Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
15 Cards in this Set
- Front
- Back
|
Atherosclerosis is commonly observed as coronary heart disease. How do lipids play a role in this?
What are the 3 ways this is clinically manifested? |
Lipid-laden plaques reduce or block blood flow to the heart, leading to MI.
1. Angina and unstable angina. 2. Acute MI 3. Sudden Death. |
|
|
CVD is the leading cause of death for men and women in the US. How do death rates differ for men and women?
Overall, do more men or women die of CV Dx? |
Men initially have higher rates, but post menopausal women catch up and have higher rates in later life.
More women overall. |
|
|
Outline some modifiable risk factors for CHD.
Non-modifiable? |
-Dyslipidemia - high LDL, low HDL, raised TG.
-Smoking - responsible for 50% of avoidable deaths. 1/2 of these due to CHD. -HT -DM (same risk as if you have had a previous MI!) -Obesity -Dietary -Thrombogenic factors -Sedentary lifestyle. Non-modifiable: family hx of premature CHD, age, sex. Note: worst combo: smoking, high serum total cholesterol, and HT = 11x risk of CHD. |
|
|
What is the relationship between...
1. Total cholesterol and CHD risk? 2. LDL cholesterol and CHD risk? 3. HDL cholesterol and CHD risk? HDL cholesterol tends to be ______ when TGI are ______. 4. TGI and CHD? What are very high TGI (> 11.3 mmol/L) associated with? |
1. Increased TC = increased CHD risk. 10% reduction in TC = 15% reduction in CHD, total morbidity by 11%
2. LDL strongly associated, and is key target of therapy...10% increase = 20% risk of CHD risk. Considerably modified by other risk factors. Note: LDL cholesterol is only 1 part of LDL. 3. HDL: strong inverse association...lower HDL = higher CHD risk. Effect is independent of LDL. <0.9 = mmol/L = major positive risk factor, >1.55 mmol/L is a negative RF. Blanks: HDL cholesterol tends to be LOW when TGI are HIGH. 4. TGI associated with increased CHD risk, but link is complex, possibly related to low HDL. Optimal levels <1.7. Very high: increased pancreatitis risk. |
|
|
The Adult Treatment Panel (ATP) guidelines and Canadian Lipid guidelines provide recommendations for tx of lipid risk factors. What is the general principle behind this?
|
The higher the number of CHD risk factors, the lower the LDL cholesterol cut points. Examining:
-Multiple risk factors: diabetes status = CHD risk equivalent to prior heart attack. -Multiple metabolic risk factors = more intense tx. |
|
|
Optimal levels of cholesterol:
LDL below... HDL below ____ is a risk factor TGI cutoffs are.... |
LDL below 2.6 mmol/L (100 mg/dL)
HDL below 1.0 mmol/L (40 mg/dL) Lower - paying attention to moderate elevation. |
|
|
For Canadian cholesterol guidelines (2006):
The Framingham Risk score calculates risk into 3 categories...what are they? What are the risk score estimates based on (5 things)? |
3 Categories: High risk (10 year risk > 20%), Moderate risk (10 y risk 10-19%), Low risk (<10%).
Based on age, total cholesterol, smoking status, HDL level, and systolic bp. Note: also recommends additional assessments - E.g. ApoB, hsCRP, La(a).... |
|
|
Non-lipid parameters can also predict CHD risk. Give examples of some of these (3).
|
Factors involved in inflammation and endothelial injury - e.g. C-reactive protein, homocysteine, and cell adhesion molecules.
|
|
|
What are apolipoproteins?
What do they do? Which apolipoproteins are measured for risk assessment? |
The protein component of lipoproteins.
Functions: facilate lipid transport - activate 3 enzymes in lipid metabolism. ApoB (indicates LDL) ApoA (indicates HDL) Apo E genotype (indicates dysbetalipoproteinemia). |
|
|
LDL particles are mainly composed of cholesterol. These contain only 1 apolipoprotein, apoB. As such, this can be measured to count the number of LDL particles in plasma.
What do higher apo and small, dense LDL particles indicate? Are smaller or larger LDL particles more atherogenic? Why? |
High APO, smaller/denser particles = hypertriglyceridemia.
Smaller! 1. Last longer in circulation 2. More susceptible to oxidation 3. More likely to enter arterial wall. |
|
|
How is ApoB used in Canada?
What is an optimal level in a high risk patient? |
To seperate high and low risk patients with moderate hypertriglyceridemia.
<0.9 g/dL |
|
|
What is C-reactive protein? (CRP)
|
An acute phase reactant produced in the liver in response to acute inflammation. A pentameric plasma proteins with Ca++ dependent ligand binding. Has the ability to precipitate pneumonococcal C-polysaccharide, induced by IL1 and IL6.
|
|
|
How is CRP used as a CHD risk biomarker?
How does it compare to other risk factors such as homocysteine, liporpotein (a) and other lipid measurements? |
There is an observed association between elevated CRP and future myocardial infarction, stroke, etc. **Marker for inflammatory state in people with atherosclerosis, but may not be directly involved in atherogenesis.
Stronger. |
|
|
According to the current recommendations for hsCRP screening (hsCRP = high sensitivity C-reactive protein)....
Should the population be screened? Should it be used to monitor tx? Who might it help? |
NO.
NO. May help intermediate risk group and predict future events in high-risk group. Canada: "may be useful for further definition of CAD risk in pt with Framingham risk score between 10%-19%. |
|
|
What is the JUPITER trial?
|
The JUPITER trial aims to answer a critical clinical question: Can statin drugs prevent cardiovascular disease among healthy people with normal low-density lipoprotein (LDL) cholesterol levels but an increased level of high-sensitivity C-reactive protein (hsCRP). **Supports CRP as an independent RF for CVD.
|
