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Cholesterol Flashcards

1
Q

Fibrates are most effective at

A

lowering plasma triglyceride

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2
Q

How does fibrates acts

A

By binding to and activating receptor in liver called PPAR-alpha (peroxisome- proliferator activated receptor alpha)

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3
Q

Effect of activation on PPAR-alpha

A

-Increase synthesis of lipoprotein lipase, enhance clearing triglyceride
-Decrease Apolipoprotein CIII, an inhibitor of lipoprotein lipase
-Increase apolipoprotein A1 and A2 lvl. Increasing HDL lvl

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4
Q

Adverse Effect of Lipase

A
  • Risk of Gallstone
  • Myopathy
  • Hepatotoxicity
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5
Q

Statins how it works

A

-inhibit the enzyme HMG CoA reductase, the rate-limiting step of cholesterol synthesis
- cause upregulation of hepatic LDL
- remove cholesterol from the blood.

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6
Q

Cholesterol Synthesis

A

Acetyl CoA converted to 3 hydroxy and 3 methylglutaryl CoA(HMG CoA)

HMG CoA then ezymetically conver to mevalonic acid by enzyme HMG Co A reductase
(rate limiting step)

Best done at night

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7
Q

Benefit of Statins

A
  • decrease LDL
  • Increase HDL
  • decrease Triglyceride
    Primary and secondary prevention of cvs diseases
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8
Q

Atorvastatin

A
  • low oral bioavilability
  • distributed to spleen as well as adrenal gland
  • Metabolized by CYP3A4
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9
Q

Rosuvastatin

A
  • low oral bioavialabilty
    -not extensively metabolized.
    -Predominantly eliminated in feces. minimal renal excretion.
  • plasma concentration are higher in asian patient
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10
Q

Adverse effect of Statin

A
  • myopathy
  • Rhabdomyolysis
  • hepatotoxicity
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11
Q

Nicotinic acid MOA

A

Inhibit hepatic synthesis of VLDL (ldl is vldl by product)
Increase blood lvl of HDL
many side effects

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11
Q

Bile Acid Sequestrants

A

Bile acid are negatively charged molecules made in liver, created by cholesterol converted by CYP7A1

Bile acid squestrants - large positively charge molecule, bind to bile acid, cause a need to synthesis bile acid, LDL is required. Create uptake of plasma LDL

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12
Q

What is coronary heart disease (CHD)?

A

CHD occurs when coronary blood circulation fails to adequately supply the heart with blood.

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13
Q

What is the primary cause of coronary heart disease?

A

Atherosclerosis – the buildup of plaque on arterial walls, leading to narrowed arteries and reduced blood flow to the heart.

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14
Q

How is cholesterol linked to coronary heart disease?

A

High blood cholesterol levels increase the risk of CHD because they contribute to atherosclerosis. Therefore, cholesterol-lowering drugs are a major focus in preventing CHD.

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15
Q

What percentage of deaths in Canada are caused by cardiovascular disease?

A

One third of all deaths – more than any other illness.

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16
Q

What is cholesterol and why is it important?

A

Cholesterol is essential for:
1. Cell membrane structure
2. Steroid hormone production (e.g., testosterone, estrogen)
3. Bile salt synthesis

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17
Q

What are the sources of cholesterol in the body?

A

Endogenous cholesterol (80%): Synthesized by the liver
Exogenous cholesterol (20%): Obtained from dietary sources

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18
Q

Why is high cholesterol a concern despite its physiological importance?

A

High blood cholesterol is associated with atherosclerosis and coronary heart disease.

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19
Q

Front

A

Back

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20
Q

What is the basic structure of lipoproteins?

A

Lipoproteins have an outer hydrophilic shell of phospholipids (soluble in plasma) and a lipophilic core made of cholesterol and triglycerides.

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21
Q

What is the primary function of lipoproteins?

A

To transport cholesterol and triglycerides in the blood. Lipophilic molecules require lipoproteins to be blood-soluble.

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22
Q

What are the three functions of apolipoproteins in lipoproteins?

A
  1. Allow recognition by cells for binding/ingestion
  2. Activate enzymes that metabolize lipoproteins
  3. Increase lipoprotein structural stability
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23
Q

What is the role of apolipoprotein A-I and B-100?

A

Apolipoprotein A-I: transports cholesterol from tissues to liver
Apolipoprotein B-100: transports cholesterol to tissues

24
How are lipoproteins classified?
By density. Higher protein % = higher density. Three key classes: VLDL, LDL, HDL.
25
What do Very Low Density Lipoproteins (VLDL) do?
VLDL delivers triglycerides from liver to adipose and muscle tissue. It has a triglyceride-rich core and carries most blood triglycerides.
26
What is the controversy regarding VLDL and atherosclerosis?
Some studies suggest high VLDL contributes to atherosclerosis, but evidence is inconsistent.
27
What do Low Density Lipoproteins (LDL) do?
LDL delivers cholesterol to non-hepatic tissues. Contains one B-100 apolipoprotein. It makes up 60–70% of blood cholesterol.
28
Why is LDL called 'bad cholesterol'?
Higher LDL is strongly linked to atherosclerosis and coronary heart disease. Lowering LDL reduces CHD risk and death.
29
What do High Density Lipoproteins (HDL) do?
HDL removes cholesterol from tissues and transports it to the liver. Promotes cholesterol clearance from blood.
30
Why is HDL called 'good cholesterol'?
HDL lowers CHD risk and is protective against atherosclerosis. It contains apolipoproteins A-I, A-II, A-IV.
31
What initiates atherosclerosis according to the role of LDL?
LDL moves into the sub-endothelial space of arteries and oxidizes, triggering immune cell recruitment and inflammation.
32
What are foam cells and how are they formed?
Macrophages ingest oxidized LDL and become enlarged and vacuolated – these are foam cells.
33
What is the progression of atherosclerotic plaque formation?
Fatty streaks form from foam cells → platelet adhesion → smooth muscle migration → collagen synthesis → fibrous plaque formation.
34
What is the primary nature of atherosclerosis?
Atherosclerosis is primarily an inflammatory process, not just a lipid disorder.
35
What role does LDL play in initiating atherosclerosis?
LDL penetration of the arterial wall causes a mild injury, triggering inflammation.
36
What is the key inflammatory response in atherosclerosis development?
Monocyte/macrophage infiltration in response to LDL accumulation leads to foam cell formation and plaque development.
37
What is the recommended age for cholesterol screening in Canada for males?
All males over age 40.
38
What is the recommended age for cholesterol screening in Canada for females?
All females over age 50, or those who are post-menopausal.
39
Besides age, who else should undergo cholesterol screening in Canada?
Patients with: diabetes, heart disease/family history, hypertension, central obesity (waist >102 cm men, >88 cm women), smokers/recent quitters, inflammatory or renal disease.
40
Front
Back
41
What is the Framingham Risk Score used for?
It estimates a patient’s 10-year risk of developing coronary heart disease using gender, age, cholesterol, smoking status, HDL, and systolic blood pressure.
42
What are the Framingham Risk Score risk categories?
High risk: >20% Moderate risk: 10–19% Low risk: <10%
43
What are the limitations of the Framingham Risk Score?
It underestimates risk in youth, women, and patients with metabolic syndrome.
44
What is the treatment guideline for HIGH cardiovascular risk?
Treat all patients. LDL target: <2 mmol/L or >50% reduction
45
When is MODERATE cardiovascular risk treated?
Treat if: - LDL > 3.5 mmol/L - Triglyceride/HDL ratio > 5.0 - Significant inflammation present LDL target: <2 mmol/L or >50% reduction
46
When is LOW cardiovascular risk treated?
Treat if LDL > 5.0 mmol/L LDL target: >50% reduction
47
What is metabolic syndrome?
A combination of disorders that increase the risk of coronary heart disease and type II diabetes.
48
What are the diagnostic criteria for metabolic syndrome (need 3 or more)?
1. Central obesity: Waist > 102 cm (men) or > 88 cm (women) 2. Triglycerides > 1.7 mmol/L 3. Low HDL: <1.03 mmol/L (men), <1.29 mmol/L (women) 4. Fasting glucose > 5.6 mmol/L 5. Blood pressure > 135/85 mmHg
49
What is the treatment goal for metabolic syndrome?
To decrease the risk of coronary heart disease and type II diabetes.
50
How common is metabolic syndrome in Canada?
It affects about 1 in 4 Canadians.
51
Is drug therapy the first-line treatment for high LDL cholesterol?
No, the primary treatment is lifestyle changes including diet, weight control, exercise, and smoking cessation.
52
What are the primary lifestyle changes recommended for lowering LDL cholesterol?
Diet modification, weight loss, regular exercise, and smoking cessation.
53
What are the dietary recommendations for lowering LDL cholesterol?
Consume less than 200 mg/day of cholesterol, <7% of total calories from saturated fats, 10–25 g/day of soluble fiber, and 2 g/day of plant stanols/sterols.
54
How does weight control impact LDL cholesterol and heart disease risk?
Weight loss through diet and exercise lowers LDL cholesterol and reduces coronary heart disease risk.
55
What are the benefits of cardiovascular exercise for cholesterol and heart health?
Exercise lowers LDL, raises HDL, reduces insulin resistance, and lowers blood pressure.
56
What are the exercise recommendations for LDL management?
Exercise 30–60 minutes per day is recommended for all individuals.
57
How does cigarette smoking affect cholesterol and heart disease risk?
Smoking decreases HDL and increases LDL cholesterol, increasing coronary heart disease risk.
58
Why is smoking cessation especially important in younger adults?
Smoking is a major risk factor for younger adults; quitting greatly reduces disease risk.

Pharm (10 decks)

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