Veterinary Medicine - September 2007 - (Page 598)

Hyperlipidemia O P E E R - R E V I E W E D You can earn two hours of Continuing Education credit from Kansas State University by answering the following questions on hyperlipidemia. Circle only the best answer for each question, and transfer your answers to the form on page 618. CE Article #1 1. Which statement is true regarding lipoprotein transport? a. Triglyceride is primarily transported as chylomicrons and VLDLs. b. Triglyceride is primarily transported as chylomicrons and LDLs. c. Cholesterol is primarily transported as VLDLs and LDLs. d. Cholesterol is primarily transported as LDLs and HDLs. e. Both A and D and thyroid-stimulating hormone measurements d. Lipoprotein electrophoresis e. Both B and D 7. A patient presents with hyperadrenocorticism and hyperlipidemia. What is the treatment of choice for the hyperlipidemia in this patient? a. A low-fat diet b. Gemfibrozil c. Niacin d. Menhaden oil e. Treat the hyperadrenocorticism first. 2. What is the most common cause of hyperlipidemia in dogs and cats? a. Diabetes mellitus b. Postprandial c. Hyperadrenocorticism d. Nephrotic syndrome e. Pancreatitis 8. Which therapy would be considered next for a patient with idiopathic hypertriglyceridemia inadequately controlled with low-fat diets? a. Gemfibrozil b. Soluble fibers c. Cholestyramine d. Thyroid hormone supplementation e. Combination therapy with gemfibrozil and lovastatin 3. To avoid confusion caused by postprandial lipidemia, how long should a patient be fasted before evaluating for hyperlipidemia? a. 30 seconds b. 5 minutes c. 1 hour d. 4 hours e. 12 hours 9. Before initiating therapy with gemfibrozil or lovastatin for idiopathic hypertriglyceridemia, what should be evaluated and frequently monitored? a. Blood urea nitrogen and creatinine concentrations b. Liver enzyme activities c. Pancreatic lipase immunoreactivity d. T4 and thyroid-stimulating hormone concentrations e. Follow-up is not necessary. 4. Which of these is not a common cause of hyperlipidemia in dogs or cats? a. Exocrine pancreatic insufficiency b. Hypothyroidism c. Diabetes mellitus d. Hyperadrenocorticism e. Pancreatitis 5. The clinical manifestations of hyperlipidemia in dogs and cats may relate to dysfunction of what organ system? a. Gastrointestinal b. Nervous c. Integumentary d. Ocular e. All of the above 10. Which statement regarding cholesterol in dogs and cats is false? a. Mild hypercholesterolemia should be managed aggressively because of the risk of atherosclerosis. b. Severe hypercholesterolemia does not affect the gross appearance of serum or plasma. c. Hypothyroidism can cause severe hypercholesterolemia. d. For severe idiopathic hypercholesterolemia, low-fat diets are the mainstay of therapy. e. Both A and B 6. A middle-aged dog presents to your clinic with the chief complaint of lethargy, weight gain, and fasting lipemia. What diagnostic test would you recommend next? a. None—begin therapy immediately for primary hyperlipidemia. b. Lipoprotein lipase activity assessment c. A complete blood count, a serum chemistry profile, urinalysis, and T4 receptors are upregulated to increase the removal of LDLs and HDLs from the blood.18 Potential side effects of this medication include constipation, interference of oral medication absorption, and increased VLDLs from uptake of LDLs.18 Because of the risk of increased VLDLs, use cholestyramine with caution in patients with concurrent hypertriglyceridemia. The statins, which are methylglutaconyl-coenzyme A (HMG-CoA) reductase inhibitors, are the most potent cholesterol-lowering drugs in people.18 HMG-CoA reductase is the rate limiting step in cholesterol synthesis.18 Statins, by inhibiting HMG-CoA reductase, reduce hepatic cholesterol synthesis. A decreased hepatic cholesterol concentration results in the upregulation of hepatic LDL receptors and increased removal of LDLs from the blood.18 The statins also decrease the hepatic production of VLDLs and are modestly effective in the treatment of hypertriglyceridemia.18 Lovastatin (10 mg orally once a day) is effective for persistent hypercholesterolemia in dogs.3 Potential adverse effects include hepatotoxicity, vomiting, diarrhea, myopathy, and hyperesthesia.18 Perform a serum chemistry profile, including creatine kinase activity, before administering any statin, and frequent monitoring for hepatotoxicosis and myopathy is a must. Serum alanine aminotransferase and alkaline phosphatase activities along with serum creatine kinase activities (myopathy) should be measured after one month and then, if normal, at sixmonth intervals. The combination of a statin plus a fibric acid derivative (gemfibrozil) may increase the risk of skeletal myopathy. These drugs should not be used or should be discontinued in any patient with hepatic disease or that develops evidence of hepatic disease or myopathy during use. The benefit of statins in dogs and cats to reduce LDL is unproven because most of their total cholesterol is transported as HDL. 598 September 2007 VETERINARY MEDICINE

Table of Contents Feed for the Digital Edition of Veterinary Medicine - September 2007

Contents Letters Leading Off The Veterinary Medicine Interview: Dr. William J. Kay Idea Exchange Practical Matters Salivary Mucoceles in Cates: A Retropspective Study of Seven Cases Hyperlipidemia in Dogs and Cats Purina Insert The Latest Management Recommendations for Cats and Dogs with Nonketotic Diabetes Mellitus CE Form Product Preview Advertiser Index Marketplace/Classifieds Mind Over Miller

Veterinary Medicine - September 2007

For optimal viewing of this digital publication, please enable JavaScript and then refresh the page. If you would like to try to load the digital publication without using Flash Player detection, please click here.