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CPT > Lecture 7 - Hyperlipidaemia > Flashcards

Lecture 7 - Hyperlipidaemia Flashcards

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1
Q

What is the function of cholesterol?

A

Maintains membrane integrity (fluid when cold, more rigid when hot)

Precursor in production of steroid hormones

Bile acid precursor
Vitamin D precursor

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2
Q

What is the clinical risk of having a high level of cholesterol?

A

Leads to high level of LDL which has the longest half-life
LDL susceptible to oxidation at damaged endothelium, ROS contributes to endothelial dysfunction increasing adherence of lipid rich deposits and foam cells formed (macrophages engulf oxidised LDL) leading to formation of atheromatous plaques

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3
Q

What is HDL?

A

Carrier of cholesterol that takes cholesterol away from circulation not tissues that need it and the liver for disposal in bile

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4
Q

How does levels of total serum cholesterol affect the risk of coronary heart disease?

A

Inc total serum cholesterol = Inc risk of coronary heart disease

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5
Q

How can you non pharmacologically modify cholesterol levels?

A

Exercise
Diet modification

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6
Q

How does a reduction in total cholesterol by 10% affect 10 year Coronary Heart disease mortality?

A

15% reduction in 10year CHD mortality and 11% total mortality

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7
Q

What are some familial forms of hypercholesterolaemia?

A

LDL receptor gene mutation (reduced reuptaake of LDL from circulation)

Apolipoprotein B gene mutation

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8
Q

How to statins work to reduce blood cholesterol?

A

Competitively inhibits the action of HMG-CoA REDUCTASE preventing the conversion of HMG-CoA to melanovate which is needed to produce cholesterol

Also increases clearance of LDL

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9
Q

Besides reducing circulating LDL (transporter for cholesterol) what are the other benefits of statin therapy?

A

Improved vascular endothelial function (inc NO, Vascular Endothelal factor decreased)

Stabilisation of atherosclerotic plaques by decreasing smooth muscle proliferation and inc collagen

Improved haemostasis - decreased fibrinogen, platelet aggregation and. Inc fibrinolysis

Anti inflammatory - dec proliferation of inflammatory cells

Antioxidant - reduced Super Oxide formation

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10
Q

What are some statins?

A

Atorvastatin
Simvastatin
Rosuvastatin

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11
Q

Why is simvastatin typically taken at night?

A

It has a relatively short half life compared to atorvastatin

Cholesterol is made in its highest quantities at night so best time for simvastatin to have the largest effect is night

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12
Q

What are the adverse effects of statins?

A

Muscle pain
GI disruption
Nausea
Headache
Rare - RHABDOMYOLYSIS
Inc liver enzymes

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13
Q

When are statins contraindicated?

A

Renal or hepatic impairment
PREGNANCY or Breast feeding

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14
Q

What are the important drug-drug interactions for statins?

A

CYP3A4 important since amiodarone, diltiazem, and macrolides increase plasma conc of Statin

Amlodipine increases plasma conc of statin

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15
Q

How would drinking grapefruit juice affect levels of statins and other drugs?
Why?

A

Levels of statin increase

Grapefruit Juice inhibits CYP3A4 which is the metaboliser for statins so statins are broken down more slowly so their levels increase

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16
Q

What is a primary prevention for Cardiovasular disease?

A

Interventions for individuals at high risk of cardiovascular disease

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17
Q

What is a secondary prevention for cardiovascular disease?

A

Intervetniosn for individuals who already have cardiovascular disease

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18
Q

What investigation must be done on a patient before prescribing statins?

A

Full lipid profile including HDL and non HDL
+
Triglycerides

19
Q

What is the primary prevention method of statin prescription to reduce risk of cardiovascular disease?

A

20mg Atorvastatin once daily

20
Q

What is the secondary prevention method of statin prescription to reduce risk of cardiovascular disease?

A

80mg once daily

Amend if ADRs or DDIs
CKD do 20mg

21
Q

What drug is often given if statins are contraindicated or not tolerated?

A

Ezetimibe

22
Q

What is the main well known adverse effect of statins?

A

Muscle pain

23
Q

What is the nocebo effect?

A

Where if you’re aware of the negative effects of a drug you are likely to experience the negative effects for the drug

E.g you know statins can cause muscle pain so when you take it you are likely to have muscle pain

24
Q

What is the function of fibrates (fibrin acid derivatives)?

A

Decrease serum triglycerides and reduce LDL cholesterol

25
Q

What is an example of a fibrate?

A

Fenofibrate

26
Q

What is the MoA of fenofibrate?

A

Activates nuclear transcription factor PPARalpha

PPARalpha leads to. Increase in production of lipoprotein lipase

27
Q

What an are the positive efffects of fenofibrate?

A

Inc triglycerides remaoval from lipoprotein in plasma
Inc fatty acid uptake by liver
Inc HDL
Inc LDL affinity for receptor (inc reuptake of LDL)

28
Q

What are the adverse effects, contraindications and drug-drug interactions of fenofibrate?

A

Adverse effects : GI upset, myositis and cholelithiasis

Contraindications: photosensitivy, gall bladder disease

DDI: warfarin increased Anticoagulation (possibly due to competing for albumin)

29
Q

What is ezetimibe?
Function and MoA:

A

A cholesterol absorption inhibitor helping reduce cholersterol levels

Inhibits NPC1L1 transporter at brush border in small intestines REDUCING ABSORPTION OF CHOLLESTEROL BY THE GUT

30
Q

Where does ezetimibe get metabolised to its active form?

A

Pro durg enters hepatic circulation then gets activated
Limits systemic exposure since excreted in bile

31
Q

What are the adverse effects, contraindications and drug-drug interactions for ezetimibe what is its MoA?

A

Adverse: abdominal pain, GI upset and angioedma
Contraindications: hepatic failure
DDI: ciclosporin, fibrates (leads to gallstones)

MoA:inhibits NPC1L1 transporter at brush border of small intestine reducing dietary absorption of cholesterol

32
Q

When is ezetimibe often used?

A

Used when patient cant tolerate a large does of statin so lower the dose of statin then add ezetimibe

33
Q

What is the benefit of combining a statin with ezetimibe?

A

Can have a lower amount of statin and still achieve an aggressive enough level of cholesterol reduction

34
Q

What is bempedoic acid?
What’s it used for?

A

ATP Citrate lyase inhibitor prevents citrate from being converted to acetyl CoA so stops cholesterol production down the line

Hypercholesterolaemia when giving with ezetimibe or mixed dyslipidaeima where statin not suitable

35
Q

Why does bempedoic acid cause fewer muscle ADR than statins?

A

Active form formed almost exclusively in the liver so since it doesn’t really make it to muscle cells doesn’t cause the pain

36
Q

What are the adverse effects, contraindications and important drug-drug interactions for bempedoic acid?

A

Adverse: hyperuricaemia, anaemia, pain in extremities

Contra: pregancy and breastfeeding

DDI: slow excretion of many drugs like statins

37
Q

What is alirocumab and how does it reduce LDL cholesterol?

A

Monoclonal antibody that target the PCSK9 protein

PCSK9 internalises and degrades LDL reuptake receptors in the liver

By alirocumab inhibiting PCSK9 proteins, LDL reuptake receptors can degrade more LDL cholesterol decreasing cholesterol levels

38
Q

How does the PCSk9 protein normally work?

A

Binds to LDL receptors in the liver degrading them

So if inhibited more LDL receptors are present to degrade LDL cholesterol

39
Q

What is the mechanism of action of inclisiran?

A

Inhibits translation of PCSK9 so less PCSK9 made whereas alirocumab just block the action of PCSK9 not reducing hte levels of it

40
Q

Why are PCSK9 targeting drugs not sued instead of statins?

A

Much more expensive

41
Q

What does caffeine interfere with to help reduce cholesterol levels?

A

PCSK9

So more LDL receptors on liver

42
Q

What are some other options to help reduce LDL cholesterol instead of drugs?

A

Plant sterols (grains, legumes)

43
Q

What is good about alcohol for cholesterol and TG?

A

Inc HDL cholesterol (good cholesterol)

Inc TG

CPT (30 decks)

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