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Home > CME > Courses

THE CME CREDIT FOR THIS ACTIVITY HAS EXPIRED.

Drug-Induced Pancreatitis

Presented by the University of Alabama School of Medicine
Division of Continuing Medical Education

Release Date: April 30, 2008
Expiration Date: April 30, 2011

Target Audience
Objectives
Source
CME Participation
Accreditation & Credit

Introduction
Case 1
Case Question #1
References

TARGET AUDIENCE:
Primary care physicians

OBJECTIVES:
Upon completion of this CME activity, participants should be able to:
  • Describe the characteristics of pancreatitis.
  • Determine the characteristics of drug-induced injury.
  • Discuss optimal management for drug-induced injuries.
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SOURCE:
FACULTY:

Donald H. Marks, MD, PhD
Director, Hepatitis Clinic
Cooper Green Mercy Hospital
Birmingham, Alabama

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DISCLOSURE:
The faculty has no commercial affiliations to disclose.

Because of the nature of preliminary studies, some products mentioned are unlabeled and investigational. Dosages, indications, and methods of use of drugs mentioned in this publication may reflect the experience of the authors, clinical literature, or other resources. Therefore, please see the full prescribing information before using any licensed product mentioned.

CME PARTICIPATION:
To participate in this online course for CME credit, please review the objectives before beginning the program. Complete the course and the self-assessment test before April 30, 2011 to receive CME credit. Your certificate will then be available online. This process should take approximately 1 hour.
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ACCREDITATION:

The University of Alabama School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The University of Alabama School of Medicine designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity.

The boards of nursing in many states, including Alabama, recognize Category 1 continuing medical education courses as acceptable activities for the renewal of license to practice nursing.

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DISCLAIMER:
Dosages, indications, and methods of use of any drug referred to in this publication may reflect the clinical experience of the authors, clinical literature, or other clinical resources. Therefore, please see the full prescribing information before using any product mentioned. UAB is an equal opportunity/affirmative action institution.
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INTRODUCTION:

Pancreatitis is a typically painful inflammation of the pancreas which can present as an acute disease or have a chronic nature. The overall incidence of pancreatitis is between 4.8 and 24.2 per 100,000 persons. It is usually caused by gallstones or alcohol, but can be idiopathic, and may on rare occasions have a hereditary nature. Less common causes of pancreatitis include infections (mumps), trauma (steering wheel injury during MVA), tumors, post-ERCP, autoimmune, and adverse effects of medication.

Pancreatitis results from an insult or injury which activates digestive zymogens such as trypsin in the pancreatic acinar cells. Pancreatic proenzymes can become activated by endotoxins, toxins, ischemia, infections and anoxia. The activated pancreatic enzymes then begin a process of autodigestion which leads to edema, interstitial hemorrhage, vascular damage, coagulation, formation of thrombi, cellular necrosis and pain. These processes end with fibrosis and pancreatic insufficiency. Local pancreatic autodigestion can extend into generalized a systemic inflammatory response resulting in shock, ARDS and multi-organ system failure. During autodigestion, fat necrosis binds calcium, causing hypocalcemia.

The diagnosis of pancreatitis is made by a combination of complaints of chronic abdominal pain, often described as radiating straight through to the back, a history of risk factors, laboratory findings (high amylase and lipase) and radiologic features (abdominal plain film and CT). Amylase, a pancreatic digestive enzyme which is also present in the salivary glands, may be elevated but is nonspecific and may even be normal in acute pancreatitis. Lipase is another digestive enzyme, also found in gastric and intestinal mucosa and hepatic tissue, but its specificity for pancreatitis is considered better than for amylase (90% vs. 75%). Because lipase is cleared by the kidney, renal failure will elevate its levels.

Films of the chest and abdomen can show the calcification of chronic pancreatitis, and for acute pancreatitis, a sentinel loop, elevated hemi-diaphragm, and pleural effusions may be present. An ultrasound can rule out gallstones, as can a CT, which is also useful for grading the severity of disease and prognosis. CT can also locate phlegmons, abscesses and pseudocysts.

Unresolved issues include chemoprevention of endoscopic retrograde cholangiopancreatography-induced acute pancreatitis, the indications for antibiotic prophylaxis in severe acute pancreatitis and nutritional supplementation with probiotics and synbiotics.

A wide range of medications have been linked to pancreatitis and, in the absence of alcohol and other obvious causes, need to be ruled out: Of all cases of acute pancreatitis, 1.2 to 1.4% are due to toxic effects of medication. Following is a list of drugs linked to pancreatitis:

Amiodarone and amlodipine
Anesthetics: propofol
Antibiotics (macrolides, sulfa, fluoroquinolones, rifampin, INH, dapsone)
Antiepileptics (carbamazepine, valproic acid, topiramate)
Antihypertensives (lisinopril)
Antineoplastic agents
Antipsychotics (risperdal)
Most antiretrovirals
NSAIDS
Diuretics such as hydrochlorothiazide (HCTZ)
GI agents, including H2 blockers and proton pump inhibitors (omeprazole)
Glucocorticoids
Hyperlipidemic drugs : statins
Interferon

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Case 1:

Mr. A is a 45-year-old heavy male with a new diagnosis of hypertension. His history is negative for gastric, hepatic or gallbladder disease. He typically consumes two espresso drinks per day, smokes, and favors Mexican restaurants. Medications include hydrochlorothiazide for 6 weeks and nicotine gum. Six weeks after starting HCTZ, he began to have vague gastric discomfort, nausea and decreased appetite, with no gastric reflux. Physical exam is unremarkable. Liver enzymes and CBC are normal. Based on symptoms and history, a primary diagnosis of gastritis is made.

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Case 1, Question 1 of 6

1. What would be the first steps in management?

A. Use of antacids +/- empiric use of PPI and H2 blockers
B. Staged conservative measures, including stopping espresso
C. Removing spicy foods from the diet
D. All of the above


 

 
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