Session 5 - Lecture 1 - Hyperlipidaemias Flashcards
1 - Intro
Hyperlipidaemias
{management and common drug classes}
2 - Lecture outline
Lecture outline
• Briefly review pathophysiology of atherosclerosis and ACS
• Discuss some evidence that demonstrates a need for lipid management
• Introduce the common lipid lowering therapeutic agents and their:
MOAs
Clinical effects and trial data
ADRs
• Alternative lipid lowering options – non POM
• Consider the consequences of national guidelines in the prescribing of lipid lowering drugs
• CVD risk
Understand the therapeutic options for managing hyperlipidaemias, the evidence that supports the use of therapeutic agents and how this can reduce incidence of ACS and CVD events
{1. couple of slides
- as useful/important to manage CV risk
3a. MOA – mechanism of action
3b. Clinical effects supporting trial data and how that’s changed
3c. Class and cross class adverse drug reactions (ADRs). - Alternatives to px only meds (POM).
- How guidelines have changed in recent years and why
- thinking about CVD risk}
3 - Cholesterol
Cholesterol
- Majority of cholesterol synthesised in the body with contribution from diet
- Essential for cell membrane integrity and precursor in production of steroid hormones, bile acids and vitamin D production
- LDL susceptible to oxidation at damaged endothelium initiated by necrotic tissue and ROS, adhere to proteoglycans - atherosclerosis
- HDL carrier of cholesterol away from circulation to liver for recycling so called “good cholesterol”
- Quantity of cholesterol transported to the peripheral tissues exceeds its catabolism and needs to be returned to the liver
- High triglycerides not particularly good but limited data to suggest it should be targeted as a modifiable risk factor
{Cholesterol (see MEH)
- majority of cholesterol produced in liver and intestines, and then a smaller amount produced in a higher rate in adrenal gland and reproductive organs.
- Cholesterol important in anchoring GPCRs within PM. also needed to be present in the skin for Vit D.
- So the LDL (bad cholesterol) - about 50% cholesterol and makes up about 70% in the plasma, typically contributes to damage in the vasculature
- HDL - about 20% cholesterol, smaller amount in terms of plasma. catabolism or recycling.
- crux to whole mechanism is that amount of cholesterol produced and sent out into circulation is greater than what’s needed in the tissues and the organs, it exceeds the catabolism at those sites. Amount returned to liver or managing this governs to some extent the atherosclerosis and damage to vasculature that ultimately leads to acute coronary syndromes in vascular disease.
- The triglyceride components – get situations with elevated triglycerides, some familial HLs, they’re in components of HDL and LDL but in terms of direct effect on cardiovascular risk as modifiable risk factor is inconclusive.}
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