Chapter 2 - Dyslipidaemia Flashcards

1
Q

What are the causes of hypercholestsrolaemia and hypertriglyceridaemia?

A

Inherited (familial hypercholestsrolaemia)
Alcohol
Fatty food
Poor glycaemic control
Smoking
Obesity
Medication - corticosteroids, immunosuppressants, antipsychotics

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2
Q

What are the aims in hypercholestsrolaemia?

A

Total cholesterol <5mmol/L
LDL <3mmol/L
HDL >1mmol/L
Triglycerides <2.3mmol/L

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3
Q

Give examples of high intensity statins

A

Atorvastatin 20, 40, 80
Rosuvastatin 10, 20, 40
Simvastatin 80

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4
Q

How much do high intensity statins reduce LDL cholesterol by?

A

> 40%

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5
Q

Give some examples of medium intensity statins

A

Atorvastatin 10
Rosuvastatin 5
Simvastatin 20, 40
Fluvastatin 80

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6
Q

How much do medium intensity statins reduce LDL cholesterol by?

A

30-40%

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7
Q

Give examples of low intensity statins

A

Simvastatin 10
Fluvastatin 20, 40
Pravastatin 10, 20, 40

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8
Q

How much do low intensity statins reduce LDL cholesterol by?

A

<30%

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9
Q

What is familial hypercholestsrolaemia and when should this be suspected?

A

This is inherited hypercholestsrolaemia

If should be suspected history
Total cholesterol is >7.5mmol/L
There is a personal or family histrionic of CHD

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10
Q

What is the lifestyle advice associated with familial hypercholestsrolaemia?

A

Stop smoking
Lose weight
Reduce alcohol consumption

This should be given to every patient affected

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11
Q

What is the first line treatment for familial hypercholestsrolaemia?

A

High intensity statin e.g. atorvastatin 20mg

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12
Q

What drugs can be considered if a statin is contraindicated, not tolerated or not effective as monotherapy?

A

Ezetimibe
Fibrates (when TG >10mmol/L)
Lipid modifying drugs

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13
Q

In hypercholestsrolaemia, who should primary prevention be given to?

A

Anyone with familial hypercholestsrolaemia

Anyone with type 1 diabetes

Anyone with CKD

Anyone with a 10 year CVD risk of >10% (QRISK score)

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14
Q

What is first line for primary hypercholestsrolaemia?

A

Atorvastatin 20mg

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15
Q

When is secondary prevention given in hypercholestsrolaemia?

A

In patients with established CVD e.g. MI, angina, stroke, TIA

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16
Q

What is the first line drug treatment for secondary hypercholestsrolaemia?

A

Atorvastatin 80mg

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17
Q

What type of cholesterol are statins best at reducing?

A

LDL-C

They are not as effective at reducing triglycerides

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18
Q

What type of cholesterol are fibrates good at reducing?

A

Triglycerides

They are usually given when TG levels are high (>10mmol/L) even after LDL-C had been reduced

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19
Q

What monitoring needs to be done before lipid modifying therapy is started?

A

TC
HDL-C
Non HDL-C
TG

Creatinine kinase (in patients with an increased risk of myopathy or unexpected muscle pain)
Renal function 
LFTs (then measure at 3 and 12 months)
Thyroid function 
HbA1c
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20
Q

What is rhabdomyolysis?

A

This is a serious syndrome caused by direct muscle injury

The muscle fibres die and release their contents into the bloodstream

This can lead to serious complications e.g. renal failure

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21
Q

What are the symptoms of rhabdomyolysis?

A

Muscle pain
Muscle weakness of trouble moving
Dare red or brown urine, or decreased urination

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22
Q

What is the mechanism of action of statins

A

They competitively inhibit HMG-CoA reductase

Which controls the synthesis of cholesterol in the liver

23
Q

What are the cautions associated with statins?

A

Elderly
Liver disease
Increased risk of myopathy

24
Q

What increases the risk of myopathy associated with statins?

A
High dose
High alcohol consumption 
Hypothyroidism 
Renal impairment 
Personal or family history or muscle disorders
25
What are the side effects of statins?
Common - myalgia, thrombocytopenia Uncommon - hepatic disorders Rare - myopathy, rhabdomyolysis, interstitial lung disease
26
Can statins be given in pregnancy?
No Discontinue statins 3 months before attempting to conceive The patient should be on adequate contraception during treatment and for 1 month afterwards
27
What patient counselling should be given for statins?
Seek advice if you develop muscle pain, weakness, tenderness or dark urine/less urine (rhabdomyolysis) Seek advice if you develop difficulty breathing, a cough or weight loss (interstitial lung disease) Statins have many interactions with food and medications e.g. grapefruit juice
28
What time should to take statins and why?
Simvastatin, pravastatin, fluvastatin Night - cholesterol synthesis is highest when dietary intake is lowest Atorvastatin, rosuvastatin Any time - it has a longer half life
29
When should the dose of rosuvastatin be reduced?
Risk factors for myopathy or rhabdomyolysis Concurrent use of fibrates, clopidogrel and some antifungals Patients aged over 70 Patients of an Asian origin
30
What are the main drug interactions of statins?
Amiodarone, verapamil, diltiazem, amlodipine- increased risk of myopathy Clarithromycin, erythromycin, ciclosporin - temporarily stop the statin during antibiotic treatment Grapefruit juice - take 12h apart At johns wort Fibrates, ezetimibe
31
Can simvastatin be sold OTC?
Yes, for primary prevention Max pack side 28 Max dose 10mg daily
32
What is the mechanism of action of ezetimibe?
They reduce the intestinal absorption of cholesterol They have a greater effect on LDL-C than they do on TGs
33
What are the main side effects of ezetimibe?
Myopathy | Pancreatitis
34
Are fibrates better at reducing LDL cholesterol or triglycerides?
Triglycerides They are used when TG levels remain high >10mmol/L
35
When are fibrates cautioned?
Myopathy Increased risk of myopathy e.g. renal impairment Hypothyroidism - correct thyroid levels before initiating
36
What additional monitoring should be carried out when fibrates and statins are used?
Hepatic function | Creatinine kinase
37
Can lomitapide be given in pregnancy?
No - it is teratogenic
38
Give some examples of bile acid suppressants
Colestryramine Colestipol Colesevelam
39
What is the mechanism of action of bile acid sequestrants?
Bind to bile acids and prevent their reabsorption | This promotes the conversion of cholesterol into bile acids
40
What is an issue associated with the long term use of bile acid sequesterants?
Deficiency of fat soluble vitamins e.g. vitamin A, D, K and folic acid
41
Which groups of lipid regulating drugs are the most effective at reducing LDL-C?
Statins
42
What is the main problem associated with bile acid seqesterants in reducing cholesterol?
They can efficiently reduce LDL-C, but can aggregate hypertriglyceridaemia
43
What is the advice surrounding bile acid sequestrants if a patient is on other medications?
Don’t take them at the same time Take other drugs 1 hour before or 4 hours after Bile acid sequestrants can affect the absorption of other medications
44
Why is it important to treat hypothyroidism before starting lipid modifying therapy?
Hypothyroidism can exacerbate hyperlipidaemia Treating hypothyroidism may reduce cholesterol and therefore the need for statins
45
What is the maximum atorvastatin dose when taking ciclosporin?
10mg
46
What creatinine kinase is a concern in a patient on a statin?
5 times the upper limit
47
What is the maximum dose of atorvastatin if a patient is also taking ciclosporin?
10mg
48
Can a statin and gemfibrozil be used together?
No - increased risk of myopathy and rhabdomyolysis
49
If a patient is on a statin, what LFT level would you stop the statin?
3 times the upper limit
50
In what patient groups would you offer statins without assessing them?
Type 1 diabetes CKD eGFR<60 Familial hypercholestsrolaemia
51
Who do we offer lipid modifying therapy to?
QRISK >10% (CV event in the next 10 years) Type I diabetics CKD Familial hypercholestsrolaemia
52
What cardiovascular risk assessment calculators do we use?
QRISK2 QRISK3 - considers additional factors e.g. migraines, corticosteroid use JBS3 - long term assessment
53
What is used for the secondary prevention of CV events
Lipid modifying therapy e.g. statin | Aspirin if atherosclerotic disease
54
Why do we tend to avoid high dose simvastatin (80mg)
Risk of myopathy and rhabdomyolysis