Cholesterol Flashcards
What is the first step in atherogenesis?
Endothelial injury caused by high LDL, smoking, hypertension, or diabetes.
What happens after lipid entry during atherogenesis?
LDL oxidizes within the vessel wall.
How do monocytes contribute to atherogenesis?
They migrate, become macrophages, and engulf oxidized LDL to form foam cells.
What is a fatty streak in atherogenesis?
Foam cell accumulation creating early lesions.
What is the role of smooth muscle cells in atherogenesis?
They migrate, proliferate, and form a fibrous cap.
What happens when a plaque ruptures in atherogenesis?
Exposes the lipid core, leading to thrombus formation and potential blockage.
What are triglycerides, and what is their function?
Energy storage molecules made of glycerol and three fatty acids.
How are triglycerides used during fasting?
Broken into free fatty acids and glycerol for energy.
What is cholesterol, and what are its functions?
A sterol used for cell membranes, hormones, bile acids, and vitamin D.
What is free cholesterol?
Active cholesterol in cell membranes and plasma, maintaining membrane fluidity.
What is esterified cholesterol?
Cholesterol combined with fatty acids for storage and transport.
What are the two sources of cholesterol?
Dietary (e.g., eggs, dairy) and liver synthesis (de novo).
What is the starting point of the mevalonate pathway?
Acetyl-CoA formation.
What enzyme converts HMG-CoA into mevalonate?
HMG-CoA reductase.
What is the target of statins in cholesterol synthesis?
HMG-CoA reductase.
What is squalene, and what is its role in cholesterol synthesis?
An intermediate processed into lanosterol and then cholesterol.
What are chylomicrons?
Large lipoproteins that transport dietary triglycerides and cholesterol to tissues.
What is the role of VLDL?
Transports triglycerides from the liver to tissues.
What is IDL, and how is it formed?
Intermediate lipoprotein formed after triglyceride delivery by VLDL.
What is LDL, and why is it considered ‘bad cholesterol’?
Derived from IDL, it delivers cholesterol to tissues and promotes plaque formation.
What is HDL, and why is it considered ‘good cholesterol’?
A protein-rich lipoprotein that removes cholesterol to the liver for excretion.
How is coronary artery disease (CAD) risk calculated?
Divide LDL by HDL.
What LDL/HDL ratio indicates low CAD risk for males?
1.0.
What LDL/HDL ratio indicates very high CAD risk for males?
7.99.
What is the target total cholesterol level?
Less than 200 mg/dL.
What are the HDL targets for men and women?
Men >40 mg/dL; women >50 mg/dL.
What is the target LDL level?
Less than 130 mg/dL.
What is the target triglyceride level?
Less than 120 mg/dL.
What are primary causes of hypercholesterolemia?
Genetic mutations, such as familial LDL receptor mutations.
What are secondary causes of hypercholesterolemia?
Obesity, Type II diabetes, hypothyroidism, CKD, or medications.
Why is dietary cholesterol control often insufficient?
The liver compensates by increasing endogenous cholesterol synthesis.
How does soluble fiber affect cholesterol?
Reduces absorption of dietary cholesterol.
What are dietary sources of omega-3 fatty acids?
Fish and flaxseed.
How do plant sterols and stanols reduce cholesterol?
Compete with cholesterol for absorption in the intestine.
What is the MOA of statins?
Inhibit HMG-CoA reductase to decrease cholesterol synthesis.
What are the side effects of statins?
Muscle pain and elevated liver enzymes.
What is the MOA of niacin?
Reduces VLDL and LDL synthesis; increases HDL.
What is the MOA of fibrates?
Activate PPAR-alpha to enhance triglyceride metabolism.
What is the MOA of bile acid resins?
Bind bile acids, forcing the liver to use cholesterol to produce more bile acids.
What is the MOA of cholesterol absorption inhibitors?
Block the NPC1L1 transporter to reduce dietary cholesterol absorption.
What is the novel MOA of PCSK9 inhibitors?
Prevent LDL receptor degradation, enhancing LDL clearance.
What are the risks of hypocholesterolemia?
Increased cancer risk, hemorrhagic stroke, anxiety, impaired healing, and preterm birth.
