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Pharmacology > Cholesterol > Flashcards

Cholesterol Flashcards

1
Q

What is the first step in atherogenesis?

A

Endothelial injury caused by high LDL, smoking, hypertension, or diabetes.

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2
Q

What happens after lipid entry during atherogenesis?

A

LDL oxidizes within the vessel wall.

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3
Q

How do monocytes contribute to atherogenesis?

A

They migrate, become macrophages, and engulf oxidized LDL to form foam cells.

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4
Q

What is a fatty streak in atherogenesis?

A

Foam cell accumulation creating early lesions.

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5
Q

What is the role of smooth muscle cells in atherogenesis?

A

They migrate, proliferate, and form a fibrous cap.

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6
Q

What happens when a plaque ruptures in atherogenesis?

A

Exposes the lipid core, leading to thrombus formation and potential blockage.

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7
Q

What are triglycerides, and what is their function?

A

Energy storage molecules made of glycerol and three fatty acids.

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8
Q

How are triglycerides used during fasting?

A

Broken into free fatty acids and glycerol for energy.

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9
Q

What is cholesterol, and what are its functions?

A

A sterol used for cell membranes, hormones, bile acids, and vitamin D.

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10
Q

What is free cholesterol?

A

Active cholesterol in cell membranes and plasma, maintaining membrane fluidity.

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11
Q

What is esterified cholesterol?

A

Cholesterol combined with fatty acids for storage and transport.

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12
Q

What are the two sources of cholesterol?

A

Dietary (e.g., eggs, dairy) and liver synthesis (de novo).

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13
Q

What is the starting point of the mevalonate pathway?

A

Acetyl-CoA formation.

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14
Q

What enzyme converts HMG-CoA into mevalonate?

A

HMG-CoA reductase.

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15
Q

What is the target of statins in cholesterol synthesis?

A

HMG-CoA reductase.

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16
Q

What is squalene, and what is its role in cholesterol synthesis?

A

An intermediate processed into lanosterol and then cholesterol.

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17
Q

What are chylomicrons?

A

Large lipoproteins that transport dietary triglycerides and cholesterol to tissues.

18
Q

What is the role of VLDL?

A

Transports triglycerides from the liver to tissues.

19
Q

What is IDL, and how is it formed?

A

Intermediate lipoprotein formed after triglyceride delivery by VLDL.

20
Q

What is LDL, and why is it considered ‘bad cholesterol’?

A

Derived from IDL, it delivers cholesterol to tissues and promotes plaque formation.

21
Q

What is HDL, and why is it considered ‘good cholesterol’?

A

A protein-rich lipoprotein that removes cholesterol to the liver for excretion.

22
Q

How is coronary artery disease (CAD) risk calculated?

A

Divide LDL by HDL.

23
Q

What LDL/HDL ratio indicates low CAD risk for males?

A

1.0.

24
Q

What LDL/HDL ratio indicates very high CAD risk for males?

A

7.99.

25
Q

What is the target total cholesterol level?

A

Less than 200 mg/dL.

26
Q

What are the HDL targets for men and women?

A

Men >40 mg/dL; women >50 mg/dL.

27
Q

What is the target LDL level?

A

Less than 130 mg/dL.

28
Q

What is the target triglyceride level?

A

Less than 120 mg/dL.

29
Q

What are primary causes of hypercholesterolemia?

A

Genetic mutations, such as familial LDL receptor mutations.

30
Q

What are secondary causes of hypercholesterolemia?

A

Obesity, Type II diabetes, hypothyroidism, CKD, or medications.

31
Q

Why is dietary cholesterol control often insufficient?

A

The liver compensates by increasing endogenous cholesterol synthesis.

32
Q

How does soluble fiber affect cholesterol?

A

Reduces absorption of dietary cholesterol.

33
Q

What are dietary sources of omega-3 fatty acids?

A

Fish and flaxseed.

34
Q

How do plant sterols and stanols reduce cholesterol?

A

Compete with cholesterol for absorption in the intestine.

35
Q

What is the MOA of statins?

A

Inhibit HMG-CoA reductase to decrease cholesterol synthesis.

36
Q

What are the side effects of statins?

A

Muscle pain and elevated liver enzymes.

37
Q

What is the MOA of niacin?

A

Reduces VLDL and LDL synthesis; increases HDL.

38
Q

What is the MOA of fibrates?

A

Activate PPAR-alpha to enhance triglyceride metabolism.

39
Q

What is the MOA of bile acid resins?

A

Bind bile acids, forcing the liver to use cholesterol to produce more bile acids.

40
Q

What is the MOA of cholesterol absorption inhibitors?

A

Block the NPC1L1 transporter to reduce dietary cholesterol absorption.

41
Q

What is the novel MOA of PCSK9 inhibitors?

A

Prevent LDL receptor degradation, enhancing LDL clearance.

42
Q

What are the risks of hypocholesterolemia?

A

Increased cancer risk, hemorrhagic stroke, anxiety, impaired healing, and preterm birth.

Pharmacology (27 decks)

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