skin rash, weight loss, and anemia. A glucagonoma is a rare islet cell tumor.

A somatostatinoma is an islet cell tumor. Somatostatin is produced by the delta cells of the islets of Langerhans. Therefore, a somatostatinoma is a tumor of the delta cells. Somatostatinoma is a rare islet cell tumor.
1 Positive transglutaminase antibodies
Dermatitis herpetiformis produces erythematous, pruriginous bullous lesions on the extensor surfaces of the elbows, knees, scalp, neck, and buttocks. These lesions, sometimes called skin celiac disease, are found in 10% of patients with celiac disease, and are highly specific for it; nearly all patients with dermatitis herpetiformis have histologic evidence of celiac disease on small-bowel biopsy. However, in many cases the enteropathy is subclinical. Histopathologic examination of the bullae reveals deposits of anti-gliadin IgA antibodies in the basal membrane of the epidermis.

In most cases, the skin lesions involute after the patient is put on a gluten-free diet. However, this can take several months. In patients with severe pruritus, the mainstay of treatment is dapsone, which is highly effective in relieving this symptom. Second-line options include sulfasalazine and sulfapyridine.

Celiac disease can present with isolated nutrient deficiencies (e.g. iron, folate, B-complex vitamins), and therefore could explain this patient's iron deficiency anemia. As transglutaminase antibodies are found in 70% of cases of celiac disease, there is a high probability that this assay will be positive in this patient, whether or not the anemia is caused by celiac disease.

The more florid presentation of celiac disease - with overt steatorrhea, weight loss, and malnutrition - is becoming less common in the United States. Therefore, the physician must be aware of the possibility of celiac disease in patients with milder symptoms, such as occasional diarrhea with bulky stools, bloating, or more rarely, isolated micronutrient deficiencies.

Anti-Saccharomyces (ASCA) antibodies are associated with Crohn's disease (60-70% of patients are positive). Lesions in these patients include oral aphthous ulcers, pyoderma gangrenosum, and rheumatoid nodules, as well as signs of non-cutaneous disease (e.g. enterocutaneous fistulas, malnutrition, micronutrient deficiencies).

A 99mTc-red cell scintigraphy could be positive because occult gastrointestinal bleeding is still a possibility. Causes of a negative iron balance include:

1) Deficient intake, which is most prevalent in poor countries.
2) Pregnancy.
3) Chronic bleeding (gynecologic, gastrointestinal, hematuria).
4) Iron deposition in tissues (e.g. cardiac hemosiderosis)

The deficiency in hemoglobin synthesis in the bone marrow tends to cause a compensatory rise in erythropoietin levels, which produces erythroid hyperplasia in the bone marrow. Other findings include absence of sideroblasts and stainable iron in the bone marrow's reticular network. However, bone marrow biopsy has been largely abandoned for diagnosis of iron-deficiency anemia because of interobserver variability and the availability of less invasive tests of iron status, particularly serum ferritin and total iron binding capacity (TIBC).
Niacin (B3)
This patient probably has niacin deficiency. Niacin (nicotinamide, nicotinic acid) deficiency is uncommon in the United States. It is often found in people who live on a diet that consists mainly of corn (maize). This is due to the fact that the niacin in corn cannot be absorbed unless it is chemically treated with alkali first. If a person consumes a diet rich in tryptophan, but low in niacin, they are able to compensate since tryptophan can be converted into niacin. Deficiency may also result from alcoholism, cirrhosis, or diarrhea. Men and women are affected equally. Symptoms of niacin deficiency include nausea, vomiting, diarrhea, rash, glossitis, stomatitis, depression, and psychosis. Niacin deficiency, also known as pellagra, manifests as the '3 Ds': diarrhea, dermatitis, and dementia. Treatment consists of niacin supplementation.

The causes of zinc deficiency include malnutrition, chronic debilitating diseases, chronic renal disease, alcoholism, drugs such as penicillamine and diuretic, and genetic disorders, such as sickle cell disease. Clinical manifestations in severe cases include alopecia, diarrhea, weight loss, infections, dermatitis, hypogonadism in men, and intercurrent infections. Supplementation with zinc is the treatment of choice.

Folate deficiency causes megaloblastic macrocytic anemia, as folate plays a key role in nucleic acid synthesis. The early manifestation of folate deficiency, especially in its suboptimal state, predisposes to occlusive vascular disease and thrombosis. These manifestations are linked to increased homocysteine levels found in folate deficiency. Neurological disturbances, such as mood disturbance and spinal cord syndromes, are also seen. It is also associated with predisposition to neoplasia and interferes with immunologic status. Folate replacement is the option to prevent and to treat the deficiency.

Vitamin B1 (or thiamine deficiency) causes beri beri, occurring mostly in the malnourished and alcoholics. The deficiency manifests with acute heart failure, neurologic deficits, and epilepsy. Empiric use of thiamine and prophylactic use in high-risk population is strongly recommended even before blood reports are obtained, as the treatment is inexpensive and prevents major catastrophes.

Vitamin B12 (or cobalamin deficiency) manifests as megaloblastic macrocytic anemia, pancytopenia, and a spectrum of neuropsychiatric disorders such as peripheral neuropathy, parasthesias, and demyelination of corticospinal tract. Nutritional deficiency, alcoholism, and malabsorption syndromes are some causes of B12 deficiency. It is also associated with homocysteinemia and atherosclerosis. Diagnosis is by serum estimation of B12, and oral supplementation is safe and effective. Intramuscular injections may also be used.
refer for emergency endoscopy
He should be referred for an emergency upper endoscopy.

This patient is most likely bleeding from a gastric ulcer. His recent NSAID use, as well as his alcohol and tobacco habits, make him at risk for peptic ulcer disease. His symptoms of melena and hematemesis, along with his anemia, make the diagnosis quite straightforward.

It appears that this patient is still actively bleeding based on the results of the nasogastric tube irrigation; therefore, the priority should be getting the ulcer to stop bleeding. Upper endoscopy should be performed so that the bleeding site can be identified and treated with electrocautery, coagulation, or injection of epinephrine or a sclerosing agent. If the bleeding cannot be stopped with endoscopic interventions, angiographic embolization should also be tried. If these interventions do not succeed, the patient has rapid deterioration, or if he requires more than 6 units of blood in a 24-hour period, then emergency surgery may be indicated.

The other choices are not the best options for immediate management. This individual cannot be followed simply with transfusions and serial CBC's because he appears to still be actively bleeding.

Helicobacter pylori infection may very well be playing a part in the etiology of this man's ulcer, but evaluation for H. pylori can be done with a biopsy at the time of his endoscopy; it will not help in his immediate management.

A barium esophagram will not identify actively bleeding ulcers and cannot treat active bleeding.

While NSAID, alcohol, and tobacco use may have precipitated this man's GI bleed, counseling about his use of these substances will not sufficiently treat his immediate bleed.
topical ntg 0.2%-0.4%
the correct response is topical nitroglycerin 0.2 - 0.4%.

The patient is likely suffering from an anal fissure. Anal fissures often affect infants as well as middle-aged individuals. The majority of fissures are considered primary, and they are caused by local trauma, such as passage of hard stool, prolonged diarrhea, vaginal delivery, or anal sex. They are described linear or rocket shaped ulcers that are usually < 5 mm in length. Common presentation of anal fissures include a tearing pain that accompany bowel movements; there is also bright red rectal bleeding that is limited to a small amount noted on the toilet paper or surface of the stool. The patient described all of these components. Patients will also note perianal pruritus or irritation, all of which the patient admits to experiencing.

Because this patient has had a several incidences very similar to the one he is currently presenting with, this episode should be categorized as a chronic anal fissure. Once a fissure is branded as such, treatments considered will include topical 0.2 - 0.4% nitroglycerin, topical 2% diltiazem ointment, or even injection of botulinum toxin directly into the internal anal sphincter. All of these treatments listed result in healing a chronic fissure 50 - 80% of the time; 40% of cases can recur after treatment.

Topical lidocaine 5% and lidocaine plus prilocaine 2.5% are topical anesthetics that are indicated fortemporary relief of what the patient is experiencing; however, they will not promote healing of the lesion. Topical bacitracin is not indicated for symptom relief or for healing of anal fissures. Topical hydrocortisone cream 1% may decrease inflammation of the lesion; however, it will not promote overall healing.
Vitamin B12 supplementation
A strict vegan diet consists of fruits, vegetables, and grains. Meat (including fish, seafood, and poultry), dairy products, and eggs are excluded. This commonly results in vitamin B12 deficiency, presenting as macrocytic, normochromic anemia/megaloblastic anemia. The clinical manifestations associated with vitamin B12 deficiency include hematological, neurological, and psychiatric manifestations. The hematological manifestations include macrocytic (megaloblastic) anemia and pancytopenia in advanced cases. Paresthesias, peripheral neuropathy, and demyelination of the corticospinal tract and dorsal columns (subacute combined systems disease) are the neurological sequelae associated with vitamin B12 deficiency. Psychiatric disorders associated with vitamin B12 deficiency include impaired memory, irritability, depression, and dementia; rarely, psychosis is a result of the deficiency. Treatment of vitamin B12 deficiency includes administration of cobalamin through oral or parenteral route. Cobalamin is administered as 1000 mcg daily intramuscular (IM) 2 times per week for 2 weeks during the initial period, which is followed by 1000 mcg/wk IM for 5 weeks; afterwards, the patient must receive maintenance therapy of 100 - 1000 mcg IM every month for life.

If iron studies indicate the need, iron supplementation may be considered in a hypochromic, microcytic anemia.

Folate supplementation should be considered in macrocytic anemia with decreased serum folate levels.

A normocytic, normochromic anemia may occur due to blood loss, aplastic anemia, sickle cell anemia, or end-stage renal disease. If severe, transfusion may be necessary.

End-stage renal disease may result in decreased production of erythropoietin (EPO), and EPO therapy may be necessary.
This patient's most concerning diagnosis is a malignant esophageal lesion. However, nonmalignant etiologies may also be responsible for this presentation.

A barium esophagography is obtained as the first study to evaluate dysphagia. In patients with progressive esophageal dysphagia, a radiographic barium study is used to differentiate between mechanical lesions (such as peptic stricture and esophageal cancer) and motility disorders (such as achalasia). The sensitivity of barium radiography for detecting esophageal strictures is greater than that of endoscopy. Barium studies also provide an assessment of esophageal function and morphology that may be undetected on endoscopy. Hypopharyngeal pathology and disorders of the cricopharyngeal muscle are better appreciated on radiographic examination, particularly with videofluoroscopic recording. Either a positive or a negative study is usually followed by an endoscopic evaluation; it is done in order to clarify findings in the case of a positive examination or to add a level of certainty in the case of a negative one.

A chest X-ray may reveal adenopathy, a widened mediastinum, metastatic lesions to the lungs or bone, or signs of tracheoesophageal fistula, such as pneumonia. It will not, however, reliably identify esophageal lesions.

Endoscopy with biopsy establishes the diagnosis of esophageal carcinoma with high reliability. It is the study of choice for evaluating persistent heartburn, odynophagia, and structural abnormalities detected on barium esophagography.

Ambulatory esophageal pH monitoring is the preferred study for documenting acid reflux. It is indicated in the following clinical scenarios: for patients being considered for anti-reflux surgery with a normal endoscopy; in patients with a normal endoscopy but with continued reflux symptoms following therapy with a proton pump inhibitor; and in the evaluation of atypical reflux symptoms that continues despite anti-reflux therapy.

Patients with alarm symptoms, such as unexplained weight loss, odynophagia, jaundice, recurrent vomiting, blood loss, a palpable mass or lymph node, or a family history of GI malignancy, should have diagnostic testing performed promptly.
GI bleed
The patient described in this question is at most risk for a gastrointestinal bleed secondary to his chronic non-steroidal use. Patients in their 60s are at an approximate 3-fold increased risk for a gastrointestinal bleed when they take non-steroidal anti-inflammatory medications compared to not taking them. The non-steroidals inhibit the prostaglandins responsible for homeostasis, and thus can lead to gastrointestinal mucosal injury.
Chronic analgesic consumption is associated with chronic kidney disease. Analgesic nephropathy is still a relatively uncommon cause of chronic kidney disease; its prevalence is higher in Europe and Australia than in the United States, where it accounts for only 2-4% of the cases of end stage kidney disease.

End stage kidney disease is the most advanced stage of kidney disease, for which patients typically require dialysis.

Some studies have debated causality, however a recent New England Journal of Medicine article addressed the risk in patients with chronic consumption and found a 2.5-5 fold increase risk of chronic renal failure in patients who chronically used acetaminophen vs. those who did not. Cumulative lifetime use increased the odds of renal failure, and results were similar for patients who took aspirin. The highest risk was noted among patients who took >500g/yr acetaminophen (>1.4g/day). Other studies have found increased risk among users of >3-5 gram per lifetime and >6 tablets/day for 3 years.

The National Kidney Foundation currently classifies 5 stages of chronic kidney disease in patients who have structural or functional damage of the kidneys for greater than or equal to 3 months, as evidenced by abnormal pathology or laboratory markers of kidney damage (blood, urine, imaging studies). Patients who have a GFR less than 60ml/min/1.73m3 for at least 3 months, with or without such markers, are also considered to have chronic kidney disease.

This patient presumably already has chronic aches (for which he takes the ibuprofen) and should not be at any additional risk for accidental injury secondary to the ibuprofen.
thiamine def
Vitamin B1 (or thiamine) deficiency results in beriberi, which is characterized by:

A bilateral symmetric peripheral neuropathy beginning in the legs. Patients may present with burning sensation in the feet and difficulty rising from a squatting position. On examination, there may be decreased vibratory and position sensation in the toes. Ankle jerk and knee jerk reflexes may be absent.
Wernicke-Korsakoff syndrome, which is comprised of nystagmus, ophthalmoplegia, ataxia, memory loss, and confabulation.
Congestive heart failure with tachycardia, peripheral edema, and cardiomegaly.

Causes include inadequate dietary intake, especially from a diet based on polished rice and alcoholism. Dietary sources rich in vitamin B1 include yeast, legumes, liver, whole grains, and enriched cereal products.

In cases of riboflavin (or Vitamin B2) deficiency, patients present with angular stomatitis and cheilosis. On examination, they are pale, have atrophic glossitis, and the tongue may appear magenta.

In cases of vitamin K deficiency, patients present with bleeding tendencies, which include epistaxis, menorrhagia, and hematuria. The prothrombin time (PT) and the activated partial thromboplastin time (aPTT) are usually prolonged.

In cases of vitamin D deficiency, children can present with inability to walk unsupported due to muscle weakness and lower limb skeletal deformities, such as genu varum and genu valgum. They may also have prominent costochondral junctions.

In cases of iron deficiency, patients can present with feeling weak, dizzy, and tired; they may experience syncope. On examination, they have pale conjunctivae and koilonychia.
barium enema
Intussusception, in which a part of the bowel telescopes into an adjacent part of the bowel, is the most common cause of bowel obstruction in children between ages 6 months and 3 years of age. Typical presenting signs include intermittent colicky, abdominal pain, vomiting, and bloody, mucousy stools sometimes described as "currant-jelly" in appearance. Some children may present with only irritability and progressive or alternating lethargy. On abdominal examination, a slightly tender, sausage-shaped palpable mass is characteristic.

Most cases are idiopathic; however, it is felt that hypertrophied Peyer's patches in the ileum stimulate peristalsis and cause the intussusception. Other causes, usually found in older children, include polyp, lymphoma, intestinal parasites, Meckel diverticulum, intramural hematoma, and hemangioma. Ileocolic intussusceptions are by far the most common, but cecocolic and ileoileal presentations may occur.

The telescoping of the bowel causes diminished venous blood flow resulting in edema and hemorrhage, leading to decreased arterial blood flow, ischemia, and infarction. Left untreated, death occurs in most cases. The diagnostic test of choice is to perform a barium enema; it helps in confirming the diagnosis because the enema shows a typical "cervix-like mass" or a "coiled spring" appearance on the evacuation film. Treatment by hydrostatic reduction with the same barium enema is successful in 50 - 90% of cases. Air contrast enemas are being used widely now, but barium enemas are still standard as well. If the intussusception is not reducible by the enema, then surgical treatment is indicated.

Imaging with CT scan is usually not indicated for establishing the diagnosis of intussusception, unless a lead point is suspected. A lead point is found in only 10% of children less than 2 years old.

Plain radiographs may be normal or show a pattern of small bowel obstruction with no gas in the right colon, indicating intussusception; however, it needs to be followed up with barium enema for confirmation.

An upper GI endoscopy would be unlikely to demonstrate any pathology at the ileocolic level, and a colonoscopy would not be as helpful in either identifying the intussusception or providing therapeutic relief.
nonalcoholic steatohepatitis
Explanation Nonalcoholic steatohepatitis (NASH) is a diagnosis of exclusion in patients who have an asymptomatic increase in liver enzymes where no other etiological factor can be determined. It is a definite clinical entity seen most commonly in patients with diabetes, obesity, or hyperlipidemia.
In this patient, her alcohol intake is not enough to cause alcoholic hepatitis. Also her ALT is higher than AST, the reverse of that seen in alcohol-related liver disease. Primary biliary cirrhosis and cholestatic hepatitis have an increase in alkaline phosphatase due to cholestasis, which is normal in this patient. Autoimmune hepatitis is usually associated with a high ANA.

NASH can also be seen, though uncommonly, with other conditions like extensive abdominal surgery, rapid weight loss or severe starvation, hyperalimentation, and certain drugs like tamoxifen and amiodarone. The pathogenesis of NASH is not fully understood, but there are several theories. Insulin resistance is the most widely accepted one, which leads to hepatic steatosis and steatohepatitis. Other oxidative injuries can also cause inflammation and stimulate steatohepatitis like hepatic iron, intestinal bacteria, deficiency of anti-oxidants, etc. Ultrasound may show fatty liver, and liver biopsy will reveal fatty change with or without fibrosis and cirrhosis. There is no particular treatment for NASH, though better diabetic control, gradual weight loss, and treatment of hyperlipidemia are recommended. Less than 25% progress to cirrhosis of the liver. It has a much better prognosis than alcoholic hepatitis.

Primary biliary cirrhosis is a chronic liver disease of middle-aged women of unknown etiology. An immunologic basis has been proposed. Alkaline phosphatase is increased due to cholestasis as well as IgM level. Early symptoms include pruritus and fatigue. Later jaundice, arthralgias, hyperpigmentation, keratconjunctivitis, steatorrhea, osteomalacia, and vitamin deficiencies may occur. Anti-mitochondrial antibodies are positive in more than 90% of patients and are diagnostic. Liver biopsy shows granulomatous inflammation of the bile ducts. Treatment includes replacement of vitamins, ursodeoxycholic acid, cholestyramine for itching, cyclosporine, colchicines, and methotrexate. Studies are ongoing with lamivudine, zidovudine, and benzafibrate.

Autoimmune hepatitis is a heterogeneous condition characterized by the presence of autoantibodies, abnormal liver enzymes, absence of other etiological factors, positive ANA, marked increase in serum gamma globulins, and piecemeal necrosis on liver biopsy. Antismooth muscle antibody, soluble liver antigen antibodies, and antibodies to liver/kidney microsomal (LKM) antigens are seen. Steroids and azathioprine are used for treatment.
Barium study
The recollection of slow progressing difficulties in initiating swallowing and regurgitation in an older patient makes you suspect Zenker diverticulum. Your clinical diagnosis is supported by bad breath and throat clearing. Definitive diagnosis is made by barium studies.

Endoscopy is actually contraindicated in this patient because the lesion is proximal and there is a risk of perforation of the pharynx.

Endoscopic ultrasound is performed in patients with esophageal carcinoma for staging. Your patient has no typical signs of esophageal carcinoma (progressive dysphagia for solid foods first, followed by liquids, with weight loss in a smoker and/or alcoholic). That diagnosis is not excluded; however, the probability of Zenker diverticulum will prevent you from choosing endoscopy as the first step in management.

24 hours pH monitoring should be considered in a patient with symptoms of gastroesophageal reflux (GERD) when the diagnosis is not clear. GERD will present with epigastric or substernal pain, sore throat, metallic taste in mouth, hoarseness, cough, and wheezing. It is not likely that your patient has GERD.

Manometry should be considered if you suspect a disorder of esophageal peristalsis, as is the case in achalasia, esophageal spasm, nutcracker esophagus, or lower esophageal sphincter diseases. These disorders can present with dysphagia for both solid foods and liquids, sometimes accompanied by pain and weight loss. Manometry includes the placement of a nasogastric tube, and the procedure will increase the risk of pharyngeal perforation. Manometry should be performed only after barium studies exclude Zenker diverticulum.
staph aureus
In cases of Staphylococcus aureus food poisoning, patients present with severe nausea and vomiting. They may also develop diarrhea, abdominal pain, and occasionally headache and fever. Stools are watery but not blood stained. The onset of symptoms is 1 to 6 hours after ingesting the contaminated food. Common culprits include processed meat, dairy products, and potato salads, especially when prepared by food handlers with skin infections that are left at room temperature. Several persons may be similarly affected. There are no fecal leukocytes or trophozoites on examination of the stool. Management includes intravenous replacement of fluid and electrolytes.

In cases of Clostridium perfringens, food poisoning, patients present with watery diarrhea 8 to 24 hours after ingesting contaminated food like inadequately cooked meat or legumes. No fecal leukocytes or trophozoites are present on stool examination.

In cases of Escherichia coli serotype O157:H7 food poisoning, patientspresent with watery diarrhea, which can become bloodstained. Sources of infection include undercooked beef. A stool examination reveals polymorphonuclear leukocytes.

Giardia lamblia can be acquired by drinking contaminated water. Patients present with watery diarrhea. The incubation period is around 1 week. There are trophozoites in the stool, but no leukocytes.

Patients with Salmonella typhi food poisoning usually present with bloody diarrhea. Sources of infection include beef, poultry, eggs, and dairy products. Examination of the stool reveals mononuclear leukocytes.
continue metroniadazole
The patient has an uncomplicated case of Clostridium difficile colitis. Current guidelines call for her to continue metronidazole for a course of 10-14 days.

C. difficile is a Gram-positive, spore-forming rod; it is accountable for 15 to 20% of antibiotic-related cases of diarrhea and almost all cases of pseudomembranous colitis. Disruption of the normal colonic micro flora is usually the precipitating event for C. difficile colitis. This disruption is generally caused by the use of broad-spectrum antibiotics, such as clindamycin, broad-spectrum penicillin, and cephalosporins. Colonization of C. difficile occurs after the micro floral disruption, during which the heat-resistant spores are converted into vegetative spores. Asymptomatic carrier state or clinical manifestations of C. difficile colitis develop depending on the host immune factor. Manifestations range from mild diarrhea to life-threatening C. difficile pseudomembranous colitis.

The use of clindamycin prior to the occurrence of the diarrhea strongly suggests pseudomembranous colitis as the cause of the diarrhea. Pseudomembranous colitis is an inflammatory bowel disorder associated with antibiotic use. It is due to toxins of Clostridium difficile. The toxins bind to intestinal mucosal epithelial cells and cause watery, secretory diarrhea, abdominal pain, fever, and dehydration. The mucosa shows yellow plaques, focal ulceration, and exudates, which form the characteristic pseudomembrane. Stool samples are positive for fecal leukocytes, and the toxin and the organism may be cultured.

Metronidazole is a first line therapeutic agent in the treatment of C. difficile colitis, given in the dose of 500 mg orally, 3 times a day for 10-14 days. It is inexpensive and has an efficacy of > than 90%. The response to treatment with metronidazole is usually rapid, with fever resolution occurring within 24 hours and diarrhea resolution within 4-5 days.

Vancomycin is approximately equally effective as metronidazole in the treatment of C. difficile colitis. Vancomycin should be initiated in patients with severe symptoms (e.g., leukocytosis >15,000 cells/uL or serum Cr 1.5 x normal). It is administered orally in the dose of 125 mg 3 times a day for 10 - 14 days. Initial treatment of severe cases of pseudomembranous colitis must be aggressive, with intravenous metronidazole and oral vancomycin given in combination. In cases where medical therapy fails, surgical intervention, such as colectomy and ileostomy, may be necessary.

Ampicillin and clindamycin, being the offending agents, should not be administered; they may cause the condition to worsen. Ciprofloxacin is not the drug of choice for treating unresolved cases of pseudomembranous colitis following metronidazole treatment.
acute appendicitis
Acute appendicitis can affect all ages and is a common cause of emergency surgery; there is a lifetime incidence of approximately 6%. While appendicitis has some very classic features, it still can be very difficult to diagnose. It is especially dfficult to diagnose in very young or old patients, in patients with concomitant pregnancy, or in patients with other diseases (e.g., diabetes or AIDS).

This patient's presentation is classic for appendicitis. The classic presentation is one of anorexia, with abdominal pain that begins in the periumbilical area. The pain becomes steady and migrates to the right lower quadrant in a 24-hour period. Nausea, emesis, and/or diarrhea are common. Rebound tenderness can be present and reflects peritoneal inflammation; rebound is less apparent in elderly or obese patients.

Fever may or may not be present, although over 80% of patients with acute appendicitis will have an elevated white blood cell count. Radiographic exams that may be useful, if positive, include plain films of the abdomen (to look for a fecalith or gas in the appendix), a barium enema (to look for non-filling of the appendix), ultrasound (especially in pregnancy, to look for a tender, immobile, non-compressible structure), or a CT scan (to look for an inflamed appendix). However, surgical evaluation with laparoscopy or laparotomy is the definitive test for appendicitis, and is the treatment of choice if suspicion is high.

Acute salpingitis and a tubo-ovarian abscess are often high on the differential diagnosis list in a young female with abdominal pain, particularly in this patient with her recent menses and new sexual partner. However, pelvic inflammatory disease is usually associated with cervical motion tenderness; the patient will usually have bilateral lower abdominal pain, since PID is an ascending infection from the cervix up through the fallopian tubes. The normal appearing cervix and cervical discharge also make PID less likely, although this patient should be tested for Neisseria gonorrhoeae and Chlamydia trachomatis during the pelvic exam.

Renal lithiasis seems less likely since the patient does not complain of flank pain and has a normal urinalysis.

Ectopic pregnancy should be a concern with any sexually active female, but the history of her recent menses makes that diagnosis less likely; a serum pregnancy test is still indicated, however, to entirely rule out the potentially life-threatening entity.
Hep C
Hepatitis C is a viral infection caused by an enveloped RNA virus belonging to the flaviviridae family. It is transmitted parenterally by sharing needles during parenteral drug use as well as from mother to child. The medical staff is also at risk of infection and sexual transmission can also occur. Other groups at risk of infection are those undergoing hemodialysis and recipients of organ transplant before 1992. Blood, blood products, and organ donors have been screened for hepatitis C since 1992 and the risk has been minimized in recipients now.

Acute hepatitis C is asymptomatic in 60 - 70% of patients. Chronic infection develops in 55 - 85% of patients, chronic liver disease in 70% of patients, and cirrhosis in 5 - 20% of patients. Combination therapy with pegylated interferon and ribavirin is the treatment of choice resulting in sustained response rates of 40 - 80%. Hepatitis C is the leading indication for liver transplant in the US.

Hepatitis A is transmitted by the feco-oral route and it has no chronic form. Once infected, it provides immunity for life. A vaccine is also available for travelers to endemic areas and other susceptible groups.

Hepatitis B is also transmitted parenterally and sexually. The risk of chronic infection varies with age; for those over 5 years of age, it is about 2 - 6%. Infants have a risk of chronic infection of 90%, and between 1 - 5 years it is about 30%.

Hepatitis D occurs as a co-infection or superinfection in patients infected with hepatitis B. It cannot infect a person by itself because it requires the envelope protein of hepatitis B. Chronic HBV carriers who acquire HDV superinfection usually develop chronic HDV infection.

Hepatitis E is transmitted feco-orally, and the most common source is contaminated water. The acute hepatitis is most severe in pregnancy, especially the 3rd trimester. It has no chronic form.

Hepatitis A and E are rare in the United States.
Celiac disease
Celiac disease is a hereditary disorder caused by gluten intolerance. Gluten is found in wheat, rye, barley, and oats. Patients may be asymptomatic or may present with diarrhea, abdominal discomfort, distention, and steatorrhea (stools are pale, malodorous, and difficult to flush because they float on the toilet water). Patients may have anemia from iron and folate deficiency, osteomalacia and bone pains from calcium deficiency, and edema from hypoproteinemia. Diagnosis is confirmed by a small intestine mucosal biopsy which shows a flat mucosa due to villous atrophy, and by subsequent improvement on a gluten-free diet. Specific treatment includes a gluten-free diet.

Whipple's disease mainly affects men; it is caused by the bacterium Tropheryma whippelii. It is a multisystemic disease that affects the small intestines, joints, brain, heart, and eyes. Patients can present with diarrhea, steatorrhea, abdominal pain, weight loss, and joint pains. On examination, patients may be pale with lymphadenopathy. Histological examination of a small bowel mucosal biopsy reveals PAS-positive foamy macrophages. Treatment is with trimethoprim-sulfamethoxazole or chloramphenicol.

Short bowel syndrome is usually the result of surgical resection of the intestines or a jejunoileal bypass. The malabsorption is a result of inadequate absorptive surface. Malabsorption of vitamin B12 results in paraesthesias; malabsorption of calcium results in bone pain and carpopedal spasms.

Tropical sprue is an acquired disease that affects both visitors and natives of tropical areas (e.g., the Caribbean and South India). Its etiology is unknown. Patients usually present with diarrhea and weight loss; they report that their stools are soft and bulky (steatorrhea). They may also develop deficiencies of folate and cobalamin. Stool microscopy should be done to look for cysts and trophozoites. Histological examination of a small bowel mucosal biopsy aids in making the diagnosis. Treatment is with tetracycline or oxytetracycline.

Lactose intolerance results from a deficiency of lactose which is a disaccharidase in the mucosal cells of the small intestine; it splits the disaccharide lactose into glucose and galactose. Patients complain of borborygmi, flatulence, nausea, abdominal cramps, pain, and diarrhea after ingesting lactose-containing food (e.g., milk). Treatment includes following a lactose-free diet.
Amitriptyline at bed time
Irritable bowel syndrome (IBS) is a disorder of gastrointestinal motility; it causes abdominal pain, constipation, diarrhea, and/or bloating. The cause of irritable bowel syndrome is unknown; however, many things may aggravate the symptoms. Some patients have mood disorders, but the gastrointestinal and psychological symptoms are not necessarily synchronous in these patients. In others, emotional factors, dietary, drug, or hormonal changes may be associated with changes in gastrointestinal motility.

There is an increased incidence of irritable bowel syndrome in individuals who were victims of physical or sexual abuse, either as children or adults; therefore, when evaluating patients with IBS, particularly those with refractory complaints, an investigation for a history of prior abuse is important.

2 major clinical types of IBS exist: constipation-predominant and diarrhea-predominant varieties. In constipation-predominant IBS, episodes of constipation are common, and many patients complain of abdominal pain, which may be intermittent and colicky or a dull constant ache. The pain may be relieved by a bowel movement. In diarrhea-predominant IBS, diarrhea often occurs after eating or upon waking. Pain and bloating are common.

Treatment of IBS is largely supportive. The chronic nature of IBS should be emphasized, and education about the disorder is important. Increasing dietary fiber can help many patients' constipation. Regular exercise is also helpful, and it can help with psychological stressors that may be exacerbating their bowel symptoms.

Tricyclic antidepressants help many patients with IBS, helping with pain, bloating, and diarrhea. They must be taken chronically, however, to be of use. Thus, amitriptyline at bedtime is the only correct choice of the options given. Selective serotonin reuptake inhibitor (SSRI) agents have also been useful in the management of IBS, but given this patient's failure of 2 such agents, a trial of amitriptyline is a better choice then trying paroxetine, which is another SSRI. Anticholinergic agents may also be useful, as may diphenoxylate or loperamide for those patients with diarrhea. Narcotics and sedatives are not good choices for therapy because they have the potential for dependency, and IBS is a chronic condition.
Vitamin D Deficiency
In cases of vitamin D deficiency, children can present with an inability to walk unsupported due to muscle weakness and lower limb skeletal deformities such as genu varum (bow legs) and genu valgum (knock knees). On examination, they may have prominent costochondral junctions (rachitic rosary) and indentation of the lower ribs at their diaphragmatic attachment (Harrison's groove). Causes include inadequate dietary intake and inadequate exposure to sunlight. They should be encouraged to be exposed to ultraviolet irradiation of the skin as well as increase their dietary sources of vitamin D which include fortified milk, fish liver oils, butter, egg yolk, and liver.

In cases of riboflavin (or Vitamin B2) deficiency, patients present with angular stomatitis and cheilosis. On examination, they are pale, have atrophic glossitis, and the tongue may appear magenta.

Vitamin B1 (or thiamine) deficiency results in beriberi, which is characterized by:

A bilateral symmetric peripheral neuropathy beginning in the legs.
Wernicke-Korsakoff syndrome, which is comprised of nystagmus, ophthalmoplegia, ataxia, memory loss, and confabulation.
Congestive heart failure with tachycardia, peripheral edema, and cardiomegaly.

In cases of vitamin K deficiency, patients present with bleeding tendencies, which include epistaxis, menorrhagia, and hematuria. The prothrombin time (PT) and the activated partial thromboplastin time (aPTT) are usually prolonged.

In cases of iron deficiency, patients can present with feeling weak, dizzy, and tired; they may experience syncope. On examination, they have pale conjunctivae and koilonychia.
Vitamin A
Vitamin A is involved in the general health of epithelial tissue. It exists in various forms that have different functions in the organism. The 11-cis-retinal form functions as a component of the vision cycle. It combines with the protein opsin to form rhodopsin, which is the photosensitive molecule in the discs of the rod cells. Upon absorption of light, the 11-cis form is converted to trans-retinal that dissociates from the opsin protein. This cascade converts light into atomic motion and then into a nerve signal. A single photon is absorbed by a rod cell and leads to hyperpolarization of the plasma membrane by closing the cation-specific channels. The trans-retinal is then isomerized back to 11-cis retinal, which can then bind opsin again and go through another cycle.

A deficiency in vitamin A leads to night blindness and eventually deterioration of the outer rod segments. Vitamin A (all-trans-retinol) is converted to 11-cis-retinal in several steps. Retinyl phosphate functions in the synthesis of some glycoproteins and mucopolysaccharides as a glycosyl donor. This is especially true for certain glycoproteins necessary for normal growth regulation and mucous secretion. Retinol and all-trans-retinoic acid bind to specific receptors in the cell, the nuclear receptor superfamily. This family of receptors includes those that bind estrogen, progesterone, glucocorticoids, vitamin D3, and thyroxine, in addition to retinol and all-trans-retinoic acid. All of these receptors contain a highly conserved DNA binding domain, a hormone-binding domain, and a variable activation domain.

β-Carotene functions as an antioxidant in the cell. β-Carotene is the precursor of retinal, the chromophore in visual pigments. Synthetic forms of vitamin A are also now available and used as drugs. 13-cis-retinoic acid is used in the treatment of acne. Etretinate, an aromatic derivative of all-trans- retinoic acid, is used in the treatment of psoriasis.

The structures of some of these important retinoids are shown in the included image.
3. Wireless capsule endoscopy
Wireless capsule endoscopy is performed by ingestion of a battery-powered capsule containing a camera and a transmitter. The capsule transmits images to sensors outside the patient during its transit in the gastrointestinal tract. Indications for capsule endoscopy are still evolving, but several series have shown that capsule endoscopy is more sensitive than small bowel radiography or push enteroscopy for locating the source of small-bowel bleeding. The most common etiologies of bleeding in this region are angioectasia and Crohn's disease. Several other small bowel lesions, such as tumors (leiomyoma, lymphomas, carcinoids, or carcinomas), varices, and polyps, have also been described.

An important concern is the possibility of capsule impaction and small bowel obstruction. Some centers are reluctant to perform capsule endoscopy in patients with partial or intermittent obstruction of the small bowel. However, capsule impaction may reveal the site of a lesion and allow its surgical removal, obviating the need for intraoperative enteroscopy. Other relative contraindications are incapacity of cooperating with the examination (e.g. dementia), swallowing disorders, esophageal stricture, gastroparesis, and poor surgical risk. In patients with obstruction or gastroparesis, the examiner may place the capsule endoscopically.

This patient has no signs of ulcer activity. Therefore, biopsy of the duodenal scar is not indicated.

A 99mTc scan is the test of choice for Meckel's diverticulum, a remnant of the embryonic omphalomesenteric duct found in 1.5% of the general population. Its most common location is the antimesenteric border of the mid-to-distal small bowel. Some diverticula contain ectopic, acid-producing gastric mucosa. Therefore, they can ulcerate and bleed. Rectal bleeding caused by Meckel's diverticulum is often maroon or brick-red in color, and its incidence decreases with age. Therefore, this diagnosis is unlikely in this case.

Angiography can be used if other less invasive procedures (i.e. small bowel radiography, push enteroscopy, or small bowel radiography) are non-diagnostic.

Computed tomography is not indicated in the absence of other symptoms indicating a specific etiology (e.g. a palpable mass or suspicion of pancreatic disease).

Of note, colonoscopy after rapid oral purging has emerged as the procedure of choice for the evaluation of acute lower GI bleeding, and it also provides a means for therapy. Scintigraphy and/or angiography also play important roles in diagnosis and embolization when colonoscopy reveals negative findings or when it is not feasible.
Ischemic Colitis
This is a classic presentation of ischemic colitis. Ischemic colitis occurs when there is obstruction of the colonic blood supply, causing ischemia with inflammation and ulceration of the colonic mucosa. The area of the splenic flexure is most at risk for ischemia because it is the watershed area of the arterial supply to the colon.

Ischemic colitis is most commonly seen in elderly individuals. These patients typically present with an acute onset of pain associated with bloody diarrhea, and they have an area of tenderness corresponding to the ischemic segment of colon. Patients may experience recurrent bouts of ischemic colitis. Sigmoidoscopy makes the diagnosis in 85% of patients; 15% will have ischemia in areas proximal to the reach of a sigmoidoscopy. The majority of these patients will improve with supportive care (hydration and prophylactic antibiotics, in case of bacterial transmigration). However, some patients have much more severe disease, which may even require emergency colectomy.

The most important condition to differentiate from ischemic colitis is that of small bowel ischemia. Small bowel ischemia can lead to gangrene of the intestine. Most commonly, these patients have developed occlusion of some of the distribution of the superior mesenteric artery, either from acute thrombosis in an area of atherosclerosis, or from embolic disease. These patients classically have pain out of proportion to their exam, at least early in the process, and they do not usually have an area of localized tenderness on palpation. These patients can have leukocytosis on the level of 20,000 to 30,000/μL, and they may exhibit a lactic acidosis and elevated amylase levels. Their stool is usually positive for occult blood, but frank blood is only rarely seen. Early diagnosis is very important, although often difficult, and urgent surgery is the only treatment.

Renal or ureteral lithiasis can cause severe abdominal pain, and these patients can have diarrhea as well, but it should not cause hematochezia or localized anterior abdominal tenderness.

Diverticulitis is more common on the left, which is the case with this patient's pain, but it typically does not cause hematochezia. Additionally, the sudden onset of very severe pain would not be typical of diverticulitis.

Infectious colitis can cause abdominal pain and hematochezia, but the improvement in her pain over such a short time period would be atypical for an enterotoxic infection. Infection should be considered in this patient because of her recent travel history.
Prescribe Ursodiol
Both morbid obesity and rapid weight loss are risk factors for development of cholecystitis. Gallstones may be present within the gallbladder and remain asymptomatic, or the gallbladder walls may become inflamed, resulting in cholecystitis. Ursodiol is approved for prevention of gallstones in obesity patients with rapid weight loss. It would be the best choice in health maintenance and delaying or preventing need for surgical cholecystectomy.

Orlistat is a prescription medication approved for treatment of obesity. Its mechanism is to block fat absorption. It does not have a direct role in health maintenance or prevention of cholecystitis or cholelithiasis. In fact, it has pronounced gastrointestinal side effects.

Over-the-counter omeprazole is a commonly used proton-pump-inhibitor (PPI); it is helpful in acid lowering in the stomach and treatment of gastroesophageal reflux disease. It has not been shown to help gallbladder disease, and there is some evidence that PPIs may worsen it.

Reducing the patient's exercise may aggravate her condition and negatively impact her weight loss. Exercise has an inverse relationship with cholecystitis and rates of cholecystectomies, so this patient should be encouraged to continue frequent exercise.

This patient should not be instructed to restrict caloric consumption further. She is already losing weight quite rapidly at around 4 pounds per week. Her daily caloric intake is low; recommending further restriction will likely discourage her, and there will not be any benefit in regard to her gallbladder disease.
Lactose intolerance
Lactose intolerance results from a deficiency of lactose, a disaccharidase in the mucosal cells of the small intestine which splits the disaccharide lactose into glucose and galactose. Patients note borborygmi, flatulence, nausea, abdominal cramps, pain, and diarrhea after ingesting lactose-containing food (e.g., milk). Laboratory investigations reveal that the diarrheal stools are acidic. When the hydrogen breath test is administered, there is elevated hydrogen content in the expired air because the colonic flora digests the unabsorbed lactose. Treatment includes following a lactose-free diet.

Celiac disease is a hereditary disorder caused by gluten intolerance; gluten is found in wheat, rye, barley, and oats. Patients may be asymptomatic or may present with diarrhea, abdominal discomfort, distention, and steatorrhea; their stools are pale, malodorous, and difficult to flush because they float on the toilet water. Patients may have anemia from iron and folate deficiency, osteomalacia and bone pains from calcium deficiency, and edema from hypoproteinemia. Diagnosis is confirmed by a small intestine mucosal biopsy which shows a flat mucosa due to villous atrophy, and by subsequent improvement on a gluten-free diet. Specific treatment includes a gluten-free diet.

Whipple's disease mainly affects men; it is caused by the bacterium Tropheryma whippelii. It is a multisystemic disease which affects the small intestines, joints, brain, heart, and eyes. Patients can present with diarrhea, steatorrhea, abdominal pain, weight loss, and joint pains. On examination, they may be pale and have lymphadenopathy. Histological examination of a small bowel mucosal biopsy reveals PAS-positive foamy macrophages. Treatment is with trimethoprim-sulfamethoxazole or chloramphenicol.

Short bowel syndrome is usually the result of surgical resection of the intestines or a jejunoileal bypass. The malabsorption is a result of inadequate absorptive surface. Malabsorption of vitamin B12 results in paresthesias; malabsorption of calcium results in bone pain and carpopedal spasms.

Tropical sprue is an acquired disease that affects both visitors and natives of tropical areas (e.g., the Caribbean and South India). Its etiology is unknown. Patients usually present with diarrhea and weight loss; they report that their stools are soft and bulky (steatorrhea). They may also develop deficiencies of folate and cobalamin. Stool microscopy should be done to look for cysts and trophozoites. Histological examination of a small bowel mucosal biopsy aids in making the diagnosis. Treatment is with tetracycline or oxytetracycline.
A 38-year-old man presents with sudden onset of acute upper abdominal pain since the previous night associated with nausea, several episodes of vomiting, and weakness. The pain is mostly in the epigastric region with constant, severe, and steady radiation to the back. He also has a low grade fever since this morning without any chills. He denies diarrhea or dysuria. His past history is significant for hypertension, for which he takes amlodipine 10 mg daily and enalapril 5 mg daily. He has smoked half a pack of cigarettes daily for the past 12 years. He initially denies drinking alcohol except on the weekends occasionally, but on further and repeated questioning he says he drinks 3-4 beers daily and had been drinking continuously for the last 2 days with his friends while watching sports on TV. Family history is unremarkable.
On examination he has a temperature of 100.6° F, pulse 106/minute, BP 150/92 mm Hg, and respiratory rate is 20/minute. There is no pallor, icterus, cyanosis, or lymphadenopathy. Mucus membranes are dry, and skin is somewhat clammy. Lungs are clear, and heart sounds normal except for sinus tachycardia. Abdominal exam reveals diffuse tenderness in the epigastric and right as well as left upper quadrants. There is some distension and mild guarding in the upper abdomen. Bowel sounds are hypoactive, but there is no ascites or hepatosplenomegaly. Rectal exam is normal. Labs reveal Hb 15g%, WBC 14,500/uL, platelets 400,000/uL, AST 42 U/L, ALT 36 U/L, AP 26 U/L, amylase 3600 U/L, lipase 546 U/L, BUN 25 mg/dL, creatinine, 1.5 mg/dL, bilirubin 1.2 mg/dL, and random blood sugar 110 mg/dL.



Question
Which of the following is one of the predictors of acute pancreatic necrosis if present at diagnosis along with 2 other factors?
Answer Choices
1 Age over 50 years
2 WBC count more than 16,000/uL
3 Blood glucose over 180mg/dL
4 Serum LDH over 300 U/L
5 AST more than 200 U/L
2 WBC count more than 16,000/uL
Explanation This patient is suffering from acute alcoholic pancreatitis. The 2 most common causes of acute pancreatitis are gallstones and alcohol. Other causes include hypertriglyceridemia, hypercalcemia, abdominal trauma, ERCP, and drugs like valproic acid, azathioprine, mercaptopurine, didanosine, thiazides, tetracyclines etc. Assessment of severity is done by either Ranson's criteria on admission and at 48 hours or by the Acute Physiology and Chronic Health (APACHE) II scoring system. Ranson's criteria include:
(1) Age more that 55 years
(2) WBC count more than 16,000/Ul
(3) Blood glucose more than 200mg/dL
(4) Serum LDH over 350 U/L
(5) AST over 250 U/L.

3 or more criteria on admission predict a complicated course with possibility of pancreatic necrosis.

At 48 hours development of any of the following indicates a worsening prognosis:

(1) Hematocrit drop of more than 10%
(2) BUN rise greater than 5 mg/dL
(3) Arterial PO2 less than 60 mm hg
(4) Serum calcium less than 8 mg/dL
(5) Base deficit over 4 meq/L
(6) Estimated fluid sequestration of more than 6 L.

An elevated C reactive protein at 48 hours suggests the development of pancreatic necrosis. A high amylase and lipase are suggestive of acute pancreatitis. Leukocytosis is usually present.

Other than the labs ordered above, imaging may also be done. Plain abdominal X-ray may show radio-opaque gallstones, the sentinel loop sign (localized ileus of a small segment of small intestine, usually in the left upper quadrant), and the colon cut-off sign (lack of air in the colon in the area of the inflamed pancreas immediately preceded by a gas filled segment of transverse colon). There may be a reactive pleural effusion with atelectasis in the lower lobes of the lungs. Ultrasound is non specific and may show gallstones. CT scan of the abdomen will show the inflamed pancreas and detect complications like necrosis or pseudocyst formation. Since Ranson's criteria and APACHE scoring systems are cumbersome and time consuming, a CT Severity Index (CTSI) has recently become popular. It uses a grading system based on unenhanced CT of the pancreas and a necrosis score based on contrast enhanced CT of the pancreas. CTSI is the unenhanced score plus the necrosis score, the maximum of which can be 10 and more than 6 indicates severe disease. MRI and MRCP are being increasingly used where available for diagnosis and management of pancreatitis.

Treatment involves bowel rest, aggressive hydration, pain control, and bed rest in a hospital. Electrolyte imbalances should be corrected, especially calcium since saponification may lower the level. Broad spectrum antibiotics are not routinely recommended, but in patients with impending necrotizing pancreatitis, antibiotics have shown to decrease mortality. Nutritional support is of utmost importance. For mild to moderate cases, IV hydration and gentle advancement of oral feeding is recommended, where as in severe cases total parenteral nutrition may be needed. Alcohol abstinence will be needed to prevent further episodes. Complications include prerenal azotemia, acute tubular necrosis, shock, pancreatic necrosis, pseudocyst formation, ARDS, and pancreatic abscess. Intra-abdominal hemorrhage may cause ecchymoses around the umbilicus (Cullen's sign) or in the flanks (Grey-Turner sign), though these are rare and not specific for pancreatitis. Prognosis is good for mild cases who abstain from drinking. Recurrences are common in alcoholics. Prognosis is poor for severe necrotizing pancreatitis, especially with multi-organ involvement.
A 53-year-old man presents with a 2-day history of jaundice and malaise. His history is significant for mucosal candidiasis, for which the patient is on oral ketoconazole 200 mg daily for the past 3 weeks. He occasionally has headaches, and sometimes takes paracetamol in a daily dose of 1 gram to achieve headache relief. Two weeks before the appearance of symptoms, the patient was treated with flucloxacillin for respiratory tract infection. Except for the appearance of jaundice and malaise, the patient denies the presence of any other symptoms, and the remainder of his personal history is unremarkable.

Physical examination reveals a mildly jaundiced patient, 180 centimeters tall, 82 kilograms in weight. His blood pressure is 110/86 mmHg, and the remainder of his general physical examination revealed no abnormalities.

Laboratory analyses reveal the presence of hyperbilirubinemia and elevated serum transaminases, normal alkaline phosphatase and γ-Glutamyl transferase levels. Other routine laboratory analyses reveal no abnormalities.

Serological testing does not reveal the presence of antibodies against human immuno-deficiency, hepatitis A, C, D and E, or viruses in patient's serum. Also, HBsAg, anti-HBs or anti-HBc antibodies are not present in patient's serum. Anti-LKM-1, antinuclear, anti-thyroid, antimitochondrial, and anti-smooth muscle antibodies are absent.



Question
What is the most likely cause of liver dysfunction in this patient?

Answer Choices
1 Paracetamol-induced hepatitis
2 Primary sclerosing cholangitis
3 Ketoconazole-caused hepatitis
4 Flucloxacillin-induced hepatitis
5 Primary autoimmune hepatitis
ketoconazole causing hepatitis
Ketoconazole is an antifungal imidazole used in treating systemic mycoses. The common adverse effect of ketoconazole is hepatotoxicity. The severity of ketoconazole-induced hepatotoxicity is linked to the exposure level of the drug. Ketoconazole-induced hepatotoxicity is probably mediated through a reactive metabolite N- deacetyl ketoconazole (DAK). The latter appears to be the major metabolite, which is a hepatic cytotoxic. Ketoconazole administration results in a significantly dose-dependent increase in serum transaminase activities, as well as cloudy swelling, ballooning degeneration and centrilobular confluent necrosis of the hepatocytes. The histological feature ranges from acute hepatitis to confluent centrilobular, or massive necrosis.

Paracetamol hepatotoxicity is dose-related (i.e., signs of liver dysfunction appear only when a high dose of paracetamol, which exceeds liver metabolizing capacity for this drug, is taken). In such a case, toxic intermediary metabolites do accumulate, causing liver damage. It is considered that a daily paracetamol dose of 10 - 15 mg/kg may be considered as a safe, therapeutic dose. Therefore, liver dysfunction, in the presented case, is not the result of paracetamol-induced hepatitis.

Primary sclerosing cholangitis is frequently accompanied with elevation of serum alkaline phosphatase, and gamma-glutamyl transferase levels. Since increased serum levels of those enzymes are not noted in the presented case, it is unlikely that the patient suffers from primary sclerosing cholangitis.

Flucloxacillin administration causes cholestatic hepatitis (i.e., liver dysfunction in patients with flucloxacillin-induced hepatitis is associated with elevated alkaline phosphatase and gamma-glutamyl transferase levels, as well as with disproportionate rise of conjugated serum bilirubin level). Since hepatitis in the presented patient is not of cholestatic type, it is unlikely that he suffers from flucloxacillin-induced hepatitis.

Autoimmune hepatitis is characterized with the appearance of auto-antibodies, including liver kidney microsomal (LKM) antibodies. LKM antibodies in patients with genuine (primary) autoimmune hepatitis are of LKM1 type, not of LKM2 type.
2 Perform sigmoidoscopy
A sigmoidoscopy should be performed.

Hemorrhoids consist of an accumulation of hemorrhoidal tissue in the perianal region. Their pathophysiology is related to constant straining and repeated trauma to the anal canal due to prolonged straining, hardened stools, lack of pelvic floor support, and increased intra-abdominal pressure. The high prevalence of these factors in Western societies makes hemorrhoids an extremely common disease, with 1 million cases per year in western civilization.

Hemorrhoids can be internal (above the dentate line) or external hemorrhoids (below the line). Internal hemorrhoids have no pain innervation and can be destroyed in an office setting without local anesthesia. Some modalities are sclerosis, banding, cryotherapy, and laser ablation.

The following classification is used for hemorrhoids:
Grade: Characteristics-
I: Enlargement; lesion remains above the dentate line
II:Protrusion with straining and spontaneous reduction
III: Protrusion with straining and manually reducible
IV: Irreducible protrusion

The most common symptoms are bleeding, usually described as painless, live bleeding, often seen on wiping; pain (usually dull and aching, caused by vascular engorgement), protrusion, and difficulties with anal hygiene. Thrombosis and strangling of a protruding hemorrhoid by the anal sphincter are very painful and require urgent attention. Some patients bleed persistently and develop iron-deficiency anemia.

Hemorrhoids are the most common cause of anal pathology; however, other causes of anal disease, such as rectal prolapse, pelvic floor dysfunction, perianal fistulas, inflammatory bowel disease, psychogenic symptoms, and (in particular) colon cancer, must be actively sought in patients presenting with anal complaints.

Painless rectal bleeding should raise suspicion of rectal cancer and screening is mandatory. Endoscopic methods such as sigmoidoscopy and colonoscopy are preferred because they permit biopsy of the lesion to confirm the diagnosis. In younger patients at low risk for colorectal cancer, it is reasonable to first treat the hemorrhoids and performing a further workup if the bleeding persists.
Intravenous hydration and antibiotics
The presence of fever, jaundice, and right-upper quadrant pain defines Charcot's triad, which is the classical presentation of acute cholangitis. Reynolds' pentad consists of Charcot's triad plus sepsis/shock and mental status changes. 95% of patients presenting with these syndromes have common duct stones.

In most cases, there is a favorable response to conservative treatment, which consists of interrupting oral feeding, analgesia, intravenous hydration, and antibiotics. The following antibiotic schemes can be used:

A third-generation cephalosporin + an aminoglycoside
Piperacillin or ampicillin + metronidazole + an aminoglycoside
Monotherapy with imipenem, meropenem, mezlocillin, ampicillin-sulbactam, ticarcillin-clavulanate, or piperacillin-tazobactam
After clinical improvement, cholecystectomy is undertaken in the first few days after the initial hospitalization in order to avoid recurrence. Surgery is warranted because the recurrence rate is as high as 10% per year in patients whose gallbladders are not removed. The use of cholestyramine is another risk factor for recurrence in this patient, and gallbladder calcifications (porcelain gallbladder) are thought to pose a risk of malignization and are considered an indication for cholecystectomy.

When the disease progresses despite the initial conservative treatment (i.e., there is worsening fever, leukocytosis, abdominal pain, and guarding), emergency biliary drainage is warranted because of the possibility of gallbladder perforation or gangrene. Some possible approaches are cholecystectomy (conventional or laparoscopic), cholecystostomy, or percutaneous drainage. The latter 2 are usually reserved for sicker patients, who are less likely to tolerate surgery well.
A 33-year-old woman presents seeking advice. She is concerned regarding the appearance of spider angiomas that are present on her trunk and face. She states that spider angiomas appeared during pregnancy and that they persist now, 9 months after delivery. Before pregnancy, she was treated with imipramine because of depression and she is currently still taking this drug. She denies alcohol intake, however she tells you that 3 years ago, she had acute infection with hepatitis C virus. She was also frequently treated with flucloxacillin during the past couple of years for recurrent respiratory tract infections. In addition, she started taking oral contraceptives after delivery. The remainder of her personal history is unremarkable.

Physical examination reveals the presence of multiple spider angiomas on the patient's face, forearms, and back. The remainder of the patient's general physical findings are unremarkable.

Routine laboratory analyses reveal normal AST (26 IU/l, reference values 8 to 27 IU/l) and ALT (22 IU/l, reference value 8 to 23 IU/l) levels. Alkaline phosphatase level is normal (43 IU/l, reference value 23-71 IU/l) and other routine laboratory analyses reveal no abnormalities. HbSAg, HbeAg, and antiHbc antibodies are not present in patient's serum. IgG antibodies to hepatitis C are present, but testing for hepatitis C virus (HCV) does not reveal the presence of HCV RNA in patient's serum.



Question
What is the most likely cause of the patient's spider angiomas?

Answer Choices
1 Flucloxacillin-induced hepatitis
2 Imipramine-induced hepatitis
3 Oral contraceptives
4 Chronic hepatitis caused by hepatitis C virus
5 Pregnancy-related appearance
Oral contraceptives
The most likely cause of this patient's spider angiomas are Oral contraceptives. In conditions when estrogen hormones are present in excess such as during pregnancy, contraceptive intake, or liver disease (due to decreased degradation of estrogens), the surplus of estrogens cause the appearance of spider nevi.

In pregnant women, spider angiomas appear from the second to fifth month of pregnancy and disappear in a short period of time (within 2 months) after the delivery. Since in the presented case, spider angiomas are present for a longer period of time, it is unlikely that they are pregnancy-related.

In untreated patients with acute Hepatitis C, disease evolves towards chronicity in about 80% of patients, while only about 20% of patients recover completely. Patients who have chronic hepatitis C also have HCV RNA in their serum, but those who have recovered completely have no HCV RNA in serum and have IgG antibodies against hepatitis C virus as the marker of past hepatitis C infection. As the presented patient satisfies criteria for the patient who had hepatitis C in the past, her spider angiomas are not related to chronic hepatitis C infection.

Imipramine seldom causes liver damage. In addition, hepatitis caused by imipramine administration is of a cholestatic type, i.e. it is associated with increased serum levels of transaminases and alkaline phosphatase. Since the alkaline phosphatase level in the presented patient is normal, imipramine-induced hepatitis is not likely.

Similar to imipramine, hepatitis caused by flucloxacillin administration is also of a cholestatic type. For the reasons presented above, the possibility of flucloxacillin-induced hepatitis is also unlikely.
barium swallow
The symptoms described let you suspect GERD (gastroesophageal reflux disease). Diagnostic measurements depend upon symptoms. If symptoms are of short duration and there are no systemic manifestations, empiric treatment should be tried. With good response to that, chronic maintenance treatment should be considered. Poor response should lead to endoscopy of the upper gastrointestinal tract. With dysphagia, the 1st diagnostic step is barium swallow. If it is normal, treatment should be empiric; if it is abnormal, an endoscopy should be performed. If the endoscopy shows reflux, chronic treatment for GERD will be necessary. With an unclear diagnosis after history and endoscopy, if empiric treatment does not show any response or surgical treatment is considered, esophageal manometry with Bernstein test and 24-hour esophageal pH monitoring need to be performed.

An ECG would be appropriate if you suspected angina pectoris as the cause of the symptoms. Angina pectoris, a common manifestation of coronary artery disease, can present as heartburn with radiating pain from the epigastrium to jaw, left shoulder, and/or left axilla. It can be triggered by physical and mental stress, cold temperatures, or heavy meals. One kind of angina, Prinzmetal's angina, typically occurs in bed at night; it is caused by coronary spasms, and it is not precipitated by cardiac work. Dysphagia, however, is not a symptom of angina.

When there is no dysphagia, but there are chronic symptoms and/or signs of blood-loss (heme-positive stool, anemia, or hematemesis), an esophagogastroscopy would be proper. Helicobacter pylori (HP) plays a role in gastritis and peptic ulcers. There is no proof of any connection to GERD. Acute HP gastritis is characterized by epigastric pain, nausea, and vomiting. Ulcus duodeni classically presents with burning epigastric pain 1 - 3 hours after meals and at night. It tends to wax and wane over months. Additionally, ulcer patients may present with hemorrhages.

Esophageal manometry, which measures intraesophageal pressure, is performed if a patient with symptoms of GERD has a normal upper endoscopy after barium swallow or empiric treatment for GERD.

Gastric secretory testing and serum gastrin measuring is indicated in patients with refractory ulcer disease; it is also indicated if Zollinger-Ellison syndrome (caused by a gastrin producing endocrine tumor, which is usually located in pancreas or duodenum) is suspected, or in patients who will undergo elective surgery for duodenal ulcers.

Treatment of GERD

First line lifestyle modification (avoid spicy foods and foods that delay gastric emptying, smaller meal sizes, weight loss, avoid lying down after meals
Second line H2-receptor antagonist for 8 - 12 weeks
Third line Proton pump inhibitors
Fourth line Surgical fundoplication
Ulcerative Colitis
Ulcerative colitis is an ulcera-inflammatory disease limited to the colon and affecting only the mucosa and submucosa, except in the most severe cases. Ulcerative colitis extends in a continuous fashion proximally from the rectum in contrast to the skip lesions in Crohn's disease. Histologically, there is mononuclear inflammatory cell infiltration of the lamina propria collection of neutrophils in the crypts, called crypt abscesses and epithelial cell necrosis. However, there are no well-formed granulomas.

Ischemic bowel disease applies to the structural changes in the colon that occur due to deprivation of blood supply .The causes for deprivation of blood could be arterial occlusion, venous occlusion and non-occlusive ischemia. The causes of non-occlusive ischemia include cardiac failure, shock, dehydration, and vasoconstrictive drugs. Depending on the severity and the presentation, it is classified into transmural, mural and mucosal infarction, and chronic ischemic colitis. The diagnosis is based on the natural history of the disease and endoscopic findings with supportive biopsy.

Crohn's disease is a chronic, relapsing inflammatory disorder of obscure origin. It is a granulomatous disease and most often involves the small intestine and colon. It is characterized by transmural inflammation affecting all layers, presence of non-caseating granulomas, fissuring with formation of fistulas, and skip lesions.

Shigellosis is a bacterial enterocolitis caused by shigella. It primarily involves distal colon with acute mucosal inflammation and erosion with purulent exudates. Stool culture is diagnostic.

Amebic colitis is caused by Entamoeba histolytica, a protozoan parasite that spreads by faeco-oral route. They form flask shaped ulcers with a narrow neck and broad base. A stool examination for ova and cyst shows trophozoites and cysts of ameba. These parasites penetrate portal vessels, embolize to the liver to produce solitary discrete hepatic abscess, some exceeding 10 cm.
It can be dx with lab analysis
This patient has a zinc deficiency, which is established by low zinc level and the associated clinical presentation. Diagnosis is usually made by laboratory analysis.

World Health Organization (WHO), the United Nations Children's Fund (UNICEF), the International Atomic Energy Agency (IAEA), and the International Zinc Nutrition Consultative Group (IZiNCG) have set the standard recommendations for functional indicators of zinc status in populations. The recommended indicator is serum zinc concentration less for the specific cut-offs for sex, age, etc.

The causes of zinc deficiency include malnutrition, chronic debilitating diseases, chronic renal disease, alcoholism, drugs such as penicillamine and diuretic, and genetic disorders, such as sickle cell disease. Clinical manifestations in severe cases include alopecia, diarrhea, weight loss, infections, dermatitis, hypogonadism in men, and intercurrent infections. Supplementation with zinc is the treatment of choice.

Zinc deficiency is not very common in the United States. The dietary intake, especially in children, exceeds the new dietary reference intakes, and the present level intake seems adequate. The World Health Organization/Food and Agriculture Organization/International Atomic Energy Agency (WHO/FAO/IAEA) and the Food and Nutrition Board/US Institute of Medicine (FNB/IOM), as well as recently the International Zinc Nutrition Consultative Group (IZiNCG) have set the average requirement for dietary zinc intake.

Zinc deficiency is not commonly known to cause cardiac irregularities, unlike low levels of copper, in which the incidence of cardiovascular disease is increased.

The effects of zinc deficiency in pregnancy, such as causing fetal skeletal malformations, have not been determined definitively; however, marginal deficiencies are found to be associated with preterm delivery, prolonged labor, etc.

Zinc deficiency seems to be more prevalent in adults, as not many studies have been made in children, except where it is associated with disease conditions, such as diarrhea and malnutrition.
A 42-year-old Hispanic man presents because his employee health fair lab results returned with several 'out of normal' range results. He is an established patient in your practice; you have seen him 4 times for illness or minor injury over the past 10 years. He reports that he is in generally good health and feels well; he does not see any other healthcare providers.

A summary of his past medical history includes:

Medications: occasional over-the-counter ibuprofen for joint pain

Allergies: none

Surgical history: open reduction of left ankle at the age of 22 years

Medical history: mild osteoarthritis

Social history: patient denies the use of tobacco or illicit drugs. He drinks 3 - 4 beers per week. He is married and has 5 kids; he works in industrial hygiene at a lab facility. He plays rugby on the weekends as a hobby.

Family history: no chronic diseases are known to the patient.

His vital signs at check-in were all in normal ranges.

This patient's laboratory results from the health fair are shown in the chart.

Complete Metabolic Panel (CMP)

Total Protein

6.3

6.4 - 8.2

g/dL

AST (SGOT)

21

15 - 37

U/L

ALT (SGPT)

17

5 - 43

U/L

Alk Phosphatase

55

50 - 136

U/L

Total Bilirubin

0.8

0.1 - 1.2

mg/dL

Anion Gap

6

6 - 16

mmol/L

eGFR

>60

>60

mL/min/1.73m2

Lipid Panel

Cholesterol

226

</=200

mg/dL

Triglyceride

864

</=150

mg/dL

HDL

42

40 - 59

mg/dL

LDL

Unable to calculate

</=100

mg/dL






Question
Assuming you have counseled the patient on his condition and recommended lifestyle changes, what is the most appropriate prescription for him at this time?

Answer Choices
1 Cholestyramine (Questran or Prevalite)
2 Clopidrigel (Plavix)
3 Ezetimibe (Zetia)
4 Lisinopril (Zestril or Prinivil)
5 Nicotinic acid (niacin)
Niacin
Out of the listed options, nicotinic acid (niacin) is the most appropriate to quickly lower this patient's highly elevated triglycerides (TG). Niacin, which is also known as vitamin B3, is inexpensive, and it is available in multiple prescription and over-the-counter preparations. Additionally, a fibrate, such as gemfibrozil or fenofibrate, is considered another first-line treatment for significantly elevated TG. This patient has other minor abnormalities in his lab results, but they do not warrant immediate treatment.

Cholestyramine is a bile acid sequestrant. It can be useful for decreasing elevated low-density lipoproteins (LDL), but it can actually increase TG.

Clopidrigel reduces platelet activation and binding. It is indicated in acute coronary syndromes and for the prevention of thrombotic events, but it is not indicated for the treatment of elevated TG. This patient exhibits a mild thrombophilia, but with a negative clinical history for thrombotic risk, no such treatment is indicated.

Ezetimibe inhibits cholesterol absorption and has a role in treating elevated LDL both alone and in combination with an HMG CoA reductase inhibitor (statin). This patient may have somewhat elevated total cholesterol and LDL (the calculation for LDL is not valid when the triglycerides are so dramatically elevated), but it is more important that his hypertriglyceridemia is treated initially. Ezetimibe is not recommended solely for hypertriglyceridemia; it can also cause pancreatitis, for which this patient is already at risk, as a side effect.

Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor. It is used primarily for hypertension, and it is also used in diabetics due to its beneficial effects on preserving renal function. It can cause hyperkalemia, but it should not be used for raising this patient's potassium. Even though it protects renal function, lisinopril can also raise the BUN and creatinine.
Pancreatic carcinoma is the correct response. Itis the 4th most common cancer causing death in the U.S. The disease is more common in men, especially those between 60 and 70 years. The cause is unknown; however, the incidence is greater in smokers. High fat diet and chemical exposures may increase the risk. Symptoms include weight loss, abdominal pain, loss of appetite, jaundice, nausea, weakness, fatigue, vomiting, diarrhea, indigestion, back pain, stools (clay colored), pallor, and depression. Tests should include a pancreatic biopsy, an abdominal CT scan, and abdominal ultrasound. Only 20% of the tumors are operable at the time of diagnosis. Palliation is generally the treatment, along with chemotherapy and radiation.

The chief causes of acute pancreatitis in adults are gallstones, other biliary diseases, or alcohol use. Viral infection (mumps, Coxsackie B, mycoplasma pneumonia, and Campylobacter), injury, pancreatic or common bile duct surgical procedures, and certain medications (especially estrogens, corticosteroids, thiazide diuretics, acetaminophen, tetracycline), are other causes. After the triggering event, the process continues with autodigestion that causes swelling, hemorrhage, and damage to the blood vessels. An attack may last for 48 hours. Symptoms include abdominal pain (mainly located in the upper abdomen) nausea, vomiting, weakness, sweating, anxiety, fever, clammy skin, and mild jaundice. General examination may show a low blood pressure and a heart rate above 90. Most cases resolve within 1 week with supportive measures such as fluid replacement.

Chronic pancreatitis is caused by alcohol abuse, hemochromatosis (a condition of excess iron in the blood), and other unknown factors. Inflammation and fibrosis cause the destruction of functioning glandular tissue in the pancreas. This results in an inability to properly digest fat due to a lack of pancreatic enzymes. The production of insulin is also affected. Symptoms include abdominal pain (mainly in the upper abdomen), nausea, vomiting, weight loss, and fatty stools. Additional symptoms may include swelling (overall), clay-colored stools, and abdominal indigestion.

Pancreatic abscess occurs in 5 to 10% of people with acute pancreatitis. An abscess may be caused by inadequate drainage of a pancreatic pseudocyst; a complication associated with pancreatitis. Symptoms include fever, chills, abdominal pain, and abdominal mass. Physical exam will show signs of pancreatitis, and tests should include abdominal CT and ultrasound. Treatment will include laparotomy with drainage and possible resection of dead tissue.

Insulinomas are generally benign tumors of the insulin-secreting cells of the pancreas, which secrete excess amounts of insulin. Risk factors include a prior history of multiple endocrine neoplasia Type I (MEN I). Symptoms include sweating, tremor, rapid heart rate, anxiety, hunger, dizziness, headache, clouding of vision, confusion, behavioral changes, convulsions, and loss of consciousness. Surgery is the treatment of choice to remove the tumor. If the tumor is not found during surgery, diazoxide may be given. A diuretic is always given with this medication to avoid retaining too much salt.