Lipid Disorders Flashcards
What is the primary function of cholesterol in the body?
Used for cell membrane synthesis, repair, and steroid hormone production.
What are triglycerides (TGs) primarily used for?
Energy source stored in adipose tissue or used by muscles.
What are lipoproteins?
Spherical particles that transport cholesterol and TGs.
What is the composition of lipoproteins?
A lipid core surrounded by water-soluble proteins and phospholipids.
What do chylomicrons transport?
Exogenous TGs from the gut to adipose tissue and muscle.
What is the role of VLDL (Very-Low-Density Lipoprotein)?
Transport endogenous TGs from the liver to adipose tissue and muscle.
What does LDL (Low-Density Lipoprotein) transport?
Cholesterol from the liver to peripheral tissues.
What is the function of HDL (High-Density Lipoprotein)?
Transport cholesterol from peripheral tissues to the liver.
What is Apoprotein A’s role?
Ligand for HDL receptors.
What does Apoprotein B do?
Ligand for LDL receptors.
What is the function of Apoprotein E?
Ligand for hepatic receptors for remnant particles.
What is the role of Apoprotein C-II?
Cofactor for lipoprotein lipase (LPL).
What is HMG CoA Reductase?
Rate-limiting enzyme in cholesterol synthesis.
What does Cholesterol Ester Transfer Protein (CETP) do?
Shuttles cholesterol esters between HDL and LDL.
What is the function of Lipoprotein Lipase (LPL)?
Breaks down TGs in chylomicrons and VLDL.
What does Lecithin Cholesterol Acyl Transferase (LCAT) do?
Esterifies cholesterol on HDL particles.
How does LDL function in the body?
Transports cholesterol to peripheral tissues and binds to LDL receptors (LDLRs) on cell surfaces.
What is the effect of excess LDL?
Cleared by scavenger macrophages.
What does Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) promote?
Degradation of LDLRs, reducing LDL clearance.
What can mutations in PCSK9 cause?
Familial hypercholesterolemia (FH).
What is reverse cholesterol transport?
Removes excess cholesterol from cells and transports it to the liver.
What are the antiatherogenic effects of HDL?
Reduces LDL oxidation, inhibits inflammation, improves endothelial function.
What forms foam cells in atherosclerosis?
Oxidized LDL engulfed by macrophages.
What leads to plaque rupture and thrombus formation?
Plaque rupture leads to platelet aggregation.
How are TGs transported in the body?
Dietary and hepatic TGs transported by chylomicrons and VLDL.
What happens to TGs broken down by LPL?
Converted into fatty acids for storage or energy.
What are the harmful effects of elevated serum TGs?
Associated with atherosclerosis and coronary disease.
What TG levels increase the risk of acute pancreatitis?
TG levels >1000 mg/dL.
What is required for a diagnosis of Metabolic Syndrome (MS)?
3 of the following: elevated fasting glucose, high TGs, low HDL, hypertension, abdominal obesity.
What is Lipoprotein(a)?
Formed when apoprotein(a) attaches to LDL.
What does Lipoprotein(a) promote?
Atherosclerosis by inhibiting thrombolysis.
What are primary dyslipidemias?
Inherited disorders of lipoprotein metabolism.
What is Familial Hypercholesterolemia (FH)?
Extreme elevations in cholesterol, normal TGs.
What mutations can cause Familial Hypercholesterolemia?
Mutations in LDLR, apoprotein B, PCSK9, or LDLRAP-1.
What is the risk associated with Familial Hypercholesterolemia?
High risk of premature coronary artery disease (CAD).
What characterizes Familial Combined Hyperlipidemia (FCH)?
Elevated cholesterol and TGs due to excessive hepatic apoprotein B synthesis.
What defines Familial Dysbetalipoproteinemia (FDL)?
Elevated cholesterol and TGs, normal HDL.
What is the cause of Familial Dysbetalipoproteinemia?
Abnormal apoprotein E phenotype (E2/E2).
What characterizes Polygenic Hypercholesterolemia?
Mild-to-moderate cholesterol elevation.
What distinguishes Familial Hypertriglyceridemia (FHT) and Familial Hyperchylomicronemia (FHC)?
FHT: moderate-to-severe TG elevation; FHC: extremely high TGs and chylomicrons.
How is Familial Combined Hyperlipidemia distinguished from Familial Dysbetalipoproteinemia?
FCH: Increased apoprotein B; FDL: E2/E2 phenotype, broad beta-band on electrophoresis.
What causes Familial Low HDL?
Mutations in APOA1, ABCA1, or LCAT genes.
What are secondary dyslipidemias caused by?
Systemic diseases or medications.
What are the causes of acquired hypertriglyceridemia?
Insulin resistance, obesity, diabetes, HIV, alcohol abuse, medications.
What is the general approach to treating dyslipidemia?
Lifestyle changes, medical therapy, apheresis, treat secondary causes.
What dietary recommendations does the ACC/AHA provide?
Emphasize vegetables, fruits, whole grains, low-fat dairy, fish, nuts; limit sweets, red meats, saturated and trans fats.
What is the primary role of statins?
Inhibit HMG CoA reductase, lower LDL.
What do PCSK9 inhibitors do?
Increase LDLR recycling, lower LDL.
What is the function of Ezetimibe?
Inhibits cholesterol absorption.
What do fibrates do?
Lower TGs, increase HDL.
What is the effect of Niacin on lipoprotein levels?
Lowers LDL, TGs, and lipoprotein(a); increases HDL.
What is the role of Omega-3 Fatty Acids?
Lower TGs.
What are the ACC/AHA treatment recommendations for high-risk groups?
Clinical ASCVD, LDL ≥190 mg/dL, LDL 70–189 mg/dL with diabetes or 10-year ASCVD risk ≥7.5%.
How do statins work?
Inhibit HMG CoA reductase, reduce cholesterol synthesis, increase LDLR-mediated LDL clearance.
What are the side effects of statins?
Myalgias, myositis, rhabdomyolysis (rare), increased risk of diabetes.
What is the efficacy of aggressive cholesterol-lowering?
Reduces myocardial infarction, stroke, cardiovascular mortality.
What is the effect of PCSK9 inhibitors on LDL and cardiovascular events?
Lower LDL by 50%–70%, reduce cardiovascular events.
What limits the use of PCSK9 inhibitors?
High cost.
What limits the use of Niacin?
Side effects (flushing) and lack of proven benefit.
What is the effect of Ezetimibe when added to statins?
Modest reduction in ASCVD events.
What are fibrates most effective at?
Lowering TGs.
What are aggressive therapies for Familial Hypercholesterolemia?
Mipomersen, Lomitapide, LDL Apheresis.
What is the role of lipoprotein(a) assessment?
Elevated levels increase ASCVD risk.
What is the management strategy for severe hypertriglyceridemia?
Immediate very low-fat diet, address contributing factors, use fibrates, niacin, fish oils, or statins.
