24. Obesity, management of patient with lipid metabolism disorders Flashcards
What are the CHD risk equivalents?
Diabetes Mellitus, Reno-vascular Disease, Chronic Nephropathy, Peripheral Vascular Disease, Established CVA, and all forms of AVD.
What are the three major causes of atherosclerosis?
Obesity (BMI over 30), Physical inactivity, and Atherogenic diet.
What are the different types of hyperlipidemias?
Primary and Secondary hyperlipidemias.
What are the different types of interventions for hyperlipidemia?
Secondary Prevention and Primary Prevention.
What are the phenotypic characteristics of familial hypercholesterolemia?
Xanthomas, Xanthelasma, and Corneal arch.
What is the recommended education for the treatment of dyslipidemias in older people?
Education on diet and exercise, increase physical activity, decrease body weight, and employ drug therapy.
What is the mechanism of action of drug therapy for dyslipidemias?
LDL-cholesterol reduction, triglyceride reduction, and HDL-cholesterol elevation.
What are the treatment goals for low-density lipoprotein cholesterol?
To reduce the risk of cardiovascular disease.
What are the recommendations for drug treatment of patients with hypertriglyceridemia?
To reduce the risk of pancreatitis, fibrates, omega-3 fatty acids, and niacin can be used.
What are the six drug therapies for cholesterol reduction?
- HMG CoA Reductase Inhibitors (Statins) 2. Ezetimibe 3. Bile Acid binding Resins 4. Nicotinic Acid (Niacin) 5. Fibric Acid derivatives (Fibrates) 6. Probucol.
What is the mechanism of action of HMG CoA Reductase Inhibitors (Statins)?
Cholesterol synthesis is reduced by enzyme inhibition, reducing LDL-C by 18-55% and TG by 7-30%, raising HDL-C by 5-15%, with no action on Lp(a).
What are the major side effects of HMG CoA Reductase Inhibitors (Statins)?
Myopathy and increased liver enzymes, with a prevalence of less than 5%.
What are the absolute and relative contraindications for HMG CoA Reductase Inhibitors (Statins)?
Absolute: liver disease. Relative: use with certain drugs.
What are the steps in the cholesterol synthesis pathway?
Acetyl CoA, HMG-CoA, mevalonic acid, mevalonate pyrophosphate, isopentenyl pyrophosphate, geranyl pyrophosphate, farnesyl pyrophosphate, squalene, cholesterol, dolichols, ubiquinones.
What is the prevalence of statin intolerance according to a meta-analysis by Bytyci et al. in 2022?
Prevalence of statin intolerance was not provided in the given text.
What is the mechanism of action of the drug described in the text?
It inhibits absorption of dietary and biliary cholesterol.
What is the primary effect of the drug described in the text?
It reduces plasma LDL-C.
What is the potential use of the drug described in the text for patients intolerant or nonresponsive to statins?
It may be useful as monotherapy.
What is the dual inhibition of the drug described in the text?
It inhibits cholesterol absorption in the intestine and biosynthesis in the liver.
How does the lipid reduction achieved by the drug described in the text compare to that achieved by statins alone?
It achieves lipid reductions greater than those with statins alone.
What is the safety profile of the drug described in the text shown in clinical trials?
It has a favorable safety profile.
What is the potential benefit of co-administration therapy with the drug described in the text and statins?
It may reduce the need for dosage adjustments of the statin.
What is the equivalent of one-step co-administration of ezetimibe to three-step statin titration, as described in the text?
Statin 10 mg + Ezetimibe 10 mg.
What is the mechanism of action of fibrates?
Fibrates inhibit triglyceride synthesis, increase lipoprotein lipase activity, increase catabolism of triglyceride-rich VLDL, and increase HDL through improved Apo A-I and Apo A-II synthesis.
What is the first-line treatment for hypercholesterolemia?
Statins are the first-line treatment for hypercholesterolemia.
What is the second-line treatment for hypercholesterolemia if statins alone are not effective?
Statins + ezetimibe is the second-line treatment for hypercholesterolemia if statins alone are not effective.
What is the first-line treatment for hypertriglyceridemia?
Gemfibrozil is the first-line treatment for hypertriglyceridemia.
What is the mechanism of action of PCSK-9 inhibitors?
PCSK-9 inhibitors work by binding to LDL receptors in the liver and removing LDL particles.
What is the mechanism of action of PCSK9 inhibitors?
They block PCSK9 and increase the availability of LDL-R to remove LDL from the circulation.
How do LDL receptors remove LDL particles from the liver?
They bind to LDL in the liver and remove LDL particles.
What is the role of PCSK9 in LDL metabolism?
It binds to LDL-R and promotes degradation.
What is LDL apheresis?
It is a treatment for hypercholesterolemic patients who are resistant to drug and conventional therapy.
What are the various techniques for performing LDL apheresis?
They include heparin-induced extracorporeal LDL precipitation (HELP), specific immunoadsorption, double membrane filtration, dextran sulphate adsorption (Liposorber), and direct adsorption of lipoproteins (DALI, Liposorber D).
