24. Obesity, management of patient with lipid metabolism disorders

Question 1

What are the CHD risk equivalents?

Answer 1

Diabetes Mellitus, Reno-vascular Disease, Chronic Nephropathy, Peripheral Vascular Disease, Established CVA, and all forms of AVD.

Question 2

What are the three major causes of atherosclerosis?

Answer 2

Obesity (BMI over 30), Physical inactivity, and Atherogenic diet.

Question 3

What are the different types of hyperlipidemias?

Answer 3

Primary and Secondary hyperlipidemias.

Question 4

What are the different types of interventions for hyperlipidemia?

Answer 4

Secondary Prevention and Primary Prevention.

Question 5

What are the phenotypic characteristics of familial hypercholesterolemia?

Answer 5

Xanthomas, Xanthelasma, and Corneal arch.

Question 6

What is the recommended education for the treatment of dyslipidemias in older people?

Answer 6

Education on diet and exercise, increase physical activity, decrease body weight, and employ drug therapy.

Question 7

What is the mechanism of action of drug therapy for dyslipidemias?

Answer 7

LDL-cholesterol reduction, triglyceride reduction, and HDL-cholesterol elevation.

Question 8

What are the treatment goals for low-density lipoprotein cholesterol?

Answer 8

To reduce the risk of cardiovascular disease.

Question 9

What are the recommendations for drug treatment of patients with hypertriglyceridemia?

Answer 9

To reduce the risk of pancreatitis, fibrates, omega-3 fatty acids, and niacin can be used.

Question 10

What are the six drug therapies for cholesterol reduction?

Answer 10

1. HMG CoA Reductase Inhibitors (Statins) 2. Ezetimibe 3. Bile Acid binding Resins 4. Nicotinic Acid (Niacin) 5. Fibric Acid derivatives (Fibrates) 6. Probucol.

Question 11

What is the mechanism of action of HMG CoA Reductase Inhibitors (Statins)?

Answer 11

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).

Question 12

What are the major side effects of HMG CoA Reductase Inhibitors (Statins)?

Answer 12

Myopathy and increased liver enzymes, with a prevalence of less than 5%.

Question 13

What are the absolute and relative contraindications for HMG CoA Reductase Inhibitors (Statins)?

Answer 13

Absolute: liver disease. Relative: use with certain drugs.

Question 14

What are the steps in the cholesterol synthesis pathway?

Answer 14

Acetyl CoA, HMG-CoA, mevalonic acid, mevalonate pyrophosphate, isopentenyl pyrophosphate, geranyl pyrophosphate, farnesyl pyrophosphate, squalene, cholesterol, dolichols, ubiquinones.

Question 15

What is the prevalence of statin intolerance according to a meta-analysis by Bytyci et al. in 2022?

Answer 15

Prevalence of statin intolerance was not provided in the given text.

Question 16

What is the mechanism of action of the drug described in the text?

Answer 16

It inhibits absorption of dietary and biliary cholesterol.

Question 17

What is the primary effect of the drug described in the text?

Answer 17

It reduces plasma LDL-C.

Question 18

What is the potential use of the drug described in the text for patients intolerant or nonresponsive to statins?

Answer 18

It may be useful as monotherapy.

Question 19

What is the dual inhibition of the drug described in the text?

Answer 19

It inhibits cholesterol absorption in the intestine and biosynthesis in the liver.

Question 20

How does the lipid reduction achieved by the drug described in the text compare to that achieved by statins alone?

Answer 20

It achieves lipid reductions greater than those with statins alone.

Question 21

What is the safety profile of the drug described in the text shown in clinical trials?

Answer 21

It has a favorable safety profile.

Question 22

What is the potential benefit of co-administration therapy with the drug described in the text and statins?

Answer 22

It may reduce the need for dosage adjustments of the statin.

Question 23

What is the equivalent of one-step co-administration of ezetimibe to three-step statin titration, as described in the text?

Answer 23

Statin 10 mg + Ezetimibe 10 mg.

Question 24

What is the mechanism of action of fibrates?

Answer 24

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.

Question 25

What is the first-line treatment for hypercholesterolemia?

Answer 25

Statins are the first-line treatment for hypercholesterolemia.

Question 26

What is the second-line treatment for hypercholesterolemia if statins alone are not effective?

Answer 26

Statins + ezetimibe is the second-line treatment for hypercholesterolemia if statins alone are not effective.

Question 27

What is the first-line treatment for hypertriglyceridemia?

Answer 27

Gemfibrozil is the first-line treatment for hypertriglyceridemia.

Question 28

What is the mechanism of action of PCSK-9 inhibitors?

Answer 28

PCSK-9 inhibitors work by binding to LDL receptors in the liver and removing LDL particles.

Question 29

What is the mechanism of action of PCSK9 inhibitors?

Answer 29

They block PCSK9 and increase the availability of LDL-R to remove LDL from the circulation.

Question 30

How do LDL receptors remove LDL particles from the liver?

Answer 30

They bind to LDL in the liver and remove LDL particles.

Question 31

What is the role of PCSK9 in LDL metabolism?

Answer 31

It binds to LDL-R and promotes degradation.

Question 32

What is LDL apheresis?

Answer 32

It is a treatment for hypercholesterolemic patients who are resistant to drug and conventional therapy.

Question 33

What are the various techniques for performing LDL apheresis?

Answer 33

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).