Tuberoeruptive Xanthoma (coalescent papulae). May be Type III Hyperlipidemia (elbow localization). Verruca is not so smooth and the spreading pattern is different.
Related self assesment question 1) You are caring for a 26-year-old man with dyslipidemia and a family history of early coronary arterial disease. Laboratory analysis reveals a low HDL. Which of the following interventions, if adopted by the patient, would raise his HDL levels to the greatest extent? A. Use alcohol in moderation B. Lose weight C. Increase dietary intake of protein D. Decrease dietary intake of cholesterol E. Reduce life stress EXPLANATION: Alcohol, in moderation, raises HDL cholesterol. (Y) Alternatively, cigarette smoking decreases HDL. Being overweight or obese decreases HDL, but weight loss may not raise HDL. ): Low dietary intake of cholesterol or high dietary intake of protein has not been shown to impact HDL. ): Stress can markedly increase LDL cholesterol, but will not impact HDL. The answer is A. 2) In an attempt to lower cholesterol through diet, you recommend that a 40-year-old male take fish oil. What is the lipid-lowering mechanism of action of fish oil? A. Sequesters bile acids B. Changes hepatic metabolism of lipoprotein C. Inhibits HMG-CoA reductase D. Interferes with cholesterol absorption in the gut E. Decreases secretion of triglycerides by the liver EXPLANATION: Fish oil is high in omega-3 fatty acids and have been shown to be beneficial in lowering cholesterol. Fish oils work by decreasing secretion of triglycerides by the liver. The answer is E.
A brief overview of the dyslipidemias Hyperlipidemias [TABLE="class: grid, width: 500"] [TR] [TD]Type[/TD] [TD]increased plasma lipoprotein[/TD] [TD]increased plasma lipid (most)[/TD] [TD]probable metabolic defect[/TD] [TD]risk of artherosclerosis[/TD] [TD]suggested treatment[/TD] [/TR] [TR] [TD]1 FCS, familial chylomicronemia syndrome[/TD] [TD]Chylomicrons[/TD] [TD]TG (triglycerides)[/TD] [TD]def. of lipoprotein lipase[/TD] [TD]may increase[/TD] [TD]low fat diet[/TD] [/TR] [TR] [TD]2 a FDBL, familial dysbetalipoproteinemia; FH, familial hypercholesterolemia; [/TD] [TD]LDL[/TD] [TD]Cholesterol[/TD] [TD]def. of LDL receptors[/TD] [TD]very high, mostly in coronary artery[/TD] [TD]low cholesterol, fat diet, bile acid sequesterants, statins, niacin[/TD] [/TR] [TR] [TD]2 b FCHL, familial combined hyperlipidemia[/TD] [TD]LDL & VLDL[/TD] [TD]TG & Cholesterol[/TD] [TD]overproduction of ApoB[/TD] [TD] - do - [/TD] [TD]low cholesterol, fat diet, statins, niacin, fibrates[/TD] [/TR] [TR] [TD]3 FDBL, familial dysbetalipoproteinemia[/TD] [TD]IDL[/TD] [TD]TG & Cholesterol[/TD] [TD]abnormality in Apo E[/TD] [TD]very high, mostly in peripheral vessels[/TD] [TD]low cholesterol, fat diet, statins, niacin, fibrates[/TD] [/TR] [TR] [TD]4 FHTG, familial hypertriglyceridemia[/TD] [TD]VLDL[/TD] [TD]TG[/TD] [TD]Increased VLDL production and Decreased elimination[/TD] [TD]may or may not increase[/TD] [TD]low cholesterol, fat diet, niacin, fibrates[/TD] [/TR] [TR] [TD]5 FHTG, familial hypertriglyceridemia[/TD] [TD]Chylomicrons & VLDL[/TD] [TD]TG[/TD] [TD]Increased VLDL production and Decreased elimination & decreased lipoprotein lipase[/TD] [TD] - do - [/TD] [TD]low cholesterol, fat diet, niacin, fibrates[/TD] [/TR] [/TABLE] Fat soluble vitamins have to be suplemented in all cases Hypolipoproteinemias 1) Familial Hypobetalipoproteinemia - impairment in the synthesis of Apo B, resulting in LDL levels being 10 - 50 % of normal. Affected individuals have healthy and long life 2) Abetalipoproteinemia - defect in the synthesis of Apo B...characterised by total absense of LDL & TG in plasma and decreased absorption of fat soluble vitamins. TG accumulate in intestine and liver. Im pairment in physical growth and mental retardation are commonly observed. 3) Familial Alpha lipoprotein def. ( Tangier disease ) - plasma HDL particles are almost absent ( defect in ABCA1 protein ). Due to this reverse transport of choesterol is severely affected leading to the accumulation of cholesterol esters in tissues. An absence of apoprotein CII is also found. Plasma TG is also elevated. Affected individuals are at increased risk of artherosclerosis. (-:
Another self assessment question You are caring for a patient with a poor lipid profile. His HDL is low, his LDL is high, and his triglycerides are also high. Which of the following medications would have the most beneficial effect on his HDL? A. Lovastatin B. Colestipol C. Ezetimibe D. Fenofibrate E. Cholestyramine EXPLANATION: The different options for medical management of hyperlipidemia include preparations that affect the total cholesterol, the HDL, the LDL, and the triglycerides. Choice of medication depends on the desired endpoint. The following table outlines the expected increase in HDL that would be expected using the medications in the answer key: [TABLE="class: grid, width: 500"] [TR] [TD]Medication[/TD] [TD]Increase in HDL[/TD] [/TR] [TR] [TD]Lovastatin [/TD] [TD]5%-10%[/TD] [/TR] [TR] [TD]Colestipol [/TD] [TD]Approximately 5%[/TD] [/TR] [TR] [TD]Ezetimibe [/TD] [TD]Approximately 5%[/TD] [/TR] [TR] [TD]Fenofibrate [/TD] [TD] 15%-25%[/TD] [/TR] [TR] [TD]Cholestyramine [/TD] [TD]Approximately 5%[/TD] [/TR] [/TABLE] Niacin is even better than fenofibrate, increasing HDL by 25% to 35% on average. The answer is D. Xtra Edge on Fenofibrate and Gemfibrozil Therapeutic Uses & Dosage Fibrates are useful drugs in hypertriglyceridemias in which VLDL predominate and in dysbetalipoproteinemia. They also may be of benefit in treating the hypertriglyceridemia that results from treatment with viral protease inhibitors. The usual dose of gemfibrozil is 600 mg orally once or twice daily. The dosage of fenofibrate (as Tricor) is one to three 48 mg tablets (or a single 145 mg tablet) daily. Absorption of gemfibrozil is improved when the drug is taken with food. Toxicity Rare adverse effects of fibrates include rashes, gastrointestinal symptoms, myopathy, arrhythmias, hypokalemia, and high blood levels of aminotransferases or alkaline phosphatase. A few patients show decreases in white blood count or hematocrit. Both agents potentiate the action of coumarin and indanedione anticoagulants, and doses of these agents should be adjusted. Rhabdomyolysis has occurred rarely. Risk of myopathy increases when fibrates are given with reductase inhibitors. Fenofibrate is the fibrate of choice for use in combination with a statin. Fibrates should be avoided in patients with hepatic or renal dysfunction. There appears to be a modest increase in the risk of cholesterol gallstones, reflecting an increase in the cholesterol content of bile. Therefore, fibrates should be used with caution in patients with biliary tract disease or in those at high risk such as women, obese patients, and Native Americans. Ref - Katzung 12th ed Drug can cause significant increases in serum transaminases. Perform regular periodic monitoring of liver function for duration of therapy; discontinue therapy if enzyme levels persist more than 3 times the normal limit. Monitoring: Evaluate serum lipids periodically (eg, 4 to 8 wk) during initial therapy to determine lowest effective dose; withdraw therapy if an adequate response is not achieved after 2 mo of treatment with the maximum dose. Perform periodic blood counts during first 12 mo of therapy to detect rare episodes of thrombocytopenia and granulocytopenia. Ref - A to Z drug facts I couldn't find any alcohol - fibrates drug interaxn...but since fibrates can have adverse effects on the liver, it's only prudent to advice patients to limit their alcohol intake. This is an article that deals with the topic Alcohol Use, Vascular Disease, and Lipid-Lowering Drugs (-:
Recently asked on Step 3 You did screening cholesterol tests on a 32-year-old man and found his results to be: Total cholesterol: 220 mg/dL (H) LDL: 125 mg/dL (H) HDL: 34 mg/dL (L) Triglycerides: 307 mg/dL (H) C-reactive protein: 2.4 mg/dL (H) Which of his laboratory results is the best predictor of an adverse outcome in this patient? A. Total cholesterol B. LDL C. HDL D. Triglycerides E. C-reactive protein EXPLANATION: Of all the lipid values, low HDL is the single best predictor of an adverse outcome. However, high HDL does not guarantee immunity from coronary artery disease. C-reactive protein levels predict risk for myocardial infarction and stroke even better than LDL levels do, but are not as beneficial as HDL. The answer is C.
Very Special Question First go thru all the self assessment questions posted above ( and read carefully ) and then solve this...if u get it right, then u should give urself a tap on ur back (Y) You are following a type 2 diabetic woman in her 50s. Six months ago, you checked her lipid profile. At that time, her total cholesterol was 245 mg/dL, her low-density lipoprotein (LDL) was 148 mg/dL, her high-density lipoprotein (HDL) was 30 mg/dL, and her triglycerides were 362. She has tried lifestyle modifications, but despite losing weight and exercising, her profile hasn't substantially changed. Which of the following is the first-line treatment for this patient? A. Continued lifestyle modifications B. A 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) [P1] reductase inhibitor (a "statin") C. Niacin D. Fibric acid derivatives E. Bile acid resin EXPLANATION: Statins are the drug of choice in treating hyperlipidemia in diabetes. They have been shown to decrease the risk of coronary events and are excellent in lowering LDL. They do have less effect on the triglyceride levels, but in many patients, the decrease is enough to get patients to goal. Niacin will decrease triglycerides, raise HDL, and lower LDL, but may increase insulin resistance. Niacin is often used in combination with a statin or alone in patients with statin side-effects. Fibric acid derivatives lower triglycerides and raise HDL, but have minimal effects on LDL. Bile acid resins sequester bile acids in the GI tract. They can increase triglyceride levels, and are generally not used in diabetics. The answer is B. Moral of the story - Niacin sounds nice but has some nasty side effects and is not nice for diabetics as it increases insulin resistance and Fibric acid derivatives does little to bring LDL down. I generally don't prescribe Fibric acid derivatives to anybody, becos of some reports of increased cancer incidence with its use ( my policy is when in doubt...keep it out ) and secondly becos it is a no,,,no with statins ( which most of my patients get ) and thirdly it is guaranteed to give gall stones...don't believe me. then - do a screening USG on ur hyperlipedemic patients and pick somebody without gallstones and with no predisposition and start him on any Fibric acid derivative and repeat US in 6 months to 1 year...even if u see only sludge...discontinue the drug, as it is a sign of things to come. (-:
What pharmacological option would you subscribe to in a patient who has responded well to statins...but is now showing elevated liver enzymes ( more than 3 times the upper limit ) and has developed proximal myopathy ? Firstly make sure it is due to statins - i.e rule out polymyalgia rheumatica and hypothyroidism - muscle enzymes are not specific....but do ask for it and if even if not elevated discontinue stains for at least 3 - 4 weeks or until the liver enzymes normalise. Then what ? Read the self assessment question below to know one of the options You are working with a 44-year-old man with difficult to manage dyslipidemia. He is taking atorvastatin (Lipitor) at maximum dosages, and you are considering adding ezetemibe (Zetia) to improve the lipid profile. How does ezetemibe work to help lower cholesterol? A. Sequestration of bile acids B. Changing hepatic metabolism of lipoproteins C. Inhibits HMG-CoA reductase D. Interferes with cholesterol absorption in the gut E. Decreases secretion of triglycerides by the liver EXPLANATION: Ezetemibe (Zetia) lowers cholesterol by interfering with the absorption of cholesterol in the gut. Used alone, it lowers LDL and triglycerides only modestly. When added to a low-dose statin, the combination lowers LDL as much as the maximum statin dose, but its combined use with a low-dose statin may produce fewer adverse effects. The answer is D. Remember combining fibric acid derivatives with statins for patients who have developed statin induced myopathy can be a disastrous option.
