CGP
- Cardiovascular
- Endocrine
- Geriatrics
- Gastrointestinal disorder
- Infectious disease
- Men’s and women’s health
- Neurology
- Oncology
- Ophthalmic and otics
- Pain management
- Psychiatric
- Renal disease / fluids & electrolytes
- Respiratory
- Skin conditions
- Pharmacokinetics/pharmacodynamics
- Biostatistics and pharmacoeconomics
- Pharmacy policy, procedure and regulations
The questions in this section are intended to test your knowledge and skills on Geriatric Pharmacy including biostatistics for practicing pharmacist and pharmacist preparing for CGP (Board Certified Geriatric Pharmacist).
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CGP | Gastrointestinal disorder
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Question 1 |
ME is a 65 YOM with past medical history of HTN, DM, hyperlipidemia and BPH, comes through the ER with sever bilateral upper quadrant and epigastric abdominal pain associated with nausea. NKDA and weighs 80 Kg. CT abdomen and pelvis with contrast confirmed advanced pancreatitis. His home medication includes Tamsulosin, Metformin, Exenatide, Ranitidine, Cholestyramine and Losartan. Pertinent labs incudes Lipase 2976 units/L, HDL 29mg/dl, LDL 79 mg/dl, Cholesterol 355mg/dl, triglyceride 1751mg/dl, calcium 6.0mg/dl, Albumin 2.3g/dl, Magnesium 1.4mg/dl, Potassium 3.6. Sodium 131 mmol/L, Phosphorus 2.0mg/dl Serum Creatinine 1.1 mg/dl, BG 380 mg/dl and WBC 7.9 x1000/ul. Vitals: RR 16, Pulse 117, Temperature 100.5 F, Blood Pressure 138/73 mm Hg, pulse oximetry 98%.
Which of the following is the best initial approach?
Early aggressive intravenous hydration with Lactate Ringer. | |
Early aggressive intravenous hydration with Normal Saline. | |
Early aggressive intravenous hydration with Dextrose 5%. | |
Early aggressive oral hydration with electrolyte balanced drink. |
Question 1 Explanation:
Aggressive hydration defined, as 250-500mL/hr of isotonic crystalloid solution should be provided to all patients, unless cardiovascular and/or renal comorbidities exist. Lactated Ringer’s solution may be the preferred isotonic crystalloid replacement fluid. Lactated Ringer’s solution appears to be more beneficial, resulting in fewer patients developing SIRS as compared with patients receiving normal (0.9%) saline. Thus, D and B, and C are incorrect.
Reference:
Management of Acute Pancreatitis, Am J Gastroenterol 2013; 108:1400–1415; doi:10.1038/ajg.2013.218; published online 30 July 2013
Reference:
Management of Acute Pancreatitis, Am J Gastroenterol 2013; 108:1400–1415; doi:10.1038/ajg.2013.218; published online 30 July 2013
Question 2 |
ME is a 65 YOM with past medical history of HTN, DM, hyperlipidemia and BPH, comes through the ER with sever bilateral upper quadrant and epigastric abdominal pain associated with nausea. NKDA and weighs 80 Kg. CT abdomen and pelvis with contrast confirmed advanced pancreatitis. His home medication includes Tamsulosin, Metformin, Exenatide, Ranitidine, Cholestyramine and Losartan. Pertinent labs incudes Lipase 2976 units/L, HDL 29mg/dl, LDL 79 mg/dl, Cholesterol 355mg/dl, triglyceride 1751mg/dl, calcium 6.0mg/dl, Albumin 2.3g/dl, Magnesium 1.4mg/dl, Potassium 3.6. Sodium 131 mmol/L, Phosphorus 2.0mg/dl Serum Creatinine 1.1 mg/dl, BG 380 mg/dl and WBC 7.9 x1000/ul. Vitals: RR 16, Pulse 117, Temperature 100.5 F, Blood Pressure 138/73 mm Hg, pulse oximetry 98%.
Which of the following drug ME is on, have reported cases of pancreatitis?
Excenatide | |
Ranitidine | |
Cholestyramine | |
All of the above |
Question 2 Explanation:
All of the above medications has reported cases of pancreatitis.
Reference:
Acute Pancreatitis. UpToDate. 2016. Available at: https://www.uptodate.com/contents/etiology-of-acute-pancreatitis . Accessed September 29, 2016.
Management of Acute Pancreatitis, Am J Gastroenterol 2013; 108:1400–1415; doi:10.1038/ajg.2013.218; published online 30 July 2013
Reference:
Acute Pancreatitis. UpToDate. 2016. Available at: https://www.uptodate.com/contents/etiology-of-acute-pancreatitis . Accessed September 29, 2016.
Management of Acute Pancreatitis, Am J Gastroenterol 2013; 108:1400–1415; doi:10.1038/ajg.2013.218; published online 30 July 2013
Question 3 |
ME is a 65 YOM with past medical history of HTN, DM, hyperlipidemia and BPH, comes through the ER with sever bilateral upper quadrant and epigastric abdominal pain associated with nausea. NKDA and weighs 80 Kg. CT abdomen and pelvis with contrast confirmed advanced pancreatitis. His home medication includes Tamsulosin, Metformin, Exenatide, Ranitidine, Cholestyramine and Losartan. Pertinent labs incudes Lipase 2976 units/L, HDL 29mg/dl, LDL 79 mg/dl, Cholesterol 355mg/dl, triglyceride 1751mg/dl, calcium 6.0mg/dl, Albumin 2.3g/dl, Magnesium 1.4mg/dl, Potassium 3.6. Sodium 131 mmol/L, Phosphorus 2.0mg/dl Serum Creatinine 1.1 mg/dl, BG 380 mg/dl and WBC 7.9 x1000/ul. Vitals: RR 16, Pulse 117, Temperature 100.5 F, Blood Pressure 138/73 mm Hg, pulse oximetry 98%.
Which of the following is most likely cause of ME’s acute pancreatitis?
Blood Glucose of 380mg/dl | |
Calcium of 6.0mg/dl | |
Triglyceride of 1751 mg/dl | |
Lipase 2976 units/L |
Question 3 Explanation:
In the absence of gallstones and/or history of significant alcohol use, a serum triglyceride should be obtained and considered the etiology if >1,000 mg/dL. Patient’s triglyceride level is 1751 mg/dL, Primary and secondary hypertriglyceridemia can cause acute pancreatitis. Serum lipase has a sensitivity and specificity for acute pancreatitis and may rise within 4-8 hours of the onset of symptoms, and peak at 24 hours. Thus answers A, B, and D are incorrect.
Reference:
Acute Pancreatitis. UpToDate. 2016. Available at: https://www.uptodate.com/contents/etiology-of-acute-pancreatitis . Accessed September 29, 2016
Reference:
Acute Pancreatitis. UpToDate. 2016. Available at: https://www.uptodate.com/contents/etiology-of-acute-pancreatitis . Accessed September 29, 2016
Question 4 |
ME is a 65 YOM with past medical history of HTN, DM, hyperlipidemia and BPH, comes through the ER with sever bilateral upper quadrant and epigastric abdominal pain associated with nausea. NKDA and weighs 80 Kg. CT abdomen and pelvis with contrast confirmed advanced pancreatitis. His home medication includes Tamsulosin, Metformin, Exenatide, Ranitidine, Cholestyramine and Losartan. Pertinent labs incudes Lipase 2976 units/L, HDL 29mg/dl, LDL 79 mg/dl, Cholesterol 355mg/dl, triglyceride 1751mg/dl, calcium 6.0mg/dl, Albumin 2.3g/dl, Magnesium 1.4mg/dl, Potassium 3.6. Sodium 131 mmol/L, Phosphorus 2.0mg/dl Serum Creatinine 1.1 mg/dl, BG 380 mg/dl and WBC 7.9 x1000/ul. Vitals: RR 16, Pulse 117, Temperature 100.5 F, Blood Pressure 138/73 mm Hg, pulse oximetry 98%.
What is the first-line agent for prevention of Hypertriglyceridemia-induced acute pancreatitis?
Niacin | |
Fibrates | |
Insulin | |
Statin |
Question 4 Explanation:
Patients with very high triglyceride levels (i.e., 500mg/dL or higher) usually require drug therapy in addition to therapeutic lifestyle changes. Fibrates or niacin is practical first0line choices for these patients. The initial goal is to decrease the risk of acute pancreatitis, especially if triglyceride levels are above 1,000mg/dL. Fibrate therapy can reduce triglyceride level by 20-50%, whereas nicotinic acid can reduce triglycerides at a much lower dose ~ 15-25%. Thus, A is incorrect. For patients with a triglyceride level below 500 mg/dL (5.7 mmol/L) in whom pharmacologic therapy is indicated, we suggest treatment with a statin rather than an agent targeted at reduction of triglycerides. Thus, D is incorrect. Insulin therapy is initiated for acute pancreatitis treatment, thus C is incorrect.
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.
Question 5 |
ME is a 65 YOM with past medical history of HTN, DM, hyperlipidemia and BPH, comes through the ER with sever bilateral upper quadrant and epigastric abdominal pain associated with nausea. NKDA and weighs 80 Kg. CT abdomen and pelvis with contrast confirmed advanced pancreatitis. His home medication includes Tamsulosin, Metformin, Exenatide, Ranitidine, Cholestyramine and Losartan. Pertinent labs incudes Lipase 2976 units/L, HDL 29mg/dl, LDL 79 mg/dl, Cholesterol 355mg/dl, triglyceride 1751mg/dl, calcium 6.0mg/dl, Albumin 2.3g/dl, Magnesium 1.4mg/dl, Potassium 3.6. Sodium 131 mmol/L, Phosphorus 2.0mg/dl Serum Creatinine 1.1 mg/dl, BG 380 mg/dl and WBC 7.9 x1000/ul. Vitals: RR 16, Pulse 117, Temperature 100.5 F, Blood Pressure 138/73 mm Hg, pulse oximetry 98%.
When Apheresis is unavailable, besides aggressive hydration, what is optimal alternative for treatment of Hypertriglyceridemia-induced acute pancreatitis?
Continuous intravenous insulin infusion with blood sugar parameters. | |
Heparin 5000 units subcutaneous twice daily | |
Fibrates | |
Statin |
Question 5 Explanation:
Answers C and D are incorrect, as they are utilized for preventative care. If apheresis is unavailable, or if the patient cannot tolerate apheresis, or if the patient's serum glucose level is >500 mg/dL, a continuous IV insulin infusion is initiated. Typically IV infusion of regular insulin is started at a rate of 0.1 to 0.3 units/kg/hour. In patients with blood sugar levels between 150 and 200 mg/dL, IV glucose supplementation with a separate 5 percent dextrose infusion to prevent hypoglycemia due to the insulin infusion is started. The serum glucose should initially be measured every hour to monitor glucose levels and the insulin infusion should be adjusted accordingly. Triglyceride levels should be monitored every 12 to 24 hours with adjustment of the insulin dosage as needed. Intravenous insulin should be stopped when triglyceride levels are <500 mg/dL, which typically occurs within a few days. Heparin’s use is controversial and is not recommended, thus B is incorrect.
Reference:
Hypertriglyceridemia-induced Acute Pancreatitis. UpToDate. 2016. Available at: https://www.uptodate.com/contents/hypertriglyceridemia-induced-acute-pancreatitis Accessed September 29, 2016.
Management of Acute Pancreatitis, Am J Gastroenterol 2013; 108:1400–1415; doi:10.1038/ajg.2013.218; published online 30 July 2013
Reference:
Hypertriglyceridemia-induced Acute Pancreatitis. UpToDate. 2016. Available at: https://www.uptodate.com/contents/hypertriglyceridemia-induced-acute-pancreatitis Accessed September 29, 2016.
Management of Acute Pancreatitis, Am J Gastroenterol 2013; 108:1400–1415; doi:10.1038/ajg.2013.218; published online 30 July 2013
Question 6 |
ME is a 65 YOM with past medical history of HTN, DM, hyperlipidemia and BPH, comes through the ER with sever bilateral upper quadrant and epigastric abdominal pain associated with nausea. NKDA and weighs 80 Kg. CT abdomen and pelvis with contrast confirmed advanced pancreatitis. His home medication includes Tamsulosin, Metformin, Exenatide, Ranitidine, Cholestyramine and Losartan. Pertinent labs incudes Lipase 2976 units/L, HDL 29mg/dl, LDL 79 mg/dl, Cholesterol 355mg/dl, triglyceride 1751mg/dl, calcium 6.0mg/dl, Albumin 2.3g/dl, Magnesium 1.4mg/dl, Potassium 3.6. Sodium 131 mmol/L, Phosphorus 2.0mg/dl Serum Creatinine 1.1 mg/dl, BG 380 mg/dl and WBC 7.9 x1000/ul. Vitals: RR 16, Pulse 117, Temperature 100.5 F, Blood Pressure 138/73 mm Hg, pulse oximetry 98%. Which of the following is/ are true statement regarding antibiotics use in acute pancreatitis?
Antibiotics should be given for an extrapancreatic infection. | |
Prophylactic antibiotics should be given to all patients with acute pancreatitis. | |
Antibiotic should be given to patients with sterile necrosis only. | |
All are true. |
Question 6 Explanation:
Antibiotics should be given for an extrapancreatic infection, such as cholangitis, catheter-acquired infection, bacteremia, urinary tract infection, and pneumonia. Routine use of prophylactic antibiotics in patients with severe acute pancreatitis is not recommended. The use of antibiotics in patients with sterile necrosis to prevent the development of infected necrosis is not recommended. Also, routine use of prophylactic antibiotics in patients with severe acute pancreatitis is not recommended. Thus, B, C, and D are incorrect.
Reference:
Management of Acute Pancreatitis, Am J Gastroenterol 2013; 108:1400–1415; doi:10.1038/ajg.2013.218; published online 30 July 2013
Question 7 |
What indication usually requires higher dose of proton pump inhibitor?
Helicobacter pylori | |
Esophagitis | |
Duodenal ulcer | |
Zollinger-Ellison syndrome |
Question 7 Explanation:
Answer D. The diagnosis of Zollinger-Ellison syndrome is suggested when plasma gastrin is > 1000 pg/ml and the basal acid output is > 15 mEq/h or when associated with a pH < 2. The treatment is focused on controlling gastric acid hypersecretion and localisation of the tumour and its metastases. Proton pump inhibitors are the most effective antisecretory drugs and can be administered at high dosages.
Reference:
The role of proton pump inhibitors in the treatment of Zollinger–Ellison syndrome. Available from: https://www.researchgate.net/publication/7339146_The_role_of_proton_pump_inhibitors_in_the_treatment_of_Zollinger-Ellison_syndrome [accessed Apr 16, 2017].
Tomassetti P, Campana D. Treatment of Zollinger-Ellison Syndrome. World J Gastroenterol 2005 Sep 21; 11(35): 5423–5432. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4320348/
Jensen RT, Gardner JD, Raufman JP, Pandol SJ, Doppman JL, Collen MJ. Zollinger-Ellison syndrome: current concepts and management. Ann Intern Med. 1983;98:59–75
Reference:
The role of proton pump inhibitors in the treatment of Zollinger–Ellison syndrome. Available from: https://www.researchgate.net/publication/7339146_The_role_of_proton_pump_inhibitors_in_the_treatment_of_Zollinger-Ellison_syndrome [accessed Apr 16, 2017].
Tomassetti P, Campana D. Treatment of Zollinger-Ellison Syndrome. World J Gastroenterol 2005 Sep 21; 11(35): 5423–5432. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4320348/
Jensen RT, Gardner JD, Raufman JP, Pandol SJ, Doppman JL, Collen MJ. Zollinger-Ellison syndrome: current concepts and management. Ann Intern Med. 1983;98:59–75
Question 8 |
Which of the following are complication associated with long term use of proton pump inhibitors?
Bone fractures | |
Hypomagnesemia | |
Vitamin B12 deficiency | |
Clostridium difficile infection | |
All of the above |
Question 8 Explanation:
Answer E. Use proton pump inhibitors (PPIs) in patients with or who have risk factors for osteoporosis cautiously. PPIs have been associated with a possible increased risk of bone fractures of the hip, wrist, and spine. Daily treatment with a gastric acid-suppressing medication over a long period of time may lead to hypomagnesemia. Vitamin B12 deficiency has been reported with long term use of PPIs in the literatures. The use of PPIs, may increase the risk of enteric infection by encouraging the growth of gut microflora and increasing susceptibility to organism including Clostridium Difficile. There are recent FDA warnings regarding C. Diff infection with use of PPIs. H. Pylori infection is not a complication of PPIs. PPIs in combination with certain antibiotics are used to treat H. pylori Infections.
Reference:
Targownik LE, Lix LM, Metge CJ, et al. Use of proton pump inhibitors and risk of osteoporosis-related fractures. CMAJ 2008;179:319—26.
Howden CW. Vitamin B12 levels during prolonged treatment with proton pump inhibitors. J Clin Gastroenterol. 2000;30:29–33.
Haag S, Andrews JM, Katelaris PH, et al. Management of reflux symptoms with over-the-counter pro-ton pump inhibitors: issues and proposed guidelines. Digestion 2009;80:226-34.
Reference:
Targownik LE, Lix LM, Metge CJ, et al. Use of proton pump inhibitors and risk of osteoporosis-related fractures. CMAJ 2008;179:319—26.
Howden CW. Vitamin B12 levels during prolonged treatment with proton pump inhibitors. J Clin Gastroenterol. 2000;30:29–33.
Haag S, Andrews JM, Katelaris PH, et al. Management of reflux symptoms with over-the-counter pro-ton pump inhibitors: issues and proposed guidelines. Digestion 2009;80:226-34.
Question 9 |
Concomitant use of warfarin and omeprazole is associated with increased INR and prothrombin time(PT). What enzyme dose the omeprazole inhibits that is metabolized by warfarin?
CYP3A4 | |
CYP2C9 | |
CYP2C19 | |
CYP2D9 |
Question 9 Explanation:
Answer C. Omeprazole is CYP2C19 inhibitor which can prolong the elimination of warfarin, particularly R-warfarin. R-warfarin is partially metabolized by CYP2C19. The combined use of omeprazole and warfarin has been associated with reports of increased INR and prothrombin time (PT).
Reference:
Prilosec (omeprazole) package insert. Wilmington, DE: AstraZeneca; 2016 Dec.
Reference:
Prilosec (omeprazole) package insert. Wilmington, DE: AstraZeneca; 2016 Dec.
Question 10 |
Which of the following are non-pharmacological measure that may control symptoms of gastroesophageal reflux disease? Select all that applies.
Remain upright after a meal | |
Increase fat intake to reduce gastric emptying time | |
Reduce intake of food or beverage that may reduce lower esophageal sphincter tone | |
Wear tight fitted cloths to increase intra-abdominal pressure. | |
Discontinue nicotine use in patients that uses tobacco product. |
Question 10 Explanation:
Answer A, C, E. Non-pharmacological measure that may control symptoms of gastroesophageal reflux disease are: Avoid aggravating foods/beverages that may reduce LES pressure alcohol, citrus juices caffeine, garlic, onions or cause direct irritation such as spicy foods or tomato juice should be avoided. Reduce fat intake, remain upright after meals, avoid meal before bedtime. Avoid tight fitted cloths, decrease intra-abdominal pressure. Discontinue nicotine use. Reduce intake of food or beverage that may reduce lower esophageal sphincter tone.
Reference:
American Gastroenterological Association Institute. Medical position statement on the management of gastroesophageal reflux disease. Gastroenterology 2008;135:1383-91.
Reference:
American Gastroenterological Association Institute. Medical position statement on the management of gastroesophageal reflux disease. Gastroenterology 2008;135:1383-91.
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