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CPT > Hyperlipidaemias > Flashcards

Hyperlipidaemias Flashcards

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1
Q

How does cholesterol enter the body?

A
  • Most synthesised in body
  • ~25% contributed by diet
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2
Q

Why is cholesterol essential in the body?

A
  • Membrane integrity
  • Precursor in production of steroid hormones
  • Bile acids
  • Vitamin D
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3
Q

Why is LDL considered to be bad cholesterol?

A
  • Susceptible to oxidation at damaged endothelium
  • ROS contributes to endothelial dysfunction
  • Increases adherence of lipid rich deposits
  • Foam cells formed (precursor to atheromatous plaques)
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4
Q

Which type of cholesterol is considered good?

A
  • HDL
  • Carries cholesterol away from circulation
  • To tissues that require it
  • To liver for disposal in bile
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5
Q

What blood tests can be done to assess CHD?

A
  • Total blood cholesterol
  • Now non-HDL cholesterol is a more reliable measure
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6
Q

Why is cholesterol targeted to reduce CVD risk?

A
  • Modifiable risk factor, like BP (other than genetic predisposition)
  • Data shows relationship between elevated cholesterol and morbidity and mortality from CHD
  • Reducing cholesterol by 10% affords ~15% reduction in 10 year CHD mortality and ~11% reduction in total mortality
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7
Q

How do we determine how aggressively to treat high cholesterol?

A
  • Take total CVD risk into account
  • Patient’s willingness to take medication and modify lifestyle
  • Familial forms of hypercholesterolaemia have specific/focused targets
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8
Q

Outline CVD risk

A
  • Additive
  • Multifactorial
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9
Q

How does high cholesterol affect blood vessels?

A
  • Causes fatty streaks
  • First develop in adults aged 20-29
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10
Q

What is the mechanism of action of statins?

A
  • Competitive inhibition of HMG-CoA reductase
  • Leads to decreased concentration of cholesterol within cells
  • Stimulates synthesis of LDL receptors
  • Increased number of LDL receptors promotes uptake of LDL from blood
  • Low intracellular cholesterol decreases secretion of VLDL
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11
Q

What are the additional benefits of statin therapy?

A
  • Improved vascular endothelial function
  • Stabilisation of atherosclerotic plaque
  • Improved haemostasis
  • Anti-inflammatory
  • Antioxidant
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12
Q

How does statin therapy improve vascular endothelial function?

A
  • Increased NO
  • Increased vascular endothelial growth factor
  • Decreased endothelin
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13
Q

How does statin therapy improve stabilisation of atherosclerotic plaques?

A
  • Decreased smooth muscle cell proliferation
  • Increased collagen
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14
Q

How does statin therapy improve haemostasis?

A
  • Decreased plasma fibrinogen
  • Decreased platelet aggregation
  • Increased fibrinolysis
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15
Q

How does statin therapy act as an anti-inflammatory?

A
  • Decreased proliferation of inflammatory cells into plaque
  • Decreased plasma CRP
  • Decreased adhesion molecules and cytokines
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16
Q

How does statin therapy act as an antioxidant?

A
  • Decreased superoxide formation
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17
Q

Name some kinds of statin

A
  • Simvastatin
  • Atorvastatin
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18
Q

What prescribing considerations need to be made with statins?

A
  • Simvastatin is a prodrug activated by first pass metabolism - half life is 2h
  • Atorvastatin - active derivatives obtained by first pass metabolism - half life is 24h
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19
Q

What are the adverse effects of statins?

A
  • GI disruption
  • Nausea
  • Headache
  • Myalgia (dose related)
  • Rarely - rhabdomyolysis
  • Increased liver enzymes
20
Q

What are the contraindications for statins?

A
  • Renal or hepatic impairment
  • Pregnancy (cholesterol important for foetal development)
  • Breastfeeding
21
Q

What are the DDIs of statins?

A
  • Anything that is also metabolised by CYP 3A4
  • Raises plasma statin concentration
  • Because other compounds are metabolised by CYP 3A4 instead of statins
  • E.g. amiodarone, diltiazem, macrolides, amlodipine, grapefruit juice
  • May be appropriate to withhold statin short-term whilst taking other agents
22
Q

How do we decide which statins to use?

A
  • Dose dependant reduction in LDL-cholesterol for all
  • Cost and side effect severity has driven prescribing choices
  • Atorvastatin and simvastatin are relatively cheap and easily accessible
23
Q

What is the recommended dose for primary prevention of CVD?

A
  • 20 mg atorvastatin once daily
  • Given to patients with 10 year risk of CVD greater tan 10%
  • Incorporate individual patient and risk/benefit discussions
24
Q

What is the recommended dose for secondary prevention of CVD?

A
  • 80 mg atorvastatin once daily
25
Q

What other steps need to be taken before prescribing statins?

A
  • Full lipid profile
  • Includes HDL and non-HDL and triglycerides
26
Q

What is the target when prescribing statins?

A
  • Broadly >40% reduction in non-HDL cholesterol at 3 months
27
Q

Why is simvastatin taken at night?

A
  • Has a relatively short half life
  • LDL receptor synthesis and activity are much greater at night
  • Drug is most effective at night when plenty of receptors are active
28
Q

What nocebo effect is associated with taking statins?

A
  • Muscle pain
  • Big challenge to adherence
  • Leads patients to decrease or stop use of statins
  • Makes patients reluctant to even begin taking statins as they are aware of the potential side effects
29
Q

What is the mechanism of action of fibrates?

A
  • Activate PPARa
  • Nuclear transcription factor that regulates expression of genes controlling lipoprotein metabolism
  • Increase production of lipoprotein lipase
  • Increases triglyceride removal from lipoproteins in plasma
  • Increase fatty acid uptake by liver
  • Increase levels of HDL
  • Increase LDL affinity for receptor
30
Q

How are fibrates prescribed?

A
  • Co-prescribed with statins
  • In mixed hyperlipidaemias
31
Q

What are the adverse side effects of fibrates?

A
  • GI upset
  • Myositis
  • Gall stones
32
Q

What are the contraindications of fibrates?

A
  • Photosensitivity
  • Gall bladder disease
33
Q

What are the DDIs of fibrates?

A
  • Warfarin
  • Causes increased anticoagulation
34
Q

Give an example of a fibrate

A
  • Fenofibrate
35
Q

What is the mechanism of action of cholesterol absorption inhibitors?

A
  • Inhibit NPC1l1 transporter at brush border in small intestines
  • Reduces absorption of cholesterol by gut
  • Hepatic LDL receptor expression increases
  • Decreases total cholesterol by ~15%
  • Decreases LDL cholesterol by ~20%
36
Q

How are cholesterol absorption inhibitors metabolised by the body?

A
  • Pro-drug
  • Hepatic metabolism
  • Enter enterohepatic circulation for recycling
  • Limits systemic exposure
  • Secreted by bile
37
Q

How are cholesterol absorption inhibitors prescribed?

A
  • Adjunct to statins
  • Beneficial in CKD and for secondary CVD prevention
  • Cannot escalate dose of ezetimibe
  • Useful in patients who can only tolerate a low dose of statins
38
Q

What are the adverse side effects of cholesterol absorption inhibitors?

A
  • Abdominal pain
  • GI upset
  • Angioedema
39
Q

What are the contraindications of cholesterol absorption inhibitors?

A
  • Hepatic failure
40
Q

What are the DDIs of cholesterol absorption inhibitors?

A
  • Need to be mindful if prescribed with a statin
  • Theoretical increased risk of rhabdomyolysis
41
Q

In which patients might we consider adding fibrates or nicotinic acids alongside statins?

A
  • Patients with familial hypercholesterolaemia
  • Not given to patients for primary/secondary prevention of CVD
42
Q

What is the mechanism of action of monoclonal antibodies designed to treat high cholesterol?

A
  • Inhibits PCSK9
  • PCSK9 signals that LDL receptors should be internalised for degradation
  • Inhibition increases uptake of LDL cholesterol into cells
43
Q

Why are monoclonal antibodies not commonly prescribed?

A
  • Very expensive
  • Long term effects yet to be determined
  • Requires lifelong injections every 3-6 months
44
Q

Give some examples of monoclonal antibodies that treat high cholesterol?

A
  • Alirocumab
  • Evolocumab
45
Q

What is the mechanism of action of inclisiran?

A
  • Inhibits hepatic translation of PCSK9
  • Very newly available to some in primary care e.g. patients with genetic causes of hypercholesterolaemia
46
Q

What non-medicinal options can help lower cholesterol?

A
  • Plant sterols (occur naturally in grains, legumes etc)
  • Fish oils/oily fish
  • Fibre, whole grains
  • Vitamin C and E

CPT (22 decks)

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