Lipid Disorders

Question 1

What is the primary function of cholesterol in the body?

Answer 1

Used for cell membrane synthesis, repair, and steroid hormone production.

Question 2

What are triglycerides (TGs) primarily used for?

Answer 2

Energy source stored in adipose tissue or used by muscles.

Question 3

What are lipoproteins?

Answer 3

Spherical particles that transport cholesterol and TGs.

Question 4

What is the composition of lipoproteins?

Answer 4

A lipid core surrounded by water-soluble proteins and phospholipids.

Question 5

What do chylomicrons transport?

Answer 5

Exogenous TGs from the gut to adipose tissue and muscle.

Question 6

What is the role of VLDL (Very-Low-Density Lipoprotein)?

Answer 6

Transport endogenous TGs from the liver to adipose tissue and muscle.

Question 7

What does LDL (Low-Density Lipoprotein) transport?

Answer 7

Cholesterol from the liver to peripheral tissues.

Question 8

What is the function of HDL (High-Density Lipoprotein)?

Answer 8

Transport cholesterol from peripheral tissues to the liver.

Question 9

What is Apoprotein A’s role?

Answer 9

Ligand for HDL receptors.

Question 10

What does Apoprotein B do?

Answer 10

Ligand for LDL receptors.

Question 11

What is the function of Apoprotein E?

Answer 11

Ligand for hepatic receptors for remnant particles.

Question 12

What is the role of Apoprotein C-II?

Answer 12

Cofactor for lipoprotein lipase (LPL).

Question 13

What is HMG CoA Reductase?

Answer 13

Rate-limiting enzyme in cholesterol synthesis.

Question 14

What does Cholesterol Ester Transfer Protein (CETP) do?

Answer 14

Shuttles cholesterol esters between HDL and LDL.

Question 15

What is the function of Lipoprotein Lipase (LPL)?

Answer 15

Breaks down TGs in chylomicrons and VLDL.

Question 16

What does Lecithin Cholesterol Acyl Transferase (LCAT) do?

Answer 16

Esterifies cholesterol on HDL particles.

Question 17

How does LDL function in the body?

Answer 17

Transports cholesterol to peripheral tissues and binds to LDL receptors (LDLRs) on cell surfaces.

Question 18

What is the effect of excess LDL?

Answer 18

Cleared by scavenger macrophages.

Question 19

What does Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) promote?

Answer 19

Degradation of LDLRs, reducing LDL clearance.

Question 20

What can mutations in PCSK9 cause?

Answer 20

Familial hypercholesterolemia (FH).

Question 21

What is reverse cholesterol transport?

Answer 21

Removes excess cholesterol from cells and transports it to the liver.

Question 22

What are the antiatherogenic effects of HDL?

Answer 22

Reduces LDL oxidation, inhibits inflammation, improves endothelial function.

Question 23

What forms foam cells in atherosclerosis?

Answer 23

Oxidized LDL engulfed by macrophages.

Question 24

What leads to plaque rupture and thrombus formation?

Answer 24

Plaque rupture leads to platelet aggregation.

Question 25

How are TGs transported in the body?

Answer 25

Dietary and hepatic TGs transported by chylomicrons and VLDL.

Question 26

What happens to TGs broken down by LPL?

Answer 26

Converted into fatty acids for storage or energy.

Question 27

What are the harmful effects of elevated serum TGs?

Answer 27

Associated with atherosclerosis and coronary disease.

Question 28

What TG levels increase the risk of acute pancreatitis?

Answer 28

TG levels >1000 mg/dL.

Question 29

What is required for a diagnosis of Metabolic Syndrome (MS)?

Answer 29

3 of the following: elevated fasting glucose, high TGs, low HDL, hypertension, abdominal obesity.

Question 30

What is Lipoprotein(a)?

Answer 30

Formed when apoprotein(a) attaches to LDL.

Question 31

What does Lipoprotein(a) promote?

Answer 31

Atherosclerosis by inhibiting thrombolysis.

Question 32

What are primary dyslipidemias?

Answer 32

Inherited disorders of lipoprotein metabolism.

Question 33

What is Familial Hypercholesterolemia (FH)?

Answer 33

Extreme elevations in cholesterol, normal TGs.

Question 34

What mutations can cause Familial Hypercholesterolemia?

Answer 34

Mutations in LDLR, apoprotein B, PCSK9, or LDLRAP-1.

Question 35

What is the risk associated with Familial Hypercholesterolemia?

Answer 35

High risk of premature coronary artery disease (CAD).

Question 36

What characterizes Familial Combined Hyperlipidemia (FCH)?

Answer 36

Elevated cholesterol and TGs due to excessive hepatic apoprotein B synthesis.

Question 37

What defines Familial Dysbetalipoproteinemia (FDL)?

Answer 37

Elevated cholesterol and TGs, normal HDL.

Question 38

What is the cause of Familial Dysbetalipoproteinemia?

Answer 38

Abnormal apoprotein E phenotype (E2/E2).

Question 39

What characterizes Polygenic Hypercholesterolemia?

Answer 39

Mild-to-moderate cholesterol elevation.

Question 40

What distinguishes Familial Hypertriglyceridemia (FHT) and Familial Hyperchylomicronemia (FHC)?

Answer 40

FHT: moderate-to-severe TG elevation; FHC: extremely high TGs and chylomicrons.

Question 41

How is Familial Combined Hyperlipidemia distinguished from Familial Dysbetalipoproteinemia?

Answer 41

FCH: Increased apoprotein B; FDL: E2/E2 phenotype, broad beta-band on electrophoresis.

Question 42

What causes Familial Low HDL?

Answer 42

Mutations in APOA1, ABCA1, or LCAT genes.

Question 43

What are secondary dyslipidemias caused by?

Answer 43

Systemic diseases or medications.

Question 44

What are the causes of acquired hypertriglyceridemia?

Answer 44

Insulin resistance, obesity, diabetes, HIV, alcohol abuse, medications.

Question 45

What is the general approach to treating dyslipidemia?

Answer 45

Lifestyle changes, medical therapy, apheresis, treat secondary causes.

Question 46

What dietary recommendations does the ACC/AHA provide?

Answer 46

Emphasize vegetables, fruits, whole grains, low-fat dairy, fish, nuts; limit sweets, red meats, saturated and trans fats.

Question 47

What is the primary role of statins?

Answer 47

Inhibit HMG CoA reductase, lower LDL.

Question 48

What do PCSK9 inhibitors do?

Answer 48

Increase LDLR recycling, lower LDL.

Question 49

What is the function of Ezetimibe?

Answer 49

Inhibits cholesterol absorption.

Question 50

What do fibrates do?

Answer 50

Lower TGs, increase HDL.

Question 51

What is the effect of Niacin on lipoprotein levels?

Answer 51

Lowers LDL, TGs, and lipoprotein(a); increases HDL.

Question 52

What is the role of Omega-3 Fatty Acids?

Answer 52

Lower TGs.

Question 53

What are the ACC/AHA treatment recommendations for high-risk groups?

Answer 53

Clinical ASCVD, LDL ≥190 mg/dL, LDL 70–189 mg/dL with diabetes or 10-year ASCVD risk ≥7.5%.

Question 54

How do statins work?

Answer 54

Inhibit HMG CoA reductase, reduce cholesterol synthesis, increase LDLR-mediated LDL clearance.

Question 55

What are the side effects of statins?

Answer 55

Myalgias, myositis, rhabdomyolysis (rare), increased risk of diabetes.

Question 56

What is the efficacy of aggressive cholesterol-lowering?

Answer 56

Reduces myocardial infarction, stroke, cardiovascular mortality.

Question 57

What is the effect of PCSK9 inhibitors on LDL and cardiovascular events?

Answer 57

Lower LDL by 50%–70%, reduce cardiovascular events.

Question 58

What limits the use of PCSK9 inhibitors?

Answer 58

High cost.

Question 59

What limits the use of Niacin?

Answer 59

Side effects (flushing) and lack of proven benefit.

Question 60

What is the effect of Ezetimibe when added to statins?

Answer 60

Modest reduction in ASCVD events.

Question 61

What are fibrates most effective at?

Answer 61

Lowering TGs.

Question 62

What are aggressive therapies for Familial Hypercholesterolemia?

Answer 62

Mipomersen, Lomitapide, LDL Apheresis.

Question 63

What is the role of lipoprotein(a) assessment?

Answer 63

Elevated levels increase ASCVD risk.

Question 64

What is the management strategy for severe hypertriglyceridemia?

Answer 64

Immediate very low-fat diet, address contributing factors, use fibrates, niacin, fish oils, or statins.